session 9: chapter 11 powerpoint presentation

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

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Page 1: Session 9: Chapter 11 PowerPoint Presentation

Lecture Notes

Classroom Activity to Accompany Diseases of the Human Body Fifth EditionCarol D. Tamparo Marcia A. Lewis

11Endocrine System

Diseases and Disorders

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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.

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To keep a lamp burning, we have to keep putting oil in it.

—Mother Teresa

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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

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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

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Hyperpituitarism• Etiology

• Benign slowing growing adenoma in the pituitary gland

• Adenoma releases high levels of hGH

• May also be genetic

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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

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Hyperpituitarism• Diagnostic procedures

• Clinical picture• Glucose tolerance test• MRI and CT scans• Bone x-rays

MRI=magnetic resonance imaging; CT=computed tomography.

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Hyperpituitarism• Treatment

• Surgical management of pituitary tumors

• Radiation to reduce or destroy tumor

• Medication to stop hGH production

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Hyperpituitarism

Complementary therapy•None indicated

Client communication•Explain nature of hormone hypersecretion

•Monitor replacement therapy

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Hyperpituitarism• Prognosis

• Dependent on how the condition has advanced

• For giantism prognosis is good• Advanced acromegaly causes serious complications

• Prevention• None known

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Hyperpituitarism• What gland produces hGH?1. Thyroid2. Pituitary3. Parathyroid4. Adrenal

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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

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Hypopituitarism• Etiology

• Pituitary or hypothalamus tumors• Congenital defect• Pituitary vascular diseases• Iatrogenic

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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

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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

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Hypopituitarism• Treatment

• Hormone replacement therapy with constant monitoring of levels

• Surgical management of pituitary tumors

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Hypopituitarism

Complementary therapy• Manage stress, maintain appropriate weight, eat healthy food, limit fat intake

Client communication• Explain nature of hormone deficits• Monitor replacement therapy

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Hypopituitarism• Prognosis

• Good with hormone replacement• Total loss of all hormonal secretions from anterior pituitary can be fatal

• Prevention• None known

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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

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Diabetes Insipidus• Etiology

• Tumors• Hypophysectomy• Skull fracture• Infection• Idiopathic

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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.

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Diabetes Insipidus• Treatment

• Increased fluid intake• Hormone replacement therapy

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Diabetes InsipidusComplementary therapy

•None

Client communication•Monitor proper fluid balance, weight gain, and recurrence of polyuria

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Diabetes Insipidus• Prognosis

• Depends upon underlying cause, success of treatment

• Normal life with vasopressin replacement therapy

• Prevention• None known

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Diabetes Insipidus• Which hormone is deficient in diabetes insipidus?1. hGH2. Thyroxine3. Prolactin4. Vasopressin

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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 T3, T4

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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

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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 T3, T4 levels normal by radioimmunoassay test

• Biopsy of the nodule

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Simple Goiter• Treatment

• Reduce goiter size• Dietary supplements of iodine• Hormone replacement therapy• Excision, if quite large, followed by lifelong hormone replacement

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Simple GoiterComplementary therapy

• Nutritional supplements• Avoid such goitrogenic foods as cabbage, spinach, peanuts, soybeans, peachesClient communication

• Use iodized salt• Teach clients how to monitor progressive thyroid enlargement

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Simple Goiter• Prognosis

• Good with successful treatment• Hormone replacement therapy may be necessary

• Prevention• Adequate dietary intake of iodine

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Hyperthyroidism (Graves Disease)• Description

• Oversecretion of thyroid hormones causes goiter, ophthalmopathy, dermopathy, thyrotoxicosis

• Affects women more than men

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Hyperthyroidism (Graves Disease)• Etiology

• Oversecretion of thyroid hormones influences metabolism of cells throughout body

• Graves may be genetic but more likely autoimmune

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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

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Hyperthyroidism (Graves Disease)• Diagnostic procedures

• Physical manifestation of disease• Radioimmunoassay to confirm increased levels of T3 and T4; nuclear thyroid scan

• Blood tests showing high levels of antithyroid immunoglobulins

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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

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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

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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

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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

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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

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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

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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

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Hypothyroidism (Cretinism, Myxedema)• Diagnostic procedures

• Radioimmunoassay reveals decreased levels of T3, T4, and elevated TSH

• Thyroid scan shows diminished iodine uptake

• High cholesterol, alkaline phosphates, triglycerides

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Hypothyroidism (Cretinism, Myxedema)• Treatment

• Lifelong hormone replacement therapy

• Infants should begin as soon as possible

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Hypothyroidism (Cretinism, Myxedema)

Complementary Therapy•None

Client Communication•Hormone replacement therapy needs continued monitoring throughout client’s life

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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

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Hypothyroidism (Cretinism, Myxedema)• Cretinism is the result of ____ deficiency of thyroid hormones?1. congenital2. adult3. iatrogenic4. secondary

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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.

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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

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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.

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Hyperparathyroidism (Hypercalcemia)• Diagnostic procedures

• Radioimmunoassay reveals increased serum PTH

• 24-hour urine shows calcium excretion

• Bone mineral density test• CT scan of bone

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Hyperparathyroidism (Hypercalcemia)• Treatment

• Varies with etiology• Goal is to reduce levels of circulating calcium

• Surgery and/or drug therapy

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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

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Hyperparathyroidism (Hypercalcemia)• Prognosis

• Good with successful treatment• Complications include organ damage, coma, cardiac arrest from severe hypercalcemia

• Prevention• None known

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Cushing Disease• Description

• Hypersecretion of the adrenal cortex of the adrenal glands resulting in production of excess cortisol

• More common in females

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Diabetes Mellitus• Description

• Chronic disorder of carbohydrate metabolism, the result of insufficient or inadequate use of insulin

• Causes hyperglycemia, diabetic ketoacidosis

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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

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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

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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

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Diabetes Mellitus• Signs and symptoms

• Polyuria• Glycosuria• Polydipsia• Weight loss; polyphagia

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Diabetes Mellitus• Signs and symptoms (cont.)

• Type 1• Ketoacidosis

• Type 2• May have hard-to-heal infections, blurred vision

• Muscle weakness, fatigue• Often asymptomatic

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Diabetes Mellitus• Diagnostic procedures

• Presenting symptoms• Hemoglobin A1C• Random blood glucose test• Fasting blood glucose test

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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

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Diabetes MellitusComplementary 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

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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

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Diabetes Mellitus• Prevention

• None known• Persons at risk should carefully manage their weight, diet; get plenty of exercise

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Diabetes Mellitus• Type 1 diabetes is the result of ____ not being produced by the pancreas. 1. calcium2. glucagon3. hGH4. insulin

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Credits

Publisher: Margaret BiblisAcquisitions Editor: Andy McPheeDevelopmental Editors: Yvonne Gillam, Julie MundenBackgrounds: Joseph John Clark, Jr.Production Manager: Sam RondinelliSenior Developmental Editor, Electronic Publishing: Kirk PedrickElectronic Publishing: Frank MusickThe 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.