Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

24 Cards in this Set

  • Front
  • Back
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)

**Enzymatic degradation of a cell resulting from exogenous injury

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

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

2) Liquefactive (brain)

3) Caseous (TB)

4) Fat (pancreas)

5) Fibrinoid

6) Gangrenous
=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
**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

=followed by "resolution"
Fluid Exudation
**Increased vascular permeability, vasodilation, endothelial injury
Leukocyte Activation
=rolling, tight binding, diapedesis

=bacterial products
=complement, chemokines

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

=characterized by persistent destruction and repair

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

Granulation Tissue
=highly vascularized, fibrotic

=fibrosis surrounding pus

=abnormal communication

=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
**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.
**Leukocyte travels between endothelial cells and exits blood vessel
**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
=superoxide dismutase
=glutathione peroxidase

2) Spontaneous decay

3) Antioxidants
=vitamins E and A

Reperfusion after anoxia induces free radical production.

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