Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

33 Cards in this Set

  • Front
  • Back
What is the difference between Cushing's disease and Cushing's syndrome
E: Cushing's syndrome refers to hypercortisolemia and its associated signs and symptoms due to any cause. Cushing's disease refers specifically to hypercortisolemia due to ACTH overproduction by a pituitary adenoma. The most common cause of Cushing's syndrome is iatrogenic due to exogenous steroid treatment for a variety of conditions (rheumatologic, organ transplant, reactive airway disease). If one excludes iatrogenic hypercortisolemia, the most common cause of Cushing's syndrome is Cushing's disease, which accounts for approximately two thirds of all cases.
A: pitutiary adenoma
What are the four steps involved in evaluating a patient with Cushing's syndrome?
E:Step 1: Screen for and document Cushing's syndrome (hypercortisolemia).
Step 2: Differentiate between ACTH-dependent and ACTH-independent causes.
Step 3: Distinguish pituitary Cushing's disease from ectopic ACTH secretion.
Step 4: Anatomic imaging and surgical resection of the tumor once identified.
A:hypercortisol,dependent,ectopic, imag
How should one screen for Cushing's syndrome?
E: First-line screening tests include the low-dose (1 mg) overnight dexamethasone test and 24-hour urine free cortisol levels.
A: low, 24
How is the low-dose dexamethasone suppression test performed?
E: Give 1 mg of dexamethasone at 11 pm the night before. This dose should suppress 8 am cortisol to < 1.8 μg/dL if a sensitive assay is used (the old cutoff value was < 5 μg/dl).
A: night
What must be measured along with cortisol in the 24 hour urine free cortisol measurement
E: This test should be normal in patients without Cushing's syndrome (most assays define normal as = < 100 mg/24 h). This test may be repeated up to three times if the first test is normal and there is a high index of suspicion. It must always be performed with a creatinine level to ensure adequacy of the urine collection.
A: creat
How do you distinguish between ACTH-dependent and independent causes of Cushing's?
E:The best method is simultaneous measurement of ACTH and cortisol. If the ACTH is >10 pg/mL, the patient most likely has an ACTH-dependent cause of Cushing's syndrome. Additionally, an ACTH value > 10 pg/mL following peripheral CRH administration suggests ACTH dependency.
A: simul
Once ACTH-dependent Cushing's syndrome has been confirmed, what is the final step in making the biochemical diagnosis?
E: The final step involves differentiating between a corticotrope adenoma and an ectopic ACTH-secreting tumor. A high-dose (8-mg) dexamethasone test can be performed. Patients with a pituitary source of ACTH retain suppressibility of cortisol to high-dose dexamethasone, whereas patients with ectopic ACTH tumors do not.
A: high
What is IPSS?
E:Many clinicians confirm the diagnosis with inferior petrosal sinus sampling (IPSS). This test takes advantage of the concentration gradient between pituitary venous drainage via the inferior petrosal sinus (IPS-central) and peripheral venous values of ACTH to further determine whether an ACTH-producing corticotroph adenoma is present in the pituitary; the inclusion of CRH stimulation adds greater sensitivity to the test.
A: sampl
What is pseudo-Cushing's syndrome?
E: This is a clinical state characterized by mild overactivity of the hypothalamic-pituitary-adrenal axis that is not associated with true Cushing's syndrome (hypercortisolemia). It is typically seen in a variety of psychiatric states (depression, anxiety), alcoholism, uncontrolled diabetes, and severe obesity. The dexamethasone-CRH stimulation test can be used to help distinguish this disorder from true Cushing's syndrome. Alternatively, an elevated midnight plasma cortisol level rules out pseudo-Cushing's because, unlike patients with true Cushing's syndrome, patients with pseudo-Cushing's retain the diurnal rhythym of cortisol secretion.
What is primary adrenal insufficiency also known as?
E: The causes can be divided into two categories: primary and central. Primary adrenal insufficiency (Addison's disease) is due to adrenal gland dysfunction. Central adrenal insufficiency includes both secondary (pituitary) and tertiary (hypothalamic) causes.
A: Addison
List the causes of primary adrenal sufficiency
E:Autoimmune destruction (70-80%), tuberculosis (20%), adrenal destruction by bilateral hemorrhage or infarction, tumor, infections (other than tuberculosis), surgery, radiation, drugs, amyloidosis, sarcoidosis, hyporesponsiveness to ACTH, and congenital abnormalities.
List the cause of central adrenal insufficiency.
E: Withdrawal of exogenous steroids (common), following cure of Cushing's syndrome, pituitary adenoma/infarction, and hypothalamic abnormalities (rare).
What are the clinical features of Addison's disease?
E: Weakness, fatigue, Vitiligo, orthostatic hypotension, hyponatremia, hyperkalemia,adrenal calcifications.
A: Vit, hypot, hyponat, hyperk, calci
What is the difference in the presentation between primary and central adrenal insufficiency?
E: Hyperpigmentation is not seen in central disease. Patients do not have hypersecretion of melanocyte-stimulating hormone (a product of the propiomelanocortin gene, like ACTH) that is responsible for the hyperpigmentation.
Electrolyte abnormalities (hyponatremia, hyperkalemia) are not typically present in central disease because the aldosterone system is largely intact.
Central disease may involve other manifestations of hypopituitarism.
Hypoglycemia is more commonly seen with central disease due to the presence of combined ACTH and GH deficiency.
A: hyperpig
Summarize the differences in treatment of primary and central adrenal insufficiency
E:In terms of treatment, patients with Addison's disease typically require replacement of both glucocorticoids (prednisone or hydrocortisone) and mineralocorticoids (Florinef), whereas patients with central adrenal insufficiency typically need only glucocorticoids. Patients with central disease do not usually require mineralocorticoids because aldosterone secretion is largely unaffected. All patients should be instructed to increase steroid replacement during times of illness and should wear medical alert jewelry. The goal of treatment is to ameliorate the signs and symptoms of adrenal insufficiency without causing Cushing's syndrome due to exogenous glucocorticoid replacement. Always use the lowest possible doses that control symptoms to avoid side effects.
What is the gold standard test for HPA axis?
E: Insulin tolerance test
What test do most clinicians use to assess adrenal insufficiency?
E: Because the ITT is cumbersome and requires close monitoring, most clinicians perform an ACTH stimulation test. In the classic test, a baseline cortisol is drawn and 250 μg of IV synthetic ACTH (Cortrosyn) is given. Blood samples for cortisol are collected at 30 and 60 minutes. A normal response is a stimulated cortisol value of > 20 μg/dL. A normal response rules out adrenal insufficiency in the majority of cases. A rare exception is the patient with acute central adrenal insufficiency (i.e., pituitary apoplexy or head trauma); since the adrenal glands have not had sufficient time to become atrophic and unresponsive to ACTH. Lack of a normal response indicates decreased adrenal reserve but does not differentiate between primary and central adrenal insufficiency.
E: stim
What is the differential diagnosis of pheochromocytoma?
E:is important to consider other potential diagnoses, including anxiety/panic attacks, alcoholism (or alcohol withdrawal), sympathomimetic drugs (cocaine, amphetamines, phencyclidine, epinephrine, phenylephrine, terbutaline, phenylpropanolamine [a popular over-the-counter decongestant]), combined ingestion of MAO inhibitor and tyramine-containing food, hyperthyroidism, menopause, hypoglycemia, and abrupt discontinuation of short-acting sympathetic antagonists (e.g., clonidine).
Describe the two main screening tests for pheochromocytoma.
E:Some clinicians recommend plasma-free normetanephrine and metanephrine levels as the initial biochemical test. If these values are more than four-fold higher than the upper limit of the normal reference range, proceed to radiographic imaging (CT of abdomen initially) to localize the tumor. Unfortunately, these tests are not always widely available. In such cases, obtain measurements of 24-hour urine normetanephrine and metanephrine.
A:metanephrine, normetanephrine
What tests other than urine metanephrine and normetanephrine levels are used to diagnose pheochromocytoma?
E: Other helpful tests include 24-hour urine fractionated catecholamines and catecholamine metabolites homovanillic acid and vanillylmandelic acid as well as plasma catecholamines. A clonidine suppression test may also be used to confirm the diagnosis. In borderline cases, multiple tests need to be performed or repeated.
A: VMA,HMA, clonidine
How do you locate a pheochromocytoma if standard imaging does not locate it?
E:he tumor is localized by using CT or MRI (first of the adrenals, then of the chest, abdomen, and pelvis). If the tumor cannot be localized with standard imaging, peform an 123I metaiodobenzylguanidine (MIBG) scan to localize functional catecholamine-rich tissue.
What is the treatment of choice for patients with pheochromocytomas?
E: Surgery
A: Surgery
What is the pre-surgical treatment of pheochromocytoma?
