michigan hypertension core curriculum - State of Michigan

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y sodium restriction or the use of diuretics. Stricter BP control is also associated with reduction in proteinuria, which independently correlates with improved renal outcomes and mortality rates 5 . Multiple studies have now shown additional decreases in proteinuria of similar magnitude in patients with diabetic nephropathy when a second RAAS inhibitor is added to an ACEI or ARB. Combinations of an ACEI and ARB 6 or addition of spironolactone 7-10 or epleronone 11 in patients already taking an ACEI or ARB, were studied. Safety concerns in patients with decreased GFR include an initial decrease in GFR of 5-10 ml/ min that correlates with the magnitude of proteinuria reduction and plateaus early during treatment. Of particular concern is an increase in the need for acute dialysis and a trend towards higher mortality that did not reach statistical significance in patients treated with an ACEI and ARB in the ONTARGET trial 12 . Many but not all studies of dual or triple RAAS inhibition report an increased risk of hyperkalemia as well. NDHP CCBs result in similar decreases in albuminuria, while most other antihypertensive drugs have little to no effect on proteinuria. The estimated lifetime risk of ESRD in patients with diabetes mellitus was approximately 16% prior to the widespread adoption of strict glycemic and BP control 13 . Doubling of serum creatinine occurred almost 78% of type I diabetics with overt proteinuria and a baseline serum creatinine ≥ 1.5 mg/dl who were randomized to receive antihypertensive medications other than ACE inhibitors or calcium channel blockers over a 4 year period. By comparison, in the group randomized to captopril, doubling of creatinine was observed in less than 36% of patients 14 . This benefit persisted after adjustment for the slightly lower BP maintained in the captopril group, and was not observed in patients with a baseline creatinine < 1.5 mg/dL (whose rate of creatinine was < 10% regardless of treatment). Target blood pressures in this 1993 study (< 140/90, or < 160 systolic and at least 10 mm Hg < baseline SBP) were higher than currently recommended targets, but probably reflective of blood pressures still commonly observed in clinical practice. Non-Diabetic Chronic Kidney Disease The management of hypertension in patients with non-diabetic CKD closely parallels that of CKD in patients with diabetes, as outlined above. Strict control of BP (≤ 130/80) reduces progression of CKD (loss of GFR) in a broad variety of non-diabetic kidney diseases as well as in diabetic nephropathy and is recommended by JNC-7 1 for patients with CKD. In contrast, the specific benefits of RAAS inhibition are limited to proteinuric (i.e., glomerular) diseases. This is largely expected in that 1) diabetes itself, 250 Hypertension Core Curriculum
the prototypic disease in which RAAS inhibition has shown to be beneficial, is a glomerular disease; and 2) experimental models of kidney disease detailing the mechanisms underlying renal protection from RAAS inhibition almost all relate to it glomerular effects (including reduction of glomerular capillary pressure, reduction of mesangial albumin trafficking, direct improvement of glomerular permselectivity to albumin, reduction of glomerular hypertrophy, and inhibition of mesangial growth factors such as TGF-β and PDGF). The remainder of this section will refer only to non-diabetic CKD with proteinuria. As in the case of diabetic nephropathy, ACEIs and ARBs generally reduce proteinuria by 35 to 45%. 15 Studies differ on whether supramaximal doses of ACEIs or ARBs (doses larger than those producing the greatest decreases in BP) result in further reductions in proteinuria. 16,17 Similarly, NDHP CCBs 18 possess significant anti-proteinuric effects in non-diabetic proteinuric CKD. The clinical relevance remains speculative in both cases; neither dual RAAS inhibition nor NDHP CCBs have been proven to preserve GFR. However, in light of multiple studies demonstrating an association between reduction in proteinuria and protection from GFR loss 19,20 , it is generally considered worthwhile to reduce albuminuria to less than 500 – 1000 mg/day when possible. The MDRD study 21 excluded patients with diabetes and contained a relatively high percentage of patients with autosomal dominant polycystic kidney disease (ADPKD). Although almost half of the patients studied received an ACEI, that decision was made by the patients’ treating physicians prior to enrollment and the results were not analyzed or stratified according to treatment or not with an ACEI. Patients in the group randomized to a “usual” MAP < 107 mm Hg (approximately 140/90) lost residual GFR more quickly than those randomized to a “low” MAP of < 92 mm Hg (approximately 125/75). The former group actually achieved a MAP of 96 mm Hg (approximately 130/80). Interestingly, the benefit of lower BP in these patients was limited to patient with moderate (1-2.9 g/day) or especially severe (≥ 3 g/day) proteinuria, suggesting to some that a BP of 1 g/day). The unique benefits of ACEIs in non-diabetic, proteinuric CKD patients were convincingly shown in the Ramipril Efficacy in Nephropathy 22 (REIN) study and in the African American Study of Kidney Disease 23 (AASK). In the REIN study both the ramipril and placebo groups were titrated to the same BP (DBP < 90 mm Hg). Patients excreting > 3 grams of protein daily randomized to ramipril showed slower rates of GFR loss (0.53 v. 0.88 ml/min per month). Apparent benefits persisted or increased for at least NKFM & MDCH 251
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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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Page 208 and 209: Table 2: (JNC VII, 2004) 208 Hypert
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Page 212 and 213: ecently published RCT investigated
Page 214 and 215: Post-test question: 35y/o male w/ h
Page 216 and 217: Orthostatic Hypotension Pretest que
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Page 220 and 221: 1- Fludrocortisone : a mineralocort
Page 222 and 223: References: 1. Hiitola P, Enlund H,
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
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Page 244 and 245: ACUTE KIDNEY INJURY (AKI) In additi
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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
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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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