49 terms

Adrenal Disorderz


Terms in this set (...)

Cortex of adrenal gland
Medulla of adrenal gland
Cortisol and corticosterone
Glucorticoids function
Regulate the metabolism of carbs, proteins, and fat
Glucorticoids bind to
Corticosteroid-binding globulin (CBG)
What increases CBG?
Oral contraceptives
Certain hematologic disorders
Familial CBG excess
What decreases CBG?
Nephrotic syndrome
Multiple Myeloma
Familial CBG deficiency
Describe regulation of cortisol secretion
CRH released from hypothalamus in response to stress or hypoglycemia and goes to anterior pituitary >>> ACTH released from anterior pituitary >>> ACTH causes secretion of cortisol from adrenal cortex
Cortisol action in target tissues
Increased fat and protein breakdown

Increased blood glucose

Anti-inflammatory effects
Negative feedback of cortisol
Inhibits CRH release from hypothalamus and ACTH secretion from pituitary
Describe some of the effects of exogenous glucorticoids
Anti-inflammatory: decreases pain, swelling, stiffness, and physical disability

Decrease endothelial dysfunction: decreases permeability

Infections, myopathy, osteoporosis, weight gain, gastric ulcers, skin thinning, hirusitism, cataracts, glaucoma, increased CV risk
Disorders of the adrenal cortex includes
Hyper and hypofunction
Disorders of the adrenal medulla includes
Hyperfunction only
Hyperfunction of the cortex that increases cortisol
Cushing's Disease
Cushing's syndrome
Hyperfunction of the cortex that increases aldosterone
Primary or secondary hyperaldosteronism
Hypofunction of the cortex
Addison's disease
Secondary hypocortisolism
What is Cushing's syndrome?
excessive cortisol level
What causes Cushing's disease?
1. Overproduction of ACTH by a pituitary adenoma

2. Lose diurnal and circadian patterns of ACTH and cortisol secretion

3. Lack of ability to increase ACTH and cortisol in response to stressors
What causes Cushing-like syndrome?
Taking exogenous glucorticoids
Hyperfunction of the cortex can be classified as
ACTH-dependent or ACTH-independent
Laboratory tests
24h urine free cortisol (UFC)

Midnight plasma cortisol

Late-night salivary cortisol

Low-dose dexamethasone suppression test (DST)
Which is the confirmatory Test?
24 hour Urinary Free Cortisol (UFC)
Describe the midnight plasma cortisol
If patient stays in the hospital, a midnight plasma cortisol is drawn
Describe the late-night salivary cortisol
Patient collects salivary samples and stores them in the fridge — brings to subsequent visit to physician
Describe the low dose dexamethasone suppression test (DST)
Using 1mg dexamethasone for the overnight test or 0.5mg/6h for the classic 2-day study
Describe the diagnostic evaluation for Cushing's syndrome
If syndrome expected: 1-mg overnight dexamethasone suppression test, 24h urinary free cortisol, or midnight salivary cortisol level

If normal: Cushing's syndrome excluded

If abnormal: plasma ACTH level requested

Low ACTH: ACTH-independent Cushing syndrome (autonomous adrenal cortisol secretion)

Normal or High ACTH: ACTH-dependent Cushing syndrome

If ACTH-dependent: inferior petrosal sinus sampling

ACTH central > peripheral: pituitary tumor

ACTH central </= peripheral: ectopic ACTH syndrome
Typical findings in Cushing syndrome
Psychiatric effects
Central obesity
Moon face
Thick neck
Fat trunk/abdomen
Think extremities
Skin atrophy
Osteoporosis (thinning bones)
Muscle wasting and weakness
Easy bruising
Delayed healing
Androgen excess in females — infertility, menstrual irregularity, acne
Treatment options fo Cushing syndrome
Adrenal inhibitors
Primary function of mineralcorticoids
Regulation of sodium excretion

Maintain normal intra-vascular volume
Principal mineralcorticoid secreted by adrenal cortex
Aldosterone protein binding
Albumin and CBG
Aldosterone metabolism
Aldosterone is regulated by

Also ACTH and plasma electrolytes
Aldosterone causes
Decreased sodium and water excretion

Increased extracellular fluid volume

Potent vasoconstrictor
What is hyperaldosteronism?
Excessive aldosterone secretion by adrenal cortex
Primary hyperaldosteronism
Conn disease

Usually a single benign aldosterone-producing adrenal adenoma
Secondary hyperaldosteronism
Caused by a extraadrenal stimulus (often Ang 2)
Clinical manifestations of hyperaldosteronism
Increased plasma volume — leads to HTN and suppressed renin-angiotensin

Increased sodium reabsorption (hypernatremia) — leads to increased potassium excretion (hypokalemia)

Hypokalemia leads to weakness/paralysis, metabolic alkalosis, polyuria
Treatment of hyperaldosteronism
Manage HTN and hypokalemia

Surgery for adenoma

Aldosterone-receptor antagonists
Addison's disease
Addison disease is caused by rare, autoimmune mechanisms. T or F
Addison's disease is caused by both
Inadequate corticosteroid and mineralocorticoid synthesis; elevated ACTH
Clinical Manifestations of Addison disease
Treatment of Addison disease
Lifetime glucorticoid and mineralocorticoid replacement therapy; diet of 150 mEq sodium per day
Secondary adrenal insufficiency is caused by
Prolonged admin of exogenous glucorticoids, which suppress ACTH secretion
Clinical Manifestations of secondary adrenal insufficiency
Similar to Addison disease — but no hyperpigmentation
Adrenal crisis is caused by
Undiagnosed ACTH deficiency

In patients receiving corticosteroids who are not given increased steroid dosage during periods of stress (infection, taupe, surgery, dehydration)
Clinical presentation of adrenal crisis
Profound weakness
N/v/d — volume depletion and dehydration
Treatment of adrenal crisis
corticosteroid therapy
IV fluids