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PoD > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

1
Q

What is the suffix for inflammation and exception to it?

A

“-itis”

  • Pneumonia (lungs)
  • Pleurisy (pleural cavity)
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2
Q

What are neutrophils?

A

Mobile phagocyte which recognise and move to antigen (chemotaxis) and adhere to it

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3
Q

Mechanism of neutrophils

A

Release granule contents into phagosome (non-specific)

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4
Q

What do neutrophil granules contain?

A

Oxidants and digestive enzymes

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5
Q

Consequences of neutrophil action

A
  • Neutrophils die (digests itself)

- Suppuration - forms fluid of digested cells, organisms & endogenous proteins

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6
Q

What is the role of fibrinogen?

A

It’s coagulation factors - forms fibrin which clots the exudate and localises it by stopping inflammation from spreading

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7
Q

What are two important plasma proteins involved in acute inflammation?

A

Fibrinogen and immunoglobulins

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8
Q

What is the mechanism of immunoglobulins (antibodies)?

A
  • Neutralisation - prevent binding
  • Opsonisation - attract phagocyte
  • Complement activation
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9
Q

What are 3 mediators?

A
  • Molecules on endothelial cell surface membrane
  • Molecules released from cells
  • Molecules in the plasma
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10
Q

Effects of mediators

A
  • Vasodilatation
  • Increased permeability - leaky vessels
  • Neutrophil chemotaxis & adhesion
  • Itch and pain
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11
Q

What mediators cause neutrophils adhesions?

A

Cell surface adhesion molecules

  • ICAM-1 helps pavementing
  • P-selectin helps adhesion to antigen
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12
Q

What inflammatory mediator is released from mast cells and what activates its release?

A

Histamine - due to local injury; IgE mediated reaction (allergic)

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13
Q

What does histamine cause?

A

Vasodilatation and increased permeability - acts on H1 receptors on endothelial cells

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14
Q

What is 5-hydrocytryptamine and where is it produced?

A

Serotonin and produced in platelets

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15
Q

What activates serotonin’s released?

A

When platelets degranulate in coagulation

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16
Q

What does serotonin cause and why?

A

Vasoconstriction to prevent leakage from damaged vessel

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17
Q

What does antihistamine do?

A

Prevents the mast cells releasing histamine

18
Q

What are cytokines and chemokine?

A

Inflammatory mediators which are produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli

19
Q

What do cytokines and chemokine do?

A

Attract inflammatory cells - pro-inflammatory

20
Q

What are the immediate systemic effects of inflammation?

A
  • Pyrexia
  • Feeling unwell (malaise)
  • Neutophilia
21
Q

What is pyrexia?

A

Raised temperature

22
Q

What is neutrophilia?

A

Raised white cell count

23
Q

What are long term effects of acute inflammation?

A
  • Lymphadenopathy - lymph node enlargement
  • Weight loss
  • Anaemia
24
Q

What does pus contain?

A

Dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris

25
Q

What is suppuration?

A

Pus formation

26
Q

What surrounds pus?

A

Pyogenic membrane - helps localisation

27
Q

What is an abscess?

A

Collection of pus (suppuration) under pressure from ingrowth of granulation tissue and when it collapses it leads to healing and repair

28
Q

What forms multiloculated abscesses?

A

Pus bursts through pyogenic membrane and forms new cavities

29
Q

What is empyema?

A

Collection of pus in a hollow viscus

  • Gall bladder
  • Pleural cavity
30
Q

What is pyaemia?

A

Discharge of pus to bloodstream

31
Q

What is organisation?

A

Granulation tissue formation - fibrosis and formation os a scar

32
Q

What is granulation tissue?

A

Repair of damage

33
Q

What is granulation tissue formed of?

A
  • Angiogenesis
  • Fibroblasts and collagen
  • Macrophages
34
Q

What is dissemination?

A

Spread of substances to the blood stream - patient “septic”

35
Q

What are examples of dissemination?

A
  • Bacteraemia - bacteria in blood
  • Septicaemia - growth of bacteria in blood
  • Toxaemia - toxic products in blood
36
Q

What are the signs of early septic shock?

A
  • Peripheral vasodilatation
  • Tachycardia - high heart rate
  • Hypotension - low BP
  • Pyrexia (temp)
  • Skin rash
37
Q

Effects of systemic infection

A

Shock - inability to perfuse tissues

38
Q

Describe pathogenesis of septic shock?

A

Systemic release of chemical mediators from cells into plasma - catecholamine release

39
Q

What is the action of catecholamine?

A

Chemical mediators which cause vasodilatation, tachycardia

40
Q

Outcome of septic shock

A
  • Tissue hypoxia - cell death

- Haemorrhae - vessel abnormality

PoD (35 decks)

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