Pathophysiology and Pharmacotherapy of Hypertension 2 Flashcards
When is a person diagnosed with hypertenstion
2-3 properly measured blood pressure reading that are over 130/80 mmHg
T/F: Blood pressure greater than or equal to 130/80 daytime (awake) is considered hypertension
True
T/F: Home blood pressure monitoring is considered the gold standard over ambulatory blood pressure monitoring
False: Worn device taken every 15 to 20 mins during the day and every 30 to 60 mins during sleep for 24-48 hours ambulatory blood pressure monitoring is considered gold standard
What is white coat hypertension, when is it clinically significant
Elevated office blood pressure but normal readings outside with either Ambulatory or home blood pressure monitoring, when SBPs and DBPs are higher than 20/10 mmHg compared to at home or Ambulatory
What is masked hypertension
Normal BP in office but Ambulatory and Home Blood pressure monitoring (ABPM/HBPM) are consistently above normal
When a patient has normal blood pressure what is the best option for them, when should they be reassessed
Promote healthy lifestyle habits, reassess in one year
When a patient has elevated BP what is the best option for them, when should they be reassessed
Lifestyle habit changes, reassess in 3 to 6 months
When a patient has stage 1 Hypertension Blood pressure levels when would they be advised lifestyle changes and BP medication
If the Patient has a clinical ASCVD risk or estimated CVD risk greater than 10%
T/F: When a patient has stage 2 Hypertension Blood pressure levels they are given lifestyle changes and BP medication and are reassessed every 3 to 6 months
False: When a patient has stage 2 Hypertension Blood pressure levels they are given lifestyle changes and BP medication and are reassessed every month until their goal is met, then they are reassessed every 3 to 6 months
T/F: It is important to individualize therapy to determine a BP goal for each individual patient due to intolerable adverse effects
True
What are the best proven nonpharmacological interventions for the prevention/treatment of hypertension
weight loss, Dash and Mediterranean diet, Decrease Na intake, increase exercise, decrease alcohol intake if excessive
What medication classes target the kidney to lower BP
Thiazides, ACEI, ARB, Aldosterone Antagonist, Renin Antagonist
What medication classes target the heart to lower BP
Beta Blockers, Non-DHP Caclium Channel Blockers
What medication classes and medications target the vasculature to lower BP
DHP Calcium Channel Blockers, Alpha Blockers, Nitrates, Minoxidil, Hydralazine
Which medications work on the central nervous system to lower BP
Clonidine and Methyldopa
What is the MOA of thiazide diuretics, what adverse reactions can they cause
Blockade of Sodium reabsorption at the distal tubule causing initial volume loss in the 1st week mostly/ electrolyte abnormalities, gout , dehydration, glucose intolerance
T/F: Thiazide diuretics can be given no matter the co-morbid condition
False: Thiazides can cause more harm and have reduced efficacy with co-morbid renal disease
T/F:Hydrochlorothiazide is the preferred thiazide for lowering BP
False: Low-dose chlorthalidone is the preferred thiazide
What is the MOA of ACE inhibitors, what adverse reactions can they cause
Block conversion of Angiotensin 1 to Angiotensin 2, reduce metabolism of bradykinin/ Hyperkalemia, cough, angioedema
What is the MOA of Angiostensin Receptor blocker, what adverse reactions can they cause
block the actions of angiotensin 2/ Hyperkalemia
What is the MOA of DHP Calcium Channel Blockers, what adverse reactions can they cause
Vasodialation of vascular smooth muscle via calcium antagonism/ Headache, light headness, flushing, dose dependent peripheral edema
What are ways to combat dose dependent peripheral edema cause by DHP Calcium Channel blockers
Decrease the dose, Switch to another agent, and/or add RAAS-blocking agent (ACE/ARB)
What is the MOA of non-DHP Calcium Channel Blockers, what are the adverse reactions they can cause
Reduction of cardiac output via decreases in heart rate via inhibition of calcium ions entering voltage sensitive areas of mycoardium during depolarization/bradycardia, heart failure exacerbation
Whait is the MOA of Beta-Blockers, what are the adverse reactions they can cause
Blockade of B1-receptors redcues cardiac output via reductions in both HR and stroke volume/ bradycardia, lethargy, sexual dysfunction
