Cardiovascular Flashcards
<p>Define abdominal aortic aneurysm.</p>
<p>Abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment, given the patient's sex and body size.</p>
<p>Explain the aetiology/risk factors of an abdominal aortic aneurysm. Summarise the epidemiology of an abdominal aortic aneurysm.</p>
<p>Cigarette smoking<br></br>Hereditary/family history<br></br>Increased age<br></br>Male sex (prevalence)<br></br>Female sex (rupture)<br></br>Congenital/connective tissue disorders<br></br>Prevalence among men is 4 to 6 times higher than in women.</p>
<p>Recognise the presenting symptoms of an abdominal aortic aneurysm.</p>
<p>AAA is usually asymptomatic and is discovered incidentally. In the minority of patients who experience symptoms, abdominal, back, and groin pain are typical.</p>
<p>Recognise the signs of an abdominal aortic aneurysm on physical examination.</p>
<p>Pulsatile, expanding abdominal pulse. There may also rarely be a palpable pulsatile abdominal mass.</p>
<p>Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results.</p>
<p>Abdominal USS</p>
<p>Define amyloidosis.</p>
<p>Any histological tissue specimen that binds the cotton wool dye, <strong>Congo red</strong>, and demonstrates <strong>green birefringence</strong> when viewed under polarised light is, by definition, an amyloid deposit. The patient with this deposit has amyloidosis. Deposits of amyloid may be localised in tissue or part of a systemic process. Progressive deposition of amyloid is disruptive to tissue and organ function and manifests its clinical sequelae by the dysfunction of those organs in which it deposits.</p>
<p>Explain the aetiology/risk factors of amyloidosis.</p>
<p>Monoclonal gammopathy of undetermined significance (MGUS)<br></br>Inflammatory polyarthropathy<br></br>Chronic infections<br></br>Inflammatory bowel disease<br></br>Familial periodic fever syndromes</p>
<p>Summarise the epidemiology of amyloidosis.</p>
<p>In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually.</p>
<p>Recognise the presenting symptoms of amyloidosis. Recognise the signs of amyloidosis on physical examination.</p>
<p>Fatigue<br></br>Weight loss<br></br>Dyspnoea on exertion<br></br>Jugular venous distention<br></br>Lower extremity oedema</p>
<p>Identify appropriate investigations for amyloidosis and interpret the results.</p>
<p>Serum immunofixation - positive in 60% of patients with amyloidosis<br></br>Urine immunofixation - positive in 80% of patients with amyloidosis<br></br>Immunoglobulin free light chain assay - >95% sensitivity<br></br>Bone marrow biopsy - done on all patients with suspected amyloidosis</p>
<p>Define aortic dissection.</p>
<p>Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.</p>
<p>Explain the aetiology/risk factors of aortic dissection.</p>
<p>Aortic dissection results from an intimal tear that extends into the media of the aortic wall. Cystic medial degeneration predisposes to intimal disruption and is characterised by elastin, collagen, and smooth muscle breakdown in the lamina media. Bleeding from the vasa vasorum can also lead to this condition.</p>
<p><br></br><strong>Marfan</strong> and <strong>Ehlers-Danlos</strong> increases the risk of aortic dissection.</p>
<p>Summarise the epidemiology of aortic dissection.</p>
<p>The worldwide incidence of aortic dissection is 0.5 to 2.95 cases per 100,000 people annually.</p>
<p>Recognise the presenting symptoms of aortic dissection.</p>
<p>Acute severe chest pain<br></br>Interscapular and lower pain</p>
<p>Recognise the signs of aortic dissection on physical examination.</p>
<p>Left/right blood pressure differential<br></br>Pulse deficit<br></br>Diastolic murmur<br></br>Hypertension</p>
<p>Identify appropriate investigations for aortic dissection and interpret the results.</p>
<p>ECG<br></br>CXR<br></br>Cardiac enzymes<br></br>CT angiography<br></br>Renal function tests<br></br>Liver function tests<br></br>Lactate<br></br>FBC</p>
<p>Define aortic regurgitation.</p>
<p>Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle. It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root. It can remain asymptomatic for decades before patients present with irreversible myocardial damage.</p>
<p>Explain the aetiology/risk factors of aortic regurgitation.</p>
<p>AR can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root. In developing countries, rheumatic heart disease (rheumatic fever during which the heart valves are damaged) is the most common cause, but congenital bicuspid aortic valve and aortic root dilation account for most of the cases in developed countries.</p>
<p>Summarise the epidemiology of aortic regurgitation.</p>
<p>AR is not as common as aortic stenosis and mitral regurgitation. One US study showed a prevalence of 13% in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in African-Americans. Prevalence increases with age in both genders.</p>
<p>Recognise the presenting symptoms of aortic regurgitation.</p>
<p>Dyspnoea<br></br>Fatigue<br></br>Weakness<br></br>Orthopnoea<br></br>Paroxysmal nocturnal dyspnoea<br></br>Pallor</p>
<p>Recognise the signs of aortic regurgitation on physical examination.</p>
<p>Mottled extremities<br></br>Rapid and faint peripheral pulse<br></br>Jugular venous distension<br></br>Basal lung crepitations<br></br>Altered mental status<br></br>Urine output <30 mL/hour<br></br>Soft S1<br></br>Soft or absent A2<br></br><strong>Collapsing (water hammer or Corrigan's) pulse</strong><br></br>Cyanosis<br></br>Tachypnoea<br></br>Displaced, hyperdynamic apical impulse</p>
<p>Identify appropriate investigations for aortic regurgitation and interpret the results.</p>
<p>ECG<br></br>CXR<br></br>Echo<br></br>Colour flow Doppler<br></br>Pulsed wave Doppler<br></br>Continuous wave Doppler</p>
<p>Define aortic stenosis.</p>
<p>Aortic stenosis (AS) represents obstruction of blood flow across the aortic valve due to pathological narrowing. It is a progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure.<br></br>Can be due to aortic calcification.</p>
<p>Explain the aetiology/risk factors of aortic stenosis.</p>
<p>Age >60 years<br></br>Congenitally bicuspid aortic valve<br></br>Rheumatic heart disease<br></br>Chronic kidney disease</p>
<p>Summarise the epidemiology of aortic stenosis.</p>
<p>AS is the most common valvular disease in the US and Europe and is the second most frequent cause for cardiac surgery. It is largely a disease of older people, and patients typically present in the seventh or eighth decade of life.</p>
<p>Recognise the presenting symptoms of aortic stenosis.</p>
<p>Dyspnoea<br></br>Chest pain<br></br>Syncope</p>
<p>Recognise the signs of aortic stenosis on physical examination.</p>
<p><strong>Ejection systolic murmur</strong><br></br>S2 diminished and single</p>
<p>Identify appropriate investigations for aortic stenosis and interpret the results.</p>
<p>Transthoracic echocardiogram (including Doppler)<br></br>ECG</p>
<p>Define arterial ulcers.</p>
<p>Arterial ulcers are caused by ischaemia to the leg. The ulcers are painful and more painful on elevation. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed.</p>
<p>Explain the aetiology/risk factors of arterial ulcers.</p>
<p>Smoking<br></br>Diabetes mellitus<br></br>Hypertension<br></br>Hyperlipidaemia<br></br>Strong family history of atherosclerotic disease<br></br>Male</p>
<p>Summarise the epidemiology of arterial ulcers.</p>
<p>Arterial ulcers are more common in males and people who have risk factors. They occur where the blood supply is the worst.</p>
<p>Recognise the presenting symptoms of arterial ulcers. Recognise the signs of arterial ulcers on physical examination.</p>
<p>Painful, especially on elevation<br></br>Deep, punched out, dry and often elliptical sore<br></br>Location: between toes, ball of foot, lateral malleolus and bony prominence<br></br>Cold, pale limbs<br></br>Poor capillary refill<br></br>Venous guttering<br></br>Absent or weak pulses<br></br>Atrophic skin changes</p>
<p>Identify appropriate investigations for arterial ulcers and interpret the results.</p>
