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Mechanisms of Disease Exam #1 > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

Acute inflammation

Onset:
Cellular filtrate:
Tissue injury, fibrosis:
Local and systemic signs:

A

Onset: fast - minutes to hours
Cellular filtrate: mainly neutrophils
Tissue injury, fibrosis: mild, self-limiting
Local and systemic signs: prominent

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2
Q

Chronic inflammation

Onset:
Cellular filtrate:
Tissue injury, fibrosis:
Local and systemic signs:

A

Onset: slow - days
Cellular filtrate: monocytes/Mo, lymphocytes
Tissue injury, fibrosis: severe, progressive
Local and systemic signs: less

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3
Q

Autoinflammatory syndromes are caused by:

What is used to treat them?

A

Gain-of-function mutations in the sensor.

IL-1 antagonists

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4
Q

What gets impacted by reactions to urate crystals, lipids, cholesterol crystals (atherosclerosis), and AD?

A

The inflammasome

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5
Q

3 major components of acute inflammation

A
  1. Dilation of small vessels leading to an increase in blood flow.
  2. Increased permeability of microvasculature allowing proteins and WBCs to leave circulation.
  3. Migration of WBCs from circulation to the site of injury.
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6
Q

Exudate vs. transudate

A

Exudate: high protein content and WBCs. Pus-like.

Transudate: low protein content w/ few cells.

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7
Q

Histamine

Source:
Action:

A

Source: mast cells, basophils, platelets.

Action: vaodilation, vascular permeability, endothelial activation.

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8
Q

PGs

Source:
Action:

A

Source: mast cells, leukocytes.

Action: vasodilation, pain, fever.

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9
Q

Leukotrienes

Source:
Action:

A

Source: mast cells, leukocytes.

Action: vascular permeability, chemotaxis, leukocyte adhesion, activation.

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10
Q

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

Source:
Action:

A

Source: Mo, endothelial cells, mast cells.

Action: upregulation of expression of adhesion molecules (locally) and fever, metabolic abnormalities, hypotension, shock (systemically).

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11
Q

Platelet-activating factor (PAF)

Source:
Action:

A

Source: leukocytes, mast cells.

Action: vasodilation, vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst.

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12
Q

Complement

Source:
Action:

A

Source: plasma.

Action: leukocyte chemotaxis and activation, MAC, vasodilation.

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13
Q

Kinins

Source:
Action:

A

Source: plasma.

Action: vascular permeability, SM contraction, vasodilation, pain.

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14
Q

What 2 molecules induce the coordinated expression of adhesion molecules during WBC migration?

A

TNF

IL-1

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15
Q

Explain the process of getting a WBC from circulation to the target site

A

TNF and IL-1 upregulate the expression of P and E-selectins on the endothelium which allows WBC to begin rolling.
ICAM-1 firmly grabs the WBC.
PECAM-1 pulls the WBC into the CT.
WBC engulfs the microbe and produces chemokines.
The chemokines stimulates other WBCs to continue producing TNF, IL-1.

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16
Q

What endogenous and exogenous agents help the WBCs find their target?

A

Exogenous agents like N-formylmethionine terminal on some AAs and lipids.

Endogenous chemoattractants like cytokines, complement, and arachidonic acid metabolites (mainly LTB4)

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17
Q

What do integrins connect? What can they trigger?

A

They link the intracellular cytoskeleton w/ the “outside world”. They can trigger signaling cascades within the cell that influences locomotion, proliferation, shape, etc.

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18
Q

What is leukocyte activation?

A

The recognition of microbes or dead cells by a receptor.

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19
Q

How does a microbe get engulfed by a Mo?

A

The mannose receptor on a macrophage binds a terminal mannose on a microbe. The microbe gets placed in a vesicle where it is degraded.

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20
Q

What are opsonins?

What are some main ones?

A

They are molecules that enhance the microbes’ ability to be phagocytosed.

IgG, C3b, MBL - all which can bind receptors on WBCs.

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21
Q

Once phagocytosed, what do Mo use to degrade the microbe? (3)

A

ROS
Reactive nitrogen species (from NO)
Lysosomal enzymes

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22
Q

What do smaller specific (secondary) granules contain?

What do azurophil (primary) granules contain?

A

Lysozyme, collagenase, gelatinase, lactoferrin, etc.

Myeloperoxidase, bacterial factors, etc.

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23
Q

Toxic granulation

What cells are most effected?

A

Changes in granulocytes on blood film in patients with inflammatory conditions (often in sepsis)

Mostly seen in neutrophils.

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24
Q

Neutrophil extracellular traps (NETs)

A

EC traps that provide a high concentration of antimicrobial substances at sites of infection and prevent the spread of microbes by trapping them in fibrils.

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25
Q

Extrinsic defects (phagocytic disorders)

What can it lead to?

A

Abnormalities in opsonization secondary to deficiencies of Ab and complement factors.

Neutropenia by suppression of granulocytes, or increased autoAbs or isoAbs directed against neutrophil Ags.

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26
Q

Intrinsic defects (phagocytic disorders)

A

Defects in granulocyte development or exit into circulation, granulocyte killing ability or chemotaxis (movement).

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27
Q

TTM for dermographism urticaria

How does it develop?

A

Anti-histamines.

Thought that trauma releases Ag that binds IgE (membrane-bound) of MCs that causes release of His.

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28
Q

What are 2 lipid mediators?

What do they do?

A

PGs and leukotrienes produced from arachidonic acid.

Stimulate vascular and cellular reactions in acute inflammation.

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29
Q

What are COX-1 and COX-2?

A

They catalyze the production of PGs from cyclooxygenase (from AAcid).

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30
Q

What do montelukast and zafirlukast inhibit?

A

Inhibit leukotriene receptors

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31
Q

What do Lipoxin A4 and Lipoxin B4 do? (LXA4, LXB4)

A

Inhibit inflammation

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32
Q

Thromboxane A2 does:

A

Vasoconstriction and promotes platelet aggregation.

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33
Q

PGD2 and PGE2 does:

A

Vasodilation and increased vascular permeability

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34
Q

Leukotriene C4, D4, E4 do:

Leukotriene B4?

A

Increased vascular permeability and bronchospasm.

Chemotaxis.

35
Q

Cytokines in acute inflammation (5)

A 
TNF
IL-1
IL-6
Chemokines
IL-17
36
Q

Cytokines in chronic inflammation (3)

A

IL-12
IFN-y
IL-17

37
Q

What cytokines act on the brain? (3)

What do they do?

A

TNF, IL-1, IL-6.

Fever

38
Q

What cytokines act on the liver? (2)

What do they do?

A

IL-1, IL-6.

Production of ACPs.

39
Q

What cytokines act on bone marrow? (3)

What do they do?

A

TNF, IL-1, IL-6.

Promote leukocyte production.

40
Q

Systemic pathological effects of TNF on the heart, endothelium and skeletal muscle:

A

Heart: low CO.
Endothelium: increase vascular permeability.
Muscle: insulin resistance (w/ IL-1)

41
Q

What is used often to treat diseases like RA?

A

TNF antagonists

42
Q

Roles of:

C5a and C3a:

C3b:

MAC:

A

C5a and C3a: inflammation

C3b: phagocytosis

MAC: lysis of microbe

43
Q

Inhereited deficiencies of complement proteins increases susceptibility of:

A

Infections and macular degeneratyion and hemolytic uremic syndrome due to excessive complement activation.

44
Q

C1 inhibitor:

Deficiency of it can cause:

A

Blocks activation of C1 (first protein of classical pathway).

Deficiency of it can cause hereditary angioedema.

45
Q

DAF and CD59:

Deficiency of it can cause:

A

Inhibits formation of MAC.

Excessive complement activation and lysis of RBCs, a disease called paroxysmal nocturnal hemoglobinuria (PNH).

46
Q

Mediators of vasodilation (2)

A

His and PGs

47
Q

Mediators of increased vascular permeability (5)

A 
His
Serotonin
C3a
C5a
Leukotrienes
48
Q

Mediators of chemotaxis, WBC recruitment and activation (6)

A 
TNF
IL-1
Chemokines
C3a
C5a
Leukotrienes
49
Q

Mediators of fever (3)

A

IL-1
TNF
PGs

50
Q

Mediators of pain (2)

A

PGs

Bradykinin

51
Q

Mediators of tissue damage (2)

A

Lysosomal enzymes of WBCs

ROS

52
Q

Serous inflammation

A

Marked by exudation of cell-poor fluid into potential body spaces –> effusion

53
Q

Fibrinous inflammation

A

When vascular permeability allows large molecules (like fibrin) to pass out of blood or there is a local procoagulant stimulus.

Occurs in lining of body cavities like meninges, pericardium and pleura.

54
Q

Purulent inflammation

A

Production of pus, mostly neutrophils. Usually in bacterial infection.

55
Q

Ulcer

A

Local defect of the surface of an organ/tissue from shedding of inflamed necrotic tissue.

56
Q

Acute inflammation involves:

Chronic inflammation involves:

A

Innate immunity

Adaptive immunity

57
Q

Dominant cells in chronic inflammation

A

Mo

58
Q

Which cytokines cause a monocyte to differentiate into an M1?

What can an M1 do after that?

A

Microbes or IFN-y.

Can produce ROS, NO, enzymes to kill microbe.
Can secrete IL-1, IL-12, IL-23 to cause inflammation.

59
Q

Which cytokines cause a monocyte to differentiate into an M2?

WHat can M2 do after that?

A

IL-13, IL-4, IL-5.

GFs and TGF-beta cause tissue repair and fibrosis.
IL-10, TGF-beta cause anti-inflammatory effects.

60
Q

IL-12 acts on:

To do what?

A

DCs and Mo.

Increase production of IFN-y.

61
Q

IFN-y acts on:

To do what?

A

T cells and NK cells.

Activate Mo (increase killing ability).

62
Q

IL-17 acts on:

To do what?

A

T cells.

Recruit WBCs.

63
Q

Eosinophils:

What do their granules contain?

A

Becomes abundant in IgE and parasitic reactions.

Major basic protein which is toxic to parasites and mammalian epithelial cells.

64
Q

What MUST be excluded when granulomas are identified in a patient?

A

Tuberculosis

65
Q

3 systemic clinical and pathological changes of the acute-phase response

A
  1. Fever
  2. Acute-phase ractants
  3. Leukocytosis
66
Q

How many degrees change characterizes a fever?

A

Change of 1-4 degrees C

67
Q

How much may acute-phase reactants increase in response to inflammatory stimulus?

A

Increase in several hundred-fold

68
Q

Elevated CRP –>

Elevated fibrinogen –>

Elevated SAA –>

Elevated hepcidin –>

A

MI

ESR

Secondary amyloidosis

Anemia of chronic disease

69
Q

Total WBC count:

Diff of:
Neutrophils
Eosinophils
Basophils
Monocytes
Lymphocytes
A

4-11K

Neutrophils 40-70%
Eosinophils 1-4%
Basophils 0-1%
Monocytes 4-8%
Lymphocytes 20-40%
70
Q

Leukemoid reaction

A

When extremely high WBC count (40-100K) looks like leukemia.

71
Q

What is a “left shift”?

A

When neutrophils are released quickly from bone marrow and are more immature.

72
Q

High levels of cytokines causes:

A

Disseminated intravascular coagulation
Hypotensive shock
Metabolic disturbances

“Septic shock”

73
Q

Primary cells mediating:

Bacterial infections:
Viral infections:
Allergies and parasites:

A

Bacterial infections: neutrophils
Viral infections: lymphocytes
Allergies and parasites: eosinophils

74
Q

2 requirements for cell repair

A

Cell must be able to divide

Must have underlying CT

75
Q

4 steps of angiogenesis

A
  1. GFs (VEGF)
  2. Notch signaling
  3. ECM proteins
  4. Enzymes
76
Q

TGF-beta is most important cytokine for:

A

The synthesis and deposition of CT proteins.

77
Q

What does TGF-beta do at the CT?

A

Stimulates fibroblast migration and prolifetion (increases collagen).
Decreases cell degredation by inhibiting metalloproteases.
Can lead to fibrosis.
TGF-beta also inhibits other WBCs and can be anti-inflammatory.

78
Q

Keloids

A

Overgrowths of scar tissue most often seen in AA populations.

79
Q

Calor
Rubor
Tumor
Dolor

A

Calor: warmth
Rubor: redness
Tumor: swelling
Dolor: pain

80
Q

Margination

A

Migration of WBCs toward the endothelial walls.

81
Q

How do chemotactic agents trigger an intracellular response?

What kinases are activated?

What protein do the kinases activate?

A

GPCR (Gq)

Rac/Rho/cdc42

Polymerize actin

82
Q

When do neutrophils predominate?

What replaces them and when?

A

First 6-24 hrs.

Replaced w/ monocytes from 24-48 hrs.

83
Q

What 3 things can bind the an Mo and trigger phagocytosis?

A
  1. Mannose receptor
  2. Scavenger receptors
  3. Opsonins (IgG, C3b, etc.)
84
Q

CRP

A

Can bind to microbial cell walls and fix opsonins and complement.
May also function in aiding in clearing necrotic nuclei.

Mechanisms of Disease Exam #1 (5 decks)

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