Bio Of Tissue Response To Disease Flashcards
Mediators
Initiation and amplification of the
inflammatory response and determination of its pattern severity, clinical and pathologic manifestations
Causes:
Inflammation
Infection, trauma, tissue death, physical,
chemical and immunologic injury
Process
. Inflammation
Process: Exudation of fluid from vessels → Attraction of leukocytes to the injury → Engulfment and
destruction of bacteria, tissue debris etc. → Activation
of chemical mediators → Proteolytic degradation of
extracellular debris → Restoration of injured tissue to
its normal structure and function
Termination of inflammation:
Termination of inflammation: By elimination of
offending agent (break down of mediators, short life span
of leukos and activation of anti-inflammatory mediators)
Inflammation may be also harmful in particular
situations, when:
- Inappropriately directed against self tissues
- Not adequately controlled
• Examples of the previous statement are: Rheumatoid arthritis, atherosclerosis, lung fibrosis, etc.
Inflammation
Cardinal Signs:
-Cardinal Signs:
1. Rubor (redness)
2. Dolor (pain)
3. Calor (heat)
4. Tumor (swelling)
5. Functio laesia (loss of function)
+ pallor??
Types of Inflammatory Cells
-▫ Neutrophils
▫ Monocytes-Macrophages
▫ Lymphocytes
▫ Eosinophils
▫ Mast cells and Basophils
Acute Inflammation
Major components:
Major components:
▫ Alterations in vascular caliber(size) → ↑ in blood flow
▫ Structural changes in microvasculature → Allows
plasma proteins and leukocytes leave the circulation ▫ Emigration of leukocytes from blood vessels to
focus of injury + their activation → Elimination of
offending agent
What causes acute inflammation?
▫ Infections (e.g. bacterial, viral, fungal, parasitic)
▫ Tissue necrosis (e.g. ischaemia, trauma, physical
and chemical injury)
▫ Foreign bodies (e.g. splinters, dirt, sutures)
▫ Immune (hypersensitivity) reactions: Directed
against self-Ags → Cause autoimmune diseases
(immune mediated inflammatory diseases)
Transudate:
▫ Ultra-filtrate of blood plasma due to imbalance btw. osmotic and hydrostatic pressure across vessel wall
▫ Characterised by the following:
Low protein content
Low specific gravity
Little or no cellular material
Exudate:
‘▫ Increase of vascular permeability
▫ Associated with inflammatory reaction
▫ Extravascular fluid with following characteristics:
High protein concentration
High specific gravity
Contains cellular debris
Reactions of Blood Vessels in AI
-Changes in Vascular Flow and Caliber:
- Increased Vascular Permeability
Changes in Vascular Flow and Caliber:
- Vasodilatation of arterioles and opening of new
capillary beds in the region → Increased blood flow → Cause of heat and redness of the affected area - Increased permeability of microvasculature →
Escape of protein-rich fluid into extravascular tissues 3. Loss of fluid + ↑ vessel diameter → Causes:
a. Slower blood flow
b. Concentration of erythrocytes in small vessels
c. Increased blood viscosity
All of the above result in dilatation of small vessels With slowly moving erythrocytes (stasis) - Accumulation of neutrophils along the vascular
endothelium and expression of adhesion
molecules by endothelial cells → Adherence of
leukocytes to the endothelium → Extravasation of
leukocytes and migration to the interstitial tissue
B. Increased Vascular Permeability
▪ Leads to the escape of protein-rich exudate into the
extravascular space → Oedema
▪ Responsible Factors:
a. Contraction of endothelial cells → Increase in inter-
endothelial spaces (mechanism known as immediate transient response; elicited by Histamine, Brady- kinin, Leukotrienes, Substance P, etc.).
b. Endothelial injury → Endothelial cell necrosis and
detachment (causes: burns, microbial action, neutros)
c. Increased transport of fluid and proteins through
endothelium (by the action of specific channels)
