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AP reviewer > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Deficiency of 21-hydroxylase: Laboratory finding.

A

Elevated 17-hydroxyprogesterone.

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2
Q

Congenital lipoid adrenal hyperplasia: Definition.

A

Severest form of congenital adrenal hyperplasia: All gonadal and adrenal cortical steroids are markedly underproduced.

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3
Q

Congenital lipoid adrenal hyperplasia: Genes (2).

A

StAR (steroidogenic acute regulatory) protein.

P-450scc.

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4
Q

Classic presentation of congenital adrenal hyperplasia in females:

A. Newborn.
B. Older (3).

A

A. Virilization.

B. Postpubertal: Oligomenorrhea, hirsutism, acne.

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5
Q

Classic presentation of congenital adrenal hyperplasia in males:

A. Newborn.
B. Older (3).

A

A. Salt-losing crisis.

B. Prepubertal: Precocious puberty.

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6
Q

Non-classic presentation of congenital adrenal hyperplasia (3).

A

Newborns: Normal.

Around puberty: Virilization.

Pregnancy: May present with adrenal insufficiency.

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7
Q

Congenital adrenal hyperplasia: Histopathology (3).

A

All three cortical layers are thickened, but especially the zona reticularis.

Loss of zonation.

Lipid-poor cells.

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8
Q

Congenital lipoid adrenal hyperplasia: Histopathology.

A

Cholesterol-overloaded cells with rupture and cholesterol esters.

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9
Q

Congenital adrenal hyperplasia: Complication.

A

Adrenal cortical adenoma or carcinoma.

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10
Q

Congenital adrenal hyperplasia: Effect on adrenal medulla.

A

Glucocorticoid deficiency can impair development of the medulla, resulting in epinephrine deficiency and hypoglycemia.

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11
Q

Autoimmune adrenal insufficiency:

A. Frequency.
B. Antibodies (3).

A

A. Accounts for 75-90% of cases of primary adrenal insufficiency.

B. 21-hydroxylase, 17-hydroxylase, P-450scc.

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12
Q

Primary vs. secondary adrenal insufficiency: Biochemical differences (3).

A

Primary: Low ACTH, low aldosterone, high renin.

Secondary: High ACTH, normal aldosterone, normal renin.

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13
Q

Primary vs. secondary adrenal insufficiency: Gross-pathology difference.

A

Primary: Small, pale adrenal gland.

Secondary: Enlarged gland.

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14
Q

Adrenal insufficiency: How much adrenal tissue is essential to normal function?

A

About 10%.

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15
Q

Primary adrenal cortical hyperplasia: Types (3).

A

ACTH-independent macronodular hyperplasia.

Primary pigmented nodular adrenal cortical disease.

Other.

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16
Q

ACTH-independent macronodular hyperplasia: Syndrome that can cause it, and its gene.

A

McCune-Albright syndrome, GNAS1.

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17
Q

Primary pigmented nodular adrenal cortical disease: Syndromes (2).

A

Carney’s complex.

Isolated primary pigmented nodular adrenal cortical disease.

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18
Q

Primary pigmented nodular adrenal cortical disease: Genes (2).

A

PRKAR1A.

PDE11A.

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19
Q

Other syndromes (2) that can cause bilateral adrenal hyperplasia.

A

MEN-1.

FAP.

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20
Q

Secondary adrenal cortical hyperplasia: Causes (2).

A

Pituitary adenoma or hyperplasia.

Ectopic ACTH.

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21
Q

Adrenal cortical hyperplasia: Presentation.

A

Primary: Various endocrine abnormalities.

Secondary due to pituitary: Severe, typical Cushing’s syndrome.

Secondary due to ectopic ACTH: Severe, atypical Cushing’s syndrome.

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22
Q

Adrenal cortical hyperplasia: Pharmacological therapy.

A

Ketoconazole and similar drugs.

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23
Q

Adrenal cortical hyperplasia: Degree of enlargement (3).

A

Severe: Ectopic ACTH, AIMAH.

Mild or moderate: Pituitary disease, PPNAD.

Grossly inapparent: Conn’s syndrome due to hyperplasia of zona glomerulosa.

Enlargement may be nodular or diffuse.

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24
Q

Hyperplasia of zona glomerulosa: Histopathology (3).

A

Involvement limited to the periphery of the gland.

Abnormal continuity of the zona.

More than 5 nests thick.

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25
Q

ACTH-independent macronodular adrenal cortical hyperplasia: Histopathology (2).

