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73 Cards in this Set

  • Front
  • Back
What are the risk factors for HTN?
increased age
obesity
diabetes
smoking
genetics
blacks > whites > Asians
What does HTN predispose?
atherosclerosis
stroke
CHF
renal failure
retinopathy
aortic dissection
Monckeberg atherosclerosis
calcification of the arteries, esp. radial or ulnar
usually benign
atreriolosclerosis
hyaline thickening of small arteries in essential HTN
hyperplastic "onion-skinning" in malignant HTN
atherosclerosis
disease of elastic arteries and large and medium-sized muscular arteries
What are the risk factors in developing atherosclerosis?
smoking
HTN
diabetes mellitus
hyperlipidemia
family history
What are the complications of atherosclerosis?
aneurysms
ischemia
infarcts
peripheral vascular disease
thrombus
emboli
Where do atherosclerotic plaques tend to form?
abdominal aorta > coronary artery > popliteal artery > carotid artery
What is the progression of atherosclerosis?
fatty streaks -> proliferative plaque -> complex atheromas
stable angina
most common form of angina
pain precipitated by exertion and is relieved by rest or vasodilators (e.g., nitroglycerine)
Prinzmetal's angina
intermittent chest pain at rest
caused by vasospasm
unstable/cresendo angina
prolonged or recurrent pain at rest
often indicative of imminent MI
Which type of angina has pain that is relieved by rest?
stable angina
Which type of angina has pain that gets worse during rest
Prinzmetal's angina
unstable/cresendo angina
Which type of angina has intermittent chest pain at rest?
Prinzmetal's angina
Which type of angina is caused by vasospasms?
Prinzmetal's angina
Which type of angina is relieved by vasodilators?
stable angina
Which type of angina is indicative of imminent MI?
unstable/cresendo angina
Which type of angina is a result of severe narrowing of atheroscclerotic coronary vessels?
stable angina
What is the most common form of angina?
stable angina
Where do red (hemorrhagic) infarcts occur?
loose tissue w/ collaterals (e.g., lungs, intestine) or following reperfusion
Where do pale infarcts occur?
in solid tissues w/ single blood supply (e.g., brain, heart, kidney, spleen)
Which coronary arteries are occluded the most? the least?
LAD > RCA > circumflex
When is an MI maximally yellow and soft?
10 days post-MI
When are contraction bands visible on an MI?
4 hours post-MI
When is ECG the best method of diagnosis of an MI?
w/in the first 6 hours post-MI
When does cardiac troponin I begin to rise? How long does it stay elevated?
rises after 4 hours
elevated for 7-10 days
What is the test of choice for MI in the first 24 hours post-MI?
CK-MB
How long does LDH stay elevated post-MI?
2-7 days
Is AST specific for liver?
no
can also be found in cardiac, liver and skeletal muscle cells
ST elevation
transmural infarct
ST depression
subendocardial infarct
Q waves
transmural infarct
What are the complications of an MI?
cardiac arrhythmia
LV failure and pulmonary edema
cardiogenic shock
rupture of ventricular free wall, interventricular septum, papillary muscle, cardiac tamponade
thromboembolism - mural thrombus
fibrinous pericarditis (friction fub)
Dressler's syndrome (autoimmune pheenomenon resulting in fibrinous pericarditis)
What is the most common cardiomyopathy?
dilated (congestive) cardiomyopathy - 90%
What type of cardiomyopathy causes systolic dysfunction?
dilated (congestive) cardiomyopathy
What type of cardiomyopathy causes diastolic dysfunction?
hypertrophic cardiomyopathy
hypertrophic cardiomyopathy
walls of LV are thickened (esp. the ventricular septum) and chamber becomes banana shaped
cause of sudden death in young athletes
50% inheriited as autosomal dominant trait
characterized microscopically by disoriented and tangled myocardial fibers
dilated cardiomyopathy
most comon form of cardiomyopathy
characterized by dilation of both ventricles and by both right- and left-sided heart failure
restrictive cardiomyopathy
caused by infiltrative processes w/in myocardium that results in stiffening of the heart muscle -> interferes w/ pumping action
exemplified by cardiac amloidosis -> right- and left-sided heart failure
mitral regurgitation
holosystolic high-pitched "blowing murmur"
loudest at apex
aortic stenosis
crescendo-decrescendo systolic ejection murmur following ejection click
LV >> aortic pressure during systole
radiates to carotids/apex
VSD
holosystolic murmur
mitral prolapse
late systolic murmuc w/ midsystolic click
most frequent valvular lesion
aortic regurgitation
immediate high-pitched "blowing" diastolic murmur
wide pulse pressure
mitral stenosis
follows opening snap
delayed rumbling late diastolic murmur
LA >> LV pressure during diastole
patent ductus arteriosus
continusos machine-like murmur
loudest at time of S2
What are the causes of serous pericarditis?
SLE
rheumatoid arthritis
infection
uremia
What are the causes of fibrinous pericarditis?
uremia
MI
rheumatic fever
What are the causes of hemorrhagic pericarditis?
TB
malignancy
What are the findings in hemorrhagic pericarditis?
pericardial pain
friction rub
ECG chances (diffuse ST elevations in all leads)
pulsus paradoxus
distant heart sounds
syphilitic heart disease
tertiary syphilis disrupts the vasa vasorum of the aorta -> dilation of the aorta and valve ring
"tree bark" appearance of the aorta
Buerger's disease
(aka thromboangiitis obliterans)
acute inflammation involving small to medium size arteries of the extremities, extending to adjacent veins and nerves
clearly assoc. w/ smoking
What is the treatment for Buerger's disease?
quit smoking
Takayasu's arteritis
inflammation and stenosis of medium and large sized arteries w/ freq. involvement of the aortic arch and its branches -> arotic arch syndrome
assoc. w/ elevated ESR
primarily affects young Asian females
What are the clinical symptoms of Tayakasu's arteritis?
(FAN ON MY SKIN On Wednesday)
Fever
Arthritis
Night sweats
MYalgia
SKIN nodules
Ocular disturbances
Weak pulses in upper extremities
Takayasu's arteritis primarily affects what population?
young Asian females
Buerger's diease affects what vessels?
small and intermediate vessels of the extremities
Takayasu's arteritis involves what vessels?
medium and large arteries w/ frequent involvement of the aortic arch and its branches
temporal arteritis
(giant cell arteritis)
most common vasculitis that affects medium and small arteries, usually branches of carotid artery
What are the clinical symptoms of temporal arteritis?
unilateral headache
jaw claudication
imparied vision (occlusion of opthalmic artery -> blindness)
What population does temporal arteritis affect most?
elderly females
Temporal arteritis is associated w/ what lab finding?
elevated ESR
polyarteritis nodosa
necrotizing immue complex inflammation of medium-sized muscular arteries, typically involving renal and visceral vessels
What is the treatment for polyarteritis nodosa?
corticosteroids
cyclophosphamide
Wegner's granulomatosis
characterized by focal necrotizing vasculitis and necrotizing granulomas in the lung and upper airway and by necrotizing glomerulonephritis
What is a strong marker for Wegner's granulomatosis?
C-ANCA
What is the treatment for Wegner's granulomatosis?
cyclophosphamide and corticosteroids
microscopic polyangiitis
similar to Wegner's granulomatosis but lacks granulomas
P- or C-ANCA
Churg-Strauss syndrome
granulomatous vasculitis w/ eosinophilia
What organs are involved in Churg-Strauss syndrome?
lung, heart, skin, kidneys, nerves
Kawasaki's disease
acute, self-limiting disease of infants/kids
acute necrotizing vasculitis of small/medium-sized vessels
People w/ Kawasaki's disease may develop what?
coronary aneurysms