Endocrine1

Question 1

If you have a patient with myalgia, proximal muscle weakness, fatigue, depressed DTR, and elevated CK in a young otherwise healthy woman, then what should be the initial test ordered?

Answer 1

TSH, and free T4. Most likely cause is hypothyroid myopathy.

Question 2

What’s the cause of Grave’s disease?

Answer 2

Hyperthyroidism due to thyroid stimulating auto-antibodies.

Question 3

What are the neurologic manifestations of hyperthyroidism?

Answer 3

Neurologic symptoms include insomnia, tremulousness, hyperreflexia, and irritability and anxiety.

Question 4

What triad of histologic findings would present in Graves disease?

Answer 4

1. Diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells: abundant call columnar cells lining the follicles.
2. Colloid appears pale with scalloped margins.
3. Lymphocytic infiltrate: germinal centers common (but normally aren’t in thyroid)

Question 5

What utility does potassium iodide have in managing hyperthyroidism?

Answer 5

Potassium iodide inhibits thyroid hormone synth and release. Used mainly in preparation for thyroidectomy in Grave’s disease and for treating thyroid storm.

Question 6

Why do you need to be careful about aggressive insulin management in treating hyperosmolar hyperglycemic syndrome?

Answer 6

Patients with HHS or DKA have a total body potassium deficit due to excessive urinary loss caused by osmotic diuresis induced by hyperglycemia. Aggressive insulin therapy for HHS can cause abrupt lowering of serum potassium levels&raquo_space; severe hypokalemia.

Question 7

What are the common cardiovascular side effects of hyperthyroidism?

Answer 7

Tachycardia, systolic HTN, increase pulse pressure, and tachyarrhythmia (a-fib)

Question 8

What is the initial management of toxic adenoma?

Answer 8

Beta blockers to alleviate Sx of hyperthyroidism, and thionamide (methimazole, PTU), to decrease thyroid hormone secretion.

Question 9

Are “hot” or “cold” thyroid nodules more likely to develop into cancer?

Answer 9

Cold nodules carry ^ risk of malignancy.

Question 10

What’s the mechanism of excess thyroid hormone induced bone loss?

Answer 10

Excess thyroid hormone&raquo_space; ^ osteoclast activation&raquo_space; hypercalcemia&raquo_space; decreased PTH secretion.

Question 11

What’s the most common congenital adrenal insufficiency?

Answer 11

Adrenoleukodystrophy = accumulation of very long chain FA in adrenal gland.

Question 12

How does the mechanism of spreading differ between papillary and follicular thyroid cancer?

Answer 12

Papillary = lymph node involvement

Follicular = hematogenous spreading (invasion of tumor capsule)

Question 13

What’s the treatment protocol for thyroid storm?

Answer 13

1. Beta blocker (propanalol) - decrease adrenergic manifestation
2. PTU followed by decreased Na+
3. Iodine (give 1 hr after PTU to prevent excessive iodine incorporation into T3) to block thyroid hormone release.
4. Glucocorticoids (hydrocortisone) to decrease peripheral conversion of T4 to T3.

Question 14

What electrolyte disturbances would you expect in a case of primary hyperaldosteronism?

Answer 14

Primary hyperaldosteronism = Conn syndrome

Usually due to adrenal adenoma or bilateral adrenal hyperplasia. Patient typically develop hypertension, mild hypernatremia, hypokalemia, and metabolic alkalosis.

Question 15

Why do you get a metabolic alkalosis with primary hyperaldosteronism?

Answer 15

In primary hyperaldosteronism, you have increased Na+ reabsorption, K+ secretion, and H+ secretion in the distal tubule. The hypokalemia also directly increases renal bicarb reabsorption&raquo_space; increased H+ secretion&raquo_space; metabolic alkalosis.

Question 16

What is the typical presentation of Subacute thyroiditis?

Answer 16

Subacute (de Quervian) thyroiditis typically follows a viral infection and presents with fever, neck pain, and a tender/diffuse goiter. Patients are typically thyrotoxic due to release of preformed thyroid hormone.

Question 17

In what patient population would you be more likely to see suppurative thyroiditis?

Answer 17

Suppurative (infectious) thyroiditis is classically seen in kids + immunocompromised Pt and presents with fever, erythema, and severe pain in the thyroid, often with an asymmetric goiter due to abscess formation.

Question 18

What is Pemberton’s sign?

Answer 18

Retrosternal extension of a thyroid tumor (as in thyroid lymphoma)&raquo_space; venous compression with distended neck veins and facial plethora. If Pt raises arms, the subclavian and right internal jugular become compressed between the thyroid tumor and clavicle&raquo_space; prominent venous distension and facial redness.

Question 19

If a patient presents with polyuria, constipation, nausea, markedly elevated serum Ca2+ and low PTH, then what would be the most likely diagnosis?

Answer 19

Humoral hypercalcemia of malignancy (HHM). This is the most common cause of PTH independent hypercalcemia.

Question 20

If a patient presents with low cortisol, low ACTH, hypogonadotropic hypogonadism, and hypothyroidism, then what is the most likely diagnosis?

Answer 20

Panhypopituitarism.

Low cortisol and low ACTH = central adrenal insufficiency. Presents as fatigue, anorexia, eosinophilia and hypoglycemia.

hypogonadotropic hypogonadism = low FSH, LH, and testosterone. Presents as low libido, ED, and testicular atrophy.

central hypothyroidism = low TSH, low free T4. Presents as cold intolerance, constipation, and bradycardia.

Question 21

Why do you get hypercalcemia with certain malignancies?

Answer 21

HHM (hypercalcemia of malignancy) is due to release of PTHrP (PTH related protein) by malignant cells and is generally assoc with squamous cell cancers. PTHrP&raquo_space; increased bone resorption and increased resorption of Ca2+ in distal tubule.

Question 22

Why do you tend to get hypercalcemia with sarcoidosis?

Answer 22

Sarcoidosis encourages increased conversion of 25 hydroxyvitamin D to 1,25 hydroxyl vitD&raquo_space; increased Ca2+ absorption from gut.

Question 23

What is the MCC of primary adrenal insufficiency in the US?

Answer 23

Autoimmune adrenalitis is the MCC of primary adrenal insufficiency in developed countries and is due to autoantibodies directed against adrenal enzymes responsible for corticosteroid synthesis.

Question 24

How do cortisol, ACTH, and aldosterone levels differ between primary vs central adrenal insufficiency?

Answer 24

Primary (adrenal) = low cortisol, high ACTH, low aldosterone

Central = [Secondary (pituitary), Tertiary (hypothalamus)] = low cortisol, low ACTH, normal aldosterone.

** In contrast to primary AI, Pt with secondary AI have glucocorticoid and androgen deficiency with preservation of mineralocorticoid (aldosterone) production (because this is primarily regulated by RAAS and not pituitary)

Question 25

What cardiac manifestations are observed in acromegaly?

Answer 25

In acromegaly, increased growth hormone&raquo_space; ^ production of IGF-1&raquo_space; concentric myocardial hypertrophy&raquo_space; diastolic dysfunction along with LV dilation and global hypokinesis.

** this is worsened by concurrent HTN, obstructive sleep apnea, and valvular heart disease common in acromegaly.