Acute inflammation and outcomes Flashcards

(61 cards)

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
Which mediators cause Neutrophil adhesion?
IL-1, IL-8, TNFa, Platelet activating factors, leukotrieneB4, C5a, Chemokines
26
Which mediators cause Neutrophil chemotaxis
C5a, LeukotrieneB4, Bacterial components, chemokines, IL-8
27
Which mediators cause fever?
IL-1, TNF, Prostaglandins
28
Which mediators cause pain?
Prostaglandins, bradykinin
29
Which mediators cause tissue necrosis?
Free radicals, lysosomal granule components
30
Name the source and action of histamine
Mast cells, basophils and platelets | Vasodilation, increased vascular permeability, endothelial activation
31
Name the source and action of serotonin
Platelets | Vasoconstriction
32
Name the source and action of prostaglandins
Mast cells, leukocytes | Vasodilation, pain, fever
33
Name the source and action of leukotrienes
Mast cells, leukocytes | Increased vascular permeability, chemotaxis, leukocyte adhesion and activation
34
Name the source and action of platelet activating factor
Leukocytes, endothelial cells | Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
35
Name the source and action of reactive oxygen species
Leukocytes | Killing of microbes, tissue damage
36
Name the source and action of nitric oxide
Endothelium, macrophages | smooth muscle relaxation, killing of microbes
37
Name the source and action of cytokines
Macrophages, lymphocytes, endothelial cells, mast cells Local: endothelial activation Systemic: Acute-phase response, septic shock
38
Name the source and action of chemokines
Leukocytes, activated macrophages | Chemotaxis, leukocyte activation
39
What are the 4 enzyme cascades activated by plasma mediators?
Coagulation system Kinin system Fibrinolytic system Complement system
40
Name the source and action of complement
Liver | Leukocyte chemotaxis and activation, opsonisation, vasodilation
41
Name the source and action of kinins
Liver | Increased vascular permeability, smooth muscle contraction, vasodilation, pain
42
Name the source and action of proteases
Liver | Endothelial activation, Leukocyte recruitment
43
What are the systemic effects of acute inflammation?
``` Increased [neutrophil] in blood Fever Fatigue Loss of appetite Increased acute phase proteins in blood ```
44
What are the acute phase proteins?
Fibrinogen C reactive protein Serum amyloid A Ferritin
45
What does SEPSIS stand for?
``` Shivering Extreme pain Pale skin Sleepy I feel like I might die Short of breath ```
46
What are the 4 main outcomes of acute inflammation?
Tissue resolution - normal tissue structure and function returned Repair by fibrosis - Scar formation Abscess formation Chronic inflammation
47
Define parenchyma and stroma
Parenchyma - Function cells | Stroma - support cells
48
What is the difference between resolution and repair?
Resolution - restore normal function with minimal or no evidence of damage Repair - remodel for strength, Lacks some function
49
What factors affect the outcome of acute inflammation?
Severity of damage Capacity of stem cells in area of damage to divide: Labile, Stable, Permanent Type of agent which caused damage
50
What are the stages of healing by fibrosis?
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
What are the stages of wound healing?
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
What does Epidermal growth factor do?
Regenerates endothelium
53
What does Fibroblast growth factor do?
Fibroblast proliferation, angiogenesis, epithelial cell regeneration
54
What does Platelet derived growth factor do?
Activate fibroblasts to secrete collagen
55
What does Transforming growth factor a do?
Regeneration of epithelial cells
56
What does Transforming growth factor b do?
Fibroblast proliferation, collagen synthesis
57
What does Insulin-like growth factor 1 do?
Synergisitc effects with other growth factors
58
What does Tumour necrosis factor do?
Stimulates angiogenesis
59
How are abscesses formed?
Collection of pus due to infection with pyogenic bacteria
60
What is chronic inflammation?
Inflammation of a prolonged duration
61
Which cells are involved in chronic inflammation?
Lymphocytes, plasma cells, eosinophils, mast cells