PACES Flashcards
Resp exam - do not forget what?
Pleural effusion, pneumothorax, lung collapse, lung fibrosis, consolidation on resp exam?
Hands/arms:
- CRT, clubbing (PF, lung cancer, CF, bronchiectasis, sarcoidosis/TB)
- Co2-retention flap (T2RF) - check pulse while doing
- RR (arm over chest while taking pulse)
Head/neck: JVP, tracheal assessment (3 fingers, palpate either side of trachea), cricosternal distance (<3 fingers = lung hyperinflation), cervical LNs
Chest:
- Apex beat
- Chest expansion (front/back)
- Percussion, auscultation, vocal resonance (front/back incl. supraclavicular + axillae)
Other: peripheral oedema, DVT

Asthma - def? Presentation? Ix? Severity? Short-term/long-term Mx incl. conservative? Mneumonic for conservative long-term Mx?
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
- 33 92 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:
- SABA (reliever)
- SABA + ICS (preventer)
- SABA + ICS + LTRA (leukotrine receptor antagonist e.g. montelukast)
- SABA + ICS + LABA (+ LTRA stopped unless good response)
- SABA + MART (ICS + LABA COMBO) (+ LTRA)
- NOTE: maintenance & reliever therapy (MART) - used as preventer & maintenance inhaler
- Specialist input (e.g. for oral steroids)

COPD - definition? Signs & Sx? New Dx & exacerbation Ix/Mx? Prognosis factors?
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)
- 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
- Conservative - stop smoking, influenza + pneumococcal vaccine, inhaler device training
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?

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

PE - def? Sx? RFs? Scoring & Ix? Mx?
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)
- Ix for cancer –> any Sx?

What area of the lungs does aspiration pneumonia normally affect? Mx?
The right bronchus is more vertical and so aspiration normally affects the right lung base = coarse crackles
Mx: O2, suction, abx, NBM until SALT review
Bronchiectasis - definition? causes? presentation? Ix? Mx?
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)

Sarcoidosis - def? presentation? Ix? Mx?
Def: a chronic multisystem disease characterized by the formation of non-caseating granulomas across various tissues
- Physiologically granulomas are supposed to form around insulting body e.g. infection but in sarcoidosis form for no apparent reason
Presentation:
- Profile - Afro-Caribbean, female, 20-40yrs
- Lungs - SoB, dry cough
- Skin - erythema nodosum & lupus pernio
- Other - dry eyes (uveitis, conjunctivitis, optic neuritis), polyarthralgia, fever/fatigue/weight loss, cardiac (cardiomyopathy, conduction defects), neuro (cranial nerve palsies)
Ix:
- Bloods:
- Serum ACE (high), serum soluble IL-2 receptor, ESR
- Serum Ca (activated macrophages in sarcoidosis prod 1alpha-hydroxylase –> excess activated vitamin D)
- CXR (bilateral hilar lymphadenopathy)
- Gold-standard: transbronchial biopsy (non-caseating granulomas)
Mx:
- Asymptomatic - NSAIDs/no Tx
- Symptomatic:
- Long-term steroids + bisphosphonates (osteoporosis protection)
- Steroid-sparing agents - Methotrexate/Azathioprine

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

Restrictive vs Obstructive lung conditions
Restrictive (belt around lungs) - reduced lung volume (restricted expansion) + FEV1/FVC ratio > 80% (normal/increased - from decrease in FVC)
- Poor breathing mechanics - Myasthenia gravis, scoliosis, obesity
- Interstitial lung disease - pulmonary fibrosis, sarcoidosis
Obstructive (hand choking airway) - increased lung volume (air trapped) + FEV1/FVC ratio < 80% (decreased - reduced expiratory volume)
- Airway obstruction (from inflammation of airways & problem exhaling) - Asthma, COPD (chronic bronchitis, emphysema), Bronchiectasis
Chronic bronchitis vs emphysema?
Chr bronchitis - defined by clinical features (productive cough for ≥ 3 months/yr for ≥ 2 yrs - excess mucus & less mobile cilia) - airflow blocked by mucus –> decreased O2, increased CO2 –> cyanosis = BLUE BLOATER
Emphysema - defined by structural changes (enlarged air spaces –> reduced gas exchange) - breath slowly through pursed lips to increase airway pressure = prevent collapse –> PINK PUFFER
- Centriacinar - proximal alveoli affected, assoc w/ smoking, upper lobes
- Panacinar - entire alveoli affected, assoc w/ alpha1-antitrypsin def, lower lobes
- Paraseptal - distal alveoli affected, lung peripheries –> can rupture –> pneumothorax
NOTE: commonly co-exist
Both = COPD –> airway obstructed –> reduced FVC (air expired in complete breath) & very reduced FVC1 (air expired in 1s) –> low FVC1/FVC ratio (<0.7 for Dx)
- COPD –> vasoconstriction to redirect blood flow to well-oxygenated areas of the lungs –> if widespread –> pul HTN –> cor pulmonale
Pleural effusion - signs? causes? Ix? Mx?
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
Pneumothorax - Def? RFs? Causes? Ix? Mx? How do you identify a Tension Pneumothorax?
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)
Lung cancer - epi? presentation? types? Ix? Mx?
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)
- Classically assoc w/ paraneoplastic hypercalcaemia, as tumour may release PTHrP
- 2nd most common in non-smokers
- 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
-
Adenocarcinoma (MOST COMMON LC)
- 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
Mneumonic for life-threatening asthma signs?
33 92 CHEST: ≤33 (PEF) ≤92 (O2 sats)
- Cyanosis
- Hypotension
- Exhaustion
- Silent chest
- Tachycardia
4Ps of respiratory conservative Mx?
Persuade to stop smoking
Pul rehab
Prick them - influenza + pneumococcal vaccine
Psych issues
Resp scars? Lobectomy/Pneumonectomy DDx? Presentation?
- Axillary thoracotomy scar - chest drains
- Postero/anterolateral thoracotomy scar - lobectomy, pneumonectomy & oesophageal surgery
- Radiotherapy-associated skin changes: dry, thickened, hypopigmented and telangiectasia
Lobectomy/pneumonectomy
- DDx:
- Lung cancer/mets
- Bronchiectasis, lung abscess(s), TB
- Sarcoidosis, COPD
- Presentation: dull percussion & absent breath sounds over affected area
- Complications:
- Fluid - pul oedema
- Bleed - haemothorax
- Inf - wound infection
Lobectomy ddx?
Pneumonectomy ddx?
Lobectomy:
- Cancer usually NSCLC or secondary,
- Infection e.g. localised bronchiectasis/CF with recurrent infection or haemoptysis, lung abscess, aspergilloma, TB,
- Infarction
- Trauma
- Inflammatory: sarcoidosis
- Bleeding,
- Pulmonary nodule
Pneumonectomy:
- Cancer involving more than 1 lobe/diaphragm/pleura/pericardium
- Infection e.g. bronchiectasis, multiple abscesses) NB: dull percussion note and reduced/absent breath sounds over the entire affected hemithorax
Fine vs coarse creps?
Vesicular vs bronchial breathing?
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
IHD - Types? Definition? Dx? Mx?
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)
- Continue DAPT
- ALL immediate:
- 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)

Heart failure def? Pathophysiology? Categories & Causes? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
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)
- Causes of ventricular stiffness:
- 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
- Causes of outflow obstruction/impaired contractility:
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)
- Reduced ejection fraction - prognostic benefit:

How does heart failure look on CXR?
Pulmonary oedema (fluffy alveolar shadowing = bilateral perihilar consolidation = batwings distribution) ±:
- Kurly B-lines (peripheral septal lines)
- Cardiomegaly (thoracic ratio >0.5)
- Upper lobe venous diversions (tubes going up towards apex instead of lines)
- Pleural effusion (costo-phrenic blunting)

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

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

Key heart murmurs?
Accentuation manoeuvres?
Causes?
Left vs right heart valve abn epidemiology?
Mx?
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)
-
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)
-
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)
- 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): Senile calcification (aortic valve)
- MR: IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- AR: acute (infective endocarditis, aortic dissection), chronic (CTD, RHD, HTN, congenital)
- 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
Management:
- AS:
- C: 6-monthly ECHO, exercise-stress test if asymptomatic
- M: RF optimisation (statins, HTN, DM), HF Sx (diuretics, ACEi)
- S: Based on severity/comorbid - STS-PROM (surgical risk calc)
- If severe AS:
- Medically fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
- Not fit = Transcatheter aortic valve replacement (TAVR)
- Acutely Sx/cardiogenic shock = Balloon valvuloplasty
- If severe AS:
- MR:
- M:
- ACEi ± B-blockers (as HTN worsens MR)
- Tx AF & anti-coagulate
- Diuretic (if refractory to surgery)
- S: for acute MR (post-MI, chordae tendinae rupture), asymptomatic LVEF <60%, symptomatic LVEF >30%
- Valve _R_epair > _R_eplacement
- M:
- AR:
- M: asym + Reassurance (good prog)
- Unfit for surgery/waiting - ACEi & vasodilators (e.g. hydralazine)
- S: acute/Sx/severe = surgery
- Valve _R_eplacement > _R_epair
- M: asym + Reassurance (good prog)
-
MS:
- C: asymptomatic - Monitor
- M:
- AF Tx, anti-coagulate & diuretics (if Sx/severe)
- S: Sx/severe - can do balloon valvuloplasty/replacement
- Valvuloplasty = lateral thoracotomy scar
- Do not do percutaneously if persistent left atrial thrombus/rigid calcified valve –> need open heart surgery (CABG, concurrent severe MS)

Atrial fibrillation (AF)
- Def? Causes? Ix? Mx?
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)
- Echo (valve check)
- Bloods - U&E, Mg (QT interval), Troponin (ischaemic), TFTs
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)
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
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)
Infective endocarditis - RFs? Ix? Dx criteria? Mx?
Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?
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)
3rd & 4th heart sounds - sounds & cause?
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)
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?
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)
Causes of raised JVP (>4cm)?
JVP + hepatojugular pressure (RUQ), rockstar hand
PQRST:
- Pul HTN/PE/Pericarditis/Pericardial effusion/PS
- Quantity of fluid (fluid overloaded)
- RHF
- SVC obstruction
- Tamponade/TR
SVC obstruction - presentation? Tx?
Presentation: swollen face and neck and distended veins on her chest in background of cancer
Mx: dexamethasone to reduce tumour swelling
- Insert EV stent if stridor (after intubation and steroids)
Bradycardia arrhythmia with a palpable pulse (peri-arrest) - Mx?
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
- Also considered unstable if:
- 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)
Heart block causes? types? Ix? Mx? Complications?
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
- Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
- 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
Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?
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:
- Prepare for DC cardioversion
- IV amiodarone, b-blocker

Types of pacemaker? When to use each type? Complications?
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)
- Primary prevention = @risk of serious ventricular arrhythmia
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
What are prominent V waves in the JVP indicative of?
What are cannon A waves in the JVP indicative of?
What is a prominent x descent in the JVP indicative of?
Tricuspid regurgitation
Complete heart block
Acute cardiac tamponade/Constrictive pericarditis
Immediate Mx of rheumatic fever?
Aspirin prn
Benzylpenicillin IM stat –> 10 day course of benzylpenicillin PO
Atrial flutter Mx?
- Treat underlying cause
- Anticoagulate as you would for atrial fibrillation
If haemodynamically unstable: rate control or cardioversion
What is an Austin Flint murmur? When in the heart cycle is an Austin flint murmur heard, and what causes it?
What:
- ‘Rumbling mid-diastolic murmur’
- Associated with severe aortic regurgitation
- Best auscultated in 5th ICS in MCL
- Caused by blood flowing back through the aortic valve and over the mitral valve
When:
- Mid-diastole
- Caused by regurgitant jet that runs over the mitral valve leaflets
Cardiac tamponade - key finding on exam? Triad? Mx?
Pulsus paradoxus - BP variation between inspiration & expiration (≥10)
Beck’s triad (50%):
- Raised JVP
- Muffled heart sounds
- Hypotension
Mx:
- IV fluids (RV filling depends on venous pressure & effusion is constricting)
- Echo –> refer to cardiology for pericardiocentesis
- Coagulation profile (to prep for pericardiocentesis)
Types of cardiac scar?
- Midline sternotomy + leg scar = CABG
- Midline sternotomy (no leg scar) = Valve replacement most likely (rarely can be CABG without vein graft)
- Left subclavicular -> pacemaker, debfibrillator, resynchronisation device
- L shaped scars under either breast -> L/R Thoracotomy
- 19yrs, SoB on exertion, one episode of AF
- Exam - fixed splitting of 2nd HS, mid-diastolic murmur in pulmonary area
- ECG - slight RAD, incomplete RBBB
Dx? Assoc conditions? Ix?
ASD - commonest is ostium secundum
- Mid-diastolic murmur + fixed split S2
- High risk of AF & paradoxical emboli (prev stroke?)
- NOTE: commonest inherited cardiac condition to present in adulthood (as can be asymptomatic in childhood)
- NOTE: this is not Eisenmenger’s syndrome as patient not cyanotic
Assoc w/ down’s syndrome (& AVSD), Turner’s & Noonan’s syndrome
Ix:
- ECG - incomplete RBBB (90%, can be normal variant), RVH (T-wave inversion V1-3), P pulmonale (tented P-waves), AF
- Ix: bubble study (+ RV dilatation)
- Also done for patent foramen ovale (PFO)
Constrictive pericarditis - def? Cause? Ix? Complication?
Def: chr inflamed pericardium (this is why colchicine is given for 3 months in normal pericarditis)
Cause: classically previous TB in the pericardium
Ix:
- (Exam - pericardial knock on auscultation (bit old school))
- Kussmaul’s sign - JVP rises on breathing in
- Small heart on CXR ± calcifications
- Low voltage ECG w/ T-wave inversion/flattening (could also be pericardial effusion)
Complication: cardiac liver cirrhosis
- Right ventricle struggles –> tricuspid regurg (pulsatile liver) –> liver failure (oedema +++)
Case:
- 26yrs, BP 180/100, femoral pulses weaker than radial pulse
- Mid-systolic murmur in infra-scapular area
- Trying to get pregnant unsuccessfully for 2yrs
What is the Dx? Assoc? What is there a risk of & what advice is given?
Young + very high BP –> must be secondary HTN (causes: endo - Conn’s, Phaeo; coarctation of Aorta (CoA), renal artery stenosis, chronic renal failure)
CoA - tissue restricting flow across aortic arch
- Murmur across the coarctation = left infrascapular area (due to turbulent BF)
- Lower body underdeveloped vs upper (97% men going to gym)
- Assoc: Turner’s (+ Marfan’s, Ehlers-Danlos)
- Short stature, webbed neck, wide-spaced eyes, lack of other secondary sexual characteristics, shield-like chest, short 4th metacarpals/tarsals
- Advice: avoid extreme isometric exercises e.g. weight-lifting –> risk of aortic dissection
- How do you Dx dissection? CT aortogram w/ contrast
How do you know this is the JVP and not the carotid pulse?
- Not palpable
- Double pulsation
- Obliterated when pressure applied at base of neck
- Rises with hepatojugular reflux
- Height changes with respiration
Causes of hepatic decompensation in CLD? Key features of decompensation?
Dx & Mx of decompensated chronic liver disease?
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 - infection - TB/inflammation - pancreatitis/malig (albumin leaking into ascites) OR nephrotic syndrome (pee out albumin so low serum albumin)
- Otherwise = transudative cause - portal HTN (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)

