michigan hypertension core curriculum - State of Michigan

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272 Hypertension Core Curriculum Case Studies Mark Britton, MD Case 1 A hypertensive patient taking multiple antihypertensive medications with poor BP control without an appropriate diuretic prescribed. Mrs. KT is a 56-year old white female who present with a difficult to control BP. Her BP has ranged between 150 to 170 mmHg systolic and 94 to 104 mmHg diastolic. PMH: Hypertension and hyperlipidemia. Medications: amlodipine 10mg daily, atentolol 50mg daily, quinapril 20mg daily and simvastatin 20mg daily. Physical Exam: BP is 174/98 mmHg without orthostatic change, heart rate of 84 beats/min, temperature 97.6 o F and RR of 12. Cardiac exam is normal except for an S4 gallop, lungs are clear and extremities have trace edema. Laboratory Studies: sodium of 138 mEq/L, potassium of 4.8 mEq/L, chloride of 100 mEq /L, bicarbonate of 24 mEq/L, BUN of 16 mg/dl and Cr of 1.8 mg/dl (estimated GFR in the low 30’s). What is the next appropriate strategy in controlling Mrs. KT BP? Why? Impression: Mrs. KT’s BP is persistently elevated despite multiple antihypertensives. However, she does not have resistant HTN because she is not taking a diuretic. There are multiple reasons to suspect that she would benefit from a diuretic: 1) likely consumption of a high sodium diet; 2) reduced renal natriuretic capacity given her depressed kidney function, and 3) multiple non-diuretic antihypertensives, especially the beta blocker and ACE inhibitor, which clearly benefit from being utilized with a diuretic to enhance their BP lowering effect. Her condition is highly suggestive of volume expansion for which she could benefit from a diuretic. A good rule of thumb is that when taking more than two non-diuretic anti-hypertensives that at least one of them should be a diuretic. Ideally the diuretic should be matched to the level of kidney function. Accordingly, a traditional thiazide diuretic like HCTZ is unlikely to be effective in this lady given it loses its effectiveness around an EGFR of 45 1 . Even chlorthalidone which works down to a GFR in the low to mid 30’s would be a gamble. Either metolazone, a long-acting thiazide-like diuretic, or furosemide would be good options. If furosemide is chosen, it must be dosed at least BID; furosemide is too short acting to be utilized once daily as it is, unfortunately, often prescribed. Plan: Start the patient on a metolazone 2.5 – 5.0 mg/d and monitor her BP response Case 2 A well controlled hypertensive patient with refractory hypokalemia despite replacement. Ms. JC is a 60-year old female who present with low potassium levels. Her BP was uncontrolled until two months when she was started on hydrochlorothiazide 25mg daily. Subsequently it was noted that her potassium levels has been 3.2 mEq /L. She has been maintained on potassium chloride 40 mEq daily for the past one month. PMH: Hypertension Medications: Hydrochlorothiazide 25mg daily amlodipine 10mg daily and potassium chloride 40 mEq daily. Physical Exam: BP of 117/74 mmHg, Heart rate of 76 beats/mm, temperature of 98.2 o F and RR of 16. Heart exam revealed a normal S1 and S2, lungs are clear and the remainder of his physical exam is normal. Laboratory studies: showed sodium of 136 mEq/L, potassium of 3.0 mEq/L, chloride of 100 meq/L, bicarbonate of 22 mEq /L, BUN of 21 mg/dl, Cr of 1.0 mg/dl and glucose of 98 mg/dl.
What is the most likely cause of this patient potassium being low? What are the steps that can be taken to prevent and treat the hypokalemia? Impression: This is a patient with well control BP while taking a thiazide diuretics and a dihydropyridine calcium antagonist. Hypokalemia refractory to potassium supplement is associated with depletion of magnesium stores. The combination of hypokalemia and magnesium depletion is usually seen in individuals receiving thiazide or loop diuretic treatment. 2 It has been suggested that potassium wasting is due to Na-K-ATPase impairment cause by magnesium deficiency. 3 Thus, a reasonable strategy would be to empirically administer magnesium replacement therapy given that her kidney function is normal. Measurement of serum levels can be misleading, especially if normal, because magnesium is primarily an intracellular ion and circulating levels are not necessarily indicative of magnesium depletion. Interestingly, some hypertensive patients will experience sleep disturbance. Magnesium is a reasonably effective sleep aid. Plan: Begin magnesium and potassium supplements together. Recheck potassium and magnesium levels after a few weeks. Case 3 A hypertensive patient with diabetes who is taking a diuretic and the steps that can be taken to minimize or prevent diuretic induced hyperglycemia. Mr. AV was started on hydrochlorothiazide for his HTN diagnosed three months ago; at the time of diagnosis his BP was 156/98 mm Hg. He has been taking glipizide for diabetes for the past 10 years which was well controlled until recently. He was recently discharged from the ED after experiencing an episode of elevated blood glucose (250 mg/dl). His BP at that time was 138/90 mmHg. PMH: Hypertension and diabetes mellitus Medications: Hydrochlorothiazide 25mg daily and glipizide 10 mg daily Physical Exam: BP of 136/92 mmHg, heart rate of 76 beat/mm, temperature 98 o F and RR 16. Cardiac exam is normal S1 and S2, Lungs are clear and extremities have no edema or cyanosis. Fasting CBG today is 140 What is the most likely reason for the elevation of Mr. AV glucose level? What is the best step to take to minimize or prevent diuretic-induced hyperglycemia? Impression: Mr. AV’s BP has responded fairly well to the diuretic. However, his physician is not practicing evidence-based medicine. The initial anti-hypertensive drug that should have been prescribed was either an ACE inhibitor or an ARB. Nevertheless, because his BP was 26/18 mm hg above baseline when anti-hypertensive therapy was initiated, it was highly unlikely that BP control to < 130/80 mm hg would be obtained. Accordingly, he should have been placed on two drug therapy initially with one of the agents being either an ACE or an ARB; the other agent should have been either a diuretic or a calcium antagonist. Hypokalemia during diuretic therapy has been significantly linked to the development of hyperglycemia. A nice advantage of ACE or ARB therapy concurrent with a diuretic is that these agents substantially reduce the likelihood of diuretic-induced hypokalemia and have also been shown, not surprisingly, to minimize thiazide-induced elevations in serum glucose levels. Plan: Start candesartan 4mg daily and continue hydrochlorothiazide. NKFM & MDCH 273
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MICHIGAN HYPERTENSION CORE CURRICUL
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April 2010 Dear Colleague: In 2005,
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Kevin L. Piggott, MD, MPH, FAAFP Pr
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Blood Pressure Measurement........
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10 Hypertension Core Curriculum Blo
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of the wrist. Additionally, there i
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asis. National guidelines recommend
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Post-Test Questions: 1. High BP is
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18 Hypertension Core Curriculum Ess
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Masked Hypertension is when the off
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TABLE 1. Prevalence of Awareness, T
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Blood Pressure, Circulatory Physiol
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side of the vascular tree. Arterial
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upon the other co-morbidities prese
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Table 3. Clinically Available Clues
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In the setting of chronic hypertens
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34 Hypertension Core Curriculum Tab
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cause greater disruption of CBF aut
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References/Suggested Reading Agabit
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40 Hypertension Core Curriculum Chr
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development of essential HTN can se
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Figures: Figure 1. Pie-chart with m
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Table 2 Table 3 Screening Test for
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References: 1. U.S. Renal Data Syst
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50 Hypertension Core Curriculum Spe
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side effects particularly well. A h
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14. Gaede P, Vedel P, Larsen N, Jen
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Learning Objectives: 56 Hypertensio
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glycemic risk factdors such as hype
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. Weight loss c. Weight gain d. A a
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References: 1. Association AD. All
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64 Hypertension Core Curriculum Spe
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foods and turn out of necessity to
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Figure 1: Table 1. Metabolic Syndro
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9. Singh GK, Kogan MD, Van Dyck PC,
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Incidence and Prevalence The overal
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access to healthy foods than their
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As a part of the approach to managi
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B Hypertensive Adults (rate, percen
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References: 1. Lewington S, Clarke
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82 Hypertension Core Curriculum
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appear to be related to access to c
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CDC MMWR Feb 24, 2006/55(07); 177-1
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Figure 1; Clinical presentation and
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90 Hypertension Core Curriculum Phe
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ANY patient, who develops paroxysma
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Figure 1: 94 Hypertension Core Curr
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Objectives: 96 Hypertension Core Cu
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Definition Prevalence Clinical Feat
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intake. 4 Figure 1; Ion transport i
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loading with 200 mmoles (4.6 grams)
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Figure 3; Endocrine Society See tex
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INTRODUCTION 106 Hypertension Core
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Renal manifestations. Renal ischemi
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to assess renal dimensions and dupl
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stenosis severity. Patients with no
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ARAS, ischemic nephropathy, and imp
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the goals of minimizing injury to t
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hemodynamically impaired renal arte
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e classified as having “renovascu
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disease of the abdominal aorta and
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Table 1. Contemporary evaluation of
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2. Screening tests for RAS RDU, MRA
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Manifestations of vital organ injur
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Table 6. Clinical evaluation of ren
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Table 9. Assessment of worsening re
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Table 11. New terminology for renal
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References: 1. Murphy TP, Soares G,
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2001;12(6):1235-1241. 40. Subramani
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78. Tami LF, McElderry MW, al-Adli
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142 Hypertension Core Curriculum Pr
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monitored hypertension screening an
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Policy Development: Public health p
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Med Clin North Am. Jan 2004;88(1):2
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mind they will have no problem iden
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Role of Race in the Selection of An
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individuals of any race or ethnicit
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Older Patients Need Elevated Systol
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sister, mother and father. A family
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ecause pressure-related retinopathy
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pulses (lower in the left arm). 4 C
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Vital signs suggestive of OSAHS. 20
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may shed light on underlying medica
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References: patients. 8 However, th
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Objectives: 170 Hypertension Core C
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and evidence that anti-hypertensive
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When subjects are given instruction
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interestingly found only a 6.0/4.6
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pressure: a meta-analysis of random
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isolated systolic hypertension have
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Compelling Indications for Specific
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3.) Beta-blockers, ACE inhibitors,
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treatment levels - albeit though at
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Preparations and Dosage: Oral antih
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Preparations and Dosages: The Oral
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patients with tachy-brady syndrome
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significant proteinuria. Pharmacolo
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the effect found by the ACE inhibit
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and nominally statistically signifi
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sensitive K+-channels in vascular s
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clonidine (Catapres†) 0.1-0.8 mg
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Learning Objectives 204 Hypertensio
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general, the response to beta-block
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Table 2: (JNC VII, 2004) 208 Hypert
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Learning objectives: 210 Hypertensi
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ecently published RCT investigated
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Post-test question: 35y/o male w/ h
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Orthostatic Hypotension Pretest que
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BP. It is important to note that la
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1- Fludrocortisone : a mineralocort
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Page 224 and 225: www.neuroanatomy.wisc.edu/.../Image
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Page 230 and 231: Treatment of Secondary Causes of Hy
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Page 234 and 235: Hypertension. Aug 2003;42(2):161-16
Page 236 and 237: emergency by virtue of the associat
Page 238 and 239: PATHOPHYSIOLOGY The underlying mech
Page 240 and 241: trials included a placebo arm. Seve
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Page 244 and 245: ACUTE KIDNEY INJURY (AKI) In additi
Page 246 and 247: Blood Pressure Research Council, an
Page 248 and 249: [ACE inhibitors (ACEIs), angiotensi
Page 250 and 251: y sodium restriction or the use of
Page 252 and 253: 44 months 24 , and were also seen i
Page 254 and 255: • Hypertension in dialysis patien
Page 256 and 257: GISEN Group (Gruppo Italiano di Stu
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Page 260 and 261: DEFINITION AND CLASSIFICATION Hyper
Page 262 and 263: etween adult socioeconomic position
Page 264 and 265: women treated with atenolol in earl
Page 266 and 267: Obstet Gynecol. Dec 12 2008. 5. Vol
Page 268 and 269: able to dissipate the pressure rise
Page 270 and 271: Use of Dihydropyridine Calcium Anta
Page 274 and 275: Case 4 Hypertensive patient with CK
Page 276 and 277: Case 6 276 Hypertension Core Curric
Page 278 and 279: year. Sodium restriction and weight
Page 280: What may be causing these new sympt
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