Flashcards in Acquired disorders of haemostasis. Deck (28):
how can you determine whether or not the acquired bleeding disorder is due to deficiency in the inhibitor.
APTT (measures the activity of the intrinsic and common pathways of coagulation)
Do one test on patients blood and a repeat test on patients blood mixed with normal blood.
If the repeat test shows significant correction then the deficiency is due to a lack of inhibitor.
acquirered bleeding disorders include
vitamin K deficiency
massive transfusion syndrome
how are patients with the possibility of a acquired bleeding disorder assessed
• Clinical history
• Date of onset, previous history of bleeding episodes and clinical pattern
• Response to challenges e.g. surgery, dental extraction
• For young children: bleeding from umbilical stump, vaccination, and circumcision.
• Requirement for medical/ surgical intervention
• Other systemic illness and drug history
• Family history
• Clinical examination: pattern of any bruising or other evidence of haemorrhagic signs, signs of underlying disease, joints, muscles and skin.
how can portal hypertension effect the blood plasma level.
portal hypertension causes congestion in the spleen and as more than 1/3 platelet are found in the spleen you will get less in the plasma.
which coagulation cascade factors are vitamin K dependent
which organ synthesises all the clotting factors
when vitamin K is used as a co-factor what does is become
VKOR- vitamin K epoxide
what enzyme converts Vitamin K to VKOR
gamma glutamyl carboxylase
which enzyme converts VKOR to vitamin K
vitamin K reducatse
which enzyme does wharfing work against
vitamin K reducatse.
what are the main causes of vitamin K deficenccy
prolonged nutritional deficiency.
Obstructive jaundice- cannot get bile salts in gut so fat uptake is reduced which reduced vitamin K uptake
what major risk do patients with liver disease have when undergoing surgery
liver typically produces the clotting factors.
what factors cause impaired haemostats is in liver disease
reduced plasma concentration
delayed fibrin monomer polymeriation
excessive plasmin activity.
which is the only clotting factor whose amount is not reduced in liver disease
define massive transfusion
Transfusion of a volume equal to the patient’s total blood volume in less than 24 hours or
50% blood volume loss within 3 hours
what causes the haemostatic abnormalities in a massive transfusion
dilutional depletion of platelets and coagulation factors (mainly V and VIII)
underlying disease, eg liver or renal drug treatment or surgery
Citrate toxicity- hypothermia
what is most likely cause of DIC
sepsis of gram -ve organism
causes damage and tissue factor exposure
what are the consequences of DIC
consumption of clotting factors and platelets, microvascular (thrombosis), tissue ischaema and organ damage.
Activation of fibrinolysis microangiopathic haemolysis.
Causes of acute DIC
acute intravascular haemolysis
fulminant liver disease.
laboratory tests for DIC
coagulation screen- PT, APTT, TCT, Fibrinogen concentration, FDP or D-dimer.
Is a coagulation screen for DIC do the tests have shortened or prolonged test results
Is the D dimer elevated or suppressed in DIC
Treatment for DIC
treat the underlying cause
supportive treatment- maintain tissue perfusion, co-ordinate treatment with fresh frozen plasma
and provide folic acid and vitamin K supplements.
define prothrombin ratio
patient’s prothrombin time/ mean normal prothrombin time.
what is ISI
Correction factor to account for sensitivity of thromboplastin compared with the international reference preparation
drugs which potentiate warfarin affect include
• Ampicillin (oral)
drugs which antagonise the warfarin effect.
• Vitamin K