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Pathophysiology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

define inflammation

A

coordinated vascular and cellular response of the body to cell injury and cell death

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2
Q

how is inflammation important?

A

has both protective (immune) and curative features

responsible for the removal of the injurious agent and cellular debris

initiates the healing process

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3
Q

T/F: without inflammation we cannot heal or have normal immune function

A

TRUE

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4
Q

List some factors that can lead to inflammation

A
  1. infection
  2. trauma/damaged tissue
  3. tissue necrosis
  4. presence of foreign bodies
  5. immune reactions
  6. ischemia
  7. cancer
  8. chemicals
  9. physical agents (heat/cold, radiation)
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5
Q

what are the goals of inflammation?

A
  1. inactivate injurious agents
  2. break down and remove dead cells and other cellular debris
  3. initate tissue healing
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6
Q

List the key components of inflammation

A
  1. blood vessels
  2. circulating blood cells
  3. CT or interstitial tissue cells
  4. chemical mediators derived from inflammatory cells or plasma cells
  5. specific ECM constituents (collagen and basement membranes)
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7
Q

what are the cardinal signs of inflammation?

A
  1. erythema
  2. heat
  3. edema
  4. pain
  5. loss of function
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8
Q

what are the events of an inflammatory reaction?

A
  1. vascular events
    1. vasodilation
    2. increased vascular permeability
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9
Q

what induces vasodilation during an inflammatory response?

A

histamine release from platelets and mast cells causing smooth muscle relaxation

explains heat and redness at site of injury

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10
Q

why is increased vascular permeability a key step in the inflammatory process?

A

allows for the passage of exudates (protein cell rich fluid) into the interstitial space

results in accumulation of blood in the area of dilation

allow for accumulation of platelets and neutrophils at site of injury

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11
Q

what WBCs respond during inflammation? Which one is the most important?

A
  1. neutrophils (most important)
  2. monocytes/monophages
  3. eosinophils
  4. basophils
  5. lymphocytes
  6. Mast cells
  7. langerhan cells
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12
Q

what is chemotaxis?

A

signaling molecules that tell WBCs to stop at the injury site

include:

  • interleukin-8 (IL-8)
  • C5a
  • fMLP
  • Leukotriene B4
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13
Q

what is diapedesis?

A

migration of WBCs through the endothelial lining of blood vessels

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14
Q

where are neutrophils the predominant cell?

A

predominant cell in pus

predominant leukocyte in area of injury for ~24 hrs

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15
Q

what is the role of monocytes in actue inflammation?

A

in response to inflammation signals, move to site of tissue injury and differentiate into macrophages and dendritic cells

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16
Q

what is the role of macrophages in acute inflammation?

A

these are a type of WBC that engulf and digest cellular debris, foreign substances, microbes, and cancer cells

when they arrive, actue inflammation will stop shortly after

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17
Q

what type of WBC produces antibodies?

A

lymphocytes

not included in WBC count

found in lymph

18
Q

what is the role of mast cells during acute inflammation?

A

release histamines, serotonin, thromboxane, prostaglandins, leukotrienes, platelet activating factor, cytokines, TNF alpha

19
Q

Describe how the inflammatory process goes wrong during RA

A
  1. increased TNF release from leukocytes entering due to increased synovial cell multiplication results in swollen synovium
  2. this attracts other WBCs which phagocytize the immune complexes
  3. causes the relase of metalloproteases which degrade cartilage
  4. causes inhibition of bone formation and stimulation of bone reabsorption
  5. results in formation of a pannus
20
Q

what cytokine is central to many inflammatory responses?

what cell produces it

what does it do?

A

TNF

secreted by macrophages, mast cells, and T-lymphocytes

stimulates macrophages to produce cytotoxic molecules

21
Q

list some ways inflammation can result in collateral damage to other tissues

A
  1. lack of specificity in immune response
  2. lysosomal enzymes
  3. free radicals/oxygen metabolites
  4. vascular damage to allow diapedesis
  5. phagocytosis of local cells
22
Q

List the systemic effects of acute inflammation

A
  1. fever
  2. somnolence, malaise
  3. anorexia
  4. hypotension
  5. accelerated degradation of skeletal muscle
  6. reflect increased circulating levels of IL-1, IL-6, and TNF
23
Q

define leukocytosis

A

increased WBC count

normal = 4000 - 10000 cells/ul

may increase to 15000-20000 cells/ul

24
Q

define leukopenia

A

decreased WBC count

25
Q

how is inflammation resolved?

A
  1. cells producing pro-inflammatory molecules produce and secrete “stop signals” or anti-inflammatory cytokines
  2. results in reduced production of signaling molecules (negative feedback loop)
  3. cells producing pro-inflammatory molecuels die
  4. as inflammation slows, tissue repair begins
26
Q

what is difference between M1 and M2 macrophages?

A

M1 = encourage inflammation

M2 = anti-inflammatory and encourage tissue repair

27
Q

what is the only cardinal sign of inflammation in an neutropenic disease?

A

fever

28
Q

what are the possible outcomes of acute inflammation?

A
  1. resolution
  2. healing by fibrosis
  3. chronic inflammation
29
Q

what must occur in order for complete resolution following an acute inflammatory response?

A

no damage to the CT framework or non-recoverable cells of any part of the body

the intracellular matrix acts as a scaffolding so it serves as a foundation for resolution, unless it has been damaged → results in scar tissue development

30
Q

how is healing by fibrosis/scarring a possible outcome for an inflammatory episode?

A

the preinjury tissue is replaced by CT because there has been damage to the parenchymal cells

since there aren’t enough parenchymal cells, CT fills in the gaps

31
Q

when you see a scar, what would you assume the intracellular matrix looks like?

A

disorganized with changes from the norm

32
Q

how can an inflammatory episode result in chronic inflammation?

A

if the neutrophils and their fast-acting molecular allies cannot remove the noxious agent there is prolonged inflammatory response

end result is continuous tissue injury with ongoing attempts at repair

33
Q

what is a hallmark tissue characteristic in chronic inflammation?

A

the tissue is infiltrated with macrophages, lymphocytes, and plasma cells

neutrophils are largely absent

34
Q

what is granulomatous inflammation?

A

a form of chronic inflammation

caused by aggregation of macrophages

TB is a type

sometimes presens with a central abscess

35
Q

compare the onset of acute vs chronic inflammation

A
  1. Acute = fast-minutes to hours
  2. Chronic = days
36
Q

compare the cellular infiltrates in acute vs chronic inflammation

A
  1. acute = mainly neutrophils
  2. chronic = monocytes/macrophages, lymphocytes
37
Q

compare the tissue injury and fibrosis formation in acute vs chronic inflammation

A
  1. acute = usually mild and self limited
  2. chronic = often severe and progressive
38
Q

compare the local and systemic signs of acute vs chronic inflammation

A
  1. acute = prominent
  2. chronic = less prominent, may be subtle
39
Q

how is diabetes related to chronic inflammation?

A
  1. adipose tissue, liver, muscle and pancreas are sites of inflammation in the presence of obesity
  2. this increases activity of pro-inflammatory cells which increases the release of pro-inflammatory-signaling molecules into the blood stream
  3. pro-inflammatory signaling molecules interfere with insulin signaling and damage pancreatic ß cells
  4. result is diabetes
40
Q

T/F: heart disease has no relation to chronic inflammation

A

FALSE
it is increasingly viewed as an inflammatory disease

Pathophysiology (18 decks)

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