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PANCE Endocrinology Exam |
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What are the clinical features of adrenal insufficiency? Nausea, vomiting, weakness, fatigue, lethargy, weight loss, anorexia, and hyperpigmentation 3 types of adrenal insufficiency?
- Primary (problem w/ adrenal gland itself)
- Secondary (steroid withdrawal or pituitary issue)
- Tertiary (hypothalamus) What is acute and chronic adrenocortical insufficiency? ● Acute adrenocortical insufficiency (adrenal crisis) is an emergency caused by insufficient cortisol ● Chronic adrenocortical insufficiency or primary adrenal insufficiency (Addison disease) is caused by dysfunction or absence of the adrenal cortices
What is secondary adrenal insufficiency? Secondary adrenal insufficiency is adrenal hypofunction due to a deficient secretion of ACTH by the pituitary gland which may be isolated or occur in conjunction with other pituitary hormone deficiencies. ACTH and cortisol levels both are low. What are causes of secondary adrenal insufficiency? ● Iatrogenic (adrenal suppression from prolonged steroid use) ● Pituitary or hypothalamic adenoma ● Long-term glucocorticoid therapy ● Sheehan syndrome (severe low blood pressure during or after childbirth) ● Traumatic brain injury ● Subarachnoid hemorrhage What is the cause of tertiary adrenal insufficiency? Tertiary adrenal insufficiency refers to impaired hypothalamic release of corticotropin- releasing hormone (CRH) with resulting decreased production of ACTH by the pituitary. The most common causes of tertiary adrenal insufficiency, also suppress corticotropin (ACTH) secretion: ● Abrupt cessation of high-dose glucocorticoid therapy ● Correction (cure) of hypercortisolism (Cushing's syndrome) What are the etiologies of primary adrenal insufficiency?
● Secondary (pituitary) - low ACTH and low cortisol - there is little or no ACTH response in patients with secondary (pituitary-related) adrenal insufficiency ● Tertiary (hypothalamic) - low ACTH and low cortisol - patients with tertiary disease due to lack of CRH from the hypothalamus usually have an exaggerated and prolonged ACTH response What are common laboratory findings associated with adrenocortical insufficiency? ● WBC count with moderate neutropenia, lymphocytosis, and total eosinophil count over 300/μL ● Low serum Na+ (due to low aldosterone) ● Elevated K+ (due to low aldosterone) ● Low fasting blood glucose (due to lack of cortisol) ↑ ACTH (from pituitary hypersecretion) + ↓ Cortisol (failure of the adrenal cortex) + ↓ Aldosterone Primary adrenocortical insufficiency (Addison's disease) ↓ Cortisol, ↓ ACTH, and normal aldosterone Secondary or tertiary
↓ Cortisol, ↓ ACTH, normal aldosterone, with little or no ACTH response during corticotropin-releasing hormone test Secondary adrenocortical insufficiency ↓ Cortisol, ↓ ACTH, normal aldosterone, with exaggerated and prolonged ACTH response (↑ ACTH) with the administration of CRH corticotropin-releasing hormone test Tertiary adrenocortical insufficiency (HPA suppression) What are causes of adrenal crisis? ● Stress (e.g., trauma, surgery, infection, hyperthyroidism, or prolonged fasting) in a patient with latent or treated adrenal insufficiency ● Sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency or temporary insufficiency (suppression by exogenous corticosteroids) ● Bilateral adrenalectomy or removal of a functioning adrenal tumor that suppressed the other adrenal ● Sudden destruction of the pituitary gland (pituitary necrosis) ● Injury to both adrenals (e.g., trauma, hemorrhage, anticoagulant therapy, thrombosis, infection, or metastatic carcinoma) ● Administration of etomidate (rapid anesthesia induction or intubation). In which forms of adrenal insufficiency is mineralocorticoid (aldosterone) secretion intact?
What is the treatment for primary adrenal insufficiency? Replacement therapy with a combination of glucocorticoids and mineralocorticoids. Hydrocortisone is the glucocorticoid of choice. Mineralocorticoid replacement (fludrocortisone) and increased dietary salt intake. Adjustments in dosage are made according to the clinical response. A proper dose usually results in a normal WBC count differential How should patients adjust their medications for when under stress (illness/surgery)? Increase glucocorticoid dose 2- to 3-fold during periods of minor illness; intravenous high-dose glucocorticoids during severe illness or major surgery Cushing's is all about an increase in what? Cortisol (glucocorticoid) Cushing's syndrome vs. Cushing's disease? ● Cushing's Syndrome: symptoms from chronic ↑ cortisol levels and doesn't specify cause or source of excess ● Cushing's Disease is Cushing's syndrome that results from excess pituitary production of adrenocorticotropic hormone (ACTH), generally secondary to a pituitary adenoma. Cushing disease accounts for about 40% of Cushing syndrome cases
Describe exogenous vs. endogenous Cushing's? Cushing syndrome can happen because of exogenous cortisol meaning that it comes from "outside" usually in the form of medications, or because of endogenous cortisol - meaning that the excess cortisol is made by the body. Is the majority of Cushing's syndrome exogenous or endogenous cause? The majority of cases of Cushing syndrome occur in individuals using exogenous steroid medications over a long period of time - often to treat autoimmune and inflammatory disorders, like asthma or rheumatoid arthritis. Because the molecular structure of exogenous steroid medications is so similar to cortisol they mimic its actions on various tissues. Exogenous steroid medications can also cause negative feedback on the hypothalamus and the pituitary gland. This causes a decrease in CRH and ACTH, which in turn, shuts down endogenous cortisol production from the zona fasciculata. What is the most common cause of endogenous Cushing's? The most common reason for increased levels of endogenous cortisol is excess ACTH caused by a pituitary adenoma, which is a benign tumor of the pituitary gland - and this is called Cushing disease
What is corticotropin-releasing hormone (CRH) and where does it come from? Normally, the hypothalamus, which is located at the base of the brain, secretes corticotropin-releasing hormone, known as CRH, which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. ACTH, then, travels to the pair of adrenal glands, on top of each kidney, where it specifically targets cells in the adrenal cortex. Describe the adrenal cortex and it's layers? The adrenal cortex is the outer part of the adrenal gland and is subdivided into three layers- the zona glomerulosa, the zona fasciculata, and the zona reticularis ACTH specifically stimulates cells in which zone to secrete what substance, which belongs to a class of steroids, called glucocorticoids? The zona fasciculata is the middle zone and also the widest zone and it takes up the majority of the volume of the whole adrenal gland. ACTH (secreted by the pituitary) stimulates cells in this zone to secrete cortisol, which belongs to a class of steroids, called glucocorticoids Is most cortisol free or bound?
Glucocorticoids are not soluble in water, so most cortisol in the blood is bound to a special carrier protein, called cortisol-binding globulin, and only about 5% is unbound or free. Only this small fraction of free cortisol is biologically active, and its levels are carefully controlled. Excess free cortisol is filtered in kidneys and dumped into the urine. Is cortisol higher or lower in the morning? Free cortisol in the blood is involved in a number of things and it's part of the circadian rhythm. Cortisol levels peak in the morning, when the body knows we need to "get up and go" and then drop in the evening, when we're preparing for sleep The body uses negative feedback, which means that high levels of cortisol tell the hypothalamus and pituitary gland to (decrease or increase) their secretion of CRH and ACTH? The body uses negative feedback, which means that high levels of cortisol tell the hypothalamus and pituitary gland to decrease their secretion of CRH (hypothalamus) and ACTH (pituitary) How does excess cortisol affect glucose and insulin levels in the blood? Excess cortisol leads to elevated blood glucose levels, and that leads to high insulin levels
excreted in the urine over a 24-hour period. Alternatively, blood or saliva tests late at night can help check if there's a normal daily rise and fall of cortisol levels. Another option for the initial diagnosis of Cushing syndrome? Another option is also the dexamethasone suppression test, which is when a person is given a low dose of dexamethasone, which is an exogenous steroid that suppresses ACTH production in the pituitary gland. Normally that should cause a decrease in serum cortisol levels, but if Cushing syndrome is caused by endogenous cortisol production, then the serum cortisol levels should remain unchanged. If that test is positive, the next step is to determine the exact cause of endogenous cortisol production, and ACTH plasma levels can be checked. How do cortisol levels which increase in times of stress affect gluconeogenesis? In times of stress, the body needs to have plenty of energy substrates around, so cortisol increases gluconeogenesis, which is the synthesis of new glucose molecules, proteolysis, which is the breakdown of protein and lipolysis, which is the breakdown of fat. What is a feature of Cushing syndrome due to cortisol-mediated break down of muscle to produce amino acids for gluconeogenesis. Muscle weakness is a feature of Cushing syndrome due to cortisol-mediated break down of muscle to produce amino acids for gluconeogenesis.
