Pharm Quiz 4 Flashcards

1
Q

What is the most effective diuretic?

A

Loop diuretics

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2
Q

When is Furosemide indicated?

A

Pulmonary Edema associated with CHF
Edema of hepatic, cardiac, or renal origin that has been unresponsive to other diuretics.
HTN that cannot be controlled with other diuretics

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3
Q

What diuretic compliments Furosemide?

A

Thiazide diuretic

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4
Q

Transient side effect of Furosemide:

A

Hearing loss

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5
Q

Drug interaction with Furosemide:

A

Digoxin with hypokalemia can lead to ventricular dysrhythmias
NSAIDs

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6
Q

What are three other loop diuretics?

A

Ethacrynic Acid
Torsemide
Bumetanide

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7
Q

Hydrochlorothiazide Dose

A

12.5-25mg/day

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8
Q

Where does Hydrochlorothiazide act?

A

It acts in the early segment of the distal convoluted tubule, which means it is dependent on flow of urine.

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9
Q

Spironolactone MOA

A

Blocks action of Aldosterone, which promotes sodium uptake in exchange for potassium secretion. The effects of Spironolactone are delayed because they act on the cells.

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10
Q

Spironolactone Dose

A

25-200 mg/day

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11
Q

What is Spironolactone used for?

A

It is usually used in combination with a thiazide or loop diuretic.
It also decreases mortality and hospital admissions with HF patients.

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12
Q

Side effect of Spironolactone:

A

Steroid derivative that can cause gynecomastia, menstrual irregularities, and impotence.

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13
Q

Triamterene and Amiluride

A

Directly inhibits secretion of Potassium. Only produce moderate diuresis. Usually used in conjunction with loop or thiazide diuretics.

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14
Q

What does Angiotensin II do?

A

Vasoconstricts and stimulates Aldosterone release

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15
Q

How does Angiotensin II change vascular and cardiac structure?

A

Hypertrophy
Remodeling
Thickens blood vessel walls`

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16
Q

Renin

A

Catalyzes angiotensin I from angiotensinogen

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17
Q

How does the RAAS act?

A

Vasoconstriction and renal retention of water and sodium.

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18
Q

Characteristics of ACE inhibitors:

A

Oral
Administered with food
Prolonged half lives
Prodrugs
Excreted by kidneys

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19
Q

Lisonopril dose

A

10-40 mg/day

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20
Q

What are benefits of ACE inhibitors?

A

Do not interfere with cardiovascular reflexes, which means they are good for exercising.
Orthostatic hypotension is minimal after first dose.
Used safely for bronchial asthma.

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21
Q

How are ACE inhibitors useful for HF?

A

Improve cardiac afterload by relaxing vessels.
Decrease pulmonary congestion.
Promote excretion of water.
Prevent pathologic cardiac changes.

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22
Q

What do ACE inhibitors prevent?

A

MI prevention and recovery
Prevents diabetic and nondiabetic nephropathy (decreases GFR pressure)
Reduce risk of diabetic retinopathy

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23
Q

Black Box Warning ACE inhibitors, ARBs, Alisirken

A

Fetal injury

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24
Q

ACE inhibitors AE:

A

Renal failure with stenosis
Cough
Hyperkalemia
Angioedema
Neutropenia

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25
Q

ACE inhibitors drug interactions

A

Lithium
NSAIDs reduce effects

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26
Q

Losartan Dose

A

50-100mg/day

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27
Q

ARB MOA

A

Block angiotensin II receptors

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28
Q

What ARBs are approved for HF?

A

Valsartan and Candesartan

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29
Q

What ARBs are approved for diabetic nephropathy?

A

Irbesartan and Losartan

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30
Q

What ARB is approved for MI?

A

Valsartan

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31
Q

What ARB is approved for stroke prevention?

A

Losartan

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32
Q

What ARB reduces the risk of MI, stroke, and death?

A

Telmisartan

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33
Q

Aliskiren

A

Binds with renin to prevent angiotensinogen into angiotensin I.
Did not improve outcomes in hospitalized patients with HF.

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34
Q

Eplerenone

A

Selective aldosterone receptor blocker with little to no effect on other steroid receptors.

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35
Q

Eplerenone Indication:

A

No information on whether it reduces morbidity and mortality, so only give to patients who have not responded to traditional antihypertensives.

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36
Q

What do CCBs do?

A

They work on arteries, decrease contractility, decrease SA and AV node speed, and are directly related to B-Adrenergic effects.

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37
Q

Nifedipine

A

Dihydropyridine that only works on vessels.

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38
Q

Verapamil and Diltiazem

A

Non-dihydropyridine that work on the vessels and the heart.

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39
Q

What are the direct effects of Verapamil?

A

Arterial Dilation
Coronary perfusion
Reduces HR
Decreases force of contraction

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40
Q

What is the net effect of Verapamil?

A

Because of the body compensating, the main effects are simply arterial dilation.

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41
Q

What is Verapamil used for?

A

Angina Pectoris
HTN
Afib/Aflutter
Paroxysmal Supraventricular Tachycardia

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42
Q

Drug interactions with Verapamil:

A

Digoxin, B-Blockers, grapefruit juice,

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43
Q

How is the barrow-reflex triggered?

A

By immediate-release Nifedipine, which can lead to increased mortality in patients with MI and unstable angina d/t reflexive effects.

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44
Q

What is Nifedipine indicated for?

A

Angina pectoris w/ a BB
HTN

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45
Q

Adverse effects of CCBs:

A

Flushing
Dizziness
Peripheral edema
Gingival hyperplasia
Rash

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46
Q

What CCB is preferred for patients with a AV block, HF, Bradycardia, or SNS?

A

Nifedipine

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47
Q

Stage 1 HTN

A

130-139 or 80-89

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48
Q

Stage 2 HTN

A

> 140 or >90

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49
Q

How can the barrow-reflex be overcome?

A

Usually with a BB. Once reset it will not oppose medications as much.

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50
Q

What drugs work on the brainstem and sympathetic ganglia?

A

Clonidine and Mecamylamine that suppress sympathetic action

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51
Q

What are the top two drugs for chronic HTN if there are no compelling indications?

A

Thiazide diuretic have been shown to decrease mortality and morbidity the most then Verapamil. (pg 21171)

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52
Q

Step-down therapy

A

After 1 year medications should be reduced or eliminated.

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53
Q

What medications should be avoided for patients with HF?

A

Diltiazem and Verapamil since they decrease contractility
Anti-dysrhythmics
NSAIDs

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54
Q

What medications should be avoided for patients with AV block?

A

BBs and CCBs since they decrease AV

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55
Q

What medication should be avoided for patients with CAD and post-MI?

A

Hydralazine can precipitate a reflex tachycardia –> anginal attack.

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56
Q

What medications should be avoided for patients who have dyslipidemia?

A

BBs and diuretics may exacerbate

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57
Q

What medications should be avoided for patients who have diabetes?

A

Thiazides promote hyperglycemia and BBs mask symptoms of hypoglycemia.

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58
Q

What should HTN patients with renal insufficiency be given?

A

ACEs and ARBs usually with a diuretic.

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59
Q

What is the preferred medication for diabetes?

A

ACEs and ARBs

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60
Q

First choice medication for African Americans?

A

Diuretics

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61
Q

What medications do AAs not respond as well to?

A

ACEs and BBs unless indicated by another condition

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62
Q

What dose should be given for elderly patients?

A

Start with half and increase slowly

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63
Q

What is the definition of chronic hypertension before pregnancy?

A

Developed before the 20th week of gestation

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64
Q

What are the drugs of choice when starting during pregnancy?

A

Methyldopa, Labetalol, Nifedipine

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65
Q

When does BP need to be treated in pregnancy?

A

> 180S and >110D

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66
Q

What is preeclampsia?

A

BP >140/90 and proteinuria >300 that develops after the 20th week of gestation

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67
Q

Do anti-hypertensives help preeclampsia?

A

Studies have failed to demonstrate any benefits from antihypertensive drugs.

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68
Q

What are the consequences of HF?

A

Tachycardia
Increased Contractility
Increased venous tone
Increased Arteriolar tone
Cardiac Dilation

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69
Q

What balances out sympathetic tone?

A

ANP and BNP

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70
Q

NYHA Scheme

A

Class 1 -no changes in activity
Class 2 -slight limitation of patient activity
Class 3 -mild activity causes symptoms
Class 4 -symptoms occur at rest

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71
Q

ACC/AHA Scheme

A

Stage A -high risk but no changes
Stage B -Structural changes but no symptoms
Stage C -structural changes with symptoms
Stage D -refractory HF requiring intervetions

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72
Q

Can Thiazide diuretics be used for HF?

A

Only work if GFR (CO) is high

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73
Q

What is the first-line treatment for HF?

A

ACEs usually combined with a diuretic and BB

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74
Q

Why do ACEs help HF?

A

Dilate veins and arteries
Suppress Aldosterone –> more H20 and Na excretion
Elevate kinins –> prevention of remodeling

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75
Q

Why are ARBs useful for HF?

A

They improve LV EF, increases exercise tolerance, reduce HF symptoms. However, they do not increase bradykinin levels (decreased remodeling and decreased coughing).

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76
Q

Entresto

A

Newly approved ARB that decreases RAAS and increases Bradykinin.

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77
Q

When should ARBs be given?

A

When patients still have symptoms with BB and ACE.

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78
Q

How does Aldosterone negatively impact HF?

A

Increases remodeling
Increases fibrosis
Increases SNS
Promotes baroreceptor dysfunction

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79
Q

Spironolactone BB

A

Tumorigenesis

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80
Q

What BB are used for HF?

A

Metropolol ER, Cavedilol, Bisoprolol

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81
Q

Digoxin

A

Reduces symptoms but does not decrease mortality. Second-line for HF.

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82
Q

Bidil

A

Isosorbide dinitrate and Hydralazine combination used only for black patients.

82
Q

What are the benefits of Digoxin?

A

Sympathetic tone declines
Urine production increases
Renin release declines

83
Q

Patient education regarding Digoxin:

A

Monitor pulses to look for dysrhythmias. Do not give for a HR below 50.

84
Q

AE Digoxin:

A

Hypokalemia

84
Q

What is the treatment for Digoxin dysrhythmias?

A

Lidocaine and Phenytoin
Fab antibody fragments decrease Digoxin toxicity.

85
Q

What is the treatment for Stage A HF?

A

Treating risks

86
Q

What is the treatment for Stage B HF?

A

ACE and BB

87
Q

What is the treatment for Stage C HF?

A

ACE, Diuretic, and BB.
Give aldosterone-blocker if symptoms are moderate or severe or after a MI.

88
Q

What is the treatment for Stage D HF?

A

They may need a heart transplant of LVAD.
BB and ACE may be tried but could start profound hypotension.

89
Q

ASCVD Risk Factors

A

Diabetes = ASCVD
Black Race
Advancing Age
HTN
Smoking

90
Q

What factors are included in the Framingham Risk Prediction Score:

A

Systolic BP
Total cholesterol
HDL
Age
Smoking Status

91
Q

Who should be treated for ASCVD?

A

Pts with ASCVD
LDL >190
40-75 with diabetes and LDL 70-189
10 year risk of >7.5%

92
Q

What is the treatment of choice for lowering Cholesterol?

A

If the goal is lowering the Cholesterol levels by 40%, then Atorvastatin or Lovastatin is best (HMG-Coa reductase inhibitor). Otherwise it doesn’t matter.

93
Q

What medications should be implemented if Atorvastatin is not enough?

A

Monoclonal antibodies
Bile acid sequestrants
Niacin

94
Q

Metabolic Syndrome Diagnosis:

A

> 2 of the following:
150 TG
<50 HDL
Hyperglycemia
130/85
Waist circumference >35

95
Q

What is the treatment for high TGs?

A

Decrease LDLs first and if still necessary give a fibrate for TGs specifically.

96
Q

When are the effects of statins seen?

A

2-6 weeks

97
Q

What do statins accomplish?

A

Lower LDL, TGs (for a short time), and increase HDLs

98
Q

What are some secondary effects of statins?

A

Promote plaque stability
Reduce inflammation at plaque site
Slow coronary calcification
Enhance ability of vessels to dilate
Decrease risk for thrombosis

99
Q

Statin MOA

A

Normalizes cholesterol production
Produces more hepatocyte LDL receptors –> metabolism
Decrease production of apolipoprotein –> decrease VLDL and TG

100
Q

What is the goal for LDL?

A

<100 or in patients with high CV risk <70

101
Q

Rosuvastatin Indications

A

For patients with normal LDLs but have advanced age, high levels of C-reactive protein, and one other risk factor for CV.
Double the level in Asian patients.

102
Q

When should diabetes patient have a statin?

A

> 40 years
LDL >100
One other risk factor

103
Q

Statin AE

A

Myopathy –> Myostisis–> Rhabdomyolysis (increased CK)
Hepatotoxicity (Fine to give to NASH)
Diabetes

104
Q

Risk factors for Rhabdomyolysis

A

CKD
Low Vit D
Hypothyroidism

105
Q

Atorvastatin Dose

A

10 mg

106
Q

What statin should be used for patients with renal impairment?

A

Atorvastatin or Fluvastatin

107
Q

Colesevelam

A

Bile Acid Sequestrant:
Better tolerated
Does not decrease absorption of DAKE
Does not decrease absorption of Digoxin, Warfarin

108
Q

Bile Acid Sequestrant MOA

A

Increases LDL receptors on hepatocytes and prevent reabsorption of of bile acids

109
Q

Gemfibrozil (Fibrate)

A

Decreases TG and increases HDL

110
Q

Alirocumab and Evolucumab

A

Inhibits PCSK9 that binds to lipid receptors preventing metabolism

111
Q

How are monoclonal antibodies administered?

A

SQ

112
Q

What is the equation for total cholesterol?

A

TG + LDL +HDL

113
Q

Hydralazine

A

Dilates arterioles and reflexively increases HR and contractility

114
Q

Acetylators

A

Patients breakdown Hydralazine through acetylation

115
Q

Hydralazine AE

A

Hydralazine-induced hypotension caused by water and Sodium retention.
Systemic Lupus Erythematosus like syndrome

116
Q

What is Hydralazine combined with in patient with HF?

A

Isosorbide dinitrate (a drug that dilates veins)

117
Q

Minodixil

A

Only used for severe hypertension d/t adverse effects

118
Q

AE Minodixil

A

Reflex Tachycardia
Na and H2O retention
Hypertrichosis

119
Q

Minodixil BB

A

Pericardial effusion

120
Q

AV Block Degrees

A

1st Degree: conduction is slowed
2nd Degree: Only some impulses pass through
3rd Degree: All traffic in the AV node stops

121
Q

Where does VT come from?

A

Usually from a previous MI

122
Q

Rate controlled treatment of Afib

A

Metoprolol
Diltiazem (Cardiac selective CCB)

123
Q

How restore Afib rate:

A

Ablation
Amiodarone, Sotalol
Cardioversion
Must take Warfarin 3 weeks before and 4 weeks after.

124
Q

Long-term anticoagulant therapy for afib

A

Eliquis
Xarelto
Pradaxa
Savysa

125
Q

Treatment for aflutter:

A

Cardioversion converts to SNS and patients will need long-term Class I or III agents to prevent recurrence.
Alternatives: Ablation or rate control with drugs that suppress AV conduction.

126
Q

Drugs that suppress AV conduction:

A

Diltiazem, Verapamil, or a BB

127
Q

What is SVT caused by?

A

A recurrent feedback loop where HR is 150-200.

128
Q

SVT Treatment:

A

Valsalva Maneuvers
IV BB or CCB
BB or CCB to prevent recurrence (or Amiodarone as a last resort).

129
Q

VT treatment:

A

Immediate Cardioversion
IV Amiodarone
Lidocaine
Long-term management: Amiodarone, Sotalol, ICD

130
Q

Treatment for Torsades de Pointes (ventricular tachydysrhythmia)

A

Cardioversion and IV Mag

131
Q

What dysrhythmias do not need to be treated?

A

Non-sustained, mildly symptomatic, and supraventriculars

132
Q

Quinidine

A

Class Ia Na ion blocker –> slower impulse conduction and delayed repolarization.
It also is anti-cholinergic, so it should be given with a BB to prevent excessive ventricular stimulation.
Used for long-term suppression of supraventricular and ventricular rates.

133
Q

How does Quinidine effect the EKG?

A

Widens the QRS complex and prolongs the QT interval.

134
Q

Quinidine BB

A

May increase mortality in afib and aflutter

135
Q

Quinidine Drug Interactions

A

Doubles amount of Digoxin

136
Q

Mexiletine (oral analogue of Lidocaine)

A

Accelerates repolarization
Little effect on EKG
Used for sustained VT or PVCs

137
Q

Class II Drug Propanolol

A

Closely related to CCBs
Used for excessive stimulation of the heart caused by exercise induced dysrhythmias, Sinus Tachycardia, and severe recurrent VT.

138
Q

Class II Drug Amiodarone

A

Potassium channel blocker
Delay repolarization of fast potentials
Prolong QT elongation

139
Q

Indications for Amiodarone

A

Hemodynamically unstable VT
Vfib
Converting Afib
First-line med for patients with HF for treating these.

140
Q

BB Amiodarone

A

Lung and Liver toxicity

141
Q

Amiodarone AE

A

Thyroid Toxicity
Ototoxicity
Dermatologic Toxicity

142
Q

Amiodarone Drug Interactions

A

Diuretics
CCBs and BBs –> severe bradycardia
Statins

143
Q

Class IV Drug Diltiazem and Verapamil

A

CCBs
Slows SA and AV and decreases contractility

144
Q

Class IV Indications

A

Treat Afib and Aflutter IV within 2-3 minutes

145
Q

Digoxin for dysrhythmias

A

Treats supraventricular dysrhythmias by decreasing speed of SA and AV nodes except for Perkinje fibers –> more dysrhythmias.

146
Q

How does Digoxin effect the EKG?

A

Prolongs PR
Shortens QT
Inverted T wave

147
Q

What drugs are used for variant angina?

A

Nitrates and CCBs

148
Q

How does nitroglycerine decrease pain?

A

In stable angina dilates veins –> decreased preload –> decreased cardiac demands
In variant angina, it relaxes the blood vessels –> increased oxygenation

149
Q

How should tolerance to Nitro be prevented?

A

Lowest Dose
At least 8 drug free hours/day

150
Q

How should long-lasting Nitro be discontinued?

A

Slowly to prevent vasospasm

151
Q

Isosorbide Mononitrate Isosorbide Dinitrate

A

Pharmacologically the same as nitroclycerin

152
Q

How do BBs help angina?

A

Decrease cardiac oxygen demand leading to increased exercise tolerance.
Blunt reflex tachycardia from Nitro.
Increase time in diastole.

153
Q

BB AE

A

Bradycardia
Decreased contractility and AV conduction means they should not be used by HF, SNS, or AV Block patients.

154
Q

How do CCBs help angina?

A

Relax variant spasm
Relax peripheral vessels

155
Q

Ranolazine AE

A

QT Prolongation
HTN

156
Q

What do Verapamil and Diltiazem do differently than Nifedipine?

A

They decrease HR, contractility, and conduction which means they should not be used for patients with HF.

157
Q

Drugs to prevent MI:

A

Anti-platelets
Cholesterol lowering
ACEs

158
Q

Flow chart for treatment of Angina

A

Nitro w/ BB –> CCB –>Long acting nitrate –> CABG

159
Q

What is the treatment flow chart for spastic angina?

A

CCB or long acting nitrate —> both —> CABG

160
Q

What are anticoagulants used for?

A

Disrupt the coagulation cascade preventing thrombosis in the veins and atria of the heart by reducing the formation of fibrin.

161
Q

What are antiplatelet used for?

A

They prevent platelet aggregation to prevent thrombosis in arteries.

162
Q

What is Heparin’s MOA?

A

Enhance the activity of antithrombin that inhibits thrombin and factor X.

163
Q

What are LMWs’ MOA?

A

Inactivate factor Xa

164
Q

What are the indications for LMW?

A

Hip, abdominal, and knee surgery
Prevention of DVT
Prevention of unstable angina

165
Q

How is LMW administered?

A

SQ but only needs to be adjusted based on weight or kidney function.

166
Q

What is the reversal for Heparin?

A

Protamine Sulfate

167
Q

Fondaparinux MOA

A

Selectively inhibits Factor Xa

168
Q

Indications for Fondaprinux:

A

Knee, hip, or abdominal surgery
Treating acute PE or DVT (with Heparin)
More effective at treating DVT than LMW but may cause more bleeding.

169
Q

MOA of Warfarin:

A

Suppresses production of factors VII, IX, and X by inhibiting the production of the active form of Vitamin K.

170
Q

Indications of Warfarin:

A

Prevention of PE
Prevention of thrombus on prosthetic valves
Prevention of thrombus in Afib

171
Q

What is the INR goal?

A

2-3 but cannot be adjusted quickly.

172
Q

When should PT be monitored?

A

Daily for the 1st 5 days
2/week for the next 2 weeks
1/week for the next 4 months
Then 1-2/month

173
Q

What foods contain Vit K?

A

Mayonnaise, canola oil, and soybean oil.
These foods do not need to be avoided but need to stay constant.

174
Q

Dabigatran

A

Reversible direct thrombin inhibitor.
Standard doses, rapid onset, no need for monitoring, few drug-food interactions, low risk for bleeding.

175
Q

Dabigatran and Xarelto Indications:

A

Prevention of stroke
Prevention of thrombus in Afib
Knee surgery
Treatment of DVT or PE

176
Q

Xarelto MOA

A

Inhibits Factor Xa

177
Q

Dabigatran and Xarelto Reversal Agents

A

Idarucizumab and Andexanet Alfa

178
Q

Aspirin MOA

A

Inhibits Cyclooxygenase necessary to create TXA

179
Q

Indications for Aspirin:

A

Ischemic Stroke
TIA
Both anginas
Stenting
MIs

180
Q

When should patients take Aspirin for MIs?

A

If the have a 10% risk for cardiovascular or colorectal cancer, have a life expectancy of 10 years, and are willing to take Aspirin for 10 years.

181
Q

Clopidogrel MOA

A

Prevent ADP aggregation. Not reversible.

182
Q

Clopidogrel Indications:

A

Prevent blockage of coronary stents
Reduce thrombus events in patients with atherosclerosis.
Should always be given with Aspirin.

183
Q

Clopidogrel BB:

A

Should not be used by poor metabolizers (determined by saliva test)

184
Q

Vorapaxar MOA

A

Inhibits thrombin. Reversible.

185
Q

Vorapaxar Indications:

A

Patients with history of MI or PAD. Used with Clopidogrel or Aspirin.

186
Q

Dipyridamole Indications:

A

Always used with Warfarin for a heart valve replacemnt

187
Q

Dipyridamole and Aspirin

A

Used for recurrent stroke

188
Q

Cilostazol Indications

A

Intermittent claudication

189
Q

How much iron does a pregnant woman need?

A

27 mg/day

190
Q

What are the labs needed for a diagnosis of IDA?

A

Microcytic hypochromic erythrocytes
Absence of Hemosiderin

191
Q

Dose of Ferrous Sulfate

A

500 mg

192
Q

How quickly does iron improve HGB?

A

In 1 month it will raise by 2g/dl

193
Q

What should be determined if the patient’s HGB does not rise after a month?

A

Bleeding
Noncompliance
Inflammatory disease
Malabsorption

194
Q

What is Vitamin B12 used for?

A

Synthesis of DNA which means it is required for all cells.

195
Q

What causes B12 deficiency?

A

Celiac Disease
Bariatric surgery
Regional Enteritis
Development of antibodies against B12

196
Q

Pernicious Anemia

A

Deficiency of B12 secondary to lack of intrinsic factor

197
Q

Megaloblastic Anemia

A

Lack of B12 for DNA prevents RBC division. Severe anemia is the primary cause of death from B12 deficiency

198
Q

What system is most likely to be affected by lack of B12?

A

Where a large number of cells turn over (bone marrow, GI)
Cause demyelination of neurons

199
Q

B12 Dose

A

1000-2000 mcg/day for 1-2 weeks

200
Q

Diagnosis of B12:

A

Megaloblasts and macrocytes in in peripheral blood

201
Q

What are the causes of folic acid deficiency?

A

Alcohol use
Malabsorption secondary to intestinal disease (Sprue)

202
Q

Folic Acid Dose

A

1-5mg daily then 400mcg daily for maintenance