NR 507 Pathophysiology Midterm Review STUDY GUIDE _Chamberlain College of Nursing.

NR 507: MIDTERM REVIEW Hematology Hematopoiesis: -process of blood cell production -Constant throughout life to replace RBCs that grow old and die, are killed by disease, or are lost through bleeding -Occurs in liver ...

NR 507: MIDTERM REVIEW Hematology Hematopoiesis: -process of blood cell production -Constant throughout life to replace RBCs that grow old and die, are killed by disease, or are lost through bleeding -Occurs in liver and spleen of fetus -Occurs in bone marrow after birth -2 stages: 1. Proliferation (mitotic division) 2. Maturation (differentiation) -Bone marrow: red (hematopoietic/active) & yellow (fatty/inactive) Hematopoietic stem cells (HSCs)- all blood cells are created from HSCs -signaled to undergo differentiation (by cytokines and chemokines, growth factors) to form RBC, WBC, & platelets · Lymphoid: T cell (T-lymphocyte) & B cell (B-lymphocyte) · Myeloid: Monocyte & Granulocytes (WBCs) · Erythrocyte (RBC) · Megakaryocyte (Platelets) Mesenchymal stem cells-develop into osteoclasts, fibroblasts, & adipocytes ? Erythropoietin: -hormone that stimulates erythrocyte production -Secreted by the kidneys in response to tissue hypoxia Erythrocyte: -most abundant cells in the body -primarily responsible for tissue oxygenation -mature erythrocytes lack a nucleus and mitochondria, cannot synthesize protein or carry out oxidative reactions. Cannot divide *anaerobic metabolism only -life span: 100-120 days -contains hemoglobin molecules o Stages: (7-day process) · Hemocytoblast (stem cell) binds with erythropoietin · Proerythroblast- committed to morph into RBC · Erythroblast- ribosome synthesis (2 phases) · Normoblast- Hgb accumulation & nucleus ejection · Reticulocyte –(immature RBC) released into circulation, no nucleus, ribosome, or mitochondria · RBC (after it has been in bone marrow 1-2 days) Hemoglobin: oxygen carrying protein of the erythrocyte -hemoglobin packed blood cells pick up oxygen in the lungs and exchange it for carbon dioxide in the tissues -composed of 2 pairs of polypeptide chains (globins) & 4 colorful iron complexes (hemes) -can carry up to 4 molecules of oxygen Oxyheoglobin- binding of oxygen to Fe in heme molecule, RED Deoxyhemoglobin- reduced hemoglobin, after it releases the oxygen to the tissues, BLUE Risk factors and causes for developing any type of anemia: -blood loss (acute or chronic) -impaired erythrocyte production -increased erythrocyte destruction -a combination of these factors Iron Deficiency Anemia- Microcytic-Hypochromic Anemia -most common nutritional disorder -occurs when iron stores are depleted reduced hemoglobin synthesis -more common in toddlers, adolescent girls and, women of childbearing age -causes: · Dietary deficiency · Impaired absorption · Increased requirement · Chronic blood loss Thalassemia-Microcytic-Hypochromic -inherited autosomal recessive disorder -impaired synthesis of one of the two chains of adult hemoglobin (alpha or beta) -common among Mediterranean descent -can be minor or major, can be asymptomatic or lethal (Cooley’s) Sickle Cell Anemia-Normocytic-normochromic/Hemolytic -inherited autosomal recessive disorder -presence of atypical hemoglobin-Hemoglobin S -amino acid change on the beta-globin chain (glutamine replaced for valine)-distort erythrocytes into sickle shape= cannot properly carry O2. -vaso-occlusive crisis (pain), aplastic crisis (anemia), sequestration crisis (blood pooling in spleen), hyperhemolytic crisis ( accelerated RBC destruction) - Stress, hypoxia, anxiety, fever, cold, dehydration = lower O2 binding -↑ risk of CVA, splenic damage, or kidney damage. Most people with sickle cell will become asplenic by adulthood. Hemolytic Anemia- -premature destruction of erythrocytes -majority occur within phagocyctes in lymphoid tissue -congenital (sickle cell or thalassemia) acquired (transfusion reaction, infection, autoimmune) -causes elevated erythropoietin to induce accelerated production of erythrocytes and in increase in the products of hemoglobin catabolism -transfusion with incorrect blood type: intravascular hemolysis by activation of complement system; extravascular hemolysis by phagocytosis of antibody-coated erythrocytes in spleen Pernicious Anemia-Macrocytic -vitamin B deficiency -Autoimmune gastritis-impaired intrinsic factor (transporter needed for vitamin B12 absorption) -can be congenital- autosomal recessive inheritance -gastric bypass, or gastrectomy - H. Pylori infection= risk factor -will need Vit B 12 injections for life Pulmonary Oxygen O2 transport involves 4 steps: 1. Air is inhaled through the process of Ventilation (mechanical movement of gas or air into and out of the lungs, necessary to ensure sufficient perfusion) through the lungs. 2. Oxygen diffuses from alveoli into pulmonary capillaries (dense network of blood vessels surrounding the alveoli), moving oxygen from the pulmonary veins (only veins which carry oxygenated blood) to the left side of the heart (atrium-ventricle) to the aorta into systemic arterial circulation. 