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Pathophysio > LabD 3 Haemostasis > Flashcards

LabD 3 Haemostasis Flashcards

1
Q

Haemostasis def

A

Name of a group of processes initiated innthe vody in order to stop bleeding in case of tissue and or blood vessel injury

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2
Q

Haemostasis test in general

A

Should be started by fast tests that can be performed by the animals side, not accurate tests, but they give a good estimation of what is wrong and it is easier to choose a more specific test to diagnose the haemostasis disorder

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3
Q

Major groups of haemostasis disorders

A

, thrombocytopathy, coagulopathy

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4
Q

Vasculopathy

A

Decreased ability of iction in case of blood vessel injury, the first step of the harmeostasis process

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5
Q

Thrombocythopathy

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

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6
Q

Thrombocytopenia

A

Decreased amount of thrombocytes in the blood

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7
Q

Coagulopathy

A

Problems withbthe extrinsic-, intrinsic- or common pathway of the coagulation cascade, which ends with the formation of polymerised fibrin network. (Which keep the thrombus at site of injury) Third step of haemostasis

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8
Q

First step of haemostasis

A

Vasoconstriction in case of injury

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9
Q

Second step of haemostasis

A

Formation of thrombocyte-thrombus

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10
Q

Third step of haemostasis

A

Formation of stabile Fibrin network to keep thrombus at site of injury

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11
Q

Signs of increased bleeding tendency on the skin and mucuos membranes

A

Anemia, petechia, ecchymosis, suffusion

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12
Q

Signs of increased bleeding in thoracic cavity

A

Haemothorax (blood in pleural cavity)

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13
Q

Signs of increased bleeding in the abdominal cavity

A

Haemoprotoneum (blood in between inner lining of abd. wall and internal abd. organs)

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14
Q

Signs of increased bleeding in the G.I tract

A

Haematemesis (vomiting blood), melena (dark sticky feces; internal bleeding or swallowing blood)

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15
Q

Petechia.

A

Small red/purple spot caused by bleeding in skin

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16
Q

Ecchymosis?

A

Discoloration of skin caused by bleeding underneath skin

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17
Q

Suffusion

A

Slow spread of blood

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18
Q

Tests performed by the side of the animals

A

Signs of increased bleeding tendency, capillary resistance, bleeding time, clotting time, clotting time on diff. surfaces , clot retraction time

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19
Q

Capillary resistance, also called Rumpel-Leed test

A

• Ligature on arm, Checking palmar side of lower arm for petechie
• Normal; after 3-5 min 3 small petechie visible
• Abnormal: more petechia appear
Because: capillary function not proper, more fragile ex. vasculitis or other disease affectibg wall

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20
Q

BT, BMBT

A

Bleeding time, Buccal mucosal bleeding time

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21
Q

Bleeding time and buccal mucosal bleeding time testing for

A

Test for thrombocytopenias, thrombocytopathies and vasopathies

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22
Q

Bleeding time and buccal mucosal bleeding time test

A
  • Sharp, sterile blade cut 0,1-0,2mm incision on skin on inner part external ear and buccal mucosal surface
  • Vipe blood under incision every 30sec
  • Measure time from first drop to cease of bleeding
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23
Q

Bleeding time and buccal mucosal bleeding time test is dependent on

A

thrombocyte function, platelet count and capillary function

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24
Q

Normal BMBT and normal platelet count up to

A
  • Normal BMBT: 3-5min

* Platelet count normal up to: 50x10^9/L

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25
Q

Coagulation time test is for

A

Coagulopathies

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26
Q

Coagulation time test

A
  • Fresh, native whole blood directly after taking them
  • Taken in proper way: one precise venipuncture to minimize damage to tissue around (otherwise cause increased factor ||| and initiating cosgulation cascade during sampling)
  • Use two syringe method (changing syringe after first drops, and use content of syringe 2
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27
Q

Coagulation time test types

A
  • Ct on watch glass
  • Ct in plastic syringe
  • Ct in glass tube
  • Ct in ACT (activated clotting time) tube
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28
Q

Coagulation time test, first appearance of fibrin strand

A
  • Sample onto glass slide
  • Move tip of needle back and forth in blood
  • Normal result: first strand within 1-2 min
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29
Q

