Table of content
Module A
1. Cardiology…………………………………………………………………………………………………...………………………………………………
2. Respiratory…………………………………………………………………………………………………...………………………………………………
3. Acute Medicine…………………………………………………………………………………………………...………………………………………
4. Endocrinology…………………………………………………………………………………………………...………………………………………….
Module B
1. Peri-operative Medicine and Anaesthetics…………………………………………………………………………………………………….
2. Trauma and Orthopaedics..………………………………………………………………………….………………………………………………..
3. Rheumatology……………………………………………………………………………………………………………………………………………….
4. Gastroenterology & Gastrointestinal surgery…………………………………………………………………………………………………
5. Vascular Surgery……………………………………………………………………………………………………………………………………………
Module C
1. ENT………………………………………………………………………………...…………………………………………………………………………….
2. Renal……………………………………………………………………………….……………………………………………………………………………
3. Infectious Diseases………………………………………………………………………………………………………………………………………..
4. Haematology………………………………………………………………………………...……………………………………………………………..
5. Neurology………………………………………………………………………………...…………………………………………………………………..
Random Bits
1. Signs………………………………………………………………………………...…………………………………………………………………….
2. Antibodies………………………………………………………………………………...…………………………………………………………….
3. vitamins…………………………………………………………………………..……………………………………………………………………..
,4. Clinical Chemistry…..……………………………………………..………………………………………………………………………………..
Mod A
Cardiology
● Aortic dissection:
- Causes:
🡺 Tear in the tunica intima (innermost layer) of the aorta due to:
o Uncontrolled Hypertension.
o Connective tissue disease e.g. Marfan's syndrome
o Valvular heart disease
o Cocaine/amphetamine use
- Signs and symptoms:
🡺 Sudden onset 'tearing' chest pain on onset or interscapular pain radiating to the back, with
improvement over time - Aortic dissection carries a mortality of 50% at 24 hours if untreated due
to coronary dissection
🡺 Aortic regurgitation - results from a proximal dissection that involves the aortic valve leaflets
🡺 Radio-radial delay – more likely in Type A
🡺 Radio-femoral delay – more likely in Type B
🡺 Blood pressure differential between arms
🡺 blood in the artery wall (false lumen) compressing branches of the aorta can lead to: paraparesis
(e.g. carotid or spinal artery involvement); anuria and loin pain (e.g. renal artery involvement);
abdominal pain (e.g. mesenteric artery involvement) and acute limb ischaemia (e.g. subclavian or
femoral artery involvement).
- Investigations:
🡺 CT angiogram used to diagnose
🡺 ECG, echocardiogram, chest x ray and bloods
- Management:
🡺 A-E assessment including giving IV labetalol to control BP
🡺 Type A (ascending aorta and aortic arch): Usually requires surgical management (e.g. aortic graft
via open surgery)
🡺 Type B (thoracic and abdominal descending aorta):
o In uncomplicated patients, normally managed conservatively with blood pressure control
(e.g. beta blockers) and opioid analgesia (e.g. morphine IV)
o If there is evidence of end organ damage then endovascular repair may be performed
● Arrhythmias:
- Acute Bradycardia = HR <60bpm
🡺 Causes:
o Sinus/AV nodal disease
o Drug induced such as beta blockers, calcium channel blockers
o Electrolyte abnormalities
🡺 Signs and symptoms:
o Dizziness, syncope, and tiredness
🡺 Investigations:
o A-E assessment
o ECG monitoring
🡺 Management
, o Haemodynamically unstable (HISS):
▪ atropine 500 micrograms IV or IO is given which can be repeated 6 times (3mg in total)
▪ OR Transcutaneous pacing whilst awaiting expert help for transvenous pacing/
permanent pacemaker insertion (definitive management)
▪ OR glucagon if bisoprolol overdose
▪ OR adrenaline 2-10micrograms/min IV or isoprenaline IV
o Haemodynamically stable or risk of asystole => check TFTs, electrolytes + observe
- Atrial flutter – aberrant re-entrant circuit in the right atrium cycling at 300bpm.
