Pathology-Endocrine Lecture

Question 1

What is the function of the hormones released by the hypothalamus on the pituitary?

Answer 1

GHRH = GH release, SST = inhibit GH release, GnRH = FSH/LH release, TRH = TSH & PRL release, DA = inhibit PRL release and CRH = ACTH release

Question 2

Hormones released by the posterior pituitary

Answer 2

ADH and oxytocin

Question 3

Etiologies of panhypopituitarism

Answer 3

Most common = benign craniopharyngioma. Additionally ischemia (Sheehan), tumor (metastatic or pit. adenoma), inflammation (sarcoid), trauma, infection (Tb) or surgery.

Question 4

What etiologies of panhypopituitarism can arise in the hypothalamus?

Answer 4

Tb and sarcoidosis.

Question 5

A 30 year old woman presents with headache and loss of vision. Imaging reveals a mass compressing the pituitary gland in the sella turcica. What are two variants of the most likely etiology?

Answer 5

Craniopharyngiomas have an adamantinomatous variant (common in children with peripheral palisading squamous epithelium and wet keratin) and a papillary variant (common in adults with solid sheets & papillae lined by squamous epithelium without keratin)

Question 6

Where do hypothalamic nerves release ADH and oxytocin?

Answer 6

Herring bodies in the posterior pituitary.

Question 7

2 causes of diabetes insipidus

Answer 7

Central (head trauma, surgical, tumor) or nephrogenic (renal tubule ADH insensitivity)

Question 8

Characteristic presentation of diabetes insipidus

Answer 8

Life-threatening dehydration from excessive urination

Question 9

Characteristic presentation of SIADH

Answer 9

Hyponatremia, cerebral edema (can lead to uncal herniation and death), total body water increase

Question 10

What cells are acidophils and what hormones do they produce?

Answer 10

Somatotrophs (GH) and lactotrophs (PRL)

Question 11

What cells are basophils and what hormones do they produce?

Answer 11

Corticotrophs (ACTH), gonadotrophs (FSH/LH) and thyrotrophs (TSH)

Question 12

Most common pituitary adenomas

Answer 12

Prolactinomas (30%) and null adenomas (20%). ACTH, thryotrophic and FSH/LH adenomas are all rare.

Question 13

How can you tell you are looking at an adenoma under the microscope?

Answer 13

There is only one cell type and no mixture of basophils and acidophils.

Question 14

Manifestations of GH adenomas

Answer 14

Acromegaly (after epiphysis have fused), gigantism (younger people)

Question 15

Typical presentation of prolactinomas in men and women?

Answer 15

Women: amenorrhea and galactorrhea. Men: lack of symptoms until mass effect

Question 16

Simple (euthyroid) diffuse nontoxic goiter complication

Answer 16

Airway obstruction and difficulty breathing

Question 17

A patient presents with cold intolerance, bradycardia, heart failure, high lipids and lethargy. What are some causes of this condition?

Answer 17

Hypothyroidism. Loss of thyroid tissue (surgery, radiation), hypothalamic failure, cretinism (infantile iodine deficiency), Hashimoto thyroiditis and granulomatous thyroiditis.

Question 18

Other conditions that are associated with Hashimoto thyroiditis

Answer 18

Type I diabetes mellitus, SLE, lymphomas (Non-Hodgkins lymphoma, marginal zone lymphomas, MALT)

Question 19

What are the types of hypersensitivities associated with Hashimoto thyroiditis?

Answer 19

II (plasma cells produce Abs) and IV (CD8+ cytotoxic reaction)

Question 20

Histologic features of early vs. late granulomatous thyroiditis.

Answer 20

Early: patchy microabscesses Late: damaged follicles, lymphocyte aggregates, multinucleate giant cells and fibrosis

Question 21

Histologic features of Graves disease

Answer 21

Tall columnar follicular cells w/papillary infolding and scalloping

Question 22

Why do multi nodular goiters cause hyperthyroidism?

Answer 22

10% of the time one autonomous toxic nodule is produced that releases large amounts of T4. Remember that <5% of the time these can develop into a neoplasm

Question 23

How do you determine if it is a multi nodular goiter or a malignancy?

Answer 23

Nodule has absence of a prominent capsule. Malignancies often have a thick capsule.

Question 24

What tumors can be derived from the different cells in the thyroid?

Answer 24

Follicular cells: follicular adenoma, follicular carcinoma and papillary carcinoma. C-cells: Medullary carcinoma

Question 25

Mutations that cause papillary carcinoma

Answer 25

RET/PTC fusion gene and BRAF.

Question 26

Mutations that cause follicular and anaplastic carcinoma

Answer 26

RAS, P13K, and PTEN. Follicular also has PAX8:PPARG

Question 27

Key item to diagnose papillary carcinoma

Answer 27

Optically clear nuclei

Question 28

Key item in distinguishing follicular adenoma from follicular carcinoma

Answer 28

Capsular invasion = carcinoma

Question 29

4 C’s of medullary carcinoma

Answer 29

Derived from C-cells, makes calcitonin, Congo red (amyloid) and carcinoembryonic antigen (CEA).

Question 30

Causes of primary hyperparathyroidism

Answer 30

1) Adenoma (90%). Hyperplasia and parathyroid carcinoma can also cause it. FHH, MEN1 and MEN2 are familial causes.

Question 31

Causes of secondary hyperparathyroidism

Answer 31

1) Chronic renal failure = low vitamin D and decreased Ca absorption = increased PTH.

Question 32

Histologic analysis of parathyroid adenoma

Answer 32

Monomorphic chief cell population

Question 33

Clinical symptoms of hyperparathyroidism

Answer 33

Painful bones, renal stone, abdominal groans and psychic moans.

Question 34

Causes of hypoparathyroidism

Answer 34

Surgery, congenital absence (DiGeorge), Autoimmune Polyendocrine Syndrome Type 1 (APS1)

Question 35

A patient presents with adrenalitis, hypoparathyroidism, hypogonadism and candidiasis. What is causing his condition?

Answer 35

APS1, an AR mutation in the AIRE gene on 21q22.3

Question 36

A patient presents with adrenal insufficiency, hypothyroidism and type 1 diabetes. What is causing his condition?

Answer 36

APS2, associated with HLA-DQ or HLA-DRB

Question 37

Most common causes of primary hyperaldosteronism

Answer 37

1) Idiopathic hyperaldosteronism 2) Adenoma of zona glomerulosa (Conn syndrome)

Question 38

Etiologies of Cushing’s syndrome

Answer 38

Pituitary adenoma, adrenal adenoma, adrenal hyperplasia, paraneoplastic and iatrogenic (most common).

Question 39

Most common cause of overactivity of the zona reticularis

Answer 39

21-hydroxylase deficiency shunts all cholesterol intermediates toward androgen synthesis and you get virilization.

Question 40

Acute loss of adrenal glands due to infection

Answer 40

Waterhouse-Friderichsen Syndrome.

Question 41

Chronic loss of adrenal glands with hyperpigmentation, weight loss and hypotension

Answer 41

Addison disease

Question 42

How would an adrenal carcinoma typically present?

Answer 42

Virilization, adenomas typically present with Cushing’s.