step 1 studying deck 2 Flashcards
what murmur radiates to the neck
aortic stenosis
calcium degeneration and impaired leaflet mobility
why don’t CCBs affect skeletal muscle
the skeletal muscle does not depend on extracellular calcium influx
skeletal muscle contraction only in reponse to acetylcholing
what is a side effect of antracyclines
antracyclines are chemo agents associated with severe cardiotoxicity (specifically dilate cardiomyopathy)
(daunorubicin, doxorubicin, epirubicin, idarubicin)
dilated cardiomyopathy is cumulative dose dependent and can present months after stopping the drug
doxorubicin associated cardiomyopathy is characterized by swelling of the sarcoplasmic reticulum as an early sign… later on you see a loss of cardiomyocytes (“myofibrillar dropout”)… symptoms are of biventricular CHF
prevention of doxorubicin cardiomyopathy= dexrazoxane (an iron chelating agent that decreases oxygen free radical formation)
what are some causes of restrictive cardiomyopathy
hemochromatosis amyloidosis sarcoidosis radiation therapy (chemo= dilated cardiomyopathy)
what are some causes of pericardial fibrosis
cardiac surgery
radiation therapy
viral infections of the pericardium
what are Janeway lesions
non tender, macular, red lesions to the palms and soles
due to micro-emboli to skin vessels
(septic embolization from IE valvular vegetations)
associated with IE (fever, SOB, new holosystolic murmur at the apex (mitral regurg)… here you can also see petechiae, splinter hemorrhages, roth spots, janeway lesions, and osler nodes (painful lesions to the fingers and toes due to immune complexes)
what vagal maneuvers can be used to acutely terminate paroxysmal supraventricular tachycardia (PSVT)
carotid sinus massage (increases baroreceptor firing)
valsalva
cold water immersion
carotid sinus:
afferent limb= from baroreceptors in sinus to the vagal nucleus and medullary centers via glossopharyngeal nerve (9)
efferent limb=parasympathetic impuses to the SA and AV nodes via the vagus nerve (10)
PNS slows conduction through the AV node and prolongs refractory period
what would cause excessive LA systolic pressure
mitral regurg
(mitral stenosis would increase LA pressure during diastole, not during systole, because there is obstruction to passive filling)
there is a characteristic upsloping “v wave” in the LA during catheterization
what does this patient have?
40 yo F with depression and HTN. found obtunded in apartment, hypotensive, and bradycardic…. IV glucagon is given and she improves
the patient overdosed on her beta blocker meds (causes a diffuse non selective blockade of beta receptors leading to depressed contractility, bradycardia, and varying AV block (end with low CO state)…. notice that depression was first in her pmh
glucagon is the drug of choice for beta blocker overdose
glucagon activates GPCR on cardiac myocytes and increases cAMP to increase intracellular calcium during muscle contraction and increase SA node firing (to increase HR and contractility in this patient independent of adrenergic receptors)
what is costosternal syndrome
aka costochondritis
aka anterior chest wall syndrome
due to repetitive activity/injury
what drugs have negative chronotropic effects
when used concomitantly, these can have additive negative affects on HR, AV node conduction, and myocardial contractility
ADRs= bradycardia, sinus arrest, hypotension
beta blockers (ex metoprolol, atenolol)
non dihydropyridine CCBs (verapamil, diltiazem)
cardiac glycosides (digoxin)
amiodarone and sotalol (class 3 antiarrhythmics)
cholinergic agonists (pilocarpine, rivastigmine)
what is the reflexive response to vasodilator medications
reflex tachycardia
example= beta blockers and non dihydropyridine CCBs both decrease HR, AV node conduction, and myocardial contractility
how do fibrates work
they reduce hepatic VLDL production
gemfibrozil
fenofibrate
they activate peroxisome proliferator-activated receptor alpha (PPAR alpha) leading to decreased hepatic VLDL production and increased LPL activity
theyre great for decreasing TGs
