What Pancreatic Disease Am I?

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cells of the pancreas that secrete insulin

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beta cells (islets of langerhaans)

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cells of the pancreas that secrete glucagon

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alpha cells

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cells of the pancreas that contain somatostatin (suppress both glucagon and insulin release)

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delta cells

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chemical of the pancrease stored in PP cells that stimulates the secretion of gastric and intestinal enzymes and inhibits intestinal motility

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pancreatic polypeptide

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pancreatic cells that elaborate vasoactive intestinal polypeptide (induces glycogenolysis and hyperglycemia)

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D1 cells

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pancreatic cells that synthesize serotonin and are the source of pancreatic tumors that cause carcinoid syndrome

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enterochrommafin cells

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countries with the largest number of diabetics

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India, China, US (risk is higher in African American, Hispanic, and Native American communities)

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Oral glucose tolerance test greater than 140 but less than 200

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impaired glucose tolerance; greater risk for progressing to diabetes over time

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absolute deficiency of insulin caused by beta cell destruction

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diabetes Type I

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diabetes caused by combo of peripheral resistance to insulin action and an inadequate secretory response by pancreatic beta cells

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diabetes Type II

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response to fasting states

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low insulin and high glucagon

hepatic gluconeogenolysis and glucneogenesis

decreased glycogen synthesis

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following a meal

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insulin rises and glucagon falls

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principal metabolic function of insulin

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increase rate of glucose transport into certain cells in the body (striated muscle and adiopcytes)

stored as glycogen or oxidized to generate ATP

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Anabolic effects of insulin

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attributable to increased synthesis and reduced degradation glycogen, lipids, and proteins

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pathway responsible for the mitogenic effects of insulin

promotes cellular proliferation and growth

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MAPK

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pathway that mediates the metabolic effects of insulin

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PI-3K

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severe lack of insulin caused by an immunologically mediated destruction of beta cells

commonly develops in childhood

most patients are dependent on insulin for survival

autoimmune disease in which islet destruction is caused primarily against beta cells

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diabetes type I

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Action of CD4+ cells in DM1

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cause tissue injury by activating macrophages

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action of CD8+ cells in DM1

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directly kill beta cells and secrete cytokines that zctivate macrophages

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cytokines implicated in CD4+ /CD8+ cell injury of beta cells

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IFN-gamma, TNF, and IL-1

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decreased ability of peripheral tissues to respond to insulin

beta cell dysfunction manifested as inadequate insulin secretion in the face of insulin resistance and hyperglycemia

decreased uptake of glucose in muscle and adipose tissue and inability to suppress hepatic gluconeogenesis

associated with central obesity

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diabetes type II

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adipokines implicated in insulin resistance

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leptin, adiponectin, and resistin

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drug class that activates the PPAR-gamma receptor in adipocytes to modulate gene expression and reduce insulin resistance

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TZD's

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Insulin secretion starts high and is eventually overwhelmed by pathology

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insulin resistance (DM2)

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diabetes caused by either a primary defect in beta cell function or a defect in insulin/insulin receptor signalling

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monogenic forms

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primary defect in beta cell function occurs without beta cell loss; affects either beta cell mass or insulin production

autosomal inheritance as monogenic defect, onset before 25, absence of obesity, lack of islet cell autoantibodies and insulin resistance syndrome

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maturity onset diabetes of the young (MODY

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enzyme expressed in the pancreatic beta cells that controls influx of glucose by controlling its entry into glycolytic cycle-> coupled to insulin secretion

inactivating can raise the threshold for insulin release

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glucokinase

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genes associated with MODY

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glucokinase, IPF-1, transcription factors influencing expression in beta cells and beta cell mass

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diabetes associated with point mutation in tRNA

primary defect in beta cell function due to lack in ATP synthesis

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mitochondrial diabetes

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effects of macrovascular disease associated with DM

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accelerated atherosclerosis, MI, stroke, lower extremity gangrene

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effects of microvascular disease in DM

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profound in the kidney, retina, and peripheral nerves

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biproducts formed as result of nonenzymatic reactions between intracellular glucose-derived dicarbonyl precursors with amino group of intracellular and extracelluar proteins

Cause host of problems in diabetics

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advanced glycation end products (AGEs)

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Dramatic reduction in number/size of islets

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DM1

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leukocytic infiltration of islets; principally T lymphocytes

sometime eosinophilic infiltrate too

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DM1 at time of clinical presentation

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Beta cell degranulation; depletion of stored insulin in already damaged cells

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DM1

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Subtle reduction of islet cell mass

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DM2

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deposition of pink, amorphous material beginning in and around capillaries and between cells

fibrosis may be observed

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longstanding type 2 or elderly nondiabetics

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increase in number and size of islets

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nondiabetic newborns born to diabetic mothers

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halmark of diabetic macrovascular disease

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accelerated atherosclerosis of the aorta and large and medium sized arteries

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most common cause of death in diabetics

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MI caused by atherosclerosis of the coronary arteries

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vascular lesion associated with hypertension

more prevelent and severe in diabetics

amorphous hyaline thinkening of the wall of the arterioles

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hyaline arteriolosclerosis

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diffuse thickening of the basment membrane of blood vessels

most evident in capillaries of the skin, skeletal muscle, renal glomeruli, retina, adn renal medula

may also be seen in non vascular structures

concentric layers of hyaline material composed predominantly of type IV collagen

capillaries are still more leaky than normal to plasma proteins

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diabetic microangiopathy

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second only to MI as cause of death in this disease

lesion encountered are glomerular lesions, renal vascular lesions, and pylonephritis

capillary basement membrane thickening, diffuse mesangial sclereosis, and nodular glomeruloscerosis

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diabetic nephropathy

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diffuse increase in the mesangial matrix that is always assocated with basement membrane thickening

found in patient with 10+ years duration

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diffuse mesangial sclerosis

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proteinuria, hypoalbuminemia, and edema

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nephrotic syndrome

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ball-like deposits of laminated matrix situated in the periphery of the glomerulus

PAS positive and usually containing trapped mesangial cells

Pathognomic of diabetes once unusual nephropathies excluded

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nodular glomerularsclerosis/Kimmelstie-Wilson lesion

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acute or chronic inflammation of the kidneys that usually begins in the interstitial tissue and spreads to affect the tubules

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pyelonephritis

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deficiency of insulin results in catabolic state that affects glucose, fat, and protein metabolism

storage of glycogen in the liver adn muscle ceases and reserves are depleted by glycogneolysis

glycosuria induces an osmotic diuresis; osmoreceptors of thirst centers are triggered

catabolism of proteins and fat induce a negative energy balance causing increased appetitie

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diabetes mellitus

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lipoprotein lipase, with resultant excessive breakdown of adipose stores, and an increase in levels of FFA in blood

FFA reach liver and are esterified to fattyacyl CoA-> produces ketone bodies causing ketonemia and ketonuria

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metabolic ketoacidosis in DM

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attacks of hypoglycemia

attacks that consist principally of CNS manifestations such as stupor , confusion, and loss of conciousness

attacks are precipitated by fasting or exercise and promptly relieved by feeding or parenteral administration

most often found within the pancreas and generally benign

encapsulated brown nodules located anywhere in the pancreas

distinctive round granules that contain polyglonal or rectangular dense crystals separated from the enclosing membrane by a distinc halo

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insulinoma

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marked hypersecretion of gastrin due to a tumor in the duodenum, pancreas, or peripancreatic tissues

extreme gastric secretion causes peptic ulceration; often unresponsive to usual modalities of therapy

Ulcers may occur in unusual locations such as the jejunum

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Zollinger-Ellison Syndrome

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Increased levels of glucagon, mild diabetes mellitus, a characteristic skin rash, and anemia

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alpha cell tumors

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diabetes mellitus, cholelithiasis, steatorrhea, and hypochorhydria

high plasma somatostatin levels required for diagnosis

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delta cell tumors

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watery diarrhea, hypokalemia, achlorhydria

tumor may be locally invasive or metastatic

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VIPoma