Chapter 11 Care of the Patient with an Endocrine Disorder Mosby items and derived items © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Chapter 11Chapter 11

Care of the Patient with

an Endocrine Disorder

Overview of Anatomy and PhysiologyOverview of Anatomy and Physiology

• Endocrine glands and hormones The endocrine system is composed of a series of

ductless glands It communicates through the use of hormones

• Hormones are chemical messengers that travel though the bloodstream to their target organ

*Exocrine=glands that secrete through ducts (sebaceous, sudoriferous)

*Endocrine= ductless glands; release secretions directly into bloodstream

• Works closely with nervous system

• Both control homeostasis

• Small amount of hormone is very powerful

• Too much or too little of one hormone can affect other hormones (interrelated)

• Controlled by negative feedback system

• Information continually exchanged between target organ and pituitary gland

• Pituitary gland—“master gland”; works closely with hypothalamus Anterior pituitary gland (6 hormones)

• TSH (growth and secretion of thyroid)

• FSH (growth of ovarian follicle, production of estrogen in females, and production of sperm in males)

• GH (also called somatropic hormone; accelerates the growth of the body)

• ACTH (growth and secretion of adrenal cortex)

• LH (stimulates ovulation and formation of corpus luteum in menstruation cycle)

• PROLACTIN (secretion of milk and influences maternal behavior)

Posterior PituitaryPosterior Pituitary

Posterior pituitary gland (2 hormones)• Oxytocin (maintains water balance by increasing the reabsorption

of water by the kidneys)

• ADH (vasopressin) maintains water balance by increasing the reabsorption of water by the kidneys.

Categorized Based on Function:

• TROPIC- target other endocrine structures to increase their growth and secretions

• SEX- influence reproductive changes

• ANABOLIC- stimulate the process of building tissues.

• Thyroid gland Butterfly shaped Thyroxine (T3), Triiodothronine (T4), Calcitonin Requires iodine for function Control metabolism, growth and development,

nervous system activity Controlled by TSH released by pituitary gland

• Parathyroid gland 4 glands in posterior surface of thyroid PTH; regulates Ca and PhosphorusCalcium: > levels=impaired heart fx, cardiac arrest

<levels=excitability of nerve cells; increased muscle stimulation; tetany

• Adrenal gland Adrenal cortex; outer section

• 3 layers; each secrete hormone (steroid) Mineralocorticoids, glucocorticoids, sex hormones

Adrenal medulla; middle section• Epinephrine (adrenaline), norepinephrine

• Pancreas Exocrine and endocrine functions Insulin and glucagon

Figure 11-2Figure 11-2

Pituitary hormones.

(From Thibodeau, G.A., Patton, K.T. [2008]. Structure and function of the body. [13th ed.]. St. Louis: Mosby.)

• Female sex glands Ovaries; estrogen & progesterone Placenta; releases estrogen & progesterone during

pregnancy

• Male sex glands Testes; testosterone

• Thymus gland Thymosin; assists with immunity during infancy

• Pineal gland Melatonin; biological clock & inhibits gonadotropic

activity

Location of the endocrine glands in the female and male bodies.

(From Thibodeau, G.A., Patton, K.T. [2008]. Structure and function of the body. [13th ed.]. St. Louis: Mosby.)

Disorders of the Pituitary GlandDisorders of the Pituitary Gland

• Acromegaly Etiology/pathophysiology

• Overproduction of growth hormone in the adult

• Causes Idiopathic hyperplasia of the anterior pituitary gland Tumor growth in the anterior pituitary gland

• Changes are irreversible

• Acromegaly (continued) Clinical manifestations/assessment

• Enlargement of the cranium and lower jaw

• Separation and malocclusion of the teeth

• Bulging forehead

• Bulbous nose

• Thick lips; enlarged tongue; hypertrophy of vocal cords

• Generalized coarsening of the facial features

• Enlarged hands and feet

• Enlarged heart, liver, and spleen

• Acromegaly (continued) Clinical manifestations/assessment (continued)

• Muscle weakness

• Hypertrophy of the joints with pain and stiffness

• Males—impotence

• Females—deepened voice, increased facial hair, amenorrhea

• Partial or complete blindness with pressure on the optic nerve due to tumor

• Severe headaches common

Right: Coarse facial features typical of acromegaly. Left: Patient’s

face several years before she developed the pituitary tumor.

(Courtesy of the Group for Research in Pathology Education.)

