Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What percent of the world’s population has DM?

A

3%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percent of patients are unaware they have DM?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the normal range of BG level?

A

70-120 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main complications of DM?

A
  • MI
  • Renal failure
  • Cerebrovascular disease
  • HTN heart disease
  • Infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of death with DM?

A

MI or heart related issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

Yes–insulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the histological findings of insulitis? (2)

A

Infiltration of PMNs and degranulation/death of beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lobated WBCs = ?

A

PMNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Are the acinar cells affected with insulitis?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Beta cell damage 2/2 chronic hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to amylin in the pathogenesis of DM II?

A

ABnormally packaged and secreted, and accumulates outside beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does Amylin resemble in DM II (histologically)?

A

Amyloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Is there an HLA haplotype associated with DM II?

A

Nah

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

DM I = viral infection

DM II = obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Yes

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?

A

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?

A

10%

48
Q

True or false: amyloid is commonly found in insulinomas

A

True

49
Q

What is the prognosis for insulinomas?

A

Good

50
Q

What are gastrinomas?

A

Proliferation of G cells that secrete G cells, causes PUDs

51
Q

Where are gastrinomas usually found?

A

Duodenum

52
Q

Are gastrinomas usually single or multiple?

A

Single

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?

A

MEN 1

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?

A

Increases

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?

A

Increases

Endocrine (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions