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USMLE World Q Bank > Endocrine > Flashcards

Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

Which organs are involved in MEN 1?

A

Pituitary, Parathyroid, Pancreas (Rhombus with all Ps)

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2
Q

Which organs are involved in MEN 2A?

A

Thyroid, Parathyroid and Pheochromocytoma (From rhombus to house, abre abajo)

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3
Q

Which organs are involved in MEN 2B?

A

Thyroid, Pheochromocytoma and Marfanoid habitus.

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4
Q

What is the presentation of 21-hydroxylase deficiency?

A

Hypotention, Hyperkalemia (low aldo), Virilization (high T)

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5
Q

What is the presentation of 17alpha-hydroxylase deficiency?

A

Can only produce mineralocorticoids. Hypertension, Hypokalemia. Lack of sexual development and pseudohermaphroditism in males.

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6
Q

What is the presentation of 11beta-hydroxylase deficiency?

A

Hypertension (Excess of 11-deoxycorticosterone which is ~ aldo), Virilization

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7
Q

Which glucocorticoid is preferred during childhood?

A

Hydrocortisone

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8
Q

Which glucocorticoid has mineralocorticoid activity?

A

Fludrocortisone

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9
Q

What is the thyroglossal duct?

A

The thyroid migrates down from the foramen cecum to it’s position. The duct is a remnant of this migration. Persistant duct is palpable. The most common location for an ectopic thyroid is sublingual.

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10
Q

How do you distinguish between Cushing disease and ectopic ACTH production?

A

High dose dexamethasone will suppress ACTH production in Cushing disease but in ectopic production (ie. small cell lung cancer) ACTH stays elevated even at high doses.

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11
Q

What is the effect of glucocorticoids on the liver?

A

They are potent activators of gluconeogenesis. (ie. hyperglycemia in Cushing syndrome)

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12
Q

What are the mechanism of action and side effects of Colchicine?

A

Colchicine affects tubulin polymerization. Nausea, abdominal pain and diarrhea.

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13
Q

What does Ras need to bind in order to activate?

A

GTP

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14
Q

What are neurophysins?

A

Carriers of Oxitocin and ADH from the thalamus to the posterior pituitary where they are secreted. Lack of neurophysins would lead to DI.

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15
Q

What is the relation between ADH and pro-opiomelanocortin (POMC)?

A

They are made from the same precursor polypeptide just cleaved in different ways. Both are made in the anterior pituitary.

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16
Q

Rank the different types of Insulin from the quickest to the slowest action. [The numbers represent the peak.]

A 
Aspart, Lispro, Glulisine (1 hour)
Regular (2.5 hours)
NPH (Neutral Protamine Hagedorn) (7 hours)
Detenir (8 hours)
Glardine (24 hours with no peak)
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17
Q

What is the neurological sign of hypocalcemia?

A

Chvostek’s Sign = Facial Nerve Hyperexcitability. Elicited by tapping on the jaw or on the Facial nerve just anterior to the ear.

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18
Q

What are the lab findings in mineralocorticoid excess?

A

hypertension, hypoK, low renin, and non-supressable aldosterone. Na is generally normal and edema is not generally seen.

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19
Q

Which glucose transporter is responsive to insulin and where is it located?

A

GLUT-4 on muscle cells and adipocytes

20
Q

Where in the cell is the T3 receptor?

A

In the nucleus

21
Q

How does TNF-alpha cause insulin resistance?

A

Activates Serine Kinases which phosphorylate IRS-1 which inhibits the Tyrosine Kinase phosphorylation of IRS-1 by the Insulin Receptor.

22
Q

What is the only pituitary hormone that is inhibited by the hypothalamus? All the other ones are activated.

A

Prolactin

23
Q

What does growth hormone excess do?

A

It causes IGF-1 secretion by the liver. If it happens before close of the growth plates it causes gigantism. If it happens in adulthood it causes acromegaly.

24
Q

What are the two types of symptoms of hypoglycemia?

A

Adrenergic (sweating, tremor, palpitations, hunger) & CNS (behavioral, confusion, vision, seizures)

25
Q

Compare and contrast PTH and Calcitriol. What about calcitonin.

