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Inflammation - B. Pharma 2nd Semester Pathophysiology notes pdf

Inflammation - B. Pharma 2nd Semester Pathophysiology notes pdf

Inflammation

Content

       Inflammation

       Types of inflammation

       Changes involved in acute inflammation

Objectives  

At the end of this PDF, student will be able to

         Define “inflammation”

        Classify inflammation 

        Describe the etiology of inflammation

         Identify the signs of inflammation

         Describe the changes involved in acute inflammation

Inflammation

“Local response of living mammalian tissues to injury due to any agent “

       Body defence reaction to eliminate or limit the spread of injurious agent, followed by removal of the necrosed cells and tissues

       Protective response

Etiology of Inflammation

       Infective agents - bacteria, viruses and their toxins, fungi, parasites

       Immunological agents -  cell-mediated and antigen antibody reactions

       Physical agents - heat, cold, radiation, mechanical trauma

       Chemical agents  - organic and inorganic poisons

Signs of inflammation

4 cardinal signs of inflammation

       Rubor (redness)

       Tumor (swelling)

       Calor (heat) and

       Dolor (pain)

Fifth sign - functio laesa (loss of function) - Virchow

Types of inflammation

Depending upon the defense capacity of host and duration of response

       Acute Inflammation

       Chronic inflammation

Acute Inflammation

       Short duration

       Represents early body reaction

       Followed by repair

Main features

       Accumulation of fluid & plasma at the affected site

       Intravascular activation of platelets

       Polymorpho nuclear neutrophills (PMN) – inflammatory cells

Chronic Inflammation

       Longer duration

       If causative agent of acute inflammation persists for long periods

       Recurrent attack of acute inflammation

Main features:

       Presence of lymphocytes, plasma cells & Macrophages as inflammatory cells

Changes in Acute inflammation

Two main events involved

1. Vascular events

       Alteration of microvasculature (arteries, capillaries & venules)

2. Cellular events

       Exudation of leucocytes

       Phagocytosis

Vascular events

       Alteration in the microvasculature - tissue injury

Haemodynamic Changes

Earliest features - vascular flow change,  calibre of small blood vessels

1.  Irrespective of the type of injury -  transient vasoconstriction of arterioles

       Mild form – blood flow -  3-5 seconds

       More severe injury the vasoconstriction -  5 minutes

Vascular changes

2.  Persistent progressive vasodilatation 

       Mainly arterioles

       lesser extent -  venules and capillaries

       Increased blood volume  - redness and warmth

3.       Progressive vasodilatation

       Elevate the local hydrostatic pressure - transudation of fluid into the extracellular space – swelling

4. Stasis of microcirculation

       Increased concentration of red cells - blood viscosity

5. Leucocytic margination

       Leucocytes stick to the vascular endothelium

       Move and migrate through the gaps between the endothelial cells into the extravascular space

       Emigration

Triple response

Flush

      Appearance of red line

      Local vasodilatation of capillaries and venules

Flare

      Bright reddish appearance or flush surrounding the red line  

      Vasodilatation of the adjacent arterioles

Wheal

      Swelling or oedema of the surrounding

      Transudation of fluid into the extravascular space

Pathogenesis of altered vascular permeability

Normal circumstances - fluid balance - two opposing sets of forces that causes:

Outward movement of fluid from microcirculation

      intravascular hydrostatic pressure

      colloid osmotic pressure of interstitial fluid

Inward movement of interstitial fluid into circulation

      intravascular colloid osmotic pressure

       hydrostatic pressure of interstitial fluid


Contraction of endothelial cells

       Increased leakiness - venules exclusively

       Endothelial cells - temporary gaps – contraction - vascular leakiness - release of histamine, bradykinin and others

       Response - immediately after injury – reversible - short duration (15-30 minutes)

       Example: immediate transient leakage is mild thermal injury of skin of forearm

Retraction of endothelial cells

       structural re-organisation of the cytoskeleton of endothelial cells - reversible retraction – intercellular junctions – venules - cytokines such as interleukin-1 (IL-1) and tumour necrosis factor (TNF)-α - response takes 4-6 hours after injury - lasts for 2-4 hours or more

       The example invitro experimental work only

Direct injury to endothelial cells

       Cell necrosis, physical gaps at the sites of detached endothelial cell - thrombosis at site initiated

       Affects – microvasculature -  immediately after injury  last for several hours or days or  delay of 2-12 hours and last for hours or days

Summary

       Inflammation is the local response of living mammalian tissues to injury due to any agent

       The four cardinal signs of inflammation are redness, swelling, heat and pain

       Inflammation is of 2 type acute and chronic inflammation

       Acute inflammation is of Shorter duration , represents early body reaction, followed by repair

       Chronic inflammation is of longer duration and occurs when the agents remains for longer time

       Acute inflammation is characterized by cellular events and vascular events

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