The level of blood pressure can be said to be abnormal when it is associated with a clear increase in morbidity and mortality from heart disease, stroke and renal failure. This level varies with age, sex, race and country. The defini-tion of hypertension is over 140/90 mmHg, based on at least two readings on separate occasions. The validity of a single blood pressure measurement is unclear (blood pressure rises acutely in certain situations, e.g. visiting the doctor) and usually several readings are required to confirm a diagnosis of hypertension. Occasionally, ambulatory blood pressure monitoring (blood pressure measured over a 24-hour period using a non-invasive technique) is used if there is doubt as to the level of blood pressure.
Essential hypertension Most patients with hypertension (80-90%) have no known underlying cause, i.e. ‘primary' or ‘essential' hypertension. Essential hypertension has a multifactorial aetiology:
■ Genetic component
■ Low birthweight
■ Excess alcohol intake
■ High salt intake
■ The metabolic syndrome (see p. 160).
Secondary hypertension This is the result of a specific and potentially treatable cause:
■ Renal disease accounts for over 80% of cases of secondary hypertension. The common causes are diabetic nephropathy, chronic glomerulo-nephritis, adult polycystic kidneys, chronic tubulointerstitial nephritis and renovascular disease
■ Endocrine disease (p. 655): Conn's syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing's syndrome and acromegaly
■ Coarctation of the aorta is a congenital narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus, i.e. distal to the left subclavian artery. There is hypertension due to decreased renal
perfusion, delayed (radiofemoral delay) pulses in the legs, a mid-late systolic murmur and ‘rib notching' (collateral arteries erode the under-surface of ribs) on X-ray
■ Pre-eclampsia occurring in the third trimester of pregnancy
■ Drugs, including oestrogen-containing oral contraceptives, other steroids, NSAIDs and vasopressin.
Hypertension is generally asymptomatic. Secondary causes of hypertension may be suggested by specific features, such as attacks of sweating and tachycardia in phaeochromocytoma. Malignant or accelerated hypertension describes a rapid rise in blood pressure with severe hypertension (diastolic blood pressure > 120 mmHg). The characteristic histological change is fibri-noid necrosis of the vessel wall and untreated it will result in end-organ damage in the kidneys (haematuria, proteinuria, Progressive kidney disease), brain (cerebral oedema and haemorrhage), retina (flame-shaped haemor-rhages, cotton wool spots, hard exudates, and papilloeodema) and cardio-vascular system (acute heart failure and aortic dissection).
Examination In most patients the only finding is high blood pressure, but in others signs relating to the cause (e.g. abdominal bruit in renal artery stenosis, delayed femoral pulses in coarctation of the aorta) or the end-organ effects of hypertension may be present, e.g. loud second heart sound, left ventricular heave, fourth heart sound in hypertensive heart disease, and retinal abnormalities. The latter are graded according to severity:
■ Grade 1 - increased tortuosity and reflectiveness of the retinal arteries (silver wiring)
■ Grade 2 - grade 1 plus arteriovenous nipping
■ Grade 3 - grade 2 plus flame-shaped haemorrhages and soft ‘cotton wool' exudates
■ Grade 4 - grade 3 plus papilloedema.
Investigations are carried out to identify end-organ damage and those patients with secondary causes of hypertension. Routine investigation should include:
■ Serum urea and electrolytes may show evidence of renal impairment, in which case more specific renal investigations (e.g. renal ultrasound, renal angiography) are indicated. Hypokalaemia occurs in Conn's syndrome
■ Urine Stix test for protein and blood, which may indicate renal disease (either the cause or the effect of hypertension)
■ Blood glucose
■ Serum lipids
■ ECG may show evidence of left ventricular hypertrophy or myocardial ischaemia.
Young patients with hypertension (< 30 years) or those where a secondary cause is suspected (e.g. from clinical examination or abnormal baseline investigations) should undergo further investigation, e.g. urinary/plasma catecholamines for phaeochromocytoma, investigation for renovascular hypertension (p. 374).
Treatment is begun immediately in patients with malignant or severe hyper-tension (BP > 180/110 mmHg). In other patients treatment is started if repeated measurements show that sustained hypertension is present (Table 10.16). For most patients target blood pressure during treatment is 140/85 mmHg. For patients with diabetes, chronic kidney disease or cardio-vascular disease a lower target of 130/80 mmHg is recommended. Non-pharmacological measures in the treatment of hypertension include:
■ Weight reduction (aim for BMI < 25 kg/m2)
■ Low-fat and low saturated fat diet
■ Low-salt diet (< 6 g sodium chloride per day)
■ Limited alcohol consumption (<21 units and <14 units per week for men and women respectively)
■ Dynamic exercise (at least 30 minutes brisk walk per day)
■ Increased fruit and vegetable consumption
■ Reduce cardiovascular risk by stopping smoking and increasing oily fish consumption.
