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FTCM Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

NSAIDs have what activities?

A

3 A’s:
antipyretic
analgesic
anti-inflammatory

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2
Q

Mechanism of NSAIDs (general)

A

inhibits COX –> inhibition of prostaglandins and thromboxanes

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3
Q

Eicosanoids synthesis:

A

PLA2 receptor makes arachidonic acid which makes:

  1. Cyclooxygenases
    - Prostaglandins
    - Prostacyclin
    - Thromboxane
  2. Lipooxygenases
    - Leukotrienes
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4
Q

COX-1

A
  • involved in tissue homeostasis

- dominant in gastric epithelial cells and main source of protective prostaglandin formation

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5
Q

COX-2

A

major source of eicosanoids in inflammation and cancer

  • kidney and brain
  • endothelial COX-2 primary source of vascular prostacyclin
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6
Q

Anti-inflammatory action of NSAIDs is mainly related to _____

A

inhibition of COX-2

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7
Q

Gastric damage is due to ___

A

inhibition of COX-1

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8
Q

Nonselective COX inhibitors

A

As Dogs I Invented Kissing No Problem (ADIIKNP)

Aspirin
Diclofenac
Ibuprofen
Indomethacin
Ketorolac
Naproxen
Piroxicam
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9
Q

COX-2 selective inhibitors

A

Cool Mom (CM)

Celecoxib
Meloxicam

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10
Q

NSAIDs uses

A
  • pain
  • inflammation
  • arthritis
  • colon cancer*
  • niacin tolerability*
  • closure of ductus arteriosus*
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11
Q

Niacin tolerability and NSAIDs

A

Niacin lowers cholesterol levels –> intense flushing

flushing mediated by PGD2 which can be inhibited with NSAID

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12
Q

AE of NSAIDs

A
  • GI
  • CV
  • Renal
  • NERD (respiratory disease)
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13
Q

GI adverse effects

A

due to:

  • inhibition of COX-1 in gastric epithelial cells
  • ulceration by local irritation of gastric mucosa
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14
Q

How due you treat the gastric damage and gastric uclers caused by NSAIDs?

A
  • misoprostrol
  • proton pump inhibitors
  • H2 blockers
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15
Q

Lowest risk GI AE drug?

A

Celecoxib

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16
Q

Highest risk GI AE drug?

A

Piroxicam

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17
Q

CV AE

A

caused by imbalance of TXA2 and PGI2

  • can lead to vasoconstriction, platelet aggregation, and thrombosis
  • more COX-2 selective NSAIDs = higher risk
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18
Q

TXA2

A

promotes platelet aggregation

vasoconstriction

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19
Q

PGI2

A

inhibits platelet aggregation

vasodilator

20
Q

Highest risk of CV AE drug?

A

Celecoxib

21
Q

Renal AE

A
  • decrease renal blood flow

- analgesic nephropathy

22
Q

Why is a decrease in renal blood flow that detrimental?

A

Pt with CHF, CKD, etc = problem bc PGs are really important in maintaining GFR

ALSO, NSAIDs can elevate BP and cause fluid retention –> worsen kidney function

23
Q

NSAIDS effect on RBF in pt with CHF, CKD, etc.

A

inhibition of PG decreases afferent flow to glomerulus and decreases GFR

24
Q

Chronic interstitial nephritis is cased by___

A

prolonged and excessive use of analgesics

associated with phenacetin

25
Q

COX-2 is active in which organ?

A

Kidney- which can cause renal toxicities

26
Q

NERD symptoms

A
  • angioedema
  • bronchial asthma
  • flushing
  • hypotension
  • shock
27
Q

NERD causes

A

increase leukotrienes by COX inhibition

28
Q

Celecoxib other AE

A

hypersensitivity reactions (like rashes)

29
Q

NSAIDs drug interactions

A
  • ACE inhibitors
  • Diuretics
  • Corticosteroids
  • Warfarin
30
Q

DI with ACEI

A

ACE-I prevent break down of kinins that stimulate PG

31
Q

DI with diuretics

A

effects are reduced by NSAIDs

32
Q

What is the triple whammy?

A

risk of acute kidney injury when ACEI or ARB is combined with diuretic and NSAID

why?
NSAID constrict afferent = reduce GFR
ACEI and ARB dilate efferent = reduce GFR

pt on combination should be monitored for creatine and potassium lvls

33
Q

DI with corticosteroids

A

increase GI ulcers

34
Q

DI with warfarin

A

increased risk of bleeding

35
Q

Contraindications

A
  • Reye’s syndrome
  • children/YA under 20 with fever and viral illness –>
    can use Acetaminophen and Ibuprofen instead
  • pregnancy
36
Q

Aspirin vs other salicylates

A

aspirin irreversibly acetylates while the others are reversible

37
Q

All salicylates

A
  • Aspirin
  • Mg salicylate
  • Na salicylate
  • Salicyl salicylate
38
Q

Aspirin and salicylate actions

A
  • uncouple oxidative phosphorylation –> elevated CO2 and increased respiration –> hyperventilation
  • inhibits TXA2 in platelets = long bleeding time
  • low dose aspirin inhibits COX-1 but not COX-2 so PG synthesis is unaffected
39
Q

High doses of aspirin are used to treat children during?

A

Acute phase of Kawasaki disease

40
Q

Salicylates at high and low doses:

A

high- anti-inflammatory

low- analgesic and antipyretic, also used for cardioprotective effects

41
Q

Aspirin metabolism

A
  • hydrolyzed in tissue and blood
  • low doses can be converted into hydrosoluble conjugates by liver and excreted in kidney
  • half life is 3.5 hours
  • first order kinetics
  • 1g dose or more –> zero order kinetics
42
Q

Aspirin and salicylates AE

A 
epigastric distress
prolonged BT
Reye's syndrome 
NERD
Reduce uric acid secretion at low doses*
Hepatic injury at high doses*
43
Q

Salicylism

A

intoxication

  • headache
  • mental confusion
  • hyperventilation
  • resp alkalosis and metabolic acidosis
44
Q

Acetaminophen

A
  • analgesic and antipyretic

- no anti-inflammatory or antiplatelet effects

45
Q

Acetaminophen uses

A
  • osteoarthritis
  • children
  • pregnancy
  • pain
46
Q

Acetaminophen AE

A

hepatotoxicity- liver failure

administer Acetylcysteine

FTCM Pharm (4 decks)

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