Pharmacology for Cardiac, HTN, HLD, HF, Arrhythmias Flashcards
“Statins”-AKA
Are HMG CoA Reductase Inhibitors
Statin -MOA
Inhibit LDL synthesis, increase LDL catabolism and have some non steroidal anti-inflammatory activity
Statin -AE
Hepatic Toxicity- elevated transaminases
Myopathy and Rhabdomyolysis
Neuropathy
Small increased risk of DM with high doses
Statin- Contra
Pregnancy category X
Lactation
Active or Chronic Liver disease
Relative-concomitant use of cycolosporins, gemfibrozil and niacin
Statin- Drug interactions
CYP substrate Atorva-3A4 Prava-None Rosuva-limited 2C9 Simva- 3A4&3A5-don't use Myopathy when used with Cyclosporine, gemfibrozil, niacin, azole antifungals and erythromycin
GrapeFruit?
Is a CYP3A4 inhibitor… inhibits metabolism of Atorva and simva causing increase in circulating blood levels
Statin- other Interactions
May potentiate oral anticoagulants
Statin Myopathy Risk Factors
Small body frame,
end stage renal disease or multi system diseases, perioperative,
multiple meds
Statin Monitoring
Check ALT and CK at baseline, document preexisting muscle symptoms
Check fasting lipid panel at 2 months and then every 6-12 months
Recheck ALT and CK as indicated
Monitor for new onset DM, consider lowering dose if 2 consecutive LDL are lower than 40mg/dL
Lipophilic
Atorvastatin
Hydrophilic
Pravastatin and Rosuvastatin
High intensity Statin
Atorvastatin 80mg daily
Rosuvastatin 40Mg Daily
Moderate Intensity Statin
Atorvastatin 20mg Dail
Rosuvastatin 10 mg daily
Low Intensity Statin
Pravastatin 10 mg daily
High intensity Statins are for
lowering LDL by 50%
Moderate statins lower
LDL 30-50%
Clinical ASCVD
Group 1
High intensity STatin if<75
Moderate Intensity if >75 or not candidate for HIS
LDL>190
Group 2
High intensity Statin , moderate if not a candidate
DM and 40-75 yoa
Group 3
High Intensity Statin with ASCVD>7.5%
Moderate intensity for ASCVD <7.5%
ASCVD>7.5%
Group 4
Moderate to high intensity based on Pt
Nonstatins
Use if Triglycerides >500mg/dL
Pt cannot tolerate recommended statin dose or achieve expected statin response
Fibric Acids
Fenofibrate 145 mg daily
Fibric Acid MOA
increases VLDL clearance and decreases VLDL synthesis
Fibric Acid Therapy
Decreases LDL5-20% increases HDL 10-20%
Get a baseline ALT, ALK Phos, repeat at 6-12 weeks
Yearly ALK and FLP
Fibric Acid-AE and Drug interactions
GI complaints
Possible increased effects of warfarin and sulfonylureas
Fibric Acid Contraindications
Hepatic and or severe renal dysfunction
Pre-existing gall bladder disease
Bile Acid Resins(BAR)
Not really used or helpful
Colestipol 4gm BID
Bile Acid Resins(BAR) MOA
Decreases LDL 15-25%
Increase in LDL catabolism, Decrease in Cholesterol absorption,
May increase TG and VLDL
Bile Acid Resins(BAR) AE
Contraindications
GI symptoms- constipation, flatulence, nausea
CI-Monotherapy in TGs>500
-Familial hyperlipidemia
-Hx of Severe constipation
Bile Acid Resins(BAR) Drug interactions
Problems with compliance
-Binds to many coadministered acidic drugs, decreases absorption of Digoxin, warfarin, thyroxine, thiazides, beta blockers, TCN, PCN, Amiodarone
Decreases bioavailability of statins
Take BAR 1 hour Before or 4 hrs after
Bile Acid Resins(BAR) Monitor
FLP at 6 weeks and yearly
Nicotinic Acid MOA
Niacin 1-2 gm TID
decreases LDL and VLDL synthesis
Lowers LDL 5-25% and Increases HDL 15-35%
Nicotinic Acid AE
Flushing of skin, glucose intolerance and increased UA
Hepatotoxicity
Nicotinic Acid contra
Liver disease(absolute cont) DM type 2 Gout and Hyperuricemia
Nicotinic Acid Monitor
Baseline AL, Alk Phos,
6-12 weeks ALT, all phos, Uric acid, BGL, and FLP
Yearly ALT, alk Pos, FLP
Ezetimibe
Zetia 10mg daily
Blocks Cholesterol absorption
Drops LDL by 15% increase HDL by 3%
Ezetimibe AE and Contra
AE- Fatigue, abd pain, diarrhea, back pain, arthralgia
Cont- Combination with statin in active liver disease or with persistent LFT elevations
PCSK9 inhibitors
Evolocumab- SQ q2-4 weeks
PCSK9 inhibitors MOA
Prevents PCSK9 from degrading Liver LDL receptors
Decreases LDL 60%
PCSK9 inhibitors Downside
$14,000/year
Fish Oil
W/O CHD eat fish 2/week
with CHD 1 gm EPA DHA preferably from fish oil
Fish Oil
