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BOARDS COPY > Lange - Pharm > Flashcards

Lange - Pharm Flashcards

1
Q

Penicillin- Pen G (IV), Pen V (O)

A
  • Structural analogs of D-Ala-D-Ala
  • Cocci (both gram + and -) and spirochetes (like syphilis)
  • Binds PBP–>inhibits peptidoglycan synthesis–>decreased peptidoglycan cross-linking in cell wall
  • SE = hemolytic anemia, allergy
  • Resistance = beta-lactamases
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2
Q

Ampicillin/Amoxicillin

A
  • “AMinoPenicillins are AMPed up penicillins:” wider spectrum
  • So all cocci, plus gram negative rods and gram positive rods (Listeria)
  • AmOxicillin has > Oral bioavailability than ampicillin
  • Ampicillin/Amoxicillin “HELPSS kill enterococci”: H flu, E coli, Listeria, Proteus, Salmonella, Shigella, enterococci
  • Penicillinase sensitive: Often add Clavulanic acid or Sulbactam
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3
Q

Piperacillin/Ticarcillin

A
  • bind PBPs blocking cross-linking
  • Tx for pseudomonas & gram (-) rods
  • Given with Tazobactam (beta lactamase inhibitor) - S. aureus infections
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4
Q

Methicillin/Nafcillin

A
  • Beta-Lactamase resistant - bulkier structure
  • MRSA is something that has alterations in the PBPs (doesn’t break methicillin down, just doesn’t let it bind)
  • “Use naf for staph:” S. aureus infections
  • But can’t use it for MRSA
  • SE = interstitial nephritis
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5
Q

Aztreonam

A
  • monocyclic Beta-Lactam ring that bind to PBPs
  • To treat severe gram (-) rod - no activity against gram (+) bacteria
  • used in patients with allergy to penicillin or in patients who cannot tolerate aminoglycosides (renal impairment)
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6
Q

Imipenem

A
  • Broad-spectrum. enterococci, gram (+) cocci + PEAR (Pseudomonas, Enterobacter, anaerobes, gram (-) rods)
  • SE= seizures high serum levels
  • Give Cilistatin too!
  • With imipenem, “the kill is lastin’ with cilistatin:” Inhibits renal dihydropeptidase 1–>prevents imipenem breakdown in renal tubules–>longer imipenem duration of action
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7
Q

Cephalosporins

A
  • Generation 1–gram + cocci & P.mirabilis, E.coli, Klebsiella
  • Generation 2–gram + cocci & Proteus, E.coli, Klebsiella, Serratia, H.influenza, & some anaerobes
  • Generation 3–serious gram (-) infections
  • Ceftriaxone–Gonorrhea and Meningitis
  • Ceftazidime–Pseudomonas
  • Generation 4–Cefepime, both gram (+)and serious gram (-) infections
  • SE = disulfiram-like reaction with EtOH; hypersensitivity rxn (10% of those allergic to penicillin will get this)
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8
Q

Aminoglycosides: Gentamicin, Streptomycin, Neomicin, Tobramycin, Amikacin

A
  • Binds 30s–>inhibits initiation complex formation–>mRNA misreading–>nonfunctional proteins
  • Use for severe infections with aerobic gram negative rods (like Pseudomonas)
  • (They require O2 uptake to get into cell so don’t work against anaerobes)
  • SE = ATN - nephrotoxicity (esp with cephalosporins); ototoxicity (esp with loop diuretics)
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9
Q

Clindamycin

A
  • Binds 50s–>inhibits initiation complex formation
  • “Severe anaerobic infections above the diaphragm.”
  • aspiration pneumonia, lung abscess
  • Endocarditis prophylaxis before dental procedures as well
  • SE = pseudomembranous colitis
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10
Q

Linezolid

A
  • inhibits 50s; Tx: MRSA and VRE (gram positive infections)
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11
Q

Chloramphenicol

A
  • Binds 50s–>inhibits peptidyl transferase–>inhibits growing peptide chain
  • Broad spectrum (H. flu, N. meningitidis, S. pneumoniae, Bacteroides, Rickettsiae)
  • alternative tx for bacterial meningitis in pts with penicillin allergy
  • SE = myelosuppression (aplastic anemia (dose independent), dose-dependent anemia); gray baby syndrome (with vomiting, shock…)
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12
Q

Macrolides (-thromycins): Erythromycin, Clarithromycin, Azithromycin

A
  • “MAC Daddy”: MAC tx and other atypical pneumonias, STDs (what MAC Daddy’s get), Diphtheriae
  • Bind 50s–>inhibit translocation, inhibits formation of initiation complex
  • Corynebacteria diptheriae, atypical pneumonias (Mycoplasma, Chlamydia, Legionella, MAC) and some STDs (Chlamydia)
  • Also for Campylobacter when it is fluoroquinolone-resistant
  • SE = GI upset, inhibits P-450 enzymes
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13
Q

Tetracycline (-cyclines): Doxycycline, Minocycline

A
  • “Lime in a four wheeler”
  • Binds 30s–>blocks aa-tRNA from binding ribosome–>inhibits protein synthesis
  • Lyme disease, Rickettsia, atypical pneumonias ( Mycoplasma or Chlamydia), STD Chlamydia
  • combination therapy for H. pylori
  • SE = teeth discoloration and bone deformity in children; Fanconi syndrome; Photosensitivity rash
  • Divalent cations (milk, antacids…) prevent its absorption, so don’t take it with those
  • Fecal elimination (so can use in renal deficient pts)
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14
Q

TMP-SMX

A
  • SMX = PABA analog, competitively inhibits dihydropterate synthetase–>decreased THF
  • TMP–inhibits dihydrofolate reductase–>decreased DNA synthesis
  • enteric bacteria (E. coli), Pneumocystis carinii pneumonia, treat UTI
  • “TMP = PCP”
  • SE = Stevens-Johnson syndrome, hemolytic anemia
  • Or in babies–kernicterus
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15
Q

Fluoroquinolones (-floxacins): Ciprofloxacin, Norfloxacin, Levofloxacin, etc.

A
  • Inhibit bacterial DNA topoisomerase 2–>DNA strand breaks–>cell death
  • For gram negative infections and some gram positive infections
  • Mostly for pneumonias, UTI’s, gonococcal infections
  • SE = tendonitis and tendon rupture in adults
  • And damage growing cartilage (so pregnant women and children should not take them)
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16
Q

Nitrofurantoin

A
  • Used for recurrent UTIs
  • internally metabolized; action similar to fluoroquinolones
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17
Q

Vancomycin

A
  • Binds D-ala-D-ala in cell wall–>inhibits transglycosylase–>weakened peptidoglycans in cell wall
  • Uses–serious gram positive multi-drug resistant infections (MRSA)
  • SE = red man syndrome, ototoxicity, nephrotoxicity
  • histamine blocker prophylaxis for red man syndrome or slow infusion
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18
Q

Metronidazole

A
  • Metabolized by bacterial proteins–>reduced reactive compounds–>damage DNA–>cell death
  • Uses = anaerobic infections below the diaphragm, C. difficile colitis
  • treatment of H. pylori infection
  • protozoans: giardia, trichomoniasis, & E. histolytica, T. vaginalis infections
  • SE = metallic taste; disulfiram-like effect with alcohol (like cephalosporins)
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19
Q

Rifampin

A
  • Inhibits bacterial DNA-dependent RNA-polymerase–>decreased RNA synthesis
  • Uses = mycobacteria (combotherapy): tuberculosis & leprosy
  • Monotherapy for–prophylaxis for contacts of pts with meningococcal meningitis and H flu type B infection
  • SE = harmless orange color to urine & excretions; hepatitis
  • induce P-450 system
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20
Q

Isoniazid

A
  • Processed by mycobacterial catalase-peroxidase–>metabolite–>inhibits synthesis of mycolic acids for mycobacterial cell wall
  • Uses = mycobacteria (combo-therapy)
  • Monotherapy = prophylaxis against active TB in pts with a positive PPD & negative Sx
  • SE = peripheral neuropathy (prevent with Vitamin B6); drug-induced lupus; hepatitis
  • serum level elevation occurs when someone is a slow acetylator in liver (decreased N-acetyltransferase activity)–>Isoniazid metabolization population distribution is bimodal
  • use with Pyridoxine (B6)
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21
Q

Dapsone

A
  • PABA antagonist (like sulfonamides)
  • Uses = combotherapy for Mycobacterium leprae
  • Also prophylaxis against PCP (in HIV pts)
  • SE = G6PD deficient hemolytic anemia
  • (Hemolysis IS D PAIN)
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22
Q

Ethambutol

A
  • Inhibits MB arabinosyl transferase–>decreased synth of MB cell wall
  • Uses = combotherapy for MB tuberculosis
  • SE = retrobulbar neuritis (red-green color blindness, decreased visual acuity)
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23
Q

Pyrazinamide

A
  • “Pyraz-inside”
  • Lowers environmental pH (active against IC TB)
  • Uses = combotherapy for MB tuberculosis (like ethambutol)
  • SE = hepatotoxicity
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24
Q

Nucleoside Reverse Transcriptase Inhibitors (NRTIs)”-vudine”: Zidovudine (AZT), Didanosine (ddI), Lamivudine (3TC), Stavudine (d4T), etc.

A
  • phosphorylated–>inhibit HIV reverse transcriptase–>inhibit DNA synthesis by being added to newly synthesized viral DNA–>defective viral particle
  • Use = HIV HAART therapy
  • Lamivudine–also used for Hepatitis B
  • SE: neutropenia
  • AZT–>megaloblastic anemia/BM suppression
  • ddI–>pancreatitis
  • ddC & d4T–>peripheral neuropathy
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25
Q

Nucleotide Reverse Transcriptase Inhibitors (-fovirs):

Tenofovir, Adefovir

A
  • Don’t need phosphorylated
  • inhibit reverse transcriptase
  • Uses = HIV and Hepatitis B infections
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26
Q

Non-Nucleoside Reverse Transcriptase Inhibitors (-vir-): Nevirapine, Efavirenz, Delavirdine

A
  • Bind specifically to reverse transcriptase–>decreased DNA synthesis
  • Use = HIV HAART therapy
  • SE:Nevirapine–>Stevens-Johnson syndrome; fulminant hepatitis, induce p-450 system
  • Efavirenz–>delusion and nightmares (CNS disturbances)
  • Delavirdine–> teratogenic, elevated LFTs
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27
Q

Protease inhibitors (-navirs):

Ritonavir, Saquinivir, Indinavir, etc.

