Endocrinology Flashcards

1
Q

what is the incidence of adrenocortical carcinoma

A

1-2 per million people per year

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2
Q

is adrenocortical carcinoma functional or nonfunctional

A

either!

functional - Cushing syndrome

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3
Q

The majority of adrenocortical carcinomas present with a clinical syndrome of

A

hormone excess or Cushing syndrome alone or are mixed with virilization syndrome

additional sx - weight gain, weakness, and insomnia that develop quickly over 3 to 6 months

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4
Q

common findings on CT for adrenocortical carcinoma

A

mass greater than 4 cm with higher attenuation
irregular borders
calcification
invasion to surrounding structures with lymph node enlargement

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5
Q

most common sites of mets for adrenocortical carcinoma

A

liver
lungs
lymph nodes
bone

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6
Q

due to mets, what other imaging do ppl w adrenocortical carcinoma need

A

CT scan of chest
CT scan of liver
Bone scan

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7
Q

can cytology of a fine-needle aspiration distinguish between a benign adrenal mass and an adrenocortical carcinoma

A

no - It can also lead to metastasis in the needle core site

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8
Q

what is the only potentially curative tx for adrenocortical carcinoma

A

surgical resection

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9
Q

when is adjuvant mitotane recommended for adrenocortical carcinoma

A

high-grade disease
intra-operative tumor spillage
large tumors with vascular or capsular invasion

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10
Q

how long would mitotane be continued in patients with adrenocortical carcinoma

A

5 years after surgical resection for high risk
3 years after surgical resection for low risk

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11
Q

symptoms of Cushing syndrome

A

due to cortisol excess

proximal muscle weakness
weight gain
headache
oligomenorrhea
erectile dysfunction
osteoporosis
central obesity
moon facies
buffalo hump
supraclavicular fat pads
thin extremities
HTN
acanthosis nigricans
hirsutism

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12
Q

Which of the following zones of the adrenal gland is responsible for the production of catecholamines

A

adrenal medulla

produces epinephrine, norepinephrine, and dopamine

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13
Q

what does the zona glomerulosa produce

A

the outermost layer
produces mineralocorticoids like aldosterone

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14
Q

what does the zona fasciculata produce

A

middle layer
produces glucocorticoids like cortisol

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15
Q

what does the zona reticula produce

A

innermost layer
produces androgens, such as dehydroepiandrosterone and androstenedione

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16
Q

Pheochromocytoma

A

a rare neuroendocrine tumor of the adrenal medulla which causes an excess production of catecholamines like epinephrine, norepinephrine, and dopamine

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17
Q

signs and symptoms of pheochromocytoma

A

paroxysmal or sustained hypertension
headache
palpitations
diaphoresis

may have cardiac manifestations which can be life-threatening

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18
Q

lab testing for pheochromocytoma

A

plasma fractionated free metanephrines
plasma fractionated catecholamines
serum CgA
clonidine suppression testing

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19
Q

what is the most sensitive lab test for pheochromocytoma

A

plasma fractionated free metanephrines

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20
Q

if there is high suspicion of pheochromocytoma and you find that they have elevated plasma fractionated free metanephrines, what tests should you do next to help confirm

A

24-hour urine for fractionated metanephrines and creatinine

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21
Q

imaging for pheochromocytoma

A

noncontrast CT of the abdomen followed by an immediate follow-up CT with nonionic contrast using a washout protocol

Pheochromocytomas typically retain > 40% of the contrast after 15 minutes

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22
Q

what must be treated prior to surgery for pheochromocytoma

A

hypertension and tachydysrhythmias

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23
Q

what can be used to treat hypertension and tachydysrhythmias in pheochromocytoma esp prior to surgery

A

Alpha-blockers, such as phenoxybenzamin
CCB
^these are given 10-14 days prior to surgery

can be used alone or in combo

Cardioselective beta-blockers, such as metoprolol XL, should be administered for control of tachydysrhythmias only after blood pressure has been controlled - given 2-3 days prior to surgery

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24
Q

what do pheochromocytomas consist of

A

chromaffin cells

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25
Q

treatment for pheochromocytomas

A

complete adrenalectomy - usually performed laparoscopically

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26
Q

what is the most common clinical (lab) presentation of hyperparathyroidism

A

hypercalcemia

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27
Q

Classical presentations of hyperparathyroidism

A

bone disease
nephrolithiasis
weakness
fatigue
neurobehavioral sx like depression or psychosis

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28
Q

how do you diagnose hyperparathyroidism

A

If an elevated serum calcium concentration is found on routine testing, confirmation by repeat lab draw is the first step
If an elevated level is found on repeat lab draw, the next step in evaluation is a serum parathyroid hormone

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29
Q

what is considered diagnostic for primary hyperparathyroidism

A

Elevated serum calcium and elevated serum parathyroid hormone

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30
Q

tx for sx hyperparathyroidism

A

parathyroidectomy

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31
Q

tx for asx hyperparathyroidism

A

surgery - if serum calcium concentration of 1.0 mg/dL or more above the upper limit of normal, bone density of hip, lumbar spine, or distal radius greater than 2.5 standard deviations below normal, previous asx vertebral fx, glomerular filtration rate (GFR) less than 60 mL/min, 24-hour urine calcium greater than 400 mg/day, nephrolithiasis on imaging, age < 50

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32
Q

what is the MC cause of primary hyperparathyroidism

A

parathyroid adenoma

33
Q

what are the most common causes of hypoparathyroidism

A

post neck surgery (thyroidectomy, parathyroidectomy) or autoimmune destruction of the parathyroid gland

