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Pharmacology > Pharm B Final > Flashcards

Pharm B Final Flashcards

1
Q

MOA of Aspirin

A

Inhibits COX-1 and COX-2, but its 170x more potent for COX-1 than COX-2. This inhibition suppresses formation of prostaglandins and thromboxanes thus inhibiting platelet aggregation and inflammation

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2
Q

Perioperative effects of aspirin

A
  • Decreased hemostasis (theoretical)
  • Renal dysfunction (theoretical)
  • GI hemorrhage
  • Poor bone healing
  • Bronchospasm
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3
Q

Aspirin is known to have cross reactivity with what other non-opioid pain reliever?

A

Tylenol

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4
Q

Which COX is responsible for bone healing?

A

COX-1

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5
Q

Before which procedure should the patient be on NO recent aspirin?

A

Tonsillectomy

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6
Q

Before which procedures should the patient discontinue aspirin 7 days prior?

A
  • Plastic surgery

- Retinal surgery

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7
Q

How many days are required for full regeneration of platelets after a dose of aspirin?

A

7-10 days

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8
Q

How long does it take for low dose aspirin (less than 650mg/day) to be completely cleared from the body?

A

24 hours

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9
Q

How many platelets does the body make per day

A

70,000 platelets/mL blood

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10
Q

How many platelets are contained in 1 unit of platelets?

A

5,000-7,000

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11
Q

By how much will 1 bag of platelets raise a patient’s platelet count?

A

30-60k because platelet bags come “pooled”

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12
Q

Options for emergency reversal of aspirin

A
  • Platelet transfusion

- DDAVP

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13
Q

How does DDAVP reverse aspirin?

A

Releases vWF and Factor 8

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14
Q

A 55 year-old-woman is having reconstructive breast surgery. She takes aspirin 650mg daily for paroxysmal atrial fibrillation. Her aspirin regimen should:

A. Be discontinued 1 week prior to surgery.
B. Be discontinued 5 days prior to surgery.
C. Be discontinued the morning of surgery.
D. Not be discontinued.

A

A. Be discontinued 1 week prior to surgery.

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15
Q

MOA of Plavix

A

Irreversibly inhibits ADP mediated platelet aggregation

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16
Q

Perioperative effects of Plavix

A
  • Decrease in surgical hemostasis
  • Increased periop blood loss
  • Increased mortality
  • Increased need for blood products
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17
Q

For most surgeries (including cardiac), how soon before surgery should the patient discontinue Plavix?

A

5-7 days

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18
Q

Which surgeries may be OK for patients to continue their Plavix?

A
  • PCI
  • Vascular
  • Cataract
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19
Q

Emergent reversal for Plavix

A

Platelet transfusion

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20
Q

Methods to monitor platelet function

A
  • TEG/ROTEM

- PFA

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21
Q

Which COX is responsible for gastric mucosa protection?

A

COX-1

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22
Q

Which COX is responsible for platelet aggregation?

A

COX-1

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23
Q

Which COX is responsible for inflammation?

A

COX-2

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24
Q

Theoretically, after a dose of Plavix, how many days must minimally pass before a patient’s platelet count is safe for neurosurgery?

A. 1 day
B. 3 days
C. 5 days
D. 7 days

A

C. 5 days

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25
Q

Which “other” anti-platelet drugs work ACUTELY by inhibiting IIb/IIIa?

A

EAT

  • Eptifibatide
  • Acbiximab
  • Tirofiban
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26
Q

Which “other” anti-platelet drugs are used for CHRONIC conditions and work by inhibiting ADP-mediated platelet aggregation?

A
  • Prasugrel

- Ticagrelor

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27
Q

Which “other” anti-platelet drug can be used for thromboembolism/stroke prophylaxis?

A

Ticagrelor

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28
Q

Which “other” anti-platelet may be used for CPB on a HIT patient?

A

Tirofiban

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29
Q

How soon before surgery should Prasurgrel be stopped?

A

7 days

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30
Q

How soon before surgery should Ticagrelor be stopped?

A

5 days

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31
Q

How soon before before surgery should the acute anti-platelet drugs (EAT) be discontinued?