3. Perfusion (exchange of O2 and CO2 in the bloodstream, which occurs via the alveoli and pulmonary capillaries) of systemic capillaries with oxygenated blood. 4. Oxygen is diffused from the systemic capillaries to each and every cell. Gas CO2 transport involves 4 steps (backwards): 1. Diffusion of blood (deoxygenated) from cells into systemic capillaries. 2. Perfusion of systemic capillaries with deoxygenated blood through the venous circulation, to the vena cava, into the right side of the heart (atrium-ventricle), to pulmonary arteries (only arteries which carry deoxygenated blood). 3. Diffusion of CO2 from pulmonary arteries into alveoli through pulmonary capillaries. 4. Exhalation of air by ventilation of the lungs for removal of CO2 Bronchioles- smallest of conducting airways -3 layers: 1. Epilthelial layer- (inner layer) mucous containing goblet cells, ciliated cells 2. Connective tissue layer- lamina propia- cartilage, WBCs 3. Smooth muscle layer- outer layer to constrict and dilate -Bronchioles branch out from the bronchi and connect to the alveoli. -Controlled by the ANS (autonomic nervous system). o Parasympathetic stimulation- mediated via vagus nerve § Releases neurotransmitter acetylcholine-binds to cholingeric receptors leading to bronchial constriction (decreased air flow) § Dominates to limit exposure to external substances (protection mechanism) o Sympathetic stimulation- stimulation of neurotransmitter epinephrine- binds to beta-2 adrenergic receptors  leading to bronchial dilation (increased air flow) Asthma- chronic inflammatory disorder of the bronchial mucosa -causes bronchial hyper-responsiveness, constriction of airways, and variable airflow obstruction that is reversible Pathophysiology: Antigen enters bronchial airway binds to sensitized mast cells and cover with IgEtriggers mast cell degranulation and release of inflammatory mediators’ histamines, bradykinins, prostaglandins, platelet- activating factors, prostaglandins, leukotrienes, interleukin. smooth muscle constriction, mucus secretion, and vasodilation  mucosal edema and migration of more WBCs to site  dendritic cells also present Ag to Th2 cells  causing interleukin release to produce more IgE to coat mast cells and facilitate Ag binding. Interleukin also activates eosinophils release of chemicals designed to rid the area of Ag, but instead damage surrounding airway tissue activated neutrophils amplify this damaging effect. Long term damage can lead to permanent airway remodeling. Asthma signs and symptoms -asymptomatic between attacks beginning of attack: o chest constriction o expiratory wheezing o dyspnea o nonproductive coughing o prolonged expiration o tachycardia o tachypnea - severe attacks: o use of accessory muscles of respiration o wheezing during both inspiration and expiration o pulsus paradoxus- decrease in SBP during inspiration >10mmHg Alveolar hyperinflation with asthma -airway obstruction increases airflow resistance and decreases flow rates. -impaired expiration causes air trapping, hyperinflation distal to obstruction, and increased WOB. - continued air trapping increases intrapleural pressure and alveolar gas pressuresdecreased alveolar perfusion -hyperventilation is triggered in response to increased lung volume and obstruction (early hypoxemia without CO2 retention and respiratory alkalosis) -with progressive obstruction of expiratory airflow, airtrapping becomes more severe  lungs and thorax hyperexanded, disadvantage to respiratory musclesdecrease in tidal volume and increase in CO2 retentionrespiratory acidosis (triggering respiratory failure) Anticholinergic drugs and the treatment for asthma -fast acting -tiotropium, ipratropium Mechanism of action of anticholinergic drugs to treat asthma -block acetylcholine bindingbronchodilation through decrease in parasympathetic response Bronchitis and associated pathogenesis -acutely caused by infection or inflammation -usually caused by a virus with a nonproductive cough Chronic:hyper secretion of mucus and chronic productive cough that continues for at least 3 months of the year (usually the winter months) for at least 2 consecutive years. -enhanced chronic inflammatory response in the airways to noxious particles or gases -inspired irritantsbronchial inflammationbronchial edema, increase in mucus glands and goblet cells in airway, smooth muscle hypertrophy with fibrosis, narrowing of airways. -hyper secretion of thick mucus, cant be cleared due to impaired ciliary function (defensive mechanisms compromised increasing susceptibility to infection contributing to airway injury and ineffective repair. -initially only affects larger bronchieventually all airways involved Chronic bronchitis and related acid/base disturbances, -narrowed airwaysobstructionventilation-perfusion mismatch with hypoxemia -Hypercapnia develops as air trapping worsens and the work of breathing increases -reduced tidal volumes, hypoventilationrespiratory