Cardiac Pathology Flashcards
Condition resulting from chronic ischemia and mitral insufficiency
- myocytes laid in series
- volume overload hypertrophy
- ventricular walk may or may not increase: ventricular dilation does occur
Condition resulting from HTN and/or aortic stenosis
Cardiac pressure overload hypertrophy
- new sacromeres laid in parallel to long axis
- aka concentric hypertrophy
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
- left side heart failure
Results in Chronic pulmonary hypertension (cor pulmonale)
Most commonly caused by left sided heart failure
Results in congestive hepatosplenomegaly, plural effusion, dependent peripheral edema
Right sided heart failure
- plural effusion: venous drainage backs up
Ischemic heard disease
- hypoxia + inadequate metabolite delivery + inadequate waste removal
- leading COD in us
- may result from fixed coronary lesion, acute plaque change, coronary artery thrombosis, vasoconstriction
Fixed coronary artery lesion
- up to 50% often subclinical
- 70~75% occlusion = stable angina
- 90% occlusion = unstable angina
- most commonly proximal LAD, then proximal LCX and RCA
Ischemic zones of coronary occlusion
- 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
Coronary artery thrombus (occlusive, non-occlusive)
- occlusive: can cause trans mural infarction
- non-occlusive: subendocardial, unstable angina, distal embolization and micro infarcts
Four syndromes of ischemic heart disease
- angina pectoris
- myocardial infarction
- sudden cardiac death
- chronic ischemic heart disease
Angina pectoris: 3 types
- stable angina: relieved by rest or nitro
- prinzmetal variant angina: vasospasm, transient
- unstable angina: caused by ruptured mural thrombus
Myocardial infarction process
- 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
Infarction process
- from endocardium outward
- healing happens from outside in (blood supply richer closer to coronaries)
- exception is proximal infarct extension
Mechanisms of infarct extension
- thrombus propagating proximally
- proximal vaso spasm
- impaired myocardial contractility
- platelet fibrin micro emboli
- arrythmias
Transmural infarct
- full thickness: more common
- typically caused by acute plaque change
- can occur for vasospasm (eg in cocaine use)
- ST elevation MI
Subendocardial infarction
- ST depression
- may be lysed thrombus, or hypotension in diffuse sclerosing athersclerosis
- circumferential infarct
MI gross tissue changes
- 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
Microscopic changes of necrosis
- 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)
Complications of MI
- contractile dysfunction (heart failure)
- arrhythmias
- myocardial rupture (3-7 days) -> tamponade
- pericarditis
- papillary dysfunction -> regurgitation
Reperfusion injury
- generation of free radicals from oxygen introduced to neutrophils
- inflammation around vessels can function poorly decreasing heart function
MI prognosis
- size and location
- large = bad
- transmural = bad
- anterior = bad
- posterior can result in arrhythmias and RV infarcts
MI labs
- 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
Valvular disease
- stenosis
- insufficiency
Mitral stenosis etiology
- rheumatic heart disease
Mitral insufficiency
- mostly due to myxomatous valvular degeneration
- may be calcification, rheumatic, endocarditis, chordae rupture
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
Aortic insufficiency
- mostly aortic root dilation from HTN/old
- may be endocarditis, myxomatous
Calcified congenital bicuspid aortic valve
- dystrophic calcification earlier than 70
- midline raphe on larger cusp
- no valve commissural fusion
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
- 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
Sequelae of GAStrep pharyngitis (10 days - 6 weeks)
- children 5-15
ARF
Joints: migratory painful polyarthritis
s chorea:
- criteria for diagnosing ARF 2* to GAS infxn
Bread and butter around the heart
- resolves
Myocarditis: Ashoff bodies with anitschcow cells and necrotic collagen
- ARF pancarditis
Verrucae on mitral and aortic valves
Fibrinoid necrosis of cusps and chordae
Vavulitis 2* to ARF pancarditis
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
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
Etiology native valve endocarditis
- s. aureus
Prosthetic valve endocarditis
- coagulate negative staph (s. saprophiticus, s. epidermidis)
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
Fever, flu like symptoms following dental procedure
- sub acute infective endocarditis (s. viridans, s. fecaelis, s. bovis)
- less destructive, good recovery with antibiotics
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
Small pink nodules of hematoxylin and fibrin on underside of valves (mainly mitral and tricuspid)
- ANAs damage DNA and for hematoxylin bodies
- SLE endocarditis
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
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
Prosthetic valve pathology
- 60% of prosthesis develop complication
- thromboemboli, anticoagulant related hemorrhage, infective endocarditis (ring endocarditis)
- bioprosthesis can develop
Three clinical cardiomyopathies
- dilated (90%) (4 chamber, young)
- hypertrophic (athlete falls dead on field)
- restrictive
Hypertrophic heart with systolic dysfunction and 4 chamber dilation
- dilated cardiomyopathy
- adults 20-50 y/o
- genetic influence less than 1/2 (AD)
Epicardial granulomas with myopathy
Dilated cardiomyopathy 2* to sarcoidosis
Vacuolar fatty change in myocytes due to membrane per oxidation
- dilated cardiomyopathy due to anthracycline use
Hemosiderin filled macs, cardiomyopathy
- dilated cardiomyopathy 2* to iron overload (hemochromatosis)
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
Wooly hair, plantopalmar keratosis, cardiomyopathy
- Naxos
- AR
- arrhythmogenic right ventricular cardiomyopathy
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
Treatment and complications for hypertrophic cardiomyopathy
- ventricular relaxation (B blocker)
- excise LV outflow obstruction
Afib, mitral valve endocarditis, cardiac failure, arrhythmias, sudden death
Morphology of hypertrophic cardiomyopathy
- thickened IV septum
- ventricular outflow obstruction
- banana ventricular cavity
- aortic outflow thickening
- anterior mitral leaflet thickening (systolic murmur)
Mild hypertrophy, biatrial dysfunction, diastolic dysfunction
- on microscopy patchy to diffuse fibrosis
Restrictive cardiomyopathy
- idiopathic, or secondary to sarcoidosis, amyloidosis, mets
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
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
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
Pericarditis
- viruses major cause, may also be bacteria
- non- infectious; SLE, ARF, scleroderma, post MI, HSN
- uremia
- neoplasms
Acute vs chronic pericarditis
- acute: serous, fibrinous, purulent/supp, hemorrhagic, caseous
- chronic: adhesive, constrictive
Non-infectious pericarditis with clear fluid that usually resolves without organization
- acute serous pericarditis
Most common form of acute pericarditis
- yellow cloudy fluid with fibrin and scant inflammatory cells
- fibrinous
- MI, uremia, radiation, ARF, trauma
- can organize
Infectious pericarditis with white exudate and lots of inflammation
- purulent/ supperative pericarditis
- typically organizes
Pericarditis typically caused by mets
Hemorrhagic,
- may also be infectious
Most frequent cause of disabling constrictive pericarditis
- caseating pericarditis 2* to TB
Delicate stringy organization of obliterated pericardium
- adhesive pericarditis
- rarely symptomatic
- adhesion to structures in mediastinum results in hypertrophy and dilation
- severely restricted CO
- obliterated pericardium organized into fiberous/calcified scar
- concretio cordis
- constrictive pericarditis reqs pericardectomy
Fibrinous pericarditis, aortic valvulitis, Rh nodules
- reheumatic heart disease
Heart tumors
- mostly mets
- primary tumors are rare
> myxoma, lipoma, papillary fibroelstoma, rhabdomyoma
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
Lipoma
- left ventricle, right atria, atrial septum
- obstruction and arrhythmias
Papillary fibroelastoma
- incidental valvular neoplasm
- hairlike projection on valve surface
- gray myocardial mass protruding into ventricle
- spider cells on microscopy
- Rhabdomyoma
- most common primary tumor in kids
- hamartoma assoc with tuberous sclerosis
Most common primary malignancy in heart
- angiosarcoma
- rare, deadly
Systolic vs diastolic HF
- systolic: outflow weakness
> co preserved at rest - diastolic: decreased volume capacity and contraction
> typically fibrotic
Common Etiology of left ventricular hypertrophic cardiomyopathy (3)
- myosin B-chain binding protein
- myosin binding protein C
- troponin C
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
Most common cause of fibrinous pericarditis
- renal failure
Right Ventricular Dilation without hypertrophy
Cor pulmonale
Notched ribs in X-ray
- coarctation of the aorta
- associated with bicuspid aortic valve
- not assoc. with PDA
Virulent endocarditis with trisucpid vegetations
- s. aureus from IV drug use
Restrictive endocarditis causes
- sarcoidosis, amyloid
- endocardio fibroelastosis (in kids)
Mid systolic click
- indicating the valve balloons backwards due to myxoid degeneration in the middle of systole
Restrictive cardiomyopathy with eosinophilia
Lauffler syndrome
Onset of chest pain 2-10 weeks after MI
- fibrinous pericarditis
- potentially autoimmune dresser syndrome
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)
