Terms in this set (97)
Ischemic heart disease is usually due to ___ of coronary arteries.
Dx: Chest pain that arises w/ exertion or emotional stress. Due to atherosclerosis of coronary arteries > 70% stenosis.
STABLE angina = reversible injury to myocytes
Chest pain (<20 min) radiates L arm or jaw
EKG for stable angina?
ST-segemnt depression (subendocardial ischemia)
Stable angina symptoms are relived by?
Rest or Nitroglycerin (vasodilator veins, dec preload heart, dec stress heart)
Chest pain occurs at rest
Due to rupture of atherosclerotic plaque w/ thrombosis + incomplete occlusion of a coronary artery
UNSTABLE angina = reversible injury to myocytes
EKG findings Unstable angina?
Unstable angina is relived by?
Unstable angina is high risk of progression to ___.
Prinzmetal angina is due to ___.
Coronary artery VASOSPASM
Episodic chest pain unrelated to exertion?
Prinzmetal angina = reversible injury to myocytes
EKG shows what for Prinzmetal angina?
ST-segment elevation due to TRANSMURAL ischemia
Prinzmetal angina is relived by ___ or ___.
Nitroglycerin or Ca2+ channel blockers
What causes MI?
Necrosis cardiac myocytes
Due to RUPTURE of atherosclerotic plaque q/ thrombosis + COMPLETE occlusion of coronary artery
Other causes: coronary artery vasospasm, emboli, vasculitis (Kawasaki's disease)
Clinical features MI
Severe crushing chest pain (> 20 min) that radiates to L arm or jaw
Symptoms not relived by Nitroglycerin
MI usually involved which side of the heart and which parts are usually spared?
LV involved (1st involved LAD usually, 2nd involved RCA, LCX)
Spares = RV + both atria
Initial phase of an MI
SUBendocardial necrosis involving < 50% of myocardial thickness
EKG ST-segment depression
Which marker is the most sensitive and specific marker for MI?
Rises 2-4 hours after infarction
Peaks at 24 hours
Returns to normal by 7-10 days
___ is useful for detecting reinfaction days after MI.
Rises 4-6 after infection
Peaks at 24 hours
Return to normal by 72 hours
Tx for MI
1. ASA/heparin (limit thrombosis)
2. Supplemental O2 (minimize ischemia)
3. Nitrates (dilate veins, DEC preload, DEC stress)
4. B-blocker (DEC HR, DEC arrhythmia)
5. ACE inhibitor
More definitive tx MI?
Fibrinolysis or angioplasty can cause:
1. Contraction band necrosis
2. Reperfusion injury (O2 can make free radicals can further injure the myocardium)
What are the microscopic changes, gross changes and complications MI < 4 hours?
NONE = micro, gross
Cardiogenic SHOCK (massive infection), CHF, arrhythmia
What are the microscopic changes and complications MI 4-24 hours?
Gross = DARK discoloration
Micro = Coagulative necrosis
What are the microscopic, gross changes and complications MI 4-7 days?
Gross = YELLOW pallor
Micro = MACROPHAGES
1. Ventricular free wall lead to cardiac tamponade
2. Inter ventricular septum (leads to shunt)
3. Papillary muscle (leads to mitral insufficiency = occlusion of RCA)
What are the microscopic, gross changes and complications MI 1-3 weeks?
Gross = RED border emerges as granulation tissue enters from edge of infarct
Micro = Granulation tissue w/ plump fibroblasts, collagen, + blood vessels
What are the microscopic, gross changes and complications MI months?
Gross = WHITE scare
Micro = FIBROSIS (type I collagen)
2. Mural thrombus
3. Dressler syndrome (pericarditis autoimmune phenomenon antibodies against own pericardium 6-8 weeks after MI)
What are the microscopic, gross changes and complications MI 1-3 days?
Gross = Yellow pallor
Micro = Neutrophils
Fibrinous pericarditis presents chest pain w/ friction rub (transmural infarction)
What is sudden cardiac death and when does it occur?
What causes this?
Unexpected death due to cardiac disease
Occurs w/o symptoms or < 1 hour after symptoms arise
Due to FATAL VENTRICULAR ARRHYTHMIA
Most common etiology of Sudden death/
ACUTE ischemia = 90% of pts have preexisting severe atherosclerosis
Less common cause include mitral valve relapse, cardiomyopathy, + cocaine abuse
What happens in chronic ischemic heart disease?
1. Poor myocardial fxn
2. Due to chronic ischemic damage (w or w/o infarction)
3. Progreses to CHF
What are some causes of L side failure?
L sided heart failure symptoms?
Pulmonary edema w/ Dyspnea
PND (paroxysmal nocturnal dyspnea)
Heart-failure cells = hemosiderin-laden macrophages in alveoli of pts w/ L sided heart failure
L sided heart failure leads to decreased forward perfusion which activates? What is the mainstay of tx?
Activation renin-angiotensin system
Tx = ACE inhibitor
Right sided heart failure is most commonly due to ___.
other causes L to R shunt + chronic lung disease (cor pulmonale)
Clinical features of R sides HF?
Painful HSM (hepatospenomegaly), may lead to cardiac cirrhosis
Dependent pitting edema
What affects children 2-3 weeks after strep throat?
Acute Rheumatic fever
What pathogen causes Acute Rheumatic fever?
Systemic complication of pharyngitis due to group A Beta-hemolytic streptococci
Acute Rheumatic Fever virulence factor?
Caused by MOLECULAR MIMICRY
Bacterial M protein resembles human tissues
How is Rheumatic fever diagnosed?
1. Evidence of prior group A B-hemolytic strep infection (ASO or anti-DNase B titer)
2. Minor criteria (fever + elevated ESR)
3. Major criteria
JONES Mnemonic stands for in Rheumatic fever diagnosis?
J = Joint
O = Heart problems (all layers = mitral endocarditis + aortic)
N = Nodules skin (subcutaneous)
E = Erythema marginatum
S = Sydenham choreas
Aschoff bodies present in?
Rheumatic fever = myocardium
Aschoff bodies = giant cells, chronic inflammation made collagen
Anitschkow cells are pathognomonic for?
Infective endocarditis due to rheumatic disease
___ is the most common cause of death during the acute phase of rheumatic disease.
Chronic rheumatic valve disease results in?
Stenosis (fish valve appearance valve) = Mitral valve, leads to thickening of chordae tendineae + cusps
Occasionally involved aortic valve = fusion commissures
Aortic stenosis the aortic orifice becomes < __ cm2
1 cm (normal 4)
Aortic stenosis causes?
Usually due to fibrosis + calcification from "wear and tear"
Late adulthood > 60
What can INK risk for aortic stenosis and hasten disease onset?
BICUSPID aortic valve INC risk and hastens disease onset
Compensation for aortic stenosis leads to?
1. Prolonged asymptomatic stage
2. Systolic ejection click followed by a crescendo-decrescendo murmur
Complications of Aortic stenosis
1. Concentric LV hypertrophy
2. Angina + syncope w/ exercise
3. Microangiopathic hemolytic anemia
Tx aortic stenosis
Valve replacement after the onset of complications only
What is the back flow of blood from aorta into LV during diastole called?
Aortic regurgitation causes?
Aortic root dilation (syphilic aneurysm)
Valve damage (IE = infectious endocarditis)
Clinical features aortic regurgitation?
Early, blowing Diastolic murmur
Pulsating nail bed
Head bobbing (HYPERdynamic circulation)
LV dilation + eccentric hypertrophy
Tx aortic regurgitation
Valve replacement when LV dysfunction develops
Ballooning of mitral valve into LA during systole.
Mitral valve prolapse
Causes Mitral valve prolapse
Due to myxoid degeneration in valve making it floppy
Etiology unknown, may be seen in MARFAN + EDS (Ehlers-Danlos syndrome)
Clinical features Mitral valve prolapse?
Mid-systolic click followed by regurgitation murmur; usually asymptomatic
Complications Mitral valve prolapse
Severe mitral regurgitation
Tx mitral valve prolapse
Reflex of blood from LV into LA during systole.
___ arises as a complication of Mitral valve prolapse.
Causes of Mitral Regurgitation
Acute rheumatic heart disease
Papillary muscle rupture after MI
Clinical features Mitral Regurgitation
Holosystolic "blowing" murmur
Louder w/ SQUATTING + EXPIRATION
Results in volume OVERLOAD + L-sided Heart failure
Narrowing of mitral valve orifice = mitral stenosis is usually due to?
Chronic Rheumatic valve disease
Acute Rheumatic HD causes mitral ___.
Chronic Rheumatic HD cause mitral___.
Acute = Mitral Regurgitation
Chronic = Mitral Stenosis
Clinical features of Mitral Stenosis
Opening snap followed by Diastolic RUMBLE
Complications of Mitral Stenosis due to volume overload leading to dilatation of the LA.
Atrial fibrillation w/ associated risk for mural thrombi
Inflammation of endocardium that lines the surface of cardiac valves?
Infectious endocarditis (inner surface heart) = usually due to bacterial infection
What is the most common cause of overall endocarditis?
S. viridans = low virulence organism infects perviously damaged valves
Small vegetations result that do not destroy valve
Pathogenesis of S. viridans in infectious endocarditis.
Damaged endocardial surface develops thrombotic vegetations (platelets + fibrin)
Transient bacteremia leads to trapping of bacteria in vegetations
Pts. dental procedures given Penicillin to reduce risk of endocarditis
Most common cause of infectious endocarditis in IV drug-abuse.
S. aureaus = high virulence organism; infects normal valves (tricuspid)
Large vegetations that destroy valve (acute endocarditis)
___ causes endocarditis of prosthetic valves.
__ endocarditis in pts w/ underlying colorectal carcinoma.
Which HACEK organisms can cause endocarditis w/ negative blood cultures.
H = Hemophilus
A = Actinobacillus
C = Cardiobacterium
E = Eikenella
K = Kingella
Clinical features of infective endocarditis?
Osler nodes (painful lesions fingers + toes)
Anemia of chronic disease
Lab findings infective endocarditis?
Positive blood cultures
Anemia of chronic disease
TEE is useful for detecting lesions on valves
Sterile vegetations that arise w/ hyper coagulable state or underlying adenocarcinoma.
Nonbacterial thrombotic endocarditis
Where do the vegetations arise in nonbacterial thrombotic endocarditis.
Mitral valve along lines of closure and result in regurgitation
Sterile vegetations associated with SLE?
Where are the vegetations present in Libman-Sacks Endocarditis.
Mitral valve both sides surface and undersurface => results in mitral regurgitation
Dilatation of all four chambers of the heart and is the most common form of cardiomyopathy.
Dilated Cardiomyopathy results in ___ dysfunction leading to _____ CHF
Complications of Dilated Cardiomyopathy
Mitral + tricuspid valve regurgitation + arrhythmia
Most commonly Dilated Cardiomyopathy causes?
Genetic mutation (autosomal
Drugs (Doxorubicin, cocaine)
Pregnancy (later preggers or soon after childbirth)
Tx of Dilated cardiomyopathy
Hypertrophic cardiomyopathy is massive hypertrophy of ____. Due to ___.
Genetic mutations in SARCOMERE proteins (mostly autosomal dominant)
Clinical features of Hypertrophic cardiomyopathy?
Sudden death due to ventricular arrhythmias, common cause of sudden death in young athletes
Syncope w/ exercise
What is a common cause of sudden death in young athletes?
Ventricular arrhythmias due to hypertrophic cardiomyopathy
Biopsy in hypertrophic cardiomyopathy what would be seen?
Myofiber hypertrophy w/ disarray
What is restrictive cardiomyopathy
DEC compliance of ventricular endomyocardium
Restricts filling during diastole
Causes of Restrictive Cardiomyopathy
Endocardial Fibroelastosis (children)
Loeffler syndrome (endomyocardial fibrosis w/ an Eosinophilic infiltrate + eosinophilia)
Restrictive cardiomyopathy will present as __ pts. EKG findings?
EKG = low-voltage and DEC QRS amplitudes
What is the most common primary cardiac tumor in adults?
MYXOMA - benign mesenchymal proliferation w/ a gelatinous appearance
Abundant ground substance on histology
What is a pedunculated mass in the LA that causes syncope due to obstruction of mitral valve?
What is the most common primary cardiac tumor in children that is associated with tuberous sclerosis?
Rhabdomyoma = benign hamartoma of cardiac muscle
Common metastases to the heart include?
More common that primary tumors and most commonly involves pericardium resulting in pericardial effusion.
Metastasis tumor to heart from breast, lung, melanoma, lymphoma
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