Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

EDRA > 7.3 Chronic Pain > Flashcards

7.3 Chronic Pain Flashcards

1
Q

Definitions of some chronic pain states

Allodynia

A

Allodynia

Pain due to a stimulus which
does not normally provoke pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dysaesthesia

A

Dysaesthesia

An unpleasant abnormal sensation,
whether spontaneous or evoked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperaesthesia I

A

Hyperaesthesia

Increased sensitivity to stimulation, excluding the special senses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hyperalgesia

A

Hyperalgesia
An increased response to a stimulus which is normally painful

may be caused by damage to nociceptors or peripheral nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Primary hyperalgesia

what is it

how does it occur

A

Primary hyperalgesia

describes pain sensitivity that occurs

directly in the damaged tissues.

This occurs by peripheral sensitisation whereby
nociceptors exhibit reduction in threshold and an increase in responsiveness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Secondary hyperalgesia

what is it

How does it occur

A

Secondary hyperalgesia

describes pain sensitivity that occurs in
surrounding or distant undamaged tissues.

This is a result of central sensitisation

wherein there is an increase in the excitability of
neurons within the central nervous system, so that normal inputs begin to produce abnormal responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanisms involved in hyperalgesia

Peripheral sensitisation

A

Abnormal nociceptor sensitivity

Spontaneous neuronal activity
and axonal sprouting

Inflammatory mediator-induced
excitation of nociceptors

Sympathetically mediated pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mechanisms involved in hyperalgesia

Central sensitisation

A

Short-term homosynaptic potentiation
(wind-up)

Long-term homosynaptic potentiation
(through NMDA and AMPA receptors)

Changes in synaptic architecture

Loss of inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pain scales for assessment of chronic pain

A

Global Impression Of Change Scale

Brief Pain Inventory

Short Form – 36 Physical Function Scale

Roland Morris Questionnaire

Health Assessment Questionnaire

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Brief Pain Inventory

A

Brief Pain Inventory

Worst, best and present pain intensity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Short Form – 36 Physical Function Scale

A

Short Form – 36 Physical Function Scale

General measure that is
intended to capture quality of life as well as
whether an individual is healthy or not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Global Impression Of Change Scale

A

Global Impression Of Change Scale

Completed by both the patient
and the
clinician

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Roland Morris Questionnaire

A

Roland Morris Questionnaire

Back/leg pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Health Assessment Questionnaire

A

Health Assessment Questionnaire

Difficulty rating of activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Syndrome-specific pain scales

A

Galer Neuropathic Pain Score

Oswestry Disability Questionnaire

American College of Rheumatology Response Criteria

Arthritis Impact Measurement Scale

Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Galer Neuropathic Pain Score

A

Galer Neuropathic Pain Score

For neuropathic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Oswestry Disability Questionnaire

A

Oswestry Disability Questionnaire

For patients with back pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

American College of Rheumatology Response Criteria

A

American College of Rheumatology Response Criteria

Rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Arthritis Impact Measurement Scale

A

Arthritis Impact Measurement Scale

Osteoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index

A

Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index

Osteoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Psychological assessment

A

McGill Pain Questionnaire

Beck’s Depression Inventory

Sickness Impact Profile

Minnesota Multiphasic Personality Inventory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

McGill Pain Questionnaire

A 
Domains: 
sensory, 
affective,
 evaluative 
and miscellaneous
 plus a painintensity
five-point scale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Beck’s Depression Inventory

A 
A 21-item self-rating scale 
that measures the severity of 
key symptoms associated with 
clinical depression 
but not with other psychological
factors aggravating pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sickness Impact Profile

A 
It is a general indicator of health status 
and health-related
dysfunction rather than pain
Best studied in the population 
with chronic back pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Minnesota Multiphasic Personality Inventory

A

This is a self-administered true–false test
.
The questionnaire consists of 567 items
and

it places patients in one
of four groups:

hypochondriacal,
reactively depressed,
‘somaticisers’
and manipulators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Glutamate receptors

where

activation

A

Glutamate receptors
(AMPA and NMDA)
have been

identified in spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

NMDA role chronic pain

A

Activation of these receptors by
nociceptive inputs from periphery
is involved in development of chronic pain.

Hence, NMDA antagonists
such as ketamine are used to
treat certain chronic pain states.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Wind up phenomena

Central sensitisation

A

Persistent nociceptive stimulation
of C fibres produces hyperalgesia and
allodynia through wind-up phenomena
and central sensitisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Axonal sprouting and neuroma formation

A

Axonal sprouting and neuroma formation

subsequent to nerve injury exhibit

altered up- regulation of sodium channels,
and down-regulation of potassium channels.

The net result is increased neuronal excitability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is there any phenotypic switching

A

Lastly, sensory Aβ undergo
phenotypic switching to C fibres

and start conducting pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Low-back pain

A

lumbosacral region

arising from the spinal
or paraspinal structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Sciatica

A

(radicular leg pain) may accompany low back

pain but is regarded as a separate entity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Is LBP commong

A

About 50%–80% of adults experience low-back pain.

Most backaches (85%–90%) are simple low-back
pain (mechanical back pain) in 
which no particular pathology exists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nonmechanical backaches may be due

A

Nonmechanical backaches may be
due to more serious conditions like

cancer,
infection
or inflammatory arthritis.

Visceral pathologies may also
lead to low back pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Causes of low-back pain

Mechanical

A

Mechanical

Lumbar strain or sprain
Degenerative disease
Spondylosis
Spondylolysis
Spondylolisthesis
Disc herniation
Facet joint arthropathy
Spinal stenosis
Osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Non-mechanical (spinal pathology)

A

Non-mechanical (spinal pathology)

Tumours
Infection
Arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Back pain ‘Red flag’ signs

A

‘Red flag’ signs:

non-mechanical pain,

thoracic pain,

history of cancer,

HIV,

weight loss,

structural deformity,

young (< 20 years) or

old
(> 55 years),

recent trauma,

osteoporosis,

night pain and
bladder/bowel dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Back pain Imaging:

A

Imaging: should be done only if the history or clinical examination is
suggestive of non-mechanical back pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Back pain Management

A

Management:

mostly early mobilisation and pain relief.

Physiotherapy may be
needed if progress is slow.

A minority will need
further evaluation and management.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

spinal disc herniation

A

affecting the spine due to

tear in the outer,
fibrous ring (annulus fibrosus)
of an intervertebral disc allowing
nucleus pulposus to bulge

out beyond the damaged outer rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

spinal disc herniation

Is severe pain nerve root compression

A

This tear causes release of inflammatory
chemical mediators which

may directly cause severe pain,

even in the absence of nerve root compression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

spinal disc herniation

result d/t

Commonest sites x2

rare @

A

They most often result
due to wear and tear,

and occur most frequently at
L4–L5 or L5–S1 levels.

The second most common site is 
lower cervical (C5–C6 or C6–C7),

while it is uncommon
at thoracic levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

spinal disc herniation worsened by what positon

A

The sitting and bending
forward position

(associated with desk jobs)

cause the highest increases
in intradiscal pressures
predisposing to prolapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Neurology in a severe lumbar disc prolapse

L2

A

L2

Hip flexion (iliopsoas)

Groin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Neurology in a severe lumbar disc prolapse

L3

A

L3

Knee extension (quadriceps)

Anterolateral thigh

Patellar reflex lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Neurology in a severe lumbar disc prolapse

L4

A

L4

Heel walking
(ankle dorsiflexors)

Medial ankle

Patellar reflex lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Neurology in a severe lumbar disc prolapse

L5

A

L5

First-toe dorsiflexion

Dorsum of foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Neurology in a severe lumbar disc prolapse

S1

A

S1

Toe walking
(ankle plantar flexors)

Lateral foot surface

Ankle reflex lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Neurology in a severe lumbar disc prolapse

Cauda equina

A

Cauda equina

Ankle weakness
Lax anal sphincter

Paresthesia of leg and perineum

Ankle reflex lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Neurology in a severe cervical disc prolapse

C5

A

C5

Arm abduction (deltoid) 
and elbow flexion (biceps)

Shoulder area and outer
upper arm

Biceps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Neurology in a severe cervical disc prolapse

