Kapitel 1 (Tobias) - Inflammatory Response Flashcards

1
Q

Vad är negavtiva effekter vid förlängad och ukontrollerad inflammation?

A

1) Smärta
2) Immunosuppression
3) Organ dysfunktion
4) Död

Akronym: DOSI

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2
Q

Vad är de klassiska makroskopiska symtom på inflammation?

A

1) Rubor (Rödma)
2) Dolor (Smärta)
3) Calor (Värma)
4) Tumor (Svullnad)
5) Functio Laesa (Förlust av funktion)

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3
Q

Vad är faserna av det akuta vaskulära respons i inflammation?

A

1) Vasodilation (Snabb vasoconstriction initiellt)
2) (Ökad) Permeabilitet
3) Stasis
4) Leukocyt extravation

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4
Q

Vilka vasoaktiva substanser stimulerar den snabba vasokonstriktion som kommer innan vasodilationen i akut inflammation?

Hur/var ifrån frigörs de?

A

Kringliggande vävnad: catecholaminer, serotonin, bradykinin, och prostaglandins

Sympatiska nervsystem: Norepinephrine

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5
Q

Vilka substanser stimulerar vasodilation i akut inflammation?

A

Nitric oxide, histamine, leukotriener, prostaglandiner och komplement faktorer

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6
Q

What are the 4 stages the leukocyte undergoes leading to extravation (after hemostasis has occured)?

Vad är de 4 faser som leukocyterna går igenom som ledar till extravation (efter hemostasen)?

A

1) Rolling
2) Integrin aktivation
3) Stabil adhesion
4) Extravasion

Acronym: RISE

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7
Q

Vad är E selektin och vad är funktionen?

A

Receptor på kärl endothelceller.

Binder till korresponderande ligander på leukocyter (och thrombocyter).

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8
Q

Vad kallar man processen där leukocyten går ut från kärlet?

Var händer det?

A

Diapedes.

Genom interendotheiala junctions i postkapillära venuler

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9
Q

Vad är den första leukocyt som ingår i inflammationen typiskt?

Efter hur lång tid har de peak population?

A

Neutrophiler

Efter24-48 timmer

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10
Q

Nämn 2 typer av makrofager

A
  • Tissue-resident Macrophages

- Monocyte-derived Macrophages

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11
Q

Vad är funktionen av tissue-resident macrophager?

A
  • Tidigt detektion av inflammatoriska stimuli och är en stor tidig producents av proinflammatoriska cytokiner.
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12
Q

Vad triggar monocyter till att extravasera iut i vävnaden?

A
  • Chemotaxiner
    (including cytokines, fibronectin, elastin, complement factors (C3a, C5a), thrombin, and growth factors (e.g., platelet-derived growth factor [PDGF], transforming growth factor-beta [TGF-β]))
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13
Q

Macrophage polarization refers to the ability of macrophages to assume two distinct functional phenotypes - which phenotypes are these?

A

M1 and M2

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14
Q

Vad aktiveras M1 makrofager av och vad är deras funktion?

A

Activated by:

  • Infectious agents
  • Proinflammatory cytokines

Function:

  • Debridement by phagocytosis of foreign material, pathogens, and damaged cells.
  • Production of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and prostaglandins, enhancing the inflammatory response
  • Secretion enzymes like collagenases and elastases to dissolve the extracellular matrix, facilitating phagocytosis and remodeling,
  • (antigen presenting cells that interact with lymphocytes.) (Adaptive immunesystem)
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15
Q

What is M2 macrophages classically activated by and what are their function?

A

Activated by:
- Anti-inflammatory cytokines

Function:

  • Aid in wound repair and healing
  • Secretion of growth factors like PDGF or TGF-β, which stimulate fibroblasts to produce collagen, further dampening the inflammatory response
  • Secretion enzymes like collagenases and elastases to dissolve the extracellular matrix, facilitating phagocytosis and remodeling,
  • (antigen presenting cells that interact with lymphocytes.) (Adaptive immunesystem)
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16
Q

What are the life-spans of Tissue derived Macrophages and circulating Monocytes - respectively?

A

Tissue-resident Macrophages:
- Months to years

Circulating Monocyte:
- Day(s)

17
Q

What are the cellular components of acute inflammation?

A
  • Neutrophils
  • Macrophages and monocytes
  • Lymphocytes
  • Mast Cells
  • Endothelial cells
  • (Antigen presenting cells like dendritic cells to cells of mesenchymal origin like fibroblasts and myocytes, the impact of these other cell types must be considered.)
18
Q

Where do we find Mast Cells?

A

Mast cells are ubiquitously distributed in all organs

19
Q

What do Mast cells degranulate in response to?

A
  • Physical trauma
  • Complement factors
  • Microbial products
  • Neuropeptides
20
Q

What do Mast cells release?

And what are their overall function?

A
  • Histamine (Primary soruce in acute inflammation)
  • Pro-inflammatory mediators like:
    • serotonin
    • leukotrienes
    • prostaglandin metabolites
    • heparin
    • cytokines

Overall function:
- Enhancing local inflammatory response

21
Q

List as many inflammatory stimuli as possible

A
  • Trauma
  • infection, foreign material
  • caustic chemicals
  • allergens
  • autoimmune disease
22
Q

What are lipopolysaccharide, lipoteichoic acid, peptidoglycan, and microbial oligonucleotides examples of?

A

PAMPS

Pathogen-associated molecular patterns

23
Q

What is the difference between DAMPS and PAMPS (Where are they produced - what do they signal?

A

PAMPS:

  • Microbial molecules
  • Recoqnized as “foreign” to the host

DAMPS:

  • Endogenous molecule released with cellular damage (ex. fibrinogen, high-mobility group B1, Heat Shock Proteins, etc.)
  • Alert the body to cellular damage initiated by infectious or noninfectious agents
24
Q

How do PAMPS and DAMPS signal the immune system?

A
  • By interacting with cell surface receptors.
25
Q

What are: toll-like receptors, scavenger receptors, mannose receptors, C-type lectin-like domain–containing receptors, peptidoglycan recognition receptors, and nucleotide-binding site–leucine-rich repeat receptors - examples of?

What are their function?

A
  • PRR´s (Pattern Recognition Receptors)

- Bind DAMPs and PAMPs -> Inflammation

26
Q

Where do we find PRR´s?

A
  • Expressed on the cell surface
  • Within the intracellular compartment
  • Soluble forms may be found in bodily fluids