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Fall Pharm Block 2 > Misc Cardiac > Flashcards

Misc Cardiac Flashcards

1
Q

List the uses of NTG.

A

angina, CHF, acute MI, pulm HTN, HTN emerg.

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2
Q

How would NTG be used in the management of HTN?

A

In combo with another HTN agent

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3
Q

What is the mechanism of action of NTG?

A

converted to nitric oxide - a vasodilator (mostly venules)

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4
Q

What are the cardiac benefits of NTG?

A

dec preload and some CA dilation

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5
Q

Why can’t NTG be given around the clock?

A

Nitric oxide must interact with a sulfahydryl group to cause vasodilation. If sulfahydryl is depleted, NTG will have no effect - requires 10-12 hour NTG free window to replenish depleted sulfahydryl.

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6
Q

List some adverse effects of NTG.

A

dizziness, facial flushing, headaches

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7
Q

How is NTG stored?

A

In a colored glass bottle - NTG sensitive to light and adheres to plastic.

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8
Q

After how many NTG tabs should a Pt call 911 if they are still experiencing chest pain?

A

3

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9
Q

How does one know the NTG tab they took is working?

A

It will sting

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10
Q

How long after the bottle is opened are NTG tabs good for?

A

6 - 12 months

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11
Q

What are some other routes of administration of NTG other than IV and SL?

A

buccal tabs, ointment, transdermal (patch)

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12
Q

Why should a transdermal NTG patch be removed prior to defib?

A

bc the patch has some metal (not bc of the NTG)

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13
Q

If a person has an allergic reaction to a transdermal patch what is the most likely culprit?

A

The adhesive&raquo_space; the drug

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14
Q

What is a significant drug interaction with NTG?

A

PDE-5 inhibitors –> severe hypotension

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15
Q

What are poppers?

A

Inhaled drugs of abuse that contain volatile nitrates and nitrites

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16
Q

What is the name of the ER form of NTG?

A

Isosorbide dintrate or mononitrate

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17
Q

What type of drug is digoxin and what is its mechanism of action?

A

cardiac glycoside that causes positive inotropy and negative chronotropy.

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18
Q

What are the primary uses of digoxin?

A

CHF and A-fib (rate control)

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19
Q

What are adverse effects of digitalis and what results from digitalis toxicity?

A

Anorexia, N/V. Dig toxicity = bradycardia, heart blocks, and yellow halo vision

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20
Q

How is digoxin cleared from the body?

A

renally

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21
Q

What is the antidote for digoxin OD? By what mechanism? And what short term effect does this have on patient assessment?

A

Digibind - Ab that binds to digoxin and makes it inactive. Lab can’t differentiate bound from unbound digoxin - can’t check dig levels for some time after.

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22
Q

What is the class and route of admin of warfarin?

A

PO anticoagulant

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23
Q

What is the mechanism of action of warfarin?

A

Inhibits 2 key enzymes that form vitamin K. Vitamin K needed for the liver to make clotting factors II, VII, IX, and X. Also inhibits protein C and S.

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24
Q

What is the action of protein C and S and how does this affect the action of warfarin?

A

C and S are anti-coagulants. Warfarin causes inc coagulation early after its admin.

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25
Q

How does one mitigate the early admin effects of warfarin administration?

A

Heparin (for a few days) to counteract early inc coagulation.

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26
Q

What is the 1/2 life of the K dependent clotting factors and how does this impact warfarin?

A

II = 60h, VII = 6h, IX = 24h, X = 40h. It will take 30-36 hours for the first clotting factor to be depleted and produce any anticoagulation.

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27
Q

At what point after administration of warfarin should INR be checked?

A

72 hours after

28
Q

What is true about warfarin administration for patients with liver disease?

A

Patients with liver disease have impaired clotting factor production = exaggerated response to warfarin. Should start admin at lower doses.

29
Q

What is the antidote for warfarin overdose?

A

vitamin K

30
Q

Describe dosing of warfarin among different patients.

A

Very individualized - different patients likely to require different doses to achieve affect.

31
Q

How does diet affect warfarin?

A

Vegetarians take in more vitamin K requiring more warfarin. Meat eaters may require less warfarin.

32
Q

How does diarrhea affect warfarin dosing?

A

Diarrhea impairs absorption of fat soluble vitamins like vitamin K. Less vitamin K = decreased warfarin dose.

33
Q

T/F: Warfarin crosses the placenta.

A

True

34
Q

Describe warfarin and drug interactions.

A

Warfarin is plasma protein bound and will interact with other PPB drugs. Warfarin also sticks to a lot of other drugs (levothyroxine for ex) impairing absorption of both drugs.

35
Q

By what admin routes is warfarin available?

A

IV and PO but IV is never used bc it is expensive and its onset of action is no faster than PO

36
Q

What does INR stand for and why is it measured to titrate warfarin rather than PT?

A

INR = International Normalized Ratio

PT is variable in different labs, INR is consistent.

37
Q

Name the three novel oral anticoagulants and how often each is dosed.

A

Dabigitran - bid
Apixiban - bid
Rivaroxaban - qd

38
Q

What are the pros and cons of the novel oral anticoagulants?

A

pros: dose specific for everyone and no INR monitoring is needed (effects predictable)
cons: tough to reverse and can’t monitor therapy (might miss dec adherence)

39
Q

Which novel oral anticoagulant can be reversed? What is the reversal agent and how does it work?

A

Dabigitran can be reversed with Idarucizumab - an antibody that binds dabigitran.

40
Q

What is the mechanism of ADP receptor antagonists?

A

Inhibits one of the many pathwyas by which platelets aggregation occurs –> platelets become less sticky

41
Q

What are the indications for use of ADP receptor antagonists?

A

CAD, PCI, Stent Placement/Coating, CVA

42
Q

What was the first ADP receptor inhibitor and why is it rarely used?

A

Ticlopidine - it causes neutropenia & thrombocytopenia

43
Q

What are three key differences between ADP receptor inhibitors?

A

All differ in the chances they over-anticoagulate
All differ in how quickly they anticoagulate
All differ in how quickly they stop anticoagulating when you d/c the drug

44
Q

Name three ADP receptor inhibitors other than the first one made.

A

Clopidogrel, Prasugrel, Ticagrelor

45
Q

What routes of administration is heparin typically administered and why not others?

A

IV and SC - heparin is too big to be given by other routes

46
Q

What animal is heparin derived from?

A

pigs - porcine derived

47
Q

How is coagulability measured after heparin administration?

A

PTT

48
Q

T/F: Heparin crosses the placenta.

A

False

49
Q

What is the antidote for heparin its dose?

A

Protamine - 1mg for every 80-100 units of heparin

50
Q

How is heparin typically dosed?

A

80 u/kg bolus, then 18 u/kg/hr. titrated to effect using PTT with a max dose of 2,000 u/hr

51
Q

How long after heparin is initiated should PTT be checked?

A

6 hours after initiation, then adjust

52
Q

Discuss the major potential adverse event related to heparin use and how it is mitigated.

A

HIT - heparin induced thrombocytopenia. Heparin acts as a haptin and binds to platelets. Sometimes the immune system does not recognize this complex and attacks the heparin-bound platelets. Must monitor platelet levels in a Pt on heparin.

53
Q

What is the advantage of using low molecular weight heparin?

A

Less likely to cause HIT

54
Q

How is LMWH cleared and what is the clinical implication?

A

Cleared renally - may need to adjust dose.

55
Q

List four drugs that are heparinoids, IE, heparin like substances that do not cause HIT.

A

Fondaparinux, Danaparoid, Hirudins, Argatroban

56
Q

Why is dopamine not used to treat parkinson’s disease?

A

It does not cross the blood-brain barrier

57
Q

What are the effects of dopamine at different dose ranges?

A

2-5 mcg/kg/min: renal artery dilation
5-10 mcg/kg/min: beta-1 agonist
> 10 mcg/kg/min: alpha-1 agonist

58
Q

What is dobutamine’s mechanism of action? How is it administered and what is its indication?

A

It is a beta-1 agonist. It is an IV only drug that is used in CHF.

59
Q

Describe the mechanism of action of glycoprotein (GP) IIB and IIIA antagonists.

A

mediates platelet aggregation by blocking the final common pathway of platelet aggregation.

60
Q

What is the route and indication of GP IIB and IIIA antagonists?

A

They are IV only and used for PCI and in stents.

61
Q

What is the primary risk of GP IIB and IIIA antagonists?

A

hemorrhage

62
Q

What is the mechanism of action of plasminogen activators?

A

In the body, activated plasminogen is converted to plasmin –> plasmin chews up existing clots.

63
Q

What is the difference between plasminogen activators and other anticoagulants?

A

Plasminogen activators eliminate existing clots where other anticoagulants only prevent new clots from forming.

64
Q

What are the indication for use of plasminogen activators?

A

MI (depending on time since onset of chest pain) and stroke.

65
Q

What is important to remember when considering use of plasminogen activators?

A

There are absolute and relative contraindication. HTN is a relative contraindication.

66
Q

What are the most commonly used plasminogen activators?

A

alteplase and streptokinase

Fall Pharm Block 2 (8 decks)

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