C6

A

C6

Elbow flexion (biceps)
Wrist extension

Index finger

Brachioradialis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Neurology in a severe cervical disc prolapse

C7

A

C7

Elbow extension (triceps)
Wrist flexion
Finger extension

Middle finger

Triceps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Neurology in a severe cervical disc prolapse

C8

A

C8

Finger flexion and adduction

Little finger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Neurology in a severe cervical disc prolapse

T1

A

T1

Finger abduction

Lateral epicondyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Regarding lumbar facet arthropathy

A

causes 15%–40% of cases of low-back pain

due to dysfunction or
inflammation of the facet
(zygapophyseal) joints

56
Q

facet (zygapophyseal) joints

What makes up the joint

A

These joints are formed by the articulation

of the articular processes of
the adjacent vertebrae.

They are innervated by
two medial branches of the
dorsal rami of the
corresponding spinal nerves

57
Q

Facet joint pain

Describe pain

A

The patient complains of
deep,
achy,

non-specific low-back pain

localised over the affected facet joint.

58
Q

Facet joint pain

Radiation?

A

Radiation to the thigh is possible, but radiation

distal to the knee is uncommon.

59
Q

Facet joint pain

worsened by

A

The pain is worse with

lumbar extension,
extensive walking

or
sitting for long periods of time.

The bowel and bladder
are not involved.

60
Q

Facet joint pain
examination

palpation

changes

A

On examination,

there is pain with deep palpation over
the affected facet joint.

Paraspinal muscle spasm,
loss of lumbar lordosis and
limited extension of spine may be noted.

61
Q

Facet joint pain

Diagnosis

A

However,

historic or physical examination findings
cannot reliably diagnose
lumbar zygapophyesal joint pain.

The most accepted method for
diagnosing pain arising from the

lumbar facet joints is
with low-volume intra-articular
injections or medial branch blocks.

62
Q

Diagnostic blocks

A

Diagnostic blocks use
only local anaesthetics,
and analgesics (opioids) for
sedation must be avoided.

63
Q

Lumbar spinal stenosis

mcq bit about walking

A

Walking uphill is easier than walking on a flat surface

64
Q

Lumbar spinal stenosis is the

A

Lumbar spinal stenosis is the

narrowing of the spinal canal

(transforaminal canal),

resulting in nerve compression
of the spinal roots laterally

65
Q

Lumbar spinal stenosis

Affects usually

symptoms

A

It usually affects middle-age patients (> 55 years).

Symptom include

leg pain,
weakness,
paraesthesia and
radicular pain

of the involved
spinal root.

66
Q

Is it the same as intermittent claudication

A

similar to vascular claudication,

but different in many respects,
hence it is called pseudoclaudication
or neurogenic claudication

67
Q

Types of claudication and factors affecting them

Neurogenic claudication Vascular claudication

Aggravating factors

A

Aggravating factors

Neuro -
Extension of spine:
standing
walking 
hyperextension of spine

IC

Any leg exercise

68
Q

Types of claudication and factors affecting them

Neurogenic claudication Vascular claudication

Relieving factors

A

Relieving factors

Neuro
Flexion of spine:
squatting/sitting
bending forward when sitting
walking uphill rather than on flat level
lying on side rather than on back
easier to cycle than to walk

IC

Rest

69
Q

Types of claudication and factors affecting them

Neurogenic claudication Vascular claudication

Other features

A

Other features

Pulse:
usually normal

Skin changes:
usually absent

Autonomic disturbances:
rare

IC

Vascular changes:
blood pressure decreased
peripheral pulses weak or absent
bruits or murmurs

Skin changes:
pallor
cyanosis
nail dystrophy

Autonomic:
impotence

70
Q

sacroiliac joint pain innervation

A

sacroiliac joint (SIJ) is innervated

posteriorly by lateral branches
of the dorsal primary rami of
L4–S3 and

71
Q

sacroiliac joint pain innervation

A

anteriorly by lateral branches
of the dorsal primary rami of
L2–S2.

72
Q

sacroiliac joint pain

A

SIJ pain accounts for 16%–30% of
cases of chronic
mechanical low-back pain.

73
Q

SIJ pain mainly involve

a/w any conditions?

