Pathology Exam 3

Chapter 13

Chapter 13 Diseases of the Cardiovascular System Congenital Cardiovascular Diseases Cause: temporary arrest or aberration of embryonic development (esp. during weeks 5-8) Most treated by surgery See table Arteriosclerosis Features o Hardening & thickening of artery walls o Atherosclerosis arteriosclerosis w/out qualification; fatty intimal plaques (atheromas) o Most frequent single cause of death in US Pathologic Anatomy o Develops over decades o Larger arteries esp. aorta, coronary aa., carotid aa., cerebral aa., iliac aa., & larger aa. of lower extremities o Artery appearance: dilated externally, slightly elongated/tortuous; narrow lumen due to thick intimal plaques (round, irregular) Plaque = superficial luminal layer (hard, pearly-gray fibrous tissue - often brittle, calcified) + deeper layer (soft, mushy orange yellow lipid (atheroma) w/ cholesterol crystals) Collagen made by smooth muscle cells (migrated into intima) Arterial intima thickened, fibrotic Causes o Common end result of a combination/variety of injuries of the arterial wall o Aging Hypertension Causative Factors: Mechanisms Senescent medial weakening: Gradual degeneration/stretching of arterial media & loss of elasticity s mechanical stress on arteries s senescent medial weakening Results Arterial dilatation (general & local) Compensatory intimal fibrosis Pulmonary hypertension ateriosclerosis of lower pressure pulmonary arteries

frequency & severity w/ age s severity of arteriosclerosis

Hyperlipidemia

Ex: hypercholesterolemia Transintimal filtration of plasma Dietary hyperlipidemia: Diets lipoproteins: source of lipids found rich in animal fat &/or excess in fatty deposits (atheromas) calories lipoproteins that cross aa. intima o intimal lipid deposits (atheromas) & intimal fibrosis augment each other creates a cycle lipid deposited in intima provokes intimal fibrosis slows normal diffusion of plasma lipoproteins into media traps lipids in deeper part of intima more atheromas provokes intimal fibrosis See Chart o Partly reversible remove causative factors Some regression can occur Major changes in diet is US could prevent development of severe, clinically significant arteriosclerosis

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Arterial narrowing

Complications o Occur mainly w/ severe arterioscleosis Causes Effects blood flow

Thrombosis

*most important complication Rupture of an arteriosclerotic plaque

Embolism Aneurysm

Softy, mushy plaque material carried in blood Medial weakening is focally excessive

Arterial Rupture

Medial weakness of sclerotic arteries

Lumen obstruction/narrowing: 1.distal edge of plaque elevates (valve-like flap) 2.Hemorrhage into plaque 3.platelet agglutinationmural or occlusive thrombosis 4.atheromatous embolism Most lodge in arterioles of lower limbs Arterial segment markedly dilatedaneurysm Most often in abdominal aorta & popliteal aa. Usu. in brain of hypertensive pt.

Results Ischemic atrophy &/or dysfunction of organs/tissues Infarctdry or viscus gangrene of an extremity Infarction of tissue Peripheral arterial occlusion: often in lower limbs of elderly & those w/ diabetes mellitus (may cause cramping or dry gangrene)

Dry gangrene of toes Multiple, fusiform aneurysms filled w/ firm, rubbery gray-brown lamellae of old thrombus

Coronary Heart Disease (CHD) Features o AKA: ateriosclerotic heart disease (ASHD) & ischemic heart disease o Predisposing factors: smoking, obesity, heavy coffee drinkers, diabetes mellitus, hypertension Coronary Circulation o Coronary arteries Right & left branches of aortic root Left branches anterior descending a. & circumflex a. Areas supplied: Anterior descending a. Ventricular septum Anterior & apical part of left ventricle Circumflex a. Lateral wall of left ventricle Right coronary a. Right ventricle Small posterobasal part of ventricular septum (AV node & Bundle of His) Posterobasal part of left ventricle o Coronary Blood Flow is influenced by: Ateriosclerosis Blood pressure esp. diastolic pressure Hypotension ischemia Myocardial anoxia causes coronary a. dilatation; adjusts blood flow to meet metabolic needs of myocardium O2 requirement of myocardium

