inflammation lab slides

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INFLAMMATION INFLAMMATION

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Page 1: Inflammation Lab Slides

INFLAMMATIONINFLAMMATION

Page 2: Inflammation Lab Slides

POLYMORPHONUCLEAR POLYMORPHONUCLEAR NEUTROPHILNEUTROPHIL

Page 3: Inflammation Lab Slides

MONOCYTE MONOCYTE

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EOSINOPHIL EOSINOPHIL

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BASOPHIL BASOPHIL

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SMALL LYMPHOCYTESMALL LYMPHOCYTE

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LARGE LYMPHOCYTELARGE LYMPHOCYTE

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PLASMA CELLPLASMA CELL

Page 9: Inflammation Lab Slides

Foreign body giant cell. The giant cell contains suture material.

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Langhans’ giant cell. Mycobacteria, which are acid-fast organisms, are present within the giant cell and stain red with a Kinyoun stain.

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A low power phomicrograph of granulomatous inflammation

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A granuloma is characterized by a collection of epithelioid macrophages with abundant pale eosinophilic cytoplasm and indistinct cell borders surrounded by a rim of lymphocytes.

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Langhan’s Langhan’s Giant Cell Giant Cell

PicturePicture

Robbins Textbook of Pathology 1971

Langhans’ giant cell

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ACUTE APPENDICITIS

Histologic hallmark are the presence of neutrophils at the muscularis layer (arrow).

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LEFT : THERE IS A DENSE DERMAL INFILTRATE

RIGHT : THE INFILTRATE IS COMPOSED OF FOAMY EPITHELIOID HISTIOCYTES KNOWN AS LEPRA CELLS

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RED STAINING TUBERCULOID ORGANISMS IN THE LEPRA CELLS ARE SEEN WITH FITE-FORACO STAIN.

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REPAIRREPAIR

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Granulation tissue is the hallmark of repair. Young granulation tissue is composed of a proliferation of blood vessels and fibroblasts in an edematous stroma. RBC exravasation is prominent because of leaky blood vessels.

Page 19: Inflammation Lab Slides

Older granulation tissue is composed of well-developed blood vessels with an inflammatory infiltrate in the interstitial tissue.

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SCAR. A scar is composed of parallel bundles of collagen with few fibroblasts and few blood vessels.

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KELOID. A keloid is composed of thick collagen bundles of whorled arrangement.

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Whole mount view of chronic peptic ulcer. The external muscle layer has been totally destroyed. Note the overhanging mucosa on one edge and the sloping mucosa on the other.

Page 24: Inflammation Lab Slides
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GASTRIC ULCER (PEPTIC ULCER). Chronic active ulcers are characterized by four distinct zones.

Page 26: Inflammation Lab Slides

The first two zones can be seen. The ulcer base is covered by fibrinopurulent debris (zone 1), beneath which is an active suppurative inflammatory infiltrate (zone 2).

Zone 1

Zone 2

Page 27: Inflammation Lab Slides

GASTRIC ULCER (PEPTIC ULCER). The third zone of a chronic active ulcer is composed of granulation tissue.

Page 28: Inflammation Lab Slides

GASTRIC ULCER (PEPTIC ULCER). The fourth zone is composed of dense fibrous tissue.

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Liver cirrhosis, gross

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Cirrhosis resulting from chronic viral hepatitis. Note the broad scar and coarse nodular surface.

Page 31: Inflammation Lab Slides

CIRRHOSIS. It is the common end point of many disease processes. Fibrous bands diffusely divide the liver into regenerative nodules. A trichrome stain accentuates the nodularity and proves that the bands are made of collagen.

Page 32: Inflammation Lab Slides

ALCOHOLIC CIRRHOSIS (LAENNEC’S CIRRHOSIS). In early alcoholic cirrhosis, bridging fibrosis with entrapped portal tracts is noted. Hepatocytes degenerate, and central veins and portal tracts become trapped in the fibrous scar. Bile plugs and fatty change is noted in the remaining hepatocytic parenchyma.

Page 33: Inflammation Lab Slides

Cirrhosis

• Most common cause is alcoholic liver disease

• Key features:

1. The parenchymal injury & consequent fibrosis are diffuse.

2. The nodularity is part of the diagnosis reflects balance between regeneration and scarring.

3. Vascular architecture is re-organized by the parenchymal damage and scarring formation of abnormal interconnections

4. Fibrosis is the key feature of progressive liver damage.

Page 34: Inflammation Lab Slides

CAUSES OF CIRRHOSIS

Page 35: Inflammation Lab Slides

Cirrhosis

• Pathogenesis:

Progressive fibrosis & re-organization of vascular micro-architecture of liver

Collagen deposition (types I & III) in the

lobule

Loss of fenestration of sinusoidal endothelial

cells

New vascular channels in the

septae

Create delicate or broad septal tracts

Impaired hepatocellular protein secretion

(albumin, clotting factors, lipoproteins)

Shunting of blood around the

parenchyma

Page 36: Inflammation Lab Slides

Cirrhosis

• Main characteristics

1. Bridging fibrous septae

link portal tracts with one another & portal tracts with terminal hepatic vein

2. Parenchymal nodules

contain proliferating hepatocytes encircled by fibrosis

micronodules - < 3 mm diameter

macronodules - > 3 mm to several cm

3. Disruption of architecture of entire liver