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Year 2 Collin > Pharm 17 - NSAIDS > Flashcards

Pharm 17 - NSAIDS Flashcards

1
Q

Use of NSAIDS are associated with deaths involving which systems?

A

GI and CVS

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2
Q

Which 3 properties of NSAIDS make them widely used?

A
  1. Analgesic
  2. Anti-pyretic
  3. Anti-inflammatory
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3
Q

Where is arachidonic acid derived from?

A

Phospholipid membranes

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4
Q

What reaction does COX-1/2 mediate

A

Conversion of Arachidonic acid into prostaglandin H2

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5
Q

NSAIDS inhibit what?

A

COX-1/2 - prevents Prostaglandin and Thromboxane A2 synthesis

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6
Q

Prostanoid receptors have 2 actions,

A
  1. Physiological
  2. Pro-inflammatory (pathological)

There are 10 known prostanoid receptors

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7
Q

PGE2 has 2 downstream mechanisms

A
  1. Ca mobilisation/immobilisation

2. cAMP increase/decrease

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8
Q

Which 4 receptors does PGE2 have?

A

EP1, EP2, EP3, EP4

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9
Q

What are 6 unwanted actions of PGE2

A
  1. Increased pain perception
  2. Increased body temperature
  3. Acute inflammatory response
  4. Immune responses
  5. Tumorigenesis
  6. Inhibition of apoptosis
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10
Q

Why may PGE2 analogues lower pain threshold

A
  1. PG receptors are stimulated

2. Peripheral PG receptor stimulation sensitises the nociceptors

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11
Q

Why might stimulation of PG receptors cause pain?

A
  1. cAMP mediated
  2. P2X3 nociceptors activated
  3. Inflammation causes Epac pathway to be activated and more PGE2 to be produced
  4. More activation of P2X3 nociceptors
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12
Q

What other reasons for pain may there be via PG receptor activation?

A
  1. EP1 /EP4 receptor activation (periphery and spine)
  2. Endocannabinoids (neuromodulators in thalamus, spine and periphery)
  3. Decreased beta-endorphins in the spine
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13
Q

What do NSAIDS do in the spine

A

Increase beta-endorphin in the spine

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14
Q

How does PGE2 have a pyrogenic effect?

A

PGE2 stimulates hypothalamic neurones - stimulates rise in temp

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15
Q

PGE2 role in inflammation is extremely complex

A

y=Y

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16
Q

What are desirable physiological actions of pGE2 and other prostanoids

A
  1. Bronchodilation
  2. Renal salt and water homeostasis
  3. Gastroprotection
  4. Vasoregulation
17
Q

Why should asthmatic patients avoid taking NSAIDS?

A

Because COX inhibition favours leukotriene production - leukotrienes = bronchoconstrictors

18
Q

How can NSAIDS cause renal toxicity

A

PGE2 (& other prostaglandins) increase renal blood flow.

NSAIDS:

  1. Constrict afferent arteriole
  2. Reduce renal artery flow
  3. Reduce GFR
19
Q

What gastroprotective features does PGE2 have?

A
  1. Downregulates HCl secretion

2. PGE2 stimulates mucus and bicarbonate secretion

20
Q

What gastric complication do NSAIDS increase the likelihood of?

A

Gastric ulceration

21
Q

What is the coxib family?

A

NSAIDS that selectively reversibly inhibit COX-2

e.g. Celecoxib (caused fewer ulcers than normal NSAIDS)

22
Q

Ibuprofen selectively inhibits which isoforms of COX?

A

Both - i.e. COX 1 and 2

23
Q

What are the unwanted CVS effects of NSAIDS

A
  1. Vasoconstriction
  2. Salt and water retention
  3. Reduced effect of antihypertensives

can cause:

  1. Hypertension
  2. Stroke
  3. MI
24
Q

Selective COX-2 inhibitors have what problem?

A

Pose higher risk of CVS disease than conventional NSAIDS

25
Q

Which prostaglandin causes vasodilation and decreases platelet aggregation

A

PGI2

26
Q

COX-1 selective NSAIDS increase what risk?

COX-2 selective NSAIDS increase what risk?

A

COX -1 = gastric

COX -2 = CVS

27
Q

How can GI side effects be reduced?

A
  1. Topical application
  2. Minimise use in GI ulceration patients
  3. Treat H pylori if present
  4. Coadminister with omeprazole or PPI
  5. Minimise NSAID use in patients with other RFs e.g. alcohol consumption / anticoagulant/glucocorticoid use
28
Q

Aspirin is selective for which COX enzyme?

A

COX-1

29
Q

How does aspirin bind to COX enzymes?

A

ASPIRIN BINDS IRREVERSIBLY BINDS TO COX ENZYMES

30
Q

Aspirin also reduces platelet aggregation. How

A
  1. COX-1 permanently inhibited (due to covalent bonding) which suppresses TxA2 production by platelets (TXA2 increases platelet aggregation)
  2. Aspirin has low capacity to inhibit COX-2.
  3. PGI2 is synthesised by both COX-1 and COX-2 in endothelial cells
  4. Therefore, there is still PGI2 synthesis as COX-2 works
  5. PGI2 decreases platelet aggregation.
31
Q

Platelets have no nucleus, so more platelets must be regenerated for TXA2 and platelet aggregation to occur (when aspirin is administered).

A

Y

Endothelial cells that produce PGI2 have a nucleus so can produce COX1/2.

32
Q

Aspirin can cause gastric irritation, bronchospasm, excess bleeding, nephrotoxicity. These side effects are likely not because aspirin is selective for COX-1, but because they:

A

Inhibit COX covalently (i.e. irreversibly)

33
Q

Why is paracetamol not an NSAID

A

It has minimal anti-inflammatory effect

but it does have a anti-pyretic action

34
Q

Overdosing on paracetamol may cause?

A

Liver failure

35
Q

How can overdosing on paracetamol cause liver failure

A
  1. Glutathione used to metabolise a toxic metabolite of paracetamol into an inactive reduced form
  2. Depleted glutathione = toxic metabolite oxidises thiol groups
  3. Thiol groups are crucial in key hepatic enzymes - hepatotoxicity results and cell death occurs

Paracetamol depletes glutathione

36
Q

What is the antidote for paracetamol poisoning

A
  1. Add compound with -SH groups (often IV acetylcysteine)

2. (Occasionally oral methionine)

Year 2 Collin (114 decks)

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