Cell injury-2. Fatty Change * Definition: abnormal accumulation of triglycerides within parenchymal...
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Transcript of Cell injury-2. Fatty Change * Definition: abnormal accumulation of triglycerides within parenchymal...
Fatty Change
* Definition: abnormal accumulation of triglycerides within parenchymal cells. * Site:
liver, most common site which has a central role in fat metabolism.
it may also occur in heart as in anaemia or starvation (anorexia nervosa)
Other sites: skeletal muscle, kidney and other organs.
* Causes:
1. Toxins (most importantly: Alcohol abuse)2. Diabetes mellitus 3. Protein malnutrition (starvation)4. Obesity5. Anoxia
* The significance of fatty change:
Depends on the severity of the accumulation. Mild: it may have no effect . Severe: form, fatty change may precede cell
death, and may be an early lesion in a serious liver disease called nonalcoholic steatohepatitis
* Morphological features of fatty liver:
*Grossly: • Size: enlarged.• Shape: preserved.• Surface: smooth.• Color: yellowish.• Consistency: soft & greasy.• Capsule: stretched (non-adherent).• C/S: bulges out with rounded edges.
*Microscopically:• The cells are swollen, the cytoplasm contains
droplets of fat (in mild cases) termed microvesicular steatosis, or vacuoles pushing the nucleus to one side in severe cases (signet ring appearance) termed macrovesicular steatosis.
• Fat appears as empty vacuoles in Haematoxyline & Eosin stained sections but stained in frozen sections by fat stains e.g. Oil Red O stain.
A. Endogenous pigmentationI. Melanin pigment
Melanin deficiency Melanin hyper pigmentation
1. Albinism-Hereditary absence of tyrosinase enzyme.-Hair is white, skin, iris, choroids are pink.2. Leucoderma-Idiopathic or 2ry to leprosy or syphilis.-White skin patches due to melanin loss.
1. Prolonged exposure to sun.2. Chloasma: brown patches on face, nipple & genitalia due to increased estrogen level.3. Melanocytic tumors.4. Addison’s disease.
II. Lipochrome (lipofuscin) pigment
• It is a yellowish brown pigment, which is found normally in heart, liver, testis, seminal vesicles & adrenals.
• Increases in old age & in atrophic conditions e.g. Brown atrophy of the heart.
Here is the centrilobular portion of liver next to a central vein. The cells have reduced in size or been lost from hypoxia. The pale brown-yellow pigment is lipochrome that has accumulated as the atrophic and dying cells undergo autophagocytosis.
III. Hemoglobin-derived pigmentBilirubin Hemozoin
(haematin)Hemosiderin
•Increases in jaundice.•-ve with Prussian blue reaction
•increases in Bilharziasis & malaria.•Released from the parasite, engulfed by the cells of RES in liver, spleen → parasitic pigmentation.•-ve with Prussian blue
•Increases with hemosiderosis. •+ve with Prussian blue.
Hemosiderosis
* Causes of Hemosiderosis:
1. Increased absorption of dietary iron
2. Hemolytic anemias
3. Repeated blood transfusions.
4. Hereditary hemochromatosis with tissue injury
including liver fibrosis, heart failure, and diabetes
mellitus
.
It is found at first in the mononuclear phagocytes of
the liver, bone marrow, spleen, and lymph nodes and
in scattered macrophages throughout other organs.
With progressive accumulation, parenchymal cells
throughout the body (principally the liver, pancreas,
heart, and endocrine organs) will be affected
Pathological calcification• It implies the abnormal deposition of calcium salts in tissues rather
than bone and teeth.
• It has 2 types:
Dystrophic calcification:
When the deposition occurs in dead or dying tissues e.g. areas of
necrosis or atherosclerotic patches.
it occurs with normal serum levels of calcium
Metastatic calcification:
The deposition of calcium salts in normal tissues
It almost always reflects hypercalcemia.
* Mechanism of irreversible cell injury:
• Persistent or severe injury (hypoxia) takes the
cell to the "point of no return" where the
injury becomes irreversible.
• At this point no intervention can save the cell.
• Severe mitochondrial damage is the hallmark
of irreversible injury.
Mitochondrial damage • Marked reduction in ATP production leads to
mitochondrial damage results in formation of high
conductance channels (Mitochondrial Permeability Transition
(MPT) channels) which Release cytochrome c into cytosol
which is a trigger for cell death (apoptosis).
MITOCHONDRIAL DYSFUNCTION or INJURY
MitochondrialPermeability
Transition (MPT)
Cytochrome C
↓ATP production
H+
Apoptosis