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week 44: hearing and vision loss > general > Flashcards

general Flashcards

1
Q

what Q’s would you want to know from a Hx with a Pcx of worsening hearing?

A
  • duration and pattern
  • uni or bilateral
  • otalgia
  • ear discharge or itch
  • tinnitus
  • vertigo or unsteadiness
  • prev ear infections or surgery
  • previous head or ear trauma
  • previous excessive noise exposure
  • previous exposure to ototoxic drugs
  • recent UPTI
  • throat or nasal symptoms
  • smoker
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2
Q

what are the red flag symptoms of worsening hearing?

A
  • Suden onset hearing loss
  • sudden deterioration in hearing
  • unilateral hearing loss
  • associated neurological symptoms
  • immunocompromised and sign of ear infection
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3
Q

split potential causes of hearing loss into conductive (disruption of the mechanical transfer of sound) and sensorineural (cochlear or neurological damage)

A

conductive:

  • otitis externa
  • middle ear effusion
  • otosclerosis
  • wax
  • trauma to the tympanic membrane or ossicles
  • CSOM

sensorineural:

  • infection e.g. meningitis/measles/mumps
  • trauma e.g. head injury
  • menieres disease
  • acoustic neuroma
  • idiopathic
  • presbycusis
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4
Q

describe how Renne test and Weber can help differentiate between conductive and sensorineural hearing loss

A

R - air and bone conduction. helps to determine whether there is a conductive component to hearing loss (heard loudest on bone)

W - midline test. help confirm whether there is a conductive component when the hearing loss is unilateral. in conductive deafness the pt will hear sounds louder in the affected ear. if the sound is heard in the unaffected ear there is a sensorineural hearing loss

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5
Q

what factors should you take into consideration before fitting a pt with a hearing aid?

A
  • motivation to war aids
  • ability to insert and manipulate aid
  • level of hearing impairment
  • unilateral or bilateral hearing loss
  • ability to purchase private device rather than using free NHS aid
  • cosmetic/personla preference
  • cognitive impairment
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6
Q

what are the most common causes of vision loss in the elderly?

A
  • cataracts
  • degeneration of the macula (ARMD)
  • glaucoma
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7
Q

what are the red flags for visual disturbance?

A
  • sudden onset
  • loss of vision
  • associated headache or weakness of the arm, face or leg
  • speech disturbance
  • associated nausea, vomiting or photophobia
  • eye pain or redness
  • history of trauma
  • scalp tenderness or jaw claudication
  • new medications
  • polyuria or polydipsia
  • problems with bright lights
  • flashes and floaters
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8
Q

what key examinations should the optometrist perform?

A
  • check visual acuity in both eyes using a shelled chart
  • perform anterior segment examination (examination of lids, conjunctiva, cornea, anterior chamber)
  • examine pupillary reactions
  • perform fundal examination
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9
Q

what are the key findings on fundal examination associated with ARMD?

A
  1. drunsen (yellow deposits) at the macula
  2. retinal atrophy at the macula
  3. haemorrhage at the macula
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10
Q

what is the different types of ARMD?

A

dry:

  • more common type
  • Develops slowly and causes gradual change in central vision
  • can take yrs to get to its final stage
  • at worst, Dry AMD causes a blank patch in the centre of your vision in both of your eyes

wet:

  • 10-15% often start with dry
  • can develop quickly, causing serious changes to your central vision in a short period of time, over days or weeks
  • macula stops working correctly and your body starts growing new blood vessels to fix the problem - as they grow in the wrong place, they cause swelling and bleeding underneath the macula… causes more damage to macula and eventually leads to scarring
  • immediate Tx crucial
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11
Q

what cells are found in the macula?

A

cone cells
(vital for seeing detail, colour and to see things straight infront. in wet ARMD, the cells have stopped working correctly and bleeding develops underneath)

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12
Q

what is the treatment of active wet ARMD?

A
  • course of intravitreal injections
  • there are 3 pharmacological agents used for this purpose:
    ranibizumab and afilibercept are licensed. bevacizumab is not licensed.
  • Tx starts for everyone with 3 injections at monthly intervals. it is then adjusted according to response and the drug used
  • typically 7-12 injections in 1st yr

RED FLAGS within 7days post injection = deteriorating vision or red, sore eye

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13
Q

what lifestyle changes can be made to help protect the macula?

A
  • smoking cessation
  • avoid bright sunlight/using sunglasses
  • increasing intake of food rich in macular carotenoids (spinach, cabbage, broccoli)
  • vit supplementation: ‘AREDS2 formula’ - lutein, zeaxanthin, vit C and E, zinc
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14
Q

what are potentially vision-threatening conditions that can present with red eye?

A
  • angle closure glaucoma
  • corneal ulcer
  • uveitis/iritis
  • scleritis
  • endophthalmitis (cloudy cornea/corneal oedema, hypopyon/level of pus in ant. chamber)
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15
Q

what are the advantages of registering a person as partially sighted/blind?

A
  • tax relief and additional benefit allowances
  • parking permit
  • travel and tv licence concessions
  • articles for the blind
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16
Q

what condition involves hallucinations occurring as a result of vision loss

A

Charles Bonnet syndrome

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17
Q

what is refraction of the eye? and describe the 3 types of refractory errors

A
  • bending of light to focus it onto the back of the eye
  • the cornea is the first and largest refractive surface with 40 dioptres of focussing power
  • the lens is the lesser Elmer with 20 dioptres, but it is dynamic/ accommodation and allows the eye to focus on things up close
  • overall, the eye has refractive power of 60 dioptres

errors:

  1. presbyopia/ long-sightedness:
    - age-related loss of ability to focus up close
    - lens hardens with ages. loss of elasticity = loss of dynamic focussing power
  2. myopia/ near-sightedness:
    - can see objects up close, but blurry far away
    - occurs when the light rays refract (bend) incorrectly, focussing the images in from of the retina instead of on it
    - physically bigger eye-ball
    - concave lense repairs this
  3. hyperopia /long-sightedness:
    - not a cause of old age
    - cause of physically smaller rugby ball-shaped eyeball
    - convex lens corrects this
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18
Q

what components make up the anterior and posterior segments of the eye?

A

anterior:
- structures infront of the vitreous humour: cornea, iris, ciliary body, lens (+suspensory ligaments), (+2 fluid/a-filled chambers separated by the iris)
- role = refraction. bending/sharpening light onto the back of the eye

posterior segment:
- anterior hyaloid membrane, vitreous humor, retina, choroid and optic nerve

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19
Q

describe the process of vision

A

collect information:
- eyeball -> optical front and retina/optic disc at the back

transfer information:
- connections -> optic nerve, chasm, optic tract, LGN, radiations

create conscious vision:
- brain -> occipital, temporal, parietal and frontal lobes

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20
Q

describe the structure of the retina

A
  • made up of complicated layers of different cells (outer nuclear layer -> ganglion layer -> plexiform layer -> outer nuclear layer -> pigmented epithelium)
  • the bottom layer is the light sensitive cells: rods and cones
  • light comes in through the layers and then information is transmitted back again via axons of ganglion cells, lateral cells and amacrine cells to provide initial processing of the visual signal
  • optic nerve with the major blood vessels providing the retina branching from the centre
  • macula = most sensitive spot on the retina
  • fovea= within the macula = provides the clearest vision
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21
Q

compare the 2 main types of photoreceptors

A

rods:

  • 120million in the retina
  • high convergence to ganglion cells
  • one type: vision in greyscale
  • very light sensitive/ sensitive to low levels of light
  • widespread distribution in retina
  • broad spectral sensitivity

cones:

  • 6million in the retina
  • low convergence to ganglion cells
  • 3 types: blue green red
  • only 1/30th the sensitivity of rods
  • concentrated in macula
  • narrow spectral sensitivity
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22
Q

discuss the optic nerve and what you should be looking out for in direct opthalmoscopy?

