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IMED2001 UWA > Lecture 11 - Inflammation and repair > Flashcards

Lecture 11 - Inflammation and repair Flashcards

1
Q

What is inflammation/

A

Response of living tissue to injury. It is a well organised of cascade of fluid and cellular changes in tissue

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2
Q

What causes inflammation?

A

Aetiologic agents such as viruses, bacteria, fungi, and parasites

Hypersensitivity

Physical and Chemical agents (trauma, sunburn, and acid)

Necrosis (anoxia, trauma)

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3
Q

What is hypersensitivity?

A

Body reacts against itself

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4
Q

What is good about inflammation?

A

It opens up the site for influx of drugs, antibodies, mediators

Fibrin and fibrosis can wall it off

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5
Q

What is bad about inflammation?

A

Persistent swelling and cytokines make you feel sick

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6
Q

What are the five principle effects of inflammation?

A

Redness (due to influx of blood)

Swelling (due to accumulation of fluid)

Heat (Increase in temperature due to increased blood flow to area)

Pain (due to stretching of skin)

Loss of function Movement inhibited by pain and welling. (this principle was added later

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7
Q

What are the general characteristics of inflammation?

A

Redundant and complex due to many mediators

Continuous over long periods of time (per-acute, sub-acute, and chronic desvribe different stages)

Caused by a stimulus and removal of stimulus should resolve it

Blood is the primary delivery system for inflammatory components

Inflammation is on a continuum with healing process

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8
Q

What are the causes of inflammation?

A

Microbial infection

Allergens

Autoimmunity

Trauma

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9
Q

What the local effects of inflammation?

A

Destruction of invading microorganisms

At other times appear to serve no effect

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10
Q

What are the beneficial effects of inflammation?

A

Dilution of toxins

Entry of antibodies

Fibrin formation

Delivery of nutrients and oxygen

Stimulation of immune response

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11
Q

What are the harmful effects of inflammation?

A

Persistent cytokine release

Destruction of normal tissues

Swelling

Inappropriate inflammatory response

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12
Q

How is inflammation grouped based on time course?

A

per acute - minutes or hours

Acute - a few hours to a few days

Sub-acute - period between acute and chronic

Chronic - weeks to months

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13
Q

How is inflammation grouped based on type of exudate?

A

Purulent

Serous

Haemorrhagic

Catarrhal

Mixed

Fibrinous

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14
Q

How is inflammation grouped based on severity?

A

Mild

Moderate

Severe

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15
Q

How is inflammation grouped based on distribution of lesion?

A

Focal (just one small part of an organ is affected)

Multifocal (several small parts affected)

Diffuse (whole organ is affected)

Focally extensive (diffuse but just in one part of organ)

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16
Q

What does pus mean?

A

heavy neutrophil response which means bacteria

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17
Q

What is the suffix related to inflammation?

A

“itis”

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18
Q

What are the categories of acute inflammation?

A

Cellular events

Vacular events

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19
Q

What are the vascular events of acute inflammation?

A

Changes in blood vessel calibre and blood flow

Increased vascular permeability

Formation of fluid exudate

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20
Q

What are the cellular events of acute inflammation?

A

Cells move out of vessels into area of inflammation via chemotaxis.

Inflammatory cells become activated and can phagocytose offending pathogens

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21
Q

How do macrophages that are activated by bacterial ingestion respond to inflammation?

A

They release cytokines and chemokines then release pain causing inflammatory mediators and vasodilators for other WBCs to join

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22
Q

What are the major chemical signals of inflammation?

A

Histamine (causes vasodilation and increased permeability)

Kinins (released from damaged tissue, chemotactic factors)

Prostaglandins (intensify effects of histamine)

Leukotrines (Promote adherence of phagocytic cells and increase vascular permeability)

Also delivers clotting elements which can wall off affected area to prevent spread of infection

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23
Q

Where are Complement proteins, kinins, and factor XII (hageman factor) produced/activated?

A

In the liver

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24
Q

Where are newly synthesized mediators produced?

