Sc02 Caroline’s Hypertension


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Sc02 Caroline’s Hypertension

  1. 1. Carolineʼs HypertensionThe Cardiac Cycle1. Draw out a diagram of pressure differences and events during the cardiac cycle includethe following: Mitral valve closes, aortic valve opens, aortic valve closes, mitral valveopens, aortic, ventricular and atrial pressures12. Where is the mitral valve and the tricuspid valve?23. What does JVP stand for?34. What to the P, QRS and T waves stand for on a normal ECG?45. What are the approximate lengths of normal P-R, QRS and Q-T sections?56. What do S1 (loudest), S2 (loud), S3 (quiet) and S4 (rarely heard except when EDPraised) heart sounds correspond to?67. A diastolic murmur could indicate stenosis (narrowing) of which valve?712 Mitral = left atrio-ventricular, tricuspid = right atrio-ventricular3 Jugular venous pressure4 P = atrial depolarisation, QRS = ventricular depolarisation, T = ventricular repolarisation (inverted becauseheart repolarises in opposite direction)5 P-R = 120ms, QRS = 80ms, Q-T = 300ms6 S1 = Initiation of ventricular systole, S2 = closure of semilunar valve and start of atrial filling, S3 = Openingof AV valve and rapid filling of ventricle, S4 = atrial systole (heard only in7 Either atrioventricular (mitral/left or tricuspid/right) because the ventricle is filling during diastole and theatrioventricular valve open and blood is rushing through it.
  2. 2. Regulation of Vascular Smooth Muscle Cells1. Describe the 4 structural layers within a typical muscular artery82. Of these features, which are also found in veins?93. By what mechanisms do (i) noradrenaline (ii) angiotensin II and (iii) nitric oxide, reachblood vessel SM?104. List 5 substances which directly cause vasoconstriction115. What is endothelin?126. What is vasopressin?137. What is bradykinin?148. List 5 substances which directly cause vasodilation159. List the differences between smooth muscle and striated (skeletal) muscle1610.In smooth muscle, what causes myosin to phosphorylate (and so induce contraction)?1711.What causes membrane depolarisation (and so induces contraction) in a smoothmuscle cell?188 Starting on the inside: 1/ endothelium, 2/ Tunica Intima (containing internal elastic lamina), 3/ Tunica media(containing SM cells connected by gap junctions), 4/Outermost lies the tunica adventitia which containsblood vessels, nerves and fibroblasts)9 Thin tunica media with sparse smooth muscle (more likely to dilate with sympathetic contraction), not asable to constrict as arteries. Well supplied with sympathetic nerves for this reason.10 Sympathetic nerves release noradrenaline, angiotensin II and nitric oxide are blood borne, nitric oxide canalso be released as a metabolite or local hormone.11 Noradrenaline, Histamine, Endothelin, Leukotrines, Adrenaline, Angiotensin II, Vasopressin12 Endothelin, produced in the lungs, is the most potent vasoconstrictor known in the body and works inantagonism with nitric oxide.13 Vasopressin is just another name for ADH, ADH causes water reabsorbtion in the collecting duct andconstricts arteries and veins to compensate for low blood volume14 Bradykinin is normally inhibited by ACE, it causes vessels to dilate, works on vessels via release of EDHFor nitric oxide15 Adenosine, bradykinin, prostaglandins (PGE2 or 1), Leukotrienes, histamine, nitric oxide, adrenaline16 SM is not under conscious control, it is slower to move and does not tire with prolonged contraction17 Myosin light chain kinase reacting with calmodulin, and increased Ca2+ (released from SR). The reverseis stimulated by phosphorylated myosin being affected by actin and starting the cross-bridge cycle18 Na+ and Ca2+ influx via a G-protein coupled receptor gated ion channel. Once the ion concentration goesabove a certain level, Ca2+ voltage gated channels open, Ca2+ floods in and adds to depolarisation.
