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Structure, function and defence > Acute inflammation and outcomes > Flashcards

Acute inflammation and outcomes Flashcards

1
Q

Define inflammation

A

Rapid response to injury in vascalarised tissue

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2
Q

What are the 2 phases of inflammation?

A

Vascular phase

Cellular phase

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3
Q

What happens in the vascular phase?

A

Vasodilation to increase permeability
Increase in blood flow to area of injury
Plasma proteins leave the capillaries and form inflammatory exudate

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4
Q

What happens in the cellular phase?

A

Cells leave the bloodstream and travel to the site of injury
Cells are recruited and activated
Phagocytosis

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5
Q

What are the 5 cardinal signs of inflammation?

A

Rubor (Redness) - Vasodilation
Calor (Heat) - increased blood flow
Tumor (Swelling) - Edema
Dolor (Pain) - Physical/chemical factors at nerve endings
Functio Laesa (loss of function) - Pain causing guarding reflex

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6
Q

What is the vascular phase mediated by?

A 
Mast cells (Histamine)
Endothelial cells (Nitric oxide)
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7
Q

What is the inflammatory exudate composed of?

A

Plasma
Proteins - Fibrinogen mainly
Neutrophils, macrophages and lymphocytes

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8
Q

What can the inflammatory exudate be described as?

A

Serous - watery/plasma
Haemorrhagic - RBCs, damaged vessels
Fibrinous - Fibrinogen, sticky
Purulent - pus

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9
Q

What do the Endothelial cells do?

A

Secrete Nitric oxide, Cytokines and other mediators

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10
Q

What do Polymorphonuclear leukocytes do?

A

Eliminate microbes and dead tissue

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11
Q

What do the plasma proteins do?

A

Mediate inflammation, eliminate microbes, release clotting factors and kininogens

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12
Q

What do the Lymphocytes do?

A

Mediate immune response

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13
Q

What do the Monocytes do?

A

Turn into macrophages and phagocytose

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14
Q

What do mast cells do?

A

Secrete mediators (Histamine)

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15
Q

What do fibroblasts do?

A

Secrete ECM

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16
Q

How do neutrophils leave the bloodstream?

A

Selectins are expressed which roll along the endothelium until a neutrophil is bound. Once bound, integrins are expressed which causes adhesion to the endothelium. CD11 and CD18 aggregate and cause a conformational change. PECAM-1 binds and mediates transendothelial emigration.

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17
Q

How does phagocytosis take place?

A

Foreign body is bound by Phagocyte
Actin-driven pseodopodium further binds the foreign body
Foreign body is engulfed by internalisation
Membrane fusion forms phagosome
Lysosomes fuse with phagosome and release digestive enzymes
Foreign body is broken down

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18
Q

What is opsonisation?

A

When a complement protein tags a foreign body for recognition by phagocytes

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19
Q

Name the 2 cell-derived preformed mediators and their origins.

A

Histamine - Mast cells, Basophils and platelets

Serotonin - Platelets

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20
Q

Name the cell-derived newly synthesised mediators and their origins.

A

Prostaglandins - Leukocytes, Mast cells
Leukotrienes - Leukocytes, Mast cells
Platelet activating factor - Leukocytes, Endothelial cells
Reactive oxygen species - Leukocytes
Nitric oxide - Macrophages, Endothelial cells
Cytokines - Macrophages, leukocytes, Mast cells, Endothelial cells
Neuropeptides - Leukocytes, nerve fibres

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21
Q

Name the plasma-protein derived mediators for complement activation.

A

C3a, C3b, C5a, C5b-9

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22
Q

Name the plasma protein derived factor XII actvators.

A

Kinin system

Fibrinolysis system

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23
Q

Which mediators cause vasodilation?

A

Histamine, Prostaglandin, Nitric oxide, bradykinin, Platelet activating factor

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24
Q

Which mediators cause increased permeability?

A

Histamine (briefly), C3a, C5a, bradykinin, leukotrienes, Platelet activating factor, nitric oxide

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25
Q

Which mediators cause Neutrophil adhesion?

A

IL-1, IL-8, TNFa, Platelet activating factors, leukotrieneB4, C5a, Chemokines

26
Q

Which mediators cause Neutrophil chemotaxis

A

C5a, LeukotrieneB4, Bacterial components, chemokines, IL-8

27
Q

Which mediators cause fever?

A

IL-1, TNF, Prostaglandins

28
Q

Which mediators cause pain?