A

In WBCs

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25
What is an exudate?
Fluid that filters from circulation into lesions or areas of inflammation
26
Which cytokines are preformed and stored in secretory granules?
Histamine Serotonin
27
Which mediatos are newly synthesized in WBCs during inflammatin?
Prostaglandins Leukotrienes Platelet-activating factor Reactive Oxygen Species Nitric oxide Cytokines Neuropeptides
28
What is a transudate?
Fluid pushed through capillaries due to high pressure within capillarie
29
What are mixed exudates?
More common than simple exudates because of inflammatory process which frequently persists long enough to evoke exudation of more than one type of exudate
30
What is serous exudate?
Outpouring of translucent, thin fluid that can accumulate on mucosal surface, skin, or in perioneal and pericardial cavities
31
When is serous exudate commonly seen?
Acute inflammation which indicates that insult is mild and transient. If it doesn't worsen the fluid is reabsorbed and inflammation is resolved
32
What is purulent/suppurative exudate?
PUS which is an accumulation of dead neutrophils. Almost all cases due to bacterial infection Pyogenic bacteria promote production of pus Neutrophils have enzymes that can liquefy surrounding tissues
33
What is pus?
an accumulation of dead neutrophils
34
What causes variation in colour and consistency of pus?
Hostm stimulus, and the duration
35
What is a pus filled lump with a fibrous wall or capsule called?
An abscess
36
What can happen to localized pus?
It can break loose and spread resulting in septicaemia
37
What happens if pyogenic bacteria is close to body surface?
discharges purulent exudate to the outside surface
38
What would happen if pus is reabsorbed?
Ill effects such as fever and general illness
39
What are the types of exudate?
Serous (mild) Pyogenic (pus field can be mild or severe) Catarrhal (can be mild or severe) Haemorrhagic (Severe most of the time often fatal) Fibrinous exudate (severe but can resolve without any sequelae)
40
What is catarrhal exudate?
Heavy mucous production and ofte associated with mucosal surfaces like intestinal, repiratory, and reproductive tracts Appears as thin grey-yellow
41
What surfaces are associated with catarrgal exudate?
Mucosal surfaces such as GI tract Resp tract and Repro tract
42
What is haemorrhagic exudate?
Blood vessel holes causing blood cells to leave in large numbers.
43
What do haemorrhagic exudates consist of?
RBCs, fibrin, serum, and leukocytes
44
What is fibrous exudate?
Occurs in more severe conditions with escape of larger fibrinogen molecules from vascular system. What hapens is fibrinogen reaches tissue and is converted to fibrin .
45
Where can fibrinous exudate be found?
Chiefly on mucous and serous membranes (respiratory tract, digestive tract, pleura, peritoneum, and pericardium)
46
How does fibrinous exudate look?
Slightly roughened appearance, slightly dull and granular
47
What happens as fibrin deposition increases?
Gets thick and yellow strands can be peeled off and if insult is repeated it can cause fibrin carpet
48
How is inflammation resolved?
It is resolved by complex cascade of steps and mediated by complex resolvin molecules. Exudate is produced and influx of neutrophils and destroy residual debris Apoptosis of neutrophils
49
What are the differences between acute and chronic responses?
Time: Chronic inflammation is acute inflammation that has not been resolved. Acute inflammation is exudative chronic inflammation which is productive and proliferative. Best indicator of chronic inflammation is deposition of fibrinogen
50
What are the characteristics of chronic inflammation?
Not usually red or hot Do not ooze Productive or proliferative Often present in infections with higher order organisms such as mycobacteria, fungo, and metazoan parasites and many autoimmune diseases.
51
How does chronic inflammation look histologically?
Primarily mononuclear cells involved Fibroblasts and new blood vessels. Together called granulation tissue
52
What is granulomateous inflammation?
Always chronic Composed predominantly of macrophages but may have multinucleate giant cells
53
What causes chronic inflammation?
Infection by organisms resistant to killing Repeated bouts of acute inflammation Prolonged exposure Autoimmune disease
54
What is granulomatous inflammation?
Inflammatory response consisting mostly of macrophages that try to phagocytose and then differentiate to become epitheloid macrophages and giant cells (fusion of several macrophages) Ring of lymphocytes around main site
55
What happens when mycobacteria resist macrophage activation effects?
A granuloma develops Chronic activation of macrophages by TH1 cells forming granulomas to contain intracellular pathogens that cannot be cleared
56
What happens during chronic inflammation of liver?
Fibroblasts migrate in and generate new fibrous connective tissue
57
When does repair and wound healing take place?
Repair starts soon after inflammation and continues during and beyond inflammatory phase.
58
When is perfect restoration of function expected?
Depends on regeneration of lost cells by similar cells
59
What happens if cells cant be replaced by their own kind?
if ordinary cells cannot be replaced by their own kind they are replaced by other cell types (often scar tissue.) If necrosis is extensive even tissues capable of regenerating are replaced by scar tissue
60
Which tissue have unique ways of repair?
Bone Nervous tissue (cannot repair) Heart myofibers
61
What are the cell types based on ability to regenerate?
Permanent cells that almost never double (nerve cells) Stable cells which divide if stimulated (eg smooth muscle) Jabile cells (such as epithelial cells of surfaces or linings of ducts)
62
What are the systemic effects of inflammation?
Leukocytosis which is an abnormally high circulation number of WBCs Fever which is an elevation of body temperature regulated by hypothalamus and involves a wide range of factors
63
What infections are associated with higher neutrophil count?
Bacterial infections
64
What infections are associated with high lymphocyte count?
Viral infections
65
Why does fever occur?
Thought to improve leukocyte killing efficiency and impairs replication of many organisms

IMED2001 UWA (44 decks)

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