Pharmacology Exam 2

Front 1

Atropine Drug Class

Back 1

Muscarinic Antagonist

Front 2

Epinephrine Drug Class

Back 2

Adrenergic Agonist

Front 3

Beta 1 physiological response

Back 3

positive chronotrope, positive inotrope, increased systolic blood pressure

Front 4

ACE-I ending

Back 4

-pril

Front 5

alpha 1, beta 1, beta 2 blockers

Back 5

carvedilol, labetalol

Front 6

beta-blockers ending

Back 6

-olol

Front 7

alpha 1 blockers ending

Back 7

-osin

Front 8

alpha 2 adrenergic agonists

Back 8

clonidine, methyldopa

Front 9

Anticholinergic Side Effects

Back 9

dry mouth, blurred vision, constipation, urinary retention, tachycardia, CNS: memory loss, confusion, restlessness, agitation, delirium, hallucination

Front 10

ARB ending

Back 10

-artan

Front 11

CCBs

Back 11

-pine, plus diltiazem, verapamil

Front 12

alpha 1 physiological response

Back 12

vasoconstriction in skin and mucous membranes; decreased respiratory secretions; urinary retention; reflex bradycardia; pupil dilation (mydriasis)

Front 13

beta 2 physiological response

Back 13

vasodilation: liver, heart, skeletal muscle, lungs; bronchodilation; hyperglycemia; increased liver sugar; increased glucagon; decreased blood pressure; uterine relaxation

Front 14

beta-blockers with proven benefits s/p MI

Back 14

propranolol, timolol, metoprolol, atenolol

Front 15

Baroreceptor Reflex

Back 15

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.

Front 16

Physiological Effects of Muscarinic Agonists

Back 16

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)

Front 17

alpha 1 main sites of action

Back 17

pupils (dilation: mydriasis), urinary tract (urinary retention), vasculature of skin (vasoconstriction)

Front 18

alpha 2 main site of action

Back 18

presynaptic neurons (stimulation decreases further norepinephrine release)

Front 19

beta 1 main site of action

Back 19

heart

Front 20

beta 2 main site of action

Back 20

lungs (bronchodilation), liver (increased sugar), uterus (relaxation), vasculature of skeletal muscle (vasodilation)

Front 21

Muscarinic agonists: drugs in this class

Back 21

bethanecol

Front 22

muscarinic agonists: MOA

Back 22

bind directly to muscarinic receptors and mimic ACh

Front 23

Muscarinic Agonists: therapeutic uses

Back 23

atonic bladder; urinary retention in postpartum and postoperative patients; rarely: GERD

Front 24

Muscarinic Agonists: side effects

Back 24

urinary incontinence, drooling, watery eyes, diarrhea, SOA, hypotension, increased stomach acid, heartburn, abdominal cramping, bradycardia

Front 25

Cholinesterase inhibitors affect

Back 25

autonomic nervous system and somatic nervous system

Front 26

Cholinesterase inhibitors: MOA

Back 26

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

Front 27

Cholinesterase Inhibitors: Therapeutic Uses

Back 27

irreversible: insecticides, pesticides, nerve gas; reversible: surgical reversal agents, treatment of myasthenia gravis, alzheimer's symptoms (alzheimer's drugs more specific for CNS)

Front 28

Cholinesterase Inhibitors: Side Effects

Back 28

SLUDGE, nausea

Front 29

Surgical Reversal Agents: drugs in this group

Back 29

edrophonium, neostigmine, physostigmine, pyridostigmine

Front 30

Cholinesterase Inhibitors used for Alzheimer's

Back 30

donepezil, rivastigmine, galantamine

Front 31

Muscarinic Antagonists: MOA

Back 31

compete with ACh for muscarinic recpetors, bind & block; leave sympathetic nervous system unopposed

Front 32

Muscarinic Antagonists: therapeutic uses

Back 32

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

Front 33

Muscarinic Antagonists: Side Effects

Back 33

Anticholinergic Side Effects

Front 34

Neuromuscular Blockers: MOA

Back 34

block nicotinic receptors; to move a single muscle ACh must stimulate thousands of nicotinic receptors

Front 35

Neuromuscular Blockers: Therapeutic uses

Back 35

cause paralysis during surgery

Front 36

Physical Complications associated with chronic HTN

Back 36

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

Front 37

Physiological Mechanisms Influencing Blood Pressure

Back 37

BP = CO x TPR

Front 38

Causes of increased cardiac output

Back 38

increased fluid volume, excess sodium intake, renal retention of sodium, overactivity of sympathetic nervous system, excess stimulation of RAAS

Front 39

Causes of increased TPR

Back 39

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

Front 40

How overactivity of sympathetic nervous system increases blood pressure

Back 40

vasoconstriction in skin, mucous membranes, and most organs

Front 41

RAAS

Back 41

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

Front 42

Commonly used meds that may cause/complicate HTN

Back 42

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)

Front 43

Why is it recommended to give alpha 1 blocker at bedtime?

Back 43

to minimize falls and prevent loss of blood pressure control in the am

Front 44

Differences between selective and non-selective beta blockers

Back 44

Selective have higher affinity for B1 than B2, but lose some selectivity at high doses

Front 45

Selective beta-blockers are safer in

Back 45

DM, PVD, asthma, COPD

Front 46

Non-selective beta blockers are more effective for

Back 46

hyperthyroidism, essential tremor, anxiety, migraine prophylaxis

Front 47

Additional side effects of non-slective beta blockers

Back 47

bronchoconstriction, peripheral vasoconstriction, hypoglycemia

Front 48

ramifications of abruptly stopping beta blocker therapy

Back 48

potentially fatal rebound HTN, tachycardia, angina, and MI

Front 49

how to properly discontinue beta blocker therapy

Back 49

taper over 1-2 weeks

Front 50

Which class of diuretics is the most powerful at removing fluid and why?

Back 50

loop diuretics because Loop of Henle is responsible for 25-30% of all Na+ reabsorption

Front 51

Why thiazides are preferred over loop diuretics for management of HTN?

Back 51

do not cause rebound vasoconstriction and do have direct-acting vasodilatory properties

Front 52

Mechanism of synergy between thiazides and loop diuretics

Back 52

block Na+ reabsorption at 2 different points

Front 53

Why higher doses of Loop diuretics needed in renally impaired patients

Back 53

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

Front 54

Smoothness Index

Back 54

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

Front 55

P:T ratio; Peak:Trough Ratio

Back 55

difference between blood pressure lowering at beginning and end of dosing interval; 2 measurements; difficult to establish fair comparisons based on P:T alone

Front 56

Calculate and discuss pulse pressure

Back 56

= SBP - DBP; may reflect extent of artherosclerotic disease and measure arterial stiffness; increased pulse pressure correlated with increased risk of cardiovascular mortality

Front 57

Calculate and discuss mean arterial pressure

Back 57

= (SBP) + (DBP x 2) / 3; used clinically to represent overall blood pressure, especially in hypertensive emergency

Front 58

Patient Education promoting compliance in hypertensive patient

Back 58

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.

Front 59

Discuss role of genetics/race in antihypertensive selection

Back 59

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

Front 60

Blood Pressure Goal for most patients

Back 60

<140/90

Front 61

Blood Pressure Goals for HTN patient with DM or CKD; and poss. pt's with HF with LVH

Back 61

<130/80

Front 62

Blood Pressure Goal for HTN patient with proteinuria

Back 62

<125/75

Front 63

Isolasted Systolic HTN goals

Back 63

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

Front 64

Common causes of CHF

Back 64

coronary heart disease, MI, uncontrolled HTN, renal failure, Arrhythmias, age >65 years old

Front 65

How compensatory mechanisms worsen heart failure

Back 65

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

Front 66

Evidence supporting the use of ACE-I in management of chronic heart failure

Back 66

proven to slow progression of heart failure and reduce mortality in patients with ejection fraction </=40%

Front 67

Evidence supporting the use of ARB in management of chronic heart failure

Back 67

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

Front 68

Evidence supporting the use of BB in management of chronic heart failure

Back 68

proven to reduce mortality in stable stage C & D

Front 69

Evidence supporting the use of diuretics in management of chronic heart failure

Back 69

symptom relief in stage C & D

Front 70

Evidence supporting the use of Digoxin in the management of chronic heart failure

Back 70

not shown to decrease mortality; may help symptoms in stage C & D if symptomatic despite ACE/BB/Diuretic therapy to decrease hospitalizations

Front 71

Evidence supporting the use of vasodilators in the management of chronic heart failure

Back 71

beneficial for patient intolerant of ACE/ARB or symptomatic stage C despite ACE/BB/Diuretic

