Hypertension, Hyperlipidemia: Are our children safe? Patrick R Hints and exam tips    HTN is a hot topic for exams – particularly, what is really malignant HTN and who needs urgent treatment. Also be sure that you know how to recognize the secondary causes of HTN Lipids are less beloved by examiners though they do like to ask about niacin and flushing Cardiovascular risk in your clinic patients    Do not approach HTN, Hyperlipidemia as individual problems. Look upon them as part of your patients cardiovascular risk profile – once your patients understand that they are changing their lifestyle and taking meds to lower their risks of stroke, heart attack, kidney disease and peripheral vascular disease they will be more likely to follow your advice Consider does your pt have the “metabolic syndrome”  Any 3 of  obesity, high TG, low HDL, HTN, impaired glucose tolerance Who are my at risk patients – who should I be screening? (basically everyone!)         Obesity Dyslipidemia – all pts need fasting lipid profile DM Smoking Lack of exercise Age >55 for men, >65 for women FHx of premature cardiovascular disease Microalbuminuria in diabetics Hypertension      Management should be based on the “JNC-7” guidelines Treatment should be instituted at >140/90 in most pts or >130/80 in pts with DM or chronic kidney disease Stage II HTN is >160/100 and only important to distinguish because these patients usually need 2 drugs to control. Making 1st diagnosis needs 2 readings at least 5 mins apart and in both arms. Many doctors will actually get two readings a week or two apart in a previously undiagnosed patient, and many patients will be resistant to start therapy without more than one reading Ambulatory BP monitoring can be used to evaluate for white coat HTN, and also helpful in assessing response to therapy, or persuading a pt that he needs treatment New diagnosis of HTN    Assess other cardiovascular risk factors Look for reversible causes of HTN Look for evidence of end organ damage Renal  Retinal  Cardiac – check EKG, consider stress test if any history of angina type symptoms  CNS – take full Hx and evaluate for previous TIA. Check for carotid bruits  Peripheral artery disease – check for AAA and distal pulses    Lifestyle modification Medication A 56-year-old man undergoes a routine physical examination. A funduscopic examination is performed. What does the funduscopic photograph show? ( A ) Arteriolar sclerosis and hypertensive retinopathy ( B ) Diabetic proliferative retinopathy ( C ) Papilledema ( D ) Malignant hypertensive retinopathy Correct Answer = A Characteristic changes are noted in the retinas of patients with longstanding hypertension. Narrowing of the terminal branches of retinal arterioles may be seen, as well as general narrowing of vessels with severe local constriction (as shown in this photograph). As the disease progresses, striate hemorrhages and soft exudates become visible. In a normal eye, retinal arterioles are transparent, so that blood flow is visible during ophthalmoscopy. A light streak from the ophthalmoscope will reflect from the convex wall of the healthy arteriole. In a sclerotic arteriole, thickening and fibrosis of the vessel wall develop as the sclerosis progresses. The central light reflex increases in width, and the walls of the vessel look like burnished copper, producing a "copper-wire" arteriole. With further progression and additional fibrosis, the entire width of the arteriole reflects the white stripe, producing "silver-wire" arteries. This patient's funduscopic photograph shows both the "copper and silver wires" characteristic of arteriolar sclerosis and the characteristic changes of hypertensive retinopathy. A 62-year-old hypertensive woman is evaluated because of headaches and confusion. After her vital signs are recorded, a funduscopic examination is performed. Based on the funduscopic examination, which of the following conditions most likely present? ( A ) Optic neuritis ( B ) Arteriolar sclerosis ( C ) Brain tumor ( D ) Malignant hypertension Correct Answer = D The retinal changes associated with malignant hypertension consist of arteriolar narrowing, severe local vasoconstriction, hemorrhages, exudates, and papilledema. The exudates are caused by fibroid necrosis of vessel walls. Papilledema associated with malignant hypertension can be differentiated from papilledema due to other causes by its clinical context. Optic neuritis, generally monocular and another cause of a disk swelling, is not associated with hypertension and will have accompanying afferent pupillary defects and loss of vision. Both papilledema associated with malignant hypertension and optic neuritis can be accompanied by loss of vision. Arteriolar sclerosis is not accompanied by papilledema. Brain tumors can be associated with papilledema but not arteriolar narrowing, vasoconstriction, hemorrhages, or exudates. Non-essential HTN  Although most cases of HTN are essential HTN, always consider whether it could be due to another process.          Sleep Apnea Drug induced (esp cocaine, also drugs like NSAIDS, OCP) Chronic renal disease Renal artery stenosis Cushing’s syndrome or treatment with steroids Hyperaldosteronism Pheochromocytoma Coarctation of aorta Thyroid and parathyroid disease A 25-year-old man is evaluated because of several months of episodic sweating, headaches, and palpitations. His medical history includes surgical repair of ankle injuries sustained in a fall while rollerblading 6 months ago; the anesthesiologist noted that the patient's blood pressure fluctuated significantly during the procedure and advised him to be evaluated for possible hypertension. On physical examination, he is 180 cm (71 in) tall and weighs 72 kg (158 lb); his pulse rate is 80/min, and his blood pressure is 135/80 mm Hg. He has no goiter, lid lag, or tremor. Plasma glucose was normal during an episode of palpitations. His thyroid function tests are normal. Measurement of which of the following is the best next step in the evaluation of this patient? ( A ) Serum insulin and insulin-like growth factor 1 ( B ) Repeat measurements of blood pressure ( C ) Catecholamines in a 24-hour urine sample ( D ) Thyroid stimulating hormone (TSH) Correct Answer C This patient has three classic symptoms that suggest pheochromocytoma: headache, sweating, and palpitations, all of an episodic nature. The diagnosis is further suggested by the history of labile blood pressure during a recent surgical procedure. The fact that he is not currently hypertensive does not argue against the diagnosis, because many patients with pheochromocytoma have hypertension only during their episodic paroxysms. Once suspected clinically, the diagnosis is established biochemically with the finding of elevated urinary secretion of catecholamines or their metabolites. Diagnostic yield is highest when the collection is initiated with the onset of an episode. Though rare, pheochromocytoma can be life threatening, and if it is considered in the differential diagnosis of a patient’s symptoms, testing should be ordered. Although some of the patient’s symptoms are suggestive of acromegaly or stress, there are no other symptoms, historical features, or physical findings that support these diagnoses. Physical examination does not suggest hypothyroidism, and the normal results of thyroid function tests exclude this diagnosis. A normal plasma glucose concentration during a symptomatic episode excludes insulinoma. A 41-year-old man is evaluated because of easy bruising. His medical history includes recent onset of borderline diabetes mellitus, which is being treated by diet. Review of systems shows a 4.6-kg (10-lb) weight gain, fatigue, muscle weakness, decreased libido, and depression. He uses no drugs, quit smoking 1 year ago, and has been drinking one to two six-packs of beer nightly. On physical examination, he is 183 cm (72 in) tall and weighs 91 kg (200 lb); his pulse rate is 88/min, and his blood pressure is 150/95 mm Hg. He has a round face and supraclavicular and posterior cervical fullness. He has plethoric facies, tinea versicolor of the chest, no petechiae, and three or four ecchymoses on the extremities. Neurologic examination is normal, except for 3/5 strength in proximal leg muscles. Which of the following is the most likely diagnosis? ( A ) von Willebrand’s disease ( B ) Platelet dysfunction ( C ) Hemochromatosis ( D ) Cushing’s syndrome ( E ) Small vessel vasculitis Correct Answer D This patient presents with clinical features suggestive of Cushing’s syndrome. Urine-free cortisol is the best test to diagnose this disorder. However, because of his recent heavy alcohol use, he may have alcoholic pseudo-Cushing’s syndrome. This disorder can mimic endogenous Cushing’s syndrome and can only be distinguished from it by having the patient abstain from alcohol for an extended period of time. No evaluation for Cushing’s syndrome should be done until after a period of abstinence. The patient’s easy bruising can be explained by excess circulating cortisol. Small vessel vasculitis would produce “palpable purpura” not found in this patient. von Willebrand’s disease could produce bruising but not his other symptoms. Platelet dysfunction would produce petechiae, not bruising. Hemochromatosis would be expected to produce liver function abnormalities, heart failure, diabetes, decreased libido, and a bronze discoloration of the skin but not the hypertension, round face, and abnormal fat deposition of Cushing’s syndrome. A healthy 52-year-old woman is evaluated for her routine annual physical examination. On physical examination, she is 162 cm (64 in) tall and weighs 60 kg (130 lb); her pulse rate is 80/min, and her blood pressure is 160/100 mm Hg. On two subsequent days, she has her blood pressure measured and the results are in the same range. Laboratory studies show the following: Serum sodium 140 meq/LSerum potassium 3.3 meq/LSerum creatinine 0.8 mg/dLPlasma glucose 78 mg/dL Which of the following is the most likely diagnosis? ( A ) Primary hyperaldosteronism ( B ) Renovascular hypertension ( C ) Pheochromocytoma ( D ) Bartter’s syndrome ( E ) Cushing’s syndrome Correct Answer = A This patient presents with the typical features of primary hyperaldosteronism (autonomous overproduction of aldosterone). Most patients with this disorder are asymptomatic, and it should be considered in all patients with hypertension and hypokalemia. A paired plasma aldosterone concentration to plasma renin activity ratio of greater than 20 is suggestive of this disorder, and referral to a specialist is advisable because some patients can be cured with unilateral adrenalectomy. Although Cushing’s syndrome may cause hypertension and hypokalemia, there are no suggestive clinical features of this disorder on the patient’s history and physical examination. Renovascular hypertension and pheochromocytoma are not associated with hypokalemia. Bartter’s syndrome is associated with hypokalemia but not hypertension. Lifestyle modifications   Should be prescribed to all patients including those in the “prehypertension” range – ie. 120-140 systolic 80-90 diastolic, and really all of your patients of a certain age with or without other cardiovascular risk factors Weight reduction    Diet     Reduce to <2.4g sodium per day can reduce BP by 2-8mmHg Exercise   Reduce saturated fat Increase fruit and vegetable content Can reduce BP by 8-14 mmHg Sodium restriction   aim for BMI 18.5-24.9 Loss of 10 Kg can reduce BP by up to 20mmHg Aerobic physical activity eg walking for 30 mins per day – can reduce BP by 4-9mmHg Limiting alcohol  <1 drink per day in women, <2 drinks per day in men can reduce BP by 24mmHg  Thiazides       Useful in cardiac pts, diabetics and certain pts with renal disease Sometimes less helpful in african americans Usually recommended that you check Chem 7 prior to starting and a couple of weeks into treatment as pts with renal artery stenosis can get rising creatinines and dangerously high K Calcium channel blockers   Useful in pts with heart failure and post MI, generally not used in diabetic patients on sulfonylureas due to concerns that the β blocker masks the symptoms of hypoglycemia. Also contraindicated in pts with bronchospasm Watch for postural hypotension, can cause impotence, pts may complain of feeling “tired” ACE inhibitors   First line in most patients, but risk of gout, impaired glucose tolerance, impotence and many pts don’t like them due to urinary effect β blockers   Drug choices Generally not first line now, but usually well tolerated. Remember that many patients need two medications to adequately control BP. Pt should be scheduled for follow up visit six weeks after starting med or changing dose and then dose titrated accordingly. A 47-year-old man who has had type 1 diabetes mellitus for 23 years is found to have hypertension that has been unresponsive to dietary salt restriction. His physical examination shows a blood pressure of 144/94 mm Hg and background retinopathy. His creatinine, blood urea nitrogen, and potassium are normal. A 24-h urine albumin excretion rate is 152 mg. A second urine sample is also positive for albumin, which measures 85 mg/24 h. Which one of the following medications should be used to treat this patient’s blood pressure? ( A ) Thiazide diuretic ( B ) Central sympatholytic agent ( C ) Angiotensin-converting enzyme (ACE) inhibitor ( D ) Calcium-channel blocker Correct Answer = C Several medications are effective in treating hypertension in patients with diabetes. Angiotensin-converting enzyme (ACE) inhibitors, however, have been shown to have selective benefit in this regard: they not only lower blood pressure, but also can retard the rate of progression of any underlying nephropathy. In this patient, the presence of microalbuminuria (albumin level greater than 40 mg/24 h) indicates the presence of early nephropathy. Because ACE inhibitors can retard the progression of nephropathy even in normotensive individuals, these agents should be given even if nonpharmacologic therapy has been successful in lowering the blood pressure to normal levels. However, such use can cause hyperkalemia, and because patients with diabetes are prone to hyporeninemic hypoaldosteronism (type IV renal tubular acidosis), it is important to check potassium levels during therapy. Other agents lack this selective benefit and are used as second-line treatment or if ACE inhibitors cannot be tolerated. A 48-year-old woman was found to have primary hypertension 6 months ago. Despite a trial of lifestyle modifications, her blood pressure remained elevated at about 158/96 mm Hg. Therapy with amlodipine, 5 mg daily, was begun. The patient returns for a follow-up visit 6 weeks after beginning amlodipine. Several blood pressures readings in the office average 152/92 mm Hg. She has also noted progressive ankle edema since therapy was begun. Which of the following is most appropriate at this time? ( ( ( ( A ) No change in therapy B ) Change to another antihypertensive agent C ) Increase the amlodipine to 10 mg daily D ) Recommend a low-salt diet and support hose Correct Answer = B This patient’s blood pressure control while on amlodipine is inadequate (blood pressure has not been reduced to < 140/90 mm Hg), and she has developed pedal edema attributable to the dihydropyridine calcium-channel blocker. Her medication should be changed to another antihypertensive agent that is unlikely to induce edema and will optimize blood pressure control. Adequate control of blood pressure to < 140/90 mm Hg is achieved in only 45% of patients treated with medication, which represents only 27% of all patients with hypertension. This has been labeled the “great hypertension disconnect.” Almost all physicians know the target blood pressure of < 140/90 mm Hg; however, we are not very successful in achieving this target. When target blood pressure is not attained there are three possible options: 1) increase the dose of the initial agent, 2) add a second agent, or 3) change to another drug or class of agent. This patient requires a change to another antihypertensive agent to achieve a target blood pressure and reduce side effects. Increasing this patient’s dihydropyridine calcium-channel blocker is not indicated because this will likely increase her edema. A recent randomized, double-blind, clinical trail demonstrated that thiazide diuretics were superior to calcium channel blockers or angiotensin-converting enzyme inhibitors in lowering systolic blood pressure. The diuretic was superior to calcium channel blockers in preventing heart failure, and superior to angiotensin-converting enzyme inhibitors in reducing combined coronary vascular disease outcomes, stroke, and heart failure. Since diuretics are less expensive and more effective in preventing 1 or more major forms of coronary vascular disease, they should be preferred for first-step anti-hypertensive therapy in most patients. Finally, salt restriction and support hose are unlikely to resolve the medication-induced edema or improve the blood pressure. A 56-year-old man is seen for routine follow-up of hypertension. He has no complaints. He denies any recent change in health status or drug use. His has been prescribed a four-drug regimen of diltiazem sustained-release (SR), captopril, atenolol, and hydrochlorothiazide. He is taking all his medications. At his last clinic visit 2 months ago, his pulse rate was 68/min, and his blood pressure was 138/86 mm Hg. He has no other medical problems. On physical examination, his pulse rate is 86/min and his blood pressure is 194/116 mm Hg. The rest of his physical examination is unremarkable. A stat complete blood count, electrolytes, blood urea nitrogen, creatinine, glucose levels, and urinalysis are all normal. Which of the following is the most reasonable, immediate office-treatment option? ( A ) Captopril and hydrochlorothiazide, orally ( B ) Nifedipine, sublingually ( C ) Lorazepam, orally ( D ) Nitroprusside, intravenously ( E ) No change in medications, follow-up in 2 weeks Correct Answer = A The most common cause of accelerated or urgent hypertension is noncompliance with prescribed therapy, despite frequent patient claims to the contrary. Reasonable blood pressure control at the previous visit suggests that the regimen was effective. The fact that the pulse rate is now 86/min casts some doubt on whether the atenolol has been taken recently. Immediate administration of some or all of the patient’s medications will help reestablish that they are effective for this patient. It is not necessary to lower the blood pressure to normal at this juncture. The use of sublingual nifedipine to lower blood pressure has been condemned by medical experts and the U.S. Food and Drug Administration. The precipitous and uncontrolled decrease in blood pressure frequently produced by sublingual nifedipine presents a risk of myocardial infarction, stroke, or death. Because the patient has no evidence of acute end-organ damage (papilledema, abnormal mental status or neurologic findings), admission to the intensive care unit for treatment of hypertensive crisis is not warranted. Anxiety is not evident, nor is it likely to produce this magnitude of blood pressure elevation; thus, treatment with lorazepam is not indicated. Asking the patient to resume treatment with all medications (option E) is reasonable, but the follow-up period of 2 weeks is unreasonably long. It would be preferable to verify that the patient’s regimen is effective before sending him home. Lipids    Check fasting lipoprotein analysis after 9-12 hour fast Should be done at first visit to you and then Ideal values:      LDL < 130 Total cholesterol <200 TG <200 HDL >40 When instituting and following Tx, your first aim should be to control LDL. If once LDL is controlled the pt still has high TG then consider adding nicotinic acid or fibrate ATP III GUIDELINES   STEP 1: Determine lipid level after 9-12 hr. fast STEP 2: Identify CHD risk equivalents     Clinical CHD AAA Symptomatic carotid artery disease PAD ATP III Guidelines  STEP 3: Determine major risk factors other than LDL      Cigarette smoking BP>140/90 or on anti-HTN Rx Low HDL (<40) Family Hx CHD (<65 females, < 55 males) Age (men >45, women >55) ATP III Guidelines  STEP 4: If 2+ risk factors (other than LDL) present without CHD/CHD risk equivalent, assess 10-year CHD risk (Framingham)    >20%: CHD risk equivalent 10-20% <10% Framingham Risk Scores    Method for assessing how aggressive you should be at lowering lipids. Based on risk factors identified in the Framingham study. Includes age, smoking, BP and both total and HDL cholesterol and assigns a score for each result, then dependent on total score you can calculate 10 year risk of having cardiovascular event ATP III Guidelines  STEP 5: Determine risk category ATP III Guidelines  STEP 6: Institute Lifestyle Changes Very High Risk of CAD  Goal LDL should be <70: -pt with established CAD PLUS -multiple risk factors (DM) OR -severe, poorly-controlled risk factors OR -multiple risk factors of the metabolic syndrome OR -acute coronary syndrome ATP III Guidelines  STEP 7: Consider adding drug therapy (simultaneously with lifestyle changes if CHD/CHD equivalents) The Drugs Drug Action Side effects HMG CoA reductase inhibitors (STATINS) Reduce LDL by 18-50% Increase HDL by 5-15% Reduce TG by 7-30% Myopathy – warn your pts to come in for CK check if muscle pain LFT abnormalities – contraindicated in liver disease Bile Acid Sequestrants (eg. Cholestyramine) Reduce LDL by 15-30% Increase HDL by 3-5% No effect on TG GI upset Affect absorption of other drugs Don’t use in high TG – other drugs are better Nicotinic Acid Reduce LDL by 5-25% Increase HDL by 15-35% Reduce TG by 25-50% Main SE is flushing – tell them to take their aspirin right before Can ppt gout, DM, hepatic toxicity Fibric acids Reduce LDL by 5-20% Increase HDL by 10-20% Reduce TG by 20-50% High risk of myopathy when combined with statins. CI in renal and liver disease Can ppt gallstones ATP III Guidelines  STEP 8: Identify metabolic syndrome, and treat, if present 3 months after TLC ATP III Guidelines  STEP 9: Treat elevated triglycerides    Therapeutic lifestyle modifications Primary aim is to reach LDL goal If still high after LDL goal is reached, set HDL goal 30 mg/dL higher than LDL goal  intensify statin or add nicotinic acid or fibrate Preguntas  1. 65 yo male with BPH, actively smoking, 210 lbs, comes for his first physical since 1978. BP: 148/92. Lipid panel: T chol: 208, LDL: 135, HDL 38, TG: 130   What are his goals? How do you get him there? What can we do to help you stop smoking?        Ask every pt at every visit whether they are smoking and how much and document in the chart Find out whether they want to quit Ask what you can do to help them quit Only 5-8% of smokers can quit on their own Advice from a doctor can improve the smoking cessation rate by 2.5% Quitting smoking can decrease risk of death from CAD by 50% in the first year of cessation Cancer risk decreases to risk of 30 to 50% compared to people who continue to smoke after 10 years Hazards of Smoking Cessation  Withdrawal symptoms    Depression   Peak in 1-3 days after cessation Cravings can last months Mild, but may still require counseling, treatment, or return to smoking Weight gain  Often 1-2 kg in first 2 weeks with additional 2-3 kg over the next 4-5 months   Integrate dietary interventions with smoking cessation Exacerbations of Ulcerative Colitis Drug Adjuncts in smoking cessation Issues Dosing Nicotine gum Main problem is compliance – they have to be using pretty much continuously. <25 cigarettes per day use 2mg, >25 cigarettes per day use 4mg Use 1-2 tabs per hour for 4-6 weeks Nicotine patch Main SE is insomnia – tell pt to remove the patch at night 21mg/d for 6weeks then 14mg/d for 2 weeks then 7mg/d for 2 weeks Wellbutrin Can be used in addtion to the patch or gum and treats the concomitant depression associated with stopping smoking Contraindicated in seizures, alcohol abuse, anorexia, 150mg bid – start 1-2 weeks prior to the quit date and continue for 712 weeks. Varenicline (Chantix)    Novel partial agonist of nicotinic acetylcholine receptors Better than bupropron and placebo at 12 wks and 52 wks Side effects: nausea, abnormal dreams Questions?