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Inflammation Flashcards

1
Q

What are the ten reasons why inflammation is important?

A
  • Pathogenic basis of many diseases
  • Roles in triggering immunity
  • A set of processes that keeps us alive
  • Most AI drugs work by preventing formation or actions of mediators
  • Works on a daily basis
  • Deficiency in a segment of inflammation can cause severe diseases
  • Complex relationship inflammation/cancer
  • Dysregulation of inflammation: lethal or chronic, debilitating diseases
  • Problems caused by AI drugs (iatrogenic)
  • Angiogenesis (ageing, tissue remodeling)
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2
Q

What is the ultimate goal after an injury?

A

Stabilization of the tissue

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3
Q

Describe the general pathway for what happens when you are exposed to microorganisms

A

Microorganism may pass epithelial or secretion barriers
Innate immune cells are ready to target anything foreign and will eliminate what they can really quickly
Macrophages may be activated for phagocytosis
The antigen may drain to the lymph node which may cause further exposure to NK cells and macrophages
Adaptive immunity will then kick in later

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4
Q

Define inflammation and list its two categories

A

“Inflammation is the reaction of vascularized living tissues to local injury or infection, characterized by the movement of fluid and leukocytes from the blood into the affected tissue”
2 main categories:
1. Acute
2. Chronic

A coordinated set of processes through which the host attempts to localize and eliminate micro-organisms, damaged cells, inanimate foreign particles, or antigens

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5
Q

List three roles of inflammation

A

Defence against microorganisms
Initiation of the healing process
Elimination of damaged cells, inanimate foreign particles

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6
Q

Acute inflammation has a ____ onset, relatively ____- lived, stereotypic response to injury or infection, characterized by the _______ out of the ____ and into the ____

A 
Rapid onset
Short-lived
Movement of fluid and neutrophils
Blood
Affected tissue
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7
Q

T/F:

Often an acute inflammatory response evolves into a chronic one

A

False
Rarely becomes chronic
Main aim is to fix the problem and not let it get worse

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8
Q

What are some negative aspects about inflammation?

A 
•	Acute inflammation:
o	Appendicitis (possibility of perforation due to excessive pus formation)
o	Meningitis (intra-cranial pressure)

• Chronic inflammation:
o Tuberculosis (impairment of lung function)
o Arthritis (incapacitation)
o Initiation of cancer?

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9
Q

List some cells involved in inflammation

A

Neutrophils
Endothelial cells
Macrophages
Fibroblasts

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10
Q

Select the wrong answer:
Neutrophils kill microorganisms
Endothelial cells regulate movement of protein from blood into the tissue
Macrophages degrade fibrin/debris, kill microorganisms and secrete cytokines (regulatory molecules)
Fibroblasts secrete collagen and express adhesion molecules

A

Fibroblasts secrete collagen BUT DON’T EXPRESS ADHESION MOLECULES

Endothelial cells express adhesion molecules to assist neutrophils to pass into cells

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11
Q

Exudate has ___ protein content

A

High

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12
Q

T/F:

Pus occurs all the time

A

False

Occurs sometimes

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13
Q

List the 4 cardinal signs of inflammation

A

Redness
Heat
Swelling
Pain

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14
Q

T/F:
The heat and redness associated with inflammation occurs because of fluid movement from blood into the tissue (exudation)

A

False
Heat and redness occurs due to increased blood flow (hyperaemia or erythema)

Swelling is caused by fluid movement from blood into tissues

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15
Q

Define pus

A

inflammatory exudate containing viable and dead neutrophils, cell debris, viable and dead micro-organisms, protein, lipid, DNA etc

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16
Q

What is supparation?

A

The formation of pus

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17
Q

What is purulent?

A

Consisting/containing/secreting pus

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18
Q

_____ causes heat and redness

A

Hyperaemia

passage of larger than normal volumes of blood through a tissue

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19
Q

T/F:

Hyperaemia is specific to inflammation

A

False

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20
Q

Hyperaemia is needed for the formation of ____

A

exudate

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21
Q

Explain the role of vasodilation during hyperaemia

A

Vasoactive mediators act on the smooth muscle cells of arterioles
Smooth muscle cells relax and the arterioles dilate= vasodilation
Capillaries that were ‘dormant’ now start to carry blood
More blood is now flowing through the microvascular bed and thus the tissue

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22
Q

For exudation to occur, there must be increased _______

A

Vascular permeability

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23
Q

T/F:

Fluid moving from blood into the affected tissue during exudation results in faster blood flow

A

False

Slower blood flow

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24
Q

During mild/moderate acute inflammation, how does exudate move into the tissue?

