Q:1 a) Classify the functional types of blood vessels and give examples of each.

b) Give the function of each type in the light of its anatomy. (2.5 + 2.5 marks) key: 1. Elastic Vessels: (AORTA & LARGE ARTERIES) 2. Resistance Vessels: (ARTERIOLES, METARTERIOLES & PRE-CAPILLARY SPHINCTERS) 3. Exchange Vessels: (CAPILLARIES) 4. Capacitance Vessels: (venules & veins) 5. Shunt Vessels: (Arterio-venous Anastomosis) (0.5 mark each) ELASTIC VESSELS: HISTOLOGY: More elastic tissue & loose collagen fibers. Aorta & large arteries expand to accommodate blood by ELASTIC RECOIL it generates & maintains diastolic B.P.

SIGNIFICANCE: if large vessels were not elastic, there wouldve been no blood flow in diastole RESISTANCE VESSELS: Size of these vessels control blood flow to tissues. Size is controlled by nerves & local metabolic factors like lactic acid & [CO2]. HISTOLOGY: Single layer of endothelial cells supported by a basement membrane EXCHANGE VESSELS: Through capillary wall, there is exchange between blood & tissues. Pre-capillary sphincter is there at the beginning of capillary CAPACITANCE VESSELS: SIGNIFICANCE: Veins accommodate 2/3 of blood volume (64%), without increase in pressure. Veins are supplied by sympathetic nerve fibers. When veins are constricted venous return increases When veins are dilated increased amount of blood is pooled up in veins.

SHUNT VESSELS / ARTERIO-VENOUS ANASTOMOSIS:

Pass from metarterioles venules & bypass the capillary network. SIGNIFICANCE: Rapid flow of blood Involved in temperature regulation. Normally blood flow through skin is slow BUT for temp. regulation, there must be quick flow of blood for heat loss. LOCATION: These are present in skin of exposed areas of body: (palm of hand, external ear & fingers). NERVE SUPPLY: These are supplied by sympathetic nerve fibers

--------------------------------------------------------------------------------------------Q:2 a) Define Blood flow. Briefly discuss its different types? b) Give a brief account of Reynolds number. Key:2 DEFINITION OF BLOOD FLOW: Quantity of blood that passes a given point in the circulation in a given period of time. UNIT OF BLOOD FLOW: ml/min or L/min or ml/sec. TYPES: STREAM-LINE / LAMINAR FLOW & TURBULENT FLOW LAMINAR BLOOD FLOW: Blood flows in layers or laminae. A thin layer of blood in contact with vessel wall does not move. Next layer moves with a slow velocity & further next with higher velocity. At centre of vessel, maximum velocity. Unidirectional & without noise or sound. TURBULENT FLOW: Blood flows in different directions. Blood mixes within itself. There are eddy currents in blood flow. This type of flow is accompanied by noise or sound. Normally in all vessels blood flow is streamlined, except ascending aorta & pulmonary trunk, where normally there is some turbulance. Turbulance can be determined & expressed in terms of REYNOLDS NUMBER.

b.Reynolds number DEFINITION: It is the unit of turbulance. VALUE: Its value is between 2000-3000. It is directly proportional to the product of velocity, change in diameter & density. It is inversely proportional to the viscosity. Re = v.d.p n When this no. is more than 3000, blood flow becomes turbulent. In hyperdynamic circulation, velocity increases Reynolds no. increases (hyperthyroidism & severe anemia) HEMIC MURMURS. Turbulence occurs incase of: high velocity of blood flow, pulsatile nature of flow , sudden change in vessel diameter & large vessel diameter.

-------------------------------------------------------------------------------------------Q:3 Define: Resistance Conductance Poiseuilles law Stroke volume Venous return (1 mark each) Key3 RESISTANCE is the impediment to blood flow in a vessel. CONDUCTANCE is a measure of blood flow through a vessel for a given pressure difference. CONDUCTANCE is the exact reciprocal of RESISTANCE: conductance = 1 / resistance

Poiseuilles law F = P r4

8nl F = Rate of blood flow, P = pressure difference, r = radius of vessel wall, n = viscosity of blood & l = length of vessel. STROKE VOLUME is the difference between EDV & ESV = 120 50 = 70ml. S.V is the amount of blood pumped out by each ventricle during each beat. When heart rate is normal (72/min), it is 70ml (60-80ml). VENOUS RETURN is the quantity of blood flowing from the veins into the right atrium each minute. Normally V.R = C.O (Frank starling law)

