LabD 3 Haemostasis Flashcards
(102 cards)
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
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
3
Q
Major groups of haemostasis disorders
A
, thrombocytopathy, coagulopathy
4
Q
Vasculopathy
A
Decreased ability of iction in case of blood vessel injury, the first step of the harmeostasis process
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
6
Q
Thrombocytopenia
A
Decreased amount of thrombocytes in the blood
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
8
Q
First step of haemostasis
A
Vasoconstriction in case of injury
9
Q
Second step of haemostasis
A
Formation of thrombocyte-thrombus
10
Q
Third step of haemostasis
A
Formation of stabile Fibrin network to keep thrombus at site of injury
11
Q
Signs of increased bleeding tendency on the skin and mucuos membranes
A
Anemia, petechia, ecchymosis, suffusion
12
Q
Signs of increased bleeding in thoracic cavity
A
Haemothorax (blood in pleural cavity)
13
Q
Signs of increased bleeding in the abdominal cavity
A
Haemoprotoneum (blood in between inner lining of abd. wall and internal abd. organs)
14
Q
Signs of increased bleeding in the G.I tract
A
Haematemesis (vomiting blood), melena (dark sticky feces; internal bleeding or swallowing blood)
15
Q
Petechia.
A
Small red/purple spot caused by bleeding in skin
16
Q
Ecchymosis?
A
Discoloration of skin caused by bleeding underneath skin
17
Q
Suffusion
A
Slow spread of blood
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
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
20
Q
BT, BMBT
A
Bleeding time, Buccal mucosal bleeding time
21
Q
Bleeding time and buccal mucosal bleeding time testing for
A
Test for thrombocytopenias, thrombocytopathies and vasopathies
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
23
Q
Bleeding time and buccal mucosal bleeding time test is dependent on
A
thrombocyte function, platelet count and capillary function
24
Q
Normal BMBT and normal platelet count up to
A
- Normal BMBT: 3-5min
* Platelet count normal up to: 50x10^9/L
25
Coagulation time test is for
Coagulopathies
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Coagulation time test
* 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
27
Coagulation time test types
* Ct on watch glass
* Ct in plastic syringe
* Ct in glass tube
* Ct in ACT (activated clotting time) tube
28
Coagulation time test, first appearance of fibrin strand
- Sample onto glass slide
- Move tip of needle back and forth in blood
- Normal result: first strand within 1-2 min
29
Clotting time on watch glass, how
- Fresh blood sample on watch glass treated with wax (scratches activate coag. cascade)
- Check time for the whole amount of blood is clotted
30
Clotting time on watch glass, normal result
7-15 min
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Clotting time in syringe, how
Fresh blood into plastic syringe, check time of complete coagulation
32
Clotting time in syringe, normal result
10-12 min
33
Clotting time in glass tube, normal result
4-5 min
34
Clotting time in ACT tube, what is ACT tube and how
- 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
35
Clotting time in ACT tube, normal result
3 min
36
Platelet (thrombocytic) count, 3 methods
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
37
Platelet (thrombolytic) count, important when, and what kind of blood
- 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
38
Platelet (thrombolytic) count method 3, Automatic cell counter.
- Particles 5-30fl are taken as platelets
What can be the false result?
- 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)
39
Platelet (thrombolytic) count, what method is best
Evaluation of blood smear -> evaluation of arrangement, morphology etc.
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General platelet count:
200-800 x10^9/L
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Major causes of thrombocytopenia
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
DIC
Disseminated intravascular coagulopathy
43
Clot retraction test? leave clot what happens, why and if not what is expected?
- 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
Platelet aggregation test, for?
When thrombocytopathy is expected, ex. von Willebrands disease
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Platelet aggregation test, how?
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
Platelet aggregation test, what kind of blood, what colour
Citrate blood sample, use upper layer (this is the platelet rich plasma).
Slightly opaque
47
Thrombocytic morphology
- 1-2um diameter
| - Centre is granulated, edge hyalomer(clear)
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What species have platelets size 3-5fl?
Horses, sheep, cattle
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What species have platelets size 7-8fl?
Dogs and swine
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What species have platelets size 10-15fl?
Cats
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Major causes of thrombocytopathies?
1. Improper development ex. hereditary glucoprotein deficiencies
2. Von Willebrands disease
3. Uraemia, liver failure, myelo- and or lymphoproliferative diseases, usage of NSAIDS,
52
Can we expect severe bleeding disorder from thrombocytopenia besides normal coagulation? And why
No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade
53
Can we expect severe bleeding disorder from thrombocytopathies besides normal coagulation? And why
No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade
54
Can we expect severe bleeding disorder from vasopathies besides normal coagulation? And why
No. These are prevented by the formation of polymerised fibrin strands at the end of coagulation cascade
55
Can we expect severe bleeding disorder from coagulopathies besides normal thrombocytic and vessel function? And why
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
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Coagulopathies can also be examined by using more specific tests, evaluating? What kind of blood used?
Which groups of factors are not functioning properly.
Citrate blood, preventing coagulation by binding calcium
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Prothrombin time test, how?
- 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
Prothrombin time test, what does it tell us?
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
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Prothrombin time test, factors involved?
VII, X, V, II, I, XIII
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Prothrombin time test, normal coagulation time
10-15 sec
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Activated partial thromboplastine time, test how and blood used
- blood: decalcinated plasma, reagent Silimat, micronised silica as activator.
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Reagent Simplastin contains
Rat uterus tissue homogenate as tissue thromboplastin (factor III) and CaCl2
( Prothrombin time)
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Reagent Silimat contains.
Rabbit brain homogenate as PF3 (platelet factor 3) and micronised silica as contact activator
(Activated partial thromboplastin time)
64
Normal activated partial thromboplastine time
20-30sec
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Activated partial thromboplastine time give sus what info
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
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Activated partial thromboplastine time, factors involved?
XI, IX, VIII, X, V, II, I, XIII
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Thrombin time, how and what kind of blood
Decalcinated plasma mixed with a reagent containing thrombin only
68
Thrombin time, coagulation time depends on
Concentration of fibrinogen and factor XIII in the plasma
69
Thrombin time test can also determine
Estimate fibrinogen concentration
70
Example of intrinsic pathway problem
Von willebrands disease, haemophilia A-factor VIII deficiency, haemophilia B-factor IX deficiency
71
Extrinsic pathway problem
Factor VII deficiency, dicumarol toxicosis - first stage
72
Common pathway problem example
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
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Dicumarol or warfarin tixicosis, what parameters increase or decrease
Early stage only prothrombin time is increased, later activated partial thromboplastin time is increased too
74
Dicumarol is a competetive antagonist of?
Vitamin K
75
Vitamin K is responsible for
The gamma carboxylation of Proconvertin (factor VII), Christmas factor (factor IX), Stuart-Prower (factor X) and prothrombin (factor II)
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Vitamin K deficiency leads to
Inability of the factors to bind calcium. They are calcium dependent
77
What factor has the shortest halflife
Factor VII, so it will be deficient first.
78
What test will show factor VII deficiency first and why?
Prothrombin time is increased when there is factor VII is deficient, so this test will show it first
79
Function of vit. K.
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
In case of vit. K deficiency , inproperly carboxylised prothrombin can be detected by
ELISA tes,t, called PIVKA II
81
PIVKA II stands for
Proteins induced by vitamin K absence
82
Fibrin degradation products, fibrinolytic pathway is responsible for?
Keeping the clot formation within normal limits
83
Clot inhibitors?
Antithrombin III, alpha 2 macroglobulin, alpha 1 antitripsin, heparin __> able to bind thrombine and neutralize it
84
After a complete coagulation, clot broken down by
By fibrinolytic enzymes
85
Fibrinolysis starts with free collagen fibers exposed at site of injury -> kininogen and kallikrein activators of factor XII (Hageman) -> XIIa activated ->
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
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?
Examination of the D-dimer level in the blood
87
D-dimer level in blood originates from?
Fibrin, not fibrinogen
88
Both FDP and D-dimer test are based on?
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
Performing FDP or D-dimer test is helpful for
In early diagnosis of disseminated intravascular coagulopathy (DIC)
90
DIC is a
Common acute disorder. Commonly a secondary problem, caused by primary sisease ex. septicaemia, pancreatitis, burn injuries, necrosisof tumours, shock, polytraumatisation
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Inncase of DIC, microthrombus formation and fibrinolysis are
Present at many different places in the body simultaneously because of severe tissue damage or necrosis, and blood vessel injury
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First sign of DIC can be
A positive FDP or D-dimer test
93
Consumptional coagulopathy?
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
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Extrinsic or intrinsic pathway? Tissue damage
Release of tissue factor -> extrinsic
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Extrinsic or intrinsic pathway? Necrosis
Release of tissue factor -> extrinsic
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Extrinsic or intrinsic pathway? Blood vessel injury
Finitiation of intrinsic pathway
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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
Up, up, down, up, up, up, up, yes
98
Diagnosis og von Willebrand disease, known innwhat soecies?
Humans, dogs (doberman pinschers)
Complete factor VIII is deficient
99
Von Willebrands disease often accompanied by disease?
Hypothyroidism
100
There are 3 main part of complete factor VIII
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
Determinable part of von Willebrand disease?
Factor VIII related antigen
102
Dogs with von Willebrands disease have what effects?
Increased BT and BMBt, decreased clot retraction ability and sometimes coagulation disorders
