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Semester 3 > NEURO > Flashcards

NEURO Flashcards

1
Q

type of humour in anterior and posterior chamber of eye

A

anterior = aqueous

posterior = vitreous

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2
Q

where does the neural retina end

A

at the ora serrata = non neural

this extends and goes under the retina (therefore retina is sitting ontop of this) this area = retinal pigment epithelium

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3
Q

what cells are the optic nerve myelinated with

A

oligodendrocytes (rather than Schwann cells)

susceptible to MS

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4
Q

scotopic vision

A

vision in dim/low lighting

rod cells work best in this lighting

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5
Q

why is central vision more detailed/clearer than peripheral

A

smaller receptor fields (no convergence)

no rods - only cones (+ MANY of them)

ganglion cells + bipolar neurones have been pushed aside to create a fovea pit - light doesn’t have to travel via multiple layers from vitreous

+ no blood vessels

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6
Q

where is LGN located and via what do they travel to the primary visual cortex

A

thalamus

via optic radiations

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7
Q

why do we have a blind spot

A

where the optic nerve lies we have no photoreceptors in this part of the retina

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8
Q

multiple sclerosis

A

only affects CNS (oligodendrocytes)

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9
Q

how might you get tunnel vision

A

glaucoma –> compresses axons of peripheral retina = loss of peripheral vision

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10
Q

lesion in optic chiasma

A

bitemporal hemianopia

because it destroys crossing NASAL fibres which normally receives projections from temporal view

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11
Q

Lesions of the visual cortex

A

(similar to lesions of optic tract) =
contralateral homonymous hemianopia

However unlike lesions of the optic tract, there is frequently macular sparing

because representation of the macular is so large in the primary visual cortex

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12
Q

consensual reflex pathway

+ why do HCPs look at this after trauma

A
  1. optic nerve
  2. chiasma
  3. optic tract
  4. pretectal nucleus
  5. BOTH edinger-westphal nuclei
  6. long pre-ganglion CN III
  7. synapses at prarasymp ciliary ganglion
    8 short ciliary parasympathetic nerve (ACH)
  8. sphincter pupillae

preganglionic fibres in cranial nerve III are vulnerable to raised intracranial pressure

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13
Q

what is dilator papillae driven by

A

NOT light

LONG ciliary sympathetic innervation (NA)

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14
Q

what nerve innervation increases refractive power of lens

A

PARASYMP

short ciliary nerve (Ach)–> contracts ciliary muscles –> relaxed suspensory ligaments –> lens bulges

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15
Q

myopia / Hypermetropia

what can you see

A

myopia - only close things

hypermetropia - distance things

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16
Q

how do you activate photoreceptors when light changes (eg. increases)

A
  1. When the amount of light (illumination) hitting the outer segment increases
  2. some of the Na+ channels close shut
  3. stops as much Na+ going into the cell while K+ continues to leak out
  4. cell hyperpolarises
  5. reduced release of glutamate

If decrease light —> more Na+ open –> depolarise –> more glutamate

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17
Q

how cell hyperpolarises when light hits

A

opsin protein + 11-cis retinal molecule(=photopigment) on membrane discs
(all carbon bonds are trans except at 11 = cis bond)

when hit by light they become all trans (= activated photopigment)

activated a chemical cascade involving g-proteins

break down of cGMP (which normally keeps the Na+ channels on the cell membrane open)

Na+ closes

cell hyperpolarises

less glutamate released

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18
Q

how is this response terminated

A

removal of all-trans retinal molecule

converted back to 11-cis by RPE

+ there is an enzyme that replenishes the cGMP levels so Na+ channels open again

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19
Q

function of RPE cells

A

they suck fluid between the gaps of photoreceptors = Keeps retina in place

act as a Blood-retinal barrier between retina and choroid(have tight junctions/control flow of substances)

converting all-trans back to cis-trans retinal

act as phagocytic cells - bite the outer segments for them to regrow (every 10days)

contains pigment granules that absorb stray light

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20
Q

explain how drusen can lead to death of photoreceptors

A

when outer segments of photoreceptors are photo-oxidised (by retinoids: high o2 conc/electromagnetic light) = damaged and not removed

causes RPE to become clogged with intracellular debris (lipofusin)

RPE will try get rid of this by depositing it onto the basement membrane

attracts cholesterol + immune cells from blood (choroid)

leads to build up of flatty plaques = drusen

drusen blocks movement of O2 from choroid to photoreceptors = death

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21
Q

Parvocellular

magnocellular ganglion cells

A

parvo = specialised for fine detail/colour information
- will only fire when there is excitation from ONE photoreceptor (no convergence)

magno = detecting fast movement/ broad outlines
- can be activated by a few photoreceptors (convergence due to little lateral inhibition )

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22
Q

how do we see colour

A

3 cones and we compare wavelengths between the light they detect

red with green
blue with yellow (red+green)

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23
Q

why are males more likely to be colour blind

A

red and green photoreceptor genes are on X chromosome

colourblind = recessive

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24
Q

what information do they receive:

  • retina and LGN
  • primary visual cortex

higher visual cortex areas:

  • inferotemporal pathway
  • parietal cortex
A

retina + LGN

  • wavelength
  • contrast (edges)

primary visual cortex

  • orientation of the edges
  • presence of corners
  • direction of motion
  • binocular disparity (3D)

inferotemporal

  • what is the visual image
  • what does it mean
  • shape + colour

parietal cortex (movement/spatial vision)

  • recieves great input from MAGNOcellular cells
  • where object is/going
  • how object relates to other objects
  • whether we are moving the object/itself
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25
Q

what controls the various gaze centre nuclei

where would horizontal /vertical gaze centres send impulses to

A

superior colliculi–>gaze centres

horizontal

  • abducens (VI) = abduction
  • oculomotor (III) = adduction

vertical

  • trochlear (IV) = depression (SO)
  • oculomotor (III) = elevation/depression
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26
Q

conjugate eye movements

A

saccadic (jumpy)

  • exploratory (looking around to recognise where we are)
  • voluntary (looking at clock)

smooth pursuit (following an object)

PONTINE NUCLEI + cerebellum –> vestibular system involved for balance due to track head movements

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27
Q

disconjugate eye movement pathway

A
  1. visual cortex (desire to look at something close)
  2. vergence centre (midbrain)
  3. oculomotor nucleus
  4. medial rectus contract
  5. eyes inwards

+ vergence centre–> edigner-westphal nucleus–> parasymp ciliary –> ganglion–> contract ciliary(refractive power) /constrict pupil (improve focus)

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28
Q

how can tilting of stereo cilia detect:

  • frequency
  • volume
  • pitch
A

FREQUENCY

  • low = back and forth tugging–> depolarisation/hyperpolarisation
  • high = continuous depolarisation

VOLUME
-loud = greater tugging of tip links = more AP

PITCH

  • low = floppy apex
  • high = stiff base
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29
Q

endolymph
where is it produced

what can happen if excess fluid is not removed

A

fills the spiral organ

high in K+

produced by stria vascularis

meniere’s disease = high endolymph pressure –> damage to cochlear (ringing/dizziness)

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30
Q

how are hair cells depolarised

A

tilting of hair cells opens K+ channels on adjacent stereocilia

entering of K+ from endolymph–> glutamate released to the afferent nerves

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31
Q

dorsal and ventral cochlear nuclei

A

(brainstem)
dorsal = discriminating sound via frequency

ventral = localisation of sound via frequency
(–>superior olivary nuclei –> inferior colliculi)

these –> inferior colliculi–> MGN(thalamus)–> primary auditory cortex

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32
Q

superior olivary nuclei

A

compares noise from the 2 ears to determine origin of sound

LATERAL = high frequency in 2 ears are compared

  • sensitive to VOLUME
  • ear sound hits first/closest = loudest

MEDIAL = low frequency

  • sensitive to TIMING
  • ear it hits first = closes to origin
33
Q

2 types of hair cells

A

inner = closer to origin of tectorial membrane

outer = lay further back

when OUTER depolarised they can shorten–> amplify the sensitivity of the auditory system

allowing the INNER to do its job of discriminating the hearing

34
Q

auditory pathways

A

hair cells depolarise–> afferents –> cochlear nuclei (brainstem) –> inferior colliculi —> MGN—> primary auditory

if ventral cochlear nuclei –> superior olivary–> inferior colliculi

35
Q

why does bilateral lesions at both primary auditory cortexes not lead to total deafness

A

other cortical areas also receive primary auditory input not just to primary auditory cortex

individual will be aware a sound has occurred but unable to discriminate between the frequencies heard

would be unable to understand a voice as they would be unable to hear the different pitches

36
Q

presbyacusis

A

As we age we lose hair cells esp. high frequency hearing

This is seen in elderly people who lose the hearing of “ss” in speech (sibilance) and so they cannot understand. It is not necessarily a loudness issue where the younger person has to shout, as the elderly person will still not understand.

solution = speak SLOWLY +CLEARLY

37
Q

acoustic neuroma

A

(anatomically = vestibular schwannoma)

most of vestibular nerve =myelinated by oligodendrocytes (CNS) but it turns into a peripheral nerve and is myelinated by Schwann cells(neurolemmocytes)

these Schwann cells can proliferate–> benign tumour (nerve tumour=neuroma)

which can compress on other nerves

  • ringing in ears first
  • then as it gets bigger = dizziness / tingling in face
38
Q

membrane labyrinth

bony labyrinth

A

membrane (cochlear duct) - filled with endolymph (K+)

Bony (scali vestibuli & scali tympani) - filled with perilymph (Na+)

39
Q

the membranous labyrinth structures in the vestibule where vestibular receptors are found

A

saccule
utricle
(which make up the otolith system)

and on ampullae = the swellings at the end of the semi-circular ducts (of the semi-circular canal) which join to the utricle

40
Q

otolith system

A

sensitive to linear movements and gravity

  • vertical macula(sensory epithelium) in saccule
  • horizontal macula in utricle

hair cells+cilia on macula

embedded in otoconia crystal + otolith(gel) giving inertia

1) at rest - fires streams of spontaneous AP
2) change in movement
3) jelly will lag due to otoconia crystals
4) tilt stereocilia
5) more firing

hair cells are orientated differently so every tallest cilia is facing a DIFFERENT direction - between utricle and saccule all directions are covered

41
Q

lateral/medial vestibulospinal tract

A

otolith system afferents—> LATERAL–> ipsilateral anti-gravity muscles in legs

semi-circular ducts—> MEDIAL–> muscles to move/stabilise head

42
Q

semi circular ducts

A

only respond to rotating movements of the head

ampulla
-ampullary crest with hair cells
-stereocilia are within CUPULA (gel)
-stereocilia in cupula are all facing the SAME way
but there are 3 canals therefore all axes are covered
-turn left you activate ONLY left but you hypepolarise the right

43
Q

reflex for stabilising head

A

turn left

  • LEFT canal/ vestibular nuclei triggered
  • signal to abducens nuclei on right side
  • CN VI to contract lateral rectus of RIGHT eye

the right abducens nuclei also–> oculomotor nuclei of LEFT

to contract medial rectus of LEFT eye

(eyes moving right as head moves left)

44
Q

in order to contract both eye muscles to look same direction with the reflex it needs to be fast - how is this achieved

A

the axon that links the two runs in the pathway =
medial longitudinal fasiculus
which is myelinated

the axon in the above example = between abducens to oculomotor

45
Q

which lobe of cerebellum interacts with vestibular system to make sure movements are accurate

A

floconodular lobe

46
Q

what does the cerebellum receive input from

and where does it project to

A

parallel fibres from

vestibular neuclei

and the inner ear afferents itself (going towards the nuclei) granule cells

purkinje cells project down to vestibular nuclei (inhibiting)

47
Q

what tells the purkinje fibres of cerebellum to increase/decrease their inhibitory control on vestibular nuclei

A

visual:
retinal ganglion cells that project to LGN also project to ACCESSORY OPTIC SYSTEM (many nuclei in brainstem)

AOS–> olive/pontine nuclei

  • olive modulate input from both vestibular nuclei and granule cells
  • pontine nuclei modulate the input from inner ear afferents (granule cells)
48
Q

nystagmus

A

damage to cerebellum/vestibular pathway

causing imbalance in left/right vestibular system

failure to fix on an object

leading to eye drift

49
Q

vertigo

A

sensation of moving around in space or having objects move around you

50
Q

Why does sensory conflict make us ill?

A

when there is the sensory conflict the brain thinks this is due to aberrant activity in the vestibular system and you’ve been poisoned, so you feel motion sickness.

vestibular system is essential for feeling motion sickness(visual isn’t essential)

51
Q

pathway for motion sickness

A
  1. conflict between vestibular organs and visual system
  2. feeding into vestibular nuclei
  3. to NTS (vomiting centre) to say there is mismatch
    4.increase in vasopressin (makes us feel nauseous)
    increase in symp activity–>gut dysthymia–>vomiting

area postrema (toxins in blood) and vagal afferents (toxins in gut)also plug into NTS to enhance nausea

52
Q

treatment for nausea/vomiting

A

muscarinic Ach antagonist
-act in vestibular nucleus

h1 histamine receptor antagonists (promethazine)

side effects of both

  • drowsiness
  • dry mouth
  • blurred vision
53
Q

baroreceptor reflex

A 
HIGH BP
stimulates baroreceptors in carotid sinus
afferents to NTS
excitatory to CVLM(inhibitory)
inhibits RVLM(symp)
low HR/SV/CO/TPR
lowering BP
54
Q

autoregulation

A

maintaining BLOOD FLOW
despite changes in BP

only between 60mmHg and 160mmHg

if high BP- constrict
if low BP- dilate
to maintain BF

below 60 - syncope/mental confusion

55
Q

metabolic auto-regulation

A

high levels of pCO2 (acidity)
can lead to dilation of vessels

as a result increased BF to cerebral vessels

when O2 levels drop, you see an increase in BF to brain to try maintain oxygen delivery to brain tissue.

56
Q

how Regional Hyperaemia in brain can lead to vasodilation of cerebral arteries

A

high AP firing
high K+ efflux
K+ in interstitial fluid–> vasodilator

57
Q

nervous control of cerebral arteries

A

no/little within brain (regulated by myogenic/auroregulation)

abundant to surrounding brain

serotonin = vasoconstrictor

substance P & CGRP = vasodilator

58
Q

Sumatriptan

A

serotonin receptor agonist

used for migraines

constricts blood vessels - reducing inflammation induced vasodilation–> reducing pain

59
Q

what substances can move past BBB

3 areas where it is not complete

A 
lipid soluble (O2/CO2)
glucose/AA via carrier mediated
  • area prostrema (to receive input from blood borne drugs/communicate with vomiting centre)
  • sub-fornicular (hypothalamus) ang II can diffuse into brain via this to increase thirst
  • periventricular osmoreceptors (hypothalamus) allows ADH to be secreted from here
60
Q

Cerebral Artery Vasospasm

A

extracerebral artery vasospasm triggered by subarachnoid haemorrhage (type of extracerebral haemorrhage)

can lead to reduced BF –> stroke/ischaemia

due to local vasoconstrictors:

  • 5-HT (from perivascular vessels)
  • neuropeptide Y (from perivascular vessels)
  • endothelin-1 (vascular endothelium)

damaged cells release K+—> gets high—> vasoconstrictor

61
Q

how to reduce vasospasm (drugs)

A

vgCa2+ blockers (e.g. amlodipine, acting on VSM)

ETA receptor blockers e.g. bosentan

62
Q

Cushings reflex

A

high BP
low HR

because of SOL–> pushes RVLM–> high BP

but bradycardia due to baroreceptor reflex from the high BP (lowering HR)

63
Q

type of aneurysms and what kind of haemorrhage

A

saccular - subarachnoid

microaneurysm (cerebral arteries) - intracerebral

abdominal aortic - intraperitoneal

stretched aortic ring - haemopericardium/cardiac tamponade

64
Q

Stroke management (anti-platelet therapy)

A
  • aspirin
  • clopidogrel
  • dipyridamole

thrombrolysis with tPA
plasminogen–>plasmin
(plasmin = fibrinolysis)

65
Q

what kind of haemorrhage with veins rupturing

A

subdural

66
Q

during REM Ach from where causes desynchronised axons in thalamus

A

pontomesencephalic tegmentum

67
Q

origins of

  • Ach
  • NA
  • Dopamine
  • Histamine
  • Orexin
  • serotonin
A

Ach

  • pontomesenphalic tegmentum
  • basal forebrain (linked with dementia - give AchEi)

NA
-locus coeruleus

dopamine

  • substantia nigra
  • ventral tegmental area

histamine
-tuberomamillary nucleus (hypothalamus)

orexin
-hypothalamus

serotonin
-raphe nuclei

68
Q

sleep–> waking

A

1) orexin–> wake histamine(hypothalamus)
2) switch on ARAS: serotoninergic/cholinergic/noradrenergic BRAINSTEM centres
3) activate basal forebrain cholinergic
4) project up into whole brain and increase cortex activity

69
Q

which hormones for :
attention/learning

pleasure/reward

anxiety and depression

A

Attention/learning

  • ach (basal forebrain)
  • orexin
  • NA

pleasure/reward

  • dopamine (v.tegmentum)
  • Nucleus accumbens (ventral striatum)

anxiety/depression

  • low dopamine (v.tegmentum)
  • low serotonin/NA from brainstem
70
Q

dysfunction in nuclei involved in waking

A

coma

except for OREXINERGIC = NARCOLEPSY

71
Q

how do we fall asleep

A

GABAergic inhibitory neurones from ventrolateral pre-optic nucleus (hypothalamus)

inhibit orexinergic/histaminergic/ARAS

+adenosine build up activates them

72
Q

medial/lateral pain pathway

A

LATERAL - to discriminate where/what the pain is

  • projects to specific thalamus nuclei VPL (same as dorsal column pathway)
  • to the primary somatosensory cortex

MEDIAL - the emotional negative feelings/response

  • projects to non-specific thalamus nuclei
  • to anterior cingulate/frontal cortex/hypothalamus/amygdala etc
73
Q

neurological pain/ pathological pain

inflammatory/nociceptive pain

A

neurological/pathological

  • eg. diabetic neuropathy
  • may be initiated by tissue damage but continues even after healing
  • associated with abnormal brain activity
  • loss of inhibitory

nociceptive

  • normal pain due to stimulation of nociceptive nerve endings
  • inflammatory pain = an example
  • they fade once tissue heals
74
Q

descending anti-pain pathway

A

5-HT (raphe Magnus)
NA (locus coeruleus)

project down from brainstem to spinal cord

stimulate inhibitory interneurones

prevent the SECONDARY afferent being activated by the nociceptor afferents

75
Q

3 places where opioids work

A

1) periphery - reducing stimulation of nociceptors
2) dorsal horn - preventing 2ndary afferents being activated
3) inhibiting the inhibitory neurone inhibiting the descending anti-pain pathway

76
Q

euphoria with opioids

A

opioid receptors on GABA inhibitory neurone that normally inhibits dopamine release

inhibition of GABA –> increase in DA

77
Q

respiratory depression with opioids

A

receptors in pre-botzinger complex–> inhibits neurones that set respiratory rate pattern

receptors in nuclei chemoreceptor region–> reduced sensitivity to pCO2

78
Q

methadone
buprenorphine
naloxone

A

methadone - full agonist

buprenorphine - partial

naloxone - antagonist

Semester 3 (6 decks)

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