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Y2 Pharmaco > NSAIDs (I & II) > Flashcards

NSAIDs (I & II) Flashcards

1
Q

Pain is..

A

The unpleasant sensory and emotional experience associated w actual or potential TISSUE DAMAGE.

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2
Q

NSAIDs inhibit..

A

COX enzymes, thus inhibiting prostaglandin pdn (thus, less potent than steroids)

Steroids inhibit phospholipase A2 (more potent)

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3
Q

Isomerases of Prostanoids:

A
  1. Prostacyclin (PGI2)
  2. Prostaglandins (PGE2)
  3. Thromboxanes (TXA2)
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4
Q

Steroids inhibit..

A

Phospholipase A2

  • inhibits process higher up
  • thus, inhibiting formation of all eicosanoids
  • in long term, it will suppress immune response
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5
Q

Uses of Aspirin

A
  1. Anti-inflammatory
  2. Analgesic (pain)
  3. Anti-pyretic (fever)
  4. Anti-platelet
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6
Q

Explain why there is an ‘analgesic ceiling’.

A

Tissue injury-> 1. Bradykinins 2. Leukotrienes 3. Prostaglandins

NSAIDs reduces sensitization by inhibiting prostaglandins pdn. In severe pain however, there will still be high levels of 1. & 2. that still sensitize the nociceptors to pain.

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7
Q

Some typical NSAIDs are..

A
  1. Naproxen
  2. Indomethacin
  3. Diclofenac
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8
Q

Aspirin is linked to (what syndrome)

A

Reye’s Syndrome

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9
Q

Reye’s syndrome occurs in ..

A

Occurs most commonly in children. Increased risk if aspirin is taken by children with viral infections.

  • chickenpox patient(child or young adult) who takes aspirin ends up w Reye’s syndrome (cuz liver gets affected by both the VZV n aspirin => buildup of ammonia in body)
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10
Q

What is Reye’s syndrome?

A
  • very rare but life-threatening condition mostly IN CHILDREN
  • swelling of brain & liver
  • increased risk if aspirin is taken by children w viral infections (e.g. chicken pox or flu)
  • symptoms: vomiting, personality changes, listlessness etc etc

Caused by Aspirin in children
(thats why aspirin is no longer avail in paediatric doses)

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11
Q

COX 1 typically produces:

A

TXA2 (thromboxane)

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12
Q

COX 2 typically produces:

A

PGI2 (prostacyclins) & PGE2 (classical prostaglandins)

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13
Q

TXA2 (thromboxanes) effects on CVS:

A

Vasoconstriction
Platelet aggregation

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14
Q

PGI2 (prostacyclin) effect on CVS

A

Vasodilation
Inhibits platelet aggregation

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15
Q

How is Aspirin anti-pyretic?

A

Physiologic rxn - COX induces hypothalamus to release PGE2 (prostaglandins)=> induces fever=> body is trying to kill virus/bacteria by increasing temp

  • NSAIDs block PGE2 production => reduce fever if too high
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16
Q

How is Aspirin Anti-inflammatory?

A
  • blocks pdn of PGI2 n PGE2 (prostacyclin & prostaglandin)
    Thus,
  • block vasodilation (PGI2) (less heating, redness n swelling)
  • blocks increased vascular permeability (PGE2) (less swelling)
  • blocks pain associated w inflammation (PGE2)
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17
Q

Effect of PGE2 (mostly)

A

Vascular permeability
Pain

18
Q

How is Aspirin analgesic?

A

Physiologic - prostaglandins sensitize the nociceptive fibres to stimulation by other inflammatory mediators

  • NSAIDs block pdn of prostaglandins (PGE2)
  • it only blocks sensitization, not direct nociceptive activation (therefore there is an analgesic ceiling, aka insufficient for severe pain)
  • typical NSAIDs also have additional analgesic actions in the CNS
19
Q

How is Aspirin Anti-platelet (stop blood from clotting)?

A
  1. TXA2
    - pdn of TXA2 via COX BY PLATELETS =>promotes platelet aggregation
    - but COX is inhibited in the platelets = no TXA2 formation
    - pdn of TXA2 can only be restored by formation of new platelets (1-2 weeks)
  2. PGI2
    - pdn of PGI2 by endothelial cells=> inhibits platelet aggregation
    - but COX inhibited in the endothelial cells = no PGI2 pdn
    - BUT PGI2 CAN be restored by synthesis of new COX enzyme (takes a few hours)

TRICKY BUT IMPT PART:
PGI2 is restored in a few hours but TXA2 is gone. Aka inhibition of platelet aggregation»»» platelet aggregation

MUST KNOW: THAT ASPIRIN IS SUPER ANTIPLATELET!!!

20
Q

Facts about Naproxen:
- more effective in _______
- long half life of ______
- often used for __________

A
  • more effective in women
  • long half life 12-14h
  • often used for dysmenorrhea (menstrual cramps)
  • issa typical NSAID
21
Q

Facts about Indomethacin:
- additional steroid-like _________________ inhibition => strongly ___________
- BUT adverse CNS effects: __________________________________

A
  • additional steroid-life phospholipase A2 inhibition => strongly anti-inflammatory
  • BUT adverse CNS effects: confusion, depression, psychosis, hallucinations
  • issa typical NSAID
22
Q

Facts about Diclofenac:
- short ______ half life (<2h) => _______ risk
- longer half life in ______________=> useful for ___________
- __________ administration

A
  • short plasma half life (<2h) => low GI risk
  • longer half life in synovial fluid => useful in inflammatory joint disease
  • topical/oral administration
23
Q

Other than for pain, inflammation & fever, Aspirin is also prescribed for….

A
  • prescribed at low doses as a ‘blood thinner’ for those at risk of cardiovascular disease
24
Q

Paracetamol has taken over _______ as a ________due to adverse effects.

A

Paracetamol has taken over Aspirin as a ‘pain killer’

25
Q

The dose-dependent effects of Aspirin can be classified into 2 categories, _______ & ________. Name some notable effects.

A
  1. COX inhibition (low dose therapeutic effects)
    - analgesic
    - anti-pyretic
    - anti-inflammatory
    - anti-platelet
    - gastric intolerance (-ve)
  2. Salicylate toxicity (high does toxic effects)
    - tinnitus
    - renal & respiratory failure
    - metabolic n respiratory acidosis
26
Q

Physiologic effect of Prostaglandins on the GIT:

A
  1. Reduce gastric acid secretions
  2. Increase mucosal blood flow /in mucosa
  3. Increase secretion of mucus
  4. Increase secretion of bicarbonate

Basically, protect the stomach
- COX 1 (constitutive) produces PGE2

Secretions, Blood flow, Mucus, Bicarbonate

27
Q

If PGE2 pdn is inhibited, what happens? (-ve effects)

A
  • dyspepsia (symptoms are acid reflux, heartburn), nausea, vomiting
  • ulcer formation & potential haemorrhage risk in chronic users

Basically, protective mech is gone, excess acid happens, stomach attacked

28
Q

Adverse effects of NSAIDs on RENAL system:

A
  • inhibition of COX= inhibition of both PGE2 n PGI2 pdn

Inhibition of PGE2 results in :
1. Sodium retention
2. Water retention
3. Peripheral oedema
4. Hypertension

Clinical implications:
- must check if patient alr has hypertension, udw to worsen their existing hypertension

Inhibition of PGI2 results in :
1. Suppression of renin n aldosterone reaction (less sodium retention)
2. Hyperkalemia
3. Acute renal failure

^ might seem contradictory that 1. Suppression of renin n aldosterone may recover 2. Sodium retention
- but nope, the processes happen at diff parts of the renal tubule
- inhibition of Na+ occurs at ascending limb (PGE2) (25% resorbed)
- aldosterone/renin suppression occurs at CD (PGI2) (1-2% decreased reabsorption)
- overall effect: NSAID causes Na+ retention (water retention)

29
Q

Renal adverse effects due to inhibition of PGI2 (prostacyclin):

A

No more prostacyclin means:
1. Suppression of renin & aldosterone secretion
- effects occur in CD
- only 1-2% reduction in reabsorption of Na+
2. Hyperkalemia
3. Acute renal failure

Think ‘cyclin’ the more complex sounding one to ‘glandin’ aka all the effects more secondary.

