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Medicine 2 > Week 1 - Pain > Flashcards

Week 1 - Pain Flashcards

1
Q

What are the characteristics of acute pain?

A

Tissue injury

Varying severity

Intensity relates to injury severity

Predictable time course

Successful treatment

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2
Q

What are the characteristics of chronic pain?

A

Pain > 3 months

Lasts after normal healing

Sometimes non-identifiable cause

No obvious pathological process

Unpredictable time course

Difficult to treat

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3
Q

What are the mechanisms of nocioceptive pain?

A

Good pain

Sensation associated with detection of damaging stimuli

Protective mechanism

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4
Q

What are the mechanisms of inflammatory pain?

A

Obvious tissue injury

Infiltration of immune cells promoting repair, causing pain until healed

Protective

Sharp/dull ache/throb

Well localised

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5
Q

What are the mechanisms of pathological pain?

A

Maladaptive

Results from abnormal NS function

Disease states caused by damage to NS (neuropathic pain) or abnormal function (nociplastic pain)

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6
Q

What are the mechanisms of neuropathic pain?

A

Cause by lesion or disease of SNS

Tissue injury not obvious

No protective function

Burning, shooting, pins and needles, numbness

Well localised

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7
Q

What are the mechanisms of nociplastic pain?

A

Substatial pain but no noxious stimuli or peripheral inflammatory pathology

No neuronal damage

Fibromyalgia, IBS, tension headache, interstitial cystitis

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8
Q

How to take a pain history?

A

PQRST

Precipitating factors

Quality of pain

Radiation

Severity

Timing

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9
Q

How to assess pain in dementia patients?

A

Assess via observation

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10
Q

What are the goals for pain reduction with analgesics?

A

>50% reduction

No worse than mild pain

Relief from related problems

No side effects

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11
Q

What are the properties of the dopamine pathway?

A

Reward

Pleasure

Motor function

Compulsion

Preservation

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12
Q

What are the properties of the serotinin pathway?

A

Mood

Memory processing

Sleep

Cognition

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13
Q

What are the properties of the brain reward pathway?

A

Meso-limbic dopamine pathway

+ drugs of abuse increase dopamine release

Some enhance serotinin 5HT function

Some block NMDA antagonists

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14
Q

What happens during opiate dependence liability and what are the chronic effects?

A

Agonist at G protein-coupled opioid receptors

Low neurotransmitter release in brain

Analgesia, euphoria, respiratory depression, dysphoria, sedation

Chronic effects = anhedonia, constipation, depression, insomnia

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15
Q

What happens in cocain dependence liability and what happens with a high dose?

A

Euphoria, excitement, + capacity to work

+ catecholamine neurotransmitter fucntion by preventing re-uptake

Sedative effects

High dose = overactivity of SNS = hypertension, tachycardia, hyperpyrexia, dilated pupil, palpitations

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16
Q

What happens in amphetamine drug dependence liability and what happens with high dose?

A

Produce wakefulness and concentration

Performance enhancing

Release monoamines from neuronal storage vesciles, blocking reuptake transporters

+ synaptic DA, NA, 5HT

Euphoria, + libido, energy, self-esteem, aggression, + power, obession, paranoia

High dose = psychosis

+Cv tone, + bp, + HR

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17
Q

WHat happens in cannabis dependence liability?

A

THC = active agent

Inhibits neurotransmitter release in brain via GI protein -coupled cannabinoid receptors

Mild euphoria

Dysphoria in high doses

+ appetite stimulation through actions on feeding centers in hypothalamus and gut, analgesic

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18
Q

Treatment for drug dependence?

A

Agonist substitution

Partial receptor agonist

Antagonist treatment

Anti-craving medicine

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19
Q

What is inflamed in meningitis?

What is inflamed in encephalitis?

A

Meninges

Brain

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20
Q

What is inflamed in myelitis?

What is inflamed in neuritis?

A

SPinal cord

Peripheral nerves

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21
Q

What are the main routes of infection?

A

Blood-borne

Parameningeal supparation

Spread through dura defect

Soread through cribiform plate

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22
Q

What are the symptoms of meningitis?

A

Meningism = headache, stiff neck and back, nausea/vomiting, photophobia

Fever

Rash

Infants = flaccid, bluging frontalle, fever, vomiting, strange cry, convulsions

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23
Q

How do you investigate meningitis?

A

Lumbar puncture (distinguish between bact. and vir.)

CSF analysis (if >5 white cells = meningitis)

Gram stain

Zn

PCR

Antigen agglutination tests

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24
Q

How do you manage meningitis?

A

Antibiotics

+ oxygenation

Prevent hypoglycaemia and hyponatraemia

Antoconvulsants

Decrease intracranial hypertension

Steroids prior to antibiotics

25
Q

What are the causes of viral meningitis?

A

Predisposition (immunosuppression, alcohol, diabetes, hyposplenism, myeloma)

Pneumonia

Impaired conscioussness

Immunocompromised, neonate, > 50

26
Q

What are the symptoms of encephalitis?

A

Cerebral irritation (irritated, altered personality, drowsiness, ataxia, brisk tendon reflexes, sluggish pupils)

Fever

Seizures

CSF pleocytosis

Abnormal neuroimaging

27
Q

What causes encephalitis?

A

Herpes simplex virus

Arboviruses and rabies

Mosquitos, ticks, sandlfies

28
Q

What are the clinical features of myelitis?

A

Vasculitis of anterior spinal artery

Primary = TB, syphilis

Post-infection = MMR

Ascending flaccid paralysis and sensory loss

29
Q

What are the clinical features of encephalomyelitis?

A

Mix of 2

Viral and non-viral

PAthogenesis = direct invasion, vasculitis, immune infection response

Entry to CNS = respiratory, GI, subcutaneous, mucosa

30
Q

What si the function of the somatosensory system?

A

Receives info from body parts

Detects + stimuli

Nociception (neural process activating C-fibres)

31
Q

What is the function of the sensory system?

A

Receptive fields on sensory receptors

Single neuron in CNS can receive + inputs = convergence

Converts natural stimulus into action potentials

32
Q

What happens during transduction?

A

Sensory nerve:

  • Deformation of membrane
  • Opening of Na+ and K+ channels
  • Receptor potential
  • Local depolarisation of receptive membrane
  • Action potential propagated to CNS
33
Q

What happens during transmission of tactile messages?

A

Central touch fibre branches ascend in dorsal columns

Synapse in dorsal column nuclei

Thalamus = synapse on cells

Sends projections to primary somatosensory cortex

34
Q

What are the properties of alpha-beta fibres?

A

Myelinated fibres

Fast conduction velocity

Terminate in intermediate lamina of dorsal horn

Responses sensitive to glutamate receptor and peptide receptor antagonists

35
Q

What are the properties of C-fibres?

A

Unmyelinated fibres

Slower conduction velocity

Terminate in superficial lamina or dorsal horn

Responses sensitive to glutamate receptor and peptide receptor antagonists

36
Q

What is the process of spinal processing in pain?

A
  • Dorsal horn of spinal cord receives innocuous and noxious messages
  • Signals from nociceptor afferents activates second order neurones in SC
  • Projection neurones project to brain
  • Pain signals set up withdrawal reflexes
37
Q

What are the spinal responses to pain?

A
  • Not fixed and proportional to intensity of stimulus
  • Enhanced responses for a given noxious stimulus are associated with repeated higher stimulation
38
Q

What makes up the ascending pain pathway?

A
  • Spinothalamic tract from laminae 1 and 5 to thalamus
  • Post-synaptic dorsal column pathway
  • Spino-reticular tract
  • Spino-mesenphalic pathway
39
Q

What happens to brainstem when in pain?

A
  • Stimulated through spinoreticular tract and branches of psinothalamic tract
  • Changes in bp, respiration, orientation
40
Q

What is the function of the thalamus in pain?

