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Endocrine II > Ch 24 - Endo Path > Flashcards

Ch 24 - Endo Path Flashcards

1
Q

hormones from lactotroph cells

A

prolactin

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2
Q

hormones from somatotroph cells

A

GH

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3
Q

hormones from mammosomatotroph cells

A

prolactin, GH

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4
Q

hormones from corticotroph cells

A

ATCH, POMC, MSHj

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5
Q

hormones from thyrotroph cells

A

TSH

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6
Q

hormones from gonadotroph cells

A

FSH, LH

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7
Q

oxytocin and ADH are made in

A

the hypothalamus

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8
Q

oxytocin and ADH are stored in

A

axon terminas of the posterior pituitary

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9
Q

acute hemorrhage into an adenoma causing rapid enlargement of the lesion

A

pituitary apoplexy

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10
Q

thyroiditis that is triggered by viral infection, usually post URI

A

granulomatous thyroiditis

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11
Q

MCC of thyroid pain

A

granulomatous thyroiditis

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12
Q

progressive destruction of thyroid parenchyma, hurthle cell change, mononuclear infiltrates with germinal centers w/ or w/out extensive fibrosis

A

hashimoto thyroiditis

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13
Q

typically painless, lymphocytic inflammation in the thyroid, postpartum thyroiditis

A

subacute lymphocytic thyroiditis

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14
Q

autoimmune disorders characterized by the production of autoantibodies against multiple thyroid proteins, esp the TSH receptor

A

graves dz

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15
Q

thyroid stimulating immunoglobulin antibody

A

seen in 90% of graves dz pts

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16
Q

4 causes of exopthalmos

A

gravez dz: 1) mononuclear cell infiltration of retroorbital space 2) EOM inflammaiton and edema 3) accumulation of hydrophilic GAGs 4) increased adipocytes

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17
Q

pale follicular lumen with scalloped edges

A

graves dz

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18
Q

lab findings of Graves dz

A

inc T3/T4, dec TSH

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19
Q

thyrotoxicosis, opthalmopathy, dermopathy

A

graves dz

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20
Q

Occurs in geographic areas where soil, water, and food supply contain low iodine levels and the condition is present in >10% of the population

A

Endemic goiter

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21
Q

MC areas of endemic goiter

A

Mountains; Andes and Himalayas

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22
Q

Substances that interfere wit thyroid hormone synthesis and examples

A

Goiter opens - cabbage, cauliflower, brussle sprouts, turnips, cassava

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23
Q

Peak incidence of sporadic goiter occurring

A

Puberty or YA life

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24
Q

Inheritance pattern of genetic causes of sporadic goiter

A

AR

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25
Q

Diffuse, symmetrical enlargement of the thyroid gland. Follicles lines by crowded columnar cells that may pile up to form projections. Follicles can be distended or small.

A

Hyperplastic phase of nontoxic goiter

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26
Q

Follicular epithelium involutes to form colloid-rich glands in thyroid

A

Colloid involution phase of nontoxic goiter

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27
Q

Goiter growing behind sternum or clavicles

A

Intrathoracic or plunging goiter

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28
Q

Long standing goiter with autonomous nodule that produces hyperthyroidism

A

Plummer syndrome (toxic multinodular goiter)

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29
Q

Radio iodine scan of multinodular goiter will show

A

Uneven iodine uptake - even an occasional hot nodule

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30
Q

somatic mutations of TSH receptor signaling pathway are found in

A

toxic adenomas and toxic multinodular goiters

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31
Q

MC mutations causing thyroid autonomy in

A

GOF mutations in TSHR and GNAS

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32
Q

hallmark of all follicular adenomas

A

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

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33
Q

nonfuxnl adenomas appar as __________ on radionuclide scanning

A

cold nodules

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34
Q

most papillary carcinomas have GOD mutations involving

A

RET, NKRT1, or BRAF

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35
Q

RET/PTC rearrangements are more frequent in papillary cancers arising from

A

radiation exposure

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36
Q

BRAF mutations in papillary carcinomas correlate with

A

adverse prognostic factors - mets and extrathyroid extension

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37
Q

acquired mutations that activate RAS or PI-3K/AKT of the RTK pathway

A

follicular carcinoma

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38
Q

(2;3)(q13;p25) translocation

A

follicular carcinoma

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39
Q

germline RET mutations

A

medullary thyroid carcinomas

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40
Q

MC form of thyroid cancer

A

papillary carcinoma

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41
Q

branching papillae w/ dense fibrovascular stalk covered by single or multiple layers of cuboidal epi cells

