Metabolic Acidosis Study Guide (Cortisol) | NUR MISC | Rasmussen College

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Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: • increased aci... d production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) • decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) • loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: • HCO3: decreased <22 • Blood pH: decreased <7.35 • CO2: <35 or normal (may be normal but if it is decreased this is the body’s way of trying to compensate). **Remember the respiratory system is causing hyperventilation. The respiratory system tries to increase the pH from its acidotic states through tachypnea with Kussmaul’s breathing. The goal is to “blow off” the CO2 which is acidic to help alleviate the already acidotic conditions in the body. Memorize these normal values for ABGs: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Metabolic Acidosis High anion gap & Normal anion gap problems: What is an anion gap? Simplified this is where the doctor look at various lab results from a patient’s lab work (such as electrolytes (chloride, bicarbonate, sodium) and calculates them to see the difference between the anions and cations. If there is a gap (>14 mEq/L from normal (normal is: 10-14 mEq/L) there is high anion gap metabolic acidosis going on. In other words the anion gap tells us what type of acidosis we have going on which is important so it can be treated appropriately. High Anion Acidosis is conditions that cause the body to produce too much acid or NOT enough bicarb (DKA, Aspirin toxicity, renal failure, high-fat diet, low carb diet, malnutrition) Normal Anion acidosis is loss of the bicarbonate from the body. Examples: diarrhea via GI fluids, ostomies or fistula drainage (ileostomies or pancreatic fistula)…which are rich in alkalotic fluids, however when lost it causes acidosis, or drugs ingestion: Diamox (diuretic)…. carbonic anhydrase inhibitor which reduces reabsorption of bicarb. Combine all of this to form the Mnemonic “Acidotic” Aspirin toxicity: (high anion gap) which increases the acid in the body and this also causes respiratory alkalosis (hyperventilation) Carbohydrates not metabolized (high anion gap): when there isn’t enough oxygen to break down carbs the pyruvic acids (that supplies the cells with energy) starts to turn into lactic acid and when you get acid building up you get acidosis Insufficiency of kidneys (high anion gap): kidneys are failing to filter out metabolic waste products, acids increase, and bicarb cannot keep up so it depletes Diarrhea (normal anion gap): profuse diarrhea leads to loss bicarbonate, DKA (diabetic ketoacidosis) body is breaking down ketones and is not metabolizing glucose correctly which leads to high blood glucose levels and breakdown of acids in the blood Ostomy drainage (excessive) ileostomies, Ureteroenterostomies (normal anion gap)… ostomies are an opening of an organ to allow drainage…depending on where the ostomy is these fluids are rich in bicarb and if loss directly at this spot (instead of travelling through the body to form into stool (which doesn’t lose much bicarb)…it can deplete the bicarb fast. fisTula (pancreatic fistula) (normal anion gap) fistula : a fistula is a passage between an hollow organ and body surface or between two organs….same concept with the ostomy…losing fluids where you shouldn’t be and they are not being absorbed by the body…you are wasting the bicarb Intake of high-fat diet: eating too much fat leads to the building-up of waste product which in turn leads to buildup of ketones and acids Carbonic anhydrase inhibitors (Diamox): diuretic which reduces the reabsorption of bicarb Signs & Symptoms of Metabolic Acidosis • ****Kussmaul’s respiration (body’s way of trying to compensate by exhaling the excessive CO2…in hopes of increasing bicarb and blood pH) • Confused, weak, low blood pressure, cardiac changes (if hyperkalemic …can happen EXCEPT with diarrhea or with Diamox usage which causes hypokalemia), n & v Nursing Interventions for Metabolic Acidosis Vary depending on the causes of acidosis: • Watch respiratory system and ABGs closely…if too bad may need intubation • Assess other electrolyte levels (esp. potassium because during active acidosis it will be high…however when it resolves there is an extracellular to intracellular shift of K+ back into the cell which will causes hypokalemia) • Watch neuro status, safety, and place in seizure precaution • Dialysis may be needed if they patient is experiencing acidosis (high anion gap issue ex: renal failure) • Diabetic ketoacidosis: administer prescribed insulin to help glucose go back into cell which will help the body start regulating how it metabolizes glucose…hence not more ketones (acids) Respiratory Acidosis What’s involved:…let’s look at normal breathing: 1. Oxygen enters through the mouth or nose 2. down through the Pharynx 3. into the Larynx (the throat) 4. then into the Trachea 5. and the Bronchus (right and left) which branches into the bronchioles and ends in alveoli sac *The alveolar sacs are where gas exchange takes place (oxygen and carbon dioxide diffuse across the membrane). The oxygen enters into your blood stream and CARBON DIOXIDE CO2 is exhaled through your nose or mouth. The diaphragm also plays a role in allowing lungs into inflate and deflate. Note: if there is any problem with the patient breathing rate (too slow), alveolar sacs (damaged), or diaphragm (weak) the patient can experience respiratory acidosis. *Main cause of respiratory acidosis is bradypnea (slow respiratory rate <12 bpm which causes CO2 to build-up in the lungs) When this happens the following lab values are affected: • Blood pH decreases (<7.35) • Carbon dioxide levels increase (>45) • **To compensate for this the Kidneys start to conserve bicarbonate (HCO3) to hopefully increase the blood’s pH back to normal…..so HCO3 becomes >26. REMEMBER (memorize) these lab values: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Respiratory Acidosis Remember “DEPRESS” Breathing (anything that causes you to breathe slowly, blocks the airway, or causes the diaphragm not to work properly will cause respiratory acidosis) Drugs (opioids (fentanyl, morphine), sedation (versed), ….causes respiratory depression “hypoventilation….retain carbon dioxide….increase PaCO2 and decreased pH” ) & Diseases of the neuromuscular system…Myasthenia gravis, Guillain–Barré syndrome (weakness of voluntary muscles affects the diaphragm….can’t expelled the carbon dioxide) Edema (pulmonary) extra fluid in the lung causes impaired gas exchange Pneumonia…excessive mucous production affect gas exchange…the alveoli are majorly affected because they are filled with pus and fluid Respiratory center of brain damaged (brain injury, stroke) Emboli (blocks the pulmonary artery or branch of the lungs causes carbon dioxide to increase) Spasms of bronchial tubes (asthma) bronchioles constrict and you have decreased gas exchange Sac elasticity of alveolar sac are damaged and this restricts air flow in and out of the lungs and this increases carbon dioxide (Emphysema & COPD) Signs and Symptoms of Respiratory Acidosis • Major neuro changes: Confused, very drowsy, and reports a headache • respiration rate less than 12 • low blood pressure Nursing Interventions for Respiratory Acidosis • Administer oxygen • encourage coughing and deep breathing • suction (pneumonia) • may need respiratory treatment (asthma) • hold respiratory depression drugs (know the category of drugs used opiods, sedatives etc) • ****Watch potassium levels that are >5.1…remember in hyperkalemia video we talked about how respiratory acidosis caused increase potassium ….can cause dysrhythmias) • administer antibiotics for infection • may need endotracheal intubation if CO2 rise above 50 mmhg or respiratory distress is present Metabolic Alkalosis Metabolic alkalosis in simple terms: a metabolic problem caused by the excessive loss of acids (H+) or increased amount of bicarb (HCO3) produced in the body that leads to an alkalotic state in the body. Disease processes and drugs can cause metabolic alkalosis. When metabolic alkalosis happens in the body other systems try to compensate by hopefully fixing the blood’s pH and bicarb level. One system that does this is the respiratory system by stimulating the respiratory system to hypoventilate (decrease respirations) which will retain PCO2 (carbon dioxide) so it will decrease the pH back to normal, hence you will start to see bradypnea in your patient. If a patient is experiencing metabolic alkalosis they will present with the following labs: • HCO3: increases >26 • Blood pH: increases >7.45 • CO2: >45 or normal (may be normal but if increased this is the body’s way of trying to compensate. Remember the respiratory system tries to decrease the pH from its alkalotic state by causing hypoventilation ( bradypnea). The respiratory system hopes that if the CO2 increase enough it will cause the pH to decrease and the kidneys will start to excrete the bicarb which will hopefully decrease the overall HCO3. Remember what normal values are: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Metabolic Alkalosis Remember: “Alkali” (**these are the most common causes) **Aldosterone production excessive (hyperaldosteronism) activates renin-angiotensin- aldosterone system : the adrenal cortex is releasing too much aldosterone which causes the renal tubule in the kidneys to keep sodium which wastes hydrogen ions (ex: potassium) and this causes you to keep bicarb (HCO3) Loop **diuretics (Lasix) or thiazide therapy: causes the kidneys to waste hydrogen ions and chloride through the urine (ALSO LOSING K+) which in turn increases the bicarb alKali ingestion of food (baking soda, milk, antacids) increases bicarb level in the blood Anticoagulant “citrate” (used as a storage agent in blood and during continuous forms of renal replacement therapy) Caused from a massive transfusion of whole blood (patient needs several bags of blood) and the body metabolizes the citrate used in the blood as bicarb which increases the HCO3 level in the body. Also, patients who undergo continuous forms of renal replacement therapy (CRRT) (an alternative therapy for patients who can’t undergo hemodialysis) are affected by the citrate used in the therapy. Loss of fluids (**vomiting and **GI suctioning) hence this fluids are rich in K+ and when you lose them you are losing hydrogen ions and this causes the body to increase the bicarb level, Low potassium levels cause reabsorption of HCO3- Increased sodium bicarb administration (trying to correct metabolic acidosis) Signs and Symptoms of Metabolic alkalosis • Bradypnea (hypoventilation) <12 bpm o Many symptoms due to low potassium (dysrhythmia), tetany, tremors, muscle weakness/cramping, tired, irritable, vomiting, Depression ST, flat or inverted T wave and prominent u-wave) Nursing Interventions for Metabolic Alkalosis • Based on the cause: vomiting (give antiemetic ex: Zofran, Phenergan), stop diuretics • Doctor may order Diamox (Carbonic anhydrase inhibitors): a diuretic which reduces the reabsorption of bicarb • Watch ABGs and signs of respiratory distress • Monitor potassium and chloride levels (wasted in this condition) Respiratory Alkalosis What’s involved:…let’s look at normal breathing: 1. Oxygen enters through the mouth or nose 2. down through the Pharynx 3. into the Larynx (the throat) 4. then into the Trachea 5. and the Bronchus (right and left) which branches into the bronchioles and ends in alveoli sac *The alveolar sacs are where gas exchange takes place (oxygen and carbon dioxide diffuse across the membrane). The oxygen enters into your blood stream and CARBON DIOXIDE CO2 is exhaled through your nose or mouth. The diaphragm also plays a role in allowing lungs into inflate and deflate. Note: if there is any problem with the patient breathing rate (too fast), alveolar sacs (damaged), hyperventilation, or a brain injury that affects the respiratory center a patient is at risk for respiratory alkalosis *Main cause of respiratory alkalosis is tachypnea (fast respiratory rate >20 bpm which causes CO2 to decrease in the lungs) When this happens the following lab values are affected: • Blood pH increases (>7.45) • Carbon dioxide levels increase (<35) • **To compensate for this the Kidneys start to excrete bicarbonate (HCO3) to hopefully decrease the blood’s pH back to normal…..so HCO3 becomes <22. REMEMBER (memorize) these lab values: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Respiratory Alkalosis Remember: TACHYPNEA (fast breathing leads to “hyperventilation” which leads to respiratory alkalosis) Temperature increase (fever) due to increased metabolic needs of the body which causes the respiratory center (medulla and pons) to try to compensate by making the respiratory rate increased…hence exhaling too much carbon dioxide (CO2) Aspirin toxicity: too much aspirin in the body leads to hyperventilation due to the stimulation of the respiratory center and fever Controlled ventilation (excessive usage)…mechanical ventilation****hyperventilates the patient with too much oxygen and depletes carbon dioxide Hyperventilation (excessive respirations) expelling too much carbon dioxide hYsteria (anxiety) leads to rapid breathing and expelling of carbon dioxide Pain…rapid breathing (blowing off too much carbon dioxide), Pregnancy (especially in 3rdtrimester due to changes of the respiratory tract), Pneumonia Neurological injuries from a head injury or stroke (affects the respiration system of the brain which is located in the medulla and pons) Embolism or Edema in the lungs Asthma due to hyperventilation (however, asthma can cause respiratory acidosis as well due to bronchospasms which is causing the alveoli to not properly deflate) Signs and Symptoms of Respiratory Alkalosis • ***Classic Assessment Sign is fast respiratory rate (normal for adult is 12- 20) TACHYPNEA(>20 bpm) • Neuro changes: Tired, lethargy, fast heart rate • **Tetany, dysrhythmias, muscle cramps, positive Chvostek’s sign due to hypocalcemia and hypokalemia Nursing Interventions for Respiratory Alkalosis • Teach patient breathing techniques to slow down breathing, holding breath…”rebreathing into a paper bag or re-breather mask • Watch potassium levels (hypokalemia..remember hyperkalemia in respiratory acidosis & hypocalcemia) and for signs and symptoms of low calcium and potassium levels. • **Closely watch patients on mechanical ventilation to ensure breaths are not hyperventilating the patient Hyponatremia Hypo: “under/beneath” Natr: Prefix for Sodium Emia: blood Meaning of Hyponatremia: low sodium in the blood Normal sodium levels: 135 to 145 mEq/L (<135 = hyponatremia) Role of sodium in the body: An important electrolyte that helps regulate water inside and outside of the cell. Remember that water and sodium loves each other and where ever sodium goes so does water. Learn about Hypertonic, Hypotonic, & Isotonic Solutions. For example, in hyponatremia sodium outside of the cell is very low and this causes water to move inside the cell. In turn, the cell will swell and you will start to see problems in the body, especially with brain cells (confusion). Sodium also play a role in muscle, nerves, and organ function. Types of Hyponatremia Euvolemic Hyponatremia is where the water in the body increases but the sodium stays the same. The causes include: SIADH (Syndrome of inappropriate antidiuretic hormone secretion) which is due to the increased amount of secretion of antidiuretic hormone. This hormone retains water in the body which dilutes sodium. Other causes: diabetes insipidus, adrenal insufficiency, Addison’s disease etc. Hypovolemic Hyponatremia is where the patient has lost a lot of fluid and sodium. Causes: vomiting, diarrhea, NG suction, diuretic therapy, burns, sweating Hypervolemic Hyponatremia is where the body has increased in fluid and sodium. However, sodium decreases due to dilution and because total body water and sodium are regulated independently in the body. Causes: congestive heart failure, kidney failure, IV infusion of saline, liver failure etc. Causes of Hyponatremia Remember “NO Na+” Na+ excretion increased with renal problems, NG suction (GI system rich in sodium), vomiting, diuretics, sweating, diarrhea, decreased secretion of aldosterone (diabetes insipidus) (wasting sodium) Overload of fluid with congestive heart failure, hypotonic fluids infusions, renal failure (dilutes sodium) Na+ intake low through low salt diets or nothing by mouth Antidiuretic hormone over secreted **SIADH (syndrome of inappropriate antidiuretic hormone secretion…remembers retains water in the body and this dilutes sodium) Signs & Symptoms of Hyponatremia Remember “SALT LOSS” Seizures & Stupor Abdominal cramping, attitude changes (confusion) Lethargic Tendon reflexes diminished, trouble concentrating (confused) Loss of urine & appetite Orthostatic hypotension, overactive bowel sounds Shallow respirations (happens late due to skeletal muscle weakness) Spasms of muscles Nursing Interventions for Hyponatremia • Watch cardiac, respiratory, neuro, renal, and GI status • Hypovolemic Hyponatremia: give IV sodium chloride infusion to restore sodium and fluids (3% Saline hypertonic solution….harsh on the veins…given in ICU usually through central line very slowly…must watch for fluid overload) • Hypervolemic Hyponatremia: Restrict fluid intake and in some cases administer diuretics to excretion the extra water rather than sodium to help concentrate the sodium. If the patient has renal impairment they may need dialysis. • Caused by SIADH or antidiuretic hormone problems: fluid restriction or treated with an antidiuretic hormone antagonists called Declomycin which is part of the tetracycline family (don’t give with food especially dairy or antacids…bind to cations and this affect absorption). • If patient takes Lithium remember to monitor drug levels because lithium excretion will be diminished and this can cause lithium toxicity. • Instruct to increase oral sodium intake and some physicians may prescribe sodium tablets. Food rich in sodium include: bacon, butter canned food, cheese, hot dogs, lunch meat, processed food, table salt Hypokalemia Hypo= low Kal= root word for potassium….. don’t get it confused with cal= calcium Emia=blood Meaning of hypokalemia: Low Potassium in the Blood Normal Potassium Level 3.5-5.1 (2.5 or less is very dangerous) Most of the body’s potassium is found in the intracellular part of the cell compared to the extracellular which is where sodium is mainly found. Blood tests measure potassium levels via the outside of the cell (extracellular fluid). Remember potassium is responsible for nerve impulse conduction and muscle contraction. Causes of Hypokalemia “Your Body is trying to DITCH potassium” Drugs (laxatives, diuretics, corticosteroids) Inadequate consumption of Potassium (NPO, anorexia) Too much water intake (dilutes the potassium) Cushing’s Syndrome (during this condition the adrenal glands produce excessive amounts of cortisol (if cortisol levels are excessive enough, they will start to affect the action of the Na+/K+ pump which will have properties like aldosterone and cause the body to retain sodium/water but waste potassium)…hence hypokalemia Heavy Fluid Loss (NG suction, vomiting, diarrhea, wound drainage, sweating) (Other causes: when the potassium moves from the extracellular to the intracellular with alkalosis or hyperinsulinism (this is where too much insulin in the blood and the patient will have symptoms of hypoglycemia) Signs & Symptoms of Hypokalemia Try to remember everything is going to be SLOW and LOW. Don’t forget potassium plays a role in muscle and nerve conduction so muscle systems are going to be messed up and effect the heart, GI, renal, and the breathing muscles for the lungs. • Weak pulses (irregular and thread) • Orthostatic Hypotension • Depression ST, flat or inverted T wave and prominent u-wave • Shallow respirations with diminished breath sounds….due to weakness of accessory muscle movement to breath) • Confusion, weak • Flaccid paralysis • Decrease deep tendon reflexes • Decreased bowel sounds Easy way to Remember 7 L’s 1. Lethargy (confusion) 2. Low, shallow respirations (due to decreased ability to use accessory muscles for breathing) 3. Lethal cardiac dysrhythmias 4. Lots of urine 5. Leg cramps 6. Limp muscles 7. Low BP & Heart Nursing Interventions for Hypokalemia Watch heart rhythm (place on cardiac monitor…most are already on telemetry), respiratory status, neuro, GI, urinary output and renal status (BUN and creatinine levels) Watch other electrolytes like Magnesium (will also decrease…hard to get K+ to increase if Mag is low), watch glucose, sodium, and calcium all go hand-in-hand and play a role in cell transport Administer oral Supplements for potassium with doctor’s order: usually for levels 2.5- 3.5…give with food can cause GI upset IV Potassium for levels less 2.5 (NEVER EVER GIVE POTASSIUM via IV push or by IM or subq routes) -Give according to the bag instruction don’t increase the rate…has to be given slow… patients given more than 10-20 meq/hr should be on a cardiac monitor and monitored for EKG changes -Cause phlebitis or infiltrations Don’t give LASIX, demadex , or thiazides (waste more Potassium) or Digoxin (cause digoxin toxicity) if Potassium level low…notify md for further orders) Physician will switch patient to a potassium sparing diuretic Spironolactone (Aldactone), Dyazide, Maxide, Triamterene Instruct patient to eat Potassium rich foods Remember POTASSIUM to help you remember the foods • Potatoes, pork • Oranges • Tomatoes • Avocados • Strawberries, • Spinach • fIsh • mUshrooms • Musk melons: cantaloupe Also included are: (carrots, raisins, bananas) Addison’s Disease vs Cushing’s Major Players in these endocrine disorders: • Adrenal Cortex • Steroid Hormones o Corticosteroids (specifically Aldosterone (mineralocorticoid) & Cortisol (glucocorticoid) Role of Adrenal Cortex: releases steroid hormones and sex hormones Role of Aldosterone: regulates blood pressure through renin-angiotensin-aldosterone system, helps retain sodium and secretes potassium (balances sodium and potassium levels). Role of Cortisol: “STRESS Hormone” helps the body deal with stress such as illness or injury, increases blood glucose though glucose metabolism, break downs fats, proteins, and carbs, regulates electrolytes. Lecture on Cushing’s vs Addison’s Disease Cushing’s (Syndrome & Disease) Cushing’s: hyper-secretion of CORTISOL (watch video for clever ways to remember this) Cushing’s Syndrome vs Cushing’s Disease Cushing’s Syndrome: caused by an outside cause or medical treatment such as glucocorticoid therapy Cushing’s Disease: caused from an inside source due to the pituitary gland producing too much ACTH (Adrenocorticotropic hormone) which causes the adrenal cortex to release too much cortisol. Signs & Symptoms of Cushing’s Remember the mnemonic: “STRESSED” (remember there is too much of the STRESS hormone CORTISOL) Skin fragile Truncal obesity with small arms Rounded face (appears like moon), Reproductive issues amennorhea and ED in male(due to adrenal cortex’s role in secreting sex hormones) Ecchymosis, Elevated blood pressure Striae on the extremities and abdomen (Purplish) Sugar extremely high (hyperglycemia) Excessive body hair especially in women…and Hirsutism (women starting to have male characteristics), Electrolytes imbalance: hypokalemia Dorsocervical fat pad (Buffalo hump), Depression Causes of Cushing’s • Glucocorticoid drug therapy ex: Prednisone • Body causing it: due to tumors and cancer on the *pituitary glands or adrenal cortex, or genetic predisposition Nursing Management for Cushing’s Syndrome • Prep patient for Hypophysectomy to remove the pituitary tumor • Prep patient for Adrenalectomy: o If this is done educate pt about cortisol replacement therapy after surgery • Risk for infection and skin breakdown • Monitor electrolytes blood sugar, potassium, sodium, and calcium levels Addison’s Disease Addison’s: Hyposecretion of Aldosterone & Cortisol (watch the video for a clever way on how to remember this and not get it confused with Cushing’s) Signs & Symptoms of Addison’s Disease Remember the phrase: “Low STEROID Hormones” (remember you have low production of aldosterone & cortisol which are STEROID hormones) Sodium & Sugar low (due to low levels of cortisol which is responsible for retention sodium and increases blood glucose), Salt cravings Tired and muscle weakness Electrolyte imbalance of high Potassium and high Calcium Reproductive changes…irregular menstrual cycle and ED in men lOw blood pressure (at risk for vascular collapse)….aldosterone plays a role in regulating BP Increased pigmentation of the skin (hyperpigmentation of the skin) Diarrhea and nausea, Depression Causes of Addison’s Disease • Autoimmune due to the adrenal cortex becoming damaged due to the body attacking itself: o Tuberculosis/infections o Cancer o Hemorrhaging of the adrenal cortex due to a trauma Nursing Management of Addison’s Disease • Watching glucose and K+ level • Administer medications to replace the low hormone levels of cortisol and aldosterone • For replacing cortisol: o ex: Prednisone, Hydrocortisone ▪ Education: Patient needs to report if they are having stress such as illness, surgery, or extra stress in life ( will need to increase dosage), take medication exactly as prescribed….don’t stop abruptly without consulting with MD. • For replacing aldosterone: • ex: Fludrocortisone aka Florinef ▪ Education: consume enough salt..may need extra salt • Wearing a medical alert bracelet • Eat diet high in proteins and carbs, and make sure to consume enough sodium • Avoid illnesses, stress, strenuous exercise Watch for Addisonian Crisis This develops when Addison’s Disease isn’t treated. In addisonian crisis, the patient has extremely LOW CORTISOL levels (life threatening). Remember the 5 S’s 1. Sudden pain in stomach, back, and legs 2. Syncope (going unconscious) 3. Shock 4. Super low blood pressure 5. Severe vomiting, diarrhea and headache • NEED IV Cortisol STAT: o Solu-Cortef and IV fluids (D5NS to keep blood sugar and sodium levels good and fluid status) • Watch for risk for infection, neuro status (confusion, agitation), electrolyte levels (sodium and potassium, glucose) Heart Failure Definition: the heart is too weak to pump efficiently so it can’t provide proper cardiac output to maintain the body’s metabolic needs. • Results on the body: organs and tissues will suffer from the decreased blood flow, pressure in the heart increases which over works the ventricles, body can become congested with fluids (enter into congestive heart failure) that can cause life-threatening complications. Note: the left ventricle is the largest of all four chambers which allows for maximum pumping power. Causes of Heart Failure: Mainly due to the heart muscle (specifically the ventricles) becoming damaged or too stiff. Remember the mnemonic: Failure Faulty heart valves: AV and SL valve problems (due to congenital issues or infection (endocarditis) that causes blood to back flow (regurgitation) or stenosis (narrowing of the valves that increases pressure of blood flow through the valves). This causes the heart to work harder and become weak over time. Arrhythmias: atrial fibrillation or tachycardia Infarction (myocardial)…coronary artery disease: part of the heart muscle dies due to a blockage in the coronary arteries…muscle become ischemic and can die (main cause of left ventricular systolic dysfunction) Lineage (congenital)…family history Uncontrolled Hypertension: overtime this can lead to stiffening of the heart walls because with untreated HTN the heart has to work harder and this causes the ventricles to become stiff. Recreational Drug Use (cocaine) or alcohol abuse Envaders (instead of Invaders): viruses or infections that attack the heart muscle Types of Heart Failures: Left & Right Side Heart Failure (can have both at the same time as well) Left-Sided Heart failure: the left side of the heart cannot pump blood out of the heart efficiently so blood starts to back-up in the lungs. • Most common type of heart failure. • Left-sided heart failure is likely to lead to right-sided heart failure. The left ventricle becomes too weak and doesn’t squeeze blood out properly….the heart failure can be either SYSTOLIC OR DIASTOLIC. • Systolic: “Left ventricular systolic dysfunction” remember systolic is the contraction or “squeezing” phase of the heart. In systolic dysfunction, there is an issue with the left ventricle being able to eject blood properly out of the ventricle and the organs can’t get all that rich-oxygenated blood it just received from the lungs. Patients will have a low ejection fraction. o What is ejection fraction? Ejection fraction is a calculation used to determine the severity of heart failure on the left side. A normal EF is 50% or greater meaning that more than half of the blood that fills inside the ventricles is being pumped out. An EF can be measured with an echocardiogram, heart cath, nuclear stress test. An EF of 40% or less is a diagnosis for heart failure. • Diastolic: “left ventricular diastolic dysfunction” remember diastole is the filling or resting phase of the heart. In diastolic dysfunction, the ventricle is too stiff to allow for normal filling of blood. Since there isn’t an issue with contraction but filling the ejection fraction is usually normal. Left-sided heart failure will present with PULMONARY Signs and Symptoms. Right-Sided Heart Failure: the right side of the heart cannot pump the “used” blood it received from the body efficiently so it can’t get the blood back to the lungs to get replenished with oxygen. The causes the blood to back up peripherally (legs, hands, feet, abdomen). • Right-sided heart failure causes congestion of blood in the heart and this increases the pressure in the inferior vena cava (which normally brings “used” blood back to the heart for re-oxygenation). This built-up pressure causes the hepatic veins to become very congested with blood which leads to hepatomegaly and swelling peripherally. o Right-sided heart failure is usually caused from left-sided heart failure because of the increased fluid pressure backing up from the