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All the things > 15.1-15.7 Endocrine > Flashcards

15.1-15.7 Endocrine Flashcards

1
Q

What is the mechanism by which a pituitary tumor produces bitemporal hemianopsia?

A

Compression of the optic chiasm

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2
Q

What are the problems that a nonfunctional pituitary adenoma can cause? (3)

A
  • Bitemporal hemianopsia
  • Hypopituitarism
  • HA
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3
Q

What is the most common type of functional pituitary adenoma?

A

Prolactinoma

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4
Q

What are the s/sx of a prolactinoma in males? Females?

A 
Males = Decreased libido and HA
Females = galactorrhea and amenorrhea
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5
Q

What is the treatment for a prolactinoma?

A

Dopamine agonists or surgery

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6
Q

Why do prolactinomas cause amenorrhea?

A

Prolactin inhibits the synthesis and release of GnRH

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7
Q

Why don’t males have galactorrhea with prolactinomas?

A

They do not have the terminal ducts necessary

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8
Q

What is the treatment for prolactinoma? Why?

A

Dopamine agonist, (e.g. bromocriptine) since dopamine inhibits the release of prolactin

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9
Q

What are the s/sx of GH adenomas in children? Adults? What other endocrine problem can be seen?

A
  • Gigantism in children
  • Acromegaly in adults
  • Secondary DM is often present
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10
Q

What is the most common cause of death in patients with GH adenomas? Why?

A
  • Cardiac failure

- Cardiomegaly from GH

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11
Q

What is the oropharyngeal finding of GH adenomas?

A

Macroglossia

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12
Q

What is the hormone produced by the liver in response to GH secretion? What does this do?

A
  • IGF-1

- Mediate the growth of tissues

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13
Q

How do you diagnose a GH adenoma? (2)

A
  • Elevated GH and IGF-1

- Lack of GH suppression by oral glucose

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14
Q

What is the normal response of GH to administration of oral glucose? What would be the response in the case of a GH adenoma?

A
  • Should decrease

- GH adenomas would not respond

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15
Q

What are the two medical treatments for GH adenomas? Why?

A
  • Octreotide since it is a somatostatin analogue, thus it blocks GHRH from acting on the anterior pituitary
  • GH receptor antagonist
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16
Q

What percent of the pituitary parenchyma must be lost for s/sx of hypopituitarism to appear?

A

75%

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17
Q

What type of growth causes hypopituitarism in children? Adults?

A
  • Children = craniopharyngioma

- Adults = pituitary adenoma

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18
Q

What is pituitary apoplexy?

A

Hemorrhage into the pituitary

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19
Q

What is Sheehan syndrome?

A

Hypopituitarism d/t pregnancy hypovolemia induced necrosis. This occurs during pregnancy since there is an increased amount of prolactin cells, meaning the pituitary is susceptible to infarction

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20
Q

What are the two classic s/sx of Sheehan syndrome?

A

No lactation and loss of pubic hair

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21
Q

What is primary empty sella syndrome?

A

Invasion of the arachnoid mater into the sella turcica destroys the pituitary

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22
Q

What is secondary empty sella syndrome?

A

Trauma kills pituitary

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23
Q

What are the two hormones released by the posterior pituitary?

A
  • ADH (vasopressin)

- Oxytocin

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24
Q

What are the six hormones released by the anterior pituitary?

A
  • Prolactin
  • GH
  • FSH/LH
  • ACTH
  • TSH
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25
Q

What is the role of oxytocin?

A

Induces milk release and uterine contractions during birthing process

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26
Q

What is the cause of central diabetes insipidus?

A

ADH deficiency d/t hypothalamic or posterior pituitary pathology

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27
Q

What are the s/sx of diabetes insipidus?

A

Polyuria and polydipsia

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28
Q

What are the electrolyte disturbances that can occur with diabetes insipidus?

A

Hypernatremia and high serum osmolality

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29
Q

What are the urinary findings of diabetes insipidus?

A

Low urine osmolality and specific gravity

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30
Q

How do you diagnose diabetes insipidus?

A

Water deprivation fails to increase urine osmolality

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31
Q

What is the MOA of desmopressin?

A

ADH analogue

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32
Q

What is the cause of nephrogenic diabetes insipidus?

A

Impaired renal response to ADH d/t inherited mutation or drugs

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33
Q

What is the major difference between nephrogenic and neurogenic diabetes insipidus?

