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CARDIOVASCULAR VIVAS2011-1What factors are thought to contribute to essential hypertension90-95% of cases of hypertension are idiopathic (essential hypertension)Cumulative effects of non-genetic environmental factors and genetic polymorphismsSodium homeostasis is a key element: primarily through increased reabsorption at the distal tubule (largely influenced by the renin-angiotensin system which regulates aldosterone)Thus factors are listed as:Genetic factors (multi-gene foci affecting Na+ resorption or the rennin-AT system, rarely single gene disorders)Reduced renal sodium excretion may be a key initialing event/final common pathway-> increased fluid, increased cardiac output, vasoconstiction, “resetting of pressure natriuresis”Vasoconstrictive influences e.g. vasoconstriction or vessel wall thickening. Role in 1 HTN also.Environmental factors: stress, smoking, obesity, inactivity, heavy salt intakeWhat are the long term consequences of essential hypertensionMajor risk factor for development of atherosclerosis leading to:Coronary artery diseaseCerebrovascular diseaseAortic dissectionRenal failureCardiac hypertrophyCardiac failureMulti infarct dementiaRetinal changesDescribe the clinical features of malignant hypertensionClinical syndrome characterised by:Severe hypertension with SBP > 200, DBP > 120Renal failureRetinal haemorrhage’sAlso may have:encephalopathyCVS abnormalitiespapilloedema Additional:Often superimposed on previous benign hypertension < 5% of hypertensive patients Rapidly rising BPUntreated -> death in 1-2 years2011-1What is the most frequent cause of subarachnoid haemorrhageRupture of a berry (saccular) aneurysm – occur in 2% of populationLess common causes include: traumatic haematoma, vascular malformations, hypertensive intracerebral bleed, tumors and haematologic disturbanceWhere are saccular aneurysms commonly located90% occur in the anterior circulation near major arterial branch points along the circle of Willis or a major vessel just beyond (= anterior cerebral circulation)40% anterior communicating artery 34% middle cerebral artery20% internal carotid/PICA4% Basilar/Posterior CerebralWhat are the genetic risk factors for saccular aneurysmsGenerally unknown, may result from congenital defects, under reasearchSome genetic risk: Polycystic kidney, collagen disorders (Ehlers Danlos type 4), Neurofibromatosis type 1, Marfan’s, Fibromuscular dysplasia, Aortic coarctationWhat are the pathological consequences of subarachnoid haemorrhageEarly: vasospasm and additional ischemic injury -> increased intracranial pressureLate: meningeal fibrosis & scarring -> CSF obstructionAdditional: rupture risk increases w/ size, >10mm = 50% annual bleed risk25-50% die with the first bleed2010-2Describe the pathogenesis of an aneurysmStructure or function of the vascular wall connective tissue is compromised:Poor intrinsic quality of the vascular wall connective tissue e.g. Marfan syndrome, Ehlers-Danlos, Scurvy (ineffective collagen cross-linking)Collagen degradation vs. synthesis by local inflammation (proteolytic enzymes = MMP) e.g. atherosclerotic plaque, vasculitisLoss of vascular smooth muscle cells or the inappropriate synthesis of non-collagenous or non-elastic ECM (cystic medial degeneration): caused by ischaemia to innermost aspect of the media (atherosclerosis), or mid-medial region when vasa-vasorum is stenosed from HTN or inflammationWhat are the clinical consequences of an AAARupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially fatal haemorrhageObstruction of a branch vessel resulting in ischemic injury, eg. iliac, renal, mesenteric, or vertebral arteriesEmbolism from atheroma or mural thrombusImpingement on an adjacent structure, e.g. ureter, vertebraeNothingWhat is the risk of rupture of an AAARelated to size:<4cm nil 4-5 cm 1% per year5-6 cm 11% per year>6 cm in diameter 25% per year2010-1Describe