Chapter 14 Hypertension Q&A

Chapter 14 Hypertension Q&A John Noviasky, PharmD

Question 2 • What is prevalence rate for hypertension among African Americans, Whites, and Mexican Americans • Why is prevalence higher among African - Americans • What are 3 important patient evaluation points for hypertensive patients

Question 3 • Table 14-2

Question 7 • Is “stress management” a reasonable alternative to pharmacologic treatment for hypertension

Question 8 • Table 14-6

Question 9 • What disease states were significantly reduced with BP reduction? • Which pattern of hypertension is most common in the elderly? • Does the reduction of ISH reduce CVD risk?

Question 11 • What is the J-curve phenomenon? • Is there any study which contradicts this phenomenon?

Question 12 • How much can SBP and DBP be reduced with 1 Kg weight loss? • Table 14-7 • Which patients respond best to decrease salt intake? • What is the effect of smoking on mortality? On hypertensive treatment? • Is there a benefit to electrolyte supplementation?

Question 15 • What percentage reduction is seen in patients on HCTZ for stroke, heart attacks, and CVD?

Question 16 • What drugs were studied in ALLHAT? • How many patients were studied in ALLHAT? • What happened to the doxazocin Arm? • Which drug looked better • in primary outcome? • In heart failure? • When compared “head to head”, which looked better for HF, ACEI or ARB?

Question 16 continued • Table 14-8 • how compliant are patients on once daily, twice daily, three-times-daily, 4 - times-daily?

Question 17 • Are the B-blockers, ACEI, and ARB more or less effective in African-American population? • Which agents are the most effective in this population?

Question 19 • Which patients should start on 2 drug regimen? • What is orthostatic hypotension (OH) • Which patient are at more risk for OH? • What 4 aspects of antihypertensive monitoring should always be considered? • When does BP start to fall after starting new agent? • When does BP reach “steady state” after starting new agent?

Question 20 • How often is goal BP achieved with HCTZ? • Usual start dose of HCTZ? • How much does HCTZ 25mg lower SBP and DBP? • When are loop diuretics preferred over HCTZ? • When should K-sparing diuretics be used? • How often do pts. on low dose HCTZ develop hypokalemia?

Question 20 continued • Hyperkalemia occurs more frequently with eplerenone or spironolactone? • Who should not take eplerenone because of concern of hyperkalemia?

Question 22 • Why should HCTZ be taken in morning? • What are signs of electrolyte abnormalities?

Question 23 • What did the TOMHS and VA study tell us about HCTZ side effects? • What metabolic changes should we watch for with HCTZ?

Question 24 • If hypokalemia occurs, how quickly does it develop? • How much does HCTZ 12.5, 25, and 50 mg usually decrease K+? • With HCTZ < or = 25 mg daily, how often do pts develop decrease K+?

Question 25 • When should diuretic-induced hypokalemia be treated? • When should serum K+ be measured after diuretic started or dose increased? • What is dose range of K+ needed to correct decrease K+?

Question 25 continued • Which K+ preparation is preferred, slow-release, EC, or liquid? And why? • What is the issue with starting K-sparing diuretic to conserve K+?

Question 26 • Is diabetes a contraindication to use of diuretics? Why or why not? • When a pt has decreased k+, they are more or less-likely to have impaired glucose tolerance? • Can k+ supplementation help prevent HCTZ-induced hyperglycemia? • What is mechanism behind increased uric-acid with HCTZ use? • What is usual increase in uric acid with HCTZ?

Question 27 • Should diuretic therapy be avoided in patients with dyslipidemia?

Question 28 • Do the loop and thiazide diuretics increase or decrease calcium? • Do the loop and thiazide diuretics increase or decrease magnesium? • What are symptom of decrease magnesium? • What impact does hypomagnesemia have on attempts to correct hypokalemia?

Question 29 • What are possible causes for hypertension resistant to therapy ? Table 14-11 • What is the impact of high vs. low dose HCTZ on BP? • Why is the combination of ACEI and diuretics a reasonable combination? (fig. 14-5) • Why is the combination of ACEI and B-blocker a “questionable” combination?

Question 30 • What are “compelling” indications for B-blockers? • How often is B-blocker monotherapy effective? • Which groups of pts have less BP reduction than young or white pts? • Should B-blockers be avoided in African-Americans? • Why are B-blockers not more universally used?

Question 31 • What are primary differences in B-blockers? • Where are B1 and B2 receptors found? • Is selectivity absolute? • What causes loss of selectivity? • What impact can non-selective B-blockers on Raynauds, peripheral arterial disease? • When are non-selective B-blockers preferred?

Question 32 • How do B-blockers with ISA differ from B-blockers without ISA? • When could B-blockers with ISA be used and when should they not be used? • How does elimination of hydrophilic B-blocker differ from lipophilic? • Do lipophilic B-blockers have more CNS side effects?

Question 34 • What effect can B-blockers have on insulin? • What options are there if B-blockers increase BG? • What hypoglycemic symptoms do B-blockers mask? • Is the risk of masking and potentiating hypoglycemia an absolute contraindication to use of B-blocker?

Question 34 continued • Are B-blockers best avoided in type 1 or type 2 diabetes? • What are effects on lipids of nonselective vs. selective B-blcokers?

Question 35 • What is minimal pulse rate when using B-blockers and why?

Question 36 • Why can rebound hypertension occur with D/C of B-blocker? • What are symptoms of rebound hypertension? • How can rebound hypertension be avoided?

Question 37 • Which ACEI is almost completely hepatically eliminated? • How long does it take to see the full effects of ACEI on BP? • Why do K+ and creatinine need to be monitored in a patient on ACEI?

Question 38 • What risk factors increase chance for “first-dose” to ACEI? • What is the adverse “first-dose” response sometimes seen with ACEI? • When should low-dose ACEI be started because of concern of “first-dose” response?

Question 39 • Why might the elderly and African-Americans have less response to ACEI? • What is usual success rate in reducing BP to goal with ACEI monotherapy in elderly and African Americans, and young whites? • Which is preferred monotherapy for African American; HCTZ or ACEI? • What is the risk of angiodedema in African-American compared to white?

Question 40 • What changes in creatinine are acceptable when starting ACEI and do not warrant change in therapy?

Question 43 • In which groups of patients are CCB more effective than B-blockers or ACEI? • What effects do CCB have on lipids, glucose, uric acid, electrolytes, asthma, or peripheral vascular disease? • What are the CCB in the dihydropyridine class? How about the non-dihydropyridine class? • What are the main differences between these 2 classes?

Question 43 continued • Which CCB does not need to be avoided in HF? • What are main side effects of dihydropyridine CCB? • What are main side effects of non-dihydropyridine CCB? • verapamil and diltiazem should be avoided in patients with this type of heart block • Which non-dihydropyridine causes less constipation?

Question 44 • Why shouldn’t nifedipine IR be given sublingually?

Question 45 • What is chronopharmacology? • Is chronotherapeutic verapamil better than HCTZ/B-blocker combination at reducing hypertension - related complication?

Question 48 • How does pharmacotherapy of ISH differ from regular hypertension? • What is the impact on mortality and morbidity in pts with ISH treated with CCB and HCTZ?

Question 50 • What type of CCB combination is reasonable? • What type of CCB combination is to be avoided?

Question 52 • What place in therapy is an alpha-blocker such as doxazocin in hypertensive therapy? • How do alpha-blockers help in BPH?

Question 55 • What are side effects of alpha-blockers? • When starting an alpha-blocker, how should the patient be counseled?

Question 56 • Why might B & alpha combo be safer in patient with peripheral arterial disease? • Are the B and alpha combos better than other meds for hypertension?

Question 57 • How do the central alpha-2 agonists work to decrease BP? • What are some examples of central alpha-2 agonists? • Why should alpha-2 agonists be used with a diuretic? • What is potential impact of clonidine on smoking? • What is potential problem of abrupt D/C of clonidine?

Question 58 • What is usual start dose of clonidine? • What is potential benefit of transderm clonidine as opposed to oral clonidine? • Negative side of transderm clonidine? • What are most bothersome side effect of clonidine?

Question 59 • What is the main role for methyldopa in hypertension?

Question 60 • Why do most clinicians avoid use of reserpine? • Is this a valid reason? • What did one study find when reserpine was compared to CCB/HCTZ combination? • What are some side effects that can occur with reserpine? • If reserpine is to be used, which drug should always be given along with it? • What pts should avoid reserpine and why?

Question 61 • What is mechanism of action of hydralazine? • What occurs over time with use of potent vasodilators such as hydralazine?

Question 62 • What 2 medications are most frequently mplicated in drug-induced lupus (DIL)? • What are symptoms of DIL? • Is DIL a dose-related response to hydralazine? • Besides a positive ANA, what are other common lab findings in DIL?

Chapter 14 Hypertension Q&A