Acute Inflammation Flashcards

1
Q

What is Acute Inflammation characterized by?

A

Neutrophils

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2
Q

Definition of inflammation

A

movements of fluid/leukocytes from tissues->blood

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3
Q

What type of immunity is present in acute inflammation?

A

Innate immunity

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4
Q

Hows is the vascular response different between acute and chronic inflammation?

A

Prominent vascular response in Acute

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5
Q

What kind of immunity is present in chronic inflammation?

A

Cell-mediated

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6
Q

What type of leukocyte is predominant in Chronic inflammation?

A

Mononuclear cell

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7
Q

Causes of Acute Inflammation (3)

A

1) Tissue necrosis
2) Immune hypersensitivity
3) Microbial infections (pyogenic bacteria)

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8
Q

Causes of chronic inflammation (3)

A

1) Autoimmune disorders
2) Primary granulatomous diseases (Chron’s, sarcoidosis)
3) Phagocytosis resistant organisms

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9
Q

Signs of inflammation (5)

A

1) Redness
2) Swelling
3) Heat
4) Pain
5) Loss of Function

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10
Q

Major manifestations of Acute Inflammation (6)

A

1) Rapid vascular response/altered microvasculature
2) Increased vascular permeability
3) Platelet stimulation
4) Chemical mediator activation
5) Neutrophil activity
6) Phagocytosis & intracellular killing

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11
Q

What are the 2 most common causes of fibrinous pericarditis?

A

1) uremia
2) renal failure

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12
Q

Define: Effusion

A

Excess fluid within body cavities

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13
Q

Define: Edema

A

Fluid accumulation within extravascular compartment and interstitium

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14
Q

Mechanisms of increased vascular permeability during inflammation (3)

A

1) Inflammatory mediators cause contraction of endothelial cells –> gaps
2) Direct injury to endothelial cells (arterioles, capillaries, venules usually)
3) Leukocyte dependent injury of endothelial cells

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15
Q

Define: Transudate

A

Edema with low protein content

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16
Q

Define: Exudate

A

Edema with high protein content

17
Q

Types of Exudate

A

1) Serious - no cellular component
2) Fibrinous - fibrin from coagulation activation
3) Purulent - cellular components , mostly neutrophils
4) Suppurative - Purulent + liquefactive necrosis

18
Q

Vasoactive Mediators of Edema

A
  1. Plasma Derived
    • Hageman factor
      • Fibrin split products
      • Kinins
    • Complement system
      • C3a, C5a
  2. Cell Derived
    1. Mast cell/basophils –> Histamine
    2. Platelets –> Serotonin
    3. Inflammatory Cells –> prostaglandins/leukotrienes
    4. Endothelium –> NO/prostaglandins
19
Q

What are the anaphylatoxins and what do they do?

A
  • C3a, C4a, C5a
  • Part of complement system
  • increases vascular permeability by activating Mast Cells (histamine, leukotrienes)
  • cause bronchoconstriction, vasoconstriction, edema
20
Q

What makes kinins? and what do kinins do?

A
  • Kallikrenin makes kinin
  • Kinin increases vascular permeability
21
Q

Vasoactive Cell Derived Mediators of Edema

A

1) Arachidonic acid metabolites
2) Platelet Activating Factor
3) Platelet Derived mediators
4) Mast Cell & basophil derived mediators

22
Q

Arachidonic acid metabolites and their functions

A
  1. Thromboxanes (TXA2)
    1. Vasoconstrictor, aggregatory, increases PMN response
  2. Prostaglandins (PGI2)
    1. Vasodilator, anti-aggregatory, decrases PMN responses
23
Q

Actions of Neutrophils during inflammatory resposne

A

1) Margination of cells along vascular wall
2) Adhereance to endothelium and basement membrane
3) Emigration through vascular wall via diapedesis
4) Chemotaxis - migration through soluble chemotactic agents
5) Haptotaxis - chemotax. along fixed insoluble chemotactic gradient

24
Q

Initial PMN recruitment depends on which two molecules?

A

1) C5a
2) LTB4

25
Q

Proglonged PMN recruitment depends on what?

A

Chemotactic cytokines

26
Q

Molecues responsible for leukocyte adhereance and emigration

A

Rolling - Selectins & addressins

Adhesion - B2 integrins & ICAM 1

Transmigration - PCAM -1

27
Q

Overall process of bacterial phagocytosis

A

Phagocytosis –> degranulation/NADPH oxidase activation –> bacterial killing and digestion

28
Q

Chediak-Higashi Syndrome

A

Defective lysosomal granules

29
Q

Chronic granulomatous disease of childhood

A

NADPH oxidase deficiency

No H2O2

recurrent bacterial infections

30
Q

Myeloperoxidase deficiency

A

NO HOCl, recurrent fungal infections