Core conditions 5 Flashcards
1
Q
Dry ARMD progression
A
- Early stages: usually unilateral, visual impairment is compensated by the other eye
- Brain is able to compensate for small scotoma
- Any disease affecting the Fovea may be noticeable
- Geographical atrophy: Atrophy in the retina can cause a large pale area in the fovea. The drusen can cause an inflammatory response causing cell death. The retinal pigment epithelium and photoreceptors die. You will then see blood vessels under the pale area from the choriocapillaris (choroid layer). Causes a central scotoma
2
Q
Wet ARMD process
A
- The inflammatory reaction set off by retinal cell degradation and hypoxia stimulates new blood vessel to grow (neovascularisation)- mediated by VEGF
- The blood vessels grow from the choroidal layer (in diabetic retinopathy they grow from retinal vessels)
- The new vessels grow under the RPE creating a lacy network (a sub retinal neovascular membrane (SRNVM). Some vessels break through the RPE. They are very fragile, prone to leakage and haemorrhage
- Sudden onset: need urgent referral to Ophthalmology
3
Q
Why is wet ARMD so dangerous
A
- Intra-retinal haemorrhages block the light from getting to the photoreceptors
- The neovascular membranes can grow through Bruch’s membrane into the sub-retinal space and into the outer retina
- Haemorrhage and leaked fluid disrupt the photoreceptor layer as the cells are pushed apart or closer together- image becomes distorted
- Fluid between the RPE and choroid reduces the oxygenation of the photoreceptors
4
Q
Progress of symptoms in ARMD
A
- None
- Mild difficulty with central vision, noticed particularly with close work
- Problems going from dark to light and light to dark (photoreceptors take longer to respond)
- Reduced visual acuity, difficulty with seeing facial features clearly
- Aware of central vision loss, patch of vision missing, particularly noticed when trying to read
- Problems with colour vision
- Distorted vision (metamorphopsia) Red Flag Symptom
- Visual hallucination- Charles Bonnet syndrome, know the images are not real
5
Q
Examination in ARMD
A
- Visual acuity using snellen chart: top number is meters from the chart and the bottom number is the lowest completed line
- Measure near vision: read from a pamphlet recorded as Nx with x being the smallest number font they could read
- Amsler chart: tests whether a patient has distorted vision
- Fundoscopy: look for drusen, oedema and haemorrhage in the macular region. Use in a dim room
6
Q
Investigations in ARMD
A
- Can be diagnosed clinically based on: drusen, geographical atrophy, subretinal neovascular membranes or haemorrhages under fundoscopy
- Fluorescein angiography: die is injected intravenously highlighting the choroidal and retinal vessels
- OCT
7
Q
What will you see on OCT with different ARMD
A
- Dry: drusen between Bruch’s membrane and the RPE
- Wet: loss of normal foveal dip, subretinal fluid confirming the presence of an active SRNVM
- Geographic: loss of photoreceptors and other neural tissue
8
Q
Common sudden onset painless visual loss in older people
A
- Wet age-related macular degeneration
- Vitreous haemorrhage
- Retinal detachment
- Central retinal artery / vein occlusion
- Anterior ischaemic optic neuropathy (arteritic or non-arteritic)
- CVA
9
Q
Common gradual onset painless visual loss in older people
A
- Dry age-related macular degeneration
- Cataract
- Diabetic retinopathy
- Glaucoma
10
Q
Management and comorbidities for dry ARMD
A
- No treatment for dry ARMD
- Wont loose all their vision: whilst their central vision can be severely damaged their peripheral will remain
Comorbidities: Falls, reduced mental health
11
Q
Rinne’s and Weber’s test
A
- Normal: Rinne’s positive (air conduction better then bone), Weber’s tone heard centrally
- Conductive: Rinne’s negative (bone conduction better than air conduction), tone lateralises to affected ear
- Sensorineural: Rinne’s positive, tone lateralises to non-affected ear
- False negative Rinne’s test: in profound sensorineural deafness. Rinne’s test might be falsely negative as the bone conducted test is heard by the other ear
12
Q
Red flag for hearing loss
A
Asymmetric hearing loss and sudden onset are red flags and can indicate significant pathologies like cholesteatoma, vestibular schwannoma and sudden sensorineural hearing loss
13
Q
Presbycusis definition
A
Age related hearing loss that affects people >65. A gradual decline in hearing ability particularly in high frequency tones. Due to genetic and environmental factors like exposure to loud music and ototoxic medications. Can experience tinnitus
14
Q
Presbycusis presents with:
A
chronic, slowly progressing history of:
- Gradual onset of hearing loss, typically affecting high-frequency sounds
- Difficulty understanding speech, especially in noisy environments
- Need for increased volume on the television or radio
- Difficulty using the telephone
- Loss of directionality of sound
- Worsening of symptoms in noisy environments
- Hyperacusis: Heightened sensitivity to certain frequencies of sound (Less common)
- Tinnitus (Uncommon): bilateral or central, non-pulsatile nature. Unilateral or pulsatile is a red flag.
