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PDA Block 2 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation and why is it important to use drugs to treat inflammation?

A
  • body’s mechanism for handling agents that could
    damage it
  • protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces
  • can be potentially damaging and thus is tightly regulated
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2
Q

Cardinal Signs of Acute Inflammation:

A
  • Rubor (red discoloration), calor (heat), dolor (pain), tumor (mass effect), and loss of function
  1. _​​_vasodilation
  2. increased vascular permeability
  3. recruitment of neutrophils
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3
Q

CHRONIC Inflammation:

A
  1. prolonged duration - weeks, months, or even indefinitely
  2. participation by lymphocytes, plasma cells, macrophages, fibroblasts and angioblasts
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4
Q

Potential harmful effects of inflammation include:

A
  • inflammatory cells release lysosomal enzymes (collagenases and proteases)
    • may digest normal tissue
  • inflammatory swelling may result in death:
    • swelling that obstructs airways
    • swelling within the cranial cavity
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5
Q

“Mediator Theory”:

A

Definition: signs and symptoms of inflammation are caused by the release of chemicals

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6
Q

Name the inflammatory mediators:

A
  1. Histamine
  2. Bradykinin
  3. Complement System
  4. C-Reactive Protein
  5. Cytokines
    • TNF-α
    • IL-1 (IL-α & IL-ß)
  6. Adenosine
  7. Cell-Adhesion Molecules
  8. Oxygen-derived free radicals
  9. Lipid Mediators
    • Prostaglandins
    • Leukotrienes
    • Steroids
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7
Q

HISTAMINE:

  • **Cellular source: **
  • Physiological response:
  • Mechanism:
  • **Pharmacology: **
A

biogenic amine

  • Cellular source: mast cells, basophils
  • Physiological response:
    1. vasodilation
    2. increased vascular permeability
    3. pain
  • Mechanism: Activation of GPCRs
  • Pharmacology: antihistamines (H1 antagonists)
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8
Q

BRADYKININ:

  • **Cellular source: **
  • Physiological response:
  • Mechanism:
  • Pharmacology:
A

peptide

  • Cellular source: endothelial cells
  • Physiological response:
    1. vasodilation
    2. increased microvessel permeability
    3. pain
  • Mechanism: Activation of GPCRs
  • Pharmacology:
    1. BK2 receptor antagonist Icatibant
    2. symptoms of localized swelling, inflammation, and pain
    3. Treatment of acute attacks of the hereditary angioedema (HAE) associated with increased production of bradykinin
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9
Q

COMPLEMENT SYSTEM:

  • Cellular Source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

plasma proteins

  • Cellular Source: synthesized by liver, circulate in blood
  • Physiological Response:
    1. Chemotaxis: recruitment of inflammatory cells to site of injury
    2. promote release of mediators from neutrophil
    3. increase vascular permeability
    4. excessive activation may contribute to tissue injury
  • Mechanism:
    • complement protein complexes cause osmotic lysis
    • activation of GPCRs
  • Pharmacology: Eculizumab, micrococept
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10
Q

C-REACTIVE PROTEIN:

  • Cellular Source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

plasma protein

  • Cellular Source: produced in liver in response to cytokines, also produced in adipocytes
  • Physiological Response:
    1. “acute-phase reactant”
    2. activates complement cascade
    3. mediates phagocytosis
    4. “marker of inflammation”
  • Mechanism: bind to phospholipids in bacteria and damaged cells
    • may be specific receptors in macrophages
  • Pharmacology:
    • Elevated CRP may be associated with increased risk of diabetes, hypertension and cardiovascular disease.
    • Drugs like statins may be effective in patients with elevated CRP.
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11
Q

CYTOKINES:

  • Cellular Source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

secreted proteins, in particular the pro-inflammatory cytokines: Interleukin-1 (IL-α and IL-β) and Tumor Necrosis Factor-α (TNF−α)

  • Cellular Source: nearly all inflammatory cells
  • Physiological Response:
    1. TNF-α: acute phase reaction, fever, sepsis
    2. IL-1: acute phase reaction, fibroblast and lymphocyte proliferation, fever
  • Mechanism: Bind to specific receptor proteins to induce gene expression of number of proteins via activation of NFκB and AP-1
    • increase cyclooxygenase (fever) and lipoxygenases
    • increase adhesion molecule expression
    • induce collagenase (fibrosis)
  • Pharmacology:
    1. Etanercept (Enbrel®)
    2. Infliximab (Remicade®)
    3. Anakinra
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12
Q

ADENOSINE:

  • Cellular Source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

purine nucleoside formed from breakdown of ATP

  • Cellular Source: all cells
  • Physiological Response:
    1. increased extracellularly during injury (anti-inflammatory)
    2. inhibit cytokine action
  • Mechanism: activation of GPCRs
  • Pharmacology:
    • Adenosine A2 agonists
    • Methotrexate: used to treat rheumatoid
    • arthritis; folic acid antagonist; also releases adenosine
    • Adenosine A3??
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13
Q

CELL ADHESION MOLECULES:

  • Cellular Source:
  • Physiological Response:
  • Mechanism:
  • Pharmcology:
A

family of proteins

  • Cellular source: endothelial cells, platelets, leukocytes
  • Physiological Response:
    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
  • Mechanism: “contact molecules”, calcium dependent
  • Pharmacology: Abciximab (Reopro®), Natalizumab (Tysabri®)
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14
Q

OXYGEN-DERIVED FREE RADICALS:

  • Cellular Source:
  • Pysiological Response:
  • Mechanism:
  • Pharmacology:
A

superoxide, hydroxy radicals

  • Cellular Source: all cells
  • Physiological Response:
    • intracellular killing of bacteria by neutrophils
  • Mechanisms:
    • protein oxidation
    • lipid peroxidation
    • DNA mutations
  • Pharmacology: anti-oxidants like Vitamin C and E
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15
Q

PROSTAGLANDINS:

  • Cellular source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A
  • Cellular source: virtually all cells
  • Physiological Response:
    1. vasodilation/vasoconstriction
    2. pain
    3. fever
    4. platelet aggregation (via thromboxane)
  • Mechanism: activation of specific GPCRs
  • Pharmacology: NSAIDS
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16
Q

LEUKOTRIENES:

  • Cellular source:
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

LEUKOTRIENES

  • Cellular source: macrophages, neutrophils
  • Physiological Response:
    1. increase vascular permeability
    2. bronchoconstriction
  • Mechanism: activation of GPCRs
  • Pharmacology:
    • 5-lipoxygenase inhibitors (Zileuton)
    • cys-leukotriene receptor antagonists (Zafirlukast)
17
Q

GLUCOCORTICOIDS:

  • **Cellular Source: **
  • Physiological Response:
  • Mechanism:
  • Pharmacology:
A

GLUCOCORTICOIDS

  • Cellular Source: adrenal cortex
  • Physiological Response:
    1. inhibition of cytokines
    2. inhibition of phospholipase A2 (via annexin/lipocortin)
    3. inhibition of COX-2
    4. inhibition of CAMs
  • Mechanism: activation of nuclear receptors
  • Pharmacology:
    • steroids most potent and effective agents for controlling chronic inflammatory diseases
    • example: inhaled steroids as first-line treatment for chronic asthma
18
Q

Anti-Inflammatory Drugs:

Steroids

A
  • Mechanism of action: bind to cytoplasmic receptors
  • activated receptor-steroid complex:
    • localizes to nucleus/binds DNA (GREs) transcription of certain target genes (induction or repression)
  • most patients with chronic inflammatory conditions respond to steroids
  • small minority of patients are steroid-resistant
  • limitations to use are side effects
19
Q

Anti-Inflammatory Drugs:

NSAIDS

A
  • Mechanism of action: inhibition of cyclooxygenase
    • probably the most widely used medications in the world
20
Q

Anti-Inflammatory Drugs:

  1. Leukotrienes Receptor Antaognist:
  2. Leukotriene Synthesis Inhibtors:
A
  1. Leukotrienes Receptor Antaognist:
    • **​zafirlukast (Accolate®): competitive antagonist **
  2. ​Leukotriene Synthesis Inhibitors:** **zileuton (Zyflo®)
21
Q

Anti-Inflammatory Drugs:

Cytokine Inhibitors

A
  1. etanercept
  2. infliximab

PDA Block 2 (15 decks)

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