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Endocrine Exam > Drugs for Diabetes > Flashcards

Drugs for Diabetes Flashcards

1
Q

What are some things that increase blood glucose?

A
  • T3/T4
  • Glucagon
  • Epinephrine
  • Glucocorticoids
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2
Q

What decreases blood glucose?

A
  • Insulin
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3
Q

How does insulin lower blood glucose levels?

A
  • Insulin binds to an insulin receptor which acts on MAP kinase pathways and PI3K-Akt pathways
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4
Q

What does the MAP kinase pathway cause after activation by insulin?

A
  • Cell growth
  • Proliferation
  • Gene expression
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5
Q

What does the PI3K-Akt pathway cause after activation by insulin?

A
  • Synthesis of lipids, proteins, glycogen
  • Cell survival and proliferation
  • Puts GLUT4 into the cell membrane to increase glucose influx
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6
Q

What is the anabolic effects of insulin on carbohydrate metabolism?

A
  • Promotes intracellular glucose transport and utilization
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7
Q

What is a part of the anabolic effect of insulin?

A
  • GLUT4 translocation to the cell membrane in skeletal muscle, cardiac myocytes, and adipocytes
  • Activation of glycolysis
  • Activation of glycogen synthesis
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8
Q

How does insulin oppose the catabolic effects of other hormonal systems?

A
  • Inhibition of gluconeogenesis

- Inhibition of glycogenolysis

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9
Q

What are some rapid acting insulins?

A
  • Aspart
  • Lispro
  • Glulisine
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10
Q

What is the clinical use of rapid acting insulins?

A
  • Postprandial hyperglycemia – taken before the meal
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11
Q

What is the onset, duration, and peak of rapid acting insulins?

A
  • Onset: 5-10 min
  • Duration: 1-3 hours
  • Peak: 30 min- 1 hr
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12
Q

What is a short acting insulin?

A
  • Regular insulin
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13
Q

What is the composition of regular insulin?

A
  • Unmodified zinc insulin crystals
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14
Q

What is the clinical use of regular insulin?

A
  • Basal insulin maintenance
  • Overnight coverage
  • If for postprandial hyperglycemia – inject 45 min before the meal
  • Can be injected IV in urgent situations
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15
Q

What is the onset, duration, and peak of regular insulin?

A
  • Onset: 30min- 1 hr
  • Duration: 10 hr
  • Peak: 3-5 hr
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16
Q

What are some long acting insulins?

A
  • Detemir

- Glargine

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17
Q

What is the composition of detemir?

A
  • Lys 29 in B chain is myristoylated
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18
Q

What is the composition of glargine?

A
  • Amino acid substitutions in both A and B chains enhance crystal stability, change pKa of insulin – soluble at low pH (4) but precipitates at pH 7
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19
Q

What is the clinical use of long acting insulins?

A
  • Basal insulin maintenance (1-2 sc injections daily)
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20
Q

What is the onset, duration, and peak of long acting insulins?

A
  • Onset: 3-4 hr
  • Duration: 24 hr
  • Peak: Detemir (3-9 hr); glargine (peakless)
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21
Q

What is important of a tight glycemic control?

A
  • Improves survival
  • Reduces diabetic complications
  • Has shown to be effective in multiple clinical trials, especially in patients with T1DM
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22
Q

What are some clinical indications of insulin?

A
  • T1DM
  • T2DM
  • Gestational diabetes
  • Severe hyperkalemia
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23
Q

Why is insulin used in severe hyperkalemia?

A
  • Insulin rapidly activated Na+/K+-ATPase to shift K+ from extracellular fluid into cells
  • Effect is transient
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24
Q

What else is done in severe hyperkalemia to help right away?

A
  • Loop diuretics are given to eliminate K+ in the urine
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25
Q

What are some insulin delivery systems?

A
  • Standard delivery – SQ injection using disposable needles and syringes
  • Portable pen injectors
  • Continuous subcutaneous insulin infusion devices (insulin pumps)
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26
Q

What are some adverse effects of insulin?

A
  • Hypoglycemia
  • Lipodystrophy
  • Resistance
  • Allergic reactions
  • Hypokalemia
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27
Q

What is lipodystrophy in insulin use?

A
  • Localized hypertrophy of subcutaneous fat at site of injection
  • Prevented by frequently changing the site of injection or by IM injections
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28
Q

How is resistance seen in insulin use?

A
  • Patients treated with exogenous insulin may develop insulin binding antibodies
  • IgG antibodies can neutralize the action of insulin
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29
Q

What are the most common causes of hypoglycemia in insulin therapy?

A
  • Delay of a meal or a missed meal
  • Exercise (exercised muscle consumes more glucose)
  • Overdose of insulin
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30
Q

What are some CNS/behavioral signs of hypoglycemia?

A
  • Confusion
  • Bizarre behavior
  • Seizures
  • Coma
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31
Q

What are some sympathetic hyperactivity signs of hypoglycemia?

A
  • Tachycardia
  • Palpitations
  • Sweating
  • Tremor
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32
Q

What are some parasympathetic hyperactivity signs of hypoglycemia?

A
  • Hunger

- Nausea

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33
Q

What is the treatment for hypoglycemia?

A
  • Glucose or sucrose (juice, candy or IV glucose)

- Glucagon (1 mg, sc)

34
Q

What is the MOA of amylin?

A
  • Enhances the action of insulin by:
  • Inhibition of glucagon secretion
  • Decreased gastric emptying (slows rate of intestinal glucose absorption)
  • Causes a feeling of satiety
35
Q

What is an amylin analog drug?

A
  • Pramlintide
36
Q

What is the onset, duration, and peak of pramlintide?

A
  • Onset: rapid
  • Duration: 3 hr
  • Peak: 20 min
37
Q

What is the clinical use of pramlintide?

A
  • T1DM
  • T2DM patients who take mealtime insulin therapy
  • Injected sc before meals as an adjunct to insulin therapy to control postprandial hyperglycemia
38
Q

What are some adverse effects of pramlintide?

A
  • GI: nausea, vomiting, diarrhea, anorexia

- Severe hypoglycemia – if used together with insulin

39
Q

What are some drug interactions with pramlintide?

A
  • Enhances effects of anticholinergic drugs on GI tract (i.e. constipation)
40
Q

What are incretins?

A
  • A group of gastrointestinal hormones that cause a decrease in blood glucose levels
41
Q

What is glucagon like peptide 1?

A
  • Synthesized by intestinal L-cells
  • Inhibits glucagon secretion
  • Causes satiety, inhibit gastric emptying
42
Q

What does glucagon like peptide 1 promote?

A
  • B cell proliferation
  • Insulin gene expression
  • Glucose dependent insulin secretion
43
Q

What is the half life of glucagon like peptide 1?

A
  • Very short (1-2 min)
44
Q

What are the two methods for incretin mimetics?

A
  • Long acting GLP-1 receptor agonists

- Dipeptidyl peptidase-4 (DDP-4) inhibitors

45
Q

What is exenatide?

A
  • Recombinant form of exendin-4, a protein from Gila monster saliva that has GLP-1 agonist activity
46
Q

What is the half life of exenatide?

A
  • 2.4 hr
47
Q

What is liraglutide?

A
  • GLP-1 analog with 97% homology to native GLP-1

- Lipid modified – rapidly absorbed, but binds to albumin

48
Q

What is the half life of liraglutide?

A
  • 11-15 hrs
49
Q

What are some adverse effects of GLP-1 receptor agonists?

A
  • GI: nausea, diarrhea, anorexia

- Hypoglycemia

50
Q

What are some DPP-4 inhibitors?

A
  • Sitagliptin
  • Linagliptin
  • Saxagliptin
  • Alogliptin
51
Q

What is the MOA of DPP-4 inhibitors?

A
  • Increase levels of GLP-1 to enhance its interactions with the cognate receptor
  • Effects similar to GLP-1 agonists
52
Q

What are the clinical indications for DPP-4 inhibitors?

A
  • Approved as adjunct therapy to diet and exercise in patients with T2DM
  • Used as both monotherapy and in combination with metformin/sulfonylureas/TZDs
  • Taken orally
53
Q

What are some adverse effects of DPP-4 inhibitors

A

Hypoglycemia

54
Q

Which generation of sulfonylureas has a high potency?

A
  • Second generation: used in low mg doses
55
Q

Which generation of sulfonylureas is used more often?

A
  • Second generation due to fewer adverse effects
56
Q

What are the clinical uses for sulfonylureas?

A
  • T2DM as a monotherapy or in combination with insulin or other anti-diabetic drugs
57
Q

What are some adverse effects of sulfonylureas?

A
  • Hypoglycemia
  • Weight gain (due to increased insulin release)
  • Secondary failure
58
Q

What are some sulfonylurea drug interactions that enhance their hypoglycemic effect?

A
  • Sulfonamides, clofibrate, salicylates, and other NSAIDs
  • Ethanol
  • Inhibiting CYP enzymes: azole antifungals, gemfibrozil, cimetidine
59
Q

What are some sulfonylurea drug interactions that decrease their glucose lowering effect?

A
  • Inhibiting insulin secretion: beta blockers, CCBs

- Inducing hepatic CYP enzymes: phenytoin, griseofulvina, rifampin

60
Q

What are some meglitinides?

A
  • Repaglinide

- Nateglinide

61
Q

What is the MOA of meglitinides?

A
  • K(ATP) channel inhibition
62
Q

What is the half life and duration of meglitinides?

A
  • Half life: 1-1.5 hr

- Duration of action: 4 to 6 hr

63
Q

What is the MOA of metformin?

A
  • Activation of AMP-activated protein kinase
64
Q

What is the clinical use of metformin?

A
  • Most commonly used oral agent to treat T2DM and is generally accepted as the first line treatment for this condition
65
Q

What are some advantages for using metformin?

A
  • Superior or equivalent glucose lowering efficacy compared to other oral meds
  • Does not cause hypoglycemia
  • Does not cause weight gain
  • Taken orally
  • Can be used alone or in combo
  • In clinical trials, decreased risk of both macro and microvascular complications
66
Q

What are the pharmacokinetics of metformin?

A
  • Half life: 1.5-3 hrs
  • Not bound to plasma proteins
  • Not metabolized
  • Excreted unchanged by kidneys
67
Q

What are some adverse effects of metformin?

A
  • Gi complications
  • Anorexia
  • Vomiting
  • Nausea
  • Diarrhea
  • Abdominal discomfort
  • Lactic acidosis (esp in hypoxia, renal and hepatic insufficiency)
68
Q

Who is metformin contraindicated in?

A
  • In conditions predisposing to tissue hypoxia (HF, COPD), renal failure, chronic alcoholism, and cirrhosis
69
Q

What are some thiazolidinediones?

A
  • Pioglitazone

- Rosiglitazone

70
Q

What is the MOA of thiazolidinediones?

A
  • Ligands of peroxisome proliferator-activated receptor-gamma (PPARg)’- - PPARg is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and enothelium
71
Q

Where are thiazolidinediones metabolized?

A
  • Liver
  • Half life reduced by CYP inducers
  • Half life prolonged by CYP inhibitors
72
Q

How long do the effects of thiazolidinediones last?

A
  • Week-months after drugs are eliminated due to delayed onset
73
Q

What are the clinical uses for thiazolidinediones?

A
  • T2DM, alone or in combo
  • Shown to delay progression from prediabetes to T2DM
  • Euglycemic drugs
74
Q

What are some adverse effects of thiazolidinediones?

A
  • Weight gain
  • Edema
  • Increase vascular permeability
  • Increase expression of ENaC – Increased sodium and water reabsorption in the collecting duct
  • Exacerbation of heart failure
  • Osteoporosis
75
Q

How can thiazolidinediones exacerbate heart failure?

A
  • Due to increased water retention
  • No direct effect on cardiac contractile function
  • Contraindicated in patients with CHF
76
Q

What are some SGLT2 inhibitors?

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
77
Q

What is the MOA of SGLT2 inhibitors?

A
  • Kidneys filter 160 to 180 g of glucose per day
  • Glucose is reabsorbed in the proximal tubule primarily by SGLT2
  • Gliflozins inihbit this transporter to increase glucose excretion and reduce hyperglycemia
78
Q

What are some other effects of SGLT2 inhibitors?

A
  • Cause osmotic diuresis
  • Induce weight loss
  • Reduced BP
  • Reduce plasma levels of uric acid
  • Do not cause hypoglycemia when used alone
79
Q

What are some clinical uses of SGLT2 inhibitors?

A
  • In adults with T2DM in combo
  • Taken orally before first meal of the day
  • In patients with hypovolemia, this condition should be corrected before start of therapy
80
Q

What are some adverse effects of SGLT2 inhibitors?

A
  • Hypotension
  • Hypovolemia
  • In hypovolemic patients, may cause orthostatic hypotension, dizziness, syncope
  • Genital and UTI
  • Hypoglycemia if combined with insulin or insulin secretagogues
81
Q

What are some alpha-glycosidase inhibitors?

A
  • Acarbose

- Miglitol

82
Q

What is the MOA of alpha-glycosidase inhibitors?

A
  • Competitive inhibition of alpha-glycosidases, a family of enzymes on the intestinal epithelium defer digestion and thus absorption of ingested starch
  • Lower postprandial hyperglycemia to create an insulin sparing effect

Endocrine Exam (11 decks)

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