AcromegalyAcromegaly

• Assessment Subjective; pain, visual disturbances, emotional

reactions Objective data; monitor bone enlargement, joint

involvement, vital signs, s/s heart failure

• Diagnosis CT, MRI, cranial radiographic evaluation Complete ophthalmic exam to determine damage to

optic nerve, Lab tests: serum GH level, oral GTT (GH usually falls

during challenge but not in acromegaly)

• Acromegaly (continued) Medical management/nursing interventions

• Pharmacological management

• Given to suppress GH release Parlodel Sandostatin Analgesics

• Cryosurgery (application of extreme cold)

• Transsphenoidal removal of tissue

• Proton beam therapy (radiation)

• Soft, easy-to-chew diet

• Prognosis: changes irreversible; prone to complications

• Gigantism Etiology/pathophysiology

• Overproduction of growth hormone

• Caused by hyperplasia of the anterior pituitary gland

• Occurs in a child before closure of the epiphyses

• Results in overgrowth of long bones

• Gigantism (continued) Clinical manifestations/assessment

• Great height

• Increased muscle and visceral development

• Increased weight

• Normal body proportions

• Weakness

GigantismGigantism

Assessment• Subjective; patient’s understanding of disease

process/ability to verbalize emotional responses

• Objective; frequent height measurement, use of adaptive coping mechanisms/family interactions

Diagnosis• GH suppression test (glucose loading test); baseline

GH levels high Medical management/nursing interventions

• Surgical removal of tumor

• Irradiation of the anterior pituitary gland

Prognosis: shorter than average life span

• Dwarfism Etiology/pathophysiology

• Deficiency in growth hormone; usually idiopathic

• Some cases attributed to autosomal recessive trait Clinical manifestations/assessment

• Abnormally short height

• Normal body proportion

• Appear younger than age

• Dental problems due to underdeveloped jaws

• Delayed sexual development`

• Assessment Subjective; pt’s understanding of disease process; emotional

response Objective; regular ht/wt measurement

• Diagnostic tests Radiographic evaluation of wrist for bone age & MRI/CT scan to

r/o pituitary tumor Plasma GH levels (will be decreased)

• Medical management/nursing interventions• Growth hormone injections• Removal of tumor, if present• Major issues with self-esteem• Prognosis: normal life span; prone to

musculoskeletal/cardiovascular problems

• Diabetes insipidus Etiology/pathophysiology

• Transient or permanent metabolic disorder of the posterior pituitary

• Deficiency of antidiuretic hormone (ADH)

• Primary or secondary

• Significant electrolyte and fluid imbalances

• Diabetes insipidus Clinical manifestations/assessment

• Polyuria; polydipsia• May become severely dehydrated• Lethargic• Dry skin; poor skin turgor• Constipation

Assessment• Subjective; embarrassment, not restricting fluids• Objective; skin turgor, I&O, urine color, daily weight

Diagnosis• Urine ADH measurement, urine specific gravity, urine

output, serum Na levels

Diabetes InsipidusDiabetes Insipidus

Medical management/nursing interventions• ADH preparations

• Limit caffeine due to diuretic properties

• Prognosis: dependant on etiology, usually dependant on medication for life, constant medical monitoring since condition may worsen with time

Disorders of the Thyroid and Parathyroid GlandsDisorders of the Thyroid and Parathyroid Glands

• Hyperthyroidism Etiology/pathophysiology

• Also called Graves’ disease, exophthalmic goiter, and thyrotoxicosis

• Overproduction of the thyroid hormones

• Exaggeration of metabolic processes

• Exact cause unknown

• Hyperthyroidism (continued) Clinical manifestations/assessment

• Edema of the anterior portion of the neck

• Exophthalmos

• Inability to concentrate; memory loss

• Dysphagia

• Hoarseness

• Increased appetite

• Weight loss

• Nervousness

• Hyperthyroidism (continued) Clinical manifestations/assessment (continued)

• Insomnia

• Tachycardia; hypertension

• Warm, flushed skin

• Fine hair

• Amenorrhea

• Elevated temperature

• Diaphoresis

• Hand tremors

HyperthyroidismHyperthyroidism

• Assessment Subjective: inability to concentrate, memory loss,

feelings of nervousness, jittery, insomnia Objective: rapid pulse, high BP, skin warm/flushed,

amenorrhea, hyperactivity, clumsiness, weight loss

• Diagnosis Decrease in TSH levels & elevated T3, T4 Elevated iodine uptake test

• Hyperthyroidism (continued) Medical management/nursing interventions

• Pharmacological management Propylthiouracil (PTU) Methimazole (Tapazole) Block production of thyroid hormones

• Radioactive iodine (ablation therapy)

• Subtotal thyroidectomy

• Hyperthyroidism (continued) Medical management/nursing interventions

(continued)• Postoperative

Voice rest; voice checks Avoid hyperextension of the neck Tracheotomy tray at bedside Assess for signs and symptoms of internal and external

bleeding Assess for tetany

o Chvostek’s and Trousseau’s signs Assess for thyroid crisis Prognosis: normal life expectancy; may develop

hypothyroidism due to treatment

• Hypothyroidism Etiology/pathophysiology

• Insufficient secretion of thyroid hormones

• Slowing of all metabolic processes

• Failure of thyroid or insufficient secretion of thyroid-stimulating hormone from pituitary gland

