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Human phys exam #3
chapter 12, 13, 14
| Question | Answer |
|---|---|
| ekg/ecg | electrocardiogram, measures heart's electrical signals |
| heart murmur | blood regurgitation, usually bc of improper function of a valve |
| going horizontal | fainting, makes it easier for blood to go to your brain bc the flow isn't going agains gravity |
| cardiac anatomy: left side of heart | pumps blood to the entire body, from head to toe, hence has thicker muscle wall, more work required |
| cardiac anatomy: right side of heart | pumps deoxygenated blood to lungs, much weaker half of heart bc requires little to no work |
| flow of blood: deoxygenated blood to the lungs | 1. superior and inferior venacava, 2.Right atrium, 3.tricuspid valve, 4.right ventricle 5. pulmonary semilunar valve, 5. pulmonary trun, 6.left and right pulmonary arteries, 7. lungs |
| flow of blood: oxygenated blood from the lungs | 1. left and right pulmonary veins, 2.left atrium, 3.bicuspid valve, 4. left ventricle, 5.aortic semilunar valve, 6.Aorta, 7. arteries |
| LAB RAT | Left atrium bicuspid, Right atrium tricuspid |
| PFO | when the flap betweem the left and right ventricles aren't sealed, its not sealed in all embryos because you don't need to separate the blood, all O2 comes from mom. as soon as embryo is born, force of air pushes the flaps together and they should seal |
| PFO continued | otherwise oxygenated and deoxygenated blood mix and the individual cannot function as well, less O2 = less energy |
| what is blood composed of? | formed elements ( cells and cell fragments) and a liquid called plasma. blood contains erthrocytes, leuckocytes and platelets |
| hematocrit | percentage of blood that is comprised of erthrocytes, ie. percentage of blood oxygen levels |
| cardiac anatomy: atrium | the two upper chambers of the heart, blood pools here until there is enough to push through the valves |
| cardiac anatomy: ventricles | lower chambers of heart, blood is actively pumped to either the lungs or the rest of the body |
| cardiac anatomy: arteries | vessels that carry blood away from the heart, think ARTERY = AWAY |
| cardiac anatomy: veins | carrying blood back to the ehart |
| cardiac anatomy: aorta | the largest artery in the body, pushes blood from the left ventricle to the entire body |
| cardiac anatomy: what's the difference between the inferior and superior venacavae?? | inferior vena cava collects blood BELOW the heart, inferior vena cava collects blood ABOVE the heart |
| cardiac conduction: route of electrical signal | to the apex of the heart. SA node fires a signal to the AV node. the signal goes to the apex of the heart and then turns on the purkinje fibers, triggering contractions. |
| cardiac conduction: order of contraction | atrium contracts first, after inital depolarization |
| cardiac conduction: SA node | sinoatrial node, located in top of right atrium, where initial depolarization arises, pacemaker for the heart, the rate at which the SA node discharges determines the heart rate, does not have a resting potential, undergoes pacemaker potential, |
| cardiac conduction: AV node | atrioventricular node, located in bottom of right atrium, receives signal from SA node and sends signal to bundle of His, action potential arises slowly through AV node, which allows atrial contraction to complete before ventricular contraction starts |
| cardiac conduction: bundle of his | the connection between the AV node and bundle of his makeup the only electrical connection between the atria and ventricles, otherwise, the wto are completely separated (conduction wise) |
| cardiac conduction: purkinje fibers | bundle of his separates into two branch bundles that connect with purkinje fibers, large conducting cells that send impulses throughout the ventricles. these fibers cause ventricular contraction |
| cardiac action potentials | sodium depolarizes the cell while, at the same time potassium permeability decreases, leaky potassium channels close, leading to overall further depolarization of the cell. sodium channels close almost immediately but instead of repolarizing, the cell |
| cardiac action potentials | remains depolarized bc potassium permeability is still decreased and there is an increased permeability to calcium |
| cardiac action potentials: L type calcium channels | l-type calcium channels, open much more slowly than Na channels, the flow of positive calcium into cell balances positive flow of potassium out of cell, keeping the membrane depolarized. |
| cardiac action potentials: after l-type calcium channels | eventually l-type channels close and more k channels open in response to the depolarization, repolarizing the cell |
| cardiac action potentials: pacemaker potentials | gradual depolarization of a membrane, controlled by slow reduction of potassium permeability, funny channels, which opens when the membrane potential is negative, and slowly brings Na in and potassium out. also controlled by T-type calcium channels, |
| cardiac action potentials: pacemaker potentials | t-type calcium channels open briefly to allow Ca in, these qualities of the pacemaker potential mean that the SA node has no resting potential constantly depolarizing and then repolarizing |
| electrical and mechanical functions during ekg: line before p wave | blood is entering the atriums |
| electrical and mechanical functions during ekg: p wave | stimulation of SA node begins as p wave begins, as the impulse goes from left to right atria, the p wave gets bigger. also atrial depolarization, atria is contracting to fill up ventricle |
| atrial systole | normally atrium fills passively but a little remaining blood is actively kicked in, ie. atrial systole |
| S1 heart sound is caused by | AV valve closing |
| S2 sound is caused by | SL valve closing |
| during isovolumetric contraction (systole) which valves are open and closed?? | iso means things are the same, therefore both valves are closed so nothing's changing |
| electrical and mechanical functions during ekg: QRS complex | purkinje fibers are stimulated, ventricles contracting by r wave. by the s wave, blood is leaving the ventricles |
| electrical and mechanical functions during ekg: t wave | heart is depolarizing/relaxing. refractory period, cycle prepares to begin again |
| cardiac cycle: what happens during systole | systole = squeeze, ventricles contract and then ventricles eject. during ventricular contraction, both AV and SL valves are closed. during ejection, SL valve opens and blood goes to either body or lungs |
| cardiac cycle: what happens during diastole | isometric ventricular contraction, AV valves and SL valves are close, atria is passively filling. then ventricular contractions begin, first ventricles fill passively, AV valve open, sl valve closed. finally atria contracts to push last bit in |
| myocardial contraction and relaxation | 1.action potential enters 2.voltage gated Ca channels open and Ca rushes in 3.Ca that rushes in binds to the ryanodine receptor, which triggers the Sarcoplasmic reticulum to release more Ca 4. the increased release of Ca leads to Ca spark, ie. more Ca |
| mycoardial contraction and relaxation | 5.Ca binds to troponin and initiates contraction 6. Ca unbinds from troponin and relaxation occurs 7.most Ca is pumped back into the SR, some is sent out in exchange for Na, to mantain the cells Na gradient |
| ventricular myocardium | extended plateau, permeability of ca keeps membrane potential high, ie. no tetanus, cannot contract over and over again, cardiac muscle must relax. as Na permeability falls, Ca permability increases to allow for plateau and K permeability decreases |
| ventricular myocardium | meaning more k stays in the cell, ie. cell will stay depolarized, heart can't reset and immediately start again |
| autorhythmic cells | as soon as they depolarize, they replarize, then depolarize again, occur with no stimulus, jsut repeast over and over again, no action potential needed to be acheived, found in the SA node |
| pacemaker potential in autorhytmic cells | depolarize slowly, funny channels open then close at 60mv, allows sodium to come in and k to come out @ same time. then Ca T and L channels open at staggered rates. at peak, Ca T and then L channels close, slow K channels open and K flows out, |
| pacemaker potential in autorhythmic cells | repolarizing cell, at -60mv, the whole thing starts again |
| brady vs tachy chardia | brady = slow, tachy = fast |
| drugs that affect the heart and where | parasympathetic: acetylcholine affects muscarinic receptors in the Atria. sympathetic: epinephrine and norepinephrine affect Beta receptors in both atria and ventricles |
| sympathetic regulation of heart | increased force of contraction and stroke volume result from sympathetic stimulation. sympathetic influence affects l type calcium channels, ryanodine receptors, thin and thick filaments and proteins that bring Ca back to the SR by speeding them all up |
| bp number | systole/ dyastole, |
| veins | veins have valves bc blood is going agains gravity, back to heart, muscles massage blood up when in action, when relaxed, blood falls back down but valves stop it from going all the way down |
| arteries | carry blood away from heart, don't have valves, except for aorta |
| albumin | its ia blood protein, too big to exit capillaries, instead creates an osmotic draw back into the capillaries |
| net filtration pressure | Pc (capillary pressure) + osmotic force of proteins in interstitium - hydrostatic pressure - osmotic draw from proteins inside the capillary |
| cardiac output | CO = HR (heart rate) * SV (stroke volume) || SV = EDV - ESV (end diastolic volume - end systolic volume) |
| end diastolic volume | how much blood you have just before systole |
| to calculate how long it takes blood from right ventricle to head you use | time = pulmonary vol/cardiac output |
| pulmonary circulation | circulation of blood between the heart and the lungs. |
| systemic circulation | circulation that supplies blood to all the body except to the lungs. |
| sympathetic regulation of the heart continued | norepinephrine triggers alpha cells in heart, causing vasoconstriction. epinephrine triggers beta 2 cells in the heart causing vasodialation |
| lymph | circulatory system for immune system, a series of vessels that collect things from interstition and return it to the blood, works by pressure, if you block lymph system, there is no pressure to move fluid, so it stays in the tissue, causing edema |
| lympedema | a condition of localized fluid retention and tissue swelling caused by a compromised lymphatic system |
| kwashiorkor | symptom is edema, caused by lack of essential proteins |
| what is blood made of?? | plasma, erthrocytes, leukocytes, platelets |
| cells in blood: erthrocytes | red blood cells |
| cells in blood: leukocytes | many kinds: neutrophils (neutral in presence of acid/base), eosinophils (turns red in presence of acid), basophils (turns blue in presence of base), monocytes (give rise to phagocytes), lymphocyte |
| hemostasis | prevention of blood loss, vessel damage triggers platelets who then release chemical mediators, contract the vascular smooth muscle, causing vasoconstriction ie less blood flow to the area, and creating a platelet plug |
| anemia | not enough red blood cells, bad bc you get no oxygen |
| polycythemia | too many blood cells, block flow, cause clots |
| dehydration | can look like polycythemia bc even though the red blood cell count is normal, the plasma is low, increasing the hematocrit percentage |
| thromboembolism | blood clot that forms in a vein deep inside a part of the body. It mainly affects the large veins in the lower leg and thigh. |
| murmer | regurgitation of blood backwards bc a valve is not closing properly |
| Heart block | disease in the electrical system of the heart, some part of the electrical system isn't working properly |
| congestive heart failure | occurs when the heart is unable to provide sufficient pump action to maintain blood flow to meet the needs of the body. Left side failure:Backup of fluid into pulmonary circuit, Rales or crackles in the lung. Pink, frothy sputum. |
| congestive heart failure | Right side failure: Backup of fluid into systemic circuit Edema, especially in the lower extremities |
| Hypertension | igh blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated.[1] This requires the heart to work harder than normal to circulate blood through the blood vessels |
| Myocardial Infarction | results from the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery |
| difference between sign and symptom | sign: something you can see. symptom: something the patient must tell you |
| signs of myocardial infarction and treatment | t wave inversion, S-T elevation, weird q wave. treated with MOAN: Morphine, O2, Asprin, nitroglycerin. why asprin: cox 1 and 2 inhibitor, interferes w protective lining of stomach and an anticoagulant |
| fetal circulation | Blood from the placenta carried to the fetus via umbilical vein. half is carried to the inferior vena cava, other half enters the liver. The blood then moves to the right atrium of the heart to left atrium via PFO and from |
| fetal circulation | there it is pumped through the aorta into the body. Some of the blood re-enters the placenta, where waste products from the fetus are taken up and enter the maternal circulation. |
| nasal cavity | primary filtering of air, heating of air, moistening of air |
| lobes of lung | 3 on the right side, only 2 on the left to make room for the heart |
| inspiration | inhalation, air from external environment comes in |
| expiration | exhalation, air from inside goes back out |
| process of inspiration | air comes in through nose/mouth into pharynx, passage for air and food. air then goes through the larynx, which has the vocal cords, goes into the trachea, which splits into two bronchi, leading to the lungs |
| functions of the respiratory system | provides O2, removes CO2, regulates pH in coordination w kidneys, assists in speech, defends against microbes, traps and dissolves blood clots |
| alveoli | hollow sacks that allow for oxygen exchange, two types. type 1:flat, epithelial cells that line air facing surfaces of lungs. type 2: produce detergent called surfactant that allows tissues to slide by each other, makes it easier for lungs to expand |
| boyles law | changes in pressure determine direction of gass flow, pressure inversely proportional to volume, as one goes up the other goes down |
| tidal volume | amount of air inhaled/exhaled in one relaxed breath |
| inspiratory reserve volume | amount of air that is inhaled w max effort |
| expiratory reserve volume | amount of air that is exhaled w max effort |
| residual volume | amount of air in lungs after maximum expiration, keeps alveoli inflated between breaths |
| vital capacity | amount of air that can be exhaled w max effort after max inspiration. expiratory reserve vol + tidal vol + inspiratory reserve vol. judges strenght of thoracic muscle and pulmonary function |
| inspiratory capacity | max amount that can be inhaled after normal tidal expiration. IRV+TV |
| functional residual capacity. a | amount of air in lungs after normal tidal expiration, RV +ERV |
| total lung capactiy | max amount of air the lungs can hold, RV +VC |
| negative pressure breathing | contraction of the diaphragm, and the relaxation of intercostal muscles, increasing the volume of the thoracic cavity, which the lungs expand to fill.still the same amount of air in the lungs, |
| negative pressure breathing | but w larger volume, so it is at a lower pressure than initially, when it was equal to ambient air pressure. As long as the airway is secured, air "flows" into the lungs along the pressure gradient, filling the lungs with air. |
| process of negative pressure breathing | external intercostal muscles and sternocleidomastoid pull the ribs up and away, increasing vol. thoracic cavity,air to flows in. internal intercostal muscles pull ribs together, decreasing thoracic cavity volume, increasing pressure thus pushing air out |
| pleural | tissue/cavity holding the lungs |
| hypoxia | deficiency of O2 |
| cyanosis | turning blue from lack of O2 |
| apnea | no breathing |
| tachypnea | fast breathing |
| eupnea | normal breathing |
| alveolar | having to do w the alveoli |
| hemoglobin | molecule in blood, carries o2, at full saturation, hemoglobin carries 4 molecules of o2 |
| where does O2 go in the body?? | o2 is inspired, goes into the alveoli, whic dissolve it and is absorbed and taken up by the hemoglobin in blood, the hemoglobin releases it in necessary areas and it enters a cell and goes to the mitochondria, |
| why does O2 go to mitochondria | WHY?? bc it is used as a final electron acceptor in the electron transport chain, ie, without oxygen the 36 atp from the etc can't be made |
| Bicarb equation | H2O+ CO2 <-> H2OCO3 <->HCO3 + H, the equation is reversible, when there's more H+, ie. more acidic, hemoglobin doesn't bind to O2 as well, when basic, hemoglobin binds to O2 very well |
| DPG | produced during glycholysis in red blood cells, binds o hemoglobin and makes it have less affinity for O2, thus, whenever there is a huge amount of DPG in the system, it triggers release of O2 from hemoglobin to where its supposed to go. |
| what causes hemoglobin to have a lower affinity for oxygen? | increased temperature, decreased pH, increased increased DPG, increased Pco2. increased activity leads to decreased hemoglobin/o2 affinity, which leads to hmore O2 released |
| what does it mean if hemoglobin has lower/higher affinity for O2?? | lower affinity = willing to give up O2 more readily. higher = less willing to give up O2 readily |
| what happens to your CO2?? | 10% of CO2 is in blood, 60-65% of CO2 is converted to HCO3 thanks to Carbonic anydrase, and then moved out of the red blood cell into the plasma in exchange for Cl ions. 25-30% bound to hemoglobin |
| what is the peripheral nervous system sensitive to? | CO2, O2, pH |
| what is the central nervous system sensitive to? | CO2 |
| minute ventilation | volume of gas inhaled or exhaled from a person's lungs per minute. increases as your exercise increases |
| Arterial Po2 | partial pressure of oxygen, stays the same bc even though you're removing O2, its being replaced just as quickly |
| Arterial CO2 | partial pressure of CO2, decreases as you exercise more bc you're starting to take in more and more oxygen |
| Arterial [H+] | concentration of H+ ions, ie. increase in acidity, increases as you exercise more |
| Chronic osbstructive pulmonary disease (COPD) | phagocytes destroy alveolar walls, causing less surface area, ie. less O2 uptake. includes chronic bhronchitis, emphysema |
| pneumothorax (collapsed lung) | A collapsed lung occurs when air escapes from the lung and fills up the space outside of the lung, inside the chest. messes up negative pressure breathing |
| hypoxia | deficiency of O2 in tissues |
| shallow water blackout | hyperventilating decreasese CO2 in blood, allowing people to go underwater for longer. however, as you stay underwater, O2 is low, yes, but CO2 is rising and the pressure to breathe comes from the build up of CO2. |
| shallow water blackout | eventually you lose conciousness and your instincts take over and make you breathe |
| Fick's law of diffusion | O2 consumption = Cardiac output*(arterial [O2]-venous[O2]) |
| kidneys are | bodyy's filtration system, made of 1 million subunits called nephrons |
| nephrons | made up of filtering component called renal corpuscule that filters stuff from blood, removing cells and proteins. this filtrate goes to the tubule that extends from renal corpusucule |
| renal corpuscule | contains glomerulus (a bunch of interconnected capillary loops, part of it jutts into the bowmans capsule where fluid exchange occurs) and bowman's capsule (a fluid filled capsule) |
| renal tubule | contains loop of henle, collecting duct and various other tubules |
| basic flow in kidneys | glomerulus -> bowman's capsule -> proximal convoluted tubule -> proximal straight tubule -> descending loop of henley -> ascending thin loop of henley -> ascending thick loop of henley -> distal convoluted tube -> collecting duct |
| afferent arteriole | brings blood to glomerulus, where it is filtered through the bowman's capsule |
| efferent arteriole | remaining stuff, after the filtering leaves through this arteriole |
| basic renal processes: glomerulus | blood enters glomerulus through afferent arterioles. it is run through the bowman's capsule where it is filtered and the remaining stuff is carried away via efferent arteriole. and enters the peritubular capillaries |
| basic renal processes: glomerulus | glomerular capillaries are fenistrated, and slit to allow everything but cells and proteins out. peritubular capillaries just surround everything afterwards, reabsorbing the whole way |
| Glomerular filtration rate (GFR) | volume of fluid filtered from glomeruli -> bowmans capsule / unit time. controlled by pressure, glomerular capillary bp- fluid pressure in bowmans space - osmotic force due to protein in plasma. |
| how do you test GFR? | inulin, and less so creatinine are both filtered but not reabsorbed by the kidney and are not (really) created in the body so measuring that in the urine allows you to measure GFR by calculating clearance rate of substance, is the kidney healthy or not??? |
| increasing/decreasing gfr?? | dilated afferent arteriole = increased gfr, dialted efferent arteriole =decreased gfr |
| reabsorbrtion vs filtrate | reabsorbed stuff goes back into the blood, filtrate is the stuff thats going to be your urine |
| reabsorption in tubules | removes substances neessary for body. things usually diffuse into the tubule or are carried through using mediated transport |
| glucose in diabetics | a person w uncontrolled diabetes has excess glucose in their kidneys. glucose is reabsorbed through transporters and the kidneys are doing it as best as they can, but if there's just too much glucose (ie. like in a diabetic) it'll end up in the urine. |
| clearance rate of a substance | (Urine concentration of s *urine volume per time)/ plasma concentration of s |
| micturition | basically peeing. two parts of the sphincter, internal (smooth muscle) and external (skeletal muscle, only part thats voluntary). sphincters are activated and detrusor muscles are not activated and when you are peeing, vice versa |
| metabolic water | water you get from the breakdwon of glucose/dehydration synthesis, basically water you get from metabolic activity |
| what exits where in the renal tubule | water exits passively in the descending loop of henle, Na exits passively in the thin ascending loop of henley, and exits actively in the thick ascending loop of henley |
| relation of water and sodium reabsorption | sodium reabsorption is active and occurs all through out the tubes except the descending loop of henley. and water reabsorption is through diffusion, dependant on sodium reabsorption |
| reabsorption in proximal tubule | Na/K atpase pumps power sodium reabsorption, decreasing intracellular sodium concentration |