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Coronary Arteriosclerosis o Has greatest effect on anterior descending branch, least effect on circumflex branch o Coronary thrombosis frequent @ sites w/ severe arteriosclerosis o Coronary arteries are usu. end arteries Rapid coronary occlusion = myocardial infarction Gradual coronary narrowing = formation of collateral circulation (final occlusion may not cause infarct) Coronary occlusion does not ALWAYS cause infarct! o Aggravated by hypotension & myocardial anoxia o Major change = multiple small foci of myocardial fibrosis scattered in left ventricle; due to healing of ischemic myocardial necrosis w/out clinical features of myocardial infarct Myocardial Infarction (MI) o Cause: severe, prolonged (> 20 min) myocardial ischemia; usu. due to occlusive thrombosis of sclerotic coronary a. o Necrosis begins in subendocardial region spreads thru epicardium Location: depends on site of coronary occlusion Anteroapical infarct occlusion of anterior descending branch (left ventricle) Posteriobasal infarct occlusion of right coronary a. Lateral infarct occlusion of circumflex branch Right ventricle & atria often not involved get nourishment from heart lumen o Size: varies w/ site of occlusion & development of collateral circulation Transmural due to recent thrombosis of large a.; extends to the epicardium & is covered by fibrinous pericarditis Subendocardial occurs w/out recent thrombosis or with thrombosis of narrowed a. that has collateral circulation; limited to inner half of myocardium; hypoperfusion due to coronary stenosis Mural thrombus forms in left ventricle over either transmural or subendocardial infarct o Anatomic Changes: Coagulative necrosis of myocardium opaque, firm, yellow-gray Acute inflammation - narrow rim of bright yellow neutrophils Ingrowing granulation tissue replaces necrotic myocardium; eventually forms a fibrous scar Forms in nearest viable myocardial tissue Sunken, soft, red-purple along edge of infarct Fibrous tissue firm, white Clinical Features o Cardinal symptom chest pain due to myocardial ischemia Poorly localized substernal pain Described as crushing, constricting, or oppressive Referred pain: left shoulder/arm, left side of neck Leads to Angina Pectoris (AP), Myocardial infarction (MI), & coronary insufficiency (unstable AP, preinfarction angina) o Angina Pectoris (AP) Due to brief, relatively mild myocardial ischemia Sudden onset of crushing substernal pain; subsides w/in 10 minutes of rest or sublingual nitroglycerin Precipitated by exertion or excitement o

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No myocardial necrosis occurs during attacks Sudden death due to ventricular fibrillation induced by myocardial ischemia; can occur w/out exertion/excitement; can be resuscitated

Myocardial Infarction (MI) Due to coronary thrombosis Occurs @ rest or under usual activity 50% - preceded by AP Symptoms: Chest pain Resembles AP, but more severe Sense of impending death Cardiogenic Abrupt in CO shock Due to (1) cessation of contraction by ischemic myocardium, (2) systolic bulging of infected area, (3) arrhythmias w/ effectiveness of ventricular contraction Often causes enlargement of infarct Arrhythmias Most common = PVCs from viable, but injured myocardium @ margins of infarct May cause VFib leading to sudden death Weak/Rapid Pulse Dyspnea Other complications: rupture of left ventricle, mitral insufficiency (due to papillary muscle dysfunction), left ventricular aneurysm (partially filled w/ mural thrombus) Lab abnormalities: creatine phosphokinase (CPK), presence of serum myocardial enzyme of CPK (CPK-MB), cardiac troponins in serum, progressive ECG changes Death occurs in 1st 2-weeks; many causes Mortality rate 5% in hospitalized patients; 1/3 of all CHD deaths Widespread focal myocardial fibrosis Occurs in pts. w/ severe coronary arteriosclerosis With or w/out scars from previous infarcts Impairs emptying & filling of left ventricle Pt develops left-sided CHF of progressively greater severity Treatment surgical procedures Percutaneous transluminal coronary angioplasty intraarterial balloon w/ or w/out stents Internal mammary artery grafts from aorta to more distal parts of coronary aa. (80-90% survival rate)

Hypertension (HT) Features o Persistent elevation of systemic arterial pressure to 150/100 mmHg or higher o Normal = 120/80 (upper limit = 140/90) o Systolic pressure usu. s more than diastolic pressure diastolic is more important in diagnosis of HT (minimal level of constant mechanical stress on vascular system) o pulse pressure o s severity of arteriosclerosis morbidity & mortality o complications CHF, cerebral hemorrhage

