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Tim's Cards > 2Pharm I > Flashcards

2Pharm I Flashcards

1
Q

Rank diuretics from most to least potent:

A

Loop

Thiazides

Carbonic anhydrase inhibitors (very mild)

Potassium sparing

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2
Q

What is the most common cardiovascular disease whose prevalence increases with age?

A

Hypertension

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3
Q

Individuals at 55 years old with NORMAL BP have a ___% lifetime risk for developing hypertension

A

90%

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4
Q

Hypertension contributes to what 2 categories of disease?

A

Coronary artery disease

Cerebral artery disease

*heart and brain

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5
Q

What are 3 categories of hypertension?

A

Essential (idiopathic - 90%)

Secondary (identifiable)

Malignant (5%, retinal/renal damage)

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6
Q

BP intervention LESS THAN 60 yrs:

BP intervention OVER 60:

A

140/90

150/90

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7
Q

AHA/ACC recommend lifestyle changes if Systolic is what range?

Diastolic?

A

140-159

90-99

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8
Q

What are the 3 basic ways to reduce overall blood pressure?

A

Reduce peripheral resistance

Reduce cardiac output

Reduce blood volume

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9
Q

How do most diuretics work?

A

Block Na+ reabsorption

Which then blocks water

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10
Q

In the US _____ are the first line of drugs in hypertension treatment

A

Diuretics

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11
Q

What was the first class of diuretics (no longer used b/c of toxicity)?

A

Mercurials

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12
Q

What is the first choice, and most commonly prescribed class of diuretic?

A

Thiazides (benzothiazides)

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13
Q

What do Thiazides block in the kidney?

2 things

A

Blocks Na+ reabsorption in Proximal and Distal tubules

Carbonic anhydrase (this decreases H+ availability for exchange with Na+)

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14
Q

With Thiazides, what is the problem in losing Na+ in the distal/proximal tubules?

A

K+ is also lost (hypokalemia)

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15
Q

When taking Thiazides, if sodium intake increases, ________ is exacerbated.

A

Potassium loss

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16
Q

Why are a lot of Diabetics not on Thiazides?

A

Hyperglycemia is side effect

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17
Q

Hypokalemia, Hyponatremia, Hypomagnesaemia, loss of carbonate, hyperuricemia, Hyperglycemia, elevated cholesterol, triglycerides, weakness, no boner.

What am I?

A

Thiazide diuretic

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18
Q

According to lectures, 2 thiazide drugs we need to know:

A

Hydrochlorothiazide (Microzide)

Chlorothiazide (Diuril)

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19
Q

What is the most powerful class of diuretic?

A

Loop

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20
Q

3 effects of Loop Diuretics

A

Major volume loss

Electrolyte imbalance (Na+ and K+ loss)

Ototoxicity

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21
Q

Loop diuretics block the _______ symporter

A

Na/K/Cl

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22
Q

Hyponatremia, hypokalemia, hyperglycemia, hypocalcemia, hyperuricemia, NEPHROTOXICITY, ototoxiciy, GI distress, CNS effect

What am I?

A

Loop diuretic

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23
Q

From lecture, 2 loop diuretics we need to know:

A

Ethacrynic acid (Edacrin)

Furosemide (Lasix)

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24
Q

What 2 classes of drugs cause the Lichenoid Drug Rxn?

A

Thiazide and Loop diuretics

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25
Q

What class of diuretic competes with aldosterone?

Where does that competition take place?

A

Potassium sparing diuretics

Distal renal tubules

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26
Q

Potassium sparing diuretics save K+ and ____.

They increase ___ and ____ excretion

A

H+

Na+ and Cl-

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27
Q

2 potassium sparing diuretics:

A

Spironolactone (Aldactone)

Triamterene (Dyrenium)

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28
Q

Adverse effects of Potassium sparing diuretics: Hyperkalemia, and what 4 other things?

A

Gynecomastia in males

Breast tenderness in young women

Menstrual irregularities

Decreased libido in males

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29
Q

What mild diuretic is now used mostly for glaucoma, and as an adjunctive therapy for congestive heart failure?

A

Carbonic anhydrase inhibitors

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30
Q

One carbonic anhydrase inhibitor we need to know:

A

Acetazolamide (Diamox)

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31
Q

What drug is used in emergencies to decrease blood volume?

Which to we need to know?

