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PathoPhys > Lecture 3 - Inflammation > Flashcards

Lecture 3 - Inflammation Flashcards

1
Q

State the main WBC in blood, and there % prevalence?

A

“Never let monkeys eat bananas”

Neutrophils - 60%
Lymphocytes - 30%
Monocytes - 6%
Eosinophils - 3% 
Basophils - 1%
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2
Q

haematoxylin:
a. ) Acidic or basic?
b. ) What stained?
c. ) basophillic or eosinophilic?

A

a. ) basic
b. ) nucleus (DNA)
c. ) basophilic

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3
Q

eosin:
a. ) Acidic or basic?
b. ) What stained?
c. ) basophillic or eosinophilic?

A

a. ) acidic
b. ) cytoplasm, muscle, collagen etc
c. ) eosinophilic

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4
Q

Which WBC are granulocytes?

A
  • eosinophils
  • basophils
  • neutrophils
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5
Q

A macrophage in the bloodstream is known as?

A

a monocyte

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6
Q

what shape is a monocyte/ macrophage nucleus?

A

kidney shape

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7
Q

t/f: a monocyte has a small perimeter of cytoplasm

A

false - these cells are phagocytic so need large amount of area for this

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8
Q

Monocytes/ macrophages often have special names in resident tissues - provide 2 examples?

A

kuppfer cells - liver

histiocytes - sinus

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9
Q

Complete the statement:

___phils are prevalent in large numbers because they are required to act at short notice, participating in ___ _____

A

neutrophils; acute inflammation

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10
Q

In a patient with acute appendicitis, the tissue is infiltrtated by large amounts of a certain type of cell initially. Which cell is this likely to be?

A

neutrophil

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11
Q

When inflammation is severe pus may form - what is this?

A

a collection of neutrophils and necrotic cells

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12
Q

which WBC is the ‘principle cell involved in acute inflammation’?

A

neutrophil

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13
Q

define abscess

A

a walled off collection of pus

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14
Q

Acute inflammation following tissue damage may go down one of two routes - explain these?

A
  1. If cells can regenerate, within days this is done and normal structure and function is regained (less likely)
  2. If cells cannot regrow as such healing occurs by repair mechanisms, this involves scar formation (‘fibrous repair’) leading to loss of specialized function. This is the more likely outcome.
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15
Q

describe the difference between regeneration and healing

A

healing - involves scar formation (more likely)

regeneration - no scar formation (less likely)

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16
Q

State some vascular events of the inflammatory process?

A

“KFCC makes the cytokine storm”

  1. Coagulation cascade
  2. Fibrinolytic cascade
  3. Kinin cascade
  4. Complement cascade

Overall leads involves many chemical mediators being released, known as ‘cytokine storm’

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17
Q

State the general purpose of inflammation

A

Inflammation is a protective response to:

  • eliminate initial cause of cell injury
  • eliminate necrotic tissue which resulted from insult
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18
Q

Contrast acute and chronic inflammation in terms of:

onset

A

acute - rapid

chronic - delayed

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19
Q

Contrast acute and chronic inflammation in terms of:

duration

A

acute - days

chronic - weeks to years

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20
Q

Contrast acute and chronic inflammation in terms of:

cardinal signs

A

acute - pain, heat, swelling, itchiness, loss function

chronic - loss function

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21
Q

Contrast acute and chronic inflammation in terms of:

specificity of response

A

acute - non-specific

chronic - specific to causative agent (thus adaptive immunity involved)

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22
Q

Contrast acute and chronic inflammation in terms of:

causative agent

A

acute - pathogens, injury (physical/ chemical), tissue necrosis, immune response
chronic - persistent infection, continued presence of foreign body, autoimmunity

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23
Q

Contrast acute and chronic inflammation in terms of:

fundamental cells involved

A

acute - neutrophils, subsequently macrophages

chronic - macrophages, lymphocytes, plasma cells

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24
Q

define acute inflammation

A

a rapid, non-specific response to injury/ microorganisms/ foreign substances which is designed to deliver WBC’s and plasma proteins to sites of injury

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25
Q

t/f: the white blood cells and chemical mediators of acute inflammation
normally circulate in the blood

A

true

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26
Q

Why do the white blood cells and chemical mediators of acute inflammation
circulate in the blood?

