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Diseases Of Heart Flashcards

1
Q

Compare high & low output failure

A

H: in conditions of increased needs, thyrotoxicosis & fever
L: in normal needs, myocradial infarction

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2
Q

Compare systolic & diastolic dysfunction (curves)

A

S: in MI, pressure volume loop & contractility curve are shifter of the right, EF may be normal at rest and dec with exercise or may be dec to 20% or less. SV & EF are resduced
D: in cardiomyopathy, hypertrophy & hypertension, pressure volume loop & diastolic pressure curve is shifter to the left and upwards. SV & EF are reduced while EDP is raised.

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3
Q

Mention term describing cardiac involvement in rheumatic fever

A

Pancrditis

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4
Q

Mention features of rheumatic pericarditis

A

Fibrinous inflammation with fibrin threads, bread & butter appearance, usually resolves may lead to fibrosis rarely

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5
Q

Mention features of rheumatic myocarditis

A

G: The heart is enlarged & flabby
M: Aschoff bodies: can be found in all layers, central fibrinoid necrosis with surrounding plasma cells & lymphocytes.
Antischkoff cells or caterpillar cells: activated macrophages with centrally disposed chromatin, giving appearnce if slender ribbon or attenuated body with innumerable finger-like projections.
Aschoff multinucleated giant cells: fused activated macrophages

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6
Q

Mention features of rheumatic endocarditis

A

Inflammation of mural endocardium esp left atrium, Mac Callum’s patch (rough wrinkled patch in post part of left atrium) denotes previous rheumatic involvement
Inflammation of valvular endocardium

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7
Q

Mention valves which are most severelt affected rheumatic fever & why?

A

Aortic & mitral more subjected to pressure & damage

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8
Q

Mention features of rheunatic vegetations

A

G: Multiple, beaded, pale, pin-head sized on line of closure, at the atrial surface of mitral & ventricular surface of aortic, never give emboli
M: aseptic, patletes & fibrin with Aschoff giant cells, plasma cells & lymphocytes in subendocardium.

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9
Q

Mention features of Chronic rheumatic valvulitis

A
  1. Aschoff bodies are replaced with fibrous scar.
  2. Valve cusps permenantly thickened and retracted
  3. Mitral valve has commisural fusion with fish mouth/buttonhole apearance.
  4. Chordae tendinae are thickened shorted and fused with fibrosis leading to funnel shaped valve
  5. Valvular stenosis & regurgitation
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10
Q

Mention extracardiac manifesttaions of rheumatic fever

A
  1. Joint involvement with fleeting arthritis & effusion
  2. Serous sac effusion
  3. Subcutaneous palpable nodules on bony prominences
  4. Erythema marginatum
  5. Chorea, involuntary spasmodic muscular movements
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11
Q

Mention complications of rheumatic fever

A
  1. Arrhythmia (atrial fibrillation)
  2. Acute heart failure
  3. Emboli (fom atrial mural thrombi)
  4. Infective endocarditis
  5. Congested lung & pulmonary hypertension
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12
Q

Mention predisposing factors to infective endocarditis

A
  1. Congenital heart disease (bicuspid aortic valve)
  2. Artificial valves
  3. Chronic rheumatic valvulitis
  4. Degenerative valve disease (mitral prolapse, calcific aortic valve)
  5. Host predisposing factor as DM, immunodeficiency, malignancy, IV drug abuse.
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13
Q

Mention features of acute infective endocarditis

A

G: bulky friable destructive vegetation on aortic & mitral valves showing ulceration, perforation & erosion. Easily detached.
M: supprative inflammation with entangled fibrin threads, platetlets & inflammatory celss & organism colonies on ulcerated valve.

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14
Q

C/P & complications of acute IE

A

CP, fever, chills, weakness, murmurs (left side), arrhythmias.
C, local: ulceration, perforation & rupture of valve or chordae tendinae.
General: septic emboli, pyaemic abscesses (systemic pyaemia), septicemia.

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15
Q

Mention features of subacute infective endocarditis

A

G: vegetation less bulky than acute, friable & easily detached on aortic & mitral valves.
M: platelets, fibrin threads, polymorphs, colonies of bacteria. Granulation tissue at base. Chronic inflammatory infiltrate, fibrosis & calcification may develop.

