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MHD > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Layers of the cortex of the adrenal gland?

A 
G: 
Zona glomerulosa 
-Aldosterone
F:
Zona Fasciculata
-Cortisol
R:
Zone Reticularis 
-Sex Steroids

Medulla=catecholamines

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2
Q

Endogenous Hypercortisolism

A
  1. Paraneoplastic cushing syndrome
    -secretion of ectopic acth; mostly by small cell carcinoma of the lung
    10% of cases of endogenous cushing syndrome
  2. Primary Adrenal Neoplasms including adenoma carcinoma and rarely hyperplasia
    -15-20% of cases of endogenous cushing syndrome
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3
Q 
How does 
Pituitary cushings 
adrenal cushing 
paraneoplastic cushings
iatrogenic cushings 
affect the adrenal gland?
A

Pituitary cushings: adrenal hyperplasia
adrenal cushing: tumor (adenoma or carcinoma) or hyperplasia (diffuse or nodular)
paraneoplastic cushing: adrenal hyperplasia
iatrogenic cushing: adrenal atrophy

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4
Q

Hyperaldosteronism

Primary and secondary causes

A
  1. Primary (independent of renin angiotensin system)
    - Bilateral idiopathic hyperaldosteronism
    - Adrenocortical Neoplasm
    - Familial hyperaldosteronism
  2. Secondary (activation of renin angiotensin system)
    - Decreased renal artery profusion
    - Arterial hypovolemia and edema
    - Pregnancy
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5
Q

Hyperaldosteronism clinical manifestations

A

Hypertension with long term cardiovascular compromise (MI and stroke)
Hypokalemia cuasing neuromuscular manifestation like weakness, paresthesias, visual disturbances and occasionally tetany

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6
Q

Adrenogenital syndromes
Etiology
Primary/Secondary

A

conditions characterized by structural or biochemical abnormalities of the adrenal cortex which which leads to a disorder of sexual differentiation(adrenal virilism)

Etiology
Primary: adrenocortical neoplasms (usually virilizing carcinoma) or congenital adrenal hyperplasia

Secondary: Pituitary causes (excess secretion of ACTH leading to increased production of adrenal androgens, may be associated with features of cushing syndrome

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7
Q

Congenital Adrenal Hyperplasia

A

Autosomal recessive
-Defect in the enzyme involved in adrenal steroid biosynthesis, particularly cortisol

  1. decreased cortisol–increased ATCH
  2. Adrenal hyperplasia–increased precursor steroids
  3. increase in synthesis of androgens
    - some enzyme defects also impair aldosterone biosynthesis–salt loss
    - 21 hydroxylase deficiency is most common CAH defect
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8
Q

Acute adrenal insufficiency in the setting of sepsis (waterhouse-friderichsen syndrome)

A
  1. septicemia, usually meninogocci
  2. hypotension, shock, DIC
  3. massive bilateral adrenal hemorrhage and destruction
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9
Q

Addison’s Disease

Clinical manifestations

A

chronic destruction of the adrenal cortex with multiple etiologies leading to hypofunction (usually occurs when 90% of cortex destroyed)

Clinical
Initial progressive weakness and easy fatigability
Gastrointestinal disturbances like anorexia, nausea, vomiting, weight loss and diarrhea
-decreased mineralocorticoids leads to loss of sodium, hyperkalemia, volume depletion and hypotension
-hypoglycemia may occur due to glucocorticoid deficiency
-stress like infection, trauma may precipitate an acute adrenal crisis

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10
Q

Autoimmune adrenalitis

Gross and Histo

A

Gross: very small glands
cortices markedly thin

Micro

  • diffuse atrophy of all cortical zones
  • lymphoplasmacytic infiltrate
  • medulla is unaffected
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11
Q

Are cushing syndrome and hyperaldosteronism most commonly caused by adenomas or carcinomas?

A

adenomas

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12
Q

Are virilization neoplasms most commonly caused by adenomas or carcinomas?

A

carcinomas

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13
Q

Adenomas of the adrenal gland
Gross
Histo

A

Gross
most are nonfunctional
1-2 cm diameter
yellow to yellow brown cut surface

Histo
Cytoplasm ranges from eosinophilic to vacuolated depending on lipid content
-not much mitotic activity seen
-minor degree of nuclear pleomorphism

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14
Q

Adrenal carcinoma

A

Rare neoplasm
any age
rare causes include Li-fraumeni sydnrome and Beckwith Wiedemann syndrome

Gross
-large poorly demarcated invasive lesions
cut surface with areas of hemorrhage and necrosis
tendency to invade the adrenal vein, vena cava and lymphatics with regional and distant metastasis
-median survival about 2 years

Histology:

  • may be composed of well differentiated cells or bizarre pleomorphic cells
  • invasion and metastasis are the most reliable indicators !
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15
Q

Adrenal medulla
Derivation
Cells
Secrete

A

neural crest derivation
chromaffin cells and their supporting sustentacular cells
-secrete catecholamines
-similar collections of cells distributed throughout the body in the extra adrenal paraganglion system

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16
Q

Pheochromocytoma

A

neoplasm arising from neuroendocrine cells (chromaffin cells) in the paraganglion system (adrenal medulla/etra-adrenal paraganglion system)
-give rise to surgically correctable form of hypertension

10% rule
10% extra adrenal 
10% bilateral
10% malignant 
25% being associated with germline mutation
  1. RET gene (MEN2 and 3)
  2. NF1
  3. VHL
  4. genes SDHB, SDHC, SDHD
17
Q

Pheochromocytoma Gross and Histology

A

Gross:
small circumscribed to large hemorrhagic masses
grey tan, focally, congested cut surface
Histology:
ZELLBALLEN!!!!!
nests composed of chromaffin cells surrounded by supporting/sustentacular cells
-rich vascular network
-metastasis is required for definitive diagnosis of malignancy

18
Q

Clinical features of pheochromocytoma

A

hypertension-sustained or paroxysms

  • headache, sweating, anxiety, tremor
  • symptoms caused by release of catecholamines which can precipitate an AMI, CHF, ventricular fibrillation, CVA
  • chemical diagnosis****-urinary catecholamine metabolites
    1. METANEPHRINE
    2. VANILLYLMANDELIC ACID (VMA)
19
Q

Neurobastoma

A

Definition: a neoplasm which arises in the adrenal medulla or extra adrenal paraganglion tissue

  • one of the most common childhood neoplasms; 90% occur before age 5
  • large abdominal mass in child
  • younger than 2 years with fever
  • older child presents with metastases

Gross

  • large bulky tumors
  • 25% in adrenal glands
  • others arise in the paravertebral regions of the posterior mediastinum and abdomen

Histo:
small, primitive appearing cells with dark nuclei, sheets or rosettes

20
Q

MEN1

A 
Autosomal dominant 
11q13 
tumor suppressor gene
3P's 
1. Parathyroid
2. Pancreas
3. Pituitary

Most common: primary hyperthyroidism (hyperplasia or adenoma)

Leading cause of death: endocrine tumors of the pancreas-functional tumors metastasize

Pituitary -most commonly has prolactin secreting macroadenomas

21
Q

MEN2A

A 
Autosomal Dominant 
Ret protooncogene (10q11.2)
  1. Thyroid-medullary carcinoma -in virtually all untreated cases in first 2 decades, may b multiple (Calcitonin)
  2. Adrenal medulla-Pheochromocytoma in 50% of patients though only 10% are malignant (Catecholamines)
  3. Parathyroid-10-20% have hyperparthyroid (Calcium)
22
Q

MEN 2B

A

Spectrum of thyroid and adrenal medullary changes similar to 2A with the following differences:

  1. Mucosal ganglioneuromatosis and marfanoid habitus are characteristic
  2. NO parathyroid

-RET mutation-prophylactic thyroidectomy to prevent development of medullary carcinomas

MHD (81 decks)

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