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Inflammation and Repair -1Inflammation and Repair -1
Dr.CSBR.Prasad, M.D.Dr.CSBR.Prasad, M.D.
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What is this about?Clinical Examples
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In Gist:Inflammed areas
are:
Red
Swollen &
Malfunction
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Essential to the survival of organisms is their ability to get
rid of damaged or necrotic tissues and foreign invaders,
such as microbes
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Unicellular organisms
Simple mechanisms• Diffusion• Phagocytosis
Mammals
Complex systems• Respiratory / CVS• Hemopoietic sys• GIT• Immune system
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Essential to the survival of organisms is their ability to get
rid of damaged or necrotic tissues and foreign invaders,
such as microbes
The host response that accomplishes these goals is
called inflammation
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InflammationInflammation
This is fundamentally a protective response
Without inflammation
• Infections would go unchecked
• Wounds would never heal
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InflammationInflammation
In clinical practice: we see sometimes…..
Inappropriately triggered or
Poorly controlled inflammation
Causing tissue injury !!!!!!
Eg: Autoimmune diseases, type-2 DM, AS
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InflammationInflammation
Inflammation is a complex reaction involving
1. Blood vessels
2. Plasma components &
3. Leukocytes
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InflammationInflammation
Inflammation is a complex reaction involving
1. Blood vessels
2. Plasma proteins &
3. Leukocytes
Changes in these structures / factors are brought about by inflammatory stimulus
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InflammationInflammation
Microbes
Necrotic cells
Hypoxia
Physical injury
Inflammatory stimuli:
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Acute inflammatory reactions are triggered by a variety of stimuli:
• Infections (bacterial, viral, parasitic) and microbial toxins• Trauma (blunt and penetrating)• Physical and chemical agents (thermal injury, e.g.,
burns or frostbite; irradiation; some environmental chemicals)
• Tissue necrosis (from any cause) • Foreign bodies (splinters, dirt, sutures) • Immune reactions (hypersensitivity reactions)
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InflammationInflammation
Can be:
Acute (a few hours to days)
Chronic (days to months / years)
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InflammationInflammation
Acute inflammation • Rapid in onset • Short duration• Exudation of fluid and plasma
proteins (edema)• Infiltrated by neutrophils• When acute inflammation is
successful in eliminating the offenders the reaction subsides, but if the response fails to clear the invaders it can progress to a chronic phase
Chronic inflammation • Follow acute inflammation • Insidious in onset• Longer duration • Infiltrated by lymphocytes and
macrophages • Proliferation of blood vessels,
fibrosis, and • Tissue destruction
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InflammationInflammation
Inflammation is terminated when the offending agent is eliminated
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The NOMENCLATURE used to describe inflammation in different tissues employs:
1-the tissue name &
2-the suffix “-itis”
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Tissue suffix Inflammed tissue
Pancreas itis Pancreatitis
Meninges itis Meningitis
Pericardium itis Pericarditis
Joint itis Arthritis
“4+4+11” Cardinal signs of (acute) inflammation
• Rubor = Redness• Tumor = Swelling• Calor = Heat• Dolor = Pain
(described by Celsus 1st. Century AD)
• Functio laesa = Loss of function
(added by R. Virchow)
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RuborTumor
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RuborTumorFunctio laesa
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RuborTumorFunctio laesa
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TumorFunctio laesa
Vessels make inflammation a reality
without vascularity there is no
inflammationV4-Nov,2013
Vascular events in Vascular events in acute inflammationacute inflammation
Changes in:Changes in:Caliber of the vessel
Porosity / permeability of vessels
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Acute inflammation involves:
Alteration of vascular caliber following very brief vasoconstriction
(seconds), vasodilation leads to increased blood flow and blood pooling creating redness and warmth (rubor and
calor)
Changes of microvasculature increased permeability for plasma
proteins and cells creating swelling (tumor). Fluid loss leads to
concentration of red blood cells and slowed blood flow (stasis)
Emigration of leukocytes from microcirculation
due to stasis and activation leads migration towards offending agent
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EXUDATION: Vascular changes and fluid leakage during acute inflammation lead to Edema in a process called Exudation
Transudate
•Result of hydrostatic
or osmotic imbalance
•Ultrafiltrate of plasma
•Low protein content
•Specific gravity < 1.015
Exudate
•Result of inflammation
•Vascular permeability
•High protein content
•Rich in cells
•Specific gravity >1.020 V4-Nov,2013
Increased vascular permeability and edema: a hallmark of acute inflammation
• Leakage is restricted to venules of 20-60m in diameter
• caused by endothelial gaps • usually an immediate and transient
response (30 min.)
• Gaps occur due to contraction of e.g myosin and shortening of the individual endothelial cell
• loss of protein from plasma leads to edema
• due to reduced osmotic pressure in the vasculature
• and increased osmotic pressure in the interstitium V4-Nov,2013
• Direct endothelial injury causing necrotic cell death will result in leakage from all levels of microcirculation (venules, capillaries and arterioles)
• This reaction is immediate and sustained
• Delayed prolonged leakage begins after 2-12 hours and can last several days due to thermal, x-ray or ultraviolet radiation (sunburn) and involves venules and capillaries
• Leakage from new blood vessels during tissue repair (angiogenesis) due to immature endothelial layer
All these described mechanisms may occur in one wound (e.g burns) and can be life threatening
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Inflammation – Components in the DEFINITION
• Response to tissue injury• chemical agents• cold, heat• trauma • invasion of microbes
• by the vascularized tissue• Serves to destroy, dilute or wall off the
injurious agent
• Protective response• Induces repair• Can be potentially harmful
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Inflammation – DEFINITION
Can be defined as Response to tissue injury by the vascularized tissue, which Serves to destroy, dilute or wall off the injurious agent.
It is a Protective response and Can be potentially harmful.
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Guess, what is the problem with this person?
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Important points
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What are the cardinal signs of inflammation?
• Rubor = redness• Tumor = swelling• Calor = heat• Dolor = pain
• (described by Celsus 1st. Century AD)
• Functio laesa = loss of function– (added by R. Virchow)
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Which sign was introduced by Virchow?
• Functio laesa = loss of function
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Which is the fifth sign of inflammation?
• Functio laesa = loss of function
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Factors that control the fluid balance between the intravascular and extravascular compartments
• OP and HP
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What happens to total white count in acute inflammation?
• Usually elevated
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Name THREE elements which make the inflammation possible?
1. Vessels
2. Plasma componentsa) Immunoglobulins
b) Complement components
3. Leucocytes
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Name THREE differences between Necrosis and Apoptosis?
In Apoptosis:
• Structures are membrane bound
• Changes occur before death [Until the last moment the cell is alive]
• Absence of inflammation
• ATP dependent process
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What makes inflammation a reality?
Blood vessels
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Why we need inflammation?
• To remove infectious / injurious agents
• To remove dead tissue form the body
• It’s protective.
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Name some instances where inflammation is damaging?
• Laryngitis
• Inflammation of the 4th ventricular area
• Encephalitis / Meningitis
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Name the acute inflammatory cells?
• Pyogenic infections – Neutrophil
• Allergic inflammation – Eosinophil
• Viral infections – Lymphocyte
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Name the chronic inflammatory cells?
• Lymphocytes
• Macrophages
• Plasma cells
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How do you differentiate acute from chronic inflammation?
• Onset / duration
• Type of inflammatory cells
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E N D
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