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
How does one mitigate the early admin effects of warfarin administration?
Heparin (for a few days) to counteract early inc coagulation.
26
What is the 1/2 life of the K dependent clotting factors and how does this impact warfarin?
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.
27
At what point after administration of warfarin should INR be checked?
72 hours after
28
What is true about warfarin administration for patients with liver disease?
Patients with liver disease have impaired clotting factor production = exaggerated response to warfarin. Should start admin at lower doses.
29
What is the antidote for warfarin overdose?
vitamin K
30
Describe dosing of warfarin among different patients.
Very individualized - different patients likely to require different doses to achieve affect.
31
How does diet affect warfarin?
Vegetarians take in more vitamin K requiring more warfarin. Meat eaters may require less warfarin.
32
How does diarrhea affect warfarin dosing?
Diarrhea impairs absorption of fat soluble vitamins like vitamin K. Less vitamin K = decreased warfarin dose.
33
T/F: Warfarin crosses the placenta.
True
34
Describe warfarin and drug interactions.
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
By what admin routes is warfarin available?
IV and PO but IV is never used bc it is expensive and its onset of action is no faster than PO
36
What does INR stand for and why is it measured to titrate warfarin rather than PT?
INR = International Normalized Ratio | PT is variable in different labs, INR is consistent.
37
Name the three novel oral anticoagulants and how often each is dosed.
Dabigitran - bid Apixiban - bid Rivaroxaban - qd
38
What are the pros and cons of the novel oral anticoagulants?
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
Which novel oral anticoagulant can be reversed? What is the reversal agent and how does it work?
Dabigitran can be reversed with Idarucizumab - an antibody that binds dabigitran.
40
What is the mechanism of ADP receptor antagonists?
Inhibits one of the many pathwyas by which platelets aggregation occurs --> platelets become less sticky
41
What are the indications for use of ADP receptor antagonists?
CAD, PCI, Stent Placement/Coating, CVA
42
What was the first ADP receptor inhibitor and why is it rarely used?
Ticlopidine - it causes neutropenia & thrombocytopenia
43
What are three key differences between ADP receptor inhibitors?
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
Name three ADP receptor inhibitors other than the first one made.
Clopidogrel, Prasugrel, Ticagrelor
45
What routes of administration is heparin typically administered and why not others?
IV and SC - heparin is too big to be given by other routes
46
What animal is heparin derived from?
pigs - porcine derived
47
How is coagulability measured after heparin administration?
PTT
48
T/F: Heparin crosses the placenta.
False
49
What is the antidote for heparin its dose?
Protamine - 1mg for every 80-100 units of heparin
50
How is heparin typically dosed?
80 u/kg bolus, then 18 u/kg/hr. titrated to effect using PTT with a max dose of 2,000 u/hr
51
How long after heparin is initiated should PTT be checked?
6 hours after initiation, then adjust
52
Discuss the major potential adverse event related to heparin use and how it is mitigated.
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
What is the advantage of using low molecular weight heparin?
Less likely to cause HIT
54
How is LMWH cleared and what is the clinical implication?
Cleared renally - may need to adjust dose.
55
List four drugs that are heparinoids, IE, heparin like substances that do not cause HIT.
Fondaparinux, Danaparoid, Hirudins, Argatroban
56
Why is dopamine not used to treat parkinson's disease?
It does not cross the blood-brain barrier
57
What are the effects of dopamine at different dose ranges?
2-5 mcg/kg/min: renal artery dilation 5-10 mcg/kg/min: beta-1 agonist > 10 mcg/kg/min: alpha-1 agonist
58
What is dobutamine's mechanism of action? How is it administered and what is its indication?
It is a beta-1 agonist. It is an IV only drug that is used in CHF.
59
Describe the mechanism of action of glycoprotein (GP) IIB and IIIA antagonists.
mediates platelet aggregation by blocking the final common pathway of platelet aggregation.
60
What is the route and indication of GP IIB and IIIA antagonists?
They are IV only and used for PCI and in stents.
61
What is the primary risk of GP IIB and IIIA antagonists?
hemorrhage
62
What is the mechanism of action of plasminogen activators?
In the body, activated plasminogen is converted to plasmin --> plasmin chews up existing clots.
63
What is the difference between plasminogen activators and other anticoagulants?
Plasminogen activators eliminate existing clots where other anticoagulants only prevent new clots from forming.
64
What are the indication for use of plasminogen activators?
MI (depending on time since onset of chest pain) and stroke.
65
What is important to remember when considering use of plasminogen activators?
There are absolute and relative contraindication. HTN is a relative contraindication.
66
What are the most commonly used plasminogen activators?
alteplase and streptokinase