ARTERIAL

HYPERTENTION

CEREBRAL VASCULAR
DISEASE
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 ARTERIAL HYPERTENSION
 DEFINITION
ARTERIAL HYPERTENSION IS TERMED
ELEVATED ARTERIAL PRESSURE
AFFECTS
WITH BOTH THE FUNCTION AND
THE SRUCTURE OF BLOOD VESSELS.

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 ARTERIAL HYPERTENSION
 TYPES
(SYSTOLIC AND DIASTOLIC ARTERIAL HYPERTENSION)
95% OF CASES IS
ESSENTIAL HYPERTENSION
5% IS SECONDARY
HYPERTENTION
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 CAUSES OF SECONDARY
HYPERTENSION
 RENAL DISEASES
 ENDOCRINE DISEASES
 CARDIOVASCULAR DISEASES
(COARCTATION OF AORTA,
POLYARTERITIS NODOSA)
 CEREBRAL DISEASES
 NEUROLOGIC DISEASES

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 MECHANISMS OF ESSENTIAL
HYPERTENSION
 RELATIONSHIP BETWEEN BLOOD
VOLUME & TOTAL PERIPHERAL
RESISTANCE IS ALTERED

 INDUCES RENIN SECRETION INITIATING

ANGIOTENSIN 2 –INDUCED
VASOCONSTRICTION AND INCREASING
PERIPHERAL RESISTANCE

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 MECHANISMS OF ESSENTIAL
HYPERTENSION

 THROUGH THE ALDOSTERONE

MECHANISM, INCREASES SODIUM
REABSORPTION AND, THEREFORE,
BLOOD VOLUME

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 ESSENTIAL HYPERTENSION
 GENETIC FACTORS PLAY AN IMPORTANT
ROLE IN DETERMINING PRESSURE LEVEL

 ENVIRONMENTAL FACTORS ARE

IMPORTANT TOO.

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The pathogenesis of essential
hypertension

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 STAGES OF ARTERIAL
HYPERTENSION
 FUNCTIONAL CHANGES

 SMALL ARTERIES AND ARTERIOLES

LESIONS

 ORGANS LESIONS

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 SMALL ARTERIES AND
ARTERIOLES LESIONS
ACUTE PHASE
 MUCOID AND FIBRINOID SWELLING

 FIBRINOID NECROSIS

 THROMBOSIS IN VASCULAR LUMEN

 RUPTURE OF THE VASCULAR WALL

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 SMALL ARTERIES AND
ARTERIOLES LESIONS
 Sometimes the small
arteries and arterioles
can be damaged so
severely in malignant
hypertension that
they demonstrate
necrosis with a pink
fibrin-like quality that FIBRINOID NECROSIS
gives this process its
name-fibrinoid
necrosis.

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 SMALL ARTERIES AND
ARTERIOLES LESIONS
 THROMBOSIS IN VASCULAR LUMEN

THROMBUS

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 SMALL ARTERIES AND
ARTERIOLES LESIONS
CHRONIC PHASE
HYALINOSIS

SCLEROSIS

ANEURISM FORMATION

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 SMALL ARTERIES AND
ARTERIOLES LESIONS

SCLEROSIS OF
THE VASCULAR WALL

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 SMALL ARTERIES AND
ARTERIOLES LESIONS

HYALINOSIS
OF VASCULAR WALL

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 CLASSIFICATION
 CARDIAC FORM
 CEREBRAL FORM
 RENAL FORM

ALL FORMS INCLUDE MYOCARDIAC

HYPERTROPHY OF LEFT VENTRICLE AS
MORPHOLOGIC SIGN OF ARTERIAL
HYPERTENSION
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 ARTERIAL HYPERTENSION
MYOCARDIAC HYPERTROPHY OF LEFT
VENTRICLE IS THE MORPHOLOGIC SIGN OF

