Parathyroid, Adrenal, and Pituitary Disorders

hyperparathyroidism

excessive production of parathyroid hormone (pth)

-associated with increased serum calcium levels and decreased phosphorus levels

Normal Serum Calcium Level

9.0-10.5

normal phosporus level

2.4-4.4

Primary hyperparathyroidism

increased secretion of pth from the parathyroid gland leading to problems with calcium, phosphorus, and bone metabolism

- associated with lithium use or benign or malignant tumors

- typical peak between 40s and 50s

Secondary hyperparathyroidism

hypocalcemia as a compensatory response to vitamin D deficiency, chronic renal failure or high phosphorus

Teritary hyperparathyroidism

enlargement of parathyroid = loss of negative feedback from circulating Ca (autonomous secretion of PTH in presence of normal Ca)

- Renal transplant pts who had a long history of dialysis

In hyperparathyroidism, expected lab values are...

increased PTH

increased calcium

decreased phosphorus

-order a PTH blood test, after electrolyte panel reveals this

If both calcium and phosphorus are high/low, you could expect...

the problem to not be associated with the endocrine system

clinical manifestations of hyperparathyroidism

1. kidney stones

3. muscle weakness/skeletal pain

3. arrthymias

4. hypertension

5. moist skin

6. weight loss

7. corneal calcification

8. anorexia, ab pain, constipation

9. osteoporosis/fractures

10. shortened attention span

or asymptomatic

complications from hyperparathyroidism

1. renal failure

2. pancreatitis

3. cardiac changes

4. long bone, rib, vertebral fractures

Nonsurgical treatment for hyperparathyroidism

-for pts with mild/asymptomatic

-annual blood and urine screenings of electrolytes/PTH

-annual X-rays/dexascans

-regular low impact exercise (walking)

-3L of fluids daily and moderate calcium diet

drug therapy for hyperparathyroidism

1. phosphorus supplements unless at risk for kidney stones

2. bisphosphonate (-dronates; upright 30 mins, full glass of water in am)

3. diuretics -> increase secretion of calcium

4. calciminetic-> cinacalcet for secondary cases

surgical intervention for hyperparathyroidism

-parathyroidectomy for primary or secondary

-autotransplatation of own healthy parathyroid tissue in arm or sterbicleidomastoid muscle

--if unsuccessful need lifelong calcium supplementation

care for a pt postop a parathyroidectomy

1. monitor for hemorrhage, fluid/electrolytes

2. calcium monitoring including chrvosteks, trousseaus, and tetany

3. have IV calcium ready

4. if experience hypocalcemia, breath in paper bag technique

Hypoparathyroidism

-uncommon condition of inadequate circulation of PTH

-commonly caused by trauma, genetic defect, hypo magnesia or an accidentally removed parathyroid gland

- exposure to heavy metals or tumors = unnatural cause

Lab values for hypoparathyroidism

Low PTH

low calcium

high phosphorus

clinical manifestations of hypoparathyroidism

1. tingling in lips/fingertips

2. spasms or tetany

3. dysphagia and larynospasms

4. chvosteks and trousseaus = +

5. anxiety

treatment of hypoparathyroidism

1. IV calcium gluconate or lifelong calcium supplementation

2. rebreathing exercises in a paper bag to temporarily raise calcium and alleviate symptoms

3. diet high in calcium, low in phosphorus

4. may need Vit D supplementation

5. PTH replacement not given long term due to expense

diet for hypoparathyroidism

1. No dairy; high in P

2. dark green leafy vegs

3. no spinach or rhubarb (inhibit absorption)

4. soybeans, soy milk, tofu

adrenal steroid hormones

1. Glucocorticoids -> cortisol

2. Mineralocorticoids -> aldosterone (Na/K)

3. Androgens-> sex hormones

-corticosteroids refers to any of these types of hormones

Cushing's syndrome causes

1. Prolonged, high dose corticosteroids

2. ACTH secreting pituitary tumor or tumor elsewhere in body

3. cortisol secreting neoplasm in adrenal cortex

Cushing syndrome and adrenal tumors most commonly seen in..

women 20-40

-tumor somewhere else in body (ectopic) more common in men

clinical manifestations of cushings

1. weight gain in trunk w thin extremities and fat on back of neck and shoulders

2. moon face

3. fragile skin, striae, bruises etc

4. hyperglycemia

5. hypokalemia, hypervolemia

6. sodium and water retention (monitor for HF)

7. irritability

8.hypertension

9. mineralocorticoid specific-> tendency for edema

10. androgen specific-> menstural irregularities, acne, facial hair growth, erectile dysfunction

diagnostic studies for cushings syndrome

Monitor Elevated plasma cortisol

1. 24-hour urine collection for free cortisol

- > 100 mcg in 24 hrs = cushings

2. Low-dose dexamethasone suppression test if 24 hr urine borderline

3. midnight salivary cortisol

4. CT or MRI to detect tumor

Lab findings for Cushings (not diagnostic)

1. leukopenia

2. lymphopenia

3. eosinopenia

3. hyperglycemia

4. glycosuria

5. hypercalciuria

care of pt with cushings syndrome

1. can shrink (radiation) or remove tumor

2. adrenalectromy for adrenal tumor

3. gradually reduce steroid use

4. drug therapy (less likely unless can't tolerate surgery

5. emotional support for disturbed body image

preop intervention for cushings syndrome

Bring pt to optimal physical condition by:

1. giving a high protein meal

2. controling hypertension and hyperglycemia

3. correct hypokalemia

postop care following adrenalectomy

1. monitor BP (on bedrest until stable), fluid/electrolytes (priority), and hemorrhage

2. may or maynot need corticosteroids to correct hormone fluctations

3. IV steroids given during and after steroids; PO if need lifelong correction

-adjust dose with doctor

taking a pt off a corticosteroid too fast can cause...

adrenal insufficiency

Adrenocortical insufficiency/Addisons disease

- all 3 adrenal corticosteroids are reduced

- commonly autoimmune with a genetic link

- usually discovered late in disease process, causing the adrenal gland to completely stop working by time of dx.

- sometimes caused by fungal inf, aids, tb, cancer, or lack of pituitary ACTH

clinical manifestations of Addisons disease

1. bronze, skin hyperpigmentation (common in joints/creases)

2. hypotension

3. hyperkalemia

4. hyponatremia

5. n&v, diarrhea, anorexia

6. progressive muscle weakness

Addisonian crisis

- caused by stress, withdrawal of corticosteroid replacement, after adrenal surgery or pituitary gland destruction

- hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, weakness, fever, confusion, GI issues, and pain

-life threatening and can lead to circulatory collapse

addisonian crisis care

1. treat underlying cause

2. high dose hydrocortisone replacement

3. high volume NSS and dextrose 5%

main treatment for pts with addisons disease

give corticosteroids

-on full stomach

- end in -one (hydrocortisone

diagnostic tests for addisons

ACTH response test: measure cortisol levels, give synthetic ACTH, and then measure again. Damaged adrenal glands do not response to ACTH.

-hyperkalemia, hyponatremia, increased BUN and hypoglycemia indicate

other interventions for pt with addisons disease

1. minor stress= double dose

2. major stress= triple dose

3. salt additives

4. monitor for signs of cushings from steriod use

5. glucocorticoid= 2/3 in morning, 1/3 in afternoon

6. mineralcorticoids= one dose in morning

effects of corticosteroid therapy

1) antiinflammatory

2) immunosuppression

3) maintenance of normal BP

4) carb and protein metabolism

side effects of corticosteroids

1. hypokalemia

2. muscle weakness

3. mood changes

4. glucose intolerance

5. fat to trunk and face

6. delayed healing

7. susceptible to infection

8. fractures from protein depletion

9. hypocalcemia

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

abnormal production and sustained secretion of ADH characterized by fluid (water) retention

SIADH is most common in...

older adults

Causes of SIADH

1) malignant tumors

2) CNS disorders/head trauma

3) drug therapy

-evaluate for cancer if otherwise unexplained

clinical manifestations of SIADH

1. hyponatremia= muscle cramps and weakness

2. decreased, concentrated urine

3. increased weight; puffy look

4. cerebral edema = lethargy, confusion, seizures, or coma

Na lower than 120 from SIADH=

1. vomiting

2. abdominal cramps

3. muscle twitching

4. seizures

-give these pts hypertonic 3 or 5% normal saline

diagnostic studies of SIADH

-simultaneous measurement of urine and serum osmolarity

-serum osmolality less than 280

-urine specific gravity greater than 1.030

-decreased NA, BUN, creatine, H&H

urine specific gravity readings

1.005= dilute, decreased (two 00 after decimal)

1.050= concentrated, increased (one 0 after decimal)

mild to moderate SIADH

-Na>125

-restrict fluids to 800-1000 mL/day

-Lasix

-gradual weight reduction

severe SIADH

-Na< 120

-hypertonic 3 or 5% saline

-diruetics

-restrict fluids to 500 mL/day

chronic SIADH

-800-1000mL/day

- med therapy

Nursing care of pts with SIADH

1. hourly VS, I&O, urine specific gravity

2. daily weights,

3. LOC and hyponatremia monitoring

4. fluid restriction

5. HOB flat

6. frequent turning

7. seizure precautions

For SIADH you should avoid medications that release ADH such as...

1. carbamazepine (tegretol)

2. certain chemo

3. general anesthesia agents

4. opioids

5. ocytocin

6. thiazide diuretics

7. SSRI

8. tricyclic antidepressants

diabetes insipidus

deficency of production or secretion of ADH or decreased renal response to ADH

-reversible or chronic depending on cause

Central Diabetes Insipidus

brain tumor, head injury, brain surgery, CNS infection

occurs suddenly with excessive fluid loss

nephrogenic diabetes insipidus

Kidneys fail to respond to ADH.

primary diabetes insipidus

Excess water intake

Examples: Structural lesion in thirst center, psychologic disorder

clinical manifestations of Diabetes insipidus

1. increased thirst

2. increased and dilute urine

3. may cause weight loss, constipation, dehydration, hypotension, tachycardia, cshock, or coma if PO intake cant keep up with urination

onset of central DI

after intracranial surgery or head trauma

Nonpharmocologic Care of central DI

replace fluids PO or IV with hypotonic saline

desmorpressin acetate (DDAVP)

hormone replacement therapy for central DI; synthetic ADH (other drugs to treat central DI end in -pressin)

-given IV, subQ or nasal

-promotes reabsorption of water

-too high a dose= SIADH symptoms

-too low a dose=DI symptoms

-monitor nasal cavity for irritaton

-monitor cardiac pts for cardiac reactions

Care for nephronic DI

low sodium diet and thiazide diuretics