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Paces UPDATED > Station 5 Paces > Flashcards

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
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
Q

Clinical presentations of sarcoidosis

A

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

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26
Q

Diagnosis of sarcoidosis

A

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

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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

Differentials for sarcoid (breathlessness, lymphadenopathy, myalgia, fever)

A

Hypersensitivity pneumonitis
Lymphoma

TB
HIV
Toxoplasmosis
Histoplasmosis

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29
Q

Management of sarcoidosis

A

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

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30
Q

History and examination of Marfans station 5

A

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

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31
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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32
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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33
Q

Examination of suspected raynauds

A

Hand inc. joints and pulses, skin changes
Lungs ??fibrosis
Heart (loud s2) - pul hypertension
Proximal muscle weakness
Rashes (butterfly / heliotrope)
Systemic sclerosis features

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34
Q

Investigating suspected Raynauds

A

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)

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35
Q

Management of Raynauds

A

Conservative
- Smoking cessation
- Heated gloves and socks
- Avoid cold precipitant
Medical
- Nifedipine
- Sildenafil
- Prostaglandins if incipient gangrene (ulcers)
- Aspirin

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36
Q

What is gestational hypertension

A

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

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37
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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38
Q

Risk factors for pre-eclampsia

A

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

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39
Q

Complications of gestational hypertension or pre-eclampsia

A

Mother (acute)
- HELLP syndrome
- Eclampsia
- AKI
- DIC
- ARDS
- Cerebrovascular haemorrhage

Mother (chronic)
- Future risk of hypertension

Baby
- Placental abruption
- IUGR
- Prematurity
- Fetal death

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40
Q

Clinical presentation of pre-eclampsia

A

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

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41
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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42
Q

Investigations for pre-eclampsia

A

Urine dipstick + 24 collection
FBC, UE, LFT
Foetal US (intrauterine growth restriction)

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43
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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44
Q

Differential diagnosis for headache in pregnancy

A

Venous sinus thrombosis
Eclampsia
Migraine
Dehydration
SOL

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45
Q

Investigating PE

A

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

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46
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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47
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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48
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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49
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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50
Q

Clinical presentation of ankylosing spondylitis

A

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

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51
Q

Investigating suspected ankylosing spondylitis

A

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

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52
Q

Radiological changes in ankylosing spondylitis

A

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

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53
Q

Management of ankylosing spondylitis

A

MDT
- physio / OT / social worker / disease education / rheumatologist
- Pt centred care - calculate BASDAI [measure of disease activity]

Medications
- NSAIDs + PPI
- Steroids
- DMARDs

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54
Q

Examining patient with suspected ank spond

A

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

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55
Q

Clinical signs of osteogenesis imperfecta

A

Fractures
Blue sclera
Hyper mobile joints
Teeth problems
Hearing problems

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56
Q

Indications for CT head before Lp

A

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

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57
Q

What is Kernigs sign

A

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

Sign of meningism

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58
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
Rash

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59
Q

Interpreting CSF

A

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

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60
Q

What causes retinitis pigmentosa?

A

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

(can be autosomal recessive / autosomal dominant / x-linked)

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61
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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62
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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63
Q

Syndromes associated with retinitis pigmentosa

A

Rentinintis pigmentosa is associated with a number of syndromes / congenital conditions

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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64
Q

Other causes of tunnel vision

A

Papilloedema
Glaucoma
Choroidoretinitis (posterior uveitis)
Retinitis pigmentosa

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65
Q

Management of retinitis pigmentosa

A

Refer to ophthalmology and geneticist
Vitamin A may slow disease progression

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66
Q

History taking with acromegaly

A

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)

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67
Q

Complications of acromegaly

A

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

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68
Q

Diagnosing acromegaly

A

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

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69
Q

Management of acromegaly

A

Surgery with transsphenoidal approach
Radiotherapy
Somatostatin analogues
Dopamine agonists (inhibit prolactin)
Growth hormone receptor antagonists

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70
Q

Causes of hypothyroidism

A

Primary
Autoimmune eg. Hashimotos
Subacute thyroiditis
Iodine deficiency
Drugs - amiodarone, lithium
Iatrogenic- radiotherapy, thyroidectomy, anti thyroid meds

Secondary
Hypopituitarism or hypothalamic dysfunction

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71
Q

Examining a patient with suspected hypothyroidism

A

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)

