CP2 - DOE

Causes of vocal cord motion impairment, including understanding of recurrent laryngeal nerve anatomy

1) 2nd commonest cause of stridor in neonate 2) unilateral: iatrogenic 3) bilateral: idiopathic, need scan 4) recurrent laryngeal nerve palsy or paresis - a) anatomy - I) recurrent laryngeal nerves (L&R) branches off vagus nerve (CN X) that supplies all intrinsic muscles of larynx, except cricothyroid muscles. L nerve loops under aortic arch, & R nerve looping under R subclavian artery then traveling upwards. Both travel alongside trachea II) supply sensation to larynx below vocal cords, gives cardiac branches to deep cardiac plexus, and branches to trachea, oesophagus and inferior constrictor muscles III) posterior cricoarytenoid muscles (only muscles that open vocal cords) innervated by RLNs b) pathology - 75% LHS, 15% RHS, 10% both c) aetiology - I) miscellaneous II) surgical trauma eg/ thyroidectomy III) malignant eg/ Ca bronchus, thyroid, oesophagus IV) idiopathic, neurological disorders

Features of 3rd, 4th and 6th cranial nerve palsies

1) 3rd CN palsy - a) affects MR, IR, SR, LPS, pupil b) SO & LR spared c) eye points down and out d) complete ptosis e) dilated pupil (efferent defect) - apparent in bright light f) no afferent defect g) course of CN3 from EWN in midbrain till enters orbit is closely associated with PCA. Painful CN3 palsy with pupil involvement due to compression if oculomotor CN with aneurysm of PCA - urgent Ix with MRI (angiography) for confirmation due to potential risk of rupture of aneurysm. Needs surgery for aneurysm tx to prevent intracranial haemorrhage +/- stroke h) aetiology - I) brain stem: tumour, CVA, demyelination II) skull: PCA aneurysm, extradural haematoma III) cavernous sinus: carotid-cavernous fistula, tumour, inflammation (other CNs also affected) IV) orbit - trauma, inflammation, tumour V) vascular III palsy - diabetes/BP, pupil spared, self-limiting NB/ CN palsy in children always abnormal - either tumour or trauma 2) 4th CN palsy - a) SO affected b) eye unable to look down & in on affected side c) so vertical diplopia - esp looking down & in d) bilateral cases with head injuries e) head tilt test on affected side causes eyeball to look up (also happens when use MR) 3) 6th CN palsy - a) LR/abducens palsy b) inability to abduct c) eye may drift medially on affected side due to pull of MR 4) 7th CN palsy - a) pt unable to close eye & blink properly - cornea dries (exposure keratitis, infection) b) may cause exposure hence: I) test corneal sensation II) test bell's phenomenon (eyeballs roll up when close eye

Different grades, diagnosis, management, effects on patient's life & how patients may be helped to cope with poor vision due to macular degeneration

1) AMD - a) progressive central visual loss - blind spot in central vision b) bilateral (1 eye involved initially) c) commonest cause of visual loss > 50 years, leading cause of blindness 2) risk factors - a) age b) smoking c) CV: HTN, hyperlipidaemia d) dec antioxidant levels in blood 3) 2 types of AMD- a) dry - I) atrophy of photoreceptors in retinal pigment cells II) Drusen +/- geographical atrophy, then - III) RPE/Choroidal atrophy & sensory detachment - gradual death of macula, then - IV) RPE & sensory haemorrhagic detachment & fibrous scar V) pigmentary changes - slow & gradual loss of central vision VI) difficulty recognising faces & reading VII) no tx yet - visual rehabilitation, visual aids b) wet - I) choroidal neovascularisation II) new BV proliferate & penetrate Bruch's membrane - leak & bleed, causing scars III) classic or occult based on FFA IV) distortion of vision & sudden loss of central vision - urgent referral, progresses to central scotoma V) 10% cases of ADM, but 80-90% severe visual loss in AMD

Identify common and significant tympanic membrane pathology including AOM, OME

1) AOM - a) acute middle ear infection (viral / bacterial/ barotrauma) b) most common specific diagnosis of a febrile illness in children c) symptoms - preceding URTI, pain, deafness, fever, ear tugging, irritability, poor feeding I) classic hx - pain, high fever, ear discharge (as TM ruptures) & pain improves (blood + pus) d) exam - hyperaemia, red full bulging (with pus) TM, perforation, pyrexia, dec TM mobility e) aetiology - S pneumoniae, H influezae, M catarrhalis (or viral - 50% eg/ RSV, parainfluenza, rhinovirus, enterovirus, CMV, barotrauma) 2) OME - a) pathology of adenoids - I) adenoids - acute infection (bacteria or virus) = II) ciliary dysfunction (also from smoking) + ET dysfunction = III) impaired mucous clearance = OME b) pathology of other causes - I) polymorphism, biofilms, allergy, reflux = II) inflammatory cytokines = mucin upregulation = viscous fluid in ME = III) impaired mucous clearance = OME c) chronic OM with effusion (aka glue ear) - fluid, no s/s of acute inflammation/infection d) peak at 3-5 yrs old e) commonest cause of deafness in children in developed world (affects up to 80% kids) f) sterile fluid in middle ear cleft = conductive deafness of 10-40 dB & flat tympanogram g) OME may follow URTI & resolve spontaneously in weeks - 50% OME follows AOM h) otoscopy - varied appearance, -ve ME pressure, horizontal handle malleus, cone-shaped PT, neo-annular fold, colour change: grey to blue, opaque PT, tympanometry i) most commonly occurs in children who may or may not have large adenoids, previous acute suppurative otitis media or a cleft palate j) problems - hearing loss, school, speech delay

Describe to a patient the management of AOM or tympanic membrane perforation may be, including ear care and how to administer drops

1) AOM - a) tx in GP - I) analgesia II) only give abx if <6/12 old, risk of infectious complications, symptoms >4 days, systemically unwell, (bilateral, perf/discharge, <2 yo) eg/ PO amoxicillin III) aminoglycoside or cipro drops if discharge IV) burst ear drum heals within 4-5 days b) ENT referral if not settling or complication (eg/ mastoiditis, facial palsy, intracranial sepsis) I) myringotomy if fails to resolve or facial nerve palsy, or other complication eg/ brain abscess 2) TM perforation - a) avoid eardrops with gentamicin, neomycin sulfate, or tobramycin b) systemic abx when otorrhea from TMP c) cauterization of edges of TMP with eg/ trichloroacetic acid d) fat-plug tympanoplasty e) tympanoplasty

Different types of OM - acute otitis media & recurrent OM

1) AOM - acute middle ear infection (viral / bacterial/ barotrauma) a) most common diagnosis of febrile illness in kids b) symptoms - preceding URTI, pain, deafness, fever, ear tugging, irritability, poor feeding I) classic hx - pain, high fever, then ear start to discharge (TM ruptures) & pain improves - blood + pus c) exam - hyperaemia, red full bulging (with pus) TM, perforation, pyrexia, dec TM mobility d) aetiology - S pneumoniae, H influezae, M catarrhalis (or viral - 50% eg/ RSV, parainfluenza, rhinovirus, enterovirus, CMV, or barotrauma) e) tx in GP - I) analgesia II) only give abx if <6/12 old, at risk of infectious complications, symptoms >4 days, systemically unwell, (consider if bilateral, perf/discharge, <2 yo) eg/ PO amoxicillin III) aminoglycoside or cipro drops if discharge IV) burst ear drum heals within 4-5 days f) ENT referral if not settling or complication (eg/ mastoiditis, facial palsy, intracranial sepsis) - myringotomy 2) recurrent AOM - ≥3 in 6 months, ≥4 in 12 months a) tx - I) mostly get better after 2 yrs old II) avoid pacifiers III) treat each episode individually - IV) long term abx eg/ azithro weekly V) grommets

Diabetic retinopathy

1) DM - a) diabetes affects 2% UK population b) diabetic retinopathy is commonest cause of visual impairment in working age (20-65yr olds) c) most blindness associated with DM preventable d) diabetics = 25x inc risk of blindness 2) diabetic retinopathy - a) retinal vasculopathy due to DM b) affects retinal precapillary arterioles, capillaries and venules c) retinal disease may be vascular leakage +/- closure & sequelae d) sequelae related to VEGF & factors released in retina after metabolic changes in DM & retinal ischaemia 3) diabetic retinopathy risk factors - a) duration of DM & level of control b) age c) smoking d) HTN & hyperlipidaemia e) renal impairment f) pregnancy 4) 3 types of diabetic retinopathy - a) non-proliferative DR (NPDR) or 'background' DR (BGR) - no proliferation of BV b) proliferative (PDR) - abnormal new BV growing c) diabetic maculopathy - special retinopathy, may occur with either NPDR or PDR

Questions relating to malignancy presentation, including hoarse voice, swallowing, pain, neck lump, stridor, airway obstruction

1) H&N cancer = malignant tumours in oral cavity, pharynx, paranasal sinuses, nasal cavity. Larynx, salivary glands, thyroid, or skin. 6th most common cancer worldwide. More common in men & elderly 2) common symptoms - a) persistent pain in throat b) odynophagia c) dysphagia d) persistent hoarseness or a change in voice e) referred otalgia f) bleeding in mouth or throat g) enlarging neck node h) persistent ulceration, leukoplakia or erythroplakia j) weight loss unusual - if present is secondary to dysphagia, or odynophagia 3) other possible s/s - a) lump or thickening in oral soft tissues b) soreness or feeling something stuck in throat c) difficulty chewing or opening of mouth d) difficulty moving tongue e) numbness of tongue or other parts of mouth f) swelling of jaw that causes dentures to fit poorly or become uncomfortable

Extraocular muscle anatomy and why the muscles have primary, secondary and tertiary actions

1) MR - adduction, insert horizontally on globe, CN 3 2) LR - abduction, insert horizontally on globe, CN 6 3) up & out = SR - elevation, secondary = intorsion, tertiary = adduction, inserts on globe at 23 degrees to medial wall of orbit, CN 3 4) up & in = IO - extrusion, 2 = depression, 3 = abduction, inserts on globe at 51 degrees to medial wall of orbit, CN 3 5) down & out = IR - depression, 2 = extorsion, 3 = adduction, inserts on globe at 23 degrees to medial wall of orbit, CN 3 6) down & in = SO - intorsion, 2 = depression, 3 = abduction, inserts on globe at 51 degrees to medial wall of orbit, CN 4 7) extraocular muscles don't work in isolation - have secondary & tertiary actions 8) LR6 SO4 AO3 (CN3 also innervated pupils & upper lid) 9) all but MR & LR have secondary and tertiary actions due to insertions at 23 and 51 degrees onto orbit

Different grades, diagnosis, management, effects on patient's life & how patients may be helped to cope with poor vision due to diabetic retinopathy

1) NPDR - a) usually asymptomatic b) after >8-10 yrs DM (occurs in all diabetics) c) mild, moderate or severe depending on risks d) microaneurysms, exudates, retinal haemorrhages, cotton wool spots, vascular dilatations, calibre variations, intraretinal microvascular abnormalities (IRMA) NB/ haemorrhages: dot (small), blot (large) from venous end of retinal capillaries deep in retina; flame shaped haemorrhage (more arterial) NB2/ exudates: yellowish-white deposits with well-defined edges; precipitation of leaked lipoproteins from diseased retinal vasculature NB3/ cotton wool spots (CWS): greyish white, poorly defined fluffy edged lesions, axoplasmic accumulations adjacent to retinal nerve fibre microinfarcts e) severe NPDR - many dark haemorrhages, irregular calibre variation (beading), dilatation of retinal veins, IRMAs. Most progress to PDR in 1yr 6) PDR - a) occurs in ~ 5% of DM b) more common in Type 1 than Type 2 DM c) neovascularisation on optic disc or retina from significant retinal ischaemia d) neovascularisation - I) v fine irregularly branching BV arising from veins II) start flat but enlarge & move forward into vitreous III) fragile, likely to bleed with slight traction = pre-retinal +/- vitreous haemorrhage e) PDR late changes - I) retinal fibrosis II) traction retinal detachment (blurred vision) III) iris neovascularisation (rubeosis iridis) and neovascular glaucoma

Role of speech therapists in management of voice and swallowing disorders, and use as part of voice MDT

1) SLT ENT service - a) assessment & rehabilitation of swallowing, voice & speech problems caused by: H&N cancer, benign organic pathology, muscle tension or imbalance, psychogenesis b) services - MDT, inpt dysphagia/voice assessment & mx, outpt swallowing diagnostic clinics & therapy, outpt laryngectomy & H&N cancer therapy, outpt voice diagnostics & therapy including laryngeal review clinic 2) outpt voice therapy - a) vocal hygiene advice b) targeted vocal function exercises c) digital manipulation d) counselling/onward referral e) environmental modification f) professional voice users workshops g) laryngeal review / biofeedback 3) voice therapy - a) successful in eliciting normal voice in 1st session of SLT (humming techniques into automatic speech tasks), 2 further sessions to consolidate b) exploration of causative and contributory factors - identified anger & stress c) referral on to clinical psychology

Be able to form a differential diagnosis based on history and examination e.g. SNHL, conductive hearing loss, subjective versus objective tinnitus, pulsatile tinnitus, presbyacusis, otosclerosis, noise induced hearing loss, ototoxicity

1) SNHL - a) problem with reception & transmission of info from cochlear. Inner hair cells convert mechanical energy of sound transmitted into cochlear into electrical activity. Electrical activity transmitted through nerves to CNS b) speech discrimination often difficult 2) conductive hearing loss - a) problem with loudness so shouting helps b) hearing aids excellent tx 3) subjective vs objective tinnitus - a) subjective tinnitus - perception of sound in absence of acoustic stimulus & heard only by pt. Most tinnitus is subjective b) objective tinnitus - uncommon, from noise generated by structures near ear. Sometimes tinnitus is loud enough to be heard by examiner 4) pulsatile tinnitus - a) rhythmic pulsing often in time with heart. Experienced as a thumping or whooshing sound. Often vascular in origin 5) presbyacusis - a) higher-pitched sounds of speech (consonants) sound unclear & indistinct - unable to understand communication in noisy places 6) otosclerosis - a) progressive conductive hearing loss, normal TM, no evidence of middle ear inflammation b) cochlear promontory may have faint pink tinge reflecting vascularity of lesion = Schwartz sign c) found on CT imaging 7) noise induce hearing loss - a) industrial noise or social noise b) if pt in one of above & their ears ring (noise induced tinnitus), they've been exposed to noise levels that could, with repeated exposure, permanently damage their hearing c) after noise exposure hearing muffled for several hours usually recovering next day d) these temporary auditory phenomena = noise induced tinnitus and temporary threshold shift 8) ototoxicity - a) abx eg/ gentamicin b) loop diuretics eg/ furosemide c) platinum-based chemo eg/ cisplatin d) some NSAIDS e) SNHL, dysequilibrium, or both f) some environmental & occupational chemicals shown to affect auditory system & interact with noise

Mx of bacterial rhinosinusitis in primary care setting

1) acute - a) mostly self-limiting b) simple analgesics, steam inhalations c) topical decongestant - dec nasal oedema & improve drainage of sinuses. Topical xylometazoline spray, for <5 days to avoid rhinitis medicamentosa d) steroid nose spray (oral steroids?) e) abx if high fever / severe pain - Penicillin or Amoxicillin for 7-14 days 2) chronic - a) aims - ventilate sinuses & restore mucociliary clearance b) trial of medical therapy - broad-spectrum oral abx eg/ coamoxiclav, clindamycin metronidazole & penicillin for >3 weeks c) topical nasal steroids eg/ betamethasone drops for 2 months, then steroid nasal spray (continue after 8 weeks if helps) d) nasal drops whilst pt lying on bed with head upside down over edge e) unusual for no response to medical tx f) nasal douching - ½ teaspoon of salt & sugar & bicarbonate of soda in 2 pints of boiled water, which has been left to cool. Draw some up with a syringe. Block off 1 nostril with finger then sniff or squeeze up solution into other nostril, letting it run out afterwards. Topical sprays and drops taken after douching g) surgery if fails after 3 months: adenoidectomy (± sinus washout)

Identify when referral to ENT is indicated e.g. failed medical management, red-flag symptoms

1) acute rhinosinusitis - a) ARS usually responds to medical treatment b) refer if: I) progressive pain - sinuses may need draining & urgent referral to an ENT surgeon II) s/s of potential complications requiring immediate referral include periorbital cellulitis, severe headaches, focal neurological signs and symptoms of meningitis 2) chronic rhinosinusitis - a) if no improvement after 8 medical tx, consider referring to ENT specialist - pt should undergo nasendoscopy to confirm diagnosis b) in persistent cases not responded to max medical tx, CT of paranasal sinuses 3) red flag signs - a) tumour mass - unilateral polyp, inflammatory polyps are pale yellow & bilateral b) forehead swelling - Potts puffy tumour, osteomyelitis of frontal sinus c) eye displaced due to mucocele - mucous cyst in sinus with mass effect d) consider other diagnosis if - unilateral symptoms, bleeding, crusting, cacosmia e) orbital symptoms - periorbital oedema/erythema, displaced globe, double or dec vision, ophthalmoplegia f) severe frontal headache - frontal swelling, signs of meningitis, neurological signs

Signs, symptoms, and mx of orbital cellulitis

1) acute sight threatening & potentially life-threatening emergency 2) infection behind orbital septum - can be secondary to ethmoiditis 3) s/s - a) severe malaise & fever b) eyelid oedema & redness c) proptosis (most frequently lateral & down) d) painful ophthalmoplegia e) optic nerve dysfunction if advanced 4) if left can have complications eg/ a) inc IOP b) retinal vasculature occlusion c) optic neuropathy d) orbital or subperiosteal abscess e) meningitis f) cavernous sinus thrombosis 5) tx - a) acute hospital admission b) systemic abx c) monitoring of optic nerve function d) indications for surgery: resistance to abx, orbital or subperiosteal abscess, optic neuropathy

Different causes of 'red eyes' and their management

1) aetiology - a) haemorrhage I) subjunctival - posterior edge of blood patch visible. Mostly not serious II) retrobulbar - posterior edge not visible, proptosis (white or red above & below iris), dec eye mvmt, inc pressure, pupil reaction (optic nerve function compromised - emergency, can = blind) III) causes - trauma, head injury, bleeding disorders, iatrogenic b) congestion - I) localised - episcleritis, phlyctenular, conjunctivitis II) generalised - conjunctivitis, keratitis, iridocyclitis, uveitis, acute glaucoma 2) uveitis - a) inflammation of iris & ciliary body b) keratic precipitates formed c) constricted pupil d) synechiae (iris adhesions) e) usually unknown aetiology f) tx - depends on cause & area of eye affected, steroids eg/ prednisolone - corticosteroid eyedrops (ant eye) or injections (middle or back) or tablets, mydriatic eyedrops (ant), anti-virals/fungals or abx, immunosuppressants, rarely a vitrectomy, symptom relief 3) conjunctival congestion - a) predominantly in conjunctival fornices b) superficial vessels c) bright red in colour d) blanch with topical vasoconstrictors e) move with conjunctival folds f) centripetal (from fornix to limbus) blood flow g) tx - rest eyelids, eye douche, if chronic - apply mild astringent eg/ solution of sulphate of zinc 4) ciliary or circumcorneal congestion - a) predominantly around cornea: b) deeper (anterior ciliary) vessels c) dusky red in colour d) do not blanch with topical vasoconstrictors e) do not move with conjunctival folds f) centrifugal blood flow g) tx - referral 5) corneal involvement - a) foreign body or trauma b) keratitis - viral, bacterial, immune mediated

Manage perforated tympanic membrane in primary care or ED, knowing when to refer to ENT

1) aetiology: direct trauma, blow, or due to AOM 2) most heal within 6 weeks 3) keep dry 4) GP follow up 6/52 5) ENT to see if: a) severe bleeding b) significant symptoms eg/ deafness, tinnitus, vertigo, facial palsy 6) chronic dry perforations usually from viral infections in childhood & scarlet fever a) unless causing significant deafness or preventing admission to some profession or sport such as swimming, they can be left alone b) if troublesome, grafting is successful in 80% of cases (Myringoplasty)

Common abnormalities of pupillary reflex pathway

1) afferent pupillary defect (APD) - a) pathology in afferent pathway (from retina to EWN, usually retina or optic nerve) b) RAPD - when shine light in non-affected side both pupils constrict, when shine in affected eye input is dec to both EWN so less constriction c) when swing eye from one to the other pupil constriction amount changes d) APD - no direct or consensual response e) RAPD - dec light & consensual response, pupil dilates on swinging light test f) cause - damaged optic nerve or severe retinal disease eg/ optic neuritis, severe glaucoma, direct optic nerve damage, infection (CMV, herpes) NB/ anisocoria = asymmetry in pupil size. Can happen physiologically, but should be <1mm 2) efferent defect - a) efferent pathway - from EWN to CNIII, along inferior division to intraocular muscles eg/ pupil & ciliary body, pathology somewhere in pathway b) pupil on affected side large irrespective of which eye light is shined in 3) Horner's syndrome - a) lesion of sympathetic pathway b) triad of - ptosis, miosis, anhidrosis c) affected pupil is smaller than normal - inequality more pronounced in dark d) may have neck scars (Pancoast tumour?) & eye may appear sunken (apparent enophthalmos) f) aetiology - I) 1st order neurone: CNS disease (tumour, syphilis, MS), cervical (syringomyelia, tumour, injury) II) 2nd order neurone: cervical rib, pancoast tumour, aneurysms, lymphadenopathy, neck trauma III) 3rd order neurone: ICA aneurysm, migraine, idiopathic

Interpret significance of specific symptoms to aid diagnosis and differentiate between allergic / non-allergic / infective rhinitis/rhinosinusitis, structural nasal obstruction (septal deviation)

1) allergic rhinitis a) nasal obstruction, may have hyposmia, nasal irritation, and sneezing b) slightly yellow nasal mucus (staining with eosinophils) but not diagnostic c) on exam - pale & swollen turbinates though mucosa can be red d) associated with certain exposures or time of yr 2) idiopathic rhinitis (non-infective, non-allergic) a) nasal obstruction, clear rhinorrhoea or post-nasal discharge b) itching & sneezing less common than in allergic rhinitis c) CRS, allergic rhinitis and idiopathic rhinitis can occur concurrently 3) infective rhinitis - systemically unwell, preceding URTI (see next) 4) structural - a) caused by trauma (septal haematoma) or complication of septoplasty b) may be as sign of Wegner's granulomatosis c) symptoms: whistling, crusting, bleeding, nasal obstruction d) obstruction - if unilateral may be mechanical obstruction from septal deviation, or polyp 5) nasal sarcoid - crusting, blocking, skin may have lupus kineo (raised skin lesions) 6) dry lining - damage of cilia or nerves in mucousa - feeling of blockage when clear nose, give nasal douching with isotonic solution, & keep moist with vasaline 7) rare causes - vasculitis (Wegeners granulotoma), sarcoid, drug induced (cocaine, some OTC nasal decongestants), autonomic (esp eldery), hormonal (1st trimester of pregnancy) 8) nasal cycle (1 nostril blocks, then switches) and axillo-nasal reflex (lower nostril blocks on side-lying) are normal phenomena

Anatomy of the pupil reflex pathways and common abnormalities associated with the same

1) anatomy - in PR pathway fibres bypass LGN & synapse in pretectile nucleus, then bilateral drive of Edingavespar nucleus 2) pupils & light reflex - a) info transmitted as electrical signal to pretectile nucleus b) then to Edinger-Westphal nucleus & opposite side are stimulated - why pupils on both sides constrict when shine pupil in 1 eye (also due to decussation at optic chiasma) c) pupillary light reflex neural pathway on each side has an afferent limb & 2 efferent limbs d) afferent limb has nerve fibers within CN II - afferent limb carries sensory input: light stimulates photoreceptors - stimulates retinal ganglion cells e) afferent limb consists of retina, optic nerve, & pretectal nucleus in midbrain, at level of superior colliculus. Ganglion cells of retina project fibers through optic nerve to ipsilateral pretectal nucleus f) each efferent limb has nerve fibers running along CN III - efferent limb is pupillary motor output from pretectal nucleus to ciliary sphincter muscle of iris g) pretectal nucleus projects crossed & uncrossed fibers to ipsilateral & contralateral EWN, also in midbrain h) each EWN gives rise to preganglionic parasympathetic fibers which exit with CN III and synapse with postganglionic parasympathetic neurons in ciliary ganglion i) postganglionic nerve fibers leave ciliary ganglion to innervate ciliary sphincter j) each afferent limb has 2 efferent limbs - 1 ipsilateral & 1 contralateral: ipsilateral efferent limb transmits nerve signals for direct light reflex of ipsilateral pupil. Contralateral efferent limb causes consensual light reflex of contralateral pupil j) inc intensity of light = pupil constricts (myosis), dec intensity of light = pupils dilate (mydriasis) k) parasympathetic innervation = pupillary constriction by sphincter pupillae. Controlled by EWN & CN3 & ciliary ganglion l) sympathetic innervation = pupillary dilation by dilator pupillae. Controlled by spinal cord & superior cervical ganglion

Signs & symptoms of dysthyroid disease

1) autoimmune inflammatory disorder of orbit & periorbital tissues - autoantibodies target fibroblasts in eye muscles - fibroblasts differentiate into adipocytes. Fat cells and muscles expand and become inflamed. Veins compressed, & unable to drain fluid, causing oedema 2) s/s - a) commonest cause of eyelid retraction - I) upper & lower lids well above limbus = scleral show II) may be due to sympathetic overactivity III) cosmetic & functional problems b) commonest cause of eyelid protrusion - proptosis c) lid lag aka Von Graefe sign - seen when pt asked to follow moving target from superior to inferior (eyelid doesn't come down quick enough) d) periorbital oedema, chemosis (frequent) e) exophthalmos (proptosis) in 1/3rd - I) proptosis due to secondary endocrine disorder II) most common cause of uni & bilateral proptosis III) permanent in 70% IV) optic neuropathy in 5% exophthalmos f) choroidal folds

Instruct a patient on voice and throat care

1) avoid shouting and whispering 2) avoid irritants eg/ smoking, air conditioning, dust 3) keep well hydrated 4) avoid large meals before bed at night 5) avoid excessive talking 6) too much alcohol, coffee, tea or cola will dry you up 7) try not to clear your throat unnecessarily 8) warm up voice if going to use it for a long time 9) have a humidifier in your workplace 10) drink at least 6-8 glasses of water per day 11) if voice sounds different for 2+ weeks, see a doctor 12) spicy foods and dairy products may affect voice 13) hormonal changes (eg/ menopause, pregnancy or menstruation) can affect voice quality 14) voice is closely linked with emotion, so tension or depression might show in your voice

Causes of facial palsy

1) bells palsy (55%) 2) idiopathic (probably viral) 3) diagnosis of exclusion 4) ramsay hunt (7%): herpes zoster virus 5) middle ear disease: AOM, cholesteatoma 6) trauma 7) tumour 8) infection, lyme disease 9) central cause: MS, CVA

Clinical features of orbital disease and investigations

1) bony orbit of eye - pyramid/pear shaped cavity divided into: a) roof - 2 bones = lessor wing of sphenoid, frontal b) lateral walls - 2 bones = greater wing of sphenoid, zygomatic bone c) floor - 3 bones = zygomatic, maxillary, palatine d) medial wall - 4 bones = maxillary, lacrimal, ethmoid, sphenoid 2) clinical signs - a) soft tissue involvement - I) lid & periorbital oedema II) ptosis III) conjunctival swelling (chemosis) & injection IV) causes - inflammation, vascular abnormalities b) proptosis (abnormal extrusion of globe) - I) direction of protrusion - intra or extra-conal II) proptosis severity - Hertel exophthalmometer III) pseudoproptosis - high myopia, contralateral enopthalmos IV) causes - thyroid eye disease, tumours, inflammation, infection c) enopthalmos (globe recessed in orbit) - causes: I) small globe - nanopthalmos, micropthalmos, phthisis bulbi II) structural bone change - blow out fracture III) atrophy or orbit content - irritation, scleroderma d) ophthalmoplegia - causes: I) tumour II) restrictive myopathy - TED, myositis III) ocular motor nerve lesions IV) trauma - longstanding blow out fractures e) visual dysfunction - I) VA - corneal exposure, ON compression, choroidal folds II) colour vision III) visual field defects IV) dec brightness sensitivity f) dynamic changes - I) inc venous pressure - TED, vascular abnormalities II) pulsation - AV communication, defect in orbital roof III) bruit - sign of carotid-cavernous fistula g) fundus changes - I) optic disc - swelling, atrophy, opticocillary shunt II) choroidal folds (thyroid eye disease) III) retinal vascular changes

Sites of development of branchial cysts / sinuses, thyroglossal duct cysts, preauricular sinuses / tags, nasal dermoid, lymphatic malformations

1) branchial cysts/sinuses - congenital, mostly in teenager/young adult, located at upper third anterior border of SCM, painless swelling 2) thyroglossal duct cysts - congenital, mid line of neck in children & move on swallowing, 80% present before age of 5 3) preauricular sinuses/tags - congenital, nodule, dent or dimple anywhere adjacent to external ear. Mostly unilateral. Result from developmental defects of 1st & 2nd pharyngeal arches 4) nasal dermoid - congenital, sit over bridge of nose. May be completely unconnected with nasal structures, within nose or both a) may have associated passage that leads to skin of nose - may discharge occasionally b) can have internal tract that leads up to coverings of brain & repeated infections may lead to meningitis. Dermoid cysts can contain hair, fluid, teeth or skin glands 5) lymphatic malformations - congenital, present at birth or by 2 years, rare, non-malignant masses consisting of fluid-filled channels or spaces caused by abnormal development of lymphatic system. Can affect any area of body (except brain), most commonly H&N. Tend to be soft, spongy, non-tender masses. Can potentially cause functional impairment of nearby structures or organs and disfigurement of affected areas

Important causes of optic disc swelling

1) central retinal vein occlusion (CRVO) - 'splashed red paint on yellow wall'. Optic disc swollen, multiple flame haemorrhages, veins dilated & tortuous. Cotton wool spots. Sudden loss of vision 2) vitritis with retinochoroiditis - optic disc swollen, yellowish material deep to retina, view blurred as inflammatory debris in vitreous. If settles see scars 3) malignant HTN 4) optic neuritis - a) retrobulbar pain esp on eye mvmt, associated with globe tenderness b) disc may not be swollen, cup & colour normal c) relative afferent pupillary defect d) red desaturation e) central scotoma on field testing f) may have transient neurological symptoms (blurring on exercise, tingling in extremities) g) risk of developing MS (demyelination)

Clinical features indicating supraglottitis / epiglottitis and their investigation and management

1) children aged 3-6 & adults, potentially life threatening (airway obstruction = resp arrest) 2) Hib is commonest - marked erythema & oedema of epiglottis, often onto larynx (dec with HIB vaccine) 3) cardinal features in children - a) may start as URTI, rapidly unwell, toxic, lethargic and febrile (>39), drooling, stridor 4) to avoid airway obstruction - don't upset child causing crying: don't examine throat, send for xray, insert IV cannula, ix & procedures carried out with experienced anaethetist to secure airway 5) ix - a) fibreoptic or direct laryngoscopy b) blood cultures 6) mx - a) endotracheal intubation for 3-4 days (rarely tracheostomy) b) Heliox (Helium and Oxygen mixture) c) IV abx eg/ ceftriaxone d) ? IV steroids

Complications of rhinosinusitis

1) chronic sinusitis 2) osteomyelitis 3) peri-orbital cellulitis & orbital abscess - commonest serious complication: a) direct or blood-borne spread b) ethmoid sinuses separated from orbit by thin plate of bone (lamina papyracea) c) ethmoiditis associated with: cellulitis, 'pre-septal cellulitis', orbital abscess d) mx - peri-orbital cellulitis: high dose abx & hospitalisation e) orbital abscess puts vision at risk from pressure on optic nerve and requires urgent drainage 4) facial cellulitis - extension of: orbital cellulitis, frontal sinusitis or 'Pott's puffy tumour', maxillary sinusitis or osteomyelitis a) tx - high dose abx & sinus drainage 5) mucoceles - late complication of acute sinusitis a) collections of sterile mucus in obstructed sinus (especially frontal & ethmoidal) b) facial swelling, visual disturbances - displacement of eye or secondary infections c) tx - surgical drainage 6) intracranial complications - a) direct spread, venous thrombophlebitis or along perineural tissue of olfactory nerve b) meningitis is commonest complication c) another is cavernous sinus thrombosis - I) spreading thrombophlebitis from frontal, ethmoidal and sphenoid sinuses II) dec venous return from eye so orbit swells & congestion of retinal vessels III) high fever with rigors, severe headache, dec consciousness and cerebral irritation IV) signs - IIIrd, IVth, VIth nerve palsies causing opthalmoplegia in addition to paraesthesia of upper 2 divisions of CNV, frequently bilateral V) tx - high dose abx d) brain abscesses secondary to frontal sinusitis - I) most commonly in the frontal lobe II) subtle changes in personality, headaches, grand mal convulsion or incidentally on CT scan III) tx - neurosurgical drainage or aspiration e) extradural abscess from frontal sinusitis - I) from dehiscence of posterior wall of frontal sinus II) drained into frontal sinus & hence externally f) subdural abscess from frontal sinusitis I) general malaise, headache, neck stiffness, signs of inc ICP II) diagnosis made on exam & CT scan g) effortless vomiting

Take a history relevant to lymphadenopathy in a child in primary care or ED, perform examination, and determine the likely aetiology and need for further investigations or referral

1) common: usually benign/reactive 2) hx - a) characteristics of LN - I) onset, size, duration II) is it painful or erythematous III) generalized or local IV) associated symptoms b) recent infections - URTI, respiratory symptoms, rashes, changes in bowel movements or voiding patterns, bone or joint pain, changes in vision, headaches c) constitutional symptoms - fever, night sweats, weight loss d) skin lesions or trauma - cat scratch, animal/insect bites, other open wounds, dental abscesses e) general health - hospitalized in the past? Ongoing medical conditions? Surgeries? Visits to ED? f) recent travel & exposures - infection while traveling? Been in contact with infected individuals? Viral respiratory exposures such as EBV/CMV? TB exposure? g) immunization status - MMR h) meds eg/ carbemazepine or phenytoin (many meds can cause lymphadenopathy) i) allergies j) adolescents - ask about IV drug use and obtain a sexual history k) cats - think of toxoplasmosis and bartonella l) food - ingestion of unpasteurized animal milk (brucellosis), or undercooked meats (toxoplasmosis, tularemia) 3) aetiology - d) otitis externa or media e) skin/scalp infections f) CMV g) EBV h) Brucella & Bartonella i) toxoplasmosis j) non-tuberculous mycobacteria common (violet skin colour in submandibular area in a well child is typical of NTM) k) laryngeal carcinoma 3) ix - a) biopsy if history of malignancy, node >2cm, supraclavicular b) otherwise CXR, FBC, and bx if suspicious 4) tx - a) give antibiotics & review 2 weeks b) biopsy if getting bigger

Symptoms and clinical signs of upper airway obstruction

1) complete blockage = respiratory distress, then cardiac arrest 2) imminent complete blockage = a) severe respiratory distress with cyanosis or O2 sats <90% b) agitation or lethargy c) tachycardia, CRT >2 seconds 3) severe blockage = a) stridor (abnormal high pitched sound on inspiration) at rest b) severe respiratory distress - I) severe intercostal & subcostal recession II) nasal flaring III) substernal retractions during inspiration IV) severe tachypnoea 4) moderate blockage = a) stridor with agitation b) moderate respiratory distress - I) mild intercostal & subcostal retractions II) moderate tachypnoea 5) mild obstruction = a) cough, hoarse voice, no respiratory distress

