Station 5 Paces Flashcards
Taking history of bloody diarrhoea
Presenting complaint
Systemic symptoms (fever, anorexia, weight loss, rash, arthralgia, aphthous ulcers)
PMHx and PSHx
Meds history
FH, SHx
Examination findings for ?IBD dx
Pallor
Nutritional status
Pulse and BP
Oral ulceration
Surgical scars/stomas
Tenderness
Palpable mass
Perianal disease
Steroid side effects
Gum hypertrophy from ciclosporin
Investigating IBD
Stool MC&S
FBC, UE, CRP, electrolytes
AXR
Flexi sig
Treatment for Crohns
Mild- moderate: oral steroids and mesalazine
Severe disease: IV steroid, IV infliximab
Maintenance therapy: oral steroids, aza, infliximab, adalimimab
Metronidazole in Crohns with orrianal infection/fistula/small bowel bacterial over growth
Nutritional support
Treatment for UC
Mild to mod: Oral or rectal steroids and mesalazine
Severe: IV steroids, IV ciclosporin
Maintainence therapy: oral steroids, mesalazine, azathioprine
Surgical management of IBD
Crohns: used for strictures, fistula or perianal disease that fails to respond to medical management
UC: emergency surgery for severe refractory disease or symptomatic relief of chronic disease or carcinoma
Complications of Crohns
Malabsorption
Anaemia
Abscess
Fistula
Obstruction
Complications of UC
Anaemia
Toxic dilatation
Perforation
Colonic carcinoma
- higher risk in patients with pancoitis and PSC
- surveillance colonoscopy 3 yearly in patients with pancolitis >10 years, increasing frequency with every decade form diagnosis
Extra- intestinal manifestations of IBD
Aphthous ulcers*
Erythema nodosum*
Pyoderma gangrenosum*
Finger clubbing*
Large joint arthritis*
Seronegative arthritis
Uveitis*
Episcleritis*
Iritis*
PSC
Systemic amyloidosis
- related to disease activity
What is dermatitis herpetiformis?
Itchy blistering rash usually in extensor surfaces secondary to an insensitivity to gliadin in gluten (hence commonly associated with coeliac disease
Diagnosis of dermatitis herpetiformis
Skin biopsy
Screen for coeliac disease:
FBC, iron, b12/folate, calcium
IgA TTG
Anti- endomysial antibodies
Small intestinal biopsy
Management of coeliac disease and dermatitis herpetiformis
Gluten free diet + dietitian referral
Oral dapsone
Aetiology of rhuematoid arthritis
Combination of genetic and environmental factors
Association with HLA-DR4
Association with smoking
Pathophysiology of RA
Disease exclusively of synovial joints
Inflammation of the synovial membranes due to the presence of immune complexes in these joints which leads to activation of the immune system and synovitis
Clinical presentation of RA
Symmetrical MCP, PIP and wrist joint synovitis
Joint pain, stiffness, swelling of joints and erythema
Cervical spine involvement
Characteristic dermformities:
- ulnar deviation of MCP joints
- boutnonniere deformities of fingers
- swan neck deformities
- Z deformity of thumbs
Extra articular features:
- rhuematoid nodules
- episcleritis
Diagnosis of RA
X-rays- periarticular osteopenia, symmetrical joint space loss, deformities, erosions, nodules)
RF (+ve in 70%)
Anti- CCP (+ve in 60%, more specific than RF)
ANA (+ve in 30%)
ESR and CRP
FBC (? Anaemia)
U&E (renal involvement and before NSAIDs)
Synovial fluid - raised wcc, raised protein, low glucose
Urine dip and PCR
ACR/ EULAR 2011 classification criteria (>6 points)
Management of RA
MDT approach
Disease education
Smoking cessation
Physiotherapy
NSAIDs with stomach protection
Steroids
Methotrexate + DMARD
Occasionally surgery
Features associated with poor prognosis in RA
Rhuematoid factor or anti- CCP antibodies
Smoking
Extra- articular features
HLA-DR4
Female
Early erosions
Severe disability at presentation
Systemic manifestations of RA
Pulmonary:
- fibrosis
- effusions
- fibrosing alveolitis
- obliterative bronchiolitis
- caplans nodules
Eyes:
Scleritis/episcleritis
Neurological:
- carpal tunnel syndrome
- Atlanto- axial subluxation
- peripheral neuropathy
Haematological:
- Feltys (RA+ splenomegaly+ neutropenia)
Skin: palmar erythema, Raynauds, pyoderma
Renal: glomerulonephritis
Aetiology of Ehlers Danlos Syndrome
Faulty genes in EDS result in abnormal phenotypical expression owing to defective collagen and extra cellular matrix proteins.
Hypermobile, classical, vascular EDS have an autosomal dominant inheritance pattern
Kyphoscoliotic, classical- like and cardio- valvular are autosomal recessive
Clinical presentation of EDS
Hyperflexible joints
Increased skin elasticity
Bruising
Joint dislocations
Widespread pain
Aortic aneurysm
Mitral valve prolapse
Blue sclera, tinnitus, hernias, prolapse
Investigation of EDS
Echo
CT
Molecular genetic testing
Management of EDS
Physiotherapy
Analgesia
CBT
Genetic counselling
Cardiovascular screening
What is the Pathophysiology of sarcoidosis?
Granulomas composed of macrophages, lymphocytes, epethelioid histiocytes fuse to form a multinucleotide giant cell
Clinical presentations of sarcoidosis
Painless rubbery lymph nodes
Splenomegaly
Hepatomegaly
Erythema nodosum
Skin plaques
Subcutaneous nodules
Lupus pernio
Anterior uveitis
Cranial nerve palsies
Diabetes insipidus
Arrhythmias
Hypercalcaemia
Nephritis
Bone cysts
Arthritis
Keratoconjuctivitis sicca ( dry eyes)
Diagnosis of sarcoidosis
CXR
CT
Tissue biopsy
Elevated ACE and calcium
U&E and urine dip
LFTs
Calcium + 24 hr urine calcium excretion
Lung function tests - restrictive
BAL - increased lymphocytes
Biopsy- non caseating granulomas
ECG
The combination of bi/hilar lymphadenopathy and erythema nodosum in a young adult is highly suggestive of sarcoidosis
Grading of sarcoidosis based on CXR
Stage 0 - clear CXR
1- bilateral hilar lymphadenopathy
2- BHL + pulmonary infiltrates
3- diffuse pulmonary infiltrates
4- pulmonary fibrosis
Management of sarcoidosis
Corticosteroids if:
- stages 2-4 CXR findings
- persistent Hypercalcaemia and hypercalciuria despite dietary calcium restriction
- ophthalmological complications
- neurological complications
With gastro and bone protection
History and examination of Marfans station 5
- PC
- affect on daily living
- exercise levels
- prev. Complications eg. Pneumothorax, aortic dilatation, lens dislocations
- examine for hypermobility, murmurs, chest surgery, chest deformity, palette, blue sclera
- drug history - ACEi and b-blocker
Causes of Raynauds
Primary (more common in younger females)
Secondary ( usually over 30)
- systemic sclerosis
- SLE
- RA
- Dermatomyositis
- smoking
- beta blockers
History for suspected raynauds
Classical triphasic colour changes (white, blue, red) with pain on reperfusion
Thumb often spared
Hx of digital ulceration
Underlying cause:
Rashes
Alopecia
Mouth ulcers
Dysphagia
Joint pain
Dyspnoea
Examination of suspected raynauds
Hand inc. joints and pulses
Lungs
Heart (loud s2)
Proximal muscle weakness
Rashes
Systemic sclerosis features
Investigating suspected Raynauds
In an otherwise healthy young woman further inv. May not be required.
Bloods inc ANA, ENA, dsDNA, complement levels, CRP, ESR
Urine dip for proteinuria or haematuria
Capillaroscopy
ECG
CXR
Lung function tests
Echo
Management of Raynauds
Stop smoking
Heated gloves and socks
Avoid cold precipitant
Nifedipine
Sildenafil
Prostaglandins if incipient gangrene
Aspirin
What is gestational hypertension
Develops after 20 weeks and may be transient or chronic
BP> 140/90
What is pre- eclampsia
Pregnancy induced hypertension + proteinuria and/or oedema
Eclampsia is the occurrence of convulsions superimposed on pre-eclampsia
Risk factors for pre-eclampsia
1st pregnancy
Age >40
BMI>30
FHx
Pregnancy interval >10 year
Multiple pregnancy
Chronic hypertension
Previous preeclampsia
Renal disease
Autoimmune disease
Diabetes
Complications of gestational hypertension or pre-eclampsia
HELLP syndrome
Eclampsia
AKI
DIC
ARDS
Future risk of hypertension
Cerebrovascular haemorrhage
Prematurity
IUGR
Placental abruption
Fetal death
Clinical presentation of pre-eclampsia
Frontal headache
Visual disturbance
Epigatric/RUQ pain
Nausea/vomiting
Rapid oedema
Clinical finding of pre-eclampsia
BP> 140/90 or 160/110 if severe
Proteinuria >300mg in 24 hr
Facial oedema
RUQ pain
Confusion
Hyperreflexia or cerebral irritation
Uterine tenderness or vaginal bleeding from placental abruption
Investigations for pre-eclampsia
Urine dipstick + 24 collection
FBC, UE, LFT
US
Management of pre/ eclampsia
If high risk take aspirin from 12 weeks
Regular monitoring
BP control with Labetolol
BP >160/110 needs admission steroids
Differential diagnosis for headache in pregnancy
Venous sinus thrombosis
Migraine
Dehydration
SOL
Investigating PE
FBC, BNP, trop
CXR
ECG
D dimer if wells </= 4
Wells Score for PE
3 points for:
Clinical signs/symptoms of DVT
PE most likely or equally most likely dx
1.5 points for:
HR >100
Immbolisation for last 3 days or surgery in last 4 weeks
Prev. PE or DVT
1 point for:
Haemoptysis or malignancy
Causes of reactive arthritis
Gastroenteritis eg. Shigella, salmonella, campylobacter
STI eg. Chlamydia
Most commonly affects young men carrying the HLA-B27 antigen
Joint symptoms usually post date infection by 4-8weeks
Investigation of suspected reactive arthritis
FBC, UE, CRP
RF
ANA
HLA-B27
Urine and genital swabs if concerning for STI
Joint aspirate for cell count, crystals, culture and sensitivity if effusion present
Management of reactive arthritis
Indentification and treatment of precipitating infection
NSAIDs
Corticosteroid injection to affected joint
Physio if ongoing symptoms
Clinical presentation of ankylosing spondylitis
Lower back pin and stiffness
Anterior chest pain
Usually young male
Extra-articular features:
- anterior uveitis
- apical lung fibrosis
- aortic regurgitation
- AV nodal heart block
- Achilles tendinitis
Investigating suspected ankylosing spondylitis
Inflamm markers
FBC
ALP
RF (-ve)
ANA
HLA-B27
Spinal X-rays/ MRI
ECG
Echo
Spiro/HRCT
Radiological changes in ankylosing spondylitis
Blurred joint margins
Subchondral erosions
Sclerosis or fusion of the sacroiliac joints
Loss of lumbar lordosis
Bamboo spine (marginal sydensmophytes bridging multiple vertebra)
Management of ankylosing spondylitis
Calculate BASDAI
NSAIDs
DMARDs
Steroids
Physio
Rheum referral
Examining patient with suspected ank spond
Fixed kyphoscoliosis
Loss of lumbar lordosis
Reduced chest expansion
Protuberant abdo due to diaphragmatic breathing
Occiput to wall distance >5cm
Reduced range of movement through out whole spine
Schobers test shows expansion <5cm on maximum forward flexion
Aortic regurgitation
Apical lung fibrosis
Achilles tendinitis
Clinical signs of osteogenesis imperfecta
Fractures
Blue sclera
Hyper mobile joints
Teeth problems
Hearing problems
Indications for CT head before Lp
Focal neurological symptoms
Reduced GCS
Signs of raised ICP eg. Papilloedema
What is Kernigs sign
Flex hip, then knee extension. Knee extension is resisted/causes pain
Examining a patient with suspected meningitis
Localising signs which may suggest cerebral abscess
Unilateral dilated pupil or papilloedema which may indicate a raised ICP
Ask to check obs
Interpreting CSF
Bacterial: low glucose, high protein, neutrophils and gram +ve cocci
Viral: normal glucose and protein, mononuclear cells
What causes retinitis pigmentosa?
Inherited disorder causing loss of photoreceptors causing progressive and severe visual loss
History of retinitis pigmentosa
Gradual visual loss
Painless
Both eyes
Tunnel vision
FHx
Affect on day to day life
Examining a case of suspected retinitis pigmentosa
Items around bed side
VA (may be normal or reduced)
VF- loss of peripheral vision
Pupils
Eye movements
Fundoscopy- bone spicule pigmentation which follows the vein and spares the macula
Syndromes associated with retinitis pigmentosa
Ushers: congenital deafness’s
Laurence- moon syndrome: polydactylyl, obese, deaf, dwarfism, renal failure
Refsum’s disease: ataxia, deaf, ichthyosis
Kearns- sayer syndrome: ophthalmoplegia, ataxia, deaf, conduction delays
Other causes of tunnel vision
Papilloedema
Glaucoma
Choroidoretinitis
Management of retinitis pigmentosa
Refer to ophthalmology and geneticist
Vitamin A may slow disease progression
History taking with acromegaly
Early morning headache
Nausea
Tunnel vision
Loss of libido
Lactation
Change in appearance/shoe size/ ring size
Complications of acromegaly
Acanthosis nigricans
BP (Hypertension)
Carpal tunnel syndrome
DM
Enlarged organs
Field defect (bitemporal hemianopia)
Goitre, GI malignancy
Heart failure, hirsuitism,
Joint arthropathy
Kyphosis
Lactation
Myopathy (proximal)
Diagnosing acromegaly
Raised plasma IGF-1
Non suppression of GH after an oral glucose tolerance test
MRI Pituitary fossa
CXR - cardiomegaly
ECG and Echo
Hypopituitary
HbA1c
Visual field testing
Sleep studies for obstructive sleep apnoea
Management of acromegaly
Surgery with transsphenoidal approach
Radiotherapy
Somatostatin analogues
Dopamine agonists
Growth hormone receptor antagonists
Causes of hypothyroidism
Autoimmune eg. Hashimotos
Iodine deficiency
Drugs - amiodarone, lithium, anti thyroid meds
Iatrogenic- radiotherapy, thyroidectomy, neck radiotherapy
Subacute thyroiditis
Genetic- pendreds syndrome (deaf)
Secondary hypothyroidism due to hypopituitarism or hypothalamic dysfunction
Examining a patient with suspected hypothyroidism
General: weight gain, dry skin
Slow pulse
Cool peripheries
Thyroid acropachy
Peri-orbital oedema
Loss of eyebrows
Xanthalasma
Hair loss
Goitre or thyroidectomy scar
Slow relaxing ankle jerk
Pericardial effusion
CCF
Carpel tunnel
Proximal myopathy
Investigating suspected hypothyroidism
FBC to exclude anaemia
U&E (hyponatraemia)
Lipid profile
TFTS
Autoimmune studies: anti- thyroid peroxidase autoantibody
Us thyroid if modules felt or asymmetry
CXR
Bp
ECG
Management of hypothyroidism
Levothyroxine 50mcg OD review at 12 weeks and titration as needed aiming for normal TSH
Note can precipitate angina or unmask Addisons resulting in crisis
Interpreting thyroid results
High TSH and low T4 = primary hypothyroidism
Low TSH and low T4 = secondary hypothyroidism
Raised TSH normal T4 = sub clinical hypothyroidism or poor compliance with T4
Wells score for DVT
1 point for each of:
Active cancer
Bedridden for 3 days or surgery in 3 months
Calf swelling >3cm
Collateral superficial veins
Entire leg swollen
Localised tenderness along deep vein
Pitting oedema to symptomatic leg
Paralysis of leg recently
Previous DVT
- 1 if alt diagnosis more likely
Clinical features of hereditary haemorrhagic telangiectasia (Osler- Weber- Rendu syndrome
Multiple telangiectasia on the face, lips and buccal mucosa
Anaemia
GI bleeding
Cyanosis and chest bruit (pulmonary vascular abnormality/shunt)
Discussion points re. Hereditary haemorrhagic telangiectasia
Autosomal dominant
Increases risk of gastro-intestinal haemorrhage
Epistaxis
Haemoptysis
Vascular malformations:
- pulmonary shunts
- intracranial aneurysms (SAH)
- cirrhosis
DVLA group 1 licence rules on syncope
Check the 3 Ps (provocation, prodrome, postural) if all present can continue to drive.
If solitary with no cause - 6 month ban
If clear cause which is treated- drive after 4 weeks
CHADSVAS
Congestive cardiac failure =1
Hypertension =1
Age >75 = 2
Diabetes = 1
Stroke/TIA = 2
Vascular disease = 1
Age 65-74 = 1
Sex (female) = 1
ORBIT score
Hb <13 if male or 12 if female = 2
Age >74 = 1
History of bleeding = 2
eGFR <60 = 1
Treatment with antiplatelets = 1
Taking history in hypertensive patient
Previous blood pressure readings
Associated symptoms: headache, visual disturbance, paroxysmal symptoms (phaeo)
Other medical history
Other cardiovascular risk factors
Drug history
Risk of pregnancy
Examining hypertension patient
Body habitus: obese, cushingoid, acromegalic
Radial pulse+ radial-radial and radio- femoral delay
BP in both arms
Evidence of heart failure
Evidence of renal disease
Fundoscopy
Grades of hypertensive retinopathy
- Silver wiring (thickened arterioles)
- AV nipping ( narrowing of veins as arterioles cross them)
- Cotton wool spots and flame haemorrhages
- Papilloedema
Causes of hypertension
94% essential
4% renal
1% endocrine
Aortic coarctation
Pre-eclampsia
Investigating hypertensive patient
Fundoscopy
Urine dip
U&E
ECG
CXR
Echo
Consider secondary screen:
Renin/aldosterone levels, plasma or urinary metanephrines
Stages of hypertension
Stage 1 > 140/90
Stage 2 > 160/100
Stage 3 > 180/110
Treat stage 1 if end organ damage, IHD, diabetes, ckd, 10 year cvd risk > 10%
Treatment of hypertension
<55 ACEi or ARB
>55 or afrocarribean CCB
Then add CCB or thiazide like diuretic
Then add the third of the above 3
Consider other cardiovascular risk modification drugs eg. Aspirin, statin
Causes of Papilloedema
SOL
IIH
Cavernous sinus thrombosis
Accelerated phase hypertension
Central retinal vein occlusion
Taking a rash history
Onset and location
Associated symptoms- itch/pain/bleeding/discharge
Change over time
Relievers and precipitants
Previous and current treatment
Constitutional symptoms
Systems review
PMH: HIV, immunosuppression, atopy
Drug history
Allergies
FHx
SHx (work, recreational drugs
Pathogenesis of psoriasis
T cell mediated disease
Epidermal proliferation
Dilation and proliferation of blood vessels in the dermis
Accumulation of neutrophils and T lymphocytes
HLA-cw6 is strongly associated with severe disease of early onset
Clinical examination of psoriasis
Well demarcated erythematous scaly plaques on extensor surfaces and scalp
Erythema at the edge of plaque indicates active disease
Kobner phenomonon: plaques at site of trauma
Post inflammatory hypo/hyperpigmentation
Nail changes: onycholysis and nail putting
Joint involvement
Management of psoriasis
Emollients
Topical vit D analogues
Topical steroids
Topical coal tar (stains brown)
UVB
PUVA (psoralen + UVA)
DMARDS
Causes of nail pitting
Psoriasis
Lichen planus
Alopecia areata
Fungal infections
Causes of koebner phenomenon
Psoriasis
Lichen planus
Viral warts
Vitiligo
Sarcoid
Pathology of eczema
Polymorphic inflammatory reaction involving epidermis and dermis
Acute phase (pruritis, erythema, vesiculation, infection
Chronic phase ( fissuring, lichenification of skin, excoriations)
Subtypes of eczema
Exogenous - irritant dermatitis
Endogenous - allergic dermatitis, atopic, discoid
Pompholyx
Seborrhoeic (history of immunosuppression or Parkinson’s disease)
Treatment of eczema
Avoid precipitants
Emollients
Steroids
Tacrolimus
Anti- histamines
Antibiotics if infection
UV light therapy
Pred or azithro in severe cases
Clinical findings to look for in venous ulcer disease
Gaiter area of lower leg
Varicose veins
Scars from vein stripping
Lipodermatosclerosis
Varicose eczema
Atrophie blanche
Pelvic or abdominal mass
Examination findings with arterial ulcer disease
Affects distal extremities and pressure points
Hairless and paper thin skin
Cold with poor cap refill
Absent distal pulses
Examination findings with neuropathic ulcers
Pressures areas
Peripheral neuropathy
Charcots joint
Causes of leg ulcers
Venous
Arterial
Neuropathic
Vasculitic
Neoplastic
Infectious eg. Syphilis
Haematological, eg. Sickle cell
Investigating ulcers
Doppler US
ABPI <0.8 implies arterial insufficiency
Arteriography
Treatment of ulcers
Wound care
Venous- compression bandaging
Arterial- angioplasty/vascular reconstruction/ amputation
Causes of neuropathic ulcers
Diabetes
Tabes dorsalis
Syringomelia
Examination findings of necrobiosis lipoidica diabeticorum
Well- demarcated plaques with waxy yellow centre and red brown edges
Typically on shins
Female predominance (90%)
Managed with topical steroids and support bandages
Causes of erythema nodosum
Sarcoidosis
Strep throat
Oral contraceptives
Pregnancy
TB
IBD
Lymphoma
Idiopathic
Examination findings of erythema nodosum
Tender red smooth shiny nodules on the shins
Caused by inflammation of subcutaneous fat
Older lesions leave a bruise
Evidence of the cause: strep throat, parotid swelling (sarcoidosis)
Clinical presentation of henloch schonlein purpura
Purpurin rash on buttocks and legs
Arthritis
Abdo pain
Can be precipitating by infection or drugs
Complications inc. renal involvement (IgA nephropathy) or hypertension
What causes henoch- schonlein purpura
Small vessel vasculitis: IgA and C3 deposition
Management of henoch schonlein purpura
Check FBC- normal or raised plts
May need no treatment or steroids may speed recovery and treat painful arthralgia
Examining patient with suspected sickle cell crisis
Fever
Dyspnoeic
Jaundice
Pale conjunctiva
Raised JVP
Pansystolic murmur loudest at the left eternal edge (tricuspid regurgitation)
Reduced chest expansion due to pain with coarse expiratory crackles
Small, crusted ulcer in lower third of legs
What causes a vaso-occlusive sickle cell crisis
Sickling in the small vessels of any organ- lungs, kidney, and bone most common
Often precipitated by viral illness, exercise or hypoxia
Investigations for patient with sickle cell crisis
Low Hb, high wcc and CRP
Renal impairement
Sickling on blood film
CXR- linear atelectasis in a chest crisis, cardiomegaly
Urinalysis - haematuria if renal involvement
ABG
Echo
CTPA
Management of sickle cell crisis
Oxygen
IV fluids
Analgesia
May require antibiotics
May require blood transfusion or exchange transfusion
Long term management of sickle cell disease
Folic acid
Penicillin (hyposlenism)
Hydroxycarbamide or exchange transfusion programme if frequent crisis or other features suggestive of poor prognosis
Addisons disease history
Fatigue
Muscular weakness
Low mood
Weight loss
Thirst
Syncope/ lightheadedness
N&V, abdo pain, diarrhoea
History of autoimmune disease
Steroid use
Travel history/TB and HIV risk factors
Addisons disease examination
Medic alert bracelet
Hyper- pigmentation
Lying and standing BP
Visual fields (bitemporal hemianopia in pituitary adenoma)
Look for other autoimmune conditions, eg. Thyroid, diabetes, pernicious anemia, RA, SLE, sjogrens)
Causes of adrenal insufficiency
Primary (impaired cortisol production)
- Addisons (80% of primary cases)
- adrenal adenomas
- HIV
- TB
- congenital adrenal hyperplasia
Secondary (low ACTH production)
- most commonly exogenous steroids
- pituitary adenoma
- hypothalamic tumor
Pathophysiology of Addisons disease
Autoantibodies are directed against the adrenal glands resulting in destruction of the adrenal cortex and decreased cortisol release
Investigsting adrenal insufficiency
U&E: hyponatraemia, hyperkalaemia
FBC: normocytic anaemia, lymphocytosis, eosinophilia
8am cortisol: <100 suggests adrenal insuffiency, 100-400 is grey area and required SST
SST: rise >500 after 30 mins
Arenal autoantibodies: +ve in 70% of Addisons cases
ACTH
Renin and aldosterone: in primary insufficiency aldosterone is low with a high renin
TFTS
CXR
Adrenal imaging if primary
Pituitary imaging of secondary
Management of adrenal crisis
Iv fluids
Hydrocortisone
Electrolyte replacement
Treat underlying precipitant
Chronic management of adrenal insufficiency
Hydrocortisone and fludrocortisone
Education
Medic alert bracelet
Autoimmune syndromes associated with Addisons disease
Autoimmune polyglandular syndrome type 2 - also includes autoimmune thyroid disease and T1DM
Features to ask for in history of suspected Cushing’s syndrome
Weakness
Skin changes/Bruising/ Stretch marks
Weight gain/increased appetite
Face changes - shape/acne
Hirsuitism
Polyuria/polydipsia
Back pain/fractures
Periods/sex drive
Mood/sleep
Recurrent infections
Visual changes/headache (pituitary)
Steroid use (iatrogenic)
Abdominal pain (adrenal)
Haemoptysis/ chest pain/cough/ smoking history (lung cancer)
Examination in patient with suspected cushings
Evidence of BM tests
Carpel tunnel
Bp
Moon shaped face
Hirsuitism
Acne
Bruised thin skin
Purple striae
Buffalo hump
Obesity
Wasting of proximal muscles
Proximal myopathy
Lung auscultation and feel for lymphadenopathy
Abdo exam for striae, adrenalectomg scars
Visual fields
What is cushings disease
Glucocorticoid excess due to ACTH secreting pituitary adenoma
Investigating suspected Cushing’s syndrome
24 hr urinary cortisol collection
Low dose or overnight dexamethadone suppression test - if suppressed would suggest pseudo cushings
High dose dex suppression test - if suppresses by >50% likely cushings disease
- proceed with MRI pituitary fossa
If no supression with high dose dex check ACTH at 9am
- if high likely ectopic so do CtCap for malignancy
- if low, likely adrenal tumour so adrenal CT
Treatment of Cushings disease
Transphenoidal removal of tumour - successful in 80%
If surgery fails then pituitary irradiation or medical management (metyrapone)
Treatment of ectopic acth secreting tumours
Tumor removal
Somatostatin analogues eg. Octreotide
What is Nelson’s syndrome
Bilateral adrenalectomy to treat cushings disease causing massive production of ACTH leading to hyper- pigmentation and pituitary overgrowth
Causes of proximal myopathy
Inherited: myotonic dystrophy or muscular dystrophy
Endocrine: cushings, hyperparathyrodism, thyrotoxicosis, diabetic amyotrophy
Inflammatory: PMR, RA
Metabolic: osteomalacia
Malignancy: paraneoplastic, lambert Eaton myasthenic syndrome
Drugs: alcohol or steroids
History taking in suspected hyperthyroidism
Weight loss
Anxiety/irritability/ restlessness/ insomnia
Sweating
Diarrhoea
Feeling hot
Tremor
Periods
Hair loss
Palpitations
Weakness
Eyes- pain, swelling, gritty/watery/itchy/photophobic
Neck swelling- breathing, OSA, voice change
Previous history of thyroid disease
Other autoimmune diseases
Examination in patient with suspected hyperthyroidism
Tremor
Warm sweaty hands
Thyroid acropachy
Palmar erythema
Tachycardia
Eye examination
- appearance
- lid lag
- eye movements
- eye closure
- visual acuity, visual fields, RAPD, colour, fundoscopy
- examine for goitre
- shins
- proximal myopathy
- brisk reflexes
Examination signs specific to Graves
Proptosis
Chemosis
Exposure keratitis
Ophthalmoplegia
Thyroid acropachy
Pretibial myxoedema
Investigating hyperthyroidism
TFTs: low TSH, high T4/T4
Thyroid autoantibodies
Radioisotope scanning: increased uptake of iodine in Graves, reduced in thyroiditis
US if nodules or assymetrical
FBC, UE, LFT,CRP, ecg, echo
Pregnancy test
Management of hyperthyroidism
Beta blocker
Carbimazole or propylthiouracil
- Block and replace or uptitration
If relapse consider surgery or radioactive iodine
Complications of thyroidectomy
Hypoparathyroidism
Damage to recurrent laryngeal nerve
Hypothyroidism
Recurrence of hyperthyroidism
What causes thyroid eye disease
Present in up to 50% of those with graves
Smoking
Female
Autoimmune against TSH receptors on orbital tissue
Oedema and inflammation of extraocular muscles and retroorbital tissues causes eye to be pushed forward
Fibrosis tethers the muscles causing ophthalmoplegia
Increased pressure on the optic nerve results in reduced visual acuity
Progression of thyroid eye disease
‘NOSPECS’
No signs
Only lid retraction/ lag
Soft tissue involvement
Proptosis
Extraocular muscle involvement
Chemosis
Sight loss
Worrying signs in thyroid eye disease
Optic neuropathy - visual acuity and colour vision
Exposure keratopathy
Double vision
Investigating thyroid eye disease
Tfts
Antibodies
CT/MRI orbits
Management of thyroid eye disease
May require high dose steroids
Can use ciclosporin as a steroid sparing agent
Orbital irradiation or surgical decompression
Joint endo-ophthalm clinic
Differential diagnosis for Proptosis
Orbital tumor
Caroticocavernous fistula
Orbital cellulitis
AVM
cavernous sinus thrombosis
Pre biologic screen for IBD
HIV
Hepatitis B and C
Quantiferon
VZV
EBV
Stages of diabetic retinopathy
Background: hard exudates, blot haemorrhages, microaneurysms
Pre-proliferative: cotton wool spots, flame haemorrhages
Proliferative: neovascularisation of the disc, panretinal photocoagulation scars
Diabetic maculopathy: macular oedema
What screening is in place for diabetic eye disease?
Annual retinal screening
BG retinopathy usually occurs 10 - 29 years after diabetes is diagnosed
Management of diabetic retinopathy
Improved glycaemic control
Treat other risk factors (hypertension, smoking)
Photocoagulation
Photocoagulation indications
Maculopathy
Preproliferative and proliferative diabetic retinopathy
Complications of proliferative diabetic retinopathy
Vitreous haemorrhage
Traction retinal detachment
Neovascular glaucoma
Causes of cataracts
Congenital:
Myotonic dystrophy
Rubella
Turners
Age
Diabetes
Steroids
Radiation exposure
Trauma
Storage disorders
Risk factors for gout
Diet
Alcohol
Red meat
Diuretics
Obesity
Hypertension
Urate stones
CKD
Lymphoproliferative disorders
Investigations for gout
Uric acid levels
Needle shaped negatively birefringent crystals on synovial aspirate
‘Punched out’ periarticular changes
Treatment of gout
Treat the cause
Increase hydration
NSAIDs or colchicine
Allopurinol
Symptoms/signs of Paget’s disease
Usually asymptomatic
Carpel tunnel syndrome
CCF (high output)
Conductive hearing loss
Bony enlargement - skull and long bones (sabre tibia)
Pathological fractures
Optic atrophy and angioid streaks
Renal stones
Investigation of Paget’s
High ALP, normal calcium and phosphate
Osteoporosis circumscripta
Increased uptake on bone scan
Treatment of Paget’s
Analgesia
Physio
Hearing aids
Bisphosphonates
Complications of Paget’s
CCF
Osteogenic sarcoma
Pathological fractures
Hydrocephalus
CN palsies
Cord compression
Hypercalcaemia
Gout
Kidney stones
Causes of sabre tibia
Paget’s
Osteomalacia
Syphilis
Causes of angioid streaks
Paget’s
Pseudoxanthoma elasticum
Ehlers- Danlos
Features of systemic sclerosis
Hands:
Sclerodactyly
Calcinosis
Face:
Tight skin
Beaked nose
Microstomia
Peri-oral furrowing
Telangiectasia
Alopecia
En coup de sabre
Other skin lesions: morphoea
Resp: interstitial fibrosis
Cardio: Htn, pulmonary hypertension, evidence of failure, pericarditis
Classification of systemic sclerosis
Limited: below the elbows, knees and face with slow progression over years. ILD after 5-10years. PAH after 10-20years associated with anti centromere antibodies
CREST: calcinosis, Raynauds, esophageal dysmotility, scerlodactyly, telangiectasia
Diffuse: widespread cutaneous and early visceral involvement, rapid progression over months
Renal crisis after 1-5 years, ILD, PAH, right heart failure
AntiRNA-pol III associated with renal crisis
Anti- Scl70 associated with ILD
Investigations for systemic sclerosis
ANA 90%
Anti-centromere 80% in limited
Scl- 70 antibody 70% in diffuse
Anti RNA-pol III
Hand radiographs showing calcinosis
Fibrosis on HRCT and lung function tests
Dysmotility on barium swallow
Glomeruneohritis indicated by U&E, urinalysis
ECG and Echo for cardiac disease
Treatment of systemic sclerosis
Standard Raynauds treatment
ACEi for renal disease
PPI for GI disease
Conditions associated with pyoderma gangrenosum
IBD
RA, SLE, GPA, APS
Myeloproliferative disorder
PBC, hep C, AIH
Idiopathic
Management of pyoderma gangrenosum
Investigate for underlying cause
Refer dermatology
TVN
Check for infection: Wound swab, bloods
Steroids cream
Tacrolimus ointment
High dose pred if severe
History taking in deteriorating vision
What is it? Blurring? Distortion?
Central or peripheral?
Onset and progression
Painful/painless
1 or both eyes
Day/ night variation?
Headache
Hx of demyelination
Temporal arteritis symptoms
Vascular risk factors
Drug history
Recent eye examination?
Examination in deterioration of vision patient
VA
Ishihara plates
VF
Pupils
Fundoscopy
Eye movements
Cerebellar signs if young (MS)
Palpate temporal arteries if relevant
Hearing aid/ bosses skull (pagets)
Causes of pale optic disc/optic atrophy
- Demyelination causing optic neuritis
- Ischaemic optic neuropathy (atherosclerosis or GCA)
- Compression
- tumor
- thyroid eye disease
- pituitary tumor/craniopharyngioma
- aneurysm
- Paget’s disease - Glaucoma
- Retinal disease eg. CRAO/CRVO
- Hereditary - fredrichs ataxia, retinitis pigmentosa
- Infective- syphilis, HIV, CMV
- Nutritional - b12, folate deficiency
- Medication - ethambutol, isoniazid, vincristine
Differential diagnosis for male hypogonadism
- Congenital
- Klinefelter’s, noonans, myotonic dystrophy - Acquired
- Orchitis, trauma, torsion, drugs eg. Spiro, ketoconazole, alcohol, marijuana, cytotoxics - Systemic
- liver disease, kidney disease - Endocrine
- kallmans, haemochromatosis, Prada-willi
- hypopit, prolactinoma,
- cushings, anorexia, obesity
Cause of klinefelter’s
Extra X chromosome (47XXY)
Complications of Klinefelters
Subfertility
Chronic bronchitis, Bronchiectasis, emphysema
Cancers - germ cell, breast
Varicose veins
SLE
Diabetes
Mitral valve prolapse
Osteoporosis
Examination findings in Klinefelters
Tall
Small tests
Sparse facial hair
Gynaecomastia
Investigation of suspected Klinefelters
Chromosomal analysis
Elevated FSH and LH (FSH>LH)
Low testosterone
Semen analysis
Echo- mitral valve prolapse
Dexa scan - osteoporosis
Causes of hair loss
- Localised non scarring
- alopecia areata
- tinea capitis
- trichotillomania
- traction - Diffuse non scarring
- androgenetic
- endocrine (thyroid)
- malnutrition (iron, zinc)
- drug (chemo, warfarin)
- stress - Scaring
- lichen planus
- discoid lupus erythematosus
- scleroderma morpheoa
- tinea capitis he c
History taking for hair loss
Onset and progression
Patchy or widespread
Scarring
Red/scaly
Does it regrow white?
Nails or skin affected?
Thyroid symptoms?
Stress/trauma/surgery
PMHx of autoimmune disease
DHx (chemo, heparin, warfarin)
FHx
SHx
Management of alopecia
Bloods
Fungal culture
Refer to derm
Steroids topical
Emotional support, wigs, ect.
Investigating HHT
Bloods inc FBC, haematinics, clotting
Look for hepatic, lung, GI, cerebral, bladder AVMs
How is a diagnosis of HHT
Curacao criteria- 3 criteria is definite, 2 is suspected, 1 is unlikely:
- epistaxis that is spontaneous and recurrent
- multiple mucocutaeous telangiectasia at characteristic sites
- visceral lesions
- FHx in first degree relative
Can do genetic testing
American college of rheumatology criteria
Morning stiffness
Arthritis in 3+ joints
Arthritis of the hands
Symmetrical arthritis
Rhuematoid nodules
+ve RF
Erosions on joint radiographs
Criteria for diagnosis of psoriatic arthritis
CASPER (score >3)
1. Psoriasis - current or past
2. Psoriatic nail dystrophy
3. Negative RF
4. Dactylitis - current or past
5. X-ray - juxtarticular new bone formation
Investigating psoriatic arthritis
RF and anti- CCP (usually -ve)
HLA-B27
ESR/ CRP
FBC, U&E, LFT
Urine dip
Joint aspiration
X-rays: assymetrical changes, DIPJ involvement, pencil in cup deformity, juxtaarticular new bone formation
Management of psoriatic arthritis
Weight loss, exercise, smoking cessation
NSAIDs
Steroid injection
DMARD if NSAIDs fail
Anti- TNF
Derm opinion
Examination for suspected GCA
Palpate temporal arteries
Scalp tenderness
Proximal weakness
Eye examination inc, fundoscopy
Management of GCA
FBC, U&E, ESR, CRP
Steroids - 40mg if uncomplicated, 60mg if complication
Stomach and bone protection
US of temporal artery (halo sign)
Refer to rhuem - may arrange biopsy
If eye signs - ophthalm review
Clinical presentation of polymyositis
Gradual onset progressive symmetrical proximal muscle weakness
Not affecting a eyes face or distal muscles, minimal pain
Typically in 50-60yr olds
Clinical presentation of dermatomyositis
Heliotrope rash and oedema: eyelids, nasolabial folds, Marla region, forehead
Gottrans papules
V sign rash (chest and neck)
Shawl sign rash (shoulders and proximal arms exacerbated by sunlight)
Holster sign rash: proximal thighs laterally
Mechanics hands
Nailfold abnormalities - periungal erythema, dilated capillary loops
Extra muscular/ dermatological manifestations of polymyositis/dermatomyositis
Constitutional symptoms
Arthralgia/arthritis
ILD
Pulmonary htn
Oesophageal dysmotility
Heart block
Raynauds
Skin ulcers
How is poly/dermatomyositis associated with cancer
Usually occurs within 3 years of disease onset
Affects >50% of those with the disease over the age of 65
Dermatomyositis > polymyositis
Breast, lung, pancreas, stomach, colon, ovary, lymphoma
Cancer screen on diagnosis and every 3-5 years
What is the anti-synthetase syndrome?
The presence of anti-Jo or anti- SRP with ILD and dermato/poly- myositis
Investigating suspected poly/dermato- myosotis
Routine bloods
Autoimmune screen inc. myositis specific antibodies (anti-synthetase, anti-jo1,ect)
CK, AST, ALT, LDH all raised
EMG - Myopathic changes
MRI muscle and muscle biopsy show inflammation
Cancer screen
Systemic assessment
Management of dermato/poly- myosotis
Derm review
Rhuem review
MDT - salt, physio
Steroids + gastro and bone protection
Steroid sparing agents
Calculating Beighton score
Hands flat on floor with knees straight
Bend elbows backwards
Bend knees backwards
Bend thumb back to touch forearm
Bend little finger to 90 degrees
How does pseudoxanthoma elasticum present?
‘Plucked chicken skin’ appearance
Hyperextensible joints
Blue sclera
Retinal angioid streaks on fundoscopy
Hypertension
Mitral valve prolapse
Premature coronary artery disease
Gastric bleed
Autosomal recessive
What is erythema nodosum?
A septal panniculitis. There is inflammation in subcutaneous septa of fat.
Raised red/purple tender plaques on the shins
Rockall score for UGIB
Age
Tachycardia and HR
Comorbidities inc renal and liver failure
Diagnosis in OGD
Degree of bleeding seen on OGD
GBS score for UGIB
Hb
Urea
Initial systolic BP
Gender
HR
Melaena
Recent syncope
Hepatica disease
Cardiac failure
Pathophysiology of Paget’s disease
Metabolic disease characterised by accelerated bone turnover and abnormal bone remodelling causing deformity and enlargement of bones.
Osteolytic phase then mixed phase then burnt out quiescent osteosclerotic phase
What hormones are involved in hypopituitarism and what symptoms to these cause
Gonadotropin deficiency
- low sex drive, no/irregular periods, infertility, hot flushes, small breast, reduced body hair
GH deficiency
- weight gain
TSH deficiency
- hypothyroidism
ACTH deficiency
- postural hypotension, tired, weak, abdo pain
Causes of hypopituitarism
Pituitary tumour
Iatrogenic - pituitary surgery or radiotherapy
Compression/infiltration due to local tumours
Pituitary apoplexy (acute infarction of a pituitary adenoma)
Head injury
Stroke
Meningitis
Sheehans - infarction of pituitary
Empty sella syndrome
Investigating hypopituitarism
Low Na
Low glucose
Low cortisol, TSH, T4, LH, FSH, morning testosterone, oestradiol, IGF-1, prolactin
Ct head/MRI head/ pituitary
Management of hypopituitarism
Hydrocortisone
Levothyroxine
Sex hormones
Growth hormone
Transphenoidal surgery of pituitary adenoma
Clinical presentation of pseudohypoparathyroidism
Symptoms of low calcium
Round face, short neck, shortened 4th and 5th metacarpals
Abnormal mouth/dentition
Neuro exam
Fundoscopy (cataracts)
Investigations for suspected pseudohypoparathyroidism
Low calcium, raised PTH, raised phosphate, low calcitriol
Check rest of electrolytes
Check TFTs, ACTH, adrenal antibodies
24 urinary calcium
ECG- QTc prolongation
Renal stones on USS
Brain MRI showing basal ganglia calcification
Genetic testing
Shortened metacarpals on xr
What causes pseudohypoparathyroidism
Type 1a: autosomal dominant
Type 1b: no phenotypic features but similar biochemistry
Type 2: no phenotypic features, normal or raised cAMP response in urine
Management of pseudohypoparathyroidism
Treat hypocalcaemia
Refer to endocrine
Investigate for other endocrinopathies
Risk factors for subarachnoid haemorrhage
Hypertension
APKD
FHx of brain haemorrhage
Hypermobility (EDS, Marfans)
Smoking
Driving advice post TIA
Can’t drive for 1 month
