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MSS Pharm Flashcards

1
Q

What does the Lipoxygenase pathway yield?

A

Leukotrienes

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2
Q

What is LTB4?

A

Neutrophil chemotatic agent

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3
Q

What do LTC4, D4 & E4 function in?

A

Bronchoconstriction, vasoconstriction, contraction of sm & inc vascular permeability

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4
Q

What do PGI2 do?

A

Inhibits platelet aggregation & promotes vasodilation

(Platelet-Gathering-Inhibitor)

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5
Q

What is the MOA of aspirin?

A

Irreversibly inhibits COX-1 & COX-2 by acetylation, which dec synthesis of both thromboxane A2 (TXA2) & PG. Inc bleeding time. Nof affect on PT, PTT. Type of NSAID

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6
Q

Clinical use of aspirin

A
  • Low dose: (
  • Indermediate dose (300-2400 mg/day) antipyretic & analgesic
  • High dose (2400-4000 mg/day) anti-inflam
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7
Q

What can aspirin toxicity cause?

A
  • Gastric ulceration
  • Tinnitus (CN VIII)
  • Chronic use can l/t acute renal failure, intersitial nephritis, & upper GI bleeding
  • Risk of Reye’s synd in children tx w/ apsirin for viral infection
  • Stim resp centers, causing hyperventilation & resp alkalosis
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8
Q

What are examples of NSAIDs?

A
  • Ibuprofen
  • Naproxen
  • Indomethacin
  • Ketoralac
  • Diclofenac
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9
Q

What is the MOA of NSAIDs?

A

Reversibly inhibits COX 1 & 2 & blocks PG synthesis

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10
Q

What are the clinical uses of NSAIDs?

A
  • Antipyrenic
  • Analgesic
  • Anti-inflam
  • Indomethacin is used to close a PDA
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11
Q

What can NSAID toxicity cause?

A
  • Interstitial nephritis
  • Gastric ulcer (PG’s protect gastric mucosa)
  • Renal ischemia (PG vasodilate afferent arteriole)
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12
Q

What is the MOA of COX-2 inhibitors (celecoxib)?

A

Reversibly inhibit specifically the COX isoform 2, which is found in inflam cells & vascular endothelium & mediates inflam & pain. Spares COX-1 & TXA2

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13
Q

What is the clinical use of COX-2 inhibitors?

A

Rheumatoid arthritis & osteoarthritis; pts w/ gastritis or ulcers

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14
Q

What can COX-2 inhibitor toxicity cause?

A

Inc risk of thrombosis; sulfa allergy

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15
Q

What is the MOA of Acetaminophen?

A

Reversibly inhibits COX, mostly in CNS. Inactivated peripherally

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16
Q

What are the clinical uses of Acetaminophen?

A
  • Antipyretic
  • Analgesic but not anti-inflam
  • Used instead of aspirin to avoid Reye’s synd in children w/ viral infection
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17
Q

What can Acetaminophen toxicity cause?

A

Overdose produces hepatic necrosis; acetaminophen metabolite depletes gluthione & forms toxic tissue adducts in liver. N-acetylcysteine is antidote-regenerates glutathione.

18
Q

What is an example of a bisophosphonates?

A

Alendronate, other -dronates

19
Q

What is the MOA of Bisphosphates?

A

Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity

20
Q

What are the clinical uses of Bisphosphonates?

A
  • Osteoporosis
  • Hypercalcemia
  • Paget’s dz of bone
21
Q

What can Bisphosphonate toxicity cause?

A

Corrosive esophagitis, osteonecrosis of the jaw

22
Q

What are the chronic gout drugs?

A
  • Allopurinol
  • Febuxostat
  • Proenecid
  • Colcchicine
23
Q

What are the Acute gout drugs?

A
  • NSAIDs (naproxen, indomethacin)
  • Glucocorticoids (oral or intraarticular)
24
Q

What is the MOA of Allopurinol?

A

Inhibits xanthine oxidase, dec conversation of xanthine to uric acid

25
Q

What is Allopurinol used for?

A
  • Gout
  • Lymphoma & leukemia to prevent tumor lysis- assoc w/ urate nephropathy
26
Q

What can Allopurinol inc conc of?

A

Azathioprine & 6-MP (both normally metabolized by xanthine oxidase)

27
Q

What can you not give Allopurinol w/?

A

Don’t give w/ salicylates; all but the highest doses depress uric acid clearance. Even high doses (5-6g/day) have only minor uriosuric activity

28
Q

What is the MOA of Febuxostat?

A

Inhibits xanthine oxidase

29
Q

What is the MOA of Probenecid?

A

Inhibits reabsorption of uric acid in PCT (also inhibits sec of penecillin)

30
Q

What is the MOA of Colchine?

A

Binds & stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis & degranulation

31
Q

What are the TNF-alpha inhibitors?

A
  • Etanercept
  • Infliximab
  • Adalimumab
32
Q

What can all TNF-alpha inhibitors cause?

A

Predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macro & destruction of phagocytosed microbes

33
Q

What is the MOA of Etanercept?

A

Fusion protein (recptor for TNF-alpha + IgG1 Fc), produced by recombiant DNA

34
Q

What are the clinical uses of Etanercept?

A
  • Rheumatoid arthritis
  • psoriasis
  • Ankylosing spondylitis
35
Q

What is the MOA of Infliximab & Adalimumab?

A

Anti-TNF-alpha monoclonal Ab

36
Q

What are the clinical uses of Infliximab & adalimumab?

A
  • Chron’s dz
  • Rheumatoid arthritis
  • Anklylosing spondylitis
  • Psoriasis
37
Q

How do you treat Osteoporosis?

A

SERMs (Estrogen)

Calcitonin

Bisphosphonates

Pulsatile PTH

38
Q

What is osteoporosis prophylaxis?

A

weight-bearing exercise

adequate Ca & Vit D throughout life

39
Q

What drugs are contraindicated in osteoporosis?

A

Glucocorticoids

40
Q
A

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