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Lymphoreticular > Platelets 2 > Flashcards

Platelets 2 Flashcards

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1
Q

Disorders of platelet function?

A

> Glanzmann’s thrombasthenia (defect in GPIIbIIIa)
- otterhounds and great Pyrenees
- quarter horses
- defective platelet aggregation and abnormal clot retraction
canine thrombopathia - abnormal GPIIbIIIa exposure and impaired degranulation
- bassett hounds
Bovine thrombopathia - defect not known
- simmentals
- mild-severe bleeding

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2
Q

Causes of thrombocytosis? LOOK

A

> physiological transient
- epinephrine induced splenic contraction
reactive (2*)
- ^ thrombopoietin +- IL6
- inflammation, haemorrhage, Fe deficinecy
essential thrombocythemia
- myeloproliferative disorder
- persistent ^ platelet nos.
- BM megakaryocytes ^ +- abnormal morphology
- function variable (may see pettechiae/echymoses or thrombosis)
- TPO normal/increased

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3
Q

What is vWF? Where is it synthesised and how does it circulate?

A
  • vWF = plasma glycoprotein for platlet adherence to collagen and formation of 1* haemostatic plug
  • synthesised by endothelial cells, platelets and megakaryocytes
  • circulates bound to FVIII (protective function for FVIII)
  • maysee concurrent v in FVIII
  • exists in small, medium and large multimers (large multimers most active in haemostasis)
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4
Q

Clinical signs of vWF dz?

A
  • mucosal bleeding (GI, epistaxis, haematuria)
  • NO peticheia
  • bleeding may be absent
  • prolonged buccal mucosal bleeding time despite no thrombocytopenia
  • clotting times usually NORMAL (PTT may be ^ d/t factor VIII decrease)
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5
Q

Which species is vWF dz common in?

A
  • common dogs
  • rare cats and horses
  • pigs used as human model
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6
Q

What forms of VW dz exist? LOOK

A

Type 1 - decreased conc of all multimers
Type 2 - qualitative abnormalities in vWF structure/function
Type 3 - absence of all vWF multimers

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7
Q

Type 1 vW dz?

A
  • all multimers present at decreased concentrations

- variable severity of bleeding (not until [vWF]

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8
Q

Type 2 vW dz?

A
  • qualitative abnormalities in vWF structure function
  • disproportionate decrease in LARGE multimers
  • severe and uncommon
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9
Q

Breeds type 1 vWD

A
  • Doberman

- autosomal inheritance so males and females == affected

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10
Q

breeds type 2 vWD

A
  • german shorthaired and wirehaired pointers
  • one horse case
  • autosomal recessive
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11
Q

type 3 vWD

A
  • absence of all vWF multimers (
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12
Q

breeds type 3 vWD

A
  • Scottish terriers, Chesapeake Bay Retrievers, Shetland Sheepdogs and Dutch Kooiker
  • autosomal recessive
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13
Q

How can vW dz be tsted for?

A

> measure levels of vWF Ag

  • collect blood into EDTA or citrate
  • if using citrate as a coagulant dilute 1:9
  • vWF decreased by clots in the sample and heamolysis but unaffected by lipaemia
  • separate plasma immediately, freeze and ship overnight w/ ice
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14
Q

Specific vWF tests?

A 
> ELISA
- Ab 
>  Immunoelectrophoresis 
- separate relative amounts of different multimers (required for diagnosis of type II disease) 
> genetic test to detect carriers
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15
Q

How is interpretation of vWF ELISA perfmored? ie. what do differneing levels of Ags indicate?

A
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16
Q

Tx vWD?

A

> transfusion to supply factor
- cryoprecipitate best (^ conc vWF) 1U/10kg
- plasma can be given @6-12ml/kg if cryo not available
- whole blood if anaemic too
desmopressin
- doesnt tx dz
- pre-op prophylaxis with type 1 dz
- causes release of vWF from endothelium
- human intranasal/1ug/kg SQ 30min pre-op

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17
Q

What type of sample is needed for coagulation tests?

A
  • citrated plasma
  • ratio of anticoag:blood 1:9
  • NB: vPCV anaemic patients will have more plasma!*
  • do not sample thorugh heparinised catheters
  • minimise trauma to prevent platelet activation and coagulation
  • centrifuge to separate plasma within an hour
  • analyse within 4hrs or freeze plasma
  • always include species specific control ???
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18
Q

What do citrate tubes look like? What should be checked in tube?

A

blue/purple/green (small)

- check for clots! Need to resample

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19
Q

What coagulation test can be used in practice with patient?

Study These Flashcards
A

ACT: Activated clotting time (=PTT in lab)

  • point of care test
  • INTRINSIC and COMMON pathways
  • 2ml whole blood into ACT tube with diatomaceous earth
  • incubate 60s @37* check for clot formation q5-10s
  • time to initial signs of clot is ACT time (s)
  • less sensitive than PTT
  • prolonged with thrombocytopenia
20
Q

What is the PTT?

Study These Flashcards
A

> partial thromboplastin time

  • intrinsic and common pathways
  • incubate citrated plasma with excess phospholipid [ usually comes from platelet cell membrane as this is NOT a test of platelet number] , contact activator and calcium
  • measure time to formation of clot
21
Q

What can interfere with PTT?

Study These Flashcards
A
  • lipemia, hemolysis, oxyglobin tx, icterus interfere with clot detection
22
Q

Can PTT be used to detect hypercoagulation?

Study These Flashcards
A

No too crude

- only look for prologed time

23
Q

What does prolonged PTT time indicate?

Study These Flashcards
A
  • defect in INTRINSIC (factors XII, XI, IX, VIII) or COMMON (X, V, II, fibrinogen) pathways
  • factor activity must be
24
Q

What is PT?

Study These Flashcards
A

= prothrombin time

  • screening test for defects in EXTRINSIC or COMMON pathway of coagulatino
  • incubate citrated plasma with tissue thromboplastin (TF) and calcium
  • measure time to clot formation
25
What does prolonged PT time indicate?
- defect in EXTRINSIC (factor VII) or COMMON | -
26
Which factor has the shortest half life? Clinical implications?
Factor VII of extrinsic pathway - will decrease first if problem with production of clotting factors - so prolonged PT will be seen first before PTT/ACT > eg. Vit K deficiency may see prolonged PT with normal PTT early on
27
If PT and PTT are both prolonged what scenarios could be occouring?
> problems - common - extrinsic + common - intrinsic + common - extrinsic + intrinsic - extrinsic+ intrinsic + common
28
What does PT elongation time indicate?
- factor VII deficiency - DIC - Vit K deficiency - LIver failure > NOT affected by thrombocytopenia
29
What further tests can be used to assess coagulation?
> specific factor analysis - detect specific factor deficiencies - usually for hereditary deficicenies - correct PT and PTT of test plasma to that of normal plasma
30
What tests of fibrinolysis are available?
> FDPs (fibrin degradation products) - use latex agglutination (special test and kit) - done on serum (needs to be separated within 30mins) - test immediately or freeze
31
What do ^ FDPs indicate?
> DIC most commonly - but not specific - may also increase with haemorrhage, jugular vein thrombosis (horse), liver dz - will be + if fibrinogen broken down as well as fibrin > more specific = D-dimers - plasmin mediated degradation of cross-linked fibrin
32
Disorders of coagulatioin - most common?
- acquired factor deficiencies - most common = vit K - rodenticide toxicity (coumarin, indanedione) or sweet clover ingestion (cattle)
33
Which factors are vit K deoendant?
- II, VII (PT affected first), IX, X
34
Mechanism of vit K deficiency?
- factors produced in the liver - activated by vit K depdednant carboxylase (requires reduced vit K) - production of reduced vit K requires activation of vit K reductase - vit K reductase inhibited by coumarin-type rodenticides - > lack of active FII, VII, IX, X -> coagulopathy
35
Random details on vit K deficiency pathway
- vit K from gut (fat soluble) - proenzyme needs to be carboxylated (2,7,9,10) /activated to take part in coagulation - vit K reduced back again once used - Coumarins block vit K recycling
36
Which pathways are affected by vit K? What coagulation tests affected first?
- all pathways | - PT see nfist as factor VII affected
37
CLinical signs of vit K deficency?
- haemorrhage - ^ PT and PTT - platelet nos and buccal mucosal bleeding time SHOULD be normal, but mild thrombocytopenia poss d/t consumption of clotting factors with haemorrhage
38
Tx vit K deficiency?
- Emetics, cathartics, activated charcoal if ingestion of rodenticide recent - transfusions (whole fresh blood/fresh frozen plasma) - +- packed RBCs if severe anaemia present > Vit K tx (K1) - orally/parenterally (SQ) - NOT IV (risk of anaphylaxis) - NOT IM (risk of haematoma) - O/D -> haemolytic anamiea - can give loading dose SQ + lower dose q8hrs - same dose gien orally w/ fatty meal - can take 12hrs before vit K tx shortens PT/decreases bleeding > if warfarin/1st gen rodenticide = 1 week tx > 2nd/3rd gen need to tx min 3 weeks ( check PT 24-48hrs after last dose, if prolonged reinstate tx for another 2 weeks and recheck
39
Causes of thrombocytopenia?
-
40
Give egs. of herediatary defects of coagulation
- factor VII deficiency - haemophilia A (factor VIII deficiency) - Haemophilia B (factor IX deficiency) - factor XI/XII deficiency
41
Tx inherited coagulation defects?
- transfusion (whole blood/plasma) to replace factors and RBCs - fresh/frozen plasma gives smaller factor - cryoprecipitate has 10x more factor VIII cf. plasma
42
What is DIC?
- mixed haemostatic defect - d/t excessive coagulation -> widespread thrombosis - haemorrhage -> consumption of clotting factors (platlets and fibrinogen both lost) - 2* to underlying diseases (neoplasia, liver dz, immune mediated dz, infectious dz) - may be chronic/acute
43
What haemostatic abnormalities are seen with DIC?
- THROMBOCYTOPENIA - PROLONGED pt AND ptt - ELEVATED fdpS - DECREASED FIBRINOGEN - DECREASED ANTITHROMBIN iii
44
Tx DIC?
> stop coagulation - heparin - transfusion whole blood/plasma/cryoprecipitate (source of antithrombin III) - aspirin to stop platelet activation > correct other underlying abnormalities > prog poor
45
Outline the approach to the bleeding patient
> haemorrhage peticheal/ecchymotic? = platlet defect > frank haemorrhage = coagulation defect - consider age and hx (toxins) > CBC - Hct and platlet count > thrombocytopenia? - check clots. smear - if >100x10^9 haemorrhage = cause of thrombocytopenia likely - if if plt within interval but haemorrhage (=vWD) or ecchymoses (platlet function) > check BMBT > assay vWF Ag > check clotting function (PTT may be ^ d/t concurrent v FVIII) > check PT and PTT - if both prolonged consider vit K deficiency/ DIC - PTT only = intrinsic pathway defects (haemophilia A/B) - OT only = early vit K deficiency, liver dz, early DIC

Lymphoreticular (31 decks)

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