Session 2 Flashcards

(49 cards)

1
Q

Suggest some causes of acute inflammation

A

Microbial infections, hypersensitivity reactions (acute phase), physical agents, chemicals, tissue necrosis

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2
Q

What are the 4 clinical features of acute inflammation?

A

Rubor (redness), Tumor (swelling), Calor (heat), and Dolor (pain and loss of function)

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3
Q

What are the 3 key changes in acutely inflamed tissues?

A

Changes in blood flow, exudation of fluid into tissues, infiltration of inflammatory cells

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4
Q

How does the blood flow changes in acute inflammation?

A

Transient vasoconstriction (few seconds) and then vasodilation of arterioles and capillaries, resulting in increased blood flow (heat and redness)

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5
Q

How does the permeability of the blood vessels change in acute inflammation?

A

Increase in permeability causes exudation of protein rich fluid into tissues and the slowing of circulation (swelling)

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6
Q

What is stasis?

A

Stagnation or cessation of blood flow

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7
Q

What changes in hydrostatic pressure and intersitium colloid osmotic pressure will cause fluid to flow out of vessels

A

Increase in hydrostatic pressure and increase in colloid pressure of interstitium cause an increase in fluid flow out of the vessel

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8
Q

How is hydrostatic pressure increased in acute inflammation?

A

Arteriolar dilation

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9
Q

Why does interstitial colloid pressure increase in acute inflammation?

A

Increased permeability of vessel walls leads to loss of fluid into the interstitium

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10
Q

What is the clinical term for an excess of fluid in the interstitium?

A

Oedema

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11
Q

What is the difference between transudate and exudate fluid loss?

A

Exudate: high protein content fluid (seen in inflammation)
Transudate: fluid loss due to hydrostatic pressure imbalance inly (low protein content)

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12
Q

Which cells is histamine released from in the immediate response to cause acute inflammation?

A

Mast cells, basophils, and platelets

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13
Q

Why is histamine released?

A

In response to many factors, such as physical damage, immunological reactions, complement proteins (C3a, C5a), interleukins, factors from neutrophils and platelets

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14
Q

What does histamine cause?

A

Vascular dilation, a transient increase in vascular permeability and pain

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15
Q

How does histamine and leukotrienes cause vascular leakage?

A

Stimulate endothelial contraction, which forms gaps in the endothelium

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16
Q

How do IL-1 and TNF cause vascular leakage?

A

Stimulate cytoskeletal reorganisation that creates gaps in the endothelium

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17
Q

How does VEGF cause vascular leakage?

A

It increases transcytosis (the channels across the endothelial cytoplasm)

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18
Q

Name the two prominent kinins. What is there general effect?

A

Bradykinin and kallidin; increase vascular permeability

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19
Q

Name two complement proteins important in the release of histamine from mast cells and which act as chemoattractants for white blood cells. Which WBC in particular do they attract?

A

C3a, and C5a; neutrophils

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20
Q

Name some general actions of prostaglandins

A

The constriction or dilation of vascular smooth muscle cells, the aggregation/disaggregation of platelets, and the control of cell growth

21
Q

What is the action of chemokines?

A

Induce chemotaxis, important in recruiting inflammatory cells to the site of infection

22
Q

What are interleukins predominantly synthesised by? What is their action?

A

CD4 T lymphocytes; they promote the development and differentiation of T, B and haematopoietic cells

23
Q

What are interferons?

A

Proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumour cells; they trigger an immune response

24
Q

What is TNF?

A

Tumour necrosis factor-alpha is a cytokine involved in systemic inflammation, produced mainly by macrophages

25
What are the actions of TNF?
Primary role of TNF is in the regulation of immune cells; TNF is able to induce fever, apoptotic cell death, inflammation and other effects in order to inhibit tumorigenesis and viral replication
26
What are leukotrienes?
Family of inflammatory mediators produced in leukocytes by the oxidation of arachidonic acid; they use lipid signalling in order to regulate an immune response, and can cause smooth muscle contraction
27
Which 2 mediators are the most important in increasing blood flow?
Histamine and prostaglandins
28
Which 2 mediators are the most important in increasing vascular permability?
Histamine and leukotrienes
29
Which 3 mediators are the most important in causing neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
30
Which mediator is the most important in stimulating phagocytosis?
C3b
31
Which is the most important cell of acute inflammation?
Neutrophils (polymorphonuclear leukocyte)
32
How do neutrophils infiltrate the interstitium? (in four words)
Margination, rolling, adhesion, emigration
33
How do neutrophils to the site of action?
Via chemotaxis, using chemoattractants
34
What is the chief action of neutrophils? What is it facilitated by?
Phagocytosis; opsonins (Fc and C3b)
35
Describe the O2 dependent killing mechanisms of neutrophils
Produces superoxide and hydrogen peroxide, and HOCl-, which cause damage to the antigen
36
Describe the O2 independent killing mechanisms of neutrophils
Involve lysozymes and hydrolases, bacterial permeability increasing protein and cationic proteins (defensins)
37
What are the three main functions of exudate in acute inflammation?
Delivers plasma proteins to area of injury, dilutes toxins, increases lymphatic drainage
38
What is the general function of the infiltrate of inflammatory cells in acute inflammation?
Removes pathogenic organisms and necrotic debris
39
What are the general functions of vasodilation in acute inflammation?
Increases delivery, increases temperature
40
What are the general functions of pain and loss of function in acute inflammation?
Enforces rest, reduces chance of further traumatic damage
41
What are the systemic effects of acute inflammation?
Fever, leucocytosis, acute phase response, shock
42
What is fever produced by in acute inflammation?
43
What is leucocytosis? Which mediators produce an accelerated release from the marrow?
White blood cell count above normal range for blood; IL1 and TNF
44
What is the acute phase response?
Decreased appetite, raised pulse, altered sleep patterns and changes in plasma concentrations of acute phase proteins
45
What are the potential outcomes of acute inflammation?
Complete resolution, chronic inflammation, death
46
What are possible mechanisms of resolution?
Mediators have short half-lives, they may be inhibited or inactivated by degradation. They may be diluted in the exudate.
47
Why is the fluid of a skin blister clear?
There are relatively few inflammatory cells, unless bacterial infection develops
48
What occurs to cause a skin blister?
Collection of fluid between epidermis and lower layers; the fluid forms a cushion for the tissue underneath, allowing it to resist further damage and undergo repair
49
What causes an abscess?
Inflammatory exudate forces tissues apart, with liquefactive necrosis in the centre