Disorders of thePituitary Gland

1. Disorders of thePituitary Gland

2. 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

3. 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

4. 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

5. 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).

6. 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

7. 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

8. Progression of Acromegaly

9. Figure 51-6 (Courtesy of the Group for Research in Pathology Education.) Right: Coarse facial features typical of acromegaly. Left: Patient’s face several years before she developed the pituitary tumor.

10. 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

11. 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

12. ACORMEGALY • Prognosis: development of complications reduce quality and length of life

13. 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

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

15. 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

16. GIGANTISM • Diagnostic Tests: • GH suppression test (glucose-loading test) • Prognosis: with new meds and surgical advances – increased life-span; though still less than the average individual

17. 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

18. 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

19. 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

22. 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

24. 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

25. 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

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

27. 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)

28. 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”. • PROCES: ↓ ADH  electrolyte & fluid imbalance  ↑ urine output secondary to ↑ plasma osmolality

29. 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

30. 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

31. DIABETES INSIPIDUS • Diagnostic Tests: • Urine specific gravity • Urine ADH • Serum Na+ • CT scan – sellaturcicca • Fluid deprivation test • Done if specific gravity < 1.003 and serum Na+>145 • Serum osmolality may be > 300 (norm. 280-300)

32. 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

33. 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

34. 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

35. SIADH = Syndrome of Inappropriate Secretion of ADH Etiology: • 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

36. SIADH • Consequently, the patient experiences: • Hyponatremia(<125 mEq/L) • Hemodilution • Fluid overload withut peripheral edema

37. 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.) Malignancies Non-malignant pulmonary disease Nervous System Disorders Misc. – Lupus, adrenal insufficiency, hypothyroidism, etc.

38. 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.

39. 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

40. 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

41. SIADH • Medical Management cont. • IV hypertonic saline solution – slow infusion to avoid to rapid a rise in Na+. Increase Na+ should pull water out of edematous brain cells • Declomycin300mg 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

42. SIADH • NursingInterventions: • CONTINUAL ASSESSMENT OF PT. CONDITION TO DETREMINE 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

43. SIADH • Nursing Diagnoses • Excess fluid volume, r / t decrease urine output • Risk for impaired oral mucous membrane r/t fluid restrictions

44. 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

45. Miscellaneous Slides

46. 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