absorbs a photon of light and is converted to trans-isomer from cis-isomer. activates opsin
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opsin
protein in rhodopsin with retinal
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bleaching
when rhodopsin spits due to retinal changing isomers, reversed by re synthesis with ATP
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ATP produced for re synthesis of rhodopsin
many mitochondria in inner segment of rod cells
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vitamin A
vitamin needed to to re synthesise retinal into rhodopsin
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iodopsin
photosynthesis pigment in cone cells which eolith absorbs red, green, or blue light
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s cone
short wave light blue light - 420nm
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m cone
medium wavelength green light - 543nm
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l cone
long wavelength red light - 564nm
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bipolar cells
synapse with many rod cells or single cone cell, and ganglion cell on other
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summate
when many rod cells combine to depolarise bipolar neurone
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glutamate
inhibitory neurotransmitter which causes the adjacent bipolar neurone to become hyper polarised
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glutamate
causes ganglion neurone to become depolarised creating generator potential
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visual acuity, colour vision, pupil response
3 aspects of eye tests
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every 2 years
routine eye test carried out
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snellen chart
letters chart, big to small, viewed at 6m, one eye covered
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20/20 visual acuity
ability to ready letters 1cm high at 6m
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near vision test
reading card with different size blocks of text at 30cm
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presbyopia
near vision loss. lens is less flexible as older (40+) so less able to focus near objects
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colour blindness
absence of one or more types of cone, recessive sex linked condition affecting makes more
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protanopia
absence of red cone cells
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deuteranopia
absence of defect in green cone cells
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Ishihara colour vision test
individuals with colour blindness don’t see numbers, different colour combinations
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Farnsworth-munsell 100 hue test
caps sorted into hue order, red, green, blue and yellow
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optical coherence tomography
OCT, non invasive, beam of near infra red light, detects reflected light, scattered removed with interferometry, 3d image of retina, map and measure thickness
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neurones die
loss of synaptic connections at about age 20
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brain volume and mass
brain decrease by 10% at 90, frontal lobe and hippocampus effected most
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thinner cortex
thins from age 20, due to loss of synaptic connections
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white matter
decreases with age, leading to reduced speed of cognitive processing like memory, attention, action, problem solving, and decision making
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ventricles
enlargement with age, more significant with dementia
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neurotransmitters
effects memory due to less synthesis of receptor proteins and…
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onset of dementia
age related memory loss is temper lapses of memory however severe disruptive loss indicates…
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slow age related memory loss
regular exercise, manage stress, crosswords
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worsen age related memory loss
smoking and alcohol
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effect of ageing on reaction times
simple involuntary reflex, different ages, unpaired t test
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presbycusis
age related hearing los, gradual from 18 years, loss of sensitive share cells in cochlea and neurone in auditory nerve
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high frequencies
frequencies most effected by age related hearing loss
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range of normal speech
autograph carried out between 250 and 8000Hz
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normal hearing level
up to 25dB
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glaucoma
tunnel vision, optic nerve damage, increased eye pressure as aqueous humour doesn’t drain, eye drops, laser, medication, or surgery
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chronic open angle
drainage channels slowly come blocked, reduced visual field
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acute closed angle
less common, rapid onset, pressure in eye pushes edge of iris against cornea blocking drainage channels
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age related macular degeneration
ARMD, loss of central vision due to degeneration of macula, dry- debris from pigments not broken down, retina detaches, wet- blood vessels grow, laser treatment, strong glasses
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cateracts
clouding of lens and loss of elasticity, blurred vision, worse in low light, denaturation and aggregation of lens proteins, age related, stronger glasses and brighter lights, replacement lens
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alzheimers
degenerative disease of nerve system effecting frontal and temporal lobes
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early Alzheimers
* minor memory loss eg names and location of objects * suffers aware of memory loss * long term memory intact
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mid-stage Alzheimers
* personality changes, physical problems * dependant on others for care * no longer aware of memory loss * impaired long term memory
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late stage Alzheimers
* deterioration of personality * loss of control over body functions * total dependency on others * speech severely effected * inability to swallow and lead to death
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multifactorial
disease with many factors contributing to it eg Alzheimers, effected by age and family history
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abnormal break down of protein
B amyloid proteins are produced from myelin sheath which accumulate and form plaques around neurones causing them to degenerate and less neurotransmitter produced.
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tau proteins
proteins which normally stabilise microtubules in cytoskeleton, defective ones aggregates forming neurofibrillary tangles in neurones. microtubules disintegrates and transport system collapse, less neurotransmitter, nerve dies
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cholinergic
reduction in acetylcholine levels, most treatments based on this
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amyloid
location of even for protein precursor on chromosome 21, links it to down syndrome. maybe derrivative called ADDLs that cause damage
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tau
abnormalities in proteins cause neurofibrillary tangles interfering with microtubules and intracellular transport in neurones
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acetylcholine inhibitors
use to prevent breakdown of acetylcholine to treat Alzheimers
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carers activities
help with eating, washing, dressing, going to toilet
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carers difficulties
financial cost, ability to work, distress, patients legal maters