the pathogenesis of an aortic dissectionMedial degeneration (cystic medial degeneration)What initiates the initmal tear is unvclerOnce torn, systemic blood pressure advances the dissection planeCan have rupture of the vasa-vasorum -> intramural haematoma (without intimal tear)How are aortic dissections classifiedType A: Ascending aorta, most common, most dangerousType B: Distal (usually to the subclavian artery)Also: Type I – ascending/descending, Type II ascending only, Type III descending onlyWhat are the potential complications of the diseaseRupture (to pericardium, thorax or abdomen) – high mortalityPericardial compression/tamponadeCoronary artery occlusion -> MIOcclusion/extension into other arteriesRe-entry into lumen-> double barreled aorta (chronic)Additional: early recognition, anti-hypertensive therapy and surgery -> 65 – 75% survival2009-1What are the characteristics of hypertrophic cardiomyopathyMyocardial hypertrophy without ventricular dilationAsymmetrical septal thickening (septum much larger than the free wall)Reduced stroke volume: impaired diastolic filling and LV outflow obstruction in 25% of casesWhat are the complications of HCMHeart failureSudden death (ventricular arrhythmias) – most common cause of SCD in young athletesAF, mural thrombus, emboliStrokeMitral valve SBE2008-2What are the causes of Aortic valve stenosisSenile calcific Ao Stenosis (common, 2% of population, usually after 70years, earlier if bicuspid valve 1% of population)Calcification of congenitally deformed valvePost-inflammatory scarring (Rheumatic fever) What is calcific aortic stenosisAo Stenosis most common valvular abnormality Wear and tear -> calcification on normal or cong bicuspid valves Clinical attention in 6-7th decade in bicusid valves, 8-9th decade in prev. normal valvesNote: Wear and tear usually cited as cause for calcific aortic stenosis, but newer data suggests chronic injury due to hypertension, hyperlipidaemia and inflammationHeaped up calcified masses within cusps -> protrude through to outflow tracts. Functional valve area decreased.What are the consequences of calcific aortic stenosis1. LV outflow obstruction -> increased pressure gradient over valve. (severe when valve area 0.5-1cm2) CO maintained by concentric LVH. Hypertrophied myocardium more contractile, but less compliant (reduced EDV) and ischaemic. Impaired systolic and diastolic function.Decompensation -> angina, CCF, syncope, SCD. If untreated mortality is 50% 2-5 years2008-2What are the causes of acute pericarditis?Infectious; viral, pyogenic bacteria Immune mediated(presumed); Rheumatic fever, SLE, Scleroderma, post cardiotomy. Post MI (Dressler’’s), Drug hypersensitivity reaction. Other; AMI, uraemia, post cardiac surgery, neoplastic, trauma, radiationWhat types of pericardial fluid exudate occur?1. Serous; usually non-infectious inflammation, RF, SLE, uraemia, tumours 2. Fibrinous/serofibrinous; (most common) post MI, Dressler’’s, trauma, post surgery but also as in 1.3. Purulent/suppurative; almost always bacterial invasion from local infection, lymphatic or blood seeding, or at operation 4. Haemorrhagic 5. CaseousDescribe the clinical features of pericarditisPericardial rub (may be absent if large effusion). Pain, fever (chills and rigors if suppurative), signs of cardiac failure,2008-2Outline the steps involved in the pathogenesis of atherosclerosis.Response to injury hypothesis:1. Endothelial injury and dysfunction2. Lipoprotein (mainly LDL) accumulation and oxidation in vessel wall3. Monocyte adhesion and migration into intima and transformation into foam cells and macrophages 4. Platelet adhesion 5. Smooth muscle cell migration from media into intima6. Subsequent smooth muscle cell proliferation in intima7. Enhanced lipid accumulation within intimal cells (macrophages and smooth muscle cells)List the potential causes of endothelial injury?Hyperlipidaemia, 2. Hypertension, 3. Smoking 4. Haemodynamic