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
what is the mechanism of action of the biguanides
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
26
what is the most common biguanide
metformin
27
what are the clinical applications of metformin
type 2 DM; polycystic ovarian syndrome (off label)
28
what are the common side effects of metformin
lactic acidosis, diarrhea, dyspepsia, cobalamin deficiency, mild GI distress
29
what are the contraindications for metformin use
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
how does metformin effect serum lipids and weight
lowers serum lipids and decreases weight
31
what are the changes made to the amylin analogue pramlintide that makes it different from amylin
3 pralines replace an alanine and 2 serines of amylin
32
what are the clinical applications of pramlintide
type 1 AND 2 DM
33
what are the common adverse effects of pramlintide
nausea, promotes saiety
34
what are the contraindications for pramlintide use
hypoglycemia, gastroparesis
35
how is pramlintide administered
IV before meals
36
what is the mechanism of action of GLP1-analogues
act on GLP-1 to enhance glucose-dependent insulin secretion, inhibit glucagon secretion, delay gastric emptying, and decrease appetite
37
what is the mechanism of action of DDP4 inhibitors
prolong GLP-1 activity enhance glucose-dependent insulin secretion, inhibit glucagon secretion, delay gastric emptying, and decrease appetite
38
what are the GLP-1 analogues
exenatide and liraglutide
39
what are the adverse effects of exenatide and liraglutide
hypoglycemia, nausea, vomiting, headache
40
what are the contraindications for exenatide and liraglutide
Type 1 DM, diabetic ketoacidosis
41
how are exenatide and liraglutide administered
subcutaneous injection
42
what are exenatide and liraglutide typically used in combination with
metformin or a sulfonylurea
43
what are the DPP-4 inhibitors
sitagliptin, saxagliptin
44
what are common side effects of sitagliptin, saxagliptin
URI, nasopharyngitis, headache, mild increase in serum creatinine level
45
what are the contraindications of sitagliptin, saxagliptin
type 1 DM, diabetic ketoacidosis
46
what can happen when sitagliptin, saxagliptin are used in combination with sulfonylureas and insulin
may cause hypoglycemia
47
what is exenatide originally isolated from
salivary gland of the gila monster
48
what is the mechanism of action of Thiazolidinediones (TZDs)
bind and stimulate the PPARgamma, thereby increasing insulin sensitivity in adipose tissue, liver, and muscle
49
what are the TZDs
ploglitazone and rosiglitazone
50
what is the clinical application of ploglitazone and rosiglitazone
type 2 DM
51
what are the common adverse effects of ploglitazone and rosiglitazone
heart failure, cholesterol hepatitis, hepatotoxicity, diabetic macular edema, increased HDL and LDL, decreased circulating triglycerides and free fatty acids
52
what are the contraindications of ploglitazone and rosiglitazone
heart failure, MI
53
what drug is restricted to use in patients that did not respond to other anti-diabetic medications
rosglitazone
54
what is the mechanism of action of diazoxide
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
what is the clinical application of diazoxide
hypoglycemia due to hyperinsulinemia, malignant HTN (off-label)
56
what are the common adverse effects of diazoxide
fluid retention, bowel obstruction, pancreatitis, thrombocytopenia, extrapyramidal disease, angina, hirsutism
57
what are the clinical applications of exogenous glucagon
hypoglycemia (severe), intestinal relaxation before radiography of GI tract
58
what are the common adverse effects of exogenous glucagon
rash, nausea, vomiting
59
what is the major contraindication of exogenous glucagon
known pheochromocytoma
60
what does the hyperglycemia action of glucagon depend on
sufficient hepatic store of glycogen
61
what secretes leptin
adipocytes
62
what is the transcription factor that serves as the master regulator of adipose cell differentiation and plays an important role in lipid metabolism
PPARgamma
63
what results from PPARgamma activation
decreases serum free fatty acid levels and increases lipogenesis in adipose tissue
64
what is the target tissue of amylin
CNS
65
what is the target system of leptin
CNS (basomedial hypothalamus)
66
what does AMPK do in low energy states
triggers shift from anabolic to catabolic activities
67
how does glucose enter beta cells
via GLUT2
68
what tetramer forms the pore of the K+/ATP channel
Kir6.2