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Pharmacology Term 6 > 8.2- NSAIDs > Flashcards

8.2- NSAIDs Flashcards

(51 cards)

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1
Q

What are the main therapeutic effects of NSAIDs?

Physiologically name 2 actions of NSAIDs

A
  • analgesia
  • anti-inflammation
  • antipyresis in fever
  • antiplatelet
  • vasoconstrictor
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2
Q

How is arachidonic acid produced?

A
  • Phospholipase A2 is needed to produce arachidonic acid from phospholipid in the cell membrane
  • acid is the biggest pro-inflammatory mediator in the body
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3
Q

What is the action of Cyclo-oxygenase?

A
  • Cyclo-oxygenase is produced from Arachidonic acid
  • produces PGH2 which produces prostaglandins and thromboxane
  • Thromboxane causes platelet proliferation
  • Prostaglandins act on endothelium
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4
Q

What is another general group of arachidonic acid metabolites?

A

LIPOXYGENASE

5- HPETE

produces leukotrienes

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5
Q

How do inflammatory mediators cause pain?

A

activate the nociceptors on Adelta and C fibres resulting in pain and sensitisation

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6
Q

Where are PGE2 released? ( prostaglandins)

A
  • brain
  • kidney
  • smooth muscle
  • Platelets
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7
Q

Where are prostglandins PGD2 used?

A
  • mast cells
  • airways
  • inflammation
  • pain
  • allergic reactions
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8
Q

How do NSAIDs act on COX2?

A

COX-2 inhibitors

therefore no prostaglandin production in endothelium

no thromboxane production—> no platelets

reduced pain

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9
Q

What are prostaglandins?

A
  • Arachidonic acid metabolits
  • produced by almost all nucleated cells
  • inflammation, immune response, muscle constriction and relaxation
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10
Q

Describe the molecular structure and pharma of prostaglandins

A
  • short half life
  • autocrine and paracrine
  • lipophilic
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11
Q

Where are PGF2alpha and PGE2 used?

A

in obstetrics to soften and shorten the cervix for pre-induction cervical ripening

- PGF2 acts on uterus, eye and smooth muscle

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12
Q

Describe the types of NSAIDs

A

NSAIDs act through inhibition of the two isoforms of cyclooxygenase ( COX) ; COX1 and COX2

  1. Non-selective NSAIDs; act on both COX1 and COX2
  2. Specific COX-2-inhibitors; act on COX-2 enzymes only
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13
Q

Describe COX 1

A
  • normal constituent in the body for homeostasis
  • continuously produced in
  1. Gastric mucosa- gastric cytoprotection
  2. Kindey-sodium and water balance/renal perfusion
  3. Platelets for aggregation
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14
Q

Describe COX2

A
  • INDUCED in presence of injury and inflammation, in inflammatory cells, producing the inflammatory mediators

also a normal constituent in kidney,brain, endothelium, ovary and uterus

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15
Q

Name one for each:

a) Non-selective NSAID
b) Semi-selective NSAID
c) COX-2 inhibitor

A

a) Aspirin, ibuprofen
b) Diclofenac
c) Celecoxib

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16
Q

What are the potential complications of the use of NSAIDs?

A
  • Prostaglandins normally MAINTAIN renal blood flow by
  • INDUCING VASODILATION in afferent arterioles

BUT

  • NSAIDs inhibit prostaglandin production–> harmful hypoperfusion of kidneys and reduced GFR
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17
Q

How is PGE2 affected by COX inhibitors?

A
  • PGE2 is involved in the protection of gastric mucosa; inhibits acid secretion and stimulates mucosal production
  • PGE2 INHIBITION by COX inhibitors will
  • increase mucosal permeability
  • decrease mucosal blood flow and protection

can damage stomach, ulceration, haemorrhage, perforation ( in high doses)

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18
Q

Give an example of :

a) Selective COX1 Inhibitor
b) Non-selective COX inhibitor
c) Selective COX 2 inhibitor

A

a) Aspirin
b) Ibuprofen, Naproxen
c) Diclofenac

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19
Q

What are some risk factors for GI adverse effects of NSAIDs? (5)

A
  • age>65
  • history of GI bleed or ulcer
  • concurrent use of drugs that increase risk of GI adverse events; steroids
  • Heavy smoking/ alcohol use
  • prolonged NSAID use
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20
Q

What are some highly protein bound drugs that can interfere with NSAIDs?

