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HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
HTN DM for 3rd Yr Clerkship Family Med
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HTN DM for 3rd Yr Clerkship Family Med

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3 hour seminar for 3rd year family medicine clerkship students

3 hour seminar for 3rd year family medicine clerkship students

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  • 50 million – number of votes each received by Gore and Bush in 2000 election, number of people who downloaded Mozilla Firefox
  • 5 to 10% of patients in the ambulatory primary care setting A: Accuracy – poor technique, white coat hypertension (20% of elevated results) Apnea - OSA Aldosteronism – primary hyperaldo – Increased urinary excretion of potassium signals hyperaldosteronism, which should be suspected in all hypertensive patients with unprovoked (i.e., not diuretic-induced) hypokalemia. B: Bruits – renovascular HTN (bruit is present in half of patients with this type of HTN) due to fibromuscular dysplasia or atherosclerosis Bad Kidneys – renal parenchymal HTN C: Catecholamines – pheochromocytoma, white coat HTN, decongestants, ma huang Coarctation of the Aorta - congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery Cushing’s Syndrome D: Drugs – steroids, OCPs, NSAIDs Diet – high sodium intake, low potassium, calcium, and magnesium intake E: Erythropoetin – caused by hypoxia in COPD or iatrogenic Endocrine Disorders – hypo/hyperthyroid, hyperparathyroid, pheo, acromegaly (elevated GH)
  • DASH Dietary approaches to stop hypertension High (4-5 servings f/v daily, 7-8 servings fiber daily, 2 servings lean meat), Ca, Mg, K Low in saturated fat, cholesterol, salt
  • * vitamin D * combination antioxidant vitamins * vitamin C * vitamin E * potassium * combination of potassium and magnesium * omega-6 fatty acids (olive oil) * dark chocolate * garlic * green coffee bean extract * guava fruit * sour milk (milk fermented with Lactobacillus helveticus, casein hydrosylate) * soy milk (but soy protein supplements had inconsistent results) * Abana * Balsamodendron mukul * grape seed polyphenol (but increased blood pressure when combined with vitamin C) * hawthorn extract * Hibiscus sabdariffa (sour tea) * stevia * L-arginine * coenzyme Q10 * melatonin (but increased blood pressure with concomitant nifedipine)
  • Mr. S. returns to your office six weeks later, as you advised, so you can answer any new questions he might have and so you can follow up on his high blood pressure and assess whether he has been able to adhere to your lifestyle modification recommendations. Mr. S. reports that despite his best efforts his diet still consists of doughnuts and beer. His wife is supportive but his kids do nothing to curb his stress. In addition to already being labeled a deadbeat and a slacker, he is worried about being labeled “hypertensive”. How do you want to spend your time during this visit?
  • People 130/80 to 139/89 are at twice the risk of progressing to hypertension (Vasan RS, Larson MG, Leip EP, et al. Assessment of frequency of progression to hypertension in nonhypertensive participants in The Framingham Heart Study. Lancet. 2001;358:1682-1686)
  • PEDIATRIC HYPERTENSION
  • Epidemiology
  • People 130/80 to 139/89 are at twice the risk of progressing to hypertension (Vasan RS, Larson MG, Leip EP, et al. Assessment of frequency of progression to hypertension in nonhypertensive participants in The Framingham Heart Study. Lancet. 2001;358:1682-1686)
  • PIH
  • Adults With Diagnosed Diabetes in 1990 In 1984, The Centers for Disease Control and Prevention (CDC) established the Behavioral Risk Factor Surveillance System (BRFSS), which was designed to collect state-level data, with a number of states from the outset stratifying their samples to allow them to estimate prevalence for regions within their respective states. CDC developed a standard core questionnaire for states to use so that data could be compared across states. The BRFSS is administered and supported by the Division of Adult and Community Health, National Center for Chronic Disease Prevention and Health Promotion at the CDC, and is an on-going data collection program in which all states, the District of Columbia, and three territories have been participating since 1994. BRFSS data are collected by telephone surveys and designed to monitor state-level prevalence of the major behavioral risks among adults associated with premature morbidity and mortality. The basic philosophy was to collect data on actual behaviors, rather than on attitudes or knowledge, that would be especially useful for planning, initiating, supporting, and evaluating health promotion and disease prevention programs. To determine diabetes status, respondents were asked, “Have you ever been told by a doctor that you have diabetes?” Classification of diabetes was not assessed. Participants with a BMI  30 were classified as obese. BMI data were derived from self-reported weight and height information. In 1990, there were 81,855 BRFSS participants. Of them, 11.1% were obese. Diabetes prevalence was 4.9%. States with the highest diabetes prevalence were Mississippi (6.9%), Missouri (6.4%), South Carolina (6.3%), and West Virginia (7.5%). States with the lowest prevalence were Colorado (3.1%), Idaho (3.2%), Minnesota (3.2%), Montana (2.8%), and Vermont (3.4%). References: Mokdad AH, Ford ES, Bowman BA, Nelson DE, Engelgau MM, Vinicor F, Marks JS. Diabetes trends in the U.S.: 1990-1998. Diabetes Care. 2000;23(9):1278-1283. Centers for Disease Control and Prevention (CDC). Behavioral Risk Factor Surveillance System Survey Data. Atlanta, Georgia: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 1990.