<p>Investigate for signs of atherosclerotic disease:<br></br>BM<br></br>FBC<br></br>Fasting lipids<br></br>Urinalysis<br></br>Biopsy<br></br><strong>Buerger’s test: </strong>Blanching of the foot on elevation to 15 degrees</p>
<p>Define atrial fibrillation.</p>
<p>Atrial fibrillation (AF) is a supraventricular tachyarrhythmia. It is characterised by uncoordinated atrial activity on the surface ECG, with fibrillatory waves of varying shapes, amplitudes, and timing associated with an irregularly irregular ventricular response when atrioventricular (AV) conduction is intact.</p>
<p>Explain the aetiology/risk factors of atrial fibrillation.</p>
<p>Coronary artery disease (CAD), hypertension, heart failure, valvular disease, diabetes, thyroid disorders, COPD and obstructive sleep apnoea, and advanced age are known risk factors for the development of new-onset AF.</p>
<p>Heavy alcohol intake can also increase the risk of atrial fibrillation.</p>
<p>Summarise the epidemiology of atrial fibrillation.</p>
<p>The incidence of AF increases progressively with age.<br></br>Incidence is higher in men butmortality is higher in women.</p>
<p>Recognise the presenting symptoms of atrial fibrillation.</p>
<p>SOB<br></br>Palpitations<br></br>Chest tightness</p>
<p>Recognise the signs of atrial fibrillation on physical examination.</p>
<p>Hypotension<br></br>Elevated jugular venous pressure<br></br>Added heart sounds</p>
<p>Identify appropriate investigations for atrial fibrillation and interpret the results.</p>
<p>ECG<br></br>Serum electrolytes<br></br>Cardiac biomarkers<br></br>Thyroid function tests<br></br>CXR<br></br>Transthoracic echocardiogram<br></br>Transoesophageal echocardiogram (TOE)</p>
<p>Generate a management plan for atrial fibrillation.</p>
<p>The 3 elements in the management of new-onset AF are:</p>
<p>Ventricular rate control<br></br>Restoration and maintenance of sinus rhythm<br></br>Prevention of thromboembolic events.</p>
<p>Identify the possible complications of atrial fibrillation and its management.</p>
<p>Acute stroke<br></br>MI<br></br>Congestive heart failure</p>
<p>Summarise the prognosis for patients with atrial fibrillation.</p>
<p>The prognosis depends on the onset, age and lifestyle of the patient.</p>
<p>Define atrial flutter.</p>
<p>Typical atrial flutter (anti-clockwise cavotricuspid isthmus-dependent atrial flutter) is a macro-reentrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm.</p>
<p>Explain the aetiology/risk factors of atrial flutter.</p>
<p>Increasing age<br></br>Valvular dysfunction<br></br>Atrial septal defects<br></br>Atrial dilation<br></br>Recent cardiac or thoracic procedures<br></br>Surgical or post-ablation scarring of atria<br></br>Heart failure<br></br>Hyperthyroidism<br></br>COPD<br></br>Asthma<br></br>Pneumonia</p>
<p>Summarise the epidemiology of atrial flutter.</p>
<p>The overall incidence has been reported as 88/100,000 person-years, with increasing rates with older age.</p>
<p>Recognise the presenting symptoms of atrial flutter. Recognise the signs of atrial flutter on physical examination.</p>
<p>Palpitations<br></br>Fatigue or lightheadedness<br></br>Jugular venous pulsations with rapid flutter waves<br></br>Chest pain<br></br>Dyspnoea<br></br>Syncope<br></br>Hypotension</p>
<p>Identify appropriate investigations for atrial flutter and interpret the results.</p>
<p>ECG: In the typical form, this entity is characterised electrocardiographically by flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1.<br></br>TFTs<br></br>Serum electrolytes<br></br>CXR</p>
<p>Generate a management plan for atrial flutter.</p>
<p>Synchronised cardioversion until stable.<br></br>Once stable:</p>
<p><strong>1st line:</strong>Beta-blocker or CCB or amiodarone<br></br><u>Plus:</u><br></br>Anticoagulation<br></br>Treat co-existing acute disease process</p>
<p>Identify the possible complications of atrial flutter and its management.</p>
<p>Myocardial ischaemia<br></br>Acute stroke</p>
<p>Summarise the prognosis for patients with atrial flutter.</p>
<p>In approximately 60% of cases, atrial flutter occurs in the setting of an acute process. Once that process has been treated, sinus rhythm is usually restored and chronic therapy is not required.</p>
<p>Define cardiomyopathy.</p>
<p>Primary disease of the myocardium. Cardiomyopathy can be split into three different categories, dilated, hypertrophic and restrictive.</p>
<p>Explain the aetiology/risk factors of dilated cardiomyopathy.</p>
<p>Flabby heart of unknown cause.</p>
<ul> <li>Alcohol</li> <li>Hypertension</li> <li>Viral infection</li> <li>Autoimmune</li></ul>
<p>Explain the aetiology/risk factors of hypertrophiccardiomyopathy.</p>
<p>Obstruction of outflow tract from asymmetric septal hypertrophy.</p>
<ul> <li>Inherited (autosomal dominant)</li></ul>
<p>Explain the aetiology/risk factors of restrictive cardiomyopathy.</p>
<ul> <li>Amyloidosis</li> <li>Haemochromatosis</li> <li>Sarcoidosis</li> <li>Scleroderma</li></ul>
<p>Summarise the epidemiology of cardiomyopathy.</p>
<p>Dilated cardiomyopathy is the most common form and affects five in 100,000 adults and 0.57 in 100,000 children. It is the third leading cause of heart failure in the United States behind coronary artery disease (CAD) and hypertension.</p>
<p>Recognise the presenting symptoms of cardiomyopathy. Recognise the signs of cardiomyopathy on physical examination.</p>
<p>Angina<br></br>Dyspnoea<br></br>Syncope<br></br>Sudden death</p>
<p>Identify appropriate investigations for cardiomyopathy and interpret the results.</p>
<p>ECG<br></br>Echocardiogram.<br></br>MRI scan.<br></br>Heart rhythm monitor (24 or 48-hour ECG monitor)<br></br>Exercise tests<br></br>Family tree/genetic screening</p>
<p>Define constrictive pericarditis.</p>
<p>This is an inflammation of the pericardium.</p>
<p>Explain the aetiology/risk factors of constrictive pericarditis.</p>
<p>Acute pericarditis can be idiopathic or due to an underlying systemic condition (e.g. systemic lupus erythematosus).</p>
<p>Summarise the epidemiology of constrictive pericarditis.</p>
<p>Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men. It is the most common disease of the pericardium encountered in clinical practice.</p>
<p>Recognise the presenting symptoms of constrictive pericarditis.</p>
<p>Chest pain<br></br>Fever</p>
<p>Recognise the signs of constrictive pericarditis on physical examination.</p>
<p>Pericardial rub<br></br>Ankle oedema<br></br>Ascites</p>
<p>Identify appropriate investigations for constrictive pericarditis and interpret the results.</p>
<p>ECG<br></br>CXR<br></br>CRP<br></br>Serum troponin<br></br>Pericardial fluid/blood culture<br></br>ESR<br></br>Serum urea<br></br>FBC<br></br>Echocardiography</p>
<p>Define deep vein thrombosis (DVT).</p>
<p>A blood clot in the deep vein of the leg.</p>
<p>Explain the aetiology/risk factors of deep vein thrombosis (DVT).</p>
<p>Being immobile for long periods<br></br>The Pill (increases chance of blood clots)<br></br>Age<br></br>Trauma<br></br>Active cancer<br></br>Pregnancy<br></br>Clotting disorder<br></br>Smoking</p>
<p>Summarise the epidemiology of deep vein thrombosis (DVT).</p>
<p>Venous thromboembolism (VTE) is a relatively common medical problem with a yearly incidence of approximately 1 in every 1000 adults. About two thirds of these cases are DVT and one third progress to a PE.</p>
<p>Recognise the presenting symptoms of deep vein thrombosis (DVT). Recognise the signs of deep vein thrombosis (DVT) on physical examination.</p>
<p>Pain in leg<br></br>Asymmetric oedema<br></br>Prominent superficial vein</p>
<p>Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results.</p>
<p>Wells' score - Risk of DVT or PE<br></br>Quantitative D-dimer level - Tells you how much FDP (fibrin degradation product), doesn’t work for pregnancy or cancer as these can affect clotting.<br></br>Proximal duplex ultrasound<br></br>Whole-leg ultrasound<br></br>INR and activated partial thromboplastin time (aPTT)<br></br>Urea and creatinine<br></br>LFTs<br></br>FBC</p>
<p>Generate a management plan for deep vein thrombosis (DVT).</p>
