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Scientific Basis of Theraputics > Non-steroidal anti-inflammatory drugs > Flashcards

Non-steroidal anti-inflammatory drugs Flashcards

1
Q

effects of NSAIDs

A

Analgesic -> prevent pain
Anti-pyretic -> lower a raised temperature (lower fever)
Anti-inflammatory -> decrease an immune response

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2
Q

what are NSAIDS used to treat

A
  1. low grade pain (chronic inflammation)
  2. bone pain (often by cancer metastases)
  3. fever (associated w/ infection)
  4. inflammation
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3
Q

examples of NSAID

A

aspirin

etodolac, meloxicam, ibuprofen, naproxen, indomethacin etc

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4
Q

briefly, what does COX do

A

converts arachidonic acid to prostaglandins and thromboxanes.

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5
Q

when is COX1 active

A

constantly active and present in platelets

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6
Q

when is COX2 active

A

inducible by factors like IL-1beta and TNFalpha

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7
Q

what is the role of COX2

A
  • producing prostanoids involved in inflammatory response .’. inhibits COX2 .’. reduce prostaglandins and thromboxanes .’. reduce inflammation
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8
Q

why is paracetamol not an NSAID

A

is analgesic WITHOUT antiinflammatory effects.

has little inhibition of COX1/2

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9
Q

how does COX2 produce fever

A

bacterial endotoxins stimulate macrophages to release IL1, IL1b, act on hypothalamus to stimulate COX2 release of PGE2.
PGE2 =depressed response of temp sensitive neurones
PGE2 = body’s set point temp elevated

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10
Q

how do NSAIDS have an antipyretic action

A

NSAIDS block COX .’. prevent PGE2 production .’. when taken, set point lowered back to NORMAL value, fever gos away.
no effect on normal body temp

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11
Q

how do NSAIDS have an analgesic action

A

block COX .’. no PG
.’. lessens activation of nocicpetors by oedema and PG itself
blocks hyperalgesia produced by synergistic PG and other substances.

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12
Q

COX in pain simulation

A

COX -> PG. PG= sensitised and stimulate nociceptors =pain.
oedema during inflammation (also caused by PG) = direct activation on nociceptive fibres causing pain
also PG act synergistcally with other substances (5HT,Histamine) = hyperalgesia

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13
Q

why may NSAIDS be useful in treating headache

A

caused by vasodilation, so NSAIDs can inhibit PG induced vasodilation

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14
Q

role of COX in inflammation

A

at insult, COX -> release of PGE2 and PGI2 (from endothelial cells).
= arteriolar dilation, inc permeability of postcapillary venules.
these processes increase the influx of inflammatory mediators and cells

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15
Q

NSAIDS in treating acute inflammation

A

inhibit formation of PGE2 and PGI2 .’. reduced redness and swelling
bc local hormones, and quickly degraded, once removed = no more production of PG .’. inflammatory process dies down

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16
Q

role of TXA2 in homeostasis

A

released from activated platelets.

stimulates platelet aggregation and vasoconstriction

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17
Q

role of NSAIDS in cvs

A

NSAIDS = inhibit COX= decr. TXA2 .’. bleeding time inc.

.’. NSAIDS eg aspirin are used in disease states where clotting is likely

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18
Q

what is thromboresistance

A

resistance by a blood vessel to thrombus formation

endothelium releases PG &prostacyclin which are potent inhibitors of platelet aggregation.

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19
Q

mechanism of thromboresistance

A

in healthy bv, we do not want thrombosis .’. endothelium sythesises and releases PGI2 and PGE2 and NO.
NO acts on platelets to to reduce aggregation anf keep lumen clear

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20
Q

what happens when there is damage to a vessel wall (eg atheroma rupture or trauma)

A

collagen and vWF is exposed.
circulating platelets bind to collagen and vWF causing them to become activated.
these release TXA2 .’. increased expression of certain gycoproteins .’. inc. platelet aggregation and vasoconstriction.
fibrinogen tethers platelets together. cleaved -> fibrin. formation of fibrin mesh clot.

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21
Q

difference between cox 1 and 2

A

Endothelial cells are anti-aggregatory and want vasodilation, they do this by using COX-2 to synthesise PGI2.

Platelets want to aggregate and cause vasoconstriction so use COX-1 to synthesise TXA2

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22
Q

why is aspirin so beneficial in cardiovascular disease?

A

lose dose aspirin daily = irreversibly inhibit COX. no PG or prostacyclin produced by endothelial cells OR TXA2 by platelets
overtime, platelets unable to synthesise new COX1 bc lack DNA. .’. irreversible inhibition .’. aggregation less likely.
endothelial cells contain DNA .’. synthesise new DNA .’. new COX .’. recover from aspirin .’. continue releaseof PGI2 and PGE2 .’. prevent aggregation and vasodilate vessels

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23
Q

how do prostoglandins with acute inflammatory effects contribute to joint pain in arthritis

A
  • Arteriolar dilatation
  • Increased microvascular permeability
  • Hyperalgesia
24
Q

role of NSAIDS to treat arthritis

A

block COX .’. block production of PG around and in the joints .’. less inflammation

