Pharm Flashcards
Methotrexate
Non-biologic DMARD:
“Drug of choice” – decr. TNF-a and T cell activity (by inhibting adenosine deaminase)
o More than 1 mechanism of action
o Risk for liver damage/contraindications = renal disease, liver disease (e.g. Hep C) or pregnancy
Adalimumab, etanercept
TNF-a inhibitor:
Bind + decr. free TNF-a; potential for serious side effects (incr. risk of lymphoma, latent TB)
Infliximab
TNF-a inhibitor:
Chimeric monoclonal Ab; not monotherapy b/c pts develop anti-chimeric Ab (HACA)
Tocilizumab
IL-6 receptor antagonist:
• Better than methotrexate, but more side effects
• If you fail TNF-a inhibitors
Anakinra
IL-1 receptor antagonist; not effective at treating RA
Tofacitinib
Equally as effective as methotrexate but with infection, cancer risks
Cimetidine
H2 antagonist (inhibits effect of histamine on H/K ATPase in stomach):
o PPIs much more effective, but cimetidine more “rapid acting” compared to omeprazole
o Inhibits multiple forms of cytochrome P450
Also inhibits dihydro-testosterone to androgen receptors and inhibits metabolism of estradiol
Thus, with chronic use can cause gynecomastia or impotence in men, and galactorrhea in women
“-tidine” – Tummy Irritated after DINE-ing
What’s the risk in giving old people 1st gen H1 antagonists?
Can cause delirium, agitation, incr. dementia, incr. risk of death
What is the underlying mechanism behind anaphylaxis?
Release of mast cell and basophil-derived mediators
Signs of anaphylaxis
Skin: hives and angioedema; Lungs: mucous secretions, bronchoconstriction; cards: hypotension, tachy, vasoconstriction, arrhythmias
Why is epinephrine used to counteract anaphylaxis (specific physiologic effects)?
alpha-1 agonist: causes vasoconstriction and dear. mucosal edema; beta-2 agonist: causes bronchodilator, decr. mast cell release
What types of diseases are treated with corticosteroids?
Allergies, asthma, inflammation, autoimmune disorders, cancer (antiemetic for chemo effects), sarcoidosis, hypercalcemia, respiratory distress syndrome (esp pregnant women)
Inhibitors and inducers of P-glycoprotein
Inhibitors: cimetidine, grapefruit juice; inducers: rifampin, St. John’s wort
Type I biotransformation reaction(s)
Type I reactions deactivate: oxidation, reduction, hydrolysis
Type II biotransformation reaction(s), with examples
Type II reactions detoxify, via conjugation; Acetylation, glycine conjugation, methylation, glucuronidation
P450 inducers/metabolism increasers
Rifampin, phenobarbital, phenytoin, carbamazepine, ethanol
P450 inhibitors
Cimetidine, grapefruit juice, disulfiram, ketoconazole, fluoxetine
4 elevated findings in RA
Anti-citrulline Ab (specific), Sed rate, CRP, rheumatoid factor
Where is gentamicin distributed in the body?
ECF
Where is heparin distributed in the body?
Plasma
Warfarin
o Interferes with synthesis of clotting factors
o A Fib pts = risk of systemic embolism, given warfarin to reduce risk
A Fib patients frequently had atrial mural thrombi = risk of embolism/stroke
Which CYPs metabolize warfarin?
2C9 (S-warfarin, which has the strongest effect on clotting), 3A4 and 2C19 (R-warfarin)
Clinical indications of hemorrhage
Hypotensive, dizzy, high INR, low Hgb
What drugs exhibit zero order clearance at saturable levels?
Ethanol, phenytoin, aspirin
COX effect of stomach
COX-1 (only) incr. bicarbonate, mucous secretion, mucosal blood flow, thus offering protection. This is why COX inhibitors cause gastric bleeding and peptic ulcers.
What are enterotoxins?
Bacterial toxins (exogenous pyrogens) for gram + bacteria
What are endotoxins?
Bacterial toxins (exogenous pyrogens) for gram - bacteria
3 prostaglandins that maintain GFR
PGI2, PGE2, PGE3
Colchicine
Binds tubulin in neutrophils, preventing chemotactic and chemokinetic responses
Inhibits formation of LTB4, prevents degranulation of mast cells
Combination or replace NSAIDS
Allopurinol
Xanthine oxidase inhibitor (stops production of uric acid from purines)
Risk of hypersensitivity rxns: Steven-Johnson, DRESS
Febuxostat
Xanthine oxidase inhibitor
Non-competitive
For patients who’ve failed allopurinol, but incr. (CVD) mortality
Probenecid
“Uricosuric” (incr. uric acid in urine by decr. kidney reabsorption)
To replace/supplement allopurinol if it’s not working/not enough
Risk for kidney stones
Pegloticase
“Uricoslytic” – converts uric acid to water soluble metabolite
For “severe, treatment-refractory gout”
Varying levels of ASA toxicity, with symptoms
1st – vomiting, hearing loss, vertigo = “salicylism”
2nd – resp. alkalosis (d/t central hyperventilation, tinnitus, bronchospasm
Mild/moderate levels – fever (ox phos uncoupling), metabolic acidosis (d/t comp. for resp alkalosis + salicylate accumulation)
Acetaminophen toxicity treatment
N-acetylcysteine
