Flashcards in HTN Pharmacology Deck (33):
1. Explain guidelines to accurate blood pressure measurement technique.
1. use a bare arm
2. cuff should be long enough to cover ⅔ length of upper arm with a 2.5 space from the 2.5cm from the antecubital fossa
3. arm should be supported with cuff at heart level
patients back should be supported, legs uncrossed and no talking (either person)
1. What is significant about getting different blood pressure measurements in different arms?
BP should always be taken in the arm with the higher pressure, a difference of >15mmHg is concerning for subclavian stenosis
1. What are important concerns to keep in mind concerning patient home blood pressure monitoring?
digital, automatic monitor with a cuff for the upper arm should be used; remember: home blood pressure of >135/85 is considered hypertensive
1. When are 24 hour blood pressure monitor's used?
in the diagnosis of HTN they can be used (taking an average) which is useful in ruling out :
white coat hypertension
2. What are the 3 primary goals during the initial assessment of a patient with a new HTN dx. (and how are these assessed)?
1. ID possible secondary causes of HTN
2. ID other CV risk factors
3. assess for target organ damage (TOD)
this is accomplished with physical exam and lab tests
2. What are important parts of the physical exam when assessing for HTN? (8)
BP in both arms
palpation and auscultation of heart
pulses, auscultate for bruits
aortic mass or pulsation
lower extremity edema
examine optic fund
2. Name lab tests and their function that are done as part of HTN assessment.
urinalysis- protein in urine
blood glucose- screen for diabetes
hematocrit- screen for anemia or elevated RBC
serum K+ - looking for secondary causes
serum Ca++- screen for parathyroidism
ECG- screen for cardiac hypertrophy
THS- check thyroid function
lipid- assess other risk factors for CVD
3. Why are >⅔ of patients on 2 or more antihypertensives?
combining a low dose of two drugs with different mechanisms of action to obtain a greater therapeutic effect; combining drugs can also limit the multiple compensatory mechanisms that may increase BP
3. Cite the 2014 HTN treatment goals.
general population < 140/ 90; if >80yo, <150/90 (systolic pressure being the major focus); specific guidelines for diabetics and those with renal disease
3. Name the 4 primary classes of drugs used in treating HTN along with 6 additional classes used less frequently.
angiotensin receptor blocker
calcium channel blockers
also: a and B blockers, direct vasodilators, aldosteron antagonists, direct renin inhibitors and central a2 agonists (anything that reduces SVR or CO- volume)
3. What is the black box warning for RAAS inhibitors
because Angiotensin II is required for normal fetal development (esp fetal kidney), do not use ACE inhibitors, angiotensin receptor blockers, or renin inhibitors in pregnant women
3. How would you expect renin and aldosterone levels to change with use of ACE inhibitor?
renin levels increase- due to feedback mechanisms
aldosterone levels decrease- due to decreased angiotensin II
3.. What is the mechanism by which ACE-inhibitors induce coughing?
increased bradykinnin, due to decreased ACE metabolism can sensitize bronchial epithelium to irritants
dry cough can begin anytime after an ACE-I is started (5-20%) and its effects are dose dependent
3. ACE inhibitors can reduce GFR which has which side effects (2)?
hyperkalemia and increase in creatinine (greater in CKD, renal artery stenosis, CHF and DM) which should stabilize after 1 week of treatment and may not be an indication to discontinue treatment
3. ACE inhibitors can cause 2 hypersensitivity type reactions to treatment including….
sulfhydryl-related effect when using captopril
angio-edema due o the potentiation of bradykinin (usually in 1st month causing swelling of tongue and laryngeal muscle (risk greater in AA) also "hives that don't itch-- 90% can safely take an angiotensin
3. What is the advantage of using AT1 blockers instead of ACE?
ARB also block pathways to angiotensin synthesis that are independent of RAS system, these selectively block AT1 receptors, ARB also have no effect on bradykinnin, reducing cough side effects
3. Direct Renin inhibitor blocks the _______ of the RAAS cascade.
"rate limiting step" ; also comes with black box warning regarding pregnancy
3. What is important to remember regarding the safety of prescribing direct renin inhibitors?
concomitant use of aliskiren (DRI) with ARBs or ACEIs in patient with diabetes (or GFR <60mL/min) is contraindicated because of the risk for renal impairment, hypotension and hyperkalemia
3. What is the action of diuretics?
increase urinary excretion of sodium, ventilation (decreases intravascular volume, lowering blood pressure
important to check electrolytes after starting, effects take a few weeks to reach treatment goals
3. Discuss side effects of diuretics.
volume depletion and orthostatic hypotension
metabolic side effects (hyper -glycemia, -cholesteremia and -uricemia)
3. Name two aldosterone antagonists.
spironolactone (nonselective) ED and gynecomastia
beneficial against HTN when combined with other diuretics, increase the risk of hyperkalemia
3. Name the mechanism of action of calcium channel blockers and the two types of drug in this category.
bind to receptors and inhibit calcium channels inhibiting Ca++ influx and smooth muscle contraction
dihydropyridine and non-dihydropyridine types (non-dihydropyridines affect the Ca++ in the heart)
can be accompanied by gingival hyperplasia and increased GERD due to inhibition of LE sphincter
3. How do B-adrenocetpor blockers reduce HTN?
decrease cardiac output, inhibit renin secretion and inhibit NE release
B1 selective have effects on the myocardium with less effect on airways
B2 are non-selective and effect both myocardium, vascular and bronchial cells
lipid soluble B-blockers are metabolized in liver and have shorter half-lives
3. What is intrinsic sympathomimetic activity?
partial agonism of B adrenergic receptors; they are less effective at slowing down resting heart rate but block the effects of catecholamine activation during stress or exercise
(B-blockers are also antagonists to a-adrenergic receptors, increasing NO release, although they are not the first line treatment for HTN)
3. WHat are the side effects of B-adrenergic blockers
bronchospasm, cold extremities (B2)
fatigue, depression, mental slowness, vivid dreams, dry mouth
ED, hyper glycemia, lipid abnormalities
3. What are direct vasodilator's role when used in combination to treat HTN
given with diuretic and B blocker to prevent pseudo tolerance (tachycardia and volume retention) as it works directly to relax smooth muscles by opening K+ channels (i.e. minoxidil)
note genetic variations in metabolism
3. How can a antagonists be used to treat HTN?
selective a1-antagonists block sites for NE and decrease the arteriolar resistance (can cause postural hypotension, reflex tachycardia, nasal congestion)
a2 agonists reduce the sympathetic outflow to the chart and blood vessels (can cause ED, sedation and dry mouth)
3. Name the drugs in the typical medication trio of HTN treatment.
calcium channel blockers
3. What are the first and second choice of drug for pt. with post MI, DM, CKD or recurrent stroke?
2. CCB or diuretic
**heart failure: ARB (or ACEI) and B-blocker, and diuretic and spironolactone
3. Contrast hypertensive urgency and hypertensive emergency.
emergency includes acute target organ damage (hospitalization) while urgency requires immediate treatment with PO therapy
4. Define resistant hypertension.
BP > 140/90 while on 3 different BP medication classes (including diuretic) or on any 4 antihypertensive drugs regardless of blood pressure (effects 12-30% of patients on HTN meds)
4. Describe the steps in diagnosis resistant hypertension.
1. exclude pseudo-resistance
2. ID and reverse contributing factors
3. discontinue/min interfering substances
4. screen for secondary causes