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PDA Block 2 > Intro to Pharm of Inflammation > Flashcards

Intro to Pharm of Inflammation Flashcards

1
Q

Etanercept

A

inhibits cytokines

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2
Q

Infliximab

A

inhibits cytokines

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3
Q

Aspirin

A

inhibits

prostaglandins

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4
Q

NSAID

A

inhibits prostaglandins

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5
Q

Zileuton

A

inhibits leukotrienes

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6
Q

Zafirlukast

A

inhibits

leukotrienes

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7
Q

Steroid

A

inhibit cytokines,
prostaglandins, leukotrienes,
cell adhesion molecules

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8
Q

Nonsteroidal anti-inflammatory

drug

A

inhibits prostaglandins

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9
Q

What are the two reasons that Inflammation is essential to survival?

A
  1. Self Protection

2. Healing Process

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10
Q

How is inflammation involved in Self-Protection

A

to rid the organism of both the initial cause of cell injury (e.g.,
microbes, toxins) and the consequences of such injury (e.g.,
necrotic cells and tissues).

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11
Q

how is inflammation involved in the healing process

A

Repair begins during inflammation but usually isn’t complete until whatever caused the injury has been neutralized. In the process of repair the injured tissue is replaced through regeneration of native parenchymal cells and or by filling in the defect with fibrous tissue

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12
Q

Why is inflammation important in medicine?

A
  1. It can be inappropriately triggered or poorly controlled
  2. inflammation can cause tissue injury in many diseases (even though it is involved in the healing process)
  3. Inflammatory reactions underlie many common chronic conditions like rheumatoid arthritis, atherosclerosis, and lung fibrosis, maybe even type II diabetes Alzheimers and cancer
  4. Inflammatory reactions underlie life threatening hypersensitivity reactions (ex: dog bites, drugs, toxins)
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13
Q

Describe what an ideal anti-inflammatory drug would do

A

Anti-inflammatory drugs would ideally control the harmful effects of inflammation yet not interfere with its beneficial effects

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14
Q

Describe the general components of an inflammatory response

A

There are several mediators that lead to inflammation and they all have different sources, targets and responses but they all work together!

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15
Q

What are the 5 signs/components of inflammation

A
  • Calor/Heat
  • Tumor/Swelling
  • Rubor/Redness
  • Dolor/Pain
  • Loss of Function
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16
Q

Physiological Responses to ACUTE inflammation

A
  • Vasodilation
  • Increase in vascular permeability
  • Accumulation of inflammatory cells
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17
Q

What is the general relationship between acute and chronic inflammation

A

Acute inflammation may progress to chronic but Chronic can also occur on its own.

ex: Viral infections, chronic infections, persistent injury, autoimmune diseases
- A trigger occurs that leads to both acute and chronic inflammation. And acute may progress into chronic

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18
Q

Acute inflammation

A

-Rapid onset (minutes)
-Short duration (hours to a few days)
-main characteristic is edema
-main cell type:leukocytes mostly neutophils (PMNs)
-triggered by:
*infection and microbial
toxins
*tissue necrosis
(ischemia, trauma,
physical and chemical
injury (burns or frostbite),
irradiation,
exposure to some
environmental
chemicals)
*foreign bodies (splinters,
dirt, sutures)

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19
Q

Chronic Inflammation

A

-Prolonged duration
(weeks or months)
may follow acute inflammation or may begin without any manifestations of an acute reaction. — 
-Main cell type: monocyte —  -Main characteristic: fibrosis

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20
Q

What are the initiators of chronic inflammation

A 
1.Immune-mediated inflammatory
diseases
2. Prolonged exposure to potentially
toxic agents, either exogenous or
endogenous.
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21
Q

Describe Immune-mediated inflammatory diseases

A

-autoimmune diseases: rheumatoid arthritis and multiple sclerosis – -

-unregulated immune responses against microbes: inflammatory
bowel disease. – 

-Immune responses against common
environmental substances: allergic diseases, such as bronchial asthma

22
Q

Describe Prolonged exposure to potentially
toxic agents, either exogenous or
endogenous.

A

– -exogenous agent is particulate silica, when inhaled for prolonged periods, results in an inflammatory lung disease. so for example people who worked around silica could have chronic inflammation
– 
-Atherosclerosis is a chronic inflammatory process of the arterial wall induced by endogenous toxic plasma lipid components.

23
Q

Why/how does propagation of chronic inflammation usually occur

A

-acute inflammation often leads to damage/apoptosis, this causes and autoamplifying loop leading to more inflammation. More inflammation leads to more damage which leads to more inflammation etc.

-Propagation of the disease
typically occurs as a result
of an autoimmune response, inducing a self-amplifying
cycle of damage. 
-once a chronic disease is
established flares are
frequent.
24
Q

Inflammation is a defensive host response to foreign invaders and
necrotic tissue, but it is itself capable of
causing….

A

tissue damage.

25
Q

Is pharmacological intervention necessary for inflamation

A

-No. In most cases, inflammation resolves without any pharmacological intervention

26
Q

When is pharmacological intervention necessary for inflammation

A

In response to potential harmful effects of inflammation

ex:
1. a release of enzymes that digest normal tissue like collagenases in severe arthritis
2. Edema/Swelling that can obstruct airways/brain swelling

27
Q

How can you treat or prevent the underlying cause of the disease in chronic inflammatory disorders

A

considering multiple effects and mediators

28
Q

Definition of Mediator Therapy

A

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

29
Q

What can be an effective target to treat inflammation

A

mediators

30
Q

Histamine

  • Cellular source
  • Response
  • Mechanism
  • Pharmacology
  • Classification
A
  1. Cellular source:
    ◦   stored in mast cells and basophils –  Non-mast cell sources (neurons,
    cells in the stomach)
2. Response
◦  vasodilation
◦  increase vascular 
   permeability
◦  pain permeability
  1. Mechanism- Via activation of GPCR to activate a variety of signaling pathways
  2. Pharmacology:
    Antihistamine/H1 receptor
    antagonist
    - diphenhydramine
  3. Biogenic Amine
31
Q

Response to histamine

A
  1. vasodilation
  2. increase vascular permeability
  3. pain
32
Q

pharmacology of histamine

A

Antihistamine/ H1 receptor antagonist

ex: diphenhydramine

33
Q

Bradykinin

  • Cellular source
  • Response
  • Mechanism
  • Pharmacology
  • Classification
A

1.Cellular source
◦   endothelial cells
–  -Series of proteolytic reactions in tissues (kininogen metabolized by kallikrein) give rise to bradykininactivated by tissue injury, allergic reactions, viral infections

— 2. Response
◦  vasodilation
◦  increase vascular permeability
◦  pain

  1. Mechanism
    - Activation of GPCRs
    - B2 receptor
  2. Pharmacology
    - BK2 receptor antagonist Icatibant
    - Treatment of acute attacks of hereditary angioedema (HAE) associated with increased production of bradykinin
    - symptoms of localized swelling, inflammation and pain.
  3. Peptide (9 amino acids; Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg)
34
Q

COMPLEMENT SYSTEM

  • Cellular source
  • Response
  • Mechanism
  • Pharmacology
  • Classification
A

—  1. Cellular Source
◦   synthesized by liver; circulate in blood
— 
2. Physiological Response
◦  chemotaxis: recruit inflammatory cells to sites of injury
◦  promote release of mediators from PMNs
◦  increase vascular permeability
◦  Too much-tissue injury

  1. ◦  Mechanism  
    -Complexes of complement proteins
    aggregate to cell surface membrane and cause osmotic lysis
    -Specific complement receptors
    *mast cell degranulation
  2. Pharmacology
    Eculizumab; mirococept
  3. Plasma Proteins C3a C5a C3b…
35
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.

36
Q

WHAT IS ACUTE PHASE PROTEIN ?

A

An acute phase protein is one whose plasma concentration

changes from baseline by at least 25% during inflammation

37
Q

C-Reactive Protein

A
  1. Cellular Source
    -synthesized by liver and
    fat cells  
    -protein that bind to the “C” polysaccharide of bacterial cell wall.
  2. Response
    -  Acute phase reactant
    - activates complement cascade
    - Mediates phagocytosis
    - INFLAMMATION MARKER
  3. Mechanism
    -Binds to phosphotidylcholine-containing
    substances in bacteria and damaged cells
    -Calcium dependent binding
  4. Pharmacology
    Too much CRP associated with
    increased risk of diabetes, hypertension, and CV disease
    -No “CRP Inhibitors” have been
    developed
    -Statins (cholesterol lowering drugs)
    reduce CRP levels/mechanism may be at transcriptional level
  5. plasma protein Pentameric shape protein/25 kDa
38
Q

Cytokines

  • Cellular source
  • Response
  • Mechanism
  • Pharmacology
  • Classification
A
  1. Cellular Source-Nearly all cells
  2. Physiological Response
    - stimulate acute phase reactants
    - TNF-α: fever, sepsis
    - IL-1: fibroblast and lymphocyte proliferation, fever
  3. Mechanism
    -Interaction with specific receptors to
    induce gene expression of number of
    proteins through activation of
    transcription factors, such as NF-κB and
    AP-1
    -Increase cyclooxygenase (fever)
    and lipoxygenases
    - Increase adhesion molecule
    expression
    - Induce collagenase (fibrosis)
  4. Pharmacology
    - Etanercept,   Inflixamab

Classification: Secreted proteins Tumor necrosis factor (TNF-α) and Interleukin-1 (IL-α and Il-β)

39
Q

Adenosine

  • Cellular source
  • Response
  • Mechanism
  • Pharmacology
  • Classification
A
  1. Cellular Source
    - All cells

2.Response
-Increases extracellularly during injury and has anti-inflammatory effect to inhibit cytokine action
-Receptor specific-because
in some cases adenosine
can be pro-inflammatory

  1. Mechanism
    - Via specific GPCRs

4.Pharmacology
-A2 agonists
- Methotrexate-releases adenosine
-Adenosine A3 antagonists in asthma/
inhibit mediator release

  1. Classification
    - Purine nucleoside formed from breakdown of ATP
40
Q

Cell Adhesion Molecules (CAMs)

A
  1. Cellular source
    - Endothelial cells, platelets, leukocytes

2.Response
-Leukocyte adhesion to endothelium is
integral to repair process
-Endothelial adhesion molecules contribute to
recruitment of activated platelets

3.Mechanism
-They are Glycoproteins expressed on
cell surface and mediate
contact between two cells or
between cells and
extracellular matrix
-“contact molecules”

4.Pharmacology
-Abciximab:platelet integrin receptor
antagonist, used as anti-platelet therapy in
heart disease
-Natalizumab:Blocks alpha-4 subunit of
integrin on activated T cells, Multiple sclerosis, Crohn’s disease

  1. Classification
    - Family of proteins including Ig-like CAMs, integrins, selectins, cadherins
41
Q

OXYGEN-DERIVED FREE RADICALS

A
  1. Cellular source
    - All cells
  2. Response
    - intracellular killing of bacteria by neutrophils
    - endogenous antioxidant mechanisms to control effect of free radicals
  3. Mechanism
    - Protein oxidation
    - Lipid peroxidation
    - DNA mutations
  4. Pharmacology
    - Antioxidants: vitamin C and E
  5. Classification
    - Superoxide, hydroxyl radicals
42
Q

What are the three lipid mediators

A
  • prostaglandins: pro-inflammatory
  • Leukotrienes: pro-inflammatory
  • Steroids: anti-inflammatory
43
Q

Prostaglandins

A

-Contribute to signs and
symptoms of inflammation
(pain, fever, vasoactive
effects)

- Increases other mediators that reach the site of injury

-PGE2/PGI2
directly increase blood flow and
indirectly enhance edema
formation and leukocyte
infiltration
44
Q

-PGE2/PGI2

A

directly increase blood flow and indirectly enhance edema formation and leukocyte infiltration

45
Q

Leukotrienes

A

-First identified as slow
reacting substance of
anaphylaxis (SRS-A)
released from mast cells

-increase vascular
permeability( LTC4/LTD4)

  • bronchoconstriction (LTC4/LTD4)
  • Chemoattractant for neutrophils (LTB4)
  • increased in allergies and asthma
46
Q

So what is the magic fix for inflammation

A

There is no one drug effective for treating inflammation bc there are so many mediators and the mediators all do so many things

47
Q

Steroids

A

-Act via gene transcription
-Bind to cytoplasmic receptors;
-form activated receptor-steroid
complex that localizes to nucleus to bind steroid-responsive elements in DNA and then induce/repress transcription of target genes (increase anti-inflammatory genes and decrease pro inflammatory genes )
-Most patients respond to steroids
-Steroid-resistance: cellular defect in steroid responsiveness
-side effects limit use

48
Q

 Non Steroidal Anti-
Inflammatory Drugs
(NSAIDs)

A

-inhibition of cyclooxygenase

- reduces production of
inflammatory
prostanoids

49
Q

Leukotriene Receptor Antagonists

A

(ZAFIRLUKAST) Montelukast

50
Q

 Leukotriene Synthesis Inhibitors

A

(ZILEUTON)

51
Q

 Cytokine (TNF-α) Inhibitors

A

ETANERCEPT (receptor analog)

INFLIXIMAB (monoclonal antibody)

PDA Block 2 (13 decks)

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