Hypertension Flashcards
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
which class of HTN can cause depression that may result from decreased catecholamine and serotonin levels in CNS
Adrenergic antagonists
CCBs are indicated for which patients?
Indicated for diabetic patients as well as those with coronary artery disease
Effective for HTN in African American population
JNC8 recommend treatment in elderly 60 and older for BP less than
150/90
Which drugs shouldn’t be given with ACE inhibitors?
Diuretics (spironolactone)
Lithium; causes lithium toxicity
NSAIDS; causes HTN to worsen
contraindications for central alpha receptor agonists
Use cautiously in pts with severe coronary insufficiency, conduction disturbances, recent MI, cerebrovascular disease, renal failure
List some factors that affect BP besides CO and TPR
Blood viscosity Heart rhythm, rate and contractility Blood vessel elasticity, diameter, thickness PNS and SNS Vasopressin/Antidiuretic hormone Baroreceptors Renin-Angiotensin-aldosterone system (**Mean Arterial Pressure does not affect BP)
MOA of ARBs (angiotensin II receptor blockers)
they block the vasoconstriction and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the receptor
they dilate arteries and veins and reduce artierla pressure, effective on preload and afterload. down regulates sympathetic andrenergic activity by blocking the effects of angiotensin II on the sympathetic nerve release and reuptake of norepinephrine
promotes renal excretion of sodium and water by blocking the effects of angiotensin II in the kidney and blocking angiotensin II stimulation of aldosterone secretion
Which HTN med can cause a uric acid retention and should be cautioned in patients with gout?
Thiazides
What is an additional use for Nondihydropyridine CCBs other than HTN?
diltiazem, verapamil
Because of negative inotropic effects:
A.fib (antiarrhythmic effects)
Angina
SVT
Side effects for CCbs
Flushing, headache, excessive hypotension, edema, reflex tachycardia- most commonly seen in the dihydropyridines
What labs should you do before starting an antihypertensive?
Baseline BP, Basic metabolic panel (BUN, creatinine, glucose)
MOA of thiazide diuretics
increase the urinary excretion of sodium and chloride in equal amounts. inhibit reabsorption of sodium and chloride in the ascending loop of Henle and distal tubules
The resulting diuresis with thiazides yields a decreased plasma volume. it affects stroke volume as well as CO, long term, the reduction in peripheral vascular resistance.
contraindications of loop diuretics
high doses are contraindicated in pts with hyperlipidemia, gout, diabetes
pts who are anuric, those who are hypersensitive to these or sulfonylureas, pts with hepatic coma or states of severe electrolyte depletion
Ethacrynic acid is contraindicated in infants
which HTN med is first line treatment in pregnancy
labetalol
Where are the two angiotensin 2 receptor sites?
- vessel walls (vasoconstriction purposes)
2. adrenal cortex (aldosterone release purposes)
Which Antihypertensive is best to avoid in diabetes? Why?
Beta blockers; mask the early signs of hypoglycemia