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Pharmacology > MCPHS PA Pharmacology EXAM 3 Thrombolytics > Flashcards

MCPHS PA Pharmacology EXAM 3 Thrombolytics Flashcards

Drugs and Mechanics

1
Q

What are the three types of Hematopoietic Agents

A

Erythropoetin Stimulating Agent

Granulocyte Stimulating Agents (G-CSF. GM-CSF)

Platelet Stimulating Agents

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2
Q

How do Erythropoetin Stimulating Agents (ESAs) work?

A

Agents that increase RBC production within 2-6 Weeks provided the body has the building blocks (namely Iron).

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3
Q

What do Erythropoetic Stimulating Agents (ESAs) treat?

A

Treat Anemia from Renal disease

Used while in Chemotherapy

Used in patients with HIV/AIDS

Used to help reduce the need for transfusion post surgery.

Used by professional athletes (blood doping).

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4
Q

Name the ESA agents we have studied in Class.

A

Epoetin

Procrit

Darbepoetin

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5
Q

What are Granulocyte Stimulating Agents (GSA)?

A

Granulocyte Colony Stimulating Factor (G-CSF)

Granulocyte Macrophage Colonly Stimulating Factor (GM-CSF)

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6
Q

What G-CSFs did we look at and what do they treat?

A

Filgrastim and Pegfilgrastim

Treat neutropenic (low neutraphile) complications in cancer PTs

Nonmyeloid malignancies

HIV

Hepatitis C

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7
Q

What do GM-CSF agents treat?

A

Acute Myelogenous Leukemia

Bone Marrow Transplant

Radiation induced Bone Marrow Suppression

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8
Q

What are Platelet Stimulating Agents?

A

Agents that increase platelet production.

Onset within a week.

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9
Q

How do Platelet Stimulating Agents work, and which ones did we look at in class?

A

Romiplostim and Eltrombopag.

These agents bind to and activate human thrombopoetin receptor increasing platelet production.

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10
Q

What can Cause Clot formation?

A

Increase in Venous stasis

Vascular endothelium Damage (Plaque rupture, erosion, trauma, surgery)

Medications

Hormones

Cancer

Genetic Disorder

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11
Q

What is Virchow’s triad?

A

A combination of 3 factors that lead to thrombosis. Stasis

Vessel wall injury

Hypercoaguability

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12
Q

Explain the Clotting Cascade

A

Intrinsic (involving factors XII, XI, IX, VIII) and Extrinsic (involving factor VII) pathways that lead to a common pathway (factors X, V, II, I, and XIII) that cause clots to form.

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13
Q

What are the dangers of clots?

A

Arterial clots affect the left side of the heart and above, can cause heart attack, stroke, ischemic bowel, liver and kidney injury.

Venous clots can cause DVT, and pulmonary embolism.

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14
Q

What types of drugs do we use to treat clots?

A

Anticoagulants (prevent propagation of clots, disrupt clotting cascade, Best treatment for Arterial and venous clots)

Antiplatelets (Prevent clots from starting, inhibit platelet activation, most preventitive measure for Arterial clots).

Thrombolytics (Break up current clots by inducing or enhancing bodies natural processes).

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15
Q

How are Erythropoetin Stimulating Agents (ESAs) administered, and what needs to be monitored while PTs are on them?

A

While using ensure Hemoglobin and Iron levels are monitiored.

Given IV or SQ.

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16
Q

How do the G-CSF Granulocyte Stimulating factors work?

A

G-CSFs increcrease production of Myelblast cells (The progenitor to Basophil, Neutrophil, Esoniphil, and Monocytes). Onset in 2-3 Days.

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17
Q

How do the GM-CSF Granulocyte Stimulating factors work?

A

GM-CSFs increase the production of Common Myeloid Progenitors (the Precursors to MegaKaryocytes, Erthrocytes, and Myelblasts), and everything that they create.

Onset in 5-7 Days.

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18
Q

How are G-CSF Granulocyte Stimulating factors administered, and how are they monitoted?

A

IV, SQ or Patch.

Monitor absolute neutrphil count (ANC).

Pegfilgrastim - Given once.

Filgrastim - Given daily.

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19
Q

How GM-CSF Granulocyte Stimulating factors monitored?

A

Monitor CBC w/ differential.

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20
Q

Which GM-CSF agent did we look at in class?

A

Sargramostim

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21
Q

How do Anticoagulants work?

A

Reduce the formation of thrombin by inhibiting clotting factor activity or synthesis.

