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Flashcards in Pharmacology Deck (36):
1

COX 1

GI
Platelets

2

COX-2

many cells in body
produces inflammation
produce - prostacyclin, prostaglandins and thromboxane

3

lipoxygenase

converts arachidonic acid into leukotrienes

4

prostacyclin (PGI2)

COX-1 product
anti-platelet (decreases platelet aggregation

5

prostaglandins

COX-1 product of arachidonic acid
PGE2 = decreased vascular tone, increased pain, increase uterine tone, increase temp

6

thromboxane (TXA2)

COX-1 dependent product of arachidonic acid
increases platelet aggregation
increased vascular tone
increased bronchial tone

7

leukotrienes

LTB4= neutrophil chemotaxis = attracts neutrophils to site of inflammation
LTC4, LTD4 = bronchoconstriction (act in lung)

8

corticosteroids

inhibit phospholipase A2
inhibit protein synthesis that produces COX enzyme

9

phospholipase A2

converts membrane lipid (phosphatidylinositol) to arachidonic acid

10

products of arachidonic acid

lipoxygenase pathway --> leukotrienes
COX pathway (COX 1 and COX 2) --> prostacyclin (PGI2), prostaglandins (PGE2, PGF2) & thromboxane (TXA2)

11

Zileuton

inhibits lipoxygenase = blocks leukotriene production

12

Zafirlukast
Montelukast

block leukotriene receptors (lung) --> decrease bronchoconstriction
use: asthma

13

NSAIDs

reversibly inhibit COX-1 and COX-2
blocks prostaglandin synthesis

14

gastric ulcer risk with aspirin

COX-1 produces prostaglandins which protect gastric mucosa
aspirin and NSAIDs increase gastric ulcers

15

Reye's syndrome

children treated with aspirin during a viral illness
liver failure
encephalopathy

16

aspirin induced asthma

block prostaglandin production = which normally cause bronchodilation
leukotrienes = cause bronchoconstriction

17

NSAIDs

reversibly block COX-1 and COX-2
decrease prostaglandin and decrease inflammation
use: anti-pyretic, analgesic, anti-inflammatory
SEs: rénal damage (interstitial nephritis, gastric ulcer, renal ischemia)

18

indomethacin

can be used to close patent ductus arterioles in an infant

19

COX-2 inhibitors

Celecoxib
reversibel COX-2 inhibitor = inflammatory cells and vascular endothelium
mediates inflammation and pain, spares COX-1 (helps maintain gastric mucosa), spares platelet function
use: RA & OA (or have gastritis or ulcers)
SEs: increase risk thrombosis, can't be used if sulfa allergy

20

acetaminophen

reversibly inhibits COX (mostly in CNS). inactivated peripherally
use: antipyretic, analgesic, NOT anti-inflammatory. used in children with viral infection instead of aspirin to avoid Reye's syndrome
toxicity: overdose causes hepatic necrosis

21

acetaminophen overdose

metabolite depletes glutathione and forms toxic tissue adducts in liver - toxic free radicals destroys liver cells
antidote = N-acetylcystein = regenerates glutathione

22

glutathione function in the liver

absorbs free radicals
protects hepatocytes

23

aspirin mechanism

irreversible inhibits COX-1 and COX-2 by acetylation
decreased synthesis of thromboxane A1 and prostaglandins
increases bleeding time
no effect on PT and PTT

24

Aspirin clinical use

low dose (<300 mg/day) = decreased platelet aggregation - baby aspirin used to reduce MI risk
moderate dose (300-2400 mg/day) = antipyretic and analgesic
high dose (2400 - 4000 mg/day) = anti-inflammatory

25

Aspirin SEs

gastic ulceration
tinnitus (CN VIII)
with chronic use
acute renal failure, interstitial nephritis, upper GI bleeding
risk Reye's syndrome in children treated with aspirin for viral infection
stimulates respiratory centers - causes hyperventilation and respiratory alkalosis

26

treatment for Gout

colchicine = chronic
NSAIDs = acute (naproxen, indomethacin - treatment of choice)
Allopurinol/probenecid = chronic

27

colchicine

chronic gout treatment
mech: binds to and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation
SEs: GI (esp when given orally)

28

allopurinol

mech: inhibits xanthine oxidase = decreases conversion of xanthine to uric acid
use: gout, lymphoma and leukemia (prevent tumor lysis-associated urate neuropathy)

29

febuxostat

inhibits xanthine oxidase
use: chronic gout treatment

30

allopurinol contraindications

azathioprine (immunosuppressant) and 6-mercaptopurine (normally metabolized by xanthine oxidase --> increases concentrations of toxic drug)
concurrent salicylate use (aspirin) - depresses uric acid clearance

31

probenecid

mech: inhibits reabsorption of uric acid in proximal collecting tubule (also inhibits secretion of penicillin)

32

inhibition of uric acid tubular secretion

diuretics and low-dose salicylates

33

inhibition of uric acid tubular reabsorption

probenecid and high-dose salicylates

34

TNF-alpha inhibitors

Etanercept = fusion protein (receptor for TNF-alpha + IgG1 Fc)
Infliximab/ adalimumab = anti-TNFalpha monoclonal Ab

35

Etanercept

TNF alpha inhibitor
use: RA, psoriasis, ankylosing spondylitis

36

Infliximab
Adalimumab

anti-TNF alpha monoclonal Ab
use: Crohn's disease, RA, ankylosing spondylitis, psoriasis