Cardiovascular System Meds

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High-ceiling loop diuretics MOA
blocks reabsorption of sodium and chloride in the loop of helen to preven the reabsorption of water
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High-ceiling loop diuretics therapeutic uses
congestive heart failure (edema caused by CHF)
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When can high-ceiling loop diuretics not be used?
Hypotension, on digoxin or antihypertensives
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Side effects associated with high-ceiling loop diuretics
frequent urination, hypotension, ototoxicity and tinnitus, hypokalemia
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High-ceiling loop diuretics common ending
-ide (oddball is ethacrynic acid)
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Thiazide-Like Diuretics common ending
-azide
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Thiazide-Like Diuretics MOA
blocks the reabsorption of sodium and chloride and prevents the reabsorption of water at this site
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thiazide-like diuretics therapeutic uses
pulmonary edema, essential hypertension
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Thiazide like diuretics side effects
dehydration, hyponatremia, hyperglycemia
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When can thiazide like diuretics not be used?
renal impairment and pregnancy
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Potassium-Sparing Diuretics MOA
block the action of aldosterone, causing potassium retention and excretion of sodium and water
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Potassium-Sparing Diuretics therapeutic use
heart failure and hypertension
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Potassium-Sparing Diuretics side effects
hyperkalemia, endocrine effects, drowsiness, metabolic acidosis
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Potassium-Sparing Diuretics drugs in class
spironolactone, triamterene, amiloride
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Osmotic diuretics MOA
reduces intracranial and intraocular pressure
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Osmotic diuretics therapeutic use
prevent kidney failure, decrease pressure, promote sodium retention
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Osmotic diuretics side effects
heart failure, pulmonary edema, rebound increased intracranial pressure, fluid and electrolyte imbalances (metabolic acidosis)
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Osmotic diuretic drug in class
mannitol
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When is mannitol not an option?
taking ginko or cardiac glycosides, pregnant
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What is the RAAS system?
renin-angiotensin-aldosterone system
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How does the RAAS system work?
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
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Side effects of ACE Inhibitors
Cough, hyperkalemia, angioedema, orthostatic hypotension, headache, dizziness
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Common ending for ACE Inhibitors
-pril
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Angiotensin II Receptor Blockers MOA
block the action of angiotensin in the body resulting in vasodilation and excretion of sodium and water
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Common ending for Angiotensin II Receptor Blockers
-sartan
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Angiotensin II Receptor Blocker Therapeutic Use
can't tolerate an ACE
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Angiotensin II Receptor Blocker Side Effects
No cough, angioedema, fetal injury, hypotension, dizziness/lightheadedness
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Aldosterone Antagonist MOA
reduce blood volume by blocking aldosterone receptors in the kidney, promoting excretion of sodium and water and retention of potassium
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How do aldosterone antagonists benefit HF and HTN patients?
reduces effort of heart muscle due to retention of potassium, diuretic
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Side effects of aldosterone antagonists
hyperkalemia, hyponatremia, flu-like symptoms, endocrine changes, dizziness fatigue
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Common ending for aldosterone antagonists
-one
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Direct Renin Inhibitor MOA
binds with renin to inhibit production of angiotensin I to decrease the production of angiotensin II and aldosterone
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Direct Renin Inhibitor Therapeutic Use
relieves HTN
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Side effects of Direct Renin Inhibitor
angioedema, rash, cough, hyperkalemia, diarrhea, hypotension
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Additional teaching for Direct Renin Inhibitors
avoid high fat foods
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Drug in Direct Renin Inhibitor Class
aliskiren
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Calcium Channel Blockers MOA
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
acute heart failure, acute angina attack
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Medications for hypertensive crisis side effects
headache, orthostatic hypotension, reflex tachycardia, tolerance, fluid retention
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Medications for hypertensive crisis (drugs in class)
nitroglycerin, nitroprusside, nicardipine, clevidipine, enalaprilat, esmolol
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Cardiac Glycosides drug in class
digoxin
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Cardiac Glycosides MOA
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
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Side effects of Adrenergic Agonists
Hypertensive crisis, cardiac complications, necrosis
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Meds in Adrenergic agonist class
epinephrine, dopamine, dobutamine, isoproterenol, norepinephrine