michigan hypertension core curriculum - State of Michigan

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Table 3. Clinically Available Clues Indicative of Poorly Controlled BP 6. Mechanisms of Blood Pressure-Related Target Organ Injury “Damage” to target-organs such as the heart, kidney, brain, and peripheral vasculature can occur at BP levels that are within the so-called normal range. This is because BP cutpoints for the diagnosis of hypertension such as > 140/90 mm Hg are arbitrary. SBP is more closely linked to target-organ injury and adverse clinical complications than DBP. Hypertension or incrementally higher levels of BP (even within the normal BP range) can injure target-organs via several mechanisms. Elevated BP can disrupt the functional and/or anatomic integrity of the vascular endothelium leading to accumulation of lipids, macrophages/monocytes, and inflammatory mediators in the subendothelium; this is the early stage of atherogenesis. As a vascular plaque grows elevated BP can create enough hemodynamic stress on the plaque to either contribute to or cause plaque rupture. Even in the absence of overt atherosclerosis, elevated BP leads to vascular remodeling/hypertrophy of arterial resistance vessels (arterioles) and causes abnormal vascular function (e.g., raised peripheral arterial resistance, endothelial dysfunction) and chronic ischemia of the involved target-organ such as the brain and kidney. Even if an atherosclerotic plaque does not rupture, its growth can be facilitated by elevated BP and it may compromise blood flow enough to cause intermittent (angina pectoris, transient ischemic attack [TIA]) or chronic ischemia of a target-organ. Sometimes the raised BP leads to weakening of the arteriolar vessel wall resulting in aneurysmal dilation of the vessel. Aneurysms are prone to rupture. Elevated BP, particularly SBP, is a major cause of left ventricular hypertrophy and ultimately both LV systolic dysfunction and diastolic heart failure. Nitric oxide is synthesized from its precursor L-arginine via the action of endothelial NO synthase (eNOS). Nitric oxide (NO) is necessary for normal vascular function. The integrity of the vasculature, both functionally and anatomically, is dependent on adequate NO effect. Pulsatile blood flow in the arterial system leads to NO release from endothelial cells. Accordingly, pulsatile blood flow during exercise leads to even greater NO release from the vascular endothelium. However, with ageing, for example, the arterial vasculature stiffens, in part because of remodeling/ hypertrophy of the arterial media. This is characteristically associated with increases in peripheral arterial resistance. This stiffening of the vasculature also has another important effect on endothelial function. The endothelium of stiff blood vessels produces less NO than elastic/ pliable vessels do. The lack of NO effect has also been termed endothelial dysfunction which can be measured, though with some difficulty, non-invasively. In several states of endothelial dysfunction, the primary physiological problem is not a lack of NO production but rather enhanced destruction via the mediators of high levels of oxidative stress. Two examples of states of high oxidative stress are obesity and diabetes. 30 Hypertension Core Curriculum
The higher the level of BP, the more likely pressure-related target-organs will sustain injury. Injury to pressure-sensitive target organs is occurs via multiple mechanisms as displayed in table 4. Endothelial dysfunction, vascular remodeling causing target-organ ischemia, accelerated atherosclerosis, cardiac remodeling/left ventricular hypertrophy and vascular rarefaction are examples of chronic pressure-related injury. An arterial tear as seen in aortic dissection or rupture of an aneurysm are very dramatic manifestations of pressure-related target-organ injury. Table 4. Mechanisms of Blood Pressure-Related Target Organ Injury 7. Mechanisms of Pressure-Related Hemodynamically-Mediated Renal Injury Hypertension has been linked both to chronic kidney disease as well as end-stage renal disease (ESRD). In fact, hypertension is the second leading cause of ESRD behind diabetes mellitus. The distinction between hypertension and diabetes mellitus is not entirely distinct. About 70 - 80% of persons with diabetes mellitus have hypertension (BP > 130/80 mm Hg and/or taking antihypertensive medications), and obesity augments the risk for both hypertension and diabetes mellitus. Transmission of systemic arterial pressure into the glomerulus, the functional unit of the kidney, is a major cause of renal injury. Under normal conditions the glomerulus protects itself from inordinate transmission of arterial pressure into the glomerular capillary loop. The mechanism by which systemic arterial transmission to the glomerulus is dampened is called autoregulation of renal GFR and blood flow. The afferent arteriole brings blood flow into the glomerulus from the renal artery where blood is filtered, urine is formed, and blood leaves the glomerulus via the efferent arteriole. Blood subsequently flows from this glomerular capillary network into another one, the peritubular capillaries. That is, the efferent arteriole branches into a peritubular capillary network that surrounds the tubules. Autoregulation of GFR and renal blood flow are accomplished via several mechanisms. Increases in afferent arteriolar luminal pressure cause constriction of this vessel; decreases in luminal pressure cause dilation of this vessel. These afferent luminal caliber changes in response to changes in pressure are accomplished via the myogenic reflex. Tubuloglomerular feedback (TGF) is another mechanism through which afferent arteriolar tone can be affected. This mechanism changes afferent arteriolar tone according to changes in sodium chloride delivery to the macula densa in the distal nephron. Increased NaCl delivery leads to increased afferent arteriolar tone while decreased delivery causes afferent arteriolar dilation. Finally, local activation of the RAS system as typically occurs in the setting of reduced renal mass (↓ nephron number) leads to Ang II -mediated efferent >> than afferent arteriole constriction that raises intraglomerular pressure. NKFM & MDCH 31
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........
Page 10 and 11: 10 Hypertension Core Curriculum Blo
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
Page 24 and 25: Blood Pressure, Circulatory Physiol
Page 26 and 27: side of the vascular tree. Arterial
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Page 32 and 33: In the setting of chronic hypertens
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Page 36 and 37: cause greater disruption of CBF aut
Page 38 and 39: References/Suggested Reading Agabit
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Page 42 and 43: development of essential HTN can se
Page 44 and 45: Figures: Figure 1. Pie-chart with m
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 58 and 59: glycemic risk factdors such as hype
Page 60 and 61: . Weight loss c. Weight gain d. A a
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Page 66 and 67: foods and turn out of necessity to
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Page 72 and 73: Incidence and Prevalence The overal
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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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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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