• Hypothyroidism (continued) Clinical manifestations/assessment

• Hypothermia; intolerance to cold

• Weight gain

• Depression

• Impaired memory; slow thought process

• Lethargic

• Anorexia

• Constipation

• Hypothyroidism (continued) Clinical manifestations/assessment

• Decreased libido

• Menstrual irregularities

• Thin hair

• Skin thick and dry

• Enlarged facial appearance

• Low, hoarse voice

• Bradycardia

• Hypotension

HypothyroidismHypothyroidism

• Assessment Subjective: depression, paranoia, impaired memory,

irritability, coping mechanisms Objective: skin, hair, facial features, voice,

bradycardia, decreased BP, weakness, menorrhagia

• Diagnosis Physical exam Lab tests: TSH, T3, T4,

• Hypothyroidism (continued) Medical management/nursing interventions

• Pharmacological management Synthroid Levothyroid Proloid Cytomel

• Symptomatic treatment

• Prognosis: require medication for life

• Simple goiter Etiology/pathophysiology

• Enlarged thyroid due to low iodine levels

• Enlargement is caused by the accumulation of colloid in the thyroid follicles

• Usually caused by insufficient dietary intake of iodine

• Simple goiter (continued) Clinical manifestations/assessment

• Enlargement of the thyroid gland• Dysphagia• Hoarseness• Dyspnea

Assessment Medical management/nursing interventions

• Pharmacological management Potassium iodide

• Diet high in iodine• Surgery—thyroidectomy• Prognosis: normal life expectancy

Simple goiter.

(Courtesy of L. V. Bergman & Associates, Inc., Cold Springs, New York.)

• Cancer of the thyroid Etiology/pathophysiology

• Malignancy of thyroid tissue; very rare Clinical manifestations/assessment

• Firm, fixed, small, rounded mass or nodule on thyroid Assessment Diagnosis; thyroid needle biopsy Medical management/nursing interventions

• Total thyroidectomy• Thyroid hormone replacement• If metastasis is present: radical neck dissection;

radiation, chemotherapy, and radioactive iodine• Prognosis: dependant on tumor type

• Hyperparathyroidism Etiology/pathophysiology

• Overactivity of the parathyroid, with increased production of parathyroid hormone

• Hypertrophy of one or more of the parathyroid glands

• Hyperparathyroidism (continued) Clinical manifestations/assessment

• Hypercalcemia

• Skeletal pain; pain on weight-bearing

• Pathological fractures

• Kidney stones

• Fatigue

• Drowsiness

• Nausea

• Anorexia

• Hyperparathyroidism (continued) Assessment Diagnosis

• X-ray-skeletal decalcification; PTH increased, serum phosphorus low, calcium high

Medical management/nursing interventions• Removal of tumor

• Removal of one or more parathyroid glands

• Prognosis: good with proper treatment unless due to carcinoma

• Hypoparathyroidism Etiology/pathophysiology

• Decreased parathyroid hormone

• Decreased serum calcium levels

• Inadvertent removal or destruction of one or more parathyroid glands during thyroidectomy

• Hypoparathyroidism (continued) Clinical manifestations/assessment

• Neuromuscular hyperexcitability

• Involuntary and uncontrollable muscle spasms

• Tetany

• Laryngeal spasms

• Stridor

• Cyanosis

• Parkinson-like syndrome

• Chvostek’s and Trousseau’s signs

• Hypoparathyroidism (continued) Assessment Diagnosis

• Decreased serum calcium and PTH, increased serum phosphorus

Medical management/nursing interventions• Pharmacological management

Calcium gluconate or intravenous calcium chloride

• Vitamin D

• Prognosis: fairly normal lifestyle and expectancy

Disorders of the Adrenal GlandsDisorders of the Adrenal Glands

• Adrenal hyperfunction (Cushing’s syndrome) Etiology/pathophysiology

• Plasma levels of adrenocortical hormones are increased

• Hyperplasia of adrenal tissue due to overstimulation by the pituitary gland

• Tumor of the adrenal cortex

• Adrenocorticotropic hormone (ACTH) secreting tumor outside the pituitary

• Overuse of corticosteroid drugs

• Adrenal hyperfunction (Cushing’s syndrome) (continued) Clinical manifestations/assessment

• Moonface

• Buffalo hump

• Thin arms and legs

• Hypokalemia; proteinuria

• Increased urinary calcium excretion

• Susceptible to infections

• Depression

• Loss of libido

• Adrenal hyperfunction (Cushing’s syndrome) (continued) Clinical manifestations/assessment

• Ecchymoses and petechiae

• Weight gain

• Abdominal enlargement

• Hirsutism in women

• Menstrual irregularities

• Deepening of the voice

• Adrenal hyperfunction (Cushing’s syndrome) (continued) Assessment Diagnosis

• Clinical appearance and lab tests; high cortisol levels, CT/ultrasound to r/o adrenal/pituitary tumor

