Dennis Christopher D.

So Chan RN TUA-SLCN

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

Endocrine System
Endocrine Glands
 

secrete their products directly to the blood stream different from exocrine glands

Exocrine glands: secrete through ducts onto epithelial

surfaces or into the GI tract

Overview of the Endocrine System

y The body s second great controlling system which

influences metabolic activities of cells by means of hormones, which are produced by endocrine glands
y Endocrine glands: pituitary, thyroid, parathyroid,

adrenal, pineal, and thymus y The pancreas and gonads produce both hormones and exocrine products y The hypothalamus has both neural functions and releases hormones y 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. 2. 3. 4. 5. 6. 7. 8.

Metabolism and tissue maturation Ion regulation Water Balance Immune system regulation Heart rate and blood pressure regulation Control of blood glucose and other nutrients Control of reproductive function 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.

Hormone Transport and Excretion

y Hormones are dissolved in plasma or bind to plasma proteins y Water-soluble hormones
y Proteins, epinephrine, and norepinephrine y Do not bind to plasma proteins or readily diffuse out of the blood y They are quickly broken down by enzymes or are taken up by tissues y These hormones regulate activities that have a rapid onset and a

short duration

y Lipid-soluble hormones and thyroid hormones

y Not quickly removed from the blood y Produce a prolonged effect

y Hormones leave the blood to reach target tissues or are excreted by the kidneys or liver

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

Hypopituitarism Hyperpituitatism

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 o e.g. Sheehan s syndrome  Infections and or inflammatory diseases o sarcoidosis o 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 May have micropenis, cryptorchidism

 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 y causes hypothyroidism with manifesations 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 vs.Somatotropinoma

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

Gigantism vs. Acromegaly

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,  Macroglossia leading to OSA  Hypertension, cardiomegaly, heart failure  Insulin resistance leading to type 2 DM  Visual field defects: bitemporal hemianopsia->complete blindness  Headaches  Arthritis  Hypogonadism

Therapeutics
 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 Diet

Nursing Interventions
 Provide emotional support=striking body change can

cause psychological stress.  Perform or assist with range of motion exercises to promote maximum joint mobility and prevent injury.  Evaluate muscle weakness, especially in the patient with late stage Acromegaly.  Keep the skin dry. Avoid using an oily lotion because the skin is already oily.

Nursing Interventions
 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  operative site is patched with muscle or fat-> sutures easily disrupted.  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  Mild analgesics for headache caused by CSF loss during surgery or paranasal pain.
 Paranasal pain typically subsides when the catheters

and packing are removed, usually 24 to 72 hours after surgery

Postoperative Care
 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.

Postoperative Care
 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 o o o Cortisol Thyroxine Estrogen or Testosterone Vasopressin

Diabetes Insipidus SIADH

Vasopressin or Antidiuretic Hormone

 Regulates water

metabolism
 Released during stress or

in response to an increase plasma osmolality to stimulate 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

Diabetes Insipidus
 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 ) Due to damage to the hypothalamus or pituitary stalk by tumor, anoxic encephalopathy, surgical or accidental trauma, infection (encephalitis, tuberculosis, syphilis), sarcoidosis, or multifocal langerhans cell (eosinophilic) granulomatosis ( histiocytosis X )

 Secondary diabetes insipidus



Diabetes Insipidus


Nephrogenic Diabetes Insipidus

Due to defect in the kidney tubules that interferes with water reabsorption Polyuria is unresponsive to vasopressin Patients have normal secretion of vasopressin

Diabetes Insipidus
Signs and Symptoms  Polyuria-> enormous daily output of very dilute urine, waterlike urine with specific gravity of 1.001 to 1.005  Intense thirst (patient tends to drink 4 to 40liters of fluid daily), especially with a craving for ice water,  Dehydration-> weight loss, poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness.  Inadequate water replacement results in  Hyperosmolality (irritability, mental dullness, coma, hyperthermia) because of dehydration and hypernatremia  Hypovolemia (hypotension, tachycardia and shock eventually)

Diabetes Insipidus
 Diagnostics  Fluid deprivation test-> to differentiate between psychogenic polydipsia and DI  Administration of desmopressin->to differentiate between central DI and nephrogenic DI  24 hour urine collection of volume, glucose, and creatinine  Serum for glucose, urea nitrogen, calcium, uric acid, potassium and sodium.

