Short clinical consultations Flashcards
Management of migraine?
Acute phase: paracetamol / NSAID + antiemetic (1st line). Sumatriptan (oral / intranasal / subcut)
Longer term: remove triggers, exercise, sleep hygiene, decrease caffeine.
Prophylaxis = topiramate, propranolol
Avoid opiates / analgesia overuse
Typical migraine history?
Unilateral
Throbbing in nature
Light aversion / phonophobia
Aura / scintillating scotoma
Triggers: behaviours / foods
Onset: acute onset, can last days
Similar episodes in the past
Headache red flags to identify in the history
Vascular: maximal intensity 1-2 mins, ‘thunderclap’ headache (SAH)
Infective: pyrexial, confused, unwell, meningism, photophobia
SOL: insidious headache onset, worse on bending over / coughing / mornings
Posterior fossa syndrome: incoordination, truncal ataxia, nystagmus
Nausea / vomiting, visual changes, focal neurological deficit
Presentation with 1st headache over 55y
Approach to fundoscopic exam?
‘ROVM’
- Red reflex - obscured in cataracts, corneal scars, vitrous haemorrhage
- Optic disc - looking for cup, colour and contour. Normal cup : disc ratio is 0.3
- Vessels - start at disc, follow vessels to all 4 quadrants, ask patient to look up, down, left and right
- Macula - temporal to disc, use green light for foveal reflex
Fundoscopy features: glaucoma
Large cup : disc ratio (>0.5) indicating cupping of disc
Superior polar notching
Nasal displacement of central blood vessels
Fundoscopy features: papilloedema
Disc margins are obscured, swollen and hyperaemic
Retinal vessels are tortuous
NB must rule out SOL, signs of increased ICP
Fundoscopy features: optic atrophy with macular scarring
Optic disc pallor with cupping
Large area of macular scarring
ARMD = most common cause of macular scarring
Fundoscopy appearances: dry age-related macular degeneration
Atrophy of retinal pigment in central macula
Drusen in macular area
NB presence of haemorrhages + oedema in macular area suggests wet macular degeneration
Fundoscopy appearances: hypertensive retinopathy grades 1-4
Grade 1: arteriolar narrowing
Grade 2: AV nipping
Grade 3: exudates, haemorrhages, cotton wool spots
Grade 4: papilloedema
NB no microaneurysms! only present in diabetic retinopathy.
Fundoscopy appearances: retinitis pigmentosa
Multiple bony spicule, retinal black pigmentations scattered in the periphery of the retina
Associated history of poor night vision / blindness
Positive FH
Reduced visual fields / tunnel vision
Fundoscopy appearances: central retinal vein occlusion (CRVO)
‘Stormy sunset’: engorged retinal vein with retinal haemorrhages
Fundoscopy appearances: central retinal artery occlusion (CRAO)
Central ‘cherry red spot’ with surrounding pale retina (due to choroidal blood supply to macula remains intact)
Attenuation of arteries + veins
Fundoscopy appearances: branch retinal vein occlusion
Tortuosity and dilatation of branch of central retinal vein with AV nipping
Multiple retinal haemorrhages
Microaneurysms + hard exudates
NB must exclude hyperviscosity!
Fundoscopy appearances: background diabetic retinopathy / maculopathy
Blot haemorrhages
Hard exudates
Microaneurysms
Circinate exudates
Fundoscopy appearances: pre-proliferative diabetic retinopathy
Retinal ischaemia = characteristic here
- Multiple dot + blot haemorrhages
- Cotton wool spots (ischaemic areas)
- IRMA: intra-retinal microvascular abnormalities
- New vessel formation on the disc
Fundoscopy appearances: proliferative diabetic retinopathy
New vessels on the disc (first sign) and elsewhere
Haemorrhages
Hard exudates
NB can get ‘myopic crescent’ at the edge of the disc with peripheral retinal pigment layer prominence (don’t confuse with retinitis pigmentosa!)
Fundoscopy appearances: pan-retinal laser photocoagulation
Multiple laser scars with areas of hyperpigmentation
Patient will likely have reduced peripheral vision and a degree of night blindness
Fundoscopy appearances: multiple retinal haemorrhages
Seen in both deep and superficial layers of the retina
Hyperviscosity states (polycythaemia, waldenstrom’s macroglobulinaemia, myeloma) can lead to this
Fundoscopy appearances: retinal detachment
Area of bullous retina showing area of elevation with fluid
Trauma or choroidal metastasis
Painless ‘curtain coming down’ over vision
Discussion: what is retinitis pigmentosa?
Inherited form of retinal degeneration characterised by loss of photoreceptors
Inherited via autosomal recessive or x-linked pattern
Loss of night vision and peripheral vision
Progressive condition: by the time patients are middle-aged they reach criteria to be registered as blind
Driving implications: pt needs to inform DVLA about diagnosis, DVLA have rules about best corrective acuity + visual field loss
Syndromes that include retinitis pigmentosa and other features to look for to identify them?
RP and..
Ataxic: Freidreich’s ataxia, abetalipoproteinaemia, Refsum’s disease, Kearns-Sayre syndrome
Deafness: Refsum’s disease, Kearns-Sayre, Usher’s disease
Ophthalmoplegia + ptosis + pacemaker: Kearns-Sayre
Polydactyly: Laurence-Moon-Biedl
Ichthyosis: Refsum’s disease
Ddx of fundoscopic appearances of retinitis pigmentosa?
Diabetic retinopathy
Laser treatment scars
Infections: toxoplasmosis, rubella
Conditions associated with retinitis pigmentosa?
Laurence-Moon-Biedl syndrome
Usher syndrome
Alstrom syndrome
Refsum disease
Kearns-Sayre syndrome
Ddx of bilateral visual loss?
Glaucoma
Cataracts
Diabetic retinopathy
Macular degeneration
Papilloedema
Leber’s optic neuropathy (rarer)
Ddx of the inherited ataxias?
Spinocerebellar ataxia (trinucleotide repeat disorder)
Friedreich’s ataxia
Ataxia-telangiectasia
Ataxia with oculomotor apraxia type 1
Ataxia with oculomotor apraxia type 2 (all autosomal recessive)
How is the diagnosis of hereditary haemorrhagic telangiectasia made?
Using the Curacao criteria: if 3 criteria are present then the diagnosis is definite. If 2 present, diagnosis is possible.
- Epistaxis that is spontaneous + recurrent
- Multiple mucocutaneous telangiectasia
- Visceral lesions: GI / hepatic / lung / cerebral AVMs
- FH in 1st degree relative with genetic testing to confirm diagnosis
Features of hereditary haemorrhagic telangiectasia?
Patient presenting with recurrent nosebleeds and / or anaemia.
Telangiectasis on face, lips and buccal mucosa.
Vascular dysplasia which causes telangiectasia.
Autosomal dominant inheritance.
Vascular malformations: pulmonary shunts and IC aneurysms which cause SAH.
Increased risk of GI bleed, epistaxis and haemoptysis.
Ddx of thyrotoxicosis?
Graves’ disease (most common)
Thyroiditis of any cause (de Quervain’s, radiation, post-partum, drug-related)
Toxic multinodular goitre
Toxic adenoma
Ectopic secretion
Excess levothyroxine replacement
Hashimoto’s: period of hyperthyroidism before hypo
Bloods to test in suspected hyperthyroidism?
Thyroid function tests:
T3/4
Autoantibodies:
Thyroid peroxidase (TPO)
Thyroglobulin
TSH-receptor antibodies
Simple patient explanation for hyperthyroidism
Overactive thyroid gland - too much thyroid hormone which causes bodily functions to speed up.
If thyroid is overactive, treat with a medication (carbimazole) to reduce level of thyroid hormone.
Should start to work within 2 weeks, most people take it for 1-2 years.
50% chance of cure, 50% chance of relapse.
Warn about smoking cessation and agranulocytosis.
Other options:
- Radioactive iodine: kills thyroid cells, 90% of people respond. Can worsen eye disease, can’t have kids for 6mo, can’t hold children / pets after
- Surgery: 90% chance of cure. Risks of nerve damage, low calcium, need thyroid replacement for life
Graves’ disease management?
Medical:
- Carbimazole / PTU
- Propranolol for symptoms
- Radioactive iodine
Surgical:
- Thyroidectomy
Investigations in suspected Graves’?
Bedside: ECG (AF)
Bloods: TFTs, thyroid autoantibodies, FBC, UE, CRP, pregnancy test
Imaging: USS thyroid, radioactive iodine uptake scan, echo (high output CCF)
Causes of hypothyroidism?
Autoimmune: Hashimoto’s + atrophic hypothyroidism
Iatrogenic: post-thyroidectomy, iodine, amiodarone, lithium, anti-thyroid drugs
Iodine deficiency: dietary
Genetic: Pendred’s syndrome (+ deafness)
Investigations in hypothyroidism?
Bedside: ECG (rule out pericardial effusion and ischaemia)
Bloods: TSH, T4, autoantibodies, short SynACTHen test to exclude Addison’s
Imaging: CXR (pericardial effusion and CCF)
What are the complications of hypothyroidism?
Cardiac: pericardial effusion, CCF
Neuro: carpal tunnel syndrome, proximal myopathy, ataxia
Management of hypothyroidism?
Thyroxine titrated to TSH suppression + clinical response.
NB: can precipitate angina and unmask Addison’s disease leading to adrenal crisis.
Pertinent features of a tiredness history
Tiredness:
- what do you mean by tiredness? physical / mental / both?
- timing: sudden / gradual / intermittent / progressing / stable?
Thyroid questions:
- weight gain, poor memory, low mood, hoarse voice, dry skin, hair loss, feeling cold, constipation, angina, muscle weakness, oedema, SOB, neck swelling
Other causes of tiredness qu’s:
- malignancy: weight loss / night sweats, bleeding
- heart failure
- COPD
- renal (CKD)
- neuro (myasthenia)
- endocrine (Addison’s, Cushing’s, diabetes)
- infection (TB, HIV)
- mental health, anxiety, depression
PMH: thyroid disorders + treatment, other AI conditions
FH: thyroid + AI conditions
DH: amiodarone, lithium, carbimazole, interferon alpha
SH: impact on life, smoking / alcohol / illicit drug use
Summarised presentation for a patient you suspect has RA?
This patient has a peripheral symmetrical deforming polyarthropathy.
The presence / absence of nodules suggests seropositive / negative RA.
Hand function was preserved / restricted by deformity and weakness.
There were / was no evidence of extra-articular manifestations: no CT syndrome, no ocular, cardiovascular, pulmonary, GI or neurological involvement
What are some of the extra-articular features of RA?
Eyes: scleritis / episcleritis / scleromalacia / keratoconjunctivitis sicca
Lungs: lung nodules, pulmonary fibrosis, MTX-related pulmonary fibrosis
Heart: constrictive pericarditis, pericardial effusions
Kidneys: nephrotic syndrome, membraneous GN, renal amyloidosis
Neuro: peripheral neuropathies, carpal tunnel syndrome
Spleen: splenomegaly + RA + neutropaenia (Felty’s)
Radiological features of rheumatoid arthritis?
‘SALP’
Soft tissue swelling
Articular erosions
Loss of joint space
Periarticular osteopenia
What could be some causes of anaemia in RA?
Anaemia of chronic disease
IDA from chronic NSAID use
Bone marrow suppression - DMARD use
Autoimmune haemolytic anaemia
Splenomegaly + RA + neutropaenia (Felty’s)
What investigations would you like to do if suspecting RA?
Bedside: peak flow, obs, history
Bloods: FBC (multifactorial anaemia), CRP/ESR (biomarker of inflammation)
Autoantibodies: rheumatoid factor (positive in 70%), anti-CCP antibodies
Imaging: hand and feet XRs, CXR if suspecting fibrosis (+/- HRCT)
Management options for rheumatoid arthritis?
Mainstay of medical management rests on early use of DMARD.
Methotrexate - 1st line. If contraindicated: leflunomide, sulfasalazine, hydroxychloroquine.
If patients fail to respond to 2 DMARDS OR if they have poor prognostic markers, then biologics to be added.
- TNF alpha (adalimumab)
- anti-CD20 (rituximab)
- T cell blocker (abatacept)
Steroids are advised as short-term bridging therapy when switching to DMARD.
Surgical options: arthroplasty, arthrodesis + synovectomy.
Ddx for rheumatoid arthritis?
Any of the seronegative spondyloarthropathies:
- psoriatic arthritis
- ankylosing spondylitis
- reactive arthritis
- enteropathic arthritis
HLA association for RA?
RA has a strong association with HLA-DR4.
Diagnosis criteria for RA?
A patient has RA if they have 3 or more of the American College of Rheumatology Criteria:
- Morning stiffness >1h
- Swelling of 3 or more joints
- Swelling of PIP, MCP, wrist joints
- Symmetrical joint swelling
- Rheumatoid nodules
- Presence of IgM rheumatoid factor
- Radiographic erosions / periarticular osteopenia
What objective tool can be used to measure disease activity in RA?