A

24 hours

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32
Q 
A 45 year-old-man is scheduled for a coronary artery bypass graft surgery 6 days after a cardiac catheterization for ACS.  During the cath, an antiplatelet drug was given.  Which antiplatelet drug will increase bleeding risk during the bypass surgery?
A.  Tirofiban (Aggrastat)
B.  Ticagrelor
C.  Abciximab
D.  Prasugrel
A

D. Prasugrel

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33
Q

MOA of Heparin

A

Upregulates anti-thrombin III which inactivates thrombin and factor Xa

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34
Q

CPB dose of heparin

A

300-400units/kg

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35
Q

Target ACT for CPB

A

Over 400-480

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36
Q

Heparin dosing for diagnostic cath

A

2500-5000u

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37
Q

Heparin dosing for interventional cardiology

A

10,000 units

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38
Q

Target ACT for interventional cardiology

A

Over 300

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39
Q

Target ACT for CEA

A

250-300

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40
Q

High risk patients that need a heparin drip

A
  • Thrombolic stroke within a year
  • Mechanical valves
  • DVT
  • PE
  • Recent coronary artery stent/PCI
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41
Q

Half life of heparin

A

1-2 hours

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42
Q

How soon before surgery should a heparin drip be discontinued?

A

4-6 hours

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43
Q

MOA of protamine

A

Directly binds to and inhibits heparin

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44
Q

How are heparin and protamine cleared?

A

Renally

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45
Q

Side effects of protamine

A
  • Vasodilation/hypotension (if pushed too quickly)
  • Bronchoconstriction
  • Increased PA pressures
  • Anaphylactic reactions
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46
Q

Protamine dosing

A

1-1.3mg protamine for every 100 units of heparin

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47
Q

What is heparin rebound

A

Protamine is cleared quicker than heparin so heparin can leech back out from tissue and into the blood

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48
Q

Emory dosing for protamine

A

(Heparin IV dose + 10,000 units) x 0.005

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49
Q

Cap dose of protamine

A

250mg

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50
Q

How much protamine should you give after the initial dose if the ACT is still more than 1.1 times the baseline ACT

A

25mg

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51
Q 
A 75kg, 65 year-old-female has a coronary artery bypass graft surgery.  Before cardiopulmonary bypass, 5000u heparin is given for vein harvest and 30000u heparin is given for bypass anticoagulation. How much protamine should be administered, post bypass, to reverse heparinization?  
A.  25mg
B.  125mg
C.  225mg
D.  325mg
A

C. 225mg

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52
Q

Percentage of patients exposed to heparin that develop HIT

A

5%

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53
Q

How soon after the initial dose of heparin does HIT begin?

A

5-14 days

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54
Q

When should you start to consider that your patient may have HIT?

A
  • Greater than 50% drop in platelets

- Platelet count under 100,000 after heparinization

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55
Q

Testing to confirm HIT

A
  • ELISA

- Serotonin platelet release assay

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56
Q

How long does it take for the heparin/immune complexes of HIT to clear?

A

3 months

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57
Q

Heparin protocol for acute HIT

A

No heparin, use alternative

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58
Q

Heparin protocol for recent HIT with strong positive ab tests and normal platelets

A

Heparin use debatable

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59
Q

Heparin protocol for recent HIT with weak positive ab tests and normal platelets

A

Heparin use probably OK

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60
Q

Heparin protocol for recent HIT with negative ab tests

A

Heparin is OK

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61
Q

When does ATIII deficiency occur

A

Heparin re-dosing causes ATIII to be cleared much more quickly, occurs when heparin binding clears out ATIII to less than 60% baseline levels

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62
Q

Diagnosis for ATIII deficiency

A
  • ACT under 450 after 500units/kg heparin

- ACT under 400 after CPB

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63
Q

Treatment for ATIII deficiency

A
  • ATIII concentrate
  • Recombinant ATIII
  • FFP
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64
Q

Advantages of LMWH (Lovenox)

A
  • Reduced dosing frequency
  • Reduced monitoring
  • Reduced bleeding tendencies
  • Reduced risk of HIT
  • Fewer effects on platelet function
  • More predictable pharmacokinetic response
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65
Q

What lab value is used to monitor the effect of Lovenox (LMWH)?

A

Factor Xa

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66
Q

Can LMWH be fully reversed with protamine?

A

No, it’s only partially effective

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67
Q

What clotting test is unaffected by Lovenox (LMWH)?

A

PTT

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68
Q

Examples of thrombin and Xa inhibitors

A
  • Dabigatran (Pradaxa)
  • Rivaroxaban (Xarelto)
  • Apixaben (Eliquis)
  • Bivalirudin
  • Argatroban
  • Fondaparinux
  • Edoxaban
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69
Q

Direct factor IIa (thrombin) inhibitors

A

BAD

  • Bivalirudin
  • Argatroban
  • Dabigatran
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70
Q

Direct factor Xa inhibitor that works via ATIII

A

Fondaparinux

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71
Q

Direct factor Xa inhibitors

A

EAR

  • Edoxaban
  • Apixaban (Eliquis)
  • Rivaroxaban (Xarelto)
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72
Q 
Which anticoagulant has a pharmacologic profile most suited for its use as a systemic anticoagulant for cardiopulmonary bypass?
A.  Bivalirudin
B.  Argatroban 
C.  Dabigatran (Pradaxa)
D.  Rivaroxaban (Xarelto)
E.  Edoxaban
A

A. Bivalirudin

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73
Q

Thrombin/Xa inhibitors that can be given for CPB for HIT patients

A
  • Argatroban

- Fondaparinux

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74
Q

MOA of Coumadin

A

Inhibits vitamin-K dependent synthesis of factors 2, 7, 9, 10 and proteins C and S

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75
Q

What clotting test monitors Coumadin

A

PT/INR

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76
Q

Medical uses for Coumadin

A

Long term anticoagulation for…

  • A fib
  • Low ejection fraction
  • Mechanical heart valves
  • DVT/PE
  • Vascular disease
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77
Q

Recommendations for pre-op discontinuation of Coumadin for most procedures

A

2-5 days (4 average) – must have normalized INR

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78
Q

For what surgeries might it be okay to continue taking Coumadin before surgery?

A

Cataract surgeries without retrobulbar blocks

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79
Q

Subacute reversal of Coumadin

A

Vitamin K - 10mg/day for 3 days

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80
Q

Methods for acute reversal of Coumadin

A
  • FFP
  • Factor VIIa
  • Factor IX Concentrate
  • Prothrombin Complex Clearance (factors II, VII, IX, X)
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81
Q

Dosage of FFP for acute reversal of Coumadin

A

5-8ml/kg

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82
Q 
A 70 year-old-man with an acute abdomen presents to the operating room for an emergent laparotomy.  Medical history includes congestive heart failure, diverticulosis, and atrial fibrillation on Coumadin.  Left ventricular ejection fraction is unknown.  Preoperative labs show an INR of 3.7.  Pre-induction lung auscultation reveals bilateral basilar crackles.   Which reversal agent is most appropriate to correct the INR?  
A.  Vitamin K
B.  FFP
C.  Factor VIIa
D.  PCC
A

D. PCC

  • Vitamin K isnt fast enough
  • Don’t want to give the volume of FFP because of the lung crackles
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83
Q

Common fibrinolytics

A
  • tPA (Tissue Plasminogen Activator)

- Urokinase

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84
Q

MOA of tPA

A

Activates fibrinolysis by converting plasminogen to plasmin (plasmin breaks down fibrin thus breaks down

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85
Q

MOA of Urokinase

A
  • Activates fibrinolysis by converting plasminogen to plasma
  • Decreases RBC aggregation
  • Decreases plasma viscosity
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86
Q

Is Coumadin used in the OR?

A

No - increases risk of periop bleeding

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87
Q

Are fibrinolytics for use in the OR?

A

No - causes profound bleeding and possible cerebral hemorrhage

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88
Q

When is tPA given for a thrombotic CVA?

A

Within 3 hours of onset - if its given over 3 hours there is risk of conversion to a hemorrhagic stroke

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89
Q

Recommendation for pre-op discontinuation of tPA

A

1-3 hours

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90
Q

Recommendation for pre-op discontinuation of Urokinase

A

1 hour

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91
Q

Options for reversal of fibrinolytics (tpa + urokinase)

A
  • Cryo

- FFP

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92
Q 
A 22 year-old female, postpartum day 2 from a NSVD, becomes hemodynamiclly unstable.  Her left leg is swollen and spiral CT reveals a saddle pulmonary embolus.  tPA is given emergently, but her condition does not improve and she is brought to the OR for emergent embolectomy.  The most appropriate strategy for the reversal of tPA is:
A.  Cryoprecipitate.  
B.  FFP.
C.  Antifibrinolytics.
D.  Expectant management.
A

D. Expectant management

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93
Q

What is TXA (tranexamic acid)

A

Antifibrinolytic

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94
Q

MOA of TXA

A

Prevents plasminogen/plasma from binding to fibrin. Promotes stability of the clot

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95
Q

Positive perioperative effects of TXA

A

-Improved clot stability and hemostasis

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96
Q

Negative potential perioperative effects of TXA

A
  • Harmful clotting in DIC patients
  • Harmful clotting in FV Leiden patients
  • Possible seizures
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97
Q

Bolus dose for TXA

A

15mg/kg over 10min on heparinization

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98
Q

Infusion dose for TXA

A

7.5mg/kg/hr until CPB is over or the bag runs out

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99
Q

How should you consider dosing TXA?

A

On ideal body weight – too much may cause seizures

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100
Q

High risk neuraxial procedures to have while on anticoagulants

A
  • Spinal cord stimulator
  • Intrathecal catheter and pump implant
  • Vertebroplasty/kyphoplasty
  • Epidural decompression
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101
Q

What is the electrophysiologic mechanism responsible for most clinically important arrhythmias?

A

Reentry

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102
Q

What causes reentry?

A

A propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after the refractory period has ended

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103
Q

Underlying causes of dysrhythmias

A
  • Myocardial ischemia
  • Arterial hypoxemia
  • Bradycardia
  • Electrolyte imbalance
  • Certain drugs
  • Acid-base changes
  • ANS changes
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104
Q

Negative effects of persistent dysrhythmias

A
  • Compromised hemodynamic function

- Predisposes to life threatening dysrhythmias such as v-tach and v-fib

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105
Q

Action of Class I antidysrhythmics

A

Membrane stabilizers

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106
Q

Action of Class II antidysrhythmics

A

Beta antagonists

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107
Q

Action of Class III antidysrhythmics

A

Prolong repolarization

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108
Q

Action of Class IV antidysrhythmics

A

Calcium channel blockers

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109
Q

Effects of Class I antidysrhythmics

A
  • Decrease automaticity
  • Decrease conduction through bypass tracts
  • Decrease phase 0 depolarization
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110
Q

MOA of Class I antidysrhythmics

A

Blocking fast Na+ channels and decreasing phase 0 depolarization

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111
Q

Class IA drugs

A
  • Quinidine
  • Procainamide
  • Disopyramide
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112
Q

Class IB drugs

A
  • Lidocaine
  • Tocainide
  • Phenytoin
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113
Q

Class IC drugs

A
  • Flecainide

- Lorcainide

114
Q

Indications for Quinidine

A
  • A-fib
  • Wolff Parkinson White syndrome
  • PVCs
115
Q

Oral dose of Quinidine

A

200-400mg QID

116
Q

IV dose of Quinidine

A

50-75mg/hour

117
Q

MOA of Quinidine

A
  • Decreases slope of phase 4

- Increases fibrillation threshold

118
Q

Side effects of Quinidine

A
  • Diarrhea (up to 40%)
  • EKG changes (can prolong QRS and cause v-fib)
  • Syncope/sudden death
  • Hypotension
  • Allergic reaction
119
Q

Uses for Procainamide

A
  • PVT
  • PVCs
  • VENTRICULAR tachydysrhythmias (not atrial)
120
Q

Bolus dose of Procainamide

A

100mg IV every 5 minutes

121
Q

Max dose of Procainamide

A

15mg/kg

122
Q

Infusion dose of Procainamide

A

2-6mg/min

123
Q

MOA of Procainamide

A
  • Decreases slope of phase 4 like Quinidine but with less QT effects
  • Prolongs QRS
124
Q

Side effects of Procainamide

A
  • Myocardial depression
  • Hypotension
  • Asystole or v-fib
  • SLE-like syndrome
  • Allergic rash
125
Q

Uses for disopyramide

A

Atrial and ventricular tachydysrhythmias

126
Q

Route of administration of Disopyramide

A

Oral

127
Q

MOA of Disopyramide

A

Like quinidine (decreases slope of phase 4)

128
Q

Side effects of Disopyramide

A
  • Direct myocardial depression
  • Anticholinergic activity
  • Prolonged QT and PVT
129
Q

Uses for lidocaine

A

-Ventricular dysrhythmias (PVC, v-tach)

130
Q

IV dose of lidocaine

A

2mg/kg

131
Q

Infusion dose for lidocaine

A

1-4mg/min

132
Q

IM dose of lidocaine

A

4-5mg/kg

133
Q

MOA of Lidocaine

A

Delays rate of phase 4 depolarization and blocks sodium channels in depolarized tissues

134
Q

Side effects from plasma concentrations of lidocaine over 5mcg/ml

A

Stimulation of CNS

135
Q

Side effects from plasma concentrations of lidocaine of 5-10mcg/ml

A
  • Seizures

- Hypotension

136
Q

Side effects from plasma concentrations of lidocaine over 10mcg/ml

A
  • CNS depression
  • Apnea
  • Cardiac arrest
137
Q

Uses of Phenytoin

A
  • Paradoxical VT
  • Torsade de Pointes
  • Digitalis toxicity
138
Q

Dosage of Phenytoin

A

1.5mg/kg every 5 minutes (10-15mg/kg)

139
Q

MOA of Phenytoin

A
  • Shortens QT interval

- Improves conduction through AV node

140
Q

Side effects of Phenytoin

A
  • CNS disturbances (cerebellar symptoms)
  • Increased blood glucose
  • Bone marrow suppression
  • Hypotension
141
Q

Uses for Mexiletine/Tocainide

A

Ventricular tachydysrhythmias

142
Q

Dose of Mexiletine

A

150-200mg PO every 8 hours

143
Q

Dose of Tocainide

A

800mg PO every 8 hours

144
Q

Side effects of Mexiletine/Tocainide

A
  • Epigastric burning

- Neurologic effects

145
Q

Rare side effects with Tocainide

A
  • Bone marrow depression

- Pulmonary fibrosis

146
Q

Uses for Flecainide

A
  • Atrial tachydysrhythmias
  • Ventricular premature beats
  • WPW
147
Q

MOA of Flecainide

A
  • Decrease conduction blocks through AV node

- May decrease SA node function

148
Q

Side effects of Flecainide

A
  • Negative inotropic effect
  • Prodysrhythmic effect
  • Vertigo
  • Visual accommadation problems
149
Q

Class II antidysrhythmic drugs

A
  • Propranolol
  • Metoprolol
  • Esmolol
150
Q

Indications for Class II antidysrhythmics

A
  • Afib
  • A-flutter
  • PAT
  • Digitalis-induced ventricular dysrhythmias
151
Q

MOA of Class II antidysrhythmics

A
  • Blocks sympathetic activity
  • Decreases rate of phase 4 depolarization
  • Decreases rate of SA node discharge
152
Q

Side effects of Class II antidysrhythmics

A
  • Bradycardia
  • CHF
  • Bronchospasm
  • Allergic rash
  • Mental depression
  • Fatigue
153
Q

Class III antidysrhythmic drug

A

Amiodarone

154
Q

Indications for Amiodarone (Class III antidysrhythmic)

A
  • Refractory SVT or V-tach

- WPW

155
Q

Oral dose of Amiodarone

A

200-400mg per day

156
Q

IV dose of Amiodarone

A

150mg over 10 minutes then 1mg/min

157
Q

MOA of Amiodarone

A

Prolongs refractory period in all cardiac tissue (atrial + ventricular)

158
Q

Side effects of Amiodarone

A
  • Pulmonary toxicity
  • Ventricular tachydysrhythmias
  • Hypotension
  • Bradycardia
  • Heart block
159
Q

Class IV antidysrhythmic drugs

A
  • Verapamil

- Diltiazem

160
Q

Indication for Class IV antidysrhythmics

A
  • PSVT

- A-fib/a-flutter

161
Q

IV dose of Verapamil

A

5-10mg

162
Q

PO dose of Verapamil

A

80-120mg PO q 6-8hrs

163
Q

IV dose of Diltiazem

A

20mg IV

164
Q

MOA of Class IV antidysrhythmics

A
  • Decrease phase 4

- Depresses AV node and slows conduction

165
Q

Metabolism and excretion of class IV antidysrhythmics

A
  • Hepatic metabolism

- Renal excretion

166
Q

Side effects of class IV antidysrhythmics

A
  • Hypotension
  • AV block
  • Direct myocardial depression
  • PR prolongation (not great for patients with 1st degree block)
167
Q

Indications for Digitalis

A
  • Atrial tachydysrhythmias

- Heart failure

168
Q

Oral dose of Digitalis

A

0.5-1mg over 12-24 hours

169
Q

MOA of Digitalis

A
  • Increase phase 4 slope

- Increase AV node refractoriness

170
Q

Side effects of Digitalis

A
  • Digitalis toxicity
  • EKG changes
  • Cardiac dysrhythmias
  • Nausea
  • Disturbances of cognitive function
171
Q

Indications for Adenosine

A
  • PSVT

- WPW

172
Q

Dose of Adenosine

A

6mg IV then repeat in 3 minutes with 6-12mg

173
Q

MOA of Adenosine

A

Hyperpolarizes cell and increases refractory period (similar to CCB)

174
Q

Side effects of Adenosine

A
  • Transient AV block
  • Bronchospasm
  • Facial flushing
  • Headache
  • Dyspnea
175
Q

What adjunct equipment should you consider when planning to use Adenosine?

A

External pacing pads

176
Q

What is COX?

A

Cyclooxygenase - enzyme that catalyzes the synthesis of prostaglandins and arachidonic acid

177
Q

Functions of prostaglandins

A
  • Inflammation
  • Renal perfusion
  • Platelet aggregation
178
Q

Where is COX-1 located?

A
  • Gastric mucosa
  • Platelets
  • Renal parenchyma
179
Q

Actions of COX-2

A

“Pain inducing enzyme” - mediates inflammation, pain, fever, and carcinogenesis

180
Q

4 main properties of NSAIDS

A
  • Analgesia
  • Antiinflammatory
  • Antipyretic
  • Platelet inhibition
181
Q

Why isn’t Tylenol considered an NSAID?

A

It isn’t anti-inflammatory

182
Q

MOA of NSAIDS

A

Inhibits both COX enzymes without specificity

183
Q

Do NSAIDS have high first pass metabolism?

A

No - limited 1st pass hepatic extraction

184
Q

Protein binding of NSAIDS

A

Highly protein bound to albumin because they are acidic

185
Q

pKa of NSAIDS

A

pK 3-5

186
Q

Why are NSAIDS good for arthritis/joint pain?

A

They sequester in synovial tissue

187
Q

How does elimination time correspond with therapeutic time of NSAIDS?

A

It doesnt – aspirin is eliminated in 1 hour but effects are seen for 24 hours

188
Q

Advantages of NSAIDS

A
  • Decreases activation of nociceptors
  • Less N/V
  • No respiratory depression
  • No addiction
  • Long duration
  • No pupil changes
  • No cognitive effects
189
Q

Disadvantages of NSAIDS

A
  • Inhibits platelet aggregation
  • Gastric ulceration
  • Renal dysfunction
  • Hepatocellular injury
  • Asthma exacerbation
  • Poor bone healing
  • Displaces drugs that are protein bound
190
Q

Adverse GI effects of NSAIDS

A
  • Dyspepsia
  • N/V
  • Stomach pain
  • Peptic ulcers
  • GI hemorrhage
191
Q

Adverse coagulation effects of NSAIDS

A
  • Platelet dysfunction

- Decreases thromboxane and makes platelets more slippery

192
Q

Clinical uses of ASA

A
  • Analgesia
  • Antipyretic
  • Antiplatelet
  • 1st line fever reducer
193
Q

Side effects of ASA

A
  • GI upset
  • Prolonged PT
  • Induces asthma
  • Prolonged bleeding
194
Q

Which NSAID is safe for renal patients?

A

ASA

195
Q

Uterine effects of ASA

A
  • Can prolong labor

- Risk of hemorrhage from placenta

196
Q

NSAID that can induce Reye’s Syndrome

A

ASA

197
Q

Which patients should not receive ASA?

A
  • Kids (Reye’s syndrome)

- Asthmatics

198
Q

Acetominophen does not have which of the following properties

A

Anti-inflammatory

199
Q

Dose of IV acetaminophen

A

1000mg every 6 hours

200
Q

Max dose of acetaminophen

A

4g in 1 day

201
Q

Per kilo dose of IV acetaminophen

A

15mg/kg (up to 75mg/kg/day)

202
Q

Adverse side effects of Tylenol

A
  • Hepatic toxicity

- Prostaglandin inhibition and decrease in renal perfusion

203
Q

Which patients should not receive tylenol?

A

Liver failure patients

204
Q

How does acetominophen differ from ASA?

A
  • No gastric irritation

- No platelet aggregation effects

205
Q

Actions of Ketorolac

A
  • Potent analgesic

- Minimal antiinflammatory

206
Q

Adult dosage of Toradol

A

30mg IM or IV every 6 hours

207
Q

Peds dose of Toradol

A

0.5mg/kg IM or IV every 6 hours

208
Q

Patients cannot have Toradol if their Creatinine is over

A

1.2

209
Q

Adverse effects of Toradol

A
  • Renal toxicity
  • Platelet inhibition
  • Affects bone growth
210
Q

Which NSAID is used to close the PDA after a baby is born?

A

Indomethacin

211
Q

What common NSAID is a propionic acid derivatives?

A

Ibuprofen

212
Q

NSAID used for gout

A

Phenylbutazone

213
Q

What is Celebrex

A

COX-2 inhibitor

214
Q

COX-2 inhibitors have a high incidence of what adverse effect

A

Thromboembolic events

215
Q

Chest compressions begin when a neonate’s heart rate drops below

A

60

216
Q

Most common cause of respiratory arrest in peds

A

Hypoxia

217
Q

Effects of pediatric renal physiology on drug administration

A

Babies have a lower GFR so medications excreted by glomerular filtration may have a prolonged half life. Less frequent dosing of antibiotics.

218
Q

Hepatic physiologic differences in peds

A
  • P450 system is 50% of adults

- Phase II is impaired in neonates

219
Q

Since phase II of drug metabolism is impaired in neonates, the excretion of what commonly used drugs are affected?

A
  • Benzos
  • Morphine
  • Caffeine
220
Q

Why do neonates have delayed excretion of medications?

A
  • Large volume of distribution due to increased total body water content
  • Lower protein binding
221
Q

How are half lives of drugs different in neonates?

A

Shortened – the half life of drugs increases as they approach adulthood

222
Q

If a patient has a mitochondrial disease, what induction drug should be avoided?

A

Propofol

223
Q

Peds propofol dosing for a pure IV induction

A

2.5-3mg/kg

224
Q

Peds propofol dosing after an inhalation induction

A

1mg/kg

225
Q

Contraindications to ketamine

A
  • Active URI
  • Increased ICP
  • Open globe injury
  • Psych/seizure disorder
226
Q

Pediatric dose for IV ketamin

A

0.5-2mg/kg

227
Q

Pediatric dose for IM ketamine

A

4-6mg/kg

228
Q

Pediatric dose for oral ketamine

A

6-10mg/kg

229
Q

Peds dosing for oral versed

A

0.5mg/kg

230
Q

Max of oral versed in pediatrics

A

15mg

231
Q

IV dose of succinylcholine in infants

A

2mg/kg

232
Q

IM dose of succinylcholine in infants

A

5mg/kg

233
Q

Im dose of succinylcholine in children over 6 months

A

4mg/kg

234
Q

Side effect of sux

A

Can cause bradycardia - treat with atropine

235
Q

What NMB may last longer in infants?

A

Roc - give 1/3 to 1/2 the usual dose

236
Q

Former preemies are prone to apnea up to __ weeks PCA

A

60

237
Q

Considerations for airway of Trisomy 21 patients

A
  • C spine instability

- Macroglossia

238
Q

Trisomy 21 patients are good candidates for what anesthetic drug?

A

Precedex

239
Q

Dose of precedex for peds

A

Under 0.5mcg/kg over an hour

240
Q

Local anesthetics commonly used in caudal blocks

A

Ropivicaine or Marcaine with epi

241
Q

What drug can be given in the caudal block to help potentiate it

A

1mcg/kg clonidine

242
Q

Common acid/base disorder in peds patients coming in for pyloromyotomy

A

Metabolic alkalosis

243
Q

Anesthetic considerations for pyloromyotomy

A
  • RSI
  • Tachypnea due to metabolic alkalosis
  • Prone to post op apnea
  • Avoid narcs or go very light
244
Q

MOA of Sulfonylureas

A

Increase insulin release from pancreatic beta cells

245
Q

MOA of biguanides

A

Reduces hepatic glucose production

246
Q

Commonly used sulfonylureas

A
  • Glipizide
  • Glyburide
  • Chlorpropamide
  • Tolbutamine
247
Q

Commonly used biguanide

A

Metform

248
Q

Rapid acting insulin drug

A

Lisopro (Humalog)

249
Q

Short acting insulin drug

A

Regular (Humulin L, Novolin R)

250
Q

Intermediate acting insulin drug

A

NPH

251
Q

Starting dose of Clevidipine

A

1-2mg/hr

252
Q

Top end for Clevidipine dosing

A

16mg/hr

253
Q

Clevidipine achieves about a __% reduction in systolic blood pressure

A

25

254
Q

Antidysrhythmic with bone marrow suppression

A

Phenytoin

255
Q

Adenosine dosage

A

6mg IV then 6-12mg

256
Q

Warfarin - mechanism of action

A

Inhibits synthesis of vitamin K factors 2 7 9 10

257
Q

Protamine - side effects

A
  • Hypotension
  • Bleeding
  • Increased pulmonary pressures
  • Bronchoconstriction
258
Q

Action of tranexamic acid

A

Antifibrinolytic that prevents clot breakdown by preventing plasminogen/plasmin from binding to fibrin

259
Q

Toradol IV and Morphine doses

A

30mg toradol=10mg morphine

260
Q

Effects of heparin - FFP

A

ATIII deficiency is caused by re-dosing heparin. This is treated with FFP

261
Q

Antidysrhythmic, class IV example

A

Verapamil, diltiazem

262
Q

Antidysrhythmic, class IV mechanism

A

Ca2+ blocker

263
Q

NSAID and renal dysfunction

A

Don’t use Toradol in patients with renal dysfunction or Cr over 1.2

264
Q

Antifibrinolytic therapy post bypass

A

TXA

265
Q

NSAID for treatment of PDA

A

Indomethacin

266
Q

Antidysrhythmic - beta blocker class

A

Class II

267
Q

Vitamin K dependent coag factors

A

2, 7, 9, 10

268
Q

Amiodarone infusion rate

A

1mg/min

269
Q

Oral anticoagulants

A

Coumadin

270
Q

Insulin - duration of action

A

6-8 hours

271
Q

Hirudin - mechanism of action

A

Direct thrombin inhibitor

272
Q

Ondansetron pediatric dosage

A

0.1mg/kg

273
Q

Predmedication: children

A

0.5mg/kg oral

274
Q

Lab value and ketorolac

A

Look at creatinine

275
Q

Heparin-versal of

A

Protamine

276
Q

INR after anticoagulation

A

2-3

277
Q

Lab values with heparin administration

A
  • PTT

- A

278
Q

Dose of heparin for CPB

A

400units/kg

279
Q

NPH abbreviation

A

Neutral Protamine Hagedorn

280
Q

Coumadin reversal

A

Subacute - Vitamin K

Acute - FFP 5-8cc/kg, Factor 7a, factor 9, PCC

Pharmacology (6 decks)

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