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Endocrinology

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What are the diagnostic tests if suspecting Cushing’s syndrome? 

  • 1) High 24 urine cortisol 

  • 2) High midnight salivary cortisol 

  • 3) low-dose dexamethasone suppression test (1 mg dex given at night results in high/normal cortisol in AM) 

  • All 3 tests have similar diagnostic accuracy. Must have ⅔ abnormal for a diagnosis of Cushing syndrome

 

Once Cushing syndrome has been established, then what is your next step? 

  • ACTH level measurement - this determines whether the Cushing syndrome is dependent on ACTH or not and will localize the source of ACTH

    • ACTH suppressed (<5) then ACTH-independent must be Primary Adrenal Cushing (15-20% of cases) → warrants abdominal CT or MRI

    • ACTH normal or elevated (>5) then must be ACTH-dependent → warrants 8-mg dex suppression test to separate Cushing disease (pituitary Cushing syndrome) (responds to negative feedback and suppresses plasma cortisol) from ectopic ACTH somewhere else in body (does not have suppressible cortisol)

Suggested Work-Up for Cushing’s Syndrome: https://www.aafp.org/pubs/afp/issues/2000/0901/p1119/jcr:content/root/aafp-article-primary-content-container/aafp_article_main_par/aafp_figure1.enlarge.html

 

What is the most reliable test to confirm hyperaldosteronism? 

  • Midmorning plasma aldosterone concentration/plasma renin activity ratio

  • Ratio less than 20 rules out primary hyperaldosteronism 

 

What medications interfere with plasma-renin aldosterone ratio if suspecting hyperaldosteronism?

  • ACE and ARB- patients taking them should have elevated renin activity. If plasma renin levels are suppressed, highly suggestive of primary hyperaldo 

  • Spironolactone/Epleronone/Amilioride should also ideally be stopped 4-6 weeks before testing for hyperaldo

 

What is the treatment in idiopathic primary hyperaldo (bilateral adrenal hyperplasia) or those that have an adenoma and are refusing surgery? 

 

Adrenal insufficiency diagnostic algorithm 

https://www.aafp.org/pubs/afp/issues/2014/0401/p563/jcr:content/root/aafp-article-primary-content-container/aafp_article_main_par/aafp_figure.enlarge.html

 

Stress dose steroid recommendations when a patient is ill?

  • If moderate stressor- hydrocortisone 25-75 mg/day orally or IV for 1-2 days as they recover from acute stressor or illness

  • Major stressor (trauma, surgery, critical illness, child birth)--> 100 mg IV hydrocortisone followed by 50 mg q6 IV. how rapidly you can taper depends on patient improvement

  • https://twitter.com/annkumfer/status/1294722893700628481

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What are the standard first line PO medications for diabetes?

  • Metformin

  • GLP-1

  • SGLT-2

 

What are two worrisome side effects associated with SGLT2s? 

 

How do you differentiate surreptitious use of insulin vs oral hypoglycemic agents?

  •  At time of hypoglycemia, c-peptide low with insulin and c-peptide high with oral hypoglycemics

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What is needed to make a diagnosis of DKA?

  • Ketones in urine, BHB in blood

  • Acidosis on blood gas and anion gap

  • Blood glucose >400 (may be <250 in euglycemic DKA from SGLT2s)

 

What are the causes of DKA?

  • Infection → Check UA, CXR

  • Ischemia → Check EKG, troponin, lactate

  • Indiscretion with sugar (non-compliance)

  • Insulin (lack thereof)

  • Infant (pregnancy)

 

How do you manage DKA?

  • Insulin → Use insulin gtt → once AG is closed can transition with SQ insulin (must overlap gtt and SQ insulin by 2 hours)

  • IVF → At least 2L upfront, then continue fluids with LR @ 200 mL/hr → switch to D5-containing fluids once BG is <200

  • Electrolytes → Aggressively replete K, Mg, Phos, check labs q4 hrs, make sure K is >3.3 prior to starting/continuing insulin gtt

  • DKA: https://twitter.com/OnePagerICU/status/1549040342371946497

 

How is HHNK different than DKA?

  • Partial insulin deficiency, no ketosis but massive volume loss (usually 8-10 L as opposed to 6-8L in DKA)

  • Give more fluids than you would in DKA

  • Higher mortality rate

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When should hypoglycemia be evaluated? 

  • If patient has symptoms, low glucose level, and glucose and symptoms that improve once glucose level is raised (AKA WHIPPLE TRIAD)

 

What are some causes of hypoglycemia? 

  • Sepsis/Critical illness, Drugs (insulin, sulfonylureas), hormone deficiency (cortisol def), non islet cell tumors, insulinoma, post gastric bypass hypoglycemia  

 

What is the work up for a patient with hypoglycemia? 

  • Initial work up should include detailed history, review medications/drugs, hx of tumors before considering lab work up 

  • At the time of hypoglycemia (if detected on POCT check), send stat BMP, Insulin, Pro-insulin, BHB and C peptide (important that these labs are sent before treatment)

  • Normal response to hypoglycemia suppression of insulin release, so the insulin, pro-insulin and C peptide should be low.

  • Abnormal response to hypoglycemia elevated insulin, pro-insulin and c peptide. If they are elevated, they can indicate possible insulinoma. Usually the BHB would be low in the presence of excess insulin because the insulin is allowing for ketone clearance

  • https://twitter.com/BrighamMedRes/status/1318184270515499008

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What can you give to reverse sulfonylurea induced hypoglycemia not responding to treatment with glucose only?

  • Octreotide

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What are some causes of hypopituitarism? 

  • Tumors, pituitary apoplexy, infection, infiltrative disease, empty sella syndrome, iatrogenic (surgery, radiation therapy, etc)

 

What are some of the features of hypopituitarism? 

  • Mass effect symptoms- headache, visual disturbances, personality changes 

  • ACTH deficiency symptoms- fatigue, N/V, weight loss/anorexia, hypoglycemia 

  • TSH deficiency symptoms- fatigue, hoarseness, dry skin, weight gain, bradycardia, AMS, constipation 

  • GnRH deficiency- infertility, loss of libido/impaired sexual function, osteoporosis

  • ADH deficiency- polyuria, polydipsia, nocturia 

 

What labs are usually checked? 

 

Why MUST you check a free T4 in central hypothyroidism? 

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What are the causes?

  • Graves, adenoma, Toxic Multinodular goiter, thyroiditis 

 

How do you interpret TFTs?

  • TSH low, free T4 high → Primary hyperthyroidism or thyrotoxicosis

    • B blocker (atenolol or propranolol) for symptom management 

    • If thyrotoxicosis based on uptake scan then treat with b-blocker +/- prednisone/NSAIDs for pain

    • Anti thyroid med- first line is methimazole (PTU used in first trimester of pregnancy or thyroid storm mostly)

  • TSH low, normal free T4, T3 high → Primary hyperthyroidism 2/2 to T3 thyrotoxicosis 

  • TSH low, free T3 and T 4 normal → subclinical hyperthyroidism 

    • Treatment is recommended if TSH<0.1 and patient is symptomatic

    • Indications to treat in TSH  <0.1: cardiac risk factors, symptomatic, osteoporosis, postmenopausal women not on bisphosphonates or estrogen therapy 

  • TSH high, free T3 and T4 high → central hyperthyroidism 

 

What is the treatment of a thyroid storm? 

  • Treat with PTU, beta blocker, glucocorticoid, potassium iodine 

 

What do you have to think of when a patient on methimazole presents with fever or sore throat?

  • Fever or sore throat in patient on anti thyroid meds is presumed to be agranulocytosis until proven otherwise

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What are the causes of Hypothryoidism?

  • Hashimoto, post radiation or radioactive iodine therapy, drug induced (amiodarone), thyroidectomy, history of radiation therapy or central (pituitary adenoma, surgery, radiation)

 

What are some lab findings associated with hypothyroidism?

  • Hyponatremia, high cholesterol, high CK, elevated AST

 

Interpreting thyroid tests:

 

When do you treat subclinical hypothyroidism? 

  • TSH >10 in symptomatic patient, patient young <30, pregnant or planning on becoming pregnant. Can also consider younger patients less than 65 with TSH 7-10

 

How to differentiate euthyroid sick syndrome from hyper/hypothyroid?

  • Euthyroid sick syndrome- low to normal T4, TSH is suppressed in initial stages and later can be elevated in the recovery phase. Normalizes in 4-8 weeks 

The key is the low to normal T4- whereas in hyperthyroidism, the T4 would be high 

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What are the symptoms of myxedema coma? 

  • Bradycardia, hypothermia, altered mental status, hypotension, hyponatremia, hypoglycemia, hypoventilation (respiratory acidosis) along with history of hypothyroidism, thyroidectomy scar, or radiation therapy 

  • Physical exam findings: facial swelling, non pitting edema of extremities, large tongue 

 

What initial labs should you get if you are suspicious of myxedema coma? 

  • TSH, free T4, and cortisol should be drawn prior to starting treatment. 

  • Myxedema score can be calculated to classify patients based on likelihood of having myxedema coma or not ch2330.Table1.pdf (clinicaladvisor.com)

  • Low T4, high TSH indicative of primary hypothyroidism. A low T4 with low, normal or slightly high TSH is more indicative of central hypothyroidism 

 

When do you start treatment? 

  • If you are highly suspicious of myxedema coma, you should start treatment before any laboratory confirmation 

 

What is the treatment for myxedema coma?

  • Steroids (until concomitant adrenal insufficiency has been ruled out) -hydrocortisone 100 mg IV q8

  • Thyroid treatment: usually start with T4 200-400 mcg IV followed by 50-100 mcg daily IV until the patient can tolerate PO intake. Lower end of dosing is preferred in those that are older, lighter, have hx of CAD/arrhythmias

    • Combined T4 and T3 treatment can also be used 

  • Supportive management- fluids, ventilation, rewarming, IV dextrose 

  • Treat underlying trigger- infection, etc

  • https://www.ncbi.nlm.nih.gov/books/NBK279007/

 

How do you monitor for improvement? 

  • Serum T4 and T3 should be checked every 2 days to follow levels and response to treatment. 

  • Clinical and biochemical improvement is usually seen as soon as a week. TSH expected to fall at approx 50% per week if receiving a full replacement dose of thyroid hormone

  • Failure of TSH to fall may be an indication of inadequate treatment 

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What is a prolactinoma?

  • It is a pituitary tumor that produces a hormone called prolactin. It is the most common pituitary adenoma.

 

What are the signs/symptoms of a prolactinoma?

  • General- headaches, visual changes, nausea/vomiting, lethargy (especially with large tumors- mass effect)

  • Women- breast tenderness, galactorrhea, reduced sexual interest, infertility, irregular periods or amenorrhea

  • Men- Reduced sex drive, erectile dysfunction, infertility, gynecomastia

 

What is considered an abnormal prolactin level?

  • Prolactin secretion is usually proportional to the size of the adenoma

  • Adenomas <1 cm are usually associated with serum prolactin levels below 200 ng/mL

  • Adenomas 1-2 cm in diameter – prolactin values range between 200-1000 ng/mL

  • Adenomas greater than 2 cm, prolactin levels can be >1000 ng/mL

 

Who should get an MRI?

  • MRI pituitary with and without contrast should be performed in a patient with any degree of hyperprolactinemia to look for mass lesion unless patient is taking medication known to cause hyperprolactinemia or has significant renal impairment

 

What is the first line treatment of a prolactinoma?

  • Cabergoline/Dopamine agonists are first line irrespective of the size of the tumor.

  • Even in large tumors, treatment with dopamine agonist will help shrink the tumor

 

How is response to therapy assessed?

  • After 1 month of therapy, patient should be evaluated for side effects and serum prolactin should be checked

  • If no side effects and prolactin normalized, continue current dose of dopamine agonist

  • If prolactin did not normalize, medication needs to be up titrated.

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