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Lab D > Lab 3 > Flashcards

Lab 3 Flashcards

1
Q

What is haemostasis?

A

Haemostasis is the name of a group of processes initiated in the body in order to stop bleeding in case of tissue
and/or blood vessel injuries.

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2
Q

What is Bleeding time?

A

Measure of the time from the appearance of the first drop of blood until the cessation of bleeding.

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3
Q

What tests can you use for coagulation time and how do you carry them out?

A

Clotting time on a watch glass,
Clotting time in plastic syringe,
Clotting time in glass tube,
Clotting time in activated clotting time tube.

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4
Q

What is coagulation in an ACT test tube?

A

Si02 with fresh blood to check the coagulation at 37c. SiO2 activates the contact Factor XII (Hagemann factor). Activated Factor XII activates Factor IX and kallikreinogen, kinigogen (fibronolytic pathway).

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5
Q

How long does each test take to coagulate?

A

Watch glass: 7-15 min
Plastic syringe: 10-12 min
Glass tube: 4-5 min
ACT tube: 3 min

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6
Q

What are the causes of thrombocytopenia?

A

Decrecreased production of thrombocytes in the bone marrow,
increased utilization of thrombocytes, (DIC),
increased destruction of thrombocytes autoimmune thrombocytopenia (AITP),
increased sequestration of thrombocytes

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7
Q

Which factors are dependent on vitamin K?

A

Proconvertin (Factor 7), Christmas (Factor 9), Stuart Prower (Factor 10), and Prothrombin (Factor 2)

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8
Q

What is prothrombin time?

A

Gives information about the function of the extrinsic pathway because the coagulation cascade is
triggered by adding tissue factor.

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9
Q

How long is a normal PT?

A

10-15 seconds

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10
Q

What is APTT?

A

Activated partial thromboplastin time – gives information on the function of the intrinsic pathway
through the provision of surface activation.

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11
Q

How long is a normal APTT?

A

20-30 seconds

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12
Q

What is the general platelet count?

A

200-800 x 10 to the 9

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13
Q

What is DIC?

A

Disseminated intravascular coagulopathy. Secondary problem where microthrombus formation
and fibrinolysis are present at many different places in the body simultaneously because of severe
tissue damage or necrosis

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14
Q

Which clotting factor was messed up with Von Willebrands disease?

A

Factor VIII is deficient

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15
Q

What are the major groups of haemostasis disorders?

A

Vasculopathy, Thrombocytopathy, Coagulopathy

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16
Q

What tests were used to investigate coagulopathies?

A

Bleeding time, (buccal mucosal bleeding time test,) clotting time, clotting time on different
surfaces, clot retraction time.

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17
Q

What tests investigate platelet count (can´t remember the exact phrasing of her question there but it´s
pretty much what she wanted.)

A

Blood smear test, automatic cell counters, Burker chamber count

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18
Q

What is the clot retraction test?

A

The measure of the decrease in clot size with a contractile protein called thrombostenin. Slower or no contraction happening is a sign of thrombocytopathy

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19
Q

In dicumarol posioning what is increased?

A

The PT and APTT is increased

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20
Q

How can you count platelets in a sample?

A

Burker chamber (haemocytometer), blood smear, automatic cell counters.

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21
Q

Which hemostatic disorder lead to more sever clinical signs, thrombocytpathys or coagulopathys?

A

Thrombocytopathy as there is no connection between thrombocyte-thrombus

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22
Q

Shortest coagulation factor life time?

A

(7) 3 minutes with the CT in ACT

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23
Q

Which factor is involved in measuring thrombin time?

A

(13)

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24
Q

Time until the first fibrin strain?

A

1-2 minutes

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25
Q

What does silicon dioxide influence in ACT?

A

The contact factor Hagemann factor

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26
Q

How does dicoumarol anticoagulant work?

A

It is the competitive antagonist of vitamin k which is responsible for the gamma carboxylation of
proconvertin(Factor 7) Christmas factor (Factor 9), Stuart Prower (Factor 10) and he Prothrombin
(Factor 2). It removes Ca2+ from these factors so they cannot activate

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27
Q

Clot retraction test

A

Measure of the effectiveness of thrombostenin for reducing the clot via the release of serum.

