Pharm Flashcards
Vasodilation mechanism
Endothelial cells have muscarinic receptors; cholinergic agonist bind -> release of NO (EDRF) -> guanylate cyclase -> dec. Ca2+ -> decreased activity of myosin light-chain kinase –> myosin light chain DEphosphorylation and SMC relaxation
Order the insulins in terms of earliest to latest peak
Aspart/lispro/glulisine, regular, NPH, detemir, glargine
Lithium toxicity symptoms? tx
Tremors, fascicular twitching, agitation, ataxia, delirium; tx with hemodialysis for acute. Can also cause hypothyroidism and nephrogenic diabetes inspidus.
Drugs that could increased Li levels?
Thiazides (increased proximal Na reabsorption as compensation to distal effects), ACEi, NSAIDs
Name the short benzos?
Alprazolam (Xanax), Triazolam, Oxazepam.
OATs. Tri- and eat your OATs quickly in the morning.
Name the long benzos?
Chlordiazepoxide (Librium), Diazepam (Valium), Flurazepam, Clorazepate. Long view: Libreate and Valor.
Name the medium benzos?
Lorazepam (Ativan), estazolam, temazepam.
live and LET die. Medium-lvl bond movie.
Reverse benzos with?
Flumazenil
Acute neonatal narcotic withdrawal?
Pupillary dilation, rhinorrhea, sneezing, d, n/v, chills. tx = diluted tincture of opium
Dobutamine?
B-adrenergic agonist B1>B2 –> Positive inotropy, weakly positive chronotropic, increases conduction velocity (arrhythmias), increases myocardial oxygen consumption
Anticholinergic toxicity?
Fever, mucosal/axillary dryness, cutaneous flushing, mydriasis (big), cycloplegia, delirium. e.g. TCA’s, atropine
What drugs more effective against HSV and VZV than CMV/EBV?
Acyclovir, famciclovir, valaciclovir. B/c dependnet on a thymidine kinase to turn into active triphosphate form.
Protease inhibitors?
Squinavir, ritonavir
Fusion inhibitors
Enfuvirtide
RT inhibitors
Efavirenz (NNRTI), tenofovir, lamivudine
Integrase inhibitors
Raltegravir
CCR5 receptor inhibitors
Maraviroc
Surgery + liver damage?
Inhaled anesthetics (e.g. halothane) associated w/ highly lethal fulminant hepatitis - aminotransferase, PTT inc, eosinophilia
Finasteride
Blocks peripheral conversion of testosterone to DHT
Flutamide/Cyproterone
Androgen hormone-receptor blocker
-mab’s
Monoclonal Ab
-cept’s
Receptor molecules
-nib’s
Kinase inhibitor
Origin substem for -mab’s
Mouse (-o-), Human (-u-), Chimeric w/ foreign variable (-xi), Humanized w/ completementarity determining regions (-zu), chimeric/humanized hybrid (-xizu)
Statin + fibrates
Myopathy risk. Simvastatin has highest risk.
Varenicline?
Partial agonist to nicotinic ACh receptors -> reduced nicotine withdrawal and reduced reward. (A4B4 nicotinic receptor)
Efficacy vs. potency
Efficacy = intrinsic ability of drug to elicit an effect (maximum effect). E.g. analgesics, abc, antihistamines, decongestants. Potency = dose of drug required to produce a given affect (Km related). Highly potent drugs include chemo, antiHTN, lipid-lowering. Potent dose, Kim! Max, more efficacious please.
HCTZ effects
Diuretic. Also side effect = increased Calcium absorption. Therefore, a nice drug for older women with HTN.
Pentazocine
Opioid designed for decreased abuse. Partial agonist and weak antagonist at mu receptors. Can lead to withdrawal symptoms in patients who are dependent on opioids.
Opioid administration -> sudden RUQ pain?
Biliary colic induced by contraction of SMC.
ACEi side effects
Decreased GFR (only care if Cr >30%), hyperKalemia, cough. Angioedema is rare but life-threatening.
Lamotrigine side effects
Used for refractor partial sz, generalized tonic-clonic, bipolar. Life-threatening HS reaction that manifests as skin rash = Stevens-Johnson
Thioridazine SE
retinal deposits that look like retinitis pigmentosa
Chlorpromazine SE
Corneal deposits.
