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ESA2 - Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What are some features of acute inflammation?

A

Innate, immediate and early, stereotyped, short-duration

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2
Q

Why is acute inflammation initiated?

A

Initiated to limit the tissue damage (preserve itself)

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3
Q

What accumulates in tissues in acute inflammation?

A

Fluid exudate and neutrophils

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4
Q

What is acute inflammation controlled by?

A

A variety of chemical mediators derived from plasma or cells

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5
Q

What are some causes of acute inflammation?

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals, tissue necrosis

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6
Q

What are the main clinical signs of acute inflammation?

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Loss of function
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7
Q

What changes occur in tissues in acute inflammation?

A

1) Changes in blood flow
2) Exudation of fluid into tissues
3) Infiltration of inflammatory cells

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8
Q

What changes in blood flow occur in acute inflammation?

A

1) Transient vasoconstriction of arteriole
2) Vasodilation of arterioles and then capillaries
3) Increased permeability of blood vessels
4) Increased viscosity of blood

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9
Q

What effect does the vasodilation of arterioles and capillaries have?

A

Increase in blood flow - heat and redness

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10
Q

What effect does the increased permeability of blood vessels have?

A

Exudation of protein-rich fluid into tissues and slowing of cirulation - swelling

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11
Q

What effect does the increased viscosity of blood have on the flow?

A

Flow slows

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12
Q

What is an example of a chemical mediator?

A

Histamine

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13
Q

What is histamine released from?

A

Mast cells, basophils and platelets

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14
Q

What is histamine released in response to?

A

Many stimuli eg physical damage, immunologic reactions, C3a, C5a, IL-1, factors from neutrophils and platelets

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15
Q

What does histamine cause?

A

Vascular dilation, transient increase in vascular permeability, pain

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16
Q

What is fluid flow across vessel walls determined by?

A

Balance of hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

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17
Q

What does increased hydrostatic pressure result in?

A

Increased fluid flow out of the vessel

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18
Q

What does increased colloid osmotic pressure of interstitium result in?

A

Increased fluid flow out of the vessel

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19
Q

What is oedema?

A

Increased fluid in tissue spaces

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20
Q

Does oedema lead to increased or decreased lymphatic drainage?

A

Increased lymphatic drainage

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21
Q

How does exudate and transudate differ?

A

Exudate = fluid loss in inflammation = high protein content

Transudate = fluid loss due to hydrostatic pressure imbalance = low protein content (usually caused by cardiac failure)

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22
Q

What are some mechanisms of vascular leakage?

A

Endothelial contraction, cytoskeletal reorganisation, direct injurt, leukocyte dependent injury and increased transcytosis

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23
Q

What contributes to endothelial contraction?

A

Histamine, leukotrienes

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24
Q

What contributes to cytoskeletal reorganisation

A

Cytokines, IL-1 and TNF

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25
What sorts of things can cause direct injury that leads to vascular leakage?
Toxic burns, chemicals - damage vessel walls | Eg sunburn
26
What is VEGF?
Vascular endothelial growth factor - leads to increased transcytosis
27
What is the primary type of white blood cell involved in inflammation?
Neutrophil leucocyte
28
What are neutrophils a type of?
Type of granulocyte (also known as polymorph)
29
What are the four stages of the infiltration of neutrophils?
1) Margination 2) Rolling 3) Adhesion 4) Emigration
30
What happens during the margination phase of neutrophil infiltration?
Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium
31
What happens during the rolling phase of neutrophil infiltration?
Neutrophils rolls along endothelium, sticking to it intermittendtly
32
What happens during the adhesion phase of neutrophil infiltration?
Neutrophils stick to endothelium more avidly
33
What happens during the emigration phase of neutrophil infiltration?
Neutrophils emigrate through blood vessel wall into tissue
34
How do neutrophils escape from vessels?
Relaxation of inter-endothelial cell junctions and digestion of vascular basement membrane
35
What is chemotaxis?
Movement along concentration gradients of chemoattractants
36
Give some examples of chemotaxins
C5a, LTB4, bacterial peptides
37
In the oxygen-dependent mechanism of killing, what is produced?
Superoxide and hydrogen peroxide
38
What does the H2O2-Myeloperoxidase-halide system produce?
HOCl
39
What are involved in the oxygen-independent killing mechanism
Lysozyme and hydrolass, BPI, cationic proteins
40
Where are proteases produced?
Liver
41
What are the 3 main families of proteases involved in acute inflammation?
Kinins, complement system and coagulation/fibrinolytic system
42
What are prostaglandins/leukotrienes metabolites of?
Arachidonic acid
43
What are cytokines/chemokines produced by?
White blood cells
44
What are 2 important cytokines?
Interleukin-1 and TNF alpha
45
What chemical mediators are important in the increase of blood flow?
Histamine and prostaglandins
46
What chemical mediators are important in vascular permeability?
Histamine and leukotrienes
47
What chemical mediators are important in neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
48
What chemical mediator is important in phagocytosis?
C3b
49
How does exudation of fluid combat injury?
Delivers plasma proteins (fibrogen, inflammatory mediators, immunoglobulins) to area of injury Dilutes toxins Increases lymphatic drainage - delivers microbes to phagocytes and antigens to immune system
50
How does infiltration of cells (polymorphs and macrophages) combat injury?
Removes pathogenic organisms and necrotic debris
51
How does vasodilation combat injury?
Increases delivery and increases temperature
52
How does pain/loss of function combat injury?
Enforces rest and reduces change of further traumatic damage
53
What are some local complications of acute inflammation?
Swelling - can lead to blockage eg of bile duct Exudate - compression eg cadiac tamponade and serositis Loss of fluid - eg burns, easy to dehydrate Pain and loss of function
54
What are some systemic effects of acute inflammation?
Fever (production of endogenous pyrogens) Leukocytosis Acute phase response (decreased appetite, raised pulse etc)
55
What are some acute phase proteins?
``` C-reactive protein a1-antitrypsin Haptoglobin Fibrinogen Serum amyloid A protein ```
56
What is shock?
A clinical syndrome of circulatory failure (can't maintain BP and HR increases)
57
What could happen after the development of acute inflammation?
1) Complete resolution 2) Continued acute inflammation with chrone inflammation (eg abscess) 3) Chronic inflammation and fibrous repair 4) Death
58
If acute inflammation is resolved, what happens to the exudate and fibrin?
Exudate drains to lymphatics, fibrin degraded by plasmin
59
What is ascites?
Oedema in peritoneum
60
What are some examples of disorders of acute inflammation?
Hereditary angio-oedema Alpha1 antitrypsin deficiency Inherited complement deficiencies Defects in neutrophil function/numbers

ESA2 - Pathological Processes (9 decks)

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