pathology sheet # 2

بسم الله الرحمن الرحيم

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On this link:

http://www.mediafire.com/file/dcyv6sqy3tei0aa/patho%20sheet%20_2.doc
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بسم الله الرحمن الرحيم

This sheet is from slide 21 to slide 43

Slide 22:
(Cellular swelling)
Hypoxia (decrease of oxygen) ATP synthesis will decrease sodium pumps in the membrane which depend on ATP will decrease in function sodium will enter the cell and the potassium will get out the cell sodium will take the water with inside the cell cellular swelling will happen

Slide 24:
(Ultrastructural changes of reversible cell injury)
a. we will not see discontinuity or rupture in plasma membrane because rupture of plasma membrane is a feature of irreversible cell injury
b. so protein synthesis will be decreased

Slide 25:
(Morphology of necrosis) by light microscope
1-b. RNA in the cytoplasm is a little bit basophilic so when the cell is rupture, RNA will go out of the cell then the cell will be eosinophillic

Slide 26:
2- Hypoxia ATP will decrease the cell will try to produce ATP by other mechanisms like glycolesis glycogen content in the cell will decrease glassy homogenous appearance of the cell

Slide 28:
Nuclear changes in necrosis
The figure showing us 3 patterns of nuclear changes in necrosis
a.pyknosis b.karyorrhexis c.karyolysis


Slide 31:

*Grossly in coagulative necrosis, the tissue will be appear firm to hard
* intracellular acidosis will increase because of increasing of lactic acid by glycolesis

Slide 32:
The figure is a kidney
There is a wedge-shaped part which will be firm and represents a (coagulative necrosis) because of cutting of the blood supply

Slide 33:
In the figure there is an abnormal part of the kidney and normal part
*abnormal part is where you see shadows of the cells but after 1 week disappearance of the architecture of the cells will happen

Slide 34:
*The enzymes which will be released by leukocytes will digest the cells from the beginning so we will not see the outline of the cells (complete disappearance from the beginning)
*we will see the inflammatory cells instead of seeing the outline of the dead cells

Slide 35:
*the figure is a tissue which had taken from the liver
* we can see a site of liquifactive necrosis where is a complete disappearance of dead hepatocytes and instead of the dead hepatocytes , we see neutrophiles (inflammatory cells)
Q: what is the cause of this type of necrosis
1- ischemia
2- bacterial infection
3- TB (Tuberculous infection)
Answer is 2




Slide 34:
(Gangrenous necrosis)
*is not a distinctive type of necrosis because it is either coagulative necrosis or is a coagulative necrosis and liquifactive necrosis with each other
*dry gangrene: it is a term used by the surgery to refer to a leg that has lost its blood supply and undergone coagulative necrosis
*diabetic patients are the most people that have gangrene

Slide 36:
Black tissue is a coagulative necrosis (dry gangrene)

Slide37:
Epithelioid histocytes is activated microphage that try to make digestion to ( ) of the tuberculous infection



Slide 38:
*the tissue is the lung
*the round structure is a lymph node affected by tubercolosis and it will be a cheesy material
*the cause is tuberculous infection TB (مرض السل)

Slide 39:
*there is a homogenous eosinophilic material ( caseous necrosis )
*and we will see epithelioid histocytes and lymphocytes
(caseous necrosis + epithelioid histocytes and lymphocytes granuloma)

Slide 41:
Foreign body rxn is an inflammatory rxn and foreign body cells is a multinucleated cells and gaint cells which will get around the fat cells

Note: *fatty acids attract the calcium
*it is dangerous if trauma happened in the breast of females and if she go to the surgery , first he will examine her situation and he will think that she has a cancer , so at this time it is important to ask if she has a history in cancer then the surgery will examine under the light microscope to distinguish between trauma and cancer

Slide 42:
Whitish to yellow structures in the figure is an enzymatic fat necrosis and have chalky appearance .




Haneen Bahzad Hasan
Pathology sheet # 2
20/9/2010