EndoPancreas

Question 1

Exocrine function

Answer 1

Acini(gut)

Question 2

Endocrine function

Answer 2

Islets of Langerhans (neuroectoderm)

Question 3

Cell types/ hormones of isles

Answer 3

A (alpha) - glucagon
B (beta)- insulin
D (delta) - somatostatin
F - pancreatic polypeptide

Question 4

what is proinsulin

Answer 4

precursor of insulin, A-B-C chains. no bio activity until active form take off the C- peptide.

Question 5

Stimulants of insulin

Answer 5

Sugars: Glucose, mannose; Amino acids: leucine; Vagus nerve stimulation; Sulfonylureas

Question 6

Amplifiers of glucose-induced insulin release:

Answer 6

Enteric hormones: eg., gastrin, secretin & cholecystokinin);
Neural amplifiers: beta-adrenergic effect of catecholamines;
Amino acids: arginine

Question 7

Inhibitor of insulin release

Answer 7

Neural: alpha-adrenergic effect of catecholamines; Humoral: somatostatin (paracrine action)

Question 8

Glucose utilization

Answer 8

in muscles, amino acids,liver, adipose tissue and brain

Question 9

What does insulin promote (4 things)

Answer 9

Glucose uptake into cells
Glycogen synthesis
Lipid synthesis
Protein synthesis by increasing amino acid uptake
Thus, insulin is anabolic

Question 10

Glucagon

Answer 10

Produced by alpha cells of Islets of Langerhans
Potent releaser of glucose
Stimulatesgluconeogenesis (production of glucose from non-glucose sources) Stimulateslipolysis

Question 11

glucagon action in liver cells

Answer 11

turn off glycogen synthase. and breaks down glycogen

Question 12

carb breakdown in muscles

Answer 12

Glycogen breakdown to glucose in muscles is unaffected by glucagon, but glucocorticoids are effective. Lactate produced by muscle goes to liver to be converted to glucose.

Question 13

lipid metabolism

Answer 13

Glucagon (cortisol, adrenalin): increase lipolysis

increase glycerol utilization decrease triglyceride synthesis

Question 14

diabetes mellitus

Answer 14

A syndrome of disordered metabolism with inappropriate hyperglycemia due to:
A deficiency of insulin, or
A reduction in effectiveness of insulin, or Both

Question 15

type 1 DM

Answer 15

destruction of beta cells
10 -20%
little to no insulin

Question 16

type 2 DM

Answer 16

metabolic syndrome
80-90% 
early would have high insulin and later would have little amounts of insulin
obese - 85%
non-obese -15

Question 17

obese type 2

Answer 17

Insulin Resistance (reduce sensitivity to insulin (receptor and post-receptor defects)
Often with hyperplasia of beta cells Beta cells insensitive to glucose Hyperglycemia and hyperinsulemia

Question 18

non-obese type 2

Answer 18

strong genetic trait

often associated with mutations in insulin, insulin receptors and/or signal transduction molecules

Question 19

glucose toxicity due to chronic hyperglycaemia

Answer 19

Oxidative stress due to increase in oxygen radicals (O2-)

Alterations of protein glycosylation (glycation) and functions (e.g. glycated haemoglobin, HbA1c)

Question 20

chronic complications of DM

Answer 20

Opthalmologic complications:
diabetic retinopathy cataracts
Renal complications: diabetic nephropathy infections
Neurological problems:
diabetic neuropathy - sensory, motor, autonomic
Cardiovascular defects: cardiomyopathy
myocardial infarction

Question 21

primary treatment of diabetes M type 1

Answer 21

Type I: insulin, nature of dietary intake

Question 22

treatments for type 2

Answer 22

Type II: Nutritional therapy - weight loss (diet, exercise) Pharmacologic therapy -
Biguanides (e.g., Metformin, 1st choice for obese patients), hypoglycemic agents that inhibit gluconeogenesis
Sulfonylureas (SU) (e.g., Glyburide), insulin secretagogues
Other secretagogues (e.g., Repaglinide)
Thiazolidinediones (e.g., Rosiglitazone), increase sensitivity to insulin
Glucosidase inhibitors (e.g., Acarbose), inhibit digestion of complex carbohydrates, hence reduce sugar availability
Insulin
*Note: Combination therapy is often used