Pancreas-Graffeo Flashcards
Complications
Nonenzymatic glycosylation
Glucose chemically attaches to amino group of proteins without enzymes
Directly related to level of glucose in blood
Type 1
Role of viruses
Release of sequestered ag
Or
Molecular mimicry: viral protein share sequences with beta cell (GAD shares sequences with coxsackie)
Nesidioblastosis
Cause
Islet cell hyperplasia
Type 2
Common presentation
May present with polyuria and polydipsia
Asymptomatic
Easier to control
Necrolytic migratory erythema ass with
Glucagonoma
DM
Chronic disorder of CHO, fat and protein metabolism
Common feature among all of groups: hyperglycemia
Insulinoma
Malignancy
90% benign
Can only determine malignancy if pt has invasion and mets
Form solitary aggregations of cell which look like giant islets
Ketoacidosis
Role of glucagon
Glucagon accelerates oxidation of free fatty acids
Ketones in blood and urine
D1 cells
Secrete
Vasoactive intestinal peptide
Type 1 vs type 2
Type 1
Onset <20
Normal wt
Dec blood insulin
Anti islet cell ab
Ketoacidosis common
Type 2
Insulin resistance
Reduced responsiveness of peripheral tissues to insulin
Seen in pregnancy and obesity
Type 1 vs type 2
Pathology
Type 2
Insulin resistance
Relative insulin deficiency
islet cells:
Focal atrophy and amyloid
Mild beta cell depletion
Genetic differences in type 1 vs 2
Type 1
30-70% concordance in twins
HLA-DR3 and/or DR4
Alpha cells
Glucagon
Induces hyperglycemia
Diabetic wound complications
Inc risk of infxn
Delayed healing
Monitor pts
Advanced glycosylation end products (AGE)
Form from glycosylation products which bind to long-live proteins
Inc deposition of LDLs on vessel wall
Lead to BM thickening in kidney
Laboratory DX
Criteria
Random glucose
> 200 mg/dl
Type 1
Islet cell abs
Role
Not causative
Marker of disease
Detected before clinical disease
Complications
Vascular system
Accelerated atherosclerosis in all vessels
MI: most common cause of death
Gangrene of vessels in lower extremities (causes morbidity)
Differential for hypoglycemia
Islet cell tumors
Insulin sensitivity
Liver disease
Xs production of glycogen
Ectopic production by certain sarcomas
Type 2
Role of obesity
80% of type 2 diabetics are obese
Abdominal obesity is highest ass
Weight loss and exercise can reverse
Type 1
Environmental factors
Viruses (coxsackie b)
Drugs
Chemical toxins
Type 1
Genetic susceptibility
Northern European descent
HLA-DR3 and/or DR4 (although most do not develop)
Alter recognition by T-cell receptor or ag presentation
Ass with DQ allele:: HLA-DQA1301-HLA-DQB10302
DM
Type 2
Non-insulin dependent
Previously adult onset (80-90% of cases)
Diabetic kidney problems
Nodular glomeruloneprhosclerosis
Characteristic kidney lesion
Peripheral glomerular nodules present (made of mucopolysaccharides)
Type 2
Deranged beta cell secretion
Changes with disease course
Insulin secretion normal early
No reduction in insulin levels
Mild insulin deficiency later
–chronic hyperglycemia may exhaust function of beta cells
D1 cells
Not in islets, but admixed with pancreatic exocrine cells
Free fatty acids metabolized by
Acetyl co-enzyme A in liver
DM
Type I
S&Sx
Polyuria and polydipsia mechanism
Dec insulin->glucose->polyuria (glucose, na, k, mg, po4-osmotic diuresis)->dec intracellular water-> trigger osmoreceptors of the thirst center in brain->
Polydipsia
Zollinger-Ellison Syndrome
Rx
H2 blockers-PPI
Resection of tumor
HBA1c
Glycosylated hemoglobin
Zollinger-Ellison Syndrome
Ulcer findings
Ulcers in 95% of pts
In unusual locations (like jejunum)
Type 2
Often older (>40) and frequently obese
Zollinger-Ellison Syndrome
When to consider
Pts with intractable jejunal ulcers
Also >50% of pts have diarrhea
Zollinger-Ellison Syndrome
Tumor characteristics
> 50% are malignant (may be multicentric)
Islet cell tumors
Functional
MC syndromes ass with functional tumors
Inc insulin
Inc gastrin
DM
Type I
S&Sx
Polyphagia mechanism
Dec insulin->catabolism of protein and fat->negative energy balance->polyphagia
Catabolic effects prevail leading to weight loss and mm weakness
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