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Endocrine > Robbins > Flashcards

Robbins Flashcards

1
Q

two morphologically and functionally distinct components of the pituitary gland

A

anterior lobe (adenohypophysis) and posterior lobe (neurohypophysis)

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2
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
SOMATOTROPHS

A

growth hormone (GH)

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3
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
MAMMOSOMATOTROPHS

A

GH and prolactin (PRL)

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4
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
LACTOTROPHS

A

PRL

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5
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
CORTICOTROPHS

A

adrenocorticotropic hormone
(ACTH), pro-opiomelanocortin (POMC), and melanocyte-
stimulating hormone (MSH)

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6
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
TYROTROPHS

A

thyroid-stimulating hormone (TSH)

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7
Q

Of these cells in the anterior pituitary, give the hormone they synthesize:
GONADOTROPHS

A

follicle-stimulating hormone (FSH)
and luteinizing hormone (LH)

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8
Q

Two peptide hormones secreted from the posterior pituitary

A

oxytocin and antidiuretic hormone (ADH)

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9
Q

most common cause of hyperpituitarism

A

adenoma arising in the anterior lobe of the pituitary

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10
Q

most common combination of hormones that pituitary adenomas secrete

A

GH and PRL

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11
Q

microadenoma size

A

<1cm

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12
Q

macroadenoma size

A

> 1cm

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13
Q

most common mutation in pituitary adenomas

A

Activating G-protein mutations

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14
Q

most common mutation in somatotroph cell adenomas

A

GNAS mutation

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15
Q

most common mutation in corticotroph cell adenomas

A

ubiquitin-specific protease 8 (USP8)

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16
Q

Most pituitary carcinomas are functional and secrete (2)

A

prolactin and ACTH

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17
Q

germline mutation in pituitary blastoma

A

DICER1

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18
Q

two distinctive morphologic features of most pituitary adenomas

A

cellular monomorphism and absence of a reticulin network

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19
Q

postpartum ischemic necrosis of the pituitary

A

Sheehan syndrome

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20
Q

These cysts, lined by ciliated cuboidal epithelium with occasional goblet cells and anterior pituitary cells, can accumulate proteinaceous fluid and expand, compromising the normal pituitary gland

A

Rathke cleft cyst

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21
Q

mutation in this results in combined pituitary hormone deficiency, characterized by deficiencies of GH, prolactin, and TSH

A

pituitary-specific gene PIT1

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22
Q

ADH deficiency causes

A

diabetes insipidus

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23
Q

Most common cause of Syndrome of inappropriate ADH (SIADH) secretion

A

secretion of ADH by malignant neoplasms (particularly small-cell carcinoma of the lung)

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24
Q

tumor thought to arise from vestigial remnants of Rathke pouch

A

craniopharyngioma

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25
Q

two distinct histologic variants of craniopharyngioma

A

adamantinomatous craniopharyngioma and papillary craniopharyngioma

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26
Q

craniopharyngioma that consists of nests or cords of stratified squamous epithelium embedded in a spongy “reticulum” that becomes more prominent in the internal layers. “Palisading” of the squamous epithelium is frequently observed at the periphery. Compact, lamellar keratin formation (“wet keratin”) is a diagnostic feature of this tumor and dystrophic calcification is common

A

Adamantinomatous

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27
Q

mutation in Adamantinomatous craniopharyngioma

A

CTNNB1 (β-catenin) gene

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28
Q

craniopharyngiomas that contain both solid sheets of cells and papillae lined by well-differentiated squamous epithelium and lack lamellar keratin, calcification, cysts, peripheral palisading of squamous cells, and a spongy reticulum

A

Papillary

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29
Q

mutation in Papillary craniopharyngiomas

A

BRAFV600E

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30
Q

chemical agents that can inhibit thyroid gland function are collectively known as

A

goitrogen

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31
Q

agent that inhibits the oxidation of iodide and thus blocks the production of thyroid hormones; also inhibits the peripheral deiodination of circulating T4 into T3

A

propylthiouracil

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32
Q

when given in large doses to individuals with thyroid hyperfunction, blocks the release of thyroid hormones by inhibiting the proteolysis of thyroglobulin

A

iodide

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33
Q

parafollicular cells, or C cells, synthesize and secrete the hormone __

A

calcitonin

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34
Q

most common cause of thyrotoxicosis and is associated with hyperfunction of the gland

A

Diffuse hyperplasia of the thyroid associated with Graves
disease

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35
Q

congenital hypothyroidism is most often the result of

A

iodine deficiency in the diet

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36
Q

mutations responsible for Genetic defects in thyroid development (3)

A

PAX8, FOXE1, TSH receptor mutations

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37
Q

most common cause of hypothyroidism in iodine-sufficient areas of the world

A

Autoimmune hypothyroidism (Hashimoto thyroiditis)

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38
Q

characterized by severe intellectual disability, short stature, coarse facial features, a protruding tongue, and umbilical hernia

A

Cretinism

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39
Q

hypothyroidism developing in the older child or adult

A

myxedema

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40
Q

exemplified by the presence of circulating autoantibodies against thyroglobulin and thyroid peroxidase and characterized by progressive destruction of thyroid parenchyma, Hürthle cell change, and mononuclear (lymphoplasmacytic) infiltrates, with germinal centers and variable degrees of fibrosis

A

Hashimoto thyroiditis

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41
Q

polymorphisms in these genes have a higher predisposition for Hashimoto thyroiditis

A

-cytotoxic T lymphocyte–associated antigen-4 (CTLA4)
-protein tyrosine phosphatase-22 (PTPN22), and -interleukin-2 receptor α chain (IL2RA)

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42
Q

characteristic features appear in the form of aggregates of lymphocytes, activated macrophages, and plasma cells associated with collapsed and damaged thyroid follicles. Multinucleate giant cells enclose pools of colloid

A

Granulomatous thyroiditis (also called De Quervain thyroiditis)

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43
Q

most common cause of thyroid pain

A

Granulomatous thyroiditis (also called De Quervain thyroiditis)

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44
Q

a rare disorder characterized by extensive fibrosis involving the thyroid and contiguous neck structures

A

Riedel thyroiditis

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45
Q

most common cause of endogenous hyperthyroidism characterized by the triad of thyrotoxicosis, ophthalmopathy, and dermopathy.

A

Graves disease

46
Q

autoimmune disorder characterized by the production of autoantibodies against multiple thyroid proteins, most importantly the TSH receptor

A

Graves disease

47
Q

most common antibody subtype observed in approximately 90% of patients with graves disease

A

thyroid-stimulating immunoglobulin (TSI)

48
Q

exopthalmos) is caused by an increase in the volume of the retro-orbital connective tissues and extraocular muscles, which occurs for several reasons (4)

A

(1) marked infiltration of connective tissue by mononuclear cells, predominantly T cells; (2) inflammation, edema, and swelling of extraocular muscles; (3) accumulation of extracellular matrix components,; and (4) increased numbers of adipocytes (fatty infiltration).

49
Q

Enlargement of the thyroid, or goiter is caused by

A

impaired synthesis of thyroid hormone

50
Q

Goiters can broadly be divided into two types

A

diffuse nontoxic and multinodular

51
Q

vegetable family that interfere with thyroid hormone synthesis at some level

A

Brassicaceae (Cruciferae) family (e.g., cabbage, cauliflower, Brussels sprouts, turnips, and cassava)

52
Q

Two phases identified in the evolution of diffuse nontoxic goiter

A

hyperplastic phase and the phase of colloid involution

53
Q

recurrent episodes of hyperplasia and involution combine to produce a more irregular enlargement of the thyroid, termed

A

multinodular goiter

54
Q

development of an autonomous nodule within a long-standing goiter that produces hyperthyroidism

A

Plummer syndrome

55
Q

3 mutations at least one being often present that cause follicular cells to secrete thyroid hormone independent of TSH stimulation (“thyroid autonomy”). This leads to hyperthyroidism and produces a functional “hot” nodule on imaging

A
  1. TSH receptor (TSHR) (more common)
  2. α-subunit of Gs (GNAS) (less common)
  3. enhancer of zeste, homolog 1 (EZH1) (1/3)
56
Q

nonfunctioning follicular adenomas harbor oncogenic mutations of

A

RAS

57
Q

histologic hallmark of all follicular adenomas

A

presence of an intact, well-formed capsule encircling the tumor

58
Q

precursor to conventional PTC

A

Papillary microcarcinoma

59
Q

precursor to invasive encapsulated follicular variant PTC

A

Noninvasive thryoid neoplasma with papillary- like nuclear features / Noninvasive follicular thyroid neoplasm with papillary-like features (NIFTP)

60
Q

precursor to follicular carcinoma

A

Nonfunctioning follicular adenoma

61
Q

Conventional PTCs have two defining genetic abnormalities namely

A

gene fusions of RET or NTRK, and point mutations in BRAF

62
Q

most commonly observed fusion partners of RET in sporadic papillary cancers

A

PTC1 and PTC2

63
Q

Between 50% and 80% of conventional PTCs harbor gain-of-function mutations in

A

BRAF gene

64
Q

most common BRAF gene mutation in conventional PTCs

A

BRAF valine-to-glutamate change in codon 600 (BRAFV600E)

65
Q

diagnostic requirement for conventional PTCs, known as “tall cell variant”

A

2-3X as tall as they are wide with at least >/=30% population and BRAFV600E mutation

66
Q

follicular neoplasms are often associated with gain-of- function mutations in

A

RAS

67
Q

fusion gene found in some follicular neoplasms

A

PAX8-PPARG fusion genes

68
Q

10% of follicular carcinomas exhibit gain-of-function mutations of

A

PIK3CA

69
Q

presence of this mutation in thyroid neoplasms is associated with reduced expression of thyroid differentiation markers (such as thyroglobulin and thyroid peroxidase) and may be associated with a higher risk of extrathyroidal extension and recurrence

A

BRAFV600E

70
Q

presence of this mutation in thyroid neoplasms is associated retention of expression of thyroid differentiation factors (e.g., thyroglobulin, thyroid peroxidase), which may contribute to their follicular growth pattern

A

RAS

71
Q

three recurrent genetic “hits” essentially restricted to poorly differentiated and anaplastic carcinomas

A

point mutations of TP53, beta-catenin (CTNNB1), and TERT

72
Q

Familial medullary thyroid carcinomas occur in this hereditary conditon

A

multiple endocrine neoplasia, type 2 (MEN-2)

73
Q

this mutation are also seen in approximately one-half of nonfamilial (sporadic) medullary thyroid cancers

A

RET

74
Q

The major risk factor predisposing to thyroid cancer is

A

exposure to ionizing radiation

75
Q

radiation exposure has a high chance to induce chromosome rearrangements that produce gene fusions and thus is commonly associated with this thyroid carcinomas with previous radiation exposure

A

PTC

76
Q

most common form of thyroid cancer

A

PTC

77
Q

is defined as an otherwise conventional papillary carcinoma, but less than 1 cm in size

A

Papillary microcarcinoma

78
Q

4 hallmarks of papillary neoplasms

A
  1. Branching papillae
  2. ground-glass or Orphan Annie eye nuclei
  3. psammoma bodies
  4. Foci of lymphatic invasion by tumor
79
Q

Tall cell variant papillary carcinomas almost always harbor these two aberrations and their co-occurrence may contribute to the aggressive behavior of this variant.

A

BRAF and RET/PTC

80
Q

these translocations are found in approximately one-half of diffuse sclerosing variant of papillary carcinoma cases

A

RET/PTC translocations

81
Q

prognosis in PTC is dependent on several factors including (3)

A

age (in general, being less favor- able among patients older than 40 years), presence of extrathyroidal extension, and presence of distant metastases (stage)

82
Q

thyroid carcinoma that often have propensity for invading lymphatics

A

PTC

83
Q

thyroid carcinoma that often have propensity for invading vasculature

A

Follicular carcinomas

84
Q

Anaplastic carcinomas demonstrate variable morphology (3)

A

(1) large, giant cells, including occasional osteoclast-like giant cells; (2) spindle cells; and (3) mixed spindle and giant cells

85
Q

one of the most aggressive thyroid cancers known; in most cases death occurs in less than 1 year

A

Anaplastic carcinomas

86
Q

thyroid neuroendocrine neoplasms derived from the parafollicular cells (C cells)

A

Medullary carcinoma

87
Q

common presentation in familial cases of medullary thyroid carcinomas

A

bilaterality and multicentricity

88
Q

a feature that is usually absent in sporadic lesions of medullary carcinoma

A

C-cell hyperplasia

89
Q

prophylactic thyroidectomy as early as possible is offered to prevent the otherwise inevitable development of medullary carcinoma in these patients

A

asymptomatic MEN-2 individuals carrying germline RET mutations

90
Q

the most common clinically significant congenital anomaly of the thyroid

A

Thyroglossal duct cyst

91
Q

The four parathyroid glands are composed of two cell types namely

A

chief cells and oxyphil cells

92
Q

most common cause of primary hyperparathyroidism is

A

solitary sporadic parathyroid adenoma

93
Q

two molecular defects that have an established role in the development of sporadic parathyroid adenomas

A

Cyclin D1 (CCDN1) gene inversions and MEN1 mutations

94
Q

mutated in ~70% of sporadic parathyroid carcinomas, but rarely in adenomas

A

CDC73

95
Q

only reliable criteria to distinguish parathyroid carcinoma from an adenoma

A

invasion of surrounding tissues and metastasis

96
Q

produced in medullary bone in cases of hyperparathyroidism

A

dissecting osteitis

97
Q

Symptomatic, untreated primary hyperparathyroidism manifests with three interrelated skeletal abnormalities namely

A

osteoporosis, brown tumors, and osteitis fibrosa cystica

98
Q

hallmark of severe hyperparathyroidism and is known as

A

generalized osteitis fibrosa cystica

99
Q

most frequent cause of symptomatic hypercalcemia in adults

A

malignancy

100
Q

most common mechanism (in ~80% of cases) through which osteolytic tumors induce hypercalcemia

A

secretion of PTH-related peptide (PTHrP) and bone mets

101
Q

most common cause of secondary hyperparathyroidism

A

Renal failure

102
Q

Unequivocal criteria for malignancy in pancreatic neuroendocrine tumors (PanNETs) (3)

A

metastases, vascular invasion, and local infiltration

103
Q

most common subtype of pancreatic endocrine neoplasms

A

insulinomas

104
Q

recurrent somatic alterations in three major genes or pathways in sporadic PanNETs

A

MEN1, Loss-of-function mutations in tumor suppressor genes such PTEN and TSC2, and Inactivating mutations in two genes, alpha-thalassemia/
mental retardation syndrome, X-linked (ATRX) and death-domain–associated protein (DAXX)

105
Q

disease associated with pancreatic islet cell lesions, hypersecretion of gastric acid and severe peptic ulceration

A

Zollinger-Ellison Syndrome

106
Q

two familial cancer syndromes are associated with a predisposition for developing adrenocortical carcinomas

A

Li-Fraumeni syndrome and Beckwith-Wiedemann syndrome

107
Q

mutation in Li-Fraumeni syndrome

A

TP53 mutations

108
Q

gene implicated in Beckwith-Wiedemann syndrome

A

gene for insulin-like growth factor 2 (IGF-2)

109
Q

neoplasms composed of chromaffin cells, which synthesize and release catecholamines and, in some instances, peptide hormones

A

Pheochromocytomas

110
Q

MEN-1 is characterized by abnormalities involving these organs (3)

A

parathyroid, pancreas, and pituitary gland

111
Q

MEN-2A is clinically and genetically distinct from MEN-1 and is caused by

A

germline gain-of-function mutations in the RET protooncogene

112
Q

T staging to Thyroid tumors:
T1a, T1b, T2, T3a,T3b, T4a, T4b

A

T1a </= 1cm
T1b >1cm </=2cm
T2 >2cm </=4cm
T3a >4cm limited to thyroid
T3b involved strap muscles
T4a involves subcutaneous tissues, larynx, trachea
T4b involves prevertebral fascia/ encasing the carotid artery

Endocrine (1 decks)

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