7. Introduction
Prof.Dr
.RS Mehta 7
• 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.
8. Introduction
Prof.Dr
.RS Mehta 8
• 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.
9. Etiology
Prof.Dr
.RS Mehta 9
• 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.
10. Types of Addison’s disease
Prof.Dr
.RS Mehta 10
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
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
Prof.Dr
.RS Mehta 11
14. Diagnostic Measures
Prof.Dr
.RS Mehta 14
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
.
15. Diagnostic measures.
Prof.Dr
.RS Mehta 15
• Serum glucose
• Serum electrolytes level
• Complete blood count
• CT
,MRI:T
o rule out pituitary and adrenal mass
16. Complications
Prof.Dr
.RS Mehta 16
• 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
17. Management
Prof.Dr
.RS Mehta 17
• 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.
18. Management
Prof.Dr
.RS Mehta 18
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.
20. Nursing assessment
Prof.Dr
.RS Mehta 20
• Patient’
s level of stress.
• Vital signs
• Assesses the skin color and turgor
• Weight changes,muscle weakness,and fatigue
21. Nursing Diagnosis
Prof.Dr
.RS Mehta 21
• Activity intolerance related to fatigue
• Risk for Deficient FluidVolume
• Risk for Imbalanced Nutrition:LessThan Body
Requirements
22. Monitoring and managing addisonian
crisis
Prof.Dr
.RS Mehta 22
• 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.
23. Restoring fluid balance
Prof.Dr
.RS Mehta 23
• 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.
27. Introduction
Prof.Dr
.RS Mehta 27
• 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.
28. Incidence
Prof.Dr
.RS Mehta 28
• 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.
29. Etiology
Prof.Dr
.RS Mehta 29
• 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
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
Prof.Dr
.RS Mehta 30
31. 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 31
37. Diagnosis
Prof.Dr
.RS Mehta 37
• 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.
38. Management
Prof.Dr
.RS Mehta 38
• Pituitary irradiation.
with pituitary-dependent
Patients
Cushing’
s
syndrome with adrenal hyperplasia may
require pituitary irradiation.
39. Drug therapy
Prof.Dr
.RS Mehta 39
• 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
.
40. Management
Prof.Dr
.RS Mehta 40
• 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.
41. Surgical Management
Prof.Dr
.RS Mehta 41
• Transsphenoidal hypophysectomy:
Surgical removal of the tumor by
transsphenoidal hypophysectomy .
• Adrenalectomy
43. Nursing assessment
Prof.Dr
.RS Mehta 43
• 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
44. Nursing diagnosis
Prof.Dr
.RS Mehta 44
• 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
45. Nursing Diagnosis
Prof.Dr
.RS Mehta 45
• 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
46. Nursing Interventions
Prof.Dr
.RS Mehta 46
• 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
47. Prognosis
Prof.Dr
.RS Mehta 47
• 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.
