Cardio Flashcards
Murmur associated with Rheumatic Fever:
Mitral stenosis
Murmur associated with Infective endocarditis:
Mitral and/or tricuspid regurgitation
Mutation on HCM:
AD mutation in the beta-myosin heavy chain
Histo of HCM:
Inappropriate hypertrophy of LV myocardium and disordered arrangement of cardiac myofibrils (myofibril disarray)
Physiological changes in HC:
Diastolic dysfunction LV outflow obstruction (increase afterload) Myocardial ischemia (d/t increased work of LV) Normal coronary arteries
Murmur associated with HCM:
Systolic crescendo-decrescendo murmur b/w apex and left sternal border, radiating to the suprasternal notch
Murmur changes in HCM:
Decrease with increased preload and afterload (to relieve obstruction)
Increase with decrease preload and afterload
Decrease with squatting
Increase with standing after squatting
A split S2 indicates:
Lengthening of the RV ejection time with delayed closure of the pulmonary valve
When can you hear an S2:
Complete RBBB, pulmonary stenosis, and pulmonary HTN
What structure lies behind the LA and esophagus on TEE?
descending aorta
fever, pericardial friction rub, ST elevations in all leads
pericarditis
tx of pericarditis
NSAIDs
distended neck veins, distant heart sounds, hypotension, pulsus paradoxus
cardiac tamponade
electrical alternans
cardiac tamponade
prevents intestinal reabsorption of bile acid and forces liver to use cholesterol to make more bile acids
bile acid resins
prevents cholesterol absorption at the intestinal brush border
ezetimbe
upreulates LPL to increase TG clearance and activates PPAR-a to induce HDL synthesis
fibrates
inhibits lipolysis (HSL) in adipose tissue and reduces hepatic VLDL synthesis
niacin
inactivates LDL-R degradation, increasing the amount of LDL removed from bloodstream
PCSK9 inhibitors
hepatotoxicity and myopathy
AEs of statins
upset GI, decreased absorption of fat soluble vitamins and drugs, increased risk of chol. gallstones
AEs of bile acid resins
increased LFTs and diarrhea
AEs of ezetimbe
myopathy, cholesterol gallstones
AEs of fibrates
red flushed face decreased by NSAIDs, hyperglycemia, hyperuricmia, rash
AE of niacin
myalgias, delirium, dementia, neurocognitive effects
AEs of PCSK9 inhibitors
renal impairment is a CI for use of…
fibrates
why you shouldn’t use fibrates in patients with severe renal impairment….
fibrates can increase serum creatinine
treatment for chronic atrial fibrillation
Calcium channel blockers and beta blockers
bioprosthetic heart valves are subject to….
wear and tear, calcification leading to stenosis, perforation or tearing, leading to insufficiency
acute rheumatic fever presents with
pancarditis and acute LV failure
most common cause of hemorrhagic pericarditis
TB and metastatic carcinoma
LA dilation, systemic abscess, arterial aneurysm
complications of staphylococcal septicemia followed by mitral endocarditis
what medications should patients who undergo mechanical prosthesis be put on to avoid thrombotic complications?
anticoagulants (warfarin)
the most common toxin producing dilated cardiomyopathy
alcohol
most important cause of LVH and failure
systemic HTN
how long does troponin I levels stay elevated?
7-10 d
sensitive marker for myocardial injury w/in the first 24-48 hrs
CK-MB
How long does it take CKMB to return to normal
72 hrs
gross findings 0-24 hr post MI
none
light microscopy findings 0-24 hrs post-MI:
early coagulative necrosis, release of necrotic cell contents into blood stream (troponin), edema, hemorrhage, wavy fibers, neutrophils appear, reperfusion injury, hypercontraction of myofibrils via increased free calcium influx
complications 0-24 hrs post MI
ventricular arrhythmia, HF, cardiogenic shock
gross findings 1-3 days post MI:
hyperemia
light microscopy findings 1-3 days post MI
extensive coagulative necrosis, acute inflammation with neutrophils
complications 1-3 days post MI:
postinfarction fibrinous pericarditis, arrhythmia
gross findings 3-14 days post MI:
hyperemic border; central brown-yellow softening
light microscopy findings 3-14 days post-MI:
macrophages and granulation tissue at borders
what comprises granulation tissue?
type III collagen (fibroblasts), capillaries, and myofibroblasts
complications 3-14 days post-MI:
free wall rupture leading to cardiac tamponade; papillary muscle rupture leading to mitral regurgitation; interventricular rupture d/t macrophage mediated structural damage; LV pseudoaneurysm
gross findings 2 wks-months post-MI:
recanalized artery, gray-white scar
light microscopy findings 2 weeks-months post-MI:
contracted scar complete, increased collagen deposition and decreased cellularity
complications 2 weeks-months post-MI:
Dressler syndrome, HF, arrhythmia, true ventricular aneurysm (w/ a risk of mural thrombus)
plaque disruption with superimposed mural thrombosis gives rise to…
unstable angina
MC of fibrinous pericarditis…
uremia following renal failure
top 3 causes of fibrinous pericarditis:
uremia, RA and Dressler syndrome
top 2 causes of serous pericarditis:
Lupus and rheumatic fever
MC cause of suppurative pericarditis:
infection of the pericardium
nonbacterial (marantic/thrombotic) vegetations can occur on any valve and is associated with…
malignancy (especially mucin-secreting adenocarcinomas)and a hypercoaguable state
along with mitral stenosis, what is an additional late complication of rheumatic fever?
aortic stenosis
mutation associated with TOF:
NOTCH pathway
pathway that plays a major role in in modulations of vascular development, including cardiac outflow tracts
NOTCH
mutation seen in long QT syndrome:
KCNQ1 mutations
