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Pharmacology > NSAIDS and Paracetemol > Flashcards

NSAIDS and Paracetemol Flashcards

1
Q

Prostaglandins are inflammatory mediators. What are their other functions? 4

A

Prostaglandins have house keeping functions in the :

  1. GIT
  2. Vasculature
  3. Platelets
  4. Kidneys
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2
Q

What do NSAIDs do?

A

NSAIDS inhibit the synthesis of prostaglandins by inhibit cyclooxygenase I and II

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3
Q

Describe the synthesis of prostaglandins

A
  1. Cyclooxygenase converts arachidonic acid into PGG2
  2. PGG2 is converted into PGH2
  3. PGH2 is converted into :

A) PGF2; uterine contraction
B) PGI2: vasodilation, gastric cytoprotection and decreased platelet aggregation
C) Thromboxane A2: increased platelet aggregation
D) PGE2: vasodilation in the kidney and gastric cytoprotection
E) PGD2

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4
Q

Describe the actions of PGF2

A

Uterine contraction

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5
Q

Describe the actions of PGI2 (prostacyclin)

A
  1. Gastric cytoprotection
  2. Vasodilation
  3. Decreased platelet aggregation
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6
Q

Describe the action of thromboxane A2

A

Increased platelet aggregation

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7
Q

Describe the action of PGE2

A
  1. Vasodilation in the kidneys

2. Gastric cytoprotection

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8
Q

Arachidonic acid is broken down by cyclooxygenase I and II. What is the difference.

A
  1. Cyclooxygenase I breaks down arachidonic acid into PG that produce housekeeping functions
  2. Cyclooxygenase II breaks down arachidonic acid into inflammatory PG
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9
Q

Elaborate the function of cyclooxygenase I 7

A
  1. House keeping enzymes
  2. Synthesis of housekeeping prostaglandins
  3. Gastric cytoprotection: mucous formation
  4. Platelet thromboxane A2 thrombus formation
  5. Uterine contraction
  6. GIT contraction
  7. Vasodilation
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10
Q

Elaborate the function of cyclooxygenase II 7

A
  1. Inducible enzyme
  2. Induces: cytokines, growth factors, bacterial lipopolysaccharides
    Functions include:
  3. Increased PG at inflammatory site
  4. House keeping
  5. Renal vasodilation
  6. Synthesis of PGI2
  7. Cardio-protective function
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11
Q

What are the adverse effects of non selective NSAIDs?

A
  1. GIT minor —> major e.g. ulceration, perforation, bleeding
  2. Prolonged bleeding time
  3. Renal vasoconstriction = ischaemia (nephrotoxicity)
  4. Pregnancy: prolonged gestation and bleeding
  5. Hypersensitivity reactions
  6. Tinnitus
  7. Drug interactions
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12
Q

What are the adverse effects of Cox II selective inhibitors? 4

A
  1. Inhibition of PGI2 -> increased TXA2 : increased risk MI and stroke
  2. Contra-indicated in heart failure! Also COX I inhibitors changes in BP -> Na+/H2O retention
  3. Inhibition of PG in renal vasculature -> vasoconstriction-> decrease GFR -> renal ischaemia

There is also a 50% reduction in GIT - ADR

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13
Q

How are NSAIDs classified?

A
  1. Non-selective

2. COX II selective

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14
Q

What are the categories of NSAIDS? 5

A
  1. Salicylates
  2. Acetic acid derivatives
  3. Propionic acid derivatives
  4. Oxicams
  5. Fenamates
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15
Q

Names the drugs in the group salicylates 1

A

Aspirin

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16
Q

Names the drugs in the group acetic acid derivatives 2

A
  1. Diclophenac (Coxib)

2. Indomethacin

17
Q

Names the drugs in the group oxicams 1

A

Piroxicam

18
Q

Names the drugs in the group propionic acid derivatives 2

A
  1. Ibuprofen

2. Naporxen

19
Q

Names the drugs in the group fenamates 1

A

Mefanamic acid

20
Q

What are the coxibs?

A
  1. Diclophenac
  2. Celecoxib
  3. Etoricoxib
21
Q

Describe the MOA of aspirin? 2

A

Aspirin adds an acetyl group to the active site of COX and causes irreversible inhibition of COX I and COX II.

Used to prevent platelet aggregation

22
Q

Describe the Kinetics of Aspirin

A
  1. Oral administration: water soluble so never IV
  2. Absorption: rapid; stomach, small intestine, pH dependent
  3. Binds plasma proteins (50% -90%)
  4. Biotransformation in the liver; glycine conjugation
  5. Urinary excretion; alkaline increased, acidic decreased
  6. T1/2 300mg = 2.4hours
  7. Toxic at T1/2 > 19 hours
23
Q

What are the adverse effects of aspirin at analgesic dose? 6

A
  1. GIT
  2. Heamatological
  3. Hypersensitivity
  4. Renal effects
  5. Children
  6. Pregnancy
24
Q

What are GIT adverse effects of aspirin? 6

A
  1. Epigastric distress
  2. N&V
  3. Occult blood loss
  4. Mucosal irritation
  5. Ulceration
  6. Haemorrhage
25
Q

What are heamatological adverse effects of aspirin? 2

A
  1. Prolonged bleeding time

2. Inhibits platelet aggregation

26
Q

What are hypersensitivity reactions adverse effects of aspirin? 2

A
  1. Angiooedema

2. Rashes

27
Q

What are renal adverse effects of aspirin?

A
  1. Salt and water retention
  2. Aggravate renal dysfunction
  3. Renal ischaemia
  4. Inhibit uric acid excretion
28
Q

Why is aspirin contraindicated in children

A

Underlying infection leads to Reys syndrome

29
Q

Why is aspirin CI in pregnancy?

A
  1. Causes premature closure of the ductus arteriosis

2. Not safe especially in the 3rd trimester

30
Q

What is the MOA of paracetamol? 3

A
  1. Inhibits cox 1 & 2 in the brain
  2. Poor peripheral cox inhibition
  3. No anti-inflammatory properties
31
Q

What are the advantages of using paracetamol? 3

A
  1. No GIT effects
  2. No bleeding
  3. Safe at therapeutic doses
32
Q

What are the kinetics of paracetamol?

A
  1. Rapid absorption

2. Hepatic conjugation

33
Q

What are the adverse effects of paracetamol at therapeutic doses?

A
  1. Skin rash

2. Allergic reactions

34
Q

What are the contraindicated of paracetamol?

A

Hepatic cirrhosis/ liver damage

35
Q

What is the overdosage of paracetamol?

A

> 10g

36
Q

In paracetamol toxicity, what causes death?

A

Hepatic necrosis

  1. GSH depletion causes accumulation of toxic metabolite (N acetyl benzoquinone)
  2. Treat with N acetylcysteine
37
Q

What are the uses of NSAIDs? 8

A
  1. Anti-pyretic
  2. Inflammatory diseases
  3. Pain
  4. Post-operative pain
  5. Closure of ductus arteriosus
  6. Primary dismenorrhea
  7. Prevention - colon cancer
  8. Aspirin - anti-platelet
38
Q

What are the strategies to prevent GIT problems associated with NSAIDS?

A
  1. Always take with food
  2. Combine NSAID with misoprostol (PGE2)
  3. Inhibitor of gastric acid secretin

Pharmacology (13 decks)

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