A

Both increase serum Ca++. Calcitriol increases GI bone absorption and decreases PTH. PTH stimulates osteoclasts, increases Calcitriol and decreases phosphorus reabsorption from the kidneys. Calcitonin directly oposes PTH.

26
Q

What is the mechanism of action of propylthiouracil?

A

1) Blocks thyroid peroxidase and 2) prevents the T4 to T3 conversion by blcoking 5’-deiodinase.

27
Q

What is the mechanism of action of methymazole?

A

It blocks thyroid peroxidase.

28
Q

What ligands use the JAK/STAT pathway?

A

Cytokines, Prolactin, Growth hormone and IL-2. These are tyrosine kinase associated receptors. (Not tyrosine kinase receptors themselves.)

29
Q

What are glitazones/thiozolidinediones used for and what is their main toxicity?

A

Used for type 2 DM and can cause hepatotoxicity. They increase insulin sensitivity by binding the PPAR-gamma transcription regulator.

30
Q

How does cortisol control catecholamine synthesis?

A

It promotes Phenylethanolamine-N-methyltransferase (PNMT) in the adrenal medulla. This protein converts NE to Epi.

31
Q

Describe the histology seen in Hashimoto’s Thyroiditis?

A

Mononuclear, parenchymal infiltration with well defined germinal centers.

32
Q

Why can patients with GU tumors have an increase in thyroid hormones?

A

Some GU tumors produce hCG, especially teratomas or other non-seminomatous germ cell tumors. hCG has slight affinity for the TSH receptor.

33
Q

What are the 6 Ps of congenital hypothyroidism?

A 
Pot-bellied
Pale
Puffy-faced
Protruding Umbilicus
Protuberant Tongue
Poor brain development
34
Q

Hypertension, opsoclonus-myoclonus and a retroperitoneal mass are suggestive of…

A

Neuroblastoma. Adrenal medulla tumor in children. Associated with N-myc mutations.

35
Q

What are the lab findings in primary adrenal insufficiency? What is a risk factor for it? (Addison’s Disease)

A

Hyperkalemia, hyponatremia, hypochloremia and metabolic acidosis. Patients with type I diabetes can get it.

36
Q

Describe the signaling pathway of the insulin receptor?

A

Tyrosine Kinase -(+)-> Protein Phosphatase 1 -(-)-> Glycogen Phosphorylase

Also…
Protein Phosphatase 1 -(-)-> fructose-1,6-bisphophatase -(+)-> Gluconeogenesis

Also…
Tyrosine Kinase -(+)-> Glycogen Synthase

37
Q

Which drugs should not be given while on radioactive iodine treatment?

A

Potassium Perchlorate and Potassium Pertechnetate because they are competitive inhibitors of the Sodium Iodine Symporter (NIS). Thionamides inhibit peroxidase.

38
Q

Describe the clinical presentation of a Medullary Carcinoma of the Thyroid?

A

Solid lump on the thyroid and increased serum calcitonin. You MUST check for Pheochromocytoma as most of these tumors are associated with MEN 2A or MEN2B.

39
Q

What is the mechanism of action of propylthiouracyl and methimazole?

A

Inhibit organification and coupling of iodotyrosines. Propylthiouracyl also prevent peripheral T4->T3 conversion.

40
Q

What is Eplerenone?

A

Aldosterone Receptor blocker. Just like Spironolactone but with fewer side effects.

41
Q

What are the Sulfonylurea drugs and what is their mechanism of action?

A

1st G: Tolbutamide, Chlorpropamide
2nd G: Glyburide, Glimepiride, Glipizide.
They work by closing K channels and thus inducing Insulin release.

42
Q

What is the typical picture of Glucagonoma?

A

DM (hyperglycemia), anemia and necrolytic erythema.

43
Q

What is the treatment for adrenal crisis?

A

High dose corticosteroids.

44
Q

Which hormone is involved in the pathogenesis of gestational diabetes?

A

Human Placental Lactogen causes insulin resistance and simultaneously increases insulin secretion.

45
Q

Which lipids are believed to increase insulin resistance?

A

Free Fatty Acids and Triglycerides.

USMLE World Q Bank (14 decks)

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