Y2S2B1 - Path - Endocrine

Front 1

Anterior lobe (adenohypophysis) of pituitary is derived from what?

Back 1

derived from Rathke’s pouch

Front 2

Posterior lobe (neurohypophysis) of pituitary is derived from what?

Back 2

derived from an outpouching of the floor of the 3rd ventricle

Front 3

The blood supply to the posterior pituitary is via the...

Back 3

inferior hypophysial artery, which is a branch from the internal carotid artery.

Front 4

proopiomelanocortin (POMC) precursor for adrenocorticotropic hormone (ACTH), a & b melanocyte stimulating hormone (MSH), b-endorphin, and b-lipotropin are secreted from what cell type?

Back 4

Corticotrophs. b-MSH is contained within ACTH (ACTH1-13). b-MSH is contained within b-lipotropin (b-LPH41-58). b-endorphin is also contained within b-lipotropin (b-LPH61-91). β-Lipotropin also stimulates lipolysis.

Front 5

What is the MC type of pleurihormonal pituitary adenoma?

Back 5

GH + Prl aka somatomammotroph

Front 6

macroadenoma is what size?

Back 6

>1 cm. micro is <1cm

Front 7

some macroadenomas can compress the pituitary stalk, impeding the delivery of dopamine from the hypothalamus to the anterior pituitary. This will free up the lactotrophs from dopaminergic inhibition resulting in increased release of prolactin from the anterior pituitary and hyperprolactinemia. This sequence of events is referred to as the what?

Back 7

“stalk effect.”

Front 8

Other causes of hyperprolactinemia (besides prolactinoma or hypothalamic dz)?

Back 8

Anti-dopaminergic drugs (e.g. phenothiazines, haloperidol)
Estrogen therapy (estrogen upregulates Prl gene)
Renal failure (b/c it is largely renally excreted)
Primary Hypothyroidism (inc TRH -> inc Prl)

Front 9

diabetes, hypertension, muscle weakness, arthritis, hypogonadism, cardiovascular disease are all manifestations of what pituitary adenoma?

Back 9

Somatotroph adenoma

Front 10

___% of somatotroph adenomas elaborate both GH and Prl (pleurihormonal adenoma). 40% express the ____ gene.

Back 10

30%; gsp gene

Front 11

You give a glucose suppression test and GH level is not suppressed one hour later. Dx?

Back 11

Somatotroph adenoma/acromegaly

Front 12

Which is better for diagnosing a somatotroph adenoma - MRI or CT?

Back 12

MRI

Front 13

In ~40% of somatotroph adenomas, there is a mutation in the alpha subunit that causes it to lose its GTPase activity. This results in persistent binding of GTP to the alpha subunit, which in turn results in constitutive activation of adenyl cyclase and unchecked proliferation of the somatotrophs. This mutation is referred to as the...

Back 13

“gsp oncogene.”

Front 14

typical somatotroph adenoma is composed of (acidophilic/basophilic) cells.

Back 14

acidophilic

Front 15

corticotroph adenomas are (acidophilic/basophilic) microadenomas

Back 15

basophilic

Front 16

How do you diagnose a corticotroph adenoma?

Back 16

24 hr urinary free cortisol level - best test
plasma ACTH level
MRI scan
Dexamethasone suppression test

Front 17

gonadotroph adenomase are usually (micro/macro)-adenomas

Back 17

macroadenomas

Front 18

Hypopituitarism accompanied by ________ is almost always of hypothalamic origin.

Back 18

diabetes insipidus

Front 19

______ encodes for a pituitary specific transcription factor. Mutations in it result in combined deficiencies of GH, prolactin, and TSH.

Back 19

POU1F1

Front 20

Types of hypothalamic (suprasellar) neoplasms?

Back 20

1- Craniopharyngioma
2- Gliomas
3- Germ cell tumors

Front 21

MC suprasellar tumor, accounts for 3- 5% of intracranial tumors. Bimodal age distribution (one peak 5 to 15 years and a second peak >65 years)
Derived from vestigial remnants of Rathke’s pouch
Benign, contain epithelial elements, often cystic with calcification
Arise in hypothalamus, may encroach on optic chiasm

Back 21

Craniopharyngioma

Front 22

Germ cell tumors arising in the suprasellar region that histologically look like seminomas in the testes and dysgerminomas in the ovaries are referred to as what?

Back 22

“germinomas.” Germ cell tumors arising in the suprasellar region are believed by some investigators to be derived from germ cells that migrated into this area during embryologic development.

Front 23

most consist of chromophobic cells or intensely eosinophilic cells (oncocytomas), usually are sparsely granular. account for 25% of pituitary adenomas and occur MCly in 4th decade

Back 23

Nonfunctioning adenoma

Front 24

compensatory inc in ____ in SIADH --> no hypervolemia, no inc BP and no peripheral edema

Back 24

ANP

Front 25

(hypo/hyper)-natremia -> cerebral edema -> inc ICP -> neurologic symptoms

Back 25

Hyponatremia

Front 26

MC cause of SIADH?

Back 26

Ectopic ADH secretion by malignant neoplasms (esp. small cell carcinoma of the lung)
Additional causes of SIADH include: non-neoplastic lung diseases, CNS trauma and infections, some drugs, and some endocrine disorders.

Front 27

A rare AD disorder caused by inherited mutations in the thyroid hormone receptor, which abolish the ability of the receptor to bind T3. Patients demonstrate a generalized resistance to thyroid hormones, despite high circulating levels of T3 and T4. Since the pituitary is also resistant to feedback from thyroid hormones, TSH levels tend to be high as well.

Back 27

Thyroid hormone resistance syndrome

Front 28

Inc susceptibility to Hashimoto is associated with polymorphisms in multiple immune regulatory genes especially...

Back 28

CTLA4 & PTPN22

Front 29

The CTLA4 gene encodes an inhibitory receptor expressed on the surface of what?

Back 29

Helper T-cells. CTLA-4 is an inhibitory receptor that prevents T-cell responses to self-antigens.

Front 30

The PTPN22 gene encodes a tyrosine phosphatase, which is expressed in _____ and also thought to inhibit ______.

Back 30

T-cells; T-cell function.

Front 31

Hashimoto is an autoimmune disorder initiated by autoreactive Helper T-cells. Activated B cells secrete wide variety of antithyroid antibodies, directed against:

Back 31

thyroid peroxidase, TSH-receptors, iodine transporter, thyroglobulin, etc.

Front 32

Thyroid histo shows lymphoid follicles with reactive germinal centers. Diagnostic of? There is also Hürthle cell metaplasia with infiltrates of lymphocytes and plasma cells

Back 32

Hashimoto

Front 33

Hashimoto pts are at increased risk for the development of what cancer?

Back 33

B-cell non-Hodgkin lymphomas, especially marginal zone lymphomas of mucosa-associated lymphoid tissues (MALT lymphomas).

Front 34

Graves pts have a familial predisposition and association with what genes?

Back 34

HLA-DR3, and polymorphisms in CTLA4 & PTPN22 genes

Front 35

papillary hyperplasia + scalloping in thyroid?

Back 35

Graves

Front 36

What are some goitrogens?

Back 36

cabbage, cauliflower, turnips, cassava root

Front 37

massive enlargement (up to >2000 gm) of thyroid, nodules, with a mixture of hyperplastic & dilated follicles, involutional changes: hemorrhage, fibrosis, calcification & cystic degeneration

Back 37

Multinodular Goiter

Front 38

Hyperthyroidism caused by a toxic multinodular goiter is also referred to as

Back 38

“Plummer syndrome.”

Front 39

Myxedema is d/t what?

Back 39

Accumulation of glycosaminoglycans

Front 40

~ 20% of thyroid adenomas have mutations in common with _______ carcinomas, which suggests that adenomas can progress to carcinoma

Back 40

follicular. Thyroid adenomas are often referred to as “follicular adenomas” since they are derived from the follicular epithelium and often form follicles.

Front 41

A fibrous capsule separates the neoplastic tissue from the surrounding compressed gland in thyroid adenomas. What are the different pattern types?

Back 41

trabecular (embryonal), microfollicular (fetal), macrofollicular and Hürthle cell (oncocytic) adenomas.

Front 42

a significant percentage of toxic adenomas have mutations in what?

Back 42

the TSH receptor signaling pathway

Front 43

Papillary CA may have gene rearrangements involving...? OR
Gain of function mutations in...?

Back 43

chromosome 10 -> constitutive expression of tyrosine kinase domain of RET protooncogene -> RET/PTC oncogene, strongly a/w radiation (20 – 40%); BRAF gene (30 – 50%) - constitutive activation of the Mitogen Activated Protein Kinase (MAP kinase) pathway. The MAP kinase pathway is involved in cellular differentiation and proliferation. Constitutive activation of the MAP kinase pathway results in the follicular epithelial cells receiving an unregulated growth signal. The presence of BRAF mutations in papillary carcinomas correlates with adverse prognostic factors like metastatic disease and extra-thyroidal extension.

Front 44

At time of Dx of papillary CA: lymph node involvement in ___% of cases, distant spread in ___%

Back 44

50%; 5%

Front 45

papillary fronds, empty looking nuclei “Orphan Annie eye”, nuclear grooves & psammoma bodies in thyroid gland. dx?

Back 45

Papillary CA. if you see psamomma in thyroid, pretty much diagnostic of papillary CA.

Front 46

Gain-of-function mutations of RAS and PIK3CA are a/w what?

Back 46

Follicular CA. Gain-of-function mutations of RAS and PIK3CA result in constitutive activation of the PI-3K/AKT signaling pathway, which results in the follicular epithelial cells receiving an unregulated growth signal.

Front 47

The PAX8-PPARG fusion gene is a/w what?

Back 47

Follicular CA

The PAX8-PPARG fusion gene is produced by a translocation. PAX8 is a homeobox gene involved in thyroid development. PPARG encodes a nuclear hormone receptor implicated in terminal differentiation of cells. The PAX8-PPARG fusion gene has been described in one third to one half of follicular carcinomas, but has not been described in other thyroid carcinomas.

Front 48

small uniform follicles in thyroid containing colloid with capsular and/or vascular invasion in a pt living in a mountainous area. dx?

Back 48

Follicular CA. may spread widely to distant organs (bones, lungs, liver, etc.), tumor tissue may take up radioactive iodine, patients often Rx’ed postop with thyroid hormones to decrease TSH

Front 49

what are variants of papillary CA?

Back 49

encapsulated, follicular tall cell

Front 50

what are variants of follicular CA?

Back 50

trabecular, Hurthle cell

Front 51

Serum ________ levels are used for monitoring tumor recurrence in follicular CA?

Back 51

serum thyroglobulin levels

Front 52

Medullary CA secretes calcitonin, but may also secrete:

Back 52

CEA, VIP, ACTH, etc. Patients followed post-op with serum calcitonin & CEA levels

Front 53

Sporadic & familial cases of medullary CA are associated with activating mutations in the _______________.

Back 53

RET protooncogene

Front 54

thyroid histo shows cell nests or trabeculae, amyloid deposits in the stroma, + for calcitonin & chromogranin, - for thyroglobulin

Back 54

Medullar CA

Front 55

Neuroendocrine type tumor cells are typically (small&uniform/large&disorganized).

Back 55

Small & Uniform

Front 56

Morphologic patterns of anaplastic CA?

Back 56

giant cell & spindle cell types

Front 57

What are the cell types in the parathyroid gland?

Back 57

Composed of chief cells and fat cells (fat up to 30%)
Chief cells may undergo transition to oxyphil cells (mitochondria), and water clear cells (glycogen)

Front 58

MC cause of hypercalcemia?

Back 58

Primary hyperparathyroidism

Front 59

overexpression of cyclin D1 or mutations in MEN 1 are a/w what?

Back 59

Parathyroid adenoma

Front 60

____________ is an AD disorder characterized by increased release of PTH from the parathyroid glands d/t decreased sensitivity of the chief cells to calcium ions. Inactivating mutations in the parathyroid calcium-sensing receptor (CASR) gene on chromosome 3q result in decreased responsiveness of the calcium-sensing receptors on the surface of the chief cells to calcium ions, resulting in increased release of PTH and hypercalcemia. CASR mutations have not been described in sporadic parathyroid tumors.

Back 60

Familial hypocalciuric hypercalcemia

Front 61

What is required to make the diagnosis of a parathyroid CA?

Back 61

cytologic features are not reliable, presence of invasion or metastases required to make Dx

Front 62

In some patients with long-standing secondary hyperparathyroidism due to chronic renal failure, the parathyroid glands may eventually become autonomous and secrete excessive amounts of PTH resulting in hypercalcemia, which closely resembles primary parathyroid hyperplasia. This condition is referred to as what?

Back 62

“tertiary” hyperparathyroidism

Front 63

AD Hypoparathyroidism is a/w what mutation?

