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PBL Spring 2015 - Block 2 > PHARM Chapter 30 - Endocrine Pancreas and Glucose Homeostasis > Flashcards

PHARM Chapter 30 - Endocrine Pancreas and Glucose Homeostasis Flashcards

1
Q

ME of
Acarbose
Miglitol
Voglibose

A

Alpha-Glucosidase Inhibitors - Carbohydrate analogues that bind avidly to intestinal brush border alpha-glucosidase enzymes - slowing breakdown and absorption of dietary carbohydrates (starch, dextrin, disaccharides)

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2
Q

Uses of
Acarbose
Miglitol
Voglibose

A

Type 2 diabetes mellitus

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3
Q

Continued use of alpha-glucosidase inhibitor associated with

A

diminishement of GI distress

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4
Q

Alpha-glucosidase inhibitors most useful for patients w

A

postrpandial hyperglycemia

new-onset patients w/ mild glycemia

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5
Q

Alpha-glucosidase ihibitors contraindicated in

A

Inflammatory bowel disease - delivery of undigested carbohydrates to distal bowel provides nutrients for colonic bacteria

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6
Q

ME of exogenous insulin

A

Classic anabolic hormone, promotes carbohydrate metabolism and facilitates glucose, amino acid, and triglyceride uptake and storage in liver, cardiac, and skeletal muscle, and adipose tissue

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7
Q

4 Prandial bolus exogenous insulins

A

Regular Insulin
Insulin lispro
Insulin aspart
Insulin glulisine

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8
Q

3 Basal “long-acting” exogenous insulins

A

NPH insulin
Insulin glargine
Insulin detemir

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9
Q

Uses of exogenous insulin

A

Diabetes mellitus

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10
Q

How are exogenous insulins delivered

A

parenternally, subcutanous is most commpon

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11
Q

Intermediate acting insulin that contains protamine which prolongs the time required for absorbtion

A

NPH insulin

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12
Q

Prandial bolus insulins

A

act rapidly, used to mimic B-cell release of insulin in response to nutreitn load

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13
Q

How is regular insulin stabilized for use and how long is it’s time of onset?

A

addition of zinc ions

30 minutes

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14
Q

NPH Insulin is formed how?

A

regular insulin suspended with zinc and protamine (arginine rich protien isolated from fish sperm) - peak activity occurs between 4-10 hours after administration, associated w/ increased hypoglycemia

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15
Q

Major SE of insulin therapy

A

in absence of carbs can result in hypoglycemia

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16
Q

What are the mainstay treatment for type 2 diabetics

A

sulfonylureas

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17
Q

4 first-generation sulfonylureas

A

acetohexamide
chlorpropamide
tolazamide
tolbutamide

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18
Q

5 second-generation sulfonylureas

A 
glimepiride
glipizide
glibenclamide (glyburide)
glicclazide
gliquidone
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19
Q

ME of Sulfonylureas

A

inhibit B-cell K/ATP channel at SUR1 subunit - stimulates insulin release form pancreatic B cells and increase circulating insulin to lvels sufficient to overcome insulin resistance

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20
Q

Major adverse effect of SUlfonylureas

A

hypoglycemia from oversecretion of insulin

can cause weight gain secodnary to increased insulin activity in adipose tissue (better for nonobese)

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21
Q

Differences between first and second generation sulfonylureas in dosing

A

first generation bind w/ lower affinity to SUR1 so they must be administered at higher doses

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22
Q

ME of meglitinides

A

Inhibit B-cell K/ATP channel at SUR1 subunit - stimulate insulin release from pancreatic B-cells and increase circulating insulin to levels sufficient to overcome insulin resistance

23
Q

2 meglitidines

A

Nateglinide

Repaglinide

24
Q

Sulfonylureas may displace endogenous ___ which binds to SUR1 to activate the channel

A

MG-ADP

25
Q

How are sulfonylureas delivered

A

orally

26
Q

ME of metformin

A

activates AMP-dependent protein kinase to block synthesis of fatty acids and to inhibit hepatic gluconeogenesis and glycogenolysis - increases insulin receptor activity and metabolic responsiveness in liver and skeletal muscle

27
Q

Uses of Metformin

A

type 2 diabetes mellitus

polycystic ovarian syndrome

28
Q

SE of metformin

A

lactic acidosis, GI distress

29
Q

Biguanides (metformin) have what additional benefit?

A

lowering of serum lipids, decrease in weight

30
Q

Why do Biguanides (metformin) cause lactic acidosis

A

decrease flux of metabolic acids through gluconeogenic pathways

31
Q

ME of pramlintide

A

Co-released w/ insulin from B-cell acts on receptors in CNS to slow gastric emptying - reduces postrpandial glucagon and glucose release - promotes satiety (amylin analogue)

32
Q

Uses of pramlintide

A

Type 1 and Type 2 diabetes

33
Q

Why can both type 1 and 2 diabetics benefit from pramlintide

A

type 1 lack endogenous amylin

type 2 deficient in amylin

34
Q

Added bonus of pramlintide

A

modest weight loss

35
Q

SE of pramlintide

A

nausea

36
Q

ME of GLP-1 analogues
Exenatide
Liraglutide

A

Act on GLP1 receptor to enhance glucose-dependent insulin secretion, inhibits glucagon secretion, delays gastric emptying and decreases appetite

37
Q

ME of DDP-4 inhibitors
Sitagliptin
Saxagliptin

A

Prolongs GLP-1 activity to enhance glucose-dependent insulin secretion, inhbits glucagon secretion, delays gastric emptying and decreases appetite

38
Q

Uses of Exenatide
liraglutidde
sitagliptin
saxagliptin

A

Type 2 diabetes mellitus

39
Q

SE of exenatide
liraglutide
sitagliptin
saxagliptin

A

hypoglycemia

40
Q

most common sideeffect of exenatide and liraglutide

A

nausea - acute pancreatitis is possible

41
Q

2 Thiazolidinediones

A

Pioglitazone

Rosiglitazone

42
Q

ME of pioglitazone and rosiglitazone

A

bind and stimulate the nuclear hormone receptor peroxisome proliferator-activated receptor-gamma (PPARy), increases insulin sensitivty in adipose tissue, liver, muscle

43
Q

Uses of pioglitazone, rosiglitazone

A

type 2 diabetes mellitus

44
Q

Why do TZDs not induce hypogycemia

A

do not increase insulin levels

45
Q

What main role do TZDs play in treatment

A

sensitizers - enhance action of insulin at target tissues

46
Q

SE of rosiglitazone

A

MI, heart failure, weight gain, edema, bone fractures

47
Q

ME of diazoxide

A

Binds to SUR1 subunit of K/ATP channels in pancreatic B-cells and stabilizes ATP-bound (open) state of the channel so that B-cells remain hyperpolarized - decreases insulin secretion by cells

48
Q

Uses of diazoxide

A

Hypoglycemia due to hyperinsulinism

malignant hypertension

49
Q

By what mechanism is diazoxide used off label to treat elevated BP in hypertensive emergencies

A

hyperpolarizes SUR2 channels in cardiac and smooth muscle cells

50
Q

Why is oral combination therapy beneficial

A

drugs have different MEs so lower doses can be used to have glycemic control

51
Q

octreotide is a ___ analogue

A

somatostatin - blocks hormone release

52
Q

What is used to treat severe hypoglycemia

A

glucagon via subcutaneous injection

53
Q

What other purposes is glucagon used for

A

intestinal relaxant before radiographic or MRI

PBL Spring 2015 - Block 2 (11 decks)

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