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STEP2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is an incidentaloma and how is it managed?

A
  • it is an incidentally discovered pituitary mass in an asymptomatic patient
  • for those less than 1cm, get a prolactin level and perform an annual MRI
  • for those more than 1cm, also get a TSH, T4, LH, FSH, 24-hr urine cortisol, IGF, visual fields exam
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2
Q

Describe the presentation, associations, and management of empty sella syndrome.

A
  • it is a disorder in which the pituitary is undersized and typically presents as an incidental finding
  • associated with surgery, obesity, pseudotumor cerebri, and radiation
  • workup necessitates checking thyroid and adrenal function
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3
Q

Describe the presentation and diagnosis of prolactin deficiency.

A
  • presents only in woman with an inability to lactate after childbirth; there are no symptoms in men
  • measure a prolactin level, which will be low, and perform a TRH stimulation test
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4
Q

What hormones control the release of prolactin?

A
  • dopamine inhibits release

- TRH stimulates release

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5
Q

Describe the presentation of LH and FSH deficiency in those with panhypopituitarism.

A
  • all will have decreased libido and decreased body hair
  • men will have erectile dysfunction and decreased muscle mass
  • women will have anovulation and amenorrhea
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6
Q

Describe the pathophysiology, presentation, and treatment of Kallmann syndrome.

A
  • a KAL-1 mutation leads failure of hypothalamic cell migration during development
  • this manifests as a GnRH deficiency and anosmia
  • presents with failure to complete puberty, infertility, anosmia, and renal agenesis
  • treat with testosterone replacement
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7
Q

What is the difference between Kallmann and Klinefelter syndromes?

A
  • both are manifestations of testosterone deficiency
  • Kallmann is a GnRH deficiency with associated anosmia and renal agenesis
  • Klinefelter is an androgen deficiency due to FSH and LH insensitivity
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8
Q

Describe the regulation and action of GH.

A
  • release is stimulated by pulsatile GHRH; levels rise with exercise, deep sleep, and hypoglycemia; they decline with hyperglycemia and somatostatin
  • it functions to stimulate linear growth and muscle mass through IGF-1 secretion and is an anti-insulin promoting insulin resistance and hyperglycemia
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9
Q

Describe the presentation and diagnosis of GH deficiency.

A
  • children will have short stature while adults have more subtle findings of central obesity, elevated LDL, and reduced lean muscle mass
  • a GH level is unhelpful because release is pulsatile, so the best initial test is GHRH stimulation
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10
Q

Why do cortisol and aldosterone levels not correlate with one another?

A

because cortisol production is regulated by ACTH while aldosterone production is regulated by the renin-angiotensin system

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11
Q

What is the stimulation test for prolactin?

A

TRH stimulation test

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12
Q

Describe the presentation, diagnosis, and treatment of diabetes insipidous.

A
  • it presents with high-volume urine and excessive thirst
  • urine electrolytes demonstrate high volume, low osmolality, and low sodium
  • serum electrolytes demonstrate hypovolemia, high osmolality, and high sodium
  • treat central cases with vasopressin; treat nephrogenic cases with HCTZ, amiloride, and NSAIDs
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13
Q

Why does diabetes insipidous result in low urine sodium and high serum sodium?

A

because absence of an ADH response causes excessive water wasting, the body attempts to compensate by re-absorbing sodium, but water cannot follow without ADH

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14
Q

Describe the etiology, presentation, diagnosis, and treatment of acromegaly.

A
  • it is due to a pituitary adenoma with GH overproduction
  • presents with enlargement of soft tissues including coarsening facial features, sweat gland hypertrophy, deepening voice, carpal tunnel, and hyperglycemia
  • the best initial test is IGF-1 because GH itself is pulsatile; the most accurate test is a glucose suppression test; follow with an MRI
  • treat with adenoma resection, cabergoline (DA agonist), octreotide, or pegvisomant (GH receptor antagonist)
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15
Q

Describe the etiology, presentation, diagnosis, and treatment of hyperprolactinemia.

