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ESA2 > MOD S3 > Flashcards

MOD S3 Flashcards

0
Q

What are some causes of acute inflammation?

A 
Microbial infections
Hypersensitivity reactions (aka allergies)
Physical agents
Chemical agents
Tissue necrosis
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1
Q

What is acute inflammation?

A

The response of living tissue to injury, initiated to limit tissue damage

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2
Q

What are the macroscopic signs of inflammation?

A

Calor - heat
Rubor - redness
Tumor - swelling
Dolor - pain

+ loss of function

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3
Q

What are the microscopic features of acute inflammation?

A 
Vasodilation
Gaps form in endothelium
Exudation
Margination and emigration
Macrophages and lymphocytes
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4
Q

Describe the changes in blood flow in acute inflammation

A

Transient vasoconstriction of arterioles (a few secs)
Vasodilation of arterioles and then capillaries
Increased blood vessel permeability
Stasis- increased concentration of RBCs in small vessels and blood viscosity

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5
Q

What are some chemical mediators of vasodilation?

A

HISTAMINE
Prostoglandins
C3a
C5a

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6
Q

Describe histamine

A

-Released ~30 mins into acute inflammation
-Many stimuli
-Released by mast cells, basophils and platelets
-Causes:
>Vasodilation
>Transient increase in vascular permeability
>Pain

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7
Q

What are some chemical mediators of increased vascular permeability?

A

HISTAMINE
Prostoglandins
Kinins

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8
Q

What determines fluid flow across blood vessel walls?

A

Starling’s Law
The balance of hydrostatic and colloid osmotic pressure
An increase in either will increase fluid movement out of blood vessel

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9
Q

What is a build up of tissue fluid called?

A

Oedema

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10
Q

What does oedema lead to?

A

Increased lymphatic drainage

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11
Q

What is a transudate?

A

Fluid loss from blood vessels due to hydrostatic pressure only
Has a low protein content
Caused by cardiac failure or venous outflow obstruction

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12
Q

What is exudate?

A

Fluid loss from blood vessels
Seen in inflammation
Has a high protein content

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13
Q

What are some chemical mediators of leukocyte emigration?

A

Leukotrienes
IL-8
C5a

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14
Q

What is another name for a neutrophil?

A

A polymorph

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15
Q

What do neutrophils do?

A

Move to the site of cell injury by chemotaxis
Phagocytose microorganisms by making contact, recognising and internalising them
Phagosomes then fuse with lysosomes to destroy contents
Activated neutrophils may release toxic metabolites and enzymes with damage host tissue

16
Q

What is the difference between transudate and exudate?

A

Transudate has a low protein content

Exudate has a high protein content

17
Q

What are some signs of the acute phase response of inflammation?

A

Decreased appetite
Tachycardia
Altered sleep patterns
Changes in plasma concentrations of acute phase proteins eg CRP, Fibrinogen and α1-anti trypsin

18
Q

What causes fever?

A

Production of endogenous pyrogens eg IL-1 TNFα and prostoglandin

28
Q

What is leukocytosis

A

The process by which white blood cell production is accelerated
By IL-1, TNFα
Colony simulating factors released by macrophages and t-lymphocytes

29
Q

What are the possible end results of acute inflammation?

A

Complete resolution
Continued acute inflammation and chronic inflammation (eg abscess)
Chronic inflammation with fibrous repair
Death

30
Q

How may the mediators of acute inflammation be inactivated?

A

Degradation
Dilution
Inhibition

(Most have short half lives so degrade normally anyway)

31
Q

Name the stages of neutrophil invasion in acute inflammation

A

Margination
Rolling
Adhesion
Emigration

32
Q

Describe margination (in acute inflammation)

A

First stage

Stasis causes neutrophils to line up along the edges of blood vessels

33
Q

Describe rolling (in acute inflammation)

A

Second stage

Neutrophils roll along endothelium, intermittently sticking to it

34
Q

Describe adhesion (in acute inflammation)

A

Third stage

The neutrophils stick more firmly to the endothelial walls of blood vessels

35
Q

Describe emigration (in acute inflammation)

A

Final stage

Neutrophils move through blood vessel walls into tissues

36
Q

When is complete resolution impossible?

A

When cell architecture of damaged cells is destroyed

37
Q

How is complete resolution achieved?

A 
All the changes of acute inflammation reverse
Mediators are inactivated
Neutrophils present die
Exudate drains via lymphatics
Fibrin is degraded by plasmin ect
Vascular changes stop:
>Neutrophils no longer marginate
>Vessel calibre and permeability returns to normal
38
Q

What are some possible complications of acute inflammation?

A 
Blockage of tubes
Compression
Loss of fluid
Pain
Loss of function
39
Q

Give a few clinical examples of acute inflammation

A

Skin blister
Abscess
Pericarditis

40
Q

What happens in the case of sun blisters?

A 
Caused by heat, sunlight or chemicals
Pain and profuse exudate
Collection of fluid strips off overlying epithelium
Resolution or scarring
Few inflammatory cells so clear exudate
41
Q

What happens in the case of abscesses?

A

Occur in solid tissues
Inflammatory exudate forces tissues apart
Liquefactive necrosis at centre
May cause high pressure so pain
May cause tissue damage or compress adjacent tissues

42
Q

What happens in pericarditis?

A

Inflammation of serous cavity

Pericardium becomes enflamed so increases pressure on heart

43
Q

Give examples of some hereditary disorders of the acute inflammation process

A

α1 anti trypsin deficiency
Complement deficiencies
Defects in neutrophil function
Defects in neutrophil numbers

44
Q

Describe α1-anti trypsin deficiency

A

α1 antitrypsin inhibits elastase
If deficient, elastase will break down elastin in lung and liver tissue
Can cause emphysema and liver sclerosis

ESA2 (39 decks)

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