Study Guide Exam 3.docx

SG Questions. *Respiration packet: Qs- 1)ventilation for inspiration- Ptp, what does that mean? 2) pg 5, hyperpnea 3)pg 6, intermittent vs. continuous 4) pg 8, steady state? Hemostasis-> #1: what directily stimulates platelet activation? What stimulates cascade of clotting. Angiogenesis->tumor angiogenesis, can you encourage inhibition? #2, #8- are prothrombin & fibrinogen released by endothelial cells? I.

Cardiovascular Disease for Exercise Physio 1. Describe Frank-Starling Relationship of Heart & draw the cure. How will heart failure affect this relationship? What effect will SNS stimulation have on the relationship. Frank-Starling curve graphs the relationship between EDV and SV, which is curve-linear (plateaus at certain point). EDV is on the x-axis, SV is on the y-axis. If heart failure, then the graph will shift downwards, with SNS stimulation it is slightly compensated. For normal with SNS it increases SV. 2. What is Coronary Artery disease (CAD)? What are the signs & symptoms? CAD is a chronic disease where accumulation of plaque in the arteries decreases blood flow so that metabolic need is not fulfilled. It can lead to an acute cardiac failure (for example a myocardial infarction). Typical signs: intense, dull, heavy pain in chest, arms, jaws. Atypical: indigestion, fatigue, back pain. Treatment options? NO, Calcium channel blockers, Beta blockers, Anti-platelet

3. Differentiate between the response to acute vs. chronic heart failure. Why can left heart failure cause lung edema? *What hemodynamic parameter is deranged? Acute- immediate blockage of artery. Decrs CO, incrs P, SNS, Renal body fluid-> irreversible cell death (COPRS)

Chronic- pathophysiological state where heart cannot pump enough blood to meet metabolic needs-> results in cardiac remodeling/pathological hypertrophy. Cause: Also CAD->MI, hypertension, immune disease Left heart failure causes lung edema because the blood from the left heart comes from the pulmonary artery which connects to the lungs. When there is a blockage in the left heart, the fluids pools back into the pulmonary artery, into the lungs. Treatment: CAABD- Cardiac glycosides, angiotensin receptor blockade, ACE inhibitors, Beta-blockers, Diuretic. The hemodynamic parameters causing edema is incrs Pc, incrs pi IF, *decrs. Pi C 4. Differentiate between diastolic dysfunction vs. systolic dysfunction Diastolic dysfunction- when heart is not fully filling Systolic dysfunction- when heart is not fully contracting

5. Describe the mechanism of each drug and common side effects: a. Diuretics: remove extra fluids, good for making edemas more bearable b. ACE inhibitors: Drugs that inhibit the pathway of Angiotensin I to Angiotensin II, prevents heart remodeling c. Angiotensis Receptor Antagonists: block angiotensinogen pathway, inhibits heart remodeling d. Nitrates- vasodilation, increases BF -> CAD e. Calcium Channel Blockers- vasodilation by blocking contr smooth muscles-> CAD f. Beta-blockers: decrs SNS response g. Anti-platelet agents: prevents plaque from getting larger h. Cardiac glycosides- Ionotropic effect, intensity of heart beat i. Anticoagulents- decrs TPR 6. Describe the Cardiovascular adjustments to aerobic exercise. What role does ANS contribute to change in cafdiovascular parameters? a. Need increase CO during aerobic exercise-> Incrs MAP, incrs EDV, incrs Systolic bp, decrs TPR. b. Also decrs BF to internal organs to muscles 7. Describe the training effects of aerobic exercise training. a. Incrs. Peak physiological function b. Active can reach higher VO2 Max c. Active has greater CO d. Active has lower rise in HR, does not reach an as high HR e. Active has greater SV

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Function of Blood & Erythrocytes (RBCs) 1. List the types of cells found in the blood and a general statement about their function: i. Erythrocytes (RBC)- red blood cells, transports oxygen ii. Leukocytes (WBC)- white blood cells, immune cells a. Neutrophils- general defense, most numerous b. Eosinophils, basophils, macrophages (2nd most) iii. Platelets- from megakaryoctes, myloid precursors, essential for hemostasis (clot formation) 2. Describe the genesis of blood cells. Differentiate between the cells of the myeloid lineage and lymphoid lineage. What role do growth and differentiation inducers play in the synthesis of a particular blood cell? What is a pluripotent stem cells? a. RBC come from myeloid precursor, WBC, come from lymphoid precursors b. RBC can differentiate in the bone marrow and in periphery (only one) c. EPO necessary for differentiation of precursor into RBC d. Thrombopoeiten important in differentiating into megakaryocytes-> fragments platelets e. Pluripotent stem cell is an undifferentiated cell that can differentiate into many different cell types. 3. Describe the major classes of plasma proteins, their source (where synthesized) & their function. a. Plasma Globulins- osmotic pressure in blood (pi C) Liver b. Plasma Albumins-transport vitamins & antibodies (Liver, except immunoglobins) c. Fibrinogen- Liver, clotting 4. Describe the synthesis, function, destruction of RBC. What is a reticulocyte? Describe the attributes of a mature RBC. a. Synthesis-> myeloid precursor encouraged to differentiate w/ EPO (w/ Hbg, Iron, Lose organeleles, Nucleus decondenses) b. Reticulocyte- is an immature RBC, wrong shape c. Mature RBC- disc shape, 5. What role does the RBC play in assisting with Acid-Base balance? Carbonic anhydrase catalyzes what important reaction in the RBC? a. RBC contains hgB which binds to H+ b. Carbonic anhydrase catalyzes the fwd and backwards rxn from CO2 +H20<>H2CO3<>H+ +HCO36. Discuss the nutritional requirements for proper synthesis and function of RBCs. Why is each of these nutrients important for proper function of the RBC? -Iron: For Hgb formation -Folic Acid & B12: DNA synthesis; esp B12 for intrinsic factor 7. Differences between transferrin & ferritin. What role does the GI play in determining total FE transferrin

Transferrin: when Fe binds to apotransferrin (protein) to travel through circulation Ferritin: located in GI tract, binds to excess Fe and releases in feces. (FErritin, Feces) Gi can regulate mRNA for ferritin/ amount of ferritin in body and therefore how much Fe will be in feces/ absorption amount 8. Describe the structure and function of hemoglobin. Where is hemoglobin synthesized? Composed of 4 Hgb chains, each one with a heme and globin portion, each hemoglobin carries 8 atoms of oxygen. It is synthesized in the. Heme synthesized in mitochondria & cytosol of RBC, globin synthesized by ribosomes. 9. Describe the function of EPO. Where is EPO synthesized and what is the major stimulus for synthesis? Give examples of situations when EPO ynthetic rate would be increased. EPO- erythropoeiten is a hormone that causes immature reticulocytes-> mature RBC. It is synthesized in the kidney, and stimulated by decrease tissue O2. In areas of low oxygen, EPO secretion reaches max in 24 hrs. 10. Define Anemia and Polycythemia Anemia: lack of RBC or hemoglobin. Results in less total oxygen perfusion to cells. Could be due to maturation failure-> hyperchromic: abnormal; hypochromic, abnormally low amounts of Hgb. Polycythemia: too many RBC, increases in viscocity that can impede BF 11. Differentiate between ABO blood classifications. Discuss basis for blood transfusion reactions. A, have A markers, anti-B anti-agglutinins. B, have B markers, anti-A anti-agglutinins. O have no markers, anti A & B. AB A&B, no anti.

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Hemostasis 1. Describe the role of vessel constriction, platelet aggregation, and thrombus formation in hemostasis. Hemostasis= stoppage of bleeding. Immediately once there is a cut, there is vasoconstriction. Injury causes collagen to be exposed which activates platelets- Platelet Factor. Platelets secrete TXA2- stimulates platelet aggregation, serotonin, ADP-> have myosin actin capabilities. Platelets bind to collagen via VWf. Fibrinogen bridges platelets. Platelets turn from liquid->gel because of thrombin-> which stimulates cascade of mesh clot, activates factor 13. Also positive feedback, and stim cascade of fibrinogen->fibrin. Both Prothrombin->thrombin, and fibrinogen->fibrin need Ca to occur. Vit K, bile salts, CA necessary. 2. Disorders of platelet aggregation-> bleeding problem, cannot stop bleeding.

Blood coagulation order-> cannot stop bleeding, scarring. 3. Describe role of each in hemostasis: i. Thrombocytes: (AKA platelets!) cells that are fragments of megakaryocytes that aggregate together over a damaged part of an endothelial cell. ii. TXA2: secreted by thrombocytes to stimulate platelet aggregation iii. VWf: factor secreted by endothelial cells and platelets to adhere to collagen. iv. Fibriongen: bridges neighboring platelets v. Thrombin: stimulates protein cascade for thrombus formation through activation of factor IV13. Also stimulates transformation of fibrinogen to fibrin.

