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Mechanisms of Disease Exam #1 > Chapter 3 LOs > Flashcards

Chapter 3 LOs Flashcards

1
Q

5 components of the inflammatory response

A 
Rubor: redness
Tumor: swelling
Calor: heat
Dolor: pain
Functio laesa: loss of function
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2
Q

What are the 5 steps (R’s) of the inflammatory reaction?

A
  1. Recognition
  2. Recruitment
  3. Removal
  4. Regulation of the response
  5. Resolution (repair)
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3
Q

Major features of the acute inflammatory response

Onset:
Cells involved:
Amount of fibrosis/injury:
Local signs?

A

Fast
Mostly neutrophils
Mild injury/fibrosis
Significant local signs

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4
Q

Major features of the chronic inflammatory response

Onset:
Cells involved:
Amount of fibrosis/injury:
Local signs?

A

Slow
Monocytes, Mo, lymphocytes
Severe and progressive
Less local signs

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5
Q

What are the triggers of the inflammatory response? (4)

A

Infection
Necrosis
Foreign bodies
Immune reactions

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6
Q

3 major components of the acute inflammation

A

Vasodilation
Increased vascular permeability
WBC recruitment

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7
Q

Exudate

A

High protein and cell content.

Due to increased vascular permeability.

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8
Q

Transudate

A

Low protein and cell content.

Due to changes in hydrostatic or colloid pressures.

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9
Q

What is in pus?

A

It is a purulent exudate w/ lots of neutrophils, dead cells, and microbes.

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10
Q

What are the most important WBCs in the acute response?

A

Mo and neutrophils.

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11
Q

Explain the process of rolling, adhesion and penetration of WBCs through the endothelial cell layer:

A

WBCs begin rolling by attaching to E and P-selectins.
WBCs adhere via integrins.
CD31/PECAMs pull the WBC into the ECM.
Collagenases degrade the ECM.
WBC engulfs the microbe.
WBC secretes IL-1 and TNF which upregulate selectins.
Chemokines act on neutrophils to increase their avidity for integrins.

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12
Q

Major exogenous chemotactic marker of chemotaxis

A

N-formylmethionine

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13
Q

Major endogenous chemotactic marker of chemotaxis

A

Cytokines
C5a
AA metabolites (LTB4)

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14
Q

What do the exo/endogenous chemotactic markers signal once they bind to WBCs?

A

They bind GPCRs and + Rac/Rho/cdc42 which induces actin polymerization.

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15
Q

What is the lifespan of a neutrophil?

Which cells predominate at which times?

A

Lifespan is 24-48 hrs.

Neutros dominate in first 6-24 hrs, then they’re replaced by monocytes at approx. 24-48 hrs.

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16
Q

What about neutrophils makes them best suited to be the first on the scene? (3)

A

They are in high concentration, they are attracted to chemokines and have a high affinity to selectins.

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17
Q

What is the pathway for WBC activation?

A

GPCR -> increased Ca++ -> + PKC and PLA2.

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18
Q

Basic steps of WBC activation (3)

A
  1. Recognize/attach
  2. Engulfment
  3. Killing
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19
Q

What are the 4 receptors on phagocytes and what can they bind?

A
  1. GPCR: N-Fmet., chemokines, AA metabolites.
  2. TLRs: LPS, etc.
  3. Cytokine Receptor: IFN-y, etc.
  4. Phagocytic receptor: microbes.
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20
Q

What can happen intracellularly once something binds the GPCR on a phagocyte? (2)

A

+ integrins -> adhesion

Chemotaxis

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21
Q

What can happen intracellularly once something binds the TLR on a phagocyte? (1)

A

+ mediators (AA metabolites, cytokines, etc).

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22
Q

What can happen intracellularly once something binds the cytokine receptor on a phagocyte? (2)

A

+ mediators (AA metabolites, cytokines, etc).

+ ROS -> killing.

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23
Q

What can happen intracellularly once something binds the phagocyte receptor on a phagocyte?

A

+ ROS

Phagocytosis into phagosome

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24
Q

What is the role of NADPH oxidase in producing ROS?

What is this called when it occurs in neutrophils?

A

Oxidizes NADPH to produce a superoxide radical (O2-*).

The respiratory burst.

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25
How do Azurophilic granules contribute to destroying microbes?
They have MPO and can take H2O2 and Cl- to make OCl2- which is antimicrobial.
26
What is the most efficient system of microbial killing in neutrophils?
H2O2 - MPO - halide system in azurophilic granules
27
What are some antioxidants? (5)
``` SOD (O2-* to H2O2) Catalase (detox H2O2 in peroxisomes) Glutathione peroxidase (detox H2O2 everywhere else) Cerruloplasmin (contains Cu) Iron-free transferrin ```
28
What is iNOS and how is it produced (especially in Mo)?
It is the type of NO that can kill cells. It is produced when Mo and neutros are activated by cytokines. In Mo, NO -> NO + O2-* -> ONOO- (very reactive).
29
Where are acid proteases and neural proteases kept? What do they degrade? What controls them?
Kept in specific and Azurophilic granules in neutrophils. Acid: degrade bacteria and debris. Neural: ECM and cleave C3 and C5 to produce anaphylatoxins. Antiproteases.
30
What is the role of alpha1-antitrypsin and alpha2-macroglobulin?
To inhibit neutrophil elastase
31
What is major basic protein?
It is released by eosinophils to kill parasites.
32
What are NETs? What makes them?
Fibrillar networks w/ lots of antimicrobials to prevent spreading. Produced by neutrophils. Consists of nuclear chromatin and nuclei of neutrophils, thus neutrophils must die.
33
How is the inflammatory response terminated? (4)
1. Removal of microbe. 2. Apoptosis of neutros. 3. Stop signals -> switch from pro to antiinflammatory cytokines (IL-10, TGF-b, etc). 4. Inhibition of TNF release from Mo.
34
Sources (3) and functions (3) of Histamine
MCs, basophils, platelets. Vasodilation, increased VP and endothelial activation.
35
Sources (1) and functions (3) of Prostacyclin
Endothelium Vasodilation, increased VP, inhibition of platelet aggregation.
36
Sources (2) and functions (2, 1, 2) of PGD2 and PGE2
MCs and WBCs Vasodilation, increased VP (both). PGD2 is a chemoattractant and PGE2 is repsonsible for fever and pain.
37
Sources (1) and functions (2) of TxA2
Platelets Platelet aggregation and vasocinstriction.
38
What does aspirin inhibit?
COX, thus the formation of PGs.
39
What do steroid inhibit?
PLA2, thus the formation of AA from CM.
40
Sources (2) and functions (3) of LTB4
MCs and WBCs. Chemoattractant, aggregation and adhesion of neutros, + ROS.
41
Sources (2) and functions (3) of LTC4, LTD4 and LTE4
MCs and WBCs. Vasoconstriction, increased VP, Bronchospasm**.
42
What do Zilueton and Montelukast antagonize?
LT receptors
43
Acute cytokines, their sources and actions (4)
TNF: Mo, MCs, T cells. Endothelial adhesion, + secretion of cytokines. IL-1: Mo and endothelium. Endothelial adhesion, + secretion of cytokines and fever. IL-6: Mo. Acute phase response. IL-17: T cells. Recruit WBCs.
44
Chronic cytokines, their sources and actions (3)
IL-12: DCs and Mo. + IFN-y secretion. IFN-y: T cells and NK cells. + Mo for killing. IL-17: T cells. Recruit WBCs.
45
Systemic acute physiological effects on 3 organs, the involved cytokines and end result:
Brain: TNF, IL-1, IL-6. -> fever. Liver: IL-1, IL-6. -> APP production. BM: TNF, IL-1, IL-6. -> WBC production.
46
Systemic pathological effects on 3 tissues, the involved cytokines and end result:
Heart: TNF -> low CO. Endothelium (BVs): TNF -> increase VP SKM: TNF, IL-1 -> insulin resistance
47
3 complement pathways and what activates them:
1. Alternative pathway: microbial surface molecules (LPS, etc). 2. Classical pathway: C1 fixing to IgG/M w/ Ag on it. 3. Lectin pathway: MBL binds ot microbe and activates C1.
48
3 outcomes once the complement cascade is triggered:
1. Inflammation: C5a and C3a to recruit other WBCs. 2. Phagocytosis and opsonization: bound C3b on microbe binds to receptor on phagocyte and they are engulfed or triggers opsonization. 3. MAC: lysis.
49
C1 inhibitors' function: What is the disease if there is a deficiency?
Inhibits C1 activation in classical pathway. Hereditary angioedema
50
What is the function of DAF? CD59? What is the disease if there is deficiency?
DAF: inhibits C3 convertase. CD59: inhibits MAC. Paroxysmal nocturnal hemoglobinuria
51
4 morphologic patterns, what causes them and examples:
1. Serous inflammation: exudation of cell poor fluid (ex - effusions, blisters). 2. Fibrinous inflammation: vascular leakage or local procoagulant stimulus (bleed in the pleura, meninges, pericardium). 3. Purulent inflammation: production of pus, exudate, etc. (ex - infection). 4. Ulcers: shedding of inflamed necrotic tissue.
52
3 possible outcomes of acute inflammation
Resolution Fibrosis Chronic inflammation
53
3 causes of chronic inflammation
Persistent infection Hypersensitivity reactions Prolonged exposure to toxins
54
Components of morphology of chronic inflammation
Infiltrate w/ Mo, lymphocytes and plasma cells (uninucleated cells). Tissue destruction Attempts at healing: CT replacement and angiogenesis -> fibrosis.
55
Outline the pathway of Mo activation
M1: microbes, IFN-y. Can then either produce ROS, NO, etc to kill OR release IL-1, 12, 23 to induce inflammation. M2: IL-4, 5, 13. Can then release GFs or TGF-b to induce fibrosis OR IL-10 and TGF-b to induce anti-inflammatory effects.
56
2 types of granulomatous inflammation
1. Foreign body granulomas: occurs in absence of T cell-mediated immune responses. Epitheliod and giant cells are apposed to surface of foreign body. 2. Immune granulomas: caused by agent that induces persistent T cell-mediated response of a microbe by + IL-2 -> + T cells and + IFN-y -> + Mo.
57
How does a fever occur?
Bacterial products (LPS, etc) activate WBCs to release IL-1 and TNF which activate COX to increase PGs.
58
4 steps of angiogenesis
1. VEGF 2. Notch signaling (sprouting of new vessels) 3. ECM proteins 4. Enzymes to degrade ECM
59
TGF-beta can inhibit what?
Metalloproteinases
60
What to metalloproteinases do?
Degrade collagens and ECM
61
What is healing by first intention?
When injury only involves the epithelial layer. | Ex - clean cut.
62
What is healing by second intention?
A combo of regeneration and scarring. Occurs on deeper wounds.
63
How does fibrosis occur?
Repeated injury -> inflammation -> T cells and M2 -> + TGF-beta -> fibrosis

Mechanisms of Disease Exam #1 (5 decks)

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