michigan hypertension core curriculum - State of Michigan

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e classified as having “renovascular hypertension”, since there is no compelling evidence that ARAS causes hypertension, and cure of hypertension after revascularization is rare. # 3: The term “renal ischemia” should be reserved for patients with RAS and abnormal renal perfusion (unilateral or bilateral). # 4: The term “renal artery stenosis” should be used for patients with “anatomic” stenosis, but has no implications regarding renal ischemia. #5: The term “nephropathy” should be reserved for patients with renal parenchymal disease. “Ischemic nephropathy” should be reserved for patients with renal parenchymal disease associated with longstanding atherosclerosis and intra-renal arteriolar disease. Other forms of nephropathy may be based on the presence of known diseases, such as diabetes (diabetic nephropathy), hypertension (hypertensive nephropathy), interstitial diseases (interstitial nephropathy), or may be acquired as a complication of revascularization (acute tubular necrosis, contrast nephropathy, and renal embolization). 120 Hypertension Core Curriculum
Medical therapies, particularly antihypertensive drug therapy and therapies to limit atherosclerosis, are the primary therapies for all patients with RAS. The optimal use of renal artery revascularization is poorly defined. Contemporary decisions about renal revascularization must include an assessment of the severity and functional significance of RAS (renal ischemia), the condition of the kidneys (nephropathy), and the association between RAS and vital organ injury. The benefits and risks of renal revascularization will be improved by careful patient selection. Better results will be achieved in patients with vital organ injury, renal ischemia, and no nephropathy. Appropriately designed randomized clinical trails are essential to define the role of renal revascularization. Such trials must incorporate assessment of renal ischemia and nephropathy, since these factors have the strongest influence on outcome. FIGURE LEGENDS Figure 1. The most common types of renal artery stenosis (RAS). Left, fibromuscular dysplasia (FMD), characterized by a beaded appearance of the mid or distal renal artery in which the beads are larger than the vessel (medial fibroplasia). Right, atherosclerotic renal artery stenosis (ARAS), characterized by stenosis of the ostium and proximal renal artery. Figure 2. Endovascular revascularization of ARAS. Left, baseline image before intervention (same as Figure 1, right panel). Middle, suboptimal angiographic result after balloon angioplasty, characterized by significant residual stenosis, elastic recoil, and dissection (arrow). Right, final result after stent placement demonstrates optimal lumen enlargement. Figure 3. Schematic representation of common configurations of renal arterial origins from the abdominal aorta. A, single renal artery occurs in 55 % of population. B, Single renal artery with early bifurcation occurs in 14 % of population. C, dual arterial circulation in which two major renal arteries supply a single kidney, occurs in 8 % of population. D, single major renal artery and one or more smaller accessory renal arteries, occur in 7 % of population. Other configurations (not shown) occur in 16 %, including aberrant origins of the renal arteries from other visceral vessels, iliac arteries, and aortic bifurcation. (Modified from Uflacker R. Atlas of Vascular Anatomy.2 nd edition. Philadelphia, PA: Lippincott, Williams, and Wilkins, 2007:609. Figure 4. Conventional abdominal aortogram using digital subtraction angiography (AP projection) demonstrating early (left), mid (middle), and late (right) phases of the contrast injection. Aortography is used to identify the configuration of the renal arterial origin (see Figure 3) as well as associated NKFM & MDCH 121
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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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Page 84 and 85: appear to be related to access to c
Page 86 and 87: CDC MMWR Feb 24, 2006/55(07); 177-1
Page 88 and 89: Figure 1; Clinical presentation and
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Page 92 and 93: ANY patient, who develops paroxysma
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Page 98 and 99: Definition Prevalence Clinical Feat
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Page 104 and 105: Figure 3; Endocrine Society See tex
Page 106 and 107: INTRODUCTION 106 Hypertension Core
Page 108 and 109: Renal manifestations. Renal ischemi
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Page 134 and 135: Table 11. New terminology for renal
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Page 138 and 139: 2001;12(6):1235-1241. 40. Subramani
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Page 144 and 145: monitored hypertension screening an
Page 146 and 147: Policy Development: Public health p
Page 148 and 149: Med Clin North Am. Jan 2004;88(1):2
Page 150 and 151: mind they will have no problem iden
Page 152 and 153: Role of Race in the Selection of An
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Page 158 and 159: sister, mother and father. A family
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Page 164 and 165: Vital signs suggestive of OSAHS. 20
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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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www.neuroanatomy.wisc.edu/.../Image
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Learning objectives: 226 Hypertensi
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controlled BP to have been victimiz
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Treatment of Secondary Causes of Hy
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4-Direct vasodilators (e.g.minoxidi
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Hypertension. Aug 2003;42(2):161-16
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emergency by virtue of the associat
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PATHOPHYSIOLOGY The underlying mech
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trials included a placebo arm. Seve
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an indication for careful and modes
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ACUTE KIDNEY INJURY (AKI) In additi
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Blood Pressure Research Council, an
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[ACE inhibitors (ACEIs), angiotensi
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y sodium restriction or the use of
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44 months 24 , and were also seen i
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• Hypertension in dialysis patien
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GISEN Group (Gruppo Italiano di Stu
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258 Hypertension Core Curriculum
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DEFINITION AND CLASSIFICATION Hyper
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etween adult socioeconomic position
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women treated with atenolol in earl
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Obstet Gynecol. Dec 12 2008. 5. Vol
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able to dissipate the pressure rise
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Use of Dihydropyridine Calcium Anta
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272 Hypertension Core Curriculum Ca
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Case 4 Hypertensive patient with CK
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Case 6 276 Hypertension Core Curric
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year. Sodium restriction and weight
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What may be causing these new sympt
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