Station 5 Paces Flashcards

1
Q

Taking history of bloody diarrhoea

A

Presenting complaint
Systemic symptoms (fever, anorexia, weight loss, rash, arthralgia, aphthous ulcers)
PMHx and PSHx
Meds history
FH, SHx

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2
Q

Examination findings for ?IBD dx

A

Pallor
Nutritional status
Pulse and BP
Oral ulceration
Surgical scars/stomas
Tenderness
Palpable mass
Perianal disease
Steroid side effects
Gum hypertrophy from ciclosporin

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3
Q

Investigating IBD

A

Stool MC&S
FBC, UE, CRP, electrolytes
AXR
Flexi sig

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4
Q

Treatment for Crohns

A

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

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5
Q

Treatment for UC

A

Mild to mod: Oral or rectal steroids and mesalazine
Severe: IV steroids, IV ciclosporin

Maintainence therapy: oral steroids, mesalazine, azathioprine

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6
Q

Surgical management of IBD

A

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

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7
Q

Complications of Crohns

A

Malabsorption
Anaemia
Abscess
Fistula
Obstruction

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8
Q

Complications of UC

A

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

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9
Q

Extra- intestinal manifestations of IBD

A

Aphthous ulcers*
Erythema nodosum*
Pyoderma gangrenosum*
Finger clubbing*
Large joint arthritis*
Seronegative arthritis
Uveitis*
Episcleritis*
Iritis*
PSC
Systemic amyloidosis

  • related to disease activity
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10
Q

What is dermatitis herpetiformis?

A

Itchy blistering rash usually in extensor surfaces secondary to an insensitivity to gliadin in gluten (hence commonly associated with coeliac disease

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11
Q

Diagnosis of dermatitis herpetiformis

A

Skin biopsy
Screen for coeliac disease:
FBC, iron, b12/folate, calcium
IgA TTG
Anti- endomysial antibodies
Small intestinal biopsy

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12
Q

Management of coeliac disease and dermatitis herpetiformis

A

Gluten free diet + dietitian referral
Oral dapsone

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13
Q

Aetiology of rhuematoid arthritis

A

Combination of genetic and environmental factors
Association with HLA-DR4
Association with smoking

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14
Q

Pathophysiology of RA

A

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

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15
Q

Clinical presentation of RA

A

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

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16
Q

Diagnosis of RA

A

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)

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17
Q

Management of RA

A

MDT approach
Disease education
Smoking cessation
Physiotherapy
NSAIDs with stomach protection
Steroids
Methotrexate + DMARD
Occasionally surgery

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18
Q

Features associated with poor prognosis in RA

A

Rhuematoid factor or anti- CCP antibodies
Smoking
Extra- articular features
HLA-DR4
Female
Early erosions
Severe disability at presentation

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19
Q

Systemic manifestations of RA

A

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

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20
Q

Aetiology of Ehlers Danlos Syndrome

A

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

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21
Q

Clinical presentation of EDS

A

Hyperflexible joints
Increased skin elasticity
Bruising
Joint dislocations
Widespread pain
Aortic aneurysm
Mitral valve prolapse
Blue sclera, tinnitus, hernias, prolapse

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22
Q

Investigation of EDS

A

Echo
CT
Molecular genetic testing

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23
Q

Management of EDS

A

Physiotherapy
Analgesia
CBT
Genetic counselling
Cardiovascular screening

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24
Q

What is the Pathophysiology of sarcoidosis?

A

Granulomas composed of macrophages, lymphocytes, epethelioid histiocytes fuse to form a multinucleotide giant cell

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25
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)
26
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
27
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
28
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
29
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
30
Causes of Raynauds
Primary (more common in younger females) Secondary ( usually over 30) - systemic sclerosis - SLE - RA - Dermatomyositis - smoking - beta blockers
31
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
32
Examination of suspected raynauds
Hand inc. joints and pulses Lungs Heart (loud s2) Proximal muscle weakness Rashes Systemic sclerosis features
33
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
34
Management of Raynauds
Stop smoking Heated gloves and socks Avoid cold precipitant Nifedipine Sildenafil Prostaglandins if incipient gangrene Aspirin
35
What is gestational hypertension
Develops after 20 weeks and may be transient or chronic BP> 140/90
36
What is pre- eclampsia
Pregnancy induced hypertension + proteinuria and/or oedema Eclampsia is the occurrence of convulsions superimposed on pre-eclampsia
37
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
38
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
39
Clinical presentation of pre-eclampsia
Frontal headache Visual disturbance Epigatric/RUQ pain Nausea/vomiting Rapid oedema
40
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
41
Investigations for pre-eclampsia
Urine dipstick + 24 collection FBC, UE, LFT US
42
Management of pre/ eclampsia
If high risk take aspirin from 12 weeks Regular monitoring BP control with Labetolol BP >160/110 needs admission steroids
43
Differential diagnosis for headache in pregnancy
Venous sinus thrombosis Migraine Dehydration SOL
44
Investigating PE
FBC, BNP, trop CXR ECG D dimer if wells
45
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
46
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
47
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
48
Management of reactive arthritis
Indentification and treatment of precipitating infection NSAIDs Corticosteroid injection to affected joint Physio if ongoing symptoms
49
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
50
Investigating suspected ankylosing spondylitis
Inflamm markers FBC ALP RF (-ve) ANA HLA-B27 Spinal X-rays/ MRI ECG Echo Spiro/HRCT
51
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)
52
Management of ankylosing spondylitis
Calculate BASDAI NSAIDs DMARDs Steroids Physio Rheum referral
53
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
54
Clinical signs of osteogenesis imperfecta
Fractures Blue sclera Hyper mobile joints Teeth problems Hearing problems
55
Indications for CT head before Lp
Focal neurological symptoms Reduced GCS Signs of raised ICP eg. Papilloedema
56
What is Kernigs sign
Flex hip, then knee extension. Knee extension is resisted/causes pain
57
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
58
Interpreting CSF
Bacterial: low glucose, high protein, neutrophils and gram +ve cocci Viral: normal glucose and protein, mononuclear cells
59
What causes retinitis pigmentosa?
Inherited disorder causing loss of photoreceptors causing progressive and severe visual loss
60
History of retinitis pigmentosa
Gradual visual loss Painless Both eyes Tunnel vision FHx Affect on day to day life
61
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
62
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
63
Other causes of tunnel vision
Papilloedema Glaucoma Choroidoretinitis
64
Management of retinitis pigmentosa
Refer to ophthalmology and geneticist Vitamin A may slow disease progression
65
History taking with acromegaly
Early morning headache Nausea Tunnel vision Loss of libido Lactation Change in appearance/shoe size/ ring size
66
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)
67
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
68
Management of acromegaly
Surgery with transsphenoidal approach Radiotherapy Somatostatin analogues Dopamine agonists Growth hormone receptor antagonists
69
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
70
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
71
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
72
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
73
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
74
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
75
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)
76
Discussion points re. Hereditary haemorrhagic telangiectasia
Autosomal dominant Increases risk of gastro-intestinal haemorrhage Epistaxis Haemoptysis Vascular malformations: - pulmonary shunts - intracranial aneurysms (SAH) - cirrhosis
77
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
78
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
79
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
80
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
81
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
82
Grades of hypertensive retinopathy
1. Silver wiring (thickened arterioles) 2. AV nipping ( narrowing of veins as arterioles cross them) 3. Cotton wool spots and flame haemorrhages 4. Papilloedema
83
Causes of hypertension
94% essential 4% renal 1% endocrine Aortic coarctation Pre-eclampsia
84
Investigating hypertensive patient
Fundoscopy Urine dip U&E ECG CXR Echo Consider secondary screen: Renin/aldosterone levels, plasma or urinary metanephrines
85
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%
86
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
87
Causes of Papilloedema
SOL IIH Cavernous sinus thrombosis Accelerated phase hypertension Central retinal vein occlusion
88
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
89
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
90
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
91
Management of psoriasis
Emollients Topical vit D analogues Topical steroids Topical coal tar (stains brown) UVB PUVA (psoralen + UVA) DMARDS
92
Causes of nail pitting
Psoriasis Lichen planus Alopecia areata Fungal infections
93
Causes of koebner phenomenon
Psoriasis Lichen planus Viral warts Vitiligo Sarcoid
94
Pathology of eczema
Polymorphic inflammatory reaction involving epidermis and dermis Acute phase (pruritis, erythema, vesiculation, infection Chronic phase ( fissuring, lichenification of skin, excoriations)
95
Subtypes of eczema
Exogenous - irritant dermatitis Endogenous - allergic dermatitis, atopic, discoid Pompholyx Seborrhoeic (history of immunosuppression or Parkinson’s disease)
96
Treatment of eczema
Avoid precipitants Emollients Steroids Tacrolimus Anti- histamines Antibiotics if infection UV light therapy Pred or azithro in severe cases
97
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
98
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
99
Examination findings with neuropathic ulcers
Pressures areas Peripheral neuropathy Charcots joint
100
Causes of leg ulcers
Venous Arterial Neuropathic Vasculitic Neoplastic Infectious eg. Syphilis Haematological, eg. Sickle cell
101
Investigating ulcers
Doppler US ABPI <0.8 implies arterial insufficiency Arteriography
102
Treatment of ulcers
Wound care Venous- compression bandaging Arterial- angioplasty/vascular reconstruction/ amputation
103
Causes of neuropathic ulcers
Diabetes Tabes dorsalis Syringomelia
104
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
105
Causes of erythema nodosum
Sarcoidosis Strep throat Oral contraceptives Pregnancy TB IBD Lymphoma Idiopathic
106
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)
107
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
108
What causes henoch- schonlein purpura
Small vessel vasculitis: IgA and C3 deposition
109
Management of henoch schonlein purpura
Check FBC- normal or raised plts May need no treatment or steroids may speed recovery and treat painful arthralgia
110
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
111
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
112
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
113
Management of sickle cell crisis
Oxygen IV fluids Analgesia May require antibiotics May require blood transfusion or exchange transfusion
114
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
115
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
116
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)
117
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
118
Pathophysiology of Addisons disease
Autoantibodies are directed against the adrenal glands resulting in destruction of the adrenal cortex and decreased cortisol release
119
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
120
Management of adrenal crisis
Iv fluids Hydrocortisone Electrolyte replacement Treat underlying precipitant
121
Chronic management of adrenal insufficiency
Hydrocortisone and fludrocortisone Education Medic alert bracelet
122
Autoimmune syndromes associated with Addisons disease
Autoimmune polyglandular syndrome type 2 - also includes autoimmune thyroid disease and T1DM
123
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)
124
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
125
What is cushings disease
Glucocorticoid excess due to ACTH secreting pituitary adenoma
126
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
127
Treatment of Cushings disease
Transphenoidal removal of tumour - successful in 80% If surgery fails then pituitary irradiation or medical management (metyrapone)
128
Treatment of ectopic acth secreting tumours
Tumor removal Somatostatin analogues eg. Octreotide
129
What is Nelson’s syndrome
Bilateral adrenalectomy to treat cushings disease causing massive production of ACTH leading to hyper- pigmentation and pituitary overgrowth
130
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
131
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
132
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
133
Examination signs specific to Graves
Proptosis Chemosis Exposure keratitis Ophthalmoplegia Thyroid acropachy Pretibial myxoedema
134
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
135
Management of hyperthyroidism
Beta blocker Carbimazole or propylthiouracil - Block and replace or uptitration If relapse consider surgery or radioactive iodine
136
Complications of thyroidectomy
Hypoparathyroidism Damage to recurrent laryngeal nerve Hypothyroidism Recurrence of hyperthyroidism
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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
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Progression of thyroid eye disease
‘NOSPECS’ No signs Only lid retraction/ lag Soft tissue involvement Proptosis Extraocular muscle involvement Chemosis Sight loss
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Worrying signs in thyroid eye disease
Optic neuropathy - visual acuity and colour vision Exposure keratopathy Double vision
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Investigating thyroid eye disease
Tfts Antibodies CT/MRI orbits
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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
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Differential diagnosis for Proptosis
Orbital tumor Caroticocavernous fistula Orbital cellulitis AVM cavernous sinus thrombosis
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Pre biologic screen for IBD
HIV Hepatitis B and C Quantiferon VZV EBV
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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
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What screening is in place for diabetic eye disease?
Annual retinal screening BG retinopathy usually occurs 10 - 29 years after diabetes is diagnosed
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Management of diabetic retinopathy
Improved glycaemic control Treat other risk factors (hypertension, smoking) Photocoagulation
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Photocoagulation indications
Maculopathy Preproliferative and proliferative diabetic retinopathy
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Complications of proliferative diabetic retinopathy
Vitreous haemorrhage Traction retinal detachment Neovascular glaucoma
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Causes of cataracts
Congenital: Myotonic dystrophy Rubella Turners Age Diabetes Steroids Radiation exposure Trauma Storage disorders
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Risk factors for gout
Diet Alcohol Red meat Diuretics Obesity Hypertension Urate stones CKD Lymphoproliferative disorders
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Investigations for gout
Uric acid levels Needle shaped negatively birefringent crystals on synovial aspirate ‘Punched out’ periarticular changes
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Treatment of gout
Treat the cause Increase hydration NSAIDs or colchicine Allopurinol
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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
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Investigation of Paget’s
High ALP, normal calcium and phosphate Osteoporosis circumscripta Increased uptake on bone scan
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Treatment of Paget’s
Analgesia Physio Hearing aids Bisphosphonates
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Complications of Paget’s
CCF Osteogenic sarcoma Pathological fractures Hydrocephalus CN palsies Cord compression Hypercalcaemia Gout Kidney stones
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Causes of sabre tibia
Paget’s Osteomalacia Syphilis
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Causes of angioid streaks
Paget’s Pseudoxanthoma elasticum Ehlers- Danlos
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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
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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
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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
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Treatment of systemic sclerosis
Standard Raynauds treatment ACEi for renal disease PPI for GI disease
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Conditions associated with pyoderma gangrenosum
IBD RA, SLE, GPA, APS Myeloproliferative disorder PBC, hep C, AIH Idiopathic
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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
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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?
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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)
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Causes of pale optic disc/optic atrophy
1. Demyelination causing optic neuritis 2. Ischaemic optic neuropathy (atherosclerosis or GCA) 3. Compression - tumor - thyroid eye disease - pituitary tumor/craniopharyngioma - aneurysm - Paget’s disease 4. Glaucoma 5. Retinal disease eg. CRAO/CRVO 6. Hereditary - fredrichs ataxia, retinitis pigmentosa 7. Infective- syphilis, HIV, CMV 8. Nutritional - b12, folate deficiency 9. Medication - ethambutol, isoniazid, vincristine
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Differential diagnosis for male hypogonadism
1. Congenital - Klinefelter’s, noonans, myotonic dystrophy 2. Acquired - Orchitis, trauma, torsion, drugs eg. Spiro, ketoconazole, alcohol, marijuana, cytotoxics 3. Systemic - liver disease, kidney disease 4. Endocrine - kallmans, haemochromatosis, Prada-willi - hypopit, prolactinoma, - cushings, anorexia, obesity
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Cause of klinefelter’s
Extra X chromosome (47XXY)
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Complications of Klinefelters
Subfertility Chronic bronchitis, Bronchiectasis, emphysema Cancers - germ cell, breast Varicose veins SLE Diabetes Mitral valve prolapse Osteoporosis
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Examination findings in Klinefelters
Tall Small tests Sparse facial hair Gynaecomastia
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Investigation of suspected Klinefelters
Chromosomal analysis Elevated FSH and LH (FSH>LH) Low testosterone Semen analysis Echo- mitral valve prolapse Dexa scan - osteoporosis
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Causes of hair loss
1. Localised non scarring - alopecia areata - tinea capitis - trichotillomania - traction 2. Diffuse non scarring - androgenetic - endocrine (thyroid) - malnutrition (iron, zinc) - drug (chemo, warfarin) - stress 3. Scaring - lichen planus - discoid lupus erythematosus - scleroderma morpheoa - tinea capitis he c
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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
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Management of alopecia
Bloods Fungal culture Refer to derm Steroids topical Emotional support, wigs, ect.
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Investigating HHT
Bloods inc FBC, haematinics, clotting Look for hepatic, lung, GI, cerebral, bladder AVMs
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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
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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
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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
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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
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Management of psoriatic arthritis
Weight loss, exercise, smoking cessation NSAIDs Steroid injection DMARD if NSAIDs fail Anti- TNF Derm opinion
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Examination for suspected GCA
Palpate temporal arteries Scalp tenderness Proximal weakness Eye examination inc, fundoscopy
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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
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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
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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
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Extra muscular/ dermatological manifestations of polymyositis/dermatomyositis
Constitutional symptoms Arthralgia/arthritis ILD Pulmonary htn Oesophageal dysmotility Heart block Raynauds Skin ulcers
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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
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What is the anti-synthetase syndrome?
The presence of anti-Jo or anti- SRP with ILD and dermato/poly- myositis
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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
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Management of dermato/poly- myosotis
Derm review Rhuem review MDT - salt, physio Steroids + gastro and bone protection Steroid sparing agents
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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
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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
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What is erythema nodosum?
A septal panniculitis. There is inflammation in subcutaneous septa of fat. Raised red/purple tender plaques on the shins
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Rockall score for UGIB
Age Tachycardia and HR Comorbidities inc renal and liver failure Diagnosis in OGD Degree of bleeding seen on OGD
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GBS score for UGIB
Hb Urea Initial systolic BP Gender HR Melaena Recent syncope Hepatica disease Cardiac failure
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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
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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
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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
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Investigating hypopituitarism
Low Na Low glucose Low cortisol, TSH, T4, LH, FSH, morning testosterone, oestradiol, IGF-1, prolactin Ct head/MRI head/ pituitary
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Management of hypopituitarism
Hydrocortisone Levothyroxine Sex hormones Growth hormone Transphenoidal surgery of pituitary adenoma
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Clinical presentation of pseudohypoparathyroidism
Symptoms of low calcium Round face, short neck, shortened 4th and 5th metacarpals Abnormal mouth/dentition Neuro exam Fundoscopy (cataracts)
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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
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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
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Management of pseudohypoparathyroidism
Treat hypocalcaemia Refer to endocrine Investigate for other endocrinopathies
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Risk factors for subarachnoid haemorrhage
Hypertension APKD FHx of brain haemorrhage Hypermobility (EDS, Marfans) Smoking
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Driving advice post TIA
Can’t drive for 1 month