A

Osmotic diuretics

Urea (Ureaphil)

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32
Q

What diuretic is rarely used - but treats hypochloremic stated and metabolic alkalosis in the ER?

*produced a lot of chloride

What preparation do we need to know?

A

Acidifying Agents

Ammonium chloride

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33
Q

Caffeine is a _______ that inhibits tubular reabsorption of Na+ by inhibiting _______ in the ______

A

Xanthine

ADH

Bowman’s capsule

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34
Q

Most diuretics cause ________ and many cause ______

A

Xerostomia

Aphthous stomatitis

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35
Q

T/F

Use of NSAIDS for greater than 3 weeks can decrease diuretic effectiveness

A

True

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36
Q

T/F
Many pts take potassium supplements to counteract the K+ loss from diuretics but this is contraindicated in case of severe renal impairment

A

True

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37
Q

Potassium supplements (salts) are contraindicated with what?

A

ACE Inhibitors

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38
Q

5 classes of drugs used to lower BP:

A

Diuretics

Sympathetic blockers (alpha, beta)

ACE inhibitors

Angiotensis II receptor blockers (ARB’s)

Calcium channel blockers (CCB’s)

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39
Q

T/F

Beta blockers decrease cardiac output even though constrict vessels via beta2

A

True

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40
Q

Beta blockers decrease _______ secretion

A

Renin

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41
Q

Cardioselective beta blockers block ______ only

A

Beta1

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42
Q

A beta2 agonist is used for ________

A

Asthma

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43
Q

Beta1 receptors are in the _____

Beta2 receptors are in the ______

A

Heart

Lungs

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44
Q

2 cardioselective Beta Blockers (blocks Beta1 only):

2 noncardioselective Beta Blockers (blocks beta1 and beta2):

A

Beta1:

Atenolol (Tenormin)

Metoprolol (Lopressor, Toprol)

Beta2:

Nadolol (Corgard)

Propranolol (Inderal)

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45
Q

What class of drugs has side effects consistent with over-activity of the parasympathetic nervous system?

A

Beta blockers

*GI upset, xerostomia, orthostatic hypotension, sexual dysfunction, etc

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46
Q

4 contraindications to beta blockers:

A

Congestive heart failure

Asthma

Heart block

Diabetes

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47
Q

What receptors are located postsynaptically and produce vasoconstriction, increasing peripheral resistance when stimulated?

A

Alpha1

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48
Q

Alpha1 blockers produce ________

A

peripheral vasodilation

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49
Q

T/F

Alpha1 blockers have big effects on cardiac output and renal blood flow

A

False

*little effect

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50
Q

T/F

Alpha1 blockers are more effective when used with diuretics and/or beta blockers

A

True

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51
Q

Other than decreasing peripheral resistance, what is another effect of Alpha1 blockers?

A

Decrease urinary resistance

*benign prostatic hypertrophy

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52
Q

Alpha1 blocker =

A

Old men

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53
Q

3 adverse effects of Alpha1 blockers:

A

Orthostatic hypotension

CNS effects

Cardiovascular effects

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54
Q

3 Alpha1 Receptor blockers:

A

doxazosin (Cardura)

prazosin (Minipress)

tamsulosin (Flomax)

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55
Q

Women shouldn’t handle Flowmax, and its chief side effect in men is…

A

severe orthostatic hypotension

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56
Q

ACE inhibitors - inhibit Angiotensin Converting Enzyme how?

A

competitively

*prevents angiotensin I to angiotensin II conversion

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57
Q

Explain ACE Inhibitor pathway/mechanism:

A

blocks Angiotensin I - Angiotensin II

Low Angiotensin II increases Renin

Renin reduces Aldosterone secretion

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58
Q

Normally aldosterone does what in the kidneys?

A

retains Na+ and water

*so ACE Inhibitors will decrease Na/Water retention (pee free water)

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59
Q

What are the 2 primary beneficial effects of ACE Inhibitors?

A

Vasodilate

Decrease Blood Volume

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60
Q

What is the most widely prescribed ACE Inhibitor in the US?

A

lisinopril (Prinivil, Zestril)

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61
Q

2 ACE Inhibitors:

A

lisinopril (Prinivil, Zestril)

enalapril (Vasotec)

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62
Q

What are 2 side effects of ACE Inhibitors?

A

Chronic Dry Cough

Angioneurotic edema with first dose

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63
Q

What causes the Chronic Dry Cough associated with ACE Inhibitors?

