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
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
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
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
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
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
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
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
8
Q
Four syndromes of ischemic heart disease
A
- angina pectoris
- myocardial infarction
- sudden cardiac death
- chronic ischemic heart disease
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
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
11
Q
Infarction process
A
- from endocardium outward
- healing happens from outside in (blood supply richer closer to coronaries)
- exception is proximal infarct extension
12
Q
Mechanisms of infarct extension
A
- thrombus propagating proximally
- proximal vaso spasm
- impaired myocardial contractility
- platelet fibrin micro emboli
- arrythmias
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
14
Q
Subendocardial infarction
A
- ST depression
- may be lysed thrombus, or hypotension in diffuse sclerosing athersclerosis
- circumferential infarct
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
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)
17
Q
Complications of MI
A
- contractile dysfunction (heart failure)
- arrhythmias
- myocardial rupture (3-7 days) -> tamponade
- pericarditis
- papillary dysfunction -> regurgitation
18
Q
Reperfusion injury
A
- generation of free radicals from oxygen introduced to neutrophils
- inflammation around vessels can function poorly decreasing heart function
19
Q
MI prognosis
A
- size and location
- large = bad
- transmural = bad
- anterior = bad
- posterior can result in arrhythmias and RV infarcts
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
21
Q
Valvular disease
A
- stenosis
- insufficiency
22
Q
Mitral stenosis etiology
A
- rheumatic heart disease
23
Q
Mitral insufficiency
A
- mostly due to myxomatous valvular degeneration
- may be calcification, rheumatic, endocarditis, chordae rupture
24
Atrial stenosis
- 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
25
Aortic insufficiency
- mostly aortic root dilation from HTN/old
| - may be endocarditis, myxomatous
26
Calcified congenital bicuspid aortic valve
- dystrophic calcification earlier than 70
- midline raphe on larger cusp
- no valve commissural fusion
27
Condition in older women or patients with myxomatous mitral valve or elevate LV pressure
- degenerative calcification of mitral ring
Mitral annular calcification
| - can increase risk of infectious endocarditis
28
- condition evidenced by mid-systolic click
| - women > men, 20-40 y/o 3% of us pop
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
29
Sequelae of GAStrep pharyngitis (10 days - 6 weeks)
| - children 5-15
ARF
30
Joints: migratory painful polyarthritis
| s chorea:
- criteria for diagnosing ARF 2* to GAS infxn
31
Bread and butter around the heart
- resolves
Myocarditis: Ashoff bodies with anitschcow cells and necrotic collagen
- ARF pancarditis
32
Verrucae on mitral and aortic valves
| Fibrinoid necrosis of cusps and chordae
Vavulitis 2* to ARF pancarditis
33
Fused valve commissures (fish mouth), mostly mitral valve (can involve the aortic and rarely tricuspid
- fused thickened cordae
- chronic rheumatic heart disease
| - results in stenosis most commonly
34
Etiology of infectious endocarditis
- 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
Etiology native valve endocarditis
- s. aureus
36
Prosthetic valve endocarditis
- coagulate negative staph (s. saprophiticus, s. epidermidis)
37
Eroding Vegitations forming ring abcesses presenting in pt with Osler nodes (painful) and janeway lesions (non-painful)
- acute infective endocarditis (s. aureus, s. epi)
| - nodules are fibrinoid and neutrophil laden
38
Fever, flu like symptoms following dental procedure
- sub acute infective endocarditis (s. viridans, s. fecaelis, s. bovis)
- less destructive, good recovery with antibiotics
39
Small non-destructive sterile vegetations of fibrin and platelets along valve closure lines
Non-bacterial thrombotic endocarditis
| - in PTs who are hypercoagulable: cancer, high estrogen, burns, sepsis
40
Small pink nodules of hematoxylin and fibrin on underside of valves (mainly mitral and tricuspid)
- ANAs damage DNA and for hematoxylin bodies
- SLE endocarditis
41
4 types of valvular vegetations
- 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
Murmur + flushing, cramps, nausea, vomiting, diarrhea
- carcinoid heart disease
- serotonin producing tumor
- right sided valvular leflet and mural intimal smooth muscle and collagen proliferation - stenosis/insufficiency
43
Prosthetic valve pathology
- 60% of prosthesis develop complication
- thromboemboli, anticoagulant related hemorrhage, infective endocarditis (ring endocarditis)
- bioprosthesis can develop
44
Three clinical cardiomyopathies
- dilated (90%) (4 chamber, young)
- hypertrophic (athlete falls dead on field)
- restrictive
45
Hypertrophic heart with systolic dysfunction and 4 chamber dilation
- dilated cardiomyopathy
- adults 20-50 y/o
- genetic influence less than 1/2 (AD)
46
