Inflammation Flashcards

1
Q

What is the classical definition of Inflammation?

A

Redness, warmth, pain, swelling and loss of function

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2
Q

Evolutionarily conserved structures on pathogens, detected by cells to initiate an immune response

A

Pathogen-associated molecular patterns (PAMPS)

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3
Q

Endogenous pathogens are detected through which germ-line receptor?

A

Pattern recognition receptors (PRRs)

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4
Q

Which cells are PRRs expressed by?

A

Myeloid cells: monocytes, macrophages, neutrophils, and dendritic cells

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5
Q

Which two cytokines induce autocrine and paracrine effects leading to local activation of neutrophils and macrophages

A

TNF and IL-1Beta

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6
Q

What are the endocrine effects of the release of TNF and IL-1Beta?

A

1) Induction of acute-phase proteins in the liver
2) Platelet activation
3) Fever
4) Fatigue
5) Anorexia

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7
Q

What happens with cytokine activation of endothelial cells?

A

Increase in vascular permeability and the entrance of immune cells into infected tissue

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8
Q

What are three complications associated with cytokine activation of endothelial cells

A

1) Capillary Leakage
2) vasodilation
3) hypotension

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9
Q

What is the primary function of Chemokines?

A

To recruit immune cells to a site of infection

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10
Q

What is the primary function of neutrophils?

A

Phagocytosis of pathogens

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11
Q

Which cell type releases INF-Gamma? And which cell type is activated by INF-Gamma

A

1) Type 1 helper cells (T1H)

2) Neutrophils

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12
Q

Which cell types release IL-22 and what does the release of IL-22 stimulate?

A

1) Helper T-cells and lymphoid cells

2) Acting on epithelial cells it stimulates the production of anti-microbial peptides and defensins

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13
Q

Which two cells types stimulate the release of prostaglandins and which symptoms do prostaglandins produce in patients?

A

1) Monocytes and neutrophils

2) Fatigue, fever and somnolence (excessive tiredness)

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14
Q

How does the complement system mediate inflammation?

A

Mediates microbial opsonization (tagging) and killing and generates inflammatory peptides such as C3a and C5a

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15
Q

Which cytokine suppresses the production of pro-inflammatory cytokines and what cell type produces it?

A

1) IL-10

2) Regulatory T-cells

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16
Q

Which two cytokines released from monocytes and platelets are broad suppressors of inflammation?

A

IL-37 of the IL-1 family and TGF-B

17
Q

How do TNFR and IL-1R limit inflammation?

A

They act as decoy receptors; binding and neutralizing respective cytokines

18
Q

What is sepsis?

A

The release of danger associated molecular patterns which gives rise to hyper inflammation. Damage is cause to tissue by the immune response

19
Q

Unrestrained activation of _______ leads to organ failure during sepsis? What improves the outcome of sepsis in experiments?

A

1) Compliment

2) C5a blockade

20
Q

During sepsis, local activation of which system can control the infection by confining a pathogen? What happens when this becomes systemic?

A

1) Local activation of coagulation

2) Systemic activation can cause intramuscular coagulation, micro vascular thrombosis and bleeding

21
Q

During sepsis, what can result from enhanced adherence of leukocytes and platelets to the endothelial surface and the subsequent transmigration?

A

1) Vascular inflammation
2) disruption of the endothelial cell barrier
3) Leakage of intravascular proteins into the extra vascular space
4) tissue edema (swelling caused by excess fluid)
5) decreased micro vascular perfusion

22
Q

In RA; which six cytokines promote the generation of pathogenic T cells and B cells

A

1) TNF
2) IL-1Beta
3) IL-6
4) IL-12
5) IL-18
6) IL-23

23
Q

What are the 4 targets of monoclonal antibodies are used to treat Crohns?

A

1) TNF
2) IL-12
3) IL-23
4) Alpha4-Beta7 integrin

24
Q

Which five cytokines and one checkpoint are targeted by monoclonal antibodies in the treatment of RA?

A

1) TNF
2) IL-1Ra
3) IL-6R
4) IL-12p40
5) IL-17A
6) JAK/STAT