Endocrinology Flashcards

1
Q

What is a Dexamethasone suppression test used to dx? What is a positive result?

A

It is used to diagnosis hypercortisolism (Cushing’s).

It is positive when a big dose of dexamethasone FAILS to decrease AM cortisol to <3

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2
Q

When do you surgically remove an adrenal ADENOMA?

As in, all the studies show that it is not secreting hormones.

A

Those at Increased risk of an adrenal malignancy having ALL of the following characteristics;

  • size >4 cm
  • density ≥10 Hounsfield units
  • absolute contrast washout <50% at 10 minutes
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3
Q

What is the most common type of thyroid cancer? What is the biggest risk factor for thyroid cancer?

A

Papillary Thyroid CA

Radiation exposure during childhood (ex: Hodgkin’s lymphoma)

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4
Q

For treatment of hyperthyroidism, when do you use Methimazole and when do you need to treat with radioactive iodine?

A

You use radioactive iodine to treat a Toxic Adenoma.

Methimazole treats graves hyperthyroidism.

Methimazole won’t work in a toxic adenoma, because the adenoma just keeps making thyroid hormones indefinitely

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5
Q

How do you manage a pt with Prolactin >200 (normal is <20) in a woman with schizophrenia on Risperdone?

A

Pituitary MRI, it’s not safe to stop this person’s antipsychotic medication.

Evaluation for pituitary hypersecretion when a patient is taking a medication known to raise the prolactin level is difficult.

If PRL is elevated, but <50, you can assume it’s the meds.

If PRL>100, either the medication needs to be withheld to further assess or a pituitary MRI obtained to evaluate for prolactinoma.

Caution is warranted when discontinuation of an antipsychotic agent is being considered, and consultation with a psychiatrist is recommended prior to discontinuation. If the medication cannot be discontinued, a pituitary MRI is required to exclude the diagnosis of pituitary tumor.

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6
Q

What hypoglycemic agent can increase vulvovaginal candidiasis?

A

Empagliflozin (SGLT-2 inhibitor)

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7
Q

What factors decrease levothyroxine absorption?

Increase?

A

Decrease: Celiac Disease, Ca, Iron, PPIs

Increase: Testosterone, Estrogen

Androgens case a reduction in thyroxine-binding globulin, which consequently increases the proportion of metabolically active free thyroxine that is available. Therefore, you may have to reduce levothyroxine when you’re on hormones to prevent iatrogenic thyrotoxicosis.

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8
Q

What changes should you make to levothyroxine level for a woman with hypothyroidism who becomes pregnant?

A

You will have to increase the dose by 30% to start, then check regularly during pregnancy

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9
Q

What type of thyroid disease?

Pt hospitalized with STEMI s/p Cath:

Laboratory studies obtained at the time of cardiac catheterization:
Thyroid-stimulating hormone (TSH): 0.2 µU/mL (0.5-5)
Thyroxine (T4), total: 6.5 µg/dL (5-12)
Thyroxine (T4), free: 1.0 ng/dL (0.9-2.4)
Triiodothyronine (T3), total: 60 ng/dL (70-195)

A

Nonthyroidal illness syndrome (euthyroid sick syndrome) is characterized by reduced serum T3, low or low-normal serum T4, and normal or low (but detectable) serum TSH levels.

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10
Q

What is the difference between non thyroidal illness (euthyroid sick syndrome) and subclinical hypothyroidism?

A

Non thyroidal illness

  • critically ill patient
  • normal or low (but detectable) serum TSH levels
  • reduced serum T3
  • low or low-normal serum T4

Subclinical Hypothyroidism: They are hypothyroid based on labs, but not symptomatic.

  • Low serum TSH level
  • total and free T4 levels are near the lower limit of the normal range
  • total T3 is reduced.
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11
Q

Besides IVF, what is the tx for myxedema coma?

