MKSAP Board Basics Endocrinology Flashcards

1
Q

What’s the difference between type 1A and 1B diabetes mellitus?

A

Type 1A - Autoimmune with specific autoantibodies (e.g. GAD-65, IA-2) detectable.
Present in more than 90% of cases.

Type 1B - Idiopathic, no autoimmune markers,
More common in those with Asian/African ancestry.

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2
Q

Is it best to give basal insulin in the morning or at night?

A

At night

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3
Q

What causes “dawn phenomenon”? (Where does the glucose come from?)

A

Hepatic gluconeogenesis

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4
Q

How do you fix (i.e. reset) hypoglycemia unawareness?

A

Allowing the average plasma glucose to increase for several weeks

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5
Q

What percentage of type 2 diabetes mellitus patients have microvascular disease at the time of presentation?

A

20%

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6
Q

What percentage of type 2 diabetes mellitus patients have macrovascular disease (e.g. CAD or peripheral vascular disease at time of presentation?

A

More than 20%

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7
Q

What percentage of patients in the United States with diabetes mellitus have MODY (maturity-onset diabetes of youth)?

A

5%

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8
Q

At what age does MODY present?

A

Below 25 years

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9
Q

USPSTF recommends screening for abnormal blood glucose as part of cardiovascular risk assessment in adults aged ________________ who are overweight or obese.

A

40 - 70 years

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10
Q

What are the risk factors for diabetes mellitus that should prompt screening?

A

Family history of diabetes mellitus
History of gestational diabetes
PCOS
Certain racial/ethnic groups.
Obese/overweight adults between 40 - 70 years old.

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11
Q

The American Diabetes Association recommends screening overweight adults with one additional risk factor, and all adults aged ____.

A

Over 35 years

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12
Q

What is the definition of overweight in Asian Americans?

A

BMI equal to or more than 23 kg/m2

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13
Q

What are the screening tests used for diabetes mellitus?

A

Fasting plasma glucose level
2-hour post-prandial glucose during oral glucose tolerance test
HbA1c

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14
Q

How many screening tests do you need to diagnosis diabetes mellitus?

A

2

If 2 simultaneous screening tests are abnormal - diagnose diabetes mellitus; if only one is abnormal then repeat the abnormal one.

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15
Q

How can you diagnose diabetes mellitus on the basis of a random glucose level?

A

A single random glucose level of > 200 mg/dL along with symptoms of hyperglycemia (polyuria, polydipsia, polyphagia) is diagnostic of diabetes mellitus.

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16
Q

What 2-hr glucose value during an OGTT is diagnostic of diabetes mellitus?

A

200 mg/dL or over

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17
Q

What 2-hr glucose value during an OGTT is diagnostic of pre-diabetes?

A

140 - 199 mg/dL

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18
Q

What reduces risk of developing diabetes mellitus in patients with pre-diabetes more - metformin or lifestyle modifications?

A

Lifestyle modifications

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19
Q

Can an insulin pump increase adherence in a patient who is not adherent to multiple daily insulin injections?

A

No

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20
Q

What percentage of patients taking metformin develop vitamin B12 deficiency?

A

5 - 10%

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21
Q

At what GFR is metformin contraindicated?

A

Less than or equal to 30 mL/min/1.73 m2

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22
Q

Which 3 diabetes mellitus drug classes cause weight loss?

A

GLP1 agonists
SGLT2 inhibitors
Amylinomimetics (pramlintide)

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23
Q

How do you screen for diabetic neuropathy?

A

10 g monofilament
128-Hz tuning fork
Pedal pulses
Ankle reflex

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24
Q

When should you start screening for complications in type 1 diabetes mellitus?

A

5 years after initial diagnosis (continue annually thereafter)

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25
Q

When should you start screening for complications in type 2 diabetes mellitus?

A

At the time of diagnosis (continue annually thereafter)

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26
Q

What are the indications for a moderate intensity statin in patients with diabetes mellitus?

A

Age over 40 years and an ASCVD risk of less than 7.5%
(AHA/ACC)

Age 40 - 75 years and an ASCVD risk of 10% or more
(USPSTF)

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27
Q

What are the indications for a high intensity statin in patients with diabetes mellitus?

A

Coronary artery disease, peripheral vascular disease or ASCVD risk of 7.5% or higher.
(AHA/ACC)

Age 40 - 75 years and an ASCVD risk of 10% or more
(USPSTF)

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28
Q

What is the goal blood pressure in patients with diabetes mellitus?

