Adrenal Disorder Flashcards
Two Types of Adrenal Glands
Adrenal Cortex and medulla
Adrenal Cortex Hormones
Mineralocorticoids – produced in Zona glomerulosa
Aldosterone
Stimulates renal tubule sodium reabsorption and potassium excretion
Goal to increase intravascular volume.
Sodium reabsorption = water retention
Glucocorticoids – produced in Zona fasciculata
Cortisol
Androgens – produced in Zona reticularis
Adrenal Medulla Hormones
Norepinephrine
Epinephrine
Dopamine
Active in fight or flight sympathetic response, stress, sepsis
Not under pituitary control
Controlled by sympathetic nervous system via
direct neural stimulation
Function of Cortisol
Inhibits insulin
Regulates the metabolism of proteins
carbohydrates, and fats
Diurnal excretion
Highest at ~0600
Lowest at ~2400
increases with exercise and stress
Increases in acute trauma, infection
Required for Angiotensin II production, maintains vascular tone
Regulates inflammatory response of immune system
Epidemiology and Etiology of Addison’s Disease
Autoimmune (idiopathic) destruction of adrenal cortex is most common cause in U.S.
Chronic use of steroids with blunting of ACTH/CRH response during physiologic stress
Women > men
30-60 yr age of onset
Infection as cause
TB is common cause in developing nations
Disseminated fungal infection
Intolerance to physiologic stress is a main concern
Other causes
Metastatic carcinoma
Iatrogenic
Drugs: ketoconazole, steroids
Pathophysiology of Addisons
Chronic deficiency of cortisol, aldosterone, and adrenal androgens/estrogens
Characterized by high ACTH and low corticosteriod
Autoimmune disease
Signs/ Symptoms of Addison’s Disease
Constitutional
Weakness, fatigability
Low grade fever
Skin
Hyperpigmentation, creases
GI
Anorexia, weight loss
Abdominal pain
Anorexia, N/V, Salt craving, Signs of dehydration
Cardiac
Hypotension
small heart
Shock
MSK
Myalgias, arthralgias
Neuro
Delayed deep tendon reflexes
Psychiatric
Lethargy, confusion, psychosis
Chronic Adrenocortical Insufficiency Signs/ Symptoms
Anxiety, irritability
Orthostatic Hypotension
Skin pigment changes – “tanning” over non-exposed and exposed areas, hand creases
Chronic Adrenocortical Insufficiency Lab and Imaging
Hypoglycemia
Plasma ACTH is elevated
Low serum Sodium
Elevated Potassium
Retains K+
Diagnosis of Chronic Adrenocortical Insufficiency
Low plasma cortisol @ 8am is diagnostic with elevated plasma ACTH level (>200 pg/mL)
Antiadrenal antibodies in autoimmune disease
Corticotropin (ACTH) Stimulation Test
Stimulates adrenal cortex to produce and secrete cortisol
Failed adrenal response (no cortisol elevation) is confirmatory
Chronic Adrenocortical InsufficiencyTreatment
Replacement of glucocorticoids and mineralocorticoids
Hydrocortisone
Give lowest effective dose to avoid Cushingnoid side effects
Increase dose during times of acute illness/stress
DHEA
Medical alert bracelet
Adrenal Crisis
Occurs in patients who stop their Steroidal medications
This is most common cause of adrenal insufficiency
abrupt cessation of glucocorticoids
Can occur in stressful periods without prior glucocorticoid dose adjustment:
Infections
Trauma
Surgery
Goal of treatment:
Reverse hypotension and electrolyte abnormalities
Intravenous infusion with isotonic normal saline
Replace glucocorticoid
Cushing’s Disease
Caused by excess secretion of ACTH usually by a pituitary adenoma
Cushing’s disease is the most common cause of endogenous hypercortisolism
Cushing’s Syndrome
Adrenocortical tumors Non-pituitary ACTH secreting tumors Small cell lung carcinoma Ectopic CRH Bronchial carcinoid Chronic exposure to Glucocorticoid hormones such as prednisone are the most common exogenous cause (Iatrogenic)
2 Cushing’s Syndrome Subcategories
ACTH Dependent
Cushing’s Disease
Non-pituitary ACTH secreting tumor
Ectopic CRH
ACTH Independent
Adrenocortical tumors
Cushing’s Syndrome Signs and Symptoms
Central obesity (90%), “Moon face”, “Buffalo hump”
Supraclavicular fat pads, protuberant abdomen, thin extremities
Hypertension (85%), Decreased glucose tolerance (80%)
Amenorrhea (↑androgens), Weakness (↓K+)
K+ excretion and Na+ retention , CA++ loss
Immunosuppression (↓ PMNs)
Hirsutism (70%); Osteoporosis (55%)
Thirst, polyuria, renal calculi
Acne, Purple striae
Impaired wound healing, susceptible to infections
Mental : poor concentration, depression, psychosis
Enhances catecholamine activity
Initial Lab Diagnosis for Cushings Syndrome
24-Hour Urinary Free Cortisol Level – levels high in Cushing’s in 3 separate collections
Late night salivary cortisol level
High in Cushing’s (normally, it is low)
Low Dose Dexamethasone Suppression Test (DST)
Dexa 1mg at 11PM. Check cortisol at 8:00 AM. Will diagnose Cushings if cortisol is high (>0.5 mcg/dL)
Normal <0.5mcg/dL
Treatment for Cushing’s Syndrome
Treatment depends on the specific reason for cortisol excess.
If the cause is long-term use of glucocorticoid hormones, the dosage is gradually reduced to the lowest dose adequate for control of the indicated disorder
Ketoconazole, Metyrapone
For pituitary adenoma/Adrenal adenoma: surgery
After surgery need to maintain on
Cushing’s Complications
Untreated, can cause death
Complications of hypertension and diabetes
Increased susceptibility to infections
Osteoporosis, nephrolithiasis, psychosis
Pheochromocytoma
Excessive catecholamines secreted from a tumor in the adrenal medulla:
norepinephrine, epinephrine, dopamine
typically norepinephrine
If familial, typically epinephrine
0.05%-0.2% hypertensive patients have a pheo
peak incidence 3rd-5th decade
Pheochromocytoma Signs/Symptoms
Hypertension, postural tachycardia and hypotension-episodic
Classic Triad: Attacks of severe headache, palpitations, profuse sweating range from monthly to multiple episodes daily Cardiac arrythmias, enlargement Intracerebral hemorrhage Hypertensive encephalopathy Epigastric pain, weakness, constipation Heart failure
People that should be examined for Pheochromocytoma
Patients with very difficult to control hypertension
Patients requiring more than 4 blood pressure medications
Patients with onset of hypertension before 35yo or after the age of 60
Symptoms: Headache, sweating and tachycardia/palpitatios and +/- high blood pressure
Labs and Treatments for Pheochromocytoma
Urinary catecholamines, total and fractionated metanephrines, vanillylmandelic acid (VMA), and creatinine – in a 24 hour urine collection
Direct plasma assay of epinephrine and norepinephrine, free metanephrines
CT/MRI of adrenals
Treatments for Pheochromocytoma
Surgical removal tumor or adrenal gland always indicated for all pts given high incidence of malignancy (unless
already metastatic)
Prognosis: complete cure if benign or if malignant caught early
