Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Semester 2 - Mechanisms of Disease > Week 2 - Acute Inflammation > Flashcards

Week 2 - Acute Inflammation Flashcards

(51 cards)

Start Studying
1
Q

What is acute inflammation?

A

The rapid response to an injurious agent

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

What are the major features of acute inflammation?

A 
Short duration
Innate
Immediate
Stereotyped (same response every time)
Main cell type = neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the aim of inflammation?

A

To deliver materials to the site of injury in order to prevent infection, clear damaged tissue and initiate tissue repair.

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

What are the 4 clinical signs of acute inflammation?

A

Rubor
Calor
Tumor
Dolor

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

Why does an inflamed tissue appear red and hot?

A

Increased perfusion

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

Why does an inflamed tissue appear swollen?

A

Entry of fluid and leukocytes into the tissue

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

Why does inflamed tissue appear painful? Is there any benefit to the pain?

A

Due to mediators such as bradykinin which stimulate the nerve endings.
Enforces rest

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

What are the 3 major changes which occur in acute inflammation?

A 
Vascular - 
Changes in blood flow
Exudation of fluid into the tissues
Cellular - 
Infiltration of inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is inflammation?

A

The response of vascularised living tissue to injury

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

Outline the sequence of changes that occur to blood flow in acute inflammation

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilatation of arterioles (mediators initiate this)
  3. Flow accelerates in capillaries - capillary pressure rises
  4. Increased permeability of venules - allows leakage of fluid into the tissues via gaps in endothelia
  5. Less fluid in blood = vascular stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the main chemical mediator involved in the vascular changes associated with acute inflammation?

A

Histamine

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

Apart from histamine, which other chemical mediator belongs to the vasoactive amine family.

A

Serotonin

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

What are the effects of histamine during acute inflammation?

A

Pain
Arteriolar dilation
Venular leakage

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

Apart from histamine, name 3 other mediators involved in the vascular changes of acute inflammation

A

Prostaglandins
Leukotrienes
Bradykinin

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

What happens to the hydrostatic and colloid osmotic pressures of the blood during inflammation? Why?

A

Hydrostatic pressure increases - arterioles dilate

Colloid osmotic pressure decreases - proteins leak out

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

Why is there a net movement of fluid out of the blood and into the tissues during acute inflammation?

A

Hydrostatic pressure exceeds colloid osmotic pressure in the blood

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

Why may the lymph nodes become infected following a cut to the finger?

A

Acute inflammation means exudate at the site of trauma. This excess fluid then drains to the lymph nodes, taking any microbes with it. They may then multiply there.

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

Define oedema

A

Excess fluid in the interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two types of oedema?

A

Transudate

Exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the difference between transudate and exudate?

A 
Transudate = fluid does not contain protein
Exudate = fluid is protein-rich
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 4 types of exudate, and how do they differ?

Study These Flashcards
A
  1. Pus/abscess - creamy and white –> contains neutrophils
  2. Haemorrhagic - contains RBCs
  3. Serous - clear –> plasma proteins only
  4. Fibrinous –> contains fibrin
22
Q

Which mediators are involved in oedema?

Study These Flashcards
A

Histamine, serotonin and bradykinin

23
Q

Are neutrophils usually present in the tissues?

Study These Flashcards
A

No - only if inflammation/infection is present

24
Q

What processes must the neutrophil undergo in order to capture and kill bacteria?

Study These Flashcards
A 
"CAMRADRAP"
Chemotaxis
Activation
Margination, Rolling and Adhesion
Diapedesis
Recognition-Attachment
Phagocytosis
25
What is chemotaxis?
The directional movement towards a chemical attractant
26
Discuss margination, rolling and adhesion.
Margination: Leukocytes assemble along the edges of the blood vessels. Rolling: Leukocytes "roll" along the endothelium, occasionally binding to selectins (adhesion molecules) Adhesion: Receptors on leukocytes adhere firmly to integrins
27
What is diapedesis?
Process whereby leukocytes "dig" their way out of venules - produce collagenase which breaks down the basement membrane.
28
Which plasma proteins facilitate phagocyte target recognition?
Opsonins
29
Describe phagocytosis
Particle engulfed and put into phagosome Phagosome fuses with lysosome - secondary lysosome Lysosomal contents injected into the phagosome (some leaks out into surrounding tissue) Organism killed by either oxidative burst or enzymes
30
What are two important features of chemical mediators?
Short-lived Have inhibitors --> allows termination of inflammation
31
Are all chemical mediators endogenous?
No - can be exogenous
32
Give 4 families of chemical mediator that are produced by the liver, and give examples of each.
1. Vasoactive amine - histamine/serotonin 2. Vasoactive peptides - kinins 3. Complement components - C3a/C5a 4. Clotting factors
33
How is bradykinin produced?
Cleaved off from kininogen
34
What family of chemical mediators do prostaglandins belong to?
phospholipid derivatives
35
Compare and contrast chemokines and cytokines?
Cytokines are bigger Cytokines act as messengers between cells, whereas chemokines are involved in chemotaxis Both are produced by white blood cells
36
Give an example of an exogenous chemical mediator
Endotoxin - produced by bacteria
37
Which chemical mediators cause increased blood flow?
Histamine, serotonin and prostaglandins
38
Which chemical mediators cause increased vascular permeability?
Histamine, bradykinins and leukotrienes
39
Which chemical mediators are involves in neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
40
Give 5 complications of acute inflammation
1. Damage to normal tissue 2. Obstruction of tubes by exudate 3. Accumulation of exudate - compression of organs 4. Loss of fluid from surface wounds (burns) 5. Pain and loss of function
41
What are the 4 major systemic effects of acute inflammation?
1. Fever 2. Leukocytosis 3. Acute phase response 4. Shock
42
Why does acute inflammation often lead to fever?
Exogenous pyrogens raise the setting of the body's thermostat by stimulating the production of endogenous pyrogens by macrophages.
43
How does acute inflammation lead to an increase in the number of leukocytes?
Macrophages/injured epithelia produce CSFs, which stimulate the bone marrow to increase leukocyte production.
44
What happens in the acute phase response?
There is a change in the plasma concentration of some proteins due to the liver changing the rate of protein synthesis, triggered by cytokines.
45
What accounts for the general feeling of illness during acute inflammation?
The acute phase response
46
What happens if chemical mediators enter the bloodstream?
Sepsis, which leads to shock. | Vasodilation and increased vascular permeability --> blood pressure falls rapidly --> circulatory failure
47
How may acute inflammation end?
1. Complete resolution 2. Inflammation persists - becomes chronic 3. Death!
48
What changes occur to allow complete resolution of acute inflammation?
``` Neutrophils cease migrating Vessel permeability returns to normal Exudate drains Fibrin degraded Neutrophils at site die Damaged tissue regenerates if architecture intact ```
49
What is hereditary angio-oedema?
Autosomal dominant condition causing deficiency of C1-esterase inhibitor. Results in attacks of oedema - if in windpipe, fatal.
50
What does a1-antritrypsin do? | What does deficiency lead to?
Deactivates proteases produced by neutrophils at inflammation site. Deficiency leads to emphysema and liver disease
51
What happens in chronic granulomatous disease?
Phagocytes cannot generate superoxide, hence engulfed bacteria cannot be killed via an oxidative burst. Leads to chronic infection.

Semester 2 - Mechanisms of Disease (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions