Download Secondary hypertension Renal diseases

SYSTEMIC
HYPERTENSION
 Hypertension
is one of the leading causes
of the global burden of disease.
 Hypertension doubles the risk of
cardiovascular diseases, including
coronary heart disease (CHD), congestive
heart failure (CHF), ischemic and
hemorrhagic stroke, renal failure, and
peripheral arterial disease.
 Although antihypertensive therapy clearly
reduces the risks of cardiovascular and
renal disease, large segments of the
hypertensive population are either
untreated or inadequately treated.
Definition
 Hypertension
currently is defined as a
usual BP of 140/90 mm Hg or higher, for
which the benefits of drug treatment
have been definitively established
Staging of Office Blood Pressure
BP STAGE
Normal
Prehypertension
Stage 1 hypertension
Stage 2 hypertension
SYSTOLIC BP (mm Hg)
<120
120-139
140-159
≥160
DIASTOLIC BP (mm Hg)
<80
80-89
90-99
≥100
Aetiology
1.
Primary (Essential) hypertension
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2.
The majority (90–95%) of patients with
hypertension have primary elevation of
blood pressure, i.e. essential hypertension of
unknown cause.
Secondary hypertension (5-10%).
Many factors may contribute
to development of essential HT
1.
Neural Mechanisms
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2.
Baroreflex control of sinus node function is
abnormal
Obesity-Related Hypertension
Obstructive Sleep Apnea
Renal Mechanisms
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acquired or inherited defect in the kidneys'
ability to excrete the excessive sodium load
Low Birth Weight
Genetic Contributions
3.
Vascular Mechanisms
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4.
Endothelial Cell Dysfunction
Vascular Remodeling: An increase in the
medial thickness relative to lumen diameter
(increased media-to-lumen ratio) is the
hallmark of hypertensive remodeling in
small and large arteries.
Hormonal Mechanisms

Activation of the renin-angiotensinaldosterone system (RAAS) is one of the
most important mechanisms contributing to
endothelial cell dysfunction, vascular
remodeling, and hypertension
Secondary hypertension
Renal diseases
These account for over 80% of the cases of
secondary hypertension.
The common causes are:
1.
■ diabetic nephropathy
■ chronic glomerulonephritis
■ adult polycystic disease
■ chronic tubulointerstitial nephritis
■ renovascular disease.
Endocrine causes
These include:
2.
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3.
Conn’s syndrome
Congenital adrenal hyperplasia
phaeochromocytoma
Cushing’s syndrome
acromegaly.
Hyperparathyroidism
Primary hypothyroidism
Thyrotoxicosis
Congenital cardiovascular causes

The major cause is coarctation of the aorta
4.
5.
6.
7.
Drugs: NSAIDs, oral contraceptives,
steroids, carbenoxolone, liquorice,
sympathomimetics and vasopressin.
Pregnancy (pre-eclampsia)
Alcohol
Obesity
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All adults should have blood pressure measured
routinely at least every 5 years until the age of 80
years.
Seated blood pressure when measured after 5
minutes’ resting with appropriate cuff size and arm
supported is usually sufficient, but standing blood
pressure should be measured in diabetic and
elderly subjects to exclude orthostatic
hypotension.
The cuff should be deflated at 2 mm/s and the
blood pressure measured to the nearest 2 mmHg.
Two consistent blood pressure measurements are
needed to estimate blood pressure, and more are
recommended if there is variation in the pressure.
When assessing the cardiovascular risk, the
average blood pressure at separate visits is more
accurate than measurements taken at a single
visit.
Assessment
History
 Family history, lifestyle (exercise, salt intake, smoking
habit) and other risk factors should be recorded.
 The patient with mild hypertension is usually
asymptomatic.
 Higher levels of blood pressure may be associated
with headaches, epistaxis or nocturia.
 Attacks of sweating, headaches and palpitations
point towards the diagnosis of phaeochromocytoma.
 Breathlessness may be present owing to left
ventricular hypertrophy or cardiac failure,
 symptoms of peripheral arterial vascular disease
suggest the diagnosis of atheromatous renal artery
stenosis.
Examination
 Findings
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related to hypertension
Loud A2
S4
Forceful sustained apical impulse (heaving)
Examination
1.
2.
3.
Secondary causes: Radio-femoral delay (coarctation
of the aorta), enlarged kidneys (polycystic kidney
disease), abdominal bruits (renal artery stenosis) and
the characteristic facies and habitus of Cushing's
syndrome are all examples of physical signs that may
help to identify causes of secondary hypertension.
Risk factors: Examination may also reveal features of
important risk factors such as central obesity and
hyperlipidaemia (tendon xanthomas etc.).
Complications:
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The optic fundi are often abnormal
and there may be evidence of generalised atheroma or
specific complications such as aortic aneurysm or
peripheral vascular disease.
Investigations
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investigation of all patients
Urinalysis for blood, protein and glucose
Blood urea, electrolytes and creatinine
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N.B. Hypokalaemic alkalosis may indicate
primary hyperaldosteronism but is usually due to
diuretic therapy
Blood glucose
Serum total and HDL cholesterol
12-lead ECG (left ventricular hypertrophy,
coronary artery disease)
investigation of selected patients
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Chest X-ray: to detect cardiomegaly, heart failure,
coarctation of the aorta
Ambulatory BP recording: to assess borderline or
'white coat' hypertension
Echocardiogram: to detect or quantify left ventricular
hypertrophy & for the diagnosis ofcoactation of aorta
Renal ultrasound: to detect possible renal disease
Renal angiography: to detect or confirm presence of
renal artery stenosis
Urinary catecholamines: to detect possible
phaeochromocytoma
Urinary cortisol and dexamethasone suppression test:
to detect possible Cushing's syndrome
Plasma renin activity and aldosterone: to detect
possible primary aldosteronism
Ambulatory blood pressure monitoring
 Indirect
automatic blood pressure measurements
can be made over a 24-hour period using a
measuring device worn by the patient.
 they are used to confirm the diagnosis in those
patients with ‘white-coat’ hypertension, i.e. blood
pressure is completely normal at all stages except
during a clinical consultation
 These devices may also be used to monitor the
response of patients to drug treatment and, in
particular, can be used to determine the
adequacy of 24-hour control with once-daily
medication
 Ambulatory
blood pressure recordings
seem to be better predictors of
cardiovascular risk than clinic
measurements.
 Analysis of the diurnal variation in blood
pressure suggests that those hypertensives
with loss of the usual nocturnal fall in
blood pressure (‘non-dippers’) have a
worse prognosis than those who retain this
pattern.
Complications
1.
Blood vessels
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2.
In larger arteries (> 1 mm in diameter), the
internal elastic lamina is thickened, smooth
muscle is hypertrophied and fibrous tissue is
deposited.
In smaller arteries (< 1 mm), hyaline
arteriosclerosis
aortic aneurysm and aortic dissection
Central nervous system
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Stroke (due to cerebral haemorrhage or
infarction).
Carotid atheroma and transient ischaemic
attacks are more common in hypertensive
patients.
Subarachnoid haemorrhage is also associated
with hypertension.
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3.
Hypertensive encephalopathy is a rare condition
characterised by high BP and neurological
symptoms, including transient disturbances of
speech or vision, paraesthesiae, disorientation, fits
and loss of consciousness. Papilloedema is
common.
Retina
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central retinal vein thrombosis
Hypertensive retinopathy
Grade I
Arteriolar thickening, tortuosity and increased reflectiveness ('silver wiring')
Grade 2
Grade 1 plus constriction of veins at arterial crossings ('arteriovenous
nipping')
Grade 3
Grade 2 plus evidence of retinal ischaemia (flame-shaped or blot
haemorrhages and 'cotton wool' exudates)
Grade 4
papilloedema
4.
Heart
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5.
Kidneys
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6.
coronary artery disease.
left ventricular hypertrophy
Atrial fibrillation
Diastolic dysfunction
LV failure.
Long-standing hypertension may cause proteinuria and
progressive renal failure by damaging the renal vasculature.
'Malignant' or 'accelerated' phase hypertension
(Diastole>130 mmgh)
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This rare condition may complicate hypertension of any
aetiology and is characterised by accelerated microvascular
damage and by intravascular thrombosis.
The diagnosis is based on evidence of high BP and rapidly
progressive end organ damage, such as retinopathy (grade 3
or 4), renal dysfunction (especially proteinuria) and/or
hypertensive encephalopathy .
Left ventricular failure may occur and, if this is untreated,
death occurs within months.