ADDISON’S DISEASE

PRESENTER: Dr. McDonald

Prepared by Dr Ghent, 2018

 OVERVIEW
 INTRODUCTION
 PATHOPHYSIOLOGY
 CAUSES
 SYMPTOMATOLOGY
 INVESTIGATIONS
 MANAGEMEN T
 SUMMARY
 REFERENCE
 INTRODUCTION
 Addison’s disease is adrenocortical insufficiency due
to the destruction or dysfunction of the entire
adrenal cortex. It affects glucocorticoid and
mineralocorticoid function. The onset of disease
usually occurs when 90% or more of both adrenal
cortices are dysfunctional or destroyed.

 Thomas Addison first described the clinical

presentation of primary adrenocortical insufficiency
in 1855 in his classic paper, On the Constitutional and
Local Effects of Disease of the Supra-Renal Capsules.
PATHOPHYSIOLOGY
 CAUSES
 AUTOIMMUNE

 INFECTIONS—TB, histoplasmosis, coccidioidomycosis

 AIDS

 HEMORRHAGE—anticoagulants, sepsis (Waterhouse–

Friderichsen syndrome, associated with
meningococcemia), trauma, anticardiolipin antibodies.
SIGNS AND SYMPTOMS CAUSED BY
MINERALOCORTICOID DEFICIENCY
 Abdominal pain, nausea, vomiting

 Dizziness, postural hypotension

 Salt craving

 Low blood pressure, postural hypotension

SIGNS AND SYMPTOMS CAUSED BY
GLUCOCORTICOID DEFICIENCY
 Fatigue, lack of energy

 Weight loss, anorexia

 Myalgia, joint pain

 Fever

 Low blood pressure, postural hypotension

 OTHER SIGNS AND SYMPTOMS

CAUSED BY ADRENAL ANDROGEN DEFICIENCY

 Lack of energy
 Dry and itchy skin (in women)
 Loss of libido (in women)
 Loss of axillary and pubic hair (in women)

OTHER SIGNS AND SYMPTOMS

 Hyperpigmentation
 BASIC INVESTIGATIONS
 LABS — CBCD (Anemia), Serum electrolytes
(Hyponatremia -due to loss of feedback inhibition of AVP
release, Hyperkaliemia)

 Kidney Function (Increased serum creatinine - due to

volume depletion) Liver Function

 DHEAS, TSH, free T4

 Hypoglycemia (more frequent in children)

 SPECIFIC TESTING

 ACTH STIMULATION TEST — obtain cortisol and

ACTH at baseline, give 250 mg of ACTH IV push,
measure cortisol at 30 and 60 min

 In primary adrenal insufficiency, increased plasma

renin will confirm the presence of
mineralocorticoid deficiency.

 MICROBIOLOGY — blood and urine cultures if

suspect sepsis
 MANAGEMENT
ACUTE ADRENAL CRISIS
 ABC

 O2

 IV. Fluids (D5NS 2–3L IV bolus)

 Corticosteroid (hydrocortisone100 mg IV q6h or

dexamethasone 4 mg IV q6h (dexamethasone
does not interfere with ACTH stimulation test).

 Treat precipitant (sepsis, viral gastroenteritis)

 LONG TERM TREATMENT
 TREATMENT—physiologic replacement (prednisone 5
mg PO qAM and 2.5 mg PO qPM, plus fludrocortisone
0.1 mg PO daily).

 STRESS DOSE REPLACEMENT (prevention)—if

patients have been taking suppressive dose of
glucocorticoids for >3 weeks during the preceding
year, they should be on stress dose during illnesses or
surgical procedures
 SUMMARY

 In principle, the clinical features of primary

adrenal insufficiency (Addison’s disease)
are characterized by the loss of both
glucocorticoid and mineralocorticoid
secretion

 Principal management include identification

of a specific cause and corticosteroid
therapy.
 REFERENCES

 Harrison’s Principles Of Medicine 19th Edition

 UPTODATE

 Approach To Internal Medicine

 MEDSCAPE