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22
Q

What Heparin and Heparin like Anticoagulants did we cover in Class?

A

Unfractioned Heparin (UFH)

Low Moleculra Weight Heparin (LMWH)

  • Dalteparin (LMWH)
  • Enoxaparin (LMWH)

Fondaparinux

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23
Q

What is Unfractioned Heparin (UFH) method of action to prevent coagulation?

A

UFH inhibits Factor Xa and thrombin equally.

UFH binds Xa and preventing prothrombin from making more thrombin, and it binds thrombin in such a way that it is unable to change fibrinogen to fibrin.

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24
Q

What are the indications to use Unfractioned Heparin (UFH)?

A

Treatment and Prevention of THrombosis.

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25
Q

What are the onset and route of administration for Unfractioned Heparin (UFH)?

A

Onset - Minutes to Hours

Route of Admin - IV or SQ

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26
Q

How is Unfractioned Heparin (UFH) Metabolised?

A

It is Metabolized hepatically then metabolites are cleared by the kidney.

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27
Q

How is Unfractioned Heparin (UFH) Dosed?

A

Bolus + continuous infusion for Clot treatment.

-Determined by Units / KG

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28
Q

How is Unfractuioned Heparin Usually monitired?

A

aPTT of anti-XA

Generally monitred va aPTT, checked every 4-6 Hrs until stable.

1.5-2x baseline seconds (can vary dependent on analyzing method)

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29
Q

What are the Adverse Effects of Unfractioned Heparin (UFH)?

A

Bleeding (PT needs to be monitored for blood loss i.e. decreased BP, increased HR, black tarry stool, red colored urine, headache, somnolence, and abdominal pain.

Spinal / epidural Hematoma (Can reduce risk by eliminating wpidural catheters, multiple anticoagulants/ antiplatelets)

Heparin induced Thrombocytopenia (HIT).

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30
Q

What is Heparin induced Thrombocytopenia (HIT)?

A

Type 1 is a transient drop in platelets approx 1-2 days post exposure that the PT will recover from.

Type 2 usually occurs approx 4-7 days post exposure and is indicated by a > 50% drop in platelets over time. It can cause a worry for thrombosis.

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31
Q

How does Type 2 Heparin Induced Thrombocytopenia (HIT) raise the concern for thrombosis when there is an indicated >50% drop in platelets?

A

In type 2 HIT the Body develops antibodies to heparin-PF4 (Platelet Factor 4). This forms a complex which can result in a thrombosis.

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32
Q

Is there a test for Heparin Induced Thrombocytopenia (HIT)?

A

A HIT antibody test can be completed with SRA assay.

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33
Q

What is the treatment for Heparin Induced Thrombocytopenia (HIT)? Can Heparin ever be used again?

A

Discontinue heparin

Initiate argatroban

May rechallenge if > 100 days since the event.

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34
Q

What is an aPTT test?

A

An aPTT test is a test of the activated Partial THromboplastin Time. It is a measure of the time it takes for the blood to clot.

The Greater the aPTT the more anticoagulation.

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35
Q

What is an anti-Xa test?

A

The anti-Xa test shows what the amount of Xa not bound by heparin is.

The Higher the level the more anticoagulation present.

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36
Q

Is there a tool to assess the likelihood of developing HIT?

A

The 4T test assesses the following with a rating of 0, 1, or 2.

Thrombocytopenia (% fall in platelet count)

Timing of platelet count fall (between 1 and 10)

Thrombosis or other sequelae (presence of thrombosis)

OTher cause for thrombocytopenia (definite / possible / none)

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37
Q

What can be done to reverse Bleeding with Unfractionated Heparin (UFH).

A

Protamine binds to Heparin immediately and lasts for 2 hours.

1 mg of protamine per 100 units of Heparin, max dose 50mg.

Give plasma or blood (if Hg<7 or Hypotensive)

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38
Q

What is Protamine, and what is it used for?

A

A highly positively charged molecule first isolated from fish sperm that binds with Heparin so it cannot bind with antithrombin.

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39
Q

What are Low-Molecular Weight Heparins (LMWH)?

A

Smaller pieces of Polysaccharides that bind to antithrombin and inactivate factor Xa (only, does not bind thrombin).

Indicated for treatment and prevention of thrombosis.

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40
Q

What Formulations of Low-Molecular Weight Heparin (LMWH) were presented to us in class?

A

Tinzaparin

Enoxaparin

Dalteparin

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41
Q

What are the routes of administration and Onset of Low-Molecular Weight Heparin (LMWH)?

A

Onset 12-18 Hours

Admin - Intermittent SQ injections

-mg/kg or unit / kg doses

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42
Q

How are Low-Molecular Weight Heparins (LMWH) monitored and cleared?

A

Monitor - anti-Xa

Renally cleared (cannot be used on PT’s with acute Kidney injury or Hemodialysis)

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43
Q

What are the adverse effects of Low-Molecular Weight Heparin (LMWH)?

A

Bleeding (less compared with UFH)

Spinal / Epidural hematoma

Thrombocytopenia (Similar to HIT)

  • Antibody mediated less likely
  • Discontinue Medication treat with Argatroban
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44
Q

What can be done to reverse bleeding with Low-Molecular Weight Heparin (LMWH)?

A

Protamine can be used (not as effective only binds about 80% of LMWH)

0.5MG per 1 mg LMWH (max dose 100MG)

Give within 12 or 24 hours after last dose LMWH

Give plasma or blood (if Hg <7 or hypotensive)

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45
Q

Does Unfractionated Heparin (UFH) have better Efficacy than Low-Molecular Weight Heparin (LMWH) for treatment of Clots?

A

No they have equal Efficacy

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46
Q

Does Low-Molecular Weight Heparin (LMWH) have any advantages over Unfractionated Heparin (UFH) for treatment of Clots

A

It deosn’t require hospitalization

Requires no routine monitoring

And can be Self administered

Due to ease of administration usually preferred for treatment / prevention of venous thrombosis.

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47
Q

Does Unfractionated Heparin (UFH) have any advantages over Low-Molecular Weight Heparin (LMWH) for treatment of Clots?

A

It’s Cheaper than LMWH

It can be used with an Acute Kidney Injury.

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48
Q

What are the disadvantages of Unfractionated Heparin (UFH) treatment?

A

It requires Hospitalization

It has to be routinely monitored

It cannot be self administered

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49
Q

What are the disadvantages of Low-Molecular Weight Heparin (LMWH) treatment?

A

It costs more than UFH

It cannot be used with an Acute Kidney Injury

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50
Q

What is Fondaparinux’s method of action to prevent coagulation?

A

Fondaparinux inhibits Factor Xa by binding to Antithrombin

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51
Q

How is Fondaparinux administered?

A

Admin:SQ with a fixed dose based on weight.

Can be used in Patients with a History of HIT.

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52
Q

How is Fondaparinux Cleared?

A

Renally eliminated (cannot use in acute kidney injury or hemodialysis)

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53
Q

What are Fondaparinux’s indications?

A

DVT/PE treatment and prevention.

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54
Q

What are the adverse effects of Fondaparinux?

A

Bleeding

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55
Q

What can be done to reverse bleeding with Fondaparinux?

A

Give plasma or blood (if HG<7 or hypotensive).

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56
Q

What Vitamin K Antagonist Anticoagulants did we cover in Class?

A

Warfarin

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57
Q

What is Warfarin’s method of action to Prevent clots?

A

Warfarin inhibits clotting factor synthesis that require Vitamin K (inhibits Vit K epoxide reductase complex 1 and vit K reductase)

-Inhibit production of: Prothrombin (FactorII), VII, IX, X, protein C and S.

2+7=9 and 1 more is 10 C&S

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58
Q

How is Warfarin administered and what is it’s onset?

A

Admin: PO or IV

Onset: Delayed, takes approx 2 days to start decreasing clotting factors.

  • Usually takes several days to achieve full therapeutic effect.
  • If drug stopped, effects linger.
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59
Q

Why does Warfarin linger even after discontinuing the medication?

A

Warfarin is extensively bound to albumin, and cannot be metabolized until it is unbound.

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60
Q

Where is Warfarin Metabolized?

A

Warfarin is metabolized in the liver by CYP2C9.

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61
Q

How is Warfarin Monitored?

A

International Normalized Ratio (INR)

Prothrombin time (PT)

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62
Q

What are Warfarin’s Goal INRs?

A

Normal INR is 1.8

Warfarin wants between 2-3 for

Acute MI, AFIB, Valvular heart disease, Pulmonary embolism, DVT, and Tissue Heart Valve.

For mechanical heart Failure we want between 2.5-3.5

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63
Q

What are the adverse effects of Warfarin?

A

Bleeding

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64
Q

What can be done to reverse uncontrolled bleeding while on Warfarin?

A

Phytonadione (Vitamine K) can be administered.

