Cardiology Flashcards

Question

What is the initial management of acute coronary syndrome?

Answer 1

MONAC M – Morphine IV for pain if required (with an antiemetic, e.g., metoclopramide) O - Oxygen if O2 sats <94% N – Nitrate (GTN) A – Aspirin 300mg C - ECG

Answer 2

Aspirin 300mg Asses whether PCI is possible within 120 mins, 2 outcomes: (1) Yes: Before PCI: give prasugrel/ticagrelor IF patient is bleeding risk or on anti-coagulants give clopidogrel instead During PCI: Give unfractionated heparin and GPIIb/IIIa inhibitor (2) No: Fibrinolysis with alteplase/streptokinase, should be offered within 12 hours onset OR if PCI is not available in120 mins + anti-thrombin - uHeparin, Fondaparinux, LMWH IF no ECG resolution within 90 mins transfer for PCI

Answer 3

They should be referred to the hospital for same-day assessment, usually seen by the medical team in the Ambulatory Care Unit. Emergency admission is required if there are ECG changes or complications (e.g., heart failure).

Answer 4

--> Primary PCI within 120 minutes of the time thrombolysis could have been given. --> Thrombolysis if PCI cannot be performed within 120 minutes. If ST elevation persists 90 minutes after thrombolysis, transfer for PCI. --> Drug therapy during PCI: unfractionated heparin for radial access or bivalirudin for femoral access.

Answer 5

Inserting a catheter into the radial or femoral artery (radial preferred) Feeding it to the coronary arteries under x-ray guidance Injecting contrast to identify blockages (angiography) Treating blockages with balloons (angioplasty) or devices Usually inserting a stent to keep the artery open

Answer 6

Thrombolysis involves injecting a fibrinolytic agent to break down fibrin in blood clots. It carries a significant risk of bleeding. Examples: Streptokinase, alteplase, tenecteplase

Answer 7

Aspirin 300mg (+fondaprinux if no immediate PCI planned) Estimate 6-month mortality with GRACE score, 2 outcomes: (1) <= 3%: - Conservative management and give ticagrelor (2) >=3: - PCI immediately if unstable (or within 72 hours if stable) + Give unfractionated heparin + Give prasugrel/ticagrelor + IF bleeding risk or IF patient is taking anti-coagulants, swap ticagrelor/prasugrel for clopidogrel

Answer 8

Only if oxygen saturation drops below 95% (in someone without COPD).

Answer 9

Unstable patients (hypotensive) should be considered for immediate angiography, similar to with a STEMI. Within 72 hours for GRACE score > 3% or new ischemia post-admission.

Answer 10

The GRACE score gives a 6-month probability of death after having an NSTEMI. using factors like age, heart rate, BP, renal function, cardiac arrest on presentation, ECG findings, and troponin levels.

Answer 11

3% or less: Low risk Above 3%: Medium to high risk

Answer 12

If not on oral anticoagulants: Prasugrel or Ticagrelor If on oral anticoagulants: Clopidogrel

Answer 13

Patients at medium or high risk (GRACE score > 3%) are considered for early angiography with PCI within 72 hours.

Answer 14

Echocardiogram to assess left ventricular function Cardiac rehabilitation Secondary prevention

Answer 15

The "6 A's": Aspirin 75mg once daily indefinitely Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months Atorvastatin 80mg once daily ACE inhibitors (e.g., ramipril) titrated as high as tolerated Atenolol (or another beta-blocker, usually bisoprolol) titrated as high as tolerated Aldosterone antagonist (e.g., eplerenone) for patients with clinical heart failure

Answer 16

Renal function and potassium levels (risk of hyperkalaemia).

Answer 17

Using spironolactone or eplerenone with an ACE inhibitor or angiotensin receptor blocker increases the risk of fatal hyperkalaemia.

Answer 18

The "DREAD" mnemonic: D – Death R – Rupture of the heart septum or papillary muscles E – "oEdema" (heart failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome

Answer 19

Dressler’s Syndrome (post-myocardial infarction syndrome) occurs 2-3 weeks after an MI due to a localised immune response causing pericarditis. Presentation: Pleuritic chest pain Low-grade fever Pericardial rub on auscultation Can cause pericardial effusion and rarely, pericardial tamponade

Answer 20

ECG: Global ST elevation, T wave inversion Echocardiogram: Pericardial effusion Raised inflammatory markers: CRP and ESR

Answer 21

NSAIDs: Aspirin or ibuprofen Steroids (e.g., prednisolone) for severe cases Pericardiocentesis for significant pericardial effusion

Answer 22

A dilation of the thoracic aorta, most commonly affecting the ascending aorta.

Answer 23

Less than 4.5 cm for the ascending aorta and less than 3.5 cm for the descending aorta.

Answer 24

The first sign may be when the aneurysm ruptures, leading to life-threatening bleeding into the mediastinum.

Answer 25

Extremely high mortality.

Answer 26

Intima, media, and adventitia.

Answer 27

A condition where the inner two layers of the aorta (intima and media) rupture, and the dilation is contained only within the outer (adventitia) layer.

Answer 28

Trauma (e.g., road traffic accidents), surgery to the aorta, or infection in the vessel.

Answer 29

A condition where all three layers of the aorta (intima, media, and adventitia) remain intact but are dilated

Answer 30

Thoracic aortic aneurysms are often asymptomatic and may be discovered incidentally on investigations such as chest x-rays, echocardiograms, or CT scans.

Answer 31

Chest or back pain Cough, shortness of breath, or stridor (from trachea or left bronchus compression) Hiccups (from phrenic nerve compression) Dysphagia (difficulty swallowing, from oesophageal compression) Hoarse voice (from recurrent laryngeal nerve compression)

Answer 32

Echocardiogram CT angiogram MRI angiogram

Answer 33

By treating modifiable risk factors: Stop smoking Healthy diet and exercise Optimising management of hypertension, diabetes, and hyperlipidaemia

Answer 34

Individual patient factors and the size of the aneurysm. The larger the aneurysm, the higher the risk of rupture.

Answer 35

Surveillance with regular imaging to monitor size Thoracic endovascular aortic repair (TEVAR) with a stent graft inserted via the femoral artery Open surgery (midline sternotomy) to remove the affected section of the aorta and replace it with a synthetic graft

Answer 36

Aortic dissection Ruptured aneurysm Aortic regurgitation (if the aortic valve is affected)

Answer 37

Rupture leads to life-threatening bleeding into the mediastinum, with a high risk of mortality

Answer 38

The risk of rupture increases with the diameter of the aneurysm.

Answer 39

Bleeding can occur into: Oesophagus (causing haematemesis) Airways or lungs (causing haemoptysis) Pericardial cavity (causing cardiac tamponade)

Answer 40

Severe chest or back pain Haemodynamic instability (hypotension, tachycardia) Collapse Death (often before reaching the hospital)

Answer 41

Emergency open surgery is required, where the affected section of the aorta is replaced with a synthetic graft.

Answer 42

AAA refers to the dilation of the abdominal aorta with a diameter of more than 3 cm

Answer 43

Patients often become aware of an AAA when it ruptures, leading to life-threatening bleeding.

Answer 44

Men are affected significantly more often and at a younger age than women. Increased age. Smoking. Hypertension. Family history of AAA. Existing cardiovascular disease.

Answer 45

Men: All men are offered a screening ultrasound at age 65 to detect asymptomatic AAA. Early detection helps prevent further expansion or rupture. Women: Screening is not routinely offered due to lower risk. NICE guidelines (2020) suggest considering screening in women over 70 with risk factors such as: - Cardiovascular disease - COPD - Family history - Hypertension - Hyperlipidaemia - Smoking Referral: If the aortic diameter is over 3 cm, referral to a vascular team is needed, with urgent referral if the diameter exceeds 5.5 cm.

Answer 46

Most patients are asymptomatic, with AAA often found on routine screening. Other possible presentations: Non-specific abdominal pain Pulsatile and expansile mass in the abdomen (palpated with both hands) Incidental finding on abdominal x-ray, ultrasound, or CT scan Rupture may be the first time patients become aware of it, leading to life-threatening bleeding.

Answer 47

Ultrasound: The usual initial investigation to establish the diagnosis. CT angiogram: Provides a more detailed picture of the aneurysm and helps guide elective surgery for repair.

Answer 48

< 3 cm: Normal → No further action 3 - 4.4 cm: Small aneurysm → Rescan every 12 months 4.5 - 5.4 cm: Medium aneurysm → Rescan every 3 months ≥ 5.5 cm: Large aneurysm → Refer within 2 weeks to vascular surgery for probable intervention Prevalence: Found in only 1 per 1,000 screened patients

Answer 49

--> stop smoking --> Healthy diet and exercise --> Optimising the management of hypertension, diabetes, and hyperlipidaemia

Answer 50

Elective repair is recommended for: Symptomatic aneurysm Aneurysm growing more than 1 cm per year Aneurysm diameter above 5.5 cm

Answer 51

Open repair via a laparotomy Endovascular aneurysm repair (EVAR) using a stent inserted via the femoral arteries

Answer 52

Must inform the DVLA if aneurysm is above 6 cm Stop driving if aneurysm is above 6.5 cm Stricter rules apply for heavy vehicle drivers

Answer 53

The risk of rupture increases with the diameter: 5% risk for a 5 cm aneurysm 40% risk for an 8 cm aneurysm

Answer 54

Around 80%.

Answer 55

-->Severe abdominal pain, possibly radiating to the back or groin --> Haemodynamic instability (hypotension and tachycardia) -->Pulsatile and expansile abdominal mass Collapse --> Loss of consciousness

Answer 56

It is a surgical emergency requiring immediate involvement of vascular surgeons, anaesthetists, and theatre teams.

Answer 57

Permissive hypotension refers to the strategy of maintaining lower blood pressure during fluid resuscitation to avoid increasing blood loss.

Answer 58

They should be transferred directly to theatre for surgical repair without delaying for imaging.

Answer 59

A CT angiogram can be used to diagnose or exclude ruptured AAA in haemodynamically stable patients.

Answer 60

If the patient has co-morbidities that make the prognosis with surgery very poor, a discussion about palliative care may be appropriate.

Answer 61

--> Back pain: In patients over 50 with acute severe back pain, consider an abdominal ultrasound to measure the aortic diameter. --> Acute pancreatitis: Measure serum amylase/lipase. If normal or mildly raised, perform an abdominal ultrasound to exclude AAA. --> Renal colic: Even with history of stones and positive urine dip for blood, consider an abdominal ultrasound to rule out AAA. --> Lower limb ischaemia: Consider abdominal imaging to check for AAA as a cause when evaluating for occlusion.

Answer 62

Aortic dissection occurs when a tear forms in the inner layer of the aorta, allowing blood to flow between the intima and media layers. This creates a false lumen full of blood within the aortic wall.

Answer 63

Stanford system: Type A: Affects the ascending aorta, before the brachiocephalic artery. Type B: Affects the descending aorta, after the left subclavian artery. DeBakey system: Type I: Begins in the ascending aorta and involves at least the aortic arch or the whole aorta. Type II: Isolated to the ascending aorta. Type IIIa: Begins in the descending aorta and involves only the section above the diaphragm. Type IIIb: Begins in the descending aorta and involves the aorta below the diaphragm.

Answer 64

Shared with peripheral arterial disease: Age, male sex, smoking, hypertension, poor diet, reduced physical activity, and raised cholesterol. Hypertension: Major risk factor, can be triggered by events like heavy weightlifting or cocaine use. Aortic conditions/procedures: Bicuspid aortic valve Coarctation of the aorta Aortic valve replacement Coronary artery bypass graft (CABG) Connective tissue disorders: Ehlers-Danlos Syndrome Marfan’s Syndrome

Answer 65

--> Classic symptom: Sudden onset, severe, “ripping” or “tearing” chest pain. Pain location: - Anterior chest pain: Ascending aorta affected. - Back pain: Descending aorta affected. Pain migration: Pain may change location over time. Other features: Hypertension: Present in many cases. Blood pressure difference: A difference >20mmHg between arms is significant. Radial pulse deficit: One arm’s radial pulse is decreased/absent compared to the apex beat. Diastolic murmur: Due to aortic regurgitation. Neurological signs: Focal deficits, e.g., limb weakness or paraesthesia. Chest/abdominal pain: Pain in both areas may be present. Collapse/syncope: Especially as the dissection progresses. Hypotension: As a late feature or sign of progression. Signs of organ malperfusion: Stroke: Carotid artery involvement. Myocardial infarction: Coronary ostia obstruction. Paraplegia: Spinal artery compromise. Mesenteric ischemia: Abdominal pain. Renal failure: Renal artery occlusion. Cardiovascular collapse: Sudden death if the ascending aorta ruptures into the pericardium.

Answer 66

Chest x-ray: Widened mediastinum may suggest aortic dissection. CT angiography of the chest, abdomen, and pelvis: Investigation of choice for stable patients. Helps with surgical planning. A false lumen is a key diagnostic finding. Transoesophageal echocardiography (TOE): Preferred for unstable patients who cannot be safely moved for a CT scan.

Answer 67

Type A (affects the ascending aorta): Surgical management is required. Blood pressure control to a target systolic of 100-120 mmHg using IV medications while awaiting surgery. Type B (affects the descending aorta): Conservative management: Bed rest. Reduce blood pressure with IV labetalol to prevent progression.

Answer 68

Myocardial infarction Stroke Paraplegia (motor or sensory impairment in the legs) Cardiac tamponade Aortic valve regurgitation Death

Answer 69

A sudden decrease in arterial blood flow to a limb, threatening its viability, with an incidence of ~1.5 cases per 10,000 per year, primarily affecting the lower limbs.

Answer 70

Thrombosis (80-85%) Embolism (10-15%) Trauma (5%)

Answer 71

Plaque rupture in atherosclerotic segments Hypovolaemia Thrombophilia Hypotension Malignancy

Answer 72

Left atrium (atrial fibrillation) Mural thrombus (myocardial infarction) Prostheses (heart valves or bypass grafts) Aneurysms (e.g., popliteal, abdominal aortic)

Answer 73

Smoking Diabetes mellitus Obesity Hypertension Hypercholesterolaemia

Answer 74

The six P's: Pain Pallor Pulselessness Perishingly cold (poikilothermia) Paraesthesia Paralysis

Answer 75

Embolic ALI: Sudden onset, no history of claudication, obvious source of embolus (AF, recent MI), no evidence of PAD, normal contralateral pulses Thrombotic ALI: Gradual onset, less severe symptoms, evidence of vascular disease (stroke, MI, TIA, previous vascular surgery), absent contralateral pulses, history of PAD

Answer 76

Stage I: Limb viable Stage IIa: Limb marginally threatened Stage IIb: Limb immediately threatened Stage III: Limb irreversibly damaged

Answer 77

Critical limb ischaemia (CLI) Acute deep vein thrombosis Peripheral neuropathy Compartment syndrome Thromboangiitis obliterans

Answer 78

Bedside: Handheld arterial Doppler US examination, ABPI, ECG Laboratory: FBC, U&E, LFTs, coagulation, serum lactate Imaging: CT/MR angiography, echocardiography

Answer 79

Emergency vascular specialist assessment IV unfractionated heparin Analgesia

Answer 80

Intra-arterial thrombolysis Bypass surgery Embolectomy Angioplasty Non-viable limbs: Amputation

Answer 81

Smoking cessation Lifestyle modifications (diet and exercise) Statin therapy Management of diabetes and hypertension Antiplatelet therapy

Answer 82

High mortality rate (15-20%) Reperfusion injury Compartment syndrome Peripheral nerve injury Psychosocial impacts of amputation

Answer 83

Chest pain Dyspnoea Syncope / presyncope (e.g., exertional dizziness) Murmur

Answer 84

An ejection systolic murmur (ESM) that radiates to the carotids and is decreased following the Valsalva maneuver.

Answer 85

Narrow pulse pressure Slow rising pulse Delayed ejection systolic murmur (ESM) Soft or absent S2 S4 gallop Thrill Prolonged duration of murmur Left ventricular hypertrophy or failure

Answer 86

Degenerative calcification (most common in patients > 65 years) Bicuspid aortic valve (most common in patients < 65 years) William's syndrome (supravalvular aortic stenosis) Post-rheumatic disease Subvalvular aortic stenosis (e.g., hypertrophic obstructive cardiomyopathy - HOCM)

Answer 87

Generally observe the patient.

Answer 88

Valve replacement is indicated.

Answer 89

If there is a valvular gradient > 40 mmHg and features such as left ventricular systolic dysfunction.

Answer 90

--> Surgical AVR: Treatment of choice for young, low/medium operative risk patients; often combined with angiogram due to potential cardiovascular disease. --> Transcatheter AVR (TAVR): Used for patients with high operative risk. --> Balloon valvuloplasty: May be used in children without aortic valve calcification and limited to adults with critical aortic stenosis who are not fit for valve replacement.

Answer 91

AR is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole.

Answer 92

Disease of the aortic valve Distortion or dilation of the aortic root and ascending aorta

Answer 93

Chronic: rheumatic fever: the most common cause in the developing world calcific valve disease connective tissue diseases e.g. rheumatoid arthritis/SLE bicuspid aortic valve (affects both the valves and the aortic root) Acute: Infective endocarditis.

Answer 94

Chronic: bicuspid aortic valve (affects both the valves and the aortic root) spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome Acute: Aortic dissection.

Answer 95

Early diastolic murmur (increased with handgrip) Collapsing pulse Wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) Mid-diastolic Austin-Flint murmur in severe AR (due to partial closure of mitral valve)

Answer 96

Suspected AR should be investigated with echocardiography.

Answer 97

Medical management of any associated heart failure Surgical indications include: Symptomatic patients with severe AR Asymptomatic patients with severe AR and LV systolic dysfunction

Answer 98

Arrhythmias are abnormal heart rhythms caused by interruptions in the normal electrical signals that coordinate heart muscle contractions.

Answer 99

Shockable rhythms: Ventricular tachycardia Ventricular fibrillation Non-shockable rhythms: Pulseless electrical activity (PEA) Asystole

Answer 100

Shockable rhythms (VT, VF) may respond to defibrillation, while non-shockable rhythms (PEA, asystole) will not.

Answer 101

Narrow complex tachycardia is a fast heart rate characterized by a QRS complex duration of less than 0.12 seconds, fitting within 3 small squares on a standard ECG.

Answer 102

Sinus tachycardia (treatment focuses on the underlying cause) Supraventricular tachycardia (treated with vagal manoeuvres and adenosine) Atrial fibrillation (treated with rate control or rhythm control) Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)

Answer 103

Sinus tachycardia maintains a normal P wave, QRS complex, and T wave pattern and usually occurs in response to an underlying cause (e.g., sepsis, pain).

Answer 104

SVT shows a regular rhythm with QRS complexes followed by T waves, but P waves are often buried in the T waves.

Answer 105

SVT has an abrupt onset and a very regular rhythm without variability. In contrast, sinus tachycardia presents with a gradual onset and greater variability in the heart rate. Sinus tachycardia often has identifiable causes (e.g., pain, fever), whereas SVT may occur at rest without an obvious reason.

Answer 106

Atrial fibrillation is characterized by absent P waves and an irregularly irregular ventricular rhythm.

Answer 107

Atrial flutter typically shows a saw-tooth pattern with an atrial rate of around 300 beats per minute, often resulting in a ventricular rate of 150 beats per minute.

Answer 108

The atrial rate in atrial flutter is usually around 300 beats per minute, creating a saw-tooth pattern on the ECG. Due to conduction from the atria, a QRS complex occurs at regular intervals, often resulting in two atrial contractions for every one ventricular contraction, leading to a ventricular rate of approximately 150 beats per minute. 2: 1 conduction

Answer 109

Patients with life-threatening features should be treated with synchronized DC cardioversion under sedation or general anesthesia, with intravenous amiodarone if initial shocks are unsuccessful.

Answer 110

Broad complex tachycardia is defined as a fast heart rate with a QRS complex duration of more than 0.12 seconds (or 3 small squares) on an ECG. It is classified into: Ventricular tachycardia or unclear cause (treated with IV amiodarone). Polymorphic ventricular tachycardia (e.g., torsades de pointes, treated with IV magnesium). Atrial fibrillation with bundle branch block (treated as AF). Supraventricular tachycardia with bundle branch block (treated as SVT). Patients with life-threatening features may require synchronized DC cardioversion and IV amiodarone if shocks are unsuccessful.

Answer 111

Atrial flutter is caused by a re-entrant rhythm in the atria, where electrical signals circulate in a self-perpetuating loop.

Answer 112

The atrial rate is usually around 300 beats per minute.

Answer 113

Atrial flutter gives a sawtooth appearance on the ECG, with repeated P waves at around 300 per minute and narrow complex tachycardia.

Answer 114

The signal may not enter the ventricles on every lap, often resulting in 2:1 conduction, giving a ventricular rate of about 150 beats per minute.

Answer 115

The conduction ratios may also be 3:1, 4:1, or variable.

Answer 116

Treatment includes anticoagulation based on the CHA2DS2-VASc score and radiofrequency ablation of the re-entrant rhythm as a potential permanent solution.

Answer 117

The QT interval is the duration from the start of the QRS complex to the end of the T wave.

Answer 118

The QTc estimates the QT interval if the heart rate were 60 beats per minute.

Answer 119

More than 440 milliseconds.

Answer 120

More than 460 milliseconds.

Answer 121

Prolonged repolarisation of the heart muscle cells (myocytes) after contraction

Answer 122

Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.

Answer 123

A type of polymorphic ventricular tachycardia characterized by a twisting appearance of the QRS complex on ECG.

Answer 124

It can be caused by prolonged QT intervals, leading to recurrent contractions without normal repolarisation.

Answer 125

Long QT syndrome Certain medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics) Electrolyte imbalances (e.g., hypokalaemia/hypomagnesemia/ hypocalcaemia)

Answer 126

Stop medications prolonging QT Correct electrolyte disturbances Consider beta-blockers (not sotalol) or devices like pacemakers.

Answer 127

Correct underlying causes Magnesium infusion Defibrillate if ventricular tachycardia occurs.

Answer 128

Premature ventricular beats caused by random electrical discharges outside the atria, often presenting as extra or missed beats.

Answer 129

They are more common in patients with pre-existing heart conditions, such as ischaemic heart disease or heart failure. common in all ages and in healthy people

Answer 130

As isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.

Answer 131

A rhythm where every other beat is a ventricular ectopic, alternating with a normal beat.

Answer 132

Reassurance and no treatment for infrequent ectopics.

Answer 133

In patients with underlying heart disease, frequent or concerning symptoms, or a family history of heart disease or sudden death.

Answer 134

Beta blockers.

Answer 135

Mobitz type 1 (Wenckebach phenomenon) and Mobitz type 2.

Answer 136

The PR interval progressively lengthens until a P wave is not followed by a QRS complex, after which the cycle resets.

Answer 137

Mobitz type 2 has intermittent failure of conduction with absent QRS complexes following P waves, while the PR interval remains normal.

Answer 138

There are two P waves for each QRS complex, with every other P wave not stimulating a QRS complex., difficult to tell whether this is mobitz type 1 or 2

Answer 139

There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block).

Answer 140

Also known as complete heart block, there is no observable relationship between P waves and QRS complexes, with a significant risk of asystole.

Answer 141

It is marked by delayed conduction through the atrioventricular node, with every P wave followed by a QRS complex. The PR interval is greater than 0.2 seconds (5 small squares or 1 big square) on ECG.

Answer 142

In second-degree heart block, some atrial impulses do not reach the ventricles, resulting in P waves that are not followed by QRS complexes.

Answer 143

Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. It can be normal in fit patients without symptoms. Common causes include medications (e.g., beta blockers), heart block, and sick sinus syndrome.

Answer 144

Sick sinus syndrome is a condition that causes dysfunction in the sinoatrial node, often due to idiopathic degenerative fibrosis. It can result in sinus bradycardia, sinus arrhythmias, and prolonged pauses.

Answer 145

Asystole refers to the absence of electrical activity in the heart, resulting in cardiac arrest. There is a risk of asystole in conditions like: Mobitz type 2 Third-degree heart block Previous asystole Ventricular pauses longer than 3 seconds.

Answer 146

Management includes --> intravenous atropine (first line), --> inotropes (e.g., isoprenaline or adrenaline) --> temporary cardiac pacing, and when available --> permanent implantable pacemaker.

Answer 147

Temporary cardiac pacing can be done via transcutaneous pacing (using pads on the chest) or transvenous pacing (using a catheter to stimulate the heart directly).

