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APHY 201 Exam 3a
Ch. 13 Blood, Heart, and Circulation
| Question | Answer |
|---|---|
| what are 3 functions of the circulatory system? (broad) | transportation (respiratory gases, nutrients, wastes), regulation (hormonal and temperature), protection (clotting and immunity) |
| about how many miles do the blood vessels comprise? | 60,000 miles |
| what organs make up the lymphatic system? | spleen, thymus, tonsils, lymph nodes, lymphatic vessels, lymphatic tissues, lymphatic organs |
| what is the average adult blood volume? | 5 liters |
| what percentage of normal hematocrit is blood cells? | 45% |
| what is the major solute in blood? | sodium |
| recognize for multiple choice which solute is not in blood | metabolites such as amino acids, nucleotides, glucose, pigments, hormones, enzymes, antibodies, proteins |
| (starred) what is the representative normal blood value for blood osmolality? | 285 to 295 mOsm (about 300 mOsm in renal physiology) |
| (starred) what is the normal blood value of blood pH? | 7.38 to 7.44 (7.35 to 7.45) |
| (starred) what are the normal hematocrit values (RBC proprotion) for male and female? | female is 36-46%, male is 41-53%. average is 42% |
| (starred) what is the normal hemoglobin (Hb) value for male and female? | female 12-16 g/100mL, male 13.5-17.5 g/100mL (female also lower due to menstruation) |
| (starred) what is the normal value for RBC count? | 4.5 to 5.9 million/mm^3 |
| (starred) what is the normal value for WBC count? | 4,500 to 11,000/mm^3 (upper end is kind of high on this one, could be closer to 9,000) |
| (starred) what is the normal/desired plasma value of cholesterol? | under 200 mg/dL (deciliter) |
| (starred) what is the normal/desired plasma value of glucose? | 75-115 mg/dL (fasting), or about 80-120 mg/dL |
| (starred) what is the normal/desired plasma value of triglyceride? | under 160 mg/dL |
| what are the important plasma proteins mentioned in our notes? | albumin, globulins (alpha/beta transporting lipids and fat-soluble vitamins, gamma antibodies that function in immunity), fibrinogen |
| what is the term for blood without fibrinogen? | serum |
| what very important plasma protein creates osmotic (oncotic) pressure to help draw water from tissues into capillaries to maintain BP and volume? | albumin |
| what are the specific functions of the specific globulins in the blood? | alpha and beta globulins transport lipids and fat-soluble vitamins while gamma globulins such as IgG/IgM/IgA/IgE,IgD are antibodies functioning in immunity |
| what is the protein that helps in clotting after becoming fibrin? (precursor to fibrin) | fibrinogen |
| list some regulatory mechanisms that maintain plasma volume to maintain blood pressure | RAAS, ADH, ANP, vasodilation/constriction |
| what sensors and where cause the release of ADH from the posterior pituitary gland if fluid is lost? | osmoreceptors in the hypothalamus |
| how many RBCs are in the blood? | 5 million/cubic millimeter |
| how long do RBCs live? | about 120 days |
| about how many million Hb molecules does EACH red blood cell contain? how many O2 molecules does this make per RBC? | about 280 million hemoglobin molecules, thus about 1-1.2 billion O2 molecules per RBC (2 billion atoms) |
| where is iron in heme recyelced from? | liver and spleen |
| what glycoprotein made by the liver carries iron to the red bone marrow? | transferrin |
| what is the general condition wherein one has abnormally low hemoglobin or RBC count? | anemia |
| what are the 3 anemias you should know? | iron-deficiency anemia, pernicious anemia, aplastic anemia |
| pernicious aniema is due to lack of intrinsic factor and thus one with this condition can't absorb vitamin B12. what cells where make intrinsic factor? | parietal cells in the stomach glands make intrinsic factor along with HCl |
| true or false, leukocytes have mitochondria | true, and nuclei also |
| what is the term for movement of leukocytes through the capillary wall into connective tissue? also called transendothelial migration or leukocyte extravasation | diapedesis |
| distinguish the types of leukocytes | granular (NEB: neutrophils, eosinophils and basophils) and agranular |
| (starred) which WBC is the largest of the WBCs; cytoplasm stains grayish-blue, agranular? | monocytes |
| (starred) which WBC cytoplasm stains pale blue; nucleus stains dark purple, agranular, 2nd-most common WBC, nucleus nearly fills cell? | lymphocytes, you need to know these also provide specific immune response (including antibodies) |
| (starred) which is the darkest staining WBC; cytoplasm and nucleus often blend into one dark mass; lobed, often obscured by dark granules, rarest WBC? | basophils, which you need to know also release the anticoagulant heparin (!) |
| (starred) which of the bilobed leukocytes have bright granules that stain intensely acidic? | eosinophils, which you also need to know help detoxify foreign substances, secrete enzymes that dissolve clots, fight parasitic infections (!) |
| (starred) which WBC is phagocytis and has a nucleus that stains dark purple; most common WBC? | neutrophils |
| what large cell breaks up into fragments called thrombocytes? | megakaryocyte |
| platelets lack nuclei. how long do platelets live? | 5-9 days |
| platelets release what substance that stimulates vasoconstriction? | serotonin (totally separate from its neurotransmitter duties here) |
| (starred) how long do granulocytes survive versus agranulocytes? | 12 hours to 3 days versus agranulocytes' 100-300 days or longer |
| (starred) which 2 WBCs are phagocytic? | neutrophils and monocytes (one granular and one agranular...) |
| what is the term for abnormally high RBC count? | polycythemia |
| what is the term for abnormally low WBC count? | leukopenia |
| what is the term for abnormally high WBC count? | leukocytosis |
| what is the term for cancer of bone marrow with high number of abnormal, immature WBCs? | leukemia |
| how many blood cells (red, white, platelets etc) are formed per day? | up to 500 billion (half a trillion) |
| what are the embryonic cells that give rise to all blood cells? these are multipotent adult stem cells that undergo mitosis and are used in bone marrow transplants | hematopoietic stem cells |
| where does hematopoiesis occur? (2 places? | myeloid tissue and lymphoid tissue plus MALT |
| what is myeloid tissue? | red bone marrow of long bones, ribs, sternum, pelvis, vertebral bodies, skull bones |
| erythroblasts->RBCs, EPO rcptrs; myeloblasts->granular leukocytes (NEB) with cytokine (G-CSF and GM-CSF rcptrs) and chemokine rcptrs, lymphoblasts -> lymphocytes w/interleukin &antigen rcptrs (T cell and B cell receptors), monoblasts -> monocytes w/M-CSF | |
| distinguish hematopoiesis versus erythropoiesis | |
| how many RBCs does red bone marrow produce? | 2.5 million RBCs/second |
| what continuous negative feedback loop is stimulated by EPO? | kidneys respond to low blood O2 levels, making EPO so that more RBCs are made |
| how long does the erythropoiesis process take and what does it involve? | takes about 3 days and involves loss of nucleus to form reticulocytes |
| what are the names of the forms in a hemocytoblast's differentiation to become an erythrocyte? | hemocytoblasts -> proerythroblast -> erythroblast, normoblast (nucleus expelled), reticulocyte, erythrocyte |
| true or false, all iron in your body is continuously coming from the diet | false, most iron is recycled from old RBCs and the rest comes from the diet |
| what is the old understanding of gastroferritin's role in the stomach and intestine? | that gastroferritin in the stomach binds Fe2+ and transports it to the intestine |
| all iron travels in blood bound to which protein? | transferrin |
| iron from intestinal cells is secreted into blood through which channels? | ferroportin channels |
| liver binds surplus iron to what in order to create an iron-containing structure called ferritin? | apoferritin |
| what is the major regulator of iron homeostais? it is a peptide hormone which removes ferroportin channels to inhibit intestinal absorption and cellular release of iron as well as lower plasma iron levels | hepcidin |
| what are the steps in hepcidin regulating the iron recycling pathway? | hepcidin binds to ferroportin, the only known cellular iron exporter. splenic/hepatic macrophages or intestinal enterocytes take bound molecule & trigger ferroportin channel to be internalized. ferroportin channel is lysosome-ized and iron is stored. |
| which proteins stimulate the production of different leukocyte subtypes during leukopoiesis? | cytokines. although these proteins are most known for regulating inflammation (cell activation), they also have a role in cell differentiation and proliferation |
| what glycoprotein hormone stimulates growth of megakyarocytes and their maturation into platelets? | thrombopoietin |
| which blood type is the universal donor and which is the universal recipient? why? | O- is the universal donor because these RBCs have no agglutinogens on them to cause agglutinization. AB is the universal recipient because this person's plasma lacks both antibody A and B |
| what is the solution to the fact that a donor's plasma may have antibodies against a recipient's red blood cells? | packed cell transfusion (PRBCs) |
| if anti-A serum is put into a blood and it agglutinates, what type of blood is it? | type A (or AB) |
| explain erythroblastosis fetalis | an Rh- mother exposed to Rh+ fetal blood produces antibodies; in future pregnancies, antibodies may cross the placenta and attack fetal RBCs, resulting in hemolytic disease of the newborn (clumping in the blood). the Rh- mother can be treated with RhoGAM |
| how does RhoGAM work? | neutralizes any stray Rh-positive fetal red blood cells in the mother’s bloodstream, preventing Rh sensitization, ensuring the mother's body does not produce active antibodies that could attack future pregnancies |
| true or false, anti-D antibodies form only in Rh- individuals who have been exposed to Rh+ blood | true, such as a blood transfusion of Rh+ blood into an Rh- person for the first time (or through birth bleeding) |
| recognize for multiple choice, which fetal symptoms occur in erythroblastosis fetalis | severe anemia, toxic brain syndrome due to excessive bilirubin in the blood, jaundice due to the Hb breaking down and building up, enlarged spleen due to going into overdrive to clear the damaged RBCs |
| what is the process of a temporary barrier to stop bleeding when a blood vessel is damaged? | hemostasis |
| what is the 3-step overview of the clotting response? | damage to collagen fibers in the blood produces vasoconstriction, formation of platelet plug (platelets stick to collagen), and formation of fibrin protein web |
| what are the 3 inhibiting factors to clotting under normal conditions? | the prostaglandin prostacyclin/PGI2, as well as NO, vasodilate the blood vessel to inhibit platelet aggregation; CD39 enzyme breaks down ADP into AMP and Pi to further inhibit platelt aggregation (ATP would be a danger signal generally) |
| when damaged endothelium exposes collagen, what is the 3-ish step process of clotting? | platelets begin to bind to collagen, Von Willebrand factor holds them there to resist shear force of blood, platelets recruit more platelets and form a plug by secreting ADP, serotonin, and thromboxane A2 (positive feedback) |
| what is the platelet release reaction? | activated platelets rapidly discharge their stored chemical messengers into the bloodstream to recruit more platelets and stabilize a forming blood clot |
| what special function does ADP have in the platelet release reaction? | ADP, which was stored in the dense granules of platelets, makes platelets stick to each other |
| what special function does serotonin have in the platelet release reaction? | vasoconstriction so clot doesn't wash away |
| what special function does thromboxane A2 have in the platelet release reaction? | thromboxane A2, which is made on demand by platelets, plays a role in the platelet aggregation as well as in vasoconstriction |
| what is thrombin? | thrombin (factor IIa) is a crucial serine protease enzyme in the blood coagulation cascade; triggers hemostasis by converting soluble fibrinogen into insoluble fibrin, which forms the meshwork of a blood clot |
| detail the extrinsic pathway of fibrin formation | 1. external trauma 2. damaged cells release FIII 3. FIII binds with FVII(a) to form VII complex incl. Ca2+ and phospholipids 4. complex converts FX to FXa |
| detail the intrinsic pathway of fibrin formation | 1. internal vessel damage 2. FXIIa activated by activators (collagen etc) 3. FXIIa activates FXI 4. FXIa in Ca2+ presence activates FIXa 5. FIXa binds with FVIIIa, Ca²⁺, and platelets to form VIII complex, which activates Factor Xa |
| detail the common pathway of fibrin formation | 1. FXa binds with FVa, Ca²⁺, and platelets 2. FV complex (WITH CALCIUM & PHOSPHOLIPIDS) converts prothrombin (FII) to thrombin (FIIa) 3. thrombin cleaves fibrinogen (FI) into soluble fibrin monomers 4. FXIIIa cross-links fibrin monomers into mesh clot |
| what is factor I's name, function, and pathway? | fibrinogen, converted to fibrin, common |
| what is factor II's name, function, and pathway? | prothrombin, converted to thrombin (enzyme), common pathway |
| what is factor III's name, function, and pathway? | tissue thromboplastin, cofactor function, extrinsic pathway |
| what is factor VIII's name, function, and pathway? | antihemophilic factor, cofactor, intrinsic |
| what is factor IX's name, function, and pathway? | Christmas factor, enzyme, intrinsic |
| what is factor X's name, function, and pathway? | Stuart-Prower factor, enzyme, common pathway |
| what is factor XII's name, function, and pathway? | Hageman factor, enzyme, intrinsic pathway |
| what produces prothrombin activator? | factor X |
| what converts prothrombin to thrombin? | prothrombin activator (FV complex with calcium and phospholipids) |
| thrombin speeds up the formation of prothrombin activator. this is associated with what kind of feedback? | positive feedback |
| true or false, genetic lack of any clotting factor affects coagulation | true |
| hemophilia A is sex-linked in 83% of cases. what factor is it missing? | VIII |
| hemophilia B is sex-linked in 15% of cases. what factor is it missing? | IX, the Christmas factor! |
| hemophilia C is autosomal and rare with equal occurrence in both genders. what factor is it missing? | hemophilia C |
| vitamin K deficiency is an acquired clotting disorder due to inadequate formation of what and other clotting factors in the liver? | prothrombin (vit K needed for factors 2, 7, 9, 10) |
| von Willebrand's disease is a dominant trait carried on an autosomal or sex-linked chromosome? | autosomal |
| Christmas disease is classed as hemophilia B. this sex-linked recessive trait carried on the X chromosome results in delayed formation of what? | fibrin |
| what are some anticoagulant drugs and what do they do? | aspirin inhibits prostaglandin production, resulting in defective platelet release reaction; coumadin inhibits activation of vitamin K; heparin inhibits activity of thrombin |
| what is the term for dissolution of clots? what enzyme digests what protein? | fibrinolysis; plasmin digests fibrin |
| (recognize for multiple choice) clotting can be prevented with what specific drugs?--and how do they work? | calcium chelators such as sodium citrate or EDTA; heparin blocks thrombin, coumadin inhibits vitamin K |
| what positive feedback occurs in dissolution of clots? | plasmin promotes formation of kallikrein with factor XII; kallikrein continues on its merry way to convert plasminogen into plasmin. plasmin does the nomnomnom and digests fibrin |
| what does the fibrous skeleton do and what are the annuli fibrosi? | the fibrous skeleton of the heart is a tough network of dense connective tissue; the annuli fibrosi are the four strong rings that make up the main part of the fibrous skeleton, holding in heart valves |
| what two "stringy" types of strucutres prevent heart valves from everting? | papillary muscles and chordae tendineae |
| where is the pulmonary valve located? | between right ventricle and pulmonary trunk |
| where is the aortic valve located? | between left ventricle and aorta |
| the S1 heart sound or "lub" happens when? | at the closing of AV valves / at ventricular systole |
| the S2 heart sound or "dub" happens when? | at the closing of semilunar valves / at ventricular diastole |
| what are the stethoscope positions for heart sounds? (hint: the four valves) | aortic valve = 2nd intercostal space on right; pulmonary valve = 2nd intercostal space on left; tricuspid valve = 5th intercostal space on right near sternum; bicuspid valve = 5th intercostal space on left away from sternum |
| what is the term for abnormal heart sounds produced by abnormal blood flow through the heart? many are caused by *incompetent* heart valves (know that term). and name a specific type of this. | heart murmur--a specific type is mitral valve stenosis |
| mitral valve stenosis calcifies and impairs flow between which atrium/ventricle? | between left atrium and ventricle--this may back up blood into the lungs, resulting in PULMONARY HYPERTENSION |
| incompetent valves may be due to damaged papillary muscles. incompetent valves may also cause what condition that is the most common cause of chronic mitral regurgitation? | mitral valve prolapse (the valve is floppy and bulges backward when the heart contracts. chordae tendineae get stretched--long and thin with danger of rupturing) |
| what is the term for holes in interventricular or interatrial septa which allows blood to cross sides from high to low (from left to right)? | septal defects |
| patent ductus arteriosus results from a failure of the ductus arteriosus to close after birth. what structures does it connect? | pulmonary artery to the aorta in a fetus |
| what is the term for the total volume of blood in the ventricles at the end of diastole? | end-diastolic volume |
| what is the term for when it's the end of the relaxation phase and ventricles are fully loaded with blood? | end-diastolic volume |
| what is the term for the amount of blood left in the left ventricle after systole? | end-systolic volume |
| what is the term for when there's 1/3 of the end-diastolic volume? | end-systolic volume |
| when do the atria contract relative to ventricular systole and diastole? | atria contract at the very end of ventricular diastole |
| (starred) what causes the first heart sound S1 and what phase of the cardiac cycle does it mark the beginning of? | cause is the closure of the AV valves due to rising pressure as the ventricles begin to contract; marks the start of isovolumetric contraction |
| (starred) during "isovolumetric contraction," what is the status of the heart's four valves, and how does End-Diastolic Volume (EDV) affect this phase? | all 4 valves are completely closed. it is a brief, early phase of ventricular systole; EDV effect: a higher EDV results in more pressure during this contraction phase |
| (starred) what must happen to the pressure inside the ventricles for the semilunar valves to open, and what phase occurs next? | pressure must build up until it exceeds the pressure in the arteries. once the semilunar valves open, blood is forced out during ventricular ejection. |
| (starred) what causes the second heart sound (S2, dub), and what is the status of the valves immediately after it happens? | cause: the closure of the semilunar valves as pressure in the ventricles begins to fall. valve status: all valves are closed again, marking the phase known as isovolumetric relaxation. |
| (starred) what physically causes the "dicrotic notch" seen in pressure readings, and what does it mark the end of? | cause: blood rushing back against the aortic valve immediately after it snaps shut. significance: it marks the exact moment the aortic valve closes, which signifies the end of systole and the transition into diastole (relaxation) |
| (starred) what pressure change must occur for the AV valves to reopen so the ventricles can start filling with blood again? | the pressure inside the ventricles must fall below the pressure of the atria. |
| (starred) what is the purpose of the atria contracting at the very end of the ventricular filling phase? | atrial contraction actively delivers the last remaining blood from the atria down into the ventricles before the cycle restarts |
| what does the P wave represent? | atrial activity / contraction |
| what does the QRS complex represent? | electrical signal moving through lower heart chambers, causing ventricles to contract |
| what does the T wave represent? | shows ventricles resetting (repolarization) and preparing for next heartbeat |
| what is the difference between an EKG/ECG and an EEG? | an EEG has to do with the brain, while an electrocardiogram has to do with the heart |
| what is the term for the automatic nature of the heartbeat? | automaticity is the intrinsic capability of heart cells to generate impulses without external nerve stimulation. the brain and cranial nerves only act as a volume knob |
| what are the secondary pacemakers? (2 structures) and how often do they depolarize per minute? | AV node (40-50x a min) and Purkinje fibers (20-40x/min--insufficient to sustain life) |
| what is the term for a slow, spontaneous depolarization between heartbeats triggered by hyperpolarization? | pacemaker potential, also called diastolic depolarization |
| at what voltage do voltage-gated Ca2+ channels open for pacemaker cells, and what does this accomplish? | -40mV, triggering action potential and contraction |
| how does repolarization occur for pacemaker cells? which channels open and what type? | voltage-gated K+ channels open to let K+ out |
| in what 2 ways are pacemaker cells' spontaneous depolarizations modulated? | epinephrine and norepinephrine (SNS) increase cAMP production, keeping pacemaker HCN channels open bc HCN channels open due to hyperpolarization (then letting sodium in); PSNS neurons secrete ACh, opening K+ channels = hyperpolarizing, to slow heart rate |
| what is the resting potential of myocardial action potentials for cardiac muscle cells? | -85mV |
| after cardiac muscle cells are depolarized to threshold by APs from the SA node, which type of channels open? | voltage-gated Na+ channels (fast Na+ channels) |
| membrane potential for cardiac muscle cells plateaus after depolarization at 15mV for 200-300 msec. what ions are responsible for this? | due to balance between slow influx of Ca2+ and efflux of K+ |
| the long plateau for cardiac muscle cells prevents what as seen in skeletal muscle? | long plateau prevents summation and tetanus |
| the Ca2+ slowly coming in during the plateau of a cardiac muscle cell triggers which process required for cardiac contraction? | the Ca2+-induced Ca2+ release |
| what are the steps of excitation-contraction coupling for cardiac muscle cells? | APs along sarcolemma and T tubules open voltage-gated Ca2+ channels in membrane; Ca2+ stimulates SR's calcium release channels; the Ca2+ (mostly from SR) binds to troponin to stimulate contraction } signaling complexes |
| Ca2+ concentration for repolarization of a cardiac muscle cell is decreased back to relaxation state by what 2 mechanisms? | active transport back into the SR, extrusion of Ca2+ through the plasma membrane by the Na2+-Ca2+ exchanger (NCX transporter) |
| true or false, the ECG/EKG records action potentials of the heart, contraction, and relaxation | false, it records the results from waves of depolarization--the electrical events leading to contraction and relaxation |
| (starred) the P wave of an EKG is associated with what? | atrial depolarization with atrial systole |
| (starred) the P-R interval of an EKG is associated with what? | atrial systole/contraction |
| (starred) the QRS wave/complex of an EKG is associated with what? | ventricular depolarization with ventricular systole plus atrial repolarization with atrial diastole |
| (starred) the S-T segment of an EKG is associated with what? | plateau phase of ventriclar systole/contraction |
| (starred) the T wave of an EKG is associated with what? | ventricular repolarization with ventricular diastole |
| (starred) at what point is the atria physically squeezing? | The P-Q segment |
| (starred) at what point of the EKG are the ventricles physically squeezing? (hint, it's a flat part) | S-T segment--the flat part before the T wave--ventricular repolarization |
| what is the term for abnormal patterns of electrical activity that result in abnormalities of the heartbeat? | arrhythmias |
| what is the tunica media of a given blood vessel composed of | smooth muscle tissue |
| what is tunica externa composed of? | connective tissue |
| what is the term for a balloon-like swelling in an artery or in a weakened ventricular wall? where does it most commonly occur? | aneurysm--most common in the aorta as a thoracic or abdominal aortic aneurysm, but can occur in cerebral and other arteries |
| what is the term for a tear in the wall of the aortic aneurysm, which often can be detected and corrected before it completely bursts? | dissected aorta |
| what are 2 causes of and 2 conditions that increase the risk of aneurysms? | congenital causes, atherosclerosis; hypertension and diabetes can increase the risk |
| what is the path of microcirculation and the path of blood flow from an artery to a vein through a metarteriole-thoroughfare channel? | as blood comes through an artery, it goes into a terminal arteriole, the metarteriole forming arteriovenous shunt, thoroughfare channel, then postcapillary venule, then vein |
| what are the types of capillaries from least leaky to most leaky? | continuous, fenestrated, discontinuous |
| where are continuous capillaries found? | muscles, adipose tissue, and CNS (add to BBB) |
| where are fenestrated capillaries found? (they have pores in vessel wall) | kidneys, intestines, and endocrine glands |
| where are sinusoid capillaries found? (aka discontinuous) | found in bone marrow, liver, and spleen; allow the passage of proteins |
| what is the thoracic pump? | flattening of the diaphragm at inhalation increases abdominal cavity pressure in relation to thoracic pressure and moves blood toward heart (deep breaths increase venous return) |
| what is the term for enlarged surface veins (generally in lower limbs) that occur when venous congestion stretches the veins to the point that the venous valves no longer close effectively? | varicose or spider veins |
| what is the term for a dangerous blood clot that forms in a deep vein, usually in your leg or thigh? what can it lead to? | deep vein thrombosis (DVT)--can lead to a venous thromboembolism (traveling blood clot) |
| anticoagulant drugs or thrombolytic agents may sometimes be needed to prevent or treat a thromboembolism so that it doesn't result in a potentially fatal what? (hint: at lungs) | pulmonary embolism |
| what is the term for a plaque that may protrude into the lumen and reduce blood flow, believed to be due to uptake of LDL protein apolipoprotein B at the subendothelial connective tissue of arteries? | atheroma(s) |
| what structures serve as sites for thrombus formation? | atheromas. plaques form in response to damage done to the endothelium of a blood vessel--smoking, HTN, diabetes, high cholesterol |
| what are the 3 steps for developing atherosclerosis? note that progress promoted by inflammation stimulated by cytokines and other paracrine regulators. | fatty streaks within the tunica interna attract lipid-filled macrophages and lymphocytes; smooth muscle layers are added; cap of connective tissue covers it... |
| what are the cholesterol-filled cells that derive from monocytes which become macrophages? | foam cells |
| which lipoproteins play a "sponge" role in carrying cholesterol away from the artery to the liver for metabolism? | HDLs (high-density lipoproteins) |
| what kind of drugs increase HDL levels? | statin drugs such as Lipitor, fibrates, and niacin |
| what protein is a better measure of inflammation and predictor for atherosclerosis than LDL levels? | C-reactive protein |
| what do endothelial cells become when they engulf LDLs? what is their danger? | oxidized LDLs that damage the endothelium |
| what is the condition characterized by inadequate oxygen due to reduced blood flow? what is its most common cause? | ischemia/ischemic heart disease, most commonly caused by atherosclerosis |
| what substernal pain is ischemia associated with? it comes with increased production of lactic acid. | angina pectoris (referred to pain to left shoulder and arm); can lead to necrosis of some areas of the heart, which then leads to MI (heart attack) |
| what substance can act as a shield to help prevent oxidative/stress and cell damage during reperfusion injury? | nitroglycerin |
| in ischemic conditions, how would return of blood flow to the damaged area cause apoptosis of neighboring cells to enlarge the infarct? what is it due to? | due to Ca2+ accumulation and free radical production by mitochondria |
| what condition is detected on an EKG by depression of the S-T segment? | myocardial ischemia |
| what proteins are tested for in detecting ischemia? | creatine phosphokinase, lactate dehydrogenase, troponin T, and troponin I (today's most sensitive test) |
| true or false, abnormal tachycardia can occur due to drugs or fast ectopic pacemakers | true |
| what condition occurs when pacemakers in the ventricles make them contract out of sync with the atria? | ventricular tachycardia, very dangerous, can lead to ventricular fibrillation and sudden death |
| what is the difference between flutter and fibrillation? | flutter is coordinated contractions at 200-300 bpm, fibrillation is uncoordinated pumping between the atria and ventricles |
| what are the characteristics of atrial fibrillation? (vs ventricular) | atrial fibrillation is sans P waves in ECG and AV node can't keep pace with speed of atrial contractions (!) and it's livable but with risk of thrombi, stroke, heart failiure |
| what are the characteristics of ventricular fibrillation? (vs atrial) | more of a concern and victim dies w/o CPR or eletrical defib; caused by circus rhythms; refractory period prevented; sudden death progresses from ventricular tachycardia, through ventricular fibrillation, ending in asystole (straight line ECG) |
| damage to the AV node can be seen in changes in what interval of an ECG? | P-R interval |
| what is first degree AV node block? | impulse conduction exceeds 0.2 seconds / delay of AP between SA and AV nodes |
| what is second degree AV node block? what does the EKG look like? | where not every electrical wave can pass to ventricles. looks like extra P waves in ECG tracing |
| what is third degree AV node block? | no SA node signals get through; an ectopic focus in the Purkinje fibers/ ventricular myocardium takes over, but this is slow (20-40 bpm), requires artificial pacemaker |
| what are the body's 2 main lymphatic vessels? | thoracic duct and right lymphatic duct |
| what are the 3 main organs of the lymphatic system? | tonsils, thymus, spleen are sites for lymphocyte production |
| what is the cisterna chyli? | main reservoir for lymph fluid in the abdomen |
| what are Peyer's patches? | small, organized clusters of lymphatic tissue in the mucosa lining of small intestine's ileum |
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