michigan hypertension core curriculum - State of Michigan

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and nominally statistically significant higher risks of stroke, angina, and coronary revascularization. The ALLHAT findings prompted termination of the doxazosin arm of the trial 2 years earlier than scheduled and has led national guideline writers and other authorities to recommend that the alpha blockers not be used as primary monotherapy for the treatment of hypertension. 10 Nonetheless, they remain useful when combined with other agents to accomplish satisfactory BP control and they are especially useful in older men with benign prostate hyperplasia in whom they are effective in reducing lower urinary tract symptoms. Additionally, the non-selective alpha-antagonists, including phenoxybenzamine and phentolamine, remain useful in hypertensive emergencies caused by pheochromocytoma. Used in conjunction with beta-blockade to blunt reflex tachycardia these medications help to control BP until the tumor can be surgically removed. Pharmacology/Mechanism of Action: The alpha blockers block noradrenaline-mediated vasoconstriction by binding to alpha- adrenoceptors located on the vascular smooth muscle. They operate as competitive antagonists to the binding of norepinephrine that is released by sympathetic nerves synapsing on smooth muscle. Alpha blockers are competitive antagonists with the exception of phenoxybenzamine, an irreversible, non- competitive antagonist at the receptor. Vascular smooth muscle has two primary types of alpha-adrenoceptors: alpha1 (α1) and alpha2 (α2). In contrast, only α2-adrenoceptors are found on the sympathetic nerve terminals. Smooth muscle α1 and α2-adrenoceptors are linked to a g-protein, which activates smooth muscle contraction through the IP3 signal transduction pathway. Prejunctional α2-adrenoceptors located on the sympathetic nerve terminals serve as a negative feedback mechanism for norepinephrine release. Toxicity/Side Effects: The most common side effects are related directly to alpha-adrenoceptor blockade and include dizziness, orthostatic hypotension, nasal congestion headache, fluid retention and reflex tachycardia (especially with non-selective alpha-blockers due to blockade of α2-prejunctional adrenoceptors which enhances release of norepinephrine). 198 Hypertension Core Curriculum
Direct Vasodilators There are 2 major direct vasodilators in clinical use today, minoxidil and hydralazine. They each have distinct mechanisms of action and are effective in lowering BP typically as adjunctive therapies. Accordingly, because of side effects and other considerations neither are considered first line in the treatment of uncomplicated hypertension. Hydralazine, along with methyldopa, is a preferred agent for the treatment of hypertension during pregnancy (e.g., for preeclampsia) and as an adjunct antihypertensive in other hypertensive populations. Long-term, high-dose (> 300 mg/day) hydralazine is not used as a primary drug for treating hypertension because it elicits a reflex cardiovascular sympathetic increase in heart rate and cardiac output, and the resulting myocardial oxygen demand can provoke angina pectoris or myocardial infarction. Minoxidil is more potent than hydralazine but has more adverse effects, including sodium and water retention and hypertrichosis. It is used primarily to reduce BP in patients who have been poorly controlled on various multi-drug regimens. Because it tends to increase pulse rate and trigger salt and water retention, minoxidil is typically administered with both a potent diuretic and a β blocker (or non- DHP CCB). Minoxidil is often a therapy of last resort in patients with chronic kidney disease (CKD) who have been unresponsive to other antihypertensive medications. In patients with established CKD, minoxidil can stabilize GFR, if not improve renal function, when BP is properly controlled. Occasionally, the edema with minoxidil can be of sufficient severity to require combination therapy with a loop diuretic and metolazone. Pharmacology: Hydralazine’s mechanism of action has not been comprehensively detailed but appears to have multiple, direct effects on vascular smooth muscle. Hydralazine’s effects are highly specific for arterial vessels and causes smooth muscle hyperpolarization likely by opening K+-channels. It also may inhibit IP3-induced release of calcium from the smooth muscle sarcoplasmic reticulum, which calcium would otherwise combine with calmodulin to activate myosin light chain kinase, which induces contraction. Finally, hydralazine stimulates the formation of nitric oxide by the vascular endothelium, leading to cGMP-mediated vasodilation. Minoxidil is a representative agent of the potassium-channel openers that activate ATP- NKFM & MDCH 199
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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
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
Page 154 and 155: individuals of any race or ethnicit
Page 156 and 157: Older Patients Need Elevated Systol
Page 158 and 159: sister, mother and father. A family
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Page 162 and 163: pulses (lower in the left arm). 4 C
Page 164 and 165: Vital signs suggestive of OSAHS. 20
Page 166 and 167: may shed light on underlying medica
Page 168 and 169: References: patients. 8 However, th
Page 170 and 171: Objectives: 170 Hypertension Core C
Page 172 and 173: and evidence that anti-hypertensive
Page 174 and 175: When subjects are given instruction
Page 176 and 177: interestingly found only a 6.0/4.6
Page 178 and 179: pressure: a meta-analysis of random
Page 180 and 181: isolated systolic hypertension have
Page 182 and 183: Compelling Indications for Specific
Page 184 and 185: 3.) Beta-blockers, ACE inhibitors,
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Page 188 and 189: Preparations and Dosage: Oral antih
Page 190 and 191: Preparations and Dosages: The Oral
Page 192 and 193: patients with tachy-brady syndrome
Page 194 and 195: significant proteinuria. Pharmacolo
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Page 204 and 205: Learning Objectives 204 Hypertensio
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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
Page 232 and 233: 4-Direct vasodilators (e.g.minoxidi
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
Page 240 and 241: trials included a placebo arm. Seve
Page 242 and 243: an indication for careful and modes
Page 244 and 245: ACUTE KIDNEY INJURY (AKI) In additi
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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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