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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
What are some insulin delivery systems?
- Standard delivery -- SQ injection using disposable needles and syringes - Portable pen injectors - Continuous subcutaneous insulin infusion devices (insulin pumps)
26
What are some adverse effects of insulin?
- Hypoglycemia - Lipodystrophy - Resistance - Allergic reactions - Hypokalemia
27
What is lipodystrophy in insulin use?
- Localized hypertrophy of subcutaneous fat at site of injection - Prevented by frequently changing the site of injection or by IM injections
28
How is resistance seen in insulin use?
- Patients treated with exogenous insulin may develop insulin binding antibodies - IgG antibodies can neutralize the action of insulin
29
What are the most common causes of hypoglycemia in insulin therapy?
- Delay of a meal or a missed meal - Exercise (exercised muscle consumes more glucose) - Overdose of insulin
30
What are some CNS/behavioral signs of hypoglycemia?
- Confusion - Bizarre behavior - Seizures - Coma
31
What are some sympathetic hyperactivity signs of hypoglycemia?
- Tachycardia - Palpitations - Sweating - Tremor
32
What are some parasympathetic hyperactivity signs of hypoglycemia?
- Hunger | - Nausea
33
What is the treatment for hypoglycemia?
- Glucose or sucrose (juice, candy or IV glucose) | - Glucagon (1 mg, sc)
34
What is the MOA of amylin?
- 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
What is an amylin analog drug?
- Pramlintide
36
What is the onset, duration, and peak of pramlintide?
- Onset: rapid - Duration: 3 hr - Peak: 20 min
37
What is the clinical use of pramlintide?
- T1DM - T2DM patients who take mealtime insulin therapy - Injected sc before meals as an adjunct to insulin therapy to control postprandial hyperglycemia
38
What are some adverse effects of pramlintide?
- GI: nausea, vomiting, diarrhea, anorexia | - Severe hypoglycemia -- if used together with insulin
39
What are some drug interactions with pramlintide?
- Enhances effects of anticholinergic drugs on GI tract (i.e. constipation)
40
What are incretins?
- A group of gastrointestinal hormones that cause a decrease in blood glucose levels
41
What is glucagon like peptide 1?
- Synthesized by intestinal L-cells - Inhibits glucagon secretion - Causes satiety, inhibit gastric emptying
42
What does glucagon like peptide 1 promote?
- B cell proliferation - Insulin gene expression - Glucose dependent insulin secretion
43
What is the half life of glucagon like peptide 1?
- Very short (1-2 min)
44
What are the two methods for incretin mimetics?
- Long acting GLP-1 receptor agonists | - Dipeptidyl peptidase-4 (DDP-4) inhibitors
45
What is exenatide?
- Recombinant form of exendin-4, a protein from Gila monster saliva that has GLP-1 agonist activity
46
What is the half life of exenatide?
- 2.4 hr
47
What is liraglutide?
- GLP-1 analog with 97% homology to native GLP-1 | - Lipid modified -- rapidly absorbed, but binds to albumin
48
What is the half life of liraglutide?
- 11-15 hrs
49
What are some adverse effects of GLP-1 receptor agonists?
- GI: nausea, diarrhea, anorexia | - Hypoglycemia
50
What are some DPP-4 inhibitors?
- Sitagliptin - Linagliptin - Saxagliptin - Alogliptin
51
What is the MOA of DPP-4 inhibitors?
- Increase levels of GLP-1 to enhance its interactions with the cognate receptor - Effects similar to GLP-1 agonists
52
What are the clinical indications for DPP-4 inhibitors?
- 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
What are some adverse effects of DPP-4 inhibitors
Hypoglycemia
54
Which generation of sulfonylureas has a high potency?
- Second generation: used in low mg doses
55
Which generation of sulfonylureas is used more often?
- Second generation due to fewer adverse effects
56
What are the clinical uses for sulfonylureas?
- T2DM as a monotherapy or in combination with insulin or other anti-diabetic drugs
57
What are some adverse effects of sulfonylureas?
- Hypoglycemia - Weight gain (due to increased insulin release) - Secondary failure
58
What are some sulfonylurea drug interactions that enhance their hypoglycemic effect?
- Sulfonamides, clofibrate, salicylates, and other NSAIDs - Ethanol - Inhibiting CYP enzymes: azole antifungals, gemfibrozil, cimetidine
59
What are some sulfonylurea drug interactions that decrease their glucose lowering effect?
- Inhibiting insulin secretion: beta blockers, CCBs | - Inducing hepatic CYP enzymes: phenytoin, griseofulvina, rifampin
60
What are some meglitinides?
- Repaglinide | - Nateglinide
61
What is the MOA of meglitinides?
- K(ATP) channel inhibition
62
What is the half life and duration of meglitinides?
- Half life: 1-1.5 hr | - Duration of action: 4 to 6 hr
63
What is the MOA of metformin?
- Activation of AMP-activated protein kinase
64
What is the clinical use of metformin?
- Most commonly used oral agent to treat T2DM and is generally accepted as the first line treatment for this condition
65
What are some advantages for using metformin?
- 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
What are the pharmacokinetics of metformin?
- Half life: 1.5-3 hrs - Not bound to plasma proteins - Not metabolized - Excreted unchanged by kidneys
67
What are some adverse effects of metformin?
- Gi complications - Anorexia - Vomiting - Nausea - Diarrhea - Abdominal discomfort - Lactic acidosis (esp in hypoxia, renal and hepatic insufficiency)
68
Who is metformin contraindicated in?
- In conditions predisposing to tissue hypoxia (HF, COPD), renal failure, chronic alcoholism, and cirrhosis
69
What are some thiazolidinediones?
- Pioglitazone | - Rosiglitazone
70
What is the MOA of thiazolidinediones?
- Ligands of peroxisome proliferator-activated receptor-gamma (PPARg)'- - PPARg is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and enothelium
71
Where are thiazolidinediones metabolized?
- Liver - Half life reduced by CYP inducers - Half life prolonged by CYP inhibitors
72
How long do the effects of thiazolidinediones last?
- Week-months after drugs are eliminated due to delayed onset
73
What are the clinical uses for thiazolidinediones?
- T2DM, alone or in combo - Shown to delay progression from prediabetes to T2DM - Euglycemic drugs
74
What are some adverse effects of thiazolidinediones?
- 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
How can thiazolidinediones exacerbate heart failure?
- Due to increased water retention - No direct effect on cardiac contractile function - Contraindicated in patients with CHF
76
What are some SGLT2 inhibitors?
- Canagliflozin - Dapagliflozin - Empagliflozin
77
What is the MOA of SGLT2 inhibitors?
- 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
What are some other effects of SGLT2 inhibitors?
- Cause osmotic diuresis - Induce weight loss - Reduced BP - Reduce plasma levels of uric acid - Do not cause hypoglycemia when used alone
79
What are some clinical uses of SGLT2 inhibitors?
- 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
What are some adverse effects of SGLT2 inhibitors?
- Hypotension - Hypovolemia - In hypovolemic patients, may cause orthostatic hypotension, dizziness, syncope - Genital and UTI - Hypoglycemia if combined with insulin or insulin secretagogues
81
What are some alpha-glycosidase inhibitors?
- Acarbose | - Miglitol
82
What is the MOA of alpha-glycosidase inhibitors?
- 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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