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Introduction to Pharmacology > Blood Drugs > Flashcards

Blood Drugs Flashcards

1
Q

What is hemostasis? Thrombosis?

A

process to prevent and stop bleeding (hemorrhage)

formation or presence of a blood clot in a vessel

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2
Q

How do vein and coronary (artery) thombi compare? What drugs are used on each?

A

VEIN = red thrombi, RBC embedded in fibrin = anticoagulants

CORONARY = white thrombi, platelets embedded in fibrin = antiplatelets

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3
Q

In what 3 ways do drugs that affect hemostasis and thrombosis act?

A
  1. blood coagulation (fibrin formation)
  2. platelet function (activation, coagulation)
  3. fibrin removal (fibrinolysis)
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4
Q

What is the difference between red blood cells, white blood cells, and platelets (thrombocytes)?

A

RBC = erythrocytes; transport oxygen

WBC = leukocytes; fight germs and infections by attacking infected cells

PLATELETS = stop bleeding by forming a blood clot

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5
Q

What is the structure of red blood cells? What is their function?

A
  • disc-shaped with a large surface area
  • no nucelus
  • contains hemoglobin, which picks up oxygen

transports oxygen from the lungs to the body and carbon dioxide from the body back to the lungs

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6
Q

What is the structure of platelets? Where do they come from?

A
  • colorless and lens-shaped with a small surface area
  • no nucleus

fragments of cytoplasm from cells of the bone marrow

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7
Q

What is the function of platelets? In which animals are they found? Where are they not found?

A

prevents excessive internal or external bleeding after an injury by forming a blood clot

  • mammals
  • birds and amphibians: present as intact mononuclear cells
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8
Q

What are the 3 types of white blood cells? What is their function?

A
  1. granulocytes - neutrophils, eosinophils, basophils
  2. monocytes
  3. lymphocytes - B- and T-lymphocytes

work together to fight illness or disease, like infections, inflammation, allergic reactions, and stress

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9
Q

What are the 4 basis steps of hemostasis?

A
  1. vascular stage
  2. platelet stage
  3. coagulation
  4. fibrinolysis
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10
Q

What is coagulation? What are the 4 steps?

A

process by which blood changes from a liquid into a gel, forming a blood clot (fibrin + platelets)

  1. activation
  2. adhesion
  3. aggregation of platelets
  4. deposition and maturation of fibrin
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11
Q

How do the phases of hemostasis work?

A
  • damaged blood vessels release clotting factors
  • clotting factors activate prothrombin into thrombin (IIa)
  • vasoconstriction limits blood flow and platelets form a sticky plug, where soluble fibrinogen is activated by thrombin into insoluble fibrin
  • fibrin strands adhere to the plug and form an insoluble clot
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12
Q

What are the 5 steps to the clotting cascade?

A
  1. wound (vascular injury) causes the endothelium to release tissue factor
  2. tissue factor activates factor VIIa
  3. factor VIIa activates factor Xa
  4. with factor Va, factor X activates prothrombin (factor II) into thrombin (factor IIa)
  5. thrombin (IIa) then is able to turn soluble fibrinogen into insoluble fibrin to form a clot
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13
Q

Blood coagulation factors:

A
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14
Q

What are the 3 major steps to clotting? What ion is important for the activation of many zymogen factors?

A
  1. activation of prothrombin activators
  2. conversion of prothrombin into thrombin
  3. conversion of fibrinogen into fibrin fibers

Ca2+

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15
Q

What is the difference between pro-coagulants and anti-coagulants?

A

PRO-COAGULANTS promote coagulation: XIIa, XIa, Xa, IXa, and thrombin (IIa)

ANTI-COAGULANTS inhibit coagulation: antithrombin III, fibrinolysis

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16
Q

What conditions require anticoagulants and antiplatelets?

A

cardiovascular disorders
- thrombosis
- pulmonary thrombosis
- acute coronary syndrome
- arterial fibrillation
- stroke
- ischemic heart disease
- thromboembolic disease in IMHA
- antithombotic prophylaxis

17
Q

What 4 drugs affect coagulation bleeding?

A
  1. anticoagulants
  2. antiplatelets
  3. fibrinolytic drugs
  4. antifibrinolytic
18
Q

How are anticoagulants used? What are the 4 main classes?

A

used to modify the coagulation cascade either when there is a defect in coagulation or when there is unwanted coagulation

  1. heparin and LMWH (Dalteparin, Enoxaparin)
  2. warfarin and coumarin derivatives (Dicumarol, Menadione, Acenocoumarol)
  3. thrombin inhibitors
  4. factor Xa inhibitors
19
Q

What is antithrombin III? What is its function? What drug potentiates it?

A

endogenous anticoagulant

inactivates factors IXa, Xa, XIa, XIIa, and thrombin (IIa)

heparin

20
Q

What is the mechanism of action of heparin? What does this result in?

A

binds to antithrombin III and causes conformational changes that significantly enhance its inhibitory effects on various activated coagulation factors (~1000-fold)

inactivation of Xa, thrombin (IIa), IXa, XIa, and XIIa

21
Q

Where is heparin derived from? When is it most commonly used?

A

proteoglycan from mast cells

excessive clotting or increased risk of clot formation in cats, dogs, and horses, especially disseminated intravascular coagulopathy (DIC)
- thromboembolic problems
- venous thrombosis
- pulmonary thromboembolism
- laminitis
- endotoxic shock
- burns

22
Q

What are the 2 types of heparin?

A
  1. unfractionated heparin (UFH): inactivates thrombin (IIa) and factor Xa
  2. low-molecular-weight heparin (LMWH): inactivates factor Xa
23
Q

Why is heparin not a one dose fits all drug? How can we tailor dosages to patients?

A
  • patients with low antithrombin III may not respond as well as those with adequate levels
  • variable PK among animals and protein binding

monitor clotting times with activated partial thromboplastin time (aPTT)

24
Q

What are the 2 most common adverse effects of heparin?

A
  1. bleeding problems
  2. heparin-induced thrombocytopenia (humans)
25
Q

What is a major sign of heparin overdose? How can this be reversed?

A

excessive anticoagulation and bleeding

protamine sulfate (found in fish sperm) - strongly basic and combines with acidic heparin to form a stable inactive salt

26
Q

What 2 drugs are low-molecular-weight heparins? How is activity monitored?

A
  1. Dalteparin
  2. Enoxaparin

anti-factor Xa / antifactor IIa ration
(the ratio for UFH is 1:1)

27
Q

What are the 2 major advantages of LMWH over UFH?

A
  1. greater activity and safety profile
  2. favorable and predictable PK
    - more complete and predictable absorption
    - longer duration
    - less frequent administration
    - reduced risk of bleeding
    - more predictable anticoagulant response
28
Q

How do the activity ratios of Dalteparin and Enoxaparin compare?

A

D = 2.7:1 (shorter half-life)

E = 3.3:1 and 5.3:1 (longer half-life)

29
Q

What is vitamin K? What are the 3 types?

A

fat-soluble vitamin essential for hepatic synthesis of prothrombin groups of coagulation factors (II, VII, IX, X)

K1 = plants
K2 = bacteria in gut
K3 = synthetic

30
Q

What do coumarin synthetic derivatives do? What 3 drugs belong to this class?

A

vitamin K inhibitors

  1. Warfarin (water and light soluble)
  2. Dicumarol
  3. Acenocoumarol
31
Q

What is the mechanism of action of coumarin synthetic derivatives? What 3 uses do they have?

A

reduce the production/activation of vitamin K-dependent factors that promote clotting (II, VI, IX, X) by inhibiting the regeneration of vitamin K

  1. decrease tendency for thrombosis (thromboprophylaxis in dogs)*
  2. treat or prevent blood clots in veins and arteries
    3 reduce the risk of stroke or heart attack
32
Q

What are the 2 most common adverse effects of coumarin synthetic derivatives? How are they reversed?

A
  1. decreased blood clotting, spontaneous bleeding, excessive bleeding from trauma or surgery, GI bleeding
  2. drug-drug interactions (aspirin, clopidogrel)
33
Q

What does vitamin K deficiency cause? What are the most common causes?

A

excessive bleeding due to failure of normal fibrin clot formation

  1. accidental poisoning by warfarin in dogs and cats (OTC rodenticide - hemorrhage after consumption)
  2. intestinal malabsorption
  3. medication containing warfarin
34
Q

How is vitamin K deficiency typically treated?

A

Menadione - synthetic vitamin K

35
Q

Heparin vs Warfarin:

A

Introduction to Pharmacology (39 decks)

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