A
  • neuro-retinal rim is made up of purely ganglion cell axons
  • central pale area = cup. non euro-retinal tissue

comment on..

  1. colour of the neuro-retinal rim
  2. how well demarcated the edge of the optic n is from the retina
  3. how big the cup is in relation to the size of the optic disc

(*increase in size of cup = neuro-retinal rim is thinner. means losing axons. losing connection between eye and brain = glaucoma!)

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23
Q

a) what is the first synapse in the visual pathway?
b) what fibres cross at the chiasm?
c) the right occipital lobe processed what visual field

A

a) lateral geniculate nucleus (in the thalamus - major relay system in the brain)
b) fibres from the nasal half or each retina
c) left visual field

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24
Q

describe visual field defects and identify where about the lesion is within the visual pathway

A

chiasm = bitemporal hemianopia

complete lesion of optic nerve (before chiasm) = complete blindness in the eye on the same side

right/left homonymous hemianopia = lesion on the opposite optic tract

Left homonymous inferior quadrantanopia due to involvement of optic radiations = upper right optic radiation

right superior quarjntanopia = lesion in left temporal lobe/meyers loop

(too confusing😖)

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25
Q

What receptors detect taste and describe their structure

A

foliate papilla:

  • poorly developed
  • short vertical folds and are present on each side of the tongue
  • just in fromt of palatoglossal folds

vallate papilla:

  • largest
  • along sulcus terminalis
  • supplied by the glossopharyngeal nerve
  • more sensitive to bitter tastes

fungiform papilla:

  • most numerous
  • supplied by facial nerve
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26
Q

where is the major location of these taste receptors?

A

taste buds are located on the oral surface of the soft palate, the posterior wall of the oropharynx, and the epiglottis

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27
Q

what are the 5 taste modalities? (six?)

A
  1. sweet (sugar, glycols, ketones)
  2. sour (H+)
  3. salty (NACl)
  4. bitter (quinine, alkaloids found in toxic plants)
  5. umami (glutamate - truffles meat, ages cheese and tomatoes)
  6. oleogustus (fatty acid - unpleasant)
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28
Q

what CN supplies each part of the tongue?

A
  • taste from the anterior 2/3 of the tongue is detected by the facial nerve (chorda tympani)
  • taste from the posterior 1/3 of the tongue and oropharynx is detected by glossopharyngeal nerve
  • motor to tongue = hypoglossal nerve
  • epiglottis and soft palate are supplied by the vagus nerve (taste).
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29
Q

what is the major neural pathway involved in taste

A
  • all these sensory fibres (vagus, glossopharyngeal and facial) come together and form the solitary tract
  • synapse in nucleus of tracts solitaires (gustatory nucleus)
  • 2nd order neurones join the medial limniscus
    and synapse on the thalamus
  • 3rd neurons project to the cortex (consciously discriminate different taste stimuli)
30
Q

where are the receptors detecting odour are located and describe their structure

A

olfactory receptors occupy a small area in the roof of the nasal cavity. they are bipolar neurones: nerve fibres that dangle and detect smell and fibres that project through the base of the skill to the olfactory bulb. they are part of the olfactory epithelium (basal cells, bowman glands, sustentacular cells)

31
Q

how to the receptors detecting odour convert detection of odour molecules into an AP?

A
  • odourants are dissolved in mucus secreted by the Bowman glands
  • cilia or receptor cells (bipolar neurone) are activated
  • certain chemicals can activate other cranial nerves as well as the olfactory nerves and cause reactions (e.g. pepper -> sneezing; ammonia -> arousal)
32
Q

what is the major neural pathway involved in olfaction?

