ANP1115 Lecture 2 Blood and Intro to Heart 2023 PDF

ANP1115B: Topic 1.1 – Blood (Part 2) 1.1.1 Describe the composition of blood (pp. 642-645) 1.1.2 Erythrocytes: describe their structure, function & life cycle (pp. 645-651) 1.1.3 Hemostasis: list the principal steps and justify the role of platelets in this process (pp. 657-660) 1.1.4 Describe bri...

ANP1115B: Topic 1.1 – Blood (Part 2) 1.1.1 Describe the composition of blood (pp. 642-645) 1.1.2 Erythrocytes: describe their structure, function & life cycle (pp. 645-651) 1.1.3 Hemostasis: list the principal steps and justify the role of platelets in this process (pp. 657-660) 1.1.4 Describe briefly the processes of clot retraction & fibrinolysis (pp.660-663) 1.1.5 Differentiate among the different blood types and explain the basis of transfusion reactions (pp. 663-666) J. Carnegie, UofO Fibrinolysis removal of clot when no longer needed key enzyme is plasmin [precursor = plasminogen, a plasma protein that also gets incorporated into the clot] - plasminogen is activated by tPA (tissue plasminogen activator) released by endothelial cells fibrinolysis begins within 2 days (outer edges) & continues until clot is dissolved http://www.intechopen.com/source/html/46041/media/image4.png Factors Limiting Clot Growth/Formation 2 homeostatic mechanisms to control size of clot: (i) swift removal of coagulation factors (ii) inhibition of activated clotting factors clot formation requires [procoagulation factors] > [anticoagulation factors] (i) normally flowing blood washes away procoagulants (hence the importance of vascular spasms in response to injury) (ii) as thrombin forms, it is adsorbed onto fibrin threads (limits clot size) (iii) antithrombin III (plasma protein) inactivates any escaping thrombin (iv) antithrombin III & protein C (plasma protein) inactivate many intrinsic pathway procoagulants (v) heparin (basophils & mast cells) – enhances activity of antithrombin III and inhibits intrinsic pathway (vi) smooth endothelial lining of undamaged blood vessels (no access to collagen) prevents undesirable clotting; also endothelial-derived NO & prostacyclin) One action of Hirudin is to inhibit the action of thrombin; http://www.bloodservices.ca/CentreApps/Internet/UW_V502_MainEngine.nsf/page/Blood+Suckers?OpenDocument Thromboembolytic conditions: (undesirable intravascular clotting) thrombus: clot that develops & persists in an unbroken blood vessel - can block critical blood circulation to those tissues What might promote thrombus formation in an unbroken blood vessel? embolus: a thrombus which has broken free → can get stuck in a vessel of small diameter (eg: pulmonary or cerebral emboli) treat with drugs such as tPA, streptokinase to dissolve clots via plasmin Why is low dose aspirin a good preventative therapy in heart attack risk patients?? http://www.nlm.nih.gov/medlineplus/ency/article/001124.htm  Bleeding Disorders (interference with normal clotting): (i) Thrombocytopenia: any condition harmful to bone marrow (malignancy, radiation, drugs) → easy bruising due to internal hemorrhage; also, petechiae > platelet count < 150,000/µl > whole blood transfusions give temporary (why temporary?) relief (ii) Impaired liver function: eg: hepatitis, cirrhosis (procoagulants come from liver) - liver disease also associated with reduced bile production; bile needed to absorb vitamin K (why and why is this important?) (iii) Hemophilias: hereditary bleeding disorders due to deficiencies in intrinsic pathway factors; hemophilia A (83% of cases) – lacking factor VIII; hemophilia B – lacking factor IX - both sex-linked & require regular transfusions Fi. 17.16 Petechiae https://healthjade.com/hemophilia/ 1.1.4 Differentiate among the different blood types (ABO, Rh factor) and explain the basis of transfusion reactions the body compensates for some blood loss by: (i) generalized vasoconstriction to decrease blood vessel volume (ii) increasing the rate of erythropoiesis loss of 15-30% 🡺 weakness, pallor; loss > 30% can induce shock whole blood transfusion: if substantial blood loss or thrombocytopenia; often packed red cells for anemia donor blood mixed with an anticoagulant (citrate dextrose – a calcium chelator) - can be stored several weeks @ 40C J. Carnegie, UofO Human Blood Groups transfusion of incompatible blood can be fatal RBC antigens promote agglutination newborn blood has only the ABO and Rh antigens cause serious no preformed agglutination problems during transfusion antibodies ABO Blood Groups: (agglutinins): begin Why is type O the universal donor? Why is type to appear within AB the universal recipient? months; reach adult Which blood type is most common? Least levels at years common? See also Table 17.4 https://www.dreamstime.com/stock-photos-abo-blood-group-diagram-image19504213 Rh Blood Groups: many different types of Rh factors (only C, D & E are fairly common) Rh D first identified in Rhesus monkeys, then in humans (~85% North Americans Rh+ (meaning??? ……………………………………………..) Rh antibodies NOT spontaneously formed in blood of Rh- individuals - individuals become sensitized upon first exposure to Rh antigens (transfusion, carrying an Rh+ fetus) → antibodies will attack donor RBCs in response to second & subsequent exposures Rh- mothers carrying second Rh+ fetus treated with RhoGAM (anti-Rh serum) to prevent erythroblastosis fetalis (hemolytic disease of the newborn) J. Carnegie, UofO Transfusion Reactions: Agglutination & Hemolysis problem is recipient’s agglutinins (antibodies), not donors - Why? (i) agglutination: clogs small blood vessels (ii) clumped RBCs rupture or are destroyed by