Inflammation acute inflammation

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Mohamed Hassany Ali 1

Inflammation- Acute Inflammation

Prepared by/ Mohamed Hassany AliB.Sc.

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Inflammation:

• When living tissue is damaged, a series of local processes are initiated in order to contain the offensive agent, to neutralize its effect, to limit spread and hopefully to eradicate.

• So, we can define it as :The mechanism by which the body deals with an

injury. Tissue injury stimulates inflammation.Inflammation known by Suffix “itis”.

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Signs and Symptoms:

• Rubor: redness• Calor: heat• Dolor: pain• Tumor: Swelling• Functio Laesae : loss of function

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Types of Inflammation:

• Acute inflammation• Chronic inflammation

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Acute inflammation:

• short duration, lasting from a few minutes to a few days and the cellular exudate is rich in neutrophil polymorphonuclear leucocytes with some macrophages arriving after the initial insult.

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Process of Acute inf.

• Microvasculature (vascular change)• Cellular mediators (cellular change)

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Microvasculature

• Vasodialation: increase the blood flow rate causing redness and heat.

• Permiability: of vessels causing swelling by outpouring of extracellular excudate. And the affected part lose the ability of proper function.

• Chemical mediator: and the stretching of tissue by exudate cause pain.

• exudate is the fluid within the extravascular spaces which is rich in protein and hence has a specific gravity of greater than 1.020.

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Cellular mediators:

• Leukocytes ingest offending agents, kill bacteria and other microbes, And get rid of necrotic tissue and foreign substances.

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This animation demonstrates the actions of neutrophils in the acute inflammatory process.

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As in the preceding diagram, here PMN's that are marginated along the dilated venule wall (arrow) are squeezing through the basement membrane (the process of diapedesis) and spilling out into extravascular space.

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Acute inflammatory cells:

• In most forms of acute inflammation, neutrophils predominate in the inflammatory infiltrate during the first 6 to 24 hours, then are replaced by monocytes in 24 to 48 hours.

• In viral infections: lymphocytes• In hypersensitivity reactions: eosinophils

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Neutrophils:

• Most abundant granulocyte and resembles (40-75%) of white blood cells in all mammals.

• Containing nucleus of 2-5 lobes.• Named due to H&E staining as it stains by neutral pink.• Polymorphonuclear cell.• Bacterial killing and phagocytosis.• Bone marrow origin.

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Eosinophils:

• Common in Allergic and parasites condition.• Named due to H&E staining as it stains by bright red

(acid-loving).• Resemble 1-6 % in normal persons.• Contain large granules.• Have two lobes.

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Basophils:

• Resembles less than 1% of all leukocytes.• Have large granules contain Histamine that cause

vasodialation.• Named due to H&E staining as it stains by dark blue

(Alkali-loving).• Bone marrow origin

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Lymphocyte:

• Agranulocyte with clear cytoplasm.• Have three types: (T cells, B cells and NK cells).• Resembles 25-35%• T cells: recognition, killing and regulation of immune

system.• Lymphoid tissue and thymus origin.• B cells: give rise to plasma cells.• Lymphoid tissue and bone marrow origin

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Monocyte:

• Resembles 6-9% of all white blood cells.• Agranulocyte large cell.• Unilobar nucleus.• Migrates to tissues to become macrophage which capable

of phagocytosis.• Bone marrow origin

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Plasma cell:

• Secretes large volumes of antibodies.• Lymphoid tissue and bone marrow origin.

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Pus cell:

a necrotic polymorphonuclear leucocyte, a major component of pus. Also called pus corpuscle.

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Acute inflammation, cytology:

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Types of Acute inflammation:

• Suppurative Acute inflammation “pus formation”.• Non suppurative Acute inflammation “no pus formation”.

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Types of suppurative inf.

• Localized• Diffuse

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Acute suppurative Inflammation:

• Def. : severe acute inf. Characterized by Pus formation.

• Causes: Pyogenic microorganisms like:» Staphylococcus aureus.» Streptococcus haemolyticus.» Pneumococcus.» Bacillus coli.

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Pus:

• Composition of Pus:– Living and dead bacteria and their toxins.– Liquefied necrotic tissue.– Cellular exudate: leucocytes, pus cells, macrophages and RBCs.– Inflammatory tissue exudate.

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Abscess:

• Acute localized suppurative inflammation.• Site: any tissue.• Cause: staphylococcus aureus

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Abscess

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Abscess

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Abscess, Brain

• Abscess is an exudative purulent localized inflammation. • In the white matter, a recent abscess consisting in pus :

neutrophils (normal or in lisis), fibrin, necrotic debris, germs. Vessels present congestion and important perivascular edema.

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Abscess, Brain

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Acute pyelonephritis

•  is an acute suppurative inflammation of the kidney caused by bacterial infections (Escherichia coli in 70 - 80 % of cases, Proteus mirabilis, Klebsiella pneumoniae, Enterococus fecalis, Staphylococcus).

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Microscopic:

• The renal presents abscesses (suppurative necrosis), consisting of purulent exudate (pus) :

• neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils).

• Tubules are damaged by exudate and may contain neutrophil casts, which can be found in urine. In the early stages, glomeruli and vessels are spared. 

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Acute Pyelonephritis

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Acute suppurative:

• The general morphology of a suppurative inflammation typically involves several layers:

A necrotic zone is a central focus of proteolytic liquefaction with lipid- rich detritus producing yellowish pus.A pus zone contains large numbers of neutrophils and surrounds the

central necrotic area.A hyperemic zone with perifocal edema of serous exudate is also

present.

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Acute suppurative appendicitis:

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Acute suppurative tonsillitis

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Purulent meningitis

• Purulent leptomeningitis (suppurative leptomeningitis) is a diffuse purulent inflammation.

• The leptomeninges (arachnoida and piamater) contain purulent exudate (pus): leukocytes (neutrophils), fibrin, germs, proteins, necrotic debris. Blood vessels in the subarachnoidian space and those intracerebral are congested and neutrophil margination is present. 

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Purulent meningitis

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Acute non-suppurative:

1. Catarrhal Inflammation: mucous membrane.2. Membranous Inflammation.3. Sero-fibrinous Inflammation.4. Fibrinous Inflammation.5. Serous Inflammation.6. Haemorrahgic Inflammation.7. Necrotizing Inflammation.8. Allergic Inflammation.

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Catarrhal Inflammation:

• Def. Acute non-suppurative secreting exudate rich in mucin.

• Site: GIT, Nose.• Ex: Catarrhal rhinitis• Causes: Common cold virus.

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Catarrhal rhinitis:

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Hemorrhagic inflammation:

• Definition: Acute inflammation involving microvascular injury with massive microvascular bleeding, producing an exudate with a high erythrocyte content ( A).

• Biologic purpose: Exudative inflammation despite severe vascular injury.

• Morphology: The inflamed area is usually necrotic and filled with blood.

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Hemorrhagic Inflammation

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Fibrinous inflammation:• Definition: Acute inflammation with exudation of fibrinogen-containing

serum that polymerizes to fibrin outside the blood vessels ( A, B). Here the exudate takes the form of serum- containing fibrinogen.

• Biologic purpose: Immediate temporary barrier against additional effects of inflammation.

• Etiologic factors include:Infectious toxic tissue injury;Tissue injury from physical trauma;Chemical and toxic tissue injury;Excretion of toxic metabolites (uremic toxins);Ischemic tissue injury.

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Fibrinous inflammation

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Fibrinous pericarditis

• Fibrinous pericarditis is an exudative inflammation. The visceral pericardium (epicardium) is infiltrated by the fibrinous exudate.

• This consists in fibrin strands and leukocytes. Fibrin describes an eosinophilic (pink) network, amorphous.

• Leukocytes (mainly, neutrophils) are found within the fibrin.

• Vascular congestion is also present.

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Fibrinous Pericarditis

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Fibrinous Pericarditis

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Psedomembranous inf:

• Acute non-suppurative inflammation charactrized by exudate rich in membrane-like material.

• Site: mucous membrane, GIT, upper respiratory tract.• Cause: Diphtheria bacilli

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Pseudomembranous Diphtheria

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Pseudomembranous colitis

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Necrotizing inflammation:

• Definition: Acute inflammation in which tissue necrosis predominates.

• Several types are differentiated according to demarcation of the inflammation or infestation with putrefactive bacteria. These include:

Ulcerous necrotizing type;Diffuse necrotizing type;Nonreactive necrotizing type;Gangrenous type.

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Necrotizing inflammation

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