Therapeutics
y 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)  Psychotherapy

DI: Nursing Management

y 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.

DI: Nursing Management

 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 Antiduretic 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, mesothelioma  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)  Normal renal function (low BUN<10mg/dL),absence of hypothyroidism and glucocorticoid deficiency and recent diuretic therapy.

SIADH: Management
 Maintain fluid balance  Restriction or water intake (<1,000ml/day).  (takes 3-10 days to work)  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.

SIADH: Management
 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.

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)

y Cluster of physical abnormalities due to excessive cortisol release y Cortisol excess is due either to:  Autonomous steroid release from adrenal  Increased ACTH release from pituitary  complication of exogenous steroid therapy y Pic of hympy dumpty

Hypercortisolism (Cushing s Syndrome)

y Altered metabolism of  CHO: hyperglycemia  CHON: muscle wasting, thin, fragile skin, impaired wound healing  Fats: central obesity, moon face, buffalo hump  Na and water retention  Hypokalemia, hypocalcemia  Acne, hirsutism, menstrual changes, decreased libido  Weakness, emotional lability

Cushing s Syndrome

Complications
 Osteoporosis  Peptic Ulcer  Immune and inflammatory response is also

compromised
 Other complications include HPN, and sexual and

psychological complications

Cushing s Syndrome: Diagnostics

 ACTH levels-> determine whether the syndrome is

ACTH dependent.  24-hour urine collection for cortisol, midnight serum cortisol  Dexamethasone suppression test-> 1mg dexamethasone given at 11 pm and serum cortisol taken at 8am the next day.
 Cortisol level <5ug/dl excludes Cushing s syndrome with

98% certainty

 Radiologic evaluation  Tumor in the pituitary or adrenal gland

Cushing s Syndorme: Management

 Transsphenoidal resection of pituitary tumor  Medications:
o Aminogluthetimide: adrenal enzyme inhibitor o Metyrapone and ketoconazole: suppress hypercortisolism in unresectable adrenal tumor

 Antihypertensives  Adrenalectomy as needed

Cushing s Syndome: 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  Prepare client for adrenalectomy if needed

Hyperaldosteronism
y Hypersecretion of aldosterone from the adrenal cortex y Two types:  Primary disease of the adrenal cortex  Secondary condition due to increased plasma renin activity y Causes:  Excessive reabsorption of sodium and water  Excessive renal excretion of potassium

Hyperaldosteronism: Causes
y Primary hyperaldosteronism: Autonomous secretion of aldosterone from the adrenals  Benign adrenal adenoma (Conn s syndrome) y Secondary hyperaldosteronism: High renin state-> stimulating aldosterone release  Renal artery stenosis  Wilm s tumor  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

Hyperaldosteronism: Diagnostics
Hypokalemia Hypernatremia Elevated serum bicarbonate and pH Hypomagnesemia Elevated plasma and urinary aldosterone Decreased Renin in 1 hyperaldosteronism Increased Renin in 2 hyperaldosteronism Low specific gravity urine (diluted urine)

Hyperaldosteronism: Treatment
y 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  Aldosterone secretion frequently continues. Nursing Alert! Adrenal crisis (addisonian crisis) is a medical emergency requiring immediate, vigorous treatment.

Adrenal Insufficiency:causes
y Autoimmune destruction of the adrenal gland,

tuberculosis, bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, or fungal infections.

y 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

y Weakness, fatigue y Weight loss, nausea and vomiting, anorexia y Chronic constipation or diarrhea y Cardiovascular abnormalities  Postural hypotension, decreased cardiac output  Weak, irregular pulse  Decreased tolerance for even minor stress

Adrenal Insufficiency: signs and symptoms

y Conspicuous bronze skin coloration, especially in

hand creases and over the metacarpophalangeal joints, elbows, and knees. y Poor coordination y Fasting hypoglycemia; and craving for salty food. y Amenorrhea y Adrenal crisis
 Profound weakness and fatigue, shock, severe nausea

and vomiting, hypotension, dehydration and high fever.

POMC: the Big Momma

y 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

y Corticosteroid replacement, usually with cortisone or

hydrocortisone-> primary lifelong treatment

y Fludrocortisone acetate: acts as a mineralocorticoid

to prevent dehydration and hypotension.

y Adrenal Crisis: prompt IV bolus of corticosteroids, 3 to

5 L of IV fluids, dextrose

Adrenal Insufficiency: Nursing Management

y 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)

Adrenal Insufficiency: Nursing Management

 If patient has diabetes, check blood glucose levels

periodically because steroid replacement may necessitate changing the insulin dosage.

Adrenal Insufficiency: Nursing Management

 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.

Adrenal Insufficiency: Nursing Management

 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.

Pheochromocytoma

Pheochromocytoma: 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

Pheochromocytoma:
y 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.

Pheochromocytoma: 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
y Resection or removal of one or both adrenal glands. y The treatment of choice For adrenal hyperfunction and hyperaldosteronism Adrenal tumors, such as adenomas and pheochromocytomas.

Adrenalectomy: Pre-op
y Correct electrolyte imbalance  Potassium, sodium, calcium Manage hypertension

Adrenalectomy: Post-Op care

y Monitor vital signs y WOF: shock and hemorrhage y Keep in mind that postoperative hypertension is

common because handling of the adrenal glands stimulates catecholamine release. y WOF: adrenal crisis-> hypotension, hyponatremia, hyperkalemia y 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

y Instruct the patient to take prescribed medication as

directed.
y If patient had unilateral adrenalectomy, explain that

he may be able to taper his medication in a few months.

y Inform patient that sudden withdrawal of steroids can

precipitate adrenal crisis.

Hyperthyroidism Hypothyroidsim

The Thyroid Gland

Thyroid gland is a butterfly-shaped organ located in the lower neck anterior to the trachea
y It consists of two lateral lobes

connected by an isthmus y The gland is about 5cm long and 3cm wide and weighs about 30g y It produces 3 hormones: T3, T4, and calcitonin

Functions of Thyroid Hormones

y T3 y T4 y Calcitonin

Tests of Thyroid Function

y 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 If TSH is normal, there is a 98% chance that the free thyroxine (FT4) is also normal. Used for monitoring thyroid hormone replacement therapy and for differentiating between disorders of the thyroid gland and disorders of the pituitary or hypothalamus.

Tests of Thyroid Function

y 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) y 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

y Thyroid scan, Radioscan, or Scintiscan  In a thyroid scan, a scintillation detector or gamma camera moves back and forth across the area to be studied and a visual image is made of the distribution of radioactivity in the area being scanned. 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.

Tests of Thyroid Function

y 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.

Tests of Thyroid Function

y Fine-Needle Aspiration

Biopsy
 Sampling Thyroid

Tissue to: detect malignancy  Initial test for evaluation of thyroid masses.

Tests of Thyroid Function

y 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

Plummer s nails

Hyperthyroidism
y Or thyrotoxicosis y Increased metabolic rate y 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 o Amiodarone-induced

Hyperthyroid: Signs and Symptoms

y y y y y y y y y y y y y

Enlarged thyroid gland Tachycardia-> atrial fibrillation, heart failure Hypertension Heat intolerance, diaphoresis Smooth, soft, warm skin Fine Soft Hair Diarrhea, weight loss inspite 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

y All s/s of thyrotoxicosis y Grave s exopthalmos-> vision

loss, diplopia
y Pretibial Edema

Hyperthyroidism

Thyroid Storm
y A medical emergency: high mortality y Marked delirium, severe tachycardia, vomiting, diarrhea,

dehydration, high fever

y Occurs in patients with existing but unrecognized

thyrotoxicosis, stressful illness, thyroid surgery, RAI administration

y Increased systemic adrenergic activity->epinephrine

overproduction and severe hypermetabolism

Hyperthyroidism: Diagnostics
y Radioimmunoassay test shows elevated T4 and T3. y Thyroid scan reveals increased radioactive iodine

(123I) uptake. y TSH in 1 hyperthyroidism y TSH in 2 hyperthyroidism y Orbital sonography and CT scan confirm subclinical ophthalmopathy

Hyperthyroidism: Management
y Propylthiouracil (PTU) and methimazole y Used for pregnant women and patient who refuse

surgery or 131I treatment. y During pregnancy PTU, is the preferred therapy y A few (1%) of the infants born to mothers receiving antithyroid medication will be hypothyroid. y Mechanism of action
 Blocks thyroid hormone synthesis

WOF: Agranulocytosis

Hyperthyroidism: Management
y Radioactive iodine (131I), potassium or sodium

iodide (Potassium iodide SSKI), strong iodine solution (Lugol s solution) y Adjunct with other antithyroid drugs in preparation for thyroidectomy y 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

y Potassium, or sodium iodide, (potassium iodide solution, y

y y y y

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.

Hyperthyroidism: Nursing Management of RAI treatment

 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

Hyperthyroidism: Management
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.

Hypothyroidism
 Weakness  Fatigue  Forgetfulness  Cold intolerance  Unexplained weight gain  Constipation  Goiter  Slow speech  Decreasing mental stability

 Cool, dry, coarse, flaky

inelastic skin.

Hypothyroidism
y Puffy face, hands and feet y Dry, sparse hair y Thick, brittle nails y Slow pulse rate y Anorexia y Abdominal distention y Menorrhagia y Decreased libido y Infertility y Ataxia y 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)) -dosage is increased q 2-3weeks

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)

Nursing Management of replacement therapy

 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.

Nursing Management of Replacement therapy

 Thyroid hormones alter thyroid function test results.  For 123I uptake studies  D/C levothyroxine 4 weeks before the test.  D/C liothyronine 7 to 10 days before the test.  Monitor prothrombin time; a patient taking these

hormones usually requires less anticoagulant

 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
y Characterized by excess

activity or one more of the four parathyroid glands, resulting in excessive secretion of parathyroid hormone(PTH) y Maybe primary or secondary

Hyperparathyroidism: causes
y 1 hyperparathyroidism:  Single adenoma, genetic disorders, or MEN 2 hyperparathyroidism:  Rickets, vitamin D deficiency, chronic renal failure, phenytoin or laxative abuse.

Hyperparathyroidism
y 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

Hyperparathyroidism
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.

Hyperparathyroidism: Signs and Symptoms

 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
 Congenital absence or malfunction of the parathyroid glands.  Autoimmune destruction  Removal of or injury to one or more parathyroid glands during     

neck surgery Rarely, from massive thyroid radiation therapy. Ischemic infarction of the parathyroids during Sx. Diseases, such as amyloidosis or neoplasms Suppression of normal gland function caused by hypercalcemia(reversible) Hypomagnesemia-induced impairment of hormone secretion(reversible)

Hypoparathyroidism: Signs and Sypmtoms

 Neuromuscular irritability  Increased deep tendon reflexes, (+) chvostek s and Trousseau s signs  Dysphagia  Paresthesia  Psychosis  Mental deficiency in children  Tetany seizures  Arrhythmias  Abdominal pain  Dry, lusterless hair, spontaneous hair loss  Brittle fingernails that develop ridges or fall out.  Dry scaly skin  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.