Different types of conjunctivitis

1) conjunctivitis - mucopurulent discharge, red eyes, eyelids stuck together in morning. Swollen, oedematous. Cornea clear hence no pain - differentiate sore eyes from painful eyes. More redness towards bottom lid 2) bacterial & viral & chlamydia s/s - a) gritty sore eyes, pre-auricular LN, bilateral (not chylamidia), lid swelling 2) viral - a) s/s - watery discharge, follicles (lymph) b) stress related c) self-limiting d) tx - no drops or ointments tx viral conjunctivitis (incl abx), can take 3/52, may have antivirals, symptoms relieved with cool compresses & artificial tear solutions. If severe topical steroid drops prescribed to dec discomfort 3) bacterial - a) s/s - purulent discharge, crusting & matting of eye lashes b) can occur any time c) tx - abx, topical & systematic 4) allergic - a) s/s - itchy burning eyes, stringy discharge, papillae, no LN, bilateral or unilateral, lid swelling b) seasonal c) self-limiting d) tx - opticrom, lodoxamide (NSAIDs & antihistamines), steroids, remove or avoid irritant, cool compresses & artificial tears if mild 5) chlamydial (bacterial) - a) itching & red eye - may be single eye, 3/52 b) green or yellow discharge, pus-like fluid from eyes with formation of crusts (on waking) - sticky eyelids difficult to keep open c) eye pain, blurred vision d) burning, stinging etc on urinating (both men & women); watery discharge from vagina e) women - may have hx of other disorders affecting reproductive system eg/ PID f) tx - topical antibac ointment, systemic abx eg/ oral tetracycline and erythromycin, warm compress, clean eye crusts with soft & wet cotton wool, eyes cleaned regularly with saline solution to remove mucus, lubricating drops (soothe eyes) NB/ in newborns any discharge is worrying eg/ ophthalmia neonatum (genital chlamydia) NB2/ contact lens wearers temporarily stop wearing lenses while condition is active. Good hygiene to control spread of conjunctivitis eg/ not touching eyes, washing hands, not sharing towels, discarding eye cosmetics eg/ mascara

Diagnostic features and presentation of H&N malignancy, with a focus on red flag symptoms and 2 week wait referral indications

1) detailed hx & exam of upper aerodigestive tract (panendoscopy) 2) FNAC in clinic on neck nodes or lumps (US or CT guidance) 3) CT / MRI of neck from skull base to thoracic inlet 4) CXR or CT chest 5) bloods - U&E, FBC, LFT, Glucose, Albumin, TFT 6) ECG 7) assess nutritional status 8) diagnosis confirmed with biopsy of suspected cancerous lesions or tumours 9) tumours of oropharynx - sore throat, odynophagia, dysphagia, otalgia, bleeding, change of voice, trismus, weight loss, mass in neck - enlarged or ulcerated tonsil 10) tumours of hypopharynx - late, sore throat, odynophagia, dysphagia, otalgia, haemoptysis, foreign body sensation in throat, spread to LN, hoarseness, stridor and occasionally weight loss if advanced, neck mass

Describe to a patient the management of otitis externa

1) diffuse type - a) analgesia b) aural toilet - removal of debris by dry mopping EAM or suction clearance c) topical meds: with abx/steroid ear drops eg/ Gentamicin + hydrocortisone, astringents eg/ Aluminium acetate or anti-infective drops eg/ Locorten-Vioform d) ribbon gauze wick or Pope otowick helps drops reach deeper aspects of EAM e) abx/steroid ointment injected or applied on a dressing in EAM f) systemic abx for gross cellulitis g) outcome - most cases respond to the above h) infection can spread to involve whole of pinna (cellulitis) requiring systemic abx i) systemic abx given without aural toilet and/or topical meds can lead to recurrence as infected debris remains in EAM 2) furuncle type - a) analgesia b) astringents (eg/ glycerin and ichthammol) c) abx if severe infections when lymphadenitis 3) malignant OE - high dose IV abx, urgent referral (also intracranial sepsis)

History and exam relevant to dizziness

1) dizziness - need to determine what pt means 2) 3 areas described as dizziness: a) presyncopal - pts complain of light headedness, faintness & weak at knees. Diagnosis & tx = CV. May be associated with, HTN, cardiac arrhythmia's, vasovagals b) disequilibrium - unsteadiness, elderly - momentary feeling of unsteadiness & have to hold onto things or when walking tend to veer to side. Small vessel disease in brain. From vestibular nuclei, brainstem & up, can be CNS or CV origin c) vertigo - sensation of either pt feeling as though they're rotating or surroundings are. Usually on horizontal plane as the sensation on a roundabout (vertical plane = floor is coming up to meet them). Accompanied by vegetative symptoms eg/ N+V, diarrhoea or pallor 3) presyncopal - light headed, faint, weak at knees 4) disequilibrium - unsteadiness 5) vertigo - rotating, N+V+D, pallor 6) hx for vertigo - a) description of 1st attack b) duration of attacks I) seconds: BPPV (positional eg/ when roll in bed) II) mins/ hrs: Meniere's (also SNHL, tinnitus, fullness III) days: vestibular neuronitis (20s with URTI) IV) variable: migraneous (phono/photophobia, personal or FHx migrane). c) temporal pattern - labyrinthitis: severe initial attack then days or weeks later have similar attack that's less severe, over time frequency of following attacks also dec until condition resolves d) precipitating factors - I) does mvmt precipitate it (esp positional vertigo) II) URTI just prior to dizziness (?viral aetiology) III) ear discharge pus (bacteria) e) other symptoms - pts suffering from migraine may get vertiginous attacks I) headaches or migraine II) CNS symptoms eg/ hearing change, tinnitus f) drugs - meds can cause dizziness or exacerbate underlying problem, esp that have CNS affects particularly sedatives & B-blockers

Explain management plan to patient, with focus on management provided by non-ENT specialists eg ear care, tinnitus advice, hearing tactics, management of common infections, management of imbalance

1) ear care - a) keep ears dry - if washing hair or showering / bathing, use special ear plugs b) don't use cotton buds or any other objects eg/ matches, hair grips, crochet hooks, knitting needles etc in ear c) if TM perforated don't have ears syringed d) if ears are itchy do not scratch or rub them, either with your finger nails or other objects 2) tinnitus advice - a) symptomatic management b) info reaching brain is incorrect - ear sends wrong info, or brain hearing pathways don't transmit info accurately c) neuro-otological assessment, esp if unilateral symptoms d) sound enrichment (TV on, music at night) e) hearing aids work well if associated hearing loss f) if getting off to sleep is a problem, using 'snooze' facility on a clock radio may be helpful, or night time sedation g) self help and support groups are useful and help to maintain morale h) tinnitus masker plays noise into ear, which for some pts is less annoying than tinnitus i) tinnitus therapy: psychological techniques based on info giving & strategies to avoid stress response 3) hearing tactics - a) attract pt's attention before talking eg/ tap on shoulder b) if a child, sit at front of class c) if hearing better in one ear - sit with that ear facing people d) listening in background noise or rooms with lots of echoing will be especially difficult

Identify presence of a suspected foreign body based on history and investigation NB/ know when to refer to ENT and with what urgency e.g. battery

1) ears - c) usally children, eg/ cotton buds d) removal - I) wax hook II) croc forceps (not for beads) III) suction IV) oil/alcohol to kill buzzing insects V) syringing best avoided VI) GA if uncooperative e) batteries need immediate removal, most other things can wait for several days f) can cause otitis externa 5) nose - a) hx - I) side II) number III) time IV) nasal discharge/ bleeding V) unilateral offensive discharge in a child is a FB until proven otherwise b) batteries need urgent removal, everything else can wait c) mx - I) "parental kiss": parent blows fast into child's mouth while occluding good nostril II) wax hook/ Jobson probe/suction as tolerated III) may need GA 6) airway - 6) foreign bodies - a) leading cause of death in 1-3 yr old b) s/s - I) feel something stick II) unable to E or D since, can't swallow own saliva III) sharp pain IV) fever/surgical emphysema/abnormal physiology V) if inhaled - coughing, choking, need rigid bronchoscopy c) common sites - tonsil, tongue base, valeculla d) swallowed coins that stick at cricopharyngeus are particularly common: complete dysphagia, drooling and distressed (need theatre) e) ix - I) lateral neck X ray, opaque FB (not all fishbones are opaque) II) = soft tissue swelling, loss of cervical lordosis, air-fluid level, air in oesophagus III) CXR IV) ENT can do flexi scope and remove FB under LA or GA V) if nil seen, advise to return if worse / persisting, fever or neck lump f) food bolus obstruction - eating large bites too fast, predisposition: edentulous, strictures, complete dysphagia g) tx - I) CXR & neck X ray to look for opaque bones as these won't pass II) consider buscopan & diazepam to relax muscle, but little evidence III) oesophagoscopy if doesn't pass

Clinical features indicating lymphadenitis and investigation and management

1) enlargement in 1+ LN, usually from infection. LN filled with WBC. Rarely due to cancer 2) normal LN is small and firm. When infected, inc in size, become tender, and may be felt in other areas of body during a physical exam 3) 2 types - a) localized lymphadenitis - common, involves nodes close to area where infection started eg/ nodes at neck enlarged from tonsil infection b) generalized lymphadenitis - occurs in 2+ LN groups, caused by infection that spreads via blood or another illness that affects whole body 4) symptoms - a) enlarged LN(s) b) nodes that are painful to touch c) nodes that are soft or matted together d) redness or red streaking of skin over nodes e) nodes filled with pus (an abscess) f) fluid that drains from the nodes to skin 5) ix - a) bloods to look for infection b) biopsy of tissue from LN or fluid from inside c) culturing LN fluid 6) tx - a) abx for infection by bacteria b) paracetamol & ibuprofen for pain, fever & swelling c) surgery to drain abscess

Role of the Orthoptist

1) eye health professionals who care for pts with eye disorders 2) crucial role in detection, diagnosis & mx of eye diseases in both adults and children 3) work in: hospitals, private practices, low vision and rehabilitation etc 4) orthoptists may prescribe mx programs for pts with conditions such as refractive error (need glasses), double vision, neurological disorders and ocular motility disorders, as well as aiding in rehab of impaired vision

Explain optometric reports, spectacle prescriptions and have a basic understanding of types of refractive errors and diagnostic tests

1) eye's cornea & crystalline lens are both powerful optical lenses - cornea accounts for 40D of convergence power while lens adds another 20D 2) 'D' = unit used to evaluate refractive power of a lens or of an optical system - called the Dioptre. Measurement of ability of a lens to converge or diverge light (also defined as unit of focal power) 3) standard equivalent power of the eye = +60.00D 4) if eye has these parameters, or a similar proportional length and power, light will come into focus directly onto macula - no optical or 'refractive' error present, eye is 'emmetropic' 5) 'refractive error' occurs when parameters of eye do not match ideal conditions above i.e length or power of eye (or both) is different - eye is 'ametropic' 6) these defects of the optics of the eye (refractive errors) can be corrected with optical lenses, which have a specific power to converge or diverge light in a certain direction 7) convergence = light bent inwards by a lens: type of lens that converges light = +'ve (see an 'against' movement, oval) 8) divergence = light is bent outwards: type of lens that diverges light = -'ve' (see a 'with' movement, candlestick) 9) 2 main types of ametropia - axial (a) & refractive (b) 10) axial ametropia a) myopia - short sighted I) light comes into focus in front of the retina II) axial length (distance from front of cornea to the back of retina) is longer than average III) can be corrected with spherical (sph or DS) concave (negative) lenses as they cause light to diverge b) hyperopia/hypermetropia - long-sighted I) light comes into focus behind the retina II) axial length is shorter than average III) can be corrected with spherical convex (+'ve) lenses that converge light

Significance of erythroplakia

1) fiery red patch that cannot be characterized either clinically or pathologically as any other definable lesion 2) smooth, velvety, granular or nodular lesions often with well-defined margins 3) mostly - soft palate, floor of mouth, ventral surface of tongue & retromolar area 4) more common if middle aged to elderly, M>F 5) associated with tobacco & alcohol. Risk factors for erythroplakia same as oral squamous cell 6) seldom multicentric & rarely covers extensive areas of mouth 7) soft on palpation & does not become indurated until invasive carcinoma develops in it 8) often asymptomatic, although may have sore, burning or metallic sensation 9) oral erythroplakia has highest risk of malignant transformation compared to all other mucosal lesions 10) histology - severe epithelial dysplasia, carcinoma in-situ or micro-invasive cancer 11) excision biopsy & histological exam as is mandatory procedure when erythroplakia diagnosed

Manage epistaxis in ED or GP setting

1) first aid as above 2) amount of blood loss estimated & pulse & BP measured while pressure applied to nose 3) pt seated so can lie down quickly if have a vasovagal attack 4) IV access & IV fluid commenced (care not to overload elderly pts). FBC, coagulation screen & Group and Save taken as a minimum 5) facial & clothing protection & gloves worn 6) clots removed & anaesthetic + vasoconstrictor spray applied to nasal mucosa (eg/ Cophenylocaine or 5% cocaine) 7) if bleeding point seen can be cauterised with silver nitrate (LA) or bipolar diathermy (GA) 8) more posterior bleeds endoscopically viewed & cauterised if experienced. Iif not possible - anterior Vaseline, Merocel or Bismuth and Iodine Paraffin Paste (BIPP) pack inserted into nasal cavity 9) if this fails a posterior balloon (or Foley urinary catheter) inserted as well as anterior pack - left in for 36-48 hours 10) often prophylactic abx 11) for bleeding diatheses - insert a less traumatising pack eg/ Calcium alginate 12) when packs removed an antiseptic cream is prescribed to dec chance of adhesions forming 13) if packing fails pt taken to theatre for further packing, insertion of postnasal pack & septal surgery if necessary (for more effective packing) 14) if this fails arterial ligation - sphenopalatine artery or external carotid in neck + anterior ethmoidal artery 15) anterior bleeding point - a) examine nose - LA + adrenaline on cotton ball b) cauterise: silver nitrate stick, bipolar diathermy c) anterior pack: Rapid Rhino / Merocel, BIPP, Fibrillar / Surgicel / Tranexamic acid / Floseal 16) posterior bleeding point - a) pack with posterior rapid rhino b) correct clotting, consider tranexamic acid c) if that fails consider EUA +/- SPA ligation d) posterior balloon pack (+/- anterior pack) or SPA ligation (better choice) 17) epistaxis advice on discharge - a) no heavy lifting/ bending b) no hot showers or drinks c) no picking & gentle nose blowing d) vaseline 18) vestibulitis (common, staph aureus infection of nasal vestibule): tx - mupirocin ointment or naseptin cream (naseptin contains peanuts so check allergies)

Manage a patient with suspected fractured nose in ED or GP setting, know when to refer to ENT and with what urgency

1) first aid epistaxis 2) check for head Injury : LOC, N+V, amnesia 3) signs of facial fractures: diplopia, malocclusion, facial numbness 4) check nasal symptoms: obstruction, epistaxis, CSF leak, cosmetic changes, septal haematoma (no imaging required for nose) 5) ENT management - a) acute: may need epistaxis intervention, treat septal haematoma b) clinic: 5-7 days post injury (allows soft tissue swelling to settle so bony nose can be assessed) c) manipulate bony deformity under LA / GA (can't manipulate cartilage - needs septorhinoplasty at later date, in children greenstick fractures common, still worth MUA) d) MUA only works within ~3 wks after injury. Delayed referral misses this window and then septorhinoplasty at later date is only option

Explain to a patient the management of glandular fever

1) form of tonsillitis 2) s/s - a) prodromal illness = sore throat & odynophagia b) enlarged erythematosus tonsils covered with white/grey exudate c) systemic illness with fever, malaise, marked cervical and generalized lymphadenopathy d) pt looks unwell with nasal congestion and sterterous breathing (noisy breathing due to naso/oropharyngeal congestion & narrowing) e) abdo pain & hepatosplenomegaly 3) ix - a) FBC, LFTs b) monospot - glandular fever test c) atypical mononuclear cells on blood film 4) aetiology - caused by EBV 5) symptomatic mx - a) oral rehydration b) analgesia (soluble useful) & antipyretics c) bed rest 6) abx if ?tonsillitis - not Ampicillin / Amoxicillin - rash 7) oral steroids (severe cases or danger of airway obstruction) 8) LFT monitoring 9) avoid contact sport / alcohol: hepatosplenomegaly-rupture 10) warn may feel washed out for some time

Explain to a patient the use of analgesia and symptomatic management in throat infections

1) gargling with warm saltwater (1 teaspoon of salt in 8 ounces of water) then spitting it out 2) drinking warm liquids (eg/ caffeine-free tea, water with honey, or warm soup broth) or eating a popsicle or ice cream 3) using a humidifier to moisten dry air 4) if due to infection drink plenty of fluids & plenty of rest 5) paracetamol or ibuprofen can provide pain relief & dec fever 6) throat lozenges & analgesic throat sprays can be beneficial for some individuals with a sore throat 7) if allergies or postnasal drip - OTC antihistamines and decongestants 8) if cough is causing sore throat - OTC cough syrup may help diminish the cough 9) abx if bacterial infection - finish course, even if start feeling better

Red flag symptoms (e.g. parotid mass, suspected CVA, progressive palsy indicating neoplasm, associated ear infection) requiring immediate, 2ww or routine referral

1) gradual onset over >2 weeks - suggests mass lesion eg/ parotid mass, neoplasm 2) forehead not involved - suggests CNS cause (supranuclear lesion) a) facial nerve motor nucleus is divided - dorsal aspect (forehead innervation) and ventral aspect (lower facial innervation), both sides of brain provide input to dorsal aspect (forehead) so lack of forehead involvement implies UMN lesion b) only 1 side of brain provides input to ventral aspect (lower face) 3) bilateral involvement - suggests autoimmune polyneuropathy 4) recent new medications (eg/ Influenza Vaccine) 5) recent tick bite - consider lyme disease 6) fever consider infectious cause eg/ Otitis Media 7) rash - vesicular rash (Herpes Zoster), erythema migrans (lyme disease) 8) associated ear infection - otitis media complications 9) suspected CVA

Different types of acute painless loss of vision commonly found in clinical practice, their investigations and management

1) hx - a) previous ocular hx, pmx incl general CV disease, fmx, dx including eye drops b) symptoms - I) monocular or binocular II) time of event - what were you doing at the time III) method of symptom awareness (accidently by covering other eye?) IV) change in symptoms V) associated symptoms eg/ flashes, floaters may predate vision loss VI) duration/recovery VII) visual loss - general, central & associated field, peripheral only, global effect on function (bump into objects, fall down steps, can't read) 2) exam - a) test visual acuity in both eyes b) test for visual field loss eg/ central only, central & peripheral, altitudinal, hemianopia c) pupil reactions d) anterior segment e) fundoscopy & red reflex f) ix - bloods, CT, MRI 3) monocular causes - a) acute corneal disease - painful (HSV), central cloudy cornea b) anterior chamber haemorrhage - rare c) acute cataract - rare d) vitreous haemorrhage - less rare, eg/ proliferative diabetic retinopathy, retinal tear, posterior vitreous detachment e) optic nerve - 'optic neuritis', ischaemic optic neuropathy (sectoral/global - can cause altitudinal visual field defect), importance of cranial arteritis (temporal arteritis) f) retina - branch or central retinal vein or artery occlusion, retinal detachment, macular haemorrhage 4) binocular causes - a) chiasm - pituitary apoplexy (rapidly expanding pituitary tumour) b) optic nerve - infiltrative, severe papilledema (IIH), optic neuritis c) cortex - migraine, CVA - patterns of field loss eg/ stroke I) lesion at optic nerve = loss of vision in 1 eye - same side as eye) II) lesion at optic chiasm = complete loss of vision of both eyes or bitemporal hemianopia III) lesion at optic tract = loss of halve each eye (vertically) - opposite side to lesion IV) lesion at optic radiation = loss of ¼ vision each eye - opposite side to lesion, top or bottom V) lesion at striate cortex = loss of halve each eye (vertically) - opposite side to lesion

Take a history relevant to a child presenting with hearing problems / otalgia / discharge

1) hx - a) hearing - I) when II) progression III) side b) tinnitus - I) pulsatile or not II) severity & sleep III) side c) dizziness - I) what they mean II) duration III) associated symptoms d) pain - I) side II) nature (cancer referred otalgia?) e) discharge - I) nature II) side III) duration f) facial nerve g) speech delay, school problems 2) otometry - a) pull pinna up and back in adults, back (or even down) in children b) hold like pen c) right hand for right ear, left hand for left ear

Take a comprehensive history in a child presenting with snoring, and perform relevant examination

1) hx - a) snoring b) obstructed breathing & apnoea c) disturbed sleep d) hyperactivity & impulsivity (not sleepiness) e) frequent URTIs f) ear infections g) hearing speech problems h) morning headaches i) impaired school performance j) delayed growth k) parental video useful 2) exam - a) enlarged tonsils & adenoids b) craniofacial abnormalities c) underweight/failure to thrive d) daytime mouth breathing e) polysomnography (PGS) - gold standard, only method that quantifies ventilatory & sleep abnormalities, diagnosis based on threshold criteria of apnoea index & degree of O2 desaturation

Differential diagnosis for dizziness

1) hx for basilar migraine (TIAs) - a) ataxia, unsteadiness, imbalance - gradual onset b) central vertigo - no N+V, hearing loss or tinnitus c) other s/s of cerebellar or brainstem or central lesion 2) presbystasis - a) elderly, unsteadiness for sec, worse on mvmt b) no LOC, N+V c) improves spontaneously 3) CV causes - a) syncope, light-headed, unsteady, faints b) blackouts (+ LOC) never associated with peripheral cause of dizziness c) fainting or light headed on long standing d) carotid sinus syndrome 4) peripheral vestibular causes - sudden vertigo, N+V, hearing loss & tinnitus (cochlea involvement), duration of vertigo, +/- hearing loss or tinnitus clues to specific diagnosis

Explain to a patient the management of Bell's palsy

1) idiopathic facial nerve palsy = Bell's palsy 2) symptoms appear over few hrs, then stabilise, and improve over weeks 3) think tumour if gradually progressive symptoms or recovery not started by 6 weeks 4) pain common 5) prognosis good, full recovery in 70-90% after 9 months, less in worse grade palsy or elderly (Ramsay Hunt has worse prognosis) 6) advise pt: a) keep affected eye lubricated - eye drops during day & eye ointment at night b) if cornea exposed after attempting to close eyes seek prompt medical advice c) if pt unable to close eye at bedtime tape it closed using microporous tape 7) for pts presenting within 72 hours of onset of symptoms, consider prescribing prednisolone 8) refer urgently to neurology or ENT if: a) any doubt regarding diagnosis b) recurrent or bilateral Bell's palsy c) if cornea remains exposed after attempting to close eyelid, refer urgently to ophthalmology d) if paralysis shows no sign of improvement after 1 month, or suspicion of serious underlying diagnosis (eg/ cholesteatoma, parotid tumour, malignant otitis externa), refer urgently to ENT e) if residual paralysis after 6-9 months, consider referral to a plastic surgeon 9) antivirals controversial, currently not used but may change

Explain the visual development period and why visual acuity is tested or screened in young children

1) in mammals, neurons in brain that process vision develop after birth based on signals from eyes 2) if cannot see out of 1 eye when born columns in primary visual cortex receiving inputs from other eye take over the areas that normally receive input from the deprived eye 3) axons & neurons in LGN have visual receptive field properties as expected in normal people, but layers of cortex deprived have less activity & fewer responses are isolated 4) if no vision in 1 eye past critical period, can never devlop connections needed to develop vision in that eye, but if adult loses then regains vision, can still see as all connections made 5) in humans, some babies born blind in 1 or 2 eyes eg/ cataracts. Even when vision is restored later by tx, sight would not function normally as for someone who had binocular vision from birth or had surgery to restore vision shortly after birth. So important to treat babies born blind soon 6) expression of protein Lynx1 associated with normal end of critical period for synaptic plasticity in visual system 7) amblyopia - dec vision in 1 eye a) due to lack of stimulation during critical period of visual development (birth - 8/12) b) stimulus deprivation, strabismic, anisometropic (difference in refractive error between 2 eyes) c) tx - can be reversed before 7, occlusion of 'good eye' eg/patch

AMD disability & evaluation

1) inc risk of falling (2x) 2) difficulty: shopping (8x), managing money (13x), preparing meals (4x), using telephone (12x), housework (9x) 3) emotional distress & depression (2x) 4) high users of healthcare 5) wet AMD has significant impact on pt's ability to undertake basic everyday activities eg/ reading, recognising faces, driving 6) can lead to anxiety, depression, anger, reduced drive, tiredness and confusion 7) AMD evaluation - a) visual acuities - distance, near b) reading speed c) contrast sensitivity d) central visual field - Amsler e) eye clinic - fundus photos, fundus fluorescein angiography, indocyanine green angiography (ICGA), Optical Coherent Tomography (OCT), ultrasonography f) CNV characterisation leakage type - I) classic - lazy pattern created with dye II) occult - not obvious with dye III) mixed

Likely allergic triggers based on history

1) industrial chemicals 2) tobacco smoke 3) some foods, medicines, insect venoms 4) if seasonal - a) late summer or spring = ragweed (also hay) b) late March/early April = tree pollen c) October & November = mould spores 5) if perennial - a) animal hair b) mould in house c) houseplants d) carpeting & upholstery e) dust mites

Symptoms indicative of acute rhinosinusitis

1) inflammation of nose & paranasal sinuses 2) 2+ symptoms: a) either nasal blockage/obstruction/congestion b) or nasal discharge (anterior/posterior nasal drip) c) ± facial pain/pressure d) ± cough (in adults loss of smell / taste) & either e) endoscopic signs of polyps and/or mucopurulent discharge from middle meatus and/or oedema/mucosal obstruction in middle meatus or f) CT changes: mucosal changes within OMC and/or sinuses 3) acute - URTI for <10 days, ARS when symptoms >10 d or get worse after 5 d, but <12 weeks a) haemophilus influenzae, strep pneumonia b) severe, unilateral pain over infected sinus, malaise, and pyrexia c) nasal obstruction, mucopurulent rhinorrhoea and poor smell d) acute facial pain without nasal symptoms highly unlikely to be due to ARS e) pain in cheek or upper teeth indicates maxillary sinus involvement, tends to be unilateral f) frontal sinusitis - pain above eye & tenderness of supraorbital margin g) sphenoid infection - retro-orbital pain or pain at vertex of head (can be referred to temporal region or to whole head) h) if periorbital swelling may be due to a periorbital cellulitis or abscess i) anterior rhinoscopy - inflamed or oedematous nasal mucosa and mucopurulent secretions in nasal cavity. Throat exam - mucopurulent secretions in posterior oropharynx

Common and important causes of stridor and airway obstruction in children e.g. laryngomalacia, epiglottitis, choanal atresia

1) laryngomalacia - a) common - "Floppy larynx" b) symptoms - inspiratory stridor, worse with feed, prone position, agitation c) ix - flexiscope: folded epiglottis & short aryepiglottic folds d) tx - I) most self-resolving, supraglottoplasty for some 2) epiglottitis - a) children aged 3-6, potentially life threatening (airway obstruction & respiratory arrest) b) Hib is commonest agent - marked erythema & oedema of epiglottis, often extending onto larynx (dec with widespread HIB vaccination) c) cardinal features in children - I) may start as URTI II) rapidly child is unwell, toxic, lethargic and febrile (>39) III) young children drool as too painful to swallow IV) stridor, rapidly followed by respiratory arrest V) voice is normal, hoarse, or muffled VI) leaning forward 3) choanal atresia - a) congenital disorder where back of nasal passage (choana) blocked, usually by abnormal bony or soft tissue (membranous) due to failed recanalization of nasal fossae as foetus b) symptoms - I) unilateral or bilateral II) if unilateral not detected until later in life as can manage with 1 nostril available for breathing III) bilateral - life-threatening as baby unable to breathe directly after birth - babies are obligate nasal breathers. Cyanosis while feeding (oral air passages blocked by tongue). Cyanosis may improve when baby cries. May require airway resuscitation soon after birth

Common causes of upper airway obstruction and know the principles of their management

1) laryngotracheobronchitis (croup) - a) oedema & vascular engorgement of airways particularly of subglottis b) s/s - I) low-grade RTI, then inspiratory stridor with general deterioration & toxicity, temp <38 II) brassy cough like bark of dog, harsh voice c) modified Wesley croup score to determine mx - (inspiratory stridor, retractions, air entry, cyanosis, level of consciousness) d) mx - I) MWCS 0-3 = home & supportive care II) MWCS 4-8 = hospital, observations, croup tents 'cool mist', nebulized racemic adrenaline, systemic steroids, +/- abx III) MWCS 8+ = hospital ICU, heliox (acute), nebulized racemic adrenaline, systemic steroids, intubation, +/- abx IV) if fail to respond endoscopy to exclude other airway problem eg/ subglottic stenosis 2) acute epiglottitis - a) children - start as URTI, rapidly unwell, toxic, lethargic and febrile (>39), drooling, stridor b) ix - fibreoptic or direct laryngoscopy, blood cultures c) mx - endotracheal intubation for 3-4 days, Heliox, IV abx eg/ ceftriaxone, ? IV steroids NB/ acute laryngitis - any age, gradual onset, temp <39, voice hoarse or aphonic, tx supportive

Identify complications of middle ear sepsis e.g. mastoiditis, intracranial sepsis, and know when to refer and whom to refer to (e.g. paediatrics, ENT, neurosurgery)

1) mastoiditis - a) fairly uncommon complication of AOM b) can cause significant morbidity & mortality c) infection spreads from middle ear cavity & pus forms in mastoid air cells causing bony erosion, pus may spread out through bone subperiosteally or into subcuticular region in postauricular region d) s/s - I) AOM fails to settle with: II) otalgia III) hearing loss IV) otorrhoea V) malaise VI) unilateral headache = alarm bells - may be a sign of intracranial complication e) exam - I) pyrexia II) post auricular swelling III) pinna-down & forwards IV) loss of post aural sulcus V) canal may be full of pus & polyp may be seen through perforated TM VI) sagging of postero-superior canal wall VII) tenderness over McEwen's triangle f) tx - I) high dose IV abx II) if doesn't settle within 48 hrs or complications eg/ subperiosteal abscess, facial nerve palsy, labyrinthitis, petrositis or spread outside temporal bone, pt to have a cortical mastoidectomy 2) intracranial sepsis - brain abscess 3) meningitis 4) cholesteatoma 5) labyrinthitis

Risk factors for congenital hearing loss

1) maternal age >35 2) asian or black ethnicity 3) low birthweight (<2500g) 4) lower social class 5) cranio-facial abnormalities 6) prematurity

Recognise development of periorbital cellulitis as a complication of rhinosinusitis, recognise need for urgent ENT referral

1) medical emergency! Pus can collect under orbital periosteum & inc pressure on posterior compartment of eye - can lead to blindness 2) symptoms - a) unilateral eyelid swelling, pain, redness b) blurred vision c) nasal obstruction/ discharge / URTI d) fever, headaches, meningism, septicaemia 3) predisposing factors - eye lid trauma, skin infection, URTI / sinusitis 4) exam - I) fever II) involve ophthalmology III) eye red/ swollen lid/ reduced opening IV) bad signs: dec eye movements, proptosis, vision loss, loss of red colour vision an early sign V) rhinoscopy: pus 5) Chandler periorbital cellulitis classification 1: pre-septal inflammation. lid erythema/oedema only, probably with open eye 2: orbital cellulitis. more severe symptoms, closed eye 3: subperiosteal abscess. severe symptoms, proptosis, ophthalmoplegia, visual impairment 4: orbital abscess 5: cavernous sinus thrombosis. bilateral symptoms, CNS signs 6) indications for CT - I) CNS symptoms/signs, drowsiness, seizure, cranial nerves II) diplopia/ophthalmoplegia/proptosis/abnormal pupil reflex III) deteriorating acuity or colour vision IV) unable to evaluate vision / unable to open eye V) bilateral periorbital oedema VI) no improvement or deterioration at 24-36 VII) swinging pyrexia not resolving within 36h 7) mx - I) analgesia II) IV antibiotics III) close observation of eye (red colour desaturation is an early sign of optic compression) IV) topical nasal decongestants V) combined ENT/ophthalmology / paeds VI) may need abscess drainage and sinus washout VII) watch for intracranial complications

Management of snoring and sleep apnoea

1) moderate-severe OSAHS - aim to eliminate episodes of (hypo)apnoeas, de-sats, & associated daytime sleepiness a) gold standard tx - Continuous positive airway pressure (CPAP) 2) simple snorer - aim to dec duration & intensity of snoring so socially acceptable - life style changes, oral devices & limited surgery 3) in UARS and mild OSAHS - aim to dec snoring & upper airway resistance & associated sleep fragmentation. Tx based on pt choice 4) behavioural changes for simple snoring eg/ allowing partner to fall asleep first, ear plugs, sleeping on side rather than the back, often suffice 5) weight loss - obesity is most important factor in inc upper airway resistance. Dec weight = dec snoring, apnoeas, inc sleep efficiency & O2. Most dramatic results with surgical weight loss (non-surgical is difficult to achieve & maintain) 6) lifestyle changes - a) dec smoking & alcohol (inc loss of pharyngeal muscle tone during sleep & airway collapse) b) for similar reasons, sleeping tablets, sedative antihistamines & tranquillizers avoided 7) Continuous Positive Airway Pressure (CPAP) - applied via a nasal mask, most effective tx for OSAHS as eliminates apnoeas, inc daytime alertness, neurocognitive functions, mood & CV sequelae: but - 1/3 pts offered CPAP unwilling to use it 8) intra-oral appliance - enlarge pharyngeal airway by moving & fixing mandible in anterior position. Improve snoring & mild OSAHS a) S/E - excessive salivation, jaw & teeth discomfort, temporomandibular joint dysfunction 9) pharmacological tx - a) protrytyline, acetozolaminde and progesterone - respiratory stimulants & suppress REM sleep (stage most prone to airway collapse). Drugs curative of OSAHS b) alerting drugs eg/ modafanil, may have some beneficial effect on dec daytime sleepiness alongside CPAP

Take a comprehensive history to assess epistaxis severity and causative / contributing factors

1) most people have had an epistaxis at some time in their lives and most are self-limiting 2) can affect children - arise from retrocolumellar vein at anterior end of Little's area 3) anterior septum is commonest site of bleeding in adults & prominent vessels, an area of excoriation or a tiny prominence (end of a vessel usually capped with a scab) can be seen 4) other sites - lateral nasal wall posteriorly 5) need to know - side/ duration/ intensity 6) often no obvious cause but occasionally after: a) URTI b) allergic rhinitis c) nose picking d) crusting in nose e) facial and nasal trauma including foreign bodies f) rarely tumours - rarely angiofibroma can cause severe unilateral epistaxes in adolescents 7) risk factors - a) HTN in older pts b) anticoagulant meds eg/ warfarin or aspirin c) rare causes - I) hereditary haemorrhagic telangiectasia (multiple abnormal capillaries throughout respiratory, GI and urogenital tract) II) coagulopathies eg/ Von Willebrand's disease, leukaemia and disseminated intravascular coagulation (DIC)

Key diagnostic features of benign voice pathology (e.g. muscle tension dysphonia, vocal cord nodules), including relevance to professional voice use

1) muscle tension dysphonia - commonest cause of voice disorder in secondary care: a) causes - strain/tension/overuse/abnormal use of larynx musculature b) diagnosis - I) variably hoarse: ranges from normal to no voice II) laryngeal appearance - patterns of supralaryngeal constriction c) tx - voice therapy, tx cause 2) vocal cord nodules - a) professional voice users, shouting, talking above background noise, ?reflux b) boys = girls, in young adults (<40): W>M c) husky voice worsens with use, loss of higher range of voice d) peri-laryngeal discomfort e) bilateral swellings in mid-membranous portion of vocal fold giving hourglass appearance f) tx - voice therapy, rarely surgery 3) infectious laryngitis - a) causes - viral - URTI, recurrent respiratory papillomatosis (RRP) due to HPV; (bacteria rare); fungi - candida secondary to steroid inhalers or immunosuppression b) acute viral or bacterial or fungal laryngitis symptoms - I) hoarse or croaky voice - aphonia if severe II) pain on voice use, coughing or swallowing III) irritant paroxysmal coughing IV) other symptoms of an URTI (not fungal) c) RRP - infants & children - aggressive & cause severe dysphonia and airway problems, in adults less aggressive but severe dysphonia d) acute viral or bacterial cases: erythematous or sloughy vocal folds e) papillomas - multiple, raised erythematous lesions on vocal folds or anywhere in larynx f) candida - white dots of leukoplakia g) tx of acute viral or bacterial laryngitis - I) usually self-limiting, settles with: voice rest, analgesia, fluids, steam inhalations, cough suppressants prn, abx may be required II) RRP - surgical excision