A

Mixture of large clear cells and small compact cells.

Nodules of cells containing dark brown pigment.

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26
Q

Primary pigmented nodular adrenal cortical disease: Histopathology.

A

Cortical tissue between nodules is atrophic and disorganized.

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27
Q

Adrenal cortical hyperplasia: Immunohistochemistry.

A

AIMAH: 3β-hydroxysteroid dehydrogenase.

PPNAD: Synaptophysin, 17α-hydroxylase.

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28
Q

Clinical findings that favor adrenal adenoma over adrenal hyperplasia (2).

A

Solitary, unilateral nodule.

Evidence of autonomous growth.

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29
Q

Adrenal cortical adenoma: Familial syndromes (3).

A

MEN-1.

Familial hyperaldosteronism.

Congenital adrenal hyperplasia.

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30
Q

Spoardic adrenal cortical adenoma associated wth Conn’s syndrome: Genes (3).

A

KCNJ5: Potassium channel.

ATP1A1, ATP2B3: Na/K-ATPases.

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31
Q

Adrenal cortical adenoma: Most common hormonal excess.

A

None: Most adenomas are nonfunctioning.

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32
Q

Adrenal cortical adenomas: Presentations of the functioning types (4).

A

Cushing’s syndrome.

Conn’s syndrome.

Virilization (rare).

Feminization (strongly suggests adenocarcinoma).

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33
Q

Adrenal cortical adenomas: Possible colors (3).

A

Golden yellow: Conn’s syndrome.

Mahogany: Oncocytic.

Black: Pigmented (lipofuscin).

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34
Q

Adrenal cortical adenoma associated with Conn’s syndrome: Histopathology (2).

A

Clear, lipid-rich cytoplasm.

Spironolactone bodies (if spironolactone has been given).

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35
Q

Adrenal cortical adenoma: Histopathology of non-adenomatous tissue (2).

A

Cushing’s syndrome: Atrophy of zona reticularis.

Conn’s syndrome: Paradoxical hyperplasia of zona glomerulosa.

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36
Q

Electron microscopy of adrenal cortical adenomas: General (3).

A

Much lipid.

Much smooth endoplasmic reticulum.

Many mitochondria.

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37
Q

Electron microscopy of adrenal cortical adenomas: Mitochondria (2).

A

Aldosterone-producing cells: Lamellar cristae.

Steroid-producing cells: Tubulovesicular cristae.

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38
Q

Epithelioid angiomyolipoma: Biological behavior.

A

Can be malignant.

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39
Q

Epithelioid angiomyolipoma: Histopathology (2).

A

Polygonal epithelioid cells with much cytoplasm and sometimes with a large nucleolus, forming nests or sheets.

Some cells may be multinucleate or bizarre.

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40
Q

Epithelioid angiomyolipoma:

A. Immunohistochemistry.
B. Electron microscopy.

A

A. Cells express melanocytic and myoid markers.

B. Melanosomes and pre-melanosomes.

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41
Q

Adrenal cortical carcinoma: Hereditary syndromes (5).

A

Li-Fraumeni.

Beckwith-Wiedemann.

MEN-1.

Carney’s complex.

Hereditary isolated glucocorticoid deficiency.

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42
Q

Adrenal cortical carcinoma: Genes mutated in sporadic tumors (6).

A

TP53.

β-Catenin.

Menin.

PRKAR1A.

IGF-II.

MC2-R.

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43
Q

Adrenal cortical carcinoma:

A. How many are functional?
B. What is the most common function?

A

A. About 79%.

B. Virilization due to secretion of 17-ketosteroids and DHEA.

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44
Q

Adrenal cortical carcinoma: Treatment (2).

A

Complete resection if possible; otherwise, mitotane.

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45
Q

Adrenal cortical carcinoma: Typical size and weight.

A

14-15 cm; 100-1000 g.

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46
Q

Adrenal cortical carcinoma: Features diagnostic for malignancy (3).

A

Weight greater than 100 g.

Vascular invasion.

Metastasis.

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47
Q

ACTH-independent macronodular hyperplasia: Other associated genes.

A

ACTH receptor.

GIP, β-adrenergic receptor, LH receptor.

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48
Q

Adrenal cortical carcinoma: Diagnostic immunohistochemistry (4,2,2).

A

Positive: Inhibin-α, steroidogenic factor-1, Melan-A, D11.

Negative: β-Catenin (aberrant loss), chromogranin,

Variable: Cytokeratins, synaptophysin.

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49
Q

Adrenal cortical carcinoma: Prognostic immunohistochemistry (2).

A

Ki-67.

Cyclin E: Positive staining implies advanced stage.

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50
Q

Vascular invasion by adrenal cortical carcinoma:

A. Definition.
B. Sites of metastasis.

A

A. Thrombus must accompany tumor cells.

B. Liver, lung, lymph nodes.

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51
Q

Adrenal medullary hyperplasia: Associations (4).

A

MEN 2a, MEN 2b.

Beckwith-Wiedemann syndrome.

Cystic fibrosis.

Not: VHL syndrome, neurofibromatosis.

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52
Q

Adrenal cortical carcinoma: Histopathologic features suggestive of malignancy (5).

A

Necrosis.

Cellular atypia.

Increased mitotic activity.

Invasion beyond the adrenal gland.

Broad fibrous bands.

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53
Q

MEN 2a:

A. Synonym.
B. Inheritance.
C. Components.

A

A. Sipple’s syndrome.

B. Autosomal dominant.

C. Pituitary hyperplasia, medullary carcinoma of the thyroid, pheochromocytoma.

54
Q

MEN 2a and MEN 2b: Gene and its location.

A

RET on chromosome 10q11.2.

55
Q

MEN 2b:

A. Inheritance.
B. Components.

A

A. Autosomal dominant.

B. Same as those of MEN 2a, plus mucosal neuromas.

56
Q

Adrenal medullary hyperplasia: Gross pathology (3).

A

Usually bilateral.

Nodular or diffuse.

By definition, nodules are less than 1 cm.

57
Q

Adrenal medullary hyperplasia: Histopathology (2).

A

Cells may be enlarged or pleomorphic; may show increased mitotic activity.

Hyperplasia is histopathologically indistinguishable from pheochromocytoma.

58
Q

Adrenal medullary hyperplasia: Special histopathologic feature.

A

Hyaline globules in MEN 2 syndromes.

59
Q

Pheochromocytoma: How many are hereditary?

A

Almost half.

60
Q

Pheochromocytoma: Genes (7).

A

VHL.

RET.

NF.

SDHA, SDHB, SDHC, SDHC.

61
Q

Pheochromocytoma: How many are asymptomatic?

A

Up to 25%.

62
Q

Pheochromocytoma: Instigators of symptoms (4).

A

Anesthesia.

Manipulation of the tumor.

Certain foods, drugs.

63
Q

Pheochromocytoma: Diagnostic tests (4).

A

Urinary and plasma catecholamines.

Urinary metanephrines.

Urinary vanillylmandelic acid.

64
Q

Pheochromocytoma: Histologic architecture.

A

Zellballen surrounded by sustentacular cells.

65
Q

Pheochromocytoma: Cytology of tumor cells (3).

A

Granular cytoplasm.

Large nucleoli.

Intranuclear cytoplasmic inclusions.

66
Q

Composite pheochromocytoma.

A

Also contains areas resembling neuroblastoma, ganglioneuroblastoma, or typical ganglioneuroma.

67
Q

Pheochromocytoma: More specific immunohistochemical stains (2).

A

Tyrosine hydroxylase.

SDHB: Expression is lost in any tumor exhibiting a mutation of any of the genes for succinate dehydrogenase.

68
Q

Pheochromocytoma: Significance of SDHB (2).

A

Usually mutated in extra-adrenal paraganglioma rather than in pheochromocytoma.

Mutation in pheochromocytoma suggests malignancy.

69
Q

Pheochromocytoma: Electron microscopy.

A

Neurosecretory granules.

70
Q

Pheochromocytoma: How to recognize a malignant one.

A

Only by the demonstration of distant metastases.

Histology does not help, even when there are bizarre tumor giant cells.

71
Q

Ganglioneuroma: Origin (2).

A

De novo.

Maturation of neuroblastoma or ganglioneuroblastoma.

72
Q

Ganglioneuroma: Possible laboratory findings (4).

A

Elevated HVA, VMA, VIP, and/or serotonin.

73
Q

Ganglioneuroma: Cellular components (3).

A

Ganglion cells.

Schwann cells.

Mature fibroblasts.

74
Q

Ganglioneuroma: Possible source of difficulty in histologic diagnosis.

A

Scarcity of ganglion cells can cause confusion with neurofibroma.

75
Q

Ganglioneuroma: Immunohistochemistry (3).

A

Positive: S-100, synaptophysin, neurofilament.

76
Q

Ganglioneuroma: Electron microscopy of ganglion cells (2).

A

Peripheral rough endoplasmic reticulum.

Neurosecretory granules.

77
Q

Ganglioneuroma: Clinical behavior.

A

Benign, unless it undergoes transformation to an MPNST.

78
Q

Ganglioneuroblastoma: Epidemiology.

A

Occurs mainly in toddlers.

79
Q

Ganglioneuroblastoma: Most common site.

A

Abdomen.

Ganglioneuroma: Posterior mediastinum.

80
Q

Ganglioneuroblastoma: Components.

A

Ganglioneuromatous component: Usually more than 50%.

Neuroblastomatous component.

81
Q

Ganglioneuroblastoma: Subtypes (3).

A

Nodular classic.

Nodular atypical.

Intermixed.

82
Q

Ganglioneuroblastoma: Nodular classic subtype.

A

Sharp demarcation between neuroblastomatous nodule and surrounding ganglioneuromatous component.

83
Q

Ganglioneuroblastoma: Nodular atypical subtype (3).

A

No gross or microscopic nodules.

Ganglioneuromatous component forms a thin rim.

Metastases resemble neuroblastoma.

84
Q

Ganglioneuroblastoma: Intermixed subtype (2).

A

No gross or microscopic nodules.

Microscopic foci of neuroblastomatous component.

85
Q

Ganglioneuroblastoma: Prognostic difference among subtypes.

A

Intermixed: Better.

Nodular: Worse.

86
Q

Ganglioneuroblastoma: Biochemical difference among subtypes.

A

Nodular subtype secretes more catecholamines.

87
Q

Neuroblastoma: Most common sites (2).

A

Adrenal gland.

Posterior mediastinum.

88
Q

Neuroblastoma: Classic signs of metastasis (3).

A

Periorbital ecchymoses.

Proptosis.

“Blueberry-muffin” skin.

89
Q

Neuroblastoma: Paraneoplastic syndromes (2).

A

Intractable diarrhea due to secretion of VIP.

Opsoclonus-myoclonus syndrome.

90
Q

Neuroblastoma: Histologic architecture.

A

Cells are arranged in vague lobules and may form Homer Wright rosettes (filled with pink fibrillary matter).

91
Q

Pheochromocytoma: Prognosis.

A

Five-year survival rate

− Benign: 95%.
− Malignant: 44%.

92
Q

Neuroblastoma: Subtypes.

A

Undifferentiated.

Undifferentiated and pleomorphic.

Poorly differentiated.

Differentiating.

93
Q

Neuroblastoma: Undifferentiated (2).

A

Neuroblasts show no differentiation toward ganglion cells.

No neuropil.

94
Q

Neuroblastoma: Undifferentiated and pleomorphic.

A

Same as undifferentiated neuroblastoma, except that neuroblasts are larger and more pleomorphic and have more cytoplasm.

95
Q

Neuroblastoma: Poorly differentiated.

A

Fewer than 5% of neuroblasts show differentiation toward ganglion cells.

96
Q

Neuroblastoma: Differentiating.

A

More than 5% of neuroblasts show differentiation toward ganglion cells.

97
Q

Mitosis-karyorrhexis index: Number of cells to be counted.

A

5000.

98
Q

Mitosis-karyorrhexis index: Ranges.

A

Low: Less than 2%.

Intermediate: 2-4%.

High: More than 4%.

99
Q

Neuroblastoma: Mutation that confers poor outcome.

A

Amplification of MYCN (more than 10 copies).

100
Q

Prognosis of neuroblastoma: Patient over 5 years of age.

A

Any neuroblastoma is considered to have unfavorable histology.

101
Q

Prognosis of neuroblastoma: Patient between 18 months and 5 years of age, inclusive (3).

A

Undifferentiated or poorly differentiated: Unfavorable histology.

Differentiating: Favorable as long as the MKI is low (i.e. not intermediate or high).

102
Q

Prognosis of neuroblastoma: Patient under 18 months of age (3).

A

Undifferentiated: Unfavorable histology.

Poorly differentiated or differentiating: Favorable as long as the MKI is low or intermediate.

Any tumor with a high MKI: Unfavorable.

103
Q

Prognosis of neuroblastoma: DNA index.

A. Use.
B. Interpretation.

A

A. Used in patients under 1 year of age.

B. Hyperdiploidy or near-triploidy is better than near-diploidy or near-tetraploidy.

104
Q

Prognosis of neuroblastoma: Expression of TRK.

A

TRK A, B, and C: Low or absent expression imparts poorer prognosis.

105
Q

Neuroblastoma: Extracellular components (2).

A

Fibrillar matrix resembling neuropil.

Delicate fibrovascular septa separating the lobules.

106
Q

Neuroblastoma: Definition of stage 4S.

A

Small, localized primary tumor with metastases to liver, skin, or bone marrow that nearly always spontaneously regress.

107
Q

Neuroblastoma: Immunohistochemistry of tumor cells (5,2).

A

Positive: NSE, synaptophysin, chromogranin, neurofilament, Neu-N.

Negative: Cytokeratins and other non-neural markers.

108
Q

Neuroblastoma: Associated hereditary syndromes (4).

A

Hirschsprung’s disease.

Congenital central hypoventilation.

Neurofibromatosis-1.

109
Q

Neuroblastoma: Electron microscopy (3).

A

Cytoplasmic filaments.

Dense-core granules.

Microtubules.

110
Q

Primary melanoma of the adrenal gland: Criteria (4).

A

Unilateral.

No previous melanoma.

No endocrine disorder.

No doubt about histology.

111
Q

Primary melanoma of the adrenal gland: Gross pathology.

A

Often locally advanced at presentation, with renal adhesions.

112
Q

Primary melanoma of the adrenal gland: Prognosis.

A

Death within 2 years.

113
Q

Primary melanoma of the adrenal gland vs. pigmented adrenal cortical adenoma: Immunohistochemistry (3).

A

Both are positive for Melan-A.

Adenoma is negative for S100, HMB-45.

114
Q

Primary melanoma of the adrenal gland vs. pheochromocytoma: Immunohistochemistry.

A

Both are positive for HMB-45.

The sustentacular cells of pheochromocytoma are positive for S-100.

115
Q

Myelolipoma: Age group.

A

Middle-aged.

116
Q

Myelolipoma: Presentation (2).

A

Usually asymptomatic.

Rarely causes Cushing’s syndrome or Conn’s syndrome.

117
Q

Myelolipoma:

A. Gross pathology.
B. Histopathology.

A

A. Red and yellow cut surface.

B. Mature bone marrow and mature fat.

118
Q

Myelolipoma: Variant.

A

Adenolipoma combines myelolipoma and adrenal cortical adenoma.

119
Q

Myelolipoma: Extraadrenal sites (3).

A

Liver.

Retroperitoneum.

Stomach.

120
Q

Adrenal cyst: Size and structure.

A

Usually small and unilocular.

121
Q

Adrenal cyst: Types (4).

A

Endothelial (most common).

Pseudocyst.

Epithelial.

Parasitic.

122
Q

Endothelial adrenal cyst: Types (3).

A

Lymphangioma.
Angioma.
Hamartoma.

123
Q

Adrenal pseudocyst:

A. Etiology.
B. Histopathology.

A

A. Previous hemorrhage.

B. Fibrous wall; no epithelial or endothelial lining.

124
Q

Epithelial adrenal cyst: Types (3).

A

Adenoma.
Glandular cyst or retention cyst.
Embryonal.

125
Q

Parasitic adrenal cyst:

A. Etiology.
B. Histopathology.

A

A. Parasites, esp. Echinococcus.

B. May contain fat or bone marrow.

126
Q

Adrenal cysts: Radiography (2).

A

Pseudocyst: Mural calcification.

Endothelial cyst: Septal calcification.

127
Q

Metastasis to the adrenal gland: Most frequent primary sites (4).

A

Lung.

Stomach.

Esophagus.

Liver.

128
Q

Metastasis to the adrenal gland: Gross pathology (2).

A

Usually multifocal but can be solitary.

Usually involve the cortex.

129
Q

Metastasis to the adrenal gland: Renal-cell carcinoma.

A

May mimic adrenal cortex histologically but does not express inhibin A or SF-1.

130
Q

Metastasis to the adrenal gland: Hepatocellular carcinoma (2).

A

May mimic adrenal cortex histologically but can show bile staining.

Positive for HepPar-1, canalicular polyclonal CEA, canalicular CD10.

131
Q

Autoimmune polyglandular syndromes.

A

APS-1: Includes candidiasis and alopecia; mutation in AIRE-1.

APS-2: Schmidt’s syndrome.

AP reviewer (17 decks)

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