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MD1 2016 - Abdominal > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Key Features of acute inflammation

A

edema
dilated vessels
infiltration by activated neutrophils (early) and macrophages (later

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2
Q

systemic effects of acute inflammation

A 
fever
neutrophilia
fatigue
Loss of appetite
increased acute phase proteins in blood
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3
Q

outcomes of acute inflammation

A

resolution
healing by fibrosis
abscess formation
chronic inflammation

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4
Q

important mediators in vasodilation

A

histamine
prostaglandins
NO

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5
Q

important mediators in increasing vascular permeability

A 
serotonin
histamine
C5a
C3a
leukotrienes
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6
Q

important mediators in leukocyte activation and chemotaxis

A

C5a
leukotriene B4
bacterial products/chemokines

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7
Q

What is inflammation?

A

universal response to tissue damage by harmful stimuli:
mechanical trauma
tissue necrosis
infection

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8
Q

What is the purpose of inflammation?

A

destroy (or contain) the damaging agent
initiate repair processes
return the damaged tissue to useful function

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9
Q

Define hyperemia

A

Relaxation of vascular smooth muscle leads to engorgement of tissue with blood in the first phase of acute inflammation

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10
Q

Which adhesion molecules are expressed by activated neutrophils to make contact with endothelial cells?

A

integrins and selectins

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11
Q

What is the regular lifespan of a mature neutrophil?

A

3 days

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12
Q

How do neutrophils kill bacteria and insulting agents before undergoing apoptosis?

A

Generate respiratory burst to produce hydrogen peroxide and other reactive oxygen species

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13
Q

How are dead neutrophils cleaned up?

A

by macrophages that arrive by 2nd/3rd day after injury

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14
Q

Which plasma proteins are involved in acute inflammation?

A

C5a
C3a
immunoglobulins
fibrinogen and fibrin

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15
Q

How long does acute inflammation last?

A

hours to days depending on the type and severity of the tissue damage

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16
Q

What is pavementing?

A

neutrophils lining up at the periphery of a vessel waiting to extravasate

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17
Q

What is the typical acute inflammatory exudate made of?

A

water
proteins (fibrin)
neutrophils

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18
Q

What are the mediators of increased vascular permeability?

A 
vasoactive amines
serotonin (5-hydroxytryptamine (5-HT)) 
histamine
C5a and C3a 
leukotrienes C4, D4, and E4
platelet activating factor (PAF).
19
Q

Describe Suppurative (purulent) inflammation

A

rich in neutrophil leukocytes

due to of infection by bacteria

20
Q

What is pus?

A

mixture of neutrophils (viable and dead), necrotic tissue, and tissue fluid in the acute inflammatory exudate

21
Q

What is an abscess?

A

a circumscribed collection of semi-liquid pus

22
Q

What is the cause of destruction of tissue in acute inflammation?

A

release of neutrophil lysosomal enzymes

destruction by bacteria

23
Q

What are pyogenic bacteria?

A

Bacteria which produce purulent inflammation

24
Q

What are examples of pyogenic bacteria?

A 
Staphylococci
Streptococcus pyogenes 
Streptococcus pneumoniae
E. Coli 
Neisseria meningitidis
Neisseria gonnorrhoeae
25
Q

What is contained in the exudate of fibrinous inflammation?

A

high plasma protein content (fibrinogen converted to fibrin)

26
Q

Where is fibrinous inflammation usually found?

A

membrane-lined cavities such as the pleura, pericardium and peritoneum, where the fibrin strands form a mat-like sheet causing adhesion between adjacent surfaces

27
Q

What is transudate?

A

fluid with a low plasma protein and cell content (transudate = specific gravity

28
Q

What is an exudate?

A

specific gravity >1.020 and protein content >25 g/L

29
Q

When is a transudate commonly seen?

A

in the skin in response to a burn

30
Q

What are the three big cytokines involved in acute inflammation (and mediates fever)?

A

interleukins 1 & 6, tumour necrosis factor (TNF) and prostaglandins

31
Q

What are the four end outcomes of acute inflammation?

A

resolution
healing by fibrosis/scar formation
abscess formation
chronic inflammation

32
Q

Describe resolution

A

complete restitution of normal tissue architecture and function that can only occur if the CT framework of the tissue is intact and the tissue involved has the capacity to replace any specialised cells that have been lost

33
Q

Describe healing by fibrosis

A

substantial damage to the CT framework and/or the tissue lacks the ability to regenerate specialised cells

defect becomes filled by ingrowth of a specialised vascular connective tissue called granulation tissue

34
Q

What is the two types of granulation tissue and what are their differences?

A

vascular granulation tissue - proliferating leaky capillaries, fibroblasts and inflammatory cells

fibrous granulation tissue - vessels regress, collagen laid down and is remodelled into orderly pattern to withstand tensile stresses
occurs for many weeks

35
Q

What is healing by primary intention?

A

wound edges are in close apposition and the actual defect is minimal, healing occurs quickly with a small amount of granulation tissue and is termed

36
Q

What is healing by secondary intention?

A

large tissue defect filled with blood clot and a variable amount of tissue debris. In this case, organization and filling of the defect by granulation tissue will take longer

37
Q

What is a feature of inactive fibrobalsts (after they have finished laying down collagen?)

A

small, condensed nuclei

38
Q

What does healing of the skin or mucous membrane require

A

epithelialization of the surface by proliferation of epithelium at the edges of the defect

39
Q

What bacteria will cause an abscess formation?

A

pyogenic bacteria

40
Q

What is liquefaction?

A

Liquefactive necrosis of the cells inside an abscess that is basically pus

41
Q

What is an abscess?

A

chronic inflammation surrounding acute inflammation (dead neutrophils and viable bacteria forming pus in the middle)

42
Q

Are the bacteria inside the abscess alive?

A

Yes

43
Q

What is a chronic abscess?

A

an abscess encapsulated by granulation and fibrous tissue

MD1 2016 - Abdominal (5 decks)

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