Station 5 Paces Flashcards

(207 cards)

1
Q

Taking history of bloody diarrhoea

A

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

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2
Q

Examination findings for ?IBD dx

A

General - Pallor, nutritional status, HR / BP
Hands: arthralgia
Face: Oral ulceration / conjunctival palor
Abdomen:
- Surgical scars/stomas
- Tenderness
- Palpable mass
- Perianal disease
Legs
- Erythema nodosum / pyoderma gangrenosum
Side effects
- Steroid side effects
- Gum hypertrophy from ciclosporin

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3
Q

Investigating IBD

A

Stool MC&S, faecal calprotectin
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

Acute
Anaemia
Toxic dilatation
Perforation

Chronic
PSC
Colonic carcinoma
- higher risk in patients with pancoitis and PSC
- Patients with pan colitis for >10 years require surveillance colonoscopy 3, increasing frequency with every decade form diagnosis

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9
Q

Extra- intestinal manifestations of IBD

A

Hands:
- Finger clubbing*
- Large joint arthritis*
- Seronegative arthritis

Face
- Aphthous ulcers*
- Uveitis*
- Episcleritis*
- Iritis*

Skin
- Erythema nodosum*
- Pyoderma gangrenosum*

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 - 90% coeliac pt
Small intestinal biopsy

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12
Q

Management of coeliac disease and dermatitis herpetiformis

A

Gluten free diet + dietitian referral
Oral dapsone [controls itching before diet takes effect]

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13
Q

Aetiology of rhuematoid arthritis

A

Combination of genetic and environmental factors
Association with HLA-DR4 [4 fingers]
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

And classic deformaties

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

Bedside:
Urine dip and PCR

Bloods:
FBC (? Anaemia)
U&E (renal involvement and before NSAIDs)
ESR and CRP
RF (+ve in 70%)
Anti- CCP (+ve in 60%, more specific than RF)
ANA (+ve in 30%)

Radiology:
X-rays- periarticular osteopenia, symmetrical joint space loss, deformities, erosions, nodules)

Extras:
Synovial fluid - raised wcc, raised protein, low glucose

ACR/ EULAR 2011 classification criteria (>6 points)

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17
Q

Management of RA

A

MDT approach
- Disease education
- Smoking cessation
- PT / OT / Social worker
Sx - NSAIDs with stomach protection

Induce remission - Steroids
Methotrexate + DMARD

Occasionally surgery

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18
Q

Features associated with poor prognosis in RA

A

Female
Smoking

Bloods
- Rhuematoid factor or anti- CCP antibodies
- HLA-DR4

Aggressive disease
- Extra- articular features
- Early erosions
- Severe disability at presentation

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19
Q

Systemic manifestations of RA

A

Order: top -> toe
Eyes:
- Scleritis/episcleritis
Pulmonary:
- fibrosis
- effusions
- fibrosing alveolitis *
- obliterative bronchiolitis*
- caplans nodules*
Haematological:
- Feltys (RA+ splenomegaly+ neutropenia)
Renal: glomerulonephritis
Skin: palmar erythema, Raynauds*, pyoderma gangrenosum
Neurological:
- carpal tunnel syndrome
- Atlanto- axial subluxation
- peripheral neuropathy

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20
Q

Aetiology of Ehlers Danlos Syndrome

A

Genetic disorder which causes abnormal expression of collagen and abnormal extra cellular matrix proteins.
There are many sub-types of EDS
- Hypermobile, classical and 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

Joints
- Hyperflexible joints
- Joint dislocations

Skin
- Increased skin elasticity
- Bruising
- Widespread pain

Cardio
- Aortic aneurysm
- Mitral valve prolapse

Other
Blue sclera, tinnitus, hernias, prolapse

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22
Q

Investigation of EDS

A

Echo
CT (aneurysm)
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
Common Sx - Breathlessness - Lymphadenopathy - Erythema nodosum Face - Anterior uveitis - Cranial nerve palsies - Keratoconjuctivitis sicca (dry eyes) Endocrine - Diabetes insipidus - Hypercalcaemia Painless rubbery lymph nodes Abdo - Nephritis - Splenomegaly - Hepatomegaly Cardiovascular - Arrhythmias Skin - Erythema nodosum - Skin plaques - Subcutaneous nodules - **Lupus pernio (purple rash over nose and cheeks)** MSK - Bone cysts - Arthritis
26
Diagnosis of sarcoidosis
Bedside: - Urine dip (prot / blood) - ECG Bloods: - LFTs, U&E - Elevated ACE (angiotensin converting enzyme) and calcium Secretions: - Bronchio-alveolar lavage - increased lymphocytes Imaging: - CXR (clear -> bilateral hilar lymphadenopathy, pul infiltrates, pul fibrosis) - CT Extras: - Tissue biopsy: non-caseating granulomas - Lung function tests - restrictive 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
Differentials for sarcoid (breathlessness, lymphadenopathy, myalgia, fever)
Hypersensitivity pneumonitis Lymphoma TB HIV Toxoplasmosis Histoplasmosis
29
Management of sarcoidosis
Corticosteroids (6-24/12) if: - stages 2-4 CXR findings - persistent Hypercalcaemia and hypercalciuria despite dietary calcium restriction - ophthalmological complications - neurological complications With gastro and bone protection If resistant to steroids immunosuppresants - methotrexate / azathioprine Severe pul disease -> lung transplant
30
History and examination of Marfans station 5
PC HPC - prev. Complications eg. Pneumothorax, aortic dilatation, lens dislocations MH - ACEi and b-blocker SH - effect on daily living - exercise levels OE - hypermobility, murmurs, chest surgery, chest deformity, palette, blue sclera
31
Causes of Raynauds
Primary (more common in younger females) Secondary ( usually over 30) - systemic sclerosis - SLE - RA - Dermatomyositis - smoking - beta blockers
32
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
33
Examination of suspected raynauds
Hand inc. joints and pulses, skin changes Lungs ??fibrosis Heart (loud s2) - pul hypertension Proximal muscle weakness Rashes (butterfly / heliotrope) Systemic sclerosis features
34
Investigating suspected Raynauds
In an otherwise healthy young woman further inv. May not be required. Bedside - Urine dip for proteinuria or haematuria - ECG Bloods - ANA, ENA, dsDNA, complement levels - CRP, ESR Radiology - CXR - Lung function tests - Echo Extras: Capillaroscopy (systemic sclerosis)
35
Management of Raynauds
Conservative - Smoking cessation - Heated gloves and socks - Avoid cold precipitant Medical - Nifedipine - Sildenafil - Prostaglandins if incipient gangrene (ulcers) - Aspirin
36
What is gestational hypertension
Develops after 20 weeks and may be transient or chronic BP> 140/90
37
What is pre- eclampsia
Pregnancy induced hypertension + proteinuria and/or oedema Eclampsia is the occurrence of convulsions superimposed on pre-eclampsia
38
Risk factors for pre-eclampsia
Features of pregnancy - 1st pregnancy - Pregnancy interval >10 year - Multiple pregnancy Risk of developing HTN - Age >40 - BMI>30 - FHx - Chronic hypertension - Previous preeclampsia - Renal disease - Autoimmune disease - Diabetes
39
Complications of gestational hypertension or pre-eclampsia
Mother (acute) - HELLP syndrome - Eclampsia - AKI - DIC - ARDS - Cerebrovascular haemorrhage Mother (chronic) - Future risk of hypertension Baby - Placental abruption - IUGR - Prematurity - Fetal death
40
Clinical presentation of pre-eclampsia
Frontal headache Visual disturbance Epigatric/RUQ pain Nausea/vomiting Rapid oedema
41
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
42
Investigations for pre-eclampsia
Urine dipstick + 24 collection FBC, UE, LFT Foetal US (intrauterine growth restriction)
43
Management of pre/ eclampsia
If high risk take aspirin from 12 weeks Regular monitoring BP control with Labetolol BP >160/110 needs admission steroids
44
Differential diagnosis for headache in pregnancy
Venous sinus thrombosis Eclampsia Migraine Dehydration SOL
45
Investigating PE
FBC, BNP, trop CXR ECG D dimer if wells
46
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
47
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
48
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
49
Management of reactive arthritis
Indentification and treatment of precipitating infection NSAIDs Corticosteroid injection to affected joint Physio if ongoing symptoms
50
Clinical presentation of ankylosing spondylitis
Usually young male Lower back pin and stiffness Anterior chest pain Extra-articular features: [ALL THE As] - anterior uveitis - apical lung fibrosis - aortic regurgitation [AR/AS - aortic regurgitation/ank spond] - AV nodal heart block - Achilles tendinitis
51
Investigating suspected ankylosing spondylitis
Bloods - FBC, U&E, LFT - ALP - RF (-ve), ANA - *HLA-B27* Radiology - lumbar X-rays - sacroiliitis - *Spinal MRI* - *Spiro/HRCT (apical fibrosis) * *Cardiac (AR) - ECG, Echo*
52
Radiological changes in ankylosing spondylitis
Sacroiliitis - sclerosis or fusion of the sacroiliac joints Loss of lumbar lordosis Bamboo spine (marginal sydensmophytes bridging multiple vertebra) Blurred joint margins Subchondral erosions
53
Management of ankylosing spondylitis
MDT - physio / OT / social worker / disease education / rheumatologist - Pt centred care - calculate BASDAI [measure of disease activity] Medications - NSAIDs + PPI - Steroids - DMARDs
54
Examining patient with suspected ank spond
Spine - Look - occiput to base of spine (talk outloud) - Feel - from occuput down - Move - at neck and back - Forward and back, side to side, rotation Wider complications - Lung apicies - fibrosis - Heart sounds - AR - Achilles tendinitis
55
Clinical signs of osteogenesis imperfecta
Fractures Blue sclera Hyper mobile joints Teeth problems Hearing problems
56
Indications for CT head before Lp
Focal neurological symptoms Reduced GCS Signs of raised ICP eg. Papilloedema
57
What is Kernigs sign
Flex hip, then knee extension. Knee extension is resisted/causes pain Sign of meningism
58
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 Rash
59
Interpreting CSF
Bacterial: low glucose, high protein, neutrophils and gram +ve cocci Viral: normal glucose and protein, mononuclear cells [monocytes, leucocytes]
60
What causes retinitis pigmentosa?
Inherited disorder causing loss of photoreceptors causing progressive and severe visual loss (can be autosomal recessive / autosomal dominant / x-linked)
61
History of retinitis pigmentosa
Gradual visual loss Painless Both eyes Tunnel vision FHx Affect on day to day life
62
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
63
Syndromes associated with retinitis pigmentosa
Rentinintis pigmentosa is associated with a number of syndromes / congenital conditions ## Footnote 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
64
Other causes of tunnel vision
Papilloedema Glaucoma Choroidoretinitis (posterior uveitis) Retinitis pigmentosa
65
Management of retinitis pigmentosa
Refer to ophthalmology and geneticist Vitamin A may slow disease progression
66
History taking with acromegaly
Raised ICP - Early morning headache, nausea Tunnel vision (bitemporal hemianopia) Change in appearance/shoe size/ ring size Loss of libido (LH/FSH) Lactation (prolactin not inhibited)
67
Complications of acromegaly
Field defect (bitemporal hemianopia) Metabolic***** - Acanthosis nigricans - BP (Hypertension) - DM - hirsuitism (LH / FSH) - Lactation (prolactin not inhibited) MSK - Carpal tunnel syndrome - Joint arthropathy - Kyphosis - Myopathy (proximal) Enlargement of organs - Enlarged organs - Goitre - GI malignancy - Heart failure
68
Diagnosing acromegaly
Bloods - Raised plasma IGF-1 - Non suppression of GH after an oral glucose tolerance test - Hypopituitary, HbA1c, TFT MRI Pituitary fossa Extras - visual field testing Complications - Cardiomegaly - CXR, ECG and Echo - Sleep studies for obstructive sleep apnoea
69
Management of acromegaly
Surgery with transsphenoidal approach Radiotherapy Somatostatin analogues Dopamine agonists (inhibit prolactin) Growth hormone receptor antagonists
70
Causes of hypothyroidism
Primary Autoimmune eg. Hashimotos Subacute thyroiditis Iodine deficiency Drugs - amiodarone, lithium Iatrogenic- radiotherapy, thyroidectomy, anti thyroid meds Secondary Hypopituitarism or hypothalamic dysfunction
71
Examining a patient with suspected hypothyroidism
General: weight gain, dry skin Hands - Slow pulse - Cool peripheries - Thyroid acropachy* - **Carpel tunnel** - **Proximal myopathy** Face - Peri-orbital oedema* - Loss of eyebrows - Xanthalasma* - Hair loss Neck - Goitre - Thyroidectomy scar Chest - Pericardial effusion - CCF Legs - **Slow relaxing ankle jerk** - **Peripheral oedema** - **Proximal myopathy (can't stand up)**
72
Investigating suspected hypothyroidism
Bedside - HR / BP / ECG Bloods - FBC to exclude anaemia - U&E (hyponatraemia) - Lipid profile - TFTS - Autoimmune studies: anti- thyroid peroxidase autoantibody Radiology - US thyroid if nodules felt or asymmetry - CXR
73
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
74
Hypothyroidism: Interpreting TFTs - Primary - Secondary - Subclinical / poor compliance
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
75
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
76
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)
77
Discussion points re. Hereditary haemorrhagic telangiectasia
Autosomal dominant Increases risk of gastro-intestinal haemorrhage Epistaxis Haemoptysis Vascular malformations: - pulmonary shunts - intracranial aneurysms (SAH) - cirrhosis
78
DVLA group 1 licence rules on syncope
Check for Sx of vasovagal (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
79
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
80
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
81
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
82
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
83
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
84
Causes of hypertension
94% essential 4% renal 1% endocrine - cushings / conns / pheochromocytoma Aortic coarctation Pre-eclampsia
85
Investigating hypertensive patient
End organ damage: * Fundoscopy * Urine dip, U&E * ECG (LV dilation) * CXR & Echo (heart failure) Consider secondary screen: * Cushings - urinary cortisol, low dose dex suppression test, ACTH levels. * Conns - blood and urine renin /aldosterone levels * Pheochromocytoma - plasma or urinary metanephrines * Acromegaly - IGR1 and OGTT * Pre-eclampsia - Pregnancy test / urine dip (proteinuria)
86
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%
87
Treatment of hypertension
DM type 2 or <55 (not black) - ACEi or ARB >55 / afrocarribean AND no DM2 - CCB Then add ACEi / CCB / thiazide like diuretic Then add the third of the above 3 Consider other cardiovascular risk modification drugs eg. Aspirin, statin
88
Causes of Papilloedema
SOL IIH Cavernous sinus thrombosis Accelerated phase hypertension Central retinal vein occlusion
89
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
90
Pathogenesis of psoriasis
T cell mediated autoimmune disease - Epidermal proliferation - Blood vessels in dermis -> dilation and proliferation of blood vessels Associated with HLA-CW6 -> earlier disease and more severe disease ## Footnote Accumulation of neutrophils and T lymphocytes HLA-cw6 is strongly associated with severe disease of early onset
91
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
92
Management of psoriasis
Topical treatments - Emollients - Topical Vit D analogues - Topical steroids - Topical coal tar (stains brown) UV treatment - UVB - PUVA (psoralen + UVA) DMARDS
93
Causes of nail pitting
Psoriasis Lichen planus Alopecia areata Fungal infections
94
Causes of koebner phenomenon
Psoriasis Lichen planus Viral warts Vitiligo Sarcoid
95
Pathology of eczema
Polymorphic inflammatory reaction involving epidermis and dermis Acute phase (pruritis, erythema, vesiculation, infection Chronic phase ( fissuring, lichenification of skin, excoriations)
96
Subtypes of eczema
Exogenous - irritant dermatitis Endogenous - allergic dermatitis, atopic, discoid Pompholyx Seborrhoeic (history of immunosuppression or Parkinson’s disease)
97
Treatment of eczema
Avoid precipitants Topical - Emollients - Steroids Systemic - Tacrolimus - Anti- histamines - Antibiotics if infection - Pred or azithro in severe cases UV light therapy
98
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
99
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
100
Examination findings with neuropathic ulcers
Pressures areas Peripheral neuropathy Charcots joint
101
Causes of leg ulcers
Venous Arterial Neuropathic Vasculitic Neoplastic Infectious eg. Syphilis Haematological, eg. Sickle cell
102
Investigating ulcers
Doppler US ABPI <0.8 implies arterial insufficiency Arteriography
103
Treatment of ulcers
Wound care Venous- compression bandaging Arterial- angioplasty/vascular reconstruction/ amputation
104
Causes of neuropathic ulcers
Peripheral neuropathy Diabetes / Alcohol / B12 / B1 deficiency
105
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
106
Causes of erythema nodosum
*Nodosum backwards* Idiopathic M - mycobacterium TB U - UC / CD S - sarcoidosis O - Oral contraceptive pill D - Drugs (other) O - Other infections - strep throat N - Nurturing - pregancy Lymphoma
107
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)
108
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
109
What causes henoch- schonlein purpura
Small vessel vasculitis: IgA and C3 deposition
110
Management of henoch schonlein purpura
Check FBC- normal or raised plts May need no treatment or steroids may speed recovery and treat painful arthralgia
111
Examining patient with suspected sickle cell crisis
Fever Anaemia - Pale conjunctiva Liver - Jaundice Resp - Dyspnoeic - Reduced chest expansion due to pain with coarse expiratory crackles Cardiac - Raised JVP - Tricuspid regurg - Pansystolic murmur loudest at the left sternal edge Small, crusted ulcer in lower third of legs
112
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
113
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
114
Management of sickle cell crisis
Oxygen IV fluids Analgesia May require antibiotics May require blood transfusion or exchange transfusion
115
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
116
Addisons disease history
Generalised - Fatigue - Low mood - Muscular weakness Weight loss Thirst N&V, abdo pain, diarrhoea Previous Hx - Autoimmune disease - Steroid use - HIV (RF) / TB (travel)
117
Addisons disease examination
Medic alert bracelet Hyper- pigmentation **LOOK IN THE MOUTH** *Lying and standing BP* Visual fields (bitemporal hemianopia in pituitary adenoma) Look for other autoimmune conditions, eg. Thyroid, diabetes, pernicious anemia, RA, SLE, sjogrens)
118
Causes of adrenal insufficiency
Primary (impaired cortisol production) - Addisons (80% of primary cases) - adrenal adenomas - HIV - TB/ sarcoid - congenital adrenal hyperplasia Secondary (low ACTH production) - most commonly exogenous steroids - pituitary adenoma - hypothalamic tumor
119
Pathophysiology of Addisons disease
Autoantibodies are directed against the adrenal glands resulting in destruction of the adrenal cortex and decreased cortisol release
120
Investigsting adrenal insufficiency
U&E: hyponatraemia, hyperkalaemia FBC: normocytic anaemia, lymphocytosis, eosinophilia TFTS VBG: metabolic acidosis with low Na and high K CXR Random cortisol: 8am cortisol: <100 suggests adrenal insuffiency, 100-400 is grey area and required SST (short synathen test) Short synathen test [administer synthetic ACTH check cortisol levels before and 30-60 mins after] - Primary insufficiency - does not rise (cannot make enough cortisol) - Normal OR secondary insufficiency - cortisol rise 500nanomol/L (adrenal can make cortisol but no stimulus normally) Renin and aldosterone: in primary insufficiency aldosterone is low with a high renin ACTH - high in primary and low in secondary adrenal insuffiency Arenal autoantibodies: +ve in 70% of Addisons cases Primary - adrenal imaging Secondary - pituitary imaging
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Management of adrenal crisis
Iv fluids Hydrocortisone Electrolyte replacement Treat underlying precipitant
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Chronic management of adrenal insufficiency
Hydrocortisone and fludrocortisone Education Medic alert bracelet
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Autoimmune syndromes associated with Addisons disease
Autoimmune polyglandular syndrome type 2 - also includes autoimmune thyroid disease, T1DM, pernicious anaemia, premature ovarian failure
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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)*
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Examination in patient with suspected cushings
General - Bruised thin skin - Obesity Hands - Evidence of BM tests - Carpel tunnel Proximal myopathy - Wasting of proximal muscles - Ask to stand with arms crossed Face - Cushingoid facies - Hirsuitism - Acne - Subcutanous fat pad between scapulae - **Visual fields** - Lymphadenopathy Lung - Auscultation Abdo - Striae - Central obesity - Adrenalectomg scars BP
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What is cushings disease
Glucocorticoid excess due to ACTH secreting pituitary adenoma
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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
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Treatment of Cushings disease
Transphenoidal removal of tumour - successful in 80% If surgery fails then pituitary irradiation or medical management (metyrapone)
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Treatment of ectopic acth secreting tumours
Tumor removal Somatostatin analogues eg. Octreotide
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What is Nelson’s syndrome
Bilateral adrenalectomy to treat cushings disease causing massive production of ACTH leading to hyper- pigmentation and pituitary overgrowth
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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
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History taking in suspected hyperthyroidism
General - Weight loss - Anxiety/irritability/ restlessness/ insomnia - Sweating - Feeling hot - Weakness - Tremor Head - Hair loss - Eyes- pain, swelling, gritty/watery/itchy/photophobic - Neck swelling- breathing, OSA, voice change Chest - Palpitations Abdo - Diarrhoea - Periods Previous history of thyroid disease Other autoimmune diseases
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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
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Examination signs specific to Graves
Proptosis- protrusion of eyeball Chemosis - swelling of the tissue that lines the eyelids and surface of the eye Exposure keratitis - damage to cornea after prolonged exposure to outside world Ophthalmoplegia Thyroid acropachy Pretibial myxoedema
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Investigating hyperthyroidism
TFTs: low TSH, high T4/T4 Thyroid autoantibodies - TSH antibodies - graves - Anti-thyroid peroxidase - hashimotos Radioisotope scanning: increased uptake of iodine in Graves, reduced in thyroiditis US if nodules or assymetrical FBC, UE, LFT,CRP, ecg, echo Pregnancy test
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Management of hyperthyroidism
Beta blocker Carbimazole or propylthiouracil - Block and replace or uptitration If relapse consider surgery or radioactive iodine Pregnancy - Trimester 1& 2 - propylthiouracil - Trimester 3 - carbimazole
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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 (TB) 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 - Congenital rubella - Turners - Storage disorders Risk factors: - Age - Diabetes - Steroids - Radiation exposure - Trauma
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Risk factors for gout
Lifestyle - Obesity - Hypertension - Diet (alcohol, red meat) Renal - Diuretics - CKD - Urate stones 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 Boney enlargement - Bony enlargement - skull and long bones (sabre tibia) - Carpel tunnel syndrome - Conductive hearing loss - Pathological fractures CCF (high output) 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 Bone - Osteogenic sarcoma - Pathological fractures - Hypercalcaemia Brain - Hydrocephalus - CN palsies - Cord compression Renal / joint - Gout - Kidney stones
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Causes of sabre tibia
Anterior bowing of 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 - area of inflammation and fibrosis (thickening and hardening) of the skin due to increased collagen deposition. Resp: interstitial fibrosis Cardio: Htn, pulmonary hypertension, evidence of failure, pericarditis
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Classification of systemic sclerosis
Limited: - Location - below the elbows, knees and face with slow progression over years - Anti centromere antibodies - Resp - ILD after 5-10yrs. PAH after 10-20yrs - CREST: calcinosis, Raynauds, esophageal dysmotility, scerlodactyly, telangiectasia Diffuse: - Location - widespread cutaneous and early visceral involvement, rapid progression over months - Anti- Scl70 - Renal - Renal crisis after 1-5 years *[AntiRNA-pol III associated with renal crisis]* Resp - ILD, PAH, right heart failure
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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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RA- 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
Bedside: Urine dip Bloods: RF and anti- CCP (usually -ve) HLA-B27 ESR/ CRP FBC, U&E, LFT X-rays: assymetrical changes, DIPJ involvement, pencil in cup deformity, juxtaarticular new bone formation Extras: Joint aspiration
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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
Painless gradual onset progressive symmetrical proximal muscle weakness Not affecting a eyes face or distal muscles 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 *similar to systemic sclerosis*
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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?
Polymyositis OR dermatomyositis + ILD + antibodies (anti-Jo or anti-SRP)
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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
Elher Danlos 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
*rare inherited disorder characterized by target organ resistance or unresponsiveness to parathyroid hormone (PTH)* 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
Clacium related: - Low calcium, raised PTH, raised phosphate, low calcitriol - 24 urinary calcium - Check rest of electrolytes Pit screen - TFTs, ACTH, adrenal antibodies Complications of hypocalcaemia - 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