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Questions and Answers
What is inflammation?
What is inflammation?
Inflammation is a protective response to injury, infection, or other harmful stimuli.
What are the 5 cardinal signs of acute inflammation?
What are the 5 cardinal signs of acute inflammation?
Chronic inflammation is characterized by a slow onset and a short duration.
Chronic inflammation is characterized by a slow onset and a short duration.
False
What are the primary cells involved in chronic inflammation?
What are the primary cells involved in chronic inflammation?
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Which of the following is NOT a characteristic of an opportunistic infection?
Which of the following is NOT a characteristic of an opportunistic infection?
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The immune system is responsible for protecting the body against only microorganisms.
The immune system is responsible for protecting the body against only microorganisms.
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What is the difference between innate and adaptive immunity?
What is the difference between innate and adaptive immunity?
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What are the four types of hypersensitivity reactions?
What are the four types of hypersensitivity reactions?
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Autoimmune disorders affect men more often than women.
Autoimmune disorders affect men more often than women.
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What is immunodeficiency?
What is immunodeficiency?
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Opportunistic infections are only caused by viruses.
Opportunistic infections are only caused by viruses.
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What is AIDS?
What is AIDS?
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Study Notes
Inflammation
- Inflammation is a protective response intended to eliminate the cause of cell injury, infectious agents, and necrotic cells, and to initiate repair.
- Components of inflammation include blood vessels, white blood cells and platelets, plasma proteins and chemical mediators (coagulation/fibrinolytic system, kinin system, complement system), and extracellular matrix and stromal cells (structural fibrous proteins, adhesive glycoproteins, proteoglycans, basement membrane).
- The immune response plays a crucial role in inflammation, with macrophages functioning in the elimination of microbes and dead tissue, along with mediators like cytokines and nitric oxide.
Components of Acute Inflammation
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Vascular Changes: Alterations in blood vessel caliber lead to vasodilation and increased blood flow. Changes in vasculature also permit plasma proteins to leave circulation (increased permeability).
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Cellular Events: Leukocytes emigrate from the microcirculation and accumulate in the focus of injury.
Increased Vascular Permeability
- Leads to protein-rich fluid and cells entering extravascular tissues.
- Increases osmotic pressure, causing more fluid to flow out of the blood into tissues, producing edema.
Edema
- Transudate: Mechanism: hydrostatic pressure imbalance across vascular endothelium; fluid content is low in protein (ultrafiltrate of blood plasma). Typical in noninflammatory conditions.
- Exudate: Mechanism: alteration in normal permeability of small blood vessels in area of injury; fluid content is high in protein. Typical in inflammatory conditions.
Types of Inflammation
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Acute Inflammation: Fast onset (minutes to hours), short duration (minutes to days), characterized by mainly neutrophils, usually mild and self-limiting tissue injury, and fibrosis.
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Chronic Inflammation: Slow onset (days to years), long duration, with infiltrates of monocytes/macrophages and lymphocytes, often severe and progressive tissue injury and fibrosis.
External Manifestations of Acute Inflammation
- Heat
- Redness
- Swelling
- Pain
- Loss of function
Systemic Effects of Inflammation
- Fever (elevated body temperature)
- Elevated plasma levels of acute phase proteins
- Increased white blood cell count (leukocytosis)
- Increased heart rate
- High blood pressure
- Decreased sweating
- Rigors/shivering
- Chills (perception of cold)
- Malaise
- Anorexia
Stimuli for Acute Inflammation
- Infections (bacteria, fungi, viruses, parasites)
- Trauma (various chemical and physical agents - heat, cold, burns, radiation)
- Chemicals (acids, alkalis, bacterial toxins, metals)
- Tissue necrosis
- Foreign bodies
- Immunologic reactions
Morphological Patterns of Acute Inflammation
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Serous: Exudation of cell-poor fluid into spaces created by injury to surface epithelia or into body cavities (e.g., skin blisters).
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Fibrinous: Consequence of more severe injuries, resulting in greater vascular permeability that allows large molecules (such as fibrinogen) to pass the endothelium.
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Suppurative (Purulent): Collection of large amounts of pus (an exudate consisting of many neutrophils, debris of necrotic cells, and edema fluid).
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Ulcer: Local defect of the surface of an organ or tissue that is produced by sloughing (shedding) of inflamed necrotic tissue.
Outcomes of Acute Inflammation
- Complete resolution
- Healing by connective tissue (scarring or fibrosis)
- Progression to chronic inflammation
Chronic Inflammation
- Inflammation of prolonged duration (weeks to years)
- Characterized by infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells), tissue destruction, and repair.
Immune Components of inflammation
- Macrophages: Dominant cells of chronic inflammation, involved in phagocytosis.
- B and T Lymphocytes: Important in cell-mediated immunity.
- Mast cells: Source of histamine in allergic reactions.
Tissue Repair
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Regeneration: Replacement of damaged cells by similar parenchymal cells, returning to a normal state. Typical in rapidly dividing epithelia (skin, intestines). Requires intact connective tissue.
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Scar Formation: Occurs when tissues are incapable of regeneration or supporting structures are severely damaged. Connective tissue is laid down.
Immunity
- The immune system protects against microorganisms and removes damaged/cancerous cells.
- Innate immunity: immediate, nonspecific protection (skin, mucous membranes).
- Adaptive immunity: takes 7-10 days to develop, specific to the antigen (cellular or humoral).
- T-cells: destroy antigen.
- B-cells: produce antibodies.
Altered Immune Responses
- Hypersensitivity: Inappropriate immune response to an antigen, leading to inflammation and destruction of healthy tissue. This includes four subtypes: type I (IgE-mediated), type II (cytotoxic), type III (immune complex-mediated), and type IV (cell-mediated).
- Autoimmune disorders: Normal defenses recognize self as foreign, leading to destruction of the body's own tissues. Examples: systemic lupus erythematosus, rheumatoid arthritis.
- Immunodeficiency: Diminished or absent immune response, increasing susceptibility to infections. Can be primary (genetic defect) or secondary (underlying disease, malnutrition, drugs).
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