What are the clinical manifestations of Cushing syndrome? Central obesity, moon facies, dewlap (under chin), dorsocervical and supraclavicular fat pad thickening Thin extremities with muscle wasting and proximal muscle weakness Thin skin, facial plethora, violaceous striae, easy bruising, slow wound healing Hyperglycemia and glucose intolerance Psychological problems (irritability, depression, psychosis, mania, anxiety, and insomnia) Osteoporosis (vertebral compression fractures, aseptic necrosis, hypercalciuria, and renal calculi) Immune suppression, cutaneous fungal infections, lymphopenia, decreased eosinophils Hyperpigmentation, lymphopenia, decreased eosinophils (if ACTH-dependent Cushing syndrome) What is the most common cause of Cushing syndrome?
How will cortisol levels respond to a dexamethasone suppression test in patients with Cushing syndrome caused by cortisol-producing adrenal tumor? Patients with Cushing syndrome caused by cortisol-producing adrenal tumor will show no change in cortisol levels following a dexamethasone suppression test. What is a drug used in Cushing syndrome that inhibits 11-beta-hydroxylase, thereby inhibiting glucocorticoid synthesis? Metyrapone is a drug used in Cushing syndrome as it inhibits 11-beta-hydroxylase, thereby inhibiting glucocorticoid synthesis. What are the causes of ectopic ACTH secretion? Small cell lung cancer (50%), pancreatic islet cell carcinoma, thymoma, carcinoid tumors, medullary thyroid carcinoma, and pheochromocytoma What is the usual presentation of ectopic ACTH production? Rather than the typical Cushingoid habitus, ectopic ACTH production tends to present with rapidly progressive hypokalemia, metabolic alkalosis, hyperpigmentation, hypertension, edema, and weakness. Does Cushing disease present with hypokalemia or hyperkalemia?
Cushing's causes increased levels of cortisol. Cortisol, at high levels, acts like a mineralocorticoid (aldosterone), stimulating absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving an excess of mineralocorticoids will cause hypokalemia. Does primary adrenocortical insufficiency from a pituitary tumor present with hypokalemia or hyperkalemia? Primary adrenocortical insufficiency (Addison's disease) results in ↑ ACTH (from pituitary hypersecretion) + ↓ Cortisol (failure of the adrenal cortex) + ↓ mineralocorticoid (aldosterone). Aldosterone normally causes absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving a decrease in mineralocorticoids will cause hyperkalemia. What 2 screening tests are used to confirm hypercortisolism? Low-dose dexamethasone suppression test (administered at 11 PM, with an 8 AM serum cortisol the next day) and 24-hour urinary free cortisol test What is the radiographic test of choice for identifying suspected pituitary adenomas? MRI of the sella turcica, with and without gadolinium (though up to 50% of adenomas may not be seen) What is the treatment for Cushing disease?
What is the treatment of dawn phenomenon? Treat with bedtime injection of long-acting Insulin (NPH) dose to blunt morning hyperglycemia, avoiding carbohydrate snacks late at night Nocturnal hypoglycemia followed by rebound hyperglycemia Somogyi effect - If the blood sugar level drops too low in the early morning hours, hormones (such as growth hormone, cortisol, and catecholamines) are released. These help reverse the low blood sugar level but may lead to blood sugar levels that are higher than normal in the morning. An example of the Somogyi effect is a person who takes insulin doesn't eat a regular bedtime snack, and the person's blood sugar level drops during the night. The person's body responds to low blood sugar by releasing hormones that raise the blood sugar level. This may cause a high blood sugar level in the early morning. Treatment of Somogyi effect? Treat with decreased nighttime NPH dose or give bedtime snack Diagnosis of Somogyi effect? Check 3 am blood sugar
● If the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect ● If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it's likely the dawn phenomenon What term is used to describe progressive rise in glucose from bed to morning Insulin waning Treatment of Insulin waning Treat with change of insulin dose to bedtime Fruity breath, weight loss, rapid respirations, hypotension Diabetic Ketoacidosis (DKA) Treatment of DKA Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist's consultation, if appropriate.
