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Pharmaco Ca2 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Pain vs nociception

A

Pain is a subjective experience. Nociception detects and signals presence of noxious stimuli

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2
Q

How do steroids and NSAIDS affect cyclooxygenase synthesis

A

Steroids inhibit phospholipids A2, preventing break down of phospholipids to arachidonic acid

NSAIDS inhibit formation of cyclooxygenase from arachidonic acid

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3
Q

Cyclooxygenase forms 3 prostanoids what are they

A

Prostacyclin
Prostaglandin
Thromboxane

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4
Q

What are the effects of prostacyclin

A

Vasodilatation, inhibit platelet aggregation

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5
Q

What are the effects of prostaglandin

A

Vasodilation
Vascular permeability
Pain

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6
Q

What are the effects of txa2 (cox 1 only vs cox 1 and 2 for pgi2 and pge2)

A

Vasoconstriction and platelet aggregation

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7
Q

Effects of aspirin

A

Anti inflammatory
Analgesic
Anti pyretic
Anti platelet

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8
Q

How does aspirin exert anti inflammatory effect

A

Block vasodilation

Block increase in vascular permeability

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9
Q

How does aspirin exert analgesic mechanism

A

Blocks production of prostaglandins which sensitise nociceptive fibres to stimulation by other inflammatory mediators eg bradykinin and leukotrienes

Ie block sensitisation rather than direct nociceptive activation hence nsaids have analgesic ceiling

Additional analgesics action in the cns. Crosses the blood brain barrier to affect pain modulataion and processing

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10
Q

How does aspirin exert anti pyretic effect

A

Inhibit cox formation, no pge2 forms. Pge2 responsible for fever

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11
Q

How does aspirin exert anti platelet function

A

Platelets tend to have cox1 which produce txa2, promoting aggregation. Endothelial cells have cox which forms pgi2 which inhibits aggregation.

Aspirin is an irreversible cox inhibitor. Platelets have no nucleus, unable to make new COX; takes 1-2 weeks to make COX to make txa2 to promote aggregation

Endothelial cells can recover in 3-4h to restore inhibition of platelet aggregation

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12
Q

Side effects of aspirin (due to salicylate chemical structure)

A

GI bleeding, tinnitus (sign of overrode), hypoprothrombinaemia (excessive lack of thrombosis, prone to bleeding)

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13
Q

Why is aspirin contraindicated in children

A

Reye’s syndrome. Increased risk when children with viral infections are exposed to salicylate eg aspirin.

Leads to encephalitis and liver swelling. Increased pressure on brain can cause delirium, convulsions, personality changes, loss of consciousness

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14
Q

What are the first gen nsaids

A

Aspirin, naproxen, indomethacin, diclofenac

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15
Q

What is naproxen used for

A

First gen nsaids used for dysmenorrhea because more effective in women and long half life of 12-14h

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16
Q

What is indomethacin used for

A

Rheumatoid arthritis, gout, closes ductus arteriosus in fetus

17
Q

Compare indomethacin to other nsaids

A

More potent than other nsaids. Strongly inflammatory as it is a phospholipase a2 inhibitor (more steroid like)

Has cns adverse effects such as hallucination, depression

18
Q

What is diclofenac used for

A

1st gen nsaid (cox2>cox1)

Low GI risk because short plasma half life

Longer half life in synovial fluid and accumulates in synovial joint fluid hence useful for inflammatory joint diseases eg rheumatoid arthritis

19
Q

What are the adverse gastrointestinal effects of NSAIDS

A

Decrease prostaglandin synthesis; prostaglandins responsible for decreasing gastric acid synthesis, increasing bicarbonate secretion, increasing mucosal blood flow and mucus secretion

NSAIDS result in dyspepsia, nausea, vomiting, ulcer formation, hemorrhage risk in chronic users

20
Q

How to avoid hemorrhage risk in chronic users of NSAIDS

A

Use for less than 7 days and use with other drugs eg antacids

But taking an antiplatelet eg aspirin will increase hemorrhage risk if preexistinf ulcer

21
Q

What are the renal side effects of NSAIDS (esp naproxen due to long duration of action 12-14h)

A

Inhibition of pge2:
Sodium and water retention leading to peripheral edema and hypertension

Act at ascending limb (25%)

Inhibition of pgi2
Suppresses renin and aldosterone secretion
Hyperkalemia that can result in acute renal failure

Act at DCT (1-2%)

22
Q

How do nsaids cause pseudoallergic reaction and asthma

A

Inhibit cox, push arachidonic acid to 5-lipoxygenase (eicosanoids). Excess leukotrienes lead to bronchospasm (asthma patients susceptible) and allergic reaction like symptoms es rashes, swelling, nasal congestion

23
Q

How do first gen nsaids cause bruising

A

Inhibit cox. Less thromboxane which promotes platelet aggregation, less haemostasis

24
Q

What are Coxibs

A

Gen 2 cox 2 selective inhibitors

25
Q

First gen vs second gen nsaids

A

Second gen nsaids are cox 2 selective

Cox 1 constitutive effects

Cox 2 is inducible in response to inflammatory stimulus, hence cox 2 selective inhibitors avoid adverse effects
(But constitutive in CNS, kidney, female reproductive tract, synovium)

26
Q

What are the adverse effects of Coxibs

A

Cox 2 still constitutive in kidney. Still have renal toxicity but less severe adverse effect

Delay follicular rupture, affecting ovulation to decrease chance of pregnancy

Premature close of ductus arteriosus in third trimester hence ALL NSAIDS CONTRAINDICATED IN 3RD TRIMESTER

Impair wound healing and exacerbate ulcers (not cause)

Increase thrombosis risk because relative shift to TXA2 (cox 1 only so not affected vs pgi2 and pge2) hence favour platelet aggregation

27
Q

What are the cox1>2 and cox2>1 nsaids

A 
Cox1>2: Kaley please i am not idiotic 
Ketoprofen 
Piroxicam 
Indomethacin 
Aspirin
Naproxen
Ibuprofen
Cox2>1: DM me cute pictures Evan
Diclofenac
Mefenamic acid
Meloxicam
Celecoxib
Parecoxib
Etoricoxib
28
Q

As cox 2 selectivity increases, drug effect becomes more

A

Anti inflammatory
Stronger analgesic property
More prothrombotic with the exception of aspirin

29
Q

Can i use nsaids in pregnancy

A

Contraindicated in third trimester

30
Q

Why does paracetamol not have adverse GI effect

A

Cns selective cox inhibitor, does not inhibit peripheral cox

31
Q

What are the uses of paracetamol

A

Analgesics, antipyretic

Weak anti inflammatory effect

32
Q

How does paracetamol cause hepatotoxicity

A

Metabolised to NAPQI. CYP2E1 (induced by alcohol) metabolised NAPQI to toxic metabolite

Glutathione converts toxic metabolite to non toxic. Glutathione is depleted by overdose and alcohol abuse, replenished by n acetylene cysteine

Pharmaco Ca2 (11 decks)

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