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Year One - Principles of Disease > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What do all inflammation names end in?

A

“itis”

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2
Q

What is inflammation?

A

Homeostatic response as a result of injury

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3
Q

What are the signs of acute inflammation?

A

Redness

Heat

Swelling

Pain

Loss of function

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4
Q

What causes acute inflammation?

A

Microorganisms that cause infection

Injury to tissue

Unstable chemical environment - unstable pH, bile or urine in an inappropriate place

Physical conditions - body exposed to extreme heat or cold, ionising radiation

Dead tissue

Hypersensitivity - allergic reaction

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5
Q

What is acute inflammation?

A

A series of localised events

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6
Q

Where does acute inflammation take place?

A

The microcirculation surrounding the affected tissue

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7
Q

What is microcirculation?

A

Defined as the capillary beds, which are fed by arterioles and drained by venules.

Also includes ECF and lymphatic channels surrounding these capillary beds

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8
Q

How is there a dynamic balance between the ECF and capillary beds?

A

Hydrostatic and colloid osmotic pressure

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9
Q

What is the first change that occurs during acute inflammation? What does this change cause?

A

Starts off with local arterial constriction which is then followed by local arterial dilation. This alters the flow of blood.

Constriction prevents blood to flow through the vessels (hypoxemia) and dilation allows more blood to flow through the vessels (hyperaemia)

Leads to the ‘triple response’ - flush, flare and wheal

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10
Q

What is the second change that occurs during acute inflammation? What is the process called? What two things does this change cause?

A

Change in the permeability of localised vessel walls, which makes them leakier and allow more molecules to flow into the surrounding tissues.

This process is called exudation. The substance that leaks out is known as the exudate.

Leads to an oedema forming, which is an accumulation of fluid in the ECF - explains swelling and pain symptoms

Increase viscosity in blood, which occurs as a result of fluid loss. The rate of blood therefore slows.

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11
Q

What happens to neutrophils in blood vessels during acute inflammation?

A

Neutrophil molecules move from the blood vessel into the extravascular space and take part in exudation.

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12
Q

Where are neutrophils and RBC’s usually found within the blood vessel?

A

Neutrophils - clustered within the centre of the lumen

RBCs - surround the cluster of neutrophils in the centre of the lumen

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13
Q

What are the three stages involved in the neutrophils moving out of the blood vessels during acute inflammation?

A
  1. Margination - movement of neutrophils to the endothelial aspect of the lumen
  2. Pavementing - adherence of neutrophils to the endothelium
  3. Emigration - movement of neutrophils between endothelial cells to extravascular tissues
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14
Q

What is the difference between diapedesis and emigration?

A

Diapedesis - passive movement of WBCs from lumen into extravascular space

Emigration - active movement of WBCs from lumen into extravascular space

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15
Q

What is the role of neutrophils in acute inflammation?

A

Mobile phagocytes - recognise foreign antigen and move towards it (chemotaxis). Bind to pathogen and release the granules in its cytoplasm into the organism. The granules are filled with enzymes. The enzymes destroy pathogen. This process is known as phagocytosis

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16
Q

What are the consequences of neutrophil action?

A

When they release their granule contents, they die

They produce pus, which can then extend into other tissues and progress inflammation

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17
Q

Other than neutrophils, which other molecules leak from the blood vessel into the extravascular space? What are their functions?

A

Plasma proteins - fibrinogen and immunglobulin

Fibrinogen - coagulation factor, involved in the formation of fibrin, cots exudate, localises processes

Immunoglobulin - induces the humoral immune response

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18
Q

What are the outcomes of acute inflammation?

A

Inciting agent is destroyed

Macrophages move from the blood into the affected tissue and clear up debris

Supparation

Epithelial surfaces regenerate

Fibrosis and formation of a scar occurs

Inflammatory exude filters away

Vascular changes return to normal

Inflammation resolves

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19
Q

What is granulation tissue?

A

New connective tissue, blood vessels, macrophages, fibroblasts and collagen that form on the surface of a wound during the healing process

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20
Q

What is supparation? What does this lead to?

A

Pus formation

Abscess forming, which can discharge pus as a result of the growth of granulation tissue placing pressure on it. When the abscess collapses, healing and repair can occur.

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21
Q

What is pus formed from?

A

Pus is formed from dead tissues, dead organisms, exudate, neutrophils, red blood cells and fibrin.

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22
Q

What surrounds pus? What happens if pus bursts through this?

A

Pyogenic membrane

It can form new cavities which means the abscess becomes multicoated

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23
Q

What is pyaemia?

A

Pus discharged into the bloodstream

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24
Q

What is empyema?

A

Pockets of pus that have collected inside the body cavity

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25
What is dissemination? What does it result in?
When the bacteria or toxin that causes inflammation spreads to the bloodstream Individual becomes septic
26
What are the three types of septicaemia?
Bacteraemia - bacteria spread to the blood Septicaemia - growth of bacteria in the blood Toxaemia - toxic products spreads to the blood
27
What can occur as a result of sepsis?
Septic shock, which can cause tissue hypoxia and necrosis.
28
What are the symptoms of septic shock?
Peripheral vasodilation Tachycardia - high heart rate Hypotension - low blood pressure Pyrexia - raised temperature
29
What causes septic shock?
The release of chemical mediators as a result of acute inflammation Chemical mediators cause vasodilation, which means that there is a loss of systemic vascular resistance. When systemic vascular resistance is loss, the hormone catecholamine is released. This hormone causes tachycardia. as this maintains cardiac output Septic shock also results in the body releasing bacterial endotoxin, which is a molecule that results in pyrexia and coagulation.
30
What are the four benefits of acute inflammation?
Rapid response to injury Neutrophils destroy organism Plasma proteins localise process Results in resolution and everything returns back to normal
31
What are the systemic effects of inflammation?
Pyrexia Generally feeling unwell Neutrophillia (raised white blood cell count) Lymphadenopathy - long term effect, due to regional lymph node enlargement Weight loss - long term effect Anaemia - long term effect
32
What five effects do chemical mediators result in?
Vasodilation Increased permeability Neutrophil adhesion to the side of a vessel Chemotaxis Itch and pain
33
Where are adhesion chemical mediators found? What is their role?
Found on the surface of endothelial cells and help the neutrophils to stick to the endothelium Allow neutrophils to move within and between cells
34
Name two adhesion chemical mediators
ICAM-1 P-selectin
35
Name six chemical mediators
Histamine Serotonin (5-hydrocytrytamine) Prostaglandins Cytokines and chemokines Nitric oxide Oxygen free radicals
36
What releases the chemical mediator histamine? What is its role?
Released from mast cells Involved in vasodilation and increased permeability
37
What releases the chemical mediator serotonin? What is its role?
Released from platelet cells Involved in vasoconstriction
38
What releases the chemical mediator prostaglandins? What is its role?
Released from various cells Involved in promoting histamine effects and also inhibiting inflammatory cells
39
What releases the chemical mediator cytokines and chemokine? What is its role?
Released from macrophages, lymphocytes and endothelium cells Involved in pro-inflammatory and anti-inflammatory effects
40
What releases the chemical mediator nitric oxide? What is its role?
Released from various cells Involved in smooth muscle relaxation, anti-platelet aggregation, regulating leukocyte to inflammatory focus
41
What releases the chemical mediator oxygen free radicals? What is its role?
Released from neutrophils during phagocytosis Involved in amplifying other mediator effects
42
Name the two signalling mediators
PAMPs - able to identify foreign antigens and alert other immune cells to destroy the initiating the innate and adaptive immune response DAMPs - able to initiate a non-infectious inflammatory response
43
How do the signalling molecules recognise antigens?
Pattern recognition
44
What are the three intracellular pathways that can be activated during the acute inflammatory response?
NF-kB pathway MAPK pathway Jak-Stat pathway
45
What is the role of the NF-kB pathway? How is it activated?
Results in the production of inflammatory cytokines Activated by extracellular molecule binding to the surface of the cell
46
What is the role of the MAPK pathway? How is it activated?
Involved in regulating pro-inflammatory cytokine production and inflammatory cell recruitment Activated by extracellular molecule binding to toll-like surface receptors (TLRs)
47
What is the role of the JAK-STAT pathway? How is it activated?
Production of inflammatory cytokines Activated by extracellular molecule binding to the surface of the cell
48
What are the four inflammatory pathways that take place in the plasma?
Blood coagulation pathway Fibrinolysis pathway Kinin pathway Complement cascade pathway
49
What is the role of the blood coagulation pathway?
Involved in clotting the exudate with fibrinogen
50
What is the role of the fibrinolysis pathway?
Breaking down fibrin and helping to maintain the blood supply
51
What is the role of the kinin pathway?
Releasing bradykinin, which causes contraction of smooth muscle and dilation of blood vessels
52
What is the role of the complement cascade pathway?
Bridges the inflammatory and the immune response together. Results in active components being stimulated which increases permeability, chemotaxis, phagocytosis and cell breakdown
53
What is the main difference between acute and chronic inflammation?
Chronic
54
What is the main difference between acute and chronic inflammation?
In chronic inflammation the damaged tissue or organ repairs, but doesn't resolve. This means that there is a loss of function Granulation tissue also forms in chronic inflammation
55
What causes chronic inflammation?
May follow from ongoing acute inflammation Primary pathology - usually results from an autoimmune disease
56
Why can chronic inflammation follow on from acute inflammation?