Epicardial granulomas with myopathy
Dilated cardiomyopathy 2* to sarcoidosis
47
Vacuolar fatty change in myocytes due to membrane per oxidation
- dilated cardiomyopathy due to anthracycline use
48
Hemosiderin filled macs, cardiomyopathy
- dilated cardiomyopathy 2* to iron overload (hemochromatosis)
49
Arrhythmogenic right ventricular cardiomyopathy
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
Wooly hair, plantopalmar keratosis, cardiomyopathy
- Naxos
- AR
- arrhythmogenic right ventricular cardiomyopathy
51
Left ventricular hypertrophy, systolic dysfunction and left ventricular obstruction
- sudden death in athletes
- may has dyspnea on exertion
Condition and etiology
- "floppy cow heart" hypertrophic cardiomyopathy
- AD inheritance
- B-myosin heavy chain mutation (most common)
- myosin binding protein C
- troponin C
52
Treatment and complications for hypertrophic cardiomyopathy
- ventricular relaxation (B blocker)
- excise LV outflow obstruction
Afib, mitral valve endocarditis, cardiac failure, arrhythmias, sudden death
53
Morphology of hypertrophic cardiomyopathy
- thickened IV septum
- ventricular outflow obstruction
- banana ventricular cavity
- aortic outflow thickening
- anterior mitral leaflet thickening (systolic murmur)
54
Mild hypertrophy, biatrial dysfunction, diastolic dysfunction
- on microscopy patchy to diffuse fibrosis
Restrictive cardiomyopathy
| - idiopathic, or secondary to sarcoidosis, amyloidosis, mets
55
Most frequent cause of restrictive cardiomyopathy
- wax drip atrial nodules
- firm rubbery endocardium
- Congo red and apple green biferingience
Amyloidosis
- transthyretin deposits: senile cardiac amyloidosis
- ANP amyloid deposits in atria: isolated atrial amyloidosis
- systemic amyloidosis: worst case
56
Infectious myocarditis
- 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
Non- infections myocarditis
- drug hsn: Abx, diuretics, antiHTNs (eosinophil infiltrate)
- immune mediated: SLE, ARF, transplant rejection
- sarcoidosis
- giant cell (poor prognosis) giant cells and extensive necrosis
58
Pericarditis
- viruses major cause, may also be bacteria
- non- infectious; SLE, ARF, scleroderma, post MI, HSN
- uremia
- neoplasms
59
Acute vs chronic pericarditis
- acute: serous, fibrinous, purulent/supp, hemorrhagic, caseous
- chronic: adhesive, constrictive
60
Non-infectious pericarditis with clear fluid that usually resolves without organization
- acute serous pericarditis
61
Most common form of acute pericarditis
| - yellow cloudy fluid with fibrin and scant inflammatory cells
- fibrinous
- MI, uremia, radiation, ARF, trauma
- can organize
62
Infectious pericarditis with white exudate and lots of inflammation
- purulent/ supperative pericarditis
| - typically organizes
63
Pericarditis typically caused by mets
Hemorrhagic,
| - may also be infectious
64
Most frequent cause of disabling constrictive pericarditis
- caseating pericarditis 2* to TB
65
Delicate stringy organization of obliterated pericardium
- adhesive pericarditis
- rarely symptomatic
- adhesion to structures in mediastinum results in hypertrophy and dilation
66
- severely restricted CO
| - obliterated pericardium organized into fiberous/calcified scar
- concretio cordis
| - constrictive pericarditis reqs pericardectomy
67
Fibrinous pericarditis, aortic valvulitis, Rh nodules
- reheumatic heart disease
68
Heart tumors
- mostly mets
- primary tumors are rare
> myxoma, lipoma, papillary fibroelstoma, rhabdomyoma
69
Most common primary heart tumor, variable presentation but classically currant jelly
Myxoma
- usually in L atria near foramen ovale
- may obstruct
- histo: myxomatous cells in mucopolysaccharide matrix
70
Lipoma
- left ventricle, right atria, atrial septum
| - obstruction and arrhythmias
71
Papillary fibroelastoma
- incidental valvular neoplasm
| - hairlike projection on valve surface
72
- gray myocardial mass protruding into ventricle
| - spider cells on microscopy
- Rhabdomyoma
- most common primary tumor in kids
- hamartoma assoc with tuberous sclerosis
73
Most common primary malignancy in heart
- angiosarcoma
| - rare, deadly
74
Systolic vs diastolic HF
- systolic: outflow weakness
> co preserved at rest
- diastolic: decreased volume capacity and contraction
> typically fibrotic
75
Common Etiology of left ventricular hypertrophic cardiomyopathy (3)
- myosin B-chain binding protein
- myosin binding protein C
- troponin C
76
Cyanosis at an early age
- 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
Most common cause of fibrinous pericarditis
- renal failure
78
Right Ventricular Dilation without hypertrophy
Cor pulmonale
79
Notched ribs in X-ray
- coarctation of the aorta
- associated with bicuspid aortic valve
- not assoc. with PDA
80
Virulent endocarditis with trisucpid vegetations
- s. aureus from IV drug use
81
Restrictive endocarditis causes
- sarcoidosis, amyloid
| - endocardio fibroelastosis (in kids)
82
Mid systolic click
- indicating the valve balloons backwards due to myxoid degeneration in the middle of systole
83
Restrictive cardiomyopathy with eosinophilia
Lauffler syndrome
84
Onset of chest pain 2-10 weeks after MI
- fibrinous pericarditis
| - potentially autoimmune dresser syndrome
85
Amyloids
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)
