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IP 2 > ophthalmic and otic disorders > Flashcards

ophthalmic and otic disorders Flashcards

1
Q

what is glaucoma?

A

a group of eye disorder in which there is a progressive damage to the optic nerve - characterised by structural abnormalities of the optic nerve head + associated patterns of visual field loss

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2
Q

how is glaucoma classified?

A

variations in the anterior segment of the eye and appearance of iridocorneal angle - resulting in elevated IOP

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3
Q

what are the 4 types of glaucoma?

A
  1. open-angle
  2. closed-angle
  3. secondary
  4. developmental
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4
Q

What is the pathophysiology of chronic open-angle glaucoma?

A
  1. overproduction/obstruction to outflow of aq humour through trabecular meshwork or schlemm’s canal
  2. Increase IOP + damage to optic nerve
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5
Q

What is the pathophysiology of acute angle-closure glaucoma?

A
  1. There is an obstruction to the outflow of aq humour
  2. Narrow angles between the anterior iris and posterior corneal surface, shallow anterior chambers and a thickened iris or bulging iris.
  3. Increase in IOP
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6
Q

What is the pathophysiology of secondary glaucoma?

A

trauma and surgery which may increase risk of obstruction of intraocular fluid outflow

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7
Q

clinical presentation of chronic open-angle

A
  1. Mild aching
  2. Pattern of visual field changes (due to compression of retinal rods and nerve fibres)
  3. Halos around lights
  4. Often missed as a diagnosis
  5. Slow progression, painless and irreversible
  6. Visual acuity and peripheral vision loss w/ mobility difficulties.
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8
Q

clinical presentation of primary angle closure

A
  1. Ocular pain
  2. Redness, blurred vision
  3. Photophobia, halos around lights
  4. Nausea and vomiting
  5. Medical emergency
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9
Q

drugs that may induce open-angle

A
  1. Ophthalmic corticosteroids (high)
  2. Systemic corticosteroids
  3. nasal/inhaled corticosteroids
  4. Ophthalmic anticholinergics
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10
Q

drugs that may induce closed-angle

A
  1. Topical sympathomimetics
  2. Systemic anticholinergics
  3. Antihistamines
  4. Ipratropium
  5. Benzodiazepines (low risk)
  6. Theophylline (low risk)
  7. Heterocyclic antidepressants
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11
Q

how is glaucoma diagnosed?

A
  1. Pressure measurement tonometry
  2. Fingertip tension - estimates IOP
  3. Gentle palpation of closed eyelids, one eye feels heavier than the other in acute)
  4. Gonioscopy - determines angle of eye’s anterior chamber = differentiates whether acute or chronic
  5. Ophthalmoscopy - shows cupping of optic disk in chronic
  6. Perimetry or visual field test
  7. Fundus photography
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12
Q

how is chronic open-angle glaucoma managed?

A

GOAL OF TREATMENT

  • Slow or halt progression so that any visual loss has least impact on QOL
  • Reducing IOP with treatment options
  • Medications should be the first choice for most patients
  • Laser therapy
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13
Q

what is the indication for treatment in chronic open-angled glaucoma?

A

INDICATION FOR TREATMENT:
IOP > 25 mm Hg
Vertical cup-disk ratio > 0.5
Central corneal thickness < 555 micrometer

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14
Q

what are the therapeutics for chronic open-angle glaucoma?

A

IOP is determined by balance between inflow and outflow of aq humour:

  • inflow is decreased by alpha2, alpha and beta adrenergic blockers; dopamine blockers; carbonic anhydrase inhibitors and adenylate
  • outflow is increased by cholinergic agents, prostaglandin analogs and alpha2-adrenergic agonists
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15
Q

initial treatment for chronic open-angle

A

prostaglandin analogues and beta-blockers eye drops - first line
if these cannot be tolerated or contraindicated - alpha2 adrenergic agonists or carbonic anhydrase inhibitor should be considered.

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16
Q

practice point for the initial treatment of chronic open-angle glaucoma

A
  1. treatment is recommended to begin in one eye only (worst eye), using other eye as a control to test for effectiveness
  2. response to lowering IOP should be checked within 2-6 weeks
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17
Q

subsequent treatment for chronic open-angle

A
  1. depending on response to first treatment - either change in medication (inadequate response) or add topical agent
  2. increase dose of initial agent NOT recommended - only increases ADE
  3. switch to alternative agent within class or alternative class
  4. prostaglandin analogues (structurally different to each other)
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18
Q

what happens if there is an inadequate response with initial medication for chronic open-angle

A
  • additional medication is added - HOWVER not from same class
  • no combination with prostaglandin analogues and best to use topical and systemic beta blockers
  • if more than 2 topical medications are required, suggest surgery or laser therapy
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19
Q

glaucoma response to therapy

A
  • target IOP is 30-50% reduction in pre-treatment IOP

- continuing evaluation of optic disk and visual field

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20
Q

who are recommended to undergo laser trabeculoplasty based on Australian Guidlines?

A

older patients with open-angle glaucoma that have high risk of visual loss, difficulty in administering eye drops and are unresponsive to medication alone or are poor candidates for incisional surgery

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21
Q

when is it recommended to undergo surgery in glaucoma

A
  1. when the target IOP is not being achieved with two or more medications
  2. adherence is problematic
  3. when laser therapy has failed or is not likely to succeed
22
Q

treatment for acute closed angle glaucoma

A
  1. ophthalmic emergency
  2. referral to ophthamologist
  3. peripheral laser iridotomy
23
Q

drug therapy for acute closed-angle glaucoma

A
  1. prostaglandin analogues OR topical beta-blockers
  2. pilocarpine (topical)
  3. acetazolamide (orally)
  4. mannitol (4) or oral glycerol
  5. antiemetics
    6/ opioid analgesia
24
Q

what is AMD - ophthalmic disorder

A

age-related macular degeneration which is a progressive disease affecting central vision

25
Q

what is the pathophysiology of AMD

A

partial breakdown of retinal pigment epithelium (RPE)

26
Q

what are the types of AMD

A
  1. dry (atrophic)

2. wet (choroidal neo-vascularisation)

27
Q

symptoms of AMD

A
  • central vision loss
  • difficulty judging heights and distances
  • blurry or fuzzy vision
28
Q

risk factors of AMD

A
  • family history (increases risk by 3-4x)
  • light eye colour
  • smoking
  • HTN, arteriosclerosis, hypercholesterolaemia
  • diet
29
Q

how to prevent AMD

A
  • watch for risk factors
  • avoid sunlight
  • regular examinations
30
Q

what are the drug therapy for AMD

A
  • verteporfin which is only available for wet AMD. It concentrates in the area of retina effected and is activated with laser for photodynamic therapy
  • ranibizumab (lucentis) Ab to VEGF-A. Monthly intravitreal injection 0.05mL or 0.03mL (0.5mg or 0.3mg)
31
Q

counselling for verteporfin therapy (AMD)

A
  • CI: allergy, severe hepatic impairment
  • AE: blurred vision, black spots, itch, photosensitivity
  • avoid sunlight for 48 hours.
32
Q

counselling for ranibizumab therapy (AMD)

A
  • injection to eye 1x monthly
  • local anaesthetic and AB given prior to injection
    antimicrobial eye drops 4x a day for 3 days before and after injection
  • AE: eye irritation and discomfort, sore throat, headache, joint pain, flu-like symptoms, fatigue, allergic reactions)
33
Q

what is otitis media

A

an inflammation of middle ear

34
Q

what are the three subtypes of otitis media

A
  1. acute otitis media
  2. otitis media with effusion
  3. chronic otitis media
35
Q

how are the three subtypes of otitis media differentiated

A

a) acute signs of infection
b) evidence of middle ear inflammation
c) presence of fluid in middle ear

36
Q

what is the epidemiology of otitis media?

A
  • usually caused by infection from bacteria such as Streptococcus pneumoniae, haemophiluc influenzae and moraxella catarrhalis
  • allergies
  • tobacco smoke or other irritants
  • infected or overgrown adenoids
  • excess mucus and saliva produced during teething
37
Q

what is the pathophysiology of otitis media?

A
  • acute otitis media is sually followed by viral upper respiratory tract infection impairing mucociliary apparatus causing eustachian tube dysfunction in middle ear.
  • blockage in eustachian tube repeatedly = chronic
38
Q

what are the signs and Sx of otitis media

A
  • acute onset
  • visible reddening and dullness of tympanic membrane
  • pain
39
Q

what are the treatment options for mild otitis media?

A
  • symptomatic treatment
  • wait and watch approach - reassess after 24 h (children < 2yrs)
  • 48 h (children > 2 yrs)
40
Q

what are the treatment options for recurrent otitis media?

A
  • major risk factor for OM with effusion

- chronic suppurative OM

41
Q

what is the approach therapy for acute otitis media

A
  1. Analgesics: paracetamol or NSAIDs, symptomatic treatment
  2. antibacterials: amoxicillin w/ clavulanic acid (5 days) or cephalosporin (cefuroxime X 5 days)
    - if pain persists > 2 days or systemic complications.
42
Q

what is OM with effusion (glue ear) - otitis media

A
  • fluid behind intact eardrum in absence of signs and Sx of acute infection lasting for > 3 months
  • may resolve spontaneously within 3 months
43
Q

what is the suppurative OM for OM with effusion

A
  • ciprofloxacin 0.3% ear drops instilled into affected ear, 12-h until middle ear has been free of discharge for at least 3 days
  • remove discharge qid
  • amoxicillin
  • systemic Ab if local fails
44
Q

what is the pathophysiology of otitis externa

A
  • usually results from the combination of heat and retained moisture with desquamation and maceration of epithelium of outer ear canal. different types but all are predominantly caused by P.aeruginosa and S. aureus
45
Q

what is the management approach of acute diffuse otitis externa (swimmers ear)

A
  • ear canal kept dry as much as possible
  • remove discharge or other debris from ear canal by dry aural toilet
  • dry mop the ear with rolled tissue spears or similar 6-hourly until external canal is dry.
  • instil combination of corticosteroid and antibiotic ear drops after performing aural toilet; use: dexamethasone + framycetin + gramicidin 0.05% + 0.005% ear drops 3 drops instilled into affected ear, 3 x daily fro 3-7 days OR flumethasone + clioquinol 0.02% + 1% ear drops 3 drops intilled into affected ear, 2x daily for 3-7 days
46
Q

what is the management approach of acute localised otitis externa (swimmers ear)

A
  • commonly caused by S. aureus, usually from boil associated with hair follicle. These can cause painful erysipelas that involve pinna and external canal. Systemic antibiotics are usually curative though surgical drainage may also be requried.
  • use: flucloxacillin OR cephalexin OR clindamycin (5 days)
47
Q

drug induced - in otic disorder

A
  • ototoxic = antibacterials e.g aminoglycosides, loopdiuretics may cause transient hearing loss - occasionally permanent, high dose of salicylates (NSAIDs) - almost always reversible
48
Q

what can be done to minimise risk of drug-induced in otic disorder

A
  • ear wick
  • limit to short term use only
  • monitor
  • not when tympanic membrane is perforated
  • avoid in pregnancy, elderly and patients with hearing problems
49
Q

what is tinnitus - otic disorder

A
  • ringing in the ears, noises, buzzing in the ears causing significant psychological distress
50
Q

what is the pathophysiology/epidemiology of tinnitus

A
  • perception of sound in absence of external sound
  • can be idiopathic or associated with hearing loss
  • may be associated with OM
  • consider drug associations
51
Q

what are the treatment options for tinnitus

A
  • treat underlying cause
  • TCA - bust adverse effects
  • hearing aids

IP 2 (4 decks)

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