A
  • inhibit HIV protease–>no mature proteins cleaved–>virus is unable to replicate
  • Uses = HIV HAART therapy
  • SE = altered body fat distribution (Cushingoid)/hyperlipidemia
  • Ritonavir - inhibit P-450–> increase serum levels of other durgs
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28
Q

Acyclovir

A
  • Viral thymidine kinase–>phosphorylates (activates) acyclovir–>dGTP analogue–>incorporates–>inhibits viral DNA synthesis
  • Uses = HSV1, HSV2, VZV, EBV (oral hairy leukoplakia)–Herpes mostly!
  • SE = nephrotoxicity (via crystallization); neurotoxicity (delirium, tremor)
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29
Q

Ganciclovir

A
  • Viral kinase–>phosphorylates (activates) ganciclovir–>guanosine analogue–>inhibits CMV DNA polymerase–>decreased CMV DNA synthesis
  • Uses = CMV infections, especially CMV retinitis
  • SE = pancytopenia
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30
Q

Foscarnet

A
  • Pyrophosphate analogue–>inhibits viral DNA polymerase
  • But does not require kinase activation!
  • Use = 2DOC for CMV infections and acyclovir-resistant HSV/VZV infections
  • SE = nephrotoxicity (–>hypoCa and hypoMg–>szs)
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31
Q

Amantadine

A
  • Binds M2–>blocks uncoating of viral RNA
  • Use = reduce length of influenza A symptoms
  • Also stimulates DA release from SN (Can help tx Parkinson’s)
  • SE = CNS sx
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32
Q

Oseltamivir (-ivirs)

A
  • Inhibits Neuraminidase–>decreased viral replication/release
  • Use = tx and prophylaxis of both influenza A and B
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33
Q

‘R’ibavirin

A
  • Guanosine analogue–>inhibits viral ‘R’NA polymerase–>inhibits viral ‘r’eplication
  • Uses = ‘R’SV bronchiolitis
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34
Q

Amphotericin B

A
  • Binds ergosterol–>pores (altered cell membrane permeability)–>cell death
  • Uses = systemic mycotic infections
  • SE = nephrotoxic (–>hypoK and hypoMg)
  • Can–>arrhythmias
  • Can’t cross BBB, so give intrathecally for fungal meningitis
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35
Q

Nystatin

A
  • Similar MOA to Amphotocerin B
  • More toxic so only used topically for oral and cutaneous Candida
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36
Q

Flucytosine

A
  • “FlU = 5FU”
  • Converted into 5-FU (nucleotide analogue) inside fungal cell–>inhibits thymidylate synthase–>inhibits fungal DNA and RNA synth
  • Use = added to amphotocerin B to combat fungal meningitis and systemic fungal infections
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37
Q

Caspofungin

A
  • Inhibits glucan synthase–>disrupts polysaccharide fungal cell wall
  • Tx of systemic fungal infections
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38
Q

Ketoconazole

A
  • Inhibits fungal P450–>inhibits ergosterol synthesis
  • Also inhibits our P450–>disrupted gonadal and adrenal steroid synth–>gynecomastia, decreased libido, etc
  • Uses = broad-spectrum antifungal
  • Can be given as an antifungal vaginal suppository (for vaginal candidiasis)
  • Also used to tx Cushing syndrome
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39
Q

Fluconazole

A
  • Same as ketoconazole (inhibits P450)
  • But doesn’t affect mammal steroid synth as much! Means no gynecomastia
  • Uses = systemic fungal infections
  • Especially cryptococcal meningitis (Lifelong prophylaxis) and Candidal sepsis
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40
Q

Griseofulvin

A
  • Interferes with microtubule function in keratin-rich tissues–>inhibits mitosis–>inhibits fungal cell replication
  • Uses = oral antifungal for dermatophytic fungal infections (like tinea corporis)
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41
Q

Terbinafine

A
  • Also for dermatophytic fungal infections
  • Inhibits squalene epoxidase–>decreased ergosterol synthesis
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42
Q

Chloroquine (-quines–exception is primaquine):

A
  • Tx of Plasmodium falciparum and blood form of the others
  • Quinine and mefloquine tx Plasmodium falciparum if it is drug resistant
  • Quinine SE = Cinchonism (tinnitus, H/A, dizziness)
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43
Q

Pyri”meth”amine

A
  • Inhibits DHFR–>decreased DNA synthesis
  • (Like Tri”meth”oprime)
  • Uses = tx and prophylaxis of Plasmodium falciparum and tx of Toxoplasma gondii
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44
Q

Primaquine

A
  • Uses = tx hepatic forms of P. vivax and P. ovale
  • Don’t give in pregnancy (–>fetal hemolytic anemia)
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45
Q

Pentamidine

A
  • Prophylaxis for PCP (like Dapsone)
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46
Q

Nifurtimox

A

Tx of Trypanosoma cruzi (Chagas)

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47
Q

Suramin

A
  • Tx of early Trypanosoma brucei infections
  • (=African sleeping sickness with recurring fever and LAD…tsetse fly)
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48
Q

Melarsoprol

A
  • Tx of late Trypanosoma brucei infections
  • (It “sure” is nice to go to sleep. And melatonin helps with sleep.)
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49
Q

Sodium stibogluconate

A
  • Tx of Leishmaniasis
  • (=spiking fevers, HSM…sandfly)
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50
Q

Epinephrine

A
  • B agonist at low doses, alpha agonist as well at high doses.
  • Note: so at low doses it decreases DBP, at high doses it increases DBP (SBP gets increased no matter what)
  • Low doses–>increased HR and contractility, bronchodilation
  • High doses–>vasoconstriction too
  • Uses = anaphylaxis, cardiac arrest, severe hypotension, bronchospasm in asthma, wide angle glaucoma (increased ciliary body aqueous humor)
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51
Q

Norepinephrine

A
  • Potent alpha1, alpha2, and beta1 agonist
  • alpha1–>vasoconstriction
  • beta1–>increased contractility and HR (but get reflex bradycardia–>HR doesn’t change)
  • Uses = tx of severe hypotension and shock
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52
Q

Dopamine

A
  • Low doses = beta1/2 and D1 agonist–>increased HR, contractility
  • D1–>increases renal and splanchnic blood flow–>promotes renal perfusion
  • High doses = alpha 1 agonist–>vasoconstriction
  • Uses = pressor in emergency tx of severe hypotension and shock, but spares kidneys!!!
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53
Q

Dobutamine

A
  • B1 agonist–>increases HR and contractility
  • Uses = tx of cardiogenic shock
  • Increases myocardial O2 consumption
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54
Q

Ephedrine

A
  • Stimulates release of NE and epi from neurons–>increased SBP and DBP and bronchodilation
  • Also stimulates CNS–>insomnia and decreased appetite
  • Uses = nasal decongestant, wt loss, athletic enhancement
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55
Q

Cocaine

A
  • Blocks NA/K ATPase that is responsible for reuptake of NE, DA, and 5-HT. Block voltage-gated Na+ channels.
  • –>euphoria (d/t DA), vasoconstriction, and cardiac ischemia
  • SE = HTN, cardiac ischemia, cardiac arrhythmias, abuse
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56
Q

Phenylephrine

A
  • A1 agonist–>vasoconstriction and pupil dilation; Nasal constriction if applied topically
  • Uses = severe hypotension and shock, dilate pupils for ophtho exam, nasal congestion (but get rebound rhinorrhea after a few days)
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57
Q

Clonidine

A
  • A2 agonist–>decreased central adrenergic activity–>decreased vasoconstriction, decreased CO and decreased HR
  • Does not decrease renal blood flow (good for HTN pts with renal dz)
  • Uses = tx of HTN
  • SE = rebound HTN (if drug is withdrawn quickly)
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58
Q

Isoproterenol

A
  • Potent B1 and B2 agonist–>increased HR/contractility, vasodilation (d/t B2), and bronchodilation
  • Uses = tx of torsades de pointes, or sometimes cardiac arrest or complete heart block
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59
Q

Albuterol (-terols)

A
  • Short-acting B2 agonist–>bronchodilation
  • B2 can also–>K shifting into cell
  • Use = asthma, including DOC for acute episodes
  • Also can be used to tx hyperkalemia at high doses
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60
Q

Amphetamine

A
  • Similar to Ephedrine.
  • –>hyperaroused state.
  • Also decreased appetite and insomnia.
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61
Q

Methylphenidate

A
  • Amphetamine derivative.
  • Uses = narcolepsy, ADHD
  • But Modafinil is DOC for narcolepsy I think
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62
Q

Sympatholytics

A
  • Reserpine:
  • Inhibits neuron’s ability to store NE, DA, and 5-HT
  • –>depletion of these NTs
  • Uses = tx of HTN, but causes serious psych depression so not used much!
  • Guanethidine–similar, for HTN, but also not used much anymore
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63
Q

Midodrine

A
  • “Middledrine”
  • A1 agonist–>vasoconstriction
  • Use = orthostatic hypotension
  • SE = supine HTN
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64
Q

Methyldopa

A
  • A2 agonist–>decreased central adrenergic activity–>decreased vasoconstriction
  • Also does not reduce renal blood flow
  • Use = tx of moderate HTN
  • SE = orthostatic HTN, dizziness
  • Very similar to Clonidine!
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65
Q

Fenol”dopa”m

A
  • D1 agonist–>splanchnic/renal vasodilation and natriuresis
  • = only available agent that improves renal perfusion while lowering bp!
  • Use = HTN emergencies
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66
Q

Salmeterol

A

Similar to Albuterol, but long-acting, so used to prevent asthma and COPD attacks

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67
Q

Terb”ut”aline

A
  • B2 agonist–>relaxes uterus and bronchodilates
  • Uses = only use if preterm labor needs to be delayed greater than 48 hours (like if CS need to be given for fetal lung maturity)
  • SE = tachycardia, tremor
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68
Q

Ritrodine

A

B2 agonist–>reduced preterm labor uterus contractions

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69
Q

Phenoxybenzamine

A
  • Irreversible alpha receptor antagonist (a1>a2)–>decreased vasoconstriction–>decreased bp
  • Use = tx of pheochromocytoma (or given before surg on pheochromocytoma)
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70
Q

Phentolamine

A
  • Reversible alpha receptor antagonist.
  • Use = to dx pheochromocytomas
  • (Pt will get a larger than expected bp decrease)
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71
Q

Prazosin (-zosins)

A
  • Selective alpha1 antagonist–>decreased vasoconstriction and decreased bladder/prostate contraction (relax internal urethral spincter)
  • Uses = HTN + BPH
  • SE = “first-dose” syncope (so start with low dose)
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72
Q

Propranolol (“N-Z”)

A
  • B1 and B2 antagonist–>decreased HR/contractility and bronchoconstriction
  • Uses = tachycardia with hyperthyroidism, HTN/CAD, chronic migraine tx
  • SE = bronchoconstriction, fasting hypoglycemia, hyperkalemia (bc interfere with B2-mediated IC K uptake)
  • Hypoglycemia bc decrease NE/epi release in response to glucose
  • So don’t use in DM pts (mask hypoglycemia sx!)
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73
Q

Timolol

A
  • “Tim-e 2 fix these eyes”
  • B1 and B2 antagonist.
  • B2 block–>decreased aqueous humor production by ciliary epithelium–> tx of wide-angle glaucoma
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74
Q

Carvedilol/Labetalol

A
  • A1 and B1/2 receptor blocker–>lower bp, lower HR/contractility, bronchoconstriction
  • –>decreased cardiac work
  • Uses = chronic CHF; HTN
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75
Q

Metoprolol (“A-M”)

A
  • B1 receptor antagonist–>decreased HR/contractility/conductance (increased PR)–>decreased CO
  • (also get a little bronchoconstriction d/t mild B2 antagonism)
  • Remember: B1 also is on renal JG cells, so this decreases renin
  • Uses = HTN, CAD, tachycardias
  • Esmolol = short-acting, for critically ill pts
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76
Q

Hexamethonium (mecamylamine and trimethaphan)

A
  • Competitive inhibition of Nicotinic receptors on the postsynaptic neuron of the autonomic ganglia.
  • Tx HTN emergencies
  • SE: hypotension
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77
Q

“P”ilo”c”arpine

A
  • M1-M2-M3 (mostly M3) agonist–>pupillary sphincter muscle contraction and ciliary muscle contraction
  • “P”upillary sphincter muscle contraction–>open canal of Schlemm–>anterior chamber gets wider–>tx of narrow angle glaucoma
  • “C”iliary muscle contraction–>open trabecular meshwork–>tx of wide angle glaucoma
  • Uses = tx of both narrow angle and wide angle glaucoma
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78
Q

Carbachol

A

Also used to tx wide-angle glaucoma (like Pilocarpine)

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79
Q

“M”ethacoline

A
  • Inhaled M1-M2-M3 (mostly “M”3) agonist–>smooth muscle contraction of bronchi
  • Use = bronchial challenge test for dx of reactive airway disease
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80
Q

“B”ethanechol

A
  • M2-M3 (mostly M3) agonist–>increases “b”ladder contraction and relaxes bladder sphincter–>promotes urination
  • Use = tx urinary retention (example: atonic bladder after surg)
  • Also used to tx neurogenic ileus
  • SE = bradycardia/HTN (d/t M2), diarrhea, sweating (d/t M3)
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81
Q

Atropine

A
  • Competitive M1-M2-M3 antagonist
  • Block M1–>psychosis
  • Block M2–>tachycardia
  • Block M3–>cycloplegia (loss of accommodation d/t paralyzed ciliary muscle), mydriasis, decreased GI motility
  • Use = tx for bradycardia during cardiac emergencies; and antidote for AChE inhibitor* poisoning (nerve gas, insecticide)
  • SE = hyperthermia, flushing, decreased salivation…tachycardia
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82
Q

Physostigmine (as antidote)

A
  • Antidote for Atropine overdose
  • Used bc it can cross the BBB
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83
Q

Scopolamine

A
  • Competitive M1-M2-M3 antagonist–>crosses BBB and blocks M1–>interferes with neuronal communication b/w vestibular ear and CTZ–>prevents motion sickness
  • Use = tx for motion sickness
  • Also can help muscarinic sx d/t stigmines (which tx MG)
  • SE = “ABCCDSS” (cholinergic blockade)
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84
Q

Benztropine

A
  • “Check your eyes: The Benz is getting balanced on Park place”
  • M1-M2-M3 antagonist–>crosses BBB and acts on M1 in SN–>decreased cholinergic activity (Ach)–>restore DA-Ach balance–>helps Parkinson’s
  • DOC for drug-induced PD
  • Use = adjuvant for PD, improves the tremor and rigidity (but not the bradykinesia)
  • C/I in pts with narrow angle glaucoma (d/t M3 inhibition)
  • –>pupil spincter muscle relaxes and blocks Canal of Schlemm
  • Other anti-PD agents = DA agonists (Bromocriptine, Amantadine, Levodopa) and MAO-B inhibitors (Selegiline)
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85
Q

Ipratropium (-tropiums)

A
  • M3 antagonist–>bronchodilation
  • Use = tx of COPD and asthma
  • Especially in pts who cannot take adrenergic agents
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86
Q

Oxybutynin

A
  • “If you’re nine you pee your pants so you need Oxybut-nine”
  • M1-M2-M3 antagonist–>constricts bladder spincter and decreases bladder contraction
  • Use = tx of urinary incontinence
  • SE = cholinergic blockage
  • Propantheline: same action. Urinary incontinence and duodenal ulcers
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87
Q

Neostigmine

A
  • Neo–3 letters = 3 uses
  • Reversibly inhibits AChE-->increased stimulation of both nicotinic and muscarinic receptors
  • Uses = tx of myasthenia gravis
  • Also, to stimulate the GI tract and bladder postoperatively
  • Also, to overcome non-depolarizing NM blockade
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88
Q

Physostigmine

A
  • Similar, but crosses BBB.
  • *Uses = tx of atropine poisoning
  • Also tx of glaucoma (decreased Ach breakdown at M3–>miosis–>open Canal of Schlemm)
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89
Q

Pyridostigmine

(“longest prefix”)

A
  • “Long”-acting reversible AChE inhibitor
  • Use = tx of myasthenia gravis
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90
Q

Edrophonium

A
  • Reversible AChE inhibitor–>increased stimulation of both nicotinic and muscarinic receptors
  • Use = Tensilon test (to dx myasthenia gravis or AChE overdosage)
  • Note: Tx overdoses of this or -stigmines with Atropine
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91
Q

Tacrine, Donepezil

A
  • “tACh”
  • Reversible AChE inhibitor–>increased nicotinic and muscarinic stimulation
  • Use = tx of Alzheimer’s disease (slows progression by 6 months)
  • It works bc a decrease in Ach has been noted in AD
  • “Tacrine Alzheimer’s Disease to slow it down”
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92
Q

“Echo”thiophate (-phates)

A
  • Inhibit AChE–>increased stimulation of nicotinic and muscarinic receptors
  • Use = ophthalmic ointment that txs wide angle glaucoma (d/t increased M3 stimulation…)
  • “Echo in the eyes”
  • Systemic SE: seizures, bradycardia, flaccid paralysis
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93
Q

AChE Poisons

A
  • “Mala = bad, and Para goes with mala”
  • Parathion/Malathion:
  • Poisons.
  • These, and the -phates, –>szs, bradycardia, flaccid paralysis, death when give systemically
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94
Q

Pralidoxime

A
  • Reverses AChE inhibitor binding to Ach–>allows AChE to function normally again
  • Use = tx of organophosphate/AChE inhibitor poisoning
  • This is the ONLY med that reverses both the muscarinic AND nicotinic side effects of organophosphates!!!
  • (Atropine only reverses muscarinic side effects)
  • “Have a Parade because your AChE is back”…weeeaak
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95
Q

SSRIs

(-oxetines, -oprams, Sertraline)

A
  • Prevent serotonin reuptake–>increased serotonin effect
  • Uses = major depression, OCD, anxiety disorders
  • SE = sexual dysfunction, and serotonin syndrome (muscle stiffness, hyperthermia, ANS instability)!
  • Serotonin syndrome occurs when SSRI is given with:
    • MAO inhibitor
    • TCA
    • Tramadol
    • Ondansetron
    • Linezolid
    • Triptans
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96
Q

Cyproheptadine

A

Use = tx for serotonin syndrome (Cyp on serotonin)

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97
Q

TCAs

(-triptylines, -ipramines, trazodone, bupropion, doxepin)

A
  • “ti-TBD”
  • Block 5-HT AND NE reuptake.
  • Also inhibit muscarinic, alpha-adrenergic, and histaminic receptors–>many side effects!
  • Uses = tx of major depression, chronic pain
  • SE = sedation, postural hypotension/wide QRS/arrhythmias (MCC of death); anticholinergic effects (ABCDs); seizures
  • Trazadone–>priapism
  • Risk of inducing mania in susceptible patients!
  • “Wide PPCAMSS”
  • Tx of overdose = sodium bicarbonate!
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98
Q

Heterocyclic antidepressants (venlafaxine, mirtazapine, nefazodone…)

A
  • Venlafaxine/Nefazodone–>block NE/5-HT reuptake–>tx depression
  • (Like TCAs)
  • Mirtazapine: inhibits alpha2 and 5-HT2 receptors–>increased NE and 5-HT release
  • Commonly used to tx depression in pts with insomnia
  • Use =general anxiety disorder, depressive disorders
  • SE = sedation, increased appetite–>wt gain
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99
Q

MAOIs

(phenelzine, isocarboxazid, tranylcypromine)

A
  • Irreversibly bind MAO–>increased levels of 5-HT, DA, and NE in the presynaptic neuron–>leak out and activate receptors
  • (Bc irreversible, cant give SSRI for 2 weeks after D/C these)
  • Use = atypical depression (characterized by mood reactivity!)
  • SE = HTN crisis with tyramine-containing foods (wine, cheese…)
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100
Q

Selegiline

A
  • Inhibits MAO-B-->increased DA in presynaptic neuron–>decreased DA degradation
  • Adjunct for PD tx (parkinson’s disease treatment)
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101
Q

Lithium

A
  • Inhibits IP3 second messenger cascade
  • Use = mood stabilizer for bipolar
  • SE = hand tremor, hypothyroidism, nephrogenic diabetes insipidus (d/t ADH antagonism)
  • Also teratogenic–>Ebstein Anomaly (apical displacement of tricuspid leafs, decreased RV volume, RV atrialization)
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102
Q

Typical antipsychotics

(-azines and Haloperidol)

A
  • Block D2 receptors in CNS (and also inhibit H1 some)
  • Uses = tx positive sx of schizophrenia, delirium…Tourette
  • SE: (everything below)
  • Sedation (d/t H1 block)
  • Low potency–>ABCCDSS (chlorpromazine, thioridazine)
  • Thioridazine–>retinitis pigmentosa (Vision problems)
  • Chlorpromazine–>Corneal deposits
  • High potency–>Extrapyramidal side effects (especially haloperidol and fluphenazine)
  • Tardive dyskinesia = irreversible
  • Hyperprolactinemia–>amenorrhea, galactorrhea
  • *Neuroleptic malignant syndrome (muscle rigidity, fever, ANS instability…)
  • Tx for NMS = Dantrolene
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103
Q

Atypical antipsychotics

(-apines and -idones)

A
  • Block DA AND 5HT2 receptors in brain (and some other receptors–>SE)
  • Use = tx positive AND negative sx of schizophrenia, bipolar; delirium tx
  • *SE = mild weight gain (especially Olanzapine); hyperprolactinemia
  • *Clozapine–>agranulocytosis
  • (Drugs CCCrush Myelocytes and Promyelocytes”)
  • So monitor WBC count
  • Risperidone = most likely to–>tardive dyskinesia
  • These have fewer EPS and anti-cholinergic SE than typicals
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104
Q

Benzodiazepines

(-zepams, -zolams)

A
  • Allosterically activate GABA receptor–>increase Cl ion flow–>membrane hyperpolarization–>decreased CNS activity
  • Uses = tx anxiety, status epilepticus, alcohol withdrawal (“szs”), insomnia
  • 1st line for status epilepticus!
  • SE = sedation
  • *Shorter acting–>more addictive and increased withdrawal
  • *Longer acting–>increased daytime drowsiness and fall risk
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105
Q

“Flu”mazenil

A
  • Competitive GABA antagonist
  • Use = tx of benzodiazepine overdose
  • “Treat Benzos with the Flu”
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106
Q

Barbiturates

(-barbitals, thiopental)

A
  • Same MOA as benzos (allosteric binding to GABA receptors), but longer half-life (more residual hangover effect)
  • Uses = Sedative for anxiety/insomnia; mgmt of szs
  • Thiopental–very lipid soluble–>rapid redistribution (muscle and fat), so used for anesthesia induction
  • Overdose–>cardiac/resp depression (tx = Use dialysis/alkalinize urine)
  • May get withdrawal if become dependent
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107
Q

Zolpidem

A
  • GABA receptor agonist (like benzos)–>decreased CNS activity
  • Use = short-term tx of insomnia (non-addictive!)
  • “zzz-olpidem”
  • SE = hallucinations, mild anterograde amnesia
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108
Q

Phenytoin

A
  • Decreases Na/Ca flow across membrane–>decreased nervous system depolarizations
  • Uses = GTCS, partial szs, status epilepticus
  • “pHeNytoin–hyperplasia, nystagmus”
  • SE = gingival hyperplasia, nystagmus; drug-induced SLE.
  • Also teratogen–>fetal hydantoin syndrome (decreased fetal growth, cardiac/palate defects)
  • (4 things)
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109
Q

Lamotrigine

A
  • Blocks fast voltage-gated Na channels of presynaptic neuron–>decreased glutamate/aspartate release
  • Use = epilepsy tx
  • SE = Stevens-Johnson syndrome
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110
Q

Valproate

A
  • MOA unknown, but does increase GABA
  • Use = GTCS/myoclonic szs (DOC), and absence szs (2DOC)
  • Also, treats mania of bipolar disorder
  • Note: myoclonic szs occur in morning and are triggered by decreased sleep
  • SE = hepatotoxic
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111
Q

Ethosuximide

A
  • Decreases Ca currents in neurons
  • Use = tx of absence szs (DOC)
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112
Q

Carbamazepine

A
  • Inhibits Na ion flow–>hyperpolarization–>decreased nerve activity
  • Uses = first-line for simple szs, complex partial szs, and GTCS
  • *DOC for complex partial szs and for trigeminal neuralgia
  • *
  • SE = agranulocytosis, aplastic anemia; hepatotoxic
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113
Q

‘Top’iramate

A
  • Block Na ion flow–>hyperpolarization, and GABA agonist
  • Use = tx epilepsy and migraines
  • “Top = head (migraines)”
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114
Q

Tiagabine

A
  • Inhibits GABA reuptake–>increasing GABA effect
  • Use = combotherapy for partial szs
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115
Q

Vigabatrin

A
  • Irreversibly inhibits GABA transaminase–>increased GABA levels in synapse (stopped breakdown)
  • Uses = tx infantile spasms (Viga”Baby”trin)
  • Or used as adjunct therapy for adults with refractory complex partial szs
  • SE = visual field constriction and even visual loss
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116
Q

Levetiracetam

A
  • “Leave-tired-acetam”
  • “Leaves”
  • May bind synaptic vesicle proteins–>interrupts nerve conduction
  • Uses = partial szs, myoclonic szs, GTCS
  • SE = drowsiness, depression
  • “Tired”
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117
Q

Succinylcholine

A
  • Depolarizing NM blocker, competes with Ach to reversibly bind nicotinic receptors
  • Key points = depolarizing and reversible
  • Train-of-four response = phases
  • Phase 1–initial binding–>Continuous depolarization
  • Phase 2 blockade–when the ion channel begins to repolarize but is desensitized d/t overstimulation
  • CAN use an AChE inhibitor to stop a Phase 2 block, but nothing can stop Phase 1
  • Use = produce quick muscle paralysis for endotracheal intubation, or for emergency procedures
  • *SE = hyperkalemia, cardiac arrythmias…
  • Malignant hyperthermia if given with halothane. Treat with dantrolene.
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118
Q

Pancuronium

(-cur-)

A
  • Non-depolarizing NM blocker that competitively binds nicotinic receptors
  • Does not activate it (unlike succinylcholine)
  • Short-acting, easily reversible
  • Use = adjunct to general anesthesia induction
  • Train-of-four response = fading pattern (not phases)
  • SE = hypotension
  • Can reverse effects with AChE inhibitor (-stigmine)
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119
Q

Local anesthetics

(-caines)

A
  • Block neuron Na channels–>decreased activity
  • Use = local anesthesia
  • *SE = seizures
  • Epinephrine (or other vasoconstrictors) are often given locally with the local anesthetic–>decreased systemic absorption rate–>more effective nerve block
120
Q

General inhaled anesthetics

(-anes)

A
  • Directly activate GABA–>decreased neuronal activity
  • Use = general anesthesia induction and maintenance
  • SE: myocardial and respiratory depression
  • Halothane–>fulminant hepatic necrosis, cardiac arrhythmias
  • Methoxyflurane and enflurane–>nephrotoxic
  • Halothane + Succinylcholine–>malignant hyperthermia
121
Q

General IV Anesthetics

(propofol, etomidate, ketamine, benzos, barbs, opioids)

A

SE:
propofol–>hypotension, o/w not very HY

122
Q

Opioids

(heroin, morphine, hydromorphone, codeine, oxycodone, hydrocodone, meperidine, fentanyl, dextromethorphan):

A
  • Bind/activate opioid receptors throughout nervous system–>increased K efflux–>hyperpolarization/decreased activity of neural cells–>blocked pain transmission
  • Uses = pain control, cough suppression (codeine/dextromethorphan–>suppress cough reflex in brainstem), diarrhea tx, acute pulm edema tx (morphine–>decreased anxiety/preload)
  • SE = cardiac/resp depression, constipation, miosis
  • Also, tolerance and dependence development–>nonfatal withdrawal
123
Q

Naloxone/Naltrexone

A
  • Opioid receptor antagonists
  • Use = to tx opioid overdoses
124
Q

Methadone

A
  • Opioid agonist with long half-life–>helps ease withdrawal sx but no high given
  • Use .= drug tx programs
125
Q

Butorphanol

A
  • Opioid with mixed agonist/antagonist activity at mu and agonist activity at kappa–>hyperpolarization and decreased activity of neural cells
  • Use = severe pain, especially for migraines (intranasal), labor pain, or postop pain
126
Q

Tramadol

A
  • Weak opioid mu agonist–>…–>decreased neuron activity
  • Also inhibits NE and 5-HT reuptake
  • Use = tx of moderate/severe chronic pain
  • Tram-“Midol” (for pain)
  • SE = seizures
  • “Flopping on the tramtrack”
127
Q

Dantrolene

A
  • Inhibits Ca release from the SR of myocytes–>muscle relaxation
  • Use = tx of malignant hyperthermia (d/t general anesthetics)
  • Also used to tx neuroleptic malignant syndrome d/t haloperidol, levodopa, or metoclopramide
  • Note: both of the above have muscle breakdown, hyperthermia, etc
  • SE = hepatotoxicity
128
Q

Levodopa

A
  • Crosses BBB–>DOPA-decarboxylase converts it into dopamine–>increased CNS dopamine
  • Use = first line for Parkinson’s
  • *SE: dyskinesia/sporadic mvmts, cardiac arrhythmias (d/t peripheral conversion)
  • Also, get predictable wearing-off phenomenon and unpredictable “off/on” phenomenon
  • Don’t take B6/multivitamin bc –>increased levodopa peripheral metabolism
129
Q

Carbidopa

A
  • Give with levodopa
  • Inhibits DOPA-decarboxylase in periphery–>increased levodopa in CNS
130
Q

Bromocriptine

A
  • Partial DA receptor agonist
  • Use = PD adjunct; also helps with hyperprolactinemia
  • Other PD drugs are:
    • DA agonists (Amantadine)
    • MAO-B inhibitors (Selegiline)
131
Q

Memantine

A
  • “Mem”-ory (related to AD)
  • *NMDA receptor antagonist–>decreased glutamate neuronal excitation–>decreased CNS damage–>AD sx improvement
  • Use = severe AD (sx improvement only!)
  • SE = agitation, H/A, dizziness (all CNS effects)
132
Q

Sumatriptan

(-triptans)

A
  • Postsynaptic 5-HT1b-1d (serotonin) receptor agonists–>decreased dura vasodilation/inflammation
  • Uses = acute migraines, cluster headaches
  • SE = coronary vasospasm (d/t 1b agonism)
  • So C/I in pts with CAD
133
Q

Smoking cessation agents

(Bupropion, *Varenicline)

A
  • Bupropion = TCA, but is also a nicotinic antagonist
  • Verenicline = partial agonist/antagonist at a4b2 nicotinic receptors in brain
  • SE= suicidality
  • By binding nicotine receptors, these interfere with the smoking reinforcement/reward loop
  • Use = smoking cessation (and bupropion also is used for depression)
  • SE = bupropion–>szs
134
Q

Buspirone

A
  • Presynaptic 5-HT1A receptor partial agonist
  • Use = for general anxiety disorder
  • No hypnotic, sedative, or euphoric effects (so low abuse potential!)
  • Onset of action can take several weeks
  • “Sara’s anxious until she’s on the Bus, but it takes a while to get here”
135
Q

Gabapentin

A
  • “GABAPENtin = GABA analogue, postherpatic neuralgia, edema (SE), neuropathic pain”
  • GABA analogue
  • Use = tx of postherpetic neuralgia, chronic neuropathic pain, and partial szs
  • SE = peripheral edema
136
Q

Pregabalin

A
  • Binds Ca channels in CNS–>decreased glutamate and NE release
  • Uses = fibromyalgia, chronic neuropathic pain
  • SE = dizziness
137
Q

Class 1A Anti-Arrhythmics

(Quinidine, Procainamide, Disopyramide)

A
  • “The Queen Proclaims Diso’s Pyramid”
  • “Double Quarter Pounder”
  • Bind activated Na channels–>block Na inflow in cardiac myocyte–>prolong Phase 0–>slowed conduction of action potential–>slowed rate of cardiac muscle contraction
  • Delayed Phase 3 repolarization (K+ channel block somewhat)–>prolonged QT–>watch out for torsades
  • Uses = Afib, WPW syndrome, Vtach
  • SE = cardiac arrythmias (including torsades)
  • Quinidine–>cinchonism
  • Procainamide–SLE
  • Use-dependent: 1C > 1A > 1B
  • (as ion channels depolarize more frequently, these become more effective)
138
Q

Class 1B Anti-Arrhythmics

(Lidocaine, Tocainide, Mexiletine):

A
  • “Lettuce, Tomato, Mexico”
  • Bind activated AND inactivated Na channels–>block Na inflow in cardiac myocyte–>prolong phase 0 and shorten phase 3–>decreased ability to stimulate contraction (bc can’t get to peak)
  • Uses = ventricular arrythmias (Vfib and Vtach)
  • Lidocaine = DOC for prevention and tx of post-MI arrythmias
  • (B/c Class 1B is least-use dependent (better in ischemic myocardium))
139
Q

Class 1C Anti-Arrhythmics

(Flecainide, Propafenone)

A
  • “Fries Please”
  • Bind activated Na channels–>block Na inflow into cardiac myocyte–>prolong phase 0 only–>slowed action potential rate (but not duration)–>slowed rate of contraction
  • Use = supraventricular arrhythmias
  • SE = life-threatening arrhythmias
  • Avoid in pts with structurally abn hearts (h/o CAD, low ejection fraction, etc)
  • “The fries are life-threatening”
  • The MOST use-dependent
  • (For example, –>longer QRS during exercise, but nl QRS at rest)
140
Q

Class 3 Anti-Arrhythmics

(Amiodarone, Ibutilide, Dofetilide, Sotalol)

A
  • “AIDS”
  • Bind K channels–>prolong phase 3 repolarization–>long QT (and long action potential)
  • Long QT so may–>torsades de pointes
  • Uses = atrial arrhythmias (Amiodarone and Sotalol also tx ventricular arrhythmias)
  • Amiodarone:
  • Actually Class 1-4 agent.
  • Side effects = pulmonary fibrosis, thyroid dysfunction, blue-grey skin discoloration
  • (But don’t usually get torsades with Amiodarone!)
141
Q

Class 4 Anti-Arrhythmics

(Verapamil, Diltiazem)

A
  • Block voltage-gated Ca channels on cardiac myocytes and on SA and AV nodes–>slow phase 4 spontaneous depolarization (= prolonged PR) and also delay repolarization (slowed HR)
  • Uses = supraventricular tachycardia (like Afib)
  • SE = heart block, constipation, gingival hyperplasia
142
Q

Adenosine

A
  • Increases K efflux in SA and AV nodes–>hyperpolarization–>less activation
  • Use = supraventricular tachycardias, and cardiac stress testing
  • DOC for paroxysmal supraventricular tachycardia
  • SE = flushing, dyspnea
143
Q

Potassium

A

Suppresses ectopic pacemakers (especially if d/t digoxin toxicity)

144
Q

Magnesium

A
  • Used to treat torsades
  • Used to tx digoxin toxicity
145
Q

Beta blockers–just remember

A

That they are the Class 2 anti-arrhythmics

146
Q

Digoxin

A
  • Inhibits Na/K pump–>increased IC Na–>decreased Na/Ca exchange–>increased IC Ca–>increased contractility
  • Also increases PSNS outflow at nodes–>decreased HR
  • Use = tx for heart failure
  • SE = blurry, yellow vision. GI upset. ECG changes (long PR, short QT, ST scooping, T wave inversion)
  • Hypokalemia makes these side effects worse (bc K usually competes with Digoxin to bind Na/K pump)
  • Renal failure (decreased excretion) and quinidine (displaces Digoxin off albumin) also make the SE worse
  • Verapamil/Diltiazem can–>digoxin toxicity by raising its levels
  • Digoxin toxicity: Tx with potassium and digoxin FAB (aby)
147
Q

Nesiritide

A
  • Synthetic hBNP. Binds guanylate cyclase receptor–>increased cGMP–>smooth muscle relaxation/dilation–>reduced preload and afterload
  • Use = rarely used for acute decompensated HF (doesn’t help mortality)
  • SE = hypotension
148
Q

Nitroglycerin

(and other nitrates)

