Inflammation A22-A25 Flashcards
A/22. Characteristics of acute inflammation (cellular events, chemical mediators, systemic effects)
What is the purpose of inflammation, what are the cellular local events and chemical mediators
Acute inflammation: the 5 characteristics: Calor, Rubor, Dolor, Tumor, Functional loss. Less than 1 week is acute inflammation.
Purpose: To deliver innate immune cells and defense mechanisms to the site of an injury. To dilute toxins and bacteria present. To increase blood flow to the damaged area.
Flow is increased by: Vasodilation, and Junctional Retraction
Main cells of acute inflammation: Neutrophils and Platelets
Major mediators of early phase:
- Vasoactive amines: Histamine (mast cells) and Serotonin (from platelets),
- Coagulation factor system -> activates –>
- Kallekrien and Bradykinin
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Arachidonic Acid derivatives:
- COX derivatives
- Prostaglandins - vasodilation and increased vasculary permeability, pain and fever
- Thromboxanes - platelet activation, thrombosis, pain.
- LOX derivatives
- Leukotrienes - vascular permeability, neutrophils
- COX derivatives
- Platelet activating factors
Late phase:
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TNF-alpha, IL-1, IL-6, IFN-gamma.
- Acute phase response, fever.
- Increased expression of Selectins, and CAMs by endothelial cells to aid in leukocyte chemotaxis.
- IL-8, MCP-1 monocyte chemotactic protein 1.
- Nitric Oxide
Leukocytes lysosomal enzymes
- Acid proteases/hydrolases,
- Neutral protesases, Elastase and Collagenase
A/22. Characteristics of acute inflammation (cellular events, chemical mediators, systemic effects)
What are the systemic effects of inflammation
The Acute Phase Reaction
Leukocytosis
Increased heart rate and blood pressure
Fever, chills, malaise, fatigue - all due to CNS effects
A/23. Morphologic patterns of acute inflammation according to the exudate
Serous inflammation: Watery transudate is formed. Vascular permeability is not greatly increased, so only small molecules can bypass, and protein is retained.
- Pleural or Pericardial Effusions.
Fibrinous inflammation: caused by more severe injuries. Large increase in permeability allows lots of fibrinogen/fibrin and proteinaceous exudate to leak out. Eisinophilic acellular meshwork histologically, brownish clumps irl.
- Seen during inflammation of the linings of body cavities pericardium, meninges, pleura (my pleural adhesions after PTX)
- After fibrin exudation, it can either become organized into a permanent scar or, fibrinolysis and macrophages can remove it.
Purulent aka Suppurative inflammation and Abcess formation
- Neutrophils, Necrotic cells, and proteinaceous exudate.
- Abcess: a pus filled core surrounded by a rim of living neutrophils, surrounded by dilated vessels and proliferative fibroblasts. Fibroblasts may eventually fully wall the abcess in connective tissue.
Hemorrhagic inflammation: Inflammation involving vessel damage and hemorrhage as well as the inflammation.
Ulcer: A local cavitation on the surface of a tissue caused by cell necrosis and subsequent loss/shedding of those cells. Usually seen in the GI mucosa, and in the subcutaneous regions of the lower limbs in compromised or elderly patients.
A/24. Chronic inflammation.
Histological characteristics
Mononuclear cell infiltration: Macrophages, lymphocytes, and some plasma cells. aka “Small round cell infiltration”
Simultaneous tissue destruction and tissue repair and angiogenesis / revascularization.
Exudation and edema are not really involved in chronic inflammation.
Granulomatous inflammation is a special case of chronic inflammation.
A/24. Chronic inflammation.
Causes of chronic inflammation
causes:
- Persistent inflammation, hepatitis C, B
- Hypersensitivity reactions, autoimmune diseases.
- Allergic reactions and chronic allergen exposure
- Prolonged toxin exposure.
Cell types of chronic inflammation:| Macrophages, T-cells, and B-cells
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Macrophages of the Reticulo-Endothelial System, aka Mononuclear Phagocyte system are the predominant cell types of chronic inflammation, along with Fibroblasts.
- Monocytes generated in the bone marrow enter periphery and become Macrophages. In the periphery macrophages can proliferate, and can form Giant Cells by fusion of multiple macrophages.
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Lymphocytes, particularly Th and Tc cells are also major mediators of chronic inflammation.
- Lymphocytes and form Germinal centers in extensively infiltrated sites of chronic inflammation, making the tissue appear to be lymphoid.
A/25. Granulomatous inflammation
What is the essential cause of granuloma formation,
Describe the structure of the two main types of granulomas
Granulomas occur because of Persistent T cell activation to a chronically present substance/microbe. T cells chronically activate local macrophages.
Structure of a Necrotizing granuloma (TB granuloma)
- Core of pus, cell debris, necrotic cells, and microbes.
- Epitheloid cells surround the core. Derived from macrophages.
- Giant cells, foam cellsare mixed in with the epitheloid macrophages.
- The rings of epitheloid cells are surrounded by T and B cells, lymphocytes.
- Very few neutrophils and NK cells may also be present.
Structure of a Non-necrotizing granuloma Crohn’s disease or Sarcoidosis granuloma:
- These do not have a necrotic core. Since there is no infectious agent. They have all of the same other changes though.
Granulomas that have been resolved/are no longer have the activating agent maintaining them may be healed and resolved but will cause extensive fibrosis.
A/25. Granulomatous inflammation
List the diseases that cause granulomas (6)
Tuberculosis
Leprosy
Syphillis
Cat-Scratch disease - Bartonella henselea
Sarcoidosis
Crohn’s disease
