Two conditions of abnormal secretion of Anti-diuretic Hormone (ADH)/arginine vasopressin

1. Diabetes Insipidus (DI) ADH A. Under secretion/ production of ADH or renal response to ADH o Polyuria (up to 2-20L/day) large quantities of bland urine resulting in kidneys ability to concentrate urine :

specific

gravity of <1.007
o Nocturia, bladder distention, hydronephrosis, ploydipsia (thirst), appetite & weight loss, constipation, sleep deprivation usually the PRIMARY cause i. fluid & electrolyte imbalance urinary output & plasma osmilarity ii. may be transient or a chronic lifelong condition

Causes of Diabetes Insipidus

o Primary 1. Cranial sugery 2. Head trauma 3. Encephalitis 4. Meningitis Additional causes: adverse effects of medications Dilantin, Lithium, Reserpine & alcohol

Complications:
o o o Hypernatremia - Na+ & LOC (neuro checks) Hypovolemia - fluid volume Na+encephalopathy CNS injury DEATH Hypervolemia b/c of H2O intake resulting from excessive thirst may result in water intoxication assess for crackles in the lung.. avoid fluid overload.

B. Inability to respond to ADH( Neurogenic DI) Adverse drug effects , CRF, chronic hypokalemia

2. Syndrome of Inappropriate ADH secretion (SIADH) o Over secretion/production of ADH

Disorder Diabetes Insipidus (DI) ADH

Definition & Causes

Excessive loss of H2O - Neurologic: insufficient ADH secretion by Post Pituitary gland. - Nephrologic: kidneys unable to respond to ADH - Medications: Lithium, thioridazine (Mellaril)& demeclocycline (can cause polyuria ADH) - Primary DI: results from inherited or idiopathic malfunction of Post Pituitary gland - Secondary DI: caused by surgery on or near pituitary gland, brain tumors, head trauma, metastatic tumors from lung or breast, cva, cvh, granulomatous disease.

Signs & Symptoms

Polyuria severe dehydration 2-20L/day Polydipsia (excess thirst) Weight & appetite loss Dry/tented skin Dry mucous membranes Severe hypotension (if excess H20 loss not replaced BP LOC, sensory & motor deficitshypernatremia Nocturia Bladder distention Hydronephrosis constipation possibly sleep deprivation

Dx tests & Treatments

Urine specific gravity < 1.007 Via dipstick - Urine osmolarity < 50-200 mOsm/kg serum ADH level - Serum Osmalarity >300 - Serum sodium > 145 mEq/L - + Positive H2O deprivation test - 3% NaCL via IV to assess H2O conservationstoring Vasopressin challenge test s.e =heart failure if suseptable

Nursing Interventions
Rehydration (Rapid 1st)-(P.O preferred) or IV 0.45% NaCL. closely monitor BP, HR & output Q1hr - 1. Admin vasopressin(pitressin IV/sub Q)-possible circulatory overload b/c urinary output s.e HTN, MI, uterine cramps, peristalsis - 2. mild antidiuretic effect Hydrochloratiazide, chlorpropamide ADH Monitor urine specific gravity - Monitor serum osmolality and Na for increases - Neurogenic DI: Desmopressin for hormone replacement; Chlorpropamide (Diabinese) or Carbamazepine (Tegretol) Patient Teaching Possible need for lifelong meds Wear a medic-Alert bracelet

F&E imbalance urinary output & serum osmilarity >300 mOsm/kg Decrease fluid volume

Syndrome of Inappropriate Antidiuretic Hormone (SIADH) ADH urination fluid retention

H2O intoxication cerebral edema hyponatremiaDEATH..

Excess fluid volumeBP assess crackles in lung

Excessive amount of serum ADH; resulting in: water intoxication (excessive water retention) and hyponatremiaNa+ <135 Usual feedback mechanism malfunction & cant tell the post Pituitary gland to decrease the secretion of ADH Elevated ADH leads to renal excretion of Na+ (sodium) - Renal excretion of Na+ water intoxication, cellular edema, & hyponatremia. - Causes:seen in Postop oncology pts & w/ multi-organ dysfunction. Trauma, AIDS pulmonary disease, malignant tumors, MEDS, intrathoracic pressure, untracranial hemorrhage.

Fluid Volume Excess Weight gain w/out edema-c/o of difficulty breathing Seizures - ICP Headache Fatigue Anorexia Nausea,diarrhea & vomiting Muscle aches Abdominal cramps Progressive altered LOC Coma 12) Small amounts of concentrted amber-color urine 13) BP 14) Dist. Jugular neck veins 15) Taut skin 16) Intake greater than output

High urine Osmolarity > 1200 Urine specific gravity > 1.030 - aldosterone secretion - plasma Osmolarity < 275 - Decreased Hematocrit - Decreased BUN - Sodium (Na+) < 135

Weight self daily & report wt loss Drink fluids & keep a log of I&O Keep follow up appointments Restrict fluids including ice chips Encourage sodium supplements or hypertonic saline IV infusion - Assess for changes in LOC Monitor I & O Weigh patient daily

Medications: IV hypertonic (3%) normal saline; Demeclocycline (Declomycin) or Litium to replace electrolytes Na+; Diuretics (to eliminate excess fluid) Patient Teaching Medication maybe life & medic alert Plan meal pattern and maintain fluid restriction Take sodium supplements as ordered - Weigh self daily and report 2 lb gain in 1 day

Disorder Adrenal Insufficiency (Addisons Disease)

Definition & Causes Insufficient level of cortisol because of the destruction of the adrenal cortex. 400 new cases/year in the US Autoimmune form 80% of all cases Tuberculosis (Until 1950 disseminated TB was primary cause) - Surgical removal of

Signs & Symptoms

Hyponatremia Hyovolemia Dehydration Weight loss Hypoglycemia Muscle weakness Postural Hypotension Hyperpigmentation (eternal skin) Delayed wound healing Cardiovascular changes: (tachycardia, dysrhythmias, postural Hypertension)

Dx tests & Treatments Lab studies that measure serum cortisol (ACTH) or pituitary levels - 24 hr Urine for 17hydroxycorticosteroids and 17-ketosteroids Hematological - BCP (Blood Chemistry profile)

Nursing Interventions
Maintain fluid & electrolyte balance Monitor lab values Monitor I & O Encourage 3k mL fluid daily Promote safety Provide foods high in sodium (Na) and low in potassium (K) D - Medicaitons: Hydrocortisone (to replace cortisol; fludrocortisones (florinef) to replace mineralcorticoids as needed

adrenal gland resulting in hyposecretion of adrenal hormones - AIDS A small but significant number of AIDS pts will develop Addisons disease Septicemia Infiltrative diseases - Sudden cessation of longterm high-dose steroid medication No currently recommended preventative measures focus is on early detection

GI disturbances: Anorexia, vomiting, nausea, diarrhea Depression, lethargy, emotional liability, confusion. Addisonians Crisis: life threatening response sudden withdrawal of steroids or exposure to any kind of stress (Severe Hypotensio, circulatory collapse, schock, & coma.

More Meds: Daily glucocorticod replacement therapy; Daily mineralcorticoid replacement therapy; Na+ replacement; fluids and dextrose Patient Teaching:

Addisonian Crisis

General Description - Sudden life-threatening

exacerbation of Addisons Disease usually triggered by STRESS. Patient experiences extremes of: hypotension, hyponatremia, dehydration / hyperkalemia Fever that may be unrelated to any other cause is not uncommon - Without immediate attention, condition will progress to coma and death

SIGNS AND SYMPTOMS HEADACHE NAUSEA ABDOMINAL PAIN DIARRHEA CONFUSION RESTLESSNESS MAY LEAD TO CIRCULATORY COLLAPSE MEDICAL EMERGENCY CYANOSIS & FEVER CLASSIC SIGNS OF SHOCK PALLOR; LOW BP APPREHENSION RAPID AND WEAK PULSE RAPID RESPIRATIONS

Medical Management
- COMBAT SHOCK - HYDROCORTISONE IV FOLLOWED BY 5% D/NS - LIFE-LONG REPLACEMENT OF CORTICOSTEROIDS AND MINERALOCORTICOIDS - MAY NEED ADDED SALT WITH VOMITING OR DIARRHEA

IV injection of hydrocortisone in NS to restore normal blood volume over a short period of time Assessment of causes that might have triggered crisis Constant monitoring of VS, neurological status, Fluid balance status

Disorder

Definition & Causes

Signs & Symptoms

Dx tests & Treatments -

Nursing Interventions
Monitor VS; daily weights Monitor lab values, glucose monitoring and CV status Observe for changes in mentation, LOC, s/s of complications Provide pre/postoperative care for

Cushings Disease
(Adrenal Cortex Hypersecretion)

Hypersecretion of cortisol - Elevated serum cortisol causes life-threatening changes in:pshychological physiological, metabolic functioning - Primary Cushings: caused by a tumor in the adrenal cortex

Affects all major systems of the body:

1) Generalized weakness

2) Hypertension 3) Hyperglycemia 4) Osteoporosis

5) Thin skin (bruised easily) 6) Emotional lability (mood swings)

Measurement of cortisol; ACTH - 24 hour Urine. Collection - Hematological; - Biochemical Profile (BCP), GTT - X-Ray, CT & MRI of head (anterior pituitary

Secondary Cushings: Disorder of the Pituitary or hypothalamus gland causing increased ACTH & Hyperplasia of the adrenal cortex - Iatrogenic: long-term use of glucocorticoid hormones such as steroids

Complications

Directly related to: hypernatremia, hypokalemia hypertension, hyperglycemia, skin breakdown and psychologic dysfunction - Untreated Cushings Syndrome may over time, lead to CAD and CHF

7) Skin infections 8) Fluid overload 9) Weight gain 10)Truncal obesity (moon facies, fat pad on back) 11) Striae 12) Hirsutism 13) Possible amenorrhea 14) Impotence 15) Decreased Libido 16) Petechiae 17) Males: Gynecomastia 18) Na+ & Fluid retention

function)

Medical Treatment: - Radiation therapy of PG - Single or bilateral adrenalectomy Hypophysectomy (removal of the pituitary gland)

patients undergoing surgical intervention Discharge Planning and instructions regarding medications, home care and follow-up Post-op surgery care: - Provide effective deep breathe exercise & hourly client coughing (Transphenoidal surgery avoid coughing) Keep HOB 30 degrees elevated Check pituitary surg for CSF Prevent Addisonian crisis by: giving IV NS infusion bolus and cortisol as ordered for: dry skin, decreased LOC Patient Teaching Eat high protein and vitam B, C

Adrenal Glands Located atop the kidneys; consisting of two glands in one Adrenal Medulla secretes the catecholamine epinephrine and the neurotransmitter norepinephrine Adrenal Cortex secretes steroids; including glucocorticoids, mineralcorticoids, and the sex hormones estrogens and androgens MINERALOCORTICOIDS CONCERNED WITH: 1) SODIUM RETENTION 2) WATER RETENTION 3) POTASSIUM EXCRETION Adrenal Gland Hormones: S Sugar (Glucocorticoids) S Salt (Mineralcorticoids) S Sex (Androgens) Disorder Definition & Causes Signs & Symptoms - Over-production of Thyroid H. Neurologic Changes Hyperthyroidism (Graves - Excessive secretion of

Dx tests & Treatments Elevated Serum T3 &

Nursing Interventions
Instruct client to drink (Radioactive iodine 131) with

Disease)

thyroid hormones from the thyroid gland leading to increased 1) basal metabolic rate; 2) cardiovascular function; 3) GI function; 4) neuro function; 5) weight loss; 6) heat intolerance - Thyroid hormones affect: metabolism of fats; carbs; and proteins Can be caused by: Excess secretion of TSH from the Pituitary gland; Autoimmune reaction (Graves Disease); thyroiditis; tumor; excessive dose of thyroid hormone Also known as exophthalmic goiter If untreated, complications of heart failure, thyrotoxic crisis, and severe psychiatric disorders can develop -

(LOC) Fatigue; Weight loss Enlarged thyroid Intolerance to heat - Localized edema Tremors Tachycardia Diarrhea - Exophthalmos (Bulging eyes) Anxiety Increased BP Muscle wasting Fine straight hair Facial flushing Amenorrhea Cardiac-related problems -

T4 (radioimmunoassay technique) Free T4 & T3 elevated in thyrotoxicosis - Decreased - TSH Levels - EKG tachycardia - RAIU (Positive) differentiates Graves disease from other forms of thyroiditis Nodular Goiter high-normal range

straw to decrease exposure to buccal cavity Monitor lab values Tell client to report weight gain fatigue, decreased pulse, and BP

Thyrodectomy Preop:
Teach deep breathing exercise & appropriate cough Tell pt to hold hands behind neck when coughing, sitting, turning, or getting up/back to bed to reduce post-pain

Nutrition: **High caloric diet**

Medication Therapy: - Antithyroid drugs for

life: Potassium iodide, methimazole (tapazole), or propylthiouracil (PTV) to reduce secretions of thyroid hormone - Ablative Radioactive I131 or with beta-adrenergic blockers (Inderal): to reduce vascularity and size of thyroid gland Analgesics to control pain

Self-admin of antithyroid drugs: to decrease vascularity and size of thyroid to minimize risk of hemorrhage Thyroidectomy Postop: - Provide comfort: analgesics, semi-fowlers with neck and head supported by pillows - Monitor for hemorrhage: check back of neck; auscultate trachea for stridor (indicates edema or narrowed airway) - Promote patent airway: Keep HOB elevated 30 degrees; Emmergency tracheostomy tray at bedside; Calcium gluconate at bedside; Deep breathing exercise hourly; maintain air humidification - Prevent tetany (early indication of hypocalcemia) numbness & tingling of toes, extremities; muscle twitching positive chvoteks & Trousseaus signs
-

Maintain patent IV site Assess for laryngeal nerve

damage ( ability to speak, quality, & tone of voice)

Graves Disease
Diffuse toxic goiter; probable autoimmune disorder Severe state of hyperthyroidism Common S/S include: Exopthalmos protrusion of the eye orbits caused by retro-orbital fat deposits that could cause pressure on optic nerve Enlarged thyroid gland (bruits and thrills usually present) Additional s/s associated with hyperthyroidism

Thyrotoxic Crisis (Thyroid Storm)

Extreme exacerbation of severe hyperthyroidism Occurs most often in patients who have previously undiagnosed and untreated hyperthyroidism Metabolic rate increased dramatically without regard to body systems May be precipitated by several factors, including stress, diabetes mellitus, infection, Treatment is very individualized according to clinical findings

Severe Hyperthyroidism Body Temp- Normal or slightly elevated CV Function Tachycardia Mental Status Restlessness, irritability Fluid Balance moist skin, increased respirations and urinary output

Thyrotoxic Crisis Body Temp very high (102 106) CV Function Severe tachycardia, atrial dysrythmias, CHF Mental Status possible psychotic or extreme manic behavior Fluid Balance extreme diaphoresis, vomiting, diarrhea; significant F & E imbalance

Disorder Hypothyroidism

Definition & Causes Under-production of thyroid hormone results in: decreased metabolic rate, decreased heat production. Other causes: thyroiditis, subacute postpartum, external radiation of the gland, infection, iodine deficiency, congenital or idiopathic - Secondary hypothyroidism: also called central hypothyroidism caused by insufficient secretion of TSH & TRH deficiency to disease of the hypothalamus

Signs & Symptoms Thyroid gland enlarges to form goiter (thickening of the gland) Lethargy Diminished DRT (reflexes) Periorbital edema Bradycardia Cold intolerance Dysrhythmias Hypotension Mennorrhagia (female) Decreased libido (male) Coarse dry hair Coarse dry skin Anemia, elevated serum lipids - Signs of slowed metabolism: (hypothermia, fatigue, weight gain, anorexia) - Assess for Myxedema (non-pitting edema, puffy face and tongue, hypothermia, cardiovascular collapse, coma)

Dx tests & Treatments

Normal T3 Decreased T4 and Free T4 - Increased TSH levels (unless secondary hypothyroidism)

Nursing Interventions
Give medication 1hr before food and 2 hrs after food to facilitate absorption - Provide comfort: warm environment adjust temp. or provide extra blankets (chilling increases metabolic rate, cardiac workload, and oxygen demand) Pace activities with rest periods Instruct patient to report SOB, fatigue, and dizziness Encourage fluids intake of 2,000 mL of H20 and high fiber diet to promote reg. bowel movements Patient Teaching: Maintain a calorie controlled diet and low-fat Report chest pain and sleep pattern disturbance Take same brand of medication Withhold meds for HR >100

Medication:
Thyroid hormone replacement:

(dessicated thyroid, thyroxine (Synthroid) or triiodothyronine (cytomel)

Diabetic ketoacidosis (DKA)

Clinical manifestations: Polyuria (frequent urination) Polydipsia (excessive thirst) Polyphagia (excessive hunger) Dehydration dry mouth, flushed dry skin DKA Metabolic acidosis

Diabetes Two-dose insulin protocol two thirds (2/3) of the dose before breakfast and one third (1/3) before the evening meal. After hyphysectomy diabetes insipidus can occur temp because of ADH deficiency. Disorder Hyperparathyroidism The nurse should assess for urine specific gravity lower (<) 1.006. Definition & Causes Signs & Symptoms Over-production of PTH from the PT gland in the neck Primary: - Hyperplasia or adenomas (tumor) of one of the Parathyroid gland increase Calcium absorption Secondary: - Gland enlargement due to chronic hypocalcemia Tertiary hyperthyroidism: - Chronic renal failure parathyroid glands to be enlarged and do not respond to changes in calcium levels - Increased resorption of calcium & increased excretion of phosphate results in hypercalcemia & hypophosphatemia - Major predisposing factors: CRF, hyperphosphatemia, Vit. D insufficiency - Kidneys increase bicarbonate excretion & decrease acid excretion leads to metabolic acidosis & hypokalemia - Bones increase rate of calcemia & phosphorus release lead to bone decalcification Polyuria (early sign) Renal calculi Anorexia Constipation - Nausea & vomiting Abdominal pain (from peptic ulcer disease) Generalized bone pain Pathologic fractures Muscle weakness & atrophy CNS signs (depressed DTR, parathesias, depression, psychosis)

Dx tests & Treatments - Elevated Calcium levels - Increased PTH - Decreased Phosphate - Skeletal X-rays & CT scan possible bone changes

Nursing Interventions
Promote comfort & safety: patient to walk with walker to prevent falls Initiate seizure precautions Check all urine to detect calcium-based urinary stones Provide 2,000 to 3,000 mL of fluids daily Provide a high-fiber diet Promote nutrition and fluid & electrolyte balance Weigh patient daily Prevent tetany caused by surg. Provide Pre- and postoperative care Monitor change in voice

Major symptoms include: Weakness, loss of appetite, constipation, increased need for rest & sleep, emotional disorders and shortened attention span Major signs include: Osteoporosis, kidney stones, neuromuscular disorders

Treatment: Acute Hypercalcemia Serum Ca. levels 15mg or Medication greater is considered life - Analgesics to threatening control pain 1. Rehydration - Diuretics 2. Saline / diuresis - Normal saline (0.9) 3. Administration of by IV infusion to excrete calcitonin, Ca+ phosphate, - Phosphate mithramycin - Calcitonin 4. Dialysis (Miacalcin) 5. IV Normal Saline & - Biphosphonates such Lasix as pamidronate 6. Possible (Aredia) and parathyroidectomy alendronate (Fosamax)

Hypercalcemia causes calcium deposits in soft tissues, renal calculi, altered neuro function, altered GI function with constipation, abdominal pain, anorexia, and altered cardiovascular system

may be used to inihibit bone reabsorption

Disorder Hypoparathyroidism

Definition & Causes Under-production of PTH leads to hypocalcemia (usually caused by surgical removal of all or part of the thyroid gland)

Signs & Symptoms GI Symptoms

Abdominal pain Nausea & vomiting diarrhea anorexia

Dx tests & Treatments Decreased serum PTH Decreased total calcium Decreased free calcium Increased serum Phosphate

Nursing Interventions Promote comfort & safety: provide walker to prevent fall Pacing activity with rest periods Promote nutrition & fluid balance - High-calcium diet & vitamin D

Hypocalcemia

Hypocalcemia signs:
Anxiety Headaches Paresthesias Neuro: tremors & muscle spasms

raises the threshold for excitability in nerve & muscle fibers (could lead to life-threatening tetany)

- Most commonly follows thyroidectomy -

Other Signs:
Difficulty swallowing Horse voice Thightness in throat Dry thin hair Patchy hair loss Ridged finger nails

Medication: - Calcium supplement

(P.O) or by (IV) infusion Vitamin D (P.O) to promote absorption of calcium

S/S are related to hypocalcemia:

paresthesia, laryngeospasms, positive Chvosteks sign, positive Trousseaus sign, seizures, EKG changes and resistance to digitalis