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Step 2 CK > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Decreased FSH and LH

Anosmia

Renal agenesis

A

Kallmann Syndrome

Failure of the hypothalamus to release GnRH

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2
Q

Central obesity

Increased LDL and cholesterol

Reduced lean muscle mass

A

Subtle findings for GH deficiency in adults

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3
Q

Causes of Nephrogenic DI?

A

Chronic pyelo

Amyloidosis

Myeloma

SCD

Lithium

Hypercalcemia and hypokalemia

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4
Q

The difference between central and nephrogenic DI is determined by…

A

the response to vasopressin

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5
Q

Treatment of central vs nephrogenic DI

A

central = long-term vasopressin (desmopressin)

nephrogenic = correct the underlying cause, HCTZ, amiloride, NSAIDs

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6
Q

Overproduction of growth hormone (pituitary adenoma) leading to soft tissue overgrowth throughout the body

A

Acromegaly

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7
Q

What else should you look for when a patient is diagnosed with acromegaly?

A

Parathyroid and Pancreatic disorders (i.e., MEN1)

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8
Q

Increased hat size

Body odor

Coarse facial features

Colonic polyps

HTN

A

Acromegaly

(Abuse of GH can also give the same presentation)

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9
Q

Best initial test for acromegaly

A

IGF-1

Most accurate test = glucose suppression test (unsuppressed GH levels)

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10
Q

Treatment for acromegaly

A
  1. Surgery: transphenoidal resection (70% effective)
  2. Medications: Pegvisomant is a GH receptor antagonist that inhibits IGF release from the liver
  3. Radiotherapy
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11
Q

What are two endocrine disorders that would cause elevated prolactin without there being an adenoma?

A

Acromegaly: prolactin is cosecreted with GH

Hypothyroidism: extremely high TRH levels will stimulate prolactin secretion

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12
Q

What is the only CCB to raise prolactin level?

A

Verapamil

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13
Q

After prolactin level is found to be high, which diagnostic tests should be performed?

A

Thyroid function tests

Pregnancy test

BUN/creatinine

LFTs

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14
Q

Treatment for hyperprolactinemia

A
  1. DA agonists: cabergoline is better tolerated than bromocriptine
  2. Transphenoidal surgery
  3. Radiation (rarely needed)
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15
Q

Patient is having symptoms of hypothyroidism, but their T4 is normal and TSH is only slightly elevated. How do you determine if they need thyroid replacement?

A

Antithyroid peroxidase antibodies

Positive = replace thyroid hormone

If TSH was double the upper limit of normal, you can replace without ordering antibodies

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16
Q

All forms of hyperthyroidism have an elevated…

A

T4 level

Only pituitary adenomas will have a high TSH level (low in all others)

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17
Q

What is the most appropriate next step if a patient presents with a palpable mass on her thyroid (i.e., a nodule)?

A

Get T4 and TSH levels

If the patient has a hyperfunctioning gland (i.e., T4 is elevated or the TSH is decreased), the patient does not need immediate biopsy because malignancy is not hyperfunctioning

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18
Q

The most common cause of hypercalcemia

A

Primary hyperparathyroidism

Primary hyperparathyroidism and cancer account for 90% of hypercalcemia patients

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19
Q

Treatment for hypercalcemia

A
  1. Saline hydration
  2. Bisphosphonates: pamidronate, zoledronic acid

If calcium levels remain elevated, give calcitonin (inhibits osteoclasts). Prednisone controls hypercalcemia when it is from sarcoidosis or any other granulomatous disease.

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20
Q

Primary hyperparathyroidism is from:

A
  1. Solitary adenoma (80-85%)
  2. Hyperplasia of all 4 glands (15-20%)
  3. Parathyroid malignancy (1%)
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21
Q

What study is best for determining the bone effects from high PTH?

A

DEXA

NOT bone x-ray

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22
Q

When surgery is not possible for hyperparathyroidism, what is another option?

A

Cinacalcet (inhibitor of PTH release)

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23
Q

Facial nerve hyperexcitability

Perioral numbness

Seizures

Tetany

Long QT

A

Signs of hypocalcemia

24
Q

Confusion

Lethargy

Short QT

A

Signs of hypercalcemia

25
Q

Causes of hypocalcemia

A

Primary hypoparathyroidism (from prior neck surgery)

Hypomagnesemia (necessary for PTH release and decreases urinary loss of Ca)

Renal failure (decreased 1,25 hydroxy-D)

For every point decrease in albumin, the calcium level decreases by 0.8

26
Q

Cushing syndrome vs Cushing disease

A

Cushing syndrome = hypercortisolism

Cushing disease = pituitary overproduction of ACTH

27
Q

Moon face/Buffalo hump

Striae

HTN

Erectile dysfunction

Polyuria

A

Signs of hypercortisolism

28
Q

The best initial test for the presence of hypercortisolism

A

24-hour urine cortisol

1 mg overnight dexamethasone suppression test is the best next choice

29
Q

What causes false positives to the 1 mg overnight dexamethasone suppression test (i.e., cortisol is still elevated in the morning)?

A

Depression

Alcoholism

Obesity

30
Q

After hypercortisolism is confirmed, what is the best test to determine the cause (source) or location?

A

ACTH

Low ACTH = adrenal source (aka ACTH-independent)

High ACTH = pituitary (suppresses with high dose dexamethasone) or ectopic

31
Q

Hyperglycemia

Hyperlipidemia

Hypokalemia

Metabolic alkalosis

Leukocytosis

A

Effects of hypercortisolism

32
Q

How far should you go in the evaluation of an unexpected, asymptomatic adrenal lesion on CT?

A

4% of the population has adrenal “incidentalomas”

Metanephrines of blood or urine to exclude pheochromocytoma

Renin and aldosterone to exclude hyperaldosteronism

1 mg overnight dexamethasone suppression test

33
Q

What is the next step when high-dose dexamethasone suppresses the cortisol level, but a pituitary mass is not seen on MRI?

A

Petrosal sinus sampling for ACTH

34
Q

Chronic hypoadrenalism is called

A

Addison disease

35
Q

Difference between Addison disease and acute adrenal crisis

A

Addison disease is caused by autoimmune destruction of the gland (rarely caused by TB, adrenoleukodystrophy, or metastatic cancer) and is a chronic condition with slow progression

Acute adrenal cirisis is caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland (sudden removal of chronic high-dose prednisone can precipitate adrenal crisis)

36
Q

Common lab findings in hypoadrenalism:

Glucose

K

Na

BUN

Metabolic

A

Hypoglycemia

Hyperkalemia

Hyponatremia

High BUN

Metabolic acidosis

Eosinophilia is also common

37
Q

The most specific test of adrenal function is

A

cosyntropin test (synthetic ACTH)

However, treatment is more important than testing in acute adrenal crisis

38
Q

Treatment for acute adrenal crisis

A

Hydrocortisone

Fludrocortisone can be useful if the patient still has evidence of postural instability (high mineralocorticoid/aldosterone-like effect)

39
Q

High BP + hypokalemia

A

Primary hyperaldosteronism

80% from solitary adenoma (most of the rest are from bilateral hyperplasia; it is rarely malignant)

40
Q

Best initial test for primary hyperaldosteronism?

A

Plasma aldosterone to plasma renin ratio (an elevated plasma renin excludes the diagnosis)

The most accurate test to confirm the presence of a unilateral adenoma is a sample of venous blood draining the adrenal (DO NOT start with CT scan d/t high prevalence of incidental lesions)

41
Q

Treatment of primary hyperaldosteronism

A

Unilateral adenoma = resection via laparoscopy

Bilateral adenoma = eplerenone or spironolactone

42
Q

Episodic HTN

Headache

Sweating

Palpitations/tremor

A

Pheochromocytoma

Nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high BP

43
Q

Diagnostic tests for pheochromocytoma

A

Best initial test = free metanephrines in plasma (confirmed with a 24-hour urine collection)

Followed by CT/MRI

MIBG scanning detects the location of pheochromocytoma that originates outside the adrenal gland

44
Q

Treatment for pheochromocytoma

A

Phenoxybenzamine (alpha blocker)

CCB and beta blockers can be used afterwards

Remove surgically

45
Q

Diabetes is defined/diagnosed by:

A

2 fasting blood glucose > 125

1 blood glucose > 200 with symptoms

Hemoglobin A1C > 6.5%

46
Q

When is metformin contraindicated?

A

In patients with renal dysfunction (can accumulate and cause metabolic acidosis)

47
Q

Sitagliptin

Saxagliptin

Linagliptin

Alogliptin

A

DPP-IV Inhibitors (block the metabolism of the incretins)

48
Q

GIP

GLP

A

“The incretins”

GIP = glucose insulinotropic peptide

GLP = glucagon-like peptide

Both increase insulin release and decrease glucagon release from the pancreas

49
Q

Exenatide

Liraglutide

Albiglutide

A

Incretin mimetics

50
Q

Nateglinide

Repaglinide

A

Stimulators of insulin release in a similar manner to sulfonylureas (but do not contain sulfa)

51
Q

Acarbose

Miglitol

A

Alpha glucosidase inhibitors

Block glucose absorption in the bowel

52
Q

Treatment for DKA

A

Large-volume saline and insulin

Replace potassium after the level comes down to a level approaching normal

53
Q

What is the best test to determine the severity of DKA?

A

Serum bicarbonate

(Hyperglycemia and ketones are NOT)

If the bicarbonate level is low, the anion gap is increased, and the patient is at risk of death

54
Q

When should patients with DM start on an ACE-i/ARB

A

If their BP is > 140/90

or

If urine tests positive for microalbuminuria

55
Q

Treatment for gastroparesis caused by DM

A

Metoclopromide and erythromycin

56
Q

Management of diabetic retinopathy

A

Tighter control of glucose

When neovascularization and vitreous hemorrhages are present (proliferative retinopathy), it can be treated with laser photocoagulation

Step 2 CK (18 decks)

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