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Mechanisms Of Disease > Session 2 > Flashcards

Session 2 Flashcards

1
Q

What is acute inflammation?

A

An innate, immediate and early stereotyped tissue reaction to injury. It has a short duration

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2
Q

What can cause acute inflammation?

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals and tissue necrosis.

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3
Q

What are the 5 main clinical signs of acute inflammation?

A 
Rubor - redness
Tumor - swelling
Calor - heat
Dolor - pain
Loss of function.
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4
Q

What are 3 main changes in tissues during acute inflammation?

A

Changes in blood flow
Exudation of fluid to tissues
Infiltration of inflammatory cells

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5
Q

What changes in blood flow occur in acute inflammation?

A

Vasoconstriction of arterioles immediately.
Followed by vasodilatation of arterioles and capillaries which increases blood flow.
The permeability of the blood vessels increases.
Increased viscosity of blood due to increased concentration of red blood cells.

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6
Q

Why does the permeability of blood vessels increase during acute inflammation?

A

Allows exudation of protein rich fluid into tissues.

Makes the circulation slow so swelling occurs.

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7
Q

What is the immediate response chemical mediator?

A

Histamine.

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8
Q

What cells release histamine?

A

Mast cells, basophils and platelets.

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9
Q

What stimulates the release of histamine?

A

Physical damage, immunological reactions and factors from neutrophils and platelets.

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10
Q

What does histamine cause?

A

Vascular dilatation, pain and increase vascular permeability.

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11
Q

What are the persistent response chemical mediators?

A

Many and varied chemical mediators that interlink and have varying importance.

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12
Q

What is Starling’s law?

A

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure. Comparing plasma and interstitial fluid.

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13
Q

According to Starlings law, what will happen when you increase the hydrostatic pressure in a vessel?

A

The fluid flow out of the vessel will increase.

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14
Q

According to Starlings law, what will happen if you increase the colloid osmotic pressure of the interstitium?

A

The fluid flow out of the vessel will increase.

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15
Q

What is the NET flow of fluid in the tissues during acute inflammation?

A

It is out of the vessel into the tissue spaces. Causes an Oedema.
This is because of arteriolar dilatation and increased permeability.

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16
Q

What is an oedema?

A

Excess fluid in the interstitium - can be transudate or exudate.
It leads to increased lymphatic drainage.

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17
Q

What is an exudate oedema?

Extra point - what causes it?

A

High protein content oedema.

Extra point - fluid loss in inflammation.

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18
Q

What is a transudate oedema?

Extra point - what causes it?

A

A oedema with low protein content.
Extra point - due to fluid loss because of hydrostatic pressure imbalance.
Eg in cardiac failure.

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19
Q

What are the main mechanisms of vascular leakage?

A

Endothelial contraction, increased transcytosis, cytoskeletal reorganisation, direct injury and leukocyte dependent injury.

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20
Q

War chemical mediators cause endothelial contraction?

A

Histamine and leukotrienes.

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21
Q

What is leukocyte dependent injury?

A

Where injury occurs due to toxic oxygen species and enzymes from leukocytes.

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22
Q

What chemical mediator causes increased transcytosis?

A

VEGF.

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23
Q

What plasma protein goes to the site of injury?

A

Fibrin.

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24
Q

What are the 2 main cells that migrate to the site of acute inflammation?

A

Neutrophils! And macrophages.

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25
Q

What is margination?

A

Where stasis causes neutrophils to line up at the edge of blood vessels along the endothelium.

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26
Q

What is it called when neutrophils roll along the endothelium of a blood vessel, sticking to it intermittently?

A

Rolling.

27
Q

What happens after neutrophils have finished ‘rolling’?

A

The stick more avidly, called adhesion.

28
Q

What is the final step in neutrophil infiltration?

A

The emigrate through the blood vessel wall.

29
Q

How do neutrophils escape from tissues after the acute inflammation phase?

A

There is relaxation of inter endothelial cell junctions, leading to digestion of the vascular basement membrane and movement out.

30
Q

What is chemotaxis?

A

Movement along a concentration gradient of chemoattractants. Eg C5a

31
Q

What do neutrophils do?

A

Phagocytosis. Contact, recognition and internalisation.

32
Q

What facilitates neutrophils phagocytosing?

A

Opsonins - Fc and C3b.

33
Q

What are the 2 main types of neutrophillic killing mechanisms?

A

O2 dependent and O2 independent.

34
Q

What are the types of O2 dependent neutrophillic killing mechanisms?

A

Production of super oxide/hydrogen peroxide.

Producing HOCL-

35
Q

What are the types of O2 independent neutrophillic killing systems?

A

Lysozyme and hydrolases.
BPI protein.
Catatonic proteins.

36
Q

What may activated neutrophils release?

A

Toxic metabolites and enzymes to damage the host tissue.

37
Q

What are the 3 main types of chemical mediators of acute inflammation?

A

Proteases - plasma proteins produced in the liver. Coagulative/fibrinolytic system.
Prostaglandins/Leukotrienes - metabolites of arachidonic acid
Cytokines/Chemokines - produced by WBCs. TNF alpha.

38
Q

Where in the body are proteases made?

A

In the liver.

39
Q

Which mediators of acute inflammation increase blood flow?

A

Histamine and prostaglandins.

40
Q

Which mediators of acute inflammation increase vascular permeability?

A

Histamine and leukotrienes.

41
Q

Which chemical mediators of acute inflammation aid neutrophil chemotaxis?

A

C5a, LTB4 and bacterial peptides.

42
Q

Which chemical mediators of acute inflammation aid phagocytosis?

A

C3b.

43
Q

What is the 2 main histological signs of acute inflammation?

A

Exudate of oedema fluid.

Infiltrate of inflammatory cells.

44
Q

How does exudate on of fluid combat injury?

A

Delivers plasma proteins to the area of injury. (Fibrinogen, inflammatory mediators.)
Dilutes toxins.
Increases lymphatic drainage. (Delivers micro organisms to phagocytes and antigens to immune system)

45
Q

How does infiltration of cells combat injury?

A

It removes pathogenic organisms and necrotic debris.

46
Q

How does vasodilatation combat injury?

A

It increases delivery of cells within the blood and increases the temperature.

47
Q

How does pain and loss of function combat injury?

A

It enforces rest in the person and reduces the chance of further traumatic damage.

48
Q

What are the local consequences of acute inflammation?

A

Swelling - can lead to blockage of tubes.
Exudate - compression and serositis.
Loss of fluid - in burns.
Pain and loss of function.

49
Q

What are the systemic effects of acute inflammation?

A

Fever - can be due to TNF alpha.
Leukocytes - reduce an accelerated release from the marrow. Macrophages and T lymphocytes produce colony stimulating factors.

50
Q

Which cell is released for a bacterial infection and viral infection?

A

Bacterial - neutrophils

Viral - lymphocytes

51
Q

What are the signs of a systemic acute phase response to acute inflammation?
Extra point - what are the proteins?

A

A decreased appetite
Raised pulse rate
Altered sleeping patterns
Changes in plasma concentration of proteins.
Extra point - CRP, alpha 1 antitrypsin, fibrinogen.

52
Q

What is shock?

A

A clinical syndrome of circulatory failure.

53
Q

What are the sequelae of acute inflammation?

A

1) Resolution.
2) Abscess (due to continued acute inflammation with chronic inflammation.)
3) Chronic inflammation with fibrous repair and tissue regeneration.
4) Death.

54
Q

What happens in resolution of acute inflammation?

A

The changes gradually reverse and vascular changes stop;
Neutrophils no longer marginate
Vessel permeability returns to normal
Vessel calibre returns to normal

55
Q

Under what circumstances is complete tissue resolution not possible?

A

If tissue architecture has been destroyed.

56
Q

How are mediators of acute inflammation degraded?

A 
Some have short half lives
Inactivated by degradation eg heparinase
Inhibitors may bind
They may be unstable
Can be diluted in the exudate
57
Q

What is bacterial meningitis?

A

Acute inflammation in the meninges. Causes vascular thrombosis, reduces cerebral perfusion.

58
Q

What do the alveoli get filled with in lobar pneumonia?

A

Exudate instead of air.

59
Q

What causes lobar pneumonia?

A

Streptococcus pneumoniae.

60
Q

What is the clinical course of lobar pneumonia?

A

A worsening fever, prostration, hypoxaemia and a dry cough with breathlessness.

61
Q

What is the pathophysiology of a skin blister?

A

The collection of fluid strips off underlying epithelium. There are relatively few inflammatory cells so the exudate is clear unless bacterial infection develops.

62
Q

What is the pathophysiology of an abscess?

A

The inflammatory exudate forces tissues apart.
Liquefactive necrosis is in the centre.
There is usually a high pressure so painful.
Can cause tissue damage by squashing the adjacent structures.

63
Q

What is the pathophysiology of pericarditis?

A

Inflammatory exudate pours into the cavity, get effusion. There is impairment of function and localised fibrin deposition.

64
Q

Name a disorder of acute inflammation.

A

Alpha 1 antitrypsin deficiency.

Mechanisms Of Disease (11 decks)

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