Cases

Question 1

80 yo female

Remarkable features:

• HR: 70-75 bpm
• Sinus rhythm

Answer 1

• First degree AV block
• Non-specific ST and/or T wave anomolies
• Prolonged QT interval

HYPOCALCEMIA (pt’s calcium was 6.8 mg/dl)

(when not enough calcium, channels are sluggest)

Question 2

What rules out an RTA?

Answer 2

Hypokalemia + metabolic acidosis + acidified urine

Question 3

What do you suspect with loss of fluid, electrolyte and bicarb?

Answer 3

chronic diarrhea, laxitive abuse

Question 4

65 yo male with edema, dyspnea, tachycardia, aortic systolic murmur detected

Answer 4

• CHF
  
  • what causes edema?
    
    • “sick pump”
    • RAAS
• Blood panel:
  
  • hyponatremia with hypervolemic (cirrosus, HF)

Question 5

59 yo female - Hyperparathyroidism and unmanaged HTN

Answer 5

• Hypercalcemia
• Predict low blood phosphate
• Urine:
  
  • relatively deplete in calcium
  • relatively rich in phosphate
• Manage essential HTN:
  
  • usually thiazide diuretic, but we won’t give that to her bc we don’t wnat to mess up her Ca2+ situtation
    
    • also won’t use loop diuretic
  • give Calcium channel blocker (amlodopine)

Question 6

80 yo man, fell: head injury; polyuria and hypodipsia (decreased thirst)

Dx: central (neurgenic) DI

What would blood labs reveal?

Answer 6

(can’t make/recognize ADH)

• hypernatremia
• hyperchloremia
• hypoosmotic urine (reabsorbing all the water)

Question 7

What are likely candidates diagnosis in a person with polydipsia?

Answer 7

• DI - (hypernatrimia)
• SIADH (even though reabsorbing all the water - look out for hyponatrimia)

Question 8

How do you treat a euvolemic hyponatrimic pt?

Answer 8

H2O restriction

(something has caused inordinate retention of H2O)

Question 9

What are 2 types of pts that get hypervolemic hyponatremia?

Answer 9

heart failure

marathon runners

Question 10

What are characteristics of mineralocorticoid HTN?

Answer 10

• hypokalemia
• kaliuresis
• metabolic alkalosis
• decreased plasma [renin]

Commonly caused by aldosterone excess that stimulates ENaC

• could be primary or secondary hyperaldosteronism
• NB: aldosterone has been shown to induce cell signaling linked to inflammation and development of fibrosis in CV tissues

Question 11

What is Pseudohypoaldoseronism?

Answer 11

Type I hypoaldosteronism

• causes salt-wasting
• mutations in ENaC gene (SCNN1)
  
  • Na+ reabsorption impaired causing a mass excretion of Na+ (natriuresis) and H2O