Pathology Exam 3

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o often occurs w/ CHD left ventricular hypertrophy & coronary arteriosclerosis Causes o Abnormality in regulation of cardiovascular function = MULTIPLE CAUSES Essential HT Primary HT, HT w/out qualification No Known Cause Renal HT Complication of chronic diseases of kidneys or renal aa. Endocrine HT Seen w/ Cushings disease, primary aldosteronism, or pheochromocytoma Pill HT Complication of use of oral contraceptives containing estrogen Other Part of preeclampsia-eclampsia Essential HT Baroreceptor reflex mechanism is reset to maintain elevated BP Immediate cause - arteriolar vasomotor tone (persistent in total peripheral resistance) due to arteriolar hypertrophy Normal pulse rate, CO, & blood volume Accelerates arteriosclerosis & hyaline arteriolosclerosis Initiating causes: unknown Important factors: hereditary predisposition, psychoemotional influences, salt intake, obesity Pathologic Anatomy o Left ventricular hypertrophy - weight of heart (normal = 200-400g) o Arteriosclerosis leads to ischemia o Hyaline arteriolosclerosis most severely affects renal arterioles o Arteriolar nephrosclerosis ischemic atrophy of kidneys & renal tubules; shrunken, finely granular Clinical Features o Initially asymptomatic o Headaches, fatigue, insomnia, dizzy spells, palpitation o Diagnosis by BP measurement o Heart enlarged, loud 2nd aortic sound, hard/full pulse o Course of disease: several decades, not often related to cause of death; treatable, but NOT CURABLE o Malignant Hypertension o Accelerated HT o Extreme elevation of BP (>200/120) o Rapid development of hyperplastic arteriosclerosis hyperplasia of arterial intima & severe luminal narrowing o Most severe in kidneys renal ischemia o Death w/in 1 year due to uremia, CHF, or cerebral hemorrhage

Vulvar Heart Diseases Features o Valve deformities interfere w/ normal valve function; usu. involve mitral or aortic valves Valvular stenosis valve leaflets are rigid &/or inadherent @ their commissures valve cannot open properly valvular orafice reduced in size heart chamber behind valve must work harder hypertrophy dilatation & CHF Valvular insufficiency valve leaflets cannot close properly, blood regurgitates thru valve Heart chamber behind valve must pump normal SV + additional

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regurgitated blood hypertrophy & dilatation CHF Clinical Features heart murmurs & CHF o Heart Murmurs Mitral stenosis Rumbling APICAL DIASTOLIC murmur Mitral insufficiency Blowing APICAL SYSTOLIC murmur, transmitted to left axilla Aortic stenosis Harsh SYSTOLIC murmur @ BASE of heart, transmitted to neck Aortic insufficiency Blowing decrescendo DIASTOLIC murmur @ BASE of heart o usu. produces left-sided CHF

Bacterial Endocarditis bacterial infection of heart may be bacteria of limited virulence considered valvular heart disease effective inflammatory reaction is precluded no significant localization of leukocytes vegetation bulky, friable valvular mass composed of necrotic debris, bacterial colonies, & thrombus o progresses to valve perforation/destruction valvular insufficiency can occur on prosthetic valve (Staph aureus or Staph epidermidis) occurs in drug addicts (Staph aureus, Staph epidermidis, or Candida albicans) involves tricuspid valve Cardiomyopathy (CMP) Features o Myocardiopathy, primary myocardial disease o Group of heart diseases resulting from chronic intrinsic dysfunction of myocardium o Hypertrophy of myocardial cells (poor function) o Leads to CHF, arrhythmias, &/or emboli Causes o Chronic alcoholism toxic effect of ethanol on myocardium o Chronic viral myocarditis usu. due to coxsackievirus o Heredity o Peripartum state o Idiopathic CMP = no known cause Pathologic Anatomy o Major lesion severe myocardial hypertrophy (weight = 600-1000g) of all four heart chambers o Heart may be dilated; may have mural thrombi Clinical Features o Early cardiomegaly, cardiac arrhythmias, CHF (left-sided 1st) o Complications: arrhythmias, AFib, PVCs, systemic or pulmonary embolism o Clinical course: unpredictable; progressive or erratic Aortic Aneurysms Dissecting Aneurysm of the Aorta o Initial tear - Transverse tear of aortic intima & inner media; Usu. located in ascending aorta above aortic valve Creates hematoma w/in aortic media o Dissecting Hematoma splits media around aortic circumference o External rupture produces fatal hemorrhage; usu. @ aortic root producing hemopericardium w/ fatal cardiac tamponade Arteriosclerotic Aneurysm fusiform aneurysm; lower abdominal aorta b/t renal aa. & aortic

Pathology Exam 3

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birfurcation Syphilitic Aneurysm saccular aneurysm; ascending aorta or aortic arch