Pathology - Inflammation and repair 1 Flashcards

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1
Q

what is inflammation?

A

a responsive process to perceived aggression: infection, tissue damage, non-self recognition

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2
Q

What happens to the concentration of cells and molecules during inflammation?

A

Concentration of cells and molecules of immunity increase to the sites where the trigger of inflammation happens

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3
Q

Why is inflammation is important?

A

Inflammation is important to fight infection, to heal wounds, to repair injury

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4
Q

What are the changes in vascular flow during inflammation?

A
  • Arteriolar dilatations (vascular ectasia/dilation) and opening of capillary bed
  • Localized increased blood flow: increased pressure (heat and redness)
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5
Q

What happens to vascular permeability during inflammation ?

A

Increased vascular permeability (vascular leakage) (leakage of palsma proteins that creates edema)

  • Endothelial gaps
  • Endothelial injury (endothelial cell death)
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6
Q

Describe a normal vascular environment

A

hydrostatic pressure = colloid osmotic pressur, plasma protein stays in the lumen. No net fluid or protein leakage

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7
Q

Describe the formation of exudate

A

Increased interendothelial space, along with vasodilation and stasis leads to fluid and protein leakage

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8
Q

describe the formation or transudate

A

Increased (++) pressure (venous outflow obstruction, like in congestive heart failure)

+

Decreased colloid osmotic pressure (decresed protein synthesis; increased protein loss; protein malnutrition) leads to fluid leakage

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9
Q

What is exudate

A

High protein content and may contain some white and red cells

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10
Q

What is transudate

A

Low protein content, few cells.

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11
Q

Consequences of the vascular leakage

A
  1. Outpouring of protein-rich fluid in the extravascular tissues: exsudative edema (tumor)
  2. Localized increased viscosity: blood stasis
  3. Leukocyte migration
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12
Q

Process of leukocyte migration

A
  1. Rolling along the endothelium
  2. Adhesion to the endothelium
  3. Transmigration across the endothelium (diapedesis)
  4. Piercement of the basement membrane
  5. Migration and cell-matrix interactions
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13
Q

Caracteristics of a neutrophil (4)

A
  • Innate immune system
  • Nucleus divided in 2-5 lobes
    Type of phagocytes
  • Migrate through interstitial tissue
  • Predominate during the first 6-24 hrs
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14
Q

Caracteristics of a monocyte (5)

A
  • Innate immune system
  • Bean-shaped nucleus, unilobar
  • Change into macrophages after entering the tissue spaces
  • Phagocytosis
  • Replace neutrophils in 24-48 hrs
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15
Q

Phases of phagocytosis

A
  • Recognition and attachement of the particle to be ingested by the leukocyte: mannose receptors
  • Engulfment: phagocyte membrane zips up around particle
  • Killing and degradation within neutrophils and macrophage.
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16
Q

Process of killing and degradation within neutrophils and macrophages

A
  • Fusion of phagosome with lysosomes
  • Killing by lysosomial enzymes
  • Killing by ROIs and NO (oxygen compounds)
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17
Q

What happens after phagocytosis

A

Neutrophils undergo apoptosis and are ingested by macrophages

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18
Q

Why are toll-like receptors (TLRs) are important players in leukocyte activation

A

They recognize pathogen-associated signatures and initiate the inflammatory response of the innate immune system

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19
Q

What are TLRs

A

receptors expressed at the surface of leukocytes involved in their activation (i.e., TLR3, ligand: viral double-strand RNA)

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20
Q

Name some chemical mediators of inflammation

A
  • Vasoactive amines (i.e., histamine, serotonine)
  • Complement and kinin systems
  • Clotting system (i.e., FXII, FX, fibrin, plasmin)
  • Arachidonic acid metabolites.
  • IFN-gamma by NK cells and T lymphocytes
  • Reactive Oxygen Intermediates (ROIs), Nitric Oxyde (NO), Lysozymes, O2 free radicles
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21
Q

How is the acute inflammatory response is terminated

A
  • Many chemical mediators have a short half-life: rapid decline
  • Stop signals:
    Switch in the production of pro-inflammatory to anti-inflammatory products from arachidonic acid
    Secretion of TGF beta
    Inhibition of TNF
  • Tissue macrophages half-life is prolonged (months or years)
22
Q

What is the outcome of acute inflammation?

A
  • Resolution
  • Fibrosis after healing (i.e., hypertrophic scar)
  • Progression to chronic inflammation:
    Angiogenesis
    Mononuclear cell infiltrate
    Fibrosis
23
Q

Example of a serous inflammation

A

Skin blister

24
Q

Example of fibrinous inflammation

A

fibrin (large molecule) extravasation needs severe vascular modification; more often associated with secondary fibrosis

25
Q

example of Suppurative inflammation

A

Suppurative acute appendicitis

26
Q

Morphologic patterns of acute inflammation

A
  1. Serous inflammation
  2. Fibrinous inflammation
  3. Suppurative inflammation
  4. Ulcer
27
Q

What di you have instead of vasodilation in chronic inflammation?

A

angiogenesis and then fibrosis

28
Q

Players in chronic inflammation

A
  • macrophage
  • Lymphocytes
  • Plasma cells
  • Antigen presenting cells
  • eosinophils: rarely.
  • mast cells
29
Q

What is a macrophage

A

Component of the mononuclear phagocyte system

30
Q

What does a macrophage secretes?

A

Mediators of inflammation (TNF)

31
Q

What antigens do macrophage display?

A

Displays antigens to T lymphocytes

32
Q

(HY) What is the difference between clasically activated macrophage (M1) vs alternatively activated macrophage (M2)

A

M1 leads to microbicidal actions, phagocytosis and killing bacteria and fungi
M2 leads to anti-inflammatory effects, wound repair, fibrosis

33
Q

Where do B and T lymphocytes migrate

A

Into inflammatory sutes

34
Q

How can B cell (lymphocyte) can differentiate?

A

into plasma cells which secrete antibodies

35
Q

What CD4+ T produces?

A

cytokines

36
Q

Physical characteristic of a lymphocyte

A

Large dark-staining nucleus, little cytoplasm

37
Q

What is the distinctive pattern of chronic inflammation

A

Granulomatous inflammation

38
Q

what is a granulomatous inflammation

A

It is a distinctive pattern of chronic inflammation: Activated macrophages acquiring an epitheloid appearance

39
Q

In what diseases granulomatous inflammation is present?

A
  • tuberculosis, sacoidosis, inflammatory bowel diseases
40
Q

Is there necrosis when there is granulomatous inflammation?

A

Sometimes yes: necrotizing granuloma

41
Q

What do lymphocytes and plasma cells look like when there is granulomatous inflammation?

A

Peripheral rim of lymphocytes and plasma cells

42
Q

4 systemic effects of inflammation

A
  1. Fever
  2. production of acute-phase proteins
  3. leukocytosis
    5 in severe situations: septic shock, disseminated intravascular coagulation (DIVC)
43
Q

Process of fever

A

central process, production of prostaglandins in hypothalamus, under the control of TNF and IL-1. Antipyretics can act in reducing the production of PGs.

44
Q

What protein can we test to measure inflammation?

A

C-reactive protein produced by the liver

45
Q

Two essential characteristics of stem cells in regeneration

A
  • Self-renewal capacity
  • Asymmetric replication: one daughter cell differentiates, the other retains self-renewal capacity
46
Q

What are the 2 kind of stem cells

A
  • ES (embryonic stem cells): stable
  • Adult stem cells: admixed with differentiated cells, specialized (i.e., can differentiate in one type). Involved in chemoresistance?
47
Q

What is the mechanical support in the extra-cellular matrix ? (for regeneration)

A
  • collagen and elastin
48
Q

how much of the liver can be removed and why?

A

up to 40-60% for primary tumor or metastasis, transplantation

49
Q

By what is initiated the regeneration of the liver?

A

By TNF and IL6

50
Q

Steps of a scar formation

A
  • Hemostatic plug
  • Inflammation (acute and chronic) and macrophages are central
  • Cell proliferation
  • Remodeling
51
Q

What can delay tissue repair? (5)

A

-Infection
-Protein deficiency
-Treatments: glucocorticoids
-Poor perfusion: diabetes
-Increased ECM production in keloids