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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