Common drug interactions in serotonin syndrome
SSRIs, SNRIs, MAOIs, TCAs, Tramadol, Ondansetron, Linezolid, Triptans
Thionamides
Methimazole and propylthiouracil. Inhibit thyroid peroxidase (which oxidizes iodine).
What is half-life given Vd and clearance?
t1/2 = (Vd x 0.7) / clearance
Efficacy vs. potency
Efficacy = intrinsic ability of drug to elicit an effect (maximum effect). E.g. analgesics, abc, antihistamines, decongestants. Potency = dose of drug required to produce a given affect (Km related). Highly potent drugs include chemo, antiHTN, lipid-lowering. Potent dose, Kim! Max, more efficacious please.
Vd = ?
= amount of drug given (mg) / plasma concentration of drug (mg/L) = theoretical volume occupied by total absorbed drug amount at plasma concentration.
CYP 450 Inducers
Chronic alcohol, Modafinil, St. John’s wort, Phenytoin, Phenobarbital, Nevirapine, Rifampin, Griseofulvin, Carbamazepine. “Grisly St. John Nevir Riffs the Phen-Phen w/o Carbs, Chronic Alcohol, or Modafinil.”
CYP 450 inhibitors
Acute alcohol, Gemfibrozil, Ciprofloxacin, INH, grapefruit, quinidine, amiodarone, ketoconazole, macrolides, sulfonamides, cimetidine, ritonavir. “‘Cip A-Cute Macro Grapefruit at the NIH,’ (w)Rit an Amiable Keto Quinn w/ a Sulfur-colored Gem’d Cimetar.”
Two major variables in M-M kinetics?
Km = 1 / affinity. Vmax is proportional to enzyme concentration. At Km concentration, 1/2 Vmax velocity.
Lineweaver-Burk
y-intercept = 1/Vmax. X-intercept = -1/Km (Closer to 0, greater the Km, weaker affinity)
Competitive vs. non-competitive inhibitors on Lineweaver-Burk
Competitive inhibitors do NOT affect Vmax = same y-intercept. Non-comp inhibitors do NOT affect affinity -> same x-intercept
Reversible, non-reversible comp inhibitors, and non-comp inhibitors potency vs. efficacy?
Reversible comp - don’t change Vmax but change Km. decreased potency. Non-reversible competitive and non-competitive inhibitors change Vmax -> decrease efficacy.
Pharmacokinetics vs. Pharmacodynamics
Kinetics are body’s effect on drug. ADME = absorption, distribution, metabolism, excretion. Dynamics is affect of drug on body - receptor binding, efficacy, potency, toxicity.
Bioavailability
Fraction (F) of drug that reaches systemic circulation unchanged. IV is 100%.
Low, Middle, High Vd tells you what?
Vd is LOW (4-8L) if drug remains in plasma (bound to plasma proteins, hydrophilic b/c charged). High Vd (e.g. 41) are small MW AND uncharged; in all tissues + fat. Medium Vd (teens) for small MW and hydrophilic b/c in interstitium (ECF). High Vd drugs tend to be cleared hepatically.
What do I need to know about half-life?
t1/2 = 0.7 x Vd / clearance. Drug infused at constant rate takes 4-5 half-lives to reach SS. (3.3 half-lives to reach 90% of SS). 1:50% remaining, 2:25%, 3:12.5%, etc.
Clearance
Volume of plasma cleared of drug per unit time = rate of elimination of drug / plasma concentration = Vd x Ke (elimination constant)
Loading dose calculation
Cp x Vd / F where Cp = target plasma concentration at SS.
Maintenance dose calculation
Cp x CL x tau / F where tau = dosage interval.
Zero-order elimination vs. 1st-order elimination
Constant rate of elimination (e.g. PEA - Phenytoin, Ethanol, Aspirin) vs. constant fraction is eliminated
Trapping drugs in urine?
Ionized forms are trapped and cleared quickly. Weakly acidic drugs (e.g. phenobarbital, MTX, ASA) can be cleared with bicarbonate. Weakly basic drugs (e.g. amphetamines) can be cleared with ammonium chloride.
Phase I vs. phase II drug metabolism.
I - CYP450 reduction, oxidation, and hydrolysis leading to slightly polar, water-soluble metabolites. II - GAS (Glucorinidation, Acetylation, and Sulfation) leading to VERY polar, inactive metabolites.
Therapeutic index
TITE = TD50/ED50 = median toxic dose / median effective dose. Higher therapeutic index is a SAFER drug.
Sympathetic vs. parasympathetic pathway for cardiac and smooth muscle, gland cells, and nerve terminals
Sympathetic - pre-ganglion to chain (ACh). Post-ganglion to muscle (NE, alpha and beta adrenergic receptors). Parasympathetic - pre-ganglionic from medulla. Synapse (ACh), then post-ganglion to muscle (ACh, M receptor)
Sympathetic sweat glands pathway?
Chain w/ ACh. Post-ganglionic w/ ACh, M.
Sympathetic renal vasculature pathway?
Chain w/ ACh. Post-ganglionic with D, D1. Kidneys are dope, sweat is musty, and the rest is adrenergic.
Adrenal medulla pathway?
Directly ACh -> Epi and NE release
Nictonic vs. Muscarinic receptors?
Both are ACh receptors. N are ligand-gated Na+/K+ channels. Nn in autonomic ganglia. Nm in NMJ. Muscarinic receptors are GPCRs that act thru 2nd messengers. M1-5.
Dopamine GPCRs?
D1 - Gs, relaxes renal vascular SMC. D2 - Gi, modulates transmitter release (esp. brain). Kidneys are DOPE. Brain is okay.
Histamine GPCRs
H1 - Gq, increase mucus production, vascular permeability,, contraction of bronchioles, pruritus and pain. H2 - Gs, increased gastric acid secretion. H1 is allergies. H2 is ranitidine.
Vasopressin GPCRs
V1 - Gq, increased vascular SMC contraction. V2 - Gs, increased water permeability and reabsorption in collecting tubules of kidney.
Parasympathetic GPCRs
M1 - Gq, CNS and enteric (brain is first). M2 - Gi, decreased HR and contractility of atria (heart is second). M3 - Gq, inc. exocrine gland secretion, inc. peristalsis, inc. bladder contraction, bronchoconstriction, miosis, accomodation
Sympathetic GPCRs
a1- Gq, vasc SMC contraction, mydriasis, increased intestinal and bladder sphincter contraction. a2 - Gi, decreased sympathetic outflow, decreased insulin, dec lipolysis, inc. PLT aggregation. B1 - Gs, inc HR, inc contractility, inc renin (juxtaglomerular), inc lipolysis. B2 - Gs, vasodilation, bronchodilation, inc HR, inc contractility, inc lipolysis, inc insulin, TOCOlysis, ciliary muscle relaxation (un-accmodate), inc. aqueous humor
Acronym for GPCR systems
Sympathetics, Parasympathetics (M1-M3), Dopamine, Histamine, Vasopress. Qiss and Qiq till your siq of sqs
Amphetamines
Activates NE release and inhibits reuptake. For narco, obesity, ADHD
NE reuptake inhibitors
Amphetamines, cocaine, TCAs
Modulation of NE release?
NE negatively feedbacks via alpha-2 receptors. Angiotensi-II activates NE release.
Where do ACh esterase inhibitors act?
Post-synaptic membrane
Gq GPCR receptors?
HAVe 1 M&M - H1, alpha1, V1, M1, M3
Gi GPCR receptors?
MAD 2’s - M2, alpha2, D2
Cholinomimetic agents
Bethanechol, carbachol, pilocarpine, methacholine.
Bethanechol
Postop ileus, neurogenic ileus, urinary retention. Activates Bowel and Bladder SMC. Resistant to AChe. Bethany, let it go!
Carbachol
Glaucoma, pupillary constriction, intraocular pressure.
Pilocarpine
Stimulator of sweat, tears, saliva. Open (contracts ciliary muscle) and closed-angle glaucoma (constricts pupillary sphincter).
Methacholine
Asthma challenge.
Indirect agonists for ACh
Neostigmine, Pyridostigmine, Physostigmine, Donepezil/rivastigmine/galatamine, Edrophonium
Neostigmine
Post-op and neurogenic ileum, urinary retention, myasthenia gravis, reverse NMJ blockade. Neo = NO CNS penetration.
Pyridostigmine
Long-acting for Myasthenia. No CNS. Gets RID of Myasthenia Gravis. Physostigmine gets rid of the stigma f ACh poisoning.
