Uveitis

Background

  • NB Uveitis can refer to inflammation of the iris (iritis), ciliary body (cyclitis) and/or choroid (chorioretinitis)
    • Anterior uveitis is inflammation of the anterior segment i.e. iritis and iridocyclitis (anterior chamber inflammation)
    • Intermediate uveitis is inflammation of the ciliary body, pars plana and anterior vitreous
    • Posterior uveitis is inflammation of the choroid or retina
    • Panuveitis can also occur
    • All can be acute (< 3 months), recurrent or chronic
  • Potentially blinding; accounts for 10% of blindness in the developed world; 17-52/100,000/year

Aetiology

  • Systemic autoimmune conditions e.g. seronegative spondyloarthropathies (ankylosing spondylitis; Reiter’s/reactive arthritis; inflammatory bowel disease); Behcet’s; Sarcoidosis; Psoriasis; Multiple sclerosis
    • Associated with HLA-B27
  • Infection e.g. HSV, VZV, CMV, toxoplasmosis (also syphilis and tuberculosis)
  • Trauma

Presentation

  • Unilateral (usually)
  • Pain is the main symptom
    • In AU, this is often accompanied by redness; in PU redness may be absent
      • Redness is often strongest at the iris border (circumcorneal injection)
  • Dimished or blurred vision
  • Watering of the eye
  • Photophobia
  • Flashes or floaters may be seen in posterior uveitis
  • In chronic cases, there may be an unreactive and/or irregularly shaped pupil due to synechiae (adhesions)
  • On examination with a slit-lamp, deposits of white blood cells are often seen in the anterior chamber and are a diagnostic feature
    • Often graded (from 0 to +4- >50 cells)
    • aqueous may be cloudy (flare)- also graded from 0 to +4 (fibrin deposition)
  • Where possible a full examination of inside the eye (slit lamp or fundoscopy) should be attempted to look for evidence of intermediate (cells in vitreous) or posterior (deposits in the retina)

Investigations

  • Often clinical diagnosis but investigation of an underlying cause may be useful
  • Imaging (OCT or fluorescein angiography) may be helpful too.

Management

  • The mainstay of management is eyedrops
    • Corticosteroid drops
    • Cycloplegic-mydriatic (dilating) drops e.g. cyclopentolate or atropine)
      • paralysis the ciliary body, relieving pain and preventing adhesions between the iris and lens
  • If there is suspicion of infection, topical antibiotics (chloramphenicol) can also be given
  • If an underlying cause e.g. systemic disease, is identified, manage this appropriately to prevent recurrence
  • If patients do recur, systemic steroids may be a possibility.
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Hordeolum (stye) and Chalazion (meibomian cyst)

Hordeolum/Stye

  • A small abscess collection in the Meibomian glands (internal) or eyelash follicle/associated gland (external); usually caused by staphylococcus
  • Causing pain, redness, swelling within the eye lid
  • Often managed with reassurance +/- hot compression; topical antibiotics are not recommended and incision and drainage are rarely required (most resolve within a couple of days)
    • Eyelash epilation can be done for troublesome external styes

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Chalazion/Meibomian cyst

  • Chronic lipogranulomatous inflammation of the meibomian gland usually caused by blockage
  • Painless, nodular lesion; nontender, firm, within the eyelid (NB can appear identical to stye)
    • Can rarely become large enough to press on the globe (may impair vision)
  • Management is with hot compression (antibiotics not advised)

The Protection of the Eye

Eyelid

  • Skin
    • Thinner and more elastic/mobile than elsewhere in the body
    • Little or no subcutaneous fat (good source of skin graft)
    • Extremely good blood supply (heals quickly)
  • Muscles
    • Orbicularis oculi- Eyelid closure (CNVII)
    • Levator Palpebrae- elevates eyelid (CNIII)
    • Muller’s muscle- helps to retract the upper lid (cervical sympathetic innervation)
  • Tarsal plates
    • Composed of dense fibrous tissue, keeping the eyelid rigid/firm
    • Contains meibomian glands, which open at the lid margin and makes oily secretion that forms part of the tear film