34
Q

what other electrolyte abnormality can cause hypoparathyroidism

A

hypomagnesemia

35
Q

signs and sx of hypoparathyroidism

A

tingling around the perioral area
paresthesias and muscle cramping of the hands and feet (carpopedal spasm)
tetany
laryngospasm
seizures
hyperactive DTR
Chvostek sign (facial twitching that is induced by tapping the facial nerve on the same side)
Trousseau sign (spasm in the hands after inflating a blood pressure cuff above the systolic pressure)

36
Q

triad for diagnosis of hypoparathyroidism

A

hypocalcemia
low PTH
increased phosphate

37
Q

what will EKG show for hypoparathyroidism

A

prolonged QT interval (increased risk of arrhythmia)

38
Q

tx for hypoparathyroidism - acute vs non-acute

A

acute - IV calcium gluconate plus oral calcitriol (activated vitamin D)

non-acute - calcium (500 mg to 2,000 mg two to four times daily) and vitamin D

39
Q

normal range for calcium

A

8.5-10 mg/dL

40
Q

when is a thyroid nodule more likely to be benign

A

if the nodule is painful or tender to touch and if it is soft, smooth, and mobile upon palpation

41
Q

how are thyroid nodules evaluated

A

thyroid scintigraphy (radionuclide scanning) - describes nodule as hot, warm, cold, depending on its uptake of the radioactive isotope

42
Q

Hot thyroid nodules

A

Hot nodules take up more of the radioactive isotope than surrounding thyroid tissue and are indicative of autonomously functioning nodules, such as toxic adenomas or toxic multinodular goiters, and are rarely found to be malignant

43
Q

Warm thyroid nodules

A

Warm nodules indicate normal thyroid function

44
Q

Cold thyroid nodules

A

cold nodules indicate low functional or nonfunctional thyroid tissue. Cold nodules will have a decreased uptake of radioactive isotope compared to surrounding thyroid tissue on scintigraphy

45
Q

what thyroid nodules carry the highest risk of malignancy

A

cold nodules

46
Q

how to fully evaluate thyroid nodules

A

if there is a lower than normal TSH finding –> scintigraphy next

If the serum TSH is high or normal –> thyroid ultrasound

A fine-needle aspiration should be performed if there is any suspicion for malignancy on ultrasound

47
Q

what do follicular cells secrete

A

thyroxine (or T4) and triiodothyronine (T3)

48
Q

what do parafollicular cells secrete

A

thyrocalcitonin

49
Q

Sonographic features of thyroid nodules suspicious for malignancy

A

microcalcifications
irregular borders
hyper echoic areas
increased vascularity

50
Q

what are the 4 main types of thyroid carcinoma

A

anaplastic
follicular
medullary
papillary

51
Q

what are thyroid hormone levels commonly like in thyroid carcinoma

A

normal TSH and T4 levels

52
Q

The most common type of thyroid cancer

A

papillary thyroid cancer

53
Q

what is the least aggressive thyroid cancer

A

papillary thyroid cancer

54
Q

The greatest risk factor for papillary thyroid cancer is

A

head or neck radiation exposure as a child

55
Q

what is a tumor marker for papillary thyroid cancer and follicular thyroid cancer

A

Thyroglobulin

56
Q

second most common thyroid cancer

A

follicular thyroid cancer

57
Q

what is follicular thyroid cancer associated with

A

iodine deficiency

58
Q

what thyroid cancer is associated with MEN2

A

medullary thyroid cancer

59
Q

what is used to monitor for residual disease after treatment or for recurrence of medullary thyroid cancer

A

calcitonin levels

60
Q

what is the most aggressive type of thyroid cancer

A

anaplastic thyroid cancer

61
Q

The most common cause of primary hypothyroidism in the United States

A

Hashimoto

62
Q

what is the MC cause of primary hypothyroidism in the world

A

iodine deficiency

63
Q

subclinical hypothyroidism

A

A normal T4 level and high TSH level

64
Q

what antibody is positive in majority of people with Hashimoto

A

thyroid peroxidase antibody

65
Q

how often should TSH be tested after starting levothyroxine

A

every 6 weeks

66
Q

what can be used in addition to levothyroxine for hypothyroidism

A

Some patients may have impaired conversion of T4 to T3 and may benefit from liothyronine

67
Q

The most common cause of hyperthyroidism

A

Grave’s disease - an autoimmune disease that affects TSH receptors by stimulating or blocking antibodies to the thyrotropin receptor

68
Q

T3 toxicosis

A

T4 is normal and T3 is elevated –> more favorable prognosis

69
Q

what antibodies may be present in grave’s disease

A

Thyroid-stimulating immunoglobulin antibodies - most sensitive
peroxidase antibodies
antithyroglobulin antibodies

70
Q

what can be used to treat cardiac sx in hyperthyroidism

A

beta blockers

71
Q

contraindication of Radioactive iodine ablation

A

pregnancy

72
Q

Diabetes insipidus (DI) is characterized by

A

excretion of a large volume of dilute urine through the kidneys

73
Q

Central DI

A

decreased secretion of antidiuretic hormone (ADH)

74
Q

nephrogenic DI

A

decreased sensitivity to ADH in the kidneys, leading to decreased urine concentration

75
Q

sx of DI

A

polyuria, polydipsia, and nocturia

76
Q

Water deprivation followed by administration of vasopressin (ADH) to differentiate btwn nephrogenic and central DI

A

central DI: the ADH administered will act on the kidneys to concentrate the urine, leading to an increased urinary osmolality

nephrogenic DI: the urine osmolality will remain unchanged because the kidneys are already insensitive to ADH

77
Q

drug of choice for central DI

A

desmopressin (ADH analog)

78
Q

drugs of choice for nephrogenic DI

A

Nonsteroidal anti-inflammatory drugs, such as indomethacin, and thiazide diuretics

79
Q
A