adrenals

Question 1

ACTH independent Cushing’s

Answer 1

1. Adrenal adenoma or carcinoma
2. Macronodular hyperplasia
3. Primary pigmented nodular adrenal disease
4. McCune‐Albright syndrome

Question 2

ACTH dependent Cushings

Answer 2

ACTH dependent
– Cushing disease – pituitary adenoma
– Ectopic corticotropin syndrome (ACTH)

Question 3

ACTH‐Secreting Pituitary Adenoma

Answer 3

ACTH‐Secreting Pituitary Adenoma

~70% of cases of endogenous hypercortisolism

W>M

Most frequently seen in young adults

Majority are microadenomas

Macroadenoma also possible

Rarely corticotroph cell hyperplasia without a discrete adenoma

1. Primary
2. Secondary from excessive stimulation from a hypothalamic corticotrophin‐releasing hormone (CRH)‐producing tumor

Question 4

Secretion of Ectopic ACTH by Nonpituitary Tumors

•

Answer 4

Secretion of Ectopic ACTH by Nonpituitary Tumors

1. ~10% of ACTH‐dependent Cushing syndrome
2. Most often seen with small‐cell carcinoma of the lung
   
   1. Other neoplasms
   2. Carcinoids
   3. Medullary thyroid carcinoma
   4. Islet cell tumors
3. Sometimes neuroendocrine neoplasm produces ectopic corticotrophin releasing hormone (CRH)
   
   1. → ACTH secretion and hypercortisolism

Question 5

Primary Adrenal Neoplasms and Primary Cortical hyperplasia

Answer 5

1. Primary Adrenal Neoplasms
   
   1. Most common cause of ACTH‐independent Cushing syndrome
   2. Adrenal adenoma (~10%)
   3. Adrenalcarcinoma(~5%)
      
      1. Produce most profound hypercortisolism
   4. See ↑ cortisol and ↓ ACTH
2. Primary cortical hyperplasia
   
   1. Uncommon
   2. Vast majority of hyperplastic adrenals are ACTH dependent

Question 6

Cushing Syndrome: Morphology of the Adrenal Gland

Answer 6

Cushing Syndrome Morphology of the Adrenal Glands

1. Cortical atrophy
   
   1. Seen when exogenous glucocor coids → suppression of ACTH → lack of stimulation of the zonae fasciculata and reticularis
2. Diffuse hyperplasia (both glands enlarged)
   
   1. Endogenous hypercortisolism
   2. ACTH‐dependent Cushing syndrome
   3. Cortex can be variably nodular

Question 7

Macronodular hyperplasia

Answer 7

Macronodular hyperplasia

1. Endogenous hypercortisolism
2. Adrenals almost entirely replaced by prominent nodules of varying sizes (≤3 cm)
3. Areas between the macroscopic nodules also demonstrate evidence of microscopic nodularity

Question 8

Micronodular hyperplasia

Answer 8

Micronodular hyperplasia

1. Endogenous hypercortisolism
2. Composed of 1‐ to 3‐mm darkly pigmented (brown to black) micronodules, with atrophic intervening areas
3. Pigment is thought to be lipofuscin

Question 9

Primary Adrenocortical Neoplasms: classifications

Answer 9

Primary Adrenocortical Neoplasms

1. Functional (Cushing syndrome) or non‐functional
2. Morphologically indistinguishable
3. Functional tumors: adjacent adrenal cortex and the contralateral adrenal gland are atrophic

Question 10

1. Yellow tumors surrounded by thin or well‐developed capsules
2. Most weigh <30 gm
3. Microscopically see cells that look like normal zona fasciculata

What tumor, and who is most likely to be seen with it?

Answer 10

Primary adrenal adenoma

1. Most commonly seen in women aged 30‐50
2. Adenomas (benign)
3. Yellow tumors surrounded by thin or well‐developed capsules
4. Most weigh<30 gm
5. Microscopically see cells that look like normal zona fasciculata

Question 11

primary adrenal neoplasms: adenoma vs carcinoma

Answer 11

functional/nonfunctional: Morphologically indistinguishable

Functional tumors: adjacent adrenal cortex and the contralateral adrenal gland are atrophic. Most commonly seen in women aged 30‐50

Adenomas (benign): Yellow tumor ssurrounded by thin or well‐developed capsules and most weigh<30 gm. Microscopically see cells that look like normal zona fasciculata