  • Adults With Diagnosed Diabetes in 2000 In 1984, The Centers for Disease Control and Prevention (CDC) established the Behavioral Risk Factor Surveillance System (BRFSS), which was designed to collect state-level data, with a number of states from the outset stratifying their samples to allow them to estimate prevalence for regions within their respective states. CDC developed a standard core questionnaire for states to use so that data that could be compared across states. The BRFSS is administered and supported by the Division of Adult and Community Health, National Center for Chronic Disease Prevention and Health Promotion at the CDC, and is an on-going data collection program in which all states, the District of Columbia, and three territories have been participating since 1994. BRFSS data are collected by telephone surveys and designed to monitor state-level prevalence of the major behavioral risks among adults associated with premature morbidity and mortality. The basic philosophy was to collect data on actual behaviors, rather than on attitudes or knowledge, that would be especially useful for planning, initiating, supporting, and evaluating health promotion and disease prevention programs. To determine diabetes status, respondents were asked, “Have you ever been told by a doctor that you have diabetes?” Classification of diabetes was not assessed. Participants with a BMI  30 were classified as obese. BMI data were derived from self-reported weight and height information. In 2000, there were 184,450 BRFSS participants from 50 states. By 2000, obesity and diabetes prevalence had increased to 19.8% and 7.3%, respectively. The prevalence of diabetes and obesity combined was 2.9%. States with the highest diabetes prevalence were Alabama (8.0%), California (8.4%), Maryland (8.0%), Mississippi (8.8%), and South Carolina (8.5%). Several of these states had an obesity prevalence of  22.0%, including Alabama (23.5%) and Mississippi (24.3%), in addition to Arkansas (22.6%), Kentucky (22.3%), Louisiana (22.8%), Tennessee (22.7%), Texas (22.7%), and West Virginia (22.8%). The lowest rate of diabetes was in Alaska (4.4%); the lowest rate of obesity was in Colorado (13.8%). References: Mokdad AH, Bowman BA, Ford ES, Vinicor F, Marks JS, Koplan JP. The continuing epidemics of obesity and diabetes in the United States. JAMA. 2001;286(10):1195-1200. Centers for Disease Control and Prevention (CDC). Behavioral Risk Factor Surveillance System Survey Data. Atlanta, Georgia: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 2000.
  • UKPDS Outcomes by Treatment Group for Patients Randomized to Tight Blood Pressure Control In the UK Prospective Diabetes Study (UKPDS), a total of 1,148 patients aged 25 to 65, with newly diagnosed diabetes, were randomized to a tight blood pressure control group [(n=758) goal of <150/85 mmHg] or a less tight control group [(n=390) goal of <180/105 mmHg]. Of the 758 patients in the tight control group, 400 were randomized to receive the ACE inhibitor, captopril, as initial therapy, and 358 to receive the beta-blocker, atenolol, as initial therapy. Primary outcomes, including any diabetes-related endpoint (myocardial infarction, heart failure, angina, sudden death, stroke, amputation, retinal photocoagulation, renal failure, vitreous hemorrhage), death-related to diabetes, and death from all causes, as well as secondary outcomes that included myocardial infarction, stroke, amputation or death from peripheral vascular disease, and microvascular complications, were compared in patients randomized to each therapeutic group. Captopril and atenolol were equally effective in reducing blood pressure to a mean of 144/83 mmHg and 143/81 mmHg, respectively, over a median of 8.4 years of follow-up. There were no significant differences in either the primary or secondary outcomes when the captopril-treated and atenolol-treated groups were compared. Reference: Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. UK Prospective Diabetes Study Group. BMJ. 1998;317(7160):713-720.
  • Mrs. S is SYMPTOMATIC (and so you are no longer screening)
  • What do you order?
  • TREATMENT
  • Oral hypoglycemic agents have limited effectiveness when plasma glucose is very high (i.e., >300)
  • Oral hypoglycemic agents have limited effectiveness when plasma glucose is very high (i.e., >300)
  • STARTING INSULIN
  • DKA case You’ve started Mrs. S on insulin, NPH 10 units subcutaneously at bedtime.
  • Transcript

    • 1. Hypertension & Diabetes: A Family-Centered Approach Third-Year Clerkship in Family Medicine Michael Mendoza, MD, MPH Clinical Assistant Professor Department of Family Medicine Pritzker School of Medicine The University of Chicago
    • 2. OBJECTIVES <ul><li>Briefly review the public health and epidemiological significance of hypertension and diabetes. </li></ul><ul><li>Use clinical examples to illustrate relevant pathophysiology and approach to outpatient adults, children and pregnant women with elevated blood pressure and diabetes. </li></ul><ul><li>Summarize important treatments, including medications, to treat both hypertension and diabetes. </li></ul><ul><li>Emphasize the benefit of continuity of care in the management of patients with hypertension and diabetes, including psychosocial and systems-based principles of care. </li></ul>
    • 3. Hypertension <ul><li>Prevalence: 50,000,000 (US); 1,000,000,000 (Worldwide) </li></ul><ul><li>One in three U.S. adults has high blood pressure. </li></ul><ul><li>Thirty percent of people with high blood pressure don't know they have it. </li></ul><ul><li>Direct cost to US health system is $12 billion dollars </li></ul>
    • 4. Pathophysiology of Hypertension <ul><li>Essential (or primary) hypertension – generally not well understood </li></ul><ul><ul><li>Impaired renal salt excretion leading to secretion of natriuretic factors which raise total peripheral resistance </li></ul></ul><ul><ul><li>Overactivity of the renin/angiotensin system which leads to vasoconstriction and sodium and water retention </li></ul></ul><ul><ul><li>Overactivity of the sympathetic nervous system </li></ul></ul><ul><li>Secondary Hypertension – generally very well understood </li></ul><ul><li>Progression to congestive heart failure, hypertensive nephropathy, retinopathy, vascular disease </li></ul>
    • 5. JAMA.  2003;289:2560-2571
    • 6. Clinical Case <ul><li>Mr. S is a 38 year old gentleman. Although he has had obesity for many years, he has never had a regular doctor. The father of three, Mr. S leads a sedentary lifestyle. Although he is employed as a safety officer at the local power plant, he spends much of his day eating doughnuts and other foods high in cholesterol and simple sugars. He presents to your clinic to establish primary care. He denies tobacco use but admits to “occasional” alcohol use. His exam is notable for a BMI of 34 and a blood pressure of 138/88. He is concerned because his neighbor is a health nut and told him he has hypertension. </li></ul><ul><li>What is your assessment? How do you proceed with managing Mr. S’ condition? </li></ul>
    • 7. Secondary Hypertension <ul><li>A: </li></ul><ul><ul><li>Accuracy </li></ul></ul><ul><ul><li>Apnea (OSA) </li></ul></ul><ul><ul><li>Aldosteronism (1° hyperaldo) </li></ul></ul><ul><li>B: </li></ul><ul><ul><li>Bruits (atherosclerosis, FMD) </li></ul></ul><ul><ul><li>Bad Kidneys </li></ul></ul><ul><li>C: </li></ul><ul><ul><li>Coarctation of the aorta </li></ul></ul><ul><ul><li>Catecholamines (pheo, whitecoat, decongestants, ma huang, cocaine) </li></ul></ul><ul><ul><li>Cushing’s Syndrome </li></ul></ul><ul><li>D: </li></ul><ul><ul><li>Drugs (OCPs, steroids, NSAIDs) </li></ul></ul><ul><ul><li>Diet </li></ul></ul><ul><li>E: </li></ul><ul><ul><li>Erythropoetin </li></ul></ul><ul><ul><li>Endocrine Disorders </li></ul></ul>
    • 8. Benefits of Lifestyle Modification <ul><li>A 5 mmHg reduction in SBP has been associated with </li></ul><ul><ul><li>a 15% reduction in mortality from stroke </li></ul></ul><ul><ul><li>a 9% reduction in mortality from heart disease </li></ul></ul><ul><ul><li>a 7% reduction in all-cause mortality </li></ul></ul><ul><li>A 10 lb weight loss can reduce or prevent hypertension </li></ul>
    • 9. Benefits of Lifestyle Modification *Strength of recommendation=C, good evidence, but not clinical trials documenting morbidity or mortality benefit Associated Reduction in SBP Nonpharmacologic Intervention*  2 to 4 mmHg Limit daily alcohol consumption (<2 for men, <1 for women)  4 to 9 mmHg Exercise 30 minutes aerobic at least four days per week  2 to 8 mmHg Low sodium diet, < 2.4g Na / day  8 to 14 mmHg “ DASH” diet high in fruits, veggies and low in fat  5 to 20 mmHg Weight loss (BMI < 25)
    • 10. Alternative Treatments <ul><li>Yoga, Tai Chi </li></ul><ul><li>Relaxation (e.g., 15-minutes slow breathing daily for 8 weeks) </li></ul><ul><li>Herbal therapies (e.g., Rauwolfia serpentina [snakeroot], Stephania tetrandra [tetrandrine], Panax notoginseng [ginseng], and Crataegus species [hawthorn]) </li></ul><ul><ul><li>AVOID licorice, ephedra (Ma Huang) and yohimbine (from the bark of a West African tree) </li></ul></ul><ul><li>Supplements coenzyme Q10 (CoQ10), omega-3 fatty acids, and two amino acids: L-arginine and L-taurine. </li></ul>
    • 11. Clinical Case (cont’d) <ul><li>Mr. S returns to your office six weeks later, as you advised, so you can follow up on his high blood pressure. As you assess whether he has been able to adhere to your lifestyle modification recommendations, you discover that his diet still consists of doughnuts and beer. His wife is supportive but his kids do nothing to curb his stress. He is worried about being labeled “hypertensive”. His blood pressure is 134/85. </li></ul><ul><li>How would you address your patient’s worry about being labeled as hypertensive? </li></ul>
    • 12. Classification of Hypertension > 100 or > 160 Hypertension, Stage 2 90 – 99 or 140 – 159 Hypertension, Stage 1 80 – 89 or 120 – 139 Pre-hypertension <80 and <120 Normal DBP (mmHg) SBP (mmHg)
    • 13. Diagnosis of Hypertension <ul><li>Equipment </li></ul><ul><ul><li>Mercury or calibrated aneroid sphygmomanometer </li></ul></ul><ul><ul><li>Cuff should encircle 80% of arm. </li></ul></ul><ul><ul><li>Small cuff OVERESTIMATES BP by 10-15 mmHg </li></ul></ul><ul><li>Patient </li></ul><ul><ul><li>Relaxed and seated for five minutes. </li></ul></ul><ul><ul><li>Avoid tobacco, caffeine, full bladder. </li></ul></ul><ul><ul><li>Bare arm </li></ul></ul><ul><li>Technique </li></ul><ul><ul><li>Single reading SBP>200 and/or DBP>120 </li></ul></ul><ul><ul><li>Otherwise, take average of three readings over six weeks </li></ul></ul>
    • 14. Initial Diagnostic Workup <ul><li>History and Physical </li></ul><ul><ul><li>Age, malignant course, lack of response to therapy </li></ul></ul><ul><ul><li>Chest pain, orthopnea, claudication, DM, smoking, FH CAD </li></ul></ul><ul><ul><li>HR, BMI, cardiac size, rhythm, S3, JVD, pulses, renal arteries </li></ul></ul><ul><li>Laboratory tests (not all at once!) include </li></ul><ul><ul><li>Urinalysis (proteinuria, hematuria) </li></ul></ul><ul><ul><li>Electrolytes (BUN/Cr, R/O hyperaldo) </li></ul></ul><ul><ul><li>Urine albumin to creatinine ratio </li></ul></ul><ul><ul><li>Electrocardiogram (LVH, conduction) </li></ul></ul><ul><ul><li>Echocardiogram (structural or valvular heart disease) </li></ul></ul><ul><ul><li>Fasting blood glucose level </li></ul></ul><ul><ul><li>Screening fasting lipid panel </li></ul></ul>
    • 15. Rationale for Initiating Treatment <ul><li>How do you decide what is an appropriate endpoint of therapy? </li></ul><ul><ul><li>Presence of comorbid risk factors (dysrhythmia, lipids, DM) </li></ul></ul><ul><ul><li>Projected life expectancy </li></ul></ul><ul><ul><li>Potential benefit and risk of treatment </li></ul></ul><ul><ul><li>Patient’s attitudes, values, and preferences </li></ul></ul><ul><ul><li>Risk of delaying treatment </li></ul></ul><ul><li>Diagnosis and treatment of hypertension is a series of evidence-based clinical judgments that reflect the patient’s unique circumstances </li></ul>
    • 16. Choice of Initial Medication Thiazide + ACE or ARB Yes 160/100 Hypertension, Stage 2 Thiazide Monotherapy Yes 140 / 90 Hypertension, Stage 1 None Yes 120 / 80 Pre-hypertension None Encourage <120/80 Normal Initial Medication (no compelling indications) Lifestyle Modification BP (mmHg)
    • 17. Compelling Indications + + CCB + + + + Recurrent stroke prevention + + + + + CKD + + + + + + + + + DM + + + High CAD Risk + + ++ + + + + + + + Post-MI + + + + + + + + + + + + CHF Aldo Antagonist ARB ACE-I B-blocker Thiazide
    • 18. Preparation for Antihypertensive Tx <ul><li>Know your patient </li></ul><ul><li>Education about side effects </li></ul><ul><ul><li>Remind the patient that he may not necessarily feel better. </li></ul></ul><ul><ul><li>In fact he may feel somewhat worse initially. </li></ul></ul><ul><li>Allow room for mistakes </li></ul><ul><li>Emphasize why treatment is important </li></ul><ul><li>Ambulatory self-monitoring </li></ul>
    • 19. Clinical Case (cont’d) <ul><li>Four weeks later, you notice that Mr. S has missed his appointment with you. You instruct your medical assistant to call him and remind him to reschedule his appointment. </li></ul><ul><li>Later that day, Mr. S presents to your clinic as a walk-in patient. He appears more disheveled than usual. He denies any new symptoms, except for a mild diffuse headache. In addition, you notice that Mr. S is not his usual self. On further questioning, you discover that he was fired from his job. His medication bottle is full despite having been dispensed over a month ago. His blood pressure is 220/120. </li></ul><ul><li>How do you proceed? </li></ul>
    • 20. Evaluation for HTN Emergency <ul><li>Focused history, think about “end-organs” </li></ul><ul><li>Focused physical exam including focused neurological exam </li></ul><ul><li>Review medication list and medication adherence </li></ul><ul><li>Screen for illicit substance use </li></ul><ul><li>Urinalysis </li></ul><ul><li>Urine pregnancy test if appropriate </li></ul>
    • 21. HTN Emergency vs. HTN Urgency <ul><li>Elevated blood pressure associated with evidence of end-organ damage </li></ul><ul><ul><li>Brain (SAH, intracerebral hemorrhage, encephalopathy) </li></ul></ul><ul><ul><li>Eyes (blindness, retinal hemorrhage, papilledema) </li></ul></ul><ul><ul><li>Heart (myocardial ischemia or infarction) </li></ul></ul><ul><ul><li>Lungs (acute pulmonary edema) </li></ul></ul><ul><ul><li>Kidneys (acute renal failure) </li></ul></ul><ul><ul><li>Aortic dissection </li></ul></ul><ul><li>Hypertensive URGENCY is asymptomatic (except perhaps headache) elevation of blood pressure </li></ul>
    • 22. Management <ul><li>Admit to the hospital vs. careful outpatient management </li></ul><ul><ul><li>Hypertensive emergency requires careful and expeditious blood pressure lowering </li></ul></ul><ul><ul><li>Hypertensive urgency can be managed on outpatient basis but only with appropriate monitoring, medications and with very careful attention to patient adherence and follow-up. </li></ul></ul><ul><ul><li>Rapid blood pressure has no proven benefit and can lead to end organ hypoperfusion and worse outcomes </li></ul></ul><ul><li>Explore reasons for treatment failure </li></ul>
    • 23. Clinical Case (cont’d) <ul><li>The following day Mr. S’s son, B.S., presents to your clinic with his mother because he wants to try out for his school’s badminton team. B.S. is a troublemaker at school. Like his father, he is also quite sedentary with a BMI of 18.3 which is 85th percentile for his age of 8. His blood pressure is 120/80. Apart from a crude sense of humor, physical exam is notable for a III/VI murmur that is worse with Valsalva. </li></ul><ul><li>Do you give B.S. clearance to participate in interscholastic sports and physical education? </li></ul>
    • 24. HOCM
    • 25. Hypertension in Children 75 +/- 15 120 +/- 20 >12 yr 68 +/- 15 112 +/- 20 10-12 yr 65 +/- 15 100 +/- 20 6-9 yr 65 +/- 20 99 +/- 20 4-5 yr 64 +/- 25 99 +/- 25 2-3 yr 66 +/- 25 96 +/- 30 1 yr 60 +/- 10 89 +/- 29 6 month 46 +/- 16 80 +/- 16 1 month 37 +/- 8 60 +/- 10 Newborn DBP SBP Age
    • 26. Classification of Pediatric HTN SBP or DBP greater than or equal to 95th percentile Hypertension SBP or DBP greater than 99th percentile plus 5 mm Hg Hypertension, Stage 2 SBP or DBP from 95th percentile to 99th percentile plus 5 mm Hg Hypertension, Stage 1 SBP or DBP greater than or equal to 90th percentile but less than 95th percentile. Blood pressure levels greater than or equal to 120/80 mm Hg for adolescents. Pre-hypertension SBP and DBP less than the 90th percentile Normal
    • 27.  
    • 28. Secondary vs. Essential HTN <ul><li>Secondary HTN is far more common in kids. Essential hypertension is a diagnosis of exclusion if < 10 years old </li></ul><ul><li>Renal parenchymal disease comprises 60 – 70% of pediatric patients with hypertension </li></ul><ul><li>Essential hypertension </li></ul><ul><li>Iatrogenic illness </li></ul><ul><li>Renal parenchymal disease </li></ul><ul><li>Renal vascular disease </li></ul><ul><li>Endocrine causes </li></ul><ul><li>Coarctation of the aorta </li></ul><ul><li>Renal parenchymal disease </li></ul><ul><li>Essential hypertension </li></ul><ul><li>Renal vascular disease </li></ul><ul><li>Endocrine causes </li></ul><ul><li>Coarctation of the aorta </li></ul><ul><li>Iatrogenic illness </li></ul><ul><li>Renal parenchymal disease </li></ul><ul><li>Renal vascular disease </li></ul><ul><li>Endocrine causes </li></ul><ul><li>Coarctation of the aorta </li></ul><ul><li>Essential hypertension </li></ul>12 – 18 years 6 – 12 years 1 – 6 years
    • 29. Diagnostic Workup and Treatment <ul><li>Diagnosis </li></ul><ul><ul><li>Be wary of labeling the child </li></ul></ul><ul><ul><li>CBC, BMP, UA, urine tox, renal ultrasound. Consider echo, sleep study, dilated funduscopic exam. Others as indicated. </li></ul></ul><ul><ul><li>Workup is similar to that of adults, but with greater attention to renal parenchymal and renovascular etiologies. </li></ul></ul><ul><li>Treatment </li></ul><ul><ul><li>Lifestyle changes (Prehypertension and Stage 1 HTN) </li></ul></ul><ul><ul><li>Pharmacotherapy </li></ul></ul><ul><ul><ul><li>ACE, ARB, B-blocker, CCB, thiazide diuretic </li></ul></ul></ul><ul><ul><ul><li>Be aware of side effects in young active children </li></ul></ul></ul>
    • 30. Clinical Case <ul><li>Things just got worse for B.S. and his father, Mr. S. Mrs. S comes to visit you because her last menstrual period was about 5 months ago. You diagnose pregnancy at 20 weeks gestational age. Although you find it curious that she has waited until now to come to see you, as her family physician you avoid passing judgment. You order prenatal labs and make plans to deliver her baby. </li></ul><ul><li>You notice on this visit that her blood pressure is 140/80. Prior to her pregnancy, her blood pressure has always been somewhat elevated, but never this high. Because she is pregnant you wonder whether she has chronic hypertension or gestational hypertension. Urinalysis is negative for proteinuria. </li></ul>
    • 31. Hypertension in Pregnancy <ul><li>Hard to diagnose, physiologic decrease in BP during pregnancy </li></ul><ul><li>Chronic pre-pregnancy hypertension </li></ul><ul><ul><li>high blood pressure documented before conception, before 20w gestation or that persists 6 weeks postpartum) </li></ul></ul><ul><li>Preeclampsia / Eclampsia </li></ul><ul><ul><li>a syndrome uniquely of pregnancy characterized by hypertension and proteinuria, possibly edema </li></ul></ul><ul><li>Chronic hypertension with superimposed pre-eclampsia </li></ul><ul><li>Gestational hypertension or PIH </li></ul><ul><ul><li>non preeclamptic elevation of blood pressure after 20 weeks gestation that usually resolves by postpartum week 12) </li></ul></ul>
    • 32. Preeclampsia / Eclampsia <ul><li>Preeclampsia (6%) </li></ul><ul><ul><li>Risk factors are nulliparity, African-American, maternal age < 20 or > 35, low SES, multiple gestation, polyhydramnios, obesity, diabetes, chronic hypertension </li></ul></ul><ul><ul><li>Severe: SBP>160 or DBP>110 on 2 occasions 6 hrs apart, proteinuria >2g in 24hr or 2-4% on dipstick, Cr>1.2, oliguria, visual disturbances, liver enzymes, thrombocytopenia… </li></ul></ul><ul><ul><li>Mild: everything else </li></ul></ul><ul><ul><li>THE CAUSE IS UNKNOWN </li></ul></ul><ul><li>Eclampsia (0.2-0.5%) </li></ul><ul><ul><li>Rule of Thirds </li></ul></ul>
    • 33.  
    • 34. Management of HTN in Pregnancy <ul><li>Prepregnancy counseling and risk stratification </li></ul><ul><ul><li>Assess for target organ damage which can progress in pregnancy (renal disease, LVH, retinopathy) </li></ul></ul><ul><li>May withhold antihypertensive medication in patients provided that SBP < 150 and DBP < 100. </li></ul><ul><li>Avoid ACE and ARB medications </li></ul><ul><li>Methyldopa preferred for its long track record in pregnancy </li></ul><ul><li>Proteinuria screening, watch for preeclampsia </li></ul>
    • 35. BREAK
    • 36. Diabetes Mellitus <ul><li>Prevalence of 17 million in US alone, the majority of which are Type 2. Total cost to US health care system is $100 billion </li></ul><ul><li>Type 1 diabetes (formerly known as IDDM or JDM) is caused by autoimmune destruction of pancreatic beta cells. There is an absolute insulin deficiency. </li></ul><ul><li>Type 2 diabetes (NIDDM or AODM) is encompasses a heterogeneous spectrum of hyperglycemic conditions. There is insulin resistance and relative insulin deficiency. </li></ul><ul><li>Gestational diabetes is glucose intolerance detected during pregnancy. </li></ul><ul><li>90% of patients with diabetes are managed in the primary care setting . </li></ul>
    • 37. Adults With Diagnosed Diabetes* *Includes women with a history of gestational diabetes. 1990 No data available Less than 4% 4%-6% Above 6% www.hypertensiononline.org Mokdad AH, et al. Diabetes Care. 2000;23(9):1278-1283 .
    • 38. Adults With Diagnosed Diabetes* 2000 www.hypertensiononline.org 4%-6% Above 6% *Includes women with a history of gestational diabetes. Mokdad AH, et al. JAMA. 2001;286(10):1195-1200.
    • 39. Pathophysiology of Diabetes <ul><li>A heterogeneous spectrum of disorders resulting from the combination of environmental and host factors </li></ul><ul><li>DM, Type 1 </li></ul><ul><ul><li>Immune mediated Beta-cell destruction </li></ul></ul><ul><li>DM, Type 2 </li></ul><ul><ul><li>Beta-cell dysfunction impairs insulin secretion (MODY) </li></ul></ul><ul><ul><li>Mutations of insulin receptors (peripheral resistance) </li></ul></ul><ul><li>Obesity, diet, physical inactivity </li></ul><ul><li>Trauma, pancreatitis, infection, pancreatic cancer </li></ul><ul><li>Mean reduction in life expectancy with diabetes mellitus in persons ≥ 50 years old </li></ul><ul><ul><li>7.5 years in men, 8.2 years in women </li></ul></ul>
    • 40. Native Beta Cell Dysfunction
    • 41. Landmark Diabetes Studies <ul><li>Diabetes Control and Complications Trial (DCCT) - 1993 </li></ul><ul><ul><li>Enrolled 1441 patients with type 1 diabetes </li></ul></ul><ul><ul><li>Showed that keeping blood glucose levels as close to normal as possible slows the onset and progression of eye, kidney, and nerve diseases caused by diabetes. </li></ul></ul>
    • 42. Retinopathy Nephropathy
    • 43. Landmark Diabetes Studies <ul><li>United Kingdom Prospective Diabetes Study (UKPDS) - 1998 </li></ul><ul><ul><li>Randomized clinical trial of over 5,102 patients with type 2 diabetes over 20 years in 23 clinical centers based in England, Northern Ireland and Scotland. </li></ul></ul><ul><ul><li>Showed that lowering elevated blood glucose and blood pressure levels, reduces the risk of heart disease, stroke and death from diabetes-related diseases as well as diabetic eye disease and early kidney damage </li></ul></ul><ul><ul><li>Provided conclusive evidence for the rationale for treating diabetes and hypertension in diabetes </li></ul></ul>
    • 44. UKPDS Outcomes by Treatment Group for Patients Randomized to Tight Blood Pressure Control* *The differences between the treatment groups were not statistically significant † For captopril compared to atenolol 1.29 (0.80-2.10) 28 40 Microvascular complications 1.48 (0.35-6.19) 3 5 Peripheral vascular disease 1.12 (0.59-2.12) 17 21 Stroke 1.20 (0.82-1.76) 46 61 Myocardial infarction 1.14 (0.81-1.61) 59 75 All-cause mortality 1.27 (0.82-1.97) 34 48 Diabetes-related death 1.10 (0.86-1.41) Relative Risk † (95% CI) 118 Atenolol (n=358) 141 Captopril (n=400) Any DM-related endpoint
    • 45. Clinical Case (cont’d) <ul><li>Mrs. S, a G3P2 continues to suffer from pregnancy-induced hypertension. She is now in her 26 th week of gestation and presents for her routine prenatal appointment. She has no new complaints. She feels her baby moving but is thankful that she has not yet begun to feel or look “pregnant”. </li></ul><ul><li>Her exam is unremarkable with a uterine fundal height of 27 cm from the pubic symphysis. You doppler her fetal heart tones which are 140 with normal variability. </li></ul><ul><li>Her screening exams are notable for an abnormal one hour glucose challenge test of 150. What is the next most appropriate course of action? </li></ul>
    • 46. Gestational Diabetes Mellitus (GDM) <ul><li>Whom do you screen? </li></ul><ul><ul><li>ADA: </li></ul></ul><ul><ul><ul><li>Age greater than 25 years </li></ul></ul></ul><ul><ul><ul><li>Above average weight before pregnancy </li></ul></ul></ul><ul><ul><ul><li>Members of an ethnic group with a higher prevalence of GDM (e.g., Hispanic, African, Native American, South or East Asian, Pacific Islander) </li></ul></ul></ul><ul><ul><ul><li>First degree relative with diabetes mellitus </li></ul></ul></ul><ul><ul><ul><li>History of abnormal glucose tolerance </li></ul></ul></ul><ul><ul><ul><li>History of poor obstetric outcome </li></ul></ul></ul><ul><ul><li>ACOG: </li></ul></ul><ul><ul><ul><li>All pregnant women (more practical) </li></ul></ul></ul>
    • 47. Screening and Diagnosis of GDM <ul><li>Screening </li></ul><ul><ul><li>Widely practiced by obstetricians and family physicians despite lack of evidence for improvement in perinatal outcomes </li></ul></ul><ul><ul><li>24 to 28 weeks gestation, earlier if high risk </li></ul></ul><ul><ul><li>50g oral glucose challenge test (“glucola” or “1-hr GLT”) </li></ul></ul><ul><ul><li>Plasma glucose > 130 is a positive screen </li></ul></ul><ul><li>Diagnosis </li></ul><ul><ul><li>100g glucose tolerance test (“GTT”) </li></ul></ul><ul><ul><ul><li>Fasting > 95, 1 hr > 180, 2 hr > 155, 3 hr>140 </li></ul></ul></ul><ul><ul><ul><li>Screen is positive if two or more of the four criteria are met </li></ul></ul></ul>
    • 48. Significance of GDM <ul><li>Prenatal </li></ul><ul><ul><li>Polyhydramnios a possible risk for preterm labor, preeclampsia </li></ul></ul><ul><li>Intrapartum </li></ul><ul><ul><li>Preeclampsia </li></ul></ul><ul><ul><li>Birth trauma from macrosomia (mom and baby) </li></ul></ul><ul><ul><li>Operative delivery </li></ul></ul><ul><li>Neonatal </li></ul><ul><ul><li>Hypoglycemia, hyperbilirubinemia, polycythemia </li></ul></ul><ul><ul><li>Obesity and hyperactivity (later) </li></ul></ul><ul><li>Postpartum </li></ul><ul><ul><li>Maternal progression to diabetes </li></ul></ul>
    • 49. Management of GDM <ul><li>Goal fasting capillary glucose less than 140. </li></ul><ul><li>Dietary and lifestyle modifications for all patients. </li></ul><ul><li>Insulin therapy for those not at target. </li></ul><ul><li>Antenatal testing (NST and AFI) is recommended beginning at 32 weeks </li></ul>
    • 50. Clinical Case (cont’d) <ul><li>It is now seven years since you delivered Mrs. S’s baby daughter, Maggie. Mrs. S has since returned to her job at a local convenience store but, unfortunately Mrs. S’s husband is still not gainfully employed and the family has now lost health insurance. Because you work at a federally qualified health center, you are able to see Mrs. S regardless of her ability to pay. </li></ul><ul><li>She presents to re-establish primary care. Today she reports a two week history of vaginal discharge. She denies fever, abdominal pain or new sexual partners. She reports having had frequent UTIs diagnosed by multiple providers, but on further history it appears that none of these “UTIs” was properly confirmed by culture. </li></ul><ul><li>What is the next most appropriate course of action? </li></ul>
    • 51. Screening for Diabetes <ul><li>How to screen? </li></ul><ul><ul><li>Fasting plasma glucose > 126 (usually confirmed by repeat test) </li></ul></ul><ul><li>Whom do you screen? </li></ul><ul><ul><li>Consider for >45 years and above, particularly if BMI > 25. Intervals of 3 years </li></ul></ul><ul><ul><li>Consider for younger patients and/or at shorter frequency if at higher risk </li></ul></ul><ul><ul><ul><li>First-degree relative with DM, physical inactivity, known h/o HTN, high cholesterol </li></ul></ul></ul><ul><ul><ul><li>High risk ethnic group (African-American, Latino, Native American, Pacific Islander) </li></ul></ul></ul><ul><ul><ul><li>History of GDM or history of macrosomic infant </li></ul></ul></ul>
    • 52. Diagnosis of Diabetes <ul><li>Screening of asymptomatic individuals (very common) </li></ul><ul><li>Signs and symptoms </li></ul><ul><ul><li>Fatigue, excessive thirst, frequent urination, unexplained weight loss, blurred vision, acanthosis nigricans </li></ul></ul><ul><ul><li>Recurrent fungal infections, poor wound healing </li></ul></ul><ul><ul><li>Periodontal disease </li></ul></ul><ul><ul><li>Nonspecific peripheral neuropathy </li></ul></ul><ul><ul><li>Diabetic ketoacidosis (not just Type 1 anymore) or HHS </li></ul></ul><ul><li>Diagnostic Criteria </li></ul><ul><ul><li>Fasting plasma glucose > 126 </li></ul></ul><ul><ul><li>Random plasma glucose > 200 with classic symptoms </li></ul></ul><ul><ul><li>Plasma glucose > 200 at 2 hours after 75g oral glucose load </li></ul></ul>
    • 53. Clinical Case (cont’d) <ul><li>A random plasma glucose is 345. You are almost certain this is diabetes and you counsel Mrs. S appropriately about this possibility. In anticipation of your treatment, you send a battery of lab tests and provide essential health care maintenance services. </li></ul><ul><li>What counseling do you offer to Mrs. S today? What labs and services are appropriate for Mrs. S? </li></ul>
    • 54. Rationale for Management in DM <ul><li>A chronic illness characterized by periods of good control punctuated by periods of exacerbation </li></ul><ul><li>Education, education, education! </li></ul><ul><li>Treatment is almost always NOT urgent </li></ul><ul><li>Multi-modal treatment (behavioral, medication, psychosocial, family systems, alternative therapies) </li></ul><ul><li>Frequent visits initially </li></ul><ul><li>Diabetes self-management is the goal of therapy </li></ul>
    • 55. Goals for Glycemic Control (ADA) <180 Postprandial <8 <7 <6 HbA1c (%) <110 / >180 110 – 150 <120 Bedtime <90 / >150 90 – 130 <110 Preprandial Plasma (venipuncture) <100 / >160 100 – 140 <110 Bedtime <80 / >140 80 – 120 <100 Preprandial Whole blood (“finger stick”) Add’l Action Suggested Goal Normal
    • 56. Initial Evaluation <ul><li>Physical Examination </li></ul><ul><ul><li>Height and weight (BMI) </li></ul></ul><ul><ul><li>Blood pressure </li></ul></ul><ul><ul><li>Ophthalmologic exam or referral </li></ul></ul><ul><ul><li>Foot exam or referral </li></ul></ul><ul><ul><li>Proprioception, touch and vibratory sensation </li></ul></ul><ul><li>Laboratory Evaluation </li></ul><ul><ul><li>Basic metabolic panel (creatinine) </li></ul></ul><ul><ul><li>Hemoglobin A1c (three month average) </li></ul></ul><ul><ul><li>Urinalysis (protein, ketones) </li></ul></ul><ul><ul><li>Liver function tests </li></ul></ul><ul><ul><li>Fasting lipid panel </li></ul></ul><ul><ul><li>Consider Hepatitis B Serology </li></ul></ul>
    • 57. Health Care Maintenance in DM < 130/80 Every visit Blood Pressure Vaccinate very five years Pneumococcal Vaccinate annually Influenza Prevention or identification of neuropathy, infection Baseline then annually Foot Examination Prevention or identification of diabetic retinopathy Baseline, annual if at target glycemic control, quarterly if not Ophthalmologic LDL < 100 (? < 70) Baseline, q3mo until normal, then q6mo Lipids < 6% usually (must tailor to patient) Baseline, q3mo until normal, then q6mo HbA1c Goal Frequency
    • 58. Hemoglobin A1c <ul><li>Every 1% reduction in HgA1c results in: </li></ul><ul><ul><li>21% reduction in any diabetes-related end point </li></ul></ul><ul><ul><li>14% decrease in risk of myocardial infarction </li></ul></ul><ul><ul><li>12% decrease in risk of stroke </li></ul></ul><ul><ul><li>37% decrease in risk of microvascular disease </li></ul></ul>16* 41* Macrovascular Disease 60 Neuropathy 24-33 54 Nephropathy 17-21 63% Retinopathy 8 --> 7 9 --> 7 A1c reduction UKPDS DCCT
    • 59. Clinical Case (cont’d) <ul><li>Mrs. S. returns to see you for the first time since you made the diagnosis of diabetes. She has many questions which you spend time answering. One of these questions is “Do I need to take medication?”. In addition to reminding her that the cornerstone of diabetic treatment is diet self-monitoring and a regular exercise program, you begin to discuss with her possibilities for treatment with medication. </li></ul><ul><li>In addition to recommending a pneumococcal vaccination and an appointment to visit the ophthalmologist, how do you proceed with regard to treatment for Mrs. S? </li></ul>
    • 60. Diet and Exercise in Diabetes <ul><li>Improved nutrition, increased physical activity and weight loss improve peripheral glucose uptake, decrease postprandial hyperglycemia and inhibit hepatic gluconeogenesis. </li></ul><ul><li>Even a five kilogram weigh loss can improve insulin resistance. Some benefit is realized even without weight loss. </li></ul>
    • 61. Pharmacologic Treatment of DM <ul><li>Blood pressure control!!! </li></ul><ul><li>Lipid control </li></ul><ul><li>Lifestyle modifications (1-2% decrease in A1c) </li></ul><ul><li>Selected oral hypoglycemic agents </li></ul><ul><ul><li>Biguanides (metformin) (1.5% decrease in A1c)* </li></ul></ul><ul><ul><ul><li>Suppresses hepatic gluconeogenesis </li></ul></ul></ul><ul><ul><ul><li>Improves sensitivity of muscle to insulin </li></ul></ul></ul><ul><ul><ul><li>Decreases LDL </li></ul></ul></ul><ul><ul><ul><li>Weight loss </li></ul></ul></ul>
    • 62. Pharmacologic Treatment of DM <ul><li>Selected oral hypoglycemic agents (cont’d) </li></ul><ul><ul><li>Sulfonylureas (glyburide, glipizide) (1.5 decrease in A1c) </li></ul></ul><ul><ul><ul><li>Stimulate insulin secretion by beta-cells (“secretagogues”) </li></ul></ul></ul><ul><ul><ul><li>Improve hepatic and peripheral insulin sensitivity </li></ul></ul></ul><ul><ul><li>Thiazolidinediones (rosiglitazone, pioglitazone) (0.5 – 1.4% decrease) </li></ul></ul><ul><ul><ul><li>Improves insulin sensitivity in muscle, liver, adipose tissue </li></ul></ul></ul><ul><ul><ul><li>Increases both HDL and LDL cholesterol </li></ul></ul></ul><ul><ul><ul><li>Weight gain </li></ul></ul></ul>
    • 63. New Pharmacologic Options <ul><li>Incretins (e.g., GLP-1, CCK, GIP) - gut factors that promote insulin secretion in response to nutrients </li></ul><ul><li>Oral agents </li></ul><ul><ul><li>Sitagliptin (Januvia®), Vildagliptin (Galvus®) </li></ul></ul><ul><ul><ul><li>blocks DPP-4 (enzyme that inactivates incretins) to enhance incretin levels </li></ul></ul></ul><ul><li>Injectable agents (0.3-0.7% improvement in HbA1c) </li></ul><ul><ul><li>Pramlintide (Symlin®) </li></ul></ul><ul><ul><ul><li>Synthetic analog of human amylin delays gastric emptying and inhibits glucagon secretion </li></ul></ul></ul><ul><ul><li>Exenatide (Byetta®) </li></ul></ul><ul><ul><ul><li>GLP-1 agonist enhances insulin secretion (Type 2 only) </li></ul></ul></ul>
    • 64. Clinical Case <ul><li>Although Mrs. S’ blood pressure is well-controlled with benazepril and hydrochlorothiazide, her HbA1c has risen over the last few months to 8.4%, despite maximal therapy with a glipizide, metformin and rosiglitazone. </li></ul><ul><li>She presents today asking about what she should do next? Specifically she wants to know if she needs to be on insulin. She is worried that needing insulin is a sign of worsening health and the first step toward dialysis. </li></ul><ul><li>What are the key points you want to address during this visit? </li></ul>
    • 65. Insulin <ul><li>Is the pathophysiology insulin resistance or insulin deficiency? </li></ul><ul><li>Key points </li></ul><ul><ul><li>Supplemental insulin is inevitable, even obese patients become insulinopenic </li></ul></ul><ul><ul><li>Insulin improves peripheral uptake of glucose and inhibits hepatic gluconeogenesis </li></ul></ul><ul><ul><li>Insulin is cleared by the kidney, so patients who undergo renal failure may need less supplemental insulin </li></ul></ul><ul><ul><li>Knowing the pharmacokinetics of the different types of insulin is empowering to physicians and confusing to patients </li></ul></ul>
    • 66. Physiologic Insulin Secretion
    • 67. Clinical Case (cont’d) <ul><li>It has been several months since Mrs. S began taking insulin. She now takes a combination of lente insulin 20 units BID and lispro insulin with meals as needed. </li></ul><ul><li>After returning from a one week family vacation with the Flanders family, Mr. S. brings his wife to see you because she is talking crazy and smells funny. You evaluate her and her blood sugar is 400. </li></ul><ul><li>What do you do next? </li></ul>
    • 68. Diabetic Emergencies <ul><li>Diabetic ketoacidosis </li></ul><ul><ul><li>A disorder developing over several days arising from relative insulin deficiency, impaired glucose metabolism resulting in modest hyperglycemia, lipolysis, acidosis, ketosis, and dehydration </li></ul></ul><ul><ul><li>Must rule out infection, MI, illicit drug use. Frequently a result of medication nonadherence. </li></ul></ul><ul><ul><li>Frequently occurs in Type 2 diabetics </li></ul></ul><ul><li>Hyperosmolar hyperglycemic </li></ul><ul><ul><li>A disorder developing over weeks arising from glucosuric diuresis, marked dehydration, marked hyperglycemia with little to no ketosis or acidosis </li></ul></ul><ul><ul><li>In hospital mortality is much higher than in DKA </li></ul></ul><ul><ul><li>Must rule out precipitating factors above (as in DKA) </li></ul></ul>
    • 69. Summary <ul><li>Hypertension and diabetes are chronic illnesses that are best managed when patients are active and engaged in managing their condition </li></ul><ul><li>Treatment of HTN and DM is not simply achieving a target blood pressure or HbA1c </li></ul><ul><li>HTN and DM can present problems in pregnancy, so knowing a patient and properly counseling her before pregnancy is ideal </li></ul><ul><li>Be aware of emergencies in HTN and DM that warrant urgent management and possible transfer to a higher level of care </li></ul>
    • 70.  
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