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SBM Endocrine > 01-21 Endocrine HTN > Flashcards

01-21 Endocrine HTN Flashcards

1. To understand the role of hormones in the maintenance of blood pressure and in the genesis of secondary hypertension. 2. To understand the association of specific endocrine abnormalities and hypertension. 3. To know how to initiate appropriate endocrine work-up to identify secondary causes of hypertension related to endocrine disorders. 4. To be able to recognize the clinical features of patients with a pheochromocytoma and primary hyperaldosteronism and be familiar with the appropriate e

1
Q

When should you consider working up 2° cause of HTN?

A

—when people first present, if you don’t do it then, it will likely never happen
—when HTN is hard to control with multiple medications
—when it occurs at an odd time

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2
Q

1°HyperPTH and HTN
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—30-60% of these pts

ETIOLOGY
—hyperCa2+ → vasoconstriction
—nephrocalcinosis → kidney dz → HTN
—hyeprCa2+ is assoc’d w/ plasma renin activity

TX
—parathyroidectomy may or may not fix (b/c there can be permanent kidney damage)

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3
Q

Acromegaly and HTN
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—10-50% of these pts

ETIOLOGY
—unclear
—GH may ↑ Na+ reabs +/- ↑ symp tone
—GH causes insulin resistance
—severity correlates w/ GH

TX
—usually DBP > SBP & easily treatable

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4
Q

Hyperthyroidism
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—30%
—SBP is elevated

ETIOLOGY
—↑ HR and contractility
—↑ PRA (plasm renin activity)
—yet,

TX
—usu. resolves w/ tx of hyperthyroidism

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5
Q

Hypothyroidism
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—15-30%
—¡D! BP is elevated, though these pts can be hypo-, hyper-, or normo- tensive

ETIOLOGY
—↑ peripheral resistance (vs. hyperthyroidism)
—yet, low PRA

TX
—May or may not resolve w/ L-thyroxine

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6
Q

Obesity and HTN
Etiology?
Tx?

A

ETIOLOGY
—PseudoHTN: falsely high w/ small cuff
—Increasing wt increases BP esp w/ metab syndrome (↑ gut-to-butt ratio)
—multiple possible molecular mechanisms: insulin resistance, ↑ intravascular FV, ↑ Na+ reabs

TX
—BP usually falls w/ weight loss

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7
Q

DM and HTN
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—DM2: 50% @ time of dx
—DM1: usu. normotensive @ dx; later w/ nephropathy (and only 40% get nephropathy)

ETIOLOGY
BOTH: hyperglycemia ‪↓‬ eNO activity → constrict
—nephropathy

DM2-specific:
—obestity
—insulin resist & hyperinsulin ∆s endothelial cells
— ↑ Na+ reabs probs from hyperglycemia

TX
—Treat HTN w/ ACEIs or ARBs (kidney protection)
—Stay on top of BP

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8
Q

Cushing’s Syndrome and HTN
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—80% of these pts have HTN

ETIOLOGY
—cortisol also stim’s MR-receptor → Na+ reabs
—also some incr aldo and A-II but ^^ is main pt

TX
—usually resolves w/ tx of Cushing’s

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9
Q

OCPs and HTN
Prevalence?
Etiology?
Tx?

A

PREVALENCE
—most ♀ have slight increase (3-6/2-5)

ETIOLOGY
—?estrogens ↑ angiotensinogen

TX
—usually resolves w/ d/c of OCPs
—d/c OCPs when >35y/o and/or smoker

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10
Q

CAH and HTN

A

Only rare 11β-hydroxylase mutation causes HTN

—b/c cortisol precursors (deoxycortisol) are made and bind the mineralocorticoid receptor like aldosterone would

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11
Q

Pheochromocytoma and HTN
% cause of HTN cases?
Etiology?
Tx?

A

PREVALENCE
—Causes only 0.1% of HTN cases
—Watch out in pts w/ familial endocrine syndromes like MEN
—If you have a MTC you’ll likely get a pheo

ETIOLOGY
—Catechol. vasoconstrict (via α) and ↑ HR (via β)
—25% are familial and caused by RET, NF1, VHL, etc genes

TX
—Tx the pheo w/ laproscopic resection

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12
Q

HTN and hypokalemia think?

A

hyperaldosteronism

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13
Q

PHA (Primary Hyperaldosteronism)
—Etiology
—Dx?

A

ETIOLOGY
—autonomous adrenal adenoma secreting aldosterone

DX
—noting low K+ (not very sensitive)
—new test: aldo-to-renin ratio
—Saline suppression test
—Bilateral adrenal vein sampling

TX
—if adenoma: spiro works well; not for hyperplasia

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14
Q

Renin-Secreting Tumors

A

—super rare
—HTN + hypokalemia
—elevated aldo AND PRA

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15
Q

Glucocorticoid-Remediable Aldosteronism

A

—ACTH activator onto aldosterone synthase gene
—HTN + hypokalemia
—elevated aldo; suppressed PRA

Tx: dexamethasone

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16
Q

11β-hydroxysteroid DH Deficiency
—A.K.A.?
—ETIOLOGY
—TX

A

A.K.A.
—”apparent MR excess”

ETIOLOGY:
—cortisol —11β-H-DH→ cortisone (inactive)
—when blocked (mutation, black licorice) → HTN

TX
—dexamethasone or spiro

17
Q

Liddle’s Syndrome

A

A.K.A.
“pseudoaldosteronism”

LAB
—low aldo and PRA

ETIOLOGY
—d/o of renal tubules → mutated sodium channel
—↑ Na+ reabs and ‪K+ excretion

TX
—amiloride

18
Q

What should you order when evaluating someone w/ new dx HTN?

—Say why for each one =)

A 
1. Serum aldo : renin ratio
—1° hypersaldosteronism would have ↑ ratio
2. serum K+
—sign of HPA axis dysfxn or renal tubule dysfxn
3. serum Ca2+
—hyperPTH
4. TSH
—duh
5. Serum Cr
—kidney dz

Others if suspicious: plasma free metanephrines, GH, HbA1c, etc.)

19
Q

1 Which of the following is the best example of hypertension caused purely by vasoconstriction?

  1. Essential hypertension
  2. Adrenal adenoma producing aldosterone
  3. Hyperthyroidism
  4. Pheochromocytoma
  5. Cushing’s Syndrome
20
Q

2 Patients presenting with clinical and laboratory evidence of primary hyperparathyroidism who also have significant hypertension should also have which of the following tests before having parathyroid surgery?

  1. Renal ultrasound to evaluate for RAS
  2. Plasma free metanephrine level
  3. Thyroid function tests
  4. HbA1c level
  5. None of the above
A

2: Plasma free metanephrine leve
—assoc’d w/ pheo rarely (MEN2)
—want to know that before surgery!

21
Q 
#3 Pheochromocytomas always originate in one of the adrenal glands?
—True or False
A

False, 10% are para-ganglionic pheos

22
Q

4 A 45 year old man presents with a TSH of 80 and a low free T4 level. His BP is most likely ___ ?

  1. High
  2. Low
  3. Normal
  4. Any of the above
A

4 “Any of the above”

23
Q

5 A 35 year old woman presents to your clinic with new onset of hypertension. Which of the following findings or test results would be LEAST sensitive in determining whether she had primary hyperaldosteronism?

  1. Low potassium level
  2. Non-stimulatable renin level and non-suppressible aldosterone level
  3. Non-suppressible aldosterone level after saline infusion
  4. Abnormally high serum aldosterone-renin ratio (renin suppressed)
  5. All of the above are equally very sensitive
A

1 is LEAST sensitive

24
Q

6 Which of the following is not true about pheochromocytomas?

  1. Most occur within the adrenal glands
  2. Can be associated with MEN 2a and 2b syndromes
  3. Hypertension should immediately be treated with a beta-blocker to prevent serious cardiac arrhythmias
  4. 90% are benign
  5. Patients are usually volume depleted when they initially present
A
  1. Hypertension should immediately be treated with a beta-blocker to prevent serious cardiac arrhythmias

TX WITH α-BLOCKER! Prevents vasoconstriction

25
Q

7 Patients with untreated congenital adrenal hyperplasia caused by 21-hyroxylase deficiency usually demonstrate all of the following except:

  1. Elevated 17-hydroxyprogesterone levels
  2. Hypertension due to elevated mineralocorticoids
  3. Elevated androgen levels
  4. Normal or low-normal cortisol levels
  5. A decrease in DHEAS level when treated with a glucocorticoid
A
  1. Hypertension due to elevated mineralocorticoids
26
Q

8 All of the following conditions could routinely be expected to cause a patient to present with hypertension except?

  1. Type 2 diabetes mellitus
  2. Primary hyperparathyroidism
  3. Addison’s disease
  4. Acromegaly
  5. Obesity
A
  1. Addison’s disease

—expect that to cause HYPOtension

27
Q

9 Which one of the following mechanisms appears to be the most important factor leading to hypertension in a patient with Cushing’s Disease?

  1. Arterial vasoconstriction
  2. Elevated [ACTH] throughout day and night
  3. Increased activation of the mineralocorticoid receptors by excess cortisol
  4. Renal damage from elevated cortisol levels 5. Elevated serum aldosterone levels
A
  1. Increased activation of the mineralocorticoid receptors by excess cortisol
28
Q

10 A 29 year old man presents with recently discovered hypertension (BP 170/110). He says his HBP was discovered after becoming “addicted to old-fashioned black licorice”. Which of the following is most likely NOT true?

  1. He has often been told that his teeth are black.
  2. His serum aldosterone level is very high.
  3. The black licorice contained glycyrrhizic acid. 4. His serum PRA is suppressed.
  4. His hypertension will most likely disappear if he cures his addiction for black licorice.
A
  1. His serum aldosterone level is very high.

SBM Endocrine (26 decks)

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