6) ear, eye, nose, skin, throat (ie special senses) Flashcards
OTITIS EXTERNA
- what is it?
- time definition of acute and chronic?
- group of organisms more likely to cause acute?
- group of organisms more likely to cause chronic?
inflammation of external ear canal
Acute = < 3 weeks (aka “Swimmer’s” Ear)
- norm bacterial (norm staph aureus)
Chronic = >3 months
- norm fungal (norm aspergillus)
OTITIS EXTERNA
- age most affected?
- lifestyle risk factors? 3
- medical conditions that are risk factors? 3
age (peaks between 7-12 years)
- Moisture (swimming)
- Trauma (ear clearance w finger/cotton bud)
- Hearing aids
- Wax build up
- DM
- Immunocompromised
OTITIS EXTERNA
- two main initial symptoms? 2
- main finding on examination? 1
- late severe signs/symptoms? 3
MAIN SYMPTOMS
- pruritic/itchy ear
- otalgia (esp on movement of tragus)
O/E
-erythema AND oedema of ear canal + ear
(Also mobile tympanic membrane)
LATE SIGNS
- pre-auricular lymphadenopathy
- discharge
- hearing loss
nb can also get a fever but not common
OTITIS EXTERNA
- possible investigation? 1 (when do?)
- ear hygiene advice?
- medication treatment options? 3
- additional medication to help with symptoms? 1
Can do EAR SWAB (rarely useful unless Sx are persistent/recurrent)
- Olive oil for ear wax
- if swollen/narrow ear canal: can put wick/gauze soaked in sofradex
- Avoid cotton buds!
Mild = TOP Acetic acid spray 2%
Mod = TOP Abx ± Steroids
Nb TOP Abx include neomycin and clioquinol (then TOP steroids have same names as PO/IV ones)
advice SIMPLE ANALGESIA (paracetamol/nsaids)
Nb most resolve within a few days!
OTITIS EXTERNA
- differential diagnosis? (3 common, 3 rarer)
= contact eczema / dermatitis
= impacted ear wax
- foreign body
= perforated otitis media (or chronic secretory OM)
- cholesteatoma
- malignancy (if unresponsive to Mx)
OTITIS EXTERNA
- most common complications? 3
- rare, but serious type of otitis externa? 1
- hearing loss
- narrowed ear canal
- abscess
NECROTIZING (MALIGNANT) OTITIS EXTERNA =immunocompromised its (90% are pseudomonas) -severe pain -exudate + oedema -micro-abscesses -headache +/- facial nerve palsy
Can spread to bone causing osteomyelitis + death
Need urgent admission and ENT referral
IMPACTED EAR WAX:
- most common symptom? 1
- other symptoms? 4
hearing loss = MOST COMMON
- blocked ears / feeling of fullness
- ear discomfort / earache
- tinnitus
- itchiness
nb ?vertigo (although that not confirmed!)
nb can also get cough (dt stimulation of vagus nerve)
IMPACTED EAR WAX:
- main exam to do?
- main DDx? 4
look with otoscope (if impacted, won’t see ear drum)
DDx
- otitis externa (esp if inflammation of external ear)
- foreign bodies (esp in children)
- polyp of ear canal
- osteoma of ear canal
nb can also get rare thing called: keratosis obturans (see pearly white plug of keratin)
EAR WAX:
- when should it be removed? 5
- 1st line management?
- 2nd line management?
- 3rd line management?
If earwax is totally occluding the ear canal AND any of the following are present:
- Hearing loss
- Earache
- Tinnitus
- Vertigo
- Cough suspected to be due to earwax
nb if suspected perforated ear drom, don’t do these things!
1ST LINE
- olive oil or sodium bicarb ear drops for a week
2ND LINE
- ear irrigation
can return and have more drops then more irrigati9on etc but if really can’t clear:
3RD LINE
- refer to ENT for manual removal
nb if recurrent, can have regiular drops and/or irrigation etc (basically whatever works!
always safety net for infection!!
DEAFNESS
- causes of conductive? (4 common, 4 rarer)
- causes of sensorineural? (3 common, 4 rarer)
CONDUCTIVE
= ear wax
= otitis externa
= otitis media
= glue ear
- otosclerosis
- cholesteatoma (see other flashcard)
- foreign body
- perforated tympanic mebrane (eg from trauma)
SENSORINEURAL
= presbycusis
= noise induced hearing loss (NIHL) (60% also have tinnitus)
= congenital (eg Alports)
- meniere’s disease
- acoustic neuroma
- drug ototoxicity
- damage to brain (eg meningitis, multiple sclerosis, infarct)
OTOSCLEROSIS
- what is it?
- main risk factor?
- age of onset?
- two main symptoms?
get replacement of normal bone by vascular spongy bone.
Autosomal dominant - FHx main risk factor!
Onset is usually at 20-40 years
MAIN SYMPTOMS:
- conductive deafness
- tinnitus
nb 10% of patients may have a ‘flamingo tinge’ on tympanic membrane, caused by hyperaemia
GLUE EAR
- what is it?
- age of peak onset?
- main presenting symptom?
Effectively chronic otitis media with effusion (aka secretory otitis media)
age 2-7 (normally around 2)
symptom:
= conductive HEARING LOSS (often picked up as inattention, language delay at school!)
nb can also present as behavioural problems or balance problems
PRESBYCUSIS:
- cause?
- conductive or sensorineural hearing loss?
- bilateral or unilateral?
- what do patients often complain of?
AGE-RELATED
BILATERAL
SENSORINEURAL hearing loss
Patients may describe difficulty following conversations
Audiometry shows bilateral HIGH-FREQUENCY hearing loss
MENIERE’S DISEASE
- age at presentation?
- four main symptoms? (which norm most prominent?)
- how long do episodes last?
- what clinical test is positive?
middle-aged adults
recurrent episodes of:
- vertigo (most prominent)
- tinnitus
- hearing loss (sensorineural)
- sensation of fullness or pressure (in one or both ears)
episodes last minutes to hours!
ROMBERG test is positive (close eyes and fall)
nb may also have nystagmus!
ACOUSTIC NEUROMA
- aka?
- which cranial nerves affected? 3 (and what symptoms does this then give?)
- diagnostic investigation? 1
aka vestibular schwannoma
(actually more accurate as is a benign tumour of the schwann cells surrounding the vestibular nerve)
cranial nerve EIGHT
- hearing loss (sensorineural)
- vertigo
- tinnitus
cranial nerve FIVE
- absent corneal reflex (IMPORTANT SIGN!)
(can also get trigeminal neuralgia)
cranial nerve SEVEN
- facial palsy (less common)
diagnosis = MRI cerebello-pontine angle
(nb also norm do audiometry too to quantify hearing loss)
ALWAYS refer to ENT surgeons if suspect! (they will manage conservatively or with microsurgery)
nb Bilateral acoustic neuromas are seen in neurofibromatosis type 2
Which common drugs are potentially ototoxic? 5
- gentamicin (and other amino glycosides - anything ending in MYCIN)
- furosemide
- aspirin (and some other nsaids)
- quinine
- some cytotoxics (eg cisplatin and carboplatin)
HEARING LOSS
- first clinical exam to do?
- two clinical tests to do to determine if conductive or sensorineural? (which is which and what does a ‘positive’ test for each mean?)
- when are these tests NOT useful?
OTOSCOPY (see if you can visualise any wax or middle ear effusions etc)
RHINNES TEST
= put tuning fork next to ear then on mastoid
- if air conduction (AC) > bone conduction (BC) then it is positive (means either normal hearing or sensorineural hearing loss)
- if BC >AC then is negative (means conductive hearing loss in that ear)
WEBBERS TEST
= put tuning fork on mid forehead
- lateralises to midline: normal hearing OR bilateral disease (conductive or sensorineural)
- lateralises to AFFECTED ear in CONDUCTIVE hearing loss
- lateralises to UNAFFECTED ear in SENORINEURAL hearing loss
NOT useful if bilateral or mixed hearing loss!!
HEARING LOSS
- after otoscopy + rinnes + webers tests, what is next line investigation? 1
- other investigation to consider if unsure of cause? 1
- what to do if suddent unilateral hearing loss?
AUDIOMETRY (refer for)
- in all pts to quantify hearing loss
consider imagine (eg CT if unsure of cause - esp if conductive)
refer to ENT urgently if sudden unilateral hearing loss!
HEARING LOSS
- management option for people with moderate-severe sensorineural hearing loss? 1
- if patients are deaf from birth, other management option? 1
Pathology excluded & Patients 50-80 years old? –
refer for HEARING AID (or “assess & fit”) appointments
- nb can also give to younger pts
deaf patients can have COCHLEAR IMPLANTS
nb for conductive hearing loss you treat the cause - eg gromits for glue ear, surgery for any mass
VERTIGO:
- what is it?
- most important causes? 6
- other rarer causes? 4
Vertigo may be defined as the false sensation that the body or environment is moving
= viral labyrinthitis
= vestibular neuronitis
= BPPV
= meniere’s
= vertebrobasilar ischaemia
= acoustic neuroma
- posterior circulation stroke
- trauma
- multiple sclerosis
- ototoxicity e.g. gentamicin
For each of these causes of vertigo:
- viral labyrinthitis
- vestibular neuronitis
- BPPV
- meniere’s
- vertebrobasilar ischaemia
- acoustic neuroma
describe:
1) speed of onset? (and if any preceeding events)
2) what triggers vertigo attacks? (+ how long last)
3) any associated hearing loss or tinnitus? (and any other associated symptoms)
VIRAL LABYRINTHITIS
1) SUDDEN onset (following recent viral infection)
2) no recognised trigger
3) HEARING may be affected, incl tinnitus (also get NAUSEA and vomiting!)
VESTIBULAR NEURONITIS
1) recurrent attacks (following recent viral infection)
2) no recognised trigger
3) NO hearing loss (distinguishes from above! - as only affects vestibular nerve!) (also get nausea and vomiting)
BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV`)
1) Gradual onset
2) triggered by change in head position (each episode lasts 10-20 seconds)
3) NO hearing loss or tinnitus (may get some nausea)
MENIERE’S
1) gradual onset recurrent episodes
2) no trigger although exacerbated by movement, episodes lasts minutes to hours
3) associated with hearing loss, tinnitius and fullness/pressure in ears
VERTEBROBASILAR ISCHAEMIA
1) elderly patients
2) vertigo on EXTENSION of neck
3) no associated symptoms
ACOUSTIC NEUROMA
1) gradual onset
2) no known trigger
3) associated with hearing loss, vertigo, tinnitus (and absent corneal reflex!)
LABYRINTHITIS
- how to distinguish from vestibular neuronitis? 1
- three groups of causes? (which is by far most common?)
- average age at presentation?
get hearing loss +/- tinnitus as well as vertigo (in vestibular neuronitis only the vestibular nerve is affected so only get vertigo + nausea)
LABYRINTHISITIS CAUSES
- VIRAL (by far most common!)
- bacterial (have pus, more unwell)
- systemic infection (obs are off)
viral is normally secondary to a recent URTI or herpes!
average age of presentation is 40-60
LABYRINTHITIS
- Main symptom? (describe onset and severity)
- associated symptoms? 3
- clinical sign on examination? other sign you may see?
- possible prodrome?
VERTIGO
- not triggered by movement (but is exacerbated by it!)
