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2 Inflammation, Inflammatory Disorders, and Wound Healing > 2.1 Acute Inflammation > Flashcards

2.1 Acute Inflammation Flashcards

1
Q

Main difference between acute and chronic inflammation

A

Acute: Neutrophils enter tissue
chronic: lymphocytes enter tissue

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2
Q

Acute inflammation: main hallmarks

A
  1. edema

2. neutrophils

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3
Q

Acute inflammation: what causes it (2 major stimuli)

A
  1. infection

2. tissue necrosis

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4
Q

Acute inflammation is mediated by several factors. List them (5 categories)

A
  1. TLRs
  2. Arachidonic acid metabolites (prostaglandins and leukotrienes)
  3. Mast cells (histamine, as well as AA metabolites)
  4. Complement
  5. Hageman factor (Factor XII)
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5
Q

CD14

A

A TLR on macrophages that recognizes LPS on the outer membrane of G- bacteria. Mediates acute inflammation.

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6
Q

How does TLR mediate acute inflammation?

A

TLR binds PAMP and then upregulates NF-KB, a TF that activates immune response genes.

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7
Q

NF-KB

A

Molecular switch that turns on acute inflammation. It’s a TF that activates expression of immune response genes.

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8
Q

Arachidonic acid mediators:

  • mech of production
  • products
A
  • PLA releases AA from membrane
  • Prostaglandins made from COX
  • Leukotrienes made from 5-lipoxygenase
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9
Q

Prostaglandins:

  • types
  • what do they do
  • made from what enzyme
A
  • PGI2, PGD2, PGE2
  • all cause vasodilation and increase vascular permeability
  • PGE2 also mediates fever and pain
  • made from COX enzyme
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10
Q

Leukotrienes:

  • types
  • what do they do
  • made from what enzyme
A
  • LTB4: attracts and activates neutrophils
  • LTC4, LTCD4, LTE4: vasoconstriction, bronchospasm, increased vascular permeability
  • made from 5-lipoxygenase
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11
Q

Mast cells: immediate and delayed response

A
  • immediate: release histamine

- delayed: release AA metabolites (PGs, LTs). This occurs several hours later

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12
Q

Histamine, functions

A
  • vasodilation

- increase vascular permeability

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13
Q

Complement pathways

A
  1. Classical
    - C1 binds IgG, IgM bound to antigen
  2. Mannose-binding Lectin (MBL) pathway
    - MBL binds to mannose on microorganisms and activates complement.
  3. Alternative pathway -directly activated by microbials
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14
Q

What key products do complement pathways produce?

A
  • C3 convertase
  • C5 convertase
  • C5b, C6-9: MAC
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15
Q

C3a, C5a: combined effect

A

Anaphylatoxins.

  • trigger mast cell histamine release
  • C5a also is chemotactic for neturophils
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16
Q

MAC

A
  • formed from C5b, C6-9

- lyses microbes

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17
Q

Hageman factor (Factor XII):

  • what is it
  • how activated
  • what it activates
  • is especially important in what disease
A
  • Inactive proinflammatory protein produced in liver
  • activated when exposed to subendothelial or tissue collagen
  • Activates: Coagulaiton and fibrinolytic systems, complement, and Kinin system (produces bradykinin–vasodilation, vascular permeability, pain)
  • important thing to know: plays important role in DIC by G- Sepsis
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18
Q

What vessels does vasodilation and increase in vascular permeability occur during inflammation?

A
  • vasodilation occurs at arteriole

- vascular permeability occurs at post-capillary venule

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19
Q

What mediators attract and activate neutrophils? (4)

A
  • LTB4
  • C5a
  • IL8
  • Bacterial products
  • (LTB4 and C5a also upregulate integrins.)
20
Q

Causes of mast cell activation (3)

A
  1. Tissue trauma
  2. C3a, C5a
  3. cross-linking of cell-surface IgE by antigen
21
Q

C3b

A

-opsonin for phagocytosis

22
Q

C5a

A
  • trigger mast cell histamine release with C3a

- also chemotactic for neutrophils

23
Q

Bradykinin, functions

A
  • vasodilation
  • increase vascular permeability
  • pain
24
Q

What mediates pain?

A
  • PGE2 (fever and pain)

- Bradykinin

25
Q 
Key mediators of each:
Rubor-redness
calor-warmth
tumor-swelling
dolor-pain
fever
A 
1, 2. Redness, warmth
-caused by vasodilation: Histamine, Bradykinin, PGs
3. swelling:
-Vascular permeability:
Histamine, Tissue damage
4. Pain
PGE2, Bradykinin
5. Fever
-PGE2 released by COX in hypothalamus, activated by IL1 and TNF from macrophages
26
Q

Mediators of fever

A
  • PGE2 released by COX in hypothalamus, activated by IL1 and TNF from macrophages
  • Pyrogens stimulate macrophages (eg LPS rom bacteria)
27
Q

Neutrophil arrival (Diapedesis): 4 steps, briefly describe each

A
  1. Margination–vasodilation causes cells to marginate from center of flow to periphery
  2. Rolling–selectin speed bumps
  3. Adhesion–Integrins bind CAMs on endothelium
  4. Transmigration and Chemotaxis–neutrophils cross epithelium, attracted to 4 chemotactic mediators.
28
Q

Selectins:

  • types
  • what increases them
  • what does it bind to
A
  • “speed bumps” of Rolling step in diapedesis
  • P selectin: released from Weibel-palade bodies, mediated by histamine
  • E selectin, induced by TNF and IL1
  • binds to Sialyl Lewis X on leukocytes
29
Q

Neutrophil function after diapedesis. 3 steps

A
  1. Phagocytosis
  2. Destruction of phagocytosed material
  3. Resolution
30
Q

Adhesion step of Diapedesis

A
  • CAMs on epithelium bind to Integrins on leukocytes

- Cell adhesion molecules–ICAM and VCAM

31
Q

What upregulates CAMs

A

TNF, IL1

32
Q

What upregulates Integrins

A

C5a, LTB4 (which also are chemotactic for neutrophils)

33
Q

Leukocyte Adhesion deficiency:

  • mech
  • name of specific protein
  • clinical features (3)
A
  • Integrin defect, CD18 subunit
  • auto recessive
    1. higher neutrophil level in blood (1/2 of neutrophils normally hang on vessels, like bats in a cave)
    2. delayed separation of umbilical cord (lack of neutrophils in acute inflammation means cord cells are delayed in necrosis)
    3. recurrent bacterial infections without pus
34
Q

Main opsonins

A
  • IgG

- C3b

35
Q

Chediak-Higashi syndrome

-mech

A
  • protein trafficking defect, microtubules (think Railroad track defect!)
  • Impaired phagolysosome formation–cannot destroy phagocytized particles
36
Q

Chediak-Higashi syndrome

-clinical features (6)

A
  1. increased risk of pyogenic infections
  2. neutropenia (railroad track defects make it tough to separate components in mitosis of neutrophils)
  3. Giant granules in leukocytes (railroad track defects–granules pile up)
  4. Defective primary hemostasis (platelets depend on granule function, same as 3)
  5. Albinism (melanocyte cannot use tracks to distribute melanin to many keratinocytes)
  6. Peripheral neuropathy (nerves rely on tracks for protein transportation)
37
Q

Destruction of phagocytosed material in neutrophils: name the 2 methods

A
  1. O2 dependent (oxidative burst). More effective

2. O2 independent (enzymes such as lysozyme)

38
Q

Oxidative burst, biochem reactions/enzymes

A

O2 to .O2- to H2O2 to HOCl (bleach)

  • H2O2 to HOCl is by MPO (myeloperoxidase)
  • Catalase can also take away H2O2
39
Q

Chronic granulomatous disease

A
  • Lack of NADPH oxidase leads to no H2O2 to make HOCl, so H2O2 must be taken from bacteria. However, catalase can react with H2O2, so Cat+ bacteria removes H2O2 that could be made into HOCl for respiratory burst
  • leads to infection and granuloma formation
  • Test: nitroblue tetrazolium test to screen CGD to test enzyme
40
Q

MPO deficiency

A
  • myeloperoxidase deficiency
  • cannot convert H2O2 to HOCl (bleach) for oxidative burst
  • similar to CGD
41
Q

Resolution of neutrophil function:

  • what happens
  • time frame
A
  • neutrophils undergo apoptosis, create pus

- within 24 hours

42
Q

Phases of acute inflammation

A
  1. Fluid
  2. Neutrophils (peak 24 hours)
  3. Macrophage (peak 2-3 days)
43
Q

How do macrophages ‘manage’ the next stages of inflammation?

A

Options that macrophage can do:

  • Stop acute inflammation, IL10 and TGF-B
  • Continue acute inflammation, IL8
  • Abscess formation–Wall off the infection and continue acute inflammation
  • Call in chronic inflammation–when they know that lymphocytes are needed (eg virus infection)
44
Q

Which cytokines shut down inflammation? Secreted by what?

A

Macrophages (as ‘managers’ of inflammation) secrete IL10 and TGF-B if they think inflammation should end.

45
Q

Which cytokine does macrophage secrete to recruit more neutrophils?

A
  • IL8

- Clinical sign is pus formation. This means acute inflammation is still happening, even if many weeks have passed

46
Q

Transudate vs Exudate

A

transudate–fluid leakage

exudate–fluid with protein and maybe cells

2 Inflammation, Inflammatory Disorders, and Wound Healing (6 decks)

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