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Semester 3 > NEURO > Flashcards

NEURO Flashcards

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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
what controls the various gaze centre nuclei where would horizontal /vertical gaze centres send impulses to
superior colliculi-->gaze centres horizontal - abducens (VI) = abduction - oculomotor (III) = adduction vertical - trochlear (IV) = depression (SO) - oculomotor (III) = elevation/depression
26
conjugate eye movements
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
27
disconjugate eye movement pathway
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)
28
how can tilting of stereo cilia detect: - frequency - volume - pitch
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
29
endolymph where is it produced what can happen if excess fluid is not removed
fills the spiral organ high in K+ produced by stria vascularis meniere's disease = high endolymph pressure --> damage to cochlear (ringing/dizziness)
30
how are hair cells depolarised
tilting of hair cells opens K+ channels on adjacent stereocilia entering of K+ from endolymph--> glutamate released to the afferent nerves
31
dorsal and ventral cochlear nuclei
(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
32
superior olivary nuclei
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
2 types of hair cells
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
auditory pathways
hair cells depolarise--> afferents --> cochlear nuclei (brainstem) --> inferior colliculi ---> MGN---> primary auditory if ventral cochlear nuclei --> superior olivary--> inferior colliculi
35
why does bilateral lesions at both primary auditory cortexes not lead to total deafness
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
presbyacusis
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
acoustic neuroma
(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
membrane labyrinth | bony labyrinth
membrane (cochlear duct) - filled with endolymph (K+) Bony (scali vestibuli & scali tympani) - filled with perilymph (Na+)
39
the membranous labyrinth structures in the vestibule where vestibular receptors are found
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
otolith system
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
lateral/medial vestibulospinal tract
otolith system afferents---> LATERAL--> ipsilateral anti-gravity muscles in legs semi-circular ducts---> MEDIAL--> muscles to move/stabilise head
42
semi circular ducts
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
reflex for stabilising head
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
in order to contract both eye muscles to look same direction with the reflex it needs to be fast - how is this achieved
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
which lobe of cerebellum interacts with vestibular system to make sure movements are accurate
floconodular lobe
46
what does the cerebellum receive input from and where does it project to
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
what tells the purkinje fibres of cerebellum to increase/decrease their inhibitory control on vestibular nuclei
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
nystagmus
damage to cerebellum/vestibular pathway causing imbalance in left/right vestibular system failure to fix on an object leading to eye drift
49
vertigo
sensation of moving around in space or having objects move around you
50
Why does sensory conflict make us ill?
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
pathway for motion sickness
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
treatment for nausea/vomiting
muscarinic Ach antagonist -act in vestibular nucleus h1 histamine receptor antagonists (promethazine) side effects of both - drowsiness - dry mouth - blurred vision
53
baroreceptor reflex
``` 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
autoregulation
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
metabolic auto-regulation
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
how Regional Hyperaemia in brain can lead to vasodilation of cerebral arteries
high AP firing high K+ efflux K+ in interstitial fluid--> vasodilator
57
nervous control of cerebral arteries
no/little within brain (regulated by myogenic/auroregulation) abundant to surrounding brain serotonin = vasoconstrictor substance P & CGRP = vasodilator
58
Sumatriptan
serotonin receptor agonist used for migraines constricts blood vessels - reducing inflammation induced vasodilation--> reducing pain
59
what substances can move past BBB 3 areas where it is not complete
``` 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
Cerebral Artery Vasospasm
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
how to reduce vasospasm (drugs)
vgCa2+ blockers (e.g. amlodipine, acting on VSM) ETA receptor blockers e.g. bosentan
62
Cushings reflex
high BP low HR because of SOL--> pushes RVLM--> high BP but bradycardia due to baroreceptor reflex from the high BP (lowering HR)
63
type of aneurysms and what kind of haemorrhage
saccular - subarachnoid microaneurysm (cerebral arteries) - intracerebral abdominal aortic - intraperitoneal stretched aortic ring - haemopericardium/cardiac tamponade
64
Stroke management (anti-platelet therapy)
- aspirin - clopidogrel - dipyridamole thrombrolysis with tPA plasminogen-->plasmin (plasmin = fibrinolysis)
65
what kind of haemorrhage with veins rupturing
subdural
66
during REM Ach from where causes desynchronised axons in thalamus
pontomesencephalic tegmentum
67
origins of - Ach - NA - Dopamine - Histamine - Orexin - serotonin
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
sleep--> waking
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
which hormones for : attention/learning pleasure/reward anxiety and depression
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
dysfunction in nuclei involved in waking
coma | except for OREXINERGIC = NARCOLEPSY
71
how do we fall asleep
GABAergic inhibitory neurones from ventrolateral pre-optic nucleus (hypothalamus) inhibit orexinergic/histaminergic/ARAS +adenosine build up activates them
72
medial/lateral pain pathway
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
neurological pain/ pathological pain | inflammatory/nociceptive pain
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
descending anti-pain pathway
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
3 places where opioids work
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
euphoria with opioids
opioid receptors on GABA inhibitory neurone that normally inhibits dopamine release inhibition of GABA --> increase in DA
77
respiratory depression with opioids
receptors in pre-botzinger complex--> inhibits neurones that set respiratory rate pattern receptors in nuclei chemoreceptor region--> reduced sensitivity to pCO2
78
methadone buprenorphine naloxone
methadone - full agonist buprenorphine - partial naloxone - antagonist

Semester 3 (6 decks)

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