Download Hypertensive Vascular Disease

Types and Causes of Hypertension
(Systolic and Diastolic)
 ESSENTIAL
HYPERTENSION
 90% TO 95% OF CASES
 SECONDARY
HYPERTENSION
 Renal
 Endocrine
 Cardiovascular
 Neurologic
Renal

Acute glomerulonephritis

Chronic renal disease

Polycystic disease

Renal artery stenosis

Renal vasculitis

Renin-producing tumors
Endocrine



Adrenocortical
hyperfunction

Acromegaly

Hypothyroidism
(myxedema)

Hyperthyroidism
(thyrotoxicosis)

Pregnancy-induced
Exogenous
hormones
Pheochromocytoma
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
 95%
 Idiopathic
 Generally
problems.
does not cause short-term
Essential hypertension
 When
controlled
 Compatible with long life
 Asymptomatic
 Unless
○ A myocardial infarction,
cerebrovascular accident, or other
complication supervenes.
Accelerated / Malignant
Hypertension
 5%
of hypertensives
 Rapidly
rising blood pressure
 If
untreated  death within a year or
two.
 May
develop in previously
normotensives
Accelerated / Malignant
Hypertension
Systolic pressure >200 mm hg,
Diastolic pressure >120 mm hg
Renal failure
Retinal hemorrhages and
exudates
With or without papilledema.
a complex, multifactorial
disorder
 Genetic
factors
 Reduced renal sodium excretion
 Vasoconstrictive influences
 Environmental factors
Genetic factors
 play
a definite role
 several
single-gene disorders
 cause relatively rare forms of
hypertension (and hypotension)
 through several mechanisms
Gene defects affecting
1.
Enzymes involved in Aldosterone
Metabolism (e.g., aldosterone synthase,
11β-hydroxylase, 17α-hydroxylase).
○
○
○
○
increase in secretion of aldosterone
increased salt and water resorption
plasma volume expansion
ultimately, hypertension
2.
proteins that influence Sodium
Reabsorption
○
epithelial Na+ channel protein
○
increased distal tubular
reabsorption of sodium induced by
aldosterone
○
Liddle syndrome
 Inherited
variations in BP may
also depend on the cumulative
effects of polymorphisms in
several genes that affect blood
pressure.
 For
example
○ variations in the genes
encoding components of the
renin-angiotensin system
Reduced renal sodium
excretion

may be a key initiating event in
essential hypertension

may lead sequentially to an increase in
 fluid volume
 cardiac output
 peripheral vasoconstriction
 thereby elevating blood pressure.
Vasoconstrictive influences
 increase
 chronic
peripheral resistance
or repeated
vasoconstrictive influences could
cause  thickening and rigidity
of the involved vessels.
Environmental factors
 can
modify the impact of genetic
determinants.
 Stress
 Obesity
 Smoking
 physical inactivity
 heavy consumption of salt
Renovascular Hypertension
Renal artery stenosis causes

 Decreased glomerular flow and pressure in the
afferent arteriole of the glomerulus.

(1) induces renin secretion initiating angiotensin ii
–mediated vasoconstriction  increased
peripheral resistance

