3rd apoptosis, fat degeneration Flashcards
basis of cell injury?
living cell point of no return NECROSIS
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degeneration
The point of no return is the point where Ca2+ influx occurs, membrane integrity destroyed = enzyme leakage.
- reversible cell injury
- accumulation
what happens during the point of no return?
- Calcium influx occur
- membrane integrity is dissolved
- enzyme leakage occurs
3 morphological changes of cell injury?
- cellular swelling / hydropic degeneration
- parenchymel degeneration
- fatty degeneration/accumulation
cellular swelling / hydropic degeneration appearance/cause?
ATP insufficiency and Na pump is not working and the cell takes up water. the cell becomes bigger. the organ is pale.
increased cytoplasm and vacular appearance of the organelles.
-increase in size do to water uptake
-pale appearance of the organ
parenchymel degeneration description.
Characteristic for the toxic affects on parenchymal organs.
characteristic fats of parenchymal organs like the liver and kidney. In microscopy the cell is very similar to hydropic degeneration do to the dilated mitochondria is the characteristic of the cell
-its MACROscopic appearance is like boiled meat: gray and fragile.
fatty degeneration / fat accumulation description?
characteristic of parenchymal organs also (liver and kidney and muscle) those cells of organs that have high lipid metabolism.
define parenchymal vs stroma?
The parenchyma is the functional parts of an organ in the body. This is in contrast to the stroma, which refers to the structural tissue of organs, namely, the connective tissues.
fatty acid transport process?
FA = fatty acids
TAG = triacylgrlycerol
- free FA taken up from circulation by liver,
- goes through esterification forming TAG.
- apoprotein is added forming lipoproteins.
- lipoproteins are released to the circulation
-catabolism of FA by the liver forms cholesterin used up for cell membranes. ketone bodies via oxidation are also formed from FA.
where can the process of fatty acid transport be targeted resulting problems?
-obesity/starvation, overloading FA accumulation in liver.
- diabetic patients (glucose resistance) glucose cannot be taken up so the body mobilizes fatty acids instead.
- During oxygen deprivation the whole catabolism is blocked
- alcohol consumption blocked catabolism of FA.
alcohol and malnutrition may block apoprotein adding and lipoprotein synthesis.
CELL ACCUMULATES FAT do to the liver being overloaded by fat or is inhibited from metabolizing fat.
Morphological changes during cell fat accumulation?
cytoplasm fat accumulation, cell nuclei is pushed to the side and the fat accumulation my cause rupture of the cell.
Macroscopy: the organ is yellow colored
microscopy: the cell has a large clear cytoplasm do to the dissolved fat.
causes of fat degeneration/accumulation?
- toxic effect
- protein malnutrition
- diabetes
- obesity
- anoxia
types of fat accumulation?
A. diffuse fat accumulation (occurs in toxic effect)
B. mottled (spotty) (related to anoxia)
Diseases of fat accumulation?
- Steatosis hepatis diffuse
- steatosis diffuse myocardia
Steatosis hepatic diffuse definition?
Diffuse steatosis of liver, the whole liver is enlarged, diffusely colored yellow, caused by alcohol before the cytosis there is steatosis.
steatosis definition?
infiltration of liver cells with fat, associated with disturbance of the metabolism by, for example, alcoholism, malnutrition, pregnancy, or drug therapy.
steatosis diffuse myocardia definition?
fat degeneration of the heart, mostly related toxic degeneration.
Bacteria
degeneration adipose insularis myocaria (tiger heart), definition?
papillary muscle have cross striation fat accumulation. Endocardial fat accumulation.
subendocardial fat accumulation. Sub-acute ischemia (acute oxygen deprivation) do to for example pneumonia. it starts in the subendocardial because of 2 reasons:
1. pressure is higher compressing the capillaries more.
2. subendocardial muscles work harder then the epicardium.
infiltration adipose myocardium definition?
high risk in the operation room because they cannot stand as much stress a healthy person with a normal heart
(NOTE: this is not a degeneration, but infiltration) the epicardial fat tissue, can accumulate if you are overweight. The fat surrounding the heart will penetrate the right ventricle, because the left ventricle is pumping harder preventing the fat to grow into the muscles, but the pressure on the right side is less.
the difference between between degeneration and infiltration?
- degeneration: fat accumulation inside the cell.
- infiltration: fat comes from an outside source. (extracellular accumulation of fat.
Nutmeg Liver (degeretio adiposa insularis hepatis)
Nutmeg is a type of spice
circulation in the liver occurs from the portal triad to the central vein. In the event there is some sort of pulmonary disease, or any disease that increases resistance of the blood flow, (fibrosis of the lungs). The heart will adapt, but if it fails to adapt the back-pressure end up in the splanchnic area, to the liver. The high resistance and pressure increases in the liver coming from the central vein.
an oxygen gradient forms from the peripheral to the central vein, highest in the peripheral, lowest in the central. The pericentral vein hepatocytes are effected by 2 things; higher pressure lower oxygen, and the fatty generation will occur in the central vein (Nutmeg liver)
cor pulmonale
abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.
define apoptosis?
apoptosis is an active way of cell death, in contrast to necrosis which is a passive way of cell death.
apoptosis vs necrosis?
necrosis: the integrity of the membrane is dissolved (enzymes leakage)
Apoptosis: the integrity of the membrane is preserved. (no enzyme leakage, enzymatic degradation of protein)
morphology of apoptosis?
- blebs/fragment of cell, membrane bound vesicles, which are removed by the macrophage system.
- Nuclear shrinking (pyknosis) and end up in the apoptotic bodies.
- organelles can also end up in the apoptotic bodies
the process/mechanism of apoptosis?
based off of the activation of caspases which are proteases, cysteine protease. This proteases cleave up the aspartic acid in a well preserved manner.
2 pathway mechanism of caspases activation
intrinsic and extrinsic pathway.
sequence of events in apoptosis? (intrinsic pathway)
the intrinsic pathway starts in the mitochondria. Bcl2 sensor detect DNA damage (radiation), and they may go to the mitochondria to effector molecules in the mt. membrane; Bax and Bud. These effector molecules form homodimers which forms channels on mitochondria membrane and thus, cytotochrome c is released which actives which procaspase 9 which activates the effector caspases, 3,6,7 and apoptosis occurs.
Bcl2 and Bclx regulate the Bax-Bax and Bud-Bud homodimers.
sequence of events in apoptosis? (extrinsic pathway)
extrinsic pathway is related to the tumor necrosis factor receptor (TNF-R) and tumor necrosis factor.
FAS-Receptor, FAS-Ligand (produced by B-cells), which acitvate procasase 8 which activated effector caspase.
NOTE: that FAS-ligand is produced by B-cells.
follicular lymphoma (neoplastic disease of lymphoid cells)
Neoplastic = abnormal growth of tissue/cancer
carries T-14,18 translocation
14: immunoglobulin heavy chain genes
18: Bcl-2
immunoglobulin gene joining to the bcl2 gene which upregulates the bcl2 producing lots of bcl2. As a result in the apoptotic pathway the BAX makes bcl2 and the BUD makes bcl2 heterodimers;
BAX-bcl2
BUD-bcl2
[bcl2]-[bcl2] suspending the monomer components and BLOCK the apoptosis = cancer
define autophagia?
when cells are starving they try to survive be digesting themselves. ergastoplasm contains the most amount of energy in the cell and can fuse with lysosomes. This produced a phagolysosomes which can use its own energy to survive. Apoptosis occurs when the cell is no longer able to save itself.
3 forms of cell death?
- apoptosis
- necrosis
- autophagia.
define ergastoplasm?
ribosome-studded endoplasmic reticulum
