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🫀 Cardiology
Diseases by anatomy:
This is a fluid-filled sac that surrounds and protects the heart, preventing friction during heart contractions.
Infection:
- Viruses (more common): Coxackie B, CMV, echovirus, HIV, influenza
- Although bacteria can also cause it:
- Streptococcuus → Rheumatic heart disease
- Tuberculosis
- Pneumococcus
- Haemophilus
- Pericarditis occurring 1–4 weeks—although can be longer—after an MI secondary to myocardial or pericardial damage. Occurs in ~ 7% of MI patients.
- ESR
- Antimyocardial antibodies as it is an autoimmune reaction against damaged myocardial tissue.
- Secondary immune processes (e.g. rheumatic fever, post-cardiotomy syndrome)
- Metabolic disorders (e.g. uraemia, myxoedema)
- Radiotherapy
- Cardiac surgery
- Percutaneous cardiac interventions
- Malignancy
- Rheumatology: SLE, RA, sarcoidosis, vasculitis (Behçet's)
- Sharp chest pain relieved by leaning forwards, and worse when lying flat
- Friction rub heard on auscultation of the heart
- Fever
- ECG:
- 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.
- 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).
BMJ Best Practice:
- NSAIDs
- Ibuprofen 600mg PO for (+ PPI)
- PPI for gastroprotection
- Aspirin is preferred for patients developing pericarditis after a myocardial infarction
- Colchicine (if idiopathic or viral pericarditis) to prevent recurrent pericarditis, improve response, and increase remission rates.
- Lifestyle: Restrict strenuous physical activities
- If not resposive: Consider corticosteroids
This results from pericardial scarring.
- Acute pericarditis leading to inflammation & scarring
- 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
Relieve pressure on the heart exerted by the pericardium, and treat underying cause.
- Pericardiectomy.
- NSAIDs, steroids, diuretics and other medications can be useful.
Accumulation of fluid within the pericardial space → ↑ intra-pericardial pressure → Restriction of cardiac filling → ↓ cardiac output.
- Quiet heart sounds
- Hypotension
- Raised JVP
- Kussmaul's sign: JVP rises with inspiration
- Pulsus paradoxus: Drop in systolic BP with inspiration
- 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
- Bloods
- FBC: ? inflammatory cause
- ESR
- Troponin
- CXR: Enlarged cardiac shadow
- Transthoracic echocardiogram, looking for:
- Pericardial effusion (and size of it).
- Chamber collapse and respiratory variation of ventricular filling.
- Anti-inflammatory treatment, gastroprotection and observation.
- Pericardiocentesis
- Send fluid for culture and cytology to identify cause
- Surgical drainage.
- Blood is associated with malignancy or traumatic effusion.
This is the middle muscular layer of the heart, made up of specialized muscle cells called cardiomyocytes.
The following patients have chest pain at rest and the following:
- STEMI
- STEMI
- Unstable angina
- NSTEMI
We classify ACS using symptoms, ECG & cardiac biomarkers.
ST elevation OR new LBBB is present on the ECG.
Acute:
- Morphine
- Oxygen (if SpO₂ < 95%)
- Nitrates (GTN spray)
- Aspirin 300mg STAT
- Primary PCI
- Has to be available within 2 hours of presentation.
- 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.
- Thrombolysis (e.g. with alteplase)
- If PCI not available within 2 hours of presentation, thrombolysis is indicated.
Long-term:
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:
- RCA - Inferior
- Proximal LAD - Septal
- LAD - Anterior
- Distal LAD, LCx, RCA - Apex
- LCx - Lateral
- 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
- ST elevation in II, III, aVF → Inferior MI
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.
BATMAN
- Beta-blockers
- Aspirin 300mg STAT
- Ticagrelor 180mg STAT (OR prasugrel OR clopidogrel 300mg)
- Morphine for pain
- Anticoagulant: Fondaparinux (but need to assess bleeding risk)
- Nitrates (e.g. GTN)
- Slow heart down to reduce demand of muscles → Beta-blockers
- Prevent more platelet aggregation → Dual antiplatelet therapy
- Control pain for patient comfort and to prevent tachycardia → Morphine
- Break down clot → Anticoagulant
- Stop coronary artery spasm → Nitrates
Chest pain is present at rest. There are no ECG changes and there is not a dynamic rise in troponin.
General:
- ST elevation
- Bundle branch blocks
- ST depression
- T-wave inversion (but this is normal in aVR)
- Pathological Q waves (although this is a late sign)
- Ensuring you have serial troponins. Troponins can be released from the myocardium during ischaemia, but also from elsewhere. Dynamic rise is key for diagnosis.
- Baseline (arrival to hospital/onset of pain)
- 6–12 hours after onset of symptoms
- CKD
- Sepsis
- Pulmonary embolism
- FBC
- Anaemia could contribute to a type 2 MI. This is cardiac ischaemia due to:
- increased demand (tachycardia) or,
- reduced supply (anaemia/hypotension).
- LFT
- Baseline for starting statin therapy
- U&E
- Need to know renal function for CT angio with contrast and if we’re going to start an ACEi
- TFT
- Lipid profile
- 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:
- Interventricular septal rupture → VSD (HF makes this more likely)
- Papillary muscle rupture → Mitral regurgitation
- Cardiac tamponade
- Dressler's syndrome: Immune response following MI causing pericarditis.
- NSAIDs (e.g. aspirin / ibuprofen)
- Steroids (e.g. prednisolone)
- Pericardiocentesis
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.
- When using GTN spray.
- When resting.
- CT coronary angiogram (Gold standard)
- Contraindicated if patient has poor renal function due to the contrast needed to carry this out.
- Stress echocardiogram / Myocardial perfusion SPECT / MRI
- Short-term relief:
- GTN spray (nitrates stimulate vasodilation)
- Long-term relief:
- Bisoprolol
- Amlodipine/nifedipine & bisoprolol
- Isosorbide mononitrate
- Ivabradine/nicorandil
- Percutaneous coronary intervention (PCI)
- Balloon dilation of the artery +/- stent insertion.
- 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.
There are two ways to classify this:
HFrEF vs HFpEF:
Systolic failure (EF < 40%) → Impaired contraction.
- MI → Muscle hypoxia → Muscle ischaemia → Cardiac muscle dysfunction
- Idiopathic
- Alcoholic
- Cocaine
- Doxorubicin
- Cyclophosphamide
- Clozapine
- Infiltrative
- Haemochromatosis
- Sarcoidosis
- Amyloidosis
- Infective
- Secondary to myocarditis
- HIV
- Lyme disease
- Chagas disease: Caused by Trypanzoma cruzi parasite prevalent in Central/South America
- Takotsubo
- Stress-induced. Psychological stress → LV ballooning.
Diastolic failure (EF > 50%) → Impaired filling.
- Autosomal dominant
- Genetic abnormality in the proteins making up the heart sarcomere leading to septal hypertrophy
- Impaired outflow → LV hypertrophy → Low preload volume
- 25%
- Ventricular arrhythmia
- Young patient presenting with exertional syncope. Can have chest pain and SOB.
- Unexplained syncope is a poor prognostic factor
- Exercise restriction, β-blockers
- ICD for those at risk of sudden cardiac death
- Surgical: Myomectomy or septal ablation
Deposits within the heart cause it to become stiff → Less heart muscle compliance → Poor filling.
- Amyloidosis: Amyloid deposits within the heart.
- ECHO shows "sparkling appearance"
- Renal dysfunction due to amyloid deposition
- Haemochromatosis
- Sarcoidosis
- Post-radiation fibrosis
Acute vs Chronic:
Acute decompensation of the LV → Back-pressure into the lungs → Pulmonary oedema (transudative mechanism) → Impaired gas exchange.
- Rapid onset SOB
- Worsened SOB lying back
- T1RF
- ↓ SpO₂
- Bibasal crackles (pleural effusion)
- Ensure they’re sat up.
- Diuretics to clear the fluid from their lungs.
- Oxygen to make sure they maintain saturations.
- 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.
- 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?’
- Ramipril/valsartan & bisoprolol
- Spironolactone
- If causes GI upset/gynaecomastia → Switch to eplerenone
- Hydralazine/isosorbide dinitrate
- Digoxin/ivabradine
- Surgical: Cardiac resynchronisation therapy or transplant
- LBBB
- EF < 30%
- NYHA III
- Furosemide 40mg OD
- Lifestyle advice.
- Manage underlying cause, if possible.
- Low-dose furosemide to manage oedema.
- Ramipril if hypertensive.
This is right-sided HF secondary to respiratory disease.
- COPD
- ILD
- PE
- CF
- 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)
- Symptoms: SOB, syncope, chest pain.
- Signs: Raised JVP, peripheral oedema, murmurs, hepatomegaly, ascites
- LV failure causing backpressure and increased afterload
- Pulmonary stenosis
- Pulmonary hypertension (as discussed in cor pulmonale)
- Treat the underlying cause of hypoxia & pulmonary hypertension (see Respiratory)
- Manage symptoms, e.g. oedema
General:
NYHA classification:
- No limitation to daily life
- Slight limitation on physical activity
- Marked physical activity limitation, comfortable at rest
- Symptoms at rest
ABCDE
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Upper lobe Diverson
- Pleural Effusions
- BNP (if > 2000 → urgent referral to cardiology)
- Hypertrophic cardiomyopathy
- Ischaemic cardiomyopathy (CAD)
- Dilated cardiomyopathy
- Takotsubo cardiomyopathy
Inflammation of the myocardium → Infiltration of lymphocytic cells → Myocardial necrosis & degeneration.
- Presents with shortness of breath and mild palpitations, had an upper respiratory infection (viral picture) a couple of months ago.
- Coxackie viruses (A/B)
- Lyme disease
- SLE
- Drug-associated
- Marked troponin elevation
- No relief on sitting forward or pericardial rub on examination
- Cardiac biopsy (only perform if this information would alter the treatment plan as it’s risky).
Noncancerous tumor that arises from connective tissue, commonly located in the atria, affecting blood flow and electrical conduction.
- Fever
- Weight loss
- Clubbing
- Audible tumour 'plop' - Variable with position
- ECG: May reveal AF
- Echocardiogram: Help to visualise lesion and blood flow
- CXR: Cardiomegaly, pulmonary oedema
- Open heart surgery to remove the tumour.
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.
- Ejection systolic (crescendo-decrescendo)
- Mechanical stress over time
- Risk factor that makes this worse is a biscuspid aortic valve
- Rheumatic heart disease
- Syncope (insufficient oxygen supply to brain)
- Exertional dyspnoea (back pressure into lungs)
- Angina (insufficient oxygen supply to heart)
- Hypertrophic cardiomyopathy
- Louder standing, quieter supine due to LV outflow obstruction.
- Heard louder on LLSE due to septum causing obstruction not the valve
- Aortic flow murmur
- Hyperdynamic circulation due to infection, anaemia, thyrotoxicosis or pregnancy
Widening of the aortic valve → Backflow through the valve during diastole → Increased preload within the LV → Dilation of LV.
- Early diastolic, louder leaning forward and on LLSE
- Degenerative
- Rheumatic fever
- Connective tissue disease (e.g. Marfan’s)
- Endocarditis
- Aortic root dilatation
- Mid-diastolic murmur with opening ‘snap’.
- Malar flush
- AF
- P-mitrale on ECG (Bifid P-wave) due to atrial hypertrophy
- Rheumatic fever (most common): Inflammation → Leaflet fusion
- Age-related calcification
- Systemic disease: RA/SLE
- Congenital
- Pan-systolic murmur / Late-systolic murmur
- 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
- Pulmonary hypertension → RVF
- Left atrial dilatation → Pacemaker cell irritation → AF
These are less commonly tested, but covered in paediatric cardiology, where they are more relevant.
- Pulmonary stenosis
- Pulmonary regurgitation
- Tricuspid stenosis
- Tricuspid regurgitation
Investigations & Management:
- ECG: Looking for ventricular hypertrophy,
- Echocardiogram: Flow across valves (regurgitation, pressure gradients), calcification of the valves, atria/ventricular size.
- CXR: Cardiomegaly
- Often you watch and ensure that hypertension is managed well.
Surgical:
- Valve replacement
- Transcatheter aortic/mitral valve replacement via femoral artery catheter
- Bioprosthetic valve replacement
- Balloon valvuloplasty for stenotic valves (inflate a balloon in the valve to open it)
Infection of the endocardium +/- heart valves.
- S. aureus (IVDU)
- S. viridans (Dental hygiene)
- S. epidermis (Prosthetic valve surgery/infected catheter)
- S. bovis (from GI tract)
- Roth spots (eyes)
- Osler nodes (painful finger lesions)
- Janeway lesions (painless palm lesions)
- Anaemia
- Splinter haemorrhages
Duke's criteria:
- Pathological criteria positive, OR
- 2 major criteria, OR
- 1 major & 3 minor criteria, OR
- 5 minor criteria
Major criteria:
- Two positive blood cultures
- Persistent bacteraemia from two blood cultures taken > 12 hours apart
- Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
- Positive echocardiogram
- New valvular regurgitation
Minor criteria:
- Predisposing heart condition or intravenous drug use
- Microbiological evidence does not meet major criteria
- Fever > 38ºC
- Vascular phenomena: Major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
- Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
Investigations & Management:
- 3 sets of blood cultures from 3 different sites at 3 different times
- ECG
- CXR
- Transoesophageal echocardiogram → Valvular pathology
- Medical: IV antibiotics
- Central line infection: IV vancomycin
- Surgical: Valve repair
- Severe sepsis despite antibiotics
- Heart failure
- Haemodynamic instability
- Rheumatic fever
- Group A haemolytic Streptococci → Autoimmune inflammatory disease
- Streptococci proteins cross-react with myocardial, valvular, joint and brain proteins
- 2-4 weeks following a throat infection, they develop SOB, fever & chest pain. Pericardial rub and joint pain.
- Anti-Streptolysin O (ASO) titre
- STAT IV benzylpenicillin - Covers this group A beta-haemolytic streptococcal infection
- PO Pen V for 10 days
- Libman-Sacks endocarditis
- SLE/RA antigen-antibody complexes settle in endocardium → Endocardial damage → Valve regurgitation
- Non-bacterial thrombotic endocarditis
- Damage to valve exposes collagen → Platelets & fibrin adhere to form clots → Mitral valve regurgitation.
What are the causes of:
- HTN
- Pulmonary HTN
- Hyperdynamic states
- ASD
- Aortic stenosis
- ASD
- Deep inspiration (increased VR causes tricuspid to close after mitral)
- RBBB
- Pulmonary stenosis
- Severe MR
Name the diagnosis based on the following ECGs:
- Hypertrophic cardiomyopathy
- Wolff-Parkinson White
- Hyperkalaemia
Shockable:
- Ventricular tachycardia
- Ventricular fibrillation
Non-shockable:
- Pulseless electrical activity
- Asystole
Arrhythmias:
This indicates that this is a Supraventricular Tachycardia (SVT).
Types:
- Sinus tachycardia: Usually compensating for a decreased stroke volume, or from sympathetic stimulation caused by pain, fear or catecholamines.
- AVNRT: Slow & fast pathway through AVN causes circuit to form
- AVRT (Wolff-Parkinson-White syndrome): Electricity travels down the accessory pathway and up AVN: 𝝳 wave, broad QRS
- Atrial flutter: Characterised by flutter waves on ECG, which are a saw-tooth pattern of atrial activation.
- There is a re-entrant circuit within the atria causing repetitive contractions.
- 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.
- AVN blocker: Bisoprolol/verapamil
- Electrical cardioversion
- Medical cardioversion: IV ibutilide
Management:
- Vagal manoeuvres: Carotid sinus massage
- IV adenosine 6mg
- CI in asthma: Give verapamil instead
- Paroxysmal: Lasts < 7 days
- Persistent: Lasts > 7 days, electrical cardioversion works to resolve
- Permanent: Lasts > 7 days, electrical cardioversion doesn't resolve symptoms
Mrs. SMITH
- Sepsis
- Mitral stenosis
- Ischaemic HD
- Thyrotoxicosis
- HTN
- Ventricular ectopics - Disappear when exercising
- Rate control (Mostly first-line)
- Bisoprolol
- Asthmatics: Verapamil
- Digoxin
- Asthmatics with heart failure
- Rhythm control (Cardioversion)
- There is a reversible cause (e.g. sepsis)
- New onset (< 48 hours)
- Causing HF
- Remain symptomatic despite rate control
- Immediate: AF < 48 hours OR severe haemodynamic instability
- Transoesophageal ECHO looking for left atrial thrombus.
