Acute inflammation

Formation of acute inflammatory exudateFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Chemical mediators acting on nearby blood vessels from inflammatory focus Fig.5.1.

Vasodilation and increased permiability Fig.5.2.

Neutrophils margination and emigration Fig.5.3.

Neutrophil margination, emigration and emigration in acute inflammationFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Neutrophil margination, emigration and emigration in acute inflammation Fig.5.4.

Neutrophil margination and emigration in acute inflammation Fig.5.5.

Neutrophil margination, emigration and emigration in acute inflammationFig.5.6.

Neutropil phagocytosis

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.5.7.

Mechanisms involved in inflammation-From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.5.8.

Acute serous inflammation

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Acute amigdalitis Fig.5.9.

Herpetic inflammation Fig.5.10.

Serous alveolitisFrom cases of the Pathology Department U.M.F. “Gr. T. Popa” Iasi

Fig.5.11.

Serous alveolitis: (1) Alveolar walls (congestion of parieto-alveolar capillaries); (2) Alveolar lumen: serous exudate.

Fig.5.12.

Mallory staining

Fibrinous inflammationFrom cases of the Pathology Department

U.M.F. “Gr. T. Popa” Iasi

Fig.5.13.

Mallory staining

Fibrinous alveolitis: (1) alveolar walls (congestion of parieto-alveolar capillaries); (2) alveolar lumen: fibrinous exudate.

Fig.5.14.

Fibrinous pericarditisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Fibrinous deposits on parietal pericardium

Fig.5.15.

Fibrinous pericarditis:

(1) Epicardium is covered by fibrinous exudate forming intense eosinophilic fibrin network; (2) Epicardium with vascular congestion and neutrophils.

From cases of the Pathology Department U.M.F. “Gr. T. Popa” Iasi

Fig.5.16.

Acute purulent inflammation

Pus smear (May Grunwald Giemsa)

Purulent exudate (pus) is composed of: neutrophiles; macrophages; eritrocytes; necrotic debris; fibrin; bacteria.

Fig.5.17.

Pus smear (MGG)

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.5.18.

Acute diffuse purulent inflammationFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Purulent leptomeningitisFig.5.19.

Purulent leptomeningitis: (1) meninges is diffusely thickened by purulent exudate and vascular congestion. (2) - congested vessels (leukocyte margination and diapedesis).

HE staining

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.5.20.

Vascular congestion and leukocyte diapedesis

HE staining Fig.5.21.

Leukocyte margination and diapedesis

HE staining

From cases of the Pathology Department - U.M.F. “Gr. T. Popa

Fig.5.22.

Acute localised purulent inflammation Lung acute and chronic abscesses

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.5.23.

Pulmonary abscessFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.5.24. Pulmonary abscess: (1) the cavity: contains a suppurative material and air content (in case of communication with air conducts); (2) wall: (a) acute abscess – the wall has irregular borders reprezented by suppurative necrotic lung parenchyma; (b) chronic abscess - the wall is a pyogenic membrane that becomes fibrotic by connective organization.

Localised purulentinflammation (abscess)

• Abscess:

– Localized purulent

Inflammation;

• Types

– acute / recent

– chronic

Recent cerebral abscess

• center:

– purulent exudate;

• periphery:

– fibrin wall.

HE stainingFrom cases of the Pathology Department U.M.F. “Gr. T. Popa” Iasi

Fig.5.25.

Cronic hepatic abscess

• central cavity contains• purulent exudate;

peripheral wall - pyogenic membrane

external layer connective-vascular

tissue of neoformation internal layer

fibrin network neutrophils

From cases of the Pathology Department U.M.F. “Gr. T. Popa” Iasi

Fig.5.26.