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72
Q

Investigating suspected hypothyroidism

A

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

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73
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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74
Q

Hypothyroidism: Interpreting TFTs
- Primary
- Secondary
- Subclinical / poor compliance

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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75
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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76
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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77
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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78
Q

DVLA group 1 licence rules on syncope

A

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

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79
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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80
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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81
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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82
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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83
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
84
Q

Causes of hypertension

A

94% essential
4% renal
1% endocrine - cushings / conns / pheochromocytoma
Aortic coarctation
Pre-eclampsia

85
Q

Investigating hypertensive patient

A

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
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%

87
Q

Treatment of hypertension

A

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
Q

Causes of Papilloedema

A

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

89
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

90
Q

Pathogenesis of psoriasis

A

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

Accumulation of neutrophils and T lymphocytes
HLA-cw6 is strongly associated with severe disease of early onset

91
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

92
Q

Management of psoriasis

A

Topical treatments
- Emollients
- Topical Vit D analogues
- Topical steroids
- Topical coal tar (stains brown)

UV treatment
- UVB
- PUVA (psoralen + UVA)

DMARDS

93
Q

Causes of nail pitting

A

Psoriasis
Lichen planus
Alopecia areata
Fungal infections

94
Q

Causes of koebner phenomenon

A

Psoriasis
Lichen planus
Viral warts
Vitiligo
Sarcoid

95
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)

96
Q

Subtypes of eczema

A

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

97
Q

Treatment of eczema

A

Avoid precipitants

Topical
- Emollients
- Steroids

Systemic
- Tacrolimus
- Anti- histamines
- Antibiotics if infection
- Pred or azithro in severe cases

UV light therapy

98
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

99
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

100
Q

Examination findings with neuropathic ulcers

A

Pressures areas
Peripheral neuropathy
Charcots joint

101
Q

Causes of leg ulcers

A

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

102
Q

Investigating ulcers

A

Doppler US
ABPI <0.8 implies arterial insufficiency
Arteriography

103
Q

Treatment of ulcers

A

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

104
Q

Causes of neuropathic ulcers

A

Peripheral neuropathy

Diabetes / Alcohol / B12 / B1 deficiency

105
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

106
Q

Causes of erythema nodosum

A

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
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)

108
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

109
Q

What causes henoch- schonlein purpura

A

Small vessel vasculitis: IgA and C3 deposition

110
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

111
Q

Examining patient with suspected sickle cell crisis

A

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
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

113
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

114
Q

Management of sickle cell crisis

A

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

115
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

116
Q

Addisons disease history

A

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
Q

Addisons disease examination

A

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
Q

Causes of adrenal insufficiency

A

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
Q

Pathophysiology of Addisons disease

A

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

120
Q

Investigsting adrenal insufficiency

A

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

121
Q

Management of adrenal crisis

A

Iv fluids
Hydrocortisone
Electrolyte replacement
Treat underlying precipitant

122
Q

Chronic management of adrenal insufficiency

A

Hydrocortisone and fludrocortisone
Education
Medic alert bracelet

123
Q

Autoimmune syndromes associated with Addisons disease

A

Autoimmune polyglandular syndrome type 2 - also includes autoimmune thyroid disease, T1DM, pernicious anaemia, premature ovarian failure

124
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)

125
Q

Examination in patient with suspected cushings

A

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

126
Q

What is cushings disease

A

Glucocorticoid excess due to ACTH secreting pituitary adenoma

127
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

128
Q

Treatment of Cushings disease

A

Transphenoidal removal of tumour - successful in 80%

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

129
Q

Treatment of ectopic acth secreting tumours

A

Tumor removal
Somatostatin analogues eg. Octreotide

130
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

131
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

132
Q

History taking in suspected hyperthyroidism

A

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

133
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

134
Q

Examination signs specific to Graves

A

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

135
Q

Investigating hyperthyroidism

A

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

136
Q

Management of hyperthyroidism

A

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

137
Q

Complications of thyroidectomy

A

Hypoparathyroidism
Damage to recurrent laryngeal nerve
Hypothyroidism
Recurrence of hyperthyroidism

138
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

139
Q

Progression of thyroid eye disease

A

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

140
Q

Worrying signs in thyroid eye disease

A

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

141
Q

Investigating thyroid eye disease

A

Tfts
Antibodies
CT/MRI orbits

142
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

143
Q

Differential diagnosis for Proptosis

A

Orbital tumor
Caroticocavernous fistula
Orbital cellulitis
AVM
cavernous sinus thrombosis

144
Q

Pre biologic screen for IBD

A

HIV
Hepatitis B and C
Quantiferon (TB)
VZV
EBV

145
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

146
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

147
Q

Management of diabetic retinopathy

A

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

148
Q

Photocoagulation indications

A

Maculopathy
Preproliferative and proliferative diabetic retinopathy

149
Q

Complications of proliferative diabetic retinopathy

A

Vitreous haemorrhage
Traction retinal detachment
Neovascular glaucoma

150
Q

Causes of cataracts

A

Congenital:
- Myotonic dystrophy
- Congenital rubella
- Turners
- Storage disorders

Risk factors:
- Age
- Diabetes
- Steroids
- Radiation exposure
- Trauma

151
Q

Risk factors for gout

A

Lifestyle
- Obesity
- Hypertension
- Diet (alcohol, red meat)

Renal
- Diuretics
- CKD
- Urate stones

Lymphoproliferative disorders

152
Q

Investigations for gout

A

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

153
Q

Treatment of gout

A

Treat the cause
Increase hydration
NSAIDs or colchicine

Allopurinol

154
Q

Symptoms/signs of Paget’s disease

A

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

155
Q

Investigation of Paget’s

A

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

156
Q

Treatment of Paget’s

A

Analgesia
Physio
Hearing aids
Bisphosphonates

157
Q

Complications of Paget’s

A

CCF

Bone
- Osteogenic sarcoma
- Pathological fractures
- Hypercalcaemia

Brain
- Hydrocephalus
- CN palsies
- Cord compression

Renal / joint
- Gout
- Kidney stones

158
Q

Causes of sabre tibia

A

Anterior bowing of tibia

Paget’s
Osteomalacia
Syphilis

159
Q

Causes of angioid streaks

A

Paget’s
Pseudoxanthoma elasticum
Ehlers- Danlos

160
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
- 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

161
Q

Classification of systemic sclerosis

A

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

162
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

163
Q

Treatment of systemic sclerosis

A

Standard Raynauds treatment
ACEi for renal disease
PPI for GI disease

164
Q

Conditions associated with pyoderma gangrenosum

A

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

165
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

166
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?

167
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)

168
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
169
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
170
Q

Cause of klinefelter’s

A

Extra X chromosome (47XXY)

171
Q

Complications of Klinefelters

A

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

172
Q

Examination findings in Klinefelters

A

Tall
Small tests
Sparse facial hair
Gynaecomastia

173
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

174
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
175
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

176
Q

Management of alopecia

A

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

177
Q

Investigating HHT

A

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

178
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

179
Q

RA- 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

180
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

181
Q

Investigating psoriatic arthritis

A

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

182
Q

Management of psoriatic arthritis

A

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

183
Q

Examination for suspected GCA

A

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

184
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

185
Q

Clinical presentation of polymyositis

A

Painless gradual onset progressive symmetrical proximal muscle weakness
Not affecting a eyes face or distal muscles
Typically in 50-60yr olds

186
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

187
Q

Extra muscular/ dermatological manifestations of polymyositis/dermatomyositis

A

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

similar to systemic sclerosis

188
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

189
Q

What is the anti-synthetase syndrome?

A

Polymyositis OR dermatomyositis + ILD + antibodies (anti-Jo or anti-SRP)

190
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

191
Q

Management of dermato/poly- myosotis

A

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

192
Q

Calculating Beighton score

A

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

193
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

194
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

195
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

196
Q

GBS score for UGIB

A

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

197
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

198
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

199
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

200
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

201
Q

Management of hypopituitarism

A

Hydrocortisone
Levothyroxine
Sex hormones
Growth hormone

Transphenoidal surgery of pituitary adenoma

202
Q

Clinical presentation of pseudohypoparathyroidism

A

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)

203
Q

Investigations for suspected pseudohypoparathyroidism

A

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

204
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

205
Q

Management of pseudohypoparathyroidism

A

Treat hypocalcaemia
Refer to endocrine
Investigate for other endocrinopathies

206
Q

Risk factors for subarachnoid haemorrhage

A

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

207
Q

Driving advice post TIA

A

Can’t drive for 1 month

Paces UPDATED (7 decks)

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