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Pathology 1 - Cell, Tissue, Inflammation > Lecture 4 - Inflammatory Mediators I > Flashcards

Lecture 4 - Inflammatory Mediators I Flashcards

1
Q

What do inflammatory mediators do? (4 things)

A
  • activate cells
  • localize process
  • communicate between cells
  • activate inflammation
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2
Q

List some cell responses that are activated (4):

A
  • Expression of adhesion molecules
  • Contraction of cytoskeleton (endothelial contraction, chemotaxis)
  • Synthesis of arachidonic acid (aa) mediators
  • Gene transcription (NFk-B, cell division)
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3
Q

Inflammation is largely local. Exceptions?

A

IL-1, IL-6, TNF are systemic

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4
Q

5 steps of evolution of inflammation:

A
  • Vasodilation and increased vascular permeability
  • Chemotaxis and cellular activation
  • Phagocytosis
  • Activation of immune processes
  • Resolution and regeneration
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5
Q

The 4 types of mediators?

A
  • Pre-formed (minutes)
  • Plasma-derived (min-hours)
  • aa-derived and chemokines (hrs-days)
  • Cytokines and GFs (days-weeks)
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6
Q

Preformed mediators initiate inflammation in minutes. They are:

A

Histamine, serotonin, lysozymes

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7
Q

Plasma-derived mediators augment inflammation. They are:

A

Complement, kinins, coagulation factors

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8
Q

Arachidonic acid metabolites maintain inflammation, chemotaxis. They are:

A

Prostaglandins, leukotrienes, PAF (platelet activating factor)

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9
Q

Cytokines and chemokines primarily activate cells and intercellular signaling. They include:

A

Cytokines, interleukins, chemokines

yeah, ik this card kind of sucks.

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10
Q

Growth factors influence cell division and tissue regeneration. They include:

A

Colony-stimulating factors, growth factors (…)

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11
Q

Why are histamine and serotonin fast-acting?

A

Small (from single amino acid), diffuse rapidly, metabolize rapidly

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12
Q

Histamine comes from __________ and is derived from _______.

A

Mast cells and basophils; histidine

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13
Q

Serotonin comes from ______ and is derived from _______.

A

Platelets; tryptophan

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14
Q

What causes histamine release?

A
  • Trauma, cold
  • Cross-linking of IgE
  • C3a, C5a complement receptors
  • Factors from neutrophils, monocytes, platelets
  • IL-1
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15
Q

What do histamine’s 4 receptors do?

A

H1: mediate inflammatory rxns and increase vascular permeability
H2: increase GI secretion
H3: CNS
H4: bone marrow and white blood cells

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16
Q

Why can anti-histamines make you drowsy?

A

Most block H1; cross-reactivity with H3 receptor (CNS)

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17
Q

List inflammatory responses to histamine (4):

A
  • Vasodilation
  • Increased venous vascular permeability (local tissue swelling)
  • Stimulate pain, itching
  • Contraction of smooth muscle (asthma - bronchial)
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18
Q

List some plasma-derived mediators (4):

minutes-hours (just a reminder)

A
  • Coagulation proteins (Hageman/Factor XII)
  • Complement (C3a, C5a, C3b)
  • Fibrinolytic peptides (activation of plasmin)
  • Kinins
19
Q

What activates Hageman factor?

A

Local signals

  • Negatively charged surfaces - basement membranes, collagen (like in a torn vessel)
  • Bacterial LPS
  • Enzymes (trypsin, plasmin)
20
Q

What are general goals of plasma-derived proteins?

A
  • Augment/maintain histamine response

- Coordinate coagulation, endothelial activation, leukocyte adhesion/migration, phagocytosis

21
Q

Hageman factors is central to activating: (4 things)

A
  • Coagulation
  • Fibrinolytic pathways
  • Kinin
  • Complement pathways
22
Q

What does plasmin do?

A
  • Cleave fibrin, augment vascular permeability in skin and lung
  • Generate C3a and C5a (also increase vascular permeability)

Also activate Hageman factor, kininogens, itself…response amplification.

23
Q

What does the kallikrein/kinin system do?

A

Increase vascular permeability, smooth muscle contraction, dilate blood vessels, pain

24
Q

What is thought to inactivate bradykinin?

A

ACE

Bradykinin levels increase with ACE-inhibitors (dry cough in ACE-inhibitor therapy)

25
Q

What are anaphylatoxins?

A

C3a, C4a, C5a

  • Mast cell, basophil degranulation
  • Smooth muscle contraction
  • Increased vascular permeability
26
Q

Besides its role as an anaphylatoxin, what else does C5a do?

A

Chemotactic for PMNs

  • Neutrophil degranulation
  • Superoxide production
27
Q

What is C3b good for?

A

Opsonization!

28
Q

In inflammation, newly-synthesized products are either from _____ or _____.

A
  • Lipids; membrane-released fatty acids (hours-days)

- New proteins (days to weeks)

29
Q

New synthesis of cytokines begins…

A

18-72 hours

30
Q

What produce cytokines?

A

Endothelial cells, monocytes (macrophages), lymphocytes, fibroblasts

31
Q

Membrane fatty acids will yield:

A

Prostaglandins, leukotrienes, and platelet-activating factor

short-acting, local, metabolized quickly

32
Q

What are the eicosanoids?

A

Prostaglandins, leukotrienes, thromboxanes

33
Q

What are the two mechanisms for release of arachidonic acid?

A
  • Direct action by phospholipase A2

- Phopholipase C, then diacylglycerol lipase

34
Q

Cyclooxygenases transform aa to:

A

Prostaglandins and thromboxanes

35
Q

Lipoxygenases transform aa to:

A

Leukotriene A…then further to LTB4 or LTC/LTD/LTE

36
Q

Arachidonic Acid Derivatives in Inflammation

From macrophage:

A

PGE, PGF, PGD

Vasodilation, increased vascular permeability, enhance pain

37
Q

Arachidonic Acid Derivatives in Inflammation

From neutrophil:

A

LTB4

Chemotaxis of neutrophils

38
Q

Arachidonic Acid Derivatives in Inflammation

From mast cell:

A

LTC, LTD, LTE

Bronchoconstriction (asthma), vascular leakage
aka SRS-A’s

39
Q

Arachidonic Acid Derivatives in Inflammation

From platelets:

A

Thromboxanes (TXA2)

Platelet aggregation, blood clotting

40
Q

Arachidonic Acid Derivatives in Inflammation

From endothelial cells:

A

Prostacyclin (PGI2)

Anti-thrombotic

41
Q

What is lipoxin (another aa derivative)?

A

Anti-inflammatory, late in inflammmation

Block LTC/LTD/LTE activity

42
Q

Lipoxins can be formed from leukotriene precursors, or as product of ________

A

acetylated cyclooxygenase (aspirin therapy)

Aspirin inhibits prostaglandin synthesis and promotes lipoxin synthesis

43
Q

What is PAF?

A

Platelet-activating factor

  • acetylated lysophospholipid
  • from mast cells, basophils, neutrophils, macrophages
44
Q

What does PAF do?

A

Platelet aggregation/degranulation, histamine and serotonin release, increased vascular permeability, leukocyte adhesion, chemotaxis

Pathology 1 - Cell, Tissue, Inflammation (5 decks)

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