- Affects both the cochlear hair cells and (to a lesser extent) the vestibulocochlear nerve
- Dizziness: can cause vertigo and falls
15
Q
Presbycusis management
A
- Hearing aids:These devices amplify sounds according to the patient’s specific hearing loss profile. Selecting appropriate hearing aids should consider factors such as cosmetic preferences, manual dexterity limitations, and cost constraints.
- Assistive listening devices (ALDs):ALDs can enhance speech understanding in challenging listening environments by reducing background noise levels.
- Cochlear implants:In cases of severe-to-profound bilateral presbycusis who dont respond to other methods
- Tinnitus management: a multidisciplinary approach involving sound therapy, cognitive behavioural therapy (CBT), and relaxation techniques may be beneficial.
16
Q
Aural rehabilitation
A
- Hearing aid orientation:Ensure patients receive thorough guidance on the use, maintenance, and troubleshooting of their hearing aids. Above 40dB is indicated, make sure aren’t incorrectly set too high
- Auditory training:Encourage patients to engage in regular auditory training exercises to improve speech perception in noise and enhance overall listening skills.
- Communication strategies:Educate patients about effective communication tactics such as optimal seating arrangements, utilising visual cues, and advocating for their needs in social settings.
- Support groups:online or in person
17
Q
Presbycusis risk factors
A
- Caucasian
- Low socioeconomic status
- Noise exposure
- Ototoxic drugs: Aminoglycosides (eg Gentamicin), Chemotherapeutic agents (eg Cisplatin)
- Heavy metals
- Infections
- Smoking
- Hypertension
- Diabetes
- Vascular disease
- Immunologic disorders
- Hormonal factors eg estrogen
- Genetic component
18
Q
Conditions associated with Presbycusis
A
dementia, mild cognitive impairment, learning disability, tinnitus, vertigo, dizziness and falls
19
Q
Causes of hearing loss grouped by anatomical region
A
- External auditory canal: wax impaction, otitis externa, otomycosis, foreign body, trauma
- Tympanic membrane: perforation, tympanosclerosis
- Middle ear: acute otitis media, chronic otitis media, chronic suppurative otitis media, otitis media with effusion, cholesteatoma
- Ossicles: Otosclerosis, Ossicular chain damage
- Inner ear: vestibular schwannoma, ototoxic drugs, hereditary hearing loss, Meniere’s disease, Meningitis, noise
20
Q
Audiometry
A
Use an audiogram to confirm diagnosis. Can use Pure tone audiometry and Word recognition. Pure Tone Audiometry involves playing a pure tone in a person’s ear at different frequencies and recording the lowest decibel volume they can hear it. Normal threshold is below 25dB, in presbycusis there is a poor high frequency hearing threshold.
