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Circulation1. Regarding the rapid control of blood pressure all of the following are true EXCEPT:a. Noradrenaline and adrenaline are secreted in response to a fall in blood pressure - trueb. Vasopressin is released from the supraoptic nuclei – ADH or vasopressin is made in the cell bodies in the SON, but the axons project to the posterior pituitary for release of the hormone.c. The renin angiotensin system is brought into play - trued. The kidneys bring the blood pressure to near normal – via the atrial reflexes (the volume reflex) -> dilatation of afferent glommerular ateriole -> rise in GFR. Also signals from atria to hypothalamus -> ADH causing reduced reabsorption of fluid in the renal tubule, increasing urine output and reducing blood volume. Also, release of atrial natriuretic peptide increases urine output and thus reduces blood volume.e. The baroreceptor mechanism operates best during fluctuations of blood pressure - true2. Which of the following pairs are correctly matched?a. Bradykinin – vasoconstrictionb. Vasopressin – vasodilationc. Noradrenaline – vasoconstrictiond. Nitric oxide – vasoconstrictione. Prostacyclin – vasoconstriction3. With regards to heart soundsa. The first heart sound is caused by closure of the aortic valve – of the AV valvesb. The second heart sound is caused by closure of the aortic and mitral valves – of the aortic and pulmonaryc. The fourth heart sound can be heard when the ventricle is hypertrophied – also when the arial pressure is highd. The third heart sound is always pathological – heard in many normal young individualse. The third heart sound is due to rapid ventricular ejection – caused by rapid ventricular filling4. Regarding changes in cardiac function during strenuous exercisea. Oxygen usage may increase up to 10 times – correctb. Cardiac output it less than 6.4L/min – may be up to 20.9L/minc. Stroke volume may double – stroke volume levels off (shortening diastole)d. A-V difference is ten times greater than at rest – maybe 3-4xe. Pulse rate is between 60 and 100 beats/min – up to 170+5. All of the following are characteristics of haemoglobin EXCEPT:a. It contains four haem moietiesb. It has a lower affinity for oxygen in its relaxed state – up to 500x higher w/ more binding sites expc. It contains 38 histidine residuesd. When fully saturated it carries 1.39mL of O2 per gram haemoglobine. Each molecule of adult haemoglobin contains 2 α and 2 β polypeptide chains6. Regarding factors which affect arteriolar calibrea. kinins cause vasoconstriction - dilateb. serotonin causes vasodilation - constrictc. histamine causes vasoconstriction - dilated. lactate causes vasoconstriction - dilatese. neuropeptide Y causes vasoconstriction - true7. On standing the typical cardiovascular response isa. an increase in total peripheral resistance by 75% - Increased peripheral SNS activity stimulates arteriolar vasoconstriction – increasing the TPR by 1:1.4 (i.e. 40%)b. an increase in stroke volume by 10% - venous return will drop, thus cardiac outputc. an increase in cardiac output by 50%d. a decrease in central bloodpool by 400ml – this is the main issue with standing, and why the reflexes exist to maintain BP. Note BP = CO x resistance, so BP = SV X HR x resistance. Thus on standing, the stroke volume drops (because reduced venous return/EDV) but there is a decrease in vagal stimulation and increase in sympathetic stimulation -> increase HR and increased peripheral resistance so it balances out.e. a decrease intra-abdominal vascular resistance – it will increase because intra-abdominal pressure will rise8. with regard to the calibre of arterioles, the following substance causes vasoconstrictiona. nitric oxide - dilatesb. kinins - dilatesc. histamine - dilatesd. angiotensin II – constricts (as the name implies)e. VIP - dilates9. regarding the cardiac cyclea. closure of the A-V valve occurs at the start of isovolumic relaxation – at the start of isovolumetric contractionb. closure of the aortic valve occurs at the end of isovolumic contraction – at the start of isovolumetric relaxationc. V-wave corresponds with ventricular antiaction – V wave is the rise in atrial pressure prior to the tricuspid valve openingd. A wave corresponds with atrial contraction - correcte. Jugular venous pressure demonstrates a dicrotic notch – the carotid/arterial wave form has a dicrotic notch caused by the aortic valve snapping shut at the end of systole causing an occilation10. causes of increased interstitial fluid volume and oedema include all of the following EXCEPT:a. arteriolar dilationb. decreased plasma protein levelc. histamined. increased lymph flow – clears oedemae. venular constriction11. the decreased tension developed in cardiac muscle at high levels of stretch (descending limb of Starling curve) is caused bya. decreasing available calciumb. decrease in the number of cross bridges between actin and myosinc. increased muscarinic transmission associated with high diastolic intraventricular pressuresd. disruption of myocardial fibres – The Frank-Starling curve has a "descending limb" at high filling volumes. In this region further stretching of the cardiac fibres leads to a break down in their structural integrity and subsequent drop in cardiac output. A catastrophe would occur: The diminished cardiac output would be unable to pump away all the blood that fills the ventricle during diastole. As the blood accumulates, the cardiac output falls still further until cardiac failure occurred.e. mechanical closure of calcium channels12. at an arterial blood pressure of 70mmHga. carotid sinus receptors are strongly stimulated – the stretch receptors will be very weakly stimulated, they are stimulated by high pressures not lowb. carotid body receptors are strongly stimulated – they will be poorly perfused and therefore activated by a reduction in PO2 (stagnant anoxia). These receptors are responsible for the Mayer Waves seen in hypotension: 20-40s fluctuations in BP as feedback is looped.c. central nervous system ischaemia response is activated - <40mmHgd. both carotid body and carotid sinus receptors are strongly stimulatede. none of the above are true13. The c wave of the jugular venous pressure corresponds toa. Atrial systole – a waveb. Rise in atrial pressure point prior to tricuspid opening – v wavec. Aortic valve snapping shut – the dicrotic notch of carotid/arterial pulsed. Bulging of the tricuspid valve into the atrium – correct, during isovolumetric ventricular contractione. Atrial diastole 14. with respect to the cardiac cycle and the ECGa. the start of systole is marked by the P waveb. the PR interval represents atrial relaxationc. the ST segment represents absolute refractory period of the ventricles - The T wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period (or vulnerable period).d. the T wave is synchronous with the third heart sounde. none of the above 15. vascular compliancea. is equal to increase in pressure divided by increase in volume – C = ΔV/ΔPb. is the same as vascular distensibility - Compliance is a measure of the tendency of a hollow organ to resist recoil toward its original dimensions upon removal of a distending or compressing force. It is the reciprocal of "elastance". Distensibility is simply the ability to stretch and hold more volume. They are elated, but not the same.c. is 24 times greater in a vein than a corresponding artery - Venous compliance is approximately 30 times larger than arterial complianced. is increased by sympathetic stimulation in the arterial system - decreasede. is increased by sympathetic stimulation in the venous system - decreased16. factors affecting the activity of the vasomotor area in the medulla area. inhibitory inputs from carotid and aortic chemoreceptors – excitatory inputsb. direct stimulation by CO2 – correct, also hypoxia directly stimulatesc. excitatory inputs from the carotid, aortic and cardiopulmonary baroreceptors - inhibitoryd. excitatory inputs from lungs - inhibitorye. inhibitory input from cortex via hypothalamus – excitatory or inhibitory?17. regarding Frank-Starling curvesa. the extent of afterload is proportionate to end diastolic volumeb. cardiac muscle fibres are lengthened by decreased ventricular compliancec. contractility of myocardium is increased on standing – this is correct because the drop in BP -> decreased baroreceptor stimulation -> decreased inhibition of RVLM -> increased sympathetic response -> increased HR and contractilityd. sympathetic stimulation shifts the length/tension curve upward and to the right – upward and to the lefte. increased negative intrathoracic pressure increases contractility - Contractility describes the ability of the myocardium to contract in the absence of any changes in preload or afterload. In other words, it is the "power" of the cardiac muscle. The most important influence on contractility is the sympathetic nervous system. as per Ganong: lung inflation afferents + cardiopulmonary baroreceptors (venous return) inhibits the RVLM -> reduces sympathetic stimulation (lowers BP/HR)… however studies do show the contractility increases, likely through reduced vagal stimulation.18. regarding coronary blood flowa. in most people, the left coronary artery supplies the sinoatrial node – (R)CAb. coronary blood flow occurs only during systole - diastolec. coronary blood flow is about 15% of cardiac output – 5% of output, 11% O2 consumptiond. the coronary sinus drains into the right atrium - correcte. B1 receptors in the arterial wall cause vasoconstriction – vasodilation (alpha receptors vasocontrict, sympathetic stimulation -> vasodilation because of metabolites from increased HR/contractility, however if b-blocked it would cause vasocontriction)19. Regarding Starlins forcesa. Capillary pressure at the arteriole end is 15mmHg - dependsb. Hydrostatic pressure exceeds oncotic pressure throughout the capillaryc. Capillary pressure at the venule end is 5mmHg - dependsd. Interstitial colloid osmotic pressure is usually negligiblee. Capillary filtration coefficient decreases with capillary permeability20. concerning capillary fluid exchangea. venule constriction reduces filtration pressure - increasesb. hypoproteinaemia decreases fluid shift out of capillaries - increasesc. lymphoedema fluid has a low protein count – high, caused my inadequate lymph draininaged. substance P increases capillary permeability – after noxious stimuli, via the axon reflexe. kinins reduce capillary permeability – histamine and bradykinin increase21. Regarding Starlings forcesa. Hydrostatic pressure gradient is the only force involvedb. Interstitial fluid pressure remains the samec. Osmotic pressure gradient is not involvedd. Total diffusion is not flow limitede. Transfer for substances that do not reach equilibrium is diffusion limited22. during the cardiac cyclea. ventricular systole starts with opening of the aortic valveb. rapid ejection occurs at the end of systolec. phase 3 corresponds to ventricular ejectiond. with a rate of 75bpm, diastole is 0.27 secondse. the V wave relates to rise in atrial pressure before the closure of the tricuspid valve23. With regards to cerebral blood flowa. Autoregulation is not a typical featureb. It is increased with raised intracranial pressurec. It is unaffected by sympathetic stimulationd. It is maintained at normal flow limits with arterial pressures ranging from 35 to 160mmHge. It is maintained in times of increased intracranial pressure by the Cushing reflex24. the vasomotor centre receivesa. excitatory inputs from the lungsb. excitatory and inhibitory inputs from the carotic chemoreceptorsc. direct stimulation from the heartd. excitatory input from the kidneyse. inhibitory input from the pain pathways25. the slowest conduction speed in cardiac tissue is found ina. Purkinje systemb. AV nodec. Ventricular muscled. Bundle of Hise. Atrial pathways26. circulatory changes in exercise includea. total cessation of skeletal muscle blood flow at 50% of its maximal tension – 70%b. a drop in stroke volume with isotonic muscle contractionc. a decrease in venous returnd. “rebound” hypotension post-exercise <- due to metabolitese. An initial bradycardia at the start of isometric muscle contraction27. the plateau phase of the cardiac action potential is due to the opening ofa. calcium channelsb. sodium channelsc. chloride channelsd. potassium channelse. hydrogen channels28. which of the following changes will produce a transient decrease in cerebral blood flowa. a decrease in intracranial pressureb. an increase in cardiac outputc. dilation of cerebral arteriolesd. a rise in mean venous pressure at brain levele. decreased blood viscosity29. the biggest influence of blood flow in a tube isa. viscosityb. systolic pressurec. length of vesseld. radius of vessele. diastolic pressure30. With a K+ of 8.5meq/L the ECG usuallya. Shows a prominent U waveb. Shows no evidence of atrial activityc. Has T wave inversiond. Is completely normale. Will have a QRS interval of approximately 0.06 seconds31. Which factors increase myocardial contractility?a. Hypoxiab. Hypercapniac. Acidosisd. Digitalise. Decreased cAMP32. vasodilating hormones include all of the following EXCEPT:a. VIPb. Atrial natriuretic peptidec. Vasopressind. Bradykinine. Kalidin33. lympha. protein content is lower than plasma <- and 25-50% circulating returned each day (2-4L drain)b. drains into blood via SVCc. is clear after a fatty meald. doesn’t contain clotting factorse. contains circulating neutrophils34. arteriolar dilatation in muscle is mediated by all excepta. histamineb. kininsc. circulating adrenalined. circulating noradrenalinee. atrionatriuretic factor35. during exercisea. the amount of blood in the arterial portion of the circulation may increase by as much as 30%b. blood flow to the brain is increasedc. blood flow to the kidney is increasedd. blood flow to the brain is decreasede. the oxyhaemoglobin dissociation curve (for blood in the muscular bed) is decreased in proportion to the CO2 level36. what is common to all capillary beds?a. All are patentb. Are 10-20mm in diameterc. Have a continuous basement membraned. Have intracellular fenestratione. ?37. with regard to lympha. has no clotting factorsb. its protein content depends on the area it is fromc. is not dependent on the colloid pressure of the capillaryd. ?e. ?38. during isovolumetric contractiona. mitral valve opensb. decreased aortic pressurec. may have reversed flow in the aortad. ?e. ?39. flow through a narrow tube is proportional toa. viscosityb. lengthc. average pressure in the tubed. pressure gradiente. ?40. regarding cardiac output in exercisea. it can increase 200%b. it can increase 500%c. it can increase 700%d. it can increase 300%e. it can increase 400%41. in exercise in a fit healthy young malea. stroke volume increases less than 200%b. stroke volume increases more than 300%c. stroke volume increases more than 400%d. stroke volume increases more than 700%e. ?42. regarding the blood supply of the hearta. the heart receives 15% of CO at restb. left ventricular supply may be decreased by tachycardiac. ?d. ?e. ?43. regarding granulocytesa. all have cytoplasmic granculesb. basophils are identical to mast cellsc. eosinophils phagocytose virusesd. neutrophils have a half life of 4 dayse. ?44. regarding the Rhesus antigen systema. Rh positive individuals have C, D and E antigensb. 50% of caucasians are D+c. Do not develop anti-D antibodies without prior exposure of D –ve individuals to D +ve red cellsd. ?e. ?45. the major cause of oedema isa. increased hydrostatic pressureb. increased lymph flowc. increased intravascular oncotic pressured. ?e. ?46. Regarding capillariesa. Arterioles have a lower ratio of smooth muscle to diameter than large arteriesb. Capillary flow is regulated by precapillary sphincters on metarteriolesc. Have the largest corss-sectional aread. Contain 8% of the total blood volumee. ?47. the slowest conducting type of cardiac tissue isa. bundle of Hisb. ventricular musclec. Purkinje systemd. Atrial pathwayse. AV node48. the part of the CVS with the largest total cross sectional area isa. arteriesb. large veinsc. capillariesd. arteriolese. venules49. with respect to the cardiac action potentiala. the plateau phase of repolarisation may be up to 200 times longer than the depolarisation phaseb. unlike the nerve action potential there is no overshootc. ?d. ?e. ?50. cardiac output is changed accordingly in all of the following circumstances excepta. increased by up to 700% in exerciseb. increased on eatingc. decreased by sleepd. ?e. ?51. all of the following produce vasodilatation excepta. local K+ accumulationb. systemic hypoxiac. lactated. increased CO2 tensione. decreased pH52. the c wave of the jugular venous pulse is due toa. the rise in atrial pressure before the tricuspid valve opens in diastoleb. transmitted pressure due to tricuspid bulging in isovolumetric contractionc. atrial systoled. atrial contraction against a closed tricuspid valve in complete heart blocke. the increase in intrathoracic pressure during expiration53. during the Valsalva manoeuvre bradycardia occursa. at the onset of strainingb. as the intrathoracic pressure reaches a maximumc. as a result of an initial increase in cardiac outputd. when the glottis is opened and intrathoracic pressure returns to normale. if the patient has autonomic insufficiency54. which of the following are not part of the compensatory mechanisms activated by haemorrhagea. increased erythropoietin secretionb. increased insulin secretionc. increased vasopressin secretiond. increased glucocorticoid secretione. increased renin secretion55. the most rapid conduction of electrical impulses occurs ina. atrial pathwaysb. AV nodec. Bundle of Hisd. Purkinje systeme. Ventricular muscle56. with regard to cardiac action potentialsa. cholinergic stimulation increases the slope of the prepotentialb. the resting membrane potential is increased by vagal stimulationc. phase 0 and phase 1 are steepest in the AV noded. the T wave is the surface ECG manifestation of phase 1e. the action potential in the AV node is largely due to calcium fluxes57. with regard to the 12 lead ECGa. lead II is at 90° for vector analysisb. +130° is still a normal cardiac axisc. The standard limb leads record the potential difference between 2 limbsd. V2 is placed in the left 3rd interspacee. Septal Q waves are predictable in V258. with regard to the cardiac cyclea. phase 1 represents atrial systoleb. the aortic valve opens at the beginning of phase 2c. the T wave of the ECG occurs during phase 4d. the second heart sound is due to mitral valve closuree. the c wave is due to tricuspid valve opening59. cardiac output is decreased bya. sleepb. eatingc. pregnancy in the first trimesterd. sitting from a lying positione. all of the above60. myocardial contractility is decreased by all of the following EXCEPT:a. acidosisb. barbituratesc. hypercarbiad. bradycardiae. glucagon61. the greatest percentage of the circulating blood volume is contained withina. capillariesb. larger arteriesc. venules and veinsd. pulmonary circulatione. the heart62. The Poiseuille-Hagen formula tells us thata. Longer tubes can sustain higher flow ratesb. Flow is directly proportional to resistancec. Flow will be doubled by a 20% increase in vessel diameterd. Why the venous capacitance system is important in cardiac outpute. Turbulent flow is predicted in high velocity vessels63. all of the following explain venous blood flow EXCPTa. intrathoracic pressure variationsb. the pumping action of the heartc. skeletal muscle contractiond. oncotic pressure gradient <-e. smooth muscle contraction - ?64. endothelium derived relaxing factora. shares a similar mechanism of action to glyceryl trinitrateb. activates adenyl cyclasec. is the common pathway in the action of adenosine and histamined. antagonises the action of thromboxanee. is synthesised by a magnesium dependent enzyme65. the R wave of the ECG is due toa. calcium influxb. chloride influxc. sodium influxd. potassium influxe. chloride efflux66. haemoglobina. the globin portion is a porphyrinb. the difference between haemoglobin and myoglobin is haemc. fetal haemoglobin has no beta chainsd. ?e. ?67. Regarding Poiseuille-Hagen flow in vessels, the flow in a vessel is proportional toa. Pressure difference between the two endsb. Radiusc. Viscosityd. ?e. ?68. with respect to isovolumetric contraction of the ventricle it is associated witha. decreasing aortic pressureb. aortic back flowc. open mitral and tricuspid valvesd. open aortic and pulmonary valvese. none of the above69. which of the following organs receives the largest amount of the blood’s circulation per kg of tissuea. heartb. kidneyc. braind. livere. adrenal70. a fit young man goes from sitting to running with full exertion. His stroke volume will increase bya. 400%b. 700%c. 2000%d. Less than 200%e. 1000%71. with respect to the cardiac cyclea. ?b. ?c. ?d. Isovolumetric contraction phase immediately follows the phase of atrial systolee. ?72. which of the following is a compensatory response to shocka. decreased ADHb. ?c. ?d. Increased thoracic pumpinge. ?73. lympha. has an increased protein content compared with plasmab. has a differing protein in different areasc. fats cannot enter lymphd. has no lymphocytese. contains no clotting factors74. Which of the following is true regarding Starling’s law of the hearta. It relates stroke volume to afterloadb. Changes in myocardial contractility do not influence the Frank Starling curvec. Explains the increase in heart rate produced by exercised. Explains the increase in cardiac output that occurs when venous return is increasede. Acidosis improves contractility ................
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