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Endo/Repro II Block 2 > Adrenal Gland Pathology > Flashcards

Adrenal Gland Pathology Flashcards

1
Q 
Adrenal Gland Functional Histology
Cortical Zones (3) Medullary Cell with Secretions
A

Glomerulosa: Aldosterone
Fasciculata: Cortisol
Reticularis: Androgens

Chromaffin cells: Catecholamines, Epi/NE

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2
Q

Cushing Syndrome

Pathogenesis, Presentation (6) Diagnosis (2)

A

Hypercortisolism: either endogenous or exogenous

Obesity/weight gain
Moon facies
Abdominal striae
Decreased libido
Thin skin
Muscle atrophy

Elevated cortisol on 24 hour urine test
Loss of diurnal cortisol secretion

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3
Q

Iatrogenic Hypercortisolism

Description, Morphology

A

Exogenous hypercortisolism caused by long term use of corticosteroid drugs

Bilateral adrenal cortical atrophy

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4
Q

Endogenous Hypercortisolism
Etiologies (3) with Diagnostic Tests (3)
ACTH Dependent vs Independent Morphology (2)

A

ACTH-secreting pituitary adenomas (most common)
ACTH decreases after high dose dexamethasone

Ectopic corticotropin syndrome (paraneoplastic)
Elevated ACTH unchanged by dexamethasone

Adrenal adenoma or carcinoma (ACTH independent)
Low ACTH and high Cortisol levels

Diffuse Adrenal cortical hyperplasia if dependent
Macronodular hyperplasia if independent

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5
Q 
Hyperaldosteronism
Pathogenesis (2) Clinical Features (4) Diagnosis (2) and Treatment
A

Primary: autonomous aldosterone overproduction
Secondary: Aldosterone release in response to RAAS

Hypertension
Hypernatremia
Hypokalemia
Hypomagnesemia

Elevated plasma aldosterone
(+) Aldosterone suppression test

Sprionolactone

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6
Q

Primary Hyperaldosteronism Etiologies
Idiopathic, Neoplasia, Glucocorticoid Mediated
Population, Morphology and Genetics

A

Bilateral Idiopathic (most common)
Older people
Bilateral Nodular hyperplasia of adrenals
KCNJ5 mutation

Aldosterone-Producing Neoplasia (Conn Syndrome)
Middle aged women
Tumors contain Spironolactone Bodies
KCNJ5 mutation

Glucocorticoid Mediated
Familial syndrome
CYP11B2 under CYP11B1 control
Aldosterone under ACTH control

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7
Q

Secondary Hyperaldosteronism Etiologies (5)

A 
Renal Artery stenosis
Diuretic use
Arterial hypovolemia/edema
Pregnancy
Renin-secreting tumors
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8
Q

Adrenogenital Syndrome

Pathogenesis (2) and Etiologies (3)

A

Excess secretion of DHEA and Androstenedione
Excess androgens causes virulization or feminization

Corticotroph Pituitary Adenomas
Androgen-Secreting Adrenal Carcinomas
Congenital Adrenal Hyperplasia

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9
Q

Congenital Adrenal Hyperplasia

Pathogenesis (4) Diagnosis (2) and Treatment (2)

A

CYP21A2 mutation causing deficiency of 21-hydroxylase

Without 21-h, Aldosterone and Cortisol production is shunted towards making Testosterone

Decreased levels of Aldosterone and Cortisol feed back to pituitary, causing even more Testosterone production

Sustained elevated ACTH causes bilateral adrenal hyperplasia

Diagnosed via routine neonatal metabolic screening
Elevated serum 17-hydroxyprogesterone

Treated with exogenous glucocorticoids
Mineralcorticoid supplements in Salt wasting variant

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10
Q

Congenital Adrenal Hyperplasia Presentations

Classic (6) Simple Virilizing (2) Non-Classic (5)

A

**Neonatal ambiguous genitalia is seen in all forms

Classic (Salt Wasting)
Total lack of 21-hydroxylase
Hyponatremia, Hyperkalemia
Hypotension, acidosis and cardiovascular collapse

Simple Virilizing
Partial 21-hydroxylase deficiency
Elevated testosterone causing virilization

Non-Classic (most common)
Partial 21-hydroxylase deficiency
Precocious puberty
Hirsutism, acne, menstrual irregularities

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11
Q

Primary Acute Adrenocortical Insufficiency

Etiologies (3) and Presentation (7)

A

Adrenal Crisis
Rapid Steroid Withdrawal
Adrenal Hemorrhage: Waterhouse Friederichson Syndrome

Fever
N/V
Abdominal Pain
Hypotension
Hyponatremia
Hypoglycemia
Hyperkalemia
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12
Q

Waterhouse Friederichson Syndrome

Etiologies (3) Presentation (4) Gross Morphology

A

Sepsis from: Neisseria meningitidis, Pseudomonas, Haemophilus influenzae

Rapid hypotension leading to shock
Disseminated intravascular coagulation
Widespread purpura
Acute Adrenocortical Insufficiency from hemorrhage starting in adrenal medulla