A

Increased Bradykinin release in bronchial tree

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64
Q

Angiotensin Receptor Blockers, aka…

A

Angiotensin II Receptor Blockers

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65
Q

T/F
ARB’s block vasoconstrictor and aldosterone-secreting effects of Angiotensin II

Resulting in…

A

True

increased Renin, vasodilation, decreased Na/Water retention, and reduction in BP

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66
Q

What is often preferred over ACE inhibitors b/c the action is at the receptor and there are fewer side effects

*better tolerated

A

ARB’s

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67
Q

What may decrease the effectiveness of ARB’s?

A

NSAIDS

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68
Q

CNS, Upper respiratory infections, GI effects, cramps, angioedema, teratogenicity - what am I?

A

ARB’s

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69
Q

2 common ARB’s:

A

losartan (Cozaar)

valsartan (Diovan)

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70
Q

What is the new, expensive class of drugs for Hypertension?

A

Renin Inhibitor

*binds to Renin, decreasing levels of Angiotensin I - II - Aldosterone

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71
Q

Calcium Channel Blockers prevent Ca++ from entering…

A

slow channels

select voltage-sensitive areas

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72
Q

T/F
Calcium Channel Blockers relax coronary vascular smooth muscle and cause coronary vasodilation, increasing myocardial oxygen delivery

A

True

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73
Q

Calcium Channel Blockers are used for what 3 CV purposes?

A

Hypertension

Angina

Arrhythmias

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74
Q

Calcium’s role in muscle contraction - it binds ______

which turns on ______

which phospholrylates ________

so that it can better bind ______ and produce muscle contraction

A

calmodulin

myosin kinase

myosin

actin

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75
Q

3 Calcium Channel blockers:

A

amlodipine (Norvasc)

nifedipine (Adalat, Procardia)

verapamil (Calan)

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76
Q

verapamil (Calan) has major effects on the ______

nifedipine (Procardia) has more of an effect on _______

A

heart

blood vessels

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77
Q

What Calcium channel blocker is (most) associated with gingival hyperplasia?

What % have the responder gene that results in hyperplasia from this drug?

A

nifedipine (Procardia)

33%

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78
Q

T/F

Good oral hygiene will limit the extent and severity of a lesion due to a Calcium Channel Blocker

A

True

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79
Q

Why are Centrally Acting Antihypertensives used less often?

A

Less tolerated

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80
Q

clonidine (Catapres) is a centrally acting antihypertensive that is a ______ Agonist, that activates _____ neuron, which decreases _______

A

Alpha2

Inhibitory

Sympathetic outflow

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81
Q

Xerostomia, Parotid gland swelling/pain, Dysgeusia:

A

clonidine (Catapres)

*Centrally acting antihypertensive

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82
Q

What class of drug blocks granular uptake and storage of norepinephrine (decreasing sympathetic activity due to lack of neurotransmitter supply)

A

Catecholamine Release Blockers

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83
Q

2 Catecholamine Release Blockers:

A

reserpine (Serpasil)

guanethidine (Ismelin)

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84
Q

Antihypertensive meds react with general anesthetics and CNS depressants by enhancing _______

A

hypotention

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85
Q

Antihypertensive meds have a _____ response to vasoconstricting drugs

A

potentiated

*this why use epi w/ caution, take BP prior to locals

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86
Q 
T/F
OTC sympathomimetics (like cold capsules) counteract antihypertensive therapy
A

True

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87
Q

Use of NSAIDS longer than _____ may decrease effectiveness of diuretics, beta blockers, and ACE inhibitors

A

3 weeks

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88
Q

T/F

Nicotine constricts blood vessels and increases BP

A

True

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89
Q

With Antihypertensive meds, prevent sudden changes in _____ with pts.

impregnated gingival retraction cord (vasopressors) is ______

Rebound hypertension develops when agents withdrawn, which happens often in men b/c ____ is severe

A

posture

contraindicated

impotence

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90
Q

Diuretics make you _____ potassium

ACE Inhibitors and ARB’s make you ______ potassium

A

lose

gain (increase)

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91
Q

According to published guidelines, what 4 factors should be addressed when managing CV disease?

*HTN, obesity, and cholesterol…

A

Lifestyle

Obesity

Cholesterol

Risk assessment

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92
Q

The Risk Assessment portion of managing DV disease includes what 3 tiers?

A

Lifestyle changes

Drugs for under 60 140/90, over 60 150/90

Drugs for 160/100 + BP

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93
Q

The primary indication for diuretics is _______

or life threatening edema (loop diuretics) or renal failure (osmotic diuretic - urea)

A

Hypertension

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94
Q

All Hypertension drugs have what 4 side effects?

A

Xerostomia

Weakness/fatigue

Sexual impotence/libido in men

Fake lichen planus

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95
Q

Antihypertensive meds have what drug interactions that are significant in dentistry?

(4 things)

A

Epinephrine

Vasoconstrictors

General anesthetics/CNS depressants

Prolonged analgesics, sedatives, and tranquilizers (CNS)

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96
Q

Use of NSAIDS longer than ____ weeks may decrease effectiveness of some diuretics, beta blockers, and ACEi

A

3 weeks

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97
Q

3 precautions to take during dental procedures when treating Hypertensive pts:

A

Fainters/Fallers (orthostatic hypotension)

Compliance

NSAID popping - diuretics don’t work as well

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98
Q

What is the term for pain when the heart becomes Anoxic?

A

Angina

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99
Q

T/F

Angina is an ischemic heart disease, often involving the coronary arteries, and is greater if there is Hx of MI

A

True

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100
Q

Angina can be brought on by triggers, but absent that the pain occurs most often when?

A

Nighttime

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101
Q

Typical angina (exertional) is caused by the _____ arteries causing ischemia

A

coronary

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102
Q

If the demand exceeds available oxygen, then necrosis occurs =

A

myocardial infarction

103
Q

Typical angina is ______

Atypical angina (variant), aka….

A

extertional

Prinzmetal’s

104
Q

Normally there are Beta2 receptors in coronary arteries, in Prinzmetal’s angina there are more _____ receptors

A

Alpha 1

*causes vasoconstriction w/ epinephrine

105
Q

Variant (Prinzmetal’s) angina shows an elevated ______ segment on an EKG that is not present in normal angina

A

S-T

106
Q

Nitrites and Nitrates work on endothelial cells to produce______ that cause ______ via _______

A

nitric oxide

***arterial/venous vasodilation

relaxation of all smooth muscle

107
Q

T/F

Nitrates/NItrites produce vasodilation and increase venous return to the heart

A

False

*decrease venous return

108
Q

Why do NItrates/Nitrites cause headache?

A

vasodilation is intense and fast

109
Q

Other than headache, what are 5 side effects of Nitrites/Nitrates?

A

Postural hypotension and syncope

Flush/Rash

tachycardia/increased peripheral resistance (due to sympathetic reflex)

methemoglobin

decrease oxygen carrying in large doses

110
Q

T/F
There is rapid onset to Nitrites/Nitrates and also rapid tolerance, which is why there is usually a 12 hrs on 12 hrs off schedule

A

True

111
Q

What is the fastest onset Nitrite/Nitrate preparation?

A

Amyl nitrate snorted

112
Q

Nitroglycerin is considered a “rescue” drug and is often in emergency kits

A

True

113
Q

Why is nitroglycerine stored in a small brown vial?

A

Photosensitive

114
Q

T/F

Nitroglycerin is very caustic and leaves a sublingual burn

A

True

115
Q

What is the longer duration option for nitroglycerin?

A

Patch (up to 12 hours)

116
Q

Two Nitrites/Nitrates we need to know:

A

Isosorbide dinitrate (Isordil)

Isosorbide mononitrate (Imdur)

117
Q

Beta blockers decrease cardiac ______, which decreases oxygen demand and decreases Angina

A

output (afterload)

118
Q

inotropic:

chronotropic:

A

force

timing

119
Q

T/F

Beta blockers have negative chronotropic and inotropic effects

A

True

120
Q

Pts with a history of MI will always be taking_______

A

beta blockers

121
Q

Beta blockers cause vasodilation

A

False

122
Q

Beta blockers are contraindicated for some forms of congestive heart failure and ________

A

Variant/Prinzemetal’s Angina

123
Q

Why are beta blockers often combined with diuretics?

A

Prevent sodium retention

124
Q

Cardioselective agents are preferred for insulin-dependent diabetics and _______

A

Asthmatics

125
Q

What does epinephrine do if the pt is taking a beta blocker?

A

Won’t stimulate the heart

Will vasoconstrict Alpha1 receptors

126
Q

Non-selective Beta blockers enhance what response to epinephrine?

