Neuroblastoma: Neuroblastoma:

Pink-gray hemorrhagic surface. Neuroblastoma: Differentiating neuroblastoma:

Ganglioneuroma:

Calcification is common in these tumors. A plain radiograph of the abdomen may permit a prospective diagnosis.

Above: Classic morphology – neuroblastic cells, show no perceptable differentiation. Sometimes arranged in circumferential fashion w/the central portion filled w/eosinophilic fibrillary material. Known as Homer-Wright rosette. Background consists of axons and dendrites that are being formed by the tumor cells – neurofibrillary matrix.

Above: There are multiple, small neuroblastic cells that don’t exhibit any perceptable differentiation. Also larger cells w/appreciable cytoplasm – beginning to resemble ganglion cells. Differentiating neuroblastoma or ganglioneuroblastoma – associated w/improved outcome as compared to pure neuroblastoma.

Occasionally, neuroblastoma will totally mature – not only will see ganglion cells focally (as in ganglioneuroblastoma) – but they will progress from there. All of those cells are converted either to differentiated Schwann cells or ganglion cells. Ganglioneuroma = benign. So neuroblastoma spontaneously matures to benign neoplasm. Surgical excision is curative. Note: For test q’s about neuroblastoma, see “Pediatric Neoplasia” lecture.

Endocrine Review 11/05/10 I included the answers from Dr. Davis’s “Answers to Endocrine” file in addition to what he said in class. The given answers include some abbreviations – I left them as they were in his document. Normal pituitary:

Normal pituitary: Neurohypophysis + Adenohypophysis Anterior pituitary (adeno) is where most of the action is. Case 1: 28y/o female, 8 months postpartum with amenorrhea, loss of pubic hair and hypotension. She will need:

A) Iron supplements B) Iron, B12 and Folate supplements C) RBC transfusion D) Life-long hormone replacement Old test q – REPEATED x3! E) A psychiatric consultation

D; Sheehan Syndrome; PR inhibited by estrogen/progesterone during pregnancy. Takes time for Sheehan syndrome to develop – could be several months after birth to present. Test q: Cessation of menses following child birth is a hallmark of: Sheehan syndrome.

Case 2: 32 y.o. female with breast D/C, amenorrhea and bitemporal hemianopsia. You order: A) Serum prolactin and brain MRI B) Urine FSH and LH C) Adrenal and kidney ultrasound D) Chest xray and sputum cytology E) Pelvic examination and ovary ultrasound

A; PR inhibits G-RH and therefore FSH/LH (amenorrhea); males = impotence Sounds like patient might have pituitary adenoma – making prolactin. Must measure prolactin levels and get a brain MRI. Pituitary gland adenoma: Pituitary adenoma (Eosinophilic proliferative cells)

In a normal pituitary, there are 3 different cell types – basophils (blue), eosinophils (pink), chromophobes (no color). B-FLAT – Basophils make FSH, LH, ACTH, or Thyrotropin.

Figure: Infarction in anterior pituitary (Sheehan Syndrome). In the pituitary, the blood supply is venous – have a thin-walled blood vessel that runs against the skull. When the patient is stimulated by childbirth, the anterior pituitray undergoes hyperplasia. Big gland squeezing against a thin-walled blood vessel right against the bone. Every time a woman gives birth, she loses 1-2g of hemoglobin – sometimes more than that. So hypotension, venous supply, and hyperplasia of the pituitary infarction. No recovery because it is an infarction.

Making prolactin (eosinophils). No mixture of the 3 cell types – they are all eosinophilic. Most adenomas are microadenomas (<1cm).

Case 3 Very small, 8 y.o. female has lateral visual field defects. The sella turcica is calcified. You suspect: A. ALL B. Hodgkin Disease C. Neuroblastoma D. Craniopharyngioma E. Sheehan’s syndrome

D; Craniopharyngioma; childhood hypopituitarism; cyst, hemorrhage, Ca++; bitemporal hemianopsia; diabetes insipidus. Something is pressing on the pituitary – interfering w/vision and probably affecting GH too. Also sella is calcified – classic for craniopharyngioma. Craniopharyngiomas do not have a hormone product – they just give defects. Craniopharyngioma:

Moth-eaten, irregular. Filled w/viscous fluid. Kids w/calcified lesion in the sella = craniopharyngioma

Normal Thyroid: Thyroiditis:

Follicles lined by cuboidal epithelium – filled w/colloid. Some size variation – very little.

Nothing else in the pituitary looks like this – resembles a basal cell carcinoma. Peripheral palisading around the edge – almost looks like skin. Doesn’t look anything like a gland.

Can get different kinds of inflammation – thyroiditis. Some are lymphocytic, some have giant cells, some are more fibroblastic. But only one is classic – Hashimoto’s disease (MUST BE ABLE TO RECOGNIZE)

Case 4: 48 y.o. female with lethargy, weight gain and loss of lateral eyebrows. Thyroid histology? A. Papillary hyperplasia B. Tall columnar epithelium C. Colloid scalloping D. Lymphoid nodules E. Neuroendocrine cells with amyloid

D; Hashimoto; HLA Dr3 and 5. Gained weight even though diet hasn’t changed. Hashimoto’s – will look like lymph node – will have lymphoid nodules. Test q: A 45F is clinically hypothyroid and develops antibodies directed against TSH receptors and thyroglobulin. On biopsy you would expect to see: Lymphoid nodules Hashimoto’s thyroiditis, acute. Hashimoto’s thyroiditis:

Note the enlargement of the gland. Atrophy of the gland.

Above: Hashimoto’s thyroiditis. See some residual follicles. Prominent finding will be infiltration of lymphocytes – forming germinal centers (rim of blue cells), mixture of lymphocytes in the middle w/macrophages. Same follicles we saw in follicular hyperplasia in the lymph node. Also have big pink modified follicle cells – Hurthle cells (above, right). Case 5 You would expect to find autoantibodies directed against all the following EXCEPT___?

A. Thyroglobulin B. Microsomes (peroxidases) C. TSH receptors D. Iodine

D; anti- TSH-R, thyroglobulin, peroxidase (microsomal). In Hashimoto’s, have antibodies again A, B, and C (TSH receptors, as in Grave’s disease. However, in this case, they block the effect of TSH – not amplify it.)

Case 6: 45 y.o. male with heat intolerance, palpitations and an diffusely enlarged thyroid. Expected labs:

A. High TSH, High T4 B. High TSH, Low T4 C. Low TSH, High T4 D. Low TSH, Low T4 E. Normal TSH and T4

In Hashimoto’s thyroiditis, gland may be enlarged. With time, will burn out and become atrophic.

C; Graves; anti TSH-R (++); HLA Dr3; exopthalmos; tibial myxedema. Hyperthyroid: T4 high, TSH low. Hypothyroid: T4 low, TSH high.

Test q: In a hyperthyroid patient: the free thyroxine (FT4) is increased but the TSH is decreased. (Other choices: T4 and TSH are both increased; T4 is increased but TSH is normal; FT4 and TSH are both increased; FT4 is increased but the TSH is normal) Grave’s Disease:

Papillary hyperplasia. Have finger-like projections Cells are no longer cuboidal – are columnar. sticking into follicle. Also see scalloping of the Can see the pink material being secreted colloid around the projections. into the follicle. Case 7: 60 y.o. female with small lumps in neck. Thyroid is irregularly enlarged and the gland is “toxic”. The patient is: A. Hyperthyroid B. Hypothyroid C. Euthyroid D. Infected A; nodule becomes TSH-independent (autonomous); no exop. and no tib. myx. Toxic = hyperthyroid. Goiter – gland is focally involved (focal nodules of hyperplasia). In Grave’s, everything is making thyroxin. In nodular hyperplasia, nodules may make thyroxin or may not. Goiter: enlarged thyroid. Goiter:

Irregular – nodular, one lobe bigger than other. Case 8: 52 y.o. male has thyroid biopsy. Histology reveals malignant follicles and vesicular nuclei with “grooves”. Dx? A. Papillary CA B. Follicular CA C. Medullary CA D. Anaplastic CA A; nuclear features indicate Papillary Carcinoma. Thyroid mass made up of follicles w/a special kind of nuclei – vesicular/groove/Orphan Annie = papillary carcinoma. Nuclear appearance trumps the architecture. Papillary carcinomas don’t have to be papillary – could look like follicles, but if Orphan Annie nuclei are present, it’s a PC. It will invade regional lymph nodes, but will not go through the blood to bones and lung. Relatively benign as opposed to follicular carcinoma. Seeing Orphan Annie eyes = good thing.

Goiter:

Goiter: varying follicle diameter. Huge variation in follicle size. When examined at higher power, they are still cuboidal. No hyperplasia, no finger-like projections, and nodular – not diffuse.

