Fou 6 - Cellular Suffering and Death Flashcards
How many pathway are there for apoptosis ?
Two: Intrinsic and extrinsic.
Which is the final step for apoptosis?
Activation of cytosolic caspases that mediate cellular breakdown.
What histological findings characterize Apoptosis?
Deeply eosinophilic cytoplasm, cell shrinkage, Nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, Nuclear fragmentation (Karyorrhexis), and formation of apoptotic bodies.
What is Pyknosis?
Nuclear shrinkage
What is Karyorrhexis?
Nuclear fragmentation.
In the Intrinsic pathway, what happened with the proportion of the Anti- and Pro- apoptotic factors?
Changes in proportion more pro- than anti-.
Which are the Pro- and Anti- apoptotic factors?
Pro- BAX and BAK proteins.
Anti- Bcl-2
What is the BAX and BAK’ functions?
Increased mitochondrial permeability and Cytochrome C release.
What is the function of the Apaf-1?
Normally induces the activation of caspases.
Which is the process of the Follicular lymphoma?
Occurs when Bcl-2 is overexpressed, then decrease caspase activation and tumorigenesis.
Which is the function of the BCL-2?
It is the major anti-apoptotic regulator of the mitochondrial permeability.
What is the primary initiator of the apoptosis?
Caspases.
Which is the pathway characterized by death receptors?
Extrinsic pathway.
Which are the two death receptors?
Fas receptor activated by FasL (Fas ligand). TNF receptor activated by TNF-Alpha
What is the function of Granzyme B?
Activate caspases directly.
Which defective interaction of the apoptosis process contribute to autoimmune disorders?
Defective Fas-FasL interactions.
What is the protein that is use by Killer T cells to make holes in plasma membrane?
Perforin punches holes in membrane.
Definition of necrosis:
Enzymatic degradation and protein denaturation of cell due to exogenous injury produce intracellular components leak. Inflammatory process (unlike apoptosis).
What does apoptosis mean?
Programmed cell death or orderly cell death process.
How many types of necrosis are there?
Coagulative, Liquefactive, Caseous, Fat, Fibrinoid, Gangrenous.
What is Coagulative necrosis?
Seen in: ischemia/infarcts in most tissues(except brain). Due to: ischemia/infarction; proteins denature, enzymatic degradation.
Histology: Cell outlines preserved; increased cytoplasmic binding of acidophilic dyes.
What is Liquefactive necrosis.
Seen in: Bacterial abscesses, Brain infarcts (due too increase fat content).
Due to: Neutrophils releasing lysosomal enzymes that digest the tissue.
Histology: Early (cellular debris and macrophages) and Late (cystic spaces and cavitation brain).
What is Caseous Necrosis
Seen in: TB, systemic fungi (histoplasma capsulatum), Nochardia. Due to: Macrophages wall off the infecting microorganism, that produces granular debris. Histology: Fragmented cells and debris surrounded by lymphocytes and macrophages.
What is Fat Necrosis?
Seen in: Enzymatic (acute pancreatitis, saponification) and Nonenzymatic (Breast trauma). Due to: Damaged cells release lipase, which breaks down fatty acids in cell membranes. Histology: outlines of dead cells without peripheral nuclei;saponification of fat (with calcium) appears dark blue on H&E stain.
What is Fibrinoid?
Seen in: immune reaction in vessels.
Due to: immune complexes combine with fibrin produce vessel wall damage.
Histology: Vessel walls are thick and pink.
What is Gangrenous necrosis?
Seen in: Distal extremity, after chronic ischemia. Due to: Dry (ischemia) and Wet (superinfection). Histology: Dry (coagulative) and Wet (Liquefactive).
Which are the two types of cell injury?
Reversible with O2 and Irreversible.
Reversible(R) and Irreversible (I):
1) ATP depletion. 2)Nuclear chromatin clumping. 3)Lysosomal rupture. 4)Fatty change. 5)Plasma membrane damage. 6)Nuclear pyknosis, Karyorrhexis and karyolisis.
1)R. 2)R. 3)I. 4)R. 5)I. 6)I.
What does infarction mean?
It is a tissue death caused by a lack of O2
How many types of infarcts are there?
Two type: Red and Pale or white
What is a Red infarcts?
Red (hemorrhagic) infarcts occur in venous occlusion and tissues with multiple blood supplies, such a liver, lung etc.
Reperfusion injury is due to damage by free radicals.
What is a Withe or pale infarcts?
This occur in solid organs with a single blood supply, such a heart, kidney and spleen.
What cellular by-products might you detect in the serum when the cardiac myocytes are injured?
Myoglobin, CPK, CKMB and Troponin I. Cardiac enzymes
What cellular by-products might you detect in the serum when the skeletal myocytes are injured?
CPK, Aldolase and myoglobin.
What cellular by-products might you detect in the serum when the Hepatocytes are injured?
AST, ALT, Alkaline phosphatase and GGT.
What cellular by-products might you detect in the serum when the Salivary gland cells are injured?
Amylase.
What cellular by-products might you detect in the serum when the pancreatic exocrine cells are injured?
Amylase and Lipase.
What cellular by-products might you detect in the serum when the Red blood cells (RBCs) are injured?
Heme -> Bilirubin.
What histology can feature are seen in apoptotic liver cells?
Cellular shrinkage, pyknosis, Karyorrhexis, membrane blebbing and apoptotic bodies.
What substances do cytotoxic T cells and NK cells use to induce apoptosis in the cells infected with a virus?
Perforin and Granzyme B.
What highly damagin events can cause irreversible cell injury?
Calcium influx, damage to the plasma membrane, rupture of the lysosome, mitochondrial permeability, pyknosis, Karyorrhexis and karyolisis.
What cellular enzymes are responsible for handling oxygen free radicals?
1)Catalase degrades H2O2 to O2 and H2O. 2)Superoxide Dismutase converts O2 radicals to H2O2. 3)Glutathione per oxidase catalyzes free radical breakdown.