Answer 148

Atropine is an antimuscarinic medication that inhibits the parasympathetic nervous system, leading to side effects such as pupil dilation, dry mouth, urinary retention, and constipation.

Answer 149

AF is a condition where the electrical activity in the atria becomes disorganised, leading to fibrillation (random muscle twitching) of the atria and an irregularly irregular pulse.

Answer 150

Irregularly irregular ventricular contractions Tachycardia (fast heart rate) Heart failure due to impaired ventricular filling Increased risk of stroke

Answer 151

The sinoatrial node normally produces organised electrical activity that coordinates atrial contraction.

Answer 152

Chaotic atrial electrical activity overrides the sinoatrial node's regular impulses, passing to the ventricles and causing irregularly irregular ventricular contraction.

Answer 153

Uncoordinated atrial activity may cause blood stagnation and thrombus formation in the atria. A thrombus in the left atrium can travel to the brain, causing an ischaemic stroke.

Answer 154

The mnemonic "SMITH" helps remember common causes of atrial fibrillation: Sepsis Mitral valve pathology Ischaemic heart disease Thyrotoxicosis Hypertension.

Answer 155

Alcohol and caffeine are lifestyle causes of atrial fibrillation.

Answer 156

Patients may be asymptomatic or present with palpitations, shortness of breath, dizziness, syncope, or symptoms related to associated conditions like stroke, sepsis, or thyrotoxicosis. The key examination finding is an irregularly irregular pulse.

Answer 157

Atrial fibrillation and ventricular ectopics.

Answer 158

Ventricular ectopics tend to disappear when the heart rate increases, such as during exercise, unlike atrial fibrillation.

Answer 159

ECG findings in atrial fibrillation include absent P waves, narrow QRS complex tachycardia, and an irregularly irregular ventricular rhythm.

Answer 160

An echocardiogram may be required when investigating valvular heart disease, heart failure, or before planning cardioversion.

Answer 161

Paroxysmal atrial fibrillation refers to episodes of AF that reoccur and spontaneously resolve back to sinus rhythm, lasting between 30 seconds and 48 hours.

Answer 162

Further investigations include a 24-hour ambulatory ECG (Holter monitor) or a cardiac event recorder lasting 1-2 weeks.

Answer 163

Valvular atrial fibrillation occurs with significant mitral stenosis or a mechanical heart valve, where the valvular pathology has likely caused the AF.

Answer 164

NICE 2021 recommends referral to a cardiologist for further assessment and management of patients with valvular atrial fibrillation.

Answer 165

1. Rate or rhythm control 2. Anticoagulation to prevent strokes

Answer 166

A beta blocker, such as atenolol or bisoprolol, is the first-line treatment for rate control.

Answer 167

Beta blockers (first-line, e.g., atenolol, bisoprolol) Calcium-channel blockers (e.g., diltiazem, verapamil) Digoxin (in sedentary patients)

Answer 168

Rhythm control is preferred when there is: A reversible cause New onset AF (<48 hours) AF causing heart failure Symptoms despite rate control

Answer 169

Cardioversion: Immediate or delayed Pharmacological agents: Flecainide, amiodarone Electrical cardioversion

Answer 170

To prevent stroke by reducing the risk of dislodging a thrombus formed in the atria.

Answer 171

Immediate Cardioversion: Used if AF is present for <48 hours or causes life-threatening hemodynamic instability. Delayed Cardioversion: Used if AF has been present for >48 hours and the patient is stable; requires anticoagulation for at least 3 weeks prior to reduce stroke risk.

Answer 172

Pharmacological Cardioversion Options: Flecainide Amiodarone (especially in structural heart disease) Electrical Cardioversion: Uses a defibrillator to deliver controlled shocks, usually done under sedation or general anesthesia.

Answer 173

Beta blockers (first-line) Dronedarone (second-line for maintaining normal rhythm) Amiodarone (useful in patients with heart failure or left ventricular dysfunction)

Answer 174

The "pill-in-the-pocket" (Flecainide) approach allows patients to take medication to terminate atrial fibrillation symptoms as they arise. This method is suitable for patients with infrequent episodes and no structural heart disease, who can recognize AF signs and when to take treatment. Flecainide is commonly used for this approach, but it carries the risk of converting AF to atrial flutter with rapid ventricular rates.

Answer 175

Patients with paroxysmal atrial fibrillation should be anticoagulated based on their CHA₂DS₂-VASc score, similar to those with permanent atrial fibrillation.

Answer 176

Left atrial ablation - A catheter-based procedure to destroy abnormal electrical pathways in the left atrium using radiofrequency energy. Atrioventricular node ablation - Destroys the connection between the atria and ventricles, requiring a permanent pacemaker to manage ventricular contraction.

Answer 177

Left atrial ablation is performed under general anaesthesia or sedation in a catheter laboratory. A catheter is inserted via a femoral vein and guided to the heart, where it punctures the septum into the left atrium. The operator identifies abnormal electrical pathways and applies radiofrequency ablation to create scar tissue that disrupts the arrhythmia.

Answer 178

After atrioventricular node ablation, a permanent pacemaker is needed to control ventricular contractions since the irregular electrical activity from the atria cannot reach the ventricles. Anticoagulation remains necessary to prevent strokes.

Answer 179

Anticoagulation is essential because uncontrolled atrial activity can lead to blood stagnation in the left atrium, resulting in thrombus formation. This thrombus can mobilize and cause an ischaemic stroke by traveling to the brain. Anticoagulation reduces the risk of stroke in these patients from about 5% annually to 1-2% by interfering with the clotting cascade, lowering stroke risk by approximately two-thirds.

Answer 180

Anticoagulation treatment carries a risk of serious bleeding ranging from 2.5% to 8% per year, depending on individual factors.

Answer 181

The NICE guidelines recommend using direct-acting oral anticoagulants (DOACs) as the first-line treatment. Warfarin is recommended as a second-line option if DOACs are contraindicated.

Answer 182

DOACs do not require INR monitoring, making them suitable for most patients, including those with cancer. They have a half-life of 6-14 hours. Common DOACs include apixaban, edoxaban, rivaroxaban (all direct factor Xa inhibitors), and dabigatran (a direct thrombin inhibitor). Apixaban and dabigatran are taken twice daily, while edoxaban and rivaroxaban are taken once daily.

Answer 183

DOACs require no monitoring, have no time in therapeutic range issues (with good adherence), and fewer major interactions. They are equally or slightly more effective than warfarin in preventing strokes in atrial fibrillation and have an equal or slightly lower risk of bleeding.

Answer 184

DOACs are commonly indicated for stroke prevention in atrial fibrillation, treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE), and prophylaxis of venous thromboembolism after hip or knee replacements.

Answer 185

Warfarin is a vitamin K antagonist that blocks vitamin K, essential for the functioning of several clotting factors. This action prolongs the prothrombin time, increasing the time it takes for blood to clot.

Answer 186

The effectiveness of warfarin is monitored using the INR (international normalized ratio), which compares the patient's prothrombin time to that of a healthy adult. The target INR for atrial fibrillation (AF) is between 2 and 3.

Answer 187

INR levels can be affected by medications influencing the cytochrome P450 system, dietary changes, particularly those involving vitamin K-rich foods, and the consumption of substances like cranberry juice and alcohol.

Answer 188

TTR indicates the percentage of time the INR is in the target range. Low INR increases stroke risk; high INR increases bleeding risk. Frequent monitoring is necessary for dose adjustments.

Answer 189

Warfarin metabolism involves the cytochrome P450 system, meaning that medications affecting this system (e.g., certain antibiotics) can alter INR levels, requiring close monitoring and dose adjustments.

Answer 190

Foods high in vitamin K (like leafy greens) and substances that affect the P450 system (like cranberry juice and alcohol) can influence INR levels, necessitating careful dietary management.

Answer 191

The effects of warfarin can be reversed using vitamin K in cases of significantly high INR or major bleeding.

Answer 192

Warfarin has a half-life of 1-3 days, affecting the duration of its anticoagulant effect.

Answer 193

CHA2DS2-VASc is an acronym for risk factors: Congestive heart failure Hypertension Age > 75 (2 points) Diabetes Stroke or TIA (2 points) Vascular disease Age 65-74 and Sex (female).

Answer 194

A score of 0 indicates no anticoagulation; a score of 1 suggests considering anticoagulation in men (women automatically score 1); a score of 2 or more warrants offering anticoagulation.

Answer 195

Aspirin alone is not recommended for stroke prevention in atrial fibrillation; it was an option in the past but is now considered ineffective compared to anticoagulants.

Answer 196

O - Older age (≥75), R - Renal impairment (GFR < 60), B - Bleeding history (GI or intracranial), I - Iron deficiency (low hemoglobin/hematocrit), T - Taking antiplatelet medication.

Answer 197

Left atrial appendage occlusion is a procedure for patients with contraindications to anticoagulation and a high stroke risk, preventing blood from entering the left atrial appendage to reduce thrombus formation.

Answer 198

SVT refers to a fast heart rate caused by abnormal electrical signals from above the ventricles.

Answer 199

SVT is caused by the electrical signal re-entering the atria from the ventricles, creating a self-perpetuating electrical loop.

Answer 200

SVT is characterized as "narrow complex" tachycardia, with a QRS complex duration of less than 0.12 seconds.

Answer 201

Paroxysmal SVT describes recurrent episodes of SVT that remit and return over time in the same patient.

Answer 202

Atrioventricular nodal re-entrant tachycardia Atrioventricular re-entrant tachycardia Atrial tachycardia

Answer 203

It is a type of SVT where the re-entry point is back through the atrioventricular node, and it is the most common type of SVT.

Answer 204

This type involves an accessory pathway that allows electrical signals to re-enter the atria from the ventricles, often associated with Wolff-Parkinson-White syndrome.

Answer 205

Atrial tachycardia occurs when the electrical signal originates in the atria, not from re-entering signals from the ventricles, indicating abnormally generated electrical activity.

Answer 206

--> Atrioventricular nodal re-entrant tachycardia: Re-entry through the AV node; most common type. --> Atrioventricular re-entrant tachycardia: Involves an accessory pathway allowing signals to re-enter from the ventricles; associated with Wolff-Parkinson-White syndrome. --> Atrial tachycardia: Abnormal electrical activity originates in the atria, not from re-entry from the ventricles.

Answer 207

Wolff-Parkinson-White (WPW) syndrome is caused by an extra electrical pathway (Bundle of Kent) connecting the atria and ventricles, bypassing the AV node. It may cause episodes of SVT.

Answer 208

ECG Changes: Short PR interval (<0.12 seconds) Wide QRS complex (>0.12 seconds) Delta wave (slurred upstroke in QRS) Treatment: The definitive treatment is radiofrequency ablation of the accessory pathway.

Answer 209

Vagal manoeuvres Adenosine Verapamil or a beta blocker Synchronized DC cardioversion Note: Continuous ECG monitoring is essential during management.

Answer 210

Life-Threatening Features: Use synchronized DC cardioversion under sedation or general anesthesia. If initial shocks fail, add IV adenosine/amiodarone. Wolff-Parkinson-White Syndrome: Avoid adenosine, verapamil, or beta blockers. Use procainamide or electrical cardioversion if unstable. as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms

Answer 211

Valsalva Maneuver: Increases intrathoracic pressure by having the patient blow hard against resistance (e.g., into a 10ml syringe for 10-15 seconds). Carotid Sinus Massage: Stimulates baroreceptors by massaging one side of the neck (not both) but is contraindicated in carotid artery stenosis. Diving Reflex: Involves briefly submerging the patient's face in cold water to activate the reflex.

Answer 212

Adenosine slows cardiac conduction through the AV node, effectively "resetting" it to sinus rhythm. Its half-life is under 10 seconds, requiring rapid IV bolus administration. Common side effects include brief asystole or bradycardia. Contraindications: Asthma COPD Heart failure Heart block Severe hypotension Potential atrial arrhythmia with pre-excitation Dosing: Start with 6 mg, then 12 mg, and finally 18 mg as needed.

Answer 213

Synchronized DC cardioversion delivers an electric shock to the heart to restore normal sinus rhythm, timed with the R wave on the ECG. It is used in patients with a pulse to avoid shocks during the T wave, which can cause ventricular fibrillation. In cases of pulseless ventricular tachycardia or ventricular fibrillation, synchronization is not necessary

Answer 214

Management options for recurrent SVT include long-term medication (e.g., beta blockers, calcium channel blockers, or amiodarone) and radiofrequency ablation to prevent further episodes.