Vesicular nuclei- sometimes “grooved” Papillary Carcinoma of the Thyroid:

Can see finger-like projections above.

Papillary Carcinoma – papillary projections: Papillary Thyroid Carcinoma:

Finger-like structures. See papillary projections, residual Psammoma bodies. Case 8A: What identifies a follicular thyroid tumor as malignant? A. Increased mitoses B. Production of thyroxine C. Anti-TSH receptor antibodies D. Irregular follicle shapes E. Vascular invasion E. Vascular invasion or extension through the capsule Thyroid Follicular Adenoma: Follicular Carcinoma: Metastatic Follicular Carcinoma:

Above (middle): Carcinoma – identified invasion. Will not have to do on a practical exam. WILL have to identify papillary carcinoma and medullary carcinoma. If you see follicular, call it follicular neoplasm (unknown malignant potential). Above (right): Follicular carcinomas are more aggressive – tend to spread through blood bone, lung (distant sites). Very aggressive tumor. Papillary carcinomas are most common – most likely to metastasize, but only go to regional lymph nodes – do not kill patient (like follicular carcinoma).

Case 9: A 42 y.o. female has medullary CA of the thyroid. Serum Ca++ is: A. Elevated B. Decreased C. Normal D. Not detectable E. A, B, or C A, B or C; IIa (MC, Pheo, hyperparathyroid); IIb (MC, Pheo, mucosal neuromas). For boards, pick B. Medullary carcinomas make pro-calcitonin – sometimes it’s biologically active, sometimes not. When it is, it lowers the Ca. However, at least half the time, it doesn’t. Thyroid Medullary Carcinoma: Thyroid Medullary Carcinoma

Above (both pics): See proliferation of little blue cells. All the pink acellular material is amyloid. Do not confuse w/nodular sclerosing Hodgkin’s Disease. But in HD, proliferation of cells is mostly benign cells – lymphocytes, plasma cells, eosinophils, and sometimes a big malignant cell. Here, these are all malignant. See tumor cell nests. Amyloid = pro-calcitonin.

Metastatic Medullary Carcinoma: Renal Cell Carcinoma (metastatic to thyroid):

Medullary carcinomas can metastasize – All endocrine organs may accept metastases. See thyroid tissue at bottom, clear cell to lymph nodes or through blood. carcinoma at top (renal cell carcinoma). - Anaplastic carcinoma of thyroid is worst – do not survive. Best – papillary – always survive. - Medullary carcinoma and follicular carcinoma – moderately aggressive, may be treatable or may kill you. Case 10: 45 y.o. female, post-thyroidectomy has carpal spasm and facial twitching if you tap her facial nerve. Labs expected? A. Hypercalcemia, low serum phosphate B. Hypercalcemia, high serum phosphate C. Hypocalcemia, hypophosphatemia D. Hypocalcemia, hyperphosphatemia (high serum phosphate) Old test q! E. Elevated PTH levels D; hypocalcemia and hyperphosphatemia; ↓PTH; other causes of low Ca++ are pancreatitis and low Vitamin D Thyroidectomy - #1 cause of hypoparathyroidism. In Case 10, took out parathyroid too (or didn’t leave enough behind).

Case 11: Patient has high serum Ca++. Surgeon removes 2 parathyroids, both have no fat. Dx? A. Double adenoma B. Hyperplasia C. Normal, biopsy more glands D. Carcinoma, remove thyroid and all 4 parathyroids B; hyperplasia. Normal is 50/50 cells-to-fat. When it’s an adenoma, only one is abnormal. If it’s two, it’s hyperplasia. Normal Parathyroid: Normal Parathyroid on left; Adenoma on right.

Lots of parathyroid cells – chief, oxyphil, water-clear. Capsule separating. All make parathormone. Most is made by chief cells. Half fat. Parathyoid Hyperplasia: Parathyroid Hyperplasia:

Microscopically, can’t tell adenoma from hyperplasia – Bottom left – cut in half, put half back in the patient (put in either case, all fat is gone. Must look at more than one. into muscles somewhere). Case 12: Hi Ca++ patient. Surgeon removes 4 parathyroids all with fat. There is no 5th gland detected in the thyroid. Dx? A. Hyperplasia B. Quadrupple adenoma C. Normal, do total thyroidectomy to remove all possible parathyroid tissue D. Rule out lung cancer D; high Ca++ causes: high Vitamin D; bone mets.; PTH by SCCA; sarcoid; hctz. We thought this patient had a parathyroid problem, but they all look normal. The most likely other thing to make parathormone-like substance would be lung cancer. Test q: A man presents w/hypercalcemia. A surgeon removes 4 parathyroids all with abundant fat. There is no 5th gland detected in the thyroid. What is the diagnosis: Unknown, rule out lung cancer.

