Transcript Hypertensive

Hypertensive Vascular
Disease
Hypertensive Heart
Disease
Introduction
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Systemic and local blood pressure must be tightly
regulated
Low pressure
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Inadequate perfusion of organs
Dysfunction and death
High pressure
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No additional benefit
Induces damage
Introduction
• Elevated blood pressure is called Hypertension
• Mechanisms of normal blood pressure
• Mechanisms of Hypertension
• Pathologic changes in small blood vessels
Mechanisms of normal
blood pressure
• Continuously distributed variable
• Hypertension is one end of spectrum
• A sustained diastolic pressure of more than 90 mm
Hg
• A sustained systolic pressure of more than 140 mm
Hg
• 25% in general population have hypertension
Types of Hypertension
• Essential or Primary Hypertension
• Secondary Hypertension
• Renal
• Endocrine
• Cardiovascular
• Neurologic
Types of Hypertension
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Secondary Hypertension
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Renal
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Acute glomerulonephritis
Chronic renal disease
Polycystic kidney disease
Renal artery stenosis
Renin Producing tumors
Types of Hypertension
• Secondary Hypertension
• Endocrine
• Adrenocortical hyperfunction
• Exogenous hormones
• Pheochromocytoma
• Acromegaly
• Hypothyroidism
• Hyperthyroidism
Types of Hypertension
• Secondary Hypertension
• Cardiovascular
• Coarctation of Aorta
• Polyarteritis Nodosa
• Increased intravascular
volume
• Increased cardiac output
• Rigidity of Aorta
Types of Hypertension
• Secondary Hypertension
• Neurologic
• Psychogenic
• Increased intracranial pressure
• Sleep apnea
• Acute stress including surgery and EXAMS!!!
Regulation of normal
blood pressure
• Blood pressure is proportional to cardiac output
and peripheral vascular resistance.
• Cardiac output and Peripheral resistance
determined by
• Genetic factors
• Environmental factors
• Demographic factors
Hypertension
• Major factors that determine blood pressure are
• Age
• Gender
• Body mass index
• Diet (sodium intake)
Normal pressure
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Kidney plays an important role
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Renin angiotensin mechanism
Kidney produces Prostaglandins and NO counter
balance the effect of angiotensin
When blood volume decreases, GFR decreases which
leads to reabsorption of sodium
Natriuretic factors - inhibit sodium reabsorption and
cause diuresis
When renal excretory function is impaired, increased
arterial pressure is a compensatory mechanism
Secreted by liver
Circulates in blood
11
Renin
Juxta Glomerular Apparatus
Angiotensinogen
Angiotensin 1
11
Medulla Oblangata
to increase CO
Angiotensin 11
Vasoconstriction
ACE
Walls of capillaries
Adrenal gland
Stimulates secretion
Aldosterone
Of ADH
Sodium
Mineralocorticoids
Constrictors
Dilators
Angiotensin11 Prostaglandins
Catecholamines
Kinins
Blood Volume
Humoral factors
=
Blood pressure
Cardiac factors
0
90
Cardiac factors
X
Peripheral
resistance
0
90
0
90
Cardiac
output
Heart rate
Contractility
Constrictors
Dilators
Alpha adrenergicBeta adrenergic
Mechanism in Essential
Hypertension
• Results from an interaction of genetic and
environmental factors that affect cardiac output and
peripheral resistance
Cardiac
output
X
Peripheral
resistance
=
Blood pressure
Genetic disorders
• Gene defects in enzymes: Aldosterone synthase,
11b-Hydroxylase
• Mutations in proteins: Liddle syndrome
Defects in renal
sodium balance
Defects in vascular
Smooth muscle growth and
structure
Vasoconstriction
Inadequate sodium
excretion
Salt and water retention
Increased Plasma and ECF
volume
Increased cardiac output
360
Increased vascular wall
thickness
Increased vascular
reactivity
Increased total
peripheral resistance
HYPERTENSION
Pathology of Hypertension
• Accelerates atherogenesis
• Causes degenerative changes in the wall of large
and medium sized arteries
• Also affects small blood vessels
• Hyaline aretriolosclerosis
• Hyperplastic arteriolosclerosis
Hyaline arteriolosclerosis
• Consists of homogeneous, pink, hyaline thickening
of the walls of arterioles, with loss of underlying
structural details and narrowing of lumen
• Frequently in elderly, normotensive and
hypertensive
• Common in diabetes
• Major morphologic characteristic of Benign
Nephrosclerosis
Hyaline arteriolosclerosis
• Lesions reflect
• leakage of plasma proteins
• Excessive ECM production
Hyperplastic
arteriolosclerosis
• Related to more severe and acute elevations of
blood pressure
• Characteristic of but not limited to Malignant
hypertension (Diastolic pressure > 120 mmHg)
• Onion skin, concentric laminated thickening of the
walls of arterioles with progressive narrowing of the
lumen
• If associated deposits of fibrinoid necrosis
necrotizing arteriolitis
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Hyaline arteriolosclerosis
Hyperplastic
arteriolosclerosis
Necrotizing arteriolitis
•Consequences of Hypertension:
• Blood Vessels
• Atherosclerosis, Arteriolosclerosis.
• Heart
• Enlarge, Ischemia, Infarction.
• Kidney
• Ischemia, Infarction, Nephrosclerosis.
• Eyes:
• Retinopathy – Ischemia, infarction.
• Brain:
• Ischemia, infarction, Haemorrhages.
Malignant Hypertension:
•Rapidly progressive end organ damage.
•May complicate any type of HTN.
•Artery necrosis with thrombosis.
•Rapidly developing renal failure.
•Hypertensive encephalopathy.
•Left ventricular failure.
•less time  No hypertrophy …!
COMPARISON BETWEEN BENIGN AND MALIGNANT HYPERTENSION
•characteristic - benign : malignant
•aetiology - usually primary : primary or secondary
•age - middle age, elderly : young, middle age
•incidence - common : uncommon
•course - very slow (years) : rapid (months)
•blood pressure - diastolic 90-120, very slow rise : diastolic >120, very rapid rise
Hypertensive heart
disease
• Hypertensive heart disease is the response to
increased demand induced by systemic
hypertension
Hypertensive heart
disease
• Systemic (left sided) hypertensive heart disease
• Pulmonary (right sided) hypertensive heart disease
(cor pulmonale)
Hypertensive heart
disease
• Systemic (left sided) hypertensive heart disease
• Pressure overload can lead to
• Myocardial dysfunction
• Cardiac dilation
• CHF
• Sudden death
Hypertensive heart
disease
• Systemic (left sided) hypertensive heart disease
• Criteria for diagnosis of Hypertensive heart
disease
• Left ventricular hypertrophy
• History or pathologic evidence of hypertension
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Hypertensive heart
disease
Systemic (left sided) hypertensive heart disease
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Morphology
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Overload hypertrophy
No dilation of left ventricle
Increased ratio of wall thickness to radius
Increased weight of the heart disproportionate to
the size (wt may exceed 500 gms)
Left ventricle over time becomes stiff and impairs
ventricular filling leading to left atrial dilation
Hypertensive heart
disease
• Systemic (left sided) hypertensive heart disease
• Morphology - Microscopy
• Earliest change - increase in the transverse
diameter of myocyte (difficult to appreciate on
LM)
• Later - cellular and nuclear enlargement
• Variation in cell size
• Interstitial fibrosis
Hypertensive heart
disease
• Systemic (left sided) hypertensive heart disease
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Clinical features
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Compensated HHD may be asymptomatic
May present with atrial fibrillation or CHF with cardiac
dilation
Consequences
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Normal longevity
Progressive ischemic heart disease
Progressive renal or cerebral damage
Hypertensive heart
disease
• Pulmonary (right sided) hypertensive heart disease
• Cor Pulmonale
• Right ventricular hypertrophy
• Dilation
• Failure secondary to pulmonary hypertension
Hypertensive heart
disease
• Pulmonary (right sided) hypertensive heart disease
• May be acute or chronic
• Acute - Massive pulmonary embolism
• Chronic - implies right ventricular hypertrophy
secondary to prolonged pressure overload
Hypertensive heart
disease
• Pulmonary (right sided) hypertensive heart disease
• Morphology
• Rt ventricular shape is converted to ovoid
• Rt ventricular wall thickens
• Outflow tract muscle bundle hypertrophy
• Secondary compression of left ventricular
chamber
• Tricuspid regurgitation
•Define essential hypertension?
•Briefly describe pathogenesis of renal damage in
hypertension.
•Classify hypertension, briefly describe pathogenesis in each?
•Summarize common complications of hptn?
•What is nephrosclerosis? Briefly describe its pathogenesis?
•What is meant by malignant hypertension? Briefly describe
clinical and pathological features?
•What are lacunar infarcts? arteriolosclerosis?
•How does hptn cause stroke? Damage heart?
Lacunar infarcts
•Chronic hypertension
•Arteriolosclerosis of deep
penetrating arterioles of
brain stem.
Single or multiple cavitary
infarcts – lacunes.
Lenticular nucleus,
thalamus
Slit Haemorrhages.
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• Are there any question?