acidosis Polycythemia vera -Marked hypoxemia (e.g. chronic bronchitis) leads to polycythemia (overproduction of erythrocytes) and cyanosis. -PV is a chronic neoplastic, nonmalignant condition characterized by overproduction of red blood cells (frequently with increased levels of white blood cells [leukocytosis] and platelets [thrombocytosis]) and splenomegaly. -Erythrocytosis is the essential component of PV. Clonal proliferation of erythroid progenitors occurs in the bone marrow independent of erythropoietin, although the cells express a normal erythropoietin receptor Cardiac ?Blood flow between heart and lungs -The superior & inferior vena cava carry systemic DEOXYgenated blood to the right atrium. -The tricuspid valve opens to allow blood flow into the right ventricle. -The pulmonary semilunar valve opens to allow blood flow into the pulmonary trunk, a large blood vessel which divides to form the left and right pulmonary arteries that carry blood to the lungs and eventually into the alveolar capillaries where gas exchange will occur. -The pulmonary veins return the OXYgenated blood to the left atrium. -The bicuspid valve opens to allow blood flow into the left ventricle. The aortic semilunar valve opens to allow blood flow into the aorta,a large blood vessel that divides to form the brachiocephalic, left common carotid, and subclavian arteries that will further branch to carry blood to the rest of the body. Cardiac cycle: 1. Atrial systole, atria contract blood pushes through open tricuspid and mitral valves into ventricles. Semilunar vavles are closed 2. Beginning of ventricular systole, ventricles contract, increased pressure in ventricles. Tricuspid and mitral valves close, (1st heart sound) 3. As pressure rises, semilunar valves open when ventricular pressure>atrial pressure blood pushed into aorta and pulmonary arteries 4. Beginning of ventricular diastole, pressure in relaxing ventricles drop below that in the arteries and semilunar valves close (2nd heart sound) 5. As pressure falls, blood flows from veins into relaxed atria. Tricuspid and mitral valves open when pressure in ventricle falls below atrial pressure Heart Valves -One-way blood flow through the heart is ensured by the four heart valves - Atrioventricular valves -mitral (left AV valve) and tricuspid (right AV valve) -During ventricular relaxation (diastole) the two AV valves open and blood flows from higher pressure in the atria to the lower pressure in the relaxed ventricle - With increasing ventricular pressure these valves close and prevent backflow into the atria as the ventricles contract. -closure= 1st heart sound (S1) -Semilunar valves -pulmonic and aortic -open when intraventricular pressure > aortic and pulmonary pressures and blood flows out of the ventricles and into the systemic and pulmonary circulations -After ventricular contraction and ejection, intraventricular pressure decreases and the semilunar valves close when pressure in the vessels > pressure in the ventricles, preventing backflow into the right and left ventricles - Pulmonary (RV  lung) -Aortic (LV  body) -closure= 2nd heart sound (S2) Cardiac output (CO) -HR(bpm) x SV(L/beat) -normal CO of a healthy adult is about 5L/min -4 factors affect CO directly - preload - afterload - heart rate - myocardial contractility Ejection Fraction- -SV/End Diastolic Volume (EDV) - increased by factors that increase contractility, (sympathetic nervous system activity) -A decrease in ejection fraction may indicate ventricular failure Stroke Volume--volume of blood ejected per beat during systole - depends on the force of contraction, the myocardial contractility, or the degree of myocardial fiber shortening (afterload, contractility, preload) - Inverse relationship with HR (↑HR=shorter fill time=↓SV, ↓HR=longer fill time=↑SV) -normally 70 ml Cardiac contractility -factors that determine force of contraction: - changes in preload - inotropic stimuli changes o SNS Neurotransmitters: epinephrine, norepinephrine (POSITIVE inotropic agents) § INCREASED contractility § Fever, anxiety, o Vagus nerve: Acetylcholine (NEGATIVE inotropic agent) § DECREASED contractility - O2 and CO2 levels o Severe hypoxemia= contractility is decreased o Moderate hypoxemia=catecholamines can increase contractility -determined by available Ca+ and its interaction with actin-myosin -actin/myson turn inward (inotropic) and react together to create muscle fiber contraction -troponin releases Ca+= myocardial relaxation -decreased in ischemia, hypoxia, decreased ATP Calcium binding and troponin: -in resting muscle, calcium ions are stored in sarcoplamic reticulum. -action potential reaches the muscle cellT tubules carry action potential deep into sarcoplasmcauses sarcoplasm reticulum to release store of calcium ions -In resting muscle, myosin binding sites are covered by troponin and tropomyosin. Calcium ions released into sarcoplasm as a result of action potential bind to troponintropomyosin and troponin move out of the way of the