Metastatic Calcification:

Case 13 60 y.o. female with hypercalcemia, kidney stones, bone pain, polyuria, weakness and constipation and low serum phosphate. A bone biopsy reveals? A. Metastatic parathyroid carcinoma B. Metastatic thyroid carcinoma C. Metastatic prostate carcinoma D. Osteitis fibrosa cystica E. DiGeorge syndrome D; brown tumors; also peptic ulcers and pancreatitis- enzyme activation by Ca++. Hyperparathyroidism leads to hypercalcemia (most common presentation – kidney stones). People w/hyperparathyroidism develop bone disorder called osteitis fibrosa cystica. Test q: A 60F shows bone pain, polyuria, weakness, constipation, and low serum phosphate. A bone biopsy reveals? Osteitis fibrosa cystica

Case 14 5 y.o. short, “overprotected” boy has bowed legs, broad sternum and square head. You should: A. Order a CT of the head B. Order TSH and T4 C. Prescribe synthroid D. Prescribe vitamin supplements E. Tell the parents to avoid sun exposure D; no sunshine so low Vitamin D; non-mineralized osteoid; Rickets. Overprotected = no/little exposure to sunlight. Deficiency of vitamin D – need to get out in the sun and convert some of the Vit D precursors in his skin.

Bowed legs

Normal pancreas: Chronic Pancreatitis:

If the patient from Case 12 is hypercalcemic, can get metastatic calcification (deposited on living tissue). Most common – lung and kidney. Metastatic calcification – will see nuclei (living cells) mixed in with the calcium. Test q: Which of the following is an example of metastatic calcification? Parathyroid hyperplasia with calcified alveolar septae. (Other choices: Psammoma bodies, Ferruginous bodies, Calcified atheromatous plaque, or Calcified heart valve in rheumatic heart disease)

Osteitis Fibrosa Cystica with “Brown tumors”:

See remodeling of bone – lots of osteoclastic activity (purple spots = osteoclasts). Frequently a lot of hemorrhage, so called brown tumors.

Normal pancreas: acinar pancreas makes lipases, amylases, etc. When damaged, will release enzymes fat necrosis. Also has islets (where islet cell tumors develop), ducts (where adeno-carcinomas develop). There are no neoplasms that occur in the acinar pancreas.

Chronic Pancreatitis: Fibrosis, chronic inflammation (see previous picture). DOES NOT DAMAGE ISLETS. Do not become diabetic, but do malabsorb because the acinar pancreas gets destroyed. Case 15: 10 y.o. girl is confused and exhibits rapid breathing. She has fruity breath. Parents say she eats a lot, but has lost weight. You expect: A. Hypoglycemia B. Ketonemia C. Low TSH D. High TSH E. Possible hyperosmolar coma B; ketoacidosis in type I DM. Typical in children. In contrast, hyperosmolar coma is a condition seen in type II diabetic older people – come into hospital dehydrated, out of it, glucose is 7-800, urinating all the glucose dehydrated. Case 16: 48 y.o. obese man with increased thirst and urinary volume. You expect to find: A. Increased sensation in fingers and toes B. Increased dorsalis pedis pulses C. Hypoglycemia D. Proliferative retinopathy E. High risk for ketoacidosis D; arteriolosclerosis in kidney and retina. Sounds like older type II diabetic. Answer choice E – no, not ketoacidosis. Risk for hyperosmolar coma.

Type II islet – filled w/amylin protein Case 17: 60 y.o. male with 20 year history of type II DM. Labs show proteinuria, hyperlipidemia and hypercholesterolemia. Renal biopsy shows? A. Lymphocytic infiltrate in glomeruli B. Granulomatous inflammation C. Micronodular glomerulosclerosis D. Aschoff bodies E. Normal glomeruli Old test q REPEATED x3 C; KW lesions are diagnostic in both Type I and Type II (Kimmelstiel-Wilson lesion) Nodules of mesangial matrix (Kimmelstiel-Wilson lesions) Also see thickened arterioles. In time, will become diffuse glomerulosclerosis. Case 17A. 40 y.o. female has watery diarrhea, midepigastric pain and shallow ulcers in the duodenum. Antacids and cimetidine give no relief. What test is likely to be elevated? A. Insulin B. Somatostatin C. Glucagon D. Vasoactive intestinal peptide (VIP) E. Gastrin E; gastrin; Zollinger Ellison Syndrome (islet cell tumor). Duodenal ulcers – associated w/gastrinoma. ZE syndrome – can be a part of MEN1 (3 P’s – parathyroid, pancreas, pituitary – add a 4th P: peptic ulcer = ZE)

Insulitis:

Type I DM – infiltration of islets by lymphocytes.

Old test q REPEATED x2

Pancreatic Islet Cell Tumor:

Normal pancreas (top right) and proliferative islet cells (bottom left). Usually, islet cell tumors make insulin.

Case 18: Male Cushings pt.; 1 mg Dm = no suppression; 8 mg Dm = suppression. Cause? A. Pituitary adenoma B. Adrenal adenoma C. Adrenocorticocarcinoma D. Ectopic ACTH (lung cancer) E. Germ cell tumor of testis

A; Cushing Disease (low dose -/no supression; high dose +/supression). No suppression = patient has Cushing’s. Go on to high dose if suppressed, it is a pituitary adenoma (Cushing’s disease). Here, it was suppressed, so pituitary adenoma. Adrenal glands: Atrophic Adrenal: Normal Adrenal:

Addison disease (top – atrophic cortex), normal (middle), hyperplasia/Cushing’s (bottom). Cushing’s – Adrenal Cortical Hyperplasia: cortex stimulated to make more cortisol, so yellow area is increased. Not adenoma because the whole thing is involved. If adenoma, would see nodule. Case 19: Male Cushings pt.; 1 and 8 mg fail to suppress. What next? A. *Give 16 g dexamethosone* B. Measure serum cortisol C. Measure urine cortisol D. Measure serum ACTH E. Ultrasound of testes D; ectopic tumor- ACTH is high; adenoma/hyperplasia-ACTH is low. Some people would do A, but we will rule it out for this question. We cannot suppress it, so the problem is not pituitary. The patient has Cushing’s syndrome, but not Cushing’s disease (not pituitary in origin). Next, should measure serum ACTH. If high = produced by ectopic tumor. If low = adrenal is the problem – making tons of cortisol, which feeds back on the pituitary and shuts down ACTH.

Test q: A 34M is suspected to have Cushing’s Syndrome. Urine cortisol excretion is not suppressed by 1mg or 8mg of dexamethosone. What should be done next? Measure serum ACTH. (Other choices: same as this case)

Test q: At the end of a six day dexamethosone suppression test (high dose test): 1) the urine free cortisol did not suppress and 2) the serum ACTH is increased. This most likely results from: Ectopic ACTH production.

Test q: Following the overnight dexamethasone suppression screening test, the patient has a very low serum cortisol concentration. Interpretation? Cushing’s syndrome is excluded.

Test q: A 45F presents w/hypertension and hyperglycemia. She also exhibits truncal obesity, hirsutism, and “moon” facies. The Dexamethosone suppression test fails to lower urine cortisol and the ACTH level is elevated. The most likely etiology is: Lung cancer.

Test q: A patient presents w/fatigue and trouble walking up steps for several months. A dexamethosone suppression test shows no high dose suppression of urine cortisol level and elevated plasma ACTH. Which clinical history is most consistent w/this data? 60F w/30yr history of smoking. (Other choices: 28F w/6mo history of bitemporal hemianopsia; 19M w/2yr history of steroid therapy for asthma; 28F w/2mo history of amenorrhea and galactorrhea; 34F w/1yr history of abdominal distention and constipation)

Case 20: 35 y.o. male with diarrhea, skin flushing, cyanosis and heart murmur. Dx? A. Cushing Syndrome B. Addison Syndrome C. Hashimoto Syndrome D. Graves disease E. Carcinoid syndrome E; usually have liver mets.; skin flush, diarrhea; serotonin; TriCusp/Pulmon valves damaged. Portrait of a carcinoid syndrome patient. Test q: A 35M presents w/diarrhea, skin flushing, cyanosis, and heart murmur. Small tumors are discovered in the duodenum and liver. You suspect: Carcinoid syndrome. Case 21: 47 y.o. female with nausea and fatigue. Knees and elbows are hyperpigmented. BP is low. ?? A. Acanthosis nigricans B. Type I DM C. Type II DM D. Autoimmune disease E. Adrenocorticocarcinoma D; autoimmune 65%; other causes histoplasmosis/TB; adrenogenital S.; mets. Addison’s – making too little cortisol. Adrenal Infarction: Adrenal Cryptococcal Infection:

Case 22: What are causes/etiologies of W-F Syndrome (Waterhouse-Friderichsen)? A. N. meningitidis and N. gonorrhoeae B. N. meningitidis and H. influenzae C. S. aureus and S. epidermadis D. Salmonella and Shigella E. Cryptococcus neoformans B; N. men and H flu; tissue thromboplastin/DIC; hemorrhage and infarction. W-F is a disastrous complication of a bact infection – usually NM but can be H influenzae. Develop DIC, massive hemorrhage into adrenals, infarct fingers/toes, rarely survive.

Adrenal – Waterhouse-Friderichsen: Waterhouse-Friderichsen Syndrome:

Filled w/blood. Diffuse hemorrhage. Case 23 25 y.o. male (not obese or diabetic) with headache and palpitations. BP is 200/110. ?? A. 90% of these patients are MEN II or III B. Most of these cases are sporadic C. The most sensitive test is urine VMA D. The most sensitive test is urine metanephrines E. The most specific test is urinary metanephrines B and D are correct; urine metanephrines most sensitive for pheochromocytoma. No other reason to be hypertensive – think pheochromocytoma. Not very common. Some people think that serum metanephrine test is most sensitive. “Let’s forget this question because there’s not a consensus on what it should be.” Test q: Which of the following is the most sensitive test of pheochromocytoma: Plasma metanephrines. (Other choices: Urine catecholamine, Urine metanephrines, Urine vanillymandelic acid (VMA), Plasma VMA.) The plasma metanephrines test measures the amount of metanephrine and normetanephrine in the blood (these substances are metabolites of epinephrine and norepinephrine – catecholamine hormones). Pheochromocytoma: Paraganglioma: Paraganglioma in Small Bowel:

Packets of Zellballen. Atypical cells, hemorrhage. Zellballen (left). If outside the adrenal gland, pheochromocytomas are called extra-adrenal pheochromocytomas or paragangliomas. Look the same microscopically. Pheochromocytomas in the adrenal gland usually make epinephrine because they have both the enzymes for conversion. Paragangliomas only have 1 of the enzymes, so usually make norepinephrine. Cells may be very atypical-looking, but it doesn’t mean they are malignant. With endocrine tumors, they are malignant only if they metastasize. Case 24: 2 m.o. child with calcified abdominal mass (that crosses midline) suddenly shrinks before Rx. ? A. Wilm’s tumor B. Neuroblastoma C. Burkitt lymphoma D. Renal Cell carcinoma B; neuroblastoma; differentiation to ganglioneurblastoma/ganglioneuroma. Neuroblastomas undergo spontaneous maturation.

Adrenal Neuroblastoma: Ganglioneuroblastoma:

Consists of little blue cells and neuropil (ACELLULAR – Both ganglia and neuroblastoma cells – less malignant. no nuclei in it – don’t confuse w/Wilm’s). Ganglioneuroma: Higher power of ganglioneuroblastoma (above)

Ganglioneuroma – all benign. Case 25: The tumor in this case (flashback to Case 24 – neuroblastoma) would show: A. C-myc overexpression B. Triphasic growth pattern C. Homer-Wright pseudorosettes D. Small blue cells and stroma E. WT-1 gene deletion C; Homer Wright Rosettes. Choice A – Burkitt’s; B – Wilm’s tumor; D – Wilm’s tumor; E – Wilm’s tumor

Psuedorosettes and neuropil Case 26 Adrenocorticocarcinomas are identified as malignant by: A. Nuclear atypia B. Mitotic count C. Nucleoli count D. Metastasis E. Size D; if >10 cm they may be malignant; >20 cm they are usually malignant; BUT only mets define malignancy absolutely

27. Wilm’s Tumor is identified by: A. Homer Wright Rosettes B. Procalcitonin C. Small blue cells and neuropil D. Tubules, stroma and blastema E. N-myc overexpression D. Triphasic tumor: glomeruli or tubules (epithelium), stroma (nuclei, fibroblasts), blastema or small blue cells Wilm’s Tumor: Wilm’s Tumor:

Small round blue cells, “glands”, and stroma of Wilms tumor. Blastema (blue cells); epithelium (tubules); stroma (with nuclei). Young kids typically get Wilm’s tumor, neuroblastoma, Burkitt’s.