(2) increases aldosterone  sodium reabsorption
 blood volume
VASCULAR PATHOLOGY IN
HYPERTENSION
 Accelerates
atherogenesis
 Causes
degenerative changes in the
walls of large and medium arteries
that can lead to
- Aortic dissection and
- Cerebrovascular hemorrhage.
Morphology
 Two
forms of small blood vessel
disease:
Hyaline arteriolosclerosis &
Hyperplastic arteriolosclerosis.
Hyaline Arteriolosclerosis
 Arterioles
show
Homogeneous
pink hyaline thickening
luminal narrowing
Hyaline Arteriolosclerosis
 Plasma
protein leakage across
injured endothelial cells
 Increased
smooth muscle cell
matrix synthesis in response to
chronic hemodynamic stress.
Hyaline Arteriolosclerosis
 In
Nephrosclerosis due to chronic
hypertension, the arteriolar
narrowing of hyaline
arteriosclerosis causes
○ diffuse impairment of renal blood
supply
○ glomerular scarring
Hyaline Arteriolosclerosis
 Vessels
of elderly persons (either
normo- or hypertensive)
 Diabetic
microangiography
Morphology
 Two
forms of small blood vessel
disease:
Hyaline arteriolosclerosis &
Hyperplastic arteriolosclerosis.
Hyperplastic Arteriolosclerosis.
 in
severe (malignant) hypertension
 vessels exhibit “onion-skin lesions,”
 characterized by
○ concentric
○ laminated thickening of the walls
and
○ luminal narrowing
 The
laminations consist of
○ smooth muscle cells with
○ thickened, reduplicated
basement membranes
 In
malignant hypertension they
are accompanied by
○ fibrinoid deposits &
○ vessel wall necrosis
(necrotizing arteriolitis),
particularly in the kidney.
Hypertensive Heart Disease
 stems
from
○ the increased demands placed
on the heart by hypertension,
which causes
-pressure overload
-ventricular hypertrophy
 Systemic
(Left-sided)
Hypertensive Heart Disease

Pulmonary (Right-sided)
Hypertensive Heart Disease
(Cor Pulmonale)
SYSTEMIC (LEFT-SIDED)
HYPERTENSIVE HEART DISEASE

In hypertension, hypertrophy of the
heart is an
 adaptive response to pressure overload
 that can lead to
myocardial dysfunction
cardiac dilation
CHF
in some cases sudden death.
The minimal criteria for the diagnosis
of systemic HHD are the following:
(1)
Left ventricular hypertrophy


(2)
(usually concentric)
In the absence of other
cardiovascular pathology
A history or pathologic evidence
of hypertension.
Morphology
 Hypertension
induces left ventricular
pressure overload hypertrophy
 Initially without ventricular
dilation
 Increases the weight of the heart
disproportionately to the increase
in overall cardiac size
 The
thickness of
the left ventricular
wall may exceed
2.0 cm
 The
heart weight
may exceed 500
gm.
 In
time the increased thickness

 imparts
a stiffness
 impairs diastolic filling
 often inducing left atrial enlargement
Microscopy

The earliest change of systemic HHD
○ An increase in the transverse diameter
of myocytes
○ May be difficult to appreciate on routine
microscopy.

At a more advanced stage
○ cellular and nuclear enlargement
become apparent
○ often accompanied by interstitial
fibrosis.
Compensated systemic HHD
 may be asymptomatic
 producing only electrocardiographic or
echocardiographic evidence of left ventricular
enlargement.
 In
many, systemic HHD comes to
attention due to new atrial fibrillation
 induced by left atrial enlargement or
CHF.

Depending on the severity, duration, and
underlying basis of the hypertension, and on the
adequacy of therapeutic control, the patient may
○ enjoy normal longevity
○ develop IHD due to the potentiating effects
of hypertension on coronary atherosclerosis
○ suffer renal damage or cerebrovascular
stroke as direct effects of hypertension
○ experience progressive heart failure or SCD.
 Effective
control of hypertension
 can prevent or
 lead to regression of cardiac
hypertrophy and its associated risks
PULMONARY (RIGHT-SIDED) HYPERTENSIVE
HEART DISEASE (COR PULMONALE)

stems from pressure overload of the right
ventricle

characterized by
○ right ventricular hypertrophy
○ dilation
○ potentially failure

The most frequent causes are
○ disorders of the lungs
Disorders Predisposing to Cor
Pulmonale

DISEASES OF THE PULMONARY
PARENCHYMA
 Chronic obstructive pulmonary
disease
 Diffuse pulmonary interstitial
fibrosis
 Pneumoconioses
 Cystic fibrosis
 Bronchiectasis

DISEASES OF THE PULMONARY
VESSELS
 Recurrent pulmonary
thromboembolism
 Primary pulmonary hypertension
 Extensive pulmonary arteritis (e.g.,
Wegener granulomatosis)
 Drug-, toxin-, or radiation-induced
vascular obstruction
 Extensive pulmonary tumor
microembolism
 DISORDERS
AFFECTING
CHEST MOVEMENT
Kyphoscoliosis
Marked obesity (sleep apnea,
pickwickian syndrome)
Neuromuscular diseases
 DISORDERS
INDUCING
PULMONARY ARTERIAL
CONSTRICTION
 Metabolic acidosis
 Hypoxemia
 Chronic altitude sickness
 Obstruction of major airways
 Idiopathic alveolar
hypoventilation

Cor pulmonale may be
 acute or chronic.

Acute cor pulmonale
○ can follow massive pulmonary
embolism.

Chronic cor pulmonale results from
○ right ventricular hypertrophy (and
dilation)
○ secondary to prolonged pressure
overload
Morphology

In Acute Cor Pulmonale there is
 marked dilation of the right ventricle
 without hypertrophy.
 On cross-section the normal crescent
shape of the right ventricle is
transformed to a dilated ovoid.
 In
chronic cor pulmonale
○ the right ventricular wall thickens
○ sometimes up to 1.0 cm or more
 More
of
subtle RVH may take the form
 thickening of the muscle
bundles in the outflow tract,
immediately below the
pulmonary valve, or
 thickening of the moderator
band
 Sometimes,
the hypertrophied
right ventricle
○ compresses the left ventricular
chamber, or
○ leads to regurgitation and
fibrous thickening of the
tricuspid valve.
 Normally,
the myocytes of the
right ventricle are
 haphazardly arranged and
 the wall contains transmural fat
 In
right ventricular hypertrophy,
 fat in the wall disappears
 the myocytes align themselves
circumferentially.
Renal changes
Benign Nephrosclerosis
 Associated with long-standing
hypertension and diabetes. Patients
are usually old.
 This
infrequently causes Uremia and
death
 A mild proteinuria is present.
 GFR mildly diminished.
Benign nephrosclerosis.
(Morphology- Gross)
Symmetrically atrophic kidney
( weighing 110 to 130 g)
The smaller arteries in the kidney
have become thickened and
narrowed -
This leads to patchy ischemic
atrophy with focal loss of
parenchyma that gives the
surface of the kidney the
characteristic granular
appearance as seen here.
Granular Surface
Benign nephrosclerosis.
(Morphology- Microscopy)
Hyaline
arteriolosclerosis
is usually present with
hypertension and
diabetes mellitus.
Hyaline thickening of the
walls of the small
arteries & arterioles.
Homogenous, pink
hyaline is deposited,
lumen is narrowed with
loss of underlying
cellular detail.
Malignant nephrosclerosis
IT IS A CASE OF MEDICAL EMERGENCY
Grossly kidney demonstrates focal small hemorrhages.
(flea-bitten appearance)
This is due to an accelerated phase of hypertension in which blood
pressure is very high (such as 300/150 mm Hg).
Small,
pinpoint
petechial
hemorrhage
on cortex.
Morphology
Microscopy of Malignant hypertension shows
fibrinoid necrosis of small arteries . The
damage to the arteries leads to formation of
pink fibrin--hence the term "fibrinoid".
Fibrinoid
Deposit
around
Blood
vessel
Another microscopic appearance
Thickening of the arterial wall with malignant
hypertension also produces a hyperplastic arteriolitis. The
arteriole has an "onion skin" appearance
.
Thickening
of the
arterial
Wall
Lumen
of the
Artery
Malignant Nephrosclerosis
Clinical Features.
 Characterized
by Diastolic pressure
more than 120mm Hg.( Hypertension)
 Patient
may present with: 1.Papilledema, encephalopathy,
cardiovascular abnormality
and
 2.Renal failure.
Malignant Nephrosclerosis
clinical Symptoms.




Nausea, vomiting
Marked proteinuria
Hematuria.
Visual impairment
50% - survive for at least 5 years.
90% - death – caused by Uremia
10%- death – by Cerebral Hemorrhage
IT IS CASE OF TRUE MEDICAL EMERGENCY