Term
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Definition
1.) oxidize iodide to iodine
2.) attach I to thyroglobulin
3.) couple MIT/DIT to create T3/T4 |
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Term
levothyroxine (4 brand names)
DDI, ADR, MOA |
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Definition
Synthroid, Levothroid, Unithroid, Levoxyl
MOA: synthetic T4
DDI: minerals (take am preprandially)
ADR: insomnia, tachy<3 |
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Term
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Definition
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Term
|
Definition
Thyrolar
Synthetic T3/T4 mix |
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Term
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Definition
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Term
|
Definition
MOA: inhibit TPO (3 fxn)
OOA: delayed due to thyroid gland stores; T4 t1/2
ADR: alopecia, arthralgia, agranulocytosis |
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Term
propylthiouracil (PTU)
MOA, OOA, ADR |
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Definition
MOA: inhibit TPO & 5'de-iodonase
OOA: delayed
ADR: alopecia, arthralgia, agranulocytosis |
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Term
|
Definition
ionic thyroid gland inhibitor
blocks I- symporter
byproduct of nitroprusside detox |
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Term
|
Definition
ionic thyroid gland inhibitor
blocks I- symporter |
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Term
excess iodide (2 brand names)
MOA, OOA, Use (&offlabel) |
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Definition
Lugol's Solution, SSKI
MOA: "freeze" thyroid gland
OOA: immediate
Use: thyroid storm, expectorant, prevent radiation absorption |
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Term
Radioactive Iodine
MOA, C.I. |
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Definition
MOA: uptaken into gland -> kills cells -> give levothyroxine
C.I.: pregnancy, children |
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Term
|
Definition
Xolair
MOA: binds IgE to prevent mast cell implantation
(-): $$$$$ |
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Term
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Definition
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Term
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Definition
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Term
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Definition
MOA: alpha-1 -> vasocon; beta-2 -> bronchodil
Use: anaphylaxis (hypoTN, bronchocon) |
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Term
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Definition
Benadryl
1st Gen H-1 Antag |
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Term
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Definition
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Term
|
Definition
Dramamine
1st Gen H-1 Antag |
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Term
|
Definition
Chlor-Trimeton
1st Gen H-1 Antag |
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Term
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Definition
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Term
|
Definition
Atarax, Vistaril
1st Gen H-1 Antag & antiemetic |
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Term
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Definition
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Term
|
Definition
Antivert
1st Gen H-1 Antag & anti-emetic |
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Term
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Definition
Phenergan
1st Gen H-1 Antag & anti-emetic |
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Term
|
Definition
Periactin
1st Gen H-1 Antag & 5HT2 Antag for serotonin syndrome |
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Term
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Definition
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Term
|
Definition
Claritin
2nd Gen H-1 Antag |
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Term
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Definition
Clarinex
2nd Gen H-1 Antag |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
Cytotec
PGE2 agonist ->
on proton pump: decrease p+
on mucus cell: increase mucus & bicarb |
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Term
|
Definition
| misoprostol + NSAID (why.) |
|
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Term
sucrasulfate
MOA, ADR, DDI |
|
Definition
MOA: activated by acid!!; attaches to ulceration
-take before meal
ADR: constipation
DDI: binds other drugs (esp digoxin) so space out |
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Term
|
Definition
Overcompensation -> Tolerance
while histamine is blocked, G cell releases more gastrin -> more histamine is released -> histamine competes with antag
Rebound acidity: if sudden d/c; too much histamine all binds |
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Term
|
Definition
Tagamet
H2 Blocker
*DON'T USE! CYP inhibition decreases cholesterol -> androgens |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
| Produce gastrin; blocked by SST |
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Term
|
Definition
| Produce SST to inhibit gastrin |
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Term
|
Definition
| produce histamine in response to gastrin binding CCK recep |
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Term
| 3 Anti-emetic 1st Gen H-1 Antags |
|
Definition
| promethazine, meclizine, hydroxyzine |
|
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Term
|
Definition
1.) CCK: activated by gastrin -> increase P+
2.) M2: activated by PNS -> increase P+
3.) H2: activated by histamine -> increase P+
4.) PG: activated by PGE2 -> decrease P+ |
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Term
PPIs
MOA, OOA, ADR, Formulation |
|
Definition
MOA: absorbed in GIT -> blood -> parietal cell -> activated by acid -> covalently binds p+pump
OOA: delayed
ADR: risk for CAP, HA, Diarrhea, reduced Ca++ absorp
*enteric-coated to avoid local stomach axn |
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Term
|
Definition
Prilosec, Zegerid
DDI: CYPi -> decreased efficacy of Plavix (prodrug) |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
|
Definition
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Term
metaclopromide
Use
MOA (2)
ADR |
|
Definition
Use: GERD, Anti-Emetic
MOA:
1.) D2 Blocker -> increase sphincter tone & prokinetic
2.) 5HT3 Blocker -> (brain) decrease CTZ stim, (GIT) decrease CTZ signal
ADR: longterm -> EPS, tardive dyskinesia |
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Term
| GERD & Vomiting & IBS Receptors (5) |
|
Definition
1.) D2
in Brain: CTZ stim -> N/V
in Upper GIT: decreased sphincter tone&peristalsis
2.) 5HT3
in Brain: CTZ stim -> N/V
in Upper GIT: 5HT storing cells -> nerve signal to CTZ
in Lower GIT: increase secretion & motility
3.) NK-1
in Brain: CTZ stim -> immediate vomit (substance P)
in GIT: we dk
4.) CB-1 (cannabinoid)
in Brain: anti-emesis, analgesia, euphoria (THC)
5.) H1 & Muscarinic
in vestibular apparatus -> motion sickness |
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Term
D2 Antagonists
Use, MOA, ADR, Selectivity |
|
Definition
Use: 1st Line anti-emetics
MOA: decreased vomit reflex, increased sphincter tone&prokinetic
ADR: EPS, Tardive Dyskinesia
Nonselective -> H1 & Muscarinic antag -> decreased motion sickness |
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Term
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Definition
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Term
|
Definition
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Term
|
Definition
Phenergan
D2 Antag, H1 Antag |
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Term
5HT3 Antagonists
Use, MOA, ADR |
|
Definition
Use: 1st Line CINV
MOA: block CTZ stim; block CTZ signal
ADR: constipation, dizziness |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
|
Definition
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Term
arepipant
Use, MOA, Admin ADR |
|
Definition
Emend
NK-1 Antag
Use: CINV
MOA: block CTZ
Admin: must give before chemo (then after)
ADR: fatigue, loss of appetite |
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Term
|
Definition
Use: Last resort CINV
MOA: prevents emesis
ADR: tachycardia, euphoria, dependence/withdrawal |
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Term
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Definition
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Term
|
Definition
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Term
|
Definition
Lotronex
5HT3 Antag
Use: IBS-D
MOA: blocks Lower GIT receptor -> decreased secretion & motility |
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Term
|
Definition
Amitizia
Use: IBS-S
MOA: activate GIT Cl channels to increase secretion |
|
|
Term
| 7 Mechanisms of Cancer Resistance |
|
Definition
1.) decreased uptake by drug transporter
2.) Pgp efflux pump overexpression (multidrug)
3.) increased/mutated drug target
4.) repaire of dna damage
5.) drug metabolism
6.) change in membrane lipids
7.) compartmentalization (drug cannot reach hypoxic core) |
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Term
| Mechanisms of DNA Repair (3) |
|
Definition
1.) Base Excision Repair: remove mismatched base (glycosylase); replace with new (dnapol); religate. Cell cycle arrest will occur if mech is overwhelmed
2.) Mismatch Repair: proteins identify mismatch & replace large sections. If damage is too great it will trigger apoptosis
3.) Nonhomo Endjoining Repair: reseals ds break |
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Term
|
Definition
| Nitrogen Mustard alkylating agent |
|
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Term
|
Definition
| Activated in vivo by CYP -> covalently bind with SH, N, O (commonly N7 guanine) -> crosslinks DNA |
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Term
|
Definition
| Nitrogen Mustard alkylating agent |
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Term
|
Definition
| Nitrogen Mustard alkylating agent |
|
|
Term
cyclophosphamide
& prodrug iphosphamide |
|
Definition
Nitrogen Mustard alkylating agent
metabolism:
1.) aldehyde dehydrogenase -> inactive
2.) nonenz -> acrolein
*Acrolein accum -> hemorrhagic cystitis. Hydrate & give MESNA (free -SH detoxes) |
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|
Term
| Nitrogen Mustard unique resistance |
|
Definition
| Upregulation of enz that synth Glutathione -> inactivates active metabolite |
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Term
|
Definition
| nitrosourea alkylating agent |
|
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Term
|
Definition
| nitrosourea alkylating agent |
|
|
Term
|
Definition
| triazene alkylating agent |
|
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Term
|
Definition
| PO triazene alkylating agent |
|
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Term
|
Definition
platinum compound
tox: irreversible nephrotox due to glomerular filtration & copper transporters (run NS before & after) |
|
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Term
|
Definition
platinum compound
tox: neutropenia |
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|
Term
|
Definition
platinum compound
tox: neurotoxicity |
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|
Term
| Cisplatin Mechanisms of Resistance (6) |
|
Definition
1.) uptake defect (mutation of copper transporter)
2.) increased efflux
3.) glutathione inactivation
4.) P53 mutation (prevents apoptosis)
5.) increased dna repair
6.) replicative bypass |
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|
Term
methotrexate
MOA(3), Toxicity in RA, Cancer |
|
Definition
MOA:
1.) inhibit DHFR (converstion of DHF->THF for use in converting dUMP to TMP by TS)
2.) inhibit TS directly
3.) inhibit enzymes of purine synthesis
-> therefore inhibits purines & pyrimidines both
Tox; hepatotoxicity
RA Tox: (chronic PO dose): give folic acid
Cancer Tox: (high dose IV): give leukovorin rescue w/in 24-48 hours to replenish THF |
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Term
|
Definition
inactivates 6MP & 6TG
-genetic testing: phenotype (rbc) & genotype |
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Term
|
Definition
inactivates 6MP
-gout pt can get neutropenia if dose not adjusted |
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Term
|
Definition
|
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Term
|
Definition
purine analogs (guanine)
MOA: inhibit GMP(&) synth |
|
|
Term
| Drugs that cause myelosuppression (5) |
|
Definition
Carboplatin
Purine Analog
Arthracyclines
Hydroxyurea
Topotecan |
|
|
Term
fludarabine & cladiribine
MOA
ADR |
|
Definition
purine analogs (adenine)
MOA: activated via tri-P -> incorp into DNA -> chain term
**like acyclovir
ADR: CD4+ bone marrow suppression (OI susceptible) |
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Term
|
Definition
enzyme that inactivates 5-FU
-genetic test |
|
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Term
|
Definition
capecitabine(PO) -> 5-FU -> fdUMP -> inhibit TS
*must give leukovorin(->MTHF cofactor) to stabilize interaction |
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Term
|
Definition
| cytidine analog -> triP -> DNA incorp -> chain term |
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Term
|
Definition
cytidine analog;
triP -> DNA incorp -> inhibit DNA methyl transferase
"differentiating agents" |
|
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Term
|
Definition
inhibit ribonucleotide reductase
tox: myelosuppression |
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|
Term
vinca alkaloids
moa, resistance |
|
Definition
MOA: bind open GTP site on B tubule to prevent elongation
resistance: Pgp, B tubule mutation, increased B tubules |
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Term
|
Definition
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Term
|
Definition
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Term
|
Definition
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Term
|
Definition
|
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Term
|
Definition
|
|
Term
|
Definition
taxane
albumin-bound nanoparticle increases solubility (thus decreased hypersensitivity) and efficacy |
|
|
Term
|
Definition
taxane-like
decreased resistance due to slightly diff binding site |
|
|
Term
|
Definition
MOA: bind side B-tubule site to stabilize to decrease collapse
Resitance: Pgp, decreased penetration of drug, B tubule mutatoin, increased B tubules |
|
|
Term
|
Definition
S Phase
MOA: inhibit TopoI after ss break but before religation |
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|
Term
|
Definition
|
|
Term
irinotecan
unique toxicity
metabolism |
|
Definition
topo I inhibitor
tox: neutropenia, diarrhea
activated by carboxyl esterase -> detox by UGT1A1 -> enterohepatic recirculation -> de-gluc'd by bacteria -> can act in SMINT |
|
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Term
|
Definition
Detox SN38 (irinotecan active) by glucuronidation
**genetic test |
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