  3. 3. 12. What is the other name for Endothelium Derived Hyperpolarising Factor (EDHF)1913.Which second messenger does Nitric Oxide activate leading to relaxation (vasodilation)in vascular SM cells?2014.What do reactive oxygen species do to NO mediated vasodilation?2115.Which 3 organs in particular are protected by myogenic response (contraction/stabilizing of arteries in response to increase in internal pressure.2216.What is hyperaemia and what might cause it?23Regulation of the Vascular System1. What is cardiac output in L/min at rest compared to during intense exercise?242. What is the name of the effector arm of the ANS which aims to direct blood to where it isneeded by constriction or dilation?253. What does stimulation of B1, A1 and B2 receptors do?264. Which receptors does adrenaline affect?275. Which receptors does noradrenaline affect286. Where (anatomically) is ACE produced and kept?297. What are the two functions of ADH (vasopressin)?3019 Nitric Oxide20 Cyclic GMP, pretty much the same effect as Cyclic AMP. Cyclic GMP opens K+ channels in the cellmembrane meaning the cell hyperpolarises and relaxes because Ca2+ leaves the cell.21 React with nitric oxide to prevent it from mediating vasodilation, so oxidative stress therefore tends tointerfere with the ability of blood vessels to dilate22 Kidney, brain and heart23 Hyperaemia is increased blood flow to the tissues, it might be brought on my a metabolic cause (i.e.increased metabolism during exercise) or a reactive cause (if local blood flow is cut off, metabolites build upand cause vasodilation).24 6L/min at rest, 24L/min during exercise25 The baroreceptor reflex26 B1 = increased HR and contractility, A1 = vasoconstriction, B2 = bronchodilation, vasoconstriction in skinand diversion of blood from skin and viscera to skeletal muscle27 B1, B2 and A128 Only A1 and B1 (so does not cause vasodilatation in skin)29 On the surface of endothelial cells, which is why so much of it is found in the lungs (because they have alot of endothelium)30 Water reabsorbtion in the collecting duct, vasoconstriction more generally
  4. 4. 8. The high capillary flow to the brain allows it to have how many times more blood thanthe average tissue elsewhere in the body?319. Which tissue comprises the largest vascular bed, making the largest contribution toTPR?32Short and Long Term Control of Blood Pressure1. How is MAP calculated?332. What does the diastolic pressure tell you about the circulation?343. What should MAP be in (i) Head, (ii) Thorax and (iii) Feet354. Which nerves innervate the baroreceptors and where are they?365. Describe what happens to cause syncope (fainting) in terms of baroreceptorresponses.376. What is pressure natriuresis with reference to control of blood volume?387. Atrial stretch receptors detect a rise in blood volume and secrete ANP, what is this andwhat does it do?39Treatment of Hypertension1. Define hypertension402. What proportion of the UK population are affected by hypertension, and what % of theover 50ʼs population?4131 Circle of Willis and high cerebral capillary density provide the brain with 10x more blood than the averagetissue32 Muscle33 Diastolic pressure + ((systolic - diastolic)/3)34 The diastolic pressure reflects total peripheral resistance35 Head = 60mmHg, Thorax = 90mmHg, Feet = 180mmHg36 Baroreceptors are located in aortic arch --> aortic nerve --> X cranial nerve/vagus nerve, carotid sinus -->carotid sinus nerve --> glossopharyngeal nerve37 Fright response --> sympathetic stimulation --> baroreceptors detect high BP and CO and so stimulateoverwhelming parasympathetic response, BP and CO fall, inadequate blood supply and fall over.38 Increased pressure in renal artery leads to increased excretion of Na+ and water39 ANP = Atrial naturetic peptide, causes decreased reabsorbtion of sodium and water40 Where systolic and/or diastolic blood pressure exceeds 140/90, such that it increases the risk of CVD41 25% of general population, 50% of population over 50
  5. 5. 3. What is the difference between ʻprimaryʼ and ʻsecondaryʼ hypertension?424. Identify 3 main theories for the cause of hypertension435. What is vascular remodeling in relation to hypertension?446. What is ischemia?457. Give an example of a thiazide type diuretic468. What is the mechanism of thiazide type diuretics479. What is a major adverse affect of thiazide type diuretics?4810.Name the type (e.g. non-selective/selective) of each of the following beta adrenergicreceptor blockers: pindolol, atenolol, carvedilol, propanolol4911.What is the result of stimulation of each of the following receptors: A1, A2, B1, B25012.What kind of B adrenergic receptor blockers should not be used on asthmatic patients& why?5113.Describe the effect of ACE inhibitors on RAS5242 Primary hypertension is 90% of total and is where there is no obvious cause, secondary hypertension(10%) is where an identified cause can be determined, e.g. renal or endocrine43 Overactive RAS, Overactive SNS, Kidney is damaged and canʼt excrete Na+ properly44 Thickening of arterial wall due to sustained hypertension, increasing TPR45 Restriction of blood supply to a particular tissue (e.g. cardiac)46 chlorthalidone or indapamide47 Block sodium transporters in the kidneys, reducing Na+ reabsorbtion and so water reabsorbtion48 Hypokalaemia (low plasma K+), Increased plasma cholesterol49 pindolol = partial agonist (blocks B1 but stimulates B2), atenolol = B1 selective blocker, carvedilol = B1and A1 blocker, propanolol = non-selective B-blocker50 A1 = Constricts veins and coronary arteries, constricts vascular SM in skin, increases CVP and hence COA2 = Constricts both arteries and veins, increases TPR and reduces noradrenalineB1 = Increases CO by increasing contractility and HRB2 = Dilates SM in arteries to skeletal muscle, relaxes bronchial SM (bronchodilation)51 Non-selective blocker like propanolol, because it blocks B2 receptors causing bronchoconstriction(Salbutamol is a B2 agonist)52 Blocking ACE prevents the synthesis of angiotensin II (a vasoconstrictor) from angiotensin, which alsoprevents the release of aldosterone (which increases reabsorbtion). So the effect of ACE inhibitors is toreduce TPR and reduce blood volume.
  6. 6. 14.What effect does a K+ channel agonist have on vascular tone and why?5315.What type of drug is enalapril?5416.What is bradykinin and what effect does ACE have on it?5517.Which (afferent or efferent) arteriole does angiotensin constrict most in order toincrease Na+ reabsorbtion?5618.What are the new group of drugs which are similar to ACE inhibitors but do not causethe cough because they do not increase bradykinin levels?5719.What is the first line of treatment for a hypertensive individual >55 years old?5820.What is the first line of treatment for a hypertensive individual <55 years old?5921.What are the negative side effects of calcium channel antagonists?6022.What is the physiological effect of a1 adrenergic receptor blockers?6123. What kind of patientʼs would you use methyldopa on?6253 K+ agonist would promote hyperpolarisation and so would reduce vasoconstriction and therefore TPR54 ACE (Angiotensin converting enzyme) inhibitor55 Bradykinin is a vasodilator (which also causes coughing) which is broken down by ACE. So ACE inhibitorsincrease bradykinin levels.56 Increases GFR because efferent arteriole is constricted. Therefore greater rate of reabsorbtion of NA+ andH20 overall due to higher pressure in nephron. Other ions are lost in greater volume which can result inhypokalaemia.57 Angiotensin receptor blockers e.g. losartan58 Calcium channel blocker, then combined with an ACE Inhibitor or Ang II antagonist (failing that all 3)59 Initially an ACE inhibitor or Ang II antagonist and then add a calcium channel blocker (failing that all 3)60 Because of their effect on muscle contraction, they can cause bradycardia and negative inotropy61 A1 receptors are responsible for constriction of veins and coronary arteries, so blocking them reduces riskof CVD and also reduces CO by reducing CVP.62 pregnant women suffering from hypertension, because it is a false transmitter it cannot cross placenta