Pathology Of The Heart Flashcards

Question

What are extra-cardiac lesion of RF

Answer 1

Subcutaneous nodules •Polyarthritis( migratory) •Pleural oedema and fibrinous exudates •CNS Sydenham’s chorea characterized by rapid, irregular and purposeless movement ( basal ganglia haemorrhage,oedema,perivascular lymphocytic reaction)

Answer 2

•Stenosis of the valve implies narrowing of the valve. •Isolated mitral & aortic stenosis account for close to half of all valvular heart lesions. •Stenotic valve impose volume overload as well as pressure overwork on the heart chamber involved. Insufficiency or regurgitation occurs when a valve fails to close completely during systole. •May occur as a result of intrinsic valvular dx or damage to the supporting structures •Stenosis & regurgitation produce noisy movement of blood because of turbulence called cardiac murmur. •Right heart valve disease is due to Carcinoid syndrome or congenital malformations.

Answer 3

Invasion of the heart valve or the mural endocardium by infective agents. 2 FORMS. •Acute – fatal fulminant infection. Occurs in a previously normal valve with highly virulent organism. •Subacute. – smouldering, indolent illness. occurs in previously damaged valve. •Distinction vague because of antibiotics. Xterised by deposition of friable bulky, bacterial-laden (infective) vegetations on the heart valve. Epidemiology &pathogenesis. •Congenital heart dx e.g Tetralogy of Fallot,PDA. •RHD •Valvular defects. Prosthetic valve •Immunosuppresion eg HIV,drug induced •Diabetes Mellitus •Chronic alcoholics •Intravenous drug abuse •Commoner in males above 50yrs Commoner in males. •50-75% affect previously damaged valve •Valves distorted by congenital malformations. Factors predisposing to development of IE •Seeding of blood with microbes. •Haemodynamic disturbance occuring across deformed heart valve Activation of clotting cascade •Production of agglutinating antibodies leading to clumping of organism within the vegetation. Heart—perforation of valve •myocardial abscess •suppurative pericarditis •Congestive cardiac failure •Fragmentation& embolization of septic vegetation to sites like brain, spleen, coronary arteries & kidneys •Immune complex dx-focal GN •OSTEOMYELITIS

Answer 4

Marantic endocarditis or non-bacteria thrombotic endocarditis •Libman-Sacks dx or non-bacteria verrucous endocarditis.

Answer 5

Debilitated and Cachetic patients •Vegetations on line of closure of valves. •Larger and softer than those of RF •Frequency: mitral, aortic, tricuspid and pulmonary. •Source of emboli to brain, lungs, kidney and spleen. •Most common cause of coronary emboli.

Answer 6

Granular flat verrucae, both surfaces of valves. •Mitral and Tricuspid valves commonly. •Fibrinous, granular, sterile vegetations •Valvulitis, immune complex mediated •May appear in patients with SLE(50%). •Usually does not deform the valves.

Answer 7

Fibrinous •Serous •Serofibrinous •Fibrinopurulent •Purulent •Haemorrhagic •Cholesterol •Granulomatous •Adhesive •Constrictive.

Answer 8

Infections: Bacterial,viral & fungal. •Neoplastic •Systemic disease •Rheumatic fever •Uraemia •Myocardial infarction

Answer 9

Heart disease caused by reduction in blood supply to the myocardium assoc. with diseases of the coronary arteries. In IHD, coronary atherosclosis is diffuse involving more than one major arterial branch typically involving the proximal 2cm in the epicardial region •Due to presence of collateral vessels, the cross-sectional area of the vessels must be reduced by >75% to significantly affect perfusion •Hypertension is an important risk factor for coronary atherosclerosis.

Answer 10

Myocardial infarction (heart attack) •Angina pectoris •Chronic ischaemic heart dx •Sudden cardiac death.

Answer 11

Coronary atherosclerosis 90-95%. •Coronary vasospasm alone or superimposed on atherosclerosis •Coronary artery embolism •Ostial stenosis e.g syphilitic aortitis •Coronary thrombosis •Aneurysms. Medial Calcification.(rare) •Congenital anomalies.

Answer 12

Caused by an imbalance between the myocardial blood flow and the metabolic demand •In majority of cases, the reduction in coronary blood flow is related to progressive atherosclerosis with increasing occlusion of the coronary arteries •Coronary artery perfusion depends on the differences between the pressure at the ostia and the coronary sinus •Due to compression of intramuscular arteries and coronary orifices during systole, Cardiac Blood Flow reduces in systole

Answer 13

Decrease aortic diastolic pressure •Increased intraventricular pressure & myocardial contraction •Coronary artery stenosis –Fixed coronary stenosis –Acute plague rupture or haemorrhage –Coronary artery thrombosis –Vasoconstriction •Aortic valve stenosis and regurgitation •Increased atrial pressure

Answer 14

Angina pectoris –Stable angina- –Variant or prinzmetal angina –Unstable angina- –Sudden cardiac death •Myocardial infarction

Answer 15

Stable angina- •subendocardial ischaemiaparoxysms of pain related to exertion and reduced by vasodilators(ST-segment depression on ECG) –Variant or prinzmetal angina- •reversible spasm in normal to severe atherosclerotic coronary Apain occurs at rest(ST-segment elevation or depression) –Unstable angina- •prolonged pain at rest in a patient with stable angina or worsening of pain of stable angina(usually ST-segment depression) –Sudden cardiac death- •high stroke stenosis with acute coronary changesunexpected death within an hour of a cardiac event

Answer 16

Occlusive intracoronary thrombus-i.e complicated atheromatous plaque either by ulceration or fissured (90%) •Vasospasm of CA with or without atherosclerosis (platelet aggregation implicated) •Emboli from: –Left sided mural thrombus –Vegetative endocarditis –Paradoxical emboli from right side of the heart(foramen ovale)

Answer 17

Transmural infarct- –involve entire thickness of the LV wall from endocardial to epicardium –usually anterior free wall •Posterior free wall and septal infarct with extension into the RV wall •Subendocardial infarct-multifocal areas of necrosis confined to inner 1/3-1/2 of the LV wall •Isolated infarcts of the RV and RA are extremely rare •The last 3 do not show the same evolution with transmural infarct

Answer 18

18-24hrs—pallor of the myocardium •24-72hrs—pallor with some hyperaemia •3-7days—central yellowish area surrounded by hyperaemic borders •10-21days—maximally yellow and soft with vascular margins •7weeks—white area of fibrosis

Answer 19

1-3hrs-wavy myocardial fibers •2-3hrs-staining defect with tetrazolium or basic fuschin dye– nitro blue tetrazolium test •4-12hrs- –coagulative necrosis with loss of cross striations and contraction bands, –oedema, haemorrhage and early neutrophilic infiltrate •18-24hrs- –continuing coagulative necrosis with nuclear Pyknosis –marginal macrophage and mononuclear inflammatory cell infiltrate and –Fibrovascular tissue response begin 10-21days-fibrovascular response with prominent granulation tissue •7weeks-fibrosis •These changes can vary depending on the size of the infarct, being slower in larger ones

Answer 20

Arrhythmias and conduction defects with possible sudden death •Extension of infarct or re-infarction •Congestive Cardiac Failure •Cardiogenic shock •Pericarditis •Mural thrombus with possible Embolization •Myocardial wall rupture with possible valvular insufficiency •Ventricular aneurysm Sudden death- –death occurring within an hour of onset of symptoms –Occurs in severe coronary atherosclerosis with >75% Lumina narrowing –Associated complication such as thrombus or plaque haemorrhage or rupture –Mechanism is usually an arrhythmia •Aortic dissection can also cause sudden collapse. Ishaemic cardiomyopathy- can also be a complication severe atherosclerosis of all major arteries inadequate vascular supply myocyte loss + fibrosis decreased compliancecompensatory hyperplasia & hypertrophydecompensation and heart failure

Answer 21

Size of the myocardial bed at risk and its metabolic/oxygen needs • Duration of obstruction • Coronary artery anatomy,dominance/collaterals • Site of coronary artery obstruction • Severity of obstruction • Rate at which obstruction developed

Answer 22

Signs and symptoms of severe pump failure/cardiogenic shock generally occur with large infarcts (> 40% of the left ventricle involved). •Cardiogenic shock indicates –a poor prognosis (70% mortality) and –accounts for 2/3 of hospital deaths.

Answer 23

It is important to consider these: •None of the available test is specific nor sensitive •The tests must be correlated with clinical symptoms, ECG and angiography •Timing is very important

Answer 24

Total creatinine is from both skeletal and cardiac origin; non specific •MB, MM,BB fractions –MM-cardiac & skeletal- has isoenzymes –MB-specific for cardiac, 2% is skeletal –BB-found in brain, bowel & bladder and not measured routinely) •CK-MB-is measured every 2-4hrs for 9-12hrs after patient is first seen. Rising levels indicates myocardial injury •Useful to diagnose re-infarction as level falls after a day dissipating in 1-3days

Answer 25

Troponins-I and T are structural components of cardiac muscle and released into blood with myocardial injury •Very specific; much more than CK-MB •Begins to rise within 3-12hrs, remain elevated to 5-9days for troponin I and up to 2weeks for troponin T •Difficult to diagnose re-infarction because of the above •Troponin T not very specific as it can appear with skeletal myopathies or renal failure

Answer 26

Myoglobin –is a protein found in skeletal & cardiac muscle –It is elevated before CK-MB but not specific •LD- – begins to rise in 12-24hrs, peaks in 2-3days and dissipating in 5-14days –LDH isoenzymes is more specific. –Normally isoenzyme 2 is higher than 1, but in MI, this is reversed. –LDH-5 is from liver and may increase in centrilobular necrosis of chronic liver congestion that follows CCF

Answer 27

Control of hypertension & diabetes •Drug and dietary treatment of hypercholesterolemia •Dietary reduction of plasma cholesterol & LDL •Reduction of fat intake •Avoidance of obesity •Moderation of salt intake •Cessation of smoking •Exercise

Answer 28

Sudden cardiac death •Acute ventricular fibrillation •Myocardial rupture •CCF •Thrombo-embolism •Aneurysm of the heart muscle wall

Answer 29

Myocarditis Cardiomyopathies

Answer 30

Viruses •Riketssia. •Chlamydia •Bacteria eg diphtheria. •Fungi eg candida •Parasites: Trypanosoma cruzi Toxoplasma •Trichinella. •Echinococcus. •African Trypanosomiasis Incidence variable, depends on the endemicity of certain diseases. Trypanosomiasis, diphteria.

Answer 31

Immune mediated reactions •RHD •SLE •Transplant rejection TOXINS eg alcohol ,cytotoxic drugs

Answer 32

Acute phase ----enlarged, flabby heart •Cut surface shows mottling of venticular wall, microhaemorrhages

Answer 33

Histology depends on the causative agent. •Chronic fibrosis & burnt out inflamm reaction.

Answer 34

•DILATED •HYPERTROPHIC •RESTRICTIVE

Answer 35

Xterised by gradual development of heart failure associated with 4 chamber hypertrophy & dilatation of the heart •Familial occurrence 20% •AD in most cases, AR, X-Linked mitochondrial inheritance less common •X-linked has been associated with Duchene muscular dystrophy. •Previous myocarditis •Alcohol or toxins. •Child bearing or peripartum

Answer 36

Cardiomegaly •Dilated chambers •Hypertrophy of myocytes •Patchy atrophy •Mural thrombi •Primary abnormality is impaired LV myocardial contractility.

Answer 37

Asymmetrical septal hypertrophy •Xterised by heavy hypercontracting heart •AD in 50% of cases •Associated With HLA B12,&HLA B5 •Most cases of mutation are due to mutation in the heavy chain of B myosin protein

Answer 38

Dis-proportional hypertrophy of LV muscle predominantly affecting the septum •Reduction in chamber volume •Microscopy myofibers disarray

Answer 39

Endomyocardial fibrosis EMF •Loeffler’s endocarditis •Endocardial fibroelastosis •EMF& Loeffler’s endocarditis are xterised by fibrosis of the ventricular endocardium and the subendocardial tissue.extends from the apex to the outflow tract.

Answer 40

Has been associated with malnutrition, viral infection & microfilaria infection •Excessive consumption of plantain. •Mural thrombi •Eosinophilia.

Answer 41

Xterised by focal or diffuse cartilage-like fibroelastic thickening usually involving the mural LV endocardium •Most common first 2years of life •Associated with cong.heart anomaly most often aortic valve obstruction.

Answer 42

Primary tumours are rare •Metastatic tumours –5% of patients dying of cancer •Metastasis commonly affect the pericardium.

Answer 43

Myxoma •Fibroma •Lipoma •Papillary fibroelastoma •Rhabdomyoma •Angiosarcoma

Answer 44

Most common primary tumour in adults •90% occur in the atrial •Lt :Rt 4:1 •Single tumour •1-10cm in diameter •Sessile or pedunculated, gelatinous mass •Histology; stellate cells,myxoma cells & endothelial cells in a background of acid mucopolysaccharide.

Answer 45

Most common primary heart tumour in infants •Small gray-white myocardial masses protruding into ventricular chamber •Histology: round to polygonal cells contain numerous glycogen vacuoles.

Answer 46

Trisomy 21 (Downs) VSD •Trisomy 18 (Edward’s) •Trisomy 13 (Patau’s) •Turners synd. Coartation of the aorta Environmental factors • Maternal infection eg Rubella •Cardiac teratogens: hypoxia,ionizing radiation,drugs eg thalidomide, alcohol.

Answer 47

1. Acyanotic with shunt (Lt to Rt shunt) • a) PDA, b) VSD, c) ASD •2) Cyanotic (Rt to Lt shunt ) • a) tetralogy of Fallot • b) late cyanotic VSD (Eisenmenger complex) • c) transposition of great vessel d) Total anomalous pulmonary venous connection e) Persistent truncus arteriosus f) Tricuspid atresia •3) Acyanotic (no shunt ) • a) Coarctation of the aorta • b) Aortic stenosis and atresia C) Pulmonary stenosis and atresia •

Answer 48

CYANOSIS •Pulmonary hypertension •Myocardial hypertrophy/dilatation •Failure to thrive •Cerebral thrombosis •Paradoxical embolism •Predisposition to infective endocarditis

Answer 49

Most common CHD. •The defect is most commonly in the membraneous part of the ventricular septum •Xterised by loud systolic murmur •Complication: pulm. hypertension • Reversal of shunt

Answer 50

Constriction of the ascending aorta or the arch •Pre-ductal i.e constriction just proximal to the origin of ductus arteriosus. Survival depends on the patency of the ductus. •Post-ductal i.e constrition is distal to the ductus. Less severe , may be asymtomatic.

Answer 51

Differences in the blood pressure in the upper and lower extremities •Development of collateral channels •Dilatation of intercoastal vessel leading to rib notching

Answer 52

Large VSD •Overriding aorta •Pulm. stenosis •RVH

Answer 53

Central cyanosis •Dyspnoea with blue spells •Squatting •Failure to thrive •Recurrent respiratory infection.

Pathology Of The Heart Flashcards

(79 cards)