Chronic liver disease
- Functions of liver? Outcome of failure?
- Causes? Ix?
- Important complication?
- Scoring?
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
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)

Jaundice breakdown & causes by type & Ix to differentiate
Pre-hepatic - unconjugated bilirubin comes from breakdown of RBCs
- Haemolysis related-causes (excess prod) - AIHA, SCD, G6PD def, malaria
- Ix:
- Bloods: excess unconjugated bilirubin (exceeds capacity of liver to conjugate it)
- Urine: normal (unconjugated bilirubin is insoluble)
- Stool: normal as liver functioning normally
Hepatic - bilirubin absorbed into liver –> conjugated –> excreted via biliary tract into duodenum
- Liver disease related-causes - cirrhosis, hepatitis, Gilbert’s syndrome, drugs
- Ix:
- Bloods: high unconjugated (liver less able to conjugate quickly) & conjugated bilirubin (leakage of conjugated bilirubin into circulation)
- Urine: dark (leaked conjugated bilirubin is soluble)
- Stool: slightly pale (reduced conjugated bilirubin to GI tract)
Post-hepatic - conjugated bilirubin –> soluble urobilingogen (yellow): 1) Absorbed into circulation –> excreted via kidneys 2) Remaining –oxidised–> stercobilin (brown)
- Biliary disease related-causes (prevent bile outflow) - gallstones, head of pancreas tumour, cholangiocarcinoma, PSC/PBC
- Ix:
- Bloods: high conjugated bilirubin (backlog as obstruction at biliary tree so can’t reach duodenum and instead leaks into blood)
- Urine: dark (leaked conjugated bilirubin is soluble)
- Stool: very pale (no conjugated bilirubin reaches GI tract –> no stercobilin generated)

Chronic diarrhoea - ddx? Sx? Distribution? Histology? Ix? Mx?
IBD
- Truelove & Witts’ severity index = severity criteria for 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)
- Induction:
-
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)
- Induction:
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

Interpreting LFTs + causes
Liver - raised AST + ALT
- Causes: viral/alcoholic hepatitis, hepatotoxic drugs
- Most causes increase in ALT > increase in AST EXCEPT Alcoholic hepatitis - AST 2x > ALT
- AST also rises in muscle damage e.g. MI (normal ALT)
Biliary - raised GGT + ALP
- Causes: gallstones, cholecystitis, cholangitis, PSC/PBC
- NOTE: acute alcohol intake increases GGT
- NOTE: ALP can come from BONE (& placenta) - only biliary if GGT also raised
Most common reason to do AXR? Most common causes of this reason by type?
AXR interpretation?
Key volvulus signs on AXR?
Reason to do AXR: worried about bowel obstruction (small/large bowel)
Small bowel obstruction on AXR:
- valvulae conniventes (from one wall to other)
- Central to image
- >3cm distension
- Causes: adhesions (surgery, sepsis), hernia, neoplasm, volvulus, IBD
Large bowel obstruction on AXR:
- Haustra (Not full width of bowel)
- Outsides of image
- >6cm distension
- Causes: neoplasm, diverticular disease, volvulus, faecal impaction
NOTE: 3/6/9 rule = upper limits of normal for bowel (small = 3cm, large = 6cm, caecum = 9cm)
Volvulus signs (twisting of loop of bowel on mesentery –> balloon animal):
- Coffee bean sign - sigmoid volvulus (large bowel just before rectum)
- Embryo sign - caecal volvulus (large bowel just after small bowel)

Primary Sclerosis Cholangitis (PSC) vs Primary Biliary Cholangitis (PBC)
- Associations? Ix? Tx?
-
PSC - intrahepatic & extrahepatic (horrible & progressive disease, obstructive jaundice)
- Associations: UC (10% but 80% PSC have UC), Cholangiocarcinoma
-
Ix: MRCP, pANCA
- ‘Beads on string’ on ERCP
- Tx: supportive, liver transplant
-
PBC - intrahepatic only (benign condition - middle-aged female, intractable itching)
-
Associations: AI diseases (RA, Sjogren’s, hypothyroidism)
- Sicca syndrome (70%) - dry eyes & mouth (like Sjogren’s syndrome)
- Fat malabsorption w/ steatorrhoea (incl vitamins ADEK):
- Low vit D can cause osteomalacia & proximal myopathy e.g. difficulty climbing stairs & pain in lower back
- Low vit K can cause coagulopathy
- Ix: anti-mitochondrial Ab (AMA), high cholesterol
- Tx: ursodeoxycholic acid (prognostic benefit)
-
Associations: AI diseases (RA, Sjogren’s, hypothyroidism)

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?
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
- Mild - conservative (IV abx, fluids, bowel rest, DM control)
Causes of hepatomegaly, splenomegaly & enlarged kidney(s)?
Hepatomegaly causes:
- Hepatitis (infective and non-infective)
- Hepatocellular carcinoma/hepatic mets
- Wilson’s disease, Haemochromatosis
- Primary biliary cirrhosis
- Leukaemia, Myeloma, haemolytic anaemia
- Glandular fever
- Tricuspid regurgitation
Splenomegaly causes:
- Portal HTN secondary to liver cirrhosis
- Splenic mets
- Haemolytic anaemia, Congestive HF, Glandular fever
Large kidney causes:
- Bilaterally enlarged: polycystic kidney disease, amyloidosis
- Unilaterally enlarged: renal tumour

Different kinds of erythema?
Nodosum - pain over shins
Multiforme - target lesions (life-threatening = Steven’s Johnson Syndrome)
Ab igne - hot water bottle (chr heat exposure)
Marginatum - acute rheumatic fever
Chronicum migrans - lyme disease

Viral hepatitis
Hep A: faecal-oral –> acute
Hep B: blood-borne –> acute/chronic –> serology
- Contains: Core Ag (cAg), E Ag (eAg), DS-DNA, surface antigens (sAg)
- eAg present if active & infective
- Infection response –> generate sAb (surface) + cAb (core)
- Vaccination gives sAg (no reproductive capacity) –> develop sAb (but not cAb)
- Serology:
- HBsAg/HBeAg - actively infecte
- IgM = acute; IgG = chronic
- eAg = highly infective
- HBsAb - protective (cleared/vaccinated)
- HBcAb - only if previously cleared
- HBsAg/HBeAg - actively infecte
- Can be assoc with Polyarteritis Nodosa (vasculitic rash) & mononeuritis multiplex
- Tx: IFN-alpha & lamivudine
Hep C: blood-borne –> chronic –> HCV RNA
- More likely to become chronic than Hep B
- Assoc w/ mixed cryoglobulinaemia (purpuric skin lesions, Raynaud’s phenomenon)
- RF +ve, low C4, normal C3
- Can have +ve anti-LKM1 ab (also in AI hep)
- Tx: PEG-IFN alpha & ribavirin
Hep D: blood-borne –> co/superinfection w/ Hep B virus
Hep E: faecal-oral –> acute, pregnancy

At the end of abdo exam what do you offer to do?
GOR(D)
- external Genitalia
- hernial Orificies
- digital Rectal
AI hepatitis - RFs? Ix? Mx? Complications?
RFs:
- Immune dysregulation (thyroiditis, T1DM, UC, Coeliac, RA)
- Genetic predisposition:
- For T1 AIH - HLA-DR3/4
- For T2 AIH - HLA-DQB1/DRB1
Ix:
- Anti-smooth muscle Ab (SMA), ANA
- T1: Anti-soluble liver antigen or liver/pancreas (SLA/LP), pANCA
- T2: anti-LKM1
Mx: high-dose prednisolone + long-term azathioprine
Complications:
- Cirrhosis in 40%, relapse high if stop IS
How do you tell between spleen & kidney on examination?
Spleen (vs kidney):
- Moves down with inspiration
- You can’t get above it
- Has a notch
- Dull to percussion & not ballotable
Upper GI bleed - scoring for need for intervention? Mx?
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
- F1 Essentials:
- 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
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?
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
-
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 H. pylori -ve: treat underlying cause + PPI (4-8wks, 2nd line = H2 antagonist)
- If recurrent/refractory ulcers –> long-term PPI/H2 antagonist
Young female with unilateral leg tremor
- Psychiatric issues
- Exam: tremor, bradykinesia, dark circles round iris
Dx? Ix? Mx?
Dx: Wilson’s disease (AR)
- Neuropsych issues + liver involvement (no increased risk of HCC unlike haemochromatosis)
- Basal ganglia degeneration - movement disorders, dysarthria
Ix:
- Conservative:
- Urinalysis - elevated urinary copper
- Kayser-Fleischer rings on slit-lamp exam
- Bloods: hepatic bloods, reduced serum ceruloplasmin
- Genetic testing (trinucleotide repeat) - condition appears earlier & earlier each generation
Mx: chelation w/ penicillamine
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?
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
Anal fissure - def? RFs? Presentation? Ix? Mx?
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)
Haemorrhoids - presentation, grading, Ix, Mx?
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
- 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?
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
Acute abdomen sieve
ABC->P
- Appendix
- Bleeding/bowel obstruction/BV obstruction
- GI bleed
- Obstruction - small/large, mechanical/non-mechanical, complete/incomplete
- Ischaemia/infarct
- Cholecystitis/angiitis
- Pancreatitis/Perforation (upper/lower GI)
Hernia (surgery) - def? types? Mx?
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

What are the borders of Hesselbach’s triangle?

Abdominal scars
- Midline sternotomy - AAA, laparotomy
- Rooftop scar - liver transplant, Whipple’s procedure, gastric surgery, oesophagectomy
- Kocher – open gallbladder surgery
- Nephrectomy can also be subcostal (like Kocher) or Rutherford-Morrison (hockey stick)
- Lanz/McBurney’s = Appendicectomy
- Pfannenstiel = C-section/prostatectomy/cystectomy

Colorectal cancer - Presentation? Ix? Mx? Screen?
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)

Gallstone - RFs? Types? DDx?
Biliary colic - Def? Presentation?
Cholecystitis - Def? Presentation? Ix?
Ascending cholangitis - Def? Presentation? Acute Mx?
RFs (5Fs): Fat, Female, Fertile, Forty, Fair
Types of gallstone: mixed (80%), cholesterol (10%, bigger & smaller in #), pigment (10%, smaller & more numerous)
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)
-
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

Appendicitis - presentation? DDx? Scoring? Mx?
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

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

Stoma differentiation & examination
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)
Oesophageal cancer - Presentation? Types? Mx?
Presentation: progressive dysphagia (solids –> then liquids) + FLAWS
Types:
- Squamous cell carcinoma (SCC) - less common in UK, middle oesophagus, RFs: alcohol, smoking
- Adenocarcinoma - most common in UK, lower oesophagus, assoc w/ GORD (long-term –> metaplasia - Barrett’s oesophagus –> eventually become dysplastic/ malignant)
Mx: SURGICAL
- Ivor Lewis oesophagectomy - involves midline laparotomy + right thoracotomy (stomach is mobilised and pushed through oesophageal hiatus)
- McKeown oesophagectomy - as above + left neck incision (oesophagus can be pulled up through neck incision)
Acute pancreatitis - causes? Patterns of injury? Pathophysiology? Ix? Mx? Complications? Severity score?
- 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
-
Periductal – cause: duct obstruction
-
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)
Diverticulosis vs Diverticular disease vs Diverticulitis? Acute diverticulitis classification?
Presentation? Ix? Mx?
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:
- a) Pericolic phlegmon & inflammation, no fluid collection b) pericolic abscess <4cm
- Pelvic/interloop abscess/abscess >4cm
- Purulent peritonitis
- 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:
- Conservative:
- Increased fibre & fluids
- Excercise, weight loss, stop smoking
- Medical:
- Fybogel - if constipated
- PO Dicycloverine = anti-spasmodic (for abdo cramping)
- Acute diverticulitis:
- Uncomplicated: oral abx (amoxicillin)
- Complicated:
- Excess bleeding - resus + endoscopic Tx (e.g. band ligation, 2nd = surgery)
- Abscess/perf/fistulae/obstruct - radiological drainage/surgery + IV abx
- Reccurent = open/laparoscopic resection
Ix for acute abdomen?
Bedside: urine dip
Bloods: VBG, FBC, U&E, CRP, LFTs + Bone profile, Amylase, Clotting, G&S ± BC (if temp)
Imaging: erect CXR, AXR
- CTKUB if thinking renal stones
- CTAP if collecting/perforation/obstruction
- CT angiogram if ischaemia/bleeding/AAA
- USS/MRCP if cholecystitis/gall stones
Neuroanatomy - lobes
Lobes
-
Frontal:
- Primary motor cortex (posterior frontal lobe) - initiates + regulates movement
- NOTE: in motor cortex face/arms are lateral, legs are medial
- Broca zone - speech production (defect –> expressive dysphasia)
- Primary motor cortex (posterior frontal lobe) - initiates + regulates movement
-
Parietal:
- Primary somatosensory cortex (anterior parietal lobe)
-
Occipital:
- Primary visual cortex (posterior occipital lobe)
- Optic nerve pathways to lateral geniculate nucleus –> optic radiations through temporal and parietal lobes –> primary visual cortex
- Primary visual cortex (posterior occipital lobe)
-
Temporal:
- Wernicke’s zone - understanding language (defect –> receptive dysphasia)

