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PDA Block 2 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

What explains the GI complaints associated with aspirin use?

A

Decreased production of PGs that promote mucus secretion

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2
Q

Why does aspirin increase bleeding time

A

TXA2 production in platelet decreases

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3
Q

General properties of NSAIDS

A
  • Anti-inflammatory
  • Anti-pyretic
  • Analgesic
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4
Q

Mechanism of action of all NSAIDS

A

Inhibition of cyclooxygenase

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5
Q

Acetylsalicylic Acid/Aspirin mechanism of action

A

Irreversible inhibitor of Cox 1 and 2

Acetylation of a serine moiety - Serine 230

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6
Q

Why doesn’t protein synthesis occur in both Endothelial cells AND platelets

A

Platelets have no nucleus - once inhibited, cannot create more protein

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7
Q

Aspirin

Absorption:

Distribution:

A

Absorption: Oral absorption

  • Rapidly absorbed from stomach and small intestine
  • limited by dissolution rate (chewing increases)
  • Buffered (substances which neutralize acid) vs. enteric coated (dissolves in intestines)

Distribution:

  • Highly bound to plasma proteins
  • Crosses BBB and placental barrier
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8
Q

Aspirin Metabolism

A

Renal Elimination

Plasma half life is dose-dependent

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9
Q

Unique effects specific to Aspirin/Salicylates

A

Uric Acid Excretion

CNS

Respiration

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10
Q

Uricosuric Effects

A
  • Any agent that increases rate of excretion of uric acid
  • Uptake of uric acid from renal tubules via a transporter that acts as an anion exchanger
  • Uriosuric agents compete with the urate transporter
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11
Q

What is the dose dependent Uricosuric effect of Aspirin?

A

Low doses - decrease uric acid exretion

  • Secretory component for urate sensitive to low concentrations of salicylates

Large doses - Increase uric acid excretion

  • Normal mechanism to block reabsorption via interaction with transpoter (OAT)
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12
Q

CNS effects of high doses of Salicylates (Toxicity)

A
  • Stimulation followed by depression
  • Tinnitus, high tone deafness, confusion, dizziness, delirium, psychosis, coma
  • Nausea and vomiting
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13
Q

_________ are a major limitation to long term therapy with NSAIDs

A

GI side effects

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14
Q

PGs and their function in the GI

A
  • Inhibit acid secretion by the stomach
  • Promote secretion of cytoprotective mucus in the intestine
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15
Q

NSAID GI Side Effects

A

Block the production of cytoprotective PGs

  • GI ulceration and irritation
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16
Q

NSAIDs and Platelets

A
  • All NSAIDs increase bleeding time by inhibiting platelet TXA2
  • Platelets lack nucleus so new COX only with new platelets since ASA irreversible inhibition of COX
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17
Q

Aspirin Hypersensitivity

A

Blocking COX forces arachidonic acid to follow other pathways leading to products which promote allergy, bronchoconstriction. inflammation and mucus production

  • Treated as analphylactic shock (epinephrine)
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18
Q

NSAID renal side effects

A
  • Decrease renal blood flow
  • Promote salt and water retention
  • Effects more prominant in individuals dependent on vasodilatory PGs
    • Elderly
19
Q

NSAIDs and pregnancy

A
  • Prolongation of gestation
  • Prolonged labor
  • Increased risk of postpartum hemorrhage
  • Intrauterine closure of the Patent Ductus Arteriosus
    • NSAIDS still used
20
Q

Dose needed for Salicylate poisoning

Asprin:

Methyl Salicylate:

A

Aspirin: dose 10 to 30 grams

Methyl Salicylate: dose of 4.7 grams in children

21
Q

Aspirin Half Life During Over Dose

A

15-30 hours

22
Q

Reye’s Syndrome

A
  • Specific to aspirin
  • Most often in children (6-11)
  • Acute encephalopathy; Liver degeneration
  • Often follows a viral illness
  • Mechanism unknown (Mitochondrial damage?)
23
Q

Drug Interactions for NSAIDs

A
  1. Alcohol
  2. NSAIDS
  3. Steroids
  4. Anticoagulants
  5. Methotrexate
24
Q

NSAID therapeutic uses:

  • Low Dose:
  • Intermediate Dose:
  • High Dose:
A

Low Dose (80 mg/day): CV disease

Intermediate Dose (325 mg to 1g/day): Low intensity pain/fever

High Dose (5-8 grams/day): Chronic inflammatory disease/ rheumatoid arthritis

25
Q

Side Effects Associated with all Non-Selective NSAIDs

A
  • GI irritation
  • Inhibition of platelet aggregation/ bleeding
  • Decrease in RBF in patients dependent on vasodilatory PGs
  • Hypersensitivity
26
Q

Propionic Derivatives

A
  1. Ibuprofen
  2. Naproxen
27
Q

Indomethacin

Function:

Administration:

Therapeutic Uses:

Side Effects:

A

Function: Reversible inhibition of COX1 and COX2

Administration: Both oral and IV

Therapeutic Uses: Gout; preterm labor; close PDA

Side Effects: Severe frontal headache

  • Better tolerated if given at night
28
Q

Ketorolac

Function:

Administration:

Therapeutic Uses:

Side Effects:

A

Function: Reversible inhibitor of COX1 and COX2

Administration: Oral, IV, and IM administration

Therapeutic Uses: Used as alternative for opioid analgesics in the treatment of post-operative pain

Side Effects: Possibility of serious adverse GI, renal, bleeding, and hypersensitivity

29
Q

Piroxicam

Metabolism:

Administration (per day):

Therapeutic Uses:

A

Metabolism: Metabolized by CYP2C9 (extremetly long t½)

Administration (per day): Oral administration/ once a day

Therapeutic Uses: Symptomatic treatment of acute and chronic rheumatoid arthritis and osteoarthritis

30
Q

Nabumetone (pro-drug)

Administration (per day):

Function:

Therapeutic Use:

A

Administration (per day): Oral administration/ once a day

Function: Active metabolite that may be more COX2 specific

Therapeutic Use: Management of osteoarthritis and rheumatoid arthritis

31
Q

Sulfasalazine - Mechanism of Action

A
  • Effect is independent of COX inhibition
  • Inhibition of cytokine production
  • Inhibition of lipoxygenase
  • Free radical scavenger
32
Q

Sulfasalazine

Pharmacokinetics:

Pharmacological effects:

Adverse effects:

Therapeutic Uses:

A

Pharmacokinetics: Azo bond prevents absorption in upper GI tract

Pharmacological effects: Local effect in GI to inhibit inflammation

Adverse effects: Occur in high % of patients (sulfa moiety)

Therapeutic Uses: Ulcerative colitis; Rheumatoid arthritis

33
Q

Benefit of developing COX2 specific inhibitors

A

If only block COX2, can treat inflammation without risk of GI side effects

34
Q

What does Celecoxib (Celebrex) inhibit?

A

COX-2 selectively

35
Q

Celecoxib mechanism of action

A
  • Binds tightly to a distinct hydrophilic side pocket region of COX-2
    • Close proximity to COX2 binding site
  • COX 2 specific because this site is not present in COX1
36
Q

Celecoxib

Administration:

Absorption:

Metabolism:

A

Administration: Oral administration

Absorption: Highly bound to plasma proteins

Metabolism: Metabolized via CYP2C9 to inactive metabolites

37
Q

Celecoxib

Major adverse effects:

Major Contraindications:

A

Major adverse effects: Increase risk of GI irritation, ulceration, bleeding

Major Contraindications: History of GI bleeding; deficiency of CYP2C9

38
Q

Celecoxib Therapeutic Uses

A
  • Signs/symptoms of rheumatoid arthritis and osetoarthritis
  • Primary dysmenorrhea
  • Acute pain
  • Colorectal polyps
39
Q

Acetaminophen Mechanism of Action

A

Not fully understood

No affinity for active site of COX (may be selective for brain COX)

May prevent reduction of COX to peroxidase form

  • inhibition by acetaminophen would be more effective under reducing conditions of low peroxide concentration
  • High levels of peroxide (inflammatory sites) are resistant to the action of acetaminophen
40
Q

Acetaminophen

Administration:

Metabolism:

Excretion:

A

Administration: Oral administration

Metabolism: Partially by liver microsomal system

  • CYP2E1, CYP1A2, CYP3A4 - half life is 2 hours
  • Mainly undergoes glucoronidation and sulfation

Excretion: Renal excretion

41
Q

Acetaminophen: Toxicity

A
  • Well tolerated at normal doses
  • Little to no GI issues
  • Most serious is hepatic toxicity
42
Q

Hepatic Toxicity with Acetaminophen

Symptoms?

Management?

A
  • Symptoms
    • Liver injury - elevated liver enzymes
    • Severe cases: liver failure; death
  • Management
    • N-Acetylcysteine (replenishes gluathione stores)
      • Earlier is better < 36 hours
43
Q

Role of alcohol in acetaminophen toxicity

A
  • Alcohol induces the P450 involved in production of toxic metabolite
  • Alcohol depletes glutathione
44
Q

Therapeutic use of Acetaminophen

A
  1. Acute pain and fever
  2. No anti inflammatory effects

PDA Block 2 (15 decks)

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