Nursing III
Exam 3 Content Guide
1. Acromegaly – gigantism; caused by hypersecretion of pituitary GH over a long period of time (or childhood).
Hyperprolactinemia is a prolactin secreting pituitary tumor (most commonl
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Nursing III
Exam 3 Content Guide
1. Acromegaly – gigantism; caused by hypersecretion of pituitary GH over a long period of time (or childhood).
Hyperprolactinemia is a prolactin secreting pituitary tumor (most commonly d/t ingestion of dopamine antagonist dugs;
haloperidol, risperidone). In some incidences, pituitary prolactinomas secrete GH simultaneously and cause acromegaly. This
condition is associated with a decrease in estrogen – so s/s in women: vaginal dryness, hot flashes, galactorrhea, amenorrhea,
oligomenorrhea, anovulation (infertility). In men: causes ↓testosterone s/s: ↓facial and body hair, ED, ↓libido, small testis, and
infertility. Tx: cabergoline (Dostinex)
Diagnosis often missed or delayed (~ 42yrs). Undertreated ↑morbidity and mortality d/t the chronic effect of GH on
body organs = ↑ cardiovascular, cerebrovascular, and respiratory disease; malignancies; and diabetes. In children
and adolescents: GH stimulates growth in all body tissues prior to fusion of the growth plate. In adults: GH causes
continued growth of soft tissues and small bones of the hands/feet & the membranous bones of the skull and face.
Signs and symptoms of: Child 7ft tall. Changes in facial features. Obesity, carpal tunnel, enlarged tongue, glucose
intolerance. 30% will have some form of cardiac disease, (CAD, cardiac dysrhythmias, left ventricular hypertrophy
(LVH), or cardiomyopathy) also associated with colon polyps.
Treatment: Surgical removal of the tumor, radiotherapy, or medical therapy.
Common medications: Octreotide (Sandostatin) – usually for residual GH after surgery. SQ 3x/day or IM in long
acting Q4weeks. ORAL med: bromocriptine (Parlodel) – less effective but cheaper and can be taken PO.
Assessment of: Labs: hGH, prior to the hGH test the patient should fast, and the test should be drawn at 8.00 a.m.
b/c of circadian cycle. Normally (hGH ) MEN: < 5 ng/mL WOMEN: <10 ng/mL Acromegaly = hGH > 10 ng/mL .
The glucose suppression test: measuring GH following the admin of 100 g of glucose. Normally, GH secretion is
lowered to less than 2 ng/mL. A result greater than 2 ng/mL is considered conclusive of a diagnosis of acromegaly.
- Plain films will often show sella turcica enlargement due to a pituitary tumor. Thickening of the calvarium, and
enlargement of the sinuses, jaw, and heel pads can also be seen on X-ray. MRI = show tumor location and size.
Patient education: If Pt is hyperglycemic d/t hypersecretion of GH = diabetic management. Cardio (↑cholest, or
HTN) tx needed. Teaching in prevention of complications of disease.
2. Cushing’s syndrome – Hypercortisolism is most often caused by excessive production and release of ACTH by a
pituitary secreting adenoma. Commonly occurs in women 20-40 and are approximately 20% of the pituitary tumors.
Signs and symptoms of: Many of the clinical manifestations of hypercortisolism = exaggerated action of cortisol,
which affects glucose, protein, and fat metabolism. Bruising, poor wound healing, excess hair growth in females,
HTN, edema of extremities, accumulation of fat in the face (moon face), voice changes, hyperlipidemia,
dysrhythmias, emotional liability, irritability, depression, poor memory, euphoria, psychosis, suicidal tendencies,
protein breakdown and muscle wasting, osteopenia, osteoporosis, renal calculi, polyuria, amenorrhea in females,
decrease in libido, impotence, decrease in body hair (males), protruding abdomen, subclavicular fat pads (buffalo
hump), hyperinsulinemia, Potassium and Sodium imbalances, and abnormal glucose tolerance test.
Assessment: Fluid and electrolyte imbalances, sx of heart failure (diuretics, BP meds, cardiotonic meds). SOB,
weakness (hypokalemia) – assist with ADL’s. Prevent infection (compromised immune sys) – watch for low grade
temp. – Poor wound healing, opportunistic infections.
Common treatment: No drugs are avail to successfully suppress pituitary ACTH secretion. Ketoconazole, metyrapone,
and aminoglutethimide are expensive drugs, with limited success in treating Cushing’s. Treatment of choice is
selective transsphenoidal resection with tumor removal to correct the hypercortisolism. Radiotherapy may be
prescribed. In extreme cases, bilateral adrenalectomy has been done when all other therapies have failed with
lifelong hormone replacement therapy.
