Adrenal Gland

Question 1

Why adrenal glands are important?

Answer 1

The adrenal glands are important in the synthesis and regulation of key hormones.
They play a crucial role in water and electrolyte homeostatsis, as well as regulation of blood pressure, carbohydrate and fat metabolism, physiologic response to stress, and sexual development and differentiation.

Question 2

The adrenal medulla secretes…

Answer 2

The adrenal medulla secretes the catecholamines epinephrine (also called adrenaline) and norepineprhine (also called noradrenaline), which are involved in regulation of the sympathetic nervous system.

Question 3

The adrenal cortex consists of:

Answer 3

The adrenal cortex consists of three histologically distinct zones:
zona glomerulosa, zona fasciculata, and an innermost layer called the zona reticularis.

Question 4

Whats the role of zone glomerulosa?

Answer 4

The zona glomerulosa is responsible for the production of the mineralocorticoids aldosterone, deoxycorticosterone, and 18-hydroxy-deoxycorticosterone.

Question 5

Whtas the role of zone fasiciculata?

Answer 5

The zona fasciculata produces the glucocorticoid hormone cortisol.
The normal rate of cortisol production is approximately 8 to 15 mg/day.
Its production increases markedly during physiologic stress, such as during acute illness, surgery, or trauma.
Cortisol is converted in the liver to an inactive metabolite known as
cortisone.

Question 6

What’s the role of zone reticularis?

Answer 6

The zona reticularis produces the androgens androstenedione, dehydroepiandrosterone (DHEA), and the sulfated form of dehydroepiandrosterone (DHEA-S).

Question 7

Androstenedione and DHEA are converted to…

Answer 7

Androstenedione and DHEA are converted in the

periphery, largely to testosterone and estrogen.

Question 8

What controls the adrenal hormone production?

Answer 8

Adrenal hormone production is controlled by the

hypothalamus and pituitary gland.

Question 9

What happens when sufficient or excessive cortisol levels are reached?
Adrenal androgen same mechanism

Answer 9

When sufficient or excessive cortisol levels are
reached, a negative feedback is exerted on the
secretion of CRH and ACTH, thereby decreasing
overall cortisol production.

Question 10

What does Adrenal insufficiency refer to?

Answer 10

Adrenal insufficiency generally refers to the inability of
the adrenal glands to produce adequate amounts of
cortisol for normal physiologic functioning or in times of
stress.

Question 11

Classification of Adrenal Insufficiency

Answer 11

The condition is usually classified as primary,

secondary, or tertiary

Question 12

When are these insufficiencies diagnosed?

Answer 12

Primary adrenal insufficiency usually is diagnosed in the
third to fifth decades of life, whereas secondary adrenal
insufficiency is commonly detected during the sixth
decade.

Question 13

Prevalence of Adrenal Insufficiency?

Answer 13

More in women

Question 14

What causes A.Insufficiency?

Answer 14

It occurs from destruction of the adrenal cortex, usually from an autoimmune process.

Question 15

What causes Secondary adrenal insufficiency ?

Answer 15

Secondary adrenal insufficiency occurs as a result of a
pituitary gland dysfunction whereby decreased production and
secretion of ACTH leads to a decrease in cortisol synthesis.

Question 16

What causes Tertiary adrenal insufficiency ?

Answer 16

Tertiary adrenal insufficiency is a disorder of the
hypothalamus that results in decreased production and release of CRH, which, in turn, decreases pituitary ACTH production and release.

Question 17

What causes Acute adrenal insufficiency (i.e., adrenal crisis)?

Answer 17

Acute adrenal insufficiency (i.e., adrenal crisis) results from the body’s inability to increase endogenous cortisol sufficiently during periods of excessive physiologic stress.

Question 18

A. Insufficiency signs and symptoms

Answer 18

weakness and fatigue requiring rest

periods, gastrointestinal symptoms, weight loss, and hypotension.

Question 19

Association with A.Insufficiency

Answer 19

Patients with autoimmune adrenal insufficiency may have other autoimmune disorders such as type 1 diabetes mellitus and autoimmune thyroiditis.
• Dehydration, hypovolemia, and hyperkalemia (in primary adrenal insufficiency only).
• Decreased serum sodium and chloride levels. • Increased serum blood urea nitrogen (BUN) and creatinine owing to dehydration.
• Hyperpigmentation of skin.
• Personality changes (irritability and restlessness)
• Loss of axillary and pubic hair in women owing to decreased androgen
production.
• Blood count abnormalities.

Question 20

Laboratory Test for Chronic A.Insufficiency

Answer 20

Decreased basal and stress-induced cortisol levels. • Decreased aldosterone level (in primary adrenal
insufficiency only). • Lack of increase in cortisol and aldosterone level after ACTH stimulation.

Question 21

Diagnostic Tests for Adrenal Glands

Answer 21

Computed tomography (CT) or magnetic resonance
imaging (MRI).
The presence of anti-adrenal antibodies.

Question 22

TTT for A. insuffciency?

Answer 22

Lifelong glucocorticoid replacement therapy may be necessary for patients with adrenal insufficiency, and mineralocorticoid
replacement therapy usually is required for those with
Addison’s disease.

Question 23

Whats prescribed for Chronic A. Insufficiency

Answer 23

Hydrocortisone often is prescribed because it most closely resembles endogenous cortisol (with its relatively high mineralocorticoid activity and short half-life) and allows the design of regimens that simulate the normal circadian cycle.

Question 24

What are the immediate goals of Acute A.Insufficiency?

Answer 24

The immediate treatment goals are to correct volume depletion, manage hypoglycemia, and provide glucocorticoid replacement.

Question 25

Acute A. Insufficiency and Stress?

Answer 25

Patients who experience excessive stress should be
educated regarding the need for additional
glucocorticoid replacement and prompt medical
attention.

Question 26

When should we give hydrocortisone?

Answer 26

common recommendation is to double
the maintenance dose of hydrocortisone if the patient
experiences fever or undergoes invasive dental or
diagnostic procedures.

Question 27

Whats Cushings Syndrome?

Answer 27

Cushing’s syndrome refers to the pathophysiologic
changes associated with exposure to supraphysiologic
cortisol concentrations (endogenous
hypercortisolism) or pharmacologic doses of
glucocorticoids (exogenous hypercortisolism).

Question 28

Who’s at risk for developing Cushings Syndrome?

Answer 28

Patients receiving chronic supraphysiologic doses of
glucocorticoids, such as those with rheumatologic
disorders.

Question 29

What’s the classification of Cushings Syndrome?

Answer 29

ACTH-dependent

ACTH-independent

Question 30

ACTH-dependent Cushing’s syndrome results from

Answer 30

ACTH-dependent Cushing’s syndrome results from ACTHsecreting (or rarely, CRH-secreting) adenomas.

Question 31

ACTH-independent Cushing’s syndrome is due to

Answer 31

ACTH-independent Cushing’s syndrome is due either to excessive cortisol secretion by the adrenal glands (independent of ACTH stimulation) or to exogenous glucocorticoid administration.

Question 32

What can be useful in diagnosis of Cushing’s Syndrome?

Answer 32

Circadian rhythm is lost in most patients with Cushing’s syndrome. As such, detection of elevated midnight cortisol concentrations.
Leads to cardiovascular disease

Question 33

Cushing Syndrome Signs and Symptoms

Answer 33

Hypertension, hyperglycemia, and hyperlipidemia are common findings and can be associated with cardiac hypertrophy,atherosclerosis, and hypercoagulability.
Osteopenia, osteoporosis, and increased fractures also have been
reported.

Question 34

Clinical Presentation and Diagnosis of Cushing’s Syndrome:

Answer 34

Weight gain and obesity.
• A rounded and puffy face.
• Dorsocervical (“buffalo hump”) and supraclavicular fat accumulation.
• Hirsutism (75%).
• Thin skin.
• Facial plethora (70%).
• Skin striae.
• Acne (35%).
• Hyperglycemia.
• Hyperlipidemia (70%).
• Polyuria (30%).
• Hypertension.
• Menstrual irregularities (amenoria) (70%).
• Erectile dysfunction (85%).
• Psychiatric changes (85%).

Question 35

Laboratory Tests for Cushing’s Syndrome:

Answer 35

Laboratory Tests:
1- 24-hour urinary free cortisol determination. 2- Overnight low-dose dexamethasone
suppression test (DST). 3- Imaging studies may be used to distinguish
between pituitary, ectopic, and adrenal tumors.

Question 36

What’s the goal of treatment in patients with Cushing’s syndrome ?

Answer 36

The goal of treatment in patients with Cushing’s syndrome is reversal of hypercortisolism and management of the associated comorbidities, including the potential for long-term sequelae
such as cardiac hypertrophy.

Question 37

Whats the treatment of choice for Cushings Syndrome if

tumor localized or what if exogenous cause?

Answer 37

Surgical resection is considered the treatment of choice for Cushing’s syndrome from endogenous causes if the tumor can be localized and if there are no contraindications.
• The treatment of choice for Cushing’s syndrome from
exogenous causes is gradual discontinuation of the offending agent.

Question 38

Non pharmacologial treatment of Cushings Syndrome

Answer 38

Nonpharmacologic Therapy:
1- Transsphenoidal pituitary microsurgery.
2- Pituitary irradiation or bilateral adrenalectomy.
3- Bilateral adrenalectomy.
4- Bilateral laparoscopic adrenalectomy.
5- Unilateral laparoscopic adrenalectomy.

Question 39

Pharmacotherapy of Cushing’s Syndrome

Answer 39

Pharmacotherapy generally is reserved for
patients:
1- With ectopic ACTH-secreting tumor cannot be
localized.
2- who are not surgical candidates.
3- who have failed surgery.
4- who have had a relapse after surgery.
5- in whom adjunctive therapy is required to achieve
complete remission.

Question 40

Pharmacological treatment of cushing syndrome

includes the following classes:

Answer 40

1- Inhibitors of Adrenal Steroidogenesis (as
aminoglutethimide, Ketoconazole, Metyrapone,
Etomidate, Adrenolytic Agent Mitotane.
2- Central Neuromodulators of ACTH Release as
Bromocriptine, Cyproheptadine, Octreotide,
Ritanserin, Sodium valproate.
3- Peripheral Glucocorticoid Antagonist as
Mifepristone.