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375 Cards in this Set
- Front
- Back
what usually supplies sa node
|
rca
|
|
what usually supplies av node
|
rca
|
|
what is right dominant heart
|
inf portion of heart served by rca
|
|
what supplies right ventricle
|
rca
|
|
what supplies posteromedial papillary m of mitral valve
|
rca
|
|
what part of septum does lad serve
|
ant 2/3
|
|
most common area of occlusion in heart
|
lad
|
|
dilation of left atrium can lead to
|
dysphagia, hoarseness
|
|
what part of septum carries most of the conduction bundles
|
ant 2/3
|
|
from ascending to descending aorta, what is the order of the branching vessels
|
BCS (brachiocephalic, l carotid, l subclavian)
|
|
reynolds number
|
density * diameter * velocity / viscosity
|
|
effect of changing radius vs velocity in reynolds number
|
radius has a bigger effect than velocity
|
|
what can increase pulse pressure
|
increasing stroke volume
|
|
effect of extracellular sodium on contractility
|
decreased sodium means less contractility cuz na/ca pump can't work as well
|
|
how does digoxin raise intracellular calcium
|
blocking na/k pump results in increased intracellular sodium means na/ca pump works better
|
|
what physiologic factors can decrease contractility
|
hypoxia, acidosis
|
|
what increases mvo2
|
increased afterload, increase contractility, increase hr, increase heart size
|
|
what tissue has the highest rate of oxygen extraction
|
cardiac
|
|
what does preload correspond to
|
ventricular EDV / RAP
|
|
venodilator vs vasodilator - preload vs afterlolad
|
venodilator decreases preload, vasodilator decreases afterload
|
|
normal EF
|
>55%
|
|
tension equation
|
T = P*r/w
|
|
what factors can increase viscosity
|
polycythemia, hyperprotein states, hereditary spherocytosis
|
|
effect of the following on cardiac and vascular curves: blood volume, anaphylaxis, exercise, AV shunt, hemorrhage
|
blood volume will alter the mean systemic pressure, anaphylaxis will decrease mean systemic pressure (increased perm) & shift VR curve CW & shift CO curve up, exercise and AV shunt will shift CO up & CW rot of VR, hemorrage decreases mean systemic pressure & shifts CO down & rotates VR CCW
|
|
what can change the mean systemic pressure (i.e. x intercept of VR curve)
|
increased BV and decreased venous compliance increases mean systemic pressure
|
|
effect of TPR on VR and CO
|
increased TPR shifts VR down (more blood in arteries) and shifts CO down
|
|
draw the flow diagram for cardiac cycle and label the points with valve closure/opening
|
p257
|
|
when is s3 normal
|
pregnancy and children
|
|
draw the venous pulse curve and label a c v x y
|
p257
|
|
what is wide splitting associated with
|
RV empties slower - could be due to pulmonary hypertension or stenosis, or rbbb
|
|
does wide splitting change with expiration/inspiration
|
yes
|
|
what causes fixed splitting
|
flow from left heart to right heart through asd increases amount of time it takes RV to empty
|
|
when is paradoxical splitting seen
|
LV empties slower - aortic stenosis, lbbb
|
|
what do you hear on paradoxical splitting
|
on inspiration, the p2 and a2 come close together, eliminating the split
|
|
describe the following maneuvers on preload and afterload: handgrip, inspiration vs expiration, standing vs sqat, valsalva vs rlease, lying down during pregnancy
|
p258
|
|
describe where the following is best heard: AS, AR, PR, hypertrophic cardiomyopathy, PS, asd, vsd, MR, MS, TR, TS
|
p258
|
|
describe "shape" of MR/TR
|
holosystolic
|
|
name causes of MR
|
ischemic heart dz, MVP, LV dilation, IE, papillary mm rupture, LS, rheumatic fever
|
|
what could cause giant c,v- waves on venous pulse
|
TR
|
|
what is the shape of VSD-related heart murmur (ie during what type, and shape)
|
holosystolic
|
|
shape of MVP
|
midsystolic click followed by late systolic crescendo
|
|
what causes midsystolic click in MVP
|
sudden tensing of cordae tendinae
|
|
most common cause of microangiopathic hemolytic anemia
|
as
|
|
what substance is increased in the valve of MVP
|
dermatan sulfate
|
|
