Drugs Acting on the Blood Flashcards

1
Q

Name 4 types of drugs that act on the blood.

A

Antianemic drugs, Colony Stimulating Factors, Drugs affecting hemostasis (Tx hemorrhage), Treatment of thromboembolism in cats (antithrombotics)

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2
Q

What causes Microcytic anemia?

A

Iron deficiency

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3
Q

What causes Normocytic anemia?

A

Chronic diseases, endocrine anemia, bone marrow failure.

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4
Q

What causes Macrocytic (megaloblastic) anemia?

A

B12 deficiency, folic acid deficiency

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5
Q

What causes Hemolytic anemia?

A

Autoimmune diseases, drug-induced, hemoglobinopathies, membrane disorders, metabolic abnormalities, Glucose-6-phosphate dehydrogenase deficiency, infections.

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6
Q

What do you treat microcytic anemia with?

A

Iron Preparations or Copper preparations

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7
Q

How does iron deficiency cause anemia?

A

Because iron is a main component of RBCs.

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8
Q

What routes can we use to administer iron preparations?

A

Parenteral or oral.

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9
Q

Can we use IV iron preparations?

A

No because they are more likely to cause hypersensitivity.

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10
Q

What cause the GI side-effects of oral iron preparations?

A

Irritation and astringent properties (causes constipation).

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11
Q

What is a chelating complex?

A

An agent that is readily secreted in the urine and decreases toxic effects.

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12
Q

What is the order of preference for iron preparations?

DOUBLE CHECK WITH SHOCKRY.

A

Organic>Ferrous>Ferric

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13
Q

Why do we treat microcytic anemia with copper preparations?

A

Because Cu is important for the absorption of Fe AND Cu is a component is cytochrome oxidase which is important in oxidation of Fe.

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14
Q

What iron preparation would you administer parenterally?

A

Iron carbohydrate complexes

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15
Q

What iron preparation would you administer orally?

A

Ferrous chloride, Ferrous phosphate, Ferrous sulfate.

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16
Q

What copper preparation can you give orally?

A

Copper sulfate.

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17
Q

How do you give copper glycinate?

A

SQ or IM

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18
Q

Can you give cupper preparations IV?

A

No, it’s irritating.

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19
Q

What is another name for Macrocytic anemia?

A

Megaloblastic anemia

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20
Q

What is a common cause of macrocytic anemia in ruminants?

A

Cobalt deficiency.

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21
Q

What is a common cause of normocytic/normoplastic anema?

A

It is commonly a side effect of anti-cancer drugs because they target rapidly dividing cells (kills marrow before it kills the cancer cells).

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22
Q

How does EPO play a role in normocytic anemia?

A

EPO from the kidneys stimulates RBC production.

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23
Q

What can you do for immune mediated hemolytic anemia (IMHA)?

A

Supportive therapy (fluids, acid/base balance, etc), blood transfusions, immunosuppressives, IV gamma globulin.

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24
Q

Name 4 immunosuppressives.

A

Glucocorticoids (prednisone, prednisolone), cytotoxic drugs (azathioprine, cyclophosphamide), Danazol, Cyclosporin A.

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25
Q

What are the two types of colony stimulating factors?

A

Granulocyte CSF (G-CSF) and Granulocyte-macrophage colony stimulating factor (GM-CSF).

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26
Q

What CSF type does Filgrastim fall under?

A

G-CSF

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27
Q

What CSF type does Sargramostim fall under?

A

GM-CSF

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28
Q

What is the use of CSF drugs?

A

Helps decrease the negative effects of cancer treatment by promoting growth of granulocytes.

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29
Q

What is the difference between G-CSF nd GM-CSF?

A

GM-CSF isn’t as specific, it acts on granulocytes, platelets and RBCs. G-CSF only acts on granulocytes.

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30
Q

How does Filgrastim work at therapeutic doses?

A

Stimulates progenitors of neutrophils.

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31
Q

How does Sargramostim work?

A

Stimulates the growth and development of neutrophils, eosinophils, basophils, erythrocytes and macrophages.

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32
Q

What is the clinical use of a CSF?

A

To help treat anticancer chemotherapy-induced neutropenia.

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33
Q

What are the adverse effects of CSF use?

A

Bone pain, and Sargramostim can also cause fever and cardiopulmonary toxicity.

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34
Q

What are the two drug types that affect hemostasis?

A

Hemostatics and antithrombotics.

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35
Q

What are the 5 steps in hemostasis?

A

Vascular injury > contraction of the vessel > primary hemosstasis (platelet plug) > secondary hemostasis (protein plug) > fibrinolysis.

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36
Q

What are the two types of hemostatics?

A

Local (styptic) and systemic hemostatics.

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37
Q

What can happen if you use a local hemostatic systemically?

A

Can cause emboli.

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38
Q

What are the four types of local hemostatics?

A

Vasoconstrictors
Astringents (tannic acid, ferric chloride)
Surgical (oxidized cellulose, gelatin sponge, collagen)
Physiological (thromboplastin, thrombin, fibrinogen, fibrin foam)

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39
Q

How can you tell if a drug is an amide or an ester?

A

If there’s an “-i-“ before “-caine” it’s an amide.

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40
Q

What are the 5 types of systemic hemostatics?

A

Clotting factors (blood transfusion, fresh frozen plasma)
Vitamin K
Protamine sulfate
Aminocaproic acid
Desmopressin (DDAVP) - (synthetic analog of vasopressin)

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41
Q

Of the three types of vitamin K (K1, K2, K3) which are used clinically?

A

Vit. K1 and K3

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42
Q

What is Phytonadione?

A

Vit. K1

43
Q

What is Menaquinone?

A

Vit. K2

44
Q

What is Menadione?

A

Vit. K3

45
Q

Where does Vit. K1 come from?

A

Plant origin.

46
Q

Where does Vit. K2 come from?

A

Bacteria in the GIT.

47
Q

Where does Vit. K3 come from?

A

Synthetic.

48
Q

What is the mechanism of action for Vit. K1?

A

Stimulates the formation of prothrombin (Factor II), and factors VII, IX, and X in the liver.

49
Q

How does Warfarin block clotting?

A

Warfarin blocks the reductase enzyme that reduces inactive Vitamin K epoxide to activated Vitamin K which is the cofactor required to activate factors II, VII, IX, and X.

50
Q

How is Vit. K1 given?

A

Orally for maintenance or parenterally (IV, IM, SQ) in an emergency.

51
Q

What are some considerations when giving Vit. K1 parenterally?

A

Use a small gauge needle (will bleed at site)

IM=SQ>IV (causes hypersensitivity)

52
Q

What are the 4 clinical uses of Vit. K1?

A

Warfarin poisoning
Treatment of spoiled sweet clover poisoning in cattle
Vit. K deficiency
Combined with local hemostatics for treatment of epistaxis in dogs and horses.

53
Q

Why is Vit. K deficiency so rare?

A

Food has lots of Vit. K

54
Q

What are two things that can cause Vit. K deficiency?

A

Absorption problems, treatment with broad spectrum ABs ( affects gut flora), or liver disease.

55
Q

What is a very important thing to remember when treating an animal with Vit. K1 for Warfarin poisoning?

A

Vit. K takes about a day to take effect, so animal will keep bleeding. Will need to give a transfusion to provide missing coag. factors immediately.

56
Q

What is Protamine sulfate used for?

A

Specific antidote for heparin.

57
Q

How does protamine sulfate work?

A

binds with heparin to form a salt.

58
Q

How do you give protamine sulfate?

A

Given slowly IV.

59
Q

Why can’t protamine sulfate be given orally?

A

Has a short half-life and poor penetration of membranes.

60
Q

Why must you be careful with your dose of protamine sulfate?

A

Has anticoagulant effect if given as an overdose.

61
Q

How does aminocaproic acid work?

A

It inhibits the conversion of plasminogen to plasmin.

62
Q

What are two clinical uses for aminocaproic acid?

A

To treat hemorrhage due to fibrinolysis

To treat degenerative myelopathy in GSD (peripheral neuronal degeneration.

63
Q

What does desmopressin do?

A

Increases the vWF levels for about two hours in dogs.

64
Q

What are 2 clinical uses for desmopressin?

A

Controlling bleeding in dogs with vWD

During surgery in dogs with vWD

65
Q

What are the three classes of antithrombotic drugs?

A

Anticoagulants
Thrombolytic agents
Antiplatelet drugs

66
Q

What are the two anticoagulants?

A

Warfarin

Heparin

67
Q

What is Herparin’s mechanism of action?

A

Activates antithrombin III, inhibiting thrombin and activated coag. factors IXa, Xa, XIa, and XIIa in the liver.

68
Q

How is heparin absorbed?

A

IV or SQ

NOT IM
NOT absorbed orally

69
Q

Is heparin absorbed orally?

A

No

70
Q

Can heparin be given IM?

