Podcast
Questions and Answers
What is the characteristic feature of reversible cell injury in parenchymatous cells?
What is the characteristic feature of reversible cell injury in parenchymatous cells?
Accumulation of excess neutral fat
Which organs are commonly affected by reversible cell injury?
Which organs are commonly affected by reversible cell injury?
Liver, Kidney, Heart, Skin
What is the microscopic feature of reversible cell injury in the liver?
What is the microscopic feature of reversible cell injury in the liver?
Fine granules in the cytoplasm
What is the clinical picture of reversible cell injury in the kidney?
What is the clinical picture of reversible cell injury in the kidney?
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What is the fate of cells with reversible cell injury if injurious agents persist?
What is the fate of cells with reversible cell injury if injurious agents persist?
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What are the gross characteristics of the liver in hepatic bilharziasis?
What are the gross characteristics of the liver in hepatic bilharziasis?
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What is the microscopic picture of portal tracts in hepatic bilharziasis?
What is the microscopic picture of portal tracts in hepatic bilharziasis?
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What is the pathogenesis of portal hypertension in hepatic bilharziasis?
What is the pathogenesis of portal hypertension in hepatic bilharziasis?
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What is the consequence of ammonia escape through the open porto-systemic collaterals in hepatic bilharziasis?
What is the consequence of ammonia escape through the open porto-systemic collaterals in hepatic bilharziasis?
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What are the common causes of death in hepatic bilharziasis?
What are the common causes of death in hepatic bilharziasis?
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Study Notes
Cell Injury
- Definition: A sequence of events (biochemical and morphologic) upon exposure of the cell to injurious agents.
- Causes:
- Injurious agents
- Excess fat in diet
- Viral hepatitis
Types of Cell Injury
- Reversible cell injury (Degeneration)
- Irreversible cell injury (Cell Death)
Reversible Cell Injury
- Definition: Characterized by accumulation of excess water or fat in cells.
- Microscopic picture:
- Cellular swelling (cloudy swelling and hydropic swelling)
- Accumulation of water in the cell (small amount)
- Cytoplasm: fine granules
- Organs affected:
- Liver
- Kidney
- Heart
- Clinical Picture:
- Liver: no significant change
- Kidney: proteinuria
- Heart: dilatation
- Fate:
- Can recover with removal of injurious agent
- Persistence of injurious agent leads to irreversible cell injury
Irreversible Cell Injury (Cell Death)
- Definition: Death of large groups of cells or tissues within the living body.
- Causes:
- Injurious agents
- Microscopic picture:
- Nuclear changes
- Cytoplasmic changes
- Fate:
- Cell death
Bilharziasis (Schistosomiasis)
- Chronic, specific, granulomatous infection caused by Schistosoma species, endemic in Egypt
- Life cycle and pathogenesis:
- Acute schistosomiasis: severe febrile illness, peak after 2 months
- Early stage: TH1 cells dominate, producing IFN-γ, stimulating macrophages to secrete cytokines TNF, IL-1, and IL-6, leading to fever
- Chronic schistosomiasis: dominant TH2 response, although TH1 cells persist
- Parasite egg proteins stimulate mast cells to produce IL-4, leading to TH2 differentiation
- Both TH1 and TH2 cells contribute to granuloma formation around eggs
- Acute schistosomiasis: severe febrile illness, peak after 2 months
Bilharzial Lesions
- Lesions produced by Cercaria:
- Acute allergic dermatitis at skin penetration sites
- Gross picture: maculopapular skin rash
- Microscopic picture: dilated capillaries, neutrophils, eosinophils, and macrophages
- Lesions produced by adult worms:
- Dead worms: severe inflammation, necrosis, and thrombophlebitis
- Living worms: brown bilharzial pigment in liver, spleen, and other tissues
- Lesions produced by ova:
- Recurrent bleeding due to injury by ova spines, leading to anemia
- Trapped ova: sensitization of T lymphocytes, leading to inflammatory response and granuloma formation
Bilharzial Antigens
- From worms or ova, causing hyperplasia of lymphoid and reticuloendothelial cells
Liver Bilharziasis
- Common in patients with intestinal bilharziasis
- Portal tracts show major changes:
- Ova are carried as emboli through the portal vein and trapped in small and large portal tracts
- Granulomas form, leading to fibrosis
- Dead worms: trapped in venules, leading to thrombophlebitis
- Angiomatoids: dilated capillaries in fibrotic portal tracts, representing dilated collateral channels between branches of the hepatic artery and portal veins
- Hepatic lobules: minimal lesions, preserved architecture, and minimal steatosis
- Fine bilharzial periportal fibrosis:
- Gross picture: normal-sized liver with finely granular surface and dark brown cut surface
- Microscopic picture: portal tracts show ova, granulomatous inflammation, and fibrosis
- Coarse bilharzial periportal fibrosis:
- Gross picture: reduced liver size, firm with irregular surface, and dark brown cut surface
- Microscopic picture: portal tracts show ova, granulomatous inflammation, and fibrosis
Effects and Complications
-
- Portal Hypertension:
- Pathogenesis: portal fibrosis leads to compression of portal veins, and angiomatoids convey high pressure of the hepatic artery to the portal veins
- Effects: splenomegaly, ascites, and opening of porto-systemic venous collaterals
-
- Portal Vein Thrombosis: may occur due to vascular stasis
-
- Mild disturbances of liver functions: lowering of plasma proteins
-
- Ascites: due to portal hypertension and lowering of plasma proteins
-
- Ammonia Encephalopathy: hepatic portal fibrosis allows ammonia to escape through open porto-systemic collaterals, leading to encephalopathy and coma
- Causes of death in hepatic bilharziasis:
- Bleeding (hematemesis)
- Superimposed chronic viral hepatitis (relatively common) leading to cirrhosis and liver failure
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Description
This quiz covers the different types of cell injury, their causes, and effects on various organs such as the liver, heart, kidney, and muscles. It also touches on related diseases like viral hepatitis.