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401 Exam 3 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Calor

A

Heat

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2
Q

Rumor

A

Redness

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3
Q

Tumor

A

Swelling

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4
Q

Dolor

A

Pain

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5
Q

Functiolaesa

A

Loss of function

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6
Q

3 steps of inflammation

A

Sensing - by macrophages, DC, mast cell; recruitment - by plasma proteins (cytokines, chemokines), monocyte (for macrophages) and granulocytes (for leukocytes); action/inflammation = by vasodilation, vascular permeability

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7
Q

Explain normal fluid movement: hydrostatic vs. colloid

A

Interstitium is constantly bathed in fluid from circulation. Hydrostatic pressure pushing fluid out in the arterial end, colloid osmotic pushing fluid in in the venous end. Must have intact endothelial cells.

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8
Q

What level change in blood chemistry in a dehydrated patient?

A

ALB

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9
Q

Why does lymph nodes get bigger during infection?

A

Infiltration of cells. Macrophages and lymphocytes travel to LN to start recruitment processs.

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10
Q

What causes retraction of endothelial cells?

A

Histamine and other mediators. Rapid, short-lived.

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11
Q

What is the result of retraction of endothelial cell?

A

Increase cell permeability, fluid leakage, neutrophils form NET and degranulate.

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12
Q

What causes endothelial injury during inflammation?

A

By burns, toxins. Endothelial injury happened because of the involvement of PMN (WBCs, neutrophils).

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13
Q

What is the duration of retraction of endothelial cell compared to endothelial cell injury?

A

Retraction is short, injury is long lived.

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14
Q

What is the result of endothelial injury?

A

Fluid leakage. Variations in proteins vs. cells (acellular vs. very cellular).

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15
Q

Compare exudate vs. transudate

A

Exudate = high protein, high cells, happened during inflammation
Transudate = low protein, few cells, happened as a result of decreased colloid osmotic pressure.

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16
Q

Why causing endothelial injury?

A

For cells to exit circulation in response to inflammation.

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17
Q

4 steps of leukocyte migration through blood vessel

A

Margination, rolling, pavementing (sticking), migration

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18
Q

Describe margination

A

cells “fall out” of circulation - impact endothelium. This brings cells into contact with endothelium.

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19
Q

Describe rolling

A

WBCs begin contacting specific ligands (selectin, integrin) expressed on activated endothelial cells. These ligands tell WBCs where to head over to.

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20
Q

Describe pavementing

A

WBCs strongly bind to activated (damaged) endothelial cells. Stronger bind for next step!

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21
Q

Describe migration

A

WBCs migrate between endothelial cells or through damaged endothelium, and out into the interstitium

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22
Q

Why vasodilation during inflammation?

A
  1. more blood flow through for more leukocytes (cause rubor); 2. slow movement, contact endothelial cells for margination.
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23
Q

What makes fibrin?

A

Fibrinogen

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24
Q

What does fibrin mean in inflammation?

A

Fibrin = acute inflammation. Fibrin in a local product to indicate local inflammation. It is non-specific to what causes inflammation.

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25
Q

Why is there vascular congestion/vasodilation?

A

To get more cells to site of inflammation

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26
Q

How did leukocytes get out of circulation?

A

Endothelial injury, vasodilation

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27
Q

why are the alveoli filled with fluid?

A

Leakage leads to edema

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28
Q

How does fibrin appears under microscope?

A

Pale pink.

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29
Q

What are the goals for acute inflammation?

A

Get cells to the source; release neutrophils&raquo_space;> lymphocytes > macrophages; vascular leakage leads to fluid, heat, redness; presence of fibrin and exudate (pus). Think neutrophils = kills!

30
Q

What are the goals for chronic inflammation?

A

Repair!
Presence of macrophages, lymphocytes, plasma cells&raquo_space;> neutrophils; Fibroblast making fibrosis (scar), granulomas, granulation tissue.

31
Q

How do endothelium be activated?

A

1- Cytokines released from WBCs.
2- By themselves, when they detect PAMPs and DAMPs.

32
Q

What does Weibel Palade body do?

A

Endothelium will upregulate Weibel Palade body which it will upregulate selectin body.

33
Q

What is selectin?

A

Selectin binds with glycolipid that expressed on leukocyte. Selectin mediate transient, low-affinity binding. Selectin = rolling. Selectin does not appear on leukocyte.

34
Q

What is intergrin?

A

Integrins swap low affinity for high affinity. It mediates firm adhesion to endothelial cells, mediates migration, mediates “trapping” of leukocytes.
Integrin is how cell interact with ECM and knows where to go.

35
Q

What is PECAM-1?

A

Platelet endothelial cell adhesion molecule. Expressed on platelets, endothelial cells, leukocytes. They are the stickiness.

36
Q

What mutation causes leukocyte adhesion deficiencies?

A

Mutation CD18 affects integrin function, firm adhesion defects - explains neutrophilia (neutrophiles accumulation) around the margin of blood vessel because leukocyte cannot stick and marginate out.

37
Q

Function of neutrophils in inflammation

A

Kill via phagocytosis and degranulation/secretion via NETs (neutrophilic extracellular traps) by releasing ROS.

38
Q

Function of mast cells in inflammation

A

Prominent within respiratory tract and GI tract. Express IgE on surface antibodies. If bind an antigen, degranulate and release histamine, serotonin, and cytokines.

39
Q

Function of eosinophils in inflammation

A

See a lot of eosinophils in parasitic infestation and allergic diseases. They attracted to eotaxin - seen within canine mast cell tumors.

40
Q

Explain complement cascade in inflammation

A

Complement proteins circulate as intact, quiescent forms. Activation result in cleavage of comp. protein 3 (C3) into C3a and C3b [bigger]

41
Q

Effector function of complement cascade

A
  1. Recruitment and activation of leukocytes; 2. Recognition of bound C3b by phagocyte C3b receptor leading to phagocytosis of microbe; 3. formation of membrane attack complex (MAC) for microbe lysis.
42
Q

Explain fibrosis in CHRONIC inflammation

A

Occurs when damage is too severe, effecting basement membrane, causes low oxygen. This is default mechanism and natural healing of a wound. Think of Leia’s scar.

43
Q

Explain granulation tissue in CHRONIC inflammation

A

“Second intention healing,” preceded fibrosis. Composed of fibroblasts mixed with new blood vessels growth. Allow for controlled maintenance of chronic, ongoing inflammation while promoting healing.

44
Q

Explain granuloma in CHRONIC inflammation

A

A discrete entity with epithelioid macrophages and giant cells. It is a nodule of macrophages surrounding a inciting agent (nidus) with a rim of fibrosis.

45
Q

What causes granulomatous inflammation? List 5.

A

1) Higher order bacteria
2) Fungi/yeast organisms (Coccidioides immitis, Blastomyces dermatiditis, histoplasma capsulatum)
3) Parasites
4) Foreign material
5) Intracellular bacteria (rhodococcus equi, Mycobacterium spp. causing Johne’s disease)

46
Q

Opsonization

A

coating of a ppathogen with something (antibody or C3b) to aid phagocytes in recognizing and engulfing it.

47
Q

Proud flesh

A

Granulation tissues tends to be proliferative

48
Q

What is cytokine?

A

Are small proteins that may be pro or anti-inflammatory using source cell, target cell, or effector mechanism; involves in cell-cell signaling during immune response.

49
Q

What is chemokine?

A

Chemotactic cytokine
“Bread crumbs” for WBCs to follow lead to site of infection
Play role in homeostatic or inflammatory.

50
Q

What is growth factor?

A

Molecules that involves in cell proliferation and differentiation.

51
Q

Name classes of cytokines

A

1) Interleukins, 2) interferons, 3) tumor necrosis factors (TNF), 4) chemokines

52
Q

Name 2 types of IFN

A

Type 1 consists of >20 members. Type 2 consist of 1 member TNF gamma.

53
Q

Pro-inflammatory cytokines

A

IL-1, TNF, IFN gamma

54
Q

Anti-inflammatory cytokines

A

IL-10, TGF(beta)

55
Q

What determine the exact outcome of immune stimulation?

A

The balance of pro and anti-inflammatory cytokines.

56
Q

Pro-inflammatory vs. anti-inflammatory pathway

A

DC activated, travelled to lymph node to educate T cell by secreting interleukins. T cell secretes IL for pro or anti-inflammatory reaction. (Lecture 54)

57
Q

Major cytokines driving acute inflammation

A

TNF, IL-1, IL-6

58
Q

Major cytokines driving chronic inflammation

A

IL-12, IFN-gamma

59
Q

Interferons type 1 (alpha and beta) role?

A

antiviral activity

60
Q

Interferon type 2 (gamma) role?

A

Pro-inflammatory response

61
Q

What does TGF-beta do?

A

Promote fibrosis

62
Q

Why are corticosteroids such potent immunosuppressants?

A

Corticosteroid inhibits phospholipase to make arachidonic acid. Hence, inhibit cyclooxygenase (COX) and lipooxygenase (LOX).

63
Q

Vasoactive amines?

A

They are preformed molecules, rapid release, causes vasodilation, increased permeability, smooth muscle contraction in airways, and pain.

64
Q

Nitric oxide?

A

Inducible (iNOS) induced upon inflammation (vasodilation, microbe killing); endothelial (eNOS) always on, repels platelets.

65
Q

Four effects of bradykinin

A
  1. Increased PLA2 activity
  2. Pain
  3. Vasodilation
  4. Vascular permeability
    (extra: clotting cascade, produce kallikrein enzyme)
66
Q

Morphology includes

A
  • Severity (mild, mod, severe)
  • Duration (acute, chronic)
  • Distribution (focal, multifocal, focally extensive, diffuse)
  • Organ involved
  • Process (-itis, -osis, -opathy)
67
Q

Liquefactive caused by

A

extracellular bacteria

68
Q

Caseous caused by

A

intracellular bacteria

69
Q

Tissue appears red means

A

hemorrhage, vasodilation, acute disease, necrosis, necrotic tissue appears pale pink in histology.

70
Q

Tissue appears lumpy bumpy

A

firm, chronic, histology has scar tissue (collagen+fibrosis)

71
Q

What is abscess?

A

Neutrophilic equivalent of granuloma. Pus filled center surrounded by capsule made up of fiberblast.

72
Q

Compare erosion and ulcer

A

Erosion: epithelium gone, but basement membrane still present.
Ulcer: epithelium and basement membrane GONE!

401 Exam 3 (4 decks)

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