michigan hypertension core curriculum - State of Michigan

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In the setting of chronic hypertension, the afferent arteriole anatomically remodels and becomes functionally incapable of maximally dilating (figure 4). This causes the lower end of the normal sigmoidal relationship between MAP and intraglomerular pressure to move to a higher level of BP. In contradistinction to the effect of chronic hypertension on the cerebral blood flow autoregulatory curve, as kidney function deteriorates and nephron number drops, the upper limit of autoregulation moves to a lower BP level resulting in intraglomerular pressure (and GFR) varying in a more direct relationship with systemic arterial pressure. In other words, the relationship between glomerular pressure and GFR becomes more linear. 32 Hypertension Core Curriculum Figure 4 As nephron number falls, the demands on the remaining glomeruli increase to make up for the lost glomeruli. GFR is maintained, at the expense of high intraglomerular pressure, as a consequence of local activation of the RAS system that causes Ang II-mediated efferent arteriolar constriction; at the afferent arteriole, vasodilatory prostaglandins and nitric oxide mediate vasodilatation. These changes in afferent and efferent arteriolar tone, in aggregate, lead to intraglomerular capillary hypertension. There is also increased glomerular endothelial permeability resulting in excess filtration of plasma proteins in direct relation to the increased glomerular pressure that is, in turn, elevated because of transmission of systemic arterial pressure into a dilated afferent arteriole. A final common pathway leading to further nephron destruction is glomerusclerosis and tubulointerstitial fibrosis. To understand the above pathophysiology is to also understand how to protect the kidney from further loss of functioning mass. Attainment of low levels of BP as well as lowering intraglomerular pressure with drugs such as angiotensin converting enzyme (ACE) inhibitors and/ or angiotensin receptor blockers (ARB’s) are proven ways to protect kidney function (figure 5).
Figure 5. Chronic Kidney Disease The aforementioned renal pathophysiology has important therapeutic implications. A note of caution, given that intraglomerular pressure in persons with reduced kidney function is more directly linked to systemic arterial pressure, lowering BP and/or lowering intraglomerular pressure can lead to a rise in serum creatinine that occurs as a result of lowering of GFR. Essentially the compromised kidney is letting you know that it can’t autoregulate its GFR, at least over the shortterm. Nevertheless, the compromised kidney maintains function longer, even if GFR falls in the short-term, when BP is lowered and intraglomerular pressure falls. In fact, the very conditions where autoregulation of GFR is abnormal - reduced renal mass, diabetes mellitus, proteinuric kidney disease - are indications for the type of pharmacological interventions (angiotensin converting enzyme inhibitor or angiotensin receptor blocker therapy) that may lead to a rise in serum creatinine. Thus, due to systemic circulatory and renal micro-circulatory effects, lowering BP with regimens containing ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors, will often lead to a rise in the serum creatinine indicative of a drop in the global GFR. If the patient has been over-diuresed and has a contracted plasma volume, the rise in creatinine will be even more prominent. 7. Clinically Recognizable Manifestations of BP-Related Target-Organ Injury Table 5 displays common clinically recognizable manifestations of BP-related target-organ injury. These complications represent micro- and macro-vascular complications as well as targetorgan dysfunction/failure. Careful clinical assessment and examination will detect many of these complications. The fundoscopic examination is often either poorly executed or not done in clinical situations, yet it provides great insight into the prior level of BP control and is one of the easiest ways to determine the presence of BP-related target-organ injury. Though retinopathy is linked to the level of BP, most retinal abnormalities are not specific, per se, to hypertension as some of these changes also occur, for example, in diabetes mellitus. Control of BP can prevent or forestall virtually all of these complications. NKFM & MDCH 33
Page 1: MICHIGAN HYPERTENSION CORE CURRICUL
Page 4 and 5: April 2010 Dear Colleague: In 2005,
Page 6 and 7: Kevin L. Piggott, MD, MPH, FAAFP Pr
Page 8 and 9: Blood Pressure Measurement........
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Page 12 and 13: of the wrist. Additionally, there i
Page 14 and 15: asis. National guidelines recommend
Page 16 and 17: Post-Test Questions: 1. High BP is
Page 18 and 19: 18 Hypertension Core Curriculum Ess
Page 20 and 21: Masked Hypertension is when the off
Page 22 and 23: TABLE 1. Prevalence of Awareness, T
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Page 26 and 27: side of the vascular tree. Arterial
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Page 30 and 31: Table 3. Clinically Available Clues
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Page 36 and 37: cause greater disruption of CBF aut
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Page 42 and 43: development of essential HTN can se
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Page 46 and 47: Table 2 Table 3 Screening Test for
Page 48 and 49: References: 1. U.S. Renal Data Syst
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Page 52 and 53: side effects particularly well. A h
Page 54 and 55: 14. Gaede P, Vedel P, Larsen N, Jen
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Page 60 and 61: . Weight loss c. Weight gain d. A a
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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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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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