A

This enables rapid delivery of these things to site of infection - rapid response

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27
Q

Heat, redness and swelling are often observed during acute inflammation. Explain this physiologically?

A

Due to increased permeability of blood vessels & increased blood supply to area of infection

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28
Q

Why does pain occur during acute inflammation?

A

Due to release of certain chemical mediators

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29
Q

Acute inflammation is (specific/ non-specific). What does this infer about the response brought about?

A

Acute inflammation is non-specific to causative agent, meaning regardless of causative agent the response (the inflammation) will be the same

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30
Q

State the main types of inciting agents for acute inflammation?

A
  1. Endogenous - tissue necrosis, immune Rn

2. Exogenous - infection, trauma, physical and chemical damage, foreign body’s

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31
Q

What is necessary for acute inflammation to begin? What cells are involved with this?

A

Recognition of the injurious agent is necessary

macrophages and mast cells resident in tissues responsible for this

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32
Q

Describe the two main components of acute inflammation?

A
  1. Cellular changes - leucocyte activation/ recruitment, phagocytosis
  2. Vascular changes - permeability, vasodilation
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33
Q

Detail vascular changes which occur in acute inflammation?

A
  1. Vasodilatation:
    - caused by chemical mediators (Histamine from mast cell)
    - leading to increased blood flow
    - leads to redness and heat
  2. Increased permeability:
    - allowing plasma proteins and cells to leave circulation (enter extravascular space)
    - leads to swelling
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34
Q

Detail cellular changes which occur in acute inflammation?

A
  1. Leucocyte activation
  2. Leucocyte recruitment - via chemotaxis (?)
  3. Phagocytosis & degradation
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35
Q

what’s the consequence of vasodilation in acute inflammation (clinically)?

A

heat and redness

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36
Q

what’s the consequence of increased permeability in acute inflammation (clinically)?

A

swelling

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37
Q

physiologically how does the BV become more permeable?

A

by retraction of endothelial cells, which is controlled by chemical mediators (histamine, bradykinin, leukotrienes)

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38
Q

for the following mediator, state the source (cells) and action:
histamine

A

mast cells, platelets, basophils

vasodilate, increase permeability

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39
Q

for the following mediator, state the source (cells) and action:
serotonin

A

platelets

vasodilate, increase permeability

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40
Q

for the following mediator, state the source (cells) and action:
prostoglandins

A

mast cells, leucocytes

increase permeability

41
Q

for the following mediator, state the source (cells) and action:
leukotrienes

A

Leucocytes, mast cells

Increase permeability

42
Q

for the following mediator, state the source (cells) and action:
Platelet-activating factor

A

leucocytes (Inc. eosinophils), mast cells

vasodilate, increase permeability, activate platelets

43
Q

for the following mediator, state the source (cells) and action:
kinins

A

plasma (prod. in liver)

vasodilate, increase permeability

44
Q

explain how leucocyte recruitment occurs?

A
  1. cytokines & chemokines released from macrophages in damaged tissue. These cause expression of selectins (endothelial cells) and integrins (leucocytes), allowing adhesion of WBC to vascular walls
  2. leucocytes move from vascular lumen to extravascular space toward site
45
Q

define chemotaxis

A

movt. organism in response to chemical stimulus: WBC’s move along a chemical gradient to site

46
Q

define chemokine

A

chemotactic cytokine = chemokine, binds to cell surface receptor on leucocytes

47
Q

What are integrins/ selectins? Contrast their purpose?

