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lab diagnostics > haemostasis > Flashcards

haemostasis Flashcards

1
Q

What is primary haemostasis?

A

Primary Haemostasis
• This stage occurs within seconds
• 1. Vasospasm: Vasoconstriction of the blood vessel by
Prostacyclin (PI2), Thromboxane A2 (TXA2) and serotonin
(5-HT). Slows down the bleeding.
• 2. Platelet Plug: Adherence of platelets to collagen of
damaged endothelial cells. Platelet aggregation: Role of
thrombin, adenosine diphosphate (ADP), PI2, TXA2, 5-HT
and prostaglandins.

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2
Q

What is secondary haemostasis?

A

Secondary Haemostasis
• This stage takes several minutes. Stabilizes the soft clot
and maintains vasoconstriction.
• 3. Fibrin Clot: Conversion of prothrombin to thrombin.
Thrombin stimulates the conversion of fibrinogen (Blood
protein) to polymerized fibrin (mesh).
• 4. Dissolution of the clot by fibrinolysis: Plasminogen
is converted to plasmin, the enzyme that dissolves the
fibrin.

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3
Q

What is the role of thrombin in coagulation?

A

Tissue factor provides stimulus for initial thrombin production
Thrombin activates platelets and clotting factors required for its own production
The conversion of fibrinogen to fibrin by thrombin is the critical step in clot formation

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4
Q

What are the steps in thrombus formation?

A
  1. stimulus
  2. initiation(platelet activation) and thrombin initiation(activation of coagulation factors): thrombin is the most potent platelet activator
  3. thrombin amplification (takes place on surface of activated platelets)
  4. thrombus formation(large quantities of thrombin are needed for converting fibrinogen to fibrin)
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5
Q

What is the process of blood coagulation?

A

• Initiated by the Extrinsic Pathway
– VII binds TF exposed by vascular injury
– VIIa can also activate IX in the presence of TF
– Activation of XII not required for hemostasis
• Each step of the cascades involves:
– Protease (from previous step)
– Zymogen
– Non-enzymatic cofactors
• V (Xa)
• VIII (IXa)
• TF (VIIa)
– Ca2+
– Organizing surface (platelets)
• Thrombin cleaves peptides from fibrinogen to produce fibrin monomers(gel)
• XIIIa crosslinks fibrin monomers with transglutamination

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6
Q

What is the normal range for Activated Partial Thromboplastin Time (aPTT)?

A

• aPPT normal range: 25-37 seconds

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7
Q

What causes pathophysiologic variability when testing aPTT?

A

• Age, Stress, Physical exercise, Surgery (post-op) can mask other hemostatic defects!
• Prolonged : Acquired conditions (DIC, drugs - heparin), lupus anticoagulant antobodies, VIII or iX inhibitors, Inherited: intrisic Factors deficiency
(FVIIi, FIX, FXII, prekallicrein, HWWK), vWD
• Shortened in Pregnancy/post-partum, during oral contraceptives (due to increased FVIII), after Physical exercise and stress.
• normal APTT does not exclude mild hemophilia A or B or weak inhibitors

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8
Q

How is Prothrombin Time; Prothrombin Ratio (PR) and Internationalized Ratio (INR) tested?

A

– Measures of the extrinsic/common pathway
• PT reference range: 12-15 sec; measures factors II, V, VII, X and fibrinogen.;
Used in conjunction with aPTT

• INR (International Standardize Ratio) normal range: 0.8-1.2

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9
Q

What causes pathological variability in PT and INR?

A

Pathophysiologic variability
• Circardial rythms
• Vitamin K deficiency and malabsorption (leading to vitamin K deficiency)
• Liver disease
• Afibrinogenaemia and dysfibrinogenemia
• Dilutional coagulopathy e.g. massive blood transfusion
• Multiple clotting factor deficiencies e.g. FV and FVIII deficiency including DIC

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10
Q

What is the interpretation for isolated prolonged PT?

A

Factor VII deficiency

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11
Q

What is the interpretation for Prolonged PT in

association with other coagulation abnormalities?

A

• Vitamin K deficiency
• Vitamin K antagonists e.g. warfarin, phenindione, rodenticides
• Liver disease
• Malabsorption (leading to vitamin K deficiency)
• High concentrations of unfractionated heparin
• Direct thrombin inhibitors e.g. Lepirudin, argatroban,
dabigatran
• Afibrinogenaemia and dysfibrinogenemia
• Dilutional coagulopathy e.g. massive blood transfusion
• Multiple clotting factor deficiencies e.g. FV and FVIII
deficiency
• Abnormalities of the vitamin K cycle e.g. mutations within the VKORC1 gene
• Chromosomal aberrations - the F7 and F10 genes are located on the long arm of chromosome 13 - deletions of which are associated with reduced FVII and FX levels.

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12
Q

What is the interpretation for a shortened PT?

A

Following treatment with rVIIa

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13
Q

What do problems associated with PT, aPTT and TT imply?

A

• PT Prothrombin Time
=> Exogenous coagulation (extrinsic system)
• APTT Activated Partial Thromboplastin Time
=> Endogenous coagulation (intrinsic system)
• TT Thrombin Time
=> Fibrinogen / fibrin conversion

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14
Q

What is the reference range for fibrinogen?

A

1.5-4.0 g/L

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15
Q

In which instances would the fibrinogen level be decreased?

A

• DIC due the consumption of clotting factors
• Liver disease due to decreased synthesis
• Massive transfusion leading to a dilutional coagulopathy
Inherited deficiencies e.g. hypofibrinogenaemia,
afibrinogenaemia and dysfibrinogenaemia
• Following thrombolytic therapy
In some patients following treatment with asparaginase

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16
Q

In which instances would the fibrinogen level be increased?

A
  • Increasing age
  • Female sex, pregnancy, oral contraception
  • In post-menopausal women
  • Acute phase reaction
  • Disseminated malignancy
17
Q

What is hemophilia A?

A

Factor VIII deficiency
X linked recessive
occurs in 1/10 000 males

18
Q

What is hemophilia B?

A

Factor IX deficiency
X linked recessive
occurs in 1/50 000 males

19
Q

What is the severity of bleeding in hemophilia?

A

Related to factor level
<1% - Severe - spontaneous bleeding
1-5% - Moderate - bleeding with mild injury
5-30% - Mild - bleeding with surgery or trauma

20
Q

What are D-dimers indicative of?

A

end product of fibrinolysis

reference value of <500 ug/ml

21
Q

In which situations can D-dimers be raised?

A 
Pregnancy; Burns
Malignancy; Liver disease
Infection; Snake bites
DIC; Atrial fibrillation
Vaso-occlusive sickle; Renal failure
Cell crisis; Cardiac failure,
Surgery; Venous thromboembolic disease [VTED]
Pulmonary embolism; Aortic dissection
22
Q

What are common clinical conditions associate with DIC? Activation of both coagulation and fibrinolysis triggered by these initiating events

A 
• Sepsis
• Trauma
– Head injury
– Fat embolism
• Malignancy
• Obstetrical complications
– Amniotic fluid embolism
– Abruptio placentae
• Vascular disorders
• Reaction to toxin (e.g. snake venom, drugs)
• Immunologic disorders
– Severe allergic reaction
– Transplant rejection
23
Q

What is von willebrand factor?

A 
Synthesized in endothelial cells & megakaryocytes
Functions:
1) Stabilizes Factor VIII
2) Essential for platelet adhesion
deficiency causes mucosal bleeding
24
Q

How does liver disease affect hemostasis?

A
  1. Decreased synthesis of II, VII, IX, X, XI, and fibrinogen
  2. Dietary Vitamin K deficiency (Inadequate intake or
    malabsortion)
  3. Dysfibrinogenemia
  4. Enhanced fibrinolysis (Decreased alpha-2-antiplasmin)
  5. DIC
  6. Thrombocytoepnia due to hypersplenism
25
Q

How do all anti coagulants work?

A
  • Reducing thrombin production and/or

* Inhibiting thrombin activity

26
Q

What is the mechanism of some drugs that indirectly inhibit thrombin?

A
  • Heparins: Impair thrombin production, Inhibit thrombin through antithrombin (AT)
  • Vitamin K antagonists: Non-selectively inhibit thrombin production
  • Inhibitors of thrombin production: Block specific “upstream” factor in thrombin production
27
Q

What is the mechanism of some drugs that directly inhibit thrombin?

A

• Direct thrombin inhibitors (DTIs): Specifically and directly block thrombin activity

28
Q

What is the range of INR in healthy patients?

A

healthy people: 0.8-1.2

29
Q

What is thrombocytopenia?

A

Small or normal-sized platelets in association with
thrombocytopenia suggest that the cause is a failure of
bone marrow production, whereas thrombocytopenia
with large platelets is more likely to be caused by
peripheral destruction or consumption of platelets with
the bone marrow responding by increasing platelet
production

30
Q

What is pseudothrombocytopenia?

A

Decreased no of platelets may be a result of spontaneous platelet aggregation due to anti-platelet
antibodies (EDTA dependent Ab)
also indicative of artifacts in platelet assessment

31
Q

What is drug induced thrombocytopenia?

A 
Three different mechanisms:
 bone marrow suppression
 immune-mediated destruction
 platelet aggregation
 Testing for Immune-Mediated
Testing for Drug-Induced Thrombocytopenia:
 Serotonin Release (HIT)
 PF4-heparin-IgG immune
complex (HIT)
 Drug-Specific Platelet Ab
32
Q

How is thrombocytosis diagnosed?

A

In reactive thrombocytosis (e.g. caused by severe
infection or inflammation) the platelets are usually of normal size whereas when thrombocytosis is a feature of
a myeloproliferative disorder (chronic myeloid leukaemia,
essential thrombocythaemia or polycythaemia vera)
platelet size is generally increased and some giant
platelets are present.

lab diagnostics (8 decks)

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