Endocrine Clinicals

Question 1

2* hyper aldosteronism

Answer 1

Commonly caused by heart failure. Kidney blood flow is decreased. This causes release of renin, increases Ang 2, increases aldosterone and increase blood volume. The heart can’t handle the increases blood flow. Treat the heart failure with a diuretic (spironolactone)

Question 2

Paraneoplastic syndrome

Answer 2

Secondary cause to cancer. Commonly small cell lung cancer (oat cell). The tumors over express ACTH. This causes increase in cortisol (cushinoid). Increased aldosterone. Use dexamethasone test for diagnosis.

Question 3

Pheochromocytoma

Answer 3

Adrenal tumor of the medulla. Causes over expression of epi/norepinephrine. Increases BP, increases HR. Both are not constant. Risk of stressing heart and blood vessels, leading to stroke and aneurysm. Remove tumor surgically. Give phenoxybenzamine before surgery to block alpha receptors (dec BP). Give beta-blocker to stabilize HR.

Question 4

Pituitary Dwarfism

Answer 4

Lack of GH production, no IGF production. Doesn’t present until puberty. Will have a short stature. Treat with synthetic growth hormone (Somatrem). If no response, then treat with (Mecasermin) an IGF synthetic.

Question 5

Pituitary Gigantism

Answer 5

Overproduction of GH that occurs before/during puberty. Give somatostatin (octreotide).

Question 6

Acromegaly

Answer 6

Overproduction of GH after puberty. Causes bones to grow thicker, not longer. Increases connective tissue. Give somatostatin (Octreotide)

Question 7

Cretinism

Answer 7

Mother has low thyroid function, generally due to iodine deficiency. Fetus isn’t exposed to thyroid hormone during fetal development. Born small and mentally retarted. Defects are irreversible.

Question 8

Infant Hypothyroidism

Answer 8

Fetus is exposed to normal thyroid hormone levels during fetal development. After birth thyroid levels drop. T3 is permissive to GH.

Question 9

Conn syndrome (1* hyper aldosteronism)

Answer 9

Tumor in adrenal cortex, usually glomerulosa. Increased aldosterone, increased blood volume, increased bp, elevated Na, decreased K. Treat by surgically removing tumor or give spironolactone ( mc-r antagonist)

Question 10

Iodine Deficiency

Answer 10

Lacking iodine in diet. Iodine is needed for thyroid hormone synthesis. Low T4, elevated TSH, elevated TRH. Columnar like follicular cells. Increased size of colloid, increased size of thyroid gland, leads to goiter.

Question 11

Hashimoto’s thyroiditis

Answer 11

Autoimmune destruction of thyroid gland. Most common hypothyroidism in the US. Decreased T4, elevated TSH, elevated TRH. No follicular cells to consider size of.

Question 12

Graves Disease

Answer 12

Autoimmune disease. Anti-TSH-antibodies bind to TSH receptor on follicular cells. Causes overstimulation of T4, decreased TSH, decreased TSH. Most common hyperthyroidism in the US. Increased stimulation of TSH receptors leads to columnar like follicular cells. Either remove thyroid or treat with radioactive iodine and treat with T4 for life.

Question 13

Shelan’s syndrome

Answer 13

Hypothyroidism due to infarction of the pituitary gland. Commonly caused due to severe blood loss during labor and delivery. No TSH, low T4, elevated TRH. Follicular cells will be squamous like.

Question 14

Levothyroxine

Answer 14

Synthetic T4, commonly given for hypothyroidism.

Question 15

Liothyronine

Answer 15

Synthetic T3 given when there is a deficiency in 5’/3’-deiodinase. Given for hypothyroidism.

Question 16

Perchlorate and Pertechnitate

Answer 16

Given for hypothyroidism. Blocks the Na/Iodine symporter. Decreased iodine levels, thus decreased T4. Given for hyperthyroidism.

Question 17

PTU and Methimazole

Answer 17

Blocks peroxide and deiodinase. Blocks iodine from thyronine and blocks conversion to T3. Given for hyperthyroidism.

Question 18

Cushing’s disease

Answer 18

Overproduction of cortisol. Can be caused by pituitary tumor and ectopic ACTH. Elevated cortisol, central adiposity, peripheral wasting, moon face, buffalo hump, purple striae, increased BS, insulin resistance, increased BP and risk for osteoporosis b/c vitamin D activation is blocked. Diagnose with Dexamethasone test. Remove tumor.

Question 19

Iatrogenic Cushing’s

Answer 19

Most common form of Cushing’s. Caused by long term synthetic cortisol use for AI or inflammatory issues.

Question 20

Addison’s Disease

Answer 20

Autoimmune destruction of adrenal cortex, causing adrenal insufficiency. Decreased cortisol, decreased aldosterone, elevated ACTH, very thin, weak, decreased BP, decreased BS, hyperkalemia, tanned skin b/c of overproduction of MSH. Give glucocorticoid and fludrocortisone (mineralcorticoid).

Question 21

Adrenal Crisis

Answer 21

Looks like addison’s. Occurs when patient is given glucocorticoids for long term use. Decreased ACTH will eventually cause atrophy of adrenal cortex. If pt undergoes major stress, they can no longer produce endogenous cortisol. Increase pt’s cortisol during stressful event.

Question 22

PTHrP (neoplastic syndrome)

Answer 22

This peptide is overproduced in squamous cell carcinomas (lung, head, neck and bladder). The peptide will bind with the PTH receptors and cause overproduction of PTH. Will cause hypercalcemia.

Question 23

1* hyperparathyroidism

Answer 23

Usually caused by benign tumor in the parathyroid. Will cause increased Ca plasma levels. Give Cinacalcet ( CaSR agonist), stimulates the receptor, which inhibits PTH synthesis.

Question 24

2* hyperparathyroidism

Answer 24

Generally due to chronic kidney failure. Loss of 1-alpha-hydroxylase. Thus, low vitamin D and Ca levels. Body will produce more PTH and pull more Ca from bone. Give Calcitrol (synthetic 1,25-hydroxy Vit D).

Question 25

Macrosomy

Answer 25

Large fetus born at full term, due to mothers gestational DM. Baby is exposed to high insulin levels, high blood sugar levels. Blood sugar can crash after birth.

Question 26

R-defect in insulin receptor

Answer 26

Defect in insulin receptor development during fetal development. Causes leprachonism, don’t survive.