NURSING 210 Pharmacology Compete Drug List Graded A

Hypertension 1 Cont. Hypertension 2
Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s
1
GN: Furosemide  Block Na+ & Cl-­­ in the loop of  HTN  Hypokalemia (< 3.5 mEq/L) GN: Spironolactone  Aldosterone Antagonist  HTN  Hyperkalemia (> 5 mEq/L)
TN: Lasix Henle  greatest amount of  Pulmonary Edema  due to  Risk of fatal dysrhythmias TN: Aldactone  Blocks a Transcription factor  Edema  Risk of dysrhythmias
diuresis High Filtration  Dehydration & electrolyte receptor  Blocks protein  Offset K+ loss  Endocrine effects:
Class: Loop Diuretics Class: K+ Sparing Diuretics
 High Ceiling  Higher  Edema (Hepatic & Renal imbalance  Low Na+, K+, Cl-­­ synthesis causes =  Heart Failure -­­ Gynecomastia,
dysfunction)  Hypotension AA  Delayed action (48hours) (heart & vasculature) -­­ Menstrual irregularities
maximum efficacy  achieves
 Hyperglycemia (diabetes)  Endocrine effects  anti-­­androgen Blocking Aldosterone blunts -­­ Impotence
plateau at a higher doses
 Hyperuricemia (gout)  Retention of K+ & Excretion of cardiac remodeling DDI’s
 Occurs even if GFR is low
Pregnancy Category C  Kidney disease preferred  OTOTOXICITY Pregnancy Category C Na+  Hirsutism & Acne (endocrine effects) (+) combo with Thiazide or Loop
(i.e. Poor Kidney functions)
 Massive/Rapid fluid removal (when meds push to fast)  Poor diuresis Diuretic to offset K+ loss
DDI’s (--) Ace-­­I (increase K+ levels) 
 Decrease Electrolytes: Hyperkalemia
 K offset by K+ Sparing
+

Diuretics drugs  advantageous  Directly Inhibits Na+ Channel  HTN  Hyperkalemia (> 5 mEq/L)
GN: Triamterene
 K+  Digoxin toxicity  Faster Onset  Edema Risk of dysrhythmias
 Na+   Li toxicity
TN: Dyrenium
 No Endocrine effects  Offset K+ loss
 NSAIDS decrease diuretic effect Class: K+ Sparing Diuretics  Poor diuresis  NO EFFECT ON HF
Block Prostaglandin synthesis ↓renal blood flow
Prostaglandins vasodilate
Combo toxicity Nursing Implications: K+ Level (3.5--5.5 mEq/L)  COMMIT TO MEMORY
Monitor baseline and ongoing: Weight, Blood Pressure, Pulse, Respiration, Electrolytes, Blood Glucose Edema, Hearing Loss
 Ototoxic drugs
 Other anti-­­hypertensive drugs
K+ Loss K+ Gain
Loop Diuretics & Thiazides Spironolactone & Triamterene
GN: Hydrochlorothiazide  Block Na+ & Cl-­ in early DCT  HTN  Same as Loop Diuretics but
TN: HydroDIURIL  Require functional GFR   Edema LESS SEVERE Signs of Hypokalemia (Low K+) Signs of Hyperkalemia (High K+)
because it acts in the tubule  Most widely used & first to  Hypokalemia (< 3.5 mEq/L) • Irregular heart beat  Dysrhythmias & Hypotension •Muscle twitching and weakness
Class: Thiazide Diuretics
 Lower amount of diuresis prescribe  Risk for dysrhythmias
•Muscle weakness/cramping/flaccid paralysis •Numbness in hands and feet and around mouth
than Loops Diuretics  NO OTOTOXICITY
Pregnancy Category B  Has a dosage plateau  Lower amount of dehydration •Leg cramps •Nausea and diarrhea
and electrolytes changes than •Extreme thirst
Loops Diuretics •Confusion
Eat K+ Rich Foods No K+ supplements needed
• Spinach, citrus, bananas and nuts




3 4

Cont. Hypertension 3 Cont. Hypertension 4
Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s

GN: Verapamil  Vasodilatations on blood  HTN  Bradycardia GN: Propranolol  Beta1  HTN  Beta1-­­
TN: Calan VESSELS (smooth muscle of blood  Coronary Artery Disease  Shortness of Breath TN: Inderal Heart:  Decreases C.O.  Angina Pectoris Heart Failure & mask the sign of
vessels  VSM)  Dysrhythmias  Weight gain (HR &  Force of Contractility)  Dysrhythmias hypoglycemia
Class: Ca2+ Channel Blocker  HEART (myocardium, SA & AV node) Class: Beta Blockers Kidney:  Renin =  BP
(SVT, Atrial Flutter, A-­­Fib)  Peripheral Edema Adrenergic Antagonist Beta1 & Beta 2
 Myocardial Infraction (which is dysrhythmias )
Non-­­Dihydropyridine Reduced HR (SA node)  Diabetes (i.e. swelling of ankles or feet)  Beta2  Beta2
NDH CCB Reduced Conduction Velocity BB Lungs:  Bronchoconstriction Bronchoconstriction
Most Widely used
(AV node)
Reduced contractility (Myocardium) Notify Prescriber Blood Vessel:  Vasoconstriction Anti--Hypertension Inhibition of glycogenolysis 
 Negative Inotropic Agent  Constipations Liver & Skeletal Muscle:  Medications hypoglycemia when pt is on
 Negative Chronotrope DDI’s Glycogenesis insulin
 Beta Blockers (Less effective in African Americans) DDI’s
 Negative Dromotrope
(reduces cardiac activity) Asthma: Activation of Beta 2
BETA BLOCKERS
 Digoxin arteriole restriction in Lungs 
 Grapefruit Juice REDUCES VASCULAR bronchoconstriction
(Inhibits elevates drug level= toxicity) RESISTANCE
Cardiac Suppression  Beta1  HTN  Bradycardia
GN: Metoprolol
GN: Nifedipine  Vasodilatations on blood  HTN  Reflex Tachycardia Heart:  Decreases C.O.  Angina Pectoris (Chest PX)  AV Heart Block
VESSELS (smooth muscle of blood  Stable & Variant Angina (Fact acting formulation drugs has worst TN: Lopressor
TN: Adalat vessels (VSM)  reduces BP) effect on heart  baroreceptor has no time Class: Beta Blockers
(HR &  Force of Contractility)  Mask signs of hypoglycemia
Pectoris Kidney:  Renin =  BP but does not affect glycogenolysis
Class: Ca2+ Channel Blocker to re-­­adjust) Selective Adrenergic Antagonist Beta1
Dihydropyridine  Peripheral Edema Mainly used for HTN
BB
(i.e. swelling of ankles or feet) BETA BLOCKERS
CCB
No affect on cardiac cells REDUCES VASCULAR
Notify Prescriber (Less effective in African Americans)
RESISTANCE

GN: Prazosin  Competitive antagonist of  HTN  Orthostatic Hypotension
 Chronotrope--  HR (SA Node) Dromotrope--  Heart Conductance (AV Node) Inotrope--  Heart Contractility TN: MiniPress alpha1 adrenergic receptor   Benign Prostatic Hyperplasia  Reflex Tachycardia
Positive you will increase Negative you will decrease. dilation of arterioles & veins (BPH) (because of muscle relaxation
Class: Alpha Blockers
Selective Adrenergic Antagonist  Decrease BP effects in bladder)
Negative Chronotrope Decrease HR (e.g. BB’s, Verapamil, Digoxin) Alpha1  Relaxation of smooth muscle
Positive Chronotrope Increase HR (e.g. Epinephrine) in bladder  promotes
Negative Dromotrope Decrease AV nodal activity and Heart conductance (e.g. BB’s, Verapamil, Digoxin) Mainly used for HTN
voiding
Positive Dromotrope Increases AV nodal activity (e.g. Epinephrine)
Negative Inotrope Decreases Heart contractility (e.g. BB’s & Verapamil)
Positive Inotrope Increases Heart contractility (e.g. Digoxin, Epinephrine)

, 5 6

Cont. Hypertension 5 Cont. Hypertension 6
Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s

GN: Captopril will end with  ACE--Inhibitor/Kinase   Treatment  First Dose Orthostatic GN: Lebetalol  Block Both Alpha1 & Beta HTN  Similar to Non-­ Selective BB’s
Enalapril 🢙decreases Angiotensin II HTN, HF, Nephropathy & MI Hypotension TN: Trandate receptors Bradycardia,
TN: Capoten production = preventing: ⮎ Angiotensin II • Vascular Alpha1 blocks = Slowed AV conduction,
 Prevent Class: BOTH Alpha & Beta
⚫ Peripheral & Renal Monitor BP daily promotes dilation Bronchoconstriction/Asthma
Class: ACE Inhibitor or Vasoconstriction a MI & Stroke Persistent Cough Adrenergic  Similar to Alpha Blocker
• Cardiac Beta1 reduces =
ACE-­­I  ⮮ Blood Volume big reason why patients would stop using it
HR & Contractility Orthostatic Hypotension
 ⮮Cardiac & Vascular Reduce Risk of CV Mortality  Decrease ACE/Kinase II • Juxtaglomerular cell Beta1
 leads to  increase Bradykinin blocks = decreases Renin
remodeling
(Bradykinin irritates the throat)
 K+ Retention Diabetes & Asthma Pt’s: GN: Sodium Nitroprusside  Breaks down to release Nitric HTN Emergencies  Minimal Reflex Tachycardia
 Hyperkalemia
⚫ 🠅 Increase Bradykinin level No Hypoglycemia TN: Nipride Oxide Potent venous and  Excessive Hypotension
Pregnancy Category D No Bronchoconstriction
 Aldosterone if too rapidly administered
Class: Vasodilators arterial vasodilator Fastest Acting
like Beta Blockers GI Upset  Thiocyanate toxicity in kidney
No Hyperglycemia
(Take with food)
Administration: IV Infusion Antihypertensive Agent after prolonged administration greater
 Angioedema than 3 days
like Loop and Thiazides
Bradykinin induced increase in
Immediate onset and Short
Diuretics  Cyanide poisoning
capillary permeability  duration if too rapidly administered
Giant wheals, edema of tongue, (>5 ug/kg/min)
(Less effective in African Americans)
glottis and pharynx
Drugs for Pre--Eclampsia Renal Disease
Rare but fatal! Preferred meds are Alpha/Beta Blockers Preferred meds are ACE--I and ARB's.
Treat with Epinephrine Loop diuretic better than Thiazides diuretic.
(e.g. Labetalol)
GN: Losartan will end with  Angiotensin II Receptor Similar to ACE--I  Angioedema MgSO4-­­ prevent and treat eclampsia via multifactorial
TN: Cozaar Blockers  leads to  Treatment Bradykinin induced increase in MOA (vasodilation and diuretic activities)
Heart: Reduces Heart Rate HTN, HF, Nephropathy & MI capillary permeability  NO ACE--I, ARB’s, or Diuretics! K+ Sparing Diuretics is not recommended.
Class: Angiotensin II
VSM  Vasodilation Giant wheals, edema of tongue, Diabetes African American Elderly
Receptor Blocker or PNS/CNS: Reduced Afterload  Prevent glottis and pharynx
ARB’s MI & Stroke Preferred meds are ACE inhibitors, ARB's, CCBs, Diuretics, CCBs & Diuretics & Beta Blockers
Kidney: Reduces Na+ & Cl-­
reabsorption Rare but fatal!
Not: Alpha/Beta Blockers are most tested and shown
Pregnancy Category D No Cough Treat with Epinephrine  Diuretics only in low doses b/c promotes more effective than ACE--I efficacious
No Significant Hyperkalemia hyperglycemia or Beta Blockers Monitor for hypotension
 Beta Blockers promote Hypoglycemia & Mask signs
of hypoglycemia




