Consultation Flashcards
Acromegaly
PC:
Early morning headache, nausea, bitemporal hemianopia, loss of libido, galactorrhoea, change in appearance, tight-fitting jewellery, increase in shoe size, sweaty coarse skin
PMH:
DM?
Complications:
A acanthosis and apnoea
B high BP
C carpal tunnel
D DM
E enlarged organs
F field defect (BH)
G goitre and GI malignancy
H heart failure and hypopituitary
I IGF-1
J joint arthropathy
K kyphosis
L lactation
M proximal myopathy
Ix:
-IGF1 raised
-OGTT (GH not suppressed)
-MRI pituitary
-Assess for other pituitary functions (TSH, ACTH, PRL, testosterone)
Ix for complications:
-CXR (cardiomegaly)
-ECG (ischaemia)
-Glucose
-Visual perimetry
-OSA investigations (Epworth sleep score)
Mx:
-Trans-sphenoidal surgery or RTx (SE: panhypopituitarism)
-Medical treatment with somatostatin analogues or dopamine agonists or GH receptor antagonists
-DVLA
Follow-up:
Annual GH, PLT, ECG, visual fields and MR head
N.B. Causes of acanthosis nigricans obesity, T2DM, acromegaly, Cushing’s, malignancy (gastric carcinoma)
N.B. Causes of macroglossia include acromegaly, amyloidosis, hypothyroidism, Down’s
Causes of galactorrhea
Prolactinoma
Drugs e.g. dopamine receptor blockers
Physiological
Amenorrhea
PC:
Primary (never had period) or secondary
?Pregnancy
Extreme exercise (hypothalamic), dietary changes, weight changes, hot/cold intolerance, headache, visual field loss (pituitary adenoma e.g. PLToma), loss of libido, excessive thirst, galactorrhoea (PLToma), anosmia (Kallmann’s)
PMH:
Gynaecological
?Parathyroidectomy and thyroid disorders
DH:
Antipsychotics, antidepressants
FH:
MEN1 or ovarian failure/premature menopause
DDx:
-If primary, think Turner’s
-Pituitary adenoma (most commonly prolactinoma, link MEN1)
-Pregnancy or post-partum
-PCOS
-POF
-Poor intake i.e. eating disorder
-Pills i.e. drug causes
Ix:
-PT
-Prolactin, FSH, estradiol, TSH, androgens
-PTH, Ca, glucose
-US abdomen (PCOS or structural cause)
-MR head
-Karyotyping (AIS, Turner’s)
Mx:
-Observe, hormonal treatment, RTx, trans-sphenoidal surgery
-Genetic counselling if MEN1
-Fertility specialist if pituitary lesion ruled out
-Bone health
N.B. MEN1 is AD = Parathyroid hyperplasia Pancreatic tumours Pituitary tumours
N.B. Turner’s is diagnosed on karyotyping (45X)
Short stature, webbed neck, low-set ears and hairline, widely spaced nipples, ASD, bicuspid AV, coarctation, deafness, DM
Diabetes drugs
Metformin
Increases liver sensitivity to insulin
SE: GI, renal
SGLT-2i
Dapagliflozin
Increases glucose excretion in urine
SE: UTI, euglycaemic KA
Sulphonylurea
Gliclazide
Stimulates pancreatic β-islet cells increasing endogenous insulin
SE: hypoglycaemia, weight gain, SIADH
GLP-1 analogues
Ozempic
“Incretin effect” to enhance GLP-1 action
SE: WL, pancreatitis
DPP4i
Gliptins
Increases incretins (e.g. GLP1) increase insulin
SE: less effective, pancreatitis, weight neutral
Neurofibromatosis type 1 (BMJ) (Final)
PC:
Headache, vision (optic glioma), seizures (epilepsy), BP (RAS, phaeochromocytoma), palpitations (phaeochromocytoma), hearing (acoustic neuroma), school (reduced IQ), GI symptoms, back pain (scoliosis), pain due to peripheral nerve neurofibromas
FH
Ix:
-Genetic testing to confirm
-BP (phaeochromocytoma, RAS)
-NCS/EMG
-Ophthalmology assessment
-MR or CT scans (may demonstrate features compatible with optic pathway gliomas, other brain tumours, hydrocephalus, paraspinal neurofibromas, or MPNSTs)
-Consider biopsy (if concerns regarding malignant peripheral nerve sheath tumours)
Mx:
-MDT geneticist, neurologist, plastic surgeon, orthopaedic surgeon, opthalmologist
-Annual review, monitoring BP, for malignant change, compressive symptoms etc.
-Treat epilepsy and hypertension
-Consider surgery for selected lesions
-Emergency surgical removal in phaeochromocytoma or malignant peripheral nerve sheath tumours
NF1 is chromosome 17
NF2 is 22
N.B. In NF2 there will be bilateral vestibular schwannomas, intracranial meningiomas and NO café au lait
Orthostatic hypotension
Ix:
SBP >20 mmHg (>30 mmHg in patients with hypertension) DBP >10 mmHg within 3 minutes of standing
Tilt table test
Mx:
-Avoid drugs such as alpha-blockers, TCAs, PDE-5 inhibitors, BB
-Sit before going to standing and avoid straining or Valsalva
-Hot environments may worsen
-Fluid and Na intake
-Consider short acting pressor such as midodrine
-In those without HF or HTN, consider fludrocortisone (may need Sando-K)
Cushing’s
PC:
Fatigue, bruising, weight gain, menstrual changes, lack of libido, acne, hirsutism, psychiatric symptoms, infections, depression, proximal myopathy, bitemporal hemianopia and skin hyperpigmentation (if endogenous), DM, HTN
PMH:
Any steroids?
ETOH excess (pseudo-Cushing’s)?
Cause:
-Exogenous steroids most common
-ACTH-dependent: Cushing’s disease (ACTH-secreting pituitary adenoma) OR ectopic ACTH (e.g. bronchogenic carcinoma)
-ACTH-independent adrenocortical adenomas or carcinomas
Complications:
HTN, DM, osteoporosis, proximal myopathy
Ix to diagnose:
-Confirm high cortisol with e.g. 1mg overnight dexamethasone suppression test, low dose dexamethasone suppression test (if suppressed cortisol could be alcohol or obesity i.e. pseudo)
-ACTH level (if high, ACTH-dependent, if low adrenal tumour)
-MRI pituitary +/- adrenal CT +/- CT-TAP (ectopic)
-Bilateral inferior petrosal sinus vein sampling (in some centres) if no obvious pituitary lesion on MR
Other Ix:
-PT (can cause high cortisol)
For complications:
-Urine dip and U+Es (Na) (hypertension)
-ECG and echo (hypertension)
-Bone disease (DEXA)
-Glucose +/- HbA1c (diabetes)
Tx:
-Refer to endocrine
-Trans-sphenoidal surgery for pituitary
-OR medical therapy alone e.g. somatostatin analogue or dopamine agonist or steroidogenesis inhibitor
-Adrenalectomy for adrenal disease
-Treat underlying cause of ectopic ACTH
-Pituitary irradiation
N.B. Nelson’s bilateral adrenalectomy in Cushing’s causing +++ACTH (and MSH) and pituitary overgrowth
Hyperthyroidism
PC:
Goitre (if tender = thyroiditis), anxiety, insomnia, impaired concentration, heat, sweaty, weight loss, increased appetite, tremor, palpitations, pruritis
Ask about eye problems:
Gritty, water eye with photophobia and pain, red eye, pressure, keratitis
Loss of colour vision followed by central scotoma = compressive optic neuritis = sight threatening!
Eye signs: proptosis, chemosis, exposure keratitis, opthalmoplegia, lid retraction, lid lag
Peripheral signs: acropachy, pretibial myxoedema, sweating, tremor, palmar erythema, tachycardia or AF, brisk reflexes, HTN, proximal myopathy
Bold = specific to Graves’
Causes:
-Graves’
-Toxic nodular goitre
-Transient hyperthyroid phase in De Quervain’s or post-partum thyroiditis
-Iodine induced (e.g. contrast or amiodarone)
-Pituitary adenoma (TSH-producing)
Ix:
-TFTs, antibodies
-ECG
-PT
-Radioisotope scanning (increased uptake in Graves’, decreased in thyroiditis)
-Thyroid US (to detect thyroid nodules, Doppler will show increased flow in Graves’)
Tx:
-Propranolol for symptoms
-Block and replace (thionamide plus thyroxine)
-If fails, consider radioiodine or thyroidectomy
-Severe opthalmoplegia may require high-dose steroids, irradiation or surgery
-Stop smoking
N.B.
Treatment of thyrotoxic strorm should be ITU/endocrine led
Anti-thyroid drugs, beta blockers, steroids, iodine solution
Anti-thyroid drugs associated with agranulocytosis and ANCA vasculitis
N.B. Graves’ patients can be hyper- eu- or hypothyroid depending on stage
Other differentials would be carcinoid or phaeochromocytoma
Differentials for a thyroid mass:
-Colloid nodule
-Grave’s
-Hashimoto
-De Quervain’s
-Multinodular goitre
-Adenoma
-Thyroglossal or thyroid cyst
-Thyroid malignancy (primary or metastases)
-Parathyroid malignancy
Differentials for thyroid cancer:
-Papillary (most common)
-Follicular (2nd most common)
-Medullary (MEN)
-Anaplastic (rapidly enlarging and painful with poor prognosis)
-Lymphoma
Hypothyroidism
PC:
Fatigue, cold, weight gain, constipation, hair loss, brittle nails, oedema, oligomenorrhoea, low libido
PMH:
Previously treated thyroid disease, autoimmune disease (vitiligo and Sjogren’s linked to Hashimoto’s), hypercholesterolaemia, IHD
DH:
Amiodarone, lithium
Causes:
-Autoimmune: e.g. Hashimoto’s (lymphocytic infiltration)
-Iatrogenic: post-thyroidectomy or iodine, amiodarone, lithium
-Iodine deficiency (globally most common cause)
-Genetic: Pendred’s syndrome which causes SNHL
-De Quervain’s thyroiditis
-Post-partum thyroiditis
-Central hypothyroidism (pituitary adenomas most common)
Ix:
-TFTs and autoantibodies, FBC, U+Es, lipids
-ECG and CXR (IHD, pericardial effusion, CCF)
-Consider thyroid US +/- FNA
Mx:
-Thyroxine (can precipitate angina or Addison’s)
-Check TSH every 8-12 weeks after dose change
N.B. In subclinical, many experts treat if TSH >10
Diabetic retinopathy*
Background retinopathy:
-Hard exudates
-Flame and dot haemorrhages
-Microaneurysms
Pre-proliferative:
-Cotton wool spots
-Venous beading
-IRMA
Proliferative:
-NVD
-NVE
-Pan-retinal photocoagulation
Diabetic maculopathy:
Macular oedema or hard exudates within one disc space from the fovea
Refer to ophthalmology if pre-proliferative or proliferative or clinically significant changes near the macula
Tx:
-Tight glycaemic control (may transiently worsen)
-Treat other risk factors
-VEGF inhibitors
-Photocoagulation if maculopathy or proliferative (pan-retinal versus focal)
Complications of proliferative:
Vitreous haemorrhage, retinal detachment, neovascular glaucoma
Causes of cataracts?*
Congenital: rubella, Turner’s, myotonic dystrophy
Acquired: age, DM, steroids, radiation, trauma, storage disorders
Tx:
Phacoemulsification with prosthetic lens implantation
Necrobiosis lipoidica*
Well-demarcated plaques with waxy-yellow centre and red-brown edges and telangiectasia
Topical steroids
Good glucose control doesn’t help
Syncope
PC:
Before, during, after
DDx:
-Cardiac: arrhythmia or cardiac lesion (AS, HOCM)
-Neurological: epilepsy or SOL
-Vascular: vertebrobasilar insufficiency, subclavian steal syndrome, carotid sinus hypersensitivity
-Mtabolic: hypoglycaemia, ETOH withdrawal seizures
-Orthostatic hypotension (drugs)
-Vasovagal syncope
-NEAD
OE:
Cardiac
Neurologial
Ix:
-ECG and echo +/- Holter or ILR +/- EP study or ETT
-L/S BP +/- tilt table test
-BM
-CT brain or EEG
Types of seizure
-Generalised (absence, tonic-clonic, atonic)
-Partial (simple (when patient is aware), complex)
Epilepsy is diagnosed when 2 or more unprovoked seizures >24 hours apart
Seizure causes
-Epilepsy (infection, drugs reducing threshold)
-Hypoglycaemia or other metabolic causes (e.g. uraemia)
-ETOH withdrawal or drugs
-SOL or stroke (haemorrhagic or ischaemic)
-Meningitis
Lyme disease
Tick bite borrelia burgdorferi
-Erythema migrans, fever, headache, joint pain sometimes facial palsy
-Lyme carditis (heart block, CP, SOB)
-Diagnosed by positive antibody several weeks after infection
-Antibiotics and consider pacing
Differentials for SOB
ILD
Pulmonary HTN
Asthma/COPD
PE/PTX
Malignancy
Bronchiectasis
Infection
HF/valve disease/arrhythmia
Anaemia
Haemoptysis
PC:
Haemoptysis, SOB, CP, weight loss, bone pain or liver pain, fatigue, neurology (brain mets), paraneoplastic e.g. neuropathy, pneumonia symptoms
PMH:
Smoking, occupational
Previous VTE, surgery, long haul flights, immobility, Ca, pregnancy, COCP
OE:
Loud P2
JVP
Lymphadenopathy, trachea, effusion
Look for hepatomegaly, spine tenderness, focal neurology
Ix:
If PE:
Well’s then d-dimer or CT-PA depending on pre-test probability
Also BNP, troponin and lactate and echo to look for RH strain
If Ca:
See respiratory
Mx:
If PE:
Consider thrombolysis for massive life threatening PE
Otherwise, anticoagulate
If CI to anticoagulation consider IVC filter
If unprovoked look for:
Nephrotic syndrome
Examine for malignancy
Further investigation for malignancy should be based on history and examination
Consider thrombophilia screen (includes factor V Leiden, protein C and S)
Ensure follow-up
CTPA versus VQ
CTPA scan higher dose radiation to breast tissue
Higher dose to foetus in VQ scan
Usually VQ preferred in pregnancy
Paget’s
PC:
Usually asymptomatic change in bone shape
Can get entrapment neuropathy e.g. CTS, deafness, fragility fractures, high OP CCF
Ix:
-Very high ALP, calcium may may normal or mildly elevated, normal phosphate
-X-ray ‘moth-eaten’ i.e. osteoporosis circumscripta
-Increase uptake on bone scan
Tx:
-Bisphosphonates (Ca and vitamin D should be normal before starting)
-PT/OT/orthotics
-Symptomatic
Complications:
CTS, osteosarcoma, cord compression, kidney stones, deafness, CCF
Osteoporosis
Ix:
-Bone profile, ALP, PTH, Ca, vitamin D
-Diagnosis is based on a history of prior fragility fracture or low bone mineral density (T-score ≤-2.5)
-FRAX predicts the 10-year probability of a patient having a major osteoporotic fracture
-Think about other causes (hyperthyroidism, Cushing’s, hypogonadism, myeloma, CKD, bone metastases)
Mx:
-Bisphosphonates
-Denosumab, PTH analogue
-Ca and vitamin D
-Exercise
Risk factors:
Age
Female
White ancestry
Low BMI
Steroids
Hypogonadism
Secondary amenorrhoea
Smoking and alcohol
Vitamin D deficiency
Aromatase inhibitor treatment (in women)
N.B.
OP = low bone density and micro-architectural defects in bone tissue
Osteomalacia = incomplete mineralisation of the underlying mature osteoid
Hypercalcaemia
PC:
Bones, stones, abdominal groans and moans (plus thirst and polyuria (nDI) and weakness)
Underlying cause: malignancy, sarcoidosis (dry cough), Addison’s (if other autoimmune conditions)
MH:
Thiazides, lithium, Ca or vitamin D
FH:
Familial hypocalciuric hypercalcaemia
MEN
Causes:
-Primary hyperparathyroidism
-Malignancy: MM, bony metastases, PTH-rP secretion
-Medications: thiazides, lithium, Ca or vitamin D, milk-alkali syndrome
-Sarcoidosis
-Familial
Ix:
-Bone profile (phosphate), PTH, vitamin D, FBC, U+E, TFTs, LFTs (ALP), myeloma screen, serum ACE
-Urinary calcium
-ECG to look at QT
-CXR (masses, effusions, hilar lymphadenopathy)
-Consider CT imaging if suspected solid organ malignancy
-Consider parathyroid US and Sesta-MIBI scan
-Consider DEXA
Mx:
-If >3.0, IV rehydration and IV bisophosphonates (nadir at 3 days)
-Consider calcitonin or denosumab but under specialist guidance
-Treat underlying cause
Ankylosing spondylitis
PC:
Back and joint pain and stiffness (exacerbated by immobility) for >3 months
Fever and fatigue
Ask about SOB (ILD, AR, anaemia, kyphosis causing restriction)
Associated problems:
-Anterior uveitis
-Apical fibrosis, kyphosis
-AR
-AV block
-Arthritis (may be psoriatic)
-IBD
-Osteoporosis (ask about fragility fractures)
-Ask about cauda equina
OE:
-Fixed kyphoscoliosis, loss of lumbar lordosis and extension of cervical spine (?)
-Reduced chest expansion
-Increased occiput-wall distance (>5 cm)
-Reduced ROM throughout whole spine
-Schober’s test (2 points 15cm apart expand <5cm on maximum forward flexion)
Ix:
-XR spine vertebral fusion
-MR sacroiliac joints
-Consider HLA B27 testing
-Consider PFTs
Tx:
-Smoking cessation
-Exercise, PT
-Manage osteoporosis with bisphosphonates
-Analgesia e.g. NSAIDs
-DMARDS e.g. steroids, anti-TNF, mAb, JAKi
-Surgery e.g. to correct kyphosis
Back pain differentials
-Osteoporosis with compression fracture
-Cauda equina
-Malignancy e.g. primary, MM, metastases
-Inflammatory e.g. ankylosing spondylitis
-Infection e.g. discitis or OM
-Intervertebral disc herniation
-Spinal stenosis
-Intra-abdominal pathology
Pseudoxanthoma
PC:
Loose skin, hyper-extensible joints, VA reduced, HTN, premature CAD, CVA, MV prolapse, gastric bleed
FH:
80% autosomal recessive, due to degenerative elastic fibres in skin, blood vessels and eyes
OE:
‘Loose skin folds at neck and axillae with yellow pseudo-xanthomatous plaques’
Associated blue sclera and retinal angioid streaks
DDx:
EDS (no CAD, FH more apparent as is AD) (defect in collagen causing increased skin elasticity)
TIA
Referral to specialist within 24 hours
DAPT for 21 days (load first)
Followed by clopidogrel monotherapy
Headache
PC:
Meningism, N+V, fever, rash, neurology, immunosuppressed, close contacts, foreign travel, check chance of pregnancy
PMH:
HTN, smoking, bleeding disorders
FH:
PCKD
DDx:
-Migrainous
-Tension
-Cluster
-Trigeminal
-Medication-overuse
-Meningitis
-SAH
-CVST
-GCA
-SOL
-Malignant hypertension
-Pre-eclampsia
Ix:
