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Step 1 Pharmacology > Musculoskeletal, Skin, and Connective Tissue > Flashcards

Musculoskeletal, Skin, and Connective Tissue Flashcards

1
Q

What does the Lipoxygenase pathway yield?

A

Leukotrienes

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2
Q

What is LTB4?

A

A neutrophil chemotactic agent

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3
Q

What do LTC4, D4, and E4 function in?

A

Bronchoconstriction, vasoconstriction, contraction of smooth muscle, and ↑ vascular permeability

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4
Q

What does PGI2 do?

A

Inhibit platelet aggregation and promotes

vasodilation. It also ↓ bronchial tone and ↓ uterine tone.

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5
Q

What do corticosteroids do?

A

Block protein synthesis and inhibit Phospholipase A2 (so membrane lipids don’t turn into Arachidonic Acid)

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6
Q

What does Zileuton do?

A

Inhibits Lipoxygenase so Arachidonic acid doesn’t turn into Hydroperoxides (HPETEs)

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7
Q

What do Zafirlukast and Montelukast do?

A

Leukotriene receptor agonsists. They ↑ bronchial tone.

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8
Q

What do NSAIDS, aspirin, acetaminophen, COX-2 inhibitors do?

A

Inhibit Cyclooxygenase (COX-1, COX-2) so Arachidonic acid doesn’t turn into Endoperoxides (PGG2, PGH2).

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9
Q

What do Prostaglandins (PGE2 and PGF2a) do?

A

↑ uterine tone and ↓ bronchial tone

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10
Q

What does Thromboxane (TXA2) do?

A

↑ platelet aggregation
↑ vascular tone
↑ bronchial tone

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11
Q

What is the mechanism of Aspirin?

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation, which ↓ synthesis of both thromboxane A2 (TXA2) and prostaglandins. ↑ bleeding time until new platelets are produced (∼ 7 days). No effect on PT, PTT. A type of NSAID.

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12
Q

What is the clinical use of Aspirin?

A

Low dose (< 300 mg/day): ↓ platelet aggregation. Intermediate dose (300–2400 mg/day): antipyretic and analgesic. High dose (2400–4000 mg/day): anti-inflammatory.

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13
Q

What is the toxicity of Aspirin?

A

Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Risk of Reye syndrome in children treated with aspirin for viral infection. Also stimulates respiratory centers, causing hyperventilation and respiratory alkalosis.

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14
Q

What are the NSAIDs?

A

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

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15
Q

What is the mechanism of NSAIDs?

A

Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block PG synthesis.

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16
Q

What is the clinical use of NSAIDs?

A

Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

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17
Q

What is the toxicity of NSAIDs?

A

Interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole).

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18
Q

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

A

Reversibly inhibit specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on COX-1.

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19
Q

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

A

Rheumatoid arthritis and osteoarthritis; patients with gastritis or ulcers.

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20
Q

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

A

↑ risk of thrombosis. Sulfa allergy.

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21
Q

What is the mechanism of Acetaminophen?

A

Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

22
Q

What is the clinical use of Acetaminophen?

A

Antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndrome in children with viral infection.

23
Q

What is the toxicity of Acetaminophen?

A

Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in liver. N-acetylcysteine is antidote—regenerates glutathione.

24
Q

What are the Bisphosphonates?

A

Alendronate, other -dronates.

25
Q

What is the mechanism of Bisphosphonates?

A

Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity.

26
Q

What is the clinical use of Bisphosphonates?

A

Osteoporosis, hypercalcemia, Paget disease of bone.

27
Q

What is the toxicity of Bisphosphonates?

A

Corrosive esophagitis (patients are advised to take with water and remain upright for 30 minutes), osteonecrosis of the jaw.

28
Q

Chronic gout drugs (preventive) - What are the key features of Allopurinol?

A

Inhibits xanthine oxidase, ↓ conversion of xanthine to uric acid. Also used in lymphoma and leukemia to prevent tumor lysis–associated urate nephropathy. ↑ concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase).

Do not give salicylates; all but the highest doses depress uric acid clearance. Even high doses (5–6 g/day) have only minor uricosuric activity.

29
Q

Chronic gout drugs (preventive) - What are the key features of Febuxostat?

A

Inhibits xanthine oxidase.

30
Q

Chronic gout drugs (preventive) - What are the key features of Probenecid?

A

Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin). High dose salicylates also inhibit reabsorption of uric acid in PCT.

31
Q

Acute gout drugs - Which NSAIDs are used to treat acute gout?

A

Naproxen, indomethacin

32
Q

Acute gout drugs - Which glucocorticoids are used to treat acute gout?

A

Oral or intraarticular

33
Q

Acute gout drugs - What are the key features of Colchicine?

A

Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation.
Acute and prophylactic value. GI side effects.

34
Q

What are the key universal features of TNF-α inhibitors?

A

All TNF-α inhibitors predispose to infection, including reactivation of latent TB, since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes.

35
Q

TNF-α inhibitors - What is the mechanism of Etanercept?

A 
Fusion protein (receptor for TNF-α + IgG1 Fc),
produced by recombinant DNA.

Etanercept is a TNF decoy receptor.

36
Q

TNF-α inhibitors - What is the clinical use of Etanercept?

A

Rheumatoid arthritis, psoriasis, ankylosing

spondylitis

37
Q

TNF-α inhibitors - What is the mechanism of Infliximab and adalimumab?

A

Anti-TNF-α monoclonal antibody

38
Q

TNF-α inhibitors - What is the clinical use of Infliximab and adalimumab?

A

IBD, rheumatoid arthritis, ankylosing spondylitis, psoriasis

39
Q

What is the treatment for Type II Osteoporosis?

A

Bisphosphonates, PTH, SERMs, rarely calcitonin; denosumab (monoclonal antibody against RANKL)

40
Q

What is the treatment for Osteoarthritis?

A

NSAIDs, intra-articular glucocorticoids

41
Q

What is the treatment for Rheumatoid arthritis?

A

NSAIDs, glucocorticoids, disease-modifying agents (methotrexate, sulfasalazine, TNF-α inhibitors)

42
Q

What drugs can exacerbate Gout?

A

Thiazide diuretics

43
Q

What is the treatment for Pseudogout?

A

NSAIDs for sudden, severe attacks; steroids and colchicine

44
Q

What is the treatment for Systemic lupus erythematosus?

A

NSAIDs, steroids, immunosuppressants, hydroxychloroquine

45
Q

What is the treatment for Sarcoidosis?

A

Steroids

46
Q

What is the treatment for Polymyalgia rheumatica?

A

Rapid response to low-dose corticosteroids

47
Q

What is the treatment of fibromyalgia?

A

Regular exercise, antidpressants (TCAs, SNRIs), and anticonvulsants

48
Q

What is the treatment of Polymyositis/dermatomyositis?

A

Steroids

49
Q

What does AChE inhibitor administration do for Myasthenia gravia?

A

Reversal of symptoms

50
Q

What does AChE inhibitor administration do for Lambert-Eaton myasthenic syndrome?

A

Minimal effect

51
Q

What drugs are associated with Erythema multiforme?

A

Sulfa drugs, β-lactams, phenytoin

52
Q

Patients with metastatic or unresectable melanoma in patients with BRAF V600E mutation may benefit from what drug?

A

Vemurafenib, a BRAF kinase inhibitor

Step 1 Pharmacology (18 decks)

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