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pharmaco > nsaids > Flashcards

nsaids Flashcards

1
Q

what do nsaids do?

A

inhibit cox

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2
Q

what do prostacyclin do

A

causes vasodilation, inhibit platelet aggregation

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3
Q

What do prostaglandins do

A

vasodilation, vascular permeability, pain

Has certain roles on GI as well
- reduce gastric acid secretion
- increase mucosal blood flow
- increase mucus secretion
- increase bicarbonate secretion

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4
Q

whatdo thromboxanes do

A

increase platelet aggregation and vasoconstriction

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5
Q

What is aspirin

A

acetylsalicylic acid

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6
Q

What does aspirin do

A

analgesic, anti pyretic, antiplatelet

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7
Q

how does aspirin achieve its analgesic effect

A

block prostaglandin which sensitises the nociceptive fibers to stimulation by other inflammatory mediators

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8
Q

why is there an analgesic ceiling for aspirin

A

because other mediators like bradykinin and leukotriene can also activate and stimulate the nociceptive fibers

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9
Q

What are the adverse effects of aspirin

A

normal dose can cause Gastric intolerance, bleeding, hypersensitivity.

mild dose can cause
- tinnitus, uricosuric, fever dehydration, metabolic acidosis, central hyperventilation respiratory alkalosis

sever can cause coma, vasomotor collapse, hypothrombinaemia, renal and respiratory failure.

Reye’s syndrome- encephalitis and liver, vomitting, personality changes, delirium, listlessness, convulsions.

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10
Q

When is reyes syndrome’s risk increased

A

when taken by children with viral infections

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11
Q

What are some other examples of NSAIDS

A
  1. Naproxen
  2. indomethacin
  3. diclofenac
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12
Q

What are the properties of indomethacin

A

strongly anti-inflammatory due to additional steroid like phospholipase A inhibition

can have CNS effect 15-25% confusion or depression, psychosis, hallucination

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13
Q

What is naproxen used for

A

dysmenorrhoea

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14
Q

What is diclofenac used for

A

used for inflammatory joint disease as they have longer half life in synovial fluid

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15
Q

What are the GI effects when NSAIDS block COX

A
  • dyspepsia, nausea vomiting
  • ulcer formation, potential hemorrhage risk in chronic ulcers
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16
Q

What are the renal effects of NSAIDS

A

inhibiting PGE2 results in sodium retention. Because PGE2 inhibits Na+ reabsorption in the thick ascending limb where 25% of Na is reabsorbed.

inhibiting PGI2 results in suppression of renin and aldosterone secretion, as well as acute renal failure.
- Leading to hyperkalemia. Because aldosterone increase K+ excretion, suppressing it results in K+ retention in the blood

17
Q

Why does inhibiting PGI2 results in supression of aldosterone, but Na+ reabsorption is still increased?

A

Because it prevents reabsorption of only 1-2% at teh DCT, cannot correct for the absorption of 25% in the thick ascending limb

18
Q

What are some other adverse effects of NSAIDS

A
  1. pseudo allergic reactions
  2. bleeding, failure of hemostasis which leads to bleeding
  3. asthma, can trigger bronchospasms
19
Q

why might effects be stronger for aspirin as compared to other nsaids

A

because aspirin is a irreversible cox inhibitor

20
Q

when is cox 2 induced

A

when there is an inflammation

21
Q

What are some examples of COX2

A

parecoxib, parecoxib, etoricoxib

22
Q

why are cox 2 selective inhibitors better

A

they reduce adverse GI effects

23
Q

Where is cox 2 constitutive in

A

CNS, Kidney, female reproductive tract, synovium of joint

24
Q

which of the following do cox-2 inhibitors inhibit?

TXA2, PGI2, PGE2

A

PGI2, PGE2

25
Q

What are some adverse effect of COX-2 inhibition

A
  1. renal toxicity due to the expression of both cox 1 and 2 in the kidney
  2. effect on ovulation, including delayed follicular rupture
  3. premature closure of ductus arteriosus in late pregnancy
  4. impaired wound healing
  5. increased risk of thrombosis
26
Q

what is paracetamol

A

acetaminophen

27
Q

Why is paracetamol good

A

a good analgesic, potent antipyretic, spares the GI tract, relatively safe for pediatric use, few drug drug interaction, likely involve CNS COX inhibition

28
Q

What are the cons of paracetamol

A

weak anti inflammatory,

toxic doses causes nausea vomiting liver damage.

29
Q

What does alcohol do to the metabolism of paracetamol

A

alcohol induces minor pathway of metabolism of paracetamol via CYP2E1 to generate a toxic metabolite. Glutathion converts the toxic metabolite to non toxic metabolite.

Glutathione depleted by paracetamol overdose and alcohol

Glutathion is replenished by N-acetyl cysteine

pharmaco (19 decks)

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