Be familiar with neonatal hearing screening & diferent methods to assess hearing in children

1) newborn hearing screening - a) helps identify babies with permanent hearing loss ASAP b) 1-2/1,000 babies born with permanent hearing loss in one or both ears c) if give birth in hospital, offered a newborn hearing test for baby before discharged d) ideally test done in first 4-5 weeks, but can be done at up to 3 months of age e) test = automated otoacoustic emission (AOAE) test - lasts few mins, small earpiece placed in baby's ear & gentle clicking sounds played. When ear receives sound, cochlea responds - picked up by screening equipment f) if clear response not received may use automated auditory brainstem response (AABR) - 3 small sensors on baby's head and neck. Soft headphones placed over baby's ears and gentle clicking sounds played. Test takes 5-15 minutes 2) hearing test timings - a) newborn screening - ideally at 4-5 weeks b) 8-12 months - follow-up to newborn hearing screen required for some children c) 4-5 years - most children have a hearing test when start school, at school or an audiology department 3) hearing tests for older babies & young children - a) visual reinforcement audiometry - tests hearing in children from 7 months to 2.5 years old. Baby taught to link the sound to a visual reward eg/ toy or computer screen lighting up. Once child can associate sound & visual reward the volume and pitch of the sound varied to determine quietest sounds child is able to hear b) play audiometry - children 2-5, sounds played through headphones or speakers & child asked to perform a simple task when they hear the sound eg/ putting a ball in a bucket, completing a puzzle. Volume & pitch of sound varied to determine quietest sounds child can hear c) pure tone audiometry - screen child's hearing before start school ("sweep test"). Machine generates sounds at different volumes & frequencies through headphones. Child presses button when hears sound d) bone conduction test - device passes sound directly to inner ear through bones in head - identifies which part of ear isn't working properly if child having hearing problems e) speech perception test - assesses child's ability to recognise words. Some performed using voice and others may involve playing speech through headphones or a speaker. Child identifies words they hear by pointing at a toy, picture, or repeating what they hear f) tympanometry - assesses how flexible eardrum is. If eardrum is too rigid eg/ fluid behind it (glue ear) - sounds bounce back off eardrum instead of passing through it. Soft rubber tube placed at entrance of ear, air is gently blown down tube & sound played through small speaker inside it. Tube measures sound that's bounced back from ear

Role of MDT in assessment and management of H+N cancer, including role of oncologists, speech therapists, dietician, specialist nurse

1) oncologist - a) manages a pt's care and tx once they're diagnosed with cancer b) medical oncologist treats cancer using chemotherapy or other meds c) surgical oncologist - removes tumor & nearby tissue during operations d) radiation oncologist - tx cancer with radiation therapy e) role involves: explaining cancer diagnosis & stage, discussing all relevant tx options & oncologist's recommendations, helping pt manage cancer-related pain & other symptoms or tx SE 2) oncology nurse - a) monitor pts physical & emotional status b) keep track of pts laboratory, pathology and imaging studies c) administer meds, fluids & tx (eg/ chemo) d) help pt understand disease, tx plan & SE 3) speech therapist - a) work with pts having difficulty swallowing or speaking following tx for head and neck cancer. Also voice rehabilitation after total removal of larynx b) involved in pt care throughout cancer pathway - from point of diagnosis (info & advice prior to tx), & continues through to rehab of speech, voice and swallow once tx finished 4) dietician - pts can be malnourished at presentation, & majority of pts undergoing treatment for head and neck cancer will need nutritional support

Optic disc

1) optic disc - optic nerve head, all blood vessels come out of centre of optic disc a) 2 types of blood vessels - thinner (artery) & thicker (vein) which run symmetrically b) arteries leave optic disc & immediately branch into superior & inferior branches, then into temporal & nasal branches, continue branching towards periphery c) veins join from peripheries to optic disc d) 1:3 diameter of artery: vein e) BVs avoid fovea (central part of retina responsible for fine detail vision) - foveal avascular zone gets nutrients from diffusion from retinal BV + choroidal BV. Avascular as lots of cone photoreceptors so no BVs interfere with light 2) optic disc 3 Cs - a) colour: pink b) contour of disc margin: well defined c) cup: excavated part of disc as compared to total disc diameter - where BV kinks. Obvious when more cupping - optic nerve tissue lost & BV becomes unsupported. Normal cupping ratio = 0.3 (or <). Inc shows higher excavation - significant loss of optic nerve tissue 3) optic atrophy - well defined contour, cup normal, but pale colour of disc 4) swollen disc - a) can't determine cup, contour not well defined (obliterated), pale colour eg/ giant cell arteritis, needs ESR to confirm diagnosis b) tx - high dose steroids until dec ESR (maintain tx for 2 yrs). Without quick tx other eye affected within 2 weeks

History and examination for otitis externa

1) otitis externa - a) inflammation of ear canal b) risk factors - cotton buds, water exposure, foreign bodies, usually adults/teens c) hx - I) severe ear pain II) discharge III) itching IV) hearing loss d) exam - I) pinna tender to move II) tragus tender III) ear canal filled with discharge, canal swollen IV) TM often not seen e) diffuse type - I) diffuse - generalized inflammation of ear canal II) may be part of generalized skin condition eg/ eczema, psoriasis, seborrhoeic dermatitis or neurodermatitis or III) localized due to trauma from cotton buds, instrumentation, scratching etc IV) infective due to Pseudomonas, Staph aureus, Candida, Aspergillus, Herpes zoster V) non-infective causes - allergic/irritant eg/ shampoos, medicated ear drops VI) symptoms - itchiness, irritation, pain & swelling, otorrhoea, deafness from occlusion of EAM VII) signs - pain of moving pinna or inserting aural speculum to examine ear, otorrhoea bacterial: pus & debris in EAM fungal: dry or wet debris, or yellow or black spores (Aspergillus flavum or niger respectively) viral: vesicles around introitus of EAM (Herpes zoster), soft palate or haemorrhagic vesicles on TM ('bullous myringitis') with thin, watery blood-stained discharge VIII) enlarged pre- and postauricular and upper deep cervical LN may be present f) furuncle type - I) painful infection of 1 of hair follicles of outer 1/3 of EAM, usually Staphylococcus II) arises after hairs plucked or EAM scratched III) red swelling from one aspect of outer wall of EAM bulging into meatus

Anatomy and physiology of hearing and balance (outer / middle / inner ear, conductive vs sensorineural hearing loss, interaction between inner ear, proprioception, cerebellum and vision)

1) outer ear - sound amplification, protection of TM 2) middle ear - sound/energy transformer 3) inner ear - hearing (SN)/ balance 4) balance - a) balance or vestibular system has 2 functions - I) keep us upright & avoid injury despite movement of individual or surroundings II) maintain visual fixation despite movement of head, body or surroundings eg/ when walking head moves up and down slightly with each pace but we do not perceive this b) sensory inputs arise from 3 sites: proprioceptors, vision, and labyrinth. Can maintain balance as long as any 2 are intact c) vestibular system - I) input centres: labyrinths = semi-circular canal, macula, saccule; eyes; somatosensors = joints, skin & muscle proprioceptors; cerebellum = co-ordination II) higher centres: vestibular nuclei - info from labyrinths + cerebellum, brain - info from eyes, brain stem - info from somatosensors 5) central hearing loss - pathology of higher centres 6) conductive hearing loss - a) see with use of tuning forks b) prevention or partial prevention of sound pressure waves in air reaching inner ear 7) sensorineural hearing loss - a) problem with reception & transmission of info from cochlear. Inner hair cells convert mechanical energy of sound transmitted into cochlear into electrical activity. This electrical activity is transmitted through the nerves to the CNS b) speech discrimination often difficult 8) interaction with inner ear - 9) hearing loss severity: a) mild: 20-40 dB b) moderate: 40-70 c) severe: 70-90 d) profound: >90

Take a competent history relating to ear pain and discharge

1) pain - a) SOCRATES b) does it keep them awake at night c) fleeting, or chronic d) temperature 2) discharge - a) type eg/ mucous, pus - if pus how smelly? Colour? b) any smell (eg/ cholesteatoma) c) fever d) hx of trauma to upper body e) cleaning ears eg/ cotton buds f) URTI symptoms g) recent air travel or diving h) hearing loss

Theory behind patch testing, its method and indications

1) patch test - method to determine if a specific substance causes allergic inflammation of pt's skin (delayed-type allergic reaction) 2) done on pts suspected of allergic contact or atopic dermatitis 3) may identify allergens not identified by bloods or skin prick testing 4) produce a local allergic reaction on small area of pt's back, where diluted chemicals planted. Chemicals included in the patch test kit are offenders in 90% contact allergic eczema eg/ nickel, rubber, leather, formaldehyde, lanolin, fragrance, toiletries, hair dyes, medicine, pharmaceutical items, food, drink, preservative, and other additives 5) patch test uses type IV hypersensitivity reaction - a) 1st step in becoming allergic is sensitization - when skin exposed to an allergen, APCs (aka Langerhans or Dermal Dendritic Cell) - phagocytize substance, break it down & present them on their surface bound to major histocompatibility complex type two (MHC-II) molecules b) APC then travels to LN & presents displayed allergen to CD4+ T-cell, or T-helper. T-cell undergoes clonal expansion & some clones of the newly formed antigen specific sensitized T-cells travel to site of antigen exposure c) when skin again exposed to antigen, memory T-cells in skin recognize antigen & produce cytokines = more T-cells migrate from blood vessels d) starts a complex immune cascade = skin inflammation, itching, & typical rash of contact dermatitis e) takes 2-4 days for a response in patch testing to develop 6) patches stay in place for at least 48 hours. Vigorous exercise or stretching may disrupt the test 7) at 2nd appointment (48hrs) patches are removed & back is marked with black felt tip to identify the test sites, and a preliminary reading is done. Sites rechecked at 72hrs for response. Reading at 7 days may be requested, especially if a special metal series is tested 8) weak +ve - slightly elevated pink or red plaques, mild vesiculation 9) strong +ve - 'papulovesicles' and extreme reactions have spreading redness, severe itching, and blisters or ulcers 10) relevance determined by exposure to +ve allergen(s), & rated as definite, probable, possible, past, or unknown

History and exam relevant to ear disease

1) perception of noise in absence of external stimulus, probably due to internal aberrant electrical activity in auditory system or outer hair cells 2) pulsatile or not 3) unilateral or bilateral 4) nature of tinnitus 5) associated symptoms eg/ hearing loss, vertigo 6) timings - if <10-15 minutes = physiological, if > = pathological 7) ix - a) pulsatile: bruits, anaemia, hyperthyroidism b) consider CT/MR angiogram (glomus jugulare tumour) 8) non pulsatile (scan if unilateral) - often associated with SNHL NB/ unilateral or pulsatile tinnitus or unilateral/asymmetric SNHL need ix for possible acoustic neuroma NB2/ sudden SNHL requires urgent ENT referral ix for a possible vestibular schwannoma

Key diagnostic features of globus, and its management

1) persistent sensation of having phlegm or some other obstruction in throat when there is none. Swallowing is normal - not true dysphagia, but can become irritating. May feel mild (or severe) chest pain, or clicking sensation when swallowing 2) aetiology - a) inflammation of 1+ parts of throat eg/ larynx or hypopharynx b) due to cricopharyngeal spasm c) gastroesophageal reflux (GORD) or laryngopharyngeal reflux d) oesophageal versatility e) psychogenic cause eg/ somatoform, anxiety 2) red flags - a) pain (throat or ear) b) dysphagia c) persistent hoarseness d) lateralising symptoms 3) diagnostic features - a) clinical diagnosis based on hx b) often exacerbated by stress c) usually non-smokers d) may have reflux symptoms 4) primary care mx - a) reassurance b) address life issues c) discourage throat clearing - ice water sips d) if reflux - raise end of bed, consider b.d. PPI + gaviscon advance 3/12 5) refer is red flags or symptoms >3/12

Hx, exam & mx, with emphasis on requires urgent action - pinna haematoma, trauma to middle ear, acoustic trauma, recognising what requires ENT referral, what can be managed in primary care or Emergency Department

1) pinna haematoma - a) collection of blood between cartilage & perichondrium = inc diffusion distance between cartilage and perichondrium & infection risk b) causes - boxing or rugby injury c) risk: if not drained can become infected - perichondritis, necrosis, atrophy, distortion of pinna & cosmetic deformity (hard to reverse) d) tx - aspiration / drainage, prophylactic abx 2) trauma to middle ear - a) poking things into ear to remove wax or relieve itch, sudden changes in pressure (barotrauma) eg/ loud explosion, slap across ear b) rupture of TM, ossicular chain disrupted eg/ fracture of stapes c) associated conductive hearing of 50-60dB d) if shock wave large can rupture Reissner's membrane = severe SNHL e) uncomplicated traumatic perforations have irregular edge & 10-20dB conductive loss f) usually heal spontaneously 3) acoustic trauma - a) small arms gunfire, explosions, long-term noise exposure >85dB b) progressive hearing loss c) legislation - pts working in such conditions to have ear protectors available d) acoustic trauma causes hearing loss marked at 4KHz. Acute noise exposure eg/ standing next to a loudspeaker at a rock concert or a jet engine revving up can cause damage to outer hair cells - 'temporary threshold shift' - hearing loss returns to normal within 24 hours e) tinnitus often felt during (& after) noise exposure f) susceptibility of cochlea to noise induced hearing loss has genetic component

Sensorineural hearing loss

1) problem with reception & transmission of info from cochlear. Inner hair cells convert mechanical energy of sound transmitted into cochlear into electrical activity - then transmitted through nerves to CNS 2) speech discrimination difficult 3) noise induced typically worst at 4kHz 4) aetiology - anything that causes loss of outer hair cells or damage to nerves to cochlear a) idiopathic (60%) - presbyacusis I) bilateral & symmetrical II) audiometry shows high frequency loss = constants so loss of message ('muffled') III) function well 'one to one' basis but difficulty with group conversation & background noise IV) lack of high frequencies so shouting doesn't help V) tx - reassurance they won't completely lose hearing, explain condition, fitted hearing aid b) AIDS - I) external ear - Kaposi's, fungal OE, necrotizing ('malignant') otitis II) middle ear - AOM, SOM, mastoiditis III) inner ear - neuropathy of auditory nerve, iatrogenic (vincristine, antifungals), hearing loss progresses. Exclude neurosyphilis

Instruct a patient on first aid management of epistaxis

1) pt should lean forward, pinch fleshy part of nose (not bridge) for 10 mins 2) spit out any blood (not swallow as liable to vomit) 3) apply an ice back to the bridge of the nose or back of the neck

Accomodation reflex pathway

1) pupils constrict when look at things close 2) info from the light on each retina is taken to the occipital lobe via the optic nerve and optic radiation (after a synapse in the lateral geniculate body of the posterior thalamus), where it is interpreted as vision 3) peristriate area 19 interprets accommodation, and sends signals via EWN & CN 3 to the ciliary muscle, the medial rectus muscle and (via parasympathetic fibres) the sphincter pupillae muscle 4) even blind people have near reflex (doesn't require vision) 5) in accommodation pupil constricts to inc depth of focus of eye by blocking light scattered by the periphery of the cornea. Lens inc its curvature to become more biconvex, to inc refractive power - caused by ciliary muscles

Emergency management of acute upper airway obstruction

1) respiratory arrest - clear mouth & oropharynx of vomit, dentures or foreign bodies by suction or sweeping airway with gloved finger 2) if cyanosed and still breathing - give Heliox to buy time while getting expert help 3) brown IV cannula(e) - a) attach syringe to IV cannula b) palpate thyroid cartilage & find cricothyroid groove beneath lower edge of thyroid cartilage c) insert cannula through cricothyroid membrane d) remove syringe & place high flow O2 (or Heliox) over cannula e) penknife & plastic tube if really desperate 4) percutaneous cricothyroidotomy kit - a) anaesthetise skin, scalpel blade - stab incision into lumen of airway in midline over cricothyroid membrane, insert stillette, thread narrow endotracheal tube over stillette & remove stillette, attach Ambu bag & O2 supply to tube, ventilate as necessary 5) endotracheal intubation vs tracheostomy - a) airway assessed with fibreoptic nasoendoscope if possible b) whether endotracheal intubation or a tracheostomy is performed depends on: nature of obstruction, severity of condition, expertise available (anaesthetist and surgeon), equipment available, anxiety of pt

Mx of rhinitis & nasal polyps in primary care setting

1) rhinitis - a) allergic rhinitis - I) allergen avoidance II) oral antihistamines (non-sedating): itch, sneezing, runny (antihistamines don't work well for blockage) eg/ antihistamine nose spray-azelastine possible add-on to steroid spray III) regular nasal topical steroids for obstruction IV) s/c immunotherapy in solitary grass pollen allergen - 6 occasions, b) steroids: blockage, itch, sneezing, runny. Spray (any condition), drops (CRS), oral (CRS esp polyps); drops more potent than spray, restrict use to ~2 months c) topical decongestants: blockage (only 1/52, otherwise rhinitis medicamentosa) d) nasal douching (all conditions) e) ipratropium spray: discharge (vasomotor rhinitis) f) clarithromycin 3 months (CRS without polyps) g) rhinology surgery (blockage symptoms) - I) septoplasty, septorhinoplasty, rhinoplasty II) submucous resection III) nasal polypectomy IV) functional endoscopic sinus surgery 3) nasal polyps - idiopathic nasal polyps associated with chronic rhinosinusitis - polyp is not a diagnosis but a sign of swollen mucosa a) mild or moderate - topical steroids, failure = CT, consider surgery b) severe - oral steroids + topical, surgery c) post-op - douche, topical steroids d) if purulent secretions at any point 2/52 amoxycillin/clavulanic acid

Conductive hearing loss

1) see with use of tuning forks 2) prevention or partial prevention of sound pressure waves in air reaching inner ear 3) aetiology: a) some genetic but rare b) ear canal - I) impacted wax - cotton buds II) inflammation of ear canal eg/ otitis externa - very common, only if inc oedema & mucco pus is filling lumen (may be secondary to OM) c) middle ear - I) acute suppurative OM - pus in middle ear II) glue ear - mucus rich fluid in middle ear dampens mvmt of TM & ossicles III) chronic mastoiditis IV) perforation of TM - dec collecting power of TM so less sound energy is collected V) haemotympanum - blood in middle ear, drum looks dark red or blue, may be lacerated. Conductive loss of 30 dB or less. Resolves spontaneously & TM will heal VI) ossicular discontinuity eg/ head injury - incus displaced or erosion of long process of incus in cholesteatoma. Hearing loss ~50 dB & no resolution. If tx delayed ossicle resorbed VII) fixation eg/ otosclerosis - familial, stapes fixed with over growth of spongy bone in oval window impeding transmission of sound into inner ear. Tx - stapedectomy or hearing aid VIII) dysfunction of Eustachian tube IX) retraction pockets - indrawing of TM, self-cleansing; when debris accumulates = cholesteatoma. ENT out-pt follow-up X) tympanosclerosis - calcification of collagenous scar tissue from infection or trauma XI) tumours - benign or malignant (SCC) tumours v rare. Usually where previous mastoid surgery. Discharge may be blood & painful d) tx - I) problem perceiving loudness so shouting helps II) hearing aids excellent tx III) some need surgery to tx underlying pathology

Identify a septal haematoma

1) septal haematoma caused by bleeding underneath mucoperichondrium of septum 2) rare in children 3) soft bluish bulge on either side of septum 4) does not cause unusual amount of discomfort but usually blocks both nasal air passages (distinguish from septal deviation which is unilateral & hard) 5) if in doubt bulging area prodded gently with side of a forceps - haematoma feels soft while a deformed cartilage will feel hard 6) causes - trauma, post op (septoplasty most common) 7) septal haematomas nearly always get infected producing a septal abscess and subsequent necrosis of cartilage = gross collapse of nasal bridge & "saddle deformity" - septal haematoma therefore drained (GA) ASAP. Broad spectrum abx covering Staphlyococci given for >10 days

Appropriate investigations and principles of treatment for salivary gland disorders

1) sialectasis - a) ix - plain-Xray, sialogram b) tx - remove calculus & marsupialise duct, occasionally gland needs to be excised 2) Sjorgen syndrome - a) ix - HLA: AI, B8, DR3l antigens: SSA/B, Schirmer's Test (lacrimation), Carlsson-Crittendon (salivary flow), labial biopsy - diagnostic for Sjögren's b) risks: 1 in 6 with Sjögren's develop Non-Hodgkin's B-Cell Lymphoma c) tx - I) steroids for bouts of parotid swelling II) artificial tears, artificial saliva, lubricants III) rapid growth: diagnostic parotidectomy 3) pleomorphic adenomas - a) ix - fine needle aspiration cytology, USS or CT b) histology - superficial lobe, often in tail of gland, cystic, lobulated, and bosselated false capsule, c) tx - parotid: superficial parotidectomy or tumour excision with complete cuff of normal tissue, occasionally total parotidectomy d) prognosis - if incomplete removal tendency for multiple tumour recurrence 4) Warthin's tumour or 'adenolymphoma' - a) ix - as PA histology: papillary elements lining cystic spaces in lymphoid stroma b) tx - as for pleomorphic 5) mucoepidermoid carcinoma - a) ix - histology: well-differentiated, well circumscribed. Composed of 3 cell types: mucin-secreting, epidermoid and intermediate b) tx - low grade tumours = local resection & prolonged follow up, high grade = radical resection & adjuvant radiotherapy c) prognosis - 30% recurrence rate, cure rate at 15 years ~50% for low grade & 25% for higher 6) acinic cell - a) ix - histology: well circumscribed by a large layer of dense fibrous tissue, basophilic cytoplasm, sparse stroma & lymphoid infiltrate b) tx - local resection with VII nerve preservation & prolonged follow up c) prognosis - recur locally (35%), occasionally metastasise to LN (10%). Cure rate 55% at 15 yrs

Common viral corneal infections such as herpes simplex keratitis and adenoviral conjunctivitis

1) similarities - a) lid swelling, pressure feels normal 2) adenoviral conjunctivitis - a) sore eye, discharge, conjunctival congestion b) vision + cornea + ant chamber + pupil = normal c) causes - allergic, viral, bacterial d) tx - abx, steroids 2) herpes simplex keratitis - a) red around cornea or limbus as pathology affects cornea b) multiple dendrites come together to form amoebic pattern in eye. c) pt won't have lots of discharge - some watering d) vision - rapidly progressing loss (blurring) e) severe sense of pain f) congestion is circumcorneal g) cornea - necrotic white areas, epithelial defect, fluorescein h) anterior chamber - cells: hypopyon i) pupil - constricted j) causes - viral: dots & dendrites; bacterial; necrosis; fungal; organic trauma; amoebic (contact lens) k) tx - refer, culture, intensive topical abx, atropine 3) adverse effects of topical steroid therapy on herpetic corneal infections - ocular SE eg/ cataract, inc IOP & suppression of immune response sp infection more likely & dec wound healing. Steroids can trigger central serous chorio-retinopathy (CSCR) if susceptible 4) herpes virus infection of corneal epithelium (dendritic ulcer) - if did nothing or gave steroid eye drops cornea becomes opaque - neovascularisation on cornea = scarring. Cornea avascular so low immune defences made worse by topical steroids (enhance viral replication & ability to invade cornea = full thickness involvement)

Risk factors for H&N cancer

1) smoking (including marijuana) 2) alcohol 3) pipe smokers and people who hold cigarettes between their lips for long periods have a higher risk of cancers in the lip area 4) long periods of sun exposure = inc risk of cancer of the lip and the skin of the head and neck, especially the ear 5) chewing tobacco or betel nuts and those who use pahn have inc risk of cancers in oral cavity 6) breathing in certain chemicals & hardwood dusts inc risk of cancers of nose & sinuses eg/ textiles, woodworking, nickel refinery 7) leukoplakia (white spots or patches in mouth) may be considered a risk factor, as it becomes cancerous in approximately 1/3 pts 8) HPV infection 9) 'Plummer-Vinson syndrome' 10) iron deficiency anaemia in older women

Differentiate between simple snoring and obstructive sleep apnoea

1) snoring and Obstructive Sleep Apnoea form opposite ends of obstructive sleep related breathing disorders (SRBD) spectrum 2) simple snoring is disruptive snoring without any impact on pts sleep pattern or inc daytime sleepiness 3) as severity of obstruction inc, greater respiratory effort required = inc sleep disruption & resultant daytime sleepiness 4) upper airways resistance syndrome (UARS) - inc respiratory effort identified by oesophageal pressure analysis 5) obstructive sleep apnoea hypopnoea syndrome (OSAHS) - excess daytime sleepiness + interrupted & repeated collapse of upper airway during sleep, usually with associated de-sats. Collapse is complete with total cessation of airflow (apnoea) or partial with significant hypo-ventilation (hypopnoea) 6) frequency of apnoeas and hypopnoeas used to assess severity of OSAHS - apnoea/hypopnoea index (AHI) or respiratory disturbance index (RDI). OSAHS is categorised as: mild (5-14 events per hour), moderate (15-30), severe (> 30) 7) OSAHS only likely when AHI > 15 events per hr + unexplained day time sleepiness or 2+ of. a) impaired concentration b) snoring c) unrefressed sleep d) choking episodes during sleep or witnessed apnoeas e) restless sleep f) irritability/personality change g) nocturia h) decreased libido

Explain snoring and sleep apnoea in children to their parents

1) snoring indicates some degree of partial obstruction - hypertrophy of tonsils & adenoids is major cause of SRBDs in children. Adenoidal hypertrophy peaks at 5-6 years 2) snoring & obstructive apnoea only occur during sleep. Airway between back end of nose & larynx is unprotected by cartilaginous or bony structures so reliant on muscle tone for patency. With sleep, pharyngeal muscle tone dec progressively as sleep progresses - present in all humans and yet not all humans snore or have OSAHS 3) snoring - a) noisy breathing during sleep, caused by vibration of 1+ areas of upper airway b) very common - 45% population time to time & 25% are habitual snorers

Effect of having a squint in a child and in an adult

1) squint = permanent deviation in direction of gaze of 1 eye 2) manifest squint - inward, outward, upward or downward deviation of 1 eye a) causes diplopia (double vision) b) children can ignore squinting eye so show suppression 3) latent squint - tendency for eyes to deviate (many have this - normally pt can control) 4) concomitant - strabismus remains same in all positions of gaze (up, down, left, right etc), kids 5) incomitant strabismus - strabismus which changes in different positions of gaze, due to extraocular muscle imblanace, adults 6) refractive error - shape of eye does not bend light correctly = blurred image. Main types of refractive errors are myopia (near-sightedness), hyperopia (far-sightedness), presbyopia (loss of near vision with age), and astigmatism 7) tx - a) refractive error - convex lenses (long-sighted) help convergent deviation, concave lenses (short-sighted) help divergent deviations b) surgery (no refractive error, surgery on extraocular muscles)

Differentiate between stridor and stertor

1) stertor - noisy breathing caused by partial obstruction of airway above larynx (level of oro/nasopharynx. Sounds like snoring) a) tonsillitis b) nasal obstruction c) foreign body d) angioedema e) inspiratory stridor: laryngeal level f) expiratory stridor: wheeze of asthma (bronchi/bronchioles) g) mixed inspiratory & expiratory stridor: tracheal or laryngeal and lower airways 2) stridor - noisy breathing caused by partial obstruction of airway at or below larynx a) congenital - I) laryngomalacia II) vocal cord palsy or web III) subglottic stenosis b) acquired - I) supraglottitis / epiglottitis II) laryngitis & croup (LTB) III) malignancy eg/ laryngeal carcinomas, subglottic stenosis, laryngeal papillomata, large laryngeal polyps/cysts, external compression eg/ thyroid mass IV) angioedema V) trauma eg/ fracture of larynx VI) foreign body

Limitations of surgery in the treatment of snoring and OSA

1) surgery for snoring is last resort & only considered if simple non-surgical alternatives have been tried (and failed) 2) aim of palatal surgery is to dec or stop collapsibility of oropharyngeal segment (area around throat). Dec amount of soft palate and/or removing tonsils. Surgery also undertaken to remove uvula = chief vibratory tissue 3) 4 basic surgical procedures: a) uvulopalatopharyngoplasty (UPPP) b) laser-assisted uvuloplatoplasty (LAUP) c) platal stiffening operations (CAPSO) d) radio-frequency ablation (Somnoplasty) 4) other procedures: injection Snoreplasty, septoplasty, pillar procedure 5) surgery counselling: a) after operation pt will experience pain b) surgery for snoring never carried out without a prior sleep study c) surgery is last resort; try everything else first d) no guarantee of success e) even if initially successful, snoring can return after a few months f) snoring may not be associated with soft palate at all - could occur at base of tongue. Without full diagnostic procedures not possible to differentiate. Surgery will not eradicate tongue based snoring g) if pt puts on weight after surgery esp around neck area, likely to resume snoring h) surgery may mask development of OSA i) surgery is always effective in pts with a deep oropharynx where side walls collapse towards each other j) surgery is non-reversible, may experience unwanted SE as a result of surgery k) surgery is very rarely undertaken for tx of sleep apnoea. CPAP recommended course for OSA, but also affective for snoring if simple remedies not worked

Stages of swallowing and how these will be affected by disease

1) swallowing is a complex co-ordinated reflex action, initiated voluntarily mostly completed as an orderly sequence of reflexes over seconds 2) primary function of deglutition is transfer of solid & liquid food from buccal cavity to stomach. Swallowing mechanism has 3 stages: a) oral or voluntary stage b) pharyngeal stage - involuntary stage c) oesophageal stage - involuntary stage 3) these 3 stages correspond to 3 anatomical regions which bolus of food passes, but swallowing is a continuous & integrated manoeuvre - initiation of 1st phase inevitably leads to completion of whole process 4) dysphagia: difficulty with swallowing, precipitated by pharyngeal movement, occurring within 5 seconds of initiating movement. Symptom is active & associated with swallowing 5) globus pharyngeus: sensation of pressure or tightness of or in throat, not associated with swallowing & frequently relieved by swallowing (distinct from true dysphagia where food sticks)

Specific questions related to salivary gland disease e.g. swelling after meals, lump, pain, facial palsy, xerostomia, associated arthritis, dry eyes, trismus, displaced tonsil

1) swelling after meals 2) lump - unilateral or bilateral, swelling constant or intermittent 3) pain - constant, intermittent, related to food? 4) facial palsy 5) xerostomia 6) associated arthritis 7) dry eyes, mouth, arthritis 8) trismus 9) displaced tonsil 10) foul taste in mouth 11) other associated conditions 12) sudden change

Clinical features indicating deep neck space infection and investigation and management

1) throat infection - lymphadenopathy - suppuration - neck abscess in deep neck space/DNSI (parapharyngeal = lateral to pharynx, retropharyngeal = behind pharynx) 2) s/s - a) sore throat & odynophagia b) dysphagia c) trismus & drooling d) muffled voice e) septic & fever f) poor head movement & neck mass g) airway compromise, displaced pharynx, tongue swelling h) brawny induration 3) ix - a) CT - deep neck infections b) U/S - abscess vs cellulitis (for superficial masses) c) OPG: often dental cause 4) mx - a) airway protection: observation / intubation / trachy b) IV abx c) surgical drainage/aspiration 5) complications - airway compromise, rupture: pneumonia, empyema, lung abscess, mediastinitis, Lemierre's: IJV thrombosis, carotid artery erosion

Anatomical and physiological differences between adults and children relevant to ENT e.g. head size, normal heart rate parameters

1) tongue - larger in comparison to adults 2) nasal & oral passages - smaller in comparison to adults 3) Eustachian tube - short & straight & short distance between trachea & bronchi in children, longer in adults 4) tonsils & adenoids large during childhood 5) respiratory tract obstruction occurs commonly in children as short airway 6) inc RR (30/min vs 15/min), HR (140bpm vs 85bpm) 7) dec BP (100/60 vs 120/80) 8) larger head size compared to body in children

Discuss with a patient indications for tonsillectomy and expected recovery

1) tonsillectomy indication - a) recurrent ie > 7 episodes per year in 1 year, 5/yr for 2 yrs, 3/yr for 3 yrs or more b) or a significant time is being missed off school or work) c) recurrent quinsy 2) painful for 1-2 weeks; advise regular analgesia and normal diet 3) post tonsillectomy bleed common a) usually 2-10 days post-op b) primary bleed may need theatre c) most secondary bleeds settle conservatively on admission d) preceded by child being unwell, fevers, dec oral intake e) FBC, coag, G&S f) IV antibiotics, (no evidence for H2O2) g) post-op appearance: white and slough, fever, pain and bad breath indicate infection NB/ other reasons to refer - child has guttate psoriasis exacerbated by recurrent tonsillitis, hx of sleep apnoea, daytime drowsiness & failure to thrive

Tonsillitis & peritonsillar abscess s/s, management, and when to refer a child with tonsillitis to ENT

1) tonsillitis - acute or recurrent bacterial infection, presents in childhood or young adults a) aetiology - B-haemolytic streptococcus A, corynebacteria diphtheria b) s/s - I) throat pain - usually bilateral & odynophagia II) enlarged erythematous tonsils with exudates from tonsillar crypts (white spots) III) systemic upset, pyrexia, cervical lymphadenopathy, and lethargy IV) halitosis V) rarely unilateral, exceptional in pts >35 years c) mx - I) usually self-limiting, resolve in 5 days, otherwise: II) analgesia (soluble) & antipyretics III) Po abx eg/ penicillin (or erythromycin) IV) rarely need ENT admission: IVI, IV antibiotics 2) referral - to ENT if considering tonsillectomy 3) quinsy (peritonsillar abscess) - a) may develop out of acute tonsillitis b) abscess in peritonsillar space (between tonsil & faucial pillar) c) s/s - I) severe unilateral tonsillar pain & odynophagia II) trismus & drooling - maybe absolute dysphagia III) referred otalgia IV) general malaise & fever V) pus in soft tissues superolateral to tonsil displace tonsil & uvula inferomedially VI) bulging of paratonsillar tissues & soft palate e) tx - I) drainage of abscess by lancing or aspiration II) abx III) analgesia & antipyretics & fluids

Different types of tracheostomy tubes and indications for their use

1) tracheostomy (trach) tube - curved tube inserted into tracheostomy stoma 2) commonly used tracheostomy tube consists of 3 parts: outer cannula with flange (neck plate), inner cannula, & obturator a) outer cannula - outer tube that holds tracheostomy open b) inner cannula - fits inside outer cannula c) obturator - used to insert a tracheostomy tube 3) cuffed tube - used to obtain closed circuit for ventilation 4) cuffless tube - used for pts with tracheal problems or ready for decannulation 5) fenestrated cuffed tracheostomy tube - used for pts who are on ventilator but not able to tolerate a speaking valve to speak 6) fenestrated cuffless tracheostomy tube - used for pts who have difficulty using a speaking valve 7) metal tracheostomy - rare, pts who received a tracheostomy years ago 8) short term tracheostomy tubes have a 15mm connector to allow attachment to airway equipment. Long term tracheostomy tubes have a low profile flange - more discreet but cannot be attached to airway equipment 9) non-fenestrated single cannula tube with an air-filled cuff - adult pts for temporary tracheostomy 10) dual cannula tubes safer as inner cannula may be removed quickly if obstruction & therefore preferred for pts who continue to require a tracheostomy tube after discharge from ICU 11) fenestrated tubes considered for pts undergoing weaning from ventilation 12) cuffed tubes - if pt can't protect their own airway, don't have adequate cough reflex, or can't mnage their own secretions

Indications for tracheostomy

1) tracheostomy - a) small hole made through skin over lower part of neck into trachea & 'tracheostomy tube' inserted into hole to keep it open b) when severe obstruction to breathing in throat or mechanical assistance with breathing eg/ in ICU c) breathing - air passes through nose or mouth on breathing - nasal passage on inspiration warms, moistens & removes dust particles from air before it passes through open vocal cords into lungs. On expiration air passes in reverse direction but if vocal cords are brought together airflow causes them to vibrate & allows voice. With a tracheostomy in place most air passes in and out through hole in neck so these important functions are lost or dec. Warming, humidification & filtering functions replaced artificially by filters. Speaking possible by 1-way valve on end of trachey tube - so air passes directly into lungs on inspiration but out through vocal cords on expiration 2) indications - a) bypass obstruction in throat or voice box - infections (eg/ epiglottitis), growths, anaphylaxis or inhaled objects, severe OSA b) prevent breathing problems from swelling of tissues after major op on tongue, throat etc c) removal of secretions from air passages & prevent scarring of larynx from long-term artificial ventilation eg/ ICU pts d) prevent overspill of secretions into lungs - certain neurological diseases (eg/ motor neurone disease) affect ability to swallow & cough so saliva, liquids & food spill over into trachea & lungs, can cause chest infections. 'Cuffed tracheostomy tube' - prevent leakage into lungs by sealing off space between tube & tracheal wall with balloon e) alternative means of air entry into lungs after laryngectomy - 'end-tracheostomy': trachea cut across just below larynx & lower end brought out to form a permanent stoma ('skin hole')

Tonsillitis complications s/s, management

1) trismus - a) inability to open mouth because pterygoid muscles in spasm from local inflammation, aka hot potato voice b) unilateral swelling: above & lateral to tonsil so tonsil & uvula pushed to opposite side c) tx - IVI, IV ax, aspiration 2) pharyngitis - a) symptoms usually trivial and self-limiting eg/ dry sore throat in mornings at level of tonsils, no general malaise, nocturnal nasal obstruction b) exam - inspection of oropharynx & hypopharynx - erythema, sometime granular nobbles in posterior oropharyngeal wall. If erythema laterally at or behind posterior faucial pillar consider a post-nasal cause eg/ chronic suppurative sinusitis c) acute or chronic - both relatively non specific d) if acute then often viral eg/ coryza, adenovirus, EBV, enterovirus, CMV, herpes simplex e) bacterial eg/ B-haemolytic streptococcus, pneumococcus f) fungal eg/ Candida g) often associated with steroid asthma sprays, dentures, immune suppression eg/ AIDS, radiotherapy encompassing oral cavity/oropharynx h) throat swabs occasionally useful if persistent or atypical

Differentiate SNHL from conductive hearing loss based on clinical assessment

1) tuning fork tests distinguish clinically between conductive & SNHL - Weber's test & Rinné's test 2) equipment: 512 Hz or 256 Hz fork (not 128 Hz) 3) technique: a) strike on bony prominence: avoids overtones (YOUR bony prominence not pts) b) AC: acoustic axis in line with EAC c) BC: firmly on mastoid process/vertex 4) Weber test - a) bone conduction to differentiate conductive vs. sensorineural in unilateral HL b) place firmly on forehead c) ask: do you hear it louder on one side? left or right? Or is it equal in both ears? d) interpretation - I) normal = sound is central or midline (equal hearing/hearing loss in both ears) II) abnormal - lateralises to one side: III) conductive = louder in affected ear IV) sensorineural = louder in normal ear 5) Rinne test - a) compares air & bone conduction in same ear b) tests for chronic hearing loss c) technique - I) place activated fork - 1st: at EAM (sideways on) - inform pt this is no1. 2nd: place it on mastoid process - no2 II) then ask: was it louder at the 1 or 2 d) interpretation - I) normal = +ve Rinne - louder at EAM (AC > BC), can also be SNHL II) abnormal = -ve Rinne - BC > AC, or louder at mastoid III) true -ve = conductive loss IV) false -ve = severe SNHL (sound transmitted to other ear) V) overcome false -ve by masking ear not being tested (tragal rub or barany box)

Discuss with pts principles of H+N cancer management, radiotherapy, chemotherapy, surgery, laryngectomy, neck dissection

1) tx divided into curative or palliative 2) combined modality therapy is method of tx if locally advanced H&N cancer 3) staging - extent to which cancer has spread from origin. Used to assess prognosis & determine choice of treatment (T, N, M) a) stage I cancers are small, localized & usually curable, stage II+ are locally advanced and/or have spread to local LN and/or distant metastasis 4) oral cavity carcinoma tx - surgery to primary site +/- neck, adjuvant post-op radiotherapy if high risk 6) oropharyngeal cancer tx - combined surgery with adjuvant radiation, challenge = preservation of normal speech & swallowing function 7) laryngeal cancer tx - a) early laryngeal cancer (T1/2) - laser resection, radiation, partial laryngectomy (rare) b) advanced laryngeal cancer (T3/4) - total laryngectomy +/- postop radiation c) laryngectomy & tracheostomy - tracheostomy always needs a tube, laryngectomy does not need but may have a moisture exchange device or speaking valve d) neck dissection: surgical procedure to remove LN in neck +/- other structures (SCM, IJV, XI) 8) hypopharynx cancer tx - early (T1/T2) = radiation, advanced = as advanced laryngeal carcinoma a) factors affecting tx - TNM stage, nutrition, airway, mental state of pt, speech, swallowing b) prognosis - 50% alive at 5 years, 70-90% alive at 5 years if early, 20-40% at 5 years if late 9) thyroid cancer tx - a) papillary & follicular cancer - total thyroidectomy & central compartment neck dissection, +/- radio-iodine, excellent prognosis b) medullary - surgery c) anaplastic - palliative (lymphoma is DD in rapidly progressive thyroid mass & better tx options)

Basic interpretation of audiometric assessment and tympanometry

1) tympanometry - a) normal - peak at 0 (~900), tails at 200 both sides b) type B - flat. TM perf or effusion. If perf, external canal volume (EVC) large eg >1.3 mls) c) type C: -ve pressure. Eustachian dysfunction or effusion d) type Ad: ossicular discontinuity e) type As: stiff, otosclerosis 2) pure tone audiogram - a) graphic representation of thresholds of hearing sensitivity b) different symbols for if response heard or not c) ANSI/ASHA threshold - lowest intensity at which listener can identify a signal at least 50% of time d) normal threshold adult: 0-25 dB, children - 0-15 dB e) conductive hearing loss - I) AC thresholds >25 dB level. BC thresholds within normal limits of 0-25 dB II) air-bone gap - when >10 dB difference between AC and BC thresholds = conductive loss f) sensorineural hearing loss - I) AC & BC > 25 dB, AC & BC within 10 dB II) SNHL doesn't indicate where problem lies - needs advanced diagnostics g) mixed hearing loss - I) sensorineural & conductive components II) AC and BC thresholds >25 dB III) air-bone gap of >10 dB h) configuration of hearing loss - I) flat - little or no change in thresholds (+ or - 20 dB) across frequencies II) sloping - as frequency inc, degree of hearing loss inc III) rising - as frequency inc, degree of hearing loss dec IV) trough (cookie bite) - greatest hearing loss in mid frequencies

Take a comprehensive history in a child with nasal obstruction or discharge

1) uni or bilateral 2) to distinguish if URTI (children have ~8 URTI per year) - a) often fever, malaise & possibly cough b) serous discharge at first, becomes mucopurulent before settling in ~10 days c) unlike adults often have persistent mucosal oedema secretions for >15 days d) immunity improves after age of 7 3) key question - does child have any periods when nose is clear? If yes - likely having recurrent URTI (normal) 4) features such as sneezing, nasal itch, hayfever - constant or seasonal 5) pressure or pain in cheeks, forehead, across bridge of nose 6) if rhinosinusitis - a) nasal obstruction, rhinorrhoea, hyponasal speech & snoring b) exam often not diagnostic - secretions may not be infected (green secretions may be due to stagnation rather than infection) c) bacterial rhinosinusitis can occur - can lead to peri-orbital cellulitis or intracranial complications. Majority bacterial clear of own accord 7) if nasal tumour - a) unilateral epistaxis b) blood stained nasal discharge c) facial pain or swelling 8) anosmia, cachosmia 9) factors contributing to nasal obstruction - a) frequency of URTI b) immature immune system c) prevalence of allergic rhinitis (NB/ majority with allergic rhinitis have hayfever, some have perineal rhinitis - usually house dust mites)

Be able to take a competent history relating to hearing problems

1) unilateral or bilateral 2) sudden or gradual 3) fmx eg/ otosclerosis is a Mendelian dominant with incomplete penetrance, familial causes of sensorineural hearing loss 4) any other medical history that may be contributing to their hearing loss 5) previous noise exposure 6) birth or neonatal trauma 7) serious childhood infection 8) settings in which hearing is worst 9) worse with specific frequencies 10) otalgia 11) exudate from ear 12) phonophobia 13) tinnitus 14) vertigo 15) vision loss 16) headache 17) use of hearing aids

Significance of leukoplakia

1) unusual-looking patches inside mouth. Can vary in appearance, may be: a) white or gray color b) thick, hard, raised surface c) hairy (hairy leukoplakia only) d) red spots (rare) - see doctor right away e) most often on tongue, inside cheeks & gums f) patches take several weeks to develop, rarely painful 2) smoking is most common cause, other irritants eg/ injury to inside of cheek - biting, rough, uneven teeth, dentures; inflammatory conditions; HPV 3) mild leukoplakia usually harmless & often resolves. More serious cases linked to oral cancer 4) hairy leukoplakia - EBV. More common if HIV or other immune problems 5) most resolve spontaneously & don't need tx, avoid triggers eg/ tobacco use 6) if biopsy +ve for oral cancer, patch must be removed immediately 7) small patches removed by a more extensive biopsy using laser therapy or a scalpel. Large leukoplakia patches require oral surgery 8) hairy leukoplakia - antivirals to stop growth. Topical ointments containing retinoic acid 9) in most cases, leukoplakia isn't life threatening. Patches don't cause permanent damage, lesions usually clear within a few weeks after source of irritation removed 10) hx of leukoplakia can inc risk for oral cancer

History and exam relevant to facial palsy

1) upper or lower motor neurone lesion - a) LMN: all face affected (eyebrow raise) b) UMN: lower face involved with preservation of bilateral eyebrow raise 2) onset - congenital, rapid or slowly progressive 3) severity - complete or incomplete 4) symptoms related to VII palsy a) eye closure b) drooling 5) otological symptoms a) deafness & hyperacusis b) otorrohea c) otalgia d) vertigo & tinnitus 6) neurological eg/ CVA, MS, Guillain-Barré 7) parotid disease - masses, pain 8) systemic - symptoms of infection, sarcoid 9) head, facial trauma - # skull base, stab injuries 10) exam - a) VII nerve - main facial mvmts to test - raising eyebrow, closure of eye & smile. Facial nerve function graded using House-Brackman scale b) House Brackmann Scale - I = normal, II = slight weakness noticeable on close inspection, III = obvious weakness but not disfiguring, IV = severe dec in mvmt - incomplete eye closure, V = asymmetry at rest - motion barely perceptible, VI = asymmetry at rest - no facial movement c) CNS: Vth, VIIIth and lower CNs, cerebellar d) ear: signs of infection or tumour e) parotid: if mass present - malignant until proven f) oral cavity: look in mouth for vesicles, palatal weakness, oropharynx: displaced tonsil

Signs, symptoms, and mx of orbital tumours

1) vascular - a) capillary haemangioma - I) most common orbital tumour in children, 30% seen at birth, 100% by 6 months II) most commonly in superior anterior orbit III) may enlarge on coughing or straining IV) systemic - high output cardiac failure, Kasabach-Merritt or Maffuci syndrome. V) associated strawberry nevus VI) may have spontaneous resolution VII) tx - steroids b) cavernous haemangioma - I) most common orbital tumour in adults II) 70% female pts, 40-50 years old III) normally just behind globe IV) slowly progressive axial proptosis, choroidal folds VI) tx- surgical excision 2) lacrimal gland tumours - a) pleomorphic adenomas - I) painless & very slow growing, smooth mass in lacrimal fossa II) inferonasal globe displacement III) post extension = proptosis & ophthalmoplegia IV) smooth encapsulated outline V) tx - excavation of lacrimal gland fossa b) lacrimal gland carcinoma - I) presents at 40-60 II) very poor prognosis III) painless fast-growing mass in lacrimal fossa IV) inferio-nasal globe displacement V) post extension = proptosis, ophthalmoplegia & episceleral congestion VI) trigeminal hypoesthesia in 25% VII) tx - biopsy, radical surgery & radiotherapy 3) neural tumours - a) optic nerve glioma - I) young females at end of 1st decade II) associated with NF1 III) gradual vision loss IV) tx - observation (low grade), excision (poor vision & cosmesis), radiotherapy (intracranial extension) b) optic nerve sheath meningioma - I) middle aged women II) gradual vison loss, optic nerve compression III) proptosis due to intracranial spread IV) tx - observation (slow), excision (aggressive tumours & poor vision), radiotherapy (slow-growing tumours & good vision) 4) miscellaneous tumours - a) metastases - breast, lung, prostate, skin, bowel, kidney b) invasion from sinuses

Explain to a patient in simple terms management of vestibular neuronitis, multisensory imbalance, BPPV, Meniere's, migrainous vertigo, with emphasis on management by non-ENT specialist

1) vestibular neuronitis - a) managed by GP, only lasts a few days-weeks b) tx symptomatic - fluids, rest c) avoid: alcohol, bright lights, noise, stress d) vestibular sedatives (benzos)/antiemetics, abx if bacterial infection 2) multisensory imbalance - combined vestibular, proprioceptive and fall-prevention training a) vestibular rehabilitation - balance can be improved by exercise (eg/ ice dancer spins) 3) BPPV - a) reassurance - likely to go away in a few weeks b) positioning manoeuvres Epley, Semont, Cawthorne-Cooksey exercises to move particles from semi-circular canals inner ear to stop vertigo c) vestibular suppressants (eg/ antihistamines, sedatives, scopolamine) if symptoms severe d) antiemetics to dec associated N+V e) rarely surgery may be used to treat BPPV f) prognosis: usually resolves in 12-18 months 4) Meniere's disease - a) spontaneous resolution in 70% - reassurance b) medical- acute phase: I) bed rest II) vestibular sedatives (diazepam best) III) antiemetics for N+V eg/ Prochlorperazine IV) for vertigo - Cinnarizine or Betahistine c) prophylaxis: ? Cinnarizine and betahistine d) low salt & caffeine e) surgery - resistant cases, tx not helped: grommets, intratympanic gentamicin (Chemical neurectomy), Endolymphatic Sac Decompression, vestibular nerve section, labyrinthectomy 5) migranious vertigo - a) prophylactic - amitryptyline or B-blockers, Ca-channel blockers b) Pitozifen - major SE is weight gain c) dietary restrictions - MSG, some alcohols eg/ red wine & port, aged cheese, chocolate, aspartame d) vestibular rehabilitation therapy - if movement-associated dysequilibrium present

Physiology of voice production and how these are affected by disease

1) voice = acoustic output of vocal tract as a result of vocal fold vibration a) brain controls - lungs + vocal folds + vocal tract - creates voice 2) voice is a repeating (periodic) longitudinal sound wave consisting of compressions & rarefaction of air molecules 3) kinetic energy from mvmt of air molecules causes mucosa of membranous part of vocal folds to oscillate - generates sound wave 4) oscillation of mucosa is possible due to layered structure of vocal cord (aka vocal fold) 5) Reinke's space (superficial lamina propria) allows epithelial layer to oscillate backwards & forwards 6) sound produced by vocal folds is periodic and has a fundamental frequency (F0) of vibration (in Hertz) and intensity or pressure (in dB) 7) frequency (pitch of voice): a) determined by mass per unit length of vocal folds - changed by tensioning of vocal fold & muscle contraction b) adult males speak at a lower F0 than women as vocal folds are bigger (inc mass per unit length) c) any pathological condition which inc mass per unit length eg/ Reinke's oedema (q.v.) will lower F0 d) average F0 during speech: adult male 110Hz, adult female 190Hz, child 300Hz

Management of snoring and sleep apnoea contd.

10) upper airway surgery - designed to widen upper airway: nasal, oropharyngeal or retrolingual. Procedures single site & non-invasive for simple snoring, multiple level & invasive for OSAHS a) tracheostomy - rare b) nasal surgery - nasal pathology inc upper airway resistance & inc -ve pressure in pharynx during inspiration. Surgery - correct deviated septum, nasal polyposis & turbinate hypertrophy c) uvulopalatopharyngoplasty (UPPP) - tonsillectomy, uvulectomy & excision of some of soft palate. Used when suspected obstruction solely at level of soft palate/oropharynx, or simple snoring d) Laser-Assisted Uvulopalatoplasty (LAUP) - more effective than doing nothing in OSAHS, but less effective than conventional UPPP e) radiofrequency (RF) - procedures of tonsil, palate and tongue base, submucosal application of low frequency radiowaves to create thermic lesions & thus volume dec & scarring - mucosal sparing & volume dec rather than resection. 80% dec in subjective snoring at 1 yr f) maxillofacial and multilevel surgery - pts with moderate-severe OSAHS. Range of procedures to improve retrolingual airway & retropalatal airway. Extremely invasive so limited to pts who fail to use CPAP

Explain optometric reports, spectacle prescriptions and have a basic understanding of types of refractive errors and diagnostic tests contd.

11) refractive ametropia - refractive power of eye, i.e. its ability to bend light rays to bring them into focus on the retina, is either stronger or weaker than norm of ~60 dioptres. Due to either corneal power being stronger or weaker than 40 dioptres, or power of the crystalline lens being stronger or weaker than 20 dioptres, or a combination of both a) myopia - short-sightedness: light comes into focus before retina, refractive power of eye >60D, spherical concave (-'ve) lenses are used to correct b) hyperopia/hypermetropia - long-sightedness: light comes into focus behind retina, refractive power of the eye <60D, spherical convex (+'ve) lenses 12) astigmatism - a) astigmatic eye is not spherical (rugby ball rather than tennis ball) b) has 2 meridians (in regular astigmatism these are at 90 degrees to each other) so asymmetrical shape of cornea bends light rays unevenly so they come into focus at 2 different points in relation to retina. If one or both of these points is behind or in front of the retina, the retinal image will be blurred c) cylindrical (cyl or DC), or toric lenses (have spherical & cylindrical power) used to correct this error d) light rays in one meridian are now focused onto the retina so this part of the image will be clear. Light rays in the other meridian become focused behind it so that at the retina they are not yet in focus and this part of the image remains blurred e) remaining part of image, formed along meridian (b) needs different powered lens to correct it. However, adding appropriate spherical lens to place point 2 onto retina, would put point 1 out of focus again as alters effective power of lens correcting meridian (a). So lens required which will only bend light in direction of uncorrected meridian (here meridian b) f) cylindrical lens bends rays of light in a certain meridian only g) toric lens - spherical power & bends light along every meridian, except 1 of cyl or second power, where has power to correct 2nd meridian. Axis of cylinder tells us where the second meridian is 13) examples - a) -3.00DS = prescription of a myope b) +3.00 / -0.75 x 180 = prescription of astigmatic hyperope, corrected by +2.25DS c) -9.50 / -1.25 x 30 = prescription of high myope with oblique astigmatism

Diagnostic features and presentation of H&N malignancy, with a focus on red flag symptoms and 2 week wait referral indications contd.

11) tumours of larynx - change of voice/hoarseness, dyspnoea/stridor, pain/odynophagia, dysphagia, neck mass 12) oral cavity carcinoma - non-healing ulcers, local pain, referred otalgia, loose teeth or poor fitting dentures, later: spread to LN - affects speech, swallowing, taste & appearance 13) glottis cancer - early, good prognosis: constant gruff voice, progressive, later invade supraglottis or subglottis, airway obstruction, pain, dysphagia, spread to regional LN 14) supraglottic cancer - late, local pain, referred otalgia, change in voice, dysphagia, spread to LN 15) thyroid cancer - neck lump in thyroid area, may have airway compromise due to invasion of trachea, or recurrent laryngeal nerves causing pvocal cord palsy. Risk factors - Previous radiation exposure, thyroiditis a) Ix: USS +/- FNA 16) 2 weeks wait for suspected laryngeal cancer if: >45 + persistent unexplained hoarseness or unexplained lump in neck 17) 2 weeks wait for suspected oral cancer if: unexplained ulceration in oral cavity (or lip) lasting >3 weeks or persistent & unexplained lump in neck or red/red & white patch in oral cavity consistent with erythroplakia or erythroleukoplakia 18) 2 weeks wait for suspected thyroid cancer if unexplained thyroid lump

History and exam relevant to facial palsy contd.

11) want to exclude - a) children I) congenital - Moebius Syndrome (bilat VI, bilat VII with uni or bilat XII N palsies), hemifacial microsomia (unilat VII with microtia, hemifacial hypoplasia) II) acquired - forceps delivery, chicken pox, AOM b) adults I) trauma - forceps delivery, penetrating injury II) iatrogenic III) damage from parotid or submandibular gland surgery IV) tumours - malignant parotid tumours V) mastoid surgery of any kind VI) if having ear surgery warned of risk to nerve VII) infection VIII) discharging ear & facial palsy is medical emergency - cholesteatoma must be excluded. Tx - abx, surgical exploration of mastoid to remove cholesteatoma X) AOM - tx = abx, myringotomy XI) mastoiditis, herpes zoster XII) glomus jugulare or glomud tympanicum 12) ix - pure tone audiogram, stapedial reflexes, electroneuronography

Common causes of upper airway obstruction and know the principles of their management contd. 2

13) trauma to larynx - a) severe laryngeal injuries rare (car crash) b) stab wounds, kick boxing etc c) stridor is ominous sign. No security if no stridor as delayed laryngeal oedema & obstruction can occur d) any open injury of larynx requires exploration, & CT. If airway compromised intubate. Abx to prevent perichondritis e) smoke inhalation - can have delayed laryngeal oedema. CXR & 24 hours' observation. Pts who ingest caustic agents, can have laryngeal oedema & airway problems 14) general mx - a) simple manoeuvres to open airway eg/ jaw thrust (triple airway manoeuver) b) oropharyngeal airway or nasopharyngeal airway if unconscious pt c) if not immediately intubated coma position (semi-prone, slightly head down) used d) endotracheal intubation - I) direct laryngoscopy & tracheal intubation if unconscious, apnoeic pt II) awake = fiberoptic intubation e) surgical airway - indicated when endotracheal intubation not possible, or unstable cervical spine: percutanous transtracheal jet ventilation, cricothyroidotomy, emergency trachey

Common causes of upper airway obstruction and know the principles of their management contd. 3

15) tx of extrinsic airway compression - eg/ haemorrhage, infections & tumours a) haematomas after surgery - suture removal and haematoma evacuation. Or artificial airway immediately secured b) if coagulation abnormalities - intubation over surgical airway 16) tx of retropharyngeal abscesses causing partial UAO - a) awake drainage under LA b) gentle fibreoptic exam & intubation 17) tx of inhalational injury - a) UAO from progressive supraglottic oedema usually develops within 24 hours of injury b) intubated early c) if stridor, hoarseness, or hypoxaemia - immediately intubated 18) tx of allergic manifestations - a) immediately ensure adequate airway & administration of O2, IV fluids, epinephrine, antihistamines and steroids b) likely to recur so agent or drugs responsible thoroughly ix

History and examination for necrotising / malignant otitis externa, and mastoiditis

2) necrotising/malignant otitis externa - a) aggressive form of OE b) due to Pseudomonas aeruginosa c) more common in diabetics or immunocompromised pts d) spreads from EAM to bone causing osteitis, severe pain and VII, IX,X and XI cranial nerve palsies as spreads across skull base e) severe unrelenting pain with canal granulation 3) mastoiditis - a) complication of OE, child with red/tender mastoid and pinna protrusion. IV abx

Different types of OM - OME, CSOM

3) chronic OM with effusion (aka glue ear) - fluid, no s/s of acute inflammation/infection a) peak at 3 & 5 yrs old b) commonest cause of deafness in children in developed world c) sterile collection of fluid in middle ear cleft = conductive deafness of 10-40 dB & flat tympanogram d) OME may follow an URTI or AOM e) otoscopy: -ve ME pressure, horizontal handle malleus, cone-shaped PT, neo-annular fold, colour change: grey to blue, opaque PT f) most commonly in children with large adenoids, previous ASOM or cleft palate g) problems - hearing loss, school problems, speech delay h) tx - I) high spontaneous resolution rate - in 3/12, 50% improve (90% resolve in 3 months) II) can try Valsalva or Otovent III) if persists >3/12, with symptomatic hearing loss, speech, behaviour problems = grommets or hearing aids. Grommets ventilate middle ear to dry up effusion (stay in for 1 yr) IV) persistent OME may result in thinning of TM = retraction pockets & collapse of TM V) not use for decongestants & antihistamines VI) adenoidectomy if recurrent VII) autoinflation (Valsalva or otovent balloon) VIII) infected grommet: cipro drops i) adult with glue ear - could be sign of nasopharynx tumour 4) chronic suppurative otitis media - inflammation, TM perforation 5) cholesteatoma - squamous epithelium in middle ear 6) hearing tactics - a) attract child's attention before talking eg/ tap on shoulder b) sit at front of class, if hearing better in one ear - sit with that ear facing teacher c) listening in background noise or rooms with lots of echoing will be especially difficult

Indications for, management and complications of a tracheostomy

3) mx - 2 types of tracheostomy: a) end tracheostomy - performed as part of laryngectomy b) side tracheostomy - larynx still in place & small hole created between skin over lower neck & trachea. 2 main methods: e) time in hospital - 5-10 days, depends on why tracheostomy performed. If pt needs to go home with tracheostomy tube, tube is changed at 5 days. Pt needs to be confident in being able to look after the tube at home 4) complications - a) early: I) tube displacement II) blocked tube (dried secretions, blood clot) III) pneumothorax (especially in babies) IV) surgical emphysema b) rare (late): I) tracheo-cutaneous or -oesophageal fistula II) tracheal stenosis - too much cartilage removed 5) prognosis - aim in most cases to remove tracheostomy ASAP. Ensure pt can breathe normally again before taking tube out. Often pt instructed to keep tube blocked off for 24-48 hrs before tube removed. If all is OK tube is removed & large occlusive dressing applied over hole. Hole closes within a week

Identify common and significant tympanic membrane pathology including myringosclerosis, perforation

3) myringosclerosis - a) calcification of collagenous scar tissue from previous infection or trauma b) rarely causes symptoms, tympanosclerosis can cause hearing loss (50dB) or chalky, white patches on middle ear or TM c) tx - I) hearing aids II) excise sclerotic areas & repair ossicular chain 4) perforation - a) dec collecting power of TM so less sound energy collected b) aetiology: mostly infection, otherwise traumatic perforations from blows to ear, atmospheric overpressure, exposure to excessive water pressure (eg/ divers), cotton buds c) perforations without infection or cholesteatoma not painful - audible whistling sounds during sneezing & nose blowing, dec hearing, & tendency to infection during colds if water in ear canal d) perforation with infection - copious purulent drainage, may be sanguineous e) ix - otoscopy, small perforations need otomicroscopy, screening tympanometry f) tx - I) avoid eardrops with gentamicin, neomycin sulfate, or tobramycin II) systemic abx when controlling otorrhea from TMP III) cauterization of edges of TMP IV) fat-plug tympanoplasty V) tympanoplasty

Common causes of upper airway obstruction and know the principles of their management contd.

3) rare infective conditions of larynx - recurrent respiratory papillomatosis (HPV), TB, diptheria, herpes 4) neurological causes - a) CNS depression, OSA b) PMS & NM abnormalities eg/ I) RLN problem (postop, inflammatory, tumour) II) laryngospasm, hypocalcaemia, tetanus III) myasthenia gravis, Guillain-Barre 5) angioedema 6) foreign body 7) tumour - pharyngeal, laryngeal & tracheobronchial carcinoma, vocal cord polyposis 8) laryngeal oedema - allergic, hereditary angioedema 9) haemorrhage and haematoma - post op, anticoagulation therapy, coagulopathy 10) burns 11) congenital - vascular rings, laryngeal webs, laryngocoele 12) other - crico-arytenoid arthritis, achalasia of oesophagus, hysterical stridor, myxoedema

Clinical features of orbital disease and investigations contd.

3) symptoms - a) double vision, dec vision b) pain/discomfort 4) ix - a) CT or MRI, plain x-ray b) fine needle biopsy c) TFT, search for primaries-secondaries 5) diplopia in 10% - a) restrictive myopathy - 50% have permanent diplopia b) oedema causes diplopia in active stage & fibrosis in late stage c) most frequent muscle = inferior rectus, then medial, superior, lateral 6) idiopathic orbital inflammatory disease (IOID) - a) diagnosis of exclusion, non-neoplastic, non-infectious orbital lesion (pseudotumor), involves any or all soft tissue components b) presentation - I) 20-50 years old II) abrupt painful unilateral onset III) periorbital swelling & chemosis IV) proptosis & ophthalmoplegia e) early spontaneous remission - no tx f) prolonged intermittent activity with eventual remission - tx = anti-inflams eg/ NSAIDs, steroids, cytotoxic (steroid spring drugs), radiotherapy

Mx of dysthyroid disease

3) tx - a) some - spontaneous remission within 1 yr b) regulation of thyroid hormone levels I) thionamides (stop thyroid producing excess hormones) - carbimazole & propylthiouracil. Take for 1-2 months before notice any benefit. Dec dose over time, but may need to take it whole life II) B-blocker quickly relieve symptoms c) radioiodine tx - radiation damages thyroid, dec hormones it can produce (drink), not if pregnant or breastfeeding or causing severe eye problems d) surgery - partial or total thyroidectomy if: large goitre, severe eye problems from overactive thyroid, pt can't have other tx, recurrance of symptoms, pt needs meds for rest of life to make up for not having a thyroid eg/ levothyroxine e) topical lubrication of ocular surface to avoid corneal damage caused by exposure. Tarsorrhaphy is an alternative option f) corticosteroids to dec orbital inflammation g) stop smoking, as pro-inflammatory substances are found in cigarettes (dec inflammation) h) surgery to decompress orbit, improve proptosis & address strabismus causing diplopia - when stable for at least six months or if severe to prevent blindness from optic nerve compression i) eyelid surgery is most common surgery performed on Graves ophthalmopathy pts - lid-lengthening, marginal myotomy of levator palpebrae muscle +/- lateral tarsal canthoplasty, müllerectomy, eyelid spacer grafts, recession of lower eyelid retractors, blepharoplasty

Common abnormalities of pupillary reflex pathway contd.

4) Adies syndrome - a) pt often young & female b) efferent pupillary defect on direct and consensual testing (absent light reflex) c) sluggish pupil responses d) pupil constriction on convergence slow but miosis eventually occurs (light near dissociation) e) pt may demonstrate abnormal tendon reflexes (dec, Holmes Adie syndrome) f) denervation of postganglionic parasympathetic nerve, benign process 5) Argyll Robertson pupils - a) congenital syphilis (tertiary neurosyphilis) - may be blind from optic atrophy b) pupils small & irregular - may be asymmetrical c) sluggish light responses d) light near dissociation (constrict with accommodation) 6) traumatic mydriasis (dilated pupil) - may have facial scars & signs of pupil rupture (irregular pupil margins). Blunt trauma, damage to iris sphincter muscle 7) posterior synechiae - a) after iritis, adhesion of iris pigment epithelium to lens b) symptoms - irregular-shaped, fixed pupil 8) optic atrophy - a) end stage eye disease, optic nerve pale & loss of capillaries on optic disc b) associated with afferent pupillary defect 9) pupil exam - a) inspect for anisocoria (asymmetric pupil size) b) direct/consensual response c) swinging flashlight test d) near response - I) pupil constriction II) convergence III) accommodation

Symptoms indicative of chronic rhinosinusitis

4) chronic - >12 weeks a) anaerobes b) nasal obstruction, discoloured discharge (mucky green, nasal or post-nasal) for >12 weeks c) may have anosmia or cacosmia (unpleasant smell) or intermittent frontal pain d) key points in hx of sinogenic pain: exacerbation of pain during URTI, association with rhinological symptoms, pain worse when flying & response to medical tx e) facial pain or pressure without nasal s/s unlikely to be due to rhinosinusitis (DD - midfacial segment pain, migraine, cluster headaches, atypical facial pain) f) hx of constant purulent secretions (not like smoker or snorers when just first thing in morning) g) physical signs - mucosal swelling, inflammation, discharge h) anterior rhinoscopy or nasendoscopy - inflammation, mucopus, or nasal polyps 5) more indicative (hard) symptoms - a) nasal obstruction b) purulent discharge throughout the day c) unilateral pain d) hyposmia (dec sense of smell) 6) less indicative (soft) symptoms - a) catarrh (feeling of post-nasal mucous) b) headache c) bilateral/general d) lethargy

Key diagnostic features of benign voice pathology (e.g. muscle tension dysphonia, vocal cord nodules), including relevance to professional voice use contd.

4) non-infectious laryngitis - a) causes - extra-oesophageal reflux: damage from acid and pepsin, allergies (rare), heartburn b) variable huskiness, voice may worsen with use, loss of higher range of voice c) chronic throat clearing, cough, excess mucus in throat, choking, globus, difficulty swallowing food or pills (no true dysphagia) d) general erythema & oedema of vocal folds and larynx e) tx - vocal hygiene and dietary advice, PPI 2x/day before breakfast and evening meal for a minimum of 2 months +/- alginates and H2 antagonists 5) Reinke's oedema - a) smoking, excess talking, extra-oesophageal reflux b) M=F (more noticeable in women) c) deep pitched gravelly voice (women mistaken for men on phone) d) if severe may cause choking episodes e) bilateral grey or erythematous swellings along whole length of membranous portion of vocal fold f) tx - stop smoking, surgically dec polypoid swelling +/- medical txt of reflux +/-voice therapy 6) polyps - a) shouting with a cold or extra-oesophageal reflux b) M>F 30s-50s c) husky voice worsens with use, may be deeper d) voice cuts out during speaking, choking episodes if very large e) unilateral grey or haemorrhagic swelling from mid-membranous portion of vocal fold, smooth edge f) tx - surgical excision +/- medical tx +/-voice therapy 7) cysts - a) cause not known, some develop after laryngeal inflammation, some may be congenital b) 2 types: mucus retention & epidermoid cysts c) M=F d) husky voice, pitch breaks, loss of range of voice, inc effort to produce voice e) unilateral nodular swelling or localised bulge or stiffness of vocal fold f) tx - voice therapy to dec secondary muscle tension, surgical excision

Explain snoring and sleep apnoea in children to their parents contd.

4) obstructive sleep apnoea - a) prevalence: 1-5%, M=F, no inc with age b) peak prevelance is 2-5 when adenoids & tonsils largest in relation to oropharyngeal size c) poor growth: usually thin d) symptoms similar to adults but without daytime sleepiness - impulsivity & hyperactivity, can have secondary enuresis e) aetiology - associated with adenotonsillar hypertrophy, but unlikely to be only cause I) anatomical factors predisposing to OSAHS - choanal stenosis/atresia, macroglossia, micrognathia, mid face hypoplasia (eg/ Down's, Crouzon's) and Mandibular Hypoplasia (eg/ Pierre-Robin & Cornelle De Lange syndrome) f) medical sequaele eg/ pulmonary, systemic HTN, cor pulomonale and congestive heart failure a g) neurobehavioural & developmental consequences eg/ poor school performance, poor learning skills, ADHD, behaviour problems 5) ix - a) sleep studies - indicated in all pts presenting with snoring or suspected sleep apnoea b) polysomnography (PSG) - gold standard for diagnosis of OSAHS. In-patient study involving overnight assessment of parameters eg/ EEG, electromyogram, respiratory airflow etc on video c) ambulatory pulse oximetry - screening tool for OSAHS 6) tx - a) adenotonsillectomy - most improve (>70%. Inc persistent of OSA if obese, bad OSA before treatment, >7 years old b) CPAP c) nasal steroid spray (mild OSA) d) airway/craniofacial surgery if pathology e) jaw repositioning devices & orthodontic tx NB/ refer snoring child to ENT when suspect sleep apnoea eg/ hyperactivity

Hx, exam & mx, with emphasis on requires urgent action - skull base fracture, intracranial complications, recognising what requires ENT referral, what can be managed in primary care or Emergency Department

4) skull base fracture - a) fracture of petrous temporal bone of skull base often passes through middle ear producing a conductive loss and a haemotympanum b) drum - purple, occasionally external auditory canal stenosed from fracture of tympanic ring c) CSF leakage short-lived in longditudinal fracture (80%) & damage to facial nerve is rare - abx cover indicated (CSF leakage looks like rhinorrhoea d) transverse fractures (20%) - from frontal or occipital blows - pass through labyrinth or internal auditory meatus = SNHL, vestibular damage with vertigo and facial nerve palsy e) partial or delayed facial nerve palsies recover spontaneously, complete immediate palsies may require surgical decompression f) nystagmus seen, Weber's heard in better hearing ear if cochlear damage g) urgent CT scan to define site of injury h) palsy which develops after initial injury is due to oedema + bruising around nerve - systemic steroids 5) less severe head trauma can result in 'labyrinthine concussion' eg/ tinnitus, vertigo, permanent hearing loss and BPPV 6) intracranial complication of temporal bone infections - a) brain abscess - pus surrounded by region of encephalitis within cerebrum or cerebellum b) otogenic brain abscess - any age I) from venous thrombophlebitis & develops as solitary lesion in temporal lobe or cerebellum II) aerobes, anaerobes or mixed, gram-ve bacilli III) associated mortality of 10% IV) diagnosis - suspect in anyone with ear sepsis. Develops over weeks or months V) symptoms - low grade fever, drowsiness, malaise, aphasia, visual field defects, ataxia, motor or sensory paralysis, seizures, fever, lethargy, LOC, headache and vomiting, papilloedema VI) tx - CT or MRI scan, IV penicillin, metronidazole. Abscess aspirated (burr hole)

Common and important causes of stridor and airway obstruction in children e.g. vocal cord palsy, croup, foreign body

4) vocal cord palsy - a) problem bringing vocal folds together b) symptoms - weak breathy voice c) scan of full course of RLN for aetiology 5) croup - a) common infective condition affecting larynx in children aged 1-8 b) oedema & vascular engorgement of airways particularly of subglottis c) s/s - I) low-grade RTI (eg/ with para-influenza virus), then inspiratory stridor with general deterioration and toxicity (gradual onset), temp <38 II) brassy cough like bark of dog, harsh voice III) inspiratory stridor with recession = significant subglottic oedema & potentially life-threatening NB/ features on exam of significant airway obstruction - feeding, weight 6) foreign body - diagnosed from hx & x-ray

Differential diagnosis for dizziness contd (BPPV)

5) Benign Paroxysmal Positional Vertigo - a) spontaneous, occasionally head injury b) normally middle aged or older c) hx of recurrent episodes vertigo - sudden d) associated with N+V on head movement to particular side, esp turning over in bed, turning head while driving, bending down e) usually lasts at most 1-2 mins f) no otological symptoms at all g) exam - I) Dix-Hallpike's Positional Head Test +ve in initial stage with vertigo & rotatory nystagmus stimulated by turning head to affected side. Vertigo & nystagmus disappear after 30-40 secs if head kept in position II) ENT & neurological exam otherwise normal

Identify common and significant tympanic membrane pathology including suppurative otitis media, cholesteatoma, mastoid cavity

5) acute suppurative otitis media - a) bacterial infection of middle ear. Pus, inflamed eardrum bulges outwards, pain b) drum ruptures & pus (+blood), drains into external auditory meatus c) eardrum heals within 4-5 days d) tx - I) amoxycillin + clavulanic acid (Augmentin) II) myringotomy if fails to resolve or facial nerve palsy or other dire neuro-otological complications III) brain abscesses due to neglect or inadequate tx - potentially fatal 6) chronic suppurative otitis media - a) disease of middle ear mucosa which gets repeatedly infected, often hypersecretory & hypertrophic, forming micro abscess b) may or may not be a perforation present c) odourless chronic discharge if perforation present - discharge clear mucus to mucopus d) conductive deafness usually present e) tx - I) if confined to middle ear myringoplasty curative II) if mastoid involved cortical mastoidectomy indicated as well as myringoplasty f) complications - intracranial sepsis 7) cholesteatoma - a) bag of deep meatal skin that protrudes into middle ear, continuing to produce keratin which fills the bag; the bag gets bigger etc b) anaerobic bacteria, foul smelling discharge c) tx - radical mastoidectomy v effective d) complications - bag can erode through: I) ossicles = conductive deafness 50+ dB II) into lateral semicircular canal = vertigo III) into 7th (facial) nerve canal = facial palsy IV) into cochlea = sensorineural deafness V) through tegmen into brain = intracranial abscess or sepsis VI) into sigmoid sinus = thrombose

Different types of acute painless loss of vision commonly found in clinical practice, their investigations and management contd.

5) common retinal causes of monocular APVL using HEIR: history, exam, ix, referral - a) branch retinal vein occlusion (BRVO) - H - variable vision, esp on waking, central blur E - retinal signs: variable haemorrhage, cotton wall spots, limited to 1 sector of retina - check other eye for asymptomatic BRVO I - bloods: FBC, ESR, glucose, BP R - routine outpt appt (tx soon after occlusion), if severe prognosis not good, if mild may get good resolution via collaterals Tx - sectoral panretinal photocoagulation (laser), macular laser tx, injections - steroid implants or anti-VEGF eg/ Lucentis/Ranibizuman b) central retinal vein occlusion (CRVO) - H - present on waking, global - variable (mild only central) E - acuity variable, may have RAPD if severe, retinal signs (haemorrhage, optic disc oedema), other eye for disc exams, especially optic disc (glaucomatous optic atrophy) I - BP, bloods, IOP R - eye casualty (new tx beneficial in early stages, monitoring for complications) Tx - blocked vein cannot be unblocked, sectoral panretinal photocoagulation (laser), macular laser tx, injections - steroid implants or anti-VEGF eg/ Lucentis/Ranibizuman NB/ complications - permanent severe visual loss, rubeotic glaucoma c) central retinal artery occlusion (CRAO) - H - may have absolute loss of vision, ask if previous events of intermittent prodromal phase (shutter effect - goes then comes back) E - acuity: from counting fingers to no perception of light, APD (no light) or RAPD, retinal oedema, cherry red spot, emboli, carotid bruits I - primary care: BP, tx = rebreathe into paper bag + ocular massage Secondary care: ESR (cranial arteritis), carotid USS, cardiac echo, tx = rebreathe & ocular massage, acetazolamide (dec intraocular pressure), paracentesis, steroids if cranial arteritis R - eye casualty (retina will die within 12 hrs) Tx - ocular emergency, giant cell arteritis - IV steroids, firm ocular massage may dislodge obstruction, dec IOP with anterior chamber paracentesis or drugs eg/ apraclonidine, mannitol and B-blockers, dilatation of artery eg/ sublingual isosorbide dinitrate, inhaled carbogen, intra-arterial fibrinolysis, enhanced external counterpulsation (EECP)

Important causes of optic disc swelling contd.

5) papilloedema - swelling of optic disc due to inc intracranial pressure, so bilateral a) s/s - transient visual obscurations, headaches b) splinter haemorrhages, exudates, cotton wool spots & retinal folds near disc c) enlarged blind spots d) gradually progressive field loss e) eventual atrophic changes (disc doesn't swell, Foster-Kennedy syndrome) 6) arteritic anterior ischaemic optic neuropathy (AION) - inflammation of arteries to optic disc: a) from giant cell or temporal arteritis b) temporal headache, jaw claudication, weight loss, myalgia c) sudden visual loss from inflammatory infarction of posterior ciliary artery d) inc CRP & ESR e) urgent treatment with high dose steroids f) temporal artery biopsy within 1/52 of starting tx g) tx continues for at least 2 years 7) non-arteritic AION - a) infarction of posterior communicating artery aneurysm eg/ due to atherosclerosis b) ESR not raised c) HTN in 50%, others - DM, hyperlipidaemia d) no associated systemic symptoms e) tx - low dose aspirin

Differential diagnosis for dizziness contd (Meniere's)

6) Meniere's disease - a) over diagnosed b) middle aged (between 35-55) with classical triad of symptoms: I) recurrent vertigo lasting 10 mins to 24 hours II) tinnitus (usually low frequency type) III) fluctuating but progressive SNHL c) attacks preceded by feeling of fullness in affected ear then sudden onset of vertigo - associated with N+V, sudden loss of hearing & inc loudness of tinnitus in affected ear d) at end of attack hearing recovers, not to pre-attack levels = progressive SNHL eventually e) attacks occur in clusters or widely spaced f) exam during attack - distressed pt with vertigo, N+V, just lie on bed, horizontal nystagmus, tuning forks show SNHL on affected side, pt unable to stand. ENT and neurological otherwise normal g) acoustic neuroma & otosyphilis can mimic Meniere's so ruled out with MRI & VDRL h) cause - unknown, expect due to excess fluid (hydrops) in endolymphatic fluid compartment i) ix - I) pure tone audiometry II) electric response audiometry (to exclude acoustic neuroma) & electrocochleography III) blood to exclude syphilitic ear disease IV) CT & MRI for acoustic neuroma

Clinical features of different types of glaucoma including the changes in the optic disc contd.

6) acute angle closure 'glaucoma' - a) acute high-pressure eye from obstruction to aqueous outflow (drainage) due to closure of angle by peripheral iris b) symptoms - pain + blurred vision + vomiting, more common in females (4:1) c) signs - corneal oedema (abnormal light reflex), red eye, fixed mid-dilated pupil d) risk factors - hypermetropia, fmx, shallow anterior chamber 7) rubeotic glaucoma - a) secondary cause of glaucoma b) new vessels occlude angle (grow over periphery or iris, crossing trabecular meshwork, causing scar tissue, which contracts closing off angle = inc IOP) c) causes - CRVO or diabetic retinopathy d) symptoms - pain + dec vision e) signs - red eye, corneal oedema, rubeosis, pupil distortion 8) optic disc - a) cup or not? colour clues & clues from position of BV as dive down edge of cup, measure cup-disc ratio (% of vertical height of disc occupied by cup) b) ISNT rule - should have: inferior neuroretinal rim > superior neuroretinal rim > nasal rim > temporal rim. Should apply for all cupping of optic disc c) very large cup suggests may have glaucoma, may also see optic disc haemorrhage 9) visual field & glaucoma - a) at start - loss of vision superiorly between 12 & 16 degrees from fixation - 2nd blind spot b) supranasal area has restriction of field (not noticeable for pt) c) later on - extension of loss of vision = scotoma, from blind spot, around to horizontal raphe. Inferiorly have new scotoma - same distance away from fixation as superior d) then loss of vision to brightest targets in arcuate distribution - notice if in both eyes, but not if in 1 e) eventually severe - central vision & area on temporal side (temporal island) only are left, but pt still has good visual acuity - pt knows they have disease by now f) if no surgery - loss central vision & only have the temporal island g) speed of progression of stages depends on IOP - can range from decades to months 10) Humphrey printout plot - darker at points of defects. Defects don't cross horizontal midline in optical nerve disease NB/ normal blind spot = temporal side of eye eg/ LHS on left eye - no rods or cones at optic nerve head NB2/ 20mmHg is upper limit of normal IOP

Different clinical presentations of psoriasis contd.

6) chronic plaque psoriasis (90%) - a) salmon pink (red, pink or purple) symmetrical patches & plaques b) well demarcated with loosely adherent silvery scales c) extensor surfaces eg/ knees, elbows, buttocks, knuckles d) nail changes - pitting, onycholysis, subungal hyperkeratosis, onychodystrophy e) Koebner phenomenon & Auspitz sign 7) flexural (inverse) psoriasis DD - a) due to friction & maceration b) colonisation by candida & bacteria can lead to tinea cruris, contact dermatitis 8) guttate psoriasis - a) more common in children/adolescents b) post acute streptococcal infection (group A strep) c) rain drop-like lesions (small), scaling not so prominent d) self-resolving (months), but can recur e) may preceded chronic plaque psoriasis f) mainly truncal & limbs 9) erythrodermic psoriasis - a) erythroderma - >90% body SA affected b) uncommon c) likely pmx of psoriasis, may not have other features of psoriasis d) may be systemically ill eg/ dehydration, electrolyte disturbance, renal failure, hypothermia, cardiac failure, protein loss, sepsis due to - loss of heat, protein and fluid from inflamed skin 10) pustular psoriasis - a) palmoplantar (localised to palms & soles) - I) F > M, adults (older age of onset than generalised) & smoking II) symmetrical - typical well-demarcated plaques associated with scaling, but scaling can often be very thick III) sterile pustules - very painful IV) may not have typical psoriasis elsewhere b) generalised - I) rare, precipitated by steroid withdrawal II) acute generalised pustular psoriasis (von Zumbusch) - painful III) can occur with ordinary psoriasis IV) sheets of sterile pustules, background erythema V) may be systemically unwell eg/ fever, malaise, inc WCC NB/ can affect flexures only eg/ under breasts, vulva, groin-folds & axillae. Psoriasis looks different & often do not get scaling, but very shiny, but still well demarcated, erythema

Different causes of 'red eyes' and their management contd.

6) differential diagnosis - a) conjunctivitis b) keratitis c) iridocyclitis - I) iris ballooned forward due to pupil being stuck to lens behind it II) vision - blurred/impaired III) ache in eye/pain IV) congestion is circumcorneal V) pupil constricted & oval VI) causes - usually immune mediated HLA B27 VII) tx - refer, eye drops to dilate pupil, steroid eye drops if not an infection 4) acute angle closure glaucoma - I) vision - sudden severe loss, halos, red eye II) very painful III) headache, N+V IV) congestion is circumcorneal V) pupil - dilated & fixed VI) pressure - high, feels hard VII) tx - refer, acetazolamide, topical B-blocker eg/ mannitol, and a topical steroid, analgesics & antiemetics, may need osmotics & iridotomy. Pilocarpine (causes opening of angle) every 15 min, prophylactic iridectomy other eye

Hx, exam & mx, with emphasis on requires urgent action - intracranial complications, sudden SNHL, recognising what requires ENT referral, what can be managed in primary care or Emergency Department

6) intracranial complication of temporal bone infections - c) extradural abscess - infection of extradural space (between dura & bone), pus, granulation tissue or effusion. Asymptomatic, can cause sigmoid sinus thrombophlebitis, thrombosis, otitic hydrocephalus d) sigmoid sinus thrombophlebitis - localised phlebitis causes mural thrombus formation, may occlude lumen & can propagate into internal jugular vein. If infected can cause septicaemia. Malaise, headache, spiking fever, rigors, inc ICP e) subdural abscess - circumscribed collection of pus, walled off from remaining subdural space f) meningitis - bacterial infection causing inflammation of meninges and CSF. 85% have 1+ episode of AOM. Cholesteatomas other cause 7) sudden SNHL - a) medical emergency b) mx early - I) bed rest II) vasodilators III) Carbogen gas IV) steroids c) mx late - exclude an acoustic neuroma or other disease (eg/ syphilis) in auditory system d) prognosis: low frequency losses recover better than high frequency, severe vertigo is bad prognosis 8) persistent offensive discharge = referral 9) anyone with ear sepsis or sinusitis who develops headache, malaise, LOC etc. should be suspected of having intra cranial sepsis 10) discharging ear & VII nerve palsy is emergency: cholesteatoma until proven otherwise NB/ persistent offensive discharge requires referral

Stages of swallowing and how these will be affected by disease contd.

6) touch sensation present in pharynx up to level of cricoid. Thermal sensation present in pharynx & whole length of oesophagus. Pain receptors (free naked nerve terminals) in pharynx & oesophagus 7) usual noxious, traumatic stimuli, cutting, crushing, burning & inflammation produce pharygeal pain, which cause cutaneous pain. Inflammation of pharynx lowers pain threshold locally & light contact or swallowing movements will cause pain from the inflamed mucosa 8) ix - radiology, Barium Swallow (structural abnormalities), Dynamic Contrast Swallow (physiological abnormalities) 10) prandial aspiration - classified by phases of pharyngeal swallow, 1 type or mixed phases: a) pre-prandial - before act of swallowing eg/ cleft palate, post-tonsillectomy, tongue tumour surgery b) prandial - during swallowing when inadequate airway protection during bolus transit through pharynx eg/ vocal cord palsy or after stroke c) post-prandial - after swallowing & occurs due to inhalation of residue which remains near laryngeal inlet eg/ pharyngeal pouch, oesophageal stenosis

Clinical features of orbital disease and investigations contd. 2

6) vascular orbital disorders - a) orbital venous anomalies (varices) - I) congenital enlargements of pre-existing venous channels II) usually unilateral III) may bleed or become thrombosed IV) isolated orbital varices or combined orbital & external varices b) carotid-cavernous fistula - I) abnormal communications between carotid artery & cavernous sinus II) causes - trauma, spontaneous (HTN) III) s/s - ptosis, chemosis & conjunctival injection, ophthalmoplegia, inc IOP, pulsatile proptosis with bruit & thrill, abolished by ipsilateral carotid compression, retinal venous congestion & haemorrhaging IV) direct - rapid flow shunt, caused by trauma V) indirect - slow flow shunt, congenital or spontaneous rupture, indirect communication between meningeal branches of ICA or ECA and cavernous sinus. Dilated episcleral vessels, inc IOP with wide pulsation, occasional ophthalmoplegia & mild proptosis VI) encephalocele - herniation of intracranial contents through congenital skull defects. Transmission of CSF = pulsating proptosis without bruit. Meningocele = only contains dura. Meningoencephalocele = dura + brain matter

Different grades, diagnosis, management, effects on patient's life & how patients may be helped to cope with poor vision due to macular degeneration contd.

6) wet AMD natural history - a) variable, dependent on type b) after 1 yr: 41% severe visual loss (> 6 lines), after 5yr: 64% severe visual loss, after 5yr: 54% recurrence in treated eyes 7) tx of CNV (wet) - a) focal laser photocoagulation - small extrafoveal lesions (<5% cases), non-selective thermal laser destroys choroidal neovascular lesions, can damage overlying retina I) eligibility: extrafoveal or juxtafoveal lesions, classic CNV, well-demarcated lesions II) limitations - only 13-26% pts with neovascular AMD eligible, can cause irreversible retinal damage - absolute scotoma & loss of VA b) photodynamic therapy (PDT) with Visudyne - inject visudyne into pt, shine low energy laser into back of eye - selective absorption causes choroidal BV to shrink. Tx repeated at 3 months, use in idiopathic polypoidal choroidopathy (IPCV) c) pharmacologic agents - interrupt factors stimulating or maintaining growth of endothelial cells in CNV (especially VEGF) - injected into vitreous at regular intervals. Anti-VEGF 1st line in mx of AMD: Macugen, Ranibzuman, Aflibercept d) surgery - vitrectomy & submacular excision of CNV + replacing 'sick' RPE or macular rotation to lie foveal retina on 'normal' RPE. Selected cases as salvage e) radiotherapy f) combination tx - I) similar to cancer therapy II) PDT + anti-VEGF eg/ Lucentis or Macugen III) PDT + angiostatic steroids eg/ Triamcinolone or Anecortave g) AMD rehabilitation - essential if vision subnormal, with or without tx I) registered as visually impaired, support groups eg/ Macular Disease Society, RNIB

Describing non-pigmented lesions

7 Ss Size Site Side Symmetry Surface Surrounding area Shape also - type & colour

Appropriate investigations and principles of treatment for salivary gland disorders contd.

7) adenoid cystic carcinoma - a) ix - histology: macroscopically = well circumscribed by a large layer of dense fibrous tissue, same consistency and colour as normal parotid tissue. Small cells arranged in nests fenestrated by round/oval spaces creating a cribriform pattern b) tx - wide local resection sometimes with sacrifice of VII nerve, radiotherapy controversial, prolonged follow up c) prognosis - 15 year survival 10-26%, local recurrence 50%, also to bone, liver and lung, distant metastases (e.g. lungs) can be associated with prolonged survival (up to 5 years) 8) lymphoma - ix by open biopsy, tx depends on stage & histological type 9) general ix - a) routine blood, virology, x-ray, Sialogram, CT-Sialogram, USS, Doppler, MRI b) Schirmer's, Carlsson-Crittenden, SSA/B 10) histological - a) FNAC most likely b) biopsy gland (if skin ulcerated) c) sublabial biopsy for non neoplastic disease 11) operations - a) partial superficial parotidectomy: I) complications: facial nerve palsy or paresis, Frey's syndrome, fistula (settles with time), numbness of ear lobe (permanent - division of greater auricular nerve for access to gland) b) submandibular gland excision: I) complications: haemorrhage, nerve damage (marginal mandibular - asymmetrical smile by causing weakness muscles at corner of lower mouth)

Differential diagnosis for dizziness contd. 2

7) benign vestibulopathy - a) cause unknown b) middle-aged, clusters of attacks of vertigo c) similar to Meniere's but no otological symptoms (hearing loss or tinnitus), also resolves in 2 yrs d) tx - reassurance, Cawthorne-Cooksey exercises 8) acute labyrinthine failure - a) cause usually idiopathic? viral? local vascular occlusion? autoimmune b) obvious causes - fracture of temporal bone through labyrinth, occasionally post-op c) any age, sudden deafness, severe vertigo, N+V d) vertigo prostrating & pt confined to bed e) audiogram - moderate-profound SNHL f) exam - distressed pt, afraid to move, nystagmus. Tuning fork tests show SNHL on affected side g) attack lasts 10 days to 3 weeks, with gradual improvement in vertigo. SNHL - not recover h) tx - admit for symptomatic tx of vertigo eg/ IV fluids, anti-emetics and vestibular sedatives. Plasma expanders (eg/ Dextran 70) IV & inhaled Carbogen to improve blood supply to labyrinth 9) vestibular neuronitis - a) probably viral in aetiology b) sudden onset of vertigo with N+V and nystagmus but, no hearing loss or tinnitus c) lasts a few days, often bed ridden 10) migrainous vertigo - peripheral vertigo + migrainous headaches at time of attack (uncommon) or occurring in migraine sufferers 11) central causes - space occupying lesion, degenerative disease, post-trauma, alcohol intoxication, vascular process

Different grades, diagnosis, management, effects on patient's life & how patients may be helped to cope with poor vision due to diabetic retinopathy contd.

7) diabetic maculopathy - a) specific type of DR: macular involvement b) may occur with either NPDR or PDR c) more common in type 2 than type 1 DM d) leads to visual loss if untreated e) 3 types may occur in different combos: I) focal - focal leakage from microaneurysms or dilated capillaries from focal retinal thickening & surrounding exudates II) diffuse - diffuse leak from dilated capillaries = diffuse retinal oedema, maybe some retinal haemorrhages but usually no exudates III) ischaemic - closure of perifoveal capillary network; diffuse oedema + dark haemorrhages. Fluorescein angiography confirms ischaemia 8) mx of DR - a) control of diabetes & risk factors b) laser photocoagulation - stops focal leaks as in focal maculopathy II) grid laser indicated in diffuse macular oedema; not for ischaemic maculopathy III) mixed maculopathies rneed combo strategies IV) pan-retinal photocoagulation (PRP) is recommended treatment for PDR c) future: anti-VEGFs etc d) vitrectomy - I) clears persistent vitreous haemorrhage, or retinal fibrosis or traction retinal detachment threating the macula, or causing dec in vision II) when non-response or inadequate response to laser photocoagulation for PDR 9) other ocular involvement in DM - a) inc incidence of eyelid infections, cataracts b) cranial nerve palsies: III, IV, VI c) delayed healing of corneal abrasions & ulcers d) more severe post-op intraocular inflammation eg/ FF cataract surgery e) abnormal wound healing

History and exam relevant to dizziness contd.

7) exams - a) always examine ears (middle ear infection) b) test for nystagmus c) check CN, lesions of audiovestibular nerve eg/ acoustic neuromas, may extend upwards & compress CNV, VII, IX, X, XI, XII d) pass pointing test followed by Romberg Test e) Romberg Test - if vestibular (peripheral) lesions, when close eyes in Romberg Test either sway - noticeable or gets worse when eyes open f) Dix-Hallpike Test - diagnosing BPPV g) then test for disdidokynesis, heel to toe walking, Unterberger test h) head impulse test - aka head thrust test - detects unilateral hypofunction of peripheral vestibular system eg/ vestibular neuronitis (acute vestibulopathy)

Differentiate between simple snoring and obstructive sleep apnoea contd.

8) factors that inc risk of SRBD - a) age - inc prevalence up to 60-70 b) gender - M:F = 4:1 c) obesity - most important risk factor. Central obesity indicators eg/ neck circumference index and waist:hip ratio better predictors of OSAHS than obesity or BMI in general d) smoking & alcohol inc risk e) anatomy - craniofacial abnormalities eg/ retro or micrognathia, midfacial or mandibular hypoplasia and macroglossia. Adenotonsillar hypertrophy in children, turbinate hypertrophy, septal deviations or nasal polyposis f) others - 1st degree relatives, hypothyroidism and acromegaly, neuromuscular diseases, drugs associated with central depression eg/ hypnotics & opioids 9) consequences of SRBD - a) simple snoring has a significant social impact but no detrimental impact on health. OSAHS known to have significant CV consequences: b) neurocognitive- excessive day time sleepiness, cognitive performance impaired with deterioration in memory, intellectual capacity & motor co-ordination c) CV consequences - systemic HTN (CPAP dec BP), may be coronary artery disease & cerebrovascular events d) others - potentially impotence & GOR

Physiology of voice production and how these are affected by disease contd.

8) intensity or sound pressure level (loudness of voice) - a) determined by subglottic pressure i.e. pressure beneath vocal folds - determined by degree & length of time of vocal fold closure during a vibratory cycle b) any pathological condition that dec contact between vocal folds i.e. recurrent laryngeal nerve palsy, results in dec subglottic pressure as air escape = weak voice, difficult to hear 9) vocal fold vibration leads to vowel production a) actual vowel sound (a,e,i,o,u) determined by modulation of sound by vocal tract b) determined by shaping tongue in mouth, pharynx & shaping of lips 10) consonants produced by air being 'squirted' through narrowings in vocal tract producing turbulent airflow 11) when assessing pts with voice & speech disorders each part of mechanism analysed to see whether it is causing or contributing to problem 14) dysphonia: any impairment of voice or difficulty speaking 15) dysarthria: imperfect articulation of speech due to disturbances of muscular control or incoordination 16) dysphasia: impairment of speech & verbal comprehension (sensory/receptive dysphasia) or speech and verbal production (expressive dysphasia) esp if associated with brain injury 17) hoarseness: perceived rough, harsh or breathy quality to voice

Key presentation of inflammatory disease and both benign and malignant salivary gland tumours

SCC = most common H&N cancer 1) Sjogren's syndrome - a) dry eyes & mouth & vagina, keratoconjunctivitis, glossitis, secondary candidiasis, stomatitis, dental caries, parotid gland enlargement (inc chance of lymphoma) 2) Warthin's tumour or 'adenolymphoma' (2nd most common) - a) males >40, soft, cystic masses in tail of parotid, may be bilateral 3) mucoepidermoid carcinoma - a) females >50, or children b) well differentiated (low grade) tumours grow slowly and painlessly c) poorly differentiated (high grade) tumours grow rapidly, painfully, invade local structures and metastasise to LN, lungs, bones & brain 4) acinic cell - a) middle-age & elderly females, can occur in children, mostly unilateral 5) adenoid cystic carcinoma - a) pts 40-60, tumours in submandibular gland = women, minor salivary gland tumours: M=F, grows slowly and insidiously, propensity for perineural infiltration so presents with palsies and pain 6) carcinoma pleomorphic adenoma - a) present 10 - 15 yrs after pleomorphic adenomas, pain or a palsy 7) lymphoma - a) 50-70, present firm rapidly enlarging masses & occasionally lymph node metastases

Sensorineural hearing loss contd.

c) herpes zoster oticus (Ramsay Hunt syndrome) I) herpes zoster attacks spiral or vestibular ganglion in inner ear II) intense pain in ear, later vesicular eruption on pinna & external ear III) sensorineural deafness, vertigo & facial paralysis may ensue (Ramsay Hunt) IV) tx - acyclovir to dec risk of post herpetic neuralgia d) acoustic neuroma - benign tumours from auditory nerve I) earliest symptom = unilateral hearing loss or tinnitus, mortality & morbidity from surgery directly related to tumour size II) ix - pure tone audiometry, MRI or CT, electric response audiometry III) tx - surgical removal e) globus tumours - I) rare benign tumours from non-chromaffin paraganglionic tissue, wide distribution in H&N. In neck, these cells give rise to carotid body tumours II) s/s - tinnitus synchronous with pulse, hearing loss (conductive or sensorineural), facial paralysis, paralysis of cranial nerves IX to XII III) exam - pulsatile red mass behind ear drum, audible bruit over temporal bone, facial paralysis, paralysis of cranial nerves IX to XII IV) tx - surgery, radiation or combo

Name and recognise the different types of skin conditions that can be caused by Streptococcus pyogenes contd.

b) erysipelas - I) infection of dermis & upper subcut tissue II) form of cellulitis which commonly affects the face III) mostly GAS, very rarely S. Aureus, young children = Hib IV) sources of infection on the face - nose, throat, sinuses, conjunctivae V) acute severe onset of fever, malaise and well-defined erythema of skin of the face which is usually tender and painful VI) ix - nasal, throat, ear and conjunctival swabs considered VII) tx - oral or IV Benzylpenicillin (1.2g) for 10-14 days (4-6 weeks if severe). In young children Hib should always be covered. Recurrent - prophylaxis with low dose Penicillin V VIII) severe episodes - chronic facial lymphoedema and recurrent infections. In young children orbital cellulitis may lead to meningitis and death. c) necrotizing fasciitis - black & purple rash, pt looks unwell, high fever, intense pain in affected area. Rash progresses rapidly. Deep infection caused by synergistic infection with staphylococci and streptococci. Life-threatening surgical emergency -affected tissue must be debrided, IV Abx d) Henoch- Schönlein purpura - purple rash, non-blanching lesions. Post-streptococcal phenomenon or meningococcal sepsis, viral infection, drugs or CT disease. Tx - underlying problem 10) disease from secondary infection with GAS (less frequent than S. Aureus) a) Infected atopic eczema, leg ulcers 11) disease due to Group A Streptococcal Toxins - a) Scarlet Fever - I) incubation of 2-5 days is followed by fever, severe tonsillitis and painful cervical lymphadenopathy II) erythematous rash - trunk to limbs with redness (like acute sunburn). Scaling and desquamation of skin. Strawberry tongue III) complications - due to allergic hypersensitivity reaction eg/ myocarditis, arthritis, osteomyelitis, rheumatic fever and glomerulonephritis IV) tx - 10-14 days of Benzylpenicillin + supportive care if unwell b) rarely Toxic-Shock-Like-Syndrome - similar to Staphylococcal Toxic Shock Syndrome but due to GAS. Tx - penicillin & IV gammaglobulin 13) tx - a) topically: not recommended except Chlorhexidine antiseptics b) orally: amoxycillin, Penicillin V, Erythromycin c) IV: Benzylpenicillin 14) hypersensitivity to streptococcal antigens - a) erythema nodosum & multiforme b) guttate psoriasis c) glomerulonephritis

Different types of acute painless loss of vision commonly found in clinical practice, their investigations and management contd. 2

d) branch retinal artery occlusion (BRAO) - H - any time - sectoral +/- central E - acuity variable, may have RAPD, carotid bruits, field defect, fundoscopy - embolus, signs of hypertensive retinopathy (AV nipping, flame shaped haemorrhage, cotton wools) I - BP, carotid US, bloods, cardiac echo R - eye casualty for confirmation & onward referral for ix & tx (inc risk of stroke if CV origin) Tx - urgent refer, no effective tx, long-term management is as for CRAO - assessment of CV system, carotid endarterectomy or anticoagulation, assessment for coagulopathies if no embolic source found e) retinal detachment/vitreous haemorrhage - H - floaters +/- flashes of light +/- field loss E - acuity: normal if macula on, field loss pattern depending on how much retina detached, RAPD if extensive, red reflex abnormality, fundoscopy I - N/A in primary care R - eye casualty Tx - laser surgery (photocoagulation), cryopexy (freezing), surgery eg/ scleral buckle, pneumatic retinopexy, vitrectomy, some retinal detachments cannot be fixed NB/ vitreous suddenly collapses forward & downwards from posterior, mostly benign & floaters settle down, abnormal vitreous attachment to weak area of retina can cause retinal tear - vitreous fluid can get in tear & peel off retina off pigment epithelium = visual field defect f) macular haemorrhage - H - distortion, +ve scotoma E - acuity: variable, no RAPD, full peripheral field, central haemorrhage, signs of primary disease I - BP R - eye casualty NB/ main causes - age related maculodegeneration, diabetic retinopathy, microaneurysm

Causes of vocal cord motion impairment, including understanding of recurrent laryngeal nerve anatomy contd.

d) presentation - I) weak high pitched voice that tires on prolonged talking II) perilaryngeal discomfort III) choking with fluids IV) diplophonia V) weak ('bovine') cough e) hx - I) was onset related to specific event? II) other local or systemic symptoms? III) respiratory, upper GI, neuro IV) ENT/head & neck/skull base f) exam - I) listen to voice & cough II) H&N - larynx, cranial nerves III) other systems g) ix - I) CXR - exclude mediastinal mass II) CT skull base to midthorax - lesions along path of nerve III) ?Ba swallow - oesophageal lesion or aspiration h) tx - I) unilateral = none - await spontaneous recovery, voice therapy - encourages compensation II) bilateral = tracheostomy (with speaking valve), lateralisation of cord

Sensorineural hearing loss contd

f) barotrauma and perilymph fistula - I) sudden pressure changes eg/ flying or diving may rupture membranes = leakage of perilymph into middle ear cavity or mixing of biochemically different fluids in inner ear = combo of sensorineural hearing loss, tinnitus & vertigo II) leaks into middle ear so repaired surgically g) temporal bone fractures - longitudinal (80%) or transverse (20%): transverse cause more damage to inner ear & CNVII h) noise induced - I) inner ear damage - sudden acoustic trauma (blast, gunfire etc) or prolonged excessive noise II) prolonged exposure eg/ heavy industry, hearing loss may be reversible initially - due to cochlear fatigue = temporary threshold shift. With further exposure, a permanent threshold shift occurs. Typical audiogram - notch at 4Khz with gradual involvement of the lower frequencies i) Menieres disease j) ototoxic drugs - aminoglycosides, diuretics (eg/ furosemide), salicylates, chemotherapeutics, prevention is key as little reversibility k) central cause eg/ CVA, autoimmune l) if sudden hearing loss, do tuning forks 5) sudden SNHL - medical emergency a) mx early - bed rest; vasodilators, Carbogen gas (mix of 5% CO2 and 95% O2), steroids b) mx late - exclude acoustic neuroma or other disease (eg/ syphilis) in auditory system c) prognosis: low frequency losses recover better than high frequency 6) mx - a) oral steroids ASAP b) hearing aids c) cochlear implant - when hearing aids ineffective NB/ congenital SNHL common - neonatal hearing screening

Explain the types and application of different types of LVAs as issued in the Hospital Eye Service

low vision devices - 1) children - a) bar or dome bright magnifier b) bifocal spectacles with high adds for reading c) distance binoculars or monoculars 2) adults - a) hand or stand magnifiers (HM, SM) - both can be illuminated b) binoculars/monoculars c) spectacle mounted devices 3) electrical devices - a) CCTV (higher magnification on TV) b) compact devices c) software for PCs d) voice activated devices e) screen/scanner readers f) braille keyboards 4) non-optical devices - a) talking books, watches b) large print text c) typoscopes d) bump-ons e) illumination f) tinted lenses g) kitchen aids h) reverse contrast text

Understand what commensal bacteria are

most of these bacteria can, under certain circumstances cause disease, but often merely inhabit the skin without causing any problems eg/ Staphylococci, Micrococci, Corynebacteria, Propionibacteria

Know how to apply topical treatments correctly and be familiar with the fingertip unit

1) 1 FTU = amount of topical steroid squeezed out from a standard tube along an adult's fingertip - a fingertip is from the very end of the finger to the first crease in the finger a) 1 FTU is enough to treat an area of skin 2x size of the flat of an adult's hand with the fingers together b) 2 FTUs = same as 1 g topical steroid 2) examples: a) to treat an area of skin the size of 8 adult hands = 4 FTUs for each dose (2 g per dose, if dose is 1x/day, then a 30 g tube should last for about 15 days of treatment) b) to treat 1 hand and fingers (front and back) = 1 FTU (~2 adult hands) 3) fingertip units and children - again, 1 FTU is used to treat an area of skin on a child, equivalent to 2x size of flat of an adult's hand with fingers together. Can gauge amount of topical steroid to use by using your (adult) hand to measure the amount of skin affected on the child. From this you can work out the amount of topical steroid to use

2nd line treatment option of phototherapy & be able to discuss the risks and benefits for patients with psoriasis

1) 2nd line = phototherapy (sunlight) a) narrow-band ultraviolet B (UVB) therapy - given 2-3x/week for 7 weeks I) drawbacks - time commitment, accessibility of UVB equipment II) advise against sunbeds as UV source for self-treatment (special lamps) III) exposure time controlled to avoid over exposure & burning skin - small inc rates of cancer from tx (melanoma, SCC, BCC) IV) can combine with tar or dithranol or calcipotriol for guttate psoriasis b) psoralen & UVA phototherapy (PUVA - photochemotherapy) combines oral or topical administration of psoralen (8-MOP, 5-MOP - photosensitizing agent) with exposure to UVA light I) S/E - nausea, headache, fatigue, burning, redness, itching, SCC with multiple courses. Therapy 2-3x/week, maintenance tx 2-4 weeks until remission

Recognise and describe clinical features of malignant lesion: basal cell carcinoma (including different subtypes)

1) BCC & SCC are non-melanoma skin cancers (most common skin cancer) 2) BCC - a) ~ 80% of all NMSC - malignancy of basal cells of the skin b) BCC infiltrates surrounding skin in a contiguous 3-D fashion - slow growing, locally invasive & relatively benign. Metastases are very rare c) mortality is low d) occurs mainly on sun-exposed sites of Caucasians eg/ head and neck e) presentation - I) typical pt has fair hair, light coloured eyes and fair skin II) pts may have spent a considerable part of their lives outdoors III) most are small (~1cm diameter), well-defined, erythematous, "pearly" or flesh-toned papulonodules or plaques IV) may be a central ulcer encircled by a rolled edge with surrounding telangiectasia. BCC can mimic an ulcer - may bleed followed by crusting V) can become fibrotic and resemble a scar VI) varying types - superficial, nodular, cystic, nodulo-ulcerated, morphoeic (lighter, sclerosing), keratotic or pigmented VII) large or neglected BCC can behave like a "rodent" ulcer gnawing their way through skin, muscle, bone & meninges VIII) need biopsy to establish diagnosis f) superficial BCC - erythematous patch or plaque, most commonly on trunk & face, with fine scale and visible telangiectasis. BCC may be slightly ulcerated, show central fibrosis and have an ill defined geographic border g) nodular BCC - round, spherical, oval or dome-shaped papule or nodule with a pearly translucent appearance. Slow growth and may ulcerate centrally ("rodent ulcer") or appear cystic h) morpheic or sclerosing BCC - resembles scar tissue, edges poorly defined i) inc risk of BCC recurrence - inc tumour size, tumour site - central face, esp around eyes, nose, lips, ears, poorly defined margins, subtype - morphoeic, perineural and/or perivascular invasion, previous tx failure - recurrent lesions at inc risk of recurrence

Cinical presentation of skin conditions caused by HPV (and other warts) & discuss management

1) HPV - viral genital warts: a) v. common growth of skin caused by infection with HPV types 1-77 b) particularly common if: school-aged, eczema, immunosuppression c) spread by direct contact or indirect inoculation eg/ shower room floors 2) cutaneous warts - hard, keratinous surface 3) common wart - elevated multiple papules with a rough, papillomatous and hyperkeratotic surface, vary in size. Most often on backs of fingers or toes, around nails & knees. Can resemble a cauliflower 3) plantar wart (verrucas) - inwardly growing and painful on sole of foot, & clusters of less painful mosaic warts. HPV 1, 2, 4, 57. More tx resistant 4) plane wart - flat, mostly on face, hands and shins. Often numerous. HPV 3 5) filiform wart - hyperkeratotic papillomatous warts, eyelids, neck, face and body folds. Electrocautery +/- curettage recommended 6) mucosal wart - oral warts on lips & inside cheeks = squamous cell papillomas 7) mosaic warts - confluent crops of warts, hands/feet, v resistant to tx 8) anogenital warts (HPV-6 & 11) - predispose to cervical neoplasia, all females should have cervical cytology. Referral to GU for pt + partner for screening for STDs 9) prognosis - most viral warts spontaneously resolve within a few months to years. In young children tx often more painful than disease m) tx - I) topical paints (from pharmacists) - as effective as cryotherapy if applied daily for 8-12 weeks. Contain salicyclic & lactic acid as keratolytic agents. Applied after 5 min soak in warm water and after removal of excess keratin using an emery board or nail file II) cryotherapy with liquid nitrogen - effective if used as a double freeze-thaw cycle on 3+ occasions. Freezing of 1mm of surrounding skin (takes 5-30 seconds). Can be very painful and commonly produces blistering III) curettage & cautery - curettage followed by haemostasis using silver nitrate or electrocautery. LA needed, histology to confirm diagnosis. SCC & melanomas may mimic cutaneous warts. Warts should never be excised as frequently recur in the scar IV) formalin soaks and podophyllin - resistant warts. Podophyllin v. effective for anogenital warts

Cinical presentation of skin conditions caused by Herpes simplex & discuss management

1) HSV Type I (cold sores) - 50% population, HSV Type II (anogenital) 2) both persist in sensory root ganglia after primary infection & can be shed asymptomatically (especially in 1st year). Viral shedding inc in active lesions 3) cold sores - commonly on vermillion border of lip. Pain & tingling followed by acute vesicular eruption. If primary, incubation period is 5 days. Lymphadenopathy common 4) genital herpes - HSV I or II. 1st attack - significant pain, discomfort and vesiculation occurring after prodromal pain and tingling. Common STD - referred to STD clinics for exclusion of other diseases. Recurrent genital HSV infection can be difficult to manage requiring long-term prophylactic oral aciclovir 5) complications: a) herpes gingivostomatitis - severe oral HSV infection with pain, fever and vesicles affecting gingiva, tongue, pharynx, palate and buccal mucous membranes. Lasts 5-10 days. Common in infants 1-5 b) keratoconjunctivitis - primary HSV of eye with superficial corneal ulcer which lasts several weeks. Opthalmological mx as risk of permanent scarring c) Bell's Palsy - primary or recurrent facial nerve paralysis without vesiculation may be due to HSV infection of the nerve d) eczema herpeticum - severe HSV infection affecting pts with atopic eczema. Sudden deterioration of eczema with multiple punched-out erosions on skin. Systemic tx & admission to hospital e) herpetic whitlow - direct inoculation of virus into abrasion or by a needle = acute localised herpes infection with vesiculation and blistering, can recur f) disseminated HSV - if immunocompromised, may be life threatening 6) tx - a) cold sores - topical aciclovir and rarely require systemic tx b) genital herpes and complicated infections - oral aciclovir for 5+ days

Cinical presentation of skin conditions caused by pox virus & discuss management

1) ORF virus - member of parapox virus family - widespread in lambs/goats a) usually in farmers, vets or those in contact with affected animals b) initial incubation of 5-6 days, followed by small reddish-purple papule on finger which often blisters. May become secondarily affected c) self-limiting lasting 2-3 weeks. Secondary infection - oral Flucloxacillin 2) molluscum contagiosum - self-limiting infection caused by pox virus a) common in children b) worse in atopic dermatitis c) crops of small umbilicated papules on trunk. Inflammatory changes = suppuration, crusting and intense erythema around individual lesions d) secondary infection may occur and rarely giant mollusca can be present. e) self-limiting but may last 4-18 months. Contagious in children but does not require tx. In older children or adults, lesions tx with cryotherapy or topical podophyllin

Name and recognise the different types of skin conditions that can be caused by Staphylococcus aureus

1) Staph Aureus - regarded as pathogenic but may be commensal (eg/ anterior nares, perineum, axillae and toe webs) 2) disease - direct invasion of epidermis, hair follicle, or toxin made 3) if atopic dermatitis prone to infection as abnormal skin surface lipids 4) diseases from primary infection with S. Aureus - a) impetigo - I) contagious superficial pyogenic infection of skin II) most common in young children, epidemics observed in infant schools III) mostly due to S. Aureus (sometimes Group A Streptococci) IV) single or isolated skin lesions with yellow-crusted surface often around mouth, nose and limbs. Regional lymphadenopathy, rarely bullae V) tx - topical Mupirocin partially effective, oral Flucloxacillin (or erythromycin) for 7-10 days. Should bathe separately and use their own towel VI) impetigo from streptococci associated with complications eg/ scarlet fever, urticaria, erythema multiforme, post-strep glomerulonepritits b) ecthyma - I) chronic infection of skin - ulcers with adherent crust, may have scarring II) often due to mixed infection with S. Aureus and Group A Strep III) common sites - lower leg, buttocks, thighs, occasionally face IV) tx - flucoxacillin for 14 days (500mg), or clindamycin c) superficial folliculitis - I) infection of superficial hair follicle producing small pustules which heal without scarring II) mostly S. Aureus infection, otherwise - P. aeruginosa III) small pustules centred around hair follicles on legs, buttocks or beard IV) may occur in families, sometimes in association with impetigo. May be recurrent in some young adults V) tx - oral Flucloxacillin for 2 weeks. Difficult cases may require prolonged courses of oral antibiotics and topical antiseptic washes eg/ Chlorhexidine d) pseudofolliculitis - I) apparent folliculitis of beard due to penetration & entrapment of hairs II) penetration of sharp tip of hair induces a foreign body reaction which may become infected. More common with curly short hairs III) thought to be secondary colonization IV) tx - stop shaving for several weeks but relapse will often on resumption. Emollients and topical steroid-antimicrobial combinations may be of benefit eg/ long-term lose dose Erythromycin and Chlorhexidine washes e) furunculosis - boil: I) acute necrotic infection of a single hair follicle due to S. Aureus II) young children and adults III) often carriage of S.A on skin may be an important factor IV) can have recurrent episodes in family members over weeks to months V) tx - swabs, oral Flucloxacillin for 14 days. Carriage in nose - prolonged topical abx (eg Mupirocin) applied to nose & topical antiseptic washes f) carbuncle - collection of boils: I) deep infection of multiple hair follicles with S. Aureus II) middle-aged or elderly men often in association with diabetes, malnutrition, cardiac failure, drug addiction or with prolonged steroid therapy III) deep seated abscess forms in skin with multiple drainage sites (eg/ back of neck, buttocks, thighs, shoulders) IV) fever, tenderness & pain are pronounced V) tx - swabs, oral Flucloxacillin for 14 days g) sycosis barbae, cellulitis 6) diseases due to secondary infection with S. Aureus - a) infected atopic eczema, infected wounds, infected leg ulcers

How to recognise visual acuity

1) VA = most common measure of visual function a) measure of pt's ability to resolve fine detail b) determined by size of smallest line of letters or symbols in test chart read by pt after any defects of focusing, other than aberrations, corrected 2) VA - normally using a Snellen chart at 6 m - measures acuity within central 5 degrees of visual field, so macula region used to fixate on each letter in turn (macular region resolvex fine detail) 3) another chart used is Log MAR 4) notation for Snellen chart = eg/ 6/6: (distance from chart in m)/ (distance at which letters subtend 5 minutes of arc) a) VA of 6/6 is normal (particularly if < 50), but many can read 6/4 or 6/3, so record VAs accurately to monitor them as small drop in VA may indicate early ocular pathology b) 6/6 (normal), 6/60 (defective), 6/5 (above average) c) VA recorded as Snellen fraction + any extra letters or minus any errors eg/ 6/12 -2 or 6/24 +1 d) sometimes pt can pick out letters at end of line but unable to see ones in middle due to crowding. Affects amblyopes, esp when reading

Recognise and describe the cutaneous manifestations of internal cancers eg/ acanthosis nigricans, acquired ichthyosis, pyoderma gangrenosum and dermatomyositis

1) acanthosis nigricans - hyperpigmented velvety changes of flexural (intertriginous) surfaces a) associations: I) adenocarcinoma of stomach/GI tract - rapid onset, suspect malignancy if occurs on palms, soles, and oral or ocular mucosa II) diabetes (insulin resistance), obesity 2) acquired (late onset) ichthyosis - a) non-hereditary - dry and rough skin with scaling - "fish scale skin" I) dry small fine scales which are often lifted up at the edges II) colour differs from white, brown to grey III) severity varies from barely visible lesions to strong horny plates IV) lesions most often on knees and elbows, can also be trunk b) usually appears for the first time in early adult life c) most common cancer associated is Hodgkin's lymphoma d) other cancers: non-Hodgkin's lymphoma; cutaneous T cell lymphoma; lymphomatoid papulosis; multiple myeloma; breast, lung, cervical and liver cancers; and sarcomas 3) pyoderma gangrenosum - chronic recurrent ulcerative disease a) painful ulcers - lower legs, mucous membranes, peristomal sites b) inflamed nodule that ulcerates - I) rapidly expanding II) gunmetal-coloured border (purplish nodule or ulcer) III) heals with atrophic cribriform scar c) system symptoms - fever & signs of toxicity d) associations - I) IBD (ulcerative colitis, Crohn's disease II) myelodysplasia & myeloproliferative disorders III) rheumatoid disease, diabetes (& Bechet's)

Explaining acne

1) acne vulgaris - commonest clinical variant a) common disease of pilosebaceous unit characterised by comedones, papules & pustules b) affects 85% between 12-24, onset usually at puberty (most resolve by early 20s) c) M>F in adolescents 2) normal pilosebaceous unit - a) sebaceous gland secretes sebum (oil) into hair follicle canal or duct which acts as an emollient to skin b) P. acnes and other bacteria also live within hair follicles (commensals) c) pilosebaceous units in acne have larger sebaceous glands & small residual hair follicles, mainly on face, chest and upper back 3) obstruction of pilosebaceous follicle (microcomedo formation) produces a comedone (blackhead - impacted with keratin and lipid) a) P. acnes causes inflammation = papule, pustule or nodule (or non-inflammatory eg/ closed comedones - whiteheads) 4) myths - a) acne is not just a disease of teenagers b) poor hygiene does not cause acne & no good evidence fatty foods c) drinking copious amounts of water doesn't improve acne either 5) aggravating factors - a) occlusive cosmetics/hair products b) heat/humidity c) excessive/vigorous washing d) manipulation of lesions e) exogenous meds eg/ OCP, steroids

Systemic disease and the skin

1) adrenal disease - a) striae: Cushing's (inc cortisol) eg/ adrenal hyperplasia, adrenal carcinoma or benign adenoma (or oral steroids) b) hyperpigmentation of palmar creases or buccal mucosa: hypoadrenalism (low cortisol) - idiopathic autoimmune disease (commonest), adrenal infarction, infiltration (tumour and TB), or iatrogenic (surgery). Pigmentation due to compensatory increase in ACTH and other pituitary hormone c) Cushing's symptoms - truncal obesity, moon face, buffalo hump, telangiectasia, ecchymoses, hypertrichosis 2) hyperlipidaemia - a) xanthelasma, eruptive xanthoma, tuberous xanthoma, tendinous xanthoma b) xanthomas: deposition of abnormal lipid in skin (normally primary hyperlipidaemia) c) secondary hyperlipidaemia - xanthelasmata, eruptive xanthomata, tuberous xanthomata or tendinous xanthoma, due to eg/ DM, hypothyroidism, pancreatitis, obstructive liver disease, renal failure

Classifying eczema

1) atopic eczema - a) familial predisposition to eczema, asthma, hayfever b) debilitating, chronic, itchy inflammatory disorder, with relapses c) infants = face & exposed surfaces, children = flexural sites d) most pts seen in hospital have inc circulating IgE. Skin prick testing to environmental allergies such as house dust mite are often positive e) diagnostic criteria - itchy skin + 3 of: I) pmx or fmx of atopy II) visible flexural dermatitis (cheeks <10 yrs) III) dry skin in last year IV) early onset (< 2 years old) f) prevalence in children 10-20% g) dec with age - 50% gone by 2, 80% by adolescence h) cause unclear - mutations in fillagrin gene? Combination of genetics & environment? i) exacerbations: illness, skin infection, teething, stress, change in weather 2) discoid (nummular) eczema - a) seen at any age (mostly middle-aged men) b) discrete plaques - disc like, well demarcated lesions c) any site (often limbs) d) may be manifestation of atopic eczema (pathogenesis not understood) e) often secondarily infected f) tx - potent steroid (betnovate/dermovate) 3) seborrhoeic eczema - a) any age (often young-middle aged adults) b) exacerbated by alcohol or immunosuppression c) pathogenesis not fully understood, associated with Pityrosporum spp e) adult symptoms - I) affects areas rich in sebaceous glands eg/ scalp, sides of nose, eyebrows and ears, upper trunk II) erythema and scaling, dandruff III) folliculitis and flexural variants IV) often recurs f) infant symptoms - I) first few weeks of life II) moist, shiny erythema in body folds III) scalp - yellowish scales g) tx - I) adults - ketoconozole shampoo, imidazole +/- 1% hydrocortisone II) infants - emollients, 1% hydrocortisone +/- antifungal III) scalp tx - Salicylic acid in aqueous cream, olive oil

Differential diagnosis of benign and malignant pigmented lesions

1) atypical moles (compare with other moles, junctional, compound, intradermal stages) 2) blue naevus 3) seborrheic wart 4) pigmented BCC 5) dermatofibroma 6) pyogenic granuloma 7) congenital naevi 8) halo naevus 9) naevus spilus 10) spitz naevus

Clinical features & different types of cataracts

1) cataracts - a) any opacity on or within lens b) incidence inc with age, by age of 100 has 100 % incidence - major cause of blindness c) total cataract - surface wrinkles as cortical matter liquified - sign of long-standing cataract d) aetiology (7) - age-related, traumatic, metabolic, toxic, secondary (complicated), maternal infection or drug ingestion, hereditary 2) age related cataract: a) subcapsular cataract - I) anterior - just below capsule of lens II) posterior - behind nucleus. Trouble with bright sunlight - reading vision affected more than distance vision b) nuclear sclerotic cataract - exaggeration of normal ageing leads to myopic shift c) cortical cataract - opacification of lens cortex, opacities assume a radial spoke-like configuration 3) congenital cataract: a) opacity in lens - starts at middle (nucleus) b) disrupted red reflex - light down pupil is reflected from retina, any opacity within path of light (cornea-lens-vitreous), disrupts red reflex - cataract gives blocked (total or partial) red reflex c) senile cataracts affect whole lens (cortex) 4) metabolic cataract: a) diabetes - I) T2DM - age-related cataract appears earlier (may have coexisting retinopathy - affects tx) II) true diabetic cataract - osmotic overhydration of lens = post or ant lens opacities = snowflake opacities b) galactosaemia - mannosidosis, Fabry's disease, Lowe's, Wilson's c) hypocalcaemic syndromes 5) traumatic cataract: a) penetrating eye injuries - direct damage to lens b) blunt injury - iris pigment imprinted on to lens (Vossius Ring) c) glass blowers' cataract - infrared radiation affects anterior lens capsule d) electric shock, ionising radiation

Management of cataracts

1) cataracts mx - a) degree of disability - reading, driving? occupation? impact on household work etc b) pt's opinion c) best corrected visual acuity i.e. after a recent refraction d) coexisting ocular pathology eg/ macular degeneration, advanced glaucoma e) general health, cardiac or resp disease - wait until health is better (age - not a CI) f) no need to wait until cataract 'matures' 2) cataract mx biometry - a) calculation of required intraocular lens power based on corneal diopteric power, axial length of eye & IOL formula b) can potentially make any refraction pt desires, so high myope may be made emmetropic c) most patients are made slightly myopic to enable some reading vision 3) cataract types of operations - a) intracapsular cataract extraction (ICCE) - very rarely performed I) large corneal/limbal wound (10-12mm), whole lens extracted, pt left 'aphakic' (no lens in eye) - need to wear thick aphakic glasses + 10 diopters c) extracapsular cataract extraction - becoming less common I) large corneal/limbic wound (10-12mm), anterior lens capsule opened to deliver lens nucleus via wound, remaining intracapsular lens material aspirated, posterior chamber 'PMMA' lens placed in front of remaining posterior lens capsule, wound sutured - astigmatism & post-op recovery

Cinical presentation of skin conditions caused by Varicella zoster virus & discuss management

1) chicken pox - transmitted by VZV in respiratory droplets a) incubation is 14-17 days & pts infective 2 days before & for 5 days after eruption b) common amongst children, can be severe in adults associated with significant complications eg/ pneumonia, hepatitis and encephalitis c) children develop headache, fever and malaise for 1-2 days followed by onset of vesicles on trunk, face and scalp. Oral lesions may be present. Rash lasts 10-14 days with crusting and occasionally scarring d) pregnancy: chicken pox in first 20 weeks of pregnancy associated with 2% risk of foetal damage including neurological, ocular and limb defects e) disseminated infection: fatality if oral pred or immunocompromised e) tx - adults, immunocompromised or on pred = oral aciclovir 5-7 days 2) shingles - dermatomal varicella-zoster infection due to reactivation of virus in nervous tissue in dorsal root ganglion cells and schwann cells a) pain & tingling for 24-48 hrs then dermatomal eruption of vesicles b) thoracic, cervical, ophthalmic branch of CN V, lumbosacral c) if immunocompromised zoster may be disseminated and haemorrhagic d) most zoster reactions heal without scarring but persistent pain common e) pts with shingles are infectious and active virus is contained in vesicles 3) complications of shingles - a) post-herpetic neuralgia - persistent pain > 3 months b) secondary Infection - common, risk of septicaemia and skin necrosis c) motor nerve palsy - facial nerve (Ramsay-Hunt Syndrome): facial palsy, ear pain and vesicles external ear; vestibulocochlear nerve: sensorineural deafness, dizziness, vertigo; ocular muscle palsies d) eye complications: ileitis, keratinise, conjunctivitis e) encephalitis and meningoencephalitis 4) tx of shingles - if within 72 hours of pain/tingling: oral aciclovir for 5 days

Principles and various investigations for colour vision

1) color vision possible due to photoreceptors in macula of retina of eye known as cones a) cones have light-sensitive pigments that enable us to recognize color b) cones in macula - each cone sensitive to either red, green or blue light (different wavelengths) c) pigments inside cones register different colors & send info through optic nerve to brain, enabling pts to distinguish countless shades of color d) if cones don't have 1+ light-sensitive pigments, pts unable to see 1+ of the 3 primary colors 2) color vision deficiency - inability to distinguish certain shades of color aka "color blindness" a) most with color vision deficiency can see colors, but have difficulty differentiating between: particular shades of reds and greens (most common), blues & yellows b) pts totally color blind - achromatopsia, only black and white or in shades of gray c) aetiology - I) usually inherited X-linked recessive condition II) diabetes III) glaucoma, macular degeneration IV) Alzheimer's, Parkinson's disease, MS V) chronic alcoholism VI) leukemia, sickle cell anemia VII) meds eg/ drugs for hear, BP, infections, nervous disorders and psychological problems 3) diagnosis - Ishihara colour chart a) pt shown a series of specially designed pictures composed of colored dots = pseudoisochromatic plates - pt asked to look for numbers among various colored dots b) pts with normal color vision see a number, while those with a deficiency do not. On some plates, a person with normal color vision sees one number & pt affected sees a different number c) pseudoisochromatic plate testing can determine if a color vision deficiency exists & type of deficiency, but additional testing needed to determine exact nature & degree of color deficiency 4) early detection of color deficiency vital as many learning materials rely heavily on color perception or color coding 5) tx - no cure for inherited color deficiency, if due to illness or eye injury tx cause a) special tinted eyeglasses or red-tinted contact lens on 1 eye can inc some people's ability to differentiate between colors, though nothing can make them truly see the deficient color

Pathophysiology of acne

1) comedogenesis - a) inc keratin & sebum production causes corneocytes to stick together b) shed corneocytes & sebum form a plug = closed commedone (whitehead) or open comedone (blackhead) 2) sebhorroea - a) inc sebum (inc sebum excretion rate) b) ? response to androgens ? due to abnormal sebum composition 3) Propionibacterium acnes - a) thrives in sebum so colonises pilosebaceous duct (follicle) c) organism or products interact with host cells = inflammation 4) inflammation - a) reaction to P. acnes & sebum lipids b) changes in epidermal barrier function c) ductal cells secrete cytokines

Management of venous leg ulcers

1) compression - 3 or 4 layer compression at 40mmHg (ankle) a) low-adherent dressings are applied and replaced weekly b) alternative dressings may be considered, to help with pain (hydrocolloid), heavy exudate (alginate), or slough (hydrogels) c) graduated compression dec venous reflux & ankle oedema & inc venous blood flow, improving microcirculation and encouraging healing d) no compression if ABPI <0.8, active phlebitis, DVT, or cellulitis 2) superficial venous surgery 3) skin grafting 4) cleansing and debridement - ulcer irrigated at each dressing change with warm tap water or saline & dried, also - slough, necrotic, fibrous, or excess granulation tissue removed 5) pentoxifylline - effective adjunct to compression bandaging for venous leg ulcers, may be effective in absence of compression 6) self help - a) keep mobile with regular walking - exercise calf muscle pump function b) elevate legs when immobile c) avoid trauma and wear appropriate (well-fitting) footwear d) use an emollient frequently e) examine legs regularly for broken skin, blisters, swelling, or redness f) healthy lifestyle eg/ lose weight, balanced diet (malnutrition impairs ulcer healing), and drink alcohol within recommended levels. Stop smoking NB/ can be managed in community by specialist in ulcers & dressings eg/ district nurse or tissue viability nurse

Correct application of graduated external compression for venous ulcers

1) compression aims to counteract the force of gravity and promote normal flow of venous blood up leg - acts on venous and lymphatic systems to improve venous and lymph return and reduce oedema 2) compression therapy systems categorised according to pressure produced on a model limb at the ankle during laboratory testing 3) category pressure - a) mild <20mmHg b) moderate 20-40mmHg c) strong 40-60mmHg d) very strong >60mmHg 4) effective compression should provide some compression at rest, but work effectively during exercise 5) pts with ABPI <0.8, diabetic foot ischaemia/neuropathy or cardiac failure need specialist referral before compression therapy considered 6) additional bandaging skills - pts with abnormal limb shape, abnormal peripheral circulation, skin problems and previous bandage-related problems 7) bandages applied with maximum dorsiflexion of ankle (toe towards nose) 8) ensure compression over the calf muscles 9) additional padding may be required beneath compression to adjust shape & protect an area at risk of pressure damage or to manage excessive exudate

Different types of benign melanocytic naevi

1) congenital - a) 1% children have small naevi (less common than acquired moles) b) can vary in size, rare giant 'bathing trunk' naevi: high risk of malignancy d) Mongolian blue spot: melanocytes in dermis - Asians, benign 2) acquired - develops after birth, usually <25: a) atypical moles (abnormal ABC so often excised. Genetics + childhood sun exposure) - I) acquired moles appear late childhood to adolescence - natural involution with age: II) at start - flat & dark, see nests of melanocytes in junctions of dermis & epidermis = junctional naevus III) with age some nests go deeper into epidermis = compound naevus (melanocytes can be in epidermis & dermis), dome shaped, brown papule IV) with age nests drop into dermis = intradermal naevus. Dome shaped & skin coloured. Most common on face b) halo naevus - undergoing regression, benign c) blue naevus - melanocytes in dermis, usually benign, often extremities 3) failed maturation/migration of melanocytes in utero

Recognise and describe clinical features of benign lesions: dermatofibroma & neurofibroma

1) dermatofibroma - a) common benign fibrous nodule, most often on lower legs or arms b) dermatofibromas occur at all ages and in every ethnicity. F>M c) lesions made of a proliferation of fibroblasts. May have histiocytes d) firm nodules tethered to skin surface & mobile over subcut tissue - skin dimples on pinching lesion e) pink to light brown if white, and dark brown to black in dark skin f) usually asymptomatic, sometimes painful or itchy. g) dermatofibroma is harmless - reassurance. If nuisance or causing concern, lesion can be removed surgically 2) neurofibroma - a) neurofibromatosis is a genetic disorder that causes tumors to form on nerve tissue anywhere in nervous system b) neurofibromatosis 1 - I) signs evident at birth or shortly afterward, s/s often mild to moderate II) >6 flat, light brown spots on skin (cafe au lait spots) III) freckling in armpits or groin area. Freckles smaller than cafe au lait spots & occur in clusters in skin folds IV) Linsch nodules - tiny bumps on iris of eye. Don't affect vision V) neurofibromas - soft bumps on or under skin c) neurofibromatosis 2 - less common but more seveve I) s/s - gradual hearing loss, ringing in the ears, poor balance, headaches

Recognise and describe the cardinal physical signs of dermatophyte infection of the skin and nails

1) dermatophytes - invade & multiply in keratinised tissue: a) 3 genera: Microsporum, Trichophyton (most common), Epidermophyton b) transmission - anthropophilic, zoophilic, geophilic c) lay term = ring worm, medical term is tinea (corporis, manuum etc). Unilateral with clear border d) body = tinea corporis I) scaly plaques, outward spread with red scaly border and central clearing, pruritis, glabrous skin (non-hairy skin) e) groin = tinea cruris I) fungal infections very common in groin with an annular scaly edge, extending out from creases f) hands = tinea manuum I) asymmetrical involvement with scaling, much more prominent in one palm, spreading out from wrist proximally g) feet = tinea pedis/athlete's foot I) white maceration between toe webs, more severe = scaling, pustules and erythema on sole of foot, over time can spread, with more widespread bilateral involvement = moccasin feet h) scalp = tinea capitis I) more common in Afro-Caribbeans, scaling, pustules, alopecia, can have scarring, broken hairs II) persistence of fungus and reaction to it can lead to a boggy swelling known as kerion i) nails = tinea unguium/onychomycosis I) extremely common, especially on feet, various forms with distal white discolouration (yellow & thickened nail), loss of nail plate, onycholysis with nail lifting up from its bed and hyperkeratosis 2) differentiating from candidiasis - a) important clinical features - small satellite lesions and sometimes pustules at the edges of the eruption, unlike the clear, well defined edge of tinea 3) ix - a) for any suspected fungal infections need skin scrapings (scales) b) nail infections - nail clippings with sub-ungual debris c) scalp - infections which enter shaft of hair need a hair sample d) Wood's light - UV light filtered by Wood's glass

Framework for describing skin eruptions and lesions, and recording such clinical findings

1) describing pigmented lesion (to exclude melanoma) - a) Asymmetry - if you folded the lesion in half would it look the same b) Border - smooth & regular, irregularly irregular, or regularly irregular c) Colour - uniform colour, darker in centre, haphazard colour mix d) Diameter & distribution e) Elevation & evolution f) If A, B, C abnormal is more likely to be a melanoma NB/ always compare against other moles on body - look for the mole that sticks out 2) melanoma - a) major features - changing colour, shape, size b) minor features - bleeding, inflammation, itching, >7mm in size 3) ABC doesn't help with 2 skin cancers - a) BCC - well demarcated lesion, slightly shiny border - pearly & irregular, some telangtasia, small area of crusting, areas exposed to sun (tx with excision) b) SCC

Be able to diagnose erythema nodosum and suggest a list of possible triggers

1) diagnosis - inflammation of fat cells (panniculitis) under skin a) results in tender red nodules usually on both shins & calves b) typically resolves spontaneously within 30 days c) common inbetween 12-20 years of age (especially women) d) pre-eruptive - flu-like symptoms eg/ fever, cough, malaise, aching joints e) eruptive stage - 1-2-inch (25-51 mm) nodules below skin surface - I) subcutaneous nodules can appear anywhere on body, most commonly shins, arms, thighs, and torso II) new nodule appears red & hot & firm & painful to touch IV) joint pain & inflammation can continue for several weeks or months after nodules appear 2) triggers - a) IBD b) sarcoidosis (CXR shows hilar lymphadenopathy - good prognosis) c) Bechet's disease d) infection - streptococcal (allergic hypersensitivity to group A streptococcal antigens), TB, M. pneuomiae, EBV e) drugs - sulphonamides, OCP, penicillin, hep B vaccine f) cancers - non-Hodgkin's lymphoma, carcinoid tumours, pancreatic cancer g) idiopathic NB/ tx of underlying condition & NSAIDs NB2/ Ix: hx, exam, CXR, throat swab, ASO titre

Recognise and describe skin eruptions which may be caused by drugs such as urticaria, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis

1) drug eruptions (v common in hospitalised patients) a) non-allergic - I) intrinsic drug action on skin due to pharmacological properties (so predictable & dose related) eg/ striae & systemic steroids, photosensitivity & tetracyclines II) exacerbation of pre-existing disease eg/ lithium and psoriasis III) idiosyncratic eg/ fixed drug eruption from phenolphthalein b) allergic - I) unpredictable (don't occur in all) - latent period or 2nd exposure II) IgE mediated, cytotoxic, immune complex mediated or cell mediated III) internal organs may be involved & can be life threatening IV) most common = morbilliform rash affecting trunk & thighs (abx, sulphonamides) c) usual suspects - anticonvulsants, Abx esp sulphonamides & penicillins, NSAIDs, allopurinol, thiazide diuretics, gold and penicillamine d) usually within 8-21 days of initiation, need drug hx including OTC. Can occur if drug taken for a long time as well 2) Stevens-Johnson syndrome - a) prodrome of fever & respiratory symptoms b) 2+ mucosal sites - may be severe eye & oral involvement c) <10% body SA affected d) prolonged course e) painful red or purplish macules that spreads & blisters, then top layer of affected skin dies, sheds then heals (epidermal necrosis) 3) urticaria - a) raised, itchy rash. May be confined or widespread, size varies b) rash usually settles within a few days c) may be acute (rash clears completely within 6 weeks) or chronic urticaria (rash persists or comes and goes for >6 weeks, often over many years) e) cause - salicylates or ACEI (urticarial reaction), immunisations (transient)

Recognise and describe the cutaneous manifestations of diabetes

1) ecthyma - skin infection characterised by ulcers covered by crusted sores: deep form of impetigo - same bacteria, deep erosions of skin into dermis 2) tinea pedis - dermatophyte infection of feet aka Athlete's foot a) s/s - itching, scaling, and redness, in rare cases skin may blister b) fungus may infect any part of foot, but mostly between toes or bottom of foot or nails 3) necrobiosis lipoidica - necrotising skin condition (T1DM), also associated with RA a) most frequently appears on shins, sometimes bilateral, may also occur on forearms, hands, trunk, and, rarely, nipple, penis, and surgical sites b) lesions often asymptomatic, can be tender & ulcerate when injured c) 1st symptom = erythema not necessarily associated with a known injury d) plaques (hardened, raised area of skin), center of affected area usually has a yellowish tint while area surrounding is a dark pink, also central atrophy & telangiectasia e) more common in women 4) acanthosis nigricans - hyperpigmented velvety changes of flexural surfaces 5) fungal & bacterial infections 6) granuloma annulare - commonly presents <18, chronic a) can initially occur at any age, F>M b) aside from visible rash (may burn or itch), granuloma annulare is usually asymptomatic c) ring of papules over backs of forearms, hands or feet, often centered on joints or knuckles e) papules start as very small, pimple looking bumps, which spread over time from that size to dime, quarter, half-dollar size and beyond

Develop a management plan for a patient with atopic eczema

1) education, support, career advice 2) avoid exacerbating factors 3) treat dry skin - emollient prn 1st line a) emollients come in many forms and degrees of greasiness - soap substitute & applied directly to skin b) creams eg/ aqueous, ointments eg/ oilatum (bath), white soft paraffin c) emollients dec inflammation by vasoconstriction and inactivation of inflammatory mediators. Strength depends on age, site and type/severity of eczema 4) treat active eczema - a) 1st line - I) topical steroids II) ? antihistamines - old generation (sedative) for short periods only III) Abx erythromycin or flucox if infected (bright red, exudate, pustules) IV) topical tacrolimus and pimecrolimus - calcineurin inhibitors, do not cause skin thinning. Tacrolimus = same efficacy as potent topical steroid, facial eczema or those 'stuck' on strong steroids. Pimecrolimus = same strength as 1% hydrocortisone & 20x cost. Role unclear at present V) bandaging - occlusive bandaging: tar, zinc paste, wet wraps. Helpful with itching & excoriated eczema. Wet wraps useful in children with excoriation g) 2nd line tx - I) UV light II) oral prednisolone short term III) cyclosporine A (monitor BP, renal function, risk malignancy) IV) azathioprine V) ? diet ? Chinese herbs ? psychological interventions 5) topical steroid potency - a) mild = hydrocortisone 1% b) moderate = eumovate (hydrocortisone butyrate) c) potent = elocon, betnovate (betamethasone/mometasone) d) very potent = dermovate (clobetasone) 6) complications of atopic eczema: a) infection - I) bacterial - staphyloccus aureus, streptococcus II) viral - molluscum, HSV, warts b) psychological morbidity - teasing at school, missing games, sleep loss c) children - poor growth in those with severe disease or inadequate diets d) eczema herpeticum - virus colonises eczematous and normal skin, painful, punctate erosions, need oral/IV aciclovir

Features of an eczematous rash

1) erythema & pain & pruritis - acute & chronic 2) oedema of skin - acute 3) vesicles/blisters - acute 4) bleeding, weeping - acute 5) scaling, dryness - chronic 6) fissures & lichenification - chronic 7) most common on: flexors eg/ knees (backs) & elbows (insides), hands (especially fingers), face and scalp in children 8) bilateral eczema rare

Concept of skin failure

1) event in which skin & underlying tissue die due to hypoperfusion that occurs concurrent with severe dysfunction or failure of other organ systems 2) hypoperfusion of skin due to shunting to vital organs 3) hypothermia resulting from hypoperfusion 4) metabolic abnormalities of toxic metabolites from catabolism 5) acute, chronic, or end stage a) acute: "an event in which skin and underlying tissue die due to hypoperfusion concurrent with a critical illness" eg/ sepsis, MI, etc. b) chronic: "an event in which skin and underlying tissue die due to hypoperfusion with a chronic disease state" eg/ nephropathy/HD, neuropathy, PVD, MS c) end stage: "an event in which skin and underlying tissue die due to hypoperfusion concurrent with the end of life" eg/ cancer, ALS, MS

Main types of endogenous and exogenous eczema

1) exogenous - a) irritant b) infective allergic contact 2) endogenous - a) atopic b) seborrhoeic c) asteatotic d) gravitational e) discoid

Ocular anatomy and identify different ocular regions and its supporting structures with aid of diagrams and model of the eye

1) eye ball - a) anterior & posterior parts b) anterior has clear glassy cornea which is continuous with white part of eye (sclera) c) cornea & sclera form outer part of eye d) inside this is iris, ciliary body & choroid e) innermost = retina (lines inside of choroid). No retina on ciliary body f) lens suspended by ligaments to ciliary body g) space between cornea & iris = anterior chamber. Continuous with this is posterior chamber h) eye takes light in through cornea - travels through anterior segment to pupil, which allows an amount of light to pass through to lens. Lens focuses light onto macular region of retina, from which nerve fibres take the image formed to the brain 2) eyelids - a) upper lid is longer than lower b) poisoning - lower lid at junction of cornea & sclera (limbus @ 6 o clock), upper lid crosses onto cornea ~2-3mm (cross limbus by 2-3 mm). eyelid position changes as look up or down c) inside of eyelid lined by thick conjunctiva (fine mucous membrane), folded onto sclera - 'cul de sacs' at either end = fornix. No conjunctiva over cornea d) cornea anterior surface = stratified squamous, non-keratinising epithelium. Posterior = single layer endothelial cells (maintains hydration). Bulk of thickness from corneal stroma with regularly arranged collagen fibres (maintains clarity of cornea) e) lie in front of eyeball, eyeballs in bony socket, with nose between 2 eyeballs, so pathology of nose or paranasal sinuses can affect orbit or eye f) lacrimal drainage - lower & upper canaliculi join to form common canaliculus, opens into nasal lacrimal sack, which drains into nose - blockage in any part causes watering eyes. Also reason that eyes can water when have cold 3) fundoscopy - a) look for 3 Cs - colour (normally pink), cupping (normally 0.3) and contour (normally well defined border) b) exudates - 'salt sprinkling on pink blotting paper'. Well defined & granular. Lipoproteins precipitated from retinal BV fluid. Fluid reabsorbed & lipoprotein deposited in tissue. Can merge together c) cotton wool spots - poorly defined, edges are woolly. Microinfarcts of nerve fibre layer of retina d) look for laser scars - dec ischaemic drive to make BV shrink so can't bleed e) AV nipping/AV crossing defects - when arterials cross vein they share common adventitia, so hardening of arterial wall presses on vein which narrows- in atherosclerosis, HTN (also cotton wool spots) etc

Physiology and function of the eye

1) eye enables one to see the outside world - 2 eyes provide stereoscopic vision 2) tear film keeps anterior surface of eye moist and clear 3) intraocular pressure maintains shape of eye - shape essential for normal optics of eye 4) extraocular muscles keep the visual images in alignment 5) cornea & lens refract light 6) pupil size regulates amount of light entering eye 7) vitreous provides a clear optical media 8) light falling on retina is converted into neural impulses, which travel along visual pathway into visual areas of the cerebral cortex - V1, also V2-3 10) V1 - performs edge-detection to understand spatial organization 11) V2 - forwards pulses to V1 and receives them. Pulvinar - saccade and visual attention. V2 serves same as V1, but also handles illusory contours, determining depth by comparing L&R pulses & foreground distinguishment. V2 connects to V1 - V5 12) V3 - helps process 'global motion' (direction and speed) of objects. V3 connects to V1 (weak), V2, & inferior temporal cortex 13) V4 - recognizes simple shapes, gets input from V1 (strong), V2, V3, LGN, and pulvinar. V5's outputs - eye-movement motor cortices (frontal eye-field and lateral intraparietal area) 14) V5 - functionality similar to the others, but integrates local object motion into global motion on a complex level. V5 analyzes self-motion, whereas V6 analyzes motion of objects relative to the background 15) inferior temporal gyrus - recognizes complex shapes, objects, and faces or, in conjunction with hippocampus, creates new memories a) pretectal area - anterior, posterior and medial pretectal nuclei inhibit pain, aid in REM, and aid accommodation reflex, respectively b) Edinger-Westphal nucleus moderates pupil dilation and aids convergence of eyes & lens adjustment c) nuclei of optic tract involved in smooth eye movement & accommodation reflex, as well as REM

Risk factors for skin cancer

1) fair skin - less melanin in skin provides less protection from damaging UV radiation. Blond or red hair & light-colored eyes, freckle or sunburn easily 2) hx of sunburns - 1+ blistering sunburns as a child or teenager inc risk of developing skin cancer. Sunburns in adulthood also are a risk factor 3) excessive sun exposure, especially if skin isn't protected by sunscreen or clothing. Tanning, including exposure to tanning lamps and beds, also inc risk - tan = skin's injury response to excessive UV radiation 4) sunny or high-altitude climates (exposed to more sunlight) 5) moles - having many, or abnormal moles (dysplastic nevi) 6) precancerous skin lesions - AK or IEC 7) fmx or pmx of skin cancer 8) weakened immune system eg/ HIV/AIDS, immunosuppressants 9) exposure to radiation 10) exposure to certain substances eg/ arsenic

Risk factors for the development of malignant melanoma

1) fmx or pmx of melanoma 2) severe sunburn in childhood 3) inc UV exposure eg/ sunbeds, phototherapy 4) multiple dysplastic naevi 5) large congenital naevi 6) immunosuppression 7) fair skin type 8) genetic (e.g. Gorlin's syndrome, xeroderma pigmentosum) 9) inc age 10) human papillomavirus (SCC)

Name and recognise the different types of skin conditions that can be caused by Streptococcus pyogenes

1) group A Streptococcus - always pathogenic 2) may coinfect with Staphylococcus but step infections tend to have a more acute onset of action & more rapid effect 3) diseases due to primary infection with Group A Streptococci - a) cellulitis (including perianal) - I) acute, subacute or chronic infection of loose connective tissue II) most commonly GAS although other can be other streptococci eg/ G, C and B. Rarely S. Aureus III) acute streptococcal cellulitis - fever, malaise and systemic upset. Affected limb (mainly lower) normally erythematous, hot, painful and tender IV) look for underlying cause eg/ trauma, tinea pedis, ulceration, bites V) if very severe blistering may occur and skin necrosis of dermis. Rarely infection may rapidly extend into deep dermal tissues = Necrotizing Fasciitis VI) ix - blisters or possible sites of portal entry should be swabbed VII) tx - oral or IV Benzylpenicillin (1.2g) or Flucloxacillin (1g iv qds) for 10-14 days (4-6 weeks if severe). Recurrent - prophylaxis with Penicillin V VIII) if severe - death from septicaemia, myocarditis or renal failure due to nephritic toxins. Local complications - skin necrosis, necrotizing fasciitis, subcutaneous abscesses and permanent lymphoedema

General mechanisms by which ocular trauma is sustained

1) history - a) how & when did the injury occur b) any non-ocular injury c) first aid given d) past ocular hx & pmx e) dx inc allergies & last tetanus shot 2) exam - a) ABC - life threatening conditions take priority b) visual acuity with and without pin hole c) assess each ocular structure: orbit, eyelids, lacrimal apparatus, conjunctiva, cornea, anterior chamber, iris, lens, vitreous, retia, optic nerve, IOP d) pupils, eye position (proptosis), eye movements, visual fields, sensation (paraesthesia - corneal, maxillary) 3) ix - a) chemical injury - pH b) orbital injury - orthoptic assessment, CT c) penetrating eye injury - x-ray for intraocular foreign body, CT, USS 4) perforating injury - breach in ocular coats 5) non-perforating - contusion, blunt injury 6) corneal foreign body - a) hx - grinding injury b) exam - metallic foreign body on cornea +/- rust ring, anterior uveitis c) beware hammering metal injury - high velocity, may be intraocular foreign body - check with x-ray 8) blunt injury - a) symptoms - visual disturbance or loss of vision, pain, tenderness at rest or on movement, diplopia, rule out presence of penetrating injury, use of eye protection b) exam - I) VA, visual fields, IOP assessment II) external ocular exam - for lid trauma; periorbital bruising; facial fractures III) slit lamp exam for anterior segment exam of cornea, conjunctiva, sclera, anterior chamber for presence of hyphaemia IV) pupil exam for RAPD, traumatic mydriasis V) fundus exam - absence of red reflex = vitreous haemorrhage, retinal detachment VI) extraocular mvmt - restriction of ocular mvmt may be due to fracture of orbital floor or wall, retrobulbar haematoma, cranial nerve plexus c) ix - ocular USS, x-ray or CT of orbits in suspected cases of blow out fracture of orbital floor, or other orbital walls - rule out presence of head injuries

Differences between different types of contact lenses and their uses

1) indications for use - a) visual - anisometropia, high myopia, aphakia, irregular cornea, scarring, keratoconus, corneal grafts, refractive surgery failure b) others - occupational eg/ theatre, sports; cosmetic eg/ avoid spectacles (psychological?), change eye colour; medical eg/ therapeutic, bandage; physical inability to wear spectacles eg/ allergy to frame materials, shape of facial features 2) 2 main types of contact lenses: a) soft lenses - generally fitted in high street practices, also silicon hydrogel lenses - newer, type of soft lens - extended or continuous wear b) rigid gas permeable lenses (RGPLs) - generally fitted in hospital eye service 3) soft lenses - a) disadvantages - I) can split II) deposition from tears III) more expensive IV) dehydrate if left out of solution or not in situ b) advantages - I) flexible & easy to fit (large diameter so stay secure) II) good initial comfort III) good VA if low level astigmatism IV) safer for sport V) may be used for extended wear

Different clinical presentations of psoriasis

1) inflammatory skin disorder causing inc turnover of skin due to inc keratinocyte proliferation, chronic & relapsing a) red scaly plaques b) most commonly extensor surfaces & scalp 2) epidemiology - a) 2% population, prevalence dec in Orientals, M=F b) 2 age groups of onset - late teens to early 20s (earlier in females), 50s 3) aetiology - a) genetic & environmental b) fmx c) HLA - CW6 4) histology - a) acanthosis (thickening of epidermis) b) collections of neutrophils within epidermis = Munro micro abscesses c) rete ridges of epidermis are elongated and dip into dermis d) bits of dermis between rete ridges = papillae and, in psoriasis, these are quite thin, known as supra-papillary thinning e) blood vessels within these papillae are often quite dilated f) absent granular layer g) subcorneal microabcesses

Clinical features of different types of glaucoma including the changes in the optic disc

1) intraocular pressure - normal distribution in population, with a shift towards R, mean IOP in >50 = 15.5mmHg 2) to view where aqueous drains from need to view eye with contact lens eg/ golden single mirror contact lens - allows to see into angle of eye. In a normal eye angle is open (meshwork all visible) 3) glaucoma = disorders where IOP is inc to damage normal visual process. Factors that influence level of IOP in eye - rate of aqueous humour production & resistance of drainage of aqueous humour 4) classification of glaucoma - a) primary - open angle or angle closure glaucoma b) secondary - due to pathologies (not drainage apparatus) including trabecular meshwork: I) inflammatory eg/ uveitis II) neovascular eg/ diabetic retinopathy, CRVO III) pigment dispersion syndrome, pseudoexfoliation syndrome, traumatic hyphaemia 5) progressive open angle glaucoma - a) epidemiology - commonest cause of treatable blindness after cataracts, 1% >40, 5% >75 b) risks - inc IOP, fmx, myopia, black race, diabetes c) pathology - I) inc IOP +/- vascular factors (optic nerve head susceptible to damage) = II) loss of retinal nerve fibres (photography) = III) optic disc excavation (cupping) = IV) visual field defects = tunnel vision = blindness V) main cause is inc in IOP due to inc resistance of drainage channels in angles of eye eg/ trabecular meshwork d) characterised by - I) inc IOP of >21 mmHg II) open angle III) glaucomatous cupping & visual field loss e) diagnosis - I) asymptomatic until almost blind (can lose 40% nerve fibres before visual field defect & 90% before symptomatic) II) unilateral - brain can compensate until field defect approaches centre of vision III) detect early to prevent serious visual disability - opportunistic screening: optic disc exam (slit lamp), IOP reading (Goldmann or non-contact tonometry), visual field analysis (Humphrey visual field analyser), visual acuity

Common exacerbating factors for atopic eczema

1) irritants (eg/ soap, nylon, wool, detergent) 2) illness/teething 3) skin infection 4) stress 5) change in weather eg/ cold & dry, dampness 6) allergens eg/ house dust mites, pet fur, pollen and moulds, cow's milk, eggs, peanuts, soya, wheat 7) hormonal changes eg/ in days before period, or during pregnancy

Different sub-types of melanoma

1) lentigo maligna (melanoma in situ) - a) begins as tan irregular macule (large freckles) that extends, with differing shades throughout b) occurs on sun-damaged atrophic skin in elderly (usually 70+) c) ~40% lentigo maligna progress to invasive lentigo maligna melanoma d) lesion grows slowly for 5-15 yrs in precursor form before invasion e) neoplastic melanocytes along the basal layer 2) superficial spreading melanoma - 70% all melanomas, most common type of cutaneous melanoma in light-skinned people a) affects adults of all ages, peaks 40-50 b) can arise in a preexisting melanocytic nevus c) slowly changing mole over 1-5 yrs in intermittently sun-exposed areas with greatest nevus density eg/ upper backs & lower legs d) starts as deeply pigmented macule or plaque with intact skin markings - thin. Earliest change = focal area of darkening within a preexisting nevus e) pigment ranges from black & blue-gray to pink or gray-white. Absence of pigmentation within an SSM often represents regression of melanoma f) neoplastic melanocytes throughout the epidermis

Pathophysiology of venous leg ulcers

1) loss of valve competency in deep veins - valves normally allow blood to flow up leg towards heart & also prevent backflow down leg. Causes: a) hereditary b) damaged after venous thrombosis (DVT, thrombophlebitis) c) age related damage (eg/ varicose veins) d) childbirth or surgery 2) back pressure in small vessels 3) resulting oedema further impairs blood flow 4) persistent high pressure in leg veins = damage to tiny BV in skin 5) skin becomes dry, itchy & inflamed 6) poor blood supply so skin doesn't heal well so can easily break down to leave open wound after minimal trauma = ulcer forms 7) may also be due to calf-pump failure - neuromuscular dysfunction a) constantly high pressure b) white cell trapping? c) microcirculatory failure (ischaemia, inflammatory mediators) d) liposclerosis e) ulceration

Recognise and describe the cutaneous manifestations of SLE

1) lupus erythematous - SLE (divided into acute, subacute or chronic) a) acute lupus: I) photosensitivity: macular erythema - butterfly distribution from sun II) transient & non-scarring III) associated with anti-dsDNA IV) scarring alopecia V) multi-system involvement (erythema nodulosum) b) may be associated with inc ASOT (eg/ Henoch schenlein purpura) c) cutaneous small vessel vasculitis - I) palpable purpura 1mm-cms, lesions on ankles/lower legs II) leucocytoclastic vasculitis III) systemic symptoms raises suspicion of systemic vasculitis IV) causes - infection, drugs, CT disease, neoplasm d) Henoch Schonlein Vasculitis/Purpura (type of small vessel vasculitis) - I) small vessel vasculitis - resp infection, purpuric lesions on limbs & buttocks II) common in children & young adults III) can cause arthralgia, arthritis, haematuria & abdo pain IV) IgA immune deposits V) inc risk - nephrotic syndrome, renal failure e) types of vasculitis - cutaneous (including HSP), CT disease (eg/ rheumatoid, Wegener's granulomatosis), lupus erythematous, infection (eg/ meningococcal septicaemia, post-streptococcal, hep C, drugs - sulphonamides, indomethacin) f) cause of vasculitis - allergic hypersensitivity reaction to group A streptococcal antigens g) ix for cutaneous vasculitis - I) FBC, U&Es, LFTs, ESR II) ANA, ANCA, RhF III) HCV culture, urine dipstick, ASO titre/throat swab

Defining morphology

1) macules - flat (impalpable), discrete areas of altered colour, any size 2) papules - raised, felt on palpation, <0.5cm. many subtypes: flat topped, sessile, pedunculated, umbilicated, filiform, warty 3) nodules - raised, palpable between finger and thumb, >0.5cm 4) cyst - papule or nodule lined by epithelium containing fluid, pus or keratin, fluctuant 5) plaques - any size, predominantly flat-topped, palpable, most are elevated (occasionally a plaque can be depressed/atrophic) a) can be polycylic, annular etc 6) wheals - dermal plaque or papule, due to dermal oedema so non-scaly, puncturing will not cause leakage of fluid 7) blisters - a) vesicles - fluid filled lesions <5mm, single or multiple b) bullae - fluid filled lesions >5mm c) eg/ unilocular e.g. friction blister, multilocular e.g. pompholytic eczema 8) pustules - pus filled blisters, yellow or green if older, dry to brownish scabs 9) abscess - large collection of pus 10) erosion - skin break of epidermis only 11) ulcer - skin break of epidermis extending into the dermis 12) excoriations - erosion or ulcer caused by scratching 13) fissure - skin break causing small slit

How to distinguish irritant contact from allergic contact dermatitis

1) main difference between rash caused by allergic contact dermatitis & one caused by irritant contact dermatitis is that the latter tends to be confined to the area where the trigger touched the skin, whereas in allergic contact dermatitis the rash is more likely to be more widespread on the skin 2) allergic contact dermatitis rash usually appears after a 1-2 days after exposure to allergen, unlike irritant contact dermatitis that appears immediately after contact with trigger

Treatment of fungal infections of the skin and nails, and recognize when systemic therapy is required

1) most localised skin infections respond to topical anti-fungal agents eg/ Azoles (Miconazole) or topical Terbinafine 2) for nail, scalp and hair infection or widespread skin infection (esp if immunocompromised) = systemic agent eg/ Terbinafine or Itraconazole 3) topical - for localised skin infections - a) terbinafine - fungicidal I) given orally & topically II) most effective oral agent for dermatophyte infection III) adverse SE rare IV) duration - 12 weeks (toenails), 6-12 weeks (fingernails), 2 weeks (skin) b) azoles (Ketoconazole) - fungicidal I) metabolised by liver: cytochrome P450 - care if pt has pre-existing liver disease; LFTs monitored (inc effect of ciclosporin, phenytoin) II) plasma concentration dec by concurrent use of rifampicin III) 2 types - imidazoles eg/ Ketoconazole, Miconazole; triazoles eg/ Fluconazole, Itraconazole IV) Ketoconazole - risk of hepatitis, inhibition of androgen synthesis (gynaecomastia, so rarely used systemicaly), usually topical. Can be shampoo V) systemic agents, such as Fluconazole and Itraconazole are very effective & have few SE c) polyenes (Nystatin) 5) systemic - nails, scalp, hair, widespread infection, immunocompromised - a) terbinafine b) azoles (Itraconazole) c) griseofulvin - fungistatic I) long duration - 6 weeks for skin/hair, 6-12 months for toenails II) SE - may induce photosensitive rash, nausea, headaches, hepatic enzyme inducer (phenobarbitone, coumarins) III) only licensed treatment for tinea in under twelves 6) candidiasis tx - a) polyenes eg/ Nystatin or Amphotericin B if systemic infection b) other common tx - topical Azoles eg/ Clotrimazole or oral Fluconazole

Recognise and describe the cutaneous manifestations of thyroid disease

1) myxoedema (pretibial) aka Graves' dermopathy a) almost always preceded by ocular signs in Graves' disease b) mucin deposition = waxy, discolored induration nodules or plaques—peau d'orange appearance, on anterior aspect of lower legs, spreading to dorsum of feet, or non-localised, non-pitting oedema c) advanced cases may extend to upper trunk, arms, face, neck etc d) may be painful or pruritic e) lesions resolve very slowly 2) xerosis a) occurs most commonly on scalp, lower legs, arms, hands, knuckles, sides of abdomen, and thighs b) s/s - scaling (visible peeling of outer skin layer), itching, and skin cracking

Different therapies for glaucoma and their side effects, the importance of patient compliance and the consequences of delayed diagnosis and treatment failure

1) open angle glaucoma mx - a) natural history of early field loss I) IOP > 30 = blind in 3 years, IOP 25-30 = blind in 6 years, 21-25 = blind in 15 yrs b) want to prevent significant loss of visual function with minimum disruption to pts' lifestyle (ie if they won't lose much vision, might be better to leave it) 2) medical mx - a) drops to dec IOP, started in 1 eye & IOP remeasured after 3-6 weeks - effectiveness determined by comparing eyes: I) prostaglandin analogues eg/ latanoprost. SE - lash growth, iris pigmentation II) B-blockers eg/ timolol. SE - cardiac & resp. CI - asthma, COPD III) carbonic anhydrase inhibitors eg/ dorzolamide. SE - taste, acidosis IV) a-agonists eg/ brimonidine. SE - dizziness, syncope, allergy V) cholinergic/miotics eg/ pilocarpine. SE - eye ache, dim vision b) tablet to dec IOP - carbonic anhydrase inhibitor c) topical drops - I) long acting eg/ timolol LA, nyogen II) combinations eg/ prostaglandin analogue or a-agonist or CAI + B-blocker III) preservative free drops (if pt allergic to preservatives)

Role and relationship of the diverse team of healthcare professionals involved in ophthalmic care

1) ophthalmologist - medical physician who specializes in medical & surgical care of eyes & prevention of eye disease. Diagnoses & treats refractive, medical, and surgical problems related to eye diseases and disorders 2) optometry - vision care specialty concerned with health of the eyes, visual system & related structures 3) optometrist - health care professional who specializes in function and disorders of eye, detection of eye disease, and some types of eye disease mx. Optometrist conducts eye exams, prescribes corrective contact lenses and glasses, and diagnoses and treats eye disorders 4) low vision specialist - many optometrists and some ophthalmologists have additional credentials or specialization in low vision testing, diagnosis, and tx. Trained to conduct low vision eye exams and prescribe special low vision optical devices 5) orthoptist - allied health professional who works under supervision of ophthalmologist to evaluate & treat disorders of visual system with an emphasis on binocular vision (using both eyes to see) and eye movement problems 6) optician - health professional trained to supply, prepare, and dispense optical appliances through interpretation of written prescriptions. Fits and finishes eyeglass lenses and frames and may also dispense low vision devices, contact lenses, and artificial eyes NB/ appreciate the value and implications of registration of the visually impaired

Lesions in optic pathways & associated deficits

1) optic nerve defect before chiasm = blind spot (early) or complete loss of vision in 1 eye (late) 2) at chiasm = cutting nasal retinas so lose peripheral vision: bitemporal hemianopia eg/ pituitary adenoma 3) after chiasm = half of eye affected is opposite to side affected 4) optic tract = opposite half of eye to that side eg/ left superior quadrantanopia 5) optic radiations = opposite side, top or bottom quadrant depending on if top (Meyer's loop) or bottom radiation is cut 6) lesion on visual cortex = macular sparing - loss of hemifield on opposite side, apart from vision in fovea, or bilateral blind spots

Sensory and motor pathways of the eye

1) pathways - a) vision generated by photoreceptors in retina - layer of cells at the back of the eye b) information leaves the eye by optic nerve c) partial crossing of axons at optic chiasm d) after the chiasm, axons are called the optic tract e) optic tract wraps around midbrain then to lateral geniculate nucleus (LGN), where all axons must synapse f) LGN axons fan out through deep white matter of brain as optic radiations, ultimately travel to primary visual cortex, at the back of the brain 2) visual fields - a) info enters both eyes with a great deal of overlap b) image projected onto retina can be cut down the middle, with the fovea defining the center c) now have 2 halves of the retina - referred to as temporal half (next to temple) and a nasal half d) visual images are inverted as they pass through the lens, so in R eye, the nasal retina sees R half of the world, while temporal retina sees L half of the world e) if drew a line through world at your nose, you'd see everything to R of line. That field of view = R hemifield f) each eye gets info from both hemifields. For everything you see, both eyes actually seeing it - crucial for depth perception - but the image falls on one nasal retina and one temporal retina g) L half of brain controls RHS of body, and vice versa, so LHS of brain is only interested in visual input from RHS of world. To insure brain doesn't get extraneous info, fibers from the retina sort themselves out to separate R&L hemifield. Specifically, fibers from nasal retinas cross over at optic chiasm - whereas temporal retinas, already positioned to see the opposite side of the world, do not cross h) practical consequences of crossing - damaging visual system before chiasm affects 1 eye, both hemifields - like closing 1 eye. Damaging pathway after chiasm, damages parts of both eyes, and only 1 hemifield i) record visual fields by perimetry charts

Recognise and describe clinical features of the pre-malignant lesions: actinic (solar) keratosis

1) precursors of SCC 2) actinic keratosis (aka solar keratosis) - a) very common, esp on sun-exposed fair-skinned Caucasians b) >80% occur on back of hands, forearms and on head & neck c) risk factors - inc age, male, outdoor occupation or hobbies d) dysplastic lesions with small risk of progression to SCC e) lesions - single or multiple, present as macules or patches of scaling & erythema on sun-exposed skin, normally papules < 1cm in diameter f) may be flesh-toned, pink or brown g) often asymptomatic but may occasionally be sore or itch h) result of long-term sun overexposure

Discuss prognosis and management of pigmented lesions with patients

1) prognosis of invasive melanoma - depends of depth of invasion (Breslow thickness), 5 yr survival: in situ = 100%, <1 mm = 95%, 1-3 mm = 70%, >3 mm = 40% 2) mx of melanoma - a) wide local excision using 1-2 cm margin (depends on tumour thickness) b) LN clearance for regional metastasis (possibly sentinel node biopsy) c) no specific tx for distant metastasis 3) mx of BCC: want to eradicate tumour with gd cosmetic outcome - a) surgical options (most common) - I) simple excision, Moh's micrographic surgery II) Mohs micrographic surgery - high risk tumours. Bulk of tumour removed with a curette, then affected skin removed. Tumour is excised, divided and stained. 5 yr cure rates of 99% for primary and 95% for recurrent BCCs III) curettage & cautery, cryotherapy (both if low risk as no histological samples can be taken) IV) excised with at least 4mm margins & and at least as deep as subcut fat Specimen sent for testing. 5 yr recurrence rate following surgery = <2% b) non-surgical tx options - I) radiotherapy - sole tx or as adjuvant tx. Risk of radionecrosis & late complication of SCC at site of treatment limit its use II) Imiquimod (Aldara) - topical immune-response modulator, causes inflammation to destroy tumour III) photodynamic therapy - application of a photosensitiser to lesion followed by an activating (visible) light source - phototoxic reaction to destroy tumour IV) imiquimod + phototherapy - low risk tumours. Inc recurrence rates but cosmetic results are good

Systemic complications of severe psoriasis

1) psoriasis associations - a) 10% have arthritis, can occur before, after or without skin involvement b) peak age of onset of psoriatic arthropathy 40-60 years 2) 5 types of psoriatic arthritis - a) monoarticular or asymmetrical oligoarticular (knees, ankles, MCPs, oligo = involvement of < 5 joints) b) DIP (affecting distal interphalangeal joints) c) symmetrical RA like d) axial AS (ankylosing spondylosis) or RA like (affecting axial skeleton and sacro-iliac joints) e) arthritis mutilans (rare - all small joints of hand are affected and they telescope into one another, large functional impairment) 3) course of plaque psoriasis is unpredictable & relapsing 4) pustular flares provoked by systemic corticosteroids - can be fatal 5) adverse effects of systemic treatments (eg/ hepatic fibrosis from methotrexate) & phototherapy (eg/ PUVA-induced skin cancers) 6) psoriasis can affect pts differently - some learn to live with their psoriasis and find that it does not affect ADL; whereas others can't a) may have symptoms eg/ pain, itch and bleeding b) appearance often bothers pts & some are troubled by scales that fall from their skin and scalp eg/ avoiding wearing black, long sleeves & trousers c) some describe a lack of self-confidence and feelings of being 'unclean' d) tx can be problematic as messy & takes a lot of time to apply 7) participation in sports, certain occupations, & caring for family members can become difficult for those with plaques on hands & feet 8) prejudice - incorrect belief that psoriasis is contagious. Psychological distress can lead to depression & social isolation 9) psoriasis associated with obesity, CV (heart attack etc), DM, metabolic - inc rate of IBD, coeliac disease, lung & bronchus & upper GI & urinary tract & liver & pancreatic cancers, also non-melanoma skin cancers (SCC & BCC)

Skin biopsy techniques

1) punch biopsy - most used technique for skin biopsy a) diagnostic & therapeutic purposes - can be used for any solid lesion and small vesicle that can be contained within punch b) for non-facial lesions, a 4-mm punch is sufficient; in granulomatous conditions or with atypical features, biopsies of 5+ mm preferable c) area anaesthetized, skin stretched, punch rotated, resultant wound sutured or left to heal by secondary intention. Areas with good vasculature, viz. face, genitals, mucosa, heal rapidly with minimal scarring d) advantages - easy, obtaining uniformly shaped tissue e) disadvantages - biopsy may be inadequate & not have deeper tissue 2) shave biopsy - portion of lesion above level of surrounding skin is shaved off using a blade, superficial lesions eg/ seborrheic keratosis. Normally avoided as it does not include deeper tissues 3) saucerization biopsy - for vesiculobullous disorders & epidermal neoplasms like seborrheic keratosis - plane of cleavage passes through reticular dermis & occasionally through s/c tissue. Performed using a shaving blade 4) wedge biopsy - large lesions where length & breadth & depth of specimen is important eg/ subcut mycosis, margin of SCC. After anaesthetizing skin, a stab incision in a V or a triangular shape performed with scalpel blade. Most often lesion is left to heal by secondary intention 5) incisional biopsy - itaking a part of tissue for confirming diagnosis, commonly employed when inflammatory dermatosis suspected 6) excisional biopsy - entire lesion is completely and deeply removed till subcutis plane. Wound can be closed primarily by sutures. Preferred when a neoplasm is suspected

Appropriate supportive care for patients with skin failure

1) regular cleaning and removal of crusts from oral & nasal cavities 2) care of the eyes, genitalia, perianal region 3) 1-2x daily bathing in lukewarm water (35°-38°C) 4) IV line & urinary catheter 5) NG tube if severe mucosal involvement restricting intake or severely ill 6) hourly HR, RR, BP, and urine volume and osmolality 7) body temperature & gastric emptying (volume of gastric aspiration) recorded every 3-4 hours. Daily intake-output chart 8) adequate oral intake & pain relief 9) high protein diet: 2-3 g/kg body weight per day in adults and 3-4 in kids NB/ erythroderma (skin failure) causes impaired temperature regulation, and inc fluid loss = cardiac failure, tachycardia, anaemia, dehydration, electrolyte and protein loss, hypothermia and death from sepsis

Identify scabies and head lice infection using information from history and examination

1) scabies caused by sarcoptes scabiei mite 2) human-human transmission (& close contact) eg/ young children who hold hands, elderly patients visited by relatives - not clothing or dirty items 3) clinical features - a) itchy erythematous papules which become excoriated with time b) can detect burrows which are small tracks - in children may be associated with blistering of palms & soles due to severe host response to infestation c) common sites - finger webs, flexures, axillae, breasts, ankles and insteps d) severe form = crusted (Norwegian) scabies, more in immuno-compromised or elderly with a high mite load. Large nos. of mites, due to dec scratching (physical, mental, sensory disability), immunosuppression 4) head lice - a) v common, live on hair and feed on blood within scalp b) spread by close contact eg/ children or family members when playing c) transmit Staph aureus and Strep pyogenes d) presentation - I) persistent itching in scalp (pruritis), erythema, excoriations II) egg casings or nits - occasionally can see live lice on hair III) secondary eczema

Treatments for scabies and head lice, and describe how to use them properly

1) scabies tx - a) careful use of (scabicides) Permethrin (leave on for 12hrs) or Malathion (leave on for 24hrs). Repeat 1/52 after initial therapy (days 1 & 8) b) treat any close contacts ie members of family, all members of a ward c) wash clothes and bed linen d) inform pts that following tx itching may persist for several weeks - may lead to eczema (tx = potent steroid for a short period) 2) head lice tx - a) tx changes from time to time depending on local tx policy guidelines b) most important aspect of tx is fine combing to remove nit casings & using a suitable hair conditioner c) pediculocides eg/ Malathion, Permethrin and Carbaryl not very effective & resistance reported - leave on scalp for 12h, repeat in 10 days d) hair checked on a regular basis to make sure all nits are removed e) if no other tx works may need to shave head

Psychological importance of skin disease to patients

1) skin conditions can have a detrimental effect on relationships, work, social functioning, sports and ultimately mental health 2) psychodermatology - professional marriage of dermatology & psych 3) potential pts include: a) those with primary psych diseases who present to dermatology eg/ with delusional infestation, body dysmorphic disease, or dermatitis artefacta b) those with primary skin diseases eg/ psoriasis, alopecia areata, and vitiligo who have associated anxiety, depression, or even suicidal ideation c) those with skin conditions secondary to psychotropic drugs (eg/ psoriasis induced by lithium or β blockers); and those with psychiatric disease following drug treatment for dermatological disease (eg/ suicidal ideation after isotretinoin for acne vulgaris) 4) skin disease may elicit psychosocial comorbidities - stigma, look etc 5) psychosocial stresses may elicit skin disease 6) can lead to: a) low self-esteem, depression, social isolation b) anger/frustration c) embarrassment d) poor academic performance & higher unemployment

Recognise the large social and economic burden of skin disease to the community

1) skin disease is common 2) huge psychological disability 3) occasionally life threatening 4) key to unlocking systemic disease 5) epidemiology - affects 23-33% population, one of top 4 conditions seen by GPs

Give appropriate sun protection advice

1) spend time in the shade when sun is strongest - 11-3pm, March-October 2) make sure you never burn - at least factor 15 sunscreen 3) cover up with suitable clothing and sunglasses 4) no safe or healthy way to get a tan - tan doesn't protect skin 5) balance between protecting skin from sun & getting enough vitamin D 6) if plan to be out in sun long time apply sunscreen 2x - 30 mins before going out & just before going out 7) top up sunscreen after been in water, towel drying or sweating 8) extra care to protect babies & children as their skin is much more sensitive & damage from repeat exposure to sunlight could lead to skin cancer in later life (if <6 months keep out of direct strong sunlight) 9) take extra care if: pale, freckles, red or fair hair, tend to burn rather than tan, have many moles, have skin problems from medical condition, only exposed to intense sun occasionally eg/ on holiday, fmx of skin cancer 10) don't use sunbeds or sunlamps

Main side effects of topical steroids and the measures needed to safeguard against these

1) steroid SE (rare if appropriately used) - a) site dependant - face, axillae, upper thighs, age & SA dependant - young children, elderly b) striae & thinning of skin c) telangiectasia & perioral dermatitis d) glaucoma & cataracts e) adrenal suppression 2) prescribing steroids - a) ointment vs cream - ointments generally used rather than creams in eczema as inc efficacy & less likely to develop medicament allergy long term b) steroid applied 1-2x/day in bursts of a few days to allow steroid free intervals c)tx of active areas only

Aggravating factors of psoriasis

1) sunlight - dec severity during periods of inc sun exposure (improves in summer & worse in winter) but sunburn can lead to an exacerbation 2) infection & illness: a) streptococcal infection (guttate psoriasis) b) HIV & AIDS 3) psychological stress 4) postpartum hormonal changes 5) drugs eg/ lithium, antimalarials, withdrawal of systemic steroids, B-blockers, NSAIDs, ACEI, trazodone, terfenadine, gemfibrozil, Abx eg/ tetracycline, penicillin, imiquimod 6) smoking & alcohol 7) trauma - may be spread to uninvolved skin by trauma, friction NB/ 30% have fmx

3 common complications of chronic venous ulceration

1) superficial infection (give topical antiseptics) 2) cellulitis - (give systemic antibiotics iv antibiotics) 3) lymphoedema - (give compression etc for - risk of continued ulceration and infection)

Management of ocular trauma

1) superficial injuries - topical abx & analgesia 2) eye lacerations may require suturing 3) ocular injuries that need immediate referral to ophthalmologist - a) ocular chemical burns b) perforation of cornea or rupture globe c) traumatic hyphaemia d) lens subluxation or dislocation e) lacerated lid +/- nasolacrimal duct system f) traumatic optic neuropathy g) retrobulbar haemorrhage with inc IOP 4) corneal abrasion - a) if superficial - topical abx eye ointment to prevent secondary infection b) lamenellar superficial lacerations of cornea - ix with sodium fluorescein eye drop to detect leakage of aqueous (Seidel's sign) c) mx - bandage contact lens & topical abx for 2/52 5) traumatic iritis - topical cycloplegics steroid eye drops 6) traumatic hyphaemia - tx with bed rest with head elevation for 4 days to prevent rebleeding. Topical mydriatics & steroids for 2/52. Associated inc IOP tx with topical & oral antiglaucoma tx 7) traumatic cataracts - tx with phacoemulsification, cataracts with zonular dehiscence may need iris fixation Intraocular Lens implantation or scleral fixated lens implantation 8) retinal tears with or without retinal detachment - mx with retinal lasers & retinal detachment surgery 9) important effects of blunt injury - a) blood in anterior chamber - hyphaemia may be associated with inc IOP b) iridodialysis - detachment of iris root from ciliary body, may need direct surgical closure of defect c) iridocorneal angle resection diagnosed with gonioscopy may cause secondary glaucoma d) vitreous haemorrhage e) retinal oedema & haemorrhage - Commotio Retinae f) blow out fracture 10) perforating eye injury - lid laceration: full thickness, involving lacrimal canalicular system 11) corneal lacerations - intraocular foreign body, previous ocular surgery - wound dehiscence 12) chemical injury - washout with water/saline immediately, continue to irrigate & check pH a) acids coagulate proteins & have less penetration - alkali penetrate to anterior chamber & may lead to more damage

Describe 2 treatment options for scarring

1) tx for acne scarring done once active disease has completely settled 2) selected pts may have microdermabrasion or dermabrasion for superficial scarring, but not done routinely on NHS 3) laser resurfacing to improve appearance of atrophic scars, but risks leaving permanent pigmentory changes (eg/ hypopigmentation). No NHS funding 4) large ice-pick scars may be removed with punch biopsy and keloid scars may be treated with intralesional steroids

Be able to diagnose a leg ulcer by correctly interpreting clinical signs (differentiating venous & arterial leg ulcers)

1) venous ulceration - a) large b) superficial c) gaiter area d) signs of chronic venous disease eg/ varicose veins, lipodermatosclerosis, atrophic blanche, chronic oedema, venous eczema, haemosiderin colour e) may or may not be painful 2) arterial ulceration - a) typically painful b) often small, punched out ulcers c) tend to be deep (necrotic) d) occur over bony prominences & where there are end arteries e) usually dry base without granulation tissue f) symptoms of arterial disease eg/ hairless skin, dec or absent pulses & doppler flow measurement, cold leg, poor capillary return

Indication for and be able to discuss the risk and benefit of the following systemic therapies: cyproterone acetate, isotretinoin for acne

2) cyproterone acetate - a) hormonal - Dianette (OCP) - combination of cyproterone acetate (anti-androgen) and ethinyl oestradiol b) effective in women although slow onset - as effective as oral abx c) moderate-severe acne if failed to respond to systemic Abx, signs of hyperandrogenism, acne flares at menstrual periods d) S/E: CI if pregnant or breast-feeding, fmx or pmx of idiopathic venous thromboembolism & current venous thrombotic or embolic disorder 3) Isotretinoin (Roaccutane) - a) derivative of vitamin A - retinoid highly effective for tx of acne as tackles the root of the problem in acne development: sebaceous gland, so affects all subsequent pathogenic stages b) used when - persistent acne, pt fed up of taking tablets, severe inflammatory acne and significant scarring, tx pt with psychiatric disease, resistant acne c) dose based on body weight 0.5-1.0 mg/kg d) given for 16 weeks, continued improvement after stopping drug, followed by prolonged remissions e) dec SER by 90% f) 22-30% relapse rate g) S/E: I) mucocutaneous - dry skin & mucosa, dermatitis, itching II) teratogenic (females must be on effective contraception - 2 types) III) inc lipids, deranged liver function - fasting lipids, LFTs, FBC in all pts before tx, & repeated one month into treatment. Females must have -ve urinary pregnancy test and monthly pregnancy tests performed IV) arthralgia/myalgia V) initial flare of acne VI) depression?

Recognise and describe clinical features of malignant lesion: squamous cell carcinoma

3) SCC - a) malignant epithelial neoplasm of keratinocytes b) 2nd most common skin cancer (20% of NMSC) & incidence is rising c) presentation - I) individuals at greatest risk are fair skinned with excess sun exposure II) sun-exposed sites eg/ H&N, hands & legs most commonly affected. Can arise de novo or from sites of chronic skin inflammation eg/ discoid lupus erythematosus, old burn scars, sinus tracts, chronic leg ulcers III) can develop from precursors (AK or IEC). Can invade & metastasise IV) smoking, arsenic & immunosuppression inc risk for SCC. V) firm, flesh-toned, endophytic or exophytic indurated papule or nodule or a "non-healing lump". Painful, oozes, bleeds or enlarging rapidly, usually on sun-exposed site. Often has keratinized surface or keratin plug hx shows rapid growth VI) lesion may be smooth, scaly & ulcerated, crusted or hyperkeratotic VII) biopsy to include base so invasiveness & thickness established d) 5-year survival rates for cutaneous SCC - 75%-90%, metastatic = 25% e) "bad" prognosis - site (ear, lip), size>2cm, thick depth, non-sun exposed sites, areas of chronic inflammation, poorer differentiation, immunosuppression, mucosal SCC, perineural invasion 4) cutaneous horn - a) compacted keratin that may have AK/IEC/SCC at base b) can be benign eg/ seborrheic keratosis c) excise lesion - histology 5) other types of NMSC - a) Merkel cell carcinoma (2-yr survival rate = 50-70%) b) microcystic adnexal carcinoma lymphoma NB/ skin cancer MDT - dermatologists, plastics, histopatholigists, radiotherapists & specialist nurses. Premalignant skin lesions, and sometimes low risk BCCs managed by GPs if trained. Give sun protection advice

Recognise and describe clinical features of benign lesions: epidermoid and pilar cysts, keratoacanthoma, haemangioma (strawberry naevus, cherry angioma, pyogenic granuloma), seborrhoeic keratosis

3) epidermoid & pilar cysts - a) look like small smooth lumps under surface of skin b) generally benign & cause no harm or problems c) if required, can usually be removed surgically d) epidermoid cyst - cyst sac forms from cells normally on epidermis. Mostly in young and middle-aged adults on H&N, chest, upper back & genitals e) pilar cyst - cyst sac forms from cells similar to those in bottom of hair follicles. Middle-aged women on scalp. Several develop at once f) both made of keratin g) look very similar but distinguished from microscopy 4) haemangioma - a) haemangioma = collection of small blood vessels that form a lump under skin, aka 'strawberry marks' as surface of haemangioma may look like the surface of a strawberry b) superficial or deep - some are a combination with a raised, red area on surface of skin & bluish swelling of abnormal blood vessels deeper in skin c) 1/10 babies has a haemangioma, F>M d) superficial haemangiomas - raised, bright red area of skin, feels warm as abnormal blood vessels close to surface. Superficial haemangioma may appear initially as a small area of pale skin on which a red spot develops e) deep haemangiomas - may appear bluish as abnormal blood vessels deeper in skin. Sometimes not noticeable for weeks, only appearing as a lump as haemangioma grows f) not usually present at birth but develop a few days or weeks later. Often grow rapidly in first three months g) most children only develop 1 haemangioma (can have many) h) haemangiomas can appear anywhere on the body - mainly H&N, particularly cheek, lips or upper eyelid. Can also be on organs inside body (US) 5) sebhorroeic keratosis - a) harmless warty spot appears during adult life as a common sign of skin aging. Some people have hundreds of them b) can arise on any area of skin except palms & soles & mucous membranes c) highly variable appearance - flat or raised papule or plaque, vary in size, varying colour eg/ skin, yellow, grey, brown etc, smooth, waxy or warty surface, solitary or grouped eg/ scalp, under breasts, over spine or in groin d) stick on to skin surface like barnacles 6) keratoacanthoma - a) starts as small papule and undergoes rapid growth into a symmetrical dome shaped, flesh-toned nodular tumour with a central crateriform core filled with a keratinous material. Often on face b) telangiectasia often visible around tumour c) size at presentation is 1-2 cm d) after initial rapid growth, indolent plateau phase followed by involution e) aetiology - sun or tar exposure, pitch and petroleum oils f) differentiating tumours from SCC difficult - incisional biopsy or formal excision. Symmetry, a shoulder of epidermis over sides of central crater, epidermal proliferation beneath crater favour KA

Systemic disease and the skin contd.

3) gastroenterology - a) dermatitis herpetiformis - I) typical sites: bilateral, symmetric distribution on extensor elbows and knees, scapula, sacrum and buttock-intensely itchy vesicles, usually excoriated III) perform anti-gliadin antibodies, TTG antibodies, skin biopsy b) hereditary haemorrhagic telangiectasia - I) HHT - mucosal telangiectasia: commonly get epistaxis, AV malformations may occur in cerebrum or lungs etc (could be a site for infection - abscess formation), may get anaemia from GI bleeds 4) hepatology - jaundice, pruritus, spider naevi, palmar erythema, nail changes a) chronic liver disease: meds can cause cirrhosis eg/ methotrexate 5) toxic erythema - a) morbilliform rash - erythematous macules, begins on trunk, confluent, pruritis, malaise, fever b) give abx, sulphonamides (allergy) 6) phototoxic reaction - non-allergic, photosensitivity from: amiodarone, furosemide, nalidixic acid, psoralens, sulphonamides, tetracyclines, thiazide diuretics, retinoids

Recognise and describe clinical features of the pre-malignant lesion: intra-epithelial carcinoma (Bowen's disease)

3) intraepidermal carcinoma (IEC)/Bowen's disease - a) dysplasia that extends the full thickness of the epidermis b) classically presents on lower legs of elderly women (can occur elsewhere), and as with superficial BCC can mimic a patch of eczema or psoriasis c) asymptomatic slow growing, usually solitary, sharply demarcated, scaly erythematous patch or plaque on sun-exposed site d) surface may be flat, scaly, eroded, velvety or verrucous e) risk of malignant transformation in IEC is higher than AK (4%) f) cutaneous horn - lesion which often arises on face & comprised of compacted keratin. Needs histological exam as SCC may lie at the base

Different therapies for glaucoma and their side effects, the importance of patient compliance and the consequences of delayed diagnosis and treatment failure contd.

3) laser (tx trabecular meshwork so drains more fluid) - argon laser or selective laser trabeculoplasty 4) surgery: trabeculectomy - a) intolerant to drops, laser doesn't work, needs extreme dec in IOP b) controlled fistula for aqueous to seep out, creates drainage bleb (SE - direct pathway for noxious bacteria to enter eye under conjunctiva - needs urgent referral) c) success rates 50-90% d) risk factors for failure - previous surgery, black, long-term topical meds (esp pilocarpine), coexisting uveitis (past or present), diabetes (esp with retinopathy) e) success = IOP <21 mmHg on no tx h) advances in surgery: antimetabolites (5FU, mitomycin), laser suture lysis/releasable, microtrabeculetomy, phacotrabeculectomy (deep sclerectomy/visocanalostomy) 5) acute angle closure glaucoma - a) emergency - needs urgent dec in IOP to avoid irreversible damage to optic nerve b) 4% pilocarpine eye drops every 5 mins + IV or oral acetazolamide c) anti-emetics & analgesia d) after acute attack managed - laser iridotomy or trabeculectomy 6) associated disability - a) significant peripheral field loss may result in pt unable to legally drive b) advanced glaucoma results in permanent blindness

Different subtypes of melanoma contd.

3) nodular melanoma - 2nd most common subtype, ~15% all melanomas a) median age at onset is 53 years b) uniform blue-black, blue-red, or amelanotic nodule (5%). Move vertically c) most common sites - trunk, head, and neck d) rapid growth is also a hallmark of nodular melanoma - poor prognosis 3) acral lentiginous melanoma - ~10% melanomas a) median age = 65 years, M=F b) most commonly feet (subungual or plantar lesions), palms, soles, nails c) tan, brown-black, flat macule with color variegation and irregular borders. Unlike lentigo maligna melanoma, not associated with sun exposure d) more common in dark skinned individuals 4) subungual melanoma - rare variant of acral lentiginous melanoma a) great toe or thumb & generally arise from nail matrix b) Hutchinson's sign - pigmentation on posterior nail fold, associated with advanced subungual melanoma

Recognise and describe the cutaneous manifestations of thyroid disease contd.

3) pruritis (itchy skin) a) depending on cause, may appear normal, or red, rough, bumps or blisters. Repeated scratching = raised, thickened areas of skin, can bleed or become infected 4) diffuse hair loss (chronic telogen effluvium) - inc rate of hair fall and thinning all over scalp. Hair appears thinner, but no loss of follicles (loss of hair from whole scalp, not just one area) 5) periorbital & facial oedema (Grave's opthalmopathy) - autoimmune inflammatory disorder of orbit & periorbital tissues a) upper eyelid retraction, lid lag, swelling, erythema, conjunctivitis, and exopthalmos 6) thyroid acropachy - dermopathy associated with Graves' disease a) soft-tissue swelling of hands & clubbing of fingers b) radiographic imaging of affected extremities - periostitis, most commonly of metacarpal bone

Recognise and describe the cutaneous manifestations of internal cancers eg/ acanthosis nigricans, acquired ichthyosis, pyoderma gangrenosum and dermatomyositis contd.

4) dermatomyositis: CT disorder - a) disorder of skin & muscle, proximal muscle weakness b) violaceous poikiloderamtous rash or helioptrope rash I) photosensitive distribution II) nail fold changes (telangiectasia) III) Gottron's papules - erythematous papules over bony prominences c) adult & juvenile forms (adult associated with internal malignancy) d) diagnosis: serum CK, EMG, muscle biopsy, antibodies (anti-Jo 1) e) malignancy - ovarian, lung, colorectal, pancreatic, Hodgkin's lymphoma 5) other signs of internal malignancy - Paget's disease of the nipple, superficial thrombophlebitis (pancreas), generalised pruritus (lymphoma) 6) liver disease signs - pruritus, spider naevi, palmer erythema, jaundice, white nails

Recognise and describe skin eruptions which may be caused by drugs such as urticaria, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis contd.

4) erythema multiforme a) rash comes on suddenly & develops over a few days. Tends to start on hands or feet, before spreading to limbs, upper body and face. b) starts as small red spots - may become raised patches cms in size c) often target lesions or "bulls-eye", with a dark red centre that may have a blister or crust, surrounded by a pale pink ring and a darker outermost ring. True target lesions have 3+ different colours in them (often on acral sites) d) may be slightly itchy or uncomfortable e) usually fades naturally over 2-4 weeks f) if severe, patches may join together to form large, red areas - painful g) also - fever, headache, malaise, oral sores, swollen lips covered in crusts, gential sores, red eyes, sensitivity to light and blurred vision e) hypersensitivity to streptococcal antigen (group A strep) 5) erythema multiforme & SJS triggers a) sulphonamides (co-trimazole) b) phenylbutazone & other NSAIDs c) immunisations, barbiturates, HSV, GAS (EM) d) mycoplasma infection 6) toxic epidermal necrolysis a) early symptoms - fever, flu-like symptoms, pain b) few days later skin begins to blister & peel forming painful raw areas. c) extension of SJS: widespread blistering (Nikolsky sign), with mucosal membrane involvement & malaise d) 7-21 days initiation e) >30% body SA, mortality 35% f) NSAIDs, Abx, anticonvulsants (lamotrigine, carbamazepine), allopurinol, sulfonamide antibiotics, nevirapine, barbiturates g) skin failure - needs ITU/burns unit, greasy emolients (50/50) and bandaging, opthalmologist and ENT review 7) tx if drug induced - a) stop drug & consider measures to reduce drug in system b) supportive care eg/ hydration, nutritional support

Discuss prognosis and management of pigmented lesions with patients contd.

4) prognosis of squamous cell carcinoma - a) overall 5 year survival - 75%-90%, for metastatic disease - 25% b) factors inc metastatic potential: site - ear or lip, size >2cm, thicker depth, non-sun exposed sites, areas of chronic inflammation, poorly differentiated, immunosuppression, mucosal SCC, perineural invasion 5) mx of SCC - a) majority of SCC low risk so surgical excision - clinically well defined tumours <2cm diameter, at least 4mm margin. Larger/thicker tumours, high-risk sites or poor differentiation use wider margins - Mohs' micrographic surgery b) radiotherapy - selected individuals & certain lesions when extensive or mutilating surgery would be unacceptable or surgical morbidity high c) curettage and cautery - if small, primary, <1cm, well differentiated, slow growing on sun exposed sites. 2 or 3 cycles of curettage then cautery 6) mx of actin keratosis or IEC (Bowen's) - a) cryotherapy (discrete lesions) b) 5-fluorouracil cream (Efudix) - warn pts of inflammatory reaction at site of AK = prolonged erythema and unsightly and sore erosion c) curettage & cautery d) photodynamic therapy (as effective as 5-fluorouracil) e) diclofenac gel (Solaraze), Imiquimod, laser NB/ 25% AK spontaneously disappear without tx NB2/ Bowen's - excision and radiotherapy also possible 8) mx for NMSC - a) skin cancers should be managed by skin cancer MDT eg/ dermatologist, plastic surgeon, histopathology, radiotherapist, specialist nurses b) sun protection advice to anybody with skin cancer/pre-malignant skin problems

Differences between different types of contact lenses and their uses contd.

4) rigid gas permeable lenses - a) disadvantages - I) poor initial comfort II) smaller diameter so prone to falling out b) advantages - I) fixed shape and durable II) fewer problems with deposits & easy to clean III) good for all day wear IV) smaller diameter so less corneal invasion V) VA for irregular corneas and high astigmatism 5) requirements of any contact lens a) stable accurate VA b) good comfort throughout wear c) easy to insert and remove d) easy to clean / replace / reproduce e) reasonable cost f) maintain healthy corneal physiology g) minimal lid interference and tear film disruption 6) contact lens assessment - a) initial refraction - determines spectacle prescription b) keratometry - measures curvature of cornea so amount of corneal astigmatism present c) pt then examined on slit lamp to check health of cornea, lids and tear film 7) contact lens complications - a) giant papillary conjunctivitis (GPC) b) corneal abrasion or ulcers or hypoxia c) infective keratitis d) neovascularisation e) solution hypersensitivity

Classifying eczema contd.

4) venous/varicose/stasis/gravitational eczema - a) older pts on lower limbs b) combo of inc dryness of skin (asteototic eczema) & varicose veins c) occurs around varicose veins, signs of chronic venous disease d) tx - emollients and mild/moderate topical steroids, compression hosiery e) at risk of ulceration if severe 5) asteatotic aka xerotic eczema - occurs when skin becomes abnormally dry, itchy & cracked. Often in elderly or pts in 20s. Tx - topical steroids then long-term emollients (aqueous cream/diprobase). Avoid excessive washing 6) pompholyx - development of intensely itchy watery blisters, mostly on sides of fingers, palms or soles. Can occur at any age but mostly <40 7) irritant contact dermatitis - a) direct effect of irritant substances affecting skin integrity (chemical damage rather than immune-related) b) usually hands (dorsum & finger webs) c) common in certain occupations eg/ hairdressers, chefs, housewives, cleaners, nurses, engineers d) atopic individuals more susceptible e) tx - avoid irritant, cotton gloves, emollients, topical steroids 8) allergic contact dermatitis (eczema & dermatitis are synonymous) - a) eczema following type 4 delayed cell mediated allergic reaction to contact with substance b) commonly - nickel (jewellery & buckles), hair dye, plants, topical meds, fragrance, occupational eg/ builders, engineers, surgeons c) diagnosis confirmed by patch testing d) distribution eg/ cut off point on forearms from rubber glove dermatitis e) tx - allergen avoidance, emollients, topical steroids etc 9) hand dermatitis - a) endogenous, irritant or contact allergy - often multi-factorial b) W:M = 2:1 c) aetiology from hx - atopic, occupation, hobbies etc & patch testing d) morphology is variable, if unilateral, think fungal e) tx difficult as chronic and relapsing, difficult to avoid allergens. Pt education on hand care. Can lead to loss of employment in manual workers h) tx - I) acute vesicular: KMnO4 soaks, emollients, topical steroids II) chronic: avoid irritant or allergen, emollients, topical steroids +/- occlusion, retinoids, attention to hand care

How to recognise visual acuity contd.

5) notation for LogMar = decimal eg/ 0.0 (normal), 1.0 (defective), -0.1 (above average) 6) 4 other methods of measuring visual function - contrast sensitivity, colour vision, stereopsis, V.E.P.s 7) pinhole - certain pathologies can also dec vision, to determine if pt's dec in vision is due to pathology or refractive error use pinhole test a) occluder with a tiny hole in the middle - see if any improvement made to pt's vision b) works by dec size of retinal blur circle to improve vision (provided pt has no pathology), i.e. provides a point focus c) give best VA by removing aberrations, some level of astigmatic errors and improves depth of focus d) if helps vision to within normal parameters, dec vision is probably due to refractive error. If no improvement, probably pathology present eg/ lens opacity or AMD 8) VA testing (all get progressively smaller) - a) young children - preferential looking (look towards black/white stripes if can see them) b) Cardiff cards - pictures, see if child can see picture c) Kay's pictures - if they can name or patch pictures d) logMAR crowded & uncrowded - when can read letters e) bailey Lovie (4m LogMAR) - similar to Snellen but more up-to-date

Clinical features & different types of cataracts contd.

6) toxic cataract: a) corticosteroids (systemic/topical) - causes posterior subcapsular cataract b) chlorpromazine - fine yellow deposits in anterior lens capsule c) chemotherapy eg/ busulphan 7) secondary complicated cataract: a) anterior uveitis b) hereditary retinal degenerations eg/ retinitis pigmentosa, gyrate atrophy, Stickler's syndrome c) high myopia d) glaucomflecken - small grey white anterior subcapsular cataract, seen in acute angle closure cataract 8) maternal infection & drug ingestion cataract: a) rubella - cataracts in 50% when mother infected during 1st & 2nd trimester. After 6 weeks gestation virus can cross lens capsule b) toxoplasmosis c) CMV d) drugs: thalidomide, corticosteroids 9) presenile cataract causes: a) dystrophia myotonica - cortical polychromatic cataract/posterior subcapsular stellate cataract b) atopic dermatitis - bilateral posterior stellate opacities 10) syndrome associated with cataract (4) - Down's, Alport's, Werner's, Rothmund's 11) cataract classification according to stage of development - a) immature cataract - hasn't involved whole lens b) mature cataract - cortex totally opaque, can't see behind it c) hyper mature - mature cataract, lens material smaller & wrinkles lens capsule due to leakage of water out of lens

Recognise and describe the cutaneous manifestations of diabetes contd.

7) diabetic dermopathy (aka "shin spots") - skin lesion characterized by dull-red papules that progress to well-circumscribed, small, round, atrophic hyperpigmented skin lesions usually on shins 8) neuropathic ulcer - caused by peripheral neuropathy due to its effects on sensory, motor & autonomic nerves: a) loss of sensation due to sensory neuropathy so pts vulnerable to physical, chemical and thermal trauma, risk factor - associated with 7x inc risk b) foot deformities caused by motor neuropathy (eg/ hammer toes and claw foot) may lead to abnormal pressures over bony prominences c) dry skin from autonomic neuropathy = fissures, cracking and callus d) always feet, usually plantar aspect under metatarsal heads or plantar aspects of toes g) diabetic ulcer is deep, painless & infected, 'punched out' = 'perforating ulcers'

Name and recognise the different types of skin conditions that can be caused by Staphylococcus aureus contd.

7) diseases due to toxins - a) Staphylococcal Scalded Skin Syndrome due to epidermolytic toxins ET-A and ET-B - I) relatively rare disease affecting infants and young children II) unwell child with fever, irritability and widespread erythema. Blisters with multiple areas of denuded tissue III) tx - supportive care & IV Flucloxacillin or Erythromycin for 7-14 days b) Toxic Shock Syndrome due to TSST-1 and TSST-2 toxins - I) associated with tampon use in menstruating women but can occur following any staphylococcal infection, including GIT infections II) pt very unwell with acute onset of fever, vomiting and diarrhoea & severe circulatory collapse. Widespread macular erythema may clear by day 3. Desquamation 10-21 days later is characteristic. Mucosal oedema and ulceration III) tx - IV Flucloxacillin or Erythromycin with intensive support c) Staphylococcal Scarlatina due to an erythrogenic toxin d) Bullous Impetigo - rarely, impetigo due to S. aureus associated with blisters (2-3cm). Tx - oral Flucloxacillin or Erythromycin 8) ix - skin swabs, blood cultures (only +ve if severe sepsis due to S. Aureus septicaemia) 9) tx - a) topically: Mupirocin (Bactroban), Fusidic acid b) orally: Flucloxacillin 7-14 days, Erythromycin 10-14 days c) IV: flucloxacillin 500mg-1000mg iv qd

Recognise and describe the features of a typical melanoma (using the ABCD rule)

A - Asymmetrical: melanomas often irregular, or not symmetrical, in shape. Benign moles usually symmetrical B - Border: benign moles have smooth, even borders. Melanomas have irregular borders difficult to define C - Color: 2+ colors (blue, black, brown, tan, etc.) or uneven distribution of color can indicate melanoma. Benign moles usually single shade D - Diameter: melanomas often >6mm diameter (~ size of a pencil eraser) E - Evolution: most important factor to consider when diagnosing a melanoma. If a mole has gone through recent changes in color and/or size, bring it to the attention of a dermatologist immediately NB/ always compare with other moles & other skin cancers

Framework for describing a rash

DCM - 1) distribution - where is it? Eg/ flexural, extensors, unilateral, symmetry 2) configuration - how are the lesions grouped? Eg/ line, circle (annular), cluster 3) morphology - what sort of lesions? Eg/ papules, pustules, plaques, lichenification, well demarcated border? Difference in colour between inside & border, is there a base (eg/ erythematous)

2 common skin conditions attributed to Malassezia furfur & suggest appropriate treatments for these

Malassezia or pityrosporum species are commensals. 2 most common cutaneous manifestations - pityriasis vesicolor & seborrhoeic dermatitis 1) pityriasis versicolor - a) finely scaling yellowish or brown macules, mostly on trunk b) hypo or hyper-pigmented patches depending on racial skin type - repigmentation takes months c) relapse is common d) tx - I) selenium sulphide or ketoconazole shampoo 1st line (applied overnight and washed off on 3 consecutive days) II) topical anti-fungals eg/ Miconazole, terbinafine, imidazoles III) Itraconazole for 7 days, for severe disease or if immunosuppressed 2) seborrheic dermatitis - a) mild eczematous (dermatitis) condition - red, scaly, greasy, itchy, and inflamed skin b) affects - face, scalp (cradle cap, dandruff, complicated by pitysporum folliculitis), flexures (scaling may be lost with just erythema visible) c) recurrence common d) tx - I) may clear by itself II) topical azoles (shampoo, cream) - ketoconazole, ciclopirox III) low potency topical corticosteroids (short term for rapid tx) IV) topical tacrolimus, pimecrolimus (immune-modulators, used when long term topical steroids have been difficult to withdraw) V) antiandrogens VI) others - coal tar, isotretinoin

Management of cataracts contd.

d) lens extraction by phacoemulsification (PHACO) - standard method in UK (80% cataract operations in the UK) I) 3mm incision, anterior lens capsule is 'peeled' - Capsulorrhexis, use of high frequency US probe to fragment & aspirate lens nucleus, lens cortex is aspirated, foldable silicone intraocular lens inserted through wound & unfolds in remaining lens capsule II) advantages - fast recovery, see 6/6 within 2 weeks, gd refractive results, very little astigmatism, quick op (5-20 mins in uncomplicated cases) III) complications - Posterior Capsule Opacification (20%), vitreous loss (4%), retinal detachment, endophthalmitis (0.1%) 4) acute bacterial endophthalmitis - a) complication of cataract surgery (infection), 1:1000 cases b) s/s - pain & marked visual loss, absent or poor red reflex, corneal haze, fibrinous exudate and hypopyon d) common cause - Staph. Epidermidis or Aureus, Pseudomonas sp. NB/ cataracts extraction affects ability to accommodate

2nd line treatment option - systemic optics: aciterin, methotrexate, ciclosporin and be able to discuss the risks and benefits of each for patients with psoriasis contd.

for severe or refractory psoriasis. Either: extensive psoriasis (>10% body SA), localized & causing functional impairment/distress, phototherapy ineffective 1) non-biologic systemic treatments a) methotrexate (most common) - psoriasis & psoriatic arthroplasty. Take 1x/week I) S/E - long term effects on liver (not alcoholics), teratogenicity, N + GI upset, marrow suppression II) need LFT + FBC (folic acid antagonist) b) ciclosporin - short term control (1-2 yrs) I) S/E - HTN, nephrotoxicity, carcinogenesis, hypertrichosis, tingling peripheries, need BP + U&E c) retinoids (acitretin) - teratogenic (2 years) so not if young women, dry skin & lips, hyperlipidaemia, hepatotoxicity I) need fasting lipids, LFTs NB/ methotrexate & ciclosporin suppress immune system; retinoids are synthetic forms of vit A - 1st-line for psoriatic erythroderma. 4-12 week course 2) oral corticosteroids not used as rebound psoriasis

3rd line agents for psoriasis

manufactured proteins that interrupt immune process involved in psoriasis. Generally well-tolerated, but immunosuppressive actions so small inc risk for infection 1) monoclonal antibodies eg/ TNF-α antagonists = infliximab, etanercept 2) efalizumab (s/c) = humanised monoclonal antibody 3) surgery - removal of tonsils may benefit chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis 4) diet - may benefit from fish oils eg/ salmon, herring 3) guttate psoriasis - emollients, coal tar, calcipotriol (Dovonex), narrowband UVB tx 4) erythrodermic psoriasis & generalised pustular psoriasis - a) admit, supportive tx with careful monitoring of BP, temp, and urine output b) liberal emollients eg/ white soft paraffin/liquid paraffin 50/50 & potent topical steroids c) consider systemic tx

Topical treatment options of psoriasis (including coal tar, dithranol, vitamin D analogues, steroids, retinoids) and be able to discuss the pros and cons of each

no cure for psoriasis - aim to control so minimal skin involvement. Topical agents = mild disease, phototherapy = moderate, systemic = severe 1) 1st line - topical corticosteroid for 8 weeks eg/ beclometasone 0.1%, Eumovate, or combination product with calcipotriol eg/ Dovobet a) use on face & flexures b) complications eg/ erythroderma or generalised pustular psoriasis 2) 1st line - vit D analogues eg/ Calcipotriol (Dovonex) a) may cause irritation, hypercalcaemia, PTH suppression 3) 1st line - moisturisers & emollients eg/ E45, mineral oil, petroleum jelly, calcipotriol, and decubal (oil-in-water emollient) a) inc clearance of psoriatic plaques, esp with phototherapy 4) combination therapy with vitamin D & corticosteroid best 5) tazarotene gel - vit A analogue, clean & odourless a) S/E - irritation is common, risk of teratogenicity 6) short contact dithranol - 30-min exposures in pts with few but relatively large plaques, building from 0.1-10%. Only for plaque psoriasis a) S/E - irritation & temporary skin staining (brown) 7) retinoids & coal tar limited benefit a) coal tar eg/ Alphosyl or Carbo-Dome in guttate psoriasis b) S/E - irritation, folliculitis, messy 8) keratolytics eg/ 5% salicylic acid for thicker plaques. Can cause irritation 9) scalp - cocois ung (tar + salicylic acid), coal tar shampoo (eg/ polytar), vit D3 analogue scalp application or topical corticosteroid scalp application 10) face - mild/moderate topical corticosteroid short term 11) flexures - mild/moderate topical corticosteroid, Calcitriol (Silkis) ointment NB/ education - assess pts expectations, often chronic lifelong, no cure, assess impact on life, pt concerns, compliance

Indication for and be able to discuss the risk and benefit of the following systemic therapies: tetracyclines and other antibiotics for acne

oral & topical therapy: moderate and severe acne, depressed pts, acne scarring, involvement of chest and back or topical tx hasn't worked with exception of isotretinoin, most tx continued for at least 6 weeks before maximum effect seen & often helpful to use combination therapy 1) abx - a) always commenced with 1+ topical agents eg/ retinoid and BPO, to inc likelihood of complete control b) if beneficial after 6 weeks, minimum treatment period 6 months c) success (with topical therapy) - 80-90% improve in 6/12 d) 1st line = cyclines: CI in pregnancy, breast-feeding & children (effects on bone growth in foetus & discolouration of growing teeth) e) 1st line = Minocycline. S/E - inc post-inflammatory hyperpigmentation, vestibular disturbance, hypersensitivity, lupus-like syndrome, renal/hepatic toxicity, skin or teeth staining g) 1st line = Doxycycline, Lymecycline, Tetracycline g) 2nd line = Erythromycin (macrolide) - preferred in females who may conceive and in infantile acne (rare), GI S/E h) 3rd line = Trimethoprim i) mode of action of abx not fully understood - anti-inflammatory? affect function of P.acnes? inhibit enzymes? j) biggest problem with abx = bacterial resistance - more common with erythromycin. Resistance dec by combining with topical non-antibiotics & limiting duration of tx to <6 months

Indication and potential side effects of following topical treatments: benzoyl peroxide, Abx, retinoids for acne

topical therapy: mild-moderate acne, mixed lesions, applied 1-2x/day overall aim of all therapy is to treat problem & dec scarring 1) benzyl peroxide (Panoxyl) - a) antimicrobial - dec number of P. acnes bacteria and inflammation b) no resistance c) available OTC in variety of forms eg/ soaps, washes, lotions, creams d) S/E: irritation, bleaching (clothes) 2) topical abx - a) erythromycin & clindamycin b) cause less irritation than BPO & do not bleach clothes c) but possibility of bacterial resistance - tx limited to 6 months only d) combination tx with BPO available & more effective than single agents 3) retinoids (Retin A, Isotrex) - a) vit A derivatives: retinoic acid b) comedolytic - remove surface keratin, unblocking pores for drainage of microcomedonal contents c) secondarily prevent formation of new acne lesions d) 1st line for comedonal acne e) various strengths and preparations (gels and creams) f) S/E: teratogenicity (topical and systemic), erythema and irritation, photosensitivity NB/ pt education - cause, dispel myths, assure of potential success of tx