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Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

How can hypertension be treated

A

Lifestyle changes (most effective), medications

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2
Q

Lifestyle modifications for hypertension

A 
Weight reduction and exercise
Diet changes
Relaxation techniques
Smoking cessation
Medications
Encourage self monitoring
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3
Q

What are antihypertensive medications

A

Diuretics, beta blocks, angiotensin receptor blockers, calcium channel blockers, ACE inhibitors

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4
Q

Diuretics

A

Lower bp by reducing circulating fluid volume.

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5
Q

What are the types of diuretics

A 
Thiazides (hydrochlorothiazide)
Loop diuretics (furosemide, ethracrynic acid) and potassium sparing diuretics (spironolactone)
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6
Q

Beta blockers

A

Block sympathetic nerve impulses in the heart leading to a reduction in heart rate…decreasing cardiac output

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7
Q

Examples of beta blockers

A

Atenolol
Propranolol
Metoprolol

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8
Q

Angiotensin receptor blockers (ARB)

A

Specifically blocks angiotensin II from binding to vessel receptors, preventing vasoconstriction

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9
Q

Examples of ARB

A

Losartan

Olmesartan

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10
Q

Calcium channel blockers

A

Cause systemic vasodilation resulting in a reduced peripheral vascular resistance

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11
Q

Examples of calcium channel blockers

A

Diltiazem
Verapamil
Nifedipine

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12
Q

ACE inhibitors

A

Decreases the amount of angiotensin II and aldosterone in the system resulting in vasodilation and lowering circulating fluid volume. Slow progression of renal damage in patients with diabetes

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13
Q

Examples of ACE inhibitors

A

Captopril
Lisinopril
Enalapril

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14
Q

Nitroprusside

A

Nitrate drug with potent venodilator and vasodilator properties. It is administered via IV and is broken down in the blood into NO, which in turn increases cGMP, leading to smooth muscle relaxation . Translating into vasodilation and venodilation which is helpful in rapidly reducing the blood pressure, as this drug is rapid acting and has a short half life

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15
Q

Why is nitroprusside given during malignant hypertension

A

Properties

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16
Q

What is malignant hypertension

A

Severe increase in bp causing impairment of one or more organ systems

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17
Q

Side effect nitroprusside

A

Cyanide toxicity

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18
Q

Nitroprusside administration can lead to iatrogenic cyanide toxicity if overused.

A

Sodium nitroprusside has 5CN ligand in its molecule, and breaks down into thiocyanate. This is usually detoxified in the blood, but can reach toxic levels in the blood

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19
Q

The half life of thiocyante is not as __ as nitroprusside, but is several days, and patients are at risk for toxicity and effects for longer

A

Short

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20
Q

Nitroprusside MOA

A
  1. direct release of NO(vasodilation and venodilation)
  2. Increased cGMP (NO activates guanyl cyclase in SM increasing cGMP)
  3. CGMP inactivated myosin light chains and causes SM relaxation or arteriosus action. This drug is a potent dilator of venues and arterioles
  4. the drug has a half life of 1-2 min and is rapidly acting
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21
Q

Indications nitroprusside

A

Malignant hypertension

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22
Q

How is nitroprusside administered

A

IV

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23
Q

Side effects nitroprusside

A

Cyanide toxicity

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24
Q

How does nitroprusside give canine toxicity

A

Sodium nitroprusside has 5 CN ligand in its molecules and breaks down into thiocyanate. This is usually detoxified in the blood but can reach toxic levels in the blood.

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25
Q

Symptoms of cyanide toxicity

A

Vertigo, confusion, difficulty breathing and headaches at low doses.

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26
Q

Minoxidil (loniten, rogaine)

A

Vasodilator that acts primarily on arterioles

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27
Q

Although minoxidil causes more severe adverse reactions than hydralazine it also does what

A

More intense arteriolar vasodilation

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28
Q

Indication for minoxidil

A

Severe hypertensiona nd baldness

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29
Q

Side effects minoxidil

A

Reflex tachycardia, blood volume expansion, and pericardial effusion, excessive hair growth or a rash

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30
Q

How minimize adverse effects of minoxidil

A

Give with beta blockers and diuretics and diuretics

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31
Q

MOA minoxidil

A

Vasodilator arterioles
By dilating the resistance vessels, the medication decreases afterload and subsequently cardiac workload. This action causes cardiac output and tissue perfusion to increase.

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32
Q

Does minoxidil have venous effects

A

No

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33
Q

Indications for minoxidil

A

Severe hypertension and baldness

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34
Q

Baldness and minoxidil

A

Topical

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35
Q

Side effects minoxidil

A

Reflex tachycardia, blood volume expansion, hypertrichosis, pericardial effusion, rash

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36
Q

Reflex tachycardia and minoxidil

A

As baroreceptors in the aortic arch and carotid sinus sense a decrease in bp, the vasomotor center of the medulla tries to restore normal blood pressure by increasing heart rate and myocardial contractility

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37
Q

Blood volume expansion and minoxidil

A

Chronic use of vasodilator causes prolonged reduction of bp, which triggers adrenal glands to secrete aldosterone to promote sodium and water retention. In addition, decreasing arterial pressure leads to decreased renal blood flow and reduced GFR. Decreasingthe filtrate volume increases the kidneys ability to reabsorbed sodium and water and leads to blood volume expansion

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38
Q

Minoxidil and hypertrichosis

A

Vasodilator effects cause proliferation of epithelial cells at the base of the hair follicle. Hair growth begins on the face and progresses to arms, legs, and back.

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39
Q

Minoxidil and pericardial effusion

A

Fluid retention lead to fluid accumulation underneath the pericardium and develop pericardial effusion. May compress the heart and lead to cardiac tamponade

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40
Q

Why give minoxidil with beta blocker and diuretic

A

Minimize reflex tachycardia, so premeditate with beta blocker to prevent sympathetic stimulation of the heart. Since blood volume increase negates the effect of vasodilation, diuretics also given to prevent fluid retention and volume expansion (if diuretic therapy inadequate will need dialysis)

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41
Q

Hydralazine

A

Vasodilator that helps to relax smooth muscle and decrease peripheral resistance helping to lower blood pressure and reduce afterload

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42
Q

MOA hydralazine

A

Increases cGMP , leading to SM relaxation, and arteriodilation with a slight amount of venodilation. So it directly relaxes arteriolar muscle

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43
Q

Indications for hydralazine

A

Severe hypertension and CHF

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44
Q

What is hydralazine often combined with

A

Methyldopa to treat hypertension in pregnancy

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45
Q

Side effects hydralazine

A

Drug induced lupus
With anti histone antibodies
Reflex tachycardia due to the drugs sudden pressor actions and is often co-administered with a B blocker to prevent this

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46
Q

Indications for hydralazine

A

Reduce afterload, severe hypertension , CHF

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47
Q

How does hydralazine reduce afterload

A

Relaxes SM and preferentially vasodilator arterioles,creating an afterload reduction. It is indicated in diseases where there is a cardiac failure or excess systemic resistance

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48
Q

Severe hypertension and hydralazine

A

Not for essential hypertension

First line of hypertension during pregnancy

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49
Q

Hydralazine is indicated for pregnancy hypertension along with ___

A

Methyldopa

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50
Q

MOA hydralazine

A

Increase cGMP which inhibits contraction in SM and leads to bv relaxation
(Grater vasodilation of arterioles than veins)

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51
Q

Side effects hydralazine

A 
Drug induced lupus(have antihistone antibodies)
Reflex tachycardia (compensatory response to sudden decreased bp to maintain cardiac output.)
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52
Q

How prevent reflex tachycardia with hydralazine

A

Give with beta blocker

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53
Q

Who is hydralazine contraindicated in

A

Angina, CAD

It can also cause angina

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54
Q

Calcium channel blockers (verapamil and diltiazem)

A

Verapamil belongs to the phenylalkylamines class and diltiazem belongs to a class called the benzothiazepines

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55
Q

How are verapamil and diltiazem different from other calcium channel blockers

A

Have direct action on cardiac tissue at therapeutic levels

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56
Q

Verapamil and diltiazem are also classified as type IV antiarrhythmics and

A

Work to slow AV conduction

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57
Q

Indications calcium channel blockers (verapamil and diltiazem)

A

Angina pectoris, essential hypertension and arrhythmias

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58
Q

MOA calcium channel blockers

A

Block coltage dependent calcium channels. Since these channels are concentrated in SA and AV this drug class helps by decreasing conduction through the AV node.

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59
Q

Calcium channel blockers are contraindicated in

A

Heart block, espicially 2nd degree block and complete heart block

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60
Q

Indications for calcium channel blockers

A

Angina pectoris
Essential hypertension
Arrhythmias

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61
Q

Angina pectoris and calcium channel blockers

A

Calcium channels in SM or vasculature and blocking them allows blood vessels to dilate.

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62
Q

Essential hypertension and calcium channel blockers

A

Decrease blood pressure by dilation of the arterioles.

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63
Q

What calcium channel blocker is first line for treating chronic hypertension

A

Verapamil

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64
Q

Arrhythmias and calcium channel blockers

A

Espicially atrial tachyarrhythmias as they slow impulse conduction through the AV node

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65
Q

Side effects calcium channel blocker

A 
Bradycardia
Hypotension
Constipation
Peripheral edema
Gingival hyperplasia
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66
Q

Calcium channel blockers bradycardia

A

Slow impulse conduction through the AV node to the ventricles

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67
Q

Hypotension and calcium channel blockers

A

Relaxing SM in vasculature, these medications can lead to the side effect of hypotension

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68
Q

Constipation and calcium channel blockers

A

Leads to decreased smooth muscle motility and can manifest as constipation (more so with verapamil)

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69
Q

Peripheral edema and calcium channel blockers

A

Arteriolar dilation leading to capillary hypertension which causes fluid extravasation into tissues

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70
Q

Gingival hyperplasia calcium channel blockers (verapamil)

A

Enlargement of the gums

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71
Q

Class I antiarrhythmics (Na channel blockers)

A

Treat tachyarrhythmias by blocking fast Na channels and there are several subcategories of drug based not heir specific effect on cardiac action potentials

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72
Q

class I antiarrhythmatics do what

A

Restore normal pacemaker and conduction activity and are selective for depolarized tissue, which is known as state dependent

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73
Q

MOA class I antiarrhythmics

A

Block Na channels to reduce rate of phase I depolarizationand prolong effective refractory period. This increases the threshold for firing within abnormal pacemaker cells.