What does this response entail? (2 things)

A

Pressor

hypertension, reflex bradycardia

127
Q

T/F

It’s ok to use epi with cardioselective beta blockers

A

True

128
Q

T/F
Epinephrine dilates large vessels/muscles

Epinepherine constricts small vessels/muscles

A

True

129
Q

If a pt is on heart meds, it’s most likely a Beta blocker - what 2 things do you ask?

A

Are you a diabetic?

Asthma?

130
Q

Inotropic effect of Calcium Channel blockers:

A

Negative

131
Q

Some Ca++ channel blockers cause smooth muscle relaxation (vasodilation) where?

A

Coronary arteries

132
Q

2 Calcium channel blockers that have a negative inotropic effect:

A

verapamil

diltiazem

133
Q

Ca++ channel blocker that vasodilates coronary arteries:

A

amlodipine

134
Q

Calcium channel blocker that vasodilates peripherally:

A

nifedipine

nicardipine

135
Q

What 2 things to limit in visit from pt on anti-anginals?

A

Extent of procedures/visit

epinephrine

136
Q

If a pt is on an Antianginal, consider local aneshtetics without _____

A

vasoconstrictor

137
Q

What are the practical side effects of antiarhythmic drugs?

A

Arrhythmic manifestations

138
Q

Most Antiarrhythmics prolong _______

others affect the ______ system

A

Prolong

electrical

139
Q

Cardiac arrhythmias produce abnormalities of the heartbeat and all denote something wrong with the _________ system

They are caused by disease, cardiac injury, or drugs

A

electrophysiologic

140
Q

Arrhythmias result from abnormal impulse ______, abnormal impulse ______, or a combination of the two

A

formation

conduction

141
Q

The type of arrhythmia that begins at the nodal level can be Supraventricular, Vetricular, or ______

A

Ectopic foci (preempt SA/AV node)

142
Q

When the His Purkinje system is cut in half and atria/ventricles work independently it is know as a….

A

Heart Block

143
Q

Antiarrhythmic medications ____ parts of the heart that are beating abnormally

A

Depress

144
Q

What are 3 pharmacologic effect of antiarrhythmic medications?

A

Change slope of depolarization

Raise threshold for depolarization

Alter conduction velocity

145
Q

Antiarrhythmic meds work on one or more of the _____ transmembrane phases of the cardiac cycle

A

5

146
Q

What are the 3 areas of the heart that have pacemaker activity?

A

SA node (main)

AV node

Purkinje fibers

147
Q

The spontaneous opening and closing of K+ channels is what drives _______

A

automaticity

148
Q

Where is Effective Refractory Period longer - pacemaker areas or myocardial cells?

*different arrhythmias require ERP be longer/shorter

A

Pacemaker areas

149
Q

In what 2 situations would you want to induce an arrhythmia with epi, isoproterenol (beta agonist) or hypokalemic diuretics?

A

Ventricular arrhythmias due to AV node block

Temporary heart block until pacemaker insertion

150
Q

4 contraindications for Antiarrhythmics

A

Complete AV heart block

Congestive heart failure

Hypotension

Known hypersensitivity to drug

151
Q

A partial heart block is when the _______ is not in sync

A

atria/ventricles

152
Q

T/F
Indications for antiarrhythmic drugs are arrhythmia, flutters, fibrillations, tachycardias, ectopic arrhythmia, or digoxin induced arrhythmia

A

True

153
Q

What are 4 Contraindications to Antiarrhythmics?

A

Complete AV block

CHF

Hypotension

Known hypersensitivity to drug

154
Q

What are the 4 classes of Antiarrhythmics?

A

!a, 1b, 1c

2

3

4

155
Q

Class Ia Antiarrhythmics:

3 drugs, 3 actions

A

1a (medium) = quinidine, (*procainamide, Pronestryl), (disopyramide, Norpace)

blocks Na conduction

Slows ERP

Slows AP

156
Q

Class Ib Antiarrhythmics:

1 drug, 2 actions

A

FAST = lidocaine

blocks Na conduction

Decrease relative refractory period

157
Q

Class Ic Antiarrhythmics:

(2 drugs, 2 actions)

***life threatening ventricular arrhythmias only

A

Slow = flecainide (Tambocor), propafenone (Rhythmol)

blocks Na conduction

conduction velocity

158
Q

Quinidine can lead to what clinical manifestation?

A

Cinchonism

*from cinchona tree

159
Q

Class II Antiarrhythmics:

1 drug, 1 class

A

propanolol

beta blockers

160
Q

Class III Antiarrhythmics:

3 drugs, mechanism

A

amiodarone (Cordarone, Pacerone), bretyllium, sotalol

K+ channel blockers

***sotalol (Betapace) is nonselective beta crossover

161
Q

Class IV Antiarrhthmics:

5 drug, mechanism

A

nifedipine, verapamil, diltiazem, adenosine, Digoxin (cardiac glycoside)

Calcium channel blockers

162
Q

Describe cinchonism from quinidine:

A

nausea, vomiting, headache, TINNITIS

deafness, vertigo, visuals

FATAL arrhythmias

163
Q

What is the site of action of cinchonism (quinidine)?

A

atrial tissues

164
Q

If a patient is taking antiarrhythmics, what do we NOT give them?

What is ok to give them?

A

Atropine (may cause tachycardia)

Lidocaine solutions

***not the same lidocaine as anti-arrhythmic med

165
Q

Prinzmetal angina is seen in ______ men most commonly

A

Japanese

166
Q

Nitrites/Nitrates are _______ vasodilators

A

direct

167
Q

T/F

CCB’s block calcium channels so that calcium trickles more slowly, decreasing the rate and strength of contractions

A

True

168
Q

What two side effects of taking NItrites/Nitrates is accentuated with alcohol?

A

Syncope

Postural hypotension

169
Q

What is the fastest acting Nitrite/Nitrate and how long does it last?

What is the second fastest?

A

Vaporole - (snort) onset 1 minute, lasts 3-15 minutes

Nitroglycerin - onset 1-3 minutes, half life 10 minutes

170
Q

A Transdermal pouch can last up to ___hrs

A

12

171
Q

What are the 2 long acting nitrates?

other than transdermal pouch

A

Isosorbide dinitrate (4-6 hrs)

Isosorbide mononitrate (1/2 life 4 hrs)

172
Q

procainamide (Pronestyl) is a class Ia antiarrhythmic that has reversible _____ like syndrome in ___% of pts

(nickname: novacaine)

A

lupus

25%

173
Q

Class Ib antiarrhythmics (lidocaine, phenytoin, mexiletine, tocainide) are are used to treat ______ arrhythmias

A

ventricular

174
Q

4 class Ib antiarrhythmics:

A

lidocaine

phenytoin (Dilantin)

mexiletine

tocainide

175
Q

amiodarone (Cordarone, Pacerone) contains iodine causing blue skin and may cause _____ disease

*Class III antiarrhythmic

A

thyroid

176
Q

Digoxin is a Class IV antiarrhythmic that increases _____ and ______

A

intracellular Ca

contractility

177
Q

T/F

atropine and isoproteronol treat Bradyarrhythmias

A

True

178
Q

T/F

Potassium and Magnesium treat Ectopic Pacemakers

A

True

179
Q

T/F
The vagal blocking effects of anntiarrhythmic drugs (anticholinergics like atropine) can act synergistically to lead to tachycardia

A

True

180
Q

Congestive heart failure is the inability of the heart to provide the necessary ______

A

output

181
Q

What do drugs target in CHF?

A

Reflex sympathetic output

182
Q

T/F
Right sided heart failure will manifest in fatigue and edema while left side will be more acute and result in pulmonary congestion

A

True

183
Q

T/F

With CHF you want to slow the heart and increase the contractile force

A

True

184
Q

What is the drug of choice in treatment of CHF?

A

digoxin (Digitek, Lanoxin)

aka Cardiac Glycosides

185
Q

Digoxin inhibits __________, resulting in more ________ inside the cell.

This has a positive ______ effect

A

Na/K pump

Ca

inotropic

186
Q

Digoxin has a positive inotropic effect and a negative ______ effect due to directly suppressing ______

A

chronotropic

AV node

187
Q

Digoxin has 3 mechanisms of action: positive inotropic effect through increased Ca, negative chronotropic effect by suppressing the AV node, and what else?

A

Diuresis

*pee excessively, decreasing venous return

188
Q

The increased vagal output caused by cardiac glycosides (digoxin) can be blockes by ________

A

Atropine

189
Q

T/F

Digoxin has a low therapeutic index and can lead to uncoordinated arrhythmias

A

True

190
Q

Few drugs cause sensory side effects - which causes a green/yellowish aura?