left side to the right. This causes the right side of the heart to become overworked. o Other causes: pulmonary heart disease “cor pulmonale” as a complication from pulmonary hypertension or COPD. Right-sided heart failure presents with PERPHIERAL SIGNS AND SYMPTOMS. Signs and Symptoms of Heart Failure Know the difference between the signs and symptoms of left vs. right sided heart failure. Left-sided heart failure: Remember the mnemonic DROWNING (these patients are literally drowning in their own fluid from the heart’s failure to pump efficiently) Difficulty breathing Rales (crackles) Orthopnea (cannot tolerate lying down…must sit-up to breath, especially while sleeping) Weakness (extremely tired and fatigued due to shortness of breath and heart can’t compensate for increased activity) Nocturnal Paroxysmal dyspnea (awaking during sleep with extreme dyspnea) Increased heart rate (due to fluid overload and the heart is trying to get the blood to organs but it can’t because of muscle failure) Nagging cough (can be frothy or blood-tinged sputum from fluid overload in the lungs… very bad sign) Gaining weight from the body retaining fluid…2 to 3 lb in a day or 5 lbs in a week Right-Sided Heart Failure: Remember the mnemonic SWELLING (fluid is backing up in the right side of the heart which causes fluid to back-up in the hepatic veins and peripheral veins) Swelling of legs, hands, liver, abdomen Weight gain Edema (pitting) Large neck veins (jugular venous distention) Lethargic (weak and very tired) Irregular heart rate (atrial fibrillation) Nocturia (frequent urination at night) lying down elevates the legs and allows the extra fluid to enter into the vascular system which allows the kidneys to eliminate the extra fluid. Girth of abdomen increased (from swelling of the liver and building up fluid in the abdomen)…can’t breathe well and this causes nausea and anorexia. Tests used to Diagnose Heart Failure: • BNP (b-type natriuretic peptide) blood test: a biomarker released by the ventricles when there is excessive pressure in the heart due to heart failure. o <100 pg/mL no failure o 100-300 pg/mL present o 300 pg/mL mild o 600 pg/mL moderate o 900 pg/mL severe ▪ Source ClevelandClinic.org • Chest x-ray • Echocardiogram • Heart cath • Nuclear stress test Heart failure can be acute or chronic and can be triggered/exacerbated with: • High salt intake or fluid (watch fluids) • Infection • Uncontrolled atrial fibrillation • Renal failure Nursing Interventions for Heart Failure Role: Assessing, monitoring, intervening, and educating Assessing: • Assess patient for worsening symptoms (right-sided failure…peripheral swelling vs left-sided failure…pulmonary edema) • Patient responsiveness to medication treatment: o watch heart rate (Digoxin) o respiratory status o blood pressure (vasodilators cause hypotension) o diuretics (strict intake and output, daily weights, monitor electrolyte levels, especially K+) Monitoring: • Fluid status (may be ordered a Foley catheter, if on diuretics) • Cardiac diet (low in salt and fats) • Fluid restriction (no more than 2 L per day) • Lab values: watching BNP, kidney function BUN & creatinine, troponins levels, electrolytes (especially potassium…if on Lasix: waste potassium and low potassium increases risk of digoxin toxicity) • Edema in leg: Keep legs elevated and patient in high Fowler’s to help with breathing • Safety (at risk for falls due to fluid status changes, swelling in legs and feet, and orthostatic hypotension) Educating: • Early signs and symptoms heart failure exacerbation o Shortness of breath o Weight gain o Orthopnea • Low salt (allowed 2-3 G sodium per day) and fluid restriction (no more than 2 L per day) • Vaccination to prevent illness, such as annual flu and to be up-to-date with pneumonia vaccine • Exercise aerobic (as tolerated) • Daily weights (watch for no more than 2-3 lb per day and 5 lbs per week) • Compliance with medications • Smoking cessation • Limiting alcohol Administering medications: Know the drug categories a patient will be taking with heart failure and what drugs are included in that category, the pharmacodynamics, and side effects: To remember the groups of drugs use this mnemonic: Always Administer Drugs Before A Ventricle Dies! Ace Inhibitors (angiotensin-converting-enzyme inhibitors): • first line of treatment for heart failure with beta blockers • end in “pril” Lisinopril, Ramipril, Enalapril, Captopril • works by allowing more blood to get to the heart muscle which allows it to work easier. Also, blocks the conversion of Angiotensin I or Angiotensin II (this causes vasodilation, lowers blood pressure, allows kidneys to secrete sodium because it decreases aldosterone) • side effects: dry, nagging cough and can increase potassium (inhibiting angiotensin II which decreases aldosterone in the body which causes the body to retain more potassium and excrete sodium) ARBs (Angiotensin II receptor blockers): • end in “sartan” like Losartan, Valsartan • used in place of ACE inhibitors if patient can’t tolerate them • blocks angiotensin II receptors which causes vasodilation. This lowers blood pressure and helps the kidneys to excrete sodium and water (due to the affects that blocking angiotensin II has on the kidneys…decreases aldosterone). • side effects: increases potassium levels….NO dry nagging cough Diuretics: • used along with ACE inhibitors or ARBs to decrease water and sodium retention which will decrease edema in the body and lungs. This allows the heart to pump easier. • Patients will urinate a lot! • Loop diuretics (most common) like Lasix or Furosemide (watch potassium level because they will waste potassium) • Potassium-sparing diuretics like “Aldactone” (can cause hyperkalemia, especially if taking with ACE or ARBs) Beta Blockers: • blocks norepinephrine and epinephrine effects on the heart muscle • given in stable heart failure with ACE inhibitors • end in “lol” like Metoprolol, Carvedilol and Bisoprolol • not for acute heart failure because the negative inotropic effect on the heart. The negative inotropic effect causes decrease myocardial contractility (slows heart) and decreases cardiac work load. • used in stable heart failure in people with ventricular systolic dysfunction (there is a contraction problem with the left ventricle) and to treat diastolic heart failure (remember there is a problem with the heart filling in diastolic dysfunction). It will help the heart rest so the stiff ventricle can fill properly and the volume of blood pumped out increases. • side effects: check pulse (bradycardia), no grape juice; mask hypoglycemic signs in diabetics, respiratory issues in asthmatics and patients with COPD Anticoagulants: • not used in all patients with heart failure • Typically, used in patients with heart failure who are in a-fib because they are at risk for blood clot formation or certain scenarios of left ventricular systolic heart failure when there is a low ejection fraction of <35%. Vasodilators: • (arterial dilator) Hydralazine…prescribed with a nitrate like Isordil (venous dilator) • sometimes used in place of an ACE or ARB, if patient can’t tolerate them • this causes vasodilation in the arteries and veins to help decrease the amount of blood and fluid going back which helps decrease the work load on the heart • side effects: low blood pressure, orthostatic hypotension Digoxin: • Positive inotropic effect that increases the heart’s ability to contract stronger and it has a negative chronotropic action that causes the heart to beat slower • So, the heart slows down and contracts stronger which allows the heart to pump more blood. • treatment for patients with left ventricular systolic dysfunction (however, not usually the first line of treatment due to side effects and toxicity risks)…used alongside ACE/beta blockers, and diuretics • toxicity issues: monitor patient potassium level (hypokalemia <3.5 mEq/L) because hypokalemia increases digoxin toxicity • S & S of toxicity: nausea, vomiting, visual changes yellowish green halos • normal Digoxin range 0.5 to 2 ng/mL • not for patients with a second or third degree heart block • check apical pulse before giving….>60 bpm • antidote: Digibind Hyperphosphatemia Hyper: “excessive” Phosphat: prefix for phosphate Emia: blood Meaning of Hyperphosphatemia: High levels of phosphate in the blood Normal Phosphate levels: 2.7 to 4.5 mg/dL (>4.5 is hyperphosphatemia) Role of phosphate in the body: helps build bones and teeth and nerve/muscle function. Stored mainly in the bones. The kidneys and parathyroid play a role in the regulation of calcium and phosphate. **Calcium and phosphate influence each other in opposite way. For example, when calcium levels increase in turn phosphate levels decrease (vice versa). Vitamin D plays an important role in phosphate absorption. Causes of Hyperphosphatemia (**main cause is Renal Failure) Remember “PhosHi” (there is a drug called Phoslo (calcium acetate) which is prescribed for patients in end stage renal failure (ESRF) to help keep phosphate levels low. Phoslo is a phosphate binder and it prevents the GI system from absorbing phosphate. Phospho-soda overuse: phosphate containing laxatives or enemas (Sodium Phosphate/Fleets Enema) ….do not administer to patients with renal failure Hypoparathyroidism due to under secretion of parathyroid hormone. The parathyroid plays a role in maintaining calcium and phosphate levels and it normally inhibits reabsorption of phosphate by the kidneys. In hypoparathyroidism, there is under secretion of PTH which causes phosphate to become over absorbed by the kidneys. Overuse of Vitamin D (remember Vitamin D helps with phosphate absorption. Too much vitamin-d would cause too much phosphate to be absorbed) Syndrome of Tumor Lysis is a metabolic problem that mainly occurs with treatment of cancer with chemotherapy. It causes the electrolytes to imbalance due to the cell dying and releasing intracellular contents into the blood, hence too much phosphate is released into the blood rHabdomyolysis is rapid necrosis of the muscles and this leads to myoglobin being released into the bloodstream which affects the kidneys and causes renal failure. In renal failure, you start to have phosphate excretion decreased. Insufficiency of Kidneys (end renal failure) causes phosphate to not be excreted Signs & Symptoms of Hyperphosphatemia Will have many of the same symptoms as hypocalcemia because remember phosphate and calcium function oppositely. Remember CRAMPS (same mnemonic used for hypocalcemia) Confusion Reflexes hyperactive Anorexia Muscle spasms in calves or feet, tetany, seizures Positive Trousseau’s Signs, Pruritis Signs of Chvostek Nursing Interventions of Hyperphosphatemia • **Administer phosphate-binding drugs (PhosLo) which works on the GI system and causes phosphorus to be excreted through the stool.*** NCLEX: Give with a meals or right after eating meal • Avoid using phosphate medication such as laxatives and enema • Restrict foods high is phosphate ***eat, poultry, fish, dairy, nuts, sodas, oatmeal • Prepare patient for dialysis if patient in renal failure Hypophosphatemia Hypo: “below” Phosphat: prefix for phosphate Emia: blood Meaning of Hypophosphatemia: Low levels of phosphate in the blood Normal Phosphate levels: 2.7 to 4.5 mg/dL (<2.7 is hypophosphatemia) Role of phosphate in the body: helps build bones/teeth and nerve/muscle function. Stored mainly in the bones. The kidneys and parathyroid play a role in the regulation of calcium and phosphate. **Calcium and phosphate influence each other in opposite way. For example, when calcium levels increase in turn phosphate levels decrease (vice versa). Vitamin D plays an important role in phosphate absorption. Causes of Hypophosphatemia Remember phrase: Low “Phosphate” Pharmacy: drugs such as aluminum hydroxide-based or magnesium based antacids cause malabsorption in the GI system, so no phosphate is absorbed through the GI track and the lack of vitamin d (which plays a role in phosphate absorption). Hyperparathyroidism: due to over secretion of parathyroid hormone (parathyroid plays a role in maintaining calcium and phosphate levels and it normally inhibits re-absorption of phosphate by the kidneys). However, in hyperparathyroidism there is an over secretion of PTH which causes phosphate to NOT be reabsorbed at all. Oncogenic osteomalacia: kidneys start to waste phosphate which leads to low phosphate levels and softening of the bones (this puts the patient at risk for bone fractures). Syndrome of Refeeding (aka Refeeding Syndrome): causes electrolytes and fluid problems due to malnutrition or starvation. **Watch patients who are on TPN (total parenteral nutrition). This happens when food is reintroduced after the body being in starvation mode (hence the body went into survival mode and is depleted of almost everything). When the nutrition is introduced, the body releases insulin due to the increased blood sugar from the food which causes the body to rapidly use the already low stores of phosphate, magnesium, and potassium to help with synthesizing. This depletes phosphate levels. Pulmonary issues such as respiratory alkalosis (under alkalotic conditions phosphate moves out of the blood into the cell which causes phosphate blood levels to decrease) Hyperglycemia leads to symptoms of glycosuria, polyuria, ketoacidosis which causes the kidneys to waste phosphate Alcoholism: alcohol affects the body’s ability to absorb phosphate and many alcoholics are already malnourished (hence already have low phosphate level to begin with) Thermal Burns due to the shifting of phosphate intracellularly Electrolyte imbalances: hypercalcemia, hypomagnesemia, hypokalemia also cause phosphate levels to decrease Signs & Symptoms of Hypophosphatemia Remember the word: “BROKEN” These patients are at risk for broken bones and the systems of the body are breaking down (respiratory, muscles, neuro, immune etc.) Breathing problems due to muscle weakness Rhabdomyolysis which is caused by an electrolyte disorder. This happens which there is rapid necrosis of the skeletal muscles which leads to renal failure. **These patients will have tea-colored looking urine due to myoglobin in the urine and will have muscle weakness/pain. The renal failure occurs because when the muscle dies, myoglobin is released into the blood which is very toxic to the kidneys. Reflexes (deep tendon) decreased Osteomalacia (softening of the bones) fractures and decreased bone density (alteration in bone shape), cardiac Output decreased Kills immune system with immune suppression and decreases platelet aggregation (which leads to increased bleeding) Extreme weakness, Ecchymoses from decreased platelets Neuro status changes (irritability, confusion, seizures) Nursing Interventions for Hypophosphatemia **Administer oral phosphorus with Vitamin-D supplement (remember vitamin-d helps with absorbing phosphate) If patient is receiving TPN watch for patient complaints of muscle pain or weakness (may be due to rhabdomyolysis or refeeding syndrome) Ensure patient safety due to risk of bone fractures Encourage foods high is phosphate but low in calcium: **Foods high in phosphate are fish, organ meats, nuts, pork, beef, chicken, whole grains If phosphate levels less than 1mg/dL, the doctor may order IV phosphorous which affects calcium levels causing hypocalcemia or increase phosphate levels (Hyperphosphatemia). ***Also, assess renal status (BUN/creatintine normal) before administering phosphorous because if the kidneys are failing the patient won’t be able to clear phosphate). Place on cardiac monitor and watch for EKG changes. Hypermagnesemia NCLEX Review Notes Are you studying hypermagnesemia and need to know some mnemonics on how to remember the causes, signs & symptoms, nursing interventions? This article will give you some clever mnemonics on how to remember hypermagnesemia for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate hypomagnesemia from hypermagnesemia. Don’t forget to take the hypomagnesemia & hypermagnesemia quiz. In this article you will learn: Normal Magnesium Level Causes of Hypermagnesemia Signs & Symptoms of Hypermagnesemia Nursing Interventions for Hypermagnesemia Teaching Tutorial on Hypermagnesemia Hypermagnesemia Hyper: “excessive” Magnes: prefix for magnesium Emia: blood Meaning of Hypermagnesemia: High levels of magnesium in the blood Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (>2.6 hypermagnesemia) Magnesium plays a role in: major cell functions like transferring and storing energy, regulation of parathyroid hormone PTH (which also plays a role in calcium levels). In hypermagnesemia, the release of calcium is inhibited and that is why you will see hypocalcemia if you have a high magnesium level. Magnesium also plays a role in the metabolism of carbs, lipids, and proteins, and blood pressure regulation. Magnesium is absorbed in the small intestine and excreted via the kidneys (any issues with these systems can cause magnesium level issues). Causes of Hypermagnesemia Remember “MAG” Hypermagnesemia is less common than hypomagnesemia. It typically happens when you are trying to correct hypomagnesemia with magnesium sulfate IV infusion. However, other causes can include: Magnesium containing antacids and laxatives***(Mylanta, Maalox) Addison’s disease (adrenal insufficiency) Glomerular filtration insufficiency (<30mL/min) renal failure. This is because the kidneys are keeping too much magnesium. Signs & Symptoms Hypermagnesemia Remember: Every system of the body is “Lethargic” (opposite of hypomagnesemia where the body systems are experiencing hyper-excitability) Note: You will typically only see symptoms in severe cases of hypermagnesemia (mild cases patient will be asymptomatic) Lethargy (profound) EKG changes with prolonged PR & QT interval and widened QRS complex Tendon reflexes absent/grossly diminished Hypotension Arrhythmias (bradycardia, heart blocks) Respiratory arrest GI issues (nausea, vomiting) Impaired breathing (due to skeletal weakness) Cardiac arrest Nursing Interventions for Hypermagnesemia • Monitor cardiac, respiratory, neuro system, renal status. Put patient on cardiac monitor (watch for EKG changes) • Ensure safety due to lethargic/drowsiness • Prevention: 1. Avoid giving Magnesium containing antacids/laxative to patients with renal failure 2. Assess for hypermagnesemia during IV infusions of magnesium sulfate for hypomagnesemia (sign and symptom would be diminished/absent deep tendon reflexes) 3. Withhold foods high in magnesium, such as: Remember: “Always Get Plenty Of Foods Containing Large Numbers of Magnesium” • Avocado • Green leafy vegetables • Peanut Butter, potatoes, pork • Oatmeal • Fish (canned white tuna/mackerel) • Cauliflower, chocolate (dark) • Legumes • Nuts • Oranges • Milk • Administer diuretics that waste magnesium (if patient is not in renal failure) such as Loop and Thiazide diuretics • Patient in renal failure patient prep for dialysis • IV calcium may be order to reverse side effects of Magnesium (watch IV for infiltration…prefer central line) Hypomagnesemia Hypo: “under” Magnes: prefix for magnesium Emia: blood Meaning of Hypomagnesemia: Low levels of magnesium in the blood Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (<1.6 hypomagnesemia) Magnesium plays a role in: major cell functions like transferring and storing energy, regulation of parathyroid hormone PTH (which also plays a role in calcium levels). In hypomagnesemia, the release of calcium is inhibited and that is why you will see hypocalcemia if you have low magnesium level. Magnesium also plays a role in the metabolism of carbs, lipids, and proteins, and blood pressure regulation. Magnesium is absorbed in the small intestine and excreted via the kidneys (any issues with these systems can cause magnesium level issues). Causes of Hypomagnesemia Remember “Low Mag” Limited intake Mg+ (starvation) Other electrolyte issues cause low mag levels (hypOkalemia, hypOcalcemia) Wasting Magnesium kidneys (loop and thiazide diuretics & cyclosporine…stimulates the kidneys to waste Mag) Malabsorption issues (Crohn’s, Celiac, proton-pump inhibitors drugs “Prilosec, Nexium, Protonix”…drug family ending in “prazole” Omeprazole, diarrhea/vomiting) Alcohol (due to poor dietary intake, alcohol stimulates the kidneys to excreted mag, acute pancreatitis) Glycemic issues (Diabetic Ketoacidosis, insulin administration) Signs & Symptoms of Hypomagnesemia Remember “Twitching” because the body is experiencing neuromuscular excitability. This is the OPPOSITE in hypermagnesemia where everything system of the body is lethargic. Trouesseau’s (positive due to hypocalcemia) Weak respirations Irritability Torsades de pointes (abnormal heart rhythm that leads to sudden cardiac death…seen in alcoholism) Tetany (seizures) Cardiac changes (moderate loss: Tall T-waves and depressed ST segments*** severe loss: prolonged PR & QT interval (prolong of QT interval increases patient’s risk for Torsades de pointes) with widening QRS complex, flattened t-waves, Chvostek’s sign (positive which goes along with hypocalcemia) Hypertension, hyperreflexia Involuntary movements Nausea GI issues (decreased bowel sounds and mobility) Nursing Interventions for Hypomagnesemia • Monitor cardiac, GI, respiratory, neuro status. Place on a cardiac monitor (watching for any EKG changes prolonging of PR interval and widening QRS complex) • May administer potassium supplements due to hypokalemia (hard to get magnesium level up if potassium level is down) • Administering calcium supplements (oral calcium supplements w/ Vitamin-D or 10% Calcium Gluconate) • Administer Magnesium Sulfate IV route. Monitor Mg+ level closely because patient can become magnesium toxic (***Watch for depressed or loss of deep tendon reflexes) • Place patient in seizure precautions • Oral forms of Magnesium may cause diarrhea which can increase magnesium loss so watch out for this • Watch other electrolyte levels like calcium and potassium • Encourage foods rich in Magnesium: “Always Get Plenty Of Foods Containing Large Numbers of Magnesium” • Avocado • Green leafy vegetables • Peanut Butter, potatoes, pork • Oatmeal • Fish (canned white tuna/mackerel) • Cauliflower, chocolate (dark) • Legumes • Nuts • Oranges • Milk Hypernatremia Hyper: “excessive” Natr: Prefix for Sodium Emia: blood Meaning of Hypernatremia: excessive sodium in the bloodisotonic, hypotonic, and hypertonic tonicity. Normal sodium levels: 135 to 145 mEq/L (>145 sodium is hypernatremic) Hypernatremia is a water problem rather than a sodium problem. This is because when the body collects sodium it causes a lot of water retention and this is what causes the patient problems. Role of sodium in the body: It’s an important electrolyte that helps regulate the amount of water inside and outside of the cell (water and sodium loves each other). Where ever sodium goes, so does water. Watch my video on hypotonic, hypertonic, and isotonic tonicity. For example, in hypernatremia there is a lot of sodium outside the cell and this attracts the water from inside the cell which will cause water to move outside the cell and dehydrate the cell. Sodium also plays a role in muscle, nerves, and organ function. Causes of Hypernatremia Remember the phrase “HIGH SALT” Hypercortisolism (Cushing’s Syndrome), hyperventilation Increased intake of sodium (oral or IV route) GI feeding (tube) without adequate water supplements Hypertonic solutions Sodium excretion decreased (body keeping too much sodium) and corticosteroids Aldosterone overproduction (Hyperaldosteronism) Loss of fluids (dehydrated) infection (fever), sweating, diarrhea, and diabetes insipidus Thirst impairment Signs & Symptoms of Hypernatremia Remember: “No FRIED foods for you!” (too much salt) Fever, flushed skin Restless, really agitated Increased fluid retention Edema, extremely confused Decreased urine output, dry mouth/skin Nursing Interventions for Hypernatremia • Restrict sodium intake! Know foods high in salt such as bacon, butter, canned food, cheese, hot dogs, lunch meat, processed food, and table salt. • Keep patient safe because they will be confused and agitated. • Doctor may order to give isotonic or hypotonic solutions such as 0.45% NS (which is hypotonic and most commonly used). Give hypotonic fluids slowly because brain tissue is at risk due to the shifting of fluids back into the cell (remember the cell is dehydrated with hypernatremia) and the patient is at risk for cerebral edema. In other words, the cell can lyse if fluids are administered too quickly. • Educate patient and family about sign and symptoms of high sodium level and proper foods to eat. Hyponatremia Hypo: “under/beneath” Natr: Prefix for Sodium Emia: blood Meaning of Hyponatremia: low sodium in the blood Normal sodium levels: 135 to 145 mEq/L (<135 = hyponatremia) Role of sodium in the body: An important electrolyte that helps regulate water inside and outside of the cell. Remember that water and sodium loves each other and where ever sodium goes so does water. Learn about Hypertonic, Hypotonic, & Isotonic Solutions. For example, in hyponatremia sodium outside of the cell is very low and this causes water to move inside the cell. In turn, the cell will swell and you will start to see problems in the body, especially with brain cells (confusion). Sodium also play a role in muscle, nerves, and organ function. Types of Hyponatremia Euvolemic Hyponatremia is where the water in the body increases but the sodium stays the same. The causes include: SIADH (Syndrome of inappropriate antidiuretic hormone secretion) which is due to the increased amount of secretion of antidiuretic hormone. This hormone retains water in the body which dilutes sodium. Other causes: diabetes insipidus, adrenal insufficiency, Addison’s disease etc. Hypovolemic Hyponatremia is where the patient has lost a lot of fluid and sodium. Causes: vomiting, diarrhea, NG suction, diuretic therapy, burns, sweating Hypervolemic Hyponatremia is where the body has increased in fluid and sodium. However, sodium decreases due to dilution and because total body water and sodium are regulated independently in the body. Causes: congestive heart failure, kidney failure, IV infusion of saline, liver failure etc. Causes of Hyponatremia Remember “NO Na+” Na+ excretion increased with renal problems, NG suction (GI system rich in sodium), vomiting, diuretics, sweating, diarrhea, decreased secretion of aldosterone (diabetes insipidus) (wasting sodium) Overload of fluid with congestive heart failure, hypotonic fluids infusions, renal failure (dilutes sodium) Na+ intake low through low salt diets or nothing by mouth Antidiuretic hormone over secreted **SIADH (syndrome of inappropriate antidiuretic hormone secretion…remembers retains water in the body and this dilutes sodium) Signs & Symptoms of Hyponatremia Remember “SALT LOSS” Seizures & Stupor Abdominal cramping, attitude changes (confusion) Lethargic Tendon reflexes diminished, trouble concentrating (confused) Loss of urine & appetite Orthostatic hypotension, overactive bowel sounds Shallow respirations (happens late due to skeletal muscle weakness) Spasms of muscles Nursing Interventions for Hyponatremia • Watch cardiac, respiratory, neuro, renal, and GI status • Hypovolemic Hyponatremia: give IV sodium chloride infusion to restore sodium and fluids (3% Saline hypertonic solution….harsh on the veins…given in ICU usually through central line very slowly…must watch for fluid overload) • Hypervolemic Hyponatremia: Restrict fluid intake and in some cases administer diuretics to excretion the extra water rather than sodium to help concentrate the sodium. If the patient has renal impairment they may need dialysis. • Caused by SIADH or antidiuretic hormone problems: fluid restriction or treated with an antidiuretic hormone antagonists called Declomycin which is part of the tetracycline family (don’t give with food especially dairy or antacids…bind to cations and this affect absorption). • If patient takes Lithium remember to monitor drug levels because lithium excretion will be diminished and this can cause lithium toxicity. • Instruct to increase oral sodium intake and some physicians may prescribe sodium tablets. Food rich in sodium include: bacon, butter canned food, cheese, hot dogs, lunch meat, processed food, table salt Hypercalcemia Hyper: excessive Calc: prefix for calcium Emia: blood Meaning of Hypercalcemia: excessive calcium in the blood Normal calcium levels in the blood: 8.6 to 10.0 mg/dL (>10.0 is hypercalcemia) Calcium plays a huge role in bone and teeth health along with muscle/nerve function, cell, and blood clotting. Calcium is absorbed in the GI system and stored in the bones and then excreted by the kidneys. Vitamin D helps play a role calcium absorption. Causes of Hypercalcemia Remember “High Cal” Hyperparathyroidism (high parathyroid hormone causes too much calcium to be released into the blood) Increased intake of calcium (excessive use of oral calcium or Vitamin D supplements) Glucocorticoids usage (suppresses calcium absorption which leaves more calcium in the blood) Hyperthyroidism Calcium excretion decreased with Thiazide* diuretics & renal failure, cancer of the bones Adrenal insufficiency (Addison’s Disease) Lithium usage (affects the parathyroid and causes phosphate to decrease and calcium to increase) Signs & Symptoms of Hypercalcemia “The body is too WEAK” Weakness of muscles (profound) EKG changes shortened QT interval (most common) and prolonged PR interval Absent reflexes, absent minded (disorientated), abdominal distention from constipation Kidney Stone formation Nursing Interventions for Hypercalcemia Mild cases of Hypercalcemia • Keep patient hydrated (decrease chance of renal stone formation) • Keep patient safe from falls or injury • Monitor cardiac, GI, renal, neuro status • Assess for complaints of flank or abdominal pain & strain urine to look for stone formation • Decrease calcium rich foods and intake of calcium-preserving drugs like thiazides, supplements, Vitamin D To help you remember foods high in calcium remember the phrase: “Young Sally’s calcium serum continues to randomly mess-up” Yogurt Sardines Cheese Spinach Collard greens Tofu Rhubarb Milk Moderate cases of Hypercalcemia Administer calcium reabsorption inhibitors: Calcitonin, Bisphosphonates, prostaglandin synthesis inhibitors (ASA, NSAIDS) Severe cases of Hypercalcemia Prepare patient for dialysis Hypocalcemia Hypo: low Calc: pre-fix is calcium Emia: blood Meaning of hypocalcemia: Low calcium in the blood Normal calcium level: 8.6 mg/dL to 10.0 (<8.6 mg/dL) Role of Calcium: plays a huge role in bone and teeth health along with muscle/nerve function, cell, and blood clotting. Calcium is absorbed in the GI system and stored in the bones and then excreted by the kidneys. Vitamin D helps play a role in calcium absorption. In addition, phosphorus and calcium affect each other in the opposite way. For instance, if phosphorus levels are high in the blood, calcium will decrease and vice versa. They are always doing the opposite (remember this because it is important for the causes of hypocalcemia. Causes of Hypocalcemia Remember “Low Calcium” Low parathyroid hormone due. This is due to the destruction or removal parathyroid gland (any surgeries of the neck ex: thyroidectomy you want to check the calcium level) Professors love to ask this on an exam. Oral intake inadequate (alcoholism, bulimia etc.) Wound drainage (especially GI System because this is where calcium is absorbed) Celiac’s & Crohn’s Disease cause malabsorption of calcium in the GI track Acute Pancreatitis Low Vitamin D levels (allows for calcium to be reabsorbed) Chronic kidney issues (excessive excretion of calcium by the kidneys) Increased phosphorus levels in the blood (phosphorus and calcium do the opposite of each other) Using medications such as magnesium supplements, laxatives, loop diuretics, calcium binder drugs Mobility issues Signs & Symptoms of Hypocalcemia Remember “CRAMPS” Confusion Reflexes hyperactive Arrhythmias (prolonged QT interval and ST interval) Note: definitely remember prolonged QT interval…another major test question Muscle spasms in calves or feet, tetany, seizures Positive Trousseau’s! You will see this before Chvostek’s sign or before tetany. This sign may be positive before other manifestations of hypocalcemia such as hyperactive reflexes. (KNOW How to elicit a positive Trousseau’s. You do this by using a blood pressure cuff and place it around the upper arm and inflate it to a pressure greater than the systolic blood pressure and hold it in place for 3 minutes. If it is positive the hand of the arm where the blood pressure is being taken will start to contract involuntarily (see the teaching tutorial on a demonstration). Signs of Chvostek’s (nerve hyperexcitability of the facial nerves. To elicit this response you would tap at the angle of the jaw via the masseter muscle and the facial muscles on the same side of the face will contract momentarily (the lips or nose will twitch). Nursing Interventions for Hypocalcemia • Safety (prevent falls because patient is at risk for bone fractures, seizures precautions, and watch for laryngeal spasms) • Administer IV calcium as ordered (ex: 10% calcium gluconate)….give slowly as ordered (be on cardiac monitor and watch for cardiac dysrhythmias). Assess for infiltration or phlebitis because it can cause tissue sloughing (best to give via a central line). Also, watch if patient is on Digoxin cause this can cause Digoxin toxicity. • Administer oral calcium with Vitamin D supplements (given after meals or at bedtime with a full glass of water) • If phosphorus level is high (remember phosphorus and calcium do the opposite) the doctor may order aluminum hydroxide antacids (Tums) to decrease phosphorus level which in turn would increase calcium levels. • Encourage intake of foods high in calcium: Young Sally’s calcium serum continues to randomly mess-up. • Yogurt • Sardines • Cheese • Spinach • Collard greens • Tofu • Rhubarb • Milk Hypoparathyroidism and Hyperparathyroidism Nursing Hypoparathyroidism Definition: low secretion of parathyroid hormone by the parathyroid gland Presents with HYPOcalcemia and HYPERphosphatemia (due to the role of PTH on the bones and kidneys…PTH is unable to stimulate them to increase calcium levels in the blood) Causes of Hypoparathyroidism • Damage or manipulation of the thyroid or parathyroid gland (thyroidectomy) • Low magnesium level (hypomagnesemia): parathyroid gland doesn’t function properly if there are low magnesium levels • Autoimmune: body attacks the gland • Body resistant: parathyroid gland working great but the bones and kidneys not receptive to PTH Signs & Symptoms of Hypoparathyroidism Mainly due to hypocalcemia..remember PTH • Parathesia, Positive Trousseau and Chvostek’s Sign • Tetany (involuntary muscle cramping/contraction) • Hypocalcemia and Hyperphosphatemia Nursing Interventions for Hypoparathyroidism • Monitor VS, airway, labs, educate diet (high calcium, low phosphate) • Administer Medications: Goal of medications are to increase calcium levels and decrease phosphate levels o IV calcium (if severe) Calcium Gluconate o Oral calcium supplements with vitamin D (side effects: GI upset, constipation, increase risk of renal stones) o Phosphate-binders: Aluminum carbonate to remove phosphate into stool (take after meal) o Parathyroid replacement: Natpara (injection)…watch calcium levels, GI upset, or parathesia Hyperparathyroidism Definition: high secretion of parathyroid hormone by the parathyroid gland Presents with HYPERcalcemia and HYPOphosphatemia (due to the role of PTH on the bones and kidneys…overstimulates them to increase calcium levels in the blood) Causes of Hyperparathyroidism • Primary: something is wrong with the parathyroid gland itself o Hyperplasia (enlarged), adenoma, cancerous tumor • Secondary: disease is causing the parathyroid gland to not work properly o Hypocalcemia, Vitamin-D deficiency…main cause is Chronic Renal Failure (remember kidneys play a huge role in increasing calcium levels and activating vitamin-d….the parathyroid becomes overworked) Signs & Symptoms of Hyperparathyroidism Mainly due to hypercalcemia • Bone fractures (bones become depleted of calcium) • Constipation (GI system slows down …remember calcium plays a role in muscle contraction) • Renal calculi formation (concentrated amounts of calcium in the blood) • Nausea and vomiting with epigastric pain Nursing Interventions for Hyperparathyroidisim • Monitor VS, urine for kidney stones, encourage fluids to prevent dehydration and stone formation, monitor labs, educate on diet (low calcium, high phosphate…but watch phosphate in renal patients) • Prep for Parathyroidectomy: treatment in primary hyperparathyroidism • Administered Medications: goal decrease calcium levels and keep hydrated o IV solutions: normal saline for hydration o Calcimimetics: “Senispar” decreases PTH, calcium, and phosphate levels (treatment for secondary hyperparathyroidism for patients with chronic kidney disease) o Calcitonin: lowers calcium levels and protects bones o Lasix: loop diuretics decrease calcium levels by inhibiting calcium resorption in the renal tubules (watch potassium levels because Lasix wastes potassium) o Bisphosphonates: Pamidronate (Aredia) or Alendronate (Fosamax) helps protect bones from losing calcium by slowing down osteoclasts (which break down bones) and allow osteoblasts to work (to help build bones) Hypo and Hyperthyroidism Hyperthyroidism Definition: Excessive production of thyroid hormones • Thyroid hormones play a role in burning calories, stimulating sympathetic nervous system (reflex, responses), increasing heart rate/blood pressure, and how fast we digest food Causes: • Too much Iodine • Grave’s Disease (autoimmune disorder where the body produces TSI which the body thinks is TSH…and this causes the thyroid gland to release excessive amounts of T3 and T4) • Toxic Nodular Goiter (nodular growths that produce excessive thyroid hormone) • Thyroid replacement medication toxicity Life-threatening Complications: Thyroid Storm Signs and Symptoms: • Weight Loss • Heat intolerance • Goiter (both) • Restless, irritable • Fast Heart Rate • Hair Loss • Diarrhea • Unable to focus mentally • Oily skin • Nervousness • Menstrual problems (both) Treatments: • Antithyroid medications such as: o Tapazole “Methimazole” o PTU o Iodide solution “lugol’s solution • Beta blockers: Inderal • Radioactive iodine therapy • Thyroidectomy -Avoid Salicylates and foods/supplement with iodine (increases thyroid hormone). Hypothyroidism Definition: Low production of thyroid hormones Thyroid hormones play a role in burning calories, stimulating sympathetic nervous system (reflex, responses), increasing heart rate/blood pressure, and how fast we digest food Causes: • Not enough Iodine • Hashimotos: (autoimmune disorder where the body attacks the thyroid gland) • Antithyroid medication toxicity used to treat hyperthyroidism • Thyroidectomy • Pituitary tumor (stop the anterior pituitary gland from secreting TSH which stimulates the thyroid to release T3 and T4) Life-threatening Complications: Myxedema Coma Signs and Symptoms: • Weight Gain • Unable to tolerate cold • Possible goiter from constant thyroid stimulation to get the thyroid gland to produce T3 and T4 MOST COMMON SIGN IN HASHIMOTO’S • Extremely tired and fatigued • Slow heart rate • Thinning and brittle hair • Constipation • Memory loss • Myxedema: swelling of the skin (eyes and face) that gives it a waxy appearance • Dry skin • Depression • Menstrual problems (irregular or heavy periods) Treatments: • Thyroid Hormone replacement (Synthroid, Thyrolar, Cytomel) • Avoid sedatives and narcotics because these patients are very sensitive to them and they increase the chances of myxedema coma Thyroid Storm Definition: Life-threatening complication that develops in someone who has hyperthyroidism which is an excessive secretion of thyroid hormones (T3 and T4). It is usually because hyperthyroidism is not being treated properly, the patient is undiagnosed, or the patient experienced an illness. In addition, thyroid storm can develop after a thyroidectomy due to the thyroid being manipulated during removal which can cause high amounts of T3 and T4 to enter into the blood stream. However, it is rare because today patients are placed on medications to help combat this. Causes of Thyroid Storm Patients will already have hyperthyroidism along with any of the following: • got an illness or experienced trauma/stress (septic, DKA, surgery, trauma to the gland) • suffers from Grave’s Disease that is under treated or they became sick • not taking antithyroid medications properly • taking medications that increase thyroid hormones (Salicylates: ASA) • pregnancy • radioactive iodine therapy (CT scan or as treatment) remember the thyroid loves iodine and uses it to make thyroid hormone Signs & Symptoms of Thyroid Storm The patient will have typical hyperthyroidism symptoms but they will be SEVERE to the point of death…remember the function of T3 and T4 is to increase body’s metabolism and temperature and to stimulate the sympathetic nervous system (this will be happening at an accelerated rate). Remember this condition as: A violent storm on the body at an accelerated rate. • Fever (not just heat intolerance) • Hypertension—going to exhaust the heart to the point of failure (CHF or MI) • Tachycardia— going to exhaust the heart to the point of failure (CHF or MI) • Increase respirations—due to the body working so hard and it needs more oxygen and nutrients…will get respiratory failure if not treated fast • Very restless, irritable, confused …this will progress to seizures, delirium, coma • Diarrhea Nursing Interventions for Thyroid Storm • Monitor HR, BP, RR (respiratory failure…may need mechanical ventilation), EKG, Temperature • Keep environment quiet and patient cool (cooling blankets and sedatives as prescribed) • No foods containing iodine (seafood…seaweed, dairy, eggs) Pharmacological Management of Thyroid Storm Goals: 1. Need to decrease the thyroid hormone: • Antithyroid medications (block synthesis) : o Tapazole “Methimazole”: has fewer side effects than PTU…not for first trimester of pregnancy o PTU “Propylthiouracil”: can be used during 1st trimester…watch for liver failure Side Effects with these medications: Agranulocytosis and thrombocytopenia and watch for toxicity which will present as signs and symptoms of HYPOTHYROIDISM: slow heart rate, intolerance to cold, drowsy • Iodide solution (block secretion) o Lugol’s solution: Side effects: taste changes metal taste in mouth 2. Decrease fever: Tylenol NO Salicylates or cooling blankets 3. Decrease effects of thyroid hormones on the body by blocking peripheral conversion of T3 and T4: • Beta Blockers: Inderal (not for people with asthma or history of bronchospasm…watch in diabetics can mask hypoglycemia) 4. Prevent further secretion and conversion of thyroid hormones by suppressing immune system with: • Glucocorticoids (Dexamethasone ) Adrenal Crisis (Addisonian Crisis) Adrenal crisis in a nutshell is extremely low CORTISOL levels. Key Players in Adrenal Crisis: • Adrenal Cortex: produces CORTISOL • Pituitary Gland (anterior): regulates CORTISOL production by releasing ACTH (adrenocorticotropic hormone)…when this is released it causes the adrenal cortex to release cortisol. • CORTISOL: a steroid hormone which is a glucocorticoid know as the “STRESS Hormone” . This helps the body deal with stress such as illness or injury by increasing blood glucose though glucose metabolism, breaking down fats, proteins, and carbs, and regulating electrolytes. Lecture on Adrenal Crisis Causes of Adrenal Crisis • Damage to the adrenal cortex: o Addison’s Disease which is under treated (not taking medication properly or they are taking it properly, but there is extra stress on the body and the medication needs to be increased…surgery, illness, emotional stress) • Adrenalectomy: o A treatment for Cushing’s (removal of the adrenal gland) and patient must take oral cortisol because body isn’t producing it. If the patient fails to take the medication or the medication isn’t enough they could enter into adrenal crisis. • Pituitary gland is damaged and isn’t producing enough ACTH. Remember the negative feedback loop (watch the video for details on it) Signs and Symptoms of Addisonian Crisis Remember the 5’S & 3 H’s 1. Super low blood pressure (nothing will bring it up) 2. Sudden pain in stomach, back, and legs 3. Syncope (going unconscious) 4. Shock 5. Severe vomiting, diarrhea and headache 1. Hyponatremia 2. Hyperkalemia 3. Hypoglycemia Nursing management of Adrenal Crisis • Administer some cortisol STAT via fastest route which is IV!! o Most commonly prescribed is Solu-Cortef “hydrocortisone”, along with IV fluids which will help replenish sodium and glucose (D5NS). • Start on PO glucocorticoids and mineralocorticoid: o For replacing cortisol: ex: prednisone, hydrocortisone ▪ Education: patient to report if they are having stress such as illness, surgery, or extra stress in life…… will need to increase dosage, take medication exactly as prescribed….don’t stop abruptly without consulting with md. • For replacing aldosterone: Fludrocortisone aka Florinef • Education: consuming enough salt..may need extra salt • Watch sodium, potassium and glucose levels and ensure clean environment to prevent infection Lecture on Diabetic Ketoacidosis Diabetic Ketoacidosis Define: a complication of diabetes mellitus that is life-threatening, if not treated. It is due to the breakdown of fats which turn into ketones because there is no insulin present in the body to take glucose into the cell. Therefore, you will see hyperglycemia and ketosis and acidosis. Key Players of DKA: Glucose: fuels the cells so it can function. However, with DKA there is no insulin present to take the glucose into the cell…so the glucose is not used and the patient will experience hyperglycemia >300 mg/dL. Insulin: helps take glucose into the cell so the body can use it for fuel. In DKA, the body isn’t receiving enough insulin…so the GLUCOSE can NOT enter into the cell. The glucose floats around in the blood and the body starts to think it is starving because it cannot get to the glucose. Therefore, it looks elsewhere for energy. Liver & Glucagon: the body tries an attempt to use the glucose stores in the liver (because it doesn’t know there is a bunch of glucose floating around in the blood and thinks the body is experiencing hypoglycemia). In turn, the liver releases glucagon to turn glycogen stores into more GLUCOSE….so the patient becomes even more hyperglycemic. Ketones: a byproduct of fat break down. In DKA, the body needs FUEL to function so it starts to break down FATS since it cannot use the glucose in the body. The patient will experience increased ketones in the body which are LIFE-THREATENING to a diabetic patient because it causes the blood to become acidic (metabolic acidosis) Kidneys: plays a role in reabsorbing glucose in the renal tubules. However, there is too much glucose present in the blood and it cannot be reabsorbed. So, it leaks into the urine and this causes OSMOTIC DIURESIS which causes polyuria and excretion of electrolytes (sodium,potassium, chloride) Happens mainly in TYPE 1 Diabetics…rare in type 2 but possible if they are experiencing a severe illness. Causes of DKA • Undetected diabetes: patient doesn’t know they are diabetic and this is the first sign, usually. • More Insulin needed by the body than normal: the body needs more units of insulin than it is actually receiving from injections. o Example: when a diabetic become sick (INFECTION) with illness or recovering from surgery or experiences some type of stress on the body like certain drugs such as, corticosteroids or thiazide diuretics. • Not eating (skipping meals): body starts to go into “starvation” mode and begins to burn ketones (normally in nondiabetics when the body goes into starvation mode it can cope when ketones are released by regulating insulin and glucagon to maintain sugar levels…but in the diabetic they don’t have that ability and ketones production is dangerous). • Not taking insulin as scheduled: therefore the blood glucose levels are not controlled…ketones are produced and the cycle of acidosis starts to take place in the body. Signs & Symptoms of Diabetic Ketoacidosis: Recap of what is going on: • Hyperglycemia (intracellular to extracellular shifting takes place which will lead to electrolyte imbalances) • Ketones in the blood (leads to metabolic acidosis, weight loss because of all the fat burning, electrolyte shifting as well) • Metabolic Acidosis (blood pH <7.35 and HCO3 <15 mEq/L) Happens suddenly (there may be warning signs present if the patient is monitoring their blood glucose which will be elevated consistently (>300 mg/dL) • Polyuria: due to the extreme levels of glucose in the body that causes the water inside the cells to shift to the extracellular area. The kidneys try to compensate by increasing urinary production to eliminate this extra fluid but the kidneys cannot reabsorb all the glucose so it leaks into the urine. This causes OSMOTIC DIURESIS which causes SODIUM AND POTASSIUM (along with calcium, phos) TO BE EXCRETED. *NOTE potassium levels typically stay normal or elevated in DKA because of the shifting of potassium from the inside of the cell to the outside BUT WHEN TREATMENT STARTS TO BE INITATED WITH INSULIN IT WILL CAUSES THE K+ TO MOVE BACK INTO THE CELL. Therefore, you have to watch POTASSIUM LEVELS closely during treatment. • Polydipsia: frequent drinking due to extreme thirst….vicious cycle of frequent urination and the body is trying to keep itself hydrated. • Dehydration: dry mucous membranes, decreased skin turgor (the extreme drinking doesn’t work) • Nausea & vomiting, Abdominal pain-> (especially children…causes not 100% known but could be due to the ketones present in the blood) • Kussmaul Breathing: due to metabolic acidosis….the respiratory system tries to compensate by getting rid of extra acid in the body by blowing off carbon dioxide which is an acid…this is rapid deep breathing • Acetone Smell of the Breath “fruity”: due to the breakdown of ketones • Ketones present in the urine • Tachycardia, hypotension, confusion, fatigue Nursing Interventions of DKA *Get treatment early because DKA is fatal* Teach patient early signs and when to seek treatment: • Monitor glucose and ketones during illness every 4 hours, especially if dealing with illness/infection • If vomiting and cannot eat food or drink liquids notify doctor (if can tolerate drink liquids every hour) • Notify medical doctor if blood sugars are higher than normal or greater than 300 mg/dL consistently • Ketones present in the urine • Excessive thirst, frequent urination, abdominal pain, nausea and vomiting, acetone breath Treatment of DKA Goal: Hydrate, decrease blood glucose, monitor Potassium level and cerebral edema (esp. in children), correct acid-base imbalance • Administering IV fluids: (depending on MD order) such as 0.9% normal saline (start out with a bolus of this) and progress with 0.45% NS to hydrate the cells (depends on how dehydrated the patient is) o 5% dextrose may be added to the 0.45% NS when glucose is around 250 to 300 mg/dL. This will help gradually bring the blood sugar down and help the insulin do its job by removing the ketones. • Administered insulin: REGULAR (only type given IV) and make sure K+ is normal >3.3 o Typically started out by giving unit IV bolus…then start an infusion (checking blood glucoses around the clock…hospital protocols)…you will be titrating the insulin base on blood glucose checks. ▪ NOTE: if you rapidly bring a patient’s blood glucose down (or up) the brain can’t cope and water will be moved from the blood to the CSF and you will get cerebral edema and increased intracranial pressure Tip for insulin administration: when priming tubing for insulin infusion waste 50cc to 100cc (per institution protocol) because insulin absorbs into the plastic lining of the tubing. • Watch potassium levels very closely because insulin causes K+ to move back into the cell • Administer Potassium solution IV to combat this….note renal function before administering. Diabetes Mellitus Lecture Notes for NCLEX Review Key Players: Glucose: • “Sugar” (body needs it to survive) fuels the cells of your body so they can work properly, BUT IT CAN NOT ENTER THE CELL WITHOUT THE HELP OF INSULIN • It is stored mainly in the liver in the form of glycogen Insulin: • “deals with high blood sugar levels” • A hormone that helps regulate the amount of glucose in the blood (too much glucose is very toxic to the body). • It allows your body to use glucose by allowing it to enter the cells (without insulin glucose would just float around in your body) • Secreted by the BETA cells of the pancreas from the islets of Langerhans Glucagon: • “deals with low blood sugar levels” • A peptide hormone that causes the liver to turn glycogen into glucose…does the opposite as insulin. • Also secreted by the pancreas Pancreas: • Releases insulin and glucagon Liver: • Sensitive to insulin levels and stores and turns glycogen into glucose when the pancreas secretes glucagon. Example: (if the body has increased blood glucose/increased insulin in the blood the liver with absorb and store the extra glucose for later….if there is low blood sugar/low insulin levels the liver will release glycogen which turns into glucose to help increase the blood sugar level) Glucagon and Insulin Feedback Loop 1. Increased blood sugar -> pancreas releases insulin -> causes glucose to enter into the cells to be used or be saved as glycogen for later (stored mainly in the liver) 2. Decrease blood sugar -> pancreas release glucagon -> causes the liver to release glycogen which turns into glucose to increase the low blood sugar level What happens in diabetes mellitus? The body is unable to use glucose due to either the absence of insulin or the body’s resistance to use insulin. Therefore, the patient becomes HYPERGLYCEMIA (the glucose just hangs out in the blood stream which affects major organs of the body) The body starts to metabolize FATS for energy (since it can’t get to the glucose… remember glucose can NOT enter the cell without the help of INSULIN)….which happens in Type 1 diabetics OR there is a moderate amount of insulin to deal with fats and proteins BUT carbs cannot be used (Type 2). Causes of Diabetes Mellitus Divided into types: Type 1: the beta cells located in the islet of Langerhans don’t work (been destroyed) therefore the body doesn’t release anymore insulin. For treatment, the patient MUST USE INSULIN. Risk factors: Genetic, auto-immune (virus) NOT RELATED TO LIFESTYLE (like type 2) What do patients look like clinically? Patients are young and thin….happens suddenly; ketones will be present in the urine Type 2: cells quit responding to insulin (won’t let insulin do its job by taking the glucose into the cell). Therefore, the patient has INSULIN RESISTANCE. This leaves all the glucose floating around in the blood and the pancreas senses there’s a lot of glucose present in the blood so it releases even more insulin. Due to this the patient starts to experience hyperinsulinemia which caused metabolic syndrome Treatment: diet and exercise (first line treatment)…when that doesn’t work oral medications are started Note: The type 2 diabetic may NEED INSULIN DURING STRESS, SURGERY, OR INFECTION Risk Factors: Lifestyle- being obese, sedentary, poor diet (sugary drinks), stress AND genetic What do patients look like clinically? Patients are overweight, it happens overtime, rare to have ketones (remember issues with carb metabolism) adult aged Gestational: similar to type 2 diabetes where the cells are not receptive to insulin… typically goes away after birth Complications of Diabetes Mellitus Hypoglycemia: • Blood glucose less than 60 mg/dL or drops rapidly from an elevated level. • Remember the mnemonic: “I’m sweaty, cold, and clammy….give me some candy” • Signs and Symptoms: Sweating, clammy, confusion, light headedness, double vision, tremors • Treatment: Need simple carbs if they can eat, or if unconscious IV D50 • Simple carbs include: hard candies, fruit juice, graham crackers, honey Organ Problems: Hardens the vessel (atherosclerotic….makes vessels hard from all the glucose that sticks on the proteins of the vessels and it forms plaques). So the patient can develop heart disease, strokes, hypertension, neuropathy, poor wound healing (FROM DECREASE circulation), eye trouble, infection. DKA (Diabetic Ketoacidosis): • Happens in Type 1 diabetics (rare to happen in type 2) • There is no insulin in the body and the body starts to burn fats for energy since it can’t get to the glucose • Due to this the ketones, which are acids, start to enter into the body and this causes life-threatening situation, such as acid/base imbalances • Signs and Symptoms of DKA: N&V, excessive thirst, hyperglycemia, Kussmaul breathing HHNS Hyperglycemic hyperosmolar nonketotic syndrome: • Happens mainly in Type 2 diabetics • This presents with hyperglycemia without the breakdown of ketones…so there isn’t acidosis/ketosis because there is just enough insulin present in the body to prevent the breakdown of fats • Signs and Symptoms of HHNS: very dehydrated, thirsty, hyperglycemic, mental status changes Assessment Findings of DM 3 of Hyperglycemia P’s & SUGAR Hyperglycemia: Three P’s Polyuria: (frequent urination) Why? elevated levels of glucose in the body causes the body to remove the water from inside the cell (remember in the hypertonic, hypotonic video about OSMOSIS). The water will move to an area of higher concentration which will be the blood stream and this causes more fluid to enter the blood stream. The kidneys will secrete the extra water. HOWEVER, normally your kidneys could handle all of the glucose by reabsorption but there is too much so it leaks into the urine…. GLYCOSURIA Polydipsia: very thirsty Why? the blood is trying to prevent the body from becoming dehydrated from the excessive urination so it signals to the patient to drink more water…but it doesn’t work because the kidneys will remove the excess water Polyphagia: very hunger Why? the body is burning FAT for energy since it doesn’t have any glucose to use so the body signals to the person to keep eating so there will be food to use for energy. The patient will have WEIGHTLOSS! *The 3 P’s present mainly in Type 1 Diabetics Other Assessment findings of the Diabetic Patient Remember “Sugar” Slow wound healing blUrry vision (damaged from glucose on eyes) Glycosuria (kidneys can’t reabsorb all the extra glucose) Acetone smell of breath (from burning ketones) *type 1 Rashes on skin DRY and itchy, repeated vaginal infections (yeast….loves glucose) Sickle Cell Anemia NCLEX Review What is Sickle Cell Anemia? It is where a person has abnormal hemoglobin S (normal hemoglobin is hemoglobin A) on their red blood cell. This type of hemoglobin is very sensitive to oxygen changes, which causes the red blood cell to change it’s shape. This can lead to many complications (sickle cell crisis). Sickle cell anemia is the most common and severe form of sickle cell disease. How do people get sickle cell anemia? They’re born with it! The person inherited two hemoglobin S genes from EACH parent. Therefore, it is an autosomal recessive disorder. Again, this means in order for sickle cell disease to occur in a person they must have received TWO abnormal hemoglobin S genes for each of their parents (one from each). This disease is HOMOGYZOUS (Hemoglobin SS). The parents normally don’t show signs and symptoms of the disease. They will each possess Hemoglobin A and S (one NORMAL hemoglobin and one ABNORMAL hemoglobin). This is known as SICKLE CELL TRAIT. It is rare for people who have sickle cell trait to show signs and symptoms of the disease because they usually have just enough normal hemoglobin to prevent sickling of the red blood cells. However, if two people with sickle cell trait have a child, there is a 25% chance the child will develop sickle cell disease. Which patient population is most affected by sickle cell anemia? Sickle cell anemia is most common in African-Americans. WHY? According to the CDC.gov, it’s because 1 in 12 African-Americans in the US have the sickle cell trait, so it can easily be passed to their offspring. Other patient populations affected by this genetic disorder include: Middle Eastern, Asian, Caribbean, and Eastern Mediterranean. How