Clotting time on watch glass, how

A
  • Fresh blood sample on watch glass treated with wax (scratches activate coag. cascade)
  • Check time for the whole amount of blood is clotted
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30
Q

Clotting time on watch glass, normal result

A

7-15 min

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31
Q

Clotting time in syringe, how

A

Fresh blood into plastic syringe, check time of complete coagulation

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32
Q

Clotting time in syringe, normal result

A

10-12 min

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33
Q

Clotting time in glass tube, normal result

A

4-5 min

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34
Q

Clotting time in ACT tube, what is ACT tube and how

A
  • ACT tube: contains silisiumoxide
  • Put in 37C
  • Activates factor X|| Hageman factor (contact factor), activated fcator X|| activates factor |X and kallikreinogen and kininogen (fibronolytic pathway)
  • Coagulation checked by slowly moving tube every 20sec
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35
Q

Clotting time in ACT tube, normal result

A

3 min

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36
Q

Platelet (thrombocytic) count, 3 methods

A
  1. Burker chamber (haemocytometer) count. - EDTA anticoagulated blood in physio saline.
    - Sediment and use upper layer, count 10 rectangles, multiply number by 10^9 —> number of platelets in 1L blood
    - Process quicker if NaCl is sentrifuged beforehand
  2. Blood smear.
    - See one platelet in one view by 1000x magnification —> 20x10^9/L platelet count
    - Variation in placement of thrombocytes, big aggregates of thrombocytes is good. Look around
  3. Automatic cell counter.
    - Particles 5-30fl are taken as platelets
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37
Q

Platelet (thrombolytic) count, important when, and what kind of blood

A
  • Important when BT/BMBT is increased, or petechia is visible on skin or mucuos membrane
  • Platelet count should be measured from anticoagulated blood, Na2 or K2 EDTA tube
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38
Q

Platelet (thrombolytic) count method 3, Automatic cell counter.
- Particles 5-30fl are taken as platelets

What can be the false result?

A
  • Regenerative processes of bone marrow, or in general many big (young) platelets circulating -> can be taken as RBC
    —> ex. in chronic blood loss, cats, king charles spaniels
  • RBC can also be taken as thrombocytes
  • Thrombocytic aggregates can be taken as WBC (platelet is then measured normal and high WBC)
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39
Q

Platelet (thrombolytic) count, what method is best

A

Evaluation of blood smear -> evaluation of arrangement, morphology etc.

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40
Q

General platelet count:

A

200-800 x10^9/L

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41
Q

Major causes of thrombocytopenia

A
  1. Decreased production of thrombocytes in the bone marrow
  2. Increased utilisation of thrombocytes: DIC
  3. Increased destruction: autoimmune thrombocytopenia
  4. Increased sequestration: chronic splenomegaly
  5. Increased loss: subacute/chronic bleeding
42
Q

DIC

A

Disseminated intravascular coagulopathy

43
Q

Clot retraction test? leave clot what happens, why and if not what is expected?

A
  • Leave clot —> resolve to serum around clot. 25 percent after 1 hour.
  • Reason: platelets contain protein thrombostenin
  • if slower or not happening: can suspect thrombocytopathy
44
Q

Platelet aggregation test, for?

A

When thrombocytopathy is expected, ex. von Willebrands disease

45
Q

Platelet aggregation test, how?

A

Aggregometers to estimate aggregation ability of platelets.

Put sample to cuvette and add exxagerating drugs ex. Elinephrine -> platelet aggregation induced and sample clear up.

Then photospectometer

Speed and rate is analyzed

46
Q

Platelet aggregation test, what kind of blood, what colour

A

Citrate blood sample, use upper layer (this is the platelet rich plasma).

Slightly opaque

47
Q

Thrombocytic morphology

A
  • 1-2um diameter

- Centre is granulated, edge hyalomer(clear)

48
Q

What species have platelets size 3-5fl?

A

Horses, sheep, cattle

49
Q

What species have platelets size 7-8fl?

A

Dogs and swine

50
Q

What species have platelets size 10-15fl?

A

Cats

51
Q

Major causes of thrombocytopathies?

