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Exam 1 > Inflammation & Resolution workshop > Flashcards

Inflammation & Resolution workshop Flashcards

1
Q

Different stages of inflammation.

A
  • Vasodilation
  • Margination - binding of macrophages, phagocytes
  • Migration - phagocytes & mø force into tissue
  • Phagocytosis
  • tissue repairing/Resolution - by resolvins or lipoxins
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2
Q

Vasodilation occurs how?

A
  • Compliment system, C3A, C5A activate mast cells.
  • mø/ mast cells react to tissue damage & release inflammatory mediators inc. histamine, kinin, prostaglandin, leukotrienes.
  • These act on endothelial cells, causing separation from nearby capillaries.
  • endothelial cells release nitric oxide = vasodilation.
  • Capillary more permeable.
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3
Q

Cytokines role?

A
  • activate cells in local environment & allow immune cells to enter the environment & attack intruding toxin/pathogen
  • growth factors
  • endogenous pyrogens - drive immune response & change body temp.
  • induce acute phase protein in liver
  • Eg? IL1, IL6, chemokines: CCL8- attract neutrophils, CCL5 - attract mø,
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4
Q

Process leading to fever?

A
  • macrophage ingests the toxin
  • broken down in vacuole.
  • endotoxins released so mø release IL1.
  • IL1 goes into blood stream. hypothalamus.
  • IL1 induces production of prostaglandins which increase body’s thermostat.
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5
Q

Margination?

A
  • adhesion molecules roll down with phagocytes/leukotrienes
  • force themselves between the endothelial cells
  • squeeze into site via emigration.
  • chemotaxis guide them through tissue
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6
Q

vascular stage of inflammation

A
  • arterioles & venules near site of injury constrict briefly then dilate.
  • dilation = congestion , capillary permeability
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7
Q

Phagocytosis - cellular stage?

A
  • leukotrienes engulf & degrade bacteria & cellular debris.

* products/ exudates cause swelling & pain

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8
Q

Exudates are?

A
  • serous fluid
  • RBC
  • fibrinogen
  • tissue debris
  • WBC breakdown products
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9
Q

pain how?

A

brady kinins increase capillary permeability and stimulate pain receptors

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10
Q

Cytokines eg

A
  • Pro-inflammatory TNF, IL-1, IL6 etc

  • Chemokines – CXCL-8, CCL2, CCL5 etc
  • Growth factors – M-CSF, GM-CSF etc
  • Adhesion molecules – VCAM-1, ICAM-1

• Matrix metalloproteinases - MMP-1, 2, 9 - changes extracellular matrix to allow cells to migrate

  • Clotting factors -
  • Prostaglandins – local
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11
Q

What are acute phase proteins?

A
  • made by hepatocytes in liver
  • made in response to pro-inflammatory cytokines
  • fluctuate due to infections & tissue injury
  • eg. C reactive protein, fibrinogen, complement factors eg opsonin, haptoglobin, ferritin
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12
Q

Acute phase protein eg?

A
  • C reactive protein
  • Fibrinogen
  • serum amyloid A
  • complement factors - chemotaxis, opsonin
  • haptoglobin, ferritin
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13
Q

C reactive protein fn?

A

opsonin - labels pathogen so immune cells can detect it easily

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14
Q

fibrinogen fn?

A

• coagulation factors - stops bleeding

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15
Q

serum amyloid A fn?

A
  • cell recruitment & MMP/matrix metalloid proteoids inducer.
  • allows cells to move through extracellular matrix.
  • allows tissue to change
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16
Q

Haptoglobin & ferritin fn?

A

bind Hb or Fe - blood cells.

17
Q

Role of adhesion molecules in inflammation

A
  • Cells travelling high speed due to BP.
  • Endothelial cells release MCP-1 & IL8, which attracts leukocytes.
  • Selections slow down leukocyte.
  • Adhesion molecules ICAM1 VCAM1 cause them to adhere onto endothelial cells.
  • adhesion molecule & leukocyte roll along vessel wall to site.
  • PCAM1 and CD99 are responsible for taking the leukocyte down into the site of inflammation.
18
Q

PCAM1 & CD99 are?

A

responsible for taking leukocyte down into site of inflammation

19
Q

endothelial cells release MCP-1 & IL8 which?

A

Attracts leukocytes.

20
Q

adhesion molecule eg?

A

ICAM1 & VCAM1

21
Q

How is NFkB activation in inflammation?

A
  • NFkB controls cytokines, chemokine & their receptor, adhesion molecules, MMPs, growth factors and acute phase proteins.
  • normally found in cytoplasm, bound to inhibitor IkB.
  • IkB kinase protein activated by sensing pro-inflammatory cytokines, bacterial components, viruses, DNA damaging agents.
  • IkB kinase phosphorylates IkB into smaller molecules. NFkB released & migrates into nucleus
  • NFkB binds to DNA & transcribes RNA.
  • RNA translates to proteins involved in apoptosis. inflammation, eg adhesion molecules etc
22
Q

how NFkB released?

A
  • bound to inhibitor IkB
  • IkB kinase activated by sensing pro-inflammatory cytokines, etc.
  • IkB kinase phosphorylates IkB into smaller molecules.
23
Q

NFkB controls?

A

cytokines, chemokine & their receptor, adhesion molecules, MMPs, growth factors and acute phase proteins.

24
Q

NFkB found in?

A

cytoplasm, bound to inhibitor IkB.

25
Q

Mediators in resolution & fn?

A
  • Cytokines such as TGFß, IL4,
  • IL10 - regulates release of TH2 cells, can slow down & stop mø so that they cant differentiate & engulf cells.
  • Soluble adhesion molecules - cover the cells & leukotrienes cant bind to adhesion molecules on the membrane anymore.
  • TIMPS - inhibit metallomatrix proteins/MMP
  • Lipoxins/resolvins - counteract inflammatory mediators which are present in the blood.
  • Internal opioids - counteract pain by increasing blood flow.
26
Q

Mediators in resolution list

A
  • Cytokines TGFß, IL4, IL10
  • . soluble adhesion molecules
  • TIMPS
  • lipoxins, resolvins
  • i nternal opioids
27
Q

Events that drive autoimmune diseases

A
  • Genetics MHC2 gene
  • failure of self tolerance/ central tolerance system
  • sustained infection/ inflammation
  • environmental triggers,
  • ongoing acute to chronic
  • high levels of auto antibodies
28
Q

Why central & peripheral tolerance?

A
  • Central = thymus & bone marrows
  • peripheral = regulated auto-reactive cells in circulation.
  • In central lymphoid organs/ peripheral tolerance, not all self antigens are expressed thus may not undergo negative selection
  • maintaining T cell tolerance = B cell tolerance to same antigen
  • T cell only activated by foreign molecule.
  • If both central tolerance not there then both cant target correct antigens.
29
Q

conventional immune disease treatments?

A
  • Anti-inflammatory drugs: corticosteroids, aspirin and ibuprofen. NSAIDS. Block TNF & IL1.
  • Immunosuppressants - inhibit proliferation of lymphocytes and ciclosporin-A (to flood inflammatory response)
  • Non-specific control of autoantibodies.
  • Infusion of IV immunoglobulin (IV-IG): antibodies of multiple specificity from a group of healthy donors, how it works = not clear
  • Plasmapheresis - remove circulating antibodies, short term
  • Organ specific:
  • Insulin in diabetes
  • Acetylcholinesterase inhibitor in Myasthenia gravis

Exam 1 (11 decks)

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