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Case 1 > Inflammation in Response to Injury > Flashcards

Inflammation in Response to Injury Flashcards

1
Q

What is the cellular response to stress and noxious stimuli

A

Hyperplasia, hypertrophy, atrophy, metaplasia

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2
Q

What is hyperplasia

A

Increase in number of cells

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3
Q

What is an example of hyperplasia

A

BPH (prostate metaplasia)

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4
Q

What is hypertrophy

A

Increase in size of cells

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5
Q

What is an example of hypertrophy

A

Heart cells responding to injury

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6
Q

What is atrophy

A

Decrease in number of cells/ size of cells

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7
Q

What is metaplasia

A

Abnormal changes in nature of a tissue

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8
Q

What is an example of metaplasia

A

Non-keratinised squamous epithelium of the oesophagus replaced for columnar epithelium which can secrete mucous

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9
Q

What are the two types of inflammation that occur when cells die

A

Necrosis and apoptosis

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10
Q

What is necrosis

A

Cells lose cell membrane and the cytoplasmic remnants and debris collect

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11
Q

What is apoptosis

A

Cells shrivel and split into similar droplets which are phagocytosed by WBCs

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12
Q

What are cell injury agents

A

Oxygen deprivation (hypoxia or ischaemia= decreased blood supply), physical agents, chemic agents or drugs

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13
Q

What are infectious agents

A

immunological reactions, genetic derangements, nutritional imbalances

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14
Q

What do stimuli that cause cell injury also do

A

induce inflammation in vascularised tissue

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15
Q

Why wouldn’t you see inflammation in the lens

A

It is avascular

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16
Q

What is the aim of inflammation

A

neutralise the offending agent and start the process of repair

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17
Q

What are cardinal signs of inflammation

A

Rubor, tumor, dolor, calor, functio laesa

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18
Q

What are the major components of inflammation

A

Vascular changes and cellular changes

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19
Q

Why do vascular changes occur in inflammation

A

Blood cells in circulation need to reach damaged tissues

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20
Q

How do vascular changes occur in inflammation

A

Vasodilation via histamine and NO, increased permeability and stasis

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21
Q

What is the role of vasodilation in inflammation

A

Slows down blood flow, margination must occur (cells have to move from middle of flow to the margin in order to leave vessel) -> stasis

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22
Q

What is the role of increased permeability in inflammtion

A

WBCs exit blood vessels, would normally be blocked by endothelial cells but they retract during inflammation. This occurs normally in venules and is a short lived process. Retraction is induced by NO and histamine

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23
Q

What happens when an injury to the endothelial lining occurs

A

The retraction of endothelial cells is a longer lived process so more passes through (including plasma)

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24
Q

Why does ribor occur

A

Due to dilation

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25
Why does tumur occur
Due to leaky capillaries leaking plasma
26
Why does calor occur
increase in circulation results in increase in temperature
27
Why does dolor occur
release of chemicals stimulate nerve endings (substance P)
28
Why does the amount of swelling determine how bad an injury is
it indicates the length of time the endothelium has been leaky/ amount of blood substance that has passes through
29
What are the features of a normal venule
Intact basement membrane, endothelial cell and tight junction
30
What are the features of vasoactive mediator induced injury
Endothelial retraction and gap formation
31
What is the time course of changes in permeability in a vasoactive mediator-induced injury
1 hour
32
What are the features of direct injury to endothelium
Denuded basement membrane, blebbing
33
What is the time course of changes in permeability in direct injury to epithelium
Severe changes peak at around 2.5 hours and last longer than 5 hours. Mild changes peak straight away and have stopped completely by one hour then start again from 2-5 hours.
34
How do WBCs leave vessels
Rolling, firm adhesion and transmigration
35
Describe rolling
Mediated by selectins (expressed on endothelium and WBC wall)
36
Describe firm adhesion
Mediated by beta-1 and beta-2 integrins
37
Describe transmigration
Medicated by PCAM-1 etc.
38
What do the CAMS on the endothelial cell interact with
The integrins on the WBC wall
39
What are the three different options for where selectins come from
1. selectins present inside cell and are expressed on cell wall. 2. selectin is not there and has to be generated from scratch. 3. chemokines make the selectins present more sticky (increase avidity)
40
What are the 2 sources of vascular permeability factors
Plasma and cell
41
What are the plasma derived factor mediators
fibrin split products, kinins (bradykinins), C3a and C5a
42
Describe the pathway to produce fibrin split products
hageman factor activation -> clotting/ fibrinolytic system -> fibrin split factors
43
Describe the pathway to produce kinins
hageman factor activation -> clotting/ fibrinolytic system -> kinins
44
Describe the pathway to produce C3a and C5a
complement system activation -> C3a and C5a
45
What are cell derived factor mediators
Histamine; serotonin; platelet-activating factor, prostaglandins, leukotrienes; nitric oxide, prostaglandins
46
Describe the pathway to produce histamine
mast cell/ basophil degradation -> histamine
47
Describe the pathway to produce serotonin
platelets -> serotonin
48
Describe the pathway to produce platelet-activating factor, prostaglandins, leukotrienes
inflammatory cells -> platelet-activating factor, prostaglandins, leukotrienes
49
Describe the pathway to produce nitric oxide, prostaglandins
endothelium -> nitric oxide, prostaglandins
50
What do plasma derived and cell derived mediator factors result in
Increased vascular permeability -? oedema
51
What do vasocative factors do
Effect blood vessel
52
What do chemitactic factors do
attract more cells
53
What responds in acute inflammation
Neutrophil (main WBC, aided by platelet and mast cells)
54
What responds in chronic inflammation
Macrophage (main WBC, aided by lymphocytes and plasma cells
55
What are the causes of tissue injury
Trauma, ischaemia, neoplasm, infectious agent (bacterium, virus, fungi, parasite), foreign particle (e.g. asbestos)
56
What does tissue injury result in
production of inflammatory mediators
57
What does production of inflammatory mediators result in
production of vasoactive mediators and chemotactic factors
58
What are vasoactive mediators
histamine, serotonin, bradykinin, anaphylatoxins, leukotrienes/ prostaglandins, platelet activating factor, nitric oxide
59
What are chemotactic factors
C5a, lipoxygenase products: LTB4, formylated peptides, chemkines
60
What do chemotactic factors result in
acute inflammation and chronic inflammation
61
What are anaphylatoxins
They happen before inflammation (initiate it)
62
What substances are anaphylatoxins
C4a, C3a, C5a
63
What do anaphylatoxins do
trigger degranulation (release of substances) of endothelial cells, mast cells or phagocytes which produce a local inflammatory response.
64
What happens if degranulation is widespread
It can cause a shock-like syndrome similar to that of an allergic reaction
65
What do anaphylatoxins indirectly mediate
Smooth muscle cells contraction e.g. bronchospasms (most important thing to stop bleeding); increase in teh permeability of blood capillaries; chemotaxis- receptor-mediated movement of leukocytes in the direction of the increasing concentration of anaphylatoxins.
66
What results in the termination of inflammation
Mediator production and half life; neutorophil lifespan; stop signals: lipoxin (AA metabolite), anti-inflammatory cytokines (L-10, TGF-beta), lipid mediators (resolvins, protectins), cholinergic discharge (neural impulses)- inhibit TNF discharge in macrophages
67
What are the possible outcomes of acute inflamation
complete resolution, healing, chronic inflammation
68
What are morphologic patterns
specific patterns of acute and chronic inflammation seen during particular situations that arise in the body
69
What is the morphological pattern of granulamatous inflammation
formation of granulomas (TB, leprosy, sarcoidosis and syphilis)
70
What is the morphological pattern of fibrinous inflammation
increase in vascular permeability allows for fibrin to pass through blood vessels. Fibrin can be converted into a scar, particularly between serous membranes e.g. pericardium
71
What is the morphological pattern of purulent inflammation
arising from a large amount of pus
72
What is the morphological pattern of serous inflammation
effusion of non-viscous fluid e.g. blisters
73
What is the morphological pattern of ulcerative inflammation
inflammation near an epithelium, which can lead to necrosis of tissue from surface -> ulcer
74
What morphological patterns exist
Granulatomous, fibrinous, purulent, serous and ulcerative inflammation
75
When can acute inflammation become chronic inflammation
If the body is unable to remove threat or its inflammation factors (when acute inflammation doesn't terminate)
76
Describe the features of chronic inflammation
prolonged activation, active inflammation, tissue destruction, attempts at repair
77
How does chronic inflammation heal
By fibrosis
78
What is an example of an autocrine macrophage
IL-2
79
What is an example of a parocrine macrophage
chemokines, leukocyte removal
80
What is an example of an endocrine macrophage
IL-6, acute phase response, fever
81
What is the role of activated T cells in macrophages
Add cytokine (IFN-gamma) to tissue macrophages -> actiavted macrophages
82
What is the role of non-immune activation in macrophages
endotoxin, fibronectin, chemical mediators covert tissue macrophages to activated macrophages
83
What can chronic inflammation be
Non-specific or granulomatous
84
What is a granuloma
collection of fused macrophages (after neutrophils have tried to remove threat) therefore it becomes walled off
85
Whar is granulomatous inflammation
an inflammatory response with either granulomas or a dense macrophage infiltration not forming granulomas

Case 1 (10 decks)

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