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Cardio > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

0
Q

Condition resulting from chronic ischemia and mitral insufficiency
- myocytes laid in series

A
  • volume overload hypertrophy

- ventricular walk may or may not increase: ventricular dilation does occur

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1
Q

Condition resulting from HTN and/or aortic stenosis

A

Cardiac pressure overload hypertrophy

  • new sacromeres laid in parallel to long axis
  • aka concentric hypertrophy
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2
Q

Condition caused by ischemic heart disease, HTN, aortic and mitral valve disease and myocardial disease
- pulmonary congestion and edema (siderophages) resulting in pre-renal azotemia and potentially hypoxic encephalopathy

A
  • left side heart failure
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3
Q

Results in Chronic pulmonary hypertension (cor pulmonale)
Most commonly caused by left sided heart failure
Results in congestive hepatosplenomegaly, plural effusion, dependent peripheral edema

A

Right sided heart failure

- plural effusion: venous drainage backs up

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4
Q

Ischemic heard disease

A
  • hypoxia + inadequate metabolite delivery + inadequate waste removal
  • leading COD in us
  • may result from fixed coronary lesion, acute plaque change, coronary artery thrombosis, vasoconstriction
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5
Q

Fixed coronary artery lesion

A
  • up to 50% often subclinical
  • 70~75% occlusion = stable angina
  • 90% occlusion = unstable angina
  • most commonly proximal LAD, then proximal LCX and RCA
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6
Q

Ischemic zones of coronary occlusion

A
  • LAD: medial and anterior wall (corner) and half of anterior wall between lateral and LAD of left ventricle
  • LCX: lateral wall of LVent
  • PIV: posterior corner of LVent
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7
Q

Coronary artery thrombus (occlusive, non-occlusive)

A
  • occlusive: can cause trans mural infarction

- non-occlusive: subendocardial, unstable angina, distal embolization and micro infarcts

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8
Q

Four syndromes of ischemic heart disease

A
  • angina pectoris
  • myocardial infarction
  • sudden cardiac death
  • chronic ischemic heart disease
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9
Q

Angina pectoris: 3 types

A
  • stable angina: relieved by rest or nitro
  • prinzmetal variant angina: vasospasm, transient
  • unstable angina: caused by ruptured mural thrombus
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10
Q

Myocardial infarction process

A
  • anerobic glycolysis (sec)
  • loss of contractility (minutes)
  • irreversible cell injury (20-40 minutes)
  • necrosis (~2 hrs)
  • REPERFUSION in 20 minutes cause reversal of cell injury
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11
Q

Infarction process

A
  • from endocardium outward
  • healing happens from outside in (blood supply richer closer to coronaries)
  • exception is proximal infarct extension
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12
Q

Mechanisms of infarct extension

A
  • thrombus propagating proximally
  • proximal vaso spasm
  • impaired myocardial contractility
  • platelet fibrin micro emboli
  • arrythmias
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13
Q

Transmural infarct

A
  • full thickness: more common
  • typically caused by acute plaque change
  • can occur for vasospasm (eg in cocaine use)
  • ST elevation MI
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14
Q

Subendocardial infarction

A
  • ST depression
  • may be lysed thrombus, or hypotension in diffuse sclerosing athersclerosis
  • circumferential infarct
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15
Q

MI gross tissue changes

A
  • 12 hours not grossly recognizable
  • 12-24 hours coagulative necrosis
  • 1-3 days yellowing of central tissue (inflammation neuts/macs)
  • 1 week: yellow lesion with hyperemic boarder (granulation tissue)
  • 1 mo: fibrosis
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16
Q

Microscopic changes of necrosis

A
  • 12 hours: neutrophils and wavy fibers
  • 12-24 hrs: coagulative necrosis with dev of contraction bands
  • 2-3 days: dense neutrophilic infiltrate
  • 7-10 days: dense macrophage infiltrate
  • 2-8 weeks collagen deposition
  • 2 mo: dense collagenous scar (trichrome blue)
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17
Q

Complications of MI

A
  • contractile dysfunction (heart failure)
  • arrhythmias
  • myocardial rupture (3-7 days) -> tamponade
  • pericarditis
  • papillary dysfunction -> regurgitation
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18
Q

Reperfusion injury

A
  • generation of free radicals from oxygen introduced to neutrophils
  • inflammation around vessels can function poorly decreasing heart function
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19
Q

MI prognosis

A
  • size and location
  • large = bad
  • transmural = bad
  • anterior = bad
  • posterior can result in arrhythmias and RV infarcts
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20
Q

MI labs

A
  • troponin TnI more specific
    > rises 2-4 hours, peaks at 2 days 7-10 normalizes
    > reperfusion accelerate peak
  • CK-MB: 2-4 hour rise, 1 day peak 3 day normalizes
    > useful for assessment of re infarction within 10 days
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21
Q

Valvular disease

A
  • stenosis

- insufficiency

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22
Q

Mitral stenosis etiology

A
  • rheumatic heart disease
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23
Q

Mitral insufficiency

A
  • mostly due to myxomatous valvular degeneration

- may be calcification, rheumatic, endocarditis, chordae rupture

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24
Q

Atrial stenosis

A
  • mostly senile calcification aortic stenosis
    > age related dystrophic accumulation, no valve comissural fusion
    > results in LV pressure overload, angina and syncope
  • may be calcified congenital bicuspid aortic valve, rheumatic
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25
Q

Aortic insufficiency

A
  • mostly aortic root dilation from HTN/old

- may be endocarditis, myxomatous

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26
Q

Calcified congenital bicuspid aortic valve

A
  • dystrophic calcification earlier than 70
  • midline raphe on larger cusp
  • no valve commissural fusion
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27
Q

Condition in older women or patients with myxomatous mitral valve or elevate LV pressure
- degenerative calcification of mitral ring

A

Mitral annular calcification

- can increase risk of infectious endocarditis

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28
Q
  • condition evidenced by mid-systolic click

- women > men, 20-40 y/o 3% of us pop

A

Mitral valve prolapse

  • myxoid degeneration of inner spongy layer and thinning of outer fibrous layer
  • valve annular dilation
  • thrombi can form on superior surface of leaflet
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29
Q

Sequelae of GAStrep pharyngitis (10 days - 6 weeks)

- children 5-15

A

ARF

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30
Q

Joints: migratory painful polyarthritis

s chorea:

A
  • criteria for diagnosing ARF 2* to GAS infxn
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31
Q

Bread and butter around the heart
- resolves
Myocarditis: Ashoff bodies with anitschcow cells and necrotic collagen

A
  • ARF pancarditis
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32
Q

Verrucae on mitral and aortic valves

Fibrinoid necrosis of cusps and chordae

A

Vavulitis 2* to ARF pancarditis

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33
Q

Fused valve commissures (fish mouth), mostly mitral valve (can involve the aortic and rarely tricuspid
- fused thickened cordae

A
  • chronic rheumatic heart disease

- results in stenosis most commonly

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34
Q

Etiology of infectious endocarditis

A
  • 30-40% S. viridans
  • 20-35% staph
  • 15-20% strep
  • 5-18% enterococci
  • can affect normal or altered valves and can result in emboli
35
Q

Etiology native valve endocarditis

A
  • s. aureus
36
Q

Prosthetic valve endocarditis

A
  • coagulate negative staph (s. saprophiticus, s. epidermidis)
37
Q

Eroding Vegitations forming ring abcesses presenting in pt with Osler nodes (painful) and janeway lesions (non-painful)

A
  • acute infective endocarditis (s. aureus, s. epi)

- nodules are fibrinoid and neutrophil laden

38
Q

Fever, flu like symptoms following dental procedure

A
  • sub acute infective endocarditis (s. viridans, s. fecaelis, s. bovis)
  • less destructive, good recovery with antibiotics
39
Q

Small non-destructive sterile vegetations of fibrin and platelets along valve closure lines

A

Non-bacterial thrombotic endocarditis

- in PTs who are hypercoagulable: cancer, high estrogen, burns, sepsis

40
Q

Small pink nodules of hematoxylin and fibrin on underside of valves (mainly mitral and tricuspid)
- ANAs damage DNA and for hematoxylin bodies

A
  • SLE endocarditis
41
Q

4 types of valvular vegetations

A
  • small along closure lines: RHD
  • large and destructive: infectious endocarditis
  • small-medium along closure lines: NBTE
  • small not confined to closure lines, underside: SLE
42
Q

Murmur + flushing, cramps, nausea, vomiting, diarrhea

A
  • carcinoid heart disease
  • serotonin producing tumor
  • right sided valvular leflet and mural intimal smooth muscle and collagen proliferation - stenosis/insufficiency
43
Q

Prosthetic valve pathology

A
  • 60% of prosthesis develop complication
  • thromboemboli, anticoagulant related hemorrhage, infective endocarditis (ring endocarditis)
  • bioprosthesis can develop
44
Q

Three clinical cardiomyopathies

A
  • dilated (90%) (4 chamber, young)
  • hypertrophic (athlete falls dead on field)
  • restrictive
45
Q

Hypertrophic heart with systolic dysfunction and 4 chamber dilation

A
  • dilated cardiomyopathy
  • adults 20-50 y/o
  • genetic influence less than 1/2 (AD)
46
Q

Epicardial granulomas with myopathy

A

Dilated cardiomyopathy 2* to sarcoidosis

47
Q

Vacuolar fatty change in myocytes due to membrane per oxidation

A
  • dilated cardiomyopathy due to anthracycline use
48
Q

Hemosiderin filled macs, cardiomyopathy

A
  • dilated cardiomyopathy 2* to iron overload (hemochromatosis)
49
Q

Arrhythmogenic right ventricular cardiomyopathy

A

Significant cause of death in young

  • right ventricular thinning with fatty infiltration and interstitial fibrosis
  • commonly AD genetic link
  • AR assoc with Naxos syndrome
50
Q

Wooly hair, plantopalmar keratosis, cardiomyopathy

A
  • Naxos
  • AR
  • arrhythmogenic right ventricular cardiomyopathy
51
Q

Left ventricular hypertrophy, systolic dysfunction and left ventricular obstruction
- sudden death in athletes
- may has dyspnea on exertion
Condition and etiology

A
  • “floppy cow heart” hypertrophic cardiomyopathy
  • AD inheritance
  • B-myosin heavy chain mutation (most common)
  • myosin binding protein C
  • troponin C
52
Q

Treatment and complications for hypertrophic cardiomyopathy

A
  • ventricular relaxation (B blocker)
  • excise LV outflow obstruction

Afib, mitral valve endocarditis, cardiac failure, arrhythmias, sudden death

53
Q

Morphology of hypertrophic cardiomyopathy

A
  • thickened IV septum
  • ventricular outflow obstruction
  • banana ventricular cavity
  • aortic outflow thickening
  • anterior mitral leaflet thickening (systolic murmur)
54
Q

Mild hypertrophy, biatrial dysfunction, diastolic dysfunction
- on microscopy patchy to diffuse fibrosis

A

Restrictive cardiomyopathy

- idiopathic, or secondary to sarcoidosis, amyloidosis, mets

55
Q

Most frequent cause of restrictive cardiomyopathy

  • wax drip atrial nodules
  • firm rubbery endocardium
  • Congo red and apple green biferingience
A

Amyloidosis

  • transthyretin deposits: senile cardiac amyloidosis
  • ANP amyloid deposits in atria: isolated atrial amyloidosis
  • systemic amyloidosis: worst case
56
Q

Infectious myocarditis

A
  • coxsackie A primarily in US and B
  • CMV, HIV, Influenza A,B and echo
  • chlamydia
  • rickettsia
  • bacterial: c. Dipth, N. mening, Burgdof
  • Protozoa: Tcruzi (chagas) t Gondi
  • helminths: T spiralis
57
Q

Non- infections myocarditis

A
  • drug hsn: Abx, diuretics, antiHTNs (eosinophil infiltrate)
  • immune mediated: SLE, ARF, transplant rejection
  • sarcoidosis
  • giant cell (poor prognosis) giant cells and extensive necrosis
58
Q

Pericarditis

A
  • viruses major cause, may also be bacteria
  • non- infectious; SLE, ARF, scleroderma, post MI, HSN
  • uremia
  • neoplasms
59
Q

Acute vs chronic pericarditis

A
  • acute: serous, fibrinous, purulent/supp, hemorrhagic, caseous
  • chronic: adhesive, constrictive
60
Q

Non-infectious pericarditis with clear fluid that usually resolves without organization

A
  • acute serous pericarditis
61
Q

Most common form of acute pericarditis

- yellow cloudy fluid with fibrin and scant inflammatory cells

A
  • fibrinous
  • MI, uremia, radiation, ARF, trauma
  • can organize
62
Q

Infectious pericarditis with white exudate and lots of inflammation

A
  • purulent/ supperative pericarditis

- typically organizes

63
Q

Pericarditis typically caused by mets

A

Hemorrhagic,

- may also be infectious

64
Q

Most frequent cause of disabling constrictive pericarditis

A
  • caseating pericarditis 2* to TB
65
Q

Delicate stringy organization of obliterated pericardium

A
  • adhesive pericarditis
  • rarely symptomatic
  • adhesion to structures in mediastinum results in hypertrophy and dilation
66
Q
  • severely restricted CO

- obliterated pericardium organized into fiberous/calcified scar

A
  • concretio cordis

- constrictive pericarditis reqs pericardectomy

67
Q

Fibrinous pericarditis, aortic valvulitis, Rh nodules

A
  • reheumatic heart disease
68
Q

Heart tumors

A
  • mostly mets
  • primary tumors are rare
    > myxoma, lipoma, papillary fibroelstoma, rhabdomyoma
69
Q

Most common primary heart tumor, variable presentation but classically currant jelly

A

Myxoma

  • usually in L atria near foramen ovale
  • may obstruct
  • histo: myxomatous cells in mucopolysaccharide matrix
70
Q

Lipoma

A
  • left ventricle, right atria, atrial septum

- obstruction and arrhythmias

71
Q

Papillary fibroelastoma

A
  • incidental valvular neoplasm

- hairlike projection on valve surface

72
Q
  • gray myocardial mass protruding into ventricle

- spider cells on microscopy

A
  • Rhabdomyoma
  • most common primary tumor in kids
  • hamartoma assoc with tuberous sclerosis
73
Q

Most common primary malignancy in heart

A
  • angiosarcoma

- rare, deadly

74
Q

Systolic vs diastolic HF

A
  • systolic: outflow weakness
    > co preserved at rest
  • diastolic: decreased volume capacity and contraction
    > typically fibrotic
75
Q

Common Etiology of left ventricular hypertrophic cardiomyopathy (3)

A
  • myosin B-chain binding protein
  • myosin binding protein C
  • troponin C
76
Q

Cyanosis at an early age

A
  • usually a result if right to left shunting
    > ToF, truncus arteriosis, coarctation (anything that causes early r vent hypertrophy)
    >ASDs, VSDs commonly cause right to left shunting
77
Q

Most common cause of fibrinous pericarditis

A
  • renal failure
78
Q

Right Ventricular Dilation without hypertrophy

A

Cor pulmonale

79
Q

Notched ribs in X-ray

A
  • coarctation of the aorta
  • associated with bicuspid aortic valve
  • not assoc. with PDA
80
Q

Virulent endocarditis with trisucpid vegetations

A
  • s. aureus from IV drug use
81
Q

Restrictive endocarditis causes

A
  • sarcoidosis, amyloid

- endocardio fibroelastosis (in kids)

82
Q

Mid systolic click

A
  • indicating the valve balloons backwards due to myxoid degeneration in the middle of systole
83
Q

Restrictive cardiomyopathy with eosinophilia

A

Lauffler syndrome

84
Q

Onset of chest pain 2-10 weeks after MI

A
  • fibrinous pericarditis

- potentially autoimmune dresser syndrome

85
Q

Amyloids

A

AA: acute phase (amyloidosis 2nd to RA) speckling
AF: familial (single organ, no PMH)
AL: light chain (MM)
A cal: calcitonin (assoc with medullary carcinoma)

Cardio (14 decks)

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