TBL Prep

Question 1

What are some endocrine causes of secondary HTN?

Answer 1

primary aldosteronism-pretty common, may present with hypokalemia
pheochromocytoma
Cushing’s disease

Question 2

What are some differences in presentation in secondary HTN that can help distinguish it from essential HTN?

Answer 2

abrupt onset
greater severity
absent fhx
any age of onset
sometimes tachycardia & volume overload

Question 3

What is a pheochromocytoma?

Answer 3

tumor of neuroectodermal origin that causes release of a bunch of catecholamines, raises BP

Question 4

How common is pheochromocytoma as a cause of secondary HTN? People with which condition should be screened for it?

Answer 4

1% of cases of secondary HTN

screen patients with neurofibromatosis

Question 5

What is the typical triad of symptoms of pheochromocytoma? Which other symptoms may be present?

Answer 5

triad–headache, excessive sweating, palpitations

other features–pallor, weight loss, anxiety

Question 6

Give 3 possible patterns of BP elevation w/ pheochromocytoma.

Answer 6

1. sustained HTN w/o BP spikes
2. sustained HTN w/ BP spikes to a crisis level
3. normotensive w/ BP spikes

Question 7

Which symptom when seen with HTN should send off bells in your head for pheochromocytoma?

Answer 7

orthostatic hypotension

Question 8

Which symptoms are seen with a pheochromocytoma-related HTN crisis?

Answer 8

dizziness
flushing
visual disturbances
anxiety
N/V
epileptic aura

Question 9

What are some other things that should be on the ddx for pheochromocytoma?

Answer 9

paroxysmal vasodilating headaches
autonomic dysfunction
anxiety
acute hypoglycemia
CAD
cocaine

Question 10

What are some lab tests that help in the diagnosis of pheochromocytoma?

Answer 10

urinary & plasma catecholamine measurements
urinary metanephrines
urinary vanillylmandelic acid

Question 11

What used to be considered the most reliable lab test for pheochromocytoma? What is the most reliable one now?

Answer 11

Past–urinary assay of catecholamines

Current–plasma free metanephrines, most sensitive, even b/w spells of spilling out catecholamines

Question 12

What is it about plasma free metanephrines that makes them so reliable even b/w “spells” with pheochromocytoma?

Answer 12

continuous production of O-methylated metabolites from catecholamines seeping from chromaffin stores in tumors

Question 13

Which is better–measure only total metanephrines? Or measure fractionated too?

Answer 13

best to include fractionated too b/c some tumors release only one type

Question 14

How can you distinguish false positives from true positives when testing for pheochromocytoma?

Answer 14

true pos. have catecholamines 2-3X normal high end of reference range.
If b/w 1000-2000 & hard to distinguish can use the clonidine suppression test
Abdominal CT or MRI also helpful sometimes

Question 15

What is involved in the clonidine suppression test when diagnosing pheochromocytoma?

Answer 15

if the excess catecholamines are b/c of excess SNS the clonidine will decrease it.
If a pheochromocytoma–no real effect.

Question 16

Describe the treatment for pheochromocytoma.

Answer 16

surgical removal (whether benign or malignant)
with alpha & beta blockers pre-op
volume attention (often volume depleted)
1 wk for symptoms to go away
often metastasizes or recurs–f/u important.

Question 17

When do you usu see primary hyperaldosteronism?

Answer 17

30-50s

cause of resistant HTN in African Americans & Caucasians

Question 18

Which symptoms pop up in primary hyperaldosteronism? When should you think about it as a possible diagnosis?

Answer 18

hypokalemia, metabolic alkalosis & refractory HTN
weakness
polyuria, polydipsia
nocturia

Question 19

T/F Edema is a common feature of primary hyperaldosteronism b/c of the Na+ retention.

Answer 19

False. there are enough Na+ wasting forces counteracting it that it isn’t usu seen.

Question 20

What are common complications of primary hyperaldosteronism?

Answer 20

LV hypertrophy–>heart failure

perhaps b/c aldosterone is pro-fibrotic & increases oxidative stress

Question 21

Which conditions can mimic primary hyperaldosteronism?

Answer 21

licorice ingestion
Cushing’s syndrome
Liddle’s syndrome

Question 22

Why could eating a bunch of licorice cause endocrine changes?

Answer 22

glycyrrhizic acid inhibits renal 11-beta-hydroxysteroid dehydrogenase (which metabolizes steroids)
now you have more active cortisol. Na+ retention & K+ loss.

Question 23

Not all primary hyperaldosteronism patients exhibit hypokalemia…so what is the best test to check for it?

Answer 23

urinary aldosterone excretion after 3 days of salt loading

Question 24

What is an appropriate screening test for primary hyperaldosteronism? When should this test be taken ideally?

Answer 24

Morning–when aldosterone is the highest
plasma aldosterone-renin ratio
Look for ratio>30

Question 25

What are other tests to consider using in primary hyperaldosteronism?

Answer 25

plasma K+ levels
24-hour K+ excretion
Plasma aldosterone-renin ratio
fludrocortisone test
CT
adrenal vein sampling

Question 26

What is the best treatment for a unilateral adrenal adenoma, causing primary hyperaldosteronism?

Answer 26

surgical resection

Question 27

What is the best treatment for bilateral adrenal hyperplasia or adenomas?

Answer 27

medical management
including:
spironolactone
eplerenone
Diuretic
Salt & H2O control
other anti-HTN meds

Question 28

What are the drawbacks of spironolactone?

Answer 28

can cause impotence & gynecomastia in high doses

eplerenone is also an aldosterone antagonist, but has fewer of these side effects

Question 29

T/F Ca++ channel blockers are a good addition to medical management of primary hyperaldosteronism.

Answer 29

False. They don’t do anything to aldosterone.

Question 30

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

Answer 30

Cushing’s disease–ACTH-secreting adenoma

messes w/ the adrenal gland–excess of cortisol.

Question 31

What makes up the other cases of ACTH-dependent Cushing’s syndrome?

Answer 31

oat cell
small cell carcinoma of lung
carcinoid tumor of bronchus or thymus

Question 32

WHat are some examples of ACTH-independent causes of Cushing’s syndrome?

Answer 32

adrenal adenoma
adrenal carcinoma
macro or micronodular hyperplasia

Question 33

What is the most affected age group for Cushing’s syndrome? Is HTN a major feature?

Answer 33

HTN is a major feature b/c of excess cortisol

25-40

Question 34

What is the usual presentation of Cushing’s syndrome?

Answer 34

moon facies
buffalo hump
abdominal fat
striae
proximal muscle weakness/fatigue
HTN
hirsutism
easy bruising
insulin resistance
increased cardio risk
prothrombotic state
amenorrhea
loss of libido
osteoporosis

Question 35

What is the presentation of patients with Cushing’s syndrome from excess ectopic ACTH secretion?

Answer 35

hyperpigmentation from too much POMC
severe HTN
hypokalemic metabolic alkalosis

Question 36

WHat are 2 exogenous things that can look like true Cushing’s syndrome?

Answer 36

too much steroid use

chronic alcoholism

Question 37

What is an appropriate screening test for Cushing’s?

Answer 37

dexamethasone suppression test

should drop cortisol to s

Question 38

What is a good confirmatory test for cushing’s?

Answer 38

24 hour urinary free cortisol
-only a problem if renal failure
if>100–>cushing’s

Question 39

What is the 5 year survival for Cushing’s? What is the surgical approach?

Answer 39

50% b/c of excess glucocorticoids
transsphenoidal approach to the pituitary
or adrenalectomy when approrpiate

Question 40

Give some drugs used in the medical management of Cushing’s.

Answer 40

ketoconazole–good long term
mitotane–steroidogenesis inhibitor, adrenolytic
mifepristone–blocks glucocorticoid receptora ctivation

Question 41

If you’re thinking about treating the HTN of a Cushing’s patient…what should you consider?

Answer 41

K+ sparing! spironolactone, amiloride
NOT loop diuretics
careful w/ beta blockers

Question 42

Screening in HTN patients for endocrine abnormalities is really only high yield for what?

Answer 42

primary hyperaldosteronism