PACES ALL Flashcards

Question 1

Q

Reading an ABG?

Answer

A

Respiratory failure:

Low O2 = T1RF (PaO2 <8kPa)
Low O2 + High CO2 = T2RF (PaO2 <8kPa, PaCO2 >6kPa)

Determining acid: base balance:

Low pH + high CO2 = Respiratory acidosis (low CO2 = metabolic)
High pH + low CO2 = Respiratory alkalosis (high CO2 = metabolic)
NOTE: if bicarb is high in RA = chronic RA (compensation by bicarb is slow) –> this determines if should be on scale 1/2 O2 (scale 2 = 88-92%)

Causes of acid: base balance:

RA causes: COPD, ILD, hypoventilation, asthma (normally resp alkalosis but can be acidotic if severe)
MA causes: lactic acid, ketoacids (CO2 blown off to compensate –> Kussmaul breathing)

Question 2

Q

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

Answer

A

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

Presentation

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

Ix:

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

Asthma severity:

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

Short-term Mx:

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

Long-term Mx (>16yrs):

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

Question 3

Q

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

Answer

A

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

Presentation:

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

New Dx Mx:

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

Acute Exacerbation Mx:

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

Prognosis factors:

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

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

Question 4

Q

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

Answer

A

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

Presentation:

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

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

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

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

Types & Mx –> local abx guidelines

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

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

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

Question 5

Q

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

Answer

A

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

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

RFs: SICC - Surgery, Immobility, Cancer, COCP

Initial Tx:

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

Scoring & Ix: Well’s score

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

Ongoing anticoagulation - DOAC/Warfarin

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

Question 6

Q

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

Answer

A

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

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

Presentation:

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

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

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

Mx:

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

Question 7

Q

Sarcoidosis - def? presentation? Ix? Mx?

Answer

A

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)
Lofgren’s syndrome = triad: erythema nodosum + bilateral hilar lymphadenopathy + polyarthralgia

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

Question 8

Q

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

Answer

A

Interstitial lung disease

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

Causes:

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

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

Signs: find end-insp creps, clubbing

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

Investigations: spirometry, high-res CT & lung biopsy

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

Management:

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

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

Question 9

Q

Restrictive vs Obstructive lung conditions

Answer

A

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

Question 10

Q

What is FEV1 and FVC? WHat does FEV1/FVC ratio indicate?

Answer

A

FEV1 - total air expired forcibly in 1s (spirometry reading)

FVC - total air expired in a complete breath

FEV1/FVC ratio - decrease <80 indicates an obstructive condition

Question 11

Q

Cor Pulmonale Def? Dx? Mx?

Answer

A

Def? RHF secondary to lung disease

Dx: (clinical Dx –> confirm with ECHO)

Peripheral oedema
Raised JVP
Loud pul second HS
Sytolic parasternal heave

Mx:

Smoking cessation
Optimise COPD meds
If PaO2 <8 + features of Cor Pulmonale –> long-term O2 therapy (not if smoker)
- If not above –> Sx control = diuretics

Question 12

Q

Chronic bronchitis vs emphysema?

Answer

A

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

Question 13

Q

Pleural effusion - signs? causes? Ix? Mx?

Answer

A

Signs (if fluid > 300ml):

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

Causes:

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

Ix:

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

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

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

Pleural fluid features:

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

Question 14

Q

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

Answer

A

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

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

Causes: cystic pathology, parenchymal necrosis, iatrogenic, trauma

Ix: CXR

Mx:

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

Tension pneumothorax = pushes away the trachea to the opposite side

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

Location:

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

Surgery:

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

Question 15

Q

Causes of different ABGs? Resp/Met Acidosis/Alkalosis

Answer

A

Resp acidosis (not breathing out enough) - asthma, COPD, GBS

Resp alkalosis - pain, panic attack, PE, pneumothorax

Metabolic acidosis - DKA, LA, diarrhoea, renal failure

Metabolic alkalosis - vom/diarrhoea, diuretics (loop/thiazide), Conn’s syndrome, liver cirrhosis, HF

Question 16

Q

T1RF vs T2RF causes?

Answer

A

T1RF: low/normal CO2 –> pul oedema, ARDS, collapse

T2RF: high CO2 –> opiate OD, COPD, neuromusc disease

Question 17

Q

Respiratory causes of clubbing?

Answer

A

Lung cancer, bronchiectasis (& CF), pul fibrosis

NOT COPD (but if COPD is smoker with clubbing –> lung cancer)

Question 18

Q

Causes of lung consolidation? How do you know it is a consolidation?

Answer

A

Pus (infection)

Fluid (pul. oedema)

Cancer

Blood (pulm haemorrhage)

Protein (alveolar proteinosis = rare)

Consolidation has lung bronchograms

Question 19

Q

Allergic bronchopulmonary aspergillosis (ABPA) - def? presentation? Ix? Mx?

Answer

A

Def: results from T1 hypersensitivity reaction to Aspergillus spores (in exam often Hx of bronchiectasis + eosinophilia)

Presentation:

SoB, wheeze (bronchoconstriction), productive cough, recurrent chest infections
Coarse crepitations (if bronchiectasis)
RFs: asthma, CF, atopy

Ix:

Bedside - allergic skin-prick, spirometry, oxygen sats
Bloods - eosinophilia, raised total IgE (>1000), Aspergillus +ve IgE & G
Imaging - CXR, CT-chest (bronchiectasis, mucus plugging)

Mx:

Conservative - chest physio (if features of bronchiectasis)
Medical:
- Oral glucocorticoids (low-medium dose tapered over 3-12 months)
- 2nd line - Itraconazole

Question 20

Q

Cystic fibrosis - def? presentation? Ix? Mx? Prognosis?

Answer

A

Def: hereditary AR disorder caused by a mutation in CFTR gene characterised by the production of thick sticky mucus

Presentation:

Commonly presents in infancy (Muconium ileus, genetic testing)
Multi-systemic:
- Resp - recurrent chest inf
- GI - weight loss, malnutrition
- Endo - infertility, T1DM
- MSK - poor muscle mass

Ix:

Bedside:
- Immunoreactive trypsinogen test (IRT) - newborn screening, not diagnostic
- Faecal elastase - abn pancreatic function
- Sweat test (+ve if Cl >60mmol/L; -ve <30)
- Sputum culture (pseudomonas)
- Pul funct tests (obstructive pattern)
Lab:
- Genetic testing - CFTR gene mutations, ciliary genetic defects after (kartagener’s)
- Bloods - FBC, Ig, Aspergillus precipitins, nutrition status (vit, protein, Fe)
Imaging:
- CXR/CT-chest - hyperinflation, bronchiectasis
- Abdo USS - fatty liver

Mx: MDT approach

Conservative - airway clearance techniques (chest physio), GI nutritional support
Medical:
- Nebs mucolytics (Dornase alfa, hypertonic saline)
- Bronchodilator therapy (SABA/LABA)
- Long-term abx (azithromycin)
Surgical: lung transplant (if FEV1<30% predicted, refractory haemoptysis, failure of medical therapy)

Prognosis:

No cure, mean survival = 40yrs (determinant of age is severity of lung disease)
Death from chronic resp failure, cor pulmonale (from pul HTN), resp complications (pneumothorax, pneumonia)

Question 21

Q

Hypersensitivity pneumonitis aka extrinsic allergic alveolitis - Def? Ix? Mx & specific Mx of psittacosis?

Answer

A

Def: immune-mediated ILD precipitated by hypersensitivity to inhalation of micro-organisms

Examples: Mushroom worker’s lung (thermactinomyces vulgaris), Malt-worker’s lung (Aspergillus clavatus)
DDx: pulmonary fibrosis, pneumoconiosis

Ix:

Bedside - O2 sats, inflammatory markers
Imaging: CXR (90% have consolidation), CT chest (apical lung fibrosis)
Confirmation with serology (as part of atypical pneumonia screen)

Mx:

Conservative - avoidance
Acute - pred tapered for 6 weeks
Chronic - long-term low-dose pred
Psittacosis: Tetracycline e.g. Doxy (2nd line - Macrolide e.g. erythromycin)

Question 22

Q

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

Answer

A

Epi: Second most common cancer in UK

Presentation: chronic cough, haemoptysis, FLAWS

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

Types:

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

Ix:

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

Mx:

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

Question 23

Q

4Ps of respiratory conservative Mx?

Answer

A

Persuade to stop smoking

Pul rehab

Prick them - influenza + pneumococcal vaccine

Psych issues

Question 24

Q

Resp scars? Lobectomy/Pneumonectomy DDx? Presentation?

Answer

A

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

Question 25

Q

Fine vs coarse creps?

Vesicular vs bronchial breathing?

Answer

A

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

Best heard at base of lungs

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

No specific area of lungs louder

Vesicular - inspiratory > expiratory

Bronchial - inspiratory = expiratory

Question 26

Q

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

Answer

A

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

Stable angina - chest pain on exertion relieved by rest

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

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

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

Complications: FAP (failure, arrhythmias, pericarditis)

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

Question 27

Q

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

Answer

A

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

Causes:

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

Pathophysiology:

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

Categories:

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

NYHA classification:

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

Ix:

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

Mx: MON BA (out of MONA BASH)

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

Complications:

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

Question 28

Q

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

Answer

A

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

Junctional types:

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

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

Mx:

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

Question 29

Q

Key heart murmurs?

