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OPT 537 > Exam 2 -- Endocrine -- Everything but DM > Flashcards

Exam 2 -- Endocrine -- Everything but DM Flashcards

1
Q

What percentage of pituitary tumors secrete prolactin?

A

60%

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2
Q

What are some physiologic causes of hyperprolactinemia?

A

Pregnancy and stress (stress doesn’t cause very much prolactin increase)

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3
Q

What are some pathologic causes of hyperprolactinemia?

A

Prolactinoma, damage to hypothalamus or pituitary stalk (loss of dopamine inhibition of prolactin release), hypothyroidism (low TH increases TRH from hypothalamus, which increases TSH and prolactin from pituitary), dopamine antagonists (antipsychotics, verapamil, cimetidine)

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4
Q

What percentage of clinically recognized pituitary tumors are prolactinomas?

A

30-40%

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5
Q

True or false: prolactinomas are more common in women than in men

A

True.

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6
Q

What are the clinical features of hyperprolactinemia?

A

Oligomenorrhea or amenorrhea, galactorrhea (in men and women), and loss of libido. VF defects and HA can occur if the hyperprolactinemia is caused by a prolactinoma.

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7
Q

What is the treatment of choice for prolactinoma?

A

Dopamine agonists (cabergoline and bromocriptine) work rather well to decrease prolactin secretion and can actually shrink the size of the tumor.

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8
Q

Patients on dopamine agonists for treatment of prolactinoma have what procedure done every two years?

A

Cardiac ultrasound due to possibility of valvular disease.

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9
Q

Of the dopamine agonists used to treat prolactinoma, which is more efficacious? Which might be better for a woman who wishes to get pregnant?

A

Cabergoline is more efficacious and bromocriptine might be better for the woman who wishes to get pregnant.

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10
Q

After how long of dopamine agonist use can reduction of dosage begin? How long until complete drug cessation is possible?

A

1 year for reduction and 2 years for cessation

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11
Q

When might transsphenoidal adenectomy and/or raditherapy be considered in treatment of a prolactinoma?

A

If medical therapy fails, or if the tumor is larger than 3cm and the woman wishes to get pregnant

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12
Q

Excessive growth hormone causes growth of what types of tissue?

A

Soft tissue, increased bone density

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13
Q

What are the clinical features of acromegaly?

A

Headache, enlargement of jaw and separation of teeth, hand and feet enlargement, osteoarthritis, entrapment neuropathies, abnormal glucose tolerance, and heart failure

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14
Q

What percentage of deaths of patients with acromegaly are due to heart failure?

A

60%

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15
Q

What percentage of patients with acromegaly are cured through transsphenoidal adenectomy?

A

60-90% (if the tumor is small))

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16
Q

True or false: medical therapy for acromegaly is as effective as transsphenoidal adenectomy

A

False.

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17
Q

What types of medications can be used for management of acromegaly?

A

Somatostatin analogues (inhibitors of growth hormone) octreotide and lanreotide, GH receptor antagonist pegvisomant, dopamine agonist cabergoline.

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18
Q

Use of dopamine agonists to treat acromegaly is most effective in what type of tumors?

A

Tumors that secrete GH and prolactin

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19
Q

True or false: if surgery or medical therapy fail in treatment of acromegaly, radiotherapy may be used

A

True.

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20
Q

How long can radiotherapy take to normalize GH levels in the treatment of acromegaly?

A

3-10 years

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21
Q

Which hormones are secreted by the adrenal cortex?

A

Glucocorticoids (cortisol), mineralocorticoids (aldosterone), adrenocortico androgens (testosterone)

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22
Q

What is the most common cause of Cushing’s syndrome?

A

Administration of exogenous steroids (iatrogenic)

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23
Q

What would be the levels of ACTH and cortisol in a patient with Cushing’s syndrome due to exogenous steroids?

A

Low ACTH and low cortisol (the exogenous steroids resemble cortisol enough that the hypothalamus tells pituitary to stop releasing ACTH)

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24
Q

What is the most common cause of endogenous Cushing’s syndrome?

A

Cushing’s disease (usually small ACTH-secreting pituitary adenoma, though could be a hypothalamic adenoma) accounts for more than half of endogenous Cushing’s syndrome

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25
Q

True or false: males are more affected by Cushing’s disease than females, and the incidence is normally in the third to fourth decade

A

True and false: females (not males) are the more affected gender, but the peak incidence is indeed in the third to fourth decades

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26
Q

What would be the levels of ACTH and cortisol in a patient with Cushing’s disease?

A

High ACTH and high cortisol (the pituitary releases ACTH, which stimulates adrenal cortex to release cortisol)

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27
Q

Which endogenous cause of Cushing’s syndrome is considered ACTH-independent, and why?

A

Primary adrenocortical hyperplasia or neoplasm (neoplasm more commonly). The hyperplasia or neoplasm would release excess cortisol regardless of ACTH presence.

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28
Q

What percentage of endogenous Cushing’s syndrome is caused by adrenocortical hyperplasia or neoplasm?

A

15-30%

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29
Q

What would be the levels of ACTH and cortisol in a patient with Cushing’s syndrome due to adrenocortical hyperplasia or neoplasm?

A

Low ACTH and high cortisol (hyperplasia or neoplasm releases excess cortisol, which signals to hypothalamus to tell pituitary to decrease ACTH release)

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30
Q

Ectopic ACTH secretion can be a cause of endogenous Cushing’s syndrome. What type of tumor is commonly the cause of the secretion?

A

Small cell carcinoma of the lung.

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31
Q

What would be the levels of ACTH and cortisol in a patient with Cushing’s syndrome due to ectopic ACTH secretion?

A

High ACTH and high cortisol (ectopic tumor releases ACTH, which stimulates release of cortisol; though hypothalamus is stimulated to tell pituitary to decrease ACTH release, the ectopic tumor isn’t under hypothalamic control)

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32
Q

What are the early manifestations of Cushing’s syndrome?

A

HTN and weight gain

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33
Q

What are later findings of Cushing’s syndrome?

A

Truncal obesity, moon face, buffalo hump, decreased muscle mass/weakness, hyperglycemia, glucosuria, polydipsia, thinning of skin, acne, easy bruising, osteoporosis, hyperpigmentation (only if ACTH-dependent Cushing’s), increased risk for infection, mental disturbances, hirsutism, cataracts

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34
Q

What percentage of Cushing’s syndrome patients also have diabetes mellitus?

A

20%

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35
Q

What test can be used to differentiate the two ACTH-dependent Cushing’s syndrome causes (i.e., pituitary ACTH tumor from ectopic ACTH tumor)? What would this test show in a non-Cushing’s patient? In a Cushing’s disease patient? In an ectopic ACTH patient?

A

Dexamethasone suppression test; in a non-Cushing’s patient, cortisol levels would be low; in a Cushing’s disease patient, cortisol levels would drop slightly; in an ectopic ACTH patient, cortisol levels would not drop at all.

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36
Q

What is the treatment of choice for Cushing’s disease?

A

Transsphenoidal adenectomy

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37
Q

Besides the treatment of choice, what other treatment options are available for a patient with Cushing’s disease?

A

Pituitary irradiation, adrenalectomy, pasireotide (somatostatin analog)

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38
Q

Adrenalectomy is one of the treatment options for Cushing’s disease. What are some of the significant side effects?

A

Addison’s disease (adrenal insufficiency), possible Nelson’s syndrome (rapid tumor growth)

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39
Q

True or false: adrenal carcinomas are usually inoperable due to metastasis

A

True.

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40
Q

What is the most common cause of primary hyperaldosteronism? What is the cause of most other cases of primary hyperalldosteronism?

A

Idiopathic bilateral hyperplasia is the most common cause, followed by unilateral aldosterone-secreting adenoma

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41
Q

What is another name for an aldosterone-secreting adenoma?

