Pharm Final - Glucose

Front 1

(1) what is the composition of the pancreas? (2) what cells are in the pancrease?

Back 1

98% exocrine pancreas (acinar cells) & 2% endocrine pancreas (islets of langerhans)

Hint 1

alpha (a) cells, beta (B) cells, delta (D) cells, F (PP) cells, epsilon (E) cells

Front 2

a cells: (1) hormone (2) function

Back 2

glucagon

Hint 2

increase blood glucose levels, promotes glycogenolysis and gluconeogenesis

Front 3

B cells: (1) hormone (2) function

Back 3

insulin

Hint 3

decreases blood glucose levels, promotes glycogenesis and glycoloysis

Front 4

D cells: (1) hormone (2) function

Back 4

somatostatin

Hint 4

inhibits endocrine and exocrine pancreatic hormone secretions

Front 5

PP cells: (1) hormone (2) function

Back 5

pancreatic polypeptide

Hint 5

aids in self-regulation of pancreatic secretions, other function under investigation

Front 6

E cells: (1) hormone (2) function

Back 6

grehlin

Hint 6

stimulates appetite

Front 7

(1) where does insulin come from? (2) how are the products useful?

Back 7

synthesized by B cells from proinsulin > (carboxypeptidase) > insuling (51aa) + C-peptide (31aa)

Hint 7

insulins half life = 5min while C-peptide = 30min, so C-peptide can be measured (experimental)

Front 8

(1) how does insulin differ between species? (2) which are most similar?

Back 8

highly conserved between species with AA differences in <4 places

Hint 8

cat/cow, dog/pig/human

Front 9

(1) what induces insulin secretion? (2) what are GLUTs?

Back 9

in response to a rising blood glucose which enters pancratic B cells via facilitated diffusion

Hint 9

transporters with specific tissue distributions and response types

Front 10

(1) how is insulin prepared? (2) how is insulin secreted?

Back 10

packaged into secretory vesicles & cleaved by carboxypeptidase

Hint 10

glucose enters cell via GLUT-2 > glycolysis ? ATP > blocks K+ leak channels > AP > Ca++ into cell > releases insulin from vesicles

Front 11

(1) what occurs when insulin is in the blood stream? (2) what is this called?

Back 11

binds insulin receptor > tells GLUT-4 to go to plasma membrane to uptake glucose

Hint 11

insulin mediated glucose uptake

Front 12

(1) what are the actions of insulin on adipocytes? (2) liver?

Back 12

promotes uptake of glucose (GLUT-4) and synthesis of triglycerides

Hint 12

promotes glycolysis and glycogenesis

Front 13

(1) what are the actions of insulin on muslce? (2) what happens if you don't have enough insulin acting on cells?

Back 13

promotes uptake (GLUT-4), utilization and storage of glucose

Hint 13

diabetes

Front 14

What are the types of diabetes?

Back 14

insulin dependent diabetes mellitus (IDDM)

Hint 14

non-insulin dependent diabetes mellitus (NIDDM)

Front 15

IDDM: (1) cause (2) treatment

Back 15

absolue deficiency of insulin

Hint 15

requires exogenous insulin administration

Front 16

NIDDM: (1) cause (2) treatment

Back 16

relative deficiency or resistance to endogenous insulin

Hint 16

controlled via elimination of obesity, diet modification, oral hypoglycemic agents

Front 17

(1) what are the signs of diabetes mellitus? (2) what is diabetic ketoacidosis?

Back 17

polyuria (hyperglycermia leads to spillage of glucose in urine >> osmotic diuresis), polydypsia (loss of excess water via osmotic diuresis stimulates thirst), polyphagia and weight loss (inability to build up glycogen stoers or utilize blood glucose)

Hint 17

lack of insulin promotes lipolysis > end product of B-oxidation is ketone bodies (unmeasured organic anions build up in blood > nausea/malaise, acidemia), hyperglycemia = electrolyte/fluid imbalance; requires hospitalization & injectable insulin

Front 18

(1) what drugs are used to treat diabetes mellitus?