Accentuation manoeuvres?

Causes?

Left vs right heart valve abn epidemiology?

Mx?

Complications of prosthetic heart valves?

Answer

A

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:
- Acute: - IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- Chronic - myxomatous degeration
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
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
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
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)

Complications of prosthetic heart valves: FIBAT

Failure
Infection
Bleeding - MAHA
Anaemia
Thromboembolic phenomena

Question 30

Q

MI location based on ECG

Answer

A

Inferior – right coronary artery (2,3, aVF foot)
Anterior – left anterior descending artery (V1-2)
Lateral – circumflex artery (1 ,aVL, V5/6)
Posterior - ST depression in V2-4, abnormal R wave in V2

Question 31

Q

Atrial fibrillation (AF)

Def? Causes? Ix? Mx?

Answer

A

Def: rapid, chaotic, and ineffective atrial electrical conduction

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

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

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

Mx:

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

OR

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

OR

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

AND

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

Question 32

Q

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

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

Answer

A

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

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

Presentation: low-grade fevers, night sweats

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

Ix:

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

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

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

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

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

Question 33

Q

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

Answer

A

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

KEN…TU.CKY (deee. de.de)

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

TE.NE..SSEE (de.de.deee)

Question 34

Q

In the context of HF what is cardiogenic shock? How do you treat? How do you treat rate-dependent cardiogenic shock (complete heart block)?

How will they describe cardiogenic shock in question?

Answer

A

HF so severe pressure insufficient to perfuse brain & heart alone –> 100% death if untreated
Treat with inotrope - dobutamine/dopamine –> increase perfusion of coronary arteries (saves 1/10)
Temporary external pacing –> permanent pacemaker

Q: cold peripheries & low UO

Question 35

Q

Apex beat displacement vs left ventricular hypertrophy?

Answer

A

Apex beat displaced by dilation = exam finding – caused by fluid overload
LVH = ECG Dx (peaked R-waves, ST depression and T-wave inversion in lateral leads) – caused by pressure overload e.g. HTN

Question 36

Q

Indications for CABG? Vessels used for graft? Meds post-CABG?

Answer

A

Indications:

Left main-stem disease
2+ vessel disease
Failure of medical Mx
Concomitant (aortic) valvular replacement

Grafts:

Great saphenous vein
Internal thoracic (mammary) artery - NOW the most commonly used

Meds post-CABG:

DAPT - aspirin + ticagrelor (for 12 months then just aspirin) ± specialist opinion
Cardio-selective beta-blocker (bisoprolol)
ACEi (or ARB)

Question 37

Q

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

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

Causes? Dx? Ix? Mx?

Answer

A

Pericarditis

Causes:

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

Presentation:

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

Ix:

ECG: ST elevation widespread
Only slightly raised/normal troponin

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

Question 38

Q

Causes of raised JVP (>4cm)?

Answer

A

JVP + hepatojugular pressure (RUQ), rockstar hand

PQRST:

Pul HTN/PE/Pericarditis/Pericardial effusion/PS
Quantity of fluid (fluid overloaded)
RHF
SVC obstruction
Tamponade/TR

Question 39

Q

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

Answer

A

VT or SVT w/ aberrancy

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

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

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

Ix: ECG - regular broad complex tachycardia

U&E (Mg, Ca, K), TFTs, Troponins

Mx:

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

Question 40

Q

SVC obstruction - presentation? Tx?

Answer

A

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)

Question 41

Q

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

Answer

A

Innitial: A-E

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

Question 42

Q

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

Answer

A

Causes:

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

Types:

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

Ix: ECG

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

Mx:

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

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

Question 43

Q

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

Answer

A

Types:

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

When to use each type:

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

Complications:

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

Question 44

Q

Pros/cons of TAVI?

Answer

A

Pros: no bypass required, no large scars
Cons: higher risk of stroke compared to open replacement

Question 45

Q

Different pulse forms? Causes?

Answer

A

Pulsus paradoxus - greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

severe asthma, cardiac tamponade

Slow-rising/plateau

AS

Collapsing

AR, PDA
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Pulsus alternans - regular alternation of the force of the arterial pulse

severe LVF

Bisferiens pulse - ‘double pulse’ - two systolic peaks

Mixed aortic valve disease
HOCM (also causes ‘Jerky’ pulse)

Question 46

Q

Cardiac tamponade - key finding on exam? Triad? Mx?

Answer

A

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)

Question 47

Q

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?

Answer

A

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

Question 48

Q

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

Answer

A

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

Question 49

Q

Types of cardiac scar?

Answer

A

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

Question 50

Q

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

Dx & Mx of decompensated chronic liver disease?

