Cardiac Pathology (Pathoma) Flashcards
Stable angina
Chest pain that arises w/ exertion or emotional stress.
Due to atherosclerosis of coronary arteries w/ > 70%
Represents reversible injury (cellular swelling) to myocytes.
Presents w/ chest pain ( amt of time myocardium can withstand lack of blood flow) that radiates to the left arm or jaw. Diaphoresis. Shortness of breath.
Subendocardial ischemia. Shows ST segment depression.
Relieved by rest or nitroglycerin (decrease preload)
Unsatble angina
Chest pain occurs at rest (or w/ less exertion)
Due to the formation of a thrombosis which partially** blocks coronary artery.
Reversible injury to myocytes.
ST depression
Relieved by Nitro
High risk of progression to MI (part of acute coronary syndrome)
Prinzmetal angina
Due to coronary artery vasospasm that leads to episodic chest pain unrelated to exertion.
Represents reversible injury
ST elevation due to transmural ischemia.
Nitro or Ca blockers relieve sx.
Myocardial Infarction
Necrosis of cardiac myocytes.
Classically due to thrombosis and *complete occlusion of the coronary artery.
Other causes include coronary artery vasospasm (prizmetal’s >20 min), emboli, and vasculitis (Kawasaki)
Presents w/ severe crushing chest pain (>20 minutes) that radiates to the left arm or jaw. Diaphoresis. Dyspnea. Symptoms not relieved by Nitro.
Usually involves the Left Vent. LAD>RCA>Left circumflex
Initial phase - subendocardial necrosis (ST depression).
Will progress to transmural (STEMI)
Test for elevated cardiac enzymes (leaking of enzymes due to membrane damage = irreversible injury)
Troponin I is most sensitive and specific marker. Rises 2-4hrs post infarction. Peaks at 24 hrs. Returns to normal by 7-10 days.
CK-MB is useful for detecting reinfarction. Rises in 4-6 hrs and peaks at 24. Returns to n ormal by 72 hours.
Rx is ASA/heparin. Supplemental 02. Nitrates. B-blocker. ACEI.
Fibrinolysis or angioplasty(preferred). Can cause contraction band necrosis due to repurfusion post MI.
MI in LAD
Affects anterior wall of LV and anterior IV septum
MI in RCA
Affects posterior LV wall and posterior IV septum. Feeds papillary muscle –> highest risk for papillary muscle rupture in RCA MI.
MI in Left Circumflex
Affects lateral wall of LV.
Troponin I
Most sensitive and specific marker. Rises 2-4hrs post infarction. Peaks at 24 hrs. Returns to normal by 7-10 days.
CK-MB
Useful for detecting reinfarction. Rises in 4-6 hrs and peaks at 24. Returns to n ormal by 72 hours.
Contraction band necrosis
Repurfusion post MI. Returning blood flow –> large return of calcium –> large contraction of dead cells
Repurfusion injury
ROS futher injury the myocardium.
Classically seen if cardiac markers continue to rise post angioplasty.
MI complications
Gross changes = none
Microscopic changes = none
Complications - cardiogenic shock (massive infarction), CHF, and arrhythmia (MCC of death)
MI complications 4-24 hrs.
Gross = dark discoloration
Micro = coagulative necrosis (loss of nucleus –> pyknosis, karryolexis, karryolisis)
Complications - arrhythmia
MI complications 1-3 days
Gross = yellow pallor
Micro = neutrophils
Complications - fibrinous pericarditis (chest pain w/ friction rub –> can only occur in transmural infarction!)
MI complications 4-7 days
Gross = yellow pallor
Micro = macrophages
Complications - rupture of ventricular free wall (tamponade), IV septum rupture (shunt), or papillary muscle (mitral insufficiency. Esp in RCA MI.)
MI complicatiopns 1-3 weeks
Gross = red border emerges as granulation tissue enters from edge of infarct
Micro = granulation tissue w/ plump fibroblasts, collagen, and blood vessels
Months
Gross = white scar made of type I collagen
Micro = fibrosis
Complications = aneurysm (not as strong), mural thrombus (not as contractile –> stasis –> thrombus), or dressler syndrome (AI pericarditis)
Progression of Microscopic MI
1 Day - 1 Week - 1 Month
1 day of coagulative necrosis —> 1 week of inflammation (nphils –> macrophages) –> granulation tissue from one week to one month –> scar
Sudden cardiac death
Unexpected death due to cardiac disease
Occurs w/o sx or
Chronic Ischemic Heart Disease
Poor myocardial function due to chronic ischemic damage (with or without infarction)
Progresses to CHF
Left sided heart failure
Failure of the pump
Causes: Ischemia, HTN (hypertrophy –> ischemic damage) , dilated CM (stretched muscle = less contractile) , MI, restrictive CM (can’t fill)
Pulmonary conjestion is key clinical problem. Pulmonary edema w/ dyspnea, PND, orthopnea, and crackles.