A

papillary thyroid carcinoma morphology

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42
Q

optically clear or empty appearance of nuclei with invaginations of cytoplasm (“pseudo-inclusions”)

A

nuceli morphology of papillary thyroid carcinoma

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43
Q

concentrically calcified structures within cores of papillae

A

psammoma bodies - seen in papillary carcinoma of the thyroid

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44
Q

papillary carcinomas are _____ masses on scintisacans

A

cold

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45
Q

distinguish btwn follicular adenomas and minimally invasive carcinomas with

A

aval of the tumor-capsule-tyroid interface

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46
Q

common route of dissemination of follicular carcinomas and MC met sites

A

hematogenously - bone, brain, lungs, liver

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47
Q

large, pleomorphic giant cells w/ occasional multinucleate giant cells, spindle cells with sarcomatous appearance, and mixed spindle and giant cells

A

anaplastic thyroid carcinoma morphology

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48
Q

large bulky neck mass that spreads to adjacent neck structures and/or mets to the lung

A

anaplastic thyroid carcinoma

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49
Q

neuroendocrine neoplasm derived from parafollicular cells or C cells

A

medullary thyroid carcinoma

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50
Q

important marker for diagnosis and postop follow-up in pts with medullary carcinoma of the thyroid

A

calcitonin

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51
Q

morphological indicative of inherited predisposition to medullary carcinoma of the thyroid

A

multiple prominent clusters of C cell scattered throughout parenchyma of the thyroid tumor

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52
Q

polygonal ot simple-shaped cells that form nests, trabuecular, and possible follicles, acellular amyloid deposits, calcitonin demonstrable in cytoplasm

A

medullary carcinoma of the thyroid morphology

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53
Q

cases of medullary carcinoma of the thyroid are more agressive if ass’d with

A

MEN-2B

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54
Q

asymptomatic MEN-2 pts with RET mutations are offered

A

prophylactic throidectomy

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55
Q

MC b9 neoplasm of thyroid

A

follicular adenoma

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56
Q

genetic abnormality that is farily unique to thyroid cancer

A

PAX8/PPARG fusion, RAS, PI-3K, or BRAF mutations

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57
Q

midline neck mass, anterior to trachea

A

thyroglossal duct cyst

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58
Q

polygonal cells with central round uniform nuclei and light to dark pink cytoplasm

A

cheif cells in parathyroid gland

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59
Q

autonomous production of PTH usually d/t adenoma or hyperplasia

A

primary hyperthyroidism

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60
Q

compensatory hypersecretion of PTH usually from chronic renal failure

A

secondary hyperparathyroidism

61
Q

MCC of primary hyperparathyroidism

A

solitary parathyroid adenoma

62
Q

pericentromeric inversion of ch 11

A

cyclin D1 gene inversion

63
Q

location of sporadic mutations found in tumor suppressor gene of MEN1

A

ch11q13

64
Q

rare AR mutation in the CASR gene

A

familial hypocalciuric hypercalcemia

65
Q

increased osteoclast activity, peritrabecular dribrosis, cystic brown tumors

A

von Recklinghausen dz of the bone - generalized osteitis fibrosa cystric d/t severe hyperparathyroidism

66
Q

MC areas of sites of metastatic calcification

A

stomach, lungs, myocardium, and blood vessels

67
Q

hypercalcemia is MCly seen secondarily to these neoplasias

A

solid - lung, breask, head, neck; hematologic - multiple myeloma

68
Q

painful bones, renal stone, abdominal groans, psychic moans

A

s/s of primary hyperparathyroidism

69
Q

hypoparathyroidism, mucocutaneous candidiasis, primary renal insufficiency

A

autoimmune polyendocrine sydrome type 1 (APS1)

70
Q

gene mutation found in APS1

A

AIRE gene

71
Q

AD hypoparathyroidism is caused by

A

GOF mutation in CASR gene

72
Q

hallmark of hypocalcemia

A

tetany

73
Q

beta islet cells

A

insulin

74
Q

alpha islet cells

A

glucacon

75
Q

delta islet cells

A

somatostatin

76
Q

PP cells

A

pancreatic polypeptide

77
Q

D1 cells

A

VIP

78
Q

enterochromaffin cells

A

serotonin

79
Q

secretes GIP into the proximal small bowel

A

enterendocrine K cells

80
Q

secrets GLP-1 into the distal ileum and colon

A

L cells

81
Q

2 most important incretins for regulation of insulin release from pancreas

A

GIP, GLP-1

82
Q

enzymes that break down incretins

A

DPP4

83
Q

two new agents from tx of type 2 diabetes

A

GLP-1 agonists, DPP-4 inhibitors

84
Q

principal metabolic function of insulin

A

increase rate of glucose transport into certain cells in the body

85
Q

mediators of GLUT-4 transporter to the plasma membrane

A

AKT, CBL

86
Q

locus that has greatest contribution in genetic susceptibility to type 1 DM

A

HAL gene cluster on 6p21

87
Q

genetic profile of individuals with highest risk of inheriting T1 DM

A

DR3 or DR4 haplotype with a DQ8 haplotype

88
Q

islet autoantigen targets

A

insulin, GAD, ICA512

89
Q

most important environmental risk factor in development of T2 DM

A

obesity

90
Q

2 cardinal metabolic defects characterized by type 2 DM

A

1) decreased response of peripheral tissue to insulin (insulin resistance) 2) inadequate insulin secretion

91
Q

major tissues where insulin resistance manifests

A

liver, skeletal mm, and adipose tissue

92
Q

characteristic found in islet cells of long standing T2 DM pts

A

amyloid deposition

93
Q

MC mutations seen in MODY pts w/ beta cell function defects

A

GCK gene mutations

94
Q

insulin resistance, diabetes, hypertriglyceridemia, acanthosis nigricans, abnormal fat depotsition in the liver

A

lipoatrophic diabetes - impaired response to insulin

95
Q

classic triad of diabetes

A

polydipsia, polyphagia, polyuria

96
Q

severe acute metabolic complication seen MCly in T1 but can also be seen in T2 DM

A

DKA

97
Q

fatigue, N/V, severe abd pain, fruity breath, and deep, labored breathing

A

DKA s/s

98
Q

condition seen in T2 DM pts with severe dehdration and blood glucose levels that can be as high as 600-1200mg.dL

A

hyperosmolar hyperosmotic syndrome (HHS)

99
Q

MC acute metabolic complication in either type of DM

A

hypoglycemia

100
Q

recommended matinence of HbA1c in diabetics

A
101
Q

two factors that highly contribute to diabetic microangiopathy

A

AGEs and activated PKC

102
Q

leads to cataract formation in diabetics

A

accumulation of sorbitol

103
Q

decreased levels of NADPH compromises

A

GSH regeneration > decreased ROS defense

104
Q

MCC of death in diabetics

A

MI from atherosclerosis of the coronary aa

105
Q

PAS + ovoid or spherical, laminated nodules of matrix situated in the periphery of the glomerulus

A

Kimmelstiel-Wilson dz aka nodular glomerulosclerosis seen in DM pts

106
Q

pattern of acute pyelonephritis seen much MCly in diabetics than nondiabetics

A

necrotizing papillitis

107
Q

inhibits fibrinolysis and acts as a procoagulant in the formation of atherosclerotic plaques, levels are elevated in diabetics

A

PAI-1

108
Q

earliest manifestation of diabetic nephropathy

A

microalbuminuria

109
Q

LOF mutations leading to mTOR oncogenic signaling pathway in pancreatic endocrine neoplasms

A

PTEN, 2TSC

110
Q

nearly half of PanNETs have somatic mutations in either of these two genes

A

ATRX, DAXX

111
Q

pancreatic islet cell lesions, hypersecretion of gastric acid, severe peptic ulcerations