Answer

A

Cause of hepatic decompensation in CLD:

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

Decompensated CLD –> Ascites, jaundice & encephalopathy

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

Ix:

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

Mx:

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

Question 51

Q

Chronic liver disease

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

Answer

A

Functions of the liver –> failure:

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

Causes:

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

Presentation:

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

Ix:

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

Important complication = VARICES

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

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

Question 52

Q

Jaundice breakdown & causes by type & Ix to differentiate

Answer

A

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)

Question 53

Q

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

Answer

A

IBD

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

Coeliac disease

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

Irritable bowel syndrome - Dx of exclusion

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

Question 54

Q

Most common reason to do AXR? Most common causes of this reason by type?

AXR interpretation?

Key volvulus signs on AXR?

Answer

A

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)

Question 55

Q

Erythema nodosum is associated with which conditions?

Answer

A

IBD (also pyoderma gangrenosum),

Sarcoidosis

TB

Meds (OCP, sulphonamides, aspirin/NSAIDs)

Question 56

Q

Primary Sclerosis Cholangitis (PSC) vs Primary Biliary Cholangitis (PBC)

Associations? Ix? Tx?

Answer

A

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)

Question 57

Q

Causes of hepatomegaly, splenomegaly & enlarged kidney(s)?

Answer

A

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

Question 58

Q

Mesenteric ischemia:

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

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

Answer

A

Blood supply

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

__Mesenteric ischemia

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

Ischemic colitis

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

Question 59

Q

At the end of abdo exam what do you offer to do? Exposure in abdo exam?

Answer

A

GOR(D)

external Genitalia
hernial Orificies
digital Rectal

Ideally nipples to knees but in this case, I will do nipples to the groin due to possible patient discomfort

Question 60

Q

AI hepatitis - RFs? Ix? Mx? Complications?

Answer

A

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

Question 61

Q

How do you tell between spleen & kidney on examination?

Answer

A

Spleen (vs kidney):

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

Question 62

Q

Alcoholic liver disease - presentation? Bloods? Decompensated Mx?

Answer

A

Presentation: peripheral neuropathy, cerebellar, Wernicke’s, gout, parotitis, Dupuytren’s contracture

Bloods: AST > ALT (2:1)

Decompensated Mx:

Discrimination function calculated (PT/INR + bilirubin):
- <32/Inf/upper GI bleed –> no steroids
- Otherwise –> steroids

Question 63

Q

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

Answer

A

Blatchford score

Variceal bleed

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

Question 64

Q

Dysphagia DDx? Ix?

Answer

A

Dysphagia - difficulty swallowing

vs Odynophagia - painful swallowing
vs Globus sensation - lump in throat, no pain

Oropharyngeal - difficulty initiating swallowing (± cough, choking, aspirating, regurgitation) - pressure in throat

Oral:
- mastication (CN 5,7,11) e.g. CVA
- Low saliva e.g. Sjogren’s syndrome
Pharyngeal:
- Neuromuscular - CVA, Myasthenia Gravis, Parkinson’s
- Upper oesophageal sphincter - decreased relaxation

Oesophageal - difficulty after swallowing - pressure in chest

Solids & liquids - motor
- Intermittent: oesophageal dysmotility
- Progressive (solids –> both): achalasia (“birds beak”), systemic sclerosis
Solids only - obstructive
- Non-progressive: lower oesophageal rings/webs, oesophagitis
- Progressive: stricture, cancer

Ix:

Barium swallow - if a possible proximal oesophageal lesion
Upper endoscopy ± biopsy
If affects solids & liquids –> manometry

Answer 65

A

RFs:

H. pylori exposure
Aspirin/NSAID use

Types:

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

Presentation:

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

Ix:

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

Mx: consider STOPPING NSAIDs

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

Answer 66

A

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

Answer 67

A

Ischaemic liver

Massive paracetamol overdose

Very rarely: fulminant hepatitis (B/C)

Weird causes of slightly raised ALT: Addison’s coeliac, anorexia

Answer 68

A

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

Answer 69

A

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

Answer 70

A

Gastrinoma (pancreatic islet-cell tumour)

Multiple peptic ulcers & relapses
Diarrhoea
NOTE: can be good for OSCE - PUD presentation + diarrhoea

ZE syndrome - is one cause of poorly healing gastric ulcers, others:

Crohn’s, gastric Ca
Bisphosphonates
TB, CMV

Answer 71

A

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)

Answer 72

A

Portal hypertension - increase in the pressure within portal vein, which carries blood from the digestive organs to the liver

Hepatic venous pressure gradient (HPVG) = gold standard for assessing severity and a pressure > 5mmg

Causes:

Pre-hepatic – Portal/splenic vein thrombosis, congenital atresia of portal vein
Hepatic – Cirrhosis, Schistosomiasis, hepatic mets
Post-hepatic – Budd-Chiari Syndrome, Veno-occlusive disease, constrictive pericarditis