Can give Plasma or prothrombin complex concentrate (PCC) or Factor VII (Novoseven)

If you give PCC VIT K is needed as well PO preferred.

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65
Q

When reversing uncontrolled bleeding while on Warfarin how should Vit K be administered?

A

PO preferred, but IV will be used in life threatening conditions.

Takes 2-6 hours to start revesing effects, with a total effect within 24 hours.

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66
Q

What is Prothrombin Complex Concentrate(PCC)?

A

PCC - contains major clotting factors II, VII, IX, and X, all of which are low in patients treated with warfarin or other VKA anticoagulants, as well as the antithrombotic proteins C and S

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67
Q

Warfarin interactions, which drugs increase INR?

A

Bactrim

Amiodarone

Cimetidine

Acetaminophen

Metronidazole

Azol Antifungals

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68
Q

Warfarin interactions, which drugs decrease INR?

A

Phenobarbital

Rifampin

Phenytoin

Carbamazepine

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69
Q

What Method of action do Direct Thrombin inhibitors use to prevent Coagulation?

A

Direct thrombin inhibitors inhibit thrombin (IIa) to prevent conversion of fibrinogen to fibrin.

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70
Q

What direct Thrombin inhibitors did we talk about in class?

A

Bivalirudin

Argatroban

Dabigatran

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71
Q

How is Dabigatran administered?

A

PO

72
Q

How is Argatroban administered?

A

IV

73
Q

How is Bivalirudin Administered?

A

IV

74
Q

What are the indications to use Dabigatran?

A

Prophylaxis for non-valvular AFIB, treatment of DVT/PE.

75
Q

What is the onset for Dabigatran?

A

Rapid onset prodrug converted by blood esterases.

76
Q

How is Dabigatran eliminated?

A

Renally eliminated and dose adjusted for CKD. (Most common, but cannot use with Hemodialysis PTs)

77
Q

What can be done to reverse bleeding while on Dabigatran?

A

Treat life threatening bleed with Praxbind.

Dabigatran can also be removed with hemodialysis treatment.

Plasma can be given.

78
Q

What are the indications for Argatroban use?

A

HIT treatment, and Cardiac Catheterization (PCI).

Artofocially raises INR.

79
Q

How is Argatroban eliminated?

A

Metabolized by liver (Dose adjustments for Chronic Liver Disease).

80
Q

How is Argatroban monitored?

A

Monitor aPTT.

81
Q

What are the adverse events associated with Agatroban?

A

Bleeding

No specific anidote, can only give plasma.

82
Q

What are the indications for Bivalirudin use?

A

PCI with acute or remote history of HIT.

83
Q

How is Bivalirudin Eliminated?

A

Eliminated by the Kidneys (dose adjust for Renal Dysfunction).

84
Q

How is Bivalirudin monitored?

A

Monitor aPTT.

85
Q

What are the adverse events associated with Bivalirudin?

A

Bleeding (No antidote can only give plasma).

86
Q

What Direct Xa Inhibitors did we talk about in class?

A

Rivaroxaban

Apixaban

Edoxaban

Betrixaban

-Xaban

87
Q

How are Direct Xa inhibitors administered and Monitored?

A

Admin: PO

No monitoring

88
Q

What is the onset for direct Xa inhibitors?

A

Rapid Onset

89
Q

What are the indications for Apixaban?

A

DVT/PE treatment

Stroke Prophylaxis in non-valve AFIB

Post op DVT Prophylaxis

90
Q

What are the indications for Rivaroxaban?

A

DVT/PE treatment

Stroke Prophylaxis in non-valve AFIB

Post op DVT Prophylaxis

91
Q

What are the indications for Edoxaban?

A

DVT / PE treatment

Stroke prophylaxis in non-valve AFIB

92
Q

What are the indications for Betrixaban?

A

Prohylaxis for VTE

93
Q

Which direct Xa inhibitor can be used on PTs undergoinf Hemodialysis?

A

Apixaban

94
Q

What can be done to reverse uncontrolled bleeding while on Direct Xa inhibitors?

A

Administer Andexxa

Hemodialysis does not remove drug

95
Q

Which Xa inhibitors can be used on PT’s with Renal insufficiency?

A

All of them can be dose adjusted, but only Apixaban can be used with dialysis PTs.

96
Q

What drug interactions does Apixaban have?

A

Strong CYP 3A4 or PGP inhibitors or inducers.

What drug interactions does Apixaban have?

97
Q

What drug interactions does Rivaroxaban have?

A

Strong CYP 3A4 or PGP inhibitors or inducers.

98
Q

What drug interactions does Edoxaban have?

A

Strong CYP 3A4 or PGP inhibitors or inducers.

99
Q

What drug interactions does Betrixaban have?

A

Strong PGP inhibitors

100
Q

How do antiplatlets prevent Arterial Thrombosis?

A

Cox inhibition

Increase plasma adenosine

Phosphodiesterase-3 (PDE-3) inhibition

P2Y12 ADP inhibition

Glycoprotein IIb/IIIa inhibition

101
Q

Which COX inhibitors did we talk about in class?

A

Asparin

102
Q

What is the MOA for a COX inhibitor?

A

Irrisistable inhibition of cyclooxygenase (the enzyme responsible for making Thromboxane A2 (TXA2) which causes platelets to aggregate).

103
Q

What is the duration of the antiplatelet effect of Asparin?

A

The life of the platelet (7-10 days)

104
Q

What is the MOA of P2Y12 inhibitors?

A

THey Prevent platelet activation by inhibiting ADP binding to P2Y12 receptors.

105
Q

What monitoring is donw of P2Y12 inhibitors?

A

Monitor with Platelet assay Tests

106
Q

Which P2Y12 inhibitors are irreversible?

A

Clopidogrel

Prasugrel

Ticlopidone

107
Q

Which P2Y12 inhibitors are reversible?

A

Ticagrelor

Cabgrelor (IV)

108
Q

What P2Y12 Inhibitors did we cover in class?

A

Clopidogrel

Prasugrel

Tclopidone

Ticagrelor

Cangrelor (IV)

109
Q

What are the indications for Clopidogrel?

A

Prevent coronary stent thrombosis

Ischemic stroke

Peripheral Vascular disease

110
Q

What is the onset for Clopidogrel?

A

2 hours after dose

111
Q

What is the duration of action of Clopidogrel

A

5 days

112
Q

Clopidogrel is a Prodrug, what is it metabolized by?

A

CYP2C19 (genetic varience)

113
Q

What is Clopidogrel’s dosing?

A

mg (usually load given for PCI)

114
Q

What are the adverse events associated with Clopidogrel?

A

Bleeding

Thrombotic Thrombocytopenia (TTP)

TTP usually occurs within the first 2 weeks of treatment. Low platelets, hemolytic anemia, fever, and renal dysfunction.

115
Q

Does Clopidogrel have any DDIs?

A

There are many drug interactions with CYP2C19 (the metabolizer for this prodrug)

116
Q

Do you need to alter a Clopidogrel prescription prior to any surgeries?

A

Must hold medications 5 days prior to any major surgery / procedures.

117
Q

What are the indications for Prasugrel?

A

Acute coronary syndromes

118
Q

What is the onset for Prasugrel?

A

30 minutes after loading dose

119
Q

Prasugrel is a Prodrug, where is it converted?

A

The Liver (no DDIs)

120
Q

What adverse events are associated with Prasugrel?

A

Bleeding

Angioedema (rare)

121
Q

Are there any precautions for the use of Prasugrel?

A

Avoid use in PTs >75 Y/O, or with a historu of stroke / TIA.

122
Q

What are the dosing instuctions for Prasugrel?

A

Adjust dose if PT weighs <60kg

123
Q

Do you need to alter a Prasugrel prescription prior to any surgeries?

A

Hold 5 days prior to surgery.

124
Q

What are the indications for Ticlopidine?

A

Prevention of thrombotic Stroke

Reduce instent thrombosis

125
Q

What is the onset for Ticlopidine?

A

48hrs after dose

126
Q

What are the adverse effects of Ticlopidine?

A

Beutropenia / TTP

bleeding

Monitor WBC every 2 weeks for 12 weeks after initiation.

127
Q

Is there an antidote to P2Y12 inhibitors?

A

No, give platelets and possibly Blood.

128
Q

What are the indications for Ticagrelor?

A

ACS

129
Q

What is the onset of action for Ticagrelor?

A

1.5 Hours

130
Q

Is Ticagrelor a Prodrug?

A

No

131
Q

What are the adverse effects associated with Ticagrelor?

A

Bleeding

Dyspnea

Ventricular Pauses

132
Q

What DDIs does Ticagrelor have?

A

Asparin doses > 100 mg/day (make drug less effective)

CYP3A4 inhibitors / inducers

>40 mg a day of simvastatin or lovastatin

Digoxin levels may increase (PGP inhibitor)

133
Q

Are there any specific reasons not to use Ticagrelor outside of DDIs / Adverse effects?

A

Don’t use if concerned about adherence

134
Q

Do you need to alter Ticagrelor use prior to Surgery?

A

Hold 1 day prior.

135
Q

What are the indications for the use of Cangrelor?

A

Approved for PCI

136
Q

How is Cangrelor administered?

A

Admin: IV

137
Q

Do you continue Cangrelor use after IV admin?

A

No, transition to oral P2Y12 inhibitors post IV admin.

138
Q

Are there any dose adjustments for Cangrelor?

A

No

139
Q

How is Cangrelor Dosed?

A

30 mcg / kg bolus followed by infusiom 4 mcg / kg / min

140
Q

What adverse effects are associated with Cangrelor?

A

Bleeding

141
Q

Which GP IIb/IIIa inhibitors did we cover in class?

A

Abciximab

Eptifbatide

Tirofiban

142
Q

What is the onset of GP IIb/IIIa inhibitors?

A

Immediate

143
Q

What are the adverse effects associated with GP IIb/IIIa inhibitors?

A

Bleeding

144
Q

Is there an antidote available for GP IIb/IIIa inhibitors?

A

No, give platelets.

145
Q

What antiplatelets did we discuss in class that were not Cox / P2Y12 / GP IIb/IIIa inhibitors?

A

Dipyridamole

Cilostazol

Pentoxifylline

146
Q

What is the MOA of Dipyridamole?

A

Inhibits platelets by increasing plasma levels of adenosine

147
Q

Is Dipyridamole ever given with another drug?

A

Dipyridamole is always given with asparin (Aggrenox).

148
Q

What are the indications for Dipyridamole?

A

Used in combonation with ASA for Heart Valve replacement or stroke.

149
Q

What adverse events are associated with Dipyridamole?

A

Bleeding

Dyspepsia

150
Q

Is there an antidote for Dipyridamole?

A

No, give platelets.

151
Q

What is the MOA of Cilostazol?

A

It is a PDE-3 inhibitor.

152
Q

What is the onset of Cilostazol?

A

Full onset of action at 12 weeks.

153
Q

What are the adverse events associated with Colostazol?

A

Headache

154
Q

What are the Contraindications to use Cilostazol?

A

Heart Failure

155
Q

What drug interactions does Cilostazol have?

A

CYP3A4 inhibitors

156
Q

What is the MOA of Pentoxifylline?

A

Increases cAMP in RBCs, leading to increased RBC flexibility and decreased Viscosity.

157
Q

What adverse events are associated with Pentoxifylline?

A

Nausea, Vomiting, and Leukopenia.

158
Q

Does Pentoxifylline have any risk of bleeding?

A

There is no significant risk of bleeding?

159
Q

What are the clinical uses of Pentoxifylline?

A

Intermittant Claudication, liver disease, vasculitis, etc

160
Q

What are Thrombolytics?

A

Agents given to remove thrombi that have already formed.

161
Q

What are the Conraindications to use thrombolytics?

A

There are no absolute contraindications, must be considered on a case by case basis.

162
Q

What formulatiuons of Thrombolytics did we talk about in class?

A

Atlepase (tPA)

Tenecteplase

Reteplase

163
Q

What is the MOA of Alteplase?

A

Identical to plasminogen activator, binds with plasminogen to form active complex.

Complex catalyzes conversion of other plasminogen molecules into plasmin.

-Digests Fibrin meshwork.

164
Q

What are the Therapeutic uses of Alteplase?

A

Acute ischemic stroke, acute MI, Acute massive PE

165
Q

How is Alteplase Dosed?

A

Single Dose

Amount Varies based on indication

166
Q

What adverse events are associated with Alteplase?

A

Bleeding

Angioedema

167
Q

What are the indications to use Tenecteplase or Reteplase?

A

Acute MI

168
Q

How is Tenecteplase Dosed?

A

Single Dose

169
Q

Does Tenecteplase have any special characteristics?

A

It has a longer Halflife

170
Q

What are the adverse events associated with Tenecteplase?

A

Bleeding

171
Q

How is bleeding associated with Thrombolytics handled?

A

There is no Antidote, you can only give plasma.

172
Q

Does Reteplase have any special characteristics?

A

Short Half-life

173
Q

How is Reteplase dosed?

A

Given as 2 intermittent injections.

Complex dosing makes it less favorable then Tenectplase ot Alteplase

174
Q
A
175
Q
A
176
Q
A
177
Q
A

Pharmacology (14 decks)

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