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8 Cardiac Pathology Pathoma
Terms in this set (91)
What is stable angina?
Chest pain with exertion (not at rest); the chest pain can radiate to the left arm and upper jaw
What causes stable angina?
atherosclerotic plaque occluding more than 70% of blood vessel
What is the damage to the myocytes in stable angina?
reversible injury to the myocytes characterized by edema
What are EKG findings for stable angina? Why?
there is ST segment depression because flow to the subendocardium is compromised.
What is the treatment for stable angina? How does it work?
Rest and Nitroglycerine. Rest decreases demand and blood flow necessary to myocardium. Nitro dilates the veins which reduces preload and stress on myocardium
What is unstable angina?
chest pain at rest with reversible damage to the myocytes due to a rupture of the atherosclerotic plaque that causes an INCOMPLETE occlusion of the coronary vessel.
What are some findings of unstable angina? How is it treated?
EKG ST depression
*for the same reasons as stable angina
What is Prinzmetal angina?
episodic chest pain unrelated to exertion (reversible damage to myosites) from coronary artery vasospasm (whenever the vessel clamps down = chest pain)
What are some findings of prinzmetal angina?
EKG ST elevation b/c when there's a vasospasm there is a transmural occlusion
What is the treatment for prinzmetal angina?
Nitro or calcium channel blockers
What is a myocardial infarction?
complete occlusion of a coronary artery that leads to death and necrosis of myocardium (after 20 minutes of lack of flow)
What is the clinical presentation of someone with an MI?
severe, crushing chest pain that lasts >20 minutes and radiates to the left arm or jaw, dyspnea, diaphoresis.
Symptoms not relieved by Nitroglycerine
What tests can we do for MI?
- EKG = initially ST depression (NSTEMI), as ischemia progresses, transmural ischemia = ST elevation (STEMI)
- cardiac enzyme test:
1. Troponin I, rises 2-4 hours and stays high 7-10 days, most sensitive and specific
2. CK-MB - rises quickly and goes down quickly (goes down by 72 hrs) = useful for re-infarctions
What is the treatment for MI?
2. supplemental O2 if pulse ox down
5. ACE inhibitor (decrease left ventricular dilatation = blocks agiotensin II conversion)
What is contraction band necrosis?
when you use fibrinolyis or angioplasty to treat MI and return blood back to the tissue to quickly, the calcium returns and causes contraction on bands of the myocardium
What is reperfusion injury?
When give back blood post MI, the increased oxygen can cause radical formation and further injure the tissue.
What do you see microscopically 4-24 hours post MI? Gross change?
coagulative necrosis (remove the nucleus of the cell, pyknosis, karryorexis and karryolysis)
gross = dark discoloration
What happens microscopically 1-7 days post MI? gross change?
neutrophils and macrophage infiltrate (inflammation)
Grossly = yellow palor
What happens microscopically a few weeks post MI?
granulation tissue formation
grossly = red border around edge of infarct.
What happens 1 month post MI?
healing = fibrosis = white scar grossly
What artery feeds the papillary muscles of the mitral valve? What complication can happen post MI to this valve?
right coronary artery
papillary muscle rupture = cardiac insufficiency
What is a complication that can happen 1-3 days post MI?
with a transmural MI, the neutrophils that come in can also go into the pericardium causing FIBRINOUS PERICARDITIS = chest pain and friction rub
What is a complication that can happen 4-7 days post MI?
with the macrophages coming in to eat up dead tissue, there can be rupture of the wall = cardiac tamponade as the blood fills the pericardium space or rupture of the IV septum = shunt from left to right.
What is a complication that can happen months post MI?
The fibrotic heart tissue can become dilatated and can form a mural thrombus
What are some cause of left-sided heart failure?
3. dilated cardiomyopathy (can't contract as well)
5. restrictive cardiomyopathy (can't fill the heart well so can't pump out well)
What are the symptoms of left-sided heart failure?
1. pulmonary edema = dyspnea and paroxysmal nocturnal dyspnea (having trouble sleeping supine)
- hemosiderin laden macrophages in lung = heart failure cells
2. decreased forward perfusion = activation of RAS = increase blood volume and total peripheral resistance = makes matters worse!
What are some causes of right-sided heart failure?
1. left-sided heart failure
2. left to right shunt
3. chronic lung disease (cor pulmonale)
What are the clinical symptoms of right-sided heart failure?
1. peripheral pitting edema
3. liver congestion (nutmeg liver)
What is the most common cause of rhythmic disorders?
ischemic injury (MI usually cause death due to arrhythmias)
What is the essential feature of systemic hypertensive heart disease?
left ventricular hypertrophy (dilation very late in the process)
What is a histologic feature of hypertensive heart?
enlarged hyperchomic nuclei = boxcar nuclei
What is cor pulmonale?
right ventricular hypertrophy or dilation (when acute) due to primary disorders of the lung parenchyma or vasculature (eg pulm hypertension)
What defect is associated with fetal alcohol syndrome?
What is an ostium primum ASD associated with?
What physical exam feature is found with an ASD?
split S2 b/c of delayed closure of pulmonic valve due to the higher volume in the right atrium
What is a patent ductus arteriosum associated with it?
What is the treatment for a PDA?
decreasing Prostaglandin E by giving Indomethacin (b/c prostaglandin E keeps the ductus arteriosum open!)
What will patients with Tetralogy of Fallot due in response to a cyanotic episode?
they will squat down b/c this increases the pressure in the aorta, reducing the shunting from the right ventricle to the systemic circulation
What is transposition of the great vessels associated with?
What is truncus arteriosus?
when the pulmonary trunk and aorta do not fully divide causing mixing of deoxy and oxy blood going to systemic circulation leading to cyanosis
what is the infantile aortic coarctation associated with?
what are the key findings in adult coarctation of the aorta?
hypertension in the upper extremities with hypotension and weak pulses in the lower extremities
What can acute rheumatic fever cause?
damage to the heart due to molecular mimicry where antibodies to the bacteria attack heart tissue
What are the Major Jones criteria?
J - oint problems (migratory polyarthritis)
O - heart problems (myo, peri, and epicarditis = pancarditis)
N - nodules
E - erythema marginatum
S - syndeham chorea
What are the microscopic findings of cardiac rheumatic fevers?
1. mitral valve regurgitation due to myocarditis, vegetations on the mitral valve = endocarditis
2. Aschoff bodies in the myocardium with Anitschkow cells (caterpillar nucleus)= myocarditis
3. pericarditis = friction rub
If rheumatic heart disease affects the aortic valve, what findings do you have?
the commissure of the valve leaflets fuse causing fishmouth appearance of the valve which results in stenosis
* these changes also happen in the mitral valve which is affected first
What generally causes aortic stenosis?
wear and tear leading to calcification
- precipitated by bicuspid aortic valve b/c greater use of those valves
How can we distinguish stenosis of the aortic valve from rheumatic heart disease vs general stenosis?
in rheumatic valve disease there will be fusion of the commissures and mitral valve will also be stenotic while in general aortic stenosis = no commissure fusion
What are the physical exam findings of aortic stenosis?
systolic ejection click followed by a crescendo-decrescendo murmur
(b/c of the ventricle pushing the valve open = click followed by blood rushing through
What are some complications of aortic stenosis?
1. Left ventricular hypertrophy
2. microangiopathic hemolytic anemia
3. angina and syncope with exertion
What is aortic regurgitation? What is the most common cause?
back flow of the blood into the left ventricle usually due to dilatation of the aortic root (from infectious endocarditis or syphilis aneurysm)
What are the physical exam findings of aortic regurgitation?
1. blowing diastolic murmur
2. increase in systolic pressure and decrease in diastolic pressure = widening pulse pressure causing hyperdynamic circulation which presents with bounding pulses, pulsating nail beds, and head bobbing
3. dilation and eccentric hypertrophy due to increased volume in the left ventricle
What is mitral valve prolapse?
floppy mitral valve
What is the clinical presentation for mitral valve prolapse?
1. mid systolic click because as the left ventricle fills, the mitral valve balloons backward
2. perhaps regurgitation murmur
What are some causes of mitral valve regurgitation?
1. mitral valve prolapse
2. left ventricular dilatation (moves valve open)
3. infectious endocarditis
4. ACUTE rheumatic heart disease
5. Post MI papillary rupture
What physical exam findings will you get with mitral valve regurgitation?
holosystolic blowing murmur
- louder with squatting and expiration (b/c there's increased pressure in aorta causing greater blood in left ventricle and so more regurgitation)
What can lead to mitral stenosis?
CHRONIC rheumatic valve disease
What is the key physical exam finding in mitral valve stenosis?
opening snap, followed by a diastolic rumble
What are the complications of mitral valve stenosis?
pulmonary congestion, pulmonary hypertension, and atrial fibrillation (with increased risk of mural thrombi) due to volume overload in LA
What diseases is mitral valve prolapse associated with?
Marfan's and Ehler Danlos
A patient presents with migratory polyarthritis (joints pains that come and go and travel to different joints) 2-3 weeks post streptococcal pharyngitis infection. What is the likely diagnosis?
Rheumatic heart disease
How do we diagnoses acute rheumatic disease?
1. evidence of previous streptococcal infection
2. 2 or more major Jones criteria
What is endocarditis?
inflammation of the endocardium, esp around the valves
What is the most common pathogen that causes infective endocarditis?
strep viridans = infects only previously damaged valves and causes subacute endocarditis (minor vegetations b/c low virulence bug)
a patient with a prior history of rheumatic heart disease develops bilateral pitting edema, and a purpuric skin rash post a dental procedure. What is the likely diagnosis?
infective endocarditis from strep viridans
a patient with a prior history of IV drug use presents with acute endocarditis. What is the likely pathogen? What part of the heart is more likely affected?
What is the key pathogen that causes endocarditis in patients with prosthetic valves?
What is the causative agents of endocarditis in patients with colorectal carcinoma?
What are the organisms that can cause culture negative endocarditis?
What are the clinical features of endocarditis?
- nailbed hemorrhages (splinter)
- Roth spots (retinal hemorrhages)
- Janeway lesions
- Osler nodes
- Anemia or chronic disease
What are Janeway lesions? what are they associated with?
painless erythematous skin lesions on palms and toes
What are Osler lesions? What are they associated with?
painful lesions on the fingers and toes with endocarditis
what diagnostic tool is used for endocarditis?
transesophageal echo to look for vegetations
What is nonbacterial thrombotic endocarditis?
sterile vegetations due to hypercoagulable state or adenocarcinoma usually found on the mitral valve
What are libman-sacks endocarditis? What disease is it common in?
sterile vegetations on both surfaces of the mitral valve
associated with Systemic Lupus erythematous (SLE)
What is carcinoid syndrome?
flushing, diarrhea, dermatitis and bronchoconstriction caused by carcinoid tumors due to serotonin release
What is carcinoid heart disease?
disease due to mediators released by carcinoid tumor that cause glistening white intimal plaque-like thickenings on the endocardial surface of the right heart
What are the two types of prosthetic heart valves?
1. mechanical valves
2. bioprosthetic vales (bovine valves)
What are some negatives of mechanical valves?
they can cause red cell hemolysis and thrombosis
What are the negatives of bovine valves?
What is dilated cardiomyopathy? What problem does this lead to?
massive dilation of all 4 chambers of the heart
- systolic dysfunction (neither ventricle can pump too well), and mitral and tricuspid regurgitation (the valves are stretched) and arrhythmia
What are some causes of dilated cardiomyopathy?
2. drugs (cocaine and doxorubicin)
3. pregnancy (late pregnancy or post birth= peripartum cardiomyopathy)
4. myocarditis (coxsackievirus and enterovirus)
5. genetic (dystrophin gene)
How do we diagnoses a dilated cardiomyopathy from hemochromatosis?
prussian blue stain showing accumulation of intramyocardial hemosiderin
What is the treatment for dilated cardiomyopathy?
What is the most common cause of hypertrophied cardiomyopathy?
hypertrophy of the left ventricle most commonly due to mutations in the sarcomeric proteins esp B-myosin
What is the clinical presentation of hypertrophied cardiomyopathy?
- decreased cardiac output (hard to fill stiff ventircle)
- syncope with exercise
- sudden death from ventricular arrhytmias in young athletes esp (HCM)
What is the histologic presentation of hypertrophic cardiomyopathy?
hypertrophied myocytes in disarray
What are the gross changes in HCM?
grossly, septum is more hypertrophied than the free wall (asymmetric septal hypertrophy) with banana-like left ventricular cavity
What is restrictive cardiomyopathy?
decreased compliance of the ventricle so problems filling
What are some common causes of restrictive cardiomyopathies?
1. amyloidosis (transthyretin deposition in senile form)
4. endocardial fibroelastosis (children) = linked to nutritional deficiencies or Helminth infections
5. loeffler syndrome = eosinophilic infiltrate of heart walls
what presents with low-voltage EKGs with diminished QRS amplitudes?
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