A

Prostaglandins, bradykinin

29
Q

Which mediators cause tissue necrosis?

A

Free radicals, lysosomal granule components

30
Q

Name the source and action of histamine

A

Mast cells, basophils and platelets

Vasodilation, increased vascular permeability, endothelial activation

31
Q

Name the source and action of serotonin

A

Platelets

Vasoconstriction

32
Q

Name the source and action of prostaglandins

A

Mast cells, leukocytes

Vasodilation, pain, fever

33
Q

Name the source and action of leukotrienes

A

Mast cells, leukocytes

Increased vascular permeability, chemotaxis, leukocyte adhesion and activation

34
Q

Name the source and action of platelet activating factor

A

Leukocytes, endothelial cells

Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

35
Q

Name the source and action of reactive oxygen species

A

Leukocytes

Killing of microbes, tissue damage

36
Q

Name the source and action of nitric oxide

A

Endothelium, macrophages

smooth muscle relaxation, killing of microbes

37
Q

Name the source and action of cytokines

A

Macrophages, lymphocytes, endothelial cells, mast cells
Local: endothelial activation
Systemic: Acute-phase response, septic shock

38
Q

Name the source and action of chemokines

A

Leukocytes, activated macrophages

Chemotaxis, leukocyte activation

39
Q

What are the 4 enzyme cascades activated by plasma mediators?

A

Coagulation system
Kinin system
Fibrinolytic system
Complement system

40
Q

Name the source and action of complement

A

Liver

Leukocyte chemotaxis and activation, opsonisation, vasodilation

41
Q

Name the source and action of kinins

A

Liver

Increased vascular permeability, smooth muscle contraction, vasodilation, pain

42
Q

Name the source and action of proteases

A

Liver

Endothelial activation, Leukocyte recruitment

43
Q

What are the systemic effects of acute inflammation?

A 
Increased [neutrophil] in blood
Fever
Fatigue
Loss of appetite
Increased acute phase proteins in blood
44
Q

What are the acute phase proteins?

A

Fibrinogen
C reactive protein
Serum amyloid A
Ferritin

45
Q

What does SEPSIS stand for?

A 
Shivering
Extreme pain
Pale skin
Sleepy
I feel like I might die
Short of breath
46
Q

What are the 4 main outcomes of acute inflammation?

A

Tissue resolution - normal tissue structure and function returned
Repair by fibrosis - Scar formation
Abscess formation
Chronic inflammation

47
Q

Define parenchyma and stroma

A

Parenchyma - Function cells

Stroma - support cells

48
Q

What is the difference between resolution and repair?

A

Resolution - restore normal function with minimal or no evidence of damage
Repair - remodel for strength, Lacks some function

49
Q

What factors affect the outcome of acute inflammation?

A

Severity of damage
Capacity of stem cells in area of damage to divide: Labile, Stable, Permanent
Type of agent which caused damage

50
Q

What are the stages of healing by fibrosis?

A

Granulation tissue - Macrophages, fibroblasts and angiogenesis
Fibrosis and scar formation - Fibroblasts generate matrix, scar is formed from collagen
Remodelling - vessels in area are reduced and pale scar remains

51
Q

What are the stages of wound healing?

A

Inflammatory phase - Macrophages produce growth factors
Proliferative phase - Building of tissue, Fibroblasts secrete matrix components, angiogenesis, Epithelial cells grow over wounds
Wound contraction and remodelling phase - Collagen breaks down, wound contracts, decreased vacularity

52
Q

What does Epidermal growth factor do?

A

Regenerates endothelium

53
Q

What does Fibroblast growth factor do?

A

Fibroblast proliferation, angiogenesis, epithelial cell regeneration

54
Q

What does Platelet derived growth factor do?

A

Activate fibroblasts to secrete collagen

55
Q

What does Transforming growth factor a do?

A

Regeneration of epithelial cells

56
Q

What does Transforming growth factor b do?

A

Fibroblast proliferation, collagen synthesis

57
Q

What does Insulin-like growth factor 1 do?

A

Synergisitc effects with other growth factors

58
Q

What does Tumour necrosis factor do?

A

Stimulates angiogenesis

59
Q

How are abscesses formed?

A

Collection of pus due to infection with pyogenic bacteria

60
Q

What is chronic inflammation?

A

Inflammation of a prolonged duration

61
Q

Which cells are involved in chronic inflammation?

A

Lymphocytes, plasma cells, eosinophils, mast cells

Structure, function and defence (28 decks)

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