Hypertension Flashcards
(101 cards)
ARBs are best for which type of patient
heart failure, post MI, diabetes, chronic kidney disease
MOA of adrenergic antagonists
Inhibit sympathetic system by depleting norepinephrine stores in the CNS this results in a decrease in peripheral vascular resistance and a reduction in BP
side effects of thiazides
hypokalemia, hypomagnesemia, hypercalcemia, hyperuricemia, hyperglycemia
tinnitus, paresthesia, and cramps, N/V/D, muscle cramps, weakness, sexual dysfunction
1st line treatment for African Americans with or without DM
CCB or thiazide
How can you recognize an ACE inhibitor medication?
- pril ending
ie. lisinopril, captopril
MOA of beta blockers. (-olol) drugs
Beta-1 receptors are located in the heart, as well as kidneys, and involved in coardiac contractility, rate, and renin release.
Beta blockers bond to beta-1 receptors and are termed cardio selective because they do not interfere or have a major impact on beta-2 receptors
Beta blockers reduce BP by blocking central and peripheral beta receptors which results in decreased cardiac output and sympathetic outflow
central alpha receptor agonists MOA
Stimulates the alpha 2 adrenergic receptors in the brain, they block sympathetic activity by binding and activating alpha 2 adenoreceptors, this reduces sympathetic outflow to the heart, thereby decreasing cardiac output and decreasing heart rate and contractility
When should electrolyte labs be re-evaluated after initiation of diuretic treatment?
4 weeks into treatment
Calcium Channel Blockers MOA
inhibit the movement of calcium ions across the cell membrane, they relax and vasodilator the cardiovascular system
True/False: Over time baroreceptors can adapt to high BP and their responsiveness decreases
TRUE
contraindications for direct vasodilators
Use with caution in pts with CAD or mitral valve rheumatic heart disease
Hydralazine is associated with lupus like syndrome in high doses, dermatitis, drug fever, peripheral neuropathy
Steps of the Renin-Angiotensin-Aldosterone System
- Renin released by kidneys
- Converts angiotensinogen to angiotensin 1
- ACE converts angiotensin 1 to angiotensin 2
- Angiotensin 2 stimulates aldosterone release from adrenal gland
How should beta blocker therapy be discontinued?
NOT abruptly. tapered gradually over 14 days to prevent withdrawal symptoms which included unstable agina, MI, or even death. patients without CAD could experience tachycardia, palpitations, increased sweating and fatigue
MOA of ACE inhibitors
dilate arteries and veins by blocking angiotensin II formation and inhibiting bradykinin metabolism. vasodilation will reduce arterial pressure and affect both preload and afterload of the heart.
it promotes renal excretion of sodium and water by blocking the effects of angiotensin II on the kidney and blocks angiotensin II stimulation of the aldosterone secretion. ultimately it reduces blood volume, venous pressure and arterial pressure.
it inhibits cardiac and vascular remodeling thats associated with chronic hypertension, heart failure, and MI
What are the two major determinants of BP?
- Cardiac output
- Total Peripheral resistance
CO plus TPR = BP
Which Antihypertensives are considered 1st line for white pts >18yrs with HTN?
ACE, ARB, Thiazide, or CCB alone or in combo with another med.
How can you recognize ARBs?
-sartan ending
What are some risk factors for Primary HTN?
Obesity Sedentary Increased Na intake Age Stress Family history Smoking Diabetes
Drawbacks of Potassium sparing diuretics
Less diuresis than the others
Hyperkalemia
Hirsuitism, gynecomastia, menstrual irregularities
The JNC 8 goal for DM pts regardless of race is less than
140/90
MOA of nondihydropyridines CCBs
- verapamil
diltiazem (Cardizem)
decrease heart rate and slow cardiac conduction at the AV node
What are the common side effects of antihypertensives?
HA
Dizziness, syncope
Hypotension
Which pts would benefit from potassium sparing diuretics
Pts with heart failure is its true benefit but can be used for HTN
potential treatment for patients with heart failure and/or post MI
ACE inhibitors