Arterial hypertension

1. Arterial hypertension

2. Definition
Hypertension or high blood
pressure is a chronic medical
condition in which the systemic
arterial blood pressure is elevated.

3. Arterial hypertension is defined as
borderline when it reaches 140/95mmHg
and hypertensive when its 165/95mmHg.
The elevation of systolic pressure alone
(systolic hypertension) or elevation of both
systolic and diastolic pressure (diastolic
hypertension), both have an increased risk
of complication, but diastolic hypertension
is more dangerous.

4. Classification
Primary or essential hypertension in which the
cause of increase in blood pressure is unknown. This
hypertension constitutes about 90-95% patient with
hypertension.
Secondary hypertension, remaining 5–10% of
cases are caused by other conditions that affect the
kidneys, arteries, heart, or endocrine system.

5. Cause of Primary hypertension - stress
 Risk factors - sedentary lifestyle, smoking, visceral
obesity, potassium deficiency (hypokalemia), obesity
(more than 85% of cases occur in those with a body mass
index greater than 25), salt (sodium) sensitivity,
alcohol intake, and vitamin D deficiency
 Risk also increases with aging, some inherited genetic
mutations, and having a family history of hypertension. An
elevated level of renin, a hormone secreted by the
kidney, is another risk factor, as is sympathetic nervous
system over activity. Insulin resistance, which is a
component of syndrome X, is also thought to contribute
to hypertension. Recent studies have implicated low birth
weight as a risk factor for adult essential hypertension.

6.  Secondary hypertension - causes include renal
parenchymal disease (eg, chronic glomerulonephritis
or pyelonephritis, polycystic renal disease, connective
tissue disorders, obstructive uropathy), diseases of
epynephry and tyroid glands - pheochromocytoma,
Cushing's syndrome, primary aldosteronism, congenital
adrenal hyperplasia, hyperthyroidism, myxedema.
Excessive alcohol intake and use of oral contraceptives
are common causes of curable hypertension.
 Use of sympathomimetics, NSAIDs, corticosteroids,
cocaine, or licorice commonly contributes to
hypertension.

7. Signs and symptoms
 Hypertension is usually asymptomatic until complications
develop in target organs. Dizziness, flushed facies,
headache, fatigue, epistaxis, and nervousness are not
caused by uncomplicated hypertension.
 Severe hypertension can cause severe cardiovascular,
neurologic, renal, and retinal symptoms (eg, symptomatic
coronary atherosclerosis, HF, hypertensive
encephalopathy, renal failure).

8.  Pregnancy - Hypertension in pregnant women is one
symptom of pre-eclampsia. Pre-eclampsia can progress to
a life-threatening condition called eclampsia, which is the
development of protein in the urine, generalized swelling,
and severe seizures. Other symptoms indicating that
brain function is becoming impaired may precede these
seizures such as nausea, vomiting, headaches, and vision
loss. In addition, the systemic vascular resistance and
blood pressure decrease during pregnancy. The body
must compensate by increasing cardiac output and blood
volume to provide sufficient circulation in the utero-placental
arterial bed.

9. Morphological types of essential
hypertension
1. Subclinical stage (transitoric)
2. Stage with morphological changes of
blood vessels
3. Stage with morphological changes of
inner organs

10. 1-st stage
1. Hypertrophy of muscle layer of
small arteties (intimal thickening
due to proliferation of smooth
muscle cells in the intima).
2. Hypertrophy of left ventricle of
the heart.

11.  2-nd stage
Changes in the blood vessels involves
 1. arterioles and small arteries:
arteriolohyalinosis, arteriolosclerosis,
often in the brain, kidneys, pancreas, retina
of eyes, intestine.
2. elactic fibrosis (myoelastic fibrosis) of
arteries of large and middle calibre and
severe atherosclerosis

12. 3-d stage. Clinical types of essential
hypertension
Cardiovascular
Renal
Cerebral
Ischemic brain damage
Intracranial hemorrhage

13. Intracranial hemorrhage ( intracerebral and
subarachnoid hemorrhage)
 Hypertensive over middle age have microancurysm in
very small cerebral arteries in the brain tissue. Common
sites of hypertensive intracerebral hemorrhage are the
region of the basal ganglia, pons and cerebellum cortex.
40% of patient dies during the first 3-4 days of
hemorrhage, mostly from hemorrhage into the ventricles.
The outcome of intracerebral hemorrhage is cyst
formation.

14. Renal
 Renal type of hypertension may be benign or malignant.
Benign nephrosclerosis is the term used to describe the
kidney of benign phase hypertension. Both kidney are
affected equally and are reduced in size and weight. The
capsule is often adherent to the cortical surface. The
surface of the kidney is finely granular and shows V-shaped
areas of scaring. The cut surface shows firm
kidneys and narrowed cortex. Clinical features are
variable, elevation of blood pressure with headache,
dizziness, palpitation. Renal failure and uremia may occur.

15. Cardiovascular
 Hypertensive heart disease is a common form of heart
disease. The most significant findings are marked hypertrophy
of the heard especially of the left ventricle. Weight of the
heart increases to 500-700gram. The weight of the heart is
directly related to the severity of hypertension but there is no
correlation between the weight of the heart and duration of
hypertension. The left ventricular wall is thickened, the
papillary muscles are rounded and prominent and the cardiac
chamber is small, but when decompensation and cardiac
failure develops, there is an eccentric hypertrophy with
thinning of the ventricular wall and dilation of the left
ventricular and atrial cavities. There may be dilation and
hypertrophy of the right heart as well.

16. Ischemic brain damage (hypoxic
encephalopathy and cerebral infraction)
 Brain in hypoxic encephalopathy varies depending on the
duration and severity and the length of survival.
 Macroscopically there is a focal softening. The area
supplied by distal branches of the cerebral arteries suffers
from the most severe ischemic damage and may develop
border zone or watershed infracts in the adjacent zones
between the territories supplied by major arteries.
Microscopically the nerve cells die and disappear and are
replaced by reactive fibrillary glia.

17.  Cerebral infraction is a localized area of tissue necrosis
caused by local vascular occlusion. Clinically the signs and
symptoms associated with cerebral infraction depends on
the region infracted. Cerebral infracts may be anemic of
hemorrhagic.
 An anemic infract becomes evident 6-12 hours after it
occurs. The area affected is swollen and there is blurry
junction between grey and while matter. Within 2-3 days,
the infract undergoes softening and disintegration.
 A hemorrhagic infract is red and superficially resembles a
hematoma. Usually it’s the result of fragmentation of
occlusive arterial emboli or venous thrombosis.
Hemorrhage into the brain of patient with hypertension
is intracerebral hemorrhage which is usually of
hypertensive origin.

18. Photomicrographies of arteries
showing severe medial
hypertrophy
(a)Pre-acinar artery;
(b) Intra-acinar artery.
Miller elastic stain, objective
magnification 20x

20. ventricle is markedly thickened in this patient with severe
hypertension that was untreated for many years. The myocardial
fibers have undergone hypertrophy

21. This left ventricle is very thickened (slightly over 2 cm in thickness), but the
rest of the heart is not greatly enlarged. This is typical for hypertensive heart
disease. The hypertension creates a greater pressure load on the heart to
induce the hypertrophy.

22. Gross- Kidney, arterial and arteriolosclerosis
This is the cortical surface of a kidney from a patient with long-standing severe
hypertension. The cortical surface is pitted and irregular, representing focal loss of
renal cortex secondary to patchy ischemic atrophy. In between larger areas of
(arterial) scarring, the cortical surface is finely granular, reflecting ischemic injury in a
small-vessel (arteriolar) distribution. This finely granular pattern of scarring is
referred to as arteriolar nephrosclerosis.

23. Kidney, arteriolosclerosis (in medium power)
There is hyaline arteriolosclerosis of the small vessels of the kidney. Hyaline
arteriolosclerosis is encountered in diabetics, elderly patients, and patients with
hypertension. It is more generalized and severe when associated with hypertension or
diabetes. The arteriolar walls are thickened and largely replaced by a homogeneous pink
hyaline material. The lumina are narrowed. Hypertension generates some of its
pathologic effects by causing endothelial damage. The hyaline material is probably
derived from plasma proteins that have leaked across endothelial barriers and
accumulated over the years. The narrow lumina limit cortical flow. There are glomerular
atrophy and secondary changes in the dependent nephron.

24. Heart, concentric left ventricular hypertrophy
Above are two cross sections of left ventricle from a patient with severe long-standing
hypertension. There is severe left ventricular hypertrophy. The
hypertrophy is designated concentric because the left ventricle and septum are of
approximately equal thickness. The walls of the ventricles are thickened, but the
cavity size is decreased. Left ventricular hypertrophy is a response to chronically
elevated afterload (high peripheral vascular resistance).

25. Aorta, cystic medial necrosis (low power)
The aortic wall in most cases of aortic dissection is weakened by cystic medial
necrosis. This image shows a section of aorta with multiple areas of cystic medial
necrosis. The tissue is stained with an elastic stain that stains the elastic tissues black.
The areas of cystic medial necrosis can be recognized as zones in which the elastic
laminae have been lost.

26. Aorta, cystic medial necrosis (High power)
This is an aorta from a patient who died of aortic dissection. The elastic laminae are
stained black. Note the paucity of elastic fibers in this area of cystic medial necrosis.
Compare with a normal aorta. Elastic tissue is a very important component of the
arterial media. It allows the aorta to expand during systole and slowly recoil during
diastole. It also provides a framework on which the aortic smooth muscle can
attach, and, thus, imparts some strength to the arterial wall. When the elastic
laminae are missing or destroyed, the aorta loses both its elasticity and its ability to
withstand shearing forces

27. Аrteriolosclerosis
This form of arteriolar injury is seen in patients with malignant hypertension. In contrast to the
relatively acellular hyaline material of hyaline arteriolosclerosis, this is a very cellular lesion.
Smooth muscle cells are proliferating and undergoing hypertrophy in an attempt to cope with
rapidly rising blood pressure. The arteriolar and arterial lesions in malignant hypertension
appear as thickened concentric rings of media and intima surrounding narrowed vascular lumina.
Malignant hypertension is often a disease of young black males and is a medical emergency.
Renin and aldosterone are usually quite high in this disease. The extremely high pressures found
in this disease are associated with widespread endothelial injury, thrombosis, and intravascular
coagulation syndromes. There is widespread ischemic injury in multiple organ systems. Renal
failure and central nervous system hemorrhage can be rapidly fatal

28. Kidney, fibrinoid necrosis in malignant hypertension
The kidneys are dramatically affected in malignant hypertension. In addition to
hyperplastic small vessel changes, there may be fibrinoid necrosis. The vessel walls
contain a smudgy, eosinophilic, fibrin-like material. In this case, fibrinoid necrosis of
the afferent arteriole will probably lead to loss of the glomerulus and its dependent
nephron

29. Brain, thalamic hemorrhage
This brain has been cut in a plane from frontal to occipital cortex in an orientation that
attempts to match that of a CT scan. There is an area of acute hemorrhage in the
thalamus. Massive central nervous system hemorrhage and stroke are important as causes
of death in patients with longstanding severe hypertension. Hypertension-associated acute
CNS hemorrhage often begins in the deep grey matter of the cerebral hemispheres
(putamen, thalamus), in the pontine tegmentum, or cerebellar hemispheres. The
cardiovascular system and the kidney are also at risk in patients with hypertension.

30. Causes of death
Congestive heart failure
Cerebrovascular accidents
Cardiac complication
Causes related to hypertension