25
which COX is present in the gut
COX1
26
role of COX in GI tract
PGE2 act on EP3 receptor on parietal cells in paracrine manner -> stimulates mucus secretion and inhibits gastric acid. .'. protects gastric mucosa
27
Role of NSAIDS in gastric bleeding and ulceration
decreased level of PG .'. decreased mucus secretion & gastric acid secretion increases.
28
side effects of NSAIDS
Decrease mucus secretion, decrease bicarb secretion, increase acid secretion, increase leukotriene production and increase blood loss
29
examples of cox 2 selective agents
etoricoxib, celebcoxib, valdcoxib
30
why are COX-2 selective agents are less effective analgesic
mostly effective against cox2 | less effective against COX3 which is in brain and spinal cord
31
effect of overdosing on NSAIDS
paradoxical hyperpyrexia, stupor and coma may be due to massive increase in metabolism and metabolic acid production.
32
when may we use COX in menstruation
Prostaglandins cause the pain and smooth muscle spasms during menstruation and this can lead to dysmenorrhoea, that is painful periods
33
role of NSAIDS in dysmenorrhoea
inhibit cox .'. inhibit PGE2 and PGI2 .'. reduce pain and smooth muscle spasms
34
role of NSAIDS in labour
Prostaglandins PGE2 and PGF2α are released in labour and important in mediating uterine contractions in childbirth, thus if we give NSAIDs it delays contractions.
35
why may NSAIDS increase postpartum bleeding
TXA2 production is inhibited and therefore platelets are less likely to aggregate and there is less vasoconstriction of uterine vessels.
36
effect of PGE2 and PGI2 on kindey
vasodilator prostaglandins PGE2 and PGI2. NSAIDs reduce PGs and reduce renal blood flow PGI2 mediate renin release. PGE2 decreases Na+ reabsorption
37
effect of NSAIDS on kidney
inhibition of COX2 .'. decreased Na excretion and inc intravascular vol
38
why may NSAIDS interfere with antihypertensive drugs
NSAIDS - decrease Na+ excretion and inc intravascular vol. | effectiveness of antihypertensives reduced by inc blood vol .'. in CO .'. BP increased
39
effect of PG on respiratory system
have both constrictor (mainly) and dilator effects on airway smooth muscle
40
effect of NSAIDS in respiratory system
NSAIDs =no effect on normal airway tone. At toxic doses aspirin initially stimulates respiration -> Acts on respiratory centre and uncouples oxidative phosphorylation -> Causes hyperventilation leading to alkalosis due to blowing off so much CO2
41
why are NSAIDS contraindicated with asthma
NSAIDS = COX inhibition .'. arachidonic acid shunted to lipoxygenase pathway .'. proliferation of leukotrienes .'. inflammation of airways
42
use of NSAIDS in closure of a patent ductus arteriosus
if patency is being maintained innapropriately by PGE2 and PGI2 production
43
what is patent ductus arteriosus (PDA)
patent ductus arteriosus (PDA) is a condition wherein the ductus arteriosus fails to close after birth.
44
why is it important that we not give pregnant women in third trimester NSAIDS
can then stop PG production and lead to premature closure of the ductus arteriosus
45
what is the ductis arteriosus
connection between the aortic arch and pulmonary artery, it shunts any blood from the pulmonary artery into the aorta during foetal life to prevent blood flowing to the useless lungs
46
what happens in patent ductus arteriosis
pressure is now higher in the aorta and blood flows into the pulmonary artery and travels back to lungs despite being oxygenated already. Thus PDA in acute phase = abnormal blood flow and blood mixing.
47
what is Ulcerative colitis
is inflammation of the bowel (colon and rectum) and is caused by increased levels of prostaglandins in the gut
48
what is the first line treatment for ulcerative colitis
aminosalicylates (e.g. sulfasalazine and mesalazine). =decrease inflammation in mild or moderate ulcerative colitis. also use for the short-term treatment of flare-ups and maintaining remission
49
what is the mechanism of action of sulfasalazine
metabolised in the body to 5-aminosalicylic acid (5-ASA) and sulfapyridine former is active metabolite 5ASA = reduced synthesis of eicosanoids bc blocks COX and lipoxygenase in ulceration colitis, higj cox and lipoxygenase .'. inflammatory mediators. this drug blocks these pathways .'. reduces inflamation
50
side effects of sulfasalazine
- Indigestion, feeling or being sick, abdominal pain, diarrhoea - Dizziness, headache, difficulty sleeping, tinnitus - Coughing, an itchy rash, may affect your taste and cause a sore mouth
51
what is gout
a type of inflammatory arthritis caused by the accumulation of uric acid crystals in joints.
52
what is uric acid
is a by-product of the metabolism of purines and circulates in the blood is harmless at low levels and actually helps prevent damage to blood vessel linings by exerting anti-oxidant effects.
53
what happens when there is high levels of uric crystals in the blood (called hyperuricemia)
causes tiny grit-like crystals to precipitate and collect in joints which irritate the joint tissues causing inflammation and pain
54
anti-gout drugs
naproxen, diclofenac and indomethacin.
55
mechanism of action of Naproxen
inhibits COX1/COX2 enzymes .'. low PG levels, are mediators of the joint inflammation&alleviates the symptoms. exert anti-inflammatory, analgesic and antipyretic effects inhibits platelet aggregation

Scientific Basis of Theraputics (9 decks)

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