20/21: Pathology of the Endocrine Pancreas - Fang Flashcards

1
Q

“bronze diabetes”

A

hemochromatosis

due to hemosiderin deposition in pancreas

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2
Q

b-cell destruction leading to absolute insulin deficiency

A

type 1 DM

immune-mediated
idiopathic

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3
Q

insulin resistance with relative insulin deficiency

A

type 2 DM

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4
Q

MODY =

A

maturity onset diabetes of the young

genetic abnormalities which cause a primary defect in b-cell function

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5
Q

no obesity
no insulin resistance
no antibodies to gluatmic acid

A

MODY

-just a defect in b-cell function

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6
Q

normal blood glucose range

A

70-120

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7
Q

any one of four criteria for diabetes diagnosis :

A
  1. A1c greater of equal to 6.5%
  2. Fasting plasma glucose greater than 126 mg/dL
  3. 2h plasma glucose greater than 200 mg/dL during an oral glucose tolerance test
  4. random glucose greater than 200 in patient with symptoms
  • in the absence of unequivocal hyperglycemia, criteria 1-3 should be confirmed
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8
Q

most common COD in pt with DM

A

MI

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9
Q

inflammation, degranulation of b-cells, and death of b-cells

A

acute islitis
early change in type I DM

following this acute inflammation, there will eventually be a reduction in number and size of islets; thus loss of b-cells. later will be hyalinized.

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10
Q

there is a _______ lack of insulin in type 2 DM

A

relative

normal levels of insulin re circulating but cells are not appropriately responding to the insulin

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11
Q

primary beta cell defect and peripheral tissue insulin resistance –> hyperglycemia —> _______ —> type 2 DM

A

beta cell exhaustion

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12
Q

insulin, abnormally packaged and secreted, accumulating outside beta cells

A

amylin (because resembles amyloid)

sign of type 2 DM

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13
Q

does early type 2 DM show insulinitis?

A

no insulinitis present

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14
Q

“glucose toxicity”

A

later stage of Type 2 DM

mild/moderate insulin deficency due to beta cell damage/exhaustion due to chronic hyperglycemia

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15
Q

amorphous “cracked plate glass”

A

histological type II DM

amylin

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16
Q

***_____________ is the MOST common underlying cause in the pathogenesis of complications in DM

A

non-enzymatic glycosylation of extracellular matrix

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17
Q

4 pathogenic effects of AGEs

A
  1. plasma prtns can bind to glycated BM
  2. can induce cross linking in type IV collagen in BM
  3. can trap LDL particles in artery walls
  4. can bind to receptors on numerous cell types
18
Q

AGEs =

A

advanced glycation end-products

19
Q

AGEs binding to cell receptors can cause (4)

A
  • release of cytokines and growth factors from macrophages
  • increased endothelial permeability
  • increased endothelial procoagulant activity
  • increased extracellular matrix production by vascular smooth muscle cells as well as increased proliferation
20
Q

AGEs play a role in damage of BM by (2)

A
  • prtn accumulation thickening of BM

- trapping of LDL in artery wall, oxidation

21
Q

most consistent morphologic feature of diabetes

A

diffuse thickening of BM

most evident in capillaries of retina and renal glomeruli

22
Q

despite increase in thickness of BM, diabetic capillaries are _______ than normal to plasma prtns

A

more leaky

23
Q

microangiopathy underlies the development of …

A

diabetic nephropathy
diabetic retinopathy
some forms of neuropathy

24
Q

thick, narrow, and leaky SMALL blood vessels

A

diabetic microangiopathy- especially in kidneys and eyes

due to glycosylation
BM damage leak
AGE deposition

25
Q

how would you describe peripheral neuropathy caused by DM nerve damage?

A
symmetric , bilateral
progressive, irreversible
paraesthesia
pain
muscle atrophy
26
Q

damage to blood vessels in eyes is described as

A

exudative and proliferative retinopathy

27
Q

diabetic nephrosclerosis =

A

nodular kimmelstiel-wilson glomerulopathy

28
Q

gram negative bacilli –>

staphylocci –>

A

pyelonephritis

cortical infection

29
Q

what are some effects of visceral neuropathy?

A

CN - diplopia, bell palsy
GIT - constipation, diarrhea
CVS- orthostatic hypotension

30
Q

diabetic macroangiopathy =

A

accelerated atherosclerosis

due to nonenzymatic glycosylation of lipoprtns

31
Q

ischemia due to microangiopathy and atherosceleroiss serves as a stimulus for neovascular proliferation

A

diabetic retinopathy

32
Q

3 changes in retina with diabetic retinopathy

A

edema
hemorrhagic foci
neovascularization

33
Q

no insulinitis

yes amyoid

A

type 2 DM

34
Q

more concordance in twins

A

type 2 DM

35
Q

2 pancreatic neuroendocrine tumors NETs

A
  • insulinoma
  • zollinger-ellison syndrome
  • wermer syndrome
36
Q

hyperinsulinism NET

A

insulinoma

most common pancreatic NET

37
Q

hypergastrinemia NET

A

zollinger-ellison syndrome

38
Q

MEN1 syndrome NET

A

wermer syndrome

39
Q

**Whipple triad of hypoglycemia

A
  • blood glucose less than 45 mg/dL
  • CNS confusion/stupor
  • precipitated by fasting or exercise and relieved by food
40
Q

describe insulinomas

A
  • benign
  • solitary
  • small
  • encapsulated
  • “giant islets”
  • amyloid can be found
  • 10% carcinomas
41
Q

multiple peptic ulcerations in stomach, duodenum and even jejunum —>

A

suspect zollinger-ellison syndrome

result of elevated gastric acid secretion caused by a gastrinoma

42
Q

risks of zollinger-ellison syndrome

A
  • 1/2 metastasized at time of diagnosis

- 25% associated with other endocrine tumors (MEN1 syndrome)