PACES ALL concise

Question 1

Asthma - def? Presentation? Ix? Severity? Short-term/long-term Mx incl. conservative? Mneumonic for conservative long-term Mx?

Answer 1

Def: chronic inflammatory airway disease characterized by reversible airway obstruction + airway hyperresponsiveness

Presentation

• Dry cough, polyphonic wheeze ( worse@night/morning)
• Triggers: cold air, pollen, pollution, exercise
• Atopic features - eczema, nasal polyps

Ix:

• Peak flow variability (in peak flow diary)
• Spirometry (shows reversibility after bronchodilator)
• FeNO (fractional exhaled nitric oxide - a marker of airway inflamme, in uncertain Dx)
• On exacerbation:
  
  • ABG, peak flows (min x4/day), CXR
• Other:
  
  • Allergy testing - total IgE, specific IgE (RAST), serum eosinophil count

Asthma severity:

• Life-threatening: PEF <33% of baseline/SpO2 <92%/PaO2 <8/Normal or raised PaCO2 - should be low with resp alkalosis due to excess breathing only becomes acidotic when get tired
  
  • CHEST: Cyanosis, Hypotension, Exhaustion, Silent chest, Tachycardia
• Acute severe: PEF <50% of baseline/RR >25/HR >110/can’t complete sentence without taking a breath
• Moderate: PEF <75% of baseline

Short-term Mx:

• A-E approach, seek senior support (call for help if life-threatening)
• O2 - 15L NRM (if hypoxaemic)
• Burst therapy:
  
  • SABA (spacer up to 10 puffs every 20 mins –> nebs)
  • Ipratropium Bromide (add to nebs if poor response/severe, every 4-6hrs)
  • Corticosteroids (min 5-day course, give within 1 hour, give IV if can’t take orally)
• Other Tx options:
  
  • IV Magnesium sulfate (STAT dose if poor response above/severe) - consult senior before use
  • IV salbutamol (if on ventilation) - consult senior before use
  • IV Aminophylline - consult senior before use, requires ITU setting
• If less distressed/more tired/shallow breaths/confused –> call critical care outreach team (CCOT) for ITU support

Long-term Mx (>16yrs):

• Conservative: TAME
  
  • ​Technique​
  • Avoid triggers
  • Monitor peak flow
  • Educate - formulate Personalised Asthma Action Plan (PAAP), Annual flu vaccine
• Medical:
  
  1. SABA (reliever)
  2. SABA + ICS (preventer)
  3. SABA + ICS + LTRA (leukotrine receptor antagonist e.g. montelukast)
  4. SABA + ICS + LABA (+ LTRA stopped unless good response)
  5. SABA + MART (ICS + LABA COMBO) (+ LTRA)
  6. NOTE: maintenance & reliever therapy (MART) - used as preventer & maintenance inhaler
  7. Specialist input (e.g. for oral steroids)

Question 2

COPD - definition? Signs & Sx? New Dx & exacerbation Ix/Mx? Prognosis factors?

Answer 2

Def: chronic bronchitis (damaged to cilia in bronchi - blue bloater) + emphysema (damage to alveoli - pink puffer)

Presentation:

• Cough (productive), SoB (starts on exercise)
• RF exposure - smoking/pollution
• Signs:
  
  • Barrel chest
  • Hyper-resonant (air trapping)
  • Reduced breath sounds
  • Widespread expiratory wheeze
  • Coarse crackles if exacerbation (mucus in airways)
  • Other - asterixis (CO2 retention flap), raised JVP (cor pulmonale)
  • NOTE: COPD does not cause clubbing –> cancer/bronchiectasis

New Dx Mx:

• Ix:
  
  • Bedside - mMRC dyspnoea scale, O2 sats, ECG (cor pulmonale)
  • Spirometry - FEV1/FVC <0.7 (forced exp volume in 1s)
    
    • Mild - FEV1 ≥ 80%
    • Moderate - FEV1 ≥ 50%
    • Severe - FEV1 ≥ 30%
    • Very severe - FEV1 <30%
  • Bloods - FBC, ABG, eosinophil count, alpha1-antitrypsin level
  • Imaging - CXR, CT chest
  • Other: serial peak flows if asthma DDx, sputum culture (in freq exacerbation), pul funct tests
• Mx:
  
  • Conservative - stop smoking, influenza + pneumococcal vaccine, inhaler device training
    
    • Persuade to stop smoking
    • Pul rehab
    • Prick them - influenza + pneumococcal vaccine
    • Psych issues
  • Medical - depends on severity - GOLD group –> solo/combo of:
    
    • SABA e.g. salbutamol
    • SAMA e.g. Ipratropium bromide
    • LABA e.g. salmeterol
    • LAMA e.g. tiotropium
    • ± ICS e.g. beclomethasone
    • Other: mucolytic e.g. acetylcysteine, O2 therapy, theophylline
  • Medical pathway:
    
    • 1 - SABA/SAMA
    • 2a - Steroid-responsive (eosinophilia/atopy): LABA + ICS
    • 2b - Not steroid-responsive: LABA + LAMA
    • 3 - LABA + LAMA + ICS
    • 4 - specialist input e.g. theophylline
  • Surgical - lung reduction surgery (large bullae)
  • Other: long-term O2 therapy
    
    • Only if non-smoker (smoker –> burns)
    • Only if <7.3 PaO2/<8 if also pul HTN
    • Only if PaCO2 does not rise excessively on O2

Acute Exacerbation Mx:

• Ix: ABG, ECG, CXR
• Mx:
  
  • 15L O2 NRM
  • Nebs - salbutamol + IpB
  • Steroids (PO pred/IV hydrocortisone)
  • Abx if infective –> prophylactic abx if persistent infections - azithromycin

Prognosis factors:

• Body mass - worse if obese
• Obstruction - worse if reduced FEV1
• Dyspnoea
• Exercise capacity - how far can you walk in 6 minutes?

Complication –> vasoconstriction to redirect blood flow to well-oxygenated areas of the lungs –> if widespread –> pul HTN –> cor pulmonale

Question 3

Pneumonia - def? Presentation? Types? Ix? Scoring? Mx?

Answer 3

Def: inflammation of lung caused by inf w/ visible radiographic changes

Presentation:

• Decreased chest expansion, dull on percussion, increased sound vocal resonance
• Coarse crackles
• Bronchial breathing – bronchial airflow instead of alveolar airflow (due to transmission of sounds through consolidation) – check by listening to sound at the throat

Ix: ABG, CXR, sputum culture (mod/high severity)

Scoring for CAP: CURB-65 (confusion, urea ≥7mmol/L, RR ≥30, BP <90/60, ≥65yrs)

• +1 = outpatient; +2 = outpatient/inpatient, +3 = inpatient ± ITU
• NOTE: urea is no longer used

Types & Mx –> local abx guidelines

• CAP:
  
  • Typical (S. pneumo, H. influenzae) –> Amox/Co-Amox
  • Atypical (Legionella, Mycoplasma, Chlamydia) –> Clari
    
    • ​Dry cough (instead of productive), myalgia, confusion, diarrhoea
  • NOTE: if not sure often given Co-Amox + Clari
• HAP - pneumonia arising >48hrs after admission to hospital (S. pneumo, S. aureus, P. aeruginosa) –> Taxocin (pseudomonal cover)
• Aspiration - RFs: swallowing dyfunct, reduced consciousness, reduced mental status –> elderly/frail

Goes into septic shock –> give IV fluid + senior help + check abx sensitivity (ring lab) –> ITU (intropic support - NA to increase PVR)

• Other aspects of septic-6
• NOTE: dobutamine is for cardiogenic shock to increase CO - this is not relevant here

Question 4

PE - def? Sx? RFs? Scoring & Ix? Mx?

Answer 4

Def: occlusion of pulmonary vasculature characterized by sharp pleuritic chest pain

Sx: SYNCOPE, sudden SoB, pleuritic chest pain, haemoptysis

RFs: SICC - Surgery, Immobility, Cancer, COCP

Initial Tx:

• DOAC (e.g. Apixaban) or unfractionated heparin (if bleeding risk, can be reversed easily)
• Massive PE –> IV unfractionated heparin for hours before and after thrombolysis e.g. IV alteplase

Scoring & Ix: Well’s score

• ≤4 = D-Dimer –sign raised–> CTPA
• >4 = CTPA
• ECG useful - sinus tachycardia, right heart strain, S1Q3T3
• NOTE: Troponin = useful markers for PE severity (indicates right heart strain)

Ongoing anticoagulation - DOAC/Warfarin

• Provoked - 3 months (SICC)
• Unprovoked - >6 months + cancer & thrombophilia testing
  
  • Ix for cancer –> any Sx?
    
    • If yes - CT TAP
    • If no - FBC, U&E, LFTs, clotting, physical exam –> if concern –> CT TAP
    • Consider thrombophilia screen if no cancer for anti-phospholipid syndrome (anticardiolipin, lupus anticoagulant, anti-beta-2-glycoprotein)

Question 8

Bronchiectasis - definition? causes? presentation? Ix? Mx?

Answer 8

Def: obstructive lung disease characterised by permanent dilation of bronchi from the destruction of elastic & muscular components of the bronchial wall

• Results from diseases causing chronic inflammation:
  
  • Primary ciliary dyskinesia - cilia don’t move –> mucus trapped in airways –> recurrent pneumonia –> chr inflammation
  • Cystic fibrosis - mucus thick & sticky –> recurrent pneumonia –> chr inflammation
  • Airway obstruction - tumour inside/outside airway or inhaled foreign body –> mucus can’t clear –> recurrent pneumonia –> chr inflammation
  • NOTE: worse with certain infections e.g. aspergillosis –> hypersensitivity response
• Chr inflammation - has immune cells that release cytokines –> damage ciliated epithelial cells + destroys elastin –> airways dilated + clogged with mucus –> fibroblasts deposit collagen –> stiff lungs + mucus plug –> obstructive lung disease

Presentation:

• RFs: CF, PCD, congenital disorders of airway, host immunodef (incl. HIV), recurrent lung inf
  
  • Less common - inhaled foreign body, connective tissue disease, IBD, alpha1-antitrypsin def
• Productive cough (large amounts of sputum) ± haemoptysis - worse lying flat/one side
• Dyspnoea (with increased severity)
• Fever (on exacerbation)
• Crackles, inspiratory squeaks & rhonchi, clubbing (from long-term hypoxia)

Ix: CXR (ring shadows, tramlines), high-res CT (signet ring sign), FBC + sputum culture & sensitivity (inf e.g. pseudomonas), pul function tests

• Genetic testing (for possible RF causes): serum alpha1-antitrypsin, serum Ig lvls (ID), specific IgE for Aspergillus, sweat Cl test (CF), rheumatoid factor (CTD), HIV test, nasal nitric oxide (PCD)

Mx:

• Conservative:
  
  • Persuade to stop smoking
  • Pul rehab
  • Prick them - influenza + pneumococcal vaccine
  • Psych issues
• Medical:
  
  • Mucoactive agent (nebulised hypertonic saline)
  • Inhaled bronchodilator (SABA/SAMA/LABA/LAMA) - ONLY If co-existing asthma/COPD
• Surgical: depending on primary cause e.g. IFB, tumour –> lobectomy/lung transplant
• Exacerbation: short-term abx (azithromycin)

Question 9

Interstitial lung disease - causes? presentation? Ix? Mx? Prognosis?

Answer 9

Interstitial lung disease

• Refers to the tissue the gasses pass through e.g. surface of alveoli –> reducing gas exchange

Causes:

• Upper zone fibrosis: PATEN (more occupational causes)
  
  • Pneumoconiosis (not asbestosis) - caused by inorganic dust (e.g. soot)
  • Aspergillosis/ABPA
  • TB
  • Extrinsic allergic alveolitis - caused by organic dust e.g. animal shedding
  • Negative seroarthropathies
• Lower zone fibrosis: STAIR
  
  • Sarcoidosis
  • Toxins: B-MANS (Bleomycin, Methotrexate, Amiodarone, Nitrofurantoin, Sulfasalazine)
  • Asbestosis
  • Idiopathic pulmonary fibrosis
  • Rheum: SLE, RhA etc
• Signs of conditions associated w/ pulmonary fibrosis:
  
  • MCP swelling - RA
  • Malar rash - SLE​
  • Kyphosis - Ank Spond (apical fibrosis)
  • Lupus pernio - sarcoidosis
  • Thick skin/’bird beak’ nose - systemic sclerosis
  • Aphthous ulcers, abdo scars - Crohn’s
  • Grey skin - amiodarone

Main Sx: progressive SOBOE, dry cough, fatigue, weight loss

Signs: find end-insp creps, clubbing

• Other: reduced chest expansion, normal/reduced percussion, normal vocal fremitus

Investigations: spirometry, high-res CT & lung biopsy

• Bedside: spirometry (low FEV1, low FVC, FEV1/FVC>0.8 = restrictive lung disease), ECG (right heart strain), drug review
• Bloods
  
  • FBC, U&E, LFTs, CRP, ESR, ABG (T1RF)
  • AI screen - Serology (CTD): ANA, RhF, anti-CCP
  • Serum ACE for sarcoidosis
  • TB testing
• Imaging
  
  • CXR: reticulonodular shadowing (honeycombing) + rule out lung cancer
  • High-res CT: more detailed view of alveolar structure –> ‘honeycombing’ + lung biopsy
  • Echo (right heart strain/cor pulmonale)
• Invasive
  
  • Bronchoscopy + lung biopsy (gold-standard)

Management:

• Conservative (4Ps):
  
  • Persuade to stop smoking, reduce exposure (meds, EAA)
  • Pul rehab
  • Prick them - influenza + pneumococcal vaccine
  • Psych issues
• Medical: anti-fibrotic e.g. pirfenidone +/- prednisolone ± O2 (if hypoxaemic)
• Surgical: lung transplant if severe deterioration/impairment/oxygen dependent

Prognosis: 3-4yrs post-Dx (no Mx increases survival)

Question 16

Pleural effusion - signs? causes? Ix? Mx?

Answer 16

Signs (if fluid > 300ml):

• Key:
  
  • Stony dull in lung base
  • If large: tracheal deviation away
• Reduced chest expansion
• Reduced breath sounds
• Reduced vocal fremitus

Causes:

• Transudative (<30g/L protein)
  
  • HEART FAILURE
  • Hypoalbuminaemia: liver disease, nephrotic syndrome, malabsorption
  • Hypothyroidism
  • Meig’s syndrome (benign ovarian tumor + ascites + pleural effusion)
• Exudative (>30g/L protein)
  
  • Infection: PNEUMONIA, TB, subphrenic abscess
  • Connective tissue disease; RA (also low glucose), SLE
  • Neoplasia: lung cancer, mesothelioma, metastases
  • Pancreatitis: high amylase in pleural fluid
  • Pulmonary embolism

Ix:​

• Bedside: obs, urinalysis for protein
• Bloods:
  
  • ABG, BC
  • FBC, U&E, LFTs, CRP
  • Clotting (before needle aspiration), albumin (nephrotic syndrome)
  • Mantoux/ELISPOT (TB)
• Imaging:
  
  • CXR: meniscus sign, dense shadowing, pleural effusion if ≥300mL fluid
  • CT chest - identify the cause

Management: US-guided pleural aspiration = thoracocentesis (21G needle, 50ml syringe) - above rib to avoid NV bundle

• LDH & protein in pleural fluid & serum + RBCs, WBCs, cytology, culture, pH & glucose of pleural fluid
  
  • MC&S
  • Biochemistry: PPALS
    
    • ​Protein (also serum)
    • pH
    • Amylase
    • LDH (also serum)
    • Sugar (glucose)
  • Cytology
  • Immunology - if indicated (RF, ANA, complement)
• Findings:
  
  • Protein > 30g/L: exudate
  • Protein < 30g/L: transudate
  • Protein 25-35g/L: use Light’s criteria. An exudate is likely if at least 1 of:
    
    • Pleural protein/serum protein > 0.5
    • Pleural LDH/serum LDH > 0.6
    • Pleural LDH > 2/3 upper limits of normal serum LDH
• Tx cause e.g. abx for infection, furosemide for HF
• Management of recurrent pleural effusion
  
  • Recurrent aspiration (thoracocentesis)
  • Pleurodesis
  • Indwelling pleural catheter

Pleural fluid features:

• Heavy blood staining - mesothelioma, TB, PE, trauma
• Purulent/turbid/cloudy - empyema secondary to bacterial pneumonia –> insert chest tube to allow drainage
• Milky - chylothorax via lymphatic obstruction secondary to malignancy

Question 17

Pneumothorax - Def? RFs? Causes? Ix? Mx? How do you identify a Tension Pneumothorax?

Answer 17

Pneumothorax = accumulation of air in pleural space (subdivided into primary and secondary)

RFs: pre-existing lung disease, Marfan’s, RA, smoking

Causes: cystic pathology, parenchymal necrosis, iatrogenic, trauma

Ix: CXR

Mx:

• Primary (no pre-existing lung disease)
  
  • <2cm (betw lung margin & chest wall), no SoB – observe 4-6hrs ± supplemental O2
  • SoB/≥2cm – needle aspiration (16-18G) –> observe 4-6hrs
    
    • Do NOT repeat needle aspiration x2
  • Chest drain if above fails + ADMIT ± supplemental O2
    
    • NOTE: correct clotting before inserting if possible
  • Surgery
• Secondary (pre-existing lung disease) - ADMIT all secondary pneumothorax (for at least 24hrs observation)
  
  • <1cm - high-flow O2 + ADMIT (24hrs observation)
  • 1-2cm - needle aspiration (16-18G) –> high-flow O2 + ADMIT (24hrs observation)
  • ​SoB/≥2cm/previous failed - chest drain + ADMIT ± supplemental O2
  • Surgery

Tension pneumothorax = pushes away the trachea to the opposite side

• Non-traumatic:
  
  • IMMEDIATE peri-arrest call (2222)
  • Needle decompression = emergency Tx, 2nd ICS MCL (grey cannula) + high-flow O2
  • Follow-up = ADMIT + chest drain
• Traumatic:
  
  • Open thoracostomy
  • Follow-up = ADMIT + chest drain
• Traumatic non-tension pneumothorax:
  
  • High-flow O2 + ADMIT (24hrs observation)
  • If open pneumothorax/penetrating chest wound –> occlusive dressing + observe
  • Refer to thoracic surgeons - chest drain/thoracotomy

Location:

• Needle aspiration = 2nd ICS, MCL
• Chest drain = triangle of safety (axilla, pectoralis major, latissimus dorsi, 5th ICS) - 4th/5th ICS, MAL

Surgery:

• Open thoracotomy (or video-assisted thoracoscopic surgery = VATS)
• Follow-up surgery –> pleurodesis (mechanical abrasion/chemical irritation)

Question 20

Lung cancer - epi? presentation? types? Ix? Mx?

Answer 20

Epi: Second most common cancer in UK

Presentation: chronic cough, haemoptysis, FLAWS

• Monophonic wheeze, pleural effusion signs (dull on percussion, reduced BS), cachexia, SVCO (face swelling & engorged veins in venal-caval distribution), hypertrophic pulmonary osteoarthropathy (HPOA)
• RFs: smoking, asbestos exposure, FHx

Types:

• Non-small cell lung cancer (MOST)
  
  • Adenocarcinoma (MOST COMMON LC)
    
    • Non-smoking women (40% cases)
  • Squamous cell carcinoma (SCC)
    
    • Affects large airways of lungs (central)
    • Classically assoc w/ paraneoplastic hypercalcaemia, as tumour may release PTHrP
    • 2nd most common in non-smokers
    • Most common cause of Pancoast tumour
    • Keratinization (keratin pearls)
  • Large cell carcinomas (Dx of exclusion)
  • Alveolar cell carcinoma = ++sputum
  • Bronchial adenoma = mostly carcinoid
    
    • Carcinoid syndrome - flushing, diarrhoea, episodes of dyspnoea
    • Urinary 5-Hydroxyindoleacetic Acid (5-IAA) levels may be used to screen for carcinoid syndrome
• Small cell lung cancer (15%)
  
  • Almost exclusively smokers
  • Can be assoc w/ neuroendocrine syndrome (SIADH, Cushing’s)
  • Early mets BUT chemo sensitive

Ix:

• Bloods - FBC, haematinics, Ca
• Imaging - CXR, CT chest (2WW referral), CT PET scan (staging, mets)
• Interventional if suspicious CXR:
  
  • Endobronchial US-guided biopsy (EBUS) & biopsy
  • Video-assisted Tracheostomy & Biopsy (VATS - BIOPSY) of accessible nodes

Mx:

• Conservative: lung cancer MDT
  
  • Smoking cessation
  • Psych support (McMillan Nurses, specialist lung cancer nurse involvement)
  • Palliative care (if terminal, Sx control & planning)
• Medical:
  
  • Systemic chemo - esp. for small cell lung cancer (chemosensitive)
  • Adjuvant/radical radiotherapy
• Surgical - if NSCLC
  
  • VATS-lobectomy
  • Open lobectomy/Pneumonectomy

Question 21

4Ps of respiratory conservative Mx?

Answer 21

Persuade to stop smoking

Pul rehab

Prick them - influenza + pneumococcal vaccine

Psych issues

Question 22

Fine vs coarse creps?

Vesicular vs bronchial breathing?

Answer 22

FINE (inspiratory) – pulmonary oedema (HF), interstitial lung disease (pul fibrosis)

• Best heard at base of lungs

COARSE (insp & exp) – bronchiectasis, COPD (chronic bronchitis), pneumonia

• No specific area of lungs louder

Vesicular - inspiratory > expiratory

Bronchial - inspiratory = expiratory

Question 23

IHD - RFs? Types? Definition? Dx? Mx? Complications?

Answer 23

RFs: HTN, DM, Smoking, FHx IHD, Hypercholesterolaemia

Stable angina - chest pain on exertion relieved by rest

• Path - mismatch in O2 supply and demand to the myocardium
• Ix: CT-angiogram
• Mx:
  
  • B-blockers - reduces HR req for activity –> reduced likelihood of mismatch in O2 supply & demand
  • GTN spray - reduce myocardial preload + reduces strain
  • RF modification –> reduced risk of progression

Acute coronary syndrome - Sx caused by sudden reduced BF to the myocardium

• Dx:
  
  • ​ST-elevation = STEMI
  • Troponin raised = NSTEMI (+ dynamic T-wave inversion, ST depression)
  • Unstable angina pectoris (pain at rest) = ischemia NOT infarct
• Generic ACS Mx - MONA BASH
  
  • ALL immediate:
    
    • 5-10mg Morphine IV + Nitrates (GTN spray)
    • Dual antiplatelet therapy (DAPT) - 300mg Aspirin STAT + 300mg Clopidogrel STAT (or 180mg PO Ticagrelor)
  • ALL long-term:
    
    • Continue DAPT
      
      • 1 year: 75mg OD Aspirin + 75mg OD Clopidogrel (or 90mg BD Ticagrelor)
      • >1yr - 75mg OD Aspirin
    • B-blocker (1.25-10mg Bisoprolol OD)
    • ACEi (1.25-10mg Ramipril OD)
    • Statin (80mg Atorvastatin OD)
• STEMI Mx: establish coronary reperfusion ASAP
  
  • Sx <12hrs: PCI BUT if no PCI within 2hrs Dx –> thrombolysis (e.g. tPA - tissue plasminogen activator)
  • Sx >12hrs: invasive coronary angiography ± PCI if needed
  • PCI:
    
    • If having PCI give Prasugrel (instead of Clopi/Ticagrelor)
    • PCI accessed via radial (or femoral) artery, guidewire passed via X-ray guidance into the affected coronary artery AND IV unfractionated heparin during the procedure –> stent inserted impregnated with an anti-proliferative agent (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so DAPT needed for 1yr
    • If PCI with stents inserted –> DAPT 12 months
• NSTEMI Mx:
  
  • 2.5mg SC Fondaparinux (direct factor 10a inhibitor)
  • Risk stratify - GRACE criteria (& others)
  • High risk = invasive coronary angiography (within 48-72hrs)

Complications: FAP (failure, arrhythmias, pericarditis)

• Heart failure, arrhythmias (incl. VF)
• Pericarditis
  
  • Early - positional chest pain day after MI –> give NSAIDs
  • Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)

Question 24

Heart failure def? Causes? Pathophysiology? Categories & Causes? Classification? Ix? Mx?

Answer 24

Def: pumping of blood by heart insufficient to meet the demands of the body

Causes:

• RVF:
  
  • Acute: MI, inf endocarditis, PE
  • Chr: Cor pulmonale, LVF
• LVF:
  
  • Acute: MI, inf endocarditis
  • Chronic: ischaemic/hypertensive CMO, valvular HD

Pathophysiology:

• RHF - right side of the heart pumps deoxygenated blood from the body to the lungs to be reperfused - if the RH is not pumping effectively you get the fluid collection in the peripheries = PERIPHERAL OEDEMA
• LHF - left side of the heart pumps oxygenated blood from the lungs to the body - if the LH is not pumping effectively you pooling of blood in the lungs = PULMONARY OEDEMA
• Reduced CO –> shock, tachycardia, AKI
  
  • CO = SV*HR
  • Ejection fraction = SV/End-diastolic Volume

Categories:

• HF w/ preserved ejection fraction (left ventricular >50%) = inadequate filling of ventricles during diastole (from ventricular stiffness)
  
  • Causes of ventricular stiffness:
    
    • Volume overload (valve regurg)
    • Pressure overload (HTN)
    • Decreased distensibility (constrictive pericarditis)
• HF w/ reduced ejection fraction (left ventricular <40%) = inadequate emptying of ventricles during systoles (from outflow obstruction/impaired contractility)
  
  • Causes of outflow obstruction/impaired contractility:
    
    • MI, Cardiomyopathy, Arrythmia

NYHA classification:

• 1 - no limitation on activity
• 2 - comfortable at rest but dyspnoea on ordinary activity
• 3 - marked limitation on ordinary activity
• 4 - dyspnoea at rest

Ix:

• Bedside: ECG - detects if anything precipitating HF (arrhythmia/ischaemic event)
• Bloods: ABG (if resp compromise from pul oedema), troponin (ACS), BNP (HF screening)
• Imaging: CXR (visualise pul oedema, cardiomegaly), ECHO (valvular abn/regional wall mov abn)

Mx: MON BA (out of MONA BASH)

• Immediate:
  
  • Sit the patient up (reduce venous return to heart –> less strain)
  • O2 15L/min NRM
• Medical:
  
  • IV furosemide (loop diuretic) - remove excess fluid + venous dilation (reduce preload)
  • Nitrates (GTN/Isosobide Mononitrate) AND Morphine - reduce preload on the heart
• Long-term:
  
  • Reduced ejection fraction - prognostic benefit:
    
    • B-blocker (bisoprolol) - reduce strain on heart, do not give acutely if severe HF as will kill them
    • ACEi - reduce strain on heart
      
      • After the above if LVEF <35% & Sx –> mineralocorticoid antagonist e.g. spironolactone
      • 3rd line - by specialist: Sacubitril/Valsartan (entresto), Ivabradine & CRT
    • SGLT2 inhibitors (dapagliflozin)
  • RF modification - poor glycaemic control/high cholesterol
  • Sx (diuretics)

Complications:

• Reduced CO (SV*HR) –> shock, tachycardia, AKI
• Congestion –> pulmonary oedema + peripheral oedema

Question 26

SVT - Def? Types? Presentation - case example? Mx?

Answer 26

Def: regular narrow-complex tachycardia with no p-waves + supraventricular origin

Junctional types:

• AVNRT - local re-entry circuit within AV node
• AVRT - re-entry circuit between atria and ventricles –> after SVT termination = delta wave = WPW syndrome:
  
  • ​Assoc w/ HOCM
  • Avoid digoxin, verapamil, amiodarone (reduce conduction down SAN –> worsen retrograde conduction –> risk of VT)
  • Can use B-blocker/flecainide instead

Case example: 23yrs, 1-hr palpitations + SoB, 2 similar episodes prev following alcohol, this time severe chest pain

Mx:

• Unstable tachycardia (<90 BP/chest pain/acute heart failure) –> synchronised DC Cardioversion
• Vagal manoeuvres (increase parasympathetic stim via vagus nerve to slow conduction via AV node)
  
  • Valsalva manoeuvre (blow out through nose while pinching + shut mouth) - breath through 50ml syringe
• Adenosine 6mg –> 12 mg –> 12mg
  
  • NOTE: if adenosine CI (e.g. asthma) –> VERAPAMIL (rate-limiting CCB)
• Other:
  
  • IV B-blocker/amiodarone/digoxin
  • Synchronised DC Cardioversion

Question 27

Key heart murmurs? Accentuation manoeuvres?

Causes? Left vs right heart valve abn epidemiology?

Mx? Valve types? Complications of prosthetic heart valves?

Answer 27

Key murmurs:

• AS = ejection systolic + radiates to carotids, slow rising pulse, narrow pulse pressure, heaving apex beat
  
  • Sound: Wooooshhh
  • Severe AS - absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat
    
    • A longer murmur is worse (small space for blood to pass through = takes longer)
• AR = early diastolic + sitting forward (LLSE), collapsing pulse, wide pulse pressure, displaced apex
  
  • Sound: de woooshhhh
  • Severe AR –> Austin-flint murmur = ‘Rumbling mid-diastolic murmur’
    
    • Best heard at apex, caused by blood flowing back through aortic valve and over mitral valve
    • Shorter murmur is worse (quicker to flow back through large hole)
• MR = pan-_systolic_ + radiates to left axilla, AF, displaced thrusting apex, LVF/pul HTN
  
  • Sound: Woooooshhh (holosystolic)
• MS = mid-diastolic + LLP, malar flush, AF, loud/palpable S1 “tapping” apex, pul HTN (loud P2 - pul thrill)
  
  • Sound: Wooosh de (loud S1) de (early diastolic snap)
• NOTE: same pattern for pulmonary & tricuspid (pul stenosis & tricuspid regurgitation = systolic)
  
  • TR - pulsatile liver
  • PS - radiates to back, assoc w/ Noonan’s (AD, webbed neck, wide-spaced eyes etc.)

Accentuation manoeuvres:

• R-sided murmurs (tricuspid + pulmonary) –> louder on INspiration = blood goes IN to right-side of heart
• L-sided murmurs (aortic + mitral) –> louder on EXpiration = blood EXits left-side of heart
• AS radiates to the carotids + louder on leaning forward + listen on right sternal edge
• MS louder on turning to the left, MR radiates to axilla

Causes:

• AS (stenosis/sclerosis):
  
  • Older - senile calcification
  • Younger - bicuspid valve
• AR:
  
  • Acute (aortic root dilation, infective endocarditis)
  • Chronic (CTD, RHD, bicuspid aortic valve)
• MR:
  
  • Acute: - IHD (papillary-muscle dysfunction post-MI), infective endocarditis, RHD
  • Chronic - myxomatous degeneration (can be assoc with Marfan’s/Ehlers-Danlos)
• MS: rheumatic heart disease (RHD)

Left vs Right valve abn:

• Left = more common as higher pressure system, more likely in damaged valves, commonly Strep Viridans
• Right = more common in IV drug users –> tricuspid valve is first valve reached, commonly S. aureus

Ix:

• ECHO (Dx & severity) - Transthoracic incl doppler (regurg jet) ± TOE
  
  • If the above is inconclusive:
    
    • 2nd - Cardiac MRI - analysis of cardiac function
    • 3rd - Cardiac catheterization (invasive) - pressure gradient
• ECG (LVH), CXR (pul HTN)

Management:

• AS:
  
  • C: Asymptomatic –> monitor (6 monthly ECHO)
  • S: Symptomatic –> aortic valve replacement:
    
    • Fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
    • Not fit = Transcatheter aortic valve implantation (TAVI)
  • M:
    
    • HF Sx (diuretics, ACEi)
    • RF optimisation (statins, HTN, DM)
• AR:
  
  • If no left ventricular dysfunction –> medical Mx
    
    • ACEi, vasodilators e.g. nifedipine/hydralazine (if HTN)
  • If left ventricular dysfunction & low surgical risk/another indication for cardiac surgery –> aortic valve surgery (replacement > repair)
• MR - primary (valve abn/damage):
  
  • Mitral valve surgery (repair > replacement)
  • Medical - ACEi, B-blocker & diuretics
    
    • Tx AF if present (incl. anticoagulate)
• MS:
  
  • C: If non severe + asymptomatic –> monitor
  • S: Otherwise = Balloon valvuloplasty/mitral valve replacement
    
    • if C/Is (persistent left atrial thrombus/rigid calcified valve) –> need open surgery
    • NOTE: valvuloplasty = lateral thoracotomy scar
  • M: Tx AF if present (incl. anticoagulate)

Valve types:

• Tissue valve - porcine xenograft
  
  • For older patients & females of childbearing-age - lasts 10-15yrs, less if active
  • No need for Warfarin
• Mechnical valve - quiet clicking noise
  
  • Younger people (<60yrs) - no need for repeat surgery, last 30yrs+
  • Lifelong Warfarin

Complications of prosthetic heart valves: FIBAT

• Failure
• Infection
• Bleeding - MAHA
• Anaemia
• Thromboembolic phenomena

Question 29

Atrial fibrillation (AF)

• Def? Causes? Ix? Mx?

Answer 29

Def: rapid, chaotic, and ineffective atrial electrical conduction

• ECG def: irregularly irregular narrow complex tachycardia with no p waves

Causes: idiopathic, cardio (IHD, valvular disease, cardiomyopathy), resp (PE, pneumonia), hyperthyroidism, alcohol

Ix: ECG (absence of p-waves, irregularly irreg rhythm)

Mx:

• Haemodynamically unstable (≤90 BP, chest pain, acute HF) –> DC Cardioversion

OR

• Rate control –> B-blocker (bisoprolol) OR rate-limiting CCB (verapamil - asthma)

OR

• Rhythm control - ONLY if clear reversible cause
  
  • Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
    
    • NOTE: IV heparin started prior to cardioversion
  • Sx onset >48hrs –> anticoagulate for 3wks –> elective cardioversion (also anticoag for 4wks after)

AND

• Stroke risk - CHADS-Vasc Vs Orbit/HAS-BLED score –> DOAC (Apixaban)
  
  • If metallic heart valve –> warfarin INR 3-3.5
  • Otherwise DOAC
  • NOTE: if incidental non-symptomatic AF - normal rate, no other RFs, CHA2DS2-VASc 0 –> anticoagulation not recommended
  • CHF, HTN, Age ≥75rs (2), DM, Stroke (2), Vascular disease, Age 65-74, Sex - female
    
    • Score 1 - consider; ≥2 - DOAC/Warfarin needed
    • Lifetime risk = annual risk x estimated years of life left (up to 80 yrs e.g. if 60 then x annual risk by 20)

Question 33

Infective endocarditis - RFs? Ix? Dx criteria? Mx?

Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?

Answer 33

Def: infection of heart valves (typically mitral/aortic or tricuspid in IVDU)

RFs: bacteraemia (long-term lines, IVDU, dental work), abn valves (prosthetic, RHD), prev endocarditis, VSD, piercings

Presentation: low-grade fevers, night sweats

• Exam:
  
  • Splenomegaly
  • Splinter haemorrhages, osler’s nodes, Janeway lesions, petechiae, Roth spots (eyes)
  • Chronic = clubbing (rare, mostly acute now)

Ix:

• Urine dip - haematuria
• Serial BCs (x3 but start empirical abx), ESR
• Transoesophageal Echo (TOE - vegetations)

Dx: DUKE’S CRITERIA (2 major OR 1 major + 3 minor OR 5 minor):

• Major: +ve BC (typical organism), new regurg murmur/veg on echo
• Minor: RF, fever (>38), embolic (vascular) phenomena, immune phenomena, +ve BC (another organism)
• Mx: IV abx for 6wks – fluclox/vanc/gent

Acute in structurally normal heart – In IV drug user the first valve met is tricuspid valve, commonly S. aureus (also most common cause in prosthetic valve endocarditis)

Subacute in structurally abn heart – mitral & aortic valves more commonly affected as high pressure system, more likely damaged valves, commonly Strep Viridans (overall most common cause of endocarditis)

Question 34

3rd & 4th heart sounds - sounds & cause?

Answer 34

3rd = rapid ventricular filling = volume overload e.g. HF (reduced EF/systolic)

• KEN…TU.CKY (deee. de.de)

4th = atrial contraction against stiff ventricles = pressure overload e.g. longstanding AS & other causes of left ventricular hypertrophy (HTN heart disease, HOCM, HF with preserved EF/diastolic)

• TE.NE..SSEE (de.de.deee)

Question 36

2 days of chest pain following 4 days of generalised muscle aches

• Worse on inspiration & lying flat
• Low-grade fever
• Exam: pericardial rub

Causes? Dx? Ix? Mx?

Answer 36

Pericarditis

Causes:

• Viral (most common)
• MI (can be Dressler’s syndrome)
• TB (constrictive)
• Uraemia (CKD where urea high –> pericarditis) = indication for haemodialysis (HUMP)
• Hydralazine (AI pericarditis)
  
  • NOTE: also causes drug-induced lupus
• SLE, RF, radiation

Presentation:

• Pleuritic chest pain, worse lying flat
• Exam: pericardial rub - “creaking/scratching”
  
  • Tip - put on all-fours, put stethoscope on sternal edge, hold inspiration

Ix:

• ECG: ST elevation widespread
• Only slightly raised/normal troponin

Mx: colchicine (3 months) + NSAIDs (ibuprofen, max 2wks)

Question 37

Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?

Answer 37

VT or SVT w/ aberrancy

• SVT >200bpm, also often irregular
• VT more likely if LAD
• Acutely treat any broad complex tachy as VT until proven otherwise

Presentation: palpitations, light-headed, chest pain, syncope, seizure

• Tachycardia, LVF
• ACS most common cause
• NEVER IGNORE palpitations & light-headedness

Ix: ECG - regular broad complex tachycardia

• U&E (Mg, Ca, K), TFTs, Troponins

Mx:

• Unstable tachycardia (BP <90, chest pain, acute cardiac failure) = DC cardioversion
• Stable:
  
  • IV amiodarone, b-blocker –> prepare for DC cardioversion

Question 38

Bradycardia arrhythmia with a palpable pulse (peri-arrest) - Mx?

Answer 38

Innitial: A-E

• If unstable - 500mcg IV atropine (/5mins up to 3mg)
  
  • Also considered unstable if:
    
    • Recent asystole >3s/Mobitz T2 AV block/3rd degree heart block
  • Caution in acute MI, C/I if heart transplant
• If persistent –> transcutaneous pacing + analgesia/sedation (very painful)
  
  • If can’t be achieved properly –> IV isoprenaline/adrenaline (specialist help)
• Arrange transvenous pacing (temporary if recent asystole >3s/Mobitz T2 AV block/3rd degree heart block)

Question 39

Heart block causes? types? Ix? Mx? Complications?

Answer 39

Causes:

• MI/IHD (MOST COMMON)
• Inf (RHD, IE)
• Drugs (digoxin)
• Metabolic (hyperkalaemia)
• Infiltration of conducting system (e.g. sarcoidosis)
• Degeneration of conducting system

Types:

• First Degree AV block - fixed prolonged PR interval (> 0.2 s) - ASYMPTOMATIC
• Second degree AV block:
  
  • Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
    
    • Normally asymptomatic
  • Mobitz Type II - intermittently P wave NOT followed by a QRS
    
    • May be regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
    • Can cause:
      
      • Stokes-Adams Attacks (syncope caused by ventricular asystole)
      • Dizziness, palps, chest pain, HF
• Complete AV heart block - no relationship between P waves and QRS complexes
  
  • Presentation as in Mobitz T2

Ix: ECG

• Bloods: TFTs, Digoxin, cardiac enzymes (troponin, CK, BNP)
• CXR (cardiac enlargement, pulmonary oedema)
• Echo (wall motion abn, aortic valve disease, vegitations)

Mx:

• Acute block - if clinical deterioration:
  
  • IV atropine
  • Consider temporary transcutaneous pacing
• Chronic block:
  
  • 1st degree monitored
  • Permanent pacemaker in:
    
    • Symptomatic Mobitz T1
    • Advanced Mobitz T2
    • Complete heart block

Complications: asystole, cardiac arrest, HF, surgical complications of pacemaker insertion

Question 40

Types of pacemaker? When to use each type? Complications?

Answer 40

Types:

• Implantable Cardioverter Defibrillator (ICD, has a thicker end)
• Single-chamber pacemaker (right ventricle)
  
  • Used in permanent AF (no organised atrial contraction so atrial lead not required to sense contraction)
  • Rarely can have atrial lead only - if SA disease in young with good AV conduction
• Dual-chamber pacemaker (right atrium & ventricle)
  
  • Can have ICD dual-chamber pacemaker
  • Used in paroxysmal AF/all other scenarios (there is sometimes organised atrial contraction - this is sensed by the atrial lead)
• Cardiac Resynchronisation Therapy/Biventricular pacemaker (right ventricle, left ventricle ± right atrial lead)
  
  • Can have ICD biventricular pacemaker

When to use each type:

• Atrial lead only → Sino-atrial disease in young people with good AV node conduction
• RV lead only → Pacing whilst in permanent atrial fibrillation
• Dual-lead → All other scenarios (paroxysmal AF, bradycardia)
• CRT → LV dysfunction + broad QRS –> end-stage HF
• Indications for ICD:
  
  • Primary prevention = @risk of serious ventricular arrhythmia
    
    • Familial cardiac conditions (hypertrophic cardiomyopathy, long QT)
    • Previous surgical repair of congenital HD
    • Previous MI + LVEF <35% + HF Sx
  • Secondary prevention = had previous serious ventricular arrhythmia wo/ treatable cause
    
    • Cardiac arrest from VT/VT
    • Spontaneous sustained VT AND:
      
      • Syncope/haemodynamic compromise OR
      • LVEF <35% + sign HF Sx (NYHA 3+)
    • NOTE: VT/VF from STEMI has treatable cause (open occluded vessel)

Complications:

• Surgical complications - infection, bleeding, damage to underlying structures
• Displacement (of lead)
• Pacemaker syndrome (if ventricular lead with no atrial) –> AV node conducts in retrograde direction = mitral/tricuspid regurge + HF Sx

Question 42

How do you know this is the JVP and not the carotid pulse?

Answer 42

• Not palpable
• Double pulsation
• Obliterated when pressure applied at base of neck
• Rises with hepatojugular reflux
• Height changes with respiration

Question 43

Causes of hepatic decompensation in CLD? Key features of decompensation?

Dx & Mx of decompensated chronic liver disease?

Answer 43

Cause of hepatic decompensation in CLD:

• Hypokalaemia
• Constipation (given lactulose in hospital)
• Alcohol
• GI bleed (lots of protein (Hb) enters the bowel –>liver can’t cope)
• HCC

Decompensated CLD –> Ascites, jaundice & encephalopathy

• Severely scarred liver (cirrhosis) in CLD –> back pressure on portal vein –> PORTAL HTN = splenomegaly, ascites, varices - caput medusae, oesophageal & rectal

Ix:

• Serum Ascites Albumin Gradient (SAAG) - serum albumin conc vs ascites conc - 11.1g/L
  
  • <11.1g/L = exudative cause - peritonitis (infection), peritoneal malignancy OR n_ephrotic syndrome_ (pee out albumin so low serum albumin)
  • Otherwise = transudative cause - cirrhosis, renal failure, HF
• >250 neutrophils = spontaneous bacterial peritonitis (SBP) –> Tazocin/3rd gen cephalosporin
  
  • If protein conc <15g/L give prophylactic oral ciprofloxacin

Mx:

• Paracentesis (ascitic drain) –> post-paracentesis circulatory dysfunction (drops BP) SO if >5L drained give human albumin solution (HAS) 8g/L drained
• Spironolactone (2nd line - Furosemide) - to prevent fluid accumulation
• (Salt restrict)
• Hepatic encephalopathy (liver not dealing with toxins) - give Lactulose + Rifaximin to prevent
• Coagulopathy - OGD (check for varices) + vit K (needed for clotting)

Question 44

Chronic liver disease

• Functions of liver? Outcome of failure?
• Causes? Presentation? Ix?
• Important complication?
• Scoring?

Answer 44

Functions of the liver –> failure:

• Albumin (plasma oncotic pressure) –> oedema
• Bilirubin metabolism –> jaundice
• Clotting factors –> coagulopathy
• Detoxification –> encephalopathy

Causes:

• Common - alcoholic liver disease, viral hepatitis, NASH (non-alcoholic steatohepatitis)
• Less common - AI hepatitis, PSC/PBC, HF, alpha1-antitrypsin def, haemochromatosis, Wilson’s disease

Presentation:

• Spider naevi (≥5, SVC distribution, flush inside to out), palmar erythema, gynecomastia, Dupuytren’s contracture (alcoholic liver disease), clubbing
• Specific signs:
  
  • Needle marks/tattoos - hep C
  • Parotid swelling - alcohol-related liver disease
  • Bronzed complexion/insulin injection signs - haemochromatosis
  • Obesity/DM - non-alcoholic fatty liver disease
  • Xanthelasma - cholestatic disorder

Ix:

• Alcohol history
• Hep B/C serology
• Ferritin, transferrin, A1AT, ceruloplasmin (Wilson’s)
• Ig, auto-abs (ANA in AI hep, AMA in PBC)

Important complication = VARICES

• Normal venous return: GI tract –hepatic portal vein –> liver –> hepatic vein –> systemic circulation
• Physiological hepatosystemic anastomoses (connection of portal vein to systemic circulation) sites - oesophagus, spleen, umbilicus, rectum
  
  • MEMORY AID: BUTT, GUT, CAPUT
• Pathological process:
  
  • In the case of cirrhosis - nodules impede flow of blood through the liver to the hepatic vein –> reducing blood flow to the systemic circulation
  • Backflow of blood to the hepatic portal vein = increased –> backflow to hepatosystemic anastomoses:
    
    • Oesophagus –> Oesophageal varices
    • Spleen –> Splenomegaly
    • Umbilicus –> Caput Medusae
      
      • ​Only from portal HTN if running from below umbilicus up
    • Rectum –> Rectal varices

Score for prognosis & need for liver transplant = Child-pugh score (A = 5-6; B = 7-9; C = 10-15 –> C is most severe)

Question 45

Chronic diarrhoea - ddx? Sx? Distribution? Histology? Ix? Mx?

Answer 45

IBD

• Crohn’s disease
  
  • Sx: RIF pain (terminal ileum), failure to thrive (incl. between attacks)
  • Distribution: mouth to anus (esp. terminal ileum), skip lesions
  • Histology: transmural, non-caseating granuloma (also in sarcoidosis)
  • Ix:
    
    • OGD/colonoscopy/capsule endoscopy
    • Gastografin follow-through
  • Mx:
    
    • Induction:
      
      • Steroids (induce remission)
      • 5-ASA (mesalazine)
    • Maintenance:
      
      • Steroid-sparing agents (methotrexate, azathioprine, mercaptopurine)
      • Biologics e.g. Anti-TNF (infliximab)
  • Complications: strictures, obstruction, fistulae
• Ulcerative colitis
  
  • Sx: gen. abdo pain, PR blood & mucus
  • Distribution: ONLY rectum & colon, continuous
  • Histology: mucosa & submucosa, mucosal ulcers, crypt abscesses
  • Ix:
    
    • Flexible sigmoidoscopy/colonoscopy
  • Mx:
    
    • Induction:
      
      • 5-ASA
      • Steroids
    • Maintenance:
      
      • 5-ASA (mesalazine)
      • Steroid-sparing agents (azathioprine)
      • Biologics (infliximab)
    • Surgery (proctocolectomy, IJ pouch)
  • Complications: toxic megacolon, colonic carcinoma, PSC
• Extra-intestinal signs of IBD - A PIE SAC
  
  • Aphthous ulcers (crohn’s)
  • Pyoderma gangrenosum
  • Iritis, uveitis, episcleritis (Crohn’s)
  • Erythema nodosum
  • Sclerosing cholangitis (PSC in UC)
  • Arthritis
  • Clubbing fingers (CD > UC)
• Truelove & Witts’ severity index = severity criteria for IBD

Coeliac disease

• Def: inflammatory response to gluten (immune reaction to gliadin)
  
  • DQ2/8 (on HLA typing)
• Sx: abdo Sx (steatorrhoea, diarrhoea, bloating), failure to thrive
  
  • Exam: blistering rash on both knees. aphthous mouth ulcers
  • Assoc: T1DM
• Distribution: duodenum
• Histology: subtotal villous atrophy with crypt hyperplasia
• Ix: (maintain normal diet - eat gluten for 6wks before testing)
  
  • Haematinics - macrocytic anaemia, low Fe, B12/folate
  • Serological testing:
    
    • Screening: Anti-TTG & total IgA (check for selective IgA def in case this caused false ‘-ve’ anti-tTg abs)
    • If weakly +ve –> anti-endomysial abs (more sensitive & specific)
  • OGD & duodenal biopsy
    
    • Histology: sub-total villous atrophy with crypt hyperplasia
• Mx: gluten avoidance

Irritable bowel syndrome - Dx of exclusion

• Sx: bloating, related to stress, diarrhoea/constipation, relieved by defecation
  
  • “Pellet-like stools”
• Ix: faecal calprotectin (an inflammatory marker of GI tract = less likely to be IBS, more likely IBD)
• Mx: dietary changes, stress Mx, anti-spasmodics, probiotics, laxatives/loperamide, anti-depressants

Question 50

Mesenteric ischemia:

• What is the blood supply to the GI tract?
• What area of GI tract is vulnerable to ischaemia?
• Breakdown of mesenteric ischemia? Sx? Ix? Mx?

What is the difference between Mesenteric ischemia & ischemic colitis? Sx? Ix?

Answer 50

Blood supply

• Coeliac axis - oesophagus, stomach, start of small intestine
• Superior mesenteric artery (SMA) - most of the small intestines up to 2/3 transverse colon
• Inferior mesenteric artery (IMA) - from 2/3 along transverse colon down to rectym
• NOTE: area 2/3 along transverse colon @splenic flexure = WATERSHED ZONE (limited supply from superior & inferior mesenteric arteries) –> vulnerable to ischaemia!!

_​_Mesenteric ischemia

• Acute - occlusion of SMA by thrombus/embolus
  
  • Sx: severe abdo pain, normal abdo exam, shock
  • Ix:
    
    • AXR (gasless abdo)
    • VBG (lactic acidosis)
    • CT abdo with contrast (if suspect mesenteric ischaemia)/CT angiogram (if LA)
      
      • If not primary surgery –> followed by mesenteric angiography (Dx non-occlusive mesenteric ischaemia)
  • Mx: resus + CCOT + NBM
    
    • Empirical abx
    • Bypass ± bowel resection
    • Heparin post-op
• Chronic - narrowing of SMA by atherosclerosis (stable angina of bowel)
  
  • Sx: colicky post-prandial abdo pain (more work for bowel to do –> pain, just like in stable angina & exercise)
  • Ix: as above
  • Mx: medical optimisation + bypass (angioplasty + stent if not suitable for surgery)

Ischemic colitis

• Occlusion of inferior mesenteric artery (IMA) by thrombus/embolus
• Sx: abdo pain, PR bleeding
• Ix: sigmoidoscopy/colonoscopy
• Mx: seek GI & surgical input (can develop chr ulcerating IC)
  
  • Mild - conservative (IV abx, fluids, bowel rest, DM control)
    
    • Prophylactic LMWH
  • Segmental resection + stoma

Question 54

How do you tell between spleen & kidney on examination?

Answer 54

Spleen (vs kidney):

• Moves down with inspiration
• You can’t get above it
• Has a notch
• Dull to percussion & not ballotable

Question 56

Upper GI bleed - scoring for need for intervention? Mx?

Answer 56

Blatchford score

Variceal bleed

• Massive haemorrhage –> balloon tamponade
• A-E assessment –> IV fluids, blood transfusion
  
  • F1 Essentials:
    
    • 2x large bore cannula
    • VBG
    • G&S/X-match
    • Bleep the bleed reg
• Drugs with prognostic benefit:
  
  • IV Terlipressin (ADH analogue –> vasoconstriction)/Somatostatin (used for same reason)
  • Prophylactic abx - Ceftriaxone/Norfloxacin (abx)
• Intervention (discuss with on-call bleed registrar) –> endoscopic band ligation

Question 57

Peptic ulcer disease - RFs? Types? What artery is most likely to bleed in duodenal ulcer?

Presentation? Ix? Mx? Scoring to evaluate risk of re-bleed/death?

Answer 57

RFs:

• H. pylori exposure
• Aspirin/NSAID use

Types:

• Gastric - pain worsened by meal (pain 30m-1hr after meal), loose weight, vomiting, assoc w/ NSAIDs
• Duodenal - MORE COMMON, pain relieved by meal (pain 2-3hrs after meal), assoc w/ H. pylori, worse by stress/at night –> radiates to back, put weight on, malaena
  
  • Gastroduodenal artery - runs posterior to 1st/2nd parts of duodenum –> likely cause of bleeding in PUD

Presentation:

• Chr/recurrent upper abdo pain - related to eating & nocturnal
  
  • Can be severe/radiate to back in Duodenal ulcers if ulcers penetrates pancreas
• Pointing sign on exam - show where pain is with 1-finger
• NOTE: ‘Coffee grounds’ vomiting = upper GI bleed (mostly due to PUD > gastric erosions)

Ix:

• OGD endoscopy = gold-standard
  
  • Immediately if dyspepsia + upper GI bleed
  • Within 2wks if ≥55yrs + weight loss + dyspepsia/reflux/upper abdo pain –> exclude malignancy
  • Repeat within 6-8wks to ensure ulcer healing/rule out malignancy
• H. pylori stool antigen/breath test (2wk wash out period after PPI or 4wks after abx, retest 6-8wks after starting Tx)
• Bloods - FBC

Mx: consider STOPPING NSAIDs

• Active bleed:
  
  • Urgent evaluation (A-E + Blatchford score) + blood transfusion
  • OGD endoscopy (Dx & Tx) –> high-dose IV PPI afterwards (continue oral PPI for 6wks)
  • Rockall score (for risk of rebleed/death) –> if re-bleed –> repeat endoscopy & Tx endoscopically/emergency surgery
• If H. pylori +ve:
  
  • H. pylori eradication - triple therapy for 7 days (PPI + 2 abx = Amox + clari/metro) –> retest 6-8wks after starting Tx (leave washout 2wks after PPI, 4wks after abx)
    
    • If pen allergic –> PPI + Clari + Metro
  • If long-term NSAID/aspirin use:
    
    • Consider stopping NSAIDs/aspirin
    • Ulcer healing Tx - full-dose PPI/H2 antagonist for 8wks –> H. pylori eradication afterwards
• If H. pylori -ve: treat underlying cause + PPI (4-8wks, 2nd line = H2 antagonist)
• If recurrent/refractory ulcers –> long-term PPI/H2 antagonist

Question 58

• Joint pain in both knees, XR shows chondrocalcinosis
• Wakes at night frequently to urinate, PMHx T2DM, low albumen on blood

Dx? Classification? Presentation? Ix? Mx?

Answer 58

Dx: haemochromatosis

• Risk of HCC (hepatocellular carcinoma)

Classification:

• Hereditary - AR, gene on chr6 (carried by 1:10 Europeans)
• Secondary e.g. from frequent blood transfusions (SCD)

Presentation - from Fe-deposition in various tissues:

• Arthritis (esp hands), bronze DM (tan), cirrhosis
  
  • Hypogonadism (accumulates in testis)
  • Dilated cardiomyopathy (accumulates in heart)
• XR - chondrocalcinosis is assoc w/ pseudogout & haemochromatosis

Ix:

• Blood iron profile:
  
  • TF saturation high (>55% men, >50% women)
  • Ferritin normal/slightly high (>500)
  • Low TIBC (as all transferrin saturated)

Mx:

• Venesection (until transferrin saturation normal)
• Desferrioxamine (iron chelator to prevent recurring)
• Monitoring ; TF saturation <50% & serum ferritin <50ug/l

Question 59

Case:

• 57yrs, burning pain after eating & lying flat, improved with cold drinks, high BMI, smokes, drinks alcohol, occasional bitter taste in back of the mouth
• Difficulty swallowing in recent months

Dx? Presentation? Ix? Mx? Complication?

Answer 59

Dx: GORD

• Decreased lower oesophageal sphincter (LOS) pressure:
  
  • Drugs - nitrates, CCBs (smooth muscle relaxation)
  • Alcohol, smoking
  • Hiatus hernia

Presentation: RFs (above), heartburn (worse lying down/at night), reflux incl bitter taste in mouth (after meals)

Ix:

• 8wk PPI trial
• If dyspepsia consider OGD for: anaemia, weight loss, dysphagia, >55yrs
• Oesophageal pH study (<4 for >4% of time = GORD)

Mx:

• Conservative: weight loss, smoking cessation, head of bed elevation/avoid eating late at night, reduce alcohol
• Medical:
  
  • Standard-dose PPI (20mg omeprazole) - continued long-term (if Sx continue after stopping/erosive oesophagitis/Barrett’s oesophagus)
  • H2 antagonist (e.g. cimetidine)
• Surgery (only if PPIs work but don’t want long-term medical Tx) e.g. laparoscopic fundoplication

Complication: Barrett’s oesophagus –> oesophageal adenocarcinoma

Question 60

Anal fissure - def? RFs? Presentation? Ix? Mx?

Answer 60

Def: tears of the squamous lining of the distal anal canal

• <6 weeks = acute, ≥6wks = chronic
• 90% @posterior midline

RFs: constipation, IBD, STIs (HIV, syphilis, herpes)

Presentation: painful, bright red, rectal bleeding

Ix: PR exam

Mx:

• Acute <1wk:
  
  • Soften stool - high-fibre diet + high fluid intake, fybogel (2nd - lactulose)
  • Lubricants (for passing stool), topical anaesthetic, analgesia
• Chronic: maintain above + topical GTN
  
  • After 8wks (if above not effective) –> GI referral for sphincterotomy (or botulinum toxin)

Question 62

Haemorrhoids - presentation, grading, Ix, Mx?

Answer 62

Presentation: rectal bleeding & perianal pain

Grading:

• 1 - prominent BVs (no prolapse)
• 2 - prolapse on bearing down + spontaneous reduction
• 3 - manual reduction
• 4 - can’t be manually reduced

Ix:

• Bedside: Anoscopic exam, stool (occult haem)
• Bloods: FBC
• Imaging: Colonoscopy/flex sigmoidoscopy

Mx:

• Conservative - fibre, fluids
• Medical = G1 - topical CS
• Surgical:
  
  • G2/3: band ligation
  • G4: surgical haemorrhoidectomy

Question 63

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?

Answer 63

Presentation: polyuria, polydipsia, dehydration

• Ketosis - malaise, vomiting
• FHx, other endo disorders
• If known DM:
  
  • Previous DM control (hyp/hyper)
  • Micro/macrovascular complications
  • Diabetic eye disease (Dx & Tx)

RFs: overweight, FHx (DM), PMHx (GDM), PCOS, HTN, dyslipidemia, CVD

Criteria for Dx (repeat test needed for Dx):

• Fasting plasma glucose of ≥7.0 (normal ≤6)
• OGTT (BM 2hours after 75g glucose-load)/ Sx + random plasma glucose of ≥11.1mmol/l (normal <7.8)
• HbA1c ≥48mmol/mol (≥6.5%) - not for young/T1DM, acutely ill, haem disease, preg, iatrogenic

T1DM Mx: exogenous insulin to avoid DKA & long-term complications

• Diet - lower fat, higher carbs = counting carbs (adjust insulin around diet rather than limiting eating)
• Diabetic specialist nurse - EDUCATE:
  
  • Self-adjust dose - DAFNE course for T1DM (D for DM)
  • Fingerprick glucose
  • Calorie intake & carb counting
  • Phone support
• Don’t stop insulin during acute illness, maintain calorie intake
• Insulin regimens:
  
  • 1st line - Basal-bolus regimen
    
    • Basal (background) - BD insulin detemir (or Levemir/Lantus/Tresiba) as basal insulin
    • Bolus (before meals) - analogue rapid-acting insulin e.g. insulin Lispro (Humalog)/Aspart (Novorapid)/Neutral (Actrapid)
  • Other:
    
    • BD biphasic (premixed insulin, hypos common) e.g. Novomix, Humulin M3, Humalog Mix
    • OD before bed long-acting (for T2DM)
    • NOTE: intermediate-acting insulin e.g. Humulin I, Insulatard

T2DM Mx:

• 1st line - Lifestyle changes - DESMOND course for T2DM (D for DM), dietician input, self-BM monitoring (individual HbA1c target <6.5)
  
  • HbA1c targets:
    
    • No hypoglycaemics - 48mmol/mol
    • Hypoglycaemics - 53mmol/mol
    • Escalate Tx - 58mmol/mol
• Medication:
  
  • 2nd - Metformin (SEs: diarrhoea, LA - avoid if eGFR <30)
  • 3rd - ADD Sulphonylurea e.g. Gliclazide (SEs: hypoglycaemia, weight gain)
  • 4th - ADD other DM med:
    
    • Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
      
      • C/I in HF, bladder cancer
    • SGLT-2 inhibitor e.g. Empagliflozin (SEs: Hypoglycaemia, weight loss, UTI)
      
      • Not recommended in impaired renal funct
    • DPP-4 inhibitor e.g. Linagliptin (APPROVED FOR USE IN CKD, weight neutral)
    • GLP-1 analogues e.g. Exenatide/Liraglutide (SE: weight loss - useful if BMI >35; vomiting)
      
      • Not recommended in impaired renal funct
  • 5th - If on triple therapy & not providing control –> commence insulin
• CVD risk Mx - anti-HTN, anti-lipid, QRISK-3 score
• Diabetic nephropathy Mx:
  
  • Monitor albumin-creatinine ratio (ACR)
  • Consider ACEi/ARB early
• Diabetic neuropathy Mx:
  
  • Annual Sx review (erectile dysfunction, autonomic neuropathy - orthostatic hypotension, gastroparesis, bladder emptying difficulties)
  • Annual foot screen + specialist foot Mx, monitor for diabetic foot/ulcers ± amputation
• Diabetic retinopathy: retinal screen annually (age ≥12yrs)
  
  • Background: need to tighten control
    
    • Venodilation, microaneurysms (dots), hard exudates (lipid deposits)
    • Tx: tighten glycaemic control, refer if near macula
  • Pre-proliferative (mild) - soft exudates (cotton wool spots e.g. infarcts)
  • Proliferative - neovascularization (+ floaters, reduced acuity)
    
    • Tx: pan-retinal photocoagulation
  • Diabetic maculopathy - hard exudates, oedema (+ blurred vision, reduced acuity)
    
    • Tx: intravitreal triamcinolone acetonide decreases macula oedema
  • NOTE: Pre-diabetic –> refer to diabetes prevention programme (DPP)

Diabetes complications:

• Microvascular:
  
  • Eye - diabetic retinopathy (± cataracts, glaucoma)
  • Kidney - diabetic nephropathy
  • Neuropathy - damage to PNS –> diabetic neuropathy (peripheral neuropathy - glove & stockings distribution) –> diabetic ulcers/gangrene
• Macrovascular:
  
  • Brain - stroke/TIA/cog impairment
  • Heart - coronary heart disease
  • Extremities - PVD, diabetic ulcers/gangrene

Question 65

Hyperosmolar Hyperglycaemic State

• What does insulin do? Pathophysiology of HHS?
• HHS criteria? HHS Mx? HHS Mx Targets?

Answer 65

Insulin:

• High level of insulin –> reduces serum BM (pushes into surrounding tissues & hepatic glucose store)
• Low level of insulin –> switches off ketone production

Pathophysiology:

• HHS = complication of T2DM
• In HHS have enough insulin to switch of ketone production but not enough to reduce BM lvls
• High glucose - osmotically active –> polyuria –> dehydration

HHS criteria:

• Hypovolaemia
• Glucose >30mmol/L
• NO ketonaemia
• Serum osmolality >320mOsmol/kg

Mx: REHYDRATE = IV 0.9% NaCl (3-6L by 12hrs, deficit 110-220mL/kg)

• Targets:
  
  • Reduce Na by less than 10mmol/L/day (otherwise risk osmotic demyelination syndrome)
  • Reduce BM by over 5mmol/L/hr
  • NOTE: if targets not met by 0.9% saline –> 0.45% instead
• If fluid alone are not enough –> 0.05 units/kg/hr fixed-rate insulin infusion

Question 66

Diabetes insipidus - Sx? Types? Ix? Tx?

Answer 66

Sx: hypernatremia (lethargy, thirst, irritable, confusion, coma, fits), polyuria, urine plasma osmolality <2 (very dilute)

Types:

• Central (lack of ADH prod in hypothalamus) – pituitary surgery, irradiation, trauma, infarction
• Nephrogenic (resistance to ADH effects) – hypercalcaemia, hypokalaemia, meds (lithium)

Ix: rule out DDx (BM, review drugs, K/Ca lvls)

• U&E, Ca, BM, serum & urine osmolarities
• Dx: 2-step fluid deprivation test = give desmopressin (DDAVP):
  
  • Normal/primary polydipsia –> urine concentrates on fluid deprivation (>600)
  • Cranial DI - giving desmopressin allows ADH prod –> urine conc
  • Nephrogenic DI: urine never concentrates
  • NOTE: DI excluded if urine to plasma (U: P) osmolarity ratio >2:1
• Cranial MRI - if suspect cranial DI

NOTE: Fluid deprivation test process:

• Baseline urine osmolality
• Fluid deprivation for 8hrs, take urine osmolality
• Give desmopressin, wait 8hrs, take urine osmolality

Tx:

• Nephrogenic DI –> fluids (+ monitor UO) + thiazide diuretics (hydrochlorothiazide - weird/does not make sense)
• Central DI –> fluids + desmopressin

Question 67

Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?

Answer 67

Hypothyroidism:

• Causes:
  
  • Primary:
    
    • Hashimoto’s thyroiditis - most common hypothyroidism
      
      • Goitre, AI disease (vitiligo, pernicious anaemia, T1DM, Addison’s)
      • Elderly females
      • May be initial ‘Hashitoxicosis’
      • +++ Autoantibody titres
        
        • Antithyroid peroxidase (TPO) & antithyroglobulin (TG)
    • Atrophic AI thyroiditis
      
      • No goitre, anti-TPO/TSH
    • Iodine def, meds (carbimazole, lithium), thyroid surgery
  • Secondary: pituitary gland fails to produce TSH
    
    • Tumour, vascular (Sheehan syndrome), radiation, inf
• Ix:
  
  • Bedside: ECG (pericardial effusion, ischaemia)
  • Bloods: FBC, U&E, TFTs, Lipids, Prolactin, Anti-TPO/TG
  • Imaging: CXR (effusions, HF)
• Mx: thyroid replacement therapy (levothyroxine)
  
  • Monitor with serum TSH, careful with dose in elderly (prone to IHD)
  • Myxoedema coma - A-E & active warming, T3 slow IV, hydrocortisone IV
• Associated complications:
  
  • Cardiac - HF
  • Serous effusions (pleural, peritoneal, pericardial, joint)
  • Neuro - carpal tunnel, proximal myopathy, cerebellar dysfunction, myxedema coma
  • Systemic - dyslipidemia, anaemia

Hyperthyroidism:

• Presentation:
  
  • Weight loss, increased appetite
  • Heat intolerance, tremor, sweating, palpitations
  • Mood (anxious, irritable)
  • Bowel habit (diarrhoea), menses (oligomenorrhoea)
  • Goitre
  • Eye Sx (watering, gritty, red)
  • Other AI disease (vitiligo)
  • Signs:
    
    • Lid lag (eyes)
    • Palmar erythema
    • Brisk reflexes
    • Sinus tachy/AF
• Ix: TSH low, T3/4 high, TPO (may be raised), anti-TSHr ab (in Graves), technetium 99m uptake scan (diffuse/reduced)
• Causes:
  
  • High-uptake:
    
    • Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
      
      • Eye signs: proptosis –> exophthalmos, diplopia, visual loss
      • Peripheral signs: pretibial myxoedema, thyroid acropatchy, onycholysis, bruit over thyroid
    • Toxic multinodular goitre aka Plummer’s disease: hot nodules, painless
    • Toxic adenoma: 5%, single ‘hot nodule’ on isotope scan (1 area of uptake)
  • Low-uptake:
    
    • Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
      
      • Tx: NSAIDs
    • Postpartum thyroiditis (like De Quervain’s but postpartum)
• Mx:
  
  • Conservative: lifestyle changes, corneal lubricants
  • Medical:
    
    • Sx relief – B-blockers
    • Antithyroid meds - Carbimazole (or propylthiouracil)
      
      • SEs: rashes, agranulocytosis - monitor​
    • Radioiodine:
      
      • acts slowly, effective, best Tx for toxic multinodular goitre
      • Risk of permanent hypothyroidism (10%)
      • CI in preg/lactating women
  • Surgical: subtotal thyroidectomy (in large goitre/relapse)
  • Monitoring with TFTs annually
  • Thyroid storm: acute state of shock, pyrexia, confusion, vomiting
    
    • HDU/ITU support
    • Propylthiouracil 600mg –> 200mg QDS
    • Stable iodine (Lugol’s iodine) ≥1hr later
    • Propranolol, dexamethasone & IV fluids

Question 68

Adrenal anatomy? Adrenal disease breakdown? Causes? Presentations? Ix? Mx?

Answer 68

Adrenal anatomy (outside –> in):

• Zona glomerulosa –> mineralocorticoids e.g. aldosterone
• Zona fasciculata –> glucocorticoids e.g. cortisol
• Zona reticularis –> androgens e.g. testosterone
• Adrenal medulla (centre) –> catecholamines e.g. NA/adrenaline

Cushing’s #HighCortisol

• Causes:
  
  • ACTH-dependent:
    
    • Pituitary tumour (85%) = “Cushing’s disease”
    • Ectopic ACTH-prod tumour (5%) - SCLC/carcinoid tumour
  • ACTH-independent:
    
    • Adrenal tumour (10%)
    • Iatrogenic steroid use
• Presentation:
  
  • Thin skin, easy bruising, proximal myopathy, obesity (moon face, buffalo hump), other (hirsutism, acne)
  • Exam: vertical abdo striae
  • HTN, DM, osteoporosis (back/bone pain)
• Ix:
  
  • Exclude pseudo-Cushing’s - depression, alcohol excess, chr inf (no muscle weakness)
  • Confirm Dx: low-dose dex suppression test - fail to suppress cortisol in all
    
    • Overnight dexamethasone suppression test (1g @11pm) OR
    • 48hr low-dose 0.5mg/6h PO dexamethasone supression test OR
    • 24-hr urinary free cortisol (test x3 as low sensitivity)
  • Plasma ACTH measured:
    
    • High - CRH test identifies if pituitary or ectopic
      
      • Could also do bilateral inferior petrosal sinus sampling –> if no mass –> CT contrast CAP for ectopic
    • Low - adrenal tumour –> CT/MRI adrenal glands –> if nothing –> adrenal vein sampling
• Mx: treat underlying disease e.g. withhold steroids or surgical removal of the lesion
  
  • Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
    
    • 2nd - pituitary radiotherapy (also used if still high cortisol post-surgery) –> progressive anterior pituitary failure
    • Metyrapone & ketoconazole - sometimes before/after surgery
    • 3rd - laparoscopic bilateral adrenalectomy in refractory (but require lifelong glucocorticoid/mineralocorticoid replacement + risk of Nelson’s syndrome (increased skin pigment from high ACTH

Hypoadrenalism

• Causes:
  
  • AI: Addison’s disease (>70%)
  • Malig: mets (lung, breast. kidney)
  • Inf: TB (>10%), HIV (CMV adrenalitis), Fungal
  • Infiltration: granulomatous disease, hemochromatosis, amyloidosis
  • Iatrogenic: ketoconazole, rifampicin, phenytoin, bilateral adrenalectomy
  • Congenital: congenital adrenal hyperplasia (late-onset)
• Presentation:
  
  • Anorexia/weight loss, fatigue/weakness, postural dizziness, reduced libido, sweating
  • N&V, diarrhoea, salt craving
  • Signs: hyperpigmentation in skin creases/lip/mouth, vitiligo, sparse axillary/pubic hair
• Ix:
  
  • Bedside - postural hypotension, IGRA (TB inf)
  • Bloods - FBC, U&E (↑ K⁺, ↓ Na⁺), low glucose, serum Ca, AI/auto-ab screen, plasma renin & aldosterone, short snACTHen 250mcg IM test (not Addison’s if 30min cortisol rises >550nmol/L
  • Imaging: CXR (past TB), adrenal CT (for TB/mets)
• Mx:
  
  • Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
    
    • Ppt factors: inf, trauma, surgery, missed steroid doses
    • Ix: Cortisol, ACTH, U&E
    • Mx: IV hydrocortisone + IV fluids ± fludrocortisone (if primary adrenal lesion)
      
      • Monitor BM ± IV dextrose
      • Bloods, urine, sputum culture ± abx
  • Chronic: hydrocortisone + fludrocortisone (Na homeostasis), education (compliance, increase steroid dose if ppt factors, follow-up

Hyperaldosteronism (incl. Conn’s)

• Primary (HTN, ↑ Na+ ↓ K+):
  
  • ​Conn’s - aldosterone-secreting adrenal adenoma
  • Bilateral adrenal hyperplasia
• Secondary - decreased renal perfusion (high renin –> Na reabsorption –> HTN) - RAS, HF, liver failure
• Ix: aldosterone-renin ratio (ARR), CT/MRI adrenals, adrenal vein sampling
  
  • Conn’s is very high (high aldosterone, low renin) VS BAH has both high (high aldosterone, high renin)
• Mx: spironolactone, unilateral adrenalectomy (for Conn’s)

PHaeochromocytoma #HighCatecholamines

• Cause: adrenal medulla tumour –>↑ catecholamines (adrenaline/NA)
• Presentation: episodic headache, sweating, tachycardia, hypertension, arrhythmias, death if untreated
• 10% exta-adrenal, 10% bilateral, 10% malignant
• Ix: ECG (LVF, increased ST seg, VT), 24hr urinary metanephrines, abdo CT/MRI
• Mx: specialist endo centre - alpha blockade = PHenoxybenzamine then beta-blockade –> then surgery when BP controlled (after 4-6wks)

Question 71

DDx for tiredness & lethargy? Ix?

Answer 71

DDx:

• Anaemia - PUD, altered bowel habit? occult blood loss?
• Thyroid disease - thyroiditis?
• DM - polyuria, polydipsia, weight loss
• Adrenal insufficiency
• Primary hyperparathyroidism - constipation, urinary stones, abdo pain, depression
• Hypopituitarism
• Anxiety & depression - sleep disturbances, poor appetite, recent stress

Ix:

• FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics, BM, serology (anti-TSH/TPO), 9am cortisol lvls
• CXR

Question 74

Diabetic Ketoacidosis (DKA)

• Normal glucose transport & during starvation?
• The problem in insulin deficiency (diabetes)? How does this relate to Sx of DKA?
• Ix? Dx criteria? Mx? Monitoring Tx & hourly targets?

Answer 74

Normal glucose transport: diet –> blood –insulin–> hepatic glucose store –GH, Cortisol, Adrenaline, Glucagon–> blood

• During starvating - GH, Cortisol, Adrenaline, Glucagon make sure there is enough glucose in the blood BUT liver also produces ketones
• Ketones can cross BBB providing an alternative source of fuel for the brain when low glucose
• Pancreatic beta cells –> insulin prod –> reduces glucose (high glucose has–> feedback on pancreatic beta cells –> produce more insulin)
• High insulin (associated with high glucose) –> -ve feedback on ketone prod

In insulin deficiency - high glucose but unable to produce insulin + no -ve feedback on ketone prod –> high glucose, high ketones

• High glucose - osmotically active (moves along concentration gradient into urine –> pulling more water with it) –> POLYURIA –> DEHYDRATION
• High ketones - acidic (metabolic acidosis) –> enzyme dysfunction –> COMA & DEATH

DKA Ix:

• Bedside - urine dip, ECG, continuous cardiac monitoring
• Bloods - VBG, FBC, U&E, BC, BM
• Imaging - possibly CXR

DKA Dx:

• BM: ≥11mmol/L
• Ketones: ≥3mmol/L (serum) OR ≥2+ (urine)
• Acidaemia: pH <7.3 OR Bicarb <15mmol (ketoacidosis)

DKA Mx: A-E assessment

• IV FLUIDS (rehydrate)
  
  • ​Bolus –> 1L over 1hr –> 2hr –> 3hr –> 4hr
  • Add 40mmol KCL to fluids after bolus
• 0.1 U/kg/hr fixed-rate INSULIN infusion (reduce ketones)
  
  • If BM <14 –> start 125ml/hr 10% dextrose
  • Insulin infusion continues until ketones normalise (not BM) ​
• NOTE: follow local trust guidelines for DKA Tx as varies slightly between trusts

Monitor - BM, ketones, VBG (K conc)

• Hourly targets:
  
  • Fall in BM ≥3
  • Fall in ketones ≥0.5
  • Rise in HCO3 ≥3
• Continue until: blood ketones <0.6, pH >7.3, HCO3 >18

Question 75

Acromegaly cause? presentation? Ix? Mx? Complications?

Answer 75

Cause: macroadenoma in anterior pituitary

Presentation: coarse facial features

• Skin (acanthosis nigricans - thick & dark in creases), sweating, carpal tunnel syndrome (bilateral)
• Arthropathy, sleep apnoea, reduced sexual functioning, visual field defects (bitemporal hemianopia)
• Assoc: DM, HTN, MEN type 1 (15%)

Ix:

• Bedside: CN VI palsy, urine dip (glucose), ECG (cardiomyopathy)
• Bloods: elevated IGF-1, GH lvl during OGTT (not suppressed in acromegaly)
• Imaging: MRI brain (macroadenoma), sleep studies, colonoscopy (screening), visual field testing (driving)

Mx:

• Transsphenoidal hypophysectomy (curative)
• Medical: somatostatin analogue (octreotide)
• External pituitary radiotherapy (long-term 5-10yrs)

Complications:

• General: HTN, DM, carpal tunnel syndrome, sleep apnoea, colorectal cancer, LVH/cardiomyopathy/IHD
• Anterior pituitary hypofunction: hypogonadism
• Local compressive: bitemporal hemianopia

Question 81

Hyperprolactinaemia - causes? presentation? Ix? Mx

Answer 81

Causes:

• Prolactinoma (macroprolactinoma >6000)
• Adenoma (non-funct pituitary adenoma 1000-5000, from compression & DA lvls)
• DA antagonist (metoclopramide, anti-psychotics, methyldopa)
• Hypothyroidism (increased TRH stimulates prolactin prod)
• Physiological (pregnancy, breastfeeding)

Presentation: irreg periods, decreased libido, galactorrhoea

• Bilateral hemianopia

Ix:

• Bedside - pregnancy test, visual fields assessment
• Bloods - serum prolactin, TFTs, U&E
• Imaging - pituitary MRI

Mx:

• Asymptomatic pre-menopausal/post-menopausal with microadenoma - observation
• Symptomatic pre-menopausal/macroadenoma post-menopausal/male:
  
  • Dopamine agonist (Cabergoline/Bromocriptine), 2nd line - COCP (not if want pregnancy)
  • Trans-sphenoidal surgery (if visual Sx/pressure effects refractory to medical Tx)
  • Follow-up: monitor prolactin, check visual fields

Question 83

DDx for weight loss?

Answer 83

DDx:

• Thyrotoxicosis - heat intolerance, palpitations, SoB, mood (irritable/anxious), bowel habit, menses, goitre, exophthalmos, recent pregnancy
• GI-related conditions (IBD, upper GI pathology, coeliac disease, chr pancreatitis) - dysphagia, vomiting, regurgitation, abdo pain, altered bowel habit
• Eating disorders (Anorexia nervosa) - reduced eating, compulsive exercise
• Systemic conditions (malignancy) - FLAWS

Ix:

• FBC, U&E, CRP, LFTs, fasting BM, bone profile, TFTs, anti-TTG, IgA levels, haematinics
• CXR

Question 84

Compartment syndrome Key Signs & Sx? RFs? Ix? Mx?

Answer 84

Classic = 6Ps: pain, pallor, perishingly cold, pulseless, paraesthesia, paralysis (BUT these tend to be more associated with PVD than compartment syndrome)

Typical presentation: tightness in compartment + acute disproportionate pain (worse on stretching) after trauma:

• Acute is following fracture, soft tissue/reperfusion/thermal injury
• Chronic (pain on exercise) often in long-distance runners
• Other early sign = paraesthesia
• Late signs: pallor, pulseless, paralysis

RFs: Trauma, bleeding disorder (haemophilia), compartment support (tight cast/wrappings), burns, intense muscular activity (long distance runner)

Ix:

• Compartment differential pressure measurement - within 20-30mmHg = fasciotomy needed
• +/- serum CK, urine myoglobin (rhabdomyolysis)

Acute Mx: dressing release + morphine

• 2nd line = complete fasciotomy (open all 4 compartments of lower leg)
• 3rd line = amputation
• If rhabdomyolysis —> hydration +/- Na bicarbonate (urine alkalisation) +/- haemodialysis (metabolic acidosis)

Chronic Mx: limit exercise + NSAIDs

• 2nd line = fasciotomy

Question 85

Extra-articular manifestations of RA –> what would you also examine after hands?

Answer 85

NO HIVE:

• Nodules - rheumatoid nodules (25%)
• Osteoporosis (worse by steroids & immobilisation)
• Heart & haem - pericarditis, anaemia, Felty’s syndrome (RA + splenomegaly + neutropenia)
• Interstitial - pul fibrosis (& pleural effusions, Caplan’s syndrome - nodules from RA + pneumoconiosis), interstitial nephritis (nephrotic syndrome)
• Vasculitis (high titre RF)
  
  • Peripheral neuropathy presenting as mono-neuritis multiplex
    
    • Other neuro: carpal tunnel, cervical myelopathy
  • Splinter haemorrhages, cutaneous ulcers, distal gangrene
• Eye pathologies - secondary sjogren’s syndrome (dry eyes, mouth & cough), episcleritis

Question 86

RA - Def? Presentation? Ix? Findings on X-ray? Mx?

Answer 86

Def: AI process causing synovial joint inflammation (synovitis) with destruction of peri-articular structures

• Genetics: HLA DR1/4

Presentation: joint pain @rest, swelling & stiffness in morning

• Exam:
  
  • Symmetrical swelling w/ DIP sparing
  • Muscle wasting, ulnar deviation, volar subluxation @MCPs
  • Swan-neck & Boutonnieres’ & Z-thumb deformities
  • NOTE: if nail changes/extensor rash = psoriatic arthritis
• Extra-articular manifestations of RA = NO HIVE:
  
  • Nodules - rheumatoid nodules (25%)
  • Osteoporosis (worse by steroids & immobilisation)
  • Heart & Haem - pericarditis, anaemia, Felty’s syndrome (RA + splenomegaly + neutropenia)
  • Interstitial:
    
    • Pul fibrosis (& pleural effusions, Caplan’s syndrome - nodules from RA + pneumoconiosis)
    • Interstitial nephritis (nephrotic syndrome)
  • Vasculitis (high titre RF)
    
    • Peripheral neuropathy presenting as mono-neuritis multiplex
    • Other neuro: carpal tunnel, cervical myelopathy
    • Splinter haemorrhages, cutaneous ulcers, distal gangrene
  • Eye pathologies - secondary sjogren’s syndrome (dry eyes, mouth & cough), episcleritis

Ix: anti-RF/CCP, ESR/CRP, X-rays

• Findings on X-ray = LESS
  
  • Loss of joint space
  • Erosions
  • Soft tissue swelling
  • Soft bones (periarticular osteopenia)

Mx: MDT - physio & OT

• Create an end target e.g., remission
• NSAIDs for Sx relief
• Bridging pred until Sx resolved
• 1st - Monotherapy with conventional DMARD (methotrexate/sulfasalazine)
• Target met?
  
  • Yes = keep drug regime + lifestyle changes (stay active, healthy diet, weight loss if appropriate, alcohol/smoking)
  • No = titrate cDMARD/trial alternative cDMARD ± dual therapy
• Target met?
  
  • Yes = keep drug regime + lifestyle changes
  • No = biological agents if DAS28 score >5.1 (severe burden of disease)

Question 87

Osteoarthritis - presentation? Ix? Mx?

Answer 87

Pathogenesis - loss of cartilage + bone remodelling –> inflammation & osteophytes

Presentation: pain worse with activity, crepitus + reduced RoM

• Hands - DIP & PIP swelling = Heberden’s (DIP) & Bouchard’s nodules (PIP)
  
  • Common site = base of the thumb (1st carpometacarpal joint)
• Weight-bearing joints affected e.g. knees
• NOTE: midline knee scar = total knee replacement –> fixed flexion deformity post-replacement

Ix: XR (2 views e.g. AP & lateral)

• LOSS: Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts

Mx:

• Conservative – physio, exercise, weight loss
• Medical:
  
  • Analgesia (paracetamol –> topical NSAID –> oral NSAID/opioid)
  • IA CS injection
• Surgical – arthroplasty (e.g. TJR)

Question 88

Psoriatic arthritis - Signs? Types? Criteria name? Mx?

Answer 88

Signs:

• Extensor plaques with scales (scalp + behind ears)
• Nails - pitting, hyperkeratosis, onycholysis
• Other forms: guttate (drop-like), Koebner phenomenon

Types:

• Mono/oligoarthritis
• Spondylitis (back)
• Asymmetrical polyarthritis (incl DIP-specific)
• Arthritis mutilans
• Rheumatoid-like

Criteria name: CASPAR criteria - established inflame arthritis/enthesitis + ≥3 of options

Mx:

• Conservative:
  
  • Psoriasis - precipitant avoidance (alcohol, smoking, stress, B-blockers)
  • Exercise & physio for arthritis
• Medical:
  
  • Psoriasis:
    
    • Topical Tx:
      
      • Topical steroids (hydrocortisone 2.5%/betamethasone 0.05%)
      • Calcipotriol
    • PUVA = Psoralen + UVA phototherapy
• Arthritis = Methotrexate, anti-TNFs

Question 89

Septic arthritis - presentation? Mx?

Answer 89

Presentation - hot swollen joint with reduced range of motion

Mx: needle aspiration before abx –> fluids for 3Cs & G (cells, culture, crystals, gram stain) –> empirical IV abx (based on aspiration)

• S. aureus is most common
• NOTE: if prosthetic joint - biofilm can be created - early (<3m post-surgery)/delayed (>3m) –> more complicated, coag neg staph more common

Question 90

Ankle fracture rules? Classification? Ix? Mx?

Answer 90

Rules = Ottawa rules - for what ankle fractures qualify for an X-ray

• Ankle XR:
  
  • Pain over malleolar zone
  • Tenderness along distal 6cm of the posterior edge of tibia/fibula
  • Inability to weight bear
• Foot XR:
  
  • Pain over midfoot zone
  • Tenderness at base of 5th metatarsal/navicular bone
  • Inability to weight bear

Classification = Weber classification - location of the fibula fracture in relation to the Syndesmosis (Distal Tibiofibula Syndesmosis - ligament between tibia & fibula)

• Normal
• A - fracture distal to the syndesmosis
• B - fracture @level of the syndesmosis
• C - Fracture above the syndesmosis
• If also affecting the medial malleolus = bimalleolar fracture

Ix: AP, lateral & oblique ankle X-ray

• CT (distal tibia & hindfoot) - comminuted fracture
• MRI - ankle ligaments & tendons

Mx: depends on Weber classification & level of displacement

• No to all Ottawa rules = conservative Mx: RICE – rest, immobilisation, compression, elevation
• Unimalleolar:
  
  • No evidence of ligamentous injury on X-ray –> discharge w/ cast + fracture clinic follow-up X-rays
  • Evidence = UNSTABLE
• Bimalleolar/unstable –> closed reduction (if joint dislocated on X-ray) –> refer for surgical fixation

Question 95

Neck of femur anatomy? Breakdown?

RFs? Presentation? Ix? (incl. fracture type & classification) Mx?

Answer 95

NoF anatomy - blood supply:

• Deep femoral artery (the main branch of the femoral artery) - gives rise to:
  
  • Medial & lateral circumflex femoral arteries - gives rise to:
    
    • Retinacular arteries - progress superiorly up to the head of the femur
• Artery of ligamentum teres - only a very small component of perfusion of the head/neck of the femur
• NOTE: retrograde blood supply from distal to proximal

NOF anatomy - joint capsule (ligaments surrounding the head of the femur and acetabulum):

• Intracapsular - fracture within the joint capsule (proximal to the trochanteric line) - high risk of blood supply compromise as retinacular vessels sheared –> Avascular Necrosis (AVN)
• Extracapsular - fracture outside the joint capsule (distal to the trochanteric line) - less risk of blood supply compromise

RFs: elderly, freq falls, osteoporosis, high impact trauma, post-menopausal women

Presentation: externally rotated + shortened leg

• Typically old, frail, osteoporosis/malacia

Ix:

• Examine joints above & below, NV exam of lower limb
• FBC, U&E, LFTs, CRP, G&S (if NoF - need surgery)
• Hip XR –> CT/MRI (if normal X-ray but high suspicion)
  
  • NOTE: NoF fracture Xrays: Shenton line - if not smooth = likely fracture
  • NoF fracture types - based on location:
    
    • Sub-capital (slightly below the head)
    • Transcervical
    • Basicervical
    • Intertrochanteric
    • Subtrochanteric
  • Garden classification - level of displacement:
    
    • Stage 1 - incomplete (not all the way through the bone)
    • Stage 2 - complete (but fracture components intact)
    • Stage 3 - complete with some displacement
    • Stage 4 - complete with significant displacement

Mx:

• Conservative - analgesia
• Medical - bisphosphonates (bone protection) + Vit D + DEXA
• Surgical:
  
  • Subtrochanteric - internal fixation = femoral nail
  • Intertrochanteric – internal fixation = dynamic hip screw (DHS)
  • Intracapsular:
    
    • Undisplaced (Garden I&II) – cannulated hip screw or DHS
    • Displaced (Garden III & IV) - higher risk of AVN:
      
      • <55yrs – reduction & fixation w/ screws
      • >65yrs – replace:
        
        • Fit = THR (HoF & acetabulum replaced)
          
          • Independent, mobile with ≤1 stick, no cognitive impairment
        • Not fit = hemiarthroplasty (just HoF replaced)

Question 96

Wrist fracture - types? Mx?

Answer 96

Types:

• Colles’ fracture - common in A&E, fall on an outstretched hand –> fracture of distal radius, displaced dorsaly (dorsum of the wrist)
• Smith fracture - fall on flexed wrist, displaced in a palmar direction (palm of the wrist)
• NOTE: displaced in the direction that is facing upwards (e.g. in Colles’ the dorsal aspect is facing the sky; in Smith’s the palmar aspect is facing the sky)

Mx:

• Check neurovascular intact
• Imaging (visualise fracture)
• Reduction under haematoma block > Hold (e.g. cast) > Rehabilitate
• NOTE: Smith’s fracture is often more complicated –> surgical intervention

Question 99

How do you approach an MSK X-ray?

Describing a fracture on XR approach?

Answer 99

MSK X-RAY APPROACH:

• NOTE: likely knee or hip x-ray in the exam

General:

• Name, DoB ±PC
• XR - date & time, views (AP/lateral), area of body, rotation, penetration (RI_P_E)
• NOTE: always do ≥2 views, compare to previous X-rays, look at imaging for joints above and below

ABCS approach: Alignment & joint space, Bone texture, Cortices, Soft tissues

• Alignment & joint space:
  
  • Changes suggest –> fracture, subluxation (still touch) or dislocation
  • Displacement - describe the position of fragment distal to fracture site described
  • Joint space:
    
    • Narrowing due to cartilage loss/calcification (chondrocalcinosis)/new bone (osteophytes)
    • Subchondral sclerosis is increased bone density along joint lines (OA)
• Bone texture - altered density (subchondral cyst - increased density, OA)/disruption (blurry - osteomyelitis) in trabeculae (inside of bone)/cortex (outer coating)
• Cortices - trace around outside of each bone
  
  • Step = possible pathology:
    
    • Fracture
    • Bony destruction - inf or tumour (primary/secondary)
  • Periosteal reaction (new bone in response to injury/stimuli, appears as pale bone on the outside) - can be only sign of stress/healing fracture, mild osteomyelitis, tumour)
• Soft tissues - swelling, foreign bodies (lipohaemarthrosis caused by fracture), effusions

DESCRIBE A FRACTURE:

Where - what bone? location (proximal, middle, distal OR epiphysis, metaphysis, diaphysis)? Does it involve articular surface (intra/extra-articular)?

Types:

1. Simple vs Compound:

• Simple: closed fracture i.e. only bone involved
• Compound: open fracture i.e. bone exposed to the external environment - (↑risk of infection → ↑fracture non-union) Open fractures are emergencies and require urgent management with:
  
  • IV antibiotics
  • Tetanus prophylaxis
  • Wound debridement

2. Subtype:

• Complete (all the way through the bone)
  
  • Transverse: perpendicular to long axis of bone
  • Oblique: tangential to long axis of bone
  • Spiral: oblique and rotating around the shaft
  • Comminuted: > 2 fragments –> CT to further assess
  • Impacted: broken ends of bone are jammed together by the force of injury, fracture line is indistinct
  • Linear: parallel to axis of the bone
  • Avulsion: bone attached to tendon/ligament is pulled away from main bone
• Incomplete (not whole cortex, most common in children):
  
  • Greenstick: bone bends and cracks, occurs < 10yrs
  • Salter-Harris: growth plate involvement

Displacement - describe the position of distal fragment to body (anterior/posterior)

• Angulation: change in bone axis (varus/valgus, dorsal/palmar, radial/ulna)
• Translation: movement of fractured bones away from each other (% of bone width)

OVERALL: 1) Type (simple/compound > subtype) 2) Relevant region, side and name of bone 3) Displacement (& angulation, translation)

• Example: Simple oblique fracture of the proximal right tibia with posterior displacement

Question 103

Gout - presentation? Ix? Mx?

Answer 103

Presentation: 1st MTP joint, monoarticular (can be poly)

Ix: Bloods (FBC, CRP, Urate), X-ray (erosive), joint aspiration (cells, culture, crystals, gram stain)

Mx:

• Acute: NSAIDs/Colchicine/CS inj (monoarticular)/oral (polyarticular)
• Chronic:
  
  • Dietary advice - low purine, weight loss
  • Xanthine oxidase inhibitor e.g. allopurinol/febuxostat
  • Consider - uricosuric agents e.g. sulphinpyrazone, probenicid, benzbromarone
  • (NOTE: Rasburicase - tumour lysis syndromes)

Question 104

Systemic sclerosis (scleroderma) - def? Subsets? Presentation? Ix? Raynaud’s Mx?

Answer 104

Def: multisystem disease - inflammation, vascular abn, fibrosis

Presentation: digital ulcers, tight skin around hands/mouth

Subsets:

• Limited cutaneous SS (CREST) - skin changes limited to forearm/calf/distal/peri-oral area
• Diffuse cutaneous SS - more extensive, upper arms, legs, trunk

Presentation:

• Swelling of hands & feet, Reynaud’s phenomenon, skin thickening
• Heartburn/reflux/dysphagia, bloating
• Arthralgia/myalgia
• Dyspnoea & dry crackles (pul fibrosis, pul HTN)
• Scleroderma renal crisis (renal failure, marked HTN)

Ix:

• Bedside: ECG, urine dip, pulmonary function tests (pul fibrosis)
• Bloods:
  
  • FBC, U&E, LFTs, CRP/ESR,
  • Abs: ANA (also in SLE, AI hep), anti-centromere (limited cutaneous), SCL-70 aka topoisomerase (diffuse cutaneous)
• Imaging: CXR, Echo, barium swallow

Mx:

• Specialist MDT
• Conservative: smoking cessation, emollients, avoid cold/gloves (Raynaud’s), physio, OT
• Medical:
  
  • CCB (nifedipine) for Raynaud’s
  • Omeprazole, prokinetic (domperidone) for GI Sx
  • Analgesia (for joint pain)
  • ACEi (for HTN)
  • Steroids + IS (methotrexate) –> if diffuse disease/complications (pul fibrosis)
• Scleroderma renal crisis - ACEi + renal dialysis/transplant

Question 105

GCA - Presentation? Ix? Mx?

Answer 105

GCA is most common primary vasculitis

Presentation: headache, scalp pain/tenderness, aching & stiffness, jaw/limb claudication

• Loss of vision - can have amaurosis fugax, blindness if vision not treated within hrs
• Commonly associated with polymyalgia rheumatica (PMR)

Ix:

• ESR & CRP
• USS temporal artery –> bilateral temporal artery biopsies - up to 2wks after high-dose steroids

Mx: prednisolone, if visual Sx consider IV methylprednisolone

• If persistent active/relapsing - IL-6 receptor blocker (Tocilizumab)

Question 110

Polymyalgia Rheumatica (PMR) - def? presentation? Associated condition? Dx & Ix? Mx?

Answer 110

Def: inflammatory rheumatological condition

Presentation: muscle aches and joint stiffness (takes 2-3hrs to loosen up in the morning)

• Profile: elderly woman (>70yrs)
• Difficult to rise from seated/prone position
• Shoulder/hip stiffness & bursitis
• muscle tenderness & oligoarthritis

Associated with GCA (15-20% have GCA; 40-60% GCA have PMR)

• GCA is most common primary vasculitis
• Can have amaurosis fugax, blindness if vision not treated within hrs
• Ix: bilateral temporal artery biopsies - up to 2wks after high-dose steroids

Dx: clinical + ESR, CRP, FBC (to rule out haem disorders)

Mx: prednisolone + osteoporosis prevention (Ca, Vit D, Bisphosphonates)

• Other: methotrexate + folic acid

Question 111

Tenosynovitis of hand & wrist - def? RFs? Presentation of different types? Ix? Mx?

Answer 111

Tenosynovitis def:

• Involves extrinsic tendons of hand & wrist & corresponding retinacular sheath
• Characterised as tendon irritation manifesting as pain –> progress to catching and locking when tendon gliding fails.

RFs: insulin-dep DM, pregnancy/lactation, dom-hand involvement

Presentation: location over retinacular sheat, pain increases with motion,

• Trigger finger:
  
  • Painful popping on finger flexion/extension (catching of flexor tendon)
  • Palpable nodule @level of metacarpal head in palm
• De Quervain’s disease:
  
  • ​Pain, tenderness, swelling localised to radial wrist (1-2cm proximal to radial styloid)
  • Worse on thumb mov/ulnar deviation
  • Finkelstein test (thumb in hand + ulnar deviation –> pain)
• Intersection syndrome:
  
  • ​Pain & swelling 4cm proximal to wrist joint ± redness/palpable crepitus
  • Much worse on resisted wrist extension
• Extensor pollicis longus:
  
  • Thumb IP mov –> pain @Lister’s tubercle
• Extensor carpi ulnaris:
  
  • Ulnar wrist pain
  • Worse with extension/ulnar deviation against resistance
• Flexor carpi radialis:
  
  • Pain @palmar wrist crease over scaphoid tubercle + along tendon ± localised swelling/ganglion cyst
  • Worse with resisted wrist flexion, radial deviation

Ix: high-res USS

Mx:

• NSAID ±splinting
• CS injection (sheath/compartment): flexor tendon sheath (trigger finger), 1st dorsal compartment (De Quervain’s disease)
• Surgery (surgical release of compartment)

Question 119

Fibromyalgia

Answer 119

Def: chronic pain syndrome diagnosed by the presence of widespread body pain ≥ 3 months

Presentation:

• RFs: AI rheum condition (RA, SLE), female
• Chronic widespread body pain
• Diffuse tenderness on physical exam
• Fatigue, memory problems, sleep & mood disturbance

Ix: clinical Dx

• To exclude other causes: FBC, TFT, ESR/CRP, vit-D, Ab-testing (RF, anti-CCP, ANA)

Mx:

• 1st - TCA e.g. amitryptiline
• Non-pharm: education, exercise, CBT ± referral to psych

Question 120

Benign prostatic hyperplasia (BPH) - def? Sx? Ix? Mx?

Answer 120

Def: slowly progressive hyperplasia of periurethral (transition) zone of prostate gland –> urinary outflow obstruction

• Common - occuring primarily in elderly men

Sx: lower urinary tract symptoms (FUND HIPS)

Ix: urinalysis (UTI), PSA (cancer) ± US/CT (abdo/pelvis)/cystoscopy

Mx:

• Acute retention = CATHETERISE
• Conservative - watchful waiting
• Medical:
  
  • Alpha-blocker (relax sm muscle around prostatic urethra) e.g. tamsulosin
  • 5-alpha-reductase inhibitor (reduce conversion of testosterone –> dihydrotestosterone - reducing androgenic stimulation of prostate) e.g. finasteride
• Surgical: TURP (transurethral resection of the prostate - shave extra prostate), open prostatectomy
  
  • NOTE: TURP not curative - will continue to grow

Question 121

Urinary tract calculi - def? presentation? Stone types? Ix? Mx? When to ADMIT/what to do if managed @home?

Answer 121

Def: crystal deposition within the urinary tract

Presentation: severe loin to groin pain (ureteric colic - starts around back and moves towards groin)

Stone types:

• Ca oxalate (80%)
• Mg Ammonium Phosphate (struvite) - likely staghorn calculi
  
  • Associated with proteus mirabilis inf
• Urate
• Cysteine

Ix:

• Bedside - urine dip (microscopic haematuria)
• Bloods - U&E (post-renal AKI)
• Imaging - gold standard non-contrast CT KUB (kidneys, ureters, bladder)
  
  • Contrast is excreted by kidneys - looking for bright white light of Ca –> if you give contrast it will mask the finding

Mx:

• Infected & obstructed = pyonephrosis –> URGENT decompression via NEPHROSTOMY (or retrograde w/ JJ stent)
  
  • Opening between kidney & skin w/ nephrostomy bag for external collection
  • Nephro (kidney) stomy (opening)
• <5mm (on CT) - allow spontaneous passing, retain stone for analysis
• >5mm (on CT):
  
  • Ureteroscopic lithotripsy - endoscope into ureter & using mechanical force/laser to destroy stone
    
    • Uretero (through ureter) scopic (camera) Litho (stone) tripsy (crush)
  • Extracorporeal shockwave lithotripsy - external USS to destroy stone
    
    • Extra (outside) corporeal (body) shockwave (USS) Lithtripsy (crushing stone)
  • Percutaneous nephrolithotomy - ONLY if stone in kidney (e.g. staghorn calculi), extract stone through skin in back
    
    • Percutaneous (through skin) Nephro (kidney) lith (stone) otomy (cutting)

When to ADMIT:

• Pain not controlled
• Significantly impaired renal function
• Single kidney
• Pyrexia/sepsis
• Stone >5mm

If managed at home:

• High fluid intake + return if pain worsening/develop temperature
• OPA in 4 weeks with CT-KUB on arrival –> if stone still present need lithotripsy/nephrolithotomy

Question 126

AD Polycystic Kidney Disease (PCK)

Presentation? Associations? Screening? Ix? Mx?

Answer 126

Presentation: HTN, abdo discomfort, blood in urine, FHx of IC haemorrhage

• Cysts in kidneys prod renin –> HTN
• Space occupying masses in abdo (renal/liver cysts)
• Can bleed into cysts –> blood in urine

Associations:

• Hepatic cysts
• Berry aneurysms –> risk of ICH
• Mitral valve prolapse

Family screening - renal USS

Ix:

• Urine MC&S, ECG
• FBC, U&E, fasting lipid profile
• Renal USS, CT/MRI AP, CT head
• Genetic testing - PKD1/2

Mx:

• Renoprotective lifestyle - weight, exercise, no smoking
• Tolvaptan, anti-HTN
• Inf - abx, cyst drainage, nephrectomy
• End-stage renal disease - transplant, dialysis

Question 128

Intracranial bleeds - layers of the outer brain? types? Appearance on CT-head? Presentations?

Answer 128

Outer layers of the brain:

• Skull > dura mater (adherent to inside of skull) > arachnoid mater > pia mater > brain parenchyma

Types:

• Extradural haemorrhage- bleed between dura mater & skull
  
  • Most common = skull fracture of pterion (temple) –> trauma to middle meningeal artery
  • Hx: clear trauma –> transient LoC –> lucid interval –> ongoing headache –> reduced consciousness
  • Convex (EGG) appearance on CT-head as blood sealed in by dura ± soft-tissue oedema outside skull (trauma site)
  • Mx: A-E approach, refer to neurosurgery
    
    • Monitor GCS = deterioration
• Subdural haemorrhage - bleed between dura & arachnoid mater
  
  • Tearing of bridging veins going from outer surface of brain to dura mater
  • Common in elderly + alcoholics (both have cerebral atrophy)
  • Types: both concave (SICKLE) appearance on CT-head
    
    • Acute - assoc w/ trauma + blood white (hyperdense) on CT-head
    • Chronic - little/no Hx of head trauma e.g. fall several weeks ago and then not been normal since (elderly) + dark (hypodense) blood on CT-head
    • Reduced consciousness, if severe = focal neurology (esp. if midline shift)
  • Mx: A-E, neurosurgery referral
    
    • Monitor GCS, reverse Warfarin
• Subarachnoid haemorrhage - between arachnoid & pia matter
  
  • Caused by an aneurysm (berry) or trauma
  • Presentation: sudden-onset worst headache ever, photophobia, neck stiffness
  • LP 12hrs after Sx-onset (xanthochromia)
  • Mx: A-E approach
    
    • Monitor GCS and neuro obs
    • Discuss with neurosurgery
    • Other – fluids, monitor Na, nimodipine
  • Complications:
    
    • Vasospasm – presents like a stroke
    • Hyponatraemia – can be SIADH
    • Rebleed - coil ASAP if possible

Question 129

Headache - types? Ix? Mx?

Answer 129

Types:

• Tension - band-like, front of forehead, causes: dehydration, stress
• Cluster - intense pain behind/around eye (worse @night + lacrimation & ptosis during attack), daily clusters for 4-6wks then nothing for months, M>F
  
  • Mx: 100% O2 + nasal triptans
• Migraine - intense/throbbing, focal, aura, photophobia
  
  • Triggers: alcohol, chocolate, cheese, oestrogens (OCP)
  • Mx:
    
    • Acute - simple analgesia, dark room + Triptans (take as soon as Sx start)
    • Prevent - trigger avoidance + propranolol/ topiramate (anticonvulsant, terratogenic) /amitriptytline (TCA)
• Meningitis - generalised, moves down neck, neck stiffness + fever + rash (meningococcal)
  
  • Ix: CT-head, LP (type of meningitis), BC (causative organism)
  • Mx:
    
    • Suspected in primary care - IM/IV Benzypenicillin
    • Secondary care - IV Ceftriaxone ± Amoxicillin (infants/>50yrs)
    • If could be encephalitis (seizure/behavioural) - IV Aciclovir
• SAH - sudden-onset, worst headache ever ± neck stiffness, can get preceding sentinel bleed (minor), assoc w/ PCKD (Berry aneurysm in Circle of Willis)/Marfan’s
  
  • Ix: non-contrast CT –> LP for xanthochromia (after 12hrs)
  • Mx: nimodipine (CCB, give every 4hrs, reduces vasospasm in cerebral arteries)
• Giant cell (temporal) arteritis - vasculitis –> scalp tenderness, jaw claudication, vision loss, assoc w/ polymyalgia rheumatica (>50yrs)
  
  • Ix: ESR, temporal artery biopsy
  • Mx: high-dose Prednisolone (to prevent blindness, do not wait for biopsy)
• ​Trigeminal neuralgia - electric shock-like pain on touching face (extremely tender)
  
  • Divisions of trigeminal nerve (V2&3)
  • Ix: MRI brain
  • Mx: Carbamazepine (for pain), neurology referral
• Raised ICP - worse at night/on waking/coughing/straining ± N&V, visual disturbances
  
  • Mx: osmotic diuresis - mannitol/hypertonic saline
• Cerebral Venous Sinus Thrombosis (VTE in the brain) - papilloedema, 6th nerve palsy, seizures, Cushing’s reflex (HTN, bradycardia, Cheyne-Stokes breathing)
  
  • Ix: MRI w/ MR venography
  • Mx: LMWH
• Idiopathic intracranial HTN (IIH) - Obese, female, papilloedema, postural headache worse with straining, assoc w/ OCP
  
  • Ix: visual field testing, fundoscopy, MRI brain, LP (≥25 opening pressure)
  • Mx: acetazolamide (carbonic anhydrase inh), weight loss, LPs + VP/LP shunt, ophthalmology follow-up

Question 130

Cardiovascular accident (CVA) - Def? Presentation? DDx? Classification? Ix? Mx?

Answer 130

Def: better to use cardiovascular accident (CVA)

• Stroke ≥24hrs, TIA ≤24hrs

Presentation:

• Pyramidal weakness (flexors stronger than extensors in upper limb, opposite in lower limb), hypertonia, hyperreflexia
• Hemiplegic/scissor gait –> circumduction
• TIA: Amaurosis Fugax (black curtain)
  
  • If ≥2 in 1wk = high risk of stroke –> ADMIT
  • Aspirin 300mg + secondary prevention (as for stroke)

DDx:

• Cerebral lesion - 80% ischaemic, 20% haemorrhagic (reduced GCS & raised ICP)
• Neoplastic - SOL
• Rare: syphilis, Todd’s paralysis (post-ictal), migraine, MS, cerebral abscess, rheumatological (arteritis)

Classification: Bamford aka Oxford

• Total anterior circulation stroke: hemiplegia, homonymous hemianopia, higher cortical dysfunction
• Partial anterior circulation stroke: 2/3
• Lacunar circulation stroke: hemi-motor OR hemi-sensory stroke only
• Posterior stroke: cranial nerve problems, eye-movement disorder, cerebella presentation
  
  • Weber’s & Wallenberg’s (lateral medullary syndrome = posterior cerebellar artery infarct)

Ix:

• BEFORE Tx = CT-head - 80% strokes ischaemic, 20% haemorrhagic (wrong Tx will make it much worse) –> haemorrhage has an area of hyperdense (white) bleeding
• After initial Mx –> identify cause:
  
  • ​​Structural heart defect - echocardiogram
  • AF - ambulatory ECG (24hr tape if no obv sign of AF as outpatient)
  • Carotid atherosclerosis - carotid doppler –> carotid artery stenosis (70-99%) = carotid endarterectomy

Mx: A-E approach + URGENTLY contact stroke team –> dedicated stroke unit, if ischaemic:

• Immediately:
  
  • Aspirin 300mg OD + STOP anticoagulants (high risk of haemorrhagic transformation in first 2wks)
  • <4.5hrs since Sx onset: thrombolysis (Alteplase = tPA)
    
    • C/I: any sign of active bleeding, very high BP, recent surgery, raised ICP
  • >4.5hrs since Sx onset: conservative Mx:
    
    • BM - keep controlled <11 (sliding scale insulin)
    • NG tube (nutrition)
    • MDT - dietician, SALT, PT/OT
  • < 6hrs (sometimes up to 24hrs, depending on size, area, damage) –> thrombectomy (neurosurgery)
• After 2wks:
  
  • STOP aspirin –> start clopidogrel 75mg OD + consider anticoagulation (e.g. if AF) - DOAC/Warfarin
  • Manage vascular RFs (DM, HTN, QRISK etc.)

Question 131

Parkinson’s disease definition? Cardinal Sx? DDx? Ix? Mx? Complications?

Answer 131

Def: a neurodegenerative disease of dopaminergic neurones of substantia nigra (part of basal ganglia in the midbrain)

Cardinal Sx (from extrapyramidal involuntary dysfunction): resting tremor, rigidity (cogwheeling due to superimposed tremor), bradykinesia, postural instability

+ insomnia, hypomimia (mask face), depression, autonomic dysfunction

DDx:

• Benign essential tremor - bilateral, postural, FHx, alcohol improves it (in 50%)
• Drug-induced (anti-psychotic, metoclopramide) - drug chart
• MSA (multisystem atrophy) incl Shy-Drager (autonomic) - cerebellar signs
• PSP (progressive supranuclear palsy) - loss of downward gaze
• LBD (Lewy body dementia) - visual hallucinations
• Normal-pressure hydrocephalus - gait disturbance, cognitive impairment, impaired bladder control
• Other:
  
  • Corticobasal degeneration - single-arm signs, alien limb syndrome (myoclonus)
  • Wilson’s disease (copper) - motor

Ix: clinical Dx –> dopaminergic agent trial ± MRI scan/DAT scan

Mx: problem = lack of dopamine in substantia nigra –> aim of Tx is to increase dopamine here

• Dopamine agonist (cross BBB):
  
  • Good for younger patients to reduce time on levodopa (as get very sensitised)
  • Types:
    
    • Non-ergot - ropinirole, pramipexole - avoid below SEs = 1st line but still get dopamine dysregulation syndrome (hypersexuality & gambling)
      
      • SC Apomorphine for advanced disease
    • Ergot - cabergoline, bromocriptine –> retroperitoneal/pulmonary fibrosis
• ‘L-DOPA (levodopa) AND peripheral DOPA-decarboxylase enzyme (Carbidopa)’ = Sinemet/Medapar
  
  • Relevant physiology:
    
    • Substantia nigra contains dopaminergic neurones with DOPA decarboxylase (converts L-DOPA –> dopamine) - not happening as normal in Parkinson’s
    • Peripheral DOPA-decarboxylase in body
    • Chemoreceptor trigger zone (CTZ) –> triggers nausea & vomiting
  • Drug explanation:
    
    • If give L-DOPA by itself it will be broken down by peripheral DOPA-decarboxylase into dopamine - this can’t cross BBB to reach substantia nigra but can reach CTZ –> nausea/vomiting
    • Instead, give L-DOPA with peripheral DOPA-decarboxylase inhibitor to allow more L-DOPA to cross BBB to reach dopaminergic neurones in substantial nigra to be converted to dopamine (some still reaches CTZ –> SE of nausea/vomiting)
  • Other SEs: dyskinesia, on-off phenomena, postural hypotension
    
    • Amantadine - for dyskinesia secondary to levodopa
    • COMT inhibitors e.g. entacapone for tailing off betw/ doses of levodopa

Complications:

• Falls, cognitive impairment, depression
• Drool (SALT/glycopyrronium)
• Meds SEs (e.g. vomiting)

Question 135

Gait abnormalities vs normal

Answer 135

SUMMARY:

• Normal gait cycle: 1) heel strike 2) foot flat 3) mid stance 4) heel off 5) toe-off
• Antalgic gait - limping due to pain e.g. osteoarthritis, inflammatory joint disease, fracture, sciatica
• Hemi/Diplegic gait - uni/bilateral circumduction of leg - CNS lesion (bilateral is called a ‘scissoring gait’)
• Parkinsonian gait - shuffling gait, no arm swing - Parkinson’s/DLB/Antipsychotics
• Ataxic gait - wide/broad-based stance & imbalance - Cerebellar/Vestibular/Sensory neuropathy
  
  • NOTE: can’t do tandem walk
• Neuropathic gait - high-step gait (from foot drop) - motor neuropathy e.g. L5 radiculopathy (e.g. herniated disc), common peroneal neuropathy, MS, Charcot-Marie-Tooth disease
  
  • Can’t walk on heels
• Myopathic gait - waddling/Trendelenburg gait (hip sways to one/both sides - hip abductor muscles weak) - muscular dystrophy/myopathy
• Choreiform gait - involuntary movements - Basal ganglia disease e.g. Parkinson’s meds, Huntington’s, Wilson’s, Cerebral Palsy
• Stomping gait - sensory neuropathy (loss of proprioception & vibration sense = dorsal column disease)
  
  • Vibration –> proprioception (Romberg’s +ve) –> light touch (in order lost)
  • Causes: SACD (subacute combined degen cord - B12), Friedrich’s ataxia, Tabes/taboparesis & tabes dorsalis (syphilis),
• Marche à petit pas - small steps = normal pressure hydrocephalus

IN-DEPTH:

Normal gait cycle: 1) heel strike 2) foot flat 3) mid stance 4) heel off 5) toe off

Antalgic gait - limping due to pain

• Causes: osteoarthritis, inflammatory joint disease, lower limb fracture, nerve entrapment (sciatica)

Hemiplegic gait - unilateral circumduction of leg to prevent dragging foot

• CNS lesion –> unilateral weakness & spasticity (spastic flexion of upper limb vs extension of lower limb)
• Causes - UMN lesion:
  
  • Unilateral cerebral lesion e.g. stroke, SOL, trauma, MS
  • Hemisection of spinal cord (trauma)

Diplegic gait - bilateral circumduction of legs (scissoring gait_)_

• CNS lesion as above but bilateral clinical findings - spasticity worse in lower limbs vs upper limbs ± hyperreflexia, clonus, Babinski +ve, reduced power, sensory level if spinal cord pathology
• Causes:
  
  • Spinal cord lesion e.g. prolapsed intervertebral disc, spinal spondylosis, spinal tumour/infarct, transverse myelitis
  • Bilateral brain lesion - cerebral palsy, MS, bilateral brain infarcts, midline tumour (paraspinal meningioma)
  • MND - if also LMN findings (wasting, fasciculations)

Parkinsonian gait - shuffling gait

• Loss of dopaminergic neurones in substantia nigra of basal ganglia –> extrapyramidal dysregulation = rigidity, bradykinesia, resting tremor, postural instability
• Features of parkinsonian gait:
  
  • Initiation - slow to start walking
  • Step length - shuffling gait (short steps) & festinant gait (progressively smaller steps)
  • Arm swing - reduced (early feature)
  • Posture - flexed trunk & neck = stooped
  • Turning - postural instability
• Causes: Parkinson’s, Dementia w/ LBs, Parkinson’s plus syndromes (Multisystem atrophy & progressive supranuclear palsy), drug-induced (antipsychotics/emetics)

Ataxic gait - wide/broad-based stance (to maintain balance)

• Assoc w/:
  
  • Midline cerebellar disease (alcoholism/B12 def, MS, cerebellar stroke) - DANISH (dysdiadokokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia)
  • Vestibular disease (labyrinthitis, Meniere’s, acoustic neuroma) - vertigo, N&V
  • Sensory ataxia (peripheral neuropathy e.g. DM) - +ve Romberg’s, impaired proprioception, impaired vibration sense, lack of other cerebellar signs
• Features of ataxic gaint:
  
  • Stance - broad-based ataxic gait
  • Stability - staggering, slow, unsteady –> veer towards side of lesion
  • Turning - very difficult

Neuropathic gait - high-step gait (from foot drop)

• Weakness in muscles of distal limb (foot dorsiflexors) - damage to peripheral nerves providing motor innervation –> foot drop & dragging toes –> knee & hip flex excessively to compensate
• Other features: peripheral vascular disease, peripheral sensory impairment, reduced/absent reflexes
• Causes: motor neuropathy
  
  • Isolated common peroneal nerve palsy (trauma/compression)
  • L5 radiculopathy (disc prolapse)
  • Generalised polyneuropathy involving multiple nerves (DM, MND, Charcot-Marie Tooth disease)

Myopathic gait - waddling/Trendelenburg gait (hip sways to one/both sides)

• Weakness of hip abductors –> can’t stabilise pelvis –> tilts down towards unsupported side
• Assoc features: hard to stand from seat/squat/lying without arms, +ve trendelenburg’s sign (stand on one leg - if the hip on the side of the raised leg drops = +ve)
• Causes: muscular dystrophy, myopathy (e.g. in hyperthyroidism, Cushing’s, acromegaly, Polymyalgia rheumatica)

Choreiform gait - involuntary movements

• Oro-facial dyskinesia (grimacing/lip-smacking) & choreic mov of upper/lower limbs = dance-like/writhing @rest/mov
• Causes: Basal ganglia disease
  
  • Huntington’s, Sydenham’s chorea, Cerebal palsy (Choreiform type), WIlson’s disease, Dopaminergic meds (e.g. Parkinson’s)

Question 136

Cerebellar syndrome causes?

Answer 136

MAVIS:

• MS - eye (RAPD, INO), spastic paraparesis, catheterised
• Alcohol - peripheral neuropathy, liver signs
• Vascular (thromboembolic/haemorrhagic)
• Inherited (Friedrich’s ataxia)
• SOL
• Other: hypothyroidism & paraneoplastic syndrome

Question 137

MS - def? key features? DDx? Clinical courses? Ix? Mx? Poor prognostic features?

Answer 137

Def: evidence of damage to CNS that is separated in time & space

Key features:

• Profile: young, female (catheter & walking aid/wheelchair), eye & cerebellar signs
• Initial:
  
  • Ipsilateral visual disturbance - greying/blurring ± pain on eye mov/loss of red colours
  • Sensory phenomena - wetness/burning, uncomfortable band around the chest
    
    • Lhermitte’s sign - electric shock down neck and along spine & may radiate along limbs
    • Uthoff’s - neuro Sx worsen with increased temperature (hoff = hot)
• UMN Sx: hyperreflexia, hypertonia, pyramidal pattern (arm flexors stronger, leg extensors stronger)
• Dorsal column disease - reduced vibration, proprioception, Romberg’s +ve
• Eyes:
  
  • Internuclear ophthalmoplegia
    
    • Adduction paralysis and abduction nystagmus
    • From lesion in medial longitudinal fasciculus
  • Optic nerve damage:
    
    • Colour & visual acuity loss, RAPD
    • Central scotoma (central blindspot), optic atrophy
  • CN palsy (most commonly 6th - as longest)
• Cerebellar signs (imbalance, can’t tandem walk)

DDx:

• Cervical spondylosis - wo/ UMN signs but no cerebellar signs
• Subacute combined degeneration of the cord (SACD) - dorsal columns & cerebellar - if low B12
• Neuromyelitis optica aka Devic’s disease (IgG against aquaporin-4 channel) - optic neuritis & transverse myelitis but no cerebellar Sx

Clinical courses/patterns:

• Relapsing-remitting - steady decline + strong flair
• Primary progressive - steady decline without attacks
• Secondary progressive - initial relapsing-remitting becoming primary progressive
• Marburg variant - very severe, rapidly progressive

Ix:

• Bedside:
  
  • Fundoscopy (optic neuritis), full functional assessment (physio, OT)
  • Nerve conduction studies - visual evoked potentials (VEPs) - if single nerve lesion, delayed response
• Bloods - B12 (SACD), TFTs
• Imaging:
  
  • MRI (T2) head (lesions disseminated in time & space) - McDonald’s criteria
    
    • ​Periventricular white matter lesions
  • LP: IgG oligoclonal bands, high protein

Mx:

• Acute relapse: high-dose methylprednisolone (shortens acute attack) e.g. optic neuritis (painful eye mov + reduced visual acuity)
• Long-term - MDT approach (physio, OT, SALT)
  
  • Mobility - mobility aids, physio, OT
  • Spasticity –> Baclofen/Gabapentin (Dantrolene if CKD)
  • Bowel (laxatives) & bladder (oxybutynin, LT catheter)
  • Fatigue –> Amantadine
  • Oscillopsia (visual jumping when actually still) –> Gabapentin
  • Emotional lability –> Amitriptyline

Poor prognostic features:

• Brainstem/cerebellar disease at onset
• >40yrs at onset
• Primary progressive MS (no resolution

Question 139

Neurology Ix depending on UMN/LMN signs?

Answer 139

ALL: involve MDT for full functional assessment (physio & OT)

UMN:

• Imaging (brain ± spinal cord)
• CSF (LP)
• Brain biopsy

LMN:

• Nerve conduction studies & electromyography (NCS & EMG)
• Bloods (metabolic, abs)
• Muscle/nerve biopsy

Question 140

What are the nerve innovations for deep tendon reflexes in upper and lower limb neuro examination?

Answer 140

Nerve innovations:

• S1,2 - buckle my shoe - ankle jerk (Achilles tendon)
• L3,4 - kick the door - knee jerk (patellar tendon)
• C5,6 - pick up sticks - biceps, brachioradialis reflex
• C7,8 - lay them straight - triceps reflex

Question 141

Raised ICP - what is the Monro-Kellie Doctrine? Causes? Signs? Mx?

Answer 141

Monro-Kellie Doctrine: skull is a closed box, the sum of volumes of brain, CSF & IC blood is constant - increase in one should cause a decrease in one/both of others

• In brain there is little wiggle-room, the only weak point is the foramen magnum –> herniation = coning –> death

Causes: IC haemorrhage (IC blood), tumour, (brain vol), cerebral oedema (CSF)

Signs:

• Acute (pressure on brainstem): CUSHING’S TRIAD (HTN, bradycardia, irregular breathing) + reduced GCS
• Chronic: long-term headache

Mx:

• Conservative: sit up, hyperventilated (if intubated –> reduce pCO2 –> reduce vasodilation in brain)
• Medical: mannitol (osmotic diuretic), hypertonic saline –> both draw fluid out of brain –> reduce ICP
• URGENT neurosurgical input –> Burr hole surgery

Question 142

Cauda equina - def? Sx? Causes? Key Ix? Mx?

Answer 142

Def: compression of Cauda Equina (nerve fibres below L1-2)

Sx: can you feel it while you urinate/when you tug on catheter?

• Severe back pain
• Saddle anaesthesia (numb around the anus)
• Bladder/bowel dysfunction (urinary retention, faecal incontinence)
• Lower limb weakness
• Reduced anal tone (on PR exam)

Causes: large disc herniation, cancer, trauma, abscess, haematoma

• NOTE: if likely mets e.g. background of prostate cancer –> 16mg Dexamethasone (reduces swelling)

Ix: urgent MRI scan (+ PR exam)

Mx:

• In normal disc herniation (above cauda equina):
  
  • Get the patient to keep moving (or muscles will seize up)
  • Analgesia - PR Diclofenac (neuropathic pain) + Diazepam
• In cauda equina –> urgent referral to neurosurgery for decompression/laminectomy

Question 144

Meningitis & encephalitis - presentation? causes? Ix? Mx?

Answer 144

Meningitis:

• Presentation: headache, fever, photophobia, neck stiffness
• Causes:
  
  • Bacterial – N. meningitides, S. pneumo (TB; neonates/elderly – GBS/Listeria/E.coli) – Listeria also more common in alcoholics
  • Viral – enterovirus (Coxsackie, echovirus), mumps, HSV2
  • Fungal – cryptococcus neoformans (chr)
• Ix: A-E, BC, CT head, LP (CT first, if raised ICP –> LP would cause coning)
  
  • Kernig sign - flex knee & hip to 90 degrees –> extend knee (painful & limited extension)
  • Brudzinski sign - raise head while flat –> hip & knee flexion
• Mx: bacterial – IV ceftriaxone ± amoxicillin (Listeria - neonate/elderly)
  
  • IM BenPen for possible meningococcal infection (rash) in GP setting before sending to the hospital
  • Viral – supportive (self-limiting)
  • Altered consciousness (encephalitis?) –> add IV acyclovir

Encephalitis:

• Presentation: headache, fever, seizures, drowsiness, confusion (viral HSV1 affects temporal lobes –> affecting consciousness)
• Ix: BC, CT head, LP
• Mx: IV acyclovir ± anti-convulsants

Question 146

Epilepsy - def? types & Tx? Status epilepticus def & Mx?

Answer 146

Def: tendency to have recurrent, unprovoked seizures

• Seizure = episodes of abnormal uncoordinated excessive brain activity
  
  • Provoked seizures = consequence of inf/drugs
  • Unprovoked = epilepsy

Types:

• Generalised (whole brain):
  
  • Tonic-clonic, Tonic, Atonic, Myoclonic –> Tx: Na Valproate (AVOID in girls/women of childbearing age)
  • Absence –> Tx: Ethosuximide/Na Valproate
• Focal - aware (conscious) OR impaired awareness (impaired consciousness)
  
  • Tx: Lamotrigine

Status epilepticus = >5mins/repeated seizures without full recovery in between

• 1st - IV lorazepam 4mg –> repeat
• 2nd - phenytoin infusion
• 3rd - general anaesthesia
• If no IV access –> rectal diazepam/buccal midazolam

Question 150

Wasting of hand muscles - distinguishing different nerves?

Answer 150

Hand muscle wasting - dorsal guttering = first to be affected in ulnar lesions

• First dorsal interosseous (next to thumb) = ulnar nerve
• Abductor policies brevis (thenar eminence) = median nerve
• Weakness of both - suspect T1 radiculopathy
• NOTE: ulnar nerve innervates most of the intrinsic muscles of hand except median nerve serves LOAF: 2 radial Lumbricals, Opponenes pollicis, Abductor pollicis brevis & Flexor pollicis brevis

Ulnar nerve palsy = claw hand @rest (4th & 5th fingers in extension at MCP, flexion at PIP/DIP)

• Commonest site of lesion = elbow (arthritis @wrist & elbow)
• Froment’s sign (weak adductor pollicis brevis –> thumb flexion) = +ve if thumb arches to hold paper = ulnar nerve palsy
• Ulnar paradox - higher lesion causes lesser deformity as lower lesions spares flexor digitorum profundus (causes flexion at DIP)

Median nerve palsy = sign of benediction on asking to close hand (thumb, index finger can’t close, middle finger can close partially)

• Look for sensation over thenar eminence –> if lost can’t be carpal tunnel syndrome (still median nerve palsy but arises proximally to carpal tunnel)
• Bilateral carpal tunnel syndrome causes: Acromegaly, Amyloid (periorbital purpura after sneezing), DM, Hypothyroid, pregnancy

Question 156

Sensory ataxia vs Cerebellar ataxia based on Romberg’s test?

Answer 156

Postural imbalance/swaying:

• When eyes open & closed = Cerebellar ataxia
• When eyes are closed = sensory ataxia (somatosensory nerve affected)
  
  • Dorsal column loss: Tabes dorsalis (syphilis), SCDC (B12), MS
  • Sensory peripheral neuropathy

Question 159

Lumbar disc herniation vs lumbar spinal stenosis - presentation? Ix? Mx?

Answer 159

Presentation

• Disc herniation - acute unilateral radiculopathy (pain & numb in specific dermatome/weakness in muscle group)
  
  • Straight leg raise +ve
  • Worse on flexion (bending over/sitting)
• Spinal stenosis - insidious neurogenic claudication (intermittent back pain worse on walking/standing) ± pain radiating down leg/leg paraesthesia
  
  • RFs: rev back injury/surgery, manual labour
  • Worse on extension (standing/walking)

Ix:

• Disc herniation - erect lumbar x-ray & MRI spine
• Spinal stenosis - plane x-ray, MRI (T2-weighted)

Mx: surgical decompression

Question 160

Brain anatomy “rules” summary - cerebellar, motor nerves, dorsal columns, spinothalamic tract

Clues to localisation - cortical, basal ganglia, cerebellar, nerve root

Answer 160

Cerebellar signs ipsilateral

Motor nerves travel laterally in brainstem & cross @medulla

Dorsal columns are posterior & cross @medulla

Spinothalamic tract is anterior in spinal cord & cross in spinal cord

Localisation:

• Cortical - UMN pyramidal signs (hypertonia, hyperreflexia, babinski)
• Basal ganglia - rigidity, tremor, bradykinesia
• Cerebellar - DANISH
• Nerve root (dermatome/myotome)/single nerve - LMN signs (hypotonia, hyporeflexia, fasciculations, wasting, sensory loss)

Question 164

Mononeuritis multiplex causes?

Answer 164

Vasculitis - GPA, EGPA, microscopic polyangiitis, polyarteritis nodosa

Rheum - RA, SLE, Sjogren’s, Sarcoidosis

Question 165

Muscle weakness causes by location?

Answer 165

Brain: stroke, SOL, MS

Spinal cord: MS, trauma, disc herniation/spinal stenosis, spinal cord infarct, syringomyelia

• MS - weakness & paraesthesia based on UMN demyelination, disseminated in time & space
  
  • Optic neuritis, periorbital pain, RAPD, INO (damage to medial longitudinal fasciculus)
  • Ataxia, vertigo, chr constipation, blaadder dysfunct
  • Lhermitte’s sign - electric shock down back on neck flexion
  • Unhthoff’s phenomenon - worsening of Sx with increased body temp e.g. exercise, hot shower
  • Ix: MRI (brain & spinal cord) + LP (oligoclonal bands), nerve conduction study (evoked potential)
  • Mx: methypred for flare, INF-b long-term
• Trauma - extremity weakness wo/ cortical signs/facial weakness e.g. hemisection of spinal cord (Brown-Sequard syndrome) - below level of lesion:
  
  • Ipsilateral hemiparesis & loss of vibration/proprioception
  • Contralateral loss of pain & temperature
  • At level of lesion - loss of sensation + flaccid paralysis of muscles supplied by this spinal cord segment
• Herniated disc/spinal stenosis - weakness at level of lesion & lower extremities + bladder/bowel dysfunction + sciatica
• Spinal cord infarct - occlusion of anterior spinal artery (complication of aortic surgery)
  
  • Affects anterior 2/3 spinal cord in affected segment
    
    • Sudden-onset bilateral flaccid paralysis –> developing into spastic paralysis after several days
    • Loss of pain & temp
    • Light-touch, vibration & proprioception-sense spared (dorsal columns not involved)
• Syringomyelia - developmental disorder
  
  • Syrinx (cavity) grows from centre of spinal cord & spreads outwards
  • Normally affects cervical cord but can extend into brainstem
  • Early - bilateral loss of pain & temp in cape-like distribution affecting neck, shoulders, upper arms
  • Late - as syrinx expands anterior horn cells affected –> bilateral flaccid paralysis

Anterior horn (motor neurone lesions): MND, poliomyelitis

• Poliomyelitis - enterovirus infection attacking anterior horn cells
  
  • 1-2wks prodrome (fever, headache, N&V)
  • Asymmetrical weakness + can develop years after inf (post-polio syndrome) + can take place after taking live-attenuated polio vaccine
• MND
  
  • Mixed UMN/LMN presentation
  • Ix (exclude other causes): EMG/NCS, MRI - whole spine
  • Mx: no cure - MDT approach (SALT (swallowing), physio & OT)
  • Sx-control:
    
    • Quinine - muscle cramp
    • Anticholinergics e.g. hyoscine patches - drooling
  • Prognostic:
    
    • Riluzole - glutamate antagonist (extend life expectancy by 3-5 months)
    • NIV - if respiratory muscles no longer functioning

Neuropathy: diabetic neuropathy

• Polyneuropathy (multiple nerves): DANG My THeRAPIST
  
  • Diabetic neuropathy (most common, T1/2)
    
    • Sensory - glove & stocking loss of sensation/paraesthesia
    • Motor - same distribution as above + CN palsies (3rd - pupil-sparing)
    • Autonomic - orthostatic hypotension, constipation, erectile dysfunction
  • Alcoholic neuropathy (2nd most common)
  • Nutritional (B1/6/12 def)
  • GBS (AIDP - acute inflam demyelin polyneuropathy)
    
    • AI demyelination of peripheral nerves
    • 2-4wks post-inf e.g. diarrhoea with C. jejuni
    • Ascending weakness in distal lower extremities over hrs/days (worst after 4wks)
    • Flaccid paralysis with reduced/absent deep tendon reflexes
      
      • Can involve diaphragm –> resp failure
      • Bilateral facial nerve palsy
      • Difficulty swallowing –> aspiration
    • Autonomic dysfunction - sweating, orthostatic hypotension, urinary retention
    • NOTE: sensory Sx rare
    • Ix:
      
      • LP (high protein, normal WCC)
      • NCS & EMG (reduced conduction velocity)
      • Serum abs (anti-glycolipid abs)
    • Mx:
      
      • Monitor FVC <1L, NIF <20cm H2O –> intubate + mechanical ventilation
      • Monitor BP –> IV fluids for hypo, Labetalol for hyper
      • IVIG, plasma exchange
  • M(y)-edications (colchicine, cisplatin, isoniazid –> niacin def)
  • Toxins (lead)
  • Hereditary - HMSN (CMT)
    
    • Progressive hereditary (AD) motor & sensory neuropathy (HMSN)
    • Distal back & lower extremity weakness:
      
      • Foot drop (damage to common peroneal nerve)
      • High-arch foot (pes cavus) - does not flatten with weight-bearing
      • Scoliosis
    • ± pain & sensory loss (can lead to foot ulcers)
    • Ix: nerve conduction study + EMG, genetic testing (electrophoresis/FISH)
    • Mx: physio, walking aids, foot & heel-support
  • Renal failure (uraemic nephropathy)
  • Amyloidosis
  • Porphyrias
  • Inf (HIV, syphilis)
  • Systemic (hypothyroidism)
  • Tumours (multiple myeloma)
• Mononeuropathy (one nerve):
  
  • Facial nerve palsy - not forehead-sparing, crying/sensitive to noise/abnormal taste (ant 2/3 tongue)
    
    • Idiopathic = Bell’s palsy
    • Secondary:
      
      • Lyme disease
      • Ramsay-Hunt syndrome - HZV reactivation in the geniculate ganglion, causes painful eruption in auditory canal
      • Tumours - acoustic neuroma, parotid
      • Bilateral palsy - Sarcoidosis, GBS
    • Tx: treat cause or if Bell’s palsy –> pred within 72hrs Sx onset + eye protection
  • Carpal tunnel syndrome - entrapment of median nerve in flexor retinaculum
    
    • Repetitive use of wrist –> numbness & tingling in lateral 3 fingers (& 1/2 4th finger) –> weakness of thenar muscles
    • Tinel’s sign - tap nerve at wrist
    • Phalen’s sign - reverse prayer sign for 60s
    • Ix: EMG, wrist USS, MRI wrist (imaging to detect SOL e.g. ganglion cyst)
    • Tx: immobiliser wrist (splint), CS injection, carpal tunnel release

Neuromuscular junction: MG/LEMS

• Myasthenia gravis (MG) - AI condition where Abs attach to NMJ post-synaptic nicotinic AChR in skeletal muscle
  
  • FATIGUABILITY with use
  • Initial - oculobulbar weakness (diplopia, ptosis, dysphagia, nasal voice)
  • Chr:
    
    • Asymmetrical proximal limb muscle weakness
    • Resp muscle failure
  • Assoc w/ thymic hyperplasia/thymoma
  • NOTE: normal sensation, normal deep tendon & pupillary reflexes
  • Ix:
    
    • Serological testing: AChR, MUSK abs
    • Repetitive nerve stimulation (CMAPs decrease)
    • CT chest - thymoma
    • Monitoring with serial pul funct tests (FVC & negative inspiratory force) if suspect myasthenic crisis
  • Mx:
    
    • Acetylcholinesterase inhibitors (Pyridostigmine) + IS (azathioprine)
    • Surgery - thymectomy
  • Myasthenic crisis = acute respiratory failure - FVC <1L, negative inspiratory force (NIF) ≤20cm H2O
    
    • Often trigger - meds/inf
    • Accessory muscle use/weak cough = sign. exp muscle weakness
    • Mx: intubation + mechanical ventilation (& Mx above)
      
      • IVIG/Plasmapheresis
      • Stop pyridostigmine (increases secretions –> aspiration risk), stop trigger (meds)
  • Cholinergic crisis - same presentation as above (resp muscle weakness) BUT cause = excess pyridostigmine –> overstimulation of AChR –> eventually stop working
    
    • Pyridostigmine also binds to nicotinic receptors –> cholinergic Sx - SLUDGE (Salivation, Lacrimation, Urination, Diarrhoea, GI cramps, Emesis)
    • Mx: intubation + mechanical ventilation
      
      • Atropine (anti-muscarinic) for Sx but does not address resp weakness
      • Reduce dose of pyridostigmine
• Lambert-Eaton myasthenic syndrome (LEMS) - AI condition where Abs target pre-synaptic voltage-gated Ca channels –> reduces release of ACh from presynaptic vesicles
  
  • Proximal muscle weakness - IMPROVES with use
  • Reflexes reduced/absent, ± autonomic Sx
  • Assoc w/ SCLC, Hodgkin’s lymphoma
  • Ix:
    
    • NCS, repetitive nerve stimulation (CMAPs increase)
    • Serological testing: VGCC abs
    • CT chest (SCLC)
  • Mx: Tx underlying cause, Amifampridine
    
    • IVIg/plasma exchange
    • Supportive care incl. intubation + mech ventilation (if resp compromise)

Myopathy: dermatomyositis

• Inflammatory: proximal muscle weakness & pain
  
  • Dermatomyositis - skin rash (heliotropic rash & Gottron’s papules)
  • Polymyositis
  • Assoc: ILD - in 10% patients
  • Ix: CK, ab panel (anti-Jo-1, ANA)
    
    • EMG, muscle MRI + muscle biopsy
  • Mx:
    
    • Induction: CS (PO/IV) ± IVIg
    • Maintenance: IS (methotrexate/azathioprine) ± IVIg
• Inherited:
  
  • X-linked - Duchenne’s & Becker’s muscular dystrophy
  • AD - Myotonic dystrophy
    
    • Myopathic facies (facial wasting) + frontal balding
    • Distal wasting & weakness + loss of ankle jerk
    • Assoc: cataracts, dysphagia, cardiac, DM, hypogonadism
    • Exam - failure of immediate relaxation after voluntary contraction
      
      • Percussion myotonia - thumb contracts tapping thenar eminence
      • Slow releasing grip on shaking hands
    • Ix: CK, genetic testing, EMG ‘dive-bomber’ potentials, muscle biopsy
    • Mx: MDT approach
      
      • Phenytoin for myotonia, weakness has no Tx
      • Genetic counselling - trinucleotide repeat -severity/earlier with each generation
      • Avoid statins (can cause myopathy)
• Endocrine:
  
  • Hypothyroidism - proximal muscle weakness & pain, deep tendon reflexes decreased, myoedema (swelling on percussion)
  • Also possible in Addison’s Cushing’s, Vit D def
• Meds - statins (proximal muscle weakness & pain), glucocorticoids (muscle weakness)
• Ix: serum CK, TSH lvls, EMG

Question 167

Acute limb ischaemia - Def? Presentation? Ix? Mx?

Answer 167

• Def: a sudden decrease in limb perfusion that threatens the viability of limb
  
  • AF = major RF for acute limb ischemia
• Presentation - 6Ps:
  
  • Pale
  • Pulseless
  • Painful
  • Perishingly cold
  • NOTE: need immediate vascularisation (<6hrs) if:
    
    • Paralysis
    • Paraesthesia (esp worrying)
• Ix (after initial Mx):
  
  • Bedside: ABPI (PAD), ECG (AF)
  • Bloods: FBC, U&E, clotting, HbA1c, lipid profile
  • Imaging: duplex USS, CT/MR angiography
• Mx:
  
  • Initial:
    
    • A-E, IV access, analgesia
    • IV heparin infusion - reduces the chance of the clot getting worse
  • Limb viability:
    
    • Immediate - tender muscles, loss of power, loss of sensation
    • Urgent - pale, pulseless, painful, cold
    • Irreversible - fixed, mottled skin, woody, hard muscles
  • Refer to vascular surgery:
    
    • Thrombotic - local intra-arterial thrombolysis, angioplasty, bypass
    • Embolic - embolectomy/local intra-arterial thrombolysis/bypass

Question 168

Peripheral vascular disease localisation & type of bypass graft?

Answer 168

• Both sides all reduced pulse = aorta-iliac –> aorto-bifemoral
• One side reduced pulse from the popliteal down = femoro-popliteal
• One side reduced pulse distally in anterior tibial = femoro-distal
• One side reduced pulse distally in posterior tibial = femoro-distal

Question 169

AAA key Sx & ruptured Sx? Ix? Mx?

Answer 169

Sx:

• Central abdo pain
• Radiates to back
• Bloating
• Pulsatile mass on palpation (expansile - moves to sides)
• NOTE: always consider if abdo pain + RFs (male, >65yrs, HTN, smoking etc.)

Ruptured AAA Sx:

• Severe pain radiating to back
• Visible pulsating abdo mass
• Shock (circulatory compromise)

Ix:

• Abdo duplex USS if part of national screening - male age 65yrs
• CT angiography if stable but suspicious of rupture

Mx:

• <5.5cm –> Conservative: monitor w/ USS + RF modification
  
  • <4.5cm –> yearly USS
  • 4.5≤x<5.5com –> 3 monthly USS
• Medical: optimise BP control, statin, aspirin
• Sx/>5.5cm/expanding >1cm/yr –> Surgical: endovascular (catheter into aorta to insert stent)/open repair

Question 171

Peripheral vascular (arterial) disease - Def? RFs? Spectrum? Ix? Special test?

Answer 171

Def: limb ischemia (chronic) from atherosclerosis in lower limb vasculature

RFs: male, older, smoker, HTN, DM

Spectrum:

• Intermittent claudication (mild) - cramping leg pain after walking (& have to stop) + relieved by rest
  
  • NOTE: the equivalent of stable angina (worse on exertion)
  • Worse going uphill/upstairs
• Critical limb ischemia (severe) - ulcers, gangrene, night pain & rest pain
  
  • ​NOTE: the equivalent of unstable angina (present at rest)

Ix:

• Bedside:
  
  • Exam special test = Buerger’s angle - elevation pallor –> sudden drop feet down = sunset sign
  • exercise-treadmill ABPI (ankle-brachial pressure index) - <0.8 (<0.3 = CLI)
• Bloods - FBC, U&E, LFTs, CRP, clotting
• Imaging:
  
  • Arterial duplex USS
  • CT/MR angiography

Mx: dealt with by vascular surgeons –> optimise meds + surgery (bypass)

• Conservative: smoking cessation
• Medical: ACEi, clopidogrel, statin, DM control
• Surgery: angioplasty/stent/bypass graft/amputation

Question 172

Gynaecomastia - causes? presentation? Dx? Mx?

Answer 172

Causes:

• Failures:
  
  • Liver cirrhosis due to alcoholism (failure of liver to metabolise oestrogens)
  • Renal failure
• Neoplasm:
  
  • Bronchial carcinoma
  • Pituitary tumours (hyperprolactinaemia)
  • Testicular tumours
• Hyperthyroidism, Hypogonadism
• Drug-related (spironolatone)

Presentation: elderly/puberty

Dx: bilateral USS

Mx:

• Cause
• Tamoxifen
• Surgery
• NOTE: do not stop meds just because they are causing gynecomastia

Question 173

Aortic dissection - def? Sx? Ix? Mx?

Answer 173

Def: tear in tunica intima (inner layer of BV) –> blood collection between tunica intima and tunica media –> false lumen (can occlude blood flows through aorta) –> AR, myocardial ischaemia, stroke

Sx: sudden onset, central tearing chest pain –> radiating to between shoulder blades

• Hx of intermittent claudication
• Haemodynamic instability (high HR, low BP)
• Before left subclavian artery - left arm smaller than right arm
• After left subclavian artery - lower body less developed than upper body

Ix:

• BP in both arms - radio-radial delay
• ECG, CXR (widened mediastinum)
• Gold-standard: CT-aortogram w/ contrast

Mx:

• Stanford A (ascending aorta) - more WORRYING (compromise blood to brain, cause aortic regurg):
  
  • BP control - B-blockers & CCB (aim 100-120mmHg)
  • Immediate referral for vascular surgery
• Stanford B (descending aorta)
  
  • BP control - B-blockers & CCB (aim 100-120mmHg)
  • Urgent referral to vascular surgery (repair likely if complicated)

Question 174

Comparing different types of vascular ulcers:

• Hx
• Location
• Characteristics - ulcer & surrounding skin
• Tx

Answer 174

Venous:

• Hx: varicose veins, previous DVT, obesity, preg, recurrent phlebitis
• Location: lower calf-medial malleolus
• Characteristics: mild pain
  
  • Ulcer - shallow/flat margins, exudate, sloughing @base, granulation tissue
  • Surrounding skin - haemosiderin staining, eczematous, oedematous, thickening skin, (normal CRT)
• Tx: compression bandaging, leg elevation, surgical Mx

Arterial:

• Hx: HTN, DM, smoking, prev vascular disease
• Location: pressure points, toes/feet, lateral malleolus, tibia
• Characteristics: painful
  
  • Ulcer - punched-out/deep, irreg shape, necrosis, no exudate (unless inf)
  • Surrounding skin: thin, shiny, reduced hair, 6Ps (pallor, pain, perishingly cold, pulselessness, paraesthesia, paralysis)
• Tx: revascularization (e.g. bypass), anti-platelet, manage RFs

Neuropathic:

• Hx: DM (peripheral neuropathy), trauma, prolonged pressure
• Location: plantar foot, tip of toe, lateral-fifth metatarsal
• Characteristics: no pain
  
  • Ulcer - deep, surrounded by callus, insensate (no feeling)
  • Surrounding skin - dry, cracked, callus, insensate
• Tx: debridement, topical GF

Question 175

Chronic venous insufficiency & varicose veins - presentation? Ix? Mx? Complications of varicose veins?

Answer 175

Presentation:

• Oedema, haemosiderin deposition, lipodermatosclerosis (inverted-champagne bottle), eczema, venous ulcers
• Varicose veins - dilated tortuous, superficial veins
  
  • Pain, swelling, itching, restless legs, cramps
  • Feel for thrombosis (hard = thrombophlebitis)
  • Cough impulse at SFJ (for Saphena Varix - dilation of saphenous vein @junction w/ femoral vein)
  • Trendelenburg test
    
    • Lying flat, lift up leg & empty veins
    • Compression over SFJ –> stand up (maintain pressure) - if do not fill = competent valves below SFJ
    • If do fill = incompetent valves below SFJ (blood flow from deep to superficial vein via perforating veins)
    • Repeat with pressure lower down until filling stops
  • Perthe’s test - apply tourniquet to mid-thigh + walk for 5-mins –> compresses superficial vein
    
    • Less distended - normal deep veins as calf compression pushes blood into deep venous system
    • Remain distended - impaired deep veins
  • Doppler US for reflux
• Warfarin - previous DVT
• Abdo mass with compression

Ix: duplex USS (allow DVT to be ruled out)

Venous insufficiency Mx:

• ABPI > 0.8 –> Compression bandaging
• Varicose veins:
  
  • Conservative - weight loss, avoid standing for prolonged periods
  • Minimally invasive procedures - injection sclerotherapy, endovenous radiofrequency ablation
  • Surgical - vein ligation

Varicose Veins complications:

• thrombophlebitis - Tx for superficial: NSAIDs
• Eczema
• Bleeding
• Haemosiderin deposition
• Lipodermatosclerosis (champagne bottle)
• Ulceration

Question 176

Benign breast diseases - types? presentation? Dx? Mx?

Answer 176

Breast pain

• Presentation:
  
  • Benign breast pain, cyclic/non-cyclic (fibrocystic breast)
  • Other causes - inf, trauma (fat necrosis), haematoma (on anti-coag)
• Dx: nothing if no masses/concerning features on exam
• Mx:
  
  • Reassurance, supportive bra
  • Ibuprofen/voltarol gel
  • Evening primrose oil

Breast Cyst

• Presentation:
  
  • Sudden tender, small, smooth lump –> disappears after a period
  • Multiple w/ previous similar episodes
  • Younger
• Dx:
  
  • USS only <35ys; USS + MMG ≥35yrs
  • USS - fluid-filled, well-circumscribed collection
    
    • Disappears after aspiration, biopsy if solid posterior residual lesion
• Mx: USS-guided aspiration only if large + painful

Fibroadenoma - common benign breast tumours of both glandular and stromal tissue

• Presentation:
  
  • Mobile, easily palpable, can be lobulated
  • Young women
• Dx:
  
  • Age-dependent
  • Biopsy >25yrs/very large/concerns over phyllodes tumour
  • Re-scan small FAD again in 3-6 months to monitor for rapid enlargement
• Mx:
  
  • Surgical excision - if rapid enlargement/>4cm
  • Reassurance otherwise

Mammary duct ectasia (periductal mastitis)

• Presentation:
  
  • Milk ducts dilate and fill with fluid –> breast pain + green-white nipple discharge
  • Assoc w/ smoking, menopause
• Dx: can mimic breast cancer –> need triple assessment
• Mx: conservative ± abx ± surgery for complications

Breast abscess

• Presentation:
  
  • breast-feeding, DM, post-op, smokers
  • Red, hot, tender fluctuant mass, systemic (febrile, unwell)
  • Acute Hx
• Dx:
  
  • Too painful to tolerate MMG - USS only initially
  • MMG on resolution if ≥35yrs
• Mx:
  
  • USS-guided aspiration + Abx
  • Clinical review in 48hrs –> possible repeat aspiration
  • Incision & drainage under GA if overlying necrotic skin

Question 177

Nipple discharge - causes? presentation? Dx? Mx?

Answer 177

Causes:

• Physiological (90%)
• Duct ectasia - benign, normal in post-menopausal, multi-duct
• Intraductal papilloma - papilloma growth in single duct
• Epithelial hyperplasia
• Galactorrhoea - pregnancy/prolactinoma

Presentation:

• Smokers - green multi-duct
• Duct ectasia (dilated ducts) - yellow multi duct –> cheesy watery discharge ± bloodstained
• Prolactinoma/pregnancy - b/l milky, multi duct
• Underlying pathology (cancer, PCIS, papilloma) - bloody discharge from a single duct (can be watery/serous)
  
  • Epithelial hyperplasia has a similar but less severe presentation

Dx:

• Age-related ± MRI
• USS retro-areolar w/ biopsy of visible lesions

Mx:

• Treat cancer incl. excision of NAC
• Papilloma - single/total duct excision

Question 178

Breast carcinoma - RFs? types (incl. receptors, axilla involvement)? Presentation? Dx? Mx?

Answer 178

RFs:

• Increase:
  
  • FHx (breast, ovarian, colon)
  • Genetic mutations (BRCA1/2 - sign increase risk of breast/ovarian cancer)
  • Post-menopausal, ≥40yrs, early menopause/late menarche
  • OCP (decreases risk of endometrial/ovarian/colorectal)
• Decrease: pregnancy, breastfeeding

Types:

• Invasive ductal carcinoma - 70%, firm/hard
• Lobular carcinoma - 10%, bilateral in 20%, multicentric
• Tubular - 10%, small stellate lesions, picked up on screening
• Other: medullary (soft/fleshy, good prog), mucoid (rare, good prog), Paget’s (nipple excoriation, underly intraductal tumour, poor prog)

Receptor involvement: ER (oestrogen), PR (progesterone), HER2 (Herceptin)

• ER/PR-receptive = good prognostic signs
• HER2 = bad prognostic sign (but now Tx for it)

Presentation:

• Post-menopausal
• Firm mass ± skin tethering/dimpling
• LNs in axilla

Ix:

• Triple assessment:
  
  • ≥35yrs - MMG + USS + biopsy (FNA/core biopsy)
  • <35yrs - USS + biopsy –if proven cancer–> MMG + MRI
• Axilla - USS + biopsy if any abnormal LNs
• Staging CT & bone scan if >3cm/LNs involved - TNM
  
  • T1-4 (size, 4= invasive), N0/1 (no/yes), MO/1 (no/yes)
  • Mets - bone, lung, liver
  • Nottingham prognostic index - size & grade of tumour & LNs
• MRI if lobular cancer

Mx:

• ALWAYS - Surgery:
  
  • _​_Mastectomy/wide local excision - depends on tumour size vs breast size
• ALWAYS - SLNB/ALNC
  
  • ​Sentinel LN biopsy vs axillary LN clearance = remove all
• Chemo - if involve LNs/large cancer/young patient/HER2 +ve/Triple -ve disease
• Radio - >4cm, LN involvement, skin/muscle involvement
• Endo: ONLY if ER +ve
  
  • Tamoxifen pre-menopausal
  • Letrozole if post-menopausal
  • Herceptin (Trastuzumab) for HER2+
• MDT approach (incl psychological support)

Question 179

Pre-cancerous breast masses

Answer 179

Ductal carcinoma in-situ

• Def:
  
  • Limited to mammary ducts by basement membrane –> can’t metastasise
  • Can transform into invasive (ductal) malignancy
• Presentation: often not palpable, picked up on screening, can have nipple discharge (more commonly is papilloma)
• Mx: breast-conserving surgery - wide local excision

Lobular carcinoma in-situ

Question 180

Describing a lump?

Answer 180

Localise + describe lump: 3Ss, 3Cs, 3Ts

• Site, Size, Shape
• Consistency, Contours, Colour
• Tenderness, Temperature, Tethering

Question 181

DVT - def? RFs? Presentation? Scoring & Ix? Mx?

Answer 181

Def: occlusion of deep vein in lower limb

RFs: SICC - Surgery, Immobility, Cancer, COCP

Presentation: pain, swelling (if extends proximally to iliacs –> bilateral swelling), pitting oedema, warmth, erythema

Scoring & Ix: Well’s score

• 0-1= D-Dimer –sign raised–> as below
• ≥2 = proximal leg vein USS + D-Dimer
• Obtain baseline before starting anti-coag: FBC, U&E, LFTs, clotting screen

Mx:

• Ongoing anticoagulation - DOAC/Warfarin
• Provoked - 3 months (SICC)
• Unprovoked - >6 months + thrombophilia testing

Question 182

Breast Diagnostics

Answer 182

Screening MMG

• ≥50yrs - 3yrly
• >40yrs - attending clinics

USS focused:

• <40yrs USS only
• ≥40yrs USS + MMG

Biopsy:

• all breast lumps in women >25yrs
• USS-guided

Question 183

Hernia (surgery) - def? types? Mx?

Answer 183

Def: protrusion of a viscus through its wall

Types:

• Incisional hernia - iatrogenic following surgery
• Groin hernia - ASIS & pubic tubercle palpated:
  
  • Femoral (W>M) - below and lateral to the pubic tubercle, requires more urgent repair than inguinal hernia - high risk of strangulation
  • Inguinal - above & medial to the pubic tubercle
    
    • Direct = weakness in posterior wall of inguinal canal, abdo contents emerge medial to deep ring and through superficial ring
    • Indirect (75%, most common hernias in M/W) = abdo contents passes through inguinal canal through deep ring and exits via superficial ring
    • Reduce hernia & compression on deep inguinal ring ask the patient to cough if it is direct it will reappear
  • Other groin lumps:
    
    • Lymphadenopathy - along inguinal ligament
    • Vascular - pulsatile varicose veins below inguinal ligament

Mx: surgical (mesh)

NOTE: hernias are safer the larger the defect as less likely to strangulate

Question 184

Colorectal cancer - Presentation? Ix? Mx? Screen?

Answer 184

Presentation:

• Bowel habit change
• Palpable mass
• IDA, PR bleed (clots, fresh)
• Acute (obstruction, perforation)

Ix: colonoscopy

Mx: based on TNM staging post-CT

• Colon cancer
  
  • T4 (local advancement) –> neoadjuvant Tx
  • Otherwise –> colonic resection –> if T3+/nodal disease –> adjuvant chemo
• Rectal cancer
  
  • T3-4 –> neoadjuvant Tx –> colonic resection –> if T3+/nodal disease –> adjuvant chemo
  • T1-2NOMO –> transanal excision

Screen: 60-74yrs FIT testing (or FOB)

Question 188

Appendicitis - presentation? DDx? Scoring? Mx?

Answer 188

Presentation:

• Acute umbilical to RIF pain (McBurney’s point)
• Tenderness + guarding (if rigid abdo - perforated apendix)
• N&V –> anorexia (not wanting to eat anything from nausea), change in bowel habit
• Rovsig’s sign - pain in RIF on LIF palpation
• Psoas sign & Obturator sign

DDx: ectopic, ovarian torsion, IBS/D, bowel obstruction

Ix:

• Urinalysis, bloods - FBC, U&E, CRP
• USS abdo/pelvis –> consider contrast-enhanced CT-AP

Alvarado score - >4 = likely appendicitis

Mx:

• A-E (incl. fluids)
• Sepsis bundle - abx when Dx confirmed
• Laparoscopic appendicectomy
• Conservative only if uncomplicated appendicitis

Question 190

Bowel obstruction - immediate Mx, small vs large bowel obstruction - causes, features, Mx?

Answer 190

Immediate Mx:

• NBM, Ryles tube (aspirate stomach contents)
• IV fluids
• AXR -> CT (identify transition point of obstruction)

Small bowel obstruction:

• Causes: Adhesions (prev surgery?), Hernia, Malignancy (incl. non-GI e.g. ovarian)
• Features: central dilated loops of bowel, >3cm, valvulae coniventes
• Mx: surgery (but can be counterintuitive if surgery was cause), gastrografin (oral contrast medium, acts as an osmotic laxative)

Large bowel obstruction:

• Causes: tumour, volvulus
• Features: peripheral dilated loops of bowel, >6cm, haustra
• Mx: surgery, flatus tube (in sigmoid volvulus)

NOTE: 3/6/9 rule

Question 191

Right & left hemicolectomy - indications, process & what are you left with?

Panproctocolectomy - indications, process & what are you left with?

Total vs subtotal colectomy - process & what are you left with?

Hartmann procedure - indications, process & what are you left with?

Anterior vs AP resection - indications, process & what are you left with?

Urostomy (ileal conduit) - indications & process?

Answer 191

Right hemicolectomy - right colon

• Indication: problems affecting ascending colon e.g. malignancy
• Process: removing from ileocaecal valve to 1/3 the way along the transverse colon
• What are you left with:
  
  • Primary anastomoses (ileum attached to the remaining colon)
  • Sometimes left with a stoma

Left hemicolectomy - left colon

• Indication: problems affecting the descending colon e.g. tumour
• Process: removing from 2/3 the way along the transverse colon to the sigmoid area
• What are you left with: primary anastomoses from the transverse colon to the sigmoid colon

Panproctocolectomy vs total colectomy vs subtotal colectomy

• Panproctocolectomy - total colon & rectum e.g. UC
  
  • Indication: a diffuse disease affecting the full colon e.g. FAP (familial adenomatous polyposis) or UC
  • Process: remove full colon & rectum (from ileocaecal valve to the anus)
  • What are you left with: end ileostomy (loose end of ileum brought to the skin)
• Total colectomy:
  
  • Process: remove full colon but not the rectum
  • What are you left with: ileal-pouch anal anastomosis (loose end of ileum used to reform a rectum, don’t need a stoma)
• Subtotal colectomy:
  
  • Process: remove colon except for the rectum and part of the sigmoid colon
  • What are you left with: end-ileostomy & rectal/sigmoid stump

Hartmann procedure - emergency sigmoid colon

• Indication: emergency circumstances for diseases affecting sigmoid colon e.g. malignant obstruction, sigmoid volvulus, diverticular complication (e.g. perforation - healing suboptimal so don’t want to create anastomoses as unlikely to succeed)
• Process: sigmoidectomy
• What are you left with: end-colostomy and rectal stump –> at a future date can be reversed but many just stay with end-colostomy

Anterior vs AP resection - for rectal tumours (A higher; P lower)

• Anterior:
  
  • Indication: higher rectal tumours
  • Process: removing sigmoid colon + top part of the rectum
  • What are you left with: end-colostomy/primary anastomoses ± defunctioning loop ileostomy
    
    • DLI - loop of ileum brought to surface, split so 2 lumens on surface –> divert faecal stream (into stoma bag) from distal anastomosis = gives best chance of healing
  • NOTE: sometimes low anterior resection is performed where the distal margin of resection is brought down (very little rectum remains)
• AP (abdominoperineal):
  
  • Indication: low-lying rectal tumours
  • What are you left with: end-colostomy
  • Process: remove everything up to the top of the sigmoid colon

Urostomy (ileal conduit)

• Indications:
  
  • Bladder cancer (had cystectomy)
  • Neurogenic bladder
    Radiation injury to the bladder
  • Chronic pelvic pain
• Process: removing some ileum, forming pouch & bringing to surface so forms stoma - ureters are connected to this pouch

Question 192

Stoma differentiation & examination

Answer 192

Colostomy - RIF, flushed, normal faecal matter

Ileostomy - LIF, spouted (as contents irritant to skin), runny & green faecal matter

Urostomy (via ileal conduit) - if urinary flow not possible via bladder/urethra e.g. post-cystectomy with bladder cancer

• NOTE: nephrostomy is an opening created between the kidney & skin if urine flow from the kidney to the ureter is blocked e.g. in pyonephrosis (renal stones + inf)

Stoma examination:

• Hands around stoma and ask to cough –> check for hernia + check for skin changes
• Offer stoma rectal examination (finger into stoma)

Question 194

Acute abdomen - def? immediate Tx & Ix?

Answer 194

Def: sudden, severe abdo pain that requires urgent medical/surgical attention

Immediate Tx & Ix:

• Immediate Tx - NBM, IV fluids, analgesia
• Bedside - urine dip
• Bloods - basics, VBG (lactate), amylase, G&S, clotting
• Imaging - errect CXR, AXR (bowel obstruction):
  
  • USS/MRCP/ERCP - gallstones
  • CT-KUB - renal stones
  • CT-AP - perforation/obstruction
  • CT-angiogram - ischaemic/bleed/AAA

Question 200

Acute pancreatitis - causes? Patterns of injury? Pathophysiology? Ix? Mx? Complications? Severity score?

Answer 200

• Causes: alcohol, gallstones (GET SMASHED)
  
  • Duct obstruction: gallstones (50%), trauma, tumours
  • Metabolic/toxic: alcohol (33%), drugs, hypercalcaemia/hyperlipidaemia
  • Ischaemia: shock
  • Infection/inflammation: viruses (mumps), AI
• Patterns of injury:
  
  • Periductal – cause: duct obstruction
    
    • Necrosis of acinar cells near ducts
  • Perilobular – cause: ischaemia (shock)
    
    • Necrosis @edges of lobule – blood supply comes w/ ducts = periphery most affected
  • Panlobular – develops as ½ progress
• Pathophysiology: vicious cycle - activated enzymes –> acinar necrosis –> enzyme release
  
  • Lipase release –> fat necrosis (Ca ions bind to free fatty acids forming soaps = yellow/white deposits)
• Ix:
  
  • Bloods – FBC, U&E, LFTs, CRP, Amylase
  • Imaging – USS (looking for biliary problem, sentinel loop – early sign of ileus), CXR
  • NOTE: Epigastric pain –> remember to do rectal exam (looking for melaena)
• Mx - supportive (IV fluids + analgesia first)
  
  • Resus patient (IV fluids, analgesia, antiemetic, abx) –> ITU if glasgow score >3
  • VTE prophylaxis
• Complications:
  
  • Pancreatic pseudocyst – cystic space wo/ epithelial lining, lined with necrotic & granulation tissue –> can be infected –> abscess
  • Systemic: shock, hypoglycaemia, hypocalcaemia

Severity criteria = GLASGOW score (PANCREAS):

• PaO2
• Age
• Neutrophils (WBC)
• Ca
• Renal funct (urea)
• Enzymes (LDH)
• Albumin
• Sugar (glucose)

Question 201

Diverticulosis vs Diverticular disease vs Diverticulitis? Acute diverticulitis classification?

Presentation? Ix? Mx?

Answer 201

Diverticulosis: colonic outpouching in mucosa & submucosa of colon - happen @weak points in colonic wall subject to increased pressure (common in elderly, low fibre diet)

Diverticular disease: above + Sx

Diverticulitis: infection & inflammation of diverticulum

• Hinchey classification for acute diverticulitis:
  
  1. a) Pericolic phlegmon & inflammation, no fluid collection b) pericolic abscess <4cm
  2. Pelvic/interloop abscess/abscess >4cm
  3. Purulent peritonitis
  4. Faeculent peritonitis

Presentation:

• RFs: >50yrs, low dietary fibre
• LIF pain, raised WCC, fever, painless rectal bleed

Ix:

• FBC, U&E, CRP, (BC, ABG & lactate if septic)
• Contrast CT abdo (if suspected acute diverticulitis)
• Other imaging:
  
  • CXR (rule out pneumoperitoneum)
  • Colonoscopy/sigmoidoscopy (if Dx unclear, could be cancer/ischaemia)
  • CT angiogram (if excess bleeding)

Mx:

• Asymptomatic diverticulosis:
  
  • Increased fibre & fluids
  • Excercise, weight loss, stop smoking
  • Fybogel - if constipated
• Symptomatic diverticular disease:
  
  • Above + paracetamol
  • PO Dicycloverine = anti-spasmodic (for abdo cramping)
• Acute diverticulitis:
  
  • Uncomplicated: above + oral abx (amoxicillin)
  • Complicated:
    
    • Excess bleed - resus + endoscopic band ligation/surgery
    • Abscess/perf/fistulae/obstruct - radiological drainage/surgery + IV abx
  • Reccurent = open/laparoscopic resection

Question 202

RFs? Types of stone? RUQ pain Ix?

Biliary colic - Def? Presentation?

Cholecystitis - Def? Presentation? Ix?

Ascending cholangitis - Def? Presentation? Acute Mx?

Answer 202

RFs (5Fs): Fat, Female, Fertile, Forty, Fair

Types of gallstone: mixed (80%), cholesterol (10%, bigger & smaller in #), pigment (10%, smaller & more numerous)

RUQ Pain Ix:

• Abdo USS
• Stone in CBD (common bile duct) –> ERCP
• Deranged LFTs/dilated ducts –> MRCP
• None of above –> cholecystectomy

Biliary colic:

• Def: pain due to blockage of bile flow due to a gallstone
• Presentation: RUQ pain, worse after fatty meals (stimulates gallbladder contraction –> bile release for fat emulsification)

Cholecystitis:

• Def: inflammation of the gallbladder (typically in context of gallstones)
• Presentation: RUQ pain (+ tenderness - Murphy’s sign), FEVER
  
  • ​Murphy’s only +ve if not present on the left as well
• Ix:
  
  • Urine dip – infection, bHCG
  • Bloods – FBC, U&E, LFTs, CRP, amylase, clotting screen
  • Imaging – USS (want to be fasted – so gallbladder larger), erect CXR (pneumoperitoneum – perforation of duodenum)

Ascending cholangitis:

• Def: inf ascending the biliary tree, usually in the context of gallstone
• Presentation (due to obstruction of Common Bile Duct - bile stagnates and becomes infected):
  
  • Charcot’s triad - RUQ pain, fever, JAUNDICE
  • Reynold’s pentad (severe) - above + shock + confusion
• ​Surgical EMERGENCY - Mx via sepsis 6 protocol (abx = Tazocin) + drain obstruction:
  
  • Endoscopic retrograde cholangiopancreatography (ERCP) - Dx & Tx (dye can be used to enhance the obstruction) - endoscope passed up to Ampulla of Vater with wire passed into the biliary system
    
    • Complications: pancreatitis, bleeding (from dilation of AoV), perforation
  • Percutaneous transhepatic cholangiogram (PTC) - interventional radiology - passing a wire through the liver into a hepatic duct and then into the top end of the biliary tree –> dislodge stone/alternative route for bile to flow - leave in cholecystostomy
  • Cholecystostomy - interventional radiology - insert wire directly into the gallbladder and allow it to be drained - leave in cholecystostomy
  • Patients will likely require a later cholecystectomy (after dealing with the acute infection)

Question 203

Liver transplant - indications? Unsuitable group? Surgery scar? Post-transplant care?

Answer 203

Indications:

• Acute liver failure - acute viral hep, paracetamol overdose
• Chronic liver failure

Unsuitable for liver transplant:

• Sign. co-morbidity (renal/heart failure)
• Excess weight loss/malnutrition
• Active hep B/C (other inf), end-stage HIV
• Active alcohol - 6 months abstinence needed

Surgery: Rooftop/Mercedes Benz scar

Post-transplant care:

• IS - steroids, azathioprine, tacrolimus (careful drug monitoring)
• Conservative - no alcohol/smoking, monitor for disease recurrence, cancer, transplant rejection (fatigue, fever, jaundice, abn LFTs)
• Tx opportunistic inf

Question 204

Ptosis causes?

Answer 204

Bilateral:

• MG
• Myotonic dystrophy
• Tabes dorsalis (syphilis) = Argyll-Robertson pupil

Unilateral:

• 3rd nerve palsy (down & out, dilated, ptosis)
• Horner’s syndrome (ptosis, meiosis, anhydrosis)

Question 205

Proximal muscle weakness causes?

Answer 205

CONGENITAL MIND

• CONGENITAL - mitochondrial
• Metabolic - Cushing’s, hypothyroidism
• Inflammatory - dermato/poly/inclusion body myositis
• Neuromuscular - MG/LEMS
• Dystrophy - Becker