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16
Q

C/P of subacute endocarditis

A

Fever, weight loss, fatigue, flu-like symptoms, splenomegaly & complications.

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17
Q

Describe fate & complications of subacute IE

A
  1. Valvular lesions heal with scarring leading to deformity
  2. Embolic manifestations as aspectic infarcts or mycotoc aneurysm due to impaction of emboli in vasa vasorum.
  3. Capillary lesions due to vaculitis or microemboli, leading to cutaneous lesions (splinter hemorrhages, Osler’s nodes), glomerulonephritis ( hematuria, albuminuria, renal failure), petechiae.
  4. Specticemia
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18
Q

Causes of non bacterial thrombotic endocarditis

A
  1. Chronic DIC
  2. Underlying malignancy particularly mucinous adenocarcinoma
  3. Endocardial trauma
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19
Q

Fate & complications of non-bacterial thrombotic endocarditis

A
  1. Embolic manifestations

2. Bacterial colonization & IE

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20
Q

GR: Occuerrence of atypical verrucous endocaritis

A

With SLE, due ti immune complex deposition on both sides of mitral & tricuspid valves, leading to fibrinoid necrosis, fibrosis & serious deformity.

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21
Q

GR: Valvular lesions in carcinoid syndrome

A

Due to circulation of 5HT released by intestinal carcinoid with massive liver metastasis escaping liver inactivation.

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22
Q

Why is left side ususlly not ivovlved in carcinoid?

Mention conditions in which it may be involved

A

Due to inactivation of 5HT in lung

Septal defect or primary pulmonary carcinoid

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23
Q

Mention features of valvular lesions in carcinoid

A

G: plaque like thickening of tricuspid or pulmonary valves
M: smooth muscles, sparse collagen fibers embedded in acid mucopolysaccharide-rich matrix

24
Q

Mention most common cause of aortic stenosis & its pathogenesis

A

Calcific aortic stenosis
Progessive age related process, hyoerlipidemia, hypertension, inflammation and other factors implicated in atherosclerosis