is sickle cell trait diagnosed? This disorder tends to be diagnosed in the very young pediatric populations…..like at 6 to 8 months of age. Many times (usually around 6 to 7 months) a parent will notice that their baby is all of the sudden extremely fussy (like the child is in constant pain), feverish, and has unusual swelling in the hands and feet (dactylitis…hand-foot syndrome). These signs and symptoms present because the baby’s RBCs have started to sickle and cause extreme pain. The sickling decreases blood flow to the extremities (hence hands and feet) and organs. Now WHY is this occurring now and not at birth or around 2 to 3 months? Because in utero and during the first 6 months of age, the baby has fetal hemoglobin (remember this because we talk about this type of hemoglobin for the treatment of this condition with the medication Hydroxyurea) in their system that is the main carrier of oxygen. However, around the age of 6 months this type of hemoglobin diminishes and the type of hemoglobin their genetic code gave them takes over…..which is unfortunately hemoglobin SS. Sickle cell anemia testing is part of newborn screening in most hospitals. Tests used include: Dithionite (Sickledex): a blood test that assesses for abnormal hemoglobin S…it doesn’t differentiate between if the person has sickle cell trait or sickle cell disease. Therefore, a hemoglobin electrophoresis will need to be performed. This is a blood test that assesses for various types of hemoglobin. Pathophysiology of Sickle Cell Anemia How should a red blood cell NORMALLY look? It should be round, smooth, concave with flat centers on both sides and contain no nucleus. Because the RBC doesn’t contain a nucleus it can easily squeeze through our vessels to accomplish its job. What’s one of the jobs of the RBC? To carry oxygen…..and it does this with the help of HEMOGLOBIN! For a RBC to achieve this, it must have hemoglobin A present so the shape of the red blood cell won’t change. However, people with sickle cell anemia don’t have this type of hemoglobin. Yes, their red blood cells have hemoglobin, but it’s a different type called hemoglobin S, which causes the red blood cell to be stiff, sticky, and form a “sickle” type shaped, especially when there is a low amount of oxygen in the body causing the patient to experience a sickling episode (sickle cell crisis). These RBCs can stick together so well they will cause circulation problems, AND this is when signs and symptoms will manifest themselves in a sickle cell patient. It is important to remember that most patients with sickle cell anemia will usually just have anemia and they won’t have major signs and symptoms until a crisis episode. When the RBCs sickle, this abnormal shape causes the red blood cell to become stuck in vessels (blocking blood flow)…so organs and tissue suffer….which leads to many signs and symptoms, especially pain. Where does the ANEMIA part come in? Red blood cells with hemoglobin S are very weak and easily rupture. They only live 20 days compared to the normal 120 days. The bone marrow cannot keep up with producing RBCs, so the patient is anemic. Factors that can cause Sickle Cell Crisis: remember these There are various types of sickle cell crisis, which occur when there is something causing the body to increase its demands for oxygen OR there is something affecting how oxygen is transported. “Sickle” Significant blood loss…surgery, trauma etc. Illness (at risk for this due to spleen function being affected) Climbing or flying to high altitudes Keeping continued stress (physical or mental) Low fluid intake (dehydrated) Elevated temperature…..fever, strenuous exercise (extreme temperature changes like cold weather or cold water….like swimming in cold can lead cells to sickle) Types of Sickle Cell Crisis: • Vaso-occlusive: fever, pain, edema in the hand and foot (seen in babies)….RBCs sticking together blocking blood flow which can lead to decreased circulation to organs, tissues along with infarction (stroke, renal issues). • Hyperhemolytic: destruction of RBCs at an accelerated rate….remember these RBCs are weak. When RBCs rupture they release bilirubin. Normally, the body (gallbladder and spleen) can keep up with the recycling of the RBCs and clean-up of bilirubin. However, this is not the case here in SCA…the patient can experience jaundice, gallstones, anemia etc. • Aplastic: the halt of red blood cell production….bone marrow cannot keep up with producing red blood cells so the patient will cease in making RBCs….the patient will have anemia. • Non-functional spleen: the spleen helps recycle old RBCs and filters the blood to kill foreign invaders. In SCA, the spleen can become congested with sickled RBCs, which leads it to swell and not work properly. The patient is at risk for infection and many patients will need their spleen removed. Crises vary among patients….some can have them randomly, while others have them frequently. Signs and Symptoms of Crisis in Sickle Cell Anemia Dactylitis (early sign seen in babies at 6 months): hand-foot syndrome….blood flow being blocked to hands and feet…will be swollen and fever present Pain (very severe)….back, joints, chest etc. comes in episodes Anemic: RBC dying too soon: fussiness, tired, tachycardia, jaundice or pale (for dark skinned patients assess mucous membranes), delayed growth, shortness of breath Infection risk: spleen recycles old RBCs and helps us fight infection by filtering out foreign invaders….sickled RBCs become trapped in spleen and this leads it to swell and not work properly…..at risk for infection, especially pneumonia (needs pneumococcal vaccine and flu, meningococcal)….some patients need a splenectomy Gallstones: WHY? sickled RBCs are constantly breaking down and releasing bilirubin, which leads to gallstones because there is too much bilirubin for the gallbladder to manage Stroke: if sickled RBCs stick together and block blood flow to the brain…blood supply is limited to the brain leading to a decrease in brain blood supply….can cause mental and physical disabilities….NEURO checks very important. Eye problems: vision issues due to the blockage of blood flow to eye vessels from sickled cells (needs eyes checked regularly) Risk for abnormal clotting due to an increase in blood coagulation: at risk for DVT or PE Leg ulcers (older children and adults): lack of blood flow…painful and very slow healing Acute chest syndrome (happens due to infection like pneumonia or embolism or sickled cells blocking perfusion to lung tissue): chest pain, cough, fever, low oxygen saturation, new chest x-ray infiltrate….very deadly…monitor respiratory status Also, damage to the organs that depend on high blood flow: kidneys, liver, heart…blood flow limited Nursing Interventions for Sickle Cell Anemia Sickling of RBCs occuring: focus hydration, oxygen, pain, at risk for infection, monitor respiratory status, neuro checks, at risk for acute chest syndrome, prevention of future crisis episodes, medications, blood transfusions Pain: opioids around the clock (PRN not the best at this time until crisis over) IV fluids and oral fluid: dilutes blood and helps kidney function (blood flow is being limited because RBCs are sticking together) Oxygen: remember RBCs are stressed because of the lack of oxygen….this helps with alleviating the sickling Penicillin: prevents infection or other antibiotics to treat (some MDs will order some patients to take prophylactic doses of PCN to prevent infection because their risk)…. if patient develops acute chest syndrome due to pneumonia may be ordered antibiotics. Blood transfusion to replace RBCs and helps with anemia and increases oxygen levels in the body…….for multiple transfusions watch for iron overload Bed rest Educate about preventing infection (needs vaccines to be up-to-date, hand hygiene, avoid extreme weather and physical activities, mental/physical stress, staying hydrated, avoiding smoking, high altitudes) Keep extremities elevated and extended to prevent swelling and helps blood flow Remove restrictive clothing because it decreases perfusion Warm compresses (not cold leads to sickling) for painful areas Folic acid administration: helps make RBCs…..NOT iron….this doesn’t help with this type of anemia but can actually build up in the body causing toxicity and harm to organs Medication for Sickle Cell Anemia: Hydroxyurea: this helps actually treat cancer, but it will help with SCA in that it will help create fetal hemoglobin (hgb F). This helps decrease sickling episodes and this protein is present at first til 5-6 months of age, which is why babies don’t start showing signs and symptoms until after then. It will also help with anemia (decreasing the need for blood transfusions)….Side effect: lowers WBC count Stem cell transplant: to cure….bone marrow will make healthy RBCs…needs a matched donor Angiotensin II Receptor Blocker (ARBs) Review Lecture Angiotensin 2 Receptor Blockers NCLEX Review Always ask yourself these 5 questions when you see a drug name to help you understand how the drug works, your role as a nurse, and what information will be asked on an exam about the drug: Name (specifically the family name)? This will tell how the drug works. Used for? This will tell you WHY the drug was ordered…what condition is this medication treating in your patient? Responsibilities as the nurse? This will tell you what your role is as the nurse and what you need to monitor in the patient. Side effects? Know the common side effects of the medications Education pieces for the patient? As the nurse we play a HUGE role in educating our patients on how to take the drug, what to watch out for, and when to call the doctor. Now, using those 5 questions let’s go over what you need to know about ARBs for exam: Name? ARBs: Angiotensin II Receptor Blockers Medications end with “SARTAN” Examples: Losartan, Valsartan, Olmesartan, etc. How these drugs work? They affect the end result of the renin-angiotensin- aldosterone system(RAAS) by blocking the activation of angiotensin II receptor type I sites (AT1 receptors). This will prevent angiotensin II from binding to these receptors site. These receptors can be found in the vessels of smooth muscle and adrenal glands Angiotensin II receptor type I sites are responsible for VASOCONSTRICTION and triggering the release of ALDOSTERONE by the adrenal cortex, which helps increase the blood volume. There is also angiotensin II receptor type II sites but ARBs do NOT work at these sites. What are the results of Angiotensin II receptor type I activation? It causes vasoconstriction of vessels in the body , which increase the blood pressure and triggers the release of aldosterone by the adrenal cortex to increase blood volume (this causes the kidneys to keep sodium and water but excrete potassium). How do ARBs affect RAAS? Low blood pressure occurs -> Kidneys release RENIN into circulation -> causes ANGIOTENSINOGEN (a protein created and released by the liver) to convert to ANGIOTENSIN I -> then a substance called ANGIOTENSIN-CONVERTING ENZYME (ACE) converts Angiotensin I to -> ANGIOTENSIN II Angiotensin II receptors type 1 readily receive the angiotensin II produced by the RAAS, and as noted above, vasoconstriction and the release of aldosterone will occur to help increase the blood pressure. What happens in the RAAS when a patient takes an angiotensin II receptor blocker (ARB)?These medications will PREVENT the activation of the angiotensin II receptor type 1 sites. Therefore, angiotensin II can’t do its job. Since ARBs block the activation of these receptor sites, it will cause the opposite effects: • Dilate vessels (decrease SVR and blood pressure) • Decreases the secretion of aldosterone so there is no increase in blood volume but actually a decrease in blood volume because the kidneys will excrete sodium and water but keep potassium (watch for elevated potassium levels). Now, let’s quickly look at how ACE inhibitors work vs. angiotensin II receptor blockers? ACE Inhibitors tend to cause a dry, persistent cough in SOME patients. When this occurs a physician may switch the patient to an ARB. Why do some patients experience a dry, persistent cough with an ACEI rather than an ARB? First, let’s talk about ACE. ACE stands for angiotensin-converting enzyme, and its job is to convert Angiotensin I to Angiotensin II. ACE Inhibitors prevent the conversion of Angiotensin I to Angiotensin II (which is an active vasoconstrictor). ACE also inactivates bradykinin by breaking it down. Bradykinin is an inflammatory substance. However, when a patient takes an ACE Inhibitor it will prevent this inactivation process and cause bradykinin levels to increase. Bradykinin leads to a dry, persistent cough in some patients. However, this doesn’t occur with ARBs because these medications do NOT inhibit ACE (so bradykinin is inactivated). Used for? • Hypertension • Slows down the progression of diabetic nephropathy in type 2 diabetics (ACE inhibitors do this as well): diabetic nephropathy is kidney disease in diabetics. These patient’s kidneys don’t work properly and can’t manage protein so it leaks into the urine. o ARBs and ACEI decrease the blood pressure, which will decrease the amount of protein in the urine, and this will help delay the progression of the renal disease in the type 2 diabetic. • Heart failure: these medications make it easier for the heart to pump by decreasing afterload and preload. Responsibilities of Nurse? Assess blood pressure and pulse routinely (watch for hypotension…SBP less than 90, especially if the patient is also taking diuretics or other cardiac medications or if they are hypovolemic/dehydrated). Monitor labs: • Potassium level (hyperkalemia….normal potassium 3.5-5) • Renal failure (in patients at risk…example: severe heart failure patients because these patients are dependent on the RAAS for maintaining cardiac output) o Elevated BUN and Creatinine, low urinary output <30 cc/hr, fluid retention…edema o Normal BUN: 5-20 o Normal Serum creatinine: 0.6–1.2 mg/dL • increased liver enzymes….watch in patient at risk for liver failure Monitor for Angioedema (very RARE for it to occur with an ARB compared to an ACE Inhibitor): This is swelling deep in the skin (dermis and subcutaneous tissue) …..very dangerous! • Signs and symptoms: swelling on face (mouth, eyes, tongue, lips, dyspnea, swelling of extremities)….most commonly occurs in African American patients. Side effects? dizziness (change positions slowly), hypotension, high potassium level, GI upset Education? • Check blood pressure and pulse regularly (daily the best)… always record it and bring readings to check-up with doctor • Avoid salt substitutes with potassium, and if on potassium sparing diuretics like spironolactone, especially avoid consuming foods high in potassium like… potatoes, pork, oranges, tomatoes, avocados, spinach, bananas because this medication can increase potassium levels. • Don’t skip doses or abruptly quit taking because this can lead to rebound hypertension • If taking for hypertension: educate about following healthy lifestyle changes because anti-hypertensive medications do NOT cure high blood pressure (ex: exercising, healthy diet, quit smoking) • Lower chance of angioedema (very rare) but still educate about (swelling in the face, mouth, lips and difficulty breathing) ACE Inhibitors NCLEX Review Always ask yourself these 5 questions when you see a drug name to help you understand how the drug works, your role as a nurse, and what information will be asked on an exam about the drug: Name (specifically the family name)? This will tell how the drug works. Used for? This will tell you WHY the drug was ordered…what condition is this medication treating in your patient? Responsibilities as the nurse? This will tell you what your role is as the nurse and what you need to monitor in the patient. Side effects? Know the common side effects of the medications Education pieces for the patient? As the nurse we play a HUGE role in educating our patients on how to take the drug, what to watch out for, and when to call the doctor. Now, using those 5 questions let’s go over what you need to know about ACEI for exam: Name? ACE: Angiotensin-Converting Enzyme Inhibitors Medications end in PRIL • Examples: Captopril, Lisinopril, Ramipril, Quinapril, Benazepril How these drugs work? They inhibit the RAAS (renin-angiotensin aldosterone system). Goal of the RAAS? To manage our blood pressure by activating a substance that naturally occurs in our body called Angiotensin II. How it does this? Low blood pressure occurs -> Kidneys release RENIN into circulation - > causes ANGIOTENSINOGEN (a protein created and released by the liver) to produce ANGIOTENSIN I -> then a substance called ANGIOTENSIN-CONVERTING ENZYME (ACE) converts Angiotensin I to -> ANGIOTENSIN II ACE Inhibitors prevent the conversion of Angiotensin I to Angiotensin II (which is an active vasoconstrictor). Now let’s talk a little more about this ACE and Angiotensin: ACE: converts Angiotensin I to Angiotensin II and it inactivates bradykinin by breaking it down (note: inhibiting ACE will increase the amount of bradykinin) • Bradykinin: is an inflammatory substance that dilates vessels but increased amounts of it are thought to lead to the dry, persistent cough experienced with ACEI. Angiotensin II: • Causes major vasoconstriction of the vessels (increases SVR and blood pressure) • Trigger the release of ALDOSTERONE o Causes the kidneys to keep water and sodium but excrete potassium. Since ACE Inhibitors block the role of angiotensin II, it will cause the opposite effects: • Dilates vessels (decrease SVR and blood pressure) • Causes kidneys to excrete water and sodium (has somewhat of a diuretic effect) but KEEPS potassium (risk for hyperkalemia) Used for? • Heart failure (systolic dysfunction): this is when the left ventricle can’t pump blood forward out of the heart very well. This will cause the blood to back flow into the lungs, increases the work load on the ventricle which will enlarge it, and decrease cardiac output. o These medications will decrease afterload (the resistance the ventricle must overcome to pump blood out and forward). ACEI will lower the systemic vascular resistance and make it easier for the heart to squeeze blood forward. Also, they will decrease preload (the amount the ventricles stretch once they’re filled with blood at the ending of the filling phase (diastole). • Hypertension • After a myocardial infarction: these medications will help limit the damaging effects on the heart muscle caused by the damage of the infarct. Responsibilities of Nurse? Assess blood pressure and pulse routinely (watching for hypotension, especially if patient is taking diuretics or other cardiac medications). Monitor labs: • Potassium level (hyperkalemia….normal potassium 3.5-5): hyperkalemia can cause EKG changes like: Tall peaked T waves • Renal failure: Elevated BUN and Creatinine and low urinary output <30 cc/hr o Normal BUN: 5-20 o Normal Serum creatinine: 0.6–1.2 mg/dL Watch for Angioedema: This is swelling deep in the skin (dermis and subcutaneous tissue)…..it’s very dangerous! • Signs and symptoms: swelling on the face (mouth, eyes, tongue, lips, dyspnea, swelling of extremities)….can occur in any person but most commonly occurs in African American patients. Assess how patient is tolerating the medication? Is the patient having a dry, persistent cough that they can’t tolerate? Some patients can tolerate it. They should NEVER just quit taking the medication because rebound hypertension can occur, but the patient should talk with the MD about switching to another medication like an ARB (angiotensin II receptor blocker). • Also, for patients who are taking an ACEI for heart failure the nurse would need to further investigate that the persistent cough isn’t exacerbation of heart failure. When this occurs fluid builds up in the lungs because the heart is too weak to pump it forward. Signs and symptoms of this include: crackles during auscultation, decrease in oxygen saturation, difficulty breathing on excretion etc. Side effects? Persistent dry cough, dizziness (change positions slowly), hypotension, high potassium level, angioedema (life threatening) Education for Patient? • Check blood pressure and pulse regularly (daily the best)… always record it and bring readings to check-up with doctor. • Avoid salt substitutes with potassium. If also taking potassium-sparing diuretics like Spironolactone, avoid consuming foods high in potassium like…potatoes, pork, oranges, tomatoes, avocados, spinach, bananas. • Dry persistent cough can occur…if bothersome notify MD…don’t just stop taking due to rebound hypertension!! • Don’t skip doses or abruptly quit taking (some patients may quit taking due to irritating cough)….this will lead to rebound hypertension. o Missed dose? take when remembered that same day….if remembered not until the next dose take that day’s scheduled dose but never double doses due to risk of severe hypotension. • Report immediately: if experiencing any type of swelling of face or mouth, difficulty breathing…this could be angioedema. Stages of Shock NCLEX Review What is shock? This condition results from some type of cause (discussed below) that leads to decreased tissue perfusion, which causes cell hypoxia. If the cell hypoxia is severe enough it will cause organ dysfunction (MODS) and eventually lead to death. The cause of shock depends on what type of shock is presenting. The types of shock include: • Septic shock: occurs due to a severe infection • Hypovolemic shock: occurs due to severe fluid loss • Neurogenic shock: occurs due to severe damage to the neuro system (example: spinal injury) • Cardiogenic shock: occurs due to a weak heart • Anaphylactic shock: occurs due to an allergic reaction Note: Distributive shock includes septic, anaphylactic, and neurogenic shock. Stages of Shock What are the stages of shock? Initial, compensatory, progressive, and refractory Initial Stage Big Takeaway from this Stage: Cardiac output is low enough to cause the cells to experiencehypoxia. The cells will SWITCH from AEROBIC to ANAEROBIC metabolism. Anaerobic metabolism will create LACTIC ACID, which will accumulate in the blood and lead to lactic acidosis. Signs and symptoms of shock in this stage are very subtle compared to the next stages. Let’s analyze this stage: A type of shock is presenting! Therefore, we have a cause that has led to DECREASED TISSUE PERFUSION. Hence, we’re going to have LOW cardiac output. What is cardiac output? It’s the amount of blood the heart pumps each minute. It is calculated by taking the heart rate and multiplying it by the stroke volume and this equals the cardiac output. In this stage, the cardiac output is just low enough where tissue perfusion is unable to support the oxygen demands of the cells that make up the tissues/organs. Remember the cells that make up our organs and tissues have to constantly be receiving fresh oxygen and other nutrients to survive. When they don’t receive these substances, they start to take matters into their own hands by……. Switching the way they metabolize! The cells will switch to anaerobic metabolism (metabolism WITHOUT oxygen ) from aerobic metabolism (metabolism WITH oxygen). Why do they do this? Because they don’t have any oxygen to use because they aren’t receiving it…remember tissue perfusion is decreased. What’s the downside of anaerobic metabolism? It produces a waste product called LACTIC ACID. Normally, our body can deal with lactic acid via the liver, but the liver is not functioning at an optimal level because of the low amount of oxygen its cells are receiving. In better circumstances when tissue perfusion is adequate, the liver takes lactic acid and convert it to pyruvic acid and then to glucose via gluconeogenesis. Therefore, lactic acid will start to accumulate in the blood (especially as the patient advances to the other stages of shock). The accumulation of lactic acid causes the blood’s pH level to drop (hence acidosis occurs) and it further damages the cells. Important lab values to remember: • Normal serum lactate level <1 mmol/L • Abnormal indicating lactic acidosis >4 mmol/L Compensatory Stage Big Takeaway from this Stage: The body systems are coming to the RESCUE!! Hence, they are going to “try” to compensate by using the body’s natural built-in survival team: the hormonal, neural, and biochemical processes in the body. Be sure to remember what substances are being released and how they affect the body during this stage. This built-in system will try to fight the results of anaerobic metabolism. In addition, it will attempt to increase the cardiac output and blood pressure via the stimulation of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS), which will increase tissue perfusion (this is what the patient needs right now so the cells can receive oxygen and live). Let’s analyze this stage: If the cause of shock is corrected during this stage (hence a patient with hypovolemic shock receives fluid replacements that correct the fluid status of the patient), this stage is REVERSIBLE and the patient can make a full recovery. However, if the cause is NOT corrected the patient will enter the next stage. The body will succeed at first with increasing cardiac output and blood pressure via the rescue team discussed above. This will result in an increase in tissue perfusion, BUT the body is limited on how long it can maintain this rescue effort. How does the body provide compensation? As the blood pressure drops (hence cardiac output becomes very low), the body will sense this and say “Okay, the amount of blood the heart is pumping per minute it WAY too low, especially for our vital organs (mainly the heart and brain), so we must ACT now!” One of the structures to sense this drop in blood pressure is the baroreceptors, specifically the receptors in the carotid sinus and aortic arch. This will stimulate the sympathetic nervous system to release the catecholamines: epinephrine and norepinephrine. What do these catecholamines do? They cause vasoconstriction! This will result in an increase in blood pressure and heart rate. When this occurs there is increased perfusion to the vital organs. Less blood will go to the non-vital organs (GI, renal, skin, lungs), while more will go to the vital organs (heart and brain). Furthermore, because there was a drop in blood pressure (hence arterial pressure), there will be a decrease in capillary hydrostatic pressure. What does capillary hydrostatic pressure mean? In a nutshell, it’s the force of pressure the blood creates around the capillary wall. If the blood pressure and cardiac output are low, the force of pressure the blood creates around the capillary wall is definitely low. This will signal to the body to try to increase venous blood return by shifting fluid from the interstitial compartment to the intravascular compartment. Think of it this way: it’s like the body is trying to give itself a natural IV fluid bolus. By doing this, the body is attempting to increase cardiac output and the blood pressure, which will increase tissue perfusion. Now let’s talk about how other systems are affected and how they play a role in the compensatory stage: Kidneys: because blood flow is decreased to the kidneys they activate the renin- angiotensin system. What this system does? Renin stimulates angiotensinogen which creates angiotensin I. Angiotensin I turns into Angiotensin II. Angiotensin II is a very mighty vasoconstrictor. This substance will cause vasoconstriction in both the arterial and venous system. The constriction in the venous system will lead to more blood return to the heart, and the constriction in the arterial system will increase blood pressure. All this together will lead to an increase in tissue perfusion and the cells will receive more oxygen. The presence of angiotensin II will also trigger the release of ALDOSTERONE. What does aldosterone do? It makes the kidneys KEEP sodium and water. Why does this matter? It will increase blood volume! In addition, because the kidneys are keeping sodium, it will create the urine to contain a high amount of sodium, which leads it to have a high osmolality. The high osmolality signals to the posterior pituitary gland that the body is trying to keep water for some reason, so it releases ADH (antidiuretic hormone). What does ADH do? It prevents water from leaving the kidneys. Hence, further increases BLOOD VOLUME. By increasing blood volume, the cardiac output by the heart will be increased along with tissue perfusion. Notice that all the systems trying to rescue the body from shock are trying to release substances that will increase cardiac output or increase blood volume because it knows that if it can do this it will increase tissue perfusion. GI: perfusion is decreased to this system so it slows down. The patient is a risk for paralysis of the intestines in a condition called paralytic ileus. Skin: perfusion is decreased so blood flow is low, which leads the skin to be cold and clammy. Now, this is not the case during this stage in SEPTIC SHOCK. The patient’s skin will be hot and flushed due vasodilation presenting. Lungs: perfusion is decreased so parts of the lung may not be perfused. Now, ask yourself what do the lungs do? They perform gas exchange. If some parts of the lungs are not being perfused, gas exchange is not going to occur in those parts. So, there is a ventilation and perfusion mismatch and oxygen levels will become low in the blood. This will lead the patient to hyperventilate (they are trying to compensate by increasing the rate and depth of breathing in an attempt to increase the oxygen level). Progressive Stage Big Takeaway from this Stage: the rescue effort in the previous stage has FAILED, and the body can’t compensate anymore. The patient is progressing to MODS (multiple organ dysfunction syndrome). There is no more compensation in this stage. Therefore, cardiac output is low, tissue perfusion is low, and the cells are NOT receiving oxygen, which this leads to cell hypoxic injury. Think of this stage by body systems and how each system is failing because of cell hypoxic injury. The cells will start to swell (the ion pumps are failing) and CAPILLARY PERMEABILITY is increased. The patho in this