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24 Cards in this Set

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What is apoptosis?
**Programmed cell death

**Characterized by:
=cell shrinkage
=chromatin condensation
=membrane blebbing
=formation of apoptotic bodies which are then phagocytosed
When does apoptosis occur?
=during embryogenesis

=hormone induction (menstration)

=immune cell-mediated death

=injurious stimuli (radiation, hypoxia)

=atrophy
Necrosis
**Enzymatic degradation of a cell resulting from exogenous injury

**Characterized by:
=enzymatic digestion and protein denaturation with release of intracellular components

**INFLAMMATORY
Morphologically, necrosis occurs in which forms?
1) Coagulative
=heart, liver, kidney

2) Liquefactive (brain)

3) Caseous (TB)

4) Fat (pancreas)

5) Fibrinoid

6) Gangrenous
=limbs
=GI tract
Cell Injury
Can be:

1) Reversible
2) Irreversible
Reversible Cell Injury
1) Cellular swelling

2) Nuclear chromatin clumping

3) Decreased ATP synthesis

4) Ribosomal detachment

5) Glycogen depletion
Irreversible Cell Injury
1) Plasma membrane danger

2) Lysosomal rupture

3) Ca influx --> oxidative phosphorylation

4) Nuclear pyknosis, karyolysis, karyorrhexis

5) Mitochondrial permeability
Inflammation
**Characterized by:

=rubor (redness)
=dolor (pain)
=calor (heat)
=tumor (swelling)
=functio lassa (loss of function)
Components of Inflammation:
1) Fluid exudation

2) Leukocyte activation

3) Fibrosis

**Can be ACUTE or CHRONIC
=followed by "resolution"
Fluid Exudation
**Increased vascular permeability, vasodilation, endothelial injury
Leukocyte Activation
**Emigration
=rolling, tight binding, diapedesis

**Chemotaxis
=bacterial products
=complement, chemokines

**Phagocytosis and killing
Fibrosis
**Fibroblast emigration and proliferation
ACUTE Inflammation
**Neutrophil, eosinophil, and Ab mediated
CHRONIC Inflammation
**Mononuclear cell mediated:

=characterized by persistent destruction and repair

**GRANULOMA
=nodular collections of macrophages and giant cells
Resolution
**Restoration of normal structure

Granulation Tissue
=highly vascularized, fibrotic

Abscess
=fibrosis surrounding pus

Fistula
=abnormal communication

Scarring
=collagen deposition resulting in altered structure and function
Leukocyte Extravasation
**Neutrophils exit from blood vessels at sites of tissue injury and inflammation in 4 steps:

1) Rolling
2) Tight binding
3) Diapedisis
4) Migration
Rolling
**Mediated by E-selectin on vascular endothelium binding to Sialyl-Lewis on the leukocyte
Tight Binding
**Mediated by ICAM-1 on vascular endothelium binding to LFA-1 on the leukocyte.
Diapedisis
**Leukocyte travels between endothelial cells and exits blood vessel
Migration
**Leukocyte travels through the interstituium to the site of injury or infection GUIDED by chemotactic signals (=cytokines)
Free Radical Injury--what initiates it?
**Initiated via:

=radiation exposure
=metabolism of drugs (phase I)
=redox reaction
=nitric oxide
=transition metals
=leukocyte oxidative burst
How do they induce cell injury?
**Induces cell injury through:

=membrane lipid peroxidation
=protein modification
=DNA breakage
How can we degrade free radicals?
1) Enzymes
=catalase
=superoxide dismutase
=glutathione peroxidase

2) Spontaneous decay

3) Antioxidants
=vitamins E and A
Example:

Reperfusion after anoxia induces free radical production.

When is this a problem?
**This is a MAJOR cause of injury after thrombolytic therapy.