Brainscape's Knowledge GenomeTM

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


See full index

Neurology SB > Chronic Pain and Head Injury > Flashcards

Chronic Pain and Head Injury Flashcards

1
Q

what is nociceptive pain

A

an appropriate physiological response to painful stimuli via an intact nervous system

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

what is neuropathic pain

A

an inappropriate response caused by a dysfunction in the nervous system

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

what is allodynia

A

pain from a stimulus that is not normally painful e.g. cotton wool

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

what is hyperalgesia

A

more pain than expected from a painful stimulus e.g. pin prick

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

what are common causes of neuropathic pain

A 
shingles 
surgery
trauma
diabetic neuropathy 
amputation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the mode of action of NSAIDS

A

inhibition of COX

prostaglandin synthesis decrease

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

SE of NSAIDs

A

GI irritation/bleeding
Renal toxicity
Potential drug-drug interactions
CV side effects

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

SE of opioids

A 
N + V
Constipation 
Dizziness or vertigo 
Dry skin/pruritus 
Drowsiness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SE of TCAs (e.g. amytriptyline)

A 
Constipation
Dry mouth
Drowsiness
Arrhythmia 
Insomnia 
Increased appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

examples of anticonvulsants

A

carbamazepine
gabapentin
pregabalin

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

SE of anticonvulsants

A 
sedation
dizziness
ataxia
peripheral oedema
nausea
weight gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SE of SNRIs

A 
Dry mouth 
Increased sweating 
Loss of appetites
N + V
Constipation
Drowsiness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 forms of pain

A

nociceptive (acute) pain
inflammatory (prolonged) pain
pathological (neurogenic) pain

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

what are the characteristic of pain in the skin

A

Well localised

- Pricking, Stabbing, Burning

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

what are the characteristic of pain in the muscle

A

Poorly localised

- Aching, Soreness/ tenderness, cramping, stabbing, burning

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

what are the characteristic of pain in the viscera

A 
Poorly localised (often referred to a somatic structure)
- Dullness, Vagueness, Fullness, Nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is pain relayed in nociceptive pain

A
  • intense stimuli
  • release of neurotransmitters that excite second order neurones in the CNS
  • Depolarization due to noxious stimulus elicits action potentials that propagate to the CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the first order neurones in nociceptive pain pathway

A

nociceptors

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

what are the 2 types of fibres in nociceptors

A

Aδ-fibres

C-fibres

20
Q

what are the features of Aδ-fibres

A
  • mechanical/thermal nociceptors
  • thinly myelinated
  • respond to noxious mechanical and thermal stimuli.
  • Mediate ‘first’, or fast, pain
21
Q

what are the features of C fibres

A
  • nociceptors that are unmyelinated
  • respond to all noxious stimuli (i.e. they are polymodal)
  • Mediate ‘second’, or slow, pain
22
Q

are all Aδ-fibres and C-fibres nociceptors

A

No

23
Q

where is the major site of protein synthesis on a neurone

A

soma

24
Q

where is the site of calcium dependent transmitter release

A

central terminal

25
Q

what is the pathway of neurotransmission between the primary afferent and second order neurones

A
  • AP
  • opening of voltage gated calcium channels
  • calcium influx
  • glutamate release
  • activation of glutamate receptors
  • Membrane depolarization (e.p.s.p.)
  • opening of voltage gated sodium channels
  • AP
26
Q

what are the 2 distinct processes of the nociceptive pathway following tissue damage

A
  • peripheral sensitisation

- central sensitisation

27
Q

what mediates peripheral sensitisation and what does it cause

A
  • nociceptors at the site of injury/tissue inflammation

- primary hyperalgesia

28
Q

what does central sensitisation reflect and what does it cause

A
  • increase in CNS neurone activity and properties

- Causes secondary hyperalgesia and allodynia

29
Q

how does viscerosomatic pain present

A

sharp

well localised

30
Q

what are the spinal nociceptive tracts

A

The spinothalamic tract (STT)

The spinoreticular tract (SRT)

31
Q

what is the pathophysiology of what happens after a head injury

A
  • release of excitatory amino acids e.g. glutamate
  • binding to receptors e.g. NMDA
  • release of intracellular calcium, cell swelling, activation of apoptosis
32
Q

how does secondary brain injury occur

A

Loss of blood-brain-barrier, leucocyte infiltration = inflammation

Loss of cerebral autoregulation of blood pressure = ischaemia

Loss of cerebral autoregulation of blood flow = metabolic de-coupling = more ischaemia and oedema

33
Q

what is the Monro-Kellie hypothesis

A

skull consists of brain, blood and CSF

An increase in volume of one component must produce a decrease in another component otherwise the ICP will rise

34
Q

how is cerebral perfusion pressure calculated

A

CPP = MAP - ICP

Mean arterial pressure
Intracranial pressure

35
Q

what has a major influence on CPP

A

hypotension

36
Q

what is the ideal CPP after head injury

A

> 60mmHg

i.e MAP >80mmHg and ICP <20mmHg

37
Q

what is a normal adults ICP

A

9-11mmHg

38
Q

what are the 2 types of skull base fractures

A

anterior cranial fossa fracture

posterior cranial fossa fracture

39
Q

what is the physical sign of an anterior cranial fossa fracture

A

“raccoon” or “panda eyes”

40
Q

what is the physical sign of an posterior cranial fossa fracture or what other type of fracture

A

“Battle sign” over mastoid area

basilar skull fracture

41
Q

what is the definition of a coma

A

Do not open eyes
Do not obey commands
Do not speak

equates to GCS sum of 8 or less

42
Q

what kills patients with head injuries

A

hypoxia
hypotension
raised ICP

43
Q

when should you request CT head scan in trauma

A

skull fracture
GCS < 15
focal neurological signs
on anti-coagulants e.g. warfarin

44
Q

what are the types of traumatic intracranial bleeding (going from outside to inside)

A 
Extradural haematoma
Subdural haematoma
Traumatic subarachnoid haemorrhage
Intracerebral contusion
Intracerebral haematoma
Intraventricular haemorrhage
45
Q

what is a Decompressive craniectomy

A

surgical removal of part of the skull to allow a swelling brain room to expand without being squeezed

46
Q

what are late effects of head injury

A

epilepsy
- seen early, in first 2 weeks

CSF leak
- into nose or middle ear

Cognitive problems
- post-concussion syndrome

47
Q

what is post-concussion syndrome

A

poor concentration
headache
poor memory
lethargy

Neurology SB (23 decks)

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