Adrenals turned into sacs of clotted blood

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13
Q

Primary Chronic Adrenocortical Insufficiency
Addison’s Disease
Presentation (4) Etiologies (5) Morphology (2)

A

Long standing malaise and fatigue
Anorexia/Weight loss
Joint pain
Skin hyperpigmentation

Autoimmune Polyendocrine Syndrome Type 1/2
Tuberculosis
HIV
Malignancy
Adrenoleukodystrophy (congenital, X linked)

Irregularly shrunken adrenals with lymphocytic infiltrate (if autoimmune)

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14
Q 
Autoimmune Polyendocrine Syndromes
Type 1 (APECED)  and Type 2
Clinical Features (7/3)
A 
Type 1:
AIRE gene mutation
Adrenalitis
Parathyroiditis
Hypogonadism
Pernicious anemia
Mucocutaneous Candidiasis
Ectodermal dystrophy

Type 2:
Adrenalitis
Thyroiditis
Type 1 Diabetes

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15
Q

Secondary Chronic Adrenocortical Insufficiency

Pathogenesis, Presentation (3) Lab Findings (4) Diagnosis, Morphology (2)

A

Disorders of the hypothalamus or pituitary gland that decrease ACTH secretion

Malaise/Fatigue
Anorexia/Weight loss
Joint pain

Decreased cortisol
Decreased androgen output
Normal aldosterone
Low ACTH

Cortisol and androgen output responsive to exogenous ACTH

Moderate to severe cortical shrinking
Medulla unaffected

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16
Q

Functional Cortical Neoplasms
Adenomas and Carcinomas
Clinical Features (2/4)

A

Adenoma:
Cushing syndrome
Found incidentally on radiograph

Carcinomas:
Virulization
Found incidentally on radiograph
Compression/invasion of adjacent structures
Size is most important prognostic factor, often > 4cm

17
Q

Adrenal Myelolipomas Description (3)

A

Benign Lesions

Comprised of Mature adipocytes and Hematopoietic cells

18
Q

Adrenal Incidentalomas

Diagnosis, Prevalence, Prognostic Factors (3)

A

Found on advanced imaging

4% of the population with increase with age

Clinical Intervention if:
>4 cm
Positive functional assays for hypercortisolism or pheochromocytoma
Shows CT enhancement characteristics

19
Q

Adrenal Medulla Paraganglion System

Locations (3) with Functions

A

Bronchiomeric: dilates bronchi
Intravagal: inhibits intestines, increases glycogenolysis
Aorticosympathetic: affects cardiac output and BP

20
Q

Pheochromocytoma

Origin Cell, Clinical Features (5) Diagnosis, Treatment (2), 10% Rule (5)

A

Chromaffin cells

Hypertension, can be paroxysmal or chronic
Palpitations
Headache
Sweating
Anxiety
Chronic: cardiomyopathy

Urine and plasma metanephrine elevation

Anti-Adrenergic drugs
Surgical excision

10% are:
Extra-adrenal
Bilateral
In kids
Malignant
Not associated with HTN
21
Q

Common Features of Inherited Endocrine Neoplasias (5)

A 
Tumors occur at young age
Tumors involve multiple organ systems 
Tumors are multifocal
Tumors preceded by asymptomatic hyperplasia
Aggressive and Recurrent
22
Q

Multiple Endocrine Neoplasia Type 1

Neoplasias (4) Mutation, Clinical Features (4)

A

Primary Hyperparathyroidism
Pancreatic endocrine tumors
Pituitary adenomas: Lactotrophs and Somatotrophs
Gastrinomas

Germline MEN1 loss of function, decreased menin

Hypoglycemia
Intractable peptic ulcers
Hypercalcemia
Prolactin excess symptoms

23
Q

Multiple Endocrine Neoplasia Type 2A

Neoplasias (3) Mutation, Clinical Features (3) Prophylactic Treatment

A

Pheochromocytoma
Medullary Thyroid Carcinoma (very aggressive)
Parathyroid adenoma

Germline RET gain of function

Hypertension
Hypercalcemia
Elevated calcitonin

Thyroidectomy

24
Q

Multiple Endocrine Neoplasia Type 2B

Neoplasias (3) Mutation, Clinical Features (4), Prophylactic Treatment

A

Medullary Thyroid carcinoma (very aggressive)
Pheochromocytoma
Mucosal Neuromas

Germline RET gain of function

Marfanoid body
Elevated calcitonin
Hypertension
Skin/Eye/GI/Oral/Respiratory tumors

Thyroidectomy

25
Q

Familial Medullary Thyroid Cancer

Neoplasia, Clinical Features (2) Prophylactic Treatment

A

Medullary thyroid carcinoma (very aggressive)

Elevated calcitonin levels
Aggressive metastasis

Thyroidectomy

26
Q

Pineal Gland Neoplasias (3)

A

Germinomas
Pineocytomas
Pineoblastomas

Endo/Repro II Block 2 (7 decks)

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