no
no
no

Chagas disease = American trypanosomiasis

/ / / /
Chagas disease ( = American trypanosomiasis) is caused by infection with trypanosoma cruzi, which is carried by triatomine insects. It occurs predominantly in Latin America. 

Presentation: 
  • Acute disease 
    • Asymptomatic in 95% of cases
    • If symptomatic:
      • Fever 
      • muscle aches 
      • nausea/vomiting 
      • painless unilateral periorbital oedema (= Romana’s sign) 
      • hepatosplenomegaly
      • lymphadenopathy
  • Chronic disease 
    • Develops in 2/3rds of infected individuals 
    • Cardiac complications – 95% 
      • Cardiomyopathy 
      • Apical aneurysm 
    • Megaoesophagus/megacolon 

Diagnosis: 
  • Microscopy 
  • Haemoculture 
  • IgG immunological assays 

Treatment: Benznidazole or nifurtimox 


References:

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Sleeping sickness = African trypanosomiasis

/ / / / /
Sleeping sickness, AKA African trypanosomiasis, is a tropical illness spread by the tsetse fly. 

It is caused by 
  • trypanosoma brucei gambiense 
    • West and central Africa 
    • Slow progression, 1 year to reach 2nd stage disease
    • If untreated, death in 3 years 
  • trypanosoma brucei rhodesiense 
    • east and south Africa
    • fast progression, 3 weeks to reach 2nd stage disease 
    • If untreated, death in 6 to 12 months 

First stage - blood
  • Fever, headache, loss of appetite 
  • Lymphadenopathy, splenomegaly, hepatomegaly 
  • Possibly a chancre at site of bite in t.rhodesiense 
  • Treatment
    • t. gambiense – eflornithine 
    • t. rhodesiense – suramin 

Second stage - CNS
  • Sleeping during the day 
  • Headache 
  • Neuro-psychiatric signs and symptoms
  • Motor signs 
  • Treatment 
    • Melarsoprol for both 

Diagnosis is by microscopy of blood or CSF. 



Small print gem: In sleeping sickness, lympadenopathy in the posterior triangle of the neck is known as Winterbottom’s sign. 


References:

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Malignant melanoma

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Malignant melanoma is a skin cancer with potential for metastasis to multiple body organs. 

Melanomas are most common on trunk in men and on lower extremities in women. 

Types of melanoma, in order of frequency, are:
  • Superficial spreading melanoma – most common 
  • Nodular melanoma 
  • Letingo maligna melanoma
  • Acreal lentiginous melanoma – least common 

The British Association of Dermatology’s criteria for referring a mole to a dermatologist ?melanoma is:
  • Mole which is changing in shape, colour or size 
  • Any mole which has 3 or more colours or has lost its symmetry 
  • A mole which is itching or bleeding 
  • A new pigmented line in a nail
  • A lesion growing under a nail 

Factors which suggest a lesion could be a melanoma are: 
  • Asymmetry 
  • Border irregularity 
  • Colour variation 
  • Diameter greater than 6 mm 

Sun exposure and use of sunbeds increase risk of malignant melanoma. 
Pregnancy and use of OCP do not increase risk.

Other factors identified to increase risk include: 
  • Moderately increase risk 
    • Previous primary melanoma 
    • Large number of moles 
    • Organ transplant
    • 1 or 2 family members with melanoma
  • Greatly increase risk 
    • Giant congenital pigmented naevus 
    • 3 or more family members with melanoma or pancreatic cancer 

Prognosis is based on 
  • Breslow thickness = tumour thickness 
  • Clark level = histologic level of invasion 

Metastatic disease has a poor prognosis. Chemotherapy of choice for metastatic disease is dacarbazine. This has no effect on CNS mets. 


References:

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Churg Strauss syndrome

/ /
Churg Strauss is a rare, small-vessel vasculitis of unknown aetiology  

The triad for diagnosis is: 
  • Asthma 
  • Eosinophilia 
  • Vasculitis of 2 or more extrapulmonary organs 

The asthma is often late onset.

The vasculitis of Churg Strauss
  • Most commonly affects the lungs 
  • Causes mononeuritis multiplex in up to 75% of patients 
  • Affects the skin (causing vasculitic purpura, nodules or livedo reticularis) in around 60% 
  • Glomerulonephritis (focal and segmental) occurs in up to 47% of patients but renal failure is rare 

Associations of Churg Strauss include 
  • Nasal polyps 
  • Sinusitis 
  • Allergic rhinitis 
  • Abdominal pain 

ANCA is positive in around a third of patients, most commonly pANCA 

Treatment is with high-dose steroids. 


References:

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Henoch-Schonlein Purpura

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Henoch-Schonlein Purpura (HSP) is an IgA mediated small-vessel vasculitis. 

The classical features are:
  • Purpuric rash on extensor surfaces of legs and buttocks 
  • Abdominal pain 
  • Arthralgia 
  • Haematuria often with proteinuria

Other possible features include 
  • Renal involvement 
  • Abdominal complications 
    • Bloody stools 
    • Intussuception in children 
    • Bowel ischaemia
It often follows an upper respiratory tract infection 

HSP can affect all ages but is commest in children under 10. 
Males>females, 2:1 

Treatment:
Symptomatic 
? steroids for severe HSP nephritis 


References:

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Lymphoma

/ / / / / /
Lymphoma is cancer of lymphatic cells, typically presenting as a solid tumour.

Signs and symptoms include:
  • night sweats
  • fever
  • weight loss
  • fatigue
  • palpable node

Diagnosis is by lymph node biopsy.

Other investigations include:
  • CXR 
  • Staging CT 
  • Bloods – FBC, ESR, CRP, LDH, LFTs 

The classical division of lymphoma is into:
  • Hodgkins lymphoma
    • characteristic Reed-Sternberg cell
    • around 25% of lymphomas
    • males >females
  • Non-Hodgkin lymphomas

More detailed classification of lymphoma is fiendishly complex; the current system in use is the WHO classification, which divides lymphomas into B cell and T cell.  A classification which is arguably more useful for 'basic' doctors is the one below which divides lymphomas into 'low grade/indolent' and 'high grade/aggressive'

Indolent:
  • Hodgkin lymphoma - excellent prognosis, often cured
  • Non-Hodgkins 
    • Lymphoma of mucosa-assoicated lymphoid tissue (MALT)
    • Follicular lymphoma 

Aggressive: (all are non-Hodgkins)
  • Diffuse large B cell lymphoma (=30-60% of non-Hodgkins lymphomas) 
  • Mantle cell lymphoma
  • Primary effusion lymphoma 
  • Burkitt lymphoma 

Staging:
  • I: single lymph-node region or single extralymphatic site
  • II: two or more lymph node regions or sites but on same side of diaphragm
  • III: involvement of lymph nodes/regions on both sides of diaphragm
  • IV: disseminated
  • A or B: 
    • A: no B symptoms
    • B: fever, weight loss or night sweats


Increased risk of lymphoma with: 
  • Exposure to pesticides 
  • Immune deficiencies 
    • Common variably immune deficiency (lifetime risk 8%) 
    • Wiscott-Aldrich syndrome 
    • Severe combined immune deficiency 
  • Infections
    • HIV - Burkitt lymphoma, primary effusion lymphoma, DLBCL
    • EBV – Burkitt lymphoma 
    • Herpes virus 8 - primary effusion lymphoma 
    • Helicobacter pylori – MALT
    • Campylobacter jejuni – small bowel lymphoma 
  • Medications 
    • Metotrexate – DLBCL, Hodgkins 
    • Infliximab – T cell lymphoma 

Treatment: 
  • Hodgkins lymphoma:
    • ABVD chemotherapy (=adriamycine, bleomycin, vinvlastine and dacarbazine 
    • Radiotherapy
    • Exact treatment is based on a combination of the Ann Arbor staging and presence/absence of
      • 3 involved lymph node areas 
      • high ESR 
      • large mediastinal mass 
      • extranodal disease
  • High-grade Non-Hodgkins lymphoma 
    • CHOP chemotherapy (= cyclophosphamide, doxorubicin, vincristine, prednisone) 
    • rituxumab
  • Low-grade Non-Hodgkins lymphoma
    • multiple options ranging from 'watch and wait' to chlorambucil to CHOP and rituximad.
     

References:

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Haemophilia

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Haemophilia A and haemophilia B are both X linked recessive disorders of coagulation. 1/3 of cases have no family history. 

Haemophilia A 
  • Incidence 1 in 10 000 
  • Lack of factor VIII

Haemophilia B = Christmas disease 
  • Incidence 1 in 50 000 
  • Lack of factor IX 

Severity of the disease is classified according to the baseline level of clotting factor:
  • Severe <1% normal 
  • Moderate 1-4% normal
  • Mild 5 -50% normal 

Complications include: 
  • Haemarthrosis (70-80%) – commonest joint affected is the knee followed by elbow
  • Bleeds into muscle/soft tissue 
  • Haemophiliac arthropathy 
  • Intracranial haemorrhage 
  • Pseudotumours of bone

Management: 
  • Avoid use of NSAIDs/ASA 
  • Avoid IM injections 
  • Avoid contact sports 
  • Desmopressin
  • Tranexamic acid 
  • Recombinant factor VIII or IX
  • Vaccination against hepatitis A and B


Small print gem: female carriers may have menorrhagia 


References:

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Cyanide poisoning

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Cyanide is used in a variety of industries, including Perspex manufacture, vermin extermination and electroplating. 

The greatest current risk for accidental exposure outside of industry is in household fires, in which cyanide is generated by the combustion of nitrogen-containing compounds such as nylon. 

Cyanide is toxic as it inhibitis cytochrome oxidase 

Classical features of cyanide poisoning: 
  • Smell of bitter almonds (60% of people can smell this) 
  • Red skin

Other signs and symptoms: 
  • Headache 
  • Metallic taste 
  • Dizziness 
  • Hypotension
  • Arrhythmias 
  • Seizures 
  • Coma 

Treatment: 
  • 100% oxygen
  • ?amyl nitrite – may be available on site in factories etc where cyanide poisoning is a risk 
  • IV dicobalt edetate (in the UK; the newer treatment in use elsewhere is hydroxycobalamin, which has less side effects)


References:

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Behcet’s disease

/ /
Behcet’s disease is a systemic vasculitis of unknown aetiology.

It was classically described as a triad of: 
  • Uveitis 
  • Oral ulcers 
  • Genital ulcers 

The criteria for clinical diagnosis of Behcet’s disease has now extended to: 
  • Recurrent oral ulcers (at least 3 times in a year) 
  • With any 2 of:
    • Genital ulcers
    • Positive pathergy test – formation of a pustule in response to pin-prick
    • Eye involvement (such as anterior or posterior uveitis, retinal vasculitis)
    • Skin lesions (Erythema nodosum, foliculitis, other ulcerations)

Other features of Behcet’s disease can include 
  • Arthritis 
  • Gastrointestinal ulceration
  • Neurological involvement 
  • Thrombophebitis 
  • Aneurysms, especially aortic aneurysms 

Behcet’s disease is most common in patients of Mediterranean, Middle Eastern and Japanese origin. 
Males are more affected than females 
It is associated with HLA B51. 

Severe disease is managed with steroids and immunosupression. 


References:

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Retinal vein occlusion

/ / / / / /
Retinal vein occlusion is the second most common retinal vascular disorder and a cause of painless vision loss. 

It is divided into branch retinal vein occlusion (most common) and central retinal vein occlusion. Each of these subdivisions are further divided into ischaemic (worse prognosis, poorer vision) and non-ischaemic. It is worth noting non-ischaemic CRVO can transform into ischaemic in 30% of cases 

Presentation
BRVO – painless decrease in vision or visual field defect 
CRVO – usually sudden, painless unilateral visual loss 

Investigation
  • Fundoscopy
    • Retinal haemorrhages (blot and flame shaped) 
    • Increased tortuosity of retinal veins 
    • Cotton wool spots 
    • Papilloedema 
    • Macular oedema 
  • Relative afferent papillary defect 
  • ? Fluorescein angiography 

Risk factors for RVO 
  • Age 
  • Hypertension 
  • Diabetes 
  • Smoking 
  • Hyperlipideamia 
  • Open angle glaucoma 
  • Myeloproliferative disorders – 1% of those with RVO 
  • Systemic vasculitis e.g. Behcet’s disease, PAN 

Management 
  • Refer to ophthalmology:
    • Investigation and treatment of risk factors 
    • Laser photocoagulation 
    • Anti-VEGF agents (bevacizumab, ranbizumab, pegaptanib)
    • Dexamethasone intravitreal implant 

Complications 
  • Glaucoma 
  • Iris neovascularisation 

References:

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Pericardial effusion

/ /
Pericardial effusion is a collection of fluid around the heart in excess of the usual 15 to 50mls of pericardial fluid. 

It is often associated with pericarditis – 60% of cases of pericarditis are accompanied by a pericardial effusion. 

Causes include: 
  • Malignancy (especially lung, breast, leukaemia, lymphoma) 
  • Idiopathic 
  • Trauma 
  • Uraemia
  • Radiation
  • Postoperative 
  • Infection 
  • Connective tissue disease 
  • Hypothyroidism

Management 
  • Depends on aetiology 
  • Pericardiocentesis only if: 
    • Tamponade
    • Suspicion of purulent pericarditis 
    • Chronic large effusion

Complication: Cardiac tamponade


References:

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Pulsus paradoxus

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Pulsus paradoxus is an inspiratory fall in systolic BP greater than 10mmHg.

In a ‘normal’ person the systolic BP usually falls around 6mmHg in inspiration. The ‘paradox’ refers to the fact that although the radial pulse is absent, heart sounds can be auscultated.

The commonest cause of pulsus paradoxus is cardiac tamponade (sensitivity 98%, specificity 83%) 

Other causes of pulsus paradoxus include: 

Pulsus paradoxus can be measured by 
  • Cuff sphygmonanometry 
  • Arterial waveform analysis 
  • Pulse oximetry waveform analysis 


References 

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Cardiac tamponade

/ / / / / /
Cardiac tamponade occurs when fluid accumulates in the pericardium and exerts a pressure that exceeds intracardiac pressures, leading to impaired cardiac output. 

Normally the pericardial space contains 15-50mls of fluid. If fluid accumulates slowly it can accommodate up to 2l without causing tamponade; however, if it accumulates rapidly 150-200mls can result in tamponade. 

Possible causes of tamponade are any cause of a pericardial effusion. 

The classic clinical triad is Becks (present in 10 to 40% of cases): 
  • falling BP 
  • rising JVP 
  • muffled heart sounds

Other clinical signs and symptoms include:
  • Shortness of breath 
  • Chest pain 
  • Palpitations
  • Tachycardia
  • Pulsus paradoxus = increased fall in BP during inspiration >10mmHg - present in 98%
  • Raised JVP with decreased y descent 
  • Kussmaul’s sign = rising JVP on inspiration (more common in constrictive pericarditis than tamponade) 
  • Ewart’s sign = area of dullness and bronchial breathing below left scapular due to pericardial collection

Investigations 
  • ECG 
    • Low voltages complexes 
    • Electrical alternans (present in 10 to 20%) 
  • CXR
    • 'flask-like’ cardiac shadow if slow accumulation\
    • may be normal if rapid 
  • Echo 
    • RA+/-RV collapse during diastole 

Treatment: 
Pericardiocentesis or cardiothoracic surgery 


References:

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Pericarditis

/ /
Pericarditis is inflammation of the pericardium of the heart.

Presentation 
  • Pleuritic chest pain, improved on leaning forward and worse on lying supine, may radiate to trapezius
  • Prodromal illness

Aetiology: 
  • Viral infection 
    • Coxsackie, EBV, HIV, Influenza, CMV...
  • Bacterial infection 
  • Fungal infection
  • Acute MI – especially anterior MI 
    • Early = pericarditis epistenocardica = caused by direct exudation in a transmural infarct 
    • Delayed = Dressler’s syndrome – occurs one week to several months after MI 
  • Malignancy 
    • Most commonly lung, breast or leukaemia/lymphoma 
  • Renal failure 
  • Autoimmune 
  • Hypothyroidism 
  • Medications 
    • Dantrolene, doxorubicin, isoniazid, rifampicin, mesalamine, penicillin, phenytoin, hydralazine, amiodarone, streptokinase… 

Investigations
  • ECG 
    • Saddle-shaped ST elevation, reciprocal PR segment elevation and ST depression in aVR and occasionally V1, T wave inversions 
  • Auscultation may reveal a pericardial rub 
  • Echo 
  • CXR 
    • ?'water bottle’ heart shadow 
  • Bloods 
    • ESR, CRP, LDH, FBC, troponin

Treatment 
  • NSAIDs 
  • ?Colchicine
  • Corticosteroid for pericarditis caused by connective tissue disease and renal failure. 

Complications 
  • Pericardial effusion (60% of cases) 
  • Cardiac tamponade (5% of cases) 
  • Recurrent pericarditis 
  • Constrictive peridcarditis 


References:

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Osmotic demyelination syndrome

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Osmotic demyelination syndrome is a condition that can occur if hyponatraemia is corrected too rapidly. It may consist of central pontine myelinolysis, extrapontine myelinolysis or both. 

Clinical features: 
  • Confusion 
  • Dysarthria 
  • Dysphagia 
  • Quadriparesis 
  • Coma 
  • Rarely seizures 
  • If EPM – movement disorders 

Clinical features may become apparent a few days after the rapid correction of sodium 

Osmotic demyelination syndrome is rare if initial sodium >120meq/l; mainly occurs if initial sodium is 105meq/l or less

It is more common in presence of 
  • Alcoholism 
  • Malnutrition 
  • Liver disease
  • Prolonged diuretic use 
  • Hypokalaemia 
  • an organ transplant 
  • Extensive burns 

Can be detected by T2-weighted MRI scan but changes may take several weeks to become radiologically apparent 

Treatment of osmotic demyelination syndrome is difficult – best to try and prevent 

Possible management includes steroids, IV IG, thyrotrophin releasing hormone, minocycline, relowering of serum sodium or plasmapheresis


References:

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SIADH (= Syndrome of Inappropriate secretion of AntiDiuretic Hormone)

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SIADH (= Syndrome of Inappropriate secretion of AntiDiuretic Hormone) is a condition which results in hyponatraemia.

The Bartter and Schwartz criteria for SIADH is:
  • Decreased plasma osmolality (<275 mosm/kg)
  • Inappropriately concentrated urine (>100 mosm/kg) 
  • Euvolaemic 
  • Elevated urine Na (>20 mEq/L) 
  • Normal thyroid and adrenal function 
  • No diuretic use 

ADH itself is made in the supraoptic and paracentricular nuclei of the hypothalamus. It is then stored in the posterior pituitary.

ADH is usually released in response to:
  • raised plasma osmolality (detected by osmoreceptors in the hypothalamus)
  • decreased plasma volume (detected by baroreceptors in the carotids, aorta and left atrium) 
  • limbic system activation – pain, fear, nausea 

It increases synthesis and insertion of aquaporin-2 water channels in the luminal membrane of the collecting ducts, increasing water reabsorption in the kidney

As SIADH causes hyponatraemia, clinically you would expect:
  • Sodium <125mEq/l: weakness, headaches, nausea and vomiting 
  • Sodium <115mEq/l: altered consciousness, seizures, coma 

Causes of SIADH include
  • Drugs
    • Anticonvulsants - Carbamazepine, Sodium valproate
    • Antidepressants - SSRIs, MAOIs, TCAs
    • Haloperidol
    • Amiodarone
    • Ciprofloxacin
    • Chemo
    • Opiates
    • MDMA
  • Malignancy
    • Lung cancer, especially small cell carcinoma
    • Pancreatic cancer
    • lymphoma
    • Head and neck cancers
  • Pulmonary disease
  • CNS
    • Stroke
    • Infection - encephalitis, meningitis, abscess
    • Haemorrhage
    • trauma
    • MS
    • GBS
  • Porphyria

Treatment
  • Treat cause
  • Correct sodium
    • Fluid restriction
    • ? demeclocycline
    • ? hypertonic saline
    • ? furosemide
    • ? vasopressin receptor antagonists (vaptans)
    • ? urea

If acute (48 hrs or less) correction of sodium can be fast
If chronic, correction of sodium should be cautious (around 8meq/day) to avoid osmotic demyelination syndrome.


References:
Esposito, P. et al. The syndrome of inappropriate antidiuresis: pathophysiology, clinical management and new therapeutic options. Nephron Clin Pract. 2011; 119(1):c62-c73. 

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Gaucher's disease

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Gaucher's disease is the most common of the lysosomal storage disorders. It is carried on chromosome 1 and is inherited in an autosomal recessive pattern. 

Ashkenazi Jews are most affected. 

Features of Gaucher’s disease include: 
  • Splenomegaly 
  • Hepatomegaly 
  • Hepatic fibrosis 
  • Pathological fractures 
  • Pancytopenia 
  • Seizures 

Treatment 
  • Enzyme replacement therapy 
  • splenectomy 

References:

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Pick’s disease

/ / /
Pick’s disease is the eponym for frontotemporal dementia. 

Characteristics of frontotemporal dementia include: 
  • Insidious onset and gradual progression 
  • Decline in social skills and loss of inhibitions 
  • Emotional blunting 
  • Loss of insight
  • Loss of language skills 
  • Onset before age 65 

Whereas in other forms of dementia memory is impaired, in frontotemporal dementia memory remains intact. 

The histological feature of frontotemporal dementia is tau-positive neuronal cytoplasmic inclusions. 
 

References:

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Guillain-Barre Syndrome

/ / / / /
Guillain-Barre Syndrome describes a heterogeneous group of conditions characterised by distal, symmetrical paraesthesia followed by progressive limb weakness in both arms and legs and areflexia in the absence of any identifiable genetic, metabolic or toxic cause. 

Other features which support a diagnosis of Guillain-Barre syndrome include: 
  • Progression of symptoms over days, up to 4 weeks 
  • Mild sensory symptoms or signs
  • Cranial nerve involvement, especially bilateral weakness of facial muscles 
  • Autonomic dysfunction – hypo or hypertension, gastrointestinal dysmotility, arrhythmias 
  • Absent fever at onset 

It is often preceded by infection: 
  • Campylobacter jejuni (around 25%) 
  • CMV 
  • Mycoplasma pneumonia 
  • EBV 
  • HIV 
  • Varicella zoster 

Investigations:
  • CSF – elevated protein with normal cell count (note CSF is initially normal in 50%) Electrodiagnostic testing – features of demyelination (slow conduction velocities), sural sparing pattern

The 5 subtypes of GBS are: 
  • Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) 
    • Autoimmune disorder 
    • The ‘classic’ GBS and commonest form in western countries 
  • Acute motor axonal neuropathy (AMAN) 
    • Pure motor form 
    • High proportion of paediatric patients 
    • Commonest form in Japan and China 
  • Acute motor sensory axonal neuropathy (AMSAN) 
    • Minial inflammation and demyelination 
  • Miller Fisher syndrome 
    • Rare 
    • Rapidly evolving ataxia, areflexia, mild limb weakness, and ophthalmoplegia 
  • Acute panautonomic neuropathy 
    • Rarest of all 
    • Blurry vision and dry eyes
    • Often cardiovascular involvement 

Treatment
  • Regular lung function tests to check for need for ventilatory support
  • Ventilatory support 
  • Plasma exchange 
  • IVIG 
  • No evidence to support use of steroids 

Prognosis 
  • 80-90% become non-ambulatory during the disease 
  • 50% have prominent pain 
  • 30% require ventilatory support 

  • Mortality 5% 
  • Full recovery in 85% 
  • Relapse in 5% 

Factors suggesting poor outcome:
  • Rapid onset 
  • Age >60 
  • Axonal degeneration 
  • C. jejuni infection 


References:

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Acute interstitial nephritis

/ /
Acute interstitial nephritis is inflammation of the renal interstitium.   It accounts for around 15% of cases of acute renal failure. 

Presentation 
  • Acute renal failure 
  • Systemic features (present in around 5%)
    • Fever
    • Rash 
    • Arthralgia 

Causes 

Investigation 
  • ? urinary eosinophils 
  • ? renal biopsy if patient not improving – look for plasma cell and lymphocytic infiltrates. 

Treatment 
  • Supportive 
  • Stop any precipitating drugs 


Small print gem: urinary eosinophils are found in acute interstitial nephritis, prostatitis, cystitis, bladder carcinoma, renal atheroembolic disease and rapidly progressive glomerulonephritis 


References:

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Anterior uveitis

/ / / / /
Anterior uveitis is inflammation of the
  • Iris alone (=iritis) or
  • Anterior part of ciliary body (=anterior cyclitis) or
  • Iris and anterior part of ciliary body (=iridocyclitis) 

Presentation:
  • Red eye 
  • Pain 
  • Photophobia 
  • Blurred vision 
  • Lacrimation 
  • Miosis 

Recurrent cases of anterior uveitis may cause adhesions, resulting in an irregular pupil.

Investigation:
  • Slit lamp
    • Cells in anterior chamber 
    • Keratic precipitates on corneal endothelium (white in acute cases, yellow in chronic) Koeppe/Busacca nodues on iris 
    • ? hypopyon (= pus in anterior chamber) 
  • Talbot’s test 
    • Pain increases on getting patient’s eyes to converge due to constriction of pupil. Good specificity, poorer sensitivity. 

Anterior uveitis is associated with 

Treatment
  • Refer to ophthalmologist 
  • They will treat with steroids 

Possible complications 
  • Cataract 
  • Glaucoma 

References: 

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Secret collector of interesting anonymised ECGs. Fan of the Bath Photomarathon. Lover of cream teas. [Sarah Hudson] (Your Picture)