stage really deals with capillary permeability. Literally, the flood gates have been opened from the intravascular space to the interstitial space. Fluids and proteins will be drawn into this space and this will lead to major edema throughout. In addition, this will deplete blood volume (therefore undo everything the body attempted to do in the previous stage). In other words, when the blood volume decreases it decreases the cardiac output and tissue perfusion. Let’s analyze this stage: Brain: cells to the brain are not being perfused. The mean arterial pressure is < 60 mmHg. This means the cerebral perfusion pressure (CPP) is inadequate to maintain perfusion to the brain’s cells. When this happens, you will start to see major mental status changes. The patient will be very slow in their speech, restless, anxious, agitated, and not respond to stimulation. Lungs: ARDS (acute respiratory distress syndrome) will develop. In a nutshell, this occurs due to increased capillary permeability in the alveoli sacs (this is where gas exchange occurs). The alveoli sacs will collapse due to the fluid surrounding them and the lung will lose its elasticity. The patient will need intubation and mechanical ventilation to breathe. The patient will have fluid in the lungs (crackles), increase respiratory rate, decrease oxygen level, and respiratory failure. Heart: the cells that make up the heart start to die. This includes the cells that play a role in the electrical conduction system of the heart and that help the heart contract/pump. So, cardiac dysrhythmias occur along with death to myocardial tissue. GI: cells that make up the gut start to die. For example, the cells that protect the lining of the gut from its own acid, start to quit working. Consequently, ulcers can develop which can turn into massive gastrointestinal bleeding (which isn’t good because clotting abilities will be affected due to liver hypoxia). Liver: the decreased perfusion to the liver causes the cells that make up the liver to die. The liver is a very important organ that plays a role in filtering germs, waste products, and drugs from our body. In addition, it plays a role with clotting factors. Therefore, when the cells that do these jobs are malfunctioning there is a build-up of toxic waste (bilirubin, ammonia etc.), risk for infection, and bleeding problems. DIC (disseminated intravascular coagulation): small clots will form in the vessels (further compromising blood flow to organs). This depletes the body’s platelets and clotting stores and leads to massive, uncontrollable bleeding. Watch for any type of oozing, especially around IV sites, central lines, blood puncture sites etc. Refractory Stage The word “refractory” means unmanageable. Therefore, once a patient enters this stage it cannot be reversed. All organs will shut down and fail. What was happening in the previous stage is going to be WORSE until the organs quits working. Death is inevitable. NCLEX Review on COPD Definition: pulmonary disease that causes chronic obstruction of airflow from the lungs Keys Point for COPD: • Limited Airflow (due to thick and swollen bronchioles that have become deformed with excessive sputum production and this narrows the airways) • Inability to fully exhale (due to loss of elasticity of the alveoli sacs from damage and the sacs start to develop air pockets) • Irreversible once developed…cases vary among people from mild to severe… managed with lifestyle changes and medications. • Happens gradually….most people start to notice signs and symptoms middle- aged and will present with dyspnea with activity they could normally tolerate, recurrent lung infections, chronic cough etc. • COPD is a term used as a “catch all” for diseases that limit airflow and cause dyspnea. Types of COPD include: • Emphysema “pink puffers” • Chronic bronchitis “blue bloaters” Pathophysiology of COPD Normal breathing: Inhaled oxygen travels down through the trachea which splits at the carina into bronchial tubes starting with the primary bronchus then into smaller airways called secondary and tertiary bronchi which divide into bronchioles and the oxygen goes into the alveolar sacs where gas exchange happens. As the alveoli inflate and deflate with ease, inhaled oxygen attaches to the red blood cells and carbon dioxide enters the respiratory system to be exhaled. What happens in breathing with COPD? In conditions such as chronic bronchitis “blue bloaters”: The name “blue bloaters” is due to cyanosis from “hypoxia” and bloating from edema AND increase in lung volume. The bloating is from the effects of the lung disease on the heart which causes right-sided heart failure. In chronic bronchitis, the bronchioles become damaged that leads them to be thick and swollen and deformed. This is accompanied by more sputum production. This limits the ability of the person being able to completely exhale the air taken in. So, when they take another breath in, it will increase the air volume even more (because they have retained air from the previous breath), and this leads to hyperinflation. Also, less oxygen is getting into the blood and more carbon dioxide is staying in the blood. This leads to low blood levels and high carbon dioxide levels. Patients will have cyanosis due to a decreased oxygen level. To compensate, the body increases RBC production and cause blood to shift elsewhere which increases pressure in the pulmonary artery leading to pulmonary hypertension. Pulmonary hypertension leads to right-sided heart failure (which is why you will start to see bloating..edema in the abdomen and legs) In conditions such as emphysema “pink puffers”: The name comes from hyperventilation (puffing to breathe) and pink complexion (they maintain a relatively normal oxygen level due to rapid breathing) rather than cyanosis as in chronic bronchitis. In emphysema, the alveoli sacs lose their ability to inflate and deflate due to an inflammatory response in the body. So, the sac is unable to properly deflate and inflate. Inhaled air starts to get trapped in the sacs and this causes major hyperinflation of the lungs because the patient is retaining so much volume. Hyperinflation causes the diaphragm to flatten. The diaphragm plays a huge role in helping the patient breathe effortlessly in and out. Therefore, in order to fully exhale, the patient starts to hyperventilate and use accessory muscles to get the air out now. This leads to the barrel chest look and during inspect it may be noted there is an INCREASED ANTEROPOSTERIOR DIAMETER. The damage in the sacs cause the body to keep high carbon dioxide levels and low blood oxygen levels. Inhaled oxygen will not be able to enter into the sacs for gas exchange and carbon dioxide won’t leave the cells to be exhaled. The body tries to compensate by causing hyperventilation (increasing the respiratory rate…hence puffer) and the patient will have less hypoxemia “pink complexion” than chronic bronchitis who have the cyanosis because pink puffers keep their oxygen level just where it needs to be from hyperventilation. Signs & Symptoms of COPD Remember: Lung Damage Lack of energy Unable to tolerate activity (shortness of breath) Nutrition poor (weight loss) due to energy used breathing especially with emphysema Gases abnormal (high PCO2 >45 and low PO2 <90)..respiratory acidosis Dry or productive cough constant (productive with chronic bronchitis) Accessory muscle usage during breathing, Abnormal lung sounds: diminished, coarse crackles (chronic bronchitis) or wheezing Modification of skin color from pink to cyanosis in lips, mucous membranes, nail beds (“blue bloaters”) Anteroposterior diameter increased (barrel chest)….emphysema “pink puffers” Gets in the Tripod Position during dyspnea (stands leaning forward while supporting body with hands on knees or an object) Extreme dyspnea In turn over time, people with COPD will be stimulated to breathe due to low oxygen levels RATHER than high carbon dioxide levels. Complications of COPD • Heart Disease (remember heart and lungs work together in replenishing the body with oxygen)…heart failure • Pneumothorax (spontaneous due to forming of air sacs) • Risk for Pneumonia • Cancer (especially lung) How is COPD Diagnosed? Spirometry: A test where a patient breathes into a tube that measure how much volume the lungs can hold during inhalation and how much and fast air volume is exhaled. • Measuring the FVC (Forced Vital Capacity): a low reading shows restrictive breathing….it measures the largest amount of air a person exhales after breathing in deeply in one second. • Forced Expiratory Volume: measures how much air a person can exhale within one second. A low reading shows the severity of the disease. Nursing Interventions for COPD Monitor Respiratory System: • Assess lung sounds (may need suction) and sputum production…obtain a culture if ordered…at risk for pneumonia • Keep oxygen saturation (88%-93%) why between this range? o Patients with COPD are stimulated to breathe due to LOW OXYGEN SATURATION rather than high carbon dioxide levels….which is the opposite for people for healthy lungs. If they are given too much oxygen it will reduce their need to breathe…causing hypoventilation and carbon dioxide levels will increase to toxic levels. • Given oxygen as prescribed in low amounts 1-2 liters • Monitor effort of breathing and teach about pursed-lip and diaphragmatic breathing • Pursed-lip breathing: used for when patient starts to get dyspneic. This technique increases the oxygen level and encourages them to breath out longer (remember these patient don’t fully exhale very well). It is similar to like blowing out a birthday candle. • Diaphragmatic breathing: uses abdominal muscles for breathing rather than accessory muscles o helps make diaphragm stronger which is weak o slows down breathing rate to allow breathing to be easier o decreases energy used to breathe o used along with pursued breathing technique • Administering breathing treatments as needed: bronchodilators, nebulizer etc. Respiratory therapy helps play a role in this as well (medications are discussed in more detail below) Patient Education for COPD • Nutrition needs: eating high calorie, protein rich meals that are small but frequent and staying hydrated if not contraindicated….avoid large heavy meals due to compression on the lungs from the stomach • Avoiding sick people, irritants, hot humid (smothering) or very cold weather • Stop smoking or being around people who smoke • Vaccination up-to-date: annual flu shot and Pneumovax every 5 years because it is very hard for people with COPD to recover from illnesses • Pursed lip and diaphragmatic breathing techniques • Administering medications: be familiar with groups, side effects, and patient teaching Medication Regime for COPD Remember the mnemonic: Chronic Pulmonary Medications Save Lungs Corticosteroids: decreases inflammation and mucous production in airway… given: oral, IV, inhaled and used in combination with bronchodilator like: • Symbicort: combination of steroid and long acting bronchodilator • Other corticosteroids: Prednisone, Solu-medrol, Pulmicort • Side effects: easy bruising, hyperglycemia, risk of infection, bone problems (long term use) o Patient education: rinse mouth after using inhaled corticosteroids…can develop thrush, use corticosteroid inhaler AFTER using bronchodilator inhaler Methylxanthines: Theophylline (most commonly given orally) type of bronchodilator used long term in patients who have severe COPD • Remember: Narrow therapeutic range of 10 to 20 mcg/mL • Increases risk for digoxin toxicity and decreases the effects of lithium and Dilantin Phosphodiestrace-4 inhibitors: “Roflumilast” used for people who have chronic bronchitis and it works by decreasing COPD exacerbation…not a bronchodilator • Side effects: can cause suicidal thoughts (remember the word “last” in the drug’s name…it could be the patient’s last days if they are not assessed for this side effect) and can cause weight loss. Short-acting bronchodilators: relaxes the smooth muscle of the bronchial tubes and are used in emergency situations where quick relief is needed • Albuterol (beta 2 agonist) and Atrovent (anticholinergic) Long-acting Bronchodilators: relaxes the smooth muscle of the bronchial tubes (same as short-acting bronchodilators BUT their effects last longer) used over a longer period of time….taken once or twice a day • Beta 2 agonist: salmeterol, anticholinergics: Spiriva • Patient education: let them know which drug is short and long-acting, how to use inhaler and to use bronchodilator inhaler BEFORE steroid inhaler (wait 5 minutes in between) o WHY? TO OPEN UP THE AIRWAYS SO THE STEROID CAN GET IN THERE AND DO ITS JOB • Side effects of beta 2 agonist: increased heart rate, urinary retention • Side effects of anticholinergic: dry mouth, blurred vision Chronic Kidney Disease What is CKD? It is a significant decline in kidney function that happens over a long period of time that leads to the build up of waste, water, and electrolyte imbalances in the body. CKD is irreversible. Role of the Kidneys: The kidneys receive fresh blood from the heart and filters the blood via the nephrons (glomerulus), which creates a filtrate/urine that will progress through the rest of the nephron (renal tubule). The renal tubule will fine-tune the filtrate by pulling out water and ions. Then the substances left over will be excreted in the urine. Remember the glomerulus does NOT normally filter blood cells or proteins (just water, urea, creatinine, ions). In addition, creatinine is the only substance filtered by the glomerulus that is solely filtered from the bloodstream that is NOT reabsorbed within the renal tubule. Therefore, measuring creatinine levels in the urine/blood help us to determine the functionality of the kidneys, specifically the nephron. The creatinine level along with the patient’s gender, race, weight, and age can help the physician determine the patient’s glomerular filtration rate (GFR). In CKD, the filtering structure of nephron (GLOMERULUS) is unable to filter properly. Therefore, the patient’s glomerular filtration rate (GFR) is decreased. There are various stages of CKD. A normal GFR is 90 mL/min or higher. This is the rate the glomerulus filters waste, ions, and water. Stages of Chronic Kidney Disease Be familiar with the GFR for each stage, especially stage 5, which represents ESRD (end-stage renal disease). Stage 1: Kidney damage with normal renal function GFR >90 ml/min but with proteinuria (3 months or more) Stage 2: Kidney damage with mild loss of renal function GFR 60-89 ml/min with proteinuria (3 months or more) Stage 3: Mild-to-severe loss of renal function GFR 30-59 mL/min Stage 4: Severe loss renal function GFR 15-29 mL/min Stage 5: end stage renal disease GFR less 15 mL/min *Source: “Kidney Disease Statistics For The United States | NIDDK” When GFR decreases dramatically it leads to many problems (in the early stages the patient may be asymptomatic): • Increased waste in the body: Uremia (Increased BUN and Creatinine levels, neuro changes, itching, metabolic acidosis) • Hypervolemia (edema, HTN, pulmonary and cardiac problems) • Electrolyte Imbalances: hyperkalemia, hypocalcemia, hyperphosphatemia (high phosphate levels cause low calcium levels, which stimulates the parathyroid gland to produce PTH. This causes calcium to leak out of the bones…hence bone problems), hypermagnesemia • Oliguria (less than 400 ml/day) or Anuria (less than 100 mL/day) • Proteinuria and Hematuria: glomerulus is damaged so it is allowing blood cells and proteins to leak through. The patient may have lower albumin levels (more swelling) and furtheranemia. Kidneys also produce hormones: EPO (erythropoietin): helps create RBCs in the bone marrow. In CKD, the EPO decreases, which leads to anemia. Renin: plays a role in increasing blood pressure. In CKD the glomerulus is filtering less water and the kidneys think the blood pressure is low, so it releases renin, which in turn increases blood pressure even more. Kidneys activate Vitamin D Vitamin D: plays a role in helping the body reabsorb calcium from the food we eat. In CKD, the activation of vitamin D is diminished and this leads to lower calcium levels (hypocalcemia). Causes of CKD • *High blood pressure (hypertension): constant high pressure on the artery wall that supplies the kidneys causes damage. Therefore, less blood reaches the kidneys and the nephrons can’t function properly. • *Diabetes Mellitus: uncontrolled hyperglycemia causes glucose to stick to arteries walls, which damages the blood supply to the kidneys. • Acute kidney injury • Polycystic kidney disease: genetic condition where cysts grow in the kidneys • Infection • Nephrotoxic drugs: NSAIDS, aminoglycosides, chemo therapy drugs, contrast dyes for testing procedures *most common causes of chronic renal failure Treatment for Chronic Kidney Disease: Early stages with normal GFR: • Controlling blood pressure and glucose level • Medications for hypertension that help protect the kidneys, such as ACE inhibitors “pril” or ARBs “sartan” • Monitoring GFR and blood pressure regularly Advanced stages where GFR is abnormal: • Dialysis • Kidney transplant • Diet changes Nursing Interventions for Chronic Kidney Disease What is going on with this patient? Remember waste build up (uremia and metabolic acidosis), anemia, electrolyte imbalances, low urinary output, and fluid overload. Uremia (build up of waste in the blood) • Safety: patient may be confused, assess neuro status • Itching: due to deposits of urea crystals on the skin via the sweat glands. It looks like frost on the skin and is called “uremic frost” • Low protein diet: urea is a waste product of protein breakdown (patient doesn’t need any more urea). However, patient needs some protein to prevent muscle wasting. • Assess for kussmaul breathing was is deep/rapid breaths from the acid building up in the blood (metabolic acidosis). This type of breathing is a compensatory mechanism by the respiratory system to increase the blood’s pH. Anemia: low red blood cells in the blood. RBCs help transport oxygen throughout the body so it can function. • Why is anemia presenting? Due to low amounts of EPO being produced by the kidneys and possible deficiency in other minerals that help with hemoglobin production (which acts a transporter for RBCs). These minerals include: iron, folic acid, and vitamin B12 • Patient signs and symptoms: pale, extremely tired, dyspnea, confused • Treatment: Supplements of Iron (IV form if patient on dialysis rather than PO), Erythropoietin (subq injections), or blood transfusions per MD order Electrolyte Imbalances: Hyperkalemia (>5.1 mEq/L): (normal level 3.5 – 5.1 mEq/L) at risk for significant cardiac event due to the nephrons decreased ability to excrete potassium. • Nursing Role: o restrict potassium-rich foods (potatoes, avocados, strawberries, tomatoes, spinach, oranges, bananas), monitor EKG for changes (tall peaked T-waves, Wide QRS and prolonged PR interval) o monitor lab values o may be ordered to give Kayexalate orally or rectally to remove extra potassium out of the blood o place on cardiac monitor to watch rhythm Hyperphosphatemia (>4.5 mg/dL): normal level 2.7-4.5 mg/dL Hypocalcemia (<8.6 mg/dL): normal level 8.6-10 mg/dL • Phosphate builds up in the blood because it cannot be excreted out of the kidney due to a damaged nephron, which leads to the decrease of calcium “hypocalcemia”. WHY? Because phosphate binds to the calcium and when there are high amounts of phosphate in the blood it depletes calcium from the blood due to this binding. In addition, calcium levels decrease due to the inactivation of vitamin d by the kidneys. • In addition, high phosphate levels stimulate the parathyroid gland to release PTH (parathyroid hormone), which causes the bones to leak calcium in the blood stream to increase the level. This can cause bone problems. • Nursing Role: o Administer phosphate binders, such as calcium carbonate or “PhosLo (calcium acetate)” to decrease phosphate levels. These medications works by excreting phosphate in the stool found in food. Give with meals or immediately after eating. o Diet low in phosphate: Restrict foods high is phosphate: poultry, fish, dairy, nuts, sodas, oatmeal. o Safety due to weak bones. Hypermagnesemia (>2.6 mg/dL): normal 1.6-2.6 mg/dL • Patient is at risk for EKG changes, tendon reflexes diminished or absent, lethargy. • Nursing role: o Avoid administering magnesium based antacids or laxatives o Low magnesium foods o MD may order IV calcium to help decrease level LOW UOP and Fluid Overload: • Monitor intake and output (strict) • Daily weights • Assess swelling and lung sounds “crackles” • Monitor blood pressure • Low sodium diet Acute Kidney Injury NCLEX Review What is Acute Kidney Injury? It is the SUDDEN decrease in renal function that will lead to the buildup of waste in the blood, fluid overload, and electrolyte imbalances. AKI can be reversible. Basics about the kidneys: Role of the kidneys? Filters the blood which creates a filtrate called urine. In addition, the kidneys regulate electrolyte levels, removes waste, and excessive fluid in the body. The kidneys normally do NOT filter blood cells or proteins. An adult normally voids 1-2 liters of urine per day. How do the kidneys create urine? Via the nephrons in the kidneys (the heart also plays a role in this, specifically the blood flow given by the heart to supply the kidneys with blood). Each kidney contains millions of nephrons. Each nephron receives fresh blood from the heart via an afferent arteriole. The nephron consists of two main parts: • Renal Corpuscle (function is to FILTER the blood and create filtrate..hence urine) o Glomerulus o Bowman ’s capsule • Renal Tubule (function is to REABSORB and SECRETE substances IN or OUT of the filtrate with the assistance of the peritubular capillaries) • Proximal Convoluted Tubule • Loop of Henle • Distal Convoluted Tubule • Collecting Tubule *In conclusion, there is the flow of substances back in forth from the nephron to the peritubular capillaries (circulation) until the filtrate is how the body wants it, and then it will leave the body as urine. Therefore, the tubules are crucial in deciding what should stay or go back into circulation. HOWEVER, when the nephrons are damaged as in INTRARENAL failure this mechanism is damaged and the patient will experience electrolyte imbalances, decreased glomerular filtration rate, decreased urinary output, azotemia (increase of BUN and creatinine in the blood…waste products). Urine consists of: • Water • Ions: sodium, chloride, calcium, potassium, magnesium, phosphate, bicarbonate • Creatinine* • Urea Lab work for determining kidney function: • *Creatinine: is a waste product from muscle breakdown and is solely filtered from the bloodstream via the glomerulus and is NOT reabsorbed or secreted within the nephron. Therefore, the rate of filtration of creatinine by the glomerulus helps us to determine the efficiency of the kidneys, which is why we collect blood levels to measure creatinine levels. Normal Creatinine level 0.6-1.20 mg/dL Increasing Creatinine in the body = the kidneys are NOT filtering properly • Creatinine clearance: the amount of blood the kidneys can make per minute that is free of creatinine. Normal creatinine clearance: 85-125 mL/min (female) & 95-140 mL/min (men) A creatinine clearance value along with age, sex, weight, race can help determine the GFR (glomerular filtration rate). • Glomerular Filtration Rate: rate of blood flow through the kidneys (ml/min). This shows how well the glomerulus is filtering the blood….great for determining kidney function. Normal GFR in adults: 90 or higher ml/min (remember this depends on the patient’s age, weight, creatinine, sex, and race) Normal GFR = normal urine output, normal BUN and creatinine, normal electrolyte and water balance Decreased GFR = low urinary output along with an increase in waste products in the blood (creatinine and BUN), electrolyte/fluid imbalances, and buildup of fluid • BUN (blood urine nitrogen): urea (measured as blood urea nitrogen) is a waste product from protein breakdown in the liver. It is secreted in the blood and filtered out through the kidneys. Normal BUN: 6-20 mg/dL (in AKI this level becomes greater than 20 mg/dL) Causes of Acute Renal Failure Prerenal Injury: issue with perfusion to the kidneys (any injury BEFORE the kidneys) • This leads the kidney function to decrease. The kidneys are deprived of nutrients to function properly and the amount of blood it can filter. This can eventually lead to intrarenal damage where nephrons become damaged. What can lead to decreased perfusion to the kidney? • Issues with the heart in conditions that decrease cardiac output as with an acute myocardial infarction. In this condition, the heart muscle is damaged and can’t pump sufficient amounts of blood to the kidney. • Other causes: massive bleeding (internally or externally), dehydration (hypovolemia…diarrhea, vomiting), burns etc. Intrarenal Injury: damage to the nephrons of the kidney (injury in WITHIN the kidneys) • When the nephrons are damaged the kidneys can’t filter the blood, maintain electrolyte levels, and remove excessive waste and fluid from the body. What can lead to the damage of the nephrons in the kidneys? • Nephrotoxic drugs: NSAIDS o Antibiotics “aminoglycosides o Chemo drugs o Contrast dyes used in procedures • Infection “glomerulonephritis” • Injury Postrenal Injury: blockage in the urinary tract after the kidneys to the urethra (injury found AFTER the kidneys) • This prevents urine from draining out of the kidneys, which leads to build up pressure and waste in the kidney and decreases their function. What can cause a blockage in this area? • Renal calculi • Enlarged prostate • A bladder doesn’t empty properly due to neuro damage “stroke” Stages of Acute Kidney Injury • Initiation: a cause creates injury to the kidney and then signs and symptoms start to appear which leads to the next stage. This stage lasts a few hours to several days. • Oliguric: *some patients skip this stage and go straight into the diuresis stage Urine output will be less than 400 ml/day Glomerulus is NOT filtering the blood properly: DECREASED GFR which will lead to the following signs and symptoms you will see in the patient: • Increased BUN and CREATININE: neuro changes, itching o NURSING Role: low protein diet (WHY? Remember urea is a waste product from protein break down in the liver), safety • Increased Potassium (hyperkalemia) >5.1 meq/L: due to the nephrons decreased ability to excrete potassium. It builds up in the blood and the patient is at risk for a significant cardiac event o NURSING Role: restrict potassium-rich foods, monitor EKG for changes (tall peaked T-waves, Wide QRS and prolonged PR interval), monitor lab values…may be ordered to give Kayexalate orally or rectally to remove extra potassium out of the blood), place on cardiac monitor to watch rhythm. • Increased fluid in the body: edema, at risk for fluid overload (pulmonary, cardiac issues: hypertension) o NURSING Role: restrict fluid intake, STRICT I and O’s, daily weights every day, assess swelling, heart sounds, lung sounds (crackles), monitoring respiratory rate and oxygen saturation, neuro status • Metabolic acidosis: blood pH less than 7.35 due to the decrease in the excretion of hydrogen ions by the nephrons. Patient may be confused and have kussmaul breathing. This is deep and rapid breathing. The respiratory system is trying to compensate by blowing off carbon dioxide (which is an acid) to help increase the blood’s pH. o NURSING Role: monitor respiratory and neuro status, safety • Mild hyponatremia (can be normal): diluted from fluid overload and decreased ability of the nephron to reabsorb sodium • High phosphorus and low calcium: nephron can’t regulate phosphate and calcium levels • Highly concentrated urine: high urine specific gravity >1.020 How long does this stage last? A week to 2 weeks. It is important this stage is as short as possible because the longer the patient stays in this stage the more of a risk of long term damage to the kidneys. Treatment: dialysis…this is where the blood will be filtered through a special machine that will act as the nephron to remove excessive waste, water, and electrolytes from the body. • Diuresis: Nephrons can’t concentrate urine (so it can’t regulate water and electrolyte levels yet) but they can filter out waste. So, what will be found highly concentrated in the urine? WASTE…specifically urea. This will cause OSMOTIC DIURESIS. The patient will be voiding out an excessive amount of urine (3-6 Liters/day) due to osmotic diuresis. This occurs from the high amounts of urea in the newly filtered filtrate. NURSING Role: strict I and O’s, daily weights, monitor for signs and symptoms of dehydration, HYPOVOLEMIA, hypotension. As the GFR improves (still abnormal) this will allow the BUN and CREAT to decrease but the levels will still be abnormal. Therefore, the patient’s azotemia will start resolving, and the patient will become more alert and oriented. Other signs and symptoms of this stage: Hypokalemia: per MD order may give supplements and IV fluids to prevent dehydration Urine diluted: low urine specific gravity <1.020 Lasts a week to 3 weeks • Recovery: Starts when GFRreturns to normal and the kidneys start to function normally. Urine output returns to normal along with BUN and creatinine, and electrolytes level. Therefore, the body is able to maintain these values. This stage can last a year or more, and it depends on the amount of damage done to the kidney and the patient’s age. Some patients are unable to progress to the recovery phase and instead develop Chronic Kidney Disease. Labs to Know for NCLEX Review Lab values to know for NCLEX and as a nurse or nursing student! This review will target the most important lab values you need to know for NCLEX and as a nurse. When you take the NCLEX exam there is a high probability you will have some type of lab value question. WHY? Because almost every patient that walks through the doors of a hospital will have blood work drawn, and as the nurse you will need to know about the common blood tests ordered and their normal lab value ranges. Therefore, the NCLEX wants to make sure you have competent knowledge in this area before you start working as a licensed nurse. What are the common blood tests? Metabolic Panel (BMP or CMP): This test can be basic or comprehensive, and it assesses fluid and electrolytesstatus along with glucose, renal and liver function. Complete blood count (CBC):assesses the amount of cells in the blood….platelets, white blood cells, red blood cells, hemoglobin, and hematocrit. Arterial Blood Gases (ABGs): assesses for acid-base imbalances in the body…this test is very important for patients with respiratory or metabolic conditions. Coagulation Levels: assesses clotting times (PT/INR or aPTT)…this is very important for many blood disorders and for patients who are on anticoagulants. Lipid Panel (Lipid Profile): assesses for the risk of cardiovascular disease by measuring lipoproteins, triglycerides, cholesterol. Hemoglobin A1C: assesses average blood glucose level during the past 3 months… great test to check glucose management in patients with diabetes. Drug Levels: assesses the amount of drug present in a patient’s system. Many patients are on drugs that have a very narrow therapeutic drug range. Therefore, this test is helpful in determining if a drug is subtherapeutic or toxic in a patient’s system. What to expect on the NCLEX exam with these lab values? On the NCLEX exam, you will be given lab values that are noticeably abnormal. For example, a normal Magnesium level is 1.5-2.5 mg/dL. On the NCLEX, it is highly unlikely they will ask you to choose an abnormal lab result of a Magnesium level that is 1.4 mg/dL or 2.6 mg/dL because these results are way too close to normal. They will give you something you will notice like <1 or >3 mg/dL. Another important thing to point out is that normal lab value ranges vary depending on the laboratory. So, don’t get confused on if one text says a normal Magnesium level is 1.4-2.6 mg/dL, while another text says a normal Magnesium is 1.5-2.5 mg/dL. Remember to be familiar with the average range and keep in mind NCLEX will test you on something that is very abnormal. How am I going to remember all of these lab values as a nurse? When you work as a nurse you will be encountering these labs every day, and pretty soon you will be able to recite them in your sleep. Plus, when you are looking at your patient’s results you will be able to see the normal reference range from the lab that processed the blood specimen. This will tell you the exact normal range and how abnormal this lab result is. Lecture Review on Lab Values Labs to Know for NCLEX and as a Nurse Metabolic Panel Glucose: 70–100 mg/dL Calcium: 8.5–10.5mg/L Chloride: 95-105 mEq/L Magnesium: 1.5-2.5 mg/dL Phosphorus:2.5–4.5mg/dL Potassium: 3.5-5 mEq/L Sodium: 135-145 mEq/L BUN: 5-20 Serum creatinine: 0.6–1.2 mg/dL Total Protein: 6.2–8.2 g/dL Albumin: 3.4–5.4 g/dL Bilirubin: 0.1-1 mg/dL (less 1) (formed with the breakdown of RBCs…high levels in patients with jaundice) — These are 3 enzymes found in the liver. If elevated, it can indicate liver problems and other diseases.