| vasopresin * VASOPRESSIN DOES NOT INFLUENCE WATER IN ANY PART OF THE TUBULE BEFORE THE COLLECTING DUCTS || vasopressin uses second messenger (cyclic cmp) system to trigger more aquaporins to be released | major determinant of water reabsorption. stimulates aquaporins in the collecting ducts. ie. if there's a high plasma concentration of vasopressin, there is high water permeability and reabsoption in the collecting ducts, reducing volume of urine excreted. |
| water diuresis | lack of vasopressin, results in increased urine excretion but not increased solute excretion |
| osmotic diuresis | increased urine flow but due to increased solute excretion. ie. for some reason sodium isn't reabsorbed as well so you have more Na excretion, well water follows solutes so if Na goes out, so will H2O. an example is diabetes mellitus |
| what's going on in the loop of henley?? | the descending limb is more permeable to water than Na and vice versa for the ascending limb. so when Na is reabsorbed into the interstition, it shifts the concentration gradient so that water is drawn out of the descending limb, w |
| what's going on in the distal convoluted tubule?? | actively transports Na and Cl but is impermeable to water |
| Renal cortex | outer portion of the kidney. It contains the renal corpuscles and the renal tubules except for parts of the loop of Henle which descend into the renal medulla. The renal cortex is the part of the kidney where ultrafiltration occurs. |
| ultrafiltration | filtration of blood from the arteriole through the bowmans capsule, but before the peritubular capillary |
| renal medulla | contains loop of henley and collecting duct |
| vasa recta | capillary that mirrors the loop of henley, moves in the same direction but very slowly and reabsorbs a lot of the stuff |
| aldosteron | stimulates sodium reabsportion by distal convoluted tubule and cortical collecting ducts, steroid, acts slowly |
| angiotensin II | controls the secretion of aldosterone |
| renin angiotensis aldosterone system (RAAS) | renin is secreted by juxtaglomerular cells, from juxtaglomerular apparatuses in the kidney. when bp has dropped the kidney releases renin into your blood. Angiotensinogen is a giant protein thats just chilling in your blood, once renin comes in |
| renin angiotensis aldosterone system (RAAS) | it cleaves the antiotensinogen into angiotensin I which is then cut into angiontensin II which then triggers the release of aldosterone. the rate limiting factor in angiotensin II formation is the plasma renin concentration. |
| juxtraglomerular | conctains justaglomerular cells, right next to glomerulus |
| Collecting duct | made up of various portions, cortical collecting duct, in cortex, medullary collecting duct in medulla, collects all the remaining stuff that wasn't reabsorbed and takes it to bladder |
| urea | added in thin ascending loop of henley passively to create the concnetration gradient that allows sodium to leave passively |
| renal regulation of potassium | aldosterone promotes both sodium and potassium secretion/excretion. also filtered into the urine so that Na can be reabsorbed via cotransport |
| countercurrent multiplier | two sets of tubes wit flow going in opposite direction. increases the surface area and creates a concentration gradient. comprized of the loop of henley, the vasa recta |
| Ace inhibitors | lower bp by preventing Angiotensin I from breaking into Angiotensin II |
| Angiotensin II function | increases bp, causes vasoconstriction,increases vasopressin and aldosterone release |
| sources of hydrogen ion gain/loss | bicarb equation. when Hco3 is produced and H+ binds with phosphate in the lumen, you see a net increase in HCo3, therefore net increase in H+. when Hco3 is produced and H+ binds with HCO3 in the lumen, you see a decrease in Hco3 and H+ |
| bicarb equation (H2O and CO2 passively removed) | bicarb equation happens in the epithelial cells, the two products you get are H+ and Hco3-. bicarb goes to interstitial fluid. H+, through co transport, ist transported into the tubular lumen where it binds to HCO3 in the lumen and turns into H2O and CO2 |
| bicarb equation (H2O and CO2 passively removed) | there is no net gain of bicarbs here 1+ and 1-. leads to an overall decrease of bicarb and H+ |
| bicarb equation (bicarb produced) | another to get H+ into the lumen is a phosphate equation. H+ and HCO3 produced again, but the H+ then goes to the lumen and binds to HPO4. 1 bicarb created, no bicarb removed = net gain of bicarb, ie. net gain of H+ |
| Diuretics | Lasix, HCTZ, remove fluid, ie. decrease pressure on heart and arteries |
| hypertension | high blood pressure, treated w Diuretics Angiotensin-Converting Enzyme (ACE) Inhibitors Angiotensin II Receptor antagonist Beta-Blockers Calcium Channel Blocker (antagonist) |
Created by:
hsinha93
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