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74
Q

Class I antiarrhythmic contraindicated

A

Hyperkalemia states, as excess potassium increases resisting membrane potential and can produce a sodium channel block so pronounced that asystole may result in patients taking class I

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75
Q

Arrhythmias

A

Refer to abnormal heart rate or regularity. They can be caused by either or regular impulse conduction or impulse generation

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76
Q

Indications class I

A

Arrhythmias and local anesthesia

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77
Q

MOA class I antiarrhythmics

A
  1. Block slow conduction (block fast sodium channels. Halting conduction espicially in depolarized cells
  2. block na channels to reduce rate of phase I depolarization and prolongs effective refractory period
  3. raise threshold. Bc of Na channel block they increase the threshold for firing within abnormal pacemaker cells
  4. State dependent -selectively depress tissue that is frequently depolarized, versus normally polarized tissue. This can include ischemic tissue
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78
Q

Contraindications for class I antiarrhythmics

A

Hyperkalemia

Toxicity bc k increases resting membrane potential and can produce a sodium channel blockade so pronounced that asystole may result

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79
Q

Class IA antiarrhythmics (na channel blocker)

A

Treat arrhythmias through blockage of na channels, prolonging action potentials and are effective for both atrial and ventricular arrhythmias

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80
Q

Indication for classI antiarrhythmias

A

Arrhythmias-atrial and ventricular,

Recent rant and ectopic suprventricular and ventricular tachycardia, wolff parkinson white syndrome

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81
Q

MOA class IA

A

Increase PA, effective refractory period, and QT interval

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82
Q

Commonly used class IA antiarrhythmia drugs

A

Disopyramide, procainamide

Quinidine

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83
Q

Shared side effects of class IA

A

Thrombocytopenia and torsades de pointes

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84
Q

Side effect procainamide

A

Drug induced lupus

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85
Q

Side effects quinidine

A

Cinchoism

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86
Q

Indications for class IA

A

Arrhythmias (vent ansupra vent)

Recent rant and ectopic supraventricular arrhythmias, such as Wolff parkinson white syndrome

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87
Q

MOA class IA

A

Increase AP, ERP, and QT interval

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88
Q

Disopyramide

A

Similar in action to quinidine, and has the longest half life of drugs in this class. It is indicated for ventricular arrhythmias, but has pronounced anticholinergic side effects, and can possibly worsen heart block and cause severe heart failure

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89
Q

Procainamide

A

Similar in action to quinidine, but has less GI side effects and is safer to use intravenously

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90
Q

Side effect procainamide

A

Drug induced lupus , which can be catalyze by medication. Patients with drug induced lupus typically show antihistone antibodies

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91
Q

Quinidine

A

Indicated for supraventricular and ventricular arrhythmias and also may be used for prevention.it is a state dependent block, meaning at higher heart rates, the block increases while at lower heart rates, the block decreases

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92
Q

Side effect quinidine

A

Cinchonism which resents as dizziness, ringing in the ears and diarrhea

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93
Q

Shared side effects of class iA

A

Thrombocytopenia

Torsades de points

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94
Q

Why may quinidine cause thrombocytopenia

A

Destruction of platelets by antibodies developed in response to protein quinine complexes in the circulation

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95
Q

Torsades de pointes

A

Quickly transform into ventricular fibrillation which may lead to sudden death. Torsades is a ventricular tachycardia which presented with shifting sinusoid waveformed on ECG. It may occur due to the increase in QT interval associated with this drug class

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96
Q

Class IB antiarrhythmics (Na channel blockers)

A

Class of antiarrhythmic drugs for treating ventricular arrhythmias by weakly blocking sodium channels and decreasing action potential duration. They also shorten the duration of refractory period

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97
Q

Indications for class IB

A

Arrhythmias (acute ventricular and digitalis-induced arrhythmias)
After MI arrhythmias

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98
Q

Class IB preferentially affect _ or _ purkinje and ventricular tissues, and act to decrease action potential duration by blocking sodium currents

A

Ischemic

Depolarized

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99
Q

Commonly used IB antiarrhythmias

A

Mexiletine
Lidocaine
Tocainide
Phenytoin

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100
Q

Mexiletine side effect

A

GI upset

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101
Q

Lidocaine side effect

A

CNS depresssion

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102
Q

Phenytoin

A

Anti-epileptic drug which also has class IB antiarrhythmic properties.

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103
Q

Long term use of phenytoin

A

Associated with hirsuitism, but can yield many other side effects as well

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104
Q

Indications class IB

A

Acute ventricular and digitalis induced arrhythmias
Treat arrhythmias which arise from imporoper impulse conduction or impulse conduction or impulse generation

After MI as they preferentially affect ischemic tissue

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105
Q

MOA IB

A

Highly selective for ischemic or depolarized purkinje and ventricular tissue

Decrease AP duration bc of their block of sodium currents. They have fast onset/offset kinetics and have little effect on slower heart rates, but a greater effect on faster heart rates

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106
Q

Mexiletine

A

May cause GI upset

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107
Q

Lidocaine

A

IV
Treats damaged tissues and acts only on the sodium channel. It is the second line treatment for ventricular arrhythmias and has a low level of cardiotoxicity

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108
Q

Lidocaine side effect

A

CNS depression ==seizures in severe overdose

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109
Q

Tocainide

A

Orally active drug, similar to lidocaine

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110
Q

Phenytoin

A

Anti seizure drug that is occasionally used as an antiarrhythmic, specifically in digitalis overdose to reverse atrioventricular block. It is known to have many side effects, including drug induced lupus, gingival hyperplasia, teratogenic effects and hirsutism

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111
Q

Class IC antiarrhythmics

A

Treat severe ventricular tachyarrhythmias by blocking na channels and slowing conductance

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112
Q

Class IC have no effect on _ duration and are used as a last resort in ___ ___, which may become intractable or progress to ventricular fibrillation

A

AP

Refractory tachyarrhythmias

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113
Q

Examples of class IC

A

Flecainide

Propafenone

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114
Q

Propafenone

A

Acts as a b adrenergic antagonist and has the side effects of bradycardia ad CHF

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115
Q

Class IC contraindicated

A

In patients immediately after MI and in patients with structural abnormalities due to their propensity to increase mortality in these groups

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116
Q

Indications class IC

A

Last resort in refractory tachyarrhythmias

V tach which may progress to ventricular fibrillation

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117
Q

MOA class IC

A

No AP duration as opposed to other class I antiarrhymics

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118
Q

Examples of class CI

A

Propafenone

Flecainide

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119
Q

Propafenone

A

Treats rapid heart beat arrhythmias such as supraventricular arrhythmias,. Similar to quinidine, and possesses b adrenergic antagonist activity. It may also represent life threatening ventricular arrhythmias,

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120
Q

Side effects propafenone

A

CHF, bradycardia and new arrhythmias

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121
Q

Flecainide

A

Class IC antiarrhythmias drug indicated for ventricular tachyarrhythmias and for maintaining sinus rhythms in cases of paroxysmal a fib or a flutter

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122
Q

Contraindications of class IC

A

Post MI . Has proarrhythmic activity and are contraindicated post MI and after structural heart disease due to increased mortality incidence with these diseases

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123
Q

Class III antiarrhythmics (k channel blockers)

A

Used when other types of antiarrhythmics fail. Work to prevent arrhythmias and re-entrant arrhythmias by increasing myocyte action potential duration, effective refractory period and Qt interval

124
Q

Commonly used class III antiarrhythmics

A

Aminodarone
Ibutilide
Dofetilide
Sotalol

125
Q

Aminodarone

A

Dirty drug due to its multisystemic toxicities and prescribers should heck pulmonary, liver, and thyroid function tests in patients taking this drug (causes pulmonary fibrosis, hepatotoxicity, and hypo/hyperthyroidism)

126
Q

Ibutilide and dofetilide

A

Helpful in restoring a fib and flutter to normal sinus rhythm

127
Q

Sotalol

A

Nonselective b blocker which has class II antiarrhythmic properties, and use of this medication can cause excessive b block in patients

128
Q

Indications for class III

A

Arrhythmias

129
Q

MOA class III

A

Increased AP, ERP, and QT interval

DO NOT SLOW conduction veolcity, but rather, they prolong depolarization in atrio-ventricular myocytes

130
Q

Amiodarone

A

Increases refractoriness and has a long half life. It is indicated for refractory life threatening ventricular arrhythmias, and is the first line treatment for patients not responding to CPR.

131
Q

Why is amiodarone unique

A

Has class I, II, III, IV antiarrhythmic effects bc it alters the lipid membrane

132
Q

Why do liver pulmonary and thyroid function tests when taking amiodarone

A

Toxicities of the drug. Can cause pulmonary fibrosis, hepatotoxicity, and hypo/jyperthyroidism

133
Q

Why is amiodarone called a dirty drug

A

Can bind to several different targets or receptors and thus have a wide range of effects

134
Q

Side effects amiodarone

A

CV effects (CHF, heart block, bradycardia), pulmonary fibrosis, hepatotoxicity, thyroid issues, corneal deposits, skin discolorations, neurological effects, and constipation

135
Q

Ibutilide

A

Indicated for quick conversion of a flutter or a fib to a normal sinus rhythm.

136
Q

How does ibutilide work

A

Give through IV infusion and works by prolonging action potential duration. A side effect is torsades de pointes

137
Q

Side effect ibutilide

A

Torsades de pointes

138
Q

Dofetilide

A

Indicated for converting and maintaining normal sinus rhythm in the care ofatrial flutter and atrial fibrillation

139
Q

Sotalol

A

Non selective competitive b adrenergic receptor blocker , it has significant side effects, including dyspnea, dizziness, and torsades de pointes

140
Q

Class IV antiarrhythmics (ca channel blocker)

A

Can be cardioselective or vasoselective, giving them a wide array of use

141
Q

Cardioselevtive class IV

A

Verapamil
Diltiazem
Inhibit transport of Ca across the cell membrane during cardiac depolarization by blocking Ca channels, decreasing SA node discharge…decreasing conduction through AV leading to an increased PR interval and ERP

142
Q

Indication for cardioselevtive class IV

A

Recent rant supraventricular tachycardia, also protects the ventricles from arrhythmias in atrial fluttter and fibrillation. Angina, hypertension, mostly due to SM relaxation

143
Q

Vasoselective class VI

A

Nimodipine

144
Q

MOA vasoselective class VI

A

Block Ca channels in SM and decrease vasoconstriction and spasm

145
Q

Indication nimodipine

A

Treat subarachnoid hemorrhage due to its vasoselective properties

146
Q

Side effects class iv

A

Cardiovascular (sinus node depression, AV block and CHF)

Impaired Ca transport leads to decrease gastric signaling and decreased gut motility, causing constipation in patients

147
Q

Indications class IV

A

SVT (due to AV nodal reentry), atrial fib or flutter, subarachnoid hemorrhage (nimodipine has higher effects on vascular SM than on cardiac condution)

148
Q

MOA class VI

A

Ca channels in SA and AV node blocked to decrease impulse conduction and velocity through AV
Also on SM and can treat hypertension

Decrease conduction through AV leading to an increases in PR and ERP

149
Q

Verapamil

A

Cardioselective Ca channel blocker, and has higher activity on slowing AV conduction than it does on vasodilation. It is indicated for use in arrhythmia prevention, hypertension, angina, and cluster headaches

150
Q

Diltiasem

A

Cardioselective Ca channel blocker which has actions similar to verapamil. It is used for SVT, angina, atrial flutter, and firillation, as well as hypertension

151
Q

Nimodipine

A

Vasoselective Ca channel blocker and is used to treat subarachnoid hemorrhage

152
Q

Side effects class IV

A

There are numerous cardiovascular side efffects implicated with Ca channel blocker use (AV block, sinus node depression)

Constipation (esp verapamil as Ca is a 2nd messenger for gastric, which is important for gastric motility—-motility impaired)

153
Q

Adenosine (adenocard)

A

A naturally occurring nucleotide in body that works by blocking cAMP induced Ca influx in cardiac myocytes.

154
Q

Indication adenosine

A

Tachyarrhythmias to delay the PR interval and slow a patients heart rate to a normal sinus rhythm

Supraventricular tachyarrhythmias after other efforts like vagal maneuvers to slow the heart rate have failed.

155
Q

Onset of adenosine

A

Seconds and resolves in 10 seconds. Side effects resolve in a minute

156
Q

MOA adenosine

A

Slows AV conduction from the SA node through AV, which abolished tachyarrhythmias. Basically is a short term calcium channel blocker in the AV node that is induced by cAMP….causes prolonged PR

157
Q

Indications adenosine

A

Supraventricular tachycardia (paroxysmal)

Must originate above AV node

158
Q

Why does adenosine not work for a fib, a flutter, and verntricular arrhythmias

A

Do not typically involve AV node as part of the re-entrant circuit

159
Q

Side effects adenosine

A

Bradycardia, flushing, dyspnea

160
Q

Flushing with adenosine

A

Causes brief small vessel vasodilation .. could get buried hypertension, dizziness, or palpitations

161
Q

Dyspnea adenosine

A

Induce bronchoconstriction

162
Q

Caffeine and theophylline decrease effectiveness of adenosine

A

Caffeine increase HR.

Methylxanthines bocks the receptors for adenosine on the heart

163
Q

Dipyridamole may intensify effects of adenosine

A

It is an antiplatelet medication hat blocks the uptake and metabolism of adenosine and may intensify effects,,,may get more serious side effects

164
Q

How is adenosine given

A

Rapid IV push followed by a saline fracture lush. Bc it’s Half life is only a few seconds

165
Q

Lidocaine (xylocaine)

A

Sodium Channel blocker that inhibits neuronal impulses. It is indicated to treat ventricular dysrhythmias and induce local anesthesia.

166
Q

Side effects lidocaine

A

Drowsiness, confusion, paresthesia, seizures, and respiratory arrest

167
Q

Lidocaine is an __-type anesthetic and it metabolized by the liver

A

Amide

168
Q

Administering lidocaine with a ___ prolongs the duration of local anesthetic effects

A

Vasoconstrictor

169
Q

MOA lidocaine

A

Blocks na channels, preventing action potentials from creating pain perception (skin), suppresses neuronal excitability in ventricular dysrhythmias (heart) it is a class IB antiarrhythmis

170
Q

Indications for lidocaine

A

Ventricular arrhythmias, anesthetic

171
Q

Ventricular arrhythmias and lidocaine

A

Slows nerve conduction in heart. Slows depolarization and accelerates depolarization duration.

172
Q

Unlike other antidysrhthmic meds, lidocaine does not cause ___ effects

A

Anticholinergic

173
Q

Lidocaine anesthetic

A

Nonselective amide local anesthetic blocks conduction to both sensory and motor neurons.

174
Q

In what order does lidocaine block impulses

A

Autonomic, somatic, sensory, somatic motor

175
Q

Side effects lidocaine

A

Paresthesia
Seizure (CNS excitation(benzodiazepine may manage))
Respiratory depression (high IV doses suppress CNS)
Drowsiness 9CNS excitation is followed by depressive symptoms)

176
Q

Giving lidocaine with a vasoconstrictor (epi)

A

Extends the duration of the local anesthetic. By decreasing blood flow and delaying systemic absorption of the anesthetic, epi prolongs anesthesia and decreases the risk of toxicity.

177
Q

Magnesium sulfate

A

CNS depressant that inhibits release of acetylcholine at neuromuscular junctions which prevents skeletal and uterine muscle contraction.

178
Q

Indications for magnesium sulfate

A

Preterm labor contractions

Preeclampsia

179
Q

Side effects magnesium sulfate

A

Warm feeling, hypotension, decreased DTR, decreased respiratory rate, decreased urine output, paralytic ileus

180
Q

Antidote for magnesium sulfate

A

Gluconate

181
Q

MOA magnesium sulfate

A

Muscle relaxant and depresses the CNS by stopping the release of ach resulting in decreased neuromuscular irritability and cardiac conduction. The action resolves preterm labor contractions by relaxing the uterus. In addition, by depressing the CNS, magnesium sulfate can decrease hyperreflexia and prevent the onset of seizures from eclampsia

182
Q

Indications for magnesium sulfate

A

Preterm labor contractions and preeclampsia

183
Q

Preterm labor contractions and magnesium sulfate

A

Relaxes the uterine muscle and resolves preterm labor contractions

184
Q

Preeclampsia and magnesium sulfate

A

Muscle relaxant decreases presence of hyperreflexia and lowers risk of seizures

185
Q

Side effects magnesium sulfate

A

Warm feeling, hypotension, decreased DTR, creased respiratoy rate, decreased urine output, paralytic ileus,

186
Q

Antidote to magnesium sulfate overdose

A

Calcium gluconate

187
Q

Digoxin

A

Cardiac glycoside extracted from the plant deigitalis

188
Q

MOA digoxin

A

Direct inhibition of the Na/K ATPase pump in the membranes of myocytes. Leads to increased sodium ions int he myocytes which decreases the sodium concentration gradient. Inhibiting the Na/Ca exchanger, which depends on a constant inward sodium gradient to pump calcium out of myocytes

189
Q

Overall effect of digoxin

A

Decreases sodium concentration gradient and indirectly decreases subsequent calcium outflow

190
Q

Result of digoxin MOA

A

Increased calcium concentration in heart cells leading to increased contractility of the heart also called positive inotropy

191
Q

Digoxin indication

A

CHF who remain symptomatic despite adequate diuretic and ACE inhibitor treatment. Also has vagal activity thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node. Slowed conduction through AV node makes the drug commonly used in AFIB with rapid ventricular response

192
Q

In a fib, rapid ventricular rate leads to insufficient diastolic filling time. By slowing the conduction in the AV node, digoxin can do what

A

Reduce ventricular rate therefore improving ventricular filling and the pumping function of the heart

193
Q

MOA gigoxin

A

Direct inhibitor of Na/K ATPase
Indirect inhibition of Na Ca exchanger
Increase Ca in cell
Positive inotropy

194
Q

Indications for digoxin

A

CHF
Stimulation vagus nerve
Decreased conduction at AV node
A fib

195
Q

First line of CHF treatment

A

Not dogoxin

196
Q

Digoxin and vagal nerve

A

Stimulate thereby decreasing heart rate by slowing depolarization of pacemaker cels in AV node

197
Q

A fib digoxin

A

Slowed conduction through AV node makes this drug used for a fib with rapid ventricular response.

Digoxin can reduce ventricular rate therefore improving ventricular filling and the pumping function of the heart

198
Q

Acute digoxin MOA

A

Inhibit na/k atpase pump. In heart this results in increased calcium concentration in myocytes, as well as increased vagal tone

199
Q

Why get adverse drug reactions with dogoxin

A

Narrow therapeutic index

200
Q

Side effects digoxin

A

Hyperkalemia
Cholinergic
Blurry yellow green vision with halo of light
Arrhythmia(bradycardia)

201
Q

Hyperkalemia digoxin

A

Paralysis of Na/K ATPase pump

202
Q

Cholinergic digoxin

A

Cholinergic symptoms like nausea, vomiting diarrhea and GI

203
Q

Arrhythmia from digoxin

A

Increased intracellular calcium

204
Q

Pathognomonic of dogoxin toxicity

A

Combo of increased atrial arrhythmias and inhibited AV conduction like paroxysmal atrial tachycardia with AV block

205
Q

EKG changes with dogoxin

A

Prolonged PR interval
Decreased QT
Scooping of EKG
T wave inversion

206
Q

Why decreased QT

A

Increased calcium and increasedionotropy

207
Q

How treat digoxin toxicity

A

Activated charcoal and normalize k+
If that doesn’t work
Digibind (antitoxin Fab)

Rate control done with magnesium sulfate, lidocaine, and cardiac pacing

208
Q

Digibind

A

First line treatment if have. A lot of digixin.

209
Q

Beta 1 agonistdobutamine

A

Catecholamine that works as a beta 1 agonist, increasing inotropic activity of the heart.

210
Q

MOA dubatamine

A

Cardiac stimulant used to treat heart failure, or in patients who have had cardiac surgery.

211
Q

Side effects dobutamine

A

As a beta 1 sympathomimetic, it can lead to tachycardia and arrhythmias, thus, patients should be closely monitored when this medication is give.

212
Q

What meds may increase potency of dobutamine

A

MAIOs and TCAs

213
Q

MOA dobutamine

A

Beta 1 agonist

Inotropic

214
Q

Indications for dobutamine

A

Heart failure

Cardiac surgery or cardiogenic shock

215
Q

Side effects dobutamine

A

Tachycardia, arrhythmias

216
Q

Condiersations dobuatmine

A

Closed monitor patients for adverse cardiac side effects

Other meds increase potency so be aware.

217
Q

Norepinephrine

A

Ok

218
Q

Statins

A

Class of medications used in clinical setting to lower patient cholesterol levels. These emdicatios work by inhibiting the HMG-CoA reductive, a rate limiting enzyme int he cholesterol synthesis pathway.

219
Q

Effect of statins

A

Increase HDL and decrease LDL and triglycerides, which are proven to reduce the risk of cardiovascular events in high risk patients.

220
Q

Side effects statins

A

Rhabdomyolysis and hepatotoxicity

221
Q

Satstins __ HMG-CoA reductase

A

Inhibit

222
Q

What does HMG-CoA reductase do

A

Cholesterol synthesis rate limiting enzyme

223
Q

Statins decrease LDL _ times as much as they lower triglycerides

A

3

224
Q

Statins increase __

A

HDL

225
Q

Actor a statin (lipitor)

A

MNG-CoA ereductase inhibitor

226
Q

Suffix of meds that inhibit HMG-CoA reductase

A

Statin

227
Q

Indication for statins like atorvastain

A

Hypercholesterolemia

228
Q

Side effect atorvastatin

A

Rash, hepatotoxicity, myopathy, rhabdomyolysis

229
Q

You should monitor _ enzymes on statin

A

Liver

230
Q

Why avoid grapefruit juice on statins

A

Contains chemicals that inhibit CPY3A4, causing levels of the. Statin to increase

231
Q

Why give statins at bed time

A

Liver makes majority of cholesterol at night time

232
Q

Hepatotoxicity and statins

A

Liver makes cholesterol and may be harsh

Monitor for jaundice and liver function tests

233
Q

How monitor rhabdomyolysis ons tatin

A

Serum CK levels

234
Q

Why is too much CK bad for kidney

A

Plugs the glomeruli and prevents normal glom filtration

235
Q

Vitamin B3

A

Niacin

Essential vitamin used in energy reactions as a component of NAD.

236
Q

How is niacin created

A

From aa tryptophan and requires vitamin B6 in order to convert the aa to niacin

237
Q

Pellet RA

A

Niacin defiency

238
Q

4 Ds of pellegra defiency

A

Diarrhea
Dermatitis
Dementia
Death

239
Q

Niacin deficient often results from depletion of tryptophan as is seen in ___ and ___

A

Hartnup disease

Serotonin syndrome

240
Q

Niacin can also be used as a cholesterol medication

A

More significant side effects though

241
Q

Niacin and NAD

A

Niacin is an essential component of NAD which is a coenzyme found in all living cels. It is commonly used in oxidation reduction reactions.

242
Q

Hartnup diseases

A

B6 defiency
Inability ofkidney to reabsorbed aa including tryptophan. This can cause a niacin defiency bc there is no tryptophan for conversion

243
Q

Carcinoid syndrome and niacin

A

From metastatic carcinoid tumor, which actively secretes serotonin.

244
Q

How is serotonin created

A

Derived from tryptophan and can cause a niacin defiency due to depletion of tryptophan

245
Q

Pellegra niacin defiency

A

Diarrhea
Dermatitis
Dementia
Death

246
Q

Glossitis and niacin defiency

A

Tongue red? Idk

247
Q

How can flushing from niacin therapy be treated

A

Aspirin

248
Q

Niacin

A

B3

249
Q

Use of B3

A

Decrease cholesterol

250
Q

Effects of niacin therapy

A

Decrease LDL and triglycerides

Increase HDL

251
Q

MOA niacin

A

Inhibition of lipolysis in adipose tissue, as well as reduction of hepatic VLDL secretion

252
Q

Side effect of niacin

A

Red, flushed face

253
Q

Why get flushing with niacin

A

Prostaglandin activation

254
Q

How can we reduce flushing from niacin

A

Asprin by blocking the prostaglandin mediated pathway

255
Q

Side effect niacin therapy

A

Hyperglycemia and hyperuricemia

256
Q

MOA niacin B3

A
  1. Inhibits lipolysis in adipose tissue (cant make vldl and ldl)
  2. Reduces hepatic vldl secretion—->decrease in FFA also suppresses hepatic expression of apolipoprotein C3 and leads to a reduced VLDL
257
Q

Indications for niacin

A

Want to decrease triglycerides, LDL and increase HDL

258
Q

What is a triglyceride

A

Esters derived from glycerol and three fatty acids—->high levels can lead to atherosclerosis so use statins

259
Q

Side effects niacin

A

Flushing-give asprin
Hyperglycemia
Hyperuricemia(may exacerbate gout)

260
Q

Why may niacin exacerbate gout

A

May cause hyperuricemia

261
Q

Fibrates

A

Carboxylic acid medications indicated for use in hyperlipidemia and other dyslipidemias

262
Q

Action of fibrates

A

Decrease triglycerides, increase HDL (slight), decrease LDL (slight)

263
Q

MOA fibrates

A

Upregulate LPL, allowing accessibility to triglyceride-rich lipoproteins for lipolysis

Increasing hepatic uptake of fatty acids and decreasing hepatic production of triglycerides, decreasing their overall levels

264
Q

What causes a slight increase in HDL with fibrates

A

Increased amounts of apoporoteins A-1 and A-II which allow more efficient reverse cholesterol transport

265
Q

Why get slight decrease of LDL with fibrates

A

Formation of LDL with a higher affinity for its receptor, allowing it to be catabolized quicker

266
Q

Side effects of fibrates

A

Hepatotoxicity and increase LFT values as well as cholesterol gallstones, which is due to increased cholesterol content in bile. Also myagias, increased CPK and resulting acute kidney injury

267
Q

Indications for fibrates

A

Hyperlipidemia

268
Q

MOA fibrates

A

Upregulated LPL(metabolizes triglyceride)
Decrease triglycerides
Slight increase in HDL
Slight decrease in LDL

269
Q

Side effect fibrates

A

Hepatotoxicity

Cholesterol gallstones

270
Q

Why get cholesterol gallstones with fibrates

A

Increase the cholesterol content of bile

271
Q

Ezetimibe

A

Lowers the plasma cholesterol in patients with hyperlipidemia by preventing cholesterol reabsorption at the small intestine brush border

272
Q

With ezetimibe, what happens when cholesterol reabsorption at brush border is inhibited

A

LDL receptors are upregulated , causing increased LDL uptake into cells. Thus there is a lower LDL value in circulating blood

273
Q

Side effect ezetimibe

A

Diarrhea-from large amounts of cholesterol being trapped in the gut lumen
Also increased LFT values

274
Q

Indications for ezetimibe

A

Hyperlipidemia

275
Q

MOA ezetimibe

A 
Cholesterol absorption blockers at brush border
Decreases LDL (but upregulation of LDL receptors so increased LDL uptake into cells and decreased levels in bloos)
276
Q

What is ezetimibe often combined with

A

Statins

277
Q

Why is upregulating LDL receptors good with ezetimibe

A

Increase uptake into shell

278
Q

Side effects ezetimibe

A

Diarrhea and increased LFT values

279
Q

Bile acid resins

A

Sequester bile acids and disrupt enterohepatic circulation of bile

280
Q

Indication for bile acid resin

A

Hyperlipidemia

281
Q

MOA bile acid resins

A

Bind to bile acids and represent their reabsorption in the GI system, leaving them to be excreted. Circulating cholesterol is then utilized to replace the lost bile, decreasing blood levels of cholesterol.

282
Q

Bile acids: by promoting apoprotein A1 synthesis, HDL levels __ __

A

Slightly increase

283
Q

Bile acids: by activating phosphatidic acid phosphatase, triglyceride synthesis is promoted slightly ____ ___

A

Raining triglycerides

284
Q

These drugs lead to upregulation of __ receptors in hepatocytes

A

LDL. So it is taken intracellular lh, decreasing plasma LDL cholesterol levels

285
Q

Common bile acids

A

Colestipol, cholestyramine, which can be used for diarrhea treatment and toxin absorption and colesevalam

286
Q

Side bile acid resins

A

Complaint of bad taste and GI disturbances that accompany their use. These medications lead to decreased absorption of fat soluble vitamins and cholesterol gallstones aw well.

287
Q

Indications for bile acid resins

A

Hyperlipidemia -

Familial hyperlipidemia type IIa

288
Q

What is familial hyperlipidemia type IIa

A

An inherited disease where patients display xanthelasmas, arcus senilis, and tendon xanthomas

289
Q

MOA bile acid resins

A

Bile acid reabsorption prevented (bind to bile acids in GI and makes insoluble so excreted in poop)

Slight increase HDL/Triglycerides

Activate phosphatidic acid phosphatase (which promotes hepatic TG synthesis and slightly raises their levels)
Decrease LDL…upregulation of hmg coa reductase and LD reductase restulting in increase uptake of LDL particles by hepatocytes and reduction in plasma LDL

290
Q

Colestipol

A

Bile acid resin

Can bind to other medications and decrease their absorption/MOA such as digoxin, lasix and tetracycline

291
Q

Cholestyramine

A

Bile acid resin
Used for crohns who had ileal resection to prevent diarrhea

Can also be used to absorb toxins during C diff infection

292
Q

Colesevelam

A

Bile acid resin

Also used to improve glycemic control in TIID

293
Q

Side effects bile acid resins

A

Cholesterol gallstones
Decreased absorption of fat soluble vitamins
Patients hate it(taste bad and lead to GI discomfort)

294
Q

Nitroglycerin

A

I rate medication used to treat angina and pulmonary edema . Fast acting and a potent vasodilator

295
Q

Low doses of nitroglycerin

A

Angina and pulmonary edema, as it vendor lates on a larger scale than it vasodilator, causing it to decrease cardiac preload

296
Q

High doses nitroglycerin

A

Vasodilator more than venodilates and can be sued as an antihypertensive agent

297
Q

Nitroglycerin is broken down in the blood stream into __ which does what

A

NO

Activates guanyl cyclase and a resulting increase in cGMP. This acts to relax SM, decreasing venous pressure

298
Q

Side effects nitroglycerin

A

Directly related to vasodilator effects

-hypotension, reflex tachycardia, flushing and Monday disease(industrial workers mainly)

299
Q

Contraindication nitroglycerin

A

In combination with viagra (sildenafil) as it can lead to unsafe , rapid decreases in blood pressure

300
Q

Nitroglycerin indications

A 
Pulmonary edema (quick potent vasodilator to reduce preload—>>decreases amount of blood flowing into heart and decreasing edematous in lungs)
Angina
301
Q

MOA nitroglycerin

A

Decreases preload->potent vasodilator and at low doses venodilates more than vasodilates. (High doses opposite and decreases afterload to be used as an antihypertensive agent)

Releases NO in blood-activated guanyl cyclase in smooth muscle, leading to an increase in cGMP, which acts to relax muscle contraction and leads to vasodilation

302
Q

Side effects nitroglycerin

A

Hypotension, reflex tachycardia, flushing, Monday disease

303
Q

Why get reflex tachycardia with nitroglycerin

A

Compensatory mechanism for maintaining cardiac output as bp drops

304
Q

Why get flushing with nitroglycerin

A

Vasodilator effects-common face ad neck

305
Q

Monday disease and nitroglycerin

A

Usually industrial workers exposed to nitroglycerin.
Cerebral vasodilation and terrible headaches. Workers develop tolerance to nitroglycerin and feel fine throughout week. After weekend when not exposed they return to work and feel the effects of nitroglycerin on Monday

306
Q

Contraindications for nitroglycerin

A

Viagara

Both drugs potential cGMP and venodilates. This combination is unsafe due to huge drops in bp

Pharmacology (52 decks)

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