Questions to control the knowledge
1. Definition of the perinatal period, conception about periodisation and regularities of fetal development.
2. Etiology of kymatopathies. Teratogenic terminative periods.
3. Regularities of the kymatopathy pathogenesis.
4. Conception about gametopathies.
5. Etiology, pathogenesis and pathomorphology of the blastopathies.
6. Classification of the embryopathies.
7. Pathology anatomy of the congenital defects of the heart, CNS, alimentary tract, respiratory system, urinary system, muscular system.
8. Etiology, pathogenesis, pathomorphology and prognosis of the infectious and non-infectious fetopathies.
9. Age-specific changes of the placenta. What are developmental defects of the placenta do you know?
10. Main signs of the blood circulation disturbance in the placenta.
11. Name main types of the placentitis. Causes and conditions for their development.
12. Name morphological signs of the fetal immature and overmatture.
13. Etiology, pathogenesis and pathomorphology of the newborn asphyxia, pneumopathies and labor trauma.
14. Give definition for hemorrhagic disease of the newborn. Etiology, pathogenesis and pathomorphology of the disease.
Progenesis, prenatal period, gametopathy, kymatogenesis, blastopathy, embryopathy, fetopathy, teratogenic terminative periods, teratogenic agent, diplopagus, heteropagus, teratoma, craniopagus, thoracopagus, ischiopagus, anencephaly, acrania, microcephaly, hydrocephaly, porencephaly, cyclopia, rachischi-sis, Fallot's triad, tetrad and pentad, Hirschsprung's disease, meckel's diverticulum, agenesis, atresia, hypoplasia, dysplasia, epispadia, cryptorchidism, hermaphroditism, chondrodysplasia, achondroplasia, cheiloschisis, polydactylia, palatoschisis, micrognathia, hypertelorism, mucoviscidosis, endomyocardial fibroelastosis, placentitis, intervillisitis, villusitis, deciduitis, chorioamniotitis, amniochriodeciduitis, mortinatus, asphyxia, pneumopathy, pneumonia, labour trauma, cephalhematoma, hemorrhagic disease of the newborn.
DISEASES OF THE CENTRAL NERVOUS
Berry aneurysms are the most common type of aneurysm of cerebral arteries. Berry aneurysms are small saccular aneurysms that occur in about 2% of the population. Macroscopically they appear as rounded swellings arising from the cerebral arteries. Although they can be 0.2—3 cm in diameter, most are under 1 cm. Occurring particularly at the branch points of vessels around the circle of Willis, they are frequently multiple.
Aneurysms are prone to rupture, with consequent subarachnoid hemorrhage. Berry aneurysms arise because of developmental defects in the internal elastic lamina of vessels. The stress of the systolic waves causes herniation of the intima, with formation of saccular aneurysms. This is accentuated by hypertension, and aneurysms are commonly seen in association with coarctation of the aorta and adult polycystic renal disease.
Atherosclerotic aneurysms are most common in the basilar artery, where they tend to be fusiform. Infective (mycotic) aneurysms arise in cases of
infective endocarditis, when a small segment of arterial wall is acutely inflamed and dilates due to local bacterial infection from a small septic embolus.
Strokeis common in the elderly population. The clinical diagnosis of stroke is defined as a sudden onset of non-traumatic focal neurological deficit that causes death or lasts for over 24 hours.
The terms minor stroke and reversible ischemic neurological deficit are used when recovery of clinical features occurs after a period of time, usually defined as 7 days.
The causes of stroke can be divided into two main groups: ischemic, caused by cerebral infarction and hemorrhagic, caused by intracerebral and subarachnoid hemorrhage.
Regional cerebral infarcts are caused by occlusion of main arteries supplying the brain. The most common causes originate outside the cranial cavity, e.g. emboli from the heart, aorta or carotid vessels, and thrombosis in the carotid or vertebral arteries, predisposed by atheroma.
Macroscopically, cerebral infarcts correspond to the territory of supply of the occluded arteries. It is difficult to see an infarct in the first 24 hours, as changes are limited to focal swelling and blurring of the normal demarcation between grey and white matter, termed a pale or anemic infarct. If there is lysis of an occlusive thrombus, the infracted area may be reperfused with blood, resulting in a hemorrhagic
infarct. By about one week the infracted area becomes macroscopically soft.
Microscopically, it is infiltrated by macrophages, which remove dead tissue. Proliferation of astrocytes occurs around the margins of the infarct, and these partly replace the dead tissue, usually being well established by about 2 weeks. Larger regional areas of infarction invariably heal as fluid-filled cystic spaces bounded by gliosis.
Outcome: large cerebral infarcts may cause death by associated cerebral swelling, leading to herniation, and brain stem compression. Infarcts in critical sites, particularly brain stem infarcts, may interfere with vital functions and lead to death.
Lacunar infarction is caused by arteriolosclerosis of small vessels.
Lacunar infarcts are small, often slit-shaped, areas of infarction that are less than 1 cm in maximum diameter. They are an important form of cerebral infarct, particularly in patients with hypertension and diabetes, being caused by hyaline arteriolosclerosis.
Macroscopically, lesions are usually multiple and are seen in the sites normally supplied by fine perforating branches, such as the basal ganglia, internal capsule, thalamus and pons.
Multiple lacunar infarcts in the basal ganglia cause a syndrome of rigidity and abnormal gait, which superficially resembles Parkinson's disease, termed «vascular pseudo-Parkinsonism». Lacunar infarction
is also associated with ischemic white-matter degeneration, an important cause of dementia.
Cortical laminar necrosis is caused by generalized failure of perfusion. Diffuse necrosis of cerebral cortical neurons is the pattern of infarction seen in generalized failure of blood flow or oxygenation as seen, for example, following cardiac arrest, with severe hypoglycemia and after carbon monoxide poisoning.
The changes develop 24 hours after resuscitation from the damaging episode. There is widespread damage to the cerebral cortex, with death of the majority of cortical neurons. With time, there is phagocytosis of dead neurons with astrocytic gliosis. Macroscopically the cerebral cortex is shrunken and there is extensive loss of axons from the brain, causing white matter loss.
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