uworld Flashcards
methimazole (use, MOA)
- hyperthyroid
- prevents organification of coupling of iodine in the thyroid
metoclopramide (MOA, use)
- dopamine antagonist
- prokinetic and antiemetic properties: increase gastric motility and prevent nausea/vomiting
misoprostol (what is it, what is it used for)
- prostaglandin E1 analogue
- used to prevent NSAID ulcers
Sulfonylureas (MOA, use (be specific), and who you should be careful with)
- close K+ channel in beta islet cells, membrane depolarizes, triggers insulin release via increased intracellular calcium
- only useful in T2DM, need some beta function to release endogenous insulin
- risk of hypoglycemia in renal failure patients
Sulfonylureas (1st gen (2) vs 2nd gen (3) and SE of each generation)
- 1st gen: tolbutamide, chorpropramide … disulfram-like
- 2nd gen: glyburide, glimepiride, glipizide … hypoglycemia
bupropion (MOA, one bad SE, two benefits of using as opposed to other antidepressants)
- unknown MOA (sorry), but results in increased norepi and DA
- SE: Sz in bulimic pts
- benefits: smoking cessation and no sexual SE
name 4 SSRIs
-fluoxetine, paroxetine, sertraline, citalopram
name 2 SNRIs
-venlafaxine, duloxetine
name 4 MAOIs (MAO takes pride in shanghai) also what is the general MOA of MAOI’s
- tranylcypromine, phenelzine, isocarboxazid, silegiline (MAO-B selective)
- increases levels of monoamine neurotransmitters (norepi, serotonin, DA) by decreasing breakdown within neurons
alpha-glucosidase inhibitors (name 2 and MOA)
- acarbose, miglitol
- inhibit alpha glucosidase in intestinal brush border, delays hydrolysis of sugar and therefor glucose absorption
- best at lowering post-prandial hyperglycemia
acarbose and miglitol are ….. (class) used to treat ….
- alpha glucosidase inhibitors
- T2DM
nimodipine (special Ca2+ channel blocker), why?
-tx for vasospasm that is a common complication (up to 50%) 4-12 days after subarachnoid hemorrhage
B-blockers can be used in thyrotoxicosis because…
- high levels of thyroid hormone up regulate insertion of B-receptors into membranes, increasing sensitivity to sympathetic outflow (block those receptors)
- B-blockers also inhibit T4 –> T3 conversion
pyrazinamide (what is it used for, what is its unique characteristic)?
- RIPE treatment of TB
- most active in acidic environment like inside lysosomes
antidote for digoxin toxicity?
-magnesium (also effective in tornadoes de pointes)
finasteride (MOA, tx for… bonus for another use that is primarily cosmetic, but arguably as detrimental)
- 5-alpha-reductase inhibitor (prevent conversion from T- DHT)
- tx: BPH, bonus for… baldness
anastrazole (MOA)
- aromatase inhibitor
- post-menopausal women with breast cancer (shooting from the hip here, but maybe also precocious puberty or CAH to prevent early fusion of long bones)
palivizumab (MOA)
-monoclonal antibody agains F-protein in RSV
fidaxomicin (tx for) bonus for alternative option
- recurrent c. diff
- fecal implant
dobutamine (primarily affects… (receptor type) and is used in…)
- Beta 1 receptors
- cardiac stress testing
ethosuximide (MOA)
- blocks T-type Ca2+ channels
- tx for absence sz
phenytoin (MOA)
-blocks Na+ channels and delays rate of recovery
adenosine (MOA) and antagonists (2)
- opens K+ channels in cardiac pacemaker cells, prolonging K+ release and hyper polarizing them (more negative)
- prevents Ca+ T-type channels from opening, decreasing initial inward current of Ca+ (also hyper polarizing)
- caffeine and theophylline
niacin, increases levels of… name 3 side effects
- increases HDL, can lower LDL a little bit (MOA: decreases synthesis of VLDL and inhibits lipolysis in adipose)
- red, flushed face (due to prostaglandin mediated vasodilation, can be prevented with co-administration of aspirin.
- hyperglycemia.
- hyperuricema (exacerbate gout).
dapsone (MOA… generally speaking, major use, 2 side effects (one in a specific population))
- kind of like a sulfa, inhibits folate synthesis
- tuberculoid leprosy
- agranulocytosis
- hemolytic anemia in G6PD
polyethylene glycol (class)
-osmotic diuretic
procainamide (class, use, SE)
- class 1A anti-arrythmic
- best for suppressing arrhythmias from places normally responsible for automaticity
- can prolong QT, susceptible to v-tach, SLE
transpeptidases (what is it? i don’t know, i don’t know.)
-penicillin binding protein that crosslinks peptidoglycan (target of penicillins and cephalosporins)
daptomycin (tx, MOA, can’t be used in…, SE)
- tx: for for s. aureus when nothing else is working (MRSA)
- creates pores in the membrane which allows ions to leak, depolarizing cell, preventing DNA/RNA synthesis, leading to cell death
- inactivated by surfactant, no can do pneumonia
- SE: myopathy, monitor creatine kinase, careful with statins
linezolid (tx, MOA, SE)
- MRSA
- binds to 23s portion of 50s ribosomal subunit, preventing formation of 70s ribosome
- thrombocytopenia and optic neuritis
name the class 3 anti-arrythmetics (4)
- AIDS
- amiodarone, ibutilide, dofetilide, soltalol
what is DRESS syndrome
- drug reaction with eosinophilia and systemic symptoms
- 2-8 wks after starting new drug (anticonvulsants are high risk), marked eosinophilia and impressive rash that can coalesce into giant single plaque, fever, facial edema
- thought to involve reactivation of herpes virus followed by massive t-cell rxn. self resolving after a few weeks off drug
succinylcholine (MOA, SE) *sorry, its a beast
- depolarizing skeletal muscle relaxant
- acts at nicotinic ACh receptors (stimulating), but not degraded, resulting in constant stimulation and no chance for repolarization
- SE: because nicotinic ACh receptors are at non-selective channels, not only does Na+ rush in, but K+ rushes out, prolonged use in susceptible pts (people with lots of K+ around (crush, burn injuries, demyelinating dz)) can be in big trouble for cardiac arrhythmia