A
  1. Improper development ex. hereditary glucoprotein deficiencies
  2. Von Willebrands disease
  3. Uraemia, liver failure, myelo- and or lymphoproliferative diseases, usage of NSAIDS,
52
Q

Can we expect severe bleeding disorder from thrombocytopenia besides normal coagulation? And why

A

No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade

53
Q

Can we expect severe bleeding disorder from thrombocytopathies besides normal coagulation? And why

A

No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade

54
Q

Can we expect severe bleeding disorder from vasopathies besides normal coagulation? And why

A

No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade

55
Q

Can we expect severe bleeding disorder from coagulopathies besides normal thrombocytic and vessel function? And why

A

Yes, because thrombocytic thrombus are not stable without a fibrin network, and in case of big vessel injury thrombocyte thrombus can be washed away from site of injury

56
Q

Coagulopathies can also be examined by using more specific tests, evaluating? What kind of blood used?

A

Which groups of factors are not functioning properly.

Citrate blood, preventing coagulation by binding calcium

57
Q

Prothrombin time test, how?

A
  • must be performed within 1 hour after sampling
  • blood samples mixed with sodium citrate in dilution
  • centrifuge 300rpm, 10 min -> separate decalcinated plasma from sediment (use sediment). Keep in 37C
  • reagent Simplastin, kept on 37C
  • coagulometer or in test tube, note coagulation time
58
Q

Prothrombin time test, what does it tell us?

A

Gives info about function of extrinsic pathway, because the coagulation cascade is triggered by adding tissue factor and calcium ion to the decalcinated plasma sample

59
Q

Prothrombin time test, factors involved?

A

VII, X, V, II, I, XIII

60
Q

Prothrombin time test, normal coagulation time

A

10-15 sec

61
Q

Activated partial thromboplastine time, test how and blood used

A
  • blood: decalcinated plasma, reagent Silimat, micronised silica as activator.
62
Q

Reagent Simplastin contains

A

Rat uterus tissue homogenate as tissue thromboplastin (factor III) and CaCl2

( Prothrombin time)

63
Q

Reagent Silimat contains.

A

Rabbit brain homogenate as PF3 (platelet factor 3) and micronised silica as contact activator

(Activated partial thromboplastin time)

64
Q

Normal activated partial thromboplastine time

A

20-30sec

65
Q

Activated partial thromboplastine time give sus what info

A

Function of intrinsic way, becaus ethe cascade is triggered by providing surface activation and adding platelet factor 3 and Ca2+ for the activation factir X

66
Q

Activated partial thromboplastine time, factors involved?

A

XI, IX, VIII, X, V, II, I, XIII

67
Q

Thrombin time, how and what kind of blood

A

Decalcinated plasma mixed with a reagent containing thrombin only

68
Q

Thrombin time, coagulation time depends on

A

Concentration of fibrinogen and factor XIII in the plasma

69
Q

Thrombin time test can also determine

A

Estimate fibrinogen concentration

70
Q

Example of intrinsic pathway problem

A

Von willebrands disease, haemophilia A-factor VIII deficiency, haemophilia B-factor IX deficiency

71
Q

Extrinsic pathway problem

A

Factor VII deficiency, dicumarol toxicosis - first stage

72
Q

Common pathway problem example

A

Liver disease decrease production of coagulation factors, DIC, dicumarol toxicosis - second stage, factor X and or V, and or II, and or I, and or XIII deficiency

73
Q

Dicumarol or warfarin tixicosis, what parameters increase or decrease

A

Early stage only prothrombin time is increased, later activated partial thromboplastin time is increased too

74
Q

Dicumarol is a competetive antagonist of?

A

Vitamin K

75
Q

Vitamin K is responsible for

A

The gamma carboxylation of Proconvertin (factor VII), Christmas factor (factor IX), Stuart-Prower (factor X) and prothrombin (factor II)

76
Q

Vitamin K deficiency leads to

A

Inability of the factors to bind calcium. They are calcium dependent

77
Q

What factor has the shortest halflife

A

Factor VII, so it will be deficient first.

78
Q

What test will show factor VII deficiency first and why?

A

Prothrombin time is increased when there is factor VII is deficient, so this test will show it first

79
Q

Function of vit. K.

A

To exxagerate the post_synthetic gamma carboxylation of those factors in the liver

This makes the factors able to bind Ca2+, and thus become functionally active

80
Q

In case of vit. K deficiency , inproperly carboxylised prothrombin can be detected by

A

ELISA tes,t, called PIVKA II

81
Q

PIVKA II stands for

A

Proteins induced by vitamin K absence

82
Q

Fibrin degradation products, fibrinolytic pathway is responsible for?

A

Keeping the clot formation within normal limits

83
Q

Clot inhibitors?

A

Antithrombin III, alpha 2 macroglobulin, alpha 1 antitripsin, heparin __> able to bind thrombine and neutralize it

84
Q

After a complete coagulation, clot broken down by

A

By fibrinolytic enzymes

85
Q

Fibrinolysis starts with free collagen fibers exposed at site of injury -> kininogen and kallikrein activators of factor XII (Hageman) -> XIIa activated ->

A

Extrinsic pathway -> kallikrein from prekallikrein -> kallikrin activates kininogen system -> also forming bradikinin (actuvated form kininogen)-> mediator of pain —> Kallikrein th emost important activator of plasminogen-> plasmin -> cleave fibrin strands to small pieces

86
Q

Fibrin degradation products, fibrin dimers and monomers can be measured in the blood, (somw from fibrinogen also), accurate way to detect increased fibrinolysis to determine that it comes from fibrin and not from fibrinogen?

A

Examination of the D-dimer level in the blood

87
Q

D-dimer level in blood originates from?

A

Fibrin, not fibrinogen

88
Q

Both FDP and D-dimer test are based on?

A

Latexagglutination method and fresh citrated decalcinated plasma samples. Reagent contains antibodiesagainst FDPs or D-dimers attached to latex particles —> macroscopic agglutination can be seen if enoud FDPs and or D-dimers present in plasma

89
Q

Performing FDP or D-dimer test is helpful for

A

In early diagnosis of disseminated intravascular coagulopathy (DIC)

90
Q

DIC is a

A

Common acute disorder. Commonly a secondary problem, caused by primary sisease ex. septicaemia, pancreatitis, burn injuries, necrosisof tumours, shock, polytraumatisation

91
Q

Inncase of DIC, microthrombus formation and fibrinolysis are

A

Present at many different places in the body simultaneously because of severe tissue damage or necrosis, and blood vessel injury

92
Q

First sign of DIC can be

A

A positive FDP or D-dimer test

93
Q

Consumptional coagulopathy?

A

Coagulation factors and platelets are consumpted very quickly during DIC, where both extrinsic and intrinsic pathway can be cativated at same time different areas in body

94
Q

Extrinsic or intrinsic pathway? Tissue damage

A

Release of tissue factor -> extrinsic

95
Q

Extrinsic or intrinsic pathway? Necrosis

A

Release of tissue factor -> extrinsic

96
Q

Extrinsic or intrinsic pathway? Blood vessel injury

A

Finitiation of intrinsic pathway

97
Q

Laboratory diagnostics of DIC. Coagulation time, bleeding time, platelet count, prothrombin time, activated partial thromboplastin time, thrombin time, FDP and D-dimer, apperance of damaged RBC

A

Up, up, down, up, up, up, up, yes

98
Q

Diagnosis og von Willebrand disease, known innwhat soecies?

A

Humans, dogs (doberman pinschers)

Complete factor VIII is deficient

99
Q

Von Willebrands disease often accompanied by disease?

A

Hypothyroidism

100
Q

There are 3 main part of complete factor VIII

A
  1. Von Willebrand factor - responsible for platelet adhesion and aggregation
  2. VIIIc - antihaemophylic factor
  3. Factor VIII related antigen - hapten that is the determinable part and bound strongly to von Willebrand factor
101
Q

Determinable part of von Willebrand disease?

A

Factor VIII related antigen

102
Q

Dogs with von Willebrands disease have what effects?

A

Increased BT and BMBt, decreased clot retraction ability and sometimes coagulation disorders

Pathophysio (12 decks)

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