Short clinical consultations Flashcards

(366 cards)

1
Q

Management of migraine?

A

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

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2
Q

Typical migraine history?

A

Unilateral
Throbbing in nature
Light aversion / phonophobia
Aura / scintillating scotoma
Triggers: behaviours / foods
Onset: acute onset, can last days
Similar episodes in the past

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3
Q

Headache red flags to identify in the history

A

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

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4
Q

Approach to fundoscopic exam?

A

‘ROVM’

  1. Red reflex - obscured in cataracts, corneal scars, vitrous haemorrhage
  2. Optic disc - looking for cup, colour and contour. Normal cup : disc ratio is 0.3
  3. Vessels - start at disc, follow vessels to all 4 quadrants, ask patient to look up, down, left and right
  4. Macula - temporal to disc, use green light for foveal reflex
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5
Q

Fundoscopy features: glaucoma

A

Large cup : disc ratio (>0.5) indicating cupping of disc

Superior polar notching

Nasal displacement of central blood vessels

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6
Q

Fundoscopy features: papilloedema

A

Disc margins are obscured, swollen and hyperaemic

Retinal vessels are tortuous

NB must rule out SOL, signs of increased ICP

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7
Q

Fundoscopy features: optic atrophy with macular scarring

A

Optic disc pallor with cupping

Large area of macular scarring

ARMD = most common cause of macular scarring

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8
Q

Fundoscopy appearances: dry age-related macular degeneration

A

Atrophy of retinal pigment in central macula

Drusen in macular area

NB presence of haemorrhages + oedema in macular area suggests wet macular degeneration

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9
Q

Fundoscopy appearances: hypertensive retinopathy grades 1-4

A

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.

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10
Q

Fundoscopy appearances: retinitis pigmentosa

A

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

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11
Q

Fundoscopy appearances: central retinal vein occlusion (CRVO)

A

‘Stormy sunset’: engorged retinal vein with retinal haemorrhages

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12
Q

Fundoscopy appearances: central retinal artery occlusion (CRAO)

A

Central ‘cherry red spot’ with surrounding pale retina (due to choroidal blood supply to macula remains intact)

Attenuation of arteries + veins

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13
Q

Fundoscopy appearances: branch retinal vein occlusion

A

Tortuosity and dilatation of branch of central retinal vein with AV nipping

Multiple retinal haemorrhages

Microaneurysms + hard exudates

NB must exclude hyperviscosity!

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14
Q

Fundoscopy appearances: background diabetic retinopathy / maculopathy

A

Blot haemorrhages
Hard exudates
Microaneurysms
Circinate exudates

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15
Q

Fundoscopy appearances: pre-proliferative diabetic retinopathy

A

Retinal ischaemia = characteristic here

  • Multiple dot + blot haemorrhages
  • Cotton wool spots (ischaemic areas)
  • IRMA: intra-retinal microvascular abnormalities
  • New vessel formation on the disc
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16
Q

Fundoscopy appearances: proliferative diabetic retinopathy

A

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!)

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17
Q

Fundoscopy appearances: pan-retinal laser photocoagulation

A

Multiple laser scars with areas of hyperpigmentation

Patient will likely have reduced peripheral vision and a degree of night blindness

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18
Q

Fundoscopy appearances: multiple retinal haemorrhages

A

Seen in both deep and superficial layers of the retina

Hyperviscosity states (polycythaemia, waldenstrom’s macroglobulinaemia, myeloma) can lead to this

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19
Q

Fundoscopy appearances: retinal detachment

A

Area of bullous retina showing area of elevation with fluid

Trauma or choroidal metastasis

Painless ‘curtain coming down’ over vision

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20
Q

Discussion: what is retinitis pigmentosa?

A

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

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21
Q

Syndromes that include retinitis pigmentosa and other features to look for to identify them?

A

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

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22
Q

Ddx of fundoscopic appearances of retinitis pigmentosa?

A

Diabetic retinopathy

Laser treatment scars

Infections: toxoplasmosis, rubella

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23
Q

Conditions associated with retinitis pigmentosa?

A

Laurence-Moon-Biedl syndrome
Usher syndrome
Alstrom syndrome
Refsum disease
Kearns-Sayre syndrome

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24
Q

Ddx of bilateral visual loss?

A

Glaucoma
Cataracts
Diabetic retinopathy
Macular degeneration
Papilloedema
Leber’s optic neuropathy (rarer)

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25
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)
26
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. 1. Epistaxis that is spontaneous + recurrent 2. Multiple mucocutaneous telangiectasia 3. Visceral lesions: GI / hepatic / lung / cerebral AVMs 4. FH in 1st degree relative with genetic testing to confirm diagnosis
27
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.
28
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
29
Bloods to test in suspected hyperthyroidism?
Thyroid function tests: T3/4 Autoantibodies: Thyroid peroxidase (TPO) Thyroglobulin TSH-receptor antibodies
30
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
31
Graves' disease management?
Medical: - Carbimazole / PTU - Propranolol for symptoms - Radioactive iodine Surgical: - Thyroidectomy
32
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)
33
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)
34
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)
35
What are the complications of hypothyroidism?
Cardiac: pericardial effusion, CCF Neuro: carpal tunnel syndrome, proximal myopathy, ataxia
36
Management of hypothyroidism?
Thyroxine titrated to TSH suppression + clinical response. NB: can precipitate angina and unmask Addison's disease leading to adrenal crisis.
37
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
38
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
39
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)
40
Radiological features of rheumatoid arthritis?
'SALP' Soft tissue swelling Articular erosions Loss of joint space Periarticular osteopenia
41
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)
42
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)
43
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.
44
Ddx for rheumatoid arthritis?
Any of the seronegative spondyloarthropathies: - psoriatic arthritis - ankylosing spondylitis - reactive arthritis - enteropathic arthritis
45
HLA association for RA?
RA has a strong association with HLA-DR4.
46
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
47
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
48
Classical exam findings for rheumatoid arthritis?
Symmetrical deforming polyarthropathy, typically affecting MCPJs and PIPs Presence of rheumatoid nodules at elbows
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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
60
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
61
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)
62
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)
63
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.
64
What autoimmune syndromes can Addison's disease form a part of?
The autoimmune polyglandular syndromes (type 2) Autoimmune thyroid disease T1DM
65
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
66
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).
67
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
68
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
69
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.
70
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
71
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
72
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
73
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
74
Causes of neuropathic ulcers?
Diabetes mellitus Tabes dorsalis Syringomyelia
75
Investigations for leg ulcers of unknown aetiology?
Doppler USS ABPI (0.8 - 1.2 is normal, <0.8 implies arterial insufficiency) Arteriography
76
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
77
What are the different types of neurofibromatosis?
Type 1: neurofibromas Type 2: bilateral acoustic neuromas Schwannomatosis: painful schwannomas develop on spinal and peripheral nerves
78
Causes of enlarged nerves and peripheral neuropathy?
Neurofibromatosis Leprosy Amyloidosis Acromegaly Refsum's disease
79
Ddx of neurofibromatosis?
LEOPARD syndrome Legius syndrome Proteus syndrome Macrodystrophia lipomatosa
80
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.
81
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
82
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
83
What conditions can be associated with NF1?
Phaeochromocytoma (2%) Renal artery stenosis (2%)
84
Complications associated with NF1?
Epilepsy Sarcomatous change Scoliosis Cognitive delay
85
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
86
87
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
87
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
88
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
89
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
90
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
91
Name some causes of bihilar lymphadenopathy.
Sarcoidosis Infection: TB, mycoplasma, HIV Malignancy: lymphoma, lung cancer, metastasis Pneumoconiosis: silicosis, berylliosis
92
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)
93
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
94
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
95
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
96
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
97
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
98
Management for Ehlers-Danlos syndrome?
MDT approach PT to strengthen muscles Splints / orthoses to prevent joint dislocations Analgesia Activity modification (no contact sports)
99
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)
100
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)
101
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
102
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
103
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
104
Pathophysiology of HSP?
Small-vessel vasculitis: IgA + C3 deposition Normal or raised platelet count (distinguishes from other causes of purpura) Children > adults, Male > female
105
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
106
Causes of secondary hyperlipidaemia?
Hypothyroidism Nephrotic syndrome Alcohol Cholestasis
107
Treatment of necrobiosis lipoidica diabeticorum?
Topical steroid and support bandaging. Tight diabetic control does not help.
108
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
109
Features of malignant melanoma?
'ABCDE' - appearance of lesion Asymmetrical Border irregularity Colour - black, irregular pigmentation Diameter >6mm Enlarging Metastases (draining LNs, hepatomegaly, bone tenderness)
110
Management of malignant melanoma?
- Excision - Staged on Breslow thickness (maximal depth of tumour invasion into dermis) - Glass eye + ascites - think ocular melanoma!
111
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
112
Features of BCC?
Usually on face / trunk (sun-exposed areas) Pearly nodule with rolled edge Superficial telangiectasia Ulceration in advanced lesions Other lesions
113
Treatment of BCC?
Natural history: grows slowly over months, rarely metastasizes Treatment: - surgical excision +/- radiotherapy - curettage / cryotherapy if superficial
114
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.
115
Causes of sabre tibia?
Paget's Osteomalacia Syphilis
116
Complications of Paget's disease?
Osteogenic sarcoma Basilar invagination (cord compression) Kidney stones
117
Causes of angioid streaks (in the retina)?
Paget's PXE Ehlers-Danlos Syndrome
118
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
119
Management of Paget's disease?
Bisphosphonates Calcitonin Surgery (for fractures, degenerative arthritis, bone deformity)
120
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)
121
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
122
What are some indications for photocoagulation treatment in diabetic retinopathy?
Maculopathy Proliferative and pre-proliferative diabetic retinopathy
123
Complications of proliferative diabetic retinopathy?
Vitreous haemorrhage Traction retinal detachment Neovascular glaucoma
124
Clinical signs of cataracts on fundoscopy?
Loss of red reflex Cloudy lens May have RAPD with normal fundi Associations: myotonic dystrophy (with bilateral ptosis)
125
Causes of cataracts?
Congenital: Turner's, rubella Acquired: age (usually bilateral), diabetes, steroids, radiation, trauma, storage disorders
126
Treatment of cataracts?
Surgery (as an outpatient): - Phacoemulsification with prosthetic lens implantation - YAG laser capsulotomy
127
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
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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)
129
Causes of delirium?
'PINCHME' Pain Infection Nutrition Constipation Hydration Medication Environment
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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
131
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
132
What is the FRAT score used for?
Indicates a patient's risk of falling and guides further management for worsening mobility / falls. 1. Falls in the last year 2. 4+ meds per day 3. Dx stroke / PD 4. Balance issues 5. Can they get up from a chair without using arms <3 points = lower risk >3 points = higher risk
133
What is the FRAX tool used for?
FRAX predicts the 10-year probability of a patient having a major osteoporotic fracture.
133
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
134
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)
135
Which medications add to anticholinergic burden?
'PC SOAP' Promethazine Cetirizine Solifenacin Oxybutynin Amitriptyline Prochlorperazine
136
137
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.
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Ddx of TIA?
Hemiplegic migraine Hypoglycaemia Seizure Syncope GCA Electrolyte disturbances
139
List some causes of CVA in younger patients?
Antiphospholipid syndrome Extracranial dissection Vasculitis Substance abuse: cocaine / methamphetamines Metabolic / mitochondrial disease Sickle cell disease
140
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.
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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
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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
143
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
144
Management of eczema?
Avoid precipitants Topical: emollients, steroids, tacrolimus Antihistamines for itch Abx for secondary infection UV light therapy PO prednisolone in severe cases
145
Causes of nail pitting?
Psoriasis Lichen planus Alopecia areata Fungal infections
146
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
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Definition of psoriasis?
Epidermal hyperproliferation and accumulation of inflammatory cells
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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)
149
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.
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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
151
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
152
What antibodies are SLE-specific?
ANA anti-dsDNA elevated immunoglobulins
153
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
154
Drugs that can cause drug-induced lupus?
Hydralazine Procainamide Isoniazid Phenytoin Interferon
155
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)
156
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
157
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?
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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
159
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.
160
What is CREST syndrome?
CREST is a type of limited systemic sclerosis. It consists of: - Calcinosis - Raynaud's phenomenon - Esophageal dysmotility - Sclerodactyly - Telangiectasia
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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.
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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)
163
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
164
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)
165
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)
166
What pre-treatment investigations must be considered before starting anti-TNF?
Immunisations Screen for active and latent TB with CXR and blood test
167
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
168
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)
169
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
170
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
171
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
172
How is ankylosing spondylitis disease activity measured?
Using the BASDAI: Bath Ankylosing Spondylitis Disease Activity Index. - 10-point scale - anything >4 indicates active disease
173
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
174
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
175
Investigations to perform in suspected case of Cushing's syndrome?
1. Confirm high cortisol - 24h urinary collection - low dose dex suppression test (won't suppress cortisol if +ve) 2. If elevated cortisol, identify cause - ACTH level: if high, ACTH-secreting tumour / pituitary adenoma. If low, adrenal adenoma / carcinoma. 3. Other tests - MRI pituitary fossa +/- adrenal CT +/- whole body CT to identify lesion - Inferior petrosal sinus vein sampling (pituitary vs ectopic origin)
175
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
176
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
177
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)
178
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.
179
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.
180
Why do acromegalic patients get visual disturbance?
Classically, a bitemporal hemianopia occurs. This is due to compression by the adenoma on the optic chiasm.
181
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)
182
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
183
Management of the complications of acromegaly?
OSA: CPAP CCF: diuretics, ACEi's, beta blockers Diabetes: hypoglycaemic agents Anterior pituitary deficiency: hormone replacement
184
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.
185
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.
186
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)
187
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.
188
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.
189
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.
190
Causes of bilateral extra-ocular palsies
Myasthenia gravis Graves' disease Mitochondrial cytopathies (CPEO) Miller-Fisher variant of GBS Cavernous sinus pathology
191
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
192
What causes myasthenia gravis?
Anti-nicotinic ACh receptor antibodies affect neurotransmission.
193
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%)
194
Causes of bilateral facial nerve palsy?
Guillain-Barre Syndrome Sarcoidosis Lyme disease Myasthenia gravis Bilateral Bell's palsy
195
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
196
Causes of 7th nerve palsy?
Bell's palsy Ramsay-Hunt syndrome Mononeuropathy (diabetes, sarcoid) Tumour / trauma MS / stroke
197
What is Bell's phenomenon?
The eyeball rolls up on attempted eye closure (seen in Bell's palsy)
198
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)
199
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
200
Causes of central retinal artery occlusion?
Embolic: carotid plaque rupture / cardiac mural thrombus GCA: tender scalp + pulseless temporal arteries
201
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
202
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
203
Causes of central retinal vein occlusion?
HTN Hyperglycaemia / diabetes Hyperviscosity syndromes: Waldenstrom's macroglobulinaemia or myeloma Increased intraocular pressure (glaucoma)
204
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)
205
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)
206
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
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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.
208
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?
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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)
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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
211
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
212
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
213
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
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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
215
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)
216
Management of pituitary apoplexy?
Medical: hormone replacement Surgical: transsphenoidal surgery if mass effect
217
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.
218
Ddx for psoriatic arthritis?
Rheumatoid arthritis Other seronegative spondyloarthropathies: ank spond, reactive arthritis, enteropathic arthritis Osteoarthritis Crystal arthropathy (gout, pseudogout)
219
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
220
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
221
Extra-articular features of psoriatic arthritis?
Nail involvement in 80% - pitting, ridging, hyperkeratosis, onycholysis Ocular involvement - conjunctivitis, iritis
222
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
223
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
224
What two cell types are found in sarcoidosis?
Non-caseating granulomas and Langhans giant cells.
225
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
226
Features of yellow nail syndrome?
Discoloured, dystrophic and thickened nails. A condition associated with lymphoedema, pleural effusions and bronchiectasis in 40% of cases.
227
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)
228
How do you quantify a RA flare?
DAS28 1. Number of swollen/tender joints 2. Global pain score 3. ESR/CRP
229
What are the diagnostic criteria for RA?
ACR/EULAR 1. No. LARGE joints 2. No. SMALL joints 3. ESR/CRP 4. Anti-RF/CCP 5. >6 weeks duration
230
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
231
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.
232
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
233
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
234
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)
235
Genetics of HOCM?
Autosomal Dominant Several genes, all encoding sarcomeric proteins Associated with Friedrich’s ataxia, Fabry’s, WPW
236
What are the ECG findings of HOCM?
LVH criteria (S1+R6 >35mm) Deep antero-lateral TWI Deep infero-lateral Q waves
237
Which medications must you avoid in HOCM?
Drugs that reduce pre-load as this accentuates the outflow gradient: nitrates, inotropes
238
Management of HOCM?
Amiodarone if AF Beta-blockers Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis
239
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
240
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
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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
242
DDX of blue sclera?
EDS Marfan Osteogenesis Imperfecta Pseudoxanthoma elasticum Diamond Blackfan (Pure red cell aplasia)
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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
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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
245
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
246
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
247
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
248
What pregnancy complications of lupus do you know?
Auto-antibodies can cross the placenta and lead to congenital heart block (Anti-Ro)
249
What are the renal manifestations of lupus?
6 different types of lupus nephritis, most common and most severe is diffuse proliferative lupus nephritis
250
How do you treat SLE?
Mainstay is hydroxychloroquine +/- other DMARDs like AZA, MMF, calcineurin inhibtors (ciclosporin/tac) Steroids for flares ACEi if proteinuria
251
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
252
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
253
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)
254
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
255
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)
256
What are risk factors for osteoporosis?
Post-meonopausal Low calcium Alcohol Smoking Steroids Thyroxine Senile osteoporosis Reduced gravity/weight bearing excercises
257
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
258
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
259
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.
260
How do you assess disease severity in psoriasis?
Psoriasis area and severity index (PASI), and body surface area involved
261
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)
262
What variants of psoriasis do you know?
Plaque Pustular Guttate Palmoplantar Erythrodermic Inverse psoriasis (flexor surfaces)
263
What is Auspitz sign?
Stripping of skin in psoriasis reveals underlying hypertrophied dermal capillaries
264
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
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What are the manifestations of NF2?
Schwannomas (acoustic neuromas) Meningiomas Cataracts Retinal hamartomas Less frequent skin manifestations
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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
267
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
268
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.
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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+
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Complications of bacterial meningitis?
Severe morbidity Deafness Blindness Cognitive impairment Vascular - amputations due to sepsis
271
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
272
What is your differential for telangiectasia?
Systemic Sclerosis SLE HHT Mitral stenosis Polycythaemia Carcinoid syndrome Ataxia telangiectasia
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OSA symptom scoring criteria
STOP-BANG questioniarre Epworth (>11)
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OSA Diagnostic test?
Overnight polysomnography for apnoea hypopnea index
275
What are triggers for dermatomyositis?
Genetic: HLADR3/DR5 Environment: Cocksackie virus, cancers
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Which cancers are associated with dermatomyositis?
An underlying malignancy is found in 20-25% of cases of dermatomyositis. These are typically ovarian, lung, breast
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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
278
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
279
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)
280
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
281
What drugs can cause Raynaud’s?
Beta blockers OCP Ciclosporin Chemo
282
Treatment for Raynaud’s
CCB’s Prostacyclins Nitrates
283
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)
284
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
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What is the main treatment for high grade NHL?
**R-CHOP** Rituximab Cyclophosphamide Hydroxydaunorubicin Oncovincristine Prednisolone and then maintenance Rituximab
286
What is the treatment for Hodgkin’s lypmphoma?
**ABVD** Adriamycin Bleomycin Vincristine Doxarubicin
287
What are the cardinal features of anti-phospholipid syndrome?
Thrombocytopenia (antibodies against platelets) Recurrent miscarriages Arterial (stroke) and/or venous clots (DVTs) Livedo reticularis
288
What tests would you perform in suspected antiphospholipid syndrome?
Autoimmune screen anti-cardiolipin Anti-beta2glycoprotein 1 anti-phospholipid Lupus anticoagulant
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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)
290
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
291
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)
292
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
293
Name some systemic causes for livedo reticularis
Antiphospholipid syndrome Polycythaemia rubra vera SLE Polyarteritis nodosa GPA/EGPA Walendenstrom’s Cholesterol embolism
294
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
295
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
296
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
297
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
298
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
299
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
300
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
301
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)
302
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
303
What are contraindications for thrombolysis of PE?
Intracranial disease/bleed Ischaemic stroke (<3mo) Brain/spine surgery (<3mo) Internal bleeding Coag disorder Recent head trauma
304
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
305
Do you know the inheritence of Retinitis Pigmentosa?
AD, AR, X-linked recessive, and 30% are de novo.
306
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.
307
What is the treatment of proliferative diabetic retinopathy?
If disease involves fovea = anti-VEGF (benralizumab) If disease does not involve fovea = laser photocoagulation
308
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
309
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
310
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
311
What is the treatment for central retinal artery occlusion?
Occular massage IV acetazolamide/anterior segment paracentesis (reduce IOP) Treat underlying factor
312
What are the clinical signs of macular degnereation?
Dry: Drusen + atrophy Wet: Neovascularisation in choroid
313
What are the symptoms of macular degeneration?
Central visual loss Distortion
314
What is the treatment for macular degeneration?
Anti-VEGF (ranibizumab)
315
What are the clinical findings of anterior uveitis?
Red Painful Asymetric pupil
316
What conditions is uveitis associated with?
Ank Spond Behcet’s MS Infections: HSV, TB, HIV
317
What are the risk factors for acute angle closure glaucoma?
Asian, short axial eyeball, older age, pupillary dilation
318
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
319
What is the treatment for acute angle closure glaucoma?
Topical betablockers/pilocarpine IV acetazolamide Peripheral laser iridotomy (hole in iris)
320
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
321
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
322
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
323
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
324
What are the complications of spina bifida?
Urinary stasis + recurrent infections Lower limb spasticity Hydrocephalus Arnold-Chiari malformations Recurrent meningitis Syrinx
325
What conditions are associated with acanthosis nigricans?
T2DM Obesity PCOS Acromegaly Cushing’s
326
What are the features of Williams syndrome?
Spotaneous microdeletion Mild intellectual impairment Characteristic facies with broad forehead Supravalvular aortic stenosis
327
Steroids in ascending order of potency
Hydrocortisone (Mild) Betamethasone 0.025% Fluticasone/Betamethasone 0.1% Clobetasol
328
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.
329
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)
330
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)
331
Management of infective endocarditis?
1. A-E approach, stabilise pt. Blood cultures before treating if possible. Sepsis six, 3x sets of BCs from peripheral sites at different times. 2. IV abx: benzylpenicillin + gentamicin OR vancomycin if pen-allergic. If HACEK organism suspected, treat with ceftriaxone OR ciprofloxacin. 4-6 weeks of IV abx. 3. Surgery: indications include heart failure, cardiogenic shock, aortic root abscess, expanding vegetation, AV block, prevention of septic emboli 4. Temp cardiac pacing is recommended if the pt is in AV block secondary to aortic root abscess. 5. Refer to endocarditis MDT
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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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
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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.
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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)
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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.
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Management of pseudohypoparathyroidism?
Management of hypocalcaemia and refer to endocrinology. May require screening for other endocrinopathies.
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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
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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.
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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
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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
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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
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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.
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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.
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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
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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).
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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.
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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
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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).
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List some causes of pseudohyopnatraemia.
Hyperlipidaemia Hyperglycaemia Hyperproteinaemia Hyperbilirubinaemia
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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)
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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
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Treatment of idiopathic intracranial hypertension?
Medical: - Acetazolamide - Mannitol Surgical: - Optic nerve sheath fenestration - CSF shunting (VP shunt) Other: - Weight loss
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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)
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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