- Present: Treat same as delayed cardioversion
- Absent: Calculate CHADSVASc (≥ 2 → LMWH for 4 weeks. 0-1 → Immediate cardioversion)
- Delayed: AF > 48 hours & stable
- Rate control while waiting
- Anticoagulate with warfarin (& LMWH cover until INR is in range) for 3-4 weeks before cardioverting due to clot risk
- Anticoagulate for 4 weeks after cardioverting
- LMWH
- Electrical - DC cardioversion under GA
- Chemical - Flecainide / Amiodarone
- Paroxysmal AF with no heart disease or HTN
- PO flecainide is used
- Anticoagulation
- Congestive cardiac failure
- HTN
- Age > 75 years = 2
- Diabetes
- Stroke/TIA = 2
- Vascular disease
- Age 65-74
- Sc - Female
- HTN
- Abnormal liver/renal function (1 each)
- Stroke
- Bleeding tendency - Previous major bleed
- Labile INR
- Elderly > 65 years
- Drugs/alcohol (1 each)
- Warfarin: Target INR 2-3
- Alternative: DOAC
- No, stop antiplatelet
CHA2DS2-VASc: Men ≥ 1 / Women ≥ 2 → Anticoagulate
HASBLED
General:
- 12-lead ECG
- Paroxysmal:
- Holter monitor (24hr ECG)
- Continuous loop recorder (Used in patients who don't have symptoms daily)
- Bloods: FBC (anaemia), U&E (electrolyte imbalance), TFT (hyperthyroidism)
- Echocardiogram: Structural cause
- Synchronised DC cardioversion under GA
- Unstable: Shock, syncope, myocardial ischaemia, or heart failure
- Monomorphic VT
- Polymorphic VT
- Ventricular fibrillation
Causes:
- 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
- Ischaemic HD
- HTN
- Cardiomyopathy
- Aortic valve disease
- Myocarditis
WiLLiam
- Normal in tall, thin young people (narrow QRS)
- Idiopathic
- RV strain (PE/chronic respiratory disease/ASD)
- Ischaemic HD
- Myocarditis
MaRRoW:
- RSR in V1:
- R1 - Septal depolarisation
- S - LV depolarisation
- R - RV depolarisation
- Normal V6
- Physiology: Ventricular ectopics
- Causes: Chronic HD, structural HD, hypokalaemia, hypocalcaemia
- Monomorphic VT
- Polymophic VT (PVT)
- Torsades de pointes is a type of PVT occurring due to prolonged QT. Often self-terminating but can deteriorate into VF.
- DC cardioversion
- Amiodarone
- Magnesium sulphate
- Torsades = Polymorphic VT
- ECG shows polymorphic nature of the tachycardia and the long QT interval.
- Chest compressions 30:2
- Unsynchronised shock
- Adrenaline & amiodarone
- Sustained VT causing syncope
- Sustained VT with EF < 35%
- Previous cardiac arrest due to VT or VF
Irregular heart rhythm where the ventricles contact rapidly in an uncoordinated manner, meaning that there is inadequate blood supply to the body.
- Chest compression
- Unsynchronised DC cardioversion
- Adrenaline & amiodarone
- Physical fitness
- Vasovagal
- Sick sinus syndrome
- Drugs - β-blockers, digoxin, amiodarone
- Hypothyroidism
- ↑ ICP
- Hypothermia
4 types:
Prolonged, unchanging PR interval.
- Professional athletes with high vagal tone
- Drugs: β-blockers/CCB
- Inferior MI
- 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
- No.
- Low risk of complete heart block
Increasing PR, until dropped QRS.
Fixed 2:1/3:1 block.
- Ischaemic HD
- Rheumatology - SLE, RA, systemic sclerosis
- Drugs - β-blockers, CCB, amiodarone
- Surgery - Mitral valve repair, septal ablation
- Acute: Atropine 500mcg IV
- Permanent pacemaker due to risk of complete heart block
Atria & ventricles are not contracting in a coordinated manner.
- Atropine
- Pacemaker
- QT interval > 460ms in women & > 440ms in men.
- Medications: Antiepileptics
- Family history: Long-QT syndrome
- Low potassium, calcium or magnesium
- Torsades des pointes
- Ventricular fibrillation
- Intermittent periods of SAN dysfunction → Bradycardia → Dizzy spells, syncope, chest pain
- Intrinsic heart pathology likely caused by sclerosis of the conduction system
- Sinus bradycardia
- Sinus arrest
- ABCDE - ECG, electrolytes, identify reversible causes
- Atropine 500mcg - Haemodynamic instability, Mobitz II, complete heart block, recent asystole, ventricular pause > 3s
- Options: Isoprenaline, adrenaline, aminophylline, dopamine, glucagon
- Transcutaneous pacing while awaiting expert advice
Key Issues:
- 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
- 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
- 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.
- Immediate: ECG, CXR, transthoracic echocardiogram, and bloods
- Definitive: CT TAP
- Stanford type B dissection: Descending aorta
- Trans-oesophageal echocardiogram / MRI
- Stanford Type A - Urgent surgery (Aortic root replacement / sutured aortic repair)
- Stanford Type B - Medically managed
- Rupture (80% mortality)
- Control BP to prevent this with IV β-blocker
- End-organ damage due to inadequate blood supply
- Stroke, limb ischaemia, bowel ischaemia, renal failure
- Cardiac failure
- Cardiac tamponade
A permanent pathological aortic dilation with a diameter >1.5X (Usually ≥ 3cm) the expected anteroposterior (AP) diameter of that segment.
- New back pain/abdominal pain
- Haemodynamically unstable
- Loss of consciousness
- Bloods: Cross-match, FBC, U&E, clotting
- Imaging:
- Bedside aortic ultrasound then,
- CT angiography (CTA)
- Urgent surgical repair: Endovascular repair (EVAR) or open surgical repair
- AKI
- Limb ischaemia
- Graft infection
They’re often asymptomatic, therefore it’s identified:
- incidentally, or
- through aortic screening
- 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.
Narrowing in the aorta, most commonly at the site of insertion of the ductus arteriosus.
- A blood pressure differential, where the upper limb BP > lower limb BP.
- Bedside:
- ECG → RV / LV hypertrophy may be present
- Bloods: FBC, U&E, clotting, G&S
- Imaging:
- CXR
- Notching of the inferior border of the ribs: Pressure through the collateral vessels causes rib erosion.
- Cardiomegaly
- Echocardiogram → Narrowing in the thoracic aorta (with pressure gradient across narrowing)
- CT angiography/MR angiography → 3D modelling of anatomy
- Surgical repair
- Percutaneous balloon dilation / stenting
- Persistent hypertension
- Surgical site aneurysm formation
A combination of:
- Atheroma: Deposition of fat, cholesterol and blood cells in the walls of arteries.
- Sclerosis: Infiltration of inflammatory cells into the artery wall and the lipid deposition causes progressive hardening of the walls of arteries.
- 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.
- QRISK-3. It calculates a person’s risk of having a heart attack or stroke over the next 10 years.
- If risk > 10%, consider treating with a statin.
- Atorvastatin 20mg at night (as per current NICE guidelines).
- Lifestyle advice is also a key part of management in these cases.
- 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)
- LFTs at baseline, 3 months & 12 months to check for liver inflammation.
- Needs to be > 3X the upper limit of normal to stop.
BP ≥ 140/90 mmHg, with no secondary cause identified.
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)
How would you manage the following patient:
- ACEi / ARB
- CCB
- ACEi / ARB
We need to check her K⁺:
- K⁺ < 4.5 → Spironolactone
- K⁺ ≥ 4.5 → ɑ-blocker / β-blocker
- Dry cough → Swap to valsartan
- K⁺ > 5.5 → Stop. Review BP and U&E in a week.
- < 80 years: Clinic BP < 140/90mmHg (ABPM < 135/85mmHg)
- ≥ 80 years: Clinic BP < 150/90mmHg (ABPM < 145/85mmHg)
Elevated blood pressure (BP) secondary to an identifiable cause.
- 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,
How are the following situations managed:
Encephalopathy & papilloedema:
- IV labetalol, with target BP of 160/100
- IV labetalol
- Target: 100-120 systolic
Vasodilator:
- IV GTN (10 micrograms/minute), OR
- IV isosorbide dinitrate
- IV magnesium sulphate
- IV phentolamine (ɑ-blockers) then β-blockade
💩 Gastroenterology
What are the features of each?
- Fatigue
- Anorexia
- Nausea
- Abdominal pain
- Spider naevi
- Palmar erythema
- Gynaecomastia
- Pre-hepatic
- Haemolysis e.g. G6PD deficiency
- Neonatal jaundice: Rhesus haemolytic disease, ABO haemolytic disease, hereditary spherocytosis
- Intra-hepatic
- Damage: ALD, NAFLD, hepatitis, etc.
- Gilbert's syndrome
- Crigler-Najjar syndrome
- Post-hepatic
- Gallstones: Mirizzi syndrome
- PBC/PSC
- Cholangitis
- Pancreatic cancer
- Pre-hepatic: Normal urine and stools
- Hepatic: Dark urine, normal/pale stools
- Post-hepatic: Dark urine, pale stools
- Conjugated bilirubin is soluble, unconjugated is not.
- Pre/intrahepatic → ↑ unconjugated
- Post-hepatic → ↑ conjugated
- Soluble conjugated bilirubin dissolves in the urine (urobilinogen) as it cannot be excreted through the GI tract, giving urine a dark colour.
- Lack of bilirubin in the stools (due to biliary tract obstruction) make them pale.
- 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)
- Low sodium diet
- Diuretic eg Spironolactone (Spiro better than Furosemide in ascites)
- Prophylactic antibiotics eg Ciprofloxacin
- Therapeutic paracentesis (ascitic drainage)
- Transjugular intrahepatic portosystemic shunt (TIPSS)
- Indicated in refractory ascites & secondary prophylaxis of variceal haemorrhage
- Spontaneous bacterial peritonitis
- E. coli
- Klebsiella
- Temperature
- Distended tender abdomen
- Can be asymptomatic, always consider in patients who deteriorate suddenly with no obvious cause
- Prophylactic PO ciprofloxacin
- Take ascitic culture
- IV cefotaxime
- Either asymptomatic and found incidentally, or as an acute upper GI bleed.
What are each of them used for?
- Pre-endoscopy score
- Decides timing of intervention, if the score is high the patient must go straight for treatment rather than endoscopy first
- Post-endoscopy score
- Stratifies based on mortality risk: Risk of rebleed after endoscopy
- ABCDE: Fluid / blood, FFP, Plts
- Terlipressin: Splanchnic vasoconstriction → Lower portal venous pressure going through varices and decreases bleeding risk.
- Broad spectrum prophylactic antibiotics eg 7 days Ceftriaxone (dec infection risk and risk of rebleed)
- Urgent endoscopy within 24h for band ligation
Hong kong protocol:
- Omeprazole STAT then continuous infusion to reduce the rebleeding risk
- Propranolol: Reduces azygos blood flow and variceal pressure
- Ammonia build-up causing cerebral oedema
- Early: Confusion (suspect in anyone with liver failure and altered consciousness)
- Late: Fetor hepaticus, coma
- 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
First-line:
- PO lactulose: Reduces nitrogenous waste
- ↑ faecal flow through the GI tract → ↓ time for proteins to be broken down → ↓ amino acid absorption → ↓ ammonia
- IV mannitol: Reduces cerebral oedema
Second line:
- Rifaximin: Specialist treatment to decrease activity of ammonia-producing gut flora
- Morphine
- Slowed gut motility → ↑ amino acid absorption → ↑ ammonia
- ALT > 10-fold rise
- AST
- Unconjugated bilirubin
- GGT
- 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
- Albumin
- Bilirubin
- Clotting
- ALP can be raised due to both liver and bone problems, and high in pregnancy.
- Liver: Abnormal GGT & other LFTs
- Bone: Abnormal calcium +/- vitamin D
- Non-specific: Fatigue
- Liver-specific: Decompensated liver features discussed above
- INR > 1.5
- Hepatitis
- Alcohol
- Drugs
- Autoimmune hepatitis
- Budd-chiari syndrome
- AUDIT questionnaire
- SADQ questionnaire
- Drink up to 14 units per week, spread this evenly over 3 days or more
- Mild dependence: < 15 U/day / ≤ 20 on AUDIT
- CBT first-line
- Moderate dependence: > 15 U/day OR > 20 on AUDIT
- Assisted withdrawal with chlordiazepoxide
- Severe: > 30 U/day OR > 30 on SADQ OR high risk of seizures/delirium tremens
- Inpatient withdrawal
- IV pabrinex OD
- Chlordiazepoxide reducing regime
- GGT: Although not specific and so must be accompanied by other LFTs
- Obesity
- Type 2 diabetes
- High triglycerides
- Hypertension
- Smoking
- Bloods: LFT and lipids
- Liver USS: Fatty changes
- Enhanced liver fibrosis (ELF) blood test
- Combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase → Algorithm creates a score
- Biopsy (rarely done)
- Non-alcoholic steatohepatitis (NASH): Fat has caused chronic inflammation and cell death
- 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)
- A&E: Faeco-oral
- B&C: Blood & baby
- Hepatitis A & E
- Hepatitis A & B
- Hepatitis D
- Hepatitis B is a DNA virus
- The rest are RNA viruses
- Chronic HepB infection
- HepB immunoglobulin
- Accelerated HepB vaccine course
- Young females
- Anti-smooth muscle antibodies
- ANA (anti-nuclear antibodies)
- Immunosuppression: Steroids / azathioprine
- Liver transplant
- CHILD-PUGH score
- Encephalopathy
- Ascites
- Bilirubin
- Albumin
- Prothrombin time
- 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
- Treat underlying cause
- Manage complications (e.g. ascites)
- Definitive management: Liver transplant
- Increased mortality
- Ascites & SBP
- Liver failure
- Hepatocellular carcinoma
- Renal failure/Hepatorenal syndrome
- All patients with cirrhosis
- HepB / HepC: Particularly high risk
- Alpha-feto protein (AFP)
How are the following managed:
- Activated charcoal
- Start N-acetylcysteine
- Wait until 4 hrs to take a level, treat if high
- Take immediate level, treat if high
- Methotrexate
- Amiodarone
- Isoniazid
- Obstruction of venous outflow from the liver into the inferior vena cava (IVC)
- Hepatomegaly
- Abdominal pain
- Ascites
- Hepatic: Hepatitis, cirrhosis,
- Neurological: Ataxia, tremor, dystonia
- Psychiatric: Change in personality
- Other: Kayser-Fleischer rings, Coombs negative haemolytic anaemia
- Serum caeruloplasmin
- 24 hour urinary copper (screening test)
- Genetic analysis for ATP7B gene
- Copper chelators: Penicillamine, trientine
- Autosomal recessive: Mutations in the HFE gene
- Pseudogout
- Dilated cardiomyopathy
- Cirrhosis
- Diabetes - Pancreatic deposition of Fe
- Grey skin discolouration
- Hypogonadism
- FBC: ↑ Hb
- LFT: ↑ transaminases
- BM: High
- ↑ transferrin saturation (M > 55%, F > 50%)
- ↓ TIBC
- ↑ Ferritin & Fe
- Perl's stain
- Lifelong venesection & aspirin
- Desferrioxamine (Fe-chelating agent)
- Liver: Cirrhosis (clubbing, palmar erythema, spider naevi)
- Respiratory: Emphysema (inhalers)
- Exocrine: Production of enzymes that are released into the small intestine to help digest food.
- Amylase → breaks down carbohydrates
- Lipase → breaks down fats
- Proteases → break down proteins
- Endocrine: Production of hormones, including insulin and glucagon.
- Alpha cells → Glucagon → Signals the liver to convert stored glycogen into glucose.
- Beta cells → Insulin → Signals cells to take up glucose from the bloodstream and store it for energy.
Disease:
I GET SMASHED
- Idiopathic
- Gallstones
- Ethanol (alcohol)
- Trauma
- Steroids
- Metabolic
- Autoimmune
- Scorpion sting
- Hypercalcaemia
- ERCP
- Drugs: Azathioprine, sulfasalazine, valproate, diuretics (loop/thiazide), steroids, tetracyclines
- Nausea & vomiting
- Severe epigastric pain radiating to back
- Low grade fever
- Tachycardic
- Hypotensive
- Amylase
- Lipase (more sensitive, more expensive): Remains high for 12 days
- 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
- Recurrent abdominal pain
- Weight loss (malabsorption, exocrine insufficiency)
- Jaundice
- Can suffer episodes of acute-on chronic pancreatitis
- It is often normal
- Alcohol
- Cystic fibrosis
- Hereditary
- Smoking
- FH of pancreatic cancer
- Lynch syndrome or BRCA 1/2
- Courvoisier's sign: Painless palpable GB & jaundice
- Trousseau's sign: Migratory thrombophlebitis
- Recurrent episodes of blood clots causing vessel inflammation in different locations across the body
- CA 19-9
- Endoscopic USS w/ biopsy
- CT TAP
- Bile ducts:
- Intrahepatic bile ducts
- Left and right hepatic ducts
- Common hepatic duct
- Cystic duct
- Common bile duct
- Sphincter of Oddi
- Major duodenal papilla
- Gallbladder
- Right lobe of liver
- Left lobe of liver
- Spleen
- Esophagus
- Stomach
- Pancreas
- Accessory pancreatic duct
- Pancreatic duct
- Small intestine
- Duodenum
- Jejunum
- Intrahepatic ducts: Bile ducts within the liver
- Fatigue, jaundice, pruritus, RUQ pain
- Xanthoma, xanthelasma
- Signs of cirrhosis and liver failure, e.g. ascites, splenomegaly
- Inflammation of bile ducts → Bile outflow obstruction → Bile acid, bilirubin & cholesterol buildup → Pruritus, jaundice and xathelasma
- Anti-mitochondrial IgM antibodies
- ESR
- Other autoimmune diseases:
- Thyroid
- Coeliac
- Rheumatoid conditions, e.g. Systemic sclerosis, RA
- Sjogren's syndrome
- Granulomas
- Ursodeoxycholic acid: Reduces absorption of cholesterol
- Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
- Intrahepatic and extrahepatic ducts
- Ulcerative colitis
- Fatigue, jaundice, pruritus, RUQ pain, hepatomegaly, cirrhosis
- MRCP
- There are no antibodies helpful in diagnosing PSC, none are sensitive or specific enough
- p-ANCA is present the majority of the time
- Ursodeoxycholic acid: Reduces absorption of cholesterol
- Colestyramine: Binds to bile acid to prevent absorption and help with pruritus
- Cancer of the bile duct
- Intrahepatic: Affects bile ducts inside the liver.
- 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.
- Extrahepatic (Distal): Occurs below the area where the common hepatic duct and cystic duct join to form the common bile duct.
- Primary sclerosing cholangitis
- CA 19-9 (carbohydrate antigen)
- Curative surgery combined with radiotherapy and chemotherapy (only in early cases).
- Biliary stenting
- Palliative chemotherapy
- Palliative radiotherapy
- Inflammation or infection of the common bile duct
- Charcot’s triad:
- Fever
- RUQ pain
- Jaundice
- Reynolds pentad:
- Fever
- Hypotension
- Confusion
- Escherichia coli (27%)
- Klebsiella (16%)
- Enterococci (15%)
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
- USS: Bile duct dilation
- MRCP for more detailed imaging
- ERCP (diagnostic & therapeutic): Identify and remove the cause of the blocked biliary tree.
- IV fluids
- IV antibiotics (as per local guideline), e.g. co-amoxiclav & metronidazole
- Definitive:
- ERCP - Endoscopic retrograde cholangiopancreatography
- PTC - Percutaneous transhepatic cholangiography
- Inflammation of the gallbladder usually occuring when a gallstone completely obstructs the neck of the gallbladder or cystic duct.
- Sudden-onset, severe RUQ pain lasting several hours.
- Tenderness in the right upper quadrant (with or without guarding).
- Biliary colic
- Trauma from the gallstone causes prostalandin release which stimulates an inflammatory response.
- Gallbladder then becomes more distended and inflamed causing compromise of blood flow and lymphatic drainage, leading to mucosal ischemia.
- Bacterial infection of the bile may then occur.
Exact cause is poorly understood, but often in critically ill patients, associated with bile stasis or thickening.
- Bile stasis: Trauma, severe systemic illness, and prolonged total parenteral nutrition use
- Bile thickening: Fever and dehydration
- Abdominal USS to identify presence of gallstones.
- Support: IV fluids, antibiotics & analgesia
- Definitive: Laparoscopic cholecystectomy
- Necrosis of the gallbladder wall (gangrenous cholecystitis).
- Gallbladder perforation.
- Biliary peritonitis.
- Pericholecystic abscess.
- Fistula between the gallbladder and duodenum.
- Jaundice due to inflammation of adjoining biliary ducts.
- Mirizzi syndrome
- Sepsis.
- Barium swallow
- Stop 2 weeks before endoscopy as it could mask serious pathology, e.g. gastric cancer
- NSAIDs/steroids
- Bisphosphonates
- CCBs
- Nitrates
- Macrolides
- Stomach: Worse after meals
- Duodenum: Improves after meals
- Gastrinoma of the stomach → Excessive acid secretion → Ulcers
- 4-8 weeks full dose PPI
- Repeat endoscopy 6-8 weeks after being discharged
- NBM, IV fluids
- Laparotomy
- Endoscopic clipping or thermal coagulation
- Faecal antigen
- Urea breath test
Triple therapy (BD for 7 days):
- Omeprazole
- Amoxicillin
- Clarithromycin
- Triple therapy: Metronidazole replaces clarithromycin
- Refer to gastroenterology if still + after this
Rockall score:
- Age
- SBP/HR
- Comorbidities
- Post-endoscopy diagnosis
- Signs at endoscopy
- Oesophageal/gastric varices
- Mallory-Weiss tear
- Peptic ulcer
- Malignancy
- ABCDE - IV fluids, transfusion (+/- Plts +/- FFP)
- NBM
- IV PPI
- Variceal: OGD and banding
- Non-variceal: Clips with or without adrenaline
Differentials:
- Progressive difficulty through the disease:
- Hard solids → Soft solids → Liquids
- Difficulty swallowing both solids & liquids
- Triad: Dysphagia, regurgitation and halitosis
- Requires surgical repair
Muscle spasm thought to be secondary to abnormal functioning of nerves. Consider as a differential for MI and GORD.