------------------------------------------------------------------------------------------- Q4.a . How does autoregulation take place. (4 marks) b. Mention the role of EDRF (Endothelium Derived Relaxing Factor) in control of local blood flow. (1 mark) Key4 A) Autoregulation of blood flow when Arterial Pressure Changes from normal Metabolic & Myogenic Mechanisms: (1 mark) In any body tissue, acute increase in arterial pressure leads to immediate rise in blood flow then within less than a minute blood flow is returned to normal in most tissues. This return of blood flow towards normal is called Autoregulation of blood flow. (1 mark) Metabolic Theory: When arterial pressure increases there is excess flow which leads to excess oxygen & nutrients that causes vasoconstriction results in flow decreases to normal despite the increased pressure. (1 mark) Myogenic Theory: High arterial pressure causes Sudden stretch of small blood vessels that causes smooth muscle of vessel wall contracts for a few seconds (reactive vasoconstriction) result in blood flow is reduced back to normal & vice versa. (1 mark) b. Role of EDRF: Rapid flow of blood through the arteries & arterioles exert shear stress on endothelial Cells causes significant increase in release of nitric oxide (EDRF) from endothelial cells followed by relaxation of blood vessels to increase in diameter of upstream arterial blood vessels (which significantly offer resistance to blood flow otherwise), whenever microvascular blood flow increases downstream so that local blood flow control is achieved. (1 mark)

--------------------------------------------------------------------------------------Q.5a) Briefly describe the CNS ischemic response. (4 marks) b) Why it is called last ditch response of the body. (1mark). KEY: 5 a) CNS ISCHAEMIC RESPONSE It is activated when mean B.P falls below 60 mmHg (1 mark) Blood flow to the brain dec ischemia of brain ( including vasomotor centre). (1 mark) From vasomotor centre discharge excessively occurs along sympathetic nerves this leads to : Tachycardia Vasoconstriction Increased Blood Pressure (2 mark) b) It is one the most powerful stimulant of the sympathetic vasoconstrictor nerves. This response is the last attempt of body to safe life, called last ditch response. (1 mark)

Q6. What is baroreceptor reflex? Key:6 10 Reference: p 209, Guyton 11th Ed.

(5)

Baroreceptor reflex functions to maintain blood pressure relatively constant during changes in body posture and other daily activities for short-term only as the baroreceptors undergo rapid adaptation, so not able to regulate for long term. (0.5) It is mediated through baroreceptors, spray-type nerve endings located in arch of aorta and in the walls of carotid sinus (0.5) Increased pressure in blood vessels containing baroreceptors causes increased impulse firing. Stimulated in pressure range of 50 to 60 mm Hg, to 180 mm Hg/ Very rapid in response. (1) Signals are carried from carotid baroreceptors by small Hering nerves to glossopharyngeal nerve to tractus solitarius of medullary region of brain stem. (0.5) Signals from the aortic baroreceptors in the arch of the aorta are transmitted through the vagus nerves to tractus solitaries (0.5) The net effects are inhibition of vaoconstrictor area (sympathetic activity) and excitation of the vagal center (parasympathetic activity) which cause: 1. Dilation of veins and arterioles (0.5) 2. Decreased heart rate and strength of contraction. (0.5) This causes a decline in blood pressure due to decreased peripheral resistance and cardiac output. (1)

-----------------------------------------------------------------------------------------------------------Q:7 A person rises from sitting to standing position suddenly. He feels dizzy due to postural hypotension. But after sometime the condition becomes normal. a) Give the sequence of events that helped in normalizing the blood pressure in this case. b) Which nerves take part in this reflex? (3+2 marks) key:7 A) standing from sitting blood pooling in legs postural hypotension decreased pressure sensed by baro-receptors impulses to VMC Sympathetic stimulation & parasympathetic inhibition peripheral vaso-constriction, increase in contractility of heart & heart rate increase in cardiac out put increase in blood pressure back to normal B) Impulses from CAROTID BARO-RECEPTORSHering NGlossopharyngeal Nerve.

(1 mark) Those from AORTIC BARORECEPTORS carried by VAGI (1 mark) BARORECEPTOR / PRESSORECEPTOR / STRETCH RECEPTOR REFLEX: LOCATION: Present in adventitia of wall of carotid sinus & wall of arch of aorta. . Impulses from CAROTID BARO-RECEPTORSHering NGlossopharyngeal Nerve. Those from AORTIC BARORECEPTORS carried by VAGI Glossopharyngeal N & Vagi Sensory part of V.M.C Even at normal B.PBASAL STRETCH of baroreceptors discharge of impulses of glossoph & vagus N V.M.C maintain normal peripheral resistance & B.P.

When arterial B.P increasesmore stretchmore discharge of impulses To V.M.CSympathetic inhibition & parasympathetic stimulationdecreased H.R & peripheral vasodilatation. With less H.RLess C.O With periph V.DLess T.P.R So B.P falls back to normal ( B.P=C.O X TPR) When B.P falls below normalless discharge of impulses to V.M.C SYMPATHETIC STIMULATION & parasympathetic inhibition more H.R More C.O & Peripheral V.C More TPR So B.P increases back to normal

-----------------------------------------------------------------------------------------------------------Q8. Define blood pressure. What factors retain salt and water to restore a decreased blood pressure? (0.5+4.5) th Key: 8 Reference: p 223 Guyton 11 Ed. Definition of Blood pressure: Force exerted by the blood against any unit area of the vessel wall. It is normally equal to 120/80 mmHg, where 120 is Systolic & 80 is diastolic. (0.5) Factors retaining salt and water for the restoration of blood pressure: Renin Angiotensin System plays an important role in restoration of blood pressure secondary to retention of salt and water. Renin is synthesized and released by the Juxta Glomerular cells of kidney. It causes conversion of angiotensinogen (from liver) to angiotensin I, which is converted to angiotensin II (a potent vasoconstrictor) in presence of Angiotensin converting enzyme from pulmonary capillary endothelium. (0.5) Angiotensin II decreases salt and water excretion by the kidneys by: i) Constricting the efferent arterioles, thus diminishing blood flow, allowing rapid osmotic reabsorption from tubules. (1) ii) Directly stimulating the epithelial cells of the tubules to increase the reabsorption of sodium and water. (1)

iii) Stimulating adrenal glands to secrete aldosterone which increases reabsorption of water and salt by the epithelial cells of the renal tubules. (1) Acting on hypothalamus to stimulate thirst centre leading to increased desire to drink water resulting into increased intake of water, thus building the blood volume & so the blood pressure.

----------------------------------------------------------------------------------------------------

Q9. Define cardiac output? What is Frank starling law? How does it regulate cardiac output? (5) Ref: p 111 & 112, Guyton 11th Ed key9 Cardiac output: It is the amount of blood pumped into the aorta each minute by the heart and equals 5 L/minute (1) Frank Starling Law: Within physiologic limits heart pumps all the blood that returns to it by the way of the veins. (1) Regulation of cardiac output by Frank starling law: When an extra amount of blood flows into the ventricle the cardiac muscle is stretched to a greater length. (1) This in turn causes the muscle to contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. (1) Due to greater force of contraction heart is able to pump greater quantity of blood into the aorta this way increasing the cardiac output. (1)

------------------------------------------------------------------------------------------Q10. Define cardiac index. List the factors which regulate cardiac output. Give the mechanism of any one of them. (1+3+1)

Key: 10 Ref: p 111, Guyton 11th Ed & p 234 Ganong Cardiac Index: The cardiac output per square meter of body surface area. In an average human being of 70 kg average cardiac index is about 3L/min/m2. (1) Factors which regulate cardiac output: As cardiac output is the product of stroke volume and heart rate so all factors affecting these ultimately affect cardiac output. Mechanism of relation of Heart rate to cardiac output. The basic mechanisms by which cardiac output is regulated by heart are: Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart. This follows Frank Starling mechanism according to which the greater the heart muscle is stretched during filling the greater is the force of contraction and the greater the quantity of blood pumped in the aorta (0.5) The autonomic nervous system: Sympathetic stimulation increases rate and force of contraction that lead to an increase in cardiac output. Parasympathetic stimulation on the contrary causes decreased heart rate with slight effect on force of contraction as well. (0.5) HEART RATE AFFECTING FACTORS: Heart beat is autonomous but is modified by nervous mechanisms: 1) Autonomic nerves supplying the heart: a) Sympathetic b) Parasympathetic (1)

2) Vasomotor centre (affected by impulses from different parts of the body).

EDV AFFECTING FACTORS: 1. Venous return (most important factor) or Pre-load 2. M.S.F.P (Mean Systemic Filling Pressure) 3. B.P or After-load 4. SYMPATHETIC STIMULATION or peripheral resistance 5. SKELETAL MUSCLE PUMP 6. GRAVITY 7. RESPIRATORY PUMP

(Any 4 = 1 mark)

8. NEGATIVE PRESSURE IN SYSTOLE 9. FILLING TIME 10. DURATION OF DIASTOLE 11. DISTENSIBILITY OF VENTRICLE 11. ATRIAL CONTRACTION

ESV AFFECTING FACTORS: (Any 2 = 1 mark) 1. FORCE OF HEART CONTRACTION (FRANK STARLING LAW) 2. AFTER LOAD 3. SYMPATHETIC / VAGUS NERVES 4. CONDITION OF MYOCARDIUM 5. HORMONES/DRUGS WHICH INCREASE CONTRACTILITY OF HEART: Examples: Thyroxine & Glucagon 6. FACTORS WHICH DECREASE C.O.: Examples: Heart failure, Hypoxia, Acidosis, Barbiturates, Beta adrenergic blockers

