Histology - Lecture 15 & 17 - Inflammation/blood

Front 1

What are the 3 major components of acute inflammation?

Back 1

1) Vascular dilatation - relaxation of vascular smooth muscle leads to engorgement of tissue with blood (hyperemia)
2) Endothelial activation - increased endothelial permeability allows plasma proteins to “leak” into tissues; expression of adhesion molecules on the endothelial surface causes neutrophil adherence; production of factors that cause vascular dilatation
3) Neutrophil activation and migration - expression of complementary adhesion molecules; increased motility - emigration from vessels into tissues; increased capacity for bacterial killing

Front 2

What is occurring here?

Back 2

You have the dilation of vessels (engorged capillaries) and neutrophils are beginning to adhere to the endothelium (pavementing).
This is part of acute inflammation.

Front 3

What is occurring here?

Back 3

This is part of the acute inflammation where the neutrophils are beginning to migrate through the vessel walls. Pseodopods extend between adjacent endothelial cells and penetrate the endothelial basement membrane and migrate in.

Front 4

What is occurring here?

Back 4

This is the formation of acute inflammatory exudate where the neutrophils are being attracted to the damaged tissue via chemical mediators (component C5a and LTB4). Neutrophils migrate toward high concentrations (chemotaxis)

Front 5

What is opsonization?

Back 5

Involves the coating of Immunoglobulin and compliment to promote phagocytosis of organism in the tissue. This will help in the destruction of bacteria during inflammatory response.

Front 6

What is purulent acute inflammation?

Back 6

It is an acute inflammation that involves pus, that contains neutrophils, fluid and necrotic tissue - also called an abscess. This exudate will be rich in neutrophils and often results from bacterial infection .

Front 7

What are pyogenic bacteria and what are most common?

Back 7

They are bacteria that promote purulent inflammation.
Typical pyogenic bacteria include Staphylococci, some Streptococci such as S. pyogenes and S. pneumonia, Escherichia coli and Neisseria spp. (N. meningitidis, N. gonorrhea)

Front 8

What is occurring here?

Back 8

This is a slide of the lung showing lobar pneumonia on the left side. This is a form of acute purulent inflammation where the alveoli have become obliterated (consolidation) with neutrophils, fibrin and fluid (pus) in between the.
The right shows a normal lung.

Front 9

What is the diagnosis?

Back 9

This is caused by bacterial upper respiratory infection - bronchopneumonia. This is also a acute purulent inflammation with exudate rich in neutrophils and represents with yellow green septum cough.

Front 10

What is the diagnosis?

Back 10

This is acute fibrinous inflammation where the exudate has high plasma protein content and fibrinogen is converted to fibrin and deposited in the tissues.
Often occurs with serous membrane-lined cavities (pleural, pericardial and peritoneal) and the fibrin mats causes adhesion.

Front 11

What is occurring here?

Back 11

This is acute supprative (purulent) inflammation where the tissue exudate is primarily neutrophil rich.

Front 12

What kind of inflammation is this and what is the diagnosis?

Back 12

This is an example of fibrinous acute inflammation in the visceral pericardium of the heart, where the fluid filled area (Ex) exudate has replaced with fibrinous mat. The myocardium would be seen below the epicardial fat.

Front 13

What are the 3 morphological variations of acute inflammation?

Back 13

1) Suppurative or Purulent inflammation
2) Fibrinous inflammation
3) Serous Inflammation

Front 14

What is serous inflammation?

Back 14

It is a pattern of acute inflammation where main tissue response is with low plasma protein and cell content (transudate - low gravity - because of low protein).
Exudate has high specific gravity because of high protein content.
Serous inflammation is seen in skin in response to burns and serous-mrmbrane lined cavities (effusions).

Front 15

What are the cardinal signs of inflammation?

Back 15

Redness (rubor) - hyperemia (increase blood flow)
Swelling (tumor) - fluid exudation and hypemia
Heat (valor) - hyperemia
Pain (dolor) - release of bradykinin and PGE
Loss of function (fuctio laesa) - combined affects

Front 16

What is resolution in tissue repair?

Back 16

It is the complete restitution of normal tissue and function. Neutrophils and necrotic tissue is removed by phagocytosis which leave the tissue via lymphatic drainage. This is dependent on capacity to regenerate (stem cells).

Front 17

What is this?

Back 17

This is a section showing necrotic cardiac muscle following MI. Macrophages can be identified by brown pigment granules (iron containing pigment hemosideren - derived from hemoglobin)
Myocardial cells cannot heal by complete resolution because there are no stem cells.

Front 18

What is fibrinolysins?

Back 18

They are plasma proteins that break down fibrin strands during resolution repair.

Front 19

What is healing by fibrosis tissue repair?

Back 19

This involves scar formation and occurs with substantial damaged and inability to regenerate specialized cells.
The necrotic debris is removed by macrophages and the defect becomes filled by ingrowth of granulation tissue (called organization)
Granulation tissue is then replaced by collagen to form a fibrous scar.
Though there is loss of specialized cells, structural integrity is re-estabilished.

Front 20

Back 20

This is vascular granulation tissue where fibroblasts (F) are secreting collagen. The collagen then remodels in response to tensile stress (fibrous granulation tissue). Over months and years, the cellularity of the scar diminishes and there is loss of capillaries.

Front 21

What is chronic inflammation?

Back 21

This results after acute inflammation when the injury persists over prolonged period. The predominant cells in chronic inflammation are lymphocytes, macrophages and plasma cells (contrast to acute -neutrophils).
1) Non-specific - follows non-resolution acute
2) Specific (primary) - response to certain agents

Front 22

What is abscess formation?

Back 22

If acute inflammatory response fails to destroy/remove cause of tissue damage. The damage continues and produces pus and fibrin tissue from acute inflammatory response. A chronic abscess occurs when the cavity becomes encapsulated by fibrous tissue (wall becomes thick). Pyogenic bacteria may still exist and lesion may spread.

Front 23

What is non-specific chronic inflammation?

Back 23

Tissue damage, acute inflammation, granulation tissue, tissue repair and chronic inflammation coexist, with active tissue damage and acute inflammation in one area and adjacent areas of fibrosis and chronic inflammatory infiltrates.
Disease course may include acute "flares" and usually chronic inflammation is healed by fibrosis.

Front 24

What is occurring here?

Back 24

This is the infiltrate of chronic inflammation.
1) Plasma cells - identified by purplish cytoplasm (clock face)
2) Lymphocytes - dark, round nuclei (T and B cells)
3) Macrophages - oval kidney shaped
4) Eosinophils - bilobed nuclei bright eosinophilc
5) Fibroblasts - secrete collagen

Front 25

What is the diagnosis?

Back 25

This is bronchiectasis, chronic inflammation of bronchi leading to destruction of muscular and elastic components of the wall due to repeated episodes. The elastic and muscular components are replaced granulation/fibrous tissue.

Front 26

What is non-granulomatous?

Back 26

This is a specific primary chronic inflammation.
Immune Type: hepatitis B: virus infected livers cells incite immune response producing T lymphocytes which kill virus-infected hepatocytes. The tissue damage is due to the inflammatory response itself

Non-immune type - material such as silica, talc or asbestos can activate macrophages to release mediator that induce inflammation and fibrosis.
Wood, metal, beryllium or inhaled can all induce is.

Front 27

What is occurring here?

Back 27

This idopathic pulmonary fibrosis that occurs from non-specific non-granulamtous chronic inflammation where an unknown agent triggers inflammation of alveolar walls. This is leads to extensive fibrosis of walls.

Front 28

Granulomatous

Back 28

Is defined as activated epitheloid macrophages and multinucleate giant cells derived from macrophages.

Immune - delayed hypersensitivity response, T cells activated by bacterial agents leading to epithelioid and giant cells

Non-immune - by foreign body (plant material such as a thorn)

Front 29

What is the diagnosis?

Back 29

This is caseous necrosis (CN) in tuberculosis resultsing in Langhans giant cells (L) and epithelioid macrophages (M).