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22 Cards in this Set

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Intracellular target of injurious stimuli and their consequences
1. Mitochondria - disruption in aerobic respiration

2. Cell membranes - disruption in ionic and osmotic hemostasis and lysosome rupture

3. RER and ribosome - disruption in protein synthesis

4. Genetic apparatus - degradation and disruption of DNA
Effects of acute hypoxia on intracellular systems
1. Na pump failure ⇒ ↑ intracellular Na ⇒ ↑ H2O

2. Ca pump failure ⇒ ↑ intracellular Ca ⇒ ↑ activation of degrading enzymes

3. ↑ anaerobic glycolysis ⇒ ↓ glycogen, ↑ lactic acid, ↓ pH

4. ribosome detachment ⇒ ↓ protein synthesis

Restoring O2 may reverse initial effects of acute hypoxia
What are the morphological change of cells in acute hypoxia?
1. Microscopically, cells appear enlarged, swollen, and vacuolated. Vacuoles represent distended/dilated RER and mitochondria

2. Grossly, organs appear swollen, tense, heavy, and pale
Mechanisms that contribute to membrane damage include...
1. Mitochondrial dysfunction
2. Damage to cytoskeleton
3. Loss of membrane phospholipids
4. Accumulation of phopholipid degradation products
5. Generation of reactive O2
Mycardial infarction can be detected how?
↑ serum levels of MB isoenzymes of creatine kinase and cardiac troponin I and T is detected from dying cells
Reactive Oxygen Species (ROS)
1. Attack and degrade membrane lipids, DNA, and proteins

2. Generated from electron and oygen transport systems where O2 is reduced to H2O
Reactive oxygen species are generated under what circumstances?
1. O2 toxicity (O2 therapy)

2. Radiation (e.g. UV rays, x-rays)

3. Chemical/drug induced tissue injury (e.g. CCL4, acetominophen)

4. Presence of xanthne in reperfused (restoration of blood flow after ischemia) hypoxic tissues which causes radicals ⇒ xanthine oxidase inhibitors prevent toxic oxygen metabolites

5. Microbial killing by neutrophils and macrophages during inflammation
Free radical scavengers
1. Antioxidants

2. Enzymes such as catalase, superoxide dismutase and glutathione peroxidase
Necrosis
1. Unintentional or accidental cell death

2. Caused by pathological injury resulting in necrosis from degradative enzymes.

3. Autolysis - degradative enzymes that come from the dead cells themselves

4. Hemolysis - degradative enzymes coming from inflammatory cells like neurotphils and macrophages

5. Degradative enzymes cause DIGESTION of cellular structures and DENATURATION of proteins
T/F: Necrosis and apoptosis are synonomous.
FALSE: Necrosis involves area of many dead cells whereas apoptosis includes only a single or few cells
What do necrotic cells look like?
Nuclear changes

1. PYKNOSIS - shrunken nucleus that becomes basophilic (due to cessation of DNA txn)

2. KARYORRHEXIS - nucleus breaks up into frgaments

3. KARYOLYSIS - nucleus undergoes dissolution and disappears.

Cytoplasmic changes

1. ↓ basophilia and ↑ eosinophilia

2. Shrinkage of cellular plasma membrane

3. Presence of MYELIN FIGURES (large whorled masses of phopholipids) that replace dead cells
Coagulative necrosis
1. "Cooked meat" - firm and pale

2. Appearance due to denaturation of intrinsic structural and enzymative cell proteins

3. Microscopically, cell outline and architecture is intact for a few days but later becomes anuclueate with pink cytoplasm and homogenous

4. Common pattern of necrosis in hypoxic induced cell death EXCEPT the brain
Liquefactive necrosis
1. "Pudding" - soft and semi-liquid

2 Due to powerful hydrolytic enzymes

3. Microscopically, cellular architecture is obliterated and is replaced by neutrophils and tissue debris

4. Develops in hypoxic brain cell death in PYGOGENIC bacterial infections (Staphylococcus aureus, neisseria gonorrrhoeae, chlamydia tracomatis)

5. Clinically referred to as pus.
Caseous necrosis
1. "Dry parmesan cheese" - crumbly, soft, and white

2. Combination of denaturation and cell digestion

3. Cell outline and architecture is obliterated and contains pink, granular, amorphous debris

4. Is pathognomonic (characteristic of a specific disease) for TB
Fat Necrosis
1. "Droplets of wax" - appears yellow or chalky white

2. Microscopically appears like smudgy shadows w/o nuclei

3. Occurs in pancreatitis where digestive enzymes (lipase) of injured acinar cells liquefy fat cells of the omentum

4. FAT SAPONIFICATION - process where fatty acids combine with calcium to form calcium soaps
Gangrenous Necrosis (gangrene)
1. Dry gangrene - dried and shriveled necrotic tissue that has undergone coagulative necrosis due to ischemia

2. Wet gangrene - secondary bacterial infection + associated liquefactive necrosis superimposed on dry gangrene

3. Gas gangrene - gangrene associated with anaerobic bacteria (e.g. chlostridium perfringens) that cause gas bubbles in necrotic tissue
Liquefactive necrosis
1. Due to powerful hydrolytic enzymes

2. Grossly appears to be soft and semi-liquid like pudding

3. Microscopically, cellular architecture is obliterated and is replaced by neutrophils and tissue debris

4. Develops in hypoxic brain cell death in PYGOGENIC bacterial infections (Staphylococcus aureus, neisseria gonorrrhoeae, chlamydia tracomatis)

5. Clinically referred to as pus.
Apoptosis
1. Programmed intentional cell death

2. Single or small clusters of cells shrink away from surrounding cells with loss of cell surface specialization

3. "Boils" appearance from blebs on cell surface

4. "Crescents" of condensed nuclear chromatin appear and undergo karyorrhexis

5. Cytoplasm intensely eosinophilic

6. "Apoptotic bodies" - membrane bounded fragments of apoptotic cell that are phagocytosed by neighboring cells

7. DOES NOT elicit inflammatory response like necrosis
Physiological and pathological examples of apoptosis
Physiological

1. Loss of digital webbing in embryogenesis

2. Thymic involution during young adulthood

3. Shedding of skin and mucosal epithelia during normal turnover

Pathological

1. Apoptosis of virally infected cells

2. Apoptosis in cardiac myocytes in mycardial infarcation and heart failure
Apoptosis
1. Programmed intentional cell death

2. Single or small clusters of cells shrink away from surrounding cells with loss of cell surface specialization

3. "Boils" appearance from blebs on cell surface

4. "Crescents" of condensed nuclear chromatin appear and undergo karyorrhexis

5. Cytoplasm intensely eosinophilic

6. "Apoptotic bodies" - membrane bounded fragments of apoptotic cell that are phagocytosed by neighboring cells

7. DOES NOT elicit inflammatory response like necrosis
Signalling of apoptosis
1. Initiation by ligand binding to TNF "death receptor" (internal pathway) or mitochondria release of cytochrome C causing activating of caspase cascade (the "execution caspases)

DEF: Caspase - proteases that mediate apoptosis

2. Regulated by BCL-2 family proteins: BAD, BAK, BAX promote apoptosis and BCL-2 and BCL-X inhibit apoptosis

3. Failure of normal apoptosis can lead to cancer (e.g. over-expression of BCL-2 in lymphoma can lead to dysregulated cell proliferation)
T/F: Myelin figures appear in cells that have undergone apoptosis.
FALSE: Myelin figures only appear in cells that have undergone UNINTENTIONAL cell death