Exam 3- Endocrine System Flashcards

1
Q

Biguanides

A

Increases insulin sensitivity, Reduces hepatic glucose production, and decreases glucose absorption in the gut.

Caution in liver patients due to risk for lactic acidosis
Metformin (Glucophage)
•Indicated for the treatment of DMII

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2
Q

Thiazolidinediones (TZDs) (-litazone)

A

•Decrease insulin resistance through activation of insulin-responsive genes in the nuclei of tissues important for insulin action

  • Used in the treatment of type 2 DM
  • Adverse effects – peripheral edema, liver failure, heart failure

•Pioglitazone (Actos), rosiglitazone (Avandia)

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3
Q

Sulfonylureas (-ide)

A

•Reduce blood glucose by stimulating insulin release from pancreatic beta cells

•First-generation
–Chlorpropamide (Diabinese)
–Tolbutamide (Orinase)
•Second-generation
–Glyburide (Diabeta)
–Glipizide (Glucatrol)
–Glimepride (Amaryl)

Initially used as first-line drugs in the treatment of type 2 DM
•Extensively protein bound
•Side effects – hypoglycemia

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4
Q

Meglitinide Analogues

A
  • Nateglinide (Starlix), Repaglinide (Prandin)
  • Oral hypoglycemic drugs used in the treatment of type 2 DM
  • Stimulate insulin release from pancreas
  • 98% protein bound; biotransformed by CYP450
  • Drug interactions
  • Patient education
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5
Q

Alpha-glucosidase Inhibitors

A

•Acarbose (Precose), miglitol (Glyset)
•Lower postprandial BS in the treatment of type 2 DM
•Inhibit alpha-glucosidase enzymes in the intestine
–Decreases the amount of glucose available for absorption in the GI tract
•Very little absorbed systemically
•Side effects – GI

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6
Q

Amylin Agonists

A

•Pramlintide (Symlin)
•Injectable antihyperglycemic used in the treatment of type 1 and type 2 DM patients treated with insulin
•A synthetic analogue of human amylin
–Neuropeptide hormone synthesized by pancreatic beta cells
•Biotransformed in the kidneys
•Side effects – hypoglycemia, GI

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7
Q

GLP-1 Agonist (-atide)

A

An incretin
Directly Increase insulin secretion from the beta cells and inhibit the release of glucagon.
•Exanatide (Byetta), Albiglutide (Tanzeum), Tulaglutide (Trulicity), Liraglutide (Victoza)
•Indicated as adjunct therapy in patients with type 2 DM who are using metformin, a sulfonylurea (or both) who have not achieved adequate BS control
•Glucagon-like peptide 1 (GLP-1) – deficient in diabetics
•Side effects – GI, gradual weight loss

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8
Q

DPP-4 Antagonists

A

•Sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina)
•Indicated for the treatment of type 2 DM
•Inhibits dipeptidyl peptidase 4 (DDP-4)
–Enzyme responsible for degradation of incretins
•Side effects - URI

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9
Q

Thyroid replacement hormones

A

Levothyroxine (Synthroid, Levoxyl, T4), liothyronine (Cytomel T3)
•Levothyroxine is the drug of choice for replacement of thyroid hormone (T4)
•Absorption increased on an empty stomach
•Metabolized in the liver; highly protein bound
•Few adverse effects
•Patient education

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10
Q

Antithyroid drugs

A

Propylthiouracil (PTU), methimazole (Tapazole)
•First-line drugs in the treatment of hyperthyroidism or thyrotoxicosis
•Inhibit the synthesis of thyroid hormones
•Crosses placental membranes
•Side effects – rash, leukopenia
•Drug interactions

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11
Q

Radioactive iodine

A

Sodium idodide131
•Radioactive iodine (RAI) is used in the treatment of hyperthyroidism in older adults – also in diagnosis of thyroid conditions
•The thyroid gland actively absorbs iodine
–RAI disrupts the function of thyroid cells → thyroid hormones are no longer produced
•Side effects – few; iatrogenic hypothyroidism

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12
Q

Insulin

A

•Rapid-acting insulin – lispro (Humalog)
•Fast-acting insulin – regular
•Intermediate-acting insulin – Humulin N
•Long-acting insulin – insulin glargine, insulin detemir
•Indicated for the treatment of diabetes when glucose and hemoglobin A1C goals are not met with other treatments
•Insulin produced through recombinant DNA technology
Adverse effects – hypoglycemia, dawn phenomenon
•Drug interactions
•Dosage regimen
•Lab considerations
•Patient education

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13
Q

Signs of hypoglycemia

A

decreased levels of consciousness, hunger, diaphoresis, weakness, dizziness, and tachycardia. (defined as BG less than 70).

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14
Q

Signs of hyperglycemia

A

polyuria, polydipsia, polyphagia, weight loss and fatigue, vomiting, dehydration, ketone odor to the breath, and abdominal pain. Indications may precede DKA.

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15
Q

Signs of ketoacidosis

A

drowsiness, dim vision, and Kussmauls respirations. Symptoms of hyperglycemia may precede DKA and give warning of its impending occurrence include

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16
Q

How does metformin work?

A

increases peripheral glucose uptake and utilization (insulin sensitivity), decreases hepatic glucose production, and decreases intestinal absorption of glucose. Together, these actions address the primary pathological defects of type 2 diabetes to improve glucose tolerance and lower both basal and postprandial plasma glucose levels

17
Q

What diagnostic testing is needed before initiating therapy and throughout treatment with metformin?

A

Before initiating therapy and at least annually thereafter, assess renal function. Assessment is by serum creatinine and CCr initially and then by serum creatinine annually. Patients who have been previously well controlled on metformin who are no longer controlled or who develop illnesses that place them at risk for metabolic acidosis should be assessed for evidence of ketoacidosis or lactic acidosis

18
Q

What is the action of gliptin?

A

The action of gliptins is different from that of other antihyperglycemic agents because gliptins act on the incretin hormone system to have an indirect effect on increasing insulin production. Although the improvement in glycemic control is moderate and no more than with metformin, gliptins are well tolerated, have a low risk for hypoglycemia, are weight neutral, and can be given orally

19
Q

How do GLP agonists work?

A

Glucagon-like peptide-1 is a naturally occurring peptide produced in the small intestine that potentiates glucose-stimulated insulin secretion. GLP-1 agonists directly bind to the GLP-1 receptor in the pancreatic beta cell and act as an incretin mimetic.

20
Q

When should exenatide be administered?

A

Immediate-release exenatide is given about 60 minutes before morning and evening meals and doses should be at least 6 hours apart. Do not administer after a meal.

21
Q

What are the adverse effects of propylthiouracil?

A

The most common serious adverse reaction to therapy with the thionamides is agranulocytosis and possible aplastic anemia. Drug-induced hepatitis and abnormal hair loss may occur.

22
Q

What are the adverse effects of levothyroxine?

A

Adverse reactions other than those associated with hyperthyroidism due to overdose are rare. If the patient experiences indications of hyperthyroidism (increased heart rate, cardiac arrhythmias, chest pain, tremors, nervousness, insomnia, irritability, diarrhea, vomiting, weight loss, menstrual irregularities, or heat intolerance), the TSH level should be assessed and appropriate dosage adjustments made.

23
Q

What is the recommended treatment for toxic goiter?

A

Patients with toxic goiter require higher doses of antithyroid drugs. Methimazole is initiated at a dose of 60 mg/d divided into three equal doses given 8 hours apart. Propylthiouracil is initiated with 600 to 900 mg/d in three equally divided doses given 8 hours apart. Maintenance doses are the same as for hyperthyroidism. Some treatment regimens give either medication for 1 month to “calm” the thyroid and then administer a dose of radioactive iodine.

24
Q

What are the adverse effects of PTU and methimazole?

A

The most common serious adverse reaction to therapy with the thionamides is agranulocytosis and possible aplastic anemia. Drug-induced hepatitis and abnormal hair loss may occur with either drug. Less serious and less frequent adverse reactions to both thioamides include drowsiness, headache, paresthesias, vertigo, diarrhea, nausea, arthralgia, and a pruritic skin rash. The nausea and skin rash are more common with propyl -thiouracil, but there is an element of cross-sensitivity with metimazole.

25
Q

What is the dosage schedule for alpha-glucosidase inhibitors?

A

Patients are taught to take these drugs with the first bite of each meal. The need for this timing of administration must be stressed because taking it too soon reduces its effect and taking it after a meal has no effect.

26
Q

Describe the pharmacodynamics of meglitinides

A

Meglitinides close ATP-dependent potassium channels in the beta cell membrane by binding at specific receptor sites. This potassium channel blockade depolarizes the beta cell and leads to an opening of calcium channels. The resultant influx of calcium increases the secretion of insulin. Because its time in the plasma is less than 2 hours, the effect is 4 hours with peak effect in 1 hour. The ion channel mechanism is highly tissue selective, with low affinity for heart and skeletal muscle, which reduces the potential adverse effects on these tissues.

27
Q

What is the mechanism of action of propylthiouracil?

A

Propylthiouracil partially inhibits the peripheral conversion of T4 to T3.

28
Q

What are the contraindications to therapy with alpha-glucosidase inhibitors?

A

Alpha-glucosidase inhibitors should not be used for patients with bowel diseases such as inflammatory bowel disease, bowel obstruction or risk factors for it, chronic intestinal disease associated with marked digestive disorders, or conditions that may deteriorate as a result of increased gas in the intestine. Not recommended in renal failure.

29
Q

What patient education is important relative to the administration of levothyroxine?

A

Thyroid hormones are taken as a single daily dose in the morning before breakfast to prevent insomnia. Taking levothyroxine on an empty stomach enhances absorption. If more than three doses are missed, the health-care provider should be informed. Caution patients not to change brands of thyroid preparation. If brands are switched to generics, titrating of doses over several months may be required.

30
Q

What black box warning has the FDA issued regarding the administration of TZDs?

A

should be used cautiously because of the potential for cardiovascular problems, especially with rosiglitazone. TZDs are generally well tolerated, with the exception of cardiovascular effects, including weight gain (5%), hypertension (4%), heart failure (2% to 3% in patients receiving insulin), and myocardial ischemia (3%). Increases in total cholesterol, HDL cholesterol, LDL cholesterol, and weight gain occur in less than 10% of patients.

31
Q

What symptoms may indicate that a patient is taking too much thyroid replacement hormone?

A

indications of hyperthyroidism (increased heart rate, cardiac arrhythmias, chest pain, tremors, nervousness, insomnia, irritability, diarrhea, vomiting, weight loss, menstrual irregularities, or heat intolerance),

32
Q

What is the mechanism of action of metformin?

A

increases peripheral glucose uptake and utilization (insulin sensitivity), decreases hepatic glucose production, and decreases intestinal absorption of glucose. Together, these actions address the primary pathological defects of type 2 diabetes to improve glucose tolerance and lower both basal and postprandial plasma glucose levels. Metformin does not stimulate insulin release from the pancreatic beta cells, nor does it produce hypoglycemia except in specific circumstances. Metformin does not cause hyperinsulinemia. Metformin also does not cause weight gain; often patients lose weight. Because obesity is a major factor in the pathogenesis of type 2 diabetes, this is an important drug action. Metformin also inhibits platelet aggregation and reduces blood viscosity. This property is a factor in its use in metabolic syndrome, which is discussed below.

33
Q

What lab values will be used to monitor a patient on levothyroxine?

A

Thyroid function is monitored with TSH and free T4 levels. Because of the negative feedback loop between TSH and thyroid hormones, elevations in TSH indicate insufficient thyroid hormone, and TSH levels below desired levels indicate excessive thyroid hormone. TSH and free T4 levels are checked initially and at 6 weeks after the first adjustment. Recheck the levels 4 to 6 months after achieving the target dose.

34
Q

Short-acting insulin (SAIs): Lispro

A

Onset of action: 15 min
Peak of action: 1 hr
Duration of action:

35
Q

Rapid-acting insulin (RAIs): Regular

A

Onset of action: 30 min
Peak of action: 4-6 hrs
Duration of action: 8-12 hrs

36
Q

Intermediate-acting (IAIs): NPH

A

Onset of action: 1-1.5 hrs
Peak of action:
Duration of action: 12-24 hrs

37
Q

Long-acting (LAIs): glargine, detemir

A

Onset of action:
Peak of action: none
Duration of action: 24 hrs

38
Q

When changing from NPH to glargine insulin, how will you adjust the patient’s dose?

A

when patients were switched from once-daily NPH to once daily insulin glargine, the initial dose was usually not changed. If the change was from twice-daily NPH to insulin glargine, to avoid hypoglycemia the initial dose of insulin glargine was reduced by 20% and then adjusted based on patient response

39
Q

What are side effects of insulin therapy?

A

Hypoglycemia and DKA.