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MRCS B - Critical Care (Kanani and Lammy) > Disability - neuro > Flashcards

Disability - neuro Flashcards

1
Q

Outline GCS scoring?

A 
Eyes:
4 = spontaneously open
3 = open to voice
2 = open to pain
1 = won't open
Verbal:
5 = coherent
4 = inappropriate words
3 = confused
2 = sounds incomprehensible 
1 = nothing

motor:
6 = spontaneous
5 = Localise to pain
4 = withdraw from pain
3 = Flex or decorticate response to pain
2 = extensor decerebrate response to pain
1 = no response

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2
Q

Classes of analgesia?

A

Via WHO step ladder:
Step 1 = non opioid e.g. NSAID
Step 2 = Weak opioid e.g. codeine
Step 3 = Strong opioid = morphine

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3
Q

Give examples of common opioids and whether they are synthetic or non-synthetic?

A 
Synthetic = Pethidine, fentanyl
Semi-synthetic = dihydrocodeine, diamorphine 
Noun-Synthetic = morphine, codeine
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4
Q

what receptors do morphine act upon, and the effect?

A 
Mu = analgesia and miosis, reduced gut motility
K = analgesia and dissociative
Delta = Analgesia and anti-depressant
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5
Q

Systemic effects of morphine?

A

Pain - analgesia of moderate to severe pain, not good for neuropathic pain

Respiratory depression - blunt the chemoreceptor affect to PaCO2

neurological sedation

GI = N+V, reduced motility - stimulate chemoreceptor trigger zone in area postrema

Psychiatric = euphoria, dependance and tolerance

Immuno = histamine release = pruritus

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6
Q

Why not morphine in biliary pain?

A

Causes sphincteric contraction (Sphicnter of oddi) plus it stimulates gall bladder contraction = exacerbate pain

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7
Q

Which drug for opiate overdose?

A

Naloxone
Partial mu receptor antagonist
Short half life

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8
Q

How does paracetamol cause OD?

A

normally paracetamol metabolised in liver to n-acetylbenzoquinoneimine. This is the toxic metabolite, but is normally mopped up by glutathione.

Inn paracetamol OD to much for glutathione to deal with = hepatocyte injury.

NAC is a precursor of glutathione

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9
Q

How do NSAIDs work?

A

Inhibit COX, reducing prostaglandin formation.

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10
Q

Systemic SE’s of NSAIDs?

A

GI - dyspepsia, gastritis, peptic ulceration. Causes direct secretion of acid from parietal cells, and causes reduced mucus + bicarb production.

renal - Can precipitate AKI

Coagulopathy - inhibits thromboxane A2 on platelets, meaning cannot aggregate to form a platelet plug. This effect stays until new platelets made.

Bronchospasm - Inhibition of COX leads to arachidonic acid being metabolised down leukotriene pathway = bronchospasm.

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11
Q

How do NSAIDs cause renal injury?

A

Inhibition of compensatory PGI2 and PGE2. These normally vasodilate kidney when there is reduced renal perfusion, so without them cannot increase blood flow and offset the ATN.

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12
Q

When is epidural commonly used?

A

Postoperatively

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13
Q

Why is epidural often not used in ITU?

A

often have septic patients or patients with coagulopathy which are contraindications.

Also have hypovolaemic patients so giving epidural can cause further hypovolaemia.

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14
Q

systemic effects of epidural?

A

Hypotension: due to the block of sympathetic outflow = reduced SVR and CO.

Attenuates surgical stress response

Respiratory - Reduced FRC

Coagulopathy - reduces number of post-op DVT’s

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15
Q

what is CSF volume

A

150ml

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16
Q

Where is CSF produced?

A

70% in chord plexus of 3rd, 4th and lateral ventricle

remaining 30% comes directly from vessels lining ventricular wall .

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17
Q

Circulation of CSF?

A

Begins in lateral ventricle.

Travels to 3rd ventricle via foramen of Monro

Travels to nth ventricle via aqueduct of Sylvius

Travels to subarachnoid space of spinal cord via foramen of Luschka and magendie.

Then enters cranial cavity via foramen magnum and flows around brain in subarachnoid space

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18
Q

What are arachnoid villi composed of?

A

Fusion of arachnoid membrane and endothelium of dural venous sinus it has bulged into

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19
Q

Where is CSF absorbed?

A

80% is arachnoid villi

20% spinal nerve roots

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20
Q

What structures form BBB?

A

Tight junctions between endothelial cells of cerebral capillaries

Astrocytic foot processes applied to basal membrane of cerebral capillaries

21
Q

What can pass through BBB?

A

Lipids and lipid soluble substances e.g. GA, opiates

protons (H+)

22
Q

Which three parts of the brain lie outside the BBB?

A

Neurohypophysis = posterior lobe of pituitary gland - produces ADH and oxytocin

Circumventricular organs = around 3rd and 4th ventricles

Median eminence of hypothalamus

23
Q

What. pathologies can affect the BBB?

A

Infection
Trauma
Tumours
Ischaemia

24
Q

What is cerebral blood flow?

A

750ml/min = 15% CO

This flow is maintained by auto regulation, between systolic of 50mmHg and 150mmHg

25
Q

Mechanism of auto regulation?

A
  1. myogenic: Increase in wall tension due to raised MAP stimulates a reactive contraction of smooth muscle, maintaining flow
  2. Metabolic: If blood flow is increased due to rise in arterial pressure, the normal vasodilators produces are washed away, leading to increased vascular resistance and normal flow
  3. Neurogenic - sympathetic stimulation can affect arteriolar tone.
26
Q

What the factors play a role in cerebral flow regulation>

A

PaCO2 - if increases have increased vasodilation of cerebral arterioles increasing blood flow
Low CO2 causes vasoconstriction and decreased flow

PaO2 - Brain has very high demand for oxygen. Any acute hypoxia causes vasodilation to rapidly increase flow

27
Q

What is CPP?

A

MAP - ICP

Must remain above 70mmHg for adequate perfusion

28
Q

What is Cushings reflex?

A

in raised ICP, you get a hypertension to maintain CPP and a resultant bradycardia

29
Q

What is Monroe-Kelly Doctrine?

A

Cranial cavity is a fixed space, with non-compressible contents

30
Q

Draw a graph showing relationship between intracranial volume and ICP?

A

draw

31
Q

Give some causes of raised ICP?

A
  1. CSF - hydrocephalus:
    a) Increased production (RARE) Choroid tumour / hyperplasia
    b) Decreased absorption - Pseudotumor cerebri syndrome
    c) Blockage - tumour, scarring from infection
  2. Blood = SDH, EDH, SAH, intracerebral bleed
  3. Brain e.g. tumour, cerebral oedema
32
Q

Signs. and symptoms of raised ICP?

A

Headache and N+V = worse In morning
B/L papillodema - shows chronic
Reduced GCS

33
Q

How to control ICP?

A

Conservative:
Bed position and fluid restrict
Controlled ventilation - specifically CO2

medical:
Diuretics = mannitol 0.25-1g/kg over 30 mins IV
Barbiturates e.g. thiopentone

Surgical:
Drainage of CSF from ventricular catheter
Surgery - Decompressive craniectomy

34
Q

Most important complication of raised ICP?

A

Cerebral herniation

35
Q

Different types of herniation?

A

Subfalcine = cingulate gyrus herniating under the falx cerebri . Can compress ACA = coma and contralateral weakness

Tonsillar - displacement of cerebellar tonsils via foramen magnum = cerebellar signs and Resp depression

Transtentorial = Uncus of temporal lobe passes via tectorial hiatus. Compresses midbrain and PCA
Also compresses ipsilateral occulomotor = blown pupil

36
Q

Name a flash localising sign in herniation?

A

Abducens nerve palsy means cannot abduct eye.
Think this is because motor nucleus affected and is site of lesion, BUT actually herniation causes kinking of CNN6 on its long intracranial course.

37
Q

When CT?

A

Reduced GCS, or new neurology

Persisting symptoms e.g. headache or meningism

38
Q

Management of neurological compromised patient?

A

Generally - ABCDE
Tight ventilatory control
Careful fluid and electrolyte balance

Manage cause:
1. CSF = Ventriculoperitoneal shunt. But acutely may require external ventricular drain.

  1. Blood = EDH needs immediate evacuation. SDH = burr holes. SAH = coil or clipping.
  2. Brain = Steroids, PPI, laxatives and eventual debunking if possible.
39
Q

Types of spinal injury?

A

Central cord = motor weakness mainly affecting UL

Anterior cord = motor weakness and spinothalamic. Dorsal tract unaffected = Fine touch, proprioception and vibration.

Brown sequard = hemisection:
Ipsilateral motor loss and dorsal column. Contralateral spinothalamic

40
Q

Why can spinal cord trauma cause bradycardia?

A
  1. Loss of sympathetic outflow
  2. Increase in parasympathetic stimulation due to procedures such. as suctioning / intubation
  3. Cushing reflex
41
Q

Why can spinal cord lesion cause hypotension?

A

Sympathetic loss leads to reduced vascular tone

Often miss occult blood loss e.g. blunt abdo trauma

42
Q

Dangers of autonomic dysfunction in these situations?

A

Occult blood loss can be missed, and hypotension ascribed to neurogenic shock.

Overload with fluids - pulmonary oedema
Reduced CPP due to hypotension
Hypothermia

43
Q

What is spinal shock?

A

Temporary flaccid paralysis immediately after injury.

Can recover after one month.

44
Q

What drug is key in spinal cord injury?

A

High dose IV methyl Prednisolone.

Reduces free radical production causing secondary spinal cord injury.

45
Q

Important issues during long term management?

A 
Rehab
Prevention of ulcers
Chest physio 
Feeding - line insertion
Psychological therapy
46
Q

LP purpose?

A

Diagnostic:
Infection
SAH
Hydrocephalus

Therapeutic - hydrocephalus

47
Q

Pre-procedure checks for LP?

A 
Lab = platelets and PT
Radiology = CT often done before

If suspect SAH, LP must be 12 hours after

48
Q

Equipment and procedure?

A

Sterile pack, LP needle, manometer, LA, 4 universal pots.

  1. Position - on side knees up
  2. Mark between L3/L4 = iliac crests
  3. Prep and drape.

4, LA

  1. Insert LP needle
  2. Take out needle, leave catheter in and insert manometer
  3. 4 universal samples - Virology, cytology, protein and glucose, cultures
49
Q

SE’s of LP?

A

Minor = headache, pain, paraesthsia

Major = haematoma, infection, paraplegia

MRCS B - Critical Care (Kanani and Lammy) (6 decks)

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