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S3 - Pathophysiology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

INFLAMMATION: PART 1

A

INFLAMMATION: PART 1

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2
Q

Inflammation is coordinated ________ and ________ response of the body to cell injury and cell death.

A

vascular and cellular

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3
Q

Does inflammation have protective (immune) or curative features?

A

Both

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4
Q

Inflammation initiates the healing process and is responsible for the removal of what?

A
  • injurious agent

- cellular debris

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5
Q

Is inflammation the equivalent of an infection?

A

No, associate it with tissue injury

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6
Q

Can we heal and have a normal immune function without an inflammatory response?

A

No

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7
Q

What is a type of drug that reduces inflammation by being a “immune suppressive drug”?

A

Glucocorticoids

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8
Q

What are some pathologies where inflammation can “run amok”?

A
  • RA, Lupus, or SLE
  • Obesity
  • Crohn’s Disease
  • Type I Diabetes
  • Asthma
  • Cancer
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9
Q

What are factors leading to inflammation?

A
  • Infection
  • Trauma/damaged tissue (physical or chemical)
  • Tissue necrosis
  • Presence of foreign bodies
  • Immune reactions
  • Ischemia
  • Cancer
  • Chemicals
  • Physical Agents (heat/cold, radiation)
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10
Q

What are the 3 goals of an inflammatory response?

A
  1. ) Inactivate injurious agents
  2. ) Break down and remove dead cells and other cellular debris
  3. ) Initiate tissue healing
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11
Q

What are some key components of inflammation?

A
  • blood vessels
  • circulating blood cells
  • connective or interstitial tissue cells (fibroblasts, mast cells, and resident macrophages)
  • chemical mediators
  • specific extracellular matrix constituents, primarily collagen and basement membrane
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12
Q

*What are the 5 Cardinal Signs/Symptoms of Inflammation?

A
  • Erythema (redness)
  • Heat
  • Edema
  • Pain
  • Loss of Function
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13
Q

What events cause erythema?

A

Vasodilation and increased blood flow

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14
Q

What events cause heat?

A

Vasodilation and increased blood flow

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15
Q

What events cause edema?

A

Fluid and cells leaking from local blood vessels into the extravascular spaces

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16
Q

What events cause pain?

A
  • Direct trauma
  • Chemical mediation by bradykinins, histamines, serotonin
  • Internal pressure secondary to edema
  • Swelling of nerve endings
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17
Q
  • Is inflammation capable of destroying and damaging normal tissue?
  • What is the response to this?
A
  • Yes (collateral damage)

- Inflammation is TIGHTLY REGULATED to avoid excess tissue damage and spillover to normal tissue.

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18
Q

What events are the hallmark of inflammation?

A

Vascular

  • Vasodilation
  • Vascular Permeability
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19
Q

Vasodilation:

  • _________ diameter of the small vessels in the area of injury.
  • Brings more ___________ and _________ to the area.
  • Induced by _________ release from platelets and mast cells causing smooth muscle relaxation.
  • Explains ______ and _______ at site of injury.
A
  • increased
  • plasma proteins and leukocytes
  • histamine
  • heat and redness
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20
Q

Increased Vascular Permeability:

  • Smaller arterioles become “leaky” or __________.
  • Allows for the passage of a protein and cell rich fluid (________) into the interstitial spaces (IS)
  • Also results in accumulation of blood in the area of dilation and stasis resulting in localized _______ at the site and allow for accumulation of ______ and _______ at site of injury.
A
  • permeable
  • exudate
  • redness, platelets and neutrophils
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21
Q

INFLAMMATION: PART 2

A

INFLAMMATION: PART 2

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22
Q

What type of cells are involved in the inflammatory response?

A

WBC (Leukocytes)

  • Neutrophils
  • Monocytes/Macrophages
  • Eosinophils
  • Basophils
  • Lymphocytes
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23
Q

What type of cells are the first responders and are recruited within minutes on an injury?

A

Neutrophils

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24
Q
  • What directs the movement of neutrophils to an injury?

- What are some examples?

A
  • Chemotaxis

- IL-8, C5a, fMLP, Leukotrine B4

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25
Q

What is diapedesis in regards to neutrophil movement?

A

Migration of blood cells through the endothelial lining of blood vessels (in response to inflammation)

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26
Q

What is the predominant cell type found in “pus” and in the area of injury for about 24 hours?

A

neutrophils

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27
Q

What type of WBC circulates in the blood and replenishes resident macrophages by differentiation?

A

Monocytes

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28
Q

What type of WBC engulfs and digests debris, foreign substances, mibrobes, and cancer cells? It is found in blood as mature and immature cells (monocytes).

A

Macrophages

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29
Q

What are some tissue specific macrophages?

A
  • Langerhans- skin
  • Kupffer cells- liver
  • Alveolar macrophage
  • Microglia- CNS
30
Q

What type of WBC produces antibodies?

A

Lymphocytes

31
Q

What cell type plays a key role in the inflammatory process and contains large granules which hold several preformed immune mediators such as histamines, serotonin, thromboxane, prostoglandins, leukotrine, platelet activating factor, and TNF alpha.

A

Mast cells

Think antihistamines!

32
Q

Inflammation has a lot of complex processes. How are they controlled?

A
  • Pro-inflammatory signaling molecules

- Anti-inflammatory signaling molecules

33
Q

The inflammatory response occurs ________ to terminate infection. It also must halt in a timely manner to stop this reaction from inflicting _____ damage.

A
  • rapidly

- self damage

34
Q

What is the pathology of RA?

A

-Synovial cell multiply in number, influx of leukocytes from the peripheral circulation and synovium becomes edematous

35
Q

In RA, TNF increases to cause a _______ inflammatory response. This attracts leukocytes, monocytes, and lymphocytes which phagocytize the immune complexes. This causes the release of _____________ which degrades cartilage as well as inhibits bone formation and stimulates bone resorption. Results in a structure called the _______.

A
  • massive
  • metalloproteases
  • pannus
36
Q

TNF is a cytokine central to many aspects of the inflammatory response and is secreted by _________, ____ cells, and _-__________.

A
  • macrophages
  • mast
  • T-lymphocytes
37
Q

What are a few examples of Anti-TNF compounds to moderate inflammation?

A
  • Adalimumab (Humira)
  • Etanercept (Enbrel)
  • Infliximab (Remicade)
38
Q

What are some Non-TNF boilogics to moderate inflammatory response?

A
  • Tocilizumab (Actemar)

- Anakinra (Kineret)

39
Q

Why are patients receiving anti-inflammatory drugs at increased risk for developing a serious infection and are tested for the presence of TB?

A

Glucocorticoids are immune suppressive

40
Q

What are some systemic effects of acute inflammation?

A
  • Fever
  • Somnolence, malaise
  • Anorexia
  • Hypotension
  • Accelerated degradation of skeletal muscle
  • Reflect increases circulating levels of IL-1, IL-6, TNF
41
Q
  • What is an increase in WBC count called?

- What is normal WBC count?

A
  • Leukocytosis

- 4000-10000 cells/ul

42
Q

What is a decrease in WBC count called?

A

-Leukopenia

43
Q

INFLAMMATION: PART 3

A

INFLAMMATION: PART 3

44
Q

Is inflammation a positive or negative feedback system?

A

positive feedback system

45
Q
  • Pro inflammatory signaling molecules are involved in controlling inflammation. These molecules have ______ half-lives and are rapidly degraded.
  • Large concentrations of pro-inflammatory signaling molecules leads to a reduction in amount of pro-inflammatory signaling molecules (__________ feedback system).
A
  • short

- negative

46
Q

Cells producing pro-inflammatory molecules produce and secrete “___________” or anti-inflammatory cytokines.

A

Stop Signals

-IL-4,10,11,13 and TGF-beta (macrophages)

47
Q

As inflammation slows, what begins?

A

tissue repair

48
Q

M1 macrophages ________ inflammation. They are first on the scene.

A

encourage (pro-inflammatory)

49
Q

M2 macrophages are _____-inflammatory and encourage what?

A
  • anti-inflammatory

- tissue repair

50
Q

What are some neutrophil pathologies?

A
  • deficits in numbers (neutropenia)
  • failure of neutrophils to respond to chemotactic stimuli
  • defects in the leukocyte adhesion molecules or the endothelial adhesion molecules
  • inability of neutrophils to move to injury site
  • failure of neutrophils to phagocytize properly
  • defective microbial killing
51
Q

Inflammation: Summary

  • __________
  • Increased vascular ____________
  • Accumulation of __________ and cells all contributing to the destruction of “bad guys”
  • _________ damage is part of the process
  • Plethora of signaling compounds involved in initiating the inflammatory process and “Winding down” of the inflammatory process
A
  • vasodilation
  • permeability
  • neutrophils
  • collateral
52
Q

What are some possible outcomes of an inflammatory episode?

A
  • complete resolution
  • abscess formation
  • healing by fibrosis or scarring
  • progression to chronic inflammation
53
Q

If there is complete resolution of an inflammatory episode, will there be any damage to the connective tissue framework or non-recoverable cells of any part of the body? Will normal function return as well as a clearance of injurious stimuli?

A
  • No, there will be no damage to the frameworkor cells

- Yes, normal function will return and injurious stimuli will be cleared

54
Q

If there is abscess formation, there is an accumulation of pus in a _________ space that often requires draining.

A

confined

55
Q

If there is healing by fibrosis (scarring) preinjury tissue is replaced by _________ tissue. In scarring there is a lack of __________ cells that make up the functional parts of an organ and are required for normal recovery from an injury.

A
  • connective tissue (fibrotic)

- parenchymal cells

56
Q

What are the implications of inflammation for the therapist?

A
  • Does damage healthy tissue
  • Carries with it systemic effects
  • Therapists seek to limit (RICE, OTCs)
  • Return to play
  • Can lead to chronic inflammation
57
Q

INFLAMMATION: PART 4

A

INFLAMMATION: PART 4

58
Q
  • When does progression to chronic inflammation occur?

- What is chronic inflammation characterized by?

A
  • Happens when, and only when, the neutrophils and -their fast-acting molecular allies cannot remove the noxious agent.
  • Characterized by continuous tissue injury with ongoing attempts at repair.
59
Q

What can chronic inflammation arise from?

A
  • Persistent infections or presence of foreign particles
  • Hypersensitivity diseases
  • Prolonged exposure to toxic agents (silca, cholesterol, cigarette smoke, some cancers, etc.)
60
Q

The hallmark of chronic inflammation is the tissue is infiltrated by _________, _________, and __________ (antibody producing cells) while there is an absence of ___________.

A
  • macrophages
  • lymphocytes
  • plasma cells

-neutrophils

61
Q

Attempts at healing in chronic inflammation results in ___________ and _________.

A
  • angiogenesis (growth of blood vessels)

- fibrosis

62
Q

What is a form of chronic inflammation that is caused by aggregation of macrophages?

A

Granulomatous Inflammation

63
Q

Acute vs. Chronic Inflammation:

Onset

  • Acute = __________
  • Chronic = ____________

Cellular Infiltrates

  • Acute = _____________
  • Chronic = _____________

Tissue Injury, Fibrosis

  • Acute = ____________
  • Chronic = ____________
A

Onset

  • Acute = fast- minutes to hours
  • Chronic = days

Cellular Infiltrates

  • Acute = neutrophils mainly
  • Chronic = monocytes/macrophages and lymphocytes

Tissue Injury, Fibrosis

  • Acute = usually mild and self limited
  • Chronic = often severe and progressive
64
Q

Describe chronic inflammation in Diabetes.

A
  • Increased activity of pro-inflammatory cells (macrophages)
  • Increased release of pro-inflammatory signaling molecules into the blood stream
  • These signaling molecules interfere with insulin signaling (GLUT-4) and damage pancreatic beta cells
  • Results in diabetes (Type II)
65
Q

Describe chronic inflammation in Cancer.

A
  • Tumor becomes a site of chronic inflammation and pro-inflammatory marker production
  • Tumor cells secrete pro-inflammatory markers
66
Q

What are some drugs that can control pro-inflammatory state?

A
  • Aspirin

- Celebrex

67
Q

Pro-inflammatory state is ______ wide.

A

system

68
Q
  • Can cigarette smoke induce a chronic inflammatory state?

- What about smokeless tobacco?

A
  • Yes

- Yes

69
Q

Increased levels of what are associated with an increased risk for CV events?

A

C-Reactive Protein (CRP)

70
Q

Heart disease is increasingly viewed as an ____________ disease.

A

inflammatory

S3 - Pathophysiology (14 decks)

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