A

Zollinger-Ellison syndrome

112
Q

skin rash, anemia, increased levels of glucagon

A

alpha-cell tumors

113
Q

DM, cholelithiasis, steatorrhea, hypochlorhydria

A

delta-cell tumors

114
Q

watery diarrhea, hypokalemia, acholhydria

A

WDHA syndrome - VIPoma

115
Q

zona fasiculata

A

glucocorticoids (cortisol)

116
Q

zona glomerulosa

A

mineralocroticoids (aldosterone)

117
Q

zona reticularis

A

sex steroids (estrogens and androgens)

118
Q

elevated serum cortisol, low serum ACTH

A

ACTH-independent Cushing syndrome

119
Q

hormones that regulate sporadic macronodular adrenal hyperplasia

A

gastric inhibitory peptide, LH, ADH

120
Q

ACTH levels elevated and are not suppressed by admin of low dose dexamethasone, reduces ACTH with high dose

A

pituitary cushings

121
Q

ACTH levels elevated, ACTH secretion is insensitive to low or high dose dexamethazone

A

ectopic ACTH excretion

122
Q

ACTH levels low, ACTH secretion is insensitive to low or high dose dexamethazone

A

cushing’s d/t adrenal tumor

123
Q

MC manifestation of primary hyperaldosteronism

A

high blood pressure

124
Q

MCC underlying cause of primary hyperaldosteronism

A

b/l idiopathic hyperaldosteronism (IHA)

125
Q

hyperaldosteronism cause by a solitary adosterone-secreting adenoma

A

Conn syndrome

126
Q

secondary hyperaldosteronism activates RAAS and is characterized by

A

increased levels of plasma renin

127
Q

eosinophilic, laminated cytoplasmic inclusions found in aldosterone-producing adenomas

A

spironolactone bodies

128
Q

21-hydroxlase def is caused by mutations in

A

CYP21A2

129
Q

should be suspected in any neonate with ambiguous genitalia

A

CAH

130
Q

overwhelming nisseria infection, rapidly progessive hypotension, DIC ass’d with widespread purpura, rapidly developing adreocortical insufficiency

A

waterhouse friederichen syndrome

131
Q

MCC of primary adrenal insufficiency in developed countries

A

autoimmune adrenalitis

132
Q

chronic mucocutaneous candidiasis and abnormalities f the skn, dental enamal, and nails ass’d with combinations of organ-specific autoimmune disorders (ex: autoimmune adrenalitis)

A

APS1

133
Q

APS1 is ass’d with mutations of

A

AIRE

134
Q

adrenal insufficiency and autoimmune thyroiditis or DM T1

A

APS2

135
Q

inheritance pattern of congenital adrenal hypoplasia

A

x-linked

136
Q

autoantibodiees against IL-17 and IL-22

A

APS1

137
Q

MC adrenal neoplasm in children

A

carcinoma

138
Q

common carcinoma that mets to the adrenals

A

bronchogenic

139
Q

turns brown when incubated with potassium dichromate solution

A

pehochromocytoma

140
Q

definitive sis of malignancy in pehochromocytomas is based exclusively on

A

metastases

141
Q

lab diagnosis of pheo is based on increased urinary excretion of

A

free catecholamines + metabolites (VMA, metanephrines)

142
Q

MC manifestation of MEN-1

A

primary hyperparathyroidism

143
Q

leading cause of morbidity and morality in MEN-1

A

endocrine pancreatic tumors

144
Q

MC anterior pituitary tumor seen in MEN-1

A

prolactinoma

145
Q

MC site of gastrinomas in MEN-1 pts

A

duodenum

146
Q

pheo, medullary carcinoma of the thyroid, parathyroid hyperplasia

A

sipple syndrome, MEN2A

147
Q

MEN2A is clinically distinct from MEN1 d/t

A

GOF mutations in RET (ch10q11.2)

148
Q

pheo, multifocal thyroid carcinoma, ganglioneuromas, marfanoid habitus

A

MEN2B

Endocrine II (4 decks)

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