Pathology of the Pancreas

Question 1

What is MODY? When does this occur?

Answer 1

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.

Question 2

What percent of the world’s population has DM?

Answer 2

3%

Question 3

What percent of patients are unaware they have DM?

Answer 3

50%

Question 4

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

Answer 4

AD

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

Question 5

What causes gestational DM? Prognosis?

Answer 5

Child hormones increase the BG levels of the mother

Most of the time, mother does not have DM postpartum

Question 6

What is the normal range of BG level?

Answer 6

70-120 mg/dL

Question 7

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

Answer 7

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

Question 8

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

Answer 8

Test again to confirm

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

Question 9

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

Answer 9

True

Question 10

What are the main complications of DM?

Answer 10

• MI
• Renal failure
• Cerebrovascular disease
• HTN heart disease
• Infections

Question 11

What is the most common cause of death with DM?

Answer 11

MI or heart related issues

Question 12

What is the pathogenesis in DM I?

Answer 12

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

Question 13

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

Answer 13

Yes–insulitis

Question 14

What are the histological findings of insulitis? (2)

Answer 14

Infiltration of PMNs and degranulation/death of beta cells

Question 15

Lobated WBCs = ?

Answer 15

PMNs

Question 16

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

Answer 16

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

Question 17

Are the acinar cells affected with insulitis?

Answer 17

No

Question 18

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

Answer 18

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

Question 19

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

Answer 19

Beta cell damage 2/2 chronic hyperglycemia

Question 20

What happens to amylin in the pathogenesis of DM II?

Answer 20

ABnormally packaged and secreted, and accumulates outside beta cells

Question 21

What does Amylin resemble in DM II (histologically)?

Answer 21

Amyloid

Question 22

Is there an HLA haplotype associated with DM II?

Answer 22

Nah

Question 23

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

Answer 23

DM I = viral infection

DM II = obesity

Question 24

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

Answer 24

Loss of the pulsatile pattern and beta cell exhaustion

Question 25

What is the classic histological pattern associated with DM II?

Answer 25

"Cracked-plate glass"

Question 26

Will amyin show positive for congo red?

Answer 26

Yes

Question 27

What is the major pathogenesis of DM complications?

Answer 27

Non-enzymatic glycosylation of proteins

Question 28

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

Answer 28

Schiff-base formation | Fast and reversible

Question 29

How stable are AGEs? Is this reversible?

Answer 29

Very--not reversible

Question 30

What is the effect of AGEs on BM?

Answer 30

Glycosylated proteins can bind to BM and induce cross-linking

Question 31

What is the effect of AGEs on LDL?

Answer 31

Traps in the arterial walls

Question 32

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

Answer 32

Thickening of the BM d/t hyaline arteriolosclerosis Causes increased permeability of the vessels

Question 33

Where is the arteriolosclerosis of DM most prominent?

Answer 33

Retinal and glomerular capillaries

Question 34

What three things does DM microangiopathy cause?

Answer 34

Nephropathy Retinopathy Neuropathy

Question 35

What are the histological findings of DM induced nephrosclerosis?

Answer 35

Kimmelstiel-Wilson glomerulopathy

Question 36

Is the polyneuropathy of DM usually unilateral or bilateral?

Answer 36

Bilateral

Question 37

What does trichrome stain highlight?

Answer 37

Collagen/fibrosis (turns blue)

Question 38

What causes the diabetic retinopathy?

Answer 38

Neovascularization and | hemorrhagic foci

Question 39

What causes the DM neuropathy?

Answer 39

AGE formation causes occlusion of the endoneurial, causing nerve hypoxia

Question 40

What causes the DM macroangiopathy?

Answer 40

Accelerated Atherosclerosis d/t increased stickiness of collagen with AGEs

Question 41

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

Answer 41

DM I = 30-70% | DM II = 50-90%

Question 42

What are insulinomas?

Answer 42

Beta cell tumor

Question 43

What is the most common pancreatic NET?

Answer 43

Insulinoma

Question 44

What are the ssx of insulinomas?

Answer 44

Attacks of hypoglycemia with BG less than 45 mg/dL

Question 45

What are the components of Whipple's triad?

Answer 45

- Low BG - S/sx of low BG - Ssx relieved by eating

Question 46

What are the histological characteristics of insulinomas?

Answer 46

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

Question 47

What percent of insulinomas are carcinomas?

Answer 47

10%

Question 48

True or false: amyloid is commonly found in insulinomas

Answer 48

True

Question 49

What is the prognosis for insulinomas?

Answer 49

Good

Question 50

What are gastrinomas?

Answer 50

Proliferation of G cells that secrete G cells, causes PUDs

Question 51

Where are gastrinomas usually found?

Answer 51

Duodenum

Question 52

Are gastrinomas usually single or multiple?

Answer 52

Single

Question 53

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

Answer 53

Multiple, and in unusual locations

Question 54

What syndrome is associated with Zollinger-Ellison syndrome?

Answer 54

MEN 1

Question 55

True or false: periacinar inflammation is characteristic of DM I

Answer 55

False--beta cell inflammation only

Question 56

What is the effect of AGEs on macrophages?

Answer 56

Increases release of growth factors

Question 57

What is the effect of AGEs on endothelial procoagulant activity?

Answer 57

Increases

Question 58

What is the effect of AGEs on the ECM?

Answer 58

Increases its production, as well as smooth muscle proliferation

Question 59

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

Answer 59

Increases