Objective tools such as DAS28 (disease activity score), based on an assessment of:
- no. of tender joints
- no of swollen joints
- global pain score
- ESR/CRP
DAS28 score >5.1 = active disease
score <2.6 = remission
Classical exam findings for rheumatoid arthritis?
Symmetrical deforming polyarthropathy, typically affecting MCPJs and PIPs
Presence of rheumatoid nodules at elbows
Hand deformities seen in RA?
Palmar subluxation + ulnar drift of MCP
Swan-neck deformity: rupture of lateral slip of extensor in finger
Boutonniere: rupture of central slip in finger
Z-shape deformity of thumbs
Swelling + subluxation of ulnar styloid
Carpal tunnel scar, wasting of intrinsic muscles of the hands
+ pain, swelling, stiffness of affected joints
DVLA considerations for syncope?
The ‘3 P’s’: provocation, prodrome, postural - if all 3 present then likely benign cause and can continue driving.
Solitary syncope with no clear cause: 6 month ban
Clear cause that has been treated: 4 week ban
Recurrent seizures: must be fit-free for 1 year
Differential diagnosis of syncope?
Cardiac: brady/tachy, obstructive cardiac lesion (AS, MS, HOCM or PE)
Neuro: epilepsy, vertebrobasilar insufficiency
Orthostatic: postural hypotension (+ medication history)
Vasovagal: stress, cough, micturition, defecation
Investigations for a patient with syncope?
Bedside: ECG, tilt-table test if orthostatic hypotension suspected, L/S BP
Bloods: FBC, UE, LFT, CRP/ESR, TFTs, morning cortisol
Imaging: echo (structural heart defects / valves), EEG, CT/MR brain
Special: Holter monitor, loop recorder, EP study, exercise tolerance test
Management of syncopal episodes?
Dependant on cause.
Cardiac: pacemaker, ICD, revascularisation / valve surgery
Vasovagal: education on avoidance, isotonic muscle contraction
Orthostatic hypotension: salt / water replacement, support stockings, medication review, fludrocortisone / midodrine, SSRIs
Neuro: anti-epileptics
Types of AF?
Paroxysmal: <7 days, self-terminating
Persistent: >7 days, requires chemical or electrical cardioversion
Permanent: >1 year / no further attempts to restore sinus rhythm
Investigations for AF?
Confirmation of AF (12-lead ECG or 24h Holter)
Echo: for structural heart disease, LVH, LA size (>4cm, recurrence is high)
TFTs
Management of AF?
Ideally, rate control: beta-blockers, digoxin, pacemaker, AV node ablation
If rhythm control is warranted, either chemical or electrical cardioversion:
- If severe / unstable heart failure, amiodarone
- If hypertension / LVH / CAD / HF, sotalol
- If no structural heart disease, flecainide
Pulmonary vein isolation: saved for refractory, symptomatic patients
Anticoagulation: with warfarin or NOAC
Need to predict embolic risk using the CHADSVASc score
NB: patients hgh risk for bleeding + embolic complications should be considered for left atrial appendage occlusion to isolate the commonest source of thrombus in AF
What is the CHADSVASc score used for, and what are the components of it?
Used to predict systemic embolus risk in AF.
Cardiac failure = 1
HTN = 1
Age >75 = 2
Diabetes = 1
Stroke / TIA / embolus = 2
Vascular disease = 1
Age 65 - 74 =1
Female = 1
0 - low stroke risk, no anticoagulation
1 - medium, pt preference
2 - high risk, oral anticoagulation recommended
How do you assess bleeding risk in a patient with AF that you are considering for anticoagulation?
HASBLED or ORBIT score.
HASBLED:
- HTN = 1
- abnormal kidney / liver function = 1 for each
- stroke = 1
- bleeding = 1
- labile INR = 1
- elderly = 1
- drugs (NSAIDs / alcohol) = 1 for each
3 or above - high risk, avoid oral anticoagulation
4 grades of hypertensive retinopathy?
Grade 1: silver wiring
Grade 2: silver wiring + AV nipping
Grade 3: silver wiring + AV nipping + CWS + flame haemorrhages
Grade 4: silver wiring + AVN + CWS + flame haemorrhages + papilloedema
Investigations you wish to perform in a patient presenting with hypertension?
Evidence of end-organ damage:
- fundoscopy
- LVH on ECG
- U+Es (renal impairment)
- CXR (heart failure)
- echo (heart failure)
Exclude underlying cause:
- pregnancy test
- urinalysis / ACR (blood and protein)
- U+Es
- renin / aldosterone levels, plasma metanephrines
Causes of hypertension?
Essential: 94% - associated with age / obesity / salt / alcohol
Renal: 4% - underlying CKD
Endocrine: 1% - Conn’s, Cushing’s, acromegaly, phaeochromocytoma
Aortic coarctation
Pre-eclampsia (pregnancy)
Findings of papilloedema on fundoscopy?
Blurring of disc margins / elevation of disc / venous engorgement
Causes: raised ICP, SOL, IIH, CVST, malignant hypertension, CRVO
(presents with normal visual acuity but tunnel vision, bilaterally)
What is accelerated phase / malignant hypertension?
A medical emergency.
Treatment:
- Grade III + IV retinopathy + hypertension: bed rest, long-acting CCB, BP monitoring, gradual drop in BP
- If have encephalopathy / stroke / MI / LV failure: IV vasodilators + invasive BP monitoring.
Over-rapid correction can lead to watershed stroke.
What autoimmune syndromes can Addison’s disease form a part of?
The autoimmune polyglandular syndromes (type 2)
Autoimmune thyroid disease
T1DM
How do we define different types of adrenal insufficiency?
Primary and secondary.
Primary:
- problem with adrenal glands causing decreased cortisol production
- 80% Addison’s disease
- CAH, HIV, TB, adrenal adenomas
Secondary:
- due to impairment of pituitary gland to produce ACTH
- most common reason is exogenous steroid use
- could also be due to pituitary adenoma, hypothalamic tumour
Pathophysiology of Addison’s disease?
Lack of feedback inhibition by cortisol, leading to increased ACTH and increase melanocyte-stimulating hormone (and therefore increased pigmentation).
In 80% of cases, due to an autoimmune process.
Other causes = adrenal mass, adrenal TB, amyloidosis, adrenalectomy and Waterhouse-Freidrichsen syndrome (meningococcal sepsis + adrenal infarction).
Investigations to do in a case of suspected Addison’s disease?
8am cortisol: no morning elevation suggests Addison’s (unreliable)
Short SynACTHen test: excludes Addison’s if cortisol rises to adequate levels
Long SynACTHen test: diagnose Addison’s if cortisol does not rise to adequate levels
Adrenal imaging (in primary AD) and / or pituitary imaging (in secondary AD) with MR/CT
Bloods: decreased sodium, raised potassium, increased urea (dehydration), hypoglycaemia, adrenal autoantibodies, TFTs and eosinophilia
CXR: malignancy or TB
Management of Addison’s disease?
Acute (adrenal crisis)
- 0.9% saline rehydration IV + glucose
- Hydrocortisone IV 100mg 6 hourly
- Treatment may unmask diabetes insipidus
- Anti-TB treatment increases clearance of steroid, so higher doses needed
Chronic:
- Patient education: increase steroid dose if unwell, steroid card, medic alert bracelet
- Titrate maintenance hydrocortisone + fludrocortisone dose to levels / response
Management of pyrexia of unknown origin?
Fernandez et al, 2018
Supportive until cause is found - avoid early abx until identification of cause and avoid steroid trials.
Consider stopping all drugs + reinstituting them one by one.
Ensure patient is aware of the strong possibility of no diagnosis being made.
Do not perform serological testing if there is no history of exposure to the pathogen you are testing for.
Investigations for pyrexia of unknown origin?
Bedside: obs / other exams
Bloods: culture (+ extended cultures for HACEK organisms), thick and thin films (parasites), HIV test, CRP / ESR, autoantibodies, immunoglobulins, complement levels, CK (malignant hyperthermia)
Other: bone marrow aspirate, CSF, TOE, (looking for vegetations, aortic root abscess, myxoma as cause), PET-CT
Chest pain differential diagnosis?
Stable angina vs ACS
Pericarditis
Costochondritis
Aortic dissection
Respiratory cause / pleurisy
Gastro cause
Miscellanous: HSV, anaemia, sickle cell, thyroiditis, sarcoid, substance abuse, anxiety
Acute management of ACS?
DAPT (aspirin / clopidogrel), glycoprotein IIb / IIIa inhibitor (tirofiban) if high risk (TIMI score >4) + fondaparinux
Anti-anginal: GTN + beta-blocker
Risk modification: statin + ACEi
If positive trop - proceed to coronary angiography (angioplasty + stent vs CABG)
If negative trop - functional tests to confirm ischaemia:
- exercise stress test
- MIBI scan
- stress echo
- cardiac MRI
What is the TIMI risk score for unstable angina / NSTEMI?
Estimates mortality for patients with unstable angina or NSTEMI.
Age >65: 1 point
>3 risk factors: 1
Known CAD: 1
Taking aspirin on admission: 1
Severe angina: 1
Trop rise: 1
ST depression: 1
> 3 points = high mortality risk
Causes of neuropathic ulcers?
Diabetes mellitus
Tabes dorsalis
Syringomyelia
Investigations for leg ulcers of unknown aetiology?
Doppler USS
ABPI (0.8 - 1.2 is normal, <0.8 implies arterial insufficiency)
Arteriography
Management of leg ulcers?
Specialist nurse / TVN: wound care
Venous:
- 4 layer compression bandaging (if no PVD)
- varicose vein surgery
Arterial:
- angioplasty or vascular reconstruction
- amputation
What are the different types of neurofibromatosis?
Type 1: neurofibromas
Type 2: bilateral acoustic neuromas
Schwannomatosis: painful schwannomas develop on spinal and peripheral nerves
Causes of enlarged nerves and peripheral neuropathy?
Neurofibromatosis
Leprosy
Amyloidosis
Acromegaly
Refsum’s disease
Ddx of neurofibromatosis?
LEOPARD syndrome
Legius syndrome
Proteus syndrome
Macrodystrophia lipomatosa
Genetic cause of neurofibromatosis?
Neurofibromatosis type I is the most common of the three types - is caused by genetic changes in the NF1 gene located on chromosome 17 (17q11.2). This gene encodes for neurofibromin, which acts as a tumour suppressor gene.
NF1 - neurofibromas
NF2 - schwannomas are more common
NF2’s most characteristic symptom is hearing loss, due to pressures of tumours on the acoustic nerve. May also have headaches / dizziness / nausea.
Investigations you may want to perform in a patient with suspected neurofibromatosis?
Bedside: EEG
Bloods: genetic testing
Imaging: XR, MR/CT brain, slit-lamp exam
Other: histology from biopsy of neurofibromas
Clinical signs expected in neurofibromatosis?
2 or more cutaneous neurofibromas
Cafe au lait patches: 6 or more, >15mm diameter
Axillary freckling
Lisch nodules: melanocytic hamartomas of the iris
Visual acuity - optic glioma / compression
BP: hypertension (associated with RAS and phaeochromocytomas)
Resp: fine crackles (honeycombing of lung - ILD)
Neuropathy with enlarged, palpable nerves
What conditions can be associated with NF1?
Phaeochromocytoma (2%)
Renal artery stenosis (2%)
Complications associated with NF1?
Epilepsy
Sarcomatous change
Scoliosis
Cognitive delay
Pertinent points in sarcoidosis history taking
Eye problems: painful red eye / visual disturbance
Skin: bruised / tender shins (erythema nodosum)
Joint pain
Resp: SOB, cough, haemoptysis, wheeze, Lofgren’s syndrome (triad of fever, erythema nodosum and hilar lymphadenopathy)
CVS: chest pain, palps, syncope
Abdo: pain, renal stones, polyuria, thirst
Neuro: headache, face droop, swollen face glands (parotids - Heerfordt-Waldenström syndrome), weakness / numbness
Systemic: weight loss / night sweats
TB history: contacts, travel, place of birth, vaccinations, occupation
HIV risk assessment
PMH / FH / DH
Occupational: birds / farmers / metal / stone / pottery / pets
Questions to ask if a rash sounds or looks like erythema nodosum
Strep - sore throat?
Meds - COCP, abx, sulphonamides, phenytoin
IBD questions
Behcet’s: mouth / genital ulcers
Pregnancy
Travel history
Examination for suspected sarcoidosis?
Hands: joint swelling, pulse
Face: rash (lupus pernio), eyes (+ fundoscopy), parotids, facial nerve assessment, look in mouth at throat / tonsils
Neck: lymph nodes (including parotids)
Chest: listen to heart sounds, chest, look for rash and check for axillary LNs
Abdo: feel for hepatosplenomegaly and inguinal LNs
Legs: look for erythema nodosum
Neuro: power, peripheral neuropathy
Pathophysiology of sarcoidosis?
A multisystem, granulomatous disorder
Tends to affect northern europeans, females, 20-40y, black more often than white individuals
CXR is abnormal in 90% of patients
Serum ACE is used to monitor disease activity and response to treatment, but not for diagnosis
On bloods often see hypercalcaemia, high IgG, anaemia and thrombocytopaenia
Investigations for suspected sarcoidosis?
Bedside: obs, urine dip, 24h urine for calcium (if blood calcium high), slit lamp exam, visual acuity, fundoscopy, o2 sats + ambulatory oximetry, spirometry, ECG
Bloods: CRP / ESR, FBC (thrombocytopaenia), LFTs, ACE, calcium (raised as non-caseating granulomas secrete vit D), immunoglobulins, UEs, vitamin D, TFTs
Imaging: CXR (hilar lymphadenopathy), BAL / bronchoscopy (+ biopsy), HR-CT, echo, 24h Holter, USS abdomen, CT/MRI brain
What would you expect on investigations for sarcoidosis if positive?
HRCT: ground glass changes + beading
Spirometry: restrictive pattern
BAL: increased lymphocytes
Biopsy from bronchoscopy: non-caseating granulomas + wide alveolar septae
Name some causes of bihilar lymphadenopathy.
Sarcoidosis
Infection: TB, mycoplasma, HIV
Malignancy: lymphoma, lung cancer, metastasis
Pneumoconiosis: silicosis, berylliosis
Causes of erythema nodosum?
‘NODOSUM’
No - no cause / idiopathic
D - drugs: COCP, abx, sulphonamides, phenytoin
O - OCP
S - sarcoidosis / streptococcus
U - ulcerative colitis / Crohn’s disease
M - mycobacterium / maternity (pregnancy)
What is Lofgren’s syndrome?
A type of acute sarcoidosis.
Inflammatory disorder characterised by a triad of:
- Hilar lymphadenopathy
- Erythema nodosum
- Arthritis
(+ fever)
Is often HLA-DRB1*03 associated
What tests would be important if you suspect a diagnosis of erythema nodosum?
ASO titre (antistreptolysin titre - strep A)
TB tests (early morning urine / sputum for AFB)
Mycoplasma serology
Pregnancy test
Blood film / LDH
How is sarcoidosis managed?
NSAIDs for arthralgia and skin
Refer to respiratory and ophthalmology
Steroids are indicated if:
- bilateral hilar lymphadenopathy
- infiltrates
- lung fibrosis
- eye problems
- hypercalcaemia
- neurological / cardiac involvement
(Give 40mg prednisolone for 4-6 weeks, then weaning doses)
Monitor with serum ESR and ACE
Steroid-sparing agents: MTX, hydroxychloroquine, ciclosporin, cyclophosphamide, infliximab
Surgery:
- lung transplant
- pacemaker
Features of Ehlers-Danlos on examination?
Skin + joints: hyperextensible skin, fragile skin, bruises, scarring, scars on knees
Joint hypermobility + dislocation
Cardiac: mitral valve prolapse
Abdominal: scars
- aneurysm rupture / dissection
- bowel perforation / bleeding
Pathophysiology of Ehlers-Danlos syndrome?
Autosomal dominant inheritance
Defect in collagen, causing increased skin elasticity
No premature coronary artery disease (unlike PXE)
6 types (joint hypermobility most common)
Largely a clinical diagnosis
Pregnancy can be dangerous - PROM + PPH
Genetic testing and counselling
Management for Ehlers-Danlos syndrome?
MDT approach
PT to strengthen muscles
Splints / orthoses to prevent joint dislocations
Analgesia
Activity modification (no contact sports)
Differential diagnosis for stretchy skin and hypermobile joints?
Joint hypermobility syndrome
Ehlers-Danlos Syndrome
Osteogenesis imperfecta
Marfan’s syndrome
Pseudoxanthoma elasticum (PXE)
Nail-patella syndrome (NPS)
Pertinent features in the history for a patient with PXE?
Skin problems: ‘looks like smoker’s skin’, hereditary and chronic
Other issues:
- hyperextensible joints
- reduced visual acuity
- hypertension
- MI or CVA (strong hx of coronary artery disease)
- gastric bleed
Family history of PXE symptoms (skin issues and CAD)
Important elements of the exam in a patient with suspected pseudoxanthoma elasticum?
Skin: ‘plucked chicken skin’ appearance, loose folds at neck and axillae, with yellow pseudoxanthomatous plaques, skin laxity
Eyes: blue sclerae and macular degeneration
Cardiovascular: hypertension and mitral valve prolapse
Pathophysiology of PXE?
A genetic disease that causes mineralisation of elastic fibres in some tissues.
Affects skin, eyes and blood vessels.
Inheritance: 80% autosomal recessive (ABCC6 gene, chromosome 16)
Premature coronary artery disease
History features in suspected Henoch-Schonlein Purpura?
Triad: ‘PAA’
Purpuric rash (buttocks and legs)
Arthralgia
Abdominal pain
Precipitants: infections (strep, HSV, parvovirus B19), drugs (abx)
Complications: renal involvement (IgA nephropathy), hypertension
Pathophysiology of HSP?
Small-vessel vasculitis: IgA + C3 deposition
Normal or raised platelet count (distinguishes from other causes of purpura)
Children > adults, Male > female
Other skin manifestations of sarcoidosis?
Other skin manifestations:
- Nodules + papules: face / ears / nose / neck / Koebner’s phenomenon
- Lupus pernio: diffuse bluish / brown plaque with central small papules commonly affecting the nose
Causes of secondary hyperlipidaemia?
Hypothyroidism
Nephrotic syndrome
Alcohol
Cholestasis
Treatment of necrobiosis lipoidica diabeticorum?
Topical steroid and support bandaging.
Tight diabetic control does not help.
Skin features of diabetes?
Shins:
- necrobiosis lipoidica diabeticorum: well-demarcated plaques with waxy-yellow centre and red / brown edges.
- diabetic dermopathy: red/brown, atrophic lesions
Feet + legs:
- ulcers: arterial / neuropathic
- eruptive xanthomas: yellow papules on buttocks / knees
- granuloma annulare: flesh-coloured papules in annular configurations on dorsum of feet + fingers
Injection sites:
- lipoatrophy
- fat hypertrophy
Cutaneous infections
Signs of other AI diseases:
- vitiligo
- Addison’s disease
- PVD
Features of malignant melanoma?
‘ABCDE’ - appearance of lesion
Asymmetrical
Border irregularity
Colour - black, irregular pigmentation
Diameter >6mm
Enlarging
Metastases (draining LNs, hepatomegaly, bone tenderness)
Management of malignant melanoma?
- Excision
- Staged on Breslow thickness (maximal depth of tumour invasion into dermis)
- Glass eye + ascites - think ocular melanoma!
Features of SCC?
Sun exposed areas (+ lips / mouth)
Actinic keratoses: pre-malignant red scaly patches
Varied appearance: keratotic nodule, polypoid mass, cutaneous ulcer
Other lesions / previous scars
Metastases
SCC in situ = Bowen’s disease
Biopsy suspicious lesions
Features of BCC?
Usually on face / trunk (sun-exposed areas)
Pearly nodule with rolled edge
Superficial telangiectasia
Ulceration in advanced lesions
Other lesions
Treatment of BCC?
Natural history: grows slowly over months, rarely metastasizes
Treatment:
- surgical excision +/- radiotherapy
- curettage / cryotherapy if superficial
Pathophysiology of Paget’s disease?
A condition involving cellular remodelling and deformity of >1 bones.
The structural changes cause the bones to weaken, causing deformity, pain, fracture or arthritis of joints.
A frequent component of multisystem proteinopathy.
SQSTMI + RANK genes are associated with Paget’s.
Causes of sabre tibia?
Paget’s
Osteomalacia
Syphilis
Complications of Paget’s disease?
Osteogenic sarcoma
Basilar invagination (cord compression)
Kidney stones
Causes of angioid streaks (in the retina)?
Paget’s
PXE
Ehlers-Danlos Syndrome
Investigations in suspected Paget’s disease?
Grossly elevated alk phosphatase, normal calcium and phosphate.
Radiology:
- ‘moth eaten’ on plain films (osteoporosis circumscripta)
- increased uptake on bone scan
Management of Paget’s disease?
Bisphosphonates
Calcitonin
Surgery (for fractures, degenerative arthritis, bone deformity)
Diabetic retinopathy stages?
Background: ‘HBM’
- hard exudates
- blot haemorrhages
- microaneurysms
Pre-proliferative: backround features PLUS
- cotton wool spots
- flame haemorrhages
Prolierative: pre-proliferative features PLUS
- neovascularisation
- panretinal photocoagulation scars (treatment)
Screening processes for diabetic retinopathy?
Annual screening for all patients with diabetes
Refer to ophthalmology if pre-proliferative retinopathy or changes near macula
Background retinopathy usually occurs 10-20y after diagnosis of diabetes
Young people w/ T1DM usually get proliferative retinopathy
Older patients with T2DM usually get exudative maculopathy
What are some indications for photocoagulation treatment in diabetic retinopathy?
Maculopathy
Proliferative and pre-proliferative diabetic retinopathy
Complications of proliferative diabetic retinopathy?
Vitreous haemorrhage
Traction retinal detachment
Neovascular glaucoma
Clinical signs of cataracts on fundoscopy?
Loss of red reflex
Cloudy lens
May have RAPD with normal fundi
Associations: myotonic dystrophy (with bilateral ptosis)
Causes of cataracts?
Congenital: Turner’s, rubella
Acquired: age (usually bilateral), diabetes, steroids, radiation, trauma, storage disorders
Treatment of cataracts?
Surgery (as an outpatient):
- Phacoemulsification with prosthetic lens implantation
- YAG laser capsulotomy
History-taking pertinent features for a patient presenting with worsening mobility / falls
Pre-morbid social history:
- independence / dependence (carer role + frequency)
- mobility issues - PD, stroke? walks unaided or with stick or frame
- falls recently? how many?
- where do they live (impt for discharge planning)
Precipitant:
- infection: urinary sx, pneumonia sx
- drug changes: benzos, diuretics, BP meds, antipsychotics, steroids, PD drug changes
- systemic enquiry - sites of pain
Legal:
- advanced directives / living will
Exam points for a patient presenting with worsening mobility or falls?
Ask to stand / walk unaided
Proximal LL strength: rise from chair
Gait: wide-based, ataxic, hemiplegic, shuffling
Romberg’s: sensory ataxia
Assess LLs: inspection, tone, power, reflexes, sensation, coordination
Postural hypotension: assess lying and standing BP (20mmHg drop in systolic BP after 2 mins is significant)
Causes of delirium?
‘PINCHME’
Pain
Infection
Nutrition
Constipation
Hydration
Medication
Environment
Name some delirium screening tools
4AT: alertness, AMT4, attention, acute change / fluctuating course
CAM: confusion assessment method - assess the presence, severity and fluctuation of 9 delirium features
Management of delirium?
Treat reversible causes: abx, avoid polypharmacy
MDT: nurse, social worker, OT/PT
- mobility aids
- home modifications / residential care
- resus decision / ceiling of care
What is the FRAT score used for?
Indicates a patient’s risk of falling and guides further management for worsening mobility / falls.
- Falls in the last year
- 4+ meds per day
- Dx stroke / PD
- Balance issues
- Can they get up from a chair without using arms
<3 points = lower risk
>3 points = higher risk
What is the FRAX tool used for?
FRAX predicts the 10-year probability of a patient having a major osteoporotic fracture.
Investigations for a patient with worsening mobility / falls?
Bedside: obs, collateral history, urine MCS / CSU, delirium screen 4AT or CAM
Bloods: septic screen, blood cultures, bone profile and UEs (elecs), FBC, CRP (infection)
Imaging: CXR (infection), if fall and confusion / reduced consciousness, consider CT head non contrast. High risk of subdural in atrophic brain
Which medications would we worry about as a cause of falls in polypharmacy?
Antihypertensives (low BP)
Sedatives
Diuretics (elec abnormalities and low BP)
Antidepressants (hyponatraemia)
Which medications add to anticholinergic burden?
‘PC SOAP’
Promethazine
Cetirizine
Solifenacin
Oxybutynin
Amitriptyline
Prochlorperazine
Management of TIA?
Once structural causes have been ruled out with brain imaging, mgmt focuses on secondary prevention of further episodes.
Aspirin 300mg OD for 2 weeks, then clopidogrel 75mg OD lifelong.
Optimise BP, diabetes, cholesterol, diet, exercise, smoking cessation, reduce alcohol.
Surgical: carotid endarterectomy within 2 weeks if symptomatic carotid stenosis (70-99%) (ESCT criteria).
Anticoagulate if AF present.
DVLA: no driving for 1 month.
Ddx of TIA?
Hemiplegic migraine
Hypoglycaemia
Seizure
Syncope
GCA
Electrolyte disturbances
List some causes of CVA in younger patients?
Antiphospholipid syndrome
Extracranial dissection
Vasculitis
Substance abuse: cocaine / methamphetamines
Metabolic / mitochondrial disease
Sickle cell disease
Features of antiphospholipid syndrome?
