Endocrine

Question 1

What is the most common cause of hyperpituitarism? How does it present?

Answer 1

Pituitary adenoma. Presents based on the features of the hormone produced:

Prolactinoma - galactorrhea and amenorrhea in woman, headaches and loss of libido in men

Growth hormone cell adenoma - gigantism in kids, increased tongue, hand, feet, and jaw size in adults with increased organ size (heart problems) and potential DMII (GH induces liver gluconeogenesis)

ACTH tumor - Cushing syndrome

LH, FSH, and TSH tumors are less common

Question 2

Most common pituitary adenoma? Treatment?

Answer 2

Prolactinoma

Bromocriptine or cabergoline (dopamine agonists) or surgery

Question 3

How does a nonfunctional pituitary adenoma present?

Answer 3

Presentation due to mass effect: headaches, bitemporal hemianopsia (compression of optic chiasm) and hypopituitarism due to compression of normal pituitary tissue

Question 4

How do you diagnose a GH tumor? What is the treatment?

Answer 4

GH and insulin growth factor - 1 (IGF-1 - released from liver by GH, what mediates growth of tissues) are elevated. There is a lack of suppression of GH with oral glucose.

Treatment is octreotide (somatostatin analog that suppress GH release), GH antagonists or surgery

Question 5

Causes of hypopituitarism

Answer 5

• Pituitary adenoma (adults) or craniopharyngioma (children) due to mass effect or pituitary apoplexy (bleeding into adenoma)
• Sheehan syndrome
• Empty Sella syndrome

Question 6

Central diabetes insipidus vs. Nephrogenic diabetes insipidus [causes and treatments]

Answer 6

Central - ADH deficiency due to hypothalamic or pituitary pathology. Loss of free water (hypernatremia, polydipsia, polyuria, low urine osmolality). Treatment: desmopressin (ADH analog)

Nephrogenic - unresponsiveness of the kidneys to ADH. Due to inherited mutation or drugs (Lithium, demeclocyline). Treatment: not responsive to desmopressin

Question 7

What drug can cause SIADH? What are the other causes? What is the treatment?

Answer 7

Cyclophosphamide
Ectopic production (small cell carcinoma of the lung), CNS trauma, pulmonary infection
Treatment is free water restriction and demeclocyline (blocks ADH effects)

Question 8

Clinical features of SIADH

Answer 8

Hyponatremia (normal 135-145), low serum osmolality
Metnal status changes and seizures - hyponatremia leads to neuronal swelling and cerebral edema (water shifts from vascular space to intracellular space)

Question 9

What causes the increased basal metabolic rate in hyperthyroidism?

Answer 9

Increased synthesis of Na+/K+ ATPase

Question 10

Hyperthryoidism - High or low cholesterol? High or low glucose levels?

Answer 10

Hypocholesterolemia (change in lipid metabolism)

Hyperglycemia

Question 11

Graves disease is what type of hypersensitivity reaction?

Answer 11

Type II - autoantibody (IgG) that stimulates TSH receptor

Question 12

What causes the pretibial myxedema and exophthalmos in graves?

Answer 12

Fibroblasts behind the eye and over the shin express TSH receptors -> TSH activation results in glycosaminoglycan (chondroitin sulfate and hyaluronic acid) build up, inflammation, fibrosis and edema

Question 13

What is seen on histology with Graves disease?

Answer 13

Irregular follicles with scalloped colloid and chronic inflammation

Question 14

What causes a thyroid storm? How does it present? What is the treatment?

Answer 14

Due to elevated catecholamines and massive hormone excess usually in response to stress (surgery or childbirth)
Presents as arrhythmia, hyperthermia, and vomiting with hypovolemic shock
Treatment includes PTU, beta blockers, and steroids

Question 15

What is a multinodular goiter due to?

Answer 15

Relative iodine deficiency

Usually nontoxic, regions can become TSH independent leading to hyperthyroidism (rare)

Question 16

What is a dyshormonogenetic goiter?

Answer 16

A form of cretinism due to a congenital defect in thyroid hormone production; most commonly involves thyroid peroxidase

Question 17

Signs of cretinism

Answer 17

Mental retardation, short stature with skeletal abnormalities (thyroid hormone needed for normal brain skeletal development), coarse facial features, enlarged tongue and umbilical hernia

Question 18

What is myxedema? What does it result in?

Answer 18

Accumulation of GAGs in the skin and soft tissue resulting in a deepening of voice and large tongue

Question 19

What HLA is Hashimoto thryroiditis associated with? What antibodies are often present?

Answer 19

HLA-DR5

Antithryoglobulin and antithyroid peroxidase antibodies

Question 20

What is seen histologically with Hashimoto?

Answer 20

Chronic inflammation (autoimmune destruction of thyroid gland)
Germinal centers
Hurthle cells (eosinophilic metaplasia of cells that line follicles)

Question 21

Hashimoto thyroiditis - increased risk of what cancer?

Answer 21

B-cell (marginal zone) lymphoma

Presents as an enlarging thyroid gland late in disease course

Question 22

What thyroiditis follows a viral infection and presents as a tender thyroid with transient hyperthyroidism?

Answer 22

Subacute granulomatous (De Quervain) thyroiditis

Question 23

What thyroiditis presents as a non-tender ‘hard as wood’ thyroid with chronic inflammation?

Answer 23

Riedel fibrosing thyroiditis

Question 24

What is a complication of Reidel fibrosing thyroiditis? Does it present as hyper or hypothyroid?

Answer 24

Fibrosis may extend to local structures and obstruct the airway
Hypothyroid