Answer 73

A

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

Answer 74

A

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

Answer 75

A

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)

Answer 76

A

Hormone production:

Parathyroid gland - PTH –> INCREASE Ca:
- Bone resorption
- GI absorption
- Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
Vit D₃aka 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

Answer 77

A

Primary - PTH secretion from primary parathyroid tumour/ectopic secretion from another tumour (high Ca, high PTH)
Secondary - PT hyperplasia to maintain control of hypocalcemia, normally from CKD (low Ca, high PTH, normal -ve feedback)
- CKD –> bone profile, parathyroid hormone lvl every 3-6 months
Tertiary - prolonged secondary, becomes irrepressible by serum Ca lvls. Mostly kidney transplant patients (high Ca, very high PTH)

Answer 78

A

Presentation: polyuria, polydipsia, dehydration

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

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

Criteria for Dx (repeat test needed for Dx):

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

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

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

T2DM Mx:

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

Diabetes complications:

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

Answer 79

A

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

Answer 80

A

Criteria:

True hyponatraemia
High urine osmolality
Clinically euvolemic
Dx of exclusion (9am cortisol + TFTs must be normal)

Causes:

Malig (small cell lung cancer, breast cancer)
CNS disorders (encephalitis, abscess)
Chest disease (pneumonia, TB)
Drugs (opiates, SSRIs, carbamazepine)

Answer 81

A

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

Answer 82

A

Hypothyroidism:

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

Hyperthyroidism:

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

Answer 83

A

Cushing’s #HighCortisol

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

Hypoadrenalism

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

Hyperaldosteronism (incl. Conn’s)

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

PHaeochromocytoma #HighCatecholamines

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

Answer 84

A

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

Answer 85

A

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

Answer 86

A

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

Answer 87

A

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

Answer 88

A

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

Answer 89

A

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

Answer 90

A

Diffuse: Graves’ disease, Hashimoto’s thyroiditis, De Quervain’s thyroiditis

Nodular: Multinodular goitre, adenoma, carcinoma

Answer 91

A

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

Answer 92

A

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

Answer 93

A

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)

Answer 94

A

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)

Answer 95

A

Signs:

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

Types:

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

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

Mx:

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

Answer 96

A

0 to -2.5 DEXA:

Conservative - exercise, reduce alcohol, balanced diet, Tx underlying causes
Repeat DEXA @2yrs
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

Answer 97

A

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

Answer 98

A

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

Answer 99

A

NoF anatomy - blood supply:

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

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

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

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

Presentation: externally rotated + shortened leg

Typically old, frail, osteoporosis/malacia

Ix:

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

Mx:

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

Answer 100

A

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

Answer 101

A

Joint erosion
Periarticular osteopenia
Ulnar deviation
Z-thumb
Swan neck

Answer 102

A

MSK X-RAY APPROACH:

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

General:

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

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

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

DESCRIBE A FRACTURE:

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

Types:

1. Simple vs Compound:

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

2. Subtype:

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

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

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

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

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

Answer 103

A

Meniscal injury - tenderness over joint line (+ McMurray’s)

Gout/pseudogout - swollen, erythematous, tender joint

OA - pain, crepitus, limited RoM

Ligament injury based on special tests/mov

Answer 104

A

Swan neck deformity - PIP hyperextension, DIP flexion

Boutonniere’s deformity - PIP flexion, DIP hyperextension

Other signs of RA: Z-thumb, ulnar deviation

Answer 105

A

Def: hypertrophy & contracture of palmar aponeurosis (fascia retinaculum)

Causes:

Idiopathic, age, trauma, familial (AD)
Alcoholic liver disease
Epilepsy & anti-epileptics (e.g. phenytoin)

Answer 106

A

CMCs –> MCPs –> PIPs –> DIPs

Carpal bones: Some Lovers Try Positions That They Can’t Handle

Base of wrist (radial to ulnar): Scaphoid, Lunate, Triquetrum, Pisiform
CMCs (radial to ulnar): Trapezium (trapezi”thumb”), Trapezoid, Capitate, Hamate

Answer 107

A

Look at Shenton’s line (inferior pubic rami) = NoF fracture

Answer 108

A

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)

Answer 109

A

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)

Answer 110

A

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

Answer 111

A

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)

Answer 112

A

Def: inflammatory rheumatological condition

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

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

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

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

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

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

Other: methotrexate + folic acid

Answer 113

A

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)

Answer 114

A

DDx: degenerative, infective, inflammatory, traumatic, congenital

Ix: 2 views = AP & lateral views + imaging of joints above and below as well

Mx: conservative, medical, surgical

Answer 115

A

Schober’s test: gross restriction <3cm = Ankylosing Spondylitis (fusion of sacro-iliac & lower spine)

Mark midline between dimples of venus & 10cm above –> ask to touch toes –> measure distance between 2-points
Should increase by 8-10

Sciatic stretch test: pain in thigh & buttocks = sciatica (L3-S3 nerve root irritation)

Patient supine, straight leg raise while ankle dorsiflexion

Femoral nerve test: pain in thigh & buttocks = L2-4 nerve root irritation

Patient prone, extend hip

Answer 116

A

RFs:

Exposure to high-intensity global UV radiation
Treatment w/ lipid-lowering agents, D-penicillamine (Tx for RA)
HIV, prev inf/vaccine

Presentation:

Overall: insidious/acute symmetrical muscle weakness of proximal arm & leg –> difficulty getting out of chair/climbing stairs
Dermatomyositis - acute, proximal muscle weakness + rash:
- Heliotropic rash (purple discolouration of upper-eyelids)
- Gottron’s papules (erythema over knuckles)
Polymyositis - subacute, proximal muscle weakness, no rash
Inclusion body myositis (IBM) - slowly, proximal & distal muscle weakness + muscle atrophy (quadriceps, distal wrist & finger flexor)
Assoc:
- ILD - in 10% patients with dermatomyositis/polymyositis
- Malignancy (ovarian, pancreatic, NH lymphoma, lung, bladder)
- AI disease

Ix:

Bloods: CK, ANA/myositis ab panel (anti-Jo-1)
Imaging: MRI of involved muscle, electromyogram (EMG), muscle biopsy

Mx:

Induction: CS (PO/IV) ± IVIg
Maintenance: IS (methotrexate/azathioprine) ± IVIg

Answer 117

A

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

Presentation:

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

Ix: clinical Dx

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

Mx:

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

Answer 118

A

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

Answer 119

A

Def: crystal deposition within the urinary tract

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

Stone types:

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

Ix:

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

Mx:

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

When to ADMIT:

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

If managed at home:

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

Answer 120

A

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

Answer 121

A

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

Answer 122

A

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

Answer 123

A

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

Answer 124

A

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

Mx: 2wk wait urology

Muscle invasive = cystectomy (young people) or radiotherapy/chemotherapy (older)
Superficial = surveillance cystoscopies, intravesical chemo
Mets = systemic therapy

Answer 125

A

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

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

Associations:

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

Family screening - renal USS

Answer 126

A

Presentation: sudden-onset pain, high fixed position, absent cremasteric reflex

Tx: bilateral orchidopexy (both sides as increased risk of torsion in the other side)

Answer 127

A

Paraphimosis def: unable to pull back the foreskin

Causes: tight foreskin (phimosis), a complication of urinary catheter (always remember to replace foreskin after withdrawing for catheter insertion)

Pathophysiology: constrictive effect of foreskin –> oedema of distal penis –> ischaemia/necrosis (if severe)

Mx: UROLOGICAL EMERGENCY - must be reduced ASAP

Reduce with - Lubricating jelly OR dextrose-soaked gauze
If difficult - needle used to make small holes in penis –> drainage of oedema

Answer 128

A

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)

Answer 129

A

Stress-incontinence (leak on laugh/cough):

Pelvic muscle exercises
Pseudoephedrine (2nd - Duloxetine)
Retropubic suspension/colposuspension

Urge-incontinence (preceded by the urge to pass urine):

Bladder retraining
Anticholinergic e.g. Oxybutynin (not if >80yrs), Tolterodine

Overactive bladder syndrome (urge but not incontinence - increased freq + nocturia): same as urge incontinence

Answer 130

A

Identify a problem and deal with it as going along…

Airway - patent? look, listen and feel –> head tilt + chin lift, jaw thrust, airway adjunct
Breathing - RR, O2 Sats (>94% - scale 1, 88-92% - scale 2 if COPD), resp exam, ABG –> Oxygen (15L/min O2 non-rebreather mask)
Circulation - HR, BP, CRT, cardio exam –> IV fluids
Disability - BM, pupils (PEARL - pupils equal and reactive to light), GCS/AVPU, abdo/neuro exam
Exposure - assess everything but not all at the same time –> calf tenderness, bleeding, bruising, rashes etc.

NOTE: if put in intervention say to examiner I would reassess previous steps e.g. A&B if gave IV fluids are there any changes

Answer 131

A

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

Answer 132

A

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)

Answer 133

A

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

Answer 134

A

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

Answer 135

A

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.)

Answer 136

A

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

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

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

DDx:

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

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

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

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

Complications:

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

Answer 137

A

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

Answer 138

A

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)

Answer 139

A

MAVIS:

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

Answer 140

A

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

Key features:

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

DDx:

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

Clinical courses/patterns:

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

Ix:

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

Mx:

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

Poor prognostic features:

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

Answer 141

A

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

Answer 142

A

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

Answer 143

A

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

Answer 144

A

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

Answer 145

A

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

Answer 146

A

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%)

Answer 147

A

1 flicker
2 is moves with gravity removed
3 is movement against gravity
4 is reduced power against resistance
5 is normal

Answer 148

A

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

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

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

Signs:

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

Mx:

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

Answer 149

A

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

Answer 150

A

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

Answer 151

A

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

Answer 152

A

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

Answer 153

A

RFs: atherosclerosis, hypotension, aortic aneurysm, aortic dissection

Ix:

Traumatic - CT-spine (bony injury/fracture)
Non-traumatic - MRI spine (soft tissue injury)

Mx: spinal immobilisation, manage in tertiary neurosurgical centre

Answer 154

A

HTN, bradycardia, Cheyne-Stokes breathing

Indicates raised ICP (likely form herniation through foramen magnum)

Urgent referral to tertiary neurosurgical centre

Answer 155

A

Berry aneurysm (85%)

LP in 12hrs for xanthochromia (yellow from bilirubin in CSF - RBC breakdown)

Nimodipine

Answer 156

A

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
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)

Answer 157

A

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

Answer 158

A

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

Answer 159

A

C3,4,5 keep the diaphragm alive

Phrenic nerve

Answer 160

A

Ix: MRI whole spine (often multifocal lesions)

Mx:

1st line = surgical decompression (if localised, fit enough)
2nd line = radiotherapy (external beam radiotherapy)

Answer 161

A

Postural imbalance/swaying:

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

Answer 162

A

Presentation

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

Ix:

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

Mx: surgical decompression

Answer 163

A

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)

Answer 164

A

LMN presentation = muscle pathology

Face:
- Myopathic facies (sunken cheeks, bilateral ptosis, expressionless)
  - Wasting of facial & muscles of mastication
- Frontotemporal balding
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)

Answer 165

A

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)
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

Answer 166

A

RFs:

Exposure to high-intensity global UV radiation
Treatment w/ lipid-lowering agents, D-penicillamine (Tx for RA)
HIV, prev inf/vaccine

Presentation:

Overall: insidious/acute symmetrical muscle weakness of proximal arm & leg –> difficulty getting out of chair/climbing stairs
Dermatomyositis - acute, proximal muscle weakness + rash:
- Heliotropic rash (purple discolouration of upper-eyelids)
- Gottron’s papules (erythema over knuckles)
Polymyositis - subacute, proximal muscle weakness, no rash
Inclusion body myositis (IBM) - slowly, proximal & distal muscle weakness + muscle atrophy (quadriceps, distal wrist & finger flexor)
Assoc:
- ILD - in 10% patients with dermatomyositis/polymyositis
- Malignancy (ovarian, pancreatic, NH lymphoma, lung, bladder)
- AI disease

Ix:

Bloods: CK, ANA/myositis ab panel (anti-Jo-1)
Imaging: MRI of involved muscle, electromyogram (EMG), muscle biopsy

Mx:

Induction: CS (PO/IV) ± IVIg
Maintenance: IS (methotrexate/azathioprine) ± IVIg

Answer 167

A

Vasculitis - GPA, EGPA, microscopic polyangiitis, polyarteritis nodosa

Rheum - RA, SLE, Sjogren’s, Sarcoidosis

Answer 168

A

MND

B12 - SCDC (subacute combined degeneration of the spinal cord)

Friedrich’s ataxia (cause of cerebellar syndrome)

Syphilitic tabo-paresis

Answer 169

A

Bilateral:

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

Unilateral:

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

Answer 170

A

Brain: stroke, SOL, MS

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

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

Anterior horn (motor neurone lesions): MND, poliomyelitis

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

Neuropathy: diabetic neuropathy

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

Neuromuscular junction: MG/LEMS

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

Myopathy: dermatomyositis

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

Answer 171

A

CONGENITAL MIND

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

Answer 172

A

Bilateral = 3Ms

MS
MND (normal sensation)
Myelopathy (sensory level) - SOL, cervical myelopathy, disc prolapse, transverse myelitis, syringomyelia

Unilateral:

Intracranial - CVA, SOL, MS
Brainstem - MS
Spinal cord - trauma, SOL, haemorrhage

Answer 173

A

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

Answer 174

A

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

Answer 175

A

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

Answer 176

A

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

Answer 177

A

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

Answer 178

A

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)

Answer 179

A

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

Answer 180

A

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

Answer 181

A

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

Answer 182

A

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

Answer 183

A

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)

Answer 184

A

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

Answer 185

A

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

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

Answer 186

A

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

Answer 187

A

Clinical examination

Breast imaging (MMG, USS)

Breast biopsy

Answer 188

A

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
1. a) <55yrs/DM –> ACEi (ramipril)/ANG-II receptor antagonist (Losartan)
1. b) ≥55yrs/black –> CCB (amlodipine)/thiazide diuretic (bendroflumethiazide)
1. ACEi + CCB OR ACEi + thiazide diuretic
1. ACEi + CCB + thiazide diuretic
1. Add:
  * Spironolactone (or other diuretic)
  * Alpha-blocker
  * Beta-blocker
  * Specialist advice

Answer 189

A

Screening MMG

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

USS focused:

<40yrs USS only
≥40yrs USS + MMG

Biopsy:

all breast lumps in women >25yrs
USS-guided

Answer 190

A

BP cuff above ankle with leads upwards – find dorsalis pedis pulse with doppler
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

Range:

0.8-1 = normal
0.6-0.8 = claudication (may only drop to this with exercise)
Below 0.6 = critical limb ischaemia

Answer 191

A

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)

Answer 192

A

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

Answer 193

A

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

Answer 194

A

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)

Answer 195

A

Upper:

RUQ pain: cholecystitis, ascending cholangitis, acute hepatitis
Epigastric pain: PUD, GORD, pancreatitis

Middle:

Flank pain: pyelonephritis (loin to groin pain)
Umbilical pain - AAA (consider if >65yrs, HTN)

Lower:

RIF pain: appendicitis, ureteric colic, hernia, testicular torsion
Suprapubic pain: UTI
LIF pain: diverticulitis, inflammatory colitis, ischaemic colitis, ureteric colic, hernia, testicular torsion
In women - causes of lower Abdo pain: ectopic pregnancy, ovarian torsion, PID
- Ask about _P_ain, _P_regnancy, _P_V bleeding, _P_V discharge

NOTE: also consider psych cause of generalised abdo pain (esp in kids)

Answer 196

A

Right and left hepatic ducts merge to form the common hepatic duct
Gallbladder - stores & concentrates bile and releases it to emulsify fats
Cystic duct connects gallbladder to the biliary tree
Cystic duct and common hepatic duct come together to form the common bile duct
Pancreatic duct feeds into the common bile duct - where it secretes exocrine hormones
All of the above feed through the Ampulla of Vater into the duodenum –> allowing secretion of bile into the intestines

Answer 197

A

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

Answer 198

A

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

Answer 199

A

Right hemicolectomy - right colon

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

Left hemicolectomy - left colon

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

Panproctocolectomy - total colon & rectum e.g. UC

Indication: a diffuse disease affecting the full colon e.g. FAP (familial adenomatous polyposis) or UC
Process: remove full colon & rectum (from ileocaecal valve to the anus)
What are you left with: end ileostomy (loose end of ileum brought to the skin)

Total colectomy vs subtotal colectomy

Total colectomy:
- Process: remove full colon but not the rectum
- What are you left with: ileal-pouch anal anastomosis (loose end of ileum used to reform a rectum, don’t need a stoma)
Subtotal colectomy:
- Process: remove colon except for the rectum and part of the sigmoid colon
- What are you left with: end-ileostomy & rectal/sigmoid stump

Hartmann procedure - emergency sigmoid colon

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

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

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

Colostomy (ileal conduit)

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

Answer 200

A

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)

Answer 201

A

Indications:

Traumatic rupture
Idiopathic thrombocytopenia
Spherocytosis

Problem: increased risk from encapsulated bacteria e.g. strep pneumo

Prophylaxis:

Vaccines: Pneumococcus, Meningococcus, Haemophilus Influenzae Type B
Penicillin V

Answer 202

A

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

Immediate Tx & Ix:

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

Answer 203

A

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)

Answer 204

A

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

Severity criteria = GLASGOW score (PANCREAS):

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

Answer 205

A

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

Diverticular disease: above + Sx

Diverticulitis: infection & inflammation of diverticulum

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

Presentation:

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

Ix:

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

Mx:

Asymptomatic diverticulosis:
- Increased fibre & fluids
- Excercise, weight loss, stop smoking
- Fybogel - if constipated
Symptomatic diverticular disease:
- Above + paracetamol
- PO Dicycloverine = anti-spasmodic (for abdo cramping)
Acute diverticulitis:
- Uncomplicated:
  - Low-residue diet + Paracetamol + PO Dicycloverine
  - 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

Answer 206

A

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

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

RUQ Pain Ix:

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

Biliary colic:

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

Cholecystitis:

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

Ascending cholangitis:

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

Answer 207

A

Indications:

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

Unsuitable for liver transplant:

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

Surgery: Rooftop/Mercedes Benz scar

Post-transplant care:

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

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