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
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
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.
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
What are the features of Williams syndrome?
Spotaneous microdeletion
Mild intellectual impairment
Characteristic facies with broad forehead
Supravalvular aortic stenosis
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
