Disorders of the Pituitary Gland. ACROMEGALY Acromegaly (disease of anterior portion) – Etiology/pathophysiology Overproduction of growth hormone (GH)

Disorders of the Pituitary Gland

ACROMEGALY

• Acromegaly (disease of anterior portion)– Etiology/pathophysiology

• Overproduction of growth hormone (GH) in the adult (also called “somatotropin”)

• May be due to:– Idiopathic hyperplasia of the anterior pituitary

gland(increase in # of cells, unknown cause)– Tumor growth in the anterior pituitary gland

• Changes are irreversible

ACROMEGALY

• Clinical manifestations/assessment (30-40 yrs)• Enlargement of the cranium and lower jaw• Separation and malocclusion of the teeth• Bulging forehead• Bulbous nose• Thick lips; enlarged tongue• Generalized coarsening of the facial features• Enlarged hands and feet• Enlarged heart, liver, and spleen

ACROMEGALY

• Clinical manifestations/assessment (continued)• Muscle weakness• Hypertrophy of the joints with pain and stiffness• Males—impotence• Females—deepened voice, increased facial hair,

amenorrhea• Partial or complete blindness with pressure on

the optic nerve due to tumor• Severe headaches are common

ACROMEGALY

• SUBJECTIVE/OBJECTIVE DATA– Headaches or visual disturbances– Eval muscle weakness and ability to perform ADLs– Encourage pts. to share emotional responses to

sexual problems (d/t impotence in men and masculinization in women).

ACROMEGALY

• SUBJECTIVE/OBJECTIVE DATA (cont.)– Assessment of bone enlargement/joint

involvement– Gait changes; difficulty with adl’s; pain– Changes in vital signs early heart failure;

dyspnea, hypotension– Tachycardia, weak pulse

ACROMEGALY

• Diagnosed with:– CT scan– MRI– Elevated serum Growth Hormone– Cranial xrays– Ophthamalogic exam– Definitive Test: oral glucose challenge

• Normal results = GH ↓• In Acromegaly = no decrease in GH

Progression of Acromegaly

Figure 51-6

Right: Coarse facial features typical of acromegaly. Left: Patient’s

face several years before she developed the pituitary tumor.

(Courtesy of the Group for Research in Pathology Education.)

ACROMEGALY

• Medical Management– Meds to suppress GH secretion

• Dostinex, Somatostatin Analogs – esp. in pts. who are not candidates for surgery or radiation

– Surgical tx. to remove pituitary tumors• Transphenoidal approach• Cryosurgery

– Irradiation – to destroy GH-secreting tumors• Proton beam tx. using low doses of radiation

ACROMEGALY

• Nursing Interventions:– Mainly Supportive

• Safety measures with visual impairment• Monitor for cardio-respiratory changes; weight gain• ROM exercises• Soft, easy-to-chew diet• Analgesics • Self –esteem d/t disturbance in body image

ACROMEGALY

• Prognosis: development of complications reduce quality and length of life

GIGANTISM

• Etiology/pathophysiology• Overproduction of growth hormone• Caused by hyperplasia of the anterior

pituitary gland - may develop into a tumor• Defect in hypothalamus (which directs the

anterior pituitary gland to release excess amounts of GH

• *Occurs in a child before closure of the epiphyses

GIGANTISM

• Clinical manifestations/assessment– Great height– Increased muscle and visceral development– Increased weight– Normal body proportions– Weakness

GIGANTISM• Assessment:

– Subjective: • Pts. understanding of condition, disease process, and

changes• Pts. Ability to verbalize emotional responses to these

changes

– Objective:• Frequent measurement of height; pt./family coping; lab

and radiography to take bone condition and GH levels

GIGANTISM

• Diagnostic Tests: • GH suppression test (glucose-loading test)

– For a suppression test, a sample of blood is drawn after 10-12 hours of fasting. A person is then given a standard glucose solution to drink. Blood samples are drawn at timed intervals, and GH levels are tested in each to see if the pituitary gland is sufficiently suppressed by the dose of glucose.

• Prognosis: with new meds and surgical advances – increased life-span; though still less than the average individual

GIGANTISM

• Medical Management• Surgical removal of tumor• Irradiation of the anterior pituitary gland

–Hormone replacement• Observe for development of HTN, thick bones,

osteoporosis, CHF, delayed sexual development post treatment

GIGANTISM

• Nursing Interventions– Early identification of children experiencing rapid

growth rates– Alert for potential problems with self-image– Provide understanding and compassionate

support– Emphasize importance of regular follow-up with

Endocrinologist

Nursing diagnoses:

• Activity intolerance r/t physical weakness• Chronic low self-esteem r/t irreversible body changes• Ineffective coping r/t personal vulnerability• Disturbed body image r/t negative self perception• Deficient knowledge r/t age level and learning ability

DWARFISM• Etiology/pathophysiology

• Deficiency in growth hormone; usually idiopathic; few with autosomal recessive trait

• Clinical manifestations/assessment• Abnormally short height• Normal body proportion• Appear younger than age• Dental problems due to underdeveloped jaws• Normal but delayed sexual development – will produce

normal offspring unless accompanying ↓ gonadotropins

DWARFISM

• Assessment: • Subjective: pt. understanding; emotional response,

coping strategies; when did pt. first note ↓ growth; family hx.

• Objective: regular height/weight measurements; response to GH administration

• Diagnostic Tests:• Wrist xray for bone age• MRI/CT to r/o pituitary tumor• Definitive Test: ↓ plasma levels of GH

DWARFISM

• Medical management• Growth hormone injections• Removal of tumor, if present

• Nursing Interventions:• Alert for s/sx of tumor• Identification of children with growth problems• Encourage child to wear age appropriate clothing and

engage in peer activities• Support self-esteem; emphasize child’s abilities and

strengths

DWARFISM

• Prognosis: can lead normal lives; may have musculo-skeletal and cardiovascular complications

DIABETES INSIPIDUS• Diabetes: “like a sieve or siphon”• Insipidus: “tasteless”• Etiology/pathophysiology

• Metabolic disorder of the posterior pituitary

• Transient or permanent • Deficiency of antidiuretic hormone

(ADH)

DIABETES INSIPIDUS

• Etiology/Pathophysiology cont.– May be primary or secondary to other conditions

such as head injury, intracranial tumor, infections, aneurysms, etc.

– Secretion and Actions of ADH “goes awry”.– PROCESS: ↓ ADH electrolyte & fluid imbalance

↑ urine output secondary to ↑ plasma osmolality

DIABETES INSIPIDUS• Clinical Manifestations

– Polyuria; polydipsia– Urine very dilute (low specific gravity)– Urine output may exceed 5-20 L /24 hr.– May drink 4-20 L of cold or ice water /24hr.– May become severely dehydrated– ↑ serum Na+ levels– Lethargic– Dry skin; poor skin turgor– Constipation– Weight Loss

DIABETES INSIPIDUS

• If untreated hypovolemic shock• Subjective Assessment:

– Pt. understanding of relationship of symptoms with underlying cause– May restrict social contacts and work activities– Usually weak, tired, and lethargic

• Objective Assessment: – Severity of thirst– Skin turgor– Color and specific gravity of urine– I and O– Weight loss – Constipation

DIABETES INSIPIDUS

• Diagnostic Tests:– Urine specific gravity– Urine ADH– Serum Na+– CT scan – sella turcicca– Fluid deprivation test

• Done if specific gravity < 1.003 and serum Na+>145• Serum osmolality may be > 300 (norm. 280-300)

DIABETES INSIPIDUS

• Medical Management• ADH preparations/Replacements

– IV, SQ, intranasal, oral– Various preparations of Vasopressin

• Limit caffeine due to diuretic properties• If oral fluids insufficient, IV fluids administered

– Hypotonic saline or D5W

• Nursing Interventions– I and O– Skin assessment– Daily weights

DIABETES INSIPIDUS

• Nursing Interventions cont.– Increase fluid intake to 2600ml/day if possible

– Increase calories, protein, and Vit. C for healthy skin

– Test: Urine SpG drops below 1.003; Na levels above 145

• Note: Normal Sodium Blood levels 135-145Meq/L

DIABETES INSIPIDUS

• Nursing Diagnoses:– Deficient fluid volume, risk for, r/t

excessive urine production

– Impaired skin integrity, risk for, r/t altered state of hydration

SIADH

= Syndrome of Inappropriate Secretion of ADHEtiology:

– Occurs when the pituitary gland releases too much ADH.

When the body’s system of checks and balances malfunctions (whether from a tumor, medication, or unrelated disease process) ADH may be released continually kidneys reabsorb more water, therefore ↓urine output and expanding the body’s fluid volume

SIADH

• Consequently, the patient experiences:– Hyponatremia (<125 mEq/L)– Hemodilution– Fluid overload without peripheral edema

SIADH

ADH is released in response to stress – be alert to pts who have the following risk factors, &/or are in pain, or undergoing stressful procedures:

Medications (particularly general anesthetics, opiates, barbiturates, oral hypoglycemics, thyazide diuretics,

etc.)MalignanciesNon-malignant pulmonary diseaseNervous System DisordersMisc. – Lupus, adrenal insufficiency, hypothyroidism,

etc.

SIADH

• Assessments– Subjective: c/o weakness, muscle cramps, anorexia,

nausea, & headache– Objective:

• serum Na+ < 125mEq/L• diarrhea, disorientation• Weight gain• Fluid intake > urinary output but no edema

– Note: as water intoxication proceeds and serum becomes more hypotonic brain cells expand progressive lethargy, personality changes, seizures, etc.

SIADH

• Diagnostic Tests– Diagnosis made by simultaneous measurements

of urine and serum osmolality– Results: hyponatremia (Na+< 132mEq/L) and

serum osmolality < 280 mmol/kg)– Serum is diluted; urine is concentrated

SIADH

• Medical Management:– Fluid restriction of 800-1000 ml /day

• If hyponatremia is sever, fluid restriction may be 500ml/day

• Daily fluid intake should = daily fluid output. • If fluid restriction is adequate, tests show a gradual

increase in serum Na+ and decrease in body weight

SIADH

• Medical Management cont.– IV hypertonic saline solution – slow infusion to

avoid too rapid a rise in Na+. Increase Na+ should pull water out of edematous brain cells

– Declomycin 300mg qid; lithium• Both drugs interfere with antidiuretic action of ADH

and cause polyuria; Lasix is also given

• Surgical resection, radiation, or chemo for malignant neoplasms

• NOTE: Goal: prevent hypovolemia

SIADH

• Nursing Interventions:– CONTINUAL ASSESSMENT OF PT. CONDITION TO DETERMINE

IF IMPROVING OR DETERIORATING– Neuro exams q 3-4 hrs– Lung ascultation– Monitor labs– Obtain daily weight, i/o, urine checks– Fluid restrictions; oral care– IV infusions – monitor– Oral care– Skin assessment , care– Ongoing patient teaching

SIADH

• Nursing Diagnoses– Excess fluid volume, r / t decrease urine output– Risk for impaired oral mucous membrane r/t fluid

restrictions

SIADH

• Prognosis:– If r/t an adverse reaction to medication or

secondary to head trauma, it’s self limiting– If it’s the result of a metabolic condition or tumor,

it tends to become chronic– SIADH is potentially dangerous but treatable. If

s/sx recognized early and interventions started, the prognosis is good

– Without treatment, coma and death will occur

Trick to Distinguish DI from SIADH

SIADH (Too much ADH)• ↑ADH = ↓UO (High and DRY) +↓Sodium DI (Too little ADH)• ↓ ADH =↑UO (Low and Wet) + ↑ Sodium

Miscellaneous Slides

Types of diagnostic tests

• Stimulation and suppression tests:determine whether the gland is over or undersecreting the necessary hormones

• Radioactive iodine uptake (thyroid test)• T3 and T4 uptake tests• TSH: thyroid stimulating hormone• Thyroid scan; needle aspiration of tissue• Glucose tolerance test (GTT)• Glycosylated hemoglobin (A1C) for diabetes