Pharm set in addition to scholar-rx

what is the first line drug to treat ADHD in children and what is the MOA?

methylphenidate → indirect sympathomimetic agent that stimulates the release of NE and dopamine

what is this OD? how do we treat this? MOA of treatment?

child got into mothers anxiety meds, now child has unsteady gait, low respirations, slurred speech, no change in pupil size

child likely took a benzo (“pam” and “lam”) → treat with flumazenil which is a competitive antagonist that displaces the benzo from its binding site

a pt presents with increased urination and has a high serum glucose level, pt also has HTN and now we need to control it with medication. What drug and MOA is appropriate for this pts HTN?

increased urination and increased glucose = type 2 diabetes → ACE inhibitors (“pril”) which inhibit the conversion of angiotensin I to angiotensin II

note: DM can cause kidney disease and ACEi are renal-protective, this makes them a good choice for pts with both HTN and diabetes

lithium has what adverse affect in regards to the kidneys, describe it

nephrogenic diabetes insipidus → impaired response to vasopressin in the collecting duct

a pt has an EKG that shows an irregularly irregular pulse, what is this and how do we treat it long term?

atrial fibrillation → direct oral anticoagulant like “xabans” first line long term therapy

what are the cardioselective beta-blockers?

Metoprolol, atenolol, and esmolol

*note that non-selective beta blockers are contraindicated in COPD, so if a pt needs a beta blocker for their heart but also has COPD, then you need a cardioselective beta blocker)

If we prescribe a pt a beta-blocker to treat their HTN, what do we expect to happen to their renin, ATII, aldosterone, and GFR?

all go down because if you reduce the release of renin when everything else down the line goes down too

what drugs/drug classes are known to cause hyperkalemia?

K-sparing diuretics (spironolactone, etc.) and ACE inhibitors (“pril”)

note: aldosterone is what affects potassium, and both drug classes inhibit/lower aldosterone thus increasing potassium

also digoxin (bc it messed with the Na/K pump

what pathogen and drug?

pt presents with recurrent fevers, headache, and chills and recently emigrated from Sierra Leone, now pt has developed torsades

pt has malaria → plasmodium falciparum → treated with quinidine

what drug? what serum electrolyte abnormality is associated with this drug? explain

pt has congestive heart failure and is on medication for it, pt now has blurry, yellow-tinted vision, dizziness, and nausea

digoxin toxicity → hyperkalemia because digoxin inhibits the Na/K-ATPase, so if the pump doesn’t work then no K gets pumped into the cell and it stays in the blood

what is the MOA of a nonopioid drug used to rapidly relieve pain from an MI?

nitroglycerin → causes veno-dilation that reduces venous return (which decreases workload of the heart)

what is this? How do we treat this?

pt presents with chest pain and SOB and “feels like she is about to die”, dizziness, and tingling of hands; troponins are normal and normal EKG

panic attack → benzo (pam or lam)

what is this initial therapy for allergic rhinitis (itchy watery eyes and nasal congestion during spring when outside)

second-gen antihistamines (loratadine, fexofenadine, desloratadine, and cetirizine)

what drug is a potent vasodilator used as first line treatment for HTN in pregnancy? what AE is it associated with and how can we manage this?

hydralazine → can cause reflex tachycardia so it should be administered with a beta-blocker

phase 0 of the action potential in SA nodal cells is different from phase 0 of the cardiac action potential. why? what drugs act on each?

SA nodal cells: phase 0 goes with calcium channels → type IV AAs

cardiac myocytes: phase 0 goes with Na channels → type I AAs

If a pt is being treated with chemotherapy and now has hematuria but otherwise normal (some nausea after treatment), what drug?

cyclophosphamide → hemorrhagic cystitis

pt with decompensated heart failure, and CAD now has irregular rate. what is this and how to treat it initially?

atrial fibrillation → amiodarone (note long term treatment is with anticoagulant)

pt presenting with an MI needs lots of meds, if the pt is on recreational drugs like cocaine and heroin, then one treatment is absolutely contraindicated. what drug and why?

treat with beta blockers typically, but are CI with cocaine use due to unopposed alpha activation leading to unopposed vascular smooth muscle contraction

what is this? what drug and MOA treat this?

pt given haloperidol then presents with high temp, muscle rigidity, and mental status change

neuroleptic malignant syndrome (NMS) → treat with dantrolene → MOA is prevents release of Ca from the sarcoplasmic reticulum of skeletal muscle

what drug? what AE?

medication that inhibits the renal Na/K/Cl transporter

loop diuretics → loops “lose” calcium → hypocalcemia

(thiazides increase calcium)

what drug and MOA?

treat pt for altitude sickness

acetazolamide → carbonic anhydrase inhibitor that prevents HCO3 ion reabsorption

what recreational drug do we see hallucinations, dilated pupils, but normal vital signs (no tachycardia, HTN, etc.)?

LSD → lysergic acid diethylamide

How do statins affect the michealis-menten constant (Km) of HMG-COa reductase?

increase it

if a pt has a mechanical heart valve then has a baby with defects, what is the culprit?

pts with mechanical heart valves need anticoagulation (aspirin, warfarin, or heparin) → warfarin is teratogenic (baby has calcifications of vertebrae, depressed nasal bridge, etc.)

what adverse affect and likely drug?

pt is treated for schizophrenia then gets lip smacking and abnormal tongue and jaw movement

tardive dyskinesia → haloperidol

what drug?

pt is a teenager who took some pills from his friends and now has increased grunting and blinking and increased HR and BP, dilated pupils, is flushed and anxious and has episodes where is gets a “weird sense” of happiness and contentment

methylphenidate (stimulant with high misuse potential)

what molecular affect on vascular smooth muscle cells do ACE inhibitors have?

they decrease Gq activation → decreased activity of phospholipase C

what drug?

pt is taking a drug for bipolar disorder and now has developed a maculopapular rash

lamotrigine

what drug for HTN is likely to cause increased risk for gout and erectile dysfunction?

thiazide diuretics

What ECG finding do we suspect? what drug?

pt on a cardiac drug now sees yellow halos around lights (xanthopsia)

digoxin toxicity → junctional bradycardia

what is the mechanism for ACE inhibitors to cause angioedema?

accumulation of bradykinin due to decreased degradation

note hereditary angioedema is due to deficiency of C1 esterase inhibitor

How do beta blockers act on AV node cells?

decrease the Ca currents (they decrease cAMP and activate protein kinase A to do this)