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Definition: office blood pressure 140/90 mmHg or more, confirmed by repeated measurement, home or 24-hour ambulatory monitoring (home average 135/85, ambulatory daytime 135/85). Grades 1-3; white coat and masked hypertension. Secondary causes to consider in young patients or resistant hypertension: renal parenchymal and renovascular disease, primary aldosteronism, phaeochromocytoma, Cushing syndrome, coarctation, sleep apnoea, drugs. Assessment: risk factors, target organ damage (left ventricular hypertrophy, retinopathy, albuminuria, reduced eGFR). Treatment: lifestyle (salt below 5 g/day, weight loss, exercise, alcohol limits) and drugs: ACE inhibitor or ARB, calcium channel blocker, thiazide-like diuretic, usually as single-pill combinations; then add spironolactone or others for resistant hypertension. Targets: below 140/90 and, if tolerated, 120-130 systolic. Hypertensive emergency: severe hypertension with acute organ damage needs controlled intravenous lowering.

Lipid disorders: raised LDL cholesterol (familial hypercholesterolaemia: LDL receptor, APOB or PCSK9 mutations; tendon xanthomas, early coronary disease), hypertriglyceridaemia (pancreatitis risk above 10 mmol/L), low HDL. Risk estimation: SCORE2 or similar tools categorise risk as low, moderate, high and very high. LDL targets fall with risk (very high: below 55 mg/dL and at least 50 percent reduction). Treatment: statin first-line, add ezetimibe, then PCSK9 inhibitors or bempedoic acid; fibrates or omega-3 for severe hypertriglyceridaemia.

Atherosclerosis: chronic inflammatory plaque formation (see pathology). Peripheral artery disease (PAD): intermittent claudication (calf pain on walking relieved by rest), rest pain, ulcers and gangrene in chronic limb-threatening ischaemia; ankle-brachial index below 0.9 is diagnostic; duplex ultrasound and CT or MR angiography for anatomy. Management: smoking cessation, supervised exercise, statin, antiplatelet therapy (aspirin or clopidogrel; low-dose rivaroxaban plus aspirin in selected patients), blood pressure and diabetes control, revascularisation (angioplasty, stent, bypass) for lifestyle-limiting claudication or limb-threatening ischaemia. Acute limb ischaemia (the six Ps) is an emergency.

1. Give the definition of hypertension by office and home measurements. 2. List secondary causes of hypertension. 3. Which drugs are used stepwise to lower LDL cholesterol? 4. How is PAD diagnosed?

1. Office 140/90 mmHg or more; home average 135/85 mmHg or more. 2. Renal parenchymal and renovascular disease, primary aldosteronism, phaeochromocytoma, Cushing syndrome, coarctation, sleep apnoea, drugs. 3. Statin, then ezetimibe, then PCSK9 inhibitor or bempedoic acid. 4. Ankle-brachial index below 0.9, confirmed by duplex ultrasound or angiography.

Goals: HbA1c about 7 percent (individualised), blood pressure below 130/80, LDL according to risk, and prevention of complications. First-line lifestyle change and metformin; add SGLT2 inhibitors or GLP-1 receptor agonists if cardiovascular disease, heart failure or CKD, independent of HbA1c; other agents: DPP-4 inhibitors, sulfonylureas, pioglitazone, insulin. Screening for complications: annual retinal examination, urine albumin-creatinine ratio and eGFR, foot examination. Hypoglycaemia and ketoacidosis are acute complications.

Obesity is BMI 30 or more; visceral adiposity is more harmful. It drives insulin resistance, dyslipidaemia, hypertension, sleep apnoea, fatty liver and heart failure with preserved ejection fraction. The cardiovascular-kidney-metabolic (CKM) syndrome describes the health disorder due to interactions among metabolic risk factors, chronic kidney disease and cardiovascular disease, staged by risk. Management: weight loss (diet, exercise, GLP-1 receptor agonists, tirzepatide, bariatric surgery) with integrated treatment of each component.

AKI: prerenal, intrinsic or postrenal; assess volume status, urinalysis, ultrasound; stop nephrotoxic drugs, treat cause, avoid contrast when possible. CKD: eGFR below 60 for 3 months or damage markers (albuminuria); staging by GFR and albuminuria; treat with blood pressure control, ACE inhibitor or ARB, SGLT2 inhibitor, finerenone in diabetic kidney disease, treatment of anaemia and mineral bone disease, referral for renal replacement when eGFR falls below 15-20.

Hyponatraemia: assess volume status and urine osmolality and sodium (hypovolaemic, euvolaemic such as SIAD, hypervolaemic in heart failure and cirrhosis); avoid correction faster than 8-10 mmol/L in 24 hours. Hypernatraemia: water deficit; correct slowly. Hyperkalaemia: ECG changes; calcium, insulin-glucose, salbutamol, binders, dialysis. Hypokalaemia: replace potassium and magnesium. Acid-base: interpret pH, PaCO2 and bicarbonate; anion gap for metabolic acidosis (lactate, ketones, uraemia, toxins).

1. Which drug classes benefit patients with type 2 diabetes and CKD regardless of HbA1c? 2. What does CKM syndrome describe? 3. State the CKD definition. 4. Give the safe correction rate of chronic hyponatraemia.

1. SGLT2 inhibitors and GLP-1 receptor agonists (SGLT2 inhibitors and finerenone in CKD). 2. The interaction of metabolic risk factors, chronic kidney disease and cardiovascular disease. 3. eGFR below 60 mL/min/1.73 m2 or markers of kidney damage for at least 3 months. 4. No more than 8-10 mmol/L per 24 hours.

Diagnosis of suspected DVT or PE: clinical probability (Wells score), D-dimer if low or intermediate probability, then compression ultrasound or CT pulmonary angiography. Risk stratification of PE: haemodynamic stability, right ventricular dysfunction on echo or CT, troponin (PESI or sPESI score). Treatment: anticoagulation with a direct oral anticoagulant (rivaroxaban, apixaban, dabigatran, edoxaban) or LMWH then warfarin; at least 3 months; provoked (surgery, immobilisation) versus unprovoked events determine duration; thrombolysis for high-risk PE; cancer-associated VTE treated with LMWH or DOACs.

Diagnosis: symptoms, NT-proBNP, echocardiography. HFrEF: four pillars ACE inhibitor/ARNI, beta-blocker, MRA, SGLT2 inhibitor; loop diuretics for congestion; device therapy. HFpEF: SGLT2 inhibitors, diuretics, treatment of comorbidities. Look for causes: ischaemia, hypertension, valve disease, cardiomyopathy, arrhythmia. Follow-up: titration, monitoring of renal function and potassium, cardiac rehabilitation.

COPD (post-bronchodilator FEV1/FVC below 0.70): smoking cessation, LAMA/LABA, ICS if eosinophilic or frequent exacerbations, rehabilitation, oxygen for chronic hypoxaemia. Asthma: variable obstruction; inhaled corticosteroid-based stepwise therapy, biologics for severe disease. Overlap (asthma-COPD) is treated with ICS-containing regimens. Acute exacerbations: bronchodilators, systemic steroids, antibiotics if bacterial infection is likely, oxygen and ventilatory support as needed.

1. Outline the diagnostic strategy for suspected PE. 2. How long is anticoagulation given after an unprovoked VTE? 3. List the four pillars of HFrEF therapy. 4. When is an inhaled corticosteroid added in COPD?

1. Clinical probability (Wells), D-dimer if not high probability, then CT pulmonary angiography. 2. At least 3 months, then reassess for extended treatment. 3. ACE inhibitor/ARNI, beta-blocker, mineralocorticoid antagonist, SGLT2 inhibitor. 4. With frequent exacerbations or blood eosinophils of 300 per microlitre or more.