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
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
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*
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
5
Q
+Warfarin
Therapeutic Uses
(3)
A
- DVT/PE
- Afib
- heart valve replacement
6
Q
+Warfarin PK
- Bioavailability > __%
- Onset __-__hrs (full effect takes __-__ days)
- Duration ~ __-__ days
- Metabolism through what?
- _____ variations in these isoenzymes
- interpatient _____ in ___ requirements
- Highly _____ bound (~90%)
A
- 90%
- 24-72 hrs (5-7 days) bc you have to deplete all clotting factors
- 2-5 days
- Enzymes CYP450, 2C9, 3A4
- genetic
- variability, dose
- protein
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
- Lower doses of __ mg once daily for (4)
- 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
8
Q
+Warfarin
AE (4)
A
- Bruising
- Bleeding
- Skin necrosis
- Teratogenic
CANNOT TAKE IN PREGNANCY
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)
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
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
12
Q
+Afib Algorithm
- Mechanical heart _____ or moderate or severe mitral ______
- If yes -> What meds?
- If no -> Estimate ____ risk based on (2) risk factors
A
- valves, mitral stenosis
- VKA (IA)cd
- Stroke, CHA2DS1 - VASc risk factors
for heart valves and mitral stenosis -> straight to warfarin
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)
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
- ____ is indicated (assess for _____, correct reversible ___ risk factors)
A
-
> 2
- OAC, contraindications, bleeding
- LAA occluding
- NOAC
- VKA
- OAC, contraindications, bleeding
15
Q
+Afib Algorithm
NOAC (4)
A
Non Vitamin K Antagonist Oral Anticoagulants
Apixaban
Rivaroxaban
Dabigatran
Edoxaban
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
17
Q
Antiarrhythmic Medications
- Class I = ______ channel blockers
- Class II = BB (Propranolol, Metop, Esmolol)
- Class III = ______ channel blockers
- Class IV = CCB (Verapamil, Diltiazem)
- Misc = Digoxin, Adenosine
A
- Class I = Sodium Channel Blockers
- Class III = Potassium Channel Blockers
18
Q
Class I Sodium Channel Blockers
- Class Ia
- Quinidine (Quinidex)
- Procainamide (Procanbid)
- Disopyramide (Norpace)
- Class Ib
- ________
- Mexiletine (Mexitil)
- Class Ic
- ________
- ________
A
- Class Ia
- Class 2a
- Lidocaine (Xylocaine)
- Class Ic
- Flecainide (Tambocor)
- Propafenone (Rythmol)
19
Q
Class III Potassium Channel Blockers
(3)
A
Sotalol (Betapace)
Amiodarone (Cordarone)
Dofetilide (Tikosyn)
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
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
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
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*
24
Q
+Amiodarone
AE
A
Although is not very cardiotoxic in HF - effects literally every other organ in our body
25
**+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
* 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
26
**+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
* TdP, Diarrhea
* CYP 3A4 inhibitors
* QTC \> 440msec, CrCL \< 20ml/min (renally eliminated)
* Hospitalization, 2-3, EACH\*, 5
* NOT, increase MORTALITY
27
Adenosine
## Footnote
* 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)
* SVT, sinus tachycardia
* polymorphic, wide -\> Vfib
* 0.6-10 secs
* blood, endothelial
* AE
* bradycardia, cardiac arrest
* flushing, bronchospasm, HA
28
Dyslipidemia
## Footnote
Cholesterol (\_\_\_\_\_\_)
* Essential component of cell \_\_\_\_\_
* Precursor to ____ compounds
* Derived from ____ and ____ absorption
* Fuel used to generate energy for ____ contraction and _____ reactions
Lipoproteins
* membranes
* steroid
* liver, diet
* muscle, metabolic
29
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:
30
**+Drug Therapies for Dyslipidemia**
**(6)**
* **HMG-CoA reductase inhibitors**
* **Niacin**
* **Fibrates**
* **Cholesterol absorption inhibitors**
* **Omega-3 fatty acids**
* **PCSK9 Inhibitors**
31
HMG CoA Reductase Inhibitors
## Footnote
MOA
Otherwise known as "\_\_\_\_\_"
Inhibits enzyme responsible for coverting HMG-CoA to mevalonate (rate-limiting step in production of cholesterol)
"Statins"
32
HMG CoA Reductase Inhibitors
## Footnote
Indications
**Drug of Choice for LDL reduction**
* Also significantly reduces death and recurrent MI in pts with CAD
33
**+HMG CoA Reductase Inhibitors**
| (4)
**Atorvastatin (Lipitor)**
**Pravastatin (Pravachol)**
**Simvastatin (Zocor)**
**Rosuvastatin (Crestor)**
34
**+HMG CoA Reductase Inhibitors**
## Footnote
* Lowers ___ concentrations (24-60%)
* Lowers ___ concentrations (7-40%)
* ____ HDL concentrations (5-15%)
* LDL
* TG
* Raises
35
HMG CoA Reductase Inhibitors
## Footnote
AE
* \_\_\_pathy - ____ aches, pains -\> r\_\_\_\_\_\_
* Increased ____ enzmes -\> fulminant hepatic \_\_\_\_
* New onset _____ (w high intensity therapies)
* Myopathy -\> Muscle aches, pains -\> rhabdomyolysis
* liver -\> failure
* diabetes
36
HMG CoA Reductase Inhibitors
## Footnote
Contraindications (2)
Severe active liver disease
Pregnancy
37
HMG CoA Reducatse Inhibitors PK
38
**+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
* simvastatin, atorvastatin, lovastatin
* inhibitors (*GRAPEFRUIT JUICE)*
* pravastatin, rosuvastatin
* Fibrates, gemfibrozil, finofibrate
* Niacin, \>1g/day
39
Niacin
## Footnote
MOA
Inhibits mobilization of free fatty acids from peripheral adipose tissue to the liver
40
Niacin
## Footnote
Effects on lipids:
* Lowerls LDL concentrations (\_\_-\_\_%)
* Lowers TG concentrations (\_\_-\_\_%)
* Raises HDL concentrations (\_\_-\_\_%)
* 15-25%
* 20-50%
* 15-25%
41
Niacin
## Footnote
(3)
Niacin (immediate release niacin)
Slo-Niacin (sustained release niacin)
Niaspan (extended release niacin)
42
Niacin
## Footnote
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
* 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
**+Fibrates**
## Footnote
MOA
Reduces rate of lipogenesis in the liver
44
**+Fibrates**
Effects on lipids
* Lowers LDL concentrations with normal TG (\_\_-\_\_%)
* Raises LDL concentrations with very high TG (\_\_%)
* Lowers TG concentrations (\_\_-\_\_%)
* Raises HDL concentrations (\_\_-\_\_%)
* 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
**+Fibrates**
## Footnote
Agents (2)
**Gemfibrozil (Lopid)**
**Fenofibrate (TriCor)**
46
Fibrates
AE (4)
## Footnote
Contraindications (1)
* Dyspepsia
* Gallstones
* Myopathy
* Increased hepatic transaminases
* Severe renal or hepatic disease
47
**+Cholesterol Absorption Inhibitors**
MOA
Inhibits cholesterol absorption by the small intestine
48
**+Cholesterol Absorption Inhibitors**
**(1)**
**Ezetimibe (Zetia)**
49
**+Cholesterol Absorption Inhibitors**
## Footnote
Effects on Lipids
* Lowerls LDL concentrations (\_\_-\_\_%)
* Raises HDL concentrations (\_-\_%)
* Lowers TG concentrations (\_\_-\_\_%)
* 18-20%
* 1-5%
* 7-17%
50
**+Cholesterol Absorption Inhibitors**
Contraindications
* Active liver disease
* Possibly increased cancer risk, evidence conflicting
51
Omega-3 Fatty Acids
## Footnote
MOA
Uknown (reduction in TG synthesis)
52
**+Omega-3 Fatty Acids**
| (2)
**Lovaza**
**Vascepa**
*Prescribed not OTC*
53
Omega-3 Fatty Acids
## Footnote
* Lowers TG concentrations (\_\_-\_\_%)
* May raise LDL concentrations when TG concentrations are very high - only _____ (\_\_%)
* Raises HDL concentrations - only _____ (\_\_-\_\_%)
* 26-45%
* Lovaza, 45%
* Lovaza 11-14%
54
**+Vascepa**
FDA approved for?
(What type of med is it)
**CV risk reduction**
Omega 3 Fatty Acid
55
Omega-3 Fatty Acids
## Footnote
AE
Lovaza (3)
GI (burping, taste perversion, dyspepsia)
Inhibition of platelet aggregation
Bleeding
56
**+PCSK9 Inhibitors**
MOA
* mAb binds clirculating PCSK9 and prevents d\_\_\_\_\_ of \_\_\_\_\_
* _____ LDLR -\> so they can _____ blood \_\_\_\_-C
* \_\_-\_\_% LDL as a \_\_\_\_\_\*
* prevents degradation of LDLR
* increases LDLR -\> clear LDL
* **50-70%** , monotherapy
* Newest drugs*
* Inreasing recycling of LDL receptors that clears LDL*
57
Statins vs PCSK9 Inhibitors
58
Who may need PCSK9 Inhibitors?
## Footnote
(3)
* Statin intolerant
* Genetic disorder (FH)
* Uncontrolled on statins
59
Average Annual Cost of Therapy
60
**+PCSK9 Inhibitors**
| (2)
**Evolocumab (Repatha)**
**Alirocumab (Praluent)**
61
**+Evolocumab (Repatha)**
* Route
* _____ mg every 2 weeks
* _____ mg once monthly
* Is it FDA labeled for prevention of CV?
* Guideline recommended with \_\_\_\_\_\_
* SQ
* 140
* 420
* YES FDA labeled for prevention of CV events in pts with established ASCVD
* statins
62
**+Alirocumab (Praluent)**
## Footnote
* Route
* ___ mg every 2 weeks
* \_\_\_\_mg monthly
* Is it FDA labeled for prevention/reduction in CV events?
* Guideline recommended with \_\_\_\_\_
* SQ
* 75mg
* 300mg
* No *but still effective*
* statins
63
**+Major Recommendations for Statin Therapy for Atherosclerotic Cardiovascular Disease Prevention**
