Inflammation Flashcards
List of cells and molecules involved in inflammation
Leukocytes
Endothelial cells
Cells and extracellular matrix of the surrounding tissue
Plasma proteins
List of cells that releases plasma proteins
Platelets
Endothelial cella
Inflammatory cells
Types of inflammatory
Acute inflammation
Chronic inflammation
It is rapid onset, characterized by exudation of fluid and protein from vessels and emigration of neutrophils. It only last for minutes to days.
Acute inflammation
Longer time course. It involves different cell types. Tissue repair coexist with tissue destruction
Chronic inflammation
What are the different cell types involve in Chronic Inflammation?
Lymphocyte and Macrophage
5 signs/symptoms of inflammation
Heat Pain Swelling Redness Loss of function
Causes of Acute inflammation
Infection Trauma Physical and Chemical agents Necrosis Foreign bodies Immune reactions
Stages of Acute Inflammation
- Vasodilation
- Increase vascular permeability
- Movement of the WBC from the blood vessel into soft tissue at the site of inflammation
Occurs through the release of mediators from cell
Vasodilation
What cells releases Histamine
Mast cells
Basophils
Platelets
What are the three mediators that are released that causes Vasodilation
Histamine
Prostaglandin
Nitric Oxide
Mediator that is responsible for pain/fever
Prostaglandin
True or False: Vasodilation decreases the hydrostatic pressure by slowing of blood flow
False
*increases
Allows fluid to cross the interstitial tissue. Is it when retraction of endothelial cells happen.
Increase vascular permeablity
3 steps: Movement of the WBC from the blood vessel into soft tissue at the site of inflammation
▪️Rolling
▪️Pavementing
▪️Transmigration
Loose, intermittent contact of WBC. Margination of WBC from stasis of blood
Rolling
Tight, constant contact of WBC with endothelium
Pavementing
WBC crossing through the endothelial layer
Transmigration
Process by which WBC are drawn to the site of inflammation
Chemotaxis
Mediators involved,in increase vascular permeability
Histamine
Bradykinin
Leukotrienes C4, D4 and E4
Mediators involved in the movement of WBC
Exogenous- bacterial polysaccharide
Endogenous- C5a, leukotriene B4 and Interlukin-8 (IL-8)
True or False: The role of the leukocyte is to recognize foreign particles through scavenger receptors
True
Particles that bind to foreign material and signal leukocytes to remove it
Opsonins
Types of Opsonins
IgG
C3b
Collectins
Recognize by Fc receptor of WBC
IgG
Recognize by Cr 1,2,3 on leukocyte
C3b
Recognize by C2g on leukocyte
Collectins
Mildest form of Acute Inflammation. Its appearance is relatively clear, watery. Content of fluid, few cells mostly fluid
Serous
Protein-poor fluid, seen in viral infection and burn
Transudate
What is the specific gravity of Transudate?
Its appearance is finely particulate, thick fluid. Content much more protein and cells than serous
Fibrinous
Protein-rich fluid. Seen in uremic and post MI strep throat, pneumonia, pericarditis
Exudate
What is the specific gravity of Exudate
> 1.020
Inflammation that is seen in bacterial and fungal infection. Its appearance is pus-thick, white yellow fluid. The fluid contains neutrophils,protein, necrotic cells and bacteria.
Purulent inflammation
Outcomes of Acute Inflammation
Resolution (recovery)
Inciting agent is removed
All damage cells is repaired
The organ must be capable of regeneration
Walled of collection of pus
Abscess
Loss of mucosa and deeper tissues
Ulcer
Only the mucosa is lost
Erosion
What is the common site for ulcer
GIT (stomach/duodenum)
Layers of Ulcer
Fibrin
Neutrophils
Granulation tissue
Fibrosis
Anomalous patent connection between 2 organs
Fistula (Tunnel)
Complications of ulcer
Pain
Hemorrhage
Perforation
Complications of Fistula
Infection can enter other organs
Massive hemorrhage
Replacement of lost parenchyma with disorganized connective tissue
Scar formation
Prolonged inflammation consisting of active inflammation and tissue repair and destruction
Chronic inflammation
Causes of Chronic inflammation
Viral
Autoimmune dysfunction
Prolonged exposure to infection
Persistent microbial infection
Cells involved in Chronic inflammation
Macrophage
Lymphocytes
Collection of epitheloid histiocytes and collection of activated macrophage
Granulomatous Inflammation
Causes of Granulomatous Inflammation
Mycobacterium tuberculosis Fungi such as Histoplasma capsulation and Biastomyces dermatitidis Foreign material Sarcoidosis Silica
Involves regeneration of the parenchyma or replacement of damages tissue with a scar if regeneration is not possible
Repair
Regeneration of cells combined with scarring and fibrosis
Healing
Components of healing
- Induction of inflammatory process
- Formation of new blood vessels
- Production of extracellular matrix
- tissue remodeling
- wound contacture
- increasing wound strength
Inflammatory process
- acts to contain damage
- removing infecting substance
- remove dead tissue
- start deposition of extracellular matrix
4 processes of replacement by scar
- formation of new blood vessels
- migration and proliferation of fibroblasts
- deposition of extracellular matrix
- maturation and recognization of tissue/fibers
Type of healing if wound has clean edges, close reapproximation of margins and minimal tissue disruption
Healing by first intention
Type of healing if wound has unclean edges, extensive tissue disruption and tissue necrosis
Healing by second intention
2 factors that may impair the process of wound healing
General factors
Mechanical factors
General factors such as:
Infection
Nutritional deficiency
Glucocorticoid therapy
Result in decrease fibrosis
Mechanical factors such as:
Deniscence
Poor perfusion
Unintentional reopening of the wound due to pressure or torsion
Deniscence
Decrease amount of blood available for healing
Poor perfusion
Protective response to rid the body of the cause of cell injury.
Inflammation
