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Flashcards in MSK Pharm from FA Deck (47)
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1

Lipoxygenase pathway yields what (generally)?

Leukotrienes

(remember Lipoxygenase and Cycloxygenases both come from Arachidonic acid)

2

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

LTB4: attracts neutrophils ("neutrophils arrive B4 others"

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

3

what products come from the Cycloxygenase pathway?

Prostacyclin, Prostaglandins, Thromboxane

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

4

PGI2: what is it/what does it do?

what cell/tissue releases it?

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.

5

PGE2, PGF2a: what do they do?

Increase uterine tone

decrease bronchial tone

6

TXA2: what does it do?

what cell/tissue releases it?

(Thromboxane)

incr platelet aggregation, incr vasoconstriction, incr bronchial tone

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

7

Aspirin: mech?

Irreversibly inhibits COX1 and COX2 via covalent acetylation. 

--> decr synthesis of TXA2 and Prostaglandins.

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

8

Aspirin: effect on PT? PTT?

None.

only affects bleeding time.

9

Aspirin: use (3 dose levels)?

Low dose: decr platelet aggregation (<300mg)

Medium dose: anti-fever, analgesic

High dose: anti-inflammatory (>2400mg)

10

Aspirin: tox (adults)?

Gastric ulcers

Tinnitus (CN VIII)

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

Stimulates resp centers -> hyperventilation and resp alkalosis.

11

Aspirin: tox (children)?

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

(rash/vomiting/liver damage)

12

COX 1 preferentially expressed where?

GI tract, platelets

13

COX 1 blockers: general side effects?

GI ulceration, bleeding

14

COX 2 receptors preferentially expressed where?

sites of inflammation

15

advantage to COX 2-specific blockers?

avoid side effects of COX1 (ulceration, bleeding)

16

Class?

ibuprofen, naproxen, aspirin, indomethacin, ketorolac, diclofenac

NSAIDs

17

NSAIDs: mech?

reversibly inhibit COS1 and COX 2.

Block prostaglandin synthesis

exception: aspirin = IRREVERsible block.

18

NSAIDs: use?

anti-fever, analgesic, anti-inflammatory

19

Indomethacin: unique use beyond usual NSAIDs use?

Close PDA

20

NSAIDs: tox?

interstitial nephritis, gastric ulcer, renal ischemia

21

how do NSAIDs cause gastric ulcers?

renal ischemia?

NSAIDs block prostaglandin synth

-->PGs protect gastric mucosa against ulceration

-->PGs vasodilate afferent arteriole

22

Name a COX-2 specific blocker?

celecoxib

23

celecoxib: Mech?

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

Mediates inflammation and pain

does NOT block COX1 -> spares gastric mucosa. 

24

celecoxib: effect on platelet function?

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

25

celecoxib: Use?

Rheumatoid arthritis, osteoarthritis

(esp patients with gastritis or ulcers)

26

celecoxib: tox?

incr risk of thrombosis

sulfa drug: watch out for allergies

27

Acetaminophen: mech?

reversibly inhibits COX, mainly in CNS

inactivated in periphery

28

Acetaminophen: use?

anti-fever

analgesic

NOT anti-inflammatory

29

Acetaminophen: use specific to children?

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

use acetaminophen instead

30

Acetaminophen: tox?

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