Medicine

01 Dystrophy

Methodical instruction №1

of  practical pathoanatomy employments

for 1-st year students of nursing (bachelor) faculty of the distance form education

 

LESSON 1 (6 hours)

Themes: 1. Intracellular accumulations of albumens, carbohydrates and lipids. Extracellular accumulations of albumens, carbohydrates and lipids.

2. Pathology of endo- and exogenous pigments exchanges. The notion about the development of the atherosclerosis, rheumatic diseases and hepatosis.

3. Damage and death of cells and tissues. Necrosis, apoptosis. Bases of thanatology.

 

Aim: To be able  to define macro- and microscope signs of dystrophies, to explain mechanism of development and appraise importance of complications for organism.

To study the clinical and morphological signs of cell and tissue damage and necrosis, pathomorphologіcal manifestation of organ insufficiency, etiological and pathogenetic mechanisms of necropsies development. To learn the morphological signs of death.

 

 

Equipment of the lesson: Intracellular storage is a normal function of the tissues of multicellular organisms. Cells store nutritional  constituents that are used at a later time, including fat, glycogen,  vitamins, and minerals. They also store the products  of the turnover of endogenous  membranes , principally in the form of degraded phospholipids. Furthermore , storage is  be eliminated by intracellular digestion. Many processes   result in abnormal intracellular accumulations.

Many inborn errors of metabolism lead to the  accumulation of intermediate metabolites an abnormal material. A variety of  human  diseases are characterized by an exaggeration of the normal storage functions of specialized cells.

Necrosis is the result of a dynamic process, since morphologic changes  only occur  as a  consequence  of biochemical  alterations within  the cell.

Cells may also  adapt to an adverse environment by loss of cell  substance or  shrinkage, referred to as atrophy. Atrophy,  therefore, represents a accommodation to  decreased work load, disuse,  diminished blood supply or  loss of endocrine stimulation.

 

 

 

Base level of knowledge and skills:

1.     Mechanism of apoptosis.

2.     Changes in the ultrastructure of intracellular organelles.

3.     Structure and function pigments (department of medical chemistry).

4.     Structure of all organs (department of normal human anatomy)

5.     Structure  the normal cell( department of histology, cytology and embryology).

6.     Morphology  of the cytoplasm and its organells ( department of histology, cytology and embryology).

7.     Changes in the ultrastructure of intracellular organells ( department of histology, cytology and embryology).

8.     Mechanism of apoptosis ( department of pathology).

9.     Stimuli to cell proliferation ( department of pathology).

10. Structure of blood vessels (department of normal human anatomy).

 

 

Macropreparations: Dark swelling of kidney, Lipid dystrophy of liver, kidney, heart, gyalinosis of the spleen casule, renal amyloidosis, fibroelastosis of mitral valve, local amyloidosis of the splleen and diffuse amyloidosis of the spleen, fatty dystrophy of the heart, Liver in case of mechanic icterus , Brain in case of malaria, Hemosyderosis of liver.

Nephorlythiasis, hydronephrosis, hypertrophy of heart, concentric hypertrophy of left ventricle wall of the heart, excentric hypertrophy of left ventricle wall, hypereplazia of prostate and hypertrophy of urinary bladder wall, bullous emphyzema of lung, splenomegalia, goiter (strum), nodular regeneration of liver, scar after gastric ulcer, stenosis of intestine, polyp of  endometrium, calcific aortic stenosis, hematogenous-disseminated tuberculosis of lung, dry gangrene of a foot, wet gangrene of hand, tuberculosis of adrenal gland, ancreas necrosis, decubitus of larynx, gangrene of small intestine.

 

Micropreparations: Lipid dystrophy of liver, grainy dystrophy of kidney. Brown induration of lungs. Old hemorrhage in brain.  Biliar cirrhosis of liver. Acydochloric hematine on the bottom of stomach acute ulcer.  Adenoma of adrenal gland.  Malaria pigmentation of spleen (plaster cast).

 

 

Practical activity – 900 -1115 h

I. To study and to be able to describe  orally  macropreparations of the theme:

1.     Dark swelling of kidney (so called grainy dystrophy) usually occurs as a transitory process in case of intoxications, hypoxia, infections, which are accompanied by tension of intracellular metabolic and transport systems. Macroscopic changes in organs are minimal. The term “dark” reflects macroscopic manifestation, “grainy” - microscopic manifestation. Size of the kidney is a bit larger than the normal one. Surface is smooth. Consistence is flaccid. On the cut tissue is dark and reminds boil-cooked meat. Swelling is determined by the following: one makes a cut of cortical layer of the kidney, the capsule can be easily taken off the kidney, parenchyma can be torn out in the form of cylinder.

2.     Lipid dystrophy of liver, kidney, heart. These macropreparations illustrate parenchymatous lipid dystrophy. The causes can be different: congenital enzyme pathologies and acquired: intoxications, infections, disturbance of lymph and blood circulation.

a.      Lipid dystrophy of liver (goose liver). The synonym reflects the appearance of the liver – a well fed goose, meaning that one of the possible mechanisms of development of the pathology is disturbance of quantative and qualitative (unbalanced) nutrition. The liver is enlarged, flabby and of bright-yellow color. The lower edge is round-shaped.  If the organ is cut one can find fat coating on the knife. The pieces of organ don’t sink in water.

b.     Lipid dystrophy of myocardium (“tiger heart”). The synonym reflects typical coloring of endocardium of right ventricle of the heart. Endocardium has a striped appearance as a result of dominance of lipid dystrophy of cardiomyocytes which are situated near the venous link of microcirculatory system and absence of this kind of dystrophy in cardiomyocytes, situated near arterial link. It illustrates not only manifestation of lipid parenchymatous dystrophy but is also an important diagnostic criterion. Lipid dystrophy of myocardium is a synonym of cardiac insufficiency. Due to damage of cardiomyocytes dilation of heart cavity occurs, which is accompanied by functional insufficiency of tricuspid valves.

3.     The heart is enlarged, flabby. The cavities are dilated. Myocardium on the cut is dark, of yellow-brown color. From the side of endocardium one can notice yellow-white stripes, especially in the area of trabecules and papillar muscles of right ventricle.

4.      Lipid dystrophy of kidney. Macroscopic changes are also not considerable. Both congenital and acquired (intoxications, syphilis) pathologies are observed. Clinically this condition is manifested by nephrotic syndrome.

5.     The organ is enlarged, soft, the surface is smooth. Cortical layer is wide, shining, gray with yellow spots.

6.     Brown induration of lungs. This is an example of local hemosyderosis. Presence of hemosyderosis always testifies about decomposition of hemoglobin. In this case hemosyderin is produced in alveolar macrophages and tissue macrophages of stroma. Insufficiency of lymphatic system of lung causes accumulation of this pigment in stroma which gives the lung a rusty tint. Lymphostasis, presence of foreign protein, hypoxia cause development of pneumosclerosis. As a result the organ becomes hard (induration).

   Lungs are enlarged, of heard consistence, of red-brown color on the cut, with multiple brown spots. Around the vessels and bronchi there is an increased growth of connective tissue. Interlobular walls are thickened and gray. Cavity of pulmonary artery’s branches is obstructed by red thrombi.

 Such pathological process usually develops in case of chronic venous stasis (stenos of mitral aperture in case of rheumatism) or very rarely in case of idiopathic hemosyderosis of lungs.

7.      Gyalinosis of the spleen capsule. This preparation illustrated of the enlargement and fibrinal changes of the fibrous  connective  tissue. Hyaline is the  fibrilar protein. Great role  in  it’s structure belongs to fibrin. Half-transparent masses of it  resemble the hyaline  cartilage. The spleen is enlarged. In the incision  we can see  that the capsule is enlarged and white. It’s lire poured over with glaze (The saturated solution of the sugar mixed with albumen). Such situation developed after the  undergoing  of the inflammatory process   of the abdominal cavity –peritonitis, the injure of spleen, collagenossis.

8.     Fibroelastosis of mitral valve. Express the result of the connective tissues desorganisation in the case of collagen disease. The cusps of mitral valve are enlarged, white, non-transparent. The function of the  valve isn’t perfomed  properly . This acquided heart disorder is called valvular incompetence.

9.     Renal amyloidosis. This is the example of mesenchimal disproteinosis that is characterized by the formation of the innormal fibrous protein in the  intermediate part of the complex glucoprotein. His protein  is called amyloid. Amyloidosis is divided into idiopathic (primary), hereditary, acquired (secondary), gerontal and local  - out of ethiological and pathological mechanisms of amyloidosis. This macropreparation shows the secondary amyloidosis.

10. The kidney is enlarged it’s density is  high. The surface of the incision is vex-like and has «sebiferous» color. Cortex  part is  yellow-white and enlarged, the medullar is  rosy and stained. Such kidney is called «the big sebiferous kidney». We can see it in  the  case of chronic abscess of the lung, bronchiectatic disease, osteomyelitis, fibrocavernous tuberculosis, collagenosis, dlood diseases, tumors.

11. Local amyloidosis of the spleen and Diffuse amyloidosis of the spleen. They also show the macroscopic changes in organs in the  case of amyloidosis. That are the stages of the spleen’s injure by amyloid infact. The organ  is enlarged and and  of it’s  density is higt. Firstly amyloid deposites in the lymphatic follicules that resembles than the half-transparent grains of sago (sago spleen) -–this is the stage of spleen’s amyloidosis. After that the diffuse  deposition of the amyloid takes plase. The spleen is much enlarged, brown-red , has lardaseous  glitter (lardaserous spleen) – this is the second stage of amyloidosis.

12. Fatty dystrophy of the heart. This macropreparation illustrates the disorder of the neutral fats’ metabolism. The enlargement  of the  fats’ quantity in the  fatty tissue is called adiposity (obesity).  In the macropreparation  is seen the excessive development of the epidermal fatty tissue . The fatty change of the heart is  developed in the  case of any obesity (alimentary, metabolic cerebral). The size of the heart  is enlarged. The accumulation of much fat is located primary under the epicardium of the right part. The fatty tissue is also in the stroma of myocardium. It dislocates the muscular fibrous  that are atrophying . The contracting ability of the myocardium decreases in this case. The death is possible because of  decompensation or damage of the right ventricle’ wall.

13. Old hemorrhage in brain. This is also an example of local hemosyderosis. Considering that hemosyderin is produced only in “alive” cells, brown color testifies that hemorrhage occurred at some period before the death.

    In the tissue of brain there is a strict contour of source of softening of brown       color with the beginning of cyst formation. The wall of the cyst is brown.

14. Biliar cirrhosis of liver. In case of obstruction of bile tract infrahepatic icterus develops. This is related to dilation of bile tracts and separation of dysmosomes of capillaries. In such cases pigment which doesn’t contain iron – bilirubin enters blood capillaries. The liver is hardened. Surface is with small humps. On the cut parenchyma is green-brown with connective tissue net which can be easily distinguished. The bile ducts are dilated, filled with stones.

15. Acydochloric hematin on the bottom of stomach acute ulcer. In case of extravascular hemolysis in a stomach acidochloric hematin becomes to be produced. This pigment contains iron in combined form. On the mucous of the stomach one can see an oval-shaped defect. The bottom is black.

16. Adenoma of adrenal gland. The cortex of the gland is bright-yellow. There is a clear contour of the tumor of same color. The coloring is caused by adrenochrome with pigment which is proteinogenic.

17. Mallaria pigmentation of spleen (plaster cast). The spleen is enlarged. The surface of cut is gray. The coloring is caused by accumulation of hemomelanin – life product of malaria plasmodium.   

18. Old hemorrhage in brain. This is also an example of local hemosyderosis. Considering that hemosyderin is produced only in “alive” cells, brown color testifies that hemorrhage occurred at some period before the death.

19. In the tissue of brain there is a strict contour of source of softening of brown color with the beginning of cyst formation. The wall of the cyst is brown.

20. Adenoma of adrenal gland. The cortex of the gland is bright-yellow. There is a clear contour of the tumor of same color. The coloring is caused by adrenochrome with pigment which is proteinogenic.

21. Mallaria pigmentation of spleen (plaster cast). The spleen is enlarged. The surface of cut is gray. The coloring is caused by accumulation of hemomelanin – life product of malaria plasmodium.

22. Nephorlythiasis. On a sagital cut of the kidney one can observe dilated bowls and calyces, filled with stones situated by the walls. Dilation od kidney bowl is caused by obstruction of the urinary tract by a stone. Urine which is filtered in glomeruli, accumulates and creates pressure on kidney parenchyma; as a result the latter gets atrohped. Normally thickness of parenchyma (from capsule to kidney’s mucous membrane) is – 4-5cm, in the macropreparation the sickness of parenchyma doesn’t overcoome 1.5cm. If the cause of urine stasis is not eliminated, full atrophy of kidney parenchyma may develop.

23. Hydronephrosis. The kidney is enlarged and looks like a thin-wall sack filled with water. Such pathology develops due to complicated urine outfloat, the reasons may be: presence of stones with obsruction of ureters, tumors of urinary bladder, adenoma of prostate. Urine while accumulating dilates bowls and calyces and creates pressure on kidney tissue, which leads to decreasing of thickness of parenchyma and atrophy from pressure.

24. Internal hydrocephalia. Cavities of lateral ventricles of brain is enlarged 3-4 times. The tissue of brain became thinner, fissures and are smooth. Internal hydrocephalia develops due to overwhelming accumulation of liquor, produced by vascular plexus, in ventricles. The cause may be the following: disturbance of liquor outfloat due to stenosis, bifurcation or atresia of Silviy’s cavity, compression by a tumor. This leads to atrophy of brain tissue, thining of skull bones.

25. Hypertrophy of heart. To make a comparison there are two preparations: of normal-sized heart and 2-3 times enlarged heart due to increased size of right ventricle. The base of myocardium hypertrophy is hypertrophy of cadriomyocytes due to increasing of mass of muscular cells’ sarcoplasma, size of nuclei, hyperplazia of intracellular structures, simultaneously hyperplazia of stromal frame develops. The causes are: congenital or acquired heart diseases, chronic nonspecific lung diseases, essential hypertension.

26. Concentric hypertrophy of left ventricle wall of the heart. On a horizontal cut of the heart there is a thickened (about 2.5cm ) wall of left ventricle and interatrial septum, the cavity of the ventricle is not much enlarged. Normally thickness of left ventricle wall of an adult is 1.2cm. Such hypertrophy of the heart is called tonogenous or compensatory. Meaning that it provides the essential functional level of general blood circulation.

27. Excentric hypertrophy of left ventricle wall. On a horyzontal cut of the heart two times enlarged cavity of the ventricle is visualized. The wall of the ventricle is thinner comparing with the previous macropreparation. If the reason of hypertrophy is not eliminated, dystrophic changes in hypertrohphed cardiomyocytes, and sclerotic processes in stroma develop, which lead to weakening of contractive activity of myocardium. Therefore, cardiac decompensation develops and the muscle is not capable of dealing with heavy loads. In case of decompensation of hypertrophed myocardium transversal, passive and myogenous dilation of ventricles develops.

28. Hypereplazia of prostate and hypertrophy of urinary bladder wall. Tehre are two macropreparations. First – on a sagital cut there is an increased prostate (3cm in diameter) which compresses aperture of urethra. The cavity  of urinary bladder is not enlarged. The wall of urinary bladder is 5-6 times thicker than normal (2-3mm normally) at the expence of muscular layer. From the side of mucous membrane there are muscular trabecules (trabecular hypertrophy). Functional incapability of hyperterophed muscles leads to decompensation and dilation of urinary bladder cavity and urine stasis which is visualized in second macropreparation. Thus in first macropreparation compensated, tonogenous hypertrophy of urinary bladder wall is performed, and the second one depicts myogenous , decompensated, excentric hypertrophy.

29. Bullous emphyzema of lung. On the macropreparation there is lung tissue of cyanotic-gray color, the surface is uneven due to  bulls (accumulation of air in acynus which leads to blowing and thining of elastic fibers), dilation of alveolar ways, tearing of interalveolar septi with formation fo thin-wall cavities. The lung enlarges not at the account of parenchyma but due to accumulation of air in bulls which is caused by complicated exhalation. Thus false hypertrophy of lung is performed at the time when parenchyma of lung tissue is atrophed because of pressure.

30. Splenomegalia. The spleen is considerably enlarged. Enlarging of the spleen takes place in case of inflammatory processes due to hyperplazia of lymphoid tissue (increasing of lymphocytes quantity) as a result of tense defensive immune reactions: in case of diseases of blood producing organs enlarging develops due to active extramedullar blood production. The reason of size and mass increasing of spleen is hyperplazia of pulp cells.

31. Goiter (struma). On the macropreparations there are thyroid glands which are 2.5-4 times larger than normal, of meat consistence with production in some cases of nodes of various sizes, separated by wide areas of connective tissue, in other cases – cyst-like formations, filled with colloid contains. Goiter – is a disease of thyroid gland based on diffuse or nodular hypertrophy of the organ. Normally weight of the gland of adult is 17-25g, width – 3-4cm, thickness – 1.5-2cm. In case of deficiency of iodine compensatory enlarging of the organ develops due to hyperplasia of follicular epithelium (parenchymatous goiter), more often nodular or due to stretching of follicles with colloid (colloid goiter), usually diffuse.

32. Hematogenous –disseminated tuberculosis of lung. On the  background of saved lung tissue of gray color there are multiple small white areas of infiltration – areas of cheese-like (caseous) necrosis. Under the influence of toxic action of bacillus Kochii on lung tissue area of exudative inflammation appears which rapidly transforms into  necrosis of damaged area. Necrotized tissues are white, look like cheese, that’s why this kind of coagulative necrosis is called cheese-like. Cheese-like coagulative necrosis develops in case of tuberculosis, lepra, lymphogranulematosis.

33. Dry gangrene of the foot.  A considerable are of skin of the foot is  brown-black, wrinkled, with ulcers.  The tissues of the leg are dry,  similar to  tissues of a mummy, such changes are caused by  disturbance of nutrition of tissues due  to  narrowing of arteries in case of atherosclerosis, obstructing endarteritis, diabetic angiopathy,  thrombosis. Due to lack of blood the tissue are poor with water.  Sulfide of iron  stains the tissue into black color , it is  formed from free  iron of hemoglobin and hydrogen sulphide , which educes during decomposition  of protein structures.

  1.  Hematogenous-disseminated    tuberculosis    of    lung.     On    the background of saved lung tissue of gray color there are multiple small  white areas of infiltration - areas of cheese-like (caseous) necrosis. Under the influence of toxic action of bacillus Kochii on lung tissue area of exudative inflammation appears which rapidly transforms into necrosis of damaged area. Necrotized tissues are white, look like cheese, that's why this kind of coagulative necrosis is called cheese like. Cheese-like coagulative necrosis develops in case of tuberculosis, lepra, lymphogranulematosis.

35.  Dry gangrene of a foot. A considerable are of skin of the foot is brown-black, wrinkled, with ulcers. The tissues of the leg are dry, similar to tissues of a mummy, such changes are caused by disturbance of nutrition of tissues due to narrowing of arteries in case of atherosclerosis, obstructing endarteritis, diabetic angiopathy, thrombosis. Due to lack of blood the tissue are poor with water. Sulfide of iron stains the tissue into black color, it is formed from free iron of hemoglobin and hydrogen sulphide, which educes during decomposition of protein structures.

36.    Wet gangrene of hand. A considerable area of skin of the hand, partly forearm is separated; tissue of the hand is swollen and cyanotic. Wet gangrene develops as a result of putrefactive microorganisms' activity; disturbance of blood circulation (venous stasis) and lymph stasis also promote this process. Very often such colliquative necrosis takes place in case of frost-biting.

37.    Tuberculosis of adrenal gland. Thickness of the adrenal gland on the cut is 4-5 times larger than normal. Macroscopically organ can't be differentiated on cortical and medullar layers and is presented by homogenous masses of white color (caseous necrosis). This is an indirect necrosis which develops due to damage of the gland by tuberculosis. Addison's disease develops (bronze disease).

38.    Pancreas necrosis. Tissue of the pancreas is saved in singular areas of pale-pink color on the background of structureless mass, infiltrated with blood. This is a kind of colliquative necrosis, the cause of which can be disturbances of blood- and lymph-circulation, obstruction of excretory ducts with the following enzymatic self-digestion of the gland.

39. Gangrene of small intestine. The wall of small intestine is swollen and black, the mucous is dull. As a rule wet gangrene develops in intestines. The wall is black because iron released from erythrocytes interacts with hydrogen sulphide which is produced due to decomposition of protein structures. The cause of development of such pathology can be thromboembolia of mesenteric vessels, twisted  bowels, jammed hernia, less often direct action of chemical substances.

  1. Decubitus of larynx. For a long period of time a probe was left in laryngeal cavity, due to this pressure ischemia of tissue developed. One can observe an ulcer on the back wall of the larynx. Such necrosis is called decubitus and develops in the place of long-lasting compression of the tissues.

20. Nodular regeneration of liver on the background of cirrhosis. The surface of organ is seen on the cut parenchyma is divided with white fibrous tissue Into separate parts. Along with this large regenerative grey-yellow nodes of liver parenchyma which don't have regular lobular structure can be found. The liver obtains such appearance in case  of postnecrotic cirrhosis. Meaning that in places of massive necrosis of liver parenchyma substitution of this necrosis with connective tissue occurs, and partly normal hepatocytes due to intracellular regeneration form abnormal pseudo-lobules. If these pseudo-lobules are 1cm in diameter - such cirrhosis is called small-lobular cirrosis, and if they reach 5 cm - than it'sbig lobular cirrosis. Liver possesses very high regenerative possibilities, after surgical extraction of 4/5 of the organ, the initial mass increase. After 1.5-2 months.

21. Scar after gastric ulcer. On the internal surface of stomach there is an  Scar which forms star-like wrinkles on mucous membrane. In case of erosions (only mucous I defect) heeling is performed as full regeneration - restitution. In case of necrosis of underlaying tissues of the wall ulcers are developing. During the period of heeling   there are necrotized tissues and purulent-fibrin exudation in center of the ulcer. Zone of necrosis is limited by granulative tissue with a large amount of thin-wall vessels, this tissue afterwards transforms into  connective tissue - scar. The surface of the scar is covered with epithelium, which indicated on full regeneration of epithelium -  restitution. Although above the scar mucous membrane morphologically differs from the surrounding mucous. Full ... of gastric structure did not occur.

22. Stenosis of intestine, one can see a part of the intestine which is  and reminds a "sand clock", above and below the  of intestinal of mucous membrane are situated horizontally. In the place of largest  is absent, the wall is  the aperture of the intestine in this place is almost twice smaller. This is the consequence of heeling of intestinal ulcer with the development of a scar. Such process is often a cause of intestinal impassability.

 

23. Polyp of endometrium. The uterus is cut sagitally. In the cavity one observes a tumor-like formation size of which is about 2 cm. This pathological growth of glandular epithelium along with the cells of connective tissue are covered with prismatic mucus-producing epithelium. Such polypous gorwthcan occur due to long-lasting inflammation of mucous membrane or in case of disturbed balance of sex hormones. There are glandular and glandular-fibrous polyps. Polyps can often be ulcerated and epidermized. Polyps are related to precancer conditions.

24Echinococcus of liver. On the cut of liver there is a round-shaped formation, 1.5-2cm in diameter, surrounded by white-gray tissue 1.5-2mm thick, with the background of dark-brown tissue. Around the parasite there is connective tissue growth which  Into fibrous, forming a capsule.

 

 

 

II. To study micropreparations of the theme.To draw the diagrams with basic pathologic process with main signs:

1.     1.Liver in case of mechanic icterus №44. Stained with hematoxylin and eosin. In dilated bile tracts and capillaries one observes bile of dark-brown color (bile thrombi). In cytoplasm of hepatocytes there are small particles of bilirubin. In some places the liver cells don’t have nuclei. Contours of hepatocytes aren’t clear. Along the bile tracts there is increased growth of connective tissue.

2.     Brain in case of malaria №130. Stained with hematoxylin and eosin. In the preparation there are spots of darker color. Under the large lens of microscope one can find pigment of black color and also absence of glia.

3.     Hemosyderosis of liver №155. Perls’ reaction. The principle is in the fact that during interaction of iron and yellow blood salt and under the influence of hydrochloric acid Berlin’s blue is produced. Iron-containing pigment – hemosyderin becomes blue. In the liver one can also see presence of particles of pigment of hemosyderin both in …, cells and in hepatocytes. The nuclei are purple.

4.     So called grainy dystrophy of kidney (dark swelling) of epithelium of canalicules of proximal and distal links of nephrone №48. Stained by hematoxyline and eosine. In epitheliocytes of  canalicules of first row one can see small grains. Grains almost cover the nucleus, volume of which is increased, nephrotehlium is also increased in size and narrows down aperture of canalicules. In these apertures small pink grains and desquamated cells are observed. Clinically this phenomenon is manifested in increased contents of protein in urine (proteinuria).

5.     Lipid dystrophy of liver №121, № 150.  Stained by sudan III. The cuts are made of frozen tissue. Drops of fat are yellow. Larger fat drops are in peripheral hepatocytes, small ones – in central hepatocytes. In peripheral section of a lobule there are hepatocytes, cytoplasm of which is totally filled with fat. Dominance of fat dystrophy in peripheral section of the lobule indicates on infiltrative mechanism of development. Fat comes into liver with blood and infiltrates primarily peripheral hepatocytes. Such mechanism develops in case of obesity, consumption of fatty food, mobilization of fat from fat depots (diabetes mellitus, chronic alcoholism). Development of fat dystrophy dominantly in central departments of liver lobule is connected with decomposition (poisoning, intoxication, hypoxia). Even fat deposition is observed in case of enzyme pathologies (lipidosis).

6.     Atrophy of pancreas № 9. Stained by hematoxylin-eosin and by van Gison’s method. In the preparation there are wide fields of connective tissue growth – light areas in the preparation, stained by hematoxylin-eosin, and the red ones in the preparation stained according to van Gison’s method. Vessels in stroma are dilated and filled with blood. Insular isles in hematoxylin-eosin stained preparation are performed by areas of cells with hyperchrome nuclei, they are rare, cells are situated crumbly (decreased quantity), somewhere they form alveolar structures. The areas are decreased in size.

7.     Atrophy of kidney because of pressure № 136 (hydronephrosis). Stained by can Gison’s method. While studying the preparation with an unarmed eye one observes considerable atrophy of kidney parenchyma (1. surface – capsule, the opposite, concaved – bowl). The thickness of parenchyma is 0.2-0.3cm, instead of 4.5-5cm normally. Under the microscope there are dilated canalicules filled with concentrated urine – “thyroid kidney” which indicates on complicated urine outfloat. Parenchyma is almost absent, sclerosed, glomeruli are also sclerosed, besides that there are small inflammated infiltrates – pyelonephritis. 

8.     Emphysema of lungs № 77. Stained by hematoxylin-eosin. Alveoli are distinctly dilated, filled with air, interalveolar septi are thin, and stretched like strings. In many places interalveolar walls are torn and form large air vesicles from several alveoli, ends of torn alveoli (interalveolar walls) are thick which indicates on remoteness of the process. Therefore, atrophy occurred because of pressure due to overfilling of the lung with air.

9.      Gangrene of the intestine N°. 47. There is fat tissue (alveolar-like structures) under peritoneum, deeper there are longitudinal and circular layers of smooth muscles. The mucous and submucous membranes are necrotized - structure (pattern) is totally absent; they are presented by homogenous mass of pink color, in some places infiltrated by fibrin, nuclei are absent, vessels are dilated, full with blood, some of them are obstructed by thrombi. Also somewhere necrosis of muscular layer is observed (absence of nuclei), round-vessels inflammatory infiltration - a large amount of nuclei of neutrophyl leucocytes.

10.                       Necrotic angina N°52. A considerable amount of tonsil tissue is necrotized - nuclei are absent, the pattern of tissue structure is effaced, only somewhere nidi of lymphoid tissue with follicles are saved (in which sources of necrosis are also present). Multi-layered flat epithelium on the surface of tonsil is also somewhere saved, there is purulent excaudate in crypts. Vessels are sharply dilated, hemorrhages are present. Necrotic angina is typical for scarlet fever.

11.                       Necrotic nephrosis. Organizations of kidney infarction N»134. There is a triangular-shaped area free of nuclei; structure of the organ is saved in this place. There is increased growth of connective tissue on the periphery of infarction. In the cortical layer, behind the infarction area there are places in which nuclei of epithelium of ... canalicules are absent or almost absent, epithelium is swollen, desquamates into cavity of canalicules. In the aperture of canalicules there is partly destroyed epithelium. In glomeruli nuclei are present.

12.                       Zenker's necrosis No 194. Muscular fibers are fragmented, sarcoplasma is homogenous and looks like "wax candles" -transversal   stripes   and   nuclei   are   absent.   There   are   massive hemorrhages,   sources   of   reactive   inflammation   in   endo-   and perimysium. This is a toxic-allergic necrosis, typical for enteric fever.

13.                        Myocardiosclerosis N°33. The preparation is stained by van Gison's method. Endo- and perimysium are thinner than normal and are presented by rough-fibered connective tissue. The walls of vessels are sclerosed. Muscular fibers are dyed into salad color, situated ... due to growth of connective tissue.

14.                       Carnification of lung N°142. The preparation is stained by hematoxylin and eosin. Presence of bronchi, alveoli, carbon dust testifies about lung tissue in the preparation. In alveoli there is infllammatory exudation in which connective tissue grows. Also there are fibrous structures which grow into from alveolar walls into inflammatory exudation, somewhere the ... of lung is totally lost.

15.                       Echinococcus of liver N°315. The preparation is stained by hematoxylin and eosin. One can see liver tissue and on the edge there is chitin cover, dyed into blue color.  Around echonococcus there are changed hepatocytes due to atrophy and growth of connective tissue.

16.                        Dysplasia of the cervical mucosa. The preparation is stained by hematoxylin and eosin.The normal epithelium is seen at upper left. Note the granular transformation into the dysplastic epithelium at lower left. The displastic cellsare smaller, more crowded together, and there is loss of the orderly maturation of the surface layers.

 

 

Seminar discussion – 1145-1315

1.     Name the morphologic mechanism of cell  damage.

2.     Name the hereditary proteinoses.

3.     What are the causes and mechanisms of intracellular fatty change.

4.     Characterize the appearance of the heart, liver and kidneys in fat accumulation.

5.     which histochemical metods (reactions) will help to  trace fat in the tissues.

6.     Definition  of  stromally-vascular  dystrophy.

7.     Causes of  stromally-vascular  dystrophy.

8.     Mechanism of dystrophias’ development.

9.     Clasification of  stromally-vascular  distrophias.

10. Forms of stromally-vascular   dystrophias.

11. Localisation of stromally-vascular   dystrophies.

12. Morphology of  mucoid swelling.

13. Morphology of  fibrinoid  swelling.

14. Morphology of hyalinosis.

15. Morphology of amyloidosis.

16. Structure of amyloid.

17. Result of   stromally-vascular  dystrophy.

18. Morphology of intracellular storage.

19. Morphology of  glycogen metabolism.

20. Morphology of  fat metabolism.

21. Morphology of  iron metabolism.

22. Morphology of  lipofuscin metabolism.

23. Morphology of  melanin  metabolism.

24. Morphology of  exogenous pigments metabolism.

25. Morphology of  calcification.

26. Dystrophic calcification

27. Metastatic calcification.

28. The morphology of necrosis.

29. The pathogenesis of coagulative necrosis.

30. The morphology coagulative necrosis.

31. The morphology liquefactive necrosis.

32. The morphology caseous necrosis.

33. The morphology fibrinoid necrosis.

34. The morphology fat necrosis.

35. The morphology of general death of body.

36. The morphology of changes after the death of body.

37.  Characteristic of repair

38. Morphology parenchymal regeneration.

39. Repair by connective tissue.

40. Morphology of bone repair.

41. Mechanisms involved in repair.

42. Morphology of epithelisation.

43. Morphology of cellular proliferation.

44. Stimuli to cell proliferation.

45. Mechanisms development metaplasia.

46. Complications of the metaplasia.

47. Morphology of calcification and incapsulation.

48. Morphology of dystrophic calcification.

49. Morphology of metastatic calcification.

 

Situational tasks:

 

1. One of manifestations of metabolic derangements in cells is:

A.Apoptosis;

B.*The intracellular accumulation of abnormal amounts of various substances;

C.Hypertrophy;

D. 4.Metaplasia;

E.Atrophy.

 

2.       One of the possible causes of intracellular accumulation of metabolic substances is:

A*Genetic defects;

B.Inflammation;

C.3.Embolism ;

D 4.Necrosis;

E 5.Activation of oncogenes.

 

3.       What substances are accumulated within parenchymal cells in steatosis?

A Cholesterol;

B 2.Apoproteins;

C 3.Triglycerides;

D.Vitamins;

E.Ketone bodies.

 

4.       Fatty change is often seen in all of the following organs, EXCEPT:

Aliver;

B 2.Heart;

C.Kidney;

D.Muscles;

E*5.Lung.

 

5.       The causes of steatosis include all of the following pathologic states, EXCEPT:

AObesity;

B .Anoxia;

C.* Inflammation;

D.Protein malnutrition;

E.Intoxication.

 

6.       The causes of fatty liver include all diseases, EXCEPT:

A. Obesity;

B.         .Alcohol abuse;

C .Diabetes mellitus;

 D.*Hepatitis virus В;

E.Anoxia.

 

7.       The stain used to identify fat is:

A.Hematoxylin and eosin stain;

B.*Sudan III stain;

C.Congo red stain;

D.PAS reaction;

B.5.Metachromatic stain.

 

8.       The stain used to identify glycogen is:

A.Hematoxylin and eosin stain;

B..Sudan III stain;

C..Congo red stain;

D..*PAS reaction;

E. .Metachromatic stain.

 

9.       The fatty liver has all pathologic features, EXCEPT:

A.Enlarged;

B..Yellow;

C.3.*Red;

D.4.Soft;

E.5.Greasy.

 

10. The fatty change is seen by light microscopy as:

A.Intracellular granules;

B..Basophilic granules;

C..Extracellular granules;

D..*Vacuoles in the cytoplasm around the nucleus;

E. .Eosinophilic granules.

 

1.  One of the following variants of necrosis can be found in myocardial infarct:

1.   Coagulative necrosis; 2.Liquefactive necrosis; 3.Caseous necrosis; 4.Gangrenous necrosis; 5.Fat necrosis.

 

2. Ischemic injury in the central nervous system results in:

1. Liquefactive necrosis; 2.Coagulative necrosis; 3.Caseous necrosis; 4.Gangrenous necrosis; 5.Fat necrosis.

 

3. One of the following variants of necrosis can be found in wet gangrene:

1. Coagulative necrosis; 2. Liquefactive necrosis; 3.Caseous necrosis; 4.Gangrenous necrosis; 5.Fat necrosis.

 

4. Apoptosis occurs in all of the following events, EXCEPT:

1.Aging; 2.Cell death in tumors; 3.Death of immune cells; 4.Pathologic atrophy; 5.Cell autolysis.

 

5. Apoptotic cell is characterized by all of the following electron micrograph features, EXCEPT:

l.Big size of the cell; 2.Small size of the cell; 3.Dense cytoplasm; 4.Normal organells; 5.Tightly packed organelles.

 

6. Apoptotic body is characterized by all of the following, EXCEPT:

1.Eosinophilic cytoplasm; 2.Tightly packed organelles; 3.Presence of nuclear fragments; 4.Absence of nuclear fragments; 5. Protein droplets in cytoplasm

 

7. Apoptotic cell is characterized by all of the following histological features, EXCEPT:

1.Round form; 2.Oval form; 3.Eosinophilic cytoplasm; 4.Basophilic cytoplasm; 5.Dense nuclear chromatin fragments

 

8. Borderline inflammation results from:

l.Necrosis; 2.Apoptosis; 3.Lipofuscinosis; 4.All of these; 5.None of these.

 

9.  The tubular epithelial cells in affected tubules in acute tubular necrosis include all of the following pathologic features, EXCEPT:

1. Karyolysis; 2.Plasmolysis; 3.Plasmorrhaxis; 4.Plasmocoagulation; 5. Mitosis.

 

 

Test-control 1415-1500

 

Practical skills:

1.            Students must be able to describe macro- and micropreparations of the theme..

2.            Students must be able to determine the pathological process in macropreparations and slides.

3.            Students must be able to explain mechanisms of development and morphological feature of dystrophy and necrosis, and estimate the functional conditions in organism.

 

 

Information sources:

A) Main

1. Emanuel Rubin, John L. Farber. Pathology.Philadelphia, 1994.

2. Robbins Contran Kumar. – Pathologic Basis of  Disease. – Philadelphia, 1984. 1607 p.

 

B) Additional

1.     Шлопов В.Г. Основи патологічної анатомії людини. – Київ, 1999. – 496 с.

2.     Струков А.И., Пальцев М.А. Патологическая анатомия. Курс лекций. – М.: «Медицина», 1998. – 639с.

1.     Шлопов В.Г. Основи патологічної анатомії людини. – К., 1999. – 493с.

2.     Благодаров В.М., Червяк П.І., Галахін Л.О., Стеченко В.А., Діброва М.Б., Хомінська М.Б., Конопчук М.А. Патологічна анатомія. – К.:Генеза”, 1997.- 507с.

 

 

Author: ass-prof. V. Voloshyn

 

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