inflammation report final 2003 ed

7/28/2019 INFLAMMATION Report Final 2003 Ed

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By: Jade A. Domasing


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Definition:

Inflammation is a protective response intended toremove injurious stimuli as well as the necrotic

cells and tissues resulting from original insert.OR

Repair process that causes the replacement of

damaged tissues by regeneration ofparenchyma cells or by filling of any residualdefect by fibrous scar tissues


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It causes destruction of microbes.

Causes detoxification of toxins.

Clears infections.

Helps in healing process.

Causes repair of damaged tissues.


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Inflammatory responses are sometimes harmfulas they cause:

Life threatening anaphylactic reactions to

insects bites, drugs and other chronic diseaseslike Rheumatoid arthritis, Atherosclerosis etc.

Inflammation of peritoneum leads to fibrous

bands that causes obstruction of intestines. Pericardial inflammation causes the formation

of dense pericardium that impairs cardiacfunctions.


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The inflammatory responses have many players. Theyinclude:

1) CIRCULATING CELLS:

I. Bone marrow derived polymorphonuclear leukocytes

e.g., Basophils, Esinophils and Neutrophils.II. Lymphocytes

III. Monocytes

IV. Platelets.

2) CIRCULATING PROTEINS:I. Clotting factors

II. Kininogens

III. Complement proteins


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3) VASCULAR WALL CELLS:

I. Connective tissue cells

II. Smooth muscle cells

III. Epithelial cells4) EXTRA CELLULAR MATRIX:

I. Fibrous structural proteins e.g., Elastin &Fibrinogen

II. Gel-forming proteoglycans

III. Adhesive glycoprotein e.g., Fibronectin, thatare cell-ECM and ECM-ECM connectors.


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Inflammatory stimulus ChemicalmediatorsInflammatory response untilinjurious stimulus is removed

When the inflammatory stimulus is removed thesemediators are then dissipated, catabolized orremoved.

TYPES OF INFLAMMATION: Acute inflammation

And Chronic inflammation


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Acute inflammation has two major components:

Vascular component

Cellular (leukocytes) component

Which result in the classic clinical pentad of:

Calor (Heat)

Rubor (Redness)

Tumor (Swelling) Dolor (Pain)

Functio laesa (Loss of funtion)


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Arteriolar vasodilation results in locally increasedblood flow, engorgement of the capillary bed, andincreased transudation

Exudationof protein-rich fluid from the lumen into the

extracellular space results in Outflow of water and ions into the interstitial

space (edema) Increased blood viscosity and decreased flow

(stasis) Stasis helps leukocytes escape the flow and attach

to the vascular endothelium (margination) Margination leads to transmigration of leukocytes out

of the vessel into the interstitial space


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1 Endothelial gap formation

Endothelial cell contraction

Cytoskeletal reorganization

2 Endothelial cell injury

Direct

Leukocyte-mediated

3 Increased transcytosis(vesicular trafficking)

4 Angiogenesis


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Margination and rolling

Adhesion and transmigration

Migration in the interstitial space


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Plasma-derived:

Complement, kinins, coagulation factors

Many in pro-form requiring activation (enzymatic

cleavage) Cell-derived:

Preformed, sequestered and released (mast cellhistamine)

Synthesized as needed (prostaglandin)


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Complete resolution

Little tissue damage

Capable of regeneration

Scarring (fibrosis) In tissues unable to regenerate

Excessive fibrin deposition organized into fibroustissue


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Abscess formation occurs with some bacterialor fungal infections

Progression to chronic inflammation


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Chronic inflammation is the inflammation withprolonged duration usually from weeks to monthsand sometimes to years in which activeinflammation, tissue injury and healing process

proceed simultaneously.DISTINGUISHING FEATURES:

Infiltration of mono-nuclear cells like lymphocytes,macrophages and plasma cells.

Destruction of tissue by inflammatory cells. Proliferation of new vessels leading to repair

(angiogenesis & fibrosis).


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ORIGIN AND PROCESS:Chronic inflammation arises from acute inflammation.This transition takes place if the acute responses cannotbe resolved either because of the persistence e.g., ofinjurious stimuli or by interference of the normalhealing process e.g., peptic ulcer.

Some types of injuries engender responses with chronicinflammation initially e.g., viral infections.

SETTINGS LEADING TO CHRONICINFLAMMATION:

I.

Viral infectionsII. Persistent microbial infectionsIII. Prolonged exposure to potentially toxic materialsIV. Autoimmune diseases


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CHRONIC INFLAMMATORY CELLS & MEDIATORS:1) MACROPHAGES:Macrophages are white blood cells within tissues, produced

by the division of monocytes. A majority of macrophages are stationed at strategic points

where microbial invasion or accumulation of dust is likelyto occur. Each type of macrophage, determined by itslocation, has a specific name:

In liver - Kupffer cells Spleen and lymph nodes - Sinus histocytes Nervous system - Microglial cells Lungs - Alveolar

macrophages


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FUNCTIONS OF MACROPHAGES:They help to: Filter the particulate matter Kill microbes Alert immune system of the body. Their life is 1-2 days.ACTIVATION OF MACROPHAGES:Activation of macrophages means: Increase in size

Increase in lysosomal content Increase in metabolism Increase in microbial killing activity


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ACTIVATION SIGNALS:Different signals required to activate macrophages are: Cytokines produced by T-lymphocytes Bacterial endotoxins

Different mediators produced during acuteinflammation

Extra cellular matrix proteins e.g., FibrinogenWhen macrophages become activated they produce

different type of biologically active substances that

either cause ;Cell injuryORFibrosis.


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2) LYMPHOCYTES:

Lymphocytes are mobilized in the setting of anyimmune stimulus as well as in non-immunemediated inflammation. They are initially

activated by interaction with macrophagespresenting processed antigen fragments on theircell surface.

3) EOSINOPHILS:

Are characteristics found in inflammation sitesaround parasitic infections or as part of immunereactions mediated by IgE, typically associatedwith allergies.


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4) MAST CELLS:

Are sentinel cells widely distributed in connectivetissues throughout the body and canparticipate in both acute and chronnicinflammatory responses.


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TYPES OF CHRONIC INFLAMMATION:

1) A GRANULOMATOUS:

Granuloma is not formed,Inflammation is characterized by all features of

chronic inflammation.

Examples:

Chronic viral infections e.g., Hepatitis

Chronic autoimmune diseases e.g., Rheumatoidarthritis and Ulcerative colitis

Chronic chemical intoxication e.g., Chronicalcoholic liver disease

Allergic reactions e.g., Bronchial asthma


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2) GRANULOMATOUS INFLAMMATION:

Characterized by aggregates of activatedmacrophages that assume a squamous cell likeepithelloid appearance.

GRANULOMA is defined as aggregates of macrophagesformed due persistant response of T-lymphocytes toparticular antigens.

This has a granular cheesy appearance called ascaseous necrosis.

Examples are:Bacterial:

Tuberculosis , Leprosy, Syphilis gumma etc.


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Serous Inflammation. This is characterized bythe outpouring of a watery, relatively proteinpoor fluid (effusion) that depending on the siteof injury, derives either from the serum or fromthe secretions of mesothelial cells lining theperitoneal, pleural and pericardial cavities.

Fibrinous Inflammation. This occurs as aconsequence of more severe injuries, with aresultant greater vascular permeabilityallowing larger molecules to pass theendothelial barrier.


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Suppurative (Purulent) Inflammation. This ismanifested by the presence of large amounts of

purulent exudate (pus) consisting ofneutrophils, necrotic cells and edema fluid.

Ulceration. This refers to a site of inflammationwhere an epithelial surface has become necrotic

and eroded, often with associated subepithelialacute and chronic inflammation.


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Anyone who has suffered through a severe boutof a viral illness has experienced the systemiceffects of inflammation, collectively calledacute-phase reaction.

Fever is only one of the more obvious of thesesystemic effects of inflammation; others include

increased somnolence. Malaise, anorexia,accelerated degradation of skeletal muscleproteins, hypotension, hepatic synthesis of avariety of proteins.


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Thank you so much for listening!

*God bless

inflammation report final 2003 ed

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