E: After tumor localization, the treatment of choice is surgery. All patients must be preoperatively treated with alpha-adrenergic (phenoxybenzamine) and beta-adrenergic (atenololView drug information) blockade to avoid stress-induced catecholamine excess and hypertensive crisis during surgery. It is critical to avoid beta-adrenergic blockade in the presence of unopposed alpha agonists because it may lead to peripheral vasoconstriction and an exacerbation of the patient's hypertension.
A: block, phenoxy
How big must a adrenal incdentaloma be to require treatment?
E: Although there are numerous approaches, evaluations should be individualized. It is important to perform a careful history and physical exam, looking for signs and symptoms of hormone excess. It is usually recommended that patients be screened for Cushing's syndrome (24-hour urine free cortisol and/or 1-mg overnight dexamethasoneView drug information suppression test) and pheochromocytoma (24-hour urine metanephrines/catecholamines or plasma metanephrines). One can consider screening for hyperaldosteronism, particularly if the patient is hypertensive and has a serum potassium < 3.9. Plasma aldosterone concentration (PAC) and plasma renin activity (PRA) may be used to test for an aldosterone-secreting tumor, looking for an PAC:PRA ratio > 20-25. Nonfunctioning tumors < 4 cm are typically observed for growth. Functional tumors or tumors > 4 cm (or growing) are typically removed by surgery.
What is the commonest cause of primary hyperaldosteronism?
E: Primary hyperaldosteronism is excessive production of aldosterone independent of the renin-angiotensin system. It is observed in approximately 0.5-2% of the population, and the differential diagnosis includes solitary aldosterone-producing adenoma (65%), bilateral or unilateral adrenal hyperplasia, adrenal carcinoma, and glucocorticoid remediable aldosteronism.
How do patients with primary hyperaldosteronism present?
E; Patients present with hypertension, hypokalemia (weakness, muscle cramping, paresthesias, headaches), low magnesium levels, and metabolic alkalosis.
A: Hypertension, hypokalemia, mag, met.*alk
What is the first test in the evaluation of primary hyperaldosteronism?
E: The first step is assess upright plasma aldosterone concentration and PRA in the absence of drugs that alter the renin-aldosterone axis (such as most antihypertensives: spironolactone, ACE inhibitors, and diuretics). A ratio of plasma aldosterone concentration (ng/dL) to PRA (ng/mL/h) of > 20-25 makes the diagnosis likely.
How is the diagnosis of primary hyperaldosteronism confirmed?
E: Confirmation requires a high 24-hour urine aldosterone level in the presence of normokalemia and adequate volume status or inadequate suppression of aldosterone levels using the saline suppression or salt-loading test. As always, biochemical diagnosis should precede diagnostic imaging. Treatment depends on the etiology but usually includes surgery except in cases of adrenal hyperplasia or glucocorticoid-remediable hyperaldosteronism.
A: urine.*aldo,(salt)|(saline)
What happens to the T3 resin uptake in hyperthyroidism (high/low)?
E: If the TBG is not low, it is low.
A: low
What is the best initial test for measuring thyroid function?
When is the TSH not a reliable measure of thyroid function?
E: TSH as a measure thyroid status is not a reliable indicator of hyperthyroidism in patients with hypothalamic or pituitary dysfunction.
A: pit
What are the causes of hyperthyroidism?
E: Hyperthyroidism results from tissue exposure to excess thyroid hormone. The excess thyroid hormone can come from thyroid gland hyperfunction (Graves' disease, autonomously functioning nodule), from inflammation and destruction of all or part of the gland with resultant release of stored hormone (thyroiditis), or from an exogenous source outside the thyroid.
A:Grave,autonom,thyroiditis, exog
What is the treatement of thyroid storm?
E: In addition to general supportive care (often in the intensive care unit), treatment involves initiation of the following medications:

* Antithyroid medication (propylthiouracilView drug information [PTU]) to block thyroid hormone synthesis and peripheral conversion of T4 to T3.
* Beta blockers to inhibit the adrenergic system (propranolol or esmolol IV).
* Saturated solution of potassium iodide or other iodine-rich compounds (Gastrograffin, ipodate) to block the release of preformed thyroid hormones.
* Glucocorticoids may also be part of the initial management because thyroid hormones increase metabolism of endogenous cortisol and steroids can inhibit conversion of T4 to T3.
A: PTU, (beta)|(prop),steroid