Disorders of adrenal gland with nursing management

2. There are two adrenal glands in the human, each
attached to the upper portion of a kidney..
INTRODUCTION

5. ADRENAL CORTEX
 Glucocorticoids, the prototype is hydrocortisone.
 Mineralocorticoids, mainly aldosterone.
 Androgens (male sex hormones).

6. GLUCOCORTICOIDS
Increases blood glucose levels by:
Glucose metabolism.
 Protein & fat metabolism.
Gluconeogenesis.

7. MINERALOCORTICOIDS
Electrolyte metabolism.
Act principally on the renal tubular and
gastrointestinal epithelium .
Helps in re-absorbtion of sodium & excretion of
potassium.

8. ADRENAL SEX HORMONES (ANDROGENS)
 Probably have little effect in normal amounts.
 Exert effects similar to those of male sex hormones.
 When in excess, cause masculinization.

9. Cushing’s syndrome.
Addison’s disease.

11. DEFINITION
Cushing's syndrome is characterized by excess
secretion of the adrenal cortex hormones.

12. ETIOLOGY
The causes are divided into three categories:
 Iatrogenic causes: excessive cortisol levels from chronic
therapy with glucocorticoids.
 Primary cause: excessive cortisol production from adrenal
neoplasms such as adenomas or carcinomas.
 Secondary cause: excessive production of adrenocorticotropic
hormone (ACTH) from the anterior pituitary gland due to
pituitary carcinomas or due to ectopic ACTH secretion by
neoplasms of lungs, kidneys, pancreas, thyroid etc.

13. RISK FACTORS
 Women are five times more likely than men.
 Women of age 20 to 40 years.
 Long term corticosteroid therapy.
 Family history.

14. Corticotropin-releasing Hormone.

15. PATHOPHYSIOLOGY
Use of corticosteroid medications and excessive
corticosteroid production by the adrenal cortex
Tumor of the pituitary gland that produces
ACTH and stimulates the adrenal cortex
The normal feedback mechanisms become
ineffective leading to loss of usual diurnal
pattern of cortisol. Oversecretion of cortical
hormones
Signs and symptoms of Cushing’s syndrome

16. Increased Glucocorticoids
• Overt
diabetes.
• Slow wound
healing.
• Infections.
• Muscle
wasting
• Osteoporosis
• Inc. blood
cholesterol
• Acne, oily
skin.
Fat
catabolism
Protein
catabolism
Increase
blood
glucose
Decreased
immunity

17. Mineralo
corticoids
Na+
retention
Water
reabsorbed
Weight gain,
Obesity,
Lethargy.
Hyper
tension
Heart
failure
Imbalance of
Na-K pump.
CNS instability

18. Increase
androgens
Loss of
libido
Voice
deepens
Amenorrhea,
Breast atrophy
Hirsutism

21. Ophthalmic
Cataracts, Glaucoma
Cardiovascular
Hypertension, Heart failure
Endocrine/Metabolic
Truncal obesity, Moon face
Buffalo hump, Sodium retention
Hypokalemia
Metabolic alkalosis
Hyperglycemia
Menstrual irregularities, Impotence
Negative nitrogen balance
Altered calcium metabolism
Adrenal suppression
Immune Function
Decreased inflammatory
responses
Impaired wound healing
Increased susceptibility to
infections
Psychiatric
Mood alterations
Psychoses
Skeletal
Osteoporosis
Spontaneous fractures
Aseptic necrosis of femur
Vertebral compression, Fractures
Dermatologic
Thinning of skin
Petechiae, Ecchymoses
Striae, Acne
Gastrointestinal
Peptic ulcer, Pancreatitis
Muscular
Myopathy, Muscle weakness

23. Diagnosis & investigations:
 Laboratory studies.
 Imaging Studies.

24. Initial Laboratory Results
 Hypernatremia, Hypokalemia, hyperglycemia,
hypercholesterolemia.
 Midnight serum cortisol level > 7.5 mg/dl.
 Increased 24-hour urinary free cortisol (>100 mg/24h).
 Corticotropin-releasing hormone (CRH) stimulation test is
useful to distinguish pituitary (ACTH-dependent) from ACTH-
independent (adrenal tumors, adrenal hyperplasia, exogenous
glucocorticoid administration) causes of Cushing's syndrome.
Low ACTH levels are consistent with adrenal adenoma.

25. Imaging Studies
 CT Scan or MRI of adrenal
glands.
 MRI of pituitary gland.
 Additional imaging studies may be
necessary to localize neoplasms of
the lung, pancreas, kidney, thyroid,
or thymus in patients with ectopic
ACTH production.

26. Treatment
 The treatment of Cushing's syndrome varies with its
cause.

27. Pituitary adenoma:
 Transsphenoidal hypophysectomy.
 Pituitary irradiation is reserved for patients not cured by
transsphenoidal surgery.
 Stereotactic radiotherapy (photon knife or gamma knife).
 Total bilateral adrenalectomy is reserved for patients not
cured by transsphenoidal surgery or pituitary irradiation.

28. Gamma knife surgery..

29. Adrenal neoplasm:
 Surgical resection of the affected adrenal gland.
 Glucocorticoid replacement for approximately 9 to 12
months after surgery to allow time for the contralateral
adrenal gland to recover from its prolonged suppression.

30. Ectopic ACTH:
 Surgical resection of the ACTH-secreting neoplasm.

31. Cushing’s disease

32. Assessment
Health history
 Ability to carry out routine and self-care activities.
 Changes in memory, attention span, or behavior.
 Sleep-wake pattern.
 Patient’s changed affect, short-term memory, emotional
instability, and ability to concentrate.
 Weight gain and changes in body proportions.
 Hirsutism, oily skin, acne, purple striae, and poor wound
healing.
 Changes in menstruation.
 Changes in libido.
 Changes in appetite and thirst.

34. Risk for injury related to muscle
weakness & fatigue.
 Establishing a protective environment.
 Assistance from the nurse in ambulating.
 Foods high in protein, calcium, and vitamin D are
recommended to minimize muscle wasting and
osteoporosis.
 Assist the patient in selecting appropriate foods that are
also low in sodium and calories.

35. Risk for infection related to
altered protein metabolism and
inflammatory response
 The patient should avoid unnecessary exposure to others
with infections.
 Frequently assess the patient for subtle signs of infection
because the anti-inflammatory effects of corticosteroids
may mask the common signs of inflammation and
infection.

36. Activity intolerance related to
weakness, fatigue, muscle wasting,
and altered sleep patterns
 Encourage moderate activity to prevent complications of
immobility.
 Help the patient plan and space rest periods throughout the
day.
 Promote a relaxing, quiet environment for rest and sleep.

37. Impaired skin integrity related to
edema, impaired healing, and
thin and fragile skin.
 Meticulous skin care.
 Use of adhesive tape is avoided.
 Assess the skin and bony prominences.
 Change positions frequently to prevent skin breakdown.

38. Disturbed body image related to altered
physical appearance, impaired sexual
functioning, and decreased activity level.
 Self- help groups.
 Listen to the patient.
 Weight gain and edema management
with diet & exercise.

39. Disturbed thought processes related
to mood swings, irritability and
depression.
 Explanations to the patient and family members about the
cause of emotional instability.
 helping them cope with the mood swings.
 Encourage the patient and family members to verbalize
their feelings and concerns.

40. COMPLICATIONS
Addisonian crisis: It is the sever hypofunction of the adrenal
cortex.
It may be due to surgical removal of the adrenals or pituitary &
abrupt stoppage of corticosteroid therapy.
Highly stressful events may lead to such crisis.
It is characterized by
 Circulatory collapse, hypotension.
 Dehydration.
 Nausea/ vomiting.
 Hypoglycemia.
 Hyperkalemia.

41. MANAGING
COMPLICATIONS
Addisonian Crisis
 Monitor closely for hypotension; rapid, weak pulse; rapid
respiratory rate; pallor; and extreme weakness.
 Identify factors that may have led to the crisis.
 Intravenous administration of fluid and electrolytes and
corticosteroids.
 Treat for circulatory collapse and shock.

42. Hyperglycemia
 Regular blood glucose monitoring.
 Report elevated blood glucose levels to the physician.

43. Teaching Patients Self-Care
 Do not stop the corticosteroid use abruptly and without
medical supervision.
 Ensure an adequate supply of the corticosteroid, because
running out of the medication and skipping doses can
precipitate addisonian crisis.
 Adequate calcium intake without increasing the risk for
hypertension, hyperglycemia and weight gain.
 Regularly monitor blood pressure, blood glucose levels
and weight.

44. Contd..
 Wearing a medical alert bracelet.
 Patient compliance with the medicine regimen.
 Regular medical follow-up.
 Health promotion activities (health screening, including
bone mineral density testing).

45. PRIMARYADRENOCORTICAL INSUFFICIENCY

46. Definition
 Primary adrenocortical insufficiency (Addison's
disease) is characterized by inadequate secretion of
corticosteroids resulting from partial or complete
destruction of the adrenal glands.

47. Etiology
 Autoimmune destruction of the adrenals.
 Carcinomatous destruction of the adrenal glands.
 Tuberculosis
 Adrenal infarction.
 Advanced stages of AIDS.

48. Pathophysiology

49. Clinical Manifestations
 Muscle weakness, emaciation (thin), anorexia, weight loss.
 Increased pigmentation.
 Hypotension.
 Gastrointestinal disturbances (abdominal pain, diarrhea, lack
of appetite).
 Hypoglycemic manifestations, salt craving.
 Mental status changes such as depression, emotional lability
and confusion.
 Amenorrhea and loss of axillary hair in women.

50. Laboratory Results
 Blood cortisol level <3 mg/dL and ACTH level >100
mg/dL.
 Hyperkalemia, hyponatremia( Sodium).
 Decreased glucose level.
 Mild normocytic, normochromic anemia, neutropenia.
 Decreased 24-hour urinary cortisol.

51. Imaging Studies
 Abdominal x-ray: adrenal calcifications may be noted
if the adrenocortical insufficiency is secondary to
tuberculosis or fungal infection.
 Abdominal CT scan: Small adrenal glands: idiopathic
atrophy or long-standing tuberculosis

52. Treatment
Chronic adrenocortical insufficiency
 Hydrocortisone, 15 to 20 mg PO every morning and 5 to 10
mg in late afternoon, or prednisone, 5 mg in morning and 2.5
mg at bedtime.
 Oral fludrocortisone 0.05 mg/day to 0.20 mg/day.
 Increase glucocorticoid replacement in times of stress.
 Parenteral glucocorticoids if diarrhea or vomiting occurs.

53. COMPLICATIONS
Addisonian crisis

54. MANAGEMENT
a. Measure plasma cortisol level.
b. Administer hydrocortisone 50 mg IV q8h for 24 hours; if
patient shows good clinical response, gradually taper dosage
and change to oral maintenance dose (usually prednisone, 7.5
mg/day).
c. Provide adequate volume replacement with D5NS solution until
hypotension, dehydration, and hypoglycemia are completely
corrected.

55. ADDISON’S DISEASE

56. ASSESSMENT
• Health history
• Physical examination.
• Monitor the blood pressure and pulse rate.
• Assess the skin color and turgor .
• Check for weight changes, muscle weakness, and
fatigue.
• Investigate any illness or stress that may have
 precipitated the acute crisis.

58. Risk of injury related to addisonian crisis as
evidenced by hypotension & other signs of shock.
• Monitor for signs and symptoms of shock. Hypotension,
rapid, weak pulse; rapid respiratory rate; pallor; and
extreme weakness.
• Avoid physical and psychological stressors exposure to
cold, overexertion, infection, and emotional distress.
• Avoid exertion.
• Monitor vital signs, weight, and fluid and electrolyte
status .
• Identify and reduce the factors that may have led to the
crisis.

59. Fluid volume deficit related to disease condition as
evidenced by decreased skin turgor & postural
hypotension.
 Assess the patient’s skin turgor, mucous membranes, and
weight loss.
 Instruct patient to report increased thirst.
 Monitor lying, sitting, and standing blood pressures.
 Encourage the patient to consume foods and fluids high in
sodium during gastrointestinal disturbances and very hot
weather.

60. Activity intolerance related to fatigue, muscle
weakness as evidenced by inability to participate in
exertional activities.
• Avoid unnecessary activity and stress.
• Detect signs of infection or the presence of other stressors.
• Maintain a quiet, nonstressful environment.
• Assist in ADLs.
• Increase activity gradually following a crisis.

61. Knowledge deficit related to self care after discharge
form the hospital as evidenced by patient & family
verbalization of doubts.
• Instruct about the rationale for replacement therapy and
proper dosage of medicines.
• How to modify the medication dosage and increase salt
intake in times of illness, very hot weather, and other
stressful situations.
• To wear a medical alert bracelet, and to carry information
at all times about the need for corticosteroids.

62. Signs of improper hormone
replacement
• The development of edema or weight gain may signify
too high a dose of hormone.
• Postural hypotension (decrease in systolic blood
pressure, lightheadedness, dizziness on standing) and
weight loss frequently signify too low dose.

65. Thanks