Pharm

Question 1

Methotrexate

Answer 1

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

Question 2

Adalimumab, etanercept

Answer 2

TNF-a inhibitor:

Bind + decr. free TNF-a; potential for serious side effects (incr. risk of lymphoma, latent TB)

Question 3

Infliximab

Answer 3

TNF-a inhibitor:

Chimeric monoclonal Ab; not monotherapy b/c pts develop anti-chimeric Ab (HACA)

Question 4

Tocilizumab

Answer 4

IL-6 receptor antagonist:
• Better than methotrexate, but more side effects
• If you fail TNF-a inhibitors

Question 5

Anakinra

Answer 5

IL-1 receptor antagonist; not effective at treating RA

Question 6

Tofacitinib

Answer 6

Equally as effective as methotrexate but with infection, cancer risks

Question 7

Cimetidine

Answer 7

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

Question 8

What’s the risk in giving old people 1st gen H1 antagonists?

Answer 8

Can cause delirium, agitation, incr. dementia, incr. risk of death

Question 9

What is the underlying mechanism behind anaphylaxis?

Answer 9

Release of mast cell and basophil-derived mediators

Question 10

Signs of anaphylaxis

Answer 10

Skin: hives and angioedema; Lungs: mucous secretions, bronchoconstriction; cards: hypotension, tachy, vasoconstriction, arrhythmias

Question 11

Why is epinephrine used to counteract anaphylaxis (specific physiologic effects)?

Answer 11

alpha-1 agonist: causes vasoconstriction and dear. mucosal edema; beta-2 agonist: causes bronchodilator, decr. mast cell release

Question 12

What types of diseases are treated with corticosteroids?

Answer 12

Allergies, asthma, inflammation, autoimmune disorders, cancer (antiemetic for chemo effects), sarcoidosis, hypercalcemia, respiratory distress syndrome (esp pregnant women)

Question 13

Inhibitors and inducers of P-glycoprotein

Answer 13

Inhibitors: cimetidine, grapefruit juice; inducers: rifampin, St. John’s wort

Question 14

Type I biotransformation reaction(s)

Answer 14

Type I reactions deactivate: oxidation, reduction, hydrolysis

Question 15

Type II biotransformation reaction(s), with examples

Answer 15

Type II reactions detoxify, via conjugation; Acetylation, glycine conjugation, methylation, glucuronidation

Question 16

P450 inducers/metabolism increasers

Answer 16

Rifampin, phenobarbital, phenytoin, carbamazepine, ethanol

Question 17

P450 inhibitors

Answer 17

Cimetidine, grapefruit juice, disulfiram, ketoconazole, fluoxetine

Question 18

4 elevated findings in RA

Answer 18

Anti-citrulline Ab (specific), Sed rate, CRP, rheumatoid factor

Question 19

Where is gentamicin distributed in the body?

Answer 19

ECF

Question 20

Where is heparin distributed in the body?

Answer 20

Plasma

Question 21

Warfarin

Answer 21

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

Question 22

Which CYPs metabolize warfarin?

Answer 22

2C9 (S-warfarin, which has the strongest effect on clotting), 3A4 and 2C19 (R-warfarin)

Question 23

Clinical indications of hemorrhage

Answer 23

Hypotensive, dizzy, high INR, low Hgb

Question 24

What drugs exhibit zero order clearance at saturable levels?

Answer 24

Ethanol, phenytoin, aspirin

Question 25

COX effect of stomach

Answer 25

COX-1 (only) incr. bicarbonate, mucous secretion, mucosal blood flow, thus offering protection. This is why COX inhibitors cause gastric bleeding and peptic ulcers.

Question 26

What are enterotoxins?

Answer 26

Bacterial toxins (exogenous pyrogens) for gram + bacteria

Question 27

What are endotoxins?

Answer 27

Bacterial toxins (exogenous pyrogens) for gram - bacteria

Question 28

3 prostaglandins that maintain GFR

Answer 28

PGI2, PGE2, PGE3

Question 29

Colchicine

Answer 29

 Binds tubulin in neutrophils, preventing chemotactic and chemokinetic responses
 Inhibits formation of LTB4, prevents degranulation of mast cells
 Combination or replace NSAIDS

Question 30

Allopurinol

Answer 30

Xanthine oxidase inhibitor (stops production of uric acid from purines)
 Risk of hypersensitivity rxns: Steven-Johnson, DRESS

Question 31

Febuxostat

Answer 31

Xanthine oxidase inhibitor
 Non-competitive
 For patients who’ve failed allopurinol, but incr. (CVD) mortality

Question 32

Probenecid

Answer 32

“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

Question 33

Pegloticase

Answer 33

“Uricoslytic” – converts uric acid to water soluble metabolite
 For “severe, treatment-refractory gout”

Question 34

Varying levels of ASA toxicity, with symptoms

Answer 34

 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)

Question 35

Acetaminophen toxicity treatment

Answer 35

N-acetylcysteine