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LECOM pharmacology notecards > chapter 30- pharm of endocrine pancreas & glucose homeostasis > Flashcards

chapter 30- pharm of endocrine pancreas & glucose homeostasis Flashcards

1
Q

what are the alpha-glucosidase inhibitors

A

acarbose, miglitol, voglibose

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2
Q

what is the clinical application of acarbose, miglitol, voglibose

A

type 2 DM

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3
Q

what are the common adverse effects of acarbose, miglitol, voglibose

A

abdominal pain, diarrhea, flatulence, elevated serum aminotransferase levels, elevated plasma triglycerides

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4
Q

what are the contraindications for acarbose, miglitol, voglibose

A

cirrhosis, diabetic ketoacidosis, severe digestive problems, IBD, bowel obstruction

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5
Q

who are acarbose, miglitol, voglibose most useful in

A

patients with predominant postprandial hyperglycemia and for new-onset hyperglycemia

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6
Q

what are the prandial bolus insulins

A

regular insulin, lisper, aspart, glulisine

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7
Q

what are the basal long-acting insulins

A

NPH, glargine, detemir

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8
Q

what basal insulin is a protamine

A

NPH insulin

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9
Q

what is the alteration of glargine from regular insulin

A

replaced asparagine A21 with glycine and added 2 arginines after B30

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10
Q

what is the alteration of determir from regular insulin

A

it is attached to the side chain of lysine B29

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11
Q

what are the common adverse effects of exogenous insulin

A

hypoglycemia, injection site reaction, lipodystrophy

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12
Q

what is the contraindication for exogenous insulin

A

hypoglycemia

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13
Q

how much time before a meal must regular insulin be administered

A

30 minutes

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14
Q

what is the intermediate acting exogenous insulin

A

NPH

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15
Q

what is the mechanism of action of sulfonylureas and meglitinides

A

inhibit the beta-cell K+/ATP channel in the SUR1 subunit, thereby stimulating insulin release from pancreatic beta cells & increasing circulating insulin to levels sufficient to overcome insulin resistance

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16
Q

what are the 1st generation sulfonylureas

A

acetohexamide, chlorpropamide, tolaxamide, tolbutamide

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17
Q

what are the 2nd generation sulfonylureas

A

glimepiride, glibepiride, glibenclamide, gliclazide, gliquidone

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18
Q

what are the adverse effects of sulfonylureas

A

hypoglycemia, rash, diarrhea, nausea, dizziness, marginal decrease in circulating lipids

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19
Q

what is the contraindication for sulfonylurea use

A

diabetic ketoacidosis

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20
Q

what metabolizes sulfonylureas

A

liver

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21
Q

how can sulfonylureas cause weight gain

A

secondary to increase insulin activity in adipose tissues

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22
Q

what are the meglitinides

A

nateglinide, repaglinide

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23
Q

what are common side effects of nateglinide, repaglinide

A

hypoglycemia, diarrhea, nausea, respiratory infection

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24
Q

what are the contraindications of nateglinide, repaglinide

A

diabetic ketoacidosis, type 1 DM

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25
Q

what is the mechanism of action of the biguanides

A

activates AMPK to block synthesis of fatty acids and to inhibit hepatic gluconeogenesis and glycogenolysis; increases insulin receptor activity & metabolic responsiveness in liver & skeletal muscle

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26
Q

what is the most common biguanide

A

metformin

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27
Q

what are the clinical applications of metformin

A

type 2 DM; polycystic ovarian syndrome (off label)

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28
Q

what are the common side effects of metformin

A

lactic acidosis, diarrhea, dyspepsia, cobalamin deficiency, mild GI distress

29
Q

what are the contraindications for metformin use

A

heart failure, septicemia, alcohol abuse, hepatic disease, respiratory disease, renal impairment, iodinated contrast media if acute alteration of renal function is suspected, as this may result in lactic acidosis, metabolic acidosis

30
Q

how does metformin effect serum lipids and weight

A

lowers serum lipids and decreases weight

31
Q

what are the changes made to the amylin analogue pramlintide that makes it different from amylin

A

3 pralines replace an alanine and 2 serines of amylin

32
Q

what are the clinical applications of pramlintide

A

type 1 AND 2 DM

33
Q

what are the common adverse effects of pramlintide

A

nausea, promotes saiety

34
Q

what are the contraindications for pramlintide use

A

hypoglycemia, gastroparesis

35
Q

how is pramlintide administered

A

IV before meals

36
Q

what is the mechanism of action of GLP1-analogues

A

act on GLP-1 to enhance glucose-dependent insulin secretion, inhibit glucagon secretion, delay gastric emptying, and decrease appetite

37
Q

what is the mechanism of action of DDP4 inhibitors

A

prolong GLP-1 activity enhance glucose-dependent insulin secretion, inhibit glucagon secretion, delay gastric emptying, and decrease appetite

38
Q

what are the GLP-1 analogues

A

exenatide and liraglutide

39
Q

what are the adverse effects of exenatide and liraglutide

A

hypoglycemia, nausea, vomiting, headache

40
Q

what are the contraindications for exenatide and liraglutide

A

Type 1 DM, diabetic ketoacidosis

41
Q

how are exenatide and liraglutide administered

A

subcutaneous injection

42
Q

what are exenatide and liraglutide typically used in combination with

A

metformin or a sulfonylurea

43
Q

what are the DPP-4 inhibitors

A

sitagliptin, saxagliptin

44
Q

what are common side effects of sitagliptin, saxagliptin

A

URI, nasopharyngitis, headache, mild increase in serum creatinine level

45
Q

what are the contraindications of sitagliptin, saxagliptin

A

type 1 DM, diabetic ketoacidosis

46
Q

what can happen when sitagliptin, saxagliptin are used in combination with sulfonylureas and insulin

A

may cause hypoglycemia

47
Q

what is exenatide originally isolated from

A

salivary gland of the gila monster

48
Q

what is the mechanism of action of Thiazolidinediones (TZDs)

A

bind and stimulate the PPARgamma, thereby increasing insulin sensitivity in adipose tissue, liver, and muscle

49
Q

what are the TZDs

A

ploglitazone and rosiglitazone

50
Q

what is the clinical application of ploglitazone and rosiglitazone

51
Q

what are the common adverse effects of ploglitazone and rosiglitazone

A

heart failure, cholesterol hepatitis, hepatotoxicity, diabetic macular edema, increased HDL and LDL, decreased circulating triglycerides and free fatty acids

52
Q

what are the contraindications of ploglitazone and rosiglitazone

A

heart failure, MI

53
Q

what drug is restricted to use in patients that did not respond to other anti-diabetic medications

A

rosglitazone

54
Q

what is the mechanism of action of diazoxide

A

binds to SUR1 subunit of K+/ATP channels in pancreatic beat cells and stabilizes the ATP-bound (open) state of the channel so that the beta cells remain hyper polarized

55
Q

what is the clinical application of diazoxide

A

hypoglycemia due to hyperinsulinemia, malignant HTN (off-label)

56
Q

what are the common adverse effects of diazoxide

A

fluid retention, bowel obstruction, pancreatitis, thrombocytopenia, extrapyramidal disease, angina, hirsutism

57
Q

what are the clinical applications of exogenous glucagon

A

hypoglycemia (severe), intestinal relaxation before radiography of GI tract

58
Q

what are the common adverse effects of exogenous glucagon

A

rash, nausea, vomiting

59
Q

what is the major contraindication of exogenous glucagon

A

known pheochromocytoma

60
Q

what does the hyperglycemia action of glucagon depend on

A

sufficient hepatic store of glycogen

61
Q

what secretes leptin

A

adipocytes

62
Q

what is the transcription factor that serves as the master regulator of adipose cell differentiation and plays an important role in lipid metabolism

63
Q

what results from PPARgamma activation

A

decreases serum free fatty acid levels and increases lipogenesis in adipose tissue

64
Q

what is the target tissue of amylin

65
Q

what is the target system of leptin

A

CNS (basomedial hypothalamus)

66
Q

what does AMPK do in low energy states

A

triggers shift from anabolic to catabolic activities

67
Q

how does glucose enter beta cells

68
Q

what tetramer forms the pore of the K+/ATP channel

LECOM pharmacology notecards (22 decks)

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