endocrine

1. Adrenal Disorders
Prof.Dr
.RS Mehta 1
Insufficiency
(Addison’
s
disease)
Excess
(Cushing’s
Syndrome)

2. ADDISON’S DISEASE
Prof.Dr
.RS Mehta 2

3. Introduction
3
• Also called chronic adrenal insufficiency,
hypocortisolism,hypoadren alism)
• is a rare, chronic endocrine system disorder in which the
adrenalglandsdo not produce sufficientsteroid hormones.

4. Introduction
4
• 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- morecommon in women than men.

5. Etiology
5
• 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 ofACTH from pitutary gland.

6. Types of Addison’s disease
Prof.Dr
.RS Mehta 6
Primary
• associated with primary
inability of the adrenal
to secrete sufficient
quantities of hormone
Secondary
• associated with a
secondary failure due to
inadequateACTH
formation or release

7. Clinical
Manifestations
7

8. Hyperpigmentation
8

9. Diagnostic Measures
Specific LAB test
• Serum cortisol
• PlasmaACTH
– IftheACTH level is high,the person probably has
primary adrenal insufficiency
.
– If theACTH level is low,the person probably has
secondary or tertiary adrenal insufficiency
.

10. Diagnostic measures.
• Serum glucose
• Serum electrolytes level
• Complete blood count
• CT
,MRI:T
o rule out pituitary and adrenal mass

11. Complications
• 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

12. 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.

13. 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.

14. NURSING MANAGEMENT
Prof.Dr
.RS Mehta 14

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

16. Nursing Diagnosis
• Activity intolerance related to fatigue
• Risk for Deficient FluidVolume
• Risk for Imbalanced Nutrition:LessThan Body
Requirements

17. 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.

18. 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.

19. Others
19
• Reliving fatigue
• Maintaining optimal nutrition

20. Prognosis
• T
reatment ofAddison's disease is lifelong.
• The prognosis depend on the underlying
cause.

21. CUSHING’S SYNDROME

22. 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.

23. 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.

24. 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

25. Clinical manifestation
• Central-type obesity
,
• Fatty“buffalo hump”
relatively
A heavy trunk,and
thin
extremities.
• “Moon-faced”
appearance
• Increased oiliness of the
skin and acne.
Prof.Dr
.RS Mehta 25

26. Prof.Dr
.RS Mehta 26

28. Contd…
• Abnormal
distribution
results in
fa
t
which
a moon
shaped face

29. Manifestations Due to:
Prof.Dr
.RS Mehta 29
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.

30. Diagnosis
Prof.Dr
.RS Mehta 30
• 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

31. Diagnosis
Prof.Dr
.RS Mehta 31
• 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.

32. Management
Prof.Dr
.RS Mehta 32
• Pituitary irradiation.
with pituitary-dependent
Patients
Cushing’
s
syndrome with adrenal hyperplasia may
require pituitary irradiation.

33. Drug therapy
Prof.Dr
.RS Mehta 33
• Adrenal enzyme inhibitors:
Metyrapone, aminoglutethimide, mitota
ne, and ketoconazole may be used to
reduce hyperadrenalism
therapy is
• Cortisol therapy Cortisol
essential during and after surgery
.

34. Management
Prof.Dr
.RS Mehta 34
• 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.

35. Surgical Management
Prof.Dr
.RS Mehta 35
• Transsphenoidal hypophysectomy:
Surgical removal of the tumor by
transsphenoidal hypophysectomy .
• Adrenalectomy

36. NURSING MANAGEMENT
Prof.Dr
.RS Mehta 36

37. Nursing assessment
Prof.Dr
.RS Mehta 37
• 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

38. Nursing diagnosis
Prof.Dr
.RS Mehta 38
• 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
physical appearance, impaired
altere
d
sexual
functioning,and decreased activity level

39. Nursing Diagnosis
Prof.Dr
.RS Mehta 39
• 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

40. Nursing Interventions
Prof.Dr
.RS Mehta 40
• 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

41. Prognosis
Prof.Dr
.RS Mehta 41
• 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.