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WEEK 9 SEM 4 > Non-Steroidal Anti-Inflammatory Drugs > Flashcards

Non-Steroidal Anti-Inflammatory Drugs Flashcards

1
Q

What is a typical NSAID?

A

aspirin

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2
Q

What do NSAID’s do?

A

analgesic
anti pyretic (lower temperature- doesnt stop fever occuring)
anti inflammatory

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3
Q

What do NSAID’s treat?

A

low grade pain (chronic inflammation, e.g. arthritis)
bone pain (cancer metastases)
fever (associated with infections)
inflammation (decreases the symptoms eg oedema, redness, to a small extent itch)

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4
Q

What does aspirin (NSAID) inhibit?

A

cyclooxygenase enzyme (COX)

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5
Q

What does COX do?

A

converts arachidonic acid to prostaglandins and thromboxanes

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6
Q

Where is COX1 found?

A

always there in the body

found in platelet

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7
Q

What is COX2 induced by?

A

IL1b, TNF alpha

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8
Q

What happens if you inhibit COX2?

A

reduction of prostaglandind and thromboxanes (especialy TXA2)

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9
Q

What does TXA2 do?

A

platelet aggregation

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10
Q

How does an NSAID prevent clotting?

A

irreversibly acts on COX1 and COX2
blocks COX in platelets
platelets dont have nuclei and cant synthesize new COX
so prevents clotting

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11
Q

Give examples of NSAIDs other than aspirin:

A

etodolac, meloxicam, ibuprofen, naproxen, indomethacin, etc

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12
Q

Is Paracetomol and NSAID?

A

NO BITCH

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13
Q

What is paracetomol?

A

analgesic without inflammatory properties

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14
Q

What does paracetomol inhibit?

A

weakly inhibits COX1, COX2, COX3

Paracetamol also inhibits COX-mediated generation of hydroxypeptides from arachidonic acid metabolism

these hydroxypeptides usually stimulate COX activity, and thus increases production of prostaglandins

blocking the production of hydroxypeptides may relieve a person off pain due to reduction in stimulation of COX

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15
Q

What pathway does paracetomol modulate?

A

serotonergic neurotransmission= important for antipain pathway

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16
Q

What are hydroxypeptides?

A

generated from arachidonic acid metabolism
they stimulate COX activity
increase prostaglandin production
blocking the production of hydroxypeptides may relieve a person off pain due to reduction in stimulation of COX

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17
Q

What do bacterial endotoxins (from infections) stimulate macrophages to release?

A

IL1b
lipolysaccharide part of bacterial wall composed of Lipid A
Lipid A stimulates macrophages to release IL1B

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18
Q

What does IL1b do?

A

acts on hypothalamus to release PGE2 via COX2

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19
Q

What does increased PGE2 cause?

A

reduces sensitivity of neurons to temperature

so you get fever

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20
Q

Why does headache occur?

A

vasodilation of the meninges in the brain
NSAIDs reduce the vasodilation
and also work on COX123 in the CNS

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21
Q

How do PGE2 and PGI2 (prostacyclin) cause inflammatory effects?

A

have acute inflammatory effects:

  • causes arteriolar dilatation which increases blood flow
  • it increases permeability in post capillary venules

these both increase influx of inflammatory mediators into the interstitial space

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22
Q

What does NF kappa B do?

A

NK kappa B =powerful transcription factor = mediates inflammation by causing the synthesis of various inflammatory genes

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23
Q

What is thromboxane A2 involved in?

A

haemostasis (keeping blood levels normal)
platelet aggregation for blood clotting
vasoconstriction

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24
Q

How does NSAID’s decrease thromboxane A2 levels?

A

inhibit enzyme thromboxane synthase and COX-1

this gives an increase in bleeding time

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25
Q

When should you not give NSAID?

A

when giving birth

bc inhibiting thromboxane synthase and COX 1 causes increase bleed time

26
Q

What chemicals from the endothelial lining prevent aggregation?

A

(PGI2 and PGE2 and NO)

27
Q

How is a clot formed?

A

endothelial lining gets damaged
collagen and Von Willebrand factor released from the damaged endothelium
also with thromboxane A2 =lead to increased platelet aggregation and reduced blood loss from the damaged blood vessel
after aggregation, fibrin forms
prevents microbes entering blood vessel

28
Q

What is TXA2?

A

in the blood vessels, platelets release TXA2
its a pro-aggregatory vasoconstrictor
made by COX1

29
Q

What is TXA2 made by?

A

COX1

30
Q

What happens if aspirin blocks TXA2?

A

the TXA2 in platelets is limited
platelets cannot resynthesize more TXA2 (as platelets do not have a nucleus)
TXA2 cant be renewed if blocked by arpirin
need to wait till new batch of platelets is released

31
Q

PGE2 and PGI2 stop clotting and are released from endothelial lining. If aspirin blocks COX, won’t it block PGE2 and PGI2 production too (so basically stops clotting)?

A

in the blood vessels, endothelial cells release PGI2 and PGE2 which are antiaggregatory vasodilators (prevent platelet aggregation)
they are made by COX2

COX2 can be stimulated to synthesize more of the PGI2 and PGE2
endothelial cells can renew the PGI2 and PGE2 even after its production is blocked by aspirin

32
Q

What do prostaglandins do in the GI?

A

Prostaglandins (PGI2 and PGE2) are important in protecting the gastric mucosa•they stimulate mucus secretion and inhibit acid secretion in the stomach

33
Q

If NSAIDs are given in the GI, what happens?

A

ulceration
bleeding bc HCl penetrating the gastric wall
bc less mucus and bicarbonate secretion and more acid secretion

34
Q

Give examples of COX 2 selective agents:

A

celecoxib, valdecoxib, etoricoxib, rofecoxib

35
Q

When taking NSAID overdose, why do you get paradoxical hyperpyrexia (high fever)?

A

bc excess NSAIDs uncouples oxidative phosphorylation in metabolism
cells begin to use lactate and pyruvate to produce energy
increases metabolic acid production (lactic acid) may lead to an increase in temperature

36
Q

What do prostaglandins cause during menstruation?

A

smooth muscle spasm and pain

so use NSAID to relieve pain

37
Q

Which prostaglandins are important in uterine contractions?

A

E2 and F2 alpha

38
Q

What are prostaglandins E2 and I2?

A

vasodilators of renal blood flow
they mediate renin release
they decrease Na+ reabsorption

39
Q

What effect does PGD2 and PGF2alpha have on smooth muscle airways?

A

Prostaglandins PGD2 and PGF2alpha have both constrictor and dilator effects on airway smooth muscle

40
Q

Why does NSAID cause wheezing in asthma patients?

A
  1. block COX route
  2. arachidonic acid gets metabolized by lipoxygenases 3. you get excess production of LTB4, C4, D4 and E4 which are slow reacting substances of anaphylaxis −they cause excess production of thick viscous mucus and also bronchoconstriction
41
Q

What does the ductus arteriosus do in foetal life?

A

connects the pulmonary artery to the aorta

closes a few days after birth

42
Q

What happens to the ductus arteriosus when born?

A

few days after birth it contracts and closes

bc of MORE oxygen tension and LESS prostaglandin levels

43
Q

What happens if a new born has a patent ductus arteriosus (not closing)?

A

low birth weight
sweats when feeding
shortness of breath
easily tired

44
Q

How do you close a patent arteriosus?

A

indomethacin and ibuprofen can be used

the ductus arteriosus can be closed surgically by a left side thoracotomy

45
Q

In what situation does the doctor want to keep the patent ductus ateriosus open for longer?

A

in certain patients with congenital heart disease, doctors may want to keep the ductus arteriosus open for longer than usual

46
Q

How do you keep a patent ductus arteriosus open for longer?

A

analogue of prostaglandin I2, alprostadil is infused

47
Q

What is the first line treatment for ulcerative colitis?

A

aminosalicylates (sulfasalazine and mesalazine)

48
Q

What is the Mechanism of Action of Sulfasalazine?

A

It is a prodrug
it gets metabolized to 5 amino salicylic acid and sulfapyridine
It reduces the synthesis of eicosanoids by blocking the activity of cyclooxygenase and lipoxygenase
the activity of COX and LOX is high in ulcerative colitis

49
Q

What happens in gout?

A

uric acid crystals in joint

type of arthritis

50
Q

What is used to treat gout?

A

anti-gout drugs are NSAIDs

allopurinol (this is not an NSAID)
naproxen, diclofenac, and indomethacin

51
Q

What does allopurinol do?

A

inhibits xanthine oxidase, thus production of uric acid is stopped-thus this does not cause accumulation of uric acid

52
Q

What does naproxin do?

A

naproxen inhibits COX1 and COX2 which lowers prostaglandin levels
analgesic effects
anti-inflammatory effects
anti-pyretic effects
inhibits platelet aggregation by inhibiting TXA2-

53
Q

What are side effects of sulfasalazine?

A

Indigestion, feeling or being sick, abdominal pain, diarrhoea,

Dizziness, headache, difficulty sleeping, tinnitus,

Coughing; itchy rash, may affect your taste and cause sore mouth

54
Q

What are other indications of NSAIDs?

A

Decrease colonic polyps and prevent colon cancer
May decrease Alzheimer’s disease risk
Post-operative pain relief
Renal colic – upper part of abdominal pain/groin usually caused by kidney stones

55
Q

How do toxic doses of aspirin stimulate respiration?

A

Actions on respiratory centre and uncoupling of oxidative phosphorylation - medulla stimulated
Respiratory alkalosis caused by hyperventilation (→CO2 washout from lungs)

56
Q

What do overdoes NSAID doses cause in the CNS?

A

In overdose NSAIDs produce paradoxical hyperpyrexia, stupor and coma
- ↑ metabolism and ↑ metabolic acid production

Reye’s syndrome risk (brain & liver damage) when used in

57
Q

What is etoricoxib?

A

most selective COX-2 inhibitor

They have no effect on TXA2 in platelets, but decrease PGI2 in blood vessels

58
Q

Why is rofecoxib not used anymore?

A

Rofecoxib – withdrawn due to CV effects

Not suitable for RA/osteoarthritis; use meloxicam, etodolac, Ketroralac etc. instead

59
Q

What does Aspirin cause in the GI tract?

A

↓ mucus secretion:
↓ HCO3-:
↑ acid secretion:
↑ LT production:

↑ blood loss:

Interfere with tissue healing (COX-2 inhibition)

Nausea, dyspepsia, GI contraction (COX-1 inhibition)

60
Q

How do PG cause joint pain?

A

Arteriolar dilatation
Increased microvascular permeability
Hyperalgesia – increased sensitivity to pain

WEEK 9 SEM 4 (9 decks)

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