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Medicine year 2 semester 2 > Case 23- Pain and Arthritis > Flashcards

Case 23- Pain and Arthritis Flashcards

1
Q

Pain definition

A

An unpleasant feeling caused by stimulus of nociceotic receptors following tissue injury. Its a protective mechanism

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2
Q

Is pain a state of mind

A

Pain may also involved higher cortical control which can reduce/increase the pain threshold. Supporting this is the placebo effect.

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3
Q

Pain characteristics

A
  • Felt in response to noxious stimuli
  • Acute (short term) and/or chronic (long term)
  • Somatic (body) or visceral (thorax/abdomen)
  • Has two phases- sharp instant pain and dull throbbing pain
  • Involves CNS modulation
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4
Q

Nociceptors

A

• Tend to be ‘free’ nerve ending
• Classified by the properties of axons
• Found in skin Nociceptors, Muscle Nociceptos and Joint Nociceptors
Pain receptors activate two types of pain fibres- A-delta and C-fibres.

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5
Q

A-delta fibres

A
  • Fast Sharp pain
  • Synapse Lamina 1 and 5 spinal cord
  • Second order neurones cross contralateral
  • Ascend to thalamus anterolateral tract
  • Thick and myelinated
  • 1-5 um, conduction speed- 20m/s
  • Responds to mechanical stimulation and painful heat/cold
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6
Q

C-fibres

A
  • Slow dull, achey pain
  • Synapse Lamina 1 and 2 spinal cord
  • Interneurones
  • Neurones cross contralateral
  • Ascend to thalamus anterolateral tract
  • Not myelinated
  • 2.5um. Conduction speed- 2ms
  • Responds to mechanical stimulation and substances from damaged tissue
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7
Q

Visual and proprioceptive input to our response to pain

A
  • We give a lot more weight to visual input over proprioceptive input
  • Rubber hand illusion - cant see real hand but can see rubber hand, stroke both hands until the brain adopts the rubber hand as its own. If the rubber hand is hit hard, an emotional response to pain is elicited but no actual pain is felt
  • Also seen in phantom limb pain
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8
Q

What happens if you lose wither A-delta or C-fibres

A
  • If you lose a-delta fibres but keep C fibres, dont experience sudden onset of pain but get dull, throbbing pain
  • If you lose C fibres but keep A-delta fibres, only get the sudden onset of pain with no dull ache pain
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9
Q

Rexed laminae

A
  • Consists of 10 histological and functionally specific regions in the spinal cord gray matter
  • Marginal zone of rexed laminae- Lamina I
  • Substantia gelatinous- Laminae II and III
  • Nucleus proprius- Lamina IV, V and VI
  • Where do C fibres synapse- Lamina I and II
  • Where do A-delta fibres synapse- Lamina I and V
  • Where do nociceptive neurones sometimes terminate- they sometimes branch off and terminate on second order neurones in layer III, IV and V
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10
Q

What type of fibres mediate pain

A

Type IV

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11
Q

Interneurons in the Laminae

A

Communicate between lamina so different sensory elements influence each other. Can be excitatory or inhibitory

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12
Q

Which lamina becomes the anterolateral pathway

A

Lamina I, IV, V and VI. Takes heat sensation to the brain

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13
Q

Crossing over of A-delta and C fibres

A
  • A-delta fibres tend to synapse straight onto 2nd order neurones and cross over to go to thalamus
  • C fibres go to interneurones which then synapse onto 2nd order neurone and cross over
  • They cross over at the level it enters and travels up in brain contra laterally
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14
Q

Gated theory of pain

A

If you feel pain, you rub it and relieve the pain. When you activate pain receptors, if you rub it then touch receptors are activated too. This inhibits the pain receptors and dampen down the pain pathway - feel less pain

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15
Q

How does the gated theory of pain work

A
  • A-delta and C fibres are excitatory and glutamatergic projections are excitatory
  • At the same time A-alpha and A-beta fibres go to the brain through the dorsal column
  • Branches terminate in lamina II and III - excitatory
  • Project to interneurones which project to A-delta and C fibres which are inhibitory
  • Pain sensation is reduced
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16
Q

How does the gated theory of pain work

A
  • A-delta and C fibres are excitatory and glutamatergic projections are excitatory
  • At the same time A-alpha and A-beta fibres go to the brain through the dorsal column
  • Branches terminate in lamina II and III - excitatory
  • Project to interneurones which project to A-delta and C fibres which are inhibitory
  • Pain sensation is reduced
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17
Q

Pain perception in the primary somatosensory cortex

A

Localisation of pain. Damage to the cortical regions limits ability to precisely localise pain. Discriminative component

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18
Q

Pain perception in the Hypothalamus and limbic system

A

Affective component, suffering

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19
Q

Pain perception in the thalamus

A
  • Ventral posteromedial and ventral posterolateral

* Deafferentation -> nerve damage/amputation, changes/plastcicity, chronic pain, phantom limb pain