- SUDDEN onset
- is incapacitating
- nausea and vomiting (frequent!)
+/- hearing loss
+/- tinnitus
see spontaneous (norm horizontal) nystagmus
other sign = Gait disturbance (fall/lean towards affected side)
(normally fine sitting)
nb may also see abnormality on inspection of the external ear canal and the tympanic membrane e.g. vesicles in herpes simplex infection
POSSIBLE PRODROME
- Viral Prodrome (coryza etc)
- Rhinorrhoea + Fever
HINTS exam
- what used to differentiate between?
- describe each section and findings?
used to distinguish between a central cause of vertigo (eg stroke) from a peripheral cause (eg labyrinthitis or vestibular neuronitis)
1) Head Impulse test
= (test for peripheral vestibular function)
- Fix pt. gaze straight ahead/at your nose. Rapidly turn pts. head 10-20° to one side and then reset back to face you.
NORMAL = patient holds fixed gaze w/ head movement.
ABNORMAL = saccades present i.e. patients eyes have to flick back to your nose (GET IF PERIPHERAL)
2) Nystagmus Type
- Ask pt. to look left & right to discern whether nystagmus (indicated by the fast phase of movement) is unidirectional & consistent nystagmus = POSITIVE (sign of peripheral cause)
- Nystagmus that changes on position i.e. fast phase to left when looking left and vice versa indicates a central cause (e.g. Stroke/TIA)
3) Skew
- Cover/uncover each eye in turn & note any skew – typically vertical skew. Movement = central causes of vertigo.
SO an abnormal head impulse test, unidirectional nystagmus and no vertical skew are sensitive markers of PERIPHERAL CAUSES of vertigo
LABBYRINTHITIS:
- how is diagnosis normally made?
- investigations to consider if diagnosis is uncertain or suspect more sinister cause? 6
Diagnosis is largely CLINICAL (ie based on hx and exam)
nb glucose is helpful in excluding hypoglycaemia.
in most patients with suspected viral labyrinthitis, no other investigation is necessary
OTHER
- pure tone audiometry (to assess hearing loss)
- FBC + blood culture (if systemic infection suspected)
- culture and sensitivity testing (if any middle ear effusion)
- temporal bone CT scan (if suspecting mastoiditis or cholesteatoma)
- MRI scan (can rule out causes such as suppurative labyrinthitis or central causes of vertigo)
- vestibular function testing (may be helpful in difficult cases and/or determining prognosis)
VIRAL LABYRINTHITIS:
- when to refer urgently to ENT?
- prognosis?
- advice to patients? 2
- medication to prescribe? 1
Emergency admission + see ENT specialist if sudden onset U/L hearing loss
prognosis for viral labyrinthitis: Good. Benign & self-limiting. Majority of cases take several days to few weeks to resolve completely
ADVICE
- Avoid driving/operating machinery
- During acute attacks, lie still w/ eyes closed
Medication: PROCHLORPERAZINE for dizziness
(nb this is a 1st gen anti-psychotic - so can haveEPSEs with it!)
Benign paroxysmal positional vertigo (BPPV)
- average age of onset?
- triggers?
- how long episode last for?
- what manouvere is positive? 1
- what manouvere is performed to treat? 1
55 years = average onset
vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
nb may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre
nb usually resolves spontaneously after a few weeks to months
Symptomatic relief may be gained by:
- EPLEY manoeuvre (successful in around 80% of cases)
nb can also teach the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises
nb Medication is often prescribed (e.g. Betahistine) but it tends to be of limited value
CHOLESTEATOMA
- what is it?
- risk factors? (age plus another 3)
- main two features? 2
a non-cancerous growth of squamous epithelium that is ‘trapped’ within the skull base causing local destruction
presents in childhood
- congenital (epithelium trapped in bone during embryogenesis)
- cleft palate (causing eustacian tube dysfunction)
- tympanic membrane trauma (norm secondary to otitis media)
main two features:
1) PROGRESSIVE unilateral conductive hearing loss
2) Painless PURULENT FOUL smelling discharge (otorrhea) – frequent + unremitting
nb depending on size, can also get:
- vertigo
- facial nerve palsy
- cerebellopontine angle syndrome
CHOLESTEATOMA
- what see on otoscopy? 1
- management? 1
Otoscopy
- ‘attic crust’ - seen in the uppermost part of the ear drum (with drum retraction or perforation)
Management
- patients are referred to ENT for surgical removal
RAMSAY HUNT SYNDROME
- what is it? (incl where affected)
- first symptom?
- subsequent symptoms? 3
- medical management? 2
aka herpes zoster oticus
is reactivation of VZV in CN7 (ie shinges in facial nerve)
1st) AURICULAR PAIN
other symptoms
- facial nerve palsy
- vesicular rash (around ear and tongue)
- vertigo + tinnitus
Mx
- PO aciclovir
- steroids
Difference between primary and secondary otalgia?
causes of primary otalgia? (3 common 2 rarer)
causes of secondary otalgia? (4 common, 3 rarer)
primary otalgia is pain orginiting from pathology in the ear
- secondary is when pts feel pain in the ear but this is actually referred from somewhere else
PRIMARY OTALGIA = infection (commonest!) = trauma + foreign bodies = impacted ear wax - ramsay hunt syndrome - otologic neoplasms
SECONDARY OTALGIA = dental inflammation / infection = temporomandibular joint disorders (pain worse w chewing) = trigeminal neuralgia = temporal arteritis - head + neck cancers - eagle's syndrome
Nb Eagle’s syndrome is a condition associated with the elongation of the styloid process or calcification of the stylohyoid ligament, clinically characterised by throat and neck pain, radiating into the ear.
ALWAYS find a cause for otalgia!!! - don’t just treat with analgesia! - if not resolving with eg Abx for suspected infection, refer to ENT
RED FLAGS in history of OTALGIA
- ear symptom? 1
- eye symptoms? 2
- other symptoms? 5
- past medical history? 2
- progressive or sudden hearing loss
- loss of vision (temporal arteritis)
- black spots in vision
- dysphagia
- odynophagia
- dysphonia
- hamoptysis
(head + neck Ca) - weight loss
- immunosuppressed
- diabetes
(rapidly proggressing infection)
describe what each of these words are describing in the eye:
- conjunctiva
- iris
- sclera
- pupil
- cornea
- anterior chamber
CONJUNCTIVA
- thin layer of tissue that covers whole eye EXCEPT cornea
IRIS
- coloured bit of the eye
SCLERA
- white of eye
PUPIL
- black bit
CORNEA
- transparent tiny lens that covers iris, pupil and anterior chamber (conjunctiva doesn’t cover this bit!)
ANTERIOR CHAMBER
- front part of the eye between the cornea and the iris
nb posterior chamber is between iris and lense (then aqueous chamber if actually in main part of your eyeball)
RED EYE findings in these conditions: - acute angle closure glaucoma - anterior uveitis (iritis) - scleritis - conjunctivitis - subconjunctival haemorrhage
1) brief hx / risk factors?
2) appearance of conjunctiva?
3) appearance of iris?
4) appearance of pupil?
5) appearance of cornea?
6) appearance of anterior chamber?
7) intraocular pressure?
ACUTE ANGLE CLOSURE GLAUCOMA = elderly, long-sited pt, sudden pain in/behind eye, reduced visual acuity, halos 2) conjunctiva: injected 3) iris: injected 4) pupil: FIXED MID-DILATED (can be oval) 5) cornea: steamy/hazy 6) anterior chamber: very shallow 7) intraocular pressure: very high!
ANTERIOR UVEITIS (iritis)
= HLA-B27: ank spond, RA, reactive arthritis, sarcoid etc, photophobia, deep boring pain - worse with acomodation
2) conjuctiva: injection most marked around cornea (ie red ring around iris)
3) iris: injected
4) pupil: SMALL +/- irregular shape(dt adhesions)
5) cornea: NAD
6) anterior chamber: TURGID (CELLS! = HYPERPYON)
7) IOP: NAD
SCLERITIS = half have rheum diseases, pain - esp on eye movement 2) conjunctiva: injection, is most marked around cornea (ie red ring around iris - nb similar to iritis) - also has BLUISH HUE 3) iris: ?? 4) pupil: NAD 5) cornea: NAD 6) anterior chamber: NAD 7) IOP: NAD
CONJUNCTIVITIS = norm bilateral, bacterial, viral or allergic 2) conjuntiva: injected (greatest towards medial and lateral corners of eyes), discharge (purulent if bacterial) 3) NAD 4) NAD 5) NAD 6) NAD 7) NAD
SUBCONJUNCTIVAL HAEMORRHAGE = norm secondary to valsalva manouvere, HTN, bleeding disorders, trauma, haemorrhagic fevers 2) bright red area of sclera 3) NAD 4) NAD 5) NAD 6) NAD 7) NAD
Initial management of each of these causes of red eye:
- acute angle closure glaucoma? 2
- anterior uveitis? 2
- scleritis? 1
- conjunctivitis? 1
- subconjunctival haemorrhage? 1
which would you refer to opthalmology?
ACUTE ANGLE CLOSURE GLAUCOMA - IV acetazolamide (500mg) - Pilocarpine eye drops (after 1 hr) (see specific flashcard for more info) = refer ASAP
ANTERIOR UVEITIS (iritis)
- steroid eye drops (eg pred)
- atropine eye drop
= refer ASAP
SCLERITIS
- oral NSAIDs is 1st line
= refer ASAP
CONJUNCTIVITIS
- depends on cause (antihistamine for allergic, consider chloramphenicol if bacterial)
= no referral needed
SUBCONJUNCTIVAL HAEMORRHAGE
- none, resolves spontaneously - check BP and if on anticoags
= refer (only if traumatic cause)
ACUTE ANGLE CLOSURE GLAUCOMA:
- pathophysiology? (ie what causes the raised intra-ocular pressure)
pupil dilates -> iris pushes against lense -> aqueous can’t drain from posterior to anterior chamber -> trabecular meshwork also blocked -> aqueous cannot drain from anterior chamber -> RAISED intraocular pressure
this is sight threatening as the raised IOP can -> death of optic nerve
nb normally aqueous humoour is produced by ciliary bodies in posterior chamber then moves to anterior chamber where it is drained in the trabecular meshwork
nb vitreous humour is is in the deeper part of the eye - different to aqueous humour)
ACUTE ANGLE CLOSURE GLAUCOMA:
- age generally affected?
- long or short-sighted people more at risk?
- medications that increase risk?
- what is normally the acute trigger?
generally elderly (also asians at higher risk)
long-sighted at higher risk (hyperopia) - dt shallow anterior chamber
nb you get more long-sighted as you age!!
drugs which can increase likelihood:
- sympathomimetics
- anticholinergics
^both dilate pupil!!
acute trigger is normally low light (eg in evening) as pupil dilates!
nb can also get it secondary to a traumatic haemorrhage (which pushes the posterior chamber anteriorly)
ACUTE ANGLE CLOSURE GLAUCOMA:
- classic prodrome symptom? 1
- main local symptom? 1
- other local symptom? 1
- systemic symptoms? 3
HALOES / rainbows around lights!!
constant aching pain develops RAPIDLY around one eye
- reduced vision
- pain radiates to forehead (headache)
- nausea and vomiting
- abdo pain
ACUTE ANGLE CLOSURE GLAUCOMA, findings on exam / SLIT LAMP:
- visual acuity?
- conjunctiva/sclera?
- iris?
- pupil?
- cornea?
- anterior chamber?
- intraocular pressure?
reduced visual acuity
perilimbal conjunctival injection (ie closest to the iris/cornea)
iris injected
pupil FIXED (ie not responsive to light) MID-DILATED
HAZY cornea (also hard on palpation)
anterior chamber: shallow but NO cells (how differentiate from anterior uveitis)
raised IOP
ACUTE ANGLE CLOSURE GLAUCOMA:
- who to refer to? how urgently?
- nursing management? 2
- two medications to give to treat? 2 (incl route)
- two medications to treat symptoms? 2
- definitive treatment provided by opthalmologists? 1
opthalmologist! - SUPER URGENT! (even OOH)
- lie patient on back (no pillows)
- DON’T put on eye mask or dim light (this will dilate pupil more, making worse!)
1) IV ACETAZOLAMIDE (500mg)
- this works by reducing aqueous secretions
2) PILOCARPINE EYE DROPS (after 1 hr)
- parasympathetic -> constricts pupil which opens trabecular meshwork, allowing drainage
nb can also give betablockers (if not CI) topically (timolol eye drops!)
ALSO PRESCRIBE
- oromorph
- ondasetron
DEFINITIVE MANAGEMENT: Peripheral iridectomy (laser or surgery) – do once IOP is controlled, involves removing iris segment at 12 oclock B/L to allow aqueous flow
DDx for ACUTE RED EYE (with normal lids)
- inflammatory/autoimmune? 3
- infectious? 2
- secondary to foreign bodies? 2
- other? 2
what is the most common cause?
INFLAM / AUTOIMMUNE
- anterior uveitis / iritis
- scleritis
- episcleritis
- allergic conjunctivitis
INFECTIOUS
- viral conjuctivitis
- bacterial conjuctivitis
SECONDARY TO FOREIGN BODIES
- corneal abrasions / foreign bodies
- bacterial or fungal keratitis / corneal ulcer (almost always secondary to contact lenses!)
OTHER
- acute angle closure glaucome
- subconjuctival haemorrhage
nb subconjunctival haemorrhage can be caused by: trauma, straining (coughing, sneezing, vomiting, Valsalva), conjunctivitis, chronic health conditions (diabetes, hypertension), and coagulopathy
CONJUNCTIVITIS is COMMONEST cause of acute red eye!
CONJUNCTIVITIS
- how is the appearance described?
- three main types?
‘BILATERAL generalised conunctival injection’
nb injections tend to be more peripheral
nb conjunctivitis = most common cause of acute red eye
- bacterial
- viral
- allergic
nb all three very common
CONJUCTIVITIS
- symptoms? 4
- how to distinguish clinically from viral and bacterial causes? 1
- additional feaqtures of allergic conjunctivitis? 2
‘uncomfortable’, gritty eyes (rather than painful)
- erythema of conjunctiva
- watery eyes
- itchy eyes
viral more ‘itchy’ and watery discharge while bacterial is more ‘sticky’ with a more purulent discharge (clinically hard to tell the difference between)
allergic
- eyelid swelling +/- conjunctival oedema
- history of other atopic disease
Management of allergic conjunctivitis:
- advice to patient?
- medication options? 2
use a cold compress
PO antihistamines
OR
TOP anti-histamines e.g. Emedastine or olopatadine
Nb can also have steroid drops if really bad - but these would be started by opthalmologist
BACTERIAL CONJUNCTIVITIS:
- 1st line management option? 1
- norm prognosis without this management?
- which groups of patients always given to? (3 clinical, 2 occupational)
CHLORAMPHENICOL eye drops (or fusidic acid)
controversial - most BACTERIAL infections resolve within 5 days without treatment
(can give delayed prescription)
ALWAYS GIVE Abx to:
- purulent, painful, red
- dry eyes / known eye disease
- contact lense user
- care / ICU / nursery workers
- children at nursery
BACTERIAL CONJUNCTIVITIS
- what to suspect and do if pt fails treatment?
- which group of patients should you refer to opthalmologist straight away?
suspect could be gonococcal or chlamydial cause!
DO EYE SWABS!! and refer to opthalm
refer NEONATES to opthalm straight away as most likely to be chlamydia/gonococcal from mothers birth canal
Three most common causative organisms for BACTERIAL conjunctivitis? 3 (other 2 rarer causes?)
commonest VIRAL cause of conjunctivitis? 1
BACTERIAL = strep pneumoniae = staph aureus = H. influenzae - gonococcal - chlamydial
VIRAL
= adenovirus (80%)
^very contagious!!
what normally preceedes a viral conjunctivitis?
How long do viral conjucntivits symptom s take to go away? when should you refer someone?
URTI norm preceeds (or contact with someone with conjunctivitis - eg in home)
1-2 weeks (but can be as long as 6 weeks!) - refer at 6 weeks
what can often preceede a bacterial conjunctivitis? 2
Otitis media or LRTI
FOREIGN BODY IN EYE:
- symptoms common for all? 5 (conjunctiva abrasian, corneal abrasian and penetrating injury)
- symptom that makes corneal involvement and/or penetrating injury more likely? 1
nb this is just symptoms, do signs on different flashcard
= red eye
= watery eye
= painful eye
= sensation of foreign body in eye
= blurred vision (nb degree of loss of visual acuity doesn’t correlate with severity)
(nb foreign body on cornea is more painful than on sclera)
PHOTOPHOBIA (always suggests corneal involvement, superficial or deep)
EYE INJURY
- sign likely to see in all? 1
- bedside investigation to look for abrasions? 1
- RED FLAG signs for penetrating corneal injury? 5
Conjunctival or ciliary injection (ALL)
FLUROSCEIN STAIN (appears green under blue light if any epithelial damage)
RED FLAGS
- distorted iris / pupil (or globe)
- air bubbles under cornea
- leaking humour
- hyphaema (blood level in iris) -BAD SIGN!
- subconjunctival haemorrhage (only if massive and hx of trauma!)
nb see many of these with eyes alone - but can use a slit lamp too (but norm would just refer to opthalm to do this if unsure!)
SHOULD ALWAY EVERT EYELIDS to look for abrasians / foreign bodies
nb also loss of red reflex (loose in blood in vitreous or large retinal detachment)
Test to do to see if aqueous humour is leaking from eye:
- name?
- what it involves?
Seidel’s test
= 10% Fluorescein (dark orange)
check if aqueous fluid is leaking (treat as open globe injury)
Who to refer to opthalmology urgently following occular trauma / foreign body?
- all high-velocity injuries caused by sharp objects
- chemical inj.
- FBs
- ↓visual acuity
- large abrasion (>60% cornea)
- corneal opacity
- rust ring
- distorted pupil
- retinal damage
- deep laceration of orbit etc.
BASICALLY REFER ANYTHING that is worse than a simple, small corneal abrasion with no foreign
Management of:
- corneal abrasion? 2
- additional management of corneal foreign body (non-penetrating)? 2
ie inaddition to above
CORNEAL ABRASION
- TOP anaesthetics
- TOP chloramphincol (fusidic acid if pregnant)
IF foreign body, ALSO:
- remove FB under TOP anaesthetic
- irrigate eye with water
(then do as above!)
Management of penetrating corneal injury:
- what NOT to do? 1
- who to refer to? 1
- how to protect eye in meantime? 1
- medication to give in ED? 1
Do NOT touch, manipulate or pad the eye
REFER IMMEDIATELY
Give rigid eye shield to protect eye and refer immediately
Give TETANUS shot
CORNEAL ULCER
- main risk factor?
- causative group of organisms?
- do you need to refer to opthalmology?
CONTACT LENSE WEARERS
can be bacterial (commonest), viral (norm HSV) or rarely fungal
YES - REFER URGENTLY!
CORNEAL ULCER
- often initial symptom?
- later symptoms? 4
may start with a ‘foreign body sensation’
then
- photophobia
- blurred vision
- discharge
- pain
CORNEAL ULCER
- signs on exam? 3
- additional bedside investigation? 1 (and what does it show?)
- severe conjunctival injection
- discharge
- eyelid swelling
corneal ulceration demonstrated by fluorescein stain
CORNEAL ULCER
- who manages?
- investigation they will do? why?
- management options? 2
opthalmologists manage
slit lamp - to determine if bacterial or vioral ulcer (look different)
- TOP chloramphenicol (or other Abx)
OR - TOP acyclovir
^depending on cause identified!
CATARACTS
- pathophysiology?
- risk factors? (2 demographic, 2 lifestyle, 2 conditions, 1 med)
nb this excludes for con genital
gradual deposiotion of opaque protein deposits onto lense
- increased age
- female
- smoking
- UV exposure
- diabetes mellitus
- inflammatory eye disease
- corticosteroids
CONGENITAL CATARACTS
- infections that can cause? 5
- other condition associated with? 1
TORCH
- toxoplasmosis
- other (VZV, syphillis, HIV)
- rubella
- CMV
- herpes simplex
down’s yndrome
nb can also get idiopathic congenital cataracts
ADULT-ONSET CATARACTS
- speed of onset?
- describe the loss of vision that occurs? (ie what goes first)
- associated symptoms? 2
GRADUAL (see nb below)
PAINLESS blurred vision, slowly -> loss of vision (esp if bilateral)
nb often both eyes but norm one worse than other
- trouble with nocturnal vision
- difficulty reading (↓Acuity)
- failure to recognise faces
- problems watching TV / see colour less clearly
= DAZZLE / GLARE (esp in sunlight or lights whilst driving at night - “is like driving with a dirty windscreen at night/bright light”)
= HALOES (around bright lights)
nb normal gradual onset ‘nuclear’ cataracts - but can get posterior sub-capsular cataracts which progress faster (norm secondary to STEROIDS)
CONGENITAL CATARACTS
- test to pick up?
- signs if missed? 3
- how quickly do you need to operate to reduce adverse effects? 1
RED REFLEX (absent in congenital cataracts and retinoblastoma) - part of newborn check!
if missed may notice:
- squint
- amblyopia (lazy eye)
- nystagmus
need to operate fast (ideally within 4 weeks) or seeing part of brain won’t develop properly!
CATARACTS
- findings on fundoscopy? 2
- investigation for definitive diagnosis?
red light reflex
- present if early
- absent if late
Lens appears brown or white if bright light shone
refer to opthamlmologist (routine) for slit lamp diagnosis if considering surgery
CATARACTS:
- conservative lifestyle changes? 2 (to prevent getting worse)
- are they allowed to drive?
- definitive management? 1 (when do? 2)
- stop smoking
- wear sunglasses
surgery is only cure
- operate on one eye at a time
can only drive if:
- In daylight be able to read a number plate at a distance of 20m
- Visual acuity must be at least Snellen 6/12 with both eyes open (or in the only eye if monocular)
^if worse than this - must inform DVLA and not drive!
operate if:
- QoL↓
- unable to read number plate @ 20m
ALWAYS DIOCUMENT VISUAL ACUITY (on any referral!)
Definition of:
- meibomian cyst (aka chalazion)
- stye (aka hordeolum)
how do they both present? (signs/symptoms)
two main differences in presentation? 2
MEIBOMIAN CYST - aka chalazion - blocked meibomian gland (norm hydrates eye) -> cyst - NON-infective = NOT tender (may be painful initially) = HARD on palpation
STYE - aka hordeolum - infected meibomian gland (internal) or lash follicle (external) = INFECTIVE (basically a mini abscess) = SOFTER on palpation
BOTH
- single lump on eyelid
- can get watering and slightly red eye
nb both can have a yellowy centre - but stye often more pronounced
nb if whole eyelid swollen, more likely blepharitis (although may have a stye on top of this)
Risk factors for STYE? (3 local conditions, 2 systemic conditions)
= chronic blepharitis
- rosacea
- seborrhoeic dermatitis
- pregnancy
- diabetes mellitus
nb most people who get one don’t have any reisk factors
How diagnosis of stye and meibomian cyst made?
when to refer to opthalmology? 2
clinical diagnosis
- EVERT the eyelid to see an internal stye!!
REFER IF:
- visual disturbance
- associated peri-orbital or orbital cellullitis
also if suspect it is actually a BCC
Management of STYE
- what should patients NOT do? 3
- conservative management? 1
- prognosis?
- other management options in primary care? 2
- when to consider topical antibiotics? 1
DON’T
- attempt to puncture / pop the stye
- wear eye make up until gone
- use contact lenses until gone
DO
- use warm compresses (5-10 mins 2-4 times a day until resolves)
(nb can also use OTC oral analgesias)
nb same advice for meibomian cyst
PROGNOSIS: SLEF-LIMITING (resolve in 1-2 weeks)
if painful external stye, can:
- pluck eyelash from infected follicle
- incision and drainage
only prescribe TOP antibiotic if clinical features of concurrent conjunctivitis (copious muco-purulent discharge)
(obvs if associated peri-orbital / orbital cellulitis then give PO/IV Abx for this)
DIABETIC RETINOPATHY features indicating: - background retinopathy? 1 - maculopathy? 1 - pre-proliferative retinopathy? 2 - proliferative retinopathy? 1
which cause reduced visual acuity?
BACKGROUND RETINOPATHY
- at least one micro-aneurysm (MA - ‘dots and blots’)
MACULOPATHY
- basically anything on the macula (OEDEMA most common, also: ischaemia, haemorrhages)
- can get reduced visual acuity
PRE-PROLIFERATVE
- ‘cotton wall spots’ (aka soft exudates)
- hard exudates
(nb in addition to dots and blots)
PROLIFERATIVE
- new vessel formation (wispy red noodles, often next to ischaemic areas)
- get reduced visual acuity!
nb maculopathy is seperate to other stages - each other stage can occur with or without maculopathy
nb it is actually much more confusion than this with categorisation etc but just learn this!
DIABETIC RETINOPATHY
- how often are people with diabetes screened for it?
- what can do in primary care to control / slow progression? 4
every year!
really important as don’t have any symptoms until far down! - and can stop getting worse but is not reversible!
- nb if get haemorrhages, these can present as painless floaters!
- good glycaemic control
- good HTN control
- good lipid control (diet + statins)
- stop smoking
Aside from diabetic retinopathy, what other eye conditions are people with diabetes at risk of? 2
- cataracts
- glaucoma
(nb also high risk for hypertensive retinopathy too!)
DIABETIC RETINOPATHY:
- management options in secondary care? 4
LASER TREATEMENT
- to obliterate new vessel growth
- slows progression but does not improve visual acuity
INRAVITREAL STEROIDS
ANTI-VASCULAR ENDOTHELIAL GROWTH FACTORS
-end in mab
SURGERY
- may need vitrectomy if have an intravitreal bleed
HYPERTENSIVE RETINOPATHY features of: - grade 1? 2 - grade 2? 2 - grade 3? 3 - grade 4? 1
possible symptoms? 2 (when do these occur?)
GRADE 1
- increased tortuosity (nb normal in small peripheral vessels)
- narrowing (dt deposits)
GRADE 2
- silver/copper wiring
- AV nipping
GRADE 3
- cotton wool spots (ischaemic areas)
- hard exudates
- flame/splinter bleeds
GRADE 4
- papilloedema
SYMPTOMS
- blurred vision
- visual field defects
OCCUR LATE in disease!!
Management of hypertensive retinopathy:
- mainstay? 1
- options if severe? 3
Treat primarily by CONTROLLING BP (meds and lifestyle)
for retinal edema, sometimes:
- laser
- intravitreal steroid injection - injeciton of antivascular endothelial growth factor drugs
ACUTE ANTERIOR UVEITIS:
- aka?
- pathophysiology?
- what conditions is it associated with? 10
- other main risk factor?
aka IRITIS
inflammation of the iris (coloured part of eye) and anterior chamber
HLA-B27 conditions:
- ankylosing spondylitis
- reactive arthritis
- JIA
- IBD (both)
- bechet’s disease (mouth and genital ulcers)
- psoriasis/psoriatic arthritis
- sarcoidosis
- MS
also
- HIV
- TB
other: POST EYE SURGERY infection/inflammation
ACUTE ANTERIOR UVEITIS
- aka? 1
- symptoms? 4
- main DDx to rule out? 1
aka IRITIS
PAINFUL (deep ‘boring’, worse with accomodation) and RED eye
- PHOTOPHOBIA (hurts when pupuil constricts)
- BLURRED VISION
nb may also have a headache and feel systemically unwell (also ask about PMHx/joints)
need to RULE OUT ACUTE GLAUCOMA (presents very similarly)
- obv also all other causes of acute red eye…
SLIT lamp findings for ACUTE ANTERIOR UVEITIS
1) appearance of conjunctiva?
2) appearance of iris?
3) appearance of pupil?
4) appearance of cornea?
5) appearance of anterior chamber?
6) intraocular pressure?
ANTERIOR UVEITIS (iritis)
1) conjuctiva: injection most marked around cornea (ie red ring around iris) = PERILIMBAL or CILIARY INJECTION
2) iris: injected
3) pupil: SMALL +/- irregular shape (dt adhesions)
4) cornea: normal
5) anterior chamber: TURGID (CELLS! = HYPERPYON)
6) IOP: normal
nb DON’T get hyperpyon in acute glaucoma!
ACUTE ANTERIOR UVEITIS
- how urgently to refer to opthalmologists?
- management in the interim? 3
URGENT REFERRAL TO OPTHALM
- ANALGESIA
- TOP steroids
- TOP cycloplegics to dilate pupil and relieve pain/photphobia and prevent formation of adhesions (TOP Atropine, cyclopentolate)
ECTROPION and ENTROPION
- definition of each?
- main symptoms? 2 each
- main causes/risk factors for each? (list a copuple for each)
ECTROPION
= Eversion of eyelid
- itchy / irritated red watery eye, dry eye
causes: old age, CN7 palsy, tumour on eyelid, congenital
ENTROPION
= INversion of eyelid
- occular irritation, foreign body sensation, tearing, redness
causes: old age, trachoma infection (developing world), congenital
Management of ECtropion:
- conservative? 2
- active option? 1
- lubricating eyedrops
- skin tape (esp at night)
- surgery
ENtropion
- main DDx?
- management of entropion? (2 conservative, 1 active)
assess eye-lashes for TRICHIASIS (misdirection of eyelashes), as this is a common differential
MANAGAEMENT
- taping eyelid to cheek (esp overnight
- botox for eyelid muscles
- surgery to correct!
BLEPHARITIS
- what is it?
- symptoms? 5
- management? 2
inflammation of eyelids (+/- super-imposed bacterial infection)
Chronic condition: symptoms get better + worse
- red/swollen eyelids
- crusty/gritty eyelids (esp when wake up)
- eyelashes falling out
- watery eyes
- feeling of something in your eye
Mx = Good eye hygiene
- warm, hot compresses
- massage
- cleaning lids with cotton buds
- clean baby shampoo
also artificial tears
nb can give course of steroid or antibiotic eyedrops if really bad, but rarely!
nb also tell peopl not to wear eye maker up, contact lenses etc when it’s bad!
EPISCLERITIS and SCLERITIS
- what are each of them?
- which vascular structure does each affect?
- what test to do to diferentiate between them? 1
(nb see other flashcard for sign/symptoms)
EPISCERITIS
= inflammation of superficial episcleral layer of eye
- affects SUPERFICIAL episcleral vascular plexus
SCLERITIS
= inflammation of sclera of eye
- affects DEEP episcleral (aka scleral) vascular plexus
give PHENYLEPHERINE eye drops:
- wait 5 mins:
- if EPIscleritis, redness will BLANCH
- if scleritis, will NOT blanch!
EPISCLERITIS vs SCLERITIS symptoms:
1) eye pain / discomfort?
2) pain on eye movement?
3) colour of sclera?
4) any visual change?
5) associated conditions?
EPISCLERITIS
EPISCLERITIS
1) mild DISCOMFORT, may be mild photophobia and watering
2) NO pain on eye movement
3) red eye (may be a patch or diffuse - no blue)
4) no visual change
5) normally idiopathic (can be associated with IBD)
SCLERITIS
1) deep, dull ACHE (at night / headache) + tender to touch, photophobia
2) pain on eye movement (sclera attached to muscles)
3) BLUISH/purple hue to sclera plus redness (that does NOT blanch w epinepherine drops)
4) may be visual change!
5) 30-50% have rheum disease (arthritis and weird vasculitises)
nb both can be unilateral or bilateral
Management of episleritis?
management of scleritis?
Episcleritis
- self-limiting so reassure
- give topical NSAIDs (diclofenac /ketorolac)
(+/- artificial tears)
Scleritis
- urgent opthalm referral (risk of sclera thinning and globe perforation)
Differential diagnosis for acute unilateral loss of vision:
- painful? 2
- painless? 6
Nb this is total loss - not just blurred vision
PAINFUL
- temporal arteritis
- migraine
PAINLESS
- retinal artery embolism
- retinal vein thrombosis
- spontaneous vitreous haemorrhage (floaters)
- retinal detachment
- posterior cerebral artery stroke
- optic neuritis (usually MS)
Relative afferent pupillary defect (RAPD)
- aka?
- what actually testing? (Ie what’s wrong if there is one?)
- what do you see?
Aka swinging light test
Tells you that either the optic nerve AND/OR retina is damaged
Get paradoxical dilation of abnormal eye when put light on it after putting light on normal eye
**check that this is right!!
OPTIC NEURITIS
- common cause / associated conditions?
- THREE core symptoms?
- findings on opthalmic exam? 3
- other investigation? 1
- management? 2
Inflammation of optic nerve
- MS
- also idiopathic, post URTI, drugs/toxins
Core symp
1) REDUCED vision (varying)
2) PAIN on eye MOVEMENT
3) impaired COLOUR vision
(For latter, show red pen lid, get cover eye and compare between normal and abnormal eye - will be duller colour in abnormal)
Exam
- red desaturation
- RAPD
- swollen optic disc (fundoscopy)
Do MRI brain if suspect MS
(Also do ESR and CRP)
Mx
- steroids (IV)
- urgent referral to opthalm
difference between:
- central retinal ARTERY occlusion
- central retinal VEIN occlusion
1) pathophysiology?
2) risk factors? (3 each)
3) presentation?
4) RAPD or not?
5) findings on fundoscopy?
6) management? (2 for each)
CENTRAL RETINAL ARTERY OCCLUSION
1) norm EMBOLI from:
2) carotid plaques, rarely sickle cell or vasculitis
3) sudden, painless COMPLETE loss of vision unilaterally
4) RAPD! (normally)
5) pale retina + bright red macula (aka cherry red spot)
6) eye drops to lower IOP, massage eye + call opthalm asap
CENTRAL RETINAL VEIN OCCLUSION
1) norm THROMBUS from:
2) IHD, HTN, high cholesterol (+other norm stroke RFs)
3) sudden, painless BLURRED -> COMPLETE loss of vision unilaterally
4) Occasionally RAPD (but rarely)
5) optic disk oedema and red dots (haemorrhages) all over macula
6) aspirin + call opthalm asap
EPISTAXIS
- two different types? (ie location of bleeding)
- which more serious?
- which occurs more in elderly?
ANTERIOR
- mild
- source of bleeding visible in 95% of cases
- almost always from nasal septum at ‘little’s area” where kiesselbach’s plexus forms
POSTERIOR
- larger volume and risk of airway compromise!
- occurs commonly in elderly
- source if from deeper structures of nose
EPISTAXIS
- two commonest causes?
- drugs which increase risk? (2 medicine, 1 recreational)
- common bleeding condition which often has nosebleeds?
- autoimmune condition where often get nosebleeds? 1
commonest causes
= trauma (incl nosepicking)
= foreign bodies
- anticoags
- antiplatelets
- cocaine
- von willebrands disease
- granulomatosis with polyangitis (wegners)
HTN also increases risk!!!
nb also obviously more likely to have in haemophilias and other bleeding conditions (incl alcohol excess) - but Von Wille most common and typical!
How to tell from Hx/exam if epistaxis is anterior or posterior? 1
bloods to consider for epistaxis? 3
what to look for in med hx? 2
what age should you suspect a more sinister diagnosis? 1
ANTERIOR
= blood running from ONE nostril
POSTERIOR
= blood running into THROAT
AND from BOTH nostrils
- FBC
- Group + save (if large)
- clotting
^nb these are to consider - don’t always do!
look for antiplatelets and anticoags
- stop (and reverse latter) if relevant
age under 2
- more likely to be 1st presentation of haemophillia or leukaemia
ALWAYS REFER IF UNDER 2!!!
EPISTAXIS MANAGEMENT:
- if clinically UNstable? 1
if clinically stable:
- 1st line? 1
- 2nd line? 1
- 3rd line? 1 (when can/can’t do this)
- 4th line? 1
- 5th line? 1
nb this is management to stop bleeding - see other flashcard for how to find underlying cause etc
if UNstable: A-E resus
if STABLE:
1st) pinch SOf bit of nose for 15 MIN
2nd) lidocaine + phenylepherine gauze OR spray
3rd) silver nitrate cauterise (ONLY if can visualise where bleeding from! - never do both sides of septum!)
4th) anterior packing!
5th) call ENT (they can do ligation or posterior packing with foley catheter)
NASAL FRACTURE:
- how is un-displaced managed? 1
- management option for displaced? 2 (incl time scales)
- advice for both types? 2
UN-DISPLACED
- no treatment required
DISPLACED
- reduction under GA/LA with post-op splint (within 2 weeks - complete setting occurs at 3 wks!)
- septoplasty (if a lot of post-traumatic deformity, do primary septal reconstruction)
BOTH
- sleep with head elevated
- apply ice (for 12hrs post-op)
NASAL TRAUMA:
- complication? 1
- what is it?
- most common symptom?
- other symptoms? 2
- what seen on examination? 1
- how to tell between this and deviated septum? 1
nasal septal haematoma
haematoma between the septal cartilage and the overlying perichondrium
may be precipitated by relatively MINOR trauma!!
main symp = SENSATION of NASAL OBSTRUCTION
also:
- pain
- rhinorrhoea
OE: classically a bilateral, red swelling arising from the nasal septum
how to differentiate between deviated nasal septum:
- gently probe the swelling
- haematomas = boggy
- septums = firm
NASAL SEPTAL HAEMATOMA
- how manage? 2
- how quickly manage?
- surgical drainage
- INTRAVENOUS antibiotics
if untreated: irreversible septal necrosis may develop within 3-4 days
nb if untreated may result in a ‘saddle-nose’ deformity
RISK FACTORS for SEPTAL PERFORATION:
- trauma? 4
- drugs (1 med, 1 recreational)
- medical conditions? 2
- surgery
- trauma
- foreign bodies
- piercings
- nasal sprays
- cocaine
- malignancy (rodent ulcer)
- chronic granulomatous disease (eg TB, sarcoidosis)
NASAL SEPTAL PERFORATION:
- main 3 symptoms? 3
Perforations irritate!
- WHISTLE noise
- Crust
- Epistaxis
Management options for nasal septal perforation?
- Rhinoplasty to close
- Saline douche for crusts
- Silastic buttons to occlude hole
CSF RHINORRHOEA
- normal cause?
- how to confirm that the rhinorrhoea is CSF at bedside?
Ethmoid (basal skull) fracture disrupting dura and arachnoid results in CSF leak!!
Nasal discharge test +ve for glucose (bed side dipstick)
nb can also send CSF sample to lab – B2 (tau) transferrin (gold standard ∆)
CSF RHINORRHOEA
- investigation? 1
- management advice?
- medical management? 2
CT head!
Conservative Mx – bed rest, self resolves 7-10 d
Cover with:
- Abx
- Pneumococcal vaccine
NASAL FOREIGN BODIES:
- normal age group affected?
- medication to use to help remove?
- how remove?
- which foreign bodies to remove urgently?
Most self-inserted by child
2.5% cocaine spray (avoid in child) can shrink mucosa to allow removal/suction
Remove foreign body with forceps carefully
BATTERIES require URGENT removal
ALLERGIC RHINITIS:
- features / symptoms? 5
- what conditions associated with?
- sneezing
- bilateral nasal obstruction
- clear nasal discharge
- post-nasal drip
- nasal pruritus
atopic conditions (eczema, asthma, allergies)
ALLERGIC RHINITIS
- conservative management?
- 1st line management? 1
- options if severe persistent symptoms? 2
ALLERGEN AVOIDANCE (easier said than done!)
1st) oral or intranasal antihistamines
if persistent mod-severe symptoms (or failure of antighistamines):
- short course intra-nasal corticosteroids
- short course topical nasal decongestants, eg oxymetazoline (see below!)
nb topical nasal decongestants (eg oxymetazoline) should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal
nb a short course of oral corticosteroids are occasionally needed to cover important life events
ACUTE SINUSITIS
- most common causative infectious agents? 3
- pre-disposing / risk factors? 4
- strep pneumoniae
- haemophilus influenza
- rhinovirus
- nasal obstruction (e.g. septal deviation or nasal polyps)
- recent local infection (e.g. rhinitis, dental extraction, URTI)
- swimming/diving
- smoking
nb: Acute sinusitis usually follows a common cold, and is defined as an increase in symptoms after 5 days, or persistence of symptoms beyond 10 days, but less than 12 weeks.
ACUTE SINUSITIS
- where do they get pain? what exarcerbates this pain?
- other 2 main symptoms? 2
FACIAL pain
- typically frontal pressure pain which is WORSE on BENDING FORWARD
- nasal discharge (norm thick and purulent)
- nasal obstruction (feeling)
ACUTE SINUSITIS
- symptomatic management for all? 1
- when to give intranasal corticosteroids?
- when to give oral antibiotics?
ANALGESIA
nb intranasal decongestants or nasal saline may be considered but the evidence supporting these is limited
INTRANASAL STEROIDS
- may be considered if the symptoms have been present for more than 10 days
ORAL ABX
- norm NOT required
- can give if SEVERE presentations (ie systemiacally unwell)
nb ‘double-sickening’ may sometimes be seen, where an initial viral sinusitis worsens due to secondary bacterial infection
CHRONIC RHINOSINUSITIS
- how long last?
- four main features? 4
lasts AT LEAST 12 WEEKS!
1) FACIAL PAIN (frontal pressure pain, worse on bending forward)
2) NASAL DISCHARGE (usually clear if allergic or vasomotor, thicker purulent discharge suggests secondary infection)
3) NASAL OBSTRUCITON
eg mouth breathing
4) POST-NASAL DRIP
- may produce a chronic cough
CHRONIC RHINOSINUSITITS
- lifestyle advice? 1
- medical management? 2
avoid allergen
- intranasal corticosteroids
- nasal irrigation with saline solution
nb irrigation not proven benefit for acute sinusitis but usefuyl for chronic
CHRONIC RHINOSINUSITIS
- red flag symptoms? 3
- unilateral symptoms
- persistent symptoms despite compliance with 3 months of treatment
- epistaxis
if get any of these - consider ENT referral
NASAL POLYPS
- age group and gender most at risk?
- common conditions that increase risk? 3
- rare conditions that increase risk? 3
- male
- adults
- asthma
- aspirin sensitivity
- infective sinusitis
nb Nasal polyps are NOT associated with allergy
- CF
- kartagener syndrome
- churg-strauss syndrome
NASAL POLYPS:
- four main symptoms/features? 4
1) Nasal obstruction – mouth breathing, snoring
2) Rhinorrhoea – watery, post-nasal drainage
3) Sneezing
4) Poor sense of taste and smell
NASAL POLYPS
- main DDx to rule out?
- two main red flags for this? 2
TUMOUR
- UNILATERAL discharge/symptoms
- EPISTAXIS
Nasal polyps tend to be bilateral. With unilateral lesions, suspect a tumour (and in children, rule out an encephalocele)
NASAL POLYPS:
- what age group may suspect underlying diagnosis? which diagnosis?
children with nasal polyps
always screen for cystic fibrosis!!
NASAL POLYPs:
- how to examine?
- medical management? 1
- when to refer to ENT surgeon? 3
use nasal speculum to examine
TOPICAL (ie nasal) steroids!
refer if:
- red flag symptoms
- significant nasal obstruction
- poor response to 3 months of nasal steroids (check technique)
nb ENT surgeons may presvribe oral steroids if bad
nb pts with persistent symptoms despite optimal medical management may be referred for surgery!
ACNE VULGARIS
- describe pathophysiology?
- three types of lesions seen?
- areas of body see lesions? 3
- how make diagnosis?
disorder of pilosebaceous follicles of face and upper trunk → at puberty androgens ↑sebum production from sebaceous glands → blocks glands → comedones may be open (blackheads) or closed (white heads) → papules, pustules, nodules
- comedones
- papules
- pustules
- face
- neck
- back
clinical diagnosis
ACNE VULGARIS
- age and gender most affected?
- syndrome (either primary or iatrogenic) which increases risk? 1
- teenagers
- M>F
cushings
- disease or anabolic steroid use!
ACNE VULGARIS
- features of mild? 1
- additional features of moderate? 1
- additional features of severe? 3
MILD
- facial comedones
MODERATE
+ inflammatory lesions, face +/- torso
SEVERE
+ nodules
+ cysts
+ scars
ACNE VULGARIS
- management options of mild? 2
- management options of moderate? 3
- management of severe? 1
MILD
- TOP Benzoyl peroxide
- TOP Azelaic acid (6 months)
MODERATE - TOP Clindamycin - TOP retinoids (eg tretinoin or adapalene) - PO doxycycline or clarithromycin (- can also consider COCP if severe!)
SEVERE
- PO Isoretinoin for 20wks
so:
- mild = TOP acids
- mod = TOP retionoid / TOP/PO abx
- severe = PO retinoid
nb low-strength benzoyl peroxide are OTC, others prescribed
Two main side effects of isoretinoin (oral retinoid used for acne treatment)? 2
- teratogenic
- depression + suicide risk!
nb topical retinoids are also slightly teratogenic (but not as much) so shouldn’t be used in people trying for baby or currently pregnant!
HPV:
- which two strains cause cancer?
- which two strains cause warts?
16+18 = cervical cancer 6+11 = warts
nb HPV enters basal epithelia of genital skin via micro abrasions during sexual contact → genital warts (benign growths)
nb cervical screening covered in GOSH notes
Risk factors for HPV:
- lifestyle? 1
- immune-related? 2
- oestrogen-related? 2
- Multiple sexual partners
- DM
- immunocomp
- pregn
- COCP
ANOGENITAL WARTS
- incubation period?
- how long last?
- recurrence risk?
- when greatest risk of recurrence?
Median incubation = 3 months
Resolves in 3 months with treatment
(Median detectability in genital skin = 1 year)
High recurrence!
Warts are most contagious when visible
Grow rapidly during pregnancy → regress after birth
ANOGENITAL WARTS
- describe appearance?
- symptoms? 3
- additional sign on examination? 1 (ie as well as visualising the warts)
soft CAULIFLOWER-LIKE growths of varying size.
(Less commonly, they are flat, plaque-like or pigmented)
colour: whitish to flesh-coloured to hyperpigmented to erythematous
norm <10 mm in diameter (but may coalesce into large plaques, esp if immunosuppressed or DM)
- local irritation or discomfort
- may get superficial dysparaunia
- may get dysurea if in urethra
- maybleed/be painful if catch on clothing!
can get INGUINAL LYMPHADENOPATHY!
need to examine using speculum for women!
nb can also get: Periungual warts are common warts around the nails that can be painful and disturb nail growth — nail biting is a risk factor
If find anogenital warts on examination, what other things should you test for? 4
other STIs!!
- chlamydia
- gonorrhoea
- syphillis
- HIV
anogenital warts:
- main management options? 2
- management in pregnancy? 1
1) PODOPHYLLOTOXIN SOLUTION
- not in preg or for anal warts
- nb also: Imiquimod or Sinecatechins cream instead
2) CRYOTHERAPY
- or excision or electrocautery
IN PREGNANCY:
- Warts may appear, recur or persist in pregnancy
- Treatment options limited
- Warts resolve after delivery – vaginal is typical
nb in about 30% of people, warts disappear spontaneously within 6 months without any treatment!
nb normn managed in sexual health clinic or by specialist GP
anogenital warts:
- advice about sex with new partners?
- lifestyle advice to reduce recurrence?
wear condoms!! (reduces risk, risk not zero!)
stop smoking (smoking increases risk of recurrence!)
WARTS + VERRUCAE (ie not anogenital)
- management options? 2
- who should refer to derm? 2
nb look the same as anogenital warts or slightly different
1) topical salicylic acid
2) cryotherapy
nb don’t have to treat - most go away within months-2 years
refer to derm:
- if on face
- if diagnostic uncertainty
BASAL CELL CARCINOMA
- 3 main risk factors?
- where on body tend to get?
- CLASSIC features of early? 2
- UV light exposure (usually arise on head, face & neck)
- Radiotherapy
- Fair skin (increased risk in Caucasians)
Arise on sun exposed areas (head, face, neck)
Early lesions are small, PEARLY & have edges w/ TELANGIECTASIA
BASAL CELL CARCINOMA:
- describe appearance of the 4 different types?
SUPERFICIAL
- Flat, well demarcated lesion +/- bleeding/weeping
- Typically >20mm on presentation
- Central clearing w/ thread like border
- Multiple erythematous lesions w/ equal distribution on face/arms/trunk
NODULAR:
- Solitary, shiny, red nodule (usually on face)
- Cystic & pearly central appearance w/ large telangiectasia
MORPHOEIC
- Thickened Yellowish plaque with irregular borders
- Usually on mid-facial site
Present late, and are quite aggressive
PIGMENTED
- Brown, black, or blueish lesions
- Present on people w/ darker skin
- May resemble malignant melanoma
nb don’t think I need to know this much depth!! - just know classical appearance!
BASAL CELL CARCINOMA:
- as well as visualising the lesion, what else should you always examine? 1
- how confirm diagnosis? 1
- additional imaging if suspect local invasion? 1
always examine nearby LYMPH NODES
refer for EXCISIONAL BIOPSY
if suspect local invasion (eg of nerves/glands) or any bone involvement suspectd = CONSIDER CT or MRI
BASAL CELL CARCINOMA:
- who to refer more urgently? 4 (/higher risk of more severe disease)
higer risk
= any immunocompromise
= under 24years old
= tumour >1cm diameter
= tumour adjacent to orifices (incl eye!)
nb refer all! - these are just the ones at highest risk and should definitely be seen in 2 weeks!
BASAL CELL CARCINOMA:
- surgical options? 2
- non-surgical options? 3
- lifestyle advice? 1
SURGERY
- wide local excision (BEST!)
- curettage (not if large or face)
NON-SURGICAL
- imiquimod cream (if small + superficial)
- phototherapy (if superficial, have good cosmetic result!))
- radiotherapy (norm for recurrence/incomplete resection)
nb prognosis is good (<0.5% metastasise, risk greater if >3cm in diameter)
do have increased risk of another one, SCC, melanoma - so advice re sun protection etc
nb would only do radiotherapy once on each site (as acts as it’s own risk factor)
differential diagnosis for BCC:
- nodular BCC? 1
- superficial BCC? 4
- Morphoeic BCC? 2
- pigmented BCC? 1
NODULAR
= molluscum contagiosum
SUPERFICIAL = SCC = discoid eczema = Bowen's disease = Psoriasis
MORPHOEIC
= scar tissue
= scleroderma
PIGMENTED
= malignant melanoma
nb Discoid eczema
= scattered, well-defined, coin-shaped and coin-sized plaques of eczema (aka nummular dermatitis)
nb Bowen’s disease (aka Intraepidermal SCC) = one or more irregular scaly plaques of up to several centimetres in diameter (often an orange-red colour but may be brown)
SQUAMOUS CELL CARCINOMA
- the two pre-malignant conditions that SCC normally devlop from?
- typical appearance? (incl features)
- what sign do you look for which may indicate metastases? 1
- bowen’s disease (squamous carcinoma in-situ)
- actinic (or solar) keratosis
SCC
= an irregular keratinous nodule or a firm erythematous plaque, and frequently ulcerates
LYMPHADENOPATHY may indicate metastases
RISK FACTORS for SQUAMOUS CELL CARCINOMA
- lifestyle? 1
- ethnicity? 1
- virus? 1
- other exposure? 2
- sun exposure
- white!
- HPV
- chemical exposure (arsenic, soot, tar)
- radiotherapy
nb having a pre-malignant condition (bowens / actinic keratosis) also increases your risk!
SQUAMOUS CELL CANCER
- investigation? 1
- most common management?
- other management options? (2 for SCC, 2 for pre-malig)
- lifestyle advice? 1
biopsy (norm just do at the time of excision!)
EXCISION = most common mx
- currettage (only if <1cm)
- radiotherapy (for inoperable or recurrent SCCs)
- TOP imiquimod cream (for actinic keratosis)
- photodynamic therapy (for actinic keratosis and bowens/in-situ)
REDUCE SUN EXPOSURE!
SQUAMOUS CELL CANCER
- rate of metastases?
- what features indicate a higher risk of metastases? 5
5%
increased risk:
- near orifices (esp lip/ear)
- > 2cm diameter
- depth >4mm
- poor differentiation
- recurrence
SQUAMOUS CELL CANCER
- main DDx? (2 pre-malig, 2 malig, 2 other)
- bowens (carcinoma in-situ)
- actinic (solar) keratosis
- BCC
- Malignant Melanoma (especially amelanotic)
- Keratoacanthoma
- Seborrheic keratosis (or warts)
nb keranthoma: skin lesion that erupts in sun-damaged skin (like a little volcano). It grows for a few months; then shrinks and self resolves (norm managed surgically as hard to differentiate clinically from SCC)
nb Seborrhoeic keratosis are harmless warty spots, appear more with age, some people have hundreds
MELANOMA
- biggest risk factor? 1
- ethnicity and gender most at risk?
- lifestyle risk? 1
Lots of Naevi!!
- Individual w/ > 100 common naevi or > 2 atypical naevi has a 5-20 fold increased risk of melanoma
- white
- female (although male have higher mortality)
- sun exposure
MELANOMA
- five features of moles which make them more likely to be melanomas? 5 (incl acronym)
- what is the glasgow 7-point checklist? (3 major features, 4 minor features)
A Asymmetry B Border irregularity C Colour variation (>2 colours) D Diameter over 6 mm E Evolving (enlarging, changing)
GLASGOW 7-POINT CHECKLIST
Major features
- Change in size
- Irregular shape
- Irregular colour
Minor features
- Diameter >7 mm
- Inflammation
- Oozing
- Change in sensation
MELANOMA
- commonest type?
- other types? 4
SUPERFICIAL MELANOMA (70%)
- Large flat, irregular pigmented lesion
- Grows laterally before vertical invasion develops
LENTIGO MALIGNA
- Patch of lentigo maligna develops a papule or nodule
NODULAR MELANOMA
- most aggressive
- Rapidly growing pigmented nodule – bleeds or ulcerates
- Very rarely amelanotic (non-pigmented)
- Metastasise early – poor prognosis
ACRAL LENTIGINOUS MELANOMA
- Pigmented lesions on palm, sole or under nail (late)
SUBUNGAL
- nailbed
nb all of these can be amelanotic
MELANOMA
- as well as examining lesion, what else should you examine for? 1
- three investigations needed for staging? 3 (nb may not need last if low stage)
examine for LYMPHADENOPATHY (means likely stage 3 or 4)
1) biopsy and histopathology
2) sentinel lymph node biopsy (if microscopic disease detected = stage 3 or 4)
3) CT staging (if stage 2c or above)
MELANOMA
- on histology, what is measured to help identify stage? 2
- what are the 5 stages?
- BRESLOW thickness (to nearest 0.1mm)
- if ulceration is present or not (poorer prognosis if is)
(nb other things on hisotlogy report too!)
STAGES 0 = in-situ 1 = <2mm thick 2 = >2mm thick (or >1mm +ulceration) 3 = local lymph node spread 4 = distant mets
nb have stage 1abc, 2abc etc too but don’t bother learning!
Genetic mutation common in melanoma?
BRAFV600
in 50% of melanomas!
do genetic testing to see if have
MELANOMA
- management of stages 0, 1 + 2?
- management of stage 3? 2
(see other flashcard for management of stage 4)
EXCISION
0 = 0.5mm margin
1 = 1cm margin
2 = 2cm margin
stage 3
= excision PLUS lymphadenectomy!! (+/- treamtnet for stage 4 - do a CT scan!
NEED follow up regularly for up to 5 years for all stages (except 0)
MELANOMA
- broad management options for stage 4? 2
nb don’t bother learning all of these but just be aware!
basically TARGETED and/or IMMUNOTHERAPY
incl targeted at BRAF gene!
Immunotherapy: interleukin-2, interferon alfa 2b
BRAF inhibitors: dabrafenib and vemurafenib
MEK inhibitors: trametinib
Combination BRAF and MEK inhibitors: dabrafenib
C-KIT inhibitors: imatinib, nilotinib
CTLA-4 antagonist: ipilimumab
PD-1 blocking antibodies: nivolumab, pembrolizumab
LEG ULCERS
- main 3 types?
- venous
- arterial
- neuropathic/diabetic
RISK FACTORS for LEG ULCERS:
- venous? (3 conditions, 3 others)
- arterial? (6 conditions, 2 lifestyle/others)
- neuropathic? (1 condition, 2 lifestyle)
VENOUS = varicose veins = previous DVT = HTN - Obesity - increasing age - immobility
ARTERIAL = IHD = PVD = HTN = Diabetes = CKD = RA - smoking - obesity
NEUROPATHIC
= diabetes
- poor foot care / badly fitting shoes
- smoking
LEG ULCERS
for each of:
- venous
- arterial
- neuropathic
describe:
1) common locations
2) appearance?
3) painful or painless?
4) associated dermatological signs or symptoms? (5 for venous, 3 arterial, 2 neuropahtic)
VENOUS
1) norm medial side of ankle
2) typically shallow with irregular sloping edges (typically wet w heavy exudate)
3) relatively painless (unless infected)
4)
- aching, swollen legs that feel more comfortable when elevated
- varicose veins
- mottled brown/black staining and/or dry, itchy and reddened skin (venous eczema)
- lipodermatosclerosis (hardened lower leg)
- swelling +/- lymphoededma
ARTERIAL
1) feet, heels or toes
2) deep with ‘punched out’ edge (typically dry and scabbed)
3) Frequently painful (esp at night in bed or whenlegs are at rest /elevated, relieved by standing)
4)
- cold, white or bluish feet
- difficulty palpating pulses
- may be intermmitenet claudication on walking
NEUROPATHIC ULCER
1) heels, tips of toes, between toes or any pressure points
2) similar to arterial but may be surrounded by thickened skin
3) not normally painful (unless infected)
4)
- poor foot care
- sensory loss on foot
What bedisde test is normally abnormal in ARTERIAL ulcers? (or people at risk of them)
Ankle Brachial Pressure Index (ABPI)
The normal value of 0.92 to 1.3. If the ABPI is less than 0.9, there is likely to be arterial disease.
Levels of less than 0.5 indicate severe arterial disease.
MANAGEMENT of LEG ULCERS
- lifestyle advice for all? 1
- systemic optimisation for neuropathic ulcers? 1
- nursing care for ALL? 1
- additional management for venous ulcers? 1 (when should this NOT be used?)
STOP SMOKING (really slows healing!)
better control of BLOOD SUGARS (if diabetic)
wound dressing for ALL
- different types available!
VENOUS = COMPRESSION BANDAGE
- but ONLY if good arterial supply (do ABPI before applying!)
Further investigations/management for leg ulcers:
- who to refer arterial ulcers to?
- who to x-ray foot? 1 (2nd line imaging?)
refer arterial ulcers to VASCULAR
- do ABPI first!
consider foot x-ray and/or MRI if neuropathic ulcer that is deep! - as high chance of osteomyelitis (MRI best!! - changes take a while to see on x-ray!)
Main complication of all leg ulcers?
- main signs/symptoms of this occuring? 5
two other complications of neuriopathic ulcers? 2
INFECTION
- erythema
- new pain
- increased swelling
- yellow surface crust or green/yellow pus
- fever
^nb this is norm cellulitis - but can progress to osteomyleitis (esp for neuropathic!)
^norm use FLUCLOX but can swab wound (only if clinically suspect infection!) and adjust abx use!
NEUROPATHIC ULCERS
- charcots foot
- ambutation (can happen with other ulcers but rare)
nb don’t swab ulcers unless signs of infection!!!
SOLAR KERATOSIS
- aka?
- appearance?
- risk of developing SCC?
aka ACTINIC KERATOSIS
may be solitary but often multiple keratoses
appearance varies:
- flat or thickened papule or plaque
- White or yellow; scaly, warty or horny surface
- Skin coloured, red or pigmented
- Tender or asymptomatic
very common on sites repeatedly exposed to the sun
rare for a solitary actinic keratosis to evolve to SCC
- but risk of SCC occurring at some stage in someone with > 10 is about 10 to 15%
A tender, thickened, ulcerated or enlarging actinic keratosis is suspicious of SCC
nb lots of different management options with cytotoxic cream, cryotherapy, excision etc!
KELOID SCARS
- what are they / describe appearance?
- biggest risk factors? 2
firm, smooth, hard growth due to spontaneous scar formation
- Raised, Irregular shape,
- Rubbery texture
- Red initially → brown/pale with age
may be uncomfortable or itchy
extend well beyond the original wound
can arise soon after an injury, or develop months later
higher risk
- FHx
- darker skin
GANGLION
- what is it?
- describe appearance?
- commonest locations?
- does it transilluminate?
a CYST typically associated with a tendon sheath or joint capsule of the HAND
(nb different to ganlgion of nerve cell bodies in neurology!)
The origin of a ganglion cyst is degeneration of the mucoid connective tissue of a joint
- most often affect scapholunate joint of dorsal wrist
- young-middle aged adults
- F>M
- unilocular or multilocular firm swelling 2–4 cm in diameter that transilluminates
nb can be painful (lies adjacent to nerve)
nb these are self-limiting (typically disappear in a few months!)
KAPOSI’S SARCOMA
- main at risk group?
- other risk factors?
- pathophysiology?
HIV +ve patients (esp MSM)
any immunosuppression (incl post-transplant patients etc) - nb can also get in some older diabetics
Caused by herpes virus 8 (HHV8) which is often sexually transmitted but doesn’t cause lesions unless immunocompromised (or very unlucky!)
nb is not actually a sarcoma! - is a disease of the endothelial cells of blood vessels + lymphatic system (multicentric vascular hyperplasia)
KAPOSI’S SARCOMA
- appearance?
- where else can they occur from, aside from the skin/mucous membranes? how might this present?
- red to purplish macules, papules and nodules
- anywhere on the skin or mucous membranes lining the mouth, nose, and throat; lymph nodes; or other organs.
- Initially, lesions are small and painless, but they can ulcerate and become painful
Kaposi sarcoma lesions can also occur internally and cause symptoms such as:
- Discomfort with swallowing
- Bleeding
- Haematemesis
- Haematochezia
- Melaena
- Bowel obstruction
- Shortness of breath
- Swollen legs
nb management: treat underlying immunosppression (eg HAART or reducing/changing immunosuppresive medications) - can also do localised treatment (eg cryotherapy, radiotherapy or excision but lesions almost always reoccur if still immunosuppressed!) - can also give systemic chemo or immunotherapy
GROIN SWELLING:
- likely DDx if the lump increases in size when coughing (cough impulse)? 2
likely diagnosis if NO cough impulse AND:
- compressible? 1
- expansile? 1
- transilluminates? 1
- hard? 1
- soft? 1
additional DDx in IVDU? 1
COUGH IMPULSE
- inguinal hernia (above + medial to pubic tubercle)
- femoral hernia (below + lateral to pubic tubercle)
NO COUGH IMPULSE
- compressible = saphina varix
- expansile = femoral artery aneurysm
- transilluminates = hydrocele of cord
- hard = lymph node
- soft = lipoma
if IVDU = consider GROIN ABSCESS!
nb enlarged lymph node could be reactive (infection) or malignant (lymphoma or met)
nb with saphina varix there’s norm varicose veins on leg as well!
NECK LUMPS:
- DDx in most areas of the neck? 1
nb see other flashcards for DDx of specific areas
cervical chain lymph nodes!
learn where these are again!!!
DDx for LUMPS in ANTERIOR TRIANGLE of neck:
- inflammes during URTI (norm unnoticed until then)? 1
- pulsatile? 1
- systemic symptoms of thyroid disease? 1
- hoarseness (+ may inflate and deflate while talking/vasalva)? 1
nb also LYMPH nodes is always on the DDx, regardless of area of the neck!
BRACHIAL CYST
- unnoticed until inflammed during URTI (are painless)
CAROTID BODY TUMOURS
- pulsatile
THYROID NODULES
- check TFTs
- systemic hypo/hyperthyroid (norm latter) symptoms
LARYNGOCELE
- hoarseness (+ may inflate and deflate while talking/vasalva)
plus LYMPH NODES!!
- look for red flag symptoms!
DDx for LUMPS in MIDLINE of neck:
- moves with swallow AND tongue protrusion? 1
- moves with swallow ONLY? 1
- doesn’t move with either? 1
nb also LYMPH nodes is always on the DDx, regardless of area of the neck! - although maybe less so if midline….
THYROGLOSSAL CYST
- moves with swallow AND tongue protrusion
^nb this makes sense as ‘glossal’ is attached to the tongue!
THYROID ISTHMUS NODULE
- moves on swallow ONLY
^makes sense as thyroid cartillage (attached to thyroid) is what moves when swallow!)
DERMOID CYST
- doesn’t move with any actions!
^as only attached to skin!
DDx for LUMPS in POSTERIOR TRAINGLE of neck:
- transilluminates? 1
- a specific lymph node? 1
- hard lump? 1
nb also LYMPH nodes is always on the DDx, regardless of area of the neck!
CYSTIC HYGROMA
- transilluminates
- sac full of lymph fluid
VIRCHOWS NODE
- internal organ malignancy (norm stomach Ca)
CERVICAL RIBS
- hard lump
- may have sx of arm pain/parasthesia with activity (called thoracic outlet syndrome)
plus LYMPH NODES!!
- look for red flag symptoms!
nb cystic hygromas can be diagnosed antenatally if large, may complicate delivery
What is the first line investigation for the majority of neck lumps? 1
what else might you do if suspect:
- thyroid nodule? 2
- lymph node? 1
who should you consider referring to head + neck surgery? 4
ULTRASOUND!!! (for all except cervical rib!)
thyroid nodule
- TFTs
- final needle aspirate (FNA)
lymph node
- core biopsy
consider referral to head + neck surgeons
- cystic hygroma
- laryngocele
- thyroglossal cyst
- dermoid cyst
RED FLAGS for a NECK LUMP:
- about the lump? 2
- associated local symptoms? 7
- associated systemic symptoms? 3
- Hard and fixed lump
- otalgia
- dysphagia
- stridor
- hoarse voice
- Epistaxis
- unilateral nasal congestion
- Cranial nerve palsies
- Unexplained weight loss
- night sweats
- fever or rigors
SQUINT
- fancy name?
meaning of:
- esotropia?
- exotropia?
- hypotropia?
- hypertropia?
strabismus
eso = looking medial (aka convergent)
exo = looking lateral (aka divergent)
hypo = looking down
hyper = looking up
SQUINT
- two main types?
(ie which account for 2 different groups of causes)
which age group tend to be affected by which?
which is more worrying for an underlying pathology?
CONCOMITANT (aka non-paralytic)
- due to imbalance in extraocular muscles (nerves and movements grossly normal)
- norm congenital
PARALYTIC
- norm acquired damage to cranial nerves (or extraocular muscles)
- almost always acquired
- more worrying
- get DIPOLOPIA
nb see paeds flashcard for info on non-paralytic (concomitant) squint
PARALYTIC SQUINT
- lesions of one or multiple of which 3 cranial nerves causes it?
- describe the squint thast is seen on paralysis of each of these 3 nerves? 3
(also say which cranial nerve controls which extra-ocular muscles)
CRANIAL NERVE THREE
= occulomotor
= all expect lateral rectus + superior oblique
- ‘down and out pupil’
- also get ptosis +/- DILATED pupil (called pupil sparing if pupil not dilated!)
CRANIAL NERVE FOUR = trochlear = superior oblique muscle (SO4) - get vertical diplopia - head tilt (as everything looks tilted to them)
CRANIAL NERVE SIX
= abducens
= lateral rectus muscle (LR6)
- horizontal diplopia (most pronounced when looking laterally towards muscle affected)
CRANIAL NERVE THREE
- pupil-sparing causes? 2
- pupil involving causes? 1 main, 2 other
PUPIL-SPARING
= ischaemic microvascular disease (HTN, DM etc)
= idopathic
PUPIL-INVOLVING
= berry aneurysm
- tumour
- trauma
nb you can get temporary 3rd nerve palsy as the result of a migraine!
(remember called pupil sparing if pupil not dilated!)
commonest causes CN lesions:
- cranial nerve FOUR? 3
- cranial nerve SIX? 1 serious, 3 common
CRANIAL NERVE 4
- trauma
- vasculopathy (norm HTN, DM)
- demyelinating disease (eg MS)
CRANIAL NERVE SIX = raised ICP (infection/inflamm or SOL) - vasculopathy (norm HTN, DM) - trauma - idiopathic
nb raised ICP is NOT most common cause (that’s vasculopathy or trauma - but is the most serious one!)
nb cranial nerve 6 can also go due to post-viral infections in kids, giant cell arteritis and MS
how long do these infections tend to las:
- acute otitis media?
- acute pharyngitis/tonsilitis?
- common cold?
- acute rhinosinusitis?
- acute cough/bronchitis?
acute otitis media: 4 days
acute sore throat/acute pharyngitis/acute tonsillitis: 1 week
common cold: 1.5
weeks
acute rhinosinusitis: 2.5 weeks
acute cough/acute bronchitis: 3 weeks
Phrayngitis:
- normal cause? 1
tonsillitis:
- causes of non-exudative? 4
- causes of exudative? 2
PHARYNGITIS
- typically viral
NON-EXUDATIVE TONSILITIS
- adenovirus
- enterovirus
- rhinovirus
- RSV
EXUDATIVE
- group A B-haemolytic strep
- EBV
nb this is why bacterial tonsilitis and EBV so often confused as they can both have exudate!
features of VIRAL tonsilitis:
- common symptoms? 6
- additional possible symptoms in infants/young children? 2
- finding on exam?
VIRAL TONSILITIS
- Pre-coryzal Sx (nasal discharge + block)
- Fever
- Cough (+ wheeze if asthmatic)
- Painful throat (2/7)
- Odynophagia
- Earache
YOUNG KIDS / INFANTS:
- Poor feeding (infant – noses blocked → obstructs breathing)
- Febrile convulsions
O/E:
- Enlarged + inflamed tonsils + uvula
nb can also get an acute exacerbation of asthma
What criteria used to assess likelihood of bacterial infection?
describe the FOUR parameters AND how many needed in order to give Abx?
nb NEED to know this!
what should you do to confirm a bacterial cause? 1
CENTOR
1) Fever >38deg
2) tonsillar exudate
3) cough ABSENT
4) cervial lymph node tenderness / swelling
must have at least THREE to give ABx! (still only 30-50% of these are bacterial)
should ALWAYS do a throat swab before givibng Abx! (this done in practice?)
nb if pt deemed at risk of developing complications: PRESCRIBE IMMEDIATELY
- systemically very unwell
- signs of complication (eg quinsy, intracranial complications)
- pre-existing co-morbidities (significant lung, heart, liver, immunosuppression, CF, premature infants)
MANAGEMENT OF TONSILITIS
- advice? 2
- symptomatic for all? 1
- which Abx do you prescribe if bacterial? 1
- which is 2nd line Abx if pen-allergic? 1
- which Abx do you NOT prescribe? 1
- when can you consider doing tonsilectomy? 1
- fluids
- rest
- analgesia (paracetamol + nsaids) for ALL
IF BACTERIAL
1st) PEN V (phenoxymethylpenicillin)
2nd) erythromycin (if pen-allergic)
NEVER: amoxicillin!!! (causes rash if EBV)
TONSILLECTOMY IF:
7 episodes in the past year, 5 episodes per year in the past 2 years or 3 episodes per year in the past 3 years,
and all infections should be culture confirmed group A strep
COMPLICATIONS of STREP PHARYNGITIS
- suppurative (pus-forming)? (2 common, 2 rare)
- non-suppurative?
describe how long after the strep throat you get each
SUPPURATIVE = peri-tonsiluar abscess (quinsy) = otitis media - meningitis - brain abscess
NON-SUPPURATIVE
SCARLET FEVER
- rash appears 1-2 days after sore throat starts)
ACUTE RHEUMATIC FEVER - several weeks after sore throat
POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
- 1-2 weeks post strep throat
nb giving Abx for strep throat doesn’t decrease the incidence of glomerulonephritis - but it does decrease incidence of all the others!
SCARLET FEVER
- 3 main symptoms?
- what may be confused for? 1
- sandpaper papular rash
- strawberry tongue
- sore throat
often confused with kawasaki! - look for fever LONGER THAN 5 days, conjunctivia involvement and hand involvement ?and some other stuff!
ACUTE RHEUMATIC FEVER:
- how long after sore thrat?
- main groups of symptoms? 6
presents SEVERAL WEEKS following the initial symptoms
- arthritis
- cardiac inflammation
- CNS involvement
- subcutaneous nodules
- fever
- rash
nb Rheumatic fever historically was a common cause of valvular heart disease (norm MITRAL regur or stenosis), however
incidence has significantly reduced with the introduction of abx therapy
POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
- how long after sore throat?
- appearance of urine? 1
- other symptoms? 3
presents 1-2 weeks following onset of
pharyngitis
- ‘cola-coloured urine’ (blood + protein - nephritic syndrome!)
- periorbital edema
- malaise
- decreased appetite
PERI-TONSILAR ABSCESS:
- features? (6 symp, 2 signs) (ie which differentiate from tonsilitis)
- management? 3
- throbbing unilateral throat pain (severe!)
- trismus (difficulty opening mouth
- dysphagia
- stridor
- coarse voice
- fever
- CONTRALATERAL deviation of uvula
- decreased neck mobility
^nb they may have a vague and non-specific Hx!
Mx
- urgent ENT review
- surgical drainage under LA
- antibiotics! (broad)
nb can do lateral neck x-ray to visualise
ACUTE EPIGLOTTITIS:
- commonest cause? 1
- age group at highest risk?
- who is most high riusk? 1
- symptoms + signs?
haemophilus influenza
- 1-6 years
high risk = unvaccinated children! (eg traveller community)
is very fast onset!!
- difficulty breahting (-> resp distress + increased HR)
- inspiratory AND expiratory soft stridor
- painful throat (can’t speak or swallow!)
- drooling saliva
- HIGH temp
- very tioxic looking!
Child sitting immobile, upright with mouth open (trying to optimise airway)
nb normally DON’T have a cough (one way to differentiate from croup!)
nb george washington died of this and/or the blood letting the drs did to attempt to treat it…
ACUTE EPIGLOTTITIS:
- what mustn’t you do?
- main investigation? 1 (when to do?)
- possible investigation?
- management?
don’t examnine thir mouth unless prepared to intubate!
- also don’t agitate the child!
blood cultures only AFTER safely stabilised airway!!
can do lateral x-ray (get thumb print) - aslthough often don’t do this or do Ppost-management!
ACUTE EPIGLOTTITIS:
- 1st thing to do? (if this is unsuccessful?)
- 2nd stage of management? (which med)
- what give prophylactically to household?
1) INTUBATE (immediately) w/ general anaesthetic – often unsuccessful
- TRACHEOSTOMY (if intubation fails) – life saving!
Often managed in ICU
2) Take Blood cultures + give IV Abx AFTER airway stabilised
- IV CEFUROXIME or CEFOTAXIME (until 3-5 d post tracheal tube removal)
give RIFAMPICIN prophylactically to all household members!
DDx for ACUTE EPIGLOTTITIS? 5
mainly in kids
- foreign body aspiration
- tonsilar abscess (quinsy)
- croup
- anaphylaxis
- laryngomalacia
Possible complications of epiglottitis? 5
- resp arrest -> death
- abscess
- sepsis
- meningitis
- pneumothorax
Main 4 symptoms / features which may point towards head + neck cancers? 4
- neck lump
- hoarseness
- persistent sore throat
- persistent mouth ulcer
nb dysphagia is more commonly oesophageal Ca
ORAL CANCER:
- who to send for a 2WW referral? 2
- who to sent for urgent referral (but not as fast as 2WW)? 2
ie what features are suggestive of Ca
2WW
= unexplained ULCERATION in the oral cavity lasting for more than THREE WEEKS
OR
= a persistent and unexplained lump in the neck
URGENT (but not 2ww)
- a lump on the lip or in the oral cavity
OR
- a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia
nb there is no lower age limit!! (oral cancers relatively common in younger ages!)
LARYNGEAL CANCER
- who to send for a 2WW referral? 2
ie what features are suggestive of Ca
people aged 45 and over
AND
- persistent unexplained hoarseness
OR - an unexplained lump in the neck
TRIGEMINAL NEURALGIA:
- most common cause?
- cranial nerve affected?
- describe attacks? (incl location, sensation, triggers and how long for)
norm idiopathic (can be from compression: cholesteatoma or acoustic neroma)
CN 5 = trigeminal
U/L shock-like pain paroxysms across CN5 distribution
- Abrupt in onset and termination
- Limited to one or more division of trigeminal
Provoked by: light touch, washing, shaving, smoking, talking, brushing
nb Nasolabial fold may act as trigger area
a/w numbness and tingling
nb 5% of peiople have bilateral symptoms
TRIGEMINAL NEURALGIA
- 1st line management? 1
- red flag symptoms/signs/features that suggest a serious underlying cause?
carbamazepine = 1st line
RED FLAGS
- sensory changes
- deafness or other ear problems
- PMHx of skin or oral lesions that could spread perineurally
- pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
- optic neuritis
- FHx of MS
- age of onset BELOW 40 years!
^refer to neurology is any of these features!
Causes of hoarse voice:
- lifestyle? 2
- malignancy? 2
- other illnesses? 3
what investigation should be considered and why? 1
- voice overuse
- smoking
- laryngeal cancer
- lung cancer
- viral illness
- hypothyroidism
- gastro-oesophageal reflux
consider doing CXR (to exclude apical lung lesions!)
GLOBUS
- what is it?
- when do patients notice sensastion the most?
- what needs to be ruled out?
Globus sensation is the feeling of having a lump in the throat when in fact there is nothing there
notice most when swallowing own saliva (can actually be improved when swallowing food)
need to make sure that this is not an organic cause of dysphagia!!
nb can be managed with reassurance, SALT pysio, CBT and managing reflux + postnasal drip which make worse