Front 72

Evidence supporting the use of Spironolactone in the management of chronic heart failure

Back 72

shown to decrease mortality in stage C & D

Front 73

Beta-blockers with specific clinical evidence of benefit in heart failure

Back 73

cavedilol, bisoprolol, metoprolol

Front 74

protein in the urine indicates

Back 74

kidney damage, frequently from HTN

Front 75

beta blocker use in a-fib is for

Back 75

rate control and to prevent transition to v-fib

Front 76

signs/symptoms of hypoglycemia

Back 76

tremor, flushed feeling, racing heart, confusion

Front 77

how diuretics do/don't work

Back 77

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

Front 78

vascular dehydration signs and symptoms

Back 78

dizziness, tachycardia, possibly hypotension

Front 79

adrenergic

Back 79

referring to or associated with adrenaline or the sympathetic nervous system

Front 80

Atrial fibrillation

Back 80

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

Front 81

cardiomyopathy

Back 81

enlargement and stiffening of the heart muscle

Front 82

cholinergic

Back 82

referring to or associated with acetylcholine or the parasympathetic nervous system

Front 83

ejection fraction

Back 83

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

Front 84

Inotropic

Back 84

relating to strength of heart muscle contraction

Front 85

Ischemia

Back 85

cell death occurring due to lack of oxygen

Front 86

lacrimation

Back 86

production of tears in the eyes, watering eyes

Front 87

miosis

Back 87

pupil constriction; pin-point pupils

Front 88

muscarinic

Back 88

referring to or affecting the parasympathetic nervous system or muscarinic receptors

Front 89

mydriasis

Back 89

pupil dilation

Front 90

myocardial infarction; MI

Back 90

heart attack; blockage of blood and oxygen supply to the heart which usually results in damage

Front 91

ischemic stroke

Back 91

blocking of blood and oxygen supply to an area of the brain that results in damage to brain tissue

Front 92

hemorrhagic stroke

Back 92

bleeding in the brain resulting in damage to brain tissue

Front 93

urinary retention

Back 93

mechanical problem with bladder or bladder sphincter making it difficult to urinate

Front 94

What 2 classes of medications can be used to enhance bronchodilation?

Back 94

beta 2 agonists and muscarinic antagonists

Front 95

Which 2 classes of drugs might cause bronchoconstriction?

Back 95

beta 2 blockers and muscarnic agonists

Front 96

Which 2 classes of medications can be used to treat (reverse) bradycardia? (meaning that the drug will cause an increase in heart rate)

Back 96

beta 1 agonists and muscarinic antagonists

Front 97

Which 2 classes of medications can be used to treat (reverse) tachycardia? (meaning that the drug will cause a decrease in heart rate)

Back 97

beta 1 blockers and muscarinic agonists

Front 98

Which class of drugs might cause diarrhea?

Back 98

muscarinic agonists

Front 99

Which class of drugs might cause constipation?

Back 99

muscarinic antagonists

Front 100

Which 2 classes of drugs might increase blood pressure and cardiac output?

Back 100

adrenergic agonists and muscarinic antagonists

Front 101

potential interaction between ASA and NSAIDS

Back 101

Ibuprofen may block antiplatelet benefits of ASA, take ASA 2 hours before or 4 hours after ibuprofen to maximize the antiplatelet benefits of ASA

Front 102

3 antiplatelet drugs

Back 102

ASA, extended release dipyridamole + aspirin, clopdrogrel

Front 103

Aspirin MOA

Back 103

irreversibly inhibits the enzyme cyclooxygenase

Front 104

Aspirin SEs

Back 104

upset stomach, GI discomfort, GI ulcers; ASA withdrawal associated with increased risk of clots

Front 105

extended release dipyridamole + aspirin MOA

Back 105

inhibits phosphodiesterase and enhances antithrombotic potential of vascular wall

Front 106

extended release dipyridamole + aspirin SEs

Back 106

headache, GI upset, N/V, diarrhea, dizziness, up to 25% of patients intolerant

Front 107

Clopidrogrel MOA

Back 107

inhibits binding of platelets to each other by interfering with ADP; 3-7 day lag time for onset of action

Front 108

Clopdirogrel SEs

Back 108

GI disturbance, diarrhea, abdominal pain, dizziness, headache, excessive bleeding

Front 109

Aspirin during AMI

Back 109

325 mg chew and swallow

Front 110

ASA + Clopidrogrel after stent, ACS, or ischemic stroke

Back 110

for 3-9 months, then 1 drug for life

Front 111

Secondary Prevention with antiplatelets

Back 111

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

Front 112

Primary Prevention with antiplatelets

Back 112

aspirin for patients >/= 50 with HTN, DM, hypercholestermia, or smoker

Front 113

fluid monitoring in heart failure

Back 113

weigh every day for early signs of fluid retention

Front 114

drugs that cause sodium and water retention

Back 114

NSAIDS, high dose salicylates, COX-II inhibitors, rosiglitazone, pioglitazone, corticosteroids, androgens, estrogens

Front 115

Electrolyte imbalances that predispose patients to digoxin toxicity

Back 115

hypkalemia, hypercalcemia, hypomagnesemia

Front 116

ACE-I dosing

Back 116

start with small test dose of captopril 6.25 mg TID, attempt to titrate up to 50 mg TID (for captopril)

Front 117

Diuretic dosing

Back 117

spironalactone starting dose 12.5 to 25 mg daily; target dose 25 mg 1-2x/day

Front 118

Therapeutic Serum levels for digoxin

Back 118

0.5-1 ng/ml for HF; >/= 0.8 for inotropic benefits

Front 119

Most common drug interactions with digoxin

Back 119

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

Front 120

why lower digoxin serum concentrations in heart failure

Back 120

neurohormonal benefits happen at lower serum levels; positive inotropic effects achieved at higher serum levels could contribute to the cycle of worsening heart failure

Front 121

when is it appropriate to use a digoxin loading dose

Back 121

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

Front 122

why digoxin loading dose not used frequently

Back 122

increases risk of toxicity

Front 123

timing of checking serum levels with digoxin

Back 123

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

Front 124

dosing for digoxin loading dose

Back 124

0.5-1 mg total dose; 1/2 now, 1/4 in 6-8 hours, 1/4 in another 6-8 hours

Front 125

management of digoxin toxicity

Back 125

give potassium supplements, treat arrhythmias with appropriate agent, digoxin Immune Fab (Digibind) for severe toxicity

Front 126

pt education promoting compliance with meds in heart failure patients

Back 126

these drugs are shown to reduce mortality

Front 127

appropriate digoxin dosing in heart failure

Back 127

0.125-0.25 mg daily is usual maintenance dose; dosing is extremely patient variable

Front 128

need to check dig level when

Back 128

questionable compliance, lack of improvement, lack of ventricular control in A-fib, changing renal function, interacting meds, abnormal EKG, suspected toxicity

Front 129

why hypokalemia predisposes to dig toxicity

Back 129

low potassium inhibits the Na+/K+ pumps on cardiac cell, so does dig; makes it much more pronounced

Front 130

Antihypertensive with unfavorable effects in DM and why

Back 130

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

Front 131

Antihypertensive with unfavorable effect in gout and why

Back 131

loop and thiazide diuretics; both can cause/exacerbate gout/hyperuricemia

Front 132

antihypertensives with unfavorable effects in PVD and why

Back 132

non-selective BB: beta2 mediated peripheral vasoconstriction

Front 133

antihypertensives with unfavorable effects in bronchospastic disease and why

Back 133

non-selective BB: beta2 mediated bronchoconstriction

Front 134

antihypertensives with unfavorable effects in pregnancy

Back 134

ACE-I and ARB contraindicated in pregnancy because they are tetragenic

Front 135

antihypertensives with unfavorable effects in renal insufficiency/CKD and why

Back 135

K+ sparing diuretics: renal failure patients often hyperkalemic; Thiazide diuretics: ineffective if ClCr <30 ml/min

Front 136

ACE-I in patients on a diuretic, volume depleted, elderly, or at risk of orthostatic hypotension dosing

Back 136

starting dose should be reduced by 50%

Front 137

reducing side effects with ACE-I

Back 137

side effects reduced by 50% by waiting 6 weeks between dose increases

Front 138

why to use a test dose of captopril in HF patients

Back 138

because they have "revved-up" RAAS

Front 139

drug of choice for edema associated with congestive heart failure

Back 139

loop diuretic

Front 140

principles of loop diuretic dosing in management of heart failure

Back 140

higher doses needed; usually need K+ supplement

Front 141

digoxin MOA for positive inotropic effects

Back 141

inhibits Na+/K+ pumps of cardiac cell membranes, which increased intracellular Na+, which facilitates Ca++ influx; increased intracellular Ca++ leads to stronger muscle contractions

Front 142

digoxin MOA for neurohormonal effects

Back 142

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

Front 143

signs and symptoms of digoxin toxicity

Back 143

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

Front 144

Antihypertensives indicated in systolic heart failure and why

Back 144

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

Front 145

Antihypertensives indicated after MI and why

Back 145

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

Front 146

Antihypertensives indicated with increased CV risk and why

Back 146

BB: reduced cardiac risk in patients with angina and ACS

Front 147

Antihypertensives indicated with CKD and why

Back 147

ACE/ARB: can prevent progression of renal failure in some patients

Front 148

Antihypertensives indicated with tachycardia and why

Back 148

BB, verapamil, diltiazem: all slow heart rate

Front 149

Antihypertensives indicated with BPH and why

Back 149

alpha1 blocker: relax the smooth muscle of the bladder neck and prostate, which improves urine flow

Front 150

MOA for alpha2 adrenergic agonists

Back 150

stimulate alpha2 receptors of brain stem which inhibits norepinephrine; results in decreased sympathetic output, decreased BP, mildly decreased heart rate

Front 151

therapeutic uses for alpha2 adrenergic agonists

Back 151

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

Front 152

Major SEs for alpha2 adrenergic agonists

Back 152

orthostatic hypotension, dizziness, h/a, impaired ejaculation, sedation, dry mouth, constipation, urinary retention, blurred vision, rebound fluid retention

Front 153

contraindications/precautions for alpha2 adrenergic agonists

Back 153

abrupt withdrawal causes severe rebound HTN, taper over 3-4 days

Front 154

evidence regarding alpha2 adrenergic agonists

Back 154

shown to decrease BP, but not shown to reduce CV risk

Front 155

alpha2 adrenergic agonists

Back 155

clonidine, methyldopa

Front 156

alpha 1 blockers

Back 156

doxazosin, terazosin, prazosin, alfuzosin, tamsulosin

Front 157

alpha1 blocker MOA

Back 157

competitive blocking of alpha1 receptors, causing vasodilation, also relaxes smooth muscle of bladder neck and prostate

Front 158

therapeutic uses of alpha1 blockers

Back 158

BPH, Raynaud's disease, only used as alternative therapy in HTN

Front 159

major SEs of alpha1 blockers

Back 159

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

Front 160

Precautions for alpha1 blockers

Back 160

First Dose Effect: syncope after 1st dose, to minimize falls instruct patient to take QHS and initiate therapy with dose titration

Front 161

drug interactions with alpha1 blockers

Back 161

use with vardenafil and sildenafil causes hypotension; alfuzosin is contraindicated with potent CYP3A4 inhibitors

Front 162

BPH specific alpha1 blockers

Back 162

alfuzosin, tamsulosin only used for BPH; doxazosin, terazosin used for BPH/HTN

Front 163

ACE-I MOA

Back 163

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

Front 164

ACE-I therapeutic uses

Back 164

HTN, hypertensive urgencies, diabetic nephropathy, persons with proteinuria, stroke prevention, CHF/LVH, AMI

Front 165

ACE-I major SEs

Back 165

hypotension (esp. 1st dose), Bradykinin-related Ses: dry hacking cough, non-allergic rash, angioedema; hyperkalemia; acute reversible renal insuficiency

Front 166

contraindications/precautions ACE-I

Back 166

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.

Front 167

ACE inhibitors

Back 167

captopril, enalapril, lisinopril, benazepril, ramipril, quinapril, fosinopril, trandolapril, moexipril, perindopril

Front 168

ARBs

Back 168

losartan, candesartan, eprosartan, valsartan, irbesartan, temisartan, olmesartan

Front 169

ARB MOA

Back 169

directly bind and block angiotensin II receptor

Front 170

ARB therapeutic uses

Back 170

alternative to ACE-I in patient who cannot tolerate bradykinin related side effects; may be superior in preventing diabetic nephropathy

Front 171

ARB major SEs

Back 171

similar to ACE-I except less likely to cause cough and rash

Front 172

contraindications/precautions with ARBs

Back 172

history of angioedema with ACE-I is precaution, but many practitioners won't use under those conditions; contraidicated in pregnancy

Front 173

tetragenic

Back 173

Any substance or agent that is capable of interfering with normal embryonic development and can produce non-heritable birth defects.

