Lange Pharmacology Flashcards
Penicillin
*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
Ampicillin/Amoxicillin
Penicillinase sensitive: Often add Clavulanic acid or sulbactam “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
Piperacillin/Ticarcillin
Tx for pseudomonas Given with Tazobactam (beta lactamase inhibitor)
Methicillin/Nafcillin
Penicillinase resistant So MRSA is something that has alterations in the PBPs (doesn’t break methicillin down, just doesn’t let it bind) “Use naf for staph:” Staph aureus that is But can’t use it for MRSA SE = interstitial nephritis
Aztreonam
To treat severe gram negative infections in pts with penicillin allergy Everything else on the card really stems off of that
Imipenem
Broad-spectrum. The usuals + PEAR (Pseudomonas, enterobacter, anaerobes, gram negative rods) SE= seizures 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
Cephalosporins
Generation 1–gram + and also PEcK Generation 2–gram + and also HEN PEcKS Generation 3–serious gram negative infections Ceftriaxone–gonorrhea and meningitis Ceftazidime–Pseudomonas Generation 4–Cefepime, both gram + and serious gram negative infections SE = disulfiram-like reaction with EtOH; hypersensitivity rxn (10% of those allergic to penicillin will get this)
Aminoglycosides (-mycins and Amikacin): Gentamicin, Streptomycin, Neomicin, Tobramycin
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 (esp with cephalosporins); ototoxic (esp with loop diuretics) (Aerobic, ATN”)
Clindamycin
Binds 50s–>inhibits initiation complex formation “Severe anaerobic infections above the diaphragam.” Like infections d/t nl mouth flora Endocarditis prophylaxis before dental procedures as well SE = pseudomembranous colitis
Linezolid
Also inhibits 50s, but txs MRSA and VRE (gram positive infections)
Chloramphenicol
Binds 50s–>*inhibits peptidyl transferase*–>amino acids can’t get added to chain Broad spectrum, but severe SE. Use = alternative tx for bacterial meningitis in pts with penicillin allergy SE = myelosuppression (*aplastic anemia* (dose independent), dose-dependent anemia) Also gray baby syndrome (with vomiting, shock…)<–(d/t lack of UDP-glucuronyl transferase in liver which is needed for chloramphenicol metabolism)
Macrolides (-thromycins)
“MAC Daddy”: MAC tx and other atypical pneumonias, STDs (what MAC Daddy’s get), Diphtheriae Bind 50s–>inhibit translocation For atypical pneumonias (Mycoplasma, Chlamydia, Legionella, MAC) and some STDs (Chlamydia) And for diphtheria Also for Campylobacter when it is fluoroquinolone-resistant SE = GI upset
Tetracycline (-cyclines)
“Lime in a four wheeler” Binds 30s–>blocks aa-tRNA from binding ribosome–>inhibits protein synthesis For Lyme disease, Rickettsia, atypical pneumonias 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 Fecally eliminated (so can use in renally deficient pts)
TMP-SMX
SMX = PABA analog, competitively inhibits dihydropterate synthetase–>decreased THF TMP–inhibits dihydrofolate reductase–>decreased DNA synthesis For Pneumocystis carinii pneumonia, E coli infections mostly “TMP = PCP” SE = Stevens-Johnson syndrome, hemolytic anemia Or in babies–kernicterus (SE = SJ, HaK)
Fluoroquinolones (-floxacins):
Inhibit bacterial DNA topoisomerase 2–>DNA strand breaks–>cell death For gram negative infections and some gram positive infections Mostly for pneumonias, UTIS, gonococcal infections (PUG) SE = tendonitis and tendon rupture in adults And damage growing cartilage (so pregnant women and children should not take them)
Nitrofurantoin
Used for recurrent UTIs Similar to fluoroquinolones
*Vancomycin
*Binds D-ala-D-ala in cell wall–>inhibits transglycosylase–>weakened peptidoglycans in cell wall Uses–serious gram positive multidrug resistant infections (MRSA) SE = (RON) red man syndrome, ototoxicity, nephrotoxicity Remember how to prevent red man syndrome? Skipped Polymyxins and Daptomycin on this card
Metronidazole
Metabolized by bacterial proteins–>reduced reactive compounds–>damage–>cell death Uses = anaerobic infections below the diaphragm Also giardia, trichomoniasis, and E histolytica infections *SE = metallic taste; disulfiram-like effect with alcohol (like cephalosporins)*
Rifampin
Inhibits bacterial DNA-dependent RNA-polymerase–>decreased RNA synthesis Uses = mycobacteria (combotherapy) Monotherapy for–prophylaxis for contacts of pts with meningococcal meningitis and H flu type B infection SE = harmless orange color to urine; hepatitis
Isoniazid
Processed by mycobacterial catalase-peroxidase–>metabolite–>inhibits synth of mycolic acids for mycobacterial cell wall Uses = mycobacteria (combotherapy) Monotherapy = prophylaxis against active TB in pts with a positive PPD SE = peripheral neuropathy (prevent with Vitamin B6); drug-induced lupus; hepatitis (HeNS) The SLE occurs when someone is a slow acetylator in liver (decreased N-acetyltransferase activity)–>Isoniazid metabolization population distribution is bimodal (Having lupus is SHIPP-E)
Dapsone
*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)
Ethambutol
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*)
Pyrazinamide
“Pyraz-inside” Lowers environmental pH (active against IC TB) Uses = combotherapy for MB tuberculosis (like ethambutol) SE = hepatotoxicity
Nucleoside Reverse Transcriptase Inhibitors (NRTIs)—“vudines” mostly
Activated by IC phosphorylation–>inhibit HIV reverse transcriptase–>messed up DNA synthesis–>defective viral particle Use = HIV tx Lamivudine–also used for Hepatitis B SE: neutropenia AZT–>megaloblastic anemia/BM suppression (Think of AZT as the biggest name) Didanosine–>pancreatitis
Nucleotide Reverse Transcriptase Inhibitors (-fovirs):
Don’t need phosphorylated Also inhibit reverse transcriptase Uses = HIV and Hepatitis B infections
Non-Nucleoside Reverse Transcriptase Inhibitors (-vir-):
Bind specifically to reverse transcriptase–>decreased DNA synthesis Use = HIV tx SE: *Nevirapine–>Stevens-Johnson syndrome; fulminant hepatitis* *Efavirenz–>delusion and nightmares (CNS disturbances)*
Protease inhibitors (-navirs):
Inhibit HIV protease–>virus is unable to replicate d/t no mature proteins for core particle made Uses = HIV SE = altered body fat distribution (“Fat PiG”)/hyperlipidemia
*Acyclovir
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)*
Ganciclovir
Viral kinase–>phosphorylates (activates) ganciclovir–>guanosine analogue–>inhibits CMV DNA polymerase–>decreased CMV DNA synthesis Uses = CMV infections, especially CMV retinitis SE = pancytopenia
Foscarnet
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)
Amantadine
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
Oseltamivir (-ivirs)
Inhibits Neuraminidase–>decreased viral replication/release Use = tx and prophylaxis of both influenza A and B
‘R’ibavirin
Guanosine analogue–>inhibits viral ‘R’NA polymerase–>inhibits viral ‘r’eplication Uses = ‘R’SV bronchiolitis
Amphotocerin B
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
Nystatin
Similar MOA to Amphotocerin B More toxic so only used topically for oral and cutaneous Candida
Flucytosine
“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
Caspofungin
*Inhibits glucan synthase*–>disrupts polysaccharide fungal cell wall Tx of systemic fungal infections
Ketoconazole
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
Fluconazole
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
Griseofulvin
Interferes with microtubule function in keratin-rich tissues–>inhibits mitosis–>inhibits fungal cell replication Uses = oral antifungal for dermatophytic fungal infections (like tinea corporis)
Terbinafine
Also for dermatophytic fungal infections Inhibits squalene epoxidase–>decreased ergosterol synthesis
Chloroquine (-quines–exception is primaquine):
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)
Pyri”meth”amine
Inhibits DHFR–>decreased DNA synthesis (Like Tri”meth”oprime) Uses = tx and prophylaxis of Plasmodium falciparum and tx of *Toxoplasma gondii*
Primaquine
Uses = tx hepatic forms of P. vivax and P. ovale Don’t give in pregnancy (–>fetal hemolytic anemia)
Pentamidine
Prophylaxis for PCP (like Dapsone)
Nifurtimox
Tx of Trypanosoma cruzi (Chagas)
Suramin
Tx of early Trypanosoma brucei infections (=African sleeping sickness with recurring fever and LAD…tsetse fly)
Melarsoprol
Tx of late Trypanosoma brucei infections (It “sure” is nice to go to sleep. And melatonin helps with sleep.)
*Sodium stibogluconate
Tx of Leishmaniasis (=spiking fevers, HSM…sandfly)
Epinephrine
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)
Norepinephrine
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
Dopamine
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!!!
Dobutamine
B1 agonist–>increases HR and contractility Uses = tx of cardiogenic shock Increases myocardial O2 consumption
Ephedrine
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
Amphetamine
Similar to Ephedrine. –>hyperaroused state. Also decreased appetite and insomnia.
Methylphenidate
Amphetamine derivative. Uses = narcolepsy, ADHD But Modafinil is DOC for narcolepsy I think
Cocaine
Blocks NA/K ATPase that is responsible for reuptake of NE, DA, and 5-HT –>euphoria (d/t DA), vasoconstriction, and cardiac ischemia SE = HTN, cardiac ischemia, cardiac arrhythmias
Sympatholytics
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
*Phenylephrine
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)
Midodrine
“Middledrine” A1 agonist–>vasoconstriction Use = orthostatic hypotension SE = supine HTN
Clonidine
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)
Methyldopa
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!
*Isoproterenol
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
Fenol”dopa”m
D1 agonist–>splanchnic/renal vasodilation and natriuresis *= only available agent that improves renal perfusion while lowering bp!* Use = *HTN emergencies*
Albuterol (-terols)
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
Salmeterol
Similar to Albuterol, but long-acting, so used to prevent asthma and COPD attacks
Terb”ut”aline
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
Ritrodine
B2 agonist–>reduced preterm labor uterus contractions
Phenoxybenzamine
Irreversible alpha receptor antagonist (a1>a2)–>decreased vasoconstriction–>decreased bp Use = tx of pheochromocytoma (or given before surg on pheochromocytoma)
Phentolamine
Reversible alpha receptor antagonist. Use = to dx pheochromocytomas (Pt will get a larger than expected bp decrease)
Prazosin (-zosins)
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)
Propanolol (“N-Z”)
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!)
Timolol
“Tim-e 2 fix these eyes” B1 and B2 antagonist. B2 block–>decreased aqueous humor production by ciliary epithelium–> tx of wide-angle glaucoma
Carvedilol/Labetalol
A1 and B1/2 receptor blocker–>lower bp, lower HR/contractility, bronchoconstriction –>decreased cardiac work Uses = chronic CHF; HTN
Metoprolol (“A-M”)
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, tachycardias, CAD Esmolol = short-acting, for critically ill pts
“P”ilo”c”arpine
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
Carbachol
Also used to tx wide-angle glaucoma (like Pilocarpine)
“M”ethacoline
Inhaled M1-M2-M3 (mostly “M”3) agonist–>smooth muscle contraction of bronchi Use = bronchial challenge test for dx of reactive airway disease
“B”ethanechol
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)
*Atropine
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
Physostigmine (as antidote)
Antidote for Atropine overdose Used bc it can cross the BBB
Scopolamine
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)
**Benztropine
“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)
Ipratropium (-tropiums)
M3 antagonist–>bronchodilation Use = tx of COPD and asthma Especially in pts who cannot take adrenergic agents
Oxybutynin
“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 Skipped Propantheline
*Neostigmine
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
*Physostigmine
Similar, but crosses BBB. *Uses = tx of atropine poisoning Also tx of glaucoma (decreased Ach breakdown at M3–>miosis–>open Canal of Schlemm)
Pyridostigmine (“longest prefix”)
“Long”-acting reversible AChE inhibitor Use = tx of myasthenia gravis
Edrophonium
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
Tacrine, Donepezil
“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”
“Echo”thiophate (-phates)
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”
AChE Poisons
“Mala = bad, and Para goes with mala” Parathion/Malathion: Poisons. These, and the -phates, –>szs, bradycardia, flaccid paralysis, death when give systemically
Pralidoxime
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
SSRIs (-oxetines, -oprams, Sertraline)
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
Cyproheptadine
Use = tx for serotonin syndrome (Cyp on serotonin)
TCAs (-triptylines, -ipramines, trazodone, bupropion, doxepin)
“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!*
Heterocyclic antidepressants (venlafaxine, mirtazapine, nefazodone…)
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
MAOIs (phenelzine, isocarboxazid, tranylcypromine)
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…)
Selegiline
*Inhibits MAO-B*–>increased DA in presynaptic neuron–>decreased DA degradation *Adjunct for PD* tx
Lithium
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)
*Typical antipsychotics (-azines and Haloperidol)
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
Atypical antipsychotics (-apines and -idones)
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
*Benzodiazepines (-zepams, -zolams)
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
“Flu”mazenil
Competitive GABA antagonist Use = tx of benzodiazepine overdose “Treat Benzos with the Flu”
Barbiturates (-barbitals, thiopental)
Same MOA as benzos, but longer half-life (more residual hangover effect) Uses = Sedative for anxiety/insomnia; mgmt of szs Thiopental–very lipid soluble–>rapid redistribution, so used for anesthesia induction Overdose–>cardiac/resp depression (tx = Use dialysis/alkalinize urine) May get withdrawal if become dependent
Zolpidem
*GABA receptor agonist (like benzos)–>decreased CNS activity* Use = short-term tx of insomnia (non-addictive!) “zzz-olpidem” *SE = hallucinations, mild anterograde amnesia*
**Phenytoin
*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)
Lamotrigine
Blocks fast voltage-gated Na channels of presynaptic neuron–>decreased glutamate/aspartate release Use = epilepsy tx SE = Stevens-Johnson syndrome
Valproate
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
Ethosuximide
Decreases Ca currents in neurons Use = tx of absence szs (DOC)
Carbamazepine
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
‘Top’iramate
Block Na ion flow–>hyperpolarization, and GABA agonist Use = tx epilepsy and migraines “Top = head (migraines)”
Tiagabine
Inhibits GABA reuptake–>increasing GABA effect Use = combotherapy for partial szs
Vigabatrin
Irreversibly inhibits GABA transaminase–>increased GABA levels in synapse 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
**Levetiracetam
“Leave-tired-acetam” “Leaves” May bind synaptic vesicle proteins–>interrupts nerve conduction Uses = partial szs, myoclonic szs, GTCS SE = drowsiness, depression “Tired”
*Succinylcholine
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
Pancuronium (-cur-)
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)
*Local anesthetics (-caines)
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
General inhaled anesthetics (-anes)
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
General IV Anesthetics (propofol, etomidate, ketamine, benzos, barbs, opioids)
SE: propofol–>hypotension, o/w not very HY
Opioids (heroin, morphine, hydromorphone, codeine, oxycodone, hydrocodone, meperidine, fentanyl, dextromethorphan):
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
Naloxone/Naltrexone
Opioid receptor antagonists Use = to tx opioid overdoses
Methadone
Opioid agonist with long half-life–>helps ease withdrawal sx but no high given Use .= drug tx programs
Butorphanol
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
Tramadol
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”
*Dantrolene
*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
*Levodopa
Crosses BBB–>DOPA-decarboxylase converts it into dopamine–>increased CNS dopamine Use = first line for PD *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
Carbidopa
Give with levodopa Inhibits DOPA-decarboxylase in periphery–>increased levodopa in CNS
Bromocriptine
Partial DA receptor agonist Use = PD adjunct; also helps with hyperprolactinemia Other PD drugs are: DA agonists (Amantadine) MAO-B inhibitors (Selegiline)
*Memantine
“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)
Sumatriptan (-triptans)
Postsynaptic 5-HT1b-1d *(serotonin) receptor agonists*–>decreased dura vasodilation/inflammation Uses = *migraines, cluster H/A( SE = coronary vasospasm (d/t 1b agonism) So *C/I in pts with CAD*
Smoking cessation agents (Bupropion, *Varenicline)
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
**Buspirone
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”
*Gabapentin
“GABAPENtin = GABA analogue, postherpatic neuralgia, edema (SE), neuropathic pain” GABA analogue Use = *tx of postherpatic neuralgia*, chronic neuropathic pain, and partial szs SE = *peripheral edema*
Pregabalin
Binds Ca channels in CNS–>decreased glutamate and NE release Uses = fibromyalgia, chronic neuropathic pain SE = dizziness
Class 1A Anti-Arrhythmics (Quinidine, Procainamide, Disopyramide)
“The Queen Proclaims Diso’s Pyramid” Bind activated Na channels–>block Na inflow in cardiac myocyte–>prolong Phase 0–>slowed conduction of action potential–>slowed rate of cardiac muscle contraction Also, these bind K channels some–>delayed Phase 3 repolarization–>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)
Class 1B Anti-Arrhythmics (Lidocaine, Tocainide, Mexiletine):
“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))
Class 1C Anti-Arrhythmics (Flecainide, Propafenone)
“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)
Class 3 Anti-Arrhythmics (Amiodarone, Ibutilide, Dofetilide, Sotalol)
“AIDS” Bind K channels–>prolong 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!)
Class 4 Anti-Arrhythmics (Verapamil, Diltiazem)
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
Adenosine
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
Potassium
Suppresses ectopic pacemakers (especially if d/t digoxin toxicity)
Mg
Used to treat torsades Used to tx digoxin toxicity
Beta blockers–just remember
That they are the Class 2 anti-arrhythmics
Digoxin
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)
**Nesiritide
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
Nitroglycerin (and other nitrates)
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, HF SE = 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
Amyl nitrate
DOC for cyanide poisoning (From the nitrate drug class)
Isosorbide mononitrate
Highest oral bioavailability of the nitrates
Nitroprusside
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))
ACE-inhibitors (-prils):
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!
ARBs (-sartans)
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
Hydralazine
Direct relaxation of arteriolar smooth muscle–>decreased bp Uses = HTN and HF (reduces afterload) DOC for HTN in pregnancy *(ecclampsia, preecclampsia)* SE = SLE
Minoxidil (Rogaine)
Direct relaxation of arteriolar smooth muscle Uses = tx of refractory HTN Also promotes hair growth
CCBs (-ipines)
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
Osmotic diuretics (Mannitol, urea, glycerin, isosorbide)
“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
*Carbonic anhydrase inhibitors (-zolamides)
“Ascent-azolamide” Inhibit CA 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*
*Furosemide/torsemide (and bumetanide):
*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
Ethacrynic acid
Diuretic, same MOA as loops, but not sulfonamide-related. Give this in pts who cannot tolerate furosemide d/t sulfa allergies.
Thiazide diuretics
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)
Spironolactone
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
Eplerenone
Same as Spironolactone, but less anti-androgen effect–>no gynecomastia
Triamterine/Amiloride
Blocks Na channels in DCT–>block Na/H2O reabsorption and therefore less K excretion Uses = combotherapy to tx volume overload and HTN SE = hyperkalemia
Milrinone (-rinones)
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)
Sildenafil (-afils)
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!
Heparin
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
Protamine sulfate
Tx of bleeding caused by heparin (Inactivates heparin)
Enoxaparin/Dalteparin
LMWHs. More active in degrading factor 10, less active in directly degrading thrombin Longer DOA (so less frequent dosing)
Fondaparinux
“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
Warfarin/Dicumarol
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)
Fresh frozen plasma, Vitamin K
Tx of Warfarin-induced bleeding
Direct thrombin inhibitors
(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
Rivaroxaban (-xabans)
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
Acetylsalicylic acid (Aspirin)
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))
Clopidrogrel/Ticlopidine
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
Prasugrel
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
Ticagrelor
Same effect as other-grels, but reversible allosteric inhibitor to P2Y receptor.
Cilostazol
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
Dipyridamole
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)
*Abciximab (and eptifibatide, tirofiban—“fiba”)
“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
Ivermectin
For river blindness (Onchocerca volvulus)
“Bendazoles”
Mebendazole or Albendazole: For whipworm (trichuris), hookworm, roundworm, and pinworm. Albendazole: For strongyloides, neurocystericosis, Echinococcus
Praziquantel
For schistosomiasis, neurocystericosis
Pyrantel pamoate
For hookworm, roundworm, and pinworm
Niclosamide
For tapeworm infections
A polar molecule
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) 2. Phase 2 metabolism = addition of polar moiety (sulfate, acetate, glucuronate) Makes drug water-soluble and kidney can excrete it
Fibrinolytic Agents “-okinases, -eplases
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
Aminocaproic acid (or tranexamic acid)
Inhibits plasminogen activation–>inhibits fibrinolysis Use = tx of post-surg bleeding and hemophilia SE = thrombosis
Synthetic EPO (or epoetin, darbepoetin)
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
Synthetic insulins
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
*Sulfonylureas (Glyburide, Glipizide, etc)
MOA: 1. Inhibit K channel in beta cells–>stimulate insulin release 2. Prolong insulin binding to target receptors–>increases insulin action on target tissues 3. 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)
Metformin
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!
Thiazolidinediones (-glitazones)
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
Alpha-glucosidase inhibitors (acarbose, miglitol)
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)
Meglitinides (-glinides)
Bind K channel in beta cell (different binding spot than sulfonylureas)–>insulin release SE = wt gain; hypoglycemia
Dipeptidyl peptidase-4 (DPP4) inhibitors (-gliptins)
Inhibit DPP4–>GLP1 doesn’t get degraded–>increases insulin secretion and decreases glucagon secretion SE = N/V
GLP1 analogues (exenatide, liraglutide)
Mimic GLP1–>increased insulin secretion, decrease glucagon secretion SE = wt loss
Atorvastatin (-statins)
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
Ezetimibe
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
*Cholestyramine, etc
= 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!!*
*Fibrates (Gemfibrozil, –fibrates)
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); abn liver function tests, *hepatotoxicity and gallstones* Also, compete with Warfarin for binding sites on plasma proteins–>effects of Warfarin may be increased
Niacin
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)
Bisphosphonates (-dronates)
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)
PTU (or methimazole)
Inhibit thyroid peroxidase–>inhibit iodotyrosine coupling–>decreased thyroid hormone synthesis and decreased T4/T3 conversion peripherally Use = tx of hyperthyroidism SE = *agranulocytosis*; hepatotoxic
Levothyroxine
Is synthetic T4. Use = tx of hypothyroidism And used to suppress TSH secretion to tx goiters/thyroid cancers Overdose–>hyperthyroidism sx
Colchicine
Binds tubulin–>induces microtubule depolymerization–>decreased WBC migration to affected site Use = tx of acute gouty attack SE = diarrhea
Probenecid
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)
Allopurinol
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
Corticosteroids (-sones, -solones)
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…
Beclomethasone
Inhaled glucocorticoid. Use = tx of chronic asthma. Make sure to do oral rinsing to prevent oral Candidiasis
Anti-Obesity Agents
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
Octreotide (Somatostatin)
Inhibits release of many hormones, reduces GI motility, causes vasoconstriction Uses: 1. Tx of esophageal varices 2. Tx of VIPoma diarrhea; tx of Zollinger-Ellison syndrome; tx of acromegaly…
Vasopressin (or Desmopressin)
3 effects: 1. V1 receptors–>vasoconstriction 2. V2 receptors–>increased collecting duct permeability to H2O 3. 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…
Oxytocin
Made in posterior pituitary–>stimulates uterine and breast contraction Uses = induce labor; stimulate milk let-down Also used to control postpartum uterine hemorrhage
**Flutamide
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…
Danazol
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)
Finasteride
Inhibits 5-alpha reductase–>decreased DHT–>decreased prostate growth Uses = tx of BPH, prostate cancer, and early male-pattern baldness
Anastrozole (or Letrozole)
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
Tamoxifen (SERM)
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)
*Raloxifene (SERM)
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
Leuprolide
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
Clomiphene
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
OCPs
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
Progestin-only pills
No increased thromboembolism risk
Emergency contraception pills
High doses of progestins Can take up to 72 hours after intercourse to inhibit ovulation
Mifepristone
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)”
Antacids (aluminum hydroxide…sodium bicarb)
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
Sucralfate
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…)
H2 receptor blockers (-tidines)
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
PPIs (-prazoles)
Irreversibly inhibit H/K pump in parietal cells–>decreased HCl secretion Uses = tx of PUD, GERD, ZE syndrome Also help tx H pylori infection
Odansetron
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
Promethazine
H1 receptor antagonist. Blocking GI H1 receptors–>decreased GI motility–>less N/V
*Metoclopramide
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
Prochlorperazine
Similar to Metoclopramide, but does not affect GI motility (D2 antagonist in CTZ–>blocks vomiting reflex)
Laxatives
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
Anti-diarrheal agents (diphenoxylate, loperamide, kaolin, bismuth subsalicylate
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
*Sulfasalazine (or Olsalazine)
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*)
Ursodiol (or Chenodiol)
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)
Anthracyclines (-rubicins):
3 MOA: 1. intercalate in DNA–>block DNA and RNA synthesis 2. Produce free radicals–>membrane damage (–>dose dependent cardiac damage (so keep lifetime dose down!!!)) 3. 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
Dexrazoxane
Decreases the free radical formation caused by the *anthrocyclines (-rubicins)–>less heart toxicity*
Dactinomycin (or Plicamycin)
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
Bleomycin
“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)
Busulfan
*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)
Cyclophosphamide (or Ifosfamide)
“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
Nitrosureas (-mustines)
*Alkylating* agents–>cross-link DNA–>inhibit DNA and RNA synthesis Uses = tx of *brain tumors* (and some more) Highly lipid-soluble and cross BBB!!
Cisplatin (and Carboplatin)
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
**Amifostine
Used to mitigate Cisplatin/Carboplatin nephrotoxicity
*MTX* FIVE STARS!
*= preferred first-line dz modifier for severe RA* Inhibits DHFR–>decreased FH4–>decreased thymidylate–>decreased DNA synth Uses: 1. Chemo for various malignancies 2. Immunosuppressant for autoimmune disorders (RA, Crohn, etc) 3. Abortifacent when given with PG (tx small *ectopic pregnancies* or missed abortions) SE = BM suppression; hepatotoxicity; teratogen; pulmonary toxicity
**Leucovorin (folinic acid)
Often given with MTX to minimize BM suppression Gets converted to TH4 (downstream of MTX block), so it bypasses the inhibited enzyme
*6-MP and 6-TG* FIVE STARS!
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* 2. 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!
*Azathioprine* FIVE STARS!
Analogue of 6-MP. Converted to 6-MP in cell. Uses = immunosuppressant for autoimmune dzs (SLE, etc)
*5-FU* (“flower”) FIVE STARS!
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
*Cytarabine* FIVE STARS!
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
E”topo”side (or Teniposide)
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
Vincristine/Vinblastine
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
Paclitaxel (or Doxetaxel)
“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
Hydr”oxy”urea
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
Pentostatin
Inhibits adenosine deaminase–>decreased purine degradation Tx for hairy cell leukemia “Five hairs”
Trastuzumab
Monoclonal aby against HER2/neu (erb-B2) receptor–>less uncontrolled cell growth Uses = HER2+ breast cancer SE = cardiac toxicity
Imatinib
Competitive inhibitor of tyrosine kinase enzymes in abl, c-KIT, PDGF-R, etc Uses = tx of CML, GISTs, and brain tumors
*Rituximab
“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 2. 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
NSAIDs (Ibuprofen, Naproxen, Indomethacin…)
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)
Celicoxib
(“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
Acetominophen
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)
Acetylcysteine
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
Zafirlukast (or Montelukast)
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
Zileuton
“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)
Cromolyn
Inhibits mast cell degranulation–>less histamine–>anti-inflammatory effects–>prevents asthma exacerbations associated with allergens or exercise
Cyclosporine
“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* 3. Tx of autoimmune dzs (like RA) *SE = nephrotoxicity; hepatotoxicity… (Most SE are dose-dependent) Metabolized by p450 (CYP3A4)
*Tacrolimus (Similar to Cyclosporine)
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)
Sirolimus
Similar to Tacrolimus, but inhibits *mTOR*–>decreased T cell proliferation
Mycophenolate Mofetil
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
Interferons
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*
*Prostaglandins (-prost-, or -prost)
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
PGI2 analogs (Treprostinil, epoprostenol, iloprost)
It’s a “PGI2 Pah-TIE” Inhibit platelet aggregation and produce vasodilation (both by increasing cAMP) Uses = tx of pulmonary arterial HTN
Etanercept
“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…
Gold salts
May be used to tx RA
Infliximab
“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
Thalidomide
(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)
First gen H1 receptor blockers (diphenhydramine, promethazine, meclizine…)
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)
2nd gen H1 receptor blockers (Fexofenadine, Loratadine, Cetirizine)
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
Theo’P’hylline
“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
Guaifenesin
–>secretion of less viscous mucous in bronchi–>thinner phlegm which helps stimulate resp tract secretion flow Use = expectorant to get phlegm out
Bosentan (-sentans)
Competitively inhibit endothelin receptors–>pulmonary vasodilation Use = tx of pulmonary arterial hypertension SE = hepatotoxicity; teratogen
Ethanol
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
Disulfiram
Used in tx of alcohol cessation. Inhibits acetaldehyde dehydrogenase–>increased acetaldehyde when drinking (toxic)–>N/V–>incentive not to drink
Iron as toxin (name the antidote)
Antidote = De”fero”xamine
Lead as toxin (name the antidote)
Antidote = Calcium EDTA; dimercaprol; penicillamine
Arsenic as toxin (name the antidote)
Antidote = Dimercaprol; penicillamine
Cyanide as toxin (name the antidote)
Antidote = Sodium thiosulfate; nitrites
Carbon monoxide as toxin (name the antidote)
Antidote = 100% oxygen
Amiodarone
Actually Class 1-4 agent. Side effects = pulmonary fibrosis, thyroid dysfunction, blue-grey skin discoloration (But don’t usually get torsades with Amiodarone!)
Fomepizole
Tx of ethylene glycol overdose Inhibits alcohol dehydrogenase (unlike disulfiram)–>decreased breakdown of ethylene glycol into toxic metabolites
Omega 3s (Fish Oils)
Lower triglycerides a lot Raise HDL and LDL a little If belch–>bad fishy taste in mouth
Hydroxychlorquine
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)
