Cards UWORLD Flashcards
access point for 3 vessel CABG
needs to access great seaphenous vein which
originates medial side of foot and courses anterior to medial malleolus and then travels up the medial aspect of leg and thigh…surgeons access just inferolateral to pubic tubercle
most common site of truamatic deceleration aortic injury
aortic isthmus just before ligamentum arteriosum (just right past initial downsloping of aortic arch)
in chronic aortic regurg from infection, what physiologic change to heart structure maintains cardiac output?
increased LV stroke volume (eccentric hypertrophy in LV from aortic regurg helps with this)
MOA fibrates
upregulate lipoprotein lipase by avtivating PPAR-alpha which leads to decreased hepatic VLDL and increaed LPL (lowers triglycerides)
omega 3 fatty acids also help with this
MOA nitrates
relaxes vascular smooth muscle causing peripheral vasodilation (venodilation) which will DECREASE PRELOAD/LVEDV, modest reduction in afterload and mild coronary artery dilation
this all decreases myocardial o2 demand
Hx of depression, tachycardia, prolonged QRS/QT
dx and rx
TCA overdose (too much blockade of fast sodium channels) causing prlonged QT treat with sodium bicarb to increase pH and favors extracellular Na which will alleviate blockade
How does embolus travel in retinal artery occlusion
internal carotid -> opthalmic -> retinal artery
biochemical MOA nitrates
increase NO -> increase cGMP -> decreases intracellular Ca -> myosin light chain DEPHOSPHORYLATION -> smooth muscle relaxation and vasodilation
MOA class III antiarrythmics and what are they?
block potassium channels which will prolong ventricular repolarization…prolongs QT and may lead to torsades
AIDS amiodarine ibulitide dofetilidude solatol
pathogenesis of pulmonary arterial hypertension
2 hit hypotehsis
AD mutation of BMPR2 gene….second insult (drugs, infection) activates disease process which involves increased endotheilin (vasconstrictor) and decreased NO and prostacyclin levels….smooth muscle proliferation
Karotkoff sounds heard first only during expiration at certain pressure….then at a lower pressure heard at all phases of respiration indicate what?
peridcardial dx…like tamponade, severe asthma, or constrictive pericarditis
this is PULSUS PARADOXUS
MOA beta agonists
bronchial smooth muscle relaxation via increased intracellular cAMP
10 year old immigrant with limited vaccine status presents with exertional dyspnea, easy fatigability, and toe cyanosis and clubbing but no finger or upper extremity abnormalities
patent ductus arteriosus
ACUTE pericarditis in otherwise healthy person associated with what physical exam finding
friction rub
NOT PULSUS (this is seen in more severe conditions like COPD, cardiac tamponade or severe asthma)
How to calculate number needed to treat/harm?
first calculate absolute risk reduction (ARR)
control rate - treatment rate
NNT = 1/ARR
How do AV shunts affect preload and afterload?
decrease afterload (blood can bypass arteriole resistance and just go stragiht into veins)….but increase preload
What does posterior descending supply?
posterior 1/3 of intraventricular septum, inferior wall of left ventricle, posterior wall of ventricle, posteriormedial part of papillary muscle
Adverse effect of statins and what can exacerbate theM?
rhabdo
cytochrome p 450 INHIBITORS can exacerbate them
SICKFACES.com
Sodium valproate, isoniazid, cimetidine, ketoconzaole, fluconazole, acute alcohol abuse, chloramphenicol, erythromycin, sulfonamides, ciprofloxacin, ondansetron, metronidazole
histologic color/hallmark of aging cells
lipofuscin (product of lipid peroxidation and free radical injury that chronically accumulates)
What at low doses can stimulate contractility in the heart and increase renal blood flow?
dopamine
infant born ok presents with new blowing holosystolic murmur a few days after birth
small vsd
combo of what two anginal drugs can cause severe bradycardia and hypotension
non-dihydropyridine Ca channel blockers (verapamil, diltiazem) and beta blockers
why does infusion of selective a1 adrenergic agonist (phenylephrine, methoxamine) eventually lead to decreased heart rate?
these drugs lead to vasoconstriction and increased systemic BP which will stimulate baroreceptors in carotid sinus and aortic arch to increase efferent firing which will increase VAGAL TONE on heart to inhibit pacemaker SA activity and slow conduction through AV node
patient comes in with hypertensive crisis…what’s a good medication that will cause arteriolar dilation, improve renal perfusion, and increase natriuersis
fenoldopam (selective D1 recepter agonist)
MOA sildenafil
phosphodiesterase5 inhibitor that decreases degradation of cGMP which will cause vasodilation of arteries….simiilar to action of nitrates and BNP
Which antiarrythmic has flushing, hypotension, chest pain, bronchospasm as adverse effects?
adenosine
useful in certain SVT, works by pushing K out of cells and hyperpolarizing cell, decreasing Ica and AV node conduction