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NSAIDs Flashcards

(48 cards)

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1
Q

what are eicosanoids made from ?

A

Arachidonic acid

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2
Q

where does arachidonic acid come from?

what does it go into?

A 
linoleic acid (veg oils) and converted in liver
phospholipids
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3
Q

what enzyme releases Arachidonic acid ?

A

Phospholipase A2

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4
Q

What does PGE2 do ?

A

GI mucosa protection

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5
Q

what does PGI2 do?
what is it balanced by ?
what can imbalance lead to ?

A

inhibits platelets , vasodilator
TXA2
Hypertnesion, MI and stroke

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6
Q

what is the difference between COX-1 and 2 ?

A

constitutively active = 1

Inducable in active/inflamed tissue = 2

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7
Q

where is arachidonic acid most abundant ?

A

muscle , liver, brain and kidneys

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8
Q

What are the 3 prostanoids for pain , pyrexia and inflammation?

A

PGE2, PGF2, PGD

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9
Q

What are the pathological functions of COX-1?

A

chronic inflammation and pain

Raised BP

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10
Q

What are the pathological functions of COX-2?

A

chronic inflammation and pain
fever , blood vessel permeability
tumour cell growth

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11
Q

what other autacoids enhance action of prostanoids ?

A

Bradykinin and histamine

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12
Q

why does fish oil reduce CVD incidence ?

A

EPA and DHA (Omega 3 FAs) convert TXA3 and PGE3 so balance shifted to prostacyclin activity

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13
Q

what is the main difference between aspirin and other NSAIDs?

A

aspirin irreversibly inhibits COX

compared to competitive inhibitors of arachidonic acid

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14
Q

why do you see reduction in platelets still when aspirin is stopped ?

A

platelets are non nucleic so new platelets take time to synthesis from megakaryocytes

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15
Q

explain the analgesic action of NSAIDs

A

local action at site due to increased efficacy at inflammation
Central action = decrease in PGE2 synthesis in dorsal horn - less neurotransmitter released = less excitability of neurones in pain

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16
Q

explain anti-inflammatory effects of NSAIDs

A

reduction in production of PGs especially PGE2 and PGD2 released during injury

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17
Q

Explain Anti-pyretic effect of NSAIDs

A

inhibition of hypothalamic COX-2 where cytokine induced PGs synthesis elevated - only lowers temp if raised

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18
Q

list the most Cox-1 selective compound to least (first 4)

A 
Aspirin 
ibuprofen 
naproxen 
diclofenac 
celecoxib (pare and etori)
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19
Q

how can leukotrienes be affected by NSAIDs?

A

Inhibition of PGE2 leads to less leukoteienes

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20
Q

which type of NSAIDs are more selective at therapeutic doses ?

Study These Flashcards
A

COX-2 inhibitors

21
Q

what are the PKs of NSAIDs?

A, D , M and E?

Study These Flashcards
A

A= GI
D= Accumulate at site of action, Small Vd so protein bound
M = don’t undergo first pass metabolism
liver converts to inactive form

22
Q

how does aspirin OD work ?

Study These Flashcards
A

converted to salicyclic acid then conjugation with glycine which saturates at high doses to go from 1st order to zero order

23
Q

what are GI ADRs of NSAIDs ?

Study These Flashcards
A

dyspepsia , nausea , peptic ulceration , bleeding and perforation
exacerbation of IBDs
local irriation and bleeding fro rectum

24
Q

what can put you at risk for GI ADRs?

Study These Flashcards
A

age, duration of use, glucocorticoid steroids, anticoagulants, smoking, alcohol, history of peptic ulceration and H Pylori

25
how does NSAIDs causes GI ADRs?
decrease in : mucus and bicarb secretion and increase in acid mucosal blood flow --> hypoxia hydrophobicity of mucus due to acidic nautre of NSAIDs
26
what are the renal ADRs of NSAIDs?
decrease ADRs and renal medullary blood flow increase in creatinine hyperkalaemia hypertension and oedema
27
why does the renal ADRs of NSAIDs occur ?
AA vasodilators are not present leading to decreased renin (hyperkalaemia) and increased salt and water retention due to NaK2Cl upregulation
28
Name 2 Cox-2 inhibitors
Celecoxib Etoricoxib Parecoxib
29
why are Cox-2 not that selective?
Polymorphisms in Cox-2 | patients often take non-selective before
30
Can Cox-2 inhibitors stop platelet aggregation ?
No, but they impair PGI2 potentially leading to unopposed aggregatory effects
31
what CVS ADRs are seen in mostly in COX-2 selectives?
salt water rentention = increase in BP Vasoconstriction - reduced inhibition of ADH by prostaglandins Efficacy of Antihypertensives reduced risk of MI with traditional as well
32
when should you not prescribe NSAIDs ?
pro-thrombotic risk coronary or cerebrovascular diseases excluding low dose aspirin
33
why does combination NSAIDs cause increase risk of ADRs?
competitive displacement due to protein binding - PK and PD affected
34
Name 4 high protein bound drugs and their increased risk of ADRs with NSAIDs
Sulfonylurea - hypoglycaemia Methotrexate - Hepatotoxicity and leukopenia Warfarin Low dose aspiring - competition for COX-1 = Decrease CVS protection also look out for diuretics
35
why cant you give aspiring to children under 12 ?
increased risk of Reye's syndrome - a rapid progressive encephalopathy
36
what are the ADRs of NSAIDs in pregnant women ?
Delayed labour increase blood loss premature closure of ductus arteriosus use paracetamol instead
37
name 4 indication for use of NSAIDs
``` Inflammatory conditions - joints and soft tissue OA- try topical / paracetamol Post op pain topical on cornea menorrhagia close ductus arteriosus ```
38
Where is COX-2 expressed constitutively ?
renal arterioles and cells following inflammation
39
what is the MOA for paracetamol? | what limits its actions ?
COX-2 inhibition in CNS = decreases pain signals to higher centres Perioxidases in peripheral inflammation = little inflammatory effect
40
what must you be careful of when prescribing paracetamol?
OTC medications that already have paracetamol = risk of OD
41
what is a metabolite of paracetamol? how it is minimised ? how does it cause damage?
NAPQI via Phase 1 (CYP450) Conjugation with glutathione Highly nucleophilic = oxidising thiol groups on enzymes leads to cell necrosis / apoptosis - 150mg/kg for OD
42
Why don't you give glutathione in paracetamol OD?
cannot enter the hepatocytes
43
How would a paracetamol OD present ?
Nausea , vomiting, abdo pain - first 24 hours | liver damage / UQ pain - 24 to 48
44
what is a good indicator of damage from paracetamol OD?
Prothrombin time
45
why are Blood tests a sort of red herring in paracetamol OD?
They do not show extent of overdose if multiple doses
46
what should you give in for paracetamol OD?
Activated charcoal if very early | acetylcystiene
47
why is alcohol bad with paracetamol ?
induces phase 1 metabolism to make more NAPQI
48
CVS ADRs are more prone to which type of NSAID?
it is not class specific so neither

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