Question of the Week # 157

157) A 25 year old woman presents to your office with complaints of muscle cramps and weakness. She smokes 1 pack cigarettes per day and chews tobacco and flavored gum. She also has history of alcoholism and ingests about one pint of vodka every day for the past 2 years. She also uses “Ecstasy”  during weekend parties. She has a history of snoring in the night. On examination,  afebrile,  heart rate is 88/min and blood pressure is 150/98.  Laboratory investigations reveal a Sodium of 144 meq/L, potassium of 3.0meq/L, Chloride 98meq/L , Bicarbonate of 34meq/L and Creatinine of 0.8mg%. Urinary chloride is 45meq/L. Which of the following points in the patient’s history is most helpful in diagnosing her condition?

A) Alcohol use

B) Chewing tobacco and flavored gum

C) Snoring in the night

D) Smoking

E) Use of Ecstasy

13 Responses

  1. bbbbbbbbbbb

  2. dr red plz answer

  3. ccc

  4. C…. high hco3 due to chronic respiratoy acidosis

  5. Sleep apnea causes a person to stop breathing periodically throughout sleep, which upsets the balance of oxygen and carbon dioxide in the blood. The brain senses the reduction in oxygen and the increase in carbon dioxide and sends a signal to resume breathing. The person wakes up in response to the breathing arousal signal from the brain. The muscles of the tongue and throat awaken to enlarge the airway and allow carbon dioxide to escape and oxygen to enter. The waking episodes are necessary to restart breathing (and save the person’s life), but they prevent the individual from getting high-quality sleep.

    On a physical level, the sleep apnea sufferer cannot breathe because they have an obstructed airway. The throat muscles and tongue relax too much and may be enlarged or misshapen, so the air passage is narrowed during sleep.

    Sleep apnea sufferers awaken frequently to restart breathing, but they remember little or nothing of being awake. Frequent waking at night may be a sign of sleep apnea. The frequency of waking episodes varies, but may be between ten and sixty per night. Severe sleep apnea may cause the sleeper to experience more than 100 waking episodes in a single night. One measure of sleep apnea is that the person must stop breathing for a period of at least ten seconds or more, five times within an hour. Sleep apnea sufferers may stop breathing for as long as two minutes.
    Obstructive sleep apnea (OSA) is an important clinical problem in the chronic kidney disease (CKD) population. OSA is associated with hypoxemia and sleep fragmentation, which activates the sympathetic nervous system, the renin-angiotensin-aldosterone system, alters cardiovascular hemodynamics, and results in free radical generation.

  6. answer C

    my explanation is that patient is suffering obstructive sleep apnoe with chronic respiratory acidosis , which is explained by her HIGH HCO3 (renal compensation ) , high urine CL (renal excretion of acid) . Patient has HTN : another complication of sleep apnoe .

    As for hypokalemia : not sure whether it is due to the chronic respiratory acidosis which causes extra and intracellular potassium shift or it’s due to chronic alcoholism which causes renal wasting of potassium or poor GI absorption .

    please enlighten us Dr. Redz

  7. Could it be that chronic obstructive sleep apnea induced hyper secretion of ALDOSTERONE leading to all the associated lab findings :

    hyperNA
    high HCO3
    Low K

    What’s the mechanism underlying that ?
    can anyone come up with a concept ?

  8. Laboratory investigations reveal a Sodium of 144 meq/L, potassium of 3.0meq/L, Chloride 98meq/L , Bicarbonate of 34meq/L and Creatinine of 0.8mg%. Urinary chloride is 45meq/L.

    Weird scenario- If Dr Redd is trying to show OSA syndrome here with a metabolic alkalosis in the morning by retention of Bicarbonate ions, he should have decreased urinary chloride. Urinary chloride should be less than 15 if this is post hypercapnea and not 45! The only causes of a chloride unresponsive Metabolic Alkalosis are Conn’s, Secondary hyperaldosteronism, Liddle’s and Barter’s syndrome.

    If this is Secondary Hyperaldosteronism with Hypokalemia and HTN and a sodium of 144 then Alcohol is the right answer. Acutely, alcohol causes anion gap MT acidosis with an osmolar gap of more than 20. Chronically it can result in secondary hyperaldosteronism. This patient cannot have respiratory alkalosis because OSA results in respiratory acidosis with metabolic alkalosis in the morning.

    My answer: A

    Moreover, she has been consuming Alcohol everyday for the last 2 years.

  9. Wow, wow, wow, i got it! Correct answer is “B”

    Dr Redd is one smart smart guy.. can’t give badwords! This is probably the best question i have come across ever in my life.

    The answer to this question is Chloride resistant Hyperaldosteronism, which is Secondary Hyperaldosteronism, where the urinary chloride is unresponsive/resistant to the metabolic alkalosis taking place. The key components of chewing tobacco and some flavoured gums is Glicyrrhizin which is derived from licourice root!

    Glicyrrhizin gives you this clear picture of the side effects which is hypertension and edema (water retention) and (Resistant) elevated urine chloride although there is retention of bicarbonate. These effects are related to the inhibition of cortisol metabolism within the kidney, and the subsequent stimulation of the mineralocorticoid receptors.

    If liquid ecstasy was given- then that could have been the correct answer because that contains Glicyrrhizin and flavanoids!

    Please, post this!

  10. wow!

  11. This guy has 20 shots of vodka daily. (10 x CDC recommendation) he has symptomatic hypokalemia. But alcoholics, people who snore, smoke or use ecstasy do not come to the clinic with symptomatic hypokalemia as frequently has people who are smokers, chew tobacco and flavoring gum.
    Urine chloride > 10mEq/L – alcohol less likely
    Hx of snoring alone, ecstasy alone, smoking alone do not conclude hyper aldosteronism;
    But chewing tobacco and flavored gum plus smoking history is a red flag for etiology. – licorice, its extract glycirrhizin found in 90% of tobacco products, also found in flavored gum; Two products with this substance, licorice. Licorice has minerocorticoid activity. This patient will have bicarbonate sparing, potassium losing effect. His urine chloride will be lower than normal range but it will be beyond the range that usually responds to saline because of aldosterone escape phenomenon. If this substance is removed from his diet and habits, his symptoms will likely resolve. If they persist, I will do PAC/PRA to exclude primary hyperaldosteronism first before considering other common causes of hypertension with hypokalemia like cushing’s syndrome, renovascular disease, pheochromocytoma. Obstructive sleep apnea is a rare cause presented as case report in 1994. There is no presented feature of this disease in this case except history of snoring which might as well be from excess alcohol (20 shots of vodka) history given in this case.

  12. B.. hypertension with hypokalemia, metabolic alkalosis = hyperaldosteonism. Tobacco chewing is one of the cause of hyperaldosteronism.

  13. Answer B. Licorice ingestion can mimic Hyperaldosteronism ( flavored gum ).

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