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Flashcards in Morphologic pattern of acute inflammation Deck (14):
1

What is serous inflammation?

Serous inflammation is marked by the exudation of cell poor-fluid into the space created by cell injury or into the body cavity. The fluid is not infected by destructive organisms and doesn’t contain large number of leukocytes. In the body cavity, the fluid may be derived from plasma or from secretion of mesothelial cells; accumulation of fluid in these cavity is called effusion.

2

What is fibrinous inflammation?

Fibrinous inflammation
With greater increase in vascular permeability, large molecules such as fibrinogen pass out of the blood, and fibrin is formed and deposited in the extracellular space. A fibrinous exudate develops when the vascular leaks are larger or there is a local procoagulatant stimulus (cancer). A fibrinous exudate is characteristic of inflammation in the lining of body cavity. Histologically, fibrin appears as an eosinophilic meshwork of threads or sometimes as an amorphous coagulum. Fibrinous exudates may be dissolved by fibrinolysis and cleared by macrophages. If the fibrin is not removed, over time it may stimulate the ingrowth of fibroblasts and blood vessels and thus lead to scarring.

3

What is purulent inflammation?

Purulent inflammation, abscess
Purulent inflammation is characterized by the production of pus, an exudate consisting of neutrophils, the liquefied debris of necrotic cells, and edema fluid. Most frequent cause of purulent inflammation is infection with bacteria that causes liquefactive tissue necrosis, such as staphylococci. Abscesses are localized collection of purulent inflammatory tissue caused by suppuration buried in a tissue, an organ, or a confined space. They are produced by seeding of pyogenic bacteria into a tissue. In time, the abscesses become walled off and replaced by connective tissue.

4

What is ulcers?

Ulcers
An ulcer is a local defect of the surface of an organ or tissue that is produced by the sloughing of inflamed necrotic tissue. It can occur only when tissue necrosis and resultant inflammation exist on or near a surface. It is encountered in (1) the mucosa of the mouth, stomach, intestine, or genitourinary tract, and (2) skin and subcutaneous tissue of the lower extremities in older persons who have circulatory disturbances that predispose to extensive ischemic necrosis.

5

What are the causes of chronic inflammation?

Causes of chronic inflammation
- Persistent infection by microorganisms that are difficult to eradicate, such as mycobacteria, viruses, fungi and parasites. These organisms often evoke an immune reaction called delayed-type hypersensitivity.
- Hypersensitivity disease caused by excessive and inappropriate activation of immune system. Autoimmune and allergic reaction are inappropriately triggered against antigens that are normally harmless, the reaction serves no useful purpose and only cause disease.
- Prolong exposure to potentially toxic agent, either exogenous or endogenous.
- Some forms of chronic inflammation may be important in the pathogenesis of diseases.

6

what are the morphological features of chronic inflammation?

Morphologic feature
- Infiltration with mononuclear cells, which include macrophage, lymphocytes and plasma cells.
- Tissue destruction, induced by the persistent of offending agent or by the inflammatory cells.
- Attempts of healing by connective tissue replace of damaged tissue, accomplished by angiogenesis and fibrosis.

7

What is granulomatous inflammation?

Granulomatous inflammation
Granulomatous inflammation is a form of chronic inflammation characterized by collection of activated macrophages, often with T lymphocytes, and sometimes with central necrosis. Granuloma formation is a cellular attempt to contain an offending agent that is difficult to eradicate. There is often strong activation of T lymphocytes leading to macrophages activation, which can cause injury to normal tissues. The activated macrophages may develop cytoplasm and begin to resemble epithelial cells, and are called epithelioid cells. Some activated macrophages may fuse, forming multinucleate giant cells.

8

What are the two types of granulomas inflammation?

There are two types of granulomas:
- Immune granulomas are caused by a variety of agents that are capable of inducing a persistent T cell–mediated immune response. This type of immune response produces granulomas usually when the inciting agent cannot be readily eliminated, such as a persistent microbe or a self-antigen. In such responses, macrophages activate T cells to produce cytokines, such as IL-2, which activates other T cells, perpetuating the response, and IFN-γ, which activates the macrophages.
- Foreign body granulomas are seen in response to relatively inert foreign bodies, in the absence of T cell– mediated immune responses. Typically, foreign body granulomas form around materials such as talc (associated with intravenous drug abuse), sutures, or other fibers that are large enough to preclude phagocytosis by a macrophage but are not immunogenic. Epithelioid cells and giant cells are apposed to the surface of the foreign body.

9

What are pyrogens?

Substance that induce fever

10

What does the acute phase response consist of?

The acute-phase response consists of several clinical and pathologic changes;
- Fever – Substances that induce fever are called pyrogens. The increase in body temperature is caused by prostaglandins that are produces in the vascular and perivascular cells of the hypothalamus. In the hypothalamus, the prostaglandins stimulate the production of neurotransmitters that reset the temperature set point at a higher level. Aspirin reduces fever by inhibiting prostaglandin synthesis.
- Acute-phase proteins- are plasma proteins including C-reactive protein (CRP), fibrinogen, and serum amyloid A (SAA) protein. CRP and SAA bind to microbial cell walls and act as opsonins and fix complement. Acute-phase proteins have beneficial effects during acute inflammation, but prolonged production of these proteins causes secondary amyloidosis. Hepcidin production is increased in the acute-phase response. Hepcidin reduce the availability of iron and are responsible for the anemia associated with chronic inflammation.
- Leukocytosis occurs because of accelerated release of cells from the bone marrow post-mitotic reserve pool (caused by cytokines, including TNF and IL-1) and is therefore associated with a rise in the number of more immature neutrophils in the blood.
- Increase pulse and blood pressure; decreased sweating, mainly because of redirection of blood flow from cutaneous to deep vascular beds, to minimize heat loss through the skin.

11

What are the classification of tissue according to regeneration?

Cell proliferation: signals and control mechanisms
- Labile (continuously dividing) tissue. Tissues (epithelium) can regenerate after injury as long as the pool of stem cells is preserved.
- Stable tissue. Cells that are in G0 stage of the cell cycle. These cells are capable of dividing in response to injury to loss of tissue mass. Stable cells constitute the parenchyma of the most solid tissue, such as liver, kidney, and pancreas. With exception of liver, stable tissues have a limited capacity to regenerate after injury.
- Permanent tissue. Cells that are terminally differentiated and non-proliferative. Injury to the brain and heart is irreversible and result in a scar, because neurons and cardiac myocytes can’t regenerate.

12

Explain the mechanism of liver regeneration!

Liver regeneration
Regeneration of the liver occur by two major mechanisms:
Proliferation of hepatocytes – It is triggered by the combined action of cytokine and polypeptide growth factors. In the first phase, cytokines such as IL-6 are produced by kupffer cells and act on hepatocytes to make the parenchymal cells competent to receive and respond to growth factor signals. In second phase, growth factors such as HGF and TGF-, produce by many cell types, act on primed hepatocytes to stimulate cell metabolism and entry of the cells into the cell cycle. Hepatocytes replication is followed by replication of non-parenchymal cells. In the final phase, hepatocytes return to quiescence.
Liver regeneration from progenitor cells- When the proliferative capacity of hepatocytes is impaired, such as after chronic liver injury, progenitor cells in the liver contribute to repopulation.

13

What are the steps in scar formation?

Angiogenesis to support the repair process. Steps:
- Vasodilation in response to NO and increased permeability induced by vascular endothelial growth factor (VEGF).
- Separation of pericytes from the abluminal surface and breakdown of the basement membrane to allow formation of a vessel sprout
- Migration of endothelial cells toward the area of tissue injury
- Proliferation of endothelial cells just behind the leading front of migrating cells
- Remodeling into capillary tubes
- Recruitment of periendothelial cells to form the mature vessel
- Suppression of endothelial proliferation and migration and deposition of the basement membrane.
Formation of granulation tissue. Migration and proliferation of fibroblasts and deposition of loose connective tissue, together with the vessel and interspersed leukocytes, form granulation tissue. Its histologic appearance is characterized by proliferation of fibroblast and new thin-walled, delicate capillaries, in a loose extracellular matrix.
Remodelling of connective tissue. Maturation and reorganization of connective tissue produce the stable fibrous scar. The amount of connective tissue increases in the granulation tissue, resulting in the formation of scar.

14

Explain the process of angiogenesis! What are the signalling pathways involved in angiogenesis?

The process of angiogenesis involves signalling pathways:
- Growth factors. VEGF-A stimulate both migration and proliferation of endothelial cells. Fibroblast growth factor stimulate the proliferation of endothelial cells. It promotes the migration of macrophages and fibroblasts to the damaged area and stimulates epithelial cells migration to cover epidermal wounds. PDGF and TGF­β participate in the stabilization process: PDGF recruits smooth muscle cells and TGF­β suppresses endothelial proliferation and migration and enhances the production of ECM proteins.
- Notch signalling regulates the sprouting and branching of new vessels and thus ensures that the new vessel that are formed have proper spacing to supply the healing tissue with blood.
- ECM proteins participate in the process of vessel sprouting angiogenesis.
- Enzymes in the ECM which degrade the ECM to permit remodelling and extension of the vascular tube.