A
  • sulphonylurea ( increased can cause HYPOGLYCAEMIA)
  • warfarin (displaced by aspirin for plasma protein binding–> therefore increased active free conc of Warfarin; INCREASED BLEEDING
  • Methotrexate
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21
Q

What 3 drugs make up the Triple Whammy?

Study These Flashcards
A

concurrent used of :

  1. ACE inhibitor
  2. NSAID
  3. Diuretic
22
Q

Explain the dangers of each drug in the Triple Whammy

Study These Flashcards
A
  • ACEi: decrease glomerular filtration by causing vasodilation of efferent renal arteriole
  • NSAIDs; block COX-2–> prevent prostacyclin synthesis; causing afferent arteriolar constriction
  • Diuretics; contribute to AKI by causing hypovolaemia
23
Q

What do you do if the triple whammy of meds cannot be avoided ie it is necessary?

Study These Flashcards
A
  • baseline testing of serum creatinine and electrolytes
  • patients should be advised to maintain adequate fluid intake

If triply whammy side effects, develop, main goals are

  • Restoration of fluid balance
  • withdrawal of nephrotoxic medicines
24
Q

Give a side effect of ns-NSAID in asthma patients

Study These Flashcards
A
  • non-specific NSAIDs can cause bronchoconstriction in sensitive asthmatic patients
    *
25
Can NSAIDs treat gout?
* yes * they inhibit the phagocytosis of urate crystals
26
Name 5 contraindications for the use of NSAIDs
* Pregnancy 3rd trimester * Hypertensive * Renal and liver disease * Asthma * Stomach ulcer
27
How do NSAIDs cause side effects?
* NSAIDs competitively block COX1 and COX2 therefore inhibiting prostaglandin synthesis * directly irritate GI tract---\> increase bleeding time ( inhibit thromboxane A2) * cause a renal glomerular vasoconstriction ( prostaglandin inhibition)
28
Give an example of: a) A protein pump inhibitor b) Histamine antagonist
a) Omeprazole b) Ranitidine
29
Give some side effects of Mefenamic acid
* acute pain including dysmenorrhoea * menorrhagia
30
Describe the pharmacology of paracetamol
* inhibits COX1 and COX2 through metabolism by peroxidase function of these isoenzymes * inhibits COX3 predominantly in the brain---\> this inhibition of prostaglandin synthesis in the CNS---\> produces its antipyretic and analgesic effect gets metabolised in liver--\> to glucoronide and sulpjaye conjugates that are then excreted renally.
31
Describe the absorption of paracetamol
* time taken to reach maximum plasma concentration (Tmax) is 15-30 minutes * well tolerated when taken orally * On oral administraton, it is absrobed from the intestine (70%), stomach and colon ( 30%) * rate of absorption is rapid and depends on the dose
32
Describe the elimination of paracetamol
paracetamol is metabolised in the liver and only 2-5% is excreted unchanged
33
What are the indications for paracetamol use?
* analgesic drug for ***mild to moderate pain*** * _First line treatment for chronic pain conditions_ e.g. *osteoarthritis, back pain*
34
Name 2 combos/ routes for paracetamol
* Paracetamol + Codeine co-codamol * Paracetamol + dihydrocodeine co-dydramo
35
What are the hepatic and renal cautions for use of paracetamol?
* if Liver impairment, use w caution or omit as it is metabolised in the liver * in patients w renal impairment, reduce dose of paracetamol
36
What are the cautions of paracetamol?
* alcohol dependency/ liver disease * malnutrition * chronic dehydration * body weight \< 50 kg * Use of liver enyme (CYP450) inducing drugs e.g. Rifampicin, carbamazepine, phenytoin * increasing age/ frailty
37
Why is paracetamol use cautioned in older people?
* with increasing age and frailty, there is a reduction in clearance * elderly people hvae comorbidities and polypharmacy--\> can increase risk of inadvertent paracetamol toxicity and overdose