🡺 Causes:
o Associated with pulmonary disease (COPD, OSA, PE, and pulmonary hypertension)
o Sepsis, alcohol, and thyrotoxicosis
🡺 Signs and symptoms:
o Asymptomatic, Palpitations, Dizziness, Chest pain
🡺 Investigations:
o ECG features:
▪ Regularly irregular heartbeat
▪ saw tooth baseline with repetition at 300bpm
▪ Narrow QRS complex (<120ms)
▪ Ventricular rate which depends on the level of AV block:
❖ 150bpm if 2:1
❖ 100bpm if 3:1
❖ 75bpm if 4:1
❖ 60bpm if 5:1
🡺 Management
o Haemodynamically unstable (HISS):
▪ A-E
▪ emergency synchronised DC cardioversion under sedation +/- amiodarone
o Haemodynamically stable:
▪ Vagal manoeuvres e.g. carotid massage or Valsalva manoeuvre (asking the patient to
blow into a syringe)
▪ Treat reversible causes, e.g. fluid resuscitation in septic or dehydrated patients
▪ Rate control, e.g. beta blocker or calcium channel blocker
▪ Cardioversion e.g. electrical cardioversion
▪ recurrent or refractory flutter in symptomatic despite rate control and those in which
cardioversion has failed = ablation of arrhythmogenic foci at cavotricuspid isthmus.
- Atrial fibrillation:
🡺 Causes:
o Cardiac e.g. IHD, HTN, rheumatic heard disease, pericarditis, heart failure
o Non-cardiac e.g. dehydration, hyperthyroidism, sepsis, pneumonia, PE, alcohol abuse,
electrolyte disturbances
🡺 Signs and symptoms:
o Palpitations, Chest pain, SOB, and Dizziness
o Single waveform on the jugular venous pressure (due to loss of a wave)
o apical to radial pulse deficit
, 🡺 Investigations:
o ECG features:
▪ Irregularly irregular heartbeat
▪ No disenable P waves
▪ 300-600 beats per minute
o Bloods, echo, troponin levels (if mildly raised + symptoms of ACS => repeat levels as they will
peak 12-24 hours of the insult)
🡺 Classification:
o Paroxysmal AF = episodes last >30 seconds but <7days (often <48 hours) and are self
terminating and recurrent
o Persistent AF = episodes last >. 7 days (spontaneous termination unlikely to occur after this
time)
o Permanent AF = AF that fails to terminate using cardioversion/AF that is terminated but
relapses within 24 hours/ longstanding AF (1 year) in which csrdioversion not been indicated
or accepted
o Lone AF = AF in <60-year olds, with no Hx or echo evidence of concomitant cardio or
pulmonary conditions or an acute trigger – more favorable prognosis
🡺 Management
o Haemodynamically unstable (HISS):
▪ A-E
▪ emergency synchronised DC cardioversion under sedation (+/- amiodarone)
▪ Reverse cause e.g. fluids, antibiotics or replace abnormal electrolytes
o Haemodynamically stable:
▪ Onset of AF <48 hours:
❖ Rate control:
⮚ First line = beta-blocker such as bisoprolol/carvedilol/propanolol – CI in
asthmatic + hypotensive patients
⮚ Or rate limiting non-dihydropyridine CCB if BB CI (e.g. Diltiazem or verapamil) –
CI in HF patients
⮚ Second line = dual therapy
⮚ Non-paroxysmal AF +HF who are sedentary = Digoxin monotherapy 250
micrograms IV followed by another 250 micrograms at 6 hours, then once daily
oral dosing – no need for routine monitoring unless... Risk of digoxin toxicity
(can be precipitated by hypokalaemia, thiazides, amiodarone, calcium channel
blockers, and quinidine):
● Signs and symptoms - Dizziness, Nausea and vomiting, Palpitations (due to
arrhythmias), Bradycardia typically without hypotension, Yellow-
green colour disturbance (Xanthopsia), Visual haloes, Confusion,
Hyperkalaemia (note that hypokalaemia is a risk factor for toxicity - less K+
competing for the same Na+/K+ ATPase receptors which digoxin binds too
=+ more digoxin binds to these receptors)
● Investigations:
◊ ECG = Shortened QT interval (shortens refractory periods of ventricles
=> ventricular cardiac cell is able to initiate another action potential
more quickly after the previous one) + down sloping ST-segment
depression with a characteristic “reverse-tick” appearance with
flattened or inverted t-waves, U waves (showing hypokalaemia)
Module A
1. Cardiology…………………………………………………………………………………………………...………………………………………………
2. Respiratory…………………………………………………………………………………………………...………………………………………………
3. Acute Medicine…………………………………………………………………………………………………...………………………………………
4. Endocrinology…………………………………………………………………………………………………...………………………………………….
Module B
1. Peri-operative Medicine and Anaesthetics…………………………………………………………………………………………………….
2. Trauma and Orthopaedics..………………………………………………………………………….………………………………………………..
3. Rheumatology……………………………………………………………………………………………………………………………………………….
4. Gastroenterology & Gastrointestinal surgery…………………………………………………………………………………………………
5. Vascular Surgery……………………………………………………………………………………………………………………………………………
Module C
1. ENT………………………………………………………………………………...…………………………………………………………………………….
2. Renal……………………………………………………………………………….……………………………………………………………………………
3. Infectious Diseases………………………………………………………………………………………………………………………………………..
4. Haematology………………………………………………………………………………...……………………………………………………………..
5. Neurology………………………………………………………………………………...…………………………………………………………………..
Random Bits
1. Signs………………………………………………………………………………...…………………………………………………………………….
2. Antibodies………………………………………………………………………………...…………………………………………………………….
3. vitamins…………………………………………………………………………..……………………………………………………………………..
,4. Clinical Chemistry…..……………………………………………..………………………………………………………………………………..
Mod A
Cardiology
● Aortic dissection:
- Causes:
🡺 Tear in the tunica intima (innermost layer) of the aorta due to:
o Uncontrolled Hypertension.
o Connective tissue disease e.g. Marfan's syndrome
o Valvular heart disease
o Cocaine/amphetamine use
- Signs and symptoms:
🡺 Sudden onset 'tearing' chest pain on onset or interscapular pain radiating to the back, with
improvement over time - Aortic dissection carries a mortality of 50% at 24 hours if untreated due
to coronary dissection
🡺 Aortic regurgitation - results from a proximal dissection that involves the aortic valve leaflets
🡺 Radio-radial delay – more likely in Type A
🡺 Radio-femoral delay – more likely in Type B
🡺 Blood pressure differential between arms
🡺 blood in the artery wall (false lumen) compressing branches of the aorta can lead to: paraparesis
(e.g. carotid or spinal artery involvement); anuria and loin pain (e.g. renal artery involvement);
abdominal pain (e.g. mesenteric artery involvement) and acute limb ischaemia (e.g. subclavian or
femoral artery involvement).
- Investigations:
🡺 CT angiogram used to diagnose
🡺 ECG, echocardiogram, chest x ray and bloods
- Management:
🡺 A-E assessment including giving IV labetalol to control BP
🡺 Type A (ascending aorta and aortic arch): Usually requires surgical management (e.g. aortic graft
via open surgery)
🡺 Type B (thoracic and abdominal descending aorta):
o In uncomplicated patients, normally managed conservatively with blood pressure control
(e.g. beta blockers) and opioid analgesia (e.g. morphine IV)
o If there is evidence of end organ damage then endovascular repair may be performed
● Arrhythmias:
- Acute Bradycardia = HR <60bpm
🡺 Causes:
o Sinus/AV nodal disease
o Drug induced such as beta blockers, calcium channel blockers
o Electrolyte abnormalities
🡺 Signs and symptoms:
o Dizziness, syncope, and tiredness
🡺 Investigations:
o A-E assessment
o ECG monitoring
🡺 Management
, o Haemodynamically unstable (HISS):
▪ atropine 500 micrograms IV or IO is given which can be repeated 6 times (3mg in total)
▪ OR Transcutaneous pacing whilst awaiting expert help for transvenous pacing/
permanent pacemaker insertion (definitive management)
▪ OR glucagon if bisoprolol overdose
▪ OR adrenaline 2-10micrograms/min IV or isoprenaline IV
o Haemodynamically stable or risk of asystole => check TFTs, electrolytes + observe
- Atrial flutter – aberrant re-entrant circuit in the right atrium cycling at 300bpm.
🡺 Causes:
o Associated with pulmonary disease (COPD, OSA, PE, and pulmonary hypertension)
o Sepsis, alcohol, and thyrotoxicosis
🡺 Signs and symptoms:
o Asymptomatic, Palpitations, Dizziness, Chest pain
🡺 Investigations:
o ECG features:
▪ Regularly irregular heartbeat
▪ saw tooth baseline with repetition at 300bpm
▪ Narrow QRS complex (<120ms)
▪ Ventricular rate which depends on the level of AV block:
❖ 150bpm if 2:1
❖ 100bpm if 3:1
❖ 75bpm if 4:1
❖ 60bpm if 5:1
🡺 Management
o Haemodynamically unstable (HISS):
▪ A-E
▪ emergency synchronised DC cardioversion under sedation +/- amiodarone
o Haemodynamically stable:
▪ Vagal manoeuvres e.g. carotid massage or Valsalva manoeuvre (asking the patient to
blow into a syringe)
▪ Treat reversible causes, e.g. fluid resuscitation in septic or dehydrated patients
▪ Rate control, e.g. beta blocker or calcium channel blocker
▪ Cardioversion e.g. electrical cardioversion
▪ recurrent or refractory flutter in symptomatic despite rate control and those in which
cardioversion has failed = ablation of arrhythmogenic foci at cavotricuspid isthmus.
- Atrial fibrillation:
🡺 Causes:
o Cardiac e.g. IHD, HTN, rheumatic heard disease, pericarditis, heart failure
o Non-cardiac e.g. dehydration, hyperthyroidism, sepsis, pneumonia, PE, alcohol abuse,
electrolyte disturbances
🡺 Signs and symptoms:
o Palpitations, Chest pain, SOB, and Dizziness
o Single waveform on the jugular venous pressure (due to loss of a wave)
o apical to radial pulse deficit
, 🡺 Investigations:
o ECG features:
▪ Irregularly irregular heartbeat
▪ No disenable P waves
▪ 300-600 beats per minute
o Bloods, echo, troponin levels (if mildly raised + symptoms of ACS => repeat levels as they will
peak 12-24 hours of the insult)
🡺 Classification:
o Paroxysmal AF = episodes last >30 seconds but <7days (often <48 hours) and are self
terminating and recurrent
o Persistent AF = episodes last >. 7 days (spontaneous termination unlikely to occur after this
time)
o Permanent AF = AF that fails to terminate using cardioversion/AF that is terminated but
relapses within 24 hours/ longstanding AF (1 year) in which csrdioversion not been indicated
or accepted
o Lone AF = AF in <60-year olds, with no Hx or echo evidence of concomitant cardio or
pulmonary conditions or an acute trigger – more favorable prognosis
🡺 Management
o Haemodynamically unstable (HISS):
▪ A-E
▪ emergency synchronised DC cardioversion under sedation (+/- amiodarone)
▪ Reverse cause e.g. fluids, antibiotics or replace abnormal electrolytes
o Haemodynamically stable:
▪ Onset of AF <48 hours:
❖ Rate control:
⮚ First line = beta-blocker such as bisoprolol/carvedilol/propanolol – CI in
asthmatic + hypotensive patients
⮚ Or rate limiting non-dihydropyridine CCB if BB CI (e.g. Diltiazem or verapamil) –
CI in HF patients
⮚ Second line = dual therapy
⮚ Non-paroxysmal AF +HF who are sedentary = Digoxin monotherapy 250
micrograms IV followed by another 250 micrograms at 6 hours, then once daily
oral dosing – no need for routine monitoring unless... Risk of digoxin toxicity
(can be precipitated by hypokalaemia, thiazides, amiodarone, calcium channel
blockers, and quinidine):
● Signs and symptoms - Dizziness, Nausea and vomiting, Palpitations (due to
arrhythmias), Bradycardia typically without hypotension, Yellow-
green colour disturbance (Xanthopsia), Visual haloes, Confusion,
Hyperkalaemia (note that hypokalaemia is a risk factor for toxicity - less K+
competing for the same Na+/K+ ATPase receptors which digoxin binds too
=+ more digoxin binds to these receptors)
● Investigations:
◊ ECG = Shortened QT interval (shortens refractory periods of ventricles
=> ventricular cardiac cell is able to initiate another action potential
more quickly after the previous one) + down sloping ST-segment
depression with a characteristic “reverse-tick” appearance with
flattened or inverted t-waves, U waves (showing hypokalaemia)
