Term
| What is the difference between apoptosis, cell degeneration and oncosis/necrosis? |
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Definition
Apoptosis: programmed cell death NOT arising from cell degeneration. This is not damaging to surrounding tissue
Cell Degeneration: cell damage (can result from changes in environment, metabolic activity etc) which can, in theory, be repaired
Necrosis: degeneration which cannot be repaired, resulting in death of the cell. This is damaging to surrounding tissue |
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Term
| Explain the phrase "malfunctioning cells will not necessarily result in a malfunctioning organ, or cause disease to the animal as a whole" |
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Definition
-some aspects of structure & function are redundant, so altered structure/function may not affect the tissue/animal health
-many physiologic feedback loops are self-correcting |
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Term
| Can necrosis occur in a dead animal? |
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Definition
| no, cell death is then called autolysis |
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Term
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Definition
| bacterial lysis & fermentation of tissue in a dead animal |
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Term
| What factors may contribute to how a normal cell responds to an injurious stimulus (e.g. lack of oxygen) |
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Definition
-type of injury
-duration of injury
-severity of stimulus
-type of cell
e.g. bone cell lack of O2 less impact than brain cell lack of O2 |
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Term
| What are intracellular inclusions? |
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Definition
| Accumulations of molecules in a cell, which can result from a change in metabolic pathways, phagocytosis, normal function (e.g. hepatocytes), aging cells etc |
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Term
True or False
Metabolically active cells are often more susceptible to injury than non-active cells |
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Definition
True
-constant import/export of molecules, synthesis of product etc
-sublethal injury can lead to accumulation of products |
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Term
| What might cause a product/molecule to accumulate in a cell in large amounts? |
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Definition
-increased production
-decreased excretion/secretion
-decreased consumption within the cell
-reduced metabolism/processing of a precursor (so the precursor accumulates)
-increased uptake from ECF
-loss of enzyme function to degrade substances (e.g. phagocytic molecule that has poor enzyme function) |
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Term
| What are the categories of intracellular material? (6) |
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Definition
-normal molecules that are present in excess e.g. protein
-foreign substances e.g. carbon from smoke inhallation
-pigments (e.g. bilirubin, lipofuscin)
-metal ions
-Calcium in necrotic cells
-microbial structures (baterial/viral/protistain) |
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Term
| Describe the pathogenesis of hepatic lipidosis |
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Definition
Lipid metabolism requires: enzymes, ATP, CHO metabolites
Excretion requires: synthesis of apoprotein & lipoprotein
Sublethal injury -> disruption of metabolic pathway, fatty acids or TG's accumulate in cytoplasm -> Hepatic lipidosis |
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Term
| Who would you describe a fatty liver? |
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Definition
Gross: enlarged, yellow, greasy
Microscopic: lots of fat vesicles |
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Term
| How can cell death be characterized? |
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Definition
physiological vs pathological
cell morphology - necrosis vs apoptosis |
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Term
| What is the difference between physiologic cell death & pathologic cell death? |
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Definition
| Physiologic = apoptosis (programmed cell death) |
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Term
| Skin cells maturing and dying is an example of (physiologic/pathologic) cell death |
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Definition
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Term
| Name some causes of cell injury/death... |
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Definition
-hypoxia
-ischemia
-loss of mmb integrity
-Fas ligand binding to Fas receptor (induces apoptosis) |
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Term
| What are the phases of apoptosis? |
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Definition
1. Signalling (transmembrane or intracellular. e.g. FAS binding to its receptor
2. Integration
-pro vs anti apoptotic factors are contrasted, outcome of cell is determined
3. Execution
Caspases mediate the process, with a bioamplification of apoptotic factors. Nucleus shrinks, cytoplasm & organelles form blebs -> apoptotic bodies
4. Membrane flipping
-apoptotic bodies preset signals on the mmb surface to promote their own phagocytosis |
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Term
| Key characteristics of apoptosis |
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Definition
-orchestrated
-does not induce inflammation
-cellular contents do not leak into extracellular compartment
-well controlled, mediated by enzymes |
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Term
| What enzymes regulate apoptosis? |
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Definition
caspases
(Cysteine-Aspartic residues) |
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Term
True or False
Apoptosis is a non-inflammatory process which does not require ATP to proceed |
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Definition
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Term
| What is the correlation between chronic high blood calcium, and the parathyroid gland? |
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Definition
| chronic high Ca leads to atrophy of the parathyroid via apoptosis |
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Term
| What are the four main mechanisms of cell injury? |
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Definition
-depletion of ATP
-damage to nucleic acids (especially DNA)
-interference with protein synthesis
-injury to cell membranes |
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Term
| Why do injured cells accumulate calcium, and what is the significance? |
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Definition
Cell injury = membrane damage = large amounts of calcium enter = enzyme activate
ATPase uses up ATP
Phospholipase & protease further reduce membrane integrity
Endonuclease causes damage to nucleus chromatin |
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Term
| What is white muscle disease? |
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Definition
| calcification of necrotic tissue (calcium accumulates in dead muscle cells) |
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Term
True or False
The transition from degneration to necrosis is visible fairly quickly after cells have passed the "point of no return" |
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Definition
False
6-8hrs before you can see necrosis microscopically |
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Term
| What are the trademark microscopic signs of necrosis? (3) |
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Definition
hypereosinophilia
homogenous cytoplasm
nuclear changes (pyknosis, karyorrhexis, karyolysis) |
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Term
| What cells will be more severely affected by ischemia, cells in Zone 1, 2 or 3 surrounding the portal triad? |
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Definition
Zone 3
-farthest away from the blood supply
BUT if it were an issue of toxicity in the blood, they would be exposed to the toxin last, and would exhibit signs of toxicity last |
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Term
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Definition
| shrunken, dark blue (hyperchromatic) nucleus |
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Term
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Definition
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Term
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Definition
| dissolution/fading of nucleus (caused by DNAses / endonucleases) |
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Term
| Compare necrosis vs apoptosis |
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Definition
Swell / Shrink
Liquify or coagulation / blebbing
Membrane fragment/intact
ATP depleted/requires ATP
Disorganized / organized
Contents leak / contained
Inflammation / no inflammation |
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Term
| What are some of the ways necrotic tissue can appear (grossly) |
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Definition
Coagulation Necrosis: looks similar to normal structure, pale/swollen/friable
Liquefactive Necrosis: loss of stucture, pale, liquid
Caseation Necrosis: structure lost, dry/cheeselike/friable |
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Term
| What causes liquifaction necrosis |
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Definition
leukocytes or bacteria release enzymes which break down cells -> liquify
may leave a hollow cavity behind (esp in brain) |
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Term
| Why is the brain prone to liquefaction necrosis? |
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Definition
| less capable of regeneration or scarring vs other tissues |
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Term
True or False
Macrophages in particular are prone to causing liquification of dead tissue |
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Definition
false
more likely to see caseation necrosis b.c. dont ahve lytic enzymes |
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Term
| Hyperadenalcorticism will cause persistent ______ which increses stores of _____ in hepatocytes |
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Definition
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Term
| What do hepatocytes with glycogen inclusions look like? |
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Definition
| cytoplasm looks moth-eaten |
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Term
| How does the colour of a renal infarct change over the course of several days |
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Definition
Initially: very pale (no blood)
24h: red as blood seeps into affected tissue
From there, low pH bc of liquifying cells = RBCs broken down = bilirubin (yellow/green) and hemosiderin (brown) released
Breakdown process starts around 36h and may take days depending on how big the infarct is |
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Term
| What is a "watershed zone"? |
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Definition
| where 2 arterial fields overlap (regions between 2 arterial supplies) |
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