Core Medicine

Core Medicine

Core Medicine

🫀 Cardiology

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❤️‍🩹 The Heart Wall
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Diagram: The Heart Wall
Blausen.com

Diseases by anatomy:

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Pericardium

This is a fluid-filled sac that surrounds and protects the heart, preventing friction during heart contractions.

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Pericarditis
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Acute pericarditis
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Causes
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What’s the most common cause of pericarditis?

Infection:

  • Viruses (more common): Coxackie B, CMV, echovirus, HIV, influenza
  • Although bacteria can also cause it:
    • Streptococcuus → Rheumatic heart disease
    • Tuberculosis
    • Pneumococcus
    • Haemophilus
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What is Dressler’s syndrome?
  • Pericarditis occurring 1–4 weeks—although can be longer—after an MI secondary to myocardial or pericardial damage. Occurs in ~ 7% of MI patients.
    • ‣
    What blood tests can be useful?
    • ESR
    • Antimyocardial antibodies as it is an autoimmune reaction against damaged myocardial tissue.
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What other things can cause it?
  1. Secondary immune processes (e.g. rheumatic fever, post-cardiotomy syndrome)
  2. Metabolic disorders (e.g. uraemia, myxoedema)
  3. Radiotherapy
  4. Cardiac surgery
  5. Percutaneous cardiac interventions
  6. Malignancy
  7. Rheumatology: SLE, RA, sarcoidosis, vasculitis (Behçet's)
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What are the classic presenting features in exams?
  1. Sharp chest pain relieved by leaning forwards, and worse when lying flat
  2. Friction rub heard on auscultation of the heart
  3. Fever
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What are the key investigations?
  • ECG:
    • ‣
    What does the following ECG show?
    ‣
    Answer
    • Widespread saddle ST elevation, not confined to a specific lead, showing that ischaemia is occurring to all areas of the myocardium due to pericardial compression.
    James Heilman, MD, CC BY-SA 3.0
    James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
  • Bloods: FBC, U&E, CRP, ESR, troponin
  • CXR: Rule out differentials (pneumonia, malignancy, etc.).
  • Transthoracic echocardiogram: Looking for thickening of pericardial layers, pericardial effusion and resultant effects of it (tamponade/restriction).
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How do you manage uncomplicated pericarditis?

BMJ Best Practice:

  1. NSAIDs
    • Ibuprofen 600mg PO for (+ PPI)
    • PPI for gastroprotection
    • Aspirin is preferred for patients developing pericarditis after a myocardial infarction
  2. Colchicine (if idiopathic or viral pericarditis) to prevent recurrent pericarditis, improve response, and increase remission rates.
  3. Lifestyle: Restrict strenuous physical activities
  4. If not resposive: Consider corticosteroids
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Constrictive pericarditis

This results from pericardial scarring.

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What often causes it?
  • Acute pericarditis leading to inflammation & scarring
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How would they present?
  • Symptoms: Fluid overload, exertional dyspnoea
  • OE: Right HF
    • Raised JVP, Kussmaul's sign (↑JVP), pulsus paradoxus (pulse wave volume decreases during inspiration).
    • Kussmaul's is specific to this, differentiates it from tamponade
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How is it treated?

Relieve pressure on the heart exerted by the pericardium, and treat underying cause.

  • Pericardiectomy.
  • NSAIDs, steroids, diuretics and other medications can be useful.
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Cardiac tamponade

Accumulation of fluid within the pericardial space → ↑ intra-pericardial pressure → Restriction of cardiac filling → ↓ cardiac output.

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What is Beck's triad?
  1. Quiet heart sounds
  2. Hypotension
  3. Raised JVP
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What examination findings suggest this? (2)
  1. Kussmaul's sign: JVP rises with inspiration
  2. Pulsus paradoxus: Drop in systolic BP with inspiration
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What is shown on this ECG:
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Answer
  • Electrical alterans (alternating tall and short QRS complexes)
    • Fluid filled pericardium → Heart moving backwards and forwards during contractions → Wandering baseline
  • Small QRS: Difficulty contracting due to pressure
CardioNetworks: Vdbilt, CC BY-SA 3.0
CardioNetworks: Vdbilt, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
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What other invetigations will you need?
  1. Bloods
    • FBC: ? inflammatory cause
    • ESR
    • Troponin
  2. CXR: Enlarged cardiac shadow
  3. Transthoracic echocardiogram, looking for:
    • Pericardial effusion (and size of it).
    • Chamber collapse and respiratory variation of ventricular filling.
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How would you manage these patients:
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Haemodynamically stable (pre-tamponade)
  • Anti-inflammatory treatment, gastroprotection and observation.
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Haemodynamically unstable patient with tamponade
  • Pericardiocentesis
    • Send fluid for culture and cytology to identify cause
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Haemopericardium
  • Surgical drainage.
  • Blood is associated with malignancy or traumatic effusion.
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Myocardium

This is the middle muscular layer of the heart, made up of specialized muscle cells called cardiomyocytes.

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Ischaemic heart disease
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Acute coronary syndrome (ACS)
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Classifying ACS
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ACS cases

The following patients have chest pain at rest and the following:

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ST elevation present on the ECG.
  • STEMI
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New LBBB present on ECG.
  • STEMI
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No ECG changes. No dynamic rise in troponin.
  • Unstable angina
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T-wave inversion in V1-3. Dynamic rise in troponin.
  • NSTEMI

We classify ACS using symptoms, ECG & cardiac biomarkers.

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STEMI

ST elevation OR new LBBB is present on the ECG.

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Coronary artery anatomy
Servier Medical Art. Annotations by Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D., CC BY 3.0
Servier Medical Art. Annotations by Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D., CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
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Management

Acute:

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What medications would you give immediately?
  1. Morphine
  2. Oxygen (if SpO₂ < 95%)
  3. Nitrates (GTN spray)
  4. Aspirin 300mg STAT
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What is the gold-standard treatment?
  • Primary PCI
    • ‣
    Within what time limits is this appropriate?
    • Has to be available within 2 hours of presentation.
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    What is it?
    • Insertion of catheter into brachial or femoral artery → Fed through arterial system into coronary arteries under XR guidance → Inject contrast to visualise the blockage → Balloon dilatation of artery +/- stent.
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What is the other definitive treatment option?
  • Thrombolysis (e.g. with alteplase)
    • If PCI not available within 2 hours of presentation, thrombolysis is indicated.

Long-term:

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What medications do we need to consider for secondary prevention?

Antiplatelets (preventing thrombus formation on plaques):

  • Aspirin 75mg OD
  • Another antiplatelet: clopidogrel / ticagrelor for ~ 12 months

Lipid lowering (helping reduce atheromatous plaques):

  • Atorvastatin 80mg OD

Antihypertensives (lowering BP to prevent damage to endothelium and high pressures pushing clots off plaques):

  • ACE inhibitor
  • Atenolol / bisoprolol
  • Aldosterone antagonist (if in HF)

Cases:

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ST elevation is found in the following leads, what artery is affected:
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II, III, aVF
  • RCA - Inferior
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V1-2
  • Proximal LAD - Septal
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V3-4
  • LAD - Anterior
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V5-6
  • Distal LAD, LCx, RCA - Apex
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I, aVL
  • LCx - Lateral
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V7-9
  • LCx/RCA - Posterolateral
    • V1-3: Reciprocal ST depression
    • V5-6: May see ST elevation as LCx affected
    • May see some inferior ST elevation depending on size of infarction
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What is present on the following ECG:
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Diagnosis
  • ST elevation in II, III, aVF → Inferior MI
Glenlarson, CC BY-SA 3.0
Glenlarson, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
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NSTEMI

Chest pain is present at rest. There is no ST elevation. There are either other ECG changes suggesting ischaemia (T-wave inversion or ST depression) or a dynamic rise in troponin.

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How is it acutely managed?

BATMAN

  1. Beta-blockers
  2. Aspirin 300mg STAT
  3. Ticagrelor 180mg STAT (OR prasugrel OR clopidogrel 300mg)
  4. Morphine for pain
  5. Anticoagulant: Fondaparinux (but need to assess bleeding risk)
  6. Nitrates (e.g. GTN)
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What are the principles underlying this management?
  1. Slow heart down to reduce demand of muscles → Beta-blockers
  2. Prevent more platelet aggregation → Dual antiplatelet therapy
  3. Control pain for patient comfort and to prevent tachycardia → Morphine
  4. Break down clot → Anticoagulant
  5. Stop coronary artery spasm → Nitrates
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Unstable angina

Chest pain is present at rest. There are no ECG changes and there is not a dynamic rise in troponin.

General:

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Investigations
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What ECG changes are you looking for?
  1. ST elevation
  2. Bundle branch blocks
  3. ST depression
  4. T-wave inversion (but this is normal in aVR)
  5. Pathological Q waves (although this is a late sign)
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When looking at serum troponin, what is key for diagnosis of MI?
  • Ensuring you have serial troponins. Troponins can be released from the myocardium during ischaemia, but also from elsewhere. Dynamic rise is key for diagnosis.
    • ‣
    When do we measure troponin to test for this dynamic rise?
    1. Baseline (arrival to hospital/onset of pain)
    2. 6–12 hours after onset of symptoms
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    What else can cause raised troponin?
    1. CKD
    2. Sepsis
    3. Pulmonary embolism
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What other bloods may be useful?
  1. FBC
    2. ‣
    Why might anaemia be relevant?
    • Anaemia could contribute to a type 2 MI. This is cardiac ischaemia due to:
      • increased demand (tachycardia) or,
      • reduced supply (anaemia/hypotension).
  2. LFT
    3. ‣
    Why?
    • Baseline for starting statin therapy
  3. U&E
    4. ‣
    Why?
    • Need to know renal function for CT angio with contrast and if we’re going to start an ACEi
  4. TFT
  5. Lipid profile
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Complications
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What score is used to stratify their risk?
  • GRACE score provides a risk of death or repeat MI within the next 6-months. Medium/high risk individuals are considered for early PCI.
    • Low Risk < 5%
    • Medium Risk 5-10%
    • High Risk > 10%

What complication has occurred:

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New pan-systolic murmur and acute HF.
  • Interventricular septal rupture → VSD (HF makes this more likely)
  • Papillary muscle rupture → Mitral regurgitation
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Muffled heart sounds, pulsus paradoxus, raised JVP.
  • Cardiac tamponade
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3 weeks later presents with chest pain and fever. Raised ESR.
  • Dressler's syndrome: Immune response following MI causing pericarditis.
    • ‣
    Management?
    • NSAIDs (e.g. aspirin / ibuprofen)
    • Steroids (e.g. prednisolone)
    • Pericardiocentesis
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Stable angina

This is coronary artery narrowing, causing exertional chest pain as the vessels supplying the heart cannot keep up with the oxygen demands of the muscle.

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When are symptoms classically relieved?
  1. When using GTN spray.
  2. When resting.
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How are they investigated?
  1. CT coronary angiogram (Gold standard)
    • Contraindicated if patient has poor renal function due to the contrast needed to carry this out.
  2. Stress echocardiogram / Myocardial perfusion SPECT / MRI
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What makes up the medical management?
  • Short-term relief:
    1. GTN spray (nitrates stimulate vasodilation)
  • Long-term relief:
    1. Bisoprolol
    2. Amlodipine/nifedipine & bisoprolol
    3. Isosorbide mononitrate
    4. Ivabradine/nicorandil
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What surgical management can be used?
  1. Percutaneous coronary intervention (PCI)
    • Balloon dilation of the artery +/- stent insertion.
  2. Coronary artery bypass graft (CABG)
    • Take a blood vessel from another part of the body, plumbing it into the coronary artery above and below the narrowed area or blockage.
    • Better in > 65y, diabetics, 3 vessel disease.
    • Usually use the great saphenous vein or the radial artery.
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Heart failure

There are two ways to classify this:

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Left-sided HF (LHF/LVF)

HFrEF vs HFpEF:

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Heart failure with reduced ejection fraction (HFrEF)

Systolic failure (EF < 40%) → Impaired contraction.

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Ischaemic cardiomyopathy
  • MI → Muscle hypoxia → Muscle ischaemia → Cardiac muscle dysfunction
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Dilated cardiomyopathy
  1. Idiopathic
  2. Alcoholic
    3. ‣
    What other drugs can cause DCM?
    1. Cocaine
    2. Doxorubicin
    3. Cyclophosphamide
    4. Clozapine
  3. Infiltrative
    4. ‣
    What are the causes?
    1. Haemochromatosis
    2. Sarcoidosis
    3. Amyloidosis
  4. Infective
    5. ‣
    What are the causes?
    1. Secondary to myocarditis
    2. HIV
    3. Lyme disease
    4. Chagas disease: Caused by Trypanzoma cruzi parasite prevalent in Central/South America
  5. Takotsubo
    6. ‣
    What causes this?
    • Stress-induced. Psychological stress → LV ballooning.
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Heart failure with preserved ejection fraction (HFpEF)

Diastolic failure (EF > 50%) → Impaired filling.

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Hypertrophic cardiomyopathy
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How is it inherited & what is it?
  • Autosomal dominant
  • Genetic abnormality in the proteins making up the heart sarcomere leading to septal hypertrophy
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How does it lead to HF?
  • Impaired outflow → LV hypertrophy → Low preload volume
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How many of these patients have HOCM?
  • 25%
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How does HOCM cause sudden death?
  • Ventricular arrhythmia
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How do they commonly present?
  • Young patient presenting with exertional syncope. Can have chest pain and SOB.
  • Unexplained syncope is a poor prognostic factor
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How are they managed?
  1. Exercise restriction, β-blockers
  2. ICD for those at risk of sudden cardiac death
  3. Surgical: Myomectomy or septal ablation
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Restrictive cardiomyopathy

Deposits within the heart cause it to become stiff → Less heart muscle compliance → Poor filling.

  1. Amyloidosis: Amyloid deposits within the heart.
    2. ‣
    What features suggest this?
    1. ECHO shows "sparkling appearance"
    2. Renal dysfunction due to amyloid deposition
  2. Haemochromatosis
  3. Sarcoidosis
  4. Post-radiation fibrosis

Acute vs Chronic:

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Acute LVF

Acute decompensation of the LV → Back-pressure into the lungs → Pulmonary oedema (transudative mechanism) → Impaired gas exchange.

