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USMLE Step 3 Master the board COPY > Endocrinology COPY > Flashcards

Endocrinology COPY Flashcards

1
Q

How is DM dignosis made?

A
  1. Two fasting glucose ≥ 126
  2. One random glucose ≥ 200 with symptoms (polyuria, polydipsia, polyphagia)
  3. Abnormal glucose tolerance test > 200mg/dL (2-hour glucose tolerance test with 75 g glucose load)
  4. Hemoglobin A1c > 6.5%

Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Locations 2896-2902). . Kindle Edition.

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2
Q

Best initial therarp for type 2 DM

A

Diet, exercise and weight loss

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3
Q

Best initial medical therapy for adult onset DM

A

Metformin

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4
Q

Why is metformin beneficial in obese DM patients?

A

Because it does not lead to weight gain

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5
Q

How does metformin work?

A

By blocking gluconeogenesis

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6
Q

What are the advantages of metformin?

A
  • No risk of hypoglycemia
  • Does not increase obesity
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7
Q

What are the contraindications to use of metformin?

A

Renal insufficiency

Use of contrast agents

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8
Q

Name the common DM medications

A

Metformin

Sulfonylureas

Dipeptidyl peptidase IV (DPP IV)

Thiazolidinidiones

Alpha glucosidase inhibitors

Insulin secretagogues

Glucagon-like peptides (GLP) analogues

Long-acting insulin

Short-acting insulin

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9
Q

Name three examples of sulfonylureas

A

Glyburide

Glimepiride

Glipizide

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10
Q

What is the mechanism of actions of sulfonylureas

A

By increasing the release of insulin from the pancreas

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11
Q

Side effects of sulfonylureas

A

Hypoglycemia

SIADH

Weight gain

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12
Q

Side effect of metformin

A

Risk of lactic acidosis in patients with renal insufficiency

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13
Q

Name three examples of Dipeptidyl peptidase IV (DPP-IV) inhibitors

A

Sitagliptin

Saxagliptin

Vildagliptin

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14
Q

Name two examples of thiazolidiones (“glitazones”)

A

Rosiglitazone

Pioglitazone

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15
Q

Side effects of thiazolidiones

A

Hepatocellular injury

Anemia

Pedal edema

CHF

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16
Q

Mechanism of action of thiazolidiones

A

Increasing peripheral insulin sensitivity

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17
Q

Name two examples of alpha-glucosidase inhibitors

A

Acarbose

Miglitol

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18
Q

Mechanism of action of alpha-glucosidase inhibitors

A

These agents block the absorption of glucose at the intestinal lining

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19
Q

Side effects of alpha-glucosidase inhibitors

A

Diarrhea

Abdominal pain

Bloating

Flatulence

Elevated LFTs

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20
Q

Name two examples of Insulin secretagogues (Meglitinides)

A

Nateglinide

Repaglinide

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21
Q

Mechanism of action of Insulin secretagogues (Meglitinides)

A

Increased release of insulin from the pancreas (similar to sulfonylureas)

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22
Q

Side effects of of Insulin secretagogues (Meglitinides)

A

Hypoglycemia

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23
Q

Name two examples of Glucagon-like peptide-1 (GLP-1) analogs

A

Exenatide

Liraglutide

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24
Q

Mechanism of action of Glucagon-like peptide-1 (GLP-1) analogs

A

Increase insulin and decrease glucagon

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25
Q

Side effects of Glucagon-like peptide-1 (GLP-1) analogs

A

Nausea

Vomiting

Weight loss

Hypoglycemia

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26
Q

When is insulin introduced in the Rx of type 2 DM

A

If other agents do not sufficiently control the level of glucose, then the patient is switched to insulin. A long-acting insulin, such as insulin glargine, which is a once-a-day injection with an extremely steady-state level of insulin, is used in combination with a very short-acting insulin at mealtime.

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27
Q

Name 4 short-acting insulin

A

Regular insulin

Lispro

Aspart

Glulisine

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28
Q

Name 3 long-acting insulin

A

NPH (Neutral Protamine Hagedorn): twice a day

Detemir

Glargine: once a day

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29
Q

Name the symptoms and signs of DKA

A

“Fruity breath”

Kussmaul hyperpnea

Dehydration

Abdominal pain

Increase annion gap

Hyperkalemia

Hyperglycemia

Ketones in blood/urine

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30
Q

Best initial test for DKA

A

Serum bicarbonate is the best way to determine the severity of illness

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31
Q

Lab findings in DKA

A

Hyperglycemia

Hyperkalemia

Decreased serum bicarbonate

Low pH, with low pCO2 as respiratory compensation

Acetone, acetoacetate, and beta hydroxybutyrate levels are elevated

Elevated anion gap

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32
Q

How is patient improvement monitored in DKA?

