Station 5 Flashcards
Ix of Sickle cell disease/ crisis?
- Blood tests: low Hb; high WCC and CRP; renal impairment; sickling on blood film
- CXR: linear atelectasis in a chest crisis; cardiomegaly: cardiac size proportional to degree of longstanding anaemia
- Urinalysis: microscopic haematuria if renal involvement in crisis
- Arterial blood gas: type I respiratory failure
- Echocardiogram: dilated right ventricle with impaired systolic function; raised peak
tricuspid regurgitant velocity: abnormal range for sickle cell patients is lower than other populations; i.e. >2.7 m/s abnormal - Computed tomography pulmonary angiography: linear atelectasis with patchy
consolidation ± acute pulmonary embolism
Acute Treatment of sickle cell crisis?
- Oxygen ± continuous positive airways pressure
- Intravenous fluids
- Analgesia
- Antibiotics if evidence of infection
- Blood transfusion/exchange transfusion depending on degree of anaemia and severity of crisis
Long term chronic management of sickle cell disease?
- Hydroxycarbamide or exchange transfusion programme if frequent crises or other features suggestive of a poor prognosis
- Long‐term treatment with folic acid and penicillin as patient will have features of hyposplenism
- May need further investigation of possible pulmonary hypertension if raised peak tricuspid regurgitant velocity, including right heart catheterization, after the acute event
Prognosis of sickle cell disease?
- HbSS ≈40–50 years old
- Worse prognosis with frequent chest crises or following development of pulmonary hypertension
Examination findings of sickle cell patient +/- crisis?
- Fever
- Dyspnoeic
- Jaundice
- Pale conjunctiva
- Raised JVP, pansystolic murmur loudest at left sternal edge (tricuspid regurgitation 2’ PH)
- Reduced chest expansion due to pain with coarse expiratory crackles
- Small, crusted ulcers on lower third of legs
- abdo scar suggesting splenectomy, splenomegaly
Features of Addisons disease?
- Fatigue, muscle weakness, low mood, loss of appetite, weight loss, thirst (dehydration) * Darkened skin (Addison’s disease)
- Fainting or cramps
Causes of Addison’s disease (cortisol insufficiency)?
- TB/ mets to adrenal
- Primary autoimmune Addison’s disease (may be assoc hypothyroidism/ T1DM/ vitiligo)
DDx secondary adrenal insufficiency: pituitary adenoma or sudden discontinuation of steroid
Examination findings of patient with known Addison’s disease?
- Medic alert bracelet
- Hyper‐pigmentation: palmar creases, scars, nipples and buccal mucosa
- Postural hypotension
- Visual fields: bitemporal hemianopia (pituitary adenoma)
cause: signs of other associated autoimmune diseases/ TB/ malignancy
What is Addison’s disease?
Primary adrenal insufficiency
- Pigmentation due to a lack of feedback inhibition by cortisol on the pituitary, leading to raised ACTH and melanocyte‐stimulating hormone
- 80%: autoimmune process. Other causes include adrenal metastases, adrenal tuberculosis, amyloidosis, adrenalectomy and Waterhouse–Friederichsen syndrome (meningococcal sepsis and adrenal infarction)
Ix of suspected Addison’s disease?
- 8 am cortisol: likely low (unreliable)
- Short Synacthen test
-> Exclude addison’s disease if cortisol rises to adequate levels - long Synacthen test
-> Diagnose addison’s disease if cortisol does not rise to adequate levels - adrenal imaging (primary) and/or pituitary imaging (secondary) with MRI or CT
Others:
Blood tests: eosinophilia, ↓ Na+ (kidney loss), ↑ K+, ↑ urea (dehydration), ↓ glucose, adrenal autoantibodies (if autoimmune cause), thyroid function tests (hypothyroidism)
CXR: malignancy/TB
Tx of acute adrenal crisis?
- 0.9% saline IV rehydration +++ and glucose
- Hydrocortisone
- Treatment may unmask diabetes insipidus (cortisol is required to excrete a water load)
- Anti‐TB treatment increases the clearance of steroid, therefore higher doses required
Prognosis of addisons disease?
normal life expectancy
Chronic tx of addison’s disease?
- Education: compliance, increase steroid dose if ‘ill’, steroid card, medic alert bracelet * Titrate maintenance hydrocortisone (and fludrocortisone) dose to levels/response
Examination findings of patient with Cushing’s syndrome?
- face: moon‐shaped, hirsute, with acne
- Skin: bruised, thin, with purple striae
- Back: ‘buffalo hump’
- abdomen: centripetal obesity
- legs: wasting (‘lemon on sticks’ body shape) and oedema
common complications of Cushing’s syndrome?
- Hypertension (BP)
- Diabetes mellitus (random blood glucose) * osteoporosis (kyphosis)
- Cellulitis
- proximal myopathy (stand from sitting)
examination findings which can suggest underlying cause of cushings syndrome?
- Exogenous steroids: signs of chronic condition (e.g. RA, COPD) requiring steroids * Endogenous: bitemporal hemianopia and hyperpigmentation (if ACTH ↑)
Cushing’s disease vs Cushings syndrome?
Cushing’s disease: glucocorticoid excess due to ACTH secreting pituitary adenoma
Cushing’s syndrome: the physical signs of glucocorticoid excess
Ix of suspected Cushings?
1. Confirm high cortisol
* 24‐hour urinary collection
* Low dose (for 48 hours) or overnight dexamethasone suppression test
> Suppressed cortisol: alcohol/depression/obesity (‘pseudo‐Cushing’s’)
**2. if elevated cortisol confirmed, then identify cause: **
* ACTH level
-> High: ectopic ACTH secreting tumour or pituitary adenoma
-> low: adrenal adenoma/carcinoma
* MRI pituitary fossa ± adrenal CT ± whole body CT to locate lesion
* Bilateral inferior petrosal sinus vein sampling (best test to confirm pituitary vs
ectopic origin; may also lateralise pituitary adenoma)
* High‐dose dexamethasone suppression test may help >50% suppressed
cortisol: Cushing’s disease
Prognosis of untreated Cushings syndrome?
Untreated Cushing’s syndrome: 50% mortality at 5 years (usually due to accelerated ischaemic heart disease secondary to diabetes and hypertension)
Causes of proximal myopathy?
- inherited:
⚬ Myotonic dystrophy
⚬ Muscular dystrophy - Endocrine:
⚬ Cushing’s syndrome
⚬ Hyperparathyroidism
⚬ Thyrotoxicosis
⚬ Diabetic amyotrophy - inflammatory:
⚬ Polymyositis
⚬ Rheumatoid arthritis - metabolic:
⚬ Osteomalacia (Low Vit D) - malignancy:
⚬ Paraneoplastic
⚬ Lambert–Eaton myasthenic syndrome - Drugs:
⚬ Alcohol
⚬ Steroids
Treatment of Cushings syndrome?
Surgical: Trans‐sphenoidal approach to remove pituitary tumours. Adrenalectomy for adrenal tumours
pituitary irradiation
medical: Metyrapone
What is Nelsons sydrome?
bilateral adrenalectomy (scars) to treat Cushing’s disease, causing massive production of ACTH (and melanocyte‐stimulating hormone), due to lack of feedback inhibition, leading to hyper‐pigmentation and pituitary overgrowth
Causes of macroglossia?
• acromegaly
• Amyloidosis
• Hypothyroidism
• Down’s syndrome
Complications of Acromegaly to look out for?
acanthosis nigricans
Bp ↑*
Carpal tunnel syndrome
Diabetes mellitus*
Enlarged organs
field defect*: bitemporal hemianopia goitre, gastrointestinal malignancy
Heart failure, hirsute, hypopituitary
iGF‐1 ↑
Joint arthropathy
kyphosis
lactation (galactorrhoea)
myopathy (proximal)
(*Signs of active disease)
Examination findings in acromegaly?
• Hands: large ‘spade like’, tight rings, coarse skin and sweaty
• face: prominent supra‐orbital ridges, prognathism, widely spaced teeth and
macroglossia
- features of OA/ DM
Ix for diagnosis of acromegaly?
• non‐suppression of GH after an oral glucose tolerance test
• Raised plasma igf‐1
• CT/MRI pituitary fossa: pituitary adenoma
• Also assess other pituitary functions
Ix for complications of acromegaly?
• CXR: cardiomegaly
• ECG: ischaemia (DM and hypertension)
• pituitary function tests: T4, ACTH, prolactin and testosterone
• glucose/ HbA1c: DM
• visual perimetry: bitemporal hemianopia
• sleep study for obstructive sleep apnoea (in 50%): due to macroglossia
Ix for complications of acromegaly?
• CXR: cardiomegaly
• ECG: ischaemia (DM and hypertension)
• pituitary function tests: T4, ACTH, prolactin and testosterone
• glucose/ HbA1c: DM
• visual perimetry: bitemporal hemianopia
• sleep study for obstructive sleep apnoea (in 50%): due to macroglossia
Management of acromegaly?
Aim is to normalize GH and IGF‐1 levels
- Surgery: trans‐sphenoidal approach Medical post‐op complications:
• Meningitis
• Diabetes insipidus
• Panhypopituitarism - medical therapy: somatostatin analogues (Octreotide), dopamine agonists (Cabergoline) and growth hormone receptor antagonists (Pegvisomant)
- Radiotherapy in non‐surgical candidates
Long term follow up of acromegaly?
Annual GH, PRL, ECG, visual fields and CXR ± CT head
Conditions associated with acanthosis nigricans
Associations:
⚬ Obesity
⚬ Type II diabetes mellitus
⚬ acromegaly
⚬ Cushing’s syndrome
⚬ Ethnicity: Indian subcontinent
⚬ Malignancy, e.g. gastric carcinoma and lymphoma
Men1?
• parathyroid hyperplasia (Ca2+ ↑)
• pituitary tumours
• pancreatic tumours (gastrinomas)
Important drug history in suspected hypothyroidism?
Amiodarone, lithium and anti‐thyroid drugs
Associated illnesses to elicit in suspected hypothyroidism?
• Previously treated thyroid disease
• Autoimmune: Addison’s disease, vitiligo and type I diabetes mellitus
• Hypercholesterolaemia
• History of ischaemic heart disease: treatment with thyroxine may precipitate angina
Examination findings in hypothyroidism?
• Hands:
⚬ Slow pulse
⚬ Dry skin
⚬ Cool peripheries
• Head/face/neck:
⚬ ‘Peaches and cream’ complexion (anaemia and carotenaemia)
⚬ Eyes: peri‐orbital oedema, loss of eyebrows and xanthelasma
⚬ Thinning hair
⚬ Goitre or thyroidectomy scar
• legs:
⚬ Slow relaxing ankle jerk (tested with patient kneeling on a chair)
Examination findings of complications associated with hypothyroidism
• Cardiac: pericardial effusion (rub), congestive cardiac failure (oedema)
• neurological: carpel tunnel syndrome (Phalen’s/Tinel’s test), proximal myopathy (stand from sitting) and ataxia
Ix of hypothyroidism?
• Blood: TSH (↑ in thyroid failure, ↓ in pituitary failure), T4 ↓, autoantibodies Associations: hyponatraemia, hypercholesterolaemia, macrocytic anaemia, consider short Synacthen test (exclude Addison’s)
• ECG: pericardial effusion and ischaemia
• CXR: pericardial effusion and CCF
Management of hypothyroidism?
• Thyroxine titrated to TSH suppression and clinical response
NB. 1. Can precipitate angina
2. Can unmask Addison’s disease → crisis
Causes of hypothyroidism?
• autoimmune: Hashimoto’s thyroiditis (+ goitre) and atrophic hypothyroidism
• iatrogenic: Post‐thyroidectomy or I131, amiodarone, lithium and anti‐thyroid drugs
• iodine deficiency: dietary (‘Derbyshire neck’)
• Dyshormonogenesis
• genetic: Pendred’s syndrome (with deafness)
History to enquire about in hyperthyroidism?
Enquire about: sleep and energy levels, heat intolerance and sweating, agitation, stress and tremor, appetite and weight loss and palpitations
Periods
Examination findings in hyperthyroidism/ Graves’ disease?
Ix of hyperthyroidism?
• Thyroid function tests: TSH and T3/T4
• Thyroid autoantibodies
• Radioisotope scanning: increased uptake of I131 in Graves’ disease, reduced in thyroiditis
Tx of hyperthyroidism?
• β‐Blocker, e.g. propranolol
• Carbimazole or propylthiouracil (both thionamides)
⚬ Block and replace with thyroxine
⚬ titrate dose and monitor endogenous thyroxine
Stop at 18 months and assess for return of thyrotoxicosis. One‐third of patients will remain euthyroid
If thyrotoxicosis returns, the options are
⚬ A repeat course of a thionamide
⚬ Radioiodine (I131): hypothyroidism common
⚬ Subtotal thyroidectomy
Management of graves eye disease?
Severe ophthalmopathy may require high‐dose steroids, orbital irradiation or surgical decompression to prevent visual loss
*stop smoking!
mnemonic for the progression of eye signs in Graves’ disease?
NOSPECS
- no signs or symptoms
- only lid lag/retraction
- Soft tissue involvement
- proptosis
- Extraocular muscle involvement
- Chemosis
- Sight loss due to optic nerve compression and atrophy
History to elicit in diabetic retinopathy?
• Ask the patient to detail their problem: duration and nature of visual disturbance
• Establish any underlying medical diagnoses: especially presence or absence of diabetes
• Previous eye problems or treatment
• If they are diabetic: do they have regular retinal screening?
Examination of diabetic retinopathy?
• Look around for clues: a white stick, braille book or glucometer
• Fundoscopy: check for red reflex (absent if cataract or vitreous haemorrhage)
Tip: find the disc (inferonasally) then follow each of the four main vessels out to the periphery of the quadrants and finish by examining the macular ‘look at the light’
• Check for coexisting hypertensive changes (they always ask!)
Features of background diabetic retinopathy?
1 Hard exudates
2 Blot haemorrhages
3 Microaneurysms
-> Routine referral to eye clinic.
Features of pre proliferative diabetic retinopathy?
Background changes plus:
4 Cotton wool spots
5 Flame haemorrhages
Also venous beading and loops and IRMAs (intraretinal microvascular abnormalities)
Urgent referral to ophthalmology.
Features of proliferative diabetic retinopathy?
Pre-proliferative changes plus
6 Neovascularization of the disc (NVD) and elsewhere
7 Panretinal photocoagulation scars (treatment)
Urgent referral to ophthalmology.
Features of diabetic maculopathy
Macular oedema or hard exudates within one disc space of the fovea.
Treated with focal photocoagulation.
Urgent referral to ophthalmology.
