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1 Medical /Surgical Endocrine System Introduction Endocrine glands form a communication network linking all body systems Hormones from glands control and regulate metabolic process Metabolism Transport of substances across cell membranes Fluid and electrolyte balance Growth and development Adaptation Reproduction Closely linked to and integrated with the nervous system Hormone receptors Specificity of hormone action is determined by the presence of specific hormone receptor on or in the target cell Receptors distinguish hormones from each other and translate the hormonal signal into a cellular response Protein hormones react with receptors on the cell surface (vasopressin, TRH, insulin, growth hormone, FSH, LH, corticotropin, ACTH, calcitonin) Steroid hormones react with receptors inside the cell (cortisol, aldosterone, estradiol, progesterone, testosterone) Amines and amino acid derivatives: norepi, epi, T3 and T4 The hormone-receptor complex initiates intracellular events that lead to the biologic effects of the hormone acting on the target cell Feedback control of hormone production Feedback control can be positive (low level of hormone stimulate the release of its controlling hormone) or negative (high level of hormone inhibit the release of its controlling hormone) Feedback control systems allow self- regulation and prevent hormonal overproduction Hypothalamus Provides the link between the nervous system Lies at the base of the brain in the diencephalon Regulates endocrine function by production of hormones, which travel to anterior pituitary to stimulate release of anterior pituitary hormones Corticotrophin releasing hormone Thyrotrophin releasing hormone Gonadotropin releasing hormone Growth hormone releasing hormone Prolactin inhibiting hormone (dopamine) Pituitary Gland Location Base of the skull in the sphenoid bone, connected to the hypothalamus by the pituitary stalk which links the nervous and endocrine system Composition Anterior lobe=75% of gland: hormones are controlled by hypothalamic releasing or inhibiting hormones in response to stimuli received by the nervous system Posterior lobe=25% of gland ADH Oxytocin

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Medical /Surgical

Endocrine System

Introduction

• Endocrine glands form a communication network linking all body systems

• Hormones from glands control and regulate metabolic process

• Metabolism • Transport of substances across cell membranes • Fluid and electrolyte balance • Growth and development • Adaptation • Reproduction

• Closely linked to and integrated with the nervous system

Hormone receptors

• Specificity of hormone action is determined by the presence of specific hormone receptor on or in the target cell

• Receptors distinguish hormones from each other and translate the hormonal signal into a cellular response

• Protein hormones react with receptors on the cell surface (vasopressin, TRH, insulin, growth hormone, FSH, LH, corticotropin, ACTH, calcitonin)

• Steroid hormones react with receptors inside the cell (cortisol, aldosterone, estradiol, progesterone, testosterone)

• Amines and amino acid derivatives: norepi, epi, T3 and T4

• The hormone-receptor complex initiates intracellular events that lead to the biologic effects of the hormone acting on the target cell

Feedback control of hormone

production

• Feedback control can be positive (low level of hormone stimulate the release of its controlling hormone) or negative (high level of hormone inhibit the release of its controlling hormone)

• Feedback control systems allow self-regulation and prevent hormonal overproduction

Hypothalamus • Provides the link between the nervous system

• Lies at the base of the brain in the diencephalon

• Regulates endocrine function by production of hormones, which travel to anterior pituitary to stimulate release of anterior pituitary hormones

• Corticotrophin releasing hormone

• Thyrotrophin releasing hormone

• Gonadotropin releasing hormone

• Growth hormone releasing hormone

• Prolactin inhibiting hormone (dopamine)

Pituitary Gland

Location • Base of the skull in the sphenoid bone,

connected to the hypothalamus by the pituitary stalk which links the nervous and endocrine system

Composition • Anterior lobe=75% of gland: hormones are

controlled by hypothalamic releasing or inhibiting hormones in response to stimuli received by the nervous system

• Posterior lobe=25% of gland • ADH • Oxytocin

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Anti-diuretic hormone

Too much=syndrome of inappropriate

antdiuretic hormone

Too little=Diabetes insipidus

Diabetes Insipidus

Three types

Neurogenic

Nephrogenic

Secondary

DI

Diabetes insipidus is caused by a deficiency in the production or release of ADH or the kidney’s ability to respond. Clinical Manifestations • Polyuria (30 to 40 L/24 hr) • Polydipsia • Hypotension • Tachycardia • Weight loss • Dehydration • Mental status changes • Seizures, constipation

Diagnostic Findings

Serum finding

• Serum sodium >145 mEq/L

• Serum osmolality > 300 mOsm/kg

• Serum ADH decreased in neurogenic DI, may be normal with nephrogenic or psychogenic diabetes insipidus

Urine findings

• Urine specific gravity <1.005

• Urine osmolality < 300 mOsm/kg

• Water deprivation

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Treatment

• Correct underlying cause and restore normal fluid volume and osmolality and electrolyte balance

• Volume replacement

• Hormone replacement

• Education

Syndrome of Inappropriate

Antidiuretic Hormone (SIADH)

• SIADH occurs when the body secretes excessive ADH unrelated to plasma osmolality; that is, a failure of the negative feedback mechanism that regulates the release and inhibition of ADH.

• The results are an inability to secrete a dilute urine, fluid retention, and dilutional hyponatremia

SIADH

Evaluation • Hyponatremia and hypo osmolality cause CNS problems • GI-decreased motility • CV-fluid overload • Pulmonary-fluid overload • Anorexia, nausea, vomiting headache,

abdominal cramps, seizures Laboratory • Hyponatremia and hypo osmolality in the • presence of an inappropriately concentrated • urine

Treatment

• Alleviate the underlying cause, if possible

• Fluid restriction

• Diuretics and drugs to decrease renal sensitivity to ADH (demeclocycline)

In a patient diagnosed with syndrome of inappropriate anti-diuretic

hormone (SIADH), the nurse would expect laboratory findings to include

which of the following?

a.Hypocalcemia

b.K+ 4.8 mEq/L

c.Na+ 110 mEq/L

d.Hypermagnesemia

Correct answer: C

• A defining characteristic of SIADH is hyponatremia due to sustained released of ADH.

• Normal serum sodium is approximately 135 to 145 mEq/L.

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Anterior Pituitary

• Tropic hormones –with hypo/hyper function being reflected in target organs

• If the target gland is involved, the pathologic problem is considered primary in nature

• If the anterior pituitary is involved, the problem is considered secondary in nature

• If the hypothalamus is involved, the problem is considered tertiary in nature

Hyperpituitarism of anterior pituitary

• Usually prolactin or growth hormone

• Commonly caused by a benign tumor such as an adenoma

• An excess of growth hormone results in acromegaly in adults and gigantism in children

• An excess of prolactin causes galactorrhea and

amenorrhea in women and gynecomastia in

men

Acromegaly

• Due to increased GH after closure of closure of epiphyses of the long bones.

• Prevalence of approximately 60 cases per million.

• Symptoms—enlargement of hands, feet, and paranasal and frontal sinuses, deformities of the spine and mandible. Enlargement of soft tissue. Increases free fatty acids and atherosclerosis, GH insulin antanogist.

Acromegaly

• Diagnosis

– Evaluation of GH

excess

– CT scanning

– Ophthalmologic

examination

• Surgery, radiation, drug therapy, or a combination of these three

– Transsphenoidal

approach

– Radiation therapy

normalizes GH in 30-70%

– Drug therapy includes the

use of bromocriptine a

dopamine agonist, or

octreotid a somatostatin

analog that reduces GH

Excess of other Tropic Hormones

• Excesses of other tropic hormones and overproduction of a single anterior pituitary hormone usually produces syndromes related to hormone excess from the target organ.

• In some cases excess secretion of a pituitary hormone may be appropriate such as when there are alterations in the negative feedback system.

• Excess FSH and LH may indicate a pathologic gonadal process such as orchitis or natural process such as menopause

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Hypofunction of anterior pituitary

• Primary may result from development or autoimmune disorders, infections, tumors, vascular disease or destruction of gland

• Hyposecretion of GH during childhood results in growth retardation.

• Other reasons

• With anorexia and bulimia body fat % fall below a critical level for normal hypothalamic-pituitary-gonadotropin function

• Postpartum hemorrhage Sheehan’s syndrome

Panhypopituitarism • No lactation

• Infertile because of prolactin, FSH, and LH deficiency

• Hypothyroidism develops and is followed by corticosteroid deficiency

• Mental disorders are common and because of lethargy and apathy are characteristic of thyroid and adrenal deficiency

• FSH and LH necessary for sexual development. In adults FSH and LH deficiencies in women menstrual irregularities, diminished libido and changes in breast size. In men testicular atrophy diminished spermatogenesis, loss of libido, impotence, and decreased facial hair and muscle mass

Thyroid

• Deficient or excessive thyroid hormones can produce dysfunction in all body systems. The thyroid hormones thyroxine (T4) and Triiodothyronine (T3) are secreted by the thyroid gland under the influence of the anterior pituitary gland via secretion of thyroid-stimulating hormone (TSH)

Hypothyroidism

• Thyroid hormone is necessary for • Metabolic activity of cells, which results

in increased oxygen consumption, increased rate of chemical reaction, and heat production

• Stimulates carbohydrate, fat, and protein metabolism

• Positive chronotropic and inotropic effects on heart

• Required for normal hypoxic and hypercapnic drive in respiratory center

• Increases erythropoiesis • Increase metabolism and clearance of

steroid hormones and insulin

Hypothyroidism

Etiology

• Thyroidal (associated with elevated TSH) includes congenital defects, idiopathic, post surgery or irradiation, biosynthethetic defects, iodine deficiency drugs, chronic throiditis (Hasimoto’s thyroiditis, failure of pituitary or hypothalamic

Drugs

• iodine deficiency, amiodarone, antithyroid drugs (PTU, metimazole, lithium)

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Signs and symptom Dry, sparse, coarse hair

Apathy, lethargy, forgetfulness, slowed mental process

Increased capillary fragility, bradycardia, weak contractility,

distant heart sounds

Decreased appetite, weight gain, constipation, enlarged, scaly tongue

Dry skin, cold, thick brittle nails, generalized edema

Jane Smith

Admits with CHF

• BP 90/60

• Pulse 45

• Temp 96

• Peripheral edema

• States tired and cold all the time

• Also c/o constipation

Myxedema Coma

• Decreased temperature, cold intolerance

• Distant heart sounds

• Bradycardia

• Pericardia effusion

• Lethargy, somnolence

• Dyspnea on exertion with decreased respiratory rate

• Mucinous edema

• Constipation

• Slow speech, coarse voice

Laboratory results

• Decreased T4 and T3

• Increased TSH unless problem from pituitary

Treatment

• Thyroid hormone replacement

• Monitoring of thyroid hormone levels

Hyperthyroidism

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Hyperthyroidism

Causes • Toxic diffuse goiter (Graves’s disease) • Toxic multinodular goiter • Toxic uninodular goiter • Other • Exogenous iodine in patients with preexisting

thyroid disease: • Thyroiditis • Postpartum thyroiditis • Rare including adenoma and malignancies,

pituitary tumors, others

Storm/Thyrotoxicosis

Most body systems are affected. Hyperthyroidism can produce a hyper-dynamic, hypermetabolic state that results in disruption of many major body functions • Tachycardia • Widened pulse pressure • Palpitations • Dysrhythmias • Agitation, delirium, psychoses • Fine tremor • Exaggerated reflexes • Dyspnea with increased respiratory rate

Thyroidectomy

Preoperative

• Obtain vital signs and weight

• Assess electrolyte levels

• Assess for hyperglycemia and glycosuria

• Administer antithyroid medications to prevent occurrence of thyroid storm

Postoperative

• Monitor for respiratory distress (have trach set, oxygen, and suction)

• Maintain in semi-Fowler • Monitor site for edema, bleeding • Monitor for laryngeal nerve damage, as

evidenced by respiratory obstruction, dysphonia, stridor, dysphagia

• Monitor for hypocalcemia • Prepare to administer calcium gluconate • Monitor for storm

Treatment

• Antithyroid drugs

• Surgical therapy (thyroidectomy)

• Radioactive iodine (131) therapy

A 74 year old male is admitted to the

surgical unit following a total

thyroidectomy. What additional

equipment should the nurse include in

the patient’s room set up?

• Chest tube insertion tray

• Central line insertion tray

• Tracheostomy tray

• Thoracotomy tray

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Correct answer: C

A tracheostomy tray should be available because of the patient’s risk of respiratory distress related to swelling of the operative site. An emergency tracheostomy would be indicated.

The next two questions pertain

to the following scenario

Bernard Webb, age 44, is transferred to

the surgical unit following total

thyroidectomy.

The nurse’s postoperative monitoring is

based on recognition of which of the

following as the MOST CRITICAL

potential complication?

a.Seizure

b.Neck stiffness

c.Bleeding

d.Pain

Correct answer: C

Postoperative bleeding can be a devastating

complication of thyroid surgery. An

recognized or rapidly expanding hematoma

can cause airway compromise and

asphyxiation. Pain would be present, but

bleeding is more crucial.

Two days after surgery. Mr. Webb complains

of muscle cramps and tingling in his lips. The

nurse will call the physician to share these

findings, which are MOST LIKELY the result

of:

a.Damage to the parathyroid glands during surgery

b.Residual effects of general anesthesia

c.Decreasing serum magnesium following surgery

d.Cervical spine compromise

Correct answer: A

Damage to the parathyroid glands is a

complication during thyroidectomy due to

their proximity to the thyroid gland. Tingling

and muscle cramps are manifestations due to

the loss of parathyroid hormone that controls

calcium.

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Parathyroid Glands

• Location: four glands on the posterior surface of the thyroid gland

• Regulation • Stimulation-decrease in serum Ca • Inhibition; increase in serum Ca and vit

D metabolites

• Physiologic activity: increases reabsorption of calcium and magnesium, decreases renal tubular reabsorption of phosphate and bicarbonate

Primary hyperparathyroidism

• Usually due to a benign adenoma or yperplasia of unknown cause

Results in

• Increased conversion of inactive to active vitamin D resulting in increased absorption of calcium and phosphate

• Increased bone reabsorption

• Increased kidney tubular reabsorption of phosphorus and bicarbonate

<

>CA 1)Depressed reflexes 2)Confusion, psychosis 3)Anorexia, nausea 4)Bone pain 5)Polyuria, dehydration 6)Stupor coma 7)Short ST segment 8)Short QT 9)Ventricular arrhythmias 10)Increased digitalis effect

Treatment

• Promotion of excretion of calcium in urine by administration of a loop diuretic and hydration of the patient with isotonic saline.

• Fluid intake oral 3000-4000ml of fluid daily to promote excretion and decrease the possibility of renal calculi formation.

• Synthetic calcitonin can also be administered to lower serum calcium levels

Hypoparathyroidism signs and

symptoms

- Due to low serum calcium levels

Tetany

Painful tonic spasms of smooth skeletal muscles

Dysphagia, Chvostek’s sign and Trousseau’s sign

Respiratory function my he compromised by accessory muscle spasm and laryngeal spasm

Anxiety and apprehension

Prolonged QT which risk for V tachycardia

<Ca 1)hyperreflexia, muscle cramps 2)Chvostek”s sign 3)Trousseau’s sign 4)Laryngeal spasm 5)Tetany, seizures 6)Elongated ST segment 7)Prolonged QT 8)VT/VF

Trousseau’s sign

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Diagnostic Treatment

• Low serum calcium and PTH

• Increased phosphate levels

• R/O other causes of low Ca

• Tetany is treated with IV infusion or slow push of calcium

• Long term therapy consists of the administration of Vit D and possibly supplemental calcium and oral phosphate binders

• Specific hormone replacement of PTH is not used

Adrenal Gland

Location: retroperitoneal, superior to the kidney

• Composition: two separate endocrine tissue that produce distinct hormones

• Cortex (90% of the gland) produces aldosterone, glucocorticoids, and adrenal androgens and estrogens

• Medulla (10% of the gland) produces catecholamines excess usually associated with pheochromocytoma

Mary Jones

Fainted while shopping

BP 70/50

Pulse 120

Blood sugar 45mg/dl

Acute Adrenal Insufficiency

Addison’s disease

Primary

• Result in both glucocorticoids and mineralocorticoids

Secondary

• Are those that interfere with adrenocorticotropic hormone (ACTH) secretion or simply suppress normal secretion of corticosteroids. These generally result in deficiencies of only glucocorticoids.

Causes of Insufficiency

Infection is one of the most common in critical care

Addison’s disease

Hemorrhagic destruction

Adrenal crisis can be precipitated in any patient with

chronic adrenal insufficiency by providing inadequate

hormone replacement during times of acute stress

Abrupt withdrawal of corticosteroids in someone who has

been chronically treated with these medications

Mineralocorticoids

• Aldrosterone

• Secreted in response to Angiotension ll

• Acts in the kidneys to increase sodium ion reabsorption and to increase K and hydrogen ion excretion.

• Increased absorption of Na creates an osmotic gradient across renal tubular membrane and activates ADH which causes water absorption

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Signs and Symptoms • Weakness, fatigue, weight loss

• Pigmentation of skin

• Hypotension

• Abdominal pain

• Diarrhea

• Constipation

• Salt craving

• Syncope

• Vitiligo (skin condition consisting of irregular patches totally lacking in pigment)

• Hyponatremia

• Hyperkalemia

• Hypoglycemia

• Hypercalcemia

• Anemia

• Eosinophilia

• Lymphocytosis

• Increased BUN

Diagnostic

• ACTH levels

• ACTH stimulation test

Treatment Pharmacology

• Rapid administration of IV fluids and electrolytes (usually NS)

• Hormone replacement

• Glucocorticoid

• mineralocorticoid

Potential complications

• Cardiovascular collapse

• Mechanism related to ACTH deficiency

• Management: CPR, inotropic support, fluid administration

Cushing’s

Syndrome

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Excess Adrenal hormones

Cushing’s syndrome

• Diabetes

• Hypertension, protein wasting

• Osteoporosis

• Inhibit growth in infants and children

• Decrease immune response

• Increased secretion of hydrochloric acid

• Retention of Na and water with loss of K

Diagnosis Treatment

Localization of cause

• Adrenal ultrasound

• Adrenal vein cath

• CT scan adrenal pituitary

• MRI adrenal and pituitary

Management

• Surgery to remove cause

• Radiation therapy

• Adrenal enzyme inhibitor (metyrapone)

• Ketaconazole—blocks the production of steroids at several levels (unlabeled use)

Primary Hyperaldosteronism

(Conn’s Syndrome)

Signs & symptoms are related to effects of aldosterone on renal sodium, reabsorption & potassium secretion

• Hypertension

• Hypokalemia

• Diagnostic tests

• Serum K

• Urinary potassium concentration

• Random simultaneous aldosterone and renin

• CT scan, MRI, Adrenal venous sampling

• Treatment

• Resection if adenoma-pretreat with spironolactone

• Spironolactone alone

•Review Questions

The pathophysiologic result of Cushing’s disease is?

a)Hypersecretion of mineral corticoids

b)The hypo secretion of aldosterone

c)Hypersecretion of glucocoticoids

d)Hypo secretion of androgens

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The pathophysiologic result of Cushing’s disease is?

a)Hypersecretion of mineral corticoids

b)The hypo secretion of aldosterone

c)Hypersecretion of glucocoticoids

d)Hypo secretion of androgens

Primary hypo function of the adrenal cortex can be caused by which of the following conditions?

