Hypertension

Hypertension
Elevated blood pressure
 Sustained diastolic pressure greater than 90 mm Hg, or a
sustained systolic pressure in excess of 140 mm Hg.
 systolic blood pressure is more important in determining
cardiovascular risk
 Hypertension is a common health problem with occasionally
devastating outcomes
 It typically remains asymptomatic until late in its course.

Hypertension
Elevated blood pressure
 It contributes to the pathogenesis of coronary heart disease
and cerebrovascular accidents, cardiac hypertrophy and
heart failure (hypertensive heart disease), aortic dissection,
and renal failure.
 The mechanisms of hypertension in the vast majority of
people remain unknown; "essential hypertension“ .
 The prevalence and vulnerability to complications increase
with age; they are also higher in African Americans.
 Reduction of blood pressure dramatically reduces the
incidence and death rates from IHD, heart failure, and
stroke

Pathogenesis of Hypertension
 Ninety percent to 95% of hypertension is idiopathic
(essential hypertension), which is compatible with long life,
unless complication supervenes.
 Most of the remainder of "benign hypertension" is
secondary to renal disease or, narrowing of renal artery,
(atheromatous plaque, renovascular hypertension).
 Infrequently, hypertension is secondary to diseases of
the adrenal glands, such as primary aldosteronism.
Cushing syndrome, pheochromocytoma, or other
disorders.

Pathogenesis of Hypertension
 About 5% of hypertensive persons show a rapidly rising
blood pressure that if untreated leads to death within 1 or 2
years.
 Termed accelerated or malignant hypertension,
 The clinical syndrome is characterized by severe
hypertension (diastolic pressure over 120mmHg), renal
failure, and retinal hemorrhages and exudates, with or
without papilledema (swelling of the optic disc).
 It may develop in previously normotensive persons but
more often is superimposed on preexisting benign
hypertension, either essential or secondary.

Types and Causes
of Hypertension
(Systolic and
Diastolic)
 Essential Hypertension (90% to 95% of Cases)
 Secondary Hypertension
 RENAL
 Acute glomerulonephritis
 Chronic renal disease
 Polycystic disease
 Renal artery stenosis
 Renal vasculitis
 Renin-producing tumors
 ENDOCRINE
 Adrenocortical hyperfunction (Cushing syndrome, primary
aldosteronism, congenital adrenal hyperplasia, licorice
ingestion)
 Exogenous hormones (glucocorticoids, estrogen [including
pregnancy-induced and oral contraceptives],
sympathomimetics and tyramine-containing foods,
monoamine oxidase inhibitors)
 Pheochromocytoma
 Acromegaly
 Hypothyroidism (myxedema)
 Hyperthyroidism (thyrotoxicosis)
 Pregnancy-induced
 CARDIOVASCULAR
 Coarctation of aorta
 Polyarteritis nodosa
 Increased intravascular volume
 Increased cardiac output
 Rigidity of the aorta
 NEUROLOGIC
 Psychogenic
 Increased intracranial pressure
 Sleep apnea
 Acute stress, including surgery

Essential Hypertension
contributing factors
 Alterations in renal sodium homeostasis and/or vessel wall
tone or structure underlie essential hypertension
 Both increased blood volume and increased peripheral
resistance contribute to the increased pressure.

Essential Hypertension
 Essential hypertension results from an interplay of multiple
genetic and environmental factors affecting cardiac output
and/or peripheral resistance.
 Genetic factors: Allelic variations in the genes encoding
components of the renin-angiotensin system.
 Hypertension is associated with polymorphisms in
both the angiotensinogen locus and the angiotensin II
type I receptor locus.
 Environmental factors: modify the expression of any
underlying genetic determinants of hypertension; stress,
obesity, smoking, physical inactivity, and heavy
consumption of salt are all implicated.

Vascular Pathology in Hypertension
 In addition to accelerating atherogenesis, hypertension-
associated degenerative changes in the walls of large and
medium arteries can potentiate both aortic dissection and
cerebrovascular hemorrhage.
 Hypertension is also associated with two forms of small
blood vessel disease:
 hyaline arteriolosclerosis
 hyperplastic arteriolosclerosis

Hyaline Arteriolosclerosis
 Characterized by
 Diffuse, homogeneous, pink hyaline thickening of the
walls of arterioles.
 Loss of underlying structural detail and narrowing of the
lumen
 Occurs typically in elderly patients.
 Advanced lesions are seen in persons with diabetes
mellitus and/or with hypertension.

 Hyaline arteriolosclerosis is typically seen in kidneys.
 Endothelial injury causes leakage of plasma components
across vascular endothelium, and excessive extracellular
matrix production by smooth muscle cells.
 This process is associated with luminal narrowing that
may induce ischemic injury
 Afferent & efferent arterioles in kidney → benign
nephrosclerosis

Markedly thickened arteriole to the lower right of
this glomerulus

Arteriolar wall is hyalinized and the lumen is
markedly narrowed

Hyperplastic Arteriolosclerosis
 Concentric laminated (onion skin) arteriolar thickening with
reduplicated basement membrane and smooth muscle
cells proliferation.
 Commonly associated with malignant hypertension
 Leads to luminal narrowing
 Frequently associated with fibrinoid necrosis
(necrotizing arteriolitis).
 Later, the vascular walls hypertrophy due to hyperplasia
of SMCs and sometimes this occurs along with
necrosis of the vessel wall.

Onion skin appearance
Narrow Lumen
Onion Skin Thickening
Of arterioles.

(Onion-Skinning) causing luminal obliteration (arrow)

Fibrinoid necrosis

Hypertensive heart disease (HHD)
 Basics for diagnosis
 History of hypertension
 Left ventricular hypertrophy in the absence of other
causes accounting for hypertrophy
 The stimulus for hypertrophy is pressure overload

 Stages of HHD
 Compensated HHD:
 With hypertrophy an adequate cardiac output is
maintained.
 Decompensated HHD:
 Thickness of muscle wall increase demand for
oxygen, decrease compliance, and role of
hypertension on atheroma, all contribute to
decompensated HHD and eventual dilatation.

 Gross
 Compensated stage ..... Concentric hypertrophy
 Decompensated stage ......... Dilatation
 Both stages, heart weight increased
 Histology: Large fibers with large nuclei, later interstitial
fibrosis.
 HHD Causes death
 CHF
 Increased risk of sudden cardiac death
 Renal disease , stroke
 Drug control leads to regression of hypertrophy.

Cor pulmonale
 Cor pulmonale consists of right ventricular hypertrophy
and dilation due to pulmonary hypertension caused by
primary disorders of the lung parenchyma or pulmonary
vasculature.
 Generally, right ventricular dilation and hypertrophy
caused by congenital heart disease or by left ventricular
failure are excluded by this definition.

Cor pulmonale
 Cor pulmonale may be acute or chronic.
 Acute cor pulmonale most commonly follows massive
pulmonary embolism with obstruction of >50% of the
pulmonary vascular bed.
 Chronic cor pulmonale occurs secondary to prolonged
pressure overload caused by obstruction of the
pulmonary vasculature, or compression or obliteration
of septal capillaries (resulting from emphysema,
interstitial pulmonary fibrosis, or primary pulmonary
hypertension).

Cor pulmonale
 In acute cor pulmonale the right ventricle is usually dilated
but does not show hypertrophy; if an embolism causes
sudden death the heart may even be of normal size.
 Chronic cor pulmonale is characterized by right ventricular
(and often right atrial) hypertrophy. In extreme cases the
thickness of the right ventricular wall may be comparable
to or even exceed that of the left ventricle.
 When ventricular failure develops the right ventricle and
atrium may also be dilated. Such dilation may mask right
ventricular hypertrophy.

Hypertension

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Hypertension