Omega 3 fatty acid can lower TG, Prescription is Lovaza($184/month)
Class 1a AAD MOA
Sodium channel blockers
Alters the myocardial cell membrane,
Slows conduction velocity, prolongs refractory phase and decreases automaticity
Class Ia AAD Example
Sodium channel blockers
Procainamide
Class Ia AAD Indication
Sodium channel blockers
Supraventricular and ventricular arrhythmias
Class 1a AAD AE
Sodium channel blockers
Widens QRS, Prolongs QT, bradycardia, hypotension, worsening CHF and torsades des pointes
Class 1a AAD Contra
Sodium channel blockers
Hypersensitivity to procainamide, 2nd and 3rd degree HB
Class 1a AAD Monitoring
Sodium channel blockers
MOnitor serum concentration especially in renal failure Pt
Class Ib AAD
Sodium channel blockers
Blocks the rapid influx of sodium ions-
Lidocaine
Class 1C AAD Example
Sodium channel blockers
Flecainide
Class IC AAD MOA
Sodium channel blockers
Conduction slows
Slows conduction in the purkinje fibers and av nodes
Class IC AAD Indications
Sodium channel blockers
SVT, converting fib to NSR
Class IC AAD AE
Sodium channel blockers
dizziness, headache, syncope, SOB, arrhythmias, worsening HF
Class IC AAD Contraindications
Sodium channel blockers
2nd/3rd degree HB, recent MI, cariogenic shock, HF and ischemic heart disease
Class IC AAD monitoring
Sodium channel blockers
monitor for drug interactions CYP system
Class II AAD Example
Beta Blockers
Metoprolol Succinate
Class II AAD MOA
Beta Blockers
Slows conduction velocity, prolongs refectory phase, decreases automaticity, slows AV node conduction
Class II AAD Indications
Beta Blockers
supra ventricular and ventricular rhythms
Class II AAD AE
Beta Blockers
Bradycardia, worsening HF, bronchospasm, hypotension
Class II AAD Contra
Beta Blockers
2nd/3rd degree HB, decompensated HF,
HR<45bpm
Class II AAD Monitoring
Beta Blockers
do not stop suddenly, reflex tacky and HTN, educate Pt on HR and BP
metoprolol tartrate
immediate release
Metoprolol Succinate
extended release
Class III AAD Examples
Potassium Channel Blockers
Amiodarone
Sotalol
Class III AAD Amiodarone-MOA
Increases the action potential
Class III AAD Amiodarone-
Indications
First line for VF/VT in cardiac arrest, stable Vtach, supra ventricular tachs,
Class III AAD Amiodarone-
AE
IV- Hypotension, bradycardia, blocks, phlebitis,
PO-Corneal deposits, optic neuritis, n/v/c, Anorexia, pulmonary fibrosis, elevated LFTs, blue discoloration
Class III AAD Amiodarone-
Contra
2nd/3rd degree HB
Sick SInus syndrome
Class III AAD Amiodarone-Monitoring
EKG monitoring, cautious with asthma Its, annual CXR, LFTs every 6mo, PFTs and Optho if symptoms
CYP interactions
Class III AAD- Sotalol MOA
Prolongs atrial and ventricular refractory period, also has Beta Blocker properties
Class III AAD- Sotalol Indications
Supraventricular and ventricular rhythms
Class III AAD- Sotalol AE
Bradycardia, Torsades, Worsening HF, blocks, bronchospasm
Class III AAD- Sotalol Contra
2nd/3rd degree HB, bradycardia, HF, asthma, and long QT syndrome
Class III AAD- Sotalol Monitoring/special
Pt must be hospitalized for 3 days for initiation of therapy, avoid other qt prolonging drugs, do not stop suddenly
Class IV AAD- Calcium Channel Blockers
Example
Diltiazem
Class IV AAD- Calcium Channel Blockers MOA
Nondihydropyridine- Slows conduction throughAV node
Class IV AAD- Calcium Channel Blockers Indications
PSVT, Afib/A flutter
Class IV AAD- Calcium Channel Blockers AE
dizzy, headaches, edema, blocks, bradycardia, worsening HF, and hypotension
Class IV AAD- Calcium Channel Blockers contra
WPW, caution in HF
Class IV AAD- Calcium Channel Blockers Special considerations
Negative inotrope, careful in combo with BB, dig or clonidine, CYP interactions
Digoxin MOA
Acts on AV node through parasympathetic simulation that increases vagal tone
Digoxin Indication
Controls ventricular rate in supra ventricular rhythms(Afib) and in HF does not convert afib into NSR
Digoxin- AE
anorexia, n/v/d, headache, vertigo, HB, brady
Digoxin- contra
2nd and 3rd degree HB
Digoxin- Special/monitoring
narrow therapeutic window,
requires loading dose
Adenosine MOA
Acts on the atrioventricular node to slow conduction and inhibit reentry pathways
adenosine Indications
PSVT