Week 2 - Acute Inflammation Flashcards

1
Q

Name some possible causes of acute inflammation.

A
  1. Foreign bodies: sutures, dirt, splinters
  2. Immune reactions
  3. Bacterial, viral or parasitic infections and microbial toxins
  4. Trauma (blunt and penetrating)
  5. Physical and chemical agents (thermal injury, e.g. burns or frostbite, irradiation, environmental chemicals)
  6. Tissue necrosis: any cause
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2
Q

List the cardinal signs of acute inflammation.

A
  1. Rubor = redness
  2. Tumour = swelling
  3. Calor = Heat
  4. Dolor = pain
  5. Loss of function = enforces rest and reduces chance of further damage
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3
Q

Which is the most important mediator which causes pain upon stimulation of specialised nerve endings?

A

Bradykinin

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4
Q

What is an important vasoactive mediator that stimulates vasodilatation of arterioles in acute inflammation? Name the other mediators that can also cause vasodilatation.

A

Histamine

  1. Prostaglandins
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5
Q

In the granules of what cells is histamine stored?

A
  1. Mast cells
  2. Basophils
  3. Platelets (serotonin is stored in the granules of platelets)
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6
Q

Outline the roles of histamine in acute inflammation.

A
  1. Produces pain
  2. Arteriolar dilation
  3. Venular leakage (increased permeability)
  4. Causes endothelial cells to contract and pull apart, creating gaps through which plasma proteins can pass
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7
Q

Describe the mechanism by which aspirin and NSAIDS reduce pain and swelling in fever.

A
  1. Block production of prostaglandins

2. They inhibit cyclo-oxygenase, the enzyme that produces prostaglandins from arachidonic acid

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8
Q

List the functions of bradykinin.

A
  1. Produce pain

2. Increase vascular permeability

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9
Q

Outline the forces involved in Starling’s Law.

A
  1. Capillary pressure
  2. Interstitial free fluid pressure
  3. Plasma colloid osmotic pressure
  4. Interstitial fluid colloid osmotic pressure
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10
Q

Why is swelling observed in acute inflammation?

A

Fluid and leucocytes occupy space within the tissue

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11
Q

Why does the site of inflammation appear hot and red?

A

Increased blood flow locally –> arteriolar dilation

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12
Q

Name the three main types of defensive protein in the exudate, and outline the functions of each.

A
  1. Opsonins: coat foreign material and make them easy to phagocytise
  2. Complement: group of proteins assembled locally to produce a bacteria perforating structure
  3. Antibodies: bind to the surface of microorganisms and also act as opsonins
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13
Q

Distinguish between an exudate and transudate.

A

An exudate is protein rich while a transudate is protein poor.

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14
Q

List the chemical mediators that induce vascular leakage.

A
  1. Histamine
  2. Serotonin
  3. Bradykinin
  4. Complement components: C3a, C4a, C5a
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15
Q

What is the main type of leucocyte involved in acute inflammation?

A

Neutrophil polymorphs

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16
Q

Chemical signals from which cells cause neutrophils to leave blood vessels and enter tissue spaces?

A
  1. Bacteria
  2. Injured cells
  3. Other inflammatory cells
17
Q

What are some examples of chemotaxins?

A
  1. Bacterial products
  2. Injured tissues
  3. Substances produced by leucocytes
  4. Spilled blood
18
Q

What is endotoxin?

A

A bacterial chemotaxin –> lipopolysaccharide from the outer membrane of gram negative bacteria

19
Q

What is the most powerful chemotaxin released by leucocytes?

A

Leukotriene B4

20
Q

State examples of opsonins.

A
  1. IgG antibody

2. C3b fragment of complement

21
Q

What are the two main mechanisms by which organisms that have been phagocytised can be killed?

A
  1. Oxygen dependent: using oxygen derived free radicals e.g. superoxide, hydrogen peroxide, hydroxyl –> released into the phagosome. This mechanism of killing is called the oxygen or respiratory burst
  2. Oxygen independent: using enzymes, e.g. proteases, phospholipases, nucleases and lysozyme
22
Q

Which cytokines are involved in production of fever?

A
  1. Interleukin-1

2. TNF-alpha

23
Q

Which cytokine is responsible for cachexia during malignancy?

A
  1. Tumour necrosis factor (also called cachectin)
24
Q

State examples of chemokines and how they are produced.

A
  1. Leukotriene B4: from leucocytes
  2. C5a and C3a: from complement plasma precursors
  3. Bacterial products: from bacterial metabolism
25
Q

Which complement protein facilitates phagocytosis?

A

C3b: opsonin

26
Q

List the local complications of acute inflammation.

A
  1. Damage to normal tissue: secondary to substances released by neutrophils during phagocytosis
  2. Obstruction of tubes, e.g. intestines or Fallopian tubes or compression of vital structures: secondary to swelling produced by inflammatory exudate. Fluid accumulation within an enclosed space is dangerous, e.g. cardiac tamponade, swelling of the brain
  3. Loss of fluid: Fluid can continuously leak from surface wounds. Extensive skin wounds such as burns can result in loss of large amounts of fluid
  4. Pain and loss of function
27
Q

Which cell types fuse to form giant cells?

A

Macrophages

28
Q

What is the traditional surgical approach for treatment of an abscess?

A

Incision + drainage

Antibiotics are not always effective against abscesses

29
Q

Describe monocytes and histiocytes.

A

Monocytes: Macrophages circulating in the blood
Histiocytes: Macrophages within tissues

30
Q

List the systemic effects of acute inflammation.

A
  1. Fever
  2. Neutrophil leucocytosis
  3. Tachycardia
  4. The acute phase response
  5. Shock
31
Q

What is CRP?

A

An acute phase reactant which is elevated in acute inflammation