Visual field defects
Bitemporal hemianopia = compression at optic chiasm
- Presentation: “I didn’t notice the bus coming”, “I didn’t see the car when I walked across the road” –> peripheral vision is gone
- Causes:
- Craniopharyngioma - compress from above
- Pituitary adenoma - compress from below
Quadrantonopias:
- Causes:
- Superior = temporal lobe lesion
- Inferior = parietal lobe lesion
- NOTE: use inverse rule - superior means that it is affecting the bottom of retina and temporal lobe is below the parietal lobe

Neuroanatomy - blood supply to the brain
Circle of Willis - perfuses brain
-
Cerebral arteries - anterior, middle, posterior (all bordering the circle)
- ACA - supplies anterior & medial brain (frontal lobe + medial motor & somatosensory cortices) –> behavioural changes, weakness legs > arms, mild sensory defect
- MCA - supplies the lateral brain (lateral motor & somatosensory cortices, language - Broca & Wernicke’s, optic tracts) –> weakness face > arms > legs, aphasia (expressive/receptive), hemisensory defect, homonymous hemianopia
- PCA - supplies inferior & posterior brain (affecting visual cortex and tracts) –> homonymous hemianopia, visual agnosia/prosopagnosia
- Major arteries giving rise to the circle of Willis:
- Vertebral artery (from the spine)
- Internal carotid artery (gives rise to A & M cerebral arteries)

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

Headache - types? Ix? Mx?
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

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

Neuroanatomy - motor function overview
Primary motor cortex –> pyramidal tracts = VOLUNTARY - include:
- Corticobulbar tracts - head & neck voluntary movement
- Corticospinal tracts - body voluntary movement
Extrapyramidal tracts = INVOLUNTARY - basal ganglia, cerebellum, vestibular nucleus
NOTE: pyramidal = GAS (starts movement), extrapyramidal = CLUTCH (smooths movement)

Parkinson’s disease definition? Cardinal Sx? DDx? Ix? Mx? Complications?
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
-
Non-ergot - ropinirole, pramipexole - avoid below SEs = 1st line but still get dopamine dysregulation syndrome (hypersexuality & gambling)
- ‘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
- Relevant physiology:
Complications:
- Falls, cognitive impairment, depression
- Drool (SALT/glycopyrronium)
- Meds SEs (e.g. vomiting)

CSF appearance for meningitis, TB, SAH, GBS

UMN vs LMN:
- Motorpathway name + route
- UMN & LMN lesion causes and signs
Corticospinal tract = voluntary motor pathway for body:
- Cortex - primary motor cortex (posterior frontal cortex)
- Medulla - tracts from PMC converge and cross over = pyramids
- Spinal cord - UMN synapases with LMN
- Peripheral nerves - LMN innervates muscle
UMN lesions
- Causes (anything affecting brain itself): stroke, SOL, MND, MS
- Signs: hypertonia, hyperreflexia, spasticity (velocity/direction-dependent), upgoing plantars, pronator drift
- NOTE: increased tone/reflexes as -ve feedback loop from the brain is removed
LMN lesions
- Causes (affect peripheral nerves): MND, trauma, polio, GBS
- Signs: hypotonia, hyporeflexia, muscle atrophy, fasciculations, fibrillations
- NOTE: reduced tone/reflexes because no nerve supply
Gait abnormalities vs normal
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)

MS - def? key features? DDx? Clinical courses? Ix? Mx? Poor prognostic features?
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)
- Internuclear ophthalmoplegia
- 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
- MRI (T2) head (lesions disseminated in time & space) - McDonald’s criteria
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

Wernicke’s encephalopathy - Def? Sx triad? Mx - in hypoglycaemia and without? Complication?
How does delirium tremens present?
Def: Acute presentation of thiamine (B1) def
Triad: confusion, ataxia, nystagmus
Complication = Korsakoff syndrome (chronic & permanent memory problems)
Delirium tremens: confusion, visual hallucinations, tachycardia, pyrexia

Neurology Ix depending on UMN/LMN signs?
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

MND - Presentation? DDx? Types of MND? Dx? Mx? Complications?
Presentation: mixed UMN/LMN (no sensory deficits, no eye involvement)
- UMN in lower limbs (spasticity, hyperreflexia, upgoing plantars)
- LMN in upper limbs (hypotonia, hyporeflexia, fasciculations, wasting)
- Bulbar/pseudo-bulbar tongue/speech (tongue fasciculations, palatal paralysis, nasal speech)
- NORMAL SENSORY EXAM
DDx mixed signs:
- Dual pathology (stroke + peripheral neuropathy)
- Conus medullaris lesion - painful, assoc with traumatic spinal injury/higher up mets)
- B12 def (subacute combined degen of spinal cord) = cofactor in myelination (as is folate)
Types:
- Amyotrophic lateral sclerosis (60%) - classic (UMN & LMN)
- Progressive Bulbar Palsy (30%) - CN 9-12 –> dysarthria (speech), dysphagia (swallowing)
- Primary Lateral Sclerosis - pure UMN onset
- Progressive Muscular Atrophy - pure LMN onset, ‘flail limb’ appearance
Dx: clinical, exclude other causes
- EMG/NCS (nerve conduction study) - chronic nerve root denervation
- Imaging - MRI (cervical, thoracic, lumbar spine) - exclude other causes
Mx: no cure - MDT approach
- Conservative - SALT (swallowing), physio & OT
- Sx-control:
- Quinine - muscle cramp
- Anticholinergics e.g. hyoscine patches - drooling
- Exercise & nutrition
- Prognostic:
- Riluzole - glutamate antagonist (extend life expectancy by 3-5 months)
- NIV - if respiratory muscles no longer functioning
Complications: resp compromise, frontal lobe dementia (2%)

Rigidity vs Spasticity
Rigidity (in Parkinson’s disease) = increased muscle tone, that is not velocity or direction-dependent
- In Parkinson’s get Cogwheeling = rigidity overlayed by tremor
Spasticity (in Stroke) = increased muscle tone, that is velocity or direction-dependent
- Flexors/extensors become imbalanced in strength - certain directions have increased muscle tone (not all) AND worse stiffness if move arm more quickly
Cauda equina - def? Sx? Causes? Key Ix? Mx?
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

Dementia - Types?
Types:
-
Alzheimer’s disease
- Progressive decline in cognitive function
- Tx: Acetylcholinesterase inhibitors (Donepezil)/NMDA receptor antagonists (Memantine)
-
Vascular dementia
- A stepwise decline in cognitive function
- Background of vascular disease (IHD, PVD)
-
Dementia with Lewy Bodies
- Triad - dementia, hallucinations, parkinsonism
- Balance - Parkinsonism = dopamine def vs hallucinations = dopamine excess
- Frontotemporal - personality changes, early onset
- Depressive pseudodementia - disinterested, low mood
Neuro examination Qs:
- Good acronym for general inspection?
- What screens do you do for upper and lower limbs?
- What are you feeling for on examining tone?
- What to do before checking power against resistance?
- How to find the tendon for each reflex?
- How do you accentuate neuro reflexes?
- What to remember when doing the finger-to-nose test?
- SWIFT - scars, wasting, involuntary mov, fasciculations, tremors
- Screens:
- Upper - hands out pronate (tremor?), supine hands and close eyes (pronator drift = UMN lesion)
- Lower:
- Stand up from chair with hands crossed (prox power)
- Gait assessment - normal, only on heels/toes (distal power), tandem walk (balance)
- Stand with both feet together (balance) –> Romberg’s test if they could do prior (eyes closed - proprioception).
- Tone:
- “Clasp-knife spasticity” = pyramidal (UMN) lesion - velocity/direction-dependent e.g. stroke/spinal cord compression/MND
- CLONUS also present in UMN lesion
- Rigidity = extrapyramidal lesion - velocity/direction independent, types:
- “Lead-pipe” = NMS (anti-psychotics)
- “Cogwheeling” = Parkinson’s (tremor on rigidity)
- “Clasp-knife spasticity” = pyramidal (UMN) lesion - velocity/direction-dependent e.g. stroke/spinal cord compression/MND
- Check power against gravity - raise arms/legs (if so MRC is 3+)
- Eliciting reflexes:
- Biceps - thumb over cubital fossa (from lateral side) while they move hand towards shoulder (should be central) - place nail over tendon and hit nail. Get patient to rest hand on knee
- Brachioradialis - first 2 fingers 1/3 up arm from wrist, lateral arm. Get patient to rest hand on knee
- Triceps - hold out patient arm at 90 degrees takin the weight of the patient’s arm, stand behind patient, hit just above the olecranon
- Knee jerk - if patient supine, support behind knee
- Ankle jerk - if patient supine, cross one leg over the other, dorsiflex foot, strike ankle tendon OR keep straight, dorsiflex foot and strike ball of the foot (just below ball under toes)
- Jendrassik maneuver - clench hands together/clench jaw at the same time as eliciting reflex
- Put finger just beyond reach so they have to stretch
What are the nerve innovations for deep tendon reflexes in upper and lower limb neuro examination?
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
Meningitis & encephalitis - presentation? causes? Ix? Mx?
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

Spinal cord anatomy
Dark matter middle (cell bodies = synapses) –> white matter on the outside (neurone tracts)
Sensory pathways (ascending - goes up):
-
Dorsal columns (posterior) - fine touch, vibration, proprioception
- Sensory receptors - 1st order neurone up spinal column along ipsilateral side
- At the medulla oblongata - synapses with 2nd order neurone that crosses the midline (decussation)
- At the thalamus synapses with 3rd order neurone to the Primary Somatosensory cortex
-
Spinothalamic tracts (anterior) - pain & temperature
- Nociceptors (pain) - 1st order neurone to Substantia Gelatinosa within grey matter of spinal cord
- Synapses with 2nd order neurone & immediately crosses midline (decussation) to ascend spinothalamic tract
- NOTE: spinothalamic tracts decussate at the level the neurone enters the spinal cord
- At the thalamus synapses with 3rd order neurone to the Primary Somatosensory cortex
- (Spinocerebellar tracts (lateral) - proprioceptive info to cerebellum)
Motor pathways (descending - goes down):
-
Corticospinal tracts (anterior = trunk, neck, shoulders; lateral - limbs) - voluntary motor control (from primary motor cortex)
- From the Primary Motor Cortex - UMN goes to the Medulla and crosses over (decussation)
- At the anterior horn for each spinal level synapses with LMN–> muscle
- NOTE: at any spinal level will be LMNs exiting the spine and UMNs that travel down further before synapsing with their respective LMN
- SO cord pathology above the level of Cauda Equina –> some UMN & LMN signs

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

MRC Power Scale
- 1 flicker
- 2 is moves with gravity removed
- 3 is movement against gravity
- 4 is reduced power against resistance
- 5 is normal
Key eye cranial nerve palsies? Causes? How to describe?
How to describe:
- Eyes disconjugate in the primary position
- Comment on the direction of globe e.g. down & out
- Where is the diplopia worst? When has the outside image disappeared? Cover each eye in turn & the outer image will disappear when eye with palsy is covered
- What is the reaction to light?
NOTE: LR6 SO4
3rd nerve palsy (oculomotor) –> down & out gaze
- All the extraocular muscles not working except 4 & 6 so LR turns eye out, SO turns eye down & out + ptosis & diplopia (to the left)
- Causes:
-
Medial (internal infarct) = pupil-sparing (PS fibres intact)
- Mononeuritis multiplex (microvascular causes) - HTN, DM
-
Surgical (external compression) = pupil dilation (PS fibres damaged as on periphery of 3rd nerve trunk)
- PCA Aneurysm (posterior communicating artery at junction with internal carotid artery), tumour, dissection
- PCAA = painful
- PCA Aneurysm (posterior communicating artery at junction with internal carotid artery), tumour, dissection
- SOL/haemorrhage in 3rd nerve nucleus –> bilateral ptosis
-
Medial (internal infarct) = pupil-sparing (PS fibres intact)
- Mx: check BP & BM, examine for 4th nerve palsy (check for cavernous sinus problem)
- Dilated pupil - CT scan & angiography (esp if painful)
- Medical palsy = self-resolve within 3 months - prism glasses (minimise double vision)
- Ask to look down - if 4th nerve intact –> mov of scleral blood vessels (as eye tries to turn inwards) = subtle
- NOTE: 3rd & 4th nerve palsy (± V1 (ophthalmic), 6th nerve) = cavernous sinus involvement (tumour/thrombosis/aneurysm)
4th nerve palsy (trochlear) - subtle up & in gaze + head tilt away from affected eye
- SO not functioning so upward deviation of the eye (opposite of 3rd nerve palsy) –> unable to depress eye in adduction (have problems when walking down stairs/reading book)
- Causes: head trauma e.g. whiplash/concussion; mononeuritis multiplex (microvascular e.g. DM, HTN), congenital
- NOTE: see above about 3rd & 4th nerve palsy
6th nerve palsy (abducens) - medial gaze (can’t look laterally) = VERY IMPORTANT TO PICK UP
- LR not functioning so medial deviation of the eye
- Causes:
- Most common: microvascular (HTN, DM)
- Raised ICP (tumour/aneurysm), demyelination/mass/vascular
-
‘false localising sign’ - can’t identify what side of the brain is affected as 6th nerve has the longest IC nerve root in the brain (+ one of first nerves to be affected)
- NOTE: vagus nerve is the longest overall CN
- Mx:
- Examine other CNs (7th, 8th) & cerebellar system (cerebellar pontine angle lesion)
- Fundoscopy - papilloedema (raised ICP)
7th nerve palsy (facial):
- Presentation:
- Bell’s phenomenon (when asked to close eyes they can’t shut eyelids and eyes will roll back)
- Loss of taste anterior 2/3 tongue, mouth droop, smooth nasolabial folds, hyperacusis (one ear louder than other as stapedius muscle supplied by facial nerve –> dampens sound normally –> louder sound)
- UMN vs LMN (UMN spares forehead)
- Causes:
- Viral/idiopathic
- Damaged facial nerve - trauma (e.g. forceps delivery)
- Inf - HZV (Ramsay-Hunt = vesicles in-ear canal), otitis media
- Compression/mass - parotid tumour/cerebellar-pontine angle (CPA) lesion
- MUST get ENT to rule out cholesteatoma & acoustic neuroma = MRI brain scan
- Mx: 50% LMN (Bell’s palsy) recover spontaneously in 6 months
- Eye drops + eye patch
- <72hrs –> steroids
- Long-term consequences:
- Synkinesis of facial muscles (when nerve regenerates –> innervate wrong muscles e.g. when scrunch eyes lip twitches upwards)
- Crocodile tears phenomena - where wrongly innervates lacrimal gland = cry when smiling