ARTERIAL HYPERTENSION

LEFT VENTRICLE

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 CLINICAL-MORPHOLOGICAL
FORMS OF ARTERIAL
HYPERTENSION

 CARDIAC FORM
SEE ISCHEMIC HEART DISEASE

 CEREBRAL FORM
SEE CEREBROVASCULAR DISEASES

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 CLINICAL-MORPHOLOGICAL
FORMS OF ARTERIAL
HYPERTENSION
 RENAL FORM

MAY BE BENIGN OR MALIGNANT

ACCORDING TO CLINICAL COURSE AND
MORPHOLOGICAL SIGNS

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BENIGN ARTERIAL HYPERTENSION
 HYALINE ARTERIOLOSCLEROSIS IS A
MAJOR MORPOLOGIC CHARACTERISTIC
OF BENIGN NEPHROSCLEROSIS
 WITH LUMEN NARROWING CAUSES DIFFUSE
IMPAIRMENT OF RENAL BLOOD SUPPLY,
 LOSS NEPHRONS AND FORMATION
 SYMMETRIC CONTRACTED KIDNEYS
 OR PRIMARY CONTRACTED KIDNEYS

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 PRIMARY CONTRACTED KIDNEYS
 KIDNEYS ARE
 SYMMETRICALLY ATROPHY
 EACH WEIGHING 110-130gr.
 With diffuse fine granularity
 Clinical diminished GFR,
Mild degree of proteinuria
 Without uremia

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 MALIGNANT ARTERIAL
HYPERTENSION
 FIBRINOID NECROSIS,
 NECROTIZING ARTERIOLITIS AND
 INTRAVASCULAR THROMBOSIS

ARE MAJOR MORPHOLOGIC

CHARACTERISTICS OF MALIGNANT
ARTERIAL HYPERTENSION

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 MALIGNANT ARTERIAL
HYPERTENSION

 FIBRINOID NECROSIS

 HYPERPLASTIC
ARTERIOLOSCLEROSIS
 AND THROMBOSIS
WITHIN LUMEN

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 MALIGNANT ARTERIAL
HYPERTENSION
 In malignant
nephrosclerosis, the
kidney demonstrates
focal small hemorrhages.
This is often due to an
accelerated phase of
essential hypertension in
which blood pressures
are very high (such as
300/150 mm Hg).

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 MALIGNANT ARTERIAL
HYPERTENSION
IS CHARACTERIZED BY
 DIASTOLIC PRESSURES GREATER THAN
120mmHg
 Papilledema of the kidneys
 Encephalopathy
 Cardiovascular abnormalities
 Renal failure
right up till
 uremia

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 Cerebrovascular diseases
There are three major categories of cerebrovascular
diseases as follow:
1 a generalized reduction in blood flow
with global hypoxic ischemic encephalopathy

2 infarcts caused by local artery obstruction

3 hemorrhages within the brain parenchyma

or the arachnoid space

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 Hypoxic ischemic encephalopathy
 Hypoxia is termed decreasing in the
oxygen available to tissue
 Ischemia is termed decreasing in tissue
perfusion
 Within the brain neurons are more
susceptible than glial cells to ischemic
hypoxic injure.

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 Hypoxic ischemic encephalopathy
 The brain may appear normal grossly and
microscopically due to cardiac arrest (a global
hypoxic-ischemic insult) in a period
immediately.
Within 1-2 days after acute insult, the brain is
softened and edematous, irregular
mottled discoloration in gray matter.

Softening and discoloration in the cortical mantle

is termed laminar cortical necrosis

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 Hypoxic ischemic encephalopathy
 Within 1-2 days after acute insult, the
brain is softened and edematous

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 Hypoxic ischemic encephalopathy
 The bilaterally symmetric
dark discolored areas
seen superiorly and just
lateral to the midline
represent recent
infarction in the
watershed zone between
anterior and middle
cerebral arterial
circulations. Such
watershed infarctions can
occur with relative or
absolute hypoperfusion of
the brain.

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 Hypoxic ischemic encephalopathy
 The neurons are the
most sensitive cells to
anoxic injury. Seen
here are red neurons
which are dying as a
result of hypoxia.

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 Hypoxic ischemic encephalopathy
 The Purkinje cells
between the
molecular and
granular layers of the
cerebellum are also
highly susceptible to
hypoxia. Those seen
here are red.

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 Infarcts

 Infarcts are caused by local interruption of

blood flow

 The lesions are the most common form of

cerebrovascular disease, accounting for
between 70%-80% of all cerebrovascular
strokes.

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 Infarcts
 Causes are atherosclerosis.
 The most severe atherosclerotic lesions
are evidence in the wall of the internal
carotid arteries, the proximal middle
cerebral arteries, and the basilar artery.
 The most common causes of vascular
occlusion in arteries with atherosclerosis
is thrombosis and embolism.

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 Infarcts
 the internal carotid artery with occlusive
thrombus

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 Infarcts

 The middle cerebral

artery is obturated by
Occlusive Thrombus

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 Infarcts
 Thromboemboli can lodge
in cerebral arteries,
particularly in the
distribution of the middle
cerebral, and peripherally
toward branch points.
Here is a
thromboembolus that
originated from mural
thrombus in the left
atrium. The heart is a
common source for such
emboli.

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 Infarcts
 The microscopic
appearance of this
acute cerebral
infarction reveals
marked edema (the
pale areas).

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 Infarcts

 Infarct of the
temporal lobe

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 Infarcts
 This magnetic resonance imaging scan
demonstrates subacute infarct near the
gray-white junction in the posterior
parietal region

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 Infarcts

This cerebral infarction

demonstrates
the presence of many
macrophages
at the right which are
cleaning up the
lipid debris from the
liquefactive necrosis.
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 Here is a large remote
cerebral infarction.
Resolution of the
infarction has left a
huge cystic space
encompassing much
of the cerebral
hemisphere.

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 Hypertension stroke
 Arterialpressure sudden raising
with organ lesion are termed
hypertension stroke
 Hypertension stroke reveals itself
as hemorrhages within the brain
parenchyma and subarachnoid
space.
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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 Mechanisms is very often rupture of the
vessels.
 The cause is hypertension first of all.

atherosclerotic aneurisms, trauma,

hyaline wall, vascular malformation,
vasculitis, amyloid deposits in the
vascular wall may be causes and
Contributions.
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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 Occur most commonly in the basal
ganglia, thalamus, cerebral white matter,
Pons, cerebellum.

Massive hemorrhage may be hematoma or

hemorrhagic infiltration

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 Hemorrhages involving
the basal ganglia area
(the putamen in
particular) tend to be
non-traumatic and caused
by hypertension, which
damages and weakens
the small penetrating
arteries. A mass effect
with midline shift, often
with secondary edema,
may lead to herniation.

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 This is a computed
tomographic (CT) scan
demonstrating a
hypertensive hemorrhage
in the right thalamus that
has extended into the
ventricular system.
Hemorrhages in this
location are not amenable
to surgical intervention
with removal of the
blood.

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 The large hemorrhage
in this adult brain
arose in the basal
ganglia region of a
patient with
hypertension. This is
one cause for a
"stroke".

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 The characteristic
location of the
hemorrhage in this brain
is consistent with a fall
backwards resulting in a
contracoup injury to the
inferior frontal and
temporal lobes. This has
resulted in extensive
contusions and
subarachnoid
hemorrhage.

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 Another cause for
hemorrhage,
particularly in persons
aged 10 to 30, is a
vascular
malformation. Seen
here is a mass of
irregular, tortuous
vessels over the left
posterior parietal
region.

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 The white arrow on the black card marks
the site of a ruptured berry aneurysm in
the circle of Willis. This is a major cause
for subarachnoid hemorrhage.

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PRIMARY BRAIN PARENCHYMAL
HEMORRHAGE
 Cyst formation as a result of hemorrhage

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THE END

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