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Pharmacology Block 2 > 01 Inflammation > Flashcards

01 Inflammation Flashcards

1
Q

Protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces

A

Inflammation

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2
Q

Restores homeostatic balance, fights disease, and drives wound-healing responses

A

“Little” Inflammation

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3
Q

Results in pathologic conditions such as asthma, rheumatoid arthritis, inflammatory bowel diseases, gout, atherosclerosis, and possibly cancer.

A

“Lot of” Inflammation

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4
Q

Cardinal Signs of Acute Inflammation

A
  • Rubor (red discoloration)
  • Calor (heat)
  • Dolor (pain)
  • Tumor (mass effect)
  • Loss of function
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5
Q

Physiological Effects of Acute Inflammation

A
  • Vasodilation
  • Increased vascular permeability
  • Recruitment of neutrophils

EDEMA

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6
Q

What causes these physiological effects?

  • Vasodilation
  • Increased vascular permeability
  • Recruitment of neutrophils
  • Edema
A

Acute Inflammation

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7
Q

What causes acute inflammation

A

microbial infection, physical agent, irritants/corrosive chemicals, tissue necrosis

Action via PMNs

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8
Q

What is the cause of chronic inflammation?

A

persistence of irritant, endogenous antigen or “factor”

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9
Q

Persistence of irritant endogenous antigen or “factor” can lead to what?

A

Chronic Inflammation

Leads to upregulation of damage/apoptosis and auto-amplification of the inflammatory response

Fibrosis

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10
Q

What are the harmful effects of inflammation?

A
  • Release of lysosomal enzymes (collagenases and proteases) may digest normal tissue
  • Inflammatory swelling may result in death from obstructing airways or swelling within the cranial cavity
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11
Q

Mediator Theory

A

signs and symptoms of inflammation are caused by the release of chemicals (mediators) from inflammatory and structural cells

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12
Q

Histamine

A

Inflammatory Mediator

Biogenic amine

Source: Mast cells, basophils

Phys:

  • vasodilation
  • increased vascular permeability
  • pain

Mech: GPCR activation

Tx: Antihistamines (H1 antagonists)

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13
Q

What inflammatory mediator is released specifically from mast cells and basophils?

A

Histamine

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14
Q

What inflammatory mediators causes:

  • vasodilation
  • increased vascular/microvessel permeability
  • pain
A

Histamine and Bradykinin

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15
Q

Bradykinin

A

Inflammatory mediator

Peptide

Source: Endothelial cells
- activated by tissue injury, allergic reactions, viral infections

Phys:

  • vasodilation
  • increased microvessel permeability
  • pain

Mech: GPCR activation

Tx: BK receptor antagonist

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16
Q

What causes increased microvessel permeability?

A

Bradykinin

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17
Q

Complement System (Inflammatory Mediator)

A

Plasma proteins

Source: Synthesized by liver, circulates in blood

Phys:

  1. Chemotaxis
  2. Promote release of mediators from neutrophils
  3. Increase vascular permeability
  4. Excessive activation leads to tissue injury

Mech:

  • Aggregate to cell surface and cause osmotic lysis
  • GPCR activation

Tx:

  • Eculizumab inhibits C5 cleavage
  • APT070 is a truncated CR1 which regulates overproduction of completment
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18
Q

What inflammatory mediators increase vascular permeability?

A

Histamine and Complement System

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19
Q

What inflammatory mediator causes chemotaxis?

A

Complement System

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20
Q

What inflammatory mediator promotes the release of mediators from neutrophils?

A

Complement System

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21
Q

What inflammatory mediator with excessive activation can contribute to tissue injury?

A

Complement System

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22
Q

C-Reactive Protein

A

Inflammatory Mediator

Plasma Protein

Source: Synthesized in liver and adipocytes in response to cytokines

Phys:

  1. Acute phase reactant
  2. Activates complement cascade
  3. Mediates phagocytosis
  4. Marker of inflammation

Mech: bind to phospholipids in bacteria and damaged cells (Ca2+ dependent)

Tx: Elevated CRP associated with inc risk of DM, HTN, CV disease. Statins may be effective.

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23
Q

What inflammatory mediator is produced in the liver in response to cytokines as well as in adipocytes?

A

C-Reactive Protein

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24
Q

What inflammatory mediators are an acute phase reactant?

A

C-Reactive Protein and cytokines TNF−α and IL−1

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25
Q

What inflammatory mediator activates complement cascade?

A

C-Reactive Protein

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26
Q

What inflammatory mediator mediates phagocytosis?

A

C-Reactive Protein

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27
Q

What inflammatory mediator is a marker of inflammation?

A

C-Reactive Protein

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28
Q

What inflammatory mediator binds to phospholipids in bacteria and damaged cells?

A

C-Reactive Protein

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29
Q

An elevated level of what inflammatory mediator is associated with an inc risk of DM, HTN, and CV disease?

A

C-Reactive Protein

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30
Q

Cytokines

A

Inflammatory Mediator

Proinflammatory cytokines: Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

Source: nearly all inflammatory cells

Phys:

  1. TNF−α: acute phase reaction, fever, sepsis
  2. IL−1: acute phase reaction, fibroblast and lymphocyte proliferation, fever

Mech: Induce gene expression of many proteins via NFkB and AP-1

  • increase cyclooxygenase (fever) and lipoxygenase
  • increase adhesion molecule expression
  • induce collagenase (fibrosis)

Tx:

  • Entanercept
  • Infliximab
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31
Q

What are the proinflammatory cytokines?

A

Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

32
Q

What inflammatory mediator causes acute phase reaction, fever, and sepsis?

33
Q

What inflammatory mediator causes acute phase reaction, fibroblast and lymphocyte proliferation, and fever?

A

Interleukin-1

34
Q

What inflammatory mediator causes the activation of NFkB and AP-1?

A

Proinflammatory cytokines: Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

35
Q

What is the result of activating NFkB and AP-1 by Interleukin-1 TNF−α?

A

Increase cyclooxygenase (fever) and lipoxygenase
Increase adhesion molecule expression
Induce collagenase

36
Q

What is treated with Etanercept or Infliximab?

A

Pro-inflammatory cytokines Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

37
Q

What causes an increase in cyclooxygenases (fever) and lipoxygenases?

A

Activation of NFkB and AP-1 by pro-inflammatory cytokines Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

38
Q

What inflammatory mediators induce collagenase (fibrosis)?

A

Activation of NFkB and AP-1 by pro-inflammatory cytokines Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

39
Q

Adenosine

A

Inflammatory Mediator

Purine nucleoside formed from ATP breakdown

Source: all cells

Phys:

  1. Anti-inflammatory: Increased extracellulary during injury
  2. Inhibits cytokine action

Mech: GPCR activation

Tx: Adenosine A2 agonists

40
Q

What inflammatory mediator is increases extracellularly during injury?

A

Adenosine (anti-inflammatory)

41
Q

What inflammatory mediator inhibits cytokine action?

A

Adenosine (anti-inflammatory) and glucocorticoids

42
Q

Cell Adhesion Molecules (CAMs)

A

Inflammatory Mediator

Family of Proteins

Source: endothelial cells, platelets, leukocytes

Phys:

  1. Leukocyte adhesion to endothelium is a pivotal event in host defense and tissue repair
  2. Endothelial adhesion molecules contribute to recruitment of activated platelets

Mech: “contact molecules” calcium dependent

Tx: Abciximab or Natalizumab

42
Q

What inflammatory mediator causes leukocyte adhesion to endothelium?

A

Cell Adhesion Molecules

42
Q

What inflammatory mediator contributes to recruitment of activated platelets?

A

Endothelial (Cell) adhesion molecules

42
Q

Oxygen-Derived Free Radicals

A

Superoxide, hydroxy radicals

Source: all cells

Phys: Intracellular killing of bacterial by neutrophils

Mech:

  • protein oxidation
  • lipid peroxidation
  • DNA mutations

Tx: anti-oxidants Vit C and E

42
Q

What inflammatory mediator causes intracellular killing of bacteria by neutrophils?

A

Oxygen-derived free radicals

42
Q

What inflammatory mediator works via protein oxidation, lipid peroxidation, and DNA mutations?

A

Oxygen-Derived Free radicals

42
Q

What are the lipid inflammatory mediators?

A

Prostaglandins, Leukotrienes, and Glucocorticoids

42
Q

Prostaglandin

A

Lipid Inflammatory Mediator

Eicosanoids, Steroids

Source: virtually all cells

Phys:

  1. Vasodilation/vasoconstriction
  2. Pain
  3. Fever
  4. Platelet aggregation (via thromboxane)

Mech: GPCR activation

Tx: NSAIDs

42
Q

What inflammatory mediator causes:

  1. Vasodilation/vasoconstriction
  2. Pain
  3. Fever
  4. Platelet aggregation (via thromboxane)
A

Prostaglandin (Lipid mediator)

42
Q

What inflammatory mediator is treatment for chronic inflammatory diseases?

A

Glucocorticoids

43
Q

What inflammatory mediator is treated with NSAIDs?

A

Prostaglandins (Lipid mediator)

43
Q

Leukotriene

A

Lipid inflammatory mediator

Source: macrophages, neutrophils

Phys:

  1. Inc vascular permeability
  2. Bronchoconstriction

Mech: GPCR activation

Tx:

  • Zileuton (5-lipoxygenase inhibitor)
  • Zafirlukast (cys-leukotriene receptor antagonist)
43
Q

What inflammatory mediator causes:

  1. Inc vasc permeability
  2. Bronchoconstriction
A

Leukotrienes (lipid mediator)

43
Q

5-lipoxygenase inhibitor

A

Zileuton (Tx of leukotriene)

43
Q

Cys-leukotriene receptor antagonist

A

Zafirlukast (Tx of leukotriene)

43
Q

Glucocorticoids

A

Lipid inflammatory mediator

Source: Adrenal cortex

Phys:

  1. Inhibition of cytokines
  2. inhibition of phospholipase A2
  3. inhibition of cyclooxygenase-2
  4. inhibition of cell adhesion molecules

Mech: nuclear receptor activation

Tx: Steroids (controlling chronic inflammatory diseases)

44
Q

What inflammatory mediator inhibits cyclooxygenase-2?

A

Glucocorticoids (lipid mediator)

45
Q

What inflammatory mediator inhibits cell adhesion molecules?

A

Glucocorticoids (lipid mediator)

60
Q

What inflammatory mediator is used to treat chronic inflammatory diseases?

A

Glucocorticoids

61
Q

What is the mechanism of steroids (glucocorticoids)?

A

Bind to cytoplasmic receptors

activated receptor-steroid complex localizes to nucleus/binds DNA (glucocorticoid response elements) resulting transcription of certain target genes (induction or repression)

Inhibits cytokines, protaglandins, leukotrienes, cell adhesion molecules

62
Q

What is the mechanism of action of non-steroidal anti-inflammatory drugs?

A

Inhibition of cyclooxygenase

63
Q

Leukotriene Antagonists

A

Zafirlukast

Zileuton

64
Q

Zafirlukast

A

competitive antagonist of leukotriene receptors

65
Q

Zileuton

A

Inhibits the synthesis of leukotrienes

66
Q

Inflammatory Cytokine Inhibitors

A

Etanercept

Infliximab

67
Q

What is the Acute Phase Reaction?

A

In response to injury, local inflammatory cells secrete cytokines that cause the liver to increase or decrease production of various proteins

68
Q

What mediator contributes to signs and symptoms of inflammations (pain, fever, vasoactive effects)?

A

Prostaglandins

69
Q

What mediator directly increases blood flow and indirectly enhances edema formation and leukocyte infiltration?

A

Prostaglandins

70
Q

What mediator releases slow reacting substance of anaphylaxis (SRS-A) from mast cells?

A

Leukotrienes

71
Q

What mediator is increased in allergies/asthma?

A

Leukotrienes

72
Q

What mediator causes vasodilation?

A

Prostaglandins

73
Q

What mediator causes increased vascular permeability?

A

Vasoactive amines
Complement Proteins
Bradykinin
Leukotriene

74
Q

What mediator causes chemotaxis?

A

Complement Protein

Leukotrienes

75
Q

What mediator causes fever?

A

Cytokines IL-1 and TNF-alpha

Prostaglandins

76
Q

What mediator causes pain?

A

Prostaglandins and Bradykinin

77
Q

What mediator causes tissues damage?

A

Neutrophil and macrophage lysosomal enzymes

Oxygen metabolites

Pharmacology Block 2 (12 decks)

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