eLCRS - 팜 > Pharm 18: NSAIDS > Flashcards

Pharm 18: NSAIDS Flashcards

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1
Q

What are some uses of NSAIDS

A
  • analgesic –> moderates pain e.g toothache/backache
  • antipyretic –> e.g influenza
  • anti inflammatory –> e.g rheumatoid arthritis/ osteoarthritis
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2
Q

describe the mechanism of action of NSAIDS

A

NSAIDS –> inhibits prostaglandin + thromboxane synthesis

  • they are lipid mediators derived from Arachidonic cAcid
  • Inhibits COX enzymes
  • receptor mediated

NSAIDS inhibit

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3
Q

Prostanoid receptors

a) how many are there
b) have both / no G protein dependent + independence effects

A 
- 10 known receptors 
DP 1 /2 
EP 1 / 2 /3 / 
FP 
IP1 / 2 
TP
  • have both G protein dependent + independence effects
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4
Q

What are the main UNWANTED actions of PGE2 ?

A
  • increased pain perception
  • increased body temp
  • acute inflammation response
  • immune response
  • tumorigenesis
  • inhibition of apoptosis
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5
Q

How do PGE2 analogues lower pain threshold?

A

o Peripheral PG receptor stimulation sensitizes nociceptors –> acute + chronic pain

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6
Q

What is the role of PGE2 in acute inflammation?

A

involves histamine release by mast cells, many receptors involved

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7
Q

what are other (good) physiological actions of PGE2 ?

A
  1. Bronchodilation
  2. Modulates Renal salt + water homeostasis
  3. Gastroprotective effects
  4. Involved in Vascular tone control (dilation + constriction depending on receptor activated)
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8
Q

What does it mean by PGE2 being pyrogenic?

A

PGE2 stimulates hypothalamic neurones –> initiating a rise in body temperature

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9
Q

What is the effect of NSAIDS on raised temp?

A

reduces raised temp

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10
Q

Note: PGE2 regulates salt + water homeostasis

  • PGE2 production is mediated by both COX 1 + COX 2 enzymes
A

-

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11
Q

What is the effect of PGE2 and NSAIDS on the glomerulus?

A

PGE2 = increases renal blood flow

NSAIDs = cause renal toxicity

  • -> Constriction of afferent renal arteriole
  • -> Reduction in renal artery flow
  • -> Reduced glomerular filtration rate
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12
Q

What is the role of PGE2 on gastric cytoprotection?

A
  • PGE2 down regulates HCl secretion
  • PGE2 stimulates mucus + bicarbonate secretion
  • -> produces alkali to increase PH
  • -> reduce Acid levels
  • -> enhances mucus layer
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13
Q

NSAIDS increase/ decrease risk of ulceration

A

NSAIDS increase risk of ulceration

note: 50% of deaths due to NSAID = GI related (e.g perforation)

new type: celecoxib –> reduced GI cases

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14
Q

What are the negative unwanted CVS effect of NSAIDS ?

A
  • Vasoconstriction
  • Salt and water retention
  • Reduced effect of antihypertensives

–> can cause hypertension / MI / Stroke

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15
Q

What are other methods that can limit GI side effects? - except COX2 selective NSAIDs.

i.e how would you reduce side effects of COX 1.

A
  • Topical application
  • Minimise NSAID use in patients with history of GI ulceration
  • Treat H pylori if present
  • If NSAID = essential, administer with omeprazole/ proton pump inhibitor
  • Minimise NSAID use in patients with other risk factors and reduce risk factors e.g.
    Alcohol consumption
    Anticoagulant or glucocorticoid steroid use
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16
Q

Aspirin is selective for COX ___

it binds irreversibly/ reversibly to COX enzymes

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A

Aspirin is selective for COX 1

it binds irreversibly to COX enzymes
–> acetylates active site

17
Q

What are the main actions of aspirin?

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A
  • anti-inflammatory,
  • analgesic
  • anti-pyretic actions
  • Reduces platelet aggregation
18
Q

Explain the effects of prostanoids on platelet aggregation ???

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A

technically aspirin works on both:

a) platelets
- -> aspirin inhibits COX 1
- -> inhibits TXA2 production
- -> reduces platelet aggregation

b) endothelial
- -> aspirin inhibits COX 1 + 2
- -> prevents Prostacyclin PGI2 production
- -> increases platelet aggregation

  • -> but Endothelial cells have nucleus (can replenish COX 2)
  • -> so aspirin affects this pathway to a lesser extent

overall effect = reduced platelet aggregation

19
Q

How can anti platelet actions of aspirin be explained?

what is a solution?

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A
  • Very high degree of COX-1 inhibition –> suppresses TxA2 production by platelets
  • Covalent binding –> permanently inhibits platelet COX-1
  • low capacity to inhibit COX-2

solution = low dose to allow endothelial resynthesis of COX-2

20
Q

What are Major side-effects of Aspirin seen at therapeutic doses?

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A
  • Gastric irritation / ulceration
  • Bronchospasm in asthmatics
  • Prolonged bleeding times
  • Nephrotoxicity

side effect = usually due to covalent inhibition

21
Q

Is Paracetamol a NSAID?

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A

it is not a NSAID

22
Q

whats the use for paracetamol?

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A
  • analgesic –> moderates pain

- has anti pyretic action

23
Q

Describe the mechanism of action of paracetamol

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A
  • possible mechanisms
    = via cannabinoid receptors
    = interaction with endogenous opioids
    = interaction with 5HT and adenosine receptor
24
Q

How can paracetamol cause irreversible liver failure?

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A
  • paracetamol overdose
  • glutathione = involved in conversion of toxic metabolite –> to inactive form
  • when you overdose:
  • glutathione = depleted
  • metabolite oxidises thiol groups of key hepatic enzymes –> cell death
25
How would you treat paracetamol poisoning ?
- Add compound with –SH groups - e.g IV Acetylcysteine or oral methionine Acetyl cysteine used in attempted suicide/ accidental poisoning If not administered early enough --> liver failure
26
Aspirin is unique amongst NSAIDS because: a) It has no effect on COX-1 b) It has no effect on COX-2 c) It binds covalently to COX enzymes d) It binds covalently to TP receptors e) It causes gastric ulceration
c) It binds covalently to COX enzymes
27
Inhibition of which enzyme will reduce platelet aggregation with fewest side effects? a) COX-1 b) COX-2 c) Prostacyclin synthase d) Prostaglandin E synthase e) Thromboxane A2 synthase
e) Thromboxane A2 synthase | Yes - Thromboxanes causes platelet aggregation, but not much else
28
Assertion: Inhibition of PGI2 synthesis by low dose aspirin decreases the risk of stroke Because : Decreased PGI2 reduces platelet aggregation a) Assertion true, reason true and explains assertion b) Assertion true, reason true but does not explain assertion c) Assertion true, reason false d) Assertion false, reason true e) Assertion false, reason false
e) Assertion false, reason false Explanation: Synthesis of PGI2 (prostacyclin) is inhibited by low dose aspirin, but it is not this action which decreases the risk of stroke, because PGI2 actually reduces platelet aggregation. It’s the inhibition of thromboxane synthesis
29
Why has the number of deaths from paracetamol overdose fallen steadily in England and Wales?
The quantity of paracetamol which can be purchased over the counter is restricted by law
30
NSAIDS cause increase GI + CVS related deaths
-
31
PGE2 can activate 4 receptors what do activation of these 4 receptors do?
EP 1 - increase ca2+ mobilisation EP 2 - increase cAMP EP 3 - increase cAMP+ increase Ca2+ mobilization EP4 - increase cAMP -->both cause increased pain / inflammation
32
NSAIDs mechanism of action: identify the underlying mechanism of action by which all NSAIDs have their therapeutic effects and the difference between the NSAIDs and paracetamol NSAIDs side effects: identify the side-effects associated with NSAID use COX-2 inhibitors: explain why COX-2 inhibitors have proved less successful than hoped
--
33
note: Although PGE2 can cause Bronchodilation asthmatic --> shouldn't take NSAIDS explanation - COX inhibition --> favors leukotriene production (bronchoconstrictors)
-
34
NSAID - irreversibly / reversibly inhibit both COX 1 + COX 2
NSAID reversibly inhibit both COX 1 + COX 2
35
Selective COX2 inhibitors have higher / lower CVD risk than non selective COX inhibitors Selective COX 1 inhibits have higher / lower GI risk than non non selective COX inhibitors
Selective COX2 inhibitors have higher CVD risk than non selective COX inhibitors Selective COX 1 inhibits have higher GI risk than non non selective COX inhibitors
36
NSAIDS - low risk of side effects (for analgesic effect) - high risk of side effect (anti inflammatory use)
-
37
what steps were taken to --> reduce cases over overdose
- reduction in pack size - limited to 16 tablets a pack --> caused a decrease in death rate
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