----------------------------------------------------------------------------------------------------------Q11. Enumerate the cause and features of neurogenic shock? Key11 Neurogenic shock: In this type of shock the vascular capacity increases so much that even the normal amount of blood becomes incapable of filling the circulatory system adequately. Cause of Neurogenic shock: One of the major causes of this is sudden loss of vasomotor tone throughout the body, resulting especially in massive dilation of the veins. The resulting decrease in blood volume reduces the mean systemic filling pressure, which reduces venous return to the heart leading to greatly decreased cardiac output causing inadequate blood flow throughout the body. Features of Neurogenic shock: Hypotension Rapid and feeble pulse Altered mental status ranging from confusion to coma Ref Guyton pg

Q.12 A 50 years old barber gradually develops elongated, tortuous & dilated veins in the legs. a. What is this condition called? b. Enlist factors that effect venous return. c. How are veins controlled by nervous system?

d. How do inspiration & expiration affect venous return? UHS MBBS (I) ANNUAL 2009, Q:3, Goal Ed. 2011 Key: 12 Reference: pp 176-178, 204, 240 Guyton 11th Ed. a. Condition: Varicose veins b. Factors affecting venous return (V.R):

(1+2+1+1)

(1) (Any 4 = 2 marks)

Basic factors affecting Venous return are: i) Arterial blood pressure: Directly proportional (V.R = ARTERIAL B.P TPR) ii) Total peripheral resistance (TPR) or resistance to venous return (RVR): Inversely proportional. (V.R = ARTERIAL B.P TPR) iii) Mean systemic filling pressure (MSFP) V.R = MSFP Rt. At. Pr RESISTANCE TO V.R (MSFP is affected by blood volume, sympathetic stimulation & contraction of skeletal muscles. It is directly proportional to all these). iv) Blood volume (More Blood volume will lead to more arterial pressure & more enous return) v) Sympathetic stimulation (Sympathetic Stimulation will cause vasoconstriction & more venous return) vi) Contraction of skeletal muscles (Skeletal muscle contraction causes more pressure & more venous return). Venous pump & venous valves (unidirectional flow) vii) Right atrial pressure (V.R = MSFP Rt. At. Pr RESISTANCE TO V.R) viii)Intra-abdominal pressure effect on venous pressure of leg (rise in intra-abdominal pressure due to pregnancy, large tumors or ascites).Increase in intra-abdominal pressure resists venous return. ix) Gravitational pressure effect on venous pressure (in standing posture, gravity negatively effects venous return) c) Control of veins by nervous system: Sympathetic nervous system stimulation causes venoconstriction & thus decreases the volume of the veins. This can push blood into heart & thus play a major role in regulation of heart pumping (1) d) Effect of Inspiration & expiration on heart rate: There is negative intra-thoracic pressure in inspiration, due to descent of diaphragm (when volume increases, pressure decreases according to Boyles law) so venous return increases due to suction effect by thoracic pump & vice versa. (1)

-----------------------------------------------------------------------------------------------------------Q.13 a) What are the pressure changes in Atria during the Cardiac Cycle? b) How are these changes related to the Jugular Venous Pulse? c) Give the clinical significance of JVP. (1+3+1 mark) key: 13 a) Pressure Changes in Atria: Right Atrial Pressure = Central Venous Pressure During wave a, c & v pressure rises. Otherwise remains almost zero. 4-6 mm Hg Rt. Atrium (during a, c, v) 7-8 mm Hg Lt. Atrium (during a, c, v) (1 mark) b) JUGULAR VENOUS PULSE: 3 waves can be recorded from atria which represent atrial pressure changes: a-wave: Due to increase in atrial pressure during atrial systole. (1 mark) c-wave: Recorded at beginning of contraction of ventricle. During isovolumetric contraction, ventricular pressure increases causes Cusps of AV valves are pushed into atrial cavity result in pressure rises in atria leads to ascent of c-wave. (0.5 mark) The top of c-wave coincides with opening of semilunar valves (Aortic & Pulmonary). With opening of semilunar valves, 2nd phase starts, which is maximum ejection phase. It is later on followed by isovolumetric relaxation of ventricle causes muscle length increases and now AV valve is pulled to ventricular cavity then atrial cavity increases and pressure falls in the atria leads to descent of c-wave. (0.5 mark) v-wave: Due to gradual increase in atrial pressure, resulting from venous filling of blood (from the venae cavae) into the atria, with closed AV valves that causes ascent of v-wave. (0.5 mark) Top of v-wave coincides with opening of AV valves then rapid inflow phase leads to decrease pressure in atria result in descent of v-wave. (0.5 mark) c) Significance of J.V.P: (Any 2 = 0.5 mark each = 1 mark) ac interval coincides with PR interval of ECG ac interval increases in delayed AV conduction. a waves are absent in: ATRIAL FIBRILLATION. (a wave) > (c wave) in COMPLETE AV BLOCK. Giant a waves in TRICUSPID & PULMONARY STENOSIS. Pulsating Neck Veins in CCF (Congestive Cardiac Failure). (1 mark)