In most hypertensive patients statins (p. 700) are also given to reduce the overall cardiovascular risk burden. Glycaemic control should be optimized in diabetics (HbA1c < 7%). For each class of anti-hypertensive there will be indications and contraindications in specific patient groups. A single anti-hypertensive drug is used initially, but combination treatment will be needed in many patients to control blood pressure. In patients without compelling reasons for a particular drug class a treatment algorithm (ACD) is used to advise on the sequencing of drugs and logical drug combinations (Fig. 10.17). This algorithm is based on the observation that younger people and Cauca-sians tend to have higher renin levels compared to older people or the black population.
Thus the ‘A' drugs which reduce blood pressure at least in part by sup-pression of the renin-angiotensin system are more effective as initial blood-pressure-lowering therapy in younger Caucasian patients.
Diuretics increase renal sodium and water excretion and directly dilate arterioles (p. 348). Loop diuretics, e.g. furosemide, and thiazide diuretics, e.g. bendroflumethiazide (bendrofluazide), are equally effective in lowering blood pressure, although thiazides are usually preferred, as the duration of action is longer, the diuresis is not so severe and they are cheaper. The major concern with thiazide diuretics is their adverse metabolic effects: increased serum cholesterol, hypokalaemia, hyperuricaemia (may precipitate gout) and impairment of glucose tolerance.
β-Adrenergic blocking agents (p. 494) are no longer a preferred initial therapy for hypertension. They are used in younger patients particularly those with an intolerance or contraindication to ACE inhibitors and angiotensin-II receptor antagonists; women of child bearing potential; or patients with evidence of increased sympathetic drive. p blockers reduce renin production and sympathetic nervous system activity. Complications include bradycardia, bronchospasm, cold extremities, fatigue and weakness.
ACE inhibitors (p. 497) e.g. captopril, enalapril, lisinopril, and ramipril, block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor, and block degradation of bradykinin, which is a vasodilator. Side-effects include first-dose hypotension and cough, proteinuria, rashes and leucopenia in high doses. ACE inhibitors are contraindicated in renal artery stenosis because inhibition of the renin-angiotensin system in this instance may lead to loss of renal blood flow and infarction of the kidney.
Angiotensin II receptor antagonists (p. 498) e.g. losartan, valsartan, irbesartan and candesartan, selectively block receptors for angiotensin II.
Fig. 10.17 Choosing drugs for patients newly diagnosed with hypertension. (National Institute for Health and Clinical Excellence (2006) Choosing drugs for patients newly diagnosed with hypertension. In: CG 34 Hypertension: management of hypertension in adults in primary care (Quick Reference Guide). London: NICE. Available from www.nice.org.uk/CG034. Reproduced with permission.)
They share some of the actions of ACE inhibitors and are useful in patients who cannot tolerate ACE inhibitors because of cough.
Calcium antagonists e.g. amlodipine and nifedipine, act predominantly by dilatation of peripheral arterioles. Side-effects are few and include brady-cardia and cardiac conduction defects (verapamil and diltiazem), headaches, flushing and fluid retention.
Other agents α-Blocking agents (e.g. doxazosin), hydralazine, and cen-trally acting agents (e.g. clonidine, moxonidine) may be indicated in specific circumstances. Aliskerin is a new anti-hypertensive and renin inhibitor. It is used alone or in combination with other agents.
Management of severe hypertension
Patients with malignant (p. 482) or severe hypertension (diastolic BP > 140 mmHg) should be admitted to hospital for treatment. The aim should be to reduce the diastolic blood pressure slowly (over 24-48 hours) to about 100-110 mmHg and this is usually achieved with oral antihypertensives, e.g. atenolol or amlodipine. Sublingual and intravenous antihypertensives are not recommended because they may produce a precipitous fall in blood pressure leading to cerebral infarction. When rapid control of blood pressure is required (e.g. aortic dissection), the agent of choice is intravenous sodium nitroprus-side (starting dose 0.3 μg/kg/min, i.e. 100 mg nitroprusside in 250 mL saline at 2-5 mL/h) or labetolol.
1. Ethics and communication
2. Infectious diseases
3. Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER DISEASE IN PREGNANCY
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS
5. Haematological disease
Assessment and treatment of suspected neutropenic sepsis
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
6. Malignant disease
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
8. Water, electrolytes and acid–base balance
WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
9. Renal disease
INVESTIGATION OF RENAL DISEASE
URINARY TRACT INFECTION
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
10. Cardiovascular disease
COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
ISCHAEMIC HEART DISEASE
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
ARTERIAL AND VENOUS DISEASE
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS
11. Respiratory disease
12. Intensive care medicine
13. Drug therapy, poisoning, and alcohol misuse
14. Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
15. Diabetes mellitus and other disorders of metabolism
16. The special senses
COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES