Morphological changes (accumulations) occur inside and outside cells

Transcription

1 MIXED ACCUMULATIONS (DEGENERATIONS)

2 Morphological changes (accumulations) occur inside and outside cells

3 The group includes: - chromoproteins metabolism disturbances; - lipoproteins metabolism disturbances; - nucleoproteins metabolism disturbances; - mineral metabolism disturbances.

4 Chromoproteins metabolism disturbances

5 Chromoproteins are colored proteins (or pigments)

6 They can be: - hemoglobinogenic; - lipidogenic; - proteinogenic

7 Hemoglobinogenic pigments normal abnormal (pathologic ) - Hemosiderin; - Ferritin; - Bilirubin - Porphirin; - Hematoidin; - Hematins

8 Hemosiderin hemosiderosis (result of increased synthesis of hemosiderin with its accumulation in organs and tissues)

9 Hemosiderosis can be: - hereditary (tesaurismosis); - acquired (local or general)

10 Acquired general Why? intravascular erythrocytes hemolysis. When? blood diseases; poisoning by hemolytic poisons (eg. snakes venom); severe infections (such as malaria); incompatible blood transfusions. Where? liver; spleen; lymphatic nodes; bone marrow. Outward appearance? enlarged, brown

11 Micro? accumulation of brown color pigment which there is in specific cells - sideroblasts

12 Sideroblast large cell with large nucleus, thin cytoplasm and lot of siderosomes, containing hemosiderin. Hemosiderin s grains consist of ferritin molecules

13 Acquired local Why? extravascular erythrocytes hemolysis. When? hemorrhages, diapedesis of erythrocytes in venous congestion. Where? everywhere Classic example lung hemosiderosis in chronic venous congestion (brown induration of lung)

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16 Brown induration of lung (Perls stain for iron)

17 Bilirubin metabolism disturbances its increased containment in blood, tissues jaundice

18 Manifestations: - hyperbilirubinaemia; - yellow color of skin, scleras, visible mucous membranes; - only in obstructive jaundice there is intoxication due to cholalaemia (bile in blood)

19 Types of jaundices - prehepatic (hemolytic) - intravascular erythrocytes hemolysis; - hepatic (parenchimatous) injury of hepatocytes hepatoses, hepatitides, liver cirrhoses; - posthepatic (obstructive) blockade or difficulties of bile outflow cholelythiasis, tumors of pancreas or bile ducts, destructive diseases of bile ducts, congenital defects of their structure, malignant tumour metastases into hepatic lymph nodes.

20 Liver in obstructive jaundice enlarged, green-yellow

21 Liver in obstructive jaundice accumulation of bilirubin into hepatocytes cytoplasm

22 Porphyrin containment disturbances porphyria congenital disease due to insufficiency of enzymes in hemoglobin metabolism Very rare Hypersensitivity to sunlight realizes as necrosis of skin and other membranes. Moonlight child

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24 Hematoidin form of hemosiderin which is synthesizing in hypoxia/ Usually is observed in old hemorrhages

25 Hematins group of pathological hemoglobinogenic pigments appearing in different specific pathological situations

26 Hemomelanin malaria pigment. Hydrochloric acid hematin peptic ulcers. Formaldehyde pigment.

27 Lipidogenic pigments: - lipofuscin; - ceroid; - pigment of vitamin E insufficiency; - lipochromine.

28 Lipofuscinosis - primary (as rule hereditary) - secondary (cachexias, atrophies, some vitamins deficiency, chronic intoxications by hydrocarbons, over- indulgence in analgetics (especially methamysolum)

29 Most perfect examples are brown atrophy of liver and myocardium (often in elderly persons): the organs are decreased in sizes and brown; at the histological examination yellowish or light-brown small grains of lipofuscin there in cellular cytoplasm are observed.

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33 Proteinogenic pigments: - melanin; - adrenochromine; - pigments of APUD-system cells grains.

34 Disturbance of melanin containment - melanosis

35 Melanosis can be: - hypermelanosis and hypomelanosis; - hereditary and acquired; - local and general.

36 General acquired hypermelanosis Addison's disease bilateral destruction of adrenal glands hypogonadism pellagra scurvy cachexia General hereditary hypermelanosis pigment xerodermia

37 Pigment xerodermia

38 Local acquired hypermelanosis melanosis of the large intestine in elderly people suffering from chronic constipation; black acanthosis (skin areas with increased pigmentation) in hypophyseal adenoma, hyperthyroidism, diabetes mellitus. Increased local formation of melanin is observed in nevus, which may turn in malignant tumors melanoma.

39 Nevus (mole, birthmark)

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43 Melanoma

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47 Hypomelanosis general (albinism) local (vitiligo)

48 albinism

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50 Nucleoproteins metabolism disturbances

51 - Urolithiasis; - Uric acid infarction of kidneys in newborns; - Gout.

52 Gout chronic disease is characterized by sedimentation of uric acid salts (urates) in organs and tissues and accompanied with hyperuricaemia and hyperuricuria. More often urates is accumulated in skin, joints, kidney, blood vessels.

53 Necrosis, chronic inflammation, sclerosis results of urates sedimentations in a tissue. Irreversible deformation of joint. Chronic renal failure (gout kidney tubulopathia).

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58 Mineral metabolism disturbances

59 Сalcium metabolism disturbances pathological calcification sedimentation of calcium salts into organs and tissues

60 Pathological calcification can be: According to the location: intracellular, extracellular and mixt. According to propagation: systemic and local. According to the mechanism of its development: metastatic, metabolic, degenerative.

61 Metastatic calcification (as rule general, widespraed) always there is hypercalcaemia. It is possible in: - thyroid gland adenomas; - parathyroid glands adenomas; - massive destruction of calcium depot (bones); - increased vitamin D containment; - kydneys diseases; - gastriontestinal tract disease. Usually calcium salts in metastatic calcification deposit in GIT mucosa, lungs, skin, blood vessels, myocardium, kidney

62 Metabolic calcification causes are unknown; result of acid-basic condition disorder in a tissue; can be local and general

63 Degenerative calcification or petrifaction it is always localized there is not hypercalcaemia calcium salts deposit in necrotic foci or zones of tissues with sharply decreased vital functions.

64 Examples: - petrifaction in thrombi; - petrifaction in atherosclerotic plaques; - petrifaction in tumor s stroma; - petrifaction in cusps in defective valvular heart diseases; - petrifaction of purulent exudate in chronic purulent inflammation; - petrifaction of caseous necrosis in tuberculosis; - petrifaction in syphilitic gummas; - petrifaction in place of dead parasites (echinococci); - petrifaction in place of dead fetus (lythopedion).

65 Petrifaction of tuberculosis foci in lung

66 Petrifaction in myocardium

67 Stoneformation

68 Stones pathological hard formations freely lying in a ducts or an organ s cavity

69 Predisposing factors of stoneformation: A) general disturbances of general metabolism; B) local chronic inflammation, slowing of outflow, changes of secretion chemical composition and its physics features.

70 Stones from urinary bladder

71 Stones from kidney pelvis

72 Stones in gallbladder

73 Stones from gallbladder

74 Stone in bronchus

75 Every stone has inorganic matrix and organic part.

76 Complications of stoneformation - difficulties or total blockade of outflow; - supporting of chronic inflammation; - necrosis, fistula, bedsore in tissue under stone.

77 Thank You!