Blood culture, CT head, LP (MC+S, glucose, protein)
Mx:
-Meningitis: antibiotics and treat close contacts
-SAH: neurosurgical review, nimodipine to reduce vasospasm
-Migraine: aspirin, NSAIDs, anti-emetics, triptans, lifestyle and preventative therapy (e.g. propranolol)
-Cluster: oxygen and triptans, prevention with verapamil
Ataxia
PC:
Speech, vision, Lhermitte’s, mood, bladder, bowel, Uthoff’s
Ask about:
Stroke RF, early morning headaches or nausea, vertigo, previous head or neck injury, alcohol or drug history (phenytoin), diet (B12), FH (FA, Wilson’s)
N.B. In vestibular ataxia, fast phase is AWAY from affected ear
Joint pain (gout)
(Go over reactive arthritis and pseudogout)
PC:
Ask about meat, seafood and beer, diuretics, CNIs, CKD, metabolic syndrome
OE:
Look for gouty tophi, HTN, history of urate stones (e.g. nephrectomy), chronic renal failure (fisulae), solid organ transplant
Ix:
-Uric acid levels (unreliable)
-Synovial fluid needle-shaped negatively bifringent (NoNo)
-Radiographic features punched out periarticular changes (PeePee)
Tx:
-Treat cause e.g. stop diuretic
-Increase fluids
-NSAIDs or colchicine or steroids
Prevention:
-Allopurinol or febuxostat (XOI) to get urate <300
-Losartan has a urate-lowering effect
Joint (OA)
OE:
-Asymmetrical DIPJ deformity with Heberden’s nodes (and Bouchard’s at PIPs)
-Diffuse atrophy of hand muscles
-Crepitations, reduced movement and function
-Replacement scars
Ix:
-XR (not needed) would show COLP (cysts, osteophytes, loss of joint space, peri-articular sclerosis)
-CT/MRI may be helpful when planning surgery
Tx:
Weight reduction, exercise, PT/OT
Oral or topical NSAIDs, intra-articular steroids
Joint replacement
Addison’s (BMJ)
PC:
Fatigue, weak, low mood, anorexia and weight loss, thirst, dark skin (raised ACTH and melanocyte stimulating hormone), fainting, cramps, bitemporal hemianopia (if pituitary adenoma)
PMH:
-Known Addison’s
-Other autoimmune disease
-TB or metastases
DDx:
Secondary adrenal insufficiency due to pituitary adenoma or tertiary adrenal insufficiency (hypothalamic suppression of ACTH release due to sudden discontinuation of exogenous steroid therapy)
Causes:
-Autoimmune process (80%)
-Adrenal metastases
-Adrenal TB or other infection
-Infiltration e.g. amyloidosis
-Adrenalectomy
-WF syndrome (adrenal infarction secondary to meningococcal sepsis)
Ix:
-8am cortisol
-Short Synacthen Test (cortisol fails to rise)
-ACTH level (if raised suggests primary adrenal insufficiency)
-Aldosterone and renin (to look for mineralocorticoid deficiency, low aldosterone and compensatory rise in renin) and low adrenal androgens
-Adrenal imaging +/- pituitary imaging with CT or MRI
Other Ix:
-Bloods including U+Es, glucose, adrenal autoantibodies, TFTs
-CXR if concerns for malignancy or TB
-L/S BP
Tx:
-IV saline and glucose
-HC
-Education on compliance, sick-day rules, steroid card, medic alert bracelet
-Titrate maintenance HC and fludrocortisone to response
N.B. Treatment may unmask DI
N.B. Anti-TB treatment increases clearance of steroid so larger doses required
Ischaemic-sounding chest pain
DDx:
-Ischaemia, dissection, AS or pericarditis
-PE, PTX or pneumonia (if pleuritic)
-MSK
-Oesophageal reflux or spasm (N.B. GTN can help in oesophageal spasm)
-Sickle cell crisis
Investigations:
ECG
CXR
Troponin, FBC, U+Es, lipids, glucose
Tx:
Treatment of ACS and further investigations
(Know how to manage coronary vasospasm)
Mention:
Risk scores
DVLA
ACS management? (Glos guidelines)
A to E
Aspirin 300mg
If STEMI:
-PPCI
-P2Y12 inhibitor and statin
If NSTEMI:
-Fondaparinux
-P2Y12 inhibitor and statin
-Consider Tirofiban
-If any high risk features, urgent PCI
-Otherwise, refer to cardiology for evaluation and risk stratification
Secondary prevention
Pericarditis
Causes:
Viral/HIV/TB, uraemic, AI, Ca, Dressler’s
Ix:
-Bloods
-Viral screen (most common is coxsackie)
-ECG: global saddle STE, PR depression, low voltage if effusion, electrical alternans (heart swinging in large effusion)
-CXR: globular heart
-Echo: bright pericardium, effusion, RV diastolic collapse, RWMA (if myopericarditis)
-Cardiac MR: epicardium LGE suggests myopericarditis
-Diagnostic pericardiocentesis
Tx:
-Usually self limited
-NSAIDs, colchicine
-Steroids in recurrent
-Tamponade is a medical emergency (Beck’s triad hypotension, JVP and muffled heart sounds)
-Constrictive pericarditis may need surgical pericardiectomy
AF
PC:
OE:
CV examination
Thyroid status
Neurological examination
Ix:
-12 lead, 24hr Holter, event recorder
-Echo LA >4cm high recurrence
-Hb, TSH, INR
Paroxysmal: <7 days usually self-terminating within 4 hours
Persistent: >7 days may require chemical or electrical CV
Permanent: >1 year or when no further attempts to restore sinus rhythm
Tx:
See cardiology section
HTN
PC:
Headache, CP, weakness, abdominal pain, polyuria and muscle cramps (Conn’s), visual, paroxysmal symptoms for phaeochromocytoma (headache, sweating , palpitations, anxiety)
PMH:
Renal, CV and PVD
CV risk factors
Thyroid
FH:
MEN
OE:
-Acromegaly? Cushingoid?
-RR delay (coarctation)
-BP different (coarctation, dissection, PVD)
-Systolic murmur in L infraclavicular (coarctation)
-Renal bruits (RAS) or ballotable kidney (PCKD)
-Visual fields and acuity
-Fundoscopy 1) silver wiring 2) AV nipping 3) cotton wool/flame haemorrhages 4) papilloedema
DDx in order of incidence:
-Essential
-Renal (CKD, ADPKD, RAS, nephrotic syndrome)
-Endocrine (Conn’s, Cushing’s, acromegaly, phaeochromocytoma)
-Coarctation
-Pre-eclampsia
-Also remember scleroderma crisis
Ix:
-End organ damage: fundoscopy, ECG and CXR and echo, urinalysis and PCR, U+Es
Then look at underlying cause:
-PT
-ARR, plasma or urinary metanephrines, dexamethasone suppression test
-Consider CT adrenals and US kidneys
-TSH, Ca (MEN)
-OSA tests
Tx:
-Lifestyle
-Anti-hypertensives (first choice depends on if >55 or Afro-Carribean)
-Other CV risk factors
Tx of HTN emergency:
-If encephalopathy, stroke, MI, LV failure etc.:
-Venodilators (give alpha and beta blockers in phaeo)
-Avoid rapid over-correction, aim for 25% in first hour SBP and the to 160/100 for next 48 hours, then slowly reduce thereafter (ACC)
N.B. Hypertensive emergencies (LV failure, HE, or dissection)
Urgencies include malignant or acclerated hypertension and pre-eclampsia
Eisenmenger’s
PC:
Worsening dyspnoea, oedema, syncope, palpitations, haemoptysis, family planning
Ask about hyperviscosity, paradoxical embolism
OE:
Loud P2, right parasternal heave, clubbing, cyanosis, scars, absent shunt murmur but TR common, signs of R heart failure
DDx:
ASD, VSD, AVSD, PDA
Ix:
FBC, BNP, ECG, CXR
Lung function tests, CT-PA, echo and R heart catheter
Tx:
-Pulmonary vasodilator
-Diuretic and oxygen
-Contraception
-Exercise training
-Avoid extreme heat or dehydration and isometric exercise
-Immunisations and prophylacic antibiotics
-Heart lung transplant
Correction of shunt is CI
Weight loss differentials (BMJ)
-Malignancy
-Gastrointestinal conditions e.g. coeliac
-Psychiatric causes
-Cachexia syndromes associated with organ failure (e.g., heart failure, chronic obstructive pulmonary disease, stage 5 chronic kidney disease)
-Endocrinopathies (e.g., hyperthyroidism, diabetes mellitus, adrenal insufficiency)
-Serious infections (e.g., tuberculosis, HIV)
-Medication adverse effects (GLP-1)
-Substance misuse
-Social factors that prevent adequate access to food
Anaemia
PC:
-Fatigue, SOB, CP
-GI: melena or steatorrhoea, weight loss, GORD/dysphasia/NSAIDs, pain/bloating
-Mensturation
-FH: malignancy or anaemia
-Travel history
-Diet
-Previous transfusions
OE:
-Koilonychia, glossitis, angular stomatitis, LNs, abdominal masses, tenderness and megaly
-Offer to perform rectal and vaginal examinations
-Look for signs HHT (telangiectasia) (AD disease with increased risk of GI bleed, epistaxis and haemoptysis, pulmonary shunts and inracranial aneurysms)
DDx:
MICRO
-IDA e.g. chronic GI bleed, malignancy, coeliac
-Anaemia of chronic disease
-Inherited haemoglobinopathy e.g. thalassaemia
NORMO
-Acute blood loss
-Haemolytic anaemia
-CKD
-Hypothyroidism
-Bone marrow failure
MACRO
-Megaloblastic (i.e. B12 or folate deficiency)
-Non-megaloblastic (e.g. alcohol or liver disease)
Ix:
-FBC, U+Es, LFTs, TFTs, iron studies, ferritin, folate, B12
-Consider Hb electrophoresis (thalassaemia and HbE) or haemolysis screen with blood film
-FOB test and endoscopy or CT abdomen
Tx:
-Treat cause
-Iron supplementation
-Blood transfusion (usually if <70)
Asthma
PC:
Wheeze, SOB, cough, triggers (allergy versus URTI), previous admissions, PEFR (best, normal, current), vaccination status, compliance and technique, urticaria, calf swelling, fever
DDx:
PE, pneumothorax, anaemia, RTI
Ix:
ABG, CXR, PT-PA
Tx:
Bronchodilators, steroids, astha specialist nurse
Life-threatening if:
-PEFR <33%
-Silent chest, cyanosis, altered consciousness, exhaustion, arrhythmia, hypotension, poor effort
-Saturations <92%
-PaO2 <8kPa
-Normal CO2
Criteria for safe discharge:
-PEFR >75%
-Asthma mx plan and inhaler technique
-Follow-up with GP/asthma nurse 2 days
-Hospital follow-up
Rash (psoriasis)
‘Multiple, well-demarcated salmon pink scaly plaques on extensor surfaces’ with ‘nail pitting and onycholysis’ with ‘associated psoriatic arthropathy’
Pathophysiology:
Epidermal hyperproliferation and accumulation of inflammatory cells
Types:
Plaque, guttate, pustular
Triggers:
Trauma (Koebner phenomenon)
Infection
Medications (e.g. beta-blockers, lithium)
Tx:
-Emollients, calcipotriol (vitamin D analogue), topical steroids, coal tar, topical tacrolimus
-Phototherapy
-Cytotoxics e.g. MTX, anti-TNF, retinoids
Complications:
Erythroderma and SEs of immunosuppression
Rash (eczema)
‘Erythematous and lichenified patches of skin predominantly affecting the flexor aspects of joints’ with ‘fissures, excoriations and some evidence of secondary bacterial infection’
Ix:
Patch testing for allergens
Tx:
-Avoid precipitants
-Emollients, topical steroids and topical tacrolimus
-Anti-histamines
-Consider antibioitcs
-Phototherapy
-Systemic immunosuppression (steroids, MTX, ciclosporin, MMF)
N.B. Also examine respiratory system for wheeze
Comment on if any signs of eczema herpeticum or bacterial infection
Steroid ladder?
Hydrocortisone
Eumovate
Betnovate
Clobetasol (Dermovate)
Rash (EN)
‘Tender, red, smooth, shiny nodules on the skins’
Granulomatous inflammation of subcutaneous fat (panniculitis)
Screen for cause:
Nodes (lymphoma)
OCP
Dunno (idiopathic)
Other drugs (streptomycin or sulphonamides)
Sarcoidosis or Streptococcal throat infection
UC or Crohn’s
Mycobacterial (TB) or maternity
Also look for lupus pernio if suspecting sarcoidosis (diffuse bluish plaque with central small papules commonly affecting the tip of the nose)
Rash (HSP)
‘Purpuric rash usually on extensor surfaces of buttocks and legs’
Small-vessel vasculitis due to IgA and C3 deposition
Associated arthralgia and abdominal pain
Precipitants: infections (streptococci, HSV, parvovirus) or antibiotics
Complications: HTN, IgA nephropathy
Ix:
Plts normal or raised (unlike other forms purpura)
Mx:
Most spontaneously recover, though steroids may help recovery
Can recur
Skin malignancy
PC:
Location, growth, recent changes, bleeding
PMH:
Sun exposure, occupation, FH, immunosuppression, bone pain, neurological or abdominal problems
BCC:
Pearly nodule with rolled edge, superficical telangiectasia, slowly growing, rarely metastasise
Tx: curettage/cryotherapy if superficial or surgical excision +/- radiotherapy
SCC:
Keratotic nodule, polypoid mass, cutaneous ulcer, metastases
Tx: surgery +/- radiotherapy
MM:
Asymmetrical
Border irregularity
Colour
Diameter >6mm
Enlarging
Metastases
Tx: excision, staged based on Breslow thickness, consider immunotherapy
Abdominal pain differentials
-Pancreatitis
-Renal colic, UTI
-Peptic ulceration, ischaemic bowel, perforation, gastroenteritis, BO, IBD, IBS, coeliac
-Hepatitis, gallstone disease
-Malignancy
-Pregnancy complications, PID, testicular torsion, endometriosis
-AAA
-DKA or Addison’s or gastroparesis
-Porphyria, PNH or FMF
Down’s features
‘This patient has some features of Trisomy 21’
Up-slanting palpebral fissures
Epicanthic folds
Low set ears
Low nasal bridge
Brushfield spots in the iris
Single palmar crease
Wide gap between 1st and 2nd toes
AVSD most common
Hypopituitarism
Sudden headache if apoplexy
Visual field defects
TSH: hypothyroidism
GH: -
ACTH: features of adrenal insufficiency
Gonadothrophins: low libido, amenorrhea
Prolactin: may have galactorrhoea if prolactinoma
DDx:
-Neoplastic (pituitary adenoma)
-Vascular (apoplexy or Sheehan’s)
-Infiltration (sarcoid)
-Infection (TB, abscess)
-Iatrogenic (RTX or surgery)
-Trauma
Ix:
-U+Es
-TFTs
-IGF-1
-9am cortisol and ACTH
-FSH and LH
-PLT
-Paired osmolarities
Imagining of pituitary
Mx:
Replace hormones
IV hydrocortisone in apoplexy
Nephrotic syndrome
PC:
Frothy urine, DM, SLE, RA, medications, VTE
Ix:
-Urinalysis and PCR
-U+Es, lipids
-Autoimmune serology (PLA2R), infections (HIV, HBV, HCV)
-CXR and underlying malignancy investigations
-Renal tract US
-Renal biopsy
Mx:
-Loop diuretics, fluid and Na restriction
-Anticoagulation if serum albumin <20
-Treat primary cause
-ACEi to reduce proteinuria
-SGLT2 inhibitors in selected cases e.g. IgA nephropathy
Nephrotic syndrome = hypoalbuminaemia + oedema + proteinuria (>3g/day or PCR >350)
Also associated with hypercholesterolaemia, increased thrombotic risk, increased susceptibility to encapsulated bacterial infections
Common causes:
Primary e.g. membranous, FSGS, minimal change, IgA
Secondary e.g. diabetic nephropathy, amyloidosis, SLE, RA, drugs e.g. NSAIDs, infections e.g. HIV, HCV, malignancy e.g. solid organ tumours, haematological malignancy
PD
See neuro
Antibodies in rheumatology
RA: RF, CCP
SLE: ds-DNA, Sm
Drug SLE: histone
Sjogren’s: Ro, La
Myositis: Jo
Mixed: RNP
Limited SS: centromere
Diffuse: topoisomerase
Scleroderma renal: RNA polymerase III
SLE
PC:
Constitutional symptoms (fever, WL, fatigue)
Photosensitive rash (malar or discoid), oral ulceration, alopecia, Raynaud’s (always ask RASHES, HAIR AND RAYNAUD’S), nail fold infarcts
Sjogren’s (sicca)
Clots, miscarriage/VTE
Anaemia, thyroid symptoms
Mood, focal neurology
Arthralgia, Jaccoud’s
Pleural effusion, pericarditis, Libman-Sacks, hypertension Frothy urine
DH:
Drug-induced e.g. hydralazine, procainamide, isoniazid
FH
Ix:
-Urinalysis and BP
-FBC, U+E, CRP/ESR, APTT
-Autoimmune screen including ANA, ds-DNA, anti-Sm (type of ENAs), complement, aPL screen
-Anti-histone if considering drug induced lupus
-Consider TFTs, CK
-CXR and PTFs
-ECG and echo
-Joint XRs
-Skin or renal biopsy
Diagnosis by ACR criteria
DDx:
-Scleroderma
-Sjogren’s
-MCTD
-RA (lupus don’t get much joint swelling, RA no rashes)
-Fibromyalgia
-Lymphoma
Tx:
-Sun cream and smoking cessation
-Occasionally watch and wait in mild disease
-Most patients started on hydroxychloroquine
-Topical steroids if severe skin disease
-MTX and steroids if inflammatory arthritis
-MMF or cyclophosphamide in severe renal disease
-Rituximab in multi-system
-Pregnancy counselling (anti-Ro heart block and IS)
-If aPL consider aspirin (prophylaxis) or anticoagulation (after venous thrombosis)
Side effects of cyclophosphamide:
-Haemorrhagic cystitis or haematological
-Infertility
-Teratogenic
N.B. aPL screen: anti-cardiolipin, lupus anticoagulant, beta2-glycoprotein
Rash (LR)
DDx:
APLS
PAN
SLE
Cholesterol embolisation
Bullous pemphigoid (1) versus pemphigus vulgaris (2)
1) AI, older, basement membrane, better prognosis, tense blisters
2) AI, mucus membranes, intraepidermal, Desmoglein, Nikolsky’s +ve, flaccid blisters
Both treated with oral and topical steroids
SSc
PC:
Raynaud’s phenomenon, ischaemic digital ulcers, hypertensive crisis, pulmonary arterial hypertension, ILD, oesophageal dysmotility, SIBO
Also: beaked nose, microstomia, peri-oral furrowing, fibrosis, pulmonary hypertension
Limited SSc: limited to face, below elbows, below knees; slow progression; CREST
Diffuse SSc: widespread cutaneous and early visceral involvement; rapid progression
Ix:
-ANA, anti-centromere (limited), anti-topoisomerase (diffuse) and anti-RNA (renal)
-FBC, B12/folate, U+Es, CK +/- myositis screen
To investigate complications:
-HR-CT, PFTs (aspiration, fibrosis)
-Consider OGD or oesophageal manometry and hydrogen breath test
-ECG, echo, right heart catheter
-NCS/EMG
-Urinalysis and consider renal biopsy
-Hand radiographs (calcinosis)
-Nailfold capillaroscopy (microvascular disease)
Tx:
-MDT (rheumatologists working closely with respiratory, renal, GI, psychologists, palliative at end-stage)
-Gloves and CCB (ERA, PDEi, prostacyclins) for Raynaud’s
-ACEi for renal and AVOID HIGH DOSE STEROIDS
-PPI for reflux and treatment of SIBO with antibiotics
-Trials suggest anti-fibrotics and immunomodulators beneficial for ILD in context SSc
-Manage pulmonary artery hypertension (ERA, PDEi, prostacyclins, LTOT)
What is scleroderma?
Multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels and fibrosis of skin and internal organs
Angioedema (NICE)
DDx:
Histaminergic or mast cell mediated:
-Allergic angio-oedema e.g. in context of anaphylaxis (serum tryptase)
Bradykinin:
-Drug-induced angioedema (ACEi, non-allergic, no urticaria)
-Hereditary angioedema (non-allergic)
-Acquired angioedema (no FH, non-allergic, history of SLE or lymphoma)
Fever in returning traveller (LITFL)
PC:
Where, food, swimming, sex, drugs, animals, insects, sick people, prophylaxis
DDx:
VIRAL:
-Viral gastroenteritis or respiratory viruses
-Arbovirus e.g. dengue
-Viral haemorrhagic fevers
-HIV and hepatitis
BACTERIAL:
-Gastroenteritis or meningitis
-Leptospirosis
-Enteric fever, Coxiella, brucella, rickettsia
OTHER:
-Malaria
-Schistosomiasis and leishmaniasis
Discussion with ID
Traveller’s diarrhoea
PC:
Duration, severity, bloody, watery, travel history, contacts, DH, water raw food, employment history (UKHSA if food handler)
Cause:
Bloody:
-Campylobacter, E. coli
-Entamoeba histolytica
Non-bloody:
-E. coli, Salmonella, Shigella, Yersinia
-Norovirus, Rotavirus
-Giardia, Cryptosporidium
-C. difficile, Staph Aureus
Ix:
FBC, CRP, U+Es, blood culture
Stool testing with O+P
Tx:
-Usually self-limiting
-IV hydration, electrolytes, loperamide
-Antibiotics not indicated in mild disease but can be considered based on ID advice and local guidelines
-Notify UKHSA
Diarrhoea differentials
-Infective
-IBD
-IBS
-Coeliac
-Thyroid disease
-Malignancy
-SIBO
-Pancreatic insufficiency
-Ischaemic colitis
Persistent fever
PC:
-Meningitis symptoms, focal weakness (think septic embolism), OM symptoms, tooth pain, LUTS, respiratory symptoms, GI symptoms, lymphoma symptoms, inflammatory symptoms (SLE, RA)
-Fever at night think malaria, over months think IE
-Contacts, vaccinations, travel, sexual history, pets, drugs
-BG ACHD
-FH FMF
-DH malignant hyperpyrexia syndrome with antipsychotics
OE:
IE, hepatosplenomegaly, joints
Ix:
-Culture
-Urine and CSF
-Viral serology
-PCT
-CRP, ESR, autoantibodies, Ig, complement
-LN biopsy
-CK
-TTE +/- TOE
-CT-AP
Further investigations guided by ID, microbiology, rheumatology or haematology teams
Mx:
-Investigate a treat the underlying cause
-IE: 6/52 antibiotics +/- surgery
-Supportive with anti-pyretics
PUO differentials
-Infective sources: IE, OM or discitis, deep-seated abdominal source, TB
-Malignancy
-Inflammatory: SLE, RA, Still’s disease
-Hereditary: FMF
-Drug-induced e.g. anti-psychotics
Confusion differentials
-Dementia/delirium/depression/drugs
-ETOH withdrawal/ears/eyes
-Low oxygen
-Infection including meningoencephalitis
-Retention (urine or faeces)
-Ictal/in pain
-Under hydration
-Metabolic (hypoglycaemia, electrolytes, thyroid, uraemia)
-Stroke (ischaemic or haemorrhage)/SOL
Delirium screening tool
4AT (alert, AMT4, attention, acute change)
Glandular fever
PC:
Sore throat, fever, malaise, cervical lymphadenopathy, travel, sexual, employment history, social contacts
Red flags: headaches, ascending weakness, jaundice (meningoencephalitis, GBS, hepatitis)
Red flags for lymphoma: weight loss, painless lymphadenopathy (alcohol-induced pain), night sweats
DDx:
EBV, CMV, HIV, viral hepatitis, toxoplasmosis, Hodgkin’s
Ix:
FBC and blood film, test for heterophile antibodies
Consider: EBV specific antibodies/PCR, CMV PCR, HIV screen, hepatitis serology
Consider: lymphoma work-up
Tx:
Symptomatic, avoid contact sports, avoid amoxicillin
Sickle cell disease
PC:
-Vaso-occlusive crisis: sudden-onset bone pain or pleuritc chest pain lasting days-weeks
-Acute chest syndrome: pneumonia-like ilness
-Anaemia may worsen after infection
-Infection due to hyposplenism
-Acute PE and pulmonary HTN and stoke or TIA
-Also leg ulcers, gallstones and priapism
-Triggers: virus, cold weather, dehydration, ETOH, smoking, stress, exercise, hypoxia, pregnancy
-Family planning: hydroxycarbamide is teratogenic, increased risk of crisis and miscarriage, genetic counselling
Ix:
-Anaemia, raised inflammatory markers, renal impairment, blood film sickling
-CXR linear atelectasis in chest crisis, cardiomegaly if long-standing anaemia
-Urinalysis haematuria if renal involvement
-ABG
-ECG and echo
-CT-PA
To treat crisis:
-Oxygen +/- CPAP, fluids, analgesia, antibiotics if infection
-Consider transfusion or exchange transfusion
Prevention advice:
-Fluids
-Warm clothes, avoid sudden temperature changes
-NSAIDs or paracetamol
-Hydroxycarbamide and folic acid
-Consider exchange transfusion programme
-Penicillin prophylaxis and vaccinations in functional hyposplenism
-Safety-netting
Coeliac
See gastro
IBD
PC:
Duration, travel, antibiotics, infectious contacts, foods, sexual history
Fever, anorexa, weight loss, pruritis, fatigue, rash, arthralgia, ulcers, FH
OE:
Remember to feel for hepatosplenomegaly and ask to examine perianal
DDx:
Crohn’s: UC, Yersinia, TB, lymphoma, IBS
UC: Crohn’s, infection, ischaemia, drugs, radiation, IBS
Jaundice
See jaundice section in abdomen station
Swollen calf
PMH:
Ca, HF, immobility, FH, previous VTE, pregnancy, OCP, IBD, nephrotic syndrome, ask about PE symptoms
OE:
10cm below tibial tuberosity >3cm difference, deep calf tenderness, superficial venous engorgement and pitting oedema, tenderness along deep veins, examine abdomen and pelvis to exclude mass, examine peripheral pulses
Ix:
Well’s
D-dimer (sensitive but not specific)
Compression US
If DVT confirmed:
PT, FBC, INR
Think about underlying cause (CXR, thrombophilia screen, CT-AP, mammography, PR and PSA)
Tx:
DOAC 3 months or lifelong if recurrent
Counsel regarding DOAC
Leg ulcer
PC:
Pain (if arterial), location, infection
PMH:
DVT, chronic venous insufficiency, varicose veins, CCF, PVD, sensory neuropathy, diabetes
Venous:
Gaiter, varicose veins, oedema, lipodermatosclerosis, varicose eczema, atrophie blanche
Arterial:
Distal and at pressure points, trophic changes, cold with poor capillary refill, peripheral pulses absent
Neuropathic:
Pressure areas, peripheral neuropathy, Charcot’s
Other causes:
Vasculitic, neoplastic, infectious, haematological, tropical
Ix:
Doppler
ABPI (<0.8 arterial insufficiency)
Arteriography
Tx:
Specialist nurse
Venous: compression bandaging if no PVD, varicose vein surgery
Arterial: angioplasty or vascular reconstruction or amputation
Rheumatoid arthritis
PC:
Joints involved, pain (early morning stiffness?), function
May have systemic involvement:
-Pulmonary
-Eyes: scleritis or Sjogren’s
-Neurological: CTS, peripheral neuropathy
-Haematological: Felty’s, anaemia
-Cardiac: pericarditis
-Renal: nephrotic syndrome (e.g. secondary AA amyloidosis, membranous)
DDx:
-Psoriatic (see below)
-Enteropathic
-Reactive (symmetrical) B27
-Ankylosing B27 (RA is DR4)
-Crystal arthopathy
-CTD: SLE (non-deforming), scleroderma
-OA (worse with exercise)
-Infective (disseminated gonococcal, Lyme, rheumatic fever)
-Still’s (largely diagnosis of exclusion)
-Sarcoid
OE:
Symmetrical and deforming small joint polyarthropathy (particularly PIP MCP) with:
-Ulnar deviation MCPJs
-Subluxation at wrist
-Swan-neck (PIP hyperextended fixed flexion DIP)
-Boutonniere’s deformity (fixed flexion PIP/hyperextended DIPs)
-‘Z’ thumbs
-Muscle wasting
-May have surgical scars e.g. CTS
-Nodules at elbows
Ix:
-Urinalysis
-FBC, U+Es, CRP/ESR, LFTs
-RF and anti-CCP (more specific)
-XR (soft tissue swelling, loss of joint space, articular erosions, periarticular osteopenia SLAP!)
-CT thorax and PFTs
Diagnosis by ACR criteria (clinical, laboratory and radiographic features)
DAS-28 to measure disease activity
Tx:
-PT/OT, counselling and support groups
-NSAIDs
-DMARDS (MTX, sulphasalazine, leflunamide, hydroxychloroquine)
-Steroids in short-term
-May require immunomodulation with anti-TNF, anti-CD20, anti-IL6
-Vaccines and infection counselling
-Surgery
Psoriatic versus rheumatoid arthritis?
Psoriatic:
-Psoriasis
-Different pattern of joint involvement e.g. DIPs
-Often monoarticular or oligoarticular (<5 joints)
-When multiple joints involved, it lacks the symmetry of RA
-Dactylitis
-Enthesitis
-Nail changes
-Spondyloarthritis
-Mostly seronegative
N.B. Can also have uveitis with psoriatic and there’s a link with IBD
Osteogenesis imperfecta
PC:
Blue eyes, recurrent fractures since birth, joint laxity, short stature, hearing loss
FH:
AD defect in collagen gene
Ix:
-Bone, vitamin D, ALP, PTH
-Skeletal survey and DEXA
-Genetics
-Audiology
-Echo (valve regurgitation)
Mx:
-MDT
-Vitamin D, Ca, bisphosphonates if indicated
-Orthopoedic input for fractures
HHT
Epistaxis
Mucocutaneus telangiectasias
AV malformations
Autosomal dominant
OSA
Fall differentials
-Mechanical: vision, footwear or home hazards
-Polypharmacy, sarcopenia and deconditioning
-Neurological: gait disorders e.g. PD, stroke, peripheral neuropathy, vestibular dysfunction
-Cardiology: valve, arrythmias, orthostatic
-Endocrine: hypoglycaemia
N.B. Timed up and go test, turn 180 degrees test can be used in clinic (NICE)
FRAT is helpful
Drugs increasing risk of falls: sedatives, tricyclics, antipsychotics, antidepressants, opiates, some PD drugs, alpha blockers, thiazides, beta blockers, anti-anginals
Vertigo
EDS
Retinitis pigmentosa differentials
Go over vision stuff
Usher syndrome
Laurence-Moon-Biedl
Kearns-Sayre (CPEO and cardiac abnormalities)
Refsum’s
MG
Muscular dystrophy
Marfan’s
See cardiology section
Charcot foot
Sarcoidosis
PC:
Chest, arthralgia, eye, EN or lupus pernio, neurology (facial palsy), CVS, weight loss, fever
FH
Occupational history (berryliosis can mimic) and ask about TB
Ix:
-Slit lamp examination eyes
-FBC, U+Es, LFTs, bone profile
-ECG
-PFTs and CXR
-Interferon gamma
-Serum ACE
-Consider skin biopsy and BAL
Mx:
-Steroids for pulmonary disease depending on symptoms and stage (otherwise observation)
-Lung transpant in end-stage
-For skin or eye involvement, topical or oral steroids used
-Other immunouppressive agents can be considered but would be guided by specialists
Lofgren’s = EN, bilateral hilar LN, arthralgia and fever
Dermatomyositis
N.B. Look for underlying cause
Ix:
-CK
-Antibodies (ANA and myositis-specific antibodies e.g. anti-Mi-2 and anti-Jo)
-EMG
-Biopsy
-PFTs and HRCT (ILD)
-ECG and echo (cardiac involvement)
-Swallow assessment
DDx:
Overlap myositis
Mx:
-MDT with neurologists, rheumatologists, respiratory, PT, SLT
-Sun cream
-Steroids or other immunosuppressive agents
Sturge Weber
Vitiligo
DKA*
PC:
Polyuria/dipsia, preceding illness, recent increased insulin requirement or high BMs, nausea, SOB, poor compliance, ETOH and drugs
Ix:
Septic screen
Glucose >11, bicarbonate <15/pH <7.3 and ketones >3
Raised anion gap
Mx:
ITU
IV fluids +/- K
FRII
pLMWH
Consider antibiotics
GCA and PMR
Discuss with opthalmology if visual symptoms
Otherwise refer on to rheumatology who will see urgently
Prednisolone 40-60mg depending on if visual symptoms
Lymphomas
Hodgkin’s (Reed-Sternberg):
Classical Hodgkin lymphoma
Nodular lymphocyte-predominant Hodgkin lymphoma
ABVD
NHL:
Most common B cell types are diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma
R-CHOP
NHL can be split into low-grade versus high grade or B cell (most common) versus T cell
Peutz-Jeghers
Rare, AD disorder characterised by hamartomatous polyposis
mucocutaneous pigmentation and gastrointestinal polyposis
High lifetime risk of intestinal and extra-intestinal malignancy
Other increased risk GI malignancy: FAP and Lynch syndrome (HNPCC) (both AD)
SOAPBRAINMD
Serositis
Oral ulcers/alopecia
Arthralgia
Photosensitivity
Blood
Renal
ANA
Immunologic inc. APL
Neurological
Malar rash
Discoid
Anaemia in RA (PPP)
Anaemia of CD
Felty’s
Myelosuppression
Pernicious (AI disease)
NSAIDS occult GIB
Renal disease
Poor prognostic factors in RA? (PPP)
RF or CCP or HLA DR4 positive
Women
