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*mod exam 1 > Ch 3 Lect: Inflammation and Repair (Dobson) > Flashcards

Ch 3 Lect: Inflammation and Repair (Dobson) Flashcards

1
Q

Define:

Inflammation

A

“Inflammation is a protective response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents”

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2
Q

What are the “5 R’s” of acute inflammation?

A
  1. Recognized
  2. Recruited
  3. Removed
  4. Regulated
  5. Repaired
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3
Q

What are the 5 hallmark signs of acute inflammation?

A

Rubor (redness)

Calor (heat)

Tumor (swelling)

Dolor (pain)

Loss of function

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4
Q

Features of Acute Inflammation

Onset?

A

Fast!!!

Minuites or hours

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5
Q

Features of Acute Inflammation

What is the Cellular Infiltrate?

A

NEUTROPHILS

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6
Q

Features of Acute Inflammation

Feature: Tissue injury, fibrosis?

A

Usually mild and self-limited

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7
Q

Features of Acute Inflammation

Feature: Local and systemic signs?

A

Prominent

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8
Q

Features of Chronic Inflammation

Feature: Onset?

A

Slow!!!

Days

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9
Q

Features of Chronic Inflammation

Feature: Cellular infiltrate?

A

Monocytes

Macrophages

Lymphocytes

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10
Q

Features of Chronic Inflammation

Feature: Tissue injury/fibrosis?

A

Otften severe and progressive

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11
Q

Features of Chronic Inflammation

Feature: Local and systemic signs?

A

Less than acute

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12
Q

Acute inflammation is one of the reactions of the type of host defense known as _______ immunity

A

Innate

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13
Q

Chronic inflammation is more prominent in the reactions of ________ immunity

A

Adaptive

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14
Q

What are the primary cells involved in recognition of foreign bodies?

A

Macrophages

Dendritic cells

Mast cells

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15
Q

What are dendritic cells?

A

Antigen presenting cells (APCs) that process antigen material and present it on the cell surface to the T Cells of the immune system.

They act as messengers between the innate and the adaptive immune systems.

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16
Q

Gain-of-function mutations in the sensor are the cause of rare diseases known as _______________

A

Autoinflammatory syndromes

–> Characterized by spontaneous inflammation

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17
Q

What is an effective treatment for autoinflammatory syndromes?

A

IL-1 antagonists

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18
Q

The inflammasome has been implicated in inflammatory reactions to?

A
  • Urate crystals
  • Lipids
  • Cholesterol crystals
  • Amyloid deposits in alzheimers
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19
Q

What are the three major components of an acute inflammation response?

A
  1. Dilation of small vessels leading to an increase in blood flow
  2. Increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation
  3. Emigration of leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
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20
Q

What is exudate?

A

High protein and cellular content

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21
Q

What is transudate?

A

Low protein content, few cells

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22
Q

Inflammatory reactions are initiated, maintained and terminated by ___________

A

Mediators of inflammation

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23
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Histamine

Source? Action?

A

Source: Mast cells, basophils, platelets

Action: Vasodilation, increased vascular permeability, endothelial activation

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24
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Prostaglandins

Source? Action?

A

Source: Mast cells, leukocytes

Action: Vasodilation, pain, fever

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25
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Leukotrienes

Source? Action?

A

Source: Mast cells, leukocytes

Action: Increased vascular permeability, chemotaxis, leukocyte adhesion and activation

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26
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Cytokines (TNF, IL-1, IL-6)

Source? Action?

A

Source: Macrophages, endothelial cells, mast cells

Action: Local [endothelial activation]

Systemic [fever, metabolic abnormalities, hypotension (shock)]

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27
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Chemokines

Source? Action?

A

Source: Leukocytes, activated macrophages

Action: Chemotaxis, leukocyte activation

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28
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Platelet-activating factor

Source? Action?

A

Source: Leukocytes, mast cells

Action: Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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29
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Complement

Source? Action?

A

Source: Plasma (produced in liver)

Action: Leukocyte chemotaxis and activation, direct target killing, vasodilation

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30
Q

Table 3-4

Principal mediators of Inflammation

Mediator: Kinins

Source? Action?

A

Source: Plasma (produced in liver)

Action: Increased vascular permeability, smooth muscle contraction, vasodilation, pain

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31
Q

Process of inflammation more prodominantly occurs in which of the following?

A) Arterioles

B) Venules

C) Lymphatics

A

A) Arterioles

B) Venules

C) Lymphatics

*Post capillary venules are the primary site where exudation occurs. Very thin layer allow materials to diffuse accross

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32
Q

What does this image reveal?

A

Lymphangitis

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33
Q

What are the 4 overarching steps of getting a leukocyte to travel from the circulation to the site of infection?

A
  1. Margination
  2. Rolling
  3. Adhesion to endothelium
  4. Diapedesis (transmigration)
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34
Q

What are the first two selections to become expressed by TNF and IL-1?

A

P-selectin

E-selectin

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35
Q

What is the major player involved in diapedesis/transmigration of the leukocyte across the endothelium?

A

PECAM-1 (CD31)

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36
Q

After the leukocyte has entered the tissue, what does it do to move toward the site of injury?

A

Utilizes chemotaxis

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37
Q

What is the major exogenous agent for chemotaxis?

A

N-formylmethionine

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38
Q

What are the major endogenous agents (3) for chemotaxis?

A
  1. Cyokines (eg. IL-8)
  2. Complement (C5a)
  3. Arachidonic acid (AA), mainly LTB4
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39
Q

What are the functions of integrins?

A
  • Focal attachment
  • Trigger signaling cascades
  • Influence cell locomotion, proliferation, shape and differentiation
40
Q

What are the different receptors involved in leukocyte activation?

A
  • GPCRs
  • Toll-like receptors
  • Cytokine receptor
  • Phagocytic receptor
41
Q

The macrophage mannose receptor is a lectin that binds…

A

Terminal mannose and fructose residues of glycoproteins and glycolipids.

*These sugars are typically part of molecules found on microbial cell walls

42
Q

The efficienty of phagocytosis is greatly enhanced when microbes are __________

A

Oponized

43
Q

What are the major opsonins?

A

IgG Antibodies

C3b breakdown product of complement

Mannose-binding lectin

44
Q

Killing of microbes is accomplished by ______________

A

Reactive oxygen species (ROS)

45
Q

Primary granules contain?

Aka?

Large or small?

A

MPO

Azurophil granules

Large

46
Q

What is this slide revealing?

A

Toxic granulation

–> Seen in patients with sepsis

–> Toxic granulations are dark coarse granules found in granulocytes, particularly neutrophils

47
Q

What is an alternative way that infections are contained?

A

Use of Neutrophil extracellular traps (NETs)

These NETs prevent the spreading of microbes by trapping them in fibrils

48
Q

Prostaglandins and leukotrienes are produced from?

A

Arachidonic acid (AA)

49
Q

What is the mechanism of aspirin?

A

Functions to inhibit cyclooxygenase enzyme so that prostaglandins are not produced

50
Q

What do COX inhibitors inhibit?

A

Cyclooxygenase

(prostaglandin production)

51
Q

What are the major cytokines involved in acute inflammation?

A

TNF

IL-1

IL-6

Chemokines

IL-17

52
Q

Acute Inflammation

What is the source and action of TNF?

A

Source: Macrophages (primarily), mast cells, T lymphocytes

Action: Stimulates expression of endothelial adhesion molecules and secretion of other cytokines (systemic effects)

53
Q

Acute Inflammation

What is the source and action of IL-1?

A

Source: Macrophages (primarily), endothelial cells and some epithelial cells

Actions: Similar to TNF; endothelial activation (initiation of P and E selectin release) and greater role in fever

54
Q

Acute Inflammation

What is the source and action of IL-6?

A

Source: Macrophages, other cells

Actions: Systemic effects (acute phase response)

55
Q

Acute Inflammation

What is the source and action of Chemokines?

A

Source: Macrophages, endothelial cells, T lymphocytes, mast cells and others

Actions: Recruitment of leukocytes to sites of inflammation; migration of cells in normal tissues

56
Q

Acute Inflammation

What is the source and action of IL-17?

A

Source: T lymphocytes

Action: Recruitment of neutrophils and monocytes

57
Q

What are the primary cytokines involved in chronic inflammation?

A

IL-12

IFN-gamma

IL-17

58
Q

Chronic Inflammation

What is the source and action of IL-12?

A

Source: ANTIGEN PRESENTING CELLS!!! Dendritic cells, macrophages

Actions: Increased production of IFN-gamma

59
Q

Chronic Inflammation

What is the source and action of IFN-gamma?

A

Source: T lympocytes, NK cells

Action: Activation of macrophages

60
Q

Chronic Inflammation

What is the source and action of IL-17?

A

Source: T lymphocytes

Actions: Recruitment of neutrophils and monocytes

61
Q

___ and ___ serve critical roles in leukocyte recruitment by promoting adhesion of leukocytes to endothelium and their migration through vessels

A

TNF

IL-1

62
Q

__________________ have been remarkably effective in the treatment of chronic inflammatory diseases; particularly rheumatoid arthritis

A

TNF antagonists

63
Q

What do complement proteins

C5a, C3a and C3b

do?

A

C5a and C3a = Add to the inflammatory response

C3b=Phagocytosis, acts as an opsonin

64
Q

What disease is associated with inhibiting C1 in the complement pathway?

A

C1 inhibitor blocks the activation of C1 that leads to hereditary angioedema

65
Q

What is paroxysmal nocturnal hemoglobinuria (PNH) associated with?

A

Decary accelerating factor (DAF)

66
Q

What are the principal mediators of:

Vasodilation?

A

Histamine

Prostaglandins

67
Q

What are the principal mediators of:

Increased vascular permeability?

A

Histamine

Serotonin

C3a

C5a

Leukotrienes C4, D4, E4

68
Q

What are the principal mediators of:

Chemotaxis, leukocyte recruitment and activation?

A

TNF

IL-1

Chemokines

C3a, C5a

Leukotriene B4

69
Q

What are the principal mediators of:

Fever?

A

IL-1

TNF

Prostaglandins

70
Q

What are the principal mediators of:

Pain?

A

Prostaglandins

Bradykinin

71
Q

What are the principal mediators of:

Tissue damage?

A

Lysosomal enzymes of leukocytes

Reactive oxygen species (ROS)

72
Q

What are the morphologic patterns of acute inflammation?

A
  1. Serous inflammation
  2. Fibrinous inflammation
  3. Purulent (suppurative) inflammation/abscess
  4. Ulcer
73
Q

Serous inflammation is marked by exudation of ___________ into spaces created by cell injury or into body cavities lined by the peritoneum, pleura or pericardium.

This is termed an: ________

A

Cell-poor fluid

Effusion

74
Q

When does a fibrinous exudate develop?

A

When vascular permeability allows large molecules such as fibrin to pass out of the blood

or

There is a local procoagulant stimulus (malignant cells)

75
Q

Where is fibrinous exudate characteristically found?

A

Lining body cavities

76
Q

What is purulent inflammation?

A

Produces pus; an exudate consisting of neutrophils, the liquefied debris of necrotic cells and edema fluid

77
Q

What is an ulcer?

A

A local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing of inflamed necrotic tissue

78
Q

What is the

Onset, Cellular infiltrate, Tissue injury and local/systemic signs of

Chronic inflammation?

A

Onset: Slow/days

Cellular infiltrate: Monocytes/macrophages and lymphocytes

Tissue injury: Often severe and progressive

Local/systemic signs: less than acute

79
Q

Monocytes have MANY names based on where they are:

State the name based on the location:

Circulating in blood =

In tissue=

Liver macrophages=

Spleen/lymph node=

CNS=

Lungs=

Skin=

A

Circulating in blood = Monocytes

In tissue= Macrophages

Liver macrophages= Kupffer cells

Spleen/lymph node= Sinus histiocytes

CNS= Microglial cells

Lungs= Alveolar macrophages

Skin= Langerhans cells

80
Q

Identify the labeled cells

A
81
Q

Classically activated Macrophage (M1)

What are the activated by?

What are they inhibited by?

What are the downstream events upon activation?

A

Activated: Microbes, IFN-gamma

Inhibited: IL-13, IL-4

Downstream: Inflammation, phagocytosis

82
Q

Alternatively activated Macrophage (M2)

What are the activated by?

What are they inhibited by?

What are the downstream events upon activation?

A

Active: IL-13, IL-4

Inhibited: Microbes, IFN-gamma

Downstream: Tissue repair, fibrosis, Anti-inflammatory effects

83
Q
A

Eosinophils

84
Q

Eosinophils have granules that contain _____________

A

Major basic protein

85
Q

What is this and what are the components?

A

Necrotizing granuloma

86
Q

Name examples of diseases with granulmatous inflammation:

A
  1. Tuberculosis
  2. Leprosy
  3. Syphilis
  4. Cat-scratch disease
  5. Sarcoidosis
  6. Crohn disease
87
Q

What are acute-phase reactants?

A

“Plasma proteins, mostly synthesized in the liver, whose plasma concentrations may increase several hundred-fold as a part of the response to inflammatory stimuli”

88
Q

What are 4 examples of acute-phase reactants?

A
  1. C reactive protein (CRP)
  2. Fibrinogen
  3. Serum amyloid associated protein (SAA)
  4. Hepcidin
89
Q

What is the most abundant cell type in the blood?

A

Neutrophils

(40-70%) of blood composition

90
Q

What is the least abundant cell type in the blood?

A

Basophils

(0-1%)

91
Q

What does a left-shift refer to?

A

A left shift is related to an accelerated release of cells from the bone marrow post mitotic reserve pool and is therefore associated with a rise in the number of more immature neutrophils in the blood = left shift

92
Q

_____________ is the process of new blood vessel development from existing vessels. It is critical in healing at sites of injury.

A

Angiogenesis

93
Q

What is the major player in the deposition of connective tissue?

A

TGF-beta

94
Q

Which method of “intention” allows for the best healing?

A

First intention

95
Q
A

*mod exam 1 (15 decks)

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