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295 Cards in this Set
- Front
- Back
Atropine Drug Class
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Muscarinic Antagonist
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Epinephrine Drug Class
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Adrenergic Agonist
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Beta 1 physiological response
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positive chronotrope, positive inotrope, increased systolic blood pressure
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ACE-I ending
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-pril
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alpha 1, beta 1, beta 2 blockers
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carvedilol, labetalol
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beta-blockers ending
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-olol
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alpha 1 blockers ending
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-osin
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alpha 2 adrenergic agonists
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clonidine, methyldopa
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Anticholinergic Side Effects
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dry mouth, blurred vision, constipation, urinary retention, tachycardia, CNS: memory loss, confusion, restlessness, agitation, delirium, hallucination
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ARB ending
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-artan
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CCBs
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-pine, plus diltiazem, verapamil
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alpha 1 physiological response
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vasoconstriction in skin and mucous membranes; decreased respiratory secretions; urinary retention; reflex bradycardia; pupil dilation (mydriasis)
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beta 2 physiological response
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vasodilation: liver, heart, skeletal muscle, lungs; bronchodilation; hyperglycemia; increased liver sugar; increased glucagon; decreased blood pressure; uterine relaxation
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beta-blockers with proven benefits s/p MI
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propranolol, timolol, metoprolol, atenolol
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Baroreceptor Reflex
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A dramatic reduction in blood pressure (such as that caused by intense vasodilation) triggers the baroreceptor reflex and results in reflex tachycardia; and vice versa.
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Physiological Effects of Muscarinic Agonists
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increased secretions, lacrimation, sweating, salivation, bronchial secretions, and secretion of gastric acid; decreased heart rate; relaxation of vascular smooth muscles can cause vasodilation and hypotension; constriction of bronchial smooth muscle = bronchial constriction; increased tone and motility of the GI smooth muscle = enhanced GI motility and defecation; contraction of the detrusor muscle of the bladder and relaxation of the urinary sphincters = increased voiding pressure and enhanced urination; miosis (pupillary constriction) and contraction of the ciliary muscle (accommodation for near vision)
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alpha 1 main sites of action
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pupils (dilation: mydriasis), urinary tract (urinary retention), vasculature of skin (vasoconstriction)
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alpha 2 main site of action
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presynaptic neurons (stimulation decreases further norepinephrine release)
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beta 1 main site of action
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heart
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beta 2 main site of action
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lungs (bronchodilation), liver (increased sugar), uterus (relaxation), vasculature of skeletal muscle (vasodilation)
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Muscarinic agonists: drugs in this class
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bethanecol
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muscarinic agonists: MOA
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bind directly to muscarinic receptors and mimic ACh
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Muscarinic Agonists: therapeutic uses
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atonic bladder; urinary retention in postpartum and postoperative patients; rarely: GERD
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Muscarinic Agonists: side effects
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urinary incontinence, drooling, watery eyes, diarrhea, SOA, hypotension, increased stomach acid, heartburn, abdominal cramping, bradycardia
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Cholinesterase inhibitors affect
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autonomic nervous system and somatic nervous system
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Cholinesterase inhibitors: MOA
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Acetylcholinesterase is an enzyme that normally inactivates ACh, these drugs inhibit the enzyme, thereby increasing ACh levels and activity and prolonging the effects of endogenously released ACh
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Cholinesterase Inhibitors: Therapeutic Uses
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irreversible: insecticides, pesticides, nerve gas; reversible: surgical reversal agents, treatment of myasthenia gravis, alzheimer's symptoms (alzheimer's drugs more specific for CNS)
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Cholinesterase Inhibitors: Side Effects
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SLUDGE, nausea
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Surgical Reversal Agents: drugs in this group
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edrophonium, neostigmine, physostigmine, pyridostigmine
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Cholinesterase Inhibitors used for Alzheimer's
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donepezil, rivastigmine, galantamine
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Muscarinic Antagonists: MOA
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compete with ACh for muscarinic recpetors, bind & block; leave sympathetic nervous system unopposed
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Muscarinic Antagonists: therapeutic uses
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Atropine: antidote for overdoses of cholinergic agonists, antisecretory, antispasmodic, antidiarrheal, code (severe bradycardia & asystole), ophthalmic: mydriatic; scopolamine: anti-motion sickness, antisecretory; Belladonna/opium: bladder and rectal antispasmodic; Urinary incontinence: solifenacin, tolterodine, oxybutynin, propantheline; GI spasms, irritable bowel, spastic bladder: hyoscyamine, hyosycamine + atropine + scopolamine + phenobarbitol; Bronchodilator: ipatropium bromide, tiotropium bromide; Parkinson's: trihexylphenidyl, benzotropine
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Muscarinic Antagonists: Side Effects
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Anticholinergic Side Effects
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Neuromuscular Blockers: MOA
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block nicotinic receptors; to move a single muscle ACh must stimulate thousands of nicotinic receptors
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Neuromuscular Blockers: Therapeutic uses
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cause paralysis during surgery
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Physical Complications associated with chronic HTN
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increased risk of stroke, TIA, dementia, retinopathy, MI, angina, heart failure, LVH, CKD (esp. African American, Hispanic, and Native American), PVD, early death from cardiovascular cause
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Physiological Mechanisms Influencing Blood Pressure
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BP = CO x TPR
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Causes of increased cardiac output
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increased fluid volume, excess sodium intake, renal retention of sodium, overactivity of sympathetic nervous system, excess stimulation of RAAS
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Causes of increased TPR
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overactivity of sympathetic nervous system, excess stimulation of RAAS, genetic alterations in cell membranes (e.g. increased intracellular Na+/Ca++ which alters vascular smooth muscle tone), endothelial-derived factors, hyperinsulinemia secondary to obesity or metabolic syndrome
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How overactivity of sympathetic nervous system increases blood pressure
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vasoconstriction in skin, mucous membranes, and most organs
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RAAS
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Renin released from kidneys secondary to low perfusion (vasoconstriction), low Na+, or low K+; renin converts Angiotensinogen into Angiotensin I; ACE from the lungs converts Angiotensin I to Angiotensin II; Angiotensin II leads to vasoconstriction, increased sympathetic nervous system output and inhibits vasodilators (bradykinin, prostacyclin, prostaglandin E2); Angiotensin also stimulates Aldosterone, which causes fluid retention and may lead to LVH, vascular smooth muscle hypertrophy, glomerular hypertrophy
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Commonly used meds that may cause/complicate HTN
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corticosteroids, oral contraceptives, NSAIDs, coxII inhibitors, oral decongestants, non-oral estrogen-containing contraceptives, some antidepressants, cocaine, cocaine withdrawl, ephedra, ma huang, herbal ecstasy, nicotine, nicotine withdrawl, anabolic steroids, narcotic or opiod withdrawl, amphetamines, (beta blocker without alpha blocker first in patient with pheochromocytoma)
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Why is it recommended to give alpha 1 blocker at bedtime?
