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Flashcards in MSK Pharm from FA Deck (47):
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 (

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)

31

Acetaminophen: antidote to an OD?

N-acetylcysteine

mech: regenerates glutathione in the liver

32

Bisphosphonates (alendronate, -dronates): mech?

inhibit osteoclast activity

pyrophosphate analogs; bind hydroxyapatite in bone, thus inhibiting osteoclasts

33

Bisphosphonates (alendronate, -dronates): use?

Osteoporosis

hypercalcemia

Paget disease of bone

34

Bisphosphonates (alendronate, -dronates): tox?

-Corrosive esophagitis (ie pill esophagitis; take water w pill and don't lie down for 30 min)

-Osteonecrosis of the jaw

35

Name 3 preventive gout drugs.

generally what is their mech?

Allopurinol, Febuxostat, Probenecid

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

36

Allopurinol, Febuxostat: mech?

(gout drugs)

Inhibit xanthine oxidase

-> less uric acid in blood

37

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

1. decreases the destruction of azathioprine and 6-MP (which are normally degraded by xanthine oxidase) 

2. prevents urate nephropathy from tumor lysis

38

what do we NOT give to pts with chronic gout?

Salicylates (aspirin)

they decrease clearance of uric acid

39

Probenecid: mech?

(gout drug)

inhibits reabsorption of uric acid in PCT

(also inhibits secretion of PCN)

40

3 drugs we give for acute gout?

NSAIDs (naproxen, indomethacin)

Glucocorticoids (oral or right into the joint!)

Colchicine

41

Colchicine: mech?

binds/stabilizes tubulin

-> inhibits microtubule polymerization

-> decr leukocyte chemotaxis and degranulation

42

Colchicine: tox?

GI side effects

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

43

3 TNF-a inhibitors?

what are they for, generally?

Etanercept

Infliximab

Adalimumab

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

44

Etanercept, Infliximab, Adalimumab: tox?

-> increased infection since TNF blockers prevents activation of macrophages and destruction of phagocytosed microbes

-> reactivation of latent TB

45

Infliximab, Adalimumab: mech? use?

anti-TNFa monoclonal antibody

PAIR: Psoriasis, Ank spond, IBD, RA

46

Etanercept: mech? use?

decoy TNF receptor

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

Use (PAR): Psoriasis, Ank Spond, RA

47

Antidote for acetaminophen tox?

How does it work (2 mechs)?

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.