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Endocrine Pharmacology > Pancreatic Islets > Flashcards

Pancreatic Islets Flashcards

15.6-15.8

1
Q

Lispro; Aspart; Glulisine - duration of action?

A

Ultra-short-acting synthetic insulin prep

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2
Q

Lispro; Aspart; Glulisine - MOA

A

Alteration of amino acid sequences that speed entry into circulation without affecting their interaction w/the insulin receptor –> decrease hexamer stability (monomer form is the active form); clear solutions w/ neutral pH; small amount of Zn for stability

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3
Q

Lispro; Aspart; Glulisine - How to Use

A

Reach peak concentration in blood quickly –> take right before a meal; permit control of postprandial glucose levels; emergency Tx of uncomplicated diabetic ketoacidosis

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4
Q

Regular (Crystalline) - AKA?

A

Humulin

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5
Q

Regular (Crystalline) - Duration of action

A

Short-acting (rapid) insulin prep; requires 1 hr before effect

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6
Q

Regular (Crystalline) - MOA; Tx

A

Regular insulin hexamer in clear solution w/ neutral pH; small amount of Zn for stability; emergencies or administered subcutaneously in ordinary maintenance regimens (alone or mixed w/intermediate or long-acting preparations)

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7
Q

NPH insulin (isophane) - Duration of action; stands for:

A

Intermediate-acting insulin prep; NPH = neutral protamine Hagedorn)

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8
Q

NPH insulin (isophane) - MOA

A

Combo of regular insulin and protamine; protamine is a highly basic protein used to reverse action of unfractionated heparin; protamine (insulin binding protein, IBP) combined w/ insulin in phosphate buffer –> IBP allows slower insulin release

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9
Q

NPH insulin (isophane) - How to Use

A

Often used as mixed injection w/ regular insulin (70% NPH, 30% regular insulin) –> allows both rapid and immediate effects

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10
Q

Glargine - Duration of action; Tx

A

Long (slow) acting insulin prep; provide a peakless basal insulin level lasting more than 20 h, which helps control basal glucose levels without producing hypoglycemia

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11
Q

Glargine - MOA

A

Amino acid substitutions allow increased hexamer stability w/ prolonged and predictable absorption from subcutaneous injection ; Clear solution w/ pH 4

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12
Q

Detemir - Duration of action; Tx

A

Long (slow) acting insulin prep; provide a peakless basal insulin level lasting more than 20 h, which helps control basal glucose levels without producing hypoglycemia

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13
Q

Detemir - MOA

A

Attachment of fatty acid to amino acid allows increased hexamer formation and increased albumin binding

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14
Q

Sulfonylureas - Class

A

Oral Type II Diabetes Agents

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15
Q

Sulfonylureas - MOA

A

Close ATP sensitive K+ channels to promote insulin release; may also directly promote exocytosis

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16
Q

Sulfonylureas - SE (2)

A

Hypoglycemia and weight gain w/ all

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17
Q

Sulfonylureas - 2nd generation (3)

A

Glyburide, glipizide, glimepiride

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18
Q

Meglitinides (2)

A

Repaglinide; Nateglinide (D-phenylalanine derivative)

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19
Q

Repaglinide; Nateglinide - Class/Tx

A

Oral type II DM agents; rapid onset and short duration of action so used just before a meal to control postprandial glucose levels

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20
Q

Repaglinide; Nateglinide - MOA

A

Close ATP sensitive K+ channels to promote insulin release w/o directly effecting exocytosis

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21
Q

Repaglinide; Nateglinide - Can be used for pts w/

A

sulfur allergies b/c these drugs lack sulfur

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22
Q

Repaglinide; Nateglinide - Compare duration of action

A

repaglinide > nateglinide

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23
Q

Metformin - Class/type/duration of action/Tx

A

Oral type II DM agent; Biguanide; 10-12 duration of action; reduces postprandial and fasting glucose levels; reduces endogenous insulin production thru enhanced insulin sensitivity (so good for those w/insulin resistance)

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24
Q

Metformin - MOA

A

Increases peripheral effects of insulin via increased AMP-stimulated protein kinase activation and decreases hepatic and renal glucose output (gluconeogenesis); stimulates glucose uptake and glycolysis in peripheral tissues, slows glucose absorption from GI tract, and reduces plasma glucagon levels; not a hypoglycemic and does not increase insulin release

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25
Q

Metformin - SE (2)

A

GI distress (nausea and diarrhea), lactic acidosis (esp. w/renal or liver disease, alcoholism or conditions that predispose to tissue anoxia and lactic acid production such as chronic cardiopulmonary dysfunction); no wt gain or hypoglycemia

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26
Q

Metformin - C/I (3)

A

Renal impairment, hepatic disease, history of lactic acidosis

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27
Q

Rosiglitazone; Pioglitazone - Class/type/Tx

A

Thiazolidinediones; oral type II DM agents; pioglitazone (15-24 duration of action); rosiglitazone (24 hours duration of action); reduce both fasting and postprandial hyperglycemia

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28
Q

Rosiglitazone; Pioglitazone - MOA

A

Binds to peroxisome proliferator-activated receptor-gamma nuclear receptor (PPAR - gamma receptor) to increase transcription of glucose transporters (GLUT4 in muscle and adipose tissue) –> increases effects of insulin (reduces insulin resistance); inhibits hepatic gluconeogenesis and have effects on lipid metabolism and distribution of body fat

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29
Q

Rosiglitazone; Pioglitazone - SE (2 for both, 1 for each, total of 4)

A

Both: fluid retention (presents as mild anemia and edema) => risk of heart failure; rosiglitazine: increased risk of MIs; pioglitazone: increased risk of bladder cancer; increased risk of bone fractures (females only)

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30
Q

Acarbose; Miglitol - Class/type

A

alpha-glucosidase inhibitors; oral type II DM agents; taken just before a meal

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31
Q

Acarbose; Miglitol - MOA

A

Alpha-glucosidase inhibitors-> decrease GI carbohydrate absorption (prevents conversion to monosaccharides so that they can be transported out GI lumen and into bloodstream); results in reduced postprandial hyperglycemia b/c of slowed absorption; have no effect on fasting blood sugar

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32
Q

Acarbose; Miglitol - SE (3)

A

Flatulence, diarrhea, abdominal pain resulting from increased fermentation of unabsorbed carb by bacteria in colon; hypoglycemia should be txed w/oral glucose (dextrose) and not sucrose b/c absorption of sucrose is delayed

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33
Q

GLP-1-Based agents (4)

A

Exenatide, liraglutide, sitagliptin and saxagliptin

34
Q

Sitagliptin - Type/Class

A

GLP-1 Based agent; Oral type II DM agent

35
Q

Sitagliptin - MOA and effects (4)

A

Inhibits dipeptidyl peptidase-4 (DPP-4) –> prevents degradation of incretins (hormones that increase insulin release such as GLP-1); increases glucose mediated insulin release, lowers glucagon levels, slows gastric emptying, and decreases appetite

36
Q

Sitagliptin - SE (3)

A

rhinitis, upper respiratory infections, allergic reactions, nasopharyngitis, headaches

37
Q

Exenatide (Exendin-4) - Class/Type/duration

A

Glucagon-like peptide 1 (GLP-1) Based agent; part of incretin family of peptide hormones (released from endocrine cells in epithelium of bowel in response to food and augment glucose-stimulated insulin release from pancreatic B cells); Type II DM agent; long acting

38
Q

Exenatide (Exendin-4) - MOA/effects (4) /how it’s given

A

Glucagon like peptide (GLP-1) analog –> increases glucagon dependent insulin secretion; increases glucose mediated insulin release, lowers glucagon levels, slows gastric emptying, and decreases appetite by producing feeling of satiety; given parenterally

39
Q

Exenatide (Exendin-4) - SE (5)

A

nausea (esp. during initial tx), headache, vomiting, mild weight loss, sometimes pancreatitis (serious and sometimes fatal); hypoglycemia (w/sulfonylurea)

40
Q

liraglutide

A

GLP-1 based agent

41
Q

saxagliptin

A

GLP-1 based agent

42
Q

Pramlintide - Class/type/tx/duration of action

A

Amylin analog (amylin is a hormone made by pancreatic B cells and activates high-affinity receptors that are a complex of calcitonin receptor and a receptor-activity modifying receptor [RANK]); type II DM agent; rapidly absorbed and short duration of action

43
Q

Pramlintide - MOA (4 effects)/How it’s given

A

Binds amylin receptor –> modulates postprandial glucose levels, suppresses glucagon release, delays gastric emptying, works in CNS to produce anorectic effects (decreases appetite); Given as preprandial subcutaneous injection with insulin to control postprandial glucose levels

44
Q

Pramlintide - SE (4)

A

nausea, anorexia, hypoglycemia, headache

45
Q

Bile Acid Binding Resin - Name of drug

A

Colesevelam

46
Q

Glucagon - Tx Use (4)

A

(1) Severe hypoglycemia (but requires intact hepatic glycogen stores) (2) endocrine diagnosis, (3) beta-blocker overdose (to reverse cardio effects), (4) bowel radiology (b/c it relaxes the intestine); Given parenterally

47
Q

Glucagon - MOA/Effects (3)

A

Hyperglycemic; Synthesized in pancreatic alpha-cells; Effects: hepatic glycogenolysis, gluconeogenesis, and ketogenesis (no effect on muscle glycogen); inotropic and chronotropic effects; intestinal smooth muscle relaxation

48
Q

Glucagon - SE

A

transient nausea/vomiting

49
Q

Diazoxide - MOA

A

Hyperglycemic; prevents closure of ATP regulated K+ channels to prevent insulin release; Opposite of sulfonylureas

50
Q

What are the 4 types of endocrine cells in the islets of Langerhans in the endocrine pancreas?

A

A (alpha, glucagon producing); B (beta, insulin and amylin producing); D (delta, somatostatin producing); F (pancreatic polypeptide producing)

51
Q

Which of the endocrine cell types are the most numerous in the endocrine pancreas?

A

B (insulin-producing cells)

52
Q

What is the most common pancreatic disease requiring Rx?

A

Diabetes mellitus (deficiency of insulin producing or effect)

53
Q

How is diabetes txed?

A

With several parenteral formulations of insulin and oral or parenteral noninsulin antidiabetic agents

54
Q

How do you tx severe hypoglycemia?

A

Glucagon (hormone that affects liver, cardio, and GI tract)

55
Q

What are 3 types of insulin?

A

rapid (short-acting); intermediate-acting; slow (long-acting)

56
Q

What are the 2 main types of rapid/short acting insulin?

A

Lispro and regular

57
Q

What are the 2 main types of intermediate acting insulin?

A

NPH and lente

58
Q

What is the main type of slow/long acting insulin?

A

Glargine

59
Q

What are the noninsulin antidiabetic drugs (6)?

A

(1) insulin secretagogues (glipizide); (2) biguanides (metformin); (3) alpha-glucosidase inhibitors (acarbose); (4) thiazolidinediones (pioglitazone); (5) amylin analogs (pramlintide); (6) incretin modulators (GLP-1 analog; DPP-4 inhibitor)

60
Q

When is the onset and cause of Type 1 DM?

A

Childhood; autoimmune destruction of pancreatic B cells

61
Q

What is the cause of Type 2 DM?

A

Progressive disorder due to increasing insulin resistance and diminishing insulin secretory capacity and often results in insulin deficiency

62
Q

What is hemoglobin A1C?

A

Glycosylated hemoglobin that serves as a marker of glycemia

63
Q

What does Type 1 DM require?

A

Tx w/insulin

64
Q

What does Type 2 DM require?

A

Early: noninsulin antidiabetic drugs; late: insulin added to regimen

65
Q

Major effect of insulin on liver

A

Increases storage of glucose as glycogen in the liver; involves insertion of additional GLUT2 glucose transport molecules in cell PMs; increased synthesis of the enzymes pyruvate kinase, phosphofructokinase, and glucokinase; and suppression of several other enzymes; decreases protein catabolism

66
Q

Major effect of insulin on skeletal muscle

A

Stimulates glycogen synthesis and protein synthesis; glucose transport into muscle cells is facilitated by insertion of GLUT4 transporters into cell PMs

67
Q

Major effect of insulin on adipose tissue

A

Facilitates triglyceride storage by activating plasma lipoprotein lipase, increasing glucose transport into cells via GLUT4 transporters and reducing intracellular lipolysis

68
Q

What is lactic acidosis?

A

Acidemia due to excess serum lactic acid; can result from excess production or decreased metabolism of lactic acid

69
Q

What is hypoglycemia?

A

Dangerously lowered serum [glucose]; a toxic effect of high [insulin] and the secretagogue class of oral antidiabetic drugs

70
Q

What is alpha-glucosidase?

A

An enzyme in the GI tract that converts complex starches and oligosaccharides to monosaccharides; inhibited by acarbose and miglitol

71
Q

What is common complication of insulin use?

A

Hypoglycemia, resulting from excessive insulin effect

72
Q

How to prevent brain damage from hypoglycemia?

A

(1) sugar/candy by mouth; glucose by vein or (2) glucagon (by IM injection)

73
Q

Who are most susceptible to effects of hypoglycemia?

A

Pts w/advanced renal disease; elderly; children younger than 7

74
Q

Most common form of insulin-induced immunologic complication?

A

Formation of antibodies to insulin or noninsulin protein contaminants, which results in resistance to action of the drug or allergic reactions (uncommon complication)`

75
Q

How do insulin secretagogues work?

A

Stimulate release of endogenous insulin by promoting closure of K channels in pancreatic B cell membrane. Channel closure depolarizes the cell and triggers insulin release; not effective in pts w/nonfunctional pancreatic B cells

76
Q

Which drugs can be used to prevent type 2 DM in prediabetic pts?

A

Metformin, thiazolidinediones, and alpha-glucosidase inhibitors

77
Q

Details about GLP-1 receptor

A

G protein-coupled receptor (GPCR) that increases AMP and also increases the free intracellular [Ca+2]

78
Q

What is Glucagon?

A

Protein hormone secreted by A cells of endocrine pancreases and acts thru G protein coupled receptors in heart, smooth muscle, and liver –> increases HR and force of contraction, increases hepatic glycogenolysis and gluconeogenesis, and relaxes smooth muscle (esp. in gut)

79
Q

Which drug is most likely to cause hypoglycemia when used as a monotherapy for type 1 DM?

A

Insulin secretagogues (e.g. sulfonylurea glyburide) can cause hypoglycemia as a result of increasing serum insulin levels; biguanides, thiazonlidinediones and alpha-glucosidase inhibitors are euglycemicas that are unlikely to cause hypoglycemia when used alone

80
Q

What is something extra special about glucagon?

A

Acts through cardiac glucagon R’s to stimulate the rate and force of contraction of heart. B/c this bypasses the cardiac beta adrenoceptors, glucagon is useful in the Tx of beta-blocker-induced cardiac depression

Endocrine Pharmacology (12 decks)

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