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What are the symptoms & signs?
  1. Rapid onset SOB
  2. Worsened SOB lying back
  3. T1RF
  4. ↓ SpO₂
  5. Bibasal crackles (pleural effusion)
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How do you manage them?
  1. Ensure they’re sat up.
  2. Diuretics to clear the fluid from their lungs.
  3. Oxygen to make sure they maintain saturations.
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Chronic heart failure
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What are the classic symptoms?
  1. Paroxysmal nocturnal dyspnoea: Suddenly waking up in the middle of the night feeling short of breath, gasping.
    • Stood up → Fluid sits in the bases of the lungs → Space for gas exchange in apex.
    • Lying back → Fluid spreads across more of the lungs → Reduced gas exchange area.
  2. Orthopnoea: Shortness of breath when lying back, they may sleep sat up.
    • History: ‘How many pillows do you use at night to prop yourself up?’
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What are the steps in HFrEF management?
  1. Ramipril/valsartan & bisoprolol
  2. Spironolactone
    • If causes GI upset/gynaecomastia → Switch to eplerenone
  3. Hydralazine/isosorbide dinitrate
  4. Digoxin/ivabradine
  5. Surgical: Cardiac resynchronisation therapy or transplant
    6. ‣
    What are the 3 indicatons that need to be present for this?
    1. LBBB
    2. EF < 30%
    3. NYHA III
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What can be used for symptomatic management?
  • Furosemide 40mg OD
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How is HFpEF managed?
  1. Lifestyle advice.
  2. Manage underlying cause, if possible.
  3. Low-dose furosemide to manage oedema.
  4. Ramipril if hypertensive.
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Right-sided HF (RHF)
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Cor pulmonale

This is right-sided HF secondary to respiratory disease.

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What respiratory diseases cause this?
  1. COPD
  2. ILD
  3. PE
  4. CF
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Why does respiratory disease cause RHF?
  • Disease → Hypoxia → Pulmonary hypertension → Increased RV afterload (pushing against a greater pressure)
    • Hypertrophy of the RV → Increased O₂ demand → Higher likelihood of ischaemia
    • RV dilatation → Tricuspid regurgitation → Increased preload → More RV dilatation (🔄 deadly cycle)
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What symptoms/signs may suggest this?
  • Symptoms: SOB, syncope, chest pain.
  • Signs: Raised JVP, peripheral oedema, murmurs, hepatomegaly, ascites
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What are the common causes?
  1. LV failure causing backpressure and increased afterload
  2. Pulmonary stenosis
  3. Pulmonary hypertension (as discussed in cor pulmonale)
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How would you manage them?
  1. Treat the underlying cause of hypoxia & pulmonary hypertension (see Respiratory)
  2. Manage symptoms, e.g. oedema

General:

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How are the symptoms classified?

NYHA classification:

  1. No limitation to daily life
  2. Slight limitation on physical activity
  3. Marked physical activity limitation, comfortable at rest
  4. Symptoms at rest
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Investigations
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What are the common CXR findings?

ABCDE

  1. Alveolar oedema
  2. Kerley B lines
  3. Cardiomegaly
  4. Upper lobe Diverson
  5. Pleural Effusions

Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
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What blood test do you need before doing an echocardiogram?
  • BNP (if > 2000 → urgent referral to cardiology)
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What diagnosis do the following echocardiogram results suggest:
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Asymmetric hypertrophy, diastolic dysfunction
  • Hypertrophic cardiomyopathy
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Regional wall motion abnormality, EF < 55%
  • Ischaemic cardiomyopathy (CAD)
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LV dilation, EF < 55%
  • Dilated cardiomyopathy
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Apical ballooning of LV
  • Takotsubo cardiomyopathy
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Myocarditis

Inflammation of the myocardium → Infiltration of lymphocytic cells → Myocardial necrosis & degeneration.

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What is the classic exam question?
  • Presents with shortness of breath and mild palpitations, had an upper respiratory infection (viral picture) a couple of months ago.
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What are the causes?
  1. Coxackie viruses (A/B)
  2. Lyme disease
  3. SLE
  4. Drug-associated
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What features differentiate it from pericarditis?
  1. Marked troponin elevation
  2. No relief on sitting forward or pericardial rub on examination

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How do you definitively diagnose it?
  • Cardiac biopsy (only perform if this information would alter the treatment plan as it’s risky).
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Cardiac myxoma

Noncancerous tumor that arises from connective tissue, commonly located in the atria, affecting blood flow and electrical conduction.

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What are the classic features?
  1. Fever
  2. Weight loss
  3. Clubbing
  4. Audible tumour 'plop' - Variable with position
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How would you investigate?
  1. ECG: May reveal AF
  2. Echocardiogram: Help to visualise lesion and blood flow
  3. CXR: Cardiomegaly, pulmonary oedema
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How would you manage it?
  • Open heart surgery to remove the tumour.
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Endocardium (Valves)
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Heart valves
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Diagram: Heart valves
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
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Name the 4 heart valves.
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Aortic
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Aortic stenosis

Thickening, calcification and stiffening of the aortic valve → Valve does not open sufficiently → Increased afterload as LV has to push against a higher pressure to maintain cardiac output.

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What murmur would you hear?
  • Ejection systolic (crescendo-decrescendo)
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What are the causes of this?
  1. Mechanical stress over time
    • Risk factor that makes this worse is a biscuspid aortic valve
  2. Rheumatic heart disease
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What is the classic triad of symptoms?
  1. Syncope (insufficient oxygen supply to brain)
  2. Exertional dyspnoea (back pressure into lungs)
  3. Angina (insufficient oxygen supply to heart)
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What are the other differentials for this type of murmur?
  1. Hypertrophic cardiomyopathy
    • Louder standing, quieter supine due to LV outflow obstruction.
    • Heard louder on LLSE due to septum causing obstruction not the valve
  2. Aortic flow murmur
    • Hyperdynamic circulation due to infection, anaemia, thyrotoxicosis or pregnancy
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Aortic regurgitation

Widening of the aortic valve → Backflow through the valve during diastole → Increased preload within the LV → Dilation of LV.

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What murmur would you hear?
  • Early diastolic, louder leaning forward and on LLSE
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What can cause this?
  1. Degenerative
  2. Rheumatic fever
  3. Connective tissue disease (e.g. Marfan’s)
  4. Endocarditis
  5. Aortic root dilatation
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Mitral
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Mitral stenosis
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What murmur would you hear?
  • Mid-diastolic murmur with opening ‘snap’.
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What are the other common features?
  1. Malar flush
  2. AF
  3. P-mitrale on ECG (Bifid P-wave) due to atrial hypertrophy
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What are the causes?
  • Rheumatic fever (most common): Inflammation → Leaflet fusion
  • Age-related calcification
  • Systemic disease: RA/SLE
  • Congenital
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Mitral regurgitation (most common valvular condition)
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What murmur would you hear in prolapse?
  • Pan-systolic murmur / Late-systolic murmur
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What are the causes?
  • Weakening of valve with age
  • LVF secondary to dilatation of the ventricle
  • Endocarditis
  • Papillary muscle rupture secondary to MI
  • Connective tissue diseases
    • Marfan's syndrome
    • Ehlers-Danlos syndrome
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What are the complications?
  • Pulmonary hypertension → RVF
  • Left atrial dilatation → Pacemaker cell irritation → AF
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Pulmonary

These are less commonly tested, but covered in paediatric cardiology, where they are more relevant.

  1. Pulmonary stenosis
  2. Pulmonary regurgitation
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Tricuspid
  1. Tricuspid stenosis
  2. Tricuspid regurgitation

Investigations & Management:

‣
What investigations are useful in assessing valvular pathology?
  1. ECG: Looking for ventricular hypertrophy,
  2. Echocardiogram: Flow across valves (regurgitation, pressure gradients), calcification of the valves, atria/ventricular size.
  3. CXR: Cardiomegaly
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What management should you consider?
  • Often you watch and ensure that hypertension is managed well.

Surgical:

  1. Valve replacement
    • Transcatheter aortic/mitral valve replacement via femoral artery catheter
    • Bioprosthetic valve replacement
  2. Balloon valvuloplasty for stenotic valves (inflate a balloon in the valve to open it)
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Endocarditis

Infection of the endocardium +/- heart valves.

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Infective
‣
What organisms can cause this?
  1. S. aureus (IVDU)
  2. S. viridans (Dental hygiene)
  3. S. epidermis (Prosthetic valve surgery/infected catheter)
  4. S. bovis (from GI tract)
‣
What signs & symptoms are you looking for?
  • Roth spots (eyes)
  • Osler nodes (painful finger lesions)
  • Janeway lesions (painless palm lesions)
  • Anaemia
  • Splinter haemorrhages
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What criteria are used to diagnose this and what are the constituents?

Duke's criteria:

  1. Pathological criteria positive, OR
  2. 2 major criteria, OR
  3. 1 major & 3 minor criteria, OR
  4. 5 minor criteria

Major criteria:

  1. Two positive blood cultures
  2. Persistent bacteraemia from two blood cultures taken > 12 hours apart
  3. Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
  4. Positive echocardiogram
  5. New valvular regurgitation

Minor criteria:

  1. Predisposing heart condition or intravenous drug use
  2. Microbiological evidence does not meet major criteria
  3. Fever > 38ºC
  4. Vascular phenomena: Major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  5. Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Investigations & Management:

‣
How do you investigate?
  1. 3 sets of blood cultures from 3 different sites at 3 different times
  2. ECG
  3. CXR
  4. Transoesophageal echocardiogram → Valvular pathology
‣
How do you manage it?
  1. Medical: IV antibiotics
    • Central line infection: IV vancomycin
  2. Surgical: Valve repair
    3. ‣
    When is this indicated?
    1. Severe sepsis despite antibiotics
    2. Heart failure
    3. Haemodynamic instability
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Non-infective
  1. Rheumatic fever
    2. ‣
    What is this caused by?
    • Group A haemolytic Streptococci → Autoimmune inflammatory disease
      • Streptococci proteins cross-react with myocardial, valvular, joint and brain proteins
    ‣
    How do they present?
    • 2-4 weeks following a throat infection, they develop SOB, fever & chest pain. Pericardial rub and joint pain.
    ‣
    How do you investigate it?
    • Anti-Streptolysin O (ASO) titre
    ‣
    How is this managed?
    1. STAT IV benzylpenicillin - Covers this group A beta-haemolytic streptococcal infection
    2. PO Pen V for 10 days
  2. Libman-Sacks endocarditis
    • SLE/RA antigen-antibody complexes settle in endocardium → Endocardial damage → Valve regurgitation
  3. Non-bacterial thrombotic endocarditis
    • Damage to valve exposes collagen → Platelets & fibrin adhere to form clots → Mitral valve regurgitation.
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Heart sounds
‣
Diagram: Heart sounds
Madhero88, CC BY-SA 3.0
Madhero88, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.

What are the causes of:

‣
Loud S2
  1. HTN
  2. Pulmonary HTN
  3. Hyperdynamic states
  4. ASD
‣
Soft S2
  • Aortic stenosis
‣
Fixed split S2
  • ASD
‣
Widely split S2
  1. Deep inspiration (increased VR causes tricuspid to close after mitral)
  2. RBBB
  3. Pulmonary stenosis
  4. Severe MR
‣
⚡️ Electrical Conduction
‣
Diagram: Electrical system of the heart
‣
Labelling the electrical anatomy.
‣
Label the key parts of the diagram below (Answers in drop down tab).
Madhero88, CC BY 3.0
Madhero88, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
Andrewmeyerson, CC BY-SA 3.0
Andrewmeyerson, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
How does the passage through the electrical circuits correspond with different parts of the ECG?
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
ECG

Name the diagnosis based on the following ECGs:

W.G. de Voogt, MD, PhD, SLAZ, The Netherlands, CC BY-SA 3.0
W.G. de Voogt, MD, PhD, SLAZ, The Netherlands, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Diagnosis 1
  • Hypertrophic cardiomyopathy
User Ksheka on en.wikipedia, CC BY-SA 3.0
User Ksheka on en.wikipedia, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
Diagnosis 2
  • Wolff-Parkinson White
Dr. Michael-Joseph F. Agbayani and Dr. Eddieson Gonzales (Manila, Philippines), CC BY 4.0
Dr. Michael-Joseph F. Agbayani and Dr. Eddieson Gonzales (Manila, Philippines), CC BY 4.0 creativecommons.org/licenses/by/4.0, via Wikimedia Commons. No changes were made.
‣
Diagnosis 3
  • Hyperkalaemia
‣
What are the 4 cardiac arrest rhythms & which are shockable?

Shockable:

  • Ventricular tachycardia
  • Ventricular fibrillation

Non-shockable:

  • Pulseless electrical activity
  • Asystole

Arrhythmias:

‣
Tachyarrhythmias
‣
Narrow complex (QRS < 120ms)

This indicates that this is a Supraventricular Tachycardia (SVT).

‣
Regular QRS

Types:

  1. Sinus tachycardia: Usually compensating for a decreased stroke volume, or from sympathetic stimulation caused by pain, fear or catecholamines.
  2. AVNRT: Slow & fast pathway through AVN causes circuit to form
  3. AVRT (Wolff-Parkinson-White syndrome): Electricity travels down the accessory pathway and up AVN: 𝝳 wave, broad QRS
  4. Atrial flutter: Characterised by flutter waves on ECG, which are a saw-tooth pattern of atrial activation.
    5. ‣
    Why does it happen?
    • There is a re-entrant circuit within the atria causing repetitive contractions.
    ‣
    What are key investigations?
    • Bedside: ECG
    • Bloods: FBC, U&E, TFT
    • Imaging:
      • CXR: Flutter is often associated with lung disease
      • Transthoracic echo: Assess the cardiac structures, atrial and ventricular function.
    ‣
    How is this managed?
    1. AVN blocker: Bisoprolol/verapamil
    2. Electrical cardioversion
    3. Medical cardioversion: IV ibutilide

Management:

‣
How are these often managed?
  1. Vagal manoeuvres: Carotid sinus massage
  2. IV adenosine 6mg
    • CI in asthma: Give verapamil instead
‣
Irregular QRS
‣
How can you classify AF?
  1. Paroxysmal: Lasts < 7 days
  2. Persistent: Lasts > 7 days, electrical cardioversion works to resolve
  3. Permanent: Lasts > 7 days, electrical cardioversion doesn't resolve symptoms
‣
What are the common causes?

Mrs. SMITH

  1. Sepsis
  2. Mitral stenosis
  3. Ischaemic HD
  4. Thyrotoxicosis
  5. HTN
‣
What are the other differentials for an irregularly irregular pulse?
  • Ventricular ectopics - Disappear when exercising
‣
What are the management principles?
  1. Rate control (Mostly first-line)
    2. ‣
    What are your options & when are they indicated?
    1. Bisoprolol
      • Asthmatics: Verapamil
    2. Digoxin
      • Asthmatics with heart failure
  2. Rhythm control (Cardioversion)
    3. ‣
    When is this used first line?
    1. There is a reversible cause (e.g. sepsis)
    2. New onset (< 48 hours)
    3. Causing HF
    4. Remain symptomatic despite rate control
    ‣
    How do you decide if you can cardiovert them now?
    • Immediate: AF < 48 hours OR severe haemodynamic instability
      • ‣
      What investigation will help determine if you can cardiovert now?
      • Transoesophageal ECHO looking for left atrial thrombus.