A
  • Converted to NO in the cell–>stimulates guanylate cyclase–>increased cGMP–>inactivation of MLC–>smooth muscle relaxation
  • Works mostly on smooth muscle of veins–>decreased preload
  • It also relaxes the coronary artery smooth muscle
  • (This may be bad if +cardiac ischemia bc–>coronary steal syndrome)
  • Uses = tx of angina, pulmonary edema, HF
  • SE = compensatory tachycardia, H/A, ortho hypotension, flushing
  • Need nitrate free interval daily to prevent tolerance
  • Amyl nitrite = DOC for cyanide poisoning
  • Isosorbide mononitrate–has highest oral bioavailability
149
Q

Amyl nitrate

A
  • DOC for cyanide poisoning
  • (From the nitrate drug class)
150
Q

Isosorbide mononitrate

A

Highest oral bioavailability of the nitrates

151
Q

Nitroprusside

A
  • IV only.
  • Converted to NO in the bloodstream–>stimulates guanylate cyclase–>inactivation of MLC–>smooth muscle relaxation of peripheral veins AND arteries–>reduced preload AND afterload
  • Uses - acute mgmt of a HTN crisis, severe HF, or cardiogenic shock
  • DOC for most HTN emergency
  • SE = cyanide toxicity
  • (Tx with thiosulfate (not amyl nitrate))
152
Q

ACE-inhibitors (-prils):

A
  • DOC if pt has DM and HTN
  • Inhibit peptidyl dipeptidase (ACE)–>decreased vasoconstriction, decreased aldosterone, etc–>decreased bp and blood volume
  • Uses = HTN and CHF
  • Also used to tx and prevent diabetic nephropathy
  • Shown to decrease mortality in post-MI pts (bc decreased aldo–>decreased cardiac remodeling)
  • SE = “CATCHH:” Cough, Angioedema, Teratogen (fetal renal malformation), Creatinine increase (decreased GFR), Hyperkalemia, Hypotension
  • Do NOT give if pt has bilat renal artery stenosis!
153
Q

ARBs (-sartans)

A
  • Block AT (AT1) receptors–>…–>decreased bp and blood volume
  • Uses = HTN and CHF
  • Also used to tx and prevent diabetic nephropathy
  • Same side effects as ACEi, but no cough/angioedema
154
Q

Hydralazine

A
  • Direct relaxation of arteriolar smooth muscle–>decreased bp
  • Uses = HTN and HF (reduces afterload)
  • DOC for HTN in pregnancy (ecclampsia, preecclampsia)
  • SE = Drug induced lupus, reflex tachycardia, headache
155
Q

Minoxidil (Rogaine)

A
  • Direct relaxation of arteriolar smooth muscle
  • Uses = tx of refractory HTN
  • Also promotes hair growth
156
Q

CCBs

(-ipines, verapamil, diltiazem)

A
  • Block voltage-gated L-type Ca channels–>decreased Ca inflow–>peripheral vasodilation
  • Uses = HTN, Prinzmetal angina, and Raynaud, and DES
  • DOC (or HCTZ) for isolated systolic HTN
  • Do not affect renal insufficiency
157
Q

Osmotic diuretics

(Mannitol, urea, glycerin, isosorbide)

A
  • “GUMI bear with bad heart and bad lungs in descending loop”
  • Act on PCT and descending loop of Henle–>keep water in tubule–>increase urine–>decrease effective circulating volume
  • Uses = decrease intracranial or intraocular pressure by volume depletion
  • SE are b/c it initially causes expansion of circulating volume (before renal elimination):
    • Pulmonary edema
  • C/I in pts with CHF
158
Q

Carbonic anhydrase inhibitors

(-zolamides)

A
  • “Ascent-azolamide”
  • Inhibit carbonic anhydrase in PCT cells–>less bicarb reabsorbed and more Na lost–>increased renal H2O and electrolyte loss
  • CA also helps produce aqueous humor in the eye!
  • Uses:
    • alkalinize the urine prn after toxin ingestion,
    • treat glaucoma,
    • tx/prevent altitude sickness
  • SE = hyperchloremic metabolic acidosis, hypokalemia, and hypocalcemia
159
Q

Furosemide/torsemide

(and bumetanide):

A
  • Sulfonamide derivative that inhibits NA/K/2Cl in thick ascending limb–>loss of water and electrolytes
  • No hyponatremia (no gradient there to reabsorb water in response to ADH)
  • Use = tx volume overloaded states a/w heart failure, liver failure, renal failure.
  • Also tx of HTN and hyperCa
  • SE = hyperuricemia (–>gout attack), ototoxic
  • Allergic rxn in pts with sulfa allergy
  • Note: the hyperuricemia is bc of increased PCT Na reabsorption
160
Q

Ethacrynic acid

A
  • Diuretic, same MOA as loops, but not sulfonamide-related.
  • Give this in pts who cannot tolerate furosemide d/t sulfa allergies.
161
Q

Thiazide diuretics

A
  • Inhibit NaCl transporter in DCT–>increased renal loss of H2O and salt
  • Uses = HTN, nephrogenic DI (decreases polyuria), and recurrent kidney Ca stones
  • SE = hypokalemia/hyponatremia and many hypers (hyperuricemia, hypercalcemia, hyperlipidemia)
  • The increased Ca can help with osteoporosis
  • DOC for essential HTN (without CHF or diabetes)
162
Q

Spironolactone

A
  • Competitive aldosterone receptor antagonist–>decreased Na and H2O reabsorption–>decreased K excretion
  • Also is a competitive androgen receptor antagonist
  • Uses = tx primary hyperaldosteronism, HF volume overload, HTN
  • Also used to tx female hirsutism a/w PCOS
  • Bc it antagonizes aldosterone–>decreased cardiac remodeling–>decreased CHF mortality
  • SE = hyperkalemia, gynecomastia
163
Q

Eplerenone

A

Same as Spironolactone, but less anti-androgen effect–>no gynecomastia

164
Q

Triamterine/Amiloride

A
  • Blocks Na channels in DCT–>block Na/H2O reabsorption and therefore less K excretion
  • Uses = combotherapy to tx volume overload and HTN
  • SE = hyperkalemia
165
Q

Milrinone

(-rinones)

A
  • Inhibit PDE5 (in cardiac/smooth muscle)–>increased cAMP levels–>opens Ca channels–>Ca flows in–>increased contractility
  • Use = tx of acute decompensated HF
  • SE = N/V
  • Note: increased cAMP also–>vasodilation in smooth muscle (so can limit usefulness in hypotensive patients)
166
Q

Sildenafil

(-afils)

A
  • Inhibits cGMP-specific PDE5 (in penis corpus cavernosum and pulm vasculature)–>increased cGMP–>smooth muscle relaxation–>increased penis blood flow/erection and pulm vasodilation
  • Uses = erectile dysfunction, pulmonary arterial HTN
  • C/I in pts on nitrates d/t risk of life-threatening hypotension!
167
Q

Heparin

A
  • Short half-life and rapid onset of action
  • Binds AT3–>accelerates its action–>degrades several clotting factors (especially thrombin)
  • Uses = acute tx for DVTs, pulmonary embolism, other thromboembolic events
  • Also used in tx of acute MI
  • SE = bleeding (tx with protamine sulfate, which inactivates heparin); HIT (d/t formation of anti-platelet abys)
  • Monitor effectiveness with PTT
168
Q

Protamine sulfate

A

Tx of bleeding caused by heparin

(Inactivates heparin)

169
Q

Enoxaparin/Dalteparin

A
  • LMWHs. More active in degrading factor 10, less active in directly degrading thrombin
  • Longer DOA (so less frequent dosing)
170
Q

Fondaparinux

A
  • “You’re Fond of it because it works even if you have HIT hx”
  • Binds AT3–>accelerates its action in degrading factor 10a–>inhibits coag cascade
  • Uses = Acute DVT or pulm embolism tx (especially in pts who have h/o HIT)
  • SE = bleeding
171
Q

Warfarin/Dicumarol

A
  • Inhibits Vitamin K-dependent carboxylation of 2,7,9,10, C and S in liver
  • Long half-life; slow onset
  • Monitor PT
  • Uses = chronic anticoagulation in pts at risk for thromboembolism
  • SE = bleeding (tx with fresh frozen plasma (fastest) or Vitamin K (slower)); teratogen
  • Also can–>skin necrosis (d/t transient hypercoagulation b/c protein C has shortest half-life and therefore goes away fastest)
  • Metabolized by p450 (drug interactions)
172
Q

Fresh frozen plasma, Vitamin K

A

Tx of Warfarin-induced bleeding

173
Q

Direct thrombin inhibitors

A
  • (argatroban, -gatrans, -irudins)
  • Directly inhibit thrombin by binding thrombin active site
  • Uses = acute and chronic anti-coagulation
  • Argatroban–DOC to tx HIT
  • SE = bleeding
  • PT and PTT are both increased
174
Q

Rivaroxaban

(-xabans)

A
  • Directly inhibit factor 5a
  • Uses = DVT prophylaxis, pulm embolism prophylaxis in pts with Afib
  • SE = bleeding
  • Can be used for anti-coagulation in heparin-allergic pts
175
Q

Acetylsalicylic acid (Aspirin)

A
  • Irreversibly inhibits COX1 and COX2–>decreased PG synthesis
  • Decreased PGE2–>analgesia, decreased fever, and decreased gastric mucus (–>ulcers)
  • Decreased PGI2 also–>gastric ulcers
  • Decreased TXA2–>decreased platelet aggregation
  • Uses = anti-platelet, anti-pyretic, analgesic, anti-inflammatory
  • SE = bleeding (especially GI), gastric ulcers, Reye syndrome, allergy
  • Overdose–>respiratory and metabolic acidosis (Tx = NaHCO3 (to alkalinize urine–>promotes excretion))
176
Q

Clopidrogrel/Ticlopidine

A
  • Irreversibly inhibits binding of ADP to platelet P2Y receptor–>decreased ADP-mediated platelet aggregation
  • This blocks the fibrinogen-platelet rxn–>blocked platelet plug formation
  • Uses = tx acute coronary syndrome (along with aspirin)
  • Also used in pts undergoing placement of a coronary stent to prevent thrombosis
  • SE = bleeding
  • Ticlopidine–>neutropenia
  • Metabolized by p450 to be activated
  • Suitable alternative to aspirin
177
Q

Prasugrel

A
  • Same MOA as Clopidrogel.
  • Use = tx acute coronary syndrome along with aspirin in pts undergoing percutaneous coronary intervention
  • SE = bleeding
  • Less metabolization by CYP2C19–>less genetic variability in platelet inhibition than with Clopidogrel
178
Q

Ticagrelor

A

Same effect as other-grels, but reversible allosteric inhibitor to P2Y receptor.

179
Q

Cilostazol

A
  • Inhibits platelet cAMP PDE3–>increased cAMP–>increased PGI2 synth and decreased TXA2 synth–>vasodilation and decreased platelet agg/thrombi
  • Use - tx of claudication in pts with PAD
180
Q

Dipyridamole

A
  • Inhibits platelet/endothelial cell adenosine uptake–>increased circulating adenosine–>activates platelet adenylate cyclase–>increased cAMP–>increased PGI2 synth and decreased TXA2 synth–>vasodilation, decreased platelet aggregation
  • Also, at high doses it inhibits cGMP PDE–>increased cGMP–>further vasodilation
  • Uses = pharm cardio stress tests; secondary prevention of stroke (if used with aspirin)
181
Q

Abciximab (and eptifibatide, tirofiban—“fiba”)

A
  • “A and B – bind 2b and 3a”
  • 2*3 = abSIX
  • Bind G2b/3a platelet receptor–>inhibit fibrinogen and vWF binding–>decreased fibrinogen cross-linking–>impaired platelet aggregation
  • Use = tx of acute coronary syndromes
  • SE = bleeding
182
Q

Ivermectin

A

For river blindness (Onchocerca volvulus)

183
Q

“Bendazoles”

A
  • Mebendazole or Albendazole:
  • For whipworm (trichuris), hookworm, roundworm, and pinworm.
  • Albendazole:
  • For strongyloides, neurocystericosis, Echinococcus
184
Q

Praziquantel

A

For schistosomiasis, neurocystericosis

185
Q

Pyrantel pamoate

A

For hookworm, roundworm, and pinworm

186
Q

Niclosamide

A

For tapeworm infections

187
Q

A polar molecule

A
  • In order for a drug to be eliminated by the kidney, it must be a polar molecule (not lipophilic):
  • Liver makes things polar through 2 sets of reactions:
    1. Phase 1 metabolism = Cytochrome p450
      * Alters the drug to make it more amenable to combining with polar molecules. (Usually oxidation, reduction, or hydrolysis)
    1. Phase 2 metabolism = addition of polar moiety (sulfate, acetate, glucuronate)
      * Makes drug water-soluble and kidney can excrete it
188
Q

Fibrinolytic Agents

“-okinases, -eplases

A
  • Promote conversion of plasminogen to plasmin–>acts to degrade fibrin->degrades the thrombus
  • Give when emergent restoration of blood flow is essential
  • Indicated in : massive PE, stroke, and acute MI
  • SE = bleeding
  • C/I in pts with active bleeding, recent surg, or h/o hemorrhagic stroke
  • Most effective if given within a few hours of sx onset
189
Q

Aminocaproic acid (or tranexamic acid)

A
  • Inhibits plasminogen activation–>inhibits fibrinolysis
  • Use = tx of post-surg bleeding and hemophilia
  • SE = thrombosis
190
Q

Synthetic EPO

(or epoetin, darbepoetin)

A
  • Stimulates BM to enhance erythroid proliferation and differentiation–>increased hematocrit
  • Use = tx of anemia a/w chronic renal insufficiency, chemo, or critical illness
  • SE = cardiovascular events and thrombotic complications if used to increase Hb levels too much
191
Q

Synthetic insulins

A
  • Lispro/Aspart:
  • Rapid onset (peak 1 hour); very short acting (3-4 hours)
  • Regular insulin:
  • Rapid onset (peak 2-3 hours); short-acting (5-7 hours)
  • Semilente:
  • Quick onset (peak 6 hours); intermediate-acting (10-12 hours)
  • Lente/NPH:
  • Intermediate onset (peak 10 hours); intermediate-acting (18 hours)
  • Ultralente/Glargine/Detemir:
  • Slow onset (peak 12 hours); long-acting (24 hours)
  • Glargine = longest and has no peak
192
Q

Sulfonylureas

(Glyburide, Glipizide, etc)

A
  • MOA:
    1. Inhibit K channel in beta cells–>stimulate insulin release
    1. Prolong insulin binding to target receptors–>increases insulin action on target tissues
    1. Increased insulin levels–>inhibition of glucagon secretion–>decreased serum glucagon levels
  • Use = DM2 tx
  • SE = hypoglycemia; disulfiram-like rxn with EtOH
  • *C/I in pregnancy–cause insulin depletion in fetal pancreas
  • *Excreted by liver/kidney (so be careful in pts with these problems)
193
Q

Metformin

A
  • Inhibits hepatic gluconeogenesis and increases peripheral glucose use–>decreased BSG
  • Use = DM2, polycystic ovarian syndrome
  • SE = GI upset; lactic acidosis
  • Kidney excretes it, so C/I in pts with renal problems
  • Does NOT cause hypoglycemia!
194
Q

Thiazolidinediones

(-glitazones)

A
  • Bind PPARgamma–>upregulates genes and adiponectin–>decreased insulin resistance
  • Takes a few weeks to start working since it is upregulating genes
  • Use = DM2
  • SE = wt gain/edema; hypoglycemia
195
Q

Alpha-glucosidase inhibitors

(acarbose, miglitol)

A
  • Inhibit alpha-glucosidase (enzyme on brush border of small intestine)–>less breakdown into monosaccharides–>decreased absorption of postprandial carbs
  • Uses = DM2 tx (and can be used in combo with insulin in DM1)
  • SE = GI upset (flatulence, diarrhea)
196
Q

Meglitinides

(-glinides)

A
  • Bind K channel in beta cell (different binding spot than sulfonylureas)–>insulin release
  • SE = wt gain; hypoglycemia
197
Q

Dipeptidyl peptidase-4

(DPP4) inhibitors (-gliptins)

A
  • Inhibit DPP4–>GLP1 doesn’t get degraded–>increases insulin secretion and decreases glucagon secretion
  • SE = N/V
198
Q

GLP1 analogues

(exenatide, liraglutide)

A
  • Mimic GLP1–>increased insulin secretion, decrease glucagon secretion
  • SE = wt loss
199
Q

Atorvastatin (-statins)

A
  • Inhibit HMG-CoA reductase–>decreased cholesterol synth
  • Also increase LDL receptor concentration on hepatocytes–>decreased serum LDL
  • Use = decrease total cholesterol, and especially LDL, levels
  • SE = myopathy (and possible rhabdomyolysis); abn liver function tests; teratogen
200
Q

Ezetimibe

A
  • Decreases cholesterol absorption in small intestine
  • Also, bc this–>decreased hepatocyte cholesterol stores, the hepatocytes upregulate LDL receptors–>decreased LDL
  • Uses = adjunct to diet or other meds to tx hypercholesterolemia (high cholesterol, high LDL)
  • SE = myalgia; elevated liver function tests; steatorrhea
201
Q

Cholestyramine, etc

A
  • = Bile acid-binding resins
  • Inhibit bile acid reabsorption in jejunum/ileum. This–>lower levels of bile acids–>increased conversion of cholesterol to bile acids–>lower IC cholesterol–>increased LDL receptors–>decreased LDL
  • Use= to lower cholesterol/LDL
  • SE = GI Upset/diarrhea; medication tastes bad; ADEK decreased absorption…
  • “tastes like a tyr-ant”
  • Also, –>hyperTG bc synth of TG also gets upregulated in liver
  • So C/I if pt already has high TG!!
202
Q

Fibrates

(Gemfibrozil, –fibrates)

A
  • Stimulate LPL–>TGs get broken down into chylomicrons and VLDL–>then removed from circulation
  • Use = decrease TG levels (also mild LDL decrease and HDL increase)
  • SE = myositis (esp if given with statin); and liver function tests, hepatotoxicity and gallstones
  • Also, compete with Warfarin for binding sites on plasma proteins–>effects of Warfarin may be increased
203
Q

Niacin

A
  • Inhibit apolipoprotein A1 breakdown–>increased HDL levels
  • And inhibits adipose tissue lipolysis–>less precursors for VLDL and LDL production
  • And inhibits liver TG synth
  • Uses = increases HDL levels; also helps decrease cholesterol, LDL, and TG levels some
  • SE = flushing mediated by PGs (decreased by also giving aspirin); hyperuricemia–>gout exacerbations; insulin resistance (so increase DM meds prn)
204
Q

Bisphosphonates

(-dronates)

A
  • Structural analogues of pyrophosphate–>inhibits and “kills” osteoclasts–>decreases osteoclastic bone reabsorption
  • Uses = prevention and tx of osteoporosis
  • Also used for Paget dz of the bone, bone metastasis a/w hypercalcemia
  • (3 things)
  • SE = GI upset (esp esophageal erosions); jaw osteonecrosis, Afib (3 things)
205
Q

PTU

(or methimazole)

A
  • Inhibit thyroid peroxidase–>inhibit iodotyrosine coupling–>decreased thyroid hormone synthesis and decreased T4/T3 conversion peripherally
  • Use = tx of hyperthyroidism
  • SE = agranulocytosis; hepatotoxic
206
Q

Levothyroxine

A
  • Is synthetic T4.
  • Use = tx of hypothyroidism
  • And used to suppress TSH secretion to tx goiters/thyroid cancers
  • Overdose–>hyperthyroidism sx
207
Q

Colchicine

A
  • Binds tubulin–>induces microtubule depolymerization–>decreased WBC migration to affected site
  • Use = tx of acute gouty attack
  • SE = diarrhea
208
Q

Probenecid

A
  • Decreases reabsorption of uric acid in PCT by blocking active transport
  • Use = to prevent further gouty attacks; also, to prevent/tx hyperuricemia (like in tumor lysis syndrome)
209
Q

Allopurinol

A
  • Inhibits xanthine oxidase–>decreased conversion of xanthine to uric acid
  • Use = same as probenecid
  • SE = both Allopurinol and Probenecid can stimulate acute attacks at first or make acute attacks worse
210
Q

Corticosteroids

(-sones, -solones)

A
  • Mimic actions of endogenous glucocorticoids (vasoconstriction, stimulation of gluconeogenesis and protein catabolism, decrease circulating WBCs, inhibit phospholipase A2–>decreased PG and LT formation, and stimulation of gastric acid and pepsin synth)
  • Uses = tx of adrenocortical insufficiency, allergic rxns, collagen-vascular disorders (RA, SLE, etc), inflammatory bowel disease, asthma, spinal cord compression…immunosuppression…etc
  • SE = Cushing syndrome sx (osteoporosis, irritable, hyperglycemia, fat redistribution).
  • Also impaired wound healing, PUD, muscle wasting…
211
Q

Beclomethasone

A
  • Inhaled glucocorticoid.
  • Use = tx of chronic asthma.
  • Make sure to do oral rinsing to prevent oral Candidiasis
212
Q

Anti-Obesity Agents

A
  • Both of these treat obesity
  • Orlistat:
  • Inhibits lipase–>decreased intestinal fat absorption
  • SE = steatorrhea, decreased ADEK
  • Sibutramine:
  • NT (serotonin, NE, DA) reuptake inhibitor
  • Not really sure how this helps
213
Q

Octreotide

(Somatostatin)

A
  • Inhibits release of many hormones, reduces GI motility, causes vasoconstriction
  • Uses:
    1. Tx of esophageal varices
    1. Tx of VIPoma diarrhea; tx of Zollinger-Ellison syndrome; tx of acromegaly…
214
Q

Vasopressin

(or Desmopressin)

A

3 effects:

    1. V1 receptors–>vasoconstriction
    1. V2 receptors–>increased collecting duct permeability to H2O
    1. V2-like–>increased Factor 8 activity b/c increase vWF release from endothelial cells
  • Uses = tx of central DI; tx of septic shock and cardiac arrest; can also help with vWF dz or Hemophilia A before minor surg procedures
  • Also can help prevent wetting your pants/bedwetting
  • SE = hyponatremia…
215
Q

Oxytocin

A
  • Made in posterior pituitary–>stimulates uterine and breast contraction
  • Uses = induce labor; stimulate milk let-down
  • Also used to control postpartum uterine hemorrhage
216
Q

Flutamide

A
  • Competitive androgen receptor antagonist–>decreased testosterone growth effects on prostate
  • Note: –>increased LH levels d/t decreased inhibition by testosterone
  • (So always give with Leuprolide)
  • “F-Leu-tamide”
  • Use = tx of prostate cancer
  • SE = gynecomastia…
217
Q

Danazol

A
  • Agonist at androgen and progesterone receptors–>decreased LH and FSH secretion–>decreased endometrium and breast growth
  • Use = tx endometriosis, hereditary angioedema
  • SE = androgenic SE in women (hirsutism, acne, etc)
218
Q

Finasteride

A
  • Inhibits 5-alpha reductase–>decreased DHT–>decreased prostate growth
  • Uses = tx of BPH, prostate cancer, and early male-pattern baldness
219
Q

Anastrozole

(or Letrozole)

A
  • Inhibits aromatase–>decreased estradiol levels
  • Use = chemo agent for ER+ breast cancer
  • SE = osteoporosis; increased incidence of CV events in pts with pre-existing CAD
220
Q

Tamoxifen (SERM)

A
  • Competitive ER antagonist.
  • But bc it is competitive, high estrogen amounts can overcome it, so it is most effective in postmenopausal women
  • Uses = chemo agent for ER+ breast cancer; can help with osteoporosis
  • SE = thromboembolism; endometrial cancer; hot flashes
  • Increased endometrial cancer risk bc it works as an agonist there (remember, it is a SERM)
221
Q

Raloxifene (SERM)

A
  • Mixed estrogen agonist/antagonist.
  • Use = osteoporosis tx (agonist), and to reduce risk of invasive breast (antagonist) cancer in postmenopausal women
  • Does NOT increase endometrial cancer risk
  • SE = thromboembolism
222
Q

Leuprolide

A
  • GnRH agonist–>initial LH/FSH release, but then down-regulation–>decreased estrogen and testosterone
  • Uses:
  • If given continuously: tx of metastatic prostate cancer, leiomyomas
  • If given in pulsatile manner: tx of infertility
223
Q

Clomiphene

A
  • Partial agonist at ER in the pituitary–>decreased nl estrogen feedback inhibition–>increased LH/FSH release–>ovulation
  • Use = infertility tx in pts with ovulatory dysfunction (like in PCOS)
  • SE = hot flashes, abd discomfort, multiple pregnancies
224
Q

OCPs

A
  • Mixtures of estrogen/progestin:
  • Synthetic progestin–>decreased GnRH release–>decreased LH and FSH
  • Low levels of synthetic estrogen–>decrease FSH release and cannot stimulate LH release
  • Decreased FSH–>inhibited follicle development
  • Decreased LH–>no ovulation
  • Use = birth control…
  • SE = Increased thromboembolism risk (especially in women > 35 who smoke)
  • Also, decrease ovarian and endometrial cancer risk
225
Q

Progestin-only pills

A

No increased thromboembolism risk

226
Q

Emergency contraception pills

A
  • High doses of progestins
  • Can take up to 72 hours after intercourse to inhibit ovulation
227
Q

Mifepristone

A
  • Steroid compound.
  • Competitive receptor antagonist at progesterone receptor.
  • Use = abortifacent at high doses (–>endometrial lining breakdown and cervical dilation)
  • “My feet press (on the progesterone receptor)”
228
Q

Antacids

(aluminum hydroxide…sodium bicarb)

A
  • Weak bases (form salt and H2O upon rxn with HCl)–>increase pH–>reduce gastric acidity.
  • Also, may decrease pepsin activity bc pepsin is inactivated at pH > 4
  • Uses = GERD tx; also promote healing of duodenal ulcers
229
Q

Sucralfate

A
  • Promote healing of duodenal ulcers by binding/providing physical protection to mucosal barrier
  • Requires acidic environment to be activated (don’t take with antacids, H2 blockers, PPIs…)
230
Q

H2 receptor blockers

(-tidines)

A
  • Reversibly block H2 receptor on parietal cells–>decrease cAMP–>decrease H/K pump–>decreased gastric acid secretion
  • Uses = GERD tx, PUD…
  • SE = gynecomastia, p450 inhibition
231
Q

PPIs

(-prazoles)

A
  • Irreversibly inhibit H/K pump in parietal cells–>decreased HCl secretion
  • Uses = tx of PUD, GERD, ZE syndrome
  • Also help tx H pylori infection
232
Q

Odansetron

A
  • Blocks 5HT3 receptors in GI tract and in CTZ–>inhibits activation of the vomiting reflex path
  • Uses = tx of N/V a/w chemo or surg
233
Q

Promethazine

A

H1 receptor antagonist.

Blocking GI H1 receptors–>decreased GI motility–>less N/V

234
Q

Metoclopramide

A
  • D2 antagonist in CTZ–>blocks vomiting reflex
  • Also, stimulates gastric and small intestinal motility
  • Uses = tx diabetic gastroparesis, and an anti-emetic
  • *SE = sedation, EPS
235
Q

Prochlorperazine

A

Similar to Metoclopramide, but does not affect GI motility (D2 antagonist in CTZ–>blocks vomiting reflex)

236
Q

Laxatives

A
  • Irritants/stimulants = Castor oil, senna
  • Bulking agents = Lactulose, Sorbitol, Polyethylene glycol, Mg salts
  • Stool softeners (get emulsified in stool)= Docusate, mineral oil
  • Uses = tx constipation, and for bowel preparation for colonoscopies
  • Note: lactulose–also helps tx hepatic encephalopathy by being degraded by gut bacteria into compounds that promote nitrogen excretion
237
Q

Anti-diarrheal agents

(diphenoxylate, loperamide, kaolin, bismuth subsalicylate

A
  • Diphenoxylate and Loperamide:
  • Activate mu2 opioid receptors in gut–>inhibit Ach release–>decreased peristalsis
  • Pepto-Bismol:
  • Binds E coli toxins, stimulates fluid absorption, and more
  • Uses = tx of diarrhea sx
238
Q

Sulfasalazine

(or Olsalazine)

A
  • Bacteria in gut break this down into sulfapyridine and aspirin
  • Aspirin acts as anti-inflammatory (inhibits COX)
  • Uses = inflammatory bowel disease (or RA or juvenile arthritis)
  • Do not give with folic acid (bc sulfapyridine inhibits folate absorption)
239
Q

Ursodiol

(or Chenodiol)

A
  • Inhibits HMG-CoA reductase, decreases cholesterol absorption, and inhibits secretion of cholesterol into bile
  • (So inhibits cholesterol gallstones in 3 ways)
  • Uses = tx of primary biliary cirrhosis, or tx of cholesterol gallstones (alternative to cholescystectomy)
240
Q

Anthracyclines

(-rubicins):

A

3 MOA:

    1. intercalate in DNA–>block DNA and RNA synthesis
    1. Produce free radicals–>membrane damage
  • (–>dose dependent cardiac damage (so keep lifetime dose down!!!))
    1. Disrupt fluid and ion transport across membranes
  • Doxorubicin:
  • For solid tumors, heme malignancies (acute leukemia, acute lymphoma, multiple myeloma), Kaposi sarcoma
  • Daunorubicin:
  • For acute leukemia (AML, ALL, CML) and neuroblastoma
  • Idarubicin:
  • For AML
  • SE = cardiac toxicity (DCM), BM suppression
  • Give Dexrazoxane to decrease free radical formation–>decreased heart toxicity
241
Q

Dexrazoxane

A

Decreases the free radical formation caused by the anthrocyclines (-rubicins)–>less heart toxicity

242
Q

Dactinomycin

(or Plicamycin)

A
  • Intercalates–>inhibits DNA-dependent RNA polymerase–>impaired RNA synthesis
  • Uses = adjunct for Wilms tumor or Ewing Sarcoma
  • SE = BM suppression
  • Plicamycin–used more for testicle cancers or Paget dz of the bone
243
Q

Bleomycin

A
  • “Blee makes you free when you pee”
  • Binds DNA–>triggers free radical formation–>strand breaks/DNA synth inhibition
  • Uses = chemo for testicular tumors (and some more)
  • SE = pulmonary fibrosis; rare myelosuppression
  • Cell-cycle specific (–> accumulation of cells in G2 phase)
244
Q

Busulfan

A
  • Alkylating agent–>cross-links DNA–>damages DNA
  • Uses = CML tx
  • (And in combo with other drugs for BM ablation before BM transplant)
  • SE = pulmonary fibrosis (and some more)
245
Q

Cyclophosphamide

(or Ifosfamide)

A
  • “Rule of twos”
  • p450 activates it–>alkylating agent–>DNA cross-links–>decreased DNA and RNA synth
  • Also, it suppresses B and T cell function
  • Uses = chemo for solid and heme malignancies
  • Also, immunosuppression for RA, SLE…
  • SE = hemorrhagic cystitis (prevent with fluids and MESNA); BM suppression
246
Q

Nitrosureas

(-mustines)

A
  • Alkylating agents–>cross-link DNA–>inhibit DNA and RNA synthesis
  • Uses = tx of brain tumors (and some more)
  • Highly lipid-soluble and cross BBB!!
247
Q

Cisplatin (and Carboplatin)

A
  • Alkylating agent–>cross-links DNA–>decreased DNA and RNA synthesis
  • Uses = GU tumors mostly
  • SE = nephrotoxicity, otoxicity
  • (Have “plates in your ears and kidneys”)
  • Mitigate nephrotoxicity by using Amifostine (scavenger of free radicals)
  • Skipped Mitomycin
248
Q

Amifostine

A

Used to mitigate Cisplatin/Carboplatin nephrotoxicity

249
Q

MTX FIVE STARS!

A
  • = preferred first-line dz modifier for severe RA
  • Inhibits DHFR–>decreased FH4–>decreased thymidylate–>decreased DNA synth
  • Uses:
    1. Chemo for various malignancies
    1. Immunosuppressant for autoimmune disorders (RA, Crohn, etc)
    1. Abortifacent when given with PG (tx small ectopic pregnancies or missed abortions)
  • SE = BM suppression; hepatotoxicity; teratogen; pulmonary toxicity
250
Q

Leucovorin (folinic acid)

A
  • Often given with MTX to minimize BM suppression
  • Gets converted to TH4 (downstream of MTX block), so it bypasses the inhibited enzyme
251
Q

6-MP and 6-TG FIVE STARS!

A
  • HGPRT converts it into thio-IMP–>acts as purine analogue–>inhibits purine synthesis through feedback inhibition of several enzymes involved in de novo purine synthesis
  • Uses:
    1. Chemo, esp for ALL
    1. Immunosuppressant for IBD and psoriasis
  • SE = BM suppression
  • Metabolized by xanthine oxidase
  • Allopurinol inhibits xanthine oxidase, so if given with 6-MP then 6-MP levels increase!!–>increased toxicity!
252
Q

Azathioprine FIVE STARS!

A
  • Analogue of 6-MP. Converted to 6-MP in cell.
  • Uses = immunosuppressant for autoimmune dzs (SLE, etc)
253
Q

5-FU (“flower”) FIVE STARS!

A
  • Converted into 5-FdUMP–>inhibits thymidylate synthase–>decreased thymines–>disrupted DNA synthesis
  • Uses = Chemo for adenocarcinomas (especially of the colon)
  • “Flower in your colon”
  • SE = BM suppression, photosensitivity, mucosal ulcers
  • “Flower in your eye and mouth”
  • Cell-cycle specific (acts during S phase)
  • Note: see Note card 197 to see how this correlates with MTX and Leucovorin!!!
  • Giving Leucovorin makes MTX less toxic, but it makes 5-FU more toxic
254
Q

Cytarabine FIVE STARS!

A
  • Converted in cell to araCTP–>competitively inhibits DNA polymerase–>impaired DNA synthesis
  • Uses = for AML and lymphomas
  • SE = BM suppression with pan”cyt”openia
  • Cell-cycle specific for S phase
255
Q

E”topo”side (or Teniposide)

A
  • Inhibits topoisomerase 2–>DNA strand breaks
  • Uses = tx of solid tumors like small cell lung carcinoma
  • SE = BM suppression
  • Cell cycle-specific for late S-G2 phase
256
Q

Vincristine/Vinblastine

A
  • Binds tubulin–>depolymerization of mitotic spindle–>can’t get past metaphase–>decreased cell proliferation
  • Vincristine–used for ALL, lymphomas (part of MOPP for Hodgkin)
  • SE = peripheral neuropathy, BM suppression is rare!!!
  • “Christine’s got nerve!”
  • Vinblastine–testicular cancer, lymphomas…
  • SE = BM suppression
  • “Blast the balls and the bone”
  • Cell cycle-specific for M phase
257
Q

Paclitaxel

(or Doxetaxel)

A
  • “Stable taxi”
  • Bind tubulin–>makes complex that promotes stabilization and polymerization of the mitotic spindle–>halt of mitosis during metaphase
  • Uses = ovarian and breast cancer…
  • Also used to coat coronary artery stents to prevent restenosis
  • SE = BM suppression
258
Q

Hydr”oxy”urea

A
  • Inhibits ribonucleotide reductase–>can’t turn riboNT into deoxyriboNT–>decreased DNA synthesis
  • Uses = tx for Myeloproliferative orders (CML, polycythemia vera) and melanoma
  • “MM hydroxyurea”
  • Also helps tx SCD bc it increases HbF
  • SE = BM suppression
  • Cell cycle-specific for S phase
259
Q

Pentostatin

A
  • Inhibits adenosine deaminase–>decreased purine degradation
  • Tx for hairy cell leukemia
  • “Five hairs”
260
Q

Trastuzumab

A
  • Monoclonal aby against HER2/neu (erb-B2) receptor–>less uncontrolled cell growth
  • Uses = HER2+ breast cancer
  • SE = cardiac toxicity
261
Q

Imatinib

A
  • Competitive inhibitor of tyrosine kinase enzymes in abl, c-KIT, PDGF-R, etc
  • Uses = tx of CML, GISTs, and brain tumors
262
Q

Rituximab

A
  • “Renal failure, Infusion rxn, Twenty (CD20)—>B cell lysis” (RITuximaB)
  • Monoclonal aby against CD20 (on B cells)–>B cell lysis

Uses:

    1. Tx of non-Hodgkin lymphoma and CLL
    1. Also used to tx autoimmune disorders (RA especially)
  • SE = infusion rxn; acute renal failure d/t tumor lysis syndrome
  • Prevent the infusion rxn by giving anti-histamine and Tylenol 30 minutes prior to admin
263
Q

NSAIDs

(Ibuprofen, Naproxen, Indomethacin…)

A
  • Reversible COX1 and 2 inhibitor–>decreased PG synth
  • Decreased PGE2–>analgesia, lower T (anti-pyretic), and decreased gastric mucous
  • Decreased PGI2–>increased gastric acid (–>ulcers)
  • Uses = anti-fever, analgesic, anti-inflammatory
  • Indomethacin–also for gout, closing PDA
  • SE = GI bleeds, interstitial nephritis
  • Does NOT have significant anti-platelet effect (bc is reversible so platelets can replenish TXA2)
264
Q

Celicoxib

A
  • (“select COX 2”)
  • Irreversibly inhibits COX2–>decreased PG synthesis
  • Note: COX2 is upregulated at sites of inflammation (like joint), COX1 is present in most tissues (stomach)
  • So this medicine minimizes gastric ulcers and other SE by leaving COX1 untouched
  • Uses = RA, OA, and other acute pains
  • SE = GI upset, interstitial nephritis; increased thrombosis risk
265
Q

Acetominophen

A
  • Reversibly inhibits COX1 and 2 in the CNS–>decreased PGE2 in CNS–>decreased pain and temp
  • (It is mostly inactive in periphery, so minimal anti-inflammatory effects!!)
  • Uses = anti-pyretic and analgesic
  • SE = fatal hepatotoxicity with overdose
  • (Acetylcysteine = antidote)
266
Q

Acetylcysteine

A
  • Antidote for Acetominophen overdose:
  • Contains SH groups which bind and inactivate Tylenol’s toxic byproducts
  • Also helps CF pts by cleaving S-S bonds in mucus
267
Q

Zafirlukast

(or Montelukast)

A
  • Reversible inhibitor of cysteinyl LT-1 receptor–>blocks LTC4-E4 binding–>decreased bronchoconstriction and decreased mucus
  • Uses = preventative tx of asthma (chronic asthma prophylaxis)
  • Zafirlukast inhibits P450
268
Q

Zileuton

A
  • “Zilch–LTs all gone”
  • Inhibits 5-lipoxygenase–>decreased LTA4–>decreased LTB4–>decreased neutrophil chemotaxis–>decreased airway inflammation
  • Note: LTA4 is what all of the LTs come from
  • Uses = chronic asthma prophylaxis (same as -lukasts)
269
Q

Cromolyn

A

Inhibits mast cell degranulation–>less histamine–>anti-inflammatory effects–>prevents asthma exacerbations associated with allergens or exercise

270
Q

Cyclosporine

A
  • “Cyclops don’t have IL2 eyes”
  • Inhibits calcineurin in T cell–>decreased IL2 transcription–>decreased IL2–>decreased T cell activation–>decreased production of other cytokines
  • “Decreased T cells–“T is for Transplant””

Uses :

    1. Immunosuppression in transplant pts
  • 2. Tx of GVHD
    1. Tx of autoimmune dzs (like RA)
  • *SE = nephrotoxicity; hepatotoxicity…
  • (Most SE are dose-dependent)
  • Metabolized by p450 (CYP3A4)
271
Q

Tacrolimus

(Similar to Cyclosporine)

A
  • Binds FKBP–>Inhibits calcineurin–>decreased IL2–>decreased T cell activation
  • Use = immunosuppression in transplant pts
  • *SE = increased infection risk; nephrotoxic; neurotoxic
  • Metabolized by p450
  • So very similar to cyclosporine (except SE profile)
272
Q

Sirolimus

A

Similar to Tacrolimus, but inhibits mTOR–>decreased T cell proliferation

273
Q

Mycophenolate Mofetil

A
  • Acts in B and T cells to inhibit inosine monophosphate (IMP) dehydrogenase–>decreased GMP in de novo purine synth–>decreased DNA synth in B and T cells–>decreased prolif of B and T cells
  • Use = immunosuppressant in transplant pts, also for autoimmune disorders
274
Q

Interferons

A
  • alpha–made by WBCs
  • beta–made by fibroblasts
  • gamma–made by CD4 T cells
  • Produced in response to viral infection.
  • Have multiple actions to boost immune system in viral infection.
  • *IFNa–tx of HBV and HCV; also tx of some cancers
  • IFNb–tx of MS (reduces exacerbations)
  • IFNgamma–tx of chronic granulomatous disease*
275
Q

Prostaglandins

(-prost-, or -prost)

A

Alprostadil: PGE1; relaxes smooth muscle and vasodilates

Use = For ED and maintaining PDA

“A” for PD’A’

Misoprostol: PGE1; increases uterine contractions; inhibits HCl secretion and increases mucus in stomach

Use = Prevents NSAID-induced gastric ulcers

Also abortifacient when given with MTX

Latanoprost: PGF2; increases aqueous humor drainage

Use = Tx of chronic glaucoma

Dinoprostone: PGE2; increases uterine contractions

Use = Abortifacient

Carboprost: PGF2; increases uterine contractions

Use = Abortifacient

276
Q

PGI2 analogs

(Treprostinil, epoprostenol, iloprost)

A
  • It’s a “PGI2 Pah-TIE”
  • Inhibit platelet aggregation and produce vasodilation (both by increasing cAMP)
  • Uses = tx of pulmonary arterial HTN
277
Q

Etanercept

A
  • “Intercepts TNFalpha”
  • Inhibits binding of TNFa and TNFb to their receptors–>decreased TNFa effects–>less release of other cytokines (IL1, IL6, IL8) is stimulated
  • Uses = autoimmune diseases (RA, etc)
  • SE = URIs…
278
Q

Gold salts

A

May be used to tx RA

279
Q

Infliximab

A
  • “Inflicts pain on TNFalpha”
  • Really very similar to Etanercept, but this actually binds TNFalpha itself
  • Chimeric aby that binds TNFa–>inhibits binding of TNFa with its receptor–>decreased other cytokines released–>anti-inflammation
  • Uses = autoimmune diseases (RA, IBD, etc)
  • SE = increased infection susceptibility
  • Adalimumab–same really, just monoclonal not chimeric
280
Q

Thalidomide

A
  • (Just need to straight up memorize this one)
  • Decreases TNFa production–>anti-inflammatory
  • Uses = tx of erythema nodosum leprae; also tx of multiple myeloma
  • C/I during pregnancy:
  • Causes phocomelia (shortening or absence of limbs)
281
Q

First gen H1 receptor blockers

(diphenhydramine, promethazine, meclizine…)

A
  • Block H1 receptors–>bronchodilation, decreased pruritis, vasodilation, decreased GI motility, etc
  • Also has anti-cholinergic and anti-adrenergic effects–>SE profile
  • Uses = tx of urticaria, allergic rhinitis, allergic rxns, motion sickness, sleep aid
  • Also used to tx acute dystonia (like from typical antipsychotics)
  • Promethazine–anti-emetic
  • Meclizine–motion sickness tx
  • SE = sedation; anticholinergic effects (ABCCDSS)
282
Q

2nd gen H1 receptor blockers

(Fexofenadine, Loratadine, Cetirizine)

A
  • Block H1 receptors–>same effects as first gen
  • Uses = tx of allergic rhinitis and seasonal allergies
  • Less sedation than Diphenhydramine bc does not cross BBB
  • Minimal side effects
283
Q

Theo’P’hylline

A
  • “The lungs ‘phylline’ up, the heart ‘phylline’ bad”
  • Inhibits ‘P’DE–>increased cAMP–>bronchodilation
  • Uses = tx of acute and chronic asthma
  • SE = cardiac arrhythmias, SEIZURES AND abd pain/N/V
  • (Happen bc theophylline has a very narrow therapeutic index)
  • Metabolized by p450
284
Q

Guaifenesin

A
  • –>secretion of less viscous mucous in bronchi–>thinner phlegm which helps stimulate resp tract secretion flow
  • Use = expectorant to get phlegm out
285
Q

Bosentan

(-sentans)

A
  • Competitively inhibit endothelin receptors–>pulmonary vasodilation
  • Use = tx of pulmonary arterial hypertension
  • SE = hepatotoxicity; teratogen
286
Q

Ethanol

A
  • Enhances flow of CL ions through GABA channels–>increasing inhibitory effects of GABA
  • (Just like benzos and barbiturates it seems)
  • Use = tx of ethylene glycol or methanol overdose
  • (Acts as competitive substrate at the enzymes that produce the toxic metabolites from the other two)
  • SE = CNS depression; GI inflammation; teratogen
287
Q

Disulfiram

A
  • Used in tx of alcohol cessation.
  • Inhibits acetaldehyde dehydrogenase–>increased acetaldehyde when drinking (toxic)–>N/V–>incentive not to drink
288
Q

Iron as toxin

(name the antidote)

A

Antidote = De”fero”xamine

289
Q

Lead as toxin

(name the antidote)

A

Antidote = Calcium EDTA;

dimercaprol; penicillamine

290
Q

Arsenic as toxin

(name the antidote)

A

Antidote = Dimercaprol; penicillamine

291
Q

Cyanide as toxin

(name the antidote)

A

Antidote = Sodium thiosulfate; nitrites

292
Q

Carbon monoxide as toxin (name the antidote)

A

Antidote = 100% oxygen

293
Q

Amiodarone

A
  • Actually Class 1-4 agent.
  • Side effects = pulmonary fibrosis, thyroid dysfunction, blue-grey skin discoloration
  • (But don’t usually get torsades with Amiodarone!)
294
Q

Fomepizole

A
  • Tx of ethylene glycol overdose
  • Inhibits alcohol dehydrogenase (unlike disulfiram)–>decreased breakdown of ethylene glycol into toxic metabolites
295
Q

Omega 3s (Fish Oils)

A
  • Lower triglycerides a lot
  • Raise HDL and LDL a little
  • If belch–>bad fishy taste in mouth
296
Q

Hydroxychlorquine

A
  • 2nd line for malaria, also 2nd line for RA
  • Metabolites build up–>inhibit sphingomyelinase (like Niemann-Pick) so do eye exams periodically (remember cherry red macula)

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