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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
Q

How do Azurophilic granules contribute to destroying microbes?

A

They have MPO and can take H2O2 and Cl- to make OCl2- which is antimicrobial.

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26
Q

What is the most efficient system of microbial killing in neutrophils?

A

H2O2 - MPO - halide system in azurophilic granules

27
Q

What are some antioxidants? (5)

A 
SOD (O2-* to H2O2)
Catalase (detox H2O2 in peroxisomes)
Glutathione peroxidase (detox H2O2 everywhere else)
Cerruloplasmin (contains Cu)
Iron-free transferrin
28
Q

What is iNOS and how is it produced (especially in Mo)?

A

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
Q

Where are acid proteases and neural proteases kept?

What do they degrade?

What controls them?

A

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
Q

What is the role of alpha1-antitrypsin and alpha2-macroglobulin?

A

To inhibit neutrophil elastase

31
Q

What is major basic protein?

A

It is released by eosinophils to kill parasites.

32
Q

What are NETs?

What makes them?

A

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
Q

How is the inflammatory response terminated? (4)

A
  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
Q

Sources (3) and functions (3) of Histamine

A

MCs, basophils, platelets.

Vasodilation, increased VP and endothelial activation.

35
Q

Sources (1) and functions (3) of Prostacyclin

A

Endothelium

Vasodilation, increased VP, inhibition of platelet aggregation.

36
Q

Sources (2) and functions (2, 1, 2) of PGD2 and PGE2

A

MCs and WBCs

Vasodilation, increased VP (both). PGD2 is a chemoattractant and PGE2 is repsonsible for fever and pain.

37
Q

Sources (1) and functions (2) of TxA2

A

Platelets

Platelet aggregation and vasocinstriction.

38
Q

What does aspirin inhibit?

A

COX, thus the formation of PGs.

39
Q

What do steroid inhibit?

A

PLA2, thus the formation of AA from CM.

40
Q

Sources (2) and functions (3) of LTB4

A

MCs and WBCs.

Chemoattractant, aggregation and adhesion of neutros, + ROS.

41
Q

Sources (2) and functions (3) of LTC4, LTD4 and LTE4

A

MCs and WBCs.

Vasoconstriction, increased VP, Bronchospasm**.

42
Q

What do Zilueton and Montelukast antagonize?

A

LT receptors

43
Q

Acute cytokines, their sources and actions (4)

A

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
Q

Chronic cytokines, their sources and actions (3)

A

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
Q

Systemic acute physiological effects on 3 organs, the involved cytokines and end result:

A

Brain: TNF, IL-1, IL-6. -> fever.

Liver: IL-1, IL-6. -> APP production.

BM: TNF, IL-1, IL-6. -> WBC production.

46
Q

Systemic pathological effects on 3 tissues, the involved cytokines and end result:

A

Heart: TNF -> low CO.

Endothelium (BVs): TNF -> increase VP

SKM: TNF, IL-1 -> insulin resistance

47
Q

3 complement pathways and what activates them:

A
  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
Q

3 outcomes once the complement cascade is triggered:

A
  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
Q

C1 inhibitors’ function:

What is the disease if there is a deficiency?

A

Inhibits C1 activation in classical pathway.

Hereditary angioedema

50
Q

What is the function of DAF? CD59?

What is the disease if there is deficiency?

A

DAF: inhibits C3 convertase.
CD59: inhibits MAC.

Paroxysmal nocturnal hemoglobinuria

51
Q

4 morphologic patterns, what causes them and examples:

A
  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
Q

3 possible outcomes of acute inflammation

A

Resolution
Fibrosis
Chronic inflammation

53
Q

3 causes of chronic inflammation

A

Persistent infection
Hypersensitivity reactions
Prolonged exposure to toxins

54
Q

Components of morphology of chronic inflammation

A

Infiltrate w/ Mo, lymphocytes and plasma cells (uninucleated cells).
Tissue destruction
Attempts at healing: CT replacement and angiogenesis -> fibrosis.

55
Q

Outline the pathway of Mo activation

A

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
Q

2 types of granulomatous inflammation

A
  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
Q

How does a fever occur?

A

Bacterial products (LPS, etc) activate WBCs to release IL-1 and TNF which activate COX to increase PGs.

58
Q

4 steps of angiogenesis

A
  1. VEGF
  2. Notch signaling (sprouting of new vessels)
  3. ECM proteins
  4. Enzymes to degrade ECM
59
Q

TGF-beta can inhibit what?

A

Metalloproteinases

60
Q

What to metalloproteinases do?

A

Degrade collagens and ECM

61
Q

What is healing by first intention?

A

When injury only involves the epithelial layer.

Ex - clean cut.

62
Q

What is healing by second intention?

A

A combo of regeneration and scarring. Occurs on deeper wounds.

63
Q

How does fibrosis occur?

A

Repeated injury -> inflammation -> T cells and M2 -> + TGF-beta -> fibrosis

Mechanisms of Disease Exam #1 (5 decks)

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