Carcinomas (malignant): Larger than the adenomas are usually > 200‐300 gm, Unencapsulated

Question 12

Cushings clinical

1. muscle: atrophy of what kind of muscle fibers?
2. metabolism: what kind of profile?
3. skin, immune system, bone

Answer 12

1. Atrophy of fast‐twitch myofibers → decreased muscle mass and proximal limb weakness
2. Glucorticoids induce gluconeogenesis and inhibit the uptake of glucose by cells
   
   1. Hyperglycemia, glucosuria and polydipsia (secondary diabetes)
3. The catabolic effects → loss of collagen and resorp on of bones
   
   1. Skin is thin, fragile, and easily bruised
   2. Poor wound healing
   3. – Cutaneous striae are particularly common in the abdominal area
   4. – Osteoporosis
   5. Increased risk of infections (imm

Question 13

Diagnosis of Cushing Syndrome (2)

Answer 13

1. Diagnosis of Cushing Syndrome
   
   1. Increased 24‐hour urine free‐cortisol
   2. Loss of normal diurnal pattern of cortisol secretion

Question 14

Determining the cause of Cushing Syndrome•

Answer 14

Determining the cause of Cushing Syndrome

• Serum ACTH
• Dexamethasone suppression test: Urinary excretion of 17‐hydroxycorticosteroids after administration of dexamethasone

Question 15

identify the etiologies described in each column

Answer 15

1. cushing’s disease (pituitary ACTH secreting microadenoma most common) (ACTH suppressed with high dose)
2. Ectopic and adrenal tumor behave the same way to the dexamethasone test

Question 16

Primary Hyperaldosteronism

Caused by

Mechanism

Answer 16

Primary Hyperaldosteronism

Caused by one of three mechanisms:

1. Adrenocortical neoplasm
2. Bilateral idiopathic hyperaldosteronism (IHA)
3. Glucocorticoid‐remediable hyperaldosteronism

Autonomous overproduction of aldosterone

1. Suppression of the renin‐angiotensin system and decreased plasma renin activity –> elevated BP is the most common manifestation

Question 17

Adrenocrotical Adenoma: name, gender, age, lateral preferences

Answer 17

Adenoma: most common cause of hyperaldosteronism

1. Called Conn Syndrome
2. 30‐40 yrs most common
3. W > M (2 : 1)
4. Left > right

Question 18

Usually solitary, Small (<2 cm in diameter), Well‐circumscribed lesions, Bright yellow grossly

Characteristic microscopic feature: spironolactone bodies

Answer 18

Adrenocortical adenoma: tumor in Conn’s syndrome

1. Usually solitary
2. Small (<2 cm in diameter)
3. Well‐circumscribed lesions
4. Bright yellow grossly
5. Characteristic microscopic feature: spironolactone bodies

Question 19

Bilateral Idiopathic Hyperaldosteronism

Answer 19

1. Bilateral Idiopathic Hyperaldosteronism
   
   1. Most common cause of primary hyperaldosteronism
   2. Pts older
   3. Less severe hypertension
   4. Pathogenesis is unclear
      
      1. Bilateral nodular hyperplasia of the adrenal glands

Question 20

Glucocorticoid‐Remediable Hyperaldosteronism

Answer 20

Glucocorticoid‐Remediable Hyperaldosteronism

1. uncommon
2. Familial hyperaldosteronism
3. Rearrangement of chromosome 8 that places the gene for aldosterone synthase under the control of the ACTH responsive gene promoter
   
   1. ACTH stimulates the production of aldosterone
   2. Suppressible by dexamethasone

Question 21

in addition to primary hyperaldosteronism, conn’s, and glucocorticoid remediable hyperaldosteronism, aldosterone released in response to activation of the renin‐angiotensin system by ↑ plasma renin is also seen in….