a)Tuberculosis

b)Increased production of corticotrophin-releasing hormone

c)Decreased ACTH production

d)Bronchiogenic carcinoma

Primary hypofunction of the adrenal cortex can be caused by which of the following conditions?

a)Tuberculosis

b)Increased production of corticotrophin-releasing hormone

c)Decreased ACTH production

d)Bronchiogenic carcinoma

Secondary hypofunction of the adrenal cortex can be caused by which of the following?

a)Removal of the pituitary

b)Tumor of the hypothalamus

c)A tumor involving the adrenal cortex

d)hypertension

Secondary hypofunction of the adrenal cortex can be caused by which of the following?

a)Removal of the pituitary

b)Tumor of the hypothalamus

c)A tumor involving the adrenal cortex

d)hypertension

Jane Smith, a 57-year old woman, has Cushing’s disease. Which of the following would not be found on an assessment of Ms Smith?

a)Hypotension

b)Osteoporosis

c)Hirsutism

d)Muscle weakness

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Jane Smith, a 57-year old woman, has

Cushing’s disease. Which of the following

would not be found on an assessment of Ms

Smith?

a)Hypotension

b)Osteoporosis

c)Hirsutism

d)Muscle weakness

Phillip James, a 40 year old man, has hypothyroidism. Which of the following clinical manifestations would be expected?

a)Nervousness, tremors, hyperkinesias

b)Heat intolerance, palmer erythema, subnormal temperature

c)Cold intolerance, slowed muscle contraction, bradycardia

d)Polyuria and polydipsia

Phillip James, a 40 year old man, has hypothyroidism. Which of the following clinical manifestations would be expected?

a)Nervousness, tremors, hyperkinesias

b)Heat intolerance, palmer erythema, subnormal temperature

c)Cold intolerance, slowed muscle contraction, bradycardia

d)Polyuria and polydipsia

You would expect Pat Cunningham, a 55 year old woman with hyperthyroidism to exhibit?

a)Nervousness, tremors, and hyperkinesia's

b)Subnormal temperature and peripheral edema

c)Cold intolerance, slowed muscle contraction, bradycardia

d)Yellow skin, slowed mentation, fine soft hair

You would expect Pat Cunningham, a 55 year old woman with hyperthyroidism to exhibit?

a)Nervousness, tremors, and hyperkinesia's

b)Subnormal temperature and peripheral edema

c)Cold intolerance, slowed muscle contraction, bradycardia

d)Yellow skin, slowed mentation, fine soft hair

About 50% of people with Grave’s disease have

eye involvement characterized by:

a)Retinal degeneration

b)Forward displacement of the eye (exophalmus)

c)Loss of color vision

d)Corneal atrophy

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About 50% of people with Grave’s disease have

eye involvement characterized by:

a)Retinal degeneration

b)Forward displacement of the eye (exophalmus)

c)Loss of color vision

d)Corneal atrophy

A life-threatening complication of

hypothyroidism that is associated with

hypothermia and respiratory depression is know

as:

a)Conn’s disease

b)Thyrotoxicosis

c)Addison’s disease

d)Myxedema coma

A life-threatening complication of hypothyroidism that is associated with hypothermia and respiratory depression is know as:

a)Conn’s disease

b)Thyrotoxicosis

c)Addison’s disease

d)Myxedema coma

Primary hyperparathyroidism is associate with:

a)Bone resorption

b)Urinary retention

c)Tremors

d)hypocalcemia

Primary hyperparathyroidism is associate with:

a)Bone resorption

b)Urinary retention

c)Tremors

d)hypocalcemia

A symptom of syndrome of inappropriate antidiuretic hormone (SIADH) is:

a)Hyponatremia

b)Urinary hypo osmolality

c)Hypernatremia

d)Polyuria

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A symptom of syndrome of inappropriate antidiuretic hormone (SIADH) is:

a)Hyponatremia

b)Urinary hypo-osmolality

c)Hypernatremia

d)Polyuria

Good Luck on Your Test