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LOCO 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Define pain

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

What is allodynia

A

Pain due a stimulus that does not usually elicit pain

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3
Q

What is hyperalgesia

A

An increased response to a stimulus is normally painful

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4
Q

How does somatic pain feel

A
  • Aching
  • Constant
  • May be dull/ sharp
  • Well localised, except when deep
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5
Q

What is Hiltons law

A

Nerve that supplies a joint capsule also supply the muscles that move the joint and the skin over the joint

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6
Q

How much of COX-2 must be inhibited for anti-inflammatory properties to work

A

80%

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7
Q

What is the main mode of action of NSAIDs

A

Inhibitions of COX enzymes (1 and 2)

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8
Q

3 properties of NSAIDS

A

Analgesic, antipyretic and anti-inflammatory

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9
Q

How do ibuprofen, duclofenac, ketoprofen differ from asprin

A

Additional mechanisms as well as asprisin

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10
Q

Name 4 selective COX-2 inhibitors

A

Roflecoxib
Celecoxib
Etoricoxib
Meloxicam

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11
Q

Name 4 NSAIDs which are mainly for pain

A

-Aceclofenax
Etoricoxib
Fenbufen
Tiaprofenic acid

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12
Q

What NSAID is mainly for pain

A

Paracoxib

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13
Q

Which NSAID comes in eye drop

A

Ketorolac

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14
Q

By inhibiting COX enzymes what is inhibited

A

Prostaglandins

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15
Q

Where are prostaglandins derived from

A

Archidonic acid

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16
Q

What happens to the arachidonic acid during prostaglandin synthesis

A
  • Injected into COX enzymes hydrophobic channel

- Interacts with molecular oxygen to produce either prostacyclins, prostaglandins or thromboxane

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17
Q

What is the action of prostaglandin E2

A

Vasodilator

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18
Q

What is the action of prostaglandin D2

A

Vasodilator

Inhibits platelet aggregation

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19
Q

What is the action of prostaglandin F2

A

Vasoconstrictors

Works on the uterus to make it contract

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20
Q

What is thromboxane

A

Thrombotic and vasoconstrictor

21
Q

What enzyme catalyses the formation of prostaglandin from arachidonic acid

A

Enzyme cyclooxygenase

22
Q

Describe how the shape of COX1/ COX2 differs

A

Cox 1 is narrower

Cox 2 is less rigid

23
Q

What is prostacylin also known as

A

PGI2

24
Q

Where do prostaglandins diffuse to

A

Very locally

25
Q

What kind of receptors are the prostaglandin receptors

A

GPCR

26
Q

How many different prostaglandin receptors are there

A

9

27
Q

What is COX 1’s function

A

‘house keeping’

contributes to homeostasis

28
Q

Which COX is inducible

A

COX 2

29
Q

What induces COX 2

A

Pro-inflammatory cytokines

30
Q

How long does COX 2 take to be induced

A

half an hour- 4 hours

31
Q

Why can COX 2 be induced and prostaglandins be produced easily

A

Looser hydrophobic channel allows more things in

32
Q

Which COX is mainly found in the stomach and where specifically in the stomach is it found

A

COX 1

Protects against injury and damage

33
Q

Where is the stomach is COX 2 found

A

Low level of COX 2 found in the superficial mucosa

34
Q

What prevents platelet aggregation

A

PGI2 from endothelial cells

35
Q

What induces platelet aggregation

A

Thromboxane A2 COX 1

36
Q

Does ibuprofen have long term or short term effect on platelets

A

Short

37
Q

In which area are both COX 1 and COX 2 found under resting location

A

CNS and spinal cord

38
Q

Where in the kidney is COX 2 found

A

In the macula densa

39
Q

When does COX 2 increase in the kidney

A

In salt deprivation

40
Q

What cell types are activated when COX 2 is induced

A

Macrophages

Synoviocytes

41
Q

How much of COX 1 does aspirin inhibit if 80% of COX 2 is inhibited

A

90

42
Q

What category of NSAID are ibuprofen/ piroxicam

A

Cateogory 1: rapid, competitive, reversible binding of COX 1/2

43
Q

What category of NSAID are diclofenac/ indomethacin

A

Rapid, lower affinity reversible followed by time dependent, high affinity slowly reversible binding of COX 1/2

44
Q

What category of NSAID is aspririn

A

Rapid reversible binding followed by covalent modification of COX 1 and or COX 2 non competitive reversible

45
Q

What are coxibs

A

Selective to COX 2 inhibitors

46
Q

What adverse effects have been reported in use of selective COX 2 inhibitors

A

Increased CV risk

47
Q

Is GI risk more significant in selective cox 2 or non selective

A

Non selective

48
Q

2 proposed mechanisms for paracetomol

A
  • Modulate endogenous cannaboid system and trpv1 by am404

- activates serotonergic descending pathways

LOCO 2 (25 decks)

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