other options are fish oil with omega 3 FA to decrease VLDL production and inhibit apo B synthesis (to decrease TGs)
what does ezetimibe, cholestyramine, and PCSK9 inhibitors do
ezetimibe blocks cholesterol absorption
cholestyramine is a bile acid binding resin (increases fecal losses)
PCSK9i are monoclonal ab’s that reduce LDL receptor degredatikon in the liver
what keeps the PDA open
prostaglandin E2 from the placenta combined with right to left blood flow across the PDA
PDA= continuous murmurm tachycardia, widened pulse pressure in large PDAs (this 12 day old BP was 41/12), and respiratory distress
after birth the separation from the placenta and rapid drop in pulmonary vasc resistance normally closes the PDA (failure to close is common in premies)
untreated PDAs can cause pulmonary edema, heart failure, or eisenmenger syndrome
tx= in babies give NSAIDS to inhibit prostaglandin E2 (indomethacin, ibuprofen)
how can you recognize pulsus paradoxus in a question stem
korotkoff sounds are what is heard when you listen with a stethoscope while taking a manual blood pressure
this question stem says:
at 120 mmHg intermittent korotkoff sounds are heard only during respiration and at 100 mmHg korotkoff sounds are heard throughout the resp cycle
(the difference between the systolic pressure at which they sounds are heard and the pressure at which they are heard throughout all the phases of respiration= 20 mmHg…. and pulsus paradoxus is an exaggerated drop in systolic BP with inspiration >10 mmHg)
pulsus paradoxis= pericardial disease
(in tamponade the RV volume increases as normal but because the RV can’t expand, the right ventricle pushes the interventricular septum into the LV causing a lower end diastolic volume and lower stroke volume and drastic change in the systolic BP)
basically seen in severe obstructive lung diseases and pericardial issues
what is the cause of pulsus parvus el tardus
slow rising low amplitude pulse due to diminished stroke volume and prolonged LV ejection time
due to a fixed LVOT (ex= from aortic stenosis)
what does valsalva doe to preload
(straining phase)
decreases preload
blowing out against a closed glottis increases intrathoracic pressure which is exerted onto the pericardium which then compresses the IVC and SCV and less blood is returned to the heart
what does pheylephrine do
selective alpha 1 agonist
what makes pitting edema become hard and non pitting
due to progressive fibrosis and thickening of the overlying skin
a 23 yo F immigrant has SOB and as a child had bilateral knee swelling. she has a murmur over the apex
mitral regurg, radiates to the axilla
knee swelling as a child= ARF as a kid
ARF in other countries almost always have significant mitral valve disease (=MR in first few decades of life)
in older patients they typically have mitral stenosis and regurg (MS would only be heard in diastole)
involuntary head bobbing is a sign of what
wide pulse pressure
caused by aortic regurg
what does the graphs look like for a noncompetitve/irreversible inhibitor vs a recersible competitive inhibitor drug
noncompetative/irreversible= Vmax is decreased... graph has a similar shape but does not peak as high vertically (ex= phenoxybenzamine is an irreversible alpha 1 and alpha 2 antagonist... used to treat a pheo which over produces norepi, and thus the graph showed norepi and then drug A which ended up with this pattern meaning the drug was inhibiting norepi and the answer was phenoxybenzamine... even high doses of norepi cant overcome phenoxygbenzamine because its irreversible)
reversible competative inhibitor= same Vmax, but the Km is increased (thus the same shape but the graph is shifted to the right)
(ex= labetalol and phentolamine are reversible competitive antagonists of alpha 1 and beta receptors… high dose norepi can overcome these drug’s inhibition)
what is coarctation of the aorta associated with
can be associated with berry aneurysms at the circle of willis
these berry aneurysms are prone to rupture when associated with coarctation due to HTN
results in spontaneous intracranial subarachnoid hemorrhage