<p>Heparin<br></br></p>
<p><u>Adjunct:</u><br></br>Stockings<br></br></p>
<p>Identify the possible complications of deep vein thrombosis (DVT) and its management.</p>
<p>The clot could travel to the lungs and cause a PE.</p>
<p>Summarise the prognosis for patients with deep vein thrombosis (DVT).</p>
<p>Patient should be fine as long as they start heparin. It depends on what caused the DVT (e.g. cancer).</p>
<p>Define gangrene.</p>
<p>Gangrene is a complication of necrosis characterised by the decay of body tissues. There are two major categories: infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene).</p>
<p>Explain the aetiology/risk factors of gangrene.</p>
<p>Diabetes<br></br>Smoking<br></br>Atherosclerosis<br></br>Renal disease<br></br>Drug and alcohol abuse<br></br>Malignancy<br></br>Trauma or abdominal surgery<br></br>Contaminated wounds<br></br>Malnutrition<br></br>Hypercoagulable states<br></br>Prolonged use of tourniquets</p>
<p>Summarise the epidemiology of gangrene.</p>
<p>Gangrene occurs equally in men and women. Type I necrotising fasciitis occurs most commonly in patients with diabetes and patients with peripheral vascular disease. It is the most common form of necrotising fasciitis in the general population.</p>
<p>Recognise the presenting symptoms of gangrene. Recognise the signs of gangrene on physical examination.</p>
<p>Pain<br></br>Oedema<br></br>Skin discoloration<br></br>Crepitus (gas gangrene)<br></br>Diminished pedal pulses and ankle-brachial index (ischaemic gangrene)<br></br>Low-grade fever and chills (infectious gangrene)</p>
<p>Identify appropriate investigations for gangrene and interpret the results.</p>
<p>FBC<br></br>Comprehensive metabolic panel<br></br>Serum LDH<br></br>Coagulation panel<br></br>Blood cultures<br></br>Serum C-reactive protein<br></br>Plain x-rays<br></br>CT of affected site<br></br>MRI of affected site<br></br>Doppler ultrasonography</p>
<p>Define heart block.</p>
<p>Cardiac electric disorder characterised by delayed (or absent) conduction from the atria to the ventricles.</p>
<p>Explain the aetiology/risk factors of heart block.</p>
<p>Hypertension<br></br>Increased vagal tone<br></br>AV-nodal blocking agents<br></br>Chronic stable CAD<br></br>Acute coronary syndrome<br></br>CHF<br></br>Hypertension<br></br>Cardiomyopathy</p>
<p>Summarise the epidemiology of heart block.</p>
<p>The epidemiology of AV block is not well characterised.</p>
<p>Advanced AV block (usually type II second-degree and third-degree) is usually anatomically infranodal and is seen in advanced His-Purkinje disease.</p>
<p>Recognise the presenting symptoms of heart block.</p>
<p>Syncope<br></br>Bradycardia <40 bpm<br></br>Fatigue<br></br>Dyspnoea<br></br>Chest pain<br></br>Palpitations<br></br>Nausea/vomiting</p>
<p>Recognise the signs of heart block on physical examination.</p>
<p>High blood pressure<br></br>Sometimes low blood pressure</p>
<p>Identify appropriate investigations for heart block and interpret the results.</p>
<p>ECG<br></br>Serum troponin<br></br>Serum potassium<br></br>Serum calcium<br></br>Serum pH<br></br>Serum digitalis level</p>
<p>Generate a management plan for first degree or second degree Type I heart block.</p>
<p><strong>Asymptomatic</strong><br></br><u>1st line:</u>Monitoring</p>
<p><strong>Symptomatic</strong><br></br><u>1st line:</u> Discontinuation of AV-nodal blocking medications.<br></br><u>2nd line:</u> Infrequently: PPM (permanent pacemaker) or cardiac resynchronisation therapy ± ICD placement.<br></br></p>
<p>Generate a management plan for second degree Type II or third degree heart block.</p>
<p><strong>Asymptomatic or mildly to moderately symptomatic</strong><br></br><u>1st line:</u> Condition-specific management and discontinuation of AV node-blocking drugs.<br></br><u>2nd line:</u> PPM or cardiac resynchronisation therapy ± ICD placement</p>
<p><strong>Severely symptomatic</strong><br></br><u>1st line:</u> Condition-specific management, discontinuation of AV-nodal blocking drugs, and temporary (transcutaneous or transvenous) pacing.<br></br><u>2nd line:</u> PPM or cardiac resynchronisation therapy ± ICD placement.<br></br></p>
<p>Identify the possible complications of heart block and its management.</p>
<p>In the short term, periprocedurally, the risks associated with pacemaker implantation are low: in the range of 2% to 3%. These include bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade, lead dislodgement, and pocket haematoma development. The risk of MI, stroke, and death is <1%.</p>
<p>Long-term complications include pulse generator or lead malfunction and infection. The pulse generators run on batteries that average 7 to 10 years in longevity. Battery depletion requires replacing the pulse generator.</p>
<p>Over a lifetime, there is some risk of infection of the lead, which may require extraction, a complex procedure that should be performed at specialised centres.</p>
<p>Summarise the prognosis for patients with heart block.</p>
<p>The prognosis is related to the degree of AV block and the severity of associated symptoms. In certain conditions, such as sarcoid or amyloid heart disease or acute anterior MI, the underlying condition strongly determines prognosis.</p>
<p>Define hypercholesterolaemia.</p>
<p>Hypercholesterolaemia, an elevation of total cholesterol (TC) and/or low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (HDL-C).</p>
<p>Explain the aetiology/risk factors of hypercholesterolaemia.</p>
<p>Insulin resistance and type 2 diabetes mellitus<br></br>Excess body weight (body mass index >25 kg/m²)<br></br>Hypothyroidism<br></br>Cholestatic liver disease</p>
<p>Summarise the epidemiology of hypercholesterolaemia.</p>
<p>Approximately 28.5 million adults or nearly 12% of the adult population in the US have total cholesterol levels ≥6.2 mmol/L (≥240 mg/dL).</p>
<p>Recognise the presenting symptoms of hypercholesterolaemia. Recognise the signs of hypercholesterolaemia on physical examination.</p>
<p>Family history of early onset of coronary heart disease or dyslipidaemia in first-degree relatives<br></br>History of cardiovascular disease<br></br>Excess body weight (especially abdominal obesity)<br></br>Xanthelasmas<br></br>Corneal arcus</p>
<p>Identify appropriate investigations for hypercholesterolaemia and interpret the results.</p>
<p>Lipid profile<br></br>Serum thyroid-stimulating hormone (TSH)<br></br>Lipoprotein(a)</p>
<p>Generate a management plan for hypercholesterolaemia.</p>
<p>Statins<br></br>Lifestyle modifications<br></br>Can use ezetimibe or PCSK9 inhibitor</p>
<p>Identify the possible complications of hypercholesterolaemia and its management.</p>
<p>Ischaemic heart disease<br></br>Peripheral vascular disease (PVD)<br></br>Acute coronary syndrome<br></br>Stroke<br></br>Erectile dysfunction</p>
<p>Summarise the prognosis for patients with hypercholesterolaemia.</p>
<p>If the treatment plan includes detection and management of other factors that contribute to the development of coronary heart disease (CHD), such as hypertension, diabetes mellitus, and smoking, the overall prognosis of hypercholesterolaemia is improved.</p>
<p>Define hypertriglyceridemia.</p>
<p>Hypertriglyceridaemia is defined by the National Cholesterol Education Program Adult Treatment Panel III as fasting plasma triglyceride level ≥2.3 mmol/L (≥200 mg/dL).</p>
<p>Explain the aetiology/risk factors of hypertriglyceridemia.</p>
<p>Family history of hyperlipidaemia<br></br>Family history of diabetes<br></br>Overweight/obese patients<br></br>High-saturated-fat diet<br></br>High-carbohydrate diet<br></br>Insulin resistance<br></br>Liver disease<br></br>Hypothyroidism<br></br>Renal disease<br></br>Excessive alcohol consumption<br></br>HIV infection<br></br>Cystic fibrosis</p>
<p>Summarise the epidemiology of hypertriglyceridemia.</p>
<p>The 90th percentile for triglyceride levels has been historically noted to be approximately 2.8 mmol/L (250 mg/dL) in the US. Because hypertriglyceridemia is related to insulin resistance,its prevalence is expected to continue to increase in industrialised countries.</p>