Blood and Blood elements tutorial Flashcards
State the mode of action, name at least 2 anticoagulants that you would use to collect blood for haematological studies
mode of action, name at least 2 anticoagulants that are used to collect blood They stop bleeding from occurring or lessen it and therefore prevents bleeding to death, it will promote the reaction from thrombogenic factors to antithrombogenic factors 2 examples of this drug is heparin and low molecule weight heparin, dabiagatran
State the mode of action, name at least 2 anticoagulants that you would be recommend for transfusion purposes
For transfusion processes you would use the ones which are in vitro, 2 examples are
ca chelators,
heparin Na,
citrate-p-dextrose-adrenine
acid citrate dextrose
they will maintain RBC integrity through pH stabilisation and the prevention of ATP, 2-3 diposphoglyceate decline
What are some of the adverse effects that are associated with using the anticoagulant in vivo?
in vivo its used to stop the formation of thrombi
its mediated by the reversible binding to antithrombin 3 which activated and inhibits several factors e.g thrombin and activated factors X therefore thrombin is the best to use
Adverse effects
- excessive anticoagulation and haemorrhage
- thrombocytopenia
- hypersensitivity and other immune mediated reactions
- increased erythrocyte destruction in horse
Name at least 3 agents that you may apply topically to stop the bleeding
They should have final or cause no tissue reaction and handle they usually have homeostatic agents, they should contain collagen and thrombin therefor use epinephrine, sponge which causes the blood to coagulate, fibrin foam, thrombin
How does fibrin foam, thrombin work?
it will trigger the coagulation system, the second the platelet come into contact with the collagen they become pissed out and shit of adhesive molecules epinephrine causes vasoconstriction this is the same as adrenaline, this will stop random nose bleeds in horses
Based on your knowledge of the mechanism of action. of this poison explain why a cat would will take 2 days for the symptoms to appear after eating a dead mouse its thought the cat has poisoning by a coumarin-derivative (bromadiolone)
you need to deplete all the the other factors to see the effects of the drug, so the effects of the drug will be behind the exposure of the drug this is for the 1st question it takes the drug to build enough to see it working
mode of action vit K converts proteins to their active forms which does clotting by ingesting antagonist of vit K, this will lock of vit K causing there to be no clotting and there will be lots of bleeding and is all over red rover
How bromadiolone acts to causes these clinical signs, please eplxain to her how this may occur
it causes internal haemorrhaging, you are losing the platelets and the clotting factors and the clinal signs are directed linked to this, it will inhibit vit K when you stop giving bromadiolone
Name one systemically used haemostatic agent that you may ad orally to this cat & explain how this agent acts to relieve these symptoms
you give vit K with a fatty meal because its fat soluble
Your supervisor that the medication you chose to be continued for at least 10 days and that if possible, you should co-administer that drug with a fatty meal. Give a reasonable explanation for these suggestions
The cat has been on meloxica why should you stop this treament?
Because vit K is fat soluble it will act faster if you give it a fatty meal and you feed it for a prelonged time to allow it to build back up
Meloxicam will stimulate Cox 1 thromboxane and inhibt Cox 2 which is prostanglandin which is the oppostie of what you want because the can will bleed to death
If you have the option of infusing fresh whole blood or packed red cells, which one wold you choose and why?
use fresh blood because it will have clotting factors present as well as blood where as packet RBC will only have blood and no clotting factors and this will only band aid the issue
Cattle present with severe bleeding from multiple orifices. Necropsy examination revealed free blood throughout the body cavities and connective tissues. This clinical probable was observed approximately 28 hours after the animal had been fed mouldy hay from pasture species. There was no history of exposure to any synthetic chemical compounds -What are the toxic principle? -What is MOA of the toxic principle? -Why is the appearance of clinical signs delayed? -More moralities observed in calves why? -What is used as an antidote and outline the MOA?
-What are the toxic principle? the toxin is bishdroxtcoumarin which is naturally occurring in mouldy sweet clover which causes haemorrhage disease -What is MOA of the toxic principle? bishdroxtcoumarin is vit K antagonists and will stop the synthesis of vit K clotting factor 2,7,9,10 from being created -Why is the appearance of clinical signs delayed? because your mature clotting factors must be used up 1st -More moralities observed in calves why? Because they would not have a good reservoir of mature clotting factors and they have less blood volume and they have not been exposed to many things and will not have any resistance or a reservoir against stuff -What is used as an antidote and outline the MOA? fresh blood and plasma and vit K
A dog is presented with signs of acute onset, progressive, peripheral neuromuscular disease. Clinical examinations reveals massive thrombosis of the caudal aorta, femoral arteries and the right femoral vein.
i) Name at least 2 specific examples of fibrinolytic agents that you may prescribe for this dog
ii) explain the vernal mode of action of these drugs to a curious owner of patient
iii) what adverse effects would you anticipate is using the name fibrinolytic agents
iv) Would you consider using anti-platelet drugs for this clinical condition and what specific drugs would you consider- out why
i) Name at least 2 specific examples of fibrinolytic agents that you may prescribe for this dog streptokinase- strepotordornase fibrinolysin
ii) explain the general mode of action of these drugs to a curious owner of patient streptokinase; promotes conversion of plasminogen into plasma applied locally conversion of inactive plasminogen to plasmin by using hormones, enzymes and epinephrine
iii) what adverse effects would you anticipate is using the name fibrinolytic agents non-selective; systemic plasmin formation and fibrinolysis infection use in combination with antibiotics antigenic may be lead ab formation and anaphylaxis
iv) Would you consider using anti-platelet drugs for this clinical condition and what specific drugs would you consider- out why; you would use ab anti-platelet drug because it prevents the formation blood clots, on the surface of platelets you there is Cox1 and Cox 2, cox 1 produces thromboxane and cox 2 produces prostacyclin which has anti-platelet properties to you want a drug which will block Cox 1 and stimulate cox 2
A dog comes in with pyrexia and splenomegaly, there was neutropenia (low levels of neutrophils), monocytosis (increase in the number of monocytes), thrombocytopenia (low levels of thrombocytes (platelets)) you suspect an autoimmune disease
i) citing modes of actions, outline at 3 classes of drugs may be used to treat this animal
ii) Explain why it was necessary to gradually decrease the dose of prednisolone
i) citing modes of actions, outline at 3 classes of drugs may be used to treat this animal
- imunophilin binding, inhibitor of cell division and nucleotide metabolism and JAK-STAT signaling inhibitors all of these are glucocorticoids,
MOA glucocorticoids have a very strong immunosuppression response
glucocorticoids role in the body is to reduces certain aspects of immune function, such as inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies
what glucocorticoids does in the body will be highen when you add it has a drug corticosteroids e.g prednisolone
ii) Explain why it was necessary to gradually decrease the dose of prednisolone MUST COME OFF THE DRUG SLOWLY OR ELSE YOU GET ADDISON’S DISEASE (opposite of cushing) because they body will not produce its own cortisol
For chemotherapy against mulicentric lymphoma outlines a rationale for administering prednisolone and describe its general mode of action
MOA; prednisolone at low doses you are effect have anti-inflammatory response and effect the production of arachidonic acid cortisol drives suppression of the immune system and loss of hair because the the cortisol is destroying the certain cell types prednisolone will drive these effects the drug enters the cell into the cytoplasm and binds to the glucocorticoid receptor when it binds its activated and goes into the nucleus of the cell it will activate genes which will either activate and suppression things like the immune system and then you will end up with things like neutrophil migration suppression and depression in production of proinflammatory cytokines
Describe how prolonged use of prednisolone without adhering to principle of glucocorticoids use may lead to Addison’s disease
because they body will not produce its own cortisol which leads to addison’s disease