A

SIJ pain mainly involves the buttocks,

although it may be referred to
the thigh, abdomen, groin or legs.

It may also occur with systemic
conditions such as

ankylosing spondylitis,
Crohn’s disease
and gout

74
Q

SIJ pain exacerbating / relieving

A

pain is worse in the morning
and can be

exacerbated by spine flexion,
prolonged sitting and
weight bearing on the painful limb.

Symptoms may be relieved by
flexing the affected leg and weight
bearing on the contralateral leg.

75
Q

SIJ Pain

Provocative manoeuvre to help distinguise

is it imaged?

A

Different provocative manoeuvres
help distinguish this condition from
others causing low back pain.

Most commonly used is the FABER

(flexion, 
abduction, 
external rotation, and 
extension of the hip to
create a figure of four: 
elicits pain) Patrick test.

This is used to increase
the predictive value and
establish the diagnosis.

Radiological imaging
is used mainly to exclude red flags.

Lasègue’s sign is not seen in SIJ pain

76
Q

SIJ Pain

A

Treatment follows a
multidisciplinary approach.

Conservative treatments include
exercise therapy and manipulation

(address gait and posture imbalance).

Intra-articular SJ infiltrations with local
anaesthetic and corticosteroids
have been found to be effective in most studies.

77
Q

The piriformis is a muscle where

Function

A

The piriformis is a muscle
in the gluteal region of the lower limb.

The piriformis muscle is part
of the
lateral rotators of the hip

and

it externally rotates the

extended thigh and
abducts the flexed thigh.

78
Q

piriformis syndrome causes

A

In about 15% of patients,

the piriformis muscle is split
and
pierced by the two components of sciatic nerve.

At other times,
overuse injury

(common in cyclists, runners,
tennis players, ballet dancers) of

this muscle may cause symptoms.

79
Q

Piriformis syndrome symptoms

worsened

A

This causes sciatic compression
and

consequent sciatica
(pain in the distribution
of sciatic nerve).

Pain worsens on squatting, climbing stairs, walking and
prolonged sitting. It is typically unilateral

80
Q

Piriformis syndrome eponymous tests

A

Diagnostic tests include:

Pace sign:
pain and weakness on
resisted abduction of flexed thigh in
seated position.

Lasègue’s sign:
pain on flexion, adduction and
internal rotation of hip
in a supine patient.

Freiberg’s sign:
pain on forced internal rotation
of the extended thigh.

81
Q

Piriformis syndrome Rx

A

Conservative management comprises

analgesics, stretching exercises and
deep heat using ultrasound.

Fluoroscopy-guided piriformis injections using
local anaesthetics and corticosteroids are effective.

Botulinum toxin injections have shown more effective pain relief.

Surgical release is the last option

82
Q

intravenous drug infusion therapy

for treatment of neuropathic pain

A 
1
uses lignocaine (Na+ channel blocker),

2
ketamine (NMDA antagonist),

3
magnesium (NMDA antagonist),

4
adenosine (presynaptic antinociception by preventing release of substance P)

5
alfentanil
(opioid)

83
Q

Phentolamine infusion used for

A

Phentolamine (α-blocker) infusion is
used as a diagnostic test for
sympathetic mediated pain.

If positive, the patient is
prescribed oral α-
blocker such as doxazocin

84
Q

Fibromyalgia syndrome

A

chronic generalised pain and allodynia,

a heightened and painful response
to pressure (tender points)
85
Q

Fibromyalgia syndrome sy

A

symptoms may

include fatigue,
sleep disturbance, 
joint stiffness, 
bowel and bladder abnormalities,
paraesthesia, 
depression and anxiety.
86
Q

Fibromyalgia syndrome sy prevelance

A

It is estimated to affect
2%–4% of the population

and is more common in females

87
Q

FM Diagnosis

A

The American College of Rheumatology
(ACR 1990)

established criteria for the diagnosis of FMS,

including the presence of

tenderness at 11 or more of 18 preselected sites
(tender points).

Additionally, the
Fibromyalgia Impact Questionnaire
is used to assess the impact of
pain on a patient’s life.

88
Q

FM rx

A

A multidisciplinary treatment
programme combining behavioural
modification, education and physical training is effective

89
Q

Post-herpetic neuralgia is a

what is it?

A

Post-herpetic neuralgia is a

debilitating neuralgia

following an acute
varicella zoster infection

(usually after 6 weeks).

90
Q

Post-herpetic neuralgia

where

Easy to Rx?

A

Typically, it is confined to a
dermatomal distribution of the skin.

It is difficult to treat once established.

Hence both childhood vaccination and early, aggressive treatment of acute
herpes zoster infection are vital.

91
Q

Post-herpetic neuralgia Rx options

A

1
Since it is a neuropathic pain,
it is treated first with antidepressants
(tricyclic antidepressants like amitryptyline)

followed by anticonvulsants (gabapentin).

2
Opioids may be needed in some
(NSAIDs are rarely useful).

3
Topical local anaesthetics and
capsaicin may also relieve pain.

4
Intrathecal methylprednisolone
with lignocaine as repeated injection
can help where non-interventional therapies fail.

92
Q

Diabetic neuropathies are thought to result

A

Diabetic neuropathies are thought to result from

microvascular injury involving vasa nervorum,

and

macrovascular processes of neuronal ischaemia and infarction.

Incidence increases with age,
duration of diabetes
and degree of hyperglycaemia

93
Q

Diabetic neuropathies Rx

A

Treatments include:

tight glycemic control

tricyclic antidepressants: amitryptyline

selective norepinephrine reuptake inhibitors: duloxetine

anticonvulsants: gabapentine and pregabalin
analgesics: opioids

topical agents: capsaicin cream and lignocaine patches

selective serotonin reuptake inhibitors (e.g. fluoxetine) have not been
found to be as efficacious.

94
Q

The neuropathic pain ladder is different from the World Health

A

The neuropathic pain ladder is different from the World Health

Organization pain ladder (cancer pain).

First line: tricyclic antidepressant or antiepileptic.

Second line: tricyclic antidepressant and antiepileptic.

Third line: strong opioid plus above, ± invasive procedures.

95
Q

To make the clinical diagnosis of complex regional pain syndrome
(CRPS),

A

the following criteria (Budapest) must be met

1
Continuing pain, which is disproportionate to any inciting event.

2
Must report at least one symptom in three of the four following categories:
/Must display at least one sign at time of evaluation in two or more of
the following categories

Sensory:

Vasomotor:

Sudomotor/oedema:

Motor/trophic:

There is no other diagnosis that better explains the signs and
symptoms.

96
Q

CRPS symptoms

sensory

vasomotor

sudomotor

motor

A

Sensory:
reports of hyperesthesia
and/or allodynia

Vasomotor:
reports of temperature asymmetry
and/or skin colour changes
and/or skin colour asymmetry

Sudomotor/oedema:
reports of oedema and/or sweating changes
and/or
sweating asymmetry

Motor/trophic:
reports of decreased range of motion
and/or motor

97
Q

Must display at least one sign at time of evaluation in two or more of
the following categories:

A

Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to
light touch and/or temperature sensation and/or deep somatic pressure
and/or joint movement)

Vasomotor: evidence of temperature asymmetry (> 1°C) and/or skin
colour changes and/or asymmetry

Sudomotor/oedema: evidence of oedema and/or sweating changes
and/or sweating asymmetry

Motor/trophic: evidence of decreased range of motion and/or motor
dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair,
nail, skin).

98
Q

The International Association for the Study in Pain divides CRPS into two types.

A

The International Association for the Study in Pain divides CRPS into two types.

Type I: 
formerly known as 
reflex sympathetic dystrophy, 
or Sudeck’s atrophy, 
it does not have demonstrable nerve lesions.

Type II:
formerly called causalgia,
it has evidence of obvious nerve damage.

99
Q

pathogenesis of CRPS

peripheral

A

pathogenesis of CRPS may include

1
peripheral mechanisms

such as

a
upregulation of axonal α2 adrenoceptors,
rendering them sensitive to catecholamines
(hence the term ‘sympathetically mediated pain’)

and
b
denervation hypersensitivity.

100
Q

pathogenesis of CRPS may include central

A

Central mechanisms such as wind-up and

central sensitisation play an important role.

101
Q

Risk factors for the development

of CRPS

A 
include previous trauma, 
nerve injury, 
previous surgery, 
workrelated injury and 
female sex.
102
Q

CRPS mainstay of management.

A

Physical therapy is the mainstay of management.

However, pain precludes this, hence pain relief becomes vital to achieve movement.

103
Q

CRPS Rx sympathetic pain

A

Sympatholysis using
intravenous regional anaesthesia
(lignocaine, guanethidine or bretylium)

or sympathetic ganglion blocks are
commonly employed to
address sympathetically mediated pain.

Surgical
resection and radiofrequency ablation of ganglia have also been tried.

104
Q

Three phenomena occur after amputation

A 
Phantom sensation (non-painful paraesthesias)
Stump pain (pain in the stump of the amputated limb)
Phantom pain (pain in the amputated limb).
105
Q

Salient features of phantom pain:

A

Salient features of phantom pain:

Incidence is up to 75% of amputees.

May start immediately but usually starts within first week after amputation.

Most complain of intermittent pain (few days in a month).

106
Q

phantom pain type

pathogenesis

A

Pain may be
shooting, cramping, burning or aching in nature.

Pathogenesis may be related
to spinal and cortical reorganisation of neurons.

107
Q

phantom pain RF

A

Risk factors for
development of phantom pain

are 
pre-amputation pain,
persistent stump pain, 
bilateral amputations 
and lower-limb amputations.

Gender and age are not known risk factors.

108
Q

Phantom pain RF

Pharm

A

Pharmacological treatment
includes

antidepressants,
antiepileptics and
analgesics.

109
Q

Nonpharmacological Phantom Pain

A

Nonpharmacological methods

include
TENS,
spinal cord stimulation and
biofeedback.

Recently
‘Ramachandran mirror box’
therapy has been used to
alleviate painful spasms of phantom limb.

Note: pre-emptive regional anaesthesia has not been shown to reduce the
incidence of phantom limb pain

110
Q

In transcutaneous electrical nerve stimulation (TENS)

Theory

A

Melzack and Wall proposed
that the transmission of
noxious information (C fibre)

could be inhibited by
activity in large-diameter
peripheral afferents (Aβ fibre)
(gate control theory of pain).

111
Q

In transcutaneous electrical nerve stimulation (TENS),

A

In transcutaneous electrical nerve stimulation (TENS),

electric current produced by a
device is used to

stimulate the nerves for therapeutic purposes
(analgesia).

112
Q

Two types of TENS are used.

A

Conventional TENS

Pulsed TENS

113
Q

Conventional TENS

A

Low intensity, high frequency

Mainly for nociceptive pain

Perceived as a paraesthesia

Relieves pain by a segmental
mechanism

114
Q

Pulsed TENS

A

High intensity, low frequency

Mainly for neuropathic pain

Perceived as a muscle twitch

Works by activating
extra segmental descending
inhibitory pain pathways

115
Q

Indications TENS

A

Indications include

acute post-operative pain, 
labour pain, 
angina,
dysmenorrhoea 
and chronic pain states
116
Q

Contraindications TENS

A

Contraindications include

cardiac pacemakers (interference),

pregnancy (can stimulate uterine contractions),

bleeding diathesis and

epilepsy (may induce seizures).

117
Q

Acupuncture theory

A

Acupuncture is a

complementary therapy that originated in China.

It assumes that health is 
achieved by maintaining a 
‘balanced state’ of the body, 
and that disease is the 
result of an internal imbalance.

This imbalance
leads to blockage in the flow of
qi (vital energy) along pathways known as
meridians.

118
Q

Acupuncture proposed MOA

A

Needling increases the
cerebrospinal fluid concentrations of the
endogenous opioids.
This may be the reason for the analgesia obtained.

119
Q

Acupuncture uses

A

Acupuncture has been found to be

effective for osteoarthritis,
chronic neck pain,
low-back pain,
and postoperative nausea and vomiting.

However, it is not more
effective than other conventional therapies

120
Q

Spinal cord stimulation (SCS) what is it

A

Spinal cord stimulation (SCS) is

the technique of stimulation of large
sensory fibres (Aβ) in dorsal column tracts

to mask the pain carried by
spinothalamic tracts
(based on the gate control theory of pain).

However, it may not be the only mechanism.

121
Q

Spinal cord stimulation (SCS) permanent?

A

It is not destructive,
unlike cordotomy,
and is reversible

122
Q

Major indications for SCS

A

Major indications for SCS are

neuropathic states like failed back surgery
(United States)

and

ischaemic pain (Europe).

123
Q

Non responsive to SCS

Poor candidates?

A

Nociceptive pain
does not respond to SCS.

Major psychiatric issues,
drug-seeking behaviour,
cardiac pacemakers and
patients with secondary gain

are poor candidates for
this technique.

124
Q

Intrathecal drug delivery systems for who

A

Intrathecal drug delivery systems (IDDSs)
are good options for patients who have

ineffective pain relief at
acceptable oral or transdermal doses,

or

for those who have intolerable side effects.

125
Q

Intrathecal drug delivery systems commonest indications

A 
1.
Cancer pain (most common),

2.
chronic non-malignant pain

  1. spasticity

are three main
indications for IDDSs.

126
Q

IDDS Gold standard

also used

A

Morphine is the gold-standard drug used for this.

Apart from 
opioids, 
clonidine (α2 blocker), 
ziconitide (Ca+ channel blocker) 
and 
local anaesthetics (Na+ channel blocker) 
are also used.
127
Q

IDDS 1st line

second ine

A

First-line drugs
include morphine, hydromorphone and ziconitide, whereas fentanyl, clonidine
and local anaesthetics are second-line agents.

128
Q

Tolerance and opioid-induced hyperalgesia result from

A

Tolerance and opioid-induced hyperalgesia result
from opioid therapy,
but are caused by
two distinct mechanisms.

129
Q

Opioid-induced hyperalgesia (OIH)

A

Opioid-induced hyperalgesia (OIH) is a phenomenon associated with the

long-term use of opioids.

Over time, individuals develop an

increasing sensitivity to noxious stimuli (hyperalgesia),

such that a non-noxious stimulus
evokes a painful response (allodynia).

130
Q

Mechanisms involved in OIH

A

Mechanisms involved in OIH are:

spinal NMDA activation,

spinal dynorphin release (KOP agonist)
and facilitation of descending
inhibitory pathways

131
Q

OIH Rx options

A

Treatment options include:

reduction of opioid dose

opioid rotation to
methadone or buprenorphine (KOP antagonist)

NMDA antagonists (ketamine).

132
Q

In tolerance,

A

In tolerance,

increasing the dose of opioid
can overcome it,

but doing
so in opioid-induced hyperalgesia
may worsen the patient’s condition

by inducing hyperalgesia
while increasing physical dependence.

133
Q

Tolerance v Pseudotolerance

A

important to make a

clinical distinction between

1
tolerance 
(reduction in effect needing 
an increase of opioid dose 
to maintain pain relief)

vs

2 pseudotolerance 
(request of more opioids by patient as the
prevalent dose is insufficient for treating the pain).
134
Q

Difference between opioid tolerance and opioid-induced hyperalgesia

A

Opioid tolerance

Due to decreased analgesic potency

Down-regulation of anti-nociceptive system Up-regulation of pro-Rightward shift of dose-response curve

Responds to dose increase

Sensory testing reveals no hyperalgesia

135
Q

Opioid-induced hyperalgesia

A

Opioid-induced hyperalgesia

Due to increased sensitivity (hyperalgesia)

Up regulation of pro nociceptive system
Downward shift of dose response curve

Sensory testing reveals hyperalgesia

136
Q

Risk factors for the development of chronic post-surgical pain (CPSP)
are:

A

1
Age: decreasing incidence with increasing age

2
Preoperative attitude: fear, anxiety or depression

3
Preoperative pain: higher incidence of CPSP

4
Operative technique: invasive and longer surgeries are more associated with CPSP than shorter non-invasive (laparoscopic) procedures

5
Genetic factors

6
Severe acute post-surgical pain

7
Anaesthesia technique:
none shown to be superior, but emphasis is
on multimodal analgesia with good pain relief provision for subacute post-operative pain as well.

EDRA (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions