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PHARMACOLOGY I > anticoagulants and hemostatic agents > Flashcards

anticoagulants and hemostatic agents Flashcards

1
Q

what breaks down clot formation

A

fibrinolysis

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2
Q

what factor activates Factor I (Fibrinogen) to form a clot

A

factor II (thrombin)

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3
Q

what is the intrinsic clotting pathway

A
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4
Q

what patients are candidates for Anticaogulants

A

Hypercoaguable/Thromboembolic states
* cats w/ hypertrophic CM
* dogs w/ immune mediated hemolytic anemia
* cushing’s dz
* acute phase inflammation
* protein losing nephropathy

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5
Q

what patients are candidates for hemostatic agents

A

Hypocoaguable states
* post Sx, trauma, intoxication
* genetic bleeding diatheses
* liver intoxication/failure
* disseminated intravascular coagulopathy

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6
Q

What is the indicated use for Warfarin sodium

A

prophylactic txt of thrombotic conditions
use is HIGLY CONTROVERSIAL

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7
Q

what it the MOA of Warfarin

A

blocks recycling of gamma glutamyl carboxylase vit k (oxidized) back into its reduced form

recycling is caused by vit k epoxide reductase

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8
Q

Warfarin toxicity

A
  • Narrow TI
  • fatal hemorrhage associated w/ anemia
  • hematomas can form in any system
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9
Q

Warfarin use requires the VERY FREQUENT monitoring of what

A

prothrombin time

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10
Q

indicated use of Vitamin K1

A
  • rodenticide toxicity and moldy sweet clover
  • prolonged sulfonamide txt of birds for coccidiosis
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11
Q

why won’t vitamin K1 work in patients w/ chronic liver failure

A

the liver synthesizes coagulation factors

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12
Q

how does vitamin K1 work

A

gets conjugated to newly synthesized gamma glutamyl carboxylase in the liver by dI-diaphorase (makes new gamma glutamyl carboxylase)

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13
Q

Vit K1 administration

A

PO in dogs w/ fatty meal
IM or SC in food animals

therapeutic effects occur 6-12 hrs post admin

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14
Q

toxicity/adverse effects of Vit K

A

ANAPHYLAXIS

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15
Q

Heparin soidum vs Enoxaparin Na & Dalteparin Na

A

Heparin is a large glycosaminoglycan compared to Enoxaparin & Dalteparin which are low molecular weight heparin fractions

Heparin has a tail that allows for the shut down of both Factor Xa and thrombin but the other drugs lack a tail and can only shut down factor Xa

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16
Q

admin of heparin

A

IV
SC if LMWH (enoxaparin / dalteparin)

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17
Q

metabolism of heparin

A

liver & reticuloendothelial system/macrophages

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18
Q

heparin distribution

A

largely confined to circulation

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19
Q

what can occur from IM and deep SC administration of heparin

A

hematomas

20
Q

heparin requires the presence of what to work

A

anti-thrombin III
so won’t work in animals w/ protein losing nephropathy

21
Q

non-specific binding of heparin to platelets causes…

A

immune mediated thrombocytopenia and platelet activation (heparin induced trhombocytopenia)

22
Q

competitive inhibitor of Factor Xa that does NOT require anti-thrombin III to work

A

Rivaroxaban

23
Q

Acetysalicylic acid is..

A

aspirin

24
Q

MOA of acetylsalicyclic acid

A

irreversible inhibition of COX1, preventing thromboxane A2 production

TxA2 is needed to make platelets angry

25
Q

administration of acetylsalicyclic acid

A

PO, 70% BA in dogs

26
Q

metabolism of acetylsalicyclic acid

A

converted to salicylate by plasma esterases
modified by secondary metabolism in the liver via glucoronidation & glycine modification

27
Q

elimination of acetylsalicyclic acid

A

renal - urinary acidifying agents reduce elimination, alkalinizing agents increase elimination

28
Q

why is the elimination time of acetylsalicyclic acid in cats so high (38hrs)

A

b/c its metabolism requires glucoronidation and cats don’t glucoronidate

29
Q

acetylsalicyclic acid overdose

A
  • life threatening metabolic acidosis, depression, V+, hyperventilation, hyperthermia
  • GI ulceration
  • nephrotoxicity
30
Q

acetylsalicyclic acid contraindications

A
  • being a cat
  • hemorrhagic disroders
  • kidney or liver insufficiency
  • other drugs w/ high plasma protein binding
  • surfical procedures
31
Q

this drug doubles survival compared to aspirin in cats w/ risk of cardiogenic embolism caused by hypertrophic cardiomyopathy

A

Clopidogrel bisulfate

32
Q

how does Clopidogrel bisulfate work

A

irreversibly inhibits platelet ADP receptors = less activated platelets = less clotting

33
Q

T/F: Clopidogrel bisulfate is a prodrug and has to be activated by first pass metabolism

A

True

34
Q

what are the 2 types of clot forming topicals

A

type 1: activate a patient’s own platelets
type 2: injection of fibrogen and an activating agent to casue quick clot formation

35
Q

what is collasate

A

type 1 collagen foam (activates patients platelets) by binding to their collagen receptor

36
Q

the process of Fibrinogen → fibrin is called

A

coagulation

37
Q

the breakdown of fibrin into fibrin breakdown products / D-dimers is called

A

Fibrinolysis

38
Q

what is tissue plasminogen activator

A
  • used for pulmonary or arterial thromboembolism (clots)
  • activates breakdown of fibrin → fibrin breakdown pdts
  • highly controversial, most patients die and if they survive, very few regain functional limb use
39
Q

what do Aminocaproic and Tranexamic acids do

A

inhibit the activity of plasmin / fibrinolysis, prevent the breakdown of clots

40
Q

what is the use of Aminocaproic acid

A

ELU in dogs and horses
- post surgery bleeding
- guttural pouch bleeding in horses

IV admin

41
Q

use of Tranexamic acid

A
  • ELU for post surgery bleeding in dogs and cats
  • IV admin
  • significantly more effective than aminocaproic acid in vitro
42
Q

Adverse effects of Tranexamic acid

A

V+ in dogs

43
Q

what are the Anti-fibrolytic drugs

A
  • Aminocaproic acid
  • Tranexamic acid
44
Q

what drugs are anti-coagulator factors

A
  • warfarin
  • heparins
  • rivaroxaban
45
Q

what drugs are used for anti-platelet formation

A
  • aspirin
  • clopidogrel

PHARMACOLOGY I (21 decks)

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