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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
Q

Why does tumur occur

A

Due to leaky capillaries leaking plasma

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26
Q

Why does calor occur

A

increase in circulation results in increase in temperature

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27
Q

Why does dolor occur

A

release of chemicals stimulate nerve endings (substance P)

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28
Q

Why does the amount of swelling determine how bad an injury is

A

it indicates the length of time the endothelium has been leaky/ amount of blood substance that has passes through

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29
Q

What are the features of a normal venule

A

Intact basement membrane, endothelial cell and tight junction

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30
Q

What are the features of vasoactive mediator induced injury

A

Endothelial retraction and gap formation

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31
Q

What is the time course of changes in permeability in a vasoactive mediator-induced injury

A

1 hour

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32
Q

What are the features of direct injury to endothelium

A

Denuded basement membrane, blebbing

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33
Q

What is the time course of changes in permeability in direct injury to epithelium

A

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.

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34
Q

How do WBCs leave vessels

A

Rolling, firm adhesion and transmigration

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35
Q

Describe rolling

A

Mediated by selectins (expressed on endothelium and WBC wall)

36
Q

Describe firm adhesion

A

Mediated by beta-1 and beta-2 integrins

37
Q

Describe transmigration

A

Medicated by PCAM-1 etc.

38
Q

What do the CAMS on the endothelial cell interact with

A

The integrins on the WBC wall

39
Q

What are the three different options for where selectins come from

A
  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
Q

What are the 2 sources of vascular permeability factors

A

Plasma and cell

41
Q

What are the plasma derived factor mediators

A

fibrin split products, kinins (bradykinins), C3a and C5a

42
Q

Describe the pathway to produce fibrin split products

A

hageman factor activation -> clotting/ fibrinolytic system -> fibrin split factors

43
Q

Describe the pathway to produce kinins

A

hageman factor activation -> clotting/ fibrinolytic system -> kinins

44
Q

Describe the pathway to produce C3a and C5a

A

complement system activation -> C3a and C5a

45
Q

What are cell derived factor mediators

A

Histamine; serotonin; platelet-activating factor, prostaglandins, leukotrienes; nitric oxide, prostaglandins

46
Q

Describe the pathway to produce histamine

A

mast cell/ basophil degradation -> histamine

47
Q

Describe the pathway to produce serotonin

A

platelets -> serotonin

48
Q

Describe the pathway to produce platelet-activating factor, prostaglandins, leukotrienes

A

inflammatory cells -> platelet-activating factor, prostaglandins, leukotrienes

49
Q

Describe the pathway to produce nitric oxide, prostaglandins

A

endothelium -> nitric oxide, prostaglandins

50
Q

What do plasma derived and cell derived mediator factors result in

A

Increased vascular permeability -? oedema

51
Q

What do vasocative factors do

A

Effect blood vessel

52
Q

What do chemitactic factors do

A

attract more cells

53
Q

What responds in acute inflammation

A

Neutrophil (main WBC, aided by platelet and mast cells)

54
Q

What responds in chronic inflammation

A

Macrophage (main WBC, aided by lymphocytes and plasma cells

55
Q

What are the causes of tissue injury

A

Trauma, ischaemia, neoplasm, infectious agent (bacterium, virus, fungi, parasite), foreign particle (e.g. asbestos)

56
Q

What does tissue injury result in

A

production of inflammatory mediators

57
Q

What does production of inflammatory mediators result in

A

production of vasoactive mediators and chemotactic factors

58
Q

What are vasoactive mediators

A

histamine, serotonin, bradykinin, anaphylatoxins, leukotrienes/ prostaglandins, platelet activating factor, nitric oxide

59
Q

What are chemotactic factors

A

C5a, lipoxygenase products: LTB4, formylated peptides, chemkines

60
Q

What do chemotactic factors result in

A

acute inflammation and chronic inflammation

61
Q

What are anaphylatoxins

A

They happen before inflammation (initiate it)

62
Q

What substances are anaphylatoxins

A

C4a, C3a, C5a

63
Q

What do anaphylatoxins do

A

trigger degranulation (release of substances) of endothelial cells, mast cells or phagocytes which produce a local inflammatory response.

64
Q

What happens if degranulation is widespread

A

It can cause a shock-like syndrome similar to that of an allergic reaction

65
Q

What do anaphylatoxins indirectly mediate

A

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
Q

What results in the termination of inflammation

A

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
Q

What are the possible outcomes of acute inflamation

A

complete resolution, healing, chronic inflammation

68
Q

What are morphologic patterns

A

specific patterns of acute and chronic inflammation seen during particular situations that arise in the body

69
Q

What is the morphological pattern of granulamatous inflammation

A

formation of granulomas (TB, leprosy, sarcoidosis and syphilis)

70
Q

What is the morphological pattern of fibrinous inflammation

A

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
Q

What is the morphological pattern of purulent inflammation

A

arising from a large amount of pus

72
Q

What is the morphological pattern of serous inflammation

A

effusion of non-viscous fluid e.g. blisters

73
Q

What is the morphological pattern of ulcerative inflammation

A

inflammation near an epithelium, which can lead to necrosis of tissue from surface -> ulcer

74
Q

What morphological patterns exist

A

Granulatomous, fibrinous, purulent, serous and ulcerative inflammation

75
Q

When can acute inflammation become chronic inflammation

A

If the body is unable to remove threat or its inflammation factors (when acute inflammation doesn’t terminate)

76
Q

Describe the features of chronic inflammation

A

prolonged activation, active inflammation, tissue destruction, attempts at repair

77
Q

How does chronic inflammation heal

A

By fibrosis

78
Q

What is an example of an autocrine macrophage

A

IL-2

79
Q

What is an example of a parocrine macrophage

A

chemokines, leukocyte removal

80
Q

What is an example of an endocrine macrophage

A

IL-6, acute phase response, fever

81
Q

What is the role of activated T cells in macrophages

A

Add cytokine (IFN-gamma) to tissue macrophages -> actiavted macrophages

82
Q

What is the role of non-immune activation in macrophages

A

endotoxin, fibronectin, chemical mediators covert tissue macrophages to activated macrophages

83
Q

What can chronic inflammation be

A

Non-specific or granulomatous

84
Q

What is a granuloma

A

collection of fused macrophages (after neutrophils have tried to remove threat) therefore it becomes walled off

85
Q

Whar is granulomatous inflammation

A

an inflammatory response with either granulomas or a dense macrophage infiltration not forming granulomas

Case 1 (10 decks)

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