Flashcards
BIOM3010
Cards in this deck (135)
- 1What are the two sets of valves in the heart?1. Atrioventricular (tricuspid and bicuspid or mitral)
2. Semilunar (aortic and pulmonic) - 2How do the sets of valves differ in anatomy?The atrioventricular valves have chordae tendineae (either two or three) that facilitate closing of the valves while the semilunar valves do not.
- 3What is the purpose of the heart valves?Enable the forward flow of blood while preventing back flow working on pressure gradients.
- 4What are the four phases of the cardiac cycle?1. Ventricular filling / atrial contraction
2. Isovolumetric ventricular contraction
3. Ventricular ejection
4. Isovolumetric ventricular relaxation - 5When does atrial pumping make a larger contribution to ventricular filling?At high heart rates when time for passive filling is reduced.
- 6Compare laminar and turbulent flow.Laminar is smooth flow that does not create sound while turbulent is rough flow and can be heard.
- 7Describe the four heart sounds and their causes.1. 'Lub' caused by closure of mitral and tricuspid valves creating two bursts of vibration
2. 'Dub' caused by closure of aortic and pulmonary valves
3. Marks end of rapid filling phase due to recoil of blood from ventricular wall
4. Coincides with atrial contraction (not usually heard) - 8Describe heart regurgitation or insufficiency.When valves can not close tightly, blood flows through the resulting gaps in an incorrect direction.
- 9Describe heart stenosis.When the passage containing valves decreases in size, blood flow in the correct direction is impeded.
- 10How are cardiac cells able to contract simultaneously?Gap junctions allow action potentials to travel between cells and contract simultaneously.
- 11Describe autorhythmic cardiac cells.Called pacemaker cells and are non contractile but are able to spontaneously generate action potentials. The pacemaker potential comes about from "funny" Na+ channels allowing slow inward movement and slow depolarisation to occur.
- 12Describe the spread of cardiac excitation.Originates from the sinoatrial (SA) node then travels to the atrioventricular (AV) node then down the left and right bundles of His and then into the purkinje fibres.
- 13Describe the action potential of cardiac contractile cells.1. Rapid depolarisation due to brief Na+ influx
2. Plateau due to decrease in K+ out and entry of Ca2+
3. Rapid repolarisation due to return of K+ permeability and closure of Ca2+ channels
4. Resting
- 14Describe the excitation- contraction coupling.1. Action potential in cardiac contractile cell travels down the T tubules
2. Entry of small amount of Ca2+ from ECF through L-type channels causes release of large amounts of Ca2+ from sarcoplasmic reticulum
3. Increase in cytosolic Ca2+ causes contraction - 15Why do ventricular cardiac cells have a long refractory period?Ensures that tetanus cannot occur
- 16Describe the three distinct waves of an ECG.1. P wave = Atrial depolarisation
2. QRS complex = Ventricular depolarisation (atrial repolarisation simultaneously)
3. T wave = Ventricular repolarisation - 17Define cardiac output.The volume of blood pumped out of the left ventricle per minute.
- 18What does cardiac output depend on?Heart rate and stroke volume
CO = HR x SV
CO = HR x (EDV - ESV) - 19How does acetylcholine (PSNS) effect the heart?Increases outward K+
Decreases inward Ca2+ and Na+
Overall slows progression of pacemaker potential - 20How does noradrenaline (SNS) effect the heart?Decreases outward K+
Increases inward Ca2+ and Na+
Overall increases progression of pacemaker potential - 21Define intrinsic control of stroke volume.Related to the extent of venous return
- 22Define extrinsic control of stroke volume.Related to the extent of sympathetic stimulation of the heart
- 23Give an example of physiological hypertrophy.Exercise increase thickness of ventricular wall.
- 24Give an example of pathological hypertrophy.Hypertension increases thickness of ventricular wall.
- 25What is the rate of spontaneous firing for the SA node?70 - 80 action potentials per minute
- 26What is the rate of spontaneous firing for the AV node?40 - 60 action potentials per minute
- 27What is the rate of spontaneous firing for the purkinje fibres?20 - 40 action potentials per minute
- 28What happens if the SA node is damaged?The pacemaker activity will then be controlled by the AV node.
- 29Define tachyarrhythmias.Heart rate is increased and includes atrial fibrillation, atrial flutter and ventricular fibrillation.
- 30Define bradyarrhythmias.Heart rate < 60bpm and includes heart blocks and asystolic arrest.
- 31Describe ectopic focus.Cells other than the SA node can exert pacemaker activity usually encouraged by sympathetic activity and partial depolarisation. This allows tachycardia to occur.
- 32Describe after depolariations.Due to a transient calcium increase action potentials are followed by a small after depolariation. As the action potential interval is decreased, after depolariations get larger until an indefinite train in triggered.
- 33Describe re-entrant circuits.Occurs when depolarisation begins to travel in a continuous loop. Where there is an area of unidirectional block and an alternative pathway around the block a loop can occur if the time taken for conduction via an alternate path is greater than the refractory period of tissue adjacent to the block.
- 34What is the target of class I drugs?Block of voltage-sensitive Na+ channels (mostly blocks channels that open frequently) to reduce maximum rate of depolarisation during phase 0.
- 35What are the sub-classes of class I drugs?Class 1a - midway between fastest and slowest in terms of association/dissociation
Class 1b - fastest in terms of association/dissociation
Class 1c - slowest in terms of association/dissociation - 36Describe class 1a drugs.E.g. Disopyramide, quinidine
Disopyramide used for ventricular tachyarrhythmias refractory to other treatment.
ADRs - worsening arrhythmias, parcipitate HF, nausea, GI disturbances - 37Describe class 1b drugs.E.g. Lignocaine
IV treatment for serious ventricular arrhythmias and those associated with MI
ADRs - bradycardia, respiratory depression, nausea, visual disturbances - 38Describe class 1c drugs.E.g. Flecainide
Reaches steady state block due to long action.
Used in treatment of atrial fibrillation, atrial flutter and SVT
ADRs - worsens arrhythmias, nausea, dizziness
Contraindicated in heart block and MI following CAST - 39What is the target of class II drugs?Beta1- selective adrenoceptor antagonist
- 40Describe class II drugs.E.g. Atenolol, metoprolol
Antiarrhythmic properties due to antisympathetic effects.
Used to reduce post MI mortality and to treat tachyarrhythmias.
ADRs - nausea, bronchospasm, cold extremities, bradycardia, hypotension - 41What is the target of class III drugs?Block outward K+ channels involved with repolarisation and thus prolongs action potential which increases refractory period
- 42Describe class III drugs.Amiodarone - first agent, complex and poorly understood MOA, ADRs include neurotoxicity, thyroid alterations, skin discolouration, highly lipophilic and long half life, multiple interactions.
Sotalol - dual class II/III drug, treatment of atrial, SV and ventricular arrhythmias, ADRs include hypotension, exacerbation of HF - 43What is the target of class IV drugs?Block voltage-sensitive L-type Ca2+ channels which slows conduction, reduces after-depolarisation and reduces contractile force
- 44Describe class IV drugs.E.g. Verapamil, diltiazem
Verapamil has greater cardiac effects while diltiazem acts on cardiac and vascular smooth muscle. Used for SVT, AF or flutter.
ADRs - peripheral oedema, bradycardia, headache - 45What can you use to treat bradyarrhythmias?Atropine - antagonist at muscarinic receptors, removes PSNS brake on heart.
Isoprenaline - beta agonist, used for heart block - 46Describe digoxin.Binds to and inhibits site on Na+/K+ ATPase which increase [Na+] which increases [Ca2+] leading to after-depolarisation and increased risk of dysrhythmias.
- 47What is blood flow dependent on?The pressure gradient (ΔP) and the resistance to blood flow (R)
F = ΔP/R - 48What is resistance to blood flow dependent on?Blood viscosity (η) – directly proportional
Vessel length (L)– directly proportional
Vessel radius (r) – inversely proportional
Resistance = η L / r^4 - 49If the radius of a vessel is doubled, how many times more is flow increased by?16 times
- 50How do arteries act as a pressure reservoir?The thick, highly elastic, muscular walls and large radil allow for stretch when pressure is high and contraction when pressure is low. This ensures that the flow in the microcirculation is constant.
- 51Define mean arterial pressure (MAP).The average pressure driving blood forward into the tissues throughout the cardiac cycle.
MAP = dP + 1/3 sP - 52What is the MAP used for?Used by the body to regulate and monitor BP
- 53Where are baroreceptors found?In the wall of the aortic arch and carotid sinus
- 54What can the baroreceptor reflex regulate?Heart rate, stroke volume and peripheral resistance
- 55Define haemostasis.The stopping of blood loss from damaged vessels and protect against haemorrhage.
- 56What are the four mechanisms involved in haemostasis?1. Vasoconstriction
2. Platelet adhesion to the exposed tissue
3. Platelet activation to form a haemostatic plug
4. Reinforcement of plug by fibrin - 57Define thrombosis.Haemostasis in the wrong place; formation of a haemostatic plug within the vasculature in the absence of bleeding.
- 58What are risk factors for thrombosis?1. Injury to vessel wall
2. Altered blood flow
3. Increased coagulability of the blood - 59Define venous thrombi.'Red clots', mainly erythrocytes and fibrin
- 60Define arterial thrombi.'White clots', predominately platelet aggregates and form under conditions of high flow
- 61Describe aspirin as an anti-platelet.Inhibits COX-1 irreversibly thus reducing TXA2 synthesis for the lifespan of the platelet. This produces a very long clotting time.
- 62Describe clopidogrel as an anti-platelet.Inhibits P2Y12 receptors irreversibly to inhibit clotting. It is a prodrug which is converted by CYP2C19.
- 63Describe dabigatran as an anticoagulant.Direct thrombin inhibitor that reversibly inhibits thrombin and thrombin mediated platelet aggregation.
Fixed doses produces predictable anticoagulant effect. - 64Describe rivaroxaban as an anticoagulant.Inhibits factor Xa to reduce thrombin production.
- 65Describe warfarin as an anticoagulant.Vitamin K antagonist and response can very significantly between patients.
- 66Describe how the skeletal pump facilitates venous return.It returns extra blood stored in the veins back to the heart and counters the effect of gravity on the venous system. Muscle contraction opens the upper valve and closes the lower valve so that blood is pumped upwards.
- 67Describe how the respiratory system facilitates venous return.During respiration the pressure surround the chest veins is lower than the pressure surrounding the veins in the extremities and abdomen. This establishes an externally applied pressure gradient on the veins which drives blood toward the heart.
- 68How can blood supply to the capillary bed be controlled?By smooth muscle structures; precapillary sphincters which respond to local metabolic changes. Blood then can bypass the capillary and flow through the metarteriole only.
- 69Define bulk flow.Bulk volume of protein free plasma filters out of the capillary, mixes with interstitial fluid and is then reabsorbed.
- 70What is bulk flow controlled by?Hydrostatic pressure and osmotic pressure.
- 71Describe capillary blood pressure.The hydrostatic pressure of blood flowing into capillaries; this pushes fluid out of capillaries. It is higher at the arteriolar end than the venular end.
- 72Describe blood colloid osmotic pressure.Plasma proteins remain in the plasma; plasma has a higher protein concentration and lower water concentration that interstitial fluid; draws the fluid back into the capillary. The pressure is constant.
- 73Describe the lymphatic system.More fluid is filtered out of capillary than is reabsorbed. The lymphatic system is the route to return excess interstitial fluid to the blood. Also has defence against disease, transport of absorbed fat and return of filtered proteins.
- 74Describe an oedema.The accumulation of interstitial fluid due to reduced concentrations of plasma proteins, increased permeability of capillary walls, increased venous pressure or blockage of lymph vessels.
- 75Describe the renin-angiotensin system.
- 76Describe hypertension.The major risk factor for CVD and is influenced by a combination of genetic and lifestyle factors.
- 77Define essential hypertension.No single underlying pathology
- 78Define secondary hypertension.Due to a specific underlying pathology
- 79What can hypertensive drugs target in treatment?TPR, CO or both
- 80What are the different drug classes that can be used for hypertension?1. ACE inhibitor
2. AT1R antagonist
3. Calcium channel blocker
4. Thiazide diuretic - 81Describe calcium channel blockers.Inhibit L-type calcium channels in vascular smooth muscle and myocardium.
- 82What class of calcium channel blockers are used for hypertension and name the drugs.Dihydropyridines - act mainly on VSM
Nifedipine, amlodipine and felodipine - 83Describe prazosin.Alpha-adrenoceptor antagonist in vascular smooth muscle to reduce vasoconstriction which reduces TPR and arterial pressure.