Bell’s palsy - def? presentation? Ix? Mx?
Def: acute, sudden-onset, unilateral facial palsy of probable viral aetiology
Presentation: URTI –> unilateral facial palsy (all branches, no-forehead sparing) with pain behind the ear & dry eye
- Bell’s sign: failure of eye closure (dryness and conjunctivitis)
- Precipitating factors (e.g., dental extraction, upper respiratory tract infection)
- Single episode (recurrence = likely alternative Dx)
- Unilateral (bilateral = likely alternative Dx e.g. Lyme disease, GBS, sarcoidosis, leukaemia)
- Involves all nerve branches (originates proximal to the geniculate ganglion so should be equal distribution)
- No constitutional Sx (would indicate Lyme disease, AI, granulomatous disease)
- Keratoconjunctiva sicca (dry eye - from inadequate blinking)
- Pain behind the ear
Ix: clinical Dx (Dx of exclusion)
- Electroneurography (ENoG, 72hrs-14 days after palsy starts)
- Needle electromyography (>90% degeneration in CMAP)
- Serology for Borrelia burgdorferi (if recent visit to Lyme disease-endemic region)
Mx:
- Pred (if <72hrs Sx onset)
- Eye protection (to prevent keratoconjunctivitis sicca progressing to exposure keratopathy)
- Severe palsy/complete paralysis –> concurrent antiviral therapy (aciclovir), surgical decompression
- Prognosis = 75% make a full recovery
What is vertigo? Vertigo Hx & general Tx? Breakdown? Presentation? Ix? Mx?
Def: The sensation of movement between person & environment: spinning sensation, N&V
Vertigo Hx:
- Vertigo (sense of motion) vs light-headed vs pre-syncope
- Assoc hearing loss? If yes = not BPPV
- Meniere’s disease - vertigo, tinnitus, hearing loss –> no driving
- Viral labyrinthitis - following URTI
- Tx:
- Vertigo - prochlorperazine (reg for 3 days)
- Tinnitus - betahistine
Detailed breakdown:
- Peripheral cause:
-
BPPV - crystals displaced in SCC
- sudden, brief, episodic, only on certain head movement
- Ix: Dix-hallpike test to confirm (up-beat torsional nystagmus)
- Mx:
- Education & reassurance (remission from 3wks - 6 months)
- Epley manoeuvre
- Betahistine (for vertigo)
-
Meniere’s disease - excessive endolymph in SCC
- Clustered attacks <12hrs: Fluctuating hearing loss, tinnitus, vertigo lasts minutes- hours (more than one episode)
- Ix:
- +ve Romberg’s test
- Pure-tone & speech audiometry
- Tympanometry
- Otoacoustic emissions (OAE)
- Mx: dietary changes + lifestyle modification (limit salt, caffeine, alcohol/smoking, stress) ± thiazide diuretic (triamterene/hydrochlorothiazide)/acetazolamide
- Vertigo - betahistine
- Tinnitus - devices
- Hearing loss - CS
-
Labyrinthitis - inflammation of otic capsule caused by viruses/bacteria affecting inner ear (cochlear & vestibular system)
- Severe vertigo, nystagmus and vomiting following an URTI
- Bacterial - severe hearing loss (irreversible)
- Viral - less severe Sx (often reversible)
- Ix: cranial nerve exam (Renne’s, Weber’s), audiometry (sensorineural hearing loss)
- Mx:
- If severe: IV prochlorperazine
- If less severe: PO cyclizine and prochlorperazine
- Tx cause e.g. bacterial
- Ongoing - vestibular rebab (physio, OT)
- NOTE: vestibular neuronitis is inflammation of the vestibular nerve = the same presentation without the hearing loss (normal audiogram) - comes on acutely but can take weeks to settle
- Ix & Mx - as above
- Severe vertigo, nystagmus and vomiting following an URTI
-
BPPV - crystals displaced in SCC
- Central cause:
- Stroke/TIA - lateral medullary syndrome (Wallenberg syndrome), cerebellar infarct/haemorrhage
- Cerebellar stroke - headache (occipital sudden & prominent), N&V, ataxia (imbalance)
-
Acoustic neuroma (vestibular schwannoma) - benign cerebellopontine angle tumour
- Unilateral sensorineural hearing loss, facial numbness, progressive intermittent unsteadiness
- Can have co-existing neurofibromatosis type 2
- Ix: audiometry, (CT head (can be missed if small)) –> gadolinium-enhanced MRI (absence of dural tail)
- Mx:
- Vestibular migraine - headache, photophobia, phonophobia, aura
- Vertebrobasilar ischaemia - reduced flow to posterior circulation of brain
- Head position provokes vertigo
- Hemifacial numbness & contralateral peripheral weakness/paraesthesia ± arm claudication (from subclavian steal)
- MS
- Stroke/TIA - lateral medullary syndrome (Wallenberg syndrome), cerebellar infarct/haemorrhage
GBS Ix? Mx?
Ix:
- Bloods (metabolic, abs), CT –> LP ± MRI spine (exclude other causes)
- Nerve conduction studies
Mx: ADMIT suspected cases - normally self-limiting course
- MDT - psychologist, SALT (if speech muscles affected)
- Plasmapheresis (plasma exchange)
- High-dose IVIG
- DVT prophylaxis
How to remember nerve innervation of the diaphragm? Nerve associated?
C3,4,5 keep the diaphragm alive
Phrenic nerve
What should I not forget in upper limb neuro exam?
Upper limb:
- Pronator drift (palms up)
- Power - stabilise joint, chicken, boxer, arms out straight, , separate fingers separate + hold paper, thumb straight up in air (abduction)
- Reflexes - nerve innovations:
- Biceps/brachioradialis - C5/6 - pick up sticks
- Brachioradialis - feel for radial tubercle then go several cm lower
- Triceps - C7/8 - lay them straight
- Biceps/brachioradialis - C5/6 - pick up sticks
- Coordination - finger-nose test (put elbow out like chicken) & dysdiadokokinesia
- Sensation - dorsal column: “does this feel normal?”
- Fine-touch - glove & stocking or dermatomal:
- C5 - deltoid area
- C6 - thumb
- C7 - middle finger
- C8 - little finger
- T1 - medial forearm
- T2 - medial upper arm
- Vibration - 128Hz tuning fork (IPJ thumb, hit on elbow to trigger, ask patient to say yes when it stops)
- Proprioception (hold either side of thumb)
- Fine-touch - glove & stocking or dermatomal:
- Sensation - spinothalamic:
- Pain - neurotip
- Temperature - prongs of tuning fork (sternum then dorsum of hand)
- Sensation pathology:
- Radiculopathy (dermatome - nerve root)
- Glove & stocking - peripheral neuropathy e.g. DM
What bits not to forget in lower limb neuro exam?
Lower limb:
- Gait & Romberg’s test
- Tone - clonus
- Power - stabilise joint (contralateral-side if hip)
- Nerve innovations of reflexes:
- Knee - L3/4 - kick the door
- Ankle - S1/2 - in the shoe
- Babinski reflex
- Coordination = heel-shin test
- Sensation - dorsal column:
- Fine-touch - glove & stocking or dermatomal: “does this feel normal?”
- (L1 - higher upper inner thigh)
- L2 - upper inner thigh
- L3 - medial just above knee
- L4 - medial upper calf
- L5 - lateral calf
- S1 - plantar aspect of the foot (sole)
- Vibration - 128Hz tuning fork (IPJ big toe, hit on elbow to trigger, ask patient to say yes when it stops)
- Proprioception (hold either side of big toe)
- Fine-touch - glove & stocking or dermatomal: “does this feel normal?”
- Sensation - spinothalamic:
- Pain - neurotip
- Temperature - prongs of tuning fork (sternum then dorsum of foot)
- Sensation pathology:
- Radiculopathy (dermatome - nerve root)
- Glove & stocking - peripheral neuropathy e.g. DM
Spinal cord compression Ix & Mx for malignancy?
Ix: MRI whole spine (often multifocal lesions)
Mx:
- 1st line = surgical decompression (if localised, fit enough)
- 2nd line = radiotherapy (external beam radiotherapy)
Autosomal dominant polycystic kidney disease is associated with what type of headache?
Thunderclap headache - SAH
Ramsay-Hunt Syndrome - cause? Presentation? Mx?
Cause: Reactivation of the varicella-zoster virus in the genticulate ganglion of CNVII
Presentation:
- Otalgia
- Facial nerve palsy
- Vesicular rash around ear
- Vertigo + tinnitus
Mx:
- Valaciclovir PO
- Steroids PO
- NOTE: If treated within 72 hours, 75% recover, otherwise only 1/3 fully recover
Brain anatomy “rules” summary - cerebellar, motor nerves, dorsal columns, spinothalamic tract
Clues to localisation - cortical, basal ganglia, cerebellar, nerve root
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)
Myasthenia Gravis Vs Lambert-Eaton Myasthenic Syndrome (LEMS)
Def? presentation? Assoc? Ix? Mx?
Myasthenia Gravis
- Def:
- Chr AI disorder of post-synaptic membrane of NMJ in skeletal muscle
- Abs to AChR on post-synaptic membrane
- Presentation:
- Muscle fatiguability incl dysphagia, rarely SoB
- Eyes - bilateral ptosis (and compensatory increased frontalis muscle activity = raised eyebrows), diplopia
- Face - dysarthria (slurred speech), facial paresis
- Curtain sign - when raising one upper eyelid the other one drops down
- Assoc: thymomas (in the chest)
- Ix:
- Abs: AChR (on post-synaptic membrane), MUSK abs
- Serial pul funct tests (FVC & negative inspiratory force)
- NOTE: do not wait for ABG findings - late in course
- CT-chest (for thymoma)
- Mx:
- Acetylcholinesterase inhibitors (Pyridostigmine) + IS (azathioprine)
- IVIG/Plasmapheresis
- Surgery - thymectomy
-
Myasthenic crisis = acute respiratory failure - FVC <1L, negative inspiratory force (NIF) ≤20cm H2O, need mechanical ventilatory support
- Accessory muscle use indicates sign inspiratory muscle weakness
- Weak cough indicates sign expiratory muscle weakness
- ABG often shows hypercapnia before hypoxia
- Low threshold for endotracheal intubation (rapid deterioration of bulbar & resp muscles)
- Mx: intubation + mechanical ventilation (& Mx above)
Lambert-Eaton Myasthenic Syndrome (LEMS)
- Def: rare AI disorder of NMJ
- Pre-synaptic membrane Ab to voltage-gated Ca-channel receptors
- 40% occur as paraneoplastic disorder assoc w/ SCLC
- Presentation:
- Limb weakness - proximal legs –> proximal arms e.g. waddling gait
- STRONGER WITH USE (vs MG get’s weaker with use)
- Hyporeflexia, NO eye involvement (compared to MG)
- Autonomic disturbance - dry mouth (& orthostatic hypotension, sweating, GI & urinary problems, visual blurring, sexual dysfunction)
- Associated with: small cell lung cancer (SCLC)
- Limb weakness - proximal legs –> proximal arms e.g. waddling gait
- Ix:
- Nerve conduction studies, EMG, serial PFTs
- Ab testing (Voltage-gated Ca-channels & AChR-abs)
- CT chest (SCLC)
- Mx: MDT support
- Tx underlying cause, Amifampridine
- IVIg/plasma exchange
- Supportive care
Case:
- Obese 30yrs, left-sided headache over 1wk, vomited this morning
- Tonic-clonic seizure in A&E –> confused, papilloedema, apyrexial, 6th nerve palsy
- Normal CT, CSF opening pressure high
What is normal CSF opening pressure? Dx? DDx? Ix? Mx?
Normal CSF opening pressure ≤25
Dx: Cerebral Venous Sinus Thrombosis (VTE in the brain)
- DDx = Idiopathic intracranial HTN - but would not make you this unstable neurologically
- Obese, female, papilloedema, postural headache worse with straining, assoc w/ OCP
- Ix: visual field testing, fundoscopy, MRI brain, LP (≥25 opening pressure)
- Mx: acetazolamide, weight loss, LPs + VP/LP shunt, ophthalmology follow-up
Presentation: headache, papilloedema, signs of raised ICP (6th nerve palsy), seizures, Cushing’s reflex (HTN, bradycardia, irregular breathing = Cheyne-Stokes)
Ix: MRI w/ MR venography
Mx: LMWH
Lumbar disc herniation vs lumbar spinal stenosis - presentation? Ix? Mx?
Presentation
- Disc herniation - acute unilateral radiculopathy (pain & numb in specific dermatome/weakness in muscle group)
- Straight leg raise +ve
- 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
Ix:
- Disc herniation - erect lumbar x-ray & MRI spine
- Spinal stenosis - plane x-ray, MRI (T2-weighted)
Mx: surgical decompression
Myotonic dystrophy - presentation? Assoc? Ix? Mx?
LMN presentation = muscle pathology
- Face:
- Myopathic facies (sunken cheeks, bilateral ptosis, expressionless)
- Wasting of facial & muscles of mastication
- Frontotemporal balding
- Myopathic facies (sunken cheeks, bilateral ptosis, expressionless)
- Distal wasting, weakness w/ loss of ankle jerks
- Associations: cataracts, dysphagia, cardiac (cardiomyopathy, heart block), DM, hypogonadism (gynaecomastia/testicular atrophy)
- Exam - failure of immediate relaxation after voluntary contraction
- Percussion myotonia - tap thenar eminence and thumb contracts
- Slow-releasing grip - SHAKE HANDS (or make a fist and then spread fingers quickly or squeeze eyes shut and open quickly)
Ix:
- Conservative: full functional assessment (incl. SALT), lung function tests (NM resp insufficiency), ECG/echo (CMO/HB), slit lamp (cataracts)
- Bloods - BM (DM assoc), CK, genetic testing
- Imaging & invasive:
- Electromyography (EMG) - ‘dive-bomber’ potentials
- Muscle/nerve biopsy
Mx: MDT approach
- Phenytoin for myotonia, weakness has no Tx
- Genetic counselling - AD w/ genetic anticipation (trinucleotide repeat - worse severity/earlier presentation with each generation)
- Avoid statins (can cause myopathy)
Hammertoes can be seen in what condition? Presentation? What do I need to check for to exclude DDx? DDx? Types? Ix? Mx?

Hammertoes - bilateral, symmetrical, distal wasting of small muscles of feet
- Advanced = dorsal guttering from distal wasting, wasting of extensor digitorum brevis at inferior border of lateral malleolus
- Similar can be seen in the hands = wasting of first dorsal interosseus
Sign of Charcot-Marie-Tooth disease aka hereditary motor & sensory neuropathy (HMSN)/peroneal muscular atrophy (PMA)
- Hx ankle sprains & scoliosis
- Motor & sensory losses (sensory milder) = classic peripheral neuropathy
- LMN pattern of weakness:
- Motor loss in anterolateral compartments of legs (ankle dorsiflexion & toe extension)
- Absent reflexes (plantar reflexes show no response)
- Sensory loss in glove & stocking distribution bilaterally
- LMN pattern of weakness:
- Pes cavus ± palpable common peroneal nerve, thickened nerves @medial malleolus
- High stepping (foot drop) & ataxic gait
- Test for foot drop = heel walking
What do I need to check for? NO scars over fibula (would indicate peroneal nerve damage from trauma e.g. car accident)
DDx:
- Common peroneal nerve palsy (inversion of foot normal)
- Sensory peripheral neuropathy: B12-def (SACD), Alcohol, DM, Hypothyroid (vitiligo?), HIV, drugs
- Motor peripheral neuropathy: lead poisoning
Types:
- Type 1 - demyelination, AD
- Type 2 - axonal, AD/AR
- Type 3 - demyelination, AR & presents as infant
Ix: full functional assessment, FHx, nerve conduction studies, genetic testing
Mx:
- Physio, walking aids with ankle & foot supports (e.g. foot splint)
Wasting of hand muscles - distinguishing different nerves?
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

Hyponatremia - Sx? Ix & Approach? What happens if you correct Na too fast?
Sx: confusion, altered GCS, headaches, seizures, encephalopathic
Ix: fluid status, U&E, paired osmolalities (urine, serum)
Fluid status:
- HYPOvolaemic (dehydrated) - WASTING (diarrhoea/vomiting, diuretics) –> IV fluids
- EUvolaemic (normal) - ENDOCRINE (SIADH, hypothyroidism, Addison’s) –> fluid restrict + Tx underlying cause
- HYPERvolaemic (fluid overload) - FAILURE (liver, renal, heart) –> fluid restrict + Tx underlying cause
Urine Na:
- <20 mmol/L –> hypovolaemia (increased Na reabsorption in kidneys –> increasing H20 retention –> reducing urine Na)
- >20 mmol/L –> SIADH (BUT if on diuretics, urine Na can’t be interpreted) –> fluid restrict
Na corrected too fast (>10) = osmotic demyelination syndrome (central pontine myelinolysis) –> pseudo-bulbar palsy, paraparesis, locked-in syndrome

Potassium homeostasis - areas involved? Hypo/hyper? Appearance on ECG? Hyper Tx?
Areas involved:
- Dietary intake
- Absorption in GI tract
- Adrenals & kidneys - regulate serum K concentration
HYPOkalaemia:
- Poor dietary intake, vomiting/diarrhoea
- Diuretics - loop/thiazide (block channels causing K reabsorption)
- Hyperadrenalism (Conn’s, bilateral adrenal hyperplasia, Cushing’s)
- Conn’s/BAH - excess aldosterone - NOTE: Aldosterone promotes reabsorption Na, excretion K
- Cushing’s = excess cortisol –> off-target effect on mineralocorticoid receptors –> mimics aldosterone
HYPERkalaemia:
- false = HAEMOLYSIS –> repeat sample
- Kidney failure e.g. on dialysis (kidneys = main route to remove K)
- Anti-HTN/diuretics
- ACEi/ARB - reduce kidney hyperfiltration, mainly a risk if CKD
- K+-sparing diuretics e.g. spironolactone/amiloride
- Addison’s disease (failure - can’t produce enough cortisol/aldosterone)
- NOTE: appearance on ECG = tented T-waves, broad QRS, prolonged PR interval
Hyperkalaemia Tx:
- Protect heart - IV 10-30ml 10% Ca Gluconate (repeat /15m, x5 MAX)
-
Reduce K+:
- 1st line - 10U Actrapid (insulin > drive K into cells) AND 100mL 20% glucose (to prevent hypo)
- 2nd line - 5mg Salbutamol NEB (b-agonist)
- Ix cause: drug chart, U&E (kidney funct), short SynACTHen test (Addison’s)

Calcium homeostasis?
Hyper Sx? Ix & causes? Mx?
Hypo Causes? Sx? Ix? Mx?
Hormone production:
-
Parathyroid gland - PTH –> INCREASE Ca:
- Bone resorption
- GI absorption
- Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
- Vit D3 aka cholecalciferol (UV)/ergocalciferol (diet)
- In Liver –> 25-OH(D) aka calcidiol
- In Kidney + 1alpha-hydroxylase –> 1,25-OH2(D) aka Calcitriol (activated vitD) –> INCREASE Ca
- GI absorption
- Kidney - decreased excretion
HYPERcalcemia
-
Sx:
- Stones - urinary tract calculi
- Bones - fractures
- (Abdo) moans - dyspepsia
- Thrones - polyuria, constipation
- (Psych) overtones - depression, psychosis
- Ix - check PTH:
- Low - hypercalcemia of malignancy (PTH axis is functioning normally) - bone mets, PTHrP (released by lung SCC), myeloma (CRAB)
- Normal/high - primary hyperparathyroidism (as if serum Ca high, PTH should be low) - adenoma, hyperplasia, MEN 1&2
- Other:
- Fluid status, ECG (short QT), protein electrophoresis, 24hr urinary Ca (familial hypocalciuric hypercalcemia)
- Bloods - bone profile (Ca, PO4), U&E
- Imaging: CXR
- Mx:
- IMMEDIATE = aggressive IV 0.9% fluid resus (4-6L over 24krs), repeat Ca
- Tx underlying cause:
- Parathyroid adenoma - minimally invasive surgery (subtotal/total parathyroidectomy)
- Malig - Zalendronate/Pamidronate (inhibit osteoclast activity), slow infusion
- Other:
- If bone mets –> bisphosphonates
- If renal failure –> Cinacalcet (reduce PTH)
- Recheck serum Ca @day 2 –> 4
HYPOcalcaemia
- Causes:
- Hypoparathyroidism (PO4 high, PTH low)
- Pseudohypoparathyroidism (PO4 high, PTH high) = PTH resistance
- CKD (high PO4, PTH high, ALP high)
- Vit D def (rickets/osteomalacia, low/normal PO4, high PTH, high ALP)
- Hypomagnesaemia (low/normal PO4, low/normal PTH, normal ALP)
- Presentation:
- Peri-oral numbness, digital paraesthesia, dermatitis
- +ve Trousseau’s (BP cuff 20 over SBP for 3mins –> salt bae hand), Chovstek signs (tap over the masseter muscle in the inferior pre-auricular area)
- Laryngospasm (wheeze, dysphagia, muscle cramps)
- Confusion, seizures, prolonged QT
- Ix: serum Ca, PO4, Mg, PTH, U&E, Vit D
- Mx: PO/IV replacement of Ca

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?
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
- 1st line - Basal-bolus regimen
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
- HbA1c targets:
- 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
-
Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
- 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)
- Background: need to tighten control
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

Hyperosmolar Hyperglycaemic State
- What does insulin do? Pathophysiology of HHS?
- HHS criteria? HHS Mx? HHS Mx Targets?
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

Hypernatremia - breakdown into different causes? Mx?
Causes:
-
Hypovolaemia (H20 loss > Na loss) - most common
- GI loss: D&V
- Skin loss: excessive sweating, burns
- Renal loss: diabetes insipidus (DI), osmotic diuresis (glucose/mannitol), loop diuretics, kidney disease
- Euovolaemia - Resp (tachypnoea), skin (sweating, fever), renal (DI)
- Hypervolaemia
- Mineralocorticoid excess – Conn’s syndrome
- Inappropriate saline
Causes thirst –> most people self-correct UNLESS: failure to ingest water (Elderly/dementia, fasting (e.g., for surgery), excess loss)
Mx: SLOW Hartmann’s (rapid correction –> cerebral oedema)

Diabetes insipidus - Sx? Types? Ix? Tx?
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

Hyperkalaemia - causes? Ix? Mx?
Causes:
- Spurious sample
- Excessive intake: oral, parenteral, stored blood transfusion
-
Transcellular mov (ICF>ECF):
- Acidosis, insulin shortage (DKA - high glucose, high ketones, metabolic acidosis)
- Tissue damage/catabolic state (rhabdomyolysis) – CK very high
-
Decreased excretion:
- AKI (oliguric phase)/CKD (late)
- Drugs (spironolactone – K-sparing diuretic, ACEi/ARB/NSAID)
- Addison’s (mineralocorticoid def)
Ix:
- Repeat sample (VBG to also look for acidosis)
- CK, Creatinine & Urea
- AM Cortisol/Short synACTHen test
-
ECG
- Loss of p-waves, tall, tented T-waves, broad QRS (+ bradycardia)
- If severe & untreated –> ECG forms ‘sine wave’
Mx (if >5.5 w/ ECG changes OR >6.5):
-
IV 10mls 10% calcium gluconate (cardioprotective, doesn’t lower K)
- If on Digoxin – IV Ca causes arrhythmias – cardiac monitoring
- IV 10ml 20% dextrose + 10 units short-acting insulin e.g., Actrapid (insulin drives K into cells, dextrose prevents hypo)
- Neb salbutamol adjunct + treat cause

Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?
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
-
Hashimoto’s thyroiditis - most common hypothyroidism
-
Secondary: pituitary gland fails to produce TSH
- Tumour, vascular (Sheehan syndrome), radiation, inf
-
Primary:
- 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)
-
Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
- 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)
-
Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
- High-uptake:
- 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

Adrenal disease breakdown? Causes? Presentations? Ix? Mx?
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
- ACTH-dependent:
- 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
- High - CRH test identifies if pituitary or ectopic
- 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
- Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
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
- Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
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)

DDx for tiredness & lethargy? Ix?

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
- CXR
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?
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

Acromegaly cause? presentation? Ix? Mx? Complications?
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
Mx of obesity?
- Conservative measures
- Medical (none proven to provide sustainable weight loss)
- Orlistat (gut lipase inhibitor, SEs: profound flatus, diarrhoea)
- Surgical – bariatric surgery (BMI >40 OR >35 w/ comorbidity assoc w/ obesity)
- Needs extensive screening + commitment to long-term follow-up
Hyperprolactinaemia - causes? presentation? Ix? Mx
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
DDx for weight loss?
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
Hand & wrist examination? DDx structure? Ix? Common hand pathology? Hand muscles anatomy?
Intro - WIPE (wash, intro, pain & position, explain)
Look
- General - RASS (Redness, Asymmetry, Swelling, Scars)
- Tops:
- Bones:
- OA - Heberden’s nodes (DIP), Bouchard’s nodes (PIP)
- RA - swan neck deformity, boutonniere’s deformity, Z-shaped thumb, ulnar deviation, MCP palmar subluxation
- Skin - scars, thinning, rashes, bruising (steroids)
- Muscle - wasting
- Nails - psoriatic changes (pitting, onycholysis), clubbing, nailfold vasculitis
- Bones:
- Palms - thenar (thumb-side), hypothenar muscle wasting, palmar erythema (RA), carpal tunnel release scar, swellings (e.g. ganglions)
- Extensor surfaces - psoriasis, rheumatoid nodules, gouty tophi (white uric acid crystals under the skin - fingers/elbows)
Feel
- TST (Temperature, Swelling, Tenderness)
- Palms:
- Bulk of thenar/hypothenar prominences
- Tendon thickening - flexor tendon sheaths (hypertrophy/contraction –> Dupytren’s)
- Flex each finger individually and then feel the tendon base as extend (trigger digit)
- Tops:
- Temp - forearm, wrist, MCP
-
Squeeze joints & feel for bony swelling, effusion, synovitis, deformity
- Distal radio-ulnar joint + radial & ulnar styloid
- Anatomical snuffbox (tender = scaphoid fracture)
- Carpals (bimanual palpation)
- MCP (squeeze along row then bimanual palpation if pain elicited)
- Base of thumb (squaring = OA)
- IP joints (bimanual palpation of each - nodes = OA)
-
Tendon tenderness
- Around radial styloid (1st extensor compartment) = de Quervain’s tenosynovitis
- Around ulnar styloid = extensor carpi ulnaris tendinitis
Move (active > passive - feel for crepitus, get a few more degrees)
- Wrist movements - active (prayer sign & reverse prayer sign) & passive (feel for crepitus)
- Finger movements - make fist (tendon, small joint involvement), straighten fully (against gravity - joint disease, extensor tendon rupture, neuro damage)
- Thumb movements - abduction (away from hand upward), adduction (thumb to palm), flexion (thumb to little finger) extension (lateral away from hand), opposition (thumb and little finger)
Functional:
- Power grip = Grip fingers
- Pincer grip on finger
- Ask about writing with pen, button-up shirt
Brief neuro hand exam:
- Motor (against resistance):
- Radial (extensor forearm) - wrist extension
- Ulnar (some of flexor forearm + hand) - finger abduction
- Median (flexor forearm + thumb) - thumb abduction
- Sensory:
- Ulnar (up to halfway through ring finger dorsum/palm) - hypothenar eminence
- Median (rest of the palm + fingertip to PIP dorsal index, middle and half of the ring finger) - thenar eminence
- Radial (dorsum of hand excluding above) - dorsal base of the thumb
Special tests
- Phalen’s test - reverse prayer sign >1 min (pain/paraesthesia = Carpal tunnel syndrome)
- Tinel’s test - median nerve at its course in the wrist - tap (paraesthesia = Carpal tunnel syndrome)
- Finkelstein’s test - hand closed around thumb + ulnar deviation (pain = de Quervain’s tenosynovitis)
To complete exam
- Examine the elbow, full neurovascular exam
DDx: degenerative, infective, inflammatory, traumatic, congenital
Ix: AP & lateral views (2 views) + imaging of joints above and below as well
Hand/wrist pathology:
- RA - chr AI disorder –> symmetrical deforming polyarthropathy
- Synovitis, bony deformities, palmar erythema, small muscle wasting, reduced RoM, tendon rupture/subluxation
- DIP joints sparred
- Mx: NSAIDs, steroids, DMARDs (methotrexate), surgery
- OA - mechanical joint degradation w/ degen of articular cartilage, periarticular bone remodelling & inflammation
- Signs: joint crepitus, limited RoM, bony deformities
- Mx: analgesia, CS injection, physio/splints, surgery
- Carpal tunnel syndrome - median nerve entrapment neuropathy from compression of the median nerve in carpal tunnel
- Intermittent paraesthesia, pain/burning & numb thumb, first, middle fingers and radial half of ring finger
- Worse @night
- Signs: loss of power + wasting of thenar eminence, sensory loss in median nerve distribution
- Mx: splints, CS inj, carpal tunnel decompression
- Trigger finger - thickening of flexor tendon sheath causing entrapment at A1 pulley
- Discomfort/bump at base of digit and catching/clicking during extension
- Mx: splints, NSAIDs, CS inj, surgical release
Hand muscles anatomy:
-
Median nerve - LOAF (all thumb muscles except adductor pollicis)
- Lateral 2 lumbricals
- Opponens pollicis
- Abductor pollicis brevis
- Flexor pollicis brevis
-
Ulnar nerve (extrinsic hand muscles except most of thumb)
- Adductor pollicis
- Lumbricals (flex MCP, extend IP)
- Palmar interossei (ADduct fingers) = PAD
- Dorsal interossei (ABduct fingers) = DAB
- Radial nerve = extensors

