Pathophysiology-B-Pharmacy-2nd-Semester.pdf

Different types of inflammation (acute, chronic, exudative, cellular)
Includes tables, flowcharts, and concise explanations suitable for B. Pharmacy 2nd Semester Pathophysiology students.

1. Patopyiology · B. Paracy 2d Seeter
Ifla atio
Presented by: Mr. Jagdeep Singh

2. Wat i Ifla atio?
Inflammation is the protective response of vascularized
tissues to injury caused by infection, toxins, or trauma. It
represents a coordinated effort by the body to eliminate
harmful agents, clear damaged tissue, and initiate the healing
process.
Priary Goal
Destroy or neutralize harmful agents
Remove necrotic (dead) tissue
Promote healing and tissue regeneration

3. Copoet Caue of Ifla atio
Vacular Reactio
Changes in blood flow and vessel
permeability that allow immune
components to reach the injury
site
Cellular Repo e
Migration and activation of white
blood cells to combat threats and
clear debris
Ceical Mediator
Release of signaling molecules
that coordinate and amplify the
inflammatory response
Co o Trigger
Microbial infections (bacteria, viruses)
Physical agents (trauma, burns, radiation)
Chemical agents (acids, toxins)
Tissue necrosis (cell death)
Foreign bodies (splinters, sutures)
Immune reactions (hypersensitivity)

4. Te Ifla atory Cacade
Understanding the sequential events from initial injury to tissue repair:
1
Ijury or Ifectio
Initial tissue damage triggers the inflammatory response
2
Mediator Releae
Cells release histamine, prostaglandins, and cytokines
3
Vaodilatio Pereability
Blood vessels widen and become more permeable
4
Leukocyte Migratio
White blood cells move from blood to injured tissue
5
Pagocytoi Repair
Immune cells destroy pathogens and initiate healing

5. Te Five Cardial Sig
Rubor (Rede )
Caused by vasodilation and increased
blood flow to the affected area
Calor (Heat)
Results from increased blood flow and
heightened metabolic activity
Tuor (Swellig)
Fluid accumulation (edema) due to
increased vascular permeability
Dolor (Pai)
Nerve endings stimulated by chemical mediators like
bradykinin and prostaglandins
Fuctio Laea (Lo of Fuctio)
Impaired movement or activity resulting from pain and
swelling

6. Type of Ifla atio
Type Onset Duration Dominant Cells Typical Outcome
Acute Rapid (minutes3
hours)
Short (few days) Neutrophils Resolution,
abscess, or chronic
Subacute Intermediate Few days to weeks Mixed cells Healing or
chronicity
Chronic Slow (weeks3
months)
Long-lasting Lymphocytes,
macrophages
Fibrosis, tissue
destruction

7. Acute Ifla atio: Rapid Repo e
Acute inflammation is the body's immediate and short-term protective reaction to injury or infection, characterized by a
rapid onset and resolution.
Iitial Trigger
Tissue damage or pathogen invasion activates sentinel
cells.
Vacular Cage
Arterioles dilate, increasing blood flow, and capillaries
become permeable, leading to fluid exudation.
Leukocyte Recruitet
Neutrophils rapidly migrate to the site to phagocytose
pathogens and cellular debris.
Reolutio/Healig
Harmful agents are eliminated, and the process
resolves, restoring normal tissue function.

8. Acute Ifla atio: Rapid Repo e
Acute inflammation represents the immediate and early response to injury, characterized by rapid onset, exudation of
plasma proteins, and neutrophil migration to the site of damage.
1
Vacular Pae
Vasodilation increases blood flow;
capillary permeability rises
2
Cellular Pae
Neutrophils and monocytes migrate from
bloodstream to tissue
3
Pagocytic Pae
Immune cells engulf and destroy
pathogens and debris
4
Reolutio/Healig
Tissue repairs or progresses to chronic
inflammation
Key Insight: The entire acute inflammatory response can develop within minutes to hours and typically resolves
within days if the triggering stimulus is eliminated.

9. Ceical Mediator: Te Sigalig Network
Chemical mediators orchestrate the inflammatory response by coordinating vascular changes, recruiting immune cells,
and triggering pain and fever responses.
Hitaie
Source: Mast cells
Action: Immediate vasodilation and increased vascular permeability
Protagladi
Source: Membrane phospholipids
Action: Induce pain sensation and fever response
Bradykii
Source: Plasma kinin system
Action: Powerful pain inducer and vasodilator
Cytokie
Source: Macrophages (IL-1, TNF-³)
Action: Systemic fever and leukocyte activation
Copleet Protei
Source: Plasma
Action: Chemotaxis and opsonization for enhanced phagocytosis

10. Croic Ifla atio: We Healig Stall
Chronic inflammation occurs when the inflammatory response
persists for weeks to months, featuring simultaneous tissue
destruction and attempted repair.
Ditigui ig Feature
Dominated by macrophages, lymphocytes, and plasma cells
Progressive fibrosis and tissue destruction
Angiogenesis (new blood vessel formation)
Slow, insidious onset without clear resolution
Co o Caue
Peritet Ifectio
Tuberculosis, hepatitis, chronic
viral infections
Autoi ue Dieae
Rheumatoid arthritis, inflammatory
bowel disease
Prologed Toxic Expoure
Silica, asbestos, cigarette smoke

11. Cliical Outcoe of Ifla atio
The inflammatory response can resolve in several distinct ways, each with different implications for tissue function and
patient health:
Coplete Reolutio
Ideal outcome with full restoration of normal tissue
structure and function
Healig by Fibroi
Tissue replaced by scar tissue when complete
regeneration isn't possible
Abce Foratio
Localized collection of pus requiring drainage or
antibiotic intervention
Croic Ifla atio
Persistent inflammation with ongoing fibrosis and
tissue damage
Key Takeaway
Acute inflammation is rapid, neutrophil-driven, and
typically self-limiting with favorable outcomes when
properly managed.
Chronic inflammation involves macrophages and
lymphocytes, leading to tissue fibrosis and potential
long-term complications.