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FINALS > ENT & OPHTHALMOLOGY > Flashcards

ENT & OPHTHALMOLOGY Flashcards

1
Q

What are some causes for conductive hearing loss?

A
  1. External canal obstruction = wax, pus, foreign body
  2. TM perforation = trauma, barotrauma, infection
  3. Ossicle defects = otosclerosis, infection, trauma
  4. Inadequate eustachian tube ventilation of the middle ear = effusion 2ndary to nasopahryngeal carcinoma
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2
Q

What are some causes of sensorineural hearing loss?

A
  1. Drugs - streptomycin, gentamycin, hydroxychloroquine
  2. Post-infective = meningitis, measles, mumps, flu, herpes, syphillis
  3. Meniere’s disease
  4. Cochlear valvular disease
  5. Acoustic neuroma
  6. Trauma
  7. Presbycusis
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3
Q

Describe briefly, what is the difference in terms of sound conduction between conductive, sensorineural + mixed hearing loss.

A
  • Sensorineural both air + bone conduction are reduced
  • In conductive, only AC impaired
  • in mixed, both AC + BC are affected, often with AC being worse
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4
Q

What is otosclerosis? Who does it tend to affect?

A

New bone formation around the stapes, which leads to fixation + consequent conductive hearing loss

  • autosomal dominant
  • typically manifests between 20-40yrs
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5
Q

What are the clinical features you would expect in a patient with otosclerosis?

A
  • bilateral conductive deafness
  • hearing IMPROVES when background noise present
  • worsened by pregnancy/menopause/menstruation
  • tinnitus
  • mild transient vertigo
  • positive FHx
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6
Q

How do you manage a patient with otosclerosis?

A
  1. Hearing aid - including BAHA
  2. Surgery - stapes implant
  3. Cochlear implant
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7
Q

What are the typical clinical features that a patient with presbyacusis will present with?

A

Tend to be over 65yrs

  • B/L hearing loss
  • Speech is difficult to understand, they struggle to use telephone + having to turn up volume of TV
  • hearing is WORSE in noisy environments
  • loss of directionality of sound
  • slow onset and may have associated tinnitus
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8
Q

What investigations would you perform in a patient with presbyacusis?

A
  1. OTOSCOPY - R/O otosclerosis, cholesteatoma, conductive hearing loss
  2. TYMAPNOMETRY - normal middle ear function
  3. AUDIOMETRY - B/L sensorineural pattern
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9
Q

How is prebyacusis managed?

A

Hearing aid

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10
Q

What are the clinical features of otitis externa?

A
  • watery discharge
  • itch
  • pain + tragal tenderness
  • on otoscopy = red, swollen, eczematous ear canal
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11
Q

When would you consider doing an ear swab in a patient with otitis externa?

A
  1. Treatment fails
  2. OE chronic or recurrent
  3. Topical treatment cannot be delivered (e.g. EAC occluded)
  4. Infection has spread beyond EAC
  5. Infection is severe enough to require oral Abx
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12
Q

How do you manage a patient with otitis externa?

A
  1. Manage aggravating/precipitating factors
  2. Consider cleaning EAC if wax/debris blocks topical med application
  3. Consider topical abx with or without steroid
    - e.g. ciprofloxacin with dexamethasone
    - use for at least 7 days. If symptoms persist can use for up to 14 days
  4. Consider earwick insertion if extensive swelling of EAC
  5. Oral abx rarely indicated
    - clarithromycin or flucloxacillin
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13
Q

What self-care advice should you give pts with otitis externa?

A
  1. Avoid damage to EAC - do NOT use cotton ear buds
  2. Keep the ears clean + dry
  3. Ensure pre-disposing conditions are controlled e.g. eczema, dermatitis
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14
Q

What patients are at risk of developing malignant/necrotizing otitis externa? Why is it life-threatening

A

Immunocompromised => 90% of pats are diabetics

  • Life-threatening as can cause temporal bone osteomyelitis
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15
Q

What investigation should be performed in suspected necrotizing OE?

A

CT

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16
Q

How is malignant/necrotizing OE managed?

A

Non-resolving OE with worsening pain = urgent ENT referral

  1. Surgical debridement
  2. IB Abx
  3. Specific immunoglobulins
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17
Q

What are some risk factors for developing otitis media?

A
  • bottle fed
  • passive smoking
  • dummy use
  • asthma
  • cleft-palate
  • GORD
  • raised BMI
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18
Q

How does acute otitis media present? Including what would be seen on ototscopy

A
  • Usually occurs in children post-URTI
  • Rapid onset ear pain, with child tugging at ear
  • Irritable, fever, vomiting
  • purulent discharge if drum perforates

O/E:

  • bulging red TM
  • loss of normal landmarks
  • may have a fluid level
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19
Q

How is acute otitis media managed?

A
  1. Advise that the usual duration is about 3 days but can be up to 1-week
  2. Optimize analgesia e.g. regular ibuprofen + paracetamol
  3. Antibiotics - amoxicillin or clarithromycin
    - only use if systemically unwell
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20
Q

When would you consider admitting someone with acute otitis media?

A
  • Severe systemic infection
  • Suspected acute complications = meningitis, mastoiditis, intracranial abscess, sinus thrombosis, facial nerve palsy
  • children under 3-months with a fever or over 38 degrees
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21
Q

What are risk factors for developing OME (glue ear)?

A
  1. Downs syndrome
  2. Cleft palate
  3. Cystic fibrosis
  4. Primary ciliary dyskinesia
    Allergic rhinitis
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22
Q

If otitis media with effusion occurs in an adult, what must be ruled out?

A

Post-nasal space tumour

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23
Q

What are the clinical features you would expect in a pt with OME (glue ear)?

A

HEARING LOSS

  • inattention at school
  • poor speech development
  • hearing impairment

O/E:

  • retracted dull TM
  • fluid level present
  • normal TM does NOT rule out OME
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24
Q

Why do we worry about persistent, foul smelling discharge?

A

?Cholesteatoma

- urgent ENT referral required

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25
Q

What investigations should be performed in patients with OME?

A
  1. Tympanometry = flat tympanogram in OME

2. Audiometry = conductive hearing deficit

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26
Q

How do you manage patients with OME?

A
  1. Active observation for 6-12 weeks
    - spontaneous resolution is common
    - include 2 hearing tests
    - consider ENT referral
  2. Autoinflation
    - balloon in young kids
    - valsalva in older children
  3. Myringotomy
    - insertion of grommets. They last about 10 months. Be aware of risk of infection
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27
Q

What is the criteria for ENT referral in patients with OME? (HINT there are 6)

A
  1. Hearing loss associated with impact on childs development/education
  2. Hearing loss is severe = 2ww to r/o sensorineural deafness
  3. Significant hearing loss on 2 or more occasions
  4. Tympanic membrane structurally abnormal
  5. Persistent smelly discharge
  6. Child has downs or cleft palate
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28
Q

What are the features of chronic suppurative otitis media?

A
  • PAINLESS discharge + hearing loss for over 2 weeks
  • Hx of AOM, ear trauma or glue ear + grommet insertion
  • Hx of allergy + URTI
  • Tinnitus/sensation of pressure in ear

O/E = TM perforation

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29
Q

What are the important red flag symptoms in a patient with CSOM which may suggest serious complications?

A

Mastoiditis or intracranial infection:

  • Headache
  • Vertigo
  • Labyrinthitis
  • Paralysis
  • Nystagmus
  • Fever
  • Swelling/tender behind ear
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30
Q

How is CSOM diagnosed?

A

Must refer to ENT as they are to make diagnosis

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31
Q

How is CSOM managed?