venous pulse findings in tricuspid stenosis
|
big a wave
|
|
functional regurgitaiton
|
regurg due to physical dilation of valve ring
|
|
head bobbing and bounding pulses
|
ar
|
|
what is austin flint murmur
|
mitral regurg from anterior leaf of mitral valve 2* to ar
|
|
what is best position to hear aortic regurg
|
sitting, leaning forward
|
|
opening of skeletal muscle sarcoplasmic channels vs cardiomyocyte sarcoplasmic channels
|
skeletal muscle is mechanically linked opening, whereas cardiocyte is calcium activated
|
|
describe channel permeabilities from phase 0-4 of ventricular contraction
|
p260
|
|
describe channel conductances for a node
|
p261
|
|
what is the effect of adenosine on rate of depolarization and heart rate
|
slows and decreases
|
|
what is the resting potential for potassium, sodium and calcium
|
-85,55,20
|
|
rank these in terms of speed of conduction: atria, av, purkinje, ventricles
|
purkinje > atria > ventricles> av
|
|
what is normal PR interval
|
<200ms
|
|
normal QRS interval
|
<120ms
|
|
what is U wave caused by
|
hypokalemia, bradykardia
|
|
ST elevation in all leads suspicious for
|
pericarditis
|
|
what predisposes to torsades de points
|
qt prolong
|
|
describe findings of congenital long qt
|
defect in na or k channel + sensineural deafness
|
|
rank pacemakers in terms of automaticity: sa, purkinje, his, ventricles, av
|
sa>av>his/purkinje/ventricles
|
|
what ectopic circuit responsible for wpw syndrome
|
bundle of kent
|
|
tx for wpw
|
procainamide, amniodarone
|
|
chads2 for afib
|
chf, htn, age, dm, stroke*2
|
|
which has faster beat: afib or aflutter
|
fib>flutter
|
|
tx for aflutter
|
1a, 1c, 3
|
|
tx for afib
|
2,4
|
|
review rules for ekg interpretation
|
p263
|
|
which mobitz is infranodal
|
2
|
|
which mobitz is in danger of complications
|
2, risk of 3* heart block
|
|
what dz can result in 3* heart block
|
lyme dz
|
|
what center in brain is responsible for increasing sympathetic activity in response to decreased bp
|
nucleus tractus solitarius
|
|
effect of ANP on renal arterioles? What is this mediated by
|
constricts efferent, dilates afferent. Cgmp
|
|
what is the major contributor to aldosterone escape
|
anp
|
|
aortic arch vs carotid baroreceptors -- differences
|
aortic arch only responds to INCREASE BP, whereas carotid response to both. Aortic arch uses cn10, cartodi uses cn9
|
|
central vs peripheral chemoreceptors
|
peripheral measures o2, co2, and ph. Central responds just to pH and co2.
|
|
what mediates cushings reachtion
|
central chemoreceptor
|
|
why might you see a triad of hypertension, bradycardia and depressed respiration in a person
|
increased ICP leads to cerebral ischemia which stimulates central chemoreceptor, which leads to activation of nucleus tractus solitarius, and then that causes hypertension, which then causes baroreceptor to promote reflex bradiacardia
|
|
what organ has the greates share of cardiac CO
|
liver
|
|
which organ has the highest proportion of blood given its size
|
kidney
|
|
how can increased oxygen be delivered to heart
|
increased coronary blood flow
|
|
what is the normal systolic & diastolic pressure in the LV
|
<130, < 10
|
|
what is the normal systolic & diastolic pressure in the RV
|
<25, <5
|
|
what does PCWP a good estimate for
|
left atrial pressure, atrial pressures, diastolic ventricular pressures
|
|
when might the pcwp > lv edp
|
mitral or pulmonic stenosis
|
|
what are the major regulators of cardiac blood flow
|
metabolites - adenosine
|
|
major regulator of brain blood flow
|
metabolites - co2
|
|
major regulator of blood flow to kidney
|
myogenic, tuberoglomerular feedback
|
|
major regulator of muscle blood flow
|
metabolites - lactate, adenosine, k
|
|
major regulator of blood flow to skin
|
sympatheticsc
|
|
what does the main oncotic pressure come from
|
proteins NOT ELECTROLYTES
|
|
what type of edema will lymphatic blockage cause
|
nonpitting cuz it's the interstitial oncotic pressure that's increased
|
|
where willl you find sinusoidal capillaries
|
bm, spleen, liver
|
|
where will you find fenestrated capillaries
|
glomerulus
|
|
mcc of early cyanosis
|
tetrology
|
|
how prevalent is patent foramen ovale
|
20-30%
|
|
what is required for a person w/ tricuspid atresia survive
|
asd, vsd
|
|
what is total anomalous pulmonary venous return
|
lungs empty into right heart without other defects
|
|
what heart defect is most assoc/ w/ fas
|
asd, vsd
|
|
how to distinguish asd vs vsd based on o2 levels
|
asd - o2 steps up in RA, vsd - o2 steps upin RV, pda - o2 steps up only in pulm art
|
|
what maneuver helps to improve oxygenation in tetrology
|
squatting (increased tpr)
|
|
what anatomic defect causes tetrology of fallot
|
anterosuperior displacement of the infundibular septum
|
|
what dzz are assoc/ w/ vsd
|
corrected transposition, tetrology, cru du chat, fas
|
|
what is aorta connected to in transposition
|
RV
|
|
where can a murmur be heard in postductal coarc
|
b/w shoulder blades
|
|
renin levels in person w/ coarc
|
incresaed, dec blood flow to kidney
|
|
most common cause of cyanosis in lower extremeties
|
reversed PDA (eisenmenger) dumping blood distal to subclavian
|
|
what is the collateral circulation w/ coarc
|
anterior intercostal (from IT) -> post intercostal (from aorta), superior epigsstric (from IT) to inferior epigastric (external iliac)
|
|
what is epstein's abnormality
|
maternal lithium use leads to atrialization of RV (cuz tricuspid leaflets are displaced onto RV -- therefore also TR). Dilation of RA can result in WPW.
|
|
what cardiac abormalities are associated w/: 22q11, down, rubella, turner, marfan, maternal diabetes
|
p269
|
|
renin levels in 1* htn
|
low (cuz increased cardiac output)
|
|
complications of htn
|
atherosclerosis, lvh, stroke, chf, renal fail, retinopathy, aortic dissection
|
|
which diurectics are best at electrolyte loss
|
hctz
|
|
mechanism of sodium related htn
|
enters resistance cells and opens calcium channels increasing tpr
|
|
what is arcus senilis
|
lipid deposits in cornea usualy with age
|
|
pathology of monkeberg
|
MEDIAL calcification
|
|
where (in body) is calcification in monkeberg
|
usualyy radial or ulnar
|
|
is intima involved in monkeberg
|
no
|
|
where do fibrous plaques and atheromas usually form
|
intima of arteries
|
|
hyaline arteriolosclerosis of kindey can lead to what appearance
|
shrunken, cobblestoned grainy leather
|
|
what type of arteries does atherosclerosis occur in
|
elastic and medium
|
|
what factors are responsible for smooth muscle migration in atherosclerosis
|
pdgf and tgfbeta
|
|
describe the order of these events in atherosclerosis: smooth muscle, fibrous plaques, endothelial injury, fatty streaks, macrophage and ldl accumulation, foam cell formation
|
p270
|
|
why might atherosclerosis cause htn
|
if its in renal a
|
|
what are the most likely sites of atherosclerosis
|
aaa>coronary>popliteal>carotid
|
|
what is a good way to detect plaque disruption
|
crp
|
|
What infection is a risk factor for atherosclerosis
|
chlamydia pneumoniae
|
|
why are rates of aortic dissection increased in pregnancy
|
inreased plasma volume leads to hypertensive state
|
|
what histological change is associated with aortic dissection
|
cystic medial necrosis
|
|
mediastinal widening on cxr
|
aortic dissection
|
|
what is type B aortic dissection
|
distal to subclavian
|
|
why might aortic dissection have absent pulses
|
compression of subclavian a
|
|
ekg changes in stable vs unstable vs prinzmetal angina
|
st elevation for prinzmetal (cuz its transmural), others are dpression
|
|
what is sudden cardiac death (acute coronary syndrome, not hypertrophic cardiomyopathy) associated with
|
smoking
|
|
what causes sudden cardiac death
|
vfib
|
|
what gender has more prinzmetal
|
w
|
|
explain why an aneurysm is likely to expand
|
increasing radius increases tension
|
|
sx of aaa
|
sudden onset of left flank pain + hypotension + pulsatile mass
|
|
why are women likely to get CAD at a higher age
|
estrogen increases hdls
|
|
what are the most prevalent sites of occlusion in the coronaries
|
LAD>RCA>circumflex
|
|
how long does it take to lose contractily after occlusion? Irreversible injury?
