Flashcards in Cellular Injury II Deck (59):
examples of bilirubin accumulation
hemolytic jaundice is associated with
destruction of red cells.
hepatocellular jaundice indicates
parenchymal liver damage
obstructive jaundice is either
intra or extrahepatic obstruction of the biliary tract
hemosiderin is an
iron-containing pigment that consists of aggregates of ferritin.
hemosiderin appears in tissues as
brown amorphous aggregates that stain blue with Prussian blue dye. It is usually in small amounts.
hemosiderin exists in small amounts within tissue macrophages of the
bone marrow, liver and spleen.
hemochronatosis is a
more extensive accumulation of hemosiderin, often within parenchymal cells, with accompanying tissue damage, scarring and organ dysfunction.
it occurs in hereditary (primary) and secondary (blood transfusion) forms.
lipofuscin is a
yellowish, fat soluble pigment that is an end product of membrane lipid peroxidation.
lipofuscin commonly accumulates in
elderly patients (hepatocytes and myocardial cells), referred to as brown atrophy.
the sum of the degradative and inflammatory reactions occurring after tissue death caused by injury.
necrosis - general chracteristics
1. occurs within living organisms and pathologic speciments but not fixed cells with well preserved morphology.
2. autolysis is the degradative reactions caused by intracellular enzymes indigenous to the cell.
3. heterolysis is the cellular degradation by enzymes derived from sources extrinsic to the cell.
postmortem autolysis occurs after
the death of an organism and is not necrosis.
degradative reactons in cells caused by intracellular enzymes indigenous to the cell.
the cellular degradation by enzymes derived from sources extrinstic to the dying cell.
main types of necrosis
coagulative necrosis results from
a sudden cutoff of blood sulpply to an organ, paricularly the heart and kidney.
in coagulative necrosis,
it is characterized by general preservation of tissue architecture (ghost cells).
increased cytoplasmic eosinophilia occurs because of protein denaturation and loss of cytoplasmic RNA
nuclear changes in coagulative necrosis are the
morphologic hallmark of irreversible injury and necrosis. Along with stainable nuclei, they include
chromatin clumping and shrinking with increased basophilia
fragmentation of chromatin
fading of chromatin material
liquefactive necrosis results from
ischemic injury to the CNS. After the death of CNS cells, it is caused by autolysis.
It is also chracterized by digestion of tissue.
liquefactive necrosis occurs in
supprative infections characterized by the formation of pus (liquefied tissue debris and neutrophils) by heterolytic mechanisms.
caseous necrosis occurs as part of
granulomatous inflammation and is a manifestation of partial immunity caused by the interaction of T lymphocytes, macrophages and cytokines, such as IFN-gamma derived.
caseous necrosis is associated most often with
caseous necrosis has features of both
coagulative necrosis and liquefactive necrosis.
caseous necrosis appearance
an amorphous eosinophilic apperanace on histologic examination, usually within the center of granulomas.
necrotic cells of caseous necros do not
maintain their cellular outlines but do not undergo lysis (as is seen in liquefactive necrosis).
fat necrosis occurs in two forms
traumatic fat necrosis
enzymatic fat necrosis
traumatic fat necrosis
occurs after a severe injury to tissue with a high fat content, such as the breast.
enzymatic fat necrosis
a complication of acute hemorrhagic pancreatitis, a severe inflammatory disorder of the pancreas.
steps of enzymatic fat necrosis
pancreatic enzymes diffuse into inflamed tissue and digest the parenchyma.
fatty acids liberated by the digestion of fat form calcium sats.
vessels are eroded, with resultant hemorrhage.
marked by deposition of fibrin-like proteinaceous material in the arterial walls, which appears smudgy and acidophilic.
It is often associated with immune-mediated vascular damage.
gangrenous necrosis when complicated by infective heterolysis and liquefactive necrosis
gangrenous necrosis when characterized by coagulative necrosis without liquefaction.
apoptosis is used to
remove cells with irreparable DNA damage, protecting against neoplastic formation.
it is also important for embryogenesis and programmed cell cycling (menstruation)
apoptosis - morphologic characteristics
1. a tendency to involve single isolated cells or small clusters of cells within a tissue.
2. Progression through a series of changes marked by a lack of inflammatory response.
3. shrinking of affected cells and cell fragments, resulting in small round eosinophilic masses often containing chromatin remnants.
the progression of changes in apoptosis
1. blebbing of plasma membrane, cytoplasmic shrinkage, chromatin condensation.
2. budding of cell and separation of apoptotic bodies (membrane bound segments)
3. phagocytosis of apoptotic bodies.
diverse injurious stimuli
foreign (viral) DNA
withdrawal of growth factors or hormones.
biochemical events of apoptosis
1. initiation of diverse injurious stimuli.
2. Activation of intrinsic/extrinsic pathway or cytotoxic T cell mediated apoptosis
3. activation of caspases
4. Neatly packaged portions of cell membrane with degraded cellular contents are pinched off and form apoptotic bodies which are engulfedby phagocytic macrophages.
endonucleases, which degrade dNA into nucleosomal chromatin ragments.
they also activate transglutaminases, which cross-link apoptotic cytoplasmic proteins.
healthy, stimulated cells contain adequate levels of
anti-apoptotic Bcl-2 (e.g. hormone stimulation)
the intrinsic pathway is activated when cells are
deprived of hormonal stimulation.
In the intrinsic pathway, lack of growth stimulation results in an excess of
Bax and Bak (pro-apoptotic) over Bcl-2 (anti-apoptotic) and cause release of cytochome-c from mitochondira, causing activation of caspases.
caspases are cytosolic cytotoxic proteases that are referred to as
major executioners - they activate intracellular endonucleases and proteases that neatly break down the cellular organelles and contents.
the apoptotic cascade is triggered by the
opening of the mitochondrial permeability transition pore and release of cytochrome c, triggering the apoptotic cascade.
In the extrinsic pathway,
molecules such as FAS ligand and TNF bind to receptors. The activated receptors signal via transmembrane death domains and activate caspases.
in cytotoxic T cell mediated apoptosis, cells that are recognized as
foreign (i.e. contain viral DNA, transplanted organs) are targeted by CD8+ cytotoxic
In T cell mediated apoptosis, CD8+ cytotoxic T cells puncture the plasma membranes of target cells via
through the perforins, _ enters
granzyme B enters the target cell and activates the caspases.
gene product that inhibits apoptosis
gene product that facilitates apoptosis
gene product that facilitates apoptosis by decreasing transcription of bcl-2 and increasing transcription of bax.
metastatic calcification is often caused by
hypercalcemia, most often resulting from many things.
hypercalcemia often results from
osteolytic tumors, with resultant mobilization of calcium and phosphorus
excess calcium intake, such as in the milk-alkali syndrome (nephrocalcinosis and renal stones caused by milk and antacid self therapy for peptic ulcer).
dystrophic calcification occurs in
previously damaged tissue, such as areas of old trauma, tuberculosis lesions, scarred heart valves and atherosclerotic lesions.