michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
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What is the most likely cause <strong>of</strong> this patient potassium being low? What are the steps that can<br />
be taken to prevent and treat the hypokalemia?<br />
Impression: This is a patient with well control BP while taking a thiazide diuretics and a dihydropyridine<br />
calcium antagonist. Hypokalemia refractory to potassium supplement is associated with depletion<br />
<strong>of</strong> magnesium stores. The combination <strong>of</strong> hypokalemia and magnesium depletion is usually seen in<br />
individuals receiving thiazide or loop diuretic treatment. 2 It has been suggested that potassium wasting<br />
is due to Na-K-ATPase impairment cause by magnesium deficiency. 3 Thus, a reasonable strategy<br />
would be to empirically administer magnesium replacement therapy given that her kidney function is<br />
normal. Measurement <strong>of</strong> serum levels can be misleading, especially if normal, because magnesium<br />
is primarily an intracellular ion and circulating levels are not necessarily indicative <strong>of</strong> magnesium<br />
depletion. Interestingly, some hypertensive patients will experience sleep disturbance. Magnesium is<br />
a reasonably effective sleep aid.<br />
Plan: Begin magnesium and potassium supplements together. Recheck potassium and magnesium<br />
levels after a few weeks.<br />
Case 3<br />
A hypertensive patient with diabetes who is taking a diuretic and the steps that can be taken to<br />
minimize or prevent diuretic induced hyperglycemia.<br />
Mr. AV was started on hydrochlorothiazide for his HTN diagnosed three months ago; at the time <strong>of</strong><br />
diagnosis his BP was 156/98 mm Hg. He has been taking glipizide for diabetes for the past 10 years<br />
which was well controlled until recently. He was recently discharged from the ED after experiencing an<br />
episode <strong>of</strong> elevated blood glucose (250 mg/dl). His BP at that time was 138/90 mmHg.<br />
PMH: Hypertension and diabetes mellitus<br />
Medications: Hydrochlorothiazide 25mg daily and glipizide 10 mg daily<br />
Physical Exam: BP <strong>of</strong> 136/92 mmHg, heart rate <strong>of</strong> 76 beat/mm, temperature 98 o F and RR 16. Cardiac<br />
exam is normal S1 and S2, Lungs are clear and extremities have no edema or cyanosis.<br />
Fasting CBG today is 140<br />
What is the most likely reason for the elevation <strong>of</strong> Mr. AV glucose level? What is the best step to<br />
take to minimize or prevent diuretic-induced hyperglycemia?<br />
Impression: Mr. AV’s BP has responded fairly well to the diuretic. However, his physician is not<br />
practicing evidence-based medicine. The initial anti-hypertensive drug that should have been<br />
prescribed was either an ACE inhibitor or an ARB. Nevertheless, because his BP was 26/18 mm hg<br />
above baseline when anti-hypertensive therapy was initiated, it was highly unlikely that BP control to<br />
< 130/80 mm hg would be obtained. Accordingly, he should have been placed on two drug therapy<br />
initially with one <strong>of</strong> the agents being either an ACE or an ARB; the other agent should have been either<br />
a diuretic or a calcium antagonist. Hypokalemia during diuretic therapy has been significantly linked to<br />
the development <strong>of</strong> hyperglycemia. A nice advantage <strong>of</strong> ACE or ARB therapy concurrent with a diuretic<br />
is that these agents substantially reduce the likelihood <strong>of</strong> diuretic-induced hypokalemia and have also<br />
been shown, not surprisingly, to minimize thiazide-induced elevations in serum glucose levels.<br />
Plan: Start candesartan 4mg daily and continue hydrochlorothiazide.<br />
NKFM & MDCH 273