Acute Inflammation Flashcards

1
Q

Main cell type involved in acute inflammation

A

Neutrophils

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

Main Cell types involved in chronic inflammation

A

Macrophages

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

Signs of acute inflammation

A

Heat, redness, swelling, pain, loss of function

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

Definition of acute inflammation

A

A redunant, complex, adaptive adn protective response of vessels, resident cells and leucocytes to noxious stimuli.
It brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents and repair the tissues.

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

How long does acute inflammation last

A

Hours to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Possible causes of acute inflammation (4)

A

infections and microbial toxins
Tissue necrosis; ischemia, trauma, physical and chemical injury, irradiation
Foreign bodies (splinters, dirt, dutures); endogenous substances, urate crystals, cholesterol crystals (in atherosclerosis) and lipids
Immune reactions (hypersensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Morphological hallmarks of acute inflammation (3)

A

Dilation of Blood vessels
Activation and recruitment of leukocytes
Active exudation of fluid in the extravascular tissues

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

Steps of acute inflammation (6 Rs)

A

Recognition of the injurious agent
Reaction of blood vessels
recruitment of leukocytes
Removal/clearance of the agent
Regulation (control) of the response
Repair (resolution)

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

Mediators in Acute Inflammation

A

Vasoactive Amines
Inflammatory Lipids
Complement
Cytokines
Others- chemokines, nitric oxide, coagulation cascade…..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of vasoactive amines and where are they produced/released

A

Histamine, serotonin
Released/produced by mast cells, basophils, platelets

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

Examples of inflammatory lipids and where are they produced/released

A

Prostaglandins, leukotrienes
Produced by mast cells, leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of complement and where are they produced

A

C5a, C3a
Produced in liver, present in plasma

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

Examples of cytokines and where are they produced

A

IL-1, TNF, IL-6
Produced by macrophages, endothelial cells, mast cells

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

Which mediators cause vasodilation

A

Inflammatory lipids (prostaglandins, leukotrienes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which mediators cause increased vascular permeability

A

Vasoactive amines
Complement (C5a, C3a)
Inflammatory lipids
Cytokines (IL-1, TNF)

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

Which mediators cause Leukocytes recruitment and activation

A

Inflammatory lipids
Complement
Cytokines

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

Which mediators cause pain

A

Inflammatory lipids

18
Q

Which mediators cause tissue damage

A

Neutrophil granule content
Reactive oxygen species (ROS)

19
Q

3 possible outcomes of acute inflammation

A

1- Complete resolution
Clearance of the offending agent and regeneration
2- Scarring, or fibrosis
Connective tissue growth into the area of damage or exudate, this occurs after substantial tissue destruction
3- Progression to chronic inflammation
Unresolved inflammatory process due to either the persistence of the injurious agent or some interference with the normal process of healing

20
Q

What is the acute phase response

A

characterised by different systemic effects of acute inflammation (and other conditions) including pyrexia, leucocytosis and metabolic changes
It also includes changes to the concentrations of plasma proteins, called acute phase proteins (APPs)

21
Q

Example of an exogenous pyrogen (trigger of pyrexia)

A

Bacteria

22
Q

Examples of endogenous triggers of pyrexia

A

Phagocytosis, tissue damage, immune complexes

23
Q

Endogenous pyrogens (3)

A

IL-1
TNF
IL-6

24
Q

How is PGE2 produced and what does it do

A

Produced in response to endogenous pyrogens
Increases the hypothalamic set point for body temperature

25
Q

How does hypothalamus increase body temperature

A

vasoconstriction and shivering

26
Q

what drugs target pyrexia pathway

A

NSAIDs

27
Q

What is a positive Acute Phase Protein

A

Production is increased in inflammation

28
Q

What is a Negative Acute Phase Protein

A

Production is decreased in inflammation

29
Q

Examples of positive APPs

A

C reactive protein (CRP)
Serum Amyloid A (SAA)-particularly dogs, cat, horse, cow
Haptoglobin- particularly cow
Fibrinogen- particularly horses
Complement (C3, C4)
Pig-Map - In PIGS (pig major acute protein)

30
Q

Examples of Negative APPs

A

Albumin
Transferrin
Transthyretin
Retinol-binding protein

31
Q

What is a biomarker

A

a biological molecule that is objectively measure and is an indicator of a normal or abnormal process, or of a condition or disease

32
Q

What is a transudate

A

Extravascular filtrate of protein and cell poor fluid
It is due to increased hydrostatic pressure or decreased colloid osmotic pressure, or combination of both
It is accumulated in body cavities and extracellular compartments
Fluid appears grossly clear and watery

33
Q

Possible causes of increased hydrostatic pressure

A

Venous outflow obstruction e.g. congestive heart failure

34
Q

Possible causes of decreased colloid osmotic pressure

A

Decreased protein synthesis e.g. liver disease
increased protein loss e.g. kidney disease

35
Q

What is an exudate

A

Extravascular fluid that has a high protein concentration and can contain leucocytes
Its presence implies the existence of an inflammatory process that has increased the permeability of blood vessels
Increased vascular permeability due to inflammation-> leakage of fluid/protein

36
Q

What is serous inflammation

A

Inflammation with exudation of fluid with low concentration of plasma protein and no to low numbers of leukocytes

37
Q

What is fibrinous inflammation

A

Inflammation with exudation of fibrinogen and fluid, and formation of thick, friable, loosely adherent fibrin

38
Q

Purulent inflammation

A

Inflammation with production of pus, viscous to creamy liquid, an exudate consisting of degenerated and necrotic neutrophils, debris and fluid
It is typically associated to bacterial infections

39
Q

What is haemorrhagic inflammation

A

Inflammation with vascular damage, loss of integrity of endothelium and/or extensive tissue necrosis, with leakage of red blood cells
Reflects and inciting stimulus

40
Q

Leukocytes
Lymphocytes
Macrophages

A

leukocyte- all white blood cells
lymphocytes- T&B= adaptive immune response
Macrophages= innate immune response- phagocytosis, antigen presenting, tissue remodelling and cytokine production