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loco > Analgesia and pain management, NSAIDs > Flashcards

Analgesia and pain management, NSAIDs Flashcards

1
Q

Describe acute pain. (type of pain, structures involved, duration etc.)

A

Nociceptive
primary afferent neurones detect noxious stimuli and information is relayed to the supraspinal structures
pain response correlates to degree of inflammation
duration: <12 weeks

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2
Q

Describe chronic pain. (type of pain, structures involved, duration etc.)

A 
duration: >12 weeks
no apparent ongoing tissue damage
ectopic focus of neural activity 
central/peripheral sensitisation 
response to treatment is less effective 
unpredictable prognosis
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3
Q

Define allodynia.

A

pain due to a non-noxious stimulus

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4
Q

Define hyperalgesia.

A

increased response to a stimulus which is normally painful

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5
Q

What are the clinical features of somatic pain?

A

Aching constant pain (can be dull or sharp)
Worsens on movement
Well localised pain

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6
Q

State Hilton’s law.

A

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

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7
Q

What is the difference between treatment of acute and chronic pain? (WHO analgesic ladder)

A

Acute: go DOWN the ladder
Chronic: go UP the ladder

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8
Q

What are the different types of NSAIDs? Give examples of each.

A
  1. Selective COX-2 inhibitors
    - celecoxib
    - etoricoxib
    - any -coxib
  2. Enolic acid derivatives
    - piroxicam
    - meloxicam
    - any -icam
  3. Salicylates
    - aspirin
    - diflunisol
  4. Fenamates
    - mefenamic acid
  5. Acetic acid derivatives
    - diclofenac
    - indomethacin
    - any -ac
  6. Propionic acid derviatives
    - ibuprofen
    - naproxen
    - ketoprofen
    - any -en
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9
Q

What is the difference between the structure of COX and COX 2?

A

COX 1 has a tighter hydrophobic channel

COX2 has a more flexible hydrophobic channel (creates a side pocket)

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10
Q

In the UK, which NSAIDs are used for main inflammation (i.e. inflammation only)?

A

Aceclofenac
Etoricoxib
Fenbufen
Tiaprofenic acid

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11
Q

In the UK, which NSAIDs are used for inflammation AND pain?

A 
acematcin 
celecoxib 
diclofenac
ibuprofen
indomethacin
naproxen
piroxicam
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12
Q

In the UK, which NSAIDs are used for mainly pain (i.e. pain only)?

A

paracoxib

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13
Q

Which NSAIDs can be used for:

  1. eye issues
  2. Cancer, CV issues and Alzheimer’s disease
A
  1. Ketorolac

2. Aspirin

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14
Q

What is the MOA of NSAIDs?

A

NSAIDs inhibit COX-1 and COX-2 enzymes

this prevents the conversion of arachidonic acid into prostaglandins

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15
Q

What is the action of phospholipase A2?

A

converts phospholipids into arachidonic acid and lyso-glycerol-phosphorylcholine

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16
Q

What are prostaglandins?

A

Tissue hormones

they do not diffuse very far - act locally

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17
Q

What are the different classes of prostaglandins?

A
  1. PG D, E and F
  2. Prostacyclin (PGI2)
  3. Thromboxane A (TXA2)
18
Q

What are the actions of PGD?

A 
acts on mast cells, brain and airways
actions:
- memory
- sensitisation of peripheral nerve endings 
- bronchoconstriction 
- vasodilation
19
Q

What are the actions of PGE?

A

acts on brain, kidney, smooth muscle, platelets
actions:
- memory
- sensitising nerve endings
- vasodilation (renal artery)*
- suppress lymphocytes*
- GI smooth muscle contraction + relaxation
- inhibits gastric acid secretion*
- increases platelet response to agonists
- uterine relaxation*

  • = important
20
Q

What are the actions of PGF?

A 
acts on uterus, airways, vascular smooth muscle, eye 
actions:
- uterus contraction
- bronchoconstriction 
- vasodilation and constriction
21
Q

What are the actions of PGI2?

A

acts on platelets, vascular smooth muscle, airways and stomach
actions:
- prevents formation of platelet plug
- bronchodilation
- vasodilation (renal artery)
- protects lining of stomach (inhibits gastric acid secretion)
- sensitisation of afferent nerve endings

22
Q

What are the actions of TXA2?

A 
acts on vascular smooth muscle, platelets, airways, uterine smooth muscle 
actions:
- vasoconstriction
- promotes platelet aggregation
- bronchoconstriction 
- uterine contraction
23
Q

What type of receptors are the prostaglandin/prostanoid receptors?

A

GPCRs

24
Q

Compare COX-1 and COX-2 in terms of:

  1. regulation
  2. rate of gene activation
  3. effects of glucocorticosteroids
  4. rate of arachidonic acid consumption
  5. effect of aspirin
A

COX-1:

  1. usually constitutive (constant low level of PG production)
  2. 24 hours
  3. Inhibits activity
  4. 34 mmol/min/mg
  5. inhibited

COX-2:

  1. inducible
  2. 0.5-4 hours
  3. inhibits activity
  4. 39 mmol/min/mg
  5. affected
25
Q

Why are COX-2 enzymes active in OA and RA?

A

IL-1, TVFalpha and IL-17 stimulates iNOS

iNOS induces COX2 expression

26
Q

What is the effect of the COX2 pathway and 5-LOX pathway in joints?

A

COX2 pathway produces prostaglandins and thromboxanes
5-LOX pathways produce leukotrienes
these contribute to joint soreness and stiffness

27
Q

What is the effect of COX enzymes in the stomach?

A 
COX2: found in low levels in superficial mucosa
COX1: lots in crypts 
- it produces PGE2 which:
1. increases mucus secretion
2. increases cell regeneration 
3. increases HCO3- releasing 
4. decreases H+ secretion
5. increases blood flow
28
Q

What are the effects of long-term use of NSAIDs on the stomach?

A

Inhibit PGE2 production resulting in:

  • pyrosis
  • dyspepsia
  • gastric pain
  • injury to mucosa
  • reduced blood flow
  • PMN
  • irregularity
  • congestion
  • haemorrhage

all of these manifest as gastritis and gastric ulcers

29
Q

What are the effects of COX enzymes on the cardiovascular system?

A
  • PGI2 from endothelial cells prevents platelet aggregation
  • TXA2 COX1 induced platelets promotes aggregation

increases CV risk due to potential platelet aggregation

30
Q

What role(s) does COX-2 play in the spinal cord and CNS?

A
  • peripheral and central role in pain perception and sensitisation
  • inflammation evoked spinal hyperexcitability might be related to the conversino of 2-arachidonolyglycerold to PGE2 subtype G via COX-2
31
Q

In the spinal cord + CNS, what is COX-2 activated/upregulated by?

A
  • cytokines
  • IL-1beta
  • NMDA
  • Ca2+ influx
  • NOS
32
Q

Why are COX enzymes important in the kidneys? What is the effect of NSAIDs on the kidneys?

A

COX enzymes protect the kidney and maintain a normal GFR

NSAIDs and selective COX-2 inhibitors reduce GFR (by constricting blood flow to the glomerulus)

33
Q

What are the effects of COX-1 and COX-2 in the kidneys?

A

COX-1: produces PGE2 and PGI2

  • PGE2: regulates sodium reabsorption
  • PGI2: increases potassium secretion (stimulates renin and RAAS)

COX-2: in small amounts in the macula densa, but increases in slat deprivation

34
Q

Give examples of COX-2 selective NSAIDs.

A

etoricoxib
diclofenac
celecoxib

35
Q

Give examples of COX-1 selective NSAIDs.

A

ibuprofen
naproxen
aspirin
indomethacin

36
Q

What % of COX-2 must be inhibited for NSAIDs to have a significant anti-inflammatory effect?

A

80%

37
Q

Describe category 1 NSAIDs and give examples.

A

rapid competitive reversible binding of COX1/2
examples:
- ibuprofen
- piroxicam

they are good for acute pain

38
Q

Describe category 2 NSAIDs and give examples.

A

rapid lower affinity reversible binding followed by time-dependent, high affinity slowly reversible binding of COX1/2
examples:
- diclofenac
- indomethacin

good for chronic pain

39
Q

Describe category 3 NSAIDs and give examples.

A

rapid reversible binding followed by covalent modifcation of COX1/2 - noncompetitive and irreversible
examples:
- aspirin

40
Q

Give an example of an atypical NSAID

A

Paracetamol

41
Q

What are the side effects of opioids/morphine?

A 
N+V
Dizziness
Sweating
Constipation
Drowsiness
Pruritis (itch)

loco (19 decks)

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