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MRCS Physiology > Neurological system > Flashcards

Neurological system Flashcards

1
Q

Which cells form the BBB in the CNS?

A

Astrocytes

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2
Q

Which cells perform a phagocytic role in the CNS?

A

Microglia

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3
Q

Which cells produce myelin in the CNS?

A

Oligodendrocytes

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4
Q

Blood flow to the brain is via which 2 main arteries?

A

Internal carotid

Vertebral arteries

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5
Q

How many % of cardiac output does the brain receive?

A

10-15%

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6
Q

What 3 mechanisms control cerebral blood flow?

A

Autoregulation: Myogenic, metabolic
Neural
Local

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7
Q

What does autoregulation mean?

A

The brain maintaining about the same blood flow over a wide range of BPs

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8
Q

How does MYOGENIC autoregulation occur?

A

When cerebral blood vessels constrict/dilate to maintain adequate cerebral perfusion

BP rise = constrict
BP drop = dilate

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9
Q

Range of autoregulation of cerebral perfusion pressure (CPP)

A

60-160 mmHg

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10
Q

What happens at the extreme ends of CPP range?

A

50mmHg: cerebral blood vessels fail to maintain flow

150-160mmHg: fail to regulate flow, become abnormally permeable and causing cerebral oedema

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11
Q

Equation for cerebral perfusion pressure (CPP)

A

CPP = MAP - ICP

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12
Q

What happens when CPP falls <50mmHg?

A

Cerebral ischaemia

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13
Q

What happens when CPP falls <30mmHg?

A

Death

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14
Q

Factors impairing myogenic autoregulation

A 
Ischaemia/hypoxia
Trauma
Cerebral haemorrhage
Tumour
Infection
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15
Q

How does METABOLIC autoregulation of cerebral blood flow (CBF) occur?

A

Increased brain activity = decreased PaO2 and increased PCO2 = local vasodilatation of cerebral blood vessels and increased perfusion

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16
Q

How does LOCAL autoregulation of CBF occur?

A

Changes in arterial PaO2 and CO2

Increase in CO2 = increase in CSF due to cerebral vasodilatation

Effect of changes in PaO2 not as marked - hypoxia only has a significant effect when it falls <8kPa

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17
Q

Factors affecting cerebral vessel response to PaO2 and PaCO2

A

Head injury
Cerebral haemorrhage
Shock
Hypoxia

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18
Q

Why is maintaining a low to normal PaCO2 level important in head injury patients?

A

To prevent increases in ICP due to cerebral vasodilatation

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19
Q

Where does CSF lie?

A

In subarachnoid space

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20
Q

Total CSF volume in brain

A

130-150mL (40mL in cerebral ventricles, 100mL around spinal cord)

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21
Q

Rate of CSF production

A

500mL per day

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22
Q

Normal CSF pressure

A

~0.5-1 kPa OR

10-15 mmHg

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23
Q

What produces CSF?

A

Ependymal cells in choroid plexus in the lateral, third and fourth ventricles (70%)

Blood vessels (30%)

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24
Q

Pathway of CSF flow within the CNS

A

Lateral ventricles –> interventricular foramina (of Munro) –> third ventricle –> cerebral aqueduct (of Sylvius) –> fourth ventricle –> foramen of Luschka (lateral) and Magendie (midline) –> subarachnoid space

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25
Q

What reabsorbs CSF back into the circulation?

A

Arachnoid villi/granulations –> project and drain into superior sagittal sinus

(small amt can be absorbed by spinal villi)

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26
Q

Composition of CSF

A

Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
White blood cells: 0-3 cells/mm3
Red blood cells: NONE

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27
Q

Examples of focal and diffuse SOLs

A

Focal = tumour, aneurysm, blood/haematoma, granuloma, tuberculoma, cyst, abscess

Diffuse = vasodilatation, oedema

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28
Q

Consequences of intracranial SOLs

A

Raised ICP
Intracranial shift and herniation
Hydrocephalus

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29
Q

What is pressure within the cranium governed by?

A

The Monroe-Kelly doctrine = considers skull as a rigid closed box with brain, blood and CSF as only contents

Hence, ICP = V(csf) + V(brain) + V(blood)

Increases in mass can be accommodated by loss of CSF. Once a critical point is reached (usually 100-120ml of CSF lost) there can be no further compensation and ICP rises sharply.

Next step: pressure will begin to = MAP + neuronal death + herniation

30
Q

Normal ICP in supine position

A

0-10mmHg (passmed: 7-15mmHg)

31
Q

Consequences of raised ICP

A

Hydrocephalus

Cerebral ischaemia (any rise in ICP will eventually exceed autoregulation)

Brain shift and herniation

Systemic effects (thought to be due to autonomic imbalance, hypothalamic overactivity due to compression and ischaemia of vasomotor area)

32
Q

Types of herniation

A

Transtentorial (lesion within 1 hemisphere causes herniation of medial part of temporal lobe over tentorium cerebelli)

Tonsillar (lesion in posterior fossa, lowest part of cerebellum pushes down into foramen magnum and compresses medulla)

Subfalcine (lesion in 1 hemisphere leads to herniation of cingulate gyrus under falx cerebri)

Diencephalic = coning (generalised brain swelling causing midbrain to herniate through the tentorium)

33
Q

Systemic effects of raised ICP

A

Cushing’s reflex = decreased RR, bradycardia, HTN
Cushing’s ulcers
Neurogenic pulmonary oedema
Preterminal events = bilateral pupil constriction followed by dilation, tachycardia, decreased RR, hypotension

34
Q

Clinical features of raised ICP

A

Headache
N+V
Papilloedema
Decreased consciousness

35
Q

Clinical features of cerebral herniation

A

Transtentorial:
Oculomotor nerve compression = ipsilateral pupil dilation
Cerebral peduncles = contralateral hemiparesis
PCA = cortical blindness
Cerebral aqueduct = hydrocephalus

Tonsillar:
Compression of cardio/resp centres in medulla = death

Subfalcine: ACA = infarction

All types:
Reticular activating system = coma
Distortion of midbrain and tearing of vessels = death

36
Q

What type of molecules can pass freely across the BBB into the interstitial space of the brain?

A

Lipid-soluble molecules

37
Q

What does the BBB prevent?

A

Free movement of ions into the brain

Release of neurotransmitters from neurons into the peripheral circulation

38
Q

What is the BBB formed by?

A

Structure of capillary endothelium with very tight cell-to-cell junctions

as opposed to the freely permeable fenestrated capillaries found in other tissues

End-feet of astrocytes also cover the basement membrane

39
Q

Areas of the BBB containing fenestrated capillaries

A

Areas in the midline including:
3rd and 4th ventricles = allow drugs and noxious chemicals to trigger the chemoreceptor trigger zone in the floor of the 4th ventricle, which in turn triggers the vomiting centre. Angiotensin II also passes to the vasomotor centre in this region to increase sympathetic outflow and causes vasoconstriction of peripheral vessels

Posterior lobe of pituitary = allow release of ADH and oxytocin into circulation

Hypothalamus = allow release of releasing/inhibitory hormones into the portal-hypophyseal tract

40
Q

Specific functions of BBB

A

Tight junctions restrict penetration of water-soluble substances

Lipid-soluble molecules e.g. CO2, O2, hormones, anaesthetics, alcohol can pass freely across

Endothelium has TRANSPORT PROTEINS (CARRIERS) for nutrients e.g. sugars, amino acids

Certain proteins e.g. insulin, albumin, may be transported by endocytosis and transcytosis

41
Q

Preconditions for Dx of brainstem death

A 
4 preconditions:
Must be in a COMA
Must be a KNOWN CAUSE for coma
Cause must known to be IRREVERSIBLE
Must be dependent on VENTILATOR
42
Q

Exclusion criteria for Dx of brainstem death

A

No residual drug effects from narcotics, hypnotics, tranquilisers, muscle relaxants, alcohol, illicit drugs
Core body temp must be >35 deg
No circulatory, metabolic or endocrine abnormality disturbance that may contribute to the coma

43
Q

Brainstem death tests

A

No direct/consensual pupillary response to light (CN 2-3)
Absent corneal reflex (CN 5 and 7)
No motor response in the CN distribution to stimuli in any somatic area (e.g. supraorbital or nailbed pressure leading to grimace)
No gag reflex (CN 9-10)
No cough reflex (CN 9-10)
No vestibulo-ocular reflex (CN 3, 6, 8)
Apnoea test

Must be done by 2 doctors (1 must be consultant) on 2 occasions, with >5 years’ experience and must be competent in the field (e.g. neuro/ITU), must not be part of transplant team

44
Q

Types of nerve fibres

A 
A-alpha
A-beta
A-gamma
A-delta
B
C
45
Q

Features of A-alpha fibre

A

Function = motor proprioception
Conduction velocity = 100m/s
Diameter = 15-20 micrometre

46
Q

Features of A-delta fibre

A

Myelinated
Function = PAIN (initial sharp), temperature, touch
Conduction velocity = 20m/s
Diameter = 2-5 micrometre

47
Q

Features of A-beta fibre

A

Function = touch, pressure
Conduction velocity = 50m/s
Diameter = 5-10 micrometre

48
Q

Features of A-gamma fibre

A

“high intensity mechanical stimuli”
Function = motor proprioception
Conduction velocity = 30m/s
Diameter = 3-6 micrometre

49
Q

Features of B fibre

A

Function = autonomic
Conduction velocity = 10m/s
Diameter = 3 micrometre

50
Q

Features of C fibre

A 
Unmyelinated
"high intensity mechanothermal stimuli"
Function = PAIN (dull, longer-lasting)
Conduction velocity = 1m/s
Diameter = 0.5-1 micrometre
51
Q

Main types of neurotransmitters

A

Acetylcholine (excitatory)
Amines: catecholamines, 5-hydroxytryptamine (serotonin), histamine
Amino acids: glycine (inhibitory), glutamate (can be converted to GABA, excitatory or inhibitory), aspartate (excitatory)
Peptides: substance P (involved in pain transmission), endorphins (inhibit pain pathways)

52
Q

Which amino acid are catecholamines formed from?

A

Tyrosine

53
Q

Which enzymes degrade catecholamines?

A

Monoamine oxidase = breaks down NT taken up by PREsynaptic neuron

Catechol-O-methyl transferase = break down NT take up by POSTsynaptic neuron

54
Q

Types of pain

A

Nociceptive (somatic, visceral) - common in surg pt
Referred - common in surg pt
Neuropathic
Psychogenic

55
Q

Stages of pain transmission

A

Transduction
Transmission
Modulation
Perception

56
Q

Inflammatory substances released after tissue damage

A 
Prostaglandins
Histamine
Serotonin
Bradykinin
Substance P
57
Q

Where do A-delta and C fibres synapse in the spinal cord?

A

Lamina I and III in the dorsal horn

58
Q

What does the ‘gate control theory’ of Melzack and Wall in the modulation of pain propose?

A

That pain impulses received in the dorsal horn can be modulated by other descending spinal inputs

E.g. inhibitory inputs from periaqueductal gray matter and nucleus raphe magnus (both release serotonin) + locus coeruleus (release NA)

Plus release of naturally occurring enkephalins and endorphins

59
Q

Effects of inadequate analgesia in surgical patients

A

Resp: increased chest wall splinting, reduced tidal volume, vital capacity and functional residual capacity, difficulty coughing, retention of secretions causing atelectasis and pneumonia

CV: increased HR and BP

Immobilisation, increased risk of VTE

Ileus
Urinary retention
Stress response
Psychological stress

60
Q

Roles of different analgesic drugs at different stages of pain transmission

A

Transduction: paracetamol, NSAIDs
Transmission: LA, TENS
Modulation: opioids

61
Q

MoA of paracetamol and NSAIDs

A

Inhibit prostaglandin production

Prostaglandin involved in sensitising nociceptive receptors in injured tissues to the effects of nociceptive compounds e.g. bradykinin, substance P

62
Q

MoA of LA

A

Prevent conduction of APs in A-delta and C fibres

63
Q

MoA of TENS

A

Stimulate A-beta fibres to inhibit pain transmission to higher centres

64
Q

MoA of opioids

A

Bind to mu receptors in higher centres e.g. periaqueductal gray matter and nucleus raphe magnus = stimulate descending inhibitory inputs to pain perception

Bind to mu receptors in dorsal horn

Inhibit substance P release

65
Q

Where do the preganglionic neurons of the parasympathetic nervous system lie?

A

In cranial nerve nuclei within the brainstem

66
Q

Which CNs is parasympathetic output derived from?

A 
CN 3, 7, 9, 10
Oculomotor
Facial
Glossopharyngeal
Vagus
67
Q

Which ganglia does the PNS feed into before being distributed to the structures it innervates?

A

CN III –> ciliary ganglion

CN VII –> sphenopalatine + submandibular ganglion

CN IX –> otic ganglion

S2-4 –> pelvic splanchnic nerve –> pelvic ganglion

68
Q

Where do the preganglionic neurons of the sympathetic nervous system lie?

A

In the lateral horn of spinal grey matter

69
Q

Where do the cell bodies of the postganglionic neurons of the sympathetic nervous system lie?

A

Either in the sympathetic chain OR

In a named plexus along the aorta (coeliac, superior and inferior mesenteric)

70
Q

Management of patient with head injury transferred to ITU and acute rise in ICP

A
  1. Position the pt head up 30deg to improve venous drainage
    (remove spinal collar only if safe)
  2. Sedate the pt with propofol/thiopental (decrease cerebral metabolism)
  3. Hyperventilation
  4. Treat with IV mannitol (reduce brain water and volume)
  5. Induce hypothermia may be protective
  6. Contact neurosurgical team = may advise re-scaning of pt to identify reason for deterioration
  7. Surgical options = CSF drainage, haematoma evacuation, craniectomy, lobectomy
71
Q

Why is paracetamol an effective analgesic and anti-pyretic but has poor anti-inflammatory action?

A

It inhibits COX-3 in the CNS causing analgesia

Little effect on COX-1 and 2 hence poor anti-inflammatory (which NSAIDs inhibit)

MRCS Physiology (6 decks)

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