A

Digoxin

191
Q

T/F
azole antifungals and macrolides like clindamycin and azythromycin could increase digoxin in the system and increase risk for toxicity

A

True

192
Q

What posture would you not want to put a pt with CHF in?

A

don’t recline fully - hard to breathe

193
Q

T/F

It’s ok to do general anesthesia in a dental setting with a pt with CHF

A

False

*hospital only

194
Q

What are 3 preparations of Bile Acid Sequestrants?

A

chelestyramine resin

colesevelan

colestipol

195
Q

What decreases liver triacylglycerol synthesis necessary for VLDL production?

(decreases plasma LDL’s - used for MILDLY elevated cholesterol)

A

Nicotinic Acid (Niacin)

196
Q

What is the side effect on Niacin?

A

facial flushing

197
Q

What lowers plasma triglycerides and increases HDL by inhibiting cholesterol synthesis in the liver?

A

Fibric Acids

198
Q

What are 3 Fibric Acids?

A

clofibrate

fenofibrate

gemfibrozil

199
Q

The most popular/effective cholesterol inhibitors:

A

statins

HMG coA reductase inhibitors

200
Q

HMG CoA reductase is the _____ step in the synthesis of ______

A

rate limiting

cholesterol

201
Q

When can’t you take a statin?

A

Liver disease

***HMG CoA reductase inhibitors alter liver function

202
Q

What is a side effect of statins?

HMG CoA reductase inhibitors

A

myalgias

**rhabdomyolysis - disintegration of muscle tissue

203
Q

What 2 types of drugs promote myalgias in pts taking statins?

A

Macrolide antibiotics (erythromycin)

Azole antifungals

204
Q

2 statins are combined with a drug that decreases intestinal absorption (only drug in class), what is the drug, and what are the combos?

A

ezetimibe

Vytorin - simvastatin + ezetimibe

Liptruzet - atorvastatin + ezetimibe

205
Q

The therapeutic dose for Digoxin is _____% of the toxic dose, which is why every pt needs to be _______

A

50-60%

Titrated

206
Q

Cardiac glycosides are used for what 3 conditions?

A

CHF

A-fib

flutter

207
Q

Cardiac glycosides (digoxin) can cause bradycardia/arrhythmia, _____ effects from stimulation of chemoreceptor zones and vagal nucleus (parasymphathetic effects)

*what other parasympathetic effects?

A

GI

*nausea, vomiting, increased saliation, anorexia, diarrhea, ab pain

208
Q

Other than a Green/Yellow aura, what are 3 other CNS effects of Digoxin?

A

Headache - edema

fatigue

visual

209
Q

Retraction cords and local anesthetics often have ________, which is contraindicated for pts with CHF

A

vasoconstrictors

210
Q

T/F

General anesthesia is dangerous for pts with CHF

A

True

211
Q

Statins should be used in pts with CV disease aged 40-75 and have a ______% or higher risk of having heart attack within 10 years

A

7.5%

212
Q

T/F

You can’t raise HDL without exercise

A

True

213
Q

T/F

Statins shouldn’t be combined with additional cholesterol lowering drugs like niacin or fibrates

A

True

*don’t reduce heart attack/stroke risk

214
Q

DVT =

A

deep vein thrombosis

215
Q

What are 3 types of acute coronary syndromes caused by blood clots in coronary arteries?

A

Unstable angina

Non-ST elevated MI (incomplete blockage)

ST elevated MI (complete blockage)

216
Q

T/F

Stroke reduction benefits of antiplatelets improve when used in combo with aspirin

A

True

217
Q

Aspirin causes _______ platelet aggregation

A

irreversible

218
Q

T/F

You should discontinue low dose aspirin therapy before dental treatment

A

False

*Stroke risk greater than bleeding

219
Q

T/F

Discontinuing aspirin use Increases MI and adverse bleedings and has worse clinical outcomes than nonusers

A

True

220
Q

Antiplatelet drugs used for short and long term stenting have ______ effects on platelets

A

Irreversible

221
Q

4 antiplatelet drugs

A

ticlopidine (Ticlid) *canadian

clopidogrel (Plavix)

prasugrel (Effenet)

ticagrelor (Brilinta)

222
Q

Aspirin blocks _____, which blocks ______

A

COX

Thromboxane A2

223
Q

clopidogrel prevents binding of ____ to collagen receptors thereby preventing platelet aggregation

A

ADP

224
Q

What is used with aspirin and heparin to treat acute coronary syndromes?

A

fibrinogen receptor inhibitors

platelet glycoprotein IIb/IIIa receptor antagonists

225
Q

3 platelet glycoprotein IIb/IIIa receptor antagonists (Fibrinogen Receptor Inhibitors)

A

abciximab (ReoPro)

eptifibatide (Integrilin)

tirofiban (Aggrastat)

226
Q

Thienopyridines prevent the binding of _____ to collagen receptors which prevents platelet aggregation.

It requires ____ to form the clot

A

ADP

Adenosine

227
Q

Percutaneous coronary intervention (stents) combined with antiplatelet therapy has numerous dental advisory guidelines, one being _____ risk of premature discontinuation.

Consult the cardiologist, and defer any procedure with significant bleeding risks until ______

A

catastrophic

thienopyridine therapy conclusion

228
Q

After a DES is placed, wait ___ months for major intervention

__ months for normal stent

A

12

1

229
Q

Leading up to a procedure the pt can go off Plavix, but must stay on ______

A

Aspirin

*restart Plavix right after procedure

**keep pt on 1 antiplatelet

230
Q

Heparin inhibits _____ and ______

produces _____ anticoagulant effect

A

Factor Xa and IIa thrombin

immediate

231
Q

Warfarin interferes with liver synthesis of ______

produced effect in _____ days

A

vitamin K dependent clotting factors

4-5

232
Q

Warfarin inhibits what 4 vitamin K dependent clotting factors?

What 2 proteins?

A

2, 7, 9, 10

C and S

233
Q

6 drugs that alter the efficacy of warfarin:

A

Phenytoin

Phenobarbital

Any liver metabolism drug

Antibiotics

Vita K (spinach)

Tylenol (enhances coagulation)

234
Q

3 antagonists to Heparin and Warfarin:

A

Vitamin K

Phenytoin

Phenobarbital

235
Q

NSAIDS cause _____ effects on platelets

A

reversible

236
Q

Heparin can cause profound bleeding, what is the antidote?

A

Protamine sulfate

237
Q

T/F

Heparin and Warfarin can be overlapped 1-2 days

A

True

238
Q

Warfarin has a mandatory blood test every 30 days b/c of low _____ indes

A

Therapeutic

239
Q

Many things throw off coumadin, _____ being one

A

diet

*vita K

240
Q

T/F
There is no need to discontinue warfarin use prior to routine dental procedures even though it is associated with increased gingival bleeding and mouth ulcers

A

True

241
Q

5 tests used to assess the effects of Heparin and Warfarin:

A

INR

Bleeding time test

PT

aPTT

Intrinsic pathway

242
Q

The International Normalized Ratio (INR) has a therapeutic range of ___ to ____

A

2-3

243
Q

______ and warfarin significantly enhance anticoagulation

A

Acetaminophen

244
Q

What causes the greatest number of drug interactions?

A

Warfarin

245
Q

What is the direct Thrombin inhibitor?

A

dabigatran (Pradaxa)

*prodrug - converted in vivo to dabigatran

246
Q

T/F

The advantages to dabigatron over warfarin is no monthly monitoring and less expensive

A

True

247
Q

What is the antidote to dabigatran (Pradaxa)

A

idarucizumab (Praxbind)

248
Q

Antithrombins drugs (not to be confused with Thrombin inhibitors) are _______ inhibitors

A

Factor Xa

249
Q

What are 3 Factor Xa inhibitors (antithrombins)

A

apixaban (Eliquis)

fondaparinux (Arixtra)

rivaroxaban (Xarelto)

250
Q

Hemorhage, no reversal agent, and loss of ____ function are the major risks to Factor Xa inhibitors (antithrombins)

A

kidney

251
Q

When would Factor Xa inhibitors be used?

antithrombins

A

post op after total hip/knee

prevent stroke

252
Q

Factor Xa inhibitors stop coagulation by preventing _____ mediated effects, including cleavage of fibrinogen to fibrin, and activation of what 4 factors?

A

thrombin

5, 8, 11, 13

253
Q

2 thrombolytic clot busting drugs:

A

streptokinast (Streptase)

urokinase

254
Q

What is the antidote for Tissue Plasminogen Activator (tPA)?

this is a clot forming IV drug = Retavase

A

Epsilon AminoCaproic Acid (Amicar)

*treats hemophilia, cerebral aneurysms

Tim's Cards (140 decks)

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