Combank path - cardio Flashcards
(27 cards)
What is occurring within 2-4 days post MI?
Abundant neutrophil emigration takes place to lyse dead myocardial cells and extensive coagulative necrosis takes place
What occurs 7-8 weeks post MI and what is the patient at risk for during this time?
Dense type I collagen replaces the primitive type III collagen; heart is at risk of a ventricular aneurysm b/c the scar tissue has diminished contractile properties that can become weak and bulge out to cause an aneurysm
What occurs 4-12 hours post MI?
Early coagulative necrosis is seen as neutrophils begin to migrate towards the recently infected area to degrade the tissue. Content of necrotic cells such as troponins, CK-MB, and CPK are then released into the bloodstream from the myocardial cells
What occurs 5-10 days post MI?
Macrophages begin to replace neutrophil degradation; there is extensive granulation tissue that is necrotic, soft and brown yellow; this soft necrotic tissue renders the heart susceptible to free wall rupture, tamponade, papillary muscle rupture and septum rupture
Name the valvular disorder — harsh systolic crescendo decrescendo murmur heard best at right upper sternal border
Aortic stenosis
What is one way that aortic stenosis is differentiated from mitral regurgitation?
aortic stenosis radiates to the carotids
What is the classic triad of symptoms that is associated with aortic stenosis?
angina, syncope, heart failure
What is the most common cause of aortic stenosis in the United States?
Aortic valve calcification – increases with age
What is the most common cause of mitral stenosis?
Rheumatic fever
What type of drugs have been shown to reduce mortality in post MI patients?
beta blockers
What is Wolff-Parkinson-White syndrome?
an accessory conduction pathway from atrial to ventricles causes premature ventricular excitation; this leads to paroxysmal tachycardia; ECG findings show short PR interval and an upward deflection before the QRS called a delta wave
A banana shaped left ventricle on echocardiogram indicates?
Hypertrophic cardiomyopathy
What type of axis deviation would show on ECG for hypertrophic cardiomyopathy?
left axis deviation
What type of dysfunction does hypertrophic cardiomyopathy cause?
asymmetrical interventricular septal hypertrophy and hypertrophy of the LV produces a diastolic dysfunction (ventricle can’t fill!)
What is hemochromatosis?
an AR d/o causing increased iron absorption in the intestines
What are the most common signs of hemochromatosis at the time of presentation?
hepatomegaly, skin pigmentation, arthritis
Which cardiomyopathy can result from hemochromatosis?
dilated cardiomyopathy due to iron deposition within the myocardium
When should surgical repair of an AAA be performed
if aneurysm is ruptured; grows > 1 cm in one year; grows beyond 5.5 cm for men or 4.5 cm for women
What is Friederich’s ataxia?
AR trinucleotide repeat d/o (GAA) that causes poor mitochondrial function; staggering gait, nystagmus, pes cavus and hammer toes are characteristic findings
What is the most common cause of death in Friedreich’s ataxia?
hypertrophic cardiomyopathy
What is multiple myeloma?
hematologic malignancy that causes neoplastic proliferation of plasma cells resulting in overproduction of monoclonal IgG, IgA and or light chains
The secreted monoclonal immunoglobulin proteins caused by multiple myeloma can form what type of amyloid and where can they deposit?
AL amyloid; can infiltrate the myocardium causing normal sized ventricular cavities to become stiff, this leads to restrictive cardiomyopathy
Digoxin toxicity is increased by quinidine because?
it decreases digoxin’s renal clearance
T/F hypercalcemia and hypokalemia increase digoxin toxicity
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