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Locomotor 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

how many major drug classes are for treating pain

A

7 major drug classes

- NSAIDS plus COX2 make up 35%

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2
Q

What is pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

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3
Q

define allodynia

A

Pain due to a stimulus which does not normally provoke pain,
e.g. Pain caused by light touch to the skin

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4
Q

define hyperalgesia

A

– An increased response to a stimulus which is normally painful

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5
Q

what are the two types of pain

A

actue

chronic

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6
Q

name 4 different types of chronic pain

A
  • Nociceptive e.g. OA and RA

Neuropathic

  • central = e.g. post stroke, MS, SCI
  • peripheral = e.g. post herpetic neuralgia and diabetic neuropathy
  • Visceral - internal organs, pancreatitis, IBS
  • Mixed - lower back, cancer, fibromyalgia
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7
Q

define chronic pain

A

Pain that lasts longer than 12 weeks

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8
Q

somatic pain

A
  • aching - often constant
  • may be dull or sharp
  • often worse with movement
  • get better at rest
  • well localised
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9
Q

When is somatic pain not well localised

A
  • when it is deep e.g. a muscle, tendon, ligament, bone, fascia, and joints
  • hiltons law - nerves that move the joint capsule also supply the muscles that move the joint and the skin over the joint
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10
Q

What is hiltons law

A

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

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11
Q

how is the WHO analgesic ladder used for chronic and acute pain

A

When you have acute pain want to start with the strongest possible therefore when it heals you want to go down the pain ladder

if there is chronic pain you might start on the bottom of the ladder and move upwards

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12
Q

what is the WHO analgesic ladder for pain

A

Step 1 - non opioid analgesics and NSAIDS

step 2
- weak opioids

Step 3
- strong opioids, methadone, oral administration, transdermal patch

step 4

  • nerve blocks
  • epidurals
  • PCA pump
  • spinal stimulators
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13
Q

describe NSAIDS

A

Effective as analgesics and for inflammation

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14
Q

How many NSAIDS are there on the market

A

Many different NSAIDs on the market

  • Fewer than 10 dominate
  • among the most used drugs in the world
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15
Q

What is the main role of NSAIDS

A

inhibition of COX enzymes

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16
Q

How does Aspirin work

A

Aspirin (COX-1 and COX-2 inhibitor): analgesic, antipyretic, anti-inflammatory)

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17
Q

What is the difference between COX-1 and COX-2 structure

A

COX1

  • bit narrower
  • not as flexible
  • does not have the hydrophobic channel

COX 2

  • larger
  • more flexible
  • has a larger hydrophobic channel
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18
Q

What is the main role of COX enzymes

A

Take arachdinonic acid and produce prostaglandins

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19
Q

what does iburprofen, diclofenac and ketoprofen do

A

(COX-1 and COX-2 inhibition, plus additional mechanisms…): analgesic and anti-inflammatory effects

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20
Q

name some selective COX-2 inhibitors

A

Rofecoxib voluntarily withdrawn 2004
Celecoxib
Etoricoxib
Meloxicam

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21
Q

what are the side effects of COX 2 inhibits

A

increase the risk of haemorragic stroke and heart attacks

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22
Q

what NSAIDS are mainly used for inflammation

A

Aceclofenac, etoricoxib, fenbufen, tiaprofenic acid

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23
Q

what NSAIDS are used for inflammation and pain

A

Acematcin, celecoxib, diclofenac, ibuprofen, indomethacin, naproxen and piroxicam

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24
Q

What NSAID that is used mainly for pain

A

Paracoxib

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25
Q

name some other NSAIDS

A

Ketorolac (eye drops)

Aspirin (cardiovascular, cancer, Alzheimer’s disease)

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26
Q

in these days when do you prescribe a COX-2

A

when the person cannot handle the NSAID

27
Q

How does prostaglandin synthesis take place

A

COX enzymes cause the conversion of arachidonic acid to prostaglandins

28
Q

name the different types of prostaglandin

A

Prostaglandins = D, E and F

Prostacyclin (PGI2)

Thomboxane A

29
Q

name what the different types of prostaglandins do

A

D = inhibit platelet aggregation, vasodilator

E = vasodilator, hyperalgesia

F = bronchoncstrictor, Myometrial contraction

30
Q

what is the action of prostacyclin

A
  • Vasodilation
  • hyperalgesia
  • stops platelet aggregation
31
Q

What is the action of thromboxane

A

Vasoconstriction, Induce platelet aggregation, Bronchoconstriction,
Uterine contraction

32
Q

describe the hydrophobic channel in COX enzymes

A

COX1 narrower

COX2 wider less rigid

33
Q

where does the arachdinonic acid bind to the COX enzymes

A

on the hydrophobic channels

34
Q

where do you want the COX inhibitors to work

A

on the hydrophobic channels where the arachdinonic acid binds to the COX enzymes

35
Q

what are prostaglandins

A

they are tissue hormones

- that are produced locally as they do not diffuse very far

36
Q

What does PGE2 do

A

Vasodilation (renal artery),

Suppress lymphocytes,

Sensitizes

peripheral nerve endings,

Inhibits gastric acid secretion,

Fever

Uterine relaxation

37
Q

What does pGD2 do

A

Vasodilation,

Bronchoconstriction (10x higher in asthmatics)

38
Q

What does PGI2 do

A

Vasodilation (renal artery),

Inhibit platelet aggregation,

Bronchodilation,

Inhibit gastric acid secretion,

Sensitize afferent nerve endings to pain

39
Q

What does PGF2alpa do

A

Mixed vascular effects (vasoconstriction and dilation), Bronchoconstriction, Uterine contraction

40
Q

what are the receptors of prostaglandins and how many receptors are there

A

G-protein-coupled receptors

9 identified receptors

41
Q

What does COX1 do

A

Housekeeping gene

always present

Contributes to homeostasis

Invovled in the GI tract, platelet function and macorophage

42
Q

What does COX2 do

A
  • inducible
  • only found in tissue that is damaged
  • found in inflammation
43
Q

describe the similarities between cox1 and cox2

A
  • same weight

- COX2 is 60% homology to cox 1

44
Q

How long does it take for gene activation in COX2

A
  1. 5 TO 4 hours compared to cox 1 gene which takes 24 hours

- therefore COX2 can be produced in higher quantities more quickly

45
Q

what is COX 2 like in the joint

A

COX2 mRNA and protein is increased in joints with osteo or rheumatoid arthritis

Pathophysiology

  • IL1, TNF and IL17 (stimulates iNOS that induces COX2)
  • these pro inflammatory cytokines either then cause either direct or indirect induction of COX2
  • thus you get vasodilation and nociceptor sensitisation leading to pain
46
Q

in the stomach what is he mean isoforms of COX enzymes

A

Mainly COX1 isoform

- there are low levels of COX2 in the superficial mucosa

47
Q

What does COX1 do in the stomach

A

In crypts where is protects against injury and damage

Normal PGE2 helps gastric mucosa (blue box)

48
Q

what does NSAIDS for long periods do in the stomach

A

NSAIDs for long periods blocks PGE2 generation (red boxes)

49
Q

what are the side effects of NSAIDS

A
  • gastric ulcers
  • gastritis
  • blood
  • haemorrhage
  • pyrosis
  • dyspepsia
50
Q

what does prostacyclin prevent

A

PGI2 (prostacyclin) from endothelial cells prevents platelet aggregation

51
Q

what does thromboxane do to platelets

A
  • Thromboxane A2 COX1 induced in platelets promotes aggregation
52
Q

How does aspirin act as a blood thinner

A

Low dose aspirin act as a blood thinner as there is a covalent change to the active site that changes the function and blocks the platelets action so arachdinonic acid cannot be converted to thromboxane as it cannot bind to the COX1 enzyme within the platelet

53
Q

Why does aspirin work less efficiently with ibuprofen

A

Ibuprofen will go into the COX enzyme and bind to a similar location and will block a short period of time the active site but it also blocks aspirin from getting in therefore aspirin works less efficiently

54
Q

what is COX important in

A

spinal nociceptive transmission

- expressed in the spinal cord in inflammation

55
Q

what is important in protecting the kidney

A

Prostaglandins important in protecting kidney

56
Q

How does COX1 work in the kidneys

A

COX1 producing PGE2 and PGI2

  • PGE2 regulates sodium reabsorption
  • PGI2 increase potassium secretion (stimulates renin and thus renin-angiotensin system)
  • In addition vasodilatory actions
57
Q

When does COX2 increase in the kidney

A

COX2 present in small amounts in macula densa but increases in salt deprivation

58
Q

for a drug to be effective at anti-inflammatory how much of the COX-2 do you have to be inhibiting

A

80%

59
Q

What are the 3 broad categories of COX inhibition mechanisms

A

Category 1: rapid competitive reversible binding of COX1/2

  • acute pain such as headaches
  • Ibuprofen, piroxicam

Category 2: rapid lower affinity reversible binding followed by time dependent, high affinity slowly reversible binding of COX1/2

  • good for musculoskeletal disorders
  • Diclofenac, indomethacin

Category 3: rapid reversible binding followed by covalent modification of COX1 and or COX2 non-competitive irreversible
- Aspirin

60
Q

why was rofecoxib withdrawn

A

increase 2 times of risk of CV events

61
Q

Describe the mechanism o faction of paracetamol

A

Does not inhibit any COX outside of CNS (reduces COX)

Could modulate endogenous cannabinoid system and TRPV1 by AM404 metabolite

Activates serotonergic descending pathways

62
Q

describe COX 3

A

Transcribed from COX1 gene retains extra intron

only found in the CNS

63
Q

why does paracetamol not work via COX 3

A

Hypothesis that this was the target for paracetamol

Sites for COX3 don’t match with fever production

Appears non-functional in humans

Locomotor 2 (30 decks)

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