phagocytes & Hb released overall result: (i) blocked flow to tissues (ii) reduced O2-carrying ability of blood (iii) Hb precipitates/clogs kidney tubules → possible kidney failure also: fever, chills, nausea, vomiting, general toxicity - critical to prevent kidney failure by administering alkaline fluids to dilute & dissolve Hb; also diuretics autologous transfusion (eg: 1 unit/4 days up to 3 days before surgery) http://www.chxa.com/a/what-is-blood-agglutination/  Anti-A serum Anti-B serum Blood Typing Type AB use serum containing anti-A or Anti-B agglutinins similar procedure for Rh factor typing Type B Don’t forget to try this! Type A Type O J. Carnegie, UofO  Topic 1.2 The Heart Chapter 18 1.2.1 Describe the internal and external anatomy of the heart 1.2.2 Trace the pathway followed by blood in both the pulmonary and systemic circuits 1.2.3 Describe the organization of the coronary circulation Mastering A and P and its interactive physiology learning exercises will be very helpful for this topic! J. Carnegie, UofO The internal and external anatomy of the heart simply a transport system pump; hollow blood vessels provide delivery routes enclosed within mediastinum of thorax extends obliquely for 12-14 cm from 2nd rib to 5th intercostal space; 2/3 of mass on left side; right side lying on diaphragm broad, flat base toward right shoulder; apex points toward left hip 3 layers: pericardium, myocardium, endocardium Fig. 18.2 1. Pericardium – outer covering of heart double-walled, fibro-serous sac a) fibrous pericardium protects and anchors heart prevents overfilling of heart b) serous pericardium: parietal & visceral (epicardium) layers + fluid-filled pericardial cavity Fig. 18.3 2. Myocardium cardiac muscle = bulk of heart branching cardiac muscle cells arranged into bundles and the connective tissue wrappings of these bundles: » reinforce myocardium internally & anchor cardiac muscle fibers » provide additional support for great vessels & valves » direct spread of action potentials across heart to specific pathways 3. Endocardium » layer of endothelium + CT layer on inner myocardial surface » continuous with endothelium of vessels leaving & entering heart J. Carnegie, UofO Fig.  2 atria & 2 ventricles; what are the interatrial & interventricular septa? 2 exterior grooves: coronary sulcus (atrioventricular groove) & anterior-posterior interventricular sulcus Anterior view J. Carnegie, UofO Fig. 18.5a  1. Atria: Receiving Chambers small, thin-walled - need only convey blood to ventricles deoxygenated, systemic blood enters right atrium via: (i) superior vena cava - systemic from ?? (ii) inferior vena cava - systemic from ?? (iii) coronary sinus - from myocardium oxygenated blood to left atrium via 4 pulmonary veins Fig. 18.5d Posterior view Fig. 18.5a – Gross anatomy of the heart; Anterior view  pectinate muscles (muscle bundles found especially the right atrium) fossa ovalis foramen ovale www.riversideonline.com Fig. 18.5e Frontal Section 2. Ventricles: Discharging Chambers these are the real pumps of the heart; walls much thicker (esp: left ventricle) (i) right ventricle pumps blood oxygen-poor to the pulmonary trunk (ii) left ventricle pumps oxygen-rich blood to the aorta internal walls have muscle bundles: trabeculae carneae, papillary muscles (the latter link the chordae tendineae) Fig. 18.5e Fig. 18.9 chordae tendineae J. Carnegie, UofO 3. Heart Valves blood flow is unidirectional; enforced by 4 heart valves realize the importance of chordae tendineae & papillary muscles to keep valves ??? 1. Atrioventricular valves: paired, between ….. & ….. (i) tricuspid valve = right atrium to right ventricle (ii) mitral (bicuspid) valve = left atrium to left ventricle 2. Semilunar valves: paired, from ventricles to either pulmonary or systemic circuits (i) pulmonary valve = right ventricle to pulmonary trunk (ii) aortic valve = left ventricle to aorta Valve problems valvular insufficiency (incompetent valves that don’t close 100%) valvular stenosis – valves stiff due to calcification and/or scar tissue J. Carnegie, UofO Fig. 18.6a Superior view; atria removed AV valves Semilunar valves Figs. 18.7 & 18.8 J. Carnegie, UofO Trace the pathway followed by a RBC from its entry into the heart to its exit; include all of the valves in the order encountered http://www.youtube.com/watc 2 4 3 h?v=JA0Wb3gc4mE 1 One tiny correction in this video: The narrator refers to the pulmonary trunk as the pulmonary artery.  2 side-by-side pumps: 1. Pulmonary circuit 2. Systemic circuit Focus Figure 18.1  Equal volumes are pumped into the pulmonary & systemic circuits; but the two ventricles have unequal workloads (1) pulmonary circuit (rt ventricle): short, low-pressure circulation (2) systemic circuit (lt ventricle):long pathway with 5X resistance Walls of left ventricle 3X thicker than those of right. Fig. 18.1 1.2.3 Describe the coronary circulation shortest, but one of the most important, circulations in the body right & left coronary arteries branch from the base of the aorta; encircle the heart in the coronary sulcus (atrioventricular groove) Fig. 18.10a  many anastomoses, which provide alternate routes for nourishment if a given artery begins to be occluded - but total occlusion means ???? (1) actively deliver blood when heart is relaxed (2) largely ineffective when ventricles contracting because?? heart ~1/200 of body but requires ~1/20 of blood supply (esp. left ventricle) Diseases of coronary vessels: angina pectoris: myocardial infarction: J. Carnegie, UofO https://medlineplus.gov/ency/article/000198.htm Coronary venous supply: begin with capillaries: