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3 IIH > 5.3 Inflammation > Flashcards

5.3 Inflammation Flashcards

1
Q

What are the 4 cardinal signs of inflammation?

A

rubor
tumor
calor
dolor

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2
Q

How are pathogens recognised?

A

Pattern Recognition Receptors recognise pattern associated molecular patterns

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3
Q

What role do mast cells play in the acute phase?

A

they start the whole thing off!

detect injury
release histamine and other mediators
initiating inflammatory response

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4
Q

What does histamine do?

A

vasodilation
endothelial junction widening (permeability)
irritation of nerve endings (itchiness)

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5
Q

What is the effect of the eicosanoids on inflammation?

How might this be targeted?

A

cause vasodilation and prolong oedema

COX may be blocked by aspirin and NSAIDs

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6
Q

What is the effect of the lipoxygenase pathway on inflammation?

How might this be targeted?

A

chemotaxins and vasoconstrictors, cause vascular permeability and bronchospasms

leukotriene receptor antagonists like monteleukast are used in asthma

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7
Q

How does increased permeability contribute to inflammation?

A

plasma proteins and cells extravasate (swelling)

fluid loss concentrated red blood cells and slows blood flow

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8
Q

How does vasodilation contribute to inflammation?

A

more blood flow and pooling cause rubor and calor

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9
Q

How does movement of white cells contribtue to inflammation?

A

blood stasis and activation signals lead to immune cells migrating towards offending agents

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10
Q

How can local inflammation cause systemic infection?

A

partly mediated by acute phase cytokines

IL-1, IL-6, TNF-alpha

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11
Q

What is the effect of acute phase cytokines on endothelium?

A

vasodilation and increased permeability to get activated cells into tissues

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12
Q

What is the effect of acute phase cytokines on the hypothalamus?

A

fever stimulation to decrease pathogen replicaiton

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13
Q

What is the effect of acute phase cytokines on fat and muscle tissues?

A

protein / energy mobilisation, for fever and immune response

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14
Q

What is the effect of acute phase cytokines on the liver?

A

increases acute phse proteins (CRP), contributing to opsonisation and complement activation

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15
Q

What is the effect of acute phase cytokines on bone marrow?

A

neutrophil mobilisation to increase phagocytosis

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16
Q

What is the effect of acute phase cytokines on dendritic cells?

A

TNF stimulates migration to lymph nodes and maturation, initiating the adaptive response

17
Q

How might we treat IBD?

A

blocking the acute phase cytokine TNF-alpha

18
Q

How might we treat rheumatoid arthritis?

A

any of the acute phase cytokines could be blocked and this would help ngl

19
Q

What might happen if you overproduce TNF-alpha and IL-1?

A

septic shock, so there is massive macrophage activation in liver and spleen in response to pathogens

20
Q

Name 5 outcomes of acute inflammation

A 
complete restitution
healing with scar formation
abscess formation 
granuloma formation
chronic inflammation
21
Q

Why might chronic inflammation occur?

A

when the acute phase can’t be resolved

22
Q

What examples of chronic inflammation are there?

A

persistent injury or infection (ulcer, TB)
prolonged toxic agent exposure (silica)
autoimmune disease states (RA, SLE)

23
Q

What are the mechanisms for chronic inflammation?

A 
cellular infiltration (granulomas)
tissues destruction by inflammatory cells (COPD)
attempts at repair with fibrosis and angiogenesis
24
Q

Why is termination of acute inflammation quite quick?

A

most mediators are very short lived and are degraded immediately

ati-inflammatory cytokines can inhibit produciton of pro-inflammatory cytokines

25
Q

Name 3 acute phase proteins

A

CRP
C3/C4
Fibrinogen Ferritin

26
Q

Name 3 negative control proteins

A

A1 antitrypsin
Albumin
Transferrin

27
Q

How do CRP levels change and why is this useful?

A

rise and fall very quickly in response to presence of infection

can be used clinically to test whether infection is present, and how the patient is responding to treatment

28
Q

What does CRP do?

A

binds to bacteria and fungal cell walls opsonising them and activating classical complement cascade by binding C1q

29
Q

What might CRP increase as a response to?

A

inflammation
injury
infection

30
Q

What is erythrocyte sedimentation rate?

A

the rate at which erythrocytes settle out of unclotted blood in one hour

31
Q

How might ESR change?

A

normally erythrocytes are negatively charged, repelling each other, low ESR

acute phase reactants cause the loss of erythrocyte negative charge resulting in increased sedimentation

32
Q

What is leukocytosis?

A

increase in WBC count, usually as a direct effect of IL-1 and IL-6 on bone marrow neutrophil stores

33
Q

What happens in leukocytosis when precurosor cells are released?

A

‘left shift’, this can result in leukaemoid reaction

3 IIH (23 decks)

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