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Assistant-prof. V.Voloshyn

According prof. Bodnar Ya.Ya. & prof. Sorokina I.V.

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Anaemias are the group of diseases or syndromes which are

characterized by the decreasing of haemoglobin and red corpuscles rate

(maintenance) in a volume unit of blood or their morphofunctional

properties

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Pathology of red corpuscles

normocytosis megaloblastes

anisocytosis, hyperchromia, hypochromia poikilocytosis

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There are 3 basic groups of anaemias in dependence from etiology and pathogeny:

1) posthemorrhagic (predefined by blood losing);2) anaemias are predefined by violations in the haemopoetic system;3) haemolitic (predefined by enhanceable destructions of hemocytes).

Anaemias classification

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Acute posthemorrhagic anaemia Acute anaemia is observed

after the massive bleeding from the vessels of stomach, varicose extended veins of oesophagus, break of pipe at extra-uterine pregnancy, corrosium branches of pulmonary artery by a tuberculosis process and others like that.

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Acute posthaemorrhagic anaemia

Anaemia as a bled result can have acute or chronic motion.

Acute posthaemorrhagic anaemia arises up at a fast and massive bleed.

The bleeding is more dangerous for life when the bleeding vessels have larger caliber and are situated nearer to the heart.

For example, at the break of aorta arc a patient loses less a 1 liter of blood, death is conditioned by the acute catastrophic falling of arterial pressure and deficit of filling of heart chambers. Death comes quickly (rapid) than anaemia develops. Consequently it does not follow to attribute the indicated state to anaemia.

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Hemopericardium

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Acute posthemorrhagic anaemia

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Acute posthemorrhagic anaemia

Death comes at the loss more than half of total volume of blood

The skin of dead body and internal organs are bloodless, pale and of corpses blots are expressed badly & almost not noticeable

Stages of development of acute posthemorrhagic anaemia: spasm of capillaries; outputting of intercellular liquid in the blood river-bed; centralization of blood circulation; disruption of compensation.

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Chronic posthemorrhagic anaemia

predefined by slow, but long duration bleed.

It is observed at the small bleeding from the tumours of digestive canal, which are having sores; haemorrhagic gastric and duodenum ulcers, haemorrhoidal veins ulcers, meno-& metrorrhagiae and others like that.

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Signs of chronic posthaemorrhagic

anaemia

pallor of skin and internalss; substituting of yellow marrow

by red, which actively regenerate in diaphysis of tubular bones;

The are appearance of the haemopoetic extramarrow (heterotopic) places in the liver, kidneys, hypoderm;

At tissues hypoxia there are cardiomyoliposis (tiger heart), lipid dystrophy in a liver, kidneys, dystrophic changes in a brain cortex;

plural point hemorrhages in serosal and mucuses membranes.

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Anaemias which are predetermined by haemopoesis violations Anaemias of this type are predetermined by the condition of the matters deficit which necessary for an erythrogenesis or pathology of regeneration of blood synthesis tissue.1.Irons scarcity:

a) as a result of alimentary insufficiency of iron; b) as a result of exogenous insufficiency of iron in connection with the

enhanceable necessities of organism; c) as a result of absorption insufficiency of iron (enteritises, enterectomy); d) idiopathic.

2.Conditioned to violations of synthesis or utilization of porphyry: a) inherited b) purchased (lead poisoning, deficit of B6 vitamin)

3.Conditioned to violations of DNA & RNA synthesis – megaloblastic anaemias. a) as a result of deficit of B12 vitamin (malignant); b) as a result of folium acid deficit: c) inherited anaemias, conditioned by violation of enzymes activity which take

part in the synthesis of purin and pyramidin bases. 4.Hypoplastic and aplastic anaemias, evocation by endogenous, exogenous or inherited factors.

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Iron deficiency anemia Iron deficiency anemia of early age. Early and late chlorosis. Symptomatic chloranemia which develops at

different pathological conditions of gastrointestinal tract (achylic, agastric, anenteral etc.) in infections (tuberculosis).

Hypochromic anemia of pregnancy. Posthemorrhagic anemia which indeed is iron

deficiency anemia. Chlorosis (called so because of pale greenish color

of skin in this disease).

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COMMONS MORPHOLOGICAL DISPLAYS OF ANAEMIAS PREDEFINED BY VIOLATION OF HAEMOPOESIS

stromal-vascular changes: stromal swelling and fibrosis in organs, diapedetic hemorrhages, hemosiderosis;

change of parenchyma elements: dystrophy and atrophy;

compensatory displays in the haemopoetic system: the yellow marrow transformated into red in tubular bones, the development of extramarrow haemopoetic places in the

lymphatic nodes, spleen, liver stromae, fatty cellulose of kidney hilus & serosas.

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Pathoanatomy of Irons scarcity anaemia

Parenchimatic dystrophy of internalss. Dryness of skin. There are cracks in the mouth corners. Atrophy of tongue papillae, gastratrophia. Hyperplasia of red marrow and. Formed

the niduses of extramarrow haemopoesis. Irons scarcity anaemia is hypochromic

always. c.i. 1.0( 0.4 – 0.5)

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There are inherited and purchased::::::::::::::::::::::::::::::::::::::::::::::::::::::::: Inherited In 1945 T. Kuli described anaemia of brothers in five generations, the decline of enzymes activity which took part in the synthesis of haemoglobin lay in basis of this anaemia. At men a defect is coupled with X-chromosome. The synthesis of porphyries is violated, that does not give to link iron, and it accumulates in an organism. The whey (cироватка) contains the iron a lot but efficiency of erythrogenesis is low. The erythrocytes are basophilic and there are a little haemoglobin in them. Plenty of sideroblasts are accumulated in marrow. A hemosiderosis appears in many organs and tissues, so as iron are taken by macrophages. In course of time a cirrhosis which clinically shows up hepatic insufficiency develops in a liver. The changes in myocardium give cardiosclerosis and heart-vessels insufficiency; sclerotic changes in a pancreas give the symptoms of saccharine diabetes, in testicles – eunuchoidism.

ANAEMIAS CONDITIONED by VIOLATION of SYNTHESIS & MASTERING (assimilation) of PORPHYRIES

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Purchased Anaemias:lead (Pb) poisoning: lead fixes on the membranes of erythrocytes and locks the sulfurichydryl groups of enzymes in the haemsynthesis. It violates activity of Na+ and K+ dependent АТFasis, that lead (conduces) to the decline Kalium in the erythrocytes. Plenty of reticulocytes (to 8%) appears in blood, and aminolevulinic acid is in urine. Metabolism of the nervous system is violated, motive polineuritis develops, especially in hands, asthenia, violation of gastroenteric canal (colics, atony). Anaemia, as a result of deficit of vitamin of B6 arises up rarely. B6 vitamin is an instrument in the porphyry synthesis, its deficit arises up sometimes at the long duration application of antituberculouss at adults, and at children on the artificial rearing.

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A. Pernicious anemia (Addison-Biermer) due to deficiency of gastromucoprotein in the gastric juice.

B. Pernicious anemia after stomach resection for cancer, polyposis.

C. Pernicious anemia in diseases of small intestine due to disturbed absorption of vitamin B12.

D. Helminthic pernicious anemia.

E. Pernicious anemia of pregnancy due to fetal growth and increased consumption of vitamin B12 and folic acid.

F. B12 achrestic anemia due to disturbances of B12 utilization in the bone marrow.

В12 vitamin folium-deficit anaemia (pernicious anemias) classification

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В12 vitamin folium-deficit anaemia

Megaloblastic type of haemopoesis. Guntr's glossitis. Funicular myelosis (the decline of myelinsyntesis is in a

spinal cord). General haemosiderosis Likegelatin marrow Anaemia. (chronic hypoxy, fatty dystrophy of

parenchimatic organs, common obesity)

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The mucous membrane of the stomach at Addison-Biermer disease

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В12 vitamin folium-deficit anaemia

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Anaemias which arise up as a result of deep oppression (depression) of haemopoetic processes by both endogenous and exogenous factors.These factors conduce to the loss to ability of marrow cells to the regeneration. As a result marrow of flat bones substitutes by fatty tissue (“consumptions” of marrow) – panmyelophtosis

Hypoplastic and aplastic anaemias

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Marrow at a haemophthisis (hypoplastic anaemia)

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Endogenic: 1. Endocrine (hypothyroidism, thymus tumors). 2. Genuine (Ehrlich's aplastic anemia). 3. Osteomyelosclerosis. Exogenic: 1. Radiation lesions (x-rays, radium radiation, atomic energy). 2. Chemical (benzene, cytostatic preparations, etc. 3. Toxicoallergic: a) medicinal (pyramidon, barbiturates, sulfanilamides); b) antibiotics (Chloromycetin).

4. Infectious.

Hypoplastic and aplastic anaemias classification (by etiology):

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Inherited (congenital) aplastic anaemias:

Endogenous: inherited family factors. Among the inherited aplastic anaemias select domestic

aplastic anaemias of Falkoni and hemophthisis of Erlich domestic aplastic anaemias of Falkoni. It has a chronic motion and characterized by:

hyperchromic anaemia, the expressed haemorragic syndrome, defects of development.

Hemophthisis of Erlich. It has acute or subacute motion and is characterized by

progressive death of active marrow, expressed hemorragic syndrome, can be complicated by a sepsis.

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Hemophthisiss are predefined by exogenous factors

a) radiation anaemia (radiation action); b) toxic matters (toxic benzol anaemia); c) medicinal anaemia:• a long duration using of wide spectrum action antibiotics which stop the mitosis not only microorganisms but also haemopoetic cells; • a long duration using of sedative preparations (violation of the neuro-humoral regulation of haemopoesis);• a long duration using of paracetamol group preparations (toxic action on red marrow);d) replacement of normal haemopoetic tissue by other (the metastases of tumours, substitution by bone tissue(osteosclerosis) osteosclerotic anaemia at marble illnesses of Albers-Schoenberg at osteomyelopoetic dysplasia)

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Haemolytic anaemia.Haemoglobin-uremic nephrosis.

In the cytoplasm of epithelium of proximal ductules are vacuoles (V) containing the corns of haemoglobin

(Gb). In separate vacuoles haemoglobin is concentrated; there we are marked high activity of

sour fosfatazy (black granules)

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Sickle-cell anemia

Normal cells Sickle-cells

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Erythroblast at haemolytic anaemia

There are plenty of granules (Gr) which contain iron in mitochondria (M)

Gr

Gr

Gr

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Thank you for attention!