Cell Injury Flashcards
Types of necrosis
Coagulative
Colliquative
Caseous
Grangrenous
Fat
Coagulative necrosis
Tissue with connective tissue —> basic arrangement preserved
Colliquative necrosis
Tissue with minimal connective tissue —> ‘liquifies’
Caseous necrosis
‘Cheese’-like necrotic debris contained within
Grangrenous necrosis
DRY – sterile coagulative necrosis e.g. distal limb
WET - coagulative necrosis with superimposed infection
Fat necrosis
Focal necrosis in fat due to action of lipases (also trauma)
Causes of cell injury
O2 deprivation
Trauma
Microbial
Immunological
Chemical
Hypoxia
Low O2 to tissues
Ischaemia
Decreased O2 to part of the body
Free radical
An atom, molecule or ion with one or more unpaired valence electron
Atrophy
Shrinkage in the size of a cell by the loss of cell substance
Hypertrophy
Increase in size of cells and organ
Hyperplasia
Increase in number of cells in an organ/tissue
Metaplasia
Reversible change in which one adult cell type is replaced by another adult cell type
Forms of cell death
APOPTOSIS - cell contents contained, no surrounding damage
NECROSIS - cell contents spill out, tissue damage
Example of Coagulative necrosis
MI
Example of caseous necrosis
Tuberculosis (TB)
Example of colliquative necrosis
Focal bacterial infections —> accumulation of pus, liquefies tissue
Often in brain
Example of Grangrenous necrosis
WET - GI tract, bacterial
DRY - Limbs (diabetic)
Autolysis
Lysis of tissues by their own enzymes —> death
“Rotting of the tissue”
Primary and secondary healing/repair intention
Primary - restitution with no/minimal residual defect (eg. Suturing leaving a fine scar)
Secondary - organisation and repair where there’s tissue loss, granulation tissue
Regeneration of labile cells
Good capacity to regenerate
eg. Surface epithelial cells
Regeneration of stable cells
Divide at slow rate, but can regenerate if needed
eg. Hepatocytes in liver
Regeneration of permanent cells
Unable
eg. Nerve cells, striated muscle cells
Bacterial exotoxins
Chemicals released by bacteria which stimulate inflammation
Bacterial endotoxins
Associated with bacterial cells walls, also stimulate inflammation
Tissue necrosis
Dead tissue releases peptides
Triggers acute inflammation
Cardinal signs of acute inflammation
Redness - vasodilation
Heat - increased blood flow
Swelling - accumulation of fluid
Pain - physical distortion of tissue
Loss of function
Stages of inflammation
- Release of chemical mediators
- Vasodilation
- Increased vascular permeability
- Fluid accumulation
- Cellular recruitment
- Phagocytosis
Cellular exudation
Increased vascular permeability
Increased net flow of fluid out of vessels = exudation
What can neutrophils do
Move/migrate
Bind to opsonised microorganisms
Phagocytosis
Emigration
Cells (neutrophils) pass between endothelial cells, through basal lamina and into adventitia
What are the early chemical events of inflammatory response
Histamine and thrombin released
Up regulation of platelet activating factor (PAF) on endothelial cells
Neutrophil adhesion to endothelial surface
Histamine
Causes vascular dilation and permeability
Released by mast cells
Chemokines
Chemicals (types of cytokines) which attract more WBC to site of inflammation
eg. IL-8 attracts neutrophils
Coagulation system in plasma
Converts soluble fibrinogen into fibrin
Benefits of inflammation
Dilution of toxins
Entry of antibodies
Transport of drugs
Fibrin formation
Delivery of nutrients and O2
Stimulation of immune response
Harmful effects of inflammation
Digestion of normal tissue
Swelling
Inappropriate inflammatory response (eg. anaphylaxis)
What is resolution
Everything is back to normal
Outcomes of inflammation
Resolution
Suppuration
Scarring or fibrosis
Chronic inflammation
Suppuration
Formation of pus - mix of neutrophils, debris, bacteria
If walled off = abscess
How does granulation tissue form
New capillaries —> more macrophages —> proliferation of fibroblasts —> fibrosis or scarring
What are neutrophils replaced by in the progression from acute to chronic inflammation
Lymphocytes
Cells of chronic inflammation
Lymphocytes - small purple dots
Plasma cells - fried eggs
Macrophages - bigger blobby ones
(Sometimes eosinophils) - tomatoes with sunglasses
B lymphocytes
Meet antigens, turn into plasma cells
Plasma cells then produce antibodies
T lymphocytes
Killer T cells (CD8+)
Helper T cells (CD4+)
Killer T cells (CD8+)
Cytotoxic function, and recruiting other immune cells
Helper T cells (CD4+)
Activate killer T and plasma cells
What are cytokines
Small proteins which:
Enhance cell mediated immunity
Enhance antibody response
Granuloma
A collection of histiocytes