Answer 21

1. Seen in:
   
   1. Decreased renal perfusion: arteriolar nephrosclerosis, renal artery stenosis
   2. Arterial hypovolemia and edema: congestive heart failure, cirrhosis, nephrotic syndrome
   3. Pregnancy: due to estrogen‐induced increases in plasma renin substrate

Question 22

Answer 22

spironalactone bodies found in aldosterone secreting adenomas (conn’s). eiosinophilic, laminated cytoplasmic inclusions

Question 23

Clinical Course of hyperaldosteronism

Answer 23

1. Hypertension (most important)
2. – ~5‐10% all hypertensive patients
3. Clinical Course
   
   1. – ~20% of treatment resistant hypertensives
   2. – Most common cause of secondary hypertension (i.e.,an identifiable cause)
4. Long‐term effects of hypertension on the CV system:
   
   1. – Left ventricular hypertrophy and reduced diastolic volumes
   2. – Stroke and myocardial infarction
5. Aldosterone also promotes sodium reabsorp on → increased reabsorption of water
   
   1. – Expands the extracellular fluid volume
   2. – Elevated cardiac output
6. Hypokalemia (↓K) typically seen
   
   1. Weakness, paresthesias, visual dist

Question 24

Screening and confirmation test and diagnosis of hyperaldosteronism

Answer 24

1. Screening test:
   
   1. Elevated ratio of plasma aldosterone concentration to plasma renin activity
2. Confirmation test:
   
   1. Aldosterone suppression test
   2. Administer: oral saline load, IV saline load, fludrocortisone
3. If aldosterone is not suppressed: confirm primary hyperaldosteronism

Question 25

tx for bilateral remediable hyperaldo and adenomas, secondary hyperaldo

Answer 25

1. Varies depending on the cause 1. Adenomas: surgical resection 2. Treatment 1. **Bilateral hyperplasia:** 1. Aldosterone antagonist (e.g. spironolactone) 2. **Secondary hyperaldosteronism:** 1. Treat underlying cause

Question 26

Adrenogenital Syndromes

Answer 26

1. Adrenogenital Syndromes 1. Disorders of sexual differentiation: Virilization or feminization 1. Primary gonadal disorders 2. Primary adrenal disoders 2. ACTH regulates adrenal androgen formation: 1. Adrenal cortex secretes dehydroepiandrosterone and androstenedione 1. Converted to testosterone in peripheral tissues 3. “Pure” syndrome or as a component of Cushing disease 1. Adrenocortical neoplasms (more likely carcinoma) 2. Congenital adrenal hyperplasia (CAH)

Question 27

Congenital Adrenal Hyperplasia (CAH)

Answer 27

Congenital Adrenal Hyperplasia (CAH) 1. **Several autosomal‐recessive, inherited metabolic errors** 2. **Deficiency or total lack of an enzyme involved in the biosynthesis of cortical steroids, esp. cortisol**

Question 28

21‐Hydroxylase Deficiency

Answer 28

1. \>90% of CAH 2. Mutations of **CYP21A2** 3. Three distinctive syndromes: 1. **Salt‐wasting syndrome** 2. **Simple virilizing adrenogenital syndrome** _without salt wasting_ 3. **Nonclassic or late‐onset adrenal virilism**

Question 29

Salt‐Wasting Syndrome 1. main problem 2. typcially presents for boys/girls 3. what it can cause

Answer 29

1. Salt‐Wasting Syndrome * **Inability to convert progesterone into deoxycorticosterone** * **Typically presents soon after birth** 1. **​****Virilization recognized in the female at birth or in uter** 2. _Males come to clinical attention 5‐15 days later because of some salt‐losing crisis_ 2. Salt wasting (hyponatremia and hyperkalemia) → acidosis, hypotension, cardiovascular collapse, and possibly death

Question 30

​girls vs boys: salt wasting syndrome

Answer 30

1. Inability to convert progesterone into deoxycorticosterone 2. Typically presents soon after birth 1. ​Virilization recognized in the female at birth or in uter 2. Males come to clinical attention 5‐15 days later because of some salt‐losing crisis 3. Salt wasting (hyponatremia and hyperkalemia) → acidosis, hypotension, cardiovascular collapse, and possibly death

Question 31

progressive virilzation

Answer 31

1. Simple Virilizing Adrenogenital Syndrome Without Salt Wasting 1. Presents as genital ambiguity 2. ~1/3 of 21‐hydroxylase deficiency 3. Progressive virilization

Question 32

most common andrenogenital 21 hydroxylase deficiency syndrome

Answer 32

1. Nonclassic or Late‐onset Adrenal Virilism 2. Most common 1. Only a partial deficiency in 21‐hydroxylase 2. function 1. Asymptomatic 2. Hirsutism, acne, and menstrual irregularities

Question 33

an xx baby is born with virilizing features, identified too late and die. autopsy is shown below. what is the condition?

Answer 33

1. congenital adrenal hyperplasia 1. **Adrenals are bilaterally hyperplastic** 2. **Cortex is thickened and nodular** 3. **Cortex looks brown** ​***due to total depletion of all lipid***

Question 34

hould be suspected in any neonate with ambiguous genitalia

Answer 34

CAH

Question 35

newborn with clitoral hypertrophy and pseudohermaphroditism in infants

Answer 35

CAH 21 oh deficiency

Question 36

adolescent girl visits your clinic and you diagnose oligomenorrhea, hirsutism, and acne in postpubertal

Answer 36

CAH 21 Oh deficiency

Question 37

in CAH, severe enzyme deficiency in infancy can be life‐threatening. describe some symptoms

Answer 37

Severe enzyme deficiency in infancy can be life‐threatening with vomiting, dehydration, and salt wasting

Question 38

CAH and the adrenal medulla

Answer 38

High levels of intra‐adrenal glucocorticoids are required to make catecholamine, epinephrine and norepinephrine Pts with severe salt‐wasting 21‐hydroxylase deficiency: 1. Low cortisol levels → adrenomedullary dysplasia (↓ catecholamine secre on) → hypotension and circulatory collapse

Question 39

Treatment of CAH

Answer 39

1. Treatment of CAH 1. Exogenous glucocorticoids 2. Replaces glucocorticoids AND Suppress ACTH levels which decreases the excessive synthesis of the steroid hormones 3. responsible for many of the clinical abnormalities 4. Mineralocorticoid supplementation

Question 40

Answer 40

addison's diz: chronic adrenal insufficiency

Question 41

Adrenocortical Insufficiency

Answer 41

_Adrenocortical Insufficiency_ ## Footnote **Primary acute adrenocortical insufficiency (adrenal crisis)** **Primary chronic adrenocortical insufficiency (Addison disease)** **Secondary from decreased stimulation of the adrenals due to a deficiency of ACTH**

Question 42

what causes adreanal insufficiency

Answer 42

1. Crisis: 1. Pt with chronic adrenocortical insufficiency precipitated by any form of stress 2. Adrenal glands can’t provide immediate increase in steroid output 2. **Exogenous corticosteroids, in whom rapid withdrawal of steroids or failure to increase steroid doses in response to an acute stress** 3. Massive adrenal hemorrhage → damage to the adrenal cortex 1. New borns following prolonged and difficult delivery with considerable trauma and hypoxia 2. Pts on anti coagulant therapy 3. Postsurgical patients who develop disseminated intravascular coagulation 4. Disseminated bacterial infection (Waterhouse‐Friderichsen syndrome)

Question 43

WHFS

Answer 43

1. Uncommon * Any age, but more common in kids 2. Overwhelming bacterial infection, classically Neisseria meningitidis septicemia * Also see with Pseudomonas species, pneumococci, Haemophilus influenzae, or even staphylococci 3. Rapidly progressive hypotension leading to shock 4. Disseminated intravascular coagulation associated 5. with widespread purpura, particularly of the skin 6. Rapidly developing adrenocortical insufficiency associated with massive bilateral adrenal hemorrhage 1. Fatal, unless promptly recognition and treated

Question 44

Progressive destruction of the adrenal cortex

Answer 44

Primary Chronic Adrenocortical Insufficiency (Addison Disease) * Uncommon * Progressive destruction of the adrenal cortex, requires up to 90% before symptoms show

Question 45

a group of autosomal recessive disorders characterized by defects in the biosynthesis of steroids

Answer 45

CAH

Question 46

Accounts for 60‐70% of Addison Disease

Answer 46

autoimmune adrenalitis

Question 47

Accounts for 60‐70% of Addison Disease

Answer 47

Accounts for 60‐70% of Addison Disease 1. Autoi-mmune destruction of steroidogenic cells 2. Autoantibodies 1. 21‐hydroxylase 2. 17‐ hydroxylase have been detected 3. Occurs in one of two clinical settings: 1. Autoimmune polyendocrine syndrome type 1 (**APS1**) 2. Autoimmune polyendocrine syndrome type 2 (**APS2)**

Question 48

APS2

Answer 48

APS2 1. Usually starts in early adulthood 2. Presents as a combination of adrenal insufficiency and autoimmune thyroiditis or type 1 diabetes

Question 49

causes of Addison's Dz

Answer 49

1. Infections 1. Particularly tuberculosis and fungal 2. AIDS at increased risk from several infectious (CMV, MAI) and noninfectious (Kaposi sarcoma) causes 2. Metastatic neoplasms 1. Lung and breast carcinomas most commonly 2. Others: GI carcinomas, melanoma, and hematopoietic neoplasms 3. Genetic causes 1. Congenital adrenal hypoplasia 4. Rare X‐linked disease 1. Adrenoleukodystrophy

Question 50

Morphology: addisons--\> primary, TB/fungal infection, metastatic causes

Answer 50

1. Morphology 1. **Primary autoimmune adrenalitis** 1. Irregularly shrunken glands, which may be difficult to 2. Histology 1. Cortex contains scattered residual cortical cells in a collapsed network of connective tissue 2. Variable lymphoid infiltrate 2. **Tuberculous and fungal disease** 1. Adrenal architecture is effaced by a granulomatous inflammatory reaction 3. **Metastatic carcinoma** 1. Normal architecture obscured by the infiltrating neoplasm

Question 51

1. Clinical symptoms of Addisons's: 2.

Answer 51

1. Begins insidiously 1. Early manifestations: progressive weakness and easy fatigability 2. Often dismissed as nonspecific complaints 3. GI disturbances 4. Anorexia, nausea, vomiting, weight loss, and diarrhea 2. Primary adrenal disease: get hyperpigmentation of the skin 1. Especially on sun‐exposed areas and at pressure points (e.g. neck, elbows, knees, and knuckles) 2. Results from elevated levels of pro‐opiomelanocortin (POMC) 1. Comes from anterior pituitary and is a precursor of both ACTH and melanocyte stimulating hormone (MSH)

Question 52

Answer 52

addisson's

Question 53

Addison's, clinical

Answer 53

Hypoglycemia can occur – From impaired gluconeogenesis Stresses can precipitate an acute adrenal crisis – E.g. infections, trauma, or surgical procedures – Intractable vomiting, abdominal pain, hypotension, coma, and vascular collapse – Death occurs rapidly unless corticosteroid therapy begins immediately

Question 55

hyperkalemia, hyponatremia, volume depletion, hyptotension: what other symptoms is this individual prone to develop?

Answer 55

adrenal insufficiency: lack of mineralcorticoids --\> sodium loss without potassium excretion. other symptoms include intractable vomiting, abdominal pain, hypotension, coma, vascular collapse.

Question 56

hypokalemia, weakness, parathesis, visual disturbances, frank tetany

Answer 56

primay hyperaldosteronism

Question 57

1. Mostareclinicallysilentanddiscovered incidentally 2. Well‐circumscribed nodular lesion 3. Up to 2.5 cm in diameter 4. Usually yellow to yellow‐brown because of the presence of lipid 5. Cortex adjacent to nonfunctional adenomas is normal

Answer 57

Adrenocortical Adenomas

Question 58

neoplasms that can occur at any age, including childhood, and more likely to be functional. Often present with virilisation. These are large, invasive lesions, often \> 20 cm in diameter. When smaller, and more‐circumscribed may be difficult to distinguish from an adenoma. Often invade nearby veins and lymphatics. Metastases to regional and periaortic nodes, lungs and other viscera common. what is the median age of survival with these cancers? what do they look like microscopically?

Answer 58

Median patient survival is about 2 years Microscopically: 1. **Look like an adenoma** (pretty bland) 2. Undifferentiated carcinoma 3. **Need to differentiate from metastases to the adrenal cortex _(much more common)_**

Question 59

~2/3 have “paroxysmal” episodes associated with sudden rise in blood pressure and palpitations (can be fatal)

Answer 59

pheochromocytomas, neoplasm of the chromaffin cells

Question 60

rule of 10s

Answer 60

“Rule of 10s” 1. 10% are **extra‐adrenal** (called paragangliomas) 2. 10% of **sporadic** pheochromocytomas are **bilateral** 3. 10% are **malignant** 1. Defined by the presence of **metastatic disease** 2. Malignancy is **more common in extra‐adrenal paragangliomas** and in some germline mutations 4. 10% **don’t have hypertension**

Question 61

Tachycardia, palpitations, headache, sweating, tremor, and a sense of apprehension Can also get abdominal pain, chest pain, nausea, and vomiting Can be precipitated by.....

