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Nursing Care for Clients with Endocrine Disorders

Endocrine System

 The endocrine system integrates body functions by the synthesis and release of hormones

 The functions of the endocrine and the nervous system are interrelated.

 Hypothalamus: link between the nervous system and the endocrine system.

Endocrine Glands

 Pituitary Gland

 Adrenal Glands

 Thyroid Glands

 Parathyroid Glands

 Gonads

Overview of the Endocrine System

The body’s second great controlling system which influences metabolic activities of cells by means of
hormones, which are produced by endocrine glands

Endocrine glands: pituitary, thyroid, parathyroid, adrenal, pineal, and thymus

The pancreas and gonads produce both hormones and exocrine products

The hypothalamus has both neural functions and releases hormones

Other tissues and organs that produce hormones: adipose cells, pockets of cells in the walls of the small
intestine, stomach, kidneys, and heart

Functions of Endocrine System

1. Metabolism and tissue maturation

2. Ion regulation

3. Water Balance

4. Immune system regulation

5. Heart rate and blood pressure regulation

6. Control of blood glucose and other nutrients


7. Control of reproductive function

8. Uterine contractions and milk release

Hormones

 Are chemical substances that are secreted by the endocrine glands.

 Can travel moderate to long distances or very short distances.

 Acts only to cells or tissues that have receptors for the specific hormone.

 Target organ: the cell or tissue that responds to a particular hormone.

Regulation of Hormones

 If the client is healthy, the concentration or hormones is maintained at a constant level.

 When the hormone concentration rises, further production of that hormone is inhibited.

 When the hormone concentration falls, the rate of the production of that hormone increases.

Diseases of the Endocrine System

 Primary Disease- problem in target gland; autonomous

 Secondary Disease-problem outside the target gland; most often due to a problem in pituitary
gland

Disorders of the Anterior Pituitary Gland

Hypopituitarism

 Caused by low levels of one or more anterior pituitary hormones.

 Lack of the hormone leads to loss of function in the gland or organ that it controls.

Causes of Primary Hypopituitarism

 Pituitary tumors

 Inadequate blood supply to the pituitary gland

 Infections and or inflammatory diseases

o Sarcoidosis, amyloidosis

 Radiation therapy

 Surgical removal of pituitary tissue


 Autoimmune diseases Congenital absence,

Causes of 2° Hypopituitarism

 Tumors of the hypothalamus

 Inflammatory disease

 Head injuries

 Surgical damage to the pituitary and/or blood vessels or nerves leading to it.

Signs and Symptoms

 Tumor: bitemporal hemianopsia on visual confrontation

 Varying signs of hormonal disturbances depending on which hormones are being under secreted

Signs and Symptoms

 Gonadotropin Deficiency

 Congenital Onset

 Delayed or absent secondary sexual characteristics

 Acquired

 Loss of body hair

 Infertility, decrease libido, impotence in males, amenorrhea in females

 Prolactin Deficiency

 Failure to lactate

Signs and Symptoms

 TSH (Thyroid Stimulating hormone) Deficiency

causes hypothyroidism with manifestations such as fatigue, weakness, weight change, and
hyperlipidemia

 Adrenocorticotropic (ACTH) hormone deficiency

• results in diminished cortisol secretion.

• symptoms include weakness, fatigue, weight loss, and hypotension

Signs and Symptoms


 Growth hormone (GH) deficiency

 In childhood: failure to grow

 In adulthood: mild to moderate central obesity, increased systolic BP and increases in LDL
cholesterol

Diagnostics

 X-ray, MRI or CT scan: pituitary tumor

 Plasma hormone levels: decreased

Therapeutics

 Hormonal Substitution: may be for life

 Corticosteroids, levothyroxine

 androgen for males, estrogen for females

 Growth hormone

 Radiation therapy for tumors


Surgery for tumors: Transphenoidal Hypophysectomy

Hyperpituitarism

 Hyperfunction of the anterior pituitary gland=oversecretion of one or more of the pituitary


hormones

 Usually caused by benign pituitary adenoma

 2 most common hormones affected:

 Prolactin

 growth hormone

Prolactinoma

 Female: galactorrhea menstrual disturbances, infertility, signs of estrogen deficit (vaginal


mucosal atrophy, decreased vaginal lubrication and libido)

 Male: Decreased libido and possible impotence, reduced sperm count and infertility,
gynecomastia

Growth Hormone Hypersecretion


 Gigantism: GH hypersecretion prior to closure of epiphyses; proportional growth

 Acromegaly: GH hypersecretion after closure of epiphyses; disproportional growth

Growth Homone Hypersecretion:


Signs and Symptoms

 Enlarged hand and feet; carpal tunnel syndrome common

 Coarsening of features esp. in Acromegaly; prominent mandible, tooth spacing widens,

 Hypertension, cardiomegaly, heart failure

 Insulin resistance leading to type 2 DM

 Visual field defects: bitemporal hemianopsia->complete blindness

 Headaches, Arthritis, Hypogonadism,

Medication

 bromocriptine and cabergoline (dopamine agonist)

 For prolactinoma and GH hypersecretion

 Octreotide (somatostatin) for GH hypersecretion

 Sx

 surgical remission is achieved in about 70% of patients followed over 3 years

 Growth hormone levels fall immediately; diaphoresis and carpal tunnel syndrome often
improve within a day post-Sx

 Radiation Therapy for large tumors

Nursing Interventions

 Provide emotional support=striking body change can cause psychological stress.

 Perform or assist with ROM exercises to promote maximum joint mobility and prevent injury.

 Keep the skin dry. Avoid using an oily lotion because the skin is already oily.

 Be aware that pituitary tumor cause visual problems. If there is hemianopsia, stand where he
can see you.

 Warn relatives that hyperpituitarism can cause inexplicable mood changes.


 If the patient is a child, explain to the parents that surgery prevents permanent soft-tissue
deformities but won’t correct bone changes that have already occurred.

 After an operation, emphasize the importance of continuing hormone replacement therapy.

Transphenoidal Hypophysectomy

 Endoscopic, transnasal, transsphenoidal pituitary microsurgery.

 Removal of adenoma while preserving anterior pituitary function in most patients.

 Surgery is usually well tolerated, but complication occur in about 10%.

Postoperative care

 WOF: Bleeding

 keep the patient on bed rest for 24 hours after surgery and encourage ambulation
thereafter

 keep the head of bed elevated (30°) to avoid placing tension or pressure on the suture
line.

 Instruct the patient not to sneeze, cough, blow his nose, or bend over for several days to
avoid disturbing the suture line.

 Arrange for visual field testing as soon as possible because visual defects can indicate
hemorrhage.

Postoperative Care

 WOF: CSF leak and infection

 reinforce measures to prevent increased ICP

 oral care, BUT the patient should not brush his teeth for 2 weeks to avoid suture line
disruption

 Signs of CSF leak

 Frequent clearing of the throat and swallowing

 Presence of halo ring on gauze

 Test for glucose

 Signs of infection

 Fever, headache, nuchal rigidity


Postoperative Care

 WOF: Post-Op pain

 Paranasal pain typically subsides when the catheters and packing are removed, usually
24 to 72 hours after surgery

 WOF: Diabetes Insipidus

 due to inadequate release of ADH

 usually happens 24 to 48 hours after surgery and may resolve within 72 hours.

 be alert for increased thirst and increased specific gravity.

Management

 I & O, urine sp. Gravity and daily weight monitoring

 Fluid replacement

 Aqueous vasopressin, sublingual desmopressin acetate.

 WOF: S/Sx of hypopituitarism

 patient may need hormonal replacement therapy due to decreased pituitary secretion
of tropic hormones.

 Necessary: cortisol immediate post-op

 Maintenance hormonal replacement as needed

o Cortisol, Thyroxine, Vasopressin

o Estrogen or Testosterone

Disorders of The Posterior Pituitary Gland

Vasopressin or Antidiuretic Hormone

 Regulates water metabolism, stimulates reabsorption of water and decreased urine output.

Diabetes Insipidus

 Disorder characterized by massive polyuria due to either lack of ADH or kidney’s insensitivity to
it.

 Types:

 Central DI, Nephrogenic DI


 Central Diabetes Insipidus: Deficiency of vasopressin

 Primary diabetes Insipidus ( without an identifiable organic lesion noted on MRI of the
pituitary and hypothalamus)

 May be familial, occurring as a dominant trait, or (“idiopathic”)

 Secondary diabetes insipidus

 Due to damage to the hypothalamus or pituitary stalk by tumor, anoxic


encephalopathy, surgical or accidental trauma, infection (encephalitis,
tuberculosis, syphilis), sarcoidosis

 “Nephrogenic Diabetes Insipidus”

 Due to defect in the kidney tubules that interferes with water reabsorption

 Patients have normal secretion of vasopressin

Signs and Symptoms

 Polyuria, Intense thirst, Dehydration.

 Diagnostics

 Fluid deprivation test-> to differentiate between psychogenic polydipsia and DI

 Administration of desmopressin->to differentiate between central DI and nephrogenic

 24 hour urine collection of volume, glucose, and creatinine

 Serum for glucose, urea nitrogen, calcium, uric acid, potassium and sodium.

Medications

 For central DI

 Desmopressin (DDAVP): intranasal

 Lypressin: intrasanal, Vasopressin tannate in oil: IM

 For nephrogenic DI:

 Indomethacin-hydrochlorthiazide (with potassium supplementation)

 Indomethacin-demopressin, Indomethacin-amiloride

 Clofibrate, chlorpropamide and thiazide diuretics (mild DI)

DI: Nursing Management


Maintain fluid and Sodium balance

 Record I & O. Weigh patient daily.

 Maintain fluid intake to prevent dehydration.

 WOF: dehydration and shock

 Keep the side rails up and assist with walking if the patient is dizzy or has muscle
weakness.

 Monitor urine specific gravity between doses. Watch for decreased specific gravity with
increased urine output->need for the next dose or a dosage increase.

 Add more bulk foods and fruit juices to the diet->to prevent constipation. Laxative (milk of
magnesia PRN).

 Provide meticulous skin and mouth care, and apply a lubricant to cracked or sore lips.

 Diet: low in sodium

 Carry out drug therapy

 caution must be used with administration of vasopressin if coronary artery disease is


present->causes vasoconstriction

 assist in searching for the underlying pathology

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

 Disorder due to excessive ADH release

 Signs and Symptoms

 persistent excretion of concentrated urine

 signs of fluid overload

 change in level of consciousness

 NO EDEMA

 HYPONATREMIA

Causes of SIADH

 Tumors: bronchogenic carcinoma, lymphoma, pancreatic cancer

 Pulmonary: TB, pneumonia, lung abscess, COPD, pneumothorax, HIV secretion


 CNS: meningitis, head injury, subdural hematoma, subarachnoid hemorrhage, neurosurgery

 Drugs: some medications (vincristine, phenotiazines, tricylic antidepressants, thiazide diuretics,


and others) and nicotine have been implicated in SIADH; they either directly stimulate the
pituitary gland or increase the sensitivity of renal tubules to circulating ADH.

