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Pharmacology (Dale Turley) > Exam 5 - ppt 2 > Flashcards

Exam 5 - ppt 2 Flashcards

1
Q

What is ECMO?

A

Extracorporeal membrane oxygenation

providing both cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of gas exchange

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2
Q

What are the two most common ECMO’s?

A

veno-arterial (VA)

veno-venous (VV)

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3
Q

ECMO has been used on ________, but it is seeing more use in ______ with cardiac and respiratory failure

A

children

adults

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4
Q

ECMO artificially removes the _____________ and ___________ red blood cells.

A

carbon dioxide

oxygenating

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5
Q

Generally it is only used in the later treatment of a person with heart or lung failure as it is solely a life-sustaining intervention.
What is it?

A

ECMO

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6
Q

_____________ _____ generally used for shorter-term treatment.

A

cardiopulmonary bypass (CPB) not ECMO

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7
Q

____ ________are typically placed in the ascending aorta and vena cavae, allowing complete bypass.

A

CPB cannulae

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8
Q

_________________ in ECMO can be placed in the femoral or internal jugular veins, limiting its size and the amount of support.

A

Venous inflow cannula

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9
Q

________ _______ (if utilized) is placed femorally.

A

Arterial cannula

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10
Q

___ (intraoperative) can also be converted to ____, in which case right atrial and ascending aortic cannulae will be utilized

A

CPB

ECMO

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11
Q

Aspirin was first introduced by the drug and dye firm ____ in 1899

A

Bayer

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12
Q

Aspirin is ___________ acid

A

Acetylsalicylic

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13
Q

Aspirin is in what class of drugs?

A

NSAIDS

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14
Q

Aspirin MOA?

A

Inhibits prostaglandin and thromboxane synthesis

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15
Q

Aspirin inhibits _________ ____ conversion to __________ __.

A

Arachidonic acid

into Prostaglandin H2

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16
Q

______ ____ of aspirin is required for effective anti-inflammatory action

A

higher dose

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17
Q

____ _______ of aspirin inhibit platelet generation resulting in an antithrombotic effect

A

Low doses

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18
Q

What is the typical lose dose ?

A

typically 75 to 81 mg/day

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19
Q

Intermediate doses of aspirin inhibit ____ and ___, blocking prostaglandin (PG) production

A

COX1

COX2

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20
Q

What is the typical intermediate dosage for Aspirin?

A

650 mg to 4 g/day

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21
Q

The anti platelet effect significantly reduces the incidence of ______ and __ in patients at risk .

A

stroke and MI

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22
Q

Aspirin prolongs ________ ____

A

bleeding time

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23
Q

How long to the inhibitory effects on platelet aggregation last ?

A

8 days

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24
Q

What is salicylism?

A

salicylate poisoning

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25
Q

patients can get what intoxication after repeated administration of high dose ?

A

mild chronic salicylate

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26
Q

Aspirins ______________ change at higher doses.

A

pharmacokinetics

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27
Q

What are salicylism symptoms?

A

Symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, nausea, vomiting, and sometimes diarrhea

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28
Q

What type of immediate tx is needed during salicylism ?

A

Gastric lavage

Activated charcoal to adsorb drug left in the stomach / dialysis

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29
Q

FDA recommends no ASA to those under the age of __?

A

16

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30
Q

An association between aspirin use and induction of ___________ exists in children

A

Reye’s syndrome

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31
Q

Reye’s syndrome is a rapidly progressive ____________ which usually begins shortly after recovery from an acute viral illness, especially _________ & _________ (chickenpox)

A

encephalopathy

influenza and varicella (chickenpox).

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32
Q

______ _____ with minimal inflammation and ________ ______ can be signs of Reyes

A

Fatty liver

cerebral edema

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33
Q

Reyes syndrome effects many organs, especially what?

A

brain and liver

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34
Q

Reyes syndrome can cause elevated blood ________ level and low _____ _____.

A

ammonia level ( hepatic encephalopathy )

and

low blood sugar

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35
Q

What are the classic features of Reyes syndrome ?

