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Sem 5 > NS 2: Environment of the brain > Flashcards

NS 2: Environment of the brain Flashcards

1
Q

how does the ICA enter the skull?

A

through the carotid canal in the petrous part of the temporal bone, allowing entry into the middle cranial fossa

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2
Q

what does the ICA branch to give in order to supply the medial surfaces of the frontal and parietal lobes?

A

the anterior cerebral arteries

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3
Q

what does the ICA branch to give in order to supply the lateral surfaces of the cerebral cortex?

A

the middle cerebral arteries

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4
Q

how do the vertebral arteries enter the skull, and where do they arise?

A

through the foramen magnum

arise from the subclavian arteries

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5
Q

what do the vertebral arteries form on entering the skull?

A

the basilar artery

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6
Q

what does the basilar artery supply?

A

the cerebellum and brainstem: midbrain, pons and medulla

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7
Q

what does the basilar artery split to give in order to supply the inferior surface of the brain and the occipital lobes?

A

paired posterior cerebral arteries

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8
Q

how are the cerebral arteries joined together to form the circle of Willis at the base of the brain?

A

by communicating branches
(anterior cerebral arteries joined by anterior communicating artery, posterior cerebral joined to ICA by posterior communicating arteries which arise from the ICA)

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9
Q

clinical importance of circle of Willis?

A

collateral circulation can be provided if arterial blockage, but this is usually inadequate following sudden occlusion of cerebral vessels e.g. with cerebral thrombosis, haemorrhage or embolism), so vascular stroke commonly occurs.

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10
Q

describe how the L and R anterior cerebral arteries arise from the arch of the aorta

A

R: brachiocephalic trunk, R common carotid, R ICA, R anterior cerebral
L: L common carotid, L ICA, L anterior cerebral

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11
Q

describe how the R posterior cerebral artery arises from the aortic arch

A

brachiocephalic trunk, R subclavian, R vertebral, joins with L vertebral to form basilar, gives rise to posterior cerebral

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12
Q

what must cerebral veins cross to enter the dural venous sinuses and why is this problematic?

A

the subarachnoid space

hamorrhage may occur in space if head trauma

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13
Q

why is CSF leakage common with fractures of the base of the skull? and why with base fractures is a CT scan required, rather than an X-ray?

A

the dura lining this region is strongly adherent to the periosteum, so dural tears are common with fracture, causing rhinorrhoea and otorrohoea, and can allow organisms to enter.
skull base is more dense and its L and R sides are superimposed.

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14
Q

how does serious bleeding from the nose occur?

A

tearing of ICA and fracture of the sphenoid

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15
Q

type of blood characterising an exxtradural haemorrhage and visual appearance on scan*?

A 
arterial- tearing of anterior branches of middle meningeal artery
lens shaped (lenticular)- flexible periosteal layer of dura mater is moved away from the cranium.
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16
Q

CSF functions?

A

cushioning, protection of brain and SC
reservoir of metabolites
buoyancy- lightens weight of brain

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17
Q

why is a meningeal haematoma more worrying if arterial blood rather than venous?

A

arterial blood= higher pressure, so more damage may result

subarachnoid haemorrhage= arterial blood- often result of a ruptured aneurysm

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18
Q

contrast effects of upper and lower motor neurone lesions on muscle tone?

A

upper e.g. stroke, causes hypertonia, presented as spastic paralysis- resistance to passive movement of a limb, maximal at beginning of movement.
lower produces hypotonia and flaccid paralysis- body limbs hand loose.

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19
Q

with what disease is cog wheel rigidity seen (result of hypertonicity with an element of tremor present)?

A

Parkinson’s disease

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20
Q

what would an absent ankle jerk in a patient with lower back pain suggest?

A

prolapsed disc at S1-S2 level

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21
Q

which vertebral arches fail to fuse in spina bifida occulta?

A

L5/S1

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22
Q

concerns with myelomeningocele?

A

neural problems

exposed neural tissue and meninges susceptible to life-threatening infections

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23
Q

describe the difference between communicating and non-communicating hydrocephalus?**

A

communicating- flow of CSF through ventricles and into SA space is not impaired, but movement from space into venous system is partly or completely blocked.
non-communicating- flow of CSF is obstructed within ventricles or between the ventricles and the subarachnoid space e.g. aqeductal stenosis due to nearby tumour in midbrain or by cellular debris following intraventricular haemorrhage or bacterial and fungal infections of CNS. obstruction may also occur in an interventricular foramen.

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24
Q

function of an epidural block?

A

anaesthetic inserted into lumbar cistern to block structures innervated by cauda equina

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25
Q

what structure is the uncus the anterior part of?

A

the parahippocampal gyrus ( an elevation of the cerebal cortex)

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26
Q

give 3 reasons why familiarity with the inferior (ventral) aspect of the brain is important?

A
  • almost all cranial nerves of brain emerge from here, and base of skull very vulnerable to impact trauma so cranial nerves and inferior aspect is just as vulnerable to these injuries aswell.
  • relationship between pituitary, hypothalamus and optic nerves clearly visible here, can therefore better understand effects of hypothalamic tumours on neuronal function.
  • uncus readily seen, so can readily see relationship between uncus and oculomotor nerve, so can understand that uncus herniation leads to impairment of peripheral targets of oculomotor nerve.
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27
Q

why are the bones of the calvaria separated in infants with hydrocephalus?

A

sutures are yet to fuse
posterior fontanelle between sagittal and lambdoid sutures closes within 6-9mnths
anterior between coronal and sagittal sutures closes within 2 years.

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28
Q

what may cause a communicating hydrocephalus throguh blockage of CSF drainage from SA space into venous sytem?

A
  • congenital absence of arachnoid granulations
  • blocked granulations by rbc due to subarachnoid haemorrhage
  • fibrosis due to meningitis
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29
Q

Intracranially, through what does the ICA pass anteriorly, alongside the abducens nerve?

A

the cavernous sinus

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30
Q

what are the terminal branches of the ICA and where do they lie?

A

anterior and middle cerebral arteries
subarachnoid space between the arachnoid mater bridging the gaps between adjacent gyri, and the pia mater which travels down into the sulci of the cerebral cortex.

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31
Q

what forms the anterior circulation of the brain?

A

the ICAs and their branches

32
Q

when the posterior communicating arteries of the ICAs join the posterior cerebral arteries, this completes the cerebral arterial circle around which structure?

A

the interpeduncular fossa: deep depression on inferior surface of midbrain between the cerebral peduncles

33
Q

through what do the cervical parts of the vertebral arteries ascend through?

A 
the transverse foramina of the first 6 cervical vertebrae
atlantic parts (related to C1) then pass through foramen magnum after perforating dura and arachnoid mater.
34
Q

where does the basilar artery form?

A

at the caudal border of the pons

35
Q

where are the superior cerebral veins and what do they drain into?

A

on superolateral surface of brain

superior sagittal sinus

36
Q

what do inferior and superficial middle cerebral veins drain into?

A

from inferior, PI, and deep aspects of cerebral hemispheres, drain into straight, transverse and superior petrosal sinuses.

37
Q

what is the great cerebral vein?

A

single midline vein formed inside brain by union of 2 internal cerebral veins, ends by merging with inferior sagittal sinus to form straight sinus.

38
Q

what is the venous drainage of the cerebellum?

A

superior and inferior cerebellar veins which drain into transverse and sigmoid sinuses.

39
Q

How do astrocytes funtion to provide nutrients to neurones?

A

glucose-lactate shuttle: glucose uptaken by astrocytes from the blood and converted to glycogen for storage as neurones have few energy reserves- cannot store or produce glycogen. Can then be converted to lactate for neurones, so have a very temporary supply of energy. Remember neurones can only respire aerobically, O2 dependent. Glucose from blood metabolised to lactate and excreted into ECF for uptake by surrounding neurones.

40
Q

how do astrocytes maintain a low EC concentration of neurotransmitter?

A

able to remove neurotransmitters through uptake via proteins in their membranes, so lots of astrocytes found at the synapse. Important for the excitatory neurotransmitter glutamate as too much=TOXIC.
glutamate coverted to glutamine via g;lutamine synthetase after uptake, then converted back to glutamate on pre-synsptic terminal by glutaminase. Glutamine also goes to inhibitory neurones for GABA synthesis.

41
Q

why can [K+] in brain ECF increase quite rapidly, and why are astrocytes important for managing this?

A

K+ release into ECF with intense neuronal activity. As membrane mainly permeable to K+ at rest as K+ channels open, the resting Em is dependent on the transmembrane K+ gradient, so high K+ would mean the Em would reset to a more +ve value, making neurones more electrically excitable, would depolarise causing inappropriate AP firing, but astrocytes have K+ channels and transporters so can redistribute K+ over non active regions, with adjacent astrocytes tightly coupled via gap junctions, allowing K+ to flow down its conc gradient from active zone to a remote site.

42
Q

what are oligodendrocytes responsible for?

A

myelination of CNS neurones, simultatenously myelinate axons of multiple neurones. Allow rapid AP transmission by saltatory conduction rather than local current flow.

43
Q

what is the brain’s main defence system?

A

microglia: cells involved in immune response. can present antigens to T cells, but don’t want this too much as rigid skull doesn’t allow volume expansion with inflammatory responses. Dendrites get thicker to allow phagocytosis of material.

44
Q

how do brain capillaries form an effective BB barrier, preventing limiting diffusion of substances from the blood into the brain ECF?

A

tight junctions between endothelial cells- formed by occludins and claudins (proteins), and end feet of astrocyte processes send messages to endothelium to form tight junctions.
basement membrane
end feet of astrocyte processes

45
Q

glucose, K+ and aa can cross BB barrier, but in a controlled manner, why is important that aa entry into ECF is controlled?

A

aa can often act as neurotransmitters and don’t want inappropriate neurone activation, but aa are needed.

46
Q

importance of CNS inhibiting initiation of pro-inflammatory T cell response?

A

rigid skull will not tolerate volume expansion

47
Q

function of swelling of cell body of a neurone, known as the axon hillock?

A

AP initiation

48
Q

4 main sections of a neurone?

A

cell body (soma)
axon
dendrites
nerve terminal

49
Q

how does neurotransmitter release occur at a synapse?

A

depolarisation of nerve pre-synaptic nerve terminal when AP arrives, causes opening of voltage-gated Ca2+ channels, so influx of Ca2+, which is bound by a Ca2+ binding protein= synaptotagmin, which is a vesicle associated protein and so transports vesicle containing neurotransmitter to the presynaptic membrane, where protein activates a SNARE-protein complex, so that veiscle can fuse with membrane at an active zone, and NT released into synaptic cleft.

50
Q

how do botulinum and tetanus toxins (produced by clostridia bacteria) parlayse individuals?

A

inhibit NT release at synapses by degrading proteins of the SNARE complex through their intrinsic protease activity

51
Q

what does the postsynaptic response depend on?

A

nature of neurotransmitter
nauture of receptor: ligand-gated (ionotropic- ion channels which mediate ion influxes when active e.g. nicotinic AChR which mediates Na+ influx) or GPCRs (metabotropic) e.g. muscarinic AchR

52
Q

3 chemical classes of NTs in CNS?

A

aa e.g. glutamate, glycine and GABA
biogenic amines e.g. Ach, noradrenaline, 5-HT, dopamine, histamine
peptides e.g. NPY and somatostatin

53
Q

major excitatory neurotransmitter in the CNS?

A

glutamate

54
Q

examples of glutamate receptors?

A 
ionotropic:
AMPA: Na+/K+ permeability
Kainate: Na+/K+
NMDA: Na+/K+/sometimes Ca2+. Blocked by Mg at rest, so must be depolarised before ions can flow through when glutamate binds. Important for learning and memory, activation increases Ca2+.
metabotropic: GPCRs
55
Q

how are fast excitatory responses generated?

A

by excitatory neurotransmitters e.g. glutamate, which bind to ligand-gated ion channels and cause depolarisation of post-synaptic cell with cation influx.
Depolarisation then causes more APs. Particular threshold reached with excitatory PS potential, which causes AP to fire.

56
Q

which receptors do glutaminergic synapses have?

A

NMDA and AMPA

57
Q

clinical importance of Ca2+ entry through glutamate NMDA ligand-gated ion channels?

A

too much glutamate can cause excitotoxicity
*STROKE: damaged areas can undergo depolarisation, which can then spread and activate NMDA receptors, causing elevated Ca2+, so if these receptros are blocked, it can limit the damage caused by a stroke.
Ca2+ entry important for inducing long term potentiation- this can be caused by strong, high frequency stimulation.

58
Q

how may AMPA receptors acted upon by glutamate be upregulated?

A

by activation of NMDAs and mGluRs

59
Q

main inhibitory neurotransmitter in brain?

A

GABA: gamma amino butyric acid

60
Q

where in the CNS does glycine mainly act as an inhibitory neurotransmitter?

A

brainstem and SC

61
Q

how do GABA and glycine act as inhibitory neurotransmitters?

A

receptors have integral Cl- channels so activation causes hyperpolarisation, producing an inhibitory post synaptic potentialand reducing AP firing

62
Q

give examples of drugs which enhance the response to GABA?

A

benzodiazepines and barbiturates
bind to GABA A receptors
benzodiazepines used to treat anxiety, sedative effects and epilepsy- suppress too much neuronal activity
barbiturates no longer used in anxiety as risk of fatal OD and tolerance, but sometimes used as anti-epileptic
also alcohol and steroids

63
Q

describe what neurotransmitters are released in the patellar (knee jerk) reflex (L3, L4)

A

glycine released from inhibitory interneurones to relax hamstrings (biceps femoris, semimembranosus and semitendinosus)
message sent to SC, glutamate released, activating motor neurone- releases ACh to cause quads to contract

64
Q

function of biogenic amines as neurotransmitters in CNS?

A

neuromodulators

most confined to specific pathways

65
Q

give 4 examples of where ACh acts as an neurotransmitter?

A

NMJ
ganglionic synpases of ANS
postganglionic parasympathetic
nicotinic and muscarinic receptors in brain
receptors often present on presynptic terminals to enhance release of other transmitters

66
Q

which are the 1st neurones to die off in Alzheimer’s?

A

those cholinergic neurones of the nucleus basalis

so can give cholinesterase inhibitors to relieve symptoms in alzheimers.

67
Q

tment for Parkinson’s disease?

A

levodopa: converted to dopamine by DOPA decarboxylase
Parkinsons: loss of dopaminergic neurones in substantia nigra

68
Q

disease caused by too much dopamine?

A

schizophrenia

anti-psychotics: antagonsits at dopamine D2 receptors

69
Q

why don’t we want too much dopamine peripherally?

A

can increase BP
so give carbadopa- can’t pass BB barrier, so dopamine reduced in blood as carbadopa inhibits DOPA decarboxylase required to convert L-DOPA to dopamine, but doesn’t affect enzyme converting L-dopa to dopamine in brain

70
Q

where are the neurones located that are responsible for most NA production in brain?

A

locus ceruleus
activity increases during behavioural arousal, inactove in sleep
amphetamines increase NA and dopamine release and increase wakefulness

71
Q

what condition may be associated with a deficiency of NA?

A

depression

72
Q

where are serotoninergic neurones located in brain?

A

raphe nuclei

73
Q

serotonin functions?

A

sleep/wakefulness, mood

serotonin selective reuptake inhibitors increase serotinin, so used in tment of depression and anxiety disorders

74
Q

describe how CSF passes from the lateral ventricles in the superior sagittal sinus?

A

passes from lateral ventricles into 3rd via intraventricular foramina of Monro
then into 4th via cerebral aqeduct
then into SA space via foramina of Luschka (2 found laterally) and Magendie ( 1 in midline)
CSF then flows rostrally over cerebral hemispheres or down into SC
reabsorption then occurs via arachnoid granulations within the superior sagittal and related venous sinuses

75
Q

name of foramina that allows CSF to pass from lateral ventricles into 3rd?

A

interventricular foramen/foramen of Monro

76
Q

which arteries are given off the vertebral arteries on route to the brain, and what do they supply?

A

anterior and posterior spinal arteries- anterior spinal= anterior 2/3 of SC, posterior spinal= dorsal column/medial lemniscal tract, arise from vertebral or indirectly from posterior inferior cerebellar.
posterior inferior cerebellar artery- lateral part of medulla and cerebellum

77
Q

4 main functions of CSF?

A

buoyancy- cerebral tissues helped from being compressed by gravity against the skull- this would impede b.flow, causing ischaemia
shock absorption and protection
volume changes- CSF allows H20 to shift from CSF to cells without causing any gross change in CNS volume
homeostasis- K+ levels tightly maintained so protecting neurons from fluctuating plasma concs, constant renewal of fluid to prevent build up of neuronal waste products, transmitters and ions, enabled by high flow rate.

Sem 5 (35 decks)

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