A

< 130/80 mmHg (ACC/AHA)

< 140/90 mmHg (ADA)

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29
Q

Urine albumin excretion higher than ______ indicates diabetic nephropathy

A

30 mg/g of creatinine

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30
Q

Dot-and-blot hemorrhages and clusters of hard, yellowish exudates are characteristic of _______

A

Non-proliferative diabetic retinopathy

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31
Q

Neovascularization (a network of new blood vessels) protruding from the optic nerve is characteristic of _______

A

Proliferative diabetic retinopathy

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32
Q

How can you prevent diabetic retinopathy?

A

Blood glucose control
Blood pressure control
Smoking cessation

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33
Q

Treatment options for severe non-proliferative diabetic retinopathy and proliferative diabetic retinopathy.

A

Panretinal laser photocoagulation

Intraocular injections of bevacizumab or ranibizumab

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34
Q

Treatment options for macular edema in diabetes mellitus patients.

A

Intraocular injections of bevacizumab or ranibizumab

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35
Q

Treatment options for gastroparesis in patients with diabetes mellitus.

A

Small feedings
Metoclopramide
Erythromycin

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36
Q

What is the treatment of diabetic mononeuropathy (e.g. third nerve palsy)?

A

Nothing.
Symptoms resolve spontaneously.

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37
Q

What is the definition of hyperglycemic hyperosmolar syndrome?

A

Plasma osmolality > 320 mOsm/kg H2O
Glucose > 600 mg/dL
No/low ketones.
No acidosis.

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38
Q

What diagnosis should be considered in any older patient with altered mental status and hypovolemia?

A

Hyperglycemic hyperosmolar syndrome

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39
Q

What fluids should you use in hyperglycemic hyperosmolar syndrome?

A

Normal saline first to replenish extracellular space.
Hypotonic fluids after blood pressure is restored and urine output is established.

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40
Q

When should you give IV insulin in patients with hyperglycemic hyperosmolar syndrome?

A

After expansion of the intravascular space has begun.

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41
Q

When should you switch to subcutaneous insulin in patients with hyperglycemic hyperosmolar syndrome?

A

Once blood glucose is less than 200 mg/dL and the patient is eating.

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42
Q

Which fluids should you give in diabetic ketoacidosis?

A

Normal saline for immediate volume replacement and switch to 0.45% saline if the sodium is high or normal after the initial bolus.

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43
Q

When should you start potassium replacement in diabetic ketoacidosis?

A

When potasstium is < 5.5 meq/L

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44
Q

When should you start the glucose infusion along with the insulin infusion in a patient with diabetic ketoacidosis?

A

When the blood glucose is less than 250 mg/dL

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45
Q

When do you replace the potassium in a patient with diabetic ketoacidosis?

A

When serum potassium is less than 5.5 mEq/L

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46
Q

What do you do if a patient with diabetic ketoacidosis presents with a serum potassium of less than 3.3 mEq/L?

A

Delay the initiation of the insulin infusion.

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47
Q

Is severe acidosis in diabetic ketoacidosis treated with bicarbonate?

A

No. Evidence of benefit is lacking.

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48
Q

What is the glucose goal for critically ill patients in the hospital?

A

140 - 180 mg/dL

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49
Q

What is the treatment for critically ill patients in the hospital with glucose levels above 180 - 200 mg/dL

A

Insulin infusion

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50
Q

Is tight inpatient glycemic control (80 - 110 mg/dL) recommended for hospitalized patients with diabetes mellitus?

A

No.
It is not consistently associated with improved outcomes and may increase mortality.

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51
Q

What is the recommended medication for hospitalized patients with diabetes mellitus?

A

Insulin

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52
Q

Can oral or non-insulin drugs be considered in hospitalized patients with diabetes mellitus type 2?

A

Only if patients are stable with no anticipated changes in nutrition or hemodynamic status.

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53
Q

How are pregnant women screened for gestational diabetes?

A

Screening at 24 - 28 weeks with 75 gram 2-hr OGTT

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54
Q

How often should patients with a history of gestational diabetes be screened for development of type 2 diabetes mellitus after delivery?

A

Annually

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55
Q

What is the target HbA1c is pregnancy to decrease risk of congenital malformations and fetal loss?

A

Within 1% of normal i.e. 6.6% or lower.

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56
Q

What are the glycemic targets during pregnancy?

A

Premeal glucose: < 95 mg/dL
1-hr post-prandial: < 140 mg/dL
2-hr post-prandial: < 120 mg/dL

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57
Q

What is the medication of choice in gestational diabetes?

A

Insulin

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58
Q

How often should patients with diabetes mellitus be screened for diabetic retinopathy during pregnancy?

A

Once per trimester

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59
Q

Which blood pressure medications can safely be used during pregnancy?

A

Methyldopa
Beta-blockers (except atenolol)
Calcium channel blockers
Hydralazine

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60
Q

When should you evaluate a patient for hypoglycemia?

A

When they meet Whipple’s triad:
- Neuroglycopenic symptoms
- Glucose < 55 mg/dL
- Resolution of symptoms with glucose ingestion

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61
Q

What are the types of hypoglycemic disorders?

A

Fasting
Post-prandial

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62
Q

What evaluation needs to be done in all patients with fasting hypoglycemia?

A

Screen for use of hypoglycemic agents e.g. insulin or sulfonylurea.

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63
Q

MEN1

A
  • Primary hyperparathyroidism (multigland)
  • Pituitary adenoma
  • Pancreatic neuroendocrine tumors
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64
Q

How is an insulinoma diagnosed?

A

72-hr fast with the following results:

Fasting plasma glucose < 45 mg/dL
Serum insulin > 5 - 6 mU/L
Elevated C-peptide level

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65
Q

What is the imaging study of choice after an insulinoma is diagnosed?

A

CT abdomen

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66
Q

What happens to the C-peptide levels in case of surreptitious use of oral hypoglycemic agents (e.g. sulfonylureas or meglitinide)?

A

Inappropriately elevated at time of hypoglycemia

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67
Q

What happens to the C-peptide levels in case of surreptitious use of insulin?

A

Low at the time of hypoglycemia

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68
Q

Are home glucometers accurate?

A

For the most part but they can be inaccurate in the hypoglycemia range.

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69
Q

Do patients who don’t have Whipple’s triad need to be evaluated for hypoglycemia?

A

No

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70
Q

How do you treat acute hypoglycemia?

A

Oral carbohydrates
IV glucose
IM glucagon

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71
Q

What is the most common cause of hypopituitarism?

A

Pituitary adenoma

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72
Q

What diagnosis should be considered when a patient presents with sudden onset headache, visual changes, ophthalmoplegia, and altered mental status?

A

Pituitary apoplexy (sudden pituitary hemorrhage or infarction)

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73
Q

What diagnosis should be considered in patients presenting with amenorrhea, post-partum inability to lactate, and fatigue?

A

Sheehan syndrome (postpartum pituitary necrosis)

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74
Q

When do most cases of lymphocytic hypophysitis occur?

A

During or after pregnancy

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75
Q

What are non-hormonal symptoms of pituitary adenomas (mass effect)?

A
  • Peripheral vision loss
  • Headache
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76
Q

What is the most accurate way to test for secondary adrenal insufficiency?

A

Metyrapone stimulation test

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77
Q

Which two steroids are measured in a metyrapone stimulation test?

A
  • Cortisol
  • 11-deoxycortisol
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78
Q

What is the imaging of choice for a pituitary problem?

A

Pituitary MRI

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79
Q

Should FSH/LH be measured in women with normal menstrual cycles when assessing for pituitary problems?

A

No

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80
Q

Should growth hormone be measured or IGF-1 - and why?

A

IGF-1
Growth hormone is pulsatile

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81
Q

What is the treatment of a pituitary apoplexy?

A

Glucocorticoids until adrenal insufficiency is ruled out.
May need urgent neurosurgical decompression.

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82
Q

What is thyroid hormone replacement based on in patients with secondary hypothyroidism?

A

Free T4 levels

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83
Q

What should you do before treating secondary hypothyroidism with thyroid hormone replacement?

A

Treat or rule out adrenal insufficiency

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84
Q

What happens to the serum sodium levels in adrenal insufficiency?

A

Stay normal or go low.
(Adrenal insufficiency is a cause of hyponatremia)

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85
Q

What is a pituitary microadenoma?

A

Pituitary adenoma less than 1 cm in size

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86
Q

What is a pituitary macroadenoma?

A

Pituitary adenoma 1 cm or larger in size

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87
Q

What non-pituitary conditions can cause enlargement of the pituitary gland?

A
  • Untreated primary hypothyroidism
  • Pregnancy
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88
Q

What is the confirmatory test for acromegaly?

A

Oral glucose tolerance test to suppress growth hormone

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89
Q

What are the tests to confirm Cushing’s disease?

A

24-hr urine collection for cortisol
Dexamethasone suppression test
Late night salivary cortisol
ACTH (elevated or inappropriately normal in Cushing’s disease)

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90
Q

Which patients with primary hyperparathyroidism need to be evaluated for a pituitary adenoma?

A

Those with a family history of MEN1

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91
Q

Can psychotropic agents cause hyperprolactinemia?

A

Yes

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92
Q

Can protease inhibitors cause hyperprolactinemia?

A

Yes

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93
Q

Can opiates cause hyperprolactinemia?

A

Yes

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94
Q

Can methyldopa cause hyperprolactinemia?

