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POD > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

1
Q

What is inflammation in the lungs called?

A

pneumonia

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2
Q

What is inflammation in the pleural cavity called?

A

pleurisy

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3
Q

What do neutrophils do?

A

-Recognise a foreign antigen, move towards it and adhere to organism.
-Granules possess oxidants (H2O2) and enzymes (proteases)
Release granule contents
-Phagocytose and destroy foreign antigen

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4
Q

What are the consequences of neutrophil action?

A
  • Neutrophils die when granule contents released
  • Produce pus filled with bits of cell, organisms and endogenous proteins
  • Inflammation might progress if extension into other tissues
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5
Q

What is the role of plasma proteins in inflammation?

A
  • Fibrinogen is a coagulation factor which forms fibrin and clots exudate. This localises the inflammatory process
  • Immunoglobulins provide a humoural immune response, plasma specific for antigen
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6
Q

What are mediators of acute inflammtion

A
  • molecules on endothelial cell surface membrane
  • molecules released from cells
  • molecules in the plasma
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7
Q

What are the collective effects of mediators?

A
  • vasodilation
  • increased permeability
  • neutrophil adhesion
  • chemotaxis
  • itch and pain
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8
Q

What does ICAM-1 do?

A

Helps neutrophils to stick

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9
Q

What does P-selectin do?

A

Interacts with neutrophil surface

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10
Q

What molecules are released from cells?

A
  • histamine
  • 5-hydroxytryptamine (serotonin)
  • prostaglandins (arachidonic acid metabolites via lipoxygenase pathway)
  • leukotrienes (arachidonic acid metabolites via cyclo-oygenase pathway)
  • omega-3 polyunsaturated fatty acids
  • platelets activating factor
  • cytokines and chemokines
  • nitric oxide
  • oxygen free radicals
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11
Q

Histamine

A
  • It is preformed in mast cells beside vessels, platelets, basophils]
  • It is released as a result of local injury: IgE mediated reactions
  • Causes vasodilation and increased permeability
  • Acts via H1 receptors on endothelial cells
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12
Q

Serotonin

A

-Preformed in the platelet
Released when platelets degranulate in coagulation
-Cause vasoconstriction

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13
Q

Prostaglandins

A
  • Released by many cells (endothelium and leukocytes).
  • Many promote histamine effects and inhibit inflammatory cells.
  • Thromboxane A2 promotes platelet aggregation and vasoconstriction- the opposite effect to PGD2, PGE2 etc.. -Latter: effectiveness of non-steroidal anti-inflammatory drugs.
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14
Q

Leukotrines

A
  • Released by neutrophils especially

- Vasoactive-dynamic effort on vessels to increase permeability and constrict smooth muscle

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15
Q

Omega-3 polyunsaturated fatty acids

A

Decrease synthesis of arachidonic acid derived inflammatory response?

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16
Q

What is platelet activating factor?

A
  • Produced by cell membranes of activated inflammatory cells

- Reduces permeability by enhancing platelet degranulation at site of injury

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17
Q

Cytokines and Chemokines

A
  • small molecules produced by macrophages, lymphocytes and endothelium in response to inflammatory stimuli
  • they attract inflammatory cells
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18
Q

Nitric Oxide

A
  • Released by various cells

- Cause relaxation of smooth muscle, anti platelet, regulate leukocyte recruitment to inflammatory response

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19
Q

Oxygen Free Radicals

A
  • Released by neutrophils on phagocytosis

- They amplify other mediator effects

20
Q

What are the 4 enzymes cascades that take place in the plasma?

A
  • blood coagulation pathways
  • fibrinolysis
  • kinin system
  • complement cascade
21
Q

Blood Coagulation Pathways

A
  • clots fibrinogen in the exudate

- interacts widely with other systems

22
Q

Fibrinolysis

A
  • breaks down fibrin to help maintain blood supply

- products of fibrin breakdown are vasoactive

23
Q

Kinin System

A

Bradykinin responsible for pain

24
Q

Complement Cascade

A
  • Ties inflammation with the immune system

- Active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown

25
Q

What are the immediate systemic effects of inflammation?

A
  • pyrexia
  • feeling unwell including malaise, anorexia, nausea, abdominal pain and vomiting
  • neutrophilia- released by bone marrow
26
Q

What are the longer term effects of acute inflammation?

A
  • lymphadenopathy
  • weight loss
  • anaemia
27
Q

What are the outcomes of acute inflammation?

A
  • resolution
  • suppuration
  • organisation
  • dissemination
  • chronic inflammation
28
Q

What is suppuration?

A
  • Formation of pus

- Pyogenic membrane surrounds pus and walls it off

29
Q

What is an abscess?

A
  • A collection of pus under pressure
  • Can be single locule or multi-loculated
  • It points and discharges before collapsing and healing
30
Q

How are multiloculated abscesses formed?

A

Pus bursts through pyogenic membrane and forms new cavities

31
Q

What is an empyema?

A

Pus in a hollow viscous such as the gall bladder or the pleural cavity

32
Q

What is pyaemia?

A

When pus is discharged into the bloodstream

33
Q

What is organisation?

A

Organisation is healing and repair. Characterised by granulation tissue and leads to fibrosis and formation of a scar.

34
Q

What is granulation tissue?

A

It is a universal patch formed of new capillaries, fibroblasts, collagen and macrophages.

35
Q

What is dissemination?

A

-Spread to the bloodstream which results in patients becoming septic

36
Q

Bacteraemia

A

bacteria in the blood

37
Q

septicaemia

A

growth of bacteria in blood

38
Q

toxaemia

A

toxic products in blood

39
Q

What are the effects of systemic infection?

A
  • shock=inability to perfuse tissues

- early septic shock

40
Q

What are the symptoms of early septic shock?

A
  • peripheral vasodilation
  • tachycardia
  • hypotension
  • pyrexia
  • sometime haemorrhagic skin rash
41
Q

What is the pathogenesis of septic shock?

A
  • There is a systemic release of chemical mediators from cells into plasma
  • Mediators cause vasodilation causing loss of systemic vascular resistance
  • Results in catecholamine release
  • Tachycardia follow to maintain CO because increased heart rate compensates CO=SV x HR
  • bacterial endotoxin released
  • activation of coagulation
42
Q

What does interleukin-1 do?

A

When released it acts on the hypothalamus and causes pyrexia

43
Q

How does the activation of coagulation result in a haemorrhagic skin rash?

A
  • Disseminated intravascular coagulation
  • Vasoactive chemical causes vasodilation
  • Results in haemorrhagic skin rash
44
Q

What happens when a raised HR is insufficient to maintain cardiac output?

A
  • SVR is low so BP falls.
  • There is reduced perfusion of tissues which results in tissue hypoxia and leads to loss of cell tissue and organ function
45
Q

What are the outcomes of septic shock?

A
  • proves rapidly fatal
  • tissue hypoxia -cell death
  • haemorrhage
  • requires urgent intervention and support- admittance to ICU

POD (54 decks)

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