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AASM > 3 - Peritoneal Pathologies > Flashcards

3 - Peritoneal Pathologies Flashcards

1
Q

What are the two types of peritoneum?

A

Parietal

Visceral

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2
Q

What is the name of a double-fold of peritoneum?

A

Mesentery

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3
Q

What 3 layers make up the peritoneum?

A

Mesothelium
Basement membrane
Submesothelial layer

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4
Q

From what tissue is the mesothelium derived from?

A

Mesoderm

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5
Q

What structure increases the SA of the mesothelium?

A

Microvilli

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6
Q

What is the peritoneum bathed in?

A

Peritoneal fluid

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7
Q

What are the 3 functions of the peritoneum?

A

1) Non-adhesive barrier (role of surfactant)
2) Solute / fluid transport
3) Immune function

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8
Q

How does the mesothelium provide an immune function?

A

Mesothelial cells can act as APC cells

Can also produce cytokines too.

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9
Q

What are 3 peritoneal pathologies ?

A

Adhesions

Endometriosis

Encapsulated peritoneal sclerosis (Long-term PD)

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10
Q

When do peritoneal adhesions form?

A

After peritoneal injury (surgery)

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11
Q

What are the 2 most common complications of adhesion formation?

A

1) Small bowel obstruction (most common cause)

2) Infertility in women (fallopian tube obstruction) - 1/3 of all cases

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12
Q

How much do adhesions cost the NHS?

A

£56 million a year

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13
Q

What are the only treatments currently to prevent adhesion formation?

A

Physical barriers to hold organs apart.

e.g. gels

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14
Q

What are 4 processes that occur for adhesions to form?

A

Inflammation
Blood vessel ingrowth
Collagen deposition
Contraction

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15
Q

What two differences seperate scar tissue from healthy tissue?

A

Scar tissue is:

1) Avascular
2) Acellular

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16
Q

What two findings resulted in the conclusion that adhesions were dissimilar to scar tissue?

A

Adhesions are well vascularised.

Adhesions contain nerves.

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17
Q

What stimuli were the nerves in adhesions capable of sensing?

What did they express?

A

Pain.

Substance P.

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18
Q

What 2 proteins are capable of cleaving plasminogen into plasmin?

A

uPA (plasminogen activator urokinase)

tPA

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19
Q

Which of the two cleavage proteins was shown to be the most important in adhesion formation?

A

tPA

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20
Q

What is the role of plasmin?

A

Breakdown of fibrin clots.

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21
Q

What is the half life of tPA?

A

30 seconds

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22
Q

What are the 3 functions of TGF-beta?

A

1) Wound healing
2) Tissue repair
3) Growth and development

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23
Q

How many types of TGF-Beta are there? What are they called?

A

3.

TGF-Beta 1/2/3

24
Q

What is TGF-beta’s effect on collagen production in wound healing process?

How does it do it?

A

Increases expression of PAI-1.

Increases collagen production.

25
Q

What two receptors does TGF-Beta signal through?

A

TGF-Beta Receptor I / II

26
Q

What is the modulatory regulator of TGF-beta function / expression?

A

Its own receptor.

27
Q

Of the 3 TGF-Betas, what is the function of 1 and 2 compared to TGF-B3 in THE SKIN?

A

TGF-B 1/2 = scar formation

TGF-B 3 = anti-scar formation

28
Q

What is the issue with placing medical therapy in the peritoneal cavity?

A

It does stay long enough!

Also need a transport vehicle.

29
Q

What are the effects of TGF-B 1/2/3 in the peritoneum?

A

Scar formation!!

30
Q

What is the omentum?

A

A fatty peritoneal fold.

31
Q

What is the name of the 2 omenta in the body?

A

Greater

Lesser

32
Q

What characteristic does the omentum have when there’s abdominal trauma?

A

Rapidly adheres to injured tissue.

33
Q

What reasons (2) does the omentum easily adhere to damaged areas?

A

High levels of:

  • Angiogenic factors
  • Neurogenic factors
34
Q

What was noticed on electron microscopy that may explain the omentum’s tendancy to stick to trauma / clots ?

A

Fenestrations which may function like a sponge - sucking up the clot.

35
Q

How many women does endometriosis affect in the UK?

A

1.5 million

36
Q

What symptoms occur in endometriosis?

A

Pain
Fatigue
Infertility

37
Q

What feature about menses can result in endometriosis?

A

Retrograde flow of menstrual effluent.

38
Q

Where endometriotic tissue bleeds, what can form?

A

Adhesion formation (due to presence of fibrin clot)

39
Q

Despite retrograde menstrual effluent occurring in ALL women, what 3 areas have been thought to potentially be linked to endometriosis occurring in some and not others?

A

1) Extended viability of endometrial tissue
2) Varied peritoneal attachment
3) Varied scope of invasion / growth

40
Q

What two options could extend viability of endometrial tissue ?

A

Reduced apoptosis

Abnormal immune response

41
Q

What 2 options may explain variance in ease of peritoneal attachment in endometriosis?

A

Peritoneal status

Altered ECM deposition

42
Q

Through GFP labelling, what was shown (Cross-talk) between implanted endometrial tissue onto peritoneum?

A

Cross-talk occurs.

Endometrial tissue:
1) Spreads across peritoneum

2) Grows deep into peritoneum

43
Q

What is the cause / biggest risk factor for developing encapsulating peritoneal sclerosis?

A

Duration of PD

44
Q

How do encapsulating peritoneal sclerosis patients present?

A

Malnutrition

Bowel obstruction

45
Q

What is the management for EPS?

A

Surgery

+ steroids

46
Q

What is the overall indication for dialysis?

A

End-stage renal disease

47
Q

What % of ESRD patients opt for PD and what % opt for haemodialysis?

A

85%

48
Q

What’s the progression of peritoneal fibrosis in PD Patients?

A

High glucose, low pH dialysate.

Creates glucose degradation products / advanced glycated products which damage peritoneum.

Constant injury / repair cycle, resulting in peritoneal fibrosis.

49
Q

What growth factor is known to be released in the pathogenesis of EPS?

A

TGF-B1

involved directly in collagen deposition / scarring

50
Q

What is the main cellular process that results in the thickening of the peritoneum, resulting in peritoneal dialysis?

A

Mesothelial-to-mesenchymal transition (MMT)

51
Q

What is the phenotype exchange that occurs in mesothelial-to-mesenchymal transition?

A

Epithelial –> mesenchymal.

52
Q

What characteristics do the epithelial phenotype of mesothelial cells (normal) include?

A

Lubricant secretion

Barrier function etc

53
Q

What is the pathophysiological changes that enable this phenotype change?

A

Loss of junctions / basement membranes..

Cells begin expressing mesenchymal markers.

Increase ECM deposition.

= fibrosis.

54
Q

What is one of the main stimulators of this transitional process?

A

TGF-Beta

55
Q

Developmentally, MMT is really important for the development of which structures?

A

Heart, lungs and gut vasculature.

56
Q

Adult MMT results in what?

A

Peritoneal thickening

Excessive matrix deposition

57
Q

Despite peritoneal sclerosis occurring following long-term PD. Why do only some people get encapsulating peritoneal sclerosis? What is the proposed hypothesis?

A

2-hit hypothesis:

1) First hit is the MMT process following peritoneal injury.
2) Calcium levels? Genetic predisposition?

AASM (8 decks)

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