Cardiac Pt 2 Arrhythmia, Dyslipidemia Flashcards

1
Q

Atrial Fibrillation

  • ___ventricular d_________ which occurs when the atria _____ instead of beating effectively
  • Results in loss of “atrial ___”
  • Also results in ____ of blood which could potentially ____
A
  • Supraventricular dysrhythmia , quiver
  • X “kick”
  • stasis, clot
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2
Q

AF Anticoagulation Statistics

  • AF accounts for 25% of all ____ in the elderly
  • AF is estimated to be responsible for 70,000 strokes/year
  • _____ ~62% RRR (regular rate and rhythm)
  • _____ ~ 22% RRR
  • Asbolute RR still depends on _____ risk
A
  • strokes
  • Warfarin
  • Aspirin
  • baseline
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3
Q

+Vitamin K Antagonists

(1)

A

Warfarin (Coumadin)

  • Warfain is a hideous drug - antiquity*
  • Factors II, VII, IX, and X all dependent on Vitamin K*
  • Fun fact: where was warfarin discovered? -* ts used in rat poison - rats eat it, bleed out, and die- Pts will say “im not gonna eat that rat poison!” you will an you’ll like it!
  • Aspirin more recently shown that it doesn’t really work bc more for arterial clots*
  • Warfarin name - Wisconsin Alumni Research Foundation = WARF*
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4
Q

+Warfarin

MOA

  • Inhibits synthesis of _____ _ dependent clotting _____ (4) and regulatory _____ (2)
  • Prevents ______ and _______ of new thrombi
  • No effect on? (2)
A
  • Vitamin K, clotting factors (II, VII, IX, X), proteins C and S
  • formation, propagation
  • circulating clotting factors, formed thrombi
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5
Q

+Warfarin

Therapeutic Uses

(3)

A
  • DVT/PE
  • Afib
  • heart valve replacement
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6
Q

+Warfarin PK

  1. Bioavailability > __%
  2. Onset __-__hrs (full effect takes __-__ days)
  3. Duration ~ __-__ days
  4. Metabolism through what?
    • ​​_____ variations in these isoenzymes
    • interpatient _____ in ___ requirements
  5. Highly _____ bound (~90%)
A
  1. 90%
  2. 24-72 hrs (5-7 days) bc you have to deplete all clotting factors
  3. 2-5 days
  4. Enzymes CYP450, 2C9, 3A4
    • genetic
    • variability, dose
  5. protein
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7
Q

+Warfarin Dosing

  • __ mg oral ____ daily
    • Lower doses of __ mg once daily for (4)
      • ex) one pt may require a very small dose (1 mg) wherease another may need higher doses (15mg) to achieve same level of anticoagulation
  • Dose adjustments based on what lab value?
A
  • 5mg once daily
    • 2 mg - elderly, frail, malnourished, liver failure
  • INR

Hideous drug bc HUGGEE interpatient variability - theres a website that helps us dose - but it even says 50% accuracy

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8
Q

+Warfarin

AE (4)

A
  • Bruising
  • Bleeding
  • Skin necrosis
  • Teratogenic

CANNOT TAKE IN PREGNANCY

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9
Q

+Warfarin

Drug and Food Interactions

A

Many drug-drug interactions

Drug-food interactions with foods high in Vitamin K - reduces effect of Warfarin (green leafy vegetables, chickpeas, tea)

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10
Q

+Reversal of Warfarin

What medication?

  • Promotes the ____ formation of _____ required for normal _____
  • Onset of action
    • PO: __-__ hrs
    • IV: __-__ hrs
  • AE (1)
  • Caution with?
A

Vitamin K

  • hepatic, factors, clotting
  • Onset
    • 6-12 h
    • 1-2 h
  • Hypersensitivity with rapid IV admin**
  • Reinstitution of warfarin therapy
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11
Q

Reversal of Warfarin

  • _____
    • Factors (4)
    • Protein (2)
  • FDA approved for urgent reversal of warfarin therapy in adult pts with acute major _____ or requring reversal for an invasive _____
  • Dose is determined by patient ____ and pretreatment ___
  • Black box warning =
A
  • Kcentra a better reversal agent compared to vitamin K - can work better acutely
    • II, VII, IX, X
    • C, S
  • bleeding, procedure
  • weight, INR
  • increased risk fo arterial/venous thromboembolic events
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12
Q

+Afib Algorithm

  1. Mechanical heart _____ or moderate or severe mitral ______
    • If yes -> What meds?
    • If no -> Estimate ____ risk based on (2) risk factors
A
  1. valves, mitral stenosis
    1. VKA (IA)cd
    2. Stroke, CHA2DS1 - VASc risk factors

for heart valves and mitral stenosis -> straight to warfarin

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13
Q

+Afib Algorithm

  • If 0 risk factors =
  • If 1 risk factor =
A
  • No antiplatelet or anticoagulant tx (IIIB)
    • Rare- only for pts with only AFIB and nothing else
  • OAC should be considered (IIaB)
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14
Q

+Afib Algorithm

  • If > 2 risk factors
    • ____ is indicated (assess for _____, correct reversible ___ risk factors)
      • _____ o_____ devices may be considered in pts with clear contraindications for OAC (IIbC)
      • Group of Drugs
      • Group of Drugs
A
  • > 2
    • OAC, contraindications, bleeding
      • LAA occluding
      • NOAC
      • VKA
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15
Q

+Afib Algorithm

NOAC (4)

A

Non Vitamin K Antagonist Oral Anticoagulants

Apixaban

Rivaroxaban

Dabigatran

Edoxaban

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16
Q

Cardiac Electrophysiology

  • Na+ currents contribute to ________ while K+ and Ca2+ channels control ___________
  • Na+ channesl are ____ channels while Ca2+ channels consist of 2 types: __ (Long lasting) and __ (Transient)
  • Channels are mainly in 3 states: R____, O____, In_____ or C_____
A
  • Depolarization, Repolarization
  • fast, 2 types: L, T
  • Resting, Open, Inactivated or Closed
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17
Q

Antiarrhythmic Medications

  1. Class I = ______ channel blockers
  2. Class II = BB (Propranolol, Metop, Esmolol)
  3. Class III = ______ channel blockers
  4. Class IV = CCB (Verapamil, Diltiazem)
  5. Misc = Digoxin, Adenosine
A
  • Class I = Sodium Channel Blockers
  • Class III = Potassium Channel Blockers
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18
Q

Class I Sodium Channel Blockers

  1. Class Ia
    • Quinidine (Quinidex)
    • Procainamide (Procanbid)
    • Disopyramide (Norpace)
  2. Class Ib
    • ________
    • Mexiletine (Mexitil)
  3. Class Ic
    • ________
    • ________
A
  1. Class Ia
  2. Class 2a
    • Lidocaine (Xylocaine)
  3. Class Ic
    • Flecainide (Tambocor)
    • Propafenone (Rythmol)
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19
Q

Class III Potassium Channel Blockers

(3)

A

Sotalol (Betapace)

Amiodarone (Cordarone)

Dofetilide (Tikosyn)

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20
Q

Class Ic Antiarrhythmics

Propafenone

  • M____ taste, di_____, acute decompensated heart ____
  • Br_____, ____cardia, heart b____ (negative ___tropic and __-blocking properties)
  • Contraindicated in pts with ____ (Class III, IV), l___ disease, and v____ disease
  • DI: d____, w____, as well as drugs that inhibit ____ 2D6, 1A2, 3A4
A
  • Metallic, dizziness, HF
  • Bronchospasm, Bradycardia, block, ino, B
  • HF, liver, valvular
  • digoxin, warfarin, CYP

Generally - many antiarrhythmics not safe for HF - only one that is safe is AMIO

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21
Q

Clas Ic Antiarrhythmics

Flecainamide

  • D_____, tr____, acute decompensated heart ____ (negative inotropic effects)
  • Contraindicated in pts with __ __, C _ _, _____ disease
  • Drug interaction with _______
A
  • Dizziness, tremor, HF
  • HF, CAD, Valvular disease
  • Digoxin
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22
Q

+Amiodarone (Cordarone)

  • Possess pharmacologic effects from ___ ____ Vaughn Williams Classes
    • Blocks _____, ______, _____ channels
    • Anti____ properties
  • Drug of _____* in patients with ____ ____*
  • Used in (2)
A
  • all three
    • sodium, potassium, calcium
    • adrenergic
  • choice*, heart failure
  • atrial and ventricular arrhythmia
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23
Q

Amiodarone (Cordarone) PK

  • Pharmacokinetics
    • Formulations (2)
    • Erratic absorption when admistered ____
    • _____ half life ~ __-__ days
    • Highly _____
    • Metabolized through the _____
  • Potent ______ of CYP 3A4 and PgP
    • Many drug-___ interactions (2)
A
  • PK
    • PO, IV
    • PO
    • prolonged, 40-60 days
    • lipophilic
    • liver
  • Inhibitor
    • drug: Digoxin, Warfarin
  • ITS TAKES MONTHSS FOR amio to wash out - highly lipophilic*
  • Reeks havoc on Drug interactions -> since many of the pts that need amio are probably on dig and warfarin - creates a problem - when pt needs amio has to reduce empiric dose of dig or warf or else will get amio toxicity*
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24
Q

+Amiodarone

AE

A

Although is not very cardiotoxic in HF - effects literally every other organ in our body

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25
Q

+Class III Antiarrhythmics

Sotalol

  • Acute decompensated __, ____cardia, AV ____, wh____, ___ within _ days of initiation, b________
  • Contraindicated in pts with baseline (2)
  • ______ mandatory for initiation, obtain ___ every _-_ hrs after first __ doses, _____-dose every __ days
A
  • HF, Bradcardia, AV block, wheezing, TdP 3, bronchospasm
  • QTC > 440msec, CrCL <40ml/min (renally eliminated)
  • Hospitalization, QTC 2-3 hrs after 5 doses, double every 3 days
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26
Q

+Class III Antiarrhythmics

Dofetilide

  • _ _ _, D_____
  • Drug interactions with? (1)
  • Contraindicated in pts with (2)
  • ______ mandatory for initiation, obtain QTC _-_ hrs after ____* of the first __ doses
  • Does ___ increase ______ in pts with HF
A
  • TdP, Diarrhea
  • CYP 3A4 inhibitors
  • QTC > 440msec, CrCL < 20ml/min (renally eliminated)
  • Hospitalization, 2-3, EACH*, 5
  • NOT, increase MORTALITY
27
Q

Adenosine

  • Indications (2)
  • Do not give fo runstable or irregular ____morphic ____ complex tachycardia bc may cause degeneration to what heart rhythm?
  • Half life:
  • Rapidly removed from plasma through cellular elements of the ____ and by the uptake of the vascular _____ wall
  • AE
    • Cardiac (2)
    • Non-Cardiac (3)
A
  • SVT, sinus tachycardia
  • polymorphic, wide -> Vfib
  • 0.6-10 secs
  • blood, endothelial
  • AE
    • bradycardia, cardiac arrest
    • flushing, bronchospasm, HA
28
Q

Dyslipidemia

Cholesterol (______)

  • Essential component of cell _____
  • Precursor to ____ compounds
  • Derived from ____ and ____ absorption
  • Fuel used to generate energy for ____ contraction and _____ reactions
A

Lipoproteins

  • membranes
  • steroid
  • liver, diet
  • muscle, metabolic
29
Q

Adult Treatment Panel III: Lipid Classification (no on exam)

  1. LDL
    • ​​Optimal:
    • Near optimal/above optimal:
    • Borderline high:
    • High:
    • Very High:
  2. HDL
    • ​​Low:
    • High:
  3. Total Cholesterol
    • ​​Desirable:
    • Borderline high:
    • High:
  4. Triglycerides​​
    • Normal:
    • Borderline High:
    • High:
    • Very High:
A
30
Q

+Drug Therapies for Dyslipidemia

(6)

A
  • HMG-CoA reductase inhibitors
  • Niacin
  • Fibrates
  • Cholesterol absorption inhibitors
  • Omega-3 fatty acids
  • PCSK9 Inhibitors
31
Q

HMG CoA Reductase Inhibitors

MOA

Otherwise known as “_____”

A

Inhibits enzyme responsible for coverting HMG-CoA to mevalonate (rate-limiting step in production of cholesterol)

“Statins”

32
Q

HMG CoA Reductase Inhibitors

Indications

A

Drug of Choice for LDL reduction

  • Also significantly reduces death and recurrent MI in pts with CAD
33
Q

+HMG CoA Reductase Inhibitors

(4)

A

Atorvastatin (Lipitor)

Pravastatin (Pravachol)

Simvastatin (Zocor)

Rosuvastatin (Crestor)

34
Q

+HMG CoA Reductase Inhibitors

  • Lowers ___ concentrations (24-60%)
  • Lowers ___ concentrations (7-40%)
  • ____ HDL concentrations (5-15%)
A
  • LDL
  • TG
  • Raises
35
Q

HMG CoA Reductase Inhibitors

AE

  • ___pathy - ____ aches, pains -> r______
  • Increased ____ enzmes -> fulminant hepatic ____
  • New onset _____ (w high intensity therapies)
A
  • Myopathy -> Muscle aches, pains -> rhabdomyolysis
  • liver -> failure
  • diabetes
36
Q

HMG CoA Reductase Inhibitors

Contraindications (2)

A

Severe active liver disease

Pregnancy

37
Q

HMG CoA Reducatse Inhibitors PK

A
38
Q

+HMG CoA Reductase Inhibitors

Drug Interactions

  • CYP3A4 substrates (3)
    • Avoid strong CYP3A4 _____
    • Preferable to use (2)
  • _______: Increased risk of myopathy/rhabdo when coadministered with statins (risk is greater with g_____ than with f_____)
  • ______: doses > __g/day increases risk of myopathy/rhabdo
A
  • simvastatin, atorvastatin, lovastatin
    • inhibitors (GRAPEFRUIT JUICE)
    • pravastatin, rosuvastatin
  • Fibrates, gemfibrozil, finofibrate
  • Niacin, >1g/day
39
Q

Niacin

MOA

A

Inhibits mobilization of free fatty acids from peripheral adipose tissue to the liver

40
Q

Niacin

Effects on lipids:

  • Lowerls LDL concentrations (__-__%)
  • Lowers TG concentrations (__-__%)
  • Raises HDL concentrations (__-__%)
A
  • 15-25%
  • 20-50%
  • 15-25%
41
Q

Niacin

(3)

A

Niacin (immediate release niacin)

Slo-Niacin (sustained release niacin)

Niaspan (extended release niacin)

42
Q

Niacin

AE

  • ____glycemia/glucose ______
  • Hyper______
  • ___ distress (so take with ___ to lessen effects)
  • Increased hepatic ______ (______ release appears to be more hepatotoxic than other preparations)
  • F______
    • extended and sustained release are ____ likely to cause flushing
    • Minimized with ___ or ____ 30 min prior to niacin, taking at ___ time, and avoiding ___ beverages, ____ foods, and __ showers at time of admin
A
  • Hyperglycemia, glucose intolerance
  • Hyperuricemia
  • GI, food
  • Transaminases (sustained)
  • Flushing *its terrible! i call BS on asa/ibup helping
    • less
    • ASA, Ibuprofen, bed, hot, spicy, hot
43
Q

+Fibrates

MOA

A

Reduces rate of lipogenesis in the liver

44
Q

+Fibrates

Effects on lipids

  • Lowers LDL concentrations with normal TG (__-__%)
  • Raises LDL concentrations with very high TG (__%)
  • Lowers TG concentrations (__-__%)
  • Raises HDL concentrations (__-__%)
A
  • 2-20%
  • 45%
  • 30-55%
  • 18-22%
  • Excessively high triglycerides for a long period of time -> pancreatitis*
  • So a lot of times used to prevent pancreatitis more than cholesterol*
45
Q

+Fibrates

Agents (2)

A

Gemfibrozil (Lopid)

Fenofibrate (TriCor)

46
Q

Fibrates
AE (4)

Contraindications (1)

A
  • Dyspepsia
  • Gallstones
  • Myopathy
  • Increased hepatic transaminases
  • Severe renal or hepatic disease
47
Q

+Cholesterol Absorption Inhibitors

MOA

A

Inhibits cholesterol absorption by the small intestine

48
Q

+Cholesterol Absorption Inhibitors

(1)

A

Ezetimibe (Zetia)

49
Q

+Cholesterol Absorption Inhibitors

Effects on Lipids

  • Lowerls LDL concentrations (__-__%)
  • Raises HDL concentrations (_-_%)
  • Lowers TG concentrations (__-__%)
A
  • 18-20%
  • 1-5%
  • 7-17%
50
Q

+Cholesterol Absorption Inhibitors

Contraindications

A
  • Active liver disease
  • Possibly increased cancer risk, evidence conflicting
51
Q

Omega-3 Fatty Acids

MOA

A

Uknown (reduction in TG synthesis)

52
Q

+Omega-3 Fatty Acids

(2)

A

Lovaza

Vascepa

Prescribed not OTC

53
Q

Omega-3 Fatty Acids

  • Lowers TG concentrations (__-__%)
  • May raise LDL concentrations when TG concentrations are very high - only _____ (__%)
  • Raises HDL concentrations - only _____ (__-__%)
A
  • 26-45%
  • Lovaza, 45%
  • Lovaza 11-14%
54
Q

+Vascepa

FDA approved for?

(What type of med is it)

A

CV risk reduction

Omega 3 Fatty Acid

55
Q

Omega-3 Fatty Acids

AE

Lovaza (3)

A

GI (burping, taste perversion, dyspepsia)

Inhibition of platelet aggregation

Bleeding

56
Q

+PCSK9 Inhibitors

MOA

  • mAb binds clirculating PCSK9 and prevents d_____ of _____
  • _____ LDLR -> so they can _____ blood ____-C
  • __-__% LDL as a _____*
A
  • prevents degradation of LDLR
  • increases LDLR -> clear LDL
  • 50-70% , monotherapy
  • Newest drugs*
  • Inreasing recycling of LDL receptors that clears LDL*
57
Q

Statins vs PCSK9 Inhibitors

A
58
Q

Who may need PCSK9 Inhibitors?

(3)

A
  • Statin intolerant
  • Genetic disorder (FH)
  • Uncontrolled on statins
59
Q

Average Annual Cost of Therapy

A
60
Q

+PCSK9 Inhibitors

(2)

A

Evolocumab (Repatha)

Alirocumab (Praluent)

61
Q

+Evolocumab (Repatha)

  • Route
  • _____ mg every 2 weeks
  • _____ mg once monthly
  • Is it FDA labeled for prevention of CV?
  • Guideline recommended with ______
A
  • SQ
  • 140
  • 420
  • YES FDA labeled for prevention of CV events in pts with established ASCVD
  • statins
62
Q

+Alirocumab (Praluent)

  • Route
  • ___ mg every 2 weeks
  • ____mg monthly
  • Is it FDA labeled for prevention/reduction in CV events?
  • Guideline recommended with _____
A
  • SQ
  • 75mg
  • 300mg
  • No but still effective
  • statins
63
Q

+Major Recommendations for Statin Therapy for Atherosclerotic Cardiovascular Disease Prevention

A