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to minimize falls and prevent loss of blood pressure control in the am
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Differences between selective and non-selective beta blockers
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Selective have higher affinity for B1 than B2, but lose some selectivity at high doses
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Selective beta-blockers are safer in
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DM, PVD, asthma, COPD
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Non-selective beta blockers are more effective for
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hyperthyroidism, essential tremor, anxiety, migraine prophylaxis
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Additional side effects of non-slective beta blockers
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bronchoconstriction, peripheral vasoconstriction, hypoglycemia
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ramifications of abruptly stopping beta blocker therapy
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potentially fatal rebound HTN, tachycardia, angina, and MI
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how to properly discontinue beta blocker therapy
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taper over 1-2 weeks
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Which class of diuretics is the most powerful at removing fluid and why?
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loop diuretics because Loop of Henle is responsible for 25-30% of all Na+ reabsorption
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Why thiazides are preferred over loop diuretics for management of HTN?
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do not cause rebound vasoconstriction and do have direct-acting vasodilatory properties
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Mechanism of synergy between thiazides and loop diuretics
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block Na+ reabsorption at 2 different points
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Why higher doses of Loop diuretics needed in renally impaired patients
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must be secreted into urine by the organic pathway of the proximal tubule to be effective; competition with endogenous organic acids such as uric acid for entrance into the urine
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Smoothness Index
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blood pressure fluctuations measured at multiple points throughout the dosing interval; ratio between average 24 hour blood pressure changes; relates better to real world than P:T ratio
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P:T ratio; Peak:Trough Ratio
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difference between blood pressure lowering at beginning and end of dosing interval; 2 measurements; difficult to establish fair comparisons based on P:T alone
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Calculate and discuss pulse pressure
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= SBP - DBP; may reflect extent of artherosclerotic disease and measure arterial stiffness; increased pulse pressure correlated with increased risk of cardiovascular mortality
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Calculate and discuss mean arterial pressure
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= (SBP) + (DBP x 2) / 3; used clinically to represent overall blood pressure, especially in hypertensive emergency
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Patient Education promoting compliance in hypertensive patient
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Even if you don't feel bad, HTN can kill you. If you stop taking suddenly, it can kill you (esp. alpha 2 antagonists, beta-blockers). Take at night.
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Discuss role of genetics/race in antihypertensive selection
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HTN affects African Americans at increased rate and they have a greater need for combination therapy to meet and maintain BP goals; thiazides and CCBs particularly effective for African Americans, higher rate of angioedema and cough from ACE-I than whites
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Blood Pressure Goal for most patients
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<140/90
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Blood Pressure Goals for HTN patient with DM or CKD; and poss. pt's with HF with LVH
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<130/80
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Blood Pressure Goal for HTN patient with proteinuria
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<125/75
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Isolasted Systolic HTN goals
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with SBP > 180, 1st goal is < 160, monitor closely for hypotension, dizziness, sweating, tachycardia, falls, fatigue, etc.; continue to aim for target BP as long as patient tolerates
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Common causes of CHF
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coronary heart disease, MI, uncontrolled HTN, renal failure, Arrhythmias, age >65 years old
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How compensatory mechanisms worsen heart failure
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HF = decreased cardiac output; body attempts to increase cardiac output leading to more damage and worse HF; specifically body increases heart rate and force of contraction via increased sympathetic activity leads to increased workload, stress, O2 demand; also decreased cardiac output can be interpreted as dehydration leading to fluid retention to raise blood pressure which strains the heart and leads to edema and pulmonary congestion; vasoconstriction leads to increased after load and oxygen demand; all these attempts to increase cardiac output lead to ventricular hypertrophy which leads to stiffening and weakened contractions
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Evidence supporting the use of ACE-I in management of chronic heart failure
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proven to slow progression of heart failure and reduce mortality in patients with ejection fraction </=40%
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Evidence supporting the use of ARB in management of chronic heart failure
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adding to ACE-I is reasonable in stage C &D who are symptomatic despite ACE/BB/diuretic therapy or in place of ACE if pt. doesn't tolerate ACE
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Evidence supporting the use of BB in management of chronic heart failure
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proven to reduce mortality in stable stage C & D
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Evidence supporting the use of diuretics in management of chronic heart failure
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symptom relief in stage C & D
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Evidence supporting the use of Digoxin in the management of chronic heart failure
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not shown to decrease mortality; may help symptoms in stage C & D if symptomatic despite ACE/BB/Diuretic therapy to decrease hospitalizations
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Evidence supporting the use of vasodilators in the management of chronic heart failure
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beneficial for patient intolerant of ACE/ARB or symptomatic stage C despite ACE/BB/Diuretic
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Evidence supporting the use of Spironolactone in the management of chronic heart failure
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shown to decrease mortality in stage C & D
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Beta-blockers with specific clinical evidence of benefit in heart failure
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cavedilol, bisoprolol, metoprolol
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protein in the urine indicates
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kidney damage, frequently from HTN
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beta blocker use in a-fib is for
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rate control and to prevent transition to v-fib
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signs/symptoms of hypoglycemia
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tremor, flushed feeling, racing heart, confusion
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how diuretics do/don't work
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they don't pull fluid out of tissues (edema), they pull fluid out of blood so that fluid in tissues can move back into the blood where it belongs
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vascular dehydration signs and symptoms
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dizziness, tachycardia, possibly hypotension
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adrenergic
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referring to or associated with adrenaline or the sympathetic nervous system
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Atrial fibrillation
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atria of the heart are not beating in a normal rhythm; not necessarily a life-threatening dysrhythmia, but puts the patient at a significantly increased risk of clots
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cardiomyopathy
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enlargement and stiffening of the heart muscle
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cholinergic
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referring to or associated with acetylcholine or the parasympathetic nervous system
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ejection fraction
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a clinical measurement used to determine level of heart function in heart failure patients; a low EF indicates poor heart function and worsened heart failure
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Inotropic
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relating to strength of heart muscle contraction
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Ischemia
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cell death occurring due to lack of oxygen
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lacrimation
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production of tears in the eyes, watering eyes
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miosis
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pupil constriction; pin-point pupils
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muscarinic
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referring to or affecting the parasympathetic nervous system or muscarinic receptors
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mydriasis
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pupil dilation
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myocardial infarction; MI
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heart attack; blockage of blood and oxygen supply to the heart which usually results in damage
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ischemic stroke
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blocking of blood and oxygen supply to an area of the brain that results in damage to brain tissue
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hemorrhagic stroke
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bleeding in the brain resulting in damage to brain tissue
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urinary retention
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mechanical problem with bladder or bladder sphincter making it difficult to urinate
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What 2 classes of medications can be used to enhance bronchodilation?
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beta 2 agonists and muscarinic antagonists
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Which 2 classes of drugs might cause bronchoconstriction?
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beta 2 blockers and muscarnic agonists
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Which 2 classes of medications can be used to treat (reverse) bradycardia? (meaning that the drug will cause an increase in heart rate)
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beta 1 agonists and muscarinic antagonists
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Which 2 classes of medications can be used to treat (reverse) tachycardia? (meaning that the drug will cause a decrease in heart rate)
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beta 1 blockers and muscarinic agonists
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Which class of drugs might cause diarrhea?
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muscarinic agonists
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Which class of drugs might cause constipation?
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muscarinic antagonists
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Which 2 classes of drugs might increase blood pressure and cardiac output?
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adrenergic agonists and muscarinic antagonists
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potential interaction between ASA and NSAIDS
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Ibuprofen may block antiplatelet benefits of ASA, take ASA 2 hours before or 4 hours after ibuprofen to maximize the antiplatelet benefits of ASA
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3 antiplatelet drugs
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ASA, extended release dipyridamole + aspirin, clopdrogrel
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Aspirin MOA
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irreversibly inhibits the enzyme cyclooxygenase
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Aspirin SEs
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upset stomach, GI discomfort, GI ulcers; ASA withdrawal associated with increased risk of clots
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extended release dipyridamole + aspirin MOA
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inhibits phosphodiesterase and enhances antithrombotic potential of vascular wall
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extended release dipyridamole + aspirin SEs
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headache, GI upset, N/V, diarrhea, dizziness, up to 25% of patients intolerant
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Clopidrogrel MOA
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inhibits binding of platelets to each other by interfering with ADP; 3-7 day lag time for onset of action
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Clopdirogrel SEs
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GI disturbance, diarrhea, abdominal pain, dizziness, headache, excessive bleeding
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Aspirin during AMI
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325 mg chew and swallow
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ASA + Clopidrogrel after stent, ACS, or ischemic stroke
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for 3-9 months, then 1 drug for life
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Secondary Prevention with antiplatelets
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any of the 3, but if cost isn't a concern then dipyridamole +ASA or Clopidrogrel; for any patient with hx of MI, CVA, TIA, ischemic stroke, or angina
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Primary Prevention with antiplatelets
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aspirin for patients >/= 50 with HTN, DM, hypercholestermia, or smoker
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fluid monitoring in heart failure
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weigh every day for early signs of fluid retention
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drugs that cause sodium and water retention
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NSAIDS, high dose salicylates, COX-II inhibitors, rosiglitazone, pioglitazone, corticosteroids, androgens, estrogens
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Electrolyte imbalances that predispose patients to digoxin toxicity
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hypkalemia, hypercalcemia, hypomagnesemia
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ACE-I dosing
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start with small test dose of captopril 6.25 mg TID, attempt to titrate up to 50 mg TID (for captopril)
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Diuretic dosing
|
spironalactone starting dose 12.5 to 25 mg daily; target dose 25 mg 1-2x/day
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Therapeutic Serum levels for digoxin
|
0.5-1 ng/ml for HF; >/= 0.8 for inotropic benefits
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Most common drug interactions with digoxin
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diuretics and laxatives can cause hypokalemia; antacids may decrease bioavailability; AV heart block with BB, diltiazem, verapamil; CYP3A4 inhibitors will increase, and could double, dig levels (quinidine, amiodarone, diltiazem, itraconazole, erythromycin, clarithromycin); oral antibiotics; colestyramine can bind intestinally and inhibit absorption
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why lower digoxin serum concentrations in heart failure
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neurohormonal benefits happen at lower serum levels; positive inotropic effects achieved at higher serum levels could contribute to the cycle of worsening heart failure
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when is it appropriate to use a digoxin loading dose
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for tachyarrhythmias to overcome large Vd and rapidly achieve adequate serum levels; only when quick onset of action is needed; usually only in hospital setting
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why digoxin loading dose not used frequently
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increases risk of toxicity
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timing of checking serum levels with digoxin
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serum level in 24 hours and 7 days, 24 hour check just to make sure it's not too high; steady state not reached for 7 days with normal renal function, 14 or more days with renal impairment; only levels drawn at steady state will accurately reflect current dose; at least 6 and optimally 12 hours after dose for lab draw
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dosing for digoxin loading dose
|
0.5-1 mg total dose; 1/2 now, 1/4 in 6-8 hours, 1/4 in another 6-8 hours
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management of digoxin toxicity
|
give potassium supplements, treat arrhythmias with appropriate agent, digoxin Immune Fab (Digibind) for severe toxicity
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pt education promoting compliance with meds in heart failure patients
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these drugs are shown to reduce mortality
|
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appropriate digoxin dosing in heart failure
|
0.125-0.25 mg daily is usual maintenance dose; dosing is extremely patient variable
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need to check dig level when
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questionable compliance, lack of improvement, lack of ventricular control in A-fib, changing renal function, interacting meds, abnormal EKG, suspected toxicity
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why hypokalemia predisposes to dig toxicity
|
low potassium inhibits the Na+/K+ pumps on cardiac cell, so does dig; makes it much more pronounced
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Antihypertensive with unfavorable effects in DM and why
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BB: may mask s/s of hypoglycemia and prolong hypoglycemic episodes, esp. non-selective or brittle type I; CAN be used safely in some persons, esp. with a compelling indication
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Antihypertensive with unfavorable effect in gout and why
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loop and thiazide diuretics; both can cause/exacerbate gout/hyperuricemia
|
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antihypertensives with unfavorable effects in PVD and why
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non-selective BB: beta2 mediated peripheral vasoconstriction
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antihypertensives with unfavorable effects in bronchospastic disease and why
|
non-selective BB: beta2 mediated bronchoconstriction
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antihypertensives with unfavorable effects in pregnancy
|
ACE-I and ARB contraindicated in pregnancy because they are tetragenic
|
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antihypertensives with unfavorable effects in renal insufficiency/CKD and why
|
K+ sparing diuretics: renal failure patients often hyperkalemic; Thiazide diuretics: ineffective if ClCr <30 ml/min
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ACE-I in patients on a diuretic, volume depleted, elderly, or at risk of orthostatic hypotension dosing
|
starting dose should be reduced by 50%
|
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reducing side effects with ACE-I
|
side effects reduced by 50% by waiting 6 weeks between dose increases
|
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why to use a test dose of captopril in HF patients
|
because they have "revved-up" RAAS
|
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drug of choice for edema associated with congestive heart failure
|
loop diuretic
|
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principles of loop diuretic dosing in management of heart failure
|
higher doses needed; usually need K+ supplement
|
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digoxin MOA for positive inotropic effects
|
inhibits Na+/K+ pumps of cardiac cell membranes, which increased intracellular Na+, which facilitates Ca++ influx; increased intracellular Ca++ leads to stronger muscle contractions
|
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digoxin MOA for neurohormonal effects
|
decreased sympathetic nervous system activation and increased parasympathetic nervous system activity leading to decreased heart rate and enhanced diastolic filling; also slow SA node conduction
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signs and symptoms of digoxin toxicity
|
N/V, loss of appetite, fatigue, weakness, dizziness, headache, neuralgia, confusion, delirium, psychosis, blurred vision, haloes, photophobia, red-green or yellow-green tinted vision, almost any cardiac dysrhythmia, sinus bradycardia
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Antihypertensives indicated in systolic heart failure and why
|
ACE-I: reduced cardiac risk when administered with a BB; ARB: used in place of ACE-I if intolerant; BB: reduced cardiac risk; Diuretics: loops are drug of choice for edema associated with CHF, K+ sparing diuretics improve morbidity and mortality and slow disease progression
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Antihypertensives indicated after MI and why
|
BB: reduced cardiac risk; ACE: reduced cardiac risk if administered with BB, prevents myocardial remodeling and cardiac hypertrophy often seen post MI, benefits are seen if started with 24 hours of MI and continued for at least 6 weeks, longer if LVH; ALD ANT: improve morbidity and mortality if LV systolic dysfunction
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Antihypertensives indicated with increased CV risk and why
|
BB: reduced cardiac risk in patients with angina and ACS
|
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Antihypertensives indicated with CKD and why
|
ACE/ARB: can prevent progression of renal failure in some patients
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Antihypertensives indicated with tachycardia and why
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BB, verapamil, diltiazem: all slow heart rate
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Antihypertensives indicated with BPH and why
|
alpha1 blocker: relax the smooth muscle of the bladder neck and prostate, which improves urine flow
|
|
MOA for alpha2 adrenergic agonists
|
stimulate alpha2 receptors of brain stem which inhibits norepinephrine; results in decreased sympathetic output, decreased BP, mildly decreased heart rate
|
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therapeutic uses for alpha2 adrenergic agonists
|
mostly resistant HTN, methyldopa is drug of choice in pregnancy-induced HTN, clonidine chewable tablet for hypertensive urgencies; adjunct therapy for ADHD, withdrawal from nicotine, opiates, benzos, and alcohol; clonidine commonly used for Tourette's
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Major SEs for alpha2 adrenergic agonists
|
orthostatic hypotension, dizziness, h/a, impaired ejaculation, sedation, dry mouth, constipation, urinary retention, blurred vision, rebound fluid retention
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contraindications/precautions for alpha2 adrenergic agonists
|
abrupt withdrawal causes severe rebound HTN, taper over 3-4 days
|
|
evidence regarding alpha2 adrenergic agonists
|
shown to decrease BP, but not shown to reduce CV risk
|
|
alpha2 adrenergic agonists
|
clonidine, methyldopa
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alpha 1 blockers
|
doxazosin, terazosin, prazosin, alfuzosin, tamsulosin
|
|
alpha1 blocker MOA
|
competitive blocking of alpha1 receptors, causing vasodilation, also relaxes smooth muscle of bladder neck and prostate
|
|
therapeutic uses of alpha1 blockers
|
BPH, Raynaud's disease, only used as alternative therapy in HTN
|
|
major SEs of alpha1 blockers
|
orthostatic HTN (less likely with BPH selective drugs), reflex tachycardia, sodium and water retention (rebound renal reaction to vasodilation), dizziness, lack of energy, drowsiness, nasal congestion, h/a, decreased libido
|
|
Precautions for alpha1 blockers
|
First Dose Effect: syncope after 1st dose, to minimize falls instruct patient to take QHS and initiate therapy with dose titration
|
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drug interactions with alpha1 blockers
|
use with vardenafil and sildenafil causes hypotension; alfuzosin is contraindicated with potent CYP3A4 inhibitors
|
|
BPH specific alpha1 blockers
|
alfuzosin, tamsulosin only used for BPH; doxazosin, terazosin used for BPH/HTN
|
|
ACE-I MOA
|
inhibit the conversion of angiotensin 1 to its more active form, angiotensin 2; counteract or inhibit all of the pharmacological effects of angiotensin 2; cause vasodilation, dec. aldosterone levels, Na+ and fluid wasting, K+ retention
|
|
ACE-I therapeutic uses
|
HTN, hypertensive urgencies, diabetic nephropathy, persons with proteinuria, stroke prevention, CHF/LVH, AMI
|
|
ACE-I major SEs
|
hypotension (esp. 1st dose), Bradykinin-related Ses: dry hacking cough, non-allergic rash, angioedema; hyperkalemia; acute reversible renal insuficiency
|
|
contraindications/precautions ACE-I
|
test dose of captopril for pts. w/ high RAAS activity: hyponatremia, diuretic use, HF; starting dose reducd by 50% in pts. on diuretic, volume depleted, @ risk of orthostatic HTN, or elderly; Side Effects reduced 50% by waiting 6 weeks b/t dosage inc.
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ACE inhibitors
|
captopril, enalapril, lisinopril, benazepril, ramipril, quinapril, fosinopril, trandolapril, moexipril, perindopril
|
|
ARBs
|
losartan, candesartan, eprosartan, valsartan, irbesartan, temisartan, olmesartan
|
|
ARB MOA
|
directly bind and block angiotensin II receptor
|
|
ARB therapeutic uses
|
alternative to ACE-I in patient who cannot tolerate bradykinin related side effects; may be superior in preventing diabetic nephropathy
|
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ARB major SEs
|
similar to ACE-I except less likely to cause cough and rash
|
|
contraindications/precautions with ARBs
|
history of angioedema with ACE-I is precaution, but many practitioners won't use under those conditions; contraidicated in pregnancy
|
|
tetragenic
|
Any substance or agent that is capable of interfering with normal embryonic development and can produce non-heritable birth defects.
|
|
Normal blood pressure
|
<120/80
|
|
Prehypertension
|
120-39/80-89
|
|
Stage 1 hypertension
|
140-159/90-99
|
|
Stage 2 hypertension
|
>/= 160 / >/= 100
|
|
Hypertensive Crisis
|
>180/120
|
|
Major determinant of SBP
|
cardiac output
|
|
Major determinant of DBP
|
TPR
|
|
Isolated Systolic HTN
|
SBP >/= 140 with DBP <90
|
|
Systolic or Diastolic greater predictor of cardiovascular risk
|
SBP
|
|
how carvedilol differs from other beta blockers
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1st BB shown to improve survival in heart failure; 65% reduced risk of death compared to placebo in addition to standard therapy ?Don't know if this is what she is looking for?
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Increased risk of orthostatic hypotension
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elderly, diabetic, severe volume depletion, baroreflex dysfunction, autonomic insufficiency, use of venodilators (BB, alpha blockers, nitrates, phosphodiesterase inhibitors)
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Orthostatic hypotension
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SBP drop >20 or DBP drop >10 when changing from supine to sitting or sitting to standing
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Cardioselective BB MOA
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selectively block beta1 receptors; dec. HR, force of contraction, cardiac workload, and O2 demand; block juxtaglomerular cells, blocking renin release
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Cardioselective BB Therapeutic Uses
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HTN, a-fib, tachycardia; reduces CV risk in pts. w/ chronic stable angina, MI, ACS, systolic HF; hyperthyroidism, essential tremor, ANS overload (anxiety, stage fright)
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Cardioselective BB Major Side Effects
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hypotension, sexual impairment, nightmares, acute heart failure, reduced cardiac output, bradycardia, AV block
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Cardioselective BB contraindications/precautions
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may mask s/s of hypoglycemia in diabetics; sig. risk of fatal rebound HTN, taper over 1-2 weeks; use caution with uncompensated HF, AV-block, or diabetes
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Cardioselective BB Other Notes
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additive AV blocking when given with digoxin, verapamil, or diltiazem; rarely used: acebutolol, does not reduce CV risk
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Cardioselective BB
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acebutolol, atenolol, betaxolol, metoprolol, bisoprolol, esmolol
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Non-selective BB
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propranolol, nadolol, pindolol
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Intrinsic Sympathomimetic Activity (ISA)
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BB that have partial agonist activity; have little effect on resting heart rate, cardiac output, and Tg levels; do not reduce cardiovascular risk like other BB and may be detrimental in post-MI; rarely used
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ISA BB
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acebutolol, pindolol
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acebutolol therapeutic use
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afib with underlying bradycardia
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Non-selective BB MOA
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block beta1 & 2 receptors
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Non-selective BB Therapeutic Uses
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same cardioselective plus: carteolol and timolol are used as eye drops to treat glaucoma; propranolol may be more effective in treating hyperthyroidism, essential tremor, ANS overload, and migraine prophylaxis
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Non-selective BB Major Side Effects
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same as cardioselective, plus: peripheral vasoconstriction, bronchoconstriction, hypoglycemia (prolonged in diabetics)
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Non-selective BB contraindications/precautions
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asthma, COPD, PVD, uncompensated HF, AV-block, diabetics
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Non-selective BB other notes
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additive AV blocking when given with digoxin, verapamil, or diltiazem; rarely used: pindolol, does not reduce CV risk; may blunt the response to albuterol and other beta2 agonists
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alpha 1, beta 1 & 2, blockers MOA
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blocks listed receptors
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alpha 1, beta 1 & 2, blockers Therapeutic Uses
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carvedilol: CHF; Labetalol: acute management of hypertensive emergencies
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alpha 1, beta 1 & 2, blockers Major Side Effects
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similar to those for alpha 1 blockers and BB separately without reflex tachycardia
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alpha 1, beta 1 & 2, blockers
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carvedilol, labetalol
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CCB MOA
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inhibit Ca++ entrance into coronary and arterial vessels; vasodilators; diltiazem and verapamil also act on heart and are negative inotropes and negative chronotropes
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CCB Therapeutic Uses
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isolated systolic HTN in elderly, african-americans, raynaud's; verapamil and diltiazem can be used for a-fib & tachycardia, but not shown to be cardio-protective
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CCB Major Side Effects
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dizziness, hyypotension, flushing, peripheral edema, h/a; nifedipine & nicardipine: also reflex tachycardia; except amlodipine: negative inotropic; verapamil & diltazem: bradycardia, AV heart block; all: constipation, gingival enlargement
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CCB contraindications/precautions
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immediate-release nifedipine is assoc. with dangerous ping-ponging BP, reflex tachycardia, arrhythmias, MI, and death; sustained-release is safe
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CCB other notes
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verapamil & diltiazem may cause AV block if given with beta blockers, and have p450 interactions (3A4)
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Thiazide Diuretics MOA
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block tubular reabsorption of Na+ at the early part of the distal convoluted tubule
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Thiazide Diuretics Therapeutic Uses
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1st line drug for most HTN, mild to mod. edema, tx of calcium-based kidney stones, red risk of osteoporosis, exc synergy with any other antihypertensive
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Thiazide Diuretics Major Side Effects
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dehydration, electrolyte imbalance, hypokalemia, hyperuricemia, may cause hyperglycemia in some diabetics
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Thiazide Diuretics contraindications/precautions
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according to package insert, contraindicated with sulfonamide allergy, but no documented case of cross-sensitivity and not considered real concern
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Thiazide Diuretics other notes
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ineffective in pts with ClCr < 30ml/min, beta blockers may increase hyperglycemic effect in DMII
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Thiazide Diuretics
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hydrochlorothiazide, chlorthalidone, metolazone, chlorothiazide, indapamide
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Loop Diuretics MOA
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block Na+ reabsorption in ascending limb of the loop of Henle
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Loop Diuretics Therapeutic Uses
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Drug of choice for edema assoc with CHF or RF, acute pulmonary edema
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Loop Diuretics Major Side Effects
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orthostatic hypotension, dehydration, hypokalemia, electrolyte imbalance, ototoxicity, prerenal azotemia
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Loop Diuretics contraindications/precautions
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Do not take QHS, higher doses may be needed in RF & HF, synergy with thiazides
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Loop Diuretics Other Notes
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onset of action: 30 min po, 5 min IV; usually require K+ supplement, hypokalemia can lead to toxicity if taking digoxin & can predispose to QT prolongation
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Loop diuretics
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furosemide, bumetanide, torsemide
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K+ sparing diuretics (aldosterone antagonists)
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spironolactone, eplerenone
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K+ sparing diuretics (not aldosterone antagonists)
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amiloride, triamterene
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K+ Sparing Diuretics (aldosterone antagonists) MOA
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synthetic aldosterone antagonist, causes Na+ elimination and K+ reabsorption
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K+ Sparing Diuretics (aldosterone antagonists) Therapeutic Uses
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slows CHF disease progression, rduce portal vein HTN, used with thiazides or loops to prevent hypokalemia, resistant HTN already on 3+ drugs
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K+ Sparing Diuretics (aldosterone antagonists) Major Side Effects
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hyperkalemia (life-threatening), spironolactone may cause gynecomastia, menstrual irregularities & deepening of voice in females
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K+ Sparing Diuretics (aldosterone antagonists) Precautions/Contraindications
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K+ > 5.5, ClCr < 30ml/min, extreme caution if receiving K+ supplements, ACE-I, ARBs, or using salt sub high in K+, eplerenone use is contraindicated with cyp3A4 inhibitors such as macrolides, ketoconazole, itraconazole & others
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K+ Sparing Diuretics (aldosterone antagonists) Note on eplerenone
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eplerenone is reserved for pts with sex hormone related side effects because it costs almost 6x as much as spironolactone
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K+ Sparing Diuretics (not aldosterone antagonists) MOA
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inhibit Na+ reabsorption and K+ elimination at the distal renal tubule
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K+ Sparing Diuretics (not aldosterone antagonists) Therapeutic Uses
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prevent hypokalemia, not used for CHF or portal vein hypertension
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K+ Sparing Diuretics (not aldosterone antagonists) Major Side Effect
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hyperkalemia
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blood pressure goal in patients with diabetes or CKD, some experts also add heart failure with LVH to this list
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<130/80
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Goal for isolated systolic HTN
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<140/90, if SBP >180, the first goal is <160, continue to attempt to reach target BP as long as patient tolerates; monitor closely for hypotension
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compelling indication: recurrent stroke prevention
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ACE + thiazide: combination shown to reduce recurrent stroke; ARB also shown to reduce risk
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compelling indication: CKD
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ACE/ARB: decreased intraglomerular pressure, decreased progression of CKD; Loop Diuretics: considered more effective than thiazides in CKD, but it is controversial
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compelling indication: left ventricular dysfunction (systolic heart failure)
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1st line regimen of choice: ACE + Diuretic; standard therapy: ACE, Diuretic, BB; ACE: decreased CV m/m; diuretics: symptom relief of edema; BB: decreased CV m/m with ACE (start at very low dose and titrate slowly to avoid acute exacerbations of HF) (bisprolol, carvedilol, metoprolol only BB proven beneficia)l; ARB: if intolerant of ACE or add-on; ALD ANT: addition can decrease CV m/m in LVD; not recommended to use both ARB and ALD ANT due to increased risk of severe hyperkalemia
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compelling indication: s/p MI
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BB without ISA and ACE; BB: decreased cardiac adrenergic stimulation and decreased risk of subsequent MI or sudden cardiac death; ACE: improve cardiac remodeling, cardiac function, and decrease CV events; ALD ANT: decreased CV m/m soon after AMI (3 to 14 days), but need diligent K+ monitoring
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Compelling Indication: CAD, increased CV risk
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BB without ISA: decreased BP, increased myocardial O2 consumption, decreased O2 demand, most evidence for benefits in these patients; CCB: diltiazem and verapamil: alternatives, pines: add-on therapy; with ACS: 1st line therapy BB & ACE; after control with BB and/or CCB, adding ACE/ARB further reduces CV risk
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Compelling Indication: DM
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1st: ACE/ARB: both provide nephroprotection as a result of vasodilation in efferent arteriole of the kidney; ACE: decreased CV risk; ARB: decreased risk of progressive kidney dysfunction; 2nd: thiazide; decreased BP and provide addt'l decreased CV risk; Add-on: CCB or BB; CCB: not as protective as ACE, diltiazem and verapamil provide more renal protection than -pines; BB: decreased CV risk in diabetic patients with caution due to masking s/s of hypoglycemia
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HMG-CoA Reductase Inhibitors MOA
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inhibit HMG-CoA Reductase in liver--the catalyst in rate limiting of cholesterol synthesis
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HMG-CoA Reductase Inhibitors therapeutic uses
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Lower LDL, Elevate HDL, Lower Tg, decrease CV m/m, MI, stroke
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HMG-CoA Reductase Inhibitors major side effects
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hepatotoxicity, myopathy, renal issues, constipation, diarrhea, dizziness, headache, contraindicated in pregnancy
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HMG-CoA Reductase Inhibitors Unproven Benefits
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Alzheimer's, macular degneration, glaucoma, MS, Osteoporosis, rheumatoid arthritis, cancer
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Dietary Cholesterol Absorption Inhibitors MOA
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prevents cholesterol absorption through intestinal villi; only works for dietary cholesterol, not genetic
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Dietary Cholesterol Absorption Inhibitors Therapeutic Uses
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decrease LDL, decrease Tg, good synergy with statin
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Dietary cholesterol absorption inhibitors major side effects
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GI upset
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Niacin MOA
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unknown
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Niacin Therapeutic Uses
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decrease LDL and Tg, most effective for increasing HDL, decrease risk of CV death & MI
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Niacin Major Side Effects
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flushing, itching, GI, N/V, diarrhea, heaptotoxicity, exacerbation of peptic ulcers and gout
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Bile Acid-Binding Resins MOA
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binds bile acids in intestines; body then must break down cholesterol to make more bile acid
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Bile Acid-Binding Resins Therapeutic Uses
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adjunct therapy or for intolerance of statins, decrease LDL
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Bile Acid-Binding Resins Major Side Effects
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may increase Tg, constipation, heartburn, nausea, gas, belching, bloating
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Fibrates MOA
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increase lipoprotein lipase activity, key enzyme in removal of Tg
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Fibrates Therapeutic Uses
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decreased risk of stroke & MI, decrease LDL, increase HDL, decrease Tg 40%
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Fibrates major side effects
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gallstones, myopathy, hepatotoxicity, clofibrate: increased risk of cancer
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HMG-CoA Reductase Inhibitors Appropriate Safety Monitoring
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monitor AST, ALT (d/c if levels 3x normal) @ 6wks, 12wks, and q6months; CPK (d/c if 10x normal); watch for muscle weakness/tenderness; Rosuvastatin: proteinuria
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Bile Acid-Binding Resins Appropriate Safety Monitoring
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monitor VLDL closely; contraindicated if Tg >500mg/dL
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Patient instructions for avoiding drug interactions with bile acid binding resins
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digoxin, warfarin, levothyroxine: prevent absorption; Vit A, E, D, K (fat soluble): decreased intestinal absorption; Take these meds 2 hours before or 4-6 hours after; colesevelam more selective and doesn't have these problems
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patient instructions for statins
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take at bedtime or with evening meal except atorvastatin, rosuvastatin, and pravastatin (these 3 can be taken at any time of day)
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patient instruction for niacin
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pre-medicate with ASA or ibuprofen 30 minutes before each dose to reduce side effects
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pt education and counseling promoting medication compliance in the hyperlipidemic patient
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reaching target LDL decreases risk of MI 30%, mortality 20%; lowering cholesterol is fundamental in decreasing m/m from heart disease; lipid lowering drugs can prevent formation, slow progression, and cause regression of atherosclerotic lesion; drugs must be continued indefinitely, lifestyle changes in addition to meds is important
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evidence supporting the use of statins
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decreased risk of CV death, MI, stroke; lower LDL and total cholesterol by 25-40%, atorvastatin lowers LDL by up to 60%; elevate HDL, lower Tg about 10%
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discuss the role of genetics in selecting individual goal LDL
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family hx of early CHD (male 1st degree relative <55, female <65) is major risk factor
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determining goal LDL by number of risk factors
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0-1 risk factors: <160; 2+ risk factors: <130; existing CHD: <100
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existing CHD when deciding target LDL
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angina, diabetes, previous MI, previous ischemic stroke
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If goal of LDL <100 achieved with standard statin dose in patient with existing CHD or very high risk
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consider aiming for <70
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Very high risk when determining target LDL
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existing CHD + diabetes/poorly controlled major risk factors/triad of dec HDL, inc Tg, inc LDL; ACS: ranging from unstable angina to AMI
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Major Risk factors for developing CHD (used in determining goal LDL)
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smoking >10 cigarettes/day; HTN (treated or not); low HDL (<40 mg/dL); family history; men 45 or older; women 55 or older; if HDL >60, subtract 1 risk factor
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determinants of myocardial O2 demand (increased demand if)
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heart rate (faster); contractility (stronger); preload (increased volume--venous); afterload (increased resistance--arterial)
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3 classes of drugs used to treat angina
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nitrates, BB, CCB
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Why BB is not useful for variant angina
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variant agina is due to vasospasms and BB do not vasodilate
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Nitrates MOA
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venous dilators
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Nitrates common side effects
|
venous pooling, headache, orthostatic hypotension, lightheadedness, dizziness, hypotension, flushing
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importance of nitrate-free interval
|
tolerance develops very quickly
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how to provide nitrate free interval
|
need 8-12 hour interval daily; take off patches at noc; for BID po take at 8 and 2, or equivalent
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treatment for acute angina attacks
|
SL nitro tabs or spray
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prophylactic treatment for angina
|
nitro ointment/patch/SR capsules, isosorbiade dinitrate tabs, isosorbide mononitrate tabs
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pt instructions for SL nitro use
|
under tongue x1 q5 minutes until pain relieved up to 3 doses; if no relief seek emergency care
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treatment goal for unstable angina
|
reduce risk of MI and death
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|
treat unstable angina with
|
IV nitrates, BB, CCB, heparin & ASA, IV morphine; EKG, coronary catheterization
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|
majority of angina is due to
|
obstruction of the coronary vessels by atherosclerotic plagues
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Stable exertional angina pectoris is
|
exertion related with a predictable pattern
|
|
variant angina pectoris (Prinzmetal's) description
|
associated with more severe pain; usually occurs at rest rather than with exertion, early morning, awakening from sleep; tends to involve the right coronary artery; apt to be associated with arrhythmias or conduction defects
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|
variant angina is caused by
|
vasospasms of the coronary artery
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treatment goal for stable exertional angina pectoris
|
reduce frequency and intensity of anginal attacks
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Drug of choice for stable angina and why
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BB, because they have been shown to reduce m/m
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Alternative treatments for stable angina
|
CCB or long-acting nitrates
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drug to use when patient doesn't respond to triple anti-anginal therapy
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ranolazine
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other drugs in the treatment plan for stable angina
|
SL nitro for acute attacks, ASA for stroke prevention, Statins to goal LDL of <100; ACE for patients with CAD and diabetes or LV systolic dysfunction
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Bottom Line: statins
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drug of choice for most patients; tolerated well; strongest evidence of reduced m/m
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Bottom Line: Niacin
|
cheap, works great, not well tolerated, decreases morbidity, doesn't decrease mortality
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Bottom Line: Bile Acid-Binding Resins
|
used for synergy, or alone in mild cases
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Bottom Line: Fibrates
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drug of choice to decrease Tg; also evidence of decreased m/m
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If cholesterol is just a little high, then
|
try lifestyle modifications alone; if not effective, then add meds
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If cholesterol is >20 points high, then
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start meds and lifestyle changes
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