Pharma Flashcards
(143 cards)
maintenance dose formula
what unit will MD be in?
and what if certain dosing interval is given?
MD = Cpss x CL / [bioavailability fraction]
MD unit is mg/min
If dosing interval given, can calc. MD based on that
(eg, 2 mg/min x 60 min/hr x 6 hrs for an MD of 2 and an interval of 6 hrs)
Cpss is steady-state plasma conc.
CL is clearance
bioavailability is 1 if IV
half life formula + how many half-lives to reach Cpss
Vd x 0.7 / CL
steady state conc reached in 4-5 half lives
loading dose formula
changes in loading dose based on organ function?
Vd x Cpss / [Bioavailability fraction]
loading dose stays say, but maintenance dose changes in case of renal/liver issue affecting elimination
anastrozole, letrozole, exemestane
MOA, uses
aromatase inhibitor
postmenopausal breast cancer (blocks aromatization of androstenedione in liver, muscle, fat)
flutamide, cyproterone acetate + spironolactone
MOA, uses
androgen receptor antagonists
tx of metastatic prostate cancer
Cytarabine + Gemcitabine
MOA, differences
both pyrimidine analog antimetabolites; incorporated into DNA > strand termination (no effect on folate metab.)
cytarabine is S-phase specific; gemcitabine is NOT + also has ribonucleotide reductase inhibition
(“cyt” has S sound; “gem” is a real gem… works better)
Fludarabine
MOA, indication
deamination-resistant purine nucleotide analog
inhibits DNA polymerase, primase, ligase and ribonucleotide reductase
used for CLL
5-Fluorouracil
MOA, leucovorin effect
pyrimidine analog that inhibits thymidylate synthetase (after conversion to floxuridine monophosphate)
binds thymidylate synthetase in presence of reduced folate > leucovorin actually INCREASES its toxicity
Interleukin-2
MOA and indications as a drug
activation + differentiation of T-cells to help tumor destruction
approved for renal cell carcinoma and melanoma
Abciximab
MOA + indication
anti-GpIIb/IIIa receptor mAb; blocks final step in platelet aggregation (GpIIb/IIIa binds fibrinogen)
used during angioplasty in ACS
Colchicine
MOA, use, sfx
binds TUBULIN and prevents microtubule polymerization (impairs WBC migration + phagocytosis to reduce gout inflammation)
2nd line in gout, for pt with renal failure, PUD, other NSAID contraindications
GI microtubule disruption > diarrhea (less common nausea, vomiting + pain)
Hepatitis 2-3 days after surgery with anesthesia
cause, s/s, histo
Halothane Hepatitis - halothane is hi-risk, fluranes lower, but still some risk; CYP450 metab > intermediates > immune-mediated hepatitis
fever, nausea, jaundice, tender hepatomegaly OR liver atrophy if severe, anorexia, my-/arthralgia, rash
high LFTs and bilirubin, prolonged PT (may have leukocytosis and eosinophilia, probably and HS rxn)
centrilobular hepatic necrosis (like viral hep)
inflammation of portal tracts and parenchyma
Nitrous Oxide
MOA and toxicity
NMDA antagonism
prolonged exposure > inhibits methionine reductase > megaloblastic anemia
Succinylcholine
MOA, toxicity
depolarizing NMJ blocker
hyperkalemia (esp. burn or SC injury pt)
malignant hyperthermia (ANS issues, rigidity, high temp)
First-line for absence seizures
Detailed MOA, SFX, and 2nd line
Ethosuximide
blocks T-type Ca channels > inhibits rhythmic burst discharges in thalamic neurons
sfx are nausea, vomit, fatigue + hyperactivity
valproate is 2nd line
4 drugs assoc. with acute pancreatitis
azathioprine
sulfasalazine
furosemide
valproate
vinca alkaloids
MOA, phase specificity?
vincristine / vinblastine
inhibit microtubule FORMATION by binding beta-tubulin and preventing polymerization of microtubules
specific to M phase of cell cycle (chromosomes can’t align and segregate)
vincristine
side effect
peripheral neuropathy
disruption of neuronal microtubules > disrupts axonal transport
Cell Cycle + its related chemo drugs
each phase
G1 - cells prepare building blocks for DNA synth
G0 - resting phase
S - DNA replication; topoisomerase I + II inhibitors (etoposide, irinotecan, topotecan) and antimetabolites (MTX, 5-FU, etc.)
G2 - DNA checked for errors + corrections made or apoptosis occurs; intercalators + ROS formers work here (bleomycin, doxorubicin, etc.)
M - division; vinca alkaloids + taxanes
Thiazolidinediones
MOA + effects
PPARy agonist
increased: FA uptake
adiponectin (adipokine that increases adipocyte insulin response + stimulates FA oxidation)
insulin sensitivity
decreased: TNF-alpha and leptin (adipokine that acts on hypothalamus to decrease appetite)
Succinylcholine side effects
Malignant Hyperthermia - especially with halothane co-admin; in genetically susceptible patients
Severe hyperkalemia + life-threatening arrhythmia - in patients with burns, myopathies, denervation or crush injuries
(upregulation of nAChR in denervation > great drug effect)
Bradycardia (PSNS stim) -or- tachycardia (SNS stim)
UFH binds both ATIII and thrombin, increasing ATIII inactivation of thrombin AND factor X
LMWH primarily affects inactivation of which factor?
Mostly just factor X
it has the AT-III binding pentasaccharide, but is shorter and doesn’t bind thrombin
inhibitor of ALCOHOL DEHYDROGENASE
inhibitor(s) of ACETALDEHYDE DH
fomepizole (alcohol DH)
disulfiram (acetaldehyde DH)
metronidazole (acetaldehyde DH)
heparin induced thrombocytopenia mechanism + tx
heparin-PLATELET FACTOR 4 complex causes IgG autoantibodies (about 3-5 days after heparin initiation)
Ab then binds Fc receptor on platelets > activation and clot formation > platelet consumption causes -penia
stop heparin and give direct thrombin inhibitors (bivalirudin or ARGATROBAN) or LMW heparinoids (fondaparinux, danaparoid) to control thrombosis
(don’t give warfarin because necrosis risk is high when thrombosis is already present!)