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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the characteristics of acute inflammation (4)?

A
  • rapid course
  • vasodilation
  • increased vascular permeability
  • accumulated neutrophils
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2
Q

What is the dominant characteristic of chronic inflammation?

A

Scar tissue formation and proliferation

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3
Q

Which kind of inflammation has predictable clinical manifestations, and which does not?

A

Predictable: acute
Unpredictable: chronic

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4
Q

What are (5) benefits of inflammation?

A
  • Localizes and dilutes damaging substances
  • promotes antibody transport
  • promotes fibrin clot formation
  • stimulates immune response
  • mobilizes phagocytes
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5
Q

What are (4) risks of inflammation?

A
  • release of lysosomal enzymes
  • prolonged vascular pooling leading to hypoxia
  • excessive swelling

Chronically can lead to excessive scarring

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6
Q

What are the (5) cardinal signs of acute inflammation?

A

S.H.A.R.P.

  • Swelling
  • Heat
  • A loss of function
  • Redness
  • Pain
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7
Q

What is the triple response of Lewis?

A
  1. Flush (red line)
  2. Red flare
  3. Wheal
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8
Q

When does the triple response of Lewis occur?

A

In the beginning of acute inflammation.

Common response to insect bites, minor skin trauma.

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9
Q

How long does the triple response of Lewis tend to last?

A

15-30 minutes

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10
Q

What is the flush, or red line stage, of Lewis response?

A

Local vasodilation - the result of histamine release

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11
Q

What is the flare stage of Lewis response?

A

Dilation of arterioles adjacent to the injury site dilate, causing a red zone.

If local nerve fibers are cut, then no flare.

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12
Q

What is the wheal stage of lewis response?

A

Local edema (swelling) caused by fluid accumulation. Fluid may persist, even if redness fades.

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13
Q

What are the (3) stages of blood flow alteration that may occur during acute inflammation?

A
  • transient vasoconstriction caused by short lived arteriole spasms in the SNS
  • vasodilation (hyperemia) leading to increased flow (up to 10x)
  • stasis (pooling) includes sludging (clumping of red blood cells)
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14
Q

What are exudates and what do they contain?

A 
Inflammatory fluids 
Contain: 
- fluid 
- plasma proteins 
- debris 
- leukocytes
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15
Q

What are transudates?

A

Non-inflammatory fluids

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16
Q

What kind of exudates are produced in mild (non-serious) injury?

What is their main component, and what color results?

A

Serous exudates

Consists of albumin

Thin, straw-colored fluid

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17
Q

What are the (5) stages of leukocyte response to injury?

A
  1. Margination & rolling - move to edge of vessels
  2. Pavementing - adhere to vessel walls
  3. Diapedesis - exit vessels / enter tissue
  4. Migration (chemotaxis) - follow chemokines to injury site
  5. Phagocytosis & degranulation - ingestion and digestion of solid particles
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18
Q

What are the (4) steps of phagocytosis?

A
  1. Adhesion of target to phagocyte
  2. Ingestion of particle via phagosome / lysosome (or phagolysosomes)
  3. Intracellular killing
  4. Digestion
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19
Q

What immune cells are the first responders during acute inflammation?

A

Neutrophils

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20
Q

Neutrophils do the best job with which kind of pathogens?

A

Bacteria

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21
Q

Macrophages (monocytes) are most common with what kind of injury?

A

Chronic inflammation (all phases)

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22
Q

Lymphocytes and plasma cells are most common with with kinds of pathogens?

A

Viruses

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23
Q

When are eosinophils and basophils most common?

A

Parasitic infection (eosin)

Hypersensitivity (baso)

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24
Q

What are the amine chemical mediators, and where are they found?

A

Histamine - mast cells, basophils, platelets

Serotonin - platelets, mast cells

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25
Q

What kinds of cells produce prostaglandins?

A
  • leukocytes
  • platelets
  • endothelium
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26
Q

What action do histamines and serotonin have on vasculature?

A

Vasoconstriction

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26
Q

When are arachidonic acids released?

A

During every phase of acute inflammation

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27
Q

What (3) eicosanoids are the main derivatives of arachidonic acid?

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
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28
Q

When arachidonic acid is released from plasma membrane phospholipids, which (2) enzymatic pathways are activated?

A
  • cyclooxygenase

- lipoxygenase

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29
Q

What kind of hormones block the phospholipase pathway that activates arachidonic acid?

A

Corticosteroids

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30
Q

What are the (2) main actions of leukotrienes?

A
  • attract neutrophils (chemotactic)

- increase vessel permeability (leakier vessels)

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31
Q

Which inflammatory pathway is inhibited by NSAIDs?

A

Cyclooxygenase

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32
Q

Which enzymatic pathway produces leukotrienes?

A

Lipooxygenase

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33
Q

Which enzymatic pathway produces prostaglandins and thromboxanes?

A

Cyclooxygenase

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34
Q

What are the (5) main actions of prostaglandins and thromboxanes?

A
  • increase vessel permeability
  • increase vascular smooth muscle activity
  • increase platelet activity
  • contribute to fever
  • potentiate pain
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35
Q

What effect do fish oils (eicosapentaetoic acids) have on the inflammation process?

A

Inhibit the production of leukotrienes by affecting the lipooxygenase pathway

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36
Q

What are the (6) categories of cell derived mediators of inflammation?

A
  1. Lysosomal agents
  2. Oxygen-derived free radicals
  3. Platelet activating factor
  4. Cytokines
  5. Neuropeptides
  6. Nitric oxide
37
Q

What (2) plasma systems act as mediators of inflammation?

A
  • kinin system

- complement system

38
Q

What do kinins (especially bradykinin) do?

A
  • enhance permeability
  • elicit pain
  • fever
39
Q

What is the classic activation pathway for the complement system?

A

Antigen-antibody complexes

40
Q

What is the alternate activation pathway for the complement system?

A

Exposure to bacterial endotoxins

41
Q

What are the (3) components of the clotting system?

A
  • fibrinopeptides
  • plasmin
  • thrombin
42
Q

In the clotting system, activation of plasmin produces what (2) effects?

A
  • lysis of fibrin clots

- activation of complement

43
Q

In mild injury, how quickly does the immediate transient response start, and how long does it last?

A

Starts within 10 minutes

Lasts 30-60 minutes

44
Q

When does a delayed-prolonged response to injury begin, and how long does it last?

A

Starts 2-3 hours post injury

Lasts several hours up to days

45
Q

What are (3) common causes of the delayed-prolonged response to injury?

A
  • sunburn
  • radiation therapy
  • moderate thermal burns
46
Q

When does injury lead to an immediate-sustained response?

A

When endothelial cells are directly damaged and undergo necrosis

47
Q

What are (3) main characteristics of chronic inflammation?

A
  • prolonged (4-6 weeks)
  • leukocytic infiltration
  • fibrosis (scarring)
48
Q

What are the clinical signs of chronic inflammation?

A

Highly variable

49
Q

What is the most common fatal infectious disease?

A

TB

50
Q

What are the (6) morphological patterns of inflammation?

A
  1. Serous
  2. Fibrinous
  3. Catarrhal
  4. Pyogenic
  5. Granulomatous
  6. Ulcer
51
Q

What are some (3) mild injuries that give rise to serous inflammation?

A
  • Rheumatoid arthritis
  • Burn injury
  • Herpetic sores
52
Q

What is the main characteristic of pyogenic response?

A

Pus generation

53
Q

What kind of inflammation leads to the formation of abscesses?

A

Pyogenic - pus formation

54
Q

What is a furuncle?

A

A boil - small, pus filled abscess

55
Q

What is a caruncle?

A

An enlarged furuncle - a pus filled boil with multiple points of discharge

56
Q

What kind of inflammation is cellulitis, and what are its (3) main characteristics?

A

A type of pyogenic inflammation - subcutaneous

It is:

  • acute
  • diffuse
  • spreading
57
Q

What are erysipelas?

A

Cellulitis in the face

58
Q

What are (2) common infections that lead to cellulitis?

A
  • strep

- staph

59
Q

What is a special kind of chronic inflammation involving deposits of non-digestible materials?

A

Granulomatous

60
Q

What are (2) infection types that lead to granulomatous inflammation?

A
  • TB

- autoimmune disorders like rheumatoid arthritis

61
Q

What is the major cell type involved in granulomatous inflammation?

A

Modified macrophages

62
Q

What is an acute ulcer?

A

A shallow crater in the surface of a tissue, resulting from sloughing of necrotic tissue

63
Q

What is pyrexia?

A

Fever

64
Q

What brain area regulates body temperature?

A

Hypothalamus

65
Q

Besides increased body temperature, what happens during fever?

A

Increased metabolic rates due to increased energy and oxygen demand of cells

66
Q

What are the (4) stages of fever?

A
  1. Prodrome
  2. Cold
  3. Flush
  4. Crisis
67
Q

What happens in the prodrome stage of fever?

A

Pre-fever: the subject feels sick and achy, but no increase in temp

68
Q

What happens in the cold stage of fever?

A

Fever begins - cutaneous blood flow is reduced to conserve heat, resulting in the skin feeling cold and possibly shivering

69
Q

What happens in the flush stage of fever?

A

Higher body temperature has been achieved, blood flow increases to the skin

70
Q

Patients may fluctuate between which two stages of fever?

A

Cold and flush

71
Q

What happens in the crisis stage of fever?

A

Fever breaks, temperature returns to normal. Sweating occurs to release heat.

72
Q

What is the upper temperature limit for non-neuronal cell function?

A

105-106 degrees

73
Q

At what temperature do CNS disturbances start to appear?

A

103-105 degrees

74
Q

At what temperature is death likely?

A

110 degrees

75
Q

Systematic manifestations of inflammation, also called acute phase reactions include what (5) symptoms?

A
  1. Somnolence
  2. Fever
  3. Poor appetite
  4. Increased neutrophils (production, release, and activity)
  5. Alterations in plasma proteins
76
Q

What is leukocytosis?

A

Elevated levels of circulating WBC, usually neutrophils >10,000 mm3

77
Q

What is leukopenia?

A

Reduced circulating WBC <3,000 mm3

78
Q

What is the ideal outcome of inflammation?

A

Resolution - tissues completely restored to normal

  • remove or inactive inflammatory stimulus
  • reverse vascular changes
  • remove exudates and debris
79
Q

What is parenchymal regeneration?

A

Replacement of damaged tissues by normal cells of the same type

80
Q

What is repair by connective tissue?

A

Replacement of damaged tissue with collagen

81
Q

What is granulation tissue and what are it’s (3) major characteristics?

A

Immature, early scar tissue

Characteristics:

  • cellular (macrophages)
  • vascular
  • edematous (fibroblasts)
82
Q

What is a primary union in wound repair?

A

The margins of clean wounds are apposed under sterile conditions - the ideal healing (stitches)

83
Q

What is secondary union in wound repair?

A

Repair of large wounds with separated edges - tissue loss has occurred and the resulting gap must be filled with granulation tissue

84
Q

What are the (3) main factors to increase tensile strength in wound repair?

A
  1. Type and quantity of collagen - Type III should be replaced by Type I
  2. Orientation and size of fibers - initially random, should be realigned and reinforced along the direction of stress
  3. Cross linkages - should form between the alpha chains of collagen
85
Q

What is a keloid?

A

Hyperplastic scar tissue covered by intact skin - an excessive proliferation of scar tissue

86
Q

When does repair by connective tissue take place?

A

When resolution or parenchymal regeneration is not possible, so damaged tissue is replaced with granulation tissue.

87
Q

What is the maximum tensile strength of primary union restoration tissue?

A

80%

88
Q

Can striated muscle fibers repair?

A

Limited repair capacity

89
Q

Can the heart muscle repair?

A

Necrosis of heart muscle generally causes scarring; diffuse, non-lethal injury may be repairable

Pathology (4 decks)

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