factors (disturbed flow patterns) 5. Homocysteine, 6. Toxins, 7. Viruses, 8. Immune reactions2007-2What is the sequence of events in acute coronary artery occlusionAtheromatous plaque rupture/erosionPlatelet adhesion, activation and aggregation -> release of aggregators (thomboxane, serotonin, platelet factors)VasospasmInstrinsic coagulation cascade activationThrombus evolves to occlude arteryDescribe the time course of myocardial injury after coronary occlusionATP depletion – secondsLoss of contractility – 2minATP reduction – 10-40minsIrreverible cell injury 20-40minsMyonecrosis after 30minsMicrovascular injury at 1 hourExtensive necosis needs 2-4 hours of ischaemia (blood flow <10%)Anaerobic metabolism begins immediately, cell death occurs after 30mins or so, extensive necrosis occurs after 2 hours2007-2What is the morphology of a berry aneurysmMedial muscular layer thins as approaches neck…What are thre common sites of beryy (saccular) aneurysmsWhat is the natural history of a ruptured berry aneurysm2007-1What is the most frequent cause of clinically significant subarachnoid haemorrhage?Rupture of a saccular (berry) aneurysmWhere are saccular aneurysms commonly located?40% ant comm art34% middle cerebral art20% int carotid/PICA4% Basilar/Posterior Cerebral (most likely to cause problems with vasospasm)What is the aetiology of saccular aneurysms?Generally unknownNot ‘congenital’,Some genetic risk (Polycystic kidney, Ehlers Danlos type 4, Neurofibromatosis type 1, Marfans),Predisposing factors (Smoking, Hypertension)What are the consequences of subarachnoid haemorrhage?Early (Vasospasm and additional ischemic injury)Later (Meningeal fibrosis & scarring, CSF obstruction)2007-11. List the major risk factors for aortic dissection.2.Describe the morphological features of aortic dissection3.What are the consequences of aortic dissection?1. Hypertension 2. Connective tissue diseases eg. Marfan Syndrome, 3. Iatrogenic: coronary artery catheterisation, Coronary artery by pass. 4. Pregnancy 1. Most frequent pre-existing = medial degeneration of elastic tissue 2. Intimal tear aorta extends into the media. 3. Haematoma spread between the middle and outer thirds along the laminar planes of the media and formed a blood filled channel. 4. Disrupts outward causing massive haemorrhage or re-rupture into the lumen of the aorta producing a false lumen.1. Dissects proximally towards the aortic valve and vessels of the neck and causes disruption of the aortic valve, cardiac tamponade, myocardial infarction, cerebral vascular accident. 2. Dissects distally into the renal, mesenteric, iliac & femoral arteries causing ischaemia.3. Compression of the spinal vessels causing transverse myelitis.2004-2What is aortic dissection?PROMPTSCOMMENTSPOINTS REQUIREDAortic dissection is the dissection of blood along the laminar planes of the aortic media, with the formation of a blood filled channel within the aortic wall, which often ruptures, causing massive haemorrhage.There is usually an intimal tear that extends into but not through the media of the ascending aorta, usually within 10 cm of the aortic valve. The dissection can extend proximally into the heart, as well as distally along the aorta into the iliac and femoral arteries. Sometime, the blood re-ruptures into the lumen of the aorta, producing a second intimal tear.There is usually no marked dilatation of the aorta. The dissection does not affect the aorta that is affected by substantial atherosclerosis.Adequate definitionto passSECOND QUESTION (if needed)What are the predisposing factors for aortic dissection?Need 1 to passPOINTS REQUIREDHypertension Connective tissue diseases (eg: Marfan) IatrogenicTHIRD QUESTIONWhat are the complications of aortic dissection?Need 3 specifics to passDeath-rupture 3 body cavities Extension/Obstruction-Carotid, renal, mesenteric arteriesRetrograde to aortic valvular apparatus (root)-Cardiac tamponade -Aortic