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Internal Medicine Board Review > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is meant by positive and negative feedback regulation in endocrine diseases?

A

Positive feedback refers to the stimulation of hormone secretion by the feedback mechanism, and in negative feedback hormone secretion is inhibited by the feedback.

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2
Q

What are the definitions of primary, secondary, and tertiary hormone diseases?

A

Primary glandular failure refers to disease of the gland that secretes the hormone. Secondary glandular disease is disease of the gland that controls the primary gland. Tertiary glandular disease is disease of the gland that controls the secondary gland that controls the primary gland.

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3
Q

What are the hormones of the anterior pituitary?

A

The hormones of the anterior pituitary gland include FSH, LH, TSH, ACTH, GH, and prolactin.

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4
Q

What are typical signs and symptoms of a pituitary tumor?

A

Historically, pituitary tumors presented with hormonal hypersecretion symptoms, hypopituitarism, and mass effect. Now, with the use of imaging, these are frequently found incidentally in imaging done for other reasons.

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5
Q

Aside from prolactinoma, what are the other causes of hyperprolactinemia?

A

Non-prolactinoma causes of hyperprolactinemia include drugs (antipsychotics, metoclopramide, and verapamil), Diseases of the hypothalamus or pituitary stalk which interfere with production or transport of dopamine (sarcoidosis, trauma), pregnancy, nipple stimulation, orgasm, chest wall injuries (piercing, shingles), hypothyroidism, and chronic kidney disease.

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6
Q

What is the best initial medical therapy for hyperprolactinemia?

A

Cabergoline is the 1st line treatment for hyperprolactinemia. This is contraindicated in known lung, heart valve, and retroperitoneal fibrotic disease. Bromocriptine is the 2nd line treatment for hyperprolactinemia, but it causes more nausea and orthostatic hypotension than cabergoline.

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7
Q

How do you test for acromegaly?

A

Screen for acromegaly with IGF-1. Growth hormone measurement is not recommended because its secretion is pulsatile and levels can fluctuate greatly.

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8
Q

What is the workup for pituitary incidentaloma?

A

The size of an incidentally found pituitary tumor depends on size. If it is <1cm evaluate for hormone hypersecretion. If >1cm evaluate for hormone hyper- and hyposecretion as well as evaluation of visual fields. To test for hypersecretion check prolactin, IGF-1, 24-hour urinary free cortisol or low-dose dexamethasone suppression test, and check TSH and free T4. Test for hyposecretion with TSH, free T4, morning cortisol, LH, FSH, and estradiol.

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9
Q

Which cancers metastasize to the pituitary?

A

Lung and breast cancers are the most common cancers to metastasize to the pituitary.

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10
Q

What is the clinical presentation of pituitary apoplexy? The treatment?

A

Pituitary apoplexy is caused by hemorrhage in a pituitary mass. It presents with severe headache, N/V, visual defects, and altered mental status. If symptoms are mild only corticosteroids may be necessary. Edema causing mass effect requires emergent neurosurgical decompression.

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11
Q

What happens to the urine osmolality and serum sodium in a patient with diabetes insipidus who is on a water restriction?

A

A DI patient on water restriction will have an elevated serum sodium and will continue to put out a dilute urine.

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12
Q

What are the urine osmolality, serum sodium, and serum osmolality in a patient with SIADH?

A

A patient with SIADH will have a concentrated urine, high urine sodium excretion, low serum sodium, and low serum osmolality.

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13
Q

What is the first screening test of choice for hyper- and hypothyroidism?

A

The first screening test for hypo- and hyperthyroidism is a TSH.

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14
Q

What is the difference between the thyroid uptake and the thyroid scan? What do the different tests tell you?

A

The thyroid uptake measures the degree of iodine uptake in percent uptake whereas the thyroid scan (scintigraphy) assesses the pattern of uptake.

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15
Q

What are the common signs and symptoms of hypothyroidism? Lab tests?

A

The common symptoms of hypothyroidism are cold intolerance, weight gain, fatigue, menstrual irregularities, mental slowness, depressed mood, constipation, hoarseness, edema, brittle nails. Common signs are goiter, cool/pale skin, coarse hair, periorbital or nonpitting edema, delayed reflexes, and bradycardia.

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16
Q

How do you make a diagnosis of secondary or tertiary hypothyroidism?

A

Secondary and tertiary hypothyroidism are diagnosed by a low TSH and low free T4, once euthyroid sick syndrome is excluded.

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17
Q

What are the risks of overtreating hypothyroidism?

A

The risks of overtreating hypothyroidism include bone loss, tachyarrhythmias (atrial fibrillation).

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18
Q

What are the signs and symptoms of myxedema coma?

A

Patients with myxedema coma present with progressive symptoms of hypothyroidism. Decreased mentation and hypothermia are the classic findings.

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19
Q

What is the treatment of myxedema coma?

A

Myxedema coma is treated with thyroid hormone (most experts recommend combined T4 and T3). Glucocorticoids should be given as well until adrenal insufficiency is ruled out.

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20
Q

What is apathetic hyperthyroidism?

A

Elderly patients may present with atrial fibrillation or depression without classic symptoms of hyperthyroidism. This is termed apathetic hyperthyroidism.

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21
Q

What specific physical findings confirm the diagnosis of Graves disease?

A

Physical findings consistent with Graves disease include diffuse goiter (sometimes with a bruit) and Graves ophthalmopathy (proptosis and periorbital edema).

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22
Q

What is the result of the thyroid uptake and scan in a patient with Graves disease?

A

The thyroid uptake and scan in Graves shows increased uptake in a diffuse pattern.

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23
Q

What are the side effects of medications used to treat Graves disease?

A

Graves disease is treated with methimazole and PTU. Methimazole cannot be given in the 1st trimester of pregnancy. PTU is associated with liver injury, vasculitis, and lupus-like syndrome. Both PTU and methimazole can cause hepatic toxicity and agranulocytosis.

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24
Q

What are the precipitating events leading to thyroid storm?

A

Precipitating events for thyroid storm include surgery, infections, or an iodine load (amiodarone or contrast).

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25
Q

In addition to PTU or MMI, beta-blockers, and iodine, which other drug is given to patients to treat thyroid storm?

A

Thyroid storm is generally associated with a relative adrenal insufficiency. Therefore, glucocorticoids should be added to treatment with PTU or MMI, beta-blockers, and iodine.

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26
Q

What causes subacute thyroiditis?

A

Subacute thyroiditis is presumed to be caused by viral infection causing granulomas in the thyroid gland.

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27
Q

What are the results of the thyroid uptake in patients with thyroiditis (all causes)?

A

Thyroid uptake is reduced in patients with thyroiditis of all causes.

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28
Q

In which situations is it appropriate to check a sick patient’s thyroid function?

A

Do not check thyroid studies in sick patients unless their illness is likely to be caused by myxedema coma or thyroid storm.

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29
Q

Workup of which nodule can cease after the thyroid uptake and scan - a hot or cold one?

A

A hot nodule on thyroid uptake and scan does not require further workup.

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30
Q

List some characteristics associated with malignant nodules.

A

Malignant nodules are usually cold on thyroid scan. However, most benign nodules are also cold.

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31
Q

If the TSH is high and an ultrasound of a solitary nodule is not concerning for malignancy, what is the most common diagnosis?

A

Hypothyroidism is the most common cause of a benign appearing nodule (on ultrasound) with a high TSH.

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32
Q

What are the 4 histologic types of thyroid cancer? Which is the most aggressive?

A

The four types of thyroid cancer are papillary, follicular, medullary, and anaplastic. The most aggressive is anaplastic thyroid cancer.

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33
Q

What is the hormone released by medullary thyroid cancer?

A

Medullary thyroid cancer is associated with an elevated calcitonin secreted by parafollicular C cells.

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34
Q

MEN2A and MEN2B are associated with which histologic type of thyroid cancer?

A

MEN2A and MEN2B are both associated with medullary thyroid cancer.

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35
Q

What is the gene associated with medullary thyroid cancer?

A

Medullary thyroid cancer is associated with point mutations in the RET oncogene.

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36
Q

Thyroid lymphoma is associated with which autoimmune disease?

A

Thyroid lymphoma is associated with chronic autoimmune thyroiditis.

37
Q

Name 3 different hormones that are produced in the adrenal cortex

A

The three hormones produced in the adrenal cortex are cortisol (zona fasciculata), aldosterone (zona glomerulosa), and DHEAS (zona reticularis).

38
Q

What is produced in the adrenal medulla?

A

The adrenal medulla produces epinephrine in the chromaffin cells.

39
Q

What do mineralocorticoid hormones do?

A

Mineralocorticoids cause sodium absorption and K/H excretion. High levels cause hypertension, hyperkalemia, and metabolic alkalosis.

40
Q

What are the effects of excess cortisol?

A

Excess cortisol causes lipolysis, gluconeogenesis, weakening of bones, and inhibition of inflammatory responses.

41
Q

What happens to a woman who overproduces adrenal androgens because of a disease process? How does she present?

A

Excess androgens in a woman cause hirsutism and virilization, and abnormal menses. If androgren excess occurs in gestation it results in ambiguous genitalia.

42
Q

Which genes control steroid synthesis in the adrenal cortex? Which cortical hormones are increased and decreased when there is a defect in 21-hydroxylase? 17-alpha-hydroxylase? 11-beta-hydroxylase?

A

The genes involved in adrenal cortical steroid synthesis include CYP17, CYP21A2, and CYP11B1. 21-hydroxylase defects lead to an increase in androgen production. 17-alpha-hydroxylase defects lead to increased aldosterone. 11-hydroxylase defects lead to excess adrenal androgens.

43
Q

Which gene defect is most commonly associated with congenital adrenal hyperplasia?

A

95% of congenital adrenal hyperplasia is due to mutations in CYP21A2.

44
Q

What is the difference between Cushing syndrome and Cushing disease?

A

Cushing syndrome refers to the condition of excess adrenal cortisol. Cushing disease is when Cushing syndrome is caused by an ACTH producing pituitary adenoma.

45
Q

What is the ACTH level in Cushing disease?

A

The ACTH level is elevated in Cushing disease.

46
Q

What are your choices for initial tests to evaluate a patient who may have Cushing syndrome?

A

The initial tests to screen for Cushing syndrome are low-dose dexamethasone suppression test, 24 hour urinary free cortisol, and late night salivary cortisol.

47
Q

What is pseudo-Cushing’s? In which situations does it occur?

A

Pseudo-Cushing’s is seen in patients who are depressed, obese, alcoholic, or sick. Patients with pseudo-Cushings will suppress with low-dose dexamethasone suppression test.

48
Q

Explain which tests are done to differentiate ACTH-Dependent Cushing syndrome vs. ACTH-independent Cushing syndrome?

A

If the ACTH is normal or high in Cushing syndrome the condition is considered ACTH-dependent. To differentiate Cushing disease from ectopic ACTH source you can use CRH stimulation test, high-dose dexamethasone suppression test, inferior petrosal sinus sampling, and HRCT of the chest and abdomen.

49
Q

How does adrenal insufficiency (both primary and secondary) present?

A

Patients with primary adrenal insufficiency presents with hypotension and hyperpigmentation. THey also commonly have mineralocorticoid deficiency as well, leading to hyponatremia and hyperkalemia. Secondary adrenal insufficiency presents without hyperpigmentation.

50
Q

Abnormal K levels occur in which type of adrenal insufficiency? Why?

A

Abnormal potassium levels are seen in primary adrenal insufficiency as there is also mineralocorticoid deficiency as well. This is not seen in secondary adrenal insufficiency.

51
Q

How do aldosterone levels affect serum Na and K?

A

Aldosterone leads to sodium absorption and potassium excretion.

52
Q

Which diseases should you be concerned about in a patient with untreated hypertension and a low K?

A

In an untreated hypertensive patient with low potassium you should consider primary hyperaldosteronism, secondary hyperaldosteronism, licorice ingestion, and Cushing syndrome.

53
Q

What are the screening tests to differentiate primary and secondary hyperaldosteronism? How do you interpret them?

A

The screening tests for primary and secondary hyperaldosteronism are the plasma aldosterone concentration and plasma renin activity which are used to calculate the PAC:PRA ratio. A PAC:PRA ratio >20 with aldosterone level >10 is consistent with primary hyperaldosteronism.

54
Q

Hypoaldosteronism is usually due to which acquired problem?

A

The most common cause of hypoaldosteronism is low renin level in a diabetic patient with mild renal disease.

55
Q

Which screenings are employed to test for pheochromocytoma?

A

If the pre-test probability is low use 24-hour urinary fractionated metanephrines and catecholamines. WIth high pre-test probability use plasma fractionated metanephrines.

56
Q

What are the first steps in working up adrenal incidentaloma?

A

The first steps in workup of adrenal incidentaloma are determining if it is making hormones and is it cancerous. Lab tests that should be done in all patients with incidentaloma are low-dose dexamethasone suppression test, plasma or urinary fractionated metanephrines, and checking of BP and potassium with evaluation for hyperaldosteronism if abnormal.

57
Q

What is the definition of primary amenorrhea, and what are the causes?

A

Primary amenorrhea is the absence of menses before 16yo or lack of secondary sex characteristics by age 14. Causes include Turner syndrome, genetic absence of a uterus, and androgen insensitivity syndrome.

58
Q

A female patient with short stature, primary amenorrhea, and little or no breast development probably has which genetic defect?

A

A female patient with primary amenorrhea and little or no breast development is likely to have Turner syndrome.

59
Q

What is the definition of secondary amenorrhea, and what are the common causes?

A

Secondary amenorrhea is defined as the absence of menses for 3-6 months in a women who was previously menstruating. Causes include pregnancy, ovarian failure, hypogonadotrophic hypogonadism, and functional hypothalamic amenorrhea (eating disorders and athletes).

60
Q

What are the initial labs for the workup of secondary amenorrhea, once pregnancy is excluded?

A

Once pregnancy is excluded the lab testing for secondary amenorrhea should include FSH, LH, prolactin, and TSH. If the woman exhibits hirsutism you should laos check testosterone, DHEAS, and 17-OH progesterone.

61
Q

What do FSH and LH levels in an amenorrheic woman tell you?

A

High FSH and LH in an amenorrheic woman are consistent with ovarian failure. Decreased FSH and LH are consistent with hypogonadotrophic hypogonadism.

62
Q

Which testing is done for a woman with secondary amenorrhea who has low FSH and LH levels?

A

Estradiol and GnRH may be checked in the woman with secondary amenorrhea with low FSH and LH.

63
Q

How does a woman with PCOS present?

A

A woman with PCOS presents with amenorrhea or oligomenorrhea and hirsutism. It is associated with obesity, insulin resistance, diabetes, and OSA.

64
Q

Patients with PCOS should be evaluated for which additional diagnosis?

A

Women with PCOS should be screening for insulin resistance.

65
Q

What is the most common cause of primary hypogonadism in males?

A

Primary hypogonadism in males is usually due to Klinefelter syndrome causing defective testosterone production.

66
Q

Differentiate Kallmann syndrome from Klinefelter’s.

A

In Kallmann syndrome the FSH, LH and GnRH are all low. In Klinefelter syndrome the FSH and LH are elevated.

67
Q

In which situations do you see gynecomastia as a normal finding? As part of a disease state?

A

Gynecomastia is normal in boys at puberty. Gynecomastia is also seen in advanced age, obesity, cirrhosis, hyperthyroidism, Klinefelter syndrome, germ cell tumors, and hyperprolactinemia.

68
Q

What are the categories of diabetes mellitus?

A

The categories of diabetes mellitus are prediabetes, type 1 diabetes, type 2 diabetes, gestational diabetes. Specific types due to other causes are MODY and LADA (latent autoimmune diabetes in adults).

69
Q

Define prediabetes and clinical diabetes.

A

Prediabetes is a fasting glucose 100-125 and hemoglobin A1C <6.5%. Clinical diabetes is diagnosed by 4 criteria: FPG >126, random glucose >200 with symptoms, A1C >6.5%, and glucose >200 after 75-gram glucose load.

70
Q

Define MODY and LADA.

A

MODY is a group of monogenetic autosomal dominant defects that cause ineffective production and or release of insulin by the beta cells of the pancreas. LADA has a late onset of immune-mediated course often in non-obese patients. They generally do not require insulin at time of diagnosis but require it later in the course of disease.

71
Q

What are the criteria for the diagnosis of prediabetes?

A

Prediabetes is a fasting glucose 100-125.

72
Q

Which diseases can lead to a false value of HgbA1C?

A

False results of A1C can be seen in hemolytic anemias, thalassemias, hemoglobinopathies, and those with hepatic or renal diseases.

73
Q

When are finger stick glucoses useful? When should they not be used?

A

Finger-stick glucose readings should not be used for diagnosis but are used for monitoring diabetes control.

74
Q

What is the significance of diagnosing prediabetes?

A

Prediabetics have a 6-fold increased risk of developing diabetes: ⅓ develop diabetes, ⅓ stay prediabetic, and ⅓ normalize. Patients with prediabetes are at risk of microvascular complications.

75
Q

Which autoimmune diseases are also associated with type 1 diabetes?

A

Type 1 diabetes is associated with other autoimmune diseases including hypothyroidism and adrenal insufficiency.

76
Q

What is the primary treatment for type 1 diabetes?

A

Type 1 diabetics require insulin therapy.

77
Q

Explain the honeymoon effect.

A

After initial insulin therapy in a newly diagnosed type 1 diabetic there may be a period of reduced insulin requirements. This is termed the honeymoon effect.

78
Q

What is the difference between dawn phenomenon and Somogyi effect?

A

The dawn phenomenon is a rise in glucose between 4-7am due to increased levels of cortisol. The Somogyi effect is morning hyperglycemia in response to compensatory mechanisms triggered by hypoglycemia during the night. If using NPH you should try giving NPH dose later (at bedtime) to allow peak to occur around awakening.

79
Q

What are the most common causes of morning hyperglycemia in DM?

A

Causes of morning hyperglycemia in type 1 diabetes include inadequate long-acting insulin, dawn phenomenon, and Somogyi effect.

80
Q

Which mechanisms lead to the development of type 2 diabetes?

A

Four mechanisms lead to the development of type 2 diabetes. These include: 1. insulin resistance in muscle and fat tissues, 2. gradual reduction of insulin secretion by the pancreas, 3. unregulated hepatic gluconeogenesis and glucagon secretion, 4. reduction in gastrointestinal incretins (glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide).

81
Q

Which conditions are associated with acanthosis nigricans?

A

Acanthosis nigricans is seen in insulin resistance. It is also seen in PCOS, Cushing’s, with certain medications (ie. niacin and corticosteroids), and acromegaly.

82
Q

What is the first treatment for type 2 diabetes?

A

The 1st treatment for type 2 diabetes is therapeutic lifestyle change including diet, exercise, and weight loss.

83
Q

What are the mechanisms of action of the main classes of oral hypoglycemics?

A

The main classes of oral hypoglycemics are the secretagogues (sulfonylureas and meglitinides), insulin sensitizers (metformin and thiazolidinediones), and the alpha-glucosidase inhibitors.

84
Q

What are the metformin side effects and contraindications? Thiazolidinediones?

A

The major side effects of metformin are diarrhea and abdominal pain. It is contraindicated with renal dysfunction and is often held for procedures which might affect renal function and lead to lactic acidosis.

85
Q

In which type 2 diabetes situations should patients be prescribed insulin early in treatment?

A

Insulin should be used early in type 2 diabetes if the patient has consistently high random glucose readings (>300), A1C>10%, A1C > 9% with symptoms, signs of ketosis on physical exam, and severe symptoms of hyperglycemia or history of DKA.

86
Q

What are the initial drugs used to treat newly diagnosed type 2 diabetes?

A

Unless contraindicated, metformin should be used in newly diagnosed diabetes along with therapeutic lifestyle change. Treatment options for those with A1C < 7.5% include metformin, GLP-1 agonist, DPP4 inhibitor, TZD, alpha-glucosidase inhibitor, SGLT-2 inhibitor, or insulin secretagogue. If A1C > 7.5% you should start two drugs including the above and possibly basal insulin.

87
Q

What are the treatment goals for glucose and HgbA1C?

A

There are two sets of goals for diabetes control. According to AACE they recommend fasting glucose < 110, 2-hour postprandial glucose < 140, and A1C < 6.5%. The ADA proposes fasting glucose 90-130, 2-hour postprandial glucose < 180, and A1C < 7.0%.

88
Q

Describe the relationship between HgbA1C and pre- and postprandial blood glucose.

A

With an elevated A1C, preprandial hyperglycemia likely contributes more to the high average blood glucose. If A1C < 7.5-8%, postprandial glucose contributes more to high average blood glucose.

Internal Medicine Board Review (13 decks)

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