Physostigmine
ACh toxicity (Crosses CNS)
Cholinesterase inhibitor poisoning
DUMBBELSS - Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of m. and CNS, Lacrimation, Sweating, Salivation. Tx = atropine (Ach antagonist working on M receptors only; won’t reverse muscle paralysis based on Nicotnic receptors) + pralidoxime (AChE regenerator)
GU Muscarinic antagonists
Reduce urgency in mild cystitis and bladder spasms. Oxybuynin, darifenacin, solifenacin
Respiratory muscarinic antagonists
Ipratropium, tiotropium - COPD, asthma
CNS muscarininc antagonists
Benztropine for Parkinsons. Scopolamine for motion sickness.
GI, resp muscarininc antagonist
Glycopyrrolate - reduce airway secretions, drooling tx, peptic ulcer tx
Atropine effects
Pupil dilation, cycloplegia, dec. airway secretions, dec. acid secretions, decreased motility, decreased urgency in cystitis. Used for heart block.
Atropine toxicity
Hot as hare, Dry as bone, Red as beet Blind as a bat (cycoplegia), Mad as a hatter.
Epinephrine
B > alpha. Inds - anaphylaxis, OA-glaucoma, asthma, hypotension
Norepinephrine
alpha1>alpha2>beta. Use for hypotension (but decreased renal perfusion)
Isoproterenol
B1=B2. Beta2-mediated vasodilation -> dec. pressure -> increased HR. Inds - for evaluating tachyarrhythmias.
Dopamine
D1 = D2 > Beta > alpha. Ind for unstable bradycardia, HF, shock. Inotropic and chronotropic alpha effects at high doses. Low dose - vasodilation to renal and mesenteric vasculature. Higher doses - inotrope via B1. Higher doses - generalized vasoconstriction via alpha-1.
Dobutamine
Beta1 > Beta2, alpha. HF, cardiac stress testing
Phenylephrine
alpha1 > alpha2. Hypotension, mydriasis, rhinitis (Decongestant)
Albuterol, salmeterol, terbutaline
B2 > B1. Acute asthma, COPD. Terbutaline for tocolysis in premature contractions.
Ephedrine
Nasal decongestion, urinary incontinence, hypotension
Sympatholytics
alpha-agonists. Clonidine and alpha-methyldopa.
Clonidine
Clonidine is used for HTN urgency, ADHD, severe pain. Toxicities include CNS depression, brady, hypo, resp depression, miosis.
alpha-methyldopa
Used for HTN in pregnancy. Tox -> Direct Coombs + hemolytic anemia.
Non-selective alpha blockers
Phenoxybenzamine and phentolamine
Phentolamine
Reversible. Used to reverse hypertensive crisis in MAOi taking patients who ate tyramine.
Phenoxybenzamine
Irreversible. Used for pehochromocytoma pre-op to prevent HTN crisis
Alpha-1 antagonist
=-osins (Prazosin, terazosin, tamsulosin). Used for BPH urinary symptoms, HTN. Tox - 1st dose hypotension.
Alpha-2 antagonist
Mirtazapine used for depression. Tox = sedation, inc. chol, inc appetite
B1>B2 selective antagonists
A to M. Atenolol, esmolol, metoprolol
Non-selective Beta blockers
N to Z. Nadolol, propanolol, timolol
Nonselective alpha AND beta-antagonists
Carvedilol and labetalol
Beta blocker toxicities
Impotence, CNS, CV, dyslipidemia (metoprolol), exacerbate asthmatics and COPD, cocaine risk-> HTN
Beta-blocker tox tx?
Glucagon
Cu, As, Au fox treatment?
Penicillamine
Cyanide treatment?
Nitrite + thiosulfate, hydroxocobalamin
Digitalis fox treatment?
Anti-digitalis Fab fragments
Fe tox treatment?
Deferoxamine, deferasirox
Lead tox treatment?
EDTA, dimeraprol, succimer, penicillamine
Mercury, arsenic, gold tox treatment?
Dimercaprol, succimer
Methanol, ethylene glycol tox treatment?
Fomepizole > ethanol, dialysis
Methemoglobin tox treatment?
Methylene blue, Vitamin C
Salicylate tox treatment?
NaHCO3, dilaysis
TCAs tox treatment?
NaHCO3 (plasma alkalinization)
tPA, streptokinase, urokinase tox treatment?
