Alquiros, Michelle Anne V.

Topic: Addison’s Disease, Cushing’s Syndrome, Pheochromocytoma

Adrenal Glands – situated retroperitoneally, each embedded in perirenal fat above the kidneys.
2 Parts:
1. Adrenal Cortex
 Outer shell of adrenal gland
 Synthesizes 3 classes of steroids:
1.a. Glucorticoids (cortisol)
o Acts primarily on carbohydrate, glucose, protein metabolism.
o Responsible for suppression of inflammatory response to injury.
o Maintains fluid and electrolyte balance.
o Controls resistance to stress

1.b. Mineralocorticoids (aldosterone)

- Affects metabolism of electrolytes
1.c. Sex hormone (androgen)
- Physiology of reproduction

2. Adrenal Medulla
- Inner core of the adrenal gland
- Produces catecholamines:
2.a. Epinephrine
- constricts vessels in the skin
- dilates vessels in the skeletal muscles
- increase cardiac activity
- dilates the bronchi by relaxing bronchi musculature
- decreases activities of the gastrointestinal tract
2.b. Nor-epinephine
- constricts the arterioles and venules
- increased resistance to blood flow
- elevated blood pressure
- slowing of heart rate

2.c. Dopamine
- dilation of systemic arteries
- increase cardiac output
- increased blood flow to kidneys
Addison’s disease

Definition :
Primary Adrenal insufficiency due to destruction or dysfunction of all the layers of adrenal
cortex. Onset of the disease usually occurs when 90% of all adrenal cortices are destroyed. It is common
in females 30-50yo and children.

Cause:
 Autoimmune (80% of cases)
 Granulomatous disease (TB)
 Bilateral adrenal hemorrhage due to anticoagulant medications or trauma
 Ketoconazole use (blocks steroid synthesis)

Manifestations:
 Hypoglycemia
 Decreased resistance to stress
 Hyperpigmentation
 Hyponatremia
 Hyperkalemia
 Dehydration
 Hypotention
 Decreased cardiac output
 Less axillary and pubic hair

Diagnostic procedures:
1. CT scan – shows intracranial lesions
2. Plasma ACTH level – decreased
3. Serum Cortisol - decreased
8am – 10 am = 5-23ug/dL
4pm – 6pm = 3-13ug/dL
4. BUN – increased (5-15mg/dL)
5. Serum Na – decresed (135-145mEq/L)
6. Serum K – increased (3.5-5.0mEq/L)
7. Serum glucose – decreased (70-100mg/dL)
8. Urine 17KS – decrease or absent
Male = 5-25mg/24hrs
Female= 5-15mg/24hrs
>65yo: 4-8mg/24hrs

Complication:
Addisonian Crisis – a life-threatening situation precipitated by stress, infection, trauma or surgery.
Signs and symptoms:
 Severe hypotension
 Generalized weakness
 Hypoglycemia, Hyponatremia, Hyperkalemia
 Severe headache
 Irritability, confusion
  shock
Cushing’s Syndrome

Definition: Hypersecretion of glucocorticoids from adrenal cortex.

3 forms of cushing’s syndrome:

1. Pituitary Form – results from excessive production of ACTH by a tumor of the pituitary gland. It is
also called Cushing’s disease.
2. Adrenal Form – caused by an adrenal tumor.
3. Ectopic cushing’s – due to a nonpituitary ACTH-secreting tumor. Such as small cell carcinoma of the
lung may secret ACTH or CRF and produce sever Cushing’s syndrome.it can also result from long-
term therapy with one of the potent pharmacological preparations of glucocorticoids. (Iatrogenic
Cushing’s Syndrome)

Manifastations:
 Hyperglycemia
 Centripetal obesity (Buffalo hump & Moon face)
 Thin extremities
 Hirsutism
 Muscle weakness
 Purple Striae/stretch marks (abdomen and thigh)
 Breast atrophy
 Amenorrhea
 Hypertension
 Hypernatremia
 Hypokalemia
 Weight gain
 Pitting edema

Diagnostic procedures:
1. Ct scan – adrenal tumors
2. Plasma ACTH level – increased
3. Serum Cortisol – increased *loss of diurnal pattern of cortisol secretion
8am – 10 am = 5-23ug/dL 3 blood samples are drawn
4pm – 6pm = 3-13ug/dL (morning, evening, following morning after
4. BUN – Normal (5-15mg/dL) a midnight dose of dexamathasone)
5. Serum Na – incresed (135-145mEq/L)
6. Serum K – decreased (3.5-5.0mEq/L)
7. Serum glucose – increased (70-100mg/dL)
8. Urine 17 KetoSteroids – increase
Male = 5-25mg/24hrs
Female= 5-15mg/24hrs
>65yo: 4-8mg/24hrs

Complication: Death
Pheochromocytoma

Definition: life-threatening tumors of chromaffin tissues (pigmented cells) in the adrenal medulla that
produce excess amounts of catecholamines that stimulate the Sympathetic nervous system (SNS).

Cause:
Incidental adrenal mass/lesions (2-3%)

Manifestation:
 Paroxysmal hypertension
 Severe pounding headaches
 Palpitations
 Tremors
 Visual disturbances
 Profuse diaphoresis
 Weight loss
 Pain on chest or abdomen with nausea and vomiting
 Hyperglycemia and glycosuria

Diagnostic procedures:
1. Blood/urine test – increase catecholamine levels
2. Histamine test – increased BP (normally, causes the blood pressure to drop)
- Given subcutaneously if BP < 170/110mmHg
- Regine test is done if BP >170/110mmHg
3. Regine test – patient should not receive any sedative, anti-hypertensive medication (Reserpine),
narcotics *may cause false-positive reactions
*Phentolamine (Regine) given IV – adrenergic-blocking agent, neutralizes
epinephrine and caused Blood pressure to drop
*Positive for Tumor if there is a Fall of atleast 35mmHg systolic and 25mmHg
diastolic within 3-5minutes
4. Urinary Vanillymandelie Acid (VMA) test
-24 hour urine for VMA (breakdown products of catecholamine metabolism)
- Foods affecting VMA excretion excluded 3 days before test
(coffee, tea, banana, vanilla, chocolate, drugs)

Complication:
 Hypertensive retinopathy and neuropathy
 Cardiac enlargement
 Congestive Heart Failure
 Cerebrovascular accident