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ENRP > Exam 2 Path > Flashcards

Exam 2 Path Flashcards

1
Q

Pituitary adenoma:

Female vs male presentation of lactotroph adenoma

A

Females present at a young age with primary amenorrhea

Males present at an older age with mass effect

*PRL is a more common workup in young females vs males, therefore caught earlier

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2
Q

Pituitary adenoma type?

stromal hyalinization w/ psammoma bodies,
dense calcifications can become pituitary stones

A

Lactotroph adenoma

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3
Q

Pituitary adenoma:

Effect of a somatotroph adenoma in a younger child who is still growing

A

Gigantism (very tall)

*GH effect on bone prior to closure of epiphyseal plates

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4
Q

Pituitary adenoma:

Effect of a somatotroph adenoma in an adult who has finished growing

A

Acromegaly (thicc bones)

  • GH effect on bone after closure of epiphyseal plates
  • large face and hands, jaw, nose, lips, organs
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5
Q

Diagnostic test for pituitary somatotroph adenoma?

A

Measure serum IGF-1 (more stable and predictable)

Oral glucose tolerance test

*oral glucose would normally inhibit GH, if IGF-1 remains high after ogt then suggestive of somatotroph adenoma

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6
Q

Diagnostic test for corticotroph adenoma?

*in setting of high ACTH

A

Dexamethasone suppression test: pituitary corticotroph adenoma will be suppressed (decreased ACTH), ectopic ACTH will not be suppressed

*inferior petrosal sinus sampling would also show increased ACTH in setting of pituitary adenoma

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7
Q

Diagnosis?

Elevated ACTH and hyperpigmentation
Surgical hx = bilateral adrenalectomy

A

Nelson syndrome

removal of adrenals leads to increase in ACTH, which stilmulates MSH (melanocyte stimulating hormone), leads to hyperpigmentation

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8
Q

Paraneoplastic syndromes:

Ectopic ACTH releasing tumor type?

A

Small cell lung cancer

*causes cushing syndrome

  • cushing and SIADH can be caused by small cell
  • hypercalcemia of malignancy caused by squamous cell
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9
Q

Paraneoplastic syndromes:

Ectopic ADH releasing tumor type?

A

Small cell lung cancer

*causes SIADH

  • cushing and SIADH can be caused by small cell
  • hypercalcemia of malignancy caused by squamous cell
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10
Q

Paraneoplastic syndromes:

Ectopic PTHrP releasing tumor type?

A

Squamous cell lung carcinoma

  • hypercalcemia of malignancy caused by squamous cell
  • cushing and SIADH can be caused by small cell
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11
Q

Typical presentation of a gonadotroph pituitary adenoma?

A

Mass effect

*minimal secretion, “silent” or “null cell” adenoma

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12
Q

Diagnosis?

HA, N/V, papilledema,
Bilateral temporal hemianopsia
Under production of all pituitary hormones except prolactin

A

Pituitary lesion mass effect

*caused by neoplasm or hemorrhage

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13
Q

What transcription factor is elevated in most pituitary adenomas? (somato-, lacto-, thyro-)

A

PIT-1 transcription factor

*less clinically useful because it does not narrow it down very much

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14
Q

What transcription factor is elevated in corticotroph pituitary adenomas? (cushings disease)

A

TPIT transcription factor

*more useful because it is specific for corticotroph adenomas

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15
Q

What SOMATIC mutation is associated with somatotroph pituitary adenomas?

A

GNAS mutation

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16
Q

Somatic GNAS mutation pathophysiology in development of pituitary somatotroph adenoma?

A
  1. GNAS mutation = loss of function in Gs-a GTPase (part of GH receptor),
  2. Leads to increased GTP (cant break it down)
  3. Uninhibited cAMP driven somatotroph proliferation
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17
Q

What SOMATIC mutation is associated with corticotroph pituitary adenomas?

A

USP8 mutation

*leads to EGFR upregulation

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18
Q

What GERMLINE mutation is associated with somatotroph pituitary adenomas?

A

AIP (FIPA)

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19
Q

Other pituitary neoplasms:

Cystic mass lined with ciliated columnar epithelium
Can cause mass effect and/or rupture (pituitary inflammation and meningitis)

A

Rathke’s cleft cyst

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20
Q

Other pituitary neoplasms:

Cyst lined with squamous epithelium,
Calcified cyst
Wet keratin
Presents with growth retardation or hypopituitarism

A

Craniopharyngeoma

*kid form (adamantinomatous)

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21
Q

Other pituitary neoplasms:

Cyst lined with squamous epithelium,
Papillary structure
Presents with increased ICP or hypopituitarism

A

Craniopharyngeoma

*adult form (papillary)

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22
Q

Infarct and death of the pituitary due to disrption of the diaphragma sella,
CSF leak into the sella that compresses the pituitary

A

Primary empty sella syndrome

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23
Q

Expansion of the pituitary leading to infarction and death, leaving empty space in sella

A

Secondary empty sella syndrome

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24
Q

Diagnosis?

New mom presents with lactational dysfunction (hypopituitarism) and empty space in sella on imaging

A

Sheehan syndrome

*postpartum necrosis of anterior pituitary (secondary empty sella syndrome: pituitary expands in pregnancy leading to infarct and death of pit)

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25
Q

Diagnosis?

Polyuria and polydipsia
Hypernatremia (excess water loss)
DDAVP administration leads to water retention

A

Central DI

  • if no response to DDAVP then it would be nephrogenic DI
  • thirst is appropriate
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26
Q

Diagnosis?

Low urine output (concentrated)
Thirsty
Hyopnatremia
Lung tumor

A

SIADH

*inappropriate thirst

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27
Q

Gross findings for cushing syndrome due to priamry adrenal disease

A

Unilateral well-circumscribed adrenal cortical adenoma

*low ACTH due to primary adrenal dz

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28
Q

Gross findings for cushing syndrome due to secondary hyperadrenalism

A

Bilateral cortical hypertrophy of adrenal glands

  • high ACTH causes hyperplasia of adrenals
  • due to neoplastic release of ACTH
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29
Q

What is Conn syndrome?

HTN, hypokalemia, hypomagnesemia

A

Primary hyperaldosteronism

*idiopathic > adenoma

30
Q

Diagnosis of hyperaldosteronism (primary vs secondary)?

HTN, hypokalemia

A

assess plasma renin activity (PRA)

  • high PRA = secondary hyperaldosteronism
  • low PRA = primary hyperaldosteronism
31
Q

Adrenocortical CARCINOMA is more likely to secrete what hormone type?

A

androgens (virilizing)

32
Q

Adrenogenital syndromes due to 21 hydroxylase def:

Complete lack of 21-hydroxylase
Virilization seen at birth
Hyponatremia, Hyperkalemia, Hypotension

A

Classic “salt wasting”adrenogenitalism

33
Q

Adrenogenital syndromes due to 21 hydroxylase def:

Partial lack of 21-hydroxylase
Virilization
Some mineralcorticoid release (no salt wasting)

A

Simple virilizing syndrome

34
Q

Adrenogenital syndromes due to 21 hydroxylase def:

Partial lack of 21-hydroxylase
Precocious puberty w/ acne and hirsutism

A

Nonclassic/ Late onset virilism

35
Q

Treatment for adrenogenital syndromes due to 21-hydroxylase def.?

A

Glucocorticoids

36
Q

Diagnosis?

Hypotension, abdominal pain
F, N/V
Hyperkalemia, Hyponatremia, Hypoglycemia

A

Acute adrenal insufficiency

*caused by rapid withdrawal of steroids, adrenal hemorrhage, stress, infection, trauma, burns, etc.

37
Q

Diagnosis?

Chronic malaise and fatigue
Anorexia, weight loss, arthralgias
Skin hyperpigmentation

A

Primary chronic adrenocortical insufficency (Addison dz)

*primary adrenal dz so there will be elevated ACTH to try and compensate, leads to hyperpigmentation due to MSH stimulation (like in Nelson synd)

38
Q

Diagnosis?

Adrenalitis (adrenal insufficiency)
Parathyroiditis
Hypogonadism
Pernicious anemia
Mucocutaneous candidiasis
Ectodermal dystrophy (teeth and nail probs)
A

Autoimmune polyendocrine syndrome type 1

*APECED

39
Q

Diagnosis?

Adrenalitis (adrenal insufficiency)
Thyroiditis
T1DM

A

Autoimmune polyendocrine syndrome type 2

40
Q

Diagnosis?

HTN, HA, palpitations, diaphoresis
Urine and plasma metanephrines elevated

A

Pheochromocytoma (or paraganglioma)

41
Q

MEN 1 tumors

A

*Pituitary adenoma
*Pancreatic endocrine tumor
Parathyroid adenoma

*=specific to this MEN syndrome

42
Q

MEN 2A tumors

A
  • Parathyroid adenoma
  • *Pheochromocytoma
  • *Medullary thyroid carcinoma
  • =shared with MEN1
  • *=shared with MEN2B
43
Q

MEN 2B tumors

A

Pheochromocytoma
Medullary thyroid carcinoma
*Mucosal neuromas

  • Marfanoid body habitus
  • =specific to this MEN syndrome
44
Q

What tumor is seen in both MEN1 and MEN2A?

A

Parathyroid adenoma

45
Q

What tumors are seen in both MEN2A and MEN2B?

A

Pheochromocytoma

Medullary thyroid carcinoma

46
Q

Pancreatic neuroendocrine tumors:

Pt presents with hypoglycemia and pancreatic mass
Labs show elevated insulin and C-peptide
Amyloid on histo

A

Insulinoma (B-cell tumor)

47
Q

Pancreatic neuroendocrine tumors:

Pt presents with epigastric pain and pancreatic mass
Gastric/duodenal ulcers unresponsive to tx

A

Gastrinoma (G-cell tumor)

*Zollinger ellison synd

48
Q

Pancreatic neuroendocrine tumors:

Pt presents with RUQ pain, steatorrhea and pancreatic mass
Labs show hyperglycemia

A

Somatostatinoma (delta-cell tumor)

*somatostatin shuts up the other hormones (decreased CCK leads to decreased gallbladder motility, decreased insulin leads to hyperglycemia)

49
Q

Pancreatic neuroendocrine tumors:

Pt presents with hyperglycemia, LE dermatitis and pancreatic mass
May also have depression, DVT

A

Glucagonoma (a-cell tumor)

50
Q

Pancreatic neuroendocrine tumors:

Pt presents with watery diarrhea and pancreatic mass
Labs show hypokalemia and achlorhydria (low HCl in gastric secretions)

A

VIPoma (D1 cell tumor)

WDHA syndrome

51
Q

Diagnosis?

Young child with impaired development, low growth, coarse facial features, umbilical hernia
Hint of living in iodine deficient area

A

Congenital hypothyroidism (cretinism)

52
Q

Diagnosis?

Young adult with mental and physical slowing, weight gain, cold intolerance, low CO and high cholesterol

A

Myxedema (hypothyroidism of the adult)

53
Q

Thyroiditis types:

Diffuse painless thyroid enlargement
TPO and Tg auto-ab
Histo: lymphocytes w/ germinal centers, atrophic follicles with eosinophilic change (Hurthle cell metaplasia)

A

Hashimoto thyroiditis

  • T-cell mediated (breakdown of self tolerance)
  • hyper then hypothyroid
54
Q

Thyroiditis types:

TRANSIENT thyroid irregularities (i.e. postpartum)
Painless enlargement

A

Subacute lymphocytic thyroiditis

*hypo or hyperthyroid

55
Q

Thyroiditis types:

PAINFUL thyroid enlargement
Histo: granulomas
?preceded by viral infection

A

Granulomatous thyroiditis

*hypo or hyperthyroid

56
Q

Thyroiditis types:

Fibrosis of thyroid tissue into nearby tissues
IgG4 related dz
Histo: fibrosis, lymphocytes, PLASMA CELLS

A

Riedel thyroiditis

*euthyroid

57
Q

Thyroid tumors:

Benign
Clonal proliferation of follicular cells w/ “thyroid autonomy”
Capsule intact, no nuclear features

A

Follicular adenoma

58
Q

Thyroid tumors:

Malignant
Histo: follicular architecture, enlarged nuclei with clear appearance (orphan annie eye)
RAS mutations

A

Papillary thyroid carcinoma: follicular variant

*nuclear features (orphan annie eye) determine papillary carcinoma!!!

59
Q

Thyroid tumors:

Malignant
Histo: papillary architecture w/ columnar-looking cells, enlarged nuclei with clear appearance (orphan annie eye)
RET or BRAF mutations
Older patients, more aggressive

A

Papillary thyroid carcinoma: tall cell variant

*nuclear features (orphan annie eye) determine papillary carcinoma!!!

60
Q

Thyroid tumors:

Malignant
Histo: papillary architecture w/ connective tissue, enlarged nuclei with clear appearance (orphan annie eye)
RET or BRAF mutations
Younger patients, metz more common

A

Papillary thyroid carcinoma: diffuse sclerosing variant

*nuclear features (orphan annie eye) determine papillary carcinoma!!!

61
Q

Thyroid tumors:

Malignant, common in areas w/ iodine deficient goiter
Histo: follicular architecture, capsule invasion, angioinvasion
RAS, PAX8/PPARG mutations

A

Follicular thyroid carcinoma

62
Q

Thyroid tumors:

Malignant, very deadly, elderly
Histo: high grade anaplastic features
p53 mutation

A

Anaplastic thyroid carcinoma

63
Q

Thyroid tumors:

Malignant
Histo: c-cell hyperplasia, blue cells with dispersed chromatin, amyloid
RET mutation

A

Medullary thyroid carcinoma

  • most are sporadic (worse prognosis)
  • familial = best prognosis
  • also think of MEN 2A & B (prophylactic thyroidectomy)
64
Q

Diagnosis?

Elevated PTH, Elevated Ca
Typically asymptomatic
Short QT

A

Primary hyperparathyroidism (hypercalcemia)

*adenoma, hyperplasia, carcinoma

65
Q

Diagnosis?

Elevated PTH, Low Ca
Stupor, numbness, cramps/spasms, Trosseau/Chovstek signs
Long QT

A

Secondary hyperparathyroidism (hypocalcemia)

*tissues dont respond to PTH => hypersecretion of PTH and hyperplasia of parathyroids

66
Q

Diagnosis?

Low PTH, Elevated Ca
Painful bones, renal stones, abdominal groans, psychiatric moans
Short QT

A

Hypercalcemia of malignancy (symptomatic hypercalcemia)

*will have elevated PTHrP or Vit D mediatied or local osteolytic (breast ca, multiple myeloma)

67
Q

Diagnosis?

Low PTH, Low Ca

A

Primary hypoparathyroidism

*can be caused by neck surgery, autoimmune dz, DiGeorge synd (3rd & 4th pharyngeal arch underdev, CaSR activating mutation, familial mutation in PTH synth)

68
Q

Effect of an activating mutation in CaSR:

PTH
Ca
Urine Ca

A

PTH: Low
Ca: Low
Urine Ca: High (renal excretion)

*AD mutation

69
Q

Effect of an inactivating mutation in CaSR:

PTH
Ca
Urine Ca

A

PTH: High
Ca: High
Urine Ca: Low (renal retention)

70
Q

Diagnosis?

nl or high PTH, Low Ca

A

Pseudohypoparathyroidism

  • tissues unresponsive to PTH
  • can lead to Albright osteodystrophy
71
Q

Diagnosis?

Child with short stature and obesity
Short fingers and toes
GNAS mutation (PTH receptor pathway)
A

Albright hereditary osteodystrophy

*results in pseudohypoparathyroidism (unresponsive to PTH)

ENRP (5 decks)

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