Aminocaproic acid
Coronary vasospasm drugs?
Cocaine, sumatriptan, ergot alkaloids
Cutaneous flushing drugs?
VANC - vancomysin (via histamine release NOT IgE HS reaction), adenosine, niacin (via prostaglandins!), Ca2+ channel blockers (Amlodopine)
Dilated cardiomyopathy drugs?
Doxorubicin, daunorubicin; Prevent with dexrazoxane = Fe-chelating agent
Torsades de pointes causing drugs?
Class II, IA, macrolides, antipsychs, TCAs
Hyperglycemia causing drugs?
Tacrolimus, PIs, Niacin, HCTZ, Beta-blockers, Corticosteroids
Hypothyroidism causing drugs?
Li, amiodarone, sulfonamides
Focal to massive hepatic necrosis drugs?
HAVAc - halothane, Amanita phalloides, Valproic acid, acetaminophen
Pancreatitis causing drugs?
Didanosine, Corticosteroids, Alcohol, Valproic, Azathioprine, Diuretics. “Drugs Causing Violent Abdominal Distress.”
Agranulocytosis causing drugs?
Dapsone, Clozapine, Carbamazepine, Colchicine, Methimazole, Propylthuiouracil
Aplastic anemia causing drugs?
Carbamazepine, Methimazole, NSAIDs, Benzene, Chloramphenicol, Propylthiouracil. “Can’t Make New Blood Cells Propylerly.”
Hemolysis in G6PD?
INH, Sulfa, Dapsone, Primaquine, ASA, Ibuprofen, Nitrofurantoin. “Hemolysis IS D PAIN”
Megaloblastic anemia causing drugs?
Phenytoin, Methotrexate, Sulfa. “Having a blast with PMS?”
Fat redistribution drugs
PIs, Glucocorticoids
Gout causing drugs?
Pyrazinamide, thiazides, furosemide, niacin, cyclosporine “Painful Tophi on Feet Need Care” in gout.
Photosensitivity drugs?
Sulfonamides, Amiodarone, Tetracyclines, 5-FU. “SAT For a photo.”
Stevens-Jonson drugs
Anti-epileptics, allopurinol, sulfa, penicillin
SLE like syndrome drugs?
Sulfa, hydralazine, INH, procainamide, phenytoin, etanercept. “Lupus is SHIPP-E”
Drugs causing seizures?
INH, bupropion, Imipenem/cilastatin, tramadol, enflurane, metoclopramide. With seizures, I BITE My tongue
Drugs causing SIADH?
Carbamazepine, cyclophosphamide, SSRIs
Drugs causing pulmonary fibrosis?
Bleomycin, amiodarone, busulfan, methotrexate
Substrates for P450?
Always Always Always Always Think When Starting Others. (Anti-eps, antideps, anti-psychs, anesthetics, theophylline, warfarin, statins, OCPs).
Sulfa drugs
Popular FACTSSS - Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamide antibiotics, Sulfasalazine, Sulfonylureas.
-Azole vs. -bendazole?
Ergosterol synthesis inhibitor vs. Antiparasitic/helmintic
Clozapine
Acts on D4 receptors, meaning it doesn’t have as bad pseudoparkinsonism, tardive dyskinesia, hyperprolactinemia
Which TB drug is more active against intracellular pathogens?
Pyrazinamide, because it requires an acidic environment (such as macrophage phagolysosomes).
Etoposide
Chemo that inhibits sealing activity of topi-II. (Topo-I relieves NEG super coil with single strand nicks. Topo-II induces transient dbl stranded breaks to relieve positive and negative supercoiling)
Glucocorticoid effects on immune system
Reduce lymphocyte counts (T>B) with redistribution to spleen, LN’s, and bone marrow. Inhibition of Ig synthesis and stimulation of lymphocyte apoptosis. Inhibit monocyte to macrophage differentiation. Decreased eosinophils. Reduced basophils. INCREASED neutrophils b/c of demargination from vessel wall.
Amiodarone side effects
Thyroid dysfunction, corneal micro-deposits, blue-gray skin discoloration, drug-related hepatitis, pulmonary fibrosisq
Streptokinase
Thrombolytic. Converts plasminogen into plasmin —> degrades fibrin.
Opioid receptors
mu - dependence, euphoria, respiratory and cardiac depression, reduced GI motility, sedation; works by opening K+ channels to hyper polarize. Kappa = miosis, dysphoria, sedation. Delta = antidepressant. Nociceptin/orphanin (N/OFQ) = anxiolysis and inc. appetite
Psoriasis treatments
Topical vitamin D analogs (calciportiene, calcitriol, tacalcitol), which prevent keratinocyte proliferation. Cyclosporine (inhibits NFAT to stop transcription of IL-2). Ustekinumab is human monoclonal Ab targeting IL-12 and 23. Inhibits differentiation of CD4+ the and Th17. Etanercept is recombinant form of human TNF receptor that binds TNF-alpha to treat mod-severe plaque-type psoriasis.
Warfarin side effect early on?
Skin and SQ fat necrosis b/c of inhibition of protein C anticoagulation and it’s half-life is shorter than the other factors leading to a transient hyper-coagulable state
Hemorrhagic cystitis after chemo?
Associated with nitrogen mustard-based chemotherapeutic agents like cyclophosphamide. Metabolized by kidney into acrolein –> urine -> necrosis. Prevent with hydration and MESNA (binds and inactivates toxic metabolites)
Leucovorin
Folinic acid. Drug used for MTX overdose b/c bypasses dihydrofolate reductase step.
Amifostine
Cytoprotective free-radical scavenger used to dec. nephrotoxicity of Platinum and alklyating chemo agents
Filgrastim
G-CSF analog for minimization of granulocytopenia after myelosuppressive chemo
Best drug for decreasing triglycerides?
Fibrates (SE - muscle tox w/ statin and gallstones). Activate PPAR-alpha -> lipoprotein lipase activity.
Cromolyn and nedocromil mech?
Inhibit mast cell DEGRANULATION. Prevention of acute attacks.
How does digoxin treat AF w/ RVR (2nd line)?
Slows conduction through AV node by acting on VAGUS nerve. Ca+ channel blockers and beta-blockers are first line.
Cytarabine
Pyrimidine analog anti-metabolite in DNA leading strand. S-phase specific. Gemcitabine is another pyrimidine analog.
Selective COX-2 inhibitors
Used to help avoid PLT and GI side effects of NSAIDs. e.g. celecoxib
Non-nucleotide reverse transcriptase inhibitors
Nevirapine, efavirenz, delavirdine. DONT require activation via intracellular phophorylation. AE’s common like flu, abdominal pain, jaundice, fever. Stevens-Johnsons.
Zidovudine (AZT)
is NOT lamivudine. 3’ prevention of elongation. Like zalcitabine, must be converted into monophosphate form via cellular thymidine kinase.
Motion sickness receptors?
M1 and H1 stimulation -> nausea and vomiting. 1st-gen antihistamines like meclizine and dimenhydrinate; Scopolamien for only anti-muscarinic. SE’s are blurry vision, dry mouth, palpitations, urinary retention, constipation
Cladribine
PURINE analog for hairy cell leukemia. Resistant to degradation by adenosine deaminase.
Dacarbazine
Cell-cycle non-specific methylating agent requiring enzymatic activation (liver)
Cyclophosphamide
Alkylating agent that must be converted to active by hepatic CYP450 2B
Lomustine
Nitrosourea agent that acts by DNA alkylation and cross-bridge formation (Requires non-enzymatic hydroxylation in liver). Penetrates CNS b/c lipophilic.
Nitroprusside
Quick onset, short duration of action w/ cyanide toxicity with prolonged use, high dose, renal problems. Direct arterial and venous vasodilator.
Fenoldopam
Benazepine derivative of dopamine that is a SELECTIVE D-1 agonist with NO effect on alpha or beta receptors. Vasodilation of arterial beds and also improves renal blood flow (and increases sodium excretion)
Class III antiarrhythmics
K+ efflux decreased, increased AP. Dofetilide, ibutilide, amiodarone, sotalol.
Class IA antiarrhythmics
Disopyramide, Quinidine, Procainamide. “Quinn is a Pro Dicer.” Intermediate inhibition of phase 0 and prolonged AP.
Class IB antiarrhythmics
Lidocaine, Tocainide, Mexiletine. “Mex The Lido” Weak inhibition of phase 0, and shortened AP.
Class 1C antiarrythmics
Moricizine, Flecainide, Propafenone. “Mori is a Pro Flexer!.” Strong inhibition of phase 0 with no change in AP.