------------------------------------------------------------------------------------------------------------

Q.14 Define Hypertension. What do mean by: Essential hypertension, Malignant hypertension, Atherosclerosis & Co-arctation of aorta. (1+4 marks)

key:14 HYPERTENSION: Persistent increase in systemic arterial blood pressure. CLINICAL DEFINITION: When systolic B.P rises above 130 mmHg and diastolic B.P above 85 mmHg. (REFERENCE: SILVER THORN) (1 mark)

ESSENTIAL HYPERTENSION: B.P is elevated in absence of an underlying disease. Arterial B.P is increased due to increased TPR. TPR is increased due to unknown pathology. (1 mark) MALIGNANT HYPERTENSION: 250/150 B.P Developed due to combined effect of primary and secondary hypertension. It produces severe renal disease & retinal hemorrhage. causes death in few years. (1 mark) ATHEROSCLEROSIS (hardening of blood vessels) COARCTATION OF AORTA (narrowing of aorta) (1 mark) (1 mark)

-------------------------------------------------------------------------------------------------------

Q15:Asim 25 year old man came with head injury in emergency. On examination his blood pressure was 160/100mmHg. There was no history of previous hypertension. On receiving antihypertensive dose from a Junior Doctor, he collapsed in a short while. a-What could be the cause of his high blood pressure? (1.5marks) b-Why did he collapsed after antihypertensive therapy? (1 mark) key15 A;a: increased intracranial pressure of CSF due to head injury-cushing reflex -increase in BP. (1.5 mark) b:Therapy decreased the BP ,decreased blood flow to brain tissues-brain ischemia-loss of consciousness. Q16 Bano with 28 weeks of pregnancy visited the Gynae outdoor for her antenatal routine examination She complained of headache and weakness. On examination her BP was 130/100 mmHg, there was odema of feet also. a-What she may be suffering from? (1 mark) b -Give the pathophysiology of this type of hypertension. key16 a- Pre-eclampsia (Toxemia of Pregnancy) (1 mark)

(1.5 mark)

b- toxic factors released from ischemic placenta-cause dysfunction of vascular endothelial cells throughout the body, including the blood vessels of the kidneys. This endothelial dysfunction decreases release of nitric oxide - causing vasoconstriction, decreased rate of fluid filtration from the glomeruli into the renal tubules, impaired renal pressure natriuresis, and development of hypertension. (1.5 mark) -----------------------------------------------------------------------------------------------------------Q17: What is normal capillary blood pressure and give the two methods to measure it. Explain the difference in values found by these two methods. (1+3+1marks) a.capillary pressure is 17 mm hg. b. two methods: key17 1. Micropipette method: A micropipette is thrust directly into the capillary and the pressure is measured using an appropriate micromanometer system 2. Isogravimetric method: (Functional method) Also called indirect method. It is measured by keeping the capillary pressure constant while simultaneously 1) decreasing the arterial pressure 2) increasing the venous pressure. Micropipette method= 25 mm Hg Isogravimetric method = 17 mm Hg

There are 2 reasons why the iso-gravimetric method gives less pressure than the micropipette method: There are far many capillaries nearer to the venules than the arterioles The venous capillaries are several times as permeable as the arterial capillaries. -----------------------------------------------------------------------------------------------------Q18: Define and draw an arterial pulse. What information can be gained from it. Mention one abnormal pulse? (2+2+1 marks) Key18 Propagated wave of expansion (due to compliance of arteries) due to pumping of blood into aorta travel through walls of arteries at speed of 3 to 5 m/sec; in the large arterial branches, 7 to 10 m/sec; and in the small arteries, 15 to 35 m/sec. (1 mark)

1-Rate and rhythm of heart, 2-volume of pulse tells about blood vol, and blood flow to the part, 3-speed of conduction of pulse and damping of pressure pulse tells about the compliance of blood vessel, 4-Character of the pulse ---heart and valvular condition, 5-condition of vessel wallabout loss of compliance and atherosclerosis in old age. 6-presence or absence of delay and Comparison the pulse with other side tells about coarctation of aorta and aortic aneurysm. (0.5 for each point = 2 marks for any 4 points) Pulsus Paradoxus. Increase in pressure during inspiration due to more negative intraplueral pressure present in: severe lung disease, constrictive pericarditis, cardiac temponade. (1 mark)

----------------------------------------------------------------------------------------------Q19: Name the vessels which constitute microcirculation? Which factors regulate local tissue blood flow? (1+4 marks)

