Acute Inflammation Flashcards

1
Q

What is pneumonitis?

A

Inflammation of the lung tissue

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2
Q

What are the functions of neutrophils?

A

Mobile phagocytes - they recognise foreign antigens
move towards it (chemotaxis)
Adhere to organisms

Their granules contain oxidants (hydrogen peroxide) and enzymes (non -specific proteases)

They release their granule contents into phagosome and destroy foreign body.

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3
Q

What are the consequences of neutrophil action?

A

Neutrophils often die when their granule contents is released.
Produce pus which might extend into other tissues causing inflammation.

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4
Q

What does pus consist of?

A

Bits of cell, organisms and endogenous proteins.

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5
Q

What is the role of fibrinogen in the inflammatory response?

A

Coagulation factor that activates and forms fibrin which acts as a scaffold trapping blood molecules allowing it to clot.

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6
Q

What is the role of immunoglobulins in the inflammatory response?

A

Specific to antigen, activate humoural immune response.

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7
Q

What are the 3 different types of mediators of acute inflammation?

A

Molecules on endothelial cell surface
Molecules released from cells
Molecules in the plasma

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8
Q

What are the collective effects of mediators?

A
Vasodilatation
Increased permeability 
Neutrophil adhesion
Chemotaxis 
Itch and pain
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9
Q

Give some properties and examples of cell surface mediators?

A

Cell surface mediators are sticky and aid in the adhesion of neutrophils. E.g P-selectin, ICAM-1

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10
Q

Give some examples of molecules released from cells?

A

Histamine is main molecule involved in inflammatory response.Preformed in mast cells beside platelets, vessels and basophils. 5-hydroxytryptamine (serotonin) is another example. It is preformed in platelets and released when they degranulate.

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11
Q

What effects does the release of histamine cause?

A

Causes vasodilatation and increased permeability.

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12
Q

What effect does serotonin cause?

A

Causes vasoconstriction.

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13
Q

What do plasma molecule mediators do?

A

They interaction and are involved in enzyme cascades.

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14
Q

Give some examples of these enzyme cascades?

A

Blood coagulation pathway - clots fibrinogen in exudate
Fibrinolysis - breaks down fibrin, helps maintain blood supply.
Kinin system - causes the pain in response.
Complement cascade - ties inflammation with immune response.

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15
Q

What is the general outcome of mediators?

A
Vasodilation and constriction
Neutrophil adhesion 
Increased permeability 
Chemotaxis 
Itch and Pain
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16
Q

What is Chemotaxis?

A

The movement of an organism in a direction corresponding to the gradient of a particular substance. Chemicals released by foreign antigen are detected and then used as a tracker so the fighter can move towards it.

17
Q

What are some immediate effects of acute inflammation?

A

Pyrexia - raised temperature
Feel unwell - malaise, anorexia, nausea, abdominal pain and vomiting in children.
Neutrophilia - raised white cell count.

18
Q

What are some longer term effects of acute inflammation?

A

Lymphadenopathy - regional lymph node enlargement.
Weight loss - catabolic reaction
Anaemia - red cell deficiency or lack of haemoglobin in blood

19
Q

What is acute inflammation suppuration?

A

Pus formation

Pyogenic membrane surrounds pus

20
Q

What is an Abscess?

A

Collection of pus (suppuration) under pressure.

21
Q

What is a multiloculated abscess?

A

When the pus from one abscess bursts through the pyogenic membrane and forms new cavities.

22
Q

What is pus in a hollow viscus referred to?

A

Empyema e.g pus in gallbladder, pleural cavity.

23
Q

What is Pyaemia?

A

Pus in the bloodstream.

24
Q

What is granulation tissue?

A

Universal patch or repair kit for damaged tissue.

Formed of new capillaries, fibroblasts, collagen and macrophages.

25
Q

What is dissemination?

A

The spread of infection to the bloodstream - sepsis

26
Q

What is bacteraemia?

A

Bacteria in the blood

27
Q

What is Septicaemia?

A

The growth of bacteria in the blood.

28
Q

What is Toxaemia?

A

Toxins in the blood

29
Q

What are the clinical symptoms of septic shock?

A
Peripheral vasodilation
Tachycardia
Hypotension
Pyrexia
Haemorrhagic skin rash
30
Q

How does septic shock occur?

A

Mediators are released causing vasodilation if cells. This vasodilation then leads to loss of systemic vascular resistance. Catecholamine is then released. Tachycardia then results as heart rate increases to compensate for cardiac output.

31
Q

What could potentially happen if this compensation fails.

A

Blood pressure falls so there is reduced perfusion to tissues. This causes tissue damage and even loss of organ function.

32
Q

What are the outcomes of septic shock?

A

Rapidly fatal
Hypoxia
Haemorrhage
Requires urgent intervention.