anticoagulants and hemostatic agents Flashcards
what breaks down clot formation
fibrinolysis
what factor activates Factor I (Fibrinogen) to form a clot
factor II (thrombin)
what is the intrinsic clotting pathway
what patients are candidates for Anticaogulants
Hypercoaguable/Thromboembolic states
* cats w/ hypertrophic CM
* dogs w/ immune mediated hemolytic anemia
* cushing’s dz
* acute phase inflammation
* protein losing nephropathy
what patients are candidates for hemostatic agents
Hypocoaguable states
* post Sx, trauma, intoxication
* genetic bleeding diatheses
* liver intoxication/failure
* disseminated intravascular coagulopathy
What is the indicated use for Warfarin sodium
prophylactic txt of thrombotic conditions
use is HIGLY CONTROVERSIAL
what it the MOA of Warfarin
blocks recycling of gamma glutamyl carboxylase vit k (oxidized) back into its reduced form
recycling is caused by vit k epoxide reductase
Warfarin toxicity
- Narrow TI
- fatal hemorrhage associated w/ anemia
- hematomas can form in any system
Warfarin use requires the VERY FREQUENT monitoring of what
prothrombin time
indicated use of Vitamin K1
- rodenticide toxicity and moldy sweet clover
- prolonged sulfonamide txt of birds for coccidiosis
why won’t vitamin K1 work in patients w/ chronic liver failure
the liver synthesizes coagulation factors
how does vitamin K1 work
gets conjugated to newly synthesized gamma glutamyl carboxylase in the liver by dI-diaphorase (makes new gamma glutamyl carboxylase)
Vit K1 administration
PO in dogs w/ fatty meal
IM or SC in food animals
therapeutic effects occur 6-12 hrs post admin
toxicity/adverse effects of Vit K
ANAPHYLAXIS
Heparin soidum vs Enoxaparin Na & Dalteparin Na
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
admin of heparin
IV
SC if LMWH (enoxaparin / dalteparin)
metabolism of heparin
liver & reticuloendothelial system/macrophages
heparin distribution
largely confined to circulation
what can occur from IM and deep SC administration of heparin
hematomas
heparin requires the presence of what to work
anti-thrombin III
so won’t work in animals w/ protein losing nephropathy
non-specific binding of heparin to platelets causes…
immune mediated thrombocytopenia and platelet activation (heparin induced trhombocytopenia)
competitive inhibitor of Factor Xa that does NOT require anti-thrombin III to work
Rivaroxaban
Acetysalicylic acid is..
aspirin
MOA of acetylsalicyclic acid
irreversible inhibition of COX1, preventing thromboxane A2 production
TxA2 is needed to make platelets angry
administration of acetylsalicyclic acid
PO, 70% BA in dogs
metabolism of acetylsalicyclic acid
converted to salicylate by plasma esterases
modified by secondary metabolism in the liver via glucoronidation & glycine modification
elimination of acetylsalicyclic acid
renal - urinary acidifying agents reduce elimination, alkalinizing agents increase elimination
why is the elimination time of acetylsalicyclic acid in cats so high (38hrs)
b/c its metabolism requires glucoronidation and cats don’t glucoronidate
acetylsalicyclic acid overdose
- life threatening metabolic acidosis, depression, V+, hyperventilation, hyperthermia
- GI ulceration
- nephrotoxicity
acetylsalicyclic acid contraindications
- being a cat
- hemorrhagic disroders
- kidney or liver insufficiency
- other drugs w/ high plasma protein binding
- surfical procedures
this drug doubles survival compared to aspirin in cats w/ risk of cardiogenic embolism caused by hypertrophic cardiomyopathy
Clopidogrel bisulfate
how does Clopidogrel bisulfate work
irreversibly inhibits platelet ADP receptors = less activated platelets = less clotting
T/F: Clopidogrel bisulfate is a prodrug and has to be activated by first pass metabolism
True
what are the 2 types of clot forming topicals
type 1: activate a patient’s own platelets
type 2: injection of fibrogen and an activating agent to casue quick clot formation
what is collasate
type 1 collagen foam (activates patients platelets) by binding to their collagen receptor
the process of Fibrinogen → fibrin is called
coagulation
the breakdown of fibrin into fibrin breakdown products / D-dimers is called
Fibrinolysis
what is tissue plasminogen activator
- 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
what do Aminocaproic and Tranexamic acids do
inhibit the activity of plasmin / fibrinolysis, prevent the breakdown of clots
what is the use of Aminocaproic acid
ELU in dogs and horses
- post surgery bleeding
- guttural pouch bleeding in horses
IV admin
use of Tranexamic acid
- ELU for post surgery bleeding in dogs and cats
- IV admin
- significantly more effective than aminocaproic acid in vitro
Adverse effects of Tranexamic acid
V+ in dogs
what are the Anti-fibrolytic drugs
- Aminocaproic acid
- Tranexamic acid
what drugs are anti-coagulator factors
- warfarin
- heparins
- rivaroxaban
what drugs are used for anti-platelet formation
- aspirin
- clopidogrel
