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196 Cards in this Set

  • Front
  • Back
primary cause of hypertension
hyaline ateriosclerosis
benign pink walled, thickened, majority of HTN
hyperplastic arteriosclerosis
malignant, nectrotizing, HTN
lab DX for vasculitis
polyarteritis nodosa
systemic vasculitis
loc: not in lungs
necrotizing, fibrinoid necrosis
systemic vasculitis
loc: upper resp/lungs
path: granulomatous inflammation
temporal vasculitis
systemic vasculitis
loc: in head
path: multinucleated histiocytes destroying lamina
tx for vasculitis
syphillitic anyeurism
thoracic aorta, plasma cell infiltrate destroys vaso vasorum
path: "tree barking"
etiology and SXs of aoritc dissections
HTN, Marfan's
excrutiating pain radiating to back, moves down with dissection
esophageal varices secondary to
portal HTN
lymph walls inflammed secondart to group A beta-hemolytic Strep
Lymphedema usually caused by
doctors (surgery, radiation)
Virchow's triad
1)stasis, 2) hypercoagulability, 3) endothelial dysfunction
leads to thrombogenesis
irreversible damage to myocardium after X min of ischemia
LAD occlusion --> (leads)
anterior wall, V1-V4
RCA occlusion -->(leads)
inferior/posterior wall (II, aVF, III)
LCX occlusion -->(leads)
lateral wall (V4-6)
MI 4-12hrs
gross: no change
path: coagulative necrosis, wavy fibers, hemorrhage, edema, PMNs
ECG: small Q wave, ST seg elevation
MI 12-24hrs
gross: dark mottling/slight pallor
path: coagulative necrosis, pyknosis, hypereosonophilia
ECG: Q wave, ST seg elevation, inverted T
MI 1-3 days
gross: mottling with yellow center
path: complete coagulative necrosis
ECG: ST normalizes, T wave inversion, Q wave
MI 3-7 days
gross: hyperemic border with soft yellow center
path: phagocytosis of macrophages
ECG: ST normalizes, T wave inversion, Q wave
MI 7-10 days
gross: yellow tan
path: young granulation tissue
ECG: ST normalizes, T wave inversion, Q wave
MI 10-14 days
gross: red grey
path: organizing granulation and beginning of fibrosis
ECG: ST normalizes, T wave inversion, Q wave
MI 2-8 weeks
gross: gray=white scar
path: fibrosis
ECG: ST normalizes, T wave reverts, Q wave persists
Acute MI
no gross/his changes
ECG: ST seg elevation
most specific to heart
peaks at 18hrs
stays around for 10-14 days
peaks at 24 hrs, out by 48-72 hrs
myocardial rupture susceptible during
lab test for venous thromboembolism
DX of venous thromboembolism with
CT angiography
CXR SXs of venous thromboembolism
Hampton's hump, Westermark sign
chest pain, dyspnea,
characteristic ECG finding of venous thromboembolism
cardiogenic stroke indicated with
multiple embolic events
What major vessel type is not included in the hilum
lower lobe pulmonary veins (drain directly to L atrium)
which hilum is superior and why
left bc pul artery goes over the L bronchus
double heart border indicative of
mitral insufficiency and stenosis(enlarged L atrium)
CHF stage 1 on CHX
pulmonary vascular congestion/redistribution
CHF stage 2 on CHX
perivascular blurring, peribronchial cuffing, kerly B lines
CHF stage 3 on CHX
alveolar edema
non-cardiogenic pul edema on CHX
batwing pattern
Aortic coarctation on CHX
figure 3
what is a good prognosis for a rt sided aortic arch
abberan left subclavian artery
what confers a larger risk for ACS in women over men
most important acquired risk factor of CHD
determinants of heart oxygen demand
afterload + preload (really wall tension)
Rate pressure product =
systolic BP * HR
Variant angina (ECG and etiology, B blockers?)
cocaine often, ST elevation usually, NO B blockers
ECG changes over time in MI
1-2 days
ACUTE: ST elevation with reciprocal depression
HOURS: ST elevation, reduced R wave, Q wave begins, reduced reciprocal ST depression
1-2days:T wave inversion, Q wave
DAYS: ST normalization, T wave inverted
WEEKS: deep Q wave only thing left
major difference between UA and NSTEMI
cardiac enzymes
major difference between STEMI and NSTEMI
ST elevationV
Ventricular rupture indicates __ MI, SX?