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20
Q

Centrifugal pathway

A
  • Descending pathway:
  • Sensory cortex, frontal, limbic cortex ->
  • Periventricular nucleus of the hypothalamus releases Enkephalin, Endorphin and Dynorphin (opioid peptides)
  • Acts on the Periaqueductal grey which releases Serotonin and Glutamate
  • This acts on the raphe nucleus -> Spinal cord
  • The Spinal cord releases Serotonin and Endorphins
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21
Q

Which neurotransmitters can alter pain

A

Noradrenaline and Serotonin can massively reduce or even eliminate the pain we feel

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22
Q

Central control of pain

A
  • Periaqueductal grey receives input from hypothalamus, amygdala and cortex
  • Periaqueductal grey matter projects down towards medulla and spinal cord and back onto pain pathway which lie on dorsal horn - brain can dampen down or intensify the pain information
  • Similar thing happens with locus ceruleus and raphe nucleus
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23
Q

Peripheral sensitisation

A
  • Normally nociceptors high threshold
  • Respond only to noxious stimuli
  • Nociceptors become sensitised (more sensitive)-Threshold lowered (non noxious stimuli, allodynia). Responsiveness increased (to noxious stimuli, hyperalgesia)
  • Reduces likelihood of further damage
  • Example- sunburn
24
Q

Peripheral sensation action

A
  • Damage and inflammation causes the release of chemicals from direct action and immune cells i.e. neutrophils
  • ATP, Histamine, Serotonin, Cytokines. Bradykinin and Neuropeptides are released
  • These act on the Sensitisation nociceptor
25
Q

Central sensitisation

A
  • Not fully understood
  • Involved sensitisation within the spinal cord/brain circuitry
  • It alters synaptic strength between neurones
  • Occurs- Spinal cord (lamina 1 and V neurones), Thalamus, Amygdala and the Anterior cingulate cortex
26
Q

Central sensitisation- action

A
  • AMPA and NMDA allow for Na+ entry, this causes Ca+ levels to increase
  • This acts on PKC and CaMKII
  • This releases the secondary messengers ERK and MAPK which cause increased production of Transcription factors
  • The transcription factors increase transcription of more NMDA/AMPA receptors
27
Q

Biopsychosocial model of pain (Bio)

A
  • Pharmacological treatments- based on patient needs
  • Physiotherapy/exercise
  • Sleep
28
Q

Biopsychosocial model of pain (Psycho)

A
  • Physiotherapy- self managing strategies

* Psychological therapy- coping mechanisms/positive attitude

29
Q

Biopsychosocial model of pain (Social)

A
  • Sociologists
  • Family support
  • Work environment
30
Q

Types of cognitive bias

A
  • Anchoring- relying too heavily on the first bit of information we are give
  • Search satisfying- we find a convenient answer that fits so we stop searching
  • Confirmational bias- we think of a hypothesis and only search for evidence that supports it and not evidence which refutes it
  • Cognitive miser function- reverting to system 1 in the dual process theory. Done in an attempt to conserve cognitive energy i.e. on a busy shift
  • Heuristics- using rules of thumb and mental shortcuts
31
Q

Avoiding cognitive bias

A
  • Remember the cognitive biases we are prone to- we are not as rational as we think
  • Gain experience and develop sound medical knowledge
  • Optimise the environment you work in- Get plenty of sleep, Eat and drink regularly, Take regular breaks
  • Be aware of your limits and ask for help when needed- but don’t take what others say at face value. Healthy scepticism.
32
Q

Inflammatory arthritis- FBC

A
  • Hb - Normochromic, normocytic anaemia (anaemia of chronic disease)
  • White Cell Count - Neutrophilia is seen in bacterial infection (e.g. septic arthritis) or if a patient is on corticosteroid treatment.
  • Lymphopenia – occurs with viral illnesses or active SLE. Neutropenia may reflect drug-induced bone marrow suppression.
  • Platelets – Thrombocythaemia occurs with chronic inflammation. Thrombocyopenia is seen in drug- induced bone marrow suppression.
33
Q

Inflammatory arthritis- ESR and CRP

A

Increased in inflammation and acute phase reactants

34
Q

Inflammatory arthritis- Bone and liver biochemistry

A
  • Raised Alkaline Phosphatase may indicate liver or bone disease.
  • Liver enzymes might be raised if there is drug-induced toxicity.
35
Q

Inflammatory arthritis- Serum uric acid

A

Used to check for gout. Has limited value it can be normal or raised, can be raised in patients who dont have gout

36
Q

Inflammatory arthritis- RF (Rheumatoid Factors)

A
  • RF positive in 70% of RA (Rheumatoid Arthritis), but it is not diagnostic. It can be detected in many autoimmune rheumatic disorders (e.g. SLE, Sjorgen’s syndrome) and in 5% general population (e.g. Elderly).
  • RF negative is a good prognostic factor for RA.
37
Q

Inflammatory arthritis Anti-CCP

A
  • Present in <80% of patients with RA.
  • Anti-CCP has been found to be more specific (90% specific in RA) than rheumatoid factor in RA and may be more sensitive in erosive disease.
38
Q

Inflammatory arthritis- ANAs (antinuclear antibodies)

A
  • About 95% of patients with SLE have a positive ANA test result
  • 30% of RA patient will be ANA positive. 8% of the normal population will be ANA positive.
39
Q

Inflammatory arthritis= HLA-B27

A
  • Positive in 95% of those with Ankylosing Spondylitis
  • Positive in 8% of general population
  • HLA-B27 may also be present in people with spondylitis associated with inflammatory bowel disease and psoriatic arthritis. It can be positive in patients with Reactive arthritis.
40
Q

Definitions- Arthralgia. Arthritis, Arthropathy and Osteoarthritis

A
  • Anthralgia= joint pain
  • Arthritis= joint inflammation
  • Arthropathy- joint pathology
  • Osteoarthritis- loss of cartilage via dysregulated chrondrocyte activity
41
Q

Joint pain assessment

A
  • What is the pattern (acute, chronic, mono/oligo/poly, symmetrical)
  • What is the character (biomechanical/inflammatory)
  • SOCRATES
42
Q

Features of Biochemical (non-inflamatory arthritis)

A
  • Pain after use
  • Early morning stiffness <30minutes
  • Chronic
  • No extra-articular features (multisystem)
43
Q

Features of inflammatory arthritis

A
  • Pain with rest, improves with use
  • Early morning stiffness >30 minutes
  • Acute/subacute
  • Multisystem/ extra-articular features
44
Q

Inflammatory arhtritis

A

Usually autoimmune mediated, therefore can be managed by immunosuppression. Early and effective treatment improves outcomes considerable

45
Q

Types of arthritis

A

Biochemical (non-inflammatory)- Osteoarthritis

Immune- Autoimmune arthritis, Crystal arthropathy, Infective arthritis (septic arthritis)

46
Q

Autoimmune arthritis

A
  • Rheumatoid
  • Spondyloarthropathies- Psoriatic arthritis, Reactive arthritis, Ankylosing spondylitits
  • Undifferentiated
  • Type of inflammatory arthirits
47
Q

Crystal arthropathy

A
  • Gout
  • Calcium Pyrophosphate crystal disease (CPPD)- Pseudogout
  • Type of inflammatory arthirits
48
Q

Classifying arthritis- How many joints

A
  • Mono- septic arthritis, Gout
  • Oligo <5- Reactive arthritis, Psoriatic arthritis, Osteoarthritis
  • Poly >5- Rheumatoid arthritis. Sometimes Osteoarthritis and Psoriatic arthrirtis
  • Axial- Ankylosing spondylitis, Psoriatic arthritis
49
Q

Classifying arthritis- Location

A
  • Peripheral- how many joints are affected

* Axial- in the spine and also the Sacoriliac joint

50
Q

Osteoarthritis

A
  • Joint pain character- non inflammatory
  • Pain with rest, improves with use
  • Early morning stiffness >30 minutes
  • Acute/subacute
  • Multi-system/extra-articular features
  • Risk factors- increasing age, female, obesity, physically demanding occupation
  • Most commonly affects hip, knees and hand
  • Clinical examination- Crepitus, Reduced range of movement, Boney growth, Sometimes swelling/effusion
  • Hand clinical signs- muscle wasting, Bouchard’s nodes, Heberden’s nodes
51
Q

Osteoarthritis- features on an x-ray

A
  • L- loss of joint space
  • O- osteophytes
  • S- Subchondral sclerosis
  • S- Subchondral cysts
52
Q

Rheumatoid arthritis (autoimmune)

A
  • Joint pain character- inflammatory
  • Pain with rest, improves with use
  • Early morning stiffness >30 minutes
  • Acute/subacute
  • Multisystem/extra-articular features
  • Risk factors- incidence age 40-60, female, family history
  • Typically involves wrists, MCP and PIP joints
  • Typically spares certain joints- Thoracolumbar spine and DIPS of the fingers and IP’s of the toes
  • Normally effects multiple joints. Usually >5 and is symmetrical
53
Q

Clinical examination- Rheumatoid arthritis

A
  • May be MCP, PIPJ swelling, warmth over these joint spared DIPJ
  • MCP squeeze- tenderness
  • Swelling is sometimes termed boggy
  • Chronic damage with MCP subluxation, Z-thumbs, swan-neck
  • Ulnar deviation
  • Buttonhole deformity- PIP flexion and DIP hyperextension
  • Swan neck deformity- PIP hyperextension and DIP flexion
54
Q

Rheumatoid arthritis investigation= X-ray

A
  • Loss of Joint Space
  • Erosions
  • Subarticular osteopenia
  • Soft tissue swelling
  • Late signs- evidence of joint damage
55
Q

Investigations into rheumatoid arthritis- bloods

A
  • Rheumatoid factor is less specific to RA but higher levels of RA is suggestive of increased likelihood of joint destruction
  • Can be present in other disease and 5-10% of the normal population
  • Anti-CCP is more specific to rheumatoid arthritis
  • Inflammatory markers (CRP, ESR) are also likely to be raised

Medicine year 2 semester 2 (47 decks)

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