A

Conn’s syndrome

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42
Q

Why does hyperaldosteronism cause hypertension and hypokalemia?

A

Aldosterone causes sodium (and hence water) retention, increasing blood pressure. Whenever more sodium is retanied, less potassium is kept.

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43
Q

Hypertension caused by _____________ and ______________ is curable by surgery. (Name the two conditions.)

A

Primary hyperaldosteronism; pheochromocytoma

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44
Q

Which gender has a higher prevalence for primary hyperaldosteronism, and at what age?

A

Female (2:1) middle age

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45
Q

What causes secondary hyperaldosteronism?

A

Renal disease or heart failure that makes the body think there is not enough blood, and so activates the renin-angiotensin system (results in increased aldosterone levels)

46
Q

What causes acute adrenal insufficiency?

A

Sudden stress placed on a patient with chronic, or sudden withdrawal of exogenous steroids.

47
Q

Chronic adrenal insufficiency is also known by what name?

A

Addison’s disease

48
Q

What is the most common cause of chronic adrenal insufficiency?

A

Autoimmune adrenalitis

49
Q

What role does tuberculosis have in the history of chronic adrenal insuffiency?

A

It used to account for the majority of cases but then decreased. It is now on the upswing again*

50
Q

Metastatic neoplasms of the adrenal gland can cause adrenal insufficiency. True or false: these neoplasms usually originate in the lungs and liver.

A

False; they usually originate from the lungs and breasts

51
Q

What are the symptoms of adrenal insuffiency?

A

Anorexia, nausea and vomiting, diarrhea, weight loss, hypotension, hyperpigmentation, weakness and fatigability.

52
Q

Hyperpigmentation of the face, axillae, nipples, palms, etc., can occur in what conditions?

A

Adrenal insuffiency and ACTH-dependent Cushing’s syndrome

53
Q

Which hormones are secreted by the adrenal medulla?

A

Catecholamines (mostly epinephrine)

54
Q

Pheochromocytoma is an uncommon tumor. It is also known as the 10% tumor. What does this mean?

A

10% are malignant, 10% are bilateral, 10% occur in children (they also tend to recur, and to run in families, and to present with stroke)

55
Q

Suppose you were to call pheochromocytoma the 90% tumor. What would that mean?

A

90% of pheochromocytomas are benign, 90% are unilateral, 90% occur in adults

56
Q

What are the clinical features of pheochromocytoma?

A

Abrupt elevation of blood pressure with heachache, sweating, palpitations, tachycardia, tremor, and sense of apprehension, increased risk of stroke, cardiomyopathy, insulin resistance, possible abdominal pain with nausea and vomiting

57
Q

What is the treatment option for pheochromocytoma?

A

Adrenalectomy

58
Q

What is another term for hyperthyroidism?

A

Thyrotoxicosis

59
Q

What is the most common cause of hyperthyroidism? What are some other causes?

A

Diffuse hyperplasia due to Graves’ disease, hyperfunctional thyroid goiter, hyperfunctional thyroid adenoma, thyroid inflammation, ingestion of excess thyroid hormone, weight-loss herbal supplements

60
Q

What are the clinical features of hyperthyroidism?

A

Increased basal metabolic rate (unexplained weight loss), nervousness, irritability, tremor, hyperreflexia, tachycardia (may lead to HF in the elderly), hypermotility of the gut with malabsorption and hyperdefecation, staring gaze with lid retraction from sympathetic innervation, heat intolerance, insomnia, oligomenorrhea

61
Q

What percentage of the US population has Graves’ disease?

A

0.4-1.0%

62
Q

True or false: Graves’ disease is the second most common cause of endogenous hyperthyroidism

A

False; it is THE most common cause of endogenous hyperthyroidism

63
Q

What age is the peak incidence of Graves’ disease?

A

Between 20 and 40 years

64
Q

Which gender has a higher prevalence for Graves’ disease?

A

Female (7x)

65
Q

What are some precipitating factors for Graves’ disease?

A

Genetic susceptibility, infection, smoking, pregnancy/stress, iodine-containing drugs in a patient with an iodine deficient diet and the autoimmune condition

66
Q

Graves’ disease is an autoimmune disorder. What type of hypersensitivity is it?

A

Type II

67
Q

Describe the effect of the antibodies in Graves’ disease.

A

Antibodies are directed against thyroid stimulating hormone receptors. These antibodies stimulate the receptor, causing the hyperthyroidism. These antibodies could also just block the receptors, potentially leading into Hashimoto’s thyroiditis

68
Q

Graves’ disease can include a triad of findings. What are these findings?

A

Thyrotoxicosis with goiter (same symptoms as any other hyperthyroidism, plus the antibody is stimulating the TSH receptors enough to cause hyperplasia and hypertrophy of the thyroid), infiltrative ophthalmopathy with exophthalmos (the antibodies against TSH receptors also attack some receptors in the EOM, causing aggregation of WBCs and swelling of EOMs; hypo deviation can be seen), localized, infiltrative dermopathy (pretibial myxedema; thickening and pigmentation of skin over lower leg)

69
Q

What sort of hormone levels would be found in a Graves’ disease patient?

A

High T3 and T4, low TSH

70
Q

Orbitopathy due to Graves’ disease can include what findings?

A

Exophthalmos, EOM weakness (particularly inferior muscles), diplopia (especially in upgaze), lid retraction (Darylmple’s sign) and lid lag, lid edema, keratitis from dry eye, compressive optic neuropathy (due to EOM compression)

71
Q

Before treating Graves’ disease itself, what class of drug would you give to help relieve some of the patient’s symptoms?

A

Beta blockers slow everything down. Heart rate goal is below 90 bpm if the blood pressure allows. Atenolol 25-50 mg/day.

72
Q

What class of drug could you use to treat Graves’ disease itself? What is the mechanism of these drugs?

A

Thionamides (methimazole and PTU); they inhibiti oxidation of iodine in the synthesis of thyroid hormone

73
Q

What dosage of methimazole would you use for a mild case of Graves’ disease? For a severe case?

A

10mg/day for mild case; 20-30 mg/day for severe case

74
Q

Which of the thionamides is preferred in the treatment of Grave’s disease? Why?

A

Methimazole: has longer duration of action, lower incidence of SE

75
Q

True or false: permanent remission of Graves’ disease occurs in more than half of patients after discontinuance of methimazole

A

False; 20-30% experience remission

76
Q

Ideally, thionamides can help the patient achieve a euthyroid state in how long?

A

3 to 8 weeks

77
Q

True or false: thionamides can be used for years, as long as they work well

A

True.

78
Q

What sort of treatment of Graves’ disease is used most commonly in the US?

A

Radioiodine ablation of the thyroid

79
Q

Radioiodine ablation of the thyroid is achieved within what time period?

A

6 to 18 weeks

80
Q

Immediately after radioiodine treatment, TSH receptor antibody concentrations initially _________ (rise/fall)

A

Rise, potentially making the orbitopathy appear worse

81
Q

What percentage of patients who undergo radioiodine treatment of Graves’ disease need to have subsequent doses?

A

10-20%

82
Q

Why is subtotal thyroidectomy is an unpopular therapy in treating Graves’ disease?

A

Surgery risk of hypothyroid and damage to laryngeal nerve

83
Q

Although subtotal thyroidectomy is an unpopular therapy in treating Graves’ disease, what are a few indications for its use?

A

Very large/obstructive goiter, active ophthalmopathy, antithyroid drug allergy, coexisting suspicious or malignant thyroid nodule

84
Q

Which is more common, hyperthyroidism or hypothyroidism?

A

Hypothyroidism

85
Q

What are a few common causes of primary hypothyroidism?

A

Thyroid ablation via surgery or radiation therapy, Hashimoto’s thyroiditis, primary idiopathic hypothyroidism

86
Q

True or false: Hashimoto’s thyroiditis is the most common cause of hypothyroidism in iodine-deficient populations

A

False; it is the most common cause of hypothyroidism in iodine-sufficient populations

87
Q

How would TSH, T3, and T4 levels be in a patient with primary hypothyroidism?

A

High TSH, low T3 and T4

88
Q

How would TSH, T3, and T4 levels be in a patient with secondary hypothyroidism?

A

Low TSH, low T3 and T4

89
Q

Hypothyroidism is more common in which gender?

A

Female 8:1

90
Q

What are some clinical features of hypothyroidism?

A

Mimics depression early on, slow speech, weight gain, fatigue, cold intolerance, bradycardia, heart failure, delayed deep tendon reflexes, decreased bowel motility with resultant constipation

91
Q

What is the treatment for hypothyroidism?

A

Fasting L-thyroxine (before breakfast)

92
Q

What causes neonatal hypothyroidism?

A

Iodine deficiency in the diet of the mother while pregnant (possible iodine deficiency in child itself after birth???)

93
Q

During which stage of pregnancy would iodine deficiency cause the most harm?

A

During the first trimester, iodine deficiency could cause severe mental impairment

94
Q

What are some clinical features of neonatal hypothyroidism?

A

Impaired development of skeletal system (short stature), mental impairment, coarse facial features

95
Q

Hashimoto’s thyroiditis is an autoimmune disease. What type of hypersensitivity is it?

A

Type IV

96
Q

Hashimoto’s thyroiditis is more common in which gender and age group?

A

Women between 45 and 65

97
Q

True or false: a patient with Hashimoto thyroiditis may first experience transient hyperthyroidism

A

True; this is due to disruption of thyroid follicles and subsequent release of the thyroid hormone they contain

98
Q

What are some precipitating factors for Hasimoto’s thyroiditis?

A

Infection, stress, pregnancy, iodine intake, radiation exposure.

99
Q

How would you treat Hashimoto’s thyroiditis?

A

L-thyroxine qd, possible q1week

100
Q

Thyroid neoplasms are not uncommon. What characteristics may indicate that a thyroid nodule is more likely to be benign?

A

Multiple nodules that do take up radioactive iodine in an older female.

101
Q

Thyroid neoplasms are not uncommon. What characteristics may indicate that a thyroid nodule is more likely to be neoplastic?

A

A solitary nodule that does not take up radioactive iodine in a younger male.

102
Q

The parathyroid glands release parathyroid hormone in response to what signal?

A

Low blood calcium levels

103
Q

True or false: primary hyperparathyroidism is one of the most common endocrine disorders

A

True.

104
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma.

105
Q

Which gender is more affected by primary hyperparathyroidism?

A

Female

106
Q

What are the symptoms of hyperparathyroidism?

A

Painful bones, renal stones, abdominal groans (constipation, nausea, peptic ulcers, pancreatitis, gallstones), psychic moans (depression, lethargy, seizures). Nonspecific symptoms include fatigue, weakness, anorexia, mild depression, missed work

107
Q

What therapy would you recommend for a patient with hyperparathyroidism?

A

Remove adenoma, increase fluid uptake, decrease calcium in diet, maintain vitamin D uptake, do physical activity

108
Q

Is hypoparathyroidism more or less common than hyperparathyroidism?

A

Much less common

109
Q

What can cause hypoparathyroidism?

A

Surgical removal of parathyroid glands (most common); autoimmune disease, though this is much less common

110
Q

What are some clinical signs of hypoparathyroidism?

A

Latent tetany such as Cvostek’s sign (tap on facial nerve, causes contraction of facial muscles, upperlip [Dick Cheney sneer]) and Trousseau’s sign (inflation of blood pressure cuff for 3 minutes causes carpal spasm)

111
Q

What sort of therapy would be recommended for a patient with hypoparathyroidism?

A

Vitamin D and calcium; synthetic parathyroid hormone is being evaluated

OPT 537 (21 decks)

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