Blood and Blood elements tutorial Flashcards

1
Q

State the mode of action, name at least 2 anticoagulants that you would use to collect blood for haematological studies

A

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

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2
Q

State the mode of action, name at least 2 anticoagulants that you would be recommend for transfusion purposes

A

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

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3
Q

What are some of the adverse effects that are associated with using the anticoagulant in vivo?

A

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
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4
Q

Name at least 3 agents that you may apply topically to stop the bleeding

A

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

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5
Q

How does fibrin foam, thrombin work?

A

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

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6
Q

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)

A

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

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7
Q

How bromadiolone acts to causes these clinical signs, please eplxain to her how this may occur

A

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

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8
Q

Name one systemically used haemostatic agent that you may ad orally to this cat & explain how this agent acts to relieve these symptoms

A

you give vit K with a fatty meal because its fat soluble

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9
Q

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?

A

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

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10
Q

If you have the option of infusing fresh whole blood or packed red cells, which one wold you choose and why?

A

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

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11
Q

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?

A

-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

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12
Q

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

A

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

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13
Q

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

A

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

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14
Q

For chemotherapy against mulicentric lymphoma outlines a rationale for administering prednisolone and describe its general mode of action

A

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

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15
Q

Describe how prolonged use of prednisolone without adhering to principle of glucocorticoids use may lead to Addison’s disease

A

because they body will not produce its own cortisol which leads to addison’s disease

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16
Q

What agent is essential for carboxylation and activation of clotting factors II, TX and X. It is also of choice in cases of bleeding and petechiation that occurs following GIT disease and bile duct obstruction

A

vitamin K

17
Q

What agent is clinically used to treat disseminated intravascular clotting reversibly binds to and activates antithrombin (fIII) leading to the inactivation of coagulation factors II and X

A

Streptokinase

18
Q

What is prescribed for atop and autoimmune destruction of the skin by targeting and the transcription and release of Janus Kinase dependent cytokines involved in allergy, inflammation and pruritus

A

Iron copper paste

19
Q

What monoclonal ab has clinical approval for neutralised interleukin-31 a cytokine that plays an important role in the pathogenies of atopic dermatitis in dogs?

A

Oclacitinib

20
Q

This drug is often incorporated in sponges or gauze and applied topically to stop spontaneous nasal bleeding (epistaxis). The primary hemostatic mechanism is the induction of vasoconstriction via alpha-1 adrenergic receptors in capillaries.

A

Epinephrine or fibrin foam

21
Q

Anti-platelet drug used to treat chronic thromboembolism in animals by targeting the release of thromboxane A2 , a pro-aggregatory prostaglandin from cell membrane activation in thrombocytes.-

A

ticlopidine

22
Q

What is used as a recombinant peptide to mange chronic anaemia resulting from chronic kidney disease in companion animals?-

A

Erythropoietin

23
Q

What drug is commonly used as an adjunct immune suppressive agent that works by targeting the incorporation of purine nucleotides during cell division and clonal lymphocyte expansion?-

A

azathioprine

24
Q

What is erythropoietin and where is it synthesised in the body?

A

What is erythropoietin and where is it synthesised in the body? hormone produced primarily by the kidneys. It plays a key role in the production of red blood cells (RBCs), which carry oxygen from the lungs to the rest of the body

25
Q

You are a consultant for an intensive pig farm. On this farm, pigs are housed in-doors, on concrete slabs and maintained on commercially provided feed. Recently, all the piglets that were born in the last 7 days are anorexic, very lethargic, have pale mucous membranes & are losing weight. The adult animals do not show any of these symptoms and, Blood & other clinical examinations reveal no parasitic infestation/infections. You suspect that this is a typical case of piglet anemia. i) What would you suspect as the most probable cause of this type of anaemia & why do you think this problem is more likely to be prevalent in this type of farm? ii) How would you attempt to correct this problem in individual piglets that are anaemic?

A

i) What would you suspect as the most probable cause of this type of anaemia & why do you think this problem is more likely to be prevalent in this type of farm?

Anemia from iron deficiency and the piglets are more susceptible by lack of exposure to alternate source of iron eg. soil

ii) How would you attempt to correct this problem in individual piglets that are anaemic?

Iron-dextran (Po or IM)

Iron-copper paste (topical on udders)

26
Q

What are some of side effects of using recombinant erythropioetin?

A

Ab formation and allergies

vomitng and seizures

systemitc hypertension- CVS effects

Absolute polycythemia (increased RBC count)

27
Q

Recombinant Erythropoietin may also be used therapeutically in horses. However caution must be exercised as this is regarded as a “DOPING” agent. Please explain why we should refrain from administering erythropoietin in horses that are about to participate in a race.

A

Erythropoiesis= increased O2 carrying capacity- unfair advantage

28
Q

Fill out this table

A
29
Q
A
30
Q
A

The answer to Q5 is Oclacitinib