Key19 Arteriole,metaarteriole, Precapillary sphincter,capillary,venules. (1 mark) Acute flow: 1-Vasodilator Theory for Acute Local Blood Flow Regulation Role of Adenosine, carbon dioxide, adenosine phosphate compounds, histamine, potassium ions, and hydrogen tons (1 mark) 2 Oxygen Lack Theory- other neutrients thiamine, niacin, and riboflavin: in their deficiency tissues become unable to take oxygen,decreased peripheral resistancevasodilatation (1.5 mark) 3. Autoregulation (0.25) 4 Vasodilatation by release of nitric oxide- Endothelium-Derived Relaxing Factor (0.25) Long term flow vascular endothelial growth factor (VEGF), fibroblast growth factor, and angiogenin: Chronic oxygen deficiency angiogenesis ------------------------------------------------------------------------------------------Q20:A:Name the organs with potent autoregulation of blood flow. Give the mechanisms . (1+2 marks) B:Compare the active and reactive hyperaemia. (3+2 marks) Key:20 A.8) there are two organs which are potent regulators 1 mark 1. kidney 2. brain Kidney : tubuloglomerular feedback composition of fluid in early distil tubule is sensed by epithelial structure of the distil tubule macula densa when too much fluid filters through the glomerulus into the tubular system macula densa causes constriction of afferent arterioles reducing renal blood flow and GFR to normal. 1 mark Brain: increase CO2 and H2 ion and decreased O2 concentration dilates the cerebral vessels and increase the blood flow to the brain for rapid washout of these gases. 1 mark

------------------------------------------------------------------------------------------------------Q.21 Ali Ahmed is a 58 year old man who is not only a chronic smoker but he is also over weight for his height. His B.P was 180/125 mm hg. Renal arteriogram showed 80 % occlusion of the left renal artery and his plasma renin activity was found to be increased. a.How did occlusion of his left renal artery lead to the increase in plasma renin activity and hypertension. b. Give three lethal complications of chronic hypertension. (2+3 marks) key:21 a- The occlusion of the left renal artery causes a decrease in the blood flow to the kidney which results in the secretion of rennin and retains salt and water. The normal right kidney than retains salt and water because of the renin secreted by the left kidney. This causes formation of aldosterone and angiotensin II both of which circulate and cause retention of salt and water. (1 marks) b- The lethal effects of chronic hypertension are. 1-Increased workload on heart as a result coronary heart disease this leads to heart failure & death 2-Increased BP damages the major blood vessels in the brain (stroke) causing death of the major portion of the brain ( cerebral infarct) . stroke leads to paralysis , dementia , blindness 3-High BP causes injury to kidney and many areas of destructionas a result renal failure , uremia and death (3 marks) -----------------------------------------------------------------------------------------------------------Q.22 Outline the special features of circulation of coronary vessels. (5 marks)

Key22 SPECIAL FEATURES: Blood flow through Rt.coronary artery is pre-dominant in 50% of humans. Blood flow through Lt.coronary artery is pre-dominant in 20% of humans. Blood flow through both coronaries is equal in 30% of humans. (0.5 mark) Coronary blood flow at rest is 225-250ml/min. It may increase 4-6 times during exercise. (0.5 mark) Myocardial O2 consumption at rest is about 8ml/100g/min. (0.5 mark)

coronary blood flow varies with phases of cardiac cycle. More than 70% coronary blood flow occurs during diastole During systole the blood flow decreases due to compression by cardiac muscle. (0.5 mark) Subendocardial vessels are compressed much more than epicardial vessels. So subendocardial portion of myocardium is more prone to ischemia. It is the most common site of M.I. (0.5 mark) Br.of Lt.coronary art. are compressed more in systole than branches of the Rt.coronary Blood flow through coronary sinus increases in systole. (0.5 mark) Collaterals are important in coronary circulation. In gradual narrowing of coronary artery, collaterals open up to compensate. (0.5 mark) Coronary blood flow is autoregulated according to O2 consumption & demand. When PO2 in myocardium fallshypoxia (due to increased consumption) (0.5 mark) Direct effect of sympathetic stimulation on coronary vessels: Coronary vasoconstriction. Indirect effect: (more important) Coronary vasodilation with more coronary blood flow. Symp. Stim. As a result More heart rate & contractility leads to More myocardial metabolism & O2 consumption leads to hypoxia vasodilator metabolites leads to Vasodilitation (0.5 mark) Direct effect of parasymp. Stim.: coronary vasodilation Indirect effect: coronary vasoconstriction with decreased coronary blood flow. Parasymp. Stim. leads to Decreased heart rate & Force of contraction as a result less myocardial metabolism & O2 consumption no hypoxia

no release of vasodilator metabolites as a result there is Vasoconstriction. (0.5 mark) ----------------------------------------------------------------------------------------------------Q.23 Give an account of circulatory changes that occur as a result of muscular exercise (5 marks) Key23

1) INCREASE IN SKELETAL MUSCLE BLOOD FLOW: At rest 3-4 ml/100g/min. During severe Ex. 20x (i-e, 50-100ml/100g/min). This is due to: a) B.P b) opening of dormant capillaries c) stimulation Of symp. Vasodilator fibers at onset of Exercise. d) Local metabolic factors is very imp in sk.muscle.Blood flow. In tissue hypoxiathere is release of Vasodilatirs: Adenosine,H+, K+, PGs, Bradykinin, ADP, ATP, Lactic acid, Pyruvic acid, temp, Ca++. All these factors are present in physical activity thus blood flow is increased. (0.5 mark) 2) EFFECT ON THE HEART: Due to SYMP.stimul. & PARASYMP inhibition there is TACHYCARDIA (H.Rate:180-200/min). Stroke vol. & thus C.O (4-6X) V.R (due to thoracoabd. & sk.mus. pump), there is venoconstriction as a result E.D.V& E.S.V (due to forceful vent. Contraction) M.S.F.Pr (0.5 mark) 3) EFFECT ON CIRCULATION: due to contraction of Liver & Splenic capsule, additional amount of blood enter into general circulation. All the blood vessel show Vasoconstricton Except Cerebral, Coronary & in the active Skeletal Muscles. (0.5 mark) 4) CUTANEOUS BLOOD SUPPLY: In the beginning of Exercise there is Cutaneous V.C. As Ex. Progresses, more heat production leading to Sweatingas a result Cutaneous V.D.(to facilitate heat loss from the body). (0.5 mark) 5) CEREBRAL BLOOD VESSELS: They remain dilated. Cerebral blood flow is UNCHANGED (0.25 mark) 6) CORONARY BLOOD FLOW:

There is Coronary V.D. Coronary blood flow 4-6x (0.25 mark) 7) SPLANCHNIC BLOOD FLOW & 8) RENAL BLOOD FLOW: There is Splanchnic & Renal V.C . Because of this about 2.5L Blood is directed towards active muscle as a result Active Skeletal Muscle V.D. (0.5 mark) EFFECT OF Ex. ON B.P: B.P varies due to: a) Severity of Ex b) Type of Ex c) Mental state of person performing Ex. A) Severity of Exercise: ( Mild, Moderate, Severe.) Mild Ex: BOTH SYSTOLIC & DIASTOLIC B.P Mod Ex: BOTH Severe : SYSTOLIC B.P BUT DIASTOLIC Due to accumulation of metabolites in sk.mus. V.D (0.5 mark) B) TYPE OF Ex:(Isotonic or Isometric) ISOTONIC Ex: Swimming, running etc. In these Exs: less in B.P because many groups of muscles are active. In these groups there is V.D. So TPR does not much Tachycardia. Systolic B.P BUT not that much ISOMETRIC Ex: (wt. lifting & body building) In this a few groups of muscles are active. In these few groups there is V.D, but V.C in remaining ones. There is marked in TPR this leads to B.P Conclusion: The wt. lifters have high B.P. (0.5 mark) Mental State of person performing Ex: - No mental tension + Exl: B.P - Mental tension + Ex:B.P e.g of hammering a nail while standing on the ground VS doing so while standing on ladder. (0.5 mark) ----------------------------------------------------------------------------------------------------Q.24 Briefly discuss the factors which alter the peripheral resistance? (5 marks) Key24

1. Vessel Diameter: Varies inversely with resistance. A 4 time increase in vessel diameter can increase the flow as much as 256 folds.

2. Total resistance to blood flow = sum of resistance of arteries, arterioles, capillaries, venules and veins (connected in series). 3. For blood vessels connected in parallel: 1/R Total = 1/R1 + 1/R2 + 1.R3 . Fig. 14-10, Guyton, 11th ed. 4. Pressure difference between ends of the vessel (delta P): Resistance is inversely proportional to pressure difference. 5. Viscosity of blood: Directly proportional. 6. Length of vessel: Directly proportional. 7. Hematocrit: Directly proportional. It also increases blood viscosity. Fig. 14-12 & Fig. 14-13, Guyton. 8. Arterial pressure: Inversely proportional to resistance, directly proportional to flow. 9. Sympathetic stimulation: leads to vasoconstriction as a result increase resistance 10. Conductance: Resistance = 1/ conductance (0.5 mark for each point)

----------------------------------------------------------------------------------------------------------Q.25 A 32 years old lady, Safia was brought semiconscious to the emergency of hospital with a history of induced abortion by a nurse at home. On examination her body temperature was 102 F, pulse was very rapid and feeble and BP was 60/50mmHg. a. What is the most likely diagnosis? b. Briefly mention the special features of her disease. (1+4 marks) key:25 a. Septic shock b. 1. High fever 2. Marked Vasodilitation in infected tissues. (1 mark) (1 mark) (1 mark)

3. May be high Cardiac output due to arteriolar dilation in infected tissues & by high metabolic rate and V.D elsewhere in the body due to bacterial toxin stimulation of cellular metabolism & from high body temperature. (0.5 mark) 4. Sludging of blood due to red cell agglutination in response to degenerating tissues. (0.5 mark) 5. Micro-blood clot development in widespread areas of body (DIC) clotting factors are used up multiple tissue hemmorhages, mainly in GIT. (1 mark)

-------------------------------------------------------------------------------------------------------Q.26 A 35 years old lady, Naziran Bibi came to the Gynae Outdoor with the history of menorrhagia (excessive bleeding during each menstrual cycle) since last 2 years.

