20/21: Pathology of the Endocrine Pancreas - Fang Flashcards
(42 cards)
“bronze diabetes”
hemochromatosis
due to hemosiderin deposition in pancreas
b-cell destruction leading to absolute insulin deficiency
type 1 DM
immune-mediated
idiopathic
insulin resistance with relative insulin deficiency
type 2 DM
MODY =
maturity onset diabetes of the young
genetic abnormalities which cause a primary defect in b-cell function
no obesity
no insulin resistance
no antibodies to gluatmic acid
MODY
-just a defect in b-cell function
normal blood glucose range
70-120
any one of four criteria for diabetes diagnosis :
- A1c greater of equal to 6.5%
- Fasting plasma glucose greater than 126 mg/dL
- 2h plasma glucose greater than 200 mg/dL during an oral glucose tolerance test
- random glucose greater than 200 in patient with symptoms
- in the absence of unequivocal hyperglycemia, criteria 1-3 should be confirmed
most common COD in pt with DM
MI
inflammation, degranulation of b-cells, and death of b-cells
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.
there is a _______ lack of insulin in type 2 DM
relative
normal levels of insulin re circulating but cells are not appropriately responding to the insulin
primary beta cell defect and peripheral tissue insulin resistance –> hyperglycemia —> _______ —> type 2 DM
beta cell exhaustion
insulin, abnormally packaged and secreted, accumulating outside beta cells
amylin (because resembles amyloid)
sign of type 2 DM
does early type 2 DM show insulinitis?
no insulinitis present
“glucose toxicity”
later stage of Type 2 DM
mild/moderate insulin deficency due to beta cell damage/exhaustion due to chronic hyperglycemia
amorphous “cracked plate glass”
histological type II DM
amylin
***_____________ is the MOST common underlying cause in the pathogenesis of complications in DM
non-enzymatic glycosylation of extracellular matrix
4 pathogenic effects of AGEs
- plasma prtns can bind to glycated BM
- can induce cross linking in type IV collagen in BM
- can trap LDL particles in artery walls
- can bind to receptors on numerous cell types
AGEs =
advanced glycation end-products
AGEs binding to cell receptors can cause (4)
- 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
AGEs play a role in damage of BM by (2)
- prtn accumulation thickening of BM
- trapping of LDL in artery wall, oxidation
most consistent morphologic feature of diabetes
diffuse thickening of BM
most evident in capillaries of retina and renal glomeruli
despite increase in thickness of BM, diabetic capillaries are _______ than normal to plasma prtns
more leaky
microangiopathy underlies the development of …
diabetic nephropathy
diabetic retinopathy
some forms of neuropathy
thick, narrow, and leaky SMALL blood vessels
diabetic microangiopathy- especially in kidneys and eyes
due to glycosylation
BM damage leak
AGE deposition
