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99 Cards in this Set
- Front
- Back
Cladribine =
|
adenosine analog R to degradation by adenosine deaminase
=> adenosine toxicity kills HCL cells |
|
MTX = folic acid analog that binds:
|
DHFR
|
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5-FU =
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pyrimidine analog that inhibits thymidylate synthesis
=> inhibits DNA synth |
|
Leucovorin = N-formyl-THF = Folinic Acid;
=> (2) |
1. "rescue" from MTX toxicity
(inhibits MTX) or 2. potentiation of 5-FU |
|
Enoxaparin =
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LMW heparin (binds and activates ATIII)
=> inactivation of 10a - less effective than unfractioned heparin |
|
main SE of Vincristine =
(vinca alkaloid) |
neurotoxicity
(due to failure of MT polym in axons) |
|
ultimately, Aminocaproic acid inhibits:
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fibrinolysis
- so does Tranexamic acid |
|
**what does desmopressin do in the blood?
(NOT at the tubules) |
***releases Factor 8 and vWF from the endothelium
(tx for vWD) |
|
what are Gardos channel blockers?
|
meds that block the efflux of K+ and water from the cell, preventing dehydration and subsequent polymerization of HbS
= tx for SCA |
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4 opioids:
|
1. Meperidine
2. Diphenoxylate 3. Dextromethorphan 4. Loperamide |
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example of a nonselective MAOI:
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Phenelzine
|
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“-dipines” =
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dihydropyridine Ca2+-chan blockers
|
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non-dihydropyridine blockers =
(2) |
1. Verapamil
2. Diltiazem |
|
SER Syndrome:
Sinners Sell Drugs That Make Me Trip |
St. John's Wort
SSRI's Dextromethorphan TCA's MAOI's Meperidine Triptans (anti-migraine) |
|
8 features of SER Syndrome:
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1. confusion
2. agitation 3. tremor 4. tachycardia 5. HTN 6. clonus 7. hyperthermia 8. diaphoresis |
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SER Syndrome is treated with:
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Cyproheptadine
- anti-H with anti-SER properties |
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Abciximab =
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GP2b3a r' blocker
- mimics Glanzman (deficiency in GP2b3a) |
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Fondaparinux =
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Factor 10a inhibitor
|
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Unfractioned heparin binds:
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BOTH ATIII and thrombin
=> inactivation of BOTH Factor 10a AND thrombin = more effective than LMW heparin (like Enoxaparin) |
|
Trastuzumab =
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AB against ERB-B2 (HER2/neu)
|
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major SE of ganciclovir =
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neutropenia,
ESP. when given with Zidovudine |
|
most prominent SE of Cisplatin =
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nephrotoxicity
- prevented with Amifostine (f.r. hunter) and hydration |
|
Ticlopidine =
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inhibitor of plat. ADP release (like Clopidogrel)
=> plats aren't activated to express GP2b/3a |
|
serious SE of Ticlopidine =
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neutropenia
=> fever and mouth ulcers |
|
another name for TNF-a =
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cachectin
- released by mP's and neoplasms ~~ systemic inflammation - cachexia and septic shock at high concentrations |
|
Rituximab =
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anti-CD20 agent
|
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vinca alkaloids act at the:
|
M phase
- prevent division |
|
Argatroban =
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DIRECT thrombin inhibitor => anticoagulation
|
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what does Sucralfate do?
|
coats ulcer base, like Bismuth
|
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what do vinca alkaloids do?
|
bind B tubulin, preventing MT polymerization
=> MT's destroyed |
|
mech. of Colchicine:
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binds tubulin => prevents MT polym.
|
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1st-gen/typical antipsychotics are either low-potency or high; respective SE's =
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non-neurologic if low-potency
(sedation, anti-cholinergic, orthostatic hypotension) neurologic if high-potency (EPS, which includes rigidity) |
|
2 low-potency neuroleptics:
(first-gen antipsychotics) |
1. Chlorpromazine
2. Thioridazine |
|
2 high-potency neuroleptics:
|
1. Haloperidol
2. Fluphenazine |
|
main SE of Lamotrigine =
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skin rash
- pot. fatal in children |
|
**improvement in strength of MG pt following Edrophonium admin. means:
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they are being under-treated
=> **inc. dose of [Neostigmine] |
|
remember that Edrophonium is a:
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rapidly-reversible ACHE inhibitor
=> inc. ACH concentration |
|
Ca2+ chan. blockers like Nimodipine can be used to prevent:
|
vasospasm following subarachnoid hemorrhage (SAH)
|
|
specific mech. of Morphine:
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acts via G/2nd messengers to INCREASE K+ efflux
=> cells hyperpolarized => no pain transmission |
|
Modafinil =
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non-amph. for NARCOLEPSY
|
|
Timolol and other B-blockers in the eye:
|
decrease production of aqueous humor [by ciliary epithelium]
- treat glaucoma |
|
drug-induced Parkinsonism is the result of blocking:
|
D2
- neuroleptics, anti-emetics |
|
drug-induced Parkinsonism is treated with:
|
Benztropine or Amantadine
- L-dopa and DOPA agonists can't be used - will ppt psychosis |
|
most effective way to reduce blood Li2+ =
|
hemodialysis
|
|
Li2+ is excreted:
|
by the kidneys
- acts JUST LIKE Na+ => anything that damages kidneys OR causes an increase in PCT Na+ reabsorption will cause Li2+ toxicity |
|
3 classes of drugs that inc. Na+ reabsorption at the PCT:
|
1. NSAIDs
2. Thiazide diuretics 3. ACEI's |
|
"-capones" =
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COMT inhibitors
=> prevent peripheral conversion of L-dopa => inc. L-dopa into brain |
|
big difference b/w Entacapone and Tolcapone:
|
Tolcapone blocks peripheral AND central conversion of L-dopa, and has an inc. risk for hepatotoxicity
|
|
Carbidopa =
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DOPA decarboxylase inhibitor,
which prevents peripheral shunting of DOPA/L-dopa (like "-capones" / COMT inhibitors |
|
caveat with prescribing COMT inhibitors:
|
**useless** by themselves
|
|
"-gelines" =
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MAOI's
|
|
Atropine does not fix muscular or CNS excitation in cholinergic syndrome, but _____________ does
|
Pralidoxime
|
|
Ceftriaxone does not cover Listeria, so you need to add:
|
Ampicllin
- Ampicillin = d.o.c. for Listeria |
|
B6 increases:
|
peripheral metabolism of L-dopa
=> Parkinson symps return |
|
main problem with Cimetidine (H2-blocker) =
|
gynecomastia
|
|
"blood/gas partition coefficient" =
|
solubility in the blood
|
|
**highly-soluble inhaled anesthetic =>
|
higher solubility in the blood
=> slower equilibrium with the brain => longer onset |
|
an inhaled anesthetic with low blood solubility =>
|
QUICK onset of action
(reaches brain faster) |
|
the lower the MAC,
|
the more potent the inhaled anesthetic
(MAC = conc. that renders 50% unresponsive to painful stimuli) |
|
what's one way to decrease tolerance to Morphine?
|
give a Glutamate (NMDA channel) inhibitor,
like Ketamine |
|
higher peripheral (lipid) solubility means:
|
**more anesthetic is extracted from the blood**
=> need GREATER concentration in order to reach brain and be effective |
|
***both blood solubility AND tissue solubility are BARRIERS to reaching the brain***
|
the higher blood and lipid solubility are, the LONGER the anesthetic will take to work, and the MORE anesthetic you need
|
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TCA's have a __________________ effect on the CV system
|
Quinidine-like
- prolong QT, arrhythmias - by blocking fast Na+ channels |
|
TCA toxicity is treated with:
|
NS and HCO3
- increases Na+, to offset inhibition of Na+ chans by TCA (with subsequent cardiac issues) |
|
sexual SE's are common to:
|
SSRI's
- use Bupropion instead |
|
almost all volatile anesthetics increase:
|
cerebral blood flow
=> inc. ICP - in all other major organs, blood flow and thus organ function is DEcreased |
|
Phenytoin toxicity:
(3) |
1. gingival hyperplasia
(via inc. PDGF) 2. ataxia (cerebellum) 3. nystagmus (vestibular syst) |
|
4 effects of Benzo's:
|
1. hypnotic
2. anxiolytic 3. anti-convulsant 4. muscle relaxant |
|
mech. of Benzo's:
|
increase Cl- channel opening
=> enhance GABA |
|
2 symps of opioid use to which tolerance does NOT occur:
|
1. constipation
2. miosis - take daily laxatives |
|
4 mechanisms of TCA's:
|
1. NOR and SER reuptake inhibitors
2. Muscarinic r' antagonists 3. α1 blockers 4. H1 blockers |
|
2 high-potency antipsychotics:
|
1. Haloperidol
2. Fluphenazine |
|
Taxanes bind B tubulin and:
|
STABILIZE MT's
=> can't depolym => arrest |
|
2 low-potency antipsychotics:
|
1. Chlorpromazine
2. Thioridazine |
|
Mirtazapine = tetracycline; mech:
(3) |
1. blocks a2
=> NOR and SER release into terminal 2. 5HT2 antagonist 3. 5HT3 antagonist |
|
chronic topical corticosteroid administration =>
|
atrophy of dermis, drying/cracking of skin, tightening, telangiectasias, and ecchymoses
|
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nucleotide =
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P'd nucleoside
|
|
nucleoside antivirals must be:
|
P'd into nucleotides in order to function
|
|
***what is the mechanism of the cyclovirs?
|
they are *viral-kinase-dependent nucleosides*
- get P'd in order to become nucleotides, => effects - nucleotides like Cidofovir and Tenofovir, and nucleosides ZDZ and Lamivudine, get phosphorylated by the HOST cell kinase |
|
what do all P'd nucleotide analogs eventually do?
(2) |
1. inhibit DNAP
2. cause chain termination |
|
Probenecid and Sulfinpyrazone are:
|
uricosuric agents, which help excrete uric acid
- NOT used in pts with renal issues, for fear of nephrolithiasis - Allopurinol CAN be used despite renal issues |
|
chronic use of steroids =>
|
osteoporosis,
among other things |
|
"-dronates" =
|
Bisphosphonates,
pyrophosphate analogs (component of hydroxyapatite) |
|
PROG is required for endometrial cells to:
|
grow, differentiate into decidual cells that can accommodate pregnancy, and stabilize
- withdrawal of PROG will result in apoptosis, => bleeding |
|
TNF-a ~~
|
systemic inflammatory response
(IL-1, IL-6 as well) - cachexia and septic shock at high concentrations |
|
6 absolute contraindications to OCP's:
|
1. Hx of thromboembolic event or stroke
2. >35 and smoke heavily 3. hyperTG 4. decompensated or acute liver dz (impaired metabolism) 5. preg 6. Hx of EST-dependent tumor |
|
what is the standard prescription for gonococcal urethritis?
|
ceftriaxone for N. gonorrhea,
Z-pak for [probably concomitant] Chlamydia |
|
B-lactam antib's can often cause:
|
acute interstitial nephritis
- duh: Penicillin is a B-lactam |
|
Azathioprine =
|
**prodrug of 6MP**
- inhibits de novo synthesis of Purines (pure As Gold) |
|
Pyridoxine = B6 =
|
nec. cofactor in any transamination (AA becomes a-keto or vice versa)
- eaten up by INH |
|
Rasburicase =
|
uric acid excreter, like Allopurinol
- couple of steps further downstream |
|
what do topoisomerases do?
|
relieve the strain of supercoiling
|
|
Arachidonic Acid is a:
|
PUFA
|
|
B-blockers __________ EF
|
INCREASE it
- via dec. AF |
|
mech, and indication of Chlorpromazine:
|
D2 r' inhibitor,
antiemetic |
|
"-mustins" and Streptozocin are:
|
alkylating agents used against brain tumors
|
|
1st-line tx for Toxoplasmosis gondii =
|
Pyrimethamine and Sulfadiazine
|
|
6 atypical antipsychotics:
|
1. Olanzapine
2. Clozapine 3. Quetiapine 4. Risperidone 5. Aripiprazole 6. Ziprasidone |
|
mechanism of typical antipsychotics/neuroleptics:
|
block D2
|