A

By monitoring anion gap

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33
Q

Outline the management of DKA

A

Admit ICU/ward

Fluid resuscitation (NS + IV insulin)

Monitor Na+ K+ phosphate and glucose

Change NS to D5NS when glucose level < 250 mg/L

Change IV insulin to an SQ insulin sliding scale once the anion gap normalizes

Continue IV insulin for at least 30 minutes following the administration of the first dose of SQ insulin

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34
Q

Name the complications of DKA

A

HTN

Retinopathy (proliferative)

Nephropathy

Neuropathy

Erectile dysfunction

Gastroparesis

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35
Q

Rx for gastroparesis in DM

A

Metoclopromide

Erythromycin

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36
Q

Rx of DM neuropathy

A

Gabapentin

Pregabalin

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37
Q

LDL goal in DM

A

< 100

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38
Q

LDL goal in CAD and DM

A

< 70

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39
Q

Rx of retinopathy in DM

A

Laser photocoagulation

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40
Q

Diagnostic criteria for hyperglycemic hyperosmolar nonketotic diabetic state/coma

A

Serum glucose > 600 mg/dL (hyperglycemia)

Serum pH > 7.3

Serum bicarbonate > 15 mEq/L

Anion gap 14 mEq/L (normal)

Serum osmolality > 310 mOsm/kg.

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41
Q

Clinical features of hypothyroidism

A

Weight Gain

intolerance Cold intolerance

Coarse hair

Dry skin

Depressed

Bradycardia

Diminished reflexes

Muscle weakness

Fatigue

Menstrual changes

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42
Q

Clinical features of hyperthyroidism

A

Weight loss

Heat intolerance

Fine hair

Moist skin

Anxious

Tachycardia, tachyarrhythmias such as atrial fibrillation

Muscle weakness

Fatigue

Menstrual changes

43
Q

Best initial tests for hypothyroidism

A

T4 (decreased)

TSH (elevated)

44
Q

Rx for hypothyroidism

A

T4 ot thyroxine replacement. T4 will be converted to T3 in the local tissues as needed

45
Q

Best initial tests for hyperthyroidism

A

T4 (increased)

TSH (often decreased)

46
Q

Name the four forms of hyperthyroidism

A

Grave’s disease

Silent thyroiditis

Subacute thyroiditis

Pituitary adenoma

47
Q

Findings in diagnostic testings for Grave’s disease

A

TSH - low

T4 - high

RAIU(radioactive iodine reuptake) - elevated

48
Q

Findings in diagnostic testings for “Silent” thyroiditis

A

TSH - low (not specific for this form of hyperthyroidism)

T4 - high

RAIU(radioactive iodine reuptake) - low

49
Q

In which form of hyperthyroidism may present with antibodies to thyroid peroxidase and antithyroglobulin antibodies

A

Silent thyroiditis

50
Q

Name the only cause of hyperthyroidism with an elevated TSH

A

Pituitary adenoma

51
Q

Rx for hypothyroidism

A

T4 or thyroxine replacement. T4 will be converted to T3 in the local tissue as needed

52
Q

Outline the Rx of thyroid storm and the role of medications used

A

Iodine: Blocks uptake of iodine into the thyroid gland

Propylthiouracil or methimazole: Blocks production of thyroxine

Dexamethasone: Blocks peripheral conversion of T4 to T3

Propranolol: Blocks target organ effect

53
Q

Most common cause of hypercalcemia

A

Primary hyperparathyroidism

54
Q

Causes of hypercalcemia

A

Primary hyperparathyroidism

Malignancy: Produces a parathyroid hormone– like particle

Granulomatous disease: Sarcoid granulomas actually make vitamin D

Vitamin D intoxication

Thiazide diuretics: These increase tubular reabsorption of calcium

Tuberculosis

Histoplasmosis

Berryliosis

55
Q

Criteria for surgical removal of the parathyroid gland

A

Any symptomatic disease (“ stones, bones, psychic moans, GI groans”)

Renal insufficiency, no matter how slight

Markedly elevated 24-hour urine calcium

Very elevated serum calcium (> 12.5)

56
Q

Normal serum calcium level

A

8.4 - 10.2 mg/dL

57
Q

Outline Rx for acute severe hypercalcemia

A
  1. Hydration: High volume (3– 4 liters) of normal saline
  2. Furosemide: Only after hydration has been given. Loop diuretics increase calcium excretion by the kidney
  3. Bisphosphonate (pamidronate) is very potent but slow, taking a week to work.
  4. Calcitonin: If hydration and furosemide do not control the calcium and you need something faster than a bisphosphonate, then calcitonin is the answer.
  5. Steroid: Use if the etiology is granulomatous disease.
58
Q

Name the clinical features of acute severe hypercalcemia

A

Confusion

Constipation

Polyuria and polydipsia from nephrogenic diabetes insipidus

Short QT syndrome on the EKG

Renal insufficiency, ATN, kidney stone

59
Q

Clinical presentation of Cushing syndrome

A

Fat redistribution: Truncal obesity, “moon face,” buffalo hump, thin arms and legs

Easy bruising and striae: Loss of collagen from the cortisol thins the skin

Hypertension: From fluid and sodium retention (look for hypokalemia in hyperaldosteronism)

Muscle wasting

Hirsutism: From increased adrenal androgen levels

60
Q

Anosmia with hypogonadism (low GnRH, FSH, and LH)

A

Kallman’s syndrome

61
Q

Clinical features of Klinefelter’s syndrome

A

Insensitivity of the FSH and LH receptors on their testicles

XXY on karyotype

The FSH and LH levels are very high, but no testosterone is produced from the testicles.

62
Q

Features common to all forms of congenital adrenal hyperplasia (CAH)

A

Elevated ACTH

Low aldosterone and cortisol levels

Treatable with prednisone, which inhibits the pituitary.

63
Q

What forms of CAH has HTN

A

11 and 17 hydroxylase deficiencies

64
Q

Virilization is seen in which of the CAH

A

21 and 11 hydroxylase deficiencies

65
Q

Diagnosis: CAH with increased 17 hydroxyprogesterone level

A

21 hydroxylase deficiency

66
Q

Cause of Hirsutism in 21 and 11 hydroxylase deficiencies

A

Increased andrenal androgens

67
Q

Most accurate diagnostic test for prolactinoma

A

MRI of the brain

68
Q

Best initial therapy for prolactinoma

A

Dopamine agonists:

  • Bromocriptine
  • Cabergoline
69
Q

Why is DM common among those with acromegaly?

A

Because growth hormone acts as an anti-insulin

70
Q

Best initial test for acromegaly

A

Insulin-like growth factor (IGF)

71
Q

Why is GH not the best initial test for acromegaly?

A

Growth hormone (GH) level is not done first, because GH has its maximum secretion in the middle of the night during deep sleep. GH also has a short half-life.

72
Q

Most acurate test to diagnose acromegaly

A

Suppression of GH by giving glucose excludes acromegaly.

73
Q

What is the place of MRI in the diagnosis of acromegaly?

A

To locate the lesion

74
Q

Outline the Rx of acromegaly

A

Surgical resection with transphenoidal removal cures 70 percent of cases

Octreotide: Somatostatin has some effect in preventing the release of growth hormone

Cabergoline or bromocriptine: Dopamine agonists inhibit growth hormone release

Pegvisomant: This is a growth hormone receptor antagonist.

75
Q

Clinical features of Turner’s syndrome

A

Short stature

Webbed neck

Wide-spaced nipples

Scant pubic and axillary hair

The XO karyotype prevents menstruation.

Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Locations 3488-3490). . Kindle Edition.

76
Q

What is the etiopathogenesis of testicular feminization syndrome?

A

The absence of testosterone receptors results in no penis, prostate, or scrotum.

Fischer, Conrad (2012-09-22). Master the Boards: USMLE Step 3 (Kindle Location 3492). . Kindle Edition.

77
Q

Name two causes of primary amenorrhea

A

Turner’s syndrome

Testicular feminization syndrome

78
Q

Enumerate the causes of secondary amenorrhea

A

Pregnancy

Exercise

Extreme weight loss

Hyperprolactinemia

Polycystic ovary syndrome

79
Q

Best initial tests for pheochromocytoma

A

High plasma and urinary catecholamine levels

Plasma-free metanephrine and VMA levels

80
Q

Most accurate test for pheochromocytoma

A

CT or MRI of the adrenal glands

81
Q

Rx outline for pheochromocytoma

A

Phenoxybenzamine (alpha blockade) first to control blood pressure. Without alpha blockade, patients’ blood pressure can significantly drop intraoperatively

Propranolol is used after an alpha blocker like phenoxybenzamine.

Surgical or laparoscopic resection

82
Q

What is the strongest indication for screening for DM

A

HTN

83
Q

Name the characteristics of MEN syndrome type 1 (Wermer’s syndrome)

A

Parathyroid hyperplasia

Pancreatic islet cell tumor

Pituitary adenoma

84
Q

Name the characteristics of MEN syndrome type 2A (Sipple’s syndrome)

A

Parathyroid hyperplasia

Thyroid medullary cancer

Pheochromocytoma

85
Q

Name the characteristics of MEN syndrome type 2B

A

Thyroid medullary cancer

Pheochromocytoma

Mucocutaneous neuromas

Ganglioneuromatosis of the colon

Marfan-like habitus

86
Q

Presentation of severe hypocalcemia

A

Seizures

Neural twitching (Chvostek’s sign and Trousseau’s sign)

Arrhythmia: prolonged QT on ECG

87
Q

Rx outline for hypocalcemia

A

Replace calcium

Calcium + Vit D (for Vit D def and hypoparathyroidism)

88
Q

Name the anterior pituitary hormones and the hypothalmic hormones that control their release

A
  • ACTH controlled by CRH
  • GH controlled by GHRH
  • TSH controlled by TRH
  • LH controlled by GnRH
  • FSH controlled by GnRH
  • PRL controlled by Dopamine (inhibits)
89
Q

Diagnosis: HTN + Low renin + Low potassium

A

Hyperaldosteronism

90
Q

Confirmatory diagnostic test for hyperaldosteronism

A

CT scan of the adrenals

91
Q

Risk factors for osteoporosis

A

Menopause

Low BMI

Family hx of osteoporosis

Early ovarian failure

Low calcium intake

Smoking

Nulliparity

Alcohol

High caffeine intake

(Source: S95)

92
Q

What are implications of prebreakfast, prelunch, predinner and bedtime glucose levels?

A

Prebreakfast glucose level: Reflects predinner NPH dose.

Prelunch glucose level: Reflects prebreakfast regular insulin dose.

Predinner glucose level: Reflects prebreakfast NPH dose.

Bedtime glucose level: Reflects predinner regular insulin dose.

93
Q

What are the time of onset, peak effect and duration of regular insulin

A

Onset: 30-60 minutes

Peak effect: 2-4 hours

Duration: 5-8 hours

94
Q

What are the time of onset, peak effect and duration of lispro

A

Onset: 5-10 minutes

Peak effect: 0.5-1.5 hours

Duration: 6-8 hours

95
Q

What are the time of onset, peak effect and duration of aspart

A

Onset: 10-20 minutes

Peak effect: 1-3 hours

Duration: 3-5 hours

96
Q

What are the time of onset, peak effect and duration of glulisine

A

Onset: 5-15 minutes

Peak effect: 1.0-1.5 hours

Duration: 1.0-2.5 hours

97
Q

What are the time of onset, peak effect and duration of NPH (Neutral Protamine Hagedorn)

A

Onset: 2-4 hours

Peak effect: 6-10 hours

Duration: 18-28 hours

98
Q

What are the time of onset, peak effect and duration of detemir

A

Onset: 2 hours

Peak effect: No discernible peak

Duration: 20 hours

99
Q

What are the time of onset, peak effect and duration of glargine

A

Onset: 1-4 hours

Peak effect: No discernible peak hour

Duration: 20-24 hours

100
Q

Possible diagnoses:

  • TSH - low
  • T4 - high
  • RAIU - decrease
A

Subacute thyroiditis (hyperthyroid stage)

Hashimoto thyroiditis (hyperthyroid stage)

Exogenous T3/T4: levothyroxine

Postpartum thyroiditis

101
Q

Possible diagnoses:

  • TSH - low
  • T4 - high
  • RAIU - increase
A
  • Graves’ disease
  • Toxic adenoma
  • Multinodular goiter
102
Q

Possible diagnoses:

TSH - low
T4 - decrease

A

Pituitary hypothyroidism

Hypothalamic hypothyroidism

103
Q

What are the predominant estrogens in reproductive years and during menopause?

A

Under the stimulation of the stimulizing leutinizing hormone (LH), the theca cells of the post-menopausal ovary produce androstenedione and testosterone.

Estrone, a product of androstenedione conversion in adipose tissue, is the predominant estrogen in menopause.

Estradiol is the most prevalent estrogen in the reproductive years, and estriol is made by the placenta during pregnancy.

Estrane is a minor estrogen

104
Q

What is hungry bone syndrome?

A

Hypocalcemia following surgical correction of hyperparathyroidism in patients with severe, prolonged disease, as calcium is rapidly taken from the circulation and deposited into the bone.

USMLE Step 3 Master the board COPY (33 decks)

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