38
Describe the overdose of paracetamol
* saturation of Phase II paracetamol pathway ( normal/ zero order) bc enzymes are saturated * drug is INSTEAD metabolised via phase I CYP450 * NAPQI intermediate is conjugated with glutathione but if glutathione reserves are depleted due to excess dose of paracetamol * Therefore the reactive intermediate (NAPQI) will exert its toxic effect
39
Give signs of paracetamol overdose
* nausea and vomiting ( but normally none) LATER FEATURES: 12-36 hrs; abdominal pain _24+ hrs;_ loin pain, haematuria and proteinuria=signs of renal failure _2-3 days;_ right subcostal pain, **vomiting and jaundice after 2-3 days are features of Hepatic Necrosis**
40
What is defined as a paracetamol overdose? How would you resolve it?
* **Single doses\> 10g ( ie 20 tablets)** potentially fatal to thsoe with **compromised** hepatic function or alcoholics * ANTIDOTE: **N-acetylcysteine (NAC) for paracetamol poisoning---\> most effective when administered within 8-10 hrs after ingestion**
41
Describe the pharmacokinetics of aspirin
- irreversibly inhibits COX enzymes and blocks the production of thromboxane - half life is less than 30 mins; rapidly hydrolysed in plasma to salicylate - absorbed from stomach - converted to salicylate acid, gut liver and plasma - 80-85% is bound to plasma proteins and crosses placenta and CSF
42
How exactly does aspirin work?
- TXA2 is synthesized in platelets - PGI2 is synthesixed in vascular endothelium When aspirin inhibits COX, the platelets cannot regenerate TXA2. The vascular endothelium, however, can synthesise PGI2.This creates a relative excess of PGI2 so inhibiting platelet aggregation.
43
How long does aspirin effect on platelets last if only given in a single dose?
7-10 days then a new cohort of platelets is produced
44
What are the respiratory effects of aspirin?
Direct Stimulation of respiratory centre---\> Hyperventilation (occurs due to uncoupling If phosphorylation ↑ CO2 in Overdose this is the cause of death – Resp. Alkalosis – Renal Compensation – ↓BP, Resp Acidosis + Metabolic Acidosis
45
What are the metabolic effects of aspirin?
* Increased Cellular Metabolism * Increased Utilization of glucose reducing Blood sugar
46
What are the most common signs of aspirin overdose?
* Hyperventilation * Respiratory alkalosis * Metabolic acidosis after resp alkalosis--\> increased anion gap bc of 1. accumulation of intracellular lactate 2. excretion of bicarbonate by kidney to compensate for resp alkalosis
47
Name some mild signs of aspirin overdose
* Nausea and vomiting • Tinnitus * Deafness * lethargy or dizziness.
48
Name 4 moderate to severe signs of aspirin overdose
* dehydration * sweating * restlessness * warm extremities
49
What is Reye syndrome?
caused by using aspirin to treat a viral condition in children/ teenagers w an underlying fatty acid oxidation disorder ## Footnote Children 4-12yrs • Presents with Encephalopathy & Liver disease • Diagnosis based on History and presentation • Medical Emergency - NO ASPIRIN FOR CHILDREN
50
Compare and contrast aspirin with Paracetamol
ASPIRIN: - Irreversible inhibitor of COX1 and COX2 - 70% absorbed from upper GI - metabolised by esterases in gut wall and liver - renal excretion PARACETAMOL: - selective inhibitor of COX3 in CNS - upper GI 70-90% absorption - metabolised in liver - renal excretion
51
Give 3 toxic effects of aspirin and 3 of paracetamol
Aspirin: 1. Reyes syndrome in children 2. Hepatic/renal impairment 3. GI upset PARACETAMOL: 1. Thrombocytopenia 2. Liver necrosis 3. GI upset

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