Medical management/nursing interventions• Treat causative factor

Adrenalectomy for adrenal tumor Radiation or surgical removal for pituitary tumors

• Lysodren• Dietary recommendations:

Low-sodium High-potassium

• Adrenal hypofunction (Addison’s disease) Etiology/pathophysiology

• Adrenal glands do not secrete adequate amounts of glucocorticoids and mineralocorticoids

• May result from Adrenalectomy Pituitary hypofunction Long-standing steroid therapy

• Adrenal hypofunction (Addison’s disease) (continued) Clinical manifestations/assessment

• Usually not detected until 90% cortex destroyed

• Related to imbalances of hormones, nutrients, and electrolytes

• Nausea; anorexia

• Postural hypotension

• Headache

• Disorientation

• Abdominal pain; lower back pain

• Anxiety

• Adrenal hypofunction (Addison’s disease) (continued) Clinical manifestations/assessment

• Darkly pigmented skin and mucous membranes

• Weight loss

• Vomiting

• Diarrhea

• Hypoglycemia

• Hyponatremia

• Hyperkalemia

• Assess for adrenal crisis

• Adrenal hypofunction (Addison’s disease) (continued) Assessment Diagnosis

• Decreased serum Na, increased K+, decreased glucose, cortisol/aldosterone levels low

Treatment• Restore fluid and electrolyte balance• Replacement of adrenal hormones• Diet high in sodium and low in potassium• Adrenal crisis

IV corticosteroids in a solution of saline and glucose Prognosis: fair with proper treatment

• Pheochromocytoma Etiology/pathophysiology

• Chromaffin cell tumor; usually found in the adrenal medulla

• Causes excessive secretion of epinephrine and norepinephrine

Clinical manifestations/assessment• Hypertension

Diagnosis: urinary metanephrines (catecholamine metabolites) elevated

Medical management/nursing interventions• Surgical removal of tumor

Disorders of the PancreasDisorders of the Pancreas

• Diabetes mellitus Etiology/pathophysiology

• A systemic metabolic disorder that involves improper metabolism of carbohydrates, fats, and proteins

• Insulin deficiency

• Risk factors Heredity Environment and lifestyle Viruses Malignancy or surgery of pancreas

• Diabetes mellitus (continued) Types of diabetes mellitus

• Type I—insulin dependent (IDDM)

• Type II—non-insulin dependent (NIDDM) Clinical manifestations/assessment

• Type I and type II “3 Ps”

o Polyuriao Polydipsiao Polyphagia

• Diabetes mellitus (continued) Clinical manifestations/assessment (continued)

• Type I Sudden onset Weight loss Hyperglycemia Under 40 years old

• Diabetes mellitus (continued) Clinical manifestations/assessment (continued)

• Type II Slow onset May go undetected for years “3 Ps” are usually mild If untreated, may have skin infections and arteriosclerotic

conditions

• Diabetes mellitus (continued) Diagnostic tests

• Fasting blood glucose (FBG)

• Oral glucose tolerance test (OGTT)

• 2-hour postprandial blood sugar

• Patient self-monitoring of blood glucose (SMBG)

• Glycosylated hemoglobin (HbA1c)

• C-peptide test

• Diabetes mellitus (continued) Medical management/nursing interventions

• Diet A goal of nutritional therapy is to achieve a blood glucose

level of <126 mg/dL Balanced diet should include proteins, carbohydrates,

and fats Type II—may be controlled by diet alone Type I—diet is calculated and then the amount of insulin

required to metabolize it is established

(continued)• Diet (continued)

American Diabetes Association (ADA) dieto Seven exchangeso Quantitative diet

Need three regular meals with snacks between meals and at bedtime to maintain constant glucose levels

(continued)• Exercise

Promotes movement of glucose into the cell Lowers blood glucose Lowers insulin needs

• Stress of acute illness and surgery Extra insulin may be required Increased risk of ketoacidosis (hyperglycemia) Glucose must be monitored closely

(continued)• Medications

Insulino Classified by action: Regular; Lente and NPH;

Ultralenteo Classified by type: beef/pork: Humulin/Novolino Injection sites should be rotated to prevent scar

tissue formationo Sliding scale

A, Rotation of sites for insulin injections.

B, Injection diagram to track rotation of injection sites.

(From Potter, P.A., Perry, A.G. [2003]. Basic nursing: essentials for practice. [5th ed.]. St. Louis: Mosby.)