Ant wall, LAD
death, demo of tamponade (deep x, blunted y)
Septal rupture indicates ___ MI, SX? thrill?
ant wall, LAD. holocystiolic murmur at LSB with THRILL
papillary muscle rupture indicates ___ MI. SX? thrill?
inferior wall (RCA), holocystolic murmur WO thrill
RV MI indicated by? SXs? TX?
ST elevation in V4R (midclavicular, 5th ICS on RIGHT)
JVD, Kussmaul's sign
TX: saline
NON-STEMI, ____ hospital mortality ____ reinfarction rate
lower, higher
what are the causes of right heart failure?
LEFT heart failure
pulmonary embolism
cor pulmonale
causes of systolic HF
decreased contractility and increased afterload
causes of diastolic HF
impaired diastolic filling (decreased compliance, decreased active relaxation)
pressure-volume loop changes for systolic and diastolic heart failure
systolic: reduced slope of ESPVR curve
diastolic: increased bottom curve
in which, diastolic or systolic, is the EF maintained
S3/S4 in systolic/diastolic
3-s, 4-d
heart dilates in systolic or diastolic HF
ADH released from where and what effect
post. pituitary, causes increased preload through water retention (and maybe vc as well)
functions of natriuretic peptide
vasodilation, na excretion, ANG II ANT
cheyne-stokes respiration
deep breathing, followed by periods of no breathing, cycles
abdomino-jugular reflex
sign of rt heart failure - push on abdomin, JVD goes up and does not come down or comes down only slowly
pulsus alternans
sign of advanced heart failure, strong/weak pulse cycle
ACUTE tx of HF
lasix (only if pt is not hypotensive)
nitrates (reduced preload)
position (sit up)
added to lasix as diuretic adjunct
lasix alternative
K sparing diuretic - aldosterone ANT
BNP analogue
AE: bad for ppl with renal failure
TX for HYPOtensive pt in acute HF
inotropic agent - dobutamine, milrinone (NOT useful in acute exacerbation of chronic HF)
TX for chronic HF
ACE inh or ARBs (or both)
hydralazine and nitrates
hydralazine - aterial vasodilator (also anti-oxidant)
nitrates - venous vasodilator
for ppl with ACE inh AEs
especially good for AAs
AE of diuretics
electrolyte disturbances --> arryhtmias
arterial vasodilator --> reduced TPR
3 agents that reduce mortality in HF
beta blockers, ACE inh, ADH inh
catecholamines diminish ability of mycoytes to reenter cell cycle
what does uric acid indicate
oxidative stress (xanthine oxidase function)
what is the effect of hydralazine in the nitroso-redux balance
hydralazine acts as an anti-oxidant
which form of cardiomyopathy --> systolic dysfunctoin
what is the etiology of dilated CM
acute viral myocarditis, ETOH, genetic
what is the major hemodynamic findingin dilated CM
low LVEF
what is the EF in HCM
unchanged or elevated
what is the etiology of HCM
AD, c1,5,14
sxs of HCM
syncope, angina, dyspnea, bifid pulse, triple apical impulse, LVH
bifid pulse is a sx in which 2 conditions
murmur of HCM? increase with?
systolic ejection
increased with reduced chamber size (increased contractility, exercise, VALSALVA, standing, after a premature beat)
predictors of SD in HCM
young age, syncope, FHX, extent of hypertrophy
etiology of restrictive CM
amyloidosis, sarcoidosis
SX of restrictive CM
Kusmmaul's sign, sq. root sign
ECG findings of arrhythmogenic RV dysplasia
vtach, LBBB, R axis deviation
epsilon and t wave inversion in v123
etiology of arrhythmogenic RV dysplasia
arrhythmogenic RV dysplasia more common in men or women
histology of HCM
disarray and fibrosis
histology of sarcoidosis
non-caseating granulomatous inflammation, usually also involves lungs
etiology of myocarditis
usually viral (Coxsackie B)
histology of chagas disease
acute histology of cardiac transplantation rejection
lymphocytic infiltrate and myocyte necrosis
late histology of cardiac transplantation rejection
thickening of coronaries, malignancy
mech of heparin
AT III amplification
mech of warfarin/coumadin
vit K ANT
factors affected by warfarin
monitor for heparin
monitor for warfarin
rapid reversal of herparin
protamine sulfate
rapid reversal of warfarin
FFP, vit K
complications of heparin
compllication of warfarin
transient hypercoagulability, displace meds on plasma proteins, TERATOGENIC
ADP ANT (anti-plate)
clopidogrel (clavix)
used with aspirin P2Y rec ANT (ADP ANT) anti plate
additive to aspirin for anti-platelet
monoclonal Ab against GPIIa/IIIb (blocks aggreg of plate)
commotio cordis
concussion of the heart, can kill especially kids with small balls (that hit them)
major difference between septic shock and all others
pathophysiology of septic shock
endotoxins from bacteria lead to host response --> septic shock
usually LPS (gram -) TSST-1 of staph, polysaccarhid capsule of strep --> monocytes release TNF, Il1 --> vasodilation, hypotension, complement cascade
septic with fluids
hypovolemic -low,low,low,high
cardiogenic - variable, high, low, high
septic - low, low, high, low
septic with fluids, normal, normal, high, low
in ASD, L or R has volume overload
clinical features of an ASD
wide split S2
ejection murmur
prominent parasternal heave
clinical features of VSD
holocystolic murmur
sxs of HF (s3)
pulmonary HTN (--> Eisenmegger)
which of the following reqs endocarditis prophylaxis? ASD, VSD, AVSD, PDA
all but ASD
PDA clinical features
wide pulse pressure, continous machinery like murmur
Down's asociated with
TGA presentation
big blue bably (neonatal cyanosis most common cause)
path of TGA
abnormal growth of the conotruncal ridges (failure to spiral)
Tetralogy of Fallot SXs and components?
VSD, pulmonary stenosis, overriding aorta, RVH
present in childhood, cyanosis, clubbing CXR boot shape
DiGeorge associated with
Tet of Fallot and truncus arteriosus
Turner's associated with
Coarctation of the Aorta
CXR of coarctation? T of Fallot
figure 3, boot shape
predisposing risk factors for aortic dissection
HTN, cystic medial necrosis, Marfan's, trauma
what kind of aortic dissection is a surgical emergency?
different pulse in each arm suggests
aortic dissection with bracheocephalic a. involvement
sxs of aortic dissection
excrutiating pain, HTN Diastolic over 140, sxs depend on which arteries are involved
management of aortic dissection
drop dp/dt with B blockers FIRST. then tx HTN
kusmmaul sign differential
RV MI, restrictive CM, cardiac tamponade
goldschmidt says post MI, pts go home on...
B blocker
Ace inhibitor or ARB
what are the clinical features of hypercholesterolemia
ldl collects in tendons(achilles heel)
corneal arcuses in the young
xanthelomas (accumulation in periorbital space)
clinical features of chylomicronemia syndrome
eruptive xanthomas, hepatosplenomegaly
familial combined hyperlipidemia mechanism?
overproduction of B100
Lipid presentation of combined hyperlipidemia
high 1/3 LDL, 1/3VLDL, 1/3 both
familial hypertriglyceridemia produces what kind of particles?
VLDL, but big VLDLs so harder to get into walls
clinical features of hyperlipidemia?
milky serum, retinal lipemia, eruptive xanthomas in the skin
how does small dense LDL get made
high TG level cause increased levels of VLDL which drives CETP causing LDL and HDL to lose cholesterol and get TG enriched. the TG enriched are then substrates for hepatic lipase.
what is the dyslipidemic triad
high TG, low HDL, small dense LDL
what is special about Apo(a)
the apo(a) inhibits fibrinolysis
familial combined etiology
AD, overproduction of B100
familial hypertriglyceridemia is a _____ disorder
important cause of low HDL
causative risk factors
Metabolic Syndrome
central obesity
glucose intolerance
low HDL
high TG
activated fat cells secrete less _____
major risk factors (ATP III)
low HDL
reducing polyunsaturated fats and saturated fats will lead to what change in HDL
leads to reduced HDL
does exercise effect LDL
effect of TG on PAI 1
function of statins
reduce LDL
doubling statins ==> increase of
mech of statins
BE R upregulated, reduced chol production
rhabdo with statins increased change with the following":
fibrates, azole antifungals, macrolide Abs, HIV protease inhibitors
inhibits cholesterol absorption
very well tolerated
drugs to tx high tg
fibrates, omega-3
fibrates mech
PPARalpha activation, suppresses synthesis of CIII
effect of fibrates
reduce TG, also increase HDL
omega 3 effects
reduce TG, little else
niacin mech, effect, AE?
effect: increased HDL
mech: inhibits lypolysis
AE: flushing, itching (Tx with aspirin)
pulsus bisferians
differentiate HCM, AR
wide PP=AR, narrow-HCM
with HOCM, which drugs to avoid?
ACE inh, nitrates, digoxin, saunas
what is syndrome X
angina pectoris WO any signs of significant atherosclerotic lesions
most likely caused by microvascular dysfunction
2 drugs that reduce remodelling
B-blockers, ACE inh
CRP increased by which cytokine
what signs are suggestive of RV MI win 1st 24 hrs
hypotension and sinus tach, CLEAR lung fields, kussmaul
in angina pectoris, the primarily goal is to _______ thourgh ___ drugs and secondary to ______ through O____
decrease demand (nitrates, beta blockers, CCBs) and increase 02 supply though Anti-platelets
to be considered sudden death, death must be caused within ___ hrs of acute onset of SXs
definition of sudden cardiac deat
irreverisble cessation of all biological function
cardiac arrest
aburpt cessation of cardiac mechanical function (can be reverisble)
mechL VT, VF, asystole, pEA
Cardiovascular collapse
seeden loss of effective blood flow (basically cardiac arrest plus some peripheral stuff)
vfib accounds for ___% events and has ___% mortality
66, 60
vtach accounds for ___% events and has ___ %mortality
5, 10
asystole accounds for ___% events and has ___% mortality
29, over 90
what is sinus arrhythmia
in a cyclical fashion, HR speed and slows.
speeds - inspiration, V return to RA, to handle V speeds up
P waves taller on inspiration and wider on expiration (normal change)
atrial flutter on ECG
sawtooth in aVF, II, III, spikes in V1, rates around 300, 2:1 or 4:1 conduction usually
which vessels can give off impulses into afib
pulmonary veins
most common cause of syncope
neurally mediated(neurocardiogenic, vagally-mediated, vasovagal)
which 2 statins are relatively hydrophilic
atorvastatin LIPITOR, simvastatin ZOCOR
which 2 statins are metabolized by CYP450 3A4
atorvastatin LIPITOR,. simvastatin ZOCOR
what drugs can exacerbate rhambdo with statins
fibrates, azole antifungals, macorlidge Ab, HIV protease inhibitors
mech of bile acid sequestrants
interfere with bile reabsorption in poo
mech of fibrates
activate PPAR alpah in liver suppressing CIII synthesis
also increase HDL
mech of niacin
inhibits lypolysis
major symptom of coarctation
HIGH BP in heart
coarctation comes from misdevelopemnt of which arches
4,6 L arches