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28
Q

Platelet count normal number?

A

200-800 x 10 to the 9.

Platelet count formula for smear (20*10^9/l)

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29
Q

Which anticoagulant used for platelet count examination?

A

EDTA, K2, Na2-

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30
Q

Dicumarol toxicosis effect on PT an APTT?

A

Increases quickly on PT then gradually on APTT

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31
Q

Ratio of anticoagulant (citrate:blood)?

A

1:9

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32
Q

Thrombocytopenia, name 3 causes

A

Decreased production of thrombocytes in the bone marrow, increased utilization of thrombocytes
DIC (disseminated intravascular coagulopathy), increased loss of thrombocytes: subacute/chronic
bleeding

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33
Q

How does sodium citrate inhibit coagulation?

A

Citrate prevents coagulation by binding calcium ions

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34
Q

DIC

A

Disseminated intravascular coagulopathy (DIC) microthrombus formation and fibrinolysis are
present at many different locations in the body due to necrosis or severe tissue damage.

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35
Q

BMBT time?

A

3-5 minutes

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36
Q

How is BMBT performed?

A

0.5 cm incision on the skin of the inner part of the external ear or the buccal mucosal surface. Wipe away excess blood under the incision until the cessation of bleeding

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37
Q

What level of platelets are considered a clinical bleeding disorder?

A

Above 50x10 to the 9/Liter

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38
Q

Function of platelets?

A

They bind thrombocytes along with fibrin to form clots in damaged blood vessels

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39
Q

What do factors need for their synthesis?

A

Calcium ion

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40
Q

Which factor is 13 and what is its function?

A

Von Willebrand Factor is responsible for plately adhesion and aggregation and anti haemophylic
factor.

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41
Q

What factor are in extrinsic pathway?

A

3, 7, 5, 10, 2, 13

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42
Q

Which factors can bind to Calcium?

A

Proconvertin (Factor 7), Christmas (Factor 9), stuart prower (Factor 10), Prothrombin (Factor 2)

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43
Q

What molecule can activate factor 12 (hagemann)?

A

Free collagen fibres, kininogen, and kallikrein

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44
Q

What is the glue that sticks the thrombocytes to each other?

A

Polymerized fibrin network

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45
Q

What factor initiates the intrinsic pathway?

A

Hagemann factor Factor 12

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46
Q

What factor is calcium?

A

Factor 4

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47
Q

Haemostasis examinations?

A

Haemostasis examinations should be started by fast tests that can be performed by
side of the animals. These are not accurate but easy to perform and give good estimation. By doing these tests we can give a direction for more specific diagnosis of haemostasis disorders.

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48
Q

Name the major groups of hemostasis disorders?

A
  1. Vasculopathy
  2. Thrombocytopathy
  3. Coagulopathy
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49
Q

Vasculopathy

A

Decreased ability of vasoconstriction in case of blood vessel injury, the first step of the
haemostasis process.

50
Q

Thrombocytopathy

A

Decreased ability of platelets to aggregate and adhere to the site of injury, and formation
of the primary thrombocyte-thrombus, the second step of haemostasis, Thrombocytopenia (decreased amount of thrombocytes in the blood)

51
Q

Coagulopathy

A

Problems with the extrinsic-, intrinsic-, or common pathway of the coagulation cascade, which ends with the formation of a polymerised fibrin network, which keeps thrombocyte thrombi at the site of injury,
the third and final step of haemostasis

52
Q

Tests performed by side of the animals?

A
  • Signs of increased bleeding tendency: on the skin and mucous membranes: anemia, petechia, ecchymosis,
    suffusion; in the thoracic cavity: haemothorax; in the abdominal cavity: haemoperotoneum; in the
    gastrointestinal tract: haematemesis, melena
  • Capillary resistance (human medicine)
  • Bleeding time (buccal mucosal bleeding time test, BMBTT)
  • Appearance of the first fibrin strand (clotting time)
  • Appearance of the clot (clotting time on different surfaces)
  • Clot retraction time
53
Q

How to take the capillary resistance test (Rumpel-Leed-test)?

A

It is performed by putting a
ligature on the arm, above the elbow and checking the palmar side (because skin is thinner there) of the lower arm for petechie.
After 3-5 min. of ligature 3 small petechie (small reddish dot, bleeding from capillaries under
the skin) should appear normally. If capillary function is not proper, more petechia appear.
Capillaries may
become more fragile for example in case of vasculitis (viral, autoimmune, etc.), or other diseases affecting the
wall of the blood vessels.

54
Q

Bleeding time, Buccal mucosal bleeding time (BT, BMBT) test?

A

The test for thrombocytopenias, thrombocythopathies and

vasopathies.

55
Q

How to take the Bleeding time, Buccal mucosal bleeding time (BT, BMBT) test?

A

Use a sharp and sterile blade and make an at least 0.1-0.2 mm deep, 0.5 cm long incision on the skin of the inner
part of the external ear or on the buccal mucosal surface. Vipe the blood drop flowing UNDER the wound carefully with a cotton wool tissue, or
paper towel in 20-30 sec. intervals.
Measure the time from the appearance of the first drop of blood until the ceasing of bleeding. BT, BMBT is dependent on
the thrombocytic function, the platelet count, and the capillary function.

56
Q

Why is it important to avoid touching the wound when collecting the sample?

A

It is important to avoid touching the wound itself, because otherwise you may
remove the small thrombocyte-thrombus from the wound, and therefore bleeding time will be longer.

57
Q

What is normal BMBT?

A

Normal BMBT: 3-5 min

58
Q

When is there a danger of clinical bleeding?

A

There is no danger of clinical bleeding (appearance of petechia) until platelet count is above 50 x 109/l.

59
Q

How to perform coagulation time (CT) test?

A

These are the tests for coagulopathies!!!
It is always important to perform these tests from fresh, native (not containing any anticoagulants!) whole
blood samples, immediately after taking them! Samples should be taken by a proper way, preferably with only
one precise venipuncture, so that we do not cause too much damage to the surrounding tissues. Otherwise we
may cause increased tissue factor (factor III.) release from the damaged cells, which leads to the initiation of the
coagulation cascade during sampling! It is advised to use the so called ”two syringe method”. In this case we do
not use the first drops of blood for coagulation measurements, we change syringe after taking these first drops,
and use the content of the second syringe for that purpose.

60
Q

Why should the sample of CT test be taken with only one precise venipuncture?

A

Samples should be taken by a proper way, preferably with only one precise venipuncture, so that we do not cause too much damage to the surrounding tissues. Otherwise we may cause increased tissue factor (factor III.) release from the damaged cells, which leads to the initiation of the
coagulation cascade during sampling!

61
Q

What is the “two syringe method”?

A

It is advised to use the so called ”two syringe method”. In this case we do not use the first drops of blood for coagulation measurements, we change syringe after taking these first drops, and use the content of the second syringe for that purpose.

62
Q

How to see the appearance of the first fibrin strand?

A

Put some drops of the blood sample onto a glass slide and sink the tip of a needle into the blood and move the
needle forward and back while carefully and slowly pulling the tip out of the blood sample. The first fibrin strand
should appear within 1-2 min. You need to have good vision for the evaluation of this test, and a properly lighted
room

63
Q

Sampling of clotting time (CT) on watch glass?

A

Put the fresh blood sample on watch glass that was previously treated with paraffin or wax (otherwise scratches
of the glass would activate the coagulation cascade). Check the complete coagulation time (until the whole
amount of blood becomes solid, like gelatine) .

64
Q

Normal clotting time on watch glass?

A

Normal is 7-15 min.

65
Q

Sampling of CT (clotting time) in plastic syringe?

A

Put the fresh blood sample into a plastic syringe (or leave some blood in it after sampling) and check the time of
the complete coagulation.

66
Q

Normal clotting time in plastic syringe?

A

Normal is 10-12 min.

67
Q

Sampling of CT in glass tube?

A

Pour some fresh blood into a glass test tube and check the time of the complete coagulation.

68
Q

Normal clotting time in glass tube?

A

Normal is 4-5 min

69
Q

Sampling of CT in ACT (activated clotting time) tube?

A

Put some fresh blood into a glass test tube that contains SiO2 (commercially available tube, called ACT tube,
usually with brown cap), put it in a thermostate (37o
C) and check the time of the complete coagulation. SiO2
activates Factor XII (Hagemann-factor, contact factor). Activated Factor XII activates Factor IX and kallikreinogen, kinigogen (fibronolytic pathway). Blood coagulation should be checked by slowly moving the
tube every 15-20 sec.

