Addison's disease and Cushing's syndrome are both adrenal disorders but with opposite causes and manifestations. Addison's disease is caused by adrenal insufficiency leading to low cortisol and aldosterone. Symptoms include fatigue, weight loss, hyperpigmentation and hypotension. Cushing's syndrome is caused by excessive cortisol secretion leading to central obesity, hypertension and hyperglycemia. Diagnosis involves blood and urine tests to measure hormone levels. Treatment of Addison's disease involves hormone replacement therapy while treatment of Cushing's focuses on reducing excess cortisol levels through surgery, radiation or drug therapy.

1. ADRENAL
DISORDERS
Addison’s disease & Cushing’s Syndrome
1Prof. Dr. RS Mehta

2. Review of
Endocrine
system
2Prof. Dr. RS Mehta

3. 3Prof. Dr. RS Mehta

4. Hormones
and its functions
- Glucocorticoids:
cortisol
- Mineralocorticoids:
aldosterone
- Androgens
- Catecholamines:
Norepinephrine and
epinephrine
4Prof. Dr. RS Mehta

5. Adrenal Disorders
Insufficiency
(Addison’s
disease)
Excess
(Cushing’s
Syndrome)
5Prof. Dr. RS Mehta

6. ADDISON’S DISEASE
6Prof. Dr. RS Mehta

7. Introduction
• Also called chronic adrenal
insufficiency, hypocortisolism,hypoadren
alism)
• is a rare, chronic endocrine system disorder in
which the adrenal glands do not produce
sufficient steroid hormones.
7Prof. Dr. RS Mehta

8. Introduction
• Thomas Addison (1793-1860) first described
the syndrome in 1855.
• Age- can affect people of any age, most
common between the ages of 30 and 50.
• Sex- more common in women than men.
8Prof. Dr. RS Mehta

9. Etiology
• Anatomic destruction of gland (chronic or acute)
• Autoimmune or idiopathic atrophy
• Surgical removal of both adrenal glands
• Infections (tuberculosis, fungal, viral—especially in
AIDS)
• Invasion: metastatic
• Congenital adrenal hyperplasia
• Inadequate secretion of ACTH from pitutary gland.
9Prof. Dr. RS Mehta

10. Types of Addison’s disease
Primary
• associated with primary
inability of the adrenal
to secrete sufficient
quantities of hormone
Secondary
• associated with a
secondary failure due to
inadequate ACTH
formation or release
10Prof. Dr. RS Mehta

11. Pathophysiology
insufficiency due to the
destruction or dysfunction of
the entire adrenal cortex
Decreased glucocorticoid:
cortisol
Liver function and digestive
enzymes is decreased, GI
disturbances
Low blood sugar results, nausea,
vomiting
decreased mineralocorticoid:
aldosterone
Increased water & sodium loss
at renal tubules: hyponatremia,
hyperkalemia
Increased water loss results in
decreased fluid volume
11Prof. Dr. RS Mehta

12. Clinical
Manifestations
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13. Hyperpigmentation
13Prof. Dr. RS Mehta

14. Diagnostic Measures
Specific LAB test
• Serum cortisol
• Plasma ACTH
– If the ACTH level is high, the person probably has
primary adrenal insufficiency.
– If the ACTH level is low, the person probably has
secondary or tertiary adrenal insufficiency.
14Prof. Dr. RS Mehta

15. Diagnostic measures.
• Serum glucose
• Serum electrolytes level
• Complete blood count
• CT, MRI:To rule out pituitary and adrenal mass
15Prof. Dr. RS Mehta

16. Complications
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• Adrenal crisis(addisonian crisis): sudden
pain in back, abdomen, legs, cyanosis and the
classic signs of circulatory shock: pallor,
apprehension, rapid and weak pulse, rapid
respirations, and low blood pressure.
• Osteoporosis
Prof. Dr. RS Mehta

17. Management
• 1. Correct fluid and electrolyte imbalances:
Directed primarily toward repletion of circulating
glucocorticoids and replacement of the sodium and
water deficits.
• 2. Correct Hypoglycemia: An IV infusion of 5%
glucose in normal saline solution(DNS) or 25%
dextrose bolus.
17Prof. Dr. RS Mehta

18. Management
3. Replace Steroids: a bolus iv infusion of 100
mg hydrocortisone.
– Maintenance100-mg bolus of hydrocortisone IV
every 6 h.
• Lifelong replacement of corticosteroids and
mineralocorticoids
• Mineralocorticoid supplementation - 0.05–0.1
mg fludrocortisone per day PO. 18Prof. Dr. RS Mehta

19. NURSING MANAGEMENT
19Prof. Dr. RS Mehta

20. Nursing assessment
• Patient’s level of stress.
• Vital signs
• Assesses the skin color and turgor
• Weight changes, muscle weakness, and fatigue
20Prof. Dr. RS Mehta

21. Nursing Diagnosis
• Activity intolerance related to fatigue
• Risk for Deficient FluidVolume
• Risk for Imbalanced Nutrition: Less Than Body
Requirements
21Prof. Dr. RS Mehta

22. Monitoring and managing addisonian
crisis
• Physical and psychological stressors must be
avoided like exposure to cold, overexertion,
infection, and emotional distress.
• Intravenous administration of fluid, glucose,
and electrolytes, especially sodium;
replacement of missing steroid hormones; and
vasopressors.
22Prof. Dr. RS Mehta

23. Restoring fluid balance
• Assesses the patient’s skin turgor, mucous
membranes, weight.
• Encourages the patient to consume foods and
fluids and select foods high in sodium
• Administer hormone replacement as
prescribed and to modify the dosage during
illness and other stressful occasions.
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24. Others
• Reliving fatigue
• Maintaining optimal nutrition
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25. Prognosis
25
• Treatment of Addison's disease is lifelong.
• The prognosis depend on the underlying
cause.
Prof. Dr. RS Mehta

26. CUSHING’S SYNDROME
26Prof. Dr. RS Mehta

27. Introduction
• Cushing’s syndrome (Hypercortisolism,
Adrenal Hyperfunction) :
is a cluster of clinical abnormalities caused by
excessive levels of adrenocortical hormones
(particularly cortisol)
• 1st described by Harvey Cushing in 1932.
27Prof. Dr. RS Mehta

28. Incidence
• Cushing’s syndrome affects 13 of every 1
million people.
• It is more common in women than in men
and occurs primarily between ages 25 and 40.
28Prof. Dr. RS Mehta

29. Etiology
• Excess. In approximately 70% of patients,
Cushing’s syndrome results from excessive
production of corticotropin and consequent
hyperplasia of the adrenal cortex.
• Pituitary hypersecretion and pituitary tumors
29Prof. Dr. RS Mehta

30. Pathophysiology
Excess due to increased production from
adrenal cortex or dysfunction of pituitary
increased glucocorticoid:
cortisol
Increased digestive enzymes,
increased glucose production
Hyperglycemia, peptic ulcer
increased mineralocorticoid:
aldosterone
Increased water & sodium
retention at renal tubules:
hypernatremia, hypokalemia
Hypertension
30Prof. Dr. RS Mehta

31. Clinical manifestation
• Central-type obesity,
• Fatty “buffalo hump”
• A heavy trunk, and
relatively thin
extremities.
• “Moon-faced”
appearance
• Increased oiliness of the
skin and acne.
31Prof. Dr. RS Mehta

32. 32Prof. Dr. RS Mehta

34. Contd…
• Abnormal fat
distribution which
results in a moon
shaped face

35. Manifestations Due to:
Excess
Glucocorticoids
• Weight gain
• Deposition of
adipose tissue
• Oily complexion.
• Muscle weakness
• osteoporosis
• Mental
disturbances
Excess
Mineralocorticoids
• Hypertension
• Hypernatremia
• Hypokalemia
• Expanded
blood volume
• Edema
Excess
androgens
• Hirsutism
• Breasts –
Atrophy.
• Amenorrhoea
• Voice –
masculine.
35Prof. Dr. RS Mehta

36. Diagnosis
• Low-dose dexamethasone suppression
test
• Imaging studies. Ultrasound, CT scan, or
angiography localizes adrenal tumors and may
identify pituitary tumors.
• Serum Electrolyte levels
• Increased blood glucose
36Prof. Dr. RS Mehta

37. Diagnosis
• Measurement of a 24-h urine free cortisol can
also be used as a screening test. A level >140
nmol/d (50 μg/d) is suggestive of cushing’s
syndrome.
37Prof. Dr. RS Mehta

38. Management
• Pituitary irradiation. Patients
with pituitary-dependent Cushing’s
syndrome with adrenal hyperplasia may
require pituitary irradiation.
38Prof. Dr. RS Mehta

39. Drug therapy
• Adrenal enzyme inhibitors:
Metyrapone, aminoglutethimide, mitota
ne, and ketoconazole may be used to
reduce hyperadrenalism
• Cortisol therapy Cortisol therapy is
essential during and after surgery.
39Prof. Dr. RS Mehta

40. Management
• Diabetes mellitus and peptic ulcer common in
the patient with Cushing’s syndrome.
Therefore, insulin therapy and medication to
treat peptic ulcer may be initiated if needed.
40Prof. Dr. RS Mehta

41. Surgical Management
• Transsphenoidal hypophysectomy:
Surgical removal of the tumor by
transsphenoidal hypophysectomy .
• Adrenalectomy
41Prof. Dr. RS Mehta

42. NURSING MANAGEMENT
42Prof. Dr. RS Mehta

43. Nursing assessment
• Health history. The history includes information
about the patient’s level of activity and ability to carry
out routine and self-care activities.
• Physical exam. The skin is observed and assessed for
trauma, infection, breakdown, bruising, and edema.
• Mental function. The nurse assesses the patient’s
mental function including mood, responses to
questions, awareness of environment, and level of
43Prof. Dr. RS Mehta

44. Nursing diagnosis
• Self-care deficit related to weakness, fatigue,
muscle wasting, and altered sleep patterns
• Impaired skin integrity related to edema,
impaired healing, and thin and fragile skin
• Disturbed body image related to altered
physical appearance, impaired sexual
functioning, and decreased activity level
44Prof. Dr. RS Mehta

45. Nursing Diagnosis
• Disturbed thought processes related to mood
swings, irritability, and depression.
• Risk for injury related to weakness
• Risk for infection related to suppression of
inflammatory response
45Prof. Dr. RS Mehta

46. Nursing Interventions
• Decreasing Risk for injury
• Decreasing risk for infection
• Preparing patient for surgery
• Encouraging rest and activity
• Promoting Skin integrity
• Improving Body image
• Improving thought process
46Prof. Dr. RS Mehta

47. Prognosis
• Without treatment, hypercortisolism persists and in
many patients worsens.
• Untreated disease carries a dismal survival rate of
50% at 5 years.
• Despite improvement of complications in most
patients, cardiovascular risk, hypertension, obesity,
and decreased quality of life may persist in some
patients.
47Prof. Dr. RS Mehta

48. Thank you so much
48Prof. Dr. RS Mehta