A
  1. Topical/systemic Abx
  2. Surgery (myringoplasty)
    - persistent discharge
    - mastoiditis
    - cholesteatoma
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32
Q

What is a cholesteatoma?

A

Locally destructive expansion of stratified squamous epithelium within the middle ear

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33
Q

What are the typical clinical features of a cholesteatoma?

A

PERSISTENT FOUL SMELLING DISCHARGE

  • Headache, pain
  • Conductive hearing loss
  • CN involvement (= disease progression) e.g. vertigo, sensorineural hearing loss, meningitis, facial paralysis
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34
Q

When would you urgently refer or semi-urgently refer patients with suspected cholesteatoma?

A

URGENT:
- with suspected cholesteatoma AND a serious complication including; facial nerve palsy or vertigo, other neurological signs (incl. pain) or signs that could be associated with the development of an intracranial abscess or meningitis

SEMI-URGENT:
- suspected cholesteatoma with NO serious complications

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35
Q

How is a suspected cholesteatoma investigated?

A
  1. Audiology assessment

2. CT head - for complications

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36
Q

How do you manage pts with cholesteatoma?

A
  1. Mastoidectomy

2. Steroid + Abx if infection

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37
Q

What are the clinical features of mastoiditis?

A
  • fever (pt is usually very unwell)
  • Protruding auricle
  • Tender, swollen + red mastoid
  • May have a hx of recurrent OM
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38
Q

What investigation should be done in suspected mastoiditis?

A

CT head

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39
Q

How do you manage pts with mastoiditis?

A
  1. IV Abx

2. Myringotomy with or without mastoidectomy

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40
Q

How do you manage Ramsay-Hunt syndrome?

A

Give oral aciclovir + prednisolone within first 72h

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41
Q

What are the 3 red flag symptoms in a patient presenting with nasal blockage?

A
  1. Unilateral
  2. Persistent despite 3 months treatment
  3. Epistaxis
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42
Q

What are some predipsosing factors to developing rhinosinusitis?

A
  1. Atopy
  2. Nasal obstruction - septal deviation or polyps
  3. Recent local infection - rhinitis, dental extraction
  4. Swimming/diving
  5. Smoking
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43
Q

What are the clinical features of acute sinusitis?

A
  1. Facial pain
    - typically frontal pressure worse on bending forwards
  2. Discharge
    - from nose. Thick + purulent
  3. Nasal obstruction/congestion
  4. Anosmia
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44
Q

How do you manage patients with acute sinusitis?

A
  1. Analgesia
  2. Intranasal decongestants or nasal saline
  3. Intranasal steroids if symptoms present for more than 10-days
  4. Phenoxymethylpenicillin if symptoms are severe
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45
Q

What are the clinical features of chronic rhinosinusitis WITH polyps?

A
  • Watery anterior rhinorrhoea
  • bilateral nasal obstruction
  • purulent post-nasal drip
  • cheek pain
  • mouth breathing
  • snoring
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46
Q

What investigations should you perform in patients with suspected chronic rhinosinusitis WITH polyps?

A
  1. Nasal endoscopy
  2. Anterior rhinoscopy
  3. RAST
  4. CT sinuses
  5. Biopsy
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47
Q

How do you manage patients with chronic rhinosinusitis WITH polyps?

A
  1. Topical nasal steroid - betamethasone 0.1%
  2. Short course of prednisolone
  3. Nasal saline irrigation
  4. Antibiotics if evidence of infection
  5. Antihistamine + allergen avoidance
  6. Endoscopic sinus surgery
    - advise NOT to blow nose + continue steroids
    - SEs = CSF leak, optic nerve damage
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48
Q

What are the clinical features of chronic rhinosinusitis WITHOUT polpys?

A
  • B/L intermittent nasal blockage
  • sneezing
  • rhinorrhoea
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49
Q

What investigations should be performed in chronic rhinosinusitis WITHOUT polyps?

A
  1. Thuddicums speculum
  2. Nasal endoscopy
  3. RAST
50
Q

How do you manage chronic rhinosinusitis WITHOUT polyps?

A
  1. Antihistamine if clear evidence of allergy e.g. loratidine
  2. Topical nasal steroid e.g. betamethasone 0.1%
  3. Saline nasal irrigation
  4. Sinus surgery if unresponsive to medical treatment
51
Q

What are the classifications of allergic rhinitis?

A
  1. Seasonal
    - symptoms around same time every year
  2. Perennial
    - symptoms throughout the year
  3. Occupational
    - Symptoms follow exposure to particular allergens within workplace
52
Q

What are the clinical features of allergic rhinitis?

A
  1. Sneezing
  2. B/L nasal obstruction
  3. Clear nasal discharge
  4. Post-nasal drip
  5. Nasal pruritus
53
Q

How do you manage allergic rhinitis?

A
  1. Allergen avoidance
  2. Oral/intranasal anti-histamines
  3. Intranasal corticosteroids
54
Q

What is the centor criteria + how is it used to manage cases of tonsillitis?

A
  1. Cough absent (+1)
  2. Exudate on tonsils (+1)
  3. Tender/swollen cervical nodes (+1)
  4. Temperature over 38 (+1)
    - also if 3-14 yrs (+1) or 45 and above (-1)

Consider Abx if score 3/4.
- Penicillin V or erythromycin

55
Q

What are some indications for a tonsillectomy?

A
  1. For recurrent tonsillitis if ALL of:
    - caused by tonsillitis
    - 5+ episodes a year
    - Episodes disabling + prevent normal functioning
    - symptoms for more than 1y
  2. Airway obstruction e.g. OSA in children
  3. Quinsy
  4. Suspicion of cancer e.g. unilateral enlargement or ulceration
56
Q

List some complications which can arise as a result of a sore throat?

A
  1. Peritonsillar abscess (Quinsy)
  2. Retropharyngeal abscess - rare
  3. Scarlet fever
  4. Rheumatic fever
  5. Post-streptococcal glomerulonephritis
    - malaise + ‘smoky’ urine 1–2 wks after pharyngitis
57
Q

How do you manage a patient with a quinsy?

A

ADMIT

  • IV Abx
  • incision + drainage under LA or tonsillectomy under GA
58
Q

What is Scarlet fever? How is it treated?

A

‘Sandpaper’ like rash on chest, axillae or behind ears 12-48h after pharyngotonsillitis

  • circumoral pallor
  • strawberry tongue

Treatment = start Penicillin V/G + notify public health

59
Q

What are the clinical features of rheumatic fever?

A
  • carditis
  • arthritis
  • subcutaneous nodules
  • erythema marginatum
  • sydenham’s chorea
60
Q

What is laryngomalacia?

A

Immature + floppy aryepiglottic folds + glottis causing laryngeal collapse on inspiration

61
Q

How does laryngomalacia tend to present?

A

STRIDOR in children

  • presents within the first few weeks of life
  • noticeable at certain times e.g. lying on back, feeding, excited/upset

Problems can occur with concurrent laryngeal infections or with feeding

62
Q

How is laryngomalacia managed?

A

Usually no treatment is required BUT severe cases may warrant surgery

63
Q

How do you manage epiglottitis?

A

Do NOT examine the throat or cause any distress

  1. Contact anaesthetists + ENT
  2. O2 + nebulised adrenaline
  3. IV Dexamethasone
  4. Cefotaxime
  5. Take to theatre to secure airway by intubation
64
Q

What is a pharyngeal pouch? What are the typical symptoms?

A

More common in OLDER men
- usually not seen but if large then a midline lump in the neck which gurgles on palpation

Symptoms = dysphagia, regurgitation, aspiration + a chronic cough

65
Q

What is a branchial cyst?

A

Oval, mobile cystic mass that develops between sternocleidomastoid muscle + pharynx

  • develop due to failure of obliteration of 2nd branchial cleft in embryonic development
  • usually present in early adulthood
66
Q

What are the clinical features of infectious mononucleosis?

A

Triad of:

  1. Fever
  2. Pharyngitis
  3. Lymphadenopathy - may be present in anterior or posterior triangles of neck (tonsilitis only involves upper anterior chain)

Others:
- lymphocytosis, malaise, anorexia, headache, hepatitis, palatal petechiae, splenomegaly (rupture can occur)

67
Q

What investigations can be performed in suspected infectious mononucleosis?

A
  1. FBC - lymphocytosis

2. Monospot test in 2nd week of illness

68
Q

How do you manage infectious mononucleosis?

A
  1. Rest in early stages, drink plenty of fluids, avoid alcohol
  2. Simple analgesia
  3. Avoid contact sports for 8 weeks
69
Q

What occurs in acute angle closure glaucoma?

A

When iris bulges forward + seals off trabeuclar meshwork from the anterior chamber preventing aqueous humour being able to drain
- causes a continual increase in pressure in eye

70
Q

What are some risk factors for AACG?

A
  • increasing age
  • females 4x more likely
  • FHx
  • Chinese + East Asian origin
  • Shallow anterior chamber
71
Q

What medications can precipitate AACG?

A
  • adrenergics e.g. noradrenaline
  • anticholinergics e.g. solifenacin
  • TCAs e.g. amitriptyline
  • Angle narrowing e.g. cyclopentolate
72
Q

What are the symptoms + signs of AACG?

A

HEADACHE + PAINFUL RED EYE
- blurred vision, haloes around lights, N+V, onset over hrs to days

O/E:

  • red eye, teary
  • hazy cornea, decreased visual acuity, dilatation of affected pupil, fixed pupil
  • decreased VA
73
Q

If you see someone in GP with suspected AACG, what do you do?

A

SAME-DAY OPHTHALMOLOGY ASSESSMENT REQ

  • will have tonometry (raised IOP over 40mmHg)
  • Gonioscopy
  • slit lamp
74
Q

How do you manage AACG?

A

Avoid dark rooms as dilatation worsens angle closure

  1. Pilocarpine - constricts
  2. Azetazolomide - decreases aqueous humour
  3. Timolol
  4. Analgesic + anti-emetic
75
Q

What is the definitive management of AACG?

A

Peripheral laser iridectomy in BOTH eyes

76
Q

What are some risk factors for retinal detachment?

A
  • previous hx
  • cataract surgery
  • trauma
  • myopia
  • DM
  • ARMD
77
Q

What are the clinical features of retinal detachement?

A 
PAINLESS 
- peripheral vision loss (like a shadow)
- blurred/distorted cision
4 F's:
- Floaters
- Flashes
- Field loss
- Fall in VA
78
Q

How do you manage retinal detachment?

A

URGENT OPHTHALMOLOGY R/V

  1. Rest
  2. Laser photocoagulation - fix tear in retina
  3. Surgery to fix detachment
    - vitrectomy or gas tamponade
79
Q

What is the most common cause of central retinal artery occlusion?

A

Atherosclerosis

- also can be caused by GCA

80
Q

What are the clinical features of central retinal artery occlusion?

A

DRAMATIC SUDDEN PAINLESS LOSS OF VISION

  • acuity is finger counting or worse
  • RAPD may precede retinal changes
81
Q

What will fundoscopy show in central retinal artery occlusion?

A

Pale retina with a cherry red spot

82
Q

How do you manage central retinal artery occlusion?

A

Attempt to restore ocular blood flow within 100 mins

  1. Ocular massage
  2. Surgical removal of aqueous humour
  3. Intraocular antihypertensives
  4. Inhaled carbogen to dilate the artery
83
Q

What does retinal vein occlusion look like on fundoscopy?

A
  • Flame + blot haemorrhages
  • Optic disc oedema
  • Macular oedema
84
Q

How do you manage retinal vein occlusion?

A

IMMEDIATE OPHTHALMOLOGY R/V

  • Aim is to treat macular oedema + prevent complications. Options:
    1. Laser photocoagulation
    2. Intravitreal steroids
    3. Anti-VEGF
85
Q

How do you differentiate between periorbital (preseptal) + orbital cellulitis?

A

periorbital is less serious + will not have any eye pain or visual problems

86
Q

What investigations + management should be performed in suspected orbital cellulitis?

A
  1. FBC - raised WCC + CRP/ESR
  2. Conjunctival swab
  3. Orbital CT
  4. Blood cultures

Management = Urgent CT + ophthalmology review + IV Abx

87
Q

What are some (i) painless (ii) painful causes of red eye?

A

(i) conjunctivitis, episleritis, subconjunctival haemorrhage
(ii) Painful:
- glaucoma
- anterior uveitis
- scleritis
- corneal abrasions/ulceration
- keratitis
- foreign body
- traumatic/chemical injury

88
Q

What are some indications for immediate Abx for conjunctivitis?

A
  • STI
  • contact lens wearer
  • immunocompromised
89
Q

How do you manage conjunctivitis?

A

Most cases resolve within 5-days without treatment:

  1. Artificial tears - hydromellose
  2. Chloramphenicol or Fusidic acid if bacterial
  3. Antihistamine if allergic
90
Q

What patient advice should you give to people with conjunctivitis?

A
  • irrigation to remove purulent discharge may be helpful
  • contact lens wear avoided until 48h post infection resolution
  • wash hands + don’t share towels
  • seek medical attention if condition deteriorates
91
Q

What conditions is episcleritis associated with?

A

Inflammatory disorders e.g. RA and IBD

92
Q

How do you differentiate between scleritis + episcleritis?

A

EPISCLERITIS
= painless/mild pain, no visual loss
SCLERITIS
= painful, gradual vision loss

93
Q

How is epislceritis managed?

A

Conservatively

  • usually resolves in 1-4wks
  • lubricating eye drops
  • analgesia + cold compress
  • safety net
94
Q

How is a subconjunctival haemorrhage managed?

A

Harmless + will resolve spontaneously within 2-weeks

- think about investigating possible causes e.g. HTN + bleeding disorders

95
Q

What conditions are associated with anterior uveitis?

A

HLA-B27

  • ankylosing spondylitis
  • IBD
  • reactive arthritis

CHRONIC

  • sarcoidosis
  • syphillis
  • Lyme disease
  • TB
  • herpes virus
96
Q

What are the clinical features of anterior uveitis?

A

Unilateral features which start spontaneously.

  • acute pain + photophobia
  • blurred vision, decreased VA
  • floaters + flashes
  • miosis, lacrimation
  • pain on movement
  • pupil dilates irregularly + hypopyon
97
Q

How is anterior uveitis managed?

A

URGENT referral + control of underlying disease

  1. Prednisolone 1% drops
  2. Cyclopentolate 1% 8-hrly to maintain pupil dilatation to prevent adhesions
98
Q

What are the clinical features of keratitis?

A
  • pain, photophobia
  • vesicles around eye
  • watering eye
  • decreased VA
  • foreign body sensation (enquire about mouth + genital ulcers)
99
Q

What condition will show dendritic corneal ulcers?

A

Keratitis

100
Q

When should you perform an MRI in pts presenting with CN6 palsy?

A
  • other CN palsies also present
  • younger than 35
  • B/L papilloedema
101
Q

How do you manage CN6 palsies?

A

Most microvascular palsies resolve within 3-6 months

  1. Temporary prisms in glasses
  2. Botox injection into medial rectus can limit the squint
102
Q

If a patient with a third nerve palsy presents with fixed pupil dilation, what should you be worried about?

A

Suggests compression from SOL

  • urgent neuroimaging required
  • suspect posterior communicating/internal carotid artery aneurysm
103
Q

What will patients with a 4th nerve palsy not be able to do?

A

Look down + in

104
Q

What are some causes of a gradual loss of vision?

A
  • cataract
  • glaucoma
  • diabetic retinopathy
  • hypertensive retinopathy
  • ARMD
  • retinitis pigmentosa
  • vit A deficiency
105
Q

What are the clinical features of ARMD?

A

Gradual loss of CENTRAL vision

  • reduced VA
  • crooked/wavy appearance of straight lines
  • difficulty reading + making out faces
  • worsening vision at night + with changing light conditions
106
Q

What is seen on examination in ARMD?

A
  • Reduced VA on snellen
  • scotoma (= central patch vision loss)
  • amsler grid shows straight line distortion
  • fundoscopy has DRUSEN in dry
107
Q

How do you manage DRY ARMD?

A

No specific treatment - lifestyle measures may slow progression

  • avoid smoking
  • controlling BP
  • vitamin supplementation
108
Q

How do you manage WET ARMD?

A
  1. Anti-VEGF medications (ranibizumab)
  2. Laser photocoagulation
  3. Photodynamic therapy
  4. Intravitreal steroids
109
Q

What are the risk factors for primary open-angle glaucoma?

A
  • aged over 50
  • IOP over 23mmHg
  • FHx glaucoma
  • myopia (short-sightedness)
  • black ethnicity
110
Q

What are the clinical features of primary open-angle glaucoma?

A

Asymptomatic rise in IOP

  • peripheral vision loss
  • tunnel vision
111
Q

How do you manage primary open-angle glaucoma?

A
  1. Topical prostaglandin analogues = lantoprost, travoprost
  2. Topical beta-blockers = betaxolol (caution asthma + HF)
  3. Topical alpha agonists = brimonidine
  4. Carbonic anhydrase inhibitors (acetazolomide)
  5. Pilocarpine
  6. Laser trabeculoplasty
  7. Trabeculoectomy/stents
112
Q

What are the clinical features of cataracts?

A

Usually asymmetrical as each eye is affected separately:

  • very slow reduction in vision
  • progressive blurring of vision
  • colour goes brown/yellow
  • starbursts around lights
  • LOSS OF RED REFLEX
113
Q

What does cataract surgery involve?

A

Drilling + breaking lens into pieces, removing pieces + then implanting an artificial lens into the eye
- usually done as a day case under LA

114
Q

What is mild NPDR classed as?

A

1 or more microaneurysm

115
Q

What is moderate NPDR classed as?

A
  • microaneurysms
  • blot haemorrhages
  • hard exudates
  • cotton wool spots, venous beading/looping + intraretinal microvascular abnormalities (IRMA)
116
Q

What is severe NPDR classed as?

A
  • blot haemorrhages + microaneurysms in 4 quadrants
  • venous bleeding in at least 2 quadrants
  • IRMA in at least 1 quadrant
117
Q

What is proliferative diabetic retinopathy classed as?

A
  • retinal neovascularisation, may lead to vitreous haemorrhage
  • fibrous tissue forming anterior to retinal disc
  • more common in T1DM
118
Q

What is maculopathy? Who is it more common in?

A
  • based on location rather than severity - any are potentially serious
  • any hard exudates or other changes on macula
  • more common in T2DM
119
Q

How do you manage non-severe NPDR?

A

Observation - strive to achieve optimum glycaemic + hypertensive control

120
Q

How do you manage severe NPDR?

A

Consider pan-retinal photocoagulation

121
Q

How do you manage proliferative diabetic retinopathy?

A

Urgent pan-retinal photocoagulation

122
Q

How is hypertensive retinopathy staged?

A

Keith-Wagener Classification

FINALS (14 decks)

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