insufficiency -Coronary ostia (AMI) -Spinal arteries2004-2What are the morphological features of an abdominal aortic aneurysm?PROMPTSCOMMENTSPOINTS REQUIREDAn aneurysm is a localised dilatation of the abdominal aorta. It is usually between the renal arterial and the bifurcation of the aorta into iliac vessels. The aneurysm often contains atheromatous ulcers covered with mural thrombi, with thinning and destruction of the media.SECOND QUESTION (if needed)List the common causes of abdominal aortic aneurysmPOINTS REQUIRED- Atherosclerosis-Congenital (cystic medial degeneration)- Mycotic - Syphilis - Trauma - Immunological - (Salmonella)Need 2 causes to passTHIRD QUESTIONWhat are the complications of an abdominal aortic aneurysm?Need 3 to pass- Rupture-Occlusion of branch – iliac, mesenteric, vert.-Embolism of atheroma/thrombi-Impingement adj. Structure (ureter, erosion vert.)-Presentation abdominal mass-Rupture Risk (2% <4cm) (5- 10% each year >5cm)-Operative mortality (unruptured 5%) (ruptured >50%)2004-2What are the causes of calcific aortic stenosis?PROMPTSCOMMENTSPOINTS REQUIRED-Senile calcific aortic stenosis -Calcification of congenitallydeformed valveNeed 1 to passSECOND QUESTION (if needed)What are the complications of aortic stenosis?Need 2 to passPOINTS REQUIREDIncreasing obstruction to left ventricular outflowCardiac output maintained (left ventricular hypertrophy)Angina (? ↓ microcirculatory myocardium) Syncope (? Poorly understood)Cardiac decompensation – congestive failure2003-2What are the causes of pericarditis?What pathological types of pericarditis can occur?Infectious, Inflammatory, Malignant., example of each.Non-infectious inflammations (Rhfever, SLE, uremia), viral; fibrinous reaction occurs with these, plus AMI, post AMI; pus from adjacent invasion, haem spread, lymphatic spread, surgical introduction; blood from TB, malignant spread, bacteria, post-surgery; caseous is TB.Serous; fibrinous/serofibrinous; purulent (suppurative); haemorrhagic; caseous2003-2Describe the pathological changes in myocardium following occlusion of a coronary artery.What are the potential consequences of reperfusion?Loss of contractility (<2mins); loss of ATP (50%at10min,10%at40min); irreversible cell injury (20-40min);microvascular injury (>1hour); coagulative necrosis.Minutes: myofibrillar relaxation, glycogen depletion, mitochondrial and cell swelling. 40minutes: sarcolemmal disruption, mitochondrial amorphous densities. Necrosis first in subendocardium, endocardium is spared. 4-12hour coag necrosis, edema, hemorrhage.Early: no damage. Later: reperfusion hemorrhage; acceleration of disintegration of damaged myocytes; exaggerated contraction of myofibrils; some new injury from oxygen free radicals. ‘Prolonged post-ischaemic ventricular dysfunction’.2003-1What are the criteria for systemic hypertensive heart diseaseCOMMENTSPOINTS REQUIRED1 Left Ventricular Hypertrophy2 Absence of another cause3 Systemic HypertensionWhat are the gross morphology findings in hypertensive heart diseasePOINTS REQUIRED1 Thick L ventricular wall3 of 42 No dilation3 L atrial enlargement4 Increased weight of heartWhat are the pathological consequencesPOINTS REQUIRED1 Stiffness2 Impaired diastolic filling3 Atrial dilation/fibrillation4 Heart failure5 Sudden Cardiac Death2003-1Draw a typical atheromatous plaqueCOMMENTSPOINTS REQUIRED1 Endothelium4 of 62 Fibrous Cap3 Necrotic Centre4 Foam Cells5 Cholesterol crystals6 CalciumWhat are the pathological consequencesPOINTS REQUIRED1 Weakening wall -Rupture of Vessel, aneurysm3 of 52 Gradual Occlusion – Ischaemia3 Disruption – Acute Occlusion4 Embolisation – Distal occlusion5 Calcification6PROMPTSPrompt for process and consequenceWhich arteries are commonly affectedPOINTS REQUIRED1 Large elastic - aorta2 Medium sized muscular3 Lower Limbs more than Upper4 Coronary5 Circle of Willis6 Carotids ................
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