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Endo > SM_187b: Diabetes Pharmacology > Flashcards

SM_187b: Diabetes Pharmacology Flashcards

1
Q

Diabetes is a group of metabolic disorders resulting in ___

A

Diabetes is a group of metabolic disorders resulting in hyperglycemia

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2
Q

Prolonged hyperglycemia in diabetes results in ____, ____, ____, and ____

A

Prolonged hyperglycemia in diabetes results in cardiovascular disease, nephropathy, retinopathy, and neuropathy

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3
Q

____ is the key to alleviated symptoms and improving outcomes in diabetes mellitus

A

Control of blood glucose is the key to alleviated symptoms and improving outcomes in diabetes mellitus

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4
Q

Proinsulin is converted to insulin via ____

A

Proinsulin is converted to insulin via cleavage of C peptide

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5
Q

___ is the primary stimulus for insulin secretion

A

Rise in blood glucose is the primary stimulus for insulin secretion

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6
Q

Insulin receptor is a ____

A

Insulin receptor is a receptor tyrosine kinase

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7
Q

Describe the mechanism of action of the insulin receptor

A

Insulin receptor mechanism of action

  1. Insulin binds to insulin receptor
  2. Tyrosine phosphorylation of substrates activates downstream signaling
  3. Activation of PI3K-AKT pathway -> increased glycogen synthase, translocation of glucose transporters to membrane
  4. Signalging through RAS-MAPK pathway results in proliferation
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8
Q

T1DM is when ___ and there is an ___

A

T1DM is when insulin is lacking and there is an absolute requirement for insulin replacement

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9
Q

T2DM is when ____ due to ____

A

T2DM is when insulin is insufficient due to inadequate secretion or target tissue resistance

(other treatments may be able to stimulate the secretion of sufficient insulin)

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10
Q

Insulin needs vary throughout the day, mainly due to ___

A

Insulin needs vary throughout the day, mainly due to blood glucose increases after meals

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11
Q

____, ____, ____, and ____ are short-acting insulins

A

Regular insulin, lispro, aspart, and glulisine are short-acting insulins

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12
Q

Lispro, aspart, and glulisine insulins have ____ onset than regular insulin because they aggregate less

A

Lispro, aspart, and glulisine insulins have faster onset than regular insulin because they aggregate less

  • Taken just before meal, activity lasts for period of meal digestion
  • Aspart and glulisine insulins are used as pumps for continuous subcutaneous insulin infusion
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13
Q

____, ____, and ____ are longer acting insulins

  • NPH insulin: protamine slows absorption
  • Glargine: aggregation results in slower absorption, peakless
  • Detemir: aggregates and binds to albumin, peakless
A

NPH insulin, glargine, and detemir are longer acting insulins

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14
Q

Basal / bolus insulin regimen involves ____

A

Basal / bolus insulin regimen involves glargine or detemir before breakfast or at bedtime, with preprandial injections of short acting insulin

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15
Q

Split-mixed insulin regimen involves ____

A

Split-mixed insulin regimen involves pre-breakfast and pre-supper injection of a mixture of short- and long-acting insulins

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16
Q

Insulin pump is used for ____ to provide ____ with ____

A

Insulin pump is used for continuous subcutaneous insulin infusion to provide a continuous basal rate with mealtime bolus injections based on size and nature of meals

  • Complications: abscesses, cellulitis, pump failures
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17
Q

Describe limitations to and alternatives for insulin administration methods

A

Limitations to and alternatives for insulin administration methods

  • Limitations: amount / type of food influence insulin requirement, r egional blood flow affected by exercise / temperature / smoking, and counterregulatory hormones / injury / infection / other drugs affect insulin requirement
  • Islet cell autotransplantation: infusion of own pancreatic islet cells into portal vein in liver
  • Generation of induced pluripotent stem cell derived beta cells for autologous replacement therapy
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18
Q

____ and ____ are major side effects of insulin

A

Hypoglycemia and weight gain are major side effects of insulin

  • Risk higher in kids
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19
Q

Treatment of insulin-induced hypoglycemia is ____

A

Treatment of insulin-induced hypoglycemia is glucose

  • Glucagon: acts through GPCR and cAMP, increases hepatic glucose production
  • Diazoxide (thiazide): no diuretics, interacts with beta cell K channel, decreases insulin secretion
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20
Q

Describe mechanisms of therapeutic effects of agents for type 2 diabetes

A

Mechanisms of therapeutic effects of agents for type 2 diabetes

  • Increase insulin secretion
  • Affect glucose metabolism directly
  • Promote insulin action
  • Decrease glucose absorption
  • Increase glucose excretion
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21
Q

Sulfonylureas (glyburide) ____

A

Sulfonylureas (glyburide) increase secretion of insulin from pancreatic beta cells

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22
Q

Glyburide is a ____

A

Glyburide is a sulfonylurea

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23
Q

Sulfonylureas (glyburide) bind to ___, ____, and ____

A

Sulfonylureas (glyburide) bind to the sulfonylurea, block the KATP channel, and depolarize the beta cell

Increase secretion of insulin

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24
Q

Describe pharmacokinetics of sulfonylureas

A

Sulfonylurea pharmacokinetics

  • Rapidly absorbed after oral administration
  • Absorption can be reduced by food and hyperglycemia
  • Highly protein bound (> 90%)
  • Plasma half life of 3-5 hour but 24 hour duration of hypoglycemic action
  • Hepatic metabolism (CYP2C9)
  • Renal excretion
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25
Q

Describe types of sulfonylureas

A

Sulfonylureas

  • First generation (e.g. chlorpropamide, tolbutamide): rarely used
  • Second generation (e.g. glyburide): more potent and fewer drug interactions
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26
Q

____ is the main adverse effect of sulfonylureas

A

Hypoglycemia is the main adverse effect of sulfonylureas

  • Weight gain, interference with alcohol metabolism, possible adverse cardiovascular effects
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27
Q

Describe drug interactions of sulfonylureas

A

Sulfonylurea drug interactions

  • Competition for plasma protein binding (especially sulfonamides) can increase [free sulfonylurea]
  • Hypoglycemic effect can be decreased by ethanol
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28
Q

Repaglinide is a ___

A

Repaglinide is a meglitinide

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29
Q

Meglitinides (repaglinide) act on ____ and have some overlap in binding sites with ____

A

Meglitinides (repaglinide) act on beta cell K channels and have some overlap in binding sites with sulfonylureas

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30
Q

Describe the pharmacokinetics of meglitinides (repaglinide)

A

Meglitinides (repaglinide) pharmacokinetics

  • Very rapid onset with oral administration
  • Stimulate insulin over period of meal digestion
  • Metabolized in liver by CYP3A4, some renal metabolism
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31
Q

Describe the mechanism of action of meglitinides (repaglinide)

A

Meglitinides (repaglinide) mechanism of action

  1. Act on beta cell K channels
  2. Increase K inside cell
  3. Depolarization
  4. Increase Ca flux into cell through voltage gated Ca channel
  5. Insulin secretion
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32
Q

____ is main toxicity of meglitinides (repaglinide)

A

Hypoglycemia is main toxicity of meglitinides (repaglinide)

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33
Q

____ has drug interactions with meglitinides (repaglinide)

A

Anti-lipidemia drug gemfibrozil (Lopid) has drug interactions with meglitinides (repaglinide)

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34
Q

GLP-1 mimetics are ____, ____, and ____

A

GLP-1 mimetics are exenatide, liraglutide, and dulaglutide

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35
Q

Describe GLP-1 mimetics

A

GLP-1 mimetics

  • Incretins: GI hormones derived from proglucagon
  • Promote glucose-dependent insulin secretion
  • Effective in patients with T2DM
  • Can result in weight loss
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36
Q

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) function to ____

A

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) function to promote glucose-dependent insulin secretion

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37
Q

Describe mechanism of action of GLP-1 mimetics (exenatide, liraglutide, and dulaglutide)

A

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) mechanism of action

  1. Act through GLP receptors (GPCRs)
  2. Act mainly through cAMP/PKA pathway but can also stimulate other signaling pathways
  3. Close K channels, increase Ca release, and increase release of insulin
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38
Q

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are rapidly absorbed after ___

A

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are rapidly absorbed after subcutaneous injection

39
Q

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are contraindicated in patients with ____

A

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are contraindicated in patients with thyroid medullary carcinomas

  • Adverse effects: nausea, vomiting, abdominal pain, pancreatitis
40
Q

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) have drug interactions with ____, ____, and ____

A

GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) have drug interactions with antibiotics, alcohol, and oral contraceptives (exenatide)

41
Q

Sitagliptin is a ____

A

Sitagliptin is a DPP-4 inhibitors

42
Q

Describe the mechanism of action of DPP-4 inhibitors (sitagliptin)

A

DPP-4 inhibitors (sitagliptin) mechanism of action

  1. Inhibit serine protease dipeptidyl peptidase-4
  2. GLP-1 activated
  3. Increased glucose-mediated insulin secretion and decreased glucagon
43
Q

DPP-4 inhibitors (sitagliptin) are ____ effective and have ____ excretion

A

DPP-4 inhibitors (sitagliptin) are orally effective and have renal excretion

44
Q

DPP-4 inhibitors (sitagliptin) adverse effects are ____, ____, and ____

A

DPP-4 inhibitors (sitagliptin) adverse effects are headaches, allergy, and nasopharyngitis

45
Q

DPP-4 inhibitor saxagliptin has ___ metabolism

A

DPP-4 inhibitor saxagliptin has CYP3A4 metabolism

46
Q

Biguanides (metformin) are ___

A

Biguanides (metformin) are oral agents that decrease glucose production

47
Q

Metformin is a ___

A

Metformin is a biguanide

48
Q

___ is a common first line treatment for T2DM

A

Metformin monotherapy is a common first line treatment for T2DM

49
Q

Biguanides (metform) activate ____ and exert ____

A

Biguanides (metform) activate AMPK and exert non-AMPK dependent actions including complex I inhibition

50
Q

Describe mechanism of action of biguanides (metformin)

A

Biguanides (metformin) mechanism of action

  1. Activate AMPK and exert non-AMPK dependent actions including complex I inhibition
  2. Decrease haptic glucose production, suppress gluconeogenesis, increases glycogen storage in muscle
51
Q

____ is less likely to cause hypoglycemia than other agents used to treat diabetes

A

Metformin is less likely to cause hypoglycemia than other agents used to treat diabetes

52
Q

Biguanides (metformin) are ___ and undergo ___ excretion

A

Biguanides (metformin) are not metabolized and undergo renal excretion

53
Q

Biguanide (metformin) main adverse effect is ____

A

Biguanide (metformin) main adverse effect is decreased vitamin B12 absorption

  • Indigestion, cramps, and diarrhea
  • Lactic acidosis, promoted by comorbidities
54
Q

____ drugs compete for the proximal tubule secretory system, elevating circulating metformin

A

Cationic drugs compete for the proximal tubule secretory system, elevating circulating metformin

55
Q

Thiazolidinediones (pioglitazone) are ___

A

Thiazolidinediones (pioglitazone) are oral agents that promote insulin action

56
Q

Pioglitazone is a ____

A

Pioglitazone is a thiazolidinediones

57
Q

Describe the mechanism of action of thiazolidinediones (pioglitazone)

A

Thiazolidinedione (pioglitazone) mechanism of action

  1. Binds to and activates PPAR-gamma in complex with RXR
  2. Promotes transcription of insulin-sensitive genes in liver, muscle, and adipose tissue
58
Q

Thiazolidinediones (pioglitazone) are ____ effective and metabolized in ____

A

Thiazolidinediones (pioglitazone) are orally effective and metabolized in liver by several CYPs

59
Q

____ is the main adverse effect of thiazolidinediones (pioglitazone)

A

Congestive heart failure is the main adverse effect of thiazolidinediones (pioglitazone)

60
Q

Thiazolidinediones (pioglitazone) have interactions with drug that target ____ such as ____

A

Thiazolidinediones (pioglitazone) have interactions with drug that target metabolism such as rifampin

61
Q

Acarbose is an ____

A

Acarbose is an alpha-glucosidase inhibitor

62
Q

Alpha-glucosidease inhibitors (acarbose) ____

A

Alpha-glucosidease inhibitors (acarbose) decrease glucose absorption

63
Q

Describe the structure and mechanism of alpha-glucosidease inhibitors (acarbose)

A

Alpha-glucosidease inhibitors (acarbose) structure and mechanism

  • High affinity for alpha-glucosideases on the brush border of epithelial cells
  • Delays absorption of glucose, interfering with hydrolysis of disaccharides
64
Q

Acarbose decreases plasma glucose increment after ____ loading

A

Acarbose decreases plasma glucose increment after sucrose loading

65
Q

Alpha-glucosidease inhibitors (acarbose) have ___ absorption and ___ excretion

A

Alpha-glucosidease inhibitors (acarbose) have minimal absorption and renal excretion

66
Q

Alpha-glucosidease inhibitors (acarbose) adverse effects are ____ and ____

A

Alpha-glucosidease inhibitors (acarbose) adverse effects are abdominal pain and flatulence due to bacterial metabolism of the glucose

(weak effect)

67
Q

Alpha-glucosidease inhibitors (acarbose) drug interaction is ____

A

Alpha-glucosidease inhibitors (acarbose) drug interaction is decreasing absorption (e.g. of digoxin)

68
Q

Pramlintide is an ____

A

Pramlintide is an amylin analog

69
Q

Amylin analogs (pramlintide) ____

A

Amylin analogs (pramlintide) decreases glucose absorption

70
Q

Amylin analog (pramlintide) binds to ____ and mimics ____

A

Amylin analog (pramlintide) binds to amylin receptor in hindbrain and mimics physiological effects of amylin (islet amyloid peptide)

71
Q

Describe the mechanism of action of amylin analogs (pramlintide)

A

Amylin analogs (pramlintide)

  1. Bind to amylin receptor in hindbrain
  2. Mimic physiological effects of amylin (islet amyloid peptide)
  3. Slows gastric emptying / decreases post-prandial glucose concentrations, anorectic effect, inhibits glucagon release
72
Q

Amylin analogs (pramlintide) are administered ____ prior to ____

A

Amylin analogs (pramlintide) are administered subcutaneously prior to meals

(renal metabolism and excretion)

73
Q

Amylin analogs (pramlintide) adverse effects are ____, ____, and ____

A

Amylin analogs (pramlintide) adverse effects are nausea, increasing insulin hypoglycemic risk, and contraindication in patients with disorder of GI motility

74
Q

Amylin analogs (pramlintide) drug interactions are with ___

A

Amylin analogs (pramlintide) drug interactions are with other agents affecting GI motility

75
Q

Colesevelam is a ____

A

Colesevelam is a bile binding resin

76
Q

Bile binding residen (colesevelam) ____

A

Bile binding residen (colesevelam) decreases glucose absorption

77
Q

Bile binding residen (colesevelam) is primarily used for treatment of ____

A

Bile binding residen (colesevelam) is primarily used for treatment of hypercholesterolemia

78
Q

Bile binding residen (colesevelam) functions to ____ and ____

A

Bile binding residen (colesevelam) functions to lower plasma glucose in patients with T2DM and lower HbA1c

79
Q

Bile acid binding resin (colesevelam) has ___ absorption

A

Bile acid binding resin (colesevelam) has minimal oral absorption

80
Q

Bile acid binding resin (colesevelam) has adverse effects of ___, ___, ___, ___, and ___

A

Bile acid binding resin (colesevelam) has adverse effects of constipation, dyspepsia, abdominal pain, nausea, and increased plasma triglycerides

81
Q

Bile acid binding resin (colesevelam) interferes with ___

A

Bile acid binding resin (colesevelam) interferes with absorption of many commonly used drugs and fat soluble vitamins

82
Q

Canagliflozin is a ____

A

Canagliflozin is a SGLT2 inhibitor

83
Q

SGLT2 inhibitors (canagliflozin) ____

A

SGLT2 inhibitors (canagliflozin) increase glucose excretion

84
Q

Describe SGLT2

A

SGLT2

  • Sodium/glucose co-transporter 2 (SGLT2) expressed in the proximal tubule
  • SGLT2 functions in reabsorption of glucose -> returned to circulation via glucose transporters 1 and 2
  • SGLT2 is low affinity, high capacity transporter
  • Loss of function mutations in SGLT2 cause glucosuria
85
Q

Describe SGLT2 inhibitors (canagliflozin) pharmacokinetics

A

SGLT2 inhibitors (canagliflozin) pharmacokinetics

  • Orally effective
  • Peak at 1-2 hour
  • Metabolized and undergoes fecal and renal excretion
86
Q

____ is the main adverse effect of SGLT2 inhibitors (canagliflozin)

A

Increased risk of amputations is the main adverse effect of SGLT2 inhibitors (canagliflozin)

87
Q

SGLT2 inhibitors (canagliflozin) have a drug interaction with ____

A

SGLT2 inhibitors (canagliflozin) have a drug interaction with gatifloxacin

88
Q

Bromocriptine is a ____

A

Bromocriptine is a dopaminergic agonist

89
Q

Describe the mechanism and action of dopaminergic agonists (bromocriptine)

A

Dopaminergic agonists (bromocriptine) mechanism and action

  • Increases dopaminergic activity in the hypothalamus
  • Mechanism for effects on blood glucose has not been established
  • Decreases postprandial glucose without increasing insulin
90
Q

Dopaminergic agonists (bromocriptine) are ___

A

Dopaminergic agonists (bromocriptine) are orally effective

  • Nausea, vomiting, headaches, fatigue, orthostatic hypotension
  • Weak effect
91
Q

Describe the treatment sequence for T2DM

A

Treatment sequence for T2DM

  1. Metformin
  2. If A1c is > 7% after 3-4 months, a second drug is added
  3. If A1c still > 7% after another 3-4 months, 2 oral agents or insulin are added
92
Q

Use of pioglitazone should be avoided in patients with ____ or ____

A

Use of pioglitazone should be avoided in patients with heart failure or acute diseases of the liver

93
Q

Summarize drugs for treating diabetes

A

Drugs for treating diabetes

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