Pharm Flashcards
Anti-muscarcinic that can be used as a treatment for drug-induced parkinsonian symptoms (cog-wheel rigidity, resting tremor, masked facies, bradykinesia) typically caused by D2 receptor blockade in the nigrostriatal pathway
Benzotropine and trihexyphenidyl
long acting insulin
Detmir (Dont), Go (Glargine)
Intermediate Acting Insulin
regular insulin (Rest), NPH (neutral protamine Hagedorn) (Now); peaks 2-3 hours after admin
Short Acting insulin (pe-prandial admin)
Glulisine (Girls) Aspart (And) Lispro (Lads)
Diuretic used to treat acute decompensated HF
Loop diuretics which work at the TaLH; inhibit NaKCl2; Furosemide and Ethacrynic Acid
diuretic primarily used to treat Hypertension
Thiazide diuretics; work at DCT inhibiting the NaCl; Hydrochlorothiazide and Chlorothalidone
Phase I Drug metabolism
Reduction, oxidation, hydrolysis with Cytochrome P450 yields slightly polar water-soluble metabolites
Phase II Drug metabolism
Conjugation (methylation, glucuronidation, acetylation, sulfanation) yields very polar inactive metabolites that can be really excreted
Drugs that can cause drug induced lupus in slow acetylators
Procainamide, isoniazid, hydralazine (increases cGMP leading to smooth muscle dilation; used in HTN emergency)
Hydralazine MOA, Use and SAE
MOA: Increases cGMP –> smooth muscle relaxation; Hypertensive emergency (smooth muscle dilation); reflexive Tachycardia, SLE, fluid retention, headache, angina
Treat for extended spectrum beta lactamase organism
Carbapanems
SAEs of Carbapenems
Diarrhea, lower seizure threshold, rash
SAEs of Amphotericin B
Infusion related: fever, chills, headache, hypotension; Long term complication: Type I renal tubular acidosis (1 cylinder), Anemia second to decreased Epo production, magnesium wasting’ seizures with intrathecal administration
Class IV Antiarr
Verapamil, Diltiazem- RATE control (SA and AV node conduction)
Adverse SAEs of Adenosine
Flushing, SOB, Chest pain, Sense of impeding doom, headache, hypotension, bronchospasm; effects are blunted by theophylline and caffeine (A1r Antagonist)
Class V Antiarrythmics
Adenosine, Digoxin, Magnesium, Potassium
MOA of Adenosine
Binds A1 receptors increased K+ efflux from the cell, decreased Ca current (Ica) –> Decreased AV node conduction
Drug that causes selective inhibition of I funny channels prolonging phase 4 of the pacemaker AP; decreases SA node firing; reduces Cardiac O2 requirement
Ivabradine
SAE of ivabradine
Visual brightness, hypertension, bradycardia
This drug causes smooth muscle relaxation by inhibiting Na current mediated action potentials; however it is less efficacious in infected tissues
Lidocaine, bupivacaine; less effective in ischemic and acidotic tissue
Conditions treated with FFP/ prothrombin Complex concentrate
Deficiencies in F II, VII, IX, X C and S; Warfarin too, rodent poisoning, etc; DIC, cirrhosis
Conditions treated with Cyoprecipitate
cry contains fibronectin, VIII, XIII and vWF; so you can treat vWF deficiency, fibrinogen deficiency and Hemophilia A.
Cholinomimetics
bethancol, pilocarpine, carbachol, methacholine
Alzheimer’s Drugs that are AChEi
Rivastigmine, Donepezil, Galantamine; penetrate the CNS
Treatment of Myasthenia Gravis
Pyridostigmine or Neostigmine (AChEi); Edrophonium for Dgx (improvement in weakness= myasthenia crisis + tension test; negative tension test is an exacerbation of sx and suggest AChEi OD)
Treatment for non-depolarizing NMJ blockade with tubocurarine, rocuronium, etc
Neostigmine (does not penetrate CNS)
Treatment for depolarizing NMJ blockade with Succinylcholine
AchEi; must be administered in Phase II of NM blockade otherwise it will potentiate effects of Succinylcholine in phase I
Symptoms of Ach Toxicity associated with AChEi and Organophosphates
DUMBBELSS: Diarrhea, Urination, Miosis, Bradycardia, bronchospasm, Emesis, Lacrimation, salivation, sweating.
Treatment of Organophosphate toxicity (irreversible AChEi)
Atropine (CNS reversal) and Pralidoxine (if organophosphate bound hasn’t aged with AchE then Pralidoxine can reverse the interaction and increase AChE reverse peripheral effects including flaccid paralysis)
Non-selective Alpha and Beta Blockers and indications
Carveidilol (HF, Variceal bleed); Labetalol (HTN emergency)
MOA of Sildenafil, -nafil suffix
PDE5 inhibitor–> increased cGMP –> Increased Smooth muscle relaxation in response to NO –> increased blood flow in the corpus cavernous and decreased pulmonary vascular resistance
SAEs of Sildenafil
Headache, flushing, dyspepsia, cyanopia, risk of life threatening hypotension when administered with nitrates (potentiates its affects)
NNRTis that inhibit Reverse Transcriptase in HIV
Delvirdine, efavirenz, Nevirapine
NRTIs that inhibit Reverse Transcriptase in HIV
Abacivir, didanosine, emtricitabine, lamuvidine, stavudine, tenofivir, zidovudine
Integrase inhibitors for HIV
Dolute(gravir), Elvite(gravir,) Ralte(gravir )
Protease Inhibitors of HIV
Atanzavir, darunavir, fosamprenavir, indinavir, lopinavir, ritonavir, saquin(avir)
Inhibits attachment of HIV to cells by blocking CCR5 and inhibiting interaction with gp120
Maraviroc
Inhibits penetration of HIV into cells
Enfuviritide binds gp41
protease inhibitor SAEs
Metabolic complications (lipodystrophy, insulin resistance, hyperglycemia, etc)
NRTI SAEs
lipodystrophy (horse) , lactic acidosis (spilled milk) , hypersensitivity with Abracavir (red bubbles from pot), pancreatitis with didanosine (sir dan holding sponge) and bone marrow suppression with zidovudine (princess izolde eating from depressed bone marrow plate)
NNRTI Saes
stevens johnsons syndrome (red mask), hepatoxicity (yellow stag with liver spot), neuropsychologist effects (holding head), teratogenic (tarantula), and Nevirapine is a CYP450 inducer
SAEs of integrate inhibitors
myopathy
Prevents catecholamine crisis in patients who are to have surgical resection of pheochromocytoma; In addition to a non-selective beta blocker like propranolol, what drug do you administer?
Think about it: Pheo– catecholamines–> adrenergic agonists–> sympathetic effects–> if you have already administered a beta blocker then you have to take care of the alpha adrenergic effects of catecholamines Phenoxybenzamine; non-selective alpha antagonist
Thyroid peroxidase inhibitors
Propylthiouracil, methimazole
Inhibitors of peripheral conversion of T3 and T4
propranolol, propylthiouracil, Ipodate (IV contrast)
inhibitors of Iodine uptake
potassium iodide; inhibits Iodine uptake and inhibits T3,T4 release
Treatment for urinary urgency
Anti-mAChR (Oxybutanin, Tolteridine)
Treatment for Overflow incontinence 2nd BPH
Alpha-1 Agonists: Prazosin, tamrulosin, terazosin;
Treatment of overflow incontinence due to detrusor under activity
bethanecol
MOA of Spironolactone and Eplerenone
Competitive aldosterone receptor antagonist (blocks aldo causing potassium wasting) at the collecting duct
MOA of Triamterence and Amiloride
Block sodium channels at the collecting duct
Indications for K+ Sparing diuretics
Hyperaldosteronism, K+ depletion, HF, hepatic ascites (spiro), nephrogenic DI (amiloride), antiandrogen
Treatment of Malignant hyperthermia and MOA
MH is caused by inhaled anesthetics/succinylcholine ; due to a mutation of the ryanodine receptor; Dantrolene is a ryandodine receptor blocker and leads to decreased Ca2+ release from the SR decreasing muscle contractions and hyperthermia
What causes uncoupling in the ETC
Thermogenin, ASA and dinitrophenol- leads to increased O2 consumption, decreased ATP production and decreased H+ inside (which is why you get less ATP); Produces heat
Blocks Complex V of ETC
Oligomycin
Blocks Complex IV of ETC
CN, CO, Azide
Blocks complex III of ETC
Antimycin A
Blocks Complex I of ETC
Rotenone
Nonbenzo that is used in the treatment of generalize anxiety disorder and is a partial 51HT agonist
Buspirone