Usmle Step 1 Review - Endocrinology

Front 1

anterior pituitary hormones secreted by acidophils

Back 1

GH, PRL

Front 2

anterior pituitary hormones secreted by basophils

Back 2

FSH, LH, ACTH, TSH (B-FLAT)

Front 3

insulin-dependent glucose transporter

Back 3

GLUT4

Front 4

glucose transporter on RBCs and brain

Back 4

GLUT1

Front 5

glucose transporter on adipose and skeletal muscle

Back 5

GLUT4

Front 6

insulin-independent (concentration sensing) glucose transporter

Back 6

GLUT2

Front 7

glucose transporter on B-islets, liver, kidney, and small intestine

Back 7

GLUT2

Front 8

What hormones trigger insulin release?

Back 8

GH, EPI, NE, glucagon

Front 9

Does alpha or beta adrenergic stimulation trigger insulin release?

Back 9

beta agonists trigger insulin release

Front 10

What hormones suppress insulin release?

Back 10

cortisol, somatostatin, alpha2 agonists

Front 11

How to B-islets regulate insulin release?

Back 11

increased glucose --> increased ATP --> closes K+ channels --> depolarization --> insulin release

Front 12

What is the effect of insulin on the kidneys?

Back 12

induces Na+ retention

Front 13

What is the effect of insulin on the plasma K+ concentration?

Back 13

reduces it, by inducing cellular K+ uptake

Front 14

In addition to stimulating release of TSH, TRH increases release of ___?

Back 14

PRL

Front 15

In addition to inhibiting PRL release, somatostatin inhibits the release of ___ and ___.

Back 15

GH, TSH

Front 16

How does PRL inhibit the secretion of LH and FSH?

Back 16

By inhibiting the secretion of GnRH.

Front 17

17a-hydroxylase deficiency: ___ mineralocorticoids, ___ cortisol, ___ adrenal androgens.

Back 17

high mineralocorticoids, low cortisol, low adrenal androgens

Front 18

Clinical presentation of 17a-hydroxylase deficiency?

Back 18

hypertension and hypokalemia (from excess aldosterone); hypocortisolism; XY pseudohermaphrodite, XX w/o secondary sex characteristics (from decreased adrenal androgens)

Front 19

What is the most common congenital adrenal hyperplasia?

Back 19

21-hydroxylase deficiency

Front 20

21-hydroxylase deficiency: ___ mineralocorticoids, ___ cortisol, ___ adrenal androgens.

Back 20

low mineralocorticoids, low cortisol, high adrenal androgens

Front 21

Clinical presentation of 21-hydroxylase deficiency?

Back 21

hypotension, hyperkalemia, high renin, volume depletion (from low aldosterone); hypocortisolism; XY precocious puberty, XX pseudohermaphroditism

Front 22

11B-hydroxylase deficiency has ___ aldosterone, ___ 11-deoxycorticosterone, ___ cortisol and ___ adrenal androgens.

Back 22

low aldosterone, high 11-deoxycorticosterone, low cortisol, and high adrenal androgens

Front 23

Clinical presentation of 11B-hydroxylase deficiency?

Back 23

hypertension (from high 11-deoxycorticosterone); XY precocious puberty; XX pseudohermaphroditism

Front 24

How does cortisol maintain blood pressure?

Back 24

by increasing the expression of alpha 1 receptors on arterioles

Front 25

What cells secrete PTH?

Back 25

Chief cells of the parathyroid gland.

Front 26

How does PTH stimulate bone reabsorption?

Back 26

By increasing osteoblasts' production of M-CSF and RANK-L, which activates osteoclasts.

Front 27

What is the effect of increased PTH secretion on serum Mg2+?

Back 27

decreases Mg2+

Front 28

What is the overall effect of PTH on serum phosphate?

Back 28

decreased, because PTH decreases phosphate reabsorption in the kidneys (which outweighs the phosphate gained from bone breakdown)

Front 29

What is the overall effect of vitamin D on serum phosphate?

Back 29

increases, because it increases reabsorption by the kidneys. This counterbalances PTH's decrease of serum phosphate.

Front 30

What hormones signal through cAMP (hint: FLAT CHAMP).

Back 30

FSH, LH, ACTH, TSH; CRH, hCG, ADH (V2R), MSH, PTH

Front 31

second messenger of FSH signal

Back 31

cAMP

Front 32

second messenger of LH signal

Back 32

cAMP

Front 33

second messenger of ACTH signal

Back 33

cAMP

Front 34

second messenger of TSH signal

Back 34

cAMP

Front 35

second messenger of CRH signal

Back 35

cAMP

Front 36

second messenger of hCG signal

Back 36

cAMP

Front 37

second messenger of ADH (V2R) signal

Back 37

cAMP

Front 38

second messenger of MSH signal

Back 38

cAMP

Front 39

second messenger of PTH signal

Back 39

cAMP

Front 40

What hormones signal though cGMP?

Back 40

The vasodilators: ANP, NO

Front 41

second messenger of nitrous oxide signal

Back 41

cGMP

Front 42

second messenger of ANP signal

Back 42

cGMP

Front 43

What hormones signal through IP3/Ca2+? hint: GOAT HAG

Back 43

GnRH, Oxytocin, ADH (V1R), TRH, histamine (H1), angiotensin II, gastrin

Front 44

second messenger of GnRH signal

Back 44

IP3/Ca2+

Front 45

second messenger of oxytocin signal

Back 45

IP3/Ca2+

Front 46

second messenger of ADH (V1R) signal

Back 46

IP3/Ca2+

Front 47

second messenger of TRH signal

Back 47

IP3/Ca2+

Front 48

second messenger of histamine (H1) signal

Back 48

IP3/Ca2+

Front 49

second messenger of angiotensin II signal

Back 49

IP3/Ca2+

Front 50

second messenger of gastrin signal

Back 50

IP3/Ca2+

Front 51

Which steroid binds its receptor in the nucleus instead of the cytoplasm?

Back 51

T3/T4

Front 52

Which hormones signal through an intrinsic tyrosine kinase, via the MAP-K pathway?

Back 52

insulin, IGF-1, FGF, PDGF

Front 53

signal mechanism for insulin

Back 53

intrinsic tyrosine kinase, MAPK

Front 54

signal mechanism for the growth factors IGF-1, FGF, PDGF

Back 54

intrinsic tyrosine kinase, MAPK

Front 55

What enzyme converts T4 to T3, and where is this enzyme located?

Back 55

5' deiodinase, in the target cell

Front 56

What is the Wolff-Chaikoff effect?

Back 56

the transient decrease in T3/T4 after excessive ingestion of iodide due to inhibition of the iodide pump

Front 57

What is the mechanism of action of methimazole?

Back 57

inhibits thyroid peroxidase

Front 58

What is the mechanism of action of propylthiouracil?

Back 58

inhibits thyroid peroxidase AND 5' deiodinase

Front 59

What tumor is 10% malignant, bilateral, extra-adrenal, calcified, pediatric, and familial?

Back 59

pheochromocytoma

Front 60

What will you find in the urine of someone with a pheochromocytoma?

Back 60

increased vanillylmandelic acid

Front 61

What do you use to treat a pheochromocytoma (besides surgery)?

Back 61

alpha antagonists like phenoxybenzamine

Front 62

What will you find in the urine of someone with neuroblastoma?

Back 62

homovanillic acid from increased dopamine. DO NOT have increased VMA like pheo.

Front 63

What is the breakdown product of epinephrine?

Back 63

metanephrine

Front 64

What is the breakdown product of dopamine?

Back 64

homovanillic acid (HVA)

Front 65

What is the breakdown product of norepinephrine?

Back 65

vanillylmandelic acid (VMA)

Front 66

What type of thyroiditis occurs secondary to a flu-like illness and is painful and granulomatous?

Back 66

de Quervain's (subacute) thyroiditis

Front 67

What is Reidel's thyroiditis?

Back 67

replacement of the thyroid with fibrous tissue

Front 68

What is a thyroid storm?

Back 68

A complication of Graves' disease in which stress-induced catecholamine surge causes death by arrhythmia.

Front 69

What causes the Jod-Basedow phenomenon?

Back 69

Iodine repletion in an iodine-deficienct person can cause thyrotoxicosis.

Front 70

What is Chovstek's sign?

Back 70

tapping the facial nerve causes contraction of the facial muscles (a sign of hypocalcemia)

Front 71

What is Trousseau's sign?

Back 71

occlusion of the brachial artery with BP cuff causes carpal spasm (a sign of hypocalcemia)

Front 72

In primary hyperparathyroidism, calcium will be ___ while phosphate will be ___.

Back 72

Calcium is high, phosphate is low.

Front 73

In secondary hyperparathyroidism, calcium will be ___ while phosphate will be ___.

Back 73

Calcium is low, phosphate is high.

Front 74

What is another name for pseudohypoparathyroidism?

Back 74

Albright's hereditary osteodystrophy

Front 75

What is the inheritance pattern for pseudohypoparathyroidism?

Back 75

autosomal dominant failure of kidneys to respond to PTH

Front 76

What is the treatment for SIADH?

Back 76

demeclocycline, an ADH receptor antagonist

Front 77

Describe the potassium abnormality in DKA.

Back 77

Hyperkalemia with depleted intracellular K+ due to low insulin.

Front 78

What are the 3 neoplasias of MEN1?

Back 78

Parathyroid, Pituitary (prolactin, GH), Pancreas (gastrinoma, VIPoma, insulinoma)

Front 79

What are the 3 neoplasias of MEN2a?

Back 79

Parathyroid, Pheochromocytoma, Medullary thyroid carcinoma

Front 80

What are the 3 neoplasias of MEN2b, and what is the other physical finding?

Back 80

Pheochromocytoma, Medullary thyroid carcinoma, oral/intestinal ganglioneuromas, and Marfanoid habitus

Front 81

Which MEN syndromes include pheochromocytoma?

Back 81

MEN 2a and 2b

Front 82

What MEN syndromes include medullary thyroid carcinoma?

Back 82

MEN 2a and 2b (ret gene!)

Front 83

What MEN syndromes include hyperparathyroidism?

Back 83

MEN 1 and MEN 2a

Front 84

If regular insulin is short-acting, what are lispro and aspart?

Back 84

Rapid-acting

Front 85

If regular insulin is defined as short-acting, what is NPH?

Back 85

intermediate-acting

Front 86

If regular insulin is defined as short-acting, what are glargine and detemir?

Back 86

long-acting

Front 87

tolbutamide

Back 87

first generation sulfonylurea

Front 88

chlorpropramide

Back 88

first generation sulfonylurea

Front 89

glyburide

Back 89

second generation sulfonylurea

Front 90

glimopiride

Back 90

second generation sulfonylurea

Front 91

glipizide

Back 91

second generation sulfonylurea

Front 92

metformin

Back 92

biguanide

Front 93

What is the mechanism of action of sulfonylureas?

Back 93

Close the K+ channel in the B-cell membrane, so the cell depolarizes. Resulting Ca2+ release stimulates INCREASED INSULIN RELEASE.

Front 94

What is the mechanism of action of biguanides like metformin?

Back 94

INCREASED INSULIN SENSITIVITY via decreased gluconeogenesis, increased glycolysis, and increased peripheral glucose uptake.

Front 95

What is the mechanism of action of thiazolidinediones (TZDs)?

Back 95

INCREASE INSULIN SENSITIVITY via binding PPAR-gamma, a nuclear transcription regulator. Also INCREASE ADIPONECTIN.

Front 96

pioglitazone

Back 96

TZD

Front 97

rosiglitazone

Back 97

TZD

Front 98

acarbose

Back 98

alpha-glucosidase inhibitor

Front 99

miglitol

Back 99

alpha-glucosidase inhibitor

Front 100

Mechanism of alpha-glucosidase inhibitors?

Back 100

Inhibit intestinal brush border alpha-glucosidases, so decrease absorption of carbohydrates.

Front 101

Mechanism of action of pramintide?

Back 101

decreases glucagon secretion

Front 102

Mechanism of action of exenatide?

Back 102

GLP1 analogue that increases insulin release and decreases glucagon release

Front 103

exenatide

Back 103

GLP1 analogue

Front 104

Major side effect of first generation sulfonylureas?

Back 104

disulfiram-like rxn when combined w alcohol

Front 105

Major side effect of second generation sulfonylureas?

Back 105

hypoglycemia

Front 106

Major side effect of metformin?

Back 106

lactic acidosis

Front 107

Major side effects of TZDs?

Back 107

weight gain, edema, CHF, hepatotoxicity (CONTRAINDICATED IN CHF!!!)

Front 108

Major side effect of alpha-glucosidase inhibitors?

Back 108

diarrhea

Front 109

Major side effect of pramintide?

Back 109

hypoglycemia, n/v, diarrhea

Front 110

Major side effect of exenatide?

Back 110

n/v, pancreatitis