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CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

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Page 1: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

CELL AND TISSUE INJURY COURSE-I

YEAR II

PATHOLOGY LABORATORY

Assist. Prof. Dr. Ipek Erbarut Seven

Assoc. Prof. Dr. Pelin Bağcı

Page 2: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

CHANGES IN THE SIZE, CONSISTENCY, COLOUR&

COMPOSITION OF ORGANS

Page 3: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-l . HYPERTROPHYORGAN: HeartGross findings: The thickness of the ventricular wall is thickened.

Page 4: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-2 HYPERPLASIAORGAN: Prostate

Gross Findings: Two prostatic lobes are seen. They are enlarged, firm and nodular. The cut surfaces are also nodular and contains some minute cysts. The size of nodules vary from 0.5 to 1.5cm.Descriptive Notes: This increase in size is in response to hormonal changes that occurs with the aging process.

NODULENormal size of the prostate

Page 5: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-3: HYPERPLASIAORGAN: Thyroid (Nodular Hyperplasia)

Gross Findings: Thyroidectomy specimen with glistening, jelatinous, nodular surfaces is seen. At cut section you can discriminate fibrous bands causing nodular structures. Descriptive Notes: In the adult, the normal thyroid gland weighs 20 to 25 gm. The most common cause of the nodular hyperplasia is lack of iodine in the diet resulting insufficient production of throid hormones. This cause increase the sythesis and release of TSH (thyroid stimulating hormone), resulting in enlargement of the thyroid.

NODULE

Page 6: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-4: LYMPHOMAORGAN: Spleen

Gross Findings: In the cut section of the spleen, you see numerous nodular masses(approximately 0.6-0.8 cm. in dimension). This leads to diffuse enlargement of the spleen.Descriptive notes: These nodular masses are formed by neoplastic proliferation of lymphocytes which are actually local cells of the spleen.

Page 7: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-4: LYMPHOMAORGAN: Spleen

Gross Findings: In the cut section of the spleen, you see numerous nodular masses(approximately 0.6-0.8 cm. in dimension). This leads to diffuse enlargement of the spleen.Descriptive notes: These nodular masses are formed by neoplastic proliferation of lymphocytes which are actually local cells of the spleen.

NODULE

Page 8: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-5: MILLIARY TUBERCULOSISORGAN: Lung

Gross Findings: There are multiple small (pin-point to a few millimeters), yellow whitedistinct foci. This leads to diffuse enlargement of the lungs.Descriptive notes: These foci are formed by granulomatous inflammation.

Granulomatous foci

Page 9: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-7: ACUTE REJECTIONORGAN: KidneyGross Findings: The kidney is larger, harder,and paler than normal.Descriptive Notes: Enlargement of the kidney caused by edema, and diffuse mononuclear cell infiltration. Result of humoral rejection extensive renal parenchymal necrosis seen.

Page 10: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-8: LINITIS PLASTICAORGAN: Stomach

Gross Findings: There is diffuse thickening of the gastric wall which has given rise to a term “leather-bottle” stomach also called linitis plastica.Descriptive Notes: Tumour cell infiltration to the gastric wall ends up with diffuse thickening of the gastric wall.

Page 11: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-9: HYPERTROPHY – DILATATIONORGAN: Urinary Bladder

Gross Findings: This is a partial cystectomy spesimen. The bladder is turned inside out so that you can see the pale mucosa. The cavity of the urinary bladder is enlarged. The bladder wall is thicker than normal.Descriptive Notes: Vesical obstruction caused hypertrophy of the muscle layer. Hypertrophy of the muscle bundles produce trabeculation. Vesical obstruction caused dilatation of the bladder and hypertrophy of the muscle layer. Hypertrophy of the muscle bundles produce trabeculation.

trabeculation

Thickened wall

Page 12: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-11: FATTY CHANGEORGAN: Liver

Gross Findings: A slice of the liver is seen. Liver is enlarged, yellow, smooth, firmer than normal and greasy. The capsule remains smooth and glistening.The lumina seen on the cut surface are the branches of the portal vein.Descriptive Notes: the normal adult liver weighs 1400 to 1600 gms. Fatty change results from defective oxidation of fatty acids and aberrant mitochondrial function.

Page 13: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-12: ANTHROCOSISORGAN: LungGross Findings: Accumulation of this pigment blacken the tissue of the lung

Descriptive Notes: The most common exogeneous pigment is carbon or coal dust, which is a virtually ubiquitous air pollutant of urban life.

Page 14: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-12: ANTHROCOSISORGAN: Lung

Gross Findings: Accumulation of this pigment blacken the tissue of the lung.Descriptive Notes: The most common exogeneous pigment is carbon or coal dust, which is a virtually ubiquitous air pollutant of urban life.

Page 15: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-13: ATHEROSCLEROSIS-CHOLESTEROL ACCUMULATIONORGAN: Vessel Wall

Gross Findings: You see an opened vessel wall. On the inner surface there are elevated areas of different diameter in size, yellow-white in colour and with irregular lipid plaques.Some plaques are calcified, these can be recognised with their white color and rigid appearance. The size of the atheromatous plaques are varible and some show coalescence.Descriptive Notes: Endothelial cell damage and increased total cholesterol and decreased HDL cholesterol cause atherosclerotic plaq formation.

LIPID PLAQUELipid plaque

Page 16: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-14: FATTY CHANGEGross Findings: The heart is enlarged and softened. It is yellow in colour. You can also see atherosclerotic yellow lipid plaques in the opened vessels.

Page 17: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-15: AMYLOIDOSlSORGAN: KidneyGross Findings; Kidney is enlarged , firm and have a waxy appearance.Descriptive Notes: Extracellular hyaline amorphous material is accumulated in glomeruli and vessel wall. Painting the cut surface with iodine imparts a yellow colour is transformed to blue violet.

Page 18: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-16: PASSIVE CONGESTIONORGAN: Ovary

Gross Findings : The organ is diffusely enlarged, firm, and cyanotic. Descriptive Notes: This is due to twisting of ovary that cause obstruction of venous return resulting in intense congestion. Ovarian torsion is uncommon.

Page 19: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-17: CHRONIC PASSIVE CONGESTION ORGAN: Liver

NUTMEG LIVER (normal adult liver weight is 1400-1600gm.) Gross Findings: There is dusky red cyanosis and diffuse increase in liver size and weight. On the cut surface the central congested areas appear darker than the pale peripheral portions of the lobules and thus compose the so-called nutmeg pattern.Descriptive Notes: Passive congestion of the liver results from right-sided heart failure or obstruction of the inferior vena cava or hepatic vein. When you think about the normal circulation of the liver you will easily understand why the central areas axe primarily affected. We see hemorrhagic necrosis in the pericentral zones. Whereas the peripheral hepatocytes, suffering from less hypoxia, develop fatty change. This zonal difference gives red [centre of the lobule) and yellow (periphery-of the lobuie) discoloration so-called "nutmeg" liver to the organ.

NUTMEG

Page 20: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-17: CHRONIC PASSIVE CONGESTION ORGAN: Liver

NUTMEG LIVER (normal adult liver weight is 1400-1600gm.) Gross Findings: There is dusky red cyanosis and diffuse increase in liver size and weight. On the cut surface the central congested areas appear darker than the pale peripheral portions of the lobules and thus compose the so-called nutmeg pattern.Descriptive Notes: Passive congestion of the liver results from right-sided heart failure or obstruction of the inferior vena cava or hepatic vein. When you think about the normal circulation of the liver you will easily understand why the central areas axe primarily affected. We see hemorrhagic necrosis in the pericentral zones. Whereas the peripheral hepatocytes, suffering from less hypoxia, develop fatty change. This zonal difference gives red [centre of the lobule) and yellow (periphery-of the lobuie) discoloration so-called "nutmeg" liver to the organ.

NUTMEG

Page 21: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-18: PASSIVE CONGESTIONORGAN: Testis (Torsion)

Gross Findings: Testis shows slight but diffuse enlargement. The organ is tense and cyanotic.Descriptive Notes: There is an impairment of venous return from the testis due to the twisting of the spermatic cord resulting compression of testicle veins.

Page 22: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-19: CONGESTIONORGAN: Brain —> Meningeal Congestion

Gross Findings: The blood vessels of the meninges are engorged with dark red blood. There is also diffuse increase in the size and weight of the organ due to secondary edema formation.

CEREBRAL LOBES

CEREBELLUM

ENGORGED VESSELS

Page 23: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-20: ABSCESS ORGAN: Spleen

Gross Findings: Spleen is enlarged. Acute inflammatory cell infiltration results with a tissue defect (arrows) that you can notice on the cut section of the spleen.Descriptive Notes: Normally in the addult spleen weighs, about 150 gm and measures 12 cm in lenght, 7 cm in width, and 3 cm in thickness.

Page 24: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-21: TUBERCULOSIS ORGAN: Apex of the LungGross Findings: At the apex of the lung there is an intraparanchymal tissue defect (arrow) .At the centre of the defect with a close inspection one can easily identify the necrosis.Descriptive Notes: Mycobacterium cause tuberculosis.The type of the necrosis is calledcaseification necrosis

Page 25: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-21: TUBERCULOSISORGAN: Lung

Gross Findings: At the apex of the lung there is an intraparanchymal tissue defect. There is a caseification necrosis at the center. Descriptive Notes: Mycobacterium cause tuberculosis.The type of the necrosis is calledcaseification necrosis.

NECROSIS

Page 26: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-22: ATROPHYORGAN: Kidney

Gross Findings: The cut section of the kidney reveals dilatation and deformation of the calyces, irregular loss of renal parenchyma with scarring. Its surface is granular with depressed scars. Descriptive Notes: Atrophy is due to progressive destruction and loss of renal parenchyma.

DILATED CALYCES

PARENCHYMAL THINNING

Page 27: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-23: HYPOPLASIA(congenital)ORGAN: KIDNEY

The size of the kidney is diffusely decreased. Its surface is smooth. There are some hemorhagic areas in cortex. The number of renal lobes and pyramids is 6 or fewer (normal kidney has about 12 pyramids).

Page 28: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-24: CHRONIC PYELONEPHRITIS WITH CALCULIORGAN: KIDNEY

The cortical surface of the kidney contains irregular, broad depressed area (scar formation) of cortical fibrosis and atrophy leading to focal decrease in size of the organ. On cut section you see dilatation of calyces with atrophy, calculi and scarring of the overlying cortex. Medullary and perirenal fatt tissue is increased.

calculi

Corcical thinning

Page 29: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-25: INFARCTION ORGAN: SPLEEN

Gross Findings: On the cut section of the spleen you see multiple, pale, wedge shaped, well deliniated infarcts beneath the capsule. The infarcts which are wedge shaped have their apex pointing toward the focus of vascular occlusion. Since all the dependent tissue out to the periphery of the organ is affected, the external aspect of the organ forms the base of the wedge.Descriptive Notes:This is an example of white infarct which is seen secondary to the arterial occlusion of the solid organs.

INFARCT

INFARCT

Page 30: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-26: INFARCTIONORGAN: Placenta

Gross Findings: On cut section of the placenta reveals a white-tan and firm area of necrosis. It is also wedge shaped with apex at maternal surface.Descriptive Notes: This is also an example of white infarct. It results from cessation of blood supply to intervillous space and necrosis of villi .

INFARCT

Page 31: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-27: TRANSMURAL INFARCT ORGAN: Small bowelGross Findings: A segment of small bowel is seen. A large part of this segment is intensly congested and dark purple. This discoloration fades gradually into the adjacent segments of the normal bowel, that is the demarcation is not sharply defined.Descriptive Notes: This is also an example of a red infarct. We see red infarct both in arterial and venous occlusions of the small bowel due to the fact that it has rich in arterial anastomoses.

Page 32: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-29: CIRRHOSISORGAN: Liver

Gross Findings: The liver is harder than normal due to fibrosis. Its surface shows diffuse nodularity that reflects nodular regeneration and scarring.Descriptive Notes: Cirrhosis of the liver is the terminal sequel of repeated injury to the liver parenchyma. The result is the formation of broad fibrous bands separating regenerative nodules that do not have the normal achitecture of liver lobules.

Fibrous bands

Page 33: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-30: BRONCHOPNEUMONIAORGAN: Lung

Gross Findings: The lung shows patchy distributed firm and gray-red to yellow colour, elevated nodular airless areas due to inflammatory infiltration.These nodules are distributed along with the bronchioles so called bronchopneumonia.Descriptive Notes: It results from aspiration of organisms causing inflammation and necrosis of underlying parenchyma.

Page 34: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

Gross Findings: Its mucosal surface shows minute yellow patches due to cholesterolaccumulation . This is called as a "strawberry gallbladder".Descriptive Notes: It is results from abnormal deposition of mixtures of cholesterol and triglyceride in macrophages in the lamina propria of the gallbladder.

HD-31: CHOLESTEROLOSISORGAN: Gall bladder

Cholesterol accumulation

Page 35: CELL AND TISSUE INJURY COURSE-I YEAR II PATHOLOGY LABORATORY Assist. Prof. Dr. Ipek Erbarut Seven Assoc. Prof. Dr. Pelin Bağcı

HD-32: FIBROMAORGAN: Ovary

Gross Findings: The tissue is harder and bigger than a normal ovary because of infiltration by neoplastic cells arising in the ovarian strorna. The ovary appears as a white firm, mass composed of interlacing bundles of fibers.Descriptive Notes:It is a benign neoplasm of the ovary.