Dermatology / ENT / Eyes Flashcards
Neck lumps:
- What is a thyroglossal cyst?
- What is a cystic hygroma?
- What is a brachial cyst?
Thyroglossal cyst - midline between thyroid and hyoid but can be anywhere along thyroglossal tract (tongue to thyroid) - moves up when sticks out tongue
Cystic hygroma - arises from jugular lymphatic sac, commonly left posterior triangle, soft painless mass transilluminate
Brachial cyst - solitary painless mass in young person, Hx intermittent swelling and tenderness during URTI, +/- discharge if associated with sinus tract
What is Livedo reticularis?
Net like discolouration of venules commonly on legs, can be triggered by cold.
Causes:
* Pregnancy
* AI - RA, SLE, Polyarteritis nodosa (PAN), polymyositis,
* Other - Raynaud’s, lymphoma, TB
What is acanthosis nigricans?
Velvety brown/black markings at groin/armpits/neck
Causes - obesity, gastric carcinoma, Hodgkin’s lymphoma, Acromegaly, Cushing’s, DM
What is this skin condition in the context of coeliac disease?
Dermatitis Herpetiformis
Itchy subepidermal blisters on elbows/scalp/shoulders/ankles assoc with coeliac disease
Often in women in 30-40s
Tx: Dapsone, gluten-free diet
Pterygium vs Pinguecula
Pterygium & Pinguecula - benign conjunctival growths due to degeneration of Bowman’s membrane of cornea extending into conjunctival epithelium - commonly from nasal-side sclera, wedge-shaped.
Difference = Pterygium can grow over edge of cornea and affect veission
Assoc w/ UV light esp in people outdoors/hot/dusty, >40yrs
Often assymptomatic, visual disturbance if affecting pupillary area
Tx: surgical removal but recurrence common
What is another name for Hordeolum? What is the difference between this and Chalazeon?
Hordeolum = stye - they can be internal or external.
Stye - infection (S. aureus) of the gland of Zeis (secrete sebum, ensure eyelashes don’t become brittle) which opens into the eyelash follicle –> erythema around eyelash root.
* Self-limmiting in 1-2wks, eyelid hygeine, warm compress, massages of lesion 10 mins QDS +/- topical abx ointment if draining/blepharoconjunctivitis.
Chalazeon - obstructed Meibomiam gland (secrete Meibum - reduced evaporation of tear film) - mostly non-tender more cosmetic issue.
Give an overview of glaucoma
Glaucoma causes progressive optic neuropathy due to increased IOP
* Increased IOP (11-21 is normal) can damage optic nerve causing visual field defect
* Leading cause of irreversible blindness (10% UK blindness)
Types:
* Occular HTN - OH (3-5% >40yrs)
* Primary open angle glaucoma - POAG (2%) - normal angle, increased IOP from clogging of drainage canals. Chronic course.
- RFs Short-sighted (myopia), T2DM, CVD, HTN, age/black/FHx.
- Secondary OAG - uncommon, causes include steroids.
* Primary angle closure glaucoma (0.4%) - iris pushes forward onto trabecular meshwork.
- RFs Long-sighted, women/asian, age.
Clinical features:
* Acute angle closure - acute eye pain = opthalmological emergency
- Painful red eye + headache/nausea/vomiting
- Reduced vision, lights-surrounded by halos - caused by hazy oedematous cornea
- Mid-dilated fixed pupil
* Sub-acute (intermittent) angle closure - as above but less severe, self-limiting, often recurrent.
- Presents on lying supine/eye closure/post-sleep.
* Chronic angle closure/POAG - asymptomatic until severe visual field defect.
- Often Dx by optometrist - increased IOP/visual field defect/cupped optic disc (+/- angle closure on gonioscopy)
Management:
* Testing:
- >60yrs - 2yrly
- >70yrs/>40yrs + FHx + OAG/>40yrs + black - 1yrly
* Suspected angle closure glaucoma - URGENT opthalmology assessment:
- GP Tx - lay flat, miotic e.g. pilocarpine 1 eye drop (2% blue eyes, 4% brown), systemic agent e.g. acetazolamide 500mg (increase acqueous humour production)
- Definitive = laser iridotomy (hole in iris allowing acq humour to flow into anterior chamber
* POAG/OH - prevent progression: lifetime monitoring, if mod/severe - topical prostoglandin analogue/prostamide (latanoprost), topical beta-blocker, sometimes - laser/surgery (trabeculoplasty)
Give an overview of conjunctivitis
Most common cause of red eye - inflammation of conjunctiva often inf/allergic.
* 80% viral - most common adenovirus (75% viral cases), bacteria - most common cause in children H. influenzae (others - S. pneumo, S. aureus), opthalmia neonatorum (first 4wks life, most commonly from C. trachomatis)
Presentation:
* Redness (hyperaemia) over sclera and inner eyelid
* Gritty/itchy in allergic
* Discharge - eyelashes stuck together
* Transient blurring (cleared on blinking)
* Photophobia/pain - indicating corneal involvement = keratoconjunctivitis
Rule out red flags: reduced vision, severe eye pain/headache/photophobia, red sticky eye in neonate, trauma/FB, copious discharge (gonorrhoea), herpes inf, soft contact lens use + conreal Sx (watering + photophobia)
Tx - largely self-limiting
* Eye hygeine, cool compress, artificial tears
* Topical abx (Chloramphenicol 0.5% drops/1% ointment or fusidic acid 1% drops)
* Contageous - inf control measures
* If contact lens - stop lens use until Sx gone/good eyelid cleaning, use topical fluorescein ?corneal staining –> opthalmology ref
NOTE: ongoing Sx - send swab for viral PCR (adeno/HSV) & bacterial culture –> empiral topical abx + opthalmology referral if >7-10d Sx after Tx.
Scleritis vs Episcleritis
Scleritis - inflammatory condition where sclera becomes oedematous/tender/tissue destruction
* Most common in women between 40-50yrs
* Classification: anterior OR posterior - both assoc w/ keratitis/uveitis/glaucoma/cataracts/exudative retinal detachment.
- 20% in RA/collagen diseases, 15% HZV/TB/Syphilis/Gout/reactive arthritis, 10% Ankylosing spondylitis
Features: severe deep pain, vision can be affected, focal/diffuse redness (vessel dilation in subconjunctival network)
Management (resistant to Tx): early referral, systemic NSAIDs (oxyphenbutazone/indomethacin)
Note topical steroids worsens condition, systemic steroids for worst cases
Episcleritis - inflammation of episclera (thin vascular layer overlying sclera), 2/3 unilateral.
* 30% in collagen disease/HZV/Syphilis/Gout, note = good indicator of disease activity in IBD.
* Types - simple (acute, mild, sectorial, recurrent), nodular (localised, raised mobile inflam near limbus, single or multiple)
Features: mild irritation, photophobia, redness
* 15% develop iritis
* Compared to conjunctivitis - episcleritis has localised response and no palpebral conjunctival response (lines the eyelid)
* Drop of phenylephrine 2.5% causes blanching of episcleral vessels - not in scleritis
Mx: self-limiting, artifical tears, oral NSAIDs if needed
Give an overview of subconjunctival haemorrhage
Bright red patch under conjunctiva following rupture of small conjunctival vessel
* Causes - spontaneuous, trauma, local congestion (cough/sneeze)
* Normally unilateral, recurrent/bilateral = HTN/blood dyscrasias (disease of blood/BM/lymph)
* No Tx needed - resolves within 2wks
Give an overview of keratitis
Keratitis is inflammation of cornea - normally infectious = occular emergency (major cause of blindness)
* RFs: contact lens, corneal trauma
Features: red eye, slight blurring, photophobia
* Hypopyon/leukocytic exudate - white/grey patch on cornea = collection of WBCs in corneal tissue
Tx: topical abx +/- pupil-dilators, CSs, systemic abx
Complications: corneal scarring, perf, endophthalmitis
What is an acoustic neuroma?
IC tumour arising from Schwann cell sheath investing the vestibular/cochlear nerve(s) - increase in size to occupy large portion of cerebellopontine angle
* Arise spontaneuous or as part of NF1
* Presentation = unilateral sensorineural hearing loss (can be fluctuating/improve with steroids) +/- headache/tinnitus/vertigo/facial numbness or weakness
* Ix: MRI-head w/ contrast
* Tx: young >2.5cm/small intact hearing -> surgery, old - small -> serial MRIs, growing -> radiotherapy/radiosurgery
Give examples of ototoxic medication?
Presents with tinnitus –> gradual sensorineural hearing loss/vertigo
Aminoglycosides (streptomycin - vestibulotoxic but cochleotoxic in kids, neumycin - cochelotoxic, gent - vestibulotoxic)
Loop diuretics (ethacrynic acid/furosemide) - by themselves reversible but combined with aminoglycosides can be irreversible
Rinne vs Weber’s tests
Rinne under the Pinne - place tuning fork on the mastoid
* +ve (normal) = air conduction > bone conduction
* -ve (abnormal) = BC > AC = Conductive Hearing Loss (CHL)
Weber did a header - place on forehead
* Normal = equal hearing in both ears
* Lateralisation - contralateral = Sensorineural hearing loss (SNHL), epsilateral = CHL
What is furunculosis?
Furunculsis affects external ear canal - infected (staph) hair follicle in distal part of meatus
* Sx: pain at lesion site/movement of pina/pressure on tragus, can be slight deafness - occulusion of meatus
* Often self-limiting in 4-10d but can required abx
What is otosclerosis?
Otosclerosis is progressive conductive deafness from fixation (ankylosis) of stapes at oval window (can’t vibrate) due to laying down of vascular spongey bone across joint
* Female, early 30s, FHx, pregnancy/oestrogen therapy
* PC: slow progressing hearing loss B/L (70%) +/- tinnitus, NAD on otoscope exam
* Ix: early disease - pure-tone audiometry = low-freq conductive hearing loss (later in disease high freq losses)
* Tx: hearing aids -> stapedectomy
What is a dermoid cyst?
Dermoid cystic = cystic teratoma containing developmentally mature skin with hair follicles & sweat glands +/- sebum/fat/bone/nails/teeth/eyes/cartilage/thyroid tissue
* Mature so normally benign
* Commonly young children, often near lateral eyebrow (if near midline will need MRI to exclude IC extension if considering excision)
What is this skin condition?
Seborrheic keratosis (basal cell papillomas) - most common benign tumour in older adults (>40yrs)
* Can appear flat/raised/pedunculated/yellow-dark brown, commonly on trunk.
* Histology - localised prolif basal layer of epidermis (often hyperkeratosis in surface crypts)
* Tx - none needed (can do cryotherapy)
What is a sebaceous cyst?
Sebaceous cyst (type of trichilemmal cyst) - cyst below skin surface filled with sebum
* Commonly on scalp/ears/face/back/upper arms (don’t affect palms of hands or soles of feet)
* If infected may required I&D/surgical excision
BCC vs SCC vs Malignant Melanoma
BCC believed to arise from pulripotent SCs in basal layer epidermis/follicular structures = most common malig, slow-growing, rarely mets
* Middle/elderly caucasians, UV exposure, male
* PC: non-healing sore “rolled-edge” on face/ears/scalp/neck/upper trunk, mild trauma -> bleeding
* Tx: Imiquimod, 5-flurouracil, curettage and cautery (if deeper needs excision, if cosmetically sensitive can do Moh’s micrographic surgery, radiotherapy if elderly and not surgical candidate)
Cutaneuous SCC is second most common skin cancer (20%) - malig tumour of epidermal keratinocytes -> can have local infiltrative growth (and to LNs/lungs)
* Elderly (rare <60yrs unless IS) , UV exposure, can arise de novo or from acitinic keratoses (pre-cancerous)
* Rapidly expanding painless ulcerated nodules, cauliflower-appearance w/ bleeding/ulceration/serous exudation often in head & neck (55%, 25% hands/arms)
* Tx: topical meds/surgery
Malignant melanoma - 4% skin cancers, biggest cause skin cancer deaths.
* GLASGOW 7 for Melanoma
- 3 Major - size, shape, colour
- 4 Minor - Diameter >7mm, inflammation, oozing/bleeding, itch/odd sensation
* Most common sites: lower leg in women, trunk in men
* Tx: surgery
Pina cellulitis vs perichondritis
Pina cellulitis is complication of acute otitis externa/eczema/psoriasis/insect bite
* Causative organism: S. aureus
* PC: involves entire ear including lobe
Pina perichondritis due to penetrating trauma e.g. ear piercing - if untreated abscess form lifting perichondrial layer from cartilage -> necrosis and cauliflower deformity -> can progress to systemic infection/nec fasc
* Causative organism: P. aeruginosa
* PC: spares ear lobe
* T2DM predisposes
Red flags - abscess/necrosis, central neuro signs including low GCS
Tx: remove piercing, in early infection abx mainstay, if abscess/necrosis for surgery, CT if cranial concerns, plastic surgery for deformity
What condition is characterised by telangiectasia, recurrent epistaxis and FHx.
Osler-Weber-Rendu Syndrome (Hereditary haemorrhagic telangiectasia) - AD characterised by telangiectasia (90% affected from 20s), recurrent epistaxis and FHx.
* Morbidity/mortality due to multiorgan AV malformations -> haemorrhage
* Main systems - nasal mucosa/skin, GI tract, pul vasculature, brain
* Tx: blood transfusions (up to 30% pts), surgery (up to 50% pts)
Please identify what is going on in each of these otoscope exams
Top left - otitis externa - canal erythematous/oedematous/swollen with exudate. Movement of tragus/auricle often causes pain
* Superficial inf skin (P. aeruginosa, S. aureus) of ear canal (from trapped moisture/trauma)
* PC: irritation (meatal tenderness on pinna mov), scanty discharge, conductive hearing loss
* Complication: necrotising (malignant) OE if IS/radiotherapy to skull base - bacteria inf deep soft tissue and can cause osteomyelitis of temporal bone
* Tx: abx ear drops
Middle bottom - otitis media, middle left - otitis media with perforation, middle bottom - otitis media with effusion (glue ear - fluid collection in middle ear space without evidence of active inflam)
* **Chronic suppurative otitis media (CSOM) **is a complication of otitis media - chronic inflam of middle ear/mastoid cavity –> over 2wks painless recurrent otorrhoea via tympanic perf +/- hearing loss (often improves)
- Unsafe if atticoantral (top, safe if tubotympanic) or involves cholesteatoma
- Mx: GP should not swab/innitiate Tx -> refer to ENT & advise keep ear dry, admit if evidence of infection, secondary care - topical abx/steroids, microsuction, surgery (myringoplasty/tympanoplasty), if persistent hearing loss for audiology.
Top right - Bullous Myringitis = inf middle ear (like otitis media) but has tympanic membrane vesicles (if vesicles elsewhere consider other Dx e.g. Ramsay-Hunt)
* Due to viral (RSV/influenza) or bacterial (strep pneumo/mycoplasma pneumo) or fungal from adjacent epidermis
* Commonly boys 2-8yrs (OM = boys <2yrs)
* PC: mod/severe ear pain & fever (both less common in OM), 50% sensorineural deafness (conductive if middle ear effusion) +/- blood otorrhoea
* Tx: same as OM but more often needs oral abx (amox), pure tone audiogram, myringotomy (if refractory)
* Prognosis: good (hearing loss/vestibular dysfunct normally transient)
Top middle - cholesteatoma - destructive lesion of expanding keratinizing squamous epithelium in middle ear/mastoid process –> local expansion can cause damage to adjacent vital structures (dura/lateral sinus/facial nerve/SC canals)
* Congenital/acquired (primary accum within retraction pocket or secondary ingrowth of skin through perf)
* Hallmark = painless constant/frequent otorrhoea (+/- conductive hearing loss, dizzyness, neck abscess, central nervous system complications)
* Otoscopy - deep retraction pockets in tympanic membrane +/- granulation tissue/skin debris. Crusty lesion (yellow) in upper membrane, pus, tympanic perforation in 90% (if congenital less common)
* Tx: surgical removal
Pt with HIV presents with this opthalmologic exam
CMV Retinitis
* Most common CMV mainfestation in HIV
* “Pizza” fundus - retinal spots and flame haemorrhages
* Decreased visual acuity, floaters, loss of visual fields on one side –> can lead to blindness
* Tx: ganciclovir
Define Uveitis
Uveitis - inflammation of uveal tract (iris, chorids, ciliary body)
* Anterior uveitis (iridocyclitis) - involves iris & ciliary body
* Posterior uveitis (choroiditis) - involves choroids (uncommon except in CMV retinitis in AIDS)
Idiopathic, trauma or assoc with diseases linked with HLA-B27:
* Ankylosing spondylitis, reactive arthritis, juvenille idiopathic arthritis, psoriasis
* IBD, Sarcoidosis, Inf (HZV, HSV, Syphilis)
PC: pain, photophobia, ciliary injection (red limbus), lacrimation, blurring
Talbot’s test +ve - pain on pupil convergence (constriction)
What is this skin condition?
Lichen Planus - pruritic papular erruption, purple colour, polygonal shape +/- fine scale
* Flexor surfaces of upper extremeties/genetalia/mucous membranes
* Cause - immunologically-mediated reaction
* Tx: antihistamines, weak coal-tar, 1-2% menthol in calamine lotion, topical steroids
What is this skin condition?
Lichen simplex chronicus - skin thickening with variable scaling secondary to scratching/rubbing - mechanical trauma to point of lichenification (often caused innitially by eczema/insect bit/scar/venous insufficiency)
PC: localised itchy demarcated plaque (>5cm) with scaling, excoriations and lichenification
* Common sites - calf, elbow, behind neck, genitalia (vulva/scrotum)
Tx: potent topical steroids (intralesion st inj if resistant), tar/ichthyol preperations, occlusive dressings, oral antihistamines
Give an overview of Bell’s Palsy vs Ramsay Hunt Syndrome
Bell’s Palsy - LMN facial palsy (affects all branches of f nerve vs UMN temporal spared)
* Cause - latent HSV1/HZV reactivated from cranial nerve ganglia
* PC: unilat/sudden - facial distortion, watery eye, hypersensitive to sound, loss of taste
* Tx: oral pred (50mg OD 10d) if presenting within 72hrs
Ramsay Hunt Syndrome
* Cause - VZV reactivation in geniculate ganglion of facial nerve (or glossopharyngeal/vagus)
* Elderly, deep pain in ear +/- sensorineural deaf/vertigo/LMN facial palsy (recovery less likely than BP)/rash or blisters (skin of ear canal/auricle)
* Tx: acyclovir/steroids
Differentials of unilat eye pain & blurring?
Give an overview of retinal detachment?
Retinal detachment is seperation of inner neurosensory retina and outer retinal pigment epithelium - gap becomes filled with subretinal fluid
* Classification: Rhegmatogenous (most common, sensory retina detaches due to retinal break), Non-R (tractional - vitreous contracts in prolif diabetic retinopathy, exudative - damage of retinal pigment epithelium (HTN) -> leaking subretinal fluid)
* RFs: posterior vitreous detachment, previous RD, high myopia, FHx, prev eye surgery, trauma
*PC: 4Fs (floaters, flashes, field loss, fall in acuity - painless curtain falling)
* Tx: Surgery
Vestibular neuritis vs Labyrinthitis?
Vestibular neuritis - recurrent vertigo lasting days
* Preceding viral illness
* Hearing not affected, no tinnitus (as in labyrinthitis)
* Complete recovery in wks
Labyrinthitis - inflam disorder of inner ear secondary to inf (URTI in 50%)/ischaemic event (elderly)
* PC: vertigo, sweating, N/V, tinnitus, SN deaf, nystagmus away from lesion
* NOTE: If recurrent attacks rare instead suspect Meniere’s
* Mx: Anti-emetic (prochlorperazine/promethazine/cyclizine), vestibular sedative (Ca-ch & histamine antag - Cinnarizine, hist analogue - betahistine)
Give an overview of Acne Vulgaris?
Pilosebaceous unit becomes blocked by keratin plug –> comodones (white/blackhead), papules/pustules, cysts/nodules affect face/chest/back
* Androgenic hormones -> high sebum production - NOTE: cutibacterium acnes prolif within sebum in hair follicles
* Starts at puberty resolves with age - affects 95% adolescents in western countries
* Conglobate acne - rare and severe in men - extensive inflam papules/supurative nodules/cysts on upper trunk/arms
* Acne fulminans - sudden severe inflam reaction -> deep ulceration/erosions +/- systemic effects (fever/arthralgia/myalgia)
* Things worsening acne: hormones (PCOS, POP), drugs (CS), makeup, trauma/stress/environ/diet, UV light
Tx:
* Topical - retinoid/azelaic acid/benzoyl peroxide/abx
* Oral - abx such as tetracyclines e.g. doxycycline
* In pregnancy - benzoyl peroxide advised
Complications: scarring, keloid scar, hyper/depigmentation
What is bacterial cause of Impetigo? What is Tx?
S. aureus
Hydrogen peroxide 1% cream
Retinal vein vs artery occlusion
Retinal vein occlusion - interruption of normal venous drainage from retinal tissue - either central vein (CRVO) or branch (BRVO) occlusion
* Painless, sudden, unilateral vision loss
* RFs: young - hypercoag/vasculitis, old - HTN/DM/atherosclerosis/glaucoma
* Tx focused on vision-threatening complications e.g. macular oedema/neovascularisation –> vascular endothelial growth factor (VEGF) inhibitors/intravitreal corticosteroids
Retinal artery occlusion - rare but common cause of blindness in elderly.
* Causes - embolus, sudden vessel narrowing (e.g. haemorrhage into atheromatous plaque) or inflam (e.g. temporal arteritis)
* PC: >60yrs, sudden painless vision loss, poor light reactivity (consensual reflex normal)
* Opthalmic exam: retina pale/opaque from oedema, retinal arteries irregular (red threads), fovea = cherry red spot, optic atrophy after wks (optic nerve white)
* Mx: OPTHALMOLOGICAL EMERGENCY -> refer to eye ED
Diabetic eye complications overview
Most common = diabetic retinopathy
* Chr progressive, sight-threatening of retinal microvasculature assoc w/ prolonged hyperglycaemia
* RFs: poor glycaemic control, HTN/CVD, renal disease, pregnancy
* Retinal findings: microaneurysms (capillary outpouching), hard exudates (resorption of retinal oedema), small dot/blot (in inner nuclear layer of retina)/flame haemorrhages (in nerve fibre layer), cotton wool spots (soft exudates), neovascularisation
* Classification DR: 1. BG (mild) non-proliferative - ≥1 microaneurysm 2-3. Moderate-severe non-prolif - prev + haemorrhages/cotton wool spots 4-5. Proliferative - prev + neovascularisation
* Diabetic maculopathy: focal/diffuse macular oedema (from capillary leak), ischaemic maculopathy (visual acuity drop + ischaemia on fluorescien angio), CSMO (clin-sig macular oedema - thick retina/hard exudates)
* PC: Painless gradual reduction in central vision/asymptomatic/floaters
* Gold standard for Dx - dilated retinal photo
* Mx:
- Screening, good glycaemic control HbA1c <7%/BP (≤140/80)/lipid
- Laser Tx (doesn’t restore lost vision), anti-VEGF intravitreal inj/steroids, vitrectomy
- Prognosis - unTx 50% lose sight in 2yrs, 90% lose all useful vision in 10yrs
Cataracts - opacification of lens (earlier in diabetics)
* Gradual vision loss +/- burred vision + glare (driving at night)/appear increasingly myopic (short-sighted)
* Tx: replace lens - can develop opacification of posterior capsule behind replacement –> Tx with neodymium-doped yttrium aluminium garnet laser (opening in opacified lens)
Less common associations:
* Premature presbyopia - from lens pliability
* Rubeosis iridis - severe ischaemia causes neovascularisation (vessels grow forward/over iris) - if block trabecular meshwork can cause acute glaucoma
Give an overview of age-related macular degeneration
- Most common cause of severe irreversible visual impairment in older adults in developed world
- Drusen (lipid material collects below retinal pigment epithelium RPE) in macula + chroidal neovascularisation (wet AMD) or geographic atrophy (dry AMD)
Types:
* Dry AMD - 90% cases -> gradual vision loss, end-stage is whole of macula affected causing central vision loss (8% chance each year of progressing to wet AMD)
* Wet AMD (exudative) - 90% cases of severe visual loss - neovascularisation under/above RPE - easily bleed/leak -> distortion/scarring retina -> severe visual impairment in 2yrs unTx - end form = disciform MD (scar formation)
PC:
* Asymptomatic
* Blurred vision >50yrs (wet - develops quickly, dry - slow)
* Metamorphopsia - straight lines appear bent
* Scotoma - black/grey patches in central vision
* Other - light glare, reduced contrast sensitivity, abn dark adaptation, photopsia (flickering light), Charles Bonnet Syndrome (visual hallucination)
Fundoscopy - drusen, macular pigment/exudative/haemorrhagic/atrophic changes
Mx: opthalmology referral (see within 1wk)
* Dry AMD - visual rehab & lifestyle advice
* Wet AMD - intravitreal inj anti-VEGF (vascular endothelial GF) e.g. ranibizumab –> side effect can be endophthalmitis (eye pain/redness/burring/discharge)
Visual field defects in temporal vs pariental lesions
Temporal lesion damages inferior optic radiations -> superior quadrantonopia of contralateral side of both eyes
Parietal lesion damages superior optic radiations -> inferior quadrantonopia of contralateral side of both eyes
Pupillary abnormalities Overview
Anisocoria (unequal pupil size)
* NAD (20%) - ≤1mm difference
* Congen iris abn
* Mechanical (iris damage)
* Pharm - mydriasis (bigger - antichol e.g. atropine, sympath e.g. adrenaline), miosis (smaller - pilocarpine, prostaglandins e.g. latanoprost, opioids)
* Horner’s syndrome (oculosympathetic palsy) = miosis, ptosis, anhidrosis, enopthalmos - causes:
- Central lesion - stroke/demyelinarting disease
- Preganglionic lesion - pancoast/mediastinal/thyroid
- Postganglionic lesion - carotid artery dissection, cavernous sinus lesion, otitis media
* Oculomotor (CNIII) nerve palsy - if pupil involved = pupil fixed and dilated, other = ptosis, ipsilateral “down and out” pupil, loss of accomodation
- Involve pupil causes (as affect superficial PS fibres innervating pupil) = compressive lesions (head trauma, IC aneurysms, uncal herniation, tumour)
- Don’t affect pupil causes = ischaemic/diabetic
* Trigeminal autonomic cephalgia - unilateral head pain + ipsilateral autonomic Sx (lacrimation/rhinorrhoea)
Impaired pupillary light reflex
* Optic nerve (II) damaged = info not received - direct light reflex lost & consensual light reflex in other eye lost (if damage at optic chiasm still ipsilateral connections intact so all light reflexes intact)
* Occulomotor (III) nerve damaged = info received but OP damaged - no direct light reflex but consensual intact
* RAPD (Marcus Gunn pupil) - unilateral lesion in affererent visual pathway anterior to chiasm = on stim of normal eye full constriction B/L then on stim of affected eye partial constriction B/L
* Non-reactive pupil
- if unilateral, fixed, dilated - injury/compression CN III/upper brainstem/pharm blockade
- If bilateral, fixed, dilated - extensive IC pathology/pharm blockade
Near-light dissociation pupils
* Argyll Robertson - B/L tonically small pupils, react poorly to light but briskly to accomodation –> neurosyphillis
* Holmes-Adie - large irregular pupil slow to constrict (& prolonged constriction) but normal on accomodation –> damage to efferent PS/idiopathic
* NOTE: most today HA as neurosyphillis very rare with modern Tx