Knee examination? Presentation? Ddx structure? Ix? Common pathologies?
Intro - WIPE (wash, intro, pain & position, explain)
Function - Gait (Antalgic, waddling = abductor dysfunction)
Look:
- General - RASS (Redness, Asymmetry, Swelling, Scars)
- Standing up - front (quads wasting, knee swelling), side (fixed flexion deformity, foot arches), back (varus/valgus deformity, baker’s cyst)
- Lying on bed - scars (TKR, arthroscopic ports on either side), wasting, deformity
Feel:
- TST (Temperature, Swelling, Tenderness)
- Effusion:
- Patellar tap (push down thigh & hold, press down on patella with middle finger)
- Sweep test (push down thigh, back of hand sweeps up medial x3, other back of hand sweeps down lateral, +ve is swelling on the medial side)
- Palpation:
- Leg straight - quadriceps tendon, medial & lateral borders of patella, patella tendon
- Knee @90 degrees:
- Patella tendon, tibial tuberosity (down from tendon), medial joint margin
- Lateral joint margin, head of the fibula (slightly lateral and distal to knee), collateral ligaments (hands around upper calf)
Move (active > passive - feel for crepitus, get a few more degrees)
- Knee extension:
- Active = push knee down into bed
- Passive = lift entire leg up @ ankle (hyperextension >10 degrees)
- Knee flexion:
- Active = bring heel towards bum (posterior sag?) then straighten
- Passive = same mov, leave knee flexed (for next part)
Special tests = 3Cs of knees – Cartilage (McMurray’s), Collaterals, Cruciates – Lachman’s, A/P-drawer)
- Anterior & posterior drawer (ant- bring towards = ACL; post - push away = PCL)
- Lachman’s test (flex knee to 30 degrees, right hand pulls, left hand stabilises the femur, checks ACL)
- Collateral ligament assessment:
- Varus stress test (LCL) - put the knee in varus positon while palpating the lateral knee joint line
- Valgus stress test (MCL) - put the knee in valgus position while palpating the medial knee joint line
- Menisci assessment - McMurray’s test - say “would consider doing but may be too painful for the patient”
- Passively flex the knee, hold the right foot with right hand apply external pressure with the left hand palpating the knee (abducting at the hip) while fixating and external rotating with the right hand, slowly extend at the knee watching for a click/discomfort = medial meniscus tear
- Opposite movements to test for lateral meniscus tear
To complete exam:
- Assess NV status
- Examine joints below and above (hip and ankle)
- Further imaging if indicated (X-ray)
Presentation:
- Normal gait, no obvious deformities of either knee, on palpation there was no pain and there was a full range of active and passive movement
- There was no evidence of laxity in the knee ligaments bilaterally
DDx: degenerative, infective, inflammatory, traumatic, congenital
Ix: AP & lateral views (2 views) + imaging of joints above and below as well
Common pathologies:
- ACL tear - twisting injury, ‘pop’ swelling within 1 hour, very painful for 2wks
- Increased laxity on anterior drawer test/Lachman’s test
- Mx: physio/surgical reconstruction (if ongoing instability)
- PCL tear - high energy trauma (multi-ligament knee injury/hip dislocation/fracture)
- Increased laxity on posterior drawer test
- Mx: physio/surgical reconstruction
- Meniscal tear - twisting injury, swelling after a few hrs, sharp localised medial/lateral pain worse on hyperflexion/twisting, knee may lock/give way
- Tender over medial/lateral joint line, good RoM unless knee locked, +ve McMurray’s
- Mx: MRI/arthroscopy to confirm, tear usually excised arthroscopically
- Collateral ligament tear
- Varus/valgus laxity, effusion, tenderness over affected ligaments
- Mx: rest, physio, hinged brace
- OA - pain & stiffness, reduced RoM, crepitus
- Prepatellar bursitis - localised swelling over patella, precipitated by period of kneeling
- Signs: tender over patella, normal RoM
- Mx: rest, NSAIDs, aspiration/CS inj

Hip examination? Presentation? DDx structure? Ix? Mx (for OA)? Common pathology?
Intro - WIPE (wash, intro, pain & position, explain)
Function - Gait (Antalgic, Trendelenburg - waddling = abductor dysfunction)
Look
- General - RASS (Redness, Asymmetry, Swelling, Scars)
- Standing inspection:
- Front (pelvic tilt, quads wasting), side (lumbar lordosis, knee flexion, foot arches), behind (scoliosis, gluteal atrophy, iliac crest alignment)
-
Trendelenburg’s test:
- Place hand resting lightly above both hips
- Bend one knee - if the hip dips on the bent side = contralateral abductor muscle weakness
- Lying inspection: compare symmetry & rotation (shortened & externally rotated = fractured NoF), hip scars, dressings, skin changes
Feel - check for pain, start on the normal side
- TST (Temperature, Swelling, Tenderness)
- Bony landmark tenderness:
- Feel around hip joint (tenderness, warmth, effusion)
- Feel along greater trochanter (lateral edge of thigh - trochanteric bursitis) run a hand up to greater trochanter (trochanteric bursitis)
- Feel ASIS –> pubic rami
- Measure true/apparent leg lengths:
- Apparent = umbilicus to medial malleolus (unequal = spinal/pelvic deformity e.g. scoliosis)
- True = ASIS to ipsilateral medial malleolus (unequal = true limb shortening e.g. fracture)
Move (active > passive - feel for crepitus, get a few more degrees)
- Roll side to side
- Flexion:
- Active (as far as can) then passive feeling for crepitus
- Passive internal & external rotation (while knee is bent to 90 degrees, lose IR early in OA)
- Passive abduction & adduction - place a hand on the contralateral pelvic crest to detect mov (crossing over leg for adduction)
- Passive extension - lie face down, scars/muscle wasting? place hand on pelvis/lumbar spine to detect mov
Special tests
-
Thomas’s test (not if hip replacement –> dislocation):
- Place a hand under the lumbar spine (check no lumbar lordosis)
- Flex hip on one side (knee bent)
- If contralateral thigh forced off the ground = fixed flexion deformity (of the side forced off the ground)
- NOTE: need to flex hip on the opposite side to that examining
To complete exam - examine shoulder and knee, full neurovascular exam distal to joint
Presentation:
- Normal gait, no obvious deformities on inspection
- On palpation, there was no pain with a full range of passive and active movement and no fixed flexion deformity and no abductor muscle weakness
DDx: degenerative, infective, inflammatory, traumatic, congenital
Ix: AP & lateral views (2 views) + imaging of joints above and below as well
Mx (for OA):
- Conservative – physio, exercise, weight loss
- Medical – analgesia, IA CS injection
- Surgical – arthroplasty
Common pathology:
- Hip OA - pain, crepitus, reduced ROM (internal rotation lost first)
- Hip fracture - shortened and externally rotated limb
- Hip dislocation - shortened and internally rotated limb
- Abductor muscle weakness - Trendelenburg’s positive
- Trochanteric bursitis - pain over the greater trochanter
- Childhood - dislocation, Perthes, SUFE
RA - Def? Presentation? Ix? Mx?
Def: AI process causing synovial joint inflammation (synovitis) with destruction of peri-articular structures
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
Mx:
- Create an end target e.g., remission
- 1st - Monotherapy with conventional DMARD (methotrexate/sulfasalazine) + bridging pred until Sx resolved
- 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)

Osteoarthritis - presentation? Ix? Mx?
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)

Psoriatic arthritis - Signs? Types? Criteria name? Mx?
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
- Topical Tx:
- Psoriasis:
- Arthritis = Methotrexate, anti-TNFs

Assessing osteoporosis risk

Osteoporosis Mx? Using bisphosphonates –> jaw pain & swelling?
0 to -2.5 DEXA:
- Conservative - exercise, reduce alcohol, balanced diet, Tx underlying causes
- Repeat DEXA @2yrs
-2.5
- 1st line - Bisphosphonates PO (e.g. alendronic acid) –> if not tolerate can trial Denosumab/Raloxifene/Teriparatide
- Vit D + Ca replacement (if inadequate sunlight/intake exposure)
- Review Tx every 3-5yrs
NOTE:
- If premature menopause –> discuss HRT
- If on high-dose CS (≥7.5mg OD for ≥3 months) –> consider bisphosphonates for bone protection
Osteonecrosis of the jaw

Septic arthritis - presentation? Mx?
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

Ankle fracture rules? Classification? Ix? Mx?
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

Ankle fracture X-ray

Compartment syndrome Key Signs & Sx? RFs? Ix? Mx?
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
Neck of femur anatomy? Breakdown?
RFs? Presentation? Ix? (incl. fracture type & classification) Mx?
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
- Medial & lateral circumflex femoral arteries - gives rise to:
- 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)
- Fit = THR (HoF & acetabulum replaced)

Wrist fracture - types? Mx?
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

RA Hand X-ray findings?
- Joint erosion
- Periarticular osteopenia
- Ulnar deviation
- Z-thumb
- Swan neck

Fracture Mx?
- Reduce (aligning fracture components) e.g. chole’s fracture - haematoma block (provides anaesthesia as you manipulate different parts of the fracture) –> traction/counter-traction
- Hold e.g. with cast
- Rehabilitate - regain function e.g. physio

How do you approach an MSK X-ray?
Describing a fracture on XR approach?
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)
- Step = possible pathology:
- 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

Gout - presentation? Ix? Mx?
Presentation: 1st MTP joint, monoarticular (can be poly)
Ix: Bloods (FBC, CRP, Urate), X-ray (errosive)
Mx:
- Acute:
- NSAIDs
- Colchicine
- Oral Pred (5 days), steroid joint injection
- 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)
Ankylosing Spondylitis is a type of what? Ix? Mx?
Axial spondylitis
Ix:
- Spinal exam: Schober’s test - gross restriction <3cm (should be 8-10cm)
- X-ray:
- Sacroiliitis
- Sclerosis
- Erosive damage
- Widening joint space
- (Fusion)
- MRI scan whole spine & sacroiliac joints - detect pre-radiographic axial spondylitis
- Sacroiliitis
- Shiny corners (Romanus lesions)
Mx:
- Analgesics + NSAIDs
- TNF-alpha blocker (or IL-17 blocker)
Systemic sclerosis (scleroderma) - def? Subsets? Presentation? Ix? Raynaud’s Mx?
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
Dermatomyositis - Presentation? Ix?
Causes muscle inflammation + skin rash
Presentation: Gottron’s papules, heliotropic rash, proximal muscle weakness
Ix: CK, ANA/myositis ab panel, MRI of involved muscle, electromyogram, muscle biopsy
GCA - Presentation? Ix? Mx?
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)
Polymyalgia Rheumatica (PMR) - def? presentation? Associated condition? Dx & Ix? Mx?
Def: inflammatory rheumatological condition
Presentation: muscle aches and joint stiffness
- 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
Tenosynovitis of hand & wrist - def? RFs? Presentation of different types? Ix? Mx?
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)
AKI - def? Severity stages? Breakdown by pathology? Ix? Mx?
Def: abrupt loss of kidney function resulting in dysregulation of fluid balance + electrolytes & retention of nitrogenous waste products
Severity defined based on creatinine/urine output:
- Stage 1: 1.5-1.9x baseline/UO <0.5mL/kg/hr for 6-12hrs
- Stage 2: 2-2.9x baseline/UO <0.5mL/kg/hr for >12hrs
- Stage 3: >3x baseline/UO <0.3mL/kg/hr for >24hrs OR anuria >12hrs
Breakdown by pathology:
-
Pre-renal - HYPOPERFUSION
- Hypovolemia (e.g. dehydration/upper GI bleed -> less circulating volume)
- Sepsis/Anaphylaxis (widespread vasodilation -> reduced perfusion pressure)
- HF (heart pumping less effectively -> less blood reaches kidneys)
- RAS (mechanical obstruction of blood flow to kidneys)
-
Renal - KIDNEY-SPECIFIC –> renal referral
- Acute tubular necrosis (following pre-renal AKI, high CK)
- Glomerulus = Glomerulonephritis
- Interstitium = acute interstitial nephritis (low-grade fever, elevated urinary eosinophils, commonly from NSAIDs)
- Blood vessels = vasculitis
- Toxin accumulation = nephrotoxic drugs (ACEi, thiazide diuretic), rhabdomyolysis (myoglobin)
-
Post-renal - OBSTRUCTION –> urology referral
- Ureteric calculus
- BPH
- Cancer (prostrate, bladder)
Ix:
- Bedside - urinalysis (haematuria, inf, BM, PCR)
- Red cell casts - glomerulonephritis
- White cell casts = pyelonephritis
- Bloods - U&E, AI screen (ANCA), CK
- Imaging - renal USS (stones, vascular thrombosis)
Mx:
- Identify & Mx the cause
- Hypovolaemic - IV fluid bolus
- Hypervolaemic - if pul oedema –> loop diuretic (furosemide) + Na restriciton

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

Urinary tract calculi - def? presentation? Stone types? Ix? Mx? When to ADMIT/what to do if managed @home?
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)
-
Ureteroscopic lithotripsy - endoscope into ureter & using mechanical force/laser to destroy stone
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

Scrotal masses - ddx?
DDx:
-
Testicular torsion - EMERGENCY & TIME-URGENT
- Elevated testis, loss of cremasteric reflex, very tender
- Tx: bilateral orchidopexy (orchidectomy - if necrotic)
-
Can you feel above swelling?
- YES - swelling separate from testis?
- YES - Epididymal cyst OR Varicocele
- NO - Tender?
- YES - Epididymo-orchitis
- NO - Hydrocele OR Tumour
- NO - Inguinal hernia
- YES - swelling separate from testis?

Nephrotic vs nephritic syndrome
- Glomerular structure and podocyte function?
- Nephritic - def? key signs? causes?
- Nephrotic - def? key signs? causes?
Kidney glomerular structure:
- Capillary > Endothelial cells > Glomerular basement membrane (GBM) > Foot processes of podocyte
- Podocyte function: prevent protein leaking into the filtrate
Nephritic = proliferative - inflammation of glomerulus & nephrons –> capillary becomes leaky –> blood & protein leak
- Key: blood, protein, increased creatinine, possible trigger (e.g. inf), acute/subacute disease progression
- Causes: often immune-mediated
-
Post-streptococcal glomerulonephritis - molecular mimicry - antigen in kidneys accidentally recognised as strep antigen after inf
- Nephritic - more HTN
- Weeks after GAS inf (pharyngitis, skin)
- Ix: ASO titre (high/low C3)
- Mx: conservative - BP control
- No long-term problems
-
IgA nephropathy (Berger’s disease) - generate abn IgA –> abs attach & form immune complexes = sticks & get stuck in glomerular capillaries –> activate compliment –> inflammation
- Nephritic - more proteinuria
- Sx: abdo pain, rash, arthritis
- Days post-resp/GI inf
- Mx: BP control, steroid
- 40% get renal failure
- Assoc w/ IgA conditions (HSP, Coeliac disease)
-
Henoch-Schonlein Purpura (HSP) - related to IgA nephropathy but is WIDESPREAD (IgA limited to kidneys)
- Purpuric rash (buttocks/extensors), arthritis, abdo pain, Hx URTI
- Mx: spontaneous resolution ± steroids
- Haemolytic Uraemic Syndrome (HUS) - MAHA, thrombocytopenia, E.Coli (O157)
- Goodpasture’s syndrome (anti-GBM disease) - pul haemorrhage, rapidly progressing glomerulonephritis + anti-GBM abs
- Granulomatosis with polyangiitis (Wegner’s) - chronic sinusitis + lung haemorrhage, PR3 (cANCA)
- SLE
-
Post-streptococcal glomerulonephritis - molecular mimicry - antigen in kidneys accidentally recognised as strep antigen after inf
Nephrotic = non-proliferative - (urinary protein loss >3.5g/day) from Podocyte effacement
- NOTE: 24-hr urine collection not commonly done so better marker is spot urine protein: creatinine ratio >300mg/mmol
- Key: high protein, hypoalbuminaemia, oedema (face), thrombosis (main coag factor loss in urine is anti-thrombin 3 = one of the bodies main anticoagulant mechanisms –> hypercoagulable state) –> VTE
-
Renal biopsy to determine type –> causes:
- Minimal change disease - children –> Tx: steroids
- Focal segmental glomerulosclerosis - most common in adults, assoc w/ obesity, DM & HIV
- Membranous glomerulonephritis - 2nd most common in adults, idiopathic
- Amyloidosis –> Ix: CONGO RED STAIN
Testicular cancer - Epidemiology & mets? Ix? Mx?
Epidemiology & mets:
- Mets to para-aortic LNs
- Most common malignancy in males 20-40yrs
Ix:
- Blood testicular tumour markers: alpha-fetoprotein, beta-hCG, LDH (necrosis, others secreted by tumour itself)
- Testicular US –> CT-CAP for staging (would likely do orchidectomy before CT)
- Urine dip (look for infection) –> culture
Mx:
- Orchidectomy – take inguinal approach (scrotal approach risks mets and inguinal is coming out the same way the testicle drops) - only time would not do this first is when respiratory compromise then would do chemo first
- BEP chemotherapy follow-up = very good response typically
- Very good prognosis - good/intermediate prognosis groups have >90% 5-yr survival

Urinary retention breakdown? Ix? Mx acute retention?
- Acute - pain
- Chronic – no pain
- Low pressure
- High pressure – renal impairment + hydronephrosis
- LUTS with nocturnal enuresis
Acute Ix:
- DRE - men & women (also PV exam)
- Urine dip + MC&S
- Bloods - FBC, U&E, PSA
- Imaging - bladder scan (for acute), US KUB (for chronic)
- Meds review:
- stop anticholinergics
- analgesia if needed
- laxatives for constipation

Hydrocele - def? Ix?
Def: collection of fluid in tunica vaginalis
Ix: US, testicular tumour markers (AFP & bHCG - secreted by tumour, LDH - necrosis), urine culture (inf)
Causes: idiopathic, inf, trauma, tumour
Varicocele - def? What side is more common? What is it associated with x2? How can I reduce swelling?
Def: distended veins of pampiniform plexus
Key points:
- More common on left (the way left testicular vein drains into left renal vein)
- Assoc w/ infertility, renal cancer
- Swelling may reduce when lying down
Bladder cancer - presentation? Ix? Mx?
Most common = transitional cell carcinoma (urothelial)
Presentation:
- Painless visible haematuria (or asymptomatic non-visible haematuria)
- Irrigative LUTS (urgency, suprapubic pain)
- Recurrent UTIs
- Pain, weight loss, lymphoedema
Ix:
- Initial:
- Urine dip (blood, leucocytes)
- MC&S (use MSU - RBCs & WBCs, no bacterial growth)
- Bloods - FBC
- Flexible cystoscopy (lower urinary tract) + CT-urogram (upper urinary track if visible haematuria –> if non-visible low-risk use US)
- Dx & staging = Transurethral Bladder Tumour Resection (TURBT) - resects full tumour + histology
- Intravesical therapy:
- Bacillus Calmette-Guerin (BCG) instilled into bladder –> reduces superficial bladder cancer recurrence (causes immune response to remaining tumour cells, same substance as in BCG vaccine)
- Mitomycin - cytotoxic chemo agent
- Intravesical therapy:
Mx: 2wk wait urology
- Muscle invasive = cystectomy (young people) or radiotherapy/chemotherapy (older)
- Superficial = surveillance cystoscopies, intravesical chemo
- Mets = systemic therapy
ANCA-assoc vasculitis breakdown? Presentation? Ix? Types based on Ix? Tx?
Presentation: ALL can cause renal impairment + rash (e.g. shins) ± low-grade pyrexia/fatigue
Ix - Rheumatological Ab screening:
- ANA
- ANCA
- biopsies of BVs/affected organs e.g. kidneys
cANCA = PR3:
-
Granulomatosis with polyangiitis (GPA) aka Wegener’s
- Nasal bridge collapse/epistaxis, chronic sinusitis
- DDx for nasal bridge collapse can be cocaine abuse
- Can develop pulmonary nodules/haemorrhage
- Granulomas
- Case: 52yrs, cough with blood, malaise, rashes, SoB, sinusitis for yrs
- ABG - reduced PaO2, raised creatinine, cANCA +ve
- Nasal bridge collapse/epistaxis, chronic sinusitis
pANCA = MPO (myeloperoxidase):
-
Eosinophilic granulomatosis with polyangiitis (EGPA) aka Churg-Strauss
- Asthma + eosinophilia + mononeuritis multiplex (e.g. weakness in hand)
- Granulomas
- Microscopic polyangiitis - no granulomas
Tx:
- Remission: cyclophosphamide + CSs
- Maintenance: low-dose CSs + methotrexate

Testicular torsion - presentation? Tx?
Presentation: sudden-onset pain, high fixed position, absent cremasteric reflex
Tx: bilateral orchidopexy (both sides as increased risk of torsion in the other side)
Prostate cancer - Ix? Mx?
Ix:
- PR exam, PSA
- FBC, U&E, LFTs
- Transrectal ultrasound (TRUS)-guided needle biopsy
- Gleason score = PC grading
- TNM staging
- Multiparametric MRI
Mx: surgery/radiotherapy
- Radial prostatectomy ± LN dissection
- External beam radiotherapy/brachytherapy
- Androgen-deprivation therapy (ADT)
Acute tubular necrosis - causes? def?
Def: renal tubular dysfunction/detachment from the basement membrane
- Most common intrinsic renal cause of AKI
- Causes:
- Chronic ischaemia of renal tubules (shock/LVF) - initially pre-renal AKI
- Nephrotoxic (lots of myo/haemoglobin, contrast, aminoglycosides e.g. gent, Ig light chains)
- Can’t concentrate urine or regulate electrolytes –> high UO, high urine sodium
Red swollen leg DDx?
Cellulitis/Erysipelas
Venous thrombosis (DVT)
Chronic venous insufficiency

Purpuric erruption DDx?
Meningococcal septicaemia
DIC
Vasculitis
Acitinic purpura

Changing pigmented lesion ddx?
Melanocytic naevi
Seborrhoeic wart
Malignant melanoma

Itchy eruption DDx?
Eczema - atopy/exacerbating factors
Scabies - contacts with Hx
Urticaria - precipitant
Lichen planus - FHx/drug-induced
general Mx: antihistamines, CS

Anaemia Ix? Mx?
Ix: FBC, haematinics, B12/folate, OGD
Blood transfusion threshold: Hb <70 or <80 AND ACS
Other options: Fe infusion, ferrous fumarate
NOTE: anaemia can exacerbate chest pain/ACS
Delirium definition? Common causes?
Delirium screen breakdown? Mx?
Def: Acute confusional state caused by a physical condition
Causes: U PINCHES ME
- Urinary retention
- Pain
- Infections
- Nutrition
- Constipation
- Hydration
- Endo & electrolytes
- Stroke
- Medications & alcohol
- Environmental
Delirium screen:
- FBC, U&E, LFT, glucose, BC, Ca, TFTs, B12/folate
- Urine dip + MC&S
- CXR, possibly CT-head
Management: Tx cause
- Conservative: lighting, clocks, 1:1 nursing, adequate hydration, laxatives, involve family/carers
- SOS (risk to themselves/others):
- Lorazepam (PO/IM/IV)
- Haloperidol (PO/IM) - be careful if Parkinson’s –> worsens Sx
Anaphylaxis Mx (acute & chronic)
ABCDE
- Stop suspected cause
- Secure airway, give 100% oxygen, +/- intubate if respiratory obstruction imminent
- IM 0.5mg adrenaline (1:1000)
- IV 10mg chlorpheniramine
- IV 100mg hydrocortisone
- Treat bronchospasm – salbutamol +/- ipratropium
Going forward:
- Maintain fluids + monitor pulse oximetry, ECG and BP
- If still hypotensive, may need transfer to ICU and an IVI of adrenaline +/- aminophylline (bronchodilator) and nebulised salbutamol
After acute episode:
- Admit to ward and monitor ECG, monitor for 6hrs for biphasic reaction
- Measure mast cell tryptase 1-6 hours after = confirm anaphylaxis
- Continue chlorpheniramine
- Suggest MedicAlert bracelet with name of culprit allergen
- Teach about self-injected adrenaline & give auto-injector
- Skin prick tests showing specific IgE to help identify allergens to avoid

What is sepsis 6?
3 in, 3 out
All within 1hr

How to Tx asystole?
IV adrenaline
Drugs for cardiac arrest?
DC shock (150J biphasic)
Adrenaline 1mg IV (10ml 1:10,000)
Amiodarone 300mg IV (if shockable rhythm)
Trauma patient initial Mx?
Airway and cervical spine
Next - CT-head + CXR
Acute limb ischaemia - Def? Presentation? Ix? Mx?
-
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
- Initial:

Peripheral vascular disease localisation & type of bypass graft?
- 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

Peripheral vascular (arterial) disease - Def? RFs? Spectrum? Ix? Special test?
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
AAA key Sx & ruptured Sx? Ix? Mx?
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

Vascular exam - upper, abdo & lower? Arterial & venous anatomy?
NOTE: if press harder and it is there = my own pulse; if press weaker and it is there = their pulse
- If can’t feel pulses can use doppler USS: triphasic signal
- 1st phase - forward rush of blood
- 2nd phase - reverse flow from elastic recoil (in arterial wall)
- Lost in arterial disease = biphasic/monophasic signal
- 3rd phase - forward flow on vessel relaxing
EXAMINATION:
General inspection – smoking, inhalers, diabetic meds, fistula, dressings, walking stick
Upper:
- Hands – splinter haemorrhages, nicotine stains, missing digits (more common in trauma, Buerger’s disease), temperature + CRT
- Supra-aortic pulses:
- Radial – rate, rhythm, radio-radial delay
- Brachial pulse – character
- Subclavian pulse, in supraclavicular fossa
- Carotid pulse
- BP
- Listen for bruits in neck, breathe in and out slowly
Abdo:
- Inspect for scars, look around sides
- Palpate for aneurysms - abdominal aortic pulse
- Listen for aortic and renal bruits (above umbilicus and to either side)
Lower:
- Inspect (colour, swelling, scars, varicose veins)
- Palpate:
- Temp in feet, calves, thighs (run back of hand along)
- Tenderness - squeeze ankles/calves (DVT)
- CRT, pitting oedema
- Measure leg diameter 10cm below tibial tuberosity (If <3cm between = not significant)
- Femoral arteries (ASIS & pubic symphysis midpoint):
- Feel simultaneously as weak femoral pulse difficult to determine
- Radio-femoral delay
- Auscultate femoral pulse for bruits (can also listen to iliacs - below umbilicus on either side) –> sometimes only picked up on exercise
- Popliteal arteries – reach around back of knee, behind the knee, slightly lateral, lift leg up to 30 degrees so weight resting on fingers
- Pedal arteries – anterior (dorsalis pedis) & posterior tibial (behind medial malleolus)
- BUERGER’S TEST (for peripheral vascular disease)
- Both feet held up – angle foot goes white is Buerger’s angle –> when foot blanches swing legs over side of bed and let them hand down –> ischaemic foot will go brick red = severe peripheral vascular disease of lower limb = SUNSET SIGN
- Ideally, I should hold feet for 1 minute but still say -ve test if no blanching
- ABPI:
- BP cuff above ankle with leads upwards – find dorsalis pedis pulse with doppler USS
- Inflate cuff until signal disappears – let down cuff until signal reappears = ankle pressure
- Repeat procedure in arm using brachial artery signal to record the brachial pressure
- ABPI = ankle pressure/brachial pressure
- 0.5-0.8 = claudication (mild-moderate disease); <0.5 = rest pain (severe disease); <0.2 = gangrene
Finally - complete relevant neuro exam, vascular exam where not been done in exam, CV & abdo exams
- Bloods - FBC, U&E, coag
- D-dimer, duplex USS (venous - DVT/arterial - perfussion) –> CTPA (PE)
- Tx: DOAC/Warfarin if high-risk DVT
Leg Anatomy:
-
Arterial:
- External iliac artery > femoral artery (pulse):
- Profunda artery (minor branch)
- Superficial femora artery (main branch) > Popliteal artery (pulse):
- Anterior tibial artery - form dorsalis pedis artery (pulse)
-
Posterior tibial artery - goes around medial malleolus (pulse)
- Peroneal artery (branch of PTA)
- External iliac artery > femoral artery (pulse):
-
Venous:
- Great-saphenous vein (medial) - meets deep femoral vein in medial upper thigh (as goes into groin)
- Small-saphenous vein (lateral)
- Connected via perforating vein

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

Aortic dissection - def? Sx? Ix? Mx?
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)

Breast anatomy? Breast exam? Triple assessment?
Breast anatomy - Lobules > ducts > nipple
- Ligaments suspending breast = Cooper’s ligaments
- Most lymphatic drainage to axilla (& intercostal, interthoracic LNs)
- Blood supply - perforating intercostal arteries
Intro - WIPE + chaperone
Inspection:
-
SITTING Positions:
- Relaxed arms
- Hands rested on thighs
- Hands-on hips - tense pectoralis
- Hands behind head - accentuate dimpling/asymmetry
- Lift breasts - submammary fold (ask patient)
- Look for:
- Asymmetry, local swelling, scars (look under breasts)
- Skin changes:
- Dimpling/puckering - tethering due to cancer
- Peau d’orange - lymphatic oedema due to cancer
- Nipple changes:
- Paget’s disease of breast - unilateral nipple = cancer
- Eczema - areola (rarely nipple), bilateral
- Inversion - normal variant/cancer
Palpation: LYING DOWN + hand on the side being examined behind head + check for pain (start on normal side)
- Use palmar surface of middle 3 fingers to feel for any lumps starting in centre and going round in concentric circles
- Pinch along axillary tail (first 2 fingers & thumb)
- Ask patient to squeeze each nipple to check for discharge
- Localise + describe lump: 3Ss, 3Cs, 3Ts
- Site, Size, Shape
- Consistency, Contours, Colour
- Tenderness, Temperature, Tethering/Transillumination
- Lymph nodes:
- Axillary - ask patient to hold bicep:
- Palpate apical, lateral, medial, anterior, posterior aspects
- Cervical LN exam
- Axillary - ask patient to hold bicep:
- Offer to examine lungs and liver for mets
Triple assessment:
- Examination
- Imaging (USS <35yrs; MMG + USS ≥35yrs)
- Biopsy (FNA if cystic, core biopsy if solid)

Comparing different types of vascular ulcers:
- Hx
- Location
- Characteristics - ulcer & surrounding skin
- Tx
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: off-loading pressure, topical GF
Pressure:
- Hx: limited mobility
- Location: bony prominence, heel
- Characteristics:
- Ulcer - deep, macerated (moist, wrinkly)
- Surrounding skin - atrophic skin, lost muscle mass
- Tx: off-loading pressure, reduced moisture, increased nutrition

Breast Diagnostics
Screening MMG
- ≥50yrs - 3yrly
- >40yrs - attending clinics
USS focused:
- <35yrs USS only
- ≥35yrs USS + MMG
Biopsy:
- all breast lumps in women >25yrs
- USS-guided
Benign breast diseases - types? presentation? Dx? Mx?
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
Nipple discharge - causes? presentation? Dx? Mx?
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
Breast carcinoma - RFs? types (incl. receptors, axilla involvement)? Presentation? Dx? Mx?
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)
Hypertension BP targets? Ix? Mx?
BP targets:
- <140/90
- <150/95 for over 80yrs
- Causes of hypertensive crisis ≥180/120: pregnancy, scleroderma, vasculitis, renovascular, endo, cocaine –> reduce BP slowly
Ix:
- Bedside - ECG, urine dip
- Bloods - FBC, U&E, lipids, BM, TFTs
Drug treatment:
- Conservative management - diet (low salt), exercise, reduce alcohol
- a) <55yrs/DM –> ACEi (ramipril)/ANG-II receptor antagonist (Losartan)
- b) ≥55yrs/black –> CCB (amlodipine)/thiazide diuretic (bendroflumethiazide)
- ACEi + CCB OR ACEi + thiazide diuretic
- ACEi + CCB + thiazide diuretic
- Add:
* Spironolactone (or other diuretic)
* Alpha-blocker
* Beta-blocker
* Specialist advice
- Add:
DVT - def? RFs? Presentation? Scoring & Ix? Mx?
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
Thyroglossal duct cyst - def? presentation? Tx?
Most common congenital neck mass
- Thyroglossal duct - embryological duct connecting back of tongue & thyroid gland
- Cyst results from failure of thyroglossal duct closing before birth
Presentation: painless fluctuant midline mass
- Often presents in childhood following inf (painful red)
- On exam moves upwards when sticking out tongue due to attachment of duct
Tx: surgical resection of cyst & duct
Pre-cancerous breast masses
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
- Mx: breast-conserving surgery - wide local excision
Lobular carcinoma in-situ
Epistaxis - RFs? Where do most nosebleeds arise from? When is it a posterior bleed? Mx of anterior nosebleed?
RFs:
- alcohol intake/excess
- bleeding/clotting disorder
- anticoag/platelets
- topical drugs (decongestants, cocaine)
- nasal polyps
- chronic sinusitis
Location: anterior nasopharynx - Little’s area (where 5 arteries come together = Kiesellbach’s plexus)
- NOTE: Posterior nose bleeds are less common but bleed more
Most anterior, suspect posterior bleed if:
- Profuse bleed, both nostrils
- The bleeding point can’t be seen on speculum exam
- Suspected anterior bleed not responsive to packing/cautery
- Mx posterior with bilateral posterior packing + abx (change packing every 48hrs)
Ix: nasal speculum examination
Mx of anterior nosebleeds:
- First aid:
- Sit up + lean forward
- Mouth open (spit blood out)
- Pinch nasal cartridge for 15mins
- Vasoconstrictors (oxymetazoline spray, adrenaline-soaked gauze) & analgesia
- Silver nitrate cautery (or electrocautery)
- Anterior nasal packing

Tonsilitis - most common causes? scoring? Ix? Mx? When to ADMIT?
Causes: EBV, GAS
Scoring:
- CENTOR (if <3 days pharyngitis):
- Cough absent
- Exudate
- Nodes (cervical anterior)
- Temp >38 at any point
- FeverPAIN score
- Fever (during previous 24 hours)
- Purulence (pus on tonsils)
- Attend rapidly (within 3 days after onset of symptoms)
- Severely inflamed tonsils
- No cough or coryza
Ix: oropharyngeal examination (unless considering epiglottitis - can cause respiratory compromise –> keep child calm with mum/dad)
Mx:
- If CENTOR 3-5/FeverPAIN 4-5 –> rapid strep test + abx (phenoxymethylpenicillin) + self-care advice
- Otherwise just self-care advice (if FeverPAIN 2-3 can give ‘back-up abx’)
- Tonsillectomy if: 7 bouts in 1yr/5 bouts per year for 2yrs/3 bouts per year for 3yrs
ADMIT if:
- Difficulty breathing
- Clinical dehydration
- Peri-tonsillar abscess (quinsy)/cellulitis
- Marked systemic illness/sepsis
- Suspected rare cause (e.g. Kawasaki disease, diphtheria)

Causes of red eye?
Painless red eye:
- Conjunctivitis:
- Diffuse conjunctival injection (unilateral or bilateral)
- Discharge (purulent if bacterial), swollen conjunctiva (chemosis) and debris
- Subconjunctival haemorrhage:
- Flat, bright red patch on conjunctiva with sharply defined borders and normal conjunctiva surrounding it.
- Episcleritis:
- Sectoral area of subconjunctival injection (unilateral)
- Superficial - moveable with swab (using topical anaesthesia)
- Dry eye:
- Deficiencies in tear production/maintenance secondary to e.g. blepharitis (obstruction of meibomian glands)
- Clinical features - diffuse conjunctival injection (unilateral/bilateral), inflamed lid margins with crusting & matted eyelashes.
Painful red eye:
- Scleritis:
- Localised conjunctival injection (unilateral), minimal watery discharge
- Visual acuity may be reduced, photophobia, tender globe (causing the patient to wake at night) –> all progressively worsen
- Commonly have CTD
- Uveitis:
- Circumciliary conjunctival injection (unilateral), hazy cornea, distorted pupil, hypopyon, watery discharge
- Reduced visual acuity, photophobia & pain
- Corneal abrasion:
- Eye redness, pain, watering and photophobia
- Epithelial defects stain brightly with fluorescein drops & cobalt blue light.
- Damage to epithelial layer of eye due to light trauma - very painful but shortlived
- Corneal ulcer:
- Pain, watering, photophobia, staining epithelial defect with associated haziness (infiltrates)
- Epithelial defect may appear fluffy, irregular and apparent even without a slit lamp.
- More common in contact-lens wearers (infection or immunological response) = more severe than abrasion
- Acute angle-closure glaucoma (AACG):
- Significant pain –> vomiting, circumciliary conjunctival injection (unilateral), reduced visual acuity, photophobia, haloes in vision, hazy cornea and a mid-dilated unreactive pupil.
- Foreign bodies:
- May be visible on the surface of the eye or embedded within the cornea or sclera
- Associated clinical features include redness, pain, watering and a ‘foreign body sensation’.
- Foreign bodies may be hidden under the top and bottom of the eyelid.

Acute angle-closure glaucoma - presentation? Ix? Mx?
Presentation: blurring of vision, painful red eye, headache, N&V
- In contrast:
- Uveitis has small pupil (& red eye, headache & visual disturbance)
- Scleritis, corneal ulcer and conjunctivitis are not associated with headache and nausea or sign drop in visual acuity
Ix:
- Gonioscopy - examination of anterior chamber angle
- Slit-lamp examination
- Automatic static perimetry
Mx:
- 1st line - Carbonic anhydrase inhibitors (acetazolamide) AND/or topical beta-blockers (timolol) AND/or topical alpha-2 agonists (brimonidine)
- When the suspected cause is pupillary block/plateau iris syndrome and IOP <40 –> topical ophthalmic anticholinergic (pilocarpine)
- Initial Tx fails/IOP >50 –> hyperosmotic agent (IV mannitol)
- 2nd line - anterior chamber paracentesis
- Surgery (after acute attack resolves in pupillary block)/chronic angle-closure glaucoma - laser peripheral iridotomy
Sinusitis - red flags? When to admit? Ix? Mx?
Red flags (need urgent ENT referral):
- Unilateral
- Persistent > 3 months despite Tx
- Epistaxis
When to admit:
- Severe systemic infection
- Signs of dangerous complications of sinusitis:
- Periorbital/orbital cellulitis
- Meningitis
- Brain abscess
Ix: anterior rhinoscopy, nasal endoscopy
Mx:
- If symptoms <10 days –> advice and safetynetting
- If symptoms >10 days –> 14-day course of high-dose nasal CS
- Can give back-up prescription of abx
Retinal detachment - RFs? Presentation? Ix? Mx?
RFs:
- Rhegmatogenous RD (small tear in retina - vitreous can get behind retina): prev Hx in other eye, prev cataract surgery, myopia (short-sighted), ocular trauma (e.g. lattice degeneration)
- Non-rhegmatogenous RF: DM, intraocular tumour, age-related macular generation
Presentation:
- Acute loss/deterioration of central vision
- Flashing lights in temporal visual fields (easier to notice in dark environment)
- Floaters (large, central)
- Numerous, small = retinal haemorrhage
Ix:
- Visual acuity testing
- Slit-lamp exam
- Indirect ophthalmoscopy
Mx:
- Prophylactic Tx - laser cerclage
- Retinal tear without detachment:
- Asymptomatic - observation/reassurance ± prophylactic Tx (laser cerclage)
- Symptomatic - cryopexy/laser retinopexy
- Scleral buckle/vitrectomy + cryopexy/laser retinopexy
Otitis media - Def? Causative organisms? Red Flags?
Def: middle ear inf, most resolve without abx
- Organisms: S. pneumo, H. influenzae
- Causes bulging tympanic membrane
- Acute suppurative otitis media (perforated ear drum): otalgia + discharge –> otalgia improves after discharge (pressure release)
Red flags:
- Mastoiditis
- Sepsis w/ post-auricular tenderness
- Mastoid air space abscess
- Facial palsy - due to oedema of facial nerve (rare)
- Meningism/altered conscious state
Hypertension BP targets? Mx?
BP targets:
- <140/90
- <150/95 if >80yrs
Drug treatment:
- a) <55yrs/DM –> ACEi (ramipril)/ANG-II receptor antagonist (Losartan)
- b) ≥55yrs/black –> CCB (amlodipine)/thiazide diuretic (bendroflumethiazide)
- ACEi + CCB OR ACEi + thiazide diuretic
- ACEi + CCB + thiazide diuretic
- Add:
* Spironolactone (or other diuretic)
* Alpha-blocker
* Beta-blocker
* Specialist advice
- Add: