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Pharmacology > Haematopoietic Pharmacology > Flashcards

Haematopoietic Pharmacology Flashcards

1
Q

EPO (epoetin Alfa, epogen, procrit)

A

Recombinant growth hormone similar to human epo and stimulates the production of rbc in bone marrow

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2
Q

Indication for epo

A

Anemia secondary to health conditions such as chronic renal failure or chemotherapy treated cancers.

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3
Q

Epo MOA

A

Simulated rbc production in bone marrow. This increases patients hemoglobin, hematocrit, and reticulocyte counts

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4
Q

Patients on epo require adequate intake of what

A

Iron, folic acid, b12

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5
Q

Indications for epo

A

Chronic renal failure

Anemia

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6
Q

Why chronic renal failure need epo

A

It is made in kidney

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7
Q

Anemia wanting epo may be caused by what

A

HIV meds, cancer, chronic renal failure

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8
Q

Side efects epo

A

Increased risk of thrombosis
Pelvic and limb pain
Hypertension

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9
Q

Epo may accelerate tumor progression

A

Yikes

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10
Q

Warfarin

A

In patients requiring chronic anticoagulation such as those with history of DVT, PE, a fib, or artificial heart valves

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11
Q

How does warfarin work

A

Inhibiting epoxied reductase, leading to interference int he synthesis of vitamin K dependent clotting factors

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12
Q

What are the vitamin dependent clotting factors

A

II, VII, IX, X, C< and S

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13
Q

Side effects warfarin

A

Bleeding, which necessitates the monitoring of patients INR as well as necrosis which is more common in protein C deficient patients..

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14
Q

What causes warfarin necrosis

A

Initial prothrombin state caused by the rapid decline in proteins C and S and manifests as gangrene and massive skin necrosis

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15
Q

How is warfarin metabolized

A

P450 pathway and providers should be cautioned of other medications effecting this pathway.

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16
Q

Pregnancy and warfarin

A

Teratogen

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17
Q

MOA warfarin : clotting factors

A

Interferes with vit k dependent clotting factors

Warfarin inhibits epoxied reductase, so vitamin k unable to reduced to its active form-hydroquinone (vitamin KH2). Prevents gamma-carboxylation of glutamic acid on the clotting factors II, VII, IX, X and C and S. Can’t bind to endothelium and become biologically inactive

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18
Q

Warfarin MOA: extrinsic pathway

A

Acts on extrinsic pathway by preventing the activation of vitamin k , which reduces production of II, VII, IX< and X

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19
Q

Why does the effect of warfarin take several days

A

Half lives of already activated factors

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20
Q

Warfarin MOA: bridge with heparin

A

Usually administered with warfarin to prevent thrombosis. This is because for the first 4-5 days, though warfarin is preventing active factors from being formed, the previously formed factors must degrade. After give,it causes a decline in factor VII, but takes more time to decrease factor II. Furthermore, proteins C and S are decreased, leading to a prothrombin state initially

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21
Q

Indications for warfarin

A

Chronic anticoagulation

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22
Q

What ailments might require chronic anticoagulation

A

Fibrillation, artificial heart valves, previous pulmonary embolism and previous DVT

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23
Q

Side effects warfarin

A

Bleeding
Necrosis
Cytochrome p450

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24
Q

Hemorrhage is the most common side effect of warfarin. What do physicians monitor

A

PT and INR to make sure only 2-4 times the normal range

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25
Q

Necrosis and warfarin

A

Can lead to massive thrombus formation, causing skin necrosis and gangrene.

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26
Q

Why get necrosis from warfarin

A

Initial inhibition of proteins C and S leading to a prothrombin state when starting this medication.

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27
Q

Who is more susceptible to necrosis when on warfarin

A

Patients who are protein c deficient

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28
Q

Cytochromep45O inhibitors

A

May lead to too much warfarin

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29
Q

Antidote to too much warfarin (or severe bleeding, reversal before surgery)

A

FFP and vitaminK

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30
Q

Warfarin/Coumadin

A

Oral anticoagulant used int he prevention of thrombosis and embolism

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31
Q

How does warfarin work

A

Inhibits vitamin k epoxied reductaseand leads to depletion of active vitamin K to be used by blood coagulation proteins.

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32
Q

Antidotes to warfarin

A

Vitamin K and fresh frozen plasma

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33
Q

Vitamin K antidote to warfarin

A

Involved int he production of coagulation factors II, VII, IX, X , protein C and S.

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34
Q

Are the effects of vitamin K reversal on warfarin immediate

A

No

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35
Q

Fresh frozen plasma (FFP)

A

Liquid portion of human blood that has been frozen and preserved after a blood donation . It replaces II, VII, V, IX, X, and helps to reverse warfarin effects much quicker than vitamin K

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36
Q

Vitamin K1 (phytonadione)

A

Essential component in the synthesis of prothrombin and clotting factors II, VII, IX, X which allow the blood to coagulate

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37
Q

Indication for vitamin K1

A

Hypoprothrombinemia, warfarin overdose, and prophylaxis of hemorrhage in new borne

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38
Q

Side effects vitamin K1

A

Bilirubin induced brain dysfunction (kernicterus), and hypersensitivity reactions such as shock and cardiac arrest.

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39
Q

To prevent a life threatening hypersensitivity reaction, vitamin K1 should not be given ___ unless other routes are contraindicated

A

IV

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40
Q

MOA vitamin K1

A

Essential in synthesis of prothrombin and clotting factors II, VII, IX, and X, whicha loow the blood to coagulate

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41
Q

Indications of vitamin K1

A

Hypoprothrombia (newborn prophylaxis)

Bleeding from warfarin overdose

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42
Q

Babies are born with a _ defiency

A

Vitamin K

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43
Q

In order to prevent hemorrhage in newborns what are they given

A

Single dose of vitamin K1 to increase prothrombinleavels and preventbleeding

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44
Q

Side effects vitamin K1

A

Shock (hypersensitivity), kernicterus (causes serum bilirubin levels to rise), cardiac arrests not give though IV)

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45
Q

___ __ are required for intestinal absorption of vitamin K1

A

Bile salts

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46
Q

Increased risk of __ with IV administration of vitamin K1

A

Hypersensitivity reaction

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47
Q

Heparin

A

Anticoagulant medication, which is a cofactors for antithrombin, working to inactivate the coagulation factors IIa (thrombin ) and Xa

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48
Q

Indication for heparin

A

Acute coronary syndrome, a fib, pulmonary embolism, and prophylaxis in hypercoagulable states.

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49
Q

Does heparin cross the placenta

A

No

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50
Q

Who is heparin commonly used in

A

Anticoagulat in pregnant patients

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51
Q

Indications for heparin

A

Acute coronary syndrome (STEMI NSTEMI-help break down clots in cases of non ST elevation)
Prophylaxis (against thrombosis(DVT risk))
Pulmonary embolism (prevent thrombi)
April fibrillation 9stop stroke and embolism)
Used in pregnancy

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52
Q

Why is heparin used during pregnancy

A

Doesn’t cross placenta no risk to fetus

Pregnant patients may become hypercoagulable as a physiologic mechanismto prevent post partum hemorrhage

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53
Q

Heparin

A

Anticoagulant which is a cofactors for antithrombin , working to inactivate the coagulation factors IIa (thrombin and Xa

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54
Q

Indication for heparin

A

Acute coronary syndrome, a fib, pulmonary embolism, prophylaxis in hypercoagulable states

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55
Q

Half life of heparin

A

Short so administered frequently or as continuous infusion

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56
Q

MOA heparin

A

Acting as a cofactor for antithrombin activation. As antithrombin is activated, it acts to decrease activation of factor IIa, or thrombin, as well as factor Xa.

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57
Q

Side effects heparin

A

Bleeding, thrombocytopenia(HIT)

58
Q

Antidote to heparin therapy

A

Positively charged reversal agent, protamine sulfate, which binds to the negatively charged heparin

59
Q

MOA heparin

A

Half life 1 hour
Binds to inhibitor antithrombin III, causing its activation.
Antithrombin now activated, leading to the inactivateion of thrombin (factor IIa) and other proteases involved in blood clotting, most notable Xa

60
Q

Antithrombin effects are increased _ fold due to the activation via heparin, leading to vastly decreased coagulability

A

1000

61
Q

Side effects heparin

A

Bleeding

HIT

62
Q

Bleeding with heparin

A

If too much

Monitor PTT

63
Q

Heparin induced thrombocytopenia (HIT)

A

5-10 days after heparin—-leading to pathological platelet activation and clearance, causing thrombocytopenia

64
Q

Antidote to heparin

A

Protamine sulfate

65
Q

Protamine sulfate

A

For rapid reversal of heparin, protamine sulfate is used as an antidote. It is highly positively charged, and binds to negatively charged heparin.

Low molecular weight heparin is not easily reversible

66
Q

HIT incidence

A

.2-5% in patients who have been treated for greater than 4 days

67
Q

__ heparin is more likely to cause HIT tha ______

A

Unfractionated

Low molecular weight heparin (LMWH)

68
Q

When does HIT occur

A

5-10 days after initiation of heparin therapy

69
Q

Early onset HIT

A

10 hours, patients who have receives heparin therapy recently and have persistent antibodies to the complex of heparin and platelet factor 4

70
Q

Heparin platelet factor 4 complex

A

Platelet factor 4 is released from the alpha granules of platelets upon platelet activation and binds to heparin

71
Q

__, __, and __ autoantibodies form against heparin platelet factor 4 complex

A

IgG IgA, IgM

72
Q

Heparin platelet factor 4 antibody complex binds __

A

Platelets—>platelet aggregation and thus thrombocytopenia and procoagulant product which can lead to thrombosis

73
Q

Platelet aggregation

A

Heparin platelet factor 4 antibody complex bound to platelets results in platelet aggregation, subsequent removal from circulation and thus thrombocytopenia

74
Q

Procoagulatn release HIT

A

Platelet aggregation also results in the release of progcoagulants which can cause thrombosis

75
Q

Symptoms of HIT

A

Thrombocytopenia

76
Q

Diagnosis of HIT

A

Serotonin release assay (SRA)

77
Q

SRA

A

High serotonin release occurs as this is a marker of platelet activation.

A CBC is always performed to determine the degree of thrombocytopenia

78
Q

Treatment of HIT

A

Stop heparin, start direct thrombin inhibitor

79
Q

Example of a direct thrombin inhibitor

A

Bivalirudin

Argatroban

80
Q

Aspirin

A

Ok

81
Q

ENOS Paris (lovenox)

A

First LMW heparin in the US.

82
Q

Use of enoxaparin (lovenox)

A

Prevents DVT while patients are int he hospital or it can be used as a bridge medication for patients starting warfarin

83
Q

What are some other LMW heparin

A

Dalteparin (fragmin)

Tinzaparin (innohep)

84
Q

Benefits of LMW heparin

A

Can be administered outpatient and do not require PTT minotoring

85
Q

MOA enoxaparin

A

LMW heparin only inactivated factor XA (standard heparin inactivated IIa and Xa)

It binds to antithrombin, forming a complex which irreversibly inactivated clotting factor Xa

86
Q

Indications for LMW heparin

A

Clot formation prevention (prevent DVT, patients with unstable angina or an acute STEMI)

87
Q

Side effects LMW heparin

A

HIT

Bleeding

88
Q

Consideration for LMW heparin

A

Educate patient on side effects

If going home on enoxaparin need to demonstrate administration.

89
Q

How is enoxaparin administered

A

Subcutaneously 2 inches away from umbilicus or any abdominal incision

90
Q

Why give enoxaparin 2 inches away from umbilicus or incision

A

Have more scar tissue and don’t absorb normally

91
Q

Antidotes for enoxaparin

A

Protamine sulfate binds directly to the free heparin in the bloodstream and inactivated it, immediately preventing further inactivation of clotting factors

92
Q

Clopidogrel (plavix)

A

Antiplatelt medication that works as an ADP receptor antagonist to prevent platelet aggregation.

93
Q

Indication for clopidogrel

A

Treatment of coronary syndrome and in order to prevent thrombotic events

94
Q

Side effects clopidogrel (plavix)

A

Coronary syndrome and in order to prevent thrombotic events.

95
Q

Side effects clopidogrel

A

Hemorrhage, abdominal pain, thrombotic thrombocytopenic purpura, and pancytopenia

96
Q

Why not give clopidogrel before surgery

A

Prevent increased bleeding

97
Q

MOA clopidogrel

A

Antagonizing ADP receptors in order to prevent ADP mediated aggregation. IRREVERSIBLE and last the full lifespan of the platelet
Prevents platelet activation

98
Q

Lifespan of platelet

A

3-7 days

99
Q

Indications for clopidogrel

A

Acute coronary syndrome (prevents blockages from forming within coronary arteries)

Prevention of thrombotic events (MI and ischemia)

100
Q

Side effects clopidogrel

A

Bleeding, Thrombotic Thrombocytopenic Purpura (TTP), pancytopenia, abdominal pain

101
Q

Thrombotic thrombocytopenic purpura

A

Cause small blood clots to form within the small vessels of the body leading to issues related to organ function. Monitor for bruising, kidney failure, fever, anemia, thrombocytopenia, and neurological symptoms

102
Q

Pancytopenia

A

Includes thrombocytopenia, leukopenia, and anemia

103
Q

Why abdominal pain on clopidogrel

A

Absorbed in the GI tract; therefore, it may cause abdominal pain related to GI bleeding. Patients taking clopidogrel should be monitored for abdominal pain and other signs of GI bleeding, such as blood in the feces

104
Q

Do not give clopidogrel _ days before surgery

A

5

105
Q

Abciximab and tirofiban and eptifibatide (GP IIb/IIIa inhibitors)

A

Glycoproteins iIb/IIIa receptor inhibitors that work by inhibiting platelet glycoproteins IIb/IIIa receptors, preventing the binding of fibrinogen

106
Q

MOA GP IIb/IIIa inhibitors

A

Prevent binding of fibrinogen, prevent aggregation of platelets, thereby preventing clot formation.

107
Q

The inhibition of platelet aggregation caused by GPIIb/IIIa receptor inhibitors can be reversed. How

A

Stopping the medication, unlike medications such as asprin and ticlopidine, which cause irreversible inhibition of platelet aggregation

108
Q

Indications for GP IIb/IIIa receptor inhibitors used to prevent thrombotic events in patients after percutaneous coronary intervention (PCI) or in those with acute coronary syndrome (ACS)

A

Ok

109
Q

Side effects of GP IIb/IIIa receptor inhibitors

A

Bleeding, espicially GI hemorrhage

110
Q

GPIIBIIIa receptor inhibitors are often administered with what

A

Heparin and asprin

111
Q

MOA IIb/IIIa receptor inhibitors

A

IIb/IIIa receptor inhibitors which prevents binding to fibrinogen, preventing platelet aggregation of platelets thereby preventing clot formation
Inhibit platelet aggregation

112
Q

Are abciximab, tirofiban and epitibatide irreversible? Do they irreversibly inhibit GPIIb/IIIa receptor

A

Abciximab-irreversible

Tirofiban and eptifibatide-reversible by stopping medication of daily zing the patient

113
Q

Indications for IIb/IIa receptor inhibitors

A

Thrombotic event prevention short term

  • acute coronary syndrome
  • percutaneous coronary intervention (PCI)
114
Q

Acute coronary syndrome

A

These patients experience a disruption of arterial plaque causing complications such as unstable angina, and MI. Treatment with GP/IIb?IIIa receptor inhibitors, with heparin and asprin decreases the likelihood that the patient will experience a thrombotic event sue to the disruption of plaque

115
Q

Percutaneous coronary intervention (PCI)

A

Wall of artery is damaged, increasing the risk of platelet aggregationa nd blood clot formation

116
Q

Side effects GP IIb/IIIa inhibitors

A

Bleeding

Espicially GI hemorrhage. If bleeding or hemorrhage occurs, the infusion should be stopped immediately

117
Q

Considerations GP IIb/IIIa inhibitors

A

Expensive, combination drug therapy( heparin and asprin!!!!!)

118
Q

What are GP IIbIIIa inhibitors given with

A

Heparin and asprin

119
Q

Ticlopidine (ticlid)

A

Antiplatelet medication designed to inhibit platelet aggregation, thereby preventing thrombotic events

120
Q

Though closely related to clopidogrel, ticlopidine causes what

A

More adverse hematologic effects, such as neutropenia and thrombotic thrombocytopenic purpura TTP

121
Q

Other side effects of ticlopidine

A

Diarrhea, abdominal pain, flatulence, nausea, heart burn, rash

122
Q

Patients taking ticlopidine should have their ___ monikered every two weeks for the first three months

A

CBC

123
Q

It is important to remember that ticlopidine must be withheld prior to surgery. Why

A

Risk of bleeding

124
Q

MOA ticlopidine

A

ADP receptor antagonist-prevents GP IIb/IIIa expression on platelets leading to an inability of platelet aggregation by inhibiting fibrinogen from binding

Irreversibly inhibits platelet aggregation -

125
Q

Bc ticlopidine inhibition of platelet aggregation is irreversible so antiplatelet action will continue until when

A

Until death or destruction of the platelet occurs

126
Q

Indications for ticlopidine

A

Thrombotic event prevention-bc a clump of platelets makes up the center of a thrombus or clot, use of ticlopidine to inhibit platelet aggregation will ultimately work to prevent a thrombotic event.

127
Q

Ticlopidine should only be used for patients who have not responded to ___ or can not tolerate the use of asprin

A

Asprin

128
Q

Side effects ticlopidine

A

Neutropenia. This condition increases a patients risk of infection; however it is not permanent.
TTP-causes clot formation throughout the body.
GI distress
Rash

129
Q

TTP presentation

A

Fever and changes in neurological function. Lab results may also reveal low platelet counts, anemia, and kidney problems

130
Q

Considerations of ticlopidine

A

Not before surgery!

  • due to increased risk of bleeding. Keep in mind that the effects of the drug remain int he body for 7-10 days after last dose, so ample time must be planned for the discontinuation of the drug prior to surgery
  • monitor CBC for neutropenia
131
Q

Alteplase

A

Thrombocytopenic medication that dissolves blood clots by fibrin lysis..known as a clot buster

132
Q

What is alteplase similar to

A

TPA

133
Q

What does tPA do

A

Breaks down the fibrin found in blood clots.

134
Q

Alteplase inc ontraindicated in who

A

History of bleeding.

135
Q

Antidote to alteplase

A

Apical

136
Q

Alteplase MOA

A

Fibronolytic medication by converting plasminogen into enzyme plasmin. Plasmin breaks down blood clots by destroying fibrin structure and therefore dissolving blood clot

137
Q

Indications for alteplase

A

Thrombosis (bc it breaks down an already formed thrombus or blood clot and is used in acute situations. The formation of a blood clot within a blood vessel or within the heart may obstruct normal blood flow and tissue perfusion. The thrombus may result in acute MI , acute ischemic stroke, or acute pulmonary embolism. In addition this drug may be given to dissolve a thrombus causing central venous Cather blockage

138
Q

Side effects alteplase

A

Bleeding

139
Q

Contraindications alteplase

A

Intracranial hemorrhage
-bc it prevents clot formation and potentiates the risk of hemorrhage

Internal hemorrhaging
-since bleeding is a major complication…the med may destroy pre existing clots and instigate bleeding in previously healing sites of injury. May also destroy clotting factors and prevent future clot formation in blood vessels

140
Q

Considerations alteplase

A

Minimize bleeding
-avoid giving anticoagulants, maintain tissue integrity by avoiding invasive procedures and needles related to subcutaneous or intramuscular injections
, monitor for shock
-internal bleeding may cause hypovolemic shock in the patient receiving alteplase.
-significant intravasculature fluid loss prevents the heart from pumping an adequate supply of blood and oxygen to the organs. It is important to frequently monitor the patient for symptoms of shock. Be alert for changing vital signs such as decreased bp, increased hr, and decreased body temperature. Assess the patient for increasing anxiety, confusion, shallow breathing, refuse sweating and weak pulse

141
Q

Antidote to alteplase if suspect bleeding

A

Stop thrombocytopenic therapy and administer aminocarproic acid (amicar) as an antidote to prevent further bleeding. This antifibrolytic drug prevents the conversion of plasminogen to plasmin and avoids fibrinoyltic activity that results in bleeding

Pharmacology (52 decks)

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