Front 174

Normal blood pressure

Back 174

<120/80

Front 175

Prehypertension

Back 175

120-39/80-89

Front 176

Stage 1 hypertension

Back 176

140-159/90-99

Front 177

Stage 2 hypertension

Back 177

>/= 160 / >/= 100

Front 178

Hypertensive Crisis

Back 178

>180/120

Front 179

Major determinant of SBP

Back 179

cardiac output

Front 180

Major determinant of DBP

Back 180

TPR

Front 181

Isolated Systolic HTN

Back 181

SBP >/= 140 with DBP <90

Front 182

Systolic or Diastolic greater predictor of cardiovascular risk

Back 182

SBP

Front 183

how carvedilol differs from other beta blockers

Back 183

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?

Front 184

Increased risk of orthostatic hypotension

Back 184

elderly, diabetic, severe volume depletion, baroreflex dysfunction, autonomic insufficiency, use of venodilators (BB, alpha blockers, nitrates, phosphodiesterase inhibitors)

Front 185

Orthostatic hypotension

Back 185

SBP drop >20 or DBP drop >10 when changing from supine to sitting or sitting to standing

Front 186

Cardioselective BB MOA

Back 186

selectively block beta1 receptors; dec. HR, force of contraction, cardiac workload, and O2 demand; block juxtaglomerular cells, blocking renin release

Front 187

Cardioselective BB Therapeutic Uses

Back 187

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)

Front 188

Cardioselective BB Major Side Effects

Back 188

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

Front 190

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

Front 191

Cardioselective BB

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acebutolol, atenolol, betaxolol, metoprolol, bisoprolol, esmolol

Front 192

Non-selective BB

Back 192

propranolol, nadolol, pindolol

Front 193

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

Front 194

ISA BB

Back 194

acebutolol, pindolol

Front 195

acebutolol therapeutic use

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afib with underlying bradycardia

Front 196

Non-selective BB MOA

Back 196

block beta1 & 2 receptors

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Non-selective BB Therapeutic Uses

Back 197

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

Front 198

Non-selective BB Major Side Effects

Back 198

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

Front 208

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

Front 209

CCB other notes

Back 209

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

Front 212

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

Front 214

Thiazide Diuretics other notes

Back 214

ineffective in pts with ClCr < 30ml/min, beta blockers may increase hyperglycemic effect in DMII

Front 215

Thiazide Diuretics

Back 215

hydrochlorothiazide, chlorthalidone, metolazone, chlorothiazide, indapamide

Front 216

Loop Diuretics MOA

Back 216

block Na+ reabsorption in ascending limb of the loop of Henle

Front 217

Loop Diuretics Therapeutic Uses

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Drug of choice for edema assoc with CHF or RF, acute pulmonary edema

Front 218

Loop Diuretics Major Side Effects

Back 218

orthostatic hypotension, dehydration, hypokalemia, electrolyte imbalance, ototoxicity, prerenal azotemia

Front 219

Loop Diuretics contraindications/precautions

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Do not take QHS, higher doses may be needed in RF & HF, synergy with thiazides

Front 220

Loop Diuretics Other Notes

Back 220

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

Front 221

Loop diuretics

Back 221

furosemide, bumetanide, torsemide

Front 222

K+ sparing diuretics (aldosterone antagonists)

Back 222

spironolactone, eplerenone

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K+ sparing diuretics (not aldosterone antagonists)

Back 223

amiloride, triamterene

Front 224

K+ Sparing Diuretics (aldosterone antagonists) MOA

Back 224

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

Front 227

K+ Sparing Diuretics (aldosterone antagonists) Precautions/Contraindications

Back 227

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

Front 228

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

Front 229

K+ Sparing Diuretics (not aldosterone antagonists) MOA

Back 229

inhibit Na+ reabsorption and K+ elimination at the distal renal tubule

Front 230

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

Front 232

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

Front 234

compelling indication: recurrent stroke prevention

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ACE + thiazide: combination shown to reduce recurrent stroke; ARB also shown to reduce risk

Front 235

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

Front 236

compelling indication: left ventricular dysfunction (systolic heart failure)

Back 236

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

Front 238

Compelling Indication: CAD, increased CV risk

Back 238

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

Front 239

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

Front 240

HMG-CoA Reductase Inhibitors MOA

Back 240

inhibit HMG-CoA Reductase in liver--the catalyst in rate limiting of cholesterol synthesis

Front 241

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

Front 244

Dietary Cholesterol Absorption Inhibitors MOA

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prevents cholesterol absorption through intestinal villi; only works for dietary cholesterol, not genetic

Front 245

Dietary Cholesterol Absorption Inhibitors Therapeutic Uses

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decrease LDL, decrease Tg, good synergy with statin

Front 246

Dietary cholesterol absorption inhibitors major side effects

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GI upset

Front 247

Niacin MOA

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unknown

Front 248

Niacin Therapeutic Uses

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decrease LDL and Tg, most effective for increasing HDL, decrease risk of CV death & MI

Front 249

Niacin Major Side Effects

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flushing, itching, GI, N/V, diarrhea, heaptotoxicity, exacerbation of peptic ulcers and gout

Front 250

Bile Acid-Binding Resins MOA

Back 250

binds bile acids in intestines; body then must break down cholesterol to make more bile acid

Front 251

Bile Acid-Binding Resins Therapeutic Uses

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adjunct therapy or for intolerance of statins, decrease LDL

Front 252

Bile Acid-Binding Resins Major Side Effects

Back 252

may increase Tg, constipation, heartburn, nausea, gas, belching, bloating

Front 253

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%

Front 255

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

Front 257

Bile Acid-Binding Resins Appropriate Safety Monitoring

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monitor VLDL closely; contraindicated if Tg >500mg/dL

Front 258

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

Front 259

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)

Front 260

patient instruction for niacin

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pre-medicate with ASA or ibuprofen 30 minutes before each dose to reduce side effects

Front 261

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

Front 262

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%

Front 263

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

Front 264

determining goal LDL by number of risk factors

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0-1 risk factors: <160; 2+ risk factors: <130; existing CHD: <100

Front 265

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

Front 269

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)

Front 270

3 classes of drugs used to treat angina

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nitrates, BB, CCB

Front 271

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

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venous pooling, headache, orthostatic hypotension, lightheadedness, dizziness, hypotension, flushing

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importance of nitrate-free interval

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tolerance develops very quickly

Front 275

how to provide nitrate free interval

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need 8-12 hour interval daily; take off patches at noc; for BID po take at 8 and 2, or equivalent

Front 276

treatment for acute angina attacks

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SL nitro tabs or spray

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prophylactic treatment for angina

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nitro ointment/patch/SR capsules, isosorbiade dinitrate tabs, isosorbide mononitrate tabs

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pt instructions for SL nitro use

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under tongue x1 q5 minutes until pain relieved up to 3 doses; if no relief seek emergency care

Front 279

treatment goal for unstable angina

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reduce risk of MI and death

Front 280

treat unstable angina with

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IV nitrates, BB, CCB, heparin & ASA, IV morphine; EKG, coronary catheterization

Front 281

majority of angina is due to

Back 281

obstruction of the coronary vessels by atherosclerotic plagues

Front 282

Stable exertional angina pectoris is

Back 282

exertion related with a predictable pattern

Front 283

variant angina pectoris (Prinzmetal's) description

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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

Front 284

variant angina is caused by

Back 284

vasospasms of the coronary artery

Front 285

treatment goal for stable exertional angina pectoris

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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

Front 287

Alternative treatments for stable angina

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CCB or long-acting nitrates

Front 288

drug to use when patient doesn't respond to triple anti-anginal therapy

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ranolazine

Front 289

other drugs in the treatment plan for stable angina

Back 289

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

Front 290

Bottom Line: statins

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drug of choice for most patients; tolerated well; strongest evidence of reduced m/m

Front 291

Bottom Line: Niacin

Back 291

cheap, works great, not well tolerated, decreases morbidity, doesn't decrease mortality

Front 292

Bottom Line: Bile Acid-Binding Resins

Back 292

used for synergy, or alone in mild cases

Front 293

Bottom Line: Fibrates

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drug of choice to decrease Tg; also evidence of decreased m/m

Front 294

If cholesterol is just a little high, then

Back 294

try lifestyle modifications alone; if not effective, then add meds

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If cholesterol is >20 points high, then

Back 295

start meds and lifestyle changes