- For surgery: Packing of nasal passage for 24-48hrs – instruct deep breathing exercises thru mouth. Liquid diet,
use toothettes for cleaning teeth. Neuro assessment Qhr. Monitor for ↑ICP, avoid straining. Risk for CSF leak –
look for clear drainage/halo ring on drip pad under nose, will test + for glucose if CSF. If + = bedrest with HOB
elevated. Normally leak will cease spontaneously. ↑Risk infection. Therefore, antibiotics are usually ordered.
Monitor fluid status. Risk for SIADH, or diabetes insipidus.
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Patient education and support: Wt gain 25 -100 pounds, acne, excess body hair, redistribution of fat, and striae on
the abdomen and breasts=Encourage the Pt to explore feelings. Prevent infection. Prevent fracture.
3. Hypothyroidism – Insufficient secretion of TH by thyroid gland, causing decreased metabolic rate and heat
production, and various effects on body system
Assessment,
Common medications: thyroid hormone replacement: dessicated thyroid, thyroxine (Synthroid),
or triiodothyronine (Cytomel). Give med in AM 1 hour b4 meal or 2 hrs after meal to facilitate absorption
Pregnant and non-pregnant treatment
Myxedema (a life-threatening crisis state of hypothyroidism): non-pitting edema in connective tissues throughout
body, puffy face and tongue, severe metabolic disorders, hypothermia, cardiovascular collapse, and coma
4. Thyroid crisis (Hyperthyroidism) – A pt with hyperthyroidism is susceptible to a thyroid crisis. Often caused by
increased medications, a thyroid crisis (thyroid storm) is a rare but often life-threatening emergency. Early
identification is essential.
Assessment: Infection, stress or emotional trauma, pregnancy, a comorbidity, or medications may precipitate it.
Clinical manifestations: extremely high fever (>102), abdominal pain, nausea, vomiting, diarrhea, tremors, severe
neurological signs and symptoms (e.g., restlessness, delirium/confusion, agitation, psychosis, and coma), and
cardiovascular problems (Tachycardia, atrial fibrillation, heart failure, and angina). Most patients will have high
systolic blood pressure with a wide pulse pressure. One of the earliest clues to the onset of a thyroid storm is high
fever and diaphoresis that are out of proportion to an infection.
possible seizure
Interventions: Respiratory support should be provided immediately. Hemodynamic instability is a major priority. IV
access is a priority to correct volume and electrolyte depletion and administer nutrition as indicated. Vasopressors to
restore or maintain BP. May implement measures to treat heart failure (digoxin, and diuretics). Reduce fever
immediately. A cooling blanket and the administration of acetaminophen as ordered is standard care. Adrenal
insufficiency with the stress related to the thyroid storm = glucocorticoids such as hydrocortisone.
Patient education: NO ASPIRIN.
5. Grave’s Disease – pronounced hyperthyroidism often associated with enlarged thyroid gland and exophthalmos;
also called thyrotoxicosis.
Signs of: . Neck goiter and exophthalmos (bulging eyes) are characteristic. Tachycardia, nervousness, insomnia,
increased heat production, and weight loss. Cardiac problems: increased systolic blood pressure, a widened pulse
pressure, and other dysrhythmias.
Treatment: Antithyroid medications: Methimazole (Tapazole), Propylthiouracil
6. Inflammatory Immune Response – is a response that is composed of several body systems, which are constantly on
alert to detect nonself and harmful intruders from the normal cells and proteins in the body. The immune system can
remember a foreign agent and develop a heightened response during a subsequent exposure. When regulation of
the immune response is controlled, the response is protective; however, when the immune response is exaggerated,
the consequences can be dangerous.
The purposes of this innate protective response are to control bleeding, remove waste products, limit infection, and
promote healing. IIR responses cause local vasodilation to aid in delivering an increased bloodflow and to bring
neutrophils, macro- phages (the major phagocytic cells of the immune system), and clotting factors to the damaged
area.
Cardinal signs of local reaction to an injury or infection as first described by Celsus, an early Roman physician:
• Rubor (redness) due to vasodilation
• Calor (heat) due to increased bloodflow to area
• Tumor (swelling) due to release of fluids containing white blood cells and proteins to the insult site
• Dolor (pain) due to swelling that stretches the surrounding tissues; pain alerts the patient to rest the affected area
to assist prevention of further damage
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7. Shock – Review all the material on different types of shock and clinical manifestations of each.
Different types: The shock syndrome, or acute circulatory failure, can be classified according to etiology into three
basic categories: hypovolemic, cardiogenic, and distributive. Sub-categories of distributive shock include neurogenic,
anaphylactic, and septic.
Causes of the different types: Progression from one stage to the other is dependent on the patient’s health status,
duration of the insult, response to therapy, and the correction of the underlying cause. The end result is always the
same; tissues fail to receive oxygen and nutrients, and are unable to eliminate waste products
- Hypovolemic shock: an insufficient intravascular volume and low cardiac output; is initiated by various causes.
Blood loss due to internal or external bleeding, fluid loss, injury or vomiting, diarrhea, severe dehydration, burns,
surgery, ascites, or peritonitis.
MANIFESTATIONS OF HYPOVOLEMIC SHOCK
Tachycardia is a compensatory helps remove accumulating lactic acid. May result in cardiac arrhythmias
and chest pain (inadequate filling of the cardiac arteries during diastole). Due to lack of tissue
perfusion, the patient’s level of consciousness is altered.
Pulse pressure narrows as the diastolic increases. Tachypnea and increase in depth of respirations
(may gasp for breath). Decline in urine output. Skin pale, cool, delayed capillary refill. Jugular veins
appear flat. Decreased cerebral perfusion and a change in LOC. Disoriented, confused, restless, anxious.
Nursing Interventions:
Minimize fluid loss. Large diameter catheter – Give Fluids (monitor FV overload), Oxygen, Meds.
Observe for changes in Respirations, heart sounds, assess lung sounds, chest pain. (Risk of Secondary
shock if given blood products = anaphylactic shock) Monitor lab results, I&O. Give pain meds. Position,
the patient with legs elevated, trunk flat, and head and shoulders above the chest (modified
Trendelenburg position). Monitor s/s infection (IV).
- Cardiogenic: a diminished cardiac output is due to loss of left ventricular pump function. It results in tissue
hypoxia even when fluid volume is adequate.
MANIFESTATIONS OF CARDIOGENIC SHOCK
Hypotension SBP < 90 mm Hg. Heart rate > 100 beats per minute. Weak thready pulse, Diminished
heart sounds. Change in level of consciousness (LOC). Cool, pale, moist skin Urine output less than 30
mL/hour Chest pain. Dysrhythmias. Tachypnea. Crackle breath sounds. ↓cardiac output.
Nursing Interventions:
Fluids, Oxygen, Meds. Observe for changes in Respirations, heart sounds, assess lung sounds, chest
pain. Monitor lab results, I&O. Give pain meds to diminish myocardial O2 consumption). Calm
environment, education to reduce anxiety. Limit activities to preserve O2. Give pain meds
- Distributive shock: • Anaphylactic shock: due to hypersensitivity to a foreign substance (antigen/antibody
reaction). • Neurogenic shock: due to disruption of outflow of sympathetic nervous system response—often due
to tissue damage in the spinal cord pathway. • Septic shock: result of overwhelming infection.
Phases of shock:
Initial - -Decreased CO, impaired tissue perfusion, elevated lactic acid. No clinical s/sx except for elevated lactic acid.
Compensatory - - Body is trying to bring us back to homeostasis.
- Neural changes: SNS activated (epi/norepi activated)
- Hormonal changes: (ACTH is released, kidneys affected, K+/Na+ affected)
- Chemical compensation (leads to respiratory alkalosis!)
Progressive - Unable to continue compensatory phase. Multi organ dysfunction syndrome (MODS). Organ
hypoperfusion
Refractory - - Death is inevitable
ASSESSMENT AND CARE OF SHOCK SYNDROME Clinical findings correlated with organs compromised by inadequate
oxygen. Regardless of the type of shock, it leads to a SBP of less than 90 mm Hg and the narrowing of pulse pressure
that is inadequate to meet the tissue needs. (SBP may be elevated initially.)
First: Position pt. to maximize o2 return to the brain (admin O2), monitor pulse & resp rates, keep normothermic.
Initial Compensatory Stage: Body mechanisms are triggered to maintain adequate BP and tissue perfusion. Subtle
changes in baseline may be observed. Monitor heart rate and pulse, blood pressure, central venous pressure (CVP),
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respiratory rate, core, and peripheral temperature, and urinary output. Pulse oximetry may also be performed.
Arterial gases are monitored for accurate assessment. Blood sampling for urea and electrolyte levels, full blood
count, and glucose levels may also be performed. Elevated glucose levels are present with release of stress
hormones such as cortisol.
Progressive Stage: Compensating mechanisms begin to fail. Symptoms are evident of inadequate organ perfusion. A
full assessment should be done to identify any signs of blood or fluid loss, fluid shift as in ascites, infection, vomiting,
or inadequate fluid intake.
Decompensated Stage: Failure of compensating mechanisms. No response to treatment. There is a great risk of
cardiac arrest. A rising serum lactate is an indicator of inadequate tissue perfusion due to metabolic acidosis. Low
arterial oxygen con- tent, chest pain, cardiac dysrhythmias, altered level of consciousness (LOC), or low urinary
output. MAPB cannot be maintained without assistance.
8. Angina –
Assessment,
Different types,
Treatment,
Patient education,
Causes
9. Myocardial Infarction –
Assessment,
Clinical manifestations,
Common medications,
Side effects of common medications,
Patient education,
Phases of rehabilitation
10. Coronary Artery Disease –
Modifiable risk factors,
Assessment,
Common treatment,
Prevention
11. Cardiac Angiograms- Coronary angiogram, or heart catheterization, is an invasive procedure that is considered the
gold standard for diagnosis of CAD.
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