Labs: Adrenal Flashcards
Laboratory data of a patient with arterial hypertension include increased Na+ and decreased K+ concentrations. Urinary aldosterone excretion is twice normal. What is the most likely diagnosis if plasma renin activity is 1) high 2) low?
High Renin: Renovascular disease, low renal blood flow: from loss of fluid volume (can be ascites, edema) or compression of renal artery. Or can be renin-secreting tumor.
Low Renin: primary hyperaldosternoism / Conn’s syndrome. Most commonly from idiopathic adrenal hyperplasia, then less commonly from aldosterone-producing neoplasms
Plasma cortisol level of a patient is lower than normal. Urinary aldosterone excretion is decreased and the patient is hypoglycemic. What is the most likely diagnosis and what tests would you order?
Primary Adrenal Insufficiency (unknown specific cause)
Tests: try ACTH stimulation test. Addison’s will not produce cortisol in response to ACTH due to autoimmune rxn anti-21-OHase and adrenal destruction. Could also be 21-OHase genetic defect.
If it was acute onset, test for infection (N. meningiditis, psuedomonas, S. pneumoniae) with Waterhouse-Friderichsen Syndrome (acute hemorrhagic necrosis of adrenals)
A 24-year-old man complains of gradually increasing weakness, weight loss and loss of appetite. He was observed to have bronzed skin, however, he reported no exposure to the sun. He was hypotensive and showed evidence of muscle wasting.
The results of the laboratory test included: serum Na+ 125 mmol/l, serum K+ 6.2 mmol/l, plasma cortisol: 4 μg/dl (8:00 a.m.) (decreased), plasma ACTH: increased above normal. An ACTH stimulation test failed to elicit response in plasma cortisol level.
What is the most likely diagnosis?
Addison’s Disease
Bronze skin (check palms too), signs of low aldosterone (low Na, high K, hypotension). ACTH increased bc no neg feedback, and no response to ACTH stimulation bc primary dysfunction of aldosterone synthesis
Addison’s usually has anti-21-OHase autoimmune rxn.
A patient with Cushing’s syndrome entered the hospital for diagnostic studies. Baseline plasma cortisol was elevated. A small dose of dexamethasone did not suppress cortisol but 50% reduction occurred when large dose of dexamethasone was given. Plasma ACTH was elevated. What is the most likely diagnosis?
ACTH-dependent Cushing Disease. Due to ACTH-producing pituitary tumor (2°) or CRH overproduction in hypothalamus (3°). [Hamar said give insulin to induce hypoglycemia to differentiate btwn them, not really sure how that works]
Small dose dexamethasone (cortisol analogue) differentiates metabolic syndrome (cortisol suppressed) from Cushing syndrome (no response)
High dose suppresses 2° and 3° forms, but not the 1° (adrenal cortex adenoma) or 4° (ectopic tumor like sm cell lung cancer producing ACTH)
A hypertensive male patient enters the hospital for medical evaluation. His blood pressure is 180/95 mmHg; Serum Na+: 148 mmol/l, K+: 3.5 mmol/l, fasting plasma glucose: 7.2 mmol/l. Baseline plasma cortisol was elevated. A small dose of dexamethasone did not suppress cortisol. A large dose of dexamethasone was given but there was little change in the blood cortisol from baseline values. Plasma ACTH was high. What is the most likely diagnosis?
Ectopic ACTH production, usually via small cell lung cancer
Not 1° hypercortisol (adrenal cortex neoplasia), which is the other one not responding to high dose dexamethosone test, because 1° is seen with low ACTH levels.
Remember cortisol has some mineralocorticoid activity, so Na+ and K+ levels are borderline on their limits of normal.
A 40-year-old woman complains of amenorrhea and emotional disturbances, perhaps partially due to her increasing obesity which is concentrated around the chest and the abdomen. Her X-ray studies show evidence of mineral bone loss (osteoporosis). Laboratory results: serum K+ 3.2 mmol/l, fasting plasma glucose: 7.7 mmol/l, plasma cortisol: 40 μg/dl (8:00 a.m.) (elevated), plasma ACTH is lower than normal. A large dose of dexamethasone did not suppress the elevated cortisol level. What is the most likely diagnosis?
Adrenal Hyperplasia or Cortisol-Producing Neoplasm.
This conclusion is from low levels of ACTH + not responding to dexamethosone. It is ACTH-independent cortisol production, differentiated from ectopic ACTH-producing tumor (which also doesn’t respond to dexamethosone) because of low ACTH levels.
A young girl develops virilization and hypertension. Plasma cortisol is low, ACTH is elevated. What is the most likely cause of this condition? How are adrenal production of glucocorticoids, mineralocorticoids and androgens affected?
Congenital Adrenal Hyperplasia (CAH) aka Adrenogenital Syndrome: 11β-hydroxylase deficiency, in which cause cortisol and aldosterone are not synthesized and can see elevated DOC (aldosterone precursor), causing hypertension and hypokalemia bc DOC is overproduced (example of a secondary hypertension cause)
A young boy develops precocious puberty and arterial hypotension. Plasma ACTH is elevated, serum Na+ is low. The deficiency of which enzyme is presumably responsible for the the above findings? Urinary excretion of 17-ketosteroids, DHEA and free cortisol are probably normal, low or elevated?
Congenital Adrenal Hyperplasia (CAH) due to 21-hydroxylase deficiency (more common form). Na+ low because of low aldosterone levels, which is indicative that it’s not the 11β-hydroxylase deficiency type of CAH which would have high [Na+].
Urinary excretion of 17-ketosteroids and DHEA would be high due to androgen overproduction
Free cortisol is probably low bc of 21-OHase deficiency meaning can’t fully make cortisol.
A 40-year-old man complains of spells of headache, profuse perspiration
(diaphoresis), nausea and palpitations. Arterial blood pressure is markedly elevated. Urinary VMA excretion is increased. What is the most likely diagnosis? What test would you order to confirm your diagnosis?
Pheochromocytoma: increased VMA (breakdown product of catecholamines) is evidence of high catecholamine synthesis
Can try suppression test with Clonidine: will not see decrease in circulating catecholamines as a result bc unregulated production.
Can also do imaging tests: US, CT, MRI. I-MIBG is radiolabeled adrenal-specific agent used to visualize tumors.
