Exam Practical Blood Flashcards

1
Q

Prothrombin Time

A

(Normal = 10-14 seconds)
This simple test measures the extrinsic pathway in addition to the common terminal sequence. Tissue thromboplastin and calcium are added to citrated plasma. The prothrombin time may also be expressed as the International Normalized Ratio (INR).

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2
Q

Activated Partial Thromboplastin Time (APTT)

A

(Normal = 30-40 seconds)
his screening test assesses the intrinsic pathway of coagulation in addition to the common terminal sequence. In this test three substances are added to citrated plasma, to initiate coagulation: phospholipid, a surface activator such as kaolin, and calcium.

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3
Q

Thrombin time (TT)

A

(Normal = 14-16 seconds)
Assesses the common terminal sequence. It is sensitive to a deficiency of fibrinogen (I) or to an inhibition of thrombin (IIa).

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4
Q

Intrinsic Factors

A
XII 
XI 
IX
XIIa
Xia
 (Calcium ions VIII + PF3)
IXa
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5
Q

Extrinsic Factors

A

Factor VII
(Calcium ions Tissue Factor)
Factor VIIa

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6
Q

Common Pathway

A
X Calcium ions V + PF3
Prothrombin (II)
Fibrinogen Fibrinogen XIII
Xa
Thrombin (IIa) Fibrin
Crosslinked Fibrin
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7
Q

Why is it rare for a Factor 13 deficiency?

A

F13 is a stabilising factor, so when we have APPT and PT we still have a clot, but if that clot were to breakdown in a little while, it may be 13.

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8
Q

Deficiency of Vitamin K- dependent factors:

A

Haemorrhagic disease of the newborn;
Biliary obstruction
Malabsorption of vitamin K e.g. coeliac disease, sprue
Vitamin K-antagonist therapy e.g. anticoagulation with coumarin

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9
Q

Inhibition of coagulation:

A

Specific inhibitors e.g. antibodies against components of factor VIII
Non-specific inhibitors e.g. autoantibodies associated with SLE and RA

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10
Q

Miscellaneous Coag disorders

A

Diseases with paraproteinaemia;
L-asparginase;
Therapy with heparin, defibrinating agents or thrombolytic drugs Massive transfusion syndrome

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11
Q

Von Willebrands

A

.People with VWD have a low level of a substance called von Willebrand factor

The main symptoms are:

bruising easily or getting large bruises
frequent or long-lasting nosebleeds
bleeding gums
heavy or long-lasting bleeding from cuts
in women, heavy periods and bleeding during or after labour
heavy or long-lasting bleeding after a tooth removal or surgery

on Willebrand Factor’s primary function is binding to other proteins, in particular factor VIII, and it is important in platelet adhesion to wound sites.[5] It is not an enzyme and, thus, has no catalytic activity.

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12
Q

Long APPT time

A

A deficiency or inhibition of one or more of the coagulation factors: XII, XI, VIII, X, V, II or I.

  1. Haemophilia A
  2. Haemophilia B
  3. Conditions above
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13
Q

Long PT Time

A

A deficiency or inhibition of one or more of the coagulation factors: VII,X,V,II or I

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14
Q

Long TT

A
  1. Deficiency or abnormality of fibrinogen
  2. Inhibition of thrombin by heparin or FDP’s

Disorder of the common pathway

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15
Q

Antibody Identification Practical

A

Red cells at the top of, or spread through the gel = positive reaction
Red cells at the bottom of the well = negative reaction

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16
Q

Warfarin

A

The chart above show that Warfarin interferes with the vitamin K cycle. It interacts with the reductase enzyme which means that oxidised vitamin K cannot be converted back to vitamin K. This in turn means, as shown above, that the amount of reduced vitamin K will also decrease. The carboxylation of Precursor Prothrombin (Factor II) to Biologically active Prothrombin requires reduced vitamin K. Hence if the amount of reduced vitamin K is decreased this means that biologically active Prothrombin will not be formed and hence the clotting pathway will be interrupted therefore leading to a reduction in blood coagulation.

Vitamin K is vital for the formation of the clotting factors II, VII, IX and X. As well as the anticoagulant proteins C and S.

17
Q

Heparin

A

It can be seen how the inhibition of the Factors II (Prothrombin), VII, IX and X have an effect on the formation of a stable fibrin clot. The inhibition of Factor VII has a direct effect on the extrinsic pathway. By inhibiting this factor the whole pathway is blocked. Factor IX and X have an effect early on in the intrinsic pathway.Inhibiting Factor X has a double effect on the extrinsic pathway because if there is still some factor VII in the blood stream it will have no factor X to react with. Hence, it is very unlikely that any Xa and V will be formed to carry on the pathway towards the stable fibrin clot. The inhibition of Prothrombin then has an effect on the production of Thrombin and hence the clot as well. Overall the inhibition of these 4 factors has a major effect on the ability of the body to form a stable fibrin clot.

18
Q

Factor 4

A

Calcium Ions

19
Q

Extrinsic Pathway

A

Tissue Factor → VIIa affects X → Xa

20
Q

Heparin vs Warfarin

A

Pregnancy: Heparin No, Warfarin SAFE

Warfarin Antidote FFP, Vit K
Heparin Antidote Protamine Sulphate

Warfarin monitor INR
Heparin monitor APPT

21
Q

Heparin affects

A
11
9
7
10
2

But the active forms.