A

Through inter-endothelial gaps in post-capillary venules only (contraction of endothelial cells)

(immediate/transient AND delayed/prolonged)

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25
During more severe inflammation, how does exudate move into the tissue?
Damage to endothelial cells in all microvesels | immediate/prolonged
26
What are the two forms of pressure acting on the microcirculation?
Colloid osmotic pressure= fluid is moving from the interstitial space into the capillary because there is high concentrations of proteins within the capillaries in comparison to the interstitial space Hydrostatic pressure= blood in arterioles meeds high resistance of capillaries, drives fluid across the endothelial wall from inside to out
27
T/F: | During normal conditions, there is generally greater hydrostatic pressure in comparison to colloid osmotic pressure
False They are both fairly equal During acute inflammation there is an imbalance between the two pressures which causes the movement of fluid/protein from the blood into the tissue
28
List three reasons for exudation
The fluid dilutes the toxins and increases the flow into lymphatics More plasma proteins are brought into the affected area: antibodies, complement system proteins, fibrin system proteins Brings in more neutrophils which can destroy micro-organisms
29
Increased blood flow _____ hydrostatic pressure and can result in ______
Increases | Exudate (swelling)
30
Chemotactic mediators results in the _______ which causes ____ or ______
results in the recruitment and stimulation of inflammatory cells Results in acute or chronic inflammation
31
Vasoactive mediators causes ______ which results in _____
Causes increased blood flow and vascular permeability to proteins Results in exudate
32
Where does histamine come from and what is its role
Comes from mast cells in tissue and platelets in blood | It is a vasoactive mediator (increases vasodilation in arterioles and vascular permeability to post capillary venules)
33
List two lipid-derived mediators that are pro-inflammatory mediators acting on blood vessels
Prostanoids | Leukotrienes
34
A2 acts on ____ to form ______
acts on the membrane phospholipid to form arachidonic acid
35
____ and ____ act on arachidonic acid to form ___ and ____. This will induce inflammation by acting on blood vessels.
Cyclooxygenases and lipoxygenases | Prostanoids and Leukotrienes
36
How do corticosteroids inhibit inflammation?
Inhibit A2 from acting on the phospholipid membrane thus prevents the inflammation pathway
37
What do NSAIDs and Zileuton do?
Non-steroidal anti-inflammatory drugs inhibit cyclyoxygenases Zileuton inhibits lipoxygenases
38
List 3 vasoactive mediators involved in inflammation
Histamine Lipid-derived mediators (prostanoides and leukotrines) Plasma derived mediators (complement fragments and kinins)
39
List four vasoactive mediators that result in vasodilation (act on arterioles)
Histamine Kinins Prostaglandin E2 Prostaglandin I2
40
List four vasoactive mediators that result in increased vascular permeability of post capillary venules
Histamine Kinins C3a, C5a Leukotrines B4 and C4
41
_____ can increase your sensitivity to pain
Prostaglandins
42
What are the two main roles of neutrophils?
Kill microorganisms | Release chemotactins to attract other neutrophils and macrophages
43
Where are neutrophils produced?
Bone marrow
44
T/F: | Neutrophils reside in tissues
False They are in the blood They enter tissues when they have been signalled to do so
45
In what order do these reach their maximum? | Oedema, monocytes/macrophages, neutrophils
First oedema Then neutrophils Then macrophages/monocytes
46
List the main neutrophil events
``` Margination in small vessels Emigration from vessel into tissue Phagocytosis of micro-organisms Killing of microorganisms Death of the neutrophil ```
47
In what stage does rolling, adhesion and emigration occur for neutrophils
First stage | Margination in small vessels- adherence to the endothelium
48
How do neutrophils adhere to the endothelium
Both neutrophils and endothelial cells express integrins
49
How do neutrophils emigrate from the vessel into the tissue?
Follow a chemogradient towards the target tissue
50
How do neutrophils kill microorganisms?
Form a phagosome Phagosome fuses with granulues to form phagolysosome Granulues released in phagolysosome to kill microorganism ROS can be directed into phagolysosome OR as neutrophils die they release a NET (neutrophil extracellular trap) - This consists of DNA and anti-microbial proteins attached - Kills the microorganism
51
T/F: | Neutrophils don't have ER or ribosomes
False | they don't have ER and golgi apparatus
52
T/F: | Neutrophils are incapable of proliferation
True
53
T/F: | Neutrophils are a long lived cell
False | Short-lived
54
What are the general roles of macrophages?
Kill microrgansisms Phagocytose debris/microorganisms Regulate other cells by producing cytokines
55
Where do monocytes originate from?
Originate in bone marrow | Become macrophages later
56
T/F: | macrophages are long lived
True | can remain in tissues for months or years
57
T/F: | macrophages have a multi lobed nucleus
False | Single lobed
58
T/F: | macrophages are incapable of proliferating and differnetiating
False
59
What are the three types of cytokine actions?
Autocrine Paracrine Systemic (endocrine)
60
What is the role of cytokines?
Regulating other cells/pathways Modify activities of cells Stimulate or inhibit cellular functions THEY ARE PROTEINS
61
What is the major source of Interleukin 1 and tumour necrosis factor?
Macrophages
62
What is over produced when you have arthritis?
TNF and IL-1
63
What are some general roles of TNF and IL-1
Make T cells proliferate Make the hypothalamus give you a fever Increase the expression of adhesion molecules Cause stem cells to differentiate into leukocytes
64
What does PAMPs and PRRs stand for?
Pathogen Associated Molecular Patterns | Pattern Recognition Receptors
65
What do PRRs recognise?
PAMPs: microbial origin Lipids, carbohydrates, nucleic acids, proteins DAMPs: - Damage associated molecular patterns - Released from damaged cells - E.g. ATP, RNA, DNA
66
What is the role of PRRs
Activate the adaptive immune response Detect microbial infection Trigger anti-microbial host defences
67
T/F: | PRRs are part of the adaptive immune response
False | Part of the innate immune response
68
Toll-like receptors are a form of ______
pattern recognition receptors (PRRs)
69
What are the 5 possible forms of progression of acute inflammation?
``` Resolution Organisation Suppuration Chronic Inflammation Longer Term Healing ```
70
A granuloma is a nodular inflammatory lesion containing mostly -_____
macrophages, lymphocytes, fibroblasts
71
What is fibrinogen?
Glycoprotein made by the liver | Converted into fibrin by thrombin during coagulation
72
Describe what must happen for outcome 1 to occur- resolution
``` Mild stimulus no tissue damage Little or no fibrin deposition Fluid drains away through lymphatics Tissue stabilized quite rapidly ```
73
Describe acute healing by fibrosis
Copious amounts of fibrin are deposited Macrophages/capillaries/fibroblasts migrate to the area and form granulation tissue macrophages will then break down the fibrin Fibroblasts will deposit collagen
74
T/F: | and abcess is superficial and an ulcer is deep
False Ulcer= superficial Abcess= deep
75
What can be found in pus?
Living/dead neutrophils, fluid, plasma proteins, living/dead microorganisms, cell debris, nucleic acids, myeloperoxidase
76
T/F: | Suppuration is almost always a response to viral infection
False | Bacterial infection
77
T/F: Chronic inflammation is inflammation of prolonged duration (weeks to years) in which active inflammation, tissue destruction and tissue repair are proceeding simulatenously
True
78
What are the three major types of chronic inflammation?
Suppuration (chronic abcess) Mixed (rheumatoid arthritis) Granulomatous (tuberculosis)
79
T/F: | Suppuration occurs during chronic granulomatous inflammation
False
80
What are some characteristics of chronic inflammatory lesions?
Persistent Cellular infiltration Destruction of normal tissue Formation of fibrous connective tissue
81
Describe chronic suppurative inflammation
Characterised by neutrophils | Inolves pus
82
Describe an abcess and what is it an example of
An example of chronic suppurative inflammation | Collection of pus within a solid tissue
83
What are the three types of chronic granulomatous inflammation
Foreign body granuloma Chronic granulomatous inflammation of unknown origin Immune type
84
Giant cells, epithelioid cells and difuse fibrosis are characteristics of _____
foreign body chronic granulomatous inflammation
85
Epithelioid cells and langhands giant cells are characteristic of _____
unknown origin chronic granulomatous inflammation
86
What is the role of a granuloma?
To contain a microorganism/irritant in order to prevent its dissemination Focuses the immune response against the initiating factor
87
What happens when mice are injected with anti-TNF?
No granulomas form Bacteria persist Mouse death
88
Briefly describe how granulomas form
Chemokines recruit monocytes into an area Cytokines cause monocytes to differentiate into macrophages or epithelioid cells Cytokines cause epithelioid cells to fuse together to form giant cells Growth factors recruit fibroblasts and they form fibrous tissue
89
What are some negative aspects of inflammation?
Complications of acute inflammation Chronic inflammation Systemic inflammation

CPAT (9 decks)

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