- 84Describe ACE inhibitors and name them.Reduces Ang II induced vasoconstriction, sodium retention and aldosterone release. It also increase bradykinin levels which is a endogenous vasodilator. It is first like therapy for hypertension. Food in GI tract can reduce absorption by 30-40%.
Captopril, enalapril, perindopril, fosinopril - 85Describe AT1R antagonists and name them.Competitively block binding of Ang II to the AT1R to reduce vasoconstriction, sodium reabsorption and aldosterone release.
Losartan, candesartan, irbesartan, telemisartan - 86Describe thiazide diuretics and name them.Act on distal tubules to prevent Na+ and Cl- reabsorption and thus reduce blood volume. In low doses they also reduce BP by vasodilation. It is first line therapy only for patients >65.
Hydrochlorothiazide - 87Define atherosclerosis.A progressive disease of the large arteries caused by the local accumulation of lipids and fibrous elements together with chronic inflammation.
- 88What is the most clinical complication of atherosclerosis?The formation of a thrombus
- 89Describe the seven stages of atherosclerosis.1. Dysfunction occurs (e.g. reduced production of NO and prostaglandins)
2. Endothelial cells express adhesion molecules which blood leukocytes (monocytes) attach, move into intima and mature into macrophages.
3. Oxidation of LDL and accumulation in macrophages form foam cells.
4. Accumulation of foam cells leads to fatty streak formation.
5. Fibroproliferative response increases synthesis of extracellular matrix macromolecules such as collagen.
6. Apoptosis of foam cells and smooth muscle cells.
7. Plaque's fibrous cap can rupture causing thrombus. - 90How are lipids and cholesterol transported through blood?As lipoproteins, central core of lipid surrounded by polar phospholipids and protein.
- 91What is the function of VLDL?Transport of TGs and cholesterol from liver to tissues.
- 92What is the function of HDL?Transport of cholesterol back to liver for use or excretion.
- 93When do VLDL become LDL?LDLs are formed after VLDLs lose TGs
- 94Describe the mechanism of action of statins.Competitively inhibit HMG Co-A reductase which is the rate limiting step in cholesterol biosynthesis.
- 95When are fibrates used?In severe hypertriglyceridemia, dyslipidemia associated with diabetes and as second line in hypercholesterolaemia.
- 96Describe the mechanism of action of ezetimibe.Cholesterol absorption inhibitor in the duodenum causing increased uptake of LDL from plasma.
- 97Define congestive heart failure.The inability of the heart to supply adequate nutrients to the metabolising tissues of the body, leading to accumulation of fluid in lungs and/or legs.
- 98How does the body compensate in heart failure?Increased activation of sympathetic NS and renin-angiotensin system.
- 99What is the mechanism of action of loop diuretics?Block Na+/K+/2Cl- symporter is ascending loop of Henle reducing reabsorption of Na+, K+ and Cl- ions.
- 100What are the four drug classes that can be used in heart failure?1. ACEI/ARBs
2. Beta blockers
3. Digoxin
4. Diuretics - 101Which beta blockers are used in heart failure?Bisoprolol
Carvedilol
Metoprolol - 102When are beta blockers recommended in heart failure?When LV ejection fraction <35% in combination with ACEI/ARB and diuretic.
- 103Define stable angina.Predictable chest pain experience with exertion due to underlying narrowing of the coronary vessels by atheroma.
- 104Define unstable angina.Pain occurring with reduced exertion, culminating in pain at rest. Similar pathology to an MI, similar treatment as for NSTEMI.
- 105Define myocardial infarction.Sudden occlusion of coronary vessel leading to death of cardiac tissue due to O2 deprivation.
- 106Describe the mechanism of action of fibrinolysis.Catalyses the conversion of plasminogen to active plasmin which breaks down the cross link between fibrinogen and fibrin in the blood and the clot dissolves.
- 107Define hypovolemic shock.Due to loss of blood, plasma, water or electrolytes.
- 108Define cardiogenic shock.When the heart cannot pump enough blood due to infarction, myopathy, pulmonary embolism.
