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Lymphoreticular > Platelets 2 > Flashcards

Platelets 2 Flashcards

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?

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?

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?

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

Can PTT be used to detect hypercoagulation?

A

No too crude

- only look for prologed time

23
Q

What does prolonged PTT time indicate?

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?

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
Q

What does prolonged PT time indicate?

A
  • defect in EXTRINSIC (factor VII) or COMMON

-

26
Q

Which factor has the shortest half life? Clinical implications?

A

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
Q

If PT and PTT are both prolonged what scenarios could be occouring?

A

> problems

  • common
  • extrinsic + common
  • intrinsic + common
  • extrinsic + intrinsic
  • extrinsic+ intrinsic + common
28
Q

What does PT elongation time indicate?

A
  • factor VII deficiency
  • DIC
  • Vit K deficiency
  • LIver failure
    > NOT affected by thrombocytopenia
29
Q

What further tests can be used to assess coagulation?

A

> specific factor analysis

  • detect specific factor deficiencies
  • usually for hereditary deficicenies
  • correct PT and PTT of test plasma to that of normal plasma
30
Q

What tests of fibrinolysis are available?

A

> 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
Q

What do ^ FDPs indicate?

A

> 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
Q

Disorders of coagulatioin - most common?

A
  • acquired factor deficiencies
  • most common = vit K
  • rodenticide toxicity (coumarin, indanedione) or sweet clover ingestion (cattle)
33
Q

Which factors are vit K deoendant?

A
  • II, VII (PT affected first), IX, X
34
Q

Mechanism of vit K deficiency?

A
  • 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
Q

Random details on vit K deficiency pathway

A
  • 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
Q

Which pathways are affected by vit K? What coagulation tests affected first?

A
  • all pathways

- PT see nfist as factor VII affected

37
Q

CLinical signs of vit K deficency?

A
  • 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
Q

Tx vit K deficiency?

A
  • 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
Q

Causes of thrombocytopenia?

A

-

40
Q

Give egs. of herediatary defects of coagulation

A
  • factor VII deficiency
  • haemophilia A (factor VIII deficiency)
  • Haemophilia B (factor IX deficiency)
  • factor XI/XII deficiency
41
Q

Tx inherited coagulation defects?

A
  • transfusion (whole blood/plasma) to replace factors and RBCs
  • fresh/frozen plasma gives smaller factor
  • cryoprecipitate has 10x more factor VIII cf. plasma
42
Q

What is DIC?

A
  • 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
Q

What haemostatic abnormalities are seen with DIC?

A
  • THROMBOCYTOPENIA
  • PROLONGED pt AND ptt
  • ELEVATED fdpS
  • DECREASED FIBRINOGEN
  • DECREASED ANTITHROMBIN iii
44
Q

Tx DIC?

A

> stop coagulation
- heparin
- transfusion whole blood/plasma/cryoprecipitate (source of antithrombin III)
- aspirin to stop platelet activation
correct other underlying abnormalities
prog poor

45
Q

Outline the approach to the bleeding patient

A

> 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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