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CGP ESA2 > MOD 2 Acute Inflammation > Flashcards

MOD 2 Acute Inflammation Flashcards

1
Q

Define ACUTE INFLAMMATION

A

The innate and stereotyped rapid response to cell injury, with the aim of delivering mediators of host defence (leukocytes & plasma proteins) to the site of injury.

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2
Q

What can cause acute inflammation?

A 
Infection
Foreign Bodies (e.g. splinters, dirt, sutures)
Immune reactions
Tissue necrosis
Trauma
Physical and chemical agents
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3
Q

What are the clinical signs of acute inflammation?

A

Rubor (red), Calor (hot), Tumour (swelling), Dolor (pain) & loss of function

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4
Q

What local mediator causes the pain associated with acute inflammation? What else causes pain?

A

Bradykinin. Histamine also causes pain.

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5
Q

Why does the site of acute inflammation swell?

A

Accumulation of leukocytes & fluid at the site.

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6
Q

What 3 steps can acute inflammation be broken down into?

A
  1. Change in blood flow
  2. Exudation of fluid
  3. Infiltration of inflammatory cells
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7
Q

What changes in blood flow are associated with acute inflammation?

A

HISTAMINE released from mast cells, basophils & platelets prompts VASODILATION of the arterioles leading to the site, causing an INCREASE IN BLOOD FLOW (rubber & calor)

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8
Q

What class of chemicals do serotonin (5HT) & histamine belong to?

A

Vasoactive amines

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9
Q

What are the effects of histamine?

A

Pain, vasodilatation and venular leakage

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10
Q

Describe how the changes in blood flow brought about by local mediators e.g. histamine cause an exudation of fluid

A

Increased capillary hydrostatic pressure because of arteriolar dilation. Venule walls become leaky due to gaps widening in the endothelium.
Thus resistance before the capillaries is decreased and after the capillaries is increased, causing greater exudation of fluid.

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11
Q

In the long term, the mediators responsible for the vasodilation switch from histamine to two others. What are they?

A

Bradykinin & Prostaglandins.

Prostaglandins are made in the cyclooxygenase pathway and thus their production can be reduced by prescribing aspirin.

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12
Q

What are the three main proteins present in the exudate?

A

Opsonins, complement and antibodies

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13
Q

What is the difference between an exudate and a transudate?

A

An exudate is rich in plasma proteins.
A transudate is largely fluid and plasma protein deprived This occurs when the vessel permeability has not been increased.

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14
Q

What is the role of Leukotrienes and how are they made?

A

Made from arachidonic acid, a product of phospholipid when acted upon by phospholipase.
The reaction requires the enzyme lipoxygenase.
Leukotrienes are PERMEABILITY INCREASERS

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15
Q

From which vessels does the exudate move out from in acute inflammation?

A

Venues & capillaries

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16
Q

What is the predominant immune cell type in acute inflammation?

A

Neutrophils

17
Q

What are the key steps in a neutrophil arriving at the correct site and performing its function?

A
  1. Chemotaxis
  2. Activation
  3. Margination
  4. Rolling
  5. Adhesion
  6. Diapedesis
  7. Recognition-attachment
  8. Phagocytosis
  9. Killing
18
Q

Describe CHEMOTAXIS

A

The movement of a neutrophil towards a chemical attractant (CHEMOTAXIN) e.g. a bacterial endotoxin.
Thrombin

19
Q

Describe the appearance and function of neutrophils.

A

Phagocytosis
Trilobular nucleus
Finite number of granules, once used the cell dies
Cannot divide

20
Q

Describe activation

A

Metabolic rate is increased
Begins on chemotaxin binding
Neutrophil becomes wedge shaped pointing in the direction of the stimulus

21
Q

List some chemotaxins

A 
FDPs
Bacterial endotoxins
clotted blood
thrombin
C3a, C4a, C5a
22
Q

Define margination, rolling and adhesion

A

When the neutrophils adopt positions around the edge of the blood vessel cross section.
The neutrophils then ROLL along the wall, bound to SELECTINS
They then ADHERE to INTEGRINS (e.g. ICAM-1)

23
Q

How do neutrophils leave the venule?

A

They don’t use endothelial gaps, they use COLLAGENASES to digest the basement membrane of the endothelium.
This process is called DIAPEDESIS & takes 3-9 minutes

24
Q

Describe the process of recognition-attachment

A

The bacterium may have been OPSONISED by IgG antibody or C3b or the neutrophil will recognise antigens

25
Q

Describe phagocytosis

A

The bacterium is engulfed by PSEUDOPODIA, and contained within a PHAGOSOME. This in turn fuses with a LYSOSOME to form a PHAGOLYSOSOME.
Granules fuse with the phagosome before it has fused off from the outside, so DEGRANULATION occurs- some hydrolytic enzymes leak into the local tissue

26
Q

How is the phagocytksed bacterium killed?

A
  1. ROS made by NADPH Oxidase

2. Lysosomal hydrolases

27
Q

What are the functions of complement?

A
  1. To make MAC (membrane attack complex)

2. Act as local mediators for chemotaxis and opsonisation

28
Q

What are the local effects of acute inflammation?

A
  1. Damage to healthy tissue because of DEGRANULATION
  2. Pain & loss of function
  3. Loss of fluid e.g. from burns
  4. Obstruction of tubes because of swelling causing compression e.g. fallopian tubes or cardiac tamponade
29
Q

What are the systemic effects of acute inflammation?

A
  1. Acute phase response - change in liver metabolism to decrease albumin production and increase protein production of the immune system e.g. FIBRINOGEN & C3, CRP & ALPHA-1 ANTITRYPSIN
  2. Leukocytosis - increased leukocytes in blood e.g. neutrophils because of G-CSF release from endothelial cells that have been damaged
  3. Toxic shock - endotoxins from bacteria cause a rapid decrease in TPR and BP causing distributive shock
  4. Fever - some of the mediators are pyrogenic e.g. TNF, interleukin 1. Some bacteria can’t survive at the higher temperatures.
30
Q

How does acute inflammation return to normal?

A

Removal of pathogenic injury causing stimulus causes a return to normal vascular permeability and the exudate is reabsorbed in venules.
Neutrophils undergo apoptosis and are phagocytosed by macrophages.
Healing continues by FIBROUS REPAIR or REGENERATION depending on the tissue type.

31
Q

What types of exudate are there?

A
  1. Pus- creamy white because dense neutrophils. Occurs when chemotactic bacteria are present
  2. Haemorrhagic- contains RBCs
  3. Serous - seen in blisters. Contains plasma proteins but not many leukocytes
  4. Fibrinous - Significant fibrin deposition.
32
Q

What is the molecular defect in hereditary angio-oedema?

A

C1-esterase inhibitor deficiency

33
Q

What are the symptoms and effects of hereditary angio-oedema? What emergency can it cause?

A

Non-itchy angio-oedema in dermis and mucosal areas
Abdominal pain due to intestinal oedema

SUDDEN DEATH due to laryngeal oedema

34
Q

Describe Alpha-1 antitrypsin deficiency

A

Misfolded alpha-1 antitrypsin causing it to accumulate in the liver
This causes liver damage but also EMPHYSEMA as the PROTEASES made by neutrophils in the lungs go unchecked.

35
Q

Discuss chronic granulomatous disease

A

NADPH oxidase is deficient. Therefore macrophages cannot make enough ROS to create a RESPIRATORY BURST.
Causes CHRONIC ABSCESSES

CGP ESA2 (7 decks)

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