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Haemotology > Week 2 part 2 > Flashcards

Week 2 part 2 Flashcards

1
Q

Disseminated intravascular coagulation

A

Simultaneous coagulation and haemorrhage caused by the initial formation of thrombi which consume clotting factors (factors 5,8) and platelets, ultimately leading to bleeding.

Disseminated intravascular coagulation (DIC) is a rare but serious condition that causes abnormal blood clotting throughout the body’s blood vessels. It is caused by another disease or condition, such as an infection or injury, that makes the body’s normal blood clotting process become overactive

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2
Q

Disseminated intravascular coagulation causes

A 
Infection
Malignancy
Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm
Liver disease
Obstetric complications
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3
Q

Management of Disseminated intravascular coagulation

A

Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure
Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased fibrinogen degradation products
Treat the underlying cause and supportive management

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4
Q

Disseminated intravascular coagulation features

A

Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure

Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased fibrinogen degradation products

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5
Q

Blood tests in Disseminated intravascular coagulation

A

Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased fibrinogen degradation products

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6
Q

Immune thrombocytopenic purpura (ITP)

A

Immune (or idiopathic) thrombocytopenic purpura (ITP) is an immune-mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.

Children with ITP usually have an acute thrombocytopenia that may follow infection or vaccination. In contract, adults tend to have a more chronic condition.

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7
Q

Features of Immune thrombocytopenic purpura (ITP)

A

may be detected incidentally following routine bloods
symptomatic patients may present with
petichae, purpura, bleeding (e.g. epistaxis)

catastrophic bleeding (e.g. intracranial) is not a common presentation

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8
Q

Immune thrombocytopenic purpura (ITP) management

A

first-line treatment for ITP is oral prednisolone
pooled normal human immunoglobulin (IVIG) may also be used - it raises the platelet count quicker than steroids, therefore may be used if active bleeding or an urgent invasive procedure is required

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9
Q

Evan’s syndrome

A

ITP in association with autoimmune haemolytic anaemia (AIHA)

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10
Q

Acquired causes of Platelet Functional Defects

A

Drugs (eg Aspirin, non-steroidal anti inflammatory drugs)

Renal failure

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11
Q

Von Willebrand’s disease

A

Von Willebrand’s disease is the most common inherited bleeding disorder. The majority of cases are inherited in an autosomal dominant fashion* and characteristically behaves like a platelet disorder i.e. epistaxis and menorrhagia are common.

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12
Q

Causes of acquired Thrombocytopenia

A

Marrow failure

Peripheral destruction

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13
Q

Commonest cause of primary haemostatic failure

A

Thrombocytopenia

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14
Q

von Willebrand factor

A

large glycoprotein which forms massive multimers up to 1,000,000 Da in size
promotes platelet adhesion to damaged endothelium
carrier molecule for factor VIII

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15
Q

Investigations for Von Willebrand’s disease

A

prolonged bleeding time
APTT may be prolonged
factor VIII levels may be moderately reduced
defective platelet aggregation with ristocetin

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16
Q

Von Willebrand’s disease management

A
  • tranexamic acid for mild bleeding
  • desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
  • factor VIII concentrate
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17
Q

Type 3 von Willebrand’s disease

A

(most severe form) is inherited as an autosomal recessive trait. Around 80% of patients have type 1 disease

total lack of vWF (autosomal recessive)

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18
Q

Type 1 Von Willebrand’s disease

A

type 1: partial reduction in vWF (80% of patients)

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19
Q

Type 2 Von Willebrand’s disease

A

abnormal form of vWF present

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20
Q

Hemophilia

A

Haemophilia is an X-linked recessive disorder of coagulation. Up to 30% of patients have no family history of the condition. Haemophilia A is due to a deficiency of factor VIII whilst in haemophilia B (Christmas disease) there is a lack of factor IX (single factor deficiency)

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21
Q

Features of hemophilia

A

haemoarthroses
haematomas
prolonged bleeding after surgery or trauma

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22
Q

Investigations in hemophilia

A

prolonged APTT

bleeding time, thrombin time, prothrombin time normal

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23
Q

Multiple clotting factor deficiencies

examples

A

Disseminated Intravascular Coagulation
Liver failure
Vitamin K Deficiency/Warfarin therapy

24
Q

Where are coagulation factors produced?

A

All coagulation factors are synthesised in hepatocytes

Reduced in liver failure

25
Q

What coagulation factors require carboxylation by Vitamin K for their function?

A

Factors II, VII, IX & X are carboxylated by vitamin K which is essential for function

26
Q

Sources of Vitamin K

A

Diet
Intestinal synthesis
Absorbed upper intestine
Requires bile salts for absorption

27
Q

Causes of Vitamin K Deficiency

A 
Poor dietary intake
Malabsorption
Obstructive jaundice
Vitamin K antagonists (warfarin)
Haemorrhagic disease of the newborn
28
Q

Haemophilia A

A

Haemophilia A (factor VIII deficiency)

29
Q

Haemophilia B

A

Haemophilia B (factor IX deficiency)

30
Q

Single Factor Deficiency examples

A

Haemophilia A and B

Isolated prolonged APTT

31
Q

Thrombotic Events

A

Arterial = Coronary, cerebral, peripheral

Venous = Deep venous thromboses, Pulmonary Embolism

32
Q

Arterial thrombosis

A

Arterial thrombosis is a blood clot in an artery, which can be very serious because it can stop blood reaching important organs. Arteries are blood vessels that carry blood from the heart to the rest of the body and the heart muscle.

Arterial thrombosis may be caused by a hardening of the arteries, called arteriosclerosis. This happens when fatty or calcium deposits cause artery walls to thicken. This can lead to a buildup of fatty material (called plaque) in the artery walls. This plaque can suddenly burst (rupture), followed by a blood clot.

33
Q

Management of Arterial thrombosis

A

Blood-thinning medicines (anticoagulants)
Catheters
Stents
Medicines to interfere with or dissolve blood clots

34
Q

Venous thromboembolism: risk factors

A 
increased risk with advancing age
obesity
family history of VTE
pregnancy (especially puerperium)
immobility
hospitalisation
anaesthesia
central venous catheter: femoral >> subclavian
35
Q

What medications increase the risk of Venous thromboembolism?

A

combined oral contraceptive pill
raloxifene and tamoxifen
antipsychotics (especially olanzapine)

36
Q

Venous thrombosis

A

Venous thrombosis is when the blood clot blocks a vein. Veins carry blood from the body back into the heart.

  • Low pressure system.
  • Platelets not activated.
  • Activates coagulation cascade - rich in fibrin clot.
37
Q

Virchow’s triad

A

Stasis
Vessel wall damage
Hypercoagulability

38
Q

Venous thrombosis management

A

Heparin/warfarin/New oral anticoagulants (e.g. rivaroxiban)

39
Q

Deep Vein Thrombosis features

A

Pain in one leg (usually the calf or inner thigh)
Swelling in the leg or arm
Chest pain
Numbness or weakness on one side of the body
Sudden change in your mental state

40
Q

Potential features of pulmonary embolism include:

A 
chest pain - typically pleuritic
dyspnoea
haemoptysis
tachycardia
tachypnoea
respiratory examination - classically the chest will be clear
41
Q

Management of PE

A

apixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a PE

if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

if the patient has antiphospholipid syndrome (specifically ‘triple positive’ in the guidance) then LMWH followed by a VKA should be used

42
Q

Hypercoagulability CAUSES

A

Associated with release of tissue factor, raised VWF and factor VIII

43
Q

Causes of inherited thrombophilia

A

factor V Leiden (activated protein C resistance): most common cause of thrombophilia

prothrombin gene mutation: second most common cause

Deficiencies of naturally occurring anticoagulants

  • antithrombin III deficiency
  • protein C deficiency
  • protein S deficiency
44
Q

Hereditary Thrombophilias

A

A group of genetic defects in which affected individuals have an increased tendancy to develop premature, unusual and recurrent thromboses.

45
Q

Consider Hereditary Thrombophilia Screening

A 
Venous thrombosis <45 years old
Recurrent venous thrombosis
Unusual venous thrombosis
Family history of venous thrombosis
Family history of thrombophilia
46
Q

Causes of acquired Thrombophilia

A

Antiphospholipid syndrome

Drugs - the combined oral contraceptive pill

47
Q

Management of Hereditary Thrombophilia

A

Advice on avoiding risk
Short term prophylaxis to prevent thrombotic events during periods of known risk

Short term anticoagulation to treat thrombotