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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
Q

Clinical presentations of sarcoidosis

A

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)

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26
Q

Diagnosis of sarcoidosis

A

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

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27
Q

Grading of sarcoidosis based on CXR

A

Stage 0 - clear CXR
1- bilateral hilar lymphadenopathy
2- BHL + pulmonary infiltrates
3- diffuse pulmonary infiltrates
4- pulmonary fibrosis

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28
Q

Management of sarcoidosis

A

Corticosteroids if:
- stages 2-4 CXR findings
- persistent Hypercalcaemia and hypercalciuria despite dietary calcium restriction
- ophthalmological complications
- neurological complications

With gastro and bone protection

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29
Q

History and examination of Marfans station 5

A
  • 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
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30
Q

Causes of Raynauds

A

Primary (more common in younger females)
Secondary ( usually over 30)
- systemic sclerosis
- SLE
- RA
- Dermatomyositis
- smoking
- beta blockers

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31
Q

History for suspected raynauds

A

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

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32
Q

Examination of suspected raynauds

A

Hand inc. joints and pulses
Lungs
Heart (loud s2)
Proximal muscle weakness
Rashes
Systemic sclerosis features

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33
Q

Investigating suspected Raynauds

A

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

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34
Q

Management of Raynauds

A

Stop smoking
Heated gloves and socks
Avoid cold precipitant
Nifedipine
Sildenafil
Prostaglandins if incipient gangrene
Aspirin

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35
Q

What is gestational hypertension

A

Develops after 20 weeks and may be transient or chronic
BP> 140/90

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36
Q

What is pre- eclampsia

A

Pregnancy induced hypertension + proteinuria and/or oedema

Eclampsia is the occurrence of convulsions superimposed on pre-eclampsia

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37
Q

Risk factors for pre-eclampsia

A

1st pregnancy
Age >40
BMI>30
FHx
Pregnancy interval >10 year
Multiple pregnancy
Chronic hypertension
Previous preeclampsia
Renal disease
Autoimmune disease
Diabetes

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38
Q

Complications of gestational hypertension or pre-eclampsia

A

HELLP syndrome
Eclampsia
AKI
DIC
ARDS
Future risk of hypertension
Cerebrovascular haemorrhage
Prematurity
IUGR
Placental abruption
Fetal death

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39
Q

Clinical presentation of pre-eclampsia

A

Frontal headache
Visual disturbance
Epigatric/RUQ pain
Nausea/vomiting
Rapid oedema

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40
Q

Clinical finding of pre-eclampsia

A

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

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41
Q

Investigations for pre-eclampsia

A

Urine dipstick + 24 collection
FBC, UE, LFT
US

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42
Q

Management of pre/ eclampsia

A

If high risk take aspirin from 12 weeks
Regular monitoring
BP control with Labetolol
BP >160/110 needs admission steroids

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43
Q

Differential diagnosis for headache in pregnancy

A

Venous sinus thrombosis
Migraine
Dehydration
SOL

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44
Q

Investigating PE

A

FBC, BNP, trop
CXR
ECG
D dimer if wells </= 4

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45
Q

Wells Score for PE

A

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

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46
Q

Causes of reactive arthritis

A

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

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47
Q

Investigation of suspected reactive arthritis

A

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

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48
Q

Management of reactive arthritis

A

Indentification and treatment of precipitating infection
NSAIDs
Corticosteroid injection to affected joint
Physio if ongoing symptoms

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49
Q

Clinical presentation of ankylosing spondylitis

A

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

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50
Q

Investigating suspected ankylosing spondylitis

A

Inflamm markers
FBC
ALP
RF (-ve)
ANA
HLA-B27
Spinal X-rays/ MRI
ECG
Echo
Spiro/HRCT

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51
Q

Radiological changes in ankylosing spondylitis

A

Blurred joint margins
Subchondral erosions
Sclerosis or fusion of the sacroiliac joints
Loss of lumbar lordosis
Bamboo spine (marginal sydensmophytes bridging multiple vertebra)

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52
Q

Management of ankylosing spondylitis

A

Calculate BASDAI
NSAIDs
DMARDs
Steroids
Physio
Rheum referral

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53
Q

Examining patient with suspected ank spond

A

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

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54
Q

Clinical signs of osteogenesis imperfecta

A

Fractures
Blue sclera
Hyper mobile joints
Teeth problems
Hearing problems

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55
Q

Indications for CT head before Lp

A

Focal neurological symptoms
Reduced GCS
Signs of raised ICP eg. Papilloedema

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56
Q

What is Kernigs sign

A

Flex hip, then knee extension. Knee extension is resisted/causes pain

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57
Q

Examining a patient with suspected meningitis

A

Localising signs which may suggest cerebral abscess
Unilateral dilated pupil or papilloedema which may indicate a raised ICP
Ask to check obs

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58
Q

Interpreting CSF

A

Bacterial: low glucose, high protein, neutrophils and gram +ve cocci
Viral: normal glucose and protein, mononuclear cells

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59
Q

What causes retinitis pigmentosa?

A

Inherited disorder causing loss of photoreceptors causing progressive and severe visual loss

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60
Q

History of retinitis pigmentosa

A

Gradual visual loss
Painless
Both eyes
Tunnel vision
FHx
Affect on day to day life

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61
Q

Examining a case of suspected retinitis pigmentosa

A

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

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62
Q

Syndromes associated with retinitis pigmentosa

A

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

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63
Q

Other causes of tunnel vision

A

Papilloedema
Glaucoma
Choroidoretinitis

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64
Q

Management of retinitis pigmentosa

A

Refer to ophthalmology and geneticist
Vitamin A may slow disease progression

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65
Q

History taking with acromegaly

A

Early morning headache
Nausea
Tunnel vision
Loss of libido
Lactation
Change in appearance/shoe size/ ring size

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66
Q

Complications of acromegaly

A

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)

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67
Q

Diagnosing acromegaly

A

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

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68
Q

Management of acromegaly

A

Surgery with transsphenoidal approach
Radiotherapy
Somatostatin analogues
Dopamine agonists
Growth hormone receptor antagonists

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69
Q

Causes of hypothyroidism

A

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

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70
Q

Examining a patient with suspected hypothyroidism

A

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

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71
Q

Investigating suspected hypothyroidism

A

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

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72
Q

Management of hypothyroidism

A

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

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73
Q

Interpreting thyroid results

A

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

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74
Q

Wells score for DVT

A

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
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75
Q

Clinical features of hereditary haemorrhagic telangiectasia (Osler- Weber- Rendu syndrome

A

Multiple telangiectasia on the face, lips and buccal mucosa
Anaemia
GI bleeding
Cyanosis and chest bruit (pulmonary vascular abnormality/shunt)

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76
Q

Discussion points re. Hereditary haemorrhagic telangiectasia

A

Autosomal dominant
Increases risk of gastro-intestinal haemorrhage
Epistaxis
Haemoptysis

Vascular malformations:
- pulmonary shunts
- intracranial aneurysms (SAH)
- cirrhosis

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77
Q

DVLA group 1 licence rules on syncope

A

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

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78
Q

CHADSVAS

A

Congestive cardiac failure =1
Hypertension =1
Age >75 = 2
Diabetes = 1
Stroke/TIA = 2
Vascular disease = 1
Age 65-74 = 1
Sex (female) = 1

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79
Q

ORBIT score

A

Hb <13 if male or 12 if female = 2
Age >74 = 1
History of bleeding = 2
eGFR <60 = 1
Treatment with antiplatelets = 1

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80
Q

Taking history in hypertensive patient

A

Previous blood pressure readings
Associated symptoms: headache, visual disturbance, paroxysmal symptoms (phaeo)
Other medical history
Other cardiovascular risk factors
Drug history
Risk of pregnancy

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81
Q

Examining hypertension patient

A

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

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82
Q

Grades of hypertensive retinopathy

A
  1. Silver wiring (thickened arterioles)
  2. AV nipping ( narrowing of veins as arterioles cross them)
  3. Cotton wool spots and flame haemorrhages
  4. Papilloedema
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83
Q

Causes of hypertension

A

94% essential
4% renal
1% endocrine
Aortic coarctation
Pre-eclampsia

84
Q

Investigating hypertensive patient

A

Fundoscopy
Urine dip
U&E
ECG
CXR
Echo

Consider secondary screen:
Renin/aldosterone levels, plasma or urinary metanephrines

85
Q

Stages of hypertension

A

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
Q

Treatment of hypertension

A

<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
Q

Causes of Papilloedema

A

SOL
IIH
Cavernous sinus thrombosis
Accelerated phase hypertension
Central retinal vein occlusion

88
Q

Taking a rash history

A

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
Q

Pathogenesis of psoriasis

A

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
Q

Clinical examination of psoriasis

A

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
Q

Management of psoriasis

A

Emollients
Topical vit D analogues
Topical steroids
Topical coal tar (stains brown)
UVB
PUVA (psoralen + UVA)
DMARDS

92
Q

Causes of nail pitting

A

Psoriasis
Lichen planus
Alopecia areata
Fungal infections

93
Q

Causes of koebner phenomenon

A

Psoriasis
Lichen planus
Viral warts
Vitiligo
Sarcoid

94
Q

Pathology of eczema

A

Polymorphic inflammatory reaction involving epidermis and dermis
Acute phase (pruritis, erythema, vesiculation, infection
Chronic phase ( fissuring, lichenification of skin, excoriations)

95
Q

Subtypes of eczema

A

Exogenous - irritant dermatitis
Endogenous - allergic dermatitis, atopic, discoid
Pompholyx
Seborrhoeic (history of immunosuppression or Parkinson’s disease)

96
Q

Treatment of eczema

A

Avoid precipitants
Emollients
Steroids
Tacrolimus
Anti- histamines
Antibiotics if infection
UV light therapy
Pred or azithro in severe cases

97
Q

Clinical findings to look for in venous ulcer disease

A

Gaiter area of lower leg
Varicose veins
Scars from vein stripping
Lipodermatosclerosis
Varicose eczema
Atrophie blanche
Pelvic or abdominal mass

98
Q

Examination findings with arterial ulcer disease

A

Affects distal extremities and pressure points
Hairless and paper thin skin
Cold with poor cap refill
Absent distal pulses

99
Q

Examination findings with neuropathic ulcers

A

Pressures areas
Peripheral neuropathy
Charcots joint

100
Q

Causes of leg ulcers

A

Venous
Arterial
Neuropathic
Vasculitic
Neoplastic
Infectious eg. Syphilis
Haematological, eg. Sickle cell

101
Q

Investigating ulcers

A

Doppler US
ABPI <0.8 implies arterial insufficiency
Arteriography

102
Q

Treatment of ulcers

A

Wound care
Venous- compression bandaging
Arterial- angioplasty/vascular reconstruction/ amputation

103
Q

Causes of neuropathic ulcers

A

Diabetes
Tabes dorsalis
Syringomelia

104
Q

Examination findings of necrobiosis lipoidica diabeticorum

A

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
Q

Causes of erythema nodosum

A

Sarcoidosis
Strep throat
Oral contraceptives
Pregnancy
TB
IBD
Lymphoma
Idiopathic

106
Q

Examination findings of erythema nodosum

A

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
Q

Clinical presentation of henloch schonlein purpura

A

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
Q

What causes henoch- schonlein purpura

A

Small vessel vasculitis: IgA and C3 deposition

109
Q

Management of henoch schonlein purpura

A

Check FBC- normal or raised plts
May need no treatment or steroids may speed recovery and treat painful arthralgia

110
Q

Examining patient with suspected sickle cell crisis

A

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
Q

What causes a vaso-occlusive sickle cell crisis

A

Sickling in the small vessels of any organ- lungs, kidney, and bone most common
Often precipitated by viral illness, exercise or hypoxia

112
Q

Investigations for patient with sickle cell crisis

A

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
Q

Management of sickle cell crisis

A

Oxygen
IV fluids
Analgesia
May require antibiotics
May require blood transfusion or exchange transfusion

114
Q

Long term management of sickle cell disease

A

Folic acid
Penicillin (hyposlenism)
Hydroxycarbamide or exchange transfusion programme if frequent crisis or other features suggestive of poor prognosis

115
Q

Addisons disease history

A

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
Q

Addisons disease examination

A

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
Q

Causes of adrenal insufficiency

A

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
Q

Pathophysiology of Addisons disease

A

Autoantibodies are directed against the adrenal glands resulting in destruction of the adrenal cortex and decreased cortisol release

119
Q

Investigsting adrenal insufficiency

A

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
Q

Management of adrenal crisis

A

Iv fluids
Hydrocortisone
Electrolyte replacement
Treat underlying precipitant

121
Q

Chronic management of adrenal insufficiency

A

Hydrocortisone and fludrocortisone
Education
Medic alert bracelet

122
Q

Autoimmune syndromes associated with Addisons disease

A

Autoimmune polyglandular syndrome type 2 - also includes autoimmune thyroid disease and T1DM

123
Q

Features to ask for in history of suspected Cushing’s syndrome

A

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
Q

Examination in patient with suspected cushings

A

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
Q

What is cushings disease

A

Glucocorticoid excess due to ACTH secreting pituitary adenoma

126
Q

Investigating suspected Cushing’s syndrome

A

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
Q

Treatment of Cushings disease

A

Transphenoidal removal of tumour - successful in 80%

If surgery fails then pituitary irradiation or medical management (metyrapone)

128
Q

Treatment of ectopic acth secreting tumours

A

Tumor removal
Somatostatin analogues eg. Octreotide

129
Q

What is Nelson’s syndrome

A

Bilateral adrenalectomy to treat cushings disease causing massive production of ACTH leading to hyper- pigmentation and pituitary overgrowth

130
Q

Causes of proximal myopathy

A

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
Q

History taking in suspected hyperthyroidism

A

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
Q

Examination in patient with suspected hyperthyroidism

A

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
Q

Examination signs specific to Graves

A

Proptosis
Chemosis
Exposure keratitis
Ophthalmoplegia
Thyroid acropachy
Pretibial myxoedema

134
Q

Investigating hyperthyroidism

A

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
Q

Management of hyperthyroidism

A

Beta blocker
Carbimazole or propylthiouracil
- Block and replace or uptitration

If relapse consider surgery or radioactive iodine

136
Q

Complications of thyroidectomy

A

Hypoparathyroidism
Damage to recurrent laryngeal nerve
Hypothyroidism
Recurrence of hyperthyroidism

137
Q

What causes thyroid eye disease

A

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

138
Q

Progression of thyroid eye disease

A

‘NOSPECS’
No signs
Only lid retraction/ lag
Soft tissue involvement
Proptosis
Extraocular muscle involvement
Chemosis
Sight loss

139
Q

Worrying signs in thyroid eye disease

A

Optic neuropathy - visual acuity and colour vision
Exposure keratopathy
Double vision

140
Q

Investigating thyroid eye disease

A

Tfts
Antibodies
CT/MRI orbits

141
Q

Management of thyroid eye disease

A

May require high dose steroids
Can use ciclosporin as a steroid sparing agent
Orbital irradiation or surgical decompression
Joint endo-ophthalm clinic

142
Q

Differential diagnosis for Proptosis

A

Orbital tumor
Caroticocavernous fistula
Orbital cellulitis
AVM
cavernous sinus thrombosis

143
Q

Pre biologic screen for IBD

A

HIV
Hepatitis B and C
Quantiferon
VZV
EBV

144
Q

Stages of diabetic retinopathy

A

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

145
Q

What screening is in place for diabetic eye disease?

A

Annual retinal screening
BG retinopathy usually occurs 10 - 29 years after diabetes is diagnosed

146
Q

Management of diabetic retinopathy

A

Improved glycaemic control
Treat other risk factors (hypertension, smoking)
Photocoagulation

147
Q

Photocoagulation indications

A

Maculopathy
Preproliferative and proliferative diabetic retinopathy

148
Q

Complications of proliferative diabetic retinopathy

A

Vitreous haemorrhage
Traction retinal detachment
Neovascular glaucoma

149
Q

Causes of cataracts

A

Congenital:
Myotonic dystrophy
Rubella
Turners
Age
Diabetes
Steroids
Radiation exposure
Trauma
Storage disorders

150
Q

Risk factors for gout

A

Diet
Alcohol
Red meat
Diuretics
Obesity
Hypertension
Urate stones
CKD
Lymphoproliferative disorders

151
Q

Investigations for gout

A

Uric acid levels
Needle shaped negatively birefringent crystals on synovial aspirate
‘Punched out’ periarticular changes

152
Q

Treatment of gout

A

Treat the cause
Increase hydration
NSAIDs or colchicine

Allopurinol

153
Q

Symptoms/signs of Paget’s disease

A

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

154
Q

Investigation of Paget’s

A

High ALP, normal calcium and phosphate
Osteoporosis circumscripta
Increased uptake on bone scan

155
Q

Treatment of Paget’s

A

Analgesia
Physio
Hearing aids
Bisphosphonates

156
Q

Complications of Paget’s

A

CCF
Osteogenic sarcoma
Pathological fractures
Hydrocephalus
CN palsies
Cord compression
Hypercalcaemia
Gout
Kidney stones

157
Q

Causes of sabre tibia

A

Paget’s
Osteomalacia
Syphilis

158
Q

Causes of angioid streaks

A

Paget’s
Pseudoxanthoma elasticum
Ehlers- Danlos

159
Q

Features of systemic sclerosis

A

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

160
Q

Classification of systemic sclerosis

A

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

161
Q

Investigations for systemic sclerosis

A

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

162
Q

Treatment of systemic sclerosis

A

Standard Raynauds treatment
ACEi for renal disease
PPI for GI disease

163
Q

Conditions associated with pyoderma gangrenosum

A

IBD
RA, SLE, GPA, APS
Myeloproliferative disorder
PBC, hep C, AIH
Idiopathic

164
Q

Management of pyoderma gangrenosum

A

Investigate for underlying cause
Refer dermatology
TVN
Check for infection: Wound swab, bloods
Steroids cream
Tacrolimus ointment
High dose pred if severe

165
Q

History taking in deteriorating vision

A

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?

166
Q

Examination in deterioration of vision patient

A

VA
Ishihara plates
VF
Pupils
Fundoscopy
Eye movements
Cerebellar signs if young (MS)
Palpate temporal arteries if relevant
Hearing aid/ bosses skull (pagets)

167
Q

Causes of pale optic disc/optic atrophy

A
  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
168
Q

Differential diagnosis for male hypogonadism

A
  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
169
Q

Cause of klinefelter’s

A

Extra X chromosome (47XXY)

170
Q

Complications of Klinefelters

A

Subfertility
Chronic bronchitis, Bronchiectasis, emphysema
Cancers - germ cell, breast
Varicose veins
SLE
Diabetes
Mitral valve prolapse
Osteoporosis

171
Q

Examination findings in Klinefelters

A

Tall
Small tests
Sparse facial hair
Gynaecomastia

172
Q

Investigation of suspected Klinefelters

A

Chromosomal analysis
Elevated FSH and LH (FSH>LH)
Low testosterone
Semen analysis
Echo- mitral valve prolapse
Dexa scan - osteoporosis

173
Q

Causes of hair loss

A
  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
174
Q

History taking for hair loss

A

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

175
Q

Management of alopecia

A

Bloods
Fungal culture
Refer to derm
Steroids topical
Emotional support, wigs, ect.

176
Q

Investigating HHT

A

Bloods inc FBC, haematinics, clotting
Look for hepatic, lung, GI, cerebral, bladder AVMs

177
Q

How is a diagnosis of HHT

A

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

178
Q

American college of rheumatology criteria

A

Morning stiffness
Arthritis in 3+ joints
Arthritis of the hands
Symmetrical arthritis
Rhuematoid nodules
+ve RF
Erosions on joint radiographs

179
Q

Criteria for diagnosis of psoriatic arthritis

A

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

180
Q

Investigating psoriatic arthritis

A

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

181
Q

Management of psoriatic arthritis

A

Weight loss, exercise, smoking cessation
NSAIDs
Steroid injection
DMARD if NSAIDs fail
Anti- TNF
Derm opinion

182
Q

Examination for suspected GCA

A

Palpate temporal arteries
Scalp tenderness
Proximal weakness
Eye examination inc, fundoscopy

183
Q

Management of GCA

A

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

184
Q

Clinical presentation of polymyositis

A

Gradual onset progressive symmetrical proximal muscle weakness
Not affecting a eyes face or distal muscles, minimal pain
Typically in 50-60yr olds

185
Q

Clinical presentation of dermatomyositis

A

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

186
Q

Extra muscular/ dermatological manifestations of polymyositis/dermatomyositis

A

Constitutional symptoms
Arthralgia/arthritis
ILD
Pulmonary htn
Oesophageal dysmotility
Heart block
Raynauds
Skin ulcers

187
Q

How is poly/dermatomyositis associated with cancer

A

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

188
Q

What is the anti-synthetase syndrome?

A

The presence of anti-Jo or anti- SRP with ILD and dermato/poly- myositis

189
Q

Investigating suspected poly/dermato- myosotis

A

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

190
Q

Management of dermato/poly- myosotis

A

Derm review
Rhuem review
MDT - salt, physio
Steroids + gastro and bone protection
Steroid sparing agents

191
Q

Calculating Beighton score

A

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

192
Q

How does pseudoxanthoma elasticum present?

A

‘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

193
Q

What is erythema nodosum?

A

A septal panniculitis. There is inflammation in subcutaneous septa of fat.
Raised red/purple tender plaques on the shins

194
Q

Rockall score for UGIB

A

Age
Tachycardia and HR
Comorbidities inc renal and liver failure
Diagnosis in OGD
Degree of bleeding seen on OGD

195
Q

GBS score for UGIB

A

Hb
Urea
Initial systolic BP
Gender
HR
Melaena
Recent syncope
Hepatica disease
Cardiac failure

196
Q

Pathophysiology of Paget’s disease

A

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

197
Q

What hormones are involved in hypopituitarism and what symptoms to these cause

A

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

198
Q

Causes of hypopituitarism

A

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

199
Q

Investigating hypopituitarism

A

Low Na
Low glucose
Low cortisol, TSH, T4, LH, FSH, morning testosterone, oestradiol, IGF-1, prolactin

Ct head/MRI head/ pituitary

200
Q

Management of hypopituitarism

A

Hydrocortisone
Levothyroxine
Sex hormones
Growth hormone

Transphenoidal surgery of pituitary adenoma

201
Q

Clinical presentation of pseudohypoparathyroidism

A

Symptoms of low calcium
Round face, short neck, shortened 4th and 5th metacarpals
Abnormal mouth/dentition
Neuro exam
Fundoscopy (cataracts)

202
Q

Investigations for suspected pseudohypoparathyroidism

A

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

203
Q

What causes pseudohypoparathyroidism

A

Type 1a: autosomal dominant
Type 1b: no phenotypic features but similar biochemistry
Type 2: no phenotypic features, normal or raised cAMP response in urine

204
Q

Management of pseudohypoparathyroidism

A

Treat hypocalcaemia
Refer to endocrine
Investigate for other endocrinopathies

205
Q

Risk factors for subarachnoid haemorrhage

A

Hypertension
APKD
FHx of brain haemorrhage
Hypermobility (EDS, Marfans)
Smoking

206
Q

Driving advice post TIA

A

Can’t drive for 1 month

Paces (6 decks)

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