Her blood pressure was 120/90mmHg. Give the mechanism by which her blood pressure was maintained at this level without any treatment.. (5 marks) Key:26 LONG TERM REGULATION OF B.P: 0.5 mark for each flow diagram

CONSTANTLY PRODUCES LIVER

ANGIOTENSINOGEN IN PLASMA

J.G CELLS OF KIDNEY B.P PRODUCE ANGIOTENSIN 1 DECAPEPTIDE IN PLASMA CONTAIN ANGIOTENSIN-CONVERTING ENZYME (A.C.E) ANGIOTENSIN 2 OCTAPEPTIDE IN PLASMA CIRCULATES IN BLOOD FOR FEW MIN. THEN DESTROYED BY ANGIOTENSINASE IN R.B.Cs etc RENIN

ENDOTHELIAL CELLS OF LUNG CAPILLARIES

OR: Same discussed in text.

 VASO-PRESSIN/ADH Mechanism: Her B.P as a result release of ADH from hypothalamo-neuro-hypophyseal system. ADH (synthesized. in hypoth) then (transported to) Post.pituitary then ADH release . ADH has 2 actions 1) V.C/VASOPRESSIN IN SHORT-TERM REGULATION & 2) ANTIDIURETIC HORMONE REABSORBS WATER FROM D.C.T FOR LONG- TERM 1 mark Renal Body Fluid Pr Control Mechanism: Her B.P as a result Renal blood flow so Glomerular pressure this leads to GFR as a result Salt & water lost in urine this leads to blood vol, V.Return Cardiac output B.P to normal. 1 mark

4 FACTORS ASSISTING RENAL BODY FLUID Pr CONTROL MECHANISM: 1) SYMP. IMPULSES TO KIDNEY. 2) RENIN ANGIOTENSIN MECH. 3) ADH MECHANISM. 4) ALDOSTERONE. 1 mark In this patient due to blood loss there is decrease in blood volume as a result decrease blood pressure SYMP. Impulses to kidney RENIN ADH ALDOSTERONE Net effect: Retention of salt & water. 1 mark Q.27 a. Define Ejection Fraction, Vascular compliance and Central Venous Pulse. b. A 10 year old boy was brought to medical outdoor with complaint of weakness, easy fatigue ability and chest pain. There is also a history of repeated sore throat. On examination he had water hammer pulse and on auscultation a blowing diastolic murmur was heard over left ventricle. 1. What is the most likely diagnosis? 2. Give the sequence of events causing this disease. (3+2 marks) key:27 a) EJECTION FRACTION: is the fraction of EDV that is ejected out by each ventricle. Normally it is 60-65%. 1 mark

 Vascular compliance is increase in volume per unit increase in pressure of blood vessel. 1 mark CVP: It is the Jugular venous pulse or the pressure changes in the right atrium. 1 mark b 1. Aortic Regurgitation. 1 mark 2. Bacterial infection sore throat antibodies formed damage aortic valve Scar formation valve cannot close aortic regurgitation. 1 mark

---------------------------------------------------------------------------------------Q.28 Define Edema and give its types. Key28 (2+3 marks)

Edema: Refers to presence of excess fluid in body tissues.

2 mark

Types: 1) Extracellular edema: Due to abnormal leakage of fluid from plasma to interstitial spaces across capillaries Due to failure of lymphatics to return fluid from interstitium back into blood 1.5 mark 2) Intracellular edema: Due to depression of metabolic system Due to lack of adequate nutrition. 1.5 mark

--------------------------------------------------------------------------------------------------------Q.29 A 23 year old boy Ali was brought to the emergency of Avicenna Hospital with the complaint of chest pain. On examination his pulse was found to be week in volume during inspiration but strong during expiration. a. Name this abnormal type of pulse. b. What possible cardiac / pulmonary disease may be responsible for it. c. Give the baseline mechanism for this finding. (1+1+3 marks) Key29 a. Pulsus paradoxus 1 mark b. Acute severe asthma / Cardiac temponade / Constrictive pericarditus / pericardial effusion 1 mark

c. Suction of right atrium decreases due to fluid collection venous return decreases less blood returns to rt. Heart less Cardiac output Histamine release in asthma this leads to vasodilitation as a result less venous return During inspiration, more negative intra thoracic pressure as a result more blood retained in lung vessels less returns to heart as a result week pulse in inspiration due to less C.O in inspiration further enhanced by disease. 3 marks