Back 63

gain of function mutations in the CASR gene
↑ sensitivity of CASR to Ca++ -> ↓ PTH -> dec Ca++

Front 64

end-organ resistance to PTH causes what dz?

Back 64

PSEUDOhypoparathyroidism

Front 65

Which type of pseudohypoparathyroidism has a dec cAMP response to PTH (defic of Gsalpha), short stature, round face, short neck, short metacarpals/metatarsals (albright hereditary osteodystrophy - 4th finger is shorter than normal, being only slightly longer than the 5th finger)?

Back 65

PHP type 1A

Front 66

Which type of pseudohypoparathyroidism has a normal cAMP response to PTH, but with dec response to cAMP, phenotypically normal?

Back 66

PHP type 1B

Front 67

Aldosterone is regulated by what levels?

Back 67

renin-angiotensin & potassium levels

Front 68

Genetic causes of primary cortical hyperplasia of adrenal?

Back 68

Overexpression of non-ACTH hormone receptors
Mutations in genes regulating cAMP levels
Germline mutations in GNAS -> constitutively active Gsα (GNAS = gene that encodes the alpha subunit of the G protein Gs)

Front 69

Ectopic secretion of CRH or ACTH can come from what tumors?

Back 69

Small cell carcinoma of the lung
Medullary carcinoma of the thyroid
Carcinoid tumors
Pancreatic islet cell tumors

Front 70

ACTH is elevated -> adrenals are bilaterally hyperplastic

Back 70

Cushing disease. changes are the same with ectopic CRH or ACTH release

Front 71

Conn syndrome is what?

Back 71

adrenocortical adenoma. causes primary hyperaldosteronism

Front 72

AD disorder, caused by fusion of the aldosterone synthase & 11b-hydroxylase genes on chromosome 8. Fusion gene results in adrenocortical cells which secrete “hybrid” steroids, as well as cortisol & aldosterone. Aldosterone secretion is stimulated by ACTH, suppressible by administration of dexamethasone

Back 72

Glucocorticoid-remediable Hyperaldosteronism. 11b-hydroxylase catalyzes the conversion of 11-deoxycortisol to cortisol in the adrenal cortex

Front 73

DIC w/ widespread purpura, massive bilateral adrenal hemorrhage causing adrenocortical insufficiency, shock (d/t rapidly progressive hypotension). What is the problem and what are some possible causes of the adrenal hemorrhage?

Back 73

Waterhouse-Friderichsen syndrome (from Meningococcal septicemia usually)

bacterial seeding of small vessels, DIC, endotoxin-induced vasculitis, HS vasculitis
High mortality rate!

Front 74

Over 90% of Addisons is d/t:

Back 74

Autoimmune adrenalitis, Tuberculosis, AIDS, Metastatic cancers

Front 75

Extra-adrenal paraganglia: The branchiomeric (carotid bodies) & intravagal paraganglia are (sympathetic/parasympathetic), and the aorticosympathetic paraganglia (organs of Zuckerkandl) are (sympathetic/parasympathetic).

Back 75

Parasympathetic; sympathetic

Front 76

Pheochromocytoma 10%'s!

Back 76

10 % extra-adrenal
10 % bilateral in sporadic cases, but up to 50% are bilateral in familial cases
10 % in children
10 % are malignant in adrenal cases, but up to 40% are malignant in extra-adrenal cases (in extraadrenal ganglia called paragangliomas)

Front 77

Familial syndromes a/w pheochromocytoma?

Back 77

MEN-2A & MEN-2B
Neurofibromatosis, type 1
Von Hippel-Lindau disease

Front 78

Dx of pheochromocytoma is done by...

Back 78

24 hour urine for catecholamines & their metabolites: metanephrines & vanillylmandelic acid (VMA)
Imaging studies

Front 79

Classic “zellballen” growth pattern is most characteristic of what? The tumor cells are arranged into rounded nests surrounded by delicate fibrovascular tissue trabeculae.

Back 79

Pheochromocytoma
Biologic behavior of a pheochromocytoma cannot be accurately assessed based solely upon the histologic features; so that the diagnosis of malignancy in pheochromocytomas is based exclusively on the presence of metastases.

Front 80

What is the MC site of gastrinomas in MEN-1 (far more than pancreatic gastrinomas)?

Back 80

Duodenum. In addition, extra-pancreatic carcinoid tumors, thyroid and adrenocortical adenomas, and lipomas are more frequent than in the general population.

Front 81

Where is MEN 1 gene located? What are the 3 p's a/w MEN1?

Back 81

chromosome 11q13
1. Parathyroid hyperplasia or adenoma (80-95%)
2. Pancreatic Islet Cell tumors (75%)
- gastrinomas: peptic ulcers (Zollinger-Ellison syndrome)
- insulinomas: hypoglycemia
- VIPomas: watery diarrhea
3. Pituitary adenoma (66%); MC is prolactinoma, also GH & ACTH-producing adenomas

Front 82

Where is the RET protooncogene of MEN-2a located? What are 3 conditions a/w MEN2a?

Back 82

chromosome 10q11.2
1. C cell hyperplasia & Medullary thyroid carcinoma (100%)
2. Pheochromocytoma (40-50%), often bilateral and may arise in the extra-adrenal paraganglia
3. Parathyroid hyperplasia (10-20%)

Front 83

The mutation in RET w/ MEN-2b is different from MEN2a. There is siginificant clinical overlap. What conditions are a/w MEN-2b?

Back 83

1 - C cell hyperplasia & Medullary thyroid carcinoma (100 %)
2 - Pheochromocytoma (34%)
Plus:
**3 - Ganglioneuromas arising in the skin, eyes, mouth, GI tract, respiratory tract & bladder (100%)
**4 - Marfanoid body habitus (65%)

Front 84

A variant of MEN-2A w/ a strong predisposition to medullary thyroid CA (older age & more indolent than 2A & 2B)? Doesn't have other manifestations of 2A or 2B.

Back 84

Familial Medullary Thyroid Cancer

Front 85

Diagnosis of DM?

Back 85

A random glucose > 200 mg/dl with classic signs & symptoms
A fasting glucose > 126 mg/dl on more than one occasion
An abnormal glucose tolerance test in which the glucose level is > 200 mg/dl 2 hours after a standard carbohydrate load

Front 86

What factors, other than glucose, stimulate insulin release (not synthesis)?

Back 86

intestinal hormones and certain amino acids (leucine and arginine)

Front 87

Ketones in DM are...?

Back 87

acetoacetic acid, b-hydroxybutyric acid and acetone

Front 88

Which MODY is d/t mutations in hepatocyte nuclear transcription factor-4alpha (HNF-4alpha) -> severe beta-cell secretory defect

Back 88

MODY 1

Front 89

Which MODY is d/t mutations in glucokinase -> mild beta-cell secretory defect -> mild hyperglycemia. Up to 50% of females with glucokinase mutations develop what?

Back 89

MODY 2. Glucokinase converts glucose to glucose 6-phosphate, which is the first step in oxidation of glucose via glycolysis resulting in production of ATP. ATP is required for insulin secretion. up to 50% of women -> gestational diabetes.

Front 90

Which MODY is d/t mutations in hepatocyte nuclear transcription factor-1alpha (HNF-1alpha) -> severe beta-cell secretory defect

Back 90

MODY 3

Front 91

Which MODY is d/t mutations in insulin promoter factor 1 (IPF-1) --> decreased betacell mass predisposing to diabetes

Back 91

MODY 4

Front 92

Which MODY is d/t mutations in hepatocyte nuclear factor 1 (HNF-1beta -> severe beta-cell secretory defect

Back 92

MODY 5

Front 93

Which MODY is d/t mutations in neurogenic differentiation factor 1 (Neuro D1) --> decreased betacell mass predisposing to diabetes. Neuro D1 is also involved in expression of the insulin gene.

Back 93

MODY 6

Front 94

AGEs! a_______ can bind to BM's modified by AGEs. They can induce crosslinking of ______ in BM's. It can result in trapping of _____ in artery walls.

Back 94

plasma proteins; type IV collagen; LDLparticles

Front 95

AGEs bind to a receptor (RAGE) on certain cell types. This can cause what effects?

Back 95

release of cytokines & growth factors from macrophages
inc ECM production -> inc proliferation of vascular smooth muscle cells
inc endothelial permeability & procoagulant activity
release of cytokines & growth factors from mesangial cells

Front 96

inc intracellular glucose -> inc diacylgylcerol -> PKC activation --> results in many things such as?

Back 96

VEGF
endothelin & DECREASED nitric oxide
profibrogenic molecules, e.g., TGF-b
plasminogen activator inhibitor-1 (PAI-1)
pro-inflammatory cytokines by endothelial cells

Front 97

What has been implicated in the neovascularization characterizing diabetic retinopathy?

Back 97

VEGF

Front 98

glucose is converted to sorbitol via what enzyme?

Back 98

aldose reductase. this process consumes NAPDPH, which is required for glutathione reductase

Front 99

What is diabetic microandiopathy?

Back 99

thickening of capillary BMs, capillary BMs are more permeable, underlies the development of diabetic nephropathy & retinopathy

Front 100

Retinal ischemia in diabetes results in release of an angiogenesis factor, vascular endothelial cell growth factor (VEGF). VEGF in the anterior chamber results in formation of a neovascular membrane over the surface of the iris, which can then do what?

Back 100

occlude the outflow of aqueous humor through the trabecular meshwork. This results in increased intraocular pressure, which can then cause damage to the optic nerve (i.e. glaucoma). In retine, can also cause Hemorrhage & Traction retinal detachment.

Front 101

capillary microaneurysm in retina of diabetics is caused by what?

Back 101

decreased pericytes (supportive SM cells of capillaries)

Front 102

Majority of pancreatic endocrine neoplasms (islet cell tumors) are (functional/nonfunctional). What is the MC type?

Back 102

Majority are functional
Insulinomas are the MC type of islet cell tumors (90% are benign!)

Front 103

necrolytic migratory erythema (erosions and crusting seen primarily in the perioral and anogenital regions) is a/w which type islet cell tumor?

Back 103

Glucagonoma. also mild diabetes & anemia

Front 104

mild diabetes, cholelithiasis, steatorrhea, hypochlorhydria are a/w which type of islet cell tumor?

Back 104

Somatostatinoma. Somatostatin inhibits release of cholecystokinin. Cholecystokinin is the major hormone responsible for gallbladder contraction (in response to fatty meal) and pancreatic enzyme secretion. Somatostatin also inhibits release of gastrin resulting in hypochlorhydria.

Front 105

Which islet cell tumor causes a so-called “atypical carcinoid syndrome,” which is distinct from the (classical) carcinoid syndrome caused by gastrointestinal carcinoids?

Back 105

Enterochromaffin Cell (Carcinoid) Tumor (facial flushing, hypotension, periorbital edema, lacrimation)

Front 106

Ectopicomas (a pancreatic endocrine neoplasm) can secrete what different substances?

Back 106

ACTH, PTH, ADH

Front 107

What drug inhibits the Na+K+ATPase pump, which results in an increase in extracellular potassium. When Na+K+ATPase is inhibited, the sodium-calcium exchanger removes accumulated intracellular sodium in exchange for calcium.

Back 107

Digitalis

This exchange increases sarcoplasmic calcium and is the mechanism thought to be responsible for the positive inotropic effect of digitalis.

Front 108

Aldosterone defic can cause (acidosis/alkalosis)

Back 108

acidosis

Front 109

What is the MC cause of intractable epilepsy in children and is a frequent cause of epilepsy in adults?

Back 109

Focal cortical dysplasia

All forms of focal cortical dysplasia lead to disorganization of the normal structure of the cerebral cortex.

Front 110

What is a rare developmental disorder characterized by abnormal slits, or clefts, in the cerebral hemispheres?

Back 110

Schizencephaly

Front 111

What is a congenital malformation of the cerebral hemispheres in which the gyri are abnormally thick?

Back 111

Pachygyria

Front 112

tumor cells in pituitary staining positive for the proliferation marker Ki-67, overexpression of cyclin D1, p53 mutations, and epigenetic silencing of RB1 is a/w what?

Back 112

atypical adenomas, they have a higher propensity for aggressive behavior, including invasion and recurrence

Front 113

HRAS mutations in pituitary are observed in what?

Back 113

rarely occurring pituitary carcinomas

Front 114

an autoimmune disorder of the anterior pituitary. It occurs most commonly in young women late in pregnancy or during the postpartum period. It often results in hypopituitarism

Back 114

Lymphocytic Hypophysitis

Front 115

Most follicular adenomas are (cold/hot) nodules on scintillation scans

Back 115

cold

Front 116

Because of their propensity for (lymph/vascular) invasion, follicular carcinomas overall have a worse prognosis than the more common papillary carcinomas.

Back 116

vascular

Front 117

Trisomy __ is the most common cytogenetic abnormality in the familial form of papillary RCC.

Back 117

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