A

rash, vomiting and liver damage

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36
Q

What are complications and precautions with ASA?

A

GI bleeding - b/c it is a cyclooxyrgenase drug

coagulation disorder

G6PD deficiency

influenza, varicella, or febrile viral infection (pts <20 yo think reyes)

caution in pts 80 yo and older - liver metabolism is narrow

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37
Q

Heart failure is a syndrome resulting in the inability of the heart to maintain adequate ________ ______ to meet metabolic needs

A

coronary output

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38
Q

Heartfailure can occur _______ congestion

A

without

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39
Q

What are some abnormalities that occur with HF?

A

Myocardial contraction (systolic dysfunction)

Ventricular relaxation (diastolic dysfunction)

or BOTH

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40
Q

What are two common causes of HF?

A

HTN

CAD

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41
Q

What is the four- staging system that focuses on the symptoms of HF?

A

American Heart Association (AHA) / American College cardiology (ACC) staging system

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42
Q

What is the staging system that has categories based on how heart failure affects a person’s ability to function?

A

New York Heart Association (NYHA) staging system

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43
Q

What staging system and is more popular and used as a tool to assess progress therapy ?

A

NYHA

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44
Q

Pharmacologic Treatment of Heart Failure is aimed at ____________ the neurohormones that are increased in heart failure (HF).

A

antagonizing

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45
Q

What are the drugs used most to treat HF?

A

Drugs used most are beta blockers, vasodilators, nitrates, diuretics, and digitalis (cardiac glycoside).

Patients are often on a multidrug regimen to prolong life and control symptoms.

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46
Q

Pharmacologic Treatment of Heart Failure targets?

A

a) reduce HF symptoms
b) reduce underlying cause
c) reverse changed body system

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47
Q

What is diastolic HF?

A

heart does not fully relax so it does not fill with blood

stiff heart muscle can’t relax normally

less blood fills the ventricles

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48
Q

What is systolic HF?

A

heart does not pump enough blood

weakening heart muscle cannot squeeze as well

Less blood pumped out of ventricles

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49
Q

Management of Diastolic HF ?

A

Angiotensin converting enzyme inhibitors (ACEI)

Beta blockers

Diuretics

Calcium channel blockers (CCB)

Negative inotrope (flecainide) CCB, BB, Class Ia, Ic)

Angiotensin receptor blockers (ARB)

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50
Q

Management of Systolic HF?

A

Digoxin

Diuretics (esp Loop)

Nitrates

ACEI’s

B-adrenergic amine (Dobutamine) (sympathometic)

PDE3 (phosphodiesterase): Amrinone, Milrinone

Standard therapy = ACEI + Loop ± Digoxin

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51
Q

What is the standard management of SHF?

A

ACEI + Loop + or - digoxin

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52
Q

What is digoxin?

A

A cardiac glycoside

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53
Q

What plant is digoxin derived from?

A

digitalis purpurea

54
Q

What are the actions of digoxin that meet the goals for SHF treatment?

A

Strengthen the heartbeat

Slow the heart rate

Convert irregular cardiac/sinus rhythms

Maintain ventricular rate between 70 and 80 beats/minute

55
Q

Digoxin MOA?

A

Inhibits NA/K/ATPass Pump

56
Q

When cardiac glycosides like ________ inhibit the Na/K ATPase pump on cardiac cells, it increases Na that is exchanged for ___ by the ___/__ exchanger.

A

digoxin

exchanges for Ca

by the Na+/Ca++ exchanger

57
Q

The accumulation of intracellular Ca++ binds to _________ which results in increased _____________ of the heart muscle

A

troponin-C

contractility

58
Q

How does digoxin work?

A

increases contraction
prolongs refractory of AV node
decreased conduction through AV and SA nodes

59
Q

Digoxin is ________ inotrope, which means it?

A

positive

it increases cardiac output

60
Q

Digoxin is a ________ chronotrope, which means it ?

A

negative

it decreases heart rate

61
Q

What are clinical considerations with digoxin ?

A

There is systemic, coronary arterial, and venous vasoconstriction (especially when given by injection … over 15–20 min).

There is some diuretic effect as it inhibits reabsorption of Na+.

Digoxin use is recommended in concert with diuretics, ACEI’s, and beta blockers to alleviate CHF symptoms.

Many interactions and contraindications!

Monitor for electrolyte imbalances!

Watch aldosterone blockers (Potassium sparing diuretics) worsening renal failure

Monitor for narrow therapeutic index which can lead to digitalis toxicity!

62
Q

How do you treat digoxin toxicity?

A

Digoxin Immune Fab ( digibind)

63
Q

Digoxin HF?

A

Half-life: 36–48 hours, increasing in elderly and with renal impairment.

64
Q

Digoxin adverse reactions EENT, META, NEURO?

A

EENT: blurry vision “yellow, green halo’s”

META: electrolyte imbalance (K+) , increase in K+

NEURO: headache, weakness, disorientation, hallucinations ( get a dig level, ASA level)

65
Q

What does digoxin decrease serum concentrations of?

A 
Aminoglycosides, antimetabolites
fibrates
antacids
bismuth
thyroid prep
Licorice
St. Johns Wort ( high fiber diet)
High fibre meal
66
Q

What does digoxin increase serum concentrations of?

A 
Use of laxatives
Use of macrolides ( Z-PAK)
Quinidine
amiodarone
benzodiazepines
verapamil
67
Q

What are contraindications to using Digoxin?

A

Geriatrics are highly sensitive ( to dig)
AV Blocks and arrhythmias
Hypersensitivities
Patients with hypocalcemia, hypokalemia, hypomagnesemia

68
Q

Patient education of digoxin?

A

Instruct patient on how to take pulse and HR

Review signs and symptoms of toxicity

Advise patient to keep away from excess sunlight

Advise patient to use original Rx container

Warn of diminished effect with high fiber meal

Advise patient to wear MedicAlert bracelet

Advise patient to increase intake of potassium

Warn that antacids and antidiarrheals diminish effect

Advise missed doses need to be taken within 12 hours of next dose

69
Q

Digoxin: Pregnancy Special Considerations?

A

Experience shows it can be used on a case-by-case situation when risk of not using it is high to mother.

70
Q

Digoxin: Geriatrics Special Considerations?

A

Age-related changes in renal function show dosage must be altered down or else toxicity can occur.

71
Q

What does the FDA category digoxin for pregnancy?

A

Category C

72
Q

What are clinical uses of Antiarrythmic Drugs?

A

Clinical uses:
Abnormalities in heart rhythm
Fast: tachyarrhythmia
Slow: bradyarrhythmia

73
Q

Goals with Antiarrythmic Drugs?

A

Restore normal sinus rhythm

Suppress the initiation of abnormal rhythms

74
Q

What are class I and what do they do?

A

Sodium Channel Blockers

Inhibit ventricular automaticity and slow conduction velocity

75
Q

What are class II and what do they do?

A

Beta Blockers

Block sympathetic action

76
Q

What are class III and what do they do?

A

Potassium Channel Blockers

Prolong action potential duration and refractoriness

77
Q

What are class IV and what do they do?

A

Calcium Channel Blockers

Slow AV and SA node conduction velocity

78
Q

Class I: sodium channel blockers MOA?

A

Inhibit ventricular automaticity and slow conduction velocity

79
Q

What do Class IA do?

A

Lengthen action potential duration

Prolong ventricular refractory period

Increase conduction rate at AV node

80
Q

What do Class IB MOA?

A

Slow conduction and shorten action potential duration in healthy cardiac tissue ( healthy tissues doing the work )

Alters signal conduction in neurons by blocking the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for signal propagation.

81
Q

What do Class IC MOA?

A

Acts in the refractory period of Purkinje fibers without altering the refractory period of the adjacent myocardium

Works by slowing the influx of sodium ions into the cardiac muscle cells, causing a decrease in excitability of the cells.

Propafenone is more selective for cells with a high rate

82
Q

Class IA: Sodium Channel Blockers examples?

A

Quinidex
Procainamide
Disopyramide

83
Q

Clinical uses of Class IA?

A

treatment of atrial arrhythmias

84
Q

Class IA has Many side effects and adverse reactions, like?

A

Cardiovascular
hematologic
neurologic

Drug-induced lupus with procainamide

Given IV

85
Q

Class IB: Sodium Channel Blockers examples?

A

Lidocaine (Xylocaine IV)
tocainide (tonocard)
mexiletine ( mexitil)

86
Q

Clinical uses of Class IB?

A

Ventricular arrhythmias, especially during an acute myocardial infarction

Digitalis-induced arrhythmias

87
Q

Class IC: Sodium Channel Blockers examples?

A

propafenone (Rythmol) flecainide (Tambocor)

88
Q

Clinical uses of Class IC?

A

treatment of sustained ventricular tachycardia and paroxysmal supraventricular tachycardia (PSVT)

89
Q

BBW for Flecainide (Tambocor)?

A

Use only for life-threatening arrhythmias

Increased risk of mortality when used for non-life-threatening ventricular arrhythmias

90
Q

Side effects and adverse reactions of class IC?

A

arrhythmias

Increased QT prolonged with Macrolides ( can progress to Torsades de Pointe)

91
Q

Class II: Beta Blockers - Beta-1 selective act mainly on?

A

cardiac muscle

92
Q

Class II: Beta Blockers - Beta-2 selective act mainly on?

A

cardiac, lung, arterial, pancreatic, kidney, adipose, liver tissues

93
Q

Class II: BB MOA?

A

Decrease heart rate, conduction velocity, and force of contraction

94
Q

Class II/lll Beta-blocker/ Potassium Channel Blockers combo example?

A

Sotalol (Betapace)

Class II and Class III drug (Combo)

95
Q

Sotalol (Betapace) is a non-selective completive ____-___________ receptor blocker that also exhibits Class __ anti arrhythmic properties.

A

beta-adrenergic

class III

96
Q

Due to the dual action of sotalol, it is often used preferentially to other beta blockers as treatment for both ventricular ____________ and ventricular ___________.

A

fibrillation

tachycardia

97
Q

Class III: Potassium Channel Blockers examples?

A

Amiodarone (Cordarone) - Vtach, Vfib, SVT maybe

98
Q

Clinical uses of Class III: Potassium Channel Blockers PO?

A

PO: Management of supraventricular tachyarrhythmias

Restricted for life-threatening arrhythmias because of potential for drug toxicity

99
Q

Clinical uses of Class III: Potassium Channel Blockers IV?

A

IV: ACLS/PALS management of ventricular fibrillation and pulseless ventricular tachycardia

Restricted for life-threatening arrhythmias because of potential for drug toxicity

100
Q

What is amiodarone (cordarone) contraindicated with?

A

many ABS

101
Q

BBW of Class III: Potassium Channel Blockers?

A

Hepatotoxicity

Pro-arrhythmic (make worse) - sometimes it can cause other arrhythmias

Pulmonary fibrosis

102
Q

Examples of Class IV: Calcium Channel Blockers?

A

verapamil (Calan)

diltiazem (Cardizem)

103
Q

Class IV: Calcium Channel Blockers give temporary control of rapid ____________ _____ in ____ or ________

A

ventricular rates

in a-fib and a-flutter ( acute Tx IV)

104
Q

Class IV: Calcium Channel Blockers achieve conversion of ____ into normal sinus rhythm?

A

PSVT

105
Q

Side effects of Class IV: Calcium Channel Blockers ?

A

Peripheral edema!

106
Q

Conscientious Prescribing of Antiarrhythmics?

A

Need thorough medication history

Monitor serum electrolytes

Refer to cardiologist for initial outpatient therapy

Monitor potassium levels

Monitor renal and hepatic function

Monitor serum levels after reaching steady state

Monitor with 12 lead electrocardiogram

107
Q

Patient/Family Education of Antiarrhythmics?

A

Instruct patient on how to take a pulse and BP

Advise to wear Medic Alert bracelet as ID for drugs

Advise to seek help if hypotensive (Buy a BO Cuff)

Advise to seek help if patient develops fever, chills, sore throat, bruising

Advise to keep follow-up appointments

Advise of side effects, especially dizziness

Caution to be careful when driving or activity that requires alertness

108
Q

what is angina cause by?

A

Thought to be caused by the imbalance between oxygen supply and demand

109
Q

Chronic stable angina symptoms and signs?

A

deep pressure or pain in the sternum that usually radiates elsewhere

Brought on by exertion

Relieved by rest or
nitroglycerine

Lasts less than 10 minutes

110
Q

Treatment goals for angina?

A

Reducing myocardial oxygen demand

Improving oxygen supply to myocardial tissue

Treating cardiac risk factors

Controlling any factors that could lead to ischemia

111
Q

Short terms treatment for angina ?

A

Nitrates

112
Q

Long terms treatment for angina ?

A

ABCDE

A: aspirin and anticoagulation

B: beta blockers and blood pressure control - reduce activity of myocardium

C: cholesterol-lowering agents and smoking cessation

D: diet

E: exercise ? make sure cardiologist screened them to make sure they can exercise and to what extent

113
Q

What is nitrates MOA?

A

Frank-Starling mechanism

Increases coronary blood flow by dilating the coronary arteries and improving collateral flow to ischemic regions

Reduces myocardial oxygen demand by decreasing preload and to a lesser extent decreasing afterload

114
Q

What is Frank-Starling mechanism?

A

Larger volume of blood flows into the ventricle

The blood will stretch the walls of the heart, causing a greater expansion during diastole

In turn this increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole

115
Q

Nitroglycerin vaso________

A

dilates

116
Q

Does Nitroglycerin work more on veins or arteries?

A

Greater in the veins than arteries

117
Q

Because Nitroglycerin works more on the veins, it results in ______ pooling and thereby ___________ left ventricular volume (preload) and ________ ventricular EDV.

A

venous

decreasing

reducing

118
Q

Nitroglycerin increases pressure in the _____?

A

brain

119
Q

Clinical uses of Nitroglycerin?

A

Acute angina (sublingual dosage forms)

Long-term prophylaxis of angina pectoris (oral, buccal, and transdermal forms)

Adjunct in the treatment of acute myocardial infarction and acute heart failure (IV form)

inferior wall MI exception of treating chest pain with NITRO - do not give them nitro - their pressure will tank and you will kill them

120
Q

Nitroglycerin _________ coronary blood flow by ________ the coronary arteries and improving collateral flow to ischemic regions

A

Increases

dilating

121
Q

Nitroglycerin has serious adverse reactions with concurrent use of ________, _________, __________.

A

sildenafil (Viagra)
tadalafil (Cialis)
vardenafil (Levitra)

122
Q

PDE5 medications have a ___________ effect that is more significant with nitroglycerin causing ___________

A

synergistic

Hypotension

123
Q

Examples of Nitrates for angina?

A

Isosorbide dinitrate (Isordil) isosorbide mononitrate (Imdur, Monoket)

124
Q

Clinical uses of Isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur, Monoket)?

A

prevention of angina

125
Q

Isosorbide denigrate and Isosorbide mononitrate are not for the treatment of _____ _______.

A

acute attacks

126
Q

Dinitrate: undergoes _____ first-pass metabolism

A

100%

127
Q

Mononitrate: _______ undergo first-pass metabolism

A

does not

128
Q

Clinical uses of Ranolazine (Ranexa)?

A

chronic angina

New 2006

Can be used in conjunction with other BP medications

nitrate for chronic use and does not react with a lot of the drugs but it does reactive with the PDE5’s

129
Q

Ranolazine increases efficiency of ___ under _______ conditions.

A

ATP

under hypoxic

130
Q

Ranolazine has Antianginal and anti-ischemic effects without ___________ change

A

hemodynamic

Pharmacology (Dale Turley) (31 decks)

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