Lecture 6: Systemic Features of Inflammation, Chronic Inflammation Flashcards

(32 cards)

1
Q

What regulates temperature/fever?

A

Preoptic area of hypothalamus (autonomic nervous system)

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2
Q

What does a higher temperature do in fever?

A

Enhance metabolism of neutrophils / inflammatory cell function, kill bacteria (?), increase phagocytosis (?)

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3
Q

What is nonpyrogenic hyperthermia?

A

Regulatory set point unchanged; physiologic mechanisms can’t dissipate heat

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4
Q

What causes nonpyrogenic hyperthermia?

A

Heat stroke (temperatures), increased head production, exercise/seizure/metabolic disorders, malfunctioning regulatory center (CNS lesion)

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5
Q

What is pyrogenic hyperthermia?

A

Change in thermoregulatory set-point in hypothalamus

Macrophages stimulated to release IL-1, TNF, IL-6 (endogenous pyrogens) –> local production of PG in hypothalamus

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6
Q

What are examples of pyrogens?

A

Toxins from bacteria, inflammation, immune response, cancer, some pharmacologic agents, viruses

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7
Q

What is thought to be a life-threatening fever?

A

Above 105.8 F

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8
Q

Adverse effects of fever:

A

Inactivity, anorexia, discomfort, seizures

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9
Q

What does acetaminophen do?

A

Block COX-3

  • Reduce fever centrally in hypothalamus
  • Inhibit central pain signals in brain

Works faster than ibuprofen for fever

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10
Q

What does ibuprofen do?

A
  • Decrease inflammation, and therefore pain
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11
Q

What causes lymphadenitis?

A

Inflammatory mediators, debris, infectious organisms draining into nodes

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12
Q

What is lymphangitis?

A

Inflammation of lymphatic channels; characterized by red streaks

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13
Q

What are acute phase proteins?

A

Proteins that appear in plasma early in inflammation; not normally present, or present in low amounts.

IL-1, TNF, and IL-6 increase production of these in the LIVER.

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14
Q

List some examples of acute phase proteins.

A

Fibrinogen, serum amyloid A, C-reactive protein, C3, haptoglobin

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15
Q

What is C-reactive protein?

A

Bind to cell surfaces to increase binding of complement proteins/bacteria

  • activate alternative pathway
  • indicate chronic inflammation
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16
Q

What inhibits inflammatory reaction?

A

alpha1-antitrypsin

17
Q

What is serum amyloid A (SAA)?

A

Acute phase protein, may be involved in secondary amyloidosis (chronic diseases)

18
Q

What is increased erythrocyte sedimentation rate?

A

Red cells fall more quickly with settling of blood in inflammation
- presence of increased fibrinogen

Indicator of chronic inflammatory disease (like lupus)

19
Q

What is leukocytosis?

A

Increases in leukocytes (primarily neutrophils) in infection (primarily bacterial, sometimes infarction)

20
Q

What are reasons for leukocytosis?

A
  • Marginated cells are stimulated by IL-1, TNF, IL-6 (and IL-8)
  • Increase in synthesis (CSF)
  • Early release from marrow (immature - bands)
21
Q

Lymphocytosis is seen in _______

A

viral infections

22
Q

Leukocytosis is a _____ fold increase usually seen in _____ hours

23
Q

What is the numerical mark for leukocytosis?

A

Total white count > 10,000

Neutrophils > 80% (8000)

Increase in bands (

24
Q

What does an increase in eosinophils look like and mean?

A

Allergies/parasites

> 5% of differential count or >500 per microliter

25
What increases eosinophils?
IL-5 (Th1 response with increased IgE due to IL-4)
26
What hypersensitivity is associated with eosinophils?
Type I Collect at sites due to chemokines from mast cells along with histamine
27
What are examples of pathology that is systemic inflammation?
Septic shock, SIRS (systemic inflammatory response syndrome), vascular leak syndrome, DIC, anaphylaxis
28
How is inflammation resolved?
- Apoptosis of neutrophils - Anti-inflammatory mediators - Removal of debris
29
What are some anti-inflammatory mediators?
Lipoxins, resolvins, protectins, acute phase reactants
30
3 outcomes for inflammation:
- complete resolution - healing and regeneration - chronic inflammation
31
What continues inflammation in the chronic state?
Macrophages - continue to stimulate immune response, especially with persistent antigen
32
What causes fibrosis?
Fibroblasts from chronic macrophage activation; collagen formation and cross-linking Scar tissue