A
  • entirely ipsilateral
  • goes to cortex first and then thalamus
  • the central processes of the receptor cells form the olfactory nerve that pass through the cribriform plate to synapse in the olfactory bulb (olfactory nerve is covered with connective tissue of meninges)
  • from olfactory bulb –> olfactory tract -> olfactory cortex -> thalamus -> orbitofrontal cortex
33
Q

how are sound waves translated to neural signals for hearing

A
  • the characteristics of sound is the frequency (responsible for pitch) and amplitude (responsible for intensity)
  1. first transduction - sound waves strike the tympanic membrane and become vibrations
  2. the sound waves energy is transferred to the ossicles of the middle ear which vibrate
  3. second transduction: the stapes is attached to the membrane of the oval window. vibrations of the oval window create fluid waves within the cochlea
  4. this transduction - the fluid waves push on the flexible membranes of the cochlear duct. hair cells bend and release neurotransmitter
  5. fourth transduction - neurotransmitter release onto sensory neutrons creates APs that travel through the cochlear nerve to the brain
  6. energy from the waves transfers across the cochlear duct into the tympanic duct and is dissipated back into the middle ear at the round window
34
Q

what are the common problems with hearing

A

2 types of pathologies related to hearing:

  1. conduction deafness:
    - a blockage in the outer ear
    - infection in either the outer or inner ear
    - ossification of the small bones in the middle ear
    - rupture of the tympanic membrane
  2. sensory-neural deafness:
    - breakdown of the cochlea and associated mechanisms
    - damage to the auditory nerve
    - damage to the auditory cortex
35
Q

what is the principles of audiogram

A
  • graph that shows the softest sounds a person can hear at different pitches an d frequencies
  • closer the mark is to the top of the graph, the softer the sounds that the person can hear.
  • top = normal hearing, as go down -> profound hearing loss
36
Q

list causes of anosmia

A
  • idiopathic anosmia
  • nasal/sinus disease (cold, polyps, other blockages)
  • head trauma (damage to frontal lobe processing, damage to ascending nerves at cribriform plate)
  • preceding alzheimers
  • congenital
37
Q

describe some of the causes of swollen optic nerve (blurred margin/ edge on nerve runs into retina)

A
  • raised intra-cranial pressure (brain tumour, idiopathic intracranial hypertension)
  • optic neuritis (MS)
  • pseudi-papilloedema
38
Q

describe the eye symptoms/ conditions associated with MS

A

optic neuritis:

  • loss of vision
  • painful eye movements
  • afferent pupil defect
  • swollen optic nerve head (not always)
  • later onset optic atrophy

eye movement abnormalities with diplopia:

  • any cranial nerve palsy (3rd, 4th, 6th)
  • inter-nuclear ophthalmoplegia pr cerebellar/brain stem lesions (cerebellar nystagmus)

intermediate uveitis:

  • floaters and blurred vision
  • sometimes red eye and photophobia
39
Q

what is the, presentation, diagnosis
and management
of anterior ischemic optic neuropathy associated with GCA

A
  • > occlusion of the blood vessels of the anterior optic n. head (swollen optic n. head)
  • > sudden profound loss of vision in one eye
  • > 2 main types:
    1. arteritic GCA; EMERGENCY!
    2. non-arteritic; usually risk-factors for CVD (like retinal vein and artery occlusion)
  • > Hx of jaw pain, tongue pain, scalp pain, loss of weight, decreased appetite, shoulder pain, night sweats
  • > older people and female more likely
  • > TREAT then Ix! to try and save vision
  • > high dose steroids
  • > Ix inflammatory markers (CRP, SER) and USS of temporal aa. ± temporal artery biopsy (giant cells)
40
Q

what disease is suggested by:

a) cupped optic nerve and rim thinning
b) pale optic nerve

A

a) glaucoma (axons are dying)
b) optic atrophy. can happen after an episode of ON in the context of MS or exposure to drugs. can also happen after a period of nerve ischemia or compression

41
Q

what is the, presentation, diagnosis
and management
of anterior ischemic optic neuropathy associated with retinal artery and vein occlusions

A
  • sudden onset, but painless (unless associated with GCA)
  • associated risk factors similar: increasing age, HTN, dyslipidaemia, obesity, smoking, poor diet, no exercise
  • arterial occluusion ->due to embolic disease: source carotids, values, chambers in arrhythmias
  • venous occlusion -> usually due to ‘nipping’ by overlying ‘hardening’ arterioles. so, much the same risk

on fundoscopy:

  • complete vein occlusion shows flame-shaped haemorrhages In all 4 quadrants of the eye. the vein is blocked, but blood is still getting into the eye . pressure builds up.
  • partial vein occlusion when only a branch of the retinal vein is occluded. in the distribution of the vein you develop flame-shaped haemorrhages and leak fluid alone with lipid which is deposited as hard exudate
  • complete artery occlusion is difficult to spot. no haemorrhage, no blood in eye. retina becomes thicker - highlighting the thin fovea of they eye. get shining through the choroid surface -> cherry red appearance. ischemic changes to the whole area
  • partial arterial occlusion occurs when an embolic blocks supply of blood in a certain area. get paleness of the retina = ischemic changes
42
Q

what is the, presentation, diagnosis
and management
of anterior ischemic optic neuropathy associated with diabetic retinopathy

A
  • damage to retinal microvasculature
  • blindness due to :
    1. vitreous haemorrhage
    2. tractional retinal detachment
    3. rubeotic glaucoma
    4. macular oedema (leakage of damage from damaged vessels)
  • > diabetes without retinopathy. good sugar control and lifestyle measures.
  • > non-proliferative diabetic retinopathy signs = hard exudate, microaneurysm, blot/dot haemorrhage, cotton wool spots. (can give anti-VEGF meds)
  • > proliferative signs of DR: new vessels, vitreous haemorrhage, retinal detachment. laser photocoagulation
43
Q

what is the main cause of blindness in the western countries?

A

diabetic retinopathy

44
Q

what are the pathological steps of diabetic eye disease

A

chronic hyperglycaemia -> glycosylation of protein/basement membrane -> loss of pericytes (control lumen or vessels) -> reduced O2 transport = tissue hypoxia -> vas-proliferative factors produced (VEGF) -> Neo vascularisation and leakage -> macular oedema, vitreous haemorrhage, retinal detachment and rubeotic glaucoma

45
Q

Describe the pathophysiology, epidemiology, treatment and complications of thyroid eye disease

A
  • antibodies to orbital contents
  • often associated with hyperthyroidism
  • common in females and smokers
  • risk of sight loss due to optic nerve compression
  • cosmetic issue
  • immunosuppression often needed then surgery
  • due to graves disease -> inflammation, swelling and hypertrophy behind the eyeball
46
Q

list the differentials of red eye

A
  • non-traumatic subconjunctival haemorrhage (bright red on cornea)
  • conjunctivitis
  • molluscumi contagiosum (harmless infection causing small dimpled spots on the skin)
  • external eye disease that might give rise to red eye (e.g. chalazion, stye)
  • blepharitis (inflammation of the eyelids)
  • corneal abraison/ulcer
  • keratitis (inflammation of the cornea)
  • uveitis
  • trichiasis
  • entropion/ectropion
  • dry eye
  • corneal foreign body
  • scleritis
47
Q

differential between different types of conjunctivitis

A

bacterial:
- red eye, swollen puffy, discharge that is sticky and dries crusty

gonococcus:

  • hyper purulent conjunctivitis
  • notifiable disease
  • can cause corneal ulceration, opacification and perforation

viral:

  • very red eye
  • adenovirus can leave punctate scars on the cornea can cause severe conjunctivitis and keratitis (inflammation of the cornea)

allergic conjunctivitis:

  • lots of papilla on upturn upper eyelid
  • itchy
  • red

follicular conjunctivitis:

  • raised lumps on bottom eyelid fleshy bit
  • STI cause
48
Q

discuss uveitis

A
  • inflammation of 1 or more parts pf the urea
  • anterior uveitis = iris and ciliary body and leads to acute painful symptoms and photophobia
  • posterior uveitis = choroid, retina, retinal vasculature and carries risk of painless vision loss

-diagnosis is clinical

  • risk factors = inflammatory disease, HLA-B27 positivity
  • redness distributed around the edge of the eye and clear cornea
  • pain worse when reading or photophobia (clues! bot action when eye is moving)

cause:

  • ant. can be idiopathic or associated with HLA-B27 related disease or viral eye disease
  • post. associated with systemic or localised infection os systemic inflammatory disease

Tx:

  • topical corticosteroids for ant. uveitis
  • local injected coticosteroids/ systemic steroids or the immunosuppression if post. uveitis
49
Q

discuss keratitis

A
  • infectious keratitis refers to microbial invasion of the cornea causing inflammation and damage to the corneal epithelium, storm or endothelium. non-infectious is rare!
  • ocular emergency –> blindness
  • RFs = corneal trauma, contant lens wearer, breakdown of corneal epithelium

Symptoms:

  • redness in the eye
  • pain
  • photophobia
  • blurring of vision
  • watery discharge from the eye

Dx:
- Hx, slit-lamps exam, corneal scraping cultures

Rx:

  • topical AB + pupil dilating agents (help relieve pain and prevent synechiae
  • analgesics
  • corticosteroids
  • systemic antibiotics
50
Q

what eye disease causes reveals a branching pattern with blue light?

A

ocular herpes

51
Q

what is hyphaema?

A

pooling or collection of blood inside the anterior chamber of the eye

52
Q

what eye condition may occur post op cataract surgery and is a medical emergency?

A

endothelitis
- immune response within the endothelium in blood vessels, on which they become inflamed.The condition can cause oedema of the surrounding tissue, including the stroma, and can cause iritis and pain. If it is within the cornea, it can result in permanent loss of vision

pain
reduced vision
red eye, discharge
floaters

inject ABs into the eye

53
Q

what genetic tumour must be excluded in children with a squint or white papillary reflex?

A

retinoblastoma

54
Q

discuss corneal abraison

A
  • corneal epithelial defects. They are common and are typically caused by mechanical trauma from external objects such as fingernails and branches, foreign bodies that become lodged underneath the eyelids, or contact lens use
  • sudden onset
  • symptoms = foreign body sensation, photophobia, excessive tearing, blepharospasm, blurry vision
  • Tx = analgesia, topical antibiotics
  • contact lens wearers at risk of pseudomonas infection
  • usually heals within 1-2 days, but complications include ulceration or keratitis
55
Q

what is meant by the term ‘flashes’ and ‘floaters’ and their clinical significance

A 
floaters = represent the perception of the patient to the back surface of the vitreous and other bits of vitreous debris free floating in the posterior segment of the eye
flashes = represent persistent traction of the vitreous to the retina leading to stimulation of the retina. this is seen as flashes

typically due to posterior vitreous detachment (PVF):

  • harmless and happens as you get older
  • the vitreous membrane separates from the retina as the jelly (vitreous) in the back of the eye ages and becomes more liquified
  • the more liquified jelly loses is attachment to the surface of the retina and pulls away either completely (floaters) or partially (flashes and floaters)

can also mean retinal tear which could progress to retinal detachment:

  • myopic pt’s are more at risk (short sighted)
  • see ophthalmologist for thorough retinal exam
56
Q

use an algorithm to different presentations fo red eye

A

unilateral red eye:

  • lashes touching = entropion or trichiasis
  • lashes not touching and no normal eyelid closure = CN VII palsy
  • corneal staining shows focally hazzy appearance = stroll keratitis
  • corneal staining is clear = epithelial keratitis
  • pupil larger on red eye side = acute angle-closure glaucoma
  • pupil same size or smaller on red eye side + photophobia resent = iritis
  • pupil same size or smaller on red eye side + no photophobia = scleritis if painful, episcleritis if not painful

bilateral red eye:

  • predominantly itch = allergic conjunctivitis
  • predominately gritty or burning and discharge = infective conjunctivitis. no discharge = dry eyes
57
Q

list some of the main causes of itchy eye

A
  • allergic eye disease is common especially in children
  • blepharitis
  • allergic rhinitis
  • itchiness is prominent
  • can be difficult to distinguish from viral conjunctivitis
  • red eye, itch, watery discharge
  • Hx can be suggestive - seasonal, specific exposure
  • certain clinical signs more prominent follicles and papillae
  • allergy Tx = cold compress and avoid precipitant
  • anti-allergy drops
58
Q

what are the differential diagnoses of a patient presenting with visual loss?

A
  • lesions along visual pathway or compressing
  • refractive error
  • cataract (gradual loss)
  • vitreous haemorrhage (sudden loss of vision)
59
Q

describe the typical features of a headache associated with raised ICP

A
  • papilloedema = swollen optic nerve head
  • can be due to brain tumour or idiopathic intra-cranial hypertension

typical headache of raised-ICP:

  • worse in the morning or after sleep
  • frontal
  • N+V
  • worse on straining or leaning forward
  • pulsatile tinnitus
  • horizontal diplopia worse in the distance or looking to the sides
  • transient visual obscurations
  • sensitive to pain relief
60
Q

what does the red reflex examination show for normal, cataract and retinoblastoma?

A

normal = red

dark opacity = cataract

white= retinoblastoma

61
Q

identify common presentations in ENT

A

ears:

  • hearing loss
  • ear discharge (otitis media/externa, cholesteatoma)
  • complications of ear infections
  • vertigo
  • foreign body

nose:

  • epistaxis
  • nasal blockage
  • sinusitis
  • foreign bodies

throat:

  • infections
  • neck lumps
  • foreign bodies
  • airway obstruction
62
Q

discuss the cause, assessment and management of hearing loss

A

hearing loss:

  • acute or chronic
  • conductive (inner ear and pathways to auditory brainstem are intact but the sound cannot get to the inner ear) or sensorneural (the ear apparatus is transmitting sound normally to cochlea, but the sound is not getting to the auditory brain stem)
  • congenital or acquired

CHL:

  • OM with effusion
  • wax/ FB impaction
  • CSOM
  • otosclerosis

SNHL:

  • noise-induced hearing loss (permanent damage and loss of hair cells in cochlea over time)
  • presbyacusis (age related hearing loss due to progressive death of the hair cells in the cochlea)
  • congenital

assessment:

  • audiometry: measures hearing acuity for variations in sounds, intensity and pitch (20D is the Lowe limit of normal)
  • tymoanometry: objective test for middle ear function.

management:

  • prevention
  • hearing aids
  • surgery: implantable bone conducting hearing aids (CHL); cochlear implant (SNHL)
  • grommets help correct CHL cause by OME
  • stapedectomy for otosclerosis
63
Q

compare otitis media, otitis external and chronic suppurative otitis media

A

OM:

  • acute, painful (less-so if perforated TM), bloody/whitish pus
  • fever and malaise
  • common in children
  • red TM, exudate/pus behind membrane
  • oral ABs. drops if systemically well or TM is ruptured
  • > complications = spread infection around middle ear and via perforating vessels into the brain. mastoiditis/ subperiosteal abscess/ meningitis/ facial nerve palsy

OE:

  • acute, painful, pus
  • usually systemically well
  • topical Tx is best AB or anti-fungal
  • red skin, discharge, building TM (but no pus behind it). debris
  • if fungal (aspergillum fumigatus) = fungal spores
  • > complications = spreading cellulitis on face/neck, osteomyelitis

CSOM:

  • chronic, painless, smelly
  • systemically well but needs ENT referral
  • perforation, skin cells get sucked into ear canal - chronic pockets of dead skin cells (smelly). discharge
  • > complications = facial nerve palsy/ conductive hearing loss/ complete sensorineural hearing loss/ meningitis
64
Q

discuss different causes of vertigo - sensation of motion of either subject or their surrounding

A

many causes e.g. cardiac, neurological, pharmacological, sight related, postural and ENT.

commentest ENT related causes =

  1. Benign paroxysmal positional vertigo - repeated symptoms that last a few seconds and related to head posture
  2. vestibular neuritis - acute severe vertigo. can’t take head off pillow. associated with sickness
  3. vestibular migrane - short Hx of a few hours and get again at another stage
  4. secondary to AOM or CSOM
  5. meniere’s disease - ear fullness, acute episodes, hearing loss and tinnitus
65
Q

discuss epistaxis - common ENT emergency

A
  • kids: nose picking, anterior nasal infections.
    settles with AB cream
  • adults: most commonly troublesome in anti coagulated (DVT/PE/cardiac) or thrombocytopenia population (e.g. cancer/haemotology)
  • if persistent and profuse need A+E/ENT management, cautery, nasal packing if source not clear
66
Q

what causes nasal blocking?

A

mechanical obstruction - septal cartilage deviation e.g. post injury, nasal polyps, FB, tumours, choanal atresia (failed recanalization of the nasal fossae during fetal development)

functional obstruction - allergic rhinitis, URTI, rhinitis medicamentosa (rebound nasal congestion suspected to be brought on by extended use of topical decongestants), drugs

67
Q

discuss sinusitis

A
  • acute (<3/12, usually following an URTI) or chronic (>3/12)
  • acure is PAINFUL, purulent discharge, needs decongestants and Abs to settle
  • chronic can be with or without nasal polyps. it is NOT PAINFUL. post nasal drip, purulent discharge, blockage, dull headache (mucosal dysfunction -> sinusitis)
  • Tx = topical ± oral steroids, long course of macrolide Abs
  • if not responsive, CT sinuses and surgery for drainage/opening of sinuses to allow deeper penetration of topical treatment

Differential = atypical facial pain

68
Q

discus potential causes of throat infectiosn

A
  1. tonsilitis
    - bacterial or viral
    - B: more sever, temp, difficulty swallowing
    - > Tx with oral Abs (penicillin) fluids and rest. symptoms x should resolve in 7-10days
    - V: glandular fever commonest, systemic malaise, severe fatigue, lymphadenopathy, hepatosplenomegaly
    - > conservative measures unless secondary bacterial infection. avoid alcohol/ contact sports
  2. peri-tonsillar abscess (quinsy):
    - bacterial tonsilitis but symptoms more unilateral and swelling ++ in throat
    - emergency ENT referral for drainage
    - 24-48hrs IV ABx
  3. supra/epiglottitis:
    - severe sore throat and fever with almost complete dysphagia. might be drooling/ difficulty breathing. throat looks normal or slightly red
    - emergency ENT. airway can obstruct quickly
  4. laryngitis:
    - usually viral
    - hoarse voice/ loss of voice but no difficulty breathing
    - normal or near normal swallow
    - acute onset of loss of voice, painless or slight sore throat and malaise
69
Q

discuss different causes of neck lumps

A
  • acute: associated with infection (nodes, salivary obstruction, abscess)
  • > acute presentation can be treated with oral antibiotics
  • chronic: benign or malignant
  • > refer urgently to ENT for further investigation
70
Q

what are the potential causes of airway obstruction?

A
  • acute: secondary to infection or foreign body inhalation
  • progressive: secondary to external compression or laryngeal/tracheal narrowing (tumours)
  • stridor may be audible, hoarseness with difficulty breathing also red flag sign

*both need emergency ENT referral for visualisation of the airway and further management

week 44: hearing and vision loss (1 decks)

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