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Y1S2 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What does the endothelium produce to inhibit thrombin production

A

thrombomodulin and heparin

sulphate

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2
Q

what does the endothelium produce to reduce platelet adhesion

A

Prostacyclin and nitric oxide (NO)

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3
Q

What are the roles of the endothelial cells

A
  • Line blood vessels and form a barrier

* Enzymes to degrade platelet granule- derived molecules

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4
Q

what stimulates the production of platelet

A

thrombopoetin (TPO)- liver derived

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5
Q

how long do platelets stay in the circulation and where are they stored

A

Circulate for 5-10 days with ?30% “stored” in spleen

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6
Q

What is the main role of platelets

A

Form a plug when attracted by lowered prostacyclin and by collagen exposure
they release granules and cause the formation of fibrin

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7
Q

what causes vasoconstriction

A

Thromboxane A2 and serotonin from platelets cause vasoconstriction

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8
Q

how to platelets adhere to the vessel wall

A

via Von Willibrand’s factor and Glycoprotein Ib

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9
Q

how do platelets adhere to each other

A

Glycoprotein IIb-IIIa and fibrinogen

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10
Q

what is protein C activated by

A

thrombomodulin-thrombin complex

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11
Q

examples of inhibitors to the protein cascade

A
  • With co-factor- Factor S- Va and VIIIa are degraded
  • Antithrombin (previously antithrombin III) inhibit Xa and IIa
  • Heparin cofactor II inhibits Ila
  • Heparin stimulates antithrombin and heparin cofactor II
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12
Q

how is plasminogen activated

A

to plasmin by tissue plasminogen activator (tPA)- from endothelial cells

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13
Q

what is fibrin broken down into

A

fibrin degradation products” including D Dimers- a measurement of fibrinolysis
• Inhibitors of fibrinolytic system

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14
Q

what is the time scale of thromolysis

A

needs to be done in <3-4 hours, some risk of bleeding afterwards

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15
Q

what test would you use to measure coagulation

A

FBC
ncludes platelet count/size/ granules but is a poor assessment of platelet function- specialised tests of aggregation can be done

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16
Q

what is the reference range for the FBC

A

Ref range 150-400 x 10 9/l
• Easy bruising and purpura when <30-50
(thrombocytopenia)
• Risk of major bleeding if <10

17
Q

Prothrombin time (PT)

A
  • All coagulation tests are done on citrated plasma- removes Ca++
  • At 37C thromboplastin (brain extract!) and Ca++ added
  • Measure time till clot forms- extrinsic and common pathway
  • Prolonged by low levels of II X VII
18
Q

what is the role of Warfarin

A

reduces active II VII IX X so a useful measure of dose- expressed as INR- international normalised index

19
Q

Activated partial thromboplastin test (APTT)

A
  • Ca++ kaolin and phospholipids added to citrated plasma • Measure of intrinsic and common pathway
  • Prolonged in haemophilia and by heparin
20
Q

Fibrinogen

A

• Final substrate for making fibrin
• Can be measured by clot density or by-
Thrombin time- thrombin and Ca++ added to citrated plasma
GOOD INDICATOR OF LIVER FUNTION

21
Q

Correction tests and factor assays

A
  • A prolonged PT or APTT can be tested further-
  • 50:50 mix with normal plasma to see if the prolongation corrects
  • Factor assays to look for specific deficiencies
22
Q

Inherited blood disorders

A
  • Haemophilia A and B- X linked defect in VIII or IX gene
  • Commonly a new mutation so no family history
  • Approx 1:5000 of males
  • Female heterozygotes (carriers) not affected
  • Can be very mild- chance finding or issue for surgery
  • Severe (<1% VIII level)- frequent bleeds into joints and soft tissues
23
Q

Haemophilia- treatment

A

no treatment other than fresh frozen plasma
Porcine and then recombinant factor replacement
• ?Prophylaxis or treatment
• Issues of Hepatitis B or C and HIV, ??nv CJD
• Gene therapy?

24
Q

Von Willebrand disease

A
  • Usually autosomal dominant
  • Defect in platelet adhesion and binding of VIII
  • Up to 1% of population
  • Mild disease- easy bruising, heavy periods
  • Severe disease- similar to haemophilia
25
Q

Acquired coagulation disease- liver

A

• Liver disease- alcohol/autoimmune/hepatitis

  • All coag factors produced in liver
  • PT and fibrinogen abnormal, later APPT abnormal -bleeding due to abnormal clotting, low platelets
  • portal hypertension causing oesophageal varices and upper GI bleeding
26
Q

disseminated intra-vascular coagulation (DIC)

A

• Activation of clotting cascade due to- -trauma
-malignancy eg prostate cancer
-sepsis
-amniotic fluid embolism
Causes depletion of clotting factors and damage due to clot Treat the cause and replace clotting factors

27
Q

Low platelets (thrombocytopenia)

A

• Could be due to –

  • under-production
  • increased use
  • abnormal distribution
28
Q

Thrombocytopenia- under production

A

• Abnormal marrow function
- acute leukaemia, metastatic tumour, aplastic anaemia
• Expected side effect of cytotoxic chemotherapy
• Idiosyncratic and unexpected drug adverse effect eg co-trimoxazole, anti-inflammatories

29
Q

Thrombocytopenia- increase use

A

• Immune thrombocytopenia (ITP)

  • autoimmune disease of children or adults
  • may be triggered by infection or drug
  • auto antibodies to platelets
  • treated by watch and wait/ steroids/ immunoglobulins/ splenectomy/ drugs to mimic thromobopoetin
30
Q

Thrombocytopenia- abnormal distribution

A
  • Splenomegally eg portal hypertension, leukaemia

* Large haemangioma

31
Q

ncreased risk of clotting- thrombophilia

A

• Inherited defects in coag inhibitors eg Protein C, S, antithrombin • Inherited defect in factor V- V Leiden
• Acquired problems- Virchow’s triad abnormal- vessel wall - flow
- blood component

32
Q

Abnormal vessel wall

A
  • Atheroma and plaque
  • Varicose veins
  • Aneurysm
33
Q

Abnormal flow

A
  • Atrial fibrillation
  • Immobile eg long distance flight, plaster cast, surgery
  • Varicose veins
34
Q

Abnormal blood component

A
  • Increased haemoglobin/red cell count- polycythaemia
  • Increased WBC or platelet count- stasis and increased clotting
  • Increased viscosity of plasma
  • Reduced coag factor inhibitors

Y1S2 (73 decks)

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