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Endocrine > Pathology of the Pancreas > Flashcards

Pathology of the Pancreas Flashcards

1
Q

What is MODY? When does this occur?

A

Maturity-onset diabetes of the young d/t loss of function of the beta cells.

Usually occurs less than 25 yo

NO insulin resistance with this.

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2
Q

What percent of the world’s population has DM?

A

3%

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3
Q

What percent of patients are unaware they have DM?

A

50%

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4
Q

What is the inheritance pattern of primary beta cell defects with MODY? What does this cause?

A

AD

Total loss of beta cells function, but no insulin resistance, and no antibodies to glutamic acid decarboxylase

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5
Q

What causes gestational DM? Prognosis?

A

Child hormones increase the BG levels of the mother

Most of the time, mother does not have DM postpartum

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6
Q

What is the normal range of BG level?

A

70-120 mg/dL

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7
Q

What are the four criteria for diagnosing DM? (HbA1C, fasting BG, 2h test, random BG).

A
  1. HbA1C more than 6.5%
  2. Fasting plasma glucose over 126
  3. 2h plasma glucose greater than 200 during an oral glucose tolerance test
  4. Random glucose of more than 200
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8
Q

What should you do with an abnormal glucose level? What is the exception to this?

A

Test again to confirm

If lab result is abnormal with ssx, then no need to repeat

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9
Q

True or false: the risk factors for DM are the same, regardless of type, are the same

A

True

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10
Q

What are the main complications of DM?

A
  • MI
  • Renal failure
  • Cerebrovascular disease
  • HTN heart disease
  • Infections
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11
Q

What is the most common cause of death with DM?

A

MI or heart related issues

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12
Q

What is the pathogenesis in DM I?

A

MHC class II defect in HLA predisposes to dz, but set off by viral infection d/t molecular mimicry.

This causes an immune response against the normal (or altered) beta cells

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13
Q

Is there inflammation with beta cells in DM I pathogenesis? What is this called?

A

Yes–insulitis

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14
Q

What are the histological findings of insulitis? (2)

A

Infiltration of PMNs and degranulation/death of beta cells

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15
Q

Lobated WBCs = ?

A

PMNs

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16
Q

What are the histological findings of chronic insulitis? (cells, tissue changes)

A

Reduction in number/size of beta cells, with fibrosis, and lymphocyte infiltration

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17
Q

Are the acinar cells affected with insulitis?

A

No

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18
Q

What are the relative insulin levels early on in the pathogenesis of DM II? What about later on?

A

Normal at first, but there is a loss of the pulsatile pattern of insulin

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19
Q

What does the term “glucose toxicity” mean in the context of DM II?

A

Beta cell damage 2/2 chronic hyperglycemia

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20
Q

What happens to amylin in the pathogenesis of DM II?

A

ABnormally packaged and secreted, and accumulates outside beta cells

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21
Q

What does Amylin resemble in DM II (histologically)?

A

Amyloid

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22
Q

Is there an HLA haplotype associated with DM II?

A

Nah

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23
Q

What is the environmental factor that influences DM I? DM II?

A

DM I = viral infection

DM II = obesity

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24
Q

What is the first sign of DM II in terms of insulin secretion?

A

Loss of the pulsatile pattern and beta cell exhaustion

25
Q

What is the classic histological pattern associated with DM II?

A

“Cracked-plate glass”

26
Q

Will amyin show positive for congo red?

27
Q

What is the major pathogenesis of DM complications?

A

Non-enzymatic glycosylation of proteins

28
Q

What is the reaction that normally glycosylates proteins? Is this fast or slow? Reversible or not?

A

Schiff-base formation

Fast and reversible

29
Q

How stable are AGEs? Is this reversible?

A

Very–not reversible

30
Q

What is the effect of AGEs on BM?

A

Glycosylated proteins can bind to BM and induce cross-linking

31
Q

What is the effect of AGEs on LDL?

A

Traps in the arterial walls

32
Q

What happens to small vessels with DM? What does this cause?

A

Thickening of the BM d/t hyaline arteriolosclerosis

Causes increased permeability of the vessels

33
Q

Where is the arteriolosclerosis of DM most prominent?

A

Retinal and glomerular capillaries

34
Q

What three things does DM microangiopathy cause?

A

Nephropathy
Retinopathy
Neuropathy

35
Q

What are the histological findings of DM induced nephrosclerosis?

A

Kimmelstiel-Wilson glomerulopathy

36
Q

Is the polyneuropathy of DM usually unilateral or bilateral?

37
Q

What does trichrome stain highlight?

A

Collagen/fibrosis (turns blue)

38
Q

What causes the diabetic retinopathy?

A

Neovascularization and

hemorrhagic foci

39
Q

What causes the DM neuropathy?

A

AGE formation causes occlusion of the endoneurial, causing nerve hypoxia

40
Q

What causes the DM macroangiopathy?

A

Accelerated Atherosclerosis d/t increased stickiness of collagen with AGEs

41
Q

What is the concordance of DM I and II in identical twins?

A

DM I = 30-70%

DM II = 50-90%

42
Q

What are insulinomas?

A

Beta cell tumor

43
Q

What is the most common pancreatic NET?

A

Insulinoma

44
Q

What are the ssx of insulinomas?

A

Attacks of hypoglycemia with BG less than 45 mg/dL

45
Q

What are the components of Whipple’s triad?

A
  • Low BG
  • S/sx of low BG
  • Ssx relieved by eating
46
Q

What are the histological characteristics of insulinomas?

A

Usually benign, solitary mass within the pancreas, with uniform cells in nests

47
Q

What percent of insulinomas are carcinomas?

48
Q

True or false: amyloid is commonly found in insulinomas

49
Q

What is the prognosis for insulinomas?

50
Q

What are gastrinomas?

A

Proliferation of G cells that secrete G cells, causes PUDs

51
Q

Where are gastrinomas usually found?

52
Q

Are gastrinomas usually single or multiple?

53
Q

Are PUDs with zollinger-Ellison syndrome usually single or multiple?

A

Multiple, and in unusual locations

54
Q

What syndrome is associated with Zollinger-Ellison syndrome?

55
Q

True or false: periacinar inflammation is characteristic of DM I

A

False–beta cell inflammation only

56
Q

What is the effect of AGEs on macrophages?

A

Increases release of growth factors

57
Q

What is the effect of AGEs on endothelial procoagulant activity?

58
Q

What is the effect of AGEs on the ECM?

A

Increases its production, as well as smooth muscle proliferation

59
Q

What is the effect of AGEs on the permeability of capillaries?

Endocrine (32 decks)

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