SIADH: diagnostic tests

 Low serum sodium (<135meqs/L)

 Low serum osmolality

 High urine sodium osmolality (urine osmolality >100 mosmol/kg)

 High urine sodium excretion (>20 mmol/L

SIADH: Management

 Maintain fluid balance

 Restriction or water intake (<1,000ml/day).

 If the patient has evidence of fluid overloading, a history of CHF, or is resistant to


treatment, loop diuretics (furosemide) may be added as well.

 Chronic treatment: lithium or demeclocycline which inhibit ADH action.

 Monitoring of body weight.

 Maintain sodium balance

 Increase sodium intake

 if the serum sodium is below 120 or if the patient is seizing, emergency treatment: 3%
NaCL. May be followed by furosemide.

 Excessively rapid correction of hyponatemia may cause central pontine myelinolysis.

 Patients with a plasma sodium concentration greater then 125 mmol/L rarely need
specific therapy for hyponatremia.

Disorders of the Adrenal Glands

Adrenal Insufficiency

Cushing’s Syndrome

Hyperaldosteronsim
Pheochromocytoma

Adrenal Cortex Hormones

 Glucocorticoids

 Cortisol, corticosterone

 Increased blood glucose levels by increasing the rate of gluconeogenesis.

 Increase protein catabolism

 Increasing mobilization of fatty acids promote Na and H2O retention

 Anti-inflammatory effect

 Aid the body in coping with stress

Adrenal Cortex Hormones

 Mineralocorticoids

 Aldosterone, corticosterone, Deoxycorticosterone

 Regulate fluid and electrolyte balance

 Stimulate reabsorption of sodium, chloride and water

 Stimulate potassium excretion.

 Under the control of the Renin-Angiotensin-aldosterone system

Adrenal cortex hormones

 Sex hormones

 Androgens, Estrogens

 Influences the development of sexual characteristics

Adrenal Medulla

 Release catecholamines

 Epinephrine, Norepinephrine

 Released during “fight or flight” situations-> SYMPATHETIC effect

Hypercortisolism (Cushing’s Syndrome)


 Cluster of physical abnormalities due to excessive cortisol release

 Cortisol excess is due either to:

 Autonomous steroid release from adrenal

 Increased ACTH release from pituitary

 complication of exogenous steroid therapy

Altered metabolism of

 CHO: hyperglycemia, Na and water retention

 CHON: muscle wasting, thin, fragile skin, impaired wound healing

 Fats: central obesity, moon face, buffalo hump

 Hypokalemia, hypocalcemia

 Acne, hirsutism, menstrual changes, decreased libido

 Weakness, emotional lability

Complications

 Osteoporosis

 Peptic Ulcer

 Immune and inflammatory response is also compromised

 Other complications include HPN, and sexual and psychological complications

Diagnostics

 ACTH levels-> determine whether the syndrome is ACTH dependent.

 24-hour urine collection for cortisol, midnight serum cortisol

 Dexamethasone suppression test-

 Radiologic evaluation- Tumor in the pituitary or adrenal gland

Management

 Transsphenoidal resection of pituitary tumor, Adrenalectomy as needed

 Medications:
o Aminogluthetimide: adrenal enzyme inhibitor

o Metyrapone and ketoconazole: suppress hypercortisolism in unresectable adrenal


tumor

 Antihypertensives

Nursing Considerations

 Monitor VS, WOF for HPN

 Safety Precaution:

 Maintain muscle tone

 Prevent accidents or falls and provide adequate rest

 Protect client from exposure to infection, monitor WBC

 Maintain skin integrity

 Minimize stress

 Provide diet low in calories, sodium and high in protein, potassium, calcium and vitamin D

 Monitor for urine glucose and acetone, administer insulin if necessary

Hyperaldosteronism

Hypersecretion of aldosterone from the adrenal cortex

Two types:

 Primary disease of the adrenal cortex

 Secondary condition due to increased plasma renin activity

Causes:

 Excessive reabsorption of sodium and water

 Excessive renal excretion of potassium

Causes

 Primary hyperaldosteronism: Autonomous secretion of aldosterone from the adrenals

 Benign adrenal adenoma (Conn’s syndrome)

 Secondary hyperaldosteronism: High renin state-> stimulating aldosterone release


 Renal artery stenosis

 Pregnancy

 Oral Contraceptive use

 Nephritic syndrome

 Cirrhosis with ascites

 Heart failure

Hyperaldosteronism: signs and sypmtoms

 Hypertension

 Headache and visual disturbance

 Hypokalemia

 Muscle weakness and fatigue, Paresthesia and Arrhytmias

 Polyuria and Polydipsia

 Tetany from alkalosis

 Hypernatremia

Diagnostics

 Hypokalemia, Hypernatremia, Hypomagnesemia

 Elevated serum bicarbonate and pH

 Elevated plasma and urinary aldosterone

 Low specific gravity urine (diluted urine)

Treatment

 Primary hyperaldosteronism:

 Unilateral adrenalectomy

 After aderenalectomy, WOF: signs of adrenal insufficiency.

• Potassium-sparing diuretic (such as spironolactone or amiloride)-> may lead to decreased libido,


gynecomastia, impotence

• Antihypertensives
• Aminogluthetimide-> inhibits synthesis of aldosterone.

• Diet: sodium restriction, increased potassium

• Treatment of secondary hyperaldosteronism: include correction of the underlying cause.

Adrenal Insufficiency

• 1° adrenal insufficiency: Addison’s disease

 The most common form of adrenal hypofunction-> occurs when more than 90% of the
adrenal gland is destroyed

 Autoimmune process-> decreased secretion of androgen, glucocorticoids, and


mineralocorticoids.

• 2 ° adrenal Insufficiency:

 It may also be caused by a disorder outside the gland

Nursing Alert! Adrenal crisis (addisonian crisis) is a medical emergency requiring immediate, vigorous
treatment.

causes

 Autoimmune destruction of the adrenal gland, tuberculosis, bilateral adrenalectomy,


hemorrhage into the adrenal gland, neoplasms, or fungal infections.

 Secondary adrenal hypofunction is caused by

 Hypopituitarism

 Abrupt withdrawal of long term corticosteroid therapy

• In a patient with adrenal hypofunction, adrenal crisis occurs when the body’s stores of
glucocorticoids are exhausted by trauma, infection, surgery, or other physiologic stressors.

Adrenal Insufficiency: signs and symptoms

Weakness, fatigue, Poor coordination

 Weight loss, nausea and vomiting, anorexia

 Chronic constipation or diarrhea

 Cardiovascular abnormalities

 Postural hypotension, decreased cardiac output, Weak, irregular pulse


 Decreased tolerance for even minor stress

Conspicuous bronze skin coloration, especially in hand creases and over the metacarpophalangeal
joints, elbows, and knees.

Fasting hypoglycemia; and craving for salty food.

Amenorrhea

Adrenal crisis

 Profound weakness and fatigue, shock, severe nausea and vomiting, hypotension,
dehydration and high fever.

MSH is produced when the ACTH production is increased-> hyperpigmentation

Adrenal Insufficiency

 Decreased plasma cortisol levels and serum sodium levels.

 Increased ACTH (in addison’s), serum potassium, and BUN level.

Adrenal Insufficiency: Treatment

Corticosteroid replacement, usually with cortisone or hydrocortisone-> primary lifelong treatment

Fludrocortisone acetate: acts as a mineralocorticoid to prevent dehydration and hypotension.

Adrenal Crisis: prompt IV bolus of corticosteroids, 3 to 5 L of IV fluids, dextrose

Adrenal Insufficiency: Nursing Management

WOF: adrenal crisis

 Hypotension and signs of shock (decreased level of consciousness and urine output)

 Watch for hyperkalemia before treatment and for hypokalemia after treatment (from
excessive mineralocorticoid effect)

 If patient has diabetes, check blood glucose levels periodically because steroid replacement may
necessitate changing the insulin dosage.

 Diet: maintain sodium and potassium balance, high protein and carbohydrates

 If the patient is anorexic, suggest six small meals per day to increase calorie intake.
 Observe the patient receiving steroids for cushingoid signs, such as fluid retention around the
eyes and face.

 Instruct on lifelong cortisone replacement therapy: “ Do not omit medications” Give 2/3 of dose
in AM and 1/3 in PM

 Instruct the patient that he’ll need to increase the dosage during times of stress.

 Warn that infection, injury, or profuse sweating in hot weather may precipitate crisis.

Pheochromocytoma

 Rare disorder, a chromaffin-cell tumor of the sympathetic nervous system, usually in the adrenal
medulla, secretes an excess of the catecholamines epinephrine and norepinephrine.

 This causes episodes of hypotension and symptoms of catecholamine excess.

 The tumor is usually benign but may be malignant in as many as 10% of patient.

Signs and Symptoms

 Think sympathetic!!!

 Persistent or paroxysmal HPN

 Palpitations, tachycardia, headache, visual disturbances, diaphoresis, pallor, warmth or


fluting, paresthesia, tremor, and excitation.

 Anxiety, fright, nervousness, feelings of impending doom, abdominal or chest pain, tachypnea,
N&V, fatigue, wt. loss, constipation, postural hypotension, paradoxical response to
antiHPNs(common), hyperglycemia

Diagnostic tests:

 Increased plasma levels of catecholamines, elevated blood sugar, glucosuria

 Elevated urinary catecholamines and urinary VMA

 Nursing considerations! Avoid coffee, nuts, chocolate, banana, vanilla.

 Tumor on CT scan.

Treatment

 Surgical removal of the tumor with sparing of the normal adrenals, if possible

 WOF: hypo or hypertension post-op

 Anti-hypertensives:
 Alpha-adrenergic blocker ( phentolamine, prazosin, or phenoxybenzamines)

 A beta-blocker (propanolol)

 Metyrosine may be used to block catecholamine synthesis.

Adrenalectomy

Resection or removal of one or both adrenal glands.

 The treatment of choice, For adrenal hyperfunction and hyperaldosteronism

 Adrenal tumors, such as adenomas and pheochromocytomas.

Pre-op

Correct electrolyte imbalance

 Potassium, sodium, calcium

 Manage hypertension

Post-Op care

 WOF: shock and hemorrhage

 Keep in mind that postoperative hypertension is common because handling of the adrenal
glands stimulates catecholamine release.

 WOF: adrenal crisis-> hypotension, hyponatremia, hyperkalemia

 Remember, glucocorticoids from the adrenal cortex are essential to life and must be replaced to
prevent adrenal crisis until the hypothalamic, pituitary, and adrenal axis resumes functioning.

Adrenalectomy: Nursing interventions

Instruct the patient to take prescribed medication as directed.

If patient had unilateral adrenalectomy, explain that he may be able to taper his medication in a few
months.

Inform patient that sudden withdrawal of steroids can precipitate adrenal crisis.

Disorders of the Thyroid Gland

It produces 3 hormones: T3, T4, and calcitonin

Tests of Thyroid Function


 Thyroid-Stimulating Hormone

 Single best screening test of thyroid function because of its high sensitivity

 Values above the normal range of 0.38 to 6.15 uU/mL are indicative of primary
hypothyroidism, and low values indicate hyperthyroidism

Tests of Thyroid Function

 Serum Free Thyroxine

 Test used to confirm an abnormal TSH is FT4

 FT4 is a direct measurement of free (unbound) thyroxine, the only metabolically active
fraction of T4.

 Normal value: 0.9 and 1.7ng/L (11.5 to 21.8pmol/L)

 Serum T3 and T4

 Normal range for T4 is between 4.5 and 11.5ug/dL (58.5 to 150 nmol/L)

 Although serum T3 and T4 levels generally increase or decrease together, the T3 level
appears to be a more accurate indicator of hyperthyroidism, which causes a greater rise
in T3 than T4 levels.

 Normal range for serum T3 is 70 to 220ng/dL (1.15 to 3.10 nmo/L)

Tests of Thyroid Function

 Thyroid scan, Radioscan, or Scintiscan

• Isotopes used:

 123I->most commonly used isotope.

 Technetium-99m pertechnetate, thallium, thallium and americanium

 Scans are helpful in determining location, size, shape, and anatomic function of the
thyroid gland, particularly when thyroid tissue is substernal or large.

 Identifying areas of increased function (“Hot”areas) or decreased function (“cold” areas)


can assist in diagnosis.

 Radioactive Iodine Uptake

 Measures the rate of iodine uptake by the thyroid gland.

 The patient is administered a tracer dose of iodine-123


 Measures the proportion of the administered dose present in the thyroid gland at a
specific time after its administration.

 Affected by the patient’s intake of iodine or thyroid hormone; therefore, a careful


preliminary clinical history is essential in evaluating results.

 Hyperthyroidism-> high uptake of the 123I

 Hypothyroidism-> very low uptake.

Fine-Needle Aspiration Biopsy

 Sampling Thyroid Tissue to: detect malignancy

 Initial test for evaluation of thyroid masses.

Nursing Implications of Thyroid Tests

 It is necessary to determine whether the patient has taken medications or agents that
contain iodine because these alter the results of some of the schedule tests.

 Assess for allergy to iodine or shellfish

 For the scans, tell patient that radiation is minimal

Hyperthyroidism

 Or thyrotoxicosis

 Increased metabolic rate

 Causes:

o Grave’s disease

o Initial manifestations of thyroiditis (hashimoto’s and subacute thyroiditis)

o Toxic adenoma

o TSH-secreting pituitary tumor

o Factitious thyrotoxicosis

o Jodbasedow disease

Hyperthyroid: Signs and Symptoms

Enlarged thyroid gland

Tachycardia-> atrial fibrillation, heart failure, Hypertension


Heat intolerance, diaphoresis

Smooth, soft, warm skin

Fine Soft Hair

Diarrhea, weight loss despite of increased appetite

Nervousness and fine tremors of hands.

Hyperactive reflexes, body weakness

Personality changes, mood swings

Osteoporosis

Clubbing and swelling of fingers, Plummer’s nails

Menstrual disturbances, decreased fertility

Signs and Symptom’s of Grave’s Disease

All s/s of thyrotoxicosis

Grave’s exopthalmos-> vision loss, diplopia

Pretibial Edema

Hyperthyroidism

Thyroid Storm

A medical emergency: high mortality

Marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, high fever

Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery
Increased systemic adrenergic activity->epinephrine overproduction and severe hypermetabolism

Hyperthyroidism: Diagnostics

Radioimmunoassay test shows elevated T4 and T3.

Thyroid scan reveals increased radioactive iodine (123I) uptake.

↓TSH in 1° hyperthyroidism

↑TSH in 2° hyperthyroidism

Orbital sonography and CT scan confirm subclinical ophthalmopathy


Management

Propylthiouracil (PTU) and methimazole

Used for pregnant women and patient who refuse surgery or 131I treatment.

During pregnancy PTU, is the preferred therapy

\Mechanism of action

 Blocks thyroid hormone synthesis

• WOF: Agranulocytosis

Radioactive iodine (131I), potassium or sodium iodide (Potassium iodide SSKI), strong iodine solution
(Lugol’s solution)

Adjunct with other antithyroid drugs in preparation for thyroidectomy

Treatment for thyrotoxic crisis:

 Inhibits the release and synthesis of thyroid hormones

 Decreases the vascularity of the thyroid gland

 Decreases thyroidal uptake of radioactive iodine following radiation emergencies or


administration of radioactive isotopes of iodine.

Hyperthyroidism: Nursing Management

Potassium, or sodium iodide, (potassium iodide solution, SSKI) strong iodine solution (Lugol’s
solution) Category D

Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the
patient, and to mask the very salty taste

Warn the patient that sudden withdrawal may precipitate thyrotoxicosis

Store in a light-resistant container

Give iodides through a straw to avoid tooth discoloration

Force fluids to prevent fluid volume deficit

Hyperthyroidism: Nursing Management of RAI treatment

Radioactive iodine (sodium iodide or 131I)-cat. X

 Food may delay absorption. The patient should fast overnight before administration
 After dose for hyperthyroidism, the patient’s urine and saliva are slightly radioactive for
24 hours; vomitus is highly radioactive for 6 to8 hours.

 Institute full radiation precautions during this time

 Instruct the patient to use appropriate disposal methods when coughing and
expectorating.

Hyperthyroidism: Nursing Management of RAI Tx

 After dose for thyroid cancer, isolate the patient and observe the following precations:

 Pregnant personnel shouldn't take care of the client

 Disposable eating utensils and linens should be used

 Instruct the patient to save all urine in lead containers for 24 to 48 hours so amount of
radioactive material excreted can be determined

 Or flush the toilet twice after urination

Hyperthyroidism: Nursing Management of RAI Treatment

 The patient should drink as much fluid as possible for 48 hours after drug administration
to facilitate excretion.

 Limit contact with the patient to 30 minutes per shift per person the 1st day; may
increase time to 1 hour on 2nd day and longer on the 3rd day.

 If the patient is discharged less than 7 days after 131I dose for thyroid cancer, warn patient:

 To avoid close, prolonged contact with small children

 Not to sleep in the same room with his spouse for 7 days after treatment-> increased
risk of thyroid cancer in persons exposed to 131I.

Hyperthyroidism

 B- blockers, Digoxin, anticoagulation

 Prednisone for opthalmopathy

 Treatment for thyroid storm:

o PTU

o I.V. propanolol to block sympathetic effects

o Corticosteroids to replace depleted cortisol levels


o Iodide to block release of thyroid hormone

Surgery: Thyroidectomy

 For exopthalmos

 Suggest sunglasses or eye patches to protect his eyes from light

 Moisten the conjunctivae often with artificial tears

 Warn the patient with severe lid retraction to avoid sudden physical movement that
might cause the lid to slip behind the eyeball.

 Elevate the head of bed to reduce periorbital edema

 Stress the importance of regular medical follow-up after discharge because


hypothyroidism may develop from 2 to 4 weeks pot-op

 Drug therapy and 131I therapy require careful monitoring and comprehensive teaching

Hypothyroidism

 A state of low serum thyroid hormone levels or cellular resistance to thyroid hormone

Causes

 May result from thyroidectomy

 Radiation therapy

 Chronic autoimmune thyroiditis ( Hashimoto’s Thyroiditis)

 Inflammatory conditions such as amyloidosis and sarcoidosis

 Pituitary failure to produce TSH

 Hypothalamic failure to produce thyrotropin-releasing hormone(TRH)

 Inborn errors of thyroid hormone synthesis

 An inability to synthesize thyroid hormone because of iodine deficiency.

 Use of antithyroid medications such as PTU.

 Weakness, FATIGUE

 Forgetfulness, Slow speech, Decreasing mental stability

 Cold intolerance
 Unexplained weight gain

 Constipation

 Goiter

 Cool, dry, coarse, flaky inelastic skin.

Puffy face, hands and feet

Dry, sparse hair, Thick, brittle nails

Slow pulse rate

Anorexia

Abdominal distention

Infertility, Decreased libido, Menorrhagia

Ataxia, Intentional tremor

Myxedema Coma

 Manifests as hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, respiratory


failure, coma

 Can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia,


surgery, hypothermia, use of opioids

Hypothyroidism : Diagnostics

 Radioimmunoassay tests: ↓ T3 & T4

 ↑TSH level with 1° hypothyroidism

 ↓TSH in 2 ° hypothyroidism

 Serum cholesterol and triglyceride levels are increased

 In myxedema coma

 Low serum Na levels

 Respiratory acidosis because of hypoventilation

Management
Prevention: Prophylactic iodine

supplements to decrease the incidence of iodine deficient goiter

Symptomatic cases:

 Hormonal replacement: synthroid

(synthetic hormone (levothyroxine))

Nursing Management of replacement therapy

 Warn the patient (especially the elderly) to tell the doctor if with

 Chest pain, palpitations, sweating, nervousness, or other signs or symptoms of


overdosage

 Signs and symptoms of aggravated cardiovascular disease (chest pain, dyspnea and
tachycardia)

 Instruct the patient to take thyroid hormones at the same time each day to maintain constant
hormone levels.

 Suggest a morning dosage to prevent insomnia

 Monitor apical pulse and BP. If pulse is >100bpm, withhold the drug. Assess to tachyarrhythmia
and chest pain.

 Thyroid hormones alter thyroid function test results.

 WOF: unusual bleeding and bruising

Hypothyroidism: Nursing Interventions

 Diet: High bulk, low-calorie diet

 Encourage activity

 Maintain warm environment

 Administer cathartics and stool softeners, as needed.

 To prevent myxedema coma, tell the patient to continue his course of thyroid medication even
if his symptoms subside:

 Maintain patent airway

 Administer meds-synthroid, glucose, corticosteroids.


 IV fluid replacement

 Wrap patient in blanket

 Treat infection or any underlying illness

Hyperparathyroidism

Characterized by excess activity or one more of the four parathyroid glands, resulting in excessive
secretion of parathyroid hormone(PTH)

Maybe primary or secondary

Hyperparathyroidism: causes

1° hyperparathyroidism:

 Single adenoma, genetic disorders, or MEN

 2 ° hyperparathyroidism:

 Rickets, vitamin D deficiency, chronic renal failure, phenytoin or laxative abuse.

Effect of PTH secretion: ↑Calcium

 Through increased bone resorption, increased GI and renal absorption of calcium

 Complications

 Renal calculi-> renal failure

 Osteoporosis

 Pancreatitis Peptic ulcer,

THINK OF HYPERCALCEMIA:

 CNS: psychomotor and personality disturbances, loss of memory for recent event, depression,
overt psychosis, stupor and possibly, coma.

 GI: anorexia, N&V dyspepsia, and constipation.

 Neuromuscular: fatigue; marked muscle weakness and atrophy, particularly in the legs.

 Renal: symptoms of recurring nephrolithiasis->renal insufficiency

 Skeletal and articular: chronic lower back pain and easy fracturing from bone degeneration,
bone tenderness, joint pain

 Others: skin pruritus, vision impairment, subcutaneous calcification.


Hyperparathyroidism: Dx

 ↑ serum PTH levels

 ↑ serum Ca and decreased Phosphorus levels.

 X-rays may show diffuse demineralization of bones

 Elevated alkaline phosphatase

Hyperparathyroidism: Treatment

 Surgery to remove the adenoma

 Force fluids; limiting dietary calcium intake

 For life threatening hypercalcemia: promote sodium and calcium excretion, using normal saline
solution (up to 6L in life-threatening situations), furosemide, and administering oral sodium or
potassium phosphate, Calcitonin

 Postmenopausal women: estrogen supplements

Hypoparathyroidism

 A deficiency of PTH

 PTH primarily regulates calcium

balance; hypoparathyroidism leads to hypocalcemia and produces neuromuscular symptoms ranging


from paresthesia to tetany.

Hypoparathyroidism: Signs and Sypmtoms

 Neuromuscular irritability

 Increased deep tendon reflexes, (+) chvostek’s and Trousseau’s signs

 Dysphagia

 Paresthesia, Tetany seizures

 Psychosis, Mental deficiency in children

 Arrhythmias

 Abdominal pain

 Dry, lusterless hair, spontaneous hair loss, Dry scaly skin

 Brittle fingernails that develop ridges or fall out.


 Weakened tooth enamel may cause teeth to stain, crack, and decay easily.

Hypoparathyroidism

 Decreased PTH and serum calcium levels

 Elevated serum phosphorus levels

 X-rays reveal increased bone density

 ECG: prolonged Qti, QRS-complex ST-elevation changes.

Disorders of the Pancreas

Diabetes Mellitus

Hormones of the Pancreas

 Insulin

 Glucagon

 Increases blood glucose by

 Causing glycogenolysis and gluconeogenesis in the liver

 Secreted in response to low blood sugar

 Found in the α-cells of the islets of langerhans

Diabetes Mellitus

 Chronic disease characterized by hyperglycemia

 It is due to total or partial insulin deficiency or insensitivity of the cells to insulin

 Characterized by disorders in the metabolism of CHO, FAT and CHON as well changes in
the structure and function of blood vessels.

Types of DM

 Type 1 or IDDM

 Usually occurs in children or in non-obese adults

 Type 2 or NIDDM

 Usually occurs in obese adult over age 40

 Gestational DM
 Secondary DM

 Induced by trauma, surgery, pancreatic disease or medications

 Can be treated as either type 1 or type 2

Comparison Bet Type 1 and Type II Diabetes Mellitus

Type 1 Type 2

Onset- Sudden Gradual

Age at Onset- Any age (typically young) Mostly in adults

Body Habitus - Usually thin Frequently obese

Ketosis- common Rare

Autoantibodies- present in most cases Absent

Endogenous insulin- low or absent Can be normal, decreased, or increased.

Pathophysiology

 Lack of insulin causes hyperglycemia (insulin is necessary for the transport across the
membrane)

 Body excretes excess glucose through kidneys ->osmotic diuresis->polyuria->dehydration-


>polydipsia

 Cellular starvation-> polyphagia

Hyperglycemia

The body turns to fats and protein for energy; but in the absence of glucose in the cell, fats cannot be
completely metabolized and ketones are produced

Chronic Complications

 Microangiopathy: retinopathy, nephropathy

 Macroangiopathy: peripheral vascular disease: peripheral vascular disease, atheroscelrosis, CAD

 Neuropathy

 f Diabetic Nephropathy
Diabetic Foot

Instruction in the care of the Feet

Hygiene of the feet

 Wash feet daily with mild soap and lukewarm water. Dry thoroughly between
toes by pressure. DO NOT RUB vigorously, as this is apt to break the delicate
skin

 Rub well with vegetable oil to keep them soft, prevent excess friction, remove
scales, and prevent dryness.

 If the feet become too soft and tender, rub them with alcohol about once a
week.

 When rubbing the feet, always rub upward from the tips of the toes. If varicose veins are
present, massage the feet very gently; never massage the legs.

