Inflammation and Innate Immune Response – Video Notes

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Question-and-answer flashcards covering definitions, mechanisms, mediators, cellular players, and outcomes of inflammation and innate immunity.

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27 Terms

1
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What is inflammation?

Protective vascular and cellular response to tissue injury that minimizes damage, removes damaged tissue, prevents spread, and prepares for healing.

2
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What does the suffix '-itis' indicate in medical terms?

Inflammation (as in pancreatitis, appendicitis, colitis, diverticulitis).

3
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What is innate immunity?

Non-specific, native defense that is rapid and present at birth; serves as the first line of defense.

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What are the two major branches of the immune response?

Innate immunity and adaptive immunity.

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What are the components of adaptive immunity?

Humoral immunity (B-lymphocytes/antibodies) and cell-mediated immunity (T-lymphocytes).

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What are the main effector cells in the inflammatory response?

Granulocytes and macrophages (phagocytes).

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What is acute inflammation?

A rapid reaction to injury lasting hours to days, with vascular and cellular stages, aiming to heal; can resolve or progress.

8
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What occurs in the vascular stage of acute inflammation?

Vasodilation and increased vascular permeability, leading to increased blood flow and exudation.

9
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What occurs in the cellular stage of acute inflammation?

Leukocyte activation, migration to the injury site, phagocytosis; chemotaxis and leukocytosis.

10
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What triggers the inflammatory response?

Pathogens or tissue injury that release inflammatory mediators and activate innate immune defenses.

11
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Name key inflammatory mediators and their effects.

Bradykinin—vasodilation; Histamine—vasodilation and increased permeability; Prostaglandins—vasodilation, pain, fever; Leukotrienes—increased permeability and leukocytosis; Cytokines—pro-inflammatory, promotes leukocytosis.

12
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What is exudate?

Mass of cells and fluid that seeps out of inflamed vessels to transport protective cells and debris; supports healing.

13
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What are the types of exudate?

Transudate/Serous (watery, mostly protein), Purulent (pus with degraded WBCs/tissue debris), Effusion (exudate in a body cavity).

14
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Which cells are granulocytes?

Neutrophils, eosinophils, basophils.

15
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What are phagocytes and which cells perform phagocytosis?

Monocytes/macrophages (and neutrophils) perform phagocytosis; monocytes mature into macrophages and secrete cytokines.

16
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What is leukocytosis and its normal range?

Elevated white blood cell count; normal range ~4,000–10,000 cells/mL; leukocytosis often 15,000–20,000+ cells/mL.

17
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How does acute vs. chronic inflammation differ in cellular infiltrates?

Acute inflammation is neutrophil-predominant; chronic inflammation features monocytes/macrophages and lymphocytes.

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What is chronic inflammation?

Recurrent, prolonged inflammatory response (>2 weeks) where the cause is not eliminated; macrophages and lymphocytes predominate; granulomas may form.

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What is a granuloma?

A mass of white blood cells, mostly macrophages, formed during chronic inflammation.

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What are common outcomes of acute inflammation?

Resolution/healing; fibrosis/scar formation; abscess formation; non-resolution with persistent trigger leading to chronic inflammation.

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What signs characterize acute vascular inflammation?

Redness, swelling, heat, pain, and impaired function; histamine is a dominant mediator.

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What signs characterize acute cellular inflammation?

Leukocytosis; systemic symptoms like pain, fever, fatigue; lymphadenopathy may occur.

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What is fever and how is it produced?

Elevation in body temperature caused by pyrogens; hypothalamus raises the set point, leading to chills and later fever; resolves when trigger ends.

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What is Systemic Inflammatory Response Syndrome (SIRS)?

Overwhelming systemic inflammation affecting multiple organs; cytokine storm; can cause organ failure; may lead to sepsis if infection is present.

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What is sepsis and septic shock?

Sepsis: severe infection with systemic inflammatory response; septic shock: sepsis with life-threatening cardiovascular collapse.

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What are common etiologies and consequences of chronic inflammation?

Unresolved/repeated infections, autoimmune disorders, prolonged irritants, poor diet, obesity; contributes to asthma remodeling, IBD-associated cancer risk, atherosclerosis.

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How does chronic inflammation relate to cancer and atherosclerosis?

Chronic inflammation can cause DNA mutations leading to cancer; leukocytes contribute to plaque formation in atherosclerosis.