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Miscellaneous > MCB Lecture 59 Inflammation II > Flashcards

MCB Lecture 59 Inflammation II Flashcards

0
Q

What are the different receptors for leukocyte activation?

A
  • 7 pass alpha-helical receptors
  • TLR
  • Cytokine receptors
  • Phagocic receptor
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1
Q

Which cells are important for removal of the cause of inflammation?

A

Neutrophils

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2
Q

Describe 7 pass alpha helical receptor activation

A

Chemokines, or other inflammatory mediators act as ligand.

Signal transduction:
Cytoskeletal changes
Increased integrin avidity

Outcome:
Chemotaxis and adhesion to endothelium

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3
Q

Describe TLR signalling in leukocyte recruitment

A
  1. PAMPs (such as LPS) bind to the TLR

2a. Production of inflammatory mediators (arachidonic acid, cytokines)
2b. Production of hydrolytic enzymes and ROS

3a. Amplification of inflammation
3b. Killing of microbes

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4
Q

Describe cytokine signalling in leukocyte activation

A
  1. Cytokines bind to the membrane bound receptor

2a. Production of inflammatory mediators (arachidonic acid and cytokines)
2b. Production of lysosomal enzymes and ROS

3a. Killing of microbe
3b. Amplification of the immune response

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5
Q

Describe phagocytic receptors role in leukocyte activation

A
  1. Opsonised microbe binds to FcR and CR
    2a. Production of ROS
    2b. Extension of pseudopods, phagocytosis
  2. Killing of microbe
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6
Q

Which are the phagocytic receptors on leukocytes, and what do they bind to?

A

CR1 and CR2: bind to complement on opsonised bacteria

Fc-gamma-R: bind to IgG on opsonised bacteria

CIq: binds to collectin on microbe

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7
Q

What is opsonisation?

A

Preparing the microbe for phagocytosis by binding complement and antibody

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8
Q

Describe phagocyte binding to opsonised pathogen

A

Phagocyte binds via its receptors (CR1 and 2, Fc-gamma-R, CIq) to antibody, C3b and collectin that are bound to the microbe

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9
Q

What are the two modes of phagocytic pathogen killing?

A

O2 dependent

O2 independent

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10
Q

Describe O2 dependent killing

A

ROS preoduced in the phagocyte which disrupt the function of the microbe

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11
Q

Which enzymes are involved in O2 dependent killing?

A

NADPH: O2 -> H2O2

Myeloperoxidase: H2O2 -> HOCl (hydrochlorus radical)

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12
Q

Describe the reactive oxygen species that are formed, and which are the most efficient at killing pathogens that have been phagocytosed

A

H2O2, not very efficient at killing microbes

HOCl-: very powerful oxidant, good at killing

Peroxynitrate: very powerful oxidant

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13
Q

Describe briefly what O2 independent pathogen killing is

A

Killing of the bacteria with enzymes released from the granules of leukocytes

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14
Q

What compounds are found in phagocytic granules, and what does each do?

A

Phospholipase: degrades the microbes’ membrane
Lysozyme: degrades the cell wall
Major basic protein: cytotoxic to parasites
Defensins: puts holes in the cell membrane

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15
Q

Describe how leukocytes can also injury healthy tissue

A

a. Released toxic products have no distinction between pathogen and host
b. toxic products released when:
- Frustrated phagocytosis
- Regurgitation
- Damage to phagolysosome by ingested irate crystals

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16
Q

Describe broadly how inflammation is regulated

A

Chemical mediators

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17
Q

What are the two derivations of mediators of inflammation?

A

Plasma and cell derived

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18
Q

What are the plasma derived enzymatic cascades that regulate inflammation? (3)

A
  1. Complement cascade
  2. Kinins
  3. Coagulation, fibrinolysis
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19
Q

What is the function of the regulatory enzymatic cascades?

A

These amplify and coordinate the immune response

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20
Q

Describe the presence of the plasma derived chemical mediators under normal and inflammatory conditions

A

Normal: present, but inactive
Inflammation: become activated at the site of injury

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21
Q

Describe the complement system

A

There pathways of activation

Cleavage of C3

Opsonisation, lysis, inflammation

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22
Q

What are the two types of cell derived chemical mediators of inflammation?

A

Preformed

Newly synthesised

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23
Q

What are the preformed cell derived chemical mediators?

A

Histamine in leukocyte granules

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24
Q

Describe histamine’s role in regulation of inflammation

A

Histamine controls vascular change:

Increases vasodilation and vascular permeability

25
Q

What are the newly synthesised chemical mediators of inflammation?

A

Arachidonic acid metabolites; Prostoglandin and leukotrienes

26
Q

What are eicosanoids?

A

These are the arachidonic acid metabolites

27
Q

What is are some important derivatives of arachidonic acid?

A

Prostoglandin and leukotrienes

28
Q

What is the function of leukotrienes and Prostoglandins?

A
  1. Synthesised locally

2. mediate the steps in inflammation (eg. vascular change)

29
Q

Describe the removal of the cell derived mediators

A

Decayspontaneously, or are degraded by enzymes afterwards

30
Q

How does aspirin work?
What does it target?
What does this bring about?

A

Aspirin targets the synthesis of eicosanoids

Without these, fever and pain is reduced

31
Q

Describe how cell derived chemical mediators of inflammation are only locally acting

A

Only cells in the area receiving the correct stimulation will degranulate

The compounds decay or are degraded rapidly

32
Q

What is the aim of resolution of inflammation?

A

Regenerate damaged tissue
Regain function
Minimal damage
Sort lived inflammation

33
Q

Describe some of the things that must happen for resolution of inflammation

A
  • Leukocytes stop being recruited
  • Vascularisation returns to normal
  • Draining of oedema
  • Decay and degredation of mediators
  • Apoptosis of leukocytes
34
Q

Describe how inhibition of inflammation works

A

Lipoxins are an arachidonic acid metabolite that inhibits PMN adhesion and chemotaxis

They negatively regulate the leukotrienes

35
Q

What are the features of systemic acute phase inflammation? (9)

A
  1. Fever
  2. Acute phase proteins
  3. High BP
  4. Fast heart rate
  5. Reduced sweating, presence of rigors and chills
  6. Anorexia
  7. Cachexia
  8. Lots of leukocytes
  9. Sepsis
36
Q

Describe what is happening in fever

A

The individual’s body the petite increases by 1-4 degrees in an aim to perhaps reduce the ability of the microbes to replicate

37
Q

Which molecules cause fever?

What are these molecules called?

A

Pyrogens cause fever
Exogenous: bacterial and viral molecules
Endogenous: cytokines

38
Q

What is thought to be the aim in fever?

A

Reduce the replication rate of the microorganisms

39
Q

What are the acute phase proteins, and why are they important?

A

SAA (serum amyloid A)
C reactive protein
Fibrinogen

These molecules in the blood are an indicator that there is inflammation

40
Q

Describe why erythrocytes sedimentation rate is important

A

Increased sedimentation rate indicates that there is fibrinogen bound to RBCs –> inflammation

41
Q

What is leukocytosis and what does it indicate?

Outline the different ones (3)

A

This is increased leukocytes in the blood
Neutrophillia: bacterial infection
Eosinophilia: hypersensitivities, parasite infection
Lymphoctosis: viral infection

42
Q

Why is there decreased sweating, rigors and chills during systemic acute phase reaction?

A

This is related to the change of the body’s temperature set point

43
Q

What causes anorexia during system acute phase reaction?

A

Cytokine action on the brain

44
Q

What is cachexia?

What is the mechanism?

A

This is mobilisation of the body’s fat stores due to TNF –> wasting

45
Q

What is sepsis?

A

This is large amounts of microbes in the blood

46
Q

What is the outcome of sepsis?

A
  • Vasodilation of the entire vascularisation –> hypotensive shock
  • Hypoglycaemia
  • Disseminated intra vascular coagulation (small blood clots)
47
Q

What causes hypotensive shock?

A

Widespread vasodilation, due to many cytokines circulating in the blood

48
Q

What are the different morphologies of acute inflammation?

A

Serous
Fibrinous
Supparative

49
Q

Describe the features of serous inflammation

A

Serous membranes (pleural, peritoneal, pericardial) surround the serous cavity, which is filled with a transudate

50
Q

When is serous inflammation seen?

A

Burns

Viral infections

51
Q

What is the mechanism of fibrinous inflammation?

A
  1. Increased vascular permeability –>

2. Large deposits of fibrinogen from the exudate

52
Q

How is fibrinous inflammation resolved?

A

Fibrinolysis

Macrophages clean up the debris

53
Q

When does fibrinous inflammation occur?

A

Meningitis
Pleurisy
Pericarditis

54
Q

What is the appearance and structure of supparative inflammation, and why is this so?

A

Abscesses of pus

The green colour is from the myeloperoxidase from the PMN

55
Q

When does supparative inflammation occur?

A

Pyogenic bacterial infection; staphylococci

56
Q

What is ulceration?

A

This is the loss of layers of tissue from the surface

57
Q

What causes ulceration?

A

Necrosis or inflammation

58
Q

Where can ulceration occur?

A

Mucosa of the mouth
Gastrointestinal tract
Genitourinary tract
Lower extremities if circulation is poor

59
Q

What are the clinical symptoms of systemic acute phase inflammation?

Broadly, what causes these symptoms?

A

Fever
Myalgia
Arthralgia
Anorexia

These are caused by the host’s response to injury, not the injury itself

60
Q

What is collectin?

A

Collectin is a protein that binds to a sugar on the coat of a microbe

Miscellaneous (109 decks)

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