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Lecture Notes Classroom Activity to Accompany Diseases of the Human Body Fifth Edition Carol D. Tamparo Marcia A. Lewis 11 Endocrine System Diseases and.

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Presentation on theme: "Lecture Notes Classroom Activity to Accompany Diseases of the Human Body Fifth Edition Carol D. Tamparo Marcia A. Lewis 11 Endocrine System Diseases and."— Presentation transcript:

1 Lecture Notes Classroom Activity to Accompany Diseases of the Human Body Fifth Edition Carol D. Tamparo Marcia A. Lewis 11 Endocrine System Diseases and Disorders

2 Copyright © 2011 by F.A. Davis Company. All rights reserved. This product is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means—electronic, mechanical, photocopying, recording, or otherwise — without written permission from the publisher.

3 3 To keep a lamp burning, we have to keep putting oil in it. —Mother Teresa

4 4 Common Signs and Symptoms of Endocrine System Diseases and Disorders Mental abnormalities Unusual change in energy level Changes in skin, nails, or hair Muscle atrophy Growth abnormalities Polyuria or polydipsia Cold/heat intolerance Unusual weight gain or loss Nausea and vomiting Irregular menstruation Erectile dysfunction

5 5 Hyperpituitarism Description Hypersecretion of human growth hormone (hGH) by the anterior pituitary gland Giantism results from hypersecretion of hGH during the growing years Acromegaly results from hypersecretion of hGH in adulthood

6 6 Hyperpituitarism Etiology Benign slowing growing adenoma in the pituitary gland Adenoma releases high levels of hGH May also be genetic

7 7 Hyperpituitarism Signs and symptoms Excessive growth of the long bones in giantism Abrupt increases in height Gradual deformation of facial features in acromegaly Enlargement of hands, feet, head, and tongue Sweating, chronic sinus congestion, weakness, joint pain, numbness or tingling

8 8 Hyperpituitarism Diagnostic procedures Clinical picture Glucose tolerance test MRI and CT scans Bone x-rays MRI=magnetic resonance imaging; CT=computed tomography.

9 9 Hyperpituitarism Treatment Surgical management of pituitary tumors Radiation to reduce or destroy tumor Medication to stop hGH production

10 10 Hyperpituitarism Complementary therapy None indicated Client communication Explain nature of hormone hypersecretion Monitor replacement therapy

11 11 Hyperpituitarism Prognosis Dependent on how the condition has advanced For giantism prognosis is good Advanced acromegaly causes serious complications Prevention None known

12 12 Hyperpituitarism What gland produces hGH? 1. Thyroid 2. Pituitary 3. Parathyroid 4. Adrenal

13 13 Hypopituitarism Description Commonly, gonadotropin and hGH are deficient in anterior pituitary Complex disorder causes metabolic dysfunction, sexual immaturity, growth retardation in childhood Can result in hyposecretion of essential “ target gland ” hormones

14 14 Hypopituitarism Etiology Pituitary or hypothalamus tumors Congenital defect Pituitary vascular diseases Iatrogenic

15 15 Hypopituitarism Signs and symptoms Depend upon age of client, deficient hormones May be dwarfism in children Slow emergence of secondary sexual characteristics Amenorrhea Infertility Decreased libido Loss of body hair in adults Fatigue, weakness, anorexia

16 16 Hypopituitarism Diagnostic procedures Clinical history Laboratory tests to measure pituitary and “ target ” gland hormone levels will confirm diagnosis CT scan, MRI to pinpoint tumors or lesions

17 17 Hypopituitarism Treatment Hormone replacement therapy with constant monitoring of levels Surgical management of pituitary tumors

18 18 Hypopituitarism Complementary therapy Manage stress, maintain appropriate weight, eat healthy food, limit fat intake Client communication Explain nature of hormone deficits Monitor replacement therapy

19 19 Hypopituitarism Prognosis Good with hormone replacement Total loss of all hormonal secretions from anterior pituitary can be fatal Prevention None known

20 20 Diabetes Insipidus Description Kidneys are unable to conserve water Insufficient secretion of vasopressin by the posterior pituitary gland Failure of the kidney to respond to vasopressin Affects men more than women; usually starts in childhood

21 21 Diabetes Insipidus Etiology Tumors Hypophysectomy Skull fracture Infection Idiopathic

22 22 Diabetes Insipidus Signs and symptoms Polyuria (4 to 16 liters of urine in 24 hours) Polydipsia Dehydration, weakness, mental confusion Diagnostic procedures UA Dehydration test to rule out other diseases UA=urine analysis.