Conjunctiva

  • Thin mucous membrane which lines the inner surface of the eye lid and outer surface of the eyeball, protecting the eye ball/cornea
    • During blinking, it lubricates the cornea with tears
    • Protects other exposed parts of the eye from infection (contains lymphocytes and macrophages)
    • Mucin from goblet cells has wetting effect of tear film
  • 3 parts
    • Tarsal- Inner eyelid area- firmly attached to tarsal plate
    • Bulbar- Lining the eyeball- loosely attached to underlying sclera
    • Fornix- part where these meet
  • NB the conjunctival epithelium is continuous with the corneal epithelium at the limbus (margin of the cornea)

Lacrimal Apparatus

  • Consists of lacrimal gland, punctum, canaliculi, nasolacrimal sac and duct

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  • The tear forms a thin film of fluid on the surface of conjunctiva/cornea, vital for their health and the transparency of the cornea
  • 3 parts of the tear film
    • Outer (lipid) layer- oily secretion from Meibomian and Zeis gland
    • Middle (aqueous) layer- Water from lacrimal gland and accessory lacrimal glands of Krause and Wolfring
    • Inner (mucinous) layer- Mucus from goblet cells of conjunctiva
  • Provides a moist environment for surface epithelial cells; washes away debris, transports metabolic products (oxygen, CO2) to and from surface cells, antimicrobial, and provides a smooth refracting surface over the cornea

Orbit

  • Made up of 7 skull bones:
    • NB the maxillary bone is the most likely to fracture in a blowout fracture
    • Roof: Frontal and sphenoid
    • Floor: Zygomatic, maxillary and palatine
    • Medial: Ethmoid, frontal, lacrimal and sphenoid
    • Lateral (strongest): zygomatic and sphenoid
  • At the orbital apex, there is the superior orbital fissure and optic canal.
    • Through the superior fissure: Superior and inferior divisions of CNIII, CNIV, Lacrimal, frontal and nasocilliary branches of CNV1, CN VI, superior branche of the ophthalmic vein, sympathetic fibres and orbital branch of the middle meningeal artery.
    • Through the Optic foramen travels the ophthalmic artery, central retinal vein and optic nerve (CN II).

In the base of the orbit is the inferior fissure

  • the inferior branch of the ophtalmic vein, infraorbital artery and nerve, as well as parasympathetic nerves to the lacrimal glands enter the orbit through this.

Mental Health Act – Scotland

Background

  • The Mental Health (Scotland) Act 2003 is a legal framework that governs the rules by which healthcare professionals may detain and treat patients who have a mental health disorder against their will
    • Remember that this is an imposition of somebodies rights, and care must be taken before deciding to detain an individual.

There are strict conditions in the Act about when these powers might be used.  These are:

  • That the person has a mental disorder.
  • Medical treatment is available which could stop their condition getting worse, or help treat some of their symptoms.
  • If that medical treatment was not provided, there would be a significant risk to the person or to others.
  • Because of the person’s mental disorder, his/her ability to make decisions about medical treatment is significantly impaired.
  • That the use of compulsory powers is necessary.
  • There are 3 main ways in which a doctor can use the MHA

Emergency Detention (sec 36)

  • Terms
    • Allows the patient to be taken to hospital and kept there for 72 hours
    • Should have the consent of the mental health officer where possible (although not required)
    • Allows medical treatment to be given if urgently necessary (in reality it should really be used for assessment- non-urgent treatment is not given)
    • Carries no right of appeal
      • NB A short term certificate should always be considered before and preferred to an emergency one
  • Criteria
    • it is likely that the patient has a mental disorder
    • it is likely that the patient has significantly impaired decision-making ability with respect to medical treatment for mental disorder
    • the doctor must be satisfied that significant risk to the patient or others exists, which would be ameliorated by detention under an emergency certificate
    • the doctor must be satisfied that the need for the certificate is urgent and that detention under a short-term detention certificatewould involve undesirable delay.

Short Term (sec 44)

  • Lasts 28 days; patients must be transferred within 3 days
  • Requires consent from MHO and, where possible, the named person for the individual
  • Can be appealed; revoked and extended (although a CTO should be considered prior to extension, which would supercede the Short term order)
  • Criteria
    • the patient is likely to have a mental disorder
    • the patient is likely to have significantly impaired decision-making ability with respect to medical treatment for mental disorder, as a result of his or her mental disorder
    • it is likely that detention in hospital is necessary to determine what medical treatment is required or to provide that treatment
    • it is likely that significant risk exists to the health, safety and welfare of the patient or to the safety of others if the patient is not detained
    • it is likely that granting of a short-term detention certificate is necessary, for example because  a patient is refusing to accept treatment on a voluntary basis.

Compulsory Treatment Order (part 7)

  • Can be hospital or community based and is used to provide treatment
  • Lasts 6 months; requires MHO consent; can also be appealed and suspended etc
  • Criteria
    • the patient must have a mental disorder
    • medical treatment would be likely to prevent the mental disorder worsening, or alleviate its effects
    • significant risk to health, safety and the welfare of the patient, or to the safety of others, exists if medical treatment is not provided
    • the patient’s ability to make decisions about his or her treatment is significantly impaired by mental disorder
    • the order is necessary

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Depression

Background

  • Characterised by persistent low mood and/or loss of pleasure in most activities and a range of associated features.
  • Extremely common: about 1 in 20 adults experience an episode of depression every year (majority mild and reactive)

Risk Factors

  • Complex interaction of:
    • Biological factors e.g. family history; head injury; physical illness
    • Psychosocial factors e.g. abuse, unemployment, lack of social relationships, poverty
    • Personality
  • High risk factors include
    • History of depression, suicide or abuse
    • Significant physical illness
    • Other mental health condition (including learning disability)
    • Family history
    • Frequent GP/A&E visits

Assessment of a patient who is at risk or presents with low mood

  • To screen ask about whether the patient has one of the core symptoms of depression
    • Have you been feeling down, depressed or hopeless recently (low mood)?
    • Do you have little pleasure or interest in doing things?
    • (Have you felt like you have no energy recently? While this is a core feature according to ICD, it is less specific for depression than the others.  NICE no longer consider it a core feature but as a minor feature)
  • Other symptoms of depression include
    • Worthlessness/excessive or inappropriate guilt
    • Suicidal ideation; recurrent thoughts of death
    • Diminished concentration/indecisiveness
    • Psychomotor agitation or retardation
    • Poor sleep pattern (insomnia/hypersomnia)
    • Loss or gain of appetite +/- weight change
    • (Reduced self-confidence)
    • (Bleak and pessimistic views of the future)
  • Ask about other psychiatric features, commonly anxiety
    • IMPORTANT to ask about mania/hypomania (e.g. feeling abnormally happy/high, irrational behaviour, expenditure etc) to exclude bipolar
    • Also eating disorders
    • Alcohol/substance misuse
    • Features of psychosis
  • ALWAYS ask about thoughts of suicide and self harm and go into detail where possible
  • Ask about possible triggers (e.g. relationship problems; employment issues; family problems etc), onset, timing, progression etc (i.e. take a full HPC)
  • It is important to take an extensive history in patients with possible depression, including HPC; Past psychiatric history; PMHx and drugs; FHx; Social Hx (drugs and alcohol are extremely important; as are housing, employment history, acitivities/hobies, relationships); Personal Hx (including developmental hx; childhood/growing up/school; family relationships; personal relationships; etc)
    • In reality, this may not be possible due to time constraints, so screening questionnaires e.g. PHQ-9 and HAD scale, may be useful
  • On MSE
    • Appearance and behaviour can vary from normal to unkempt, poor communication and eye contact, weepy, frustrated
    • Speech can be slowed and in extreme cases words may be few (word poverty)
    • Mood is often subjectively and objectively low and affect can be flat
    • There is rarely any disorder of thought or perception although the patient may obsess over ideas of suicide or self harm; guilt or worthlessness
    • Insight can be preserved or the patient may be so depressed as to be pessimistic about treatments
    • Cognition is rarely impaired significantly by depression but may be impaired by co-existent dementia

Diagnosis

  • NB Different associations have different criteria
    • NICE
      • At least 5 out of 9 NICE features (at least one out of two core symptoms)
      • Mild depression is where all symptoms are relatively mild, with little impairment of daily living
      • Moderate depression is defined as ‘symptoms and functional impairment between mild and severe depression’ (some marked symptoms)
      • Severe depression would be 7-9 symptoms, some of which are severe and impair daily living
    • ICD-10
      • At least 2 core symptoms and at least two minor symptoms (mild)
        • 3-4 minor symptoms (moderate)
        • All three core symptoms plus 4 or more minor symptoms with impairment of daily activity (severe)

Management

  • For mild/subthreshold depression- provide information and wait, giving follow-up in 2 weeks to see if they are better
    • Consider psychological therapy if symptoms persist
  • For moderate/severe depression
    • offer pharmacological therapy and high intensity psychotherapy
  • Psychological
    • Low intensity for subthreshold/mild depression
      • e.g. individual guided self-help or computerised therapy based on CBT principles (e.g. MoodJuice website and phoneline); group based activity programmes e.g. Dundonald centre/group based peer support
    • High intensity for moderate-severe depression
      • Group or individual CBT; interpersonal therapy; behavioural activation; couples therapy
  • Pharmacological
    • NB Consider toxicity and suicide risk; explain symptoms of anxiety may worsen initially and that most take some time to work
    • Usually, start with generic SSRI for most individuals (citalopram is often used first line, but fluoxetine, paroxetine and sertraline are alternatives)
      • Sertraline is often used in patients with significant physical illness due to its side effect profile
    • Antidepressant treatment should be trialled for minimum of 6 weeks (unless there are side effects after week 1)
      • If successful should be continued for 6 months before being reviewed and at least 2 years if the patient is at risk of relapse
      • If unsuccessful, trial another SSRI*
        • subsequently, other groups of antidepressants may be trialed
        • in general, stop the SSRI over 4 weeks before trialing a second (with fluoxetine, wait 4-7 days before starting alternative)
          • Venlafaxine may be cross-tapered

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Dysthymia/Persistent low mood

  • Defined as subthreshold features of depression lasting >2 years

Treatment refractory depression

  • There are multiple definitions of treatment refractory depression
    • Some quote a minimum trial of at least 2 antidepressants of different classes (i.e. if followed guidelines- at least 3)
    • Some say at least four
  • Chronic depression is defined as criteria for depression lasting >2 years
  • In any case, it is important to rule out pseudo-resistance i.e. patient not taking medications
  • Treatment options include pharmacological combination treatment (namely SSRI or venlafaxine with mirtazapine); augmentation therapy (usually with lithium, although the evidence for this is minimal); ECT which has been shown to be effective but does include side effects such as impaired cognition; Vagal nerve stimulation/DBS (rarely used due to highly specialist nature).

Psychotic depression

  • Usually, there is pervasive low mood and marked psychomotor disturbance with accompanying delusions and/or hallucinations.  Constipation may be a feature (patients can think that their bowels have been sewn up or have turned to dust.
  • Typically paranoid and mood-congruent, or hypochondriacal:
    • “People are out to get and kill me.”  “I’m being poisoned  to punish me for my sins.”  “I’ve got cancer because I deserve it.”
  • Cotard’s syndrome
    • More commonly found in the elderly, Cotard’s is characterised by classic nihilistic delusions:
      • I’m dead- the world around me isn’t real.
  • Treatment
    • For many of these patients, ECT will be an option for first line treatment (particularly effective).
    • Antipsychotic plus an antidepressent should be only used in combination with caution as both can enhance the side effect profile of the other. Careful monitoring is required.  Alternatively, drugs with dual-effects e.g. Amoxapine (TCA with D2 antagonism) or Olanzapine may be used, especially for episodic attacks.

Atypical Depression

  • Clinical features seem depressive but are atypical (funnily enough).
    • Mood is low but reactive (i.e. able to ‘enjoy’ activities- maybe not as much as usual)
  • PLUS 2 or more of
    • Hypersomnia (>10hrs/day at least 3 days/wk for 3 months)
    • Weight gain/ increase in appetite
    • Leaden paralysis (heavy arms and legs)- at least 1 hour/day, 3 days/week for 3 months
    • Over-sensitivity to perceived rejection- can result in significant social impairment/work problems.
  • It is often associated with anxiety and often responds well to treatment with phenelzine (MAOI- which are usually 3rd line in depression).

Somatiform Depression

  • This subtype of depression is often more described as ‘biological’ depression.  It can often be more severe that other forms but is also more amenable to pharmacological treatment.  ECT is also often effective in these patients
  • It can be diagnosed in the presence of 4 or more of the following clinical features:
    • Marked loss of enjoyment/pleasure/interest in activities that are normally enjoyable (anhydonia)
    • Lack of emotional reaction to events or activites that normally produce an emotional response (blunt affect)
    • Early morning waking (>2hours before normal)
    • Depression worse in morning
    • Objective evidence of marked psychomotor retardation or agitation (reports from others)
    • marked loss of appetite and weight loss (>5% of body mass in 1 month)
    • marked loss of libido

Goodpasture’s Syndrome

Co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage caused by a type II antigen-antibody reaction involving anti-glomerular basement membrane (anti-GBM) antibodies.

Background

  • Rare (incidence 1-2/1000000); accounts for 1-2% of all rapidly progressive glomerulonephritides
  • Between 60-80% have both renal and pulmonary involvement; whilst 20-40% just have renal and 10% just have pulmonary

Aetiology/Risk factors

  • Association with HLA-DR2/DR15
  • Exposure to organic solvents or hydrocarbons
  • Smoking
  • Infection (influenza A2)
  • Cocaine (inhalation)
  • Exposure to metal dusts

Pathophysiology

  • Autoimmune reaction (type II- cytotoxic) occurs in the glomerulus basement membrane and alveolar basement membrane, which causes glomerulonephritis (crescentic) and pulmonary haemorrhage

Presentation

  • Constitutional symptoms
    • Malaise, chills, fever, arthralgia, nausea/vomiting, weight loss
    • Can precede or be concurrent with renal/pulmonary symptoms
  • Haemoptysis, cough, dyspnoea, shortness of breath
    • Massive pulmonary haemorrhage may cause respiratory failure
    • Chest pain is uncommon
  • Haematuria; oedema; high blood pressure
  • Other signs include tachypnoea; inspiratory crackles (po haemorrhage); cyanosis; oedema; pallor

Investigations

  • Ideally, renal biopsy for antiGBM fluorescence or anti-GBM ELISA
    • Check other antibodies too e.g. ANCA, dsDNA (in case of SLE as cause)
  • Other lab tests
    • FBC (anaemia)
    • U&Es/renal function- be weary of AKI
    • ESR/PV (often normal in GP; but would be raised in vasculitis)
    • Clotting/coagulation study
    • Urinalysis
  • CXR
    • Patchy consolidation, often bilateral, symmetrical, perihilar and bibasal
      • Apices/costphrenic angles are often normal
      • CXR can be completely normal in ~20%
  • Occasionally, lung biopsy may be required

Management

  • IV steroids and usually cyclophosphamide alongside plasmapheresis until anti-GBM undetectable
    • Usually with human albumin solution
    • +/- fresh frozen plasma if there is severe haemorrhage
    • If there is severe AKI, dialysis is required (poor prognosis)
    • Corticosteroids are tapered down over 6-12 months
    • Cyclophosphamide is usually given for 3 months
  • In severe kidney failure, transplant may be an option

Complications

  • Pulmonary haemorrhage is a significant cause of mortality in these patients (5-year survival is >80%)
  • Some patients will require long-term dialysis (20-30%)

Whooping cough

Background

  • Also known as pertussis
  • Highly infectious disease caused by Bordatella pertussis
    • Produces pertussis toxin
    • Incubation usually around 7 days; spread via aerosol droplets; infectious for 3 weeks after initial symptoms
  • Fortunately infrequent (1 in 1000 per year during ‘peak year’ which recur every 3-5 years) in the UK due to vaccination (DTaP at 2, 3, 4 months)
    • More common in infants who have not yet received full vaccination (or unvaccinated)

Presentation

  • 3 phases of infection
    • catarrhal phase
      • dry, unproductive cough; may be preceded by prodromal symptoms typical of URTI (up to 7 days)
    • Paroxysmal phase
      • whooping (inspiratory gasp- may not be seen in adults), post-tussive (cough) vomiting is common in infants, generalised symptoms (can last a month or more)
      • between coughing fits, the patient is generally well
      • coughing fits are more common at night, can be triggered by cold/noise
        • in adults there may be associated autonomic features e.g. sweating, flushing; in children, it can cause cyanosis
    • Convalescent phase
      • Gradual improvement (can take 2+ months)
  • NB Pertussis is a notifiable disease

Investigations

  • Most cases are clinical diagnoses; but health protection may request laboratory confirmation via
    • nasopharygeal aspirate/swab
    • antipertussis toxin IgG
    • PCR positive

Management

  • Consider admission to those who are seriously unwell e.g. cyanotic, apnoea, trouble breathing
    • Low threshold in infants <6 months
    • Particularly in cases with complications e.g. pneumonia
  • Consider antibiotic treatment (macrolide- clarithromycin in <1 month; azithromycin + clarithromycin in older infants/children/adults; erythromycin in pregnancy) if symptoms started within 21 days
    • Important to treat in pregnancy to prevent transmission
  • Health protection can consider offering antibiotic prophylaxis to those at risk (priority group) contacts e.g. those with pregnant women or baby in household.  Also offer immunisation