70
Q

SiO2 activates (fibrinolytic pathway?)?

A

SiO2 activates Factor XII (Hagemann-factor, contact factor). Activated Factor XII activates Factor IX and kallikreinogen, kinigogen (fibronolytic pathway).

71
Q

Normal clotting in ACT tube?

A

Normal is 3 min.

72
Q

Platelet (thrombocytic) count examination?

A

Platelet count examination is important especially, when the BT, BMBT is increased, or petechie are visible on
the skin or mucous membranes. The platelet count should be measured from anticoagulated blood. For this
purpose Na2-, or K2 EDTA should be used.

73
Q

Method 1 of Platelet (thrombocytic) count examination?

A

Put 0.1 ml EDTA anticoagulated blood sample into 0.9 ml physiological saline solution, mix it, then let it to be
sedimented for 2 hours. Then one drop of the upper layer should be dripped into Bürker chamber (haemocytometer). Wait until the drop is spread over the network, and count the number of platelets in 10
rectangles. The number should be multiplied by 10^9
, and this is the number of platelets in 1 litre blood. The
process can be made quicker if the sample in NaCl-solution is centrifuged on 1500/min. Thrombocyte counting in
Bürker chamber is not accurate.

74
Q

Method 2Platelet (thrombocytic) count examination?

A

Platelet count can be estimated by using a blood smear. Finding one platelet in one view by 1000x magnification means 20x109/l platelet count. This method is also very uncertain, however checking a blood smear for any purpose can be very important. The arrangement of thrombocytes may be variable on a smear, so we should
check many views from the middle part and from the edges of the blood film. Finding big thrombocyte
aggreagates in the smear is suggestive of proper platelet function, and may explain low thrombocytic counts
measured by automatic cell counters

75
Q

Method 3 Platelet (thrombocytic) count examination?

A

Platelet count can be measured by using automatic cell counters. Particles of the blood between 5-30 fl volume
are taken as platelets. Sometimes in regenerative processes of the bone marrow, when there are many young (big) platelets circulating i.e. in case of chronic blood loss, or physiologically in cats and in King Charles spaniels
average thrombocytic volume can be so high, that these big platelets are taken as red blood cells by the counter.
Sometimes small red blood cells are also taken as thrombocytes. Thrombocytic aggregates can be taken as white blood cells, so the platelet count is measured to be normal or low and the white blood cell count to be increased. Evaluation of the blood smear (examination the arrangement, morphology, etc. of thrombocytes) is a very
important step of the diagnosis of thrombocytic disorders!

76
Q

General Platelet Count?

A

200-800 x109/l

77
Q

Major causes of thrombocytopenia?

A
  1. decreased production of thrombocytes in the bone marrow
  2. increased utilisation of thrombocytes: DIC (disseminated intravascular coagulopathy)
  3. increased destruction of thrombocytes : autoimmune thrombocytopenia (AITP)
  4. increased sequestration of thrombocytes: in case of (chronic) splenomegaly
  5. increased loss of thrombocytes: subacute/chronic bleeding
78
Q

Clot retraction test?

A

If you leave the blood clot in a tube for some hours, it will become smaller, and serum will appear around the clot. The reason for this clot retraction is that platelets contain a contractile protein called thrombostenin, Normally the volume of serum released by the clot within one hour is approx. 25% of the whole volume of the
initial clot. Thrombocytic function can be estimated by performing this test. If the clot retraction is slower, or does not
happen at all, we can suspect thrombocytopathy.

79
Q

Platelet aggregation test?

A

This test can be performed when we suspect thrombocytopathy , i.e. von Willebrand disease. In this case we can use aggregometers to estimate the aggregating ability of platelets correctly. There are several devices to evaluate
the aggregation of the platelet. The methods are similar. We have to prepare a citrated blood sample and the
upper layer should be used for this analysis. This is the platelet rich plasma. This fluid is slightly opaque. Then we put this sample into a cuvette and add some drugs which causes exaggerated aggregation, such as ADP, epinephrine etc. These drugs will induce platelet aggregation which will cause the clearing up of the fluid in the
cuvette. The speed and the rate of the clearing can be analysed by a spectrophotometer. The device gives numerical values to this process. Other instruments are also available which are working by different methods.

80
Q

Which drugs causes exaggerated aggregation?

A

ADP, epinephrine etc. These drugs will induce platelet aggregation which will cause the clearing up of the fluid in the cuvette.

81
Q

Thrombocytic morphology

A

Thrombocytes have 1-2 µm diameter. Their centre is the granulomer and the edge is the hyalomer part (zone).

82
Q

Different size of platelets for different species?

A

Horses, sheep, cattles, have the smallest platelets (3-5 fl), dogs and swine have bigger (7-8fl), and cats have the
biggest (10-15fl) thrombocytes.

83
Q

Major causes of thrombocytopathies?

A
  1. improper development of platelets, for example because of hereditary glucoprotein deficiencies, etc.
  2. von Willebrand’s disease
  3. uraemia, liver failure, myelo-, and/or lymphoproliferative diseases, NSAID (non-steroid anti-inflammatory
    drugs) treatment, etc.
84
Q

In which case can we expect signs of a really severe bleeding disorder (suffusion, haematoma, haemothrorax, haemoperitoneum)?

A

In case of thrombocytopenia, thrombocytopathies and vasopathies besides normal coagulation, we cannot expect it, because these are prevented by the formation of polymerised fibrin strands (fibrin thrombus) at the end of the coagulation
cascade.
But coagulopathies, besides normal thrombocytic and blood vessel function and normal platelet count may lead
to the aforementioned severe bleedings, and sometimes bleeding to death, because thrombocytic thrombi are not
stable without a fibrin network, and in case of a big blood vessel injury, the power of blood flow can sweep away
the thrombocyte-thrombus from the wound!

85
Q

What can be examined by using more specific “global” tests?

A

Coagulopathies can be examined, so that we can evaluate, which group(s) of
factors are not functioning properly. Citrated blood should be used , which means, 3,8 % Na-citrate:blood = 1:9. (Prepared tubes are commercially available, usually
blue cap)

86
Q

What is special about citrate?

A

Citrate prevents coagulation by binding calcium ions

87
Q

Sampling of Prothrombin time (PT) test?

A

This test must be performed within 1 hour after sampling. Blood samples should be mixed with 3.8% sodium
citrate in 9:1 dilution (4.5 ml of blood and 0.5 ml of Na-citrate). Then centrifuge the samples in 3000 rpm for 10min. and separate the (decalcinated) plasma from he sediment. The plasma must be kept on 37 o
C.
The reagent (Simplastin) for PT evaluation contains rat uterus tissue homogenate as tissue thromboplastin (Factor
III.), and CaCl2. The reagent must be kept on 37 o
C before using.
The evaluation can be performed by using coagulometer or in test-tube. 200 µl reagent should be mixed with 100 µl decalcinated (citrated!) plasma and the time of coagulation should be noted.

88
Q

Normal prothrombin time?

A

Normal PT: 10-15 sec.

89
Q

What can the prothrombin time test tell us?

A

This test gives information about the function of the extrinsic pathway, because the coagulation cascade is
triggered by adding tissue factor (and calcium ion) to the dacalcinated plasma sample.

90
Q

What are the factors involved in prothrombin time?

A

Factors involved in PT are: VII., X., V., II., I., XIII.

91
Q

Sampling of Activated partial thromboplastin time (APTT)?

A

For this test decalcinated plasma should be used similarly to PT. The reagent (Silimat) contains rabbit brain
homogenate as PF3 (platelet factor 3) and micronised silica as contact activator. 100 µl decalcinated plasma
should be mixed with 100 µl reagent and the mixture kept on 37 oC, then 100 µl of 0.025 mmol/l CaCl2 solution
should be added and from this moment the time of coagulation should be noted.

92
Q

Normal Activated partial thromboplastin time?

A

Normal APTT: 20-30 sec..

93
Q

What does the Activated partial thromboplastin time test tell us?

A

This test gives information on the function of the intrinsic pathway, because the cascade is triggered by providing surface activation (imitating the effect of free collagen, which appears on the inner surface of the vessels in case of blood vessel injury), and adding platelet factor 3 (PF3) and Ca 2+ for the activation of factor X. (remember the coagulation cascade!!)..

94
Q

What are the factors involved in the Activated partial thromboplastin time test?

A

Factors involved in APTT are: XI., IX., VIII., X., V., II., I., XIII.

95
Q

Sampling of Thrombin time (TT) test?

A

By performing this test, decalcinated plasma should be simply mixed with a reagent containing thrombin only .In
this case coagulation time depends on the concentration of fibrinogen and Factor XIII.in the plasma. Obviously
this test can also be used for the estimation of fibrinogen concentration (suspecting a normal factor XIII. level in
the blood).

96
Q

Vitamin K deficiency?

A

In the early stage of dicumarol (or warfarin) toxicosis only PT is increased, and later APTT is increased, too.
Dicumarol is a competitive antagonist of vitamin K. Vitamin K is responsible for the gamma carboxylation of
Proconvertin (Factor VII), Christmas (Factor IX), Stuart-Prower (Factor X) and the Prothrombin (Factor II), as
they are Ca2+ dependent factors, so vitamin K deficiency causes the inability of these factors to bind calcium.
Factor VII. has the shortest half life, so this factor will be deficient first. Prothrombin Time is increased when
there is factor VII deficicency, so this test will show the problem first.

97
Q

What is the function of Vitamin K?

A

Function of Vitamin K is to exaggerate the post-synthetic gamma carboxylation of those factors in the liver (vitamin K is the co-factor of the enzyme catalysing the attachment of a carboxyl group on the gamma C atom of the protein molecule after protein synthesis). This makes these factors to be able to bind Ca2+ , and thus become
functionally active.

98
Q

ELISA test?

A

In case of vitamin K deficiency of any origin (dicumarol toxicosis, etc.), improperly carboxylised prothrombin can be detected by using an ELISA (Enzyme Linked Immunosorbent Assay) test, called PIVKA II. (Proteins
Induced by Vitamin K Absence)

99
Q

FDP?

A

Fibrin degradation products

100
Q

What is the Fibrinolytic pathway responsible for?

A

Keeping the clot formation within normal limits. Clot inhibitors (antithrombin III., alpha2-macroglobulin, alpha1-antitripsin, heparin – the latter increases the binding of antithrombin III to thrombin) are able to bind to thrombin and neutralise it.
After a complete coagulation, the clot is usually not needed any more, so it should be broken down by fibrinolytic
enzymes.

101
Q

Activators of factor XII. (Hageman)?

A

Free collagen fibres, (exposed at the site of blood vessel injury), kininogen and kallikrein are the activators of factor XII. (Hageman). XII.a (activated form of factor XII. ) further activates the extrinsic pathway, and is also able to form kallikrein from prekallikrein. Kallikrein activates the kininogen system, also, forming bradikinin (activated form of kininogen), which is a very potent mediator of pain. Kallikrein is the most important activator of plasminogen.

102
Q

Why is FDP not a proper name?

A

Plasmin (activated form of plasminogen) is an endopeptidase, which can cleave fibrin strands into small pieces. Before the total degradation of polymerised fibrin strands, increased level of fibrinolysis-products, fibrin dimers and monomers (so called: “fibrin degradation products or proteins, FDP”) can be measured in the blood. FDP is not a proper name for these proteins, because, some of them are the breakdown products of fibrinogen, also, not just fibrin. Therefore high FDP in the blood is not necessarily the sign of increased fibrinolysis following increased clot formation, because these products can also originate from fibrinogen.

103
Q

Examination of D-dimer level in the blood?

A

More accurate way to detect increased fibrinolysis,is the examination of D-dimer level in the blood.
This derivate is originated only from fibrin, and not fibrinogen. Both tests (FDP, and D-dimer) are based on latex agglutination method, and fresh citrated (decalcinated) plasma samples should be used for it. The reagent contains antibodies (produced in research animals) against FDPs or D-dimers attached to latex particles. The reagent should be mixed with fresh citrated plasma sample and macroscopic agglutination can be seen dark (black) surface if enough FDPs and/or D-dimers are present in the plasma. Performing each of these tests (FDP, or rather D-dimer) is very helpful in the early diagnosis of disseminated intravascular coagulopathy (DIC).

104
Q

DIC?

A

DIC (disseminated intravascular coagulopathy) is a common acute disorder that requires accurate and quick laboratory diagnosis. It is usually a secondary problem, caused by primary diseases for example: septicaemia, pancreatitis, widespread burn injuries, or necrosis of big tumors, shock, polytraumatisation, etc. In case of DIC, microthrombus formation and fibrinolysis are present at many different places in the body simultaneously, because of severe tissue damage or necrosis (initiation of the extrinsic pathway, by the release of tissue factor), and blood vessel injury (initiation of the intrinsic pathway), so coagulation factors and platelets are consumpted very quickly during this process. That is why it is also called “consumptional coagulopathy”. DIC can be a life threatening complication of the
aforementioned diseases. Early diagnosis is very important in the management of this condition.

105
Q

First laboratory sign of DIC?

A

First laboratory sign of DIC can be a positive FDP or D-dimer test

106
Q

Laboratory diagnosis of DIC

A 
Coagualtion time: increase
Bleeding time: increase
Platelet count: decrease
PT: increase
APTT: increase
TT: increase
Fibrin degradation products (FDP), and D-dimer: increase
Appearance of schysocytes and/or burr-cells in blood smear
107
Q

Diagnosis of von Willebrand disease?

A

This disease is known in humans, and in case of dogs in Dobermann pinchers, often accompanied by hypothyroidism. In this disease the von Willebrand factor, or the complete Factor VIII is deficient. There are 3 main part of complete Factor VIII: von Willebrand factor – responsible for platelet adhesion and aggregation,
VIIIc – is the antihaemophylic factor, and the Factor VIII related antigen – is the hapten that is the determinable
part, and is bound strongly to von Willebrand factor. The dogs with this disease have increased BT, BMBT,
decreased clot retraction ability and sometimes coagulation disorders, too. The specific diagnosis is based upon the detection of the lack of von Willebrand related antigen.

108
Q

Major alterations of the basic tests in different haemostasis disorders: Coagulopathy?

A

Increased Coagulation time (CT)

109
Q

Major alterations of the basic tests in different haemostasis disorders: Thrombocytopenia?

A
  • Increased Bleeding time (BT)
  • Decreased Platelet count (PC)
  • Altered or not: Platelet morphology
110
Q

Major alterations of the basic tests in different haemostasis disorders: Thrombocytopathy?

A
  • Increased Bleeding time (BT)

- Altered: Platelet morphology

111
Q

Major alterations of the basic tests in different haemostasis disorders: Vasculopathy?

A
  • Increased Bleeding time (BT)
112
Q

Intrinsic pathway problem?

A

Increased Activated Partial Thromboplastin Time (APTT)

113
Q

Extrinsic pathway problem?

A

Increased Prothrombin time (PT)

114
Q

Common pathway problem?

A
  • Increased Activated Partial Thromboplastin Time (APTT)

- Increased Prothrombin time (PT)

115
Q

What happens when Thrombocytopenia?

A
  • Increased Bleeding time (BT), Buccal mucosal bleeding time (BMBT)
  • Decreased Platelet count
116
Q

What happens when Thrombocytopathy?

A

Increased Bleeding time (BT), Buccal mucosal bleeding time (BMBT)

117
Q

What happens when Intrinsic pathway disorder?

A

Increased Activated Partial Thromboplastin Time (APTT)

118
Q

What happens when Factor VII deficiency?

A

Increased Prothrombin time (PT)

119
Q

What happens when Disorder of common pathway?

A
  • Increased Activated Partial Thromboplastin Time (APTT)
  • Increased Prothrombin time (PT)
  • Increased/normal Bleeding time (BT), Buccal mucosal bleeding time (BMBT)
120
Q

What happens when DIC?

A
  • Increased Activated Partial Thromboplastin Time (APTT)
  • Increased Prothrombin time (PT)
  • Increased Bleeding time (BT), Buccal mucosal bleeding time (BMBT)
  • Decreased Platelet count
121
Q

What happens when Von Willebrand-disease?

A
  • Increased Bleeding time (BT), Buccal mucosal bleeding time (BMBT)
  • Increased/normal Activated Partial Thromboplastin Time (APTT)

Lab D (2 decks)

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