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Pharm Flashcards

1
Q

Vasodilation mechanism

A

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

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2
Q

Order the insulins in terms of earliest to latest peak

A

Aspart/lispro/glulisine, regular, NPH, detemir, glargine

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3
Q

Lithium toxicity symptoms? tx

A

Tremors, fascicular twitching, agitation, ataxia, delirium; tx with hemodialysis for acute. Can also cause hypothyroidism and nephrogenic diabetes inspidus.

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4
Q

Drugs that could increased Li levels?

A

Thiazides (increased proximal Na reabsorption as compensation to distal effects), ACEi, NSAIDs

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5
Q

Name the short benzos?

A

Alprazolam (Xanax), Triazolam, Oxazepam.

OATs. Tri- and eat your OATs quickly in the morning.

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6
Q

Name the long benzos?

A

Chlordiazepoxide (Librium), Diazepam (Valium), Flurazepam, Clorazepate. Long view: Libreate and Valor.

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7
Q

Name the medium benzos?

A

Lorazepam (Ativan), estazolam, temazepam.

live and LET die. Medium-lvl bond movie.

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8
Q

Reverse benzos with?

A

Flumazenil

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9
Q

Acute neonatal narcotic withdrawal?

A

Pupillary dilation, rhinorrhea, sneezing, d, n/v, chills. tx = diluted tincture of opium

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10
Q

Dobutamine?

A

B-adrenergic agonist B1>B2 –> Positive inotropy, weakly positive chronotropic, increases conduction velocity (arrhythmias), increases myocardial oxygen consumption

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11
Q

Anticholinergic toxicity?

A

Fever, mucosal/axillary dryness, cutaneous flushing, mydriasis (big), cycloplegia, delirium. e.g. TCA’s, atropine

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12
Q

What drugs more effective against HSV and VZV than CMV/EBV?

A

Acyclovir, famciclovir, valaciclovir. B/c dependnet on a thymidine kinase to turn into active triphosphate form.

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13
Q

Protease inhibitors?

A

Squinavir, ritonavir

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14
Q

Fusion inhibitors

A

Enfuvirtide

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15
Q

RT inhibitors

A

Efavirenz (NNRTI), tenofovir, lamivudine

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16
Q

Integrase inhibitors

A

Raltegravir

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17
Q

CCR5 receptor inhibitors

A

Maraviroc

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18
Q

Surgery + liver damage?

A

Inhaled anesthetics (e.g. halothane) associated w/ highly lethal fulminant hepatitis - aminotransferase, PTT inc, eosinophilia

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19
Q

Finasteride

A

Blocks peripheral conversion of testosterone to DHT

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20
Q

Flutamide/Cyproterone

A

Androgen hormone-receptor blocker

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21
Q

-mab’s

A

Monoclonal Ab

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22
Q

-cept’s

A

Receptor molecules

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23
Q

-nib’s

A

Kinase inhibitor

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24
Q

Origin substem for -mab’s

A

Mouse (-o-), Human (-u-), Chimeric w/ foreign variable (-xi), Humanized w/ completementarity determining regions (-zu), chimeric/humanized hybrid (-xizu)

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25
Q

Statin + fibrates

A

Myopathy risk. Simvastatin has highest risk.

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26
Q

Varenicline?

A

Partial agonist to nicotinic ACh receptors -> reduced nicotine withdrawal and reduced reward. (A4B4 nicotinic receptor)

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27
Q

Efficacy vs. potency

A

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.

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28
Q

HCTZ effects

A

Diuretic. Also side effect = increased Calcium absorption. Therefore, a nice drug for older women with HTN.

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29
Q

Pentazocine

A

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.

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30
Q

Opioid administration -> sudden RUQ pain?

A

Biliary colic induced by contraction of SMC.

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31
Q

ACEi side effects

A

Decreased GFR (only care if Cr >30%), hyperKalemia, cough. Angioedema is rare but life-threatening.

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32
Q

Lamotrigine side effects

A

Used for refractor partial sz, generalized tonic-clonic, bipolar. Life-threatening HS reaction that manifests as skin rash = Stevens-Johnson

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33
Q

Thioridazine SE

A

retinal deposits that look like retinitis pigmentosa

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34
Q

Chlorpromazine SE

A

Corneal deposits.

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35
Q

Common drug interactions in serotonin syndrome

A

SSRIs, SNRIs, MAOIs, TCAs, Tramadol, Ondansetron, Linezolid, Triptans

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36
Q

Thionamides

A

Methimazole and propylthiouracil. Inhibit thyroid peroxidase (which oxidizes iodine).

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37
Q

What is half-life given Vd and clearance?

A

t1/2 = (Vd x 0.7) / clearance

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38
Q

Efficacy vs. potency

A

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.

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39
Q

Vd = ?

A

= amount of drug given (mg) / plasma concentration of drug (mg/L) = theoretical volume occupied by total absorbed drug amount at plasma concentration.

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40
Q

CYP 450 Inducers

A

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.”

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41
Q

CYP 450 inhibitors

A

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.”

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42
Q

Two major variables in M-M kinetics?

A

Km = 1 / affinity. Vmax is proportional to enzyme concentration. At Km concentration, 1/2 Vmax velocity.

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43
Q

Lineweaver-Burk

A

y-intercept = 1/Vmax. X-intercept = -1/Km (Closer to 0, greater the Km, weaker affinity)

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44
Q

Competitive vs. non-competitive inhibitors on Lineweaver-Burk

A

Competitive inhibitors do NOT affect Vmax = same y-intercept. Non-comp inhibitors do NOT affect affinity -> same x-intercept

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45
Q

Reversible, non-reversible comp inhibitors, and non-comp inhibitors potency vs. efficacy?

A

Reversible comp - don’t change Vmax but change Km. decreased potency. Non-reversible competitive and non-competitive inhibitors change Vmax -> decrease efficacy.

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46
Q

Pharmacokinetics vs. Pharmacodynamics

A

Kinetics are body’s effect on drug. ADME = absorption, distribution, metabolism, excretion. Dynamics is affect of drug on body - receptor binding, efficacy, potency, toxicity.

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47
Q

Bioavailability

A

Fraction (F) of drug that reaches systemic circulation unchanged. IV is 100%.

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48
Q

Low, Middle, High Vd tells you what?

A

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.

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49
Q

What do I need to know about half-life?

A

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.

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50
Q

Clearance

A

Volume of plasma cleared of drug per unit time = rate of elimination of drug / plasma concentration = Vd x Ke (elimination constant)

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51
Q

Loading dose calculation

A

Cp x Vd / F where Cp = target plasma concentration at SS.

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52
Q

Maintenance dose calculation

A

Cp x CL x tau / F where tau = dosage interval.

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53
Q

Zero-order elimination vs. 1st-order elimination

A

Constant rate of elimination (e.g. PEA - Phenytoin, Ethanol, Aspirin) vs. constant fraction is eliminated

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54
Q

Trapping drugs in urine?

A

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.

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55
Q

Phase I vs. phase II drug metabolism.

A

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.

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56
Q

Therapeutic index

A

TITE = TD50/ED50 = median toxic dose / median effective dose. Higher therapeutic index is a SAFER drug.

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57
Q

Sympathetic vs. parasympathetic pathway for cardiac and smooth muscle, gland cells, and nerve terminals

A

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)

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58
Q

Sympathetic sweat glands pathway?

A

Chain w/ ACh. Post-ganglionic w/ ACh, M.

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59
Q

Sympathetic renal vasculature pathway?

A

Chain w/ ACh. Post-ganglionic with D, D1. Kidneys are dope, sweat is musty, and the rest is adrenergic.

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60
Q

Adrenal medulla pathway?

A

Directly ACh -> Epi and NE release

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61
Q

Nictonic vs. Muscarinic receptors?

A

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.

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62
Q

Dopamine GPCRs?

A

D1 - Gs, relaxes renal vascular SMC. D2 - Gi, modulates transmitter release (esp. brain). Kidneys are DOPE. Brain is okay.

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63
Q

Histamine GPCRs

A

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.

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64
Q

Vasopressin GPCRs

A

V1 - Gq, increased vascular SMC contraction. V2 - Gs, increased water permeability and reabsorption in collecting tubules of kidney.

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65
Q

Parasympathetic GPCRs

A

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

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66
Q

Sympathetic GPCRs

A

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

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67
Q

Acronym for GPCR systems

A

Sympathetics, Parasympathetics (M1-M3), Dopamine, Histamine, Vasopress. Qiss and Qiq till your siq of sqs

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68
Q

Amphetamines

A

Activates NE release and inhibits reuptake. For narco, obesity, ADHD

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69
Q

NE reuptake inhibitors

A

Amphetamines, cocaine, TCAs

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70
Q

Modulation of NE release?

A

NE negatively feedbacks via alpha-2 receptors. Angiotensi-II activates NE release.

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71
Q

Where do ACh esterase inhibitors act?

A

Post-synaptic membrane

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72
Q

Gq GPCR receptors?

A

HAVe 1 M&M - H1, alpha1, V1, M1, M3

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73
Q

Gi GPCR receptors?

A

MAD 2’s - M2, alpha2, D2

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74
Q

Cholinomimetic agents

A

Bethanechol, carbachol, pilocarpine, methacholine.

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75
Q

Bethanechol

A

Postop ileus, neurogenic ileus, urinary retention. Activates Bowel and Bladder SMC. Resistant to AChe. Bethany, let it go!

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76
Q

Carbachol

A

Glaucoma, pupillary constriction, intraocular pressure.

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77
Q

Pilocarpine

A

Stimulator of sweat, tears, saliva. Open (contracts ciliary muscle) and closed-angle glaucoma (constricts pupillary sphincter).

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78
Q

Methacholine

A

Asthma challenge.

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79
Q

Indirect agonists for ACh

A

Neostigmine, Pyridostigmine, Physostigmine, Donepezil/rivastigmine/galatamine, Edrophonium

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80
Q

Neostigmine

A

Post-op and neurogenic ileum, urinary retention, myasthenia gravis, reverse NMJ blockade. Neo = NO CNS penetration.

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81
Q

Pyridostigmine

A

Long-acting for Myasthenia. No CNS. Gets RID of Myasthenia Gravis. Physostigmine gets rid of the stigma f ACh poisoning.

82
Q

Physostigmine

A

ACh toxicity (Crosses CNS)

83
Q

Cholinesterase inhibitor poisoning

A

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)

84
Q

GU Muscarinic antagonists

A

Reduce urgency in mild cystitis and bladder spasms. Oxybuynin, darifenacin, solifenacin

85
Q

Respiratory muscarinic antagonists

A

Ipratropium, tiotropium - COPD, asthma

86
Q

CNS muscarininc antagonists

A

Benztropine for Parkinsons. Scopolamine for motion sickness.

87
Q

GI, resp muscarininc antagonist

A

Glycopyrrolate - reduce airway secretions, drooling tx, peptic ulcer tx

88
Q

Atropine effects

A

Pupil dilation, cycloplegia, dec. airway secretions, dec. acid secretions, decreased motility, decreased urgency in cystitis. Used for heart block.

89
Q

Atropine toxicity

A

Hot as hare, Dry as bone, Red as beet Blind as a bat (cycoplegia), Mad as a hatter.

90
Q

Epinephrine

A

B > alpha. Inds - anaphylaxis, OA-glaucoma, asthma, hypotension

91
Q

Norepinephrine

A

alpha1>alpha2>beta. Use for hypotension (but decreased renal perfusion)

92
Q

Isoproterenol

A

B1=B2. Beta2-mediated vasodilation -> dec. pressure -> increased HR. Inds - for evaluating tachyarrhythmias.

93
Q

Dopamine

A

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.

94
Q

Dobutamine

A

Beta1 > Beta2, alpha. HF, cardiac stress testing

95
Q

Phenylephrine

A

alpha1 > alpha2. Hypotension, mydriasis, rhinitis (Decongestant)

96
Q

Albuterol, salmeterol, terbutaline

A

B2 > B1. Acute asthma, COPD. Terbutaline for tocolysis in premature contractions.

97
Q

Ephedrine

A

Nasal decongestion, urinary incontinence, hypotension

98
Q

Sympatholytics

A

alpha-agonists. Clonidine and alpha-methyldopa.

99
Q

Clonidine

A

Clonidine is used for HTN urgency, ADHD, severe pain. Toxicities include CNS depression, brady, hypo, resp depression, miosis.

100
Q

alpha-methyldopa

A

Used for HTN in pregnancy. Tox -> Direct Coombs + hemolytic anemia.

101
Q

Non-selective alpha blockers

A

Phenoxybenzamine and phentolamine

102
Q

Phentolamine

A

Reversible. Used to reverse hypertensive crisis in MAOi taking patients who ate tyramine.

103
Q

Phenoxybenzamine

A

Irreversible. Used for pehochromocytoma pre-op to prevent HTN crisis

104
Q

Alpha-1 antagonist

A

=-osins (Prazosin, terazosin, tamsulosin). Used for BPH urinary symptoms, HTN. Tox - 1st dose hypotension.

105
Q

Alpha-2 antagonist

A

Mirtazapine used for depression. Tox = sedation, inc. chol, inc appetite

106
Q

B1>B2 selective antagonists

A

A to M. Atenolol, esmolol, metoprolol

107
Q

Non-selective Beta blockers

A

N to Z. Nadolol, propanolol, timolol

108
Q

Nonselective alpha AND beta-antagonists

A

Carvedilol and labetalol

109
Q

Beta blocker toxicities

A

Impotence, CNS, CV, dyslipidemia (metoprolol), exacerbate asthmatics and COPD, cocaine risk-> HTN

110
Q

Beta-blocker tox tx?

A

Glucagon

111
Q

Cu, As, Au fox treatment?

A

Penicillamine

112
Q

Cyanide treatment?

A

Nitrite + thiosulfate, hydroxocobalamin

113
Q

Digitalis fox treatment?

A

Anti-digitalis Fab fragments

114
Q

Fe tox treatment?

A

Deferoxamine, deferasirox

115
Q

Lead tox treatment?

A

EDTA, dimeraprol, succimer, penicillamine

116
Q

Mercury, arsenic, gold tox treatment?

A

Dimercaprol, succimer

117
Q

Methanol, ethylene glycol tox treatment?

A

Fomepizole > ethanol, dialysis

118
Q

Methemoglobin tox treatment?

A

Methylene blue, Vitamin C

119
Q

Salicylate tox treatment?

A

NaHCO3, dilaysis

120
Q

TCAs tox treatment?

A

NaHCO3 (plasma alkalinization)

121
Q

tPA, streptokinase, urokinase tox treatment?

A

Aminocaproic acid

122
Q

Coronary vasospasm drugs?

A

Cocaine, sumatriptan, ergot alkaloids

123
Q

Cutaneous flushing drugs?

A

VANC - vancomysin (via histamine release NOT IgE HS reaction), adenosine, niacin (via prostaglandins!), Ca2+ channel blockers (Amlodopine)

124
Q

Dilated cardiomyopathy drugs?

A

Doxorubicin, daunorubicin; Prevent with dexrazoxane = Fe-chelating agent

125
Q

Torsades de pointes causing drugs?

A

Class II, IA, macrolides, antipsychs, TCAs

126
Q

Hyperglycemia causing drugs?

A

Tacrolimus, PIs, Niacin, HCTZ, Beta-blockers, Corticosteroids

127
Q

Hypothyroidism causing drugs?

A

Li, amiodarone, sulfonamides

128
Q

Focal to massive hepatic necrosis drugs?

A

HAVAc - halothane, Amanita phalloides, Valproic acid, acetaminophen

129
Q

Pancreatitis causing drugs?

A

Didanosine, Corticosteroids, Alcohol, Valproic, Azathioprine, Diuretics. “Drugs Causing Violent Abdominal Distress.”

130
Q

Agranulocytosis causing drugs?

A

Dapsone, Clozapine, Carbamazepine, Colchicine, Methimazole, Propylthuiouracil

131
Q

Aplastic anemia causing drugs?

A

Carbamazepine, Methimazole, NSAIDs, Benzene, Chloramphenicol, Propylthiouracil. “Can’t Make New Blood Cells Propylerly.”

132
Q

Hemolysis in G6PD?

A

INH, Sulfa, Dapsone, Primaquine, ASA, Ibuprofen, Nitrofurantoin. “Hemolysis IS D PAIN”

133
Q

Megaloblastic anemia causing drugs?

A

Phenytoin, Methotrexate, Sulfa. “Having a blast with PMS?”

134
Q

Fat redistribution drugs

A

PIs, Glucocorticoids

135
Q

Gout causing drugs?

A

Pyrazinamide, thiazides, furosemide, niacin, cyclosporine “Painful Tophi on Feet Need Care” in gout.

136
Q

Photosensitivity drugs?