A
  • VPL = main somatosensory area of thalamus
  • Final relay before sensory signals reach cortex
41
Q

What is the function of the cortex when in pain?

A

Conscioussness of pain and limbic system for emotional response

42
Q

What is the function of the hypothalamus whe in pain?

A

Where repsonses are mediated

Neuroendocrine changes and behaviours

43
Q

What are causes of migraines?

A
  • Genetic
    • Autosomal dominant
  • Vascular origin theory
    • Hormonal disturbance = abnormal cerebral bloodflow
  • Cortical spreading depression theory
    • Cause of aura
  • Sensory nerve activation theory
      • trigeminovascular neuron activity
44
Q

How do you treat migraines?

A
  • Analgesics
  • Anti-emetics
  • Triptans
  • CGRP receptor antagonists
  • Beta-blockers, CC blockers, anti-epileptics, pre-menstrual oestrogen
  • Acupuncture
45
Q

What are the mechanisms behind vomiting?

A
  • Chemoreceptor trigger zone
  • Neurokinin = major output transmitter
  • Vestibular system = motion sickness
  • Intracranial pressure recptors
  • Vagal nerve afferents = gag reflex
  • Descending inputs = smells etc.
46
Q

How do you treat emesis?

A
  • 5HT3 antagonists
  • Eicosanoid synthesis inhibition (corticosteroids)
  • Neurokinin1 antagonists
  • Dopamine D2 antagonists
  • Muscarinin antagonists
  • Antihiastamines
  • Histamine H3 antagonist
  • Cannabinoid agonists
47
Q

What 3 agents go into anaestetics?

A

Hypnotics

Opioids

Neuromuscular blockers

48
Q

How are eicosanoids involved in inflammation and what are examples of some?

A
  • Main source = arachidonic acid
  • Sythensis is driven by + stimuli, such as cell damage

Examples = prostaglandins, thromboxanes, leukotrienes

49
Q

What are the roles of COX1 and COX2?

A

COX1 = enzyme in most tissues and blood platelets, tissue homeostasis

COX2 = induced in activated inflammatory cells, responsible for prostaglandin mediators of inflammation production

50
Q

What are mediators from COX and their functions?

A
  • Cyclic endoperoxides
    • PGI2 - hyperalgesic, vasodilator, - platelet aggregation
    • PGE2 - hyperalgesic, vasodilator
    • PGD2 - vasodilator, - platelet aggregation
    • TXA2 - thrombotic vasoconstrictor
51
Q

How do prostanoids generate prostaglandins?

A
  • Inflammatory response = prostanoid produced
  • PGD2 released by mast cells
  • Synergise with histamine and bradykinin
  • Redness and + bloodflow
  • Prostaglandins potentiate actions of bradykinin and histamine on blood vessels and peripheral nerves
52
Q

How does bradykinin generate prostaglandins?

A
  • Synthesised during tissue injury
  • Activated by enzymes
  • Activates nociceptors by B1 and B2 receptor
    • PG production
53
Q

How do NSAIDs reduce pain?

A
  • Reduce inflammation
  • Inflammation causes pain
  • Decrease in pain
54
Q

How do NSAIDs act as antipyretics?

A
  • Reset thermostat and hypothalamus actions
  • Inhibition of PG production in hypothalamus
  • Temperature regulated, so decrease in temperature
55
Q

What are NSAIDs mechanism of action?

A
  • Inhibit cyclooxygenase enzyme
  • Reduce eicosanoid generation
  • Less PGs and inflammation
56
Q

What are the opioid receptor mechanisms?

A
57
Q

What are the effects of morphine?

A
  • Act via u-receptor
  • Analgesia
  • Euphoria and dysphoria
  • Anti-tussive (prevent cough)
58
Q

What are the sites of action of opioids?

A
  • Increase descending control from brain to SC via excitation
  • Bind to GABAergic neuron
  • Blocks transmission of neurotransmitter from glutamate
  • Increases excitation at neurone

Medicine 2 (29 decks)

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