Back 18

injectable insulin, oral hypoglycemic agents, diet

Front 19

(1) how is insulin classified? (2) what are the indication for insulin Tx?

Back 19

duration of action (active hormone vs substances hindering absorption: short, intermediat, long), source (human recombinant, synthetic, beef, pork), concentration (40, 100, 500 U/ml; 1 U = 36ug of insulin)

Hint 19

diabetes mellitus (IDDM > always, NIDDM > sometimes due to glucose toxicity, DKA > always), ketosis and lipidosis in cattle, and hyperlipidemia in horses

Front 20

(1) describe short (rapid) acting insulin?

Back 20

R = regular insulin, most rapid onset (w/in 1/2h), shortest duration of action (up to 8h), only insulin that may be used IV

Hint 20

regular insulin

Front 21

(2) describe intermediate acting insulin?

Back 21

N = slightly delayed onset (0.5-3hrs), intermediate duration of action (4-24h, but peak at 4-6h, wane ~12h), typically administered SQ BID

Hint 21

NPH insulin (Humilin, Novolin) or Lente insulins (Novolin, Vetsulin)

Front 22

(1) describe long (slow) acting insulin? (2) brand names?

Back 22

slow onset of action (1-8hr, but peak around 6-12h), long duration of action (2-28h), once to twice daily SQ injections

Hint 22

Protamine Zinc Insulin (PZI), Glargine (Lantus), Detemir (Levemir)

Front 23

(1) what are adverse reactions to insulin? (2) what drug reactions occur with insulation?

Back 23

antibody formation (switch species, type, etc), hypoglycermia (overdose: roll bottle to mix, don't shake, syringe confusion)

Hint 23

antagonize insulin function or inhibit release (glucocorticoids, norepinephrine, dobutamine, thiazide diuretics, Ca channel blockers, progesterone, thyroid hormones, growth hormone) or enhance insulin function or promote release (anabolic steroid, alcohol, beta-blockers, salicylates, tetracyclines, oral hypoglycermics)

Front 24

what oral hypoglycemic agents do we use? (2) how does it work?

Back 24

sulfonylurease (glipizide/glyburide)

Hint 24

direct blockade of K+ channels leading to insulin release, decreased glucagon levels, improved tissue sensitivity to insulin

Front 25

(1) describe glipizide (glucotrol)? (2) describe Glyburide (diabeta, micronase)?

Back 25

readily absorbed from GIT, lasts 10-16h, treat NIDDM, adverse reactions include hepatotoxicity, hypoglycemia, anorexia, vomiting (low rate and reversible)

Hint 25

second generation sulfonylurea with a longer duration of action (~24 hours), administered once daily orally, well absorbed from GIT, use and adverse reactions similar to glipizide

Front 26

(1) describe biguanides (metformin, phenformin? (2) why use oral hypoglycemics?

Back 26

inhibit hepatic glucose release, improve peripheral insulin sensitivity, promote peripheral utilization of glucose, DOES NOT promote insulin release, adverse reaction of significant lactic acidosis in people

Hint 26

treatment of NIDDM; takes a minimum of 3-4 weeks, more effective in cats with moderate preprandial hyperglycermia (<200 mg/dl), can be used in combination with insulin

Front 27

(1) how is glucagon used? (2) what is glucagon used for therapeutically?

Back 27

synthesized by a cells of endocrine pancreas, maintains normal concentrations of glucose in blood (opposite of insulin), half life of 3-6min, secretion triggered by hypoglycemia, amino acids, exercise and inhiibted by hyperglycemia

Hint 27

adverse reaction treatment to insulin overdose, treatment of an insulinoma tumor

Front 28

(1) describe diazoxide?

Back 28

K channel opener, prevents depolarization (inhibit insulin release), expensive