Acute inflammation causes a large volume of debris, which is not removed Fails to get rid of the substance causing inflammation
57
What are the clinical symptoms of chronic inflammation?
Malaise Weight loss Loss of function
58
What are the outcomes of chronic inflammation?
Organisation - which involves the formation of granulation tissue and blood vessels Healing and repair Fibrosis and scar formation
59
What is angiogenesis?
Formation of new blood vessels
60
How does angiogenesis occur?
Capillary buds growing out from existing capillaries
61
Why does angiogenesis occur?
Release of VEGF from hypoxic cells, which is a growth factor that secretes enzymes which are able to break down proteins and enable space for blood supply to enter the damaged tissue
62
What does angiogenesis limit?
Thrombus propagation, which is the spread of a blood clot towards the direction of the heart Therefore it allows the reinstatement of flow
63
What is the formation of granulation tissue due to?
Capillaries growing into the inflammatory mass, which allows plasma proteins, macrophages and fibroblasts to access the mass Macrophages - clean up debris Fibroblasts - lay down collagen to repair tissue damage, replaces the inflammatory exudate
64
What is the granulation tissue formed from primary chronic inflammation called?
Pyogenic granulation tissue
65
What does granulation tissue result in?
Formation of a scar Fibrosis - which is the formation of excessive amount of fibrous connective tissue in an organ or tissue
66
What cells are involved in chronic inflammation?
Lymphocytes - B-cells involved in antibody production, Th-cells involved in the production of cytokines and Tc-cells involved in cell lysis and apoptosis Plasma cells - form B-cells which are involved in antibody production NK cells - involved in apoptosis, which means that they release enzymes from their granules into pathogens Macrophages - remove debris from the site of injury and cause phagocytosis. Forms APCs which are able to stimulate other cells. Release interferons, which stimulate other immune cells. Fibroblasts - able to make and assemble structural proteins, like collagen
67
What are epitheliod cells?
Activated macrophages
68
What are macrophage monocytes?
Macrophages formed in the blood
69
What is granulomatous inflammation?
Distinct from of chronic inflammation, where there is a presence of granulomas
70
What stimulates granulomatous inflammation?
Indigestible antigen, which is an antigen that the body cannot get rid of Serious infections
71
What are granulomas?
Collection of epitheliod macrophages in tissue, may contain giant cells, WBCs Surround dead material or lymphocytes
72
What are giant cells?
Multiple macrophages which are bound together to form a multinucleate cell with a large cytoplasm
73
What are silicone associated granulomas?
Granulomas that form as result of the body reacting to silicon. Commonly arise due to ruptures silicone implants
74
Name three giant cells
Langhan Foreign body Warthin Finkeldy
75
What are Langhan giant cells?
Classically found in TB Peripheral rim around the multiple nuclei contained within them Large eosinophilic cytoplasm
76
What are foreign body giant cells?
Often associated with pyogenic granulation tissue Smaller than Langhan cells don't contain as many nuclei Contain foreign material in cytoplasm
77
What are warthin finkeldy giant cells?
Associated with measles Nuclei cluster in the centre of the cell
78
What three serious diseases can cause granulomatous inflammation diseases?
TB Leprosy Syphillis
79
What is wound healing?
The process of repairing tissue damage
80
Describe the steps of wound healing
1. An injury occurs, which results in a blood clot and acute inflammation 2. During acute inflammation and clot formation, many growth factors and cytokines are released 3. These growth factors and cytokines result in granulation tissue growth and angiogenesis 4. Phagocytosis of fibrin (blood clot) occurs 5. The fibroblasts move into the site of injury and lay down collagen 6. A scar is formed, which leads to the process of re-epithelisation occurring.
81
How do we keep inflammation to a minimum during surgery?
Reducing the amount of tissue damage as much as possible
82
Why is it important to keep inflammation to a minimum during surgery?
Reduces the size of the scar, as less granulation tissue if formed
83
What type of healing occurs during surgery? What does it involve?
Healing by the primary intention. Keep the gap between the suture and the blood clot to minimum, which means that only a small amount of granulation tissue is formed and the patient is left with a small scar
84
What is healing by secondary intention?
Results in lots of granulation tissue forming, which grows into the blood clot. Causes the blood clot to contract and push into the collagen in the granulation tissue. This results in a puckered scar
85
What is the difference between fracture and wound healing?
The granulation tissue which forms contains osteoblasts as well as fibroblasts. Osteoblasts are involved in new bone formation, which is termed as callus. This process is then followed by bine remodelling which involves the osteoclasts removing dead bone
86
What are the steps of fracture healing?
Trauma which results in a fracture and a haematoma Acture inflammation occurs, which results in organisation Granulation tissue is formed
87
What is a haematoma?
Solid swelling of clotted blood within a tissue

Year One - Principles of Disease (15 decks)

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