Acute Inflammation & Antibodies Flashcards

1
Q

What is Acute Inflammation?

A

-Acute inflammation is a short-term process occurring in response to tissue injury, usually appearing within minutes or hours.

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2
Q

What is the Acute Phase Response?

A

-Refers to the change in plasma concentrations of ‘specific’ proteins in response to inflammation.

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3
Q

What is the C-reactive protein?

A

-Produced by liver cells to mediate the ‘Acute Phase Response’

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4
Q

How do Natural Killer Cells function in Acute Inflammation?

A
  • Recognise abnormal cells and kill them
  • Killed via release of cytokines inducing apoptosis
  • Are pro-inflammatory mediators for ‘Acute’ inflammation.
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5
Q

What X2 things does Acute Inflammation activate?

A
  • Complement System

- Dendritic Cell Activation

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6
Q

How does the Complement System work?

A

1) Low levels of ‘Inactive Complement System Proteins’ are found in the extracellular fluids.
2) If there’s pathogen in extracellular fluids these inactive proteins> activated via cleavage.
C3 > C3b +C3a
(Inactive Protein) (two activated proteins are formed)

3) Activation triggers other Protective Responses

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7
Q

Name some Protective Responses that are activated by the Complement System

A
  • Opsonisation
  • Direct Pathogen Killing
  • Acute Inflammation (via pro-inflammatory mediators)
  • Leukocyte Recruitment
  • Pathways
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8
Q

Name X3 Pathways that can activate the Complement System. (CMA)

A
  • Classical
  • Mannose-Binding Lectin
  • Alternative
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9
Q

What is the Classical Pathway?

A
  • triggered directly by pathogen or indirectly by antibody binding to the pathogen surface
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10
Q

What is the Alternative Pathway?

A
  • C3b protein (active form) binds to ligands and pathogens
  • Activates more complement proteins and a downstream series of events
  • Amplification loop occurs. This involves the enzyme, ‘Convertase’ which converts more inactive C3 protein to its active for C3b and C3a.
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11
Q

What is the Mannose-Binding-Lectin Pathway?

A
  • Lectin proteins bind to Mannose sugar

- Once bound triggers the Convertase enzyme to activate more C3 proteins t their active form.

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12
Q

What are the Physiological signs for Acute Inflammation?

A
  • Vasodilation of blood vessels (redness)
  • Increased Permeability
  • Fluid Accumulation Extravascular Space
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13
Q

What are key features of non-healthy tissues?

A
  • Vasodilation (Vascular Changes)
  • Accumulation of Neutrophils
  • Bacteria produced at site of infection
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14
Q

How do Neutrophils Accumulate at the site of infection?

A

-Trans-Endothelial Migration

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15
Q

What is Vasculature?

A

-Arrangement and systems of body

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16
Q

Name the five steps of Trans-Endothelial Migration

MBMMA

A

1) Margination
2) Binding
3) Migration
4) Movement
5) Activation

17
Q

What is Margination?

A

-Movement of neutrophils to endothelium at site of infection

18
Q

What is the Binding Step?

A

-Neutrophils bind to the Adhesion molecules (involved binding with other cells)

19
Q

What is the Migration step of Trans-Endothelial Migration?

A

-Neutrophils across membrane/capillary walls via ‘Diapedesis’

20
Q

What is Movement Step?

A

-Neutrophils move within tissue to site of infection via ‘Chemotaxis’

21
Q

How is a Neutrophil activated in final step of Trans-Endothelial Migration?

A

-The PAMPS of antigen of pathogen activates the PRRs of neutrophil

22
Q

What is Diapedesis?

A

-Passage of cells through capillary walls

23
Q

What is Chemotaxis?

A
  • Movement of an organism/cell due to a stimulus.

- Moves site of infection

24
Q

Name the X3 methods of Neutrophil Killing

A
  • Phagocytosis
  • Degranulation
  • NETs
25
Q

What is Neutrophilic Degranulation?

A
  • Neutrophils degranulate and release toxic substances to kill the pathogen
  • Release granules found inside the neutrophil
26
Q

Name the two types of Inflammation?

A

Systemic

Local

27
Q

What is Systemic Inflammation?

A
  • Infection in blood stream

- (as system type circulatory system)

28
Q

What is Local Inflammation?

A

-Infects ONLY one part of the body