michigan hypertension core curriculum - State of Michigan

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ecause pressure-related retinopathy occurs at incrementally higher BP levels within the so-called normal range, not just when BP crosses an arbitrary threshold of normalcy. 1 Prevalence rates utilizing photography ranged from 2 to 15 percent for various signs of retinopathy compared to 1 to 2 percents in studies utilizing direct opthalmoscopy. A higher prevalence of retinopathy has been reported amongst African Americans than among whites, a difference that can be plausibly attributed to their higher incidence, prevalence, and severity of hypertension as well as their greater coexistence of diabetes. 1 The presence of retinal changes in normotensive patients may be a marker of a pre-hypertensive state. 4 There is a clear association of hypertensive retinopathy with stroke. The ARIC (Atherosclerosis Risk In Community), a multisite cohort study, showed that signs of hypertensive retinopathy of photographs was associated with a risk of newly diagnosed stroke that was 2 - 4 times higher than in patients without retinal findings, even the analyses were controlled for hypertension, smoking and lipid levels. The association of hypertensive retinopathy with coronary heart disease has, however, been less robust. 3 Classification of Hypertensive Retinopathy 16 Grade of Retinopathy Retinal Signs Systemic Associations None No detectable signs None Mild Generalized arteriolar narrowing Modest association with risk of narrowing, arteriovenous nickingclinical stroke, subclinicalstroke, opacity (“copper wiring”) of coronary heart disease and death arteriolar wall, or a combination of these signs Malignant Signs of moderate retinopathy -Strong association with death Plus swelling of the optic disk, Identification of Secondary Causes of Hypertension There are multiple causes of secondary HTN. 8 Listed below are some of the more common etiologies. Please note that the historical and clinical findings suggestive of secondary HTN are neither sensitive nor specific, yet they do significantly inform clinical judgment regarding the likelihood of a given type of secondary HTN and therefore the need to pursue this diagnosis. Historical and Clinical Findings Suggestive of Secondary Hypertension 1,7,8,10 Resistant HTN HTN and unprovoked hyopkalemia or severe ( 18 inches in men] (sleep apnea) Onset of hypertension prior to puberty Abrupt rise in BP over a previously stable lower level Onset prior to age 30 with no obesity or family history of hypertension HTN in a vasculopath (unilateral or bilateral critical renal artery stenosis) Acute elevation of creatinine after initiation of ACE or ARB (bilateral critical renal artery stenosis) Flash pulmonary edema (bilateral critical renal artery stenosis) Azotemia (bilateral critical renal artery stenosis causing ischemic nephropathy) 160 Hypertension Core Curriculum
Premature stroke and/or family history (before 40 years of age), especially hemmorhagic (suspicious for glucocorticoid remedial aldosteronism [GRA]) 1, 7,8,10 Causes of Secondary or Resistant Hypertension Critical unilateral or bilateral renal artery stenosis Renal parenchymal disease Coarctation of the aorta Cushing’s syndrome and glucocorticoid excess states Drug induced and dietary causes Primary aldosteronism Hyperthyroidism Hypothyroidism Hyperparathyroidism Obstructive uropathy Pheochromocytoma Sleep apnea/sleep disordered breathing Renovascular Hypertension and CKD Renal artery stenosis and renovascular hypertension should be suspected in a number of circumstances including: Onset of hypertension before age 30, especially in the absence of family history of hypertension; onset of hypertension after age 55; an abdominal bruit, especially if a diastolic component is present; malignant/accelerated hypertension; hypertension that had been easy to control but is now resistant; recurrent flash pulmonary edema; renal failure of uncertain etiology, especially in the absence of proteinuria or abnormal urinary sediment; acute renal failure after the use of either an ACE or ARB – this is, however, controversial as not all experts concur that ACE’s or ARB’s are important causes renal dysfunction/failure in patients with critical bilateral renal artery stenosis. 4,8 Diagnosis of renal artery stenosis may be suggested by renal artery duplex doppler ultrasound (in patients without significant abdominal girth); critical stenosis of one or both renal arteries can be confirmed by one of several imaging studies such as magnetic resonance angiography (MRA) of the renal artery, or CT renal angiography or the gold standard, renal artery angiography. 8,10 In patients with depressed kidney function in whom you wish to avoid the possibility of contrast-induced nephropathy, carbon dioxide angiography can provide an anatomic assessment of the presence/absence of renal artery obstruction – albeit with lesser quality images than renal arteriography. 8,10 The most common paranchymal kidney diseases associated with hypertension are chronic glomerulonephritis, polycystic kidney disease and hypertensive nephrosclerosis. 10 Coarctation of the aorta Coarctation of the aorta accounts for 5 to 10% of congenital cardiac lesions with boys being affected 1.3 to 2 times the rate of girls. 15 Most cases are sporadic, however, there are some reports of concordance in monozygotic twins. Coarctation of the aorta is observed in 10 to 35% of patients with Turner’s syndrome but infrequently occurs in Down’s syndrome. 15 Obstruction usually occurs distal to the left subclavian artery resulting in equal arms pressures but diminished pulses in the legs. Coarctation rarely occurs before the take off of the left subclavian artery which, if it occurs, results in unequal arm BP and NKFM & MDCH 161
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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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Page 124 and 125: Table 1. Contemporary evaluation of
Page 126 and 127: 2. Screening tests for RAS RDU, MRA
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Page 136 and 137: References: 1. Murphy TP, Soares G,
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
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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 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
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Page 172 and 173: and evidence that anti-hypertensive
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Page 176 and 177: interestingly found only a 6.0/4.6
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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
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Page 208 and 209: 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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