michigan hypertension core curriculum - State of Michigan

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Case 4 Hypertensive patient with CKD with poorly controlled BP control experiencing a significant elevation in creatinine when BP is lowered below his goal BP. Mr. Bk is a 56-year old male who present with uncontrolled HTN two weeks ago 136/84 mmHg and an EGFR of 30ml/min/1.73m 2 . He has taken losartan 50mg daily, metolazone 5mg daily and diltiazem SR 240mg twice daily for the last one year. The patient was subsequently started on furosemide 20mg once daily because he developed bilateral leg swelling. Mr. BK presents to clinic today, without complaints; his EGFR is now 20. PMH: Hypertension, CKD and CVA. Medications: Losartan 50 mg daily, metolazone 5 mg daily, diltiazem SR 240 mg bid and furosemide 20 mg qd. Physical Exam: BP of 118/70 mmHg (no orthostatic change), heart rate of 92 beats /min, temperature 97.2 o F and RR 20. Heart: regular rhythm and an S4 gallop, Lungs: clear, Extremities: no edema, skin temp is normal. What is most likely cause of the patient’s reduced kidney function? What should be the appropriate step in the management at this time? Impression: Mr. BK was not at goal initially requiring additional antihypertensive medications. The deterioration in his kidney function is most likely due to his drop in BP. It is also certainly possible that over-diuresis is playing a role in the deterioration of his kidney function. In the setting of reduced renal mass the relationship between systemic BP and renal glomerular is no longer sigmoidal but becomes quasi-linear. Thus, declines in BP may result in rises in creatinine, at least over the short-term because renal autoregulation of glomerular pressure is impaired. Plasma volume contraction will aggravate this condition. Plan: Evaluate the patient for over-diuresis. In the absence of a new orthostatic BP change or a significant rise in serum HCO3 (indicative of a contraction alkalosis), you might consider ordering a BNP (brain natriuretic peptide) level. If even modestly elevated intravascular volume depletion is unlikely. A normal BP level will not be nearly as helpful. I would very likely simply follow this patient and recheck the serum creatinine over the next couple of weeks. Case 5 A hypertensive patient who is being treated with multiple antihypertensive drugs who has significant orthostatic hypotension. PC is a 68-year old male who present with a complaint of light-headedness especially when he stands. His other symptoms include change in vision, weakness and headaches. Four weeks ago his doxazosin was increased from 4mg qhs to 8mg qhs for better BP control. PMH: Hypertension, BPH and diabetes. Medications: Chlorthalidone 25mg daily, telmisartan 40mg daily, doxazosin 8mg qhs, and metformin 500mg twice daily. 274 Hypertension Core Curriculum
Physical Exam: BP sitting 120/74 mmHg and standing 100/60 mmHg. Pulse: 68 and regular (pulse rate does not change with standing) HEENT: Arteriovenous nicking but no other fundoscopic changes; Heart: RRR, normal S1 and S2; Lungs: grossly clear. Extremities: no edema. What are the risk factor(s) in this patient for orthostatic hypotension? What is the most likely cause of his orthostatic hypotension? Impression: This is a 68-year old male with multiple risk factor(s) for orthostatic hypotension – Age, diabetes, diuretics and taking both a diuretic and an alpha antagonist for control of BP. Orthostatic hypotension is defined as a drop in systolic blood pressure of > 20 mmHg which can be associated with symptoms. Nevertheless, practitioners should pay attention to orthostatic declines in BP that are even less in magnitude than a 20 mm Hg decline. His doxazosin was recently increased with a subsequent development of his symptoms for orthostatic hypotension. However, the lack of rise in his pulse on standing as his BP falls is consistent with autonomic neuropathy, a likely consequence of his diabetes. Plan: He should also be evaluated carefully for over-diuresis. And, even if over-diuresis is not detected, an empiric reduction in the diuretic dose is a meritorious consideration. Another consideration would be to switch him from chlorthalidone to HCTZ without a change in the daily dose; this would also effectively reduce his diuretic dose. It is likely that several factors have conspired to contribute to his orthostatic hypotension. Without question his dose of doxazosin should be reduced. If all of these changes do not eliminate his orthostatic BP decline, you must use his standing – not seated – BP as the guide to your therapeutic intensity. References: 1. Brater DC. Diuretic therapy. N Engl J Med. Aug 6 1998;339(6):387-395. 2. Weiner ID, Wingo CS. Hypokalemia--consequences, causes, and correction. J Am Soc Nephrol. Jul 1997;8(7):1179-1188. 3. Wong NL, Sutton RA, Mavichak V, Quamme GA, Dirks JH. Enhanced distal absorption of potassium by magnesium-deficient rats. Clin Sci (Lond). Nov 1985;69(5):625-630. NKFM & MDCH 275
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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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References: 1. Hiitola P, Enlund H,
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Page 244 and 245: ACUTE KIDNEY INJURY (AKI) In additi
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Page 260 and 261: DEFINITION AND CLASSIFICATION Hyper
Page 262 and 263: etween adult socioeconomic position
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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
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Page 276 and 277: Case 6 276 Hypertension Core Curric
Page 278 and 279: year. Sodium restriction and weight
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