 If the toenails are brittle and dry, soften them by soaking for 1 ½ hr each night in lukewarm
water containing 1 tsbp of powdered sodium borate (borax) per quart. Clean around nails
become too long, file them with an emery board. File them straight across and no shorter than
the underlying soft tissue of the toes. Never cut the corner of the nails.

 Wear low-heeled shoes of soft leather that fit the shape of the feet correctly. The shoes should
have wide toes that will cause no pressure, fit close in the arch, and grip the heels snugly. Wear
new shoes one-half hour on the first day and increase by 1 hour each day following. Wear thick,
warm, loose stockings.

Treatment of Corns and Calluses

 Corns and calluses are due to friction and pressure, most often from improperly fitted shoes and
stockings. Wear shoes that fit properly and cause no friction or pressure.

Instructions in the Care of the Feet

 To remove excess calluses or corns, soak the feet in lukewarm (not hot) water, using a mild
soap, for about 10 minutes and then rub off the excess tissue with a towel or file. Do not tear it
off. Under no circumstances must the skin become irritated.

 Do not cut corns or calluses. If they need attention it is safer to see a podiatrist.

 Prevent callus formation under the ball of the foot (a) by exercise, such as curling and stretching
the toes several times a day; (b) by finishing each step on the toes and not on the ball of the
foot. And (c) by wearing shoes that are not too short and that do not have high heels

Diagnostics: FBS, OGTT and RBS


Diagnostics: Glycosylated Hemoglobin

NV= 7.5% or less good control

7.6%--8.9% fair control

9% or greater, poor control

Therapeutic interventions

Lifestyle changes

 Weight control and exercise

 Planned diet

 50-60% of calories are complex carbohydrates, high fiber

 12-20% of daily calories is protein, 60-85g/day

 Fat intake not to exceed 30% of daily calories, more of polyunsaturated/


monounsaturated fats

 Basic tools: food exchange groups

 Self monitoring of blood glucose

 Moderation in alcohol intake

 Using artificial sweetener is acceptable

Insulin administration:

 For type 1 and type 2 dm when diet and weight control therapy failed.

 Aspirin, alcohol, oral anticoagulants, oral hypoglycemics beta blockers, TCA’s,


tetracycline, MAOI’s increase the hypoglycemic effect of insulin

 Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives increase glucose


levels

 Illness, infection and stress increase the need for insulin

Example Order for Typical Sliding Scale (HR)

CBG Insulin Dose

150-200 2 un its

201-250 4 units
251-300 6 units

301-350 8 units

351-400 10 units

>400 Refer to MROD, EFOD or Diabetology Fellow.

Complications of Insulin Therapy

Local allergic reaction, lipodystrophy, insulin resistance

“Dawn Phenomenon”- increase in blood sugar because of release of GH at around 3am;

 Tx: give NPH at 10 pm

• “Somogyi effect”-rebound hyperglycemia at 7am after a bout of hypoglycemia at 2-3am.

 Tx: Decrease the evening dose of intermediate acting insulin

Hypoglycemia

 If awake, give 10-15 g of fast acting simple carbohydrate (glucose tablets, fruit juice, and
soda)

 If unconscious, glucagon SQ or IM

 If in the hospital, 25-5o cc of D5050 (50% dextrose in 50cc vial)

Oral Hypoglycemic Agents

 For DM type 2

 May have to be shifted to insulin when sick, under stress, during surgery.

 Necessary to shift to insulin when pregnant

Oral Hypoglycemics

o Sulfonylureas

 Promotes increase insulin secretion from pancreatic beta cells through the stimulation(
requires at least 30% normally functioning beta cells)

 1st gen-agents: Tolbutamide, acetohexamide, tolzamide, chlorpropamide

 2nd gen-agents: Glipizide, Glyburide

Biguanides
 Reduces hepatic production of glucose by inhibiting glucogenolysis

 Decrease the intestinal absorption of glucose and improves lipid profile

 Agents- Phenformin, Metformin, Buformin

 Thiazolidinediones-enhances action at the cell and post receptor site decreasing insulin
resistance

 Agents: Pioglitazone (actos), Rosiglitazone (avandia)

Acute Complication: DKA

o Characterized by hyperglycemia and accumulation of ketones in the body causing metabolic


acidosis

o Occurs in insulin dependent Diabetic client

o Precipitating factors: Undiagnosed DM, neglect of treatment, infection, other physical or


emotional stress

o Onset slow, maybe hours to days

DKA: Signs and Symptoms

 Polydipsia, polyphagia, polyuria

 Nausea and vomiting, abdominal pain

 Skin warm, dry and flushed

 Dry mucous membranes

 Kussmaul’s respirations or hyperventilation; acetone breath

 Alterations in LOC

 Hypotension, tachycardia

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)

 Characterized by hyperglycemia and a hyperosmolar state w/o ketosis

 Occurs in NIDDM or non-diabetic persons (typically elderly persons

 Precipitating factors: undiagnosed DM, infection or other stress; certain medications, dialysis,
hyperalimentation, major burns
Emergency Management

For both DKA and HHNK, treat dehydration first with 0.9% or .45% saline

 Shift to d5w when glucose levels are down to 250-300mg/dl

 WOF too rapid correction, it can cause rapid fluid shifts (brain edema and increased ICP,
ARDS)

 IV regular insulin 0.1 unit/kg bolus then 0.1 u/kg/hr drip

 Correcting electrolyte imbalance. WOF hypoK as a result of treatment. For severe


acidosis (pH <7.1), DKA patients may have to be given NaHCO3