SIW ON THE TOPIC: HEART DEFECTS PERFORMED: 3-048GM CHECKED: ZHURAVLEV S.N. Karaganda State Medical University Department of pathological anatomy

Content Heart defects Classification Morphology Etiology Pathogenesis Used literature

Heart disease- is a permanent irreversible disorder in the structure of the heart, which violates its function.

Classification CongenitalAcquired Acquired heart defects are characterized by damage to the valvular apparatus of the heart and the main vessels and arise as a result of heart disease after birth. Among these diseases, rheumatism is more important, less - atherosclerosis, syphilis, bacterial endocarditis, brucellosis, and trauma. Acquired heart diseases are chronic diseases, in rare cases, for example, when valve flaps are destroyed due to ulcerative endocarditis, acutely occur. on frequency take the second place after vices of development of the central nervous system. According to different authors, they occur in 16-40% among other vices and in 3-8% of cases according to autopsies of children who died in the perinatal period.

Acquired heart diseases The mechanism of formation of acquired heart disease is closely related to the evolution of endocarditis, resulting in the organization of thrombotic masses, scarring, petrification and deformation of valves and fibrous rings. Progression of sclerotic changes is facilitated by hemodynamic disturbances that arise during the formation of a blemish. Pathological anatomy. Sclerotic deformation of the valvular apparatus leads to the failure of valves that are not able to close tightly during their closing, or narrowing (stenosis) of the atrioventricular apertures or the mouths of the main vessels. With a combination of valve failure and stenosis, the holes indicate a combined heart disease. Possible damage to the valve (isolated defect) or valvular heart valves (combined defect).

Congenital heart disease Etiology and pathogenesis. The causes of these defects are diverse and not related to the influence of any specific exogenous factors. The genetic mutations and chromosomal aberrations have an undeniable significance. Among the multiple defects observed in chromosomal diseases, heart defects are less common than CNS defects. The development of the defect is associated with the effect of the damaging agent on the embryo from the 3rd to the 11th week of intrauterine development. Different types of vices depend on the distortion of the stages of the heart's morphogenesis, of which the defects of the initially paired heart valves, the irregular bends of the primary cardiac tube, the developmental delay or the wrong arrangement of the heart part dividing it and the arterial trunk into the right and left halves, the persistence of the atrioventricular compounds that exist during fetal life. Pathological anatomy. In congenital heart defects in the process of myocardial hypertrophy, children not only increase the volume of muscle fibers with hyperplasia of their ultrastructures but also true hyperplasia of cardiomyocytes in children aged 3 months of life. At the same time, hyperplasia of reticulin argyrophilic stromal fibers develops. Subsequent dystrophic changes in the myocardium and stroma, up to the development of micronecrosis, lead to a gradual growth of connective tissue and the emergence of diffuse and focal cardiosclerosis.

TYPES OF VALVE HEART DISEASES Distinguished Isolated and associated defects of one valve (insufficiency + stenosis) and combined defects - two or three valves

Also on hemodynamics distinguish: -White vices, when there is no mixing of venous and arterial blood, that is, with the left-right direction of discharge. -Blue vices are divided into two types: With enrichment of the pulmonary circle. For example, with the Eisenmenger complex or the absolute transposition of the main vessels. With impoverishment of the pulmonary circle. For example, the anomaly of Ebstein or tetrad of Fallot.

INSUFFICIENCY OF THE MITRAL VALVE Insufficiency of the mitral valve - incomplete closure of valve flaps during ventricular systole, accompanied by regurgitation of blood from the LV to the LP. Can be functional and organic

MITRAL STENOSIS Narrowing of the left atrioventricular orifice due to fusion of the mitral valve flaps, which leads to difficulty in emptying the LA and increasing the pressure gradient between the LA and LV. Deformation of the valves and stenosis of the mitral orifice

Illusrtation Facies mitralis Swollen cervical veins

The narrowing of the aortic isthmus (coarctation), up to its atresia, is compensated by the development of collateral circulation through the intercostal arteries, the arteries of the chest and the sharp hypertrophy of the left ventricle of the heart.

Congenital heart defects with violations of the fission of the arterial trunk. The common arterial trunk with complete absence of fission of the arterial trunk is rare. In this defect, one common arterial trunk originates from both ventricles, the exit has 4 semilunar valves or less; The defect is often combined with a defect of the interventricular septum.

A complete transposition of the pulmonary artery and aorta arises when the direction of growth of the arterial wall is wrong, when it grows not in a spiral, but in the direction opposite to the other, normally developing parts of the heart.

Combined congenital heart disease. Among the combined vices more common are the triad, tetrad and pentad of Fallot. Triad Fallot has 3 signs: a defect of the interventricular septum, stenosis of the pulmonary artery and as a consequence of this hypertrophy of the right ventricle. The tetralogy of Fallot has 4 signs: the defect of the interventricular septum, the narrowing of the pulmonary artery, dextralization of the aorta (displacement of the aortic aperture to the right) and hypertrophy of the right ventricle of the heart. Penta Penta, in addition to these four, includes the 5th sign - the defect of the interatrial septum.

Used literature anatomy/32418/ anatomy/32418/ Струков А.И., Серов В.В. «Патологическая анатомия» 0%BE%D0%B6%D0%B4%D1%91%D0%BD%D0%B D%D1%8B%D0%B5_%D0%BF%D0%BE%D1%80% D0%BE%D0%BA%D0%B8_%D1%81%D0%B5%D1 %80%D0%B4%D1%86%D0%B0 0%BE%D0%B6%D0%B4%D1%91%D0%BD%D0%B D%D1%8B%D0%B5_%D0%BF%D0%BE%D1%80% D0%BE%D0%BA%D0%B8_%D1%81%D0%B5%D1 %80%D0%B4%D1%86%D0%B0

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