Презентация на тему Cerebral-vascular diseases

with the critical narrowing of heart or brain vessels

at the patients with hypertension disease

CVD - it is a cerebral variant of atherosclerosis IHD - this is a cardiac variant of atherosclerosis Common pathological changes of vessels at CVD and IHD

stroke (ischemic, hemorrhagic, ischemic infarction with haemorrhages)








VASCULAR DISEASE OF

THE NERVOUS SYSTEM

with diffuse small-part character necrosis of neurons and hyalinosis

of vessels.
IE develops at the decrease of cerebral blood-volume less then 25-10 ml on 100gr of tissue.
At the decreasing of cerebral blood-volume in 2 times the ischemic damage of neurons is observed.

The ischemic encephalopathy (IE)

spasm of vessels
Reasons of the decreasing of cerebral blood-volume

of the cerebral cortex.
Adaptive (around-neuronal) satellitosis - glial cells are

gathered round neurons.
Zones of gliofibrosis are observed in the place of necrotic changers.

The ischemic encephalopathy (IE)

expressed atherosclerosis)

Outcomes of

IE

- violations of sensitiveness
- violations of motions
- violations of memory

The ischemic encephalopathy (IE)

moment of crisis a fibrinoid necrosis of the arteriole

walls of brain is observed, it leads to vascular-genic edema of brain (acute swelling).
The dislocation (herniation) of brain begins into the natural opening (foramen magnum);
The cortex layer of brain stake is hurt in the
process of dislocation;

The hypertensive encephalopathy

(in the zone of cardio-respiratory centers).
Displacement of cerebellum

in foramen magnum leads to compression of basal artery and ischemia of cardio-respiratory center.
The diapedesis haemorrhage arises up round vessels, so the cavities with haemosiderophages are formed. They are
named - lacunar infarcts.

The hypertensive encephalopathy

mm across, typically in the
deep structures of the

brain
In fatal cases, necrotic changers of blood vessels are seen, much like in the kidney at "malignant hypertension".

The hypertensive encephalopathy

memory, sensitiveness, motions and etc
Outcomes of HE

of a permanent, localized neurologic deficit, may result either

from hemorrhage (1) or infarction (2), and has a multitude of specific causes.

thrombosis or thrombi-emboli
ischemic infarction with hemorrhages (5-10%) - at embolism

of vessels
hemorrhagic infarction - "anemic infarcts"
complicated by dissolution of an embolus or backflow of blood from the margins.
Clinic: hemiplegia and disorders of sensitiveness on the other part of defeat, and disorders of speech at the involving of cortex of brain.

The infarction of brain

in which a patient with occlusive atherosclerosis of a

proximal subclavian artery suffers brainstem syndromes upon exercising the arm on the involved
Granulomatous angiitis of the CNS
Moyamoya disease - the process in which the vessels of the Willis circle and nearby become narrowed (fibrosis of the intima) and may bleed.

Reasons of brain infarcts

area of ischemia after the occlusion of artery and

the destruction of neurons, the brain becomes slightly discolored and soft.
through the third day - Three days after the "stroke", the cerebral matter becomes very soft. Necrosis with the softening begins on the 2-3 weeks (collikvation necrosis).
after 3-d weeks - resorbtion of the necrosis, formation of cyst

The evolution of brain infarction (stages)

one hemisphere of brain brings to the rapid dislocation

of brain & death.
The haemorrhage mass can break through into the ventricles of brain on any stage that leads to coma. The second trunk syndrome develops (defeat of reticular structure).

break of artery, or aneurism, or vascular malformations ("angiomas")
bleeding

disorders
hemorrhage into brain tumors (primary, metastatic)
Congo-philic (amyloid) angiopathy (hereditary, idiopathic; "Alzheimer's amyloid angiopathy")

Brain hemorrhage. Reasons.

visual hillock, rarely in the cerebellum and trunk of

the brain
Sub-arachnoidal hemorrhage.

According to morphology features
hematoma - massive bleading
hemorrhagic infiltration.

Brain hemorrhage. Classification.

innate or acquired aneurism.

Vascular malformations - may bleed into

the subarachnoid space, the brain substance, or both. Arteriovenous malformations (masses of large blood vessels) tend to be located in the hemispheres

Germinal plate hemorrhages in premature babies - bleeds into the ventricles, rather than the subarachnoid space.

Atherosclerotic aneurysms in the head are typically fusiform dilatations of the basilar
artery.

myocardial infarction, repeated myocardial infarction, Sudden cardiac death
Chronic IHD:

stenosis and occlusion of coronary arteries, postinfarction cardiosclerosis, chronic aneurism of heart wall.

Classification of Ischemic heart disease

relative or absolute insufficiency of coronal blood supplying that

is secondary leads to irreversible changers of myocardium.
CAUSES
Atherosclerosis of coronal arteries
Concentric hyalinosis and circulation stenosis

Ischemic heart disease

its supplying to myocardium.
Reasons of

development:
1. Prolonged spasm of coronal arteries at hypertension disease. Spasm that is longer than 60 minutes leads to myocardial infarction.
2. Coronal stenosis at atherosclerosis
3. Circular hypoxia at: cardiomyopathies, arrhythmias, heart vices, heart de-compensation

Angina pectoris

in a patient with coronary atherosclerosis, and relieved by

rest.
Unstable ("acute coronary insufficiency") angina - due to a thrombus developing, by fits and starts, over a ruptured plaque. In duration less than 60 minutes.
Prinzmetal's angina - primarily attributable to vasospasm. Sudden cardiac death can be observed at this patients.
Cardiac syndrome X ("microvascular angina") classical clinical angina and wide-open coronary arteries

Angina pectoris

myocardium by coronal blood supplying.
Reasons

of development:
Brief spasm of coronal arteries (less than 60 minutes)
Brief increasing of concentration of catecholamine at stress
Physical overload at stenosis of one
artery (haemodynamic disturbances)

Acute coronal insufficiency

ions, ets.
Damage by mediators of platelets, toxins leucocytes and

lymphocytes
Local necrosis and apoptosis of cardiomyocytes
Damage of endothelium that leads to thrombi formation

Acute coronal insufficiency. Complications and outcomes:

due to sudden loss of the blood supplying.

Myocardial infarction

overlying thrombus ("coronary thrombosis"); massive haemorrhage into a plaque,

ballooning its cap against the opposite wall.
Prolonged spasm of coronal arteries - more than 60 mines in duration
Physical overloading of patient with critical stenosis of coronal arteries (more than 75%)
Thrombosis of coronal arteries
Cocaine use, Prinzmetal's coronary spasm, Vasculitis, Embolization, Syphilis ,other

Myocardial infarction. Reasons.

transmural
According to time of development: acute primary - 4

weeks from the beginning, recidivating (relapsed) - the formation of the new necrosis during 4 weeks on the background of primary infarction, repeated - the formation of the new necrosis after 4-th week from the beginning of 1-st one.
According to the stage of development: Ischemic stage - 12-18 hours
Stage of necrosis - 18-24 hours up to 5 days
Stage of organization - 5 days - 7 weeks

Myocardial infarction. Classification.

the abbreviation of myocytes is halted, but during the 1-st

days a nuclear is stored, and membranes of organell’s gradually collapse (picnosis and eosinophylia of cytoplasm)
necrosis - in a 24 hour from the beginning of ischemia (kariolysis, kariopiknosis) of about 5-7 days, grows myomalyatsia of heart walls (wall is yellow-green), on periphery - hemorragic halo.
organization - into the area of necrosis vessels grow up and migrate fibroblasts - zone of cardiosclerosis. A scar is formed by the end of 2th month.

Morphological characteristics:

Drop a slice of heart in the solution, and viable

heart, containing an oxidizing enzyme, will stain brown, and dead heart remain pale.

Diagnose of ischemic stage of infarction during autopsy

Left-sided congestive heart failure, Cardiogenic shock, Acute coronal insufficiency
Stage

of necrosis: Rupture of the heart - occur, when the damaged heart is most soft (days 3-5),
Formation of acute aneurysm,
Mural thrombus formation in aneurism and embolization,
Rupture of the wall of acute aneurism,
Dressler's pericarditis (fibrin pericarditis)

Complications of myocardial infarcts