Diabetes Mellitus

Hormones of the Pancreas

Insulin Decreases blood sugar:


  

Stimulating active transport of glucose into muscle and adipose tissue Promoting the conversion of glucose to glycogen for storage Promoting conversion of fatty acids into fat Stimulating protein synthesis

Secreted in response to high blood sugar Found in cells of the islets of langerhans

Hormones of the Pancreas

Glucagon
 Increases blood glucose by


Causing glycogenolysis and gluconeogenesis in the liver

 Secreted in response to low blood sugar  Found in the -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 Usually occurs in obese adult over age 40

Type 2 or NIDDM 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
y Onset- Sudden y Age at Onset- Any age y y y y

Type 2
y Gradual y Mostly in adults y Frequently obese y Rare y Absent y Can be normal, decreased, or

(typically young) Body Habitus- Usually thin Ketosis- common Autoantibodies-present in most cases Endogenous insulin- low or absent

increased.

PathophysiologyHyperglycemia
 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

Cont. pathophysiology
y 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

Pathophysiology of Diabetic Nephropathy

Hyperglycemia GFR Microalbumin uria Proteinuria GFR

ESRD

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.

Instruction in the Care of the Feet

Hygiene of the feet
 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 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.

Instruction in the care of the Feet

 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

Normal Glucose Tolerance Fasting Plasma Glucose 2 hours after glucose < 110 mg/dl Impaired Glucose Tolerance 11o-125 mg/dl Diabetes Mellitus 126 mg/dl on 2 occassions 200 mg/dl

< 140 mg/dl

140 but <200

Random Blood Glucose

---------

---------

>200 mg/dl plus diabetic symptoms

Diagnostics: Glycosylated Hemoglobin

y NV= 7.5% or less good control y 7.6%--8.9% fair control y 9% or greater, poor control

Therapeutic interventions
y Lifestyle changes
- Weight control and exercise - Planned diet
g

g g

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

Cont: therapeutic interventions

y 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

Insulin Ultra rapid acting insulin analog (humalog) Short acting insulin (Human regular insulin) Intermediate acting insulin (Humulin lente, Humulin NPH) Long acting Insulin (Protamine zinc, humulin ultralente) Premixed insulin (70% NPH, 30% regular)

Onset 10- 15 mins

Peak 1 hour

Duration 3 hours

30 minutes- 1 hour 2-4 hours

4-6 hours

3-4 hours

4-12 hours

16-20 hours

6-8 hours

12-16 hours

20-30 hours

30min-1 hour

2-12 hours

18-24 hours

Example Order for Typical Sliding Scale (HR)

CBG
y 150-200 y 201-250 y 251-300 y 301-350 y 351-400 y >400

Insulin Dose
y 2 units y 4 units y 6 units y 8 units y 10 units y Refer to MROD, EFOD or

Diabetology Fellow.

Complications of Insulin Therapy

y Local allergic reaction, lipodystrophy, insulin

resistance
y 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

Diabetes Mellitus: Complication of Insulin

Dawn Phenomenon S/Sx Cause Mgt Hyperglycemia at dawn
Growth hormone release at 3 AM
Give IAI at 10 PM (or adjust dose)

Somogyi Phenomenon
Rebound Hyperglycemia at early morning

Hypoglycemia at dawn
Decrease dose of IAI at 10 PM

Complications of insulin therapy Hypoglycemia

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 Sulfonyureas  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 Glypizide, Glyburide

 2nd gen-agents:


Oral Hypoglycemics
y Biguanides  Reduces hepatic production of glucose by inhibiting glucogenolysis  Decrease the intestinal absorption of glucose and improves lipid profile  Agents


Phenformin, Metformin, Buformin

Oral Hypoglycemics
 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
y 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

DKA

HHNK
Hyperglycemia Hyperosmolarity Polyuria (osmotic diuresis) Dehydration DM type II Elderly Patients on TPN, burn
Hyperglycemia (>600mg/dl) Hyperosmolarity(>320 mOsm/L) pH >7.3 (no acidosis)

S/sx

Hyperglycemia Polyuria Dehydration Acidosis DM type I

Type of patients

Lab Findings

Hyperglycemia (>250) Metabolic Acidosis ph <7.3 Ketosis

DKA Treatment Hydration Insulin NaHCO3 5% to 10%

HHNK Hydration Insulin

Mortality rate

10% to 20%

Always strive for excellence in everything that you do. Thank You Very Much DCSC RN