A

Sulfonamides, Amiodarone, Tetracyclines, 5-FU. “SAT For a photo.”

137
Q

Stevens-Jonson drugs

A

Anti-epileptics, allopurinol, sulfa, penicillin

138
Q

SLE like syndrome drugs?

A

Sulfa, hydralazine, INH, procainamide, phenytoin, etanercept. “Lupus is SHIPP-E”

139
Q

Drugs causing seizures?

A

INH, bupropion, Imipenem/cilastatin, tramadol, enflurane, metoclopramide. With seizures, I BITE My tongue

140
Q

Drugs causing SIADH?

A

Carbamazepine, cyclophosphamide, SSRIs

141
Q

Drugs causing pulmonary fibrosis?

A

Bleomycin, amiodarone, busulfan, methotrexate

142
Q

Substrates for P450?

A

Always Always Always Always Think When Starting Others. (Anti-eps, antideps, anti-psychs, anesthetics, theophylline, warfarin, statins, OCPs).

143
Q

Sulfa drugs

A

Popular FACTSSS - Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamide antibiotics, Sulfasalazine, Sulfonylureas.

144
Q

-Azole vs. -bendazole?

A

Ergosterol synthesis inhibitor vs. Antiparasitic/helmintic

145
Q

Clozapine

A

Acts on D4 receptors, meaning it doesn’t have as bad pseudoparkinsonism, tardive dyskinesia, hyperprolactinemia

146
Q

Which TB drug is more active against intracellular pathogens?

A

Pyrazinamide, because it requires an acidic environment (such as macrophage phagolysosomes).

147
Q

Etoposide

A

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)

148
Q

Glucocorticoid effects on immune system

A

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.

149
Q

Amiodarone side effects

A

Thyroid dysfunction, corneal micro-deposits, blue-gray skin discoloration, drug-related hepatitis, pulmonary fibrosisq

150
Q

Streptokinase

A

Thrombolytic. Converts plasminogen into plasmin —> degrades fibrin.

151
Q

Opioid receptors

A

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

152
Q

Psoriasis treatments

A

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.

153
Q

Warfarin side effect early on?

A

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

154
Q

Hemorrhagic cystitis after chemo?

A

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)

155
Q

Leucovorin

A

Folinic acid. Drug used for MTX overdose b/c bypasses dihydrofolate reductase step.

156
Q

Amifostine

A

Cytoprotective free-radical scavenger used to dec. nephrotoxicity of Platinum and alklyating chemo agents

157
Q

Filgrastim

A

G-CSF analog for minimization of granulocytopenia after myelosuppressive chemo

158
Q

Best drug for decreasing triglycerides?

A

Fibrates (SE - muscle tox w/ statin and gallstones). Activate PPAR-alpha -> lipoprotein lipase activity.

159
Q

Cromolyn and nedocromil mech?

A

Inhibit mast cell DEGRANULATION. Prevention of acute attacks.

160
Q

How does digoxin treat AF w/ RVR (2nd line)?

A

Slows conduction through AV node by acting on VAGUS nerve. Ca+ channel blockers and beta-blockers are first line.

161
Q

Cytarabine

A

Pyrimidine analog anti-metabolite in DNA leading strand. S-phase specific. Gemcitabine is another pyrimidine analog.

162
Q

Selective COX-2 inhibitors

A

Used to help avoid PLT and GI side effects of NSAIDs. e.g. celecoxib

163
Q

Non-nucleotide reverse transcriptase inhibitors

A

Nevirapine, efavirenz, delavirdine. DONT require activation via intracellular phophorylation. AE’s common like flu, abdominal pain, jaundice, fever. Stevens-Johnsons.

164
Q

Zidovudine (AZT)

A

is NOT lamivudine. 3’ prevention of elongation. Like zalcitabine, must be converted into monophosphate form via cellular thymidine kinase.

165
Q

Motion sickness receptors?

A

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

166
Q

Cladribine

A

PURINE analog for hairy cell leukemia. Resistant to degradation by adenosine deaminase.

167
Q

Dacarbazine

A

Cell-cycle non-specific methylating agent requiring enzymatic activation (liver)

168
Q

Cyclophosphamide

A

Alkylating agent that must be converted to active by hepatic CYP450 2B

169
Q

Lomustine

A

Nitrosourea agent that acts by DNA alkylation and cross-bridge formation (Requires non-enzymatic hydroxylation in liver). Penetrates CNS b/c lipophilic.

170
Q

Nitroprusside

A

Quick onset, short duration of action w/ cyanide toxicity with prolonged use, high dose, renal problems. Direct arterial and venous vasodilator.

171
Q

Fenoldopam

A

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)

172
Q

Class III antiarrhythmics

A

K+ efflux decreased, increased AP. Dofetilide, ibutilide, amiodarone, sotalol.

173
Q

Class IA antiarrhythmics

A

Disopyramide, Quinidine, Procainamide. “Quinn is a Pro Dicer.” Intermediate inhibition of phase 0 and prolonged AP.

174
Q

Class IB antiarrhythmics

A

Lidocaine, Tocainide, Mexiletine. “Mex The Lido” Weak inhibition of phase 0, and shortened AP.

175
Q

Class 1C antiarrythmics

A

Moricizine, Flecainide, Propafenone. “Mori is a Pro Flexer!.” Strong inhibition of phase 0 with no change in AP.

176
Q

ACEi first dose?

A

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)

177
Q

How do you treat Beta-blocker overdose?

A

Glucagon b/c it increases intracellular cAMP and cardiac contractility

178
Q

Serotonin syndrome vs. TCA tox?

A

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

179
Q

Cilostazol

A

Decreases platelet phosphodiesterase activity -> increased cAMP -> decreased PLT aggregation. Direct arterial vasodilator. Therefore, a PAD tx.

180
Q

Abciximab

A

Monoclonal Ab that inhibits PLT aggregation via IIb/IIIa receptor. Used prior to PCIs.

181
Q

Cisplatin should be used with?

A

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.

182
Q

Calcineurin inhibitors

A

Tacrolimus and cyclosporine. Calcineurin is essential for IL-2 activation for T-cells.

183
Q

Sucralfate

A

Binds base of mucosal ulcers to protect from acid for healing.

184
Q

Misoprostol

A

Prostaglandin E1 analog used to prevent NSAID-induced ulcer disease. Also used for labor induction and abortion.

185
Q

Acute gouty attack drugs?

A

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)

186
Q

Ototoxic chemo?

A

Cis-platin

187
Q

1st gen antihistaminergics names and side-effects

A

Chlorpheniramine, diphenhydramine, promethazine. Sedation, blurry vision.

188
Q

Opioid tolerance - what do I need to know?

A

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.

189
Q

What is tachyphylaxis?

A

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.

190
Q

Anti-motility anti-diarrheals

A

Bind mu opiate receptors in GI to slow motility. Diphenoxylate.

191
Q

Anti-secretory antidiarrheals

A

Bismuth subsalicylate, probiotics, octreotide

192
Q

Salicycylate poisoning

A

Initially 2 abnormalities: respiratory alkalosis 2/2 respiratory center hyperventilation + AG metabolic acidosis occuring aftewards (hours)

193
Q

Ticlodopine side effect

A

Rarely (<1%) = neutropenia

194
Q

Transplant anti-rejection regimen is generally

A

A calcineurin inhibitor (tacrolimus, sirolimus, cyclosporine) and a de novo purine synthesis inhibitor T-lymphocyte proliferation inhibitor (azothioprine, mycophenolate mofetil)

195
Q

The only FDA-approved anti-obesity medication?

A

Orlistat - inhibits intestinal lipase –> inhibiting fat absorption in the gut

196
Q

Probenacid

A

Inhibits renal tubular secretion of penicillins and most cephalosporins, limiting their excretion. Inhibits reABSORPTION of uric acid (gout, preventive drug)

197
Q

An agent that increases levodopa peripheral metabolism?

A

Vitamin B6. (Entacapone prevents peripheral methylation 2/2 COMT)

198
Q

Effects of carbidopa with levodopa?

A

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)

199
Q

What are “permissive” effects of a drug?

A

Allows another drug to achieve its full potential. NOT synergistic.

200
Q

Echinocandins and their mech?

A

Mech is blocking the synthesis of Beta (1,3) - D glucan, which is the main component of Candida and Asperillus. e.g. caspofungin

201
Q

Doxorubicin mechanism?

A

Intercalates DNA, binds cell membranes, and generate oxygen radicals (Heart is particularly sensitive b/c it lacks catalase)

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