Haemotology 2 - platelets Flashcards

1
Q

what are the 3 componenents of haemostatic reposnse

A

Vasocontstriction
Platelet adhesion and aggregation
Clotting - coagulation phase

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2
Q

Features of platelets

A

small, oval, no nucleus
2-3micrometres

contains granules
megakaryocyte cytoplasm

lifespan 7-10 days

essential for haemostasis

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3
Q

what is the desired end result after cogaultion phase?

A

conversion of soluble plasma protein to insoluble rigid fibrin

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4
Q

Process of initiation of coagulation phase (EXTRINSIC PATHWAY)

A

Tissue factor (Factor III) released after damage occurs
Binds to Factor VII (w/Ca2+)
= Tissue Factor - FVIIa complex

This binds to FX to activate it = FXa

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5
Q

Process of initiation of coagulation phase (INTRINSIC PATHWAY)

A

Activated proenzymes (usually Factor XII)
Combine with Platelet Factor and Ca2+
Then combine with Clotting Factors - Factor IX and co-factor VIII
Activates FX -> FXa

Slower than the extrinsic pathway

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6
Q

Process of common pathway

A

FXa and its co-factor FVa
Activates prothrombin to form THROMBIN

THROMBIN converts FIBRINOGEN to FIBRIN

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7
Q

How would a Ca or K deficiency affect someone whoe gets an injury

A

impairs blood clotting
Ca2+ usually incolved in speeding up the process and activates

Vit K needed to produce certain clotting factors in liver (ie prothrombin)

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8
Q

Why might babies be at risk of haemorrrage?

A

Liver not fully formed
Usually vitamin K deficient

Usually given Vit K supplements to prevent haemorrage

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9
Q

what are 2 ways the body controls clotting

A

natural anticoaglulants:

  • Antithrombin - inhibits thrombin among others
  • Heparin - released by basophils (type of WBC) and mast cells = co-factor that accelerates Antithrombin
    (can get it as a drug)
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10
Q

What is the process of breaking down the fibrin clot? and what enzyme is needed?

A

Fibrinolysis
Enzyme = plasmin -> produces fibrin

produces fibrin degrading products

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11
Q

explain structure of Group A Blood cell

A

Has A antigen

Has Anti-B antibodies in blood

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12
Q

explain structure of Group B Blood cell

A

Has B antigen

Has Anti-A antibodies in blood

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13
Q

explain structure of Group AB Blood cell

A

Has both AB antigens on surface

Has no antibodies in blood

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14
Q

explain structure of Group O Blood cell

A

Has no antigens on surface

has anti A and anti B antibodies in blood

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15
Q

What would happen if antibodies came into contact with the corresponding antigen on a RBC

A

agglutination
hemolysis

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16
Q

which blood group genes are dominant and recessive

A

A and B are dominant

O is recessive

17
Q

Which blood group is the universal donor and universal recipient

A

O = universal donor

AB = universal recipient

18
Q

What happens if someone has the D antigen

A

Rh positive

19
Q

which alleles do you need to be Rh -ve

A

inherit 2 negative alleles

20
Q

How might a Rh -ve person end up with anti RhD antibodies

A

via sensitisation, so by exposure to Rh +ve RBCs

e.g.
transfusion
or pregnancy/birth (Rh -ve mum and Rh +ve baby)

21
Q

what can mixing of the bloods in a Rh -ve mum and Rh +ve baby cause

A

haemolytic disease of the newborn (HDN)

22
Q

what can caue mixing of the foetal and maternal blood

A

usually stays seperate throughout pregnancy
but during delivery
breakdown of placental tissue
causes mixing of foetal and maternal tissue

23
Q

in a Rh -ve mum and Rh +ve baby, what happens if the blood mixes and explain HDN

A

when blood mixes
mum’s immune system mounts a response against the Rh+ve antigens

But usually at delivery there’s no time for them to react (usually takes 72hrs)
But the antibodies remain in the blood

So in first pregnancy theres no impact

BUT

In second, antibodies are already there

in second, when blood mixes, it can cause immune response and causes haemolytic disease of newborn