- Barium swallow
- Stop 2 weeks before endoscopy as it could mask serious pathology, e.g. gastric cancer
- NSAIDs/steroids
- Bisphosphonates
- CCBs
- Nitrates
- Macrolides
- Degeneration of the myenteric plexus around the LOS causing it to always contract
- Difficulty swallowing both solids & liquids
- Manometry: Tube into oesophagus that measures pressures
- High pressure in the LOS, incomplete relaxation, absence of peristalsis
- Barium swallow: 'Bird's beak appearance'
- Medical: Nifedipine & omeprazole
- Definitive:
- Unfit for surgery: Balloon dilation of the LOS
- Fit for surgery: Heller's cardiomyotomy
- Dysphagia
- WL
- Retrosternal chest pain
- Low grade: High dose omeprazole & 6 monthly endoscopy
- High grade: Endoscopic ablation
- Squamous cell
- Adenocarcinoma (if Barrett's) - Lower 1/3
- Stomach: Worse after meals
- Duodenum: Improves after meals
- Gastrinoma of the stomach → Excessive acid secretion → Ulcers
- 4-8 weeks full dose PPI
- Repeat endoscopy 6-8 weeks after being discharged
- NBM, IV fluids
- Laparotomy
- Endoscopic clipping or thermal coagulation
- Faecal antigen
- Urea breath test
Triple therapy (BD for 7 days):
- Omeprazole
- Amoxicillin
- Clarithromycin
- Triple therapy: Metronidazole replaces clarithromycin
- Refer to gastroenterology if still + after this
- Glandular: Adenocarcinoma
- H. pylori infection
- Smoking
- Obesity
- Signet ring cells
- Managed the same as gastric ulcers
- Gluten is broken down to gliadin in the small intestine → Inflammatory response → Cell destruction (lost surface area) → Malabsorption
- Common: T1DM & thyroid - All of these patients are tested for coeliac disease
- Other autoimmune: Autoimmune hepatitis, PBC, PSC
- Dermatitis herpetiformis (pruritic vesicles on the extensor surfaces)
- Malabsorption of B12/folate
- IgA anti-TTG antibodies
- Total IgA because if there's an IgA deficiency then the test will be negative but the disease may still be present
- IgG anti-TTG/anti-EMA
- Anti-EMA antibodies
- Villous atrophy
- Crypt hypertrophy
- Lifelong gluten free diet
- Dapsone antibiotic for dermatitis herpetiformis
- History of atherosclerosis / AF / HTN
- Sudden onset abdominal pain following food - Intermittent / colicky
- CT abdomen (angiogram)
- Lactate: ↑
Common:
- Abdominal pain, blood diarrhoea, mouth ulcers, other autoimmune conditions, WL, anaemia
- Systemically unwell during flares
- No/less blood or mucus in stool
- Entire bowel is affected
- Skip lesions
- Terminal ileum most affected & Transmural thickness inflammation
- Smoking makes it worse
- Continuous inflammation
- Limited to colon & rectum
- Only superficial mucosa affected
- Smoking protective
- Excrete blood & mucus
- Use aminosalicylates
- Primary sclerosing cholangitis
- Finger clubbing
- Erythema nodosum
- Pyoderma gangrenosum
- Episcleritis/iritis
- PSC in UC
- Rectum
- Skin: Erythema nodosum, pyoderma gangrenosum
- Primary sclerosin cholangitis (independent of flares)
- Eyes: Episcleritis, scleritis, anterior uveitis
- Osteoporosis (malabsorption)
- Peripheral neuropathy (B12)
Disease is limited to the mucosa, showing:
- Crypt abscesses
- Goblet cell depletion
- Mucin depletion
- Mucosal ulcers
- 'Lead pipe sign' - Loss of haustral markings on the bowel
- Toxic megacolon: AXR to investigate
- ACR (colon dilation), Temp > 38.6°C, HR > 120bpm, anaemia, ↑ neutrophils
- Age of onset is bi-modal:
- 15-40 years: Majority
- 60-80 years: Small second peak
- Cobblestone appearance
- Transmural inflammation with skip lesions
- Non-caseating granulomas
- Perianal skin tags
- Bedside: Faecal calprotectin
- Bloods: FBC - Macrocytic anaemia, LFT - PSC.
- Radiology: USS/CT/MRI - Fistulae, abscesses, strictures
- Endoscopy (GS) - OGD & colonoscopy
- 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
- Induce remission
- Steroids - PO prednisolone (mild-moderate) / IV hydrocortisone (severe)
- Add azathioprine/mercaptopurine
- Refractory: Infliximab
- Aminosalicylate - Mesalazine (mild-mod)
- Suppository/enema first
- PO if extensive disease
- Steroids - PO prednisolone (mild-mod) / IV hydrocortisone (severe)
- IV ciclosporin (severe)
- Severe attack (shock): IV hydrocortisone first-line
- Maintain remission
- Azathioprine/Mercaptopurine
- Methotrexate
- Infliximab
- Adalimumab
- Aminosalicylate - Mesalazine (PO/PR)
- Azathioprine
- Mercaptopurine
- Patient has either a permanent ileostomy or ileo-anal anastomosis (J-pouch)
May not need any medications whilst well
Surgery to remove the distal ileum if disease is only affecting here.
Panproctocolectomy - Surgery to remove the colon & rectum
- Abdominal plain: Classically central/periumbilical then moves to right iliac fossa
- Nausea and vomiting
- Loss of appetite
- Mild fever
- Can get rebound tenderness
- Palpation in left iliac fossa causes pain in right iliac fossa
- Mostly clinical presentation
- Raised inflammatory markers & WCC
- Pregnant female
- UTI
- Renal colic
- Appendicectomy
- Prophylactic IV antibiotics - Reduces wound infection
- Laparoscopic
- Open
- Herniation of colonic mucosa through muscularis causing outpouchings
- The presence of diverticula WITHOUT symptoms
- Inflamed/infected diverticula
- Very common in older people
- RFs: Low fibre diet & obesity
- Left iliac fossa colicky pain
- Diarrhoea
- PR blood or mucus
- Fever
- Can be septic and peritonitic if severe!
- Abdominal XR (or CT abdo)
- Erect CXR to identify a perforation
- Often an incidental finding on CT
- No treatment necessary: Advise high fibre diet and weight loss if necessary
- Analgesia
- Fluid resuscitation
- Antibiotics
- Unwell → Consider hospital admission
- Severe → May need surgical drainage or resection
See Colorectal Surgery
- There is no organic underlying disease. Many think it is linked to stress and the mind
- Diarrhoea or constipation predominant- fluctuating bowel habit
- Abdominal pain
- Bloating
- Worse after eating, improved by opening bowels
- FBC, ESR and CRP
- Faecal calprotectin
- Anti-TTG antibodies
- CA125
- Provide reassurance
- Low FODMAP diet
- Symptom dependent:
- Cramping: peppermint oil, buscopan (hyoscine butylbromide)
- Diarrhoea: Loperamide
- Constipation: Laxatives
Less common:
- Patient in hospital on antibiotics (broad spectrum - e.g. cephalosporins) for an infection develops watery diarrhoea & feels generally unwell
- Yellow plaques & mucosal inflammation
- PO metronidazole (mild)
- PO vancomycin (mod-sev)
- Toxic megacolon
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia
- Abnormal fluid balance
- Lanz
- Mercedes benz
- Kocher
- Pfannenstiel
- Rutherford Morrison (extended Lanz)
- Rooftop
🫁 Respiratory
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.
Classifying by anatomy:
- 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.
- Epworth Sleepiness Scale
- Snoring
- Daytime sleepiness
- Apnoea episodes (often reported by the partner)
- Waking up not feeling refreshed from sleep
- Concentration problems
- Sleep studies with ENT specialist / at a sleep clinic
- Oxygen saturation
- Heart rate
- Respiratory rate
- Breathing
- Lifestyle: Stop smoking, drinking alcohol and lose weight
- Continuous positive airway pressure (CPAP)
- Surgery: Uvulopalatopharyngoplasty (UPPP)
Sleeping while monitoring the:
- Haemophilus influenza type B infection causing swelling of the epiglottis.
- Thumbprinting sign: Shadowing caused by the swollen epiglottis
- 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:
- 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.
- COPD with respiratory acidosis
- Hypercapnic respiratory failure: Chest wall deformity, neuromuscular disease
Asthma is a chronic respiratory condition causing inflammation and narrowing of the bronchi.
- Dust
- Exercise
- Infection
- Time of day: Night or early morning
- Cold/damp
- Occurring in episodes
- Diurnal variation: Often worse at night.
- Wheeze
- Shortness of breath
- Atopy: Eczema, hayfever, food allergies
What makes up the following grades:
- PEFR: 50-75%
- PEFR: 33-50%
- RR ≥ 25
- HR ≥ 110
- Unable to complete sentences
- PEFR < 33%
- SpO2 < 92%
- Cyanosis
- Hypotension
- Exhaustion - PaCO₂ normal/high
- Silent chest
- Tachyarrhythmias
- pCO2 > 6 (Normal - represents exhaustion)
- ABCDE
- Nebulised salbutamol 5mg & ipratropium bromide
- K⁺ as can be ↓
- Steroids: PO prednisolone / IV hydrocortisone
- Antibiotics (if you suspect this is secondary to an infection)
- IV aminophylline
- IV salbutamol
- IV magnesium sulphate
- Admission to HDU/ITU for intubation & ventilation
- Stable on salbutamol inhaler for 24 hours
- PEFR > 75% predicted
Investigation:
- Fractional exhaled NO (FeNO): ↑ in airway inflammation
- Spirometry with reversibility
- 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).
- Curschmann spirals: Shed epithelium becomes whirled mucus plugs
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:
- 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.
- Reduce airway inflammation, preventing or reducing asthma attacks → Prevents airway smooth muscle hypertrophy secondary to chronic inflammation.
- Block acetylcholine receptors blocking the parasympathetic effect of bronchoconstriction, indirectly causing bronchodilation.
- Leukotrienes → Inflammation, bronchoconstriction & mucus secretion.
- Blocking these prevents this.
Based on NICE Guidelines (2017):
- SABA
- Add regular low-dose ICS
- Add LTRA (review in 4-8 weeks)
- Add LABA (discuss if LTRA has helped at all, if not stop it)
- MART (maintenance & reliever therapy): Combined ICS (low-dose) & fast-acting LABA
- MART with moderate dose ICS
- Increase ICS to high-dose OR add PO theophylline OR add LAMA.
- Refer to specialist
- SABA - Salbutamol
- SAMA - Ipratropium
- ICS - Beclometasone, budesonide, fluticasone, mometasone
- LTRA - Montelukast
- LABA - Salmeterol, formoterol
- LAMA - Tiotropium
- MART - Turbohaler, spiromax
- ICS & LABA - Symbicort, fostair, seretide
- Inhaled drugs, theophylline and prednisolone can be taken as normal during pregnancy and breast-feeding.
Atelectasis is the complete or partial collapse of the entire lung, or a lobe of the lung due to airway obstruction.
- Mucus plug
- 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
- Cystic fibrosis
- Asthma
- Foreign body: Inhaled object (e.g. peanut)
- Lung tumour within the airway
- Pleural effusion
- Pneumonia
- Pneumothorax
- Lung tissue scarring of lung tissue due to injury, lung disease or surgery.
- Tumor (non-airway) causing external compression
- Position patient upright
- Chest physiotherapy
- 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.
- Multiple thin walled cystic space (ring opacities), several of which have air-fluid levels.
- Tram track sign
- Signet ring sign
- Cluster of grapes sign
COPD is chronic inflammation of the airways causing bronchitis (airway inflammation & narrowing) and emphysema (alveoli destruction).
- Shortness of breath.
- Cough.
- Wheeze.
- Recurrent LRTI.
- 'Pink puffer': Predominantly emphysema.
- Compensate for damaged alveoli by hyperventilating.
- High VQ ratio.
- 'Blue bloater': Predominantly bronchitis.
- Compensate for lack of air getting to the alveoli by increasing cardiac output.
- Low V/Q ratio.
- MRC dyspnoea scale. Scale of 1-5, useful to remember the extremes:
- SOB on strenuous exercise = 1.
- Unable to leave house = 5.
- Obstructive picture: FEV1/FVC ratio < 0.7
Using FEV1:
- Stage 1: FEV1 > 80% predicted
- Stage 2: FEV1 50-79% predicted
- Stage 3: FEV1 30-49% predicted
- Stage 4: FEV1 <30% predicted
- ABG: ↑ HCO₃⁻ → Chronic retainer
- TLCO: Total lung diffusion capacity
- KCO: Diffusion capacity of a single alveolus
What would they be in the following diseases:
- Both low
- KCO high (compensatory), TLCO reduced
- Both low
- KCO high, TLCO low
- Lack of lung expansion → Higher pressures in alveoli → More diffusion
- 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.
- Prednisolone 30mg OD for 7-14 days
- Antibiotics (if infective cause)
- Regular inhalers
- Inhaled: Nebulised salbutamol and ipratropium
- Steroids: IV hydrocortisone or PO prednisolone
- Antibiotics (if likely infective cause)
- Chest physiotherapy to help clear sputum
- Non-invasive ventilation (BiPAP), may also need IV aminophylline
- Stage 1: SABA (salbutamol)/SAMA (ipratropium)
- Stage 2:
- No steroid features: LABA & LAMA
- Steroid features: LABA & ICS
- Stage 3:
- Triple therapy: LABA & LAMA & ICS (Trelegy ellipta, trimbo)
- Advanced management
- 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
- PaO2 of < 7.3 kPa (measured when the patient is clinically stable, on two occasions, at least 3 weeks apart)
- PaO2 of 7.3 - 8 kPa & one of the following:
- Nocturnal hypoxaemia (SaO2 < 90%)
- Secondary polycythaemia
- Pulmonary hypertension (pulmonary artery pressure > 25mmHg)
- Peripheral oedema
- Annual pneumococcal & flu vaccine
- Malignancy - 1° or 2°
- Foreign Body
- Abscess / cyst
- Granuloma - Sarcoid / TB
- Pulmonary hamartoma / AVM
- Skin tumor
- Adenocarcinoma (~ 40%)
- Presents in non-smoking women (but still in smokers too)
- Best prognosis
- Squamous cell carcinoma (~ 30%)
- Present in the mediastinum, develop from the bronchi
- Hypercalcaemia - Secretes PTH
- Hypertrophic pulmonary osteoarthropathy (affects hands & feet)
- Large cell carcinoma (~ 10%)
- Likely to metastasise
- Carcinoid
- Neuroendocrine tumour secreting serotonin, histamine & bradykinin
- Bradykinin → Facial flushing
- Histamine → SOB
- Serotonin → Diarrhoea, asthma & SOB
- Urinary 5-HIAA
- Octreotide scan
- Somatostatin analogues: Octreotide
- Mesothelioma
- Pleural tumour associated with asbestos exposure with a long latent period of up to 45 years between exposure and cancer development.
- Aggressive, quickly metastasise, strongly related to smoking.
- Release neuroendocrine hormones, meaning they commonly cause paraneoplastic syndromes.
- Metastases from other sites
Name the paraneoplastic syndrome & tumour causing it:
- Recurrent laryngeal nerve palsy
- Upper lung tumour
- SVCO
- Upper lung tumour
- Horner's syndrome
- Pancoast (apical) tumour compressing the sympathetic ganglion
- SIADH
- SCLC secreting ADH causing dilutional hyponatraemia
- Cushing's syndrome
- SCLC secreting ACTH
- Hypercalcaemia
- Squamous cell carcinoma secreting PTHrP
- Lambert-Eaton syndrome
- SCLC
- Cough
- Shortness of breath
- Weight loss
- Haemoptysis
- CXR:
- Pleural effusion (usually unilateral - exudative)
- Mass
- Atelectasis
- Contrast-enhanced CT thorax, abdomen, pelvis (CT TAP):
- Confirm diagnosis & staging
- PET-CT may also allow us to more clearly see metastases
- Bronchoscopy with EBUS (endobronchial USS) with transbronchial needle aspiration for histology
- 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
Infection of the lung tissue.
- Bacteria infect alveoli → Pulmonary membrane inflammation → Increased permeability → Blood & fluid entering alveoli causing consolidated appearance (filled with liquid)
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
- S. pneumonia (50%)
- H. influenzae (20%)
- Gram ⊖ coccobacilli
- Moraxella catarrhalis
- Immunocompromised patients
- Chronic pulmonary disease patients
Cases:
- Rash: Herpes labialis
- Pathogen: S. pneumoniae (Gram ⊕ diplococci)
- Pneumoncoccal urinary antigen
- CXR: Lobar consolidation
- H. influenzae (Gram ⊖ coccobacilli)
- Influenza
- Pseudomonas aeruginosa (Gram ⊖ bacilli)
- Staphylococcus aureus (Gram ⊕ cocci)
Lower respiratory tract infection (LRTI) developing > 48 hours after admission to hospital.
- P. aeruginosa (Gram ⊖ bacilli) - Associated with mechanical ventilation
- S. aureus (Gram ⊕ cocci)
- Enterobacteria:
- E. coli (Gram ⊖ bacilli)
- Klebsiella (Gram ⊖ bacilli)
Cases:
- S. aureus: Associated with flu, lymphoma/leukaemia, IVDU
- Klebsiella
- Stroke
- Myasthenia gravis
- Bulbar palsy
- Alcoholics
- Epileptics due to post-ictal state
- Lung abscess causing recurrent fever, finger clubbing and foul smelling breath
Pneumonia caused by an organism that cannot be cultured or detected using a gram stain.
"Legion of psittaci MCQ"
- Legionella
- Chlamydia psittaci
- Mycoplasma pneumoniae
- Chlamydydophila pneumoniae
- Q fever (coxiella burnetii)
Cases:
- Mycoplasma pneumonia. Rash → Erythema multiforme.
- Cold AIHA (see haematology) → ↑ RBC breadown → ↑ Bilirubin
- Mycoplasma serology
- Legionella
- Legionella → SIADH
- Urinary legionella antigen
- Clarithromycin
- Chlamydia psittaci
- Coxiella burnetii
- Pneumocystis jiroveci (see Infectious disease)
For all of these, the antibiotic choice depends on local guidelines. However, these are more commonly used.
- 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
- < 5 days from admission: Co-amoxiclav
- > 5 days from admission: Tazocin / ciprofloxacin
- Sepsis
- Pleural effusion (exudative)
- Lung abscess
Case:
- Empyema → Chest drain & antibiotics
Fluid collection within the alveoli.
- Cardiogenic
- ↑ hydrostatic pressure in the pulmonary vessels (due to overload) → Transudative fluid in alveoli
- Heart failure
- Non-cardiogenic
- Acute lung inflammation → ↑ vascular permeability & ↑ hydrostatic pressure (due to vascular resistance) → Exudative fluid in alveoli
- ARDS: Sepsis, trauma, pancreatitis
- High altitude
- Opioid/salicylate toxicity
- PE
- Bats wing airspace shadowing
- Signs of heart failure:
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Upper lobe diversion
- Pleural effusion
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.
Diseases:
- Coal worker's lung
- Hypersensitivity pneumonitis
- Type III hypersensitivity to environmental allergen causing tissue inflammation (extrinsic allergic alveolitis).
- Lymphocytes
- Mast cells
- Bird-fanciers lung → Bird droppings
- Farmer's lung → Hay mold spores
- Malt workers lung → Mould on barley
- Ankylosing spondylitis
- Radiation
- Tuberculosis
- Sarcoidosis
- Idiopathic
- Bibasal fine crackles
- Finger clubbing
- Pirfenidone: Antifibrotic & inflammatory
- Nintedanib
- Connective tissue disorders (except ankylosing spondylitis)
- SLE
- RA
- Systemic sclerosis
- Drug-induced:
- Methotrexate
- Cyclophosphamide
- Amiodarone
- Bleomycin
- Asbestosis
- Asbestos is fibrinogenic (so induces fibrosis in the tissues) & oncogenic
- There is a gap between exposure & mesothelioma
- CT: "Ground glass appearance" / "Honeycombing"
- Lung biopsy
- 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)
- Erythema nodosum (painful)
- Parotid gland swelling
- Lymphadenopathy
- Hypercalcaemia: Macrophages inside the granulomas causing an increased conversion of vitamin D to its active form.
- Neurological: Bilateral facial nerve palsies
- Ocular: Anterior uveitis
- Cardiovascular: Heart block/arrhythmia
- Gastrointestinal: Hepatomegaly
- Dermatological: Lupus pernio
- 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
- 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
- Biopsy showing non-caseating granulomas
- Stage 1 (hilar lymphandenopathy):
- Conservative
- Stage 2 (pulmonary infiltrates):
- Prednisolone (40mg)
- Methotrexate / azathioprine
- 60% of patients with pulmonary sarcoidosis have symptom resolution at 2 years.
- 20% respond to steroids.
- 20% show no improvement.
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.
Diseases:
This is an abnormal collection of air in the pleural space between the lung and the chest wall.
- Do they have an underlying lung condition?
- Cystic fibrosis, asthma, COPD.
- Are they short of breath?
- CXR: Size of pneumothorax
- Erect CXR
- At the level of the hilum, measure horizontally from the chest wall to the lung edge.
Cases:
- Right-sided rib fractures
How are the following patients managed:
- Conservative
- Aspirate with a 16-18G cannula under local anaesthetic
- Insert chest drain
How are the following patients managed:
- Conservative
- Aspirate
- Chest drain
- Chest drain
- 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.
- Tracheal deviation.
- Absence of lung markigs in the left upper zone.
- Collapse of the left lung secondary to the pressure exerted by the pneumothorax.
- ABCDE
- 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
- Chest drain
- Chest drain, sited within the triangle of safety.
- Triangle of safety borders: 5th intercostal space, mid axillary line, anterior axillary line.
A buildup of fluid within the pleural space.
- Triangle of safety: Space between the base of the axilla, lateral edge pectoralis major, 5th intercostal space and the anterior border of latissimus dorsi
- INR > 1.3
- Platelet count < 75
- Pulmonary bullae
- Pleural adhesions
- 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)
- 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
- Infection (most common exudate): Pneumonia, TB, subphrenic abscess
- Connective tissue disease: RA, SLE
- Neoplasia: Lung cancer, mesothelioma, metastases
- Pancreatitis
- PE
- Dressler's syndrome
- HF (most common transudate)
- Hypoalbuminaemia: Liver disease, nephrotic syndrome, malabsorption
- Hypothyroidism
- Meigs' syndrome: Ovarian tumour
- ? malignant pleural effusion
This is the system of transportation, taking de-oxygenated blood from the heart to the lungs to be re-saturated with oxygen before being dispersed into the systemic circulation.
Diseases:
Thrombus within the pulmonary arteries.
Triad of factors contributing to thrombosis:
- Endothelial injury
- Blood flow stasis
- Hyper-coagulability: Malignancy, thrombophilia, previous VTE, polycythemia
- LMWH (depends on local guidelines as to which one)
- Active bleeding
- Already anticoagulated, e.g. on warfarin
- Compression stockings: TEDS
Presentation:
- SOB
- Haemoptysis
- Pleuritic chest pain
- Well’s score, the most useful way to calculate it:
Investigations & Management:
- Bedside:
- ECG
- Sinus tachycardia
- May have S1Q3T3 (but less common)
- Bloods:
- ABG
- 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
- CT chest with IV contrast that allows us to identify clots within the pulmonary arteries
NICE guidelines (March 2020) recommend:
- Apixaban/rivaroxaban
- Low molecular weight heparin (LMWH) may be used depending on local guidelines
Massive PE causing:
- Haemodynamic instability
- Right heart strain
- Alteplase breaks down fibrin in the clots, rapidly dissolving them. This puts them at increased risk of bleeding elsewhere, e.g. intracranially.
- Warfarin
- 2-3
- DOAC
- LMWH
- Active cancer
- Pregnancy
- Provoked VTE, cause is identifiable.
- Unprovoked VTE due to unknown cause or irreversible cause.
- Active cancer
- Thrombophilia
Increased pressure within the pulmonary arteries.
- Primary pulmonary hypertension / connective tissue disease, e.g. SLE
- Heart failure (left): Poor LV function causes back pressure
- Chronic lung disease, e.g. COPD.
- Pulmonary vascular disease, e.g. PE.
- Sarcoidosis / haematological disorders
- Progressive SOB, fatigue,
- Syncope: Ventricular wall stress can cause vasovagal syncope
- Signs of right heart failure
- ECG: Right axis deviation, RBBB
- CXR: RVH
- Echocardiogram: Look at RV function & estimate pulmonary pressures
- Right heart catheterisation: Diagnostic
- ≥ 25 mmHg
- 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).
- Confusion
- N&V
- Cherry red skin
- ABG: Carboxyhaemoglobin > 20% (diagnostic)
- CXR: ARDS
- 100% O₂
- Hyperbaric (higher pressure than normal) O₂
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