Pain Flashcards

1
Q

Pain pathway

A

Nociception -> pain -> suffering -> pain behaviour

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2
Q

3 sources of pain

A
  1. trauma
  2. inflammation
  3. ischaemia
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3
Q

Physiology of trauma

A

Neuronal - free nerve endings
Conducted by A delta fibres
Myelinated - fast pain, quick reaction

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4
Q

Physiology of ischaemia and inflammation

A

Chemical - prostaglandins/histamine
Conducted by C fibres
Unmyelinated - delayed and continued pain

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5
Q

Gate control theory

A

Pain conduction is modulated at the spinal cord by peripheral nerve impulses and impulses from the brain

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6
Q

Gate-closing stimuli

A

Peripheral nerve stimulation (rubbing)

Mental state: endorphins, dynorphins and enkaphalins bind to ion-gated channels of post-synaptic nerve

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7
Q

Gate-opening stimuli

A

Glutamate (most excitatory neurotransmitter) binds to receptors
Mental stress (lack of feel good chemicals)
Bradykinin and other inflammatory mediators

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8
Q

Inflammation is caused by… in order to…

A

tissue damage

minimise consequences of damage and start repair

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9
Q

Symptoms of inflammation (5)

A
Redness
Swelling
Heat
Pain
Loss of function
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10
Q

3 stages of inflammation

A
  1. Damage to blood vessel: compromises laminar blood flow, so cells start hitting endothelium on inside of vessel
  2. Change in vascular permeability: joints in cell start leaking plasma and proteins, causing a drop in oncotic pressure and more fluid in interstial area
  3. Leukocyte accumulation: leukocytes migrate and adhere to side of blood vessel, opening gaps between cells further so they can emigrate to damaged area
  4. Phagocytosis of bacteria and damaged tissue and release of leukocyte product which dissolves foreign body
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11
Q

Biochemical process of inflammation

A
  1. Phospholipid from bilayer is acted on by phospholipase A2
  2. Creates arachidonic acid
  3. 5-lipoxygenase turns arachidonic acid into leukotrins, which attract white blood cells, cause vasoconstriction, bronchoconstriction, and vascular permeability
  4. Cycloxygenase 1+2 turn arachidonic acid into prostaglandins, anticoagulants, and platelet activator
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12
Q

Causes of ischaemic pain

A

Spasm causes blocked or narrowed blood vessels

O2 starvation

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13
Q

Process of ischaemic pain

A
  1. O2 starvation causes a lack of ATP
  2. Cells generate energy anaerobically
  3. Increased lactic acid
  4. Increase in hydrogen ions
  5. Increased acidity is perceived by pH sensitive nerves, which is converted to pain
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14
Q

Acute pain

A

Less than 3 months
Response to a natural or therapeutic process
Response to trauma

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15
Q

Chronic pain

A

More than 3 months
Typically not ‘useful’
Often caused by degeneration

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16
Q

Mechanism of local anaesthetics

A

Stop nerve conduction by preventing sodium ion channels working

17
Q

Adverse effects of local anaesthetics (5)

A
Neurological disorders
Convulsion
Restlessness
Respiratory paralysis
Cardiac disorders - reduced impulse conduction
18
Q

2 areas of pain relief

A

Epidural - between dura matter and vertebral spines

Spinal block - next to spinal cord

19
Q

Mechanism of opioids

A
  1. Mimic endorphins, dynorphins and enkaphalins
  2. Bind to receptor on pre-ganglionc nerve
  3. Prevent neurotransmitter release by opening K+ channels
  4. Prevents depolarisation
20
Q

Adverse effects of opioids (10)

A
Cough centre depression
Sweating
Pupil constriction
Euphoria
Respiratory depression
Bronchial contraction
Vasodilation
Biliary spasm
Decreased peristalisis (constipation)
Increased bladder tone
21
Q

Types of opioid

A

Morphine
Codeine (less potent)
Pethidine (doesn’t cause constriction of smooth muscle, but is metabolised quickly)
Tramadol (synthetic)

22
Q

PK/PD lag

A

With opioids, the effect of drug is felt after drug levels have peaked, not at peak

23
Q

Non-opioid analgesics (2)

A
  1. Non-steroidal anti-inflammatory drugs (NSAIDs), e.g. paracetamol or ibuprofen, inhibit cycloxygenase to reduce swelling and pressure
  2. Corticosteroids stop formation of arychonic acid from phospholipid