      ‣
      How does presence of a thrombus change your management?
      • Present: Treat same as delayed cardioversion
      • Absent: Calculate CHADSVASc (≥ 2 → LMWH for 4 weeks. 0-1 → Immediate cardioversion)
    • Delayed: AF > 48 hours & stable
      1. Rate control while waiting
      2. Anticoagulate with warfarin (& LMWH cover until INR is in range) for 3-4 weeks before cardioverting due to clot risk
      3. Anticoagulate for 4 weeks after cardioverting
    ‣
    What drug must always be given before cardioversion?
    • LMWH
    ‣
    What are the 2 options?
    1. Electrical - DC cardioversion under GA
    2. Chemical - Flecainide / Amiodarone
    ‣
    When is a 'pill-in-pocket' appoach indicated?
    • Paroxysmal AF with no heart disease or HTN
    • PO flecainide is used
  3. Anticoagulation
    4. ‣
    How do you assess whether they need anticoagulation?

    CHA2DS2-VASc: Men ≥ 1 / Women ≥ 2 → Anticoagulate

    • Congestive cardiac failure
    • HTN
    • Age > 75 years = 2
    • Diabetes
    • Stroke/TIA = 2
    • Vascular disease
    • Age 65-74
    • Sc - Female
    ‣
    How do you assess if they are at risk of bleeding?

    HASBLED

    • HTN
    • Abnormal liver/renal function (1 each)
    • Stroke
    • Bleeding tendency - Previous major bleed
    • Labile INR
    • Elderly > 65 years
    • Drugs/alcohol (1 each)
    ‣
    What would you give?
    • Warfarin: Target INR 2-3
      • Alternative: DOAC
    ‣
    If a patient with a history of MI presents with AF & a high thrombotic risk, do you give an antiplatelet and anticoagulant?
    • No, stop antiplatelet

General:

‣
How do you investigate an arrhythmia?
  1. 12-lead ECG
  2. Paroxysmal:
    • Holter monitor (24hr ECG)
    • Continuous loop recorder (Used in patients who don't have symptoms daily)
  3. Bloods: FBC (anaemia), U&E (electrolyte imbalance), TFT (hyperthyroidism)
  4. Echocardiogram: Structural cause
‣
How do you manage a haemodynamically unstable patient with an arrhythmia?
  • Synchronised DC cardioversion under general anaesthetic
    • Unstable: Shock, syncope, myocardial ischaemia, or heart failure
‣
Broad complex
‣
Which is which:
‣
ECG 1
  • Monomorphic VT
CardioNetworks: Giniger, CC BY-SA 3.0
CardioNetworks: Giniger, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
ECG 2
  • Polymorphic VT
CardioNetworks: Odesk, CC BY-SA 3.0
CardioNetworks: Odesk, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
ECG 3
  • Ventricular fibrillation
Antoine Ayer, CC BY-SA 4.0
Antoine Ayer, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Causes:

‣
Bundle branch block
‣
LBBB
‣
What is it?
  • Absence of electricity flow down the left branch supplying the left ventricle, resulting in a wide QRS due to the electrical supply from the right initiating the LV contraction
  • Caused by myocardial damage or hypertrophy around the LV
‣
What are the causes? (5)
  1. Ischaemic HD
  2. HTN
  3. Cardiomyopathy
  4. Aortic valve disease
  5. Myocarditis
‣
What is seen on ECG?

WiLLiam

Original: A._Rad Vector: Mrmw, CC0, via Wikimedia Commons.
Original: A._Rad Vector: Mrmw, CC0, via Wikimedia Commons.
‣
RBBB
‣
What can cause this? (5)
  1. Normal in tall, thin young people (narrow QRS)
  2. Idiopathic
  3. RV strain (PE/chronic respiratory disease/ASD)
  4. Ischaemic HD
  5. Myocarditis
‣
What is seen on ECG?

MaRRoW:

  1. RSR in V1:
    1. R1 - Septal depolarisation
    2. S - LV depolarisation
    3. R - RV depolarisation
  2. Normal V6
image
‣
Ventricular tachycardia
‣
What is the physiology of VT & what are the causes?
  • Physiology: Ventricular ectopics
  • Causes: Chronic HD, structural HD, hypokalaemia, hypocalcaemia
‣
What are the types?
  1. Monomorphic VT
  2. Polymophic VT (PVT)
    • Torsades de pointes is a type of PVT occurring due to prolonged QT. Often self-terminating but can deteriorate into VF.
‣
The following patients show VT on ECG, how are they managed:
‣
Patient with adverse features
  • DC cardioversion
‣
Patient with normal examination
  • Amiodarone
‣
Patient with Torsades des pointes
  • Magnesium sulphate
  • Torsades = Polymorphic VT
    • ECG shows polymorphic nature of the tachycardia and the long QT interval.
Michael Rosengarten BEng, MD.McGill, CC BY-SA 3.0
Michael Rosengarten BEng, MD.McGill, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Patient with no pulse
  1. Chest compressions 30:2
  2. Unsynchronised shock
  3. Adrenaline & amiodarone
‣
When is an ICD indicated?
  1. Sustained VT causing syncope
  2. Sustained VT with EF < 35%
  3. Previous cardiac arrest due to VT or VF
‣
Ventricular fibrillation

Irregular heart rhythm where the ventricles contact rapidly in an uncoordinated manner, meaning that there is inadequate blood supply to the body.

‣
ECG
CardioNetworks: Googletrans, CC BY-SA 3.0
CardioNetworks: Googletrans, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
How is it managed?
  1. Chest compression
  2. Unsynchronised DC cardioversion
  3. Adrenaline & amiodarone
‣
Bradyarrhythmias
‣
Types:
‣
Sinus bradycardia
‣
What are the causes?
  1. Physical fitness
  2. Vasovagal
  3. Sick sinus syndrome
  4. Drugs - β-blockers, digoxin, amiodarone
  5. Hypothyroidism
  6. ↑ ICP
  7. Hypothermia
‣
Heart block

4 types:

‣
Type I

Prolonged, unchanging PR interval.

‣
What are the causes?
  • Professional athletes with high vagal tone
  • Drugs: β-blockers/CCB
  • Inferior MI
‣
What do you see on the following ECG?
‣
Answer
  • First degree heart block (about 360ms).
  • Poor R wave progression across the precordial leads and a Q wave in V2 suggestive of a previous anterior wall infarction
Michael Rosengarten BEng, MD.McGill, CC BY-SA 3.0
Michael Rosengarten BEng, MD.McGill, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Does this require management?
  • No.
  • Low risk of complete heart block
‣
Type II (Mobitz I, ‘Wenkebach’)

Increasing PR, until dropped QRS.

‣
Type II (Mobitz II)

Fixed 2:1/3:1 block.

‣
What are the causes?
  1. Ischaemic HD
  2. Rheumatology - SLE, RA, systemic sclerosis
  3. Drugs - β-blockers, CCB, amiodarone
  4. Surgery - Mitral valve repair, septal ablation
‣
How are they managed?
  1. Acute: Atropine 500mcg IV
  2. Permanent pacemaker due to risk of complete heart block
‣
Type III (Complete)

Atria & ventricles are not contracting in a coordinated manner.

  1. Atropine
  2. Pacemaker
‣
Long-QT
‣
What is long-QT.
  • QT interval > 460ms in women & > 440ms in men.
‣
What can cause long QT?
  1. Medications: Antiepileptics
  2. Family history: Long-QT syndrome
  3. Low potassium, calcium or magnesium
‣
What are the complications?
  1. Torsades des pointes
  2. Ventricular fibrillation
‣
Sick sinus syndrome
‣
What is this?
  • Intermittent periods of SAN dysfunction → Bradycardia → Dizzy spells, syncope, chest pain
  • Intrinsic heart pathology likely caused by sclerosis of the conduction system
‣
What are the features?
  • Sinus bradycardia
  • Sinus arrest
‣
How is it managed?
  1. ABCDE - ECG, electrolytes, identify reversible causes
  2. Atropine 500mcg - Haemodynamic instability, Mobitz II, complete heart block, recent asystole, ventricular pause > 3s
  3. Options: Isoprenaline, adrenaline, aminophylline, dopamine, glucagon
    • Transcutaneous pacing while awaiting expert advice

‣
💢 Blood Vessels
‣
Aorta
‣
Diagram: Aortic Anatomy
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.

Key Issues:

‣
Aortic dissection
‣
What is this?
  • Tear in the tunica intima causing a false lumen to form in the wall of the vessel between the inner and outer layers of the media.
    • RFs: Marfan’s, Ehlers-Danlos
‣
What are the types?
  • Types:
    • A: Ascending aorta & arch
      • Stanford type A → DeBakey type 1
    • B: Ascending aorta only
      • Stanford type A → DeBakey type 2
    • C: Descending aorta only
      • Stanford type B → DeBakey type 3
J. Heuser, CC BY-SA 3.0
J. Heuser, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
‣
How do they present?
  • Typical patient (for exams): Male in his 50s with sudden onset 'tearing' chest pain radiating to the back.
  • Other features: Syncope, heart/renal failure, and mesenteric or limb ischaemia.
  • Signs: Left / right blood pressure differential.
‣
How do you investigate it?
  1. Immediate: ECG, CXR, transthoracic echocardiogram, and bloods
  2. Definitive: CT TAP
    3. ‣
    What does this show:
    ‣
    Answer
    • Stanford type B dissection: Descending aorta
    JasonRobertYoungMD, CC BY-SA 4.0
    JasonRobertYoungMD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
  3. Trans-oesophageal echocardiogram / MRI
‣
How are the different types managed?
  • Stanford Type A - Urgent surgery (Aortic root replacement / sutured aortic repair)
  • Stanford Type B - Medically managed
‣
What are the complications?
  1. Rupture (80% mortality)
    • Control BP to prevent this with IV β-blocker
  2. End-organ damage due to inadequate blood supply
    • Stroke, limb ischaemia, bowel ischaemia, renal failure
  3. Cardiac failure
  4. Cardiac tamponade
‣
Abdominal aortic aneurysm (AAA)

A permanent pathological aortic dilation with a diameter >1.5X (Usually ≥ 3cm) the expected anteroposterior (AP) diameter of that segment.

‣
Ruptured
‣
How do patients with a ruptured AAA present?
  • New back pain/abdominal pain
  • Haemodynamically unstable
  • Loss of consciousness
‣
How would you investigate?
  • Bloods: Cross-match, FBC, U&E, clotting
  • Imaging:
    • Bedside aortic ultrasound then,
    • CT angiography (CTA)
‣
How is it managed?
  • Urgent surgical repair: Endovascular repair (EVAR) or open surgical repair
    • ‣
    What are the risks of this?
    • AKI
    • Limb ischaemia
    • Graft infection
‣
Unruptured
‣
How is this usually identified?

They’re often asymptomatic, therefore it’s identified:

  • incidentally, or
  • through aortic screening
‣
How is it managed?
  • Surveillance is preferred to surgical repair if asymptomatic until the risk of rupture exceeds the risk of operative mortality.
  • Surgery is still indicated if the aneurysm is large or growing rapidly.
‣
Aortic coarctation

Narrowing in the aorta, most commonly at the site of insertion of the ductus arteriosus.

‣
Diagram: Aortic coarctation
Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436., CC BY 3.0
‣
What is the main sign indicating this?
  • A blood pressure differential, where the upper limb BP > lower limb BP.
‣
How would you investigate this?
  • Bedside:
    • ECG → RV / LV hypertrophy may be present
  • Bloods: FBC, U&E, clotting, G&S
  • Imaging:
    • CXR
      • ‣
      What are you looking for on CXR?
      • Notching of the inferior border of the ribs: Pressure through the collateral vessels causes rib erosion.
      • Cardiomegaly
      Associate Professor Frank Gaillard, CC BY-SA 3.0
      Associate Professor Frank Gaillard, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
    • Echocardiogram → Narrowing in the thoracic aorta (with pressure gradient across narrowing)
    • CT angiography/MR angiography → 3D modelling of anatomy
‣
How is it managed?
  1. Surgical repair
  2. Percutaneous balloon dilation / stenting
‣
What are the complications?
  • Persistent hypertension
  • Surgical site aneurysm formation
‣
Atherosclerosis
‣
What is it?

A combination of:

  1. Atheroma: Deposition of fat, cholesterol and blood cells in the walls of arteries.
  2. Sclerosis: Infiltration of inflammatory cells into the artery wall and the lipid deposition causes progressive hardening of the walls of arteries.
Npatchett, CC BY-SA 4.0
Npatchett, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
How do they contribute to hypertension and thrombus formation?
  • Hypertension: The sclerosis of the arteries stiffens the walls, giving them less compliance. The pressure therefore exerted on them is higher.
  • Thrombus: The plaque can cause damage to the endocardium, losing its smooth surface. This can cause activation of platelets and clotting factors, forming a thrombus. This can then break off to form emboli.
‣
What tool can we use assess somebody’s cardiovascular risk?
  • QRISK-3. It calculates a person’s risk of having a heart attack or stroke over the next 10 years.
    • ‣
    When would we consider treating with a statin?
    • If risk > 10%, consider treating with a statin.
    ‣
    What would you give?
    • Atorvastatin 20mg at night (as per current NICE guidelines).
    • Lifestyle advice is also a key part of management in these cases.
    ‣
    In what condition would we consider giving a statin to all adults with it?
    • Type 1 diabetics:
      • Offer atorvastatin 20 mg to adults > 40 years, or
      • who have had diabetes for more than 10 years, or
      • who have established nephropathy, or
      • have other CVD risk factors.
    • Chronic kidney disease (CKD)
    ‣
    If a patient is on a statin, what bloods should you monitor & when?
    • LFTs at baseline, 3 months & 12 months to check for liver inflammation.
      • Needs to be > 3X the upper limit of normal to stop.
‣
Hypertension
‣
Essential (90-95%)

BP ≥ 140/90 mmHg, with no secondary cause identified.

‣
How would you assess this in clinic to determine the hypertension stage?

Based on NICE guidelines (check which one your University uses for exams), initially do their clinic BP and if:

  • < 140/90 mmHg: Check every 5 years.
  • 140/90 – 179/119 mmHg: Offer ambulatory blood pressure monitoring (ABPM)
    • Stage 1 HTN: ABPM 135/85 – 149/94 mmHg
    • Stage 2 HTN: ABPM ≥ 150/95 mmHg
  • ≥ 180/120 mmHg: 135/85 to 149/94 mmHg (Stage 1 HTN)
‣
Draw the management algorithm.
‣
Exam: Catch you out cases

How would you manage the following patient:

‣
57 year old white man with type 2 diabetes.
  • ACEi / ARB
‣
41 year old woman of African–Caribbean family origin.
  • CCB
‣
61 year old man of African–Caribbean family origin with type 2 diabetes.
  • ACEi / ARB
‣
57 year old lady on an ACEi, CCB & thiazide-like duiretic, but BP still not under control.

We need to check her K⁺:

  • K⁺ < 4.5 → Spironolactone
  • K⁺ ≥ 4.5 → ɑ-blocker / β-blocker
‣
When should ramipril be stopped?
  • Dry cough → Swap to valsartan
  • K⁺ > 5.5 → Stop. Review BP and U&E in a week.
‣
What is the target BP for individuals, based on their age?
  • < 80 years: Clinic BP < 140/90mmHg (ABPM < 135/85mmHg)
  • ≥ 80 years: Clinic BP < 150/90mmHg (ABPM < 145/85mmHg)
‣
Secondary

Elevated blood pressure (BP) secondary to an identifiable cause.

‣
What are the potential causes?
  • Renal:
    • CKD (common)
    • Obstructive uropathy (common)
    • Nephrotic syndrome
    • Glomerulonephritis
  • Vascular:
    • Renal artery stenosis (common)
    • Aortic coarctation
  • Endocrine:
    • Pheochromocytoma
    • Hyperaldosteronism
    • Cushings syndrome
    • Hyperthyroidism
  • Other:
    • Obstructive sleep apnoea (common)
    • Pre-eclampsia
    • Medication-induced: Alcohol, cocaine, corticosteroids,
‣
Complications

How are the following situations managed:

‣
Hypertensive encephalopathy

Encephalopathy & papilloedema:

  • IV labetalol, with target BP of 160/100
‣
Aortic dissection
  • IV labetalol
  • Target: 100-120 systolic
‣
Pulmonary oedema

Vasodilator:

  • IV GTN (10 micrograms/minute), OR
  • IV isosorbide dinitrate
‣
Pregnancy-induced
  • IV magnesium sulphate
‣
Phaeochromocytoma
  • IV phentolamine (ɑ-blockers) then β-blockade

💩 Gastroenterology

‣
🥩 Hepatopancreatobiliary (HPB)
‣
Hepato - Liver
‣
How can the features of liver disease be classified?

What are the features of each?

‣
Compensated liver disease? (7)
  1. Fatigue
  2. Anorexia
  3. Nausea
  4. Abdominal pain
  5. Spider naevi
  6. Palmar erythema
  7. Gynaecomastia
‣
Decompensated liver disease? (4)
‣
Jaundice
‣
What are the differentials for a jaundiced patient?
  • Pre-hepatic
    1. Haemolysis e.g. G6PD deficiency
    2. Neonatal jaundice: Rhesus haemolytic disease, ABO haemolytic disease, hereditary spherocytosis
  • Intra-hepatic
    1. Damage: ALD, NAFLD, hepatitis, etc.
    2. Gilbert's syndrome
    3. Crigler-Najjar syndrome
  • Post-hepatic
    1. Gallstones: Mirizzi syndrome
    2. PBC/PSC
    3. Cholangitis
    4. Pancreatic cancer
‣
How do the stools and urine vary depending on the 3 classifications of jaundice?
  • Pre-hepatic: Normal urine and stools
  • Hepatic: Dark urine, normal/pale stools
  • Post-hepatic: Dark urine, pale stools
    • ‣
    Why pattern of symptoms occur in this case?
    1. Conjugated bilirubin is soluble, unconjugated is not.
      • Pre/intrahepatic → ↑ unconjugated
      • Post-hepatic → ↑ conjugated
    2. Soluble conjugated bilirubin dissolves in the urine (urobilinogen) as it cannot be excreted through the GI tract, giving urine a dark colour.
    3. Lack of bilirubin in the stools (due to biliary tract obstruction) make them pale.
‣
Ascites
‣
How is it investigated to determine cause?
  • Diagnostic tap to analyse the fluid contents
    • SAAG (Serum albumin:ascitic albumin ratio = SAAG)
      • High (transudate): Suggests low albumin
        • Raised portal pressure → Fluid shift
      • Low (exudate): Suggests high albumin
        • Cancer of abdomen
        • Infection → ↑ Vascular permeability (e.g. TB, SBP or pancreatitis)
‣
How is ascites managed?
  1. Low sodium diet
  2. Diuretic eg Spironolactone (Spiro better than Furosemide in ascites)
  3. Prophylactic antibiotics eg Ciprofloxacin
  4. Therapeutic paracentesis (ascitic drainage)
‣
If the disease is still present despite all of the management above, what is considered?
  • Transjugular intrahepatic portosystemic shunt (TIPSS)
  • Indicated in refractory ascites & secondary prophylaxis of variceal haemorrhage
‣
If there is a low SAAG & high neutrophils, what is the likely pathology?
  • Spontaneous bacterial peritonitis
    • ‣
    What pathogen is likely to be causing this?
    1. E. coli
    2. Klebsiella
    ‣
    What features make you suspect SBP?
    • Temperature
    • Distended tender abdomen
    • Can be asymptomatic, always consider in patients who deteriorate suddenly with no obvious cause
    ‣
    How can this be prevented?
    • Prophylactic PO ciprofloxacin
    ‣
    How is it managed?
    • Take ascitic culture
    • IV cefotaxime
‣
Varices
‣
How do these present?
  • Either asymptomatic and found incidentally, or as an acute upper GI bleed.
‣
What are the two scoring systems for an upper GI bleed?

What are each of them used for?

‣
Glasgow-Blatchford score
  • Pre-endoscopy score
  • Decides timing of intervention, if the score is high the patient must go straight for treatment rather than endoscopy first
‣
Rockall score
  • Post-endoscopy score
  • Stratifies based on mortality risk: Risk of rebleed after endoscopy
‣
What is given in the acute management? (4)
  1. ABCDE: Fluid / blood, FFP, Plts
  2. Terlipressin: Splanchnic vasoconstriction → Lower portal venous pressure going through varices and decreases bleeding risk.
  3. Broad spectrum prophylactic antibiotics eg 7 days Ceftriaxone (dec infection risk and risk of rebleed)
  4. Urgent endoscopy within 24h for band ligation
‣
What is the post-endoscopy protocol management?

Hong kong protocol:

  • Omeprazole STAT then continuous infusion to reduce the rebleeding risk
‣
What is given as secondary prophylaxis to prevent re-bleeding?
  • Propranolol: Reduces azygos blood flow and variceal pressure
‣
Hepatic encephalopathy (HE)
‣
What is it?
  • Ammonia build-up causing cerebral oedema
‣
What are the features- early and late?
  • Early: Confusion (suspect in anyone with liver failure and altered consciousness)
  • Late: Fetor hepaticus, coma
‣
How is it graded?
  • 0 - Normal mental status
  • I - Mild confusion (also slurred speech)
  • II - Moderate confusion (Lethargic & drowsy)
  • III - Disorientated to time & place, but rousable. Stupor, incoherent speech
  • IV - Coma, unresponsive
‣
How is it managed?

First-line:

  1. PO lactulose: Reduces nitrogenous waste
    • ↑ faecal flow through the GI tract → ↓ time for proteins to be broken down → ↓ amino acid absorption → ↓ ammonia
  2. IV mannitol: Reduces cerebral oedema

Second line:

  1. Rifaximin: Specialist treatment to decrease activity of ammonia-producing gut flora
‣
What pain management should be avoided?
  • Morphine
    • ‣
    Why does this increase risk of HE?
    • Slowed gut motility → ↑ amino acid absorption → ↑ ammonia
‣
Liver function tests (LFTs)
‣
Which LFTs are raised in liver damage?
  1. ALT > 10-fold rise
  2. AST
  3. Unconjugated bilirubin
  4. GGT
‣
Which LFTs are raised in cholestatic damage?
  • ALP > 3-fold rise
    • Isolated rise in ALP is suggestive of increased bone breakdown: Mets, vitamin D deficiency, fractures, renal osteodystrophy
  • GGT
    • Suggests biliary epithelial damage and bile flow obstruction
‣
How do you test the synthetic function of the liver?
  • Albumin
  • Bilirubin
  • Clotting
‣
Why must you be cautious when interpreting a raised ALP?
  • ALP can be raised due to both liver and bone problems, and high in pregnancy.
    • ‣
    What tests are useful to differentiate them?
    • Liver: Abnormal GGT & other LFTs
    • Bone: Abnormal calcium +/- vitamin D
‣
Name the differentials for liver disease.
‣
Acute liver failure
‣
How does this present?
  • Non-specific: Fatigue
  • Liver-specific: Decompensated liver features discussed above
‣
What investigation is most useful in determining if they have this?
  • INR > 1.5
‣
What are the common causes of this? (5)
  1. Hepatitis
  2. Alcohol
  3. Drugs
  4. Autoimmune hepatitis
  5. Budd-chiari syndrome
‣
Alcoholic liver disease
‣
What is used to assess alcohol dependence?
  1. AUDIT questionnaire
  2. SADQ questionnaire
‣
What is the advice around weekly alcoholic intake?
  • Drink up to 14 units per week, spread this evenly over 3 days or more
‣
How is chronic alcoholism managed?
  1. Mild dependence: < 15 U/day / ≤ 20 on AUDIT
    • CBT first-line
  2. Moderate dependence: > 15 U/day OR > 20 on AUDIT
    • Assisted withdrawal with chlordiazepoxide
  3. Severe: > 30 U/day OR > 30 on SADQ OR high risk of seizures/delirium tremens
    • Inpatient withdrawal
‣
How is acute alcohol withdrawal managed?
  1. IV pabrinex OD
  2. Chlordiazepoxide reducing regime
‣
What liver function test can give you an indication alcohol is the cause?
  • GGT: Although not specific and so must be accompanied by other LFTs
‣
NAFLD
‣
What features are suggestive of NAFLD? (5)
  1. Obesity
  2. Type 2 diabetes
  3. High triglycerides
  4. Hypertension
  5. Smoking
‣
How is this investigated?
  1. Bloods: LFT and lipids
  2. Liver USS: Fatty changes
  3. Enhanced liver fibrosis (ELF) blood test
    • Combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase → Algorithm creates a score
‣
How do you get a definitive diagnosis?
  • Biopsy (rarely done)
‣
What is severe NAFLD called?
  • Non-alcoholic steatohepatitis (NASH): Fat has caused chronic inflammation and cell death
‣
How is this managed?
  • Conservative: Weight loss (even 10% improves LFTs), stop smoking, avoid alcohol
  • Statins (as NAFLD and metabolic syndrome are RF for CVD)
  • If NASH: Consider pioglitazoes and vitamin E (under specialist)
‣
Hepatitis
‣
Viral
‣
How are the types transmitted?
  • A&E: Faeco-oral
  • B&C: Blood & baby
‣
Which ones can only be acute, never chronic?
  • Hepatitis A & E
‣
Which ones have vaccines available?
  • Hepatitis A & B
‣
Which type of Hepatitis doesn't exist without the presence of HepB first?
  • Hepatitis D
‣
Which of the hepatitis' is a DNA virus?
  • Hepatitis B is a DNA virus
  • The rest are RNA viruses
‣
If there is a 'ground glass appearance' on light microscopy of hepatic tissue, what does this suggest?
  • Chronic HepB infection
‣
A nurse has a needlestick from a known HepB patient, she hasn't finished her HepB course. How is this managed?
  1. HepB immunoglobulin
  2. Accelerated HepB vaccine course
‣
Autoimmune
‣
Who commonly presents in an exam history?
  • Young females
‣
What antibodies would you look for?
  1. Anti-smooth muscle antibodies
  2. ANA (anti-nuclear antibodies)
‣
How are they managed?
  1. Immunosuppression: Steroids / azathioprine
  2. Liver transplant
‣
Cirrhosis
‣
What scoring system measures the severity of cirrhosis?
  • CHILD-PUGH score
    • ‣
    What factors does it consider?
    1. Encephalopathy
    2. Ascites
    3. Bilirubin
    4. Albumin
    5. Prothrombin time
‣
How do you monitor management?
  • MELD score (6 monthly): Gives mortality rate and guides referral for transplant
  • USS & AFP (6 monthly): Screens for hepatocellular carcinoma
  • Endoscopy (3 yearly): Looking for varices
‣
How do you manage cirrhosis?
  1. Treat underlying cause
  2. Manage complications (e.g. ascites)
  3. Definitive management: Liver transplant
‣
What are the complications of cirrhosis?
  • Increased mortality
  • Ascites & SBP
  • Liver failure
  • Hepatocellular carcinoma
  • Renal failure/Hepatorenal syndrome
‣
Hepatocellular carcinoma
‣
Who is at high risk of this?
  1. All patients with cirrhosis
  2. HepB / HepC: Particularly high risk
‣
What is the screening test for this?
  • Alpha-feto protein (AFP)
‣
Drug-induced liver injury (DILI)
‣
Paracetamol overdose

How are the following managed:

‣
Ingestion < 1 hr ago
  • Activated charcoal
‣
Staggered overdose > 15 hrs ago
  • Start N-acetylcysteine
‣
Ingestion < 4 hrs ago
  • Wait until 4 hrs to take a level, treat if high
‣
Ingestion 4-15 hrs ago
  • Take immediate level, treat if high
‣
What other drugs can damage the liver?
  • Methotrexate
  • Amiodarone
  • Isoniazid
‣
Budd-Chiari syndrome
‣
What is this?
  • Obstruction of venous outflow from the liver into the inferior vena cava (IVC)
‣
What triad of features indicates this?
  1. Hepatomegaly
  2. Abdominal pain
  3. Ascites
‣
Inherited
‣
Wilson's disease
‣
What features suggest this?
  1. Hepatic: Hepatitis, cirrhosis,
  2. Neurological: Ataxia, tremor, dystonia
  3. Psychiatric: Change in personality
  4. Other: Kayser-Fleischer rings, Coombs negative haemolytic anaemia
‣
How would you investigate?
  1. Serum caeruloplasmin
  2. 24 hour urinary copper (screening test)
  3. Genetic analysis for ATP7B gene
‣
How is it managed?
  • Copper chelators: Penicillamine, trientine
‣
Haemochromatosis
‣
How is this inherited?
  • Autosomal recessive: Mutations in the HFE gene
‣
How can this present? (6)
  1. Pseudogout
  2. Dilated cardiomyopathy
  3. Cirrhosis
  4. Diabetes - Pancreatic deposition of Fe
  5. Grey skin discolouration
  6. Hypogonadism
‣
What is seen on routine bloods? (3)
  1. FBC: ↑ Hb
  2. LFT: ↑ transaminases
  3. BM: High
‣
What is a typical picture on iron studies? (3)
  • ↑ transferrin saturation (M > 55%, F > 50%)
  • ↓ TIBC
  • ↑ Ferritin & Fe
‣
What is seen on liver biopsy?
  • Perl's stain
‣
How are they managed?
  1. Lifelong venesection & aspirin
  2. Desferrioxamine (Fe-chelating agent)
‣
A1AT deficiency
‣
What features suggest this?
  1. Liver: Cirrhosis (clubbing, palmar erythema, spider naevi)
  2. Respiratory: Emphysema (inhalers)
‣
Pancreato - Pancreas
‣
What are the two functions of the pancreas?
  1. Exocrine: Production of enzymes that are released into the small intestine to help digest food.
    1. Amylase → breaks down carbohydrates
    2. Lipase → breaks down fats
    3. Proteases → break down proteins
  2. Endocrine: Production of hormones, including insulin and glucagon.
    1. Alpha cells → Glucagon → Signals the liver to convert stored glycogen into glucose.
    2. Beta cells → Insulin → Signals cells to take up glucose from the bloodstream and store it for energy.