|
60s, 30min
|
|
what causes contraction bands
|
reperfusion injury causes hypercontraction in dying myocytes
|
|
when do neutrophils start to migrate in mi
|
4 hours
|
|
when is the greatist risk for arrythmia in mi
|
first 4 days
|
|
when is greatest risk for free wall ruupture in mi
|
5-10d
|
|
when is greatest risk for papillary muscle rupture in mi
|
5-10d
|
|
when is greatest risk for IV septal rupture
|
5-10d
|
|
when is loss of nuclei and striations most prominent in mi
|
2-4 days
|
|
what is hyperemia and when is it seen in mi
|
2-4d, dilated blood vessels due to inflamation
|
|
when are you likely to see pale heart with tetrazolium stain in mi
|
first day
|
|
why is there a greater risk for rupture in 5-10d
|
cuz macrophages have digested important structural components
|
|
know the histology of mi
|
p271
|
|
when are you likely to see yellow-brown heart in mi
|
by 10 days
|
|
when is greatest risk for ventricular aneurysm
|
7w
|
|
venous thrombus vs arterial thrombus
|
arterial is mostly platelets and atherosclerosis (i.e. coagulation). Kill the platelet action w/ aspirin. Venous thrombus is mostly rbcs and fibrin "red" more coagulation. Use heparin and warfarin to kill
|
|
are mural thrombi red or white
|
mixed
|
|
what are lines of zohn
|
alternating laters of clotting factors and rbcs on thrombus
|
|
what is the main dx for mi
|
ekg in first 6h
|
|
when does cardiac troponin rise
|
after 4h, lasts 7-10 d
|
|
what is characteristic ekg finding of pulmonary embolism
|
s1q3t3
|
|
anteroseptal vs anterior vs anterolateral mi ekg findings
|
v1-v2; v1-v4; v4-v6
|
|
why is posteromedial papillary m likely to rupture
|
rca thrombus serves it
|
|
postinfarct pericarditis vs dressler
|
both are fibrinous pericarditis; but dressler is autoimmune and is several weeks post whereas postinfarct is 3-5d post MI
|
|
when would ckmb likely to reappear if reinfarct
|
3d
|
|
what is ischemic preconditioning
|
p272
|
|
what is myocardial stunning
|
p272
|
|
what is hibernating mycardium
|
p272
|
|
what factors are elevated in hibernating mycoardium
|
tnfalpha,nos
|
|
what is ventricular remodeling
|
p272
|
|
causes of dilated cardiomyopathy
|
alcohol, beriberi, cox, cocaine, chagas, doxorubicin, hemochromatosis, peripartum
|
|
mutations in dystrophin or mitochondrial genes can lead to what type of cardiomyopathy
|
dilated
|
|
eccentric vs concentric hypertrophy
|
dilated vs hypertrophic
|
|
disoriented tangled mycoardium
|
hypertrophic cardiomyoapthy
|
|
how is the murmur in hypertrophic cardiomyopathy different from as
|
outflow tract obstruction is removed by increasing preload (not true of AS)
|
|
inheritance of hypertrophic cardiomyopathy
|
ad
|
|
what dz is hypertrophic cardiomyopathy assoc w
|
freidrich
|
|
cause of death in hypertrophic cardiomyopathy
|
abnormal condunction due to disordered condunction bundles
|
|
which has pmi dislocation. Which has icnreased pmi
|
dilated. Hypertrophic
|
|
tx for hypertrophic cardiomyopathy
|
antiarrythmic 2 or 4
|
|
what gene is oft mutated in hypertrophic cardiomyopathy
|
beta myosin heavy chain
|
|
effect of digitalis on hypertrophic cardiomyopathy
|
increased vacuum created by relaxation of contracted heart results in outflow obstruction
|
|
causes of restrictive cardiomyopathy
|
sarcoid, amyloid, radiation, endocardial fibroelastosis, loffler's syndrome, hemochromatosis
|
|
mcc of restrictive cardiomyopathy in children
|
endocardial fibroelastosis
|
|
ekg changes in restrictive cardiomyopathy
|
low voltage ekg w/ st-t wave chagnes
|
|
complications of myocarditis
|
dilated cardiomyoatphy
|
|
causes of myocarditis
|
cox, echo, influenza
|
|
what maneuver can help releive pericarditis
|
sitting, leaning forward
|
|
cxr findings of pulmonary edema related to chf
|
kerley's lines (lines perpendicular to pleural edge that are parallel to one another or straight lines in upper lung that course diagnonal to hilum(
|
|
what are types of high output failure
|
septic shock, thiamine deficiency, hyperthyroidism, avm shunt, decreased viscosity
|
|
tx for acute coronary syndrome
|
morphine, o2, nitrates, aspirin (MONA) also bb, statin and ace
|
|
sx of bacterial endocarditis
|
systemic sx from emboli and IC (roth spot, osler ode, janeway lesion, nail bed hemorrhage), anemia. Be careful of the IC question missed a qbank question cuz o fit
|
|
what type of pericarditis seen with IE
|
suppurative
|
|
most common bacterial in tricuspid IE
|
saureus, pseud, candida
|
|
what congenital issue can inc risk of ie
|
ANY congenital heart defect
|
|
pt has new murmur, fever, splinter hemorrhage and pos blood culture. Does he have ie
|
need multiple blood cultures
|
|
why is vancomycin oft used to treat IE
|
cuz saureus is usually mrsa
|
|
what type of bacteria seen in subacute ie
|
viridians (sanguis)
|
|
why are valves that are injured more likely to get ie
|
deposition of fibrin and platelets leads to ie
|
|
ie and colon cancer
|
s bovis
|
|
ie and prosthetic valves
|
s epidermis
|
|
what is marantic endocarditis
|
hypercoag state leads to deposition, embolization
|
|
know the pictures for ie
|
p275
|
|
libman sacks vs other endocarditis
|
depositions on both sides of valves
|
|
libman sacks likes to hit what valve
|
mitral
|
|
what are the jones criteria
|
joints, pancarditis, nodules, erythema marginatum, syndenham
|
|
early deaths in rheumatic fever due to
|
myocarditis
|
|
late deaths in rheumatic fever due to
|
sequelae of rheumatic heart dz ESP MITRAL STENOSIS LEADING TO AFIB LEADING TO STROKE
|
|
what labs might be high in rheumatic heart dz
|
aso titers and dnase b
|
|
what are aschoff bodies
|
granuloma w/ anitschkow cells (activated histiocytes) seen in rheymatic heart dz
|
|
what is the likelihood of rheumatic heart dz following nephrogenic s pyogenes
|
none
|
|
ddx of polyarthritis in children
|
jra, rubella, rheumatic fever, henoch scholein
|
|
hypersensitivity in rheumatic heart dz
|
2
|
|
beat to beat variation in qrs of ekg
|
tamponade
|
|
neck vein distention on inpsiration
|
tamponade
|
|
what heart chambers will have the highest diastolic pressure during tamponade
|
it's all equal
|
|
when might you see a depressed systolic pulse during inspiration
|
happens normally but exaggerated in obstructive lung dz incl sleep apnea, croup, tamponade
|
|
treek barking of aorta
|
syphilis
|
|
pericardial effusion vs restrictive pericarditis
|
muffled heart sounds in effusion, pericardial knock (heart hitting pericardium) in restrictive
|
|
what dzz can cause serous pericarditis
|
autoimmune, virus, uremia
|
|
most common 1* cardiac tumor in adults
|
myxoma
|
|
can atrial myxomas embolize
|
yes
|
|
kussmaul's sign
|
increase in jvd on inspiration
|
|
what can be used to tx raynaud
|
ccb
|
|
wegener's vs goodpasture
|
goodpasture only affects lung. Wegeners affects upper airway also
|
|
what are things that can cause perforation of nasal septum
|
wegeners (saddle nose), cocaine
|
|
can someone w/ wegener's get an earache
|
yep
|
|
how to tx wegeners
|
cyclophosphamide and CS
|
|
increased marker in microscopic polyangiitis
|
panca
|
|
synchrony of lesions of microscopic polyangitis, henoch schonlein, PAN
|
PAN lesions are of different stages
|
|
granulomatous vasculitis
|
wegeners, churg strauss, takayasu, temoral arteritis
|
|
vasculitis that affects small vessels
|
raynaud, wegeners, sturge-weber, henoch schonlein
|
|
vasculitis that affects large vessels
|
takayasu and temporal arteritis
|
|
which vasculitis is associated with glaucoma
|
sturge weber
|
|
which vasculitis is associated with asthma and peripheral neuropathy
|
churg strauss
|
|
which vasculitis is associated with eosinophilia
|
churg strauss
|
|
what is cryoblobulinemia associated with
|
hcv, mpgn1, mm
|
|
name some infectious vasculitis
|
rocky mountain spotted fever. Disseminated meningococcemia. Syphilis. Mucormycosis
