1. Drugs for Endocrine Disorders31
Drugs for Endocrine Disorders

2. Directory
Classroom Response System
Lecture Note Presentation

3. Question 1
The mechanism of action of oral hypoglycemic agents includes:

4. Question 1 Choices
Decreased uptake and utilization of glucose by body cells
Stimulated insulin release from the pancreas
Increased insulin production by the pancreas
Decreased amount of insulin produced by the pancreas

5. Question 1 Answer
Decreased uptake and utilization of glucose by body cells
Stimulated insulin release from the pancreas
Increased insulin production by the pancreas
Decreased amount of insulin produced by the pancreas

6. Question 2
The patient is exhibiting hypoglycemia, fatigue, hypotension, anorexia, vomiting, and diarrhea. The nurse suspects:

7. Question 2 Choices Cushing’s syndrome Graves’ disease
Adrenal insufficiency
Diabetes mellitus

8. Question 2 Answer Cushing’s syndrome Graves’ disease
Adrenal insufficiency
Diabetes mellitus

9. Question 3
Insulin glargine (Lantus) should be administered:

10. Question 3 Choices Before meals After meals At bedtime
Before and after meals

11. Question 3 Answer Before meals After meals At bedtime
Before and after meals

12. Question 4
Which of the following is not a symptom of diabetes?

13. Question 4 Choices
Polyphagia
Polyuria
Polydipsia
Weight gain

14. Question 4 Answer
Polyphagia
Polyuria
Polydipsia
Weight gain

15. Learning Outcomes
Describe the general structure and functions of the endocrine system.
Compare and contrast the functions of the pancreatic hormones.
Compare and contrast the causes, signs, symptoms, and treatment of type 1 and type 2 diabetes mellitus.

16. Learning Outcomes Identify the five types of insulin.
Describe the signs and symptoms of insulin overdose and underdose.
Explain the primary functions of the thyroid gland.

17. Learning Outcomes
Identify the signs and symptoms of hypothyroidism and hyperthyroidism.
Explain the primary functions of the adrenal cortex.
Describe the signs and symptoms of Addison’s disease and Cushing’s syndrome.

18. Learning Outcomes
For each of the following drugs or drug classes identify representative drugs, explain the mechanisms of drug action, primary actions, and important adverse effects:

19. Core Concept 31.1
The endocrine system maintains homeostasis by using hormones as chemical messengers.

20. Figure 31.1 The endocrine system Source: Pearson Education/PH College

22. Core Concept 31.2
Hormones are used as replacement therapy, as antineoplastics, and for their natural therapeutic effects.

23. Core Concept 31.3
The hypothalamus and the pituitary gland secrete hormones that control other endocrine organs.

24. Hypothalamus and Pituitary
Hypothalamus secretes chemicals called releasing factors or releasing hormones
They travel via blood vessels a short distance to anterior pituitary gland.
The releasing factors tell the pituitary which hormone to release.
After the pituitary releases the appropriate hormone, it travels to its target organ to cause its effect.

25. Figure Hormones associated with the pituitary gland Source: Adapted by permission of Pearson Education, Inc., Upper Saddle River, NJ

26. Insulin and glucagon are secreted by the pancreas.
Core Concept 31.4
Insulin and glucagon are secreted by the pancreas.

27. Insulin
Regulated by a number of chemical, hormonal, and nervous factors.
Level of glucose in the blood
Glucose levels are high (hyperglycemia), the pancreas is stimulated to secrete insulin.
The islet cells stop secreting insulin when blood glucose is low (hypoglycemia) or when high levels of insulin send the pancreas a message to stop secreting the hormone.

28. Insulin Action Affects carbohydrate, fat, and protein metabolism
Assist in glucose transport Without insulin, glucose cannot enter cells.

29. Glucagon Blocker of insulin actions are opposite to those of insulin.
When levels of glucose are low, glucagon is secreted. primary function
Maintain adequate levels of glucose in the blood between meals.
It has a hyperglycemic effect: its presence moves glucose from cells, primarily in the liver, to the blood.

30. Figure 31.3 Insulin, glucagon, and blood glucose Source: Pearson Education/PH College

31. Core Concept 31.5
Type 1 diabetes is treated by dietary restrictions and insulin injections.

32. Type 1 Diabetes Symptoms
Hyperglycemia—fasting blood glucose greater than 126 mg/dl
Polyuria—excessive urination
Polyphagia—increase in hunger
Polydipsia—increased thirst

33. Type 1 Diabetes Symptoms
Glucosuria—high levels of glucose in the urine
Weight loss
Fatigue

34. Type 1 Diabetes Treatment
Combination of proper meal planning, exercise, and insulin.
Food must be eaten regularly, every 4 to 5 hours
Regular, moderate exercise helps the cellular responsiveness to insulin.

36. Table 31.2 (continued) Insulin Preparations

37. Core Concept 31.6
Type 2 diabetes is controlled through lifestyle changes and oral hypoglycemic agents.

38. Type 2 Diabetes
Capable of secreting insulin, although in amounts that are too small.
Insulin receptors in the target tissues have become insensitive or resistant to the hormone.

39. Type 2 Diabetes Controlled with oral hypoglycemic agents.
Proper diet and exercise can sometimes increase the sensitivity of insulin receptors to the point that drug therapy is unnecessary in type 2 diabetes.

40. Oral Hypoglycemic Medications
Sulfonylureas
Biguanides
Thiazolidinediones
Alpha-glucosidase inhibitors
Meglitinides
Dipeptidyl-peptase 4

41. Concept Review 31.1
Why are oral hypoglycemic drugs ineffective for treating type 1 diabetes?

43. Table 31.3 (continued) Oral Hypoglycemics

44. Table 31.3 (continued) Oral Hypoglycemics

45. Core Concept 31.7
The thyroid gland controls the basal metabolic rate and affects virtually every cell in the body.

46. Figure 31.4 Feedback mechanisms of the thyroid gland

47. Core Concept 31.8
Thyroid disorders may be treated by administering thyroid hormone or by decreasing the activity of the thyroid gland.

48. Hypothyroidism
Common disease caused by insufficient secretion of either TSH or thyroid hormone.
Symptoms: slowed body metabolism, slurred speech, bradycardia, weight gain, low body temperature,intolerance to cold environments.

49. Hypothyroidism
Causes: autoimmune disease, surgical removal of the gland, or aggressive treatment with antithyroid drugs.
Treatment with natural or synthetic thyroid hormone.

51. Hyperthyroidism
Symptoms: increased body metabolism, tachycardia, weight loss, high body temperature, and anxiety.
Graves’ disease. A particularly severe form of hyperthyroidism is called

52. Hyperthyroidism Treatment
Surgical removal of thyroid gland - thyroidectomy
Antithyroid medications or ionizing radiation to kill or inactivate some of the hyperactive thyroid cells
Antithyroid agents are sometimes given 10 to 14 days prior to thyroidectomy to decrease bleeding during surgery.

53. Concept Review 31.2
If thyroid hormone is secreted by the thyroid gland, how can a deficiency in this hormone be caused by disease in the hypothalamus or pituitary?

54. Core Concept 31.9
Glucocorticoids are released during periods of stress and influence carbohydrate, lipid, and protein metabolism in most cells.

55. Figure 31.5 Feedback control of the adrenal cortex

56. Core Concept 31.10
Glucocorticoids are prescribed for adrenocortical insufficiency and a wide variety of other conditions.

57. Adrenocortical Insufficiency
Lack of adequate corticosteroid production
Hyposecretion by the adrenal cortex
Inadequate secretion of ACTH from the pituitary
Symptoms:hypoglycemia, fatigue, hypotension, and GI disturbances such as anorexia, vomiting, and diarrhea.

58. Adrenocortical Insufficiency
Primary adrenocortical insufficiency Addison’s disease deficiency of both glucocorticoids and mineralocorticoids.

59. Secondary Adrenocortical Insufficiency
Result from long-term therapy with glucocorticoids.
The pituitary receives a message through the negative feedback mechanism to stop secreting ACTH
Without stimulation from ACTH, the adrenal cortex shrinks in size and stops secreting endogenous glucocorticoids

60. Secondary Adrenocortical Insufficiency
Result from long-term therapy with glucocorticoids.
If a patient abruptly discontinues the glucocorticoid medication, the shrunken adrenal glands will not be able to secrete enough glucocorticoids, and symptoms of adrenocortical insufficiency will appear.

61. Disorders That May Be Treated With Corticosteroids
Allergies,Asthma, Seasonal Rhinitis
Skin disorders - contact dermatitis and rashes
Neoplastic disease Hodgkin’s, leukemia, lymphoma
Shock
Rheumatic disorders rheumatoid arthritis, ankylosing spondylitis, bursitis

62. Disorders That May Be Treated With Corticosteroids
Post-transplant surgery
Chronic inflammatory bowel disease
Adrenal insufficiency
Hepatic, neurological, and renal disorders characterized by edema

64. Concept Review 31.3
Why does administration of glucocorticoids for extended periods result in adrenal atrophy?

65. Core Concept 31.11
Of the many pituitary and hypothalamic hormones, only a few have clinical applications as drugs.

66. Pituitary And Hypothalamic Hormones
Growth hormone somatotropin,
Stimulates the growth of nearly every cell in the body.

67. Pituitary And Hypothalamic Hormones
Antidiuretic hormone (ADH) Vasopressin
Secreted from the posterior pituitary gland
Conserves water in the body
Acts on the collecting ducts in the kidney to increase water reabsorption.
Three preparations
vasopressin (Pitressin), desmopressin (DDAVP, Stimate), and lypressin (Diapid).