- 109What are the seven major local factors that regulate blood flow?1. Decreased local O2
2. Increased local CO2
3. Increased H+
4. Increased K+
5. Osmolarity
6. Adenosine
7. Local hormones
These factors induce relaxation and vasodilation of arterioles close by. - 110What is the most important local hormone for vasodilation?Nitric oxide
- 111What are the most important chemical factors for circulation in brain?CO2 and H+
- 112What are the vascular elements of the nephron in order?Renal artery
Afferent arteriole
Glomerulus
Efferent arteriole
Peritubular capillaries
Renal vein - 113What are the tubular elements of the nephron in order?Bowman's capsule
Proximal tubule
Loop of Henle
Distal tubule/ collecting ducts
Renal pelvis - 114What are the three barriers filtered fluid must pass through in the glomerulus?1. Glomerular capillary wall
2. Basement membrane
3. Bowman's epithelia - 115What are the three forces involved in glomerular filtration?1. Glomerular capillary blood pressure (favours filtration)
2. Plasma-colloid osmotic pressure (opposes filtration)
3. Bowman's capsule hydrostatic pressure (opposes filtration) - 116In the proximal tubule, what role does Na+ reabsorption play?Facilitates reabsorption of glucose.
- 117In the ascending loop of Henle, what role does Na+ reabsorption play?Production of concentrated or dilute urine.
- 118In the distal tubule, what role does Na+ reabsorption play?Regulating ECF volume.
- 119What does active Na+ reabsorption drive in the proximal tubule?Water, Cl- and urea reabsorption.
- 120Describe how glucose is reabsorbed in the proximal tubules.Na+-glucose cotransporter uses energy from Na+ electrochemical gradient to move glucose into the cell against its concentration gradient. Glucose then diffuses out via the GLUT transported on the basolateral membrane.
- 121Describe tubular secretion of K+.K+ secretion is coupled to Na+ reabsorption in the distal tubule.
- 122Define plasma clearance.The volume of plasma that is cleared of a particular substance per minute. (Does not always equal amount of substance excreted from body)
- 123What are the three lines of defense against pH changes?1. Chemical buffer system (rapid but limited)
2. Respiratory system (moderate but not against respiratory imbalances)
3. Kidneys (powerful but slow long term) - 124Describe the water balance between ICF and ECF.Approximately 2/3 of total body water found ICF with remaining 1/3 in ECF (plasma and interstitial fluid).
- 125Describe the descending limb of the loop of Henle.Highly permeable to water, does not reabsorb Na+
- 126Describe the ascending limb of the loop of Henle.Impermeable to water but actively reabsorbs Na+
- 127Describe the actions of vasopressin.Produced in hypothalamus, stored in posterior pituitary.
Increases permeability of epithelial cells of distal tubule and collecting ducts to water by inserting aquaporins into luminal membrane. - 128What are the five classes of diuretics?1. Carbonic anhydrase inhibitors
2. Osmotic diuretics
3. Loop diuretics
4. Thiazide diuretics
5. Potassium-sparing diuretics - 129Describe carbonic anhydrase inhibitors.E.g. Acetazolamide, Brinzolamide, Metazolamide
Blocks carbonic anhydrase resulting in reduced H+ secretion and Na+ reabsorption.
Intraluminal HCO3- reacts with Na+ which is excreted along with water. - 130Describe osmotic diuretics.E.g. Mannitol
Non-reabsorbable solute causes increased osmotic pressure in proximal tubule and loop of Henle. - 131Describe loop diuretics.E.g. Furosemide
Inhibit luminal Na+/K+/2Cl- cotransporter in proximal tubule. - 132Describe thiazide diuretics.E.g. Hydrochlorothiazide
Inhibits Na+/Cl- symporter in distal convoluted tubule. Increases Ca2+ reabsorption, can be useful in treating calcium stones in kidneys. - 133What are the two types of potassium-sparing diuretics?1. Aldosterone antagonists
2. Na+ channel antagonists - 134Describe aldosterone antagonists.E.g. Spironolactone
Blocks Na+/K+ ATPase in collecting tubule to prevent Na+ reabsorption and K+ excretion. - 135Describe Na+ channel blockers.E.g. Amiloride
Directly blocks Na+ channels in collecting tubule.
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- Flashcards on BIOM3010, created by Zoe Thomas on 13/03/2017.
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- Zoe Thomas · Mar 2017
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- Jun 11, 2017
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