|
|
triad of henoch schonlein
|
skin, joints, gi
|
|
what vasculitis is associated with iga nephropathy
|
henoch schonlein
|
|
what vasculitis is associated with melena
|
henoch schonlein and pan
|
|
segmental thrombosis of medium vessels
|
buergers
|
|
vasculitis associated with peeling of palms and soles
|
kawasaki
|
|
tx for kawasaki
|
self limiting, maybe iv ig NO STEROIDS
|
|
vasculaitis associated with coronary aneurysms in children
|
kawasaki
|
|
vasculitis that involves renal and visceral vessels and avoids lungs
|
pan
|
|
vasculitis assoc w hbv
|
pan
|
|
tx for pan
|
cyclophosphamide and CS
|
|
ocular disturbances, arthritis and weak upper pulse
|
takayasu
|
|
jaw claudication and unilateral headache with elevated esr
|
temporal arteritis
|
|
what is temporal arteritis assoc/ w/
|
polymyalgia rheumatica
|
|
polymyalgia rheumatica vs polymyositis
|
both are mucle weakness, but polymyositis has increased ck
|
|
progression of strawberry hemangioma
|
grows w child then regresses
|
|
who does cherry hemangioma occur in
|
elderly
|
|
what is pyogenic granuloma and where does it occur and in who
|
capillary hemagnioma that can ulcerate, assoc/ w/ trauma and preg. Oft in gums
|
|
cystic hygroma
|
lymphangioma of neck w/ turners
|
|
glomus tumur - what does it arise from, where?
|
modified smooth muscle cells of thermoregulating glomus body, under fingernails
|
|
bacillary angiomatosis - what causes it
|
bartonella henselae
|
|
lymphangiosarcoma is oft complication of what
|
post radical mastectomy, persistent lymphedema
|
|
what causes kaposis
|
hhv8
|
|
what antihtn is good for chf
|
at2 causes modeling and reduced contractility - so ACEi, spironolactone, beta block (if compensated)
|
|
what helps to protect against diabetic nephropathy
|
acei
|
|
mechanism of hydralzine
|
increased cgmp
|
|
first line for pregnancy htn
|
hyralazine and metyhldopa
|
|
what is the only anti-HTN that can cause peripheral edema
|
ccb
|
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best drug to tx raynauds
|
ccb
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best drug to prevent complications of subarachnoid hemorrhage
|
ccb
|
|
what antihtn can cause constipation
|
ccb
|
|
bioavailablity of nitroglycerin vs isosorbide dinitrate
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isosorbide mononitrate = 100%
|
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what agent is responsible for Monday disease (tachycardia, dizziness, and headache on beginning of workweek)
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nitroglycerin
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|
triald of malig htn
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kidney dmg + papilledema + htn
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what antihtn can cause hyperglycemia
|
diazoxide
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|
which antihtn can mask sx of hypoglycemia in diabetics
|
bb
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|
what antihtn can cause cyanide tox
|
nitroprusside
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|
which antihtn acts on d1 receptors
|
fenoldopam
|
|
how do nitrates affect: edv, bp, contractility, hr, ejection time, mvo2
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down, down, up, up, down, down
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|
how do bb affect: edv, bp, contractility, hr, ejection time, mvo2
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up, down, down, down, up, down
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|
what bb's are ci in angina
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pindolol, acebutolol
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|
mechanism of minoxidil
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k+ stimulator, treats severe htn
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which antihtn can cuase hypertrichosis
|
minoxidil
|
|
mechansim of cilostazol
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PDE3 inhibit that inhibits BOTH PLATELET AGGREGATION AND VASODILATES
|
|
tox of statins
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hepatotox, rhabdotox
|
|
mechism of niacin
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inhibits adipose lipolysis, reduced hepatic vldl excretion
|
|
which antilipid can cause acanthosis nigricans
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nicain
|
|
which antilipid can cause gout
|
niacin
|
|
which antilipid increases formation of gallstones
|
resins
|
|
what is the major effect of resins
|
lowers ldls
|
|
which antilipids increase in liver ldlr expression
|
resins
|
|
which antilipids have chance of increased lfts
|
statin, ezetimibe
|
|
which antilipid can cause myositis
|
fibrate
|
|
which antilipid has strongest effect on tgs
|
fibrate
|
|
which combination of antilipid increases gallstone
|
fibrate and resins
|
|
which combination of antilipids increases myopathy
|
statin and fibrate
|
|
where does ryanodine act
|
blocks ryanodine receptor on sarcoplasmic reticulum, decreases intracellular calcium
|
|
what is phospholambam
|
protein that increases intracellular calcium
|
|
what type of calcium channels are found in the membrane of cardiomycotes
|
l-type or nondhp
|
|
what is half life of digoxin
|
40h
|
|
excretion of digoxin
|
kidney
|
|
what type of arrythmia is digoxin likely to treat
|
afib
|
|
toxicity of digoxin
|
cholinergic (INCLUDES BLURRY YELLOW VISION), ekg (increases pr, decreases qt- cuz it increases calcium, SCOOPING - scoop shape of st segment), hyperkalemia
|
|
contraindications to digoxin
|
renal failure, hypokalemia, quinidien
|
|
tx for digoxin od
|
1. normalize k,mg 2. lidocaine/pheny 3. anti fab
|
|
name some 1a drugs
|
quinidine, procainamide, disopyramide
|
|
name some 1b drugs
|
lido, mexilitine, tocainide, pheny\
|
|
name some 1c drugs
|
fecainaide, encainide, propafenone
|
|
which antiarythmic is best post mi
|
1b
|
|
which antiarythmic is worst post mi
|
1c
|
|
contraindication to class 1 drugs
|
hyperkalmeia
|
|
compared to other drugs, what are class 1 drugs more selective for
|
selectively depress tissue that is frequently depolarized (i.e. fast tachy)
|
|
what class 1 is used as last resort
|
1c
|
|
what drugs can lead to headache and tinnitus
|
quinidine
|
|
class of drugs that can prolong qt
|
1a and 3
|
|
what class of drugs affects preferentially ischemic tissue
|
1b
|
|
which drugs would have a qrs prolong? if it did not affect qt, what would it be?
|
class 1 (blocking na). 1c will not affect qt
|
|
what is the shortest acting bb
|
esmolol
|
|
which bb may cause dyslipidemia
|
metaprolol
|
|
how to tx bb overdose
|
glucagon
|
|
name some class 3 blocks
|
sotalol, ibutilide, bretylium, dofetilide, amniodarone
|
|
which class 3 block can cause hypotension
|
bretylium
|
|
what is treatment of choice for vtach
|
qbank says amiodarone
|
|
what antiarrythmic can cause photodermatitis
|
amidarone
|
|
what antiarrythmic can cause constipation
|
amnidarone
|
|
what antiarrythmic can result in corneal deposits
|
amniodarone
|
|
effect of ccb on skeletal muscle
|
nothing cuz in skeltal muscle most ca influx is from intracellular
|
|
what antiarrythmic can cause impotence
|
bb
|
|
mechaism of adenosine
|
increases gK, which hyperpolarizes the cell and decreases calcium
|
|
best drug for killing psvt
|
adenosine
|
|
what blocks effects of adenosine
|
theophylline
|
|
why will valsalva invoke a baroreceptor response
|
increased intrathoracic pressure will compress veins and reduce venous return and decreases co and map
|
|
dromotorpic effect
|
increases conduction velocity thru av
|
|
what is bowditch staircase
|
increased hr causes more and more ca to accumulate, which causes more contractility
|
|
describe cardiac output in terms of o2 consumption
|
co = o2 consumption / (arterial o2 - venous o2)
|
|
which prostaglandins dilate
|
PGE, PGI
|
|
which prostaglandins constrict
|
PGF
|
|
what is mycotic aneurysm
|
vessel weakening by pathogen usually bacterial (b fragilis, pseud, salmon)
|
|
endarteritis obliterans
|
destruction of vasa vasorum of aortic arch by syphilis
|
|
what is stasis dermatitis
|
discoloration and hemosiderin around ankle
|
|
PHLEBOTHROMBITIS vs THROMBOPHLEBITIS
|
thrombosis of vein vs not a thrombosis. Phlebothrombosis has no inflammation. Thrombephlebitis is just pain and inflammation in vein cuz of IV cannulation or infection or PANCREATIC HEAD CARCINOMA
|
|
sx of thoracic outlet syndrome
|
arm sleeping, numbness and paresthesia, no pulse when arm stretched to the side and head turned to same side
|
|
acute lymphangitis sx
|
red streak, usually cellulitis from s pyogenes
|
|
what is lymphedema
|
collection of lymph fluid due to blockage of drainage
|
|
what is canca
|
proteinase 3 ab
|
|
what is panca
|
myeloperoxidase
|
|
what vascular abormality in fetus can result in increased risk of congential abormality
|
single umbilical a
|
|
watter bottle on cxr
|
pericarditis
|
|
complications of gas embolus
|
pneumothorax, aseptic necrosis, pulmonary embolus
|
|
what cardiac pathologies can embolize
|
IE, atrial myxoma, marantic endocarditis
|
|
resistance to infarction by prior non lethal repititive ischemia
|
ischemic preconditioning
|
|
brief ischemic episodes followed by reperfusion that leads to reversible loss of contractility
|
myocardial stunning
|
|
chronic but reversible loss of contractile function w/ inc tnf and nos caused by persistent ischemia
|
hibernating myocardium
|
|
chronic change in shape of heart as compensation for changes in preload/afterload
|
ventricular remodeling
|
|
2 ways to accentuate s3
|
1. lateral decubitus 2. exhalation
|
|
3 sources of energy for the heart
|
1. FA oxidation (60%) 2. glucose oxidation 3. glycolysis
|
|
where can the posterior descending a branch from in a left dominant heart
|
circumflex
|
|
what is the order of JVP's
|
at carter's crossing, vehicles yield (acxvy)
|
|
effect of inspiration on heart murmurs
|
makes right sided heart murmurs louder
|
|
effect of hand grip on heart murmurs
|
increases TPR, so quiets AS and makes MR louder
|
|
effect of lying down while on pregnancy
|
compression of IVC leads to decreased preload and thus less CO
|
|
effect of squatting on preload
|
in the beginning, have increased preload, but after a bit, get increased TPR so less preload (that's why it helps with PDA)
|
|
effect of increasing preload on MVP murmur
|
increased filling time for LV means click moves closer to S2
|
|
what can cause a U wave
|
hypokalemia, bradykardia
|
|
what can tx wpw
|
procainamide, amniodarone
|
|
what infectious disorder can result in 3* heart block
|
lyme dz
|
|
effect of anp on renal arterioles? what is the mechanism
|
constrict efferent, dilate afferent using cgmp.
|
|
how is infundibular septum displaced in ToF
|
anterior and superior
|
|
defect where tricuspid leaflets are displaced into RV, resulting in hypoplastic RV and tricuspid murmur
|
epsteins abnormality
|
|
what electrical conduction deficit is common in epsteins abnormality
|
wpw
|
|
monday disease caused by drugs
|
nitrate exposure at workplace
|
|
when do you tx with warfarin for afib
|
chads2>=2
|
|
irregular heartbeat with no P waves
|
afib
|
|
which antiarrythmic may cause chest pain after being administered
|
adenosine
|
|
what color are roth spots
|
white surrounded by red
|
|
what kinds of cells may be seen in xanthoma
|
lipid laden histiocytes (touton giant cells) containing lipids and foamy cytoplasm
|
|
what type of necrosis is seen with small vessel vasculitis
|
fibrinoid necrosis
|
|
when do you start to see early coagulation necrosis after MI
|
after 4 hours. contraction bands seen after 12-24h.
|