A

Selectins - on endothelial cells, allow loose adhesion
integrins - on WBC, allow stable adhesion

allow leucocyte adhesion to vascular wall

48
Q

what produces chemokines?

A
  • microorgansism themselves
  • macrophages
  • WBC
49
Q

how do WBC move?

A

contractile filaments used to extend pseudopods

50
Q

state some of the main functions of WBC once activated at the site of insult?

A
  • phagocytosis
  • lysis/ killing engulfed pahogens
  • production mediators which amplify inflammation
51
Q

what activates WBC?

A
  • bacteria/ viral products

- inflammatory mediators secreted by mast cells and macrophages

52
Q

explain steps involved in phagocytosis?

A
  1. Recognition, attachment by receptors on WBC surface
  2. Engulfment, formation of phagsosome
  3. Killing and degradation - fusion of phagsosome with lysosome to form phagolysosome, degradation with enzymes and lisosomal acid hydrolases
53
Q

name a enzyme involved in phagocytosis?

A

myeloperoxidase

54
Q

for the following chemical mediator, state the source and action:
cytokines

A

macrophages, endothelial cells and mast cells

endothelial activation (expression of selectins)

55
Q

for the following chemical mediator, state the source and action:
chemokines

A

leucocytes, macrophages

chemotaxis, leucocyte activation (expression of integrins)

56
Q

for the following chemical mediator, state the source and action:
prostoglandins

A

mast cells, leucocytes

leucocyte adhesion, chemotaxis, degranulation

57
Q

for the following chemical mediator, state the source and action:
leukotrienes

A

mast cells, leucocytes

WBC adhesion and activation, chemotaxis

58
Q

for the following chemical mediator, state the source and action:
nitric oxide

A

endothelium, macrophages

killing microbes

59
Q

for the following chemical mediator, state the source and action:
Reactive oxygen species

A

WBC

killing microbes

60
Q

for the following chemical mediator, state the source and action:
Proteases

A

Plasma (made in liver)

leucocyte chemotaxis & activation

61
Q

for the following chemical mediator, state the source and action:
complement

A

plasma (made in liver)

endothelial activation, WBC recruitment

62
Q

3 possible outcomes of acute inflammation?

A
  1. Resolution - restoration to completely normal extent, only possible if noxious stimuli removed, cell death and tissue damage must be minimal
  2. Healing with scarring - injurious stimuli removed but damage is too severe to allow complete restoration
  3. Progression to chronic inflammation - when injurious stimuli persists
63
Q

what’s meant by chronic inflammation

A

inflammation persisting for weeks to years

64
Q

cause of chronic inflammation (basic)?

A

ongoing active inflammation; tissue injury and healing occur simultaneously

65
Q

what is chronic inflammation characterized by?

A

mononuclear cell infiltrate

66
Q

causes of chronic inflammation (reasons why inflammation would continue)?

A
  1. Persistent infection - by microbes difficult to kill
  2. Hypersensitivity - ie. rheumatoid arthritis
  3. prolonged exposure toxic agent - ie. silicosis
67
Q

Main cells of chronic inflammation?

A

MONONUCLEAR CELLS:

  • macrophages
  • lymphocytes
  • plasma cells

(eosinophils, neutrophils, mast cells somewhat involved)

68
Q

name the archetypal cell of chronic inflammation?

A

macrophage

69
Q

what’re macrophages derived from?

A

monocytes in blood

70
Q

what activates macrophages?

A

mainly cytokines, chemical mediators

71
Q

what’re activated macrophages called?

A

histiocytes

72
Q

how are lymphocytes involved in chronic inflammation?

A

B and T cells attracted to site by chemokines (chemotaxis), then T cells secrete more cytokines helping to activate macrophages

73
Q

how are plasma cells involved in chronic inflammation?

A

they prod. antibodies

74
Q

what’s meant by granulomatous inflammation? Explain the process of formation

A
  1. T cells release cytokines in response to persistent inflammation
  2. collection epithelioid histiocytes which fuse to form giant cell
75
Q

why do granulomas form?

A
  1. organisms which are resistant to phagolysosomal degradation cause them to form
  2. foreign bodies which immune system cannot remove (ie. splinter), this called a foreign body granuloma
76
Q

In which disease do granulomas most commonly form?

A

TB

77
Q

why do fevers occur?

A

in response to pyrogens, which may be:

  1. Exogenous (bacterial lipopolysachharide)
  2. Endogenous (cytokines, prostoglandins)
78
Q

how do prostoglandins exert there effect to cause fever?

A

resetting of the hypothalamic thermostat

79
Q

define sepsis

A

massive immune response leading to excess inflammation, potentially fatal

80
Q

what can cause sepsis

A

in severe infections, sepsis can be caused by:

  1. Exogenous (bacterial lipopolysachharide)
  2. Endogenous (cytokines, prostoglandins)
81
Q

what is sepsis characterized by?

A

hypotensive shock, disseminated intravascular coagulation

82
Q

define leucocytosis

A

elevated number WBC

83
Q

list the systemic effects of inflammation (4)

A
  1. elevated plasma levels of acute-phase proteins (can cause chronic disease)
  2. Fever
  3. sepsis
  4. Leucocytosis
84
Q

define repair

A

restoration of tissue architecture and function after injury

85
Q

ways in which repair can occur?

A
  1. regeneration (no scarring) - when damage less severe so damaged components can return to normal state
  2. healing (scarring) - when damage severe to a point where CT (scar tissue) must be laid down
86
Q

examples of ‘permanent tissues’?

A

cardiac, neurons

87
Q

t/f: permanent tissues can only heal, not regenerate

A

true

88
Q

how often does regeneration occur in labile tissues (ie. epithelium?

A

continuously

89
Q

t/f: organs with stable populations (ie. liver) cannot regenerate, only heal

A

false - they can regenerate

90
Q

explain the process of healing with scarring

A
  1. angiogenesis (formation new BV)
  2. migration and proliferation of fibroblasts
  3. deposition of extracellular matrix
  4. maturation and organisation of fibrous tissue (remodelling)

1+2= granulation tissue

91
Q

healing with scarring is the likely outcome for what circumstances (~5)

A
  1. acute inflammation (if severe)
  2. chronic inflammation
  3. ischaemic necrosis
  4. wounds in skin
  5. bone fractures
92
Q

repair is under control of growth factors - which ones specifically?

A
  • Transforming growth factor beta (TGF-B)
  • Vascular endothelial growth factor (VEGF)
  • Platelet derived growth factor (PDGF)
  • Epidermal growth factor (EGF)
  • Fibroblast growth factor (FGF)

“epidermal fibroblasts are transforming into vascular platelets”
(add growth factor on end - done!)

93
Q

which cells produce growth factors for repair?

A

macrophages and platelets at site of injury

94
Q

explain some of the actions of growth factors (not specific ones, just general)?

A
  1. chemotaxis (attracts more macrophages in chronic and late acute inflammation)
  2. fibroblast migration and proliferation
  3. angiogenesis
  4. increase synthesis extra-cellular matrix collagen
  5. stimulate epithelial proliferation (ie. skin)
95
Q

what is granulation tissue?

A

the new CT and microscopic BV’s which first forms in the process of scar formation (healing with scarring).

Specifically it is the new BV’s + fibroblasts and their depositions.

96
Q

acute inflammation is characterised by? (cellular level - not clincially)

A

rapid influx of neutrophils into injured tissue

97
Q

chronic inflammation is characterized by?

A

activated macrophages and lymphocytes

98
Q

Three growth factors controlling tissue repair after inflammation are?

A

any 3 of the following…
(“epidermal fibroblasts transform into vascular platelets”)

TGF-B = transforming type B
EGF = epidermal 
FGF = fibroblast
PDGF = platelet derived
VEGF = vascular endothelial

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