A

IV Hydrocortisone first
Then, Thyroid hormones

In patients with myxedema coma, intravenous hydrocortisone should be administered before thyroid hormones to treat possible adrenal insufficiency.

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12
Q

What is the MCC of primary amenorrhea (never get periods)?

A

Gonadal Failure (Mullerian agenesis, androgen insensitivity)

This is associated commonly with Turner Syndrome

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13
Q

What is primary ovarian insufficiency?

A

Primary ovarian insufficiency is considered when a woman younger than 40 years of age develops secondary amenorrhea with two serum FSH levels in the menopausal range (>35 mU/mL [35 U/L]).

Do not confuse this with primary amenorrhea, when a woman never starts periods, which is usually caused by mullein genesis ass’d with Turner syndrome

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14
Q

After ruling out pregnancy, if the cause of secondary amenorrhea is not obvious from the history and physical exam, what is the next step in your evaluation?

A

FSH, TSH, and prolactin

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15
Q

What is the treatment for PCOS?

A
  1. weight reduction
  2. low dose OCPs (first line) or medroxyprogesterone (↓LH and androgenesis)
  3. spironolactone (treats acne and hirsutism)
  4. clomiphene (for women who want to get pregnant)
  5. metformin (for patients with features of DM or metabolic syndrome)
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16
Q

For someone with features of PCOS, when do you need to get pelvic US?

A

When testosterone >150 to r/o tumor

Dx of PCOS 2/3 of the following;

  1. Ovulatory dysfunction (amenorrhea, oligomenorrhea, infertility)
  2. Lab or clinical evidence of hyperandrogegism (hirsutism, acne)
  3. US evidence of polycystic ovaries
17
Q

What is the definition of infertility?

A

Failure to conceive after 1 year of unprotected intercourse if <35 y/o

Failure to conceive after 6mo if >35 y/o

18
Q

After making the diagnosis of primary hyperparathyroidism, what other lab must you check before undergoing surgery and why?

A

25-Hydroxyvitamin D deficiency is important to avoid postoperative hypocalcemia, which occurs due to rapid flux of serum calcium into bone (hungry bone syndrome)

19
Q

What is the effect of Sarcoidosis on Ca/Phos/Vitamin D/PTH?

A

1,25-dihydroxyvitamin D is very high
Ca is high
Phos is high
PTH is super low

Macrophages within granulomas convert 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D without regulation by parathyroid hormone. An elevated 1,25-dihydroxyvitamin D level and suppressed parathyroid hormone is diagnostic of vitamin D-dependent hypercalcemia.

As vitamin D enhances absorption of both calcium and phosphorus, concurrent elevation of serum calcium and phosphorus is also suggestive of vitamin D-dependent hypercalcemia.

20
Q

Derangement of what electrolyte can cause hypocalcemia?

A

Hypomagnesemia

Hypomagnesemia causes functional, reversible parathyroid hypofunction. So PTH will be wnl, just not working properly and causing low Ca

21
Q

What is the cause of hypocalcemia after starting zolendronic acid for the treatment of osteoporosis?

A

Vitamin D Deficiency

This is why it is so important to check Vitamin D levels and correct deficiencies before starting these medications

22
Q

What test is used to adjust treatment for chronic hypoparathyroidism?

A

24h urine Ca

You want to raise the Ca, but also avoid the symptoms of hyperCa, mainly kidney stones and renal failure.

Complications of prolonged hypercalciuria include nephrolithiasis and impaired glomerular filtration rate. Serum calcium, magnesium, creatinine, and urine calcium levels should be assessed on a regular basis. The goal calcium levels should be low-normal without hypercalciuria. The magnesium level should ideally be greater than 2 mg/dL (0.83 mmol/L), and creatinine levels should remain in the normal range. If the urine calcium level is greater than 300 mg/24 h (hypercalciuria), calcium and/or vitamin D replacement needs to be decreased

23
Q

What are the indications for DEXA?

A
  • all women >65 y/o
  • <65 if FRAX >8.4% 10y risk
  • glucocorticoids
24
Q

What do the DEXA scores mean?

A

Osteopenia: T Score -1.0 to -2.4
Osteoporosis: T Score < -2.5

Note: Osteoporosis is also defined by a h/o a fragility fracture

25
Q

How long do we treat osteoporosis with bisphosphonate?

A

For low-risk osteoporotic women, treatment with antiresorptive therapy for 5 years is sufficient.

But continue for 10 years if they are losing weight, have a h/o of fragility fracture.

26
Q

What is different about Denosumab for the treatment of Osteoporosis?

A

Unlike the bisphosphonates which can be stopped after 5 years, the effects of Denosumab are not sustained when treatment is stopped.

Note: Denosumab, a monoclonal antibody against the receptor activator of nuclear factor κB ligand (RANKL), reduces bone resorption by inhibiting the development of osteoclasts. It circulates in the blood for up to 9 months after subcutaneous injection, but once cleared from the circulation, bone resorption transiently but dramatically increases, resulting in an abrupt decline in bone mineral density and, in some cases, vertebral fractures. Once initiated, there is no defined endpoint for cessation of denosumab therapy.

27
Q

19M just dx with T1DM. His hemoglobin A1c level at diagnosis was 11.1%, and antibodies to glutamic acid decarboxylase (GAD65) were positive. He was begun on prandial and basal insulin. He now reports progressive improvement in his glycemic control over the last 8 weeks without changes to his diet, activity level, or insulin doses. Data from his glucometer demonstrates an average fasting, preprandial, and bedtime blood glucose level of 80 mg/dL (4.4 mmol/L). He has several postprandial blood glucose values of approximately 60 mg/dL (3.3 mmol/L) associated with hypoglycemic symptoms.

His current hemoglobin A1c level is 5.0%. Medications are insulin glargine (8 U) and insulin aspart (2 U before meals).

How do you change his regimen?

A

Stop all insulin.

This is the “honeymoon” phase and if he wasn’t already having hypoglycemia you could try to continue.

The drastic reduction in endogenous insulin production secondary to pancreatic beta cell destruction in type 1 diabetes creates a glucose toxicity that induces a functional impairment of the remaining beta cells. As exogenous insulin therapy improves glycemic control, the remaining beta cells experience less metabolic stress, resulting in an improvement in the ability to produce insulin. This “honeymoon phase” may occur shortly after the diagnosis of diabetes and may last months to years.

28
Q

Besides hormones, what is important to test after transsphenoidal pituitary resection?

A

Na to test for SIADH

Sodium and water imbalance are common after pituitary surgery. Patients may exhibit findings of diabetes insipidus (DI) (polyuria, elevated or high normal serum sodium, and dilute urine) followed by syndrome of inappropriate antidiuretic hormone secretion (SIADH) followed again by DI. Central DI may be transient, lasting only a few weeks, or permanent.

29
Q

What is subclinical hypothyroidism? When do you need to treat it? How do you make the dx?

A

TSH high, T4 wnl
TSH>10
R/O transient TSH elevation by re-check in 2-3mo

30
Q

What is osteomalacia? How do you differentiate it from osteoporosis?

A

Osteomalacia is d/t vitamin D deficiency. You would expect to see high PTH, low Ca, low Phos, high Alk Phos.

Osteoporosis will have a normal biochemical profile, it’s dx with DEXA.

31
Q

What Vitamin D study do you need to get in hyperparathyroidism and why?

A

25-Hydroxyvitamin D

This is the one the PTH converts to 1,25-Dihydroxyvitamin D. The 1,25 levels will be elevated in high PTH, even if there is a deficiency in 25-Hydroxyvitamin D.

32
Q

Which DM2 medication is contraindicated in patients with pancreatitis?

A

Liraglutide/”Saxenda”/GLP-1 Agonist