— • ALP (alkaline phosphatase): 40-120 U/L (international units per liter) • ALT (alanine transaminase): 7 to 56 U/L • AST (aspartate transaminase) 10-40 U/L *this blood test can be ordered as a BMP (basic metabolic panel) or CMP (comprehensive metabolic panel). The CMP will include the liver function. Complete Blood Count RBC: 4.5–5.5 million WBC: 5,000–10,000 Platelets: 150,000–400,000 Hemoglobin: • 12–16 g/dL (women) • 14–18 g/dL (men) Hematocrit: • 37 – 47% (women) • 42 – 52% (men) Arterial Blood Gases (ABGs) pH: 7.35-7.45 pCO2: 35-45 mmHg HCO3: 22-26 mEq/L pO2: 80-100% O2 sat: 95-100% Coagulation Levels INR/PT: • PT (prothrombin time): 10-12 seconds (normal level for patients not on Warfarin) • INR (international normalized ration): Less than 1 (normal level for patients not on Warfarin). o When a patient is taking the anticoagulant Warfarin the INR should be 2-3. o The INR level is calculated from the PT level. aPTT (activated partial thromboplastin time): • Normal 30-40 seconds (not on Heparin) o If the patient is on Heparin, the aPTT needs to be 1.5 to 2.5 times the normal range. Lipid Panel (risk for cardiovascular disease) LDL (low density lipoprotein): <100 mg/dL (want it LOW) HDL (high density lipoprotein): >60 mg/dL (want it HIGH) Total Cholesterol: <200 mg/dL Triglycerides: <150 mg/ dL Hemoglobin A1C • 4-6% (target for patients without diabetes) • <7% (target for patients with diabetes) Drug Level Ranges Digoxin: 0.5-2 ng/mL Carbamazepine: 4-10 mcg/mL Dilantin: 10-20 mcg/mL Theophylline: 10-20 mcg/mL Phenobarbital: 15-40 mcg/mL Lithium: 0.5-1.2 mmol/L Valproic Acid: 50-100 mcg/mL NCLEX Review on Osteoarthritis What is osteoarthritis? It is the most common type of arthritis that develops due to the deterioration of the articular cartilage. Remember articular cartilage is hyaline cartilage. When this happens it leads to bone break down because the bones within the joint start to rub upon one another. This will cause changes inside and outside of the bone. The inside of the bone will start to experience abnormal hardening (sclerosis), and the outside of the bone will experience osteophytes formation (bone spurs). OA is from “wear and tear” on the body rather than from on overactive immune system, which is the cause in rheumatoid arthritis (it affects the synovium NOT hyaline cartilage in RA). What is bone cartilage? Bone cartilage is a rubbery, smooth tissue found within the joint that covers the end of each bone. It acts as a protective mechanism for movement by providing this slick surface for the bones to slide and glide during movement. In addition, it absorbs shock from movement. What happens in Osteoarthritis? The top layer of cartilage begins to breakdown and wear away. This leads to a loss of joint space within the joint, which allows the bones to grate upon each other. Therefore, there is no longer this environment that allows for easy gliding of bones during movement without friction. This leads to eroding of the bone and osteophyte formation. Furthermore, pieces of cartilage and bone can break off and float around in the joint space. All of this leads to extreme stiffness and pain. Key Points about Osteoarthritis to Remember: OA is also called degenerative joint disease and remember it is the CARTILAGE NOT synovium. It happens and worsens overtime. It tends to most commonly occur in the hands, knees, hips, and spine (majorly the weight-bearing joints which experience a lot of stress) and it does NOT affect other systems in the body and it’s unsymmetrical (a patient can have OA in both correlating joints or just one). Remember RA is symmetrical….it must be found in the correlating joint. Causes: • Occurs in older age 40+ • Increased risk if patient has had repeated joint injuries • Jobs that are strenuous • Overweight • Genetics There is no cure. It gets worse overtime and damage can’t be reversed (cases vary mild to severe). Managed with lifestyle changes (exercise/losing weight), medication, surgery (hip/knee joint replacement or bone realignment “osteotomy’, arthroscopic). No conclusive test to diagnose OA. Must evaluate patient’s signs and symptoms and rule out other forms of arthritis such as gout, rheumatoid arthritis. X-ray imaging may be helpful (remember a x-ray ONLY shows bones, it doesn’t show cartilage) • X-ray may show: sclerosis of bones, decreased joint space, osteophytes/bone fragments in the joint space, osteophytes (bone spur) formation. Signs and Symptoms of Osteoarthritis “Osteo” Outgrowths that are bony, especially on the hands due to bone spur formation (*remember the names of the nodes and where they are found): • Heberden’s Node (most common): found on the distal interphalangeal joint (joint closest to the finger nail) • Bouchard’s Node: found on the proximal interphalangeal joint (middle finger joint) Sunrise Stiffness (morning) LESS than 30 minutes (Remember RA is greater than 30 minutes)…pain will be the worst at the end of day from overuse than compared to morning time Tenderness when touching the joint site with bony overgrowths (joints will be BONY and HARD), NOT warm or boggy as with RA Experience grating (crepitus) of the bones when moving/flexing joint from bones rubbing together and joint pain with activity which goes away with rest Only the joints: Asymmetrical/Uneven , limited to joints (joint site will be hard and bony, NO warmth or boggy synovitis with red inflammation) along with limited mobility, not system wide, (no fever, anemia, fatigue, systemic inflammation…just the joints) Nursing Interventions for Osteoarthritis: Pain assessment: patient’s perception of the disease, effects of the disease on the patient’s activities of daily living, nonpharmalogical and pharmacological approaches Therapy: physical exercise is one of the most effective treatments for OA….may help create more lubrication to the cartilage allowing the pain and stiffness to decrease, strengthen muscles, help patient lose weight, feel better mentally Do NOT exercise painful, irritated joint but let it rest Exercise: this is the last thing most patients want to do but limiting activity and not exercising leads to more pain, increased joint damage, increased weight, and decreased mental health. • Types: o Low impact: walking, water aerobics o Strengthen training (lifting weights which helps strengthen muscles around the joint) o Range of motion exercises (ROM): improves the mobility of the joint and decreases stiffness • AVOID: high impact exercise that will increase the stress on weight bearing joints, such as running/jogging, jump rope, or any type of exercise where both feet are off the ground. Heat and cold compresses Importance of weight loss (BMI <25) Physical therapy and occupation therapy (using assistance devices to decrease weight bearing stress, exercise etc.), local support groups, structuring day to prevent overuse of joints Medications: Intra-articular injections: corticosteroids…more effective than oral: reduces the inflammation of the inflamed tendons and ligaments. Note: this is temporary relief of no more than a month or two. Glucosamine: improve symptoms and function Pain relief: topical creams, Tylenol, NSAIDs (GI bleeding/ulcers), controlled substances (opioids if severe) Rheumatoid Arthritis NCLEX Review What is rheumatoid arthritis? An autoimmune condition that causes inflammation in the joints. This inflammation specifically affects the membrane lining of the joint called the synovium. Rheumatoid arthritis can eventually lead to bone fusion. What is a joint? It is where two bones meet together. Rheumatoid Arthritis Stages: Synovitis: inflammation of the synovium WBCs invade the synovium, which causes it to become inflamed. This inflammation leads to thickening, and the formation of a pannus. Formation of a Pannus: A pannus is a layer of vascular fibrous tissue. The pannus will grow so large it will damage the bone and cartilage within the joint. The space in between the joints will disappear and anklyosis will develop. Ankylosis: This is the fusion of the bones. The patient will have major stiffness and immobility of the joint. Overview of Rheumatoid Arthritis The patient will have soft, tender, warm, and swollen joints. They will feel very tired (this leads them to be inactive) and have a fever. **Hallmark signs: RA affects the same joint bilaterally. Stiffness and pain will be worst in the mornings (>30 minutes of stiffness) or after long periods of inactivity and all types of joints can be affected. In the late stages bone deformity occurs (note the image below how the fingers are curved at the tops and it is symmetrical): Rheumatoid arthritis most commonly affects the fingers and wrist. It can also affect the neck, shoulders, elbows, ankles, knee, and feet. However, it just doesn’t affect the joints but can extend to the heart, skin, eyes, mouth, lungs, and cause anemia. Can happen at any age…most commonly 20-60 years old….not just in older adults as in osteoarthritis. Cases vary: some patient have severe chronic cases that last for life time. While others may have for a short time and it goes into remission. RA can come on suddenly or gradually over years. There is no cure for RA. This key is to catch it early to prevent the progression of joint damage. Treatment includes: • Medications: NSAIDs, corticosteroids, and DMARDs • Surgery (replacing the joint with an artificial one, removal of the synovium “synovectomy”, “arthrodesis” (joint fusion) where the joint is removed and the bones are fused together with a bone graft. It leads to the destruction of the joint within 2 years of the development of the disease, so it happens fast. Management with: • Lifestyle changes (developing plans for rest and exercise) • Joint support: splints, using assistive device • Stay healthy and low stress (cause flare-up) Cause not clear (genetic, environmental, or hormonal factors)…tends to affect women more than men Hard to diagnosis because symptoms may be associated with other diseases…tests typically ordered: • Positive rheumatoid factor, elevated erythrocyte sedimentation, C-reactive protein (inflammation is present the body…higher in people with RA), x-ray shows joint deterioration Signs and Symptoms of Rheumatoid Arthritis Seven S’s Sunrise Stiffness (severe pain) Soft feeling in the joints Swelling in the joint (warm) Symmetrical Synovium (affected and inflamed) Systemic (affects not only the joints…patient will feel achy, tired, and it can affect the lungs, heart, anemia etc) Stages (synovitis, pannus, anklyosis) Nursing Interventions for Rheumatoid Arthritis Nursing focus: • Pain (need to know how to treat the pain) • Preserving the joints (improving function and mobility, using assistive devices) • Education (medications and nonpharmacological treatment, the disease itself) • Mental status (dealing with depression and improving self-esteem, pain, alters life, no cure) Joint assessment Ask patient questions to help determine early on if this is RA: does it affect the symmetrical joints, when is the stiffness the worst? Educate patient about the disease (no cure but can be managed) and assess patient’s understanding about RA because management (exercise, medications) help improve quality of life and prevent further joint deterioration. Taking care of joints and decreasing fatigue: During flare-ups rest the joints that are inflamed (no exercise on the joint)…splints help with this along heat and cold treatments: • heat (best for stiffness)…heating pad or hot showers • cold (best for pain….helps reduce inflammation) Patient needs to maintain physical exercise as tolerated. This improves the fatigue and prevents a decrease in muscle strength. In addition, it prevents contractions by keeping the joints in motion. Patient needs to schedule times for rest and to never overexert themselves. Monitor for signs and symptoms of anemia (pale, fatigue, short of breath on excretion, palpations)….may be ordered supplements to promote RBCs production like iron, folic acid, vitamin b 12…at risk for GI bleeding due to medications NSAIDs….watch for dark, tarry stools Multidisciplinary approach: Physical therapy and occupational therapy will be part of the patient’s care to help assist with treatment plans. Patient needs to perform routinely ROM (range of motion) exercises and low impact aerobic exercise (stationary bike, walking, water aerobics) Use assistive devices (make sure the patient is using them correctly to promote safety…at risk for injury). These devices help alleviate stress on the joints. These devices include raised toilet seat, tools to help grab items, tools to help button or zip shirts, shower chair, cane, walkers etc. Medications for Rheumatoid Arthritis: combination of therapy may be used depending on the patient’s case NSAIDs: decreases inflammation and helps with pain • “Ibuprofen”: may cause GI distress…needs to be taken with food Corticosteroids: decreases inflammation • Dexamethasone (Decadron) • Methylprednisolone (Medrol) • Prednisone o Can be given by mouth, topical, IV, injection into the joint or IM o Skin become thins and fragile, bruises and tears easily….meticulous skin care o Watch for hyperglycemia, especially in diabetic patients o At risk for infection DMARDs (disease-modifying antirheumatic drugs): suppresses immune system from attacking the joint along with helping slow down the destruction of the disease on the joints and bones. • Hydroxychloroquine (Plaquenil) (monitor for vision changes…retinal damage) • Leflunomide (arava) • Methotrexate (Trexall) • Sulfasalazine (Azulfidine) DMARDS (biologic response modifiers): These drugs are still part of the DMARDs drug category but are genetically engineered and used in very severe cases. • Abatacept • Adalimumab • No live vaccines, avoid infection (handwashing, avoid crowds and sick people), keeping appointments to measure blood levels (wbcs), injection site will be sore… common to have site reaction Neurogenic Shock NCLEX Review What’s neurogenic shock? This type of shock leads to the inability of the sympathetic nervous system to stimulate nerve impulses, which causes hemodynamic problems. This leads to a decrease in tissue perfusion where the cells that make up our organs and tissue don’t receive enough oxygen. Hence, signs and symptoms of shock occur. Neurogenic shock is a type of distributive shock(anaphylactic and septic shock are the other types of distributive shock). This means that the vessels that deliver blood flow to the cells have an issue with distributing that blood flow. In neurogenic shock, it’s due to massive vasodilation because the sympathetic nervous system has lost the ability to stimulate nerves that control vessel vasomotor tone (this is the ability to regulate the diameter of the vessels…discussed in detail below). What can cause neurogenic shock? • Spinal cord injuries that are located at the cervical or upper thoracic locations (above T6) • Drugs that affect the autonomic and sympathetic nervous system • Spinal anesthesia Neurogenic shock is sometimes referred to as vasogenic shock. Pathophysiology of Neurogenic Shock Let’s talk about what is occurring in neurogenic shock, but first let’s do a quick review of the autonomic nervous system. The autonomic nervous system controls the functions we cannot consciously control like our heart rate, digestion, rate of breathing, pupil response, etc. It is divided into two systems called the: Sympathetic Nervous System (SNS) and Parasympathetic Nervous System(PSNS) The parasympathetic nervous system is known as the “rest and digest” system. It helps us relax by decreasing our heart rate and allows us to digest food, among other functions. The sympathetic nervous system is the “keep you alive or fight or flight” system! It increases the heart rate, blood pressure, dilates your pupils for better vision etc. Therefore, a HUGE role it plays is that it controls VASOMOTOR TONE. This means that the SNS regulates the diameter of our vessels. It will cause our vessels to constrict or dilate as needed, depending on the signals it receives from the body. Now, it’s very important to note that the PSNS and SNS are always balancing each other out to keep things regulate in our body. For example, if the SNS had to kick in to save your life, eventually it would have to slow down and this is where the PSNS system would help. Therefore, if one system is not working (as the case with neurogenic shock…the SNS is malfunctioning), the other system will be UNOPPOSED and in a sense take over, which is why many patients with neurogenic shock will have bradycardia. How does the sympathetic nervous system regulate the diameter of our vessels? The nerve fibers of the sympathetic nervous system branch out and hang out on the layers of the vessels. When nerve signals are fired, it will cause the neurotransmitters epinephrine and norepinephrine to be released. These neurotransmitters will cause the vessel to constrict (narrow). However, if there is a low level of nerve firing or NO firing, these neurotransmitters are NOT released, so the vessel just relaxes….hence dilates. This is the problem with neurogenic shock. The nerves are not being stimulated, so they are relaxed. This causes major problems! Why? Dilated vessels affect the blood pressure. When vasomotor tone is lost, vessel dilation occurs and this lowers systemic vascular resistance (SVR), which causes a major decrease in blood pressure (hypotension). Due to the decreased SVR and low blood pressure, blood pooling will occur in the vessels. This will DECREASE the amount of blood draining back to the heart (remember there is not pressure/resistance helping to push it back so it just hangs out away from the heart). What does this leave the heart to pump? Hardly anything at all! This will cause a DECREASE in tissue perfusion. In addition, this blood pooling will lead to a risk of deep vein thrombosis (DVT) development and lower the body core temperature (hypothermia). Why hypothermia? The blood is just sitting in the extremities cooling down and not returning to the core body to be warmed. These patients will have warm/dry extremities but a cold body. Why does this lead to a decrease in tissue perfusion? There is venous pooling of blood and not much blood will be flowing back to the heart because there isn’t any resistance making it go back. This will decrease cardiac preload (the amount the ventricle stretch at the end of diastole/filling phase) and cardiac afterload (resistance the ventricles must overcome to pump blood out of the heart and this is due to the decrease in SVR). Remember we discussed in our lecture on cardiac output that cardiac preload and afterload play a huge role with cardiac output because they affect stroke volume (the amount of blood the ventricle pumps with each BEAT), which affects cardiac output. CO is calculated by: CO = Heart Rate (HR) x Stroke Volume (SV) Cardiac output is the amount of blood the heart pumps per minute. When CO falls, so does the amount of blood that is rich in oxygen that flows to the cells that make up our tissues and organs. If cells don’t receive enough oxygen they start to die, and the patient starts to experience the classic signs and symptoms of shock. Also, hypothermia can occur due to the body’s inability to regulate the body temperature because of hypothalamus dysfunction. This is further complicated by the peripheral vasodilation and pooling of blood in the extremities (as discussed above). This will lead to heat loss because the blood isn’t returning back to the body to keep it warm. So, extremities will be warm and dry, but the body will be cold (poikilothermic: loses the ability to regular core body temperature). Bradycardia will occur too! The heart rate is controlled by both the sympathetic and parasympathetic nervous system. SNS increases the heart rate and PSNS works to decrease the heat rate. Therefore, they are both balancing out the heart rate. If we lose the function of the SNS, the PSNS will be unopposed and bradycardia will occur. Recap of the pathophysiology and the signs and symptoms in neurogenic shock: The major signs and symptoms you will see with neurogenic shock are… hypotension, bradycardia, hypothermia, warm/dry extremities but cold body Patho: One major function that is lost in neurogenic shock is the ability to regulate the diameter of the blood vessels. Therefore, the vessels are just relaxed (dilated). This will decrease systemic vascular resistance and hypotension will occur. Also, since the SNS isn’t working very well (which helps increase our heart rate) the parasympathetic system will take over (which decreases the heart rate)…so bradycardia will occur. Hypothermia occurs because of hypothalamus dysfunction and is further complicated by blood pooling in the extremities (remember this blood is sitting there and cooling off because it is not going back to the body). Warm/dry extremities can be found due to dilated vessels causing the blood to pool in the extremities. These signs and symptoms are slightly different than the other types of shock we have covered, especially in the early stages of shock. WHY? Remember during the early stages of shock in the other types of shock, the sympathetic nervous system kicks into gear to help “save” the body by causing vasoconstriction with the release of norepinephrine and epinephrine. This would increase the heart rate, blood pressure (in hope of increasing CO) etc. However, in neurogenic shock, this doesn’t occur because the body has lost the ability to stimulate the sympathetic nervous system due to this injury. Neurogenic shock is different from spinal shock because neurogenic shock causes hemodynamic changes with hypotension and bradycardia related to its injury. Whereas, spinal shock causes changes with sensation, motor, and reflexes. Neurogenic Shock Nursing Interventions and Treatments Goal: Manage patient’s ABCS (Airway, Breathing, Circulation & Spine) Protect the spine: Keep spine immobilized (don’t want to cause any more damage and decrease perfusion to the spine) Example: cervical collar, log rolling patient during transport, using a backboard May need intubation and mechanical ventilation if respiratory failure present (respiratory issues can occur depending on the location of the injury) Maintain tissue perfusion: want MAP to be 85- 90 mmHg. This helps maintain perfusion to organs, specifically the spine. (Dave and Cho, 2018) How? Intravenous fluids: crystalloids (fills the dilated vessels, increases venous return to the heart which will increase cardiac preload and cardiac output) • IVFs are used with caution because the patient usually has a normal blood volume. Therefore, monitor for fluid overload. o Example: dyspnea, crackles, swelling, increased CVP or PAWP • If no response with IVFs, then vasopressors may be used. Vasopressors: causes vasoconstriction (narrowing of vessels) which will increase SVR and increase blood pressure and cardiac output • Positive inotropes: Dopamine (vasoconstriction and increases heart rate) Bradycardia? Atropine • blocks the parasympathetic effects on the heart • If severe, the patient may need temporary pacing Rewarming devices for hypothermia: slowing with rewarming and monitor body core temperature Foley (some patients lose bladder function)…. Want urinary output 30 cc/hr or higher… this tells us how well the kidneys are being perfused Prevent DVT (blood is pooling) apply compression stockings, ROM (range-of-motion exercises), anticoagulants per MD order • Avoid crossing patient legs or placing pillow under patient’s knees because this further compromises circulation Guillain-Barré Syndrome NCLEX Review What is Guillain-Barré syndrome? It’s an autoimmune neuro condition where the immune system attacks the nerves in the peripheral nervous system and cranial nerves. What specifically is the immune system attacking? The immune system, which was attacking the illness (see more about this below), starts to confuse the cranial and PNS nerves for the illness. Therefore, the immune system begins to attack the myelin sheath (demyelination occurs) on the nerve cell. Remember the role of the myelin sheath? This structure helps with nerve transmission. The myelin sheath normally functions as an insulator to help nerve transmission. The myelin sheath are very helpful structures that unfortunately become attacked by the immune system, and when this occurs it leads to a decrease or complete absence in nerve signaling. Why is this happening? It is important to remember that GBS can happen to any person at any age! There is currently no cure, but treatment can help decrease signs and symptoms if started within 2 weeks of symptoms. With GBS, a previous infection usually has started it all! Many patients will start to have signs and symptoms of Guillain-Barré syndrome about 1-2 weeks AFTER some type of viral or bacterial infection or one of the following: So, as a nurse always complete a thorough health history: • Recent upper respiratory illness or gastrointestinal infection (especially Campylobacter jejuni) o An interesting statistic by CDC.gov, “As many as 40% of GBS cases in the United States are thought to be triggered by Campylobacter.” • Vaccine (swine flu etc.) • Surgery • Epstein-Barr virus HIV/AIDS, flu infection Various types of Guillain-Barré syndrome: Cases can vary from mild to very severe. • Acute inflammatory demyelinating polyneuropathy (AIDP): most common type in the US and what we will concentrate on in this lecture. It starts with paralysis/weakness/tingling sensation in the LOWER EXTREMIES (symmetrically) and migrates upward over time. It can be so severe the person will experience paralysis. Mnemonic for Guillain-Barré syndrome: “GBS” • Gradual • Blocking of • Sensation There is another type called: Miller Fisher Syndrome. Eye paralysis is usually the first sign and symptom with this type. What is happening in GBS? GBS: Gradual Block of Sensation Let’s talk Nerves (which helps explain signs and symptoms) Peripheral nervous system nerves are involved! Therefore, we’re talking about all the nerves outside the brain and spinal cord. The PNS creates a connection between our brain/spinal cord to the rest of our body (so our limbs, muscle, and some of the organs are involved). AIDP is the most common type of GBS in the U.S. Most patients start to have this weird tingling or numbness sensation (PARAESTHESIA) in their feet, which will gradually spread upward (symmetrically). Paralysis, absent reflexes, and loss of muscle tone is likely to follow the paresthesia. As a side note: It’s very important to note that GBS PEAKS in about 2 weeks with its severity of symptoms, and then slowly recovery occurs (remylenation of the myelin sheath). Nurse: reassure the patient and always communicate with them because patients who experience GBS are extremely fearful. In addition, it takes about 1-2 years for the patient to return to baseline (most patients have to complete some type of physical rehab after experiencing GBS due to the complications associated with it in regards to muscle atrophy and nerve damage). As the demyelination spreads, it can start to affect the autonomic nervous system of the PNS. Remember the PNS can be separated into the somatic nervous system (controls voluntary movement