Disease:

‣
Acute pancreatitis
‣
What are the causes?

I GET SMASHED

  1. Idiopathic
  2. Gallstones
  3. Ethanol (alcohol)
  4. Trauma
  5. Steroids
  6. Metabolic
  7. Autoimmune
  8. Scorpion sting
  9. Hypercalcaemia
  10. ERCP
  11. Drugs: Azathioprine, sulfasalazine, valproate, diuretics (loop/thiazide), steroids, tetracyclines
‣
What are the classic symptoms and signs?
  • Nausea & vomiting
  • Severe epigastric pain radiating to back
  • Low grade fever
  • Tachycardic
  • Hypotensive
‣
What markers are used to test for pancreatitis?
  • Amylase
  • Lipase (more sensitive, more expensive): Remains high for 12 days
‣
What are the signs of poor prognosis according to Glasgow scoring system?
  • PaO2 < 8kPa (60mmHg): ARDS
  • Age > 55 years
  • Neutrophils - WBC > 15 x109/l
  • Calcium < 2
  • Renal: Urea > 16mmol/l
  • Enzymes: AST/ALT > 200 iu/L or LDH > 600 iu/L
  • Albumin < 32g/l
  • Sugar: Glucose >10mmol/L
‣
Chronic pancreatitis
‣
What are the classic symptoms and signs?
  • Recurrent abdominal pain
  • Weight loss (malabsorption, exocrine insufficiency)
  • Jaundice
  • Can suffer episodes of acute-on chronic pancreatitis
‣
What is the importance of serum amylase with chronic pancreatitis?
  • It is often normal
‣
What are the common causes of chronic pancreatitis? (3)
  • Alcohol
  • Cystic fibrosis
  • Hereditary
‣
Pancreatic cancer
‣
What are the RFs?
  1. Smoking
  2. FH of pancreatic cancer
  3. Lynch syndrome or BRCA 1/2
‣
How might it present?
  1. Courvoisier's sign: Painless palpable GB & jaundice
  2. Trousseau's sign: Migratory thrombophlebitis
    • Recurrent episodes of blood clots causing vessel inflammation in different locations across the body
‣
What tumour marker is raised in this?
  • CA 19-9
‣
What are the most accurate imaging methods for staging?
  1. Endoscopic USS w/ biopsy
  2. CT TAP
‣
Biliary - Biliary Tree and Gallbladder
‣
Biliary anatomy
‣
Exercise: Labelling the biliary tree
‣
Answers
  1. Bile ducts
  2. Intrahepatic bile ducts
  3. Left and right hepatic ducts
  4. Common hepatic duct
  5. Cystic duct
  6. Common bile duct
  7. Sphincter of Oddi
  8. Major duodenal papilla
  9. Gallbladder
  10. Right lobe of liver
  11. Left lobe of liver
  12. Spleen
  13. Esophagus
  14. Stomach
  15. Pancreas
  16. Accessory pancreatic duct
  17. Pancreatic duct
  18. Small intestine
  19. Duodenum
  20. Jejunum
Jmarchn, CC BY-SA 3.0
Jmarchn, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Simplified Key Anatomy
Boumphreyfr, CC BY-SA 3.0
Boumphreyfr, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Biliary tree
‣
Autoimmune
‣
Primary biliary cholangitis
‣
Where does this affect the biliary tract?
  • Intrahepatic ducts: Bile ducts within the liver
‣
How can this present?
  • Fatigue, jaundice, pruritus, RUQ pain
  • Xanthoma, xanthelasma
  • Signs of cirrhosis and liver failure, e.g. ascites, splenomegaly
‣
Can you explain the pathophysiology and why those symptoms occur?
  • Inflammation of bile ducts → Bile outflow obstruction → Bile acid, bilirubin & cholesterol buildup → Pruritus, jaundice and xathelasma
‣
What antibodies are present in this?
  • Anti-mitochondrial IgM antibodies
‣
What other blood test is often raised in PBC?
  • ESR
‣
What diseases are associated with PBC often?
  • Other autoimmune diseases:
    • Thyroid
    • Coeliac
    • Rheumatoid conditions, e.g. Systemic sclerosis, RA
      • ‣
      Why may a patient with PBC have xerostomia (dry mouth)?
      • Sjogren's syndrome
‣
What is seen on biopsy?
  • Granulomas
‣
What two drugs can be used in the management?
  • Ursodeoxycholic acid: Reduces absorption of cholesterol
  • Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
‣
Primary sclerosing cholangitis
‣
What location does it affect?
  • Intrahepatic and extrahepatic ducts
‣
What is this associated with in 70% of cases?
  • Ulcerative colitis
‣
How can this present?
  • Fatigue, jaundice, pruritus, RUQ pain, hepatomegaly, cirrhosis
‣
What is the gold standard investigation?
  • MRCP
‣
What antibodies are present in this?
  • There are no antibodies helpful in diagnosing PSC, none are sensitive or specific enough
  • p-ANCA is present the majority of the time
‣
What two drugs can be used in the management?
  • Ursodeoxycholic acid: Reduces absorption of cholesterol
  • Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
‣
Cholangiocarcinoma
‣
What is it?
  • Cancer of the bile duct
‣
What are the three types?
  1. Intrahepatic: Affects bile ducts inside the liver.
  2. Perihilar (Klatskin): Occurs where the right and left hepatic ducts exit the liver and join to form the common hepatic duct. Also called a Klatskin tumor or perihilar cholangiocarcinoma.
  3. Extrahepatic (Distal): Occurs below the area where the common hepatic duct and cystic duct join to form the common bile duct.
‣
What’s the most common known predisposing factor?
  • Primary sclerosing cholangitis
‣
What tumour marker may be raised?
  • CA 19-9 (carbohydrate antigen)
‣
How do you manage?
  1. Curative surgery combined with radiotherapy and chemotherapy (only in early cases).
  2. Biliary stenting
  3. Palliative chemotherapy
  4. Palliative radiotherapy
‣
Acute cholangitis
‣
What is it?
  • Inflammation or infection of the common bile duct
‣
What are the features?
  • Charcot’s triad:
    1. Fever
    2. RUQ pain
    3. Jaundice
  • Reynolds pentad:
    1. Fever
    2. Hypotension
    3. Confusion
‣
What organisms commonly cause these infections?
  • Escherichia coli (27%)
  • Klebsiella (16%)
  • Enterococci (15%)

Investigations & Management:

‣
What bloods would you want?

Key bloods (but not all):

  • FBC: Leucocytosis is found in the vast majority of patients
  • CRP
  • LFT: Raised ALP ± GGT + raised bilirubin
  • U&E: Septic patients may have reduced renal function due to hypoperfusion
  • Procalcitonin: Bacterial infection
  • Blood culture
‣
What imaging would you consider?
  • USS: Bile duct dilation
  • MRCP for more detailed imaging
  • ERCP (diagnostic & therapeutic): Identify and remove the cause of the blocked biliary tree.
‣
Gallbladder: Cholecystitis
‣
Identifying & Classifying
‣
What is it?
  • Inflammation of the gallbladder usually occuring when a gallstone completely obstructs the neck of the gallbladder or cystic duct.
‣
What’s the typical presentation?
  • Sudden-onset, severe RUQ pain lasting several hours.
  • Tenderness in the right upper quadrant (with or without guarding).
‣
Name the two types.
‣
Calculous (90–95%)
‣
Partial: What do we call it when the obstruction is partial?
  • Biliary colic
‣
Complete: Why does the gallbladder become inflamed when outflow is completely obstructed?
  1. Trauma from the gallstone causes prostalandin release which stimulates an inflammatory response.
  2. Gallbladder then becomes more distended and inflamed causing compromise of blood flow and lymphatic drainage, leading to mucosal ischemia.
  3. Bacterial infection of the bile may then occur.
‣
Acalculous (5%)

Exact cause is poorly understood, but often in critically ill patients, associated with bile stasis or thickening.

‣
What are the risk factors?
  • Bile stasis: Trauma, severe systemic illness, and prolonged total parenteral nutrition use
  • Bile thickening: Fever and dehydration
‣
Name the key investigation.
  • Abdominal USS to identify presence of gallstones.
‣
Managing & Complications
‣
How do you manage them?
  1. Support: IV fluids, antibiotics & analgesia
  2. Definitive: Laparoscopic cholecystectomy
‣
Name 5 complications.
  1. Necrosis of the gallbladder wall (gangrenous cholecystitis).
  2. Gallbladder perforation.
  3. Biliary peritonitis.
  4. Pericholecystic abscess.
  5. Fistula between the gallbladder and duodenum.
  6. Jaundice due to inflammation of adjoining biliary ducts.
    7. ‣
    What is this called?
    • Mirizzi syndrome
  7. Sepsis.
‣
🌯 Luminal
‣
Upper GI (Mouth → Duodenum)

Anatomy:

‣
Oesophagus
‣
Gastro-oesophaegeal reflux disease (GORD)
‣
What is the best investigation for a hiatus hernia?
  • Barium swallow
‣
When going for an endoscopy, how is omeprazole management approached?
  • Stop 2 weeks before endoscopy as it could mask serious pathology, e.g. gastric cancer
‣
What drugs are associated with dyspepsia?
  1. NSAIDs/steroids
  2. Bisphosphonates
  3. CCBs
  4. Nitrates
  5. Macrolides
‣
Oesophageal varices

Dilated collateral blood vessels that develop as a result of portal hypertension, usually with a background of cirrhosis.

‣
What are the key features?
  1. Haematemesis
  2. Melaena
  3. Severe liver disease
  4. Cirrhosis (50% have varices)
  5. Spider nevi
  6. Jaundice
‣
What are differentials for haematemesis?
  1. Gastric varices
  2. Mallory-Weiss tear
  3. Peptic ulcer
  4. Upper GI malignancy
‣
What scoring systems may be useful?
  1. Rockall score: Estimate the risk of rebleeding or death in patients with upper GI bleed.
  2. Glasgow-Blatchford score: Stratifies upper GI bleeding patients who are "low-risk" and candidates for outpatient management.
‣
How would you investigate?
  1. Bloods: FBC, U&E, LFT, coagulation, HepB serology, G&S and cross match.
  2. Gastroscopy: Diagnostic of varices and allows assessment of their size.
  3. Consider:
    1. Capsule endoscopy
    2. Liver USS
‣
How do you manage them?
  1. ABCDE
  2. Consider, if appropriate:
    1. Transfusion
    2. Terlipressin / somatostatin analogue (e.g. octreotide)
    3. Prophylactic antibiotics (e.g. IV ceftriaxone)
  3. When stabilised, endoscopy & endoscopic variceal band ligation
    1. If endoscopy not immediately available, balloon tamponade or Danis stent
‣
Oesophageal cancer
‣
What are the common features?
  1. Dysphagia
  2. WL
  3. Retrosternal chest pain
‣
If a patient has Barrett's oesophagus, how are they managed if they have low-grade or high grade dysplasia, respectively?
  1. Low grade: High dose omeprazole & 6 monthly endoscopy
  2. High grade: Endoscopic ablation
‣
What cell types can they be?
  1. Squamous cell
  2. Adenocarcinoma (if Barrett's) - Lower 1/3
‣
Achalasia
‣
What is it?
  • Degeneration of the myenteric plexus around the LOS causing it to always contract
  • Difficulty swallowing both solids & liquids
‣
How is it investigated?
  1. Manometry: Tube into oesophagus that measures pressures
    • High pressure in the LOS, incomplete relaxation, absence of peristalsis
  2. Barium swallow: 'Bird's beak appearance'
‣
How is it managed?
  1. Medical: Nifedipine & omeprazole
  2. Definitive:
    1. Unfit for surgery: Balloon dilation of the LOS
    2. Fit for surgery: Heller's cardiomyotomy
‣
Stomach
‣
Peptic ulcer disease
‣
What are the two areas this can affect & the features of each?
  1. Stomach: Worse after meals
  2. Duodenum: Improves after meals
‣
What is Zollinger-Ellison syndrome?
  • Gastrinoma of the stomach → Excessive acid secretion → Ulcers
‣
How is H. pylori negative disease managed?
  • 4-8 weeks full dose PPI
‣
How are they followed up?
  • Repeat endoscopy 6-8 weeks after being discharged
‣
How are they managed if the ulcer perforates?
  1. NBM, IV fluids
  2. Laparotomy
‣
How are they managed if the ulcer causes a severe bleed?
  • Endoscopic clipping or thermal coagulation
‣
H. pylori
‣
How is this confirmed?
  • Faecal antigen
  • Urea breath test
‣
How is it managed initially?

Triple therapy (BD for 7 days):

  1. Omeprazole
  2. Amoxicillin
  3. Clarithromycin
‣
When tested 4 weeks later, how does management change if still positive?
  • Triple therapy: Metronidazole replaces clarithromycin
  • Refer to gastroenterology if still + after this
‣
Cancer
‣
What cell type is it likely to be?
  • Glandular: Adenocarcinoma
‣
What associations increase susceptibility?
  1. H. pylori infection
  2. Smoking
  3. Obesity
‣
What is seen on endoscopy?
  • Signet ring cells
‣
Duodenum
‣
Duodenal ulcers
  • Managed the same as gastric ulcers
‣
Coeliac disease
‣
What is the pathophysiology?
  • Gluten is broken down to gliadin in the small intestine → Inflammatory response → Cell destruction (lost surface area) → Malabsorption
‣
Presentation:
‣
What is coeliac disease most commonly linked with? What else is it associated with?
  • Common: T1DM & thyroid - All of these patients are tested for coeliac disease
  • Other autoimmune: Autoimmune hepatitis, PBC, PSC
‣
What is the rash may they present with?
  • Dermatitis herpetiformis (pruritic vesicles on the extensor surfaces)
‣
Why may they be anaemic?
  • Malabsorption of B12/folate
‣
What bloods will confirm your suspicions?
  1. IgA anti-TTG antibodies
    2. ‣
    What else should you test for with this?
    • Total IgA because if there's an IgA deficiency then the test will be negative but the disease may still be present
    ‣
    How can you confirm the diagnosis in those patients?
    • IgG anti-TTG/anti-EMA
  2. Anti-EMA antibodies
‣
What features are seen on intestinal biopsy? (2)
  1. Villous atrophy
  2. Crypt hypertrophy
‣
How are they managed?
  • Lifelong gluten free diet
  • Dapsone antibiotic for dermatitis herpetiformis
‣
Lower GI (Jejunum → Anus)

Common:

‣
Inflammatory bowel disease (IBD)
‣
Features:
‣
What features would make you consider IBD?
  • Abdominal pain, blood diarrhoea, mouth ulcers, other autoimmune conditions, WL, anaemia
  • Systemically unwell during flares
‣
How do you differentiate the two types?
‣
Crohn's (NESTS)
  • No/less blood or mucus in stool
  • Entire bowel is affected
  • Skip lesions
  • Terminal ileum most affected & Transmural thickness inflammation
  • Smoking makes it worse
‣
UC (CLOSEUP)
  • Continuous inflammation
  • Limited to colon & rectum
  • Only superficial mucosa affected
  • Smoking protective
  • Excrete blood & mucus
  • Use aminosalicylates
  • Primary sclerosing cholangitis
‣
What extra-intestinal manifestations would you look for?
  • Finger clubbing
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Episcleritis/iritis
  • PSC in UC
‣
What are the types?
‣
Ulcerative colitis
‣
What site is most commonly affected?
  • Rectum
‣
Name 5 extra-intestinal manifestations.
  1. Skin: Erythema nodosum, pyoderma gangrenosum
  2. Primary sclerosin cholangitis (independent of flares)
  3. Eyes: Episcleritis, scleritis, anterior uveitis
  4. Osteoporosis (malabsorption)
  5. Peripheral neuropathy (B12)
‣
What is seen on colonoscopy?

Disease is limited to the mucosa, showing:

  1. Crypt abscesses
  2. Goblet cell depletion
  3. Mucin depletion
  4. Mucosal ulcers
‣
What is seen on barium enema?
  • 'Lead pipe sign' - Loss of haustral markings on the bowel
‣
What are the complications?
  • Toxic megacolon: AXR to investigate
    • ACR (colon dilation), Temp > 38.6°C, HR > 120bpm, anaemia, ↑ neutrophils
Hellerhoff, CC BY-SA 3.0
Hellerhoff, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Crohn's disease
‣
What is the epidemiology?

Age of onset is bi-modal:

  • 15-40 years: Majority
  • 60-80 years: Small second peak
‣
Where does it commonly target?
  • Distal ileum
  • Proximal colon
‣
What features are you looking for?
  1. Abdominal pain (potentially colicky)
  2. Diarrhoea (often chronic)
  3. Oral aphthous ulcers (can be painful)
  4. Perianal disease
‣
How do you investigate it? (5)
  1. Bedside: Faecal calprotectin
  2. Bloods: FBC (macrocytic anaemia), LFT (PSC).
  3. Radiology: USS/CT/MRI (fistulae, abscesses, strictures)
  4. Endoscopy: OGD & colonoscopy
    • Take biopsies to look for microscopic features.
    • If active disease only do flexible sigmoidoscopy because of risk of perforation in colonoscopy.
    • If colonoscopy is negative in Crohn's, use MRI to assess the small bowel.
‣
What are the key principles of management? (2)
  1. Induce remission
    2. ‣
    What is used to induce remission in Crohn's? (3)
    1. Steroids - PO prednisolone (mild-moderate) / IV hydrocortisone (severe)
    2. Add azathioprine/mercaptopurine
    3. Refractory: Infliximab
    ‣
    What is used to induce remission in UC?
    1. Aminosalicylate - Mesalazine (mild-mod)
      1. Suppository/enema first
      2. PO if extensive disease
    2. Steroids - PO prednisolone (mild-mod) / IV hydrocortisone (severe)
    3. IV ciclosporin (severe)
  2. Maintain remission
    3. ‣
    What is used to maintain remission in Crohn's?

    Medical:

    1. Azathioprine/Mercaptopurine
    2. Methotrexate
    3. Infliximab
    4. Adalimumab

    Surgical:

    1. If only affecting one area of bowel severely, surgery will be considered.
    ‣
    What is used to maintain remission in UC?

    Medical:

    1. Aminosalicylate - Mesalazine (PO/PR)
    2. Azathioprine
    3. Mercaptopurine

    Surgical:

    1. Panproctocolectomy: Surgery to remove the colon & rectum. May have hemicolectomy, depends on case.
      • Patient has either a permanent ileostomy or ileo-anal anastomosis (J-pouch).
‣
Appendicitis
‣
What are the features of appendicitis?
  • Abdominal plain: Classically central/periumbilical then moves to right iliac fossa
  • Nausea and vomiting
  • Loss of appetite
  • Mild fever
  • Can get rebound tenderness
‣
What is Rovsing's sign?
  • Palpation in left iliac fossa causes pain in right iliac fossa
‣
How do you diagnose it?
  • Mostly clinical presentation
  • Raised inflammatory markers & WCC
‣
What conditions can a urine dipstick rule out?
  • Pregnant female
  • UTI
  • Renal colic
‣
How is it managed?
‣
What is the definitive management?
  • Appendicectomy
‣
What needs to be given before surgery & why?
  • Prophylactic IV antibiotics - Reduces wound infection
‣
What are the 2 options for surgery?
  • Laparoscopic
  • Open
‣
Diverticular disease
‣
Definitions:
‣
Diverticulum
  • Herniation of colonic mucosa through muscularis causing outpouchings
‣
Diverticulosis
  • The presence of diverticula WITHOUT symptoms
‣
Diverticulitis
  • Inflamed/infected diverticula
‣
Who is it common in? What are the 2 main risk factors?
  • Very common in older people
  • RFs: Low fibre diet & obesity
‣
What are the features of diverticulitis?
  • Left iliac fossa colicky pain
  • Diarrhoea
  • PR blood or mucus
  • Fever
  • Can be septic and peritonitic if severe!
‣
What investigation is important if suspect diverticulitis and why?
  • Abdominal XR (or CT abdo)
  • Erect CXR to identify a perforation
‣
How do you manage diverticulosis?
  • Often an incidental finding on CT
  • No treatment necessary: Advise high fibre diet and weight loss if necessary
‣
How do you manage diverticulitis?
  • Analgesia
  • Fluid resuscitation
  • Antibiotics
  • Unwell → Consider hospital admission
  • Severe → May need surgical drainage or resection
‣
Cancer

See Colorectal Surgery

‣
Irritable bowel syndrome (IBS)
‣
How is IBS different to the majority of GI conditions?
  • There is no organic underlying disease. Many think it is linked to stress and the mind
‣
What features can you get?
  • Diarrhoea or constipation predominant- fluctuating bowel habit
  • Abdominal pain
  • Bloating
  • Worse after eating, improved by opening bowels
‣
What investigations can you do to exclude other pathology before diagnosing?
  • FBC, ESR and CRP
  • Faecal calprotectin
  • Anti-TTG antibodies
  • CA125
‣
What is the management of IBS?
  • Provide reassurance
  • Low FODMAP diet
  • Symptom dependent:
    • Cramping: peppermint oil, buscopan (hyoscine butylbromide)
    • Diarrhoea: Loperamide
    • Constipation: Laxatives

Less common:

‣
Clostridium dificile
‣
What is a typical history?
  • Patient in hospital on antibiotics (broad spectrum - e.g. cephalosporins) for an infection develops watery diarrhoea & feels generally unwell
‣
What is seen on colonoscopy?
  • Yellow plaques & mucosal inflammation
‣
How are they managed? (2)
  1. PO metronidazole (mild)
  2. PO vancomycin (mod-sev)
‣
Name 1 severe complication.
  • Toxic megacolon
‣
Re-feeding syndrome
‣
What metabolic abnormalities occur with this?
  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Abnormal fluid balance

🫁 Respiratory

‣
😤 Airway

Many of these diseases affect multiple pieces of anatomy; these are clarified within the disease section. However, to help your understanding, they’re classified within the primary piece of anatomy they affect.

‣
Diagram: Airways
UNSHAW, CC BY-SA 4.0
UNSHAW, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Classifying by anatomy:

‣
Upper airways (Nasopharynx & Trachea)
‣
Obstructive sleep apnoea (OSA)
‣
What is this?
  • Obstructive sleep apnoea occurs due to the relaxation of the throat muscles, blocking your airway during sleep.
    • Collapse of the pharyngeal airway.
    • Apnoea episodes are where the individual will stop breathing for up to a few minutes.
‣
What scale is used to assess sleepiness?
  • Epworth Sleepiness Scale
‣
What features may suggest this?
  • Snoring
  • Daytime sleepiness
  • Apnoea episodes (often reported by the partner)
  • Waking up not feeling refreshed from sleep
  • Concentration problems
‣
How is this managed?
  1. Sleep studies with ENT specialist / at a sleep clinic
    2. ‣
    What do these involve?

    Sleeping while monitoring the:

    1. Oxygen saturation
    2. Heart rate
    3. Respiratory rate
    4. Breathing
  2. Lifestyle: Stop smoking, drinking alcohol and lose weight
  3. Continuous positive airway pressure (CPAP)
  4. Surgery: Uvulopalatopharyngoplasty (UPPP)
‣
Epiglottitis
‣
What is it?
  • Haemophilus influenza type B infection causing swelling of the epiglottis.
‣
What would you see on lateral neck X-ray?
  • Thumbprinting sign: Shadowing caused by the swollen epiglottis
‣
How do you manage it?
  • ABCDE
  • Immediate escalation to anaesthetics to secure the airway, this may be through intubation if possible or by tracheostomy as the swollen epiglottis may make intubation impossible.
  • IV antibiotics (see local guidelines)
  • Steroids, e.g. dexamethasone

Management:

‣
Non-invasive ventilation: What’s the difference between BiPAP and CPAP?
  • CPAP: Pushes only.
    • Provides a fixed positive pressure on the airways through inspiration and expiration, maintaining airway patency.
  • BiPAP: Pushes & pulls. Used in T2RF.
    • This is used in CO₂ retainers when they can no longer maintain their respiratory drive. It pulls the CO₂ from the lungs as well as pushing O₂ in.
      • ‣
      What conditions can indicate BiPAP?
      • COPD with respiratory acidosis
      • Hypercapnic respiratory failure: Chest wall deformity, neuromuscular disease
‣
Bronchi / bronchioles
‣
Asthma

Asthma is a chronic respiratory condition causing inflammation and narrowing of the bronchi.

‣
Acute exacerbation
‣
Presentation
‣
Name the common triggers.
  1. Dust
  2. Exercise
  3. Infection
  4. Time of day: Night or early morning
  5. Cold/damp
‣
What features suggest asthma?
  1. Occurring in episodes
  2. Diurnal variation: Often worse at night.
  3. Wheeze
  4. Shortness of breath
  5. Atopy: Eczema, hayfever, food allergies
‣
Grading

What makes up the following grades:

‣
Moderate
  • PEFR: 50-75%
‣
Severe
  • PEFR: 33-50%
  • RR ≥ 25
  • HR ≥ 110
  • Unable to complete sentences
‣
Life-threatening
  • PEFR < 33%
  • SpO2 < 92%
  • Cyanosis
  • Hypotension
  • Exhaustion - PaCO₂ normal/high
  • Silent chest
  • Tachyarrhythmias
‣
Near-fatal
  • pCO2 > 6 (Normal - represents exhaustion)
‣
Management
‣
Step 1: Initial
  1. ABCDE
  2. Nebulised salbutamol 5mg & ipratropium bromide
    3. ‣
    What bloods should you monitor because of this?
    • K⁺ as can be ↓
  3. Steroids: PO prednisolone / IV hydrocortisone
  4. Antibiotics (if you suspect this is secondary to an infection)
‣
Step 2: If non-responsive
  • IV aminophylline
  • IV salbutamol
‣
Step 3: Life-threatening
  1. IV magnesium sulphate
  2. Admission to HDU/ITU for intubation & ventilation

‣
After an acute asthma attack, when can the patient be discharged?
  • Stable on salbutamol inhaler for 24 hours
  • PEFR > 75% predicted
‣
Chronic

Investigation:

‣
What are the first-line investigations?
  1. Fractional exhaled NO (FeNO): ↑ in airway inflammation
  2. Spirometry with reversibility
‣
What are the second-line investigations?
  • Peak flow variability: measure peak flow multiple times a day for 2-4 weeks looking for variability throughout the day.
  • Direct bronchial challenge test (with histamine or methacholine).
‣
What can be seen on histology in asthma?
  • Curschmann spirals: Shed epithelium becomes whirled mucus plugs
‣
Diagnostic protocol: What do you need for diagnosis?

Note: Ask at your University which guideline protocol they follow in exams.

  • BTS (2016):
    • If high probability of asthma based on clinical picture, try treatment.
    • If unsure, use spirometry with reversibility testing to confirm.
    • If low probability, consider referring for other causes.
  • NICE (2017):
    • Advise not to make a diagnosis based on clinical picture.
    • Always investigate at a diagnostic hub.

Management:

‣
How do the following drugs work:
‣
β-2 adrenergic receptor agonists (SABA/LABA)
  • Activate beta 2 adrenergic receptors on the smooth muscle that surrounds the airways → Smooth muscle to relaxation → Bronchodilation.
    • SABA: Work within minutes, last several hours.
    • LABA: Lasts at least 12 hours.
‣
Inhaled corticosteroids (ICS)
  • Reduce airway inflammation, preventing or reducing asthma attacks → Prevents airway smooth muscle hypertrophy secondary to chronic inflammation.
‣
Muscarinic antagonists (SAMA/LAMA)
  • Block acetylcholine receptors blocking the parasympathetic effect of bronchoconstriction, indirectly causing bronchodilation.
‣
Leukotriene receptor antagonists
  • Leukotrienes → Inflammation, bronchoconstriction & mucus secretion.
  • Blocking these prevents this.
‣
What are the stages of management for adults (≥ 17 years)? (8)

Based on NICE Guidelines (2017):

  1. SABA
  2. Add regular low-dose ICS
  3. Add LTRA (review in 4-8 weeks)
  4. Add LABA (discuss if LTRA has helped at all, if not stop it)
  5. MART (maintenance & reliever therapy): Combined ICS (low-dose) & fast-acting LABA
  6. MART with moderate dose ICS
  7. Increase ICS to high-dose OR add PO theophylline OR add LAMA.
  8. Refer to specialist
‣
Give examples of each type of inhaler. (6)
  • SABA - Salbutamol
  • SAMA - Ipratropium
  • ICS - Beclometasone, budesonide, fluticasone, mometasone
  • LTRA - Montelukast
  • LABA - Salmeterol, formoterol
  • LAMA - Tiotropium
  • MART - Turbohaler, spiromax
  • ICS & LABA - Symbicort, fostair, seretide
‣
What drugs can be used in pregnancy?
  • Inhaled drugs, theophylline and prednisolone can be taken as normal during pregnancy and breast-feeding.
‣
Atelectasis

Atelectasis is the complete or partial collapse of the entire lung, or a lobe of the lung due to airway obstruction.

‣
How can you classify this?
‣
Obstructive: Airway blockage
‣
What are the 3 common causes of this?
  1. Mucus plug
    2. ‣
    Why does this commonly occur post-operatively?
    • Secretions build up in airways due to reduced movement and because you can’t cough → Airrway obstruction → Bibasal lung collapse → Reduced lower lobe breath sounds
    ‣
    Name 2 other causes.
    1. Cystic fibrosis
    2. Asthma
  2. Foreign body: Inhaled object (e.g. peanut)
  3. Lung tumour within the airway
‣
Non-obstructive: From pressure from outside the lung
‣
What could cause this?
  • Pleural effusion
  • Pneumonia
  • Pneumothorax
  • Lung tissue scarring of lung tissue due to injury, lung disease or surgery.
  • Tumor (non-airway) causing external compression
‣
How is it managed?
  1. Position patient upright
  2. Chest physiotherapy
‣
Bronchiectasis
‣
What is this?
  • Damage and scarring of the large airways due to recurrent infection and resulting inflammation from immune response.
  • Leads to mucus buildup and dysfunction of the mucociliary escalator.
‣
What is seen on CXR?
  • Multiple thin walled cystic space (ring opacities), several of which have air-fluid levels.
‣
What are the key features on CT?
  1. Tram track sign
  2. Signet ring sign
  3. Cluster of grapes sign
Mcgfowler, CC BY-SA 3.0
Mcgfowler, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
‣
Chronic obstructive pulmonary disease (COPD)

COPD is chronic inflammation of the airways causing bronchitis (airway inflammation & narrowing) and emphysema (alveoli destruction).

‣
Presentation
‣
What else may they present with?
  • Shortness of breath.
  • Cough.
  • Wheeze.
  • Recurrent LRTI.
‣
What are the two main presentations?
  1. 'Pink puffer': Predominantly emphysema.
    • Compensate for damaged alveoli by hyperventilating.
    • High VQ ratio.
  2. 'Blue bloater': Predominantly bronchitis.
    • Compensate for lack of air getting to the alveoli by increasing cardiac output.
    • Low V/Q ratio.
‣
How do you assess the impact of their breathlessness?
  • MRC dyspnoea scale. Scale of 1-5, useful to remember the extremes:
    • SOB on strenuous exercise = 1.
    • Unable to leave house = 5.
‣
Investigations
‣
What would you look for on spirometry?
  • Obstructive picture: FEV1/FVC ratio < 0.7
‣
How do you assess the severity (stage) of the exacerbation?

Using FEV1:

  1. Stage 1: FEV1 > 80% predicted
  2. Stage 2: FEV1 50-79% predicted
  3. Stage 3: FEV1 30-49% predicted
  4. Stage 4: FEV1 <30% predicted
‣
How do you assess if somebody is a CO₂ retainer?
  • ABG: ↑ HCO₃⁻ → Chronic retainer
‣
What are the TLCO & KCO?
  • TLCO: Total lung diffusion capacity
  • KCO: Diffusion capacity of a single alveolus

What would they be in the following diseases:

‣
COPD
  • Both low
‣
Pneumonectomy/atelectasis
  • KCO high (compensatory), TLCO reduced
‣
Lung fibrosis/fluid
  • Both low
‣
Myasthenia gravis with respiratory muscle weakness
  • KCO high, TLCO low
  • Lack of lung expansion → Higher pressures in alveoli → More diffusion
‣
What other investigations would be helpful for management?
  • Bedside:
    • Sputum culture: Tailor antibiotic regimen later.
    • ECG
  • Bloods:
    • FBC: WCC to assess if infective cause, Hb to look for secondary polycysthaemia.
    • Serum ɑ-1 antitrypsin
  • Imaging:
    • Chest X-ray: Exclude other causes.
    • CT thorax: Exclude fibrosis and cancer.
‣
Management
‣
Exacerbation
‣
What is the typical management of an exacerbation if sending the patient home?
  1. Prednisolone 30mg OD for 7-14 days
  2. Antibiotics (if infective cause)
  3. Regular inhalers
‣
If they require admission, how are they managed?
  1. Inhaled: Nebulised salbutamol and ipratropium
  2. Steroids: IV hydrocortisone or PO prednisolone
  3. Antibiotics (if likely infective cause)
  4. Chest physiotherapy to help clear sputum
‣
If they are on O₂ and they are becoming more acidotic and are also deteriorating, what do you need to do?
  • Non-invasive ventilation (BiPAP), may also need IV aminophylline
‣
Long-term management
‣
What are the stages of long-term management?
  1. Stage 1: SABA (salbutamol)/SAMA (ipratropium)
  2. Stage 2:
    • No steroid features: LABA & LAMA
    • Steroid features: LABA & ICS
  3. Stage 3:
    • Triple therapy: LABA & LAMA & ICS (Trelegy ellipta, trimbo)
  4. Advanced management
    5. ‣
    What surgical management is available & when is it indicated?
    • Bullectomy (removing the dilated airspaces)
    • Lung volume reduction surgery
    • Indicated in if on maximal medical therapy and still have marked ADL restriction. Must have:
      • FEV1 > 20% predicted
      • Upper lobe predominant emphysema
    ‣
    What are the indications for long-term O2 therapy?
    1. PaO2 of < 7.3 kPa (measured when the patient is clinically stable, on two occasions, at least 3 weeks apart)
    2. PaO2 of 7.3 - 8 kPa & one of the following:
      • Nocturnal hypoxaemia (SaO2 < 90%)
      • Secondary polycythaemia
      • Pulmonary hypertension (pulmonary artery pressure > 25mmHg)
      • Peripheral oedema
‣
What should they all have?
  • Annual pneumococcal & flu vaccine
‣
Lung cancer
‣
What are your differentials for a lung nodule on CXR? (6)
  • Malignancy - 1° or 2°
  • Foreign Body
  • Abscess / cyst
  • Granuloma - Sarcoid / TB
  • Pulmonary hamartoma / AVM
  • Skin tumor
‣
Classifying lung cancer
‣
Primary
‣
NSCLC (85%): What are the types?
  1. Adenocarcinoma (~ 40%)
      2. ‣
      How is this presentation different to the rest?
      • Presents in non-smoking women (but still in smokers too)
    1. Best prognosis
  2. Squamous cell carcinoma (~ 30%)
    • Present in the mediastinum, develop from the bronchi
      • ‣
      What is it associated with?
      • Hypercalcaemia - Secretes PTH
      • Hypertrophic pulmonary osteoarthropathy (affects hands & feet)
  3. Large cell carcinoma (~ 10%)
    • Likely to metastasise
  4. Carcinoid
    5. ‣
    What is this?
    • Neuroendocrine tumour secreting serotonin, histamine & bradykinin
    ‣
    What are the features?
    • Bradykinin → Facial flushing
    • Histamine → SOB
    • Serotonin → Diarrhoea, asthma & SOB
    ‣
    How do you investigate it?
    • Urinary 5-HIAA
    • Octreotide scan
    ‣
    How do you manage it?
    • Somatostatin analogues: Octreotide
  5. Mesothelioma
    6. ‣
    What is this?
    • Pleural tumour associated with asbestos exposure with a long latent period of up to 45 years between exposure and cancer development.
‣
SCLC (~ 20%)
  • Aggressive, quickly metastasise, strongly related to smoking.
  • Release neuroendocrine hormones, meaning they commonly cause paraneoplastic syndromes.
‣
Secondary
  • Metastases from other sites
‣
Paraneoplastic syndromes

Name the paraneoplastic syndrome & tumour causing it:

‣
Hoarse voice
  • Recurrent laryngeal nerve palsy
  • Upper lung tumour
‣
Pemberton's sign is positive
  • SVCO
  • Upper lung tumour
‣
Ptosis, miosis & anhidrosis
  • Horner's syndrome
  • Pancoast (apical) tumour compressing the sympathetic ganglion
‣
Severe hyponatraemia
  • SIADH
  • SCLC secreting ADH causing dilutional hyponatraemia
‣
Striae, weight gain, easy bruising, T2DM, interscapular fat pad, spinal tenderness, HTN
  • Cushing's syndrome
  • SCLC secreting ACTH
‣
Bone pain, renal stones, abdominal pain, confusion
  • Hypercalcaemia
  • Squamous cell carcinoma secreting PTHrP
‣
Proximal muscle weakness that improves on exercise, diplopia & ptosis
  • Lambert-Eaton syndrome
  • SCLC

‣
How might they present?
  • Cough
  • Shortness of breath
  • Weight loss
  • Haemoptysis
‣
How do you investigate a suspected lung cancer?
  1. CXR:
    • Pleural effusion (usually unilateral - exudative)
    • Mass
    • Atelectasis
  2. Contrast-enhanced CT thorax, abdomen, pelvis (CT TAP):
    • Confirm diagnosis & staging
    • PET-CT may also allow us to more clearly see metastases
  3. Bronchoscopy with EBUS (endobronchial USS) with transbronchial needle aspiration for histology
‣
What are the management options & indications for each?
  • Lifestyle:
    • Smoking cessation
  • Medical:
    • Chemotherapy: Metastases
    • Radiotherapy: Can be definitive in adenocarcinoma (but surgery is preferred)
  • Surgical:
    • Lobectomy/segmentectomy → Localised disease (T1/2 N0 M0)
    • Pneumonectomy/bi-lobectomy → Extensive disease
‣
Alveoli
‣
Pneumonia

Infection of the lung tissue.

‣
What is the pathophysiology of consolidation?
  • Bacteria infect alveoli → Pulmonary membrane inflammation → Increased permeability → Blood & fluid entering alveoli causing consolidated appearance (filled with liquid)
‣
How do you assess the severity?

CURB-65 (1 point for each of the following):

  • Confusion: New disorientation to time, place or person
  • Urea > 7
  • RR ≥ 30 bpm
  • BP < 90/60 mmHg
  • > 65 years
‣
How do you classify pneumonia?
‣
Typical
‣
Community-acquired pneumonia (CAP)
‣
What are the common causes?
  1. S. pneumonia (50%)
  2. H. influenzae (20%)
    3. ‣
    What is shown on culture?
    • Gram ⊖ coccobacilli
  3. Moraxella catarrhalis
    4. ‣
    Who presents with this?
    1. Immunocompromised patients
    2. Chronic pulmonary disease patients

Cases:

‣
A patient has signs of pneumonia and the following rash:
‣
What is the rash called and the underlying pathogen?
  • Rash: Herpes labialis
  • Pathogen: S. pneumoniae (Gram ⊕ diplococci)
‣
How can you confirm this diagnosis?
  • Pneumoncoccal urinary antigen
  • CXR: Lobar consolidation
Speifensender, CC BY-SA 3.0
Speifensender, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
What is the most common cause of an infective exacerbation of COPD?
  • H. influenzae (Gram ⊖ coccobacilli)
‣
Patient presents with headache, fever, myalgia and cough, chest clear. What is this likely to be?
  • Influenza
‣
A patient with cystic fibrosis presents with pneumonia. What organism could this be?
  • Pseudomonas aeruginosa (Gram ⊖ bacilli)
  • Staphylococcus aureus (Gram ⊕ cocci)
‣
Hospital-acquired pneumonia (HAP)

Lower respiratory tract infection (LRTI) developing > 48 hours after admission to hospital.

‣
What are the common causes of HAP? (4)
  1. P. aeruginosa (Gram ⊖ bacilli) - Associated with mechanical ventilation
  2. S. aureus (Gram ⊕ cocci)
  3. Enterobacteria:
    1. E. coli (Gram ⊖ bacilli)
    2. Klebsiella (Gram ⊖ bacilli)

Cases:

‣
A patient with leukaemia recently had the flu and now has a bacterial pneumonia. What is the cause?
  • S. aureus: Associated with flu, lymphoma/leukaemia, IVDU
‣
An alcoholic presents fever, red currant sputum & bronchial breathing in the upper zones. What is the cause?
  • Klebsiella
‣
Aspiration
‣
Who is at risk of this?
  1. Stroke
  2. Myasthenia gravis
  3. Bulbar palsy
  4. Alcoholics
  5. Epileptics due to post-ictal state
‣
What are they at risk of developing?
  • Lung abscess causing recurrent fever, finger clubbing and foul smelling breath
‣
Atypical

Pneumonia caused by an organism that cannot be cultured or detected using a gram stain.

‣
Name the 5 of them.

"Legion of psittaci MCQ"

  1. Legionella
  2. Chlamydia psittaci
  3. Mycoplasma pneumoniae
  4. Chlamydydophila pneumoniae
  5. Q fever (coxiella burnetii)

Cases:

‣
A patient presents with pneumonia but also has a rash made up of circular lesions across the body, her LFTs also show high bilirubin. Diagnosis?
  • Mycoplasma pneumonia. Rash → Erythema multiforme.
    • ‣
    Why has she got raised bilirubin?
    • Cold AIHA (see haematology) → ↑ RBC breadown → ↑ Bilirubin
    ‣
    What is the diagnostic test for this?
    • Mycoplasma serology
‣
A patient returns from holiday feeling SOB and with pleuritic chest pain. She has deranged LFTs and hyponatraemia. Diagnosis?
  • Legionella
    • ‣
    Why do they have hyponatraemia?
    • Legionella → SIADH
    ‣
    How is this diagnosis confirmed?
    • Urinary legionella antigen
    ‣
    How is it managed?
    • Clarithromycin
‣
A patient has D&V, dry cough, fever & polyarthralgia. He works at a local zoo cleaning bird cages. Pathogen?
  • Chlamydia psittaci
‣
Farmer who has been exposed to the bodily fluids of all of his animals presents with a flu-like illness. Pathogen?
  • Coxiella burnetii
‣
Fungal
‣
A patient with HIV presents with exertional dyspnoea. Likely pathogen?
  • Pneumocystis jiroveci (see Infectious disease)
‣
Management

For all of these, the antibiotic choice depends on local guidelines. However, these are more commonly used.

‣
How is CAP managed? (Depending on CURB-65)
  • 0-1: Home, PO amoxicillin / clarithromycin 5 days
  • 2: Admit, PO/IV amoxicillin & clarithromycin 7 days
    • Penicillin allergy: PO/IV clarithromycin
  • ≥ 3: ITU, IV co-amoxiclav/ceftriaxone/tazocin & clarithromycin
‣
How is HAP managed?
  1. < 5 days from admission: Co-amoxiclav
  2. > 5 days from admission: Tazocin / ciprofloxacin
‣
What complications can occur?
  1. Sepsis
  2. Pleural effusion (exudative)
  3. Lung abscess

Case:

‣
Patient with pneumonia and pleural effusion is on IV antibiotics and yet still has a fever. Pleural fluid aspirate shows pH < 7.2. Diagnosis & management?
  • Empyema → Chest drain & antibiotics
‣
Pulmonary oedema

Fluid collection within the alveoli.

‣
What are the 2 types & the differences between them?
  1. Cardiogenic
    • ↑ hydrostatic pressure in the pulmonary vessels (due to overload) → Transudative fluid in alveoli
      • ‣
      What is the cause of this?
      • Heart failure
  2. Non-cardiogenic
    • Acute lung inflammation → ↑ vascular permeability & ↑ hydrostatic pressure (due to vascular resistance) → Exudative fluid in alveoli
      • ‣
      What are the causes of this?
      1. ARDS: Sepsis, trauma, pancreatitis
      2. High altitude
      3. Opioid/salicylate toxicity
      4. PE
‣
What are you looking for on CXR?
  1. Bats wing airspace shadowing
    2. Frank Gaillard, CC BY-SA 3.0
    Frank Gaillard, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
  2. Signs of heart failure:
    • Alveolar oedema
    • Kerley B lines
    • Cardiomegaly
    • Upper lobe diversion
    • Pleural effusion
      • Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
      Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
‣
🍇 Interstitium

The interstitium is the tissue surrounding the alveoli, the tissue that oxygen moves across when passing from the alveoli to the blood, including alveolar epithelium, pulmonary capillary endothelium and basement membrane.

‣
Diagram: Anatomy
Anatomyclassproj1, CC BY-SA 4.0
Anatomyclassproj1, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Interstitial lung disease (ILD)
‣
Types:
‣
Upper lobe pulmonary fibrosis: Causes?
  1. Coal worker's lung
  2. Hypersensitivity pneumonitis
    3. ‣
    What is this?
    • Type III hypersensitivity to environmental allergen causing tissue inflammation (extrinsic allergic alveolitis).
    ‣
    What do you see on bronchoalveolar lavage?
    • Lymphocytes
    • Mast cells
    ‣
    Name 3 examples.
    1. Bird-fanciers lung → Bird droppings
    2. Farmer's lung → Hay mold spores
    3. Malt workers lung → Mould on barley
  3. Ankylosing spondylitis
  4. Radiation
  5. Tuberculosis
  6. Sarcoidosis
‣
Lower lobe pulmonary fibrosis: Causes?
  1. Idiopathic
    2. ‣
    What are 2 common exam findings?
    • Bibasal fine crackles
    • Finger clubbing
    ‣
    How is it managed?
    1. Pirfenidone: Antifibrotic & inflammatory
    2. Nintedanib
  2. Connective tissue disorders (except ankylosing spondylitis)
    3. ‣
    Examples?
    • SLE
    • RA
    • Systemic sclerosis
  3. Drug-induced: 
    4. ‣
    Examples?
    • Methotrexate
    • Cyclophosphamide
    • Amiodarone
    • Bleomycin
  4. Asbestosis
    5. ‣
    What happens here?
    • Asbestos is fibrinogenic (so induces fibrosis in the tissues) & oncogenic
    • There is a gap between exposure & mesothelioma
‣
How do you investigate this?
  1. CT: "Ground glass appearance" / "Honeycombing"
  2. Lung biopsy
‣
Sarcoidosis
‣
What is this?
  • Build up of inflammatory cells in the tissues forming non-caseating granulomas.
  • It’s triggered by the immune system reacting to foreign substances (viruses, bacteria, chemicals)
‣
Presentation:
‣
What is this associated with?
  • Erythema nodosum (painful)
  • Parotid gland swelling
  • Lymphadenopathy
‣
What electrolyte abnormality does it cause?
  • Hypercalcaemia: Macrophages inside the granulomas causing an increased conversion of vitamin D to its active form.
‣
What are the less common features?
  • Neurological: Bilateral facial nerve palsies
  • Ocular: Anterior uveitis
  • Cardiovascular: Heart block/arrhythmia
  • Gastrointestinal: Hepatomegaly
  • Dermatological: Lupus pernio
‣
Investigations:
‣
What are your initial investigations? (6)
  • Bedside:
    • Spirometry: Restrictive picture
    • ECG: Checking for heart involvement
  • Bloods:
    • FBC: Lymphopenia due to lymphocytes all clustered in tissues
    • U&E: Abnormal if renal stones
    • LFTs: Cholestasis or cirrhosis
    • Calcium: Hypercalcaemia
    • Serum ACE (Raised in 50%)
  • Imaging:
    • CXR
‣
How is it staged based on CXR?
  • Stage 0: No changes
  • Stage 1: Bilateral hilar lymphandenopathy
  • Stage 2: Lymphadenopathy with pulmonary infiltrates (presence of a substance denser than air)
  • Stage 3: Pulmonary infiltrates alone
  • Stage 4: Fibrosis
Jmh649, CC BY-SA 3.0
Jmh649, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
How is it definitively diagnosed?
  • Biopsy showing non-caseating granulomas
‣
Management:
‣
How is it managed based on stage?
  • Stage 1 (hilar lymphandenopathy):
    1. Conservative
  • Stage 2 (pulmonary infiltrates):
    1. Prednisolone (40mg)
    2. Methotrexate / azathioprine
‣
What is the prognosis?
  • 60% of patients with pulmonary sarcoidosis have symptom resolution at 2 years.
  • 20% respond to steroids.
  • 20% show no improvement.
‣
🌽 Pleura

The pleura is a double-layered serous membrane that covers each lung (visceral), and lines the thoracic cage (parietal). The pleural space sits between them contains a small amount of serous fluid.

‣
Diagram: Anatomy
Cancer Research UK, CC BY-SA 4.0
Cancer Research UK, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Pneumothorax

This is an abnormal collection of air in the pleural space between the lung and the chest wall.

‣
Simple pneumothorax
‣
What are the important history points and investigations to determine the management?
  1. Do they have an underlying lung condition?
    • Cystic fibrosis, asthma, COPD.
  2. Are they short of breath?
  3. CXR: Size of pneumothorax
‣
How do you investigate for this?
  • Erect CXR
    • ‣
    How do you assess the size of the pneumothorax?
    • At the level of the hilum, measure horizontally from the chest wall to the lung edge.

Cases:

‣
What is the cause of the following pneumothorax?
‣
Answer
  • Right-sided rib fractures
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Primary: No underlying cause

How are the following patients managed:

‣
Not SOB & CXR shows pneumothorax < 2cm on CXR?
  • Conservative
‣
SOB or pneumothorax > 2cm on CXR?
  1. Aspirate with a 16-18G cannula under local anaesthetic
  2. Insert chest drain
‣
Secondary: Underlying lung condition

How are the following patients managed:

‣
Not SOB AND the pneumothorax is < 1cm on CXR?
  • Conservative
‣
Not SOB and the pneumothorax is 1-2 cm on CXR?
  1. Aspirate
  2. Chest drain
‣
SOB OR the pneumothorax is > 2 cm on CXR?
  • Chest drain
‣
Tension pneumothorax
‣
How does this differ from a simple pneumothorax?
  • Tension pneumothorax occurs when there is a one-way valve that allows air into the pleural space, but does not allow it out. This causes the pressure to build up and is a very severe, life-threatening condition.
‣
What can you see on the following CXRs?
‣
Answer
  • Tracheal deviation.
  • Absence of lung markigs in the left upper zone.
  • Collapse of the left lung secondary to the pressure exerted by the pneumothorax.
Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D.Consent note: Written informed consent was obtained from the individual, including online publication., CC0, via Wikimedia Commons. No changes were made.
Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D.Consent note: Written informed consent was obtained from the individual, including online publication., CC0, via Wikimedia Commons. No changes were made.
‣
How is this acutely managed?
  1. ABCDE
  2. Needle decompression using a 16-gauge cannula (gray) inserted at the second intercostal space, mid-clavicular line.
    • Insert just above the third rib to avoid damage to neurovascular bundle
  3. Chest drain
‣
What definitive management will stop the pressure from building up again?
  • Chest drain, sited within the triangle of safety.
    • Triangle of safety borders: 5th intercostal space, mid axillary line, anterior axillary line.
‣
Pleural effusion

A buildup of fluid within the pleural space.

‣
Where do you insert a chest drain?
  • Triangle of safety: Space between the base of the axilla, lateral edge pectoralis major, 5th intercostal space and the anterior border of latissimus dorsi
    • ‣
    What are the contraindications?
    • INR > 1.3
    • Platelet count < 75
    • Pulmonary bullae
    • Pleural adhesions
‣
How do you investigate pleural effusion & what do you test for?
  • Thoracocentesis (aspirate fluid):
    • Exudate vs transudate
      • Protein < 25 → Transudate. Protein > 35 → Exudate
      • LDH: Pleural fluid LDH is > 2/3 the upper reference limit for serum LDH in exudative
    • Culture
    • Cytology (Malignancy)
    • Glucose (↓ in RA)
    • NT-proBNP (↑ in HF)
‣
How does investigation of a unilateral effusion differ from bilateral?
  • Unilateral always requires thoracocentesis whereas if bilateral is with HF symptoms & signs then it is only done if medical therapy is unsuccessful.
    • HF would be investigated with a transthoracic ECHO
‣
What are the causes of:
‣
Exudate (6)
  1. Infection (most common exudate): Pneumonia, TB, subphrenic abscess
  2. Connective tissue disease: RA, SLE
  3. Neoplasia: Lung cancer, mesothelioma, metastases
  4. Pancreatitis
  5. PE
  6. Dressler's syndrome
‣
Transudate (4)
  1. HF (most common transudate)
  2. Hypoalbuminaemia: Liver disease, nephrotic syndrome, malabsorption
  3. Hypothyroidism
  4. Meigs' syndrome: Ovarian tumour
‣
When would you request pleural fluid cytology?
  • ? malignant pleural effusion
‣
🩸 Pulmonary Circulation

The system transporting de-oxygenated blood from the heart to the lungs to be re-saturated with oxygen before being dispersed into the systemic circulation.

‣
Diagram: Anatomy
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Pulmonary embolism (PE)

Thrombus within the pulmonary arteries.

‣
What is Virchow's triad?

Triad of factors contributing to thrombosis:

  1. Endothelial injury
  2. Blood flow stasis
  3. Hyper-coagulability: Malignancy, thrombophilia, previous VTE, polycythemia
‣
How do we prevent VTE in hospital?
  1. LMWH (depends on local guidelines as to which one)
    2. ‣
    When do we avoid giving this?
    1. Active bleeding
    2. Already anticoagulated, e.g. on warfarin
  2. Compression stockings: TEDS

Presentation:

‣
How symptoms are key to look for in PE?
  1. SOB
  2. Haemoptysis
  3. Pleuritic chest pain
‣
What scoring system is used to assess if somebody is likely to have a VTE?

Investigations & Management:

‣
How would you investigate a potential PE? (8)
  • Bedside:
    • ECG
      • ‣
      What are you looking for?
      • Sinus tachycardia
      • May have S1Q3T3 (but less common)
  • Bloods:
    • ABG
      • ‣
      What would you find?
      • T1RF / Respiratory alkalosis (hyperventilation)
    • FBC, U&E, CRP
    • Clotting
  • Imaging:
    • CXR: Likely normal, important to rule out differentials including cancer and pneumonia.
    • CT pulmonary angiogram (CTPA)
    • VQ scan
    • Lower limb duplex scan - DVT (first-line in pregnancy)
    • Echocardiogram - If massive PE causing right heart strain
‣
How does a CTPA work?
  • CT chest with IV contrast that allows us to identify clots within the pulmonary arteries
    • James Heilman, MD, CC BY-SA 3.0
    James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Whilst waiting for investigations to confirm diagnosis, what should you administer?

NICE guidelines (March 2020) recommend:

  • Apixaban/rivaroxaban
  • Low molecular weight heparin (LMWH) may be used depending on local guidelines
‣
Thrombolysis
‣
Who is considered eligible for thrombolysis?

Massive PE causing:

  • Haemodynamic instability
  • Right heart strain
‣
How does it work & what are the risks?
  • Alteplase breaks down fibrin in the clots, rapidly dissolving them. This puts them at increased risk of bleeding elsewhere, e.g. intracranially.
‣
Long-term management:
‣
What are the options?
  1. Warfarin
    2. ‣
    Target INR?
    • 2-3
  2. DOAC
  3. LMWH
    4. ‣
    When is this used?
    • Active cancer
    • Pregnancy
‣
When would you anticoagulate for 3 months?
  • Provoked VTE, cause is identifiable.
‣
When would you anticoagulate for 6 months then review?
  • Unprovoked VTE due to unknown cause or irreversible cause.
    • Active cancer
    • Thrombophilia
‣
Pulmonary hypertension

Increased pressure within the pulmonary arteries.

‣
Name 5 causes.
  1. Primary pulmonary hypertension / connective tissue disease, e.g. SLE
  2. Heart failure (left): Poor LV function causes back pressure
  3. Chronic lung disease, e.g. COPD.
  4. Pulmonary vascular disease, e.g. PE.
  5. Sarcoidosis / haematological disorders
‣
How would they present?
  1. Progressive SOB, fatigue,
  2. Syncope: Ventricular wall stress can cause vasovagal syncope
  3. Signs of right heart failure
‣
How do you investigate it?
  1. ECG: Right axis deviation, RBBB
  2. CXR: RVH
  3. Echocardiogram: Look at RV function & estimate pulmonary pressures
  4. Right heart catheterisation: Diagnostic
    • ≥ 25 mmHg
‣
How do you manage it?
  • IV prostanoids, powerful vasodilators acting through prostaglandin system (e.g. epoprostenol).
  • Phosphodiesterase-5 inhibitors, prolonging the action of nitrous oxide causing vasodilation (e.g. sildenafil).
‣
CO poisoning
‣
How would they present?
  1. Confusion
  2. N&V
  3. Cherry red skin
‣
How do you investigate it?
  1. ABG: Carboxyhaemoglobin > 20% (diagnostic)
  2. CXR: ARDS
‣
How are they managed?
  1. 100% O₂
  2. Hyperbaric (higher pressure than normal) O₂

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