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Pharmacotherapy Preview Program
(P3)
Module 3
Hypertension
Antiarrhythmics
Brandon Dyson, PharmD, BCPS
Diuretics
• Thiazides
– HCTZ
• K sparing
– Triamterene,
amiloride
A.
B.
C.
D.
• Loop
– Furosemide,
bumetanide,
torsemide
• Aldosterone
antagonist
– Spironolactone,
eplerenone
E.
F.
G.
H.
I.
J.
MOA: Na channel blockade in collecting
duct, increased K reabsorption
MOA: inhibit Na-K-CL cotransporter in
loop of Henle
MOA: competitive antagonism of Na-Cl
transporter in distal tubule
MOA: competitive antagonist at
aldosterone receptor; inhibits
mineralcorticoid receptors
Less effective if CrCl <30
Often used with HCTZ
Alleviate congestive sxs of HF
AE: dose related ototoxicity, ↓ Mg, ↓
Ca, “sulfa” allergy
AE: hypokalemia
AE: hyperkalemia
Case Study: HTN
Reducing Sympathetic Tone
You start a hypertensive patient with asthma on low dose
Metoprolol (Lopressor).
• Why did you pick this drug from the others in its class? What
are other drugs in this class?
• What important patient education would you provide?
• What drug would be a good choice for someone with HTN and
BPH?
HTN: Case Study
A 35 y/o obese, hypertensive female comes to see you because she
is newly pregnant, and her OB was not sure whether she should
keep taking her Propranolol. You would best counsel the patient by
saying:
A. Your OB is an incompetent idiot. You should stop the
Propranolol, start Methyldopa (Aldomet) and find a new OB
B. Your OB is an incompetent idiot. Continue the Propranolol,
follow up monthly with me during pregnancy and find a new OB.
C. I’m glad your OB referred you to me for your BP management.
Stop the Propranolol, start Methyldopa and follow up with me in
1-2 weeks for BP check.
D. I’m glad your OB referred you to me for your BP management.
Continue the Propranolol and follow up monthly with me during
your pregnancy.
HTN: Case Study Cont’d
• How would you counsel the patient on Methyldopa?
• What is the MOA, clinical uses and it’s advantages?
• What is another centrally acting antihypertensive
drug?
Renin-Angiotensin Pathway
A. ACE, ACEIs
B. Renin; direct
renin inhibitors
C. Angiotensin II
receptors; ARBs
D. Aldosterone;
aldosterone
antagonists
HTN: Renin-Angiotensin Modulation
ACEI
ARB
Lisinopril, captopril, ramipril,
enalapril, fosinopril, quinapril,
benazepril
• MOA
Losartan, valsartan,
candesartan, irbesartan,
telmisartan, eprosartan
• MOA
• Clinical Use
• Clinical Use
• AE’s/CI’s
• AE’s/CI’s
Direct Renin Inhibitor: Aliskiren (Tekturna)
HTN: Calcium Channel Blockers
Dihydropyridine
Non-Dihydropyrdine
Amlodipine, felodipine,
nifedipine ER, nicardipine,
nimodipine
Verapamil, diltiazem
• MOA
• MOA
• Clinical Use
• Clinical Use
• AE’s/CI’s
• AE’s/CI’s
Drugs & Potassium Effects
Hypokalemia
Hyperkalemia
A.
B.
C.
D.
E.
F.
G.
H.
I.
J.
HCTZ
Spironolactone
Furosemide (Lasix)
Aliskiren (Tekturna)
Lisinopril
Nifedipine
Verapamil
Losartan
Metoprolol
Diltiazem
HTN: Vasodilators
Nitroprusside
Hydralazine
Fenoldopam
Minoxidil
A.
Stimulates NO formation in endothelial
cells arteriole dilation
B. Used for alopecia as well as HTN
C. K+ channel openers
D. Gives off NO  arteriovenous dilation
in smooth muscle
E. Active metabolite can cause
hypotensive effects for 24 hrs despite
short t 1/2
F. Renal and hepatic insufficiency risk
of cyanide toxicity
G. D1 stimulation  diuresis, natriuresis
H. Adverse effect – SLE
I. Rapid first-pass metabolism
J. Available parenteral form
K. Used in HTN urgency/emergency
Case Study: HTN
A 55 y/o WM with type II DM comes into your free clinic
with c/o constant headaches and BP of 160/100. He
stopped taking medications several years ago because he
couldn’t afford it.
• What would be his BP goal and the best initial
medication regimen for his HTN based on JNC8
recommendations?
• What labs would you want to monitor?
• How would you counsel him about lifestyle changes?
Case Study Cont’d
The patient comes back 2 weeks later. Labs show
normal BUN/creatinine, LDL>100. His BP is 148/90,
and he has developed a dry, hacking cough.
• What is a likely cause for the cough?
• How would you change his medication regimen?
Cardiac Conduction
ECG
ERP
Class 1 Antiarrhythmics – Na+ Channels
Class Ia
Procainamide, Quinidine,
Disopyramide
Class Ib
Lidocaine, Mexilitine
Class Ic
Flecainide, Propafenone,
Moricizine, Encainide
A. Decreases conduction velocity
B. Shortens repolarization and QT
interval
C. Prolongs repolarization
D. Prolongs QT  risk for TdP
E. Most potent Na channel blockade –
depressive and proarrhythmic
effects
F. Used for ventricular arrhythmias,
not effective for SVT
G. Anticholinergic effects
H. AEs are primarily neurological
Class II Antiarrhythmics – Beta receptors
• This class is also known as
Beta Blockers
• This class has a (+/-)
_________ inotropic
effect.
• They slow SA node firing
and conduction through
the AV node
Class III Antiarrhythmics – K+ Channels
•
Sotalol, Amiodarone, and
Dronedarone also have B-blocking
action.
• Dofetilide and Ibutilide can cause
Torsades de pointes and pts must
be monitored closely in a
hospitalized setting.
• Dronedarone is similar in structure
to amiodarone.
• Amiodarone has several CYP450
drug interactions including with
warfarin.
Case Study: AFib
You have a patient being treated for atrial fibrillation
by his cardiologist who comes into your office
complaining that his skin is turning blue.
• What drug is he likely taking that might cause this?
• How does this drug work?
• What monitoring/tests should be done while taking
this drug?
Class IV Antiarrhythmics – Ca++ Channels
• Affect depolarization via blockade
of Calcium Channel causing
slowed SA node firing and slowed
conduction through the AV node
• The __________ (nonDHP/DHP)
CCB’s are primarily used, such as
__________ and __________.
• These drugs cannot be used to
treat Ventricular arrhythmias.
• Major AEs include bradycardia,
excessive AV blockade, heart
failure, hypotension and
constipation.
Which of the following delay cardiac
cell repolarization (prolong QT), thus
increasing the risk of TdP?
A.
B.
C.
D.
E.
F.
G.
Quinidine
Procainamide
Lidocaine
Ibutilide
Sotalol
Dofetilide
Mexilitine