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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hypersensitivity?

A

Body reacts against itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is bad about inflammation?

A

Persistent swelling and cytokines make you feel sick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of inflammation?

A

Microbial infection

Allergens

Autoimmunity

Trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What the local effects of inflammation?

A

Destruction of invading microorganisms

At other times appear to serve no effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the harmful effects of inflammation?

A

Persistent cytokine release

Destruction of normal tissues

Swelling

Inappropriate inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is inflammation grouped based on type of exudate?

A

Purulent

Serous

Haemorrhagic

Catarrhal

Mixed

Fibrinous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is inflammation grouped based on severity?

A

Mild

Moderate

Severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does pus mean?

A

heavy neutrophil response which means bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the suffix related to inflammation?

A

“itis”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the categories of acute inflammation?

A

Cellular events

Vacular events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

In the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are newly synthesized mediators produced?

A

In WBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is an exudate?

A

Fluid that filters from circulation into lesions or areas of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which cytokines are preformed and stored in secretory granules?

A

Histamine

Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which mediatos are newly synthesized in WBCs during inflammatin?

A

Prostaglandins

Leukotrienes

Platelet-activating factor

Reactive Oxygen Species

Nitric oxide

Cytokines

Neuropeptides

28
Q

What is a transudate?

A

Fluid pushed through capillaries due to high pressure within capillarie

29
Q

What are mixed exudates?

A

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
Q

What is serous exudate?

A

Outpouring of translucent, thin fluid that can accumulate on mucosal surface, skin, or in perioneal and pericardial cavities

31
Q

When is serous exudate commonly seen?

A

Acute inflammation which indicates that insult is mild and transient. If it doesn’t worsen the fluid is reabsorbed and inflammation is resolved

32
Q

What is purulent/suppurative exudate?

A

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
Q

What is pus?

A

an accumulation of dead neutrophils

34
Q

What causes variation in colour and consistency of pus?

A

Hostm stimulus, and the duration

35
Q

What is a pus filled lump with a fibrous wall or capsule called?

A

An abscess

36
Q

What can happen to localized pus?

A

It can break loose and spread resulting in septicaemia

37
Q

What happens if pyogenic bacteria is close to body surface?

A

discharges purulent exudate to the outside surface

38
Q

What would happen if pus is reabsorbed?

A

Ill effects such as fever and general illness

39
Q

What are the types of exudate?

A

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
Q

What is catarrhal exudate?

A

Heavy mucous production and ofte associated with mucosal surfaces like intestinal, repiratory, and reproductive tracts

Appears as thin grey-yellow

41
Q

What surfaces are associated with catarrgal exudate?

A

Mucosal surfaces such as GI tract Resp tract and Repro tract

42
Q

What is haemorrhagic exudate?

A

Blood vessel holes causing blood cells to leave in large numbers.

43
Q

What do haemorrhagic exudates consist of?

A

RBCs, fibrin, serum, and leukocytes

44
Q

What is fibrous exudate?

A

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
Q

Where can fibrinous exudate be found?

A

Chiefly on mucous and serous membranes (respiratory tract, digestive tract, pleura, peritoneum, and pericardium)

46
Q

How does fibrinous exudate look?

A

Slightly roughened appearance, slightly dull and granular

47
Q

What happens as fibrin deposition increases?

A

Gets thick and yellow strands can be peeled off and if insult is repeated it can cause fibrin carpet

48
Q

How is inflammation resolved?

A

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
Q

What are the differences between acute and chronic responses?

A

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
Q

What are the characteristics of chronic inflammation?

A

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
Q

How does chronic inflammation look histologically?

A

Primarily mononuclear cells involved

Fibroblasts and new blood vessels. Together called granulation tissue

52
Q

What is granulomateous inflammation?

A

Always chronic

Composed predominantly of macrophages but may have multinucleate giant cells

53
Q

What causes chronic inflammation?

A

Infection by organisms resistant to killing

Repeated bouts of acute inflammation

Prolonged exposure

Autoimmune disease

54
Q

What is granulomatous inflammation?

A

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
Q

What happens when mycobacteria resist macrophage activation effects?

A

A granuloma develops

Chronic activation of macrophages by TH1 cells forming granulomas to contain intracellular pathogens that cannot be cleared

56
Q

What happens during chronic inflammation of liver?

A

Fibroblasts migrate in and generate new fibrous connective tissue

57
Q

When does repair and wound healing take place?

A

Repair starts soon after inflammation and continues during and beyond inflammatory phase.

58
Q

When is perfect restoration of function expected?

A

Depends on regeneration of lost cells by similar cells

59
Q

What happens if cells cant be replaced by their own kind?

A

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
Q

Which tissue have unique ways of repair?

A

Bone

Nervous tissue (cannot repair)

Heart myofibers

61
Q

What are the cell types based on ability to regenerate?

A

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
Q

What are the systemic effects of inflammation?

A

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
Q

What infections are associated with higher neutrophil count?

A

Bacterial infections

64
Q

What infections are associated with high lymphocyte count?

A

Viral infections

65
Q

Why does fever occur?

A

Thought to improve leukocyte killing efficiency and impairs replication of many organisms