30
Q

Renal adverse effects due to inhibition of PGE2 (prostaglandin):

A

No more PGE2 (prostaglandin) means:
1. Sodium retention
- occurs in thick ascending limb (TAL)
- 25% increase in reabsorption of Na+ back into blood
2. Water retention
3. Peripheral oedema
4. Hypertension

Urm, think ‘glandin’ -> gland -> gland of sodium water oedema hypertension shit
- more primary factor

31
Q

Name some OTHER adverse effects of typical NSAIDs:

A
  1. Pseudo-allergic reaction (skin rashes, swelling, itching)
  2. Asthma (can trigger bronchospasms in susceptible asthmatics)
  3. Bleeding (failure of haemostasis, bruising)

Note: effects elicited by Aspirin might be stronger than other NSAIDs cuz it is an IRREVERSIBLE COX inhibitor

32
Q

Why is Aspirin a unique NSAID?

A

Irreversible COX inhibitor

33
Q

Why do NSAIDs elicit an unwanted Asthma & Pseudo-allergic reaction in some ppl:

A
  • inhibition of COX=> more arachidonic acid gets converted to leukotrienes by LOX
  • excess leukotrienes => bronchospasms in asthmatics & allergic reaction-like symptoms
34
Q

All NSAIDs are _______ inhibitors!

A

All NSAIDs are COX-2 inhibitors!
- just different in what they are selective for

35
Q

NSAIDs are contraindicated in __________ of pregnancy.

A

Strongly contraindicated in third trimester of pregnancy.

  • it causes premature closure of ductus arteriosus (fetal lung bypass) in late pregnancy
  • can
36
Q

COX 2 effects on ovulation:

A
  • causes delayed follicular rupture
  • makes it harder to become pregnant, though not impossible
37
Q

Aspirin is far more ___________ than other selective COX1 COX2 inhibitor NSAIDs cuz of its ___________.

A

Aspirin is far more anti-platelet than other selective COX1 COX2 inhibitor NSAIDs cuz of its irreversible binding

38
Q

COX2 inhibitors _________ wound healing, may _________ ulcers. So how?

A

COX2 inhibitors impair wound healing, may exacerbate ulcers.
Clinical implications:
- patients w existing ulcers
- post-surgical painkillers/analgesia

Patients who were on 1st gen NSAIDs n developed ulcers did not improve aft switching to coxibs(2nd gen cox2 inhibitors)
- need to stop all NSAIDs-> let patient recover, then can start coxibs

39
Q

Why does selective COX2 inhibition increase risk of thrombosis?

A
  • relative increase in TXA2 => favours platelet aggregation => thrombosis
  • due to inhibition of COX2 => PGI2 downregulated
40
Q

Advantages of Paracetamol:

A

Paracetamol - CNS selective COX inhibitor

  1. Good analgesic
  2. Potent antipyretic
  3. Spares GIT
  4. Few & uncommon side effects
  5. Few drug-drug interactions
41
Q

Disadvantages of Paracetamol:

A

Paracetamol - CNS selective COX inhibitor

  1. Weak anti-inflammatory => does not block COX in periphery involved in inflammatory response
  2. Allergic skin rxns
  3. Toxic doses => nausea, vomiting, liver damage
    - hepatotoxicity exacerbated by overdose/chronic alcohol use
    - alcohol induces CYP2E1 & deplete glutathione => accumulate toxic metabolite
    - can replenish glutathione by NAC (N-acetyl-cysteine)

Y2 Pharmaco (22 decks)

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