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Qais Mohammad qm420@ic.ac.uk Slides by: Suraya Gafore Hypertension and HyperlipidaemiaSESSION CONTENT Blood pressure: ❑ Hypertension ❑ Pulmonary hypertension ❑ Hypotension Hyperlipidemia: ❑ Dyslipidemia ❑ Hypercholesterolemia ❑ Hypertriglyceridemia HYPERTENSION Primary Secondary hypertension hypertension Resistant hypertensionEpidemiology Diagnosis • Increases with age AND becoming • History and physical examination more common in adolescents • 1 in 4 adults (31% men; 26% of • BP measurements (ABPM vs HBPM) women) • Bloods • Peak incidence 50-60yrs • Urinalysis • Sex ratio ~1:1 Clinical features • Asymptomatic (mostcases) • Headaches Masked Isolated systolic • Dizziness, tinnitus and blurred hypertension hypertension vision White coat • Strong bounding pulse • Flushed hypertension • Underlying cause (secondary HTN) SECONDARY HYPERTENSION Severe HTN Onset Age group Common cause < 18 years old Coarctation of the aorta and renal parenchymal disease < 40 years old Thyroid disease, fibromuscular dysplasia, renal parenchymal disease 40 - 64 years old Thyroid disease, obstructive sleep apnoea, hyperaldosteronism ≥ 65 years old Renal artery stenosis MANAGEMENT Lifestyle • Step 1: Age <55 - ACE inhibitor. Age >55 or of black African or Caribbean origin - ACEi ARBs calcium channel blocker • Step 2: ACE inhibitor + calcium channel blocker CCB Thiazide • Step 3: ACE inhibitor + calcium channel blocker + thiazide-like diuretic Others like beta blockers, loop • Step 4: consider further diuretic or beta- diuretics, potassium sparing diuretics, blockade or alpha blocker and seeking renin inhibitors, alpha blockers expert advice COMPLICATIONS: • Retinopathy • Heart failurery disease • Renal failure • Stroke • Peripheralvascular diseaseHypertension Aetiology: Examination: Investigations: • Primary: idiopathic • Strong bounding Blood pressure • Secondary: pulse measurements fibromuscular • Flushed dysplasia (young women) and renal artery stenosis (old Blood and urinalysis people and bilateral) History: Management: Complications: • Asymptomatic • Lifestyle changes • Hypertensive vascular • Headaches • ACEi/ARBs/CCB/thiazides disease • Dizziness • Strokes/TIA • Tinnitus • Beta blockers, Others like beta blockers, loop • Hypertensive • Blurred vision diuretics, potassium sparing diuretics, renin inhibitors, alpha blockers nephrosclerosis • Hypertensive retinopathyPULMONARY HYPERTENSION 1. Pulmonary arterial hypertension 2. Pulmonary hypertension caused by left heart disease 3. Pulmonary hypertension caused by lung disease 4. Pulmonary hypertension caused by pulmonary artery obstruction 5. Pulmonary hypertension caused by multifactorial mechanisms SYMPTOMS SIGNS • Dyspnoea / syncope (exertional) • Jugular vein • Chest pain (exertional) distention • Cyanosis • Loud second heart • Fatigue sound • Hoarseness • Signs of RHF – • Cough, haemoptysis palpitations, hepatojugular reflex • Nail clubbing DIAGNOSIS • Transthoracic echocardiography • Right heart catheterisation • ECG Management Oxygen therapy Diuretics Pulmonary vasodilators Anticoagulants Repair cardiac valve Pulmonary Treat underlying lung CHF treatment endarterectomy pathology Lung transplantPulmonary hypertension Aetiology: Examination: Investigations: • Pulmonary artery obstruction • Jugular vein • Transthoracic distension echocardiography • Chronic lung disease • Nail clubbing • Catheterisation • Left heart problems • Loud second • Pulmonary arterial heart sound hypertension • ECG and CXR History: Management: Complications: ✶ Right heart • Dyspnea and • Acute: oxygen and diuretics enlargement → failure chest pain on • Cause dependent: pulmonary vasodilators, pulmonary exertion endarterectomy, anti-coagulants, fix cardiac valves, ✶ Organs due to • Hoarse voice treat underlying lung pathology etc systemic congestion HYPOTENSION ORTHOSTATIC HYPOTENSION • Drop in BP (>20/10 mmHg) within 3 minutes of standing • Old people AND neurodegeneration • Causes are: ➢ Hypovolaemia ➢ Autonomic dysfunction (eg. diabetes, Parkinson’s) ➢ Drugs (eg. diuretics, antihypertensives, antidepressants, sedatives) ➢ AlcoholManagement - Fluids – first-line for most causes (e.g. dehydration, sepsis) - Evaluate polypharmacy - Treat underlying cause – e.g. control arrhythmias, give antibiotics for sepsis, adrenaline for anaphylaxis. - Vasopressors – e.g. norepinephrine if unresponsive to fluids. - Blood transfusion – if bleeding - Positioning – lay flat, legs raised, sitting slowly - Autonomic/orthostatic causes – ↑salt/fluids, compression stockingsSBA 1 (question)SBA 1 (answer)SBA 2 (question)SBA 2 (answer) KEY TERMS DYSLIPIDAEMIA: abnormal serum lipids HYPERLIPIDEMIA: too much serum lipids (cholesterol, LDL and triglycerides) HYPERLIPOPROTEINEMIA: elevated lipoproteins HYPERTRIGLYCERIDEMIA: elevated serum triglycerides > 150 mg/dL HYPERCHOLESTEROLEMIA: too much serum cholesterol > 200 mg/dL AETIOLOGY SYMPTOMS Acquired Inherited • Diabetes mellitus • Obesity Fredericksonclassification • Hypothyroidism DIAGNOSIS Fasting lipid profilesCHYLOMICRONMET ABOLISM Cholesterol and fats attach to apo B48 = chylomicron; this needs MTP Chylomicrons are released into the lymphatic system → systemic circulation Lipoprotein lipase breaks down chylomicrons releasing glycerol and FFA. Apo E binds to hepatic receptors. VLDL metabolism LDL MTP VLDL IDL Apo B100 Lipoprotein lipaseHDL METABOLISM Familial Familial Familial Familial Abetalipoproteine hyperchylomicrona hypercholesterol dysbetalipoprotei hypertriglyceride mia emia emia nemia mia Inheritance pattern Autosomal recessive Autosomal Autosomal Autosomal Autosomal dominant recessive dominant recessive Pathogenesis Defect in lipoprotein Defect in LDL Defect in Liver produces too Mutation in MTP -> lipase or apo C II receptor or apo apolipoprotein E much VLDL / no apo B48 or apo B100 decrease removal 100 of it Clinical features Pancreatitis Early Early Pancreatitis Steatorrhea Hepatosplenomegaly atherosclerosis atherosclerosis No risk of early Fat soluble vitamin Xanthoma Tendon xanthoma Palmar xanthoma atherosclerosis deficiencies No risk of early atherosclerosis Serum findings High chylomicrons High LDL High IDL, High VLDL and TG No chylomicrons Elevated TG chylomicron No VLDL remnants and triglycerides Familial Familial hypertriglyceridemia hypercholesterolemia Familial hyperchylomicronaemia Abetalipoproteinemia Familial Dysbetalipoproteinemia Management • Lifestyle = low fat diet, weight loss and alcohol avoidance • Statins (+/- other lipid lowering agents) • Primary prevention – 20mg atorvastatin; Secondary prevention – 80mg atorvastatin • If not tolerated → Ezetimibe • Omega 3 fatty acids • Fibrates (eg. fenofibrate) • Moderate (ie. triglycerides of 175–500 mg/dL) – lifestyle changes + avoid triglyceride raising medications • Severe (ie. triglycerides of ≥500 mg/dL) – statins (if high risk of 10-year premature atherosclerosis)SBA 3 (question)SBA 3(answer)SBA 4 (question)SBA 4(answer)SUMMARYFeedback