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0. Step Ia > MSK Pharm from FA > Flashcards

MSK Pharm from FA Flashcards

1
Q

Lipoxygenase pathway yields what (generally)?

A

Leukotrienes

(remember Lipoxygenase and Cycloxygenases both come from Arachidonic acid)

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2
Q

Name the 4 leukotrienes in FA. What do they do?

A

LTB4: attracts neutrophils (“neutrophils arrive B4 others”

LTC4, LTD4, LTE4: incr bronchial tone, vasoconstriction, incr vascular permeability

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3
Q

what products come from the Cycloxygenase pathway?

A

Prostacyclin, Prostaglandins, Thromboxane

-these moderate vascular, bronchial, & uterine tone in different ways.

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4
Q

PGI2: what is it/what does it do?

what cell/tissue releases it?

A

Prostacyclin from COX pathway

anticoagulation & vascular dilatation

(decreases these: platelet aggregation, vascular tone, bronchial tone, uterine tone)

Released by endothelial cells. Kind of opposes TXA2 from platelets.

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5
Q

PGE2, PGF2a: what do they do?

A

Increase uterine tone

decrease bronchial tone

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6
Q

TXA2: what does it do?

what cell/tissue releases it?

A

(Thromboxane)

incr platelet aggregation, incr vasoconstriction, incr bronchial tone

Released by platelets. Kind of opposes PGI2 from endothelial cells.

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7
Q

Aspirin: mech?

A

Irreversibly inhibits COX1 and COX2 via covalent acetylation.

–> decr synthesis of TXA2 and Prostaglandins.

Effect: incr bleeding time until new platelets are synthesized (~7d).

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8
Q

Aspirin: effect on PT? PTT?

A

None.

only affects bleeding time.

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9
Q

Aspirin: use (3 dose levels)?

A

Low dose: decr platelet aggregation (<300mg)

Medium dose: anti-fever, analgesic

High dose: anti-inflammatory (>2400mg)

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10
Q

Aspirin: tox (adults)?

A

Gastric ulcers

Tinnitus (CN VIII)

Chronic use: renal failure, interstitial nephritis, upper GI bleeds.

Stimulates resp centers -> hyperventilation and resp alkalosis.

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11
Q

Aspirin: tox (children)?

A

Risk of Reye syndrome for kids treated with aspirin for viral infection.

(rash/vomiting/liver damage)

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12
Q

COX 1 preferentially expressed where?

A

GI tract, platelets

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13
Q

COX 1 blockers: general side effects?

A

GI ulceration, bleeding

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14
Q

COX 2 receptors preferentially expressed where?

A

sites of inflammation

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15
Q

advantage to COX 2-specific blockers?

A

avoid side effects of COX1 (ulceration, bleeding)

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16
Q

Class?

ibuprofen, naproxen, aspirin, indomethacin, ketorolac, diclofenac

A

NSAIDs

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17
Q

NSAIDs: mech?

A

reversibly inhibit COS1 and COX 2.

Block prostaglandin synthesis

exception: aspirin = IRREVERsible block.

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18
Q

NSAIDs: use?

A

anti-fever, analgesic, anti-inflammatory

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19
Q

Indomethacin: unique use beyond usual NSAIDs use?

A

Close PDA

20
Q

NSAIDs: tox?

A

interstitial nephritis, gastric ulcer, renal ischemia

21
Q

how do NSAIDs cause gastric ulcers?

renal ischemia?

A

NSAIDs block prostaglandin synth

–>PGs protect gastric mucosa against ulceration

–>PGs vasodilate afferent arteriole

22
Q

Name a COX-2 specific blocker?

A

celecoxib

23
Q

celecoxib: Mech?

A

reversibly inhibit COX-2 (found in inflammatory cells and vasc endothelial cells).

Mediates inflammation and pain

does NOT block COX1 -> spares gastric mucosa.

24
Q

celecoxib: effect on platelet function?

A

None because TXA2 production is dependent on COX1, not COX 2.

25
Q

celecoxib: Use?

A

Rheumatoid arthritis, osteoarthritis

(esp patients with gastritis or ulcers)

26
Q

celecoxib: tox?

A

incr risk of thrombosis

sulfa drug: watch out for allergies

27
Q

Acetaminophen: mech?

A

reversibly inhibits COX, mainly in CNS

inactivated in periphery

28
Q

Acetaminophen: use?

A

anti-fever

analgesic

NOT anti-inflammatory

29
Q

Acetaminophen: use specific to children?

A

children with viral illness: don’t give aspirin due to possible Reye’s (brain swelling -> encephalopathy & liver damage)

use acetaminophen instead

30
Q

Acetaminophen: tox?

A

OD -> hepatic necrosis (metabolite from acetaminophen = NAPQ1; depletes glutathione -> causes liver toxicity)

31
Q

Acetaminophen: antidote to an OD?

A

N-acetylcysteine

mech: regenerates glutathione in the liver

32
Q

Bisphosphonates (alendronate, -dronates): mech?

A

inhibit osteoclast activity

pyrophosphate analogs; bind hydroxyapatite in bone, thus inhibiting osteoclasts

33
Q

Bisphosphonates (alendronate, -dronates): use?

A

Osteoporosis

hypercalcemia

Paget disease of bone

34
Q

Bisphosphonates (alendronate, -dronates): tox?

A
  • Corrosive esophagitis (ie pill esophagitis; take water w pill and don’t lie down for 30 min)
  • Osteonecrosis of the jaw
35
Q

Name 3 preventive gout drugs.

generally what is their mech?

A

Allopurinol, Febuxostat, Probenecid

A, F: interrupt the process of Purine metabolism -> less uric acid in blood

36
Q

Allopurinol, Febuxostat: mech?

A

(gout drugs)

Inhibit xanthine oxidase

-> less uric acid in blood

37
Q

Allopurinol: why do we give this to people with leukemia/lymphoma?

A
  1. decreases the destruction of azathioprine and 6-MP (which are normally degraded by xanthine oxidase)
  2. prevents urate nephropathy from tumor lysis
38
Q

what do we NOT give to pts with chronic gout?

A

Salicylates (aspirin)

they decrease clearance of uric acid

39
Q

Probenecid: mech?

A

(gout drug)

inhibits reabsorption of uric acid in PCT

(also inhibits secretion of PCN)

40
Q

3 drugs we give for acute gout?

A

NSAIDs (naproxen, indomethacin)

Glucocorticoids (oral or right into the joint!)

Colchicine

41
Q

Colchicine: mech?

A

binds/stabilizes tubulin

  • > inhibits microtubule polymerization
  • > decr leukocyte chemotaxis and degranulation
42
Q

Colchicine: tox?

A

GI side effects

given in escalating doses until the patient can’t handle the GI issues

43
Q

3 TNF-a inhibitors?

what are they for, generally?

A

Etanercept

Infliximab

Adalimumab

-Used for autoimmune diseases (RA, ank spond, IBD etc)

44
Q

Etanercept, Infliximab, Adalimumab: tox?

A
  • > increased infection since TNF blockers prevents activation of macrophages and destruction of phagocytosed microbes
  • > reactivation of latent TB
45
Q

Infliximab, Adalimumab: mech? use?

A

anti-TNFa monoclonal antibody

PAIR: Psoriasis, Ank spond, IBD, RA

46
Q

Etanercept: mech? use?

A

decoy TNF receptor

fusion protein produced by recombinant DNA: receptor for TNF-a + IgG Fc region)

Use (PAR): Psoriasis, Ank Spond, RA

47
Q

Antidote for acetaminophen tox?

How does it work (2 mechs)?

A

N-acetylcysteine

  1. regenerates glutathione -> allows NAPQI (toxic metabolite) to be cleared
  2. donates sulfhydryl groups -> increases amt of acetaminophen that can be metabolized
    * Normally Acetaminophen is 90% metabolized by sulfation and glucuronide conjugation. 10% turns into NAPQI (via CP450 system, toxic, requires glutathione to be cleared). In overdose, NAPQI increases -> centrilobular necrosis.*

0. Step Ia (28 decks)

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