A

No

71
Q

T/F: Heparin has a slow onset and short duration.

A

False. Heparin has a fast onset and short duration.

72
Q

T/F: Heparin is rapidly metabolized in the liver.

A

True

73
Q

T/F: Heparin does not cross the placenta and is not excreted in milk.

A

True.

74
Q

What are 3 clinical uses of heparin?

A

Treatment of acute thromboembolism
Anticoagulant in pregnant animals
Anticoagulant in-vitro

75
Q

T/F: Heparin has a wide safety margin.

A

False. Heparin has a short safety margin. So does Warfarin.

76
Q

T/F: Heparin may cause allergic reaction.

A

True. However low molecular weight heparins (MWHs) are less antigenic.

77
Q

What type of heparin is less antigenic?

A

Low molecular weight heparin (LMWHs)

78
Q

How do you treat heparin toxicity?

A

Protamine sulfate, blood transfusion or fresh frozen plasma (FFP).

79
Q

What are the pharmacokinetics of Warfarin?

A

Given orally. It’s more lipid soluble, but not much better than heparin. Absorption is slow, but complete.

80
Q

What must you be aware of when giving warfarin?

A

It CAN cross the placenta and cause fetal bleeding. It can also be excreted into the milk a little.

81
Q

How long does Warfarin take to take effect?

A

A couple days, must first deplete the existing coag. factors.

NOTE: This means you can treat warfarin poisoning preemptively.

82
Q

T/F: Warfarin binds poorly to albumin.

A

False. Warfarin binds extensively (99%) to albumin giving it a longer half-life.

83
Q

How long is the duration of action of warfarin?

A

2-5 days due to protein binding.

84
Q

What are the two uses of warfarin?

A

Prevention in thromboembolic disease

Rodenticide

85
Q

What must you be aware of with animals being treated with warfarin?

A

Protein binding is weak and so drug is easily displaced (eg. Phenylbutazone and horses).

86
Q

Where is warfarin metabolized?

A

The liver

87
Q

Does warfarin have a wide or narrow safety margin?

A

Narrow.

88
Q

What are two toxic effects of warfarin?

A

Bleeding (this is number 1) and is also teratogenic (bone defects)

89
Q

What is the specific antidote to warfarin toxicity?

A

Vitamin K1

Whole blood or fresh frozen plasma can be used in severe cases.

90
Q

What 5 drugs increase response (displacement) of warfarin?

A
Phenylbutazone, salicylates
Heparin
Chloramphenicol
Sulfonamides and broad-spectrum antibiotics
Anabolic steroids
91
Q

What 4 drugs are thrombolytic agents?

A

Streptokinase
Urokinase
Tissue plasminogen activator (tPA, alteplase)
Anistreplase (APSAC)

92
Q

What is the mechanism of action for thrombolytic agents?

A

Activate conversion of plasminogen to plasmin which causes fibrinolysis.

93
Q

What must you be aware of with thrombolytic agents?

A

At low doses, they act on the clot. At high doses they can cause systemic bleeding.

94
Q

What do you use thrombolytic agents to treat?

A

Acute thromboembolic disorders.

95
Q

What toxic effects must you monitor for with thrombolytic treatment?

A

Narrow safety margin, must monitor hemodynamic and vital functions.

96
Q

What do you treat thromboembolic toxicity with?

A

Aminocaproic acid

97
Q

What drug is used as an antiplatelet drug?

A

Aspirin

98
Q

What is Aspirin’s mechanism of action?

A

Low doses inhibit synthesis of Thromboxane A2 by IRREVERSIBLY inhibiting cyclooxygenase (COX-1 and COX-2). Ultimately inhibiting platelet aggregation because TXA2 is the main proaggregant.

99
Q

What is the clinical use of Aspirin?

A

Low doses used to prevent thrombotic disorders.

100
Q

T/F: Large doses of Aspirin are more effective than low doses.

A

False. Low doses are more effective.

101
Q

What other mechanisms of action are there with regards to antiplatelet drugs?

A

Inhibit phosphodiesterase and increase cAMP (Dipyridamole)

Block GPIIb/IIIa receptors (Abciximab)

102
Q

What are two antiplatelet drugs?

A

Antithrombin = Lepirudin

Inhibition of ADP binding = Clopidogrel

103
Q

How do you treat acute thromboembolism in cats?

A

Heparin, thrombolytic agents (Streptokinase) and vasodilators.

104
Q

How do you prevent thromboembolism is cats?

A

Aspirin or Warfarin.