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Medicine 2 > Week 1 - Pain > Flashcards

Week 1 - Pain Flashcards

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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?

Study These Flashcards
A

Antibiotics

+ oxygenation

Prevent hypoglycaemia and hyponatraemia

Antoconvulsants

Decrease intracranial hypertension

Steroids prior to antibiotics

25
What are the causes of viral meningitis?
Predisposition (immunosuppression, alcohol, diabetes, hyposplenism, myeloma) Pneumonia Impaired conscioussness Immunocompromised, neonate, \> 50
26
What are the symptoms of encephalitis?
Cerebral irritation (irritated, altered personality, drowsiness, ataxia, brisk tendon reflexes, sluggish pupils) Fever Seizures CSF pleocytosis Abnormal neuroimaging
27
What causes encephalitis?
Herpes simplex virus Arboviruses and rabies Mosquitos, ticks, sandlfies
28
What are the clinical features of myelitis?
Vasculitis of anterior spinal artery Primary = TB, syphilis Post-infection = MMR Ascending flaccid paralysis and sensory loss
29
What are the clinical features of encephalomyelitis?
Mix of 2 Viral and non-viral PAthogenesis = direct invasion, vasculitis, immune infection response Entry to CNS = respiratory, GI, subcutaneous, mucosa
30
What si the function of the somatosensory system?
Receives info from body parts Detects + stimuli Nociception (neural process activating C-fibres)
31
What is the function of the sensory system?
Receptive fields on sensory receptors Single neuron in CNS can receive + inputs = convergence Converts natural stimulus into action potentials
32
What happens during transduction?
Sensory nerve: - Deformation of membrane - Opening of Na+ and K+ channels - Receptor potential - Local depolarisation of receptive membrane - Action potential propagated to CNS
33
What happens during transmission of tactile messages?
Central touch fibre branches ascend in dorsal columns Synapse in dorsal column nuclei Thalamus = synapse on cells Sends projections to primary somatosensory cortex
34
What are the properties of alpha-beta fibres?
Myelinated fibres Fast conduction velocity Terminate in intermediate lamina of dorsal horn Responses sensitive to glutamate receptor and peptide receptor antagonists
35
What are the properties of C-fibres?
Unmyelinated fibres Slower conduction velocity Terminate in superficial lamina or dorsal horn Responses sensitive to glutamate receptor and peptide receptor antagonists
36
What is the process of spinal processing in pain?
* 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
What are the spinal responses to pain?
* Not fixed and proportional to intensity of stimulus * Enhanced responses for a given noxious stimulus are associated with repeated higher stimulation
38
What makes up the ascending pain pathway?
* Spinothalamic tract from laminae 1 and 5 to thalamus * Post-synaptic dorsal column pathway * Spino-reticular tract * Spino-mesenphalic pathway
39
What happens to brainstem when in pain?
* Stimulated through spinoreticular tract and branches of psinothalamic tract * Changes in bp, respiration, orientation
40
What is the function of the thalamus in pain?
* VPL = main somatosensory area of thalamus * Final relay before sensory signals reach cortex
41
What is the function of the cortex when in pain?
Conscioussness of pain and limbic system for emotional response
42
What is the function of the hypothalamus whe in pain?
Where repsonses are mediated Neuroendocrine changes and behaviours
43
What are causes of migraines?
* 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
How do you treat migraines?
* Analgesics * Anti-emetics * Triptans * CGRP receptor antagonists * Beta-blockers, CC blockers, anti-epileptics, pre-menstrual oestrogen * Acupuncture
45
What are the mechanisms behind vomiting?
* Chemoreceptor trigger zone * Neurokinin = major output transmitter * Vestibular system = motion sickness * Intracranial pressure recptors * Vagal nerve afferents = gag reflex * Descending inputs = smells etc.
46
How do you treat emesis?
* 5HT3 antagonists * Eicosanoid synthesis inhibition (corticosteroids) * Neurokinin1 antagonists * Dopamine D2 antagonists * Muscarinin antagonists * Antihiastamines * Histamine H3 antagonist * Cannabinoid agonists
47
What 3 agents go into anaestetics?
Hypnotics Opioids Neuromuscular blockers
48
How are eicosanoids involved in inflammation and what are examples of some?
* Main source = arachidonic acid * Sythensis is driven by + stimuli, such as cell damage Examples = prostaglandins, thromboxanes, leukotrienes
49
What are the roles of COX1 and COX2?
COX1 = enzyme in most tissues and blood platelets, tissue homeostasis COX2 = induced in activated inflammatory cells, responsible for prostaglandin mediators of inflammation production
50
What are mediators from COX and their functions?
* Cyclic endoperoxides * PGI2 - hyperalgesic, vasodilator, - platelet aggregation * PGE2 - hyperalgesic, vasodilator * PGD2 - vasodilator, - platelet aggregation * TXA2 - thrombotic vasoconstrictor
51
How do prostanoids generate prostaglandins?
* 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
How does bradykinin generate prostaglandins?
* Synthesised during tissue injury * Activated by enzymes * Activates nociceptors by B1 and B2 receptor * + PG production
53
How do NSAIDs reduce pain?
* Reduce inflammation * Inflammation causes pain * Decrease in pain
54
How do NSAIDs act as antipyretics?
* Reset thermostat and hypothalamus actions * Inhibition of PG production in hypothalamus * Temperature regulated, so decrease in temperature
55
What are NSAIDs mechanism of action?
* Inhibit cyclooxygenase enzyme * Reduce eicosanoid generation * Less PGs and inflammation
56
What are the opioid receptor mechanisms?
57
What are the effects of morphine?
* Act via u-receptor * Analgesia * Euphoria and dysphoria * Anti-tussive (prevent cough)
58
What are the sites of action of opioids?
* Increase descending control from brain to SC via excitation * Bind to GABAergic neuron * Blocks transmission of neurotransmitter from glutamate * Increases excitation at neurone

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