Heart-failure cells (hemosiderin laden macrophages) in lungs.
Decreased forward perfusion –> activation of RAAS –> fluid overload and increased TPR –> positive feedback.
Mainstay of treatment is ACEI to lower TPR and fluid.
Right-sided heart failure
MCC is Left sided heart failure.
Other causes: L-R shunt and chronic lung disease (cor pulmonale)
Clinical features: JVD, painfuls H/Smegaly (may lead to cardiac cirrhosis), dependent pitting edema.
Cardiac Congenital Defects
Usually arise in embryogenesis from weeks 3-8.
Seen in 1% of live births.
Most are sporadic.
VSD
Defect in septum
MC congenital heart defect
*Associated w/ FAS.
Can be asx if small.
If large –> eventual pulmonary HTN –> reversal (Eisenmenger’s syndrome) –> cyanosis.
Rx: Surgery if symptomatic/larger
ASD
Defect usually from ostium secundum. Ostium primum type is associated w/ Downs*.
Presents w/ L–>R shunt w/ fixed split of S2.
Can cause paradoxical emboli.
PDA
Failure of DA to close.
*Associated w/ congenital rubella
Asx at birth w/ holocystolic “machine-like” murmur.
**Cyanosis in lower extremity later in life in Eisenmenger syndrom –> PDA attaches to aorta after the great vessels
Rx: Indomethacin
Tetrology of Fallot
4 problems: 1. Pulmonary Stenosis, 2. VSD. 3. Overriding aorta on VSD 4. RVH
R–>L shunt.
Stenosis is key for degree of shunting.
Kids become very cyanotic when exercising (relieved by squatting –> increase arterial pressure –> decrease shunting)
*Boot shaped heart on CXR
Transposition of Great Vessels
Separate circuits that don’t mix. Early cyanosis. Only survival if can create L–>R shunt (i.e. give prostaglandins and/or create ASD)
**Associated w/ maternal diabetes
Trunctus Arteriosis
One large vessel arising from both vessels. Due to truncus failing to divide.
Early cyanosis
Tricuspid Atresia
Tricuspid valve fails to develop
RV is hypolastic
Associated w/ ASD resulting in R–>L shunt
Presents w/ early cyanosis
Coarctation of aorta
Infantile Form:
Associated w/ PDA. Coarctation lies distal to aortic arch, but proximal to PDA (low pressure after block –> allows blood from PDA to enter descending aorta
Presents w/ lower extremity cyanosis
*Associated w/ Turner Syndrome
Adult form:
Coarctation lies distal to arch (not associated w/ PDA).
HTN in upper extremities and hypotension in lower extremities.
Associated w/ bicuspid aortic valve.
*Collateral circulation develops across intercostal arteries (enlarged and notching of ribs)
Acute Rheumatic Fever
Systemic complication of pharyngitis due to group A B-hemolytic strep
Affects children 2-3 weeks post strep throat
*Caused by molecular mimicry; bacterial M protein resembles human tissue. (Type II HS)
Diagnosis based on Jones criteria:
1.)Evidence of prior strep infection (ASO or anti-DNase B titer)
2.) Minor criteria (fever and elevated ESR)
3.) Major criteria:
J- Joint problems (migratory polyarthritis)
O- Heart problems (draw O as heart). Inflammation of all 3 layers of heart
N - Nodules
E - Erythema marginatum (rash that is more red at margins)
S - Sydenham’s Chorea
- Key long term sequelae are due to heart (pancarditis). 1.)Endocarditis –> vegetation on mitral valve (can involve aortic as well). –> regurge early, stenosis late.
2. ) *Myocarditis –> presence of Aschoff bodies (focus of chronic inflammation w/ Nischow cells (histiocytes w/ catepllar nucleus). MCC of death in acute phase.
3. ) Pericarditis –> frictrion rub
Acute attack resolves, but many cases become chronic disease.
Repeat exposure to strep –> relapse of acute phase. Increases the risk of valvular disease.
Can result in scarring of mitral valve –> mitral stenosis (thickening of chordae tendinae and cusps w/ **fusion of commisures) AKA fishmouth appearance of valve.
Ocasionally involves aortic valve –> fusion of commisures.
Key complication is endocarditis (Strep. mutans)
Aortic stenosis
Usually due to calcification and fibrosis (wear and tear)
Presents in late adulthood (
Aortic Regurgitation
MC arises due to isolated root dilatation. Can occur secondary to syphillitic aortic aneurysm. Or valve damage (I.e. infectious endocarditis –> valve damage)
Clinical features: Early, blowing, diastolic murmur. Bounding pulses, pulsating nail bed, headbobbing, Wide pulse pressure. (Increased SV and regurge)
LV dilitation and eccentric hypertrophy
Rx: is valve replacement when LV HF begins.
Mitral Valve Prolapse
Ballooning of MV into LA during sytole
Due to myxoid degeneration in valve making it floppy
Etiology is unknown; More common in Marfan’s and EDS.
Presents w/ mid-systolic click followed by regurge murmur; usually asymptomatic
Rare complications include: IE, Arrhythmia, severe mitral regurge.
Rx: is valve replacement when complications occur.
Mitral Regurgitation
Usually arises as a complication of MVP
Other causes include LV dilation, IE, acute rheumatic heart disease, and papillary muscle post RCA MI.
Clincally: Holosytsolic blowing murmur that gets louder w/ squatting or expiration.
Mitral stenosis
Usually doe to chronic rheumatic valve disease
Clinically: Opening snap w/ diastolic rumble.
Volume overload leads to dilitation of LA –> pulmonary congestion; pulmonary HTN; A fib.
Also dysphagia (esophagus) and hoarseness (left recurrent laryngeal nerve) due to LA being most posterior chamber.
Strep viridans
MC overall cause of IE
Low-virulence organism; infects previously damaged valves.
Results in small vegetations that do not destoy valve.
Pathogenesis - damaged endocardial surface –> thrombotic vegetations (platelets and fibrin) –> transient bactermia (dental procedure) –> trapping of bacteria in vegetations.
S. aurues
MCC in IV drug-use
High-virulence –> infects normal valves (tricuspid)
Large vegetations that destroy valve (acute endocarditis)
S. epidermidids
Endocarditis in prostetic valves
Strep bovis
Endocarditis in patients w/ underlying CRC.
HACEK Organisms
Endocarditis w/ negative blood cultures.
Hemophilus Actinobacillus Cardiobacterium Eikinella Kingella
Infectious Endocarditis
Clinically presents w/ fever, murmur , septic emboli can cause Janeway lesions (painless on palms and soles) Osler nodes (painful on fingers and toes –> ouch ouch osler), splinter hemorrhages , anemia of chronic disease.
Laboratory features: Positive blood cultures (spaced), AOCD (microcitic secondary to hepcidin) , TEE is useful for detecting lesions on valves.
Nonbacterial throbotic endocarditis
Sterile vegetations that arise w/ hypercoaguable state or underlying adenocarcinoma.
Vegetations arise on mitral valve and result in regurge
Libmann Sachs Endocarditis
LSE w/ SLE
Sterile
*Vegetations on both sides of mitral valve (results in mitral regurge)
Dilated Cardiomyopathy
Dilation of all 4 chambers resulting in sytolic dysfunction leading to biventricular CHF
Complications include mitral and tricuspid regurge and arrhytmia.
MCC of cardiomyopathy
MC is idiopathic
Can be due to genetic mutation, myocarditis (coxsackie virus), alcohol abuse (and thiamine deficiency), drugs, *pregnancy
Rx = transplant
Hypertrophic Cardiomyopahty
Massive hypertrophy of the LV. Preferrentially in septum.
Due to genetic mutations in **sarcomere proteins (most commonly AD)
Decreased CO. Diastolic dysfunction.
Sudden death due to ventricular arrhythmias; common cause of sudden death in young athletes
Syncope w/ exercise
*Biopsy shows myofiber hypertrophy w/ dissarray
Restrictive CM
Decreased compliance of ventricular endomyocardium
Restricts filling during diastole
Causes: amyloidosis, sarcoidosis, Hemochromatosis, Endocardial fibroelastosis (children), Loeffler syndrome (eosinophilc infiltrate)
Presents w/ CHF w/ low voltage EKG and Diminished QRS amplitudes
Myxoma
Mesenchymal proliferation w/ a gelatinous appearance.
Abundant ground substance on histo
MC primary cardiac tumor in adults
MC is pedunculated (off a stalk) mass in LA causing syncope due to blocking of mitral valve.
Rhabdomyoma
Benign hamartoma of cardiac muscle.
MC primary cardiac tumor in children; **Associated w/ tuberous sclerosis.
Usually arises in ventricle
Metastasis
More common than primary tumor
Common metastasis include: breast, lung, melanoma, and lymphoma
MC involves pericardium resulting in exudative pericardial effusion