(continued)• Medications

Oral hypoglycemic agentso Stimulate islet cells to secrete more insulino Only for type II diabetes mellitus

(continued)• Patient teaching

Good skin care Report any skin abnormalities to physician Special foot care is crucial

o Do not trim toenails—go to podiatristo No hot water bottles or heating pads

Assess for symptoms of hypoglycemia

(continued)• Acute complications

Comao Diabetic ketoacidosiso Hyperglycemic hyperosmolar nonketotico Hypoglycemic reaction

Infection

(continued)• Long-term complications

Diabetic retinopathy Cardiovascular problems Renal failure

Nursing ProcessNursing Process

• Nursing diagnoses Knowledge, deficient Self-esteem, risk for situational low Sensory and perceptual alterations: visual Fluid volume, deficient, risk for Infection, risk for Sexual dysfunction Body image, disturbed Coping, ineffective Nutrition, imbalanced Activity intolerance

Chapter 21

Hormones and Steroids

Chapter 21

Lesson 21.1

Learning Objectives

Describe the use of antidiabetic medications Identify preparations that act on the uterus

Overview

Hormones and steroids Natural and synthetic preparations Used to replace and/or increase natural

chemicals in the body

Endocrine System

Regulation and coordination of body systems Endocrine glands Pituitary, thyroid, parathyroid, adrenal glands,

pancreas, testes, ovaries, and placenta

Endocrine System

Male Reproductive System

Female Reproductive System

Antidiabetic Drugs

Diabetes mellitus: chronic disorder of metabolism

Insulin: necessary for the metabolism and use of glucose in the body

Pancreas Type 1 and type 2 diabetes

Insulin

Action Lowers blood glucose levels by helping

glucose move into target tissuesUses Treatment of type 1 diabetesTable 21-1

Insulin (cont.)

Adverse Reactions Lipodystrophy, local itching, swelling, erythema Hypoglycemia: serum glucose less than 60

mg/dLDrug Interactions Insulin antagonists Anabolic steroids and alcohol may increase the

hypoglycemic effects of insulin

Insulin (cont.)

Nursing Implications Assessment: polyuria, polyphagia, polydipsia,

weight loss, blurred vision, and fatigue Hyperglycemia: systemic acidosis Conditions that alter requirements for insulin

Patient Teaching

Oral Hypoglycemics

Action Stimulate insulin release from pancreatic beta cells;

decrease insulin resistanceUses Monotherapy versus combination therapy Six classes

Sulfonylureas, 1st and 2nd generation Biguanides Alpha-glucosidase inhibitors Meglitinides Thiazolidinediones Incretins

Oral Hypoglycemics (cont.)

Adverse Reactions Hypoglycemia; allergic reactions

Drug Interactions Displacement; potentiation Thiazides oppose the secretion of insulin

from beta cells and decrease the effectiveness of sulfonylureas

Oral Hypoglycemics (cont.)

Nursing Implications Assessment: health history; renal and liver

function; sulfa allergies

Patient Teaching

Selected Drugs Used with Pregnancy and Delivery

Overview Antepartum, intrapartum, and postpartum

Tocolytics Oxytocics Uterine relaxants Abortifacients

Drug Table 21-4

Selected Drugs Used with Pregnancy and Delivery (cont.)

Action and Uses Abortifacients stimulate uterine contractions and

cause the uterus to empty Oxytocic agents and ergot preparations cause

the uterus to contract Uterine relaxants act on beta-adrenergic

receptors to stop smooth-muscle contraction in the uterus

Tocolytics are used to stop preterm labor

Adverse Reactions Abortifacients: cramping and pain Tocolytics: visual disturbance, malaise, nausea, and

confusion Oxytocics: dysrhythmias, edema, fetal bradycardia,

anxiety, redness of skin during administration, nausea, vomiting, anaphylaxis, postpartum hemorrhage, cyanosis, and dyspnea

Ergots: nausea and vomiting, allergic reactions, bradycardia, hypotension, hypertension, cerebrospinal symptoms, and spasms

Drug Interactions Vasoconstrictors and local anesthetics

increase the effectiveness of oxytocics

Nursing Implications and Patient Teaching Assessment Diagnosis Planning Implementation: nursing care and monitoring

during drug administration Evaluation Patient and family teaching: adverse effects of

ergonovine

Question 1

____________________ are chemicals that are made in an organ or gland and carried through the bloodstream to another part of the body.

1. Steroids2. Hormones3. Androgens4. Estrogens

Question 2

Which of the following are NOT part of the endocrine system?

1. Pituitary gland2. Adrenal glands3. Placenta4. Sweat glands

Question 3

A lack of insulin can increase the production of free fatty acids. There may be an increase in glucagon and other hormones and a decrease in pH. This is called:

1. Lipodystrophy.2. Ketoacidosis.3. Hyperglycemia.4. Hypoglycemia.

Chapter 21

Lesson 21.2

Learning Objectives

Compare and contrast the action of adrenal and pituitary hormones

Describe at least five adverse reactions that may result from the use of glucocorticoid and mineralocorticoid steroids

Compare the actions of various male and female hormones

List the indications for the use of thyroid preparations

Pituitary and Adrenocortical Hormones

Pituitary gland: “master gland” Adenohypophysis Neurohypophysis Hormone production, control growth,

electrolyte balance, water retention or loss, and reproductive cycle

Pituitary Hormones

Anterior Pituitary Hormones HCG LH and FSH STH ACTH

Drug Table 21-5

Anterior Pituitary Hormones (cont.)