functions) and autonomic nervous system (involuntary functions). ***In severe cases of GBS, the autonomic system (parasympathetic and sympathetic nervous system) can be affected. Therefore, we’re talking about the nerves that regulate our blood pressure, heart rate/rhythm, temperature, vision, GI (constipation… decrease in motility of the GI system) and renal (retention of urine due to sphincter issues). Signs and Symptoms associated with autonomic dysfunction: • Inability to regulate body temperature • blood pressure issues (orthostatic hypotension and paroxysmal hypertension) • cardiac dysrhythmias Cranial nerves: In addition, there can be cranial nerve involvement, as it gradually migrates up to the area of the brain stem where the cranial nerves are located. This leads to vision problems, paralysis of the face, issues swallowing, trouble speaking etc. Let’s look at a typical scenario: A patient is 35 years old and has no pertinent information in their health history other than that they were sick about 2 weeks ago with a GI illness. However, they’ve recovered from it but now are presenting with this tingling, numbness, and weakness in the feet (called paresthesia) and it’s making walking difficult. They tell you they haven’t injuried themselves and the sensation is getting worst. This is how some patients may present with GBS (but this syndrome is just starting). As time goes on, you will find that these signs and symptoms start to migrate up and are symmetrical in origin. The patient’s reflexes will become majorly diminished or absent. This will affect the legs, arms, chest muscles used for breathing, face/eyes/swallowing ability (cranial nerves), and in severe cases the autonomic nervous system. As more time goes on the signs and symptoms go from weakness to paralysis (ex: paralyzed from neck down), lose muscle tone, absent reflexes, facial paralysis, issues swallowing, talking, weak cough (need suctioning, short of breath, reports they can’t breathe in very well) and autonomic issues. ****Respiratory system is a major focus for the nurse!!! When this system is affected, most patients will need to be intubated or have a tracheostomy for assistance to breathe. Monitor for signs and symptoms that this system is being affected. These signs and symptoms peak at about 2 weeks from when the symptoms started. Then slowly the signs and symptoms (remyelination of myelin sheath) start to resolve slowly. Most patients can make a full recovery within 1-2 years, but there are usually major complications afterwards due to paralysis that puts the patient on a long road to recovery. One important thing to point out that although the patient is experiencing paralysis or weakness, many patients will experience severe pain like muscle pain/ cramps. Exact reason not known….may be due to nerve damage. But it’s very important as the nurse to evaluate the patient for pain using some type of communication technique. However, because of severity of the muscle weakness most patients end up needing to be intubated (as stated above), develop infection (pneumonia from aspiration or ventilator acquired), at risk for blood clots and pressure injuries due to immobility, severe weight loss from nutrition issues, and will need intense physical therapy. How is Guillain-Barré syndrome Diagnosed? • Electromyography and nerve conduction studies: assesses for demyelination of nerves by determining muscle’s ability to respond to nerve stimulation • Lumbar puncture: elevated protein without elevated white blood cells. Nursing Role for Lumbar Puncture: • Before: empty bladder • During: position lateral recumbent with knees up to abdomen and chin to the chest • Post: lay flat per MD order (helps decrease headache)…head not to be elevated, patient needs fluids to help replenish fluid taken (help decrease a headache as well) Nursing Interventions for Guillain-Barré Syndrome Focus: Respiratory, blood clots (immobility) risk for PE and DVTs, heart rhythm, blood pressure issues, nutrition, infection (urinary retention and lung from vent or pneumonia), pain, pressure injuries, atrophy of muscles, extreme fear Collect a detailed health history Monitor for progression of the syndrome and if the patient is getting worst: • Spread of the paresthesia or paralysis? • Change in reflexes? • RESPIRATORY status (is it hard for the patient to talk, feel like they can’t breathe, can’t clear secretions, decrease respiratory rate, always having to suction patient?) o Have airway management equipment at bedside • Evaluate their swallowing…at risk for aspiration • Communication….patient is aware but can’t communicate…use a white board • Pain (severity and treat accordingly) • Pressure injuries due to immobility: need frequent turning to prevent pressure injuries • Prevent blood clots (SCDs, anticoagulants) • Intake and output (may need catheter to drain urine due to urinary retention) • Eye care due to facial paralysis (keep eyes moist with drops etc.) • Nutrition: assess bowel sounds (at risk for paralytic ileus), constipation (decrease in gastric motility )and may experience an increase in gastric residuals so always check prior to a new feeding)….most patients will have a feeding tube Management of airway with mechanical ventilation Pain control PT to work with and ROM to prevent muscle wasting and contractures Keep patient informed (this is scary…you usually have a once healthy person now experiencing severe paralysis and can’t breathe on their own….make sure you have some way to communicate because they will most likely be aware of everything going on and reassure this is most likely temporary) Treatments for Guillain-Barré syndrome Not a cure but helps speed up recovery: administered within 2 weeks from onset of symptoms….if greater than this time frame…doesn’t really help decrease signs and symptoms • PLASMAPHERESIS: machine that will filter the blood to remove the antibodies from the plasma that are attacking the myelin sheath (help decrease signs and symptoms not a cure) • Immunoglobulin therapy: IV immunoglobulin from a donor given to the patient to stop the antibodies that are damaging the nerves. Seizures NCLEX Review What are seizures? Seizures occur when abnormal electrical signals are being rapidly fired for neurons in the brain. This can happen throughout the brain affecting both sides (generalized seizure) or being located in a specific area of the brain (partial or focal seizure). Seizures can occur in anyone (children and adults) due to a severe acute condition, such as a high fever, illness (especially central nervous system types like bacterial meningitis), hypoglycemia, acid-base imbalances like acidosis, alcohol withdraw, brain tumor etc. Once the condition is corrected the seizures tend to stop. However, some patients can experience epilepsy. Epilepsy is where the patient has frequent seizures due to a chronic condition of some type like congenital brain defect, stroke, traumatic brain injury, long-lasting effects of an infection etc. Simplified Patho of Seizures In the brain, our neurons are tasked with handling and transmitting information. There are two types of neurons I want to discuss. These are excitatory and inhibitory neurons. Just like their name says, excitatory neurons produce “an action” or cause “excitement” by releasing a neurotransmitter called glutamate (this is an excitatory neurotransmitter). Inhibitory neurons “stop an action” or cause inhibition by releasing an inhibitory neurotransmitter called GABA. ***For seizure activity not to occur in a healthy brain, there needs to be a proper balance between these two types of neurons. If there is an imbalance of excitatory neurons vs. inhibitory neurons seizures will occur. For example, if there is not enough GABA (remember this is the inhibitory neurotransmitter) being released, too much excitation will occur leading to seizure activity. The reason I cover this is to help you understand how some of the anti-seizure drugs work to treat seizures. For instance, barbiturates stimulate GABA receptors which help control excitation and decreases seizure activity (more about medications below). Types of Seizures **remember these types for exams, especially their characteristics, expected duration, post ictus phase etc. Generalized: seizure is affecting both parts of the brain • Tonic-clonic (formerly called grand -mal): most common type of generalized seizure o May experience AURA (warning a seizure is about to happen) o Loses consciousness (at risk for injury) ▪ Will experience a tonic phase: body stiffens (may bite inside of the cheek or tongue….may see blood leaving mouth with foaming of saliva), breathing stops followed by cyanosis) ▪ Then a clonic phase: recurrent jerking (spasm and relaxation back- to-back) of extremities (patient may have incontinence of stool or/and urine) • Usually lasts no more than 3 minutes…..at risk for status epilepticus with this type of seizure ▪ ****if greater than 5 minutes or having multiple seizures in a row… activate emergency response team (will need immediate treatment to stop seizure (more on this in the nursing interventions) • Post ictus (duration: hours to days): this is the recovery period: patient will feel very tired, extremely sore from muscle stiffening and jerking, can’t remember what happened. Tonic seizure: (stiffening of the body….risk for falling) or Clonic seizure: (jerking….can be symmetrical or asymmetrical ) Absence Seizure (formerly called petit-mal) • Most common in pediatric patients and Hallmark is a staring like state o It will be like the child is just daydreaming but can’t be snapped out of it….can go unnoticed by others for a while because it short and the child won’t remember it. The person will look confused and won’t be able to talk during the even. • Very short…..seconds • Post Ictus: immediate…doesn’t remember staring off Atonic (drop attacks): • “A” means without and when you put the word tonic after it the meaning is: WITHOUT MUSCLE TONE o The patient goes limp and falls if standing or slumps over if sitting…at risk for head injury (may need helmet) • Usually not aware during event….post ictus: immediate…regains consciousness Myoclonic: • Quick duration of jerking of the muscles • Patient usually aware and conscious (this is what makes it different from a clonic seizure) • Very short….few seconds Focal (also called partial): affects a specific part of the brain Two types: know the main differences which is that with focal onset aware (simple partial) the patient is AWARE of their surroundings but with focal impaired awareness (complex partial) the patient is NOT aware of their surroundings AND will have motor symptoms called automatisms. Focal Onset AWARE (simple partial): symptoms vary depending on where the seizure is located • It tends to be a small area of a lobe…but patient is AWARE…example: occipital region the person may have vision changes • Also sometimes called an aura too because it can happen right before focal impaired awareness (complex partial) Focal Impaired AWARENESS (complex partial): alternation in awareness and has motor symptoms • Temporal lobe most commonly involved • Focal onset aware (aura) can happen before it • Automatisms present: this is where they are performing an action without knowing they are doing it like lip smacking, rubbing hands together, or grasping for something that isn’t there Stages of Experiencing a Seizure We can divide how a person experiences a seizure into stages (it varies depending on the seizure type, so remember that) Prodromal: when symptoms start to appear prior to the big event (hence seizure) • can start days before a seizure happens • mood changes (depression, anger, issues sleeping, anxiety, GI and urinary issues etc.) Aura: doesn’t happen with all types • happens at the very beginning of the seizure (what type: focal seizures OR in a tonic-clonic seizure) • happens within seconds to minutes before a seizure • many times it gives the patient time to prepare self for seizure. As the nurse (if you are present) help the patient lay down onto their side with a pillow under the head. • Symptoms vary among patients but can include: sudden weird smell or taste, déjà vu feeling, feeling anxious like something bad is about to happen, altered vision (lights or spots in vision) or hearing (hallucination type sounds or increased ability to hear sounds), dizzy (different for every person), inability to speak etc. Ictus: (word means seizure) this is the actual seizure • Usually lasts anywhere from 1 to 3 minutes • Time the seizure o seizures greater than 5 minutes or if the patient starts having seizure back-to-back, the patient may be experiencing status epilepticus (will need medical care and medication to make the seizure stop…it will unlikely stop on its own) Post Ictus: (after the seizure) brain is going to rest and recover from the seizure • usually last hours to days (tonic clonic)…..for some patients it is immediate (absence) • may feel extremely tired, sleepy, confused, headache etc. Nursing Interventions for Seizures Assess risk factors for seizure (remember any patient can experience this if any of the causes mentioned above are presenting…you want to be prepared. If risk factors present initiate seizure precautions: • Seizure precautions may include: o at bedside have suction and oxygen ready o IV access (to given anti-seizure medication, if needed) o padded side rails o pillow under head (to protect head) o bed in the lowest position o remove objects that can cause injury (remove any restrictive clothing or items the patient may be wearing….eye glasses etc. ) Assess if your patient has a history of seizures in the past and if so what type of seizure, ask if the patient experiences prodromal signs and symptoms or an aura before the seizure, how long does the seizure last? If patient is able to report prodromal or aura….help patient prepare by getting the patient in a safe position by lying down on their side. What to do when your patient has a seizure? Protect patient if they are standing-up or sitting down by: • gently lying the patient down and turning them onto their side. WHY? This helps prevent the tongue from covering the airway and helps saliva and blood drain from the mouth. • DO NOT restrain patient or try to hold the patient down • Protect their head and extremities (pillow and bed pads will help with this) • DO NOT put anything in the patient’s mouth • Remove anything that can impede breathing or break (eye glasses, tight clothing etc. ). ****Questions to be asking yourself during the seizure**** • Note the time it started and time it stopped (VERY IMPORTANT: if greater than 5 minutes or another seizure happens…THINK: status epilepticus and activate the emergency system response team. You will notify the MD of the seizure regardless because the seizure needs to be investigated….is the patient’s drug level for anti-seizure medications too low? • When the seizure started what was the patient’s behavior right before and during it? (did they cry out, become confused, report an aura, become unconscious) and the characteristics of the body movements (if any) presented at the beginning and throughout the seizure…..stiffening of the whole body or just the extremities and then jerking or just jerking, was it on just one side or both sides of the body….be sure to be as detailed as possible…this helps the healthcare team determine what type of seizure this was and what treatment may be needed • Did the patient become incontinent of urine or stool? Oxygen status (cyanosis present) Your role during the Post Ictus stage: Note the time the seizure stopped and how the patient is behaving afterwards: • Are they tired (let them sleep and rest), confused, can’t think or talk, have a headache (ask where it is located and pain rating), has any injuries (some patienst may bite their tongue or cheek) • Maintain airway (suction, administer oxygen) • If a tonic-clonic seizure, the patient will be very sleepy, won’t remember what happened. • Assess vital signs and neuro status: pupils, reflexes, is patient confused or oriented • Clean patient if incontinence was experienced. • Document and report it to the physician… is this your patient’s first seizure, are they on anything for seizures (is drug level not therapeutic….may need to draw a drug level if ordered by MD) EEG may be ordered: What’s an EEG?: assesses brain activity • Painless • Hold seizure medications or medications that are stimulants or depressants prior to EEG (these medications can prevent the proper assessment of abnormal brain waves associated with a seizure) • No caffeine products (a stimulant) 8 hours before • Can eat before • Make sure patient’s hair is clean (needs good attachment to scalp) • Different types of EEGs: some patients will need to experience sleep deprivation before the test by not sleeping the night before the test or only part of the night….always ask about this Education to patient about factors that can trigger a seizure: “Stop Seizure” Stress Trauma to the head Overexertion Period, pregnancy (hormones) Sleep depravation Electrolyte and metabolic issues (hypoglycemia, dehydration, acidosis) Illness (high fever) VisualiZation disturbances (strobe lights, certain smells or sounds) Under medicated with seizure med (remind patient importance of taking and coming to office visits to get drug levels drawn) Recreational drugs ETOH use Medications/Treatments Medications treat based on type of seizure: Barbiturates: Phenobarbital (used tonic-clonic or focal seizures & status epilepticus) • stimulates GABA receptors & this helps inhibitory neurotransmission • side effects: drowsiness, uncoordinated movements (ataxia) etc. • watch for: respiratory depression and hypotension • drug level 15 to 40 mcg/mL Hydantoins: Phenytoin (used in tonic-clonic or focal seizures) • watch the gums: will enlarge and easily bleed (called gingival hyperplasia….teach about good mouth care • may cause bone marrow suppression (watch platelets and WBCs) • tell patient to watch for rash or Steven-Johnson’s Syndrome and to REPORT it to their doctor immediately • don’t give with milk or antacids (interferes with absorption) • 10 to 20 mcg/mL Benzodiazepines: absence seizures, tonic clonic, focal • Diazepam or Lorazepam: status epilepticus (fast acting) • Very drowsy, tolerance can develop where it isn’t as effective, impair liver (monitor liver studies) • Reversal agent: Flumazenil Valproates: Valproic Acid • all types….monitor liver, WBC and platelets, GI issues Other treatments: • surgery: to remove an area of the brain that is causing the seizure….example: focal seizures that arise from temporal lobe (temporal lobectomy) • Meds not working: placement of a vagus nerve stimulator: an electrical device that sends electrical signals to the vagus nerve • Ketogenic diet (used in pediatric patient who have epilepsy): high fat, low carb, diet….used when seizures not controlled by medication Multiple Sclerosis NCLEX Review What is multiple sclerosis (MS)? It’s an autoimmune disease that affects the myelin sheath of the central nervous system (CNS). This leads to inflammation and scarring of the nerve, which causes a decrease in nerve transmission. This is why many patients experience sensory and motor problems. Quick Facts about Multiple Sclerosis: • It’s an autoimmune condition, which means the immune system is actually attacking the myelin sheath found on the nerve. • It affects the nerve cells in the brain and spinal cord, and this leads to many sensory and motor type problems. • Symptoms vary among patients because different areas of the central nervous system are affected. o For example, if the patient has lesions (damage to the myelin sheath)in the cerebellar area, the patient may experience tremors, dysarthria (issues with articulating words…muscles for speech aren’t working well), ataxia (trouble controlling body movements), and cognitive issues. o Furthermore, if the nerve to the eyes (optic nerve) is being affected the patient will have vision issues like blurry vision or blindness in one eye etc. • Women tend to be affected more than men, and MS seems to show up in the age category of 20-40s. • Symptoms can appear and then disappear. This is the most common form of MS where signs and symptoms come and go called: relapsing-remitting multiple sclerosis (RRMS) • Exact cause is not totally known • There is currently no cure, but there are lifestyle changes and medications that can improve signs and symptoms. How is Multiple Sclerosis Diagnosed? Diagnosing (takes time): the neurologist has to assess several things because there is not one test that can diagnose it: • Assessing patient’s symptoms…may need to rule out other diseases • MRI to assess for lesions in the brain and spinal cord • Lumbar puncture: assesses spinal fluid for specific proteins called oligoclonal bands (which are immunoglobulins). If these are present it shows there is inflammation in the CNS. • Evoked potential studies (sends electrical signals to the CNS and sees the response). Pathophysiology of Multiple Sclerosis You have to understand the anatomy and physiology of the nerve cell (neuron) in the central nervous system. Dendrites: receive the signal needed to create some type of action. This signal goes down to the: Soma: (which means body) and this structure helps pass on the signal it just received from the dendrites to the rest of the neuron. Then the signal goes down and passes where the soma of the neuron and axon connect at the axon hillock. Then the signal goes down this long area known as the axon. For the axon to be able to deliver this signal properly to either another neuron, muscle, or gland, it must be nicely be insulated and protected by the myelin sheath, which is made up of Schwann cells. These cells consist of fats and proteins. ****This is our problem with MS (the myelin sheath has experienced demyelination)…..so guess what?! The signal is NOT being transmitted properly to the area that the nerve supplies!! After the signal leaves the axon in a healthy neuron it goes to the axon terminal (the end of the axon) where it synapses (where a nerve signal passes) with another neuron, muscle or glands to cause an action of some type. So, in MS we’re talking about the nerve cells in the CNS, which is our BRAIN and SPINAL CORD…..because of this we can expect to finding sensory type problems (touch, vision), coordination, emotional, cognitive, and bowel/bladder issues For sign and symptoms let’s divide them by category. Remember signs and symptoms vary in patients depending on where the lesions have occurred due to demyelination. Signs and Symptoms of Multiple Sclerosis Emotionally and cognitive: drained (feel weak), fatigued, depressed, trouble articulating speech (issues swallowing), mood swings, trouble thinking (focusing, solving, keeping thoughts etc.) Sensation issues: • involuntary tremors, spasms (painful and strong), clumsiness (leads to unintentional injury), numbness/tingling (face and extremities) • electric shock sensation that travels down the body when moving head or neck in various position called “Lhermitte’s sign” • dizzy, muscles hard to move (stiff)….affects coordination (cerebellum area) • unable to be aware of body positon (proprioception) when eyes are closed….Romberg’s Sign…patient puts feet together and closes eye…this causes them to sway Vision: nystagmus (issues with controlling eye movement), optic neuritis (early) double vision…blurry vision or vision is gray (dull colors), blindness in one eye, and seeing dark spots in vision, painful when moving eyes Elimination (nerves are affected that control the bladder/bowel and their sphincters): • can’t hold urine….overactive bladder (incontinence) leads to nocturia • problems urinating…hesitancy leads to retaining urine (at risk for UTI’s and renal stones) • bowel: constipation/diarrhea or incontinence Early signs and symptoms of MS include: vision issues, tingling numbness, weakness, dizziness, balance issues, bladder problems, cognitive issue…issues speaking, weakness, spasms ****Symptoms can get worse due to heat called Uhthoff’s sign. Heat can be from the weather, physical exercise etc. Nursing Interventions for Multiple Sclerosis Nursing considerations: safety (vision, coordination, decrease perception with pain), RRMS (most common form of MS)….preventing symptoms from worsening, bladder and bowel issues, medications Preventing symptoms from getting worse: • Watch the heat (keep room cool, avoid heating blankets, pads etc.), avoid infection, stressful events, and getting too tired…overexertion (pace out activities and take time to have many rest periods) Very important to maintain regular exercise as tolerated…not too much because it can exacerbate symptoms (swimming…water aerobics, …keeps energy and mood level up) Use assistive devices to help with walking and preventing injury (toileting and showering) when symptoms are presenting, clutter free environment, especially when vision affected or experiencing vertigo, scan environment if experiencing blindness in one eye or dark spots Consult SLP (helps with speech if speech is slurred or hard to understand, difficult swallowing), PT (exercises, assistive devices), support groups with others who have MS Bladder and bowel: make accessibility to bathroom easy due to overactive bladder, may need to learn how to self-cath if retaining urine, plenty of fluids to prevent stasis of urine and to keep it from becoming too concentrated 1-2 L, high fiber to prevent constipation…stool softeners Medications for Multiple Sclerosis **Medications vary depending on what symptoms the patient is having…medications treat symptoms…. don’t cure disease • Beta interferon: decreases the number of relapses of symptoms by decreasing inflammation and the immune system response ….risk of infection because decreases WBC Drug Names: Avonex (interferon beta 1a), Rebif, Betaferon • Corticosteroids: for relapses of symptoms…methylprednisolone (solu-medrol), prednisone • Bladder issues: Oxybutynin: anticholinergic that helps with an overactive bladder…relaxes bladder to prevent contractions Bethanechol: cholinergic that helps with completely emptying the bladder by helping bladder contract fully. • Fatigue: Amantadine (antiviral and antiparkinson but has CNS effects. This helps improve fatigue in MS patients….another drug Modafinil (CNS stimulant) • Spasms: baclofen (skeletal muscle relaxants that act centrally), diazepam • Tremors: propranolol (beta blocker), isoniazid (antibiotic used to treat infection, especially TB…helps with certain tremors in MS) Increased Intracranial Pressure NCLEX Review What is increased intracranial pressure? It’s where pressure inside the skull has increased. This is a medical emergency! Intracranial pressure is the pressure created by the cerebrospinal fluid and brain tissue/blood within the skull. It can be measured in the lateral ventricles. What is a normal ICP: 5-15 mmHg (>20 mmHg…needs treatment) Pathophysiology of Increased Intracranial Pressure The skull is very hard and is limited on how much it can expand when something inside the skull experiences a change that leads to increased pressure. Inside the skull are three structures that can alter intracranial pressure: • brain • cerebrospinal fluid (CSF) • blood To understand the patho of increased intracranial pressure, you must understand the Monro-Kellie hypothesis. It deals with how ICP is affected by CSF, brain’s blood, and tissue and how these structures work to maintain cerebral perfusion pressure (CPP). In a nutshell, this hypothesis says that if the volume of one of these structures increases, the others must decrease their volume to help alleviate pressure. When there is an increase in intracranial pressure, the body can temporarily compensate for it by shifting CSF to other areas of the brain or spinal cord (or decrease it production), and alter blood volume going to the brain through vasocontriction, but if the pressure is continuous it is unable to compensate. Intracranial pressure fluctuates and this can depend on many factors like: • person’s body temperature • oxygenation status, especially CO2 and O2 levels • body position • arterial and venous pressure • anything that increase intra-abdominal or thoracic pressure (vomiting, bearing down etc.) For the brain to receive proper nutrients to work it must receive a certain about of cerebral blood flow. This is the amount of blood flowing to the brain’s tissue. It does this by altering the cerebral perfusion pressure via vasoconstriction or vasodilation. For example, if carbon dioxide levels are abnormally high (>45) vasodilation occurs, which allows more blood volume to enter the brain. However, this is not good if a patient has increased ICP because this will further increase the ICP. Cerebral perfusion pressure can become compromised during increased intracranial pressure. Therefore, there must be a sufficient cerebral perfusion pressure so that the brain is properly maintain. What is a normal CPP? 60-100 mmHg NOTE: When CPP falls too low the brain is not perfused and brain tissue dies. If the patient’s mean arterial pressure (MAP) starts to fall to the patient’s ICP, then the cerebral perfusion pressure will drop. Therefore, maintaining a sufficient MAP is essential. So How is CPP calculated? Equation: CPP= MAP – ICP You need to know the following: BP: 90/42 ICP: 19 First, the MAP must be calculated: MAP= Diastolic BP x 2 + SBP divided by 3 42 x 2 = 84 84 + 90 = 174 ….divided by 3= 58 (MAP) 58-19= CPP 39….very low…normal 60-100 mmHg What can cause an increased pressure within the skull that leads to increased intracranial pressure? • injury (head trauma) • increased in cerebrospinal fluid • hemorrhage (hemorrhagic stroke…aneurysm bursts) • hematoma (subdural and epidural…bleeding in between structures in the brain) • hydrocephalus: buildup of CSF in the brain…normally flows through the brain and spinal cord and enters the bloodstream (blocked, too much is made) • tumor: putting pressure on brain • encephalitis (inflammation of brain tissue) or meningitis (inflammation of membrane covering spinal cord and brain) What happens with increased intracranial pressure? Limited cerebral blood flow due to decreased cerebral perfusion from building pressure in the brain. The brain is getting squeezed and this leads to ischemia. All of this can lead to swelling and edema, which will eventually (if not treated) lead to herniation or displacement of the brain. The displacement of the brain can compress important areas of the brain like the brain stem (specifically medulla and vagus nerve). When CPP falls too low the body tries to increase systolic blood pressure to make more blood go to the brain, but this makes things worst!! During this time the arteries will start to dilate because of the retention of carbon dioxide. This causes more blood to flow to the brain but this will compress veins and limit blood flow to the heart. Hence, leading to more swelling and even more ICP. As all this progresses the patient’s signs and symptoms will start to become worst. Therefore, it is essential to know the EARLIEST signs and symptoms (mental status changes) of increased ICP. Signs and Symptoms of Increased ICP “Mind Crushed” Mental Status Changes ***Very earliest!! remember this for exam!! (restless, confused, problems performing normal movements and responding to questions) Irregular breathing (slow down of respirations and irregular…cheyne-stokes… hyperventilation then apnea cyclic)*late Nerve changes to optic and oculomotor nerve: double vision, swelling of optic nerve (papilledema), pupil changes (decreased, increased, or unequal size), abnormal doll’s eyes: oculocephalic reflex…in an unconscious patient open the eyes and move the head from side to side….if eyes don’t move in the opposite direction but stay fixed this is a very bad sign….indicates brain stem damage Decerebrate or decorticate posturing or flaccid • Decorticate (flexor posturing): brings upper extremities to the core of the body (middle) o adduction and flexion of arms, leg rotated internally, feet flexed • Decerebrate: (Extension posturing): extends upper extremities from the body *worst of the two (remember all the E’s in decerebrate and think EXTEND arms) o adduction and extension of arms with pronation, and feet flexed Cushing’s Triad: LATE SIGN…herniation of the brain stem • Increased systolic blood pressure (widening pulse pressure: increase in SBP and decrease in DBP), decreased heart rate, and abnormal breathing • Increased SBP (due to body trying to get more blood to the brain…thinks it’s helping) -> • Baroreceptor reflex (parasympathetic responds by dropping the heart rate to decrease the blood pressure and there may be compression of the vagus nerve due to compression from the swelling in the brain -> • The compression on the medulla of the brain leads to abnormal respirations cheyne-stokes Reflex positive Babinski (toe fan out…abnormal) Unconscious LATE Seizures Headache Emesis (vomiting) without nausea projectile Deterioration of motor function (hemiplegia)…weakness on one side of the body Nursing Interventions for Increased Intracranial Pressure Focus on preventing further increase ICP and monitoring ICP (if monitoring device inserted) “PRESSURE” Position head of bed: 30 to 45 degree (helps blood return to heart), proper alignment of head (midline) NO flexion of neck (decreases venous return) or hips (increases intra- abdominal/thoracic pressure)…watching moving around in bed Respiratory: Prevent HYPOXIA and HYPERCAPNIA! When blood oxygen levels drop or carbon dioxide levels increase, vasodilation occurs and this increases intracranial pressure. • monitor blood gases, oxygen level, suctioning as needed only (no longer than 15 seconds…increase ICP) hyperoxygenated before and after • mechanical ventilation to keep PaCO2 low 30-35 WHY? Vasoconstriction to help decrease ICP by decreasing blood flow….keep the PEEP low…increases intrathoracic pressure Elevated temperature PREVENT this! • Monitor temperature o If patient is unconscious best to take tympanic, temporal or rectal route NOT orally or axillary…. o Why is there a risk for hyperthermia? Patient may have damage to the hypothalamus, infection, dehydration etc….a high temp. increases ICP, cerebral blood flow, and metabolic needs of the patient o Can give antipyretics per MD order, remove extra blankets, decrease room temperature, cool baths…prevent shivering (increases metabolic needs and ICP) Systems to monitor: Glasgow Coma Scale • neuro checks per protocol • ventriculostomy (external ventricular drain): monitors ICP. It’s a catheter inserted in the area of the lateral ventricle to assess ICP and drains CSF during increased pressure readings. o monitor for ICP levels greater than 20 mmHg and report to MD…..patients with increased ICP are not a candidate for lumbar puncture….risk of brain herniation. Straining activities AVOIDED: vomiting, coughing, sneezing, Valsalva, agitation (keep environment calm), avoiding restraints as necessary Unconscious patient care: avoid over sedating with narcotic or sedatives, lung sounds and suction as needed, immobile (skin breakdown, monitor nutrition, at risk for renal stones, constipation, passive range of motion with extremities) nutrition, eye care with solutions and ointments, maintain GI tubes for feeding (monitor residuals….poor gastric emptying more than 100 ml), blood clot formation (SCDs, passive range of motion), talk to the patient as you would a conscious patient Rx: Barbiturates: to help decrease brain metabolism and BP which in turn decreases ICP, Vasopressors/IV fluids or antihypertensive to maintain SBP greater than 90 but less than 150, anticonvulsants meds, hyperosmotic drugs (leads to the next point of edema management)……. Edema management: dehydrating the brain (must be done carefully…watching blood pressure and renal function) Mannitol: it’s a concentrated type of sugar When this drug enters the blood it is very concentrated and it draws water that is pooling in the brain back into the blood. This type of diuretic is filtered through the glomerulus and not reabsorbed through the renal tubules, and because of this it creates an osmotic pressure that will pull water and electrolytes (sodium, chloride) from the blood (won’t be reabsorbed) and be excreted out. Watch for fluid overload (water intoxication) and depletion. FVO: signs and symptoms of heart failure, pulmonary edema (lung and heart sounds) • monitor renal function, UOP, electrolytes • not for patients with cerebral hemorrhage or anuria (no urine output) • patient will report dry mouth and thirsty…provide mouth care watch fluids (IV, oral), UOP, I and O’s (retention of urine?) More edema management meds that may be ordered: loop diuretics to remove fluid from brain and maintain a negative fluid balance….corticosteroids Cerebrovascular Accident (CVA) Stroke NCLEX Review What is a stroke? It is a condition that develops when blood rich in oxygen can NOT reach brain cells (due to either a blockage or bleeding). This causes the brain cells to die. Type of Strokes –Ischemic (most common): due to a blood clot within a blood vessel or stenosis of an artery that feeds the brain tissue. This limits the blood that can reach the brain cells. This type of stroke can happen due to: • Embolism: where a clot has left a part of the body (example the heart: this can happen due to a heart valve problem or atrial fibrillation). The clot develops in the heart and travels to the brain, which stops blood flow. • Thrombosis: Clot forms within the artery wall within the neck or brain. This is seen in patients with hyperlipidemia or atherosclerosis –Hemorrhagic: this occurs when there is bleeding in the brain due to a break in a blood vessel. Therefore, no blood will perfuse to the brain cells. In addition, this can lead to excessive swelling from the leakage of blood in the brain. Causes of this type of stroke includes: rupture of a brain aneurysm, uncontrolled hypertension, or aging blood vessels (older age). -TIA (transient ischemic attack) also called a mini-stroke. This is where signs and symptoms of a stroke occurs but last only a few minutes to hours and resolves. It is a warning signs an impending stroke may occur. If this occurs the patient needs to seek treatment. To understand strokes, let’s talk about the BRAIN”S function and anatomy! Blood supply to the brain? The blood supply to the brain comes for the carotid and vertebral arteries, which then branch into other arteries that feed the brain. If any of these areas of the artery become blocked or burst open it decreases the blood supply to the brain cells. Brain cells are very sensitive and within 5 minutes these cells start to become damaged, and the damage can become IRREVERSIBLE. The cells in the brain control how our body functions and depending on where the cells are located they are responsible for specific functions. Therefore, it is super important to be familiar with the function of each lobe and the difference between the right and left hemispheres of the brain. Let’s look at the lobes of the brain and their functions: Now strokes tend to affect ONE side of the body. So be familiar with the functions of the right side vs the left side: The right side of the brain is the CREATIVE side while the left side is the LOGICAL side. Right Side’s Functions: • Attention span • Showing emotions • Ability to solve every day problems by making decisions/plans • Reasoning (understanding jokes…reading in between the lines) • Making judgement calls • Memory • Music/art awareness • Control the left side of the body If a patient has right side brain damage, what do you think the patient will experience? • Left side weakness: Hemiplegia • Impairment in creativity: arts and music • Confused on date, time, place • Cannot recognize faces or the person’s name • Loss of depth perception • Trouble staying on topic when talking • Can’t see things on left side: LEFT SIDE NEGLECT (unilateral neglect) o (Ignores left side of body) • Trouble with maintaining proper grooming • Emotionally: not going to think things through….very impulsive • Poor ability to make decisions and assessing spatial qualities….shapes • Denial about limitations • Not able to read nonverbal language or understand the hidden meaning of things • Very short attention span Left Side’s Functions: • Speaking • Writing • Reading • Math skills • Analyzing info • Planning If a patient has left side brain damage, what do you think the patient will experience?: • Right side Hemiplegia • Aphasia (trouble formulating words and comprehending them) • Aware of their limits…experiences depression, anger, frustration • Trouble understanding written text • Can’t write (agraphia) • Impaired math skills • Memory intact • Issues with seeing on the right side So, as you can see when there is brain cell death in a certain area it will cause specific signs and symptoms. The amount of brain damage depends on how long it took for blood to return to the affected brain cells. Risk Factors for stroke -be familiar the risk factors and which ones are modifiable (things a person can change) vs. unmodifiable (things a person CAN’T change “Strokes Happen” Smoking Thinners (blood) Rhythm changes (a-fib/flutter) Oral Contraceptive Kin (family history) Excessive weight Senior citizens Hypertension Atherosclerosis Physical inactivity Previous TIA Elevated blood sugar (diabetes mellitus) aNeurysm (brain) Signs and Symptoms of a Stroke Happens suddenly: need to act fast as the nurse to help save brain cells • call rapid response so patient can receive appropriate treatment or call 911 (if outside of the hospital in the United States) • NOTE the exact time the signs and symptoms appears…important for stroke treatment “FAST” Face: drooping or uneven smile Arm: numbness, weakness, drift (raise both arms) Speech: can’t repeat a phrase, slurred speech Time: to call rapid response and note the time **National Stroke Association recommends using the mnemonic F.A.S.T. to help assess for signs and symptoms quickly. The patient can also have the following as well: Bowel and bladder incontinence or retention Important Stroke Terms: remember these terms because exams love to ask you about them. Aphasia: unable to speak (comprehending or producing it) • Receptive Aphasia: unable to comprehend speech (Wernicke’s area) • Expressive Aphasia: comprehends speech but can’t respond back with the correct words, if at all (Broca’s area) • Mixed Aphasia: combination of the two types of aphasia. • Global Aphasia: complete inability to understand speech or produce it. Dysarthria: unable to hear speech clearly due to weak muscles (hard to understand the patient’s speech….it may be slurred) Apraxia: can’t perform voluntarily movements (winking/moving arm to scratch an itch) even though muscles function is normal. Agraphia: loss the ability to write Alexia: loss the ability to read…doesn’t understand or recognize the words Agnosia: doesn’t understand sensations or recognize known objects or people Dysphagia: issues swallowing (weak muscles) Hemianopia: limited vision in half of the visual field Hemiparesis: weakness on one side of the body Diagnosed? • CT scan • MRI Medication for Ischemic Strokes: tPA (tissue plasminogen activator): for ischemia strokes ONLY not hemorrhagic! How does it work? It dissolves the clot within the blood vessel by activating the protein that causes fibrinolysis. REMEMBER: It must be given within 3 hours from the onset of stroke symptoms. It can be given 3 to 4.5 hours after onset IF strict criteria is met. To receive tPA the patient should have a: • CT of head that is NEGATIVE for hemorrhage • labs within normal limits (glucose, INR, platelets) • BP needs to be controlled SBP <185 and DBP <110 • glucose controlled (increases rise of hemorrhage) • not receiving heparin or other types of anticoagulants Nurse’s Role: monitor for BLEEDING, neuro checks around the clock, blood pressure medication if needed for hypertension, vital signs, labs, glucose, preventing injury (bedrest), avoid unnecessary venipunctures, avoid IM injections, will go to ICU to be monitored Nursing Interventions for Stroke Monitor vital signs and neuro status: • especially blood pressure (notify MD is hypertensive) • airway (difficulty swallowing….at risk for aspiration HOB 30’ with suction at bedside) • turn every 2 hours with proper alignment and watch for increased ICP (intracranial pressure) during acute stage o headache, nausea and vomiting, increased blood pressure and decreased HR and decreased RR, decrease in mental status from baseline, pupils don’t respond Assess with NIH Stroke Scale • Score ranges from 0 to 42 • 0: no stroke symptoms • 21-42: severe symptoms • 11 assessments area are scored • Assesses: o Level of consciousness, gaze, visual, facial palsy, motor function of extremities, sensory, best language, dysarthria, extinction/inattention Check cranial nerves: pupil responses, motor function, gag reflex Monitor bowel and bladder function (may be incontinent or retaining) Passive ROM with extremities and preventing contractions Interventions for aphasia Communication is key (just because the patient can’t communicate doesn’t mean they have a mental deficit). They just can’t get it out and it takes them time. The nurse’s role is to help bridge the gap and make it less frustrating for the patient. • Receptive Aphasia: unable to comprehend speech (Wernicke’s area) -use short phrases -use gestures or point while giving a command -be patient and not expect a fast response -remove distractions • Expressive Aphasia: comprehends speech but can’t respond back with speech (Broca’s area) -be patient and let them speak -be direct and simple when asking questions…..give options -communication via a dry erase board Stroke care is a multidisciplinary approach: need to involve family as much as possible because they will be providing care when patient is discharged. In addition, it is important to be always be communicating with the speech language pathologist, physical therapy, occupational therapy etc. Diet: evaluated by speech language pathologist • may need thicken liquids and mechanical soft foods • assist with eating and monitor for pouching of food in cheek (on the affected side). This increases risk of aspiration. • Have patient tuck in chin to their chest while swallowing. Watch for neglect syndrome: (tends to happen in right side brain damage). The patient is at risk for injury because patient ignores the affected side. • Remind patient to use and touch both sides of body daily (must make a conscious effort to do so). • Educate the patient about the importance of turning head side-to-side to prevent injuring the affected side. Hemianopsia interventions: turning head side-to-side to see all visual fields to prevent injury Myasthenic vs. Cholinergic Crisis Nursing Lecture Cholinergic Crisis How does it happen? It happens due to excessive stimulation at the neuromuscular junction by acetylcholine (too much ACh available) which leads to overdrive in cholinergic response. Causes: overmedication of anticholinesterase medication given in myasthenia gravis Why? these medications stop the breakdown of acetylcholine, so there is MORE available at the neuromuscular junction. This is great for treating myasthenia gravis, but too much of the medication can cause cholinergic crisis and overstimulates the muscle fiber where it will eventually quit contracting. Signs and Symptoms: Muscle fibers have had enough of the stimulation so they quit responding to the impulse which will lead to: Respiratory failure Muscle weakness However, other signs and symptoms that will present are similar to parasympathetic stimulation (the “rest and digest” system), but in OVERDRIVE!! • GI issues: vomiting, diarrhea, cramping • Pupil constriction • Increase salivation and tear production….blurred vision and increase respiratory secretions • Muscle fasciculation/twitching…from overstimulation eventually paralysis • Low blood pressure and heart rate So, other than the symptoms how are these conditions diagnosed? Tensilon Test: Edrophonium is given, which is an anticholinesterase inhibitor, and this will cause the patient to experience even more weakness (adding more ACh at the site…it is not needed because there is already enough ACh at the neuromuscular junction site causing overstimulation). The patient’s signs and symptoms will not respond but become worsen…..finding: NEGATIVE result Treatment: HOLD anticholinesterase medication and administer atropine (antidote) per MD order Myasthenic Crisis How does it happen? It happens due to low to no stimulation at the neuromuscular junction by acetylcholine (receptors are not available to do their job because of antibodies attacking the receptors), which leads to severe muscle weakness. Causes: insufficient amounts of anticholinesterase drug or an illness (respiratory infection) stress etc. that has created exacerbation of the disease myasthenia gravis. Signs and Symptoms: Remember no receptors are available to receive the ACh so there is NO stimulation of the muscle fiber, which leads to NO contraction but flaccidity. (note: both conditions will have): Respiratory failure Muscle weakness However, signs and symptoms will affect all voluntary muscles making them flaccid (from eyes to bowels): • pupils dilated • tachycardia/HTN • no cough or gag • aspiration (can’t swallow or cough) • incontinence (no muscle strength) of both bowel and bladder How to tell the difference other than symptoms: Tensilon Test: Edrophonium is given, which is an anticholinesterase inhibitor, and this will cause the patient to experience IMPROVED muscle strength (adding more ACh at the neuromuscular junction because it inhibits the breakdown of ACh)….signs and symptoms temporarily diminish…..findings: POSITIVE result Treatment: give more anticholinesterase medication per MD order Myasthenia Gravis NCLEX Review What is Myasthenia Gravis? It’s an autoimmune condition where the body attacks the receptors that allow for voluntary muscle control, which leads to muscle weakness. What voluntary muscles are involved? • Eyes: most likely will be the first sign something is wrong • Throat: another common sign…hoarse voice and problems swallowing • Face • Arms/Legs • Respiratory muscles for breathing (in severe cases) How does Myasthenia Gravis happen? Key Players Involved: Neuromuscular Junction: • Nicotinic Acetylcholine Receptors(NAChRs) or the function of Muscle-Specific Kinase (MuSK). MuSK helps with maintaining and building the neuromuscular junction, but for this lecture we will concentrate on the nicotinic acetylcholine receptors. • Neurotransmitter: Acetylcholine • Immune System: produces the anti-bodies against the nicotinic receptors. • Thymus gland • Acetylchoinesterase: an enzyme that breaks down acetycholine (remember this substance because it plays a role in the treatment of MG with anticholinesterace medications). In myasthenia gravis the issue arises at the neuromuscular junction. This is the place where the motor neuron and muscle fiber meet and the neurotransmitter acetylcholine is released. At this junction are receptors on the muscle fiber called nicotinic acetylcholine receptors that become stimulated when acetylcholine is released and cause contraction of the muscle fiber. However, in myasthenia gravis the nicotinic acetylcholine receptors are being attacked by antibodies the immune system has created and are not working properly. These receptors can NOT access the release of acetylcholine and cause muscle contraction, so there is muscle weakness. The thymus gland (found anteriorly in the upper part of the chest behind the sternum in between the lungs) plays a very important role in our immune system health. It’s the creator of T-cells, which are super important for immune health by fighting viruses and bacteria. In children the thymus is large (remember it will produce most of the body’s T-cells by the time a person attains puberty). It should shrink by adulthood and then in older age be like a fatty tissue. But in people with myasthenia gravis, the thymus gland tends to stay large and develops tumors or collection of immune cells in the gland. It is thought that the thymus erroneously causes immune cells to produce antibodies that will attack receptor sites on these voluntary muscle neuromuscular junctions. Signs and Symptoms of Myasthenia Gravis **HALLMARK: muscle weakness becomes worse with activity (especially repetitive activity) but will improve after resting the muscle. Patients tend to notice symptoms in the eyes due to eye muscle weakness of the extraocular muscles or have problems with speaking (slurred) or swallowing….signs and symptoms vary among patients. “WEAKNESS” Weakness neck, face, arms/legs/hands Eyelid drooping…can be one eye or both (Ptosis) Appearance mask-like: no expression…looks very sleepy Keeps choking or gagging when eating (difficulty swallowing)…many muscles help with the swallowing process and have become weak No energy…very fatigued…gets worse throughout the day as muscles are used Extraocular muscle involvement leading to double vision…strabismus Slurred speech (voice may be hoarse and very soft) Short of breath (can extend to respiratory muscles) Complications of Myasthenia Gravis Myasthenia gravis can go into remission where the patient doesn’t have signs and symptoms, but some patients can experience severe acute exacerbation with a complication called Myasthenic Crisis. This is where the disease is becoming worse and the patient may need intubation and mechanical ventilation to breathe. Risk factors for experiencing Myasthenic Crisis: improper dosage (not enough) of anticholinesterase meds to treat this condition, stress (physical…surgery or mental), and respiratory infection. That patient will have severe weakness of muscles that cause respiratory failure. How is it diagnosed? • Edrophonium (Tensilon test): During this test an anticholinesterase medication is given called Edrophonium. o How does the medication work? It prevents the breakdown of acetylcholine at the neuromuscular junction, which allows more of the neurotransmitter to be present at the neuromuscular junction. o It is used to diagnose Myasthenia Gravis AND differentiate between a myasthenic crisis and cholinergic crisis (see more about cholinergic crisis in the pharmacology part of this lecture). IMPORTANT: What will happen if Edrophonium is given to a patient with myasthenia gravis or to a patient in myasthenic crisis? The patient’s signs and symptoms will temporarily improve. Hence, the test is positive. What will happen if Edrophonium is given to a patient with cholinergic crisis? The patient’s signs and symptoms will become worse….NO improvement. Hence, the test is negative. • If this happens the nurse (per MD order) will administer the antidote for Edrophonium, which is ATROPINE! It is also important to have the patient on a cardiac monitor during the test and a crash cart within reach if an emergency arises. Nursing Interventions & Medications for Myasthenia Gravis Monitor respiratory status: effort of breathing, respiratory rate, oxygen saturation, does the patient feel like it’s hard to breathe? If hospitalized with exacerbation needs resuscitation equipment close by: suction etc. Monitor neuromuscular status: • Assessing vision (double vision?), quality of voice, swallowing (important for medication administration…ALWAYS check swallowing before giving meds), facial appearance, strength with arms/legs, cranial nerves Safety: at risk for injury….needs assistance at all times (remember the patient may have double vision (eye patch to help with this), arm and leg weakness) Speech pathologist will evaluate and recommend treatment based on findings. Patient may need or have a feeding tube and you will be managing this as the nurse. Monitor for aspiration, hob of greater than 30′ while eating Education about food because patient may have difficulty chewing and swallowing: • smaller meals that are easy to chew foods…pick food options that are soft and require minimal effort to chew • try scheduling meals during peak time of medication (30 minutes to 1 hour before eating) so chewing and swallowing muscle will have the most access to acetylcholine • Thicken liquids for swallowing • Take small bites and rest while eating and before a meal • It’s best to have large meals at the beginning of the day than at the end (remember patients with MG becomes progressively weaker throughout the day) Educate about performing most of their activities early in the day when the patient will have the most energy. Help patient identify things that makes symptoms worst: menstrual cycle, sickness, stress, extreme temperatures Medications for Myasthenia Gravis: Anticholinesterase: “Pyridostigmine” …improves symptoms…there is no cure! How does the anticholinesterase medication work? Remember the substance we talked about earlier called acetylcholinesterase? This medication will prevent it from working. Therefore, there will NOT be the breakdown of acetylcholine. Therefore, more of it will be available at the neuromuscular junction site. This will help improve muscle strength. Patient should take 30 to 60 minutes before a meal to help increase muscle strength with swallowing and chewing. Monitor: Myasthenic crisis (from not enough medication) or cholinergic crisis (too much of the medication): ….both will have respiratory failure and severe muscle weakness but from different causes. Signs and Symptoms of Cholinergic Crisis: Think of the signs and symptoms experienced during cholinergic crisis similar to the parasympathetic nervous system being in overdrive: • Pupil constriction • Bronchoconstriction….eventually respiratory failure • Increased salivation and mucous production • GI problems: abdominal cramping, vomiting, diarrhea • Bladder incontinence • Bradycardia Treatment: No anticholinesterase medications and atropine to reverse symptoms. Other drugs used to treat MG: corticosteroids and immunosuppressants Other treatments for MG: • Thymectomy: removal of the thymus gland (improves symptoms in some patients…NOT a cure) • Plasmapheresis with administration of IV immunoglobulins (severe cases): filters blood by removing antibodies that attack the receptors at the neuromuscular junction (temporary improvement for about 4 weeks to a couple of months….NOT a cure). Metabolic Panel Glucose: 70–100 mg/dL Calcium: 8.5–10.5mg/L Chloride: 95-105 mEq/L Magnesium: 1.5-2.5 mg/dL Phosphorus:2.5–4.5mg/dL Potassium: 3.5-5 mEq/L Sodium: 135-145 mEq/L BUN: 5-20 Serum creatinine: 0.6–1.2 mg/dL Total Protein: 6.2–8.2 g/dL Albumin: 3.4–5.4 g/dL Bilirubin: 0.1-1 mg/dL (less 1) (formed with the breakdown of RBCs…high levels in patients with jaundice) — These are 3 enzymes found in the liver. If elevated, it can indicate liver problems and other diseases.— • ALP (alkaline phosphatase): 40-120 U/L (international units per liter) • ALT (alanine transaminase): 7 to 56 U/L • AST (aspartate transaminase) 10-40 U/L *this blood test can be ordered as a BMP (basic metabolic panel) or CMP (comprehensive metabolic panel). The CMP will include the liver function. Complete Blood Count RBC: 4.5–5.5 million WBC: 5,000–10,000 Platelets: 150,000–400,000 Hemoglobin: • 12–16 g/dL (women) • 14–18 g/dL (men) Hematocrit: • 37 – 47% (women) • 42 – 52% (men) Arterial Blood Gases (ABGs) pH: 7.35-7.45 pCO2: 35-45 mmHg HCO3: 22-26 mEq/L pO2: 80-100% O2 sat: 95-100% Coagulation Levels INR/PT: • PT (prothrombin time): 10-12 seconds (normal level for patients not on Warfarin) • INR (international normalized ration): Less than 1 (normal level for patients not on Warfarin). o When a patient is taking the anticoagulant Warfarin the INR should be 2-3. o The INR level is calculated from the PT level. aPTT (activated partial thromboplastin time): • Normal 30-40 seconds (not on Heparin) o If the patient is on Heparin, the aPTT needs to be 1.5 to 2.5 times the normal range. Lipid Panel (risk for cardiovascular disease) LDL (low density lipoprotein): <100 mg/dL (want it LOW) HDL (high density lipoprotein): >60 mg/dL (want it HIGH) Total Cholesterol: <200 mg/dL Triglycerides: <150 mg/ dL Hemoglobin A1C • 4-6% (target for patients without diabetes) • <7% (target for patients with diabetes) Drug Level Ranges Digoxin: 0.5-2 ng/mL Carbamazepine: 4-10 mcg/mL Dilantin: 10-20 mcg/mL Theophylline: 10-20 mcg/mL Phenobarbital: 15-40 mcg/mL Lithium: 0.5-1.2 mmol/L Valproic Acid: 50-100 mcg/mL [Show More]

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