Exam 2- Steroidal/Non steroidal Anti-inflammatory Drugs

Question 1

COX-1 Actions CONSTITUTIVE

Answer 1

GI: PGs, decrease acid, increase mucous
Platelets: TXA2, pro-aggregatory effect
Kidneys: PGs, increase renal blood flow
Vascular: PGs, vasodilation, TXA2, vaso constriction

Question 2

COX-2 Actions INDUCED

Answer 2

Kidney: PGs, increase flow (volume stress)
Endothelial cells: PGs, vasodilate, anti-aggregation platelets (shear stress)
Uterine smooth muscle: PGs, contractions
Ductus arteriorsus: PGs, maintenance via vasodilation

Question 3

Thromboxanes are from COX-_?

Answer 3

COX-1

Question 4

NSAIDs want to inhibit _____ because it’s _____ and results in ______, _____, and _____. Inhibition of _____ leads to side effects

Answer 4

COX-2
Inducible
Analgesia, antipyretic, anti-inflammatory
COX-1

Question 5

tNSAID inhibition

Answer 5

reversible

COX-1 and COX-2

Question 6

Celecoxib

Answer 6

reversible

COX-2 only

Question 7

Acetaminophen

Answer 7

reversible
CNS COX-2 only
-Therefore not anti-inflammatory, but yes analgesia and antipyretic

Question 8

Asprin

Answer 8

irreversible
COX-1 and COX-2
-Therefore is only “anti-platelet”
-Bleed risk in patients, but anticlotting

Question 9

Dose dependent effects - analgesia

Answer 9

COX-2 at tissue injury

Intermediate doses - prn

Question 10

Dose dependent effects - antipyretic

Answer 10

COX-2 at hypothalamus

Intermediate doses - prn

Question 11

Dose dependent effects - anti-inflammatory

Answer 11

COX-2 at tissue injury

High doses - scheduled due to half-life

Question 12

Dose dependent effects - Antithrombotic

Answer 12

COX-1 in platelets

Low doses - daily (ex. aspirin only)

Question 13

Glucocorticoid action

Answer 13

Block PL-A2 therefore COX-1, COX-2 and LTs

Also specifically block COX-2, but not COX-1

Question 14

tNSAID vs. Acetamenophen

Answer 14

tNSAID: better pain control, inflammation control

Equal antipyretic control, no peripheral side effects with acetamenophen

Question 15

GI Risk vs. CV Risk vs. Renal

Answer 15

GI Risk: COX-1>COX-2, ibuprofen better, more COX-2
CV Risk: COX-2>COX-1, naproxen better, more COX-1
Renal: all bad, avoid NSAIDs in renal compromise

Question 16

Celecoxib risk

Answer 16

COX-2 inhibition
Low GI risk (no COX-1)
Higher CV risk (unsure of mech, same COX-2 effect)
High Renal risk (same COX-2 effect)

Question 17

GC Types

Answer 17

Hydrocortisone
Prednisone
Methyprednisolone
Triamcinolone
Dexamethasone

Question 18

GC Actions and Mech

Answer 18

Anti-inflammatory (GC and IS side effects)
Topical
Salt-retention (MC side effects)
Receptor binding and TF activation (slow onset)

Question 19

Non-topical GC’s

Answer 19

Cortisone
Prednisone
Need to go to liver to be activated

Question 20

Two reasons to taper GC’s

Answer 20

1. Long term- is adrenal suppressed?

2. Disease flare up

Question 21

Cortisol effects

Answer 21

GC
Increased gluconeogenesis (and blood glucose)
Decreased protein synth (AA to glucose)
Increased lipolysis (and FFA)
Pathologic = excess, iatrogenic Cushing’s

Question 22

MC Effects

Answer 22

Increased Na+ reabsorption
Increased BV, BP
Therefore more K+, H+ excretion
Excess: Hypertension, hypokalemia, alkalosis

Question 23

GC with MC side effects

Answer 23

Cortisol/Hydrocortisone

Prednisone

Question 24

GC therapeutic effects

Answer 24

1. Anti-inflammatory
   a. reduce vasodilation
   b. decreased exudate
   c. decrease cell activation
2. Anti-immune
   a. decrease inflammatory/immune mediator synth

Question 25

GC Structure

Answer 25

Cholesterol backbone

Need OH- at 11 carbon

Question 26

Alternate day therapy

Answer 26

Suppress inflammation/immune for 48 hrs

Suppress ACTH for 24 (reduce adrenal atrophy)