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Lymphoreticular > Platelets and Coagulopathy > Flashcards

Platelets and Coagulopathy Flashcards

1
Q

4 components of haemostasis?

A
  • endothelium
  • platlets
  • coagulation factos
  • fibrinolytic factors
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2
Q

What are endothelial cells? What action do they have ?

A
  • flattened cells lining blood vessels
  • pro and anticoagulant properties
  • normally anticoagulant - inhibit coagulation and platelet aggregation
  • act as barrier to subendothelial collagen which is procoagulant
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3
Q

What is vWF produced by? Function?

A
  • endothelial cells and platelets
  • stored in Weibel Palade bodies
  • Released early in haemostatic process
  • responsible for platelet adhesion to collagen
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4
Q

Which reticular lines have the shortest half life? CLinical impliations?

A
  • Neutrophils 6hrs
  • Platelets ~1week
  • RBC ~120d
    > if BM affected, neutrophil numbers will be affected first, then platelets, then anaemia
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5
Q

What are platelets?

A
  • small, discoid, ANUCLEAR cells
  • megalokaryocyte (precursor in BM) breaks off to form platelets = thrombopoiesis
  • mediated by thrombopoietin
  • 3-5um pale basophilic with small red granules
  • circulate for 5-9d most species
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6
Q

With generalised BM destruction what will be lost first?

A
  • Neutrophils 6hrs t1/2
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7
Q

What is present on the outer membrane of platleets?

A
  • receptors for ahesion and aggregation
    > glycoproteins
  • GP1b binds vWF
  • GP IIbIIIa binds fibrinogen on adjacent platelets allwing aggregaion
  • defects in receptors -> abnormal platelet function and clot formation*
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8
Q

What is contained within the platelets?

A
  • cytoskeleton (actin and myosin allows for shape change)
  • membrane bound granules
    > alpha granules (red) - contain vWF, finbrinogen and factors V and VIII
    > dense granules - contain ADP and calcium
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9
Q

What is primary hemostasis? 2*? What follows these?

A

1* = formation of 1* platlet plug
2* = activation of coagulation cascade and generation of insoluble fibrin which sabilises platlet plug
> Fibrinolysis - breakdown of fibrin and platelet plug

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10
Q

Outline steps of 1* haemosasis.

A
  • damage endothelium exposes subendohelial collagen
  • vWF released from damaged endothelium
  • platelet adhesion occours
  • platelets bind to collagen via receptor GPib and vWF from the endothelium
  • once platelets adhered to collagen, undergo shape change and become spherical with filipodia
  • additional receptors for vWF (GPIb) and fibrinogen (GPIIbIIIa) exposed
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11
Q

How does platelet aggregation occour?

A
  • platelets bind fibrinogen via GPIIbIIIa
  • fibrinogen generated from coagulation cascade
  • released from platelets and found in plasma
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12
Q

What do platelets secrete?

A
  • aggregating platelets degranulate
  • ADP, fibrinogen, vWF
  • TXA2 also released from platelet membrane
    > increase platelet adhesion and aggregation
  • also release factors V and VIII -> coagulation
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13
Q

What happens to the whole blood vessel whe damaged?

A
  • vasoconstriction to v blood pressure and blood flow past the area
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14
Q

2* haemostasis

A
  • involves activation of the coagulation cascade
  • happens simultaneously with formation of platelet plug
  • damage to endothelium releases tissue factor activating EXTRINSIC clotting pathway
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15
Q

What is the first and most important coagulation factors?

A

Tissue factor

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16
Q

What is the end point of the coagulation cascape?

A
  • activate thrombin tha causes fibrinogen -> fibrin
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17
Q

What are coagulation factors?

A
  • soluble enzymes (serine proteases) found in circulation
  • each step of coagulation cascade converts one of these factors from inactive state (proenzyme) to its active state
  • each step amplifies system
  • > insoluble fibrin aim
  • fibrin stablises 1* platelet plug
18
Q

Do the intrinsic, extrinsic and common pathways exist in vivo?

A

no only in vitro

19
Q

What is the intrsinc and extrinsic link -> common apthway factor?

A

factor 10 -> 10a

20
Q

What is extrinsic system also known as? What does it do?

A

= Initiation

  • most important in vivo
  • tissue factor (TF) released from damaged tissue binds to and activates FVII in presence of calcium
  • TF-FVII complex activates FX of common pathway and FIX of intrinsic pathway
21
Q

What is he intrinsic pathway?

A

= Amplification pathway

  • FXII activated by contat with negatively charged surface (cofactor HMWK)
  • activated FXII cleaves and activates FXI which in turn activates FIX(calcium required)
  • activated FIX activates FX of common pathway (calcium required)
22
Q

Outline common pathway

A
  • activation of factor X
  • activated FX binds activated FV and calcium on platelet surface
  • this converts prothrombin (FII) to thrombin (FIIa)
  • thrombin converts fibrinogen (FI) to fibrin (FIa)
  • fibrin crosslinked by activated FXIII
23
Q

What are inhibitors of coagulation?

A

> antithrombin III
- inhibits thrombin and activated FX
- activity increased by heparin from endothelium
- protein C inactivates factors V and VIII
fibrinolysis

24
Q

Outline fibrinolysis

A
  • enzymatic breakdown of fibrin by plasmin
  • plasmin from plasminogen found in the platelet membrane and plasma
  • plasmin degrades fibrinogen and fibrin to produce fibrin degradation products (FDPs)
25
Q

What is coagulation?

A

2* haemostasis

26
Q

How can platelets be evaluated in the lab?

A

> platelet conc (automated counts on EDTA)

  • good accuracy for all species except cat, sheep and goat d/t overlap between RBC and platelet size
  • platelet clumps can affect accuracy of counts d/t uneven distribution and overlap of size of clumps and RBCs
  • very common in cats!!*
27
Q

Which species must have a platelet count carried out from blood smear?

A
  • cats

- CKC spaniels, often thrombocytopenic with giant platelets which may be counted as RBCs

28
Q

What is thrombocytopenia? At what level may spontaneous haemorrhage occour?

A
29
Q

What is thrombocytosis? Clinical relevance?

A

> 1000x10^9/L

^ risk thrombotic activity

30
Q

What practical way can clotting times be evaluated?

A

> Buccal mucosal bleeding time (minutes)

  • 1* haemostasis (evaluates platelet FUNCTION more than number and doesn’t look at coagulation [2* clotting])
  • spring loaded cassette
31
Q

Is buccal mucosal bleeding time a good test? When would it be increased?

A
  • very low sensitivy
  • ^ thrombocytopenic
  • ^ vW disase and disorders of platlet function
  • will NOT be ^ with coagulation deficiecny (2* hemostasis)
32
Q

3 main dioders of platelets?

A

> thrombocytopenia
thrombocytoisis
disorders of functon

33
Q

What clinical signs may be seen with 1* clotting dz and 2*?

A

1* petichae and echymoses

2* haematoma

34
Q

Mechanisms of thrombocytopenia?

A 
> ^ platelet desruction or consumption 
- immune mediated destruction 
- haemorrhage (wont massively lower numbers) 
- DIC 
- sequestration (transient) 
> decreased production 
- look BM 
- other lines likely affected aswell 
> infectious 
- numerous causes 
- machanism unknown
35
Q

Most common casue of most severe thrombocytopenia?

A

> immune mediated
- platelet number v low often concurrent decreased production
Evan’s syndrome = concurrent immune mediated thrombocytopenia and anaemia

36
Q

What is Evan’s syndrome?

A
  • concurrent immune mediated thrombocytopenia and anaemia

- rare but bad!

37
Q

2 forms of immune-mediated thrombocytopenia?

A 
> 1* ab against platelet ag
> 2* - many causes
- other immune dz (SLE) 
- drugs/vaccine/injection 
- neoplasia
- infectious
38
Q

Clinical findings of immune-mediated thrombocytopenia

A

> clinical findings
profound thrombocytopenia (NB: always recheck numbers and look for clumps on smear and lcots in tube!!!)
peticheal or ecchymotic haemorrhage
Hx bleeding from gums, mucosal surfaces, prolonged bleedig from wounds etc.

39
Q

Dx of IMT?

A
  • hard to confrm, r/o other causes
  • response to tx most common
  • may see mehgakaryocyte hyperplasia (BM)
  • BM examination poss even if platelet nos low - rarely bleed from site
  • antiplatelet Abs (need large volume of blood as platlet numbers will be low)
40
Q

What is haemostasis?

A
  • interaction between BVs, platelets and coag factors that normally maintains blood in a fluid state and allows for formaion of platelet plugs and clots when vessels injured
41
Q

2 mechanisms of thrombocytopenia? What will be seen on coag tests?

A

> ^ consumption
- haemorrhage (numbers should stay above 100x10^9)
- DIC numbers may be v low (but should also see other signs of coagulation defects)
- PT, PTT will be prolonged
- FDPs will be increased
sequestration
- rare but may occour with splenomegaly or large cavitated mass
decreased production
- BM disease
- neoplasia
- drugs
infectious
- many causes including immune mediated and v production
- FeLV, BVD, Ehrlichia, Leishmania

Lymphoreticular (31 decks)

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