Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mechanisms of disease > Session 2 > Flashcards

Session 2 Flashcards

1
Q

Suggest some causes of acute inflammation

A

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

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

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

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

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

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

What is stasis?

A

Stagnation or cessation of blood flow

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

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

How is hydrostatic pressure increased in acute inflammation?

A

Arteriolar dilation

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

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

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

A

Oedema

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

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

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

A

Mast cells, basophils, and platelets

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

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

What does histamine cause?

A

Vascular dilation, a transient increase in vascular permeability and pain

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

How does histamine and leukotrienes cause vascular leakage?

A

Stimulate endothelial contraction, which forms gaps in the endothelium

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

How do IL-1 and TNF cause vascular leakage?

A

Stimulate cytoskeletal reorganisation that creates gaps in the endothelium

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

How does VEGF cause vascular leakage?

A

It increases transcytosis (the channels across the endothelial cytoplasm)

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

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

A

Bradykinin and kallidin; increase vascular permeability

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

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

What are the actions of TNF?

A

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
Q

What are leukotrienes?

A

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
Q

Which 2 mediators are the most important in increasing blood flow?

A

Histamine and prostaglandins

28
Q

Which 2 mediators are the most important in increasing vascular permability?

A

Histamine and leukotrienes

29
Q

Which 3 mediators are the most important in causing neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

30
Q

Which mediator is the most important in stimulating phagocytosis?

A

C3b

31
Q

Which is the most important cell of acute inflammation?

A

Neutrophils (polymorphonuclear leukocyte)

32
Q

How do neutrophils infiltrate the interstitium? (in four words)

A

Margination, rolling, adhesion, emigration

33
Q

How do neutrophils to the site of action?

A

Via chemotaxis, using chemoattractants

34
Q

What is the chief action of neutrophils? What is it facilitated by?

A

Phagocytosis; opsonins (Fc and C3b)

35
Q

Describe the O2 dependent killing mechanisms of neutrophils

A

Produces superoxide and hydrogen peroxide, and HOCl-, which cause damage to the antigen

36
Q

Describe the O2 independent killing mechanisms of neutrophils

A

Involve lysozymes and hydrolases, bacterial permeability increasing protein and cationic proteins (defensins)

37
Q

What are the three main functions of exudate in acute inflammation?

A

Delivers plasma proteins to area of injury, dilutes toxins, increases lymphatic drainage

38
Q

What is the general function of the infiltrate of inflammatory cells in acute inflammation?

A

Removes pathogenic organisms and necrotic debris

39
Q

What are the general functions of vasodilation in acute inflammation?

A

Increases delivery, increases temperature

40
Q

What are the general functions of pain and loss of function in acute inflammation?

A

Enforces rest, reduces chance of further traumatic damage

41
Q

What are the systemic effects of acute inflammation?

A

Fever, leucocytosis, acute phase response, shock

42
Q

What is fever produced by in acute inflammation?

A
43
Q

What is leucocytosis? Which mediators produce an accelerated release from the marrow?

A

White blood cell count above normal range for blood; IL1 and TNF

44
Q

What is the acute phase response?

A

Decreased appetite, raised pulse, altered sleep patterns and changes in plasma concentrations of acute phase proteins

45
Q

What are the potential outcomes of acute inflammation?

A

Complete resolution, chronic inflammation, death

46
Q

What are possible mechanisms of resolution?

A

Mediators have short half-lives, they may be inhibited or inactivated by degradation. They may be diluted in the exudate.

47
Q

Why is the fluid of a skin blister clear?

A

There are relatively few inflammatory cells, unless bacterial infection develops

48
Q

What occurs to cause a skin blister?

A

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
Q

What causes an abscess?

A

Inflammatory exudate forces tissues apart, with liquefactive necrosis in the centre

Mechanisms of disease (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions