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Step 2 CK > Endocrinology > Flashcards

Endocrinology Flashcards

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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

Study These Flashcards
A

Signs of hypocalcemia

24
Q

Confusion

Lethargy

Short QT

Study These Flashcards
A

Signs of hypercalcemia

25
Causes of hypocalcemia
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
Cushing syndrome vs Cushing disease
Cushing syndrome = hypercortisolism Cushing disease = pituitary overproduction of ACTH
27
Moon face/Buffalo hump Striae HTN Erectile dysfunction Polyuria
Signs of hypercortisolism
28
The best initial test for the presence of hypercortisolism
24-hour urine cortisol 1 mg overnight dexamethasone suppression test is the best next choice
29
What causes false positives to the 1 mg overnight dexamethasone suppression test (i.e., cortisol is still elevated in the morning)?
Depression Alcoholism Obesity
30
After hypercortisolism is confirmed, what is the best test to determine the cause (source) or location?
ACTH Low ACTH = adrenal source (aka ACTH-independent) High ACTH = pituitary (suppresses with high dose dexamethasone) or ectopic
31
Hyperglycemia Hyperlipidemia Hypokalemia Metabolic alkalosis Leukocytosis
Effects of hypercortisolism
32
How far should you go in the evaluation of an unexpected, asymptomatic adrenal lesion on CT?
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
What is the next step when high-dose dexamethasone suppresses the cortisol level, but a pituitary mass is not seen on MRI?
Petrosal sinus sampling for ACTH
34
Chronic hypoadrenalism is called
Addison disease
35
Difference between Addison disease and acute adrenal crisis
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
Common lab findings in hypoadrenalism: Glucose K Na BUN Metabolic
Hypoglycemia Hyperkalemia Hyponatremia High BUN Metabolic acidosis Eosinophilia is also common
37
The most specific test of adrenal function is
cosyntropin test (synthetic ACTH) However, treatment is more important than testing in acute adrenal crisis
38
Treatment for acute adrenal crisis
Hydrocortisone Fludrocortisone can be useful if the patient still has evidence of postural instability (high mineralocorticoid/aldosterone-like effect)
39
High BP + hypokalemia
Primary hyperaldosteronism 80% from solitary adenoma (most of the rest are from bilateral hyperplasia; it is rarely malignant)
40
Best initial test for primary hyperaldosteronism?
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
Treatment of primary hyperaldosteronism
Unilateral adenoma = resection via laparoscopy Bilateral adenoma = eplerenone or spironolactone
42
Episodic HTN Headache Sweating Palpitations/tremor
Pheochromocytoma Nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high BP
43
Diagnostic tests for pheochromocytoma
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
Treatment for pheochromocytoma
Phenoxybenzamine (alpha blocker) CCB and beta blockers can be used afterwards Remove surgically
45
Diabetes is defined/diagnosed by:
2 fasting blood glucose \> 125 1 blood glucose \> 200 with symptoms Hemoglobin A1C \> 6.5%
46
When is metformin contraindicated?
In patients with renal dysfunction (can accumulate and cause metabolic acidosis)
47
Sitagliptin Saxagliptin Linagliptin Alogliptin
DPP-IV Inhibitors (block the metabolism of the incretins)
48
GIP GLP
"The incretins" GIP = glucose insulinotropic peptide GLP = glucagon-like peptide Both increase insulin release and decrease glucagon release from the pancreas
49
Exenatide Liraglutide Albiglutide
Incretin mimetics
50
Nateglinide Repaglinide
Stimulators of insulin release in a similar manner to sulfonylureas (but do not contain sulfa)
51
Acarbose Miglitol
Alpha glucosidase inhibitors Block glucose absorption in the bowel
52
Treatment for DKA
Large-volume saline and insulin Replace potassium after the level comes down to a level approaching normal
53
What is the best test to determine the severity of DKA?
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
When should patients with DM start on an ACE-i/ARB
If their BP is \> 140/90 or If urine tests positive for microalbuminuria
55
Treatment for gastroparesis caused by DM
Metoclopromide and erythromycin
56
Management of diabetic retinopathy
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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