Consider APLS if young with TIA + recurrent miscarriages.
Requires anticoagulation: current evidence favours warfarin > DOAC.
Consider bubble echo looking for PFO in young patient.
Complications: TIA / stroke, DVT / PE, livedo reticularis, thrombocytopaenia, thrombophlebitis, recurrent miscarriages.
Pertinent examination points in suspected TIA
Visual acuity
Visual fields
Pupillary responses
Fundoscopy
H-test for eye movements
Palpate temporal arteries
Cardiovascular exam
Neuro: pronator drift, power, sensation, finger-nose testing, reflexes, speech, gait
Pertinent TIA history points
Timing: when, sudden / gradual, how long, complete recovery now? previous episodes
Vision: painful / painless, blurred, distorted, bits missing, double vision
Neuro: weakness, speech, swallow, headache
GCA: headache / scalp / jaw pain
Migraine: aura, headache, sensitive to light / noise, N+V
Seizure: LOC, drowsy after, incontinence, tongue biting
Hypoglycaemia: sweating, palps, hunger before
PMH stroke / TIA / recurrent miscarriages. CV risk factors: HTN, diabetes, high cholesterol, smoking, MI, stroke
DH / FH
SH: alcohol, drugs, smoking, CV risk factors
Examination features for suspected eczema?
Rash:
- erythematous + lichenified patches of skin
- mainly flexor aspects of joints
- fissures (hands, feet. painful)
- excoriations
- secondary bacterial infection
Associated atopy:
- respiratory exam: polyphonic wheeze of asthma
Investigations:
- patch testing for allergies
Management of eczema?
Avoid precipitants
Topical: emollients, steroids, tacrolimus
Antihistamines for itch
Abx for secondary infection
UV light therapy
PO prednisolone in severe cases
Causes of nail pitting?
Psoriasis
Lichen planus
Alopecia areata
Fungal infections
Examination pertinent points in a patient with psoriasis
Skin:
- chronic plaque type: multiple well-demarcated, pink scaly plaques on extensor surfaces
- check behind ears, scalp + umbilicus
- Koebner phenomenon: plaques at sites of trauma
- skin staining from coal tar treatment
Nails:
- pitting, onycholysis, hyperkeratosis, discolouration
Joints:
- psoriatic arthropathy
Definition of psoriasis?
Epidermal hyperproliferation and accumulation of inflammatory cells
Management options for psoriasis
Topical:
- emollients
- calcipotriol
- coal tar (stains)
- dithranol
- hydrocortisone
Phototherapy:
- UVB
- psoralen + UVA (PUVA)
Systemic:
- cytotoxics (MTX / ciclosporin)
- anti-TNF (adalimumab)
- retinoids (acitretin)
What is SLE?
A multisystem, inflammatory autoimmune disorder.
Broad spectrum of clinical presentations, affects all organs and tissues.
Demographics: Female > male, African + Latin americans, Afro-caribbeans, South Asians and Hispanic, 16-55y.
Takes a chronic, waxing and waning course.
How is SLE diagnosed?
Initially the American College of Rheumatology criteria (out of 11), and now the SLICC (2012) classification criteria (out of 17)
- 4/17 including 1 clinical and 1 immunological
- biopsy-proven lupus nephritis and ANA / anti-dsDNA
Management options for SLE?
Mild disease (cutaneous / joint only):
- topical corticosteroids
- hydroxychloroquine
Moderate disease (+ other organ involvement):
- prednisolone PO
- azathioprine
Severe disease (+ severe involvement of vital organs)
- methylprednisolone
- MMF (for lupus nephritis)
- cyclophosphamide
- azathioprine
What antibodies are SLE-specific?
ANA
anti-dsDNA
elevated immunoglobulins
Investigations to consider in a patient if SLE is suspected?
Bedside: obs, sats, ECG, skin/renal biopsy, nailfold capillaroscopy, pregnancy test
Bloods:
- FBC, UE, LFT, clotting, ESR / CRP
- ANA, RF, anti-CCP, ANCA, immunoglobulins, anti-dsDNA
- anti-Scl70, anticentromere, anti Ro/La, anti-Jo1, antihistone
- HIV / Hep B + C / CMV / EBV screen
- serum electrophoresis + urine BJ proteins
- ACE (sarcoid), ferritin (Still’s), anti-GBM (Goodpastures)
Other:
- If suspecting specific organ involvement, relevant tests for that organ
Drugs that can cause drug-induced lupus?
Hydralazine
Procainamide
Isoniazid
Phenytoin
Interferon
Which antibodies are specific to certain rheumatological conditions?
SLE: ANA, dsDNA, anti-Smith
Antiphospholipid syndrome: anti-cardiolipin, lupus anticoagulant, beta2-glycoprotein
Sjogren’s syndrome: anti-Ro (SSA), anti-La (SSB)
MCTD: anti-U1 RNP
RA: rheumatoid factor, CCP
Myositis: anti-Jo1
Scleroderma: anti-centromere, Scl-70, RNA polymerase III
ANCA vasculitis: c-ANCA (GPA), p-ANCA (EGPA)
New GOLD (2023) COPD management guidelines?
Severity of COPD is categorised on MRC dyspnoea scale, instead of previously-used FEV1.
0-1 exacerbations (not leading to hospital admission):
- mMRC 0-1, CAT <10 = single bronchodilator
- mMRC =>2, CAT =>10 = LABA + LAMA
=>2 mdoerate exacerbations or =>1 leading to hospitalisaton:
= LABA + LAMA
(consider LABA + LAMA + ICS if blood eosinophil count >300)
Key:
mMRC: modified Medical Research Council dyspnoea questionnaire
CAT: COPD Assessent Test
What questions to ask in an extra-articular features rheumatology screen? (ie if suspect SLE / MCTD / Sjogrens / scleroderma etc)
Systemic: weight loss, night sweats, fatigue, fever
Rashes: sensitive to sun? hair loss? mouth / nose ulcers? swollen / tight skin?
Eyes: Dry eyes / mouth, visual changes, painful eyes
CVS / resp: CP, SOB, orthopnoea, palps, ankle swelling, LOC, wheeze, cough, haemoptysis, exercise tolerance
Raynaud’s: fingers go cold + change colour (white, blue then red)
GI / GU: bladder and bowels, dysphagia, heartburn, abdo pain
Renal: high BP, blood / protein in urine
Neuro: headaches, double vision, LOC, dizziness, weakness, numbness
Muscle weakness / pain
Pregnancy: baby have heart block or rash?
PMH/DH: drug-induced lupus
FH of rheumatological or AI disease
SH: pregnant, breastfeeding? plans to do so?
Important examination features in suspected SLE?
Head / face / scalp: malar rash, discoid rash, oral ulceration, scarring alopecia (edges of bald patches look more ragged than alopecia areata)
Hands / nails: nailfold vasculitis, synovitis, Raynaud’s, fistula on arm, Jaccoud’s arthropathy (mimics RA but due to tendon contractures and not joint destruction)
CVS exam
Resp exam: effusion, rub, fibrosing alveolitis
Abdo: organomegaly, renal transplant
Legs: oedema, DVT
Skin: discoid lupus, vasculitic rash, photosensitivity rash, livedo reticularis
Cushingoid appearance: steroid use
Investigations in systemic sclerosis?
Autoantibodies (bloods):
- ANA +ve in 90%
- anti-centromere in limited SS
- anti-Scl70 in diffuse SS
Hand XRs: for calcinosis.
Pulmonary: CXR, HR-CT, PFTs. Expect lower lobe fibrosis and aspiration pneumonia.
GI: Contrast scans, FBC, B12 and folate. Gut dysmotility and malabsorption.
Renal: UE, urinalysis, urine microscopy (casts), consider renal biopsy.
Cardiac: ECG and echo. Myocardial fibrosis and arrhythmias.
What is CREST syndrome?
CREST is a type of limited systemic sclerosis.
It consists of:
- Calcinosis
- Raynaud’s phenomenon
- Esophageal dysmotility
- Sclerodactyly
- Telangiectasia
What is systemic sclerosis?
SS is a connective tissue disease characterised by autoimmunity, vasculopathy and fibrosis.
Most commonly affects females aged 35-65y.
Prognosis for diffuse SS is around 50% 5-year survival, most deaths are due to respiratory failure.
Classification of systemic sclerosis?
Limited SS:
- distribution below elbows, below knees and face
- slow progression (years)
Diffuse SS:
- widespread cutaneous and early visceral involvement
- rapid progression (months)
Management of systemic sclerosis?
Symptomatic treatments:
- camouflage creams
- Raynaud’s treatments: hand warmers, CCBs, ACEi’s, prostacyclin infusions
Renal: ACE’s
GI: PPI for reflux
Treat pulmonary hypertension: CCBs, diuretics, iloprost, bosentan, sildenafil, o2
Immunosuppression: MMF, MTX, cyclophosphamide, azathioprine, ciclosporin, prednisolone, rituximab
Pertinent features of exam for someone with suspected systemic sclerosis?
Hands:
- sclerodactyly ‘prayer sign’
- calcinosis (may ulcerate)
- assess function: hold pen
Face:
- tight skin
- microstomia
- beaked nose
- peri-oral furrowing, telangiectasia, alopecia
Other skin lesions:
- morphoea: focal / generalised patches of sclerotic skin
- en coup de sabre (scar down central forehead)
BP: hypertension
Resp: fibrosis (fine, bibasal crackles)
Cardiac: pulmonary hypertension (RV heave, loud P2, TR), evidence of CCF, pericarditis (rub)
Management of ankylosing spondylitis?
MDT approach!
- PT and hydrotherapy
- Analgesia: NSAIDs, paracetamol, weak opioids
- Corticosteroid injections: for sacroiliitis and enthesitis
- Biological agents: anti-TNF (adalimumab)
- Treat complications such as iritis
- Treat osteoporosis with bisphosphonates (prevent spinal fractures)
- Smoking cessation (close association with disease activity)
What pre-treatment investigations must be considered before starting anti-TNF?
Immunisations
Screen for active and latent TB with CXR and blood test
How is ankylosing spondylitis diagnosed?
Mainly from clinical history and examination with supporting radiological evidence.
Young patients (<40) with +ve FH
Plain spine XR: erosions / sclerosis of SI joints, and squaring of vetebrae (‘bamboo spine’)
Bloods: raised ESR / CRP, anaemia of chronic disease
Genetic testing: HLA-B27
CXR / HRCT if suspecting lung fibrosis, consider PFTs
What are the extra-articular manifestations of ankylosing spondylitis?
The 5 A’s:
Anterior uveitis (commonest, 30%)
Apical lung fibrosis
Aortic regurgitation (midline sternotomy)
AV node block (pacemaker)
Arthritis (may be psoriatic arthropathy)
What are the immunological associations with ankylosing spondylitis?
Seronegative spondyloarthropathy
HLA-B27 positive in >90% of individuals
TNF and interleukin-1 also implicated in disease activity
How do you differentiate on PFTs between mechanical restriction and interstitial lung disease?
Look at the TLCO (transfer factor).
Mechanical restriction - normal TLCO
ILD - reduced TLCO due to underlying damaged lung
DDx of breathlessness in ankylosing spondylitis?
Apical lung fibrosis
Anaemia: NSAIDs / anaemia of chronic disease
Mechanical restriction due to fusion of the spine causing restrictive defect
Cardiac causes: AR
How is ankylosing spondylitis disease activity measured?
Using the BASDAI: Bath Ankylosing Spondylitis Disease Activity Index.
- 10-point scale
- anything >4 indicates active disease
Pertinent examination points in suspected ankylosing spondylitis?
Spine:
- ask pt to stand up (back and chest exposed)
- kyphotic spine, hyperextension of the neck (question-mark posture) - increased occiput to wall distance
- reduced spinal movements
- increased AP diameter of chest wall
- Schober’s test: 2 points marked 15cm apart, expand by <5cm on maximum forward flexion is a positive test
Cardiac:
- listen to aortic area and left sternal edge (AR)
Chest:
- apical fibrosis, apical fine creps
Eyes: iritis, visual acuity check
Gait: likely antalgic, will make spinal deformity more obvious
What is the difference between Cushing’s disease and Cushing’s syndrome?
Cushing’s disease: glucocorticoid excess due to an ACTH-secreting pituitary adenoma
Cushing’s syndrome: the physical signs of glucocorticoid excess
Investigations to perform in suspected case of Cushing’s syndrome?
- Confirm high cortisol
- 24h urinary collection
- low dose dex suppression test (won’t suppress cortisol if +ve) - If elevated cortisol, identify cause
- ACTH level:
if high, ACTH-secreting tumour / pituitary adenoma.
If low, adrenal adenoma / carcinoma. - Other tests
- MRI pituitary fossa +/- adrenal CT +/- whole body CT to identify lesion
- Inferior petrosal sinus vein sampling (pituitary vs ectopic origin)
Management of Cushing’s
Surgical:
- transsphenoidal approach to remove pituitary tumour
- adrenalectomy for adrenal tumours
Nelson’s syndrome: bilateral adrenalectomy causes Cushing’s disease, as causes increased ACTH production and leads to pituitary overgrowth due to lack of feedback inhibition
Pituitary irradiation
Medical: metyrapone
Ddx of proximal myopathy causes?
Inherited: muscular / myotonic dystrophy
Endocrine: Cushing’s, hyperparathyroidism, thyrotoxicosis
Inflamm: polymyositis, RA
Metabolic: osteomalacia
Malignancy: paraneoplastic / LEMS
Drugs: alcohol, steroids
Pertinent examination points for suspected Cushing’s syndrome?
Spot diagnosis:
- Face: round, hirsuite, acne
- Skin: bruised, thin, purple striae
- Back: intrascapular fat pad
- Abdomen: central adiposity
- Legs: wasting and oedema
Complications:
- HTN (check BP)
- Diabetes (CBG)
- Osteoporosis (kyphosis)
- Cellulitis
- Proximal myopathy (stand from sitting)
Cause:
- Exogenous: signs of chronic condition (RA, COPD) requiring steroids
- Endogenous: bitemporal hemianopia + hyperpigmentation (if increased ACTH)
Why is OSA associated with acromegaly?
Acromegaly causes soft tissue swelling in the face / around the throat.
This can lead to respiratory compromise - especially when lying down at night.
Management of acromegaly?
1st line: surgery - transsphenoidal resection (curative)
2nd line: somatostatin analogues (ocretotide), bromocriptine if not tolerated
3rd line: radiotherapy to pituitary gland is an option if other treatments fail
NB a potential complication of surgery is panhypopituitarism - need to warn patients about this before surgery.
Why do acromegalic patients get visual disturbance?
Classically, a bitemporal hemianopia occurs.
This is due to compression by the adenoma on the optic chiasm.
Clinical findings in a patient with acromegaly?
General appearance: prognathism, prominent supraorbital ridges, coarse facial features, macroglossia, incrased teeth separation, spade-like hands, sweating, large feet
May have goitre
Bitemporal hemianopia on VF testing
Carpal tunnel syndrome
Axillae for acanthosis nigricans
Chest: gynaecomastia, galactorrhoea
Cardiovascular: increased JVP, displaced apex beat, bibasal crackles, pedal oedema (CCF)
Joints: arthropathy (Heberden’s nodes)
Offer to examine: BP, urine dip (glucose), DRE (polyps), testicular exam (hypogonadism)
What investigations would you request in a case of suspected acromegaly?
Screening: test IGF-1 levels (will be high)
Confirm diagnosis with OGTT (shows failure to suppress GH)
Look for underlying cause: MRI brain, looking for pituitary adenoma
Investigating complications:
- fasting glucose + HbA1c
- anterior pituitary hormone screen
- ECG: look for LVH and cardiac conduction defects
- TTE: assess ejection fraction
- sleep study: assess for OSA
- colonoscopy for polyps
- NCS for carpal tunnel syndrome
Management of the complications of acromegaly?
OSA: CPAP
CCF: diuretics, ACEi’s, beta blockers
Diabetes: hypoglycaemic agents
Anterior pituitary deficiency: hormone replacement
What is the underlying disease mechanism for osteogenesis imperfecta?
A problem with poorly formed type 1 collagen.
In >90% of cases, OI occurs due to mutations in COLIA1 or COLIA2 genes.
Inheritance pattern of osteogenesis imperfecta?
Predominantly inherited in an autosomal dominant pattern.
There are 8 different variations of OI, can develop spontaneously - this is the more severe form of the condition.
Clinical features of osteogenesis imperfecta?
Blue discolouration of eyes
Recurrent fractures since birth
Palpitations + abdominal discomfort
Short stature, barrel chest
Deformity of the legs
Abnormal gait / joint hypermobility / skin laxity
Discoloured, translucent teeth (dentogenesis imperfecta)
Hearing impairment (middle ear bones affected)
Investigations for suspected osteogenesis imperfecta?
Bloods: bone profile, vitamin D, genetic screening (predominantly an inherited condition)
Imaging: x-rays and DEXA to look at bone density. Echocardiogram.
NB: echo is requested as there is an association with bicuspid aortic valve in patients with OI, and they can also develop AR.
Management for osteogenesis imperfecta?
Depends on the results of relevant investigations for OI.
Replace low calcium / phosphate / vit D levels.
If DEXA shows decreased bone density, consider bisphosphonates.
Orthotics review.
PT review.
Main clinical features of LEMS?
Diminished reflexes that become brisker after exercise.
LL girdle weakness.
Associated with malignancy (SCLC).
Antibodies to pre-synaptic calcium channels.
EMG shows ‘second wind’ phenomenon on repetitive stimulation.
Causes of bilateral extra-ocular palsies
Myasthenia gravis
Graves’ disease
Mitochondrial cytopathies (CPEO)
Miller-Fisher variant of GBS
Cavernous sinus pathology
Management of myasthenia gravis?
Acute: IV immunoglobulin or plasmapharesis
Chronic:
- ACh esterase inhibitor (pyridostigmine)
- Immunosuppression: steroids / azathioprine
- Thymectomy is beneficial, even if patient does not have a thymoma
What causes myasthenia gravis?
Anti-nicotinic ACh receptor antibodies affect neurotransmission.
Investigations for myasthenia gravis?
Diagnostic tests:
- Anti-ACh receptor antibodies (+ve in 90%)
- Anti-MuSK antibodies
- EMG: decremented response to impulses
- Tensilon / edrephonium test: not done anymore as causes heart block
- CT / MRI chest (thymoma in 10%)
- TFTs (Graves’ in 5%)
Causes of bilateral facial nerve palsy?
Guillain-Barre Syndrome
Sarcoidosis
Lyme disease
Myasthenia gravis
Bilateral Bell’s palsy
Bell’s palsy features and management?
Bell’s palsy is the commonest cause of facial nerve palsy.
Rapid onset over a few days, HSV1 has been implicated. Induced swelling and compression of the nerve within the facial canal.
Management:
- Prednisolone started within 72h (+ aciclovir if severe)
- Eye protection (artificial tears, tape shut at night)
- Prognosis: 70-80% make a full recovery
- Pregnancy: Bell’s palsy is more common, outcome may be worse
Causes of 7th nerve palsy?
Bell’s palsy
Ramsay-Hunt syndrome
Mononeuropathy (diabetes, sarcoid)
Tumour / trauma
MS / stroke
What is Bell’s phenomenon?
The eyeball rolls up on attempted eye closure (seen in Bell’s palsy)
How to work out the level of the lesion in a facial nerve palsy?
Pons: + VI palsy and long tract signs (MS+stroke)
Cerebello-pontine angle: + V, VI, VIII + cerebellar signs (tumour)
Auditory / facial canal: +VIII (cholesteatoma or abscess)
Neck / face: + scars or parotid mass (tumour or trauma)
Clinical signs of retinal artery occlusion?
Pale, milky fundus with thread-like arterioles
+/- cherry red spot on macula (choroidal blood supply)
Cause: AF or carotid stenosis with bruit
Causes of central retinal artery occlusion?
Embolic: carotid plaque rupture / cardiac mural thrombus
GCA: tender scalp + pulseless temporal arteries
Clinical features of age-related macular degeneration?
Signs:
- wet (neovascular, exudative) or dry (non-neovascular, atrophic, non-exudative)
- Macular changes: drusen, geographic atrophy, fibrosis, neovascularisation (if wet)
Symptoms:
- loss of CENTRAL vision
- issues reading / driving / recognising faces
Management:
- ophthalmology referral
- wet ARMD: intravitreal anti-VEGF injections
Features of retinal vein occlusion?
Clinical signs:
- flame haemorrhages ++ radiating out from swollen disc
- engorged, tortuous veins
- cotton wool spots
Effect: rubeosis iridis causes secondary glaucoma in CRVO - visual loss or visual field defect
Causes of central retinal vein occlusion?
HTN
Hyperglycaemia / diabetes
Hyperviscosity syndromes: Waldenstrom’s macroglobulinaemia or myeloma
Increased intraocular pressure (glaucoma)
Causes of a pale optic disc?
‘PALE DISCS’
Pressure: tumour, glaucoma (most common cause)
Ataxia: Freidreich’s
LEber’s optic neuropathy
Dietary: B12, Degenerative: RP
Ischaemia: CRAO
Syphilis and other infections: CMV + toxoplasmosis
Cyanide + other toxins: alcohol, lead, tobacco
Sclerosis: MS (most common cause)
Management of sickle cell crisis?
Oxygen +/- CPAP
IV fluids, analgesia
Abx if evidence of infection
Blood transfusion / exchange transfusion depending on severity of crisis
Hydroxycarbamide / exchange transfusion programme if frequent crises / poor prognosis
Long-term folic acid + penicillin (due to hyposplenism)
Ddx for a patient with sickle cell presenting with fatigue / breathlessness / bone pain / pleuritic chest pain
Vaso-occlusive sickle crisis
Acute sickle chest crisis
Sicke cell crisis + pulmonary hypertension
Vaso-occlusive crisis with PE
Types of sickle cell crisis?
Vaso-occlusive crisis (sickling in small vessels of any organ). Often precipitated by viral illness, exercise or hypoxia.
Leg ulcers due to ischaemia.
Chest crises (high mortality associated with these in adulthood).
Priapism.
Pulmonary hypertension.
Differential diagnosis for diarrhoea?
Infectious:
- viral: norovirus, rotavirus
- bacterial: e.coli, salmonella, shigella, campylobacter, v.cholerae, c.difficile
- parasites: giardia, amoebic dysentry
IBD: UC or Crohn’s - blood, weight loss, abdominal pain, mucus
Colorectal Ca: blood, weight loss, enlarged LNs, abdominal masses
Coeliac disease: symptoms triggered by certain foods (bread, pasta)
Medication-related: abx, cytotoxics, laxatives, PPIs, digoxin, NSAIDs, beta-blockers
Thyrotoxicosis: sweating, hot, bulging eyes, neck lump, anxious
Bacterial overgrowth: post-gastroenteritis, burping / passing excess wind
Pancreatic insufficiency: steatorrhoea
Short bowel syndrome: previous bowel surgeries?
Ischaemic colitis: history of stroke / AF / cardiovascular disease?
Appropriate investigation / management for a patient with unexplained diarrhoea?
Bedside: stool sample, fluid resus. Send stool sample for:
- MC+S
- C.diff toxin
- Ova, cysts and parasites
- Faecal calprotectin
Bloods: cultures, FBC, WCC, CRP, UE, VBG (lactate), LFTs, TFTs, autoimmune screen, TTG (coeliac). Hep A/B/C and HIV.
Imaging: AXR (toxic megacolon / perforation)
Consider:
- Antibiotics + IV steroids (if suspect an IBD flare)
- Flexi-sig / colonoscopy / OGD + biopsies
- Abdo USS
- CT AP
- Faecal elastase (pancreatitis)
Features of a spot diagnosis for a patient with Down’s syndrome?
Low-set ears
Epicanthic folds
Protruding tongue
Collapsed nasal bridge
Single palmar crease
Wide gap between 1st and 2nd toes
Cardiac murmurs
Reduced IQ
Features of a spot diagnosis for a patient with acromegaly?
Face: prominent supraorbital ridges, large lips and nose, prognathism, spaced teeth
Macroglossia, large sweaty hands
Complications: carpal tunnel, diabetes, hypertension, gynaecomastia, arthropathy, cardiomegaly, acanthosis nigricans
Bitemporal hemianopia and optic atrophy
Rare causes: MEN type 1, Mc-Cune Albright syndrome and Carney complex
How does hypopituitarism / pituitary apoplexy generally present?
Sudden-onset headache behind eyes / around temples (90% of cases)
Associated nausea and vomiting
Sometimes meningism and reduced GCS
Bitemporal hemianopia visual field defect
May have 3rd nerve palsy
Usually have adrenal insufficiency (secondary) and other pituitary hormone deficiencies
Questions to ask when suspecting pituitary apoplexy?
Gonadotrophin: no / irregular periods, reduced libido, hot flushes
GH: weight gain
TSH: weight gain, feeling cold, dry skin, hair loss, fatigue, constipation, puffy face
ACTH: dizzy on standing, tired, weak, nausea / vomiting, weight loss, abdo pain
PMH: previous pituitary surgery, radiation, cancer, head injury
NB you do not get salt wasting and hyperpigmentation in secondary adrenal insufficiency as you do in primary adrenal insufficiency
Causes of hypopituitarism?
Pituitary tumour: often non-functioning macroadenoma
Iatrogenic: pituitary surgery / radiation
Compression / infiltration: meningioma, mets, sarcoid, abscess, craniopharyngioma
Pituitary apoplexy: acute infarction of a pituitary adenoma
Head injury / stroke / meningitis
Sheehan syndrome (infarction during blood loss in childbirth)
Empty sella syndrome
Investigations to request for suspected hypopituitarism?
Bedside: obs, history, CBG
Bloods: FBC, UE, 9am cortisol (low), TFTs (low), LH / FSH (low), morning testosterone / oestradiol (low), IGF-1 (low), prolactin (low or raised)
Imaging: CT or MRI head and pituitary (MRI has >90% sensitivity for detecting pituitary apoplexy)
Management of pituitary apoplexy?
Medical: hormone replacement
Surgical: transsphenoidal surgery if mass effect
How to perform Weber’s and Rinne’s tests?
Rinne’s first: to assess conduction
- If normal, air > bone
- If sensorineural deafness, air > bone
- If conductive deafness, bone > air
If Rinne’s +ve, progress to Weber’s - to assess lateralisation
- If sensorineural, will localise to good ear.
- If conductive, will localise to affected ear.
Ddx for psoriatic arthritis?
Rheumatoid arthritis
Other seronegative spondyloarthropathies: ank spond, reactive arthritis, enteropathic arthritis
Osteoarthritis
Crystal arthropathy (gout, pseudogout)
What criteria are used to diagnose psoriatic arthritis?
CASPAR criteria - to diagnose PsA, need =>3 points:
- psoriasis (current, past, FH)
- psoriatic nail dystrophy
- negative RF
- dactylitis (current or past)
- XR: juxta-articular new bone formation
Name some subtypes of psoriatic arthritis.
Asymmetrical oligoarthritis: DIPJ + PIPJ, MCPJs + MTPJs, knee + hip, dactylitis
Predominantly DIPJ with nail changes
Athritis mutilans: telescoping of fingers
RA-like: wrist involvement
Axial only: asymmetrical sacroiliitis
Extra-articular features of psoriatic arthritis?
Nail involvement in 80% - pitting, ridging, hyperkeratosis, onycholysis
Ocular involvement - conjunctivitis, iritis
Investigations in suspected psoriatic arthritis?
Bedside: obs, history, urine dip, sexual hx (reactive arthritis differential)
Bloods: RF and anti-CCP, ANA, ESR / CRP, FBC, UE, LFT, HLA-B27 testing if sacroiliitis
Imaging: XR hands / feet: asymmetrical changes, no periarticular osteopenia, DIPJ involvement, erosion of terminal tufts, ‘pencil in cup’ deformity, sacroiliitis, juxta-articular new bone formation
Management of psoriatic arthritis?
Lifestyle advice: weight loss, exercise, smoking cessation
NSAIDs
Steroid injections (but be aware this can cause skin to flare)
DMARD when NSAIDs fail, 3+ joints involved, PASI score =>10 (MTX, sulfasalazine, leflunomide)
Biologic: Anti-TNF / Ustekinumab / Apremilast
Surgical: joint replacement
Dermatology opinion on skin disease
What two cell types are found in sarcoidosis?
Non-caseating granulomas and Langhans giant cells.
Symptoms of sarcoid?
Eyes: dry eyes, blurred vision
Lymph nodes: enlarged
Lungs: dry cough, breathlessness, wheeze
Heart: chest pain, arrhythmias, heart palps
Hepatosplenomegaly
Joints: pain, arthritis, swelling
Skin: rashes, lupus pernio, erythema nodosum, skin lesions on back, subcutaneous nodules
Whole body: fatigue and weight loss
Features of yellow nail syndrome?
Discoloured, dystrophic and thickened nails.
A condition associated with lymphoedema, pleural effusions and bronchiectasis in 40% of cases.
What treatments do you know of for RA?
Bridging steroids for flares
Early DMARD’s
MTX +/- second agent, such as leflunomide, sulfasalazine
Anti-TNF (Infliximab)
Anti-CD20 (Rituximab)
T-cell co-receptor blocker (Abatacept)
How do you quantify a RA flare?
DAS28
- Number of swollen/tender joints
- Global pain score
- ESR/CRP
What are the diagnostic criteria for RA?
ACR/EULAR
- No. LARGE joints
- No. SMALL joints
- ESR/CRP
- Anti-RF/CCP
- > 6 weeks duration
Characteristic hand signs of RA?
Wrist subluxation
Thickened synovium
Ulnar deviation
Boutoiniers (PIP flex.d)
Swan neck (PIP ex.d)
Z thumb (MP hyper-ext)
Rheumatoid nodules (elbows)
Arthroplasty scars
What important extra-articular manifestations of Psoriatic arthritis are you aware of?
With all spondyloarthropathies:
- aortitis
- aortic regurgitation
- iritis
- apical lung fibrosis
- colitis
- enthesitis (specific for spondyloarthropathies)
DDx from other spondyloarthropathies by more asymmetry, and more peripheral joint involvement.
What are the key differences between PsA and RA?
Equal sex distribution (RA more common in women)
Asymmetric
Distal (with some exceptions)
Enthesitis
Spondylitis in 40%!
Early bone deformity
Majority RF / CCP negative
Which other condition can Mitral Stenosis mimic?
LVSD. If the mitral valve area is <1, this can mimic LV failure when the LV is functionally normal
Clinical signs of HOCM?
Prominent a due to septal bulging
Double carotid impulse
Reverse split S2
MR (anterior motion of valve)
Louder during Valsalva (reduced pre-load = reduced Starling = obstructed outflow)
Genetics of HOCM?
Autosomal Dominant
Several genes, all encoding sarcomeric proteins
Associated with Friedrich’s ataxia, Fabry’s, WPW
What are the ECG findings of HOCM?
LVH criteria (S1+R6 >35mm)
Deep antero-lateral TWI
Deep infero-lateral Q waves
Which medications must you avoid in HOCM?
Drugs that reduce pre-load as this accentuates the outflow gradient: nitrates, inotropes
Management of HOCM?
Amiodarone if AF
Beta-blockers
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis
What do you know about the genetics of Ehler Danlos syndrome (EDS)?
AD, AR, de novo mutations in gene encoding for collagen III
Principally affects joints, blood vessels, heart, eyes
What are the complications of EDS?
Joints = deformities, pain, impaired function
Skin = easy bruising and fragility
Heart = MVP, MR, AR, Aortic dissection, cardiac conduction abnormalities
Vascular = haemorrhage
GI = bleeding, diverticulae, diaphragmatic herniation, colonic rupture
Eyes = glaucoma, retinal detachment
What do you know about Osteogenesis imperfecta?
AD mutation usually in COL1A1/2 that codes for collagen I
This leads to
B: weak bones and atraumatic fractures
I: Eyes - blue sclera (loss of collagen = choroidal veins visible)
T: Teeth - dentinogenesis imperfecta
E: Ear: otosclerosis (conductive hearing loss)
Cardiac: Valvular disease - MVP, bicuspid aortic valve, AR/aortic root dilation
Rx:
1. Vit D/calcium/bisphosphonates
2. OT/PT
3. Hearing aids
4. Valve replacement/repair if needed
DDX of blue sclera?
EDS
Marfan
Osteogenesis Imperfecta
Pseudoxanthoma elasticum
Diamond Blackfan (Pure red cell aplasia)
What do you know about PXE?
AD/AR ABCC6
Abnormal MINERALISATION of ELASTIN
Mid-dermal deposition of calcium that triggers a metabolic response
Dermis: Pseudoxanthoma plaques and plucked chicken) in axilla/groin/neck
Eyes: Angoid streaks (85%)
Heart: AR, MR, MVP
Vessels: Early plaques, CAD, PVD, HTN, Renovascular disease
GI: haemorrhage due to friable vessels
What are the consequences of Systemic Sclerosis?
GI: Oesophogeal dysfunction, dysphagia, malaborption, SIBO, PBC
Skin: Raynaud’s, gangrene
MSK: arthritis, osteopenia (malabsorption)
Renal: HTN, scleroderma renal crisis
Resp: ILD, pleural effusions
CVD: Restrictive cardiomyopathy, pericarditis, PHTN, conduction defects
What is the usefulness of nailfold capilloroscopy in systemic sclerosis?
The nailfold is one of the few places you can visualise capillaries. There is significant capillary dropout due to microangiopathy, with regeneration of poorly constructed vessels in systemic sclerosis/Raynauds
Diagnostic criteria for SLE?
ANA >1:80 and signs/symptoms/labs suggestive of lupus:
Labs: Anti-dsDNA, Anti-smith, Anti-cardiopilin, lupus anti-coagulant, low C3/C4
Constitutional
Neurological
Mucocutaneous
Photosensitivity
MSK
Serosal
Renal
Haematological
What are the classic skin features of lupus?
Discoid lupus (sun-exposed)
Malar rash on face sparing naso-labial folds
Painless mucosal ulcers
Tender small joints
What pregnancy complications of lupus do you know?
Auto-antibodies can cross the placenta and lead to congenital heart block (Anti-Ro)
What are the renal manifestations of lupus?
6 different types of lupus nephritis, most common and most severe is diffuse proliferative lupus nephritis
How do you treat SLE?
Mainstay is hydroxychloroquine
+/- other DMARDs like AZA, MMF, calcineurin inhibtors (ciclosporin/tac)
Steroids for flares
ACEi if proteinuria
What are the systemic features of lupus?
Anaemia
Arthritis
Raynauds
Dermatomyositis
Discoid rash
Malar rash
Mouth ulcers
ILD, pleural effusions, pleurisy
pericarditis, Libman-Sacks endocarditis, PHTN
CNS involvement
Renal HTN, nephritis
Haematological - lymphadenopathy, splenomegaly
Eyes - Sjogren syndrome
What are the non-spinal features of ankylosing spondylitis?
Anterior uveitis
Aortic regurgitation
AV conduction defects
Enthesitis
Apical fibrosis
Ank spond is a rare cause of amyloidosis
Treatment of ankylosing spondylitis?
NSAIDs
Excercise
DMARD’s in severe cases
Biologics such as anti-TNF (adalimumab, etanercept) and anti-IL17
Rarely, surgery (spinal surgery is usually avoided)
What are the signs of osteomalacia?
Bone fragility
Proximal muscle werakness
Muscle spasms (low Ca)
X ray - looser zones
Bloods:
Low Vit D, Low calcium, raised ALP (trying to stimulate bone actiivty). Low calcium stimulates PTH which stimulates phosphate excretion.
Low Vit D, Low Ca, Low Pho
Raised ALP and raised PTH
What is osteoporosis and how is it different from osteomalacia?
Balance tips towards bone breakdown
Leads to reduced number of osteoid units, however the cells are functionally normal and there is preserved mineralisation (in contrast to osteomalacia where there is reduced mineralisation)
What are risk factors for osteoporosis?
Post-meonopausal
Low calcium
Alcohol
Smoking
Steroids
Thyroxine
Senile osteoporosis
Reduced gravity/weight bearing excercises
How do you assess disease severity of acute flares in UC?
Truelove and Witts’ criteria:
Mild: <4 stools a day
Mod: 4-6 stools a day, no sys upset, CRP <30
Severe: >6 and any signs of systemic upset
What are the indications for surgery in a flare of IBD?
Refractory to medical therapy
Any evidence of dilatation on imaging
Any evidence of fistulating disease
Are there concerns for malignancy in IBD?
Yes, if there is colitis there is concern for colorectal ca and PSC —> cholangiocarcinoma, particularly in UC
After 10 years - surveillance colonoscopy to detect early pre-malignant changes; further colonoscopy depending on risk level at that stage.
How do you assess disease severity in psoriasis?
Psoriasis area and severity index (PASI), and body surface area involved
What environmental triggers for psoriasis do you know?
Trauma
Sunburn
Stress
Smoking
Alcohol
Beta haemolytic strep
Drugs (Lithium, ACEi’s, beta-blockers, NSAID’s, terbinafine, anti-malarials)
What variants of psoriasis do you know?
Plaque
Pustular
Guttate
Palmoplantar
Erythrodermic
Inverse psoriasis (flexor surfaces)
What is Auspitz sign?
Stripping of skin in psoriasis reveals underlying hypertrophied dermal capillaries
What genes are implicated in NF?
NF1 on chromosome 17
NF2 on chromosome 22
Both these genes are TSG’s. Their absence leads to the fibrous tumours arising from the nerves - fibromas
What are the manifestations of NF2?
Schwannomas (acoustic neuromas)
Meningiomas
Cataracts
Retinal hamartomas
Less frequent skin manifestations
Other than skin and nerve involvement, what other organs can be affected in NF?
Lungs - apical fibrosis
Heart - restrictive cardiomyopathy
Spine - scloliosis
Adrenal - phaeochromocytoma
Kidneys - Renal artery stenosis
What are the responsible genes in Tuberous Sclerosis?
TSC1 and TSC2. Both are inherited in an autosomal dominant manner, and their absence leads to uncontrolled mTOR activity. This leads to benign tumours throughout the body (made up of various cell types) and an increased lifetime risk of cancer
Which organs are most often affected in Tuberous Sclerosis?
Brain - gliomas, epindymomas, astrocytomas
Skin - angiofibromas (face), subungal fibromas, ash leaf spots, Shagreen patches
Kidneys - angiomyolipolas (can bleed)
Lungs - lymphangioleiomyomatosis (cysts)
Eyes - reintal hamartomas.
What investigations need to be sent from an LP for suspected meningitis?
- Cell count and differential
- Protein, glucose, lactate
- Gram stain and culture
- Viral PCR
Bacterial meningitis
Raised WCC, predominantly Neutrophils
High protein
Low glucose
Positive gram strain
Viral meningitis
Raised WCC, predominantly lymphocytes
Normal/High protein
Normal glucose
Viral PCR+
Complications of bacterial meningitis?
Severe morbidity
Deafness
Blindness
Cognitive impairment
Vascular - amputations due to sepsis
What are the manifestations of hereditary haemorrhagic telangiectasia?
Skin - telangiectasia
Mucus membranes - epistaxis
GI - bleeding
Lungs - AV malformations
CNS - SAH, migraines, spinal AV = paraparesis
Liver - can lead to liver failure due to AV malformations
What is your differential for telangiectasia?
Systemic Sclerosis
SLE
HHT
Mitral stenosis
Polycythaemia
Carcinoid syndrome
Ataxia telangiectasia
OSA symptom scoring criteria
STOP-BANG questioniarre
Epworth (>11)
OSA Diagnostic test?
Overnight polysomnography for apnoea hypopnea index
What are triggers for dermatomyositis?
Genetic: HLADR3/DR5
Environment: Cocksackie virus, cancers
Which cancers are associated with dermatomyositis?
An underlying malignancy is found in 20-25% of cases of dermatomyositis.
These are typically ovarian, lung, breast
What are the clinical manifestations of dermatomyositis?
Skin:
Gottron’s papules
Heliotrope rash
Malar rash
Shawl sign
Hypertrophy of cuticles
Non-scarring alopecia.
Palmar hyperkeratosis (mechanics hands).
Photosensitive skin changes.
Muscles:
Prox weakness
Atrophy
Dysphagia
Resp muscle weakness
Lungs:
Fibrosing alveolitis
Organising pneumonia
What investigations would you perform for suspected dermatomyositis?
FBC, UE
CK
ANA, Anti Jo1, Anti SRP, Anti M2
Muscle biopsy
Directed screening for underlying malignancy
DDx for Raynaud’s
RA
SS
Lupus
Dermatomyositis
Polymyositis
Myeloproliferative disorders
Hep B/C
Thoracic outlet syndrome
Atherosclerosis
Carpel tunnel
Hypothyroidism
Drugs (beta blockers, cyclosporin)
What are the differences between Raynaud’s disease (primary) and Raynaud’s phenomenon (secondary)?
Primary (R. disease) - <40y
No associated systemic features
NO nailfold capillaries
Never necrotic
Normal ESR
Normal ANA
What drugs can cause Raynaud’s?
Beta blockers
OCP
Ciclosporin
Chemo
Treatment for Raynaud’s
CCB’s
Prostacyclins
Nitrates
Categorise lymphomas
Commonly classified as Hodgkin’s (Reed Sternberg B-cells) and non-Hodgkins.
Non-Hodgkins includes:
High-grade
Lymphoblastic (behaves like ALL)
B-cell (Burkitt’s, DLBCL, Mantle cell, Follicular)
How do you stage Hodgkin’s lymphoma?
Ann-Arbour staging
1. Single node
2. More than one node, same side of diaphragm
3. Above and below diaphragm
4. Extra-nodal
B symptoms at any stage
What is the main treatment for high grade NHL?
R-CHOP
Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Oncovincristine
Prednisolone
and then maintenance Rituximab
What is the treatment for Hodgkin’s lypmphoma?
ABVD
Adriamycin
Bleomycin
Vincristine
Doxarubicin
What are the cardinal features of anti-phospholipid syndrome?
Thrombocytopenia (antibodies against platelets)
Recurrent miscarriages
Arterial (stroke) and/or venous clots (DVTs)
Livedo reticularis
What tests would you perform in suspected antiphospholipid syndrome?
Autoimmune screen
anti-cardiolipin
Anti-beta2glycoprotein 1
anti-phospholipid
Lupus anticoagulant
How do you treat antiphospholipid syndrome?
Primary thromboprophylaxis - low dose aspirin
Secondary thromboprophylaxis - warfarin (INR 2-3, increased to 3-4 if clot on warfarin)
What causes for strokes in young patients do you know off?
Extra-cranial - neck hyperextension
Vasculitis
Cardiac - embolic (mxyoma, endocarditis, valvular pathology, AF)
Substance misuse - cocaine, methamphetamine
Antiphospholipid syndrome
Familial hyperlipidaemia
Sickle cell disease
Rare metabolic/mitochondrial causes such as MELAS
Causes for erythema nodosum?
STREP THROAT!
TB
Sarcoid (Lofgren’s - classical triad of fever, hilar lymphadenopathy and EN)
Myeloproliferative disorders
IBD
Behcet’s
Drugs (OCP, penicillin, sulphonylureas)
What causes erythema multiforme?
HSV
CMV, EBV, influenza, COVID-19
Medications - OCP, penicllin, carbamazapine
Vaccinations
SLE
Sarcoidosis
Malignancy
Mycoplasma pneumonia - now considered a distinct entity
Name some systemic causes for livedo reticularis
Antiphospholipid syndrome
Polycythaemia rubra vera
SLE
Polyarteritis nodosa
GPA/EGPA
Walendenstrom’s
Cholesterol embolism
What do you know about bullous pemphigoid?
Bullous = Basement
Autoimmune type 2 hypersensitivity reaction against hemidesmosomes that anchor basal cells to basal membrane
IgG targets BPAG1+2. This leads to mast cell degranulation and inflammation
Genetic component and environmental triggers (furosemide, penicillamine, NSAIDs, abx)
Nikolsky sign negative (no intraepidermal splitting)
Rx topical and sytemic steroids
What do you know about pemphigus vulgaris?
Autoimmune type 2 hypersensitivity reaction against intra-epidermal desmosomes that hold keratinocytes together in the stratum spinosum layer
Can either affect mucosal cells only (Desmoglein 3) or skin+mucosal cells (Desmoglein 1+3)
Histologically there is tombstoning (intra-epidermal disruption of keratinocytes)
Nikolsy sign positive (lateral pressure causes a split between upper and lower layers of epidermis)
Rx: topical and oral steroids, rituximab, oral rinses with lidocaine
What do you know about Peutz Jegher’s syndrome?
Autosomal dominant mutation in the tumour suppressor gene STK11 that is expressed throughout the GI tract and also various other tissue including skin, breast, lung, ovaries, testicles
Leads to the development of hamartomas in the GI tract that can become malignant. These can lead to bleeding and obstruction.
Skin manifestations include flat mucocutaneous melanocytic macules on the mucosal surfaces and also palms and soles
Risk of GI, breast, lung, ovarian, testicular cancer
What is necrobiosis lipoidica?
Typically affects young female diabetic patients
It is also associated with hypertension, thyroid disease and obesity
It is a disorder of BLOOD VESSELS
Starts as a red papule, becomes a plaque, and then slowly enlarges to a yellow patch with a red rim
Can ulcerate and turn into a squamous cell cancer
What is pyoderma gangrenosum?
Extremely painful
Rapidly enlarging tender full-thickness ulcer with blue borders
Non-infectious neutrophilic dermatosis
More common in over 50’s
Frequently associated with autoimmune conditions such as IBD, RA, GPA
Rx: Urgent immunosupression
Talk me through the Wells DVT score
Paralysis
Cancer
Immobilised
Prev DVT
Is an alternative diagnosis as likely?
Calf swelling, leg swelling, collaterals, tenderness along deep venous system, pitting oedema
1 = D-Dimer
>=2 Doppler
Talk me through the Wells PE score
DVT
Cancer
Immobilised
Prev DVT
Is PE as equally likely as other diagnosis
HR
Haemoptysis
1 = D-Dimer
>2 = CTPA/VQ
What are the components of a thrombophilia screen?
Factor V Leiden
Prothrombin mutation
Protein C
Protein S
Anti-thrombin III (rare but aggressive)
Drug history (OCP)
Are there any scoring criteria you can use to risk stratify patients for inpatient/outpatient Rx for PE?
PESI Score predicts 30-day mortality and takes into consideration history, and clinical findings
What are contraindications for thrombolysis of PE?
Intracranial disease/bleed
Ischaemic stroke (<3mo)
Brain/spine surgery (<3mo)
Internal bleeding
Coag disorder
Recent head trauma
VQ vs. CTPA risks to pregnant pt?
Both have radiation - CTPA radiation comes from the X-rays, VQ radiation comes from the dye.
CTPA = higher dose of X-ray radiation to breast tissue
VQ = higher dose of dye - ionising radiation to fetus, but still very small amounts
Do you know the inheritence of Retinitis Pigmentosa?
AD, AR, X-linked recessive, and 30% are de novo.
Do you know of any syndromes involving retinitis pigmentosa?
Kearns-Sayre: Mitochondrial. Ophthalmoplegia + cerebellar ataxia.
Usher: AR. Sensosineuronal deafness.
Refsum: Ataxia + muscle wasting.
Alport: X linked recessive. Type IV collagen. Haematuria + GS + SN deafness.
What is the treatment of proliferative diabetic retinopathy?
If disease involves fovea = anti-VEGF (benralizumab)
If disease does not involve fovea = laser photocoagulation
What are the clinical signs and symptoms of a retinal vein occlusion?
Reduced visual acuity
RAPD
SWOLLEN disc
Retinal haemorrhages (stormy sunset)
Might develop acute angle closure glaucoma
What are the causes of a retinal arterial occlusion?
The retinal artery is a terminal branch of the ophthalmic artery. Its occlusion can produce retinal infarction.
Can be:
1. Embolic
2. Rapid raised IOP
3. GCA
4. Profound hypotension
5. Vasospasm
6. Hypercoagulable states
What are the signs and symptoms of retinal artery occlusion?
Sudden painless visual loss
Pale retina
Cherry red spot on fovea (choroidal arteries unaffected)
RAPD
What is the treatment for central retinal artery occlusion?
Occular massage
IV acetazolamide/anterior segment paracentesis (reduce IOP)
Treat underlying factor
What are the clinical signs of macular degnereation?
Dry: Drusen + atrophy
Wet: Neovascularisation in choroid
What are the symptoms of macular degeneration?
Central visual loss
Distortion
What is the treatment for macular degeneration?
Anti-VEGF (ranibizumab)
What are the clinical findings of anterior uveitis?
Red
Painful
Asymetric pupil
What conditions is uveitis associated with?
Ank Spond
Behcet’s
MS
Infections: HSV, TB, HIV
What are the risk factors for acute angle closure glaucoma?
Asian, short axial eyeball, older age, pupillary dilation
What are the symptoms of acute angle closure glaucoma?
Extreme pain
Blurred vision
Haloes
Red eye
Mid-dilated or fixed dilated pupil
Corneal oedema
Raised IOP
What is the treatment for acute angle closure glaucoma?
Topical betablockers/pilocarpine
IV acetazolamide
Peripheral laser iridotomy (hole in iris)
What is keratitis?
Inflammation of the cornea
Sight-threatening emergency
Caused by infection (bacterial, fungal, viral) or inflammation (blepharitis induced irritation)
Ix - slit lamp and fluorescein = corneal ulcer
Scleritis vs. episcleritis?
Both associated with inflammatory conditions such as IBD and RA
Scleritis is painful, episcleritis is not
Both look pretty similar
Scleritis is associated with photophobia and gradual decrease in visual acuity
In episcleritis, injected vessels are mobile with gentle pressure and will blanch with phenylephrine drops
Scleritis needs oral NSAID’s /steroids, most cases of episcleritis can be managed conservatively
What do you know about deQuervain’s thyroiditis?
Typically post a viral illness
Phase 1: Lymphocytic infiltration: Hyperthyroidism, raised ESR
Phase 2: euthyroid
Phase 3: Hypothyroidism for weeks-months
Phase 4: Back to normal
Ix: Thyroid scintigraphy: globally reduced uptake of I-131
Rx:
Self-limiting
Pain control - NSAIDs
Steroids if hypothyroid
What classes of diabetic drugs do you know for patients with T2DM?
Biguanide: increase liver and muscle insulin sensitivity (metformin)
SGL-2 inhibitor: Inhibits re-absorption of glucose (dapaglifozin).
DPP4 inhibitors: reduce breakdown of incretins (sitagliptin, linagliptin). Caution if hx pancreatitis/pancreatic cancer. Can use linagliptin in renal impairment
Sulphonylureas: Increase insulin secretion (glizlazide) - risk of hypo’s
Pioglitazone: PPAR-gamma activator = more glucose transports - risk of fluid retention, osteoporotic fractures, and bladder cancer
What are the complications of spina bifida?
Urinary stasis + recurrent infections
Lower limb spasticity
Hydrocephalus
Arnold-Chiari malformations
Recurrent meningitis
Syrinx
What conditions are associated with acanthosis nigricans?
T2DM
Obesity
PCOS
Acromegaly
Cushing’s
What are the features of Williams syndrome?
Spotaneous microdeletion
Mild intellectual impairment
Characteristic facies with broad forehead
Supravalvular aortic stenosis
Steroids in ascending order of potency
Hydrocortisone (Mild)
Betamethasone 0.025%
Fluticasone/Betamethasone 0.1%
Clobetasol
What is the pathophysiology of eczema?
Allergen enters the dermis and triggers a Type I hypersensitivity reaction. On repeat exposure there is IgE mediated mast cell degranulation.
Self-perpetuating cycle of skin breakdown, skin dryness, and itching.
Causes of galactorrhoea?
Physiological (pregnancy)
Prolactinoma
Exercise, stress
Acromegaly (1/3 of patients)
PCOS
Hypothyroidism (Raised TRH stimulates prolactin release)
Drugs (metoclopromide, domperidone, haloperidol, rarely SSRI’s)
Tell me about sickle cell anaemia
AR
HBB gene (beta globin)
Low haptoglobin (intravasc haemolysis)
Scleral icterus, jaundice, bilirubin gallstones
Bone marrow hyperplasia - enlarged skull
Hepatomegaly (extramedullary haematopoiesis)
Autosplenectomy (R/O Strep, haemophilius, Neisseria, Salmonela)
Chest syndrome
Renal necrosis
Priapism
Rx: Prophylaxis, treat infections early, pain relief, hydroxyurea (increases gamma globin = ^ HbF)
Management of infective endocarditis?
- A-E approach, stabilise pt. Blood cultures before treating if possible. Sepsis six, 3x sets of BCs from peripheral sites at different times.
- IV abx: benzylpenicillin + gentamicin OR vancomycin if pen-allergic. If HACEK organism suspected, treat with ceftriaxone OR ciprofloxacin. 4-6 weeks of IV abx.
- Surgery: indications include heart failure, cardiogenic shock, aortic root abscess, expanding vegetation, AV block, prevention of septic emboli
- Temp cardiac pacing is recommended if the pt is in AV block secondary to aortic root abscess.
- Refer to endocarditis MDT
Key points in an alopecia history?
Timing: when did it start, getting worse, sudden/gradual, anything made it better or worse?
Patchy or widespread?
Scarring: more likely to be autoimmune-related
Red/scaly
Scalp/beard/body hair/eyebrows/eyelashes affected?
Does it re-grow white?
Nails
PMH: AI (DM, vitiligo, coeliac, thyroid), tiredness
FH: hair loss?
DH: allergies, chemo, COCP, heparin, warfarin
SH: diet, stress, illness, trauma, surgery, pregnancy
Examination features in alopecia history?
Hair: patchy/widespread, inflamed, scarring, exclamation mark hairs, white hair
Beard, brows, eyelashes, body hair
Nails
Don’t miss vitiligo!
Examine thyroid
Check for conjunctival pallor
Management of alopecia areata?
Mild: reassurance
Topical potent corticosteroid / intralesional triaminoclone
Dithranol or minoxidil 5%
If severe: topical immunotherapy, systemic steroid, PUVA
Trigger control
Support groups, wigs
Types of non-scarring and scarring alopecia?
Non-scarring
Androgenic/ageing
Telogen effluvium
Drug-induced
Areata/totalis/universalis
Scarring
Trauma
SLE
Lichen planus
Scleroderma morphoea
Investigations to perform in a case of alopecia?
Bedside: fungal culture (scraping)
Bloods: TFTs, FBC, iron/ferritin, glucose, ANA (lupus), syphilis serology
Special: dermoscopy (exclamation-mark hairs vs cadaverised hairs), skin biopsy if diagnosis unclear
Ddx of an acute joint?
Haemarthrosis
Trauma
Septic arthritis
Crystal arthritis (gout, pseudogout)
Reactive arthritis
Monoarticular presentation of RA / psoriatic / enteropathic arthritis
Bursitis / cellulitis / OM
Avascular necrosis
Investigations in suspected acute joint?
Bedside: urine dip + culture, stool culture, STI screen, ECG
Bloods: FBC, UE, LFT, CRP, ESR, Ca, Mg, ferritin, TFT, urate, Hba1c, lipids, blood cultures
(Consider: RF, anti-CCP, ANA, HLA-B27 if >1 joint involved)
Imaging: XR joint, MR joint if OM suspected
Special: aspirate joint (pre-abx)
(Contraindicated in prosthetic joints, cellulitis, overlying psoriasis, high INR, low plts)
Tell me what you know about septic arthritis
Common organisms: staph aureus, group A/B strep, gram neg bacilli, gonococcal
Blood culture +ve in 50%, aspirate is +ve in 70-90%
Cause: haematogenous spread, adjacent OM, soft tissue infection near joint, iatrogenic (arthroscopy), trauma
Tell me what you know about gout.
Crystal deposition disease
Disorder of purine metabolism, resulting in hyperuricaemia
Typically monoarthritis of 1st MTP joint, can be polyarticular
Males > females
Can become chronic, presence of tophi indicates severe, recurrent gout. Can get uric acid renal stones and nephropathy
Gout management?
Lifestyle changes: reduce red meat / purine intake, alcohol, weight loss, exercise
Acute phase:
- rest / ice joint, stop diuretics, address lifestyle factors
- NSAIDs + PPI (diclofenac) for 1-2 weeks
- Colchicine 2nd line
- Steroids 3rd line
Prophylaxis:
- Allopurinol (not during acute attack, delays resolution)
- Offer if 2 attacks in 1y / tophi / erosions / renal insufficiency / renal stones / diuretics / pre-chemo
- Aim for urate <300 micromol/L
- Monitor U+E and titrate according to urate
- Start 2wks after attack settled
- Alternative: febuxostat
Management of reactive arthritis?
Bed rest, ice, splints
Treat infection / contact tracing
NSAIDs
IA steroid / oral steroid
DMARDs: MTX, sulfasalazine
Most recover within 1y, 20% become chronic. Complications more likely if HLA-B27 positive.
Investigations for suspected pseudohypoparathyroidism?
Bedside: ECG (QT prolongation, heart block, VF), 24h urinary calcium
Bloods: calcium, magnesium, potassium, phos, pH (VBG), PTH, vit D, UE, ALP, amylase, TFTs, ACTH, adrenal abs, genetic testing
Imaging: renal USS (stones), brain MR (basal ganglia calcification), XR hands (shortened metacarpals)
Tell me about pseudohypoparathyroidism
Kidney and bone resistance to PTH: low calcium, high phos, high PTH, low calcitriol, normal UEs.
No urinary cAMP response to PTH.
Type 1a: GNAS1 mutation. Albright Hereditary Osteodystrophy (AHO) - round face, short stature, short 4th and 5th metacarpal bones, obesity, subcutaneous calcifications and developmental delay.
Type 1b: No phenotypic features of AHO, but similar biochemistry.
Type 2: No phenotypic features of AHO. Normal / raised urinary cAMP response.
Management of pseudohypoparathyroidism?
Management of hypocalcaemia and refer to endocrinology.
May require screening for other endocrinopathies.
What are some causes of hypocalcaemia?
Hypoparathyroidism (low PTH, low calcium)
PTH resistance (pseudohypoparathyroidism)
CKD
Vitamin D deficiency
Bisphosphonates, calcitonin, phenytoin
Acute pancreatitis
Blood transfusion
Rhabdomyolysis
Tumour lysis syndrome
Hyperphosphataemia
How would you localise a lesion in a suspected stroke between the MCA and PCA?
Macular sparing is usually seen in PCA lesions due to the supply from the MCA.
If there is no macular sparing within the HH, then you can localise the lesion to the MCA.
The weakness/numbness would be expected on the contralateral side to the brain lesion.
What are some of the complications that can occur in patients after acute management of ischaemic stroke?
- Thromboembolic disease - give IPC boots
- Risk of further strokes
- Risk of haemorrhagic transformation of ischaemic strokes
- In acute and long-term, there is a risk of seizures
- Swallowing difficulties - risk of aspiration pneumonia
- Higher risk of falls
- Urinary and faecal incontinence
What are the important aspects of secondary prevention in stroke?
Dual antiplatelet therapy (aspirin + clopi)
Lifestyle mods: BP, diet, statins, reduce salt intake, stop smoking, reduce alcohol intake
Further risk factors such as diabetes should be addressed using current guidelines
What is the treatment and prognosis for a reactive arthritis?
Treatment includes:
- Treating the underlying cause (diarrhoeal illness, gonococcal / chlamydial infection)
- Supportive: analgesia, re-hydration if diarrhoeal illness, abx if sexually-transmitted infection
What investigations would you suggest for a suspected reactive arthritis?
Bedside: stool culture, obs, sexual and travel hx.
Bloods: UE, LFTs, CRP/ESR, FBC, cultures, RF + anti-CCP (in case it is first presentation of RA instead).
Imaging: XR of the joint.
Special: aspirate joint, with culture and microscopy looking for crystal arthropathy or septic arthritis.
Can you think of any genetic links to reactive arthritis?
Reactive arthritis is associated with the HLA-B27 gene.
This gene is widely associated with the seronegative spondyloarthropathies which include enteropathic arthritis, reactive arthritis, ankylosing spondylitis and psoriatic arthritis.
What features on ECG would indicate right heart strain in the context of a suspected PE?
‘S1 Q3 T3’
A large S wave in lead I
Q wave in lead III
Inverted T waves in lead III
How would you investigate for suspected PE?
Bedside: observations, ECG (looking for signs of right heart strain)
Bloods: FBC, UE, coag profile, CRP (infection), LFTs
Imaging: CTPA (to exclude PE), CXR (exclude pneumonia or PTX)
Calculate Wells’ score:
- If patient <2 points - low risk, do d-dimer
- 2-5 points - consider d-dimer or CTPA
- >=6 points - do CTPA
Alternative rule-out criteria = PERC score (8-item clinical criteria who identify which pts are low risk of PE and can be discharged from ED).
How would you manage a patient with PE?
Initially start with treatment dose LMWH.
Then switch to oral anticoagulation: warfarin or NOAC.
Treatment duration
If provoked PE: 3 months
If unprovoked PE: 6 months
If acutely unwell / haemodynamically unstable, consider thrombolysis with alteplase, or surgical thrombectomy.
How do you assess hyponatraemia?
Need to assess volume status first.
If hypovolaemic - is urinary Na >20 mmol/l?
- Yes: renal Na loss
- No: loss elsewhere
If euvolaemic - is urine osmolality >300mOsm/kg?
- Yes: SIADH
- No: water intoxication, severe hypothyroidism, Addison’s disease
If hypervolaemic: nephrotic syndrome, CCF, cirrhosis, renal failure
Management of hyponatraemia?
Fundamentals: treat underlying cause + restore normal volume status.
Acute severe hyponatraemia: IV hypertonic saline bolus (100ml 3% NaCl) cautiously.
Hyponatraemia without neurological symptoms:
- correct by no more than 6mmol/L in first 6h
- then no more than 10mmol/L in first 24h
- management depends on cause + fluid status
Hypovolaemic: rehydration with 0.9% normal saline
Euvolaemic: fluid restrict 1.5L per 24h
Hypervolaemic: fluid restrict 1.5L per 24h
(All with regular monitoring of serum sodium levels - if done too fast can cause osmotic demyelination syndrome).
List some causes of pseudohyopnatraemia.
Hyperlipidaemia
Hyperglycaemia
Hyperproteinaemia
Hyperbilirubinaemia
What investigations would you like to do for suspected hyponatraemia?
Bedside:
- urine sodium (differentiates between renal vs extrarenal causes of hypoNa) - very high sodium in renal causes and SIADH
- urine osmolality (to confirm SIADH - increased urine osm + low serum osm suggests SIADH)
Bloods:
- UEs, serum osm (decrease in serum osm to be expected. If normal, suspect pseudohyponatraemia)
- LFTs (albumin), lipids (if pseudo suspected), glucose
- Cortisol (exclude Addison’s), TFTs (exclude hypothyroidism)
Causes of erythema nodosum?
‘SORE SHINS’
Streptococcal infections
OCP
Rickettsia
Eponymous (Behcet’s)
Sulphonamides
Hansen’s disease (leprosy)
IBD / Idiopathic
Non-Hodgkin’s lymphoma
Sarcoidosis
Treatment of idiopathic intracranial hypertension?
Medical:
- Acetazolamide
- Mannitol
Surgical:
- Optic nerve sheath fenestration
- CSF shunting (VP shunt)
Other:
- Weight loss
Causes of hypertension?
Essential (94% - assoc with age / obesity / salt / alcohol)
Renal - CKD
Endocrine - Conn’s, Cushing’s, Acromegaly, Phaeochromocytoma
Aortic coarctation
Pre-eclampsia (pregnancy)
Investigations for diagnosis of ank spond?
- Mainly clinical history + exam, with supporting radiological evidence
- Young patients (<40y) with positive FH
- Plain spine XRs: erosions / sclerosis of SI joints, with squaring of vertebrae
- Bloods: raised CRP / ESR, anaemia of chronic disease
- Genetic screening: HLA-B27
- CXR / HRCT: if suspecting lung fibrosis, consider PFTs