Answer 215

Radiofrequency ablation involves inserting a catheter to identify and burn abnormal electrical pathways in the heart, creating scar tissue that prevents conduction. It can permanently resolve arrhythmias such as atrial fibrillation, atrial flutter, supraventricular tachycardias, and Wolff-Parkinson-White syndrome.

Answer 216

Demographic: Male, over 60 Immobilisation: Hospitalisation (10x risk), long-haul flights (2x risk) Inflammation: Vasculitis, sepsis Malignancy: 20% of DVT/PE patients have cancer Medication: Chemotherapy, HRT, OCP Obesity: BMI >30 (2-3x risk) Pregnancy: 5x risk due to prothrombotic state Previous VTE Recent surgery/trauma Smoking, varicose veins

Answer 217

Virchow's triad includes three changes contributing to venous thrombosis: Hypercoagulability: Hereditary (e.g., factor V Leiden) and acquired (e.g., malignancy, pregnancy, OCP) causes. Stasis of blood: Immobilisation (e.g., casts, long-haul flights). Endothelial changes: Dysfunction (e.g., hypertension, smoking) or damage (e.g., trauma, central lines).

Answer 218

--> Unilateral leg pain (lower leg, cramping, or throbbing) --> Swelling, mostly in the calf (can extend to the entire leg in extensive cases) --> Pitting oedema --> Skin changes: erythema, cyanosis, or pallor --> Distended superficial veins (in ~17% of cases) --> Increased leg temperature and tenderness over deep veins --> Significant calf size difference (>3cm) DVT often coexists with pulmonary embolism in 40-50% of patients.

Answer 219

Two-level DVT Wells Score: Active cancer (1 point) Paralysis or immobilization (1) Recently bedridden or major surgery (1) Localized tenderness (1) Entire leg swollen (1) Calf swelling >3 cm (1) Pitting edema in symptomatic leg (1) Collateral veins (1) Previous DVT (1) Alternative diagnosis as likely as DVT (-2) Interpretation: Score ≥2: DVT likely; Score ≤1: DVT unlikely. Management: If DVT likely (≥2): Ultrasound within 4 hours. Positive: initiate anticoagulation (DOACs preferred). Negative: perform D-dimer; negative results suggest alternative diagnoses. If ultrasound delayed >4 hours, give interim anticoagulation (low-molecular weight heparin) until the scan. If D-dimer is positive after negative ultrasound, stop anticoagulation and repeat ultrasound in 6-8 days. If DVT unlikely (≤1): D-dimer test within 4 hours. If negative, consider alternatives. If positive, ultrasound within 4 hours; if delayed, initiate anticoagulation. D-dimer Testing: NICE recommends point-of-care or lab tests with age-adjusted cut-offs for patients >50 years.

Answer 220

Cellulitis: Cause: Staphylococci or Streptococci infection. Risk Factors: Diabetes, lymphoedema, IV drug use, chronic venous insufficiency. Similarities: Unilateral erythema, swelling, pain, warmth. Differences: Often has fever and raised inflammatory markers. Superficial Thrombophlebitis: Cause: Inflammatory response in a superficial vein. Similarities: Pain and erythema. Differences: Oedema and erythema are localized, with a palpable thrombus. Dependent Oedema: Similarities: Pitting oedema may occur. Differences: Usually bilateral and worse at day's end. Liver Cirrhosis/Nephrotic Syndrome: Similarities: Common leg oedema (hypoalbuminaemia) and possible erythema. Differences: Symptoms are typically bilateral. Ruptured Baker's Cyst: History: Swelling behind the knee. Similarities: Pain in the calf. Differences: Bruising below the medial malleolus (crescent sign). Trauma: Includes: Leg fractures, calf haematoma. Note: Should be evident from the history.

Answer 221

Anticoagulant Therapy: DOACs (apixaban, rivaroxaban) are preferred first-line. Active Cancer: Use a DOAC unless contraindicated. Renal Impairment: Use LMWH or unfractionated heparin if severe. Antiphospholipid Syndrome: LMWH followed by a VKA is recommended. Duration: Minimum 3 months; 6 months for unprovoked VTE. The decision to continue depends on VTE recurrence risk and bleeding risk (assessed with the HAS-BLED score).

Answer 222

Renal Impairment: Use LMWH or unfractionated heparin if severe. Antiphospholipid Syndrome: LMWH followed by a VKA is recommended.

Answer 223

Leg ulcers are slow-healing skin breaks that can worsen over time. The common types include: Venous Ulcers: Caused by blood pooling due to venous insufficiency. Arterial Ulcers: Result from insufficient blood supply due to peripheral arterial disease. Mixed Ulcers: Involve both arterial and venous pathology.

Answer 224

Typically, arterial ulcers: Occur distally, affecting the toes or dorsum of the foot Are associated with peripheral arterial disease, with absent pulses, pallor and intermittent claudication Are smaller and deeper than venous ulcers Have well defined borders Have a “punched-out” appearance Are pale colour due to poor blood supply Are less likely to bleed Are painful Have pain worse at night (when lying horizontally) Have pain is worse on elevating and improved by lowering the leg (gravity helps the circulation) Typically, venous ulcers: Occur in the gaiter area (between the top of the foot and bottom of the calf muscle) Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis Occur after a minor injury to the leg Are larger and more superficial than arterial ulcers Have irregular, gently sloping border Are more likely to bleed Are less painful than arterial ulcers Have pain relieved by elevation and worse on lowering the leg

Answer 225

Ankle-Brachial Pressure Index (ABPI): Assesses arterial disease in both types of ulcers. Blood Tests: Full Blood Count (FBC) and C-reactive protein (CRP) to check for infection. HbA1c for diabetes, FBC for anaemia, and albumin for malnutrition to assess co-morbidities. Charcoal Swabs: Useful for identifying the causative organism if infection is suspected. Skin Biopsy: Required if skin cancer (e.g., squamous cell carcinoma) is suspected; involves a two-week wait referral to dermatology.

Answer 226

Risk factor modification - smoking, HTN, diabetes, hyperlipidemia, regular exercise Optimise blood flow - revascularize via stenting, bypass or angioplasty Antiplatelets (aspirin and clopidogrel) and Statins manage atherosclerosis Debridement - remove necrotic tissue Dressings - protects against infection Topical/systemic antibiotics

Answer 227

Referral to Vascular Surgery: If mixed or arterial ulcers are suspected. Tissue Viability/Specialist Clinics: For complex or non-healing ulcers. Dermatology Referral: If alternative diagnoses like skin cancer are suspected. Pain Clinics: For difficult pain management. Diabetic Ulcer Services: For patients with diabetic ulcers.

Answer 228

--> Referral Needs: Vascular surgery for mixed/arterial ulcers. Tissue viability clinics for complex ulcers. Dermatology for suspected skin cancer. Pain clinics for pain management. Diabetic ulcer services for diabetic patients. --> Wound Care: Clean and debride the wound. Dress the wound appropriately. --> Compression Therapy: After excluding arterial disease (using ABPI). --> Medications: Pentoxifylline for healing (not licensed). Antibiotics for infection. Analgesia (avoid NSAIDs).

Answer 229

Osteomyelitis

Answer 230

Cardiac arrest is when the heart stops beating, leading to the absence of cardiac contractions. While there may be pulseless electrical activity (PEA), irreversible brain damage can occur in less than 5 minutes. Performing CPR aims to maintain cardiac output through chest compressions, ultimately seeking return of spontaneous circulation (ROSC) when the heart resumes beating.

Answer 231

The causes of reversible cardiac arrest include: H's: Hypoxia Hypovolaemia Hypokalaemia Hyperkalaemia Hypothermia T's: Tension pneumothorax Tamponade (cardiac) Toxins Thrombosis

Answer 232

30 chest compressions followed by 2 breaths.

Answer 233

One pad under the right clavicle and the other at the apex beat.

Answer 234

Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF).

Answer 235

After the first shock for shockable rhythms and immediately for non-shockable rhythms.

Answer 236

To help reset the heart rhythm; give 3 mg at the start of ALS

Answer 237

AHF is a life-threatening emergency characterized by the sudden onset or worsening of heart failure symptoms.

Answer 238

De-novo AHF (no prior history of heart failure) 2. Decompensated AHF (history of heart failure).

Answer 239

AHF that occurs without a background history of pre-existing heart failure.

Answer 240

AHF is usually caused by reduced cardiac output resulting from functional or structural abnormalities of the heart.

Answer 241

It is caused by increased cardiac filling pressures and myocardial dysfunction, often due to ischemia, leading to reduced cardiac output and hypoperfusion.

Answer 242

Reduced cardiac output can lead to pulmonary oedema.

Answer 243

1. Viral myopathy 2. Toxins 3. Valve dysfunction.

Answer 244

1. Acute coronary syndrome 2. Hypertensive crisis (e.g., bilateral renal artery stenosis) 3. Acute arrhythmia 4. Valvular disease.

Answer 245

It usually presents with signs of fluid congestion, weight gain, orthopnea, and breathlessness, often in patients with a history of pre-existing cardiomyopathy.

Answer 246

--> breathlessness --> Reduced excercise tolerance --> Oedema --> Fatigue

Answer 247

--> cyanosis --> tachycardia --> elevated JVP --> displaced apex beat --> chest signs: classically bibasal crackles but may also cause a wheeze --> S3 - heart sound Sometimes the presentation will be that of the underlying cause (e.g: chest pain, viral infection) Over 90% of patients with AHF have a normal or increased blood pressure (mmHg).

Answer 248

--> Blood Tests: To identify underlying abnormalities such as anaemia, abnormal electrolytes, or infection or troponin for MI. --> Chest X-ray: Findings may include pulmonary venous congestion, interstitial oedema, and cardiomegaly. ABCDE --> Echocardiogram: Used to identify pericardial effusion/ cardiac tamponade/ LV ejection fraction >50% is normal. --> B-type Natriuretic Peptide (BNP): Raised levels (>100 mg/litre) indicate myocardial damage and support the diagnosis. --> ECG - assess for ischaemia and arrhythmias

Answer 249

Sensitivity: BNP is sensitive for diagnosing heart failure; a negative result helps rule out heart failure. Specificity: BNP is not specific; elevated levels can occur in conditions other than heart failure, including: Tachycardia Sepsis Pulmonary Embolism Renal Impairment Chronic Obstructive Pulmonary Disease (COPD)

Answer 250

A: alveolar oedema (perihilar/bat-wing opacification) B: Kerley B lines (interstitial oedema) C: cardiomegaly (cardiothoracic ratio >50%) – may be difficult to assess on an AP film D: dilated upper lobe vessels E: effusions (i.e. pleural effusions – blunted costophrenic angles with meniscus sign)

Answer 251

Hospital Admission: Patients require admission, especially those with severe pulmonary oedema or cardiogenic shock, potentially to high dependency or intensive care units. Involve experienced seniors early. Mnemonic: SODIUM S – Sit Up: Helps oxygenate the lungs; reduces fluid spread. O – Oxygen: Administer for saturation < 95%; target 88-92% for COPD. D – Diuretics: IV furosemide to increase urine output and reduce fluid volume. I – IV Fluids Should Be Stopped: Avoid fluid overload. U – Underlying Causes Need Treatment: Identify and treat causes like myocardial infarction. M – Monitor Fluid Balance: Track intake/output, U&Es, and body weight. Severe Cases May Require: IV Opiates: Such as morphine (vasodilators). IV Nitrates: For severe hypertension or acute coronary syndrome. Inotropes: Dobutamine to improve cardiac output. Vasopressors: Noradrenaline to improve blood pressure. Non-Invasive Ventilation: Support breathing. Invasive Ventilation: Intubation and sedation if necessary. Key Points: Inotropes: Increase heart contractility, cardiac output, and mean arterial pressure (MAP). Vasopressors: Cause vasoconstriction, increase systemic vascular resistance, and improve MAP for better tissue perfusion.

Answer 252

Definition: Chronic heart failure refers to the clinical features of impaired heart function, specifically the left ventricle's ability to pump blood effectively. Pathophysiology: Impaired left ventricular function leads to a backlog of blood, increasing volume and pressure in the left atrium, pulmonary veins, and lungs. This can result in pulmonary oedema due to fluid leakage and inability to reabsorb excess fluid from surrounding tissues. Ejection Fraction: Normal Ejection Fraction: >50% Heart Failure with Reduced Ejection Fraction: EF < 50% Heart Failure with Preserved Ejection Fraction: Clinical features of heart failure with EF > 50%, often due to diastolic dysfunction (issues with filling during diastole).

Answer 253

Ischaemic heart disease Valvular heart disease (commonly aortic stenosis) Hypertension Arrhythmias (commonly atrial fibrillation) Cardiomyopathy

Answer 254

Breathlessness, worsened by exertion Cough, which may produce frothy white/pink sputum Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use) Paroxysmal nocturnal dyspnoea Peripheral oedema Fatigue

Answer 255

Tachycardia (raised heart rate) Tachypnoea (raised respiratory rate) Hypertension Murmurs on auscultation indicating valvular heart disease 3rd heart sound on auscultation Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck Peripheral oedema of the ankles, legs and sacrum

Answer 256

–> Clinical assessment - Hx and examination –> NT-proBNP bloods –> ECG –> Echocardiogram –> Bloods - to look for anaemia, renal function, thyroid function, liver function, lipids and diabetes –> chest X-ray and lung function tests to exclude lung pathology

Answer 257

R – Refer to cardiology A – Advise them about the condition M – Medical treatment P – Procedural or surgical interventions S – Specialist heart failures MDT input, such as the heart failure specialist nurses, for advice and support

Answer 258

A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) L – Loop diuretics (e.g., furosemide or bumetanide) additional specialist treatments - SGLT2 inhibitor (e.g., dapagliflozin) Sacubitril with valsartan (brand name Entresto) - for HF-rEF patients wo are symptomatic on ACEi/ARB Ivabradine - if on all 3 initial medications, HR >75 & Left Ventricular fraction <35% Hydralazine with a nitrate Digoxin

Answer 259

–> can treat underlying valvular heart disease –> Implantable cardioverter defibrillators - for patients who have had ventricular tachycardia or V fib before –> Cardiac resynchronization therapy CRT - severe heart failure with EF < 35%, involves bi-ventricular pacemakers - leads to the right atrium and both ventricles - aim to synchronise the contractions –> heart transplant in severe disease

Answer 260

Definition: Cardiomyopathy refers to disorders of the heart muscle. HOCM is a condition where the left ventricle becomes hypertrophic, leading to thickening of the muscle. Key Features: Asymmetric thickening, particularly affecting the septum, causes left ventricular outflow tract (LVOT) obstruction. Associated with an increased risk of: Heart failure Myocardial infarction Arrhythmias Sudden cardiac death (often during exertion) Epidemiology: Autosomal dominant genetic condition caused by defects in sarcomere protein genes. Prevalence: Approximately 1 in 500 people.

Answer 261

--> Presentation: Most patients are asymptomatic. Non-specific symptoms may occur during exertion: --> Shortness of breath --> Fatigue --> Dizziness --> Syncope --> Chest pain --> Palpitations Severe cases may present with symptoms of heart failure: --> Cough -->Shortness of breath -->Orthopnoea --> Paroxysmal nocturnal dyspnoea --> Oedema --> Family History: Important to ask about a family history of heart disease and sudden death. HOCM can occur in patients without a family history due to de novo mutations. --> Examination Findings: --> Ejection systolic murmur at the lower left sternal border (louder with Valsalva manoeuvre) --> Fourth heart sound --> Thrill at the lower left sternal border Possible signs of: --> Atrial fibrillation (irregularly irregular pulse) --> Mitral regurgitation (high-pitched, pan-systolic murmur) --> Heart failure

Answer 262

ECG: May show left ventricular hypertrophy. Chest X-ray: Usually normal; may show signs of pulmonary oedema if heart failure is present. Echocardiogram/Cardiac MRI: Used to establish the diagnosis. Genetic Testing: May be considered to identify affected genes.

Answer 263

Management Options: ABCDE Amiodarone Beta-blockers Cardioverter defibrillation Dual chamber pacemaker Endocarditis prophylaxis Heart transplant Patient Advice: Avoid intense exercise, heavy lifting, and dehydration. ACE inhibitors and nitrates are avoided as they can worsen LVOT obstruction. Genetic counselling offered; relatives may be tested.

Answer 264

Outcomes: Minimal symptoms with a normal lifespan (most patients) Complications: Arrhythmias (e.g., atrial fibrillation) Mitral regurgitation Heart failure Sudden cardiac death

Answer 265

Dilated Cardiomyopathy: Heart muscle becomes thin and dilated; may be genetic or secondary to conditions like myocarditis. Alcohol-Induced Cardiomyopathy: A type of dilated cardiomyopathy caused by long-term alcohol use. Restrictive Cardiomyopathy: Heart muscle becomes rigid and stiff, impairing ventricular filling during diastole. Arrhythmogenic Cardiomyopathy: Genetic condition where heart muscle is replaced with fibrofatty tissue, leading to ventricular arrhythmias; a notable cause of sudden cardiac death in young people. Takotsubo Cardiomyopathy: Rapid onset of left ventricular dysfunction often following severe emotional stress (known as "broken heart syndrome"); tends to resolve spontaneously.

Answer 266

Definition: PAD is the narrowing of arteries supplying the limbs, usually affecting the lower limbs, which reduces blood supply. Intermittent Claudication: A symptom of ischaemia in a limb. Occurs during exertion and is relieved by rest. Typically presents as crampy, achy pain in the calf, thigh, or buttock, with muscle fatigue when walking beyond a certain intensity. Critical Limb Ischaemia: End-stage PAD with inadequate blood supply for normal function at rest. Features: pain at rest, non-healing ulcers, gangrene. Pain is worse at night when the leg is raised. Acute Limb Ischaemia: Rapid onset of ischaemia due to a thrombus blocking arterial supply. Similar to a thrombus in coronary artery leading to myocardial infarction.

Answer 267

A symptom of ischaemia in a limb. Occurs during exertion and is relieved by rest. Typically presents as crampy, achy pain in the calf, thigh, or buttock, with muscle fatigue when walking beyond a certain intensity.

Answer 268

End-stage PAD with inadequate blood supply for normal function at rest. Features: pain at rest, non-healing ulcers, gangrene. Pain is worse at night when the leg is raised.

Answer 269

Rapid onset of ischaemia due to a thrombus blocking arterial supply. Similar to a thrombus in coronary artery leading to myocardial infarction.

Answer 270

Definition: Atherosclerosis is the hardening of arteries caused by the accumulation of atheromas (fatty deposits) and chronic inflammation in medium and large arteries. Athero-: Refers to soft or porridge-like. -Sclerosis: Refers to hardening or stiffening of blood vessel walls. Pathophysiology: Chronic inflammation activates the immune system in the artery wall. Lipids are deposited, leading to fibrous atheromatous plaque development. Effects of Atherosclerosis: Stiffening of Artery Walls: Leads to hypertension (raised blood pressure) and increased strain on the heart. Stenosis: Narrowing of arteries reduces blood flow, potentially causing conditions like angina. Plaque Rupture: Can result in thrombus formation, blocking distal vessels and causing ischaemia (e.g., in acute coronary syndrome).

Answer 271

Non-Modifiable Risk Factors (Cannot be changed): --> Older Age --> Family History --> Male Gender. --> Modifiable Risk Factors (Can be changed): --> Smoking --> Alcohol --> Poor Diet --> Low Exercise/Sedentary Lifestyle --> Obesity --> Poor Sleep --> Stress

Answer 272

The following medical co-morbidities increase the risk of atherosclerosis and should be carefully managed: --> Diabetes: Hyperglycemia can damage blood vessels and accelerate atherosclerosis. --> Hypertension: Elevated blood pressure contributes to vascular damage and plaque formation. --> Chronic Kidney Disease: Impaired kidney function can lead to fluid and electrolyte imbalances that affect heart health. --> Inflammatory Conditions: Conditions such as rheumatoid arthritis can increase systemic inflammation, promoting atherosclerosis. --> Atypical Antipsychotic Medications: These medications can cause weight gain and metabolic syndrome, increasing cardiovascular risk.

Answer 273

--> Angina: Chest pain due to reduced blood flow to the heart muscle. --> Myocardial Infarction: Heart attack caused by complete blockage of blood flow to a part of the heart. --> Transient Ischaemic Attack (TIA): Temporary disruption of blood flow to the brain, resulting in stroke-like symptoms that resolve within 24 hours. --> Stroke: Permanent damage due to prolonged lack of blood flow to the brain. Peripheral Arterial Disease (PAD): Narrowing of arteries supplying the limbs, leading to claudication and critical limb ischaemia. --> Chronic Mesenteric Ischaemia: Insufficient blood flow to the intestines, causing abdominal pain and weight loss.

Answer 274

Intermittent claudication is a symptom of peripheral arterial disease characterised by: Description: Crampy pain that occurs predictably after walking a certain distance. Location: Most commonly in the calf muscles, but can also affect the thighs and buttocks. Relief: Pain disappears after stopping and resting.

Answer 275

The features of acute limb ischaemia can be remembered using the “6 P’s” mnemonic: Pain Pallor Pulseless Paralysis Paraesthesia (abnormal sensation or “pins and needles”) Perishing cold

Answer 276

Leriche syndrome occurs due to occlusion in the distal aorta or proximal common iliac artery, presenting with a clinical triad of: Thigh/buttock claudication Absent femoral pulses Male impotence

Answer 277

Risk Factors: Tar staining on the fingers Xanthomata (yellow cholesterol deposits on the skin) Signs of Cardiovascular Disease: Missing limbs or digits after previous amputations Midline sternotomy scar (previous CABG) Scar on the inner calf for saphenous vein harvesting (previous CABG) Focal weakness suggestive of a previous stroke

Answer 278

--> Radial --> Brachial --> Carotid --> Abdominal aorta --> Femoral --> Popliteal --> Posterior tibial --> Dorsalis pedis

Answer 279

Skin pallor Cyanosis Dependent rubor (deep red color when the limb is lower) Muscle wasting Hair loss Ulcers Poor wound healing Gangrene (dark red/black color change in the skin)

Answer 280

Reduced skin temperature Reduced sensation Prolonged capillary refill time (more than 2 seconds) Changes during Buerger’s test

Answer 281

Buerger’s test is used to assess for peripheral arterial disease (PAD) in the leg. It consists of two parts that evaluate the adequacy of blood supply to the legs when subjected to gravitational changes.

Answer 282

In the first part, the patient lies supine, and the legs are lifted to an angle of 45 degrees at the hip for 1-2 minutes. Pallor indicates inadequate arterial supply to overcome gravity, suggesting peripheral arterial disease.

Answer 283

In the second part, the patient is seated with legs hanging over the side of the bed. Blood returns to the legs due to gravity: In a healthy patient, the legs remain a normal pink color. In a patient with PAD, the legs initially turn blue due to deoxygenated blood from ischaemic tissue, then dark red due to vasodilation in response to anaerobic respiration waste products.

Answer 284

Rubor refers to the dark red color observed in the legs of a patient with peripheral arterial disease after they have been hanging down, indicating a response to ischaemia and vasodilation.

Answer 285

--> Ankle-Brachial Pressure Index (ABPI) --> Duplex ultrasound (assessing speed and volume of blood flow) --> Angiography (CT or MRI using contrast to highlight arterial circulation)

Answer 286

--> ABPI measures the ratio of systolic blood pressure (SBP) in the ankle to the systolic blood pressure in the arm, providing an assessment of blood flow to the lower limbs.

Answer 287

ABPI is measured manually using a Doppler probe. For example, if the ankle SBP is 80 mmHg and the arm SBP is 100 mmHg, the ABPI is calculated as 0.8 (80/100).

Answer 288

An ABPI of 0.9 to 1.3 is considered normal.

Answer 289

An ABPI of 0.6 to 0.9 indicates mild peripheral arterial disease.

Answer 290

An ABPI of 0.3 to 0.6 indicates moderate to severe peripheral arterial disease.

Answer 291

An ABPI of less than 0.3 indicates severe disease or critical ischaemia.

Answer 292

An ABPI above 1.3 may indicate calcification of the arteries, making them difficult to compress, which is more common in diabetic patients.

Answer 293

Stopping smoking Optimising medical treatment of co-morbidities (e.g., hypertension and diabetes) Engaging in a structured exercise training program

Answer 294

The exercise training program involves regularly walking to the point of near-maximal claudication pain, then resting and repeating the process.

Answer 295

Atorvastatin 80 mg Clopidogrel 75 mg once daily (aspirin if clopidogrel is unsuitable) Naftidrofuryl oxalate (a 5-HT2 receptor antagonist that acts as a peripheral vasodilator)

Answer 296

Endovascular angioplasty and stenting Endarterectomy (removing the atheromatous plaque) Bypass surgery (using a graft to bypass the blockage)

Answer 297

Patients require urgent referral to the vascular team and analgesia to manage pain.

Answer 298

Endovascular angioplasty and stenting Endarterectomy Bypass surgery Amputation of the limb if blood supply cannot be restored

Answer 299

Patients require an urgent referral to the on-call vascular team for assessment.

Answer 300

In the clinical setting, hypertension is diagnosed with blood pressure above 140/90 mmHg. Confirmation is required with ambulatory or home readings above 135/85 mmHg.

Answer 301

Primary (essential) hypertension accounts for 90% of cases and occurs without a secondary cause. Secondary causes can be remembered with the mnemonic ROPED: R: Renal disease/ renal artery stenosis O: Obesity P: Pregnancy-induced hypertension or pre-eclampsia E: Endocrine (e.g., hyperaldosteronism) D: Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen, liquorice)

Answer 302

--> Ischaemic heart disease (angina, acute coronary syndrome) --> Cerebrovascular accident (stroke, intracranial haemorrhage) --> Vascular disease (peripheral arterial disease, aortic dissection, aortic aneurysms) --> Hypertensive retinopathy --> Hypertensive nephropathy --> Vascular dementia --> Left ventricular hypertrophy --> Heart failure

Answer 303

Genetic: RAAS gene polymorphisms. Neural: Increased sympathetic activity. Renal: Impaired sodium/water balance and RAAS abnormalities. Endocrine: RAAS dysregulation (↑ Angiotensin II, aldosterone), endothelial dysfunction (↓ Nitric oxide, ↑ Endothelin-1). Vascular: Arterial stiffness, impaired vasodilation. Lifestyle: Obesity, high salt, alcohol, inactivity.

Answer 304

Symptoms (if BP > 200/120 mmHg): Headaches, visual disturbance, seizures. Signs: Detected by measuring blood pressure; 24-hour monitoring avoids "white coat" hypertension and is more reliable for guiding treatment. Assessment: Fundoscopy: Hypertensive retinopathy. Urine dipstick: Renal disease. ECG: Left ventricular hypertrophy, ischaemic heart disease.

Answer 305

Urea and electrolytes: Check for renal disease. HbA1c: Screen for diabetes mellitus. Lipids: Assess for hyperlipidaemia. ECG: Evaluate heart function. Urine dipstick: Check for kidney involvement. 24-Hour BP Monitoring: Recommended for diagnosis. If unavailable, home readings with an automated sphygmomanometer are useful.

Answer 306

Stage 1 Hypertension: Clinic: > 140/90 Home/24-hr: > 135/85 Stage 2 Hypertension: Clinic: > 160/100 Home/24-hr: > 150/95 Stage 3 Hypertension (Severe): Clinic: > 180/120

Answer 307

Urine tests: Albumin ratio & dipstick for proteinuria/haematuria (kidney damage) Bloods: HbA1c, renal function, lipids Fundus exam: Hypertensive retinopathy ECG: Check for left ventricular hypertrophy or other cardiac abnormalities QRISK score: >10% = offer atorvastatin 20mg

Answer 308

Initial Assessment: Measure BP in both arms. If >20 mmHg difference, repeat and use the higher reading for further assessments. Take a second reading if the first is >140/90 mmHg; use the lower reading for management. Blood Pressure Monitoring: Offer ABPM for BP ≥140/90 mmHg: At least 2 measurements/hour during waking hours, average at least 14 readings. If ABPM is declined, offer HBPM: Two consecutive measurements, at least 1 minute apart, twice daily for 4-7 days (discard day 1). Treatment Thresholds: ABPM/HBPM ≥135/85 mmHg: Treat if <80 years with target organ damage, CVD, renal disease, diabetes, or 10-year cardiovascular risk ≥10%. Consider treatment for those under 60 with stage 1 hypertension and estimated 10-year risk <10%. Immediate Management: For BP ≥180/110 mmHg: consider immediate treatment. If papilloedema or retinal hemorrhages are present, refer for same-day assessment. Referral for suspected phaeochromocytoma if symptomatic (labile BP, headaches, palpitations).

Answer 309

Step 1: With Type 2 Diabetes: Start ACE inhibitor (rampiril) or Angiotensin Receptor Blocker (candersartan). Without Type 2 Diabetes: Aged <55 and not black African/African-Caribbean: Start ACEi or ARB. Aged ≥55 or black African/African-Caribbean: Start Calcium Channel Blocker (amlodipine). Step 2: With Type 2 Diabetes: Add CCB or thiazide-like diuretic (indapamide) Without Type 2 Diabetes: Add ACEi or ARB (if CCB was started) or thiazide-like diuretic. Step 3: Combine ACEi or ARB + CCB + thiazide-like diuretic. Step 4: Confirm resistant hypertension with ABPM or HBPM. Check for postural hypotension. Consider adding low-dose spironolactone if potassium level ≤4.5 mmol/L. Seek advice if BP is uncontrolled on optimal tolerated doses of 4 drugs.

Answer 310

Blood Pressure Targets: Age < 80 years: Clinic BP: <140/90 mmHg ABPM/HBPM: <135/85 mmHg Age > 80 years: Clinic BP: <150/90 mmHg ABPM/HBPM: <145/85 mmHg

Answer 311

Infective Endocarditis: Refers to infection of the endothelium (inner surface) of the heart, most commonly affecting the heart valves. Types: Acute: Rapid onset of symptoms, often caused by aggressive organisms. Subacute: Symptoms develop more gradually, usually associated with less virulent organisms. Chronic: Symptoms persist over a longer period, typically with less severe manifestations.

Answer 312

Patient Factors: --> Age > 60 years --> Male --> Intravenous Drug Use --> Intravascular Lines --> Chronic Hemodialysis. --> Immunosuppression: Conditions such as cancer or HIV, and use of immunosuppressive medications. --> Recent Dental or Surgical Procedure Cardiac Factors: --> Prior Infective Endocarditis --> Prosthetic Heart Valve or Cardiac Device: The presence of devices increases susceptibility to infection. --> Structural Heart Disease: Includes valvular heart disease or congenital heart disease.

Answer 313

Common Microbial Causes of IE: --> Staphylococcus Aureus --> Streptococcus Viridans --> Enterococci --> Streptococcus bovis: Strongly associated with ulcerative lesions in the colon (e.g., carcinoma). --> Enterococcus faecalis

Answer 314

Infective endocarditis can present acutely or subacutely with the following symptoms: Non-Specific infective symptoms: Fever (90%) with chills, anorexia, and weight loss Malaise Arthralgia Myalgia Night sweats Abdominal pain Clinical Signs: Heart murmurs (85%, usually in left-sided IE) Petechiae on extremities or mucous membranes (30%) Splinter hemorrhages (reddish-brown linear lesions on nail bed) Specific Findings: Janeway lesions (non-tender macules on palms and soles, associated with acute onset) Osler nodes (tender nodules on fingers and toes) Roth spots (haemorrhagic retinal lesions with a pale center) Complications: Congestive heart failure Systemic embolisation (e.g., embolic stroke) Pulmonary septic emboli: Most common presentation (75%) of isolated right-sided IE, may present with cough, dyspnoea, haemoptysis, or pleuritic chest pain.

Answer 315

Blood Cultures (Diagnostic): At least 3 samples from different sites over 30-60 minutes are recommended. Samples should be taken before starting any antibiotics to ensure accurate results. Echocardiogram (Diagnostic): Transthoracic Echocardiogram (TTE): Usually the first-line investigation. Transoesophageal Echocardiogram (TOE): Preferred as the first-line if available due to its higher sensitivity Additional Investigations: ECG: Identifies cardiac function issues such as heart block, conduction delay, and ischaemic changes (indicating emboli affecting coronary circulation). Chest X-Ray: Looks for pulmonary septic emboli, congestive heart failure, and abscesses; helps exclude other differentials. CT Scan (Thoracic, Abdominal, Pelvic): Useful for locating metastatic infections that may require drainage.

Answer 316

Initial blind therapy: Native valve: Amoxicillin +/- gentamicin (vancomycin + low-dose gentamicin if allergy) Prosthetic valve: vancomicin + rifampicin + gentamicin Caused by staphylococci: Native valve: Flucloxacillin (vancomycin + rifampicin if allergy) Prosthetic valve: Flucloxacillin + rifampicin + gentamicin (replace flucloxacillin with vancomycin if allergy) Caused by streptococci: Fully sensitive streptococci: Benzylpenicillin Less sensitive streptococci - Benzylpenicillin + low-dose gentamicin (Vancomycin + low-dose gentamicin if allergy) BASICALLY IF IT'S A PROSTHETIC VALVE: + rifampicin and gentamicin

Answer 317

Diagnosis Requirements: One Major plus Three Minor Criteria OR Five Minor Criteria Major Criteria: --> Persistently Positive Blood Cultures: Typical bacteria identified on multiple cultures. --> Specific Imaging Findings: Presence of vegetations seen on echocardiogram. Minor Criteria: PRoF. VIM mnemonic --> Predisposition: Examples include intravenous drug use or existing heart valve pathology. --> Fever: Body temperature above 38°C. --> Vascular Phenomena: Examples include splenic infarction, intracranial hemorrhage, and Janeway lesions. --> Immunological Phenomena: Examples include Osler’s nodes, Roth spots, and glomerulonephritis. --> Microbiological Phenomena: Positive cultures that do not meet major criteria.

Answer 318

Mesenteric ischemia is caused by a lack of blood flow through the mesenteric vessels supplying the intestines, resulting in intestinal ischemia.

Answer 319

Coeliac Artery: Supplies the foregut, including: Stomach Part of the duodenum Biliary system Liver Pancreas Spleen Superior Mesenteric Artery (SMA): Supplies the midgut, from: Distal part of the duodenum To the first half of the transverse colon Inferior Mesenteric Artery (IMA): Supplies the hindgut, from: Second half of the transverse colon To the rectum

Answer 320

Chronic mesenteric ischaemia (intestinal angina) results from the narrowing of mesenteric blood vessels due to atherosclerosis, leading to intermittent abdominal pain.

Answer 321

Central colicky abdominal pain after eating (starts ~30 minutes post-meal, lasting 1-2 hours) Weight loss (due to food avoidance to prevent pain) Abdominal bruit may be heard on auscultation

Answer 322

Increased age Family history of cardiovascular disease Smoking Diabetes Hypertension Raised cholesterol levels

Answer 323

Diagnosis is made through CT Angiography, which visualises the mesenteric blood vessels and identifies narrowing.

Answer 324

--> Reduce Modifiable Risk Factors: Stop smoking --> Secondary Prevention: Statins and antiplatelet medications --> Revascularisation: Endovascular Procedures (First-line): Percutaneous mesenteric artery stenting --> Open Surgery: Endarterectomy Re-implantation Bypass grafting

Answer 325

Acute mesenteric ischaemia is a condition caused by a rapid blockage in blood flow through the superior mesenteric artery, typically due to a thrombus or embolus.

Answer 326

It is usually caused by a thrombus (blood clot) stuck in the artery, either formed within the artery or as an embolus that has migrated from another site.

Answer 327

Atrial fibrillation is a key risk factor, as a thrombus can form in the left atrium and then mobilize, leading to blockage in the superior mesenteric artery.

Answer 328

It presents with sudden, severe non-specific abdominal pain that is disproportionate to the examination findings. Patients may develop shock, peritonitis, and sepsis.

Answer 329

Prolonged ischaemia can lead to necrosis of the bowel tissue and perforation.

Answer 330

Contrast CT is the diagnostic test of choice, allowing assessment of both the bowel and blood supply.

Answer 331

Patients typically show metabolic acidosis and elevated lactate levels due to ischaemia.

Answer 332

Remove necrotic bowel. Remove or bypass the thrombus in the blood vessel, using either open surgery or endovascular procedures.

Answer 333

Mitral regurgitation occurs when blood leaks back through the mitral valve during systole, leading to less efficient blood pumping and potential heart failure over time.

Answer 334

Causes include coronary artery disease, mitral valve prolapse, infective endocarditis, rheumatic fever, and congenital heart defects.

Answer 335

Risk factors include female sex, lower body mass, age, renal dysfunction, prior myocardial infarction, prior mitral stenosis or valve prolapse, and collagen disorders (e.g., Marfan's syndrome and ehlers danlos).

Answer 336

Most patients are asymptomatic; however, symptoms may include fatigue, shortness of breath, and edema due to left ventricle failure, arrhythmias, or pulmonary hypertension.

Answer 337

A pansystolic "blowing" murmur heard best at the apex and radiating into the axilla; S1 may be quiet, and severe MR may cause a widely split S2.

Answer 338

Diagnosis involves ECG (may show broad P wave) Chest X-ray (may show cardiomegaly enlarged left side) Echocardiography to assess the severity of regurgitation.

Answer 339

Acute management may include nitrates, diuretics, positive inotropes, and intra-aortic balloon pump support; ACE inhibitors, beta-blockers, and spironolactone may be used for heart failure. Surgery is indicated for acute severe cases.

Answer 340

Surgical repair is preferred over replacement due to lower mortality and higher survival rates; valve replacement may be considered if repair is not possible.

Answer 341

The primary cause of mitral stenosis is a history of rheumatic fever, accounting for approximately 90% of cases.

Answer 342

--> Rheumatic Fever: The primary cause, resulting from an immune-mediated inflammatory response to group A streptococcal pharyngitis, leading to damage of the mitral valve leaflets and supporting structures. --> Congenital Mitral Stenosis: Rare malformations of the mitral valve apparatus, such as parachute mitral valve, double-orifice mitral valve, and supravalvular ring. --> Calcific Mitral Stenosis: Common in elderly patients, especially women, due to calcium deposition on the mitral annulus, resulting in decreased valve mobility. --> Infective Endocarditis: Valvular destruction, scarring, or vegetation formation from infection that obstructs blood flow. --> Other Causes: Conditions such as systemic lupus erythematosus, carcinoid syndrome, and mucopolysaccharidoses may contribute to mitral valve pathology, though less frequently.

Answer 343

Obstructed Blood Flow: MS obstructs blood flow from the left atrium to the left ventricle during diastole, leading to increased left atrial pressure. Left Atrial Enlargement: The increased pressure causes left atrial enlargement, which predisposes patients to atrial fibrillation. Pulmonary Hypertension: Elevated left atrial pressure results in pulmonary venous hypertension, leading to pulmonary arterial hypertension. Right Ventricular Changes: This causes right ventricular hypertrophy and dilation, which can progress to right-sided heart failure. Impaired Cardiac Output: The reduced preload in the left ventricle impairs cardiac output, contributing to exercise intolerance.

Answer 344

--> Dyspnoea: Shortness of breath due to pulmonary venous hypertension. --> Increased Left Atrial Pressure: Leads to pulmonary venous hypertension. --> Haemoptysis: Can range from pink frothy sputum to sudden hemorrhage due to rupture of thin-walled bronchial veins. Heart Sounds: - Mid-Late Diastolic Murmur: Best heard during expiration. - Loud S1: Due to increased left atrial pressure. - Opening Snap: Indicates that mitral valve leaflets are still mobile. Low Volume Pulse: Indicative of reduced cardiac output. Malar Flush: Redness of the cheeks due to increased blood flow. Atrial Fibrillation: Secondary to increased left atrial pressure leading to left atrial enlargement. Features of Severe Mitral Stenosis: Length of Murmur Increases: The murmur duration becomes longer. Closer Opening Snap to S2: The opening snap occurs closer to the second heart sound (S2).

Answer 345

1. Echocardiography: Transthoracic Echocardiography (TTE): A valve area < 1cm² indicates significant stenosis. Transoesophageal Echocardiography (TOE): Used if TTE images are suboptimal. Helpful in identifying thrombus in the left atrium, especially in patients with atrial fibrillation. 2. ECG Signs of left atrial enlargement: Bifid P wave (P mitrale) in lead II. Broad, negative P wave in lead V1. Advanced stages may show atrial fibrillation, right ventricular hypertrophy, or signs of pulmonary hypertension. 3. Chest X-ray: Can show cardiac enlargement (specifically left atrial enlargement). Evidence of pulmonary venous congestion or pulmonary edema. Characteristic findings include straightening of the left heart border and elevation of the left main stem bronchus.

Answer 346

Patients with associated AF require anticoagulation - Warfarin for patients with moderate/severe MS Asymptomatic patients: Monitored with regular echocardiograms Symptomatic patients - Percutaneous mitral balloon valvotomy - Mitral valve surgery (commissurotomy, or valve replacement)

Answer 347

1. Atrial Fibrillation: Most common complication of MS. Increases the risk of thromboembolic events, such as stroke. 2. Pulmonary Hypertension: Elevated pulmonary artery pressure can lead to right ventricular failure and cor pulmonale. 3. Thromboembolism: Stasis of blood in the left atrium predisposes to thrombus formation, increasing the risk of systemic embolization. 4. Infective Endocarditis: Damaged mitral valve leaflets are more susceptible to infection. 5. Hemoptysis: Rupture of bronchial veins due to elevated pulmonary venous pressure may cause hemoptysis. 6. Pregnancy Complications: MS may worsen during pregnancy due to increased blood volume and cardiac output, potentially leading to maternal and fetal complications.

Answer 348

Myocarditis refers to inflammation of the myocardium and should be considered in younger patients presenting with chest pain. Causes include: Viral: Coxsackie B, HIV Bacterial: Diphtheria, clostridia Spirochaetes: Lyme disease Protozoa: Chagas' disease, toxoplasmosis Autoimmune Drugs: Doxorubicin

Answer 349

Usually young patient with acute onset Chest pain Dyspnoea Arrhythmias

Answer 350

Blood tests: ↑ Inflammatory markers (99% of cases) ↑ Cardiac enzymes ↑ BNP ECG: Tachycardia Arrhythmias ST/T wave changes (e.g. ST-segment elevation, T wave inversion)

Answer 351

treatment of underlying cause: e.g. antibiotics for bacterial infections Supportive treatment: for heart failure or arrhythmias

Answer 352

Heart failure Arrhythmia, possibly leading to sudden death Dilated cardiomyopathy (a late complication)

Answer 353

Pericardial effusion is the accumulation of excess fluid within the pericardial sac. The fluid can be: Transudate (low protein content) Exudate (associated with inflammation) Blood Pus Gas (associated with bacterial infections)

Answer 354

Pericardial effusion occurs when excess fluid fills the potential space in the pericardial cavity, creating inward pressure on the heart and making it difficult for the heart to expand during diastole. This may lead to pericardial tamponade, where the increased intra-pericardial pressure reduces cardiac output. Urgent draining required

Answer 355

Transudative effusion (increased venous pressure can reduce drainage from the pericardial cavity): --> Congestive heart failure --> Pulmonary hypertension Exudative effusion (inflammatory causes): --> Infection (e.g., tuberculosis, HIV, Coxsackievirus, Epstein–Barr virus) --> Autoimmune conditions (e.g., SLE, RA) --> Injury to the pericardium (e.g., post-MI, post-surgery) --> Uraemia --> Cancer --> Medications (e.g., methotrexate) --> Bleeding (e.g., rupture of the heart, aortic dissection)

Answer 356

Symptoms: Chest pain Shortness of breath Fullness in the chest Orthopnoea Compression of nearby structures can cause hiccups (phrenic nerve), dysphagia (oesophagus) , or hoarse voice (recurrent laryngeal nerve) Signs: Quiet heart sounds Pulsus paradoxus (an abnormally large fall in blood pressure during inspiration, notably when palpating the pulse) Hypotension Raised JVP Fever (with pericarditis) Pericardial rub (with pericarditis)

Answer 357

Echocardiogram: --> Diagnoses pericardial effusion --> Assesses the size of the effusion and its effect on heart function Fluid analysis: --> Protein content --> Bacterial culture --> Viral PCR --> Cytology and tumour markers for cancer

Answer 358

There are two components to treating a pericardial effusion: Treatment of the underlying cause (e.g., infection) Drainage of the effusion (where required) Inflammatory causes (pericarditis) may be treated with: Aspirin NSAIDs Colchicine Steroids There are two options for draining an effusion: Needle pericardiocentesis (echocardiogram guided) Surgical drainage A pericardial window is a surgical procedure where a portion of the pericardium is removed, creating a “window” or fistula, that allows fluid to drain from the pericardial cavity into the pleural cavity or the peritoneal cavity. Rarely, pericardiectomy (surgical removal of the pericardium) may be performed in recurrent cases.

Answer 359

Inflammation of the pericardium

Answer 360

The pericardium (or pericardial sac) is the membrane surrounding the heart. It has two layers with a small amount of fluid (less than 50mls) in between, providing lubrication to allow the heart to beat without generating friction.

Answer 361

The pericardial cavity is the potential space between the two layers of the pericardium. The layers usually touch each other, which is why it is called a "potential" space.

Answer 362

--> Idiopathic (no known cause) --> Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus) --> Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus, rheumatoid arthritis) --> Injury to the pericardium (e.g., after --myocardial infarction, surgery, trauma) --> Uraemia (due to renal impairment) --> Cancer --> Medications (e.g., methotrexate)

Answer 363

Pericardial effusion is the accumulation of fluid in the pericardial cavity, creating inward pressure on the heart, making it more difficult for the heart to expand during diastole (filling phase).

Answer 364

Pericardial tamponade is when the pericardial effusion becomes large enough to raise intra-pericardial pressure, compressing the heart and reducing filling during diastole. This decreases cardiac output during systole and is an emergency that requires immediate drainage.

Answer 365

Pleuritic chest pain Made worse when laying down and made better by sitting up and leaning forwards Low-grade fever Dyspnoea Non-productive cough Pericardial rub heard on auscultation

Answer 366

ECG: saddle-shaped ST elevation and PR-segment depression Bloods: CRP, ESR, FBC: Elevated inflammatory markers support diagnosis (90% sensitivity) Serum troponins: Elevated levels indicate myocardial involvement (myopericarditis) and poorer prognosis Urea: Elevated in uraemic pericarditis Imaging: Echocardiography: Mild pericardial effusion seen in 60% of patients

Answer 367

--> Myocarditis Similarities: 'Stabbing' chest pain, dyspnoea, signs of heart failure. Differences: Myocarditis alone does not show ST-elevation on ECG. If there are elevated cardiac enzymes with widespread ST-elevation, it's diagnosed as myopericarditis. --> Acute Coronary Syndromes (ACS) Similarities: Sharp chest pain, dyspnoea, may have elevated troponin levels. Differences: Pleuritic chest pain is typically different, exacerbated by inspiration and lying supine. A pericardial rub may be present. ECG is critical for diagnosis. --> Pulmonary Embolism (PE) Similarities: Sudden onset chest pain, which may be pleuritic; a pleural rub may occasionally be heard. Differences: Risk factors for PE (recent travel, immobility, surgery) differ from those for pericarditis. ECG may show tachycardia with right heart strain, not widespread ST-elevation.

Answer 368

Outpatient Management: --> The majority of patients can be managed as outpatients. --> Inpatient Management: Patients with high-risk features (e.g., fever > 38°C or elevated troponin) should be managed as inpatients. --> Treat Underlying Causes: Address any identifiable underlying cause if present. --> Viral Infection: Most cases are secondary to viral infection; thus, no specific antiviral treatment is indicated. --> Activity Restrictions: Avoid strenuous physical activity until symptoms resolve and inflammatory markers normalize. --> First-line Treatment: Use a combination of NSAIDs and colchicine for patients with acute idiopathic or viral pericarditis. Continue until symptom resolution and normalization of inflammatory markers (usually 1-2 weeks), followed by a tapering dose.

Answer 369

Pan-systolic murmur Prominent/giant V waves in the JVP Pulsatile hepatomegaly Left parasternal heave

Answer 370

Right ventricular infarction Pulmonary hypertension (e.g., COPD) Rheumatic heart disease Infective endocarditis (especially in intravenous drug users) Ebstein’s anomaly Carcinoid syndrome

Answer 371

Systolic murmurs: Aortic Stenosis (AS) Mitral Regurgitation (MR) Mnemonic: ASMR Diastolic murmurs: Aortic Regurgitation (AR) Mitral Stenosis (MS) Mnemonic: ARMS

Answer 372

The pathophysiology of shock is divided into the following groups: Septic (due to infection and systemic inflammation) Haemorrhagic (due to blood loss) Neurogenic (due to spinal cord or nerve injury) Cardiogenic (due to heart failure) Anaphylactic (due to severe allergic reaction)

Answer 373

Sepsis is an infection that triggers Systemic Inflammatory Response Syndrome (SIRS), characterized by: Body temperature < 36°C or > 38°C HR > 90 beats/min Respiratory rate > 20/min WBC > 12,000/mm³ or < 4,000/mm³ Patients with infection + 2 or more SIRS criteria are diagnosed with sepsis.

Answer 374

Severe sepsis: Sepsis with organ failure. Septic shock: Sepsis with refractory hypotension.

Answer 375

Marked immune activation with excessive cytokine release. Endothelial cell damage and neutrophil adhesion. Hallmarks: Excessive inflammation, coagulation, and fibrinolytic suppression.

Answer 376

Antibiotics: Prompt administration, broad-spectrum to cover likely pathogens. Haemodynamic stabilisation: Aggressive fluid resuscitation; aim for CVP 8-12 cm H2O, MAP > 65 mmHg. Modulate septic response: Tight glycaemic control; avoid routine steroid use.

Answer 377

Class I: < 750 mL (< 15% blood volume loss) Class II: 750-1500 mL (15-30% loss) Class III: 1500-2000 mL (30-40% loss) Class IV: > 2000 mL (> 40% loss)

Answer 378

Blood loss: < 750 mL (< 15%) Pulse rate: < 100 bpm Blood pressure: Normal Respiratory rate: 14-20 Urine output: > 30 mL/hr Symptoms: Normal

Answer 379

Blood loss: 750-1500 mL (15-30%) Pulse rate: > 100 bpm Blood pressure: Normal Respiratory rate: 20-30 Urine output: 20-30 mL/hr Symptoms: Anxious

Answer 380

Blood loss: 1500-2000 mL (30-40%) Pulse rate: > 120 bpm Blood pressure: Decreased Respiratory rate: 30-40 Urine output: 5-15 mL/hr Symptoms: Confused

Answer 381

Blood loss: > 2000 mL (> 40%) Pulse rate: > 140 bpm Blood pressure: Decreased Respiratory rate: > 35 Urine output: < 5 mL/hr Symptoms: Lethargic

Answer 382

Tension pneumothorax Spinal cord injury Myocardial contusion Cardiac tamponade

Answer 383

Maintain Hb of 7-8 g/dL in patients without risk factors for tissue hypoxia. Maintain Hb of 10 g/dL in patients with risk factors for tissue hypoxia.

Answer 384

Neurogenic shock occurs most often after a spinal cord transection, usually at a high level, resulting in an interruption of the autonomic nervous system.

Answer 385

There is decreased peripheral vascular resistance due to marked vasodilation, leading to reduced preload and cardiac output.

Answer 386

Decreased preload leads to reduced cardiac output (Starling’s law), resulting in decreased peripheral tissue perfusion and shock.

Answer 387

In neurogenic shock, peripheral vasoconstrictors are used to return vascular tone to normal, unlike many other types of shock.

Answer 388

In medical patients, the main cause of cardiogenic shock is ischaemic heart disease.

Answer 389

In trauma patients, direct myocardial trauma or contusion is more likely to cause cardiogenic shock.

Answer 390

Transthoracic echocardiography should be used to assess for pericardial fluid or direct myocardial injury.

Answer 391

Troponin levels may be measured, but they are less useful in delineating the extent of myocardial trauma than in myocardial infarction.

Answer 392

The right side of the heart is the most likely site of injury, including chamber or valve rupture.

Answer 393

Patients with cardiogenic shock and right-sided heart injury require surgery to repair defects, often needing cardiopulmonary bypass and potentially an intra-aortic balloon pump as a bridge to surgery.

Answer 394

Anaphylaxis is defined as a severe, life-threatening, generalised, or systemic hypersensitivity reaction.

Answer 395

Adrenaline is the most important drug in the treatment of anaphylaxis and should be administered as soon as possible.

Answer 396

Adrenaline can be repeated every 5 minutes if necessary during anaphylaxis.

Answer 397

The best site for IM injection is the anterolateral aspect of the middle third of the thigh.

Answer 398

Common causes of anaphylaxis include: Food (e.g., nuts, especially common in children) Drugs Venom (e.g., wasp stings)

Answer 399

Angina is primarily caused by atherosclerosis affecting the coronary arteries, which narrows the lumen and reduces blood flow to the myocardium (heart muscle).

Answer 400

The symptoms of angina are triggered during times of high demand, such as exercise, when there is an insufficient supply of blood to meet the demand.

Answer 401

Stable angina is defined as symptoms that occur only with exertion and are always relieved by rest or glyceryl trinitrate (GTN).

Answer 402

The typical symptoms of angina include constricting chest pain, which may radiate to the jaw or arms.

Answer 403

All patients with angina should have the following baseline investigations: Physical examination (heart sounds, signs of heart failure, blood pressure, and BMI) ECG (a normal ECG does not exclude stable angina) Full blood count (FBC) (to check for anaemia) Urea and electrolytes (U&Es) (required before starting an ACE inhibitor and other medications) Liver function tests (LFTs) (required before starting statins) Lipid profile Thyroid function tests (to check for hypothyroidism or hyperthyroidism) HbA1C and fasting glucose (to check for diabetes)

Answer 404

Exercise testing (e.g., walking on a treadmill) Pharmacological testing (e.g., administering dobutamine to stress the heart) Assessment methods during stress testing include: ECG Echocardiogram MRI Myocardial perfusion scan (nuclear medicine scan)

Answer 405

CT coronary angiography involves injecting contrast and taking CT images timed with heart contractions to provide a detailed view of the coronary arteries, highlighting the specific locations of any narrowing.

Answer 406

Invasive coronary angiography is performed in a catheter laboratory (cath lab). It involves: Inserting a catheter into the patient’s brachial or femoral artery. Directing it through the arterial system to the aorta and coronary arteries under x-ray guidance. Injecting contrast to visualise the coronary arteries and identify any areas of stenosis using x-ray images. This procedure is considered the gold standard for determining coronary artery disease.

Answer 407

The five principles of management for stable angina (RAMPS) are: R – Refer to cardiology A – Advise about the diagnosis, management, and when to call an ambulance M – Medical treatment P – Procedural or surgical interventions S – Secondary prevention

Answer 408

Referrals are usually sent to the Rapid Access Chest Pain Clinic (RACPC).

Answer 409

The three aims of medical management for stable angina are: Immediate symptomatic relief during episodes of angina Long-term symptomatic relief Secondary prevention of cardiovascular disease

Answer 410

Immediate symptomatic relief is achieved with sublingual glyceryl trinitrate (GTN) in the form of a spray or tablets.

Answer 411

Take GTN when symptoms start. Take a second dose after 5 minutes if symptoms remain. Take a third dose after a further 5 minutes if symptoms persist. Call an ambulance after a further 5 minutes if symptoms still remain.

Answer 412

Key side effects of GTN are headaches and dizziness, caused by vasodilation.

Answer 413

First-line options for long-term symptomatic relief include: Beta blockers (e.g., bisoprolol) Calcium-channel blockers (e.g., diltiazem or verapamil, both avoided in heart failure with reduced ejection fraction)

Answer 414

Specialist options for long-term symptomatic relief include: Long-acting nitrates (e.g., isosorbide mononitrate) Ivabradine Nicorandil Ranolazine

Answer 415

The medications for secondary prevention are: A – Aspirin 75mg once daily A – Atorvastatin 80mg once daily A – ACE inhibitor (if diabetes, hypertension, CKD, or heart failure are present) A – Already on a beta blocker for symptomatic relief

Answer 416

Syncope is defined as a transient loss of consciousness due to global cerebral hypoperfusion, characterized by: Rapid onset Short duration Spontaneous complete recovery (Note: This definition excludes other causes of collapse, such as epilepsy.)

Answer 417

--> Reflex syncope (neurally mediated) Vasovagal: triggered by emotion, pain, or stress (often called 'fainting') Situational: triggered by cough, micturition, or gastrointestinal events Carotid sinus syncope --> Orthostatic syncope Primary autonomic failure: e.g., Parkinson's disease, Lewy body dementia Secondary autonomic failure: e.g., diabetic neuropathy, amyloidosis, uraemia Drug-induced: e.g., diuretics, alcohol, vasodilators Volume depletion: e.g., haemorrhage, diarrhoea --> Cardiac syncope Arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular) Structural: e.g., valvular disease, myocardial infarction, hypertrophic obstructive cardiomyopathy Others: e.g., pulmonary embolism

Answer 418

Reflex syncope is the most common cause in all age groups, although orthostatic and cardiac causes become progressively more common in older patients.

Answer 419

Cardiovascular examination Postural blood pressure readings: A symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg, or a decrease in systolic BP < 90 mmHg is considered diagnostic. ECG for all patients Other tests depend on clinical features Patients with typical features, no postural drop, and a normal ECG do not require further investigations.

Answer 420

The guidelines recommended statins for a significant proportion of the population over the age of 60 years, particularly those with a 10-year cardiovascular disease (CVD) risk of 10% or greater, using the QRISK2 assessment tool.

Answer 421

The QRISK2 tool is used to assess the 10-year risk of CVD in patients aged ≤ 84 years. It should not be used in: Type 1 diabetics Patients with an estimated glomerular filtration rate (eGFR) < 60 ml/min and/or albuminuria Patients with a history of familial hyperlipidaemia

Answer 422

QRISK2 may underestimate CVD risk in: People treated for HIV People with serious mental health problems Those taking medications causing dyslipidaemia (e.g., antipsychotics, corticosteroids) People with autoimmune/systemic inflammatory disorders (e.g., systemic lupus erythematosus)

Answer 423

Before starting a statin, both total cholesterol and HDL levels should be checked, along with a full lipid profile (including triglycerides). The samples do not need to be fasting.

Answer 424

Familial hypercholesterolaemia should be considered if: Total cholesterol level > 7.5 mmol/L, and/or There is a personal or family history of premature coronary heart disease (an event before age 60 in the index person or first-degree relative)

Answer 425

Atorvastatin 20mg daily is the usual first line choice for lipid lowering for the majority of patients for primary and atorvastatin 80mg daily for secondary prevention

Answer 426

Statin treatment should be considered for primary prevention of CVD in all adults with type 1 diabetes who are: Older than 40 years Have had diabetes for more than 10 years Have established nephropathy Have other CVD risk factors Atorvastatin 20 mg should be offered.

Answer 427

Atorvastatin 20 mg should be offered to patients with CKD. The dose may be increased if a > 40% reduction in non-HDL cholesterol is not achieved and the eGFR > 30 ml/min. If eGFR < 30 ml/min, consult a renal specialist before increasing the dose.

Answer 428

Atorvastatin 80 mg should be offered as the first-line statin for secondary prevention in patients with CVD.

Answer 429

Patients should be followed up at 3 months with a full lipid profile. If non-HDL cholesterol has not decreased by at least 40%, concordance and lifestyle changes should be discussed. Consider increasing the atorvastatin dose up to 80 mg if necessary.

Answer 430

Diet: Total fat intake ≤ 30% of total energy intake Saturated fats ≤ 7% of total energy intake Dietary cholesterol < 300 mg/day Increase fruits, vegetables, and fish intake (including oily fish) Choose wholegrain varieties and unsalted nuts, seeds, and legumes Physical Activity: Aim for 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity aerobic activity weekly Engage in muscle-strengthening activities on 2 or more days a week Weight Management: Manage overweight patients as per relevant NICE guidance Alcohol Intake: Limit to a maximum of 14 units per week Smoking Cessation: Encourage smokers to quit.

Answer 431

Palmar xanthomas are characteristic lesions associated with hyperlipidaemia. They are often seen in remnant hyperlipidaemia and may less commonly be present in familial hypercholesterolaemia.

Answer 432

Eruptive xanthomas are due to high triglyceride levels and present as multiple red/yellow vesicles on extensor surfaces (e.g., elbows, knees). They are commonly associated with: Familial hypertriglyceridaemia Lipoprotein lipase deficiency

Answer 433

Tendon xanthoma, tuberous xanthoma, and xanthelasma are associated with familial hypercholesterolaemia and remnant hyperlipidaemia.

Answer 434

Xanthelasma are yellowish papules and plaques caused by localized accumulation of lipid deposits, commonly seen on the eyelid. They can also be found in patients without lipid abnormalities.

Answer 435

Management options for xanthelasma include: Surgical excision Topical trichloroacetic acid Laser therapy Electrodesiccation

Cardiology Flashcards

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