ACEi first dose?
First dose hypotension. Activating the Bezold-Jarisch reflex b/c of decreased AII -> vaguely mediated hypotension and bradycardia. Be careful if already taking thiazides (hyponatremia and hypovolemic)
How do you treat Beta-blocker overdose?
Glucagon b/c it increases intracellular cAMP and cardiac contractility
Serotonin syndrome vs. TCA tox?
TCA tox leads to antichol, vasodilation, conduction defects and arrhythmias, sz/tremors, sedation. Arrhythmia is the most comman cause of death 2/2 Na+ channel inhibition. Tx w NS and hypertonic NaHCO3
Cilostazol
Decreases platelet phosphodiesterase activity -> increased cAMP -> decreased PLT aggregation. Direct arterial vasodilator. Therefore, a PAD tx.
Abciximab
Monoclonal Ab that inhibits PLT aggregation via IIb/IIIa receptor. Used prior to PCIs.
Cisplatin should be used with?
Amifostine. Cisplatin can cause ATN 2/2 ROS. Amifostine is a free-radical scavenger. A Cl- diuresis via IV NS also works b/c totoplatin will be inactive in higher chloride conc.
Calcineurin inhibitors
Tacrolimus and cyclosporine. Calcineurin is essential for IL-2 activation for T-cells.
Sucralfate
Binds base of mucosal ulcers to protect from acid for healing.
Misoprostol
Prostaglandin E1 analog used to prevent NSAID-induced ulcer disease. Also used for labor induction and abortion.
Acute gouty attack drugs?
NSAIDs preferred, then colchicine. Allopurinol (Xanthine oxidase inhibitor) shouldn’t be used for acute b/c it can mobilize tissue stores of uric acid (worsen or precipitate attacks)
Ototoxic chemo?
Cis-platin
1st gen antihistaminergics names and side-effects
Chlorpheniramine, diphenhydramine, promethazine. Sedation, blurry vision.
Opioid tolerance - what do I need to know?
I need to know that b/c the body doesn’t develop a tolerance to constipation and miosis effects of opiates, ppx tx with fluids and laxatives.
What is tachyphylaxis?
A phenomenon where the drug’s effect rapidly declines after a few days b/c of decreased production of endogenous agonist. e.g. Rebound rhinorrhea after taking alpha agonists (phenylephrine, xylometazoline, oxymetazolin) for too long. e.g. Nitroglycerine.
Anti-motility anti-diarrheals
Bind mu opiate receptors in GI to slow motility. Diphenoxylate.
Anti-secretory antidiarrheals
Bismuth subsalicylate, probiotics, octreotide
Salicycylate poisoning
Initially 2 abnormalities: respiratory alkalosis 2/2 respiratory center hyperventilation + AG metabolic acidosis occuring aftewards (hours)
Ticlodopine side effect
Rarely (<1%) = neutropenia
Transplant anti-rejection regimen is generally
A calcineurin inhibitor (tacrolimus, sirolimus, cyclosporine) and a de novo purine synthesis inhibitor T-lymphocyte proliferation inhibitor (azothioprine, mycophenolate mofetil)
The only FDA-approved anti-obesity medication?
Orlistat - inhibits intestinal lipase –> inhibiting fat absorption in the gut
Probenacid
Inhibits renal tubular secretion of penicillins and most cephalosporins, limiting their excretion. Inhibits reABSORPTION of uric acid (gout, preventive drug)
An agent that increases levodopa peripheral metabolism?
Vitamin B6. (Entacapone prevents peripheral methylation 2/2 COMT)
Effects of carbidopa with levodopa?
Carbidopa inhibits peropheral conversion of levodopa -> increased dopamine in brain (worsened behavioral changes) but less dopamine in periphery (better peripheral side-effects - arrhythmias, postural hypotension, hot flashes, n/v)
What are “permissive” effects of a drug?
Allows another drug to achieve its full potential. NOT synergistic.
Echinocandins and their mech?
Mech is blocking the synthesis of Beta (1,3) - D glucan, which is the main component of Candida and Asperillus. e.g. caspofungin
Doxorubicin mechanism?
Intercalates DNA, binds cell membranes, and generate oxygen radicals (Heart is particularly sensitive b/c it lacks catalase)