23 23 Diabetes Insipidus Treatment Increased fluid intake Hormone replacement therapy

24 24 Diabetes Insipidus Complementary therapy None Client communication Monitor proper fluid balance, weight gain, and recurrence of polyuria

25 25 Diabetes Insipidus Prognosis Depends upon underlying cause, success of treatment Normal life with vasopressin replacement therapy Prevention None known

26 26 Diabetes Insipidus Which hormone is deficient in diabetes insipidus? 1. hGH 2. Thyroxine 3. Prolactin 4. Vasopressin

27 27 Simple Goiter Description Enlarged thyroid not caused by infection or neoplasm Endemic or sporadic More common in women Thyroid enlarges when it cannot secrete enough of thyroid hormones T 3, T 4

28 28 Simple Goiter Etiology Endemic goiter result of insufficient intake of iodine Sporadic goiter follows ingestion of certain drugs or foods Usually occurs in females over age 40 with a family history May be idiopathic

29 29 Simple Goiter Signs and symptoms May appear as small nodule or large, swollen mass at front of neck Diagnostic procedures Rule out other diseases Enlarged thyroid gland with T 3, T 4 levels normal by radioimmunoassay test Biopsy of the nodule

30 30 Simple Goiter Treatment Reduce goiter size Dietary supplements of iodine Hormone replacement therapy Excision, if quite large, followed by lifelong hormone replacement

31 31 Simple Goiter Complementary therapy Nutritional supplements Avoid such goitrogenic foods as cabbage, spinach, peanuts, soybeans, peaches Client communication Use iodized salt Teach clients how to monitor progressive thyroid enlargement

32 32 Simple Goiter Prognosis Good with successful treatment Hormone replacement therapy may be necessary Prevention Adequate dietary intake of iodine

33 33 Hyperthyroidism (Graves Disease) Description Oversecretion of thyroid hormones causes goiter, ophthalmopathy, dermopathy, thyrotoxicosis Affects women more than men

34 34 Hyperthyroidism (Graves Disease) Etiology Oversecretion of thyroid hormones influences metabolism of cells throughout body Graves may be genetic but more likely autoimmune

35 35 Hyperthyroidism (Graves Disease) Signs and symptoms Goiter Exophthalmos that may interfere with eye blinking Thickened patches of skin on feet or legs Nervousness, anxiety Loss of sleep Excessive perspiration, heat intolerance Muscle wasting, bone decalcification Cardiac problems

36 36 Hyperthyroidism (Graves Disease) Diagnostic procedures Physical manifestation of disease Radioimmunoassay to confirm increased levels of T 3 and T 4 ; nuclear thyroid scan Blood tests showing high levels of antithyroid immunoglobulins

37 37 Hyperthyroidism (Graves Disease) Treatment Dependent upon client ’ s age, sex, severity of disease Goal: to block thyroid hormone production with surgery or radioactive iodine therapy Short-term use of iodide compounds

38 38 Hyperthyroidism (Graves Disease) Complementary therapy Same as for goiter Cool compresses and eye drops for exophthalmos Hydrocortisone creams for dermopathy Client communication Teach clients to recognize symptoms of hypothyroidism that may result from drug therapy Drug and iodide compound therapy require monitoring

39 39 Hyperthyroidism (Graves Disease) Prognosis Varies; if treatment results in disease remission, prognosis is good Potentially fatal complication thyroid storm (medical emergency) that results from severe thyrotoxicosis Prevention None known

40 40 Hypothyroidism (Cretinism, Myxedema) Description Undersecretion of thyroid hormones Cretinism result of congenital deficiency of hormones Myxedema result of deficiency of hormones in childhood or adulthood Affects women more than men

41 41 Hypothyroidism (Cretinism, Myxedema) Etiology Insufficiency or loss of thyroid tissue Iatrogenic due to surgery, radioactive iodine therapy or congenital abnormality Common causes are inflammation and chronic autoimmune and Hashimoto thyroiditis Dietary or metabolic iodine deficiencies

42 42 Hypothyroidism (Cretinism, Myxedema) Signs and symptoms In neonate constipation and feeding problems Brain and skeleton fail to develop Retarded growth, impaired intelligence, delayed secondary sexual characteristics

43 43 Hypothyroidism (Cretinism, Myxedema) Signs and symptoms (cont. ) In children, there may be a hoarse cry, sleeping too much, feeding problems; in adults, symptoms insidious Fatigue, constipation, intolerance to cold, muscle cramps Later symptoms include mental clouding, diminished appetite and weight gain, dry skin, brittle hair and nails

44 44 Hypothyroidism (Cretinism, Myxedema) Diagnostic procedures Radioimmunoassay reveals decreased levels of T 3, T 4, and elevated TSH Thyroid scan shows diminished iodine uptake High cholesterol, alkaline phosphates, triglycerides

45 45 Hypothyroidism (Cretinism, Myxedema) Treatment Lifelong hormone replacement therapy Infants should begin as soon as possible

46 46 Hypothyroidism (Cretinism, Myxedema) Complementary Therapy None Client Communication Hormone replacement therapy needs continued monitoring throughout client ’ s life

47 47 Hypothyroidism (Cretinism, Myxedema) Prognosis Good with successful replacement therapy Myxedema coma is a life-threatening complication Prevention Only hypothyroidism due to dietary deficiency, radiation, or surgical removal of the thyroid, and drug-induced forms are preventable

48 48 Hypothyroidism (Cretinism, Myxedema) Cretinism is the result of ____ deficiency of thyroid hormones? 1. congenital 2. adult 3. iatrogenic 4. secondary

49 49 Hyperparathyroidism (Hypercalcemia) Description General disorder of calcium, phosphorus metabolism High levels of PTH cause hypophosphatemia, hypercalcemia Affects women twice as much as men PTH = parathyroid hormone.

50 50 Hyperparathyroidism (Hypercalcemia) Etiology Excessive secretion of PTH Primary cause is adenoma of a parathyroid gland Secondary causes include chronic renal failure, dietary insufficiency of calcium or Vitamin D, tuberculosis, and sarcoidosis

51 51 Hyperparathyroidism (Hypercalcemia) Signs and symptoms Gradual onset Clients may remain asymptomatic Weak, brittle bones Joint pain Kidney stones Polyuria CNS disturbances Chronic fatigue CNS = central nervous system.

52 52 Hyperparathyroidism (Hypercalcemia) Diagnostic procedures Radioimmunoassay reveals increased serum PTH 24-hour urine shows calcium excretion Bone mineral density test CT scan of bone

53 53 Hyperparathyroidism (Hypercalcemia) Treatment Varies with etiology Goal is to reduce levels of circulating calcium Surgery and/or drug therapy

54 54 Hyperparathyroidism (Hypercalcemia) Complementary therapy Monitor calcium and vitamin D supplements Avoid smoking Client communication Teach client about disease and its treatment Stress importance of follow-up care

55 55 Hyperparathyroidism (Hypercalcemia) Prognosis Good with successful treatment Complications include organ damage, coma, cardiac arrest from severe hypercalcemia Prevention None known

56 56 Cushing Disease Description Hypersecretion of the adrenal cortex of the adrenal glands resulting in production of excess cortisol More common in females

57 57 Diabetes Mellitus Description Chronic disorder of carbohydrate metabolism, the result of insufficient or inadequate use of insulin Causes hyperglycemia, diabetic ketoacidosis

58 58 Diabetes Mellitus Description Four types Immune-mediated type 1 diabetes: abrupt onset; occurs prior to age 30; complete absence of insulin secretion Type 2 diabetes: gradual onset; most common form; occurs after age of 40; pancreas has some insulin-secreting ability

59 59 Diabetes Mellitus Description ( cont.) Gestational diabetes (GDM): develops during pregnancy; resolves after delivery; increased risk to type 2 diabetes later Other types of diabetes: caused by pancreatic dysfunction as the result of drugs, chemicals, infections

60 60 Diabetes Mellitus Etiology Cause of types 1 and 2 diabetes are unknown Type 1 may be autoimmune disorder; type 2 may be genetic Type 2 risk factors are obesity, sedentary lifestyle, family member with diabetes Other types of diabetes are related to specific conditions

61 61 Diabetes Mellitus Signs and symptoms Polyuria Glycosuria Polydipsia Weight loss; polyphagia

62 62 Diabetes Mellitus Signs and symptoms (cont.) Type 1 Ketoacidosis Type 2 May have hard-to-heal infections, blurred vision Muscle weakness, fatigue Often asymptomatic

63 63 Diabetes Mellitus Diagnostic procedures Presenting symptoms Hemoglobin A1C Random blood glucose test Fasting blood glucose test

64 64 Diabetes Mellitus Treatment Diet and exercise helpful for most forms Type 1 = glucose monitoring and insulin management Type 2 = diet; may require insulin therapy Self-management of disease important

65 65 Diabetes Mellitus Complementary therapy Diet high in complex carbohydrates, fiber, and whole grains Exercise Client communication Teach clients how to monitor blood sugar levels Advise clients to pay special attention to their teeth and feet

66 66 Diabetes Mellitus Prognosis With early diagnosis, successful treatment, few complications, prognosis is good Complications can be acute, resulting in diabetic coma or insulin shock; both are life threatening Complications may come late in disease process, affecting nearly every body organ

67 67 Diabetes Mellitus Prevention None known Persons at risk should carefully manage their weight, diet; get plenty of exercise

68 68 Diabetes Mellitus Type 1 diabetes is the result of ____ not being produced by the pancreas. 1. calcium 2. glucagon 3. hGH 4. insulin

69 69 Credits Publisher: Margaret Biblis Acquisitions Editor: Andy McPhee Developmental Editors: Yvonne Gillam, Julie Munden Backgrounds: Joseph John Clark, Jr. Production Manager: Sam Rondinelli Senior Developmental Editor, Electronic Publishing: Kirk Pedrick Electronic Publishing: Frank Musick The publisher is not responsible for errors of omission or for consequences from application of information in this presentation, and makes no warranty, expressed or implied, in regard to its content. Any practice described in this presentation should be applied by the reader in accordance with professional standards of care used with regard to the unique circumstances that may apply in each situation.


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