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

Week 2 - Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

The rapid response to an injurious agent

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2
Q

What are the major features of acute inflammation?

A 
Short duration
Innate
Immediate
Stereotyped (same response every time)
Main cell type = neutrophils
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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.

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4
Q

What are the 4 clinical signs of acute inflammation?

A

Rubor
Calor
Tumor
Dolor

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5
Q

Why does an inflamed tissue appear red and hot?

A

Increased perfusion

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6
Q

Why does an inflamed tissue appear swollen?

A

Entry of fluid and leukocytes into the tissue

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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

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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
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9
Q

What is inflammation?

A

The response of vascularised living tissue to injury

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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
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11
Q

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

A

Histamine

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12
Q

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

A

Serotonin

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13
Q

What are the effects of histamine during acute inflammation?

A

Pain
Arteriolar dilation
Venular leakage

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14
Q

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

A

Prostaglandins
Leukotrienes
Bradykinin

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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

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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

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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.

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18
Q

Define oedema

A

Excess fluid in the interstitium

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19
Q

What are the two types of oedema?

A

Transudate

Exudate

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20
Q

What is the difference between transudate and exudate?

A 
Transudate = fluid does not contain protein
Exudate = fluid is protein-rich
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21
Q

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

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?

A

Histamine, serotonin and bradykinin

23
Q

Are neutrophils usually present in the tissues?

A

No - only if inflammation/infection is present

24
Q

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

A 
"CAMRADRAP"
Chemotaxis
Activation
Margination, Rolling and Adhesion
Diapedesis
Recognition-Attachment
Phagocytosis
25
Q

What is chemotaxis?

A

The directional movement towards a chemical attractant

26
Q

Discuss margination, rolling and adhesion.

A

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
Q

What is diapedesis?

A

Process whereby leukocytes “dig” their way out of venules - produce collagenase which breaks down the basement membrane.

28
Q

Which plasma proteins facilitate phagocyte target recognition?

A

Opsonins

29
Q

Describe phagocytosis

A

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
Q

What are two important features of chemical mediators?

A

Short-lived
Have inhibitors
–> allows termination of inflammation

31
Q

Are all chemical mediators endogenous?

A

No - can be exogenous

32
Q

Give 4 families of chemical mediator that are produced by the liver, and give examples of each.

A
  1. Vasoactive amine - histamine/serotonin
  2. Vasoactive peptides - kinins
  3. Complement components - C3a/C5a
  4. Clotting factors
33
Q

How is bradykinin produced?

A

Cleaved off from kininogen

34
Q

What family of chemical mediators do prostaglandins belong to?

A

phospholipid derivatives

35
Q

Compare and contrast chemokines and cytokines?

A

Cytokines are bigger
Cytokines act as messengers between cells, whereas chemokines are involved in chemotaxis
Both are produced by white blood cells

36
Q

Give an example of an exogenous chemical mediator

A

Endotoxin - produced by bacteria

37
Q

Which chemical mediators cause increased blood flow?

A

Histamine, serotonin and prostaglandins

38
Q

Which chemical mediators cause increased vascular permeability?

A

Histamine, bradykinins and leukotrienes

39
Q

Which chemical mediators are involves in neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

40
Q

Give 5 complications of acute inflammation

A
  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
Q

What are the 4 major systemic effects of acute inflammation?

A
  1. Fever
  2. Leukocytosis
  3. Acute phase response
  4. Shock
42
Q

Why does acute inflammation often lead to fever?

A

Exogenous pyrogens raise the setting of the body’s thermostat by stimulating the production of endogenous pyrogens by macrophages.

43
Q

How does acute inflammation lead to an increase in the number of leukocytes?

A

Macrophages/injured epithelia produce CSFs, which stimulate the bone marrow to increase leukocyte production.

44
Q

What happens in the acute phase response?

A

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
Q

What accounts for the general feeling of illness during acute inflammation?

A

The acute phase response

46
Q

What happens if chemical mediators enter the bloodstream?

A

Sepsis, which leads to shock.

Vasodilation and increased vascular permeability –> blood pressure falls rapidly –> circulatory failure

47
Q

How may acute inflammation end?

A
  1. Complete resolution
  2. Inflammation persists - becomes chronic
  3. Death!
48
Q

What changes occur to allow complete resolution of acute inflammation?

A 
Neutrophils cease migrating
Vessel permeability returns to normal
Exudate drains
Fibrin degraded
Neutrophils at site die
Damaged tissue regenerates if architecture intact
49
Q

What is hereditary angio-oedema?

A

Autosomal dominant condition causing deficiency of C1-esterase inhibitor. Results in attacks of oedema - if in windpipe, fatal.

50
Q

What does a1-antritrypsin do?

What does deficiency lead to?

A

Deactivates proteases produced by neutrophils at inflammation site.
Deficiency leads to emphysema and liver disease

51
Q

What happens in chronic granulomatous disease?

A

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)

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