A

Similar, but there is no response to desmopressin in nephrogenic diabetes insipidus

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34
Q

What are the two classic drugs that can cause nephrogenic diabetes insipidus?

A

Li

Demeclocycline

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35
Q

What is SIADH?

A

Too much ADH causes too concentrated urine to be produced

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36
Q

What are the electrolyte disturbances that can occur with SIADH?

A

Hyponatremia and low serum osmolality

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37
Q

What are the s/sx of SIADH?

A

Highly concentrated urine + mental status changes and szs

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38
Q

What is the classic ectopic cause of SIADH?

A

Small cell carcinoma of the lung

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39
Q

What are the drugs that can cause SIADH?

A

Cyclophosphamide

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40
Q

What sort of infection can cause SIADH?

A

Pulmonary infection

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41
Q

What sort of trauma can cause SIADH?

A

CNS trauma

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42
Q

What are the two treatments for SIADH?
——

A
  • Free water restriction

- Demeclocycline

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43
Q

What is a thyroglossal duct cyst?

A

Cystic dilation of the thyroglossal duct remnant that presents as an anterior neck mass

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44
Q

How does the thyroid develop?

A

Starts at the base of the tongue, and moves down the thyroglossal duct toward the anterior face

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45
Q

What is a lingual thyroid?

A

Persistence of thyroid tissue at the base of the tongue, that presents as a base of tongue mass

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46
Q

How does thyroid hormone increase BMR?

A

Increases the synthesis of Na/K ATPase

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47
Q

How does thyroid hormone increase SNS activity?

A

Increases beta adrenergic receptors

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48
Q

What is the classic arrhythmia that can occur with hyperthyroidism?

A

A-fib

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49
Q

What are the GI findings of hyperthyroidism?

A

Diarrhea with malabsorption

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50
Q

What are the uterine gyn findings of hyperthyroidism?

A

Oligomenorrhea

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51
Q

What happens to the bones with hyperthyroidism?

A

Bone resorption with hypercalcemia

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52
Q

What happens to muscle mass with hyperthyroidism?

A

Decreased

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53
Q

What are the lipid and carb abnormalities that can occur with hyperthyroidism? Why?

A
  • Hypercholesterolemia
  • Hyperglycemia

-Increased gluconeogenesis and glycogenolysis

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54
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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55
Q

What is the type of antibody that mediates the effects of Grave’s disease?

A

IgG

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56
Q

In whom does Grave’s disease usually occur?

A

Women of childbearing age

57
Q

What is Grave’s disease?

A

Autoimmune production of IgG for TSH receptor

58
Q

What is the cause of the goiter that can occur with Grave’s disease?

A

TSH receptor stimulation

59
Q

What causes the exophthalmos and pretibial myxedema in Grave’s disease?

A

Fibroblasts behind the eye and in front of the tibia have TSH receptors, and will secrete glycosaminoglycans

60
Q

What happens to the colloid in Grave’s disease?

A

scalloping (colloid pulls away from the epithelium)

61
Q

What are the T4 and TSH levels like in Grave’s disease?

A
  • Increased total and free T4

- Decreased TSH

62
Q

What happens to cholesterol levels with Grave’s disease? Serum glucose?

A
  • Cholesterol decreased

- Glucose increased

63
Q

What are the 3 treatments for Grave’s disease?

A
  • Beta blockers to block effect on the SNS
  • Thioamide to block peroxidase
  • Radioiodine ablation
64
Q

What is the building block for thyroglobulin?

A

Tyrosine

65
Q

What form of I is brought into the cell, and what is the form of I that attached to thyroglobulin?

A
  • Iodide (I-) goes into cell

- Iodine attaches to thyroglobulin

66
Q

What is the reasoning behind using thioamide (an inhibitor of myeloperoxidase) to treat hyperthyroidism?

A

Inhibits the coupling of I to thyroglobulin

67
Q

What is thyroid storm?

A

Elevated catecholamines and massive hormones excess

68
Q

What are the s/sx of thyroid storm?

A
  • Arrhythmia
  • Hyperthermia
  • Vomiting
69
Q

What is the treatment for thyroid storm? (3)

A
  • PTU
  • Beta blockers
  • Steroids
70
Q

What is the MOA and use of PTU?

A
  • Inhibits peroxidase coupling of iodine to thyroglobulin, and prevents the conversion of T4 to T3
  • Treats thyroid storm
71
Q

What causes multinodular goiter?

A

Relative iodine deficiency

72
Q

What are the consequences of having a multinodular goiter (hypo, hyperthyroid, or euthyroid)?

A

Euthyroid (normally functioning thyroid)

73
Q

What is the toxic goiter that can develop from a multinodular goiter?

A

TSH-independent regions of the thyroid will secrete T3/T4 without stimulation of TSH (badness)

74
Q

What is cretinism?

A

Hypothyroidism in neonates and in infants

75
Q

What are the s/sx of cretinism?

A
  • MR
  • Short stature
  • Coarse facial features
  • Macroglossia
  • Umbilical hernia
76
Q

What are the causes of cretinism? (4)

A
  • Maternal hypothyroidism during early pregnancy
  • Thyroid agenesis
  • Dyshormonogenetic goiter
  • Iodine deficiency
77
Q

What is the enzyme that is most commonly deficient in Dyshormonogenetic goiter?

A

Thyroperoxidase

78
Q

What is myxedema? S/sx?

A

Hypothyroidism in older children or adults

  • myxedema
  • Weight gain despite normal appetite
  • Muscle weakness
  • Cold intolerance
79
Q

What are the two classic symptoms of hypothyroidism in older children?

A

Deepening of the voice and macroglossia, both d/t myxedema

80
Q

What are the gyn findings with hypothyroidism?

A

Oligomenorrhea

81
Q

What are the lipid abnormalities that can be caused by hypothyroidism?

A

Hypercholesterolemia

82
Q

What are the nutritional causes of hypothyroidism?

A

Iodine deficiency

83
Q

What is the autoimmune cause of hypothyroidism?

A

Hashimoto’s thyroiditis

84
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune attack against the thyroid gland, causing destruction

85
Q

What are the drugs that can cause hypothyroidism?

A

Li

86
Q

What is the most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

87
Q

What is the HLA gene that is associated with Hashimoto’s thyroiditis?

A
  • HLA-DR5

- Pernicious anemia

88
Q

Why is there an initial hyperthyroidism in Hashimoto’s thyroiditis?

A

Destruction of the thyroid tissue causes release of preformed T3/T4

89
Q

What happens to T4 and TSH levels with Hashimoto’s thyroiditis in the ling term?

A
  • Decreased T4

- Increased TSH

90
Q

What are the antibodies that are usually present with Hashimoto’s thyroiditis? What is their role in the pathogenesis of Hashimoto’s thyroiditis?

A
  • Antithyroglobulin and antimicrosomal antibodies

- Just markers–do NOT mediate the destruction

91
Q

What are the classic histological findings of Hashimoto’s thyroiditis?

A
  • Chronic inflammation with germinal centers

- Hurthle cells (basophilic cells)

92
Q

Patients with Hashimoto’s thyroiditis are at an increased risk of developing what malignancy? Why?

A
  • B cell lymphoma

- Germinal centers develop a marginal zone

93
Q

Enlarging thyroid gland with Hashimoto’s thyroiditis is suspicious for what?

A

B cell lymphoma

94
Q

What is subacute (de Quervain) granulomatous thyroiditis?

A

Granulomatous thyroiditis that follows a viral infection

95
Q

What are the presenting s/sx of subacute (de Quervain) granulomatous thyroiditis?

A

Tender thyroid with transient hyperthyroidism

96
Q

What is the prognosis for subacute (deQuervain) granulomatous thyroiditis?

A

Self-limited; does not progress to hypothyroidism

97
Q

Tender thyroid = ?

A

subacute (de Quervain) granulomatous thyroiditis

98
Q

What is Reidel Fibrosing thyroiditis?

A

Chronic inflammation with extensive fibrosis of the thyroid

99
Q

What is the usual presentation of Reidel fibrosing thyroiditis?

A

Hypothyroidism with a “hard as wood” nontender thyroid gland

100
Q

What are some common complications of Reidel fibrosing thyroiditis?

A

Fibrosis extending to local structures (e.g. airway)

101
Q

What are the top two items in your ddx for a hard, nontender thyroid with hypothyroidism? In whom does each occur?

A
  • Anaplastic carcinoma (old people)

- Riedel Fibrosing thyroiditis (young women)

102
Q

In whom does Reidel fibrosing thyroiditis usually occur?

A

Young women

103
Q

What are thyroid nodules?

A

Distinct, solitary thyroid nodules that are likely benign

104
Q

Are thyroid nodules more likely benign or malignant?

A

Benign

105
Q

What are the characteristics of thyroid nodules?

A

distinct, solitary nodules

106
Q

What is the benefit of a radioactive uptake study when assessing for thyroid issues (what increases uptake and what decreases uptake)?

A

There is increased Iodine 131 uptake with Grave’s disease or nodular goiter, but decreased in adenomas and carcinomas

107
Q

What is the way to biopsy thyroid nodules?

A

Fine needle aspiration (FNA)

108
Q

Why is FNA used to biopsy the thyroid?

A

Extensive blood supply to the thyroid will cause it to bleed like nuts if biopsied in the usual fashion

109
Q

What are the results of radioactive Iodine uptake for adenomas/carcinomas? How about for Grave’s disease or nodular goiters?

A
  • Adenomas/carcinomas = decreased

- Graves/nodular goiter = increased

110
Q

What is the most common benign growth in the thyroid? What are the characteristics of this?

A
  • Follicular adenomas

- Usually surrounded by a fibrous capsule

111
Q

True or false: follicular adenomas usually secrete thyroid hormone

A

False

112
Q

What is the most common type of carcinoma of the thyroid?

A

Papillary carcinoma

113
Q

What are the risk factors for developing papillary carcinoma?

A

Exposure to ionizing radiation in childhood

114
Q

What are the two classic histologic findings of papillary carcinoma?

A
  • “Annie-eyed” nuclei (nuclei with a white clearing in the center)
  • Nuclear “grooves” (basophilic straight lines in the nucleus)
115
Q

What are psammoma bodies?

A

concentric. layed calcification that can be seen in papillary carcinoma

116
Q

Where does papillary carcinoma usually spread?

A

Cervical nodes

117
Q

What is the prognosis for papillary carcinoma?

A

Excellent

118
Q

What is follicular carcinoma?

A

Malignant proliferation of thyroid follicles

119
Q

What are the characteristics of follicular carcinomas?

A

Follicles surrounded by a fibrous capsule with invasion through the capsule

120
Q

What is the major difference between follicular adenomas and follicular carcinomas?

A

Carcinomas will invade through the fibrous capsule

121
Q

How do you differentiate between follicular adenoma and follicular carcinoma?

A

Need to examine the entire follicle to ensure that the tumor does not invade the capsule

122
Q

Can FNA make the distinction between follicular adenoma and follicular carcinoma? Why or why not?

A

No, because the only difference between the two is invasion of the fibrous capsule

123
Q

What is the primary means through which follicular carcinoma metastasizes?

A

Hematogenously

124
Q

What are the four carcinomas that spread hematogenously?

A
  1. Renal carcinoma
  2. Hepatocellular CA
  3. Follicular CA
  4. Choriocarcinoma
125
Q

What is medullary carcinoma?

A

Malignant proliferation of parafollicular C cells

126
Q

What endocrine disorder is produced form medullary carcinoma?

A

High levels of calcitonin leads to hypocalcemia

127
Q

Where does the calcitonin deposit with medullary carcinoma? What does it deposit as?

A

Within tumor as amyloid

128
Q

What is the classic histological finding of medullary carcinoma?

A

Follicles within an amyloid stroma

129
Q

Malignant cells within an amyloid stroma = ?

A

Medullary carcinoma

130
Q

What are the causes of familial thyroid carcinoma?

A

MEN2A and MEN2B

131
Q

What are the malignancies found in MEN2A?

A
  • Medullary carcinoma of the thyroid
  • pheochromocytoma
  • Parathyroid adenomas
132
Q

What are the malignancies found in MEN2B?

A
  • Medullary carcinoma of the thyroid
  • pheochromocytoma
  • ganglioneuromas of the oral mucosa
133
Q

What is the genetic cause of MEN2A and MEN2B?

A

Mutations in the RET oncogene

134
Q

What is warranted if the RET mutation is found?

A

Prophylactic thyroidectomy

135
Q

What is anaplastic carcinoma of the thyroid?

A

Undifferentiated tumor of the thyroid

136
Q

In whom is anaplastic carcinoma of the thyroid usually seen?

A

Elderly

137
Q

What is the prognosis for anaplastic carcinoma of the thyroid?

A

Poor

138
Q

What are the sequelae of anaplastic carcinoma of the thyroid?

A

Invasion of local structures leading to dysphagia and/or respiratory compromise

All the things (36 decks)

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