Treatment of diabetic retinopathy
tight glycaemic control
• Improved glycaemic control is associated with less retinopathy
• There may be a transient worsening of the retinopathy initially
treat other risk factors
• Hypertension; hypercholesterolaemia; smoking cessation
• Accelerated deterioration occurs in poor diabetic control, hypertension and
pregnancy
Indications for photocoagulation in diabetic retinopathy?
• Maculopathy
• Proliferative and pre‐proliferative diabetic retinopathy
Pan‐retinal photocoagulation prevents the ischaemic retinal cells secreting angiogenesis factors causing neovascularization.
Focal photocoagulation targets problem vessels at risk of bleeding.
Complications of proliferative diabetic retinopathy?
• Vitreous haemorrhage (may require vitrectomy)
• Traction retinal detachment
• Neovascular glaucoma due to rubeosis iridis
Clinical signs of cataracts
• Loss of the red reflex
• Cloudy lens
• May have relative afferent pupillary defect (with normal fundi if visible)
• Associations: dystrophia myotonica (bilateral ptosis)
Causes of cataracts?
• Congenital (pre‐senile): rubella, Turner’s syndrome
• Acquired: age (usually bilateral), diabetes, drugs (steroids), radiation exposure, trauma
and storage disorders
Management of cataracts?
Surgery (outpatient):
⚬ Phacoemulsification with prosthetic lense implantation
⚬ Yttrium aluminium garnet (YAG) laser capsulotomy
Causes of tophaceous gout?
• Diet and alcohol: xanthine‐rich foods (meat/seafood)
• Drugs: diuretics
• Other conditions: chronic renal failure
Examination findings to look for in patient with gout?
• Asymmetrical swelling of the small joints of the hands and feet (commonly first MTPJ)
• Gouty tophi (chalky white deposits) seen around the joints, ear and tendons
• Reduced movement and function
Associations:
• Obesity
• Hypertension
• Urate stones/nephropathy: nephrectomy scars
• Chronic renal failure: fistulae
• Lymphoproliferative disorders: lymphadenopathy
Ix of gout
• Uric acid levels (diagnostically unreliable)
• Synovial fluid: needle‐shaped, negatively birefringent crystals
• Radiograph features: ‘punched out’ periarticular changes
Acute mx of gout flare
⚬ Treat the cause
⚬ Increase hydration
⚬ High‐dose NSAIDs
⚬ Colchicine and high fluid intake
Prevention of gout
⚬ Avoid precipitants
⚬ Allopurinol (xanthine oxidase inhibitor)
Treatment for Osteoarthritis
• Simple analgesia
• Weight reduction (if OA affects weight‐bearing joint)
• Physiotherapy and occupational therapy
• Joint replacement
Examination findings of osteoarthritis
• Asymmetrical distal interphalangeal joint deformity with Heberden’s nodes (and sometimes Bouchard’s nodes at the proximal interphalangeal joint)
• Disuse atrophy of hand muscles
• Crepitation, reduced movement and function
• Carpal tunnel syndrome or scars
• Other joint involvement and joint‐replacement scars
X-RAY features of osteoarthritis
• Loss of joint space
• Osteophytes
• Peri‐articular sclerosis and cysts
What to ask about in history in patient with osteoarthritis?
Symptoms of OA: stiffness, disuse weakness
Functional aspect: mobility aids, ADLs, work
Treatments: previous joint replacement, side effects of analgesia eg stomach ulcer from NSAIDs
History in Pagets Disease?
Symptoms
• Usually asymptomatic
• Bone pain and tenderness (2%)
Assoc Conditions
• Entrapment neuropathy: carpal tunnel syndrome, visual problems, deafness
• CCF: breathlessness
Examination findings of Paget’s disease?
• Bony enlargement: skull and long bones (sabre tibia)
• Deafness (conductive): hearing‐aid
• Pathological fractures: scars
Cardiac
• High‐output heart failure: elevated JVP, SOA, shortness of breath
Neuro
• Entrapment neuropathies: carpal tunnel syndrome
Fundi
• Optic atrophy and angioid streaks
Ix of Pagets Disease
• Grossly elevated alkaline phosphatase, normal calcium/phosphate
• Radiology:
⚬ ‘Moth‐eaten’ on plain films: osteoporosis circumscripta
⚬ Increase uptake on bone scan
Tx of Paget’s disease
• Symptomatic: analgesia and hearing‐aid
• Bisphosphonates
Causes of sabre tibia
• paget’s
• Osteomalacia
• Syphilis
Associations of angioid streaks?
• paget’s
• Pseudoxanthoma elasticum
• Ehlers–Danlos
Complications of Paget’s disease
• Osteogenic sarcoma (1%)
• Basilar invagination (cord compression)
• Kidney stones (usually high calcium from bone breakdown)
Complications of Paget’s disease
• Osteogenic sarcoma (1%)
• Basilar invagination (cord compression)
• Kidney stones (usually high calcium from bone breakdown)
Examination findings in Marfans Syndrome?
General (Spot diagnosis)
• tall with long extremities (arm span > height)
Hands
• arachnodactyly: can encircle their wrist with thumb and little finger
• Hyperextensible joints: thumb able to touch ipsilateral wrist and adduct over the palm with its tip visible at the ulnar border
Face
• High arched palate with crowded teeth • Iridodonesis (with upward lens dislocation)
Respi
• Pectus carinatum (‘pigeon’) or excavatum
• Scoliosis
• Scars from cardiac surgery or chest drains (pneumothorax)
Cardiac
• Aortic incompetence: collapsing pulse
• Mitral valve prolapse
• Coarctation
Abdo
• Inguinal herniae and scars
CnS
• Normal IQ
High arched palate
What is Iridodonesis
condition in which the iris (coloured part of the eye) vibrates during eye movements.
Usually due to lens subluxation
Genetics of marfans syndrome
• Autosomal dominant and chromosome 15
• Defect in fibrillin protein (connective tissue)
Management of patients with Marfans Syndrome?
• Surveillance: monitoring of aortic root size with annual transthoracic echo
• treatment: β‐blockers and angiotensin receptor blocker to slow aortic root dilatation and pre‐emptive aortic root surgery to prevent dissection and aortic rupture
• Screen family members
Ddx for Marfans?
• Homocystinuria
⚬ Mental retardation and downward lens dislocation
History of ankylosing spondylitis?
Explore back symptoms
Psychosocial impact
• Work, driving, ADLs, etc.
Assoc problems
• Eye problems: anterior uveitis
• Pneumonia
• Syncope: CHB
Drugs and treatment
Examination findings in ankylosing spondylitis
• ‘?’ caused by fixed kyphoscoliosis and loss of lumbar lordosis with extension of cervical spine
• Protuberant abdomen due to diaphragmatic breathing as there is reduced chest expansion (<5 cm increase in girth)
• Increased occiput–wall distance (>5 cm)
• Reduced range of movement throughout entire spine
• Schöber’s test: Two points marked 15 cm apart on the dorsal spine expand by less than 5 cm on maximum forward flexion
Complications of ankylosing spondylitis?
• anterior uveitis (commonest 30%)
• apical lung fibrosis
• aortic regurgitation (4%): midline sternotomy
• atrio‐ventricular nodal heart block (10%): pacemaker
• arthritis (may be psoriatic arthropathy)
Treatment of ankylosing spondylitis
• Physiotherapy
• Analgesia
• Anti‐TNF eg infliximab
Genetics of ankylosing spondylitis
90% association with HLA B27
History taking in systemic sclerosis?
Hands
• Raynaud’s phenomenon
Colour change order: white (vasoconstriction) → blue (cyanosis) → red (hyperaemia)
• Ask about function: how does the condition affect ADLs/work, etc.
• Hypertension or heart problems
• Lung problems
• Swallowing problems or indigestion
Examination findings in Systemic Sclerosis
Hands
• Sclerodactyly: ‘prayer sign’
• Calcinosis (may ulcerate)
• Assess function: holding a cup or pen
Face
• Tight skin
• Beaked nose
• Microstomia
• Peri‐oral furrowing
• Telangiectasia
• Alopecia
Other skin lesions
• Morphoea: focal/generalized patches of sclerotic skin
• En coup de sabre (scar down central forehead)
Blood pressure
• Hypertension
Respiratory
• Interstitial fibrosis (fine and bibasal crackles)
Cardiac
• Pulmonary hypertension (RV heave, loud P2 and TR)
• Evidence of failure
• Pericarditis (rub)
Limited vs diffuse systemic sclerosis?
Limited
• Distribution limited to below elbows and knees and face
- slow progression (years)
Diffuse
• Widespread cutaneous and early visceral involvement
• Rapid progression (months)
CREST in systemic sclerosis
CRESt:
⚬ Calcinosis
⚬ Raynaud’s phenomenon
⚬ Esophageal dysmotility
⚬ Sclerodactyly
⚬ telangiectasia
Ix in systemic sclerosis?
• autoantibodies:
⚬ ANA positive (in 90%)
⚬ Anti‐centromere antibody = limited (in 80%)
⚬ Scl‐70 antibody = diffuse (in 70%)
• Hand radiographs: calcinosis
• pulmonary disease: lower lobe fibrosis and aspiration pneumonia:
⚬ CXR, high‐resolution CT scan and pulmonary function tests
• gastrointestinal disease: dysmotility and malabsorption
⚬ Contrast scans, FBC and B12/folate
• Renal disease: glomerulonephritis
⚬ U&E, urinalysis, urine microscopy (casts) and consider renal biopsy
• Cardiac disease: myocardial fibrosis and arrhythmias
⚬ ECG and echo
Tx of systemic sclerosis?
Symptomatic treatment only:
• Camouflage creams
• Raynaud’s therapy:
⚬ Gloves, hand‐warmers, etc.
⚬ Calcium‐channel blockers
⚬ ACE‐Is
⚬ Prostacyclin infusion (severe)
• Renal:
⚬ ACE‐Is: prevent hypertensive crisis and reduce the mortality from renal failure
• gastrointestinal:
⚬ Proton‐pump inhibitor for oesophageal reflux
Prognosis of systemic sclerosis
Diffuse systemic sclerosis: 50% survival to 5 years (most deaths are due to respiratory failure)
History taking in pt with SLE?
Rash:
* Location, appearance, other areas affected
* Photosensitivity
Associations
* Cold hands: Raynaud’s phenomenon
* Dry eyes/mucous membranes: Sjögren’s syndrome
Psychosocial impact
* Particularly important in young women
* Confidence, relationships, work
* Depression
* Family planning: infertility/teratogenicity from treatment
Systemic effects of SLE/treatment
* Renal: hypertension, haematuria, frothy urine/oedema (proteinuria)
* Immunosuppression: skin changes/infections
Examination findings of SLE pt?
Face
* Malar ‘butterfly’ rash
* Discoid rash ± scarring (discoid lupus)
* Oral ulceration
* Scarring alopecia
Hands
* Vasculitic lesions (nail‐fold infarcts)
* Jaccoud’s arthropathy (mimics rheumatoid arthritis but due to tendon contractures not
joint destruction)
Systemic effects of SLE
* Respiratory: percussion and auscultation
⚬ Pleural effusion, Pleural rub, Fibrosing alveolitis
- Neurological: finger‐nose‐finger and/or pronator drift
⚬ Focal neurology
⚬ Chorea
⚬ Ataxia - Renal: Hypertension
ix of SLE?
Diagnosis: Serum autoantibodies (ANA, anti dsDNA)
Disease activity:
- elevated ESR but normal CRP
- elevate Immunoglobulins
- reduced C3/C4
- Renal panel, urine microscopy for casts (Glomerulonephritis)
Diagnostic criteria for SLE?
4/11 of American College of Rheumatology Criteria:
- Malar rash
- Discoid rash
- Photosensitivity
- Oral ulcers
- Arthritis
- Serositis (pleuritis or pericarditis)
- Renal involvement (proteinuria or cellular casts)
- Neurological disorder (seizures or psychosis)
- Haematological disorder (autoimmune haemolytic anaemia or pancytopenia)
- Immunological disorders (positive anti‐dsDNA or anti‐Sm antibodies)
- Elevated ANA titre
Treatment of mild SLE disease (cutaneous/ joint involvement only)?
Topical corticosteroids
Hydroxychloroquine
treatment of moderate SLE disease (+organ involvement)?
Prednisolone
Azathioprine
Treatment of severe SLE disease (+ severe inflammatory involvement of vital organs)?
Methylprednisolone
MMF (Lupus nephritis)
Cyclophosphamide
Azathioprine
Cyclophosphamide side effects?
- Haematological and haemorrhagic cystitis * infertility
- teratogenicity
Prognosis of SLE?
Good: 90% survival at 10 years
History to take for RA patient?
Symptoms
* Joints involved, pain, function
Disability
* Occupation and ADLs
Drugs
* Will help assess disease activity
Systemic effects of disease and treatment
- lungs, eyes, neuropathies, haematological (Anaemia), cardiac, renal
Examination of Rheumatoid Arthritis patient?
examine hands
assess disease activity
assess function
treatment side effects
systemic manifestations of rheumatoid arthritis
Hand examination of Rheumatoid Arthritis patient?
- Symmetrical and deforming polyarthropathy
- Volar subluxation and ulnar deviation at the MCPJs
- Subluxation at the wrist
- Swan‐neck deformity (hyperextension of the PIPJ and flexion of the DIPJ)
- Boutonnière’s deformity (flexion of the PIPJ and hyperextension of the DIPJ)
- ‘Z’ thumbs
- Muscle wasting (disuse atrophy)
- Surgical scars:
⚬ Carpal tunnel release (wrist)
⚬ Joint replacement (especially thumb)
⚬ Tendon transfer (dorsum of hand) - Rheumatoid nodules (elbows)
examination findings in rheumatoid arthritis that reflect disease activity?
- Red, swollen, hot, painful hands imply active disease
examination to assess function in rheumatoid arthritis?
- power grip: ‘squeeze my fingers’
- precision grip: ‘pick up a coin’ or ‘do up your buttons’
- key grip: ‘pretend to use this key’
- Remember the wheelchair, walking aids and splints
examination to look for treatment effects in rheumatoid arthritis?
- Steroids: Cushingoid
- C‐spine stabilization scars
systemic manifestations of rheumatoid arthritis?
- pulmonary:
⚬ Pleural effusions
⚬ Fibrosing alveolitis
⚬ Obliterative bronchiolitis
⚬ Caplan’s nodules - Eyes:
⚬ Dry (secondary Sjögren’s)
⚬ Scleritis - neurological:
⚬ Carpal tunnel syndrome (commonest)
⚬ Atlanto‐axial subluxation: quadriplegia
⚬ Peripheral neuropathy - Haematological:
⚬ Felty’s syndrome: RA + splenomegaly + neutropaenia
⚬ Anaemia (all types!) - Cardiac:
⚬ Pericarditis - Renal:
⚬ Nephrotic syndrome (secondary amyloidosis or membraneous glomerulonephritis, e.g. due to penicillamine)
main differential diagnosis of rhuematoid arthritis?
Psoriatic arthropathy:
⚬ Nail changes
⚬ Psoriasis: elbows, behind ears and scalp
ix of rheumatoid arthritis?
- Elevated inflammatory markers
- Radiological changes:
⚬ Soft tissue swelling
⚬ Loss of joint space
⚬ Articular erosions
⚬ Periarticular osteoporosis - Positive rheumatoid factor in 80%
Prognosis for rheumatoid arthritis
5 years – 1/3 unable to work;
10 years – 1/2 significant disability
diagnosis of rheumatoid arthritis?
Diagnosis: 4/7 of American college of Rheumatology Criteria
- Morning stiffness
- Arthritis in 3+ joint areas
- Arthritis of hands
- Symmetrical arthritis
- Rheumatoid nodules
- Positive rheumatoid factor
- Erosions on joint radiographs
management of rheumatoid arthritis?
medical
* Symptomatic relief: NSAIDs and COX‐2 inhibitors
* Early introduction of disease‐modifying anti‐rheumatoid drugs (DMARDs) to suppress disease activity
Ongoing disease activity may require immunomodulation therapy:
* anti‐tnf therapy: Infliximab/Etanercept/Adalimumab
* B cell depletion therapy: Rituximab (anti‐CD20 mAb)
Supportive
⚬ Explanation and education
⚬ Exercise and physiotherapy
⚬ Occupational therapy and social support
Surgery
⚬ Joint replacement, tendon transfer, etc.
side effects of anti-TNF therapy?
rash, opportunistic infection (exclude TB: Heaf test and CXR)
what DMARDs are used in Rheumatoid arthritis to suppress disease activity?
what history to take in patient with pseudoxanthoma elasticum?
Explore skin problems
* Hereditary: chronic
other problems
* Hyperextensible joints
* Reduced visual acuity
* Hypertension
* MI or CVA
* Gastric bleed
family history
pseudoxanthoma elasticum
what examination findings?
Skin
* ‘Plucked chicken skin’ appearance: loose skin folds especially at the neck and axillae, with yellow pseudoxanthomatous plaques
Eyes
* Blue sclerae
* Retinal angioid streaks (cracks in Bruch’s membrane) and macular degeneration
Cardiovascular
* Blood pressure: 50% are hypertensive
* Mitral valve prolapse: EC and PSM
pseudoxanthoma elasticum
inheritance pattern?
80% autosomal recessive (ABCC6 gene, chromosome 16)
pathophysiology of pseudoxanthoma elasticum?
Degenerative elastic fibres in skin, blood vessels and eye
premature coronary artery disease
main differential for elastic skin apart from pseudoxanthoma elasticum?
Ehlers Danlos
Examination findings of ehlers danlos
Skin and joints
• Fragile skin: multiple ecchymoses, scarring – ‘fish‐mouth’ scars especially on the knees
• Hyperextensible skin: able to tent up skin when pulled (avoid doing this)
• Joint hypermobility and dislocation (scar from joint repair/replacement)
Cardiac
• Mitral valve prolapse
abdominal
• Scars:
⚬ Aneurysmal rupture and dissection
⚬ Bowel perforation and bleeding
Features/ pathophysiology of ehlers danlos
• Inheritance: autosomal dominant (family history more apparent)
• Defect in collagen causing increased skin elasticity
• No premature coronary artery disease
History taking for skin lump suspected malignancy?
Symptoms
• Location and rapidity of growth
• Recent changes or bleeding
Risk factors
• Sun exposure
• Occupation: exposure to dust/chemicals, outdoor work
• Family or past medical history of skin cancer
Associations
• Solid organ transplant: immunosuppression
Complications
• Local invasion or metastasis: bone pain, neurological or abdominal problems
Usual findings in basal cell carcinoma
• Usually on face/trunk: sun‐exposed areas
• Pearly nodule with rolled edge
• Superficial telangiectasia
• Ulceration in advanced lesions
• Slowly grow over a few months
• Local invasion only, rarely metastasize
Treatment of basal cell carcinoma
• Curettage/cryotherapy if superficial
• Surgical excision ± radiotherapy
Bowens disease?
Squamous cell carcinoma in situ
Bowens disease?
Squamous cell carcinoma in situ
Examination of pt with squamous cell carcinoma?
• Sun‐exposed areas (+ lips + mouth)
• Actinic keratoses: pre‐malignant (red and scaly patches)
• Varied appearance
⚬ Keratotic nodule
⚬ Polypoid mass
⚬ Cutaneous ulcer
• Other lesions/previous scars
• Metastases (draining lymph nodes/hepatomegaly/bone tenderness)
Treatment of squamous cell carcinoma?
• Surgery ± radiotherapy
• 5% metastasize
Examination findings of malignant melanoma
• Patient’s appearance: mention risks
⚬ Fair skin with freckles
⚬ Light hair
⚬ Blue eyes
• Appearance of lesion
asymmetrical
Border irregularity
Colour (black: often irregular pigmentation, may be colourless) Diameter >6 mm
Enlarging
• Other lesions/previous scars
• Metastases (draining lymph nodes/hepatomegaly/bone tenderness)
Diagnosis and treatment of malignant melanoma?
• Excision
• Staged on Breslow thickness (maximal depth of tumour invasion into dermis):
⚬ <1.5 mm = 90% 5‐year survival
⚬ >3.5 mm = 40% 5‐year survival
Beware the man with a glass eye and ascites: ocular melanoma!
History of henoch schonlein purpura
Triad
• Purpuric rash: usually on buttocks and legs
• Arthritis
• Abdominal pain
Precipitant
• Infections: streptococci, HSV, parvovirus B19, etc.
• Drugs: antibiotics
Complications
• Renal involvement (IgA nephropathy): visible or non‐visible haematuria, proteinuria
• Hypertension
Examination of henoch schonlein purpura?
Rash
• Purpuric rash: usually on buttocks and legs
Joints
• Arthritis
Other
• Blood pressure
• Urine dipstick
pathophysiology of henoch schonlein purpura?
- Small‐vessel vasculitis: IgA and C3 deposition
- Normal or raised platelet count (distinguishes from other forms of purpura)
- Children more than adults, males > females
prognosis of henoch schonlein purpura
90% full recovery although can recur
treatment of henoch schonlein purpura
most spontaneously recover without treatment although steroids may help
recovery and treat painful arthralgia
history in erythema nodosum
Skin
* Tender, red, smooth, shiny nodules on the shins
Causes
* Sarcoidosis
* Streptococcal throat infection
* Streptomycin, sulphonamides
* Oral contraceptive pill
* Pregnancy
* TB
* Inflammatory bowel disease
* Lymphoma
* Idiopathic
examination findings of erythema nodosum?
Skin
* Tender, red, smooth, shiny nodules commonly found on the shins (although anywhere with subcutaneous fat)
* Older lesions leave a bruise
Joints
* Tenderness and swelling
Cause
* Red, sore throat (streptococcal infection)
* Parotid swelling (sarcoidosis)
pathology of erythema nodosum?
inflammation of subcutaneous fat (panniculitis)
skin manifestations of sarcoidosis
- erythema nodosum
- nodules and papules: red/brown seen particularly around the face, nose, ears and neck. Demonstrates Koebner’s phenomenon
- lupus pernio: diffuse bluish/brown plaque with central small papules commonly affecting the nose
diabetes and skin rash?
necrobiosis lipoidica diabeticorum
history to take in diabetes patient with new rash
diabetic history/care
* Duration
* Insulin administration and glucose control: rotation of injection sites
* Foot care: podiatry
Microvascular complications of diabetes
* Neuropathy
* Retinopathy
Psychosocial
* Impact on ability to work, form relationships, body image
Rashes in diabetic patients? differentials
necrobiosis lipoidica diabeticorum
diabetic dermopathy, granuloma annulare, leg ulcers, eruptive xanthomata, vitiligo, candidiasis
examination findings in necrobiosis lipoidica diabeticorum?
Shins
* Necrobiosis lipoidica diabeticorum:
⚬ Well‐demarcated plaques with waxy‐yellow centre and red–brown edges
⚬ Early: may resemble a bruise
⚬ Prominent skin blood vessels
⚬ Female preponderance (90%)
* Diabetic dermopathy: Red/brown, atrophic lesions
Feet/legs
* Ulcers: arterial or neuropathic
* Eruptive xanthomata:
⚬ Yellow papules on buttocks and knees (also elbows)
⚬ Caused by hyperlipidaemia
* Granuloma annulare: flesh‐coloured papules in annular configurations on the dorsum feet (and more commonly fingers)
injection sites
* Lipoatrophy
* Fat hypertrophy
cutaneous infections
* Cellulitis
* Candidiasis (intertrigo): in skin creases
others
* Vitiligo (and other autoimmune diseases)
* PVD: pulses
Treatment for necrobiosis lipoidica diabeticorum?
- Topical steroid and support bandaging
- Tight glycaemic control does not help
examination findings in patient with xanthomata?
- Hypercholesterolaemia: tendon xanthomata, xanthelasma and corneal arcus
- Hypertriglyceridaemia: eruptive xanthomata and lipaemia retinalis
- other causes of secondary hyperlipidaemia:
⚬ Hypothyroidism
⚬ Nephrotic syndrome
⚬ Alcohol
⚬ Cholestasis
History taking for patient with leg ulcer?
Symptoms
• Pain: arterial (venous and neuropathic are painless)
• Location
Associated diseases
• Venous: DVT, chronic venous insufficiency, varicose veins, CCF
• Arterial: PVD
• Neuropathic: sensory neuropathy, diabetes
Complications
• Systemic signs of infection
Examination of leg ulcer?
Venous
• Gaiter area of lower leg
• Stigmata of venous hypertension: varicose veins or scars from vein stripping, oedema, lipodermatosclerosis, varicose eczema, atrophie blanche
• pelvic/abdominal mass
Arterial
• Distal extremities and pressure points
• Trophic changes: hairless and paper‐thin shiny skin
• Cold with poor capillary refill
• absent distal pulses
neuropathic
• Pressure areas, e.g. under the metatarsal heads
• peripheral neuropathy
• Charcot’s joints
Complications
• infection: temperature, pus and cellulitis
• malignant change: Marjolin’s ulcer (squamous cell carcinoma)
Other causes of leg ulcer apart from the usual venous/arterial/ neuropathic?
• Vasculitic, e.g. rheumatoid arthritis
• Neoplastic, e.g. squamous cell carcinoma
• Infectious, e.g. syphilis
• Haematological, e.g. sickle cell anaemia
• Tropical, e.g. cutaneous leishmaniasis
Ix leg ulcer
• Doppler ultrasound
• Ankle–brachial pressure index (0.8–1.2 is normal, <0.8 implies arterial insufficiency)
• Arteriography
Treatment of venous ulcers
• Four‐layer compression bandaging (if no PVD)
• Varicose vein surgery
Tx of arterial ulcers
Angioplasty or vascular reconstruction/amputation
Causes of neuropathic ulcers
• Diabetes mellitus
• Tabes dorsalis
• Syringomyelia
History taking in psoriasis
Describe the rash
• Location, appearance, pruritis
Psychosocial impact
• Particularly important in young women • Confidence, relationships, work
• Depression
Exacerbating factors
• Stress, alcohol, cigarettes, drugs (β‐blockers), trauma
treatment
• PUVA: risk of melanoma (fair skin, family history)
• Immunosuppression: intercurrent infections
• Systemic side‐effects: steroids
• Pregnancy? Some treatments are teratogenic
Examination findings in psoriasis?
Skin
• Chronic plaque (classical) type: multiple, well‐demarcated, ‘salmon‐pink’, scaly plaques on extensor surface
• Check behind ears, scalp and umbilicus
• Koebner phenomenon: plaques at sites of trauma
• Skin staining from treatment
Nails
• Pitting, onycholysis, hyperkeratosis, discoloration
Joints
• psoriatic arthropathy (10%), five forms:
⚬ DIPJ involvement (similar to OA)
⚬ Large joint mono/oligoarthritis
⚬ Seronegative (similar to RA)
⚬ Sacroilitis (similar to ankylosing spondylitis)
⚬ Arthritis mutilans
Treatment options of psoriasis?
Topicals:
Emollients, topical steroids, calcitriol, coal tar
Phototherapy: • UVB
• Psoralen + UVA (PUVA)
Systemics
• Cytotoxics (methotrexate and ciclosporin)
• anti‐tnfα (adalimumab: Humira) and other immunological
• Retinoids (Acitretin): teratogenic
Complications of psoriasis
Pustular psoriasis
GED
Causes of nail pitting
• psoriasis
• Lichen planus
• Alopecia areata
• Fungal infections
Koebner phenomenon assoc w
• psoriasis
• Lichen planus
• Viral warts
• Vitiligo
• Sarcoid
History taking in eczema
Rash
• Location, appearance, pruritis
psychosocial impact
• Particularly important in young women • Confidence, relationships, work
• Depression
atopic (Endogenous)
• Asthma, hay fever and allergy
Environmental (Exogenous)
• Primary irritant dermatitis: may just affect hands
• What is their job?
• Triggers?
Examination in eczema
Rash
• Erythematous and lichenified patches of skin
• Predominantly flexor aspects of joints
• Fissures (painful), especially hands and feet
• Excoriations
• Secondary bacterial infection
associated atopy
• Respiratory: polyphonic wheeze (asthma)
Systemic treatment Effects
• Steroids: e.g. blood pressure
Ix in eczema?
• Patch testing for allergies
Treatment options for eczema
• Avoid precipitants
• Topical:
⚬ Emollients
⚬ Steroids
⚬ Tacrolimus (protopic): small increased risk of Bowen’s disease
• Anti‐histamines for pruritis
• Antibiotics for secondary infection
• UV light therapy
• Systemic therapy (prednisolone) in severe cases
Or even azathioprine/ ciclosporin/ MTX
Immunologics: dupilumab, baricitinib, abrocitinib
History in young hypertensive patient with headache?
- Duration of symptoms, nature of headache
- Past history of hypertension: previous blood pressure readings (e.g. employment
medical, with prescription of oral contraceptive pill, during pregnancy) - Other medical history (e.g. renal disease), cardiovascular risk factors (smoking, diabetes, known ischaemic heart disease)
- Drug history (prescribed and illicit), alcohol consumption
- Visual disturbance (in accelerated phase hypertension)
- Paroxysomal symptoms (phaeochromocytoma)
- Check if pregnant!
Examination in young hypertensive patient with headaches?
- Body habitus: obese, Cushingoid, acromegalic
- Radial pulse (SR/AF), radio‐radial and radio‐femoral delay (coarctation)
- Check the blood pressure yourself, with a manual sphygmomanometer, in both arms
- Evidence of cardiac failure
- Underlying renal cause: renal bruit(s), polycystic kidney disease, current renal replacement therapy, ask to dip urine
- fundoscopy: hypertensive retinopathy
Fundoscopy in hypertensive retinopathy?
⚬ Grade 1: silver wiring (increased reflectance from thickened arterioles)
⚬ Grade 2: plus arteriovenous nipping (narrowing of veins as arterioles cross them)
⚬ Grade 3: plus cotton wool spots and flame haemorrhages
⚬ Grade 4: plus papilloedema
There may also be hard exudates (macular star)
causes of hypertension?
- Essential (94%: associated with age, obesity, salt and alcohol)
- Renal (4%: underlying chronic kidney disease secondary to glomerulonephritis, ADPKD, renovascular disease)
- Endocrine (1%: Conn’s, Cushing’s, acromegaly or phaeochromocytoma)
- Aortic coarctation
- Pre‐eclampsia: pregnancy
Ix of young hypertension?
- Evidence of end‐organ damage: fundoscopy, LVH on ECG, renal impairment, cardiac failure on CXR, echocardiography
- Exclude underlying cause:
⚬ Urine pregnancy test (where appropriate!)
⚬ Urinalysis (and urine ACR)
⚬ U&Es
⚬ Consider secondary screen: renin/aldosterone levels, plasma and/or urinary metanephrines
Diagnosis of hypertension?
Current (2011) British Hypertension Society guidelines:
⚬ Clinic BP >140/90 mm Hg: use 24h ABPM to confirm diagnosis (average of daytime
values)
Definitions;
⚬ Stage 1 hypertension: clinic BP ≥140/90 mm Hg or ABPM daytime average ≥135/85 mm Hg
⚬ Stage 2 hypertension: clinic BP ≥160/100 mm Hg or ABPM daytime average ≥150/95 mm Hg
⚬ Severe hypertension: clinic SBP ≥180 mm Hg or DBP ≥110 mm Hg
When to treat hypertension?
⚬ Treat if stage 1 hypertension and evidence of end‐organ damage, ischaemic heart
disease, diabetes, CKD or 10‐year cardiovascular risk ≥20%
⚬ Treat all with stage 2 hypertension
* Arrange same‐day admission if severe hypertension and grade 3 or 4 retinopathy (or other concerns; e.g. new renal impairment)
Management of hypertension
- Lifestyle modification (lose weight, increase exercise, stop smoking)
- Initial treatment:
⚬ ACE‐I or ARB - Aged >55 years or Afro‐Caribbean ethnicity: CCB or thiazide‐like diuretic
⚬ Titrate dose to maximum tolerated - Then add 2nd agent: CCB or thiazide‐like diuretic
- Then ACE‐I/ARB + CCB + thiazide‐like diuretic
- Consider adding spironolactone, β‐blocker, α‐blocker or seeking specialist opinion
- Consider other cardiovascular risk modification: aspirin, statin
Management of malignant hypertension with Grade III and IV retinopathy
Bed rest, oral anti‐hypertensives (long‐acting CCB) and non‐invasive blood pressure monitoring: aiming for gradual reduction in blood pressure
Management of HTN Plus encephalopathy/stroke/myocardial infarction/left ventricular failure.
⚬ Parenteral venodilators and invasive blood pressure monitoring.
⚬ Over rapid fall in blood pressure can lead to ‘watershed’ cerebral and retinal infarction.
what is papilloedema?
Blurring of disc margins/elevation of disc/loss of venous pulsation/venous engorgement
causes of papilloedema?
- Raised intracranial pressure: space‐occupying lesion, benign intracranial hypertension and cavernous sinus thrombosis
- Accelerated phase hypertension
- Central retinal vein occlusion
History taking in inflammatory bowel disease?
- Gastrointestinal symptoms
⚬ Duration
⚬ Precipitants (travel, antibiotics, infectious contacts, foods, sexual history)
⚬ Stool frequency and consistency (Bristol stool scale)
⚬ Blood: fresh PR/mixed with stools
⚬ Mucus/slime
⚬ Urgency, incontinence, tenesmus
⚬ Abdominal pain, bloating: and association with eating, defecation - Systemic symptoms
⚬ Fever
⚬ Anorexia
⚬ Weight loss
⚬ Rash, arthralgia, aphthous ulcers - Family history
Examination findings of IBD?
- General
⚬ Pallor/anaemia
⚬ Nutritional status
⚬ Pulse and BP
⚬ Oral ulceration - Abdomen
⚬ Surgical scars, including current/past stoma sites
⚬ Tenderness
⚬ Palpable masses (e.g. right iliac fossa mass in Crohn’s disease or colonic tumour
in UC)
⚬ Ask to examine for perianal disease - Evidence of treatment
⚬ Steroid side effects
⚬ Ciclosporin (gum hypertrophy and hypertension)
⚬ Hickman lines/scars
Ix in suspected IBD?
⚬ Stool microscopy and culture: exclude infective cause of diarrhoea
⚬ FBC and inflammatory markers: monitor disease activity
⚬ AXR: exclude toxic dilatation in UC and small bowel obstruction due to strictures in
Crohn’s
⚬ Sigmoidoscopy/colonoscopy and biopsy: histological confirmation
⚬ Bowel contrast studies: strictures and fistulae in Crohn’s disease
⚬ Further imaging: white cell scan and CT scan
Cause of IBD?
Genetic, environmental and other factors combine to produce an exaggerated,
sustained and mucosal inflammatory response
Differentials for IBD?
⚬ Crohn’s: Yersinia, tuberculosis, lymphoma (and UC)
⚬ UC: infection (e.g. campylobacter), ischaemia, drugs and radiation (and Crohn’s)
Extra intestinal manifestations of IBD?
Mouth: Apthous ulcers*
Skin: Erythema nodosum*
Pyoderma gangrenosum*
Finger clubbing*
Joint:
Large joint arthritis*
Seronegative arthritides
Eye: Uveitis, episcleritis and iritis*
Liver: Primary sclerosing cholangitis (UC)
Systemic amyloidosis
*related to disease activity
Complications of Crohns Disease?
Malabsorption
Anaemia
Abscess
Fistula
Intestinal obstruction
Complications of Ulcerative Colitis?
Anaemia
Toxic dilatation
Perforation
Colonic carcinoma
Which UC patients are at higher risk of developing Colon Ca?
Higher risk in patients with pancolitis (5–10% at 15–20 years), and in those with PSC
Recommended surveillance for colon ca in UC?
Surveillance: 3‐yearly colonoscopy for patients with pancolitis >10 years, increasing in frequency with every decade from diagnosis (2‐yearly 20–30 years, annually >30
years)
Overall treatment strategies for IBD?
Medical therapies: steroids/ 5-ASA etc
Antibiotics (metronidazole): in Crohn’s with perianal infection, fistulae or small bowel bacterial overgrowth
Nutritional support: high fibre, elemental and low residue diets
Psychological support
Surgery
what nutrition / diet is recommended in IBD?
high fibre, elemental and low residue diets
in what situation is antibiotic therapy with metronidazole indicated in crohns disease
Antibiotics (metronidazole): in Crohn’s with perianal infection, fistulae or small bowel bacterial overgrowth
Surgical tx options for IBD?
⚬ Crohn’s: obstruction from strictures, complications from fistulae and perianal disease and failure to respond to medical therapy
⚬ UC: chronic symptomatic relief, emergency surgery for severe refractory colitis and colonic dysplasia or carcinoma
History taking in atrial fibrillation?
• Symptoms of atrial fibrillation
⚬ Onset and offset, frequency and duration
⚬ Breathlessness, chest pain, palpitations, presyncope
⚬ Precipitants: alcohol, caffeine, exercise
• Associated conditions
⚬ Cardiac problems: valvular heart disease
⚬ Hypertension
⚬ Hyperthyroidism
⚬ Stroke or TIA (likely in this case)
⚬ Lung disease including PE
• Treatment consideration
⚬ Anticoagulation and risk factors for bleeding
⚬ Anti‐arrhythmic vs cardioversion vs pulmonary vein isolation
Examination finding in atrial fibrillation?
• Cardiovascular examination
⚬ Pulse and BP
⚬ Auscultation: murmurs – MS or MR
⚬ Signs of CCF
• Assessment of thyroid status
⚬ Tremor
⚬ Goitre
⚬ Eye disease: lid lag, exophthalmos (Grave’s disease)
• Brief neurological examination
⚬ Pronator drift
⚬ Visual fields
⚬ CN VII weakness (facial asymmetry)
⚬ CN V and upper limb sensation
⚬ Gait
Ix of new AF
⚬ Confirmation: 12‐lead ECG or 24‐hour Holter monitor
⚬ Echo: structural disease, LVH, LA size (>4.0 cm – recurrence high)
⚬ TSH
Types of AF
⚬ Paroxysmal: <7 days, self terminating
⚬ Persistent: >7 days, requires chemical or electrical cardioversion
⚬ Permanent: >1 year or when no further attempts to restore sinus
Mx of AF
⚬ Rhythm control: chemical or electrical cardioversion
⚬ Rate control: β‐blockers, digoxin, pacemaker and AVN ablation
CHADVASC
Systemic emboli risk:
C Congestive cardiac failure = 1 Hypertension = 1
A2 Age ≥75 = 2
D Diabetes = 1
S2 Stroke/TIA/embolus = 2
V Vascular disease = 1
A Age 65–74 = 1
Sc Sex category (female) = 1
0 = Low stroke risk = no anticoagulation
1 = Medium stroke risk (1.3% per annum) = patient preference
≥2 = High risk (>2.2% per annum) = oral anticoagulation recommended
Bleeding risk HASBLED score
Bleeding risk:
H A S B L E D
Hypertension = 1
Abnormal kidney or liver function = 1 for each
Stroke = 1
Bleeding = 1
Labile INR = 1
Elderly = 1
Drugs (NSAIDs) and alcohol = 1 for each
3 or more = high risk (avoid oral anticoagulation)
Patients high risk for both embolic and bleeding complications should be considered for left atrial appendage occlusion to isolate the commonest source of thrombus in AF.
• Prevalence: 8% of >80‐year‐olds have AF
History for syncope?
Description of the syncopal episode:
⚬ Provocation: micturation, cough or stressful situation (vasovagal)
⚬ Prodrome: light headed, dizziness, tunnel vision (vasovagal/orthostatic), no warning
(cardiac)
⚬ Posture: sitting/lying (cardiac) or standing (orthostatic), sudden head turning
(vertebrobasilar)
⚬ Associated symptoms: palpitations and chest pain (cardiac), headache, tongue biting
and incontinence (neuro)
⚬ Duration (transient, <5 minutes) and frequency
⚬ Recovery: immediate (cardiac) or prolonged confused state and amnesia (>5 minutes)
(neuro), red/flushed face (cardiac)
⚬ Injury (neuro or cardiac)
⚬ Eyewitness account is very useful
Past medical history of syncope/presyncope, cardiac disease or neurological conditions
Medications that may cause hypotension
Examination in syncope
• Brief cardiovascular exam
⚬ Pulse and blood pressure (lying and standing), postural drop: >20/10 mm Hg
difference
⚬ Auscultation: obstructive valvular pathology e.g. AS or MS or signs of a PE (loud P2 and left parasternal heave)
⚬ Pacemaker or ICD scars
• Brief neurological exam
⚬ Fundoscopy
⚬ Pronator drift
⚬ Reflexes
⚬ Parkinson’s plus tremor, rigidity, bradykinesia and orthostatic hypotension, e.g. multiple system atrophy
Ddx syncope
⚬ Cardiac: brady‐ or tachycardia, obstructive cardiac lesion: AS, MS, HOCM or PE
⚬ Neurological: epilepsy, vertebrobasilar insufficiency
⚬Orthostatic (postural) hypotension: particularly in combination with vasodilator
drugs
⚬ Vasovagal (neurocardiogenic): stress, cough, micturation, defecation
Ix in syncope
⚬ 12‐lead ECG, Holter monitor, implantable loop recorder, electrophysiology study, ETT
and Echo if cardiac cause suspected
⚬ Tilt table test if orthostatic hypotension suspected
⚬ EEG and/or CT MRI brain if a neurological cause is suspected
Mx of different causes of syncope
⚬ Cardiac: pacemaker, ICD, revascularisation and valvular surgery
⚬ Vasovagal: education on avoidance, isotonic muscle contraction
⚬ Orthostatic hypotension: salt and water replacement, support stockings, medication review, occasionally fludrocortisone, midodrine, SSRIs and pacemaker are helpful
⚬ Neurological: antiepileptic medication
DVLA instructions in pt w syncope?
⚬ Check the 3 P’s: provocation/prodrome/postural – if all present then likely benign and can continue driving.
⚬ Solitary with no clear cause – 6 month ban; clear cause that has been treated – resume driving after 4 weeks
⚬ Recurrent syncope due to seizures – must be fit free for 1 year to drive.
Ix in suspected asthma attack
• Arterial blood gas:
⚬ Hypoxaemia
⚬ Normal or rising PaCO2 suggests a tiring patient requiring respiratory support (should
have a respiratory alkalosis)
• CXR in exhalation (pneumothorax)
Tx asthma attack
⚬ Bronchodilators and steroids (not routine antibiotics as often viral)
⚬ Asthma specialist nurse: assess Inhaler technique
⚬ Allergy clinic
Tx pneumothorax
High flow O2
⚬ Needle aspiration or chest drain
⚬ May need talc or surgical pleurodesis if it is recurrent
examination findings of Osler Weber Rendu Syndrome aka Hereditary Haemorrhagic Telangiectasia?
- Multiple telangiectasia on the face, lips and buccal mucosa
- Anaemia: gastrointestinal bleeding
- Cyanosis and chest bruit: pulmonary vascular abnormality/shunt
features of Osler Weber Rendu Syndrome aka Hereditary Haemorrhagic Telangiectasia?
- Autosomal dominant
- Increased risk gastrointestinal haemorrhage, epistaxis and haemoptysis
- Vascular malformations:
> Pulmonary shunts
> Intracranial aneurysms: subarachnoid haemorrhage
Management of DVT?
- Anticoagulation: 3 months if provoked, 6 months if unprovoked, lifelong if recurrent/ high risk
- Compression stockings reduce post‐phlebitic syndrome
TIMI risk score for MI