Adverse Reactions (systemic or local reaction) Menotropins: enlarged ovaries; multiple births when

used for fertilization Clomiphene: abdominal discomfort, ovarian

enlargement, blurred vision, nervousness, nausea and vomiting, vasomotor flushes

Chorionic gonadotropins: headache, irritability, restlessness, fatigue, and edema

Somatotropin: antibody stimulation ACTH: adrenal gland

Posterior Pituitary Hormones

ADH Vasopressin may cause abdominal cramps,

anaphylaxis, bronchial constriction, circumoral pallor, diarrhea, flatus, intestinal hyperactivity, headache, sweating, tremors, urticaria, uterine cramps, vertigo, vomiting; large doses may produce death

Oxytocin ACTH Drug Table 21-6

Adrenocortical Hormones

Actions Manufactures glucocorticoids,

mineralocorticoids, and small amounts of sex hormones

Uses Adrenal insufficiency (Addison disease) Reduce inflammation in allergic or

immunologic responses; treat hematologic and malignant diseases

Adrenocortical Hormones (cont.)

Adverse Reactions Table 21-7Drug Interactions Increase effects of barbiturates, sedatives,

narcotics, and certain anticoagulants Decrease effects of insulin, oral

hypoglycemics, Coumadin, isoniazid, aspirin, and broad-spectrum antibiotics

Adrenocortical Hormones (cont.)

Nursing Implications and Patient Teaching Frequent medical monitoring Avoid smoking Alcohol use: ulcer development Risk for infection Increase dose during times of stress Signs and symptoms of adrenal insufficiency Do not stop drug abruptly MedicAlert bracelet Immunization considerations Diet Storage of drug Drug interactions Dosage schedule, missed dosage

Sex Hormones

Production influenced by the anterior pituitary Male: testosterone; androgens Female: estrogen; progesterone

Androgens

Actions Development of secondary sex characteristics; tissue

building

Uses Hypogonadism, hypopituitarism, dwarfism, eunuchism,

cryptorchidism, oligospermia, and male androgen deficiency

Adverse Reactions Edema due to sodium retention, acne, hirsutism, male

pattern baldness, cholestatic hepatitis with jaundice, buccal irritation, nausea and vomiting, diarrhea

Androgens (cont.)

Drug Interactions Increased effects – anticoagulants, antidiabetic agents,

and other drugs Decreased effects – barbiturates Concurrent use with corticosteroids increase edemaNursing Implications Assessment, diagnosis, planning, implementation, and

evaluationDrug Table 21-9

Androgens (cont.)

Patient and Family Teaching Administration Response time Diet Symptoms to report Administration considerations

Female Sex Hormones

Estrogens Progestins Table 21-10

Estrogens

Action and Uses Used for hormone replacement therapy in menopause

and other conditions (ovarian failure); infertility work-ups; palliative breast cancer treatment

Adverse Reactions

Drug Interactions

Progestins

ActionUses Contraception, control excessive uterine bleeding,

treatment of secondary amenorrhea, dysmenorrhea, premenstrual tension, and control of pain in endometriosis

Drug InteractionsNursing Implications and Patient Teaching

Oral Contraceptives

Combination Drugs: Estrogen and Progestin Table 21-11Action Prevent ovulationUse ContraceptionAdverse Reactions Estrogen excess, progestin excess, androgen excess,

estrogen deficiency, progestin deficiencyContraindications for Oral Contraceptives

Thyroid Hormones

Thyroid Supplements or ReplacementsAction Increase metabolic rate: increase tissue oxygen

consumption, body temperature, heart and respiratory rate, cardiac output, and carbohydrate, lipid, and protein metabolism; influence the development of the skeletal system

Uses Replacement therapy for several conditionsTable 21-12

Thyroid Hormones (cont.)

Adverse Reactions Dysrhythmias, hypertension, tachycardia,

hand tremors, headache, insomnia, nervousness, diarrhea, vomiting, weight loss, menstrual irregularities, rash, glycosuria, hyperglycemia, increase prothrombin time, and increase serum cholesterol levels

Drug Interactions

Thyroid Hormones (cont.)

Nursing Implications and Patient Teaching Assessment, diagnosis, planning,

implementation, evaluation Administration Drug action/expected outcomes Drug interactions: diabetes; anticoagulants;

checking with health care provider Signs/symptoms of hyperthyroidism and

hypothyroidism

Antithyroid Products

Action Stop the production of thyroid hormones Uses Treatment of hyperthyroidism; to improve

hyperthyroidism in preparation for surgery or radioactive iodine therapy

Adverse ReactionsDrug InteractionsNursing Implications and Patient Teaching

Williams' Basic Nutrition & Diet Therapy

Chapter 20

Diabetes Mellitus

14th Edition

Lesson 20.1: Diabetes Mellitus as a Metabolic Disorder

Diabetes mellitus is a metabolic disorder of glucose metabolism with many causes and forms.

A consistent, sound diet is a major keystone of diabetes care and control.

Introduction (p. 400)

11% of U.S. adults have diabetes Seventh leading cause of death in the United States Historically, victims died at young age With proper care, people with diabetes can live long,

fulfilling lives

Nature of Diabetes (p. 400)

Defining factor Glucose is primary source of energy for the body Insulin is needed to be taken out of blood and

transferred into cells People with diabetes either do not produce insulin

or cannot effectively use insulin produced Diabetes: group of metabolic diseases

characterized by hyperglycemia

Classification of Diabetes Mellitus and Glucose Intolerance (p. 400)

Type 1 diabetes mellitus Accounts for 5% to 10% of cases Previously called insulin-dependent or juvenile-

onset diabetes Severe, unstable form

Classification of Diabetes Mellitus and Glucose Intolerance (cont’d) (p. 401)

Type 1 diabetes mellitus (cont’d) Caused by autoimmune destruction of pancreatic

cells Can occur at any age Requires exogenous insulin

Type 2 Diabetes Mellitus (p. 401)

Accounts for 90% to 95% of cases Previously called adult-onset or non–insulin-

dependent diabetes Initial onset usually after age 40 years Now being diagnosed in children

Type 2 Diabetes Mellitus (cont’d) (p. 402)

Strong genetic link Prevalent in older, obese people Caused by insulin resistance or defect Usually treated with diet, exercise

Gestational Diabetes (p. 402)

Temporary form of disease occurring in pregnancy Presents complications for mother and fetus/infant Must be carefully monitored and controlled

Other Types of Diabetes (p. 404)

Causes Genetic defect Pancreatic conditions or disease Endocrinopathies: imbalance with other hormones

in the body Drug/toxin induced or chemical induced

Impaired Glucose Tolerance(p. 404)

Above normal fasting blood glucose but not high enough to be diabetes

A risk factor for type 2 diabetes Underlying conditions often present

Symptoms of Diabetes (p. 404)

Initial signs Increased thirst Increased urination Increased hunger Unusual weight loss (type 1) Unusual weight gain (type 2)

Symptoms of Diabetes (cont’d) (p. 405)

Laboratory test results Glycosuria (sugar in urine) Hyperglycemia (elevated blood sugar) Abnormal glucose tolerance tests

Progressive results Water, electrolyte imbalance Ketoacidosis Coma

The Metabolic Pattern of Diabetes (p. 405)

Energy supply and control of blood glucose Diabetes is especially related to metabolism of

carbohydrate and fat It is important to control blood glucose within

normal levels of 70 to 110 mg/dl

Case Study

Mr. Jones is a 45-year-old black male. He is 25 lbs overweight. He also has a family history of diabetes. His most recent lab work reveals an elevated fasting blood sugar, elevated total cholesterol, and low HDL level.

Case Study (cont’d)

List Mr. Jones’ risk factors for type 2 diabetes.

What other screening tools could be used for diabetes?

What are some signs and symptoms that Mr. Jones may be experiencing?

The Metabolic Pattern of Diabetes (cont’d) (p. 405)

Sources of blood glucose Dietary intake Glycogen from liver and muscles

Uses of blood glucose For immediate energy needs: glycolysis Change to glycogen for storage: glycogenesis Convert to fat for longer-term storage: lipogenesis

Pancreatic Hormone Control(p. 405)

Islets of Langerhans produce: Insulin Glucagon Somatostatin

Islets of Langerhans (p. 407)

Insulin (p. 405)

Controls blood sugar Helps transport glucose into cells Helps change glucose to glycogen and store it in

liver, muscles Stimulates changes of glucose to fat for storage

as body fat Inhibits breakdown of tissue fat and protein Promotes uptake of amino acids by skeletal

muscles Influences burning of glucose for energy

Glucagon (p. 407)

Acts in a manner opposite to insulin Breaks down stored glycogen and fat Raises blood glucose as needed to protect brain

during sleep or fasting

Somatostatin (p. 407)

A “referee” for several other hormones Inhibits secretion of insulin, glucagon, and other GI

hormones Also produced in other parts of the body (e.g.,

hypothalamus)

Abnormal Metabolism in Uncontrolled Diabetes (p. 407)

When insulin activity insufficient, imbalances occur in: Glucose Fat Protein

Glucose (p. 407)

Glucose normally absorbed into pancreatic cells, triggering secretion of insulin

Glucose taken up into cells Without insulin, cells starved for glucose

Fat (p. 407)

Without insulin, fat tissue formation decreases Fat tissue breakdown increases Intermediate products of fat breakdown, ketones,

accumulate in body

Protein (p. 408)

Without insulin, protein also broken down to secure energy

Long-Term Complications(p. 408)

Retinopathy: leading cause of new cases of blindness age 20 to 74

Nephropathy: leading cause of end-stage renal disease

Neuropathy: nervous system damage in legs and feet

Heart disease Dyslipidemia: Elevated triglyceride, decreased

high-density lipoprotein cholesterol Hypertension: A major comorbid condition

General Management of Diabetes (p. 409)

Early detection Prevention of complications Glucose tolerance test Goals of care

Maintaining optimal nutrition Avoiding symptoms Preventing complications

General Management of Diabetes (cont’d) (p. 411)

Self-care skills People with diabetes must treat themselves

Basic elements of diabetes management Healthy diet Physical activity Ensure adequate insulin

Special Objectives During Pregnancy (p. 411)

Usually involves team of specialists Careful monitoring of mother with diabetes Preventing fetal damage

Lesson 20.2: Care for the Person with Diabetes Mellitus

Daily self-care skills enable a person with diabetes to remain healthy and reduce risks for complications.

Blood glucose monitoring is a critical practice for blood glucose control.

A personalized care plan balancing food intake, exercise, and insulin regulation is essential to successful diabetes management.

Medical Nutrition Therapy for Individuals with Diabetes (p. 411) Individuals with prediabetes

Promote healthy food choices Increase physical activity Achieve and maintain moderate weight loss

Medical Nutrition Therapy for Individuals with Diabetes (cont’d) (p. 411)

Individuals with diabetes Blood glucose levels as safely as possible Lipid and lipoprotein profile Blood pressure levels Prevent, or at least slow, the rate of chronic

complications Address individual nutrition needs Maintain the pleasure of eating

Additional Considerations(p. 411)

Additional considerations For youth with type 1 diabetes, youth with type 2

diabetes, pregnant and lactating women, and older adults with diabetes, to meet the nutrition needs of these unique times in the life cycle

Provide self-management training for safe conduct of exercise, including the prevention and treatment of hypoglycemia and diabetes treatment during acute illness

Total Energy Balance (p. 411)

Normal growth and weight management Type 1 in childhood: use normal height/weight

charts Type 2 in adulthood: major goal is often weight

reduction/control Energy intake

Balances with needs for growth/development, physical activity, desirable lean weight

Negative balance if weight loss is goal

Nutrient Balance (p. 412)

Carbohydrate Starch and sugar: Complex and simple

carbohydrates Glycemic index Fiber Sugar substitutes: Nutritive and nonnutritive

Glycemic index Measure of a food’s ability to raise blood glucose

level Carbohydrates differ

Nutrient Balance (cont’d) (p. 412)

Fiber Normal consumption encouraged

Sugar substitute sweeteners Nutritive and nonnutritive allowed in moderation

Protein About 10% to 35% of total energy

Fat No more than 7% of kilocalories from saturated fat

Food Distribution (p. 414)

Eat even amounts of food at regular intervals Maintain even blood glucose supply Snacks may be needed Adjust eating according to activity level and stress Regulate glycemic response according to physical

activity and exercise Drug therapy

Daily Activity Schedule (p. 414)

Food distribution must be adjusted to activities Especially important for children and adolescents Stressful event can counteract insulin activity

Exercise (p. 414)

Recommendation: 150 min/week of moderate-intensity aerobic activity

Helps those with type 2 DM control blood glucose and prevent cardiovascular disease, other risks

For those using insulin, energy needs of exercise must be covered in food distribution plan

Drug Therapy (p. 415)

Affects food distribution Patient must adjust diet, medications, exercise as

needed

Diet Management (p. 415)

General planning according to type of diabetes Develop plan to meet individual needs: living

situation, background, food habits

Diet Management (cont’d)(p. 415)

Carbohydrate counting Count carbohydrates for a meal Inject appropriate amount of insulin to process

glucose Food exchange system

Organizes food into groups

Special Concerns (p. 416)

Special diet food items: usually not needed Alcohol: occasional cautious use allowed Hypoglycemia: prepare for possibility Illness: adjust food and insulin accordingly Travel: consult with dietitian first Eating out: plan ahead and choose restaurants wisely Stress: antagonistic to insulin

Diabetes Education Program(p. 419)

Goal: person-centered self-care Patients taking more active role in their care Diabetes requires daily survival skills

Diabetes Self-Management Education (DSME) Support informed decision-making Self-care behaviors Problem-solving Active collaboration with health care team

Necessary Skills (p. 419)

Healthy eating Being active Monitoring Medications

Insulin Oral hypoglycemic agents

Problem-solving Health coping Reducing risk

The physician sends Mr. Jones for nutritional counseling.

What are your recommendations for him?

Resources (p. 422)

American Diabetes Association American Dietetic Association American Association of Diabetes Educators

Staff Education (p. 422)

Success of diabetes education programs depends on sensitivity and training of staff

Continuing education essential

Chapter 11 Care of the Patient with an Endocrine Disorder Mosby items and derived items © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

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