4. Dietary nutrients required for normal blood clotting: a. Ca++: necessary for prothrombin->thrombin, and fibrinogen->fibrin b. Vit K: make prothrombin & clotting factors c. Bile: to absorb Vit K 5. Mechanisms to oppose clot formation. When are these mechanisms active? a. Endothelial cells secrete NO, PGI2 that inhibit TXA2 b. Tissue factor pathway inhibitor inhibits clotting factor X c. Thrombomodulin-> activates Protein C which inactivates clotting factors d. Antithrombin III: inactivates thrombin  Activated once clotting is active 6. What system is active to dissolve a clot? What are the important mediators that function to produce plasmin? What is the role of plasmin in the body? -Fibrinolytic system-> T-PA secreted by endothelial cells, convert plasminogen->Plasmin -Plasmin digests fibrin, dissolve clots.

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7. Describe anticlotting role of each: a. Thrombomodulin: -above b. Antithrombin III:- above c. Heparin: anticoagulant, prevents platelets from binding together 8. List the chemical mediators released from an endothelial cell & briefly state whether the mediator stimulates clotting or opposes clot formation: NO, PGI2-> oppose clot formation VWF- Clot Angiogenesis 1. Define/Describe: a. Angiogenesis: formation of blood vessels b. Activator molecules: molecules that promote growth: VEGF & bFGF (both stimulate NO release), and granulocytes colongy stimulating factor, hepatocyte GF

c. Inhibitor molecules: block vessel growth: AEPI- Angiostatin & Endostatin: increase apotosis, Platelet factor 4- clotting system, interferons- chemical messenger by WBC d. Metalloproteinases: secreted by activated endothelial cells, breaks down extracellular matrix 2. Briefly describe mechanism by which VEGF & bF promote growth- VEGF-> in vascular endothelial cells release NOS in endothelial, Basic fibroblast-> stimulates NOS in endothelial 3. Angiostatin & endostatin both promote cell apoptosis. Angiostatin are plasminogen fragments, endostatins are fragments of collagen. 4. List examples of normal angiogenesis: a. After menstruation to renew blood vessels b. Wound generation c. During growth and development 5. Describe tumor angiogenesis- what strategies are used to inhibit tumor growth? a. Tumor angiogenesis: growth blood vessels to feed a tumor, blocking VEGf and other growth factors inhibit tumor growth but causes diseases Could you incrsase angiostatin and endostatin? V. Respiratory Physiology 1. Describe the major functions of the lung. What lung functions are considered non-respiratory functions of the lung? Functions: maintain normal arteriole blood gas pressure, remove metabolic waste Non-respiratiory: defesne, removing substances from blood, adding metabolic substances, trapping and dissolving clots 2. Describe the major anatomical features of the lung. Describe the anatomical relationship of the lung to the chest wall. Describe the anatomical relationship of the lung and the diaphragm. Lung: 2 lungs, surrounded by pleural cavity filled with fluid, all together encapsulated by the chest wall. The lung’s elastic potential and alveolar ST make it so that they are always trying to collapse, while the chest wall always want to expand. Diaphragm is a sheet of skeletal muscle that lies below the lung, when contracts increases volume of thoraxic cavity= lowers Pip, also lowers Palv so that it is neg in comp to Patm and air rushes in. When relaxed, diaphragm results in exhalation. 3. Describe the components of the respiratory system. Differentiate between the structures of the conducting zone versus the respiratory zone. 4. Differentiate between the functions of the respiratory zone and the conducting zone. 5. Describe mechanisms to dilate versus constrict the airways. What effect does airway constriction have on resistance to airflow?

6. What cell type synthesizes and secretes surfactant? At what age does surfactant secretion initially begin? What is the function of surfactant? II, 3rd trimester, increase lung compliance 7. Define lung compliance. What role does surfactant play in altering lung compliance? -Change in volume/ Change in Ptp, if more surfactant good compliance -Elastic, Surface tension- incrs w/ deep breaths 8. Define intrapleural pressure. What is the nature of this pressure? -Change in pressure of intrapleural fluid 9. Define Transpulmonary pressure. What role does transpulmonary pressure play in expansion of the lungs? Ptp = Palv(alveolar) -Pip (intrapleural), incrs Ptp= inspiration, expansion in lung; decrs Ptp= expiration. -> depends all on compliance 10. Define Ventilation; what are the units of ventilation? Differentiate between Alveolar and Minute Ventilation. Describe the mechanics of ventilation beginning with contraction of the diaphragm. Include in your discussion the pertinent pressure differences between lung pressures and atmosphere pressures. -Exchange of air btw alveoli & atm over time. F= change P/Resistance, for Palv>Patm, driving force is expiration. Minute Ventilation: TV(500ml) x respiratory rate (12 breath/min); Alveolar TV-150 x respiratory rate (note different from alveolar dead space) 11. List the major muscles of inspiration and expiration. When is expiration a passive phenomenon? -Diaphragm for both, inspiration->external, expiration->internal 12. Define and describe the following lung volumes and capacities: Tidal volume- volume in and out for normal breathing Residual volume- air remaining in lungs w/ max expiration Vital capacity- max air inspired or expired Total lung capacity- VC + RV 13. Define and describe the following measurements made in pulmonary function tests: Forced expiratory volume (FEV)- volume expired using force Forced vital capacity (FVC)FEV1 – how much that can be forced out in 1 sec

FEV1/FVC ratio- should be 80%, Obstructive= decrease in ratio, decrease FEV1 & FVC Maximum expiratory flow rate 14. Differentiate between obstructive and restrictive lung diseases. Discuss in your answer the differences in total lung volume, vital capacity and pulmonary function tests. Obstructive Incrs airway R Decrs VC Decrs FEV1, decrs FEV1/FVC incrs residual V, incrs TLC (can’t expire as much air)

Restrictive Normal airway R Decrs TLC Decrs VC Decrs FEV1, Normal FEV1/FVC

15. Describe the key determinants for gas diffusion between the alveoli and lung capillaries. Describe the anatomical barrier for diffusion of gases in the lung. -Pressure difference -Area available -diffusion coeff -member thickness 02->alveolus->alveolar cell type I->meager->capillary endothelium->RBC membrane 16. Describe the differences in the composition of atmospheric versus alveolar versus expired air. What determines the composition of alveolar oxygen? What determines the composition of alveolar carbon dioxide? -alveolar: h20 saturated, constantly diffusing, **only partially replaced with each breath! -alveolar ventilation, rate of consumption 02 -alveolar ventilation, rate of excretion Co2 17. Know how to calculate alveolar ventilation, minute ventilation, PAO2. 150- PACO2/.8 R=CO2/O2; (760-47)*.21 (or.24 for full oxygen) 18. Know the normal ranges for arterial blood gases. PaO2: 98-100 PaCO2: 40

19. Define and differentiate between hyperventilation and hypoventilation. Partial pressures of gas in the_____ALV_____ are used to determine the presence of hyper vs. hypoventilation. Hyperventilation- incrs ventilation doesn’t match w/ incrs need Hypoventilation-decrs ventilation not matched w/ decrs need 20. Define hyperpnea. Incrs ventilation matches VO2 consumption, alveolar levels ok, Alveolar normal? **21. Describe the zones of the perfusion (continuous versus intermittent) in the lung. How are these zones related to position? Upper: intermittent, doesn’t get continuous blood supply (continuous during exercise) Lower: continuous, gets blood supply all the time Example: Pressure in Arterial end of capillary > Pressure in Venous end > Pressure in Alveolus *22. Describe the importance of hypoxic vasoconstriction in maintaining normal V/Q ratios. -send blood elsewhere when not adequate O2 content in blood23. What changes in airway resistance occur to correct for imbalances in alveolar carbon dioxide? 24. Describe the following terms: Physiological dead space- no blood flow (black holes to infiniti) Shunt- no air through alveoli (shun you, no entry- 0) 25. Describe the mechanisms to transport oxygen in the blood. What relationship exists between arterial partial pressures of oxygen and hemoglobin saturation? -Most bound to hgb, some dissolved. Curve-linear, shift to right incrs H, incrs temp, incrs DPG (glycolosis) 26. Describe the shape of the Oxygen-hemoglobin dissociation curve. What conditions shift this curve to the right? What effect does a right shift have on delivery of oxygen to respiring cells? 27. Describe the mechanisms for transport of carbon dioxide. Know the equation catalyzed by carbonic anhydrase. How does this equation result in the generation of plasma bicarbonate? -10% dissolved, 30% bound to protein, 60% as plasma bicarbonate ->carbonic anhydride convert 28. Describe the role of hemoglobin in the transport of oxygen, carbon dioxide, and hydrogen. -can transport all 3, affinity depends on what is bound to hemoglobin already 29. Where is the major integrative center for control of respiration? Differentiate between the roles of the peripheral versus central chemoreceptors in control of ventilation.

-medulla, peripheral looks at both PO2 & H+, central just looks at H+ and in medulla 30. Define the following terms: Hypoxia- decrs O2 levels in cells Hypoxemia- decrs PaO2 Anemic hypoxia- decrs RBC/hgb= decrs O2 Ischemic hypoxia- incrs viscocity Histotoxic hypoxia 31. Briefly describe the ventilatory response to exercise. What happens to arterial blood gas measurements during exercises there a difference between steady state or high intense exercise? -incrs ventilator, steady state= normal, high intense: decrs O2, incrs. CO2 32. Define Lactate Threshold. What ventilator response occurs when a person reaches their lactate threshold? 32. Describe how the body acclimates to Altitude. What role do the peripheral chemoreceptors play? Sense decrs O2, incrs. ventilation