A

Yes

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95
Q

Can beta-blockers cause hyperprolactinemia?

A

No

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96
Q

Can calcium channel blockers cause hyperprolactinemia?

A

Yes

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97
Q

Can domperidone cause hyperprolactinemia?

A

Yes

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98
Q

Can metoclopramide cause hyperprolactinemia?

A

Yes

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99
Q

Can tricyclic antidepressants cause hyperprolactinemia?

A

Yes

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100
Q

Can anti-seizure medications cause hyperprolactinemia?

A

Yes

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101
Q

What should you get in all women with hyperprolactinemia?

A

Pregnancy test
TSH level

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102
Q

What should you get in all patients with hyperprolactinemia?

A

TSH level
(Primary hypothyroidism causes hyperprolactinemia)

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103
Q

In patients with hyperprolactinemia - what is the usual level of prolactin if this is caused by drugs or a “non-prolactinoma” condition?

A

< 150 ng/mL

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104
Q

What kind of pituitary adenomas should you treat with “observation”?

A
  • Non-functioning pituitary microadenomas
  • Microprolactinomas in women with normal menstrual cycles
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105
Q

What kind of pituitary adenomas should you treat with a dopamine agonist?

A

Prolactinoma that is symptomatic

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106
Q

What is the recurrence rate of treated prolactinomas after they disappear off imaging?

A

Up to 50%

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107
Q

What kind of pituitary adenomas should you treat with surgery?

A
  • Secreting anything other than prolactin
  • Causing symptoms or mass effect (vision problem, hypopituitarism)
  • Prolactinomas unresponsive to dopamine agonists
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108
Q

What conditions should you test for in patients with polyuria?

A
  • Diabetes mellitus
  • Diabetes insipidus
  • Hypercalcemia
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109
Q

How is the diagnosis of diabetes insipidus confirmed?

A
  • Water deprivation test: inability to concentrate urine
  • Urine osmolality < 200 mOsm/kg H2O
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110
Q

How do you differentiate between central and nephrogenic diabetes insipidus?

A

Desmopressin challenge test

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111
Q

What is the imaging study of choice if the desmopressin challenge test is positive (i.e. urine concentrates) in diabetes insipidus?

A

MRI pituitary

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112
Q

What is the imaging study of choice if the desmopressin challenge test is negative (i.e. urine does not concentrate) in diabetes insipidus?

A

Renal ultrasound

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113
Q

What is the treatment of lithium induced nephrogenic diabetes insipidus?

A
  • Stop lithium
  • Add amiloride
114
Q

What is the treatment of non-drug-induced nephrogenic diabetes insipidus?

A
  • Thiazide diuretics
  • Salt restriction
115
Q

What laboratory tests are checked in asymptomatic patients with empty sella syndrome?

A

Cortisol
TSH
Free or total T4

116
Q

Is repeat imaging necessary in patients with empty sella syndrome who have negative hormonal work-up?

A

No

117
Q

Is it more common to have permanent hypothyroidism following post-partum thyroiditis or subacute thyroiditis?

A

Post-partum thyroiditis

118
Q

How long does it take for thyroid function tests to normalize after euthyroid sick syndrome (nonthyroidal illness syndrome)?

A

4 - 8 weeks after recovery from illness

119
Q

Which medication is used to treat hypothyroidism?

A

Levothyroxine

120
Q

When would you consider measuring a calcitonin level in a patient with no known thyroid disease?

A
  • Family or personal history of MEN2
  • Family history of medullary thyroid cancer
  • Hypercalcemia
121
Q

What is the most common cause of Cushing’s syndrome?

A

Iatrogenic (exogenous steroid use)

122
Q

What dose of prednisone typically causes hypothalamic-pituitary-adrenal axis suppression?

A

More than 10 - 20 mg/day for 3 or more consecutive weeks.

123
Q

What dose of prednisone is unlikely to cause clinically significant hypothalamic-pituitary-adrenal suppression?

A

5 mg/day or less

124
Q

Is facial plethora specific for Cushing’s syndrome?

A

Yes

125
Q

Is centripetal obesity specific for Cushing’s syndrome?

A

Yes

126
Q

Are supraclavicular or dorsocervical fat pads specific for Cushing’s syndrome?

A

Yes

127
Q

Which imaging study should you order in a Cushing’s patient if the ACTH is > 20 pg/mL and cortisol is not suppressed?

A

Pituitary MRI (or CT).

128
Q

Which imaging study should you order in a Cushing’s patient if the ACTH is < 5 pg/mL?

A

CT abdomen / adrenal CT

129
Q

What should you do if the ACTH is elevated but no pituitary tumor is identified in a Cushing’s patient?

A

High dose (8 mg) dexamethasone suppression test to differentiate between pituitary and ectopic ACTH production.

130
Q

What is the diagnosis if high dose (8 mg) fails to suppress cortisol?

A

Ectopic ACTH production

131
Q

What are the most common ACTH-secreting malignant tumors?

A
  • Small cell lung cancer
  • Bronchial carcinoid
  • Pheochromocytoma
  • Medullary thyroid carcinoma
132
Q

What is the source of ACTH if a high dose (8 mg) dexamethasone suppression test suppresses both pituitary ACTH production and adrenal cortisol production?

A

Source is pituitary

133
Q

Which study is performed if high dose dexamethasone suppression test indicates pituitary source of Cushing’s but no pituitary adenoma is seen on imaging?

A

Intrapetrosal sinus sampling (IPSS) for ACTH

134
Q

What are some (three) common reasons for a false positive dexamethasone suppression test?

A
  • Obesity
  • Alcohol use
  • Psychological disorders
135
Q

What the treatment of choice for low bone density caused by endogenous hypercortisolism?

A

Bisphosphonates

136
Q

What is the definition of an adrenal incidentaloma?

A

Adrenal adenoma of 1 cm or larger than is discovered incidentally.

137
Q

All asymptomatic patients with adrenal incidentalomas should have which tests done?

A
  • 1 mg overnight dexamethasone suppression test
  • 24-hr urine measurement of metanephrines and catecholamines
138
Q

Which patients with adrenal incidentalomas should have their plasma aldosterone and plasma renin activity ratio measured?

A

Patients with hypertension and/or spontaneous hypokalemia

139
Q

Adrenal carcinoma is more common in what size adrenal mass?

A

> 6 cm

140
Q

Is aldosterone synthesis ACTH dependent?

A

No

141
Q

What is the most common cause of primary adrenal insufficiency?

A

Autoimmune adrenalitis

142
Q

What is the most common cause of secondary adrenal insufficiency?

A

Exogenous glucocorticoids

143
Q

What 8 am cortisol level diagnoses adrenal insufficiency?

A

< 3 microgram/dL

144
Q

What 8 am cortisol level excludes adrenal insufficiency?

A

> 18 microgram/dL

145
Q

What test is commonly used to diagnose adrenal insufficiency?

A

Cosyntropin stimulation test

146
Q

What percentage of patients with Addison’s disease have other autoimmune disorders?

A

~ 50%

147
Q

Which steroid does not interfere with the serum cortisol assay?

A

Dexamethasone

148
Q

At what dose of hydrocortisone is fludrocortisone not required in case of primary adrenal insufficiency?

A

> 40 mg/day

149
Q

What genetic conditions is pheochromocytoma associated with?

A
  • MEN2
  • von Hippel-Lindau disease
  • Neurofibromatosis type 1
150
Q

Which test for pheochromocytoma is preferred when pre-test probability is low?

A

24-hr urine metanephrines and catecholamines

151
Q

Which test for pheochromocytoma is preferred when pre-test probably is high?

A

Plasma metanephrines

152
Q

Which test is used to localize a pheochromocytoma when CT and MRI scans are negative?

A

I-131 or I-123 MIBG scan

153
Q

What happens if you give beta blockade before alpha blockade in pheochromocytoma?

A

This can result in severe paroxysmal hypertension.

154
Q

What percentage of primary hyperaldosteronism is caused by aldosterone-producing adenomas?

A

40%

155
Q

What percentage of primary hyperaldosteronism is by bilateral adrenal hyperplasia?

A

60%

156
Q

What initial test results suggest primary hyperaldosteronism?

A
  • Aldosterone level > 15 ng/dL
  • Aldosterone/plasma renin ratio ratio > 20
157
Q

What aldosterone level after a salt loading test rules out primary hyperaldosteronism?

A

Less than 5 ng/dL

158
Q

Which anti-hypertensives should the patient not be on when testing for primary hyperaldosteronism?

A
  • Spironolactone
  • Eplerenone
159
Q

When is adrenal vein sampling (AVS) needed?

A

For lateralization when imaging is unrevealing or when there is an adrenal incidentaloma on one side.

160
Q

What percentage of patients with hyperaldosteronism do not have hypokalemia?

A

~ 50%

161
Q

Which additional anti-hypertensive medication should be prescribed in patients with uncontrolled hypertension because of primary hyperaldosteronism who are already on spironolactone or eplerenone?

A

Thiazide diuretics

162
Q

What percentage of cases of primary amenorrhea are caused by chromosomal disorders?

A

~ 50%

163
Q

What is the most common chromosomal disorder causing primary amenorrhea?

A

Turner’s syndrome

164
Q

What is the karyotype in Turner’s syndrome?

A

45, XO karoytype

165
Q

What is the karyotype in androgen-resistance syndrome?

A

XY karotype

166
Q

Can PCOS cause primary amenorrhea?

A

Yes

167
Q

What is the most important test in a patient presenting amenorrhea?

A

Pregnancy test

168
Q

What are some of the important investigations for primary amenorrhea?

A
  • Pregnancy test
  • Karyotype
  • FSH, LH, TSH, prolactin
  • Pelvic ultrasound
169
Q

What is the definition of secondary amenorrhea?

A

Absence of menstruation for 3 consecutive menstrual cycles or for 6 consecutive months in a woman who previously had menses.

170
Q

What is the most common cause of secondary amenorrhea?

A

Pregnancy

171
Q

What does a progesterone challenge test tell you?

A

Whether a patient with secondary amenorrhea is estrogen deficient or not.

172
Q

What do you do if there is no bleeding following a progesterone challenge test?

A

Indicates estrogen deficient state (hypogonadotrophic hypogonadism).

Measure estradiol level to confirm.

173
Q

What does bleeding after a progesterone challenge test indicate and suggest?

A

Indicates normal estrogen state; and suggests hyperandrogenic state such as PCOS.

174
Q

What are the causes of primary hypogonadism (hypergonadotrophic hypogonadism) in pre-menopausal aged women?

A
  • Premature ovarian failure/ovarian insufficiency
  • Chemotherapy
  • Pelvic radiation
175
Q

What is the most common cause of hirsutism with oligomenorrhea?

A

PCOS (polycystic ovarian syndrome)

176
Q

What is the LH/FSH ratio in PCOS?

A

Greater than 2:1

177
Q

Is PCOS a clinical diagnosis?

A

Yes

178
Q

When should a testosterone or DHEAS level be ordered for a PCOS patient?

A

When an androgen producing tumor needs to be ruled out.

179
Q

What should be suspected in a woman with acute onset of rapidly progressive hirsutism or virilization?

A

Androgen-secreting ovarian or adrenal tumor

180
Q

Which medications can you use for ovulation induction in PCOS?

A
  • Clomiphene citrate
  • Letrozole
181
Q

What is the treatment for patients with PCOS who do not desire fertility?

A
  • Intensive lifestyle modification
  • Oral contraceptive pills
182
Q

What should you do if the testosterone level is equivocal in males?

A

Measure free testosterone by equilibrium dialysis or mass spectrometry.

183
Q

What laboratory tests should you check if the testosterone level is low in males?

A

FSH
LH
Prolactin

184
Q

Which medications can cause hypogonadotrophic hypogonadism with low testosterone levels?

A

Anabolic steroids
Glucocorticoids
Opiates

185
Q

Can Kleinfelter’s syndrome cause primary hypogonadism in men?

A

Yes

186
Q

Can mumps cause primary hypogonadism in men?

A

Yes

187
Q

Can hemochromatosis cause primary hypogonadism in men?

A

Yes

188
Q

Can auto-immune destruction cause primary hypogonadism in men?

A

Yes

189
Q

Can trauma cause primary hypogonadism in men?

A

Yes

190
Q

Can prior chemotherapy cause primary hypogonadism in men?

A

Yes

191
Q

Can pelvic radiation cause primary hypogonadism in men?

A

Yes

192
Q

What is the next step after diagnosing primary hypogonadism in a man with no obvious cause?

A

Check karyotype (Kleinfelter’s syndrome)

193
Q

What should be done to evaluate men with secondary hypogonadism?

A
  • Prolactin level
  • MRI pituitary
  • Iron studies to evaluate for hemochromatosis
  • Sleep study
194
Q

Should testosterone levels be measured in patients having regular morning erections, with no gynecomastia and normal genital examination?

A

No

195
Q

What do you need to monitor other than testosterone levels in patients on testosterone replacement?

A

PSA
Hematocrit

196
Q

What can result in small testicles and male infertility?

A
  • Anabolic steroid abuse
  • Testosterone replacement therapy
197
Q

Should you treat fatigue and weakness without clear cut testosterone deficiency with testosterone replacement?

A

No

198
Q

What is the most common cause of outpatient hypercalcemia?

A

Primary hyperparathyroidism

199
Q

What is the most common cause of hypercalcemia in hospitalized patients?

A

Hypercalcemia of malignancy

200
Q

Is lithium induced hypercalcemia PTH-mediated or non-PTH-mediated?

A

PTH-mediated

201
Q

Is thiazide induced hypercalcemia PTH-mediated or non-PTH-mediated?

A

Non-PTH-mediated

202
Q

What percentage of sarcoidosis patients have hypercalcemia?

A

10%

203
Q

What percentage of sarcoidosis patients have hypercalciuria?

A

50%

204
Q

If the X-rays show chondrocalcinosis or osteitis fibrosa cystica - then what is the diagnosis?

A

Primary hyperparathyroidism

205
Q

Is PTH-related protein needed for diagnosis of hypercalcemia of malignancy?

A

No

206
Q

Is the phosphorous high, normal or low in hypercalcemia associated with multiple myeloma?

A

High

207
Q

Is the phosphorous high, normal or low in hypercalcemia associated with local osteolytic lesions?

A

Normal or low

208
Q

Is the phosphorous high, normal or low in hypercalcemia associated with granulomatous disease or B-cell lymphoma?

A

High

209
Q

Is the phosphorous high, normal or low in hypercalcemia associated with milk-alkali syndrome?

A

High

210
Q

Why does hyperthyroidism cause hypercalcemia?

A

Direct stimulation of osteoclasts by thyroid hormone

211
Q

How high does the serum calcium typically need to be to warrant acute intervention?

A

> 14 mg/dL

212
Q

How do you differentiate true hypercalcemia from pseudohypercalcemia?

A

Measure ionized calcium

213
Q

What should you do in patients with elevated PTH and calcium levels?

A

Measure 24-hr urine calcium and creatinine levels to exclude familial hypocalciuric hypercalcemia (FHH).

214
Q

What is the most common manifestation of MEN1?

A

Primary hyperparathyroidism

215
Q

What is the treatment of hypercalcemia caused by multiple myeloma or sarcoidosis?

A

Oral glucocorticoid therapy

216
Q

What is the acute treatment of symptomatic hypercalcemia?

A
  • IV fluids
  • Calcitonin
  • IV bisphosphonates
217
Q

Are loop diuretics recommended in the treatment of hypercalcemia?

A

No - except in case of heart failure or renal failure where they can be used to control the volume over-load when treating with IV fluids.

218
Q

What is the most common manifestation of MEN1?

A

Multi-gland primary hyperparathyroidism

219
Q

What is the most common manifestation of MEN2?

A

Medullary thyroid cancer

220
Q

MEN1

A
  • Primary hyperparathyroidism
  • Pituitary tumors
  • Pancreatic neuroendocrine tumors
221
Q

What is MEN2?

A
  • Medullary thyroid carcinoma
  • Pheochromocytoma
  • Primary hyperparathyroidism
222
Q

What percentage of patients with primary hyperparathyroidism have a coexisting vitamin D deficiency?

A

50%

223
Q

What, other than the calcium and PTH, should be measured in all patients with hyperparathyroidism?

A

Vitamin 25 (OH) D level

224
Q

How do you treat patients with primary hyperparathyroidism who are symptomatic but not candidates for surgery?

A

Cinacalcet
Bisphosphonates

225
Q

What are the indications of parathyroidectomy in patients with primary hyperparathyroidism?

A
  • Symptoms (anything that may be related).
  • Hypercalcemia with calcium > 1 mg/dL above the upper level of normal.
  • Osteoporosis (T-score: - 2.5)
  • Chronic kidney disease - stage 3 or worse
  • Urine calcium > 400 mg/24 hr
  • Age less than 50 years
226
Q

How much does total calcium decline by for each 1 g/dL decrement of serum albumin level?

A

0.8 mg/dL

227
Q

When are the Trousseau and Chvostek signs positive?

A

Hypocalcemia

228
Q

What is DiGeorge syndrome?

A

Congenital hypoparathyroidism

229
Q

Polyglandular autoimmune syndrome type 1

A
  • Autoimmune hypoparathyroidism
  • Adrenal insufficiency
  • Hypogonadism
  • Mucocutaneous candidiasis
  • Malabsorption
230
Q

What cardiac studies do you need in hypocalcemia?

A

EKG to evaluate for QTc interval prolongation

231
Q

Is the calcium level high, normal or low in rhabdomyolysis?

A

Low

232
Q

Is the calcium level high, normal or low in tumor lysis syndrome?

A

Low

233
Q

Is the calcium level high, normal or low in hypomagnesemia?

A

Low

234
Q

What lab values are seen in pseudohypoparathyroidism (PTH resistance)?

A

Low calcium
High phosphorous
Normal vitamin D
High PTH

235
Q

When can patients get “hungry bone” syndrome?

A

After parathyroidectomy

236
Q

What is the treatment of acute symptomatic hypocalcemia?

A

IV calcium gluconate
Vitamin D supplementation

237
Q

Which vitamin D replacement should you use when the patient has kidney disease?

A

Calcitriol (1,25 dihydroxy vitamin D)

238
Q

Which vitamin D replacement should you use when the patient has liver disease?

A

25 hydroxycholecalciferol

239
Q

Which vitamin D replacement should you use when the patient has vitamin D deficiency not caused by liver or kidney disease?

A

Ergocalciferol (D2) or Cholecalciferol (D3)

240
Q

Who should be screened with a DXA per USPSTF?

A
  • Women over 65 years of age.
  • Post-menopausal women < 65 years at increased risk based on a formal assessment took (i.e. FRAX)
241
Q

Should the DXA be repeated in post-menopausal women who have a previously normal DXA and no risk factors for osteoporosis?

A

No

242
Q

Is primary osteoporosis associated with any specific laboratory testing in the absence of fractures?

A

No

243
Q

What is a fragility fracture?

A

Fracture after fall from standing height or lower.

244
Q

What is the definition of osteoporosis?

A
  • T-score of less than - 2.5
  • History of fragility fracture
245
Q

What is the definition of osteopenia?

A

T-score of - 1 to - 2.4

246
Q

What is the most common cause of osteoporosis in women?

A

Estrogen deficiency (menopause)

247
Q

What is the most common cause of osteoporosis in men?

A

Testosterone deficiency (hypogonadism)

248
Q

Are the following lifestyle changes important for all osteoporosis patients?

  • Resistance exercises
  • Stop smoking
  • Limit alcohol
  • Adequate supplementation of calcium and vitamin D
  • Sunlight exposure
A

Yes

249
Q

Which medication can treat pain from osteoporotic fractures?

A

Calcitonin

250
Q

Which osteoporosis agents are contraindicated in chronic kidney disease or esophageal disease?

A

Oral bisphosphonates

251
Q

What happens when you stop denosumab therapy?

A

Rebound vertebral fractures (effect is not sustained)

252
Q

Is osteonecrosis of the jaw more common with oral or parenteral anti-resorptive therapy?

A

Parenteral (zoledronic acid and denosumab)

253
Q

How long can you give teriparatide for?

A

2 years maximum

254
Q

Is estrogen replacement therapy adequate treatment for osteoporosis in post-menopausal women?

A

No

255
Q

Should you combine teriparatide with a bisphosphonate?

A

No

256
Q

Can you give IV bisphosphonates in severe hypocalcemia or chronic kidney disease?

A

No

257
Q

What should you consider instead of osteoporosis when you see a fracture in a nursing home resident?

A

Osteomalacia

258
Q

Which lab value is the best indicator of vitamin D status?

A

Vitamin 25 (OH) D

259
Q

What are the USPSTF guidelines regarding screening for vitamin D deficiency?

A

Evidence is insufficient to recommend for or against in asymptomatic adults.

260
Q

Do obese patients have higher or lower levels of vitamin D?

A

Lower

261
Q

Do patients with malabsorption syndromes have higher or lower levels of vitamin D?

A

Lower

262
Q

Do patients with malabsorption syndromes have higher or lower levels of vitamin D?

A

Lower

263
Q

Do patients on orlistat have higher or lower levels of vitamin D?

A

Lower

264
Q

Do patients on glucocorticoids have higher or lower levels of vitamin D?

A

Lower

265
Q

Does vitamin D and calcium supplementation prevent fractures?

A

There is insufficient evidence that it does.

266
Q

What should you suspect if there is an isolated elevation of alkaline phosphatase in the absence of liver disease?

A

Paget’s disease

267
Q

What is the treatment of Paget’s disease?

A

Bisphosphonates

268
Q

What diagnostic scans are used to diagnose Paget’s disease in asymptomatic patients?

A

Bone scan followed by X-rays of areas that localize the radionucleotide

269
Q

What diagnostic scans are used to diagnose Paget’s disease in symptomatic patients?

A

X-rays of the symptomatic areas

270
Q

Which disease has a typical “cotton wool” appearance of skull?

A

Paget’s disease

271
Q

Is the HbA1c falsely high, falsely low or normal in hemolytic anemia?

A

Falsely low

272
Q

Is the HbA1c falsely high, falsely low or normal in kidney injury?

A

Falsely low

273
Q

Is the HbA1c falsely high, falsely low or normal in patients taking erythropoietin?

A

Falsely low

274
Q

Does starvation cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

275
Q

Does liver failure cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

276
Q

Does sepsis cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

277
Q

Does alcoholism cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

278
Q

Does adrenal insufficiency cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

279
Q

Does growth hormone deficiency cause fasting hypoglycemia due to decreased hepatic glucose production?

A

Yes

280
Q

Are wide (>1 cm) violaceous striae specific for Cushing’s syndrome?

A

Yes