Naplex (Cardiovascular Disorders)

Front 1

What drugs can cause or exacerbate hypertension?

Back 1

NSAIDs
Corticosteroids
Cyclosporine
Tacrolimus
Estrogens
Erythropoietin
Venlafaxine
Sympathomimetics
Cocaine

Front 2

What situations decrease your blood pressure goal to 130/80?

Back 2

Diabetes Mellitus
Chronic Kidney Disease
High CAD risk
Unstable Angina/ACS

Front 3

What situations decrease your blood pressure goal to 120/80?

Back 3

Heart Failure

Front 4

Thiazide diuretics inhibit Na reabsorption in the distal convoluted tubule. What are the primary side effects of these agents?

Back 4

Hypo K, Mg, Na
Hyper Ca
Hyperglycemia
Hyperuricemia

Front 5

What is the contraindication for these agents?

Back 5

Sulfa allergy

Front 6

Thiazide diuretics have a ceiling dose (Loop diuretics do not). What are the primary side effects of loop diuretics?

Back 6

Hypo K, Mg, Na, Ca
Hyperglycemia
Hyperuricemia
Metabolic alkalosis
Azotemia

Front 7

Effect on mortality in HF is not known in loop diuretics, but they decrease symptoms. What is the contraindication in these agents?

Back 7

Sulfa allergy

Front 8

What is an BUN:SCr ratio of >20:1 indicative of?

Back 8

Pre-renal azotemia/dehydration

Front 9

When using a potassium sparing diuretic, it is paramount to monitor for hyperkalemia. What other agents can increase potassium levels?

Back 9

ACEI's
ARB's
ARA's
NSAIDs

Front 10

K-sparing agent -->
Aldosterone Receptor Antagonist -->

Back 10

Triamterene
Spironolactone
***Hydrochlorothiazide often combined with K-sparing diuretics to curb K loss (Triamterene)

Front 11

What beta-blockers are approved for heart failure?

Back 11

Bisoprolol
Carvedilol
Metoprolol succinate (not tartrate)

Front 12

What are the primary side effects of beta-blockers?

Back 12

Bradycardia/Heart block
HF exacerbation
Bronchospasm
Fatigue
Decreased exercise tolerance
Depression
Glucose intolerance
Masked hypoglycemia in patients with DM

Front 13

What are the consequences of abrupt beta-blocker discontinuation?

Back 13

Angina
MI
Hypertensive emergency
***Must taper over 2 weeks***

Front 14

What are the contraindications to ACEI therapy?

Back 14

Pregnancy
History of angioedema or renal failure with prior use
Hyperkalemia
Bilateral renal artery stenosis

Front 15

Describe the primary side effects of ACEI's and differences between ARB's.

Back 15

Hyperkalemia, Renal insufficiency, Cough, Angioedema
ARB's --> Hyperkalemia, Renal insufficiency
Cough --> Switch to ARB
Angioedema --> Switch is controversial

Front 16

All calcium channel blockers have some degree of (-) inotropy except these two agents.

Back 16

Amlodipine
Felodipine

***These agents cannot cause heart failure exacerbation)

Front 17

What is a strange side effect of calcium channel blockers?

Back 17

Gingival hyperplasia

Front 18

Name the 3 alpha-1 antagonists

Back 18

Doxazosin
Prazosin
Terazosin
***Should not be first line therapy for hypertension (even in patients with BPH)

Front 19

What is the contraindication with these agents?

Back 19

PDE 5 inhibitor use (sildenafil, tadalafil, vardenafil) --> risk of hypotension

Front 20

Name the 2 alpha-2 agonists

Back 20

Clonidine
Methyldopa
***Decrease sympathetic outflow from the brain via binding to alpha-2 receptor

Front 21

What are the major side effects of alpha-2 agonists?

Back 21

Sedation
Orthostatic hypotension
Depression
Peripheral edema
Dry mouth
Bradycardia
Hepatitis (methyldopa)

Front 22

What clinical pearl is important with alpha-2 agonist therapy?

Back 22

Avoid abrupt discontinuation (as with beta blockers) and taper over 2 weeks

Front 23

What is the mechanism of hydralazine?

Back 23

Increased cyclic GMP
***Use if for refractory hypertension

Front 24

What is a strange side effect of hydralazine?

Back 24

Lupus-like syndrome
***Avoid in acute MI and aortic dissection

Front 25

Patient Education Pearls:

Back 25

Take diuretics in the morning to avoid nocturia
Diuretics can increase susceptibility to sunburn
Take alpha-1 antagonists at night to avoid orthostatic hypotension
Rise slowly when taking alpha-1 antagonists, alpha-2 agonists, or vasodilators

Front 26

What anti-hypertensives are safe to take in pregnancy?

Back 26

Methyldopa
Labetalol
Calcium channel blockers

Front 27

Dyslipidemia
Hyperlipidemia

Back 27

Refers to any lipid disorder
Refers to increased concentration of of a lipid such as cholesterol and triglycerides.

Front 28

What drugs increase your lipid concentrations

Back 28

Beta-blockers
Diuretics
Corticosteroids
Isotretinoin
Protease inhibitors
Cyclosporine
Estrogens

Front 29

Name the 5 major risk factors for coronary heart disease.

Back 29

Age > 45 (males), > 55 (females)
Cigarette smoking
HTN
HDL < 40
Family history of premature CHD (male < 55, female < 65)
(-) risk factor HDL > 60

Front 30

Name the disease states that automatically confer high CHD risk.

Back 30

PAD
Abdominal aortic aneurysm
Symptomatic carotid artery disease (ie. stroke, TIA)
DM
Stage 5 CKD
2 or more risk factors that confer 20% risk of CHD at 10 years (FRS)

Front 31

Name the 3 bile acid resins

Back 31

Cholestyramine
Colesevelam
Colestipol

Front 32

Name the primary side effects of these agents

Back 32

Constipation
Bloating
N/V
Flatulence
Increased triglycerides
***Bind to many drugs***

Front 33

What anti-lipid agents can increase LFT's and cause myopathy?

Back 33

Statins
Fibrates (Decreases TG, increases HDL)
Niacin (Most effective for increases in HDL)
***Monitor CK levels***

Front 34

What two anti-lipid drugs do you want to avoid?

Back 34

Statins - Gemfibrozil

Front 35

Which statins are 3A4 inhibitors? 2CP substrates?

Back 35

Atorvastatin, Lovastatin, Rosuvastatin, Simvastatin

Fluvastatin, Pitavastatin
***All can increase warfarin effects***

Front 36

What is ezetimibe effective in doing?

Back 36

You can add it to a statin to decrease LDL or to decrease statin dose if a patient is experiencing side effects

Front 37

What is a good counseling point for a patient taking a bile acid resin?
Niacin?

Back 37

Take other medications at least 1 hour before or 4 hours after the bile acid resin.
Administer with meals

Take at night (flushing)

Front 38

Statin potency (Greatest to Least)

Back 38

Rosuvastatin > Atovastatin > Simvastatin > Pravastatin = Lovastatin = Pitavastatin > Fluvastatin

Front 39

What is the difference between systolic and diastolic heart failure?

Back 39

systolic = contractility impaired + EF < 40%
diastolic = filling impaired + EF > 40%

Front 40

Drugs that cause/exacerbate heart failure

Back 40

Negative Inotropes (BB's, CCBs except amlo/felo, antiarrythmics (except amio, dofetilide), Na/H20 retention (NSAIDs, CS's, TZDs), sympathomimetics, direct cardiotoxins (anthracyclines, cyclophosphamide, trastuzumab)

Front 41

What should the BNP level be in acute decompensated heart failure?

Back 41

> 500 pg/mL

Front 42

Describe the NY Heart Association Functional Classifications

Back 42

I - LV dysfunction, but no physical limitations
II - Slight limitation (ordinary physical activity)
III - Marked limitation (ADL's)
IV - Symptoms at rest

Front 43

Describe the American College of Cardiology/AHA staging system

Back 43

A - High risk (HTN, CAD, DM)
B - Structural disease, no symptoms
C - Structural disease, symptoms
D - Refractory symptoms at rest despite maximal medical therapy

Front 44

What are the treatment guidelines based on? Describe them.

Back 44

ACC/AHA staging
A - Modify risk factors
B - ACEI + BB
C - ACEI + BB + diuretic (can also add on an ARA, use ARBs in those who aren't tolerating ACEI, Digoxin in patients that remain symptomatic, Hydralazine/Isosorbide dinitrate in AA's or if other agents are contraindicated)

Front 45

Continued

Back 45

D - Chronic positive inotropic therapy (Dobutamine, Milrinone), Mechanical circulatory support, Heart transplant, Hospice
***ARBs should not be considered equivalent to ACEIs in HF

Front 46

S/S of digoxin toxicity

Back 46

Visual disturbances
N/V
Confusion
Anorexia
Arrhythmia
***Predisposition to toxicity if hypokalemic, hypomagnesemic, or hypercalcemic

Front 47

Target digoxin level

Back 47

0.5-1 ng/mL (increased mortality if greater than 1)

Front 48

If you have to start amiodarone or dronedarone, what is the protocol with digoxin?

Back 48

Decrease dose by 50%
***No effect on mortality like BBs, ACEIs

Front 49

What is the difference between spironolactone and eplerenone?

Back 49

Spironolactone is a non-selective aldosterone receptor antagonist, and blocks androgen and estrogen levels (associated with endocrine side effects)

Front 50

Mechanism of Hydralazine
Mechanism of Isosorbide dinitrate

Back 50

Arterial vasodilation (Afterload)
Venous vasodilation (Preload)

Front 51

Side effect of Hydralazine, but not Isosorbide dinitrate

Back 51

Peripheral edema
Lupus-like syndrome
***Do Not use hydralazine alone (increased mortality)

Front 52

NTG
Nitroprusside
Nesiritide

Back 52

Venous vasodilation (decreased preload)
Arterial/Venous vasodilation (decreased preload/afterload)
BNP, Arterial/Venous vasodilation (decreased preload/afterload)
***Avoid nitroprusside in renal dysfunction

Front 53

Describe the effects of dopamine at varying concentrations

When do you want to avoid dopamine?

Back 53

Low - Dopamine (increased urine output)
Intermediate - Beta - 1
High - Alpha - 1
In patients with myocardial ischemia (also dobutamine)

Front 54

Mechanism of Dobutamine
Mechanism of Milrinone

Back 54

Beta - 1 and 2 agonist (increased CO and vasodilation)
PDE III Inhibitor (Increased CO and vasodilation)

Front 55

Unique side effect of dobutamine
Two other key differences between dobutamine and milrinone therapy

Back 55

Hypokalemia

Dobutamine can develop tolerance, and you do not want to use dobutamine in patients on a beta blocker

Front 56

Class 1A antiarrhythmics
Use

Back 56

Disopyramide
Procainamide
Quinidine
***All Class 1 agents are Na channel blockers to varying degrees
***Atrial/Ventricular arrhythmia

Front 57

Class 1B antiarrhythmics

Back 57

Lidocaine
Mexilitine
***Ventricular arrhythmia

Front 58

Class 1C antiarrhythmics

Back 58

Flecainide
Propafenone
***Atrial/Ventricular arrhythmia

Front 59

Important points for each Class 1 agent

Back 59

1A - Prolonged refractoriness, risk for TDP
1B - Can cause CNS toxicity
1C - Avoid in HF, structural heart disease

Front 60

Class III mechanism
Amiodarone, Dronedarone, Dofetilide, Ibutilide, Sotalol

Back 60

K channel blocker with Na, beta and Ca blocking (no effect on conduction velocity or automaticity)

Front 61

Amiodarone side effects

Back 61

Hypotension
Hypo/hyperthyroidism
Pulmonary fibrosis
Optic neuritis
Increased LFTs
Blue-gray skin discoloration

Front 62

Amiodarone indication

Back 62

Atrial/Ventricular (Stable VT, Pulseless VT, AF)
Half life 40-60 days

Front 63

Amiodarone
If LFTs increase -->
If TFTs abnormal -->
If Pulmonary abnormal -->
If vision abnormal

Back 63

Decrease dose
Treat thyroid
Discontinue
Discontinue

Front 64

Differences between Amiodarone and Dronedarone

Back 64

Dronedarone - Contraindicated in HF, concurrent use of 3A4 inhibitors or strong inducers, QT interval > 500 msec, pregnancy, severe hepatic impairment
Used only for atrial arrhythmia's
Shorter half life
Less likely to cause organ toxicity

Front 65

What is a major primary side effect of dofetilide, ibutilide, and sotalol?

Back 65

Torsades de Pointes

Front 66

Dofetilide indication
Ibutilide indication
Sotalol indication

Back 66

Atrial arrhythmia
Atrial arrhythmia
Atrial/Ventricular arrhythmia

Front 67

Difference between a NSTEMI and STEMI

Back 67

More platelets than fibrin (white clot)
More fibrin than platelets (red clot) - complete occlusion

Front 68

When are cardiac enzymes (troponin, CK-MB) present?

Back 68

Not in UA, but present in NSTEMI and STEMI

Front 69

When are EKG changes present and what are they?

Back 69

UA - ST-segment depression, T-wave inversion or nothing
NSTEMI - ST-segment depression, T-wave inversion or nothing
STEMI - ST-segment elevation

Front 70

***Acute pharmacologic management of UA/NSTEMI***
Morphine

Back 70

Given in those who continue to have chest discomfort despite the use of NTG

Front 71

NTG

Back 71

Chest discomfort/relief of symptoms
IV within the initial 48 hours if patients continue to have ischemia or present with HF or are hypertensive

Front 72

Beta-blockers

Back 72

Given within 24 hours in those without s/s of HF or have risk factors for cardiogenic shock (Age>70, systolic < 120, HR > 110 or < 60, heart block, reactive airway disease
Can use IV

Front 73

CCBs

Back 73

Non-DHP can be used if a contraindication to BB therapy exists and no evidence of LV dysfunction

Front 74

ACEIs

Back 74

Given within 24 hours to patients with pulmonary congestion or LVEF < 40% as long as they are not hypotensive/contraindicated

Front 75

ASA

Back 75

All patients should receive 162-325 mg at onset of chest pain (chewed and swallowed)
Continue daily for 1 month after baremetal stent implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation
Continue 75-162 mg indefinitely
If no stent --> 75-162 mg immediately

Front 76

Clopidogrel

Back 76

Alternative to ASA in patients who are allergic or have a major GI intolerance
Given to all patients however, regardless of PCI or conservative strategy is used and given with ASA
Continue to ASA for 12 - 15 months if bare metal stent is used, 1 months (ideally up to 1 year) if no stent is placed
D/C at least 5 days before CABG

Front 77

Prasugrel

Back 77

Alternative to clopidogrel
Faster inhibition than clopidogrel
Not recommended in patients > 75 years old or in those with prior history of stroke or TIA (bleeding risk)
D/C at least 7 days before CABG

Front 78

Glycoprotein IIb/IIIa receptor blockers (eptifibatide or tirofiban)

Back 78

PCI planned: Clopidogrel and/or a GPB can be initiated
Conservative strategy: Add eptifibatide or tirofiban to clopidogrel

Front 79

Anticoagulants

Back 79

PCI planned: UFH or enoxaparin added to antiplatelet therapy; fondaparinux or bivalirudin can be used alternatively
Conservative therapy: Either enoxaparin or fondaparinux should be added to anti-platelet therapy; UFH can be used alternatively

Front 80

***STEMI***
Others the same
Clopidogrel

Back 80

No stent: at least 14 days

Front 81

Fibrinolysis

Back 81

Should be used in patients presenting to a hospital without the capability to perform PCI or cannot perform PCI within 90 min of first medical contact (door to balloon time)
Should be initiated within 30 min of presenting to hospital (door to needle time)

Front 82

Anticoagulation

Back 82

Fibrinolysis: UFH, enoxaparin, or fondaparinux can be used and should be continued for up to 8 days
UFH should only be used if the treatment duration is < 48 hrs due to HIT risk with prolonged therapy
Primary PCI: UFH, bivalirudin, or enoxaparin

Front 83

Secondary prevention

Back 83

ASA, Clopidogrel (already stated)
BB - indefinitely
ACEI - indefinitely
ARA - patients with LVEF < 40% on optimal BB, ACEI therapy
Statins - indefinitely

Front 84

3 Glycoprotein IIb/IIIa inhibitors
Mechanism

Back 84

Abciximab
Eptifibatide
Tirofiban
Blocks GP receptor on platelets and prevents fibrinogen binding inhibiting platelet aggregation

Front 85

Med pearl for abciximab

Back 85

Abciximab is preferred to the other two in NSTEMI if there is no significant delay to PCI, otherwise the other two are preferred

Front 86

UFH mechanism

Back 86

potentiated antithrombin III thereby inactivating clotting factors IIa (thrombin), IXa, Xa, XIa, XIIa, and ultimately the conversion of fibrinogen to fibrin

Front 87

LMWH mechanism

Back 87

Similar to UFH, but primarily factor Xa

Front 88

Fondaparinux mechanism

Back 88

Selective inhibitor of factor Xa

Front 89

Bivalirudin

Back 89

Direct thrombin inhibitor

Front 90

What do you monitor for UFH, LMWH, and Fondaparinux?

Back 90

PT/aPTT (UFH)
CBC
Anti-Xa levels (LMWH)
S/S bleeding
***Fondiparinux contraindicated in CrCl < 30

Front 91

What do you monitor for Bivalirudin?

Back 91

PT/aPTT
ACT

Front 92

Protamine

Back 92

Reverses UFH, and LMWH (partially)

Front 93

If HIT is suspected

Back 93

DC UFH, and start DTI (argatroban, lepirudin)

Front 94

3 Fibrinolytics
Mechanism

Back 94

Reteplase
Tenectaplase
Tissue Plasminogen Activator (also used for ischemic stroke and PE)
Activates and converts plasminogen to plasmin, which degrades fibrin

Front 95

Antiarrhythmic drugs that you must adjust creatinine for

Back 95

Disopyramide
Procainamide
Flecainide
Sotalol
Dofetilide

Front 96

Two antiarrhythmic agents that are preferred in patients with AF who have HF

Back 96

Amiodarone
Dofetilide

Front 97

Two antiarrhythmic agents that should avoided in structural heart disease

Back 97

Flecainide
Propafenone

Front 98

Two antiarrhythmic agents that are only used in ventricular arrhythmias

Back 98

Lidocaine
Mexilitine