pujasari inflammation repair neo week 3

Inflammation & Repair

Hening P. Syahrin

Basic Science and Fundamental of Nursing Group Faculty of Nursing Universitas Indonesia2009

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Infla

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What to cover

� The purpose of inflammation� The Cardinal signs of acute inflammation &

describe the mechanisms involved in production of these signs

� The comparison of hemodynamic & cellular phases of the inflammatory response

� The difference of acute & chronic inflammation

� The types of inflammatory exudates

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What is Inflammation?�is the reaction of vascularized tissue to local injury

�is a series of changes in terminal vascular bed, in blood, in connective tissues to eliminate the offending irritant and repair the damaged tissue

�involves cellular, humoral, chemical & tissue participations

�is one of the most important & useful defense mechanism

Without an adequate inflammatory response none of us would be living; wound would not heal, minor infection would become overwhelmed

Ironically, it is also one of the most common means whereby our own tissues are injured; SLE

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Causes of InflammationExogenous

� Microbiological agents: e.g. viruses bacteria, fungi, protozoa. Microbial infections are the commonest causes of inflammation.

� Physical agents: trauma, extremes of heat and cold, irradiation

� Chemical agents (toxins): irritants or corrosive chemical substances, e.g. sulfuric acid, alkalis.

� Foreign bodies: sutures� Immunological reactions: hypersensitivity or

autoimmune- mediated inflammation and transplant rejection

Endogenous

Tissue ischemia such as myocardial infarction or pulmonary embolism

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The Roles/purposes of Inflammation

1. To neutralize & destroy invading & harmful agents

2. To limit the spread of harmful agents to other tissue

3. To prepare any damaged tissue for repair

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Inflammation may be categorized into:

1. Acute; short in duration, lasting less then 2 weeks & involves a discrete set of events

2. Chronic; more diffuse, extends over longer period & may result in the formation of scar tissue and deformity

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Events in the inflammatory process(the same regardless the cause)

� Increased vascular permeability� Emigration of leucocytes� Phagocytosis

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Acute Inflammation� Characterized by a rapid onset & the

resolution of the tissue changes & damage in a short period

� Changes occurs locally at the site of injury as well as systemically

� Acute- phase response� Vascular & cellular responses� Associated with chemical mediators� Hemodynamic & White Blood Cells (WBC)

response; inflammatory exudates

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Manifestation

1. Local signs, a classic description by Celsus named Cardinal signs

(1) Redness/ tumor(2) Swelling/ rubor(3) Heat/ calor(4) Pain/dolor(5) Loss of function/functio laesa

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Manifestation

General responses

1. Fever

2. Leukocytosis

3. Proliferation of the mononuclear phagocyte system

4. Injury of parenchyma organs.

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Vascular Response

� Immediately after injury� Vasoconstriction� vasodilation of arterioles & venules

that supply areaHyperemic response: congested, redness (erythema) & warmth

� Increased capillary permeability, allows fluid escape into the tissue�swelling (edema)

� Pain and impaired function is as a result of swelling & release of chemical mediators

� Benefits: dilute toxic&irritating agents and localizing the spread of infectious agents

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Fluid exudate

Normally the walls of small blood vessels are freely permeable to water and crystalloids but relatively impermeable to plasma proteins. The formation of protein-rich fluid exudates is facilitated by separation of the intercellular junction of the endothelium.

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The fluid exude carries into the inflamed area the following important constituents:

� Serum bactericidal factors

a. Antibodies which act by opsonising bacteria prior to phagocytosis and by neutralizing exotoxins

b. Components of the complement system

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� Interferon: a non-specific antiviral agent

� Fibrinogen which is converted to fibrin. Fibrin is important in providing:

a. Cement substance uniting severed tissuesb. Scaffold for repair processesc. Barrier to the spread of organismsd. Surface against which phagocytosis of adherent

organisms is enhanced

� Therapeutic agents-antibiotics, anti-inflammatory drugs, etc.

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Leukocyte exudates and phagocytosis

� Leukocytic margination,rolling

� Adhesion:by the binding of adhesionmolectures (selections, immunoglobulins, intergrins, mucin like

glycoproteins)

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� Emigrating

It refers to the process by which motile white cells migrate out of blood vessels.

emigration is an active, energy-dependent process.

red blood cell out of blood vessels, called diapedesis

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White cell transmigrationIt is include following handings:

�WBC margination

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�WBC adhesion with endothelial surface adhesion molecule

�

�WBC transmigration

2-12 minute

EM: White cell transmigrationEM: White cell transmigration

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� Chemotaxis

Following extravasations, leukocytes emigrate in tissues toward the site of injury by a process called chemotaxis.

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� Phagocytosis

Recognition and attachment of the particle to the surface of the phagocyte→ engulfment→ killing and degradation

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Types of leukocyte (inflammatory cells):Leukocytes are out of blood vessels that are known as inflammatory cells.

a. Neutrophils:Small phagocytic cell Commonly seen in early stage of inflammation, and acute inflammation, and purulent inflammation.

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b. Macrophages:

Tissue macrophages are derived from blood monocytes that emigrate from blood vessels under influence of chemotactic factors.

Commonly seen in later stage of inflammation, chronic inflammation, non-purulent inflammation, and viral, or protozoal, or fungal infections. And macrophages are also related to specific immune response.

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c. EosinophiliaCommonly seen in hypersensitivity reaction and human parasitological infections.

d. Lymphocytes and plasma cellsCommonly seen in virus infection and chronic inflammation.

e. Basophilic and mast cell

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Mac

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3. Proliferation

Proliferate constitution:Endothelium, macrophages, and fibroblasts commonly seen in later stage of inflammation

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Infl

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Definition:

It is the chemical substances which cause or participate in inflammation

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Main mediators function

Neutrophil and macrophage lysosomal enzymesOxygen metabolites, Nitric oxide

Tissue damage

PGE2, BradykininPain

IL-1, IL-6, TNF, PG.Fever

C5a, LTB4, bacterial products, IL-8, TNF. Chemotaxis

Histamine, Bradykinin, C3a, C5a, PAF, active oxygen metabolic products, Leukotrienes C4, D4, E4 Substance P

Vascular Leakage

Histamine, Bradykinin, Nitric oxide, Prostaglandins PGE2, PGD2,PGF2, PGI2

Vasodilation

Types of mediatorFunction

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Sig

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1. Significances

( 1 ) Inflammation is fundamentally a protective response whose ultimate goal is torid the organism of both the initial cause of cell injury and the consequences of such injury, the necrotic cells and tissues.

(2) Inflammatory response is closely intertwined with the process of repair.

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(3) The inflammatory response occurs in the vascularized connective tissue.

(4) Inflammatory response of both vascular and cellular responses are mediated by inflammatory mediators chemical factors derived from plasma or cells and triggered by the inflammatory stimulus.

(5) However, inflammatory responses are not perfect that may be potentially harmful.

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2. Aspects of inflammation

(1) Many systemic and local host factors influence the adequacy of the inflammatory- reparative response.

� Nutrition condition

� Immune condition

� Endocrine condition

� Characteristics of inflammatory organ or tissue

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What to cover

� Define parenchymal & stromal� Compare labile, stabile, permanent cell

types in terms of their capacity for regeneration

� Describe healing by primary & secondary intention

� Trace the wound healing process� Explain factors affecting wound healing

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Regeneration:

The surviving healthy cells nearby damage proliferate and move for repair.

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Type of Regeneration

(1) Complete regeneration:

The new tissue is the same with the loss in structure and faction. Commonly in physiological regeneration.

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Conditions:

� the ability of regeneration of parenchymal tissue is strong.

� damage area is small and the stromal framework of the injured tissue is preservative well.

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The regenerative capacity types of cells

(1) Labile cells: normally a continuous process of active replacement is occurring.The chances of restoration by regeneration are excellent.Examples: the covering epithelium, the bone marrow cells and the lymphoid cells.

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(2) Stable cells:Although normally the replacement requirements are minimal, they have not lost the capacity to proliferate in response to stimulation. Chances of regeneration remain.

Examples: adenocytes of parenchymal viscera (including endocrine); all stromal elements.

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(3) Permanent cells:Normally are unable to multiply after the growth early in life.

Examples: nerve cells, striated and cardiac muscle cells, smooth muscle cells.But peripheral nerve has retained the capacity for regeneration with damage.

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Rep

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Proliferation of fibroblasts and capillary buds and the subsequent laying down of collagen to produce a scar is the usual consequence of most tissue damage.

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1. Definition:This is young connective tissue, which is rich in young fibroblasts and capillaries

2. Morphology(1) gross feature: pink, soft, moist, and

granular appearance.

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(2) LM:

� fibroblasts:� new capillaries: capillary sprout and migrate

toward the wound. The new capillary endothelial cells are swollen and capillary tubes are narrow. These new vessels have leaky interendotheial junctions. Allow the passage of proteins and red cells into the extravascular space, thus, new granulation tissue is often edematous.

� inflammatory cells

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Granulation tissue

�Provided by prof. Song W.Wong�


(Provided by prof. Orr)

Scar tissue

Scar tissue


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1. Definition:Refers to the body’s replacement of destroyed tissue by living tissue

2. Stages in healing of wound

(1) Escape of blood and exudates

(2) Acute inflammation

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( 3 ) Contraction of the wound. The causes of contraction are not known but possible mechanisms are:

� Shrinkage of scab in superficial wounds

� Contraction properties of granulation tissue attributable to contraction of myofibroblasts or tissue re-modeling.

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(4) Proliferation and migration of fibroblasts and endothelial cells.

(5) Progressive increase in mature collagen fibres during the second week forming a scar.

(6) Loss vascularity and shrinkage of the scar.

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3. Type of wound healing

(1) Healing by fist intention

A clean wound with a minimum of space between the margins.

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(2) Healing by second intention

Healing by second intention differs from healing by first intention in:

� Greater tissue loss� More inflammatory exudates and necrotic material to remove� More granulation tissue therefore a bigger scar

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healing by second intention


� Wound contraction necessary

� Slower process

� Increased liability to infection

(3) Healing under scab

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4. Factors influencing wound healing

(1) Local factors adversely affecting healing

� Type of wounding agent; blunt, crushing, tearing etc.

� Infection

� Foreign bodies in wound

� Poor blood supply

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� Excessive movement

� Poor apposition of margins, e. g. large haematoma formation

� Poor wound contraction due to tissue tethering

� Infiltration by tumor.

� Previous irradiation.

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(2) General factors adversely affecting healing

� Age

� Poor nutrition� Deficiency of protein� Lack of Vitamin C results in abnormal

granulation tissue and deficient collagen production

� Zinc deficiency

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� Excessive glucocorticosteroid production or administration

� Fall in temperature

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pujasari inflammation repair neo week 3

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