Answer 61

Pheocrhomocytomas Can be precipitated by: 1. Emotional stress 2. Palpation in the region of the tumor 3. Patients with urinary bladder paragangliomas occasionally precipitate a paroxysm during micturition

Question 62

the 5 Ps of hyperadrenergic symptoms

Answer 62

1. Pressure: BP increases 2. Pain: headaches 3. Perspiration 4. Palpitations (tachycardia) 5. Pallor tumors/pheocrhomocytomas secrete epinephrine, norepinephrine, and dopamine, can cause episodic spells

Question 63

pheochromocytomas acutely precipitate:

Answer 63

**Acutely precipitate**: Congestive heart failure, pulmonary edema, myocardial infarction, ventricular fibrillation, and cerebrovascular accidents

Question 64

Up to 25% of pts with pheochromocytomas and paragangliomas

Answer 64

Up to 25% of pts with pheochromocytomas and paragangliomas * Typically **younger** * More often **bilateral – Up to 50%**

Question 65

renal cell carcinoma, hemangioblastoma, pancreatic endocrine neoplasm, pheocrhomocytoma, paraganglioma

Answer 65

VHL gene mutation

Question 66

optic nerve glioma, pheochromocytoma

Answer 66

NF1, cafe au lat spots as well

Question 67

SDHB, SDHC, SDHD

Answer 67

B- pheochromocytoma and paraganglioma, C just para, D- pheo and para

Question 68

**familial paraganlgioma _1, 3,_ _4_**

Answer 68

**1- SDHD** **3- SDHC** **4- SDHB**

Question 69

how is malignancy determined in pheochromocytoma

Answer 69

malignancy is defined by metastasis

Question 70

Tumors are usually preceded by an asymptomatic stage of hyperplasia involving the cell of origin

Answer 70

MEN tumors 1. Tumors occur at a younger age than sporadic tumors 2. Tumors arise in multiple endocrine organs 1. Synchronously (at the same time) 2. Metachronously (at different times) 3. Tumors often multifocal in an affected organ 4. Tumors are usually preceded by an asymptomatic 5. stage of hyperplasia involving the cell of origin – E.g. C‐cell hyperplasia in thyroid of MEN‐2 6. Tumors are usually more aggressive

Question 71

Answer 71

MEN 1

Question 72

Answer 72

MEN2 A

Question 73

Answer 73

MEN 2 B

Question 74

wermer syndrome, sipple syndrome

Answer 74

1. MEN-1- wermer 2. M2 A- sipple

Question 75

Primary hyperparathyroidism seen in 80‐95% , initial manifestation in most, hyperplasia and adenomas. The leading cause of death in these patients is X and the other common tumor associated with this condition is what?

Answer 75

1. MEN1 2. Pancreas endocrine tumors; prolactinomas 3. **Leading cause of morbidity and mortality:** Pancreatic neuroendocrine neoplasms 1. Usually aggressive and often present with metastatic disease 2. Can find multiple “microadenomas” scattered throughout the pancreas along with one or two dominant lesions 3. Often functional 1. **Pancreatic polypeptide is the most common** (**asymptomatic)** 4. Also see insulinomas and gastrinomas (**Zollinger‐Ellisonsyndrome**) 5. Pituitary 1. **Most often prolactinoma** 2. Some somatotrophin‐secreting tumors

Question 76

Other neoplasms of MEN1

Answer 76

**MEN-1** 1. **Duodenum: the most common site of gastrinomas** 2. **Neuroendocrine (carcinoid) tumors** 3. **Thyroid adenomas** 4. **Adrenocortical adenomas** 5. **Lipomas**

Question 77

Medullary carcinoma of the thyroid (~100%). Cause of this syndromic item?

Answer 77

MEN2A: mutation in the RET protooncogene

Question 78

salt and pepper cytoplasm clusters of polygonal spindle shaped chromaffin cells or chief cells surrounded by supporting sustentacular cells---\> creating small nests or alveoli

Answer 78

neuroendocrine (chromaffin) tumor cells have a salt and pepper appearance in pheochromocytomas zellballen are the nests of chromaffin cells surrounded by sustenatcular cells in pheochromocytomas

Question 79

s-100 antibodies

Answer 79

pheochromocytomas: antibodies against sustentacular cells