1. Renin converts angiotensinogen to angiotensin I 2. Angiotensin I --> angiotensin II (ACE enzyme) 3. Angiotensin II causes vasoconstriction which increases BP and causes release of aldosterone from adrenal gland 4. Aldosterone increases sodium reabsorption from distal and collecting tubules of nephrons 5. Water follows sodium 6. Sodium and water are retained in blood
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What does the RAAS system do?
regulates blood pressure
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What are the first line drug classes for blood pressure?
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Which types of diuretics are commonly used with HTN?
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ACE Inhibitors MOA
renin released to blood, reduces production of angiotensin II by blocking conversion of angiotensin I, triggers aldosterone release, causing vasoconstriction
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How do ACE inhibitors benefit HF and HTN patients?
proven to decrease mortality and myocardial workload
vasodilation of peripheral arteries of the heart resulting in decreased force of contraction, decreased heartrate, and slow conduction through AV node
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Calcium Channel Blockers therapeutic use
cardiac dysrhythmias
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Calcium Channel Blockers side effects
acute toxicity (hypotension, bradycardia, AV block), orthostatic hypotension, and peripheral edema
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Common ending for Calcium Channel Blockers
-ipine (but also verapamil and dilitazem)
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Therapeutic use for diltiazem
heart and vascular effects, to regulalte heart rate for A. Fib
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Alpha Adrenergic Blockers MOA
causes peripheral dilation, relaxes smooth muscle of bladder and prostate, reducing BPH symptoms
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Alpha Adrenergic Blockers therapeutic use
HTN, urinary outflow obstruction, obstruction/irritation associated with benign prostatic hyperplasia (not as strong as B-Blockers and CCBs)
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Alpha Adrenergic Blockers side effects
dizziness, asthenia, headache, edema
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Common ending for Alpha Adrenergic Blockers
-zosin
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Centrally Acting Alpha2 Agonists MOA
acts within the CNS to decrease the simulation of adrenergic receptors in the heart and the peripheral vascular system
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Centrally Acting Alpha2 Agonists therapeutic uses
Primary hypertension, severe cancer pain, management of ADHD
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Centrally Acting Alpha2 Agonists Side Effects
Decrease heart rate and dilate vessels: drowsiness and sedation, dry mouth, rebound hypertension if abruptly discontinues, constipation, dizziness
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Meds in Centrally Acting Alpha2 Agonists class
clonidine, guanfacine, methyldopa
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Beta-Adrenergic Blockers MOA
blocks effects of epinephrine B1: heart B2: lungs
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Beta-Adrenergic Blockers Therapeutic Use
primary hypertension, angina, tachydysrhythmias, heart failure, and MI (helpful in returning shape and function of LV)
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Beta-Adrenergic Blockers side effects
Bradycardia, AV block, decreased cardiac output, orthostatic hypotension, bronchoconstriction
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What to monitor before giving Beta-Adrenergic Blockers?
baseline ECG, blood glucose levels, and BP
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Instructions for taking Beta Blocker
Self monitor HR and BP daily, sit or lie down if experiencing dizziness or faintness, avoid sudden changes of position, do not d/c med without provider consultation
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When would you hold Beta Blocker?
rebound myocardium excitation, shortness of breath, edema, weight gain, fatigue
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Which patients should receive Beta Blocker with caution?
heart failure and asthma
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Beta-Adrenergic Blocker common ending
-olol
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Medications for hypertensive crisis MOA
nitroglycerin dilates veins and decreases venous return, which decreases cardiac oxygen demand
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Medications for hypertensive crisis therapeutic use
positive inotropic effect: increased force of myocardial contraction negative chronotropic effect: decreased heart rate (give ventricles more time to fill with blood, increasing stroke volume and cardiac output)
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Cardiac glycosides therapeutic use
second-line medication for heart failure
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What to monitor before giving Cardiac Glycosides?
pulse rate (hold if HR is less than 60 bpm) and blood levels of potassium (3.5-5.0)
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What to give for cardiac glycoside overdose?
digibind
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Adrenergic Agonists MOA
activation of alpha 1 receptors (vasoconstriction), beta 1 receptors, beta 2 receptors, and dopamine receptors (vasodilation, increased HR)
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Adrenergic Agonist therapeutic uses
anaphylactic shock, absorption of local anesthetics, superficial bleeding, decreased nasal congestion, increased BP, treatment of AV block, HF, shock, cardiac arrest, asthma