A
  • may be due prolactinomas, medications, renal insufficiency, acromegaly as it is co-secreted with GH, or hypothyroidism since it is under the control of TRH
  • presents with ED, decreased libido, and gynecomastia in males; galactorrhea, amenorrhea, and infertility in females
  • best initial test is B-hCG, also get thyroid function tests, BUN/Cr, LFTs, and an MRI
  • treat with cabergoline in most cases; otherwise, patients require surgery
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16
Q

Describe the treatment of hypothyroidism.

A

treat with levothyroxine once TSH is twice the upper limit of normal or patients have antithyroid peroxidase or antithyroglobulin antibodies

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17
Q

What is Hashimoto’s disease?

A
  • an autoimmune disease characterized by destruction of the thyroid gland and the most common cause of hypothyroidism
  • antithyroid peroxidase and antithyroglobulin antibodies are characteristic but don’t mediate disease
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18
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of euthyroid sick syndrome.

A
  • patients have systemic illness and are clinically euthyroid but have normal TSH, low T3, and low T4
  • this is because T4 is being converted to the inactive rT3 rather than the active T3
  • this is not true hypothyroidism and does not require treatment beyond that for the underlying illness
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19
Q

What is the most likely diagnosis for hyperthyroid patients with the following characteristics:

  • proptosis or myedema
  • tender thyroid
  • normal exam
  • involuted gland which isn’t palpable
  • high TSH
A
  • proptosis or myedema: Grave’s disease
  • tender thyroid: subacute thyroiditis
  • normal exam: silent/painless thyroiditis
  • involuted gland which isn’t palpable: exogenous thyroid
  • high TSH: pituitary adenoma
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20
Q

What is significant about the following thyroid antibodies:

  • anti-thyroglobulin
  • anti-thyroperoxidase
  • thyroid-stimulating immunoglobulin
A
  • anti-thyroglobulin: detects recurrence of thyroid cancer and is also present in those with Hashimoto’s
  • anti-thyroperoxidase: present in Hashimoto’s
  • thyroid-stimulating immunoglobulin: mediates Grave’s disease
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21
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of Grave’s disease.

A
  • it is a hyperthyroidism induced by thyroid-stimulating antibodies
  • it presents with hyperthyroidism, proptosis, and myxedema
  • diagnosis is made based on low TSH, elevated free T4, and a diffuse increase of RAIU; the most accurate test is detecting thyroid-stimulating antibodies
  • treat initially with steroids and then move to radioactive iodine ablation
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22
Q

What do the following suggest on radioactive iodine uptake studies?

  • diffuse increase
  • nodular increase
  • diffuse decrease
  • nodular decrease
A
  • diffuse increase: Grave’s disease
  • nodular increase: benign nodule
  • diffuse decrease: subacute or silent thyroiditis
  • nodular decrease: suggestive of malignancy
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23
Q

Describe the presentation, diagnosis, and treatment of subacute thyroiditis.

A
  • presents as hyperthyroidism with a tender thyroid gland
  • the diagnosis is based on low TSH, elevated free T4, and a diffuse decrease on RAIU scan
  • treat with aspirin
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24
Q

Describe the mechanism of action for drugs used in the treatment of thyroid storm.

A
  • propanolol blocks the end-organ effects and the conversion of T4 to T3
  • PTU blocks hormone production and the conversion of T4 to T3
  • methimazole blocks hormone production
  • Iodinated contrast material blocks the release of existing hormone
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25
Q

Describe the appropriate workup for a thyroid nodule.

A
  1. begin with TSH and free T4
  2. if tests are normal, perform FNA of the node
  3. if TSH is low perform an RAIU
  4. cold nodes should undergo FNA and hot nodes should be treated
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26
Q

What is the best next step if FNA of a thyroid nodule reveals follicular adenoma?

A

must perform an excision biopsy to rule out follicular carcinoma

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27
Q

What is unique about each of the following thyroid carcinomas:

  • papillary
  • medullary
  • follicular
  • anaplastic
A
  • papillary: most common, childhood radiation exposure is a risk factor, tends to spread to cervical lymph nodes
  • medullary: produces calcitonin and potentially hypocalcemia, is associated with MEN2
  • follicular: must perform excision biopsy to differentiate from follicular adenoma
  • anaplastic: tends to be locally invasive
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28
Q

Describe the most common etiologies, presentation, and treatment of hypercalcemia.

A
  • it is most often due to primary hyperparathyroidism or malignant production of PTHrP
  • other etiologies include vitamin D toxicity, granulomatous diseases, bony metastases or multiple myeloma, and thiazide diuretic use
  • presents with “stones, groans, moans, thrones, and psychiatric overtones” as well as shortened QT
  • treat initially with aggressive saline hydration; calcitonin is a great acute treatment as a bridge to bisphosphonates
  • use steroids if granulomatous diseases are responsible
29
Q

Describe the presentation, diagnosis, and treatment of hyperparathyroidism.

A
  • most often discovered as an incidental hypercalcemia
  • may present with “stones, groans, moans, thrones, psych overtones” and a shortened QT
  • labs show elevated calcium and PTH, low phosphate, elevated BUN/Cr, and elevated alkaline phosphatase
  • a DEXA scan is the best tool for identifying bone effects
  • treat with parathyroidectomy as first line; use cinacalcet as second-line (blocks PTH release)
30
Q

Describe the presentation of hypo- and hypercalcemia.

A
  • hypocalcemia presents with hyperexcitability: seizures, perioral numbness, Chvostek sign, and Trousseau sign
  • hypercalcemia presents with slowing: lethargy, constipation, bone pain, nephrolithiasis, short QT
31
Q

Describe the etiology, presentation, diagnosis, and treatment of hypocalcemia.

A
  • usually due to primary hypoparathyroidism after neck surgery; may also be due to renal failure or vitamin D deficiency
  • presents with neural hyper excitability including perioral numbness, Chvostek sign, Trousseau sign, and seizures
  • ECG shows a prolonged QT
  • treat with calcium and activated vitamin D replacement
32
Q

Describe the presentation, diagnosis, treatment, and complications of Paget disease of the bone.

A
  • most often presents with bone pain and an isolated alkaline phosphatase elevation
  • the most accurate test is a nuclear bone scan finding patchy areas of osteoblastic activity
  • asymptomatic patients don’t require therapy; use bisphosphonates followed by calcitonin for bone pain
  • complications include osteosarcoma and high-output CHF
33
Q

What are:

  • Cushing syndrome
  • Cushing disease
  • Addison disease
A
  • Cushing syndrome is hypercortisolism
  • Cushing disease is hypercortisolism secondary to a pituitary adenoma secreting ACTH
  • Addison disease is adrenal insufficiency
34
Q

What are the symptoms of hypercortisolism?

A
  • fat redistribution
  • osteoporosis
  • skin changes including thinning, poor wound healing, easy bruising, and striae
  • hypertension
  • cognitive disturbance
  • hyperglycemia and hyperlipidemia
  • hypokalemic metabolic alkalosis
  • leukocytosis
35
Q

What is the best initial test for the diagnosis of hypercortisolism?

A
  • best test is a 24-hour urine cortisol

- if this isn’t a choice then it is a low dose dexamethasone suppression test

36
Q

Describe the appropriate workup for hypercortisolism.

A
  1. begin with a 24-hour urine cortisol level
  2. follow this with a serum ACTH level
  3. if ACTH is low, this suggests an adrenal source and an adrenal CT should be completed
  4. if ACTH is high, get a high-dose dexamethasone suppression test
  5. failure of suppression suggests an ectopic ACTH source and a chest CT should be performed
  6. if cortisol is suppressed, look for a pituitary adenoma with MRI
  7. if no mass is found on MRI, perform a petrosal sinus sampling for ACTH
37
Q

What are low and high dose dexamethasone suppression tests used for?

A
  • low dose is an acceptable method for diagnosing hypercortisolism because it has high sensitivity
  • high dose is used to differentiate between a pituitary adenoma and an ectopic production of ACTH
38
Q

What is the function of the following tests in diagnosing hypercortisolism:

  • 24 hour urine cortisol
  • serum ACTH level
  • low dose dexamethasone suppression test
  • high dose dexamethasone suppression test
  • petrosal venous sampling
A
  • 24 hour urine cortisol: preferred for diagnosis of hypercortisolism
  • serum ACTH level: distinguishes primary from secondary hypercortisolism
  • low dose dexamethasone suppression test: back up test for diagnosis of hypercortisolism
  • high dose dexamethasone suppression test: distinguishes pituitary adenoma from ectopic ACTH production
  • petrosal venous sampling: used to diagnose a pituitary adenoma if no mass is seen on MRI
39
Q

What is the most important test to perform if one discovers an adrenal incidentaloma? Why?

A

metanephrines of blood or urine to exclude pheochromocytoma because without proper premeditation with phenoxybenzamine, surgery is extremely dangerous

40
Q

How is hypercortisolism treated?

A
  • surgical removal of the source is preferred
  • use pasireotide, a somatostatin analog, if resection of a pituitary adenoma fails
  • use mifepristone, a cortisol antagonists, if surgery isn’t an option
  • use mitotane, an inhibitor of steroidogenesis that is cytotoxic to adrenal tissue, for incomplete resection of an adrenal cancer or adrenal cancer metastases
41
Q

Describe the presentation of Addison disease and of acute adrenal crisis.

A

both present with:
- weakness, fatigue, altered mental status
- hypotension, hyponatremia, hyperkalemia
- nausea, vomiting, and anorexia
- eosinophiliaW
hyperpigmentation, though is more associated with Addison’s disease

42
Q

What is the most common cause of Addison disease?

A

it is typically due to autoimmune destruction of the gland

43
Q

What is the role of a cosyntropin stimulation test?

A

this is a synthetic ACTH given to diagnose hypocortisolism

44
Q

What are the two most important steps to take in the treatment of adrenal crisis?

A
  • give hydrocortisone, which has some aldosterone effect as well as a permissive effect for catecholamines on vascular tone
  • give fludrocortisone for patients with continued evidence of postural instability
45
Q

Describe the etiology, presentation, diagnosis, and treatment of primary hyperaldosteronism.

A
  • most cases are caused by a solitary adenoma or bilateral hyperplasia
  • the hallmark of presentation is refractory hypertension and hypokalemia
  • the best initial test is an aldosterone-to-renin ratio and the most accurate test for a unilateral adenoma is venous blood sampling
  • a CT should be done only after an aldosterone:renin > 20, aldosterone level greater than 15, hypokalemia, and low plasma renin levels have been confirmed
  • treat with resection of adenomas and eplerenone or spironolactone for bilateral hyperplasia
46
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of pheochromocytomas.

A
  • these are adrenal medullary tumors that autonomously overproduce catecholamines
  • presents with episodic hypertension, headache, diaphoresis, palpitations, tremor, and tachycardia
  • the best initial test is free plasma metanephrines which can then be confirmed with a 24-hour urine metanephrine
  • after this, perform an adrenal CT; if unrevealing, a MIBG scan will identify extra-adrenal pheochromocytomas
  • treat with phenoxybenzamine followed by beta blockers and surgical resection
47
Q

Describe the presentation, diagnosis, and treatment of insulinomas.

A
  • present with hypoglycemia and an inappropriately high insulin level
  • the best initial test is blood glucose and C-peptide; most accurate is 72-hr fasting with high C-peptide and absent ketosis
  • get a CT and then resect the mass
48
Q

Describe the presentation and treatment of glucagonomas.

A
  • present with easily managed hyperglycemia, weight loss, and necrolytic migratory erythema
  • treat with octreotide and surgical resection as most are malignant
49
Q

Describe the presentation, diagnosis, and treatment of VIPomas.

A
  • presents with a high-volume, secretory diarrhea, hypokalemia, and achlorhydia
  • diagnosis is based of VIP level and CT findings
  • treat with somatostatin and surgical resection
50
Q

Describe the genetics and features of MEN1.

A
  • due to an autosomal dominant mutation of the tumor suppressor gene MEN1
  • associated with parathyroid adenomas, pituitary tumors, and pancreatic islet cell tumors (3 P’s)
51
Q

Desc

A
  • due to an autosomal dominant mutation of the RET oncogene
  • MEN2A is associated with medullary thyroid carcinoma, pheochromocytoma, and parathyroid hyperplasia
  • MEN2B is associated with medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas, and Marfanoid habitus
52
Q

Describe the findings associated with sulfonylurea abuse.

A

hypoglycemia with elevated C-peptide, proinsulin, and urine metabolites of sulfonylurea

53
Q

How is the diagnosis of diabetes made?

A
  • HbA1c > 6.5
  • fasting glucose greater than 126
  • 2-hour glucose tolerance test greater than 200
  • random glucose greater than 200 with symptoms
54
Q

What are the contraindications to metformin use?

A

don’t initiate therapy if GFR is less than 45, don’t continue therapy if GFR is less than 30

55
Q

How does metformin work?

A

by blocking gluconeogenesis

56
Q

How do incretins work to manage diabetes?

A

they increase insulin release, decrease glucagon release, and slow gastric motility

57
Q

Thiazolidinediones are contraindicated in what population?

A

those with heart failure

58
Q

What are nateglinide and repaglinide?

A

these are diabetic medications that stimulate the release of insulin similar to sulfonylureas but do not contain sulfa

59
Q

What is pramlintide?

A

a diabetic medication that functions as an amylin analog to slow gastric emptying, decrease glucagon levels, and decrease appetite

60
Q

Order the following types of insulin by duration of action:

  • aspart
  • degludec
  • detemir
  • glargine
  • glulisine
  • lispro
  • NPH
  • regular
A
  • lispro, aspart, and glulisine are short acting
  • regular
  • NPH
  • detemir and glargine
  • degludec
61
Q

Describe the presentation and treatment of DKA.

A
  • presents with altered mental status, Kussmau respirations, polydipsia, polyuria, and non-specific abdominal pain
  • labs demonstrate ketones, hyperglycemia, metabolic acidosis with anion gap, and hyperkalemia
  • start treatment with IV fluids: use half normal or normal saline depending on corrected sodium and switch to 5% dextrose when glucose is less than 200
  • give insulin and replace potassium once below 5.3
62
Q

What is the most accurate measure of prognosis in those with DKA?

A

serum bicarb or anion gap

63
Q

All diabetics require what health maintenance initiatives?

A
  • pneumococcal vaccine
  • yearly eye and foot exam
  • statin for LDL > 100
  • ACEi/ARB for BP > 140/90 or microalbuminuria
64
Q

Describe the pathophysiology, presentation, and treatment of diabetic gastroparesis.

A
  • neuropathy decreases the ability of the gut to sense stretch which is the main stimulant for gastric motility
  • presents with bloating, constipation, early satiety, vomiting, and abdominal discomfort
  • treat with metoclopramide or erythromycin
65
Q

Describe the pathogenesis of diabetic neuropathy.

A

damage to microvasculature damages the vasa nervorum surrounding large peripheral nerves, which cause dysfunction

66
Q

What is the difference between hirsutism and virilization?

A
  • hirsutism is a male pattern of hair growth
  • virilization includes hirsutism, clitoromegaly, deepening of the voice, irregular menstruation, acne, and increased muscle mass
67
Q

List the lab tests used to evaluate virilization.

A

get a DHEA, testosterone, FSH, LH, 17-hydroxyprogesterone, and prolactin level

68
Q

How is hirsutism treated?

A
  • use oral contraceptives and antiandrogens like spironolactone or finasteride in all patients
  • add metformin for those with PCOS

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