Chapter 2 Flashcards

1
Q

what is acute and chronic non specific inflammation

A
  • acute inflammation: short and contained to specific area. quick repair
  • chronic: long lasting, weeks to indefinitely, continual injury to tissue (healing only when cause of injury is removed)
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2
Q

what are 5 clinical signs of local inflammation

A
  1. redness/erythema
  2. heat
  3. swelling
  4. pain
  5. loss of normal tissue function
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3
Q

what are 4 clinical signs of systemic inflammation

A
  1. fever
  2. leukocytosis
  3. elevated C-reactive protein
  4. lymphadenopathy
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4
Q

what is the sequence of microscopic events

A
  • injury to tissue
  • constriction of microcirculation
  • dilation of microcirculation
  • increase in permeability
  • ‘transudate’ leaves microcirculation (low protein plasma)
  • increased blood viscosity
  • decreased blood flow
  • margination and pavementing of white blood cells (WBCs)
  • WBCs enter tissue – emigration (white blood cells escaping blood vessels) and chemotaxis (movement of white blood cells after they escape to go to the injury)
  • ‘exudate’ leaves microcirculation (high protein plasma)
  • WBCs ingest foreign material – phagocytosis
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5
Q

why does immediate constriction of blood vessels occur

A
  • so clotting can occur
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6
Q

why does dilation of blood vessels occur during inflammation

A
  • aka hyperemia – increased blood flow

- erythema (clinically visible) and heat (hard to assess)

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7
Q

why is there an increase in permeability of blood vessels in inflammation

A
  • outflow of blood plasma and proteins

- into tissue, transudate

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8
Q

what is exudate

A
  • helps dilute injurious agents but results in excess fluid in tissues
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9
Q

what are the 2 types of edema

A
  1. serous: clear fluid – plasma (with some WBCs)

2. purulent: pus (tissue debris and many WBCs)

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10
Q

what is suppuration and what does it contain

A
  • production of pus

- contains tissue debris, white blood cells and plasma (causes white colour)

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11
Q

what are the 6 main types of cells involved in the inflammatory process

A
  1. neutrophils
  2. monocytes
  3. lymphocytes
  4. plasma cells
  5. eosinophils
  6. mast cells
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12
Q

what are neutrophils

A
  • 60-70% of white blood cells
  • multi-nucleated
  • first to arrive at injury
  • stem cell from bone marrow
  • phagocytosis
  • lysosomal enzymes
  • removed for functional healing
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13
Q

what are monocytes

A
  • circulates in blood
  • becomes macrophage once they reach injury tissue
  • second to arrive at inflammation
  • longer life span than neutrophils
  • important to immune response B cells – antigen presentation
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14
Q

what cells are present in chronic inflammation and the immune response

A
  • lymphocytes and plasma cells
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15
Q

what cells are present in the acute inflammation and immune response

A
  • eosinophils and mast cells
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16
Q

what are chemical mediators

A
  • messengers within inflammation and immune response
  • chemotaxis
  • activation
  • origin: blood, WBC, bacteria, cell membranes
17
Q

what are the 3 main systems of plasma proteins

A
  1. kinin system: includes vasodilation, early phase, induce pain
  2. clotting: blood clotting, protects, corrals foreign substances at site. responsible to forming the repair system for later
  3. complement system: complement is a system of plasma proteins that interacts with pathogens to mark them for destruction by phagocytes. aids in activation of WBC and IL and histamine. histamine increases vasodilation and vascular permeability. opsonization – enhancement of phagocytosis; proteins attach onto bacteria, which stimulates even more white blood cells to come and continue phagocytosis
18
Q

what are prostaglandins

A
  • chemical mediators
  • increase dilation and permeability
  • pain
  • redness
  • can cause damage to connective tissue and clot
  • aspirin/NSAIDs (advil) target prostaglandin synthesis (tylenol does not)
  • antihistamines reduce effects of histamine