7 8

 Heart Failure 1  Cont. Heart Failure 2
Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s

GN: Spironolactone  Aldosterone Antagonist  Heart Failure  Hyperkalemia (> 5 mEq/L) GN: Losartan will end with  Angiotensin II Receptor Similar to ACE--I  Angioedema
TN: Aldactone  Blocks a Transcription factor Blocking Aldosterone blunts  Risk of dysrhythmias
TN: Cozaar Blockers  leads to  Treat Bradykinin induced increase in
receptor  Blocks protein Cardiac Remodeling  Endocrine effects: Heart: Reduces Heart Rate  Heart Failure capillary permeability 
Class: K+ Sparing Diuretics synthesis causes =
Class: ARB’s or Angiotensin
 HTN -­­ Gynecomastia, VSM  Vasodilation HTN, Nephropathy & MI Giant wheals, edema of tongue,
AA  Delayed action (48hours)  -­­ Menstrual irregularities II Receptor Blocker
 Edema PNS/CNS: Reduced Afterload glottis and pharynx
 Endocrine effects  anti-­­androgen   To Offset K+ Loss -­­ Impotence Kidney: Reduces Na+ & Cl-­­  Prevent
 Retention of K+ & Excretion of (heart & vasculature) DDI’s: reabsorption MI & Stroke Rare but Fatal!
Na+ (+) combo with Thiazide or Loop Treat with Epinephrine
 Poor diuresis  Hirsutism & Acne (endocrine effects) Diuretic to offset K+ Loss No Cough
(--) Ace-­­I (increase K+ levels)  No Significant Hyperkalemia
Hyperkalemia
GN: Propranolol  Beta1  Heart Failure  Beta1-­­
GN: Captopril will end with  ACE--Inhibitor/Kinase   Heart Failure  First Dose Orthostatic TN: Inderal Heart:  Decreases C.O. Targets Cardiac Remodeling Heart Failure & mask the sign of
Enalapril 🢙Decreases Angiotensin II Targets Cardiac Remodeling Hypotension Class: Beta Blockers
(HR &  Force of Contractility)
 Myocardial Infraction hypoglycemia
⮎ Angiotensin II Kidney:  Renin =  BP  HTN (which is dysrhythmias )
TN: Capoten production = preventing: Adrenergic Antagonist Beta1 & Beta 2
⚫ Peripheral & Renal ACE-­­I have beneficial effects in Monitor BP daily  Beta2  Angina Pectoris  Beta2
Class: ACE Inhibitor or Heart Failure because they elevate BB Lungs:  Bronchoconstriction Bronchoconstriction
Vasoconstriction Persistent Cough  Dysrhythmias
ACE-­­I  ⮮ Blood Volume
Bradykinin  protect from big reason why patients would stop using it
Blood Vessel:  Vasoconstriction Inhibition of glycogenolysis 
Cardiac Remodeling  Decrease ACE/Kinase II
 ⮮Cardiac & Vascular Liver & Skeletal Muscle:  hypoglycemia when pt is on
 leads to  increase Bradykinin Glycogenesis insulin
remodeling Reduce Risk of CV Mortality
(Bradykinin irritates the throat) DDI’s
 K+ Retention
 Hyperkalemia Asthma: Activation of Beta 2
⚫ 🠅 Increase Bradykinin level HTN Nephropathy & MI BETA BLOCKERS
 Aldosterone arteriole restriction in Lungs 
GI Upset REDUCES VASCULAR bronchoconstriction
 Prevent (Less effective in African Americans)
MI & Stroke
(Take with food) RESISTANCE
 Angioedema GN: Metoprolol  Beta1  Heart Failure  Bradycardia
Bradykinin induced increase in Heart:  Decreases C.O. Targets Cardiac Remodeling  AV Heart Block
Diabetes & Asthma Pt’s: TN: Lopressor
capillary permeability  (HR &  Force of Contractility)
 Angina Pectoris (Chest PX)  Mask signs of hypoglycemia
No Hypoglycemia Class: Beta Blockers Kidney:  Renin =  BP
No Bronchoconstriction Giant wheals, edema of tongue,  HTN but does not affect glycogenolysis
Selective Adrenergic Antagonist Beta1
like Beta Blockers glottis and pharynx
BB BETA BLOCKERS
No Hyperglycemia
like Loop and Thiazides Rare but fatal! REDUCES VASCULAR Mainly used for HTN
Diuretics Treat with Epinephrine RESISTANCE
(Less effective in African Americans) (Less effective in African Americans)

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 HF3 Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Dysrhythmia: A--Fib
Supraventricular or Atrial Fib or Atrial Flutter Class II Beta Blockers
GN: Digoxin  Blocks Na+/ K+ ATPase   2nd Line Heart Failure  Cardiac: Dysrhythmia (Most common & not as harmful b/c does not affect C.O.) Class IV Calcium Channel Blockers
TN: Lanoxin Promotes Ca+ accumulation
(in cardiac smooth muscle)
Mainly for Symptomatic Relief Causes Fatal Dysrhythmias 
Class: Positive Inotropic Increases automaticity in: High risk of STROKE!!! Requires Anticoagulant Therapy: WARFARIN
Increased Contractility 
Agent consequences are Does Not prolong life Purkinje Fibers
(shorten in women) Ventricular Myocardium Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s
- increased C.O. Sign & Symptoms:
- decreased sympathetic tone GI effects: Anorexia, N/V
- increased urine production Treats Dysrhythmias-- but not CNS Effects: Fatigue
GN: Class II-­­Propranolol: Beta receptors and Ca2+ All Anti--Dysrhythmics Class II Propanolol:
the first line of drug because it Nonselective Beta1&2 channels are linked/coupled can CAUSE Dysrhythmias Heart (Beta1)
- Decrease Renin release Visual disturbances
cause dysrhythmias Adrenergic Antagonist in cardiac cells! •Bradycardia
No Effects on Cardiac Remodeling Class IV-­ Verapamil: Ca2+  Rate Control • AV Block
DDI’s:  Slow SA node
Channel Blockers ⮎ Drug Therapy Goal: •Heart failure
K+ Dependent Effects Drugs:  ↓ AV nodal conductance
Nursing Implications: Positive Inotropic agent Class: Class II (BB) Reduce Conductance
 Reduces myocardial
• Hypotension
Low Level of K+  Digoxin effects
Before you administer Digoxin ⮎Promote cholinergic (PNS) Therapeutic Range: Delay ventricles contraction by Lung (Beta2)
(Thiazides & Loop Diuretics) & Class IV (CCB) contractility
Check HR by taking pt’s effects on the heart  reducing 0.5--0.8 ng/ml  Commit to memory decreasing AV conductance to • Promote Bronchoconstriction
High Level K+  Digoxin effects
Apical Pulse activity in the SA node  Take levels 6-­­8 hrs after support max filling of ventricles (Contraindicated: asthma)
(ACE--I and Spironolactone) Remember the
If <60 beats/min decrease contractility administration Liver (Beta2)
negative dromotropic
Negative Chronotropic agent Ca2+ Channel Blockers effects: Negative Dromotropic agents • Hypoglycemia
WITHHOLD activity of
⮎ reduces SA node activity   Blocks the elimination = BB’s & Verapamil are why
(Contraindicated: diabetes)
& decrease HR  ECG: Prolong PR
• PK: ↑ Digoxin levels they are used for Atrial Fib
Notify Prescriber Negative Dromotropic agent ⮎Risk for Toxicity Class IV-­ Verapamil:
(Rate Control)
⮎ reduces AV node activity  • PD: ↓ Activity of Contractility in Heart
The negative dromotropic &
cardiac conductance the heart  Bradycardia
chronotropic effects of digoxin are  AV block
why you need to take the apical ⮎ Risk for Sub--therapy
pulse before administering digoxin.  Heart failure
ANTIDOTE: VSM
 Fab Antibody Fragment  Hypotension
(Digibind, Digifab)  Edema
 Stop Digoxin and K+ wasting Intestinal smooth muscle
diuretics (Loop & Thiazides)  Constipation (very common!)
 Anticholinergic drugs
(Atropine)
 Monitor K+




11 12

Dysrhythmia: V--Fib1 Cont. Dysrhythmia: V--Fib2
Ventricular Dysrhythmia or V--Fib or V--Tach Class I Sodium Channels Blockers Rhythm Control Drugs Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s
⮎Decrease ↓ C.O. VERY DANGEROUS Class III Potassium Channel Blockers
Treatment of choice: Cardioversion Outpatient Procedure Class I & III Used when drugs are indicated  Blocks  Cardio toxicity--
GN: Amioderone K+ Channel  Approved for severe
Acute vs. Long Term Therapy Prolong QT Ventricular Dysrhythmias Prolong QT – Torsade de Pointes!
TN: Cardorone ⮎Delay repolarization of fast ⮎ can use long--term
Drugs Mechanism of Actions Therapeutic Use Adverse Drug Effect’s/ DDI’s Class Potassium Channel potentials; Prolong action potential Slow elimination-- side effects
Blocker Class III duration and ERP
 BUT  Most effective drug persist for a long time
 Ventricular dysrhythmias  Cardio toxicity--  Blocks Na+, Ca2+
Channels, for Atrial Fib  Lung toxicity – LARRY
GN: Quinidine Rhythm Control Drugs Dyspnea, cough, chest pain
 Blocks Sodium Channels  Supraventricular Prolong QT – Torsade de Pointes! Beta ReceptorProlongs PR &
Class: Sodium Channels  Liver toxicity – LOVES
⮎Slows impulse conduction ⮎Long term management  Cinchonism-- (Gin & Tonic effect) Widen QRS
Blocker Class I--A Tinnitus, headache, nausea, vertigo, ⮎Reduce automaticity (SA & AV)
LFT’s, Anorexia, N/V, fatigue, jaundice,
 Blocks K+ Channels dark urine
disturbed vision Reduce conductance
⮎Delays repolarization  reducing  Cardio toxicity – CAKE
Administer: Orally Notify prescriber!! Pregnancy Category X
contractility HF-­­ SOB, poor exercise tolerance,
 Long Half-­ life  last weeks fatigue, tachycardia, wt gain
Like Class III drugs  Anticholinergic effects or months in the system
⮎Increased HR  Thyroid toxicity – TO
Pre-­ treat with CCB or BB Monitor thyroid hormone levels
ECG-- Widen QRS; Prolong QT  GI disturbances  Ophthalmic effects – Ohhh
Diarrhea report if decrease in visual acuity
take with meals for GI effects ECG-- Widen QRS; Prolong QT  Dermatologic effects -­­ Degree
DDI’s Avoid sunlamps, wear sun block
• Digoxin protein binding DDI’s
interaction and decrease  3A4 Inducers (therapeutic activity
elimination  Increase Risk for will decrease) & Inhibitors
(therapeutic activity will increase)
toxicity
⮎Grapefruit juice = toxicity
 Drugs that decrease K+
GN: Lidocaine Rhythm Control Drugs  Ventricular dysrhythmias  Sedation Diuretics Drugs-­­ Loop & Thiazide
Class: Sodium Channels  Blocks Sodium Channels ⮎Short term  Confusion increase risk for dysrhythmias
⮎Slows impulse conductance  Paresthesia  Others Drugs that prolong QT
Blocker Class I--B  Local Anesthetic  Blocks
 Reduce automaticity(?) interval (Torsade de Pointes)
⮎Unknown reason transmission of action potential in
Administration-- IV or IM nerves decreases sensation
Toxic effects
Rapid first pass metabolism  Accelerate Repolarization  Convulsions
 Respiratory depression

ECG: No significant changes