25
Cause of secondary myxomatous mitral valve
Injury to valve myofibroblasts due to chronic aberrant hemodynamic forces.
26
Mention features of myxomatous aortic valve
G: ballooning of mitral valve, chordae tendinae are thinned, elongated may rupture, tricuspid involvemnt may be present concomitanatly. M: fibrosa layer in thinned, spongiosa layer is thickened with myxomatous material deposition.
27
Complications of myxomatous mitral valve.
Infective endocarditis Sudden cardiac death from ventricular arrhythmia Stroke or systemic infarction due to emobli in keft atrium
28
Describe pathogenesis and features of hypertrophic cardiomyopathy
P: most cases are due to point mutation in genes encoding contractile apparatus of the heart, autosomal dominant, heart is hypercontractile. G: massive asymmetrical hypertrophy of left ventricle with no dilatation M: hypertrophy of myocytes with interstitial fibrosis, disarray with whorrly arrangement of muscle fibers and loss of normal cellular orientation.
29
Clinical features of HCM
Decreased stroke volume due to dec left ventricular compliance & dec chamber size Left ventricular outflow obstruction & mitral regurgitation due to asymmetrical hypertrophy Myocardial ischemia
30
Describe pathogenesis of DCM
``` 20-50% have genetic cause Coxscakie B virus Alcohol, other toxins Peripartum period Iron overload in hereditary hemochromatosis ```
31
Mention features of DCM
G: the heart is enlarges & flabby, all chamers are enlarged M: some fibers are hypertrophied others are thinned, interstitial fibrosis with chronic inflammatory cells.
32
Clinical manifestations of DCM
Congestive heart failure | 2ry mural thrombi, mitral regurgitation, arrhythmias
33
Mention causes of RCM associated with systemic disease
Amyloidosis, systemic or senile cardiac Endomyocardial fibrosis associated with nutritional deficiency states and related to helminthic infections Loeffler’s endomyocarditis, large mural thrombi, peripheral eosinophilia and eosinophilic tissue infiltrates. MBP causes necrosis
34
Mention most common pathogen causing myocarditis
Coxsackie B viruses
35
Causes of suppurative myocarditis
Organism reaching myocardium either by blood (septicemia or pyaemia) Direct extension from pericarium or endocardium or lung or pleura
36
Microscopic picture of suppurative myocarditis
Suppurative inflammation in interstitial tissue, destruction of muscle fibers & small abscesses
37
Causes if toxic myocarditis
Severe toxemia: diphtheria, typhoid, pneumonia, severe streptococcal infection. Chemical toxins: CO, antimony, arsenic, chloroform, phosphorus, sulphonamides.
38
Describe microscopic features of toxic myocarditis
Shows areas of degeneration (fatty change), interstitial edema & cellular infiltration of plasma cells, lymphocytes, eosinophils, polymorphs & macrophages Severe cases as in diphtheria show valculations & necrosis of muscle fibers esp conducting system.
39
Describe microscopic features of cardiac toxoplasmosis
Cellular infiltrate of plasma cells, lymphocytes & eosinophils, parasite cysts are presents.
40
The most common helminthic infection associated with cardiac involvement
Trichinosis
41
Mention microscopic features of interstitial myocarditis
Diffuse interstitial inflammation with plasma cells, lymphocytes & macrophages. Focal myocardial necrosis is common in severe cases.
42
Mention causative agents of fungal myocarditis & predisposing factor.
Cryptococcal, aspergillus, monilial | Therapy of malignant tumours as lymphoma & leukemia.
43
Describe microscopic features of idiopathic giant
The ventricular myocardium is esp involved with areas of complete necrosis. At perphery, there is marked mononuclear cellular infiltrate & elongated giant cells.
44
Most common cell in hypersensitivity myocarditis
Eosinophils
45
Describe causes & fate of serous pericarditis
C: viral, non-infectious (rheumatic fever, SLE, systemic scleroderma), idiopathic. F: resolution with no effect on cardiac function
46
Mention causes of fibrinous pericarditis
Rheumatic fever, uraemia, trauma, myocardial infarction, lung disease as pneumonia.
47
Fate of finrinous pericarditis
Resolution & fibrin digestion | Mild adhesive pericarditis OR plaque like thickening
48
Describe causes & fate of suppurative pericarditis
C: direct extension, blood-borne, lymphatic spread, penetrating chest wound. F: organization with marked adhesions resulting in constrictive pericartitis
49
Describe causes & microscopic features fate of tuberculous pericarditis
C: direct spread or blood-borne or lymphatic spread from pulmonary tuberculosis/tuberculous mediastinal LN M: fibribous inflammation with granukation tissue, tubercles & sometimes caseation, there may be hemorrhagic exudate. F:organization with marked adhesions resulting in constrictive pericartitis
50
Describe causes & fate of hemorrhagic pericarditis
``` C: -TB -Malignant neoplasms -Pericarditis+underlying blood disease -Severe bacterial infection F: organization with marked adhesions resulting in constrictive pericartitis ```
51
Describe the heart in constrictive pericarditis
The heart is small & cannot expand adequately during diastole. Constriction of venae cavae may occur impeding venous return leading to congestive heart failure.
52
Mention clinical features of pericarditis
1. Atypical chest pain (not related to exertion, worse with recumbency) 2. Friction rub
53
Describe cause & fate of hydropericardium
C: generalized edema (renal, cardiac, nutritional) F:absorbed with removal of cause
54
Decsribe causes & fate of haemopericardium
C: 1. Rupture of heart (traumatic/spontaneous) 2. Rupture of intrapericardial portion of aorta (aortic aneurysm, syphilitic aneurysm, traumatic) 3. Hemorrhagic diatheses F: Death occurs rapidly due to cardiac tamponade (200-300 ml is fatal)
55
Mention causes of pneumopercardium
Trauma Perforation of lung or eosophagus into pericardium Pericarditis due to gas forming organisms
56
Mention most common primary benign & malignant tumours of heart
B: myxoma M: angisarcome
57
Mention in descending order, cancers which send heart metastasis
Lung cancer, lymphoma, breast cancer, leukemia, melanoma, HCC, colon cancer

CVS Pathology (5 decks)

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