Pharm Flashcards

1
Q

Methotrexate

A

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

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2
Q

Adalimumab, etanercept

A

TNF-a inhibitor:

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

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3
Q

Infliximab

A

TNF-a inhibitor:

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

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4
Q

Tocilizumab

A

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

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5
Q

Anakinra

A

IL-1 receptor antagonist; not effective at treating RA

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6
Q

Tofacitinib

A

Equally as effective as methotrexate but with infection, cancer risks

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7
Q

Cimetidine

A

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

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8
Q

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

A

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

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9
Q

What is the underlying mechanism behind anaphylaxis?

A

Release of mast cell and basophil-derived mediators

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10
Q

Signs of anaphylaxis

A

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

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11
Q

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

A

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

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12
Q

What types of diseases are treated with corticosteroids?

A

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

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13
Q

Inhibitors and inducers of P-glycoprotein

A

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

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14
Q

Type I biotransformation reaction(s)

A

Type I reactions deactivate: oxidation, reduction, hydrolysis

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15
Q

Type II biotransformation reaction(s), with examples

A

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

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16
Q

P450 inducers/metabolism increasers

A

Rifampin, phenobarbital, phenytoin, carbamazepine, ethanol

17
Q

P450 inhibitors

A

Cimetidine, grapefruit juice, disulfiram, ketoconazole, fluoxetine

18
Q

4 elevated findings in RA

A

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

19
Q

Where is gentamicin distributed in the body?

20
Q

Where is heparin distributed in the body?

21
Q

Warfarin

A

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

22
Q

Which CYPs metabolize warfarin?

A

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

23
Q

Clinical indications of hemorrhage

A

Hypotensive, dizzy, high INR, low Hgb

24
Q

What drugs exhibit zero order clearance at saturable levels?

A

Ethanol, phenytoin, aspirin

25
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.
26
What are enterotoxins?
Bacterial toxins (exogenous pyrogens) for gram + bacteria
27
What are endotoxins?
Bacterial toxins (exogenous pyrogens) for gram - bacteria
28
3 prostaglandins that maintain GFR
PGI2, PGE2, PGE3
29
Colchicine
 Binds tubulin in neutrophils, preventing chemotactic and chemokinetic responses  Inhibits formation of LTB4, prevents degranulation of mast cells  Combination or replace NSAIDS
30
Allopurinol
Xanthine oxidase inhibitor (stops production of uric acid from purines)  Risk of hypersensitivity rxns: Steven-Johnson, DRESS
31
Febuxostat
Xanthine oxidase inhibitor  Non-competitive  For patients who’ve failed allopurinol, but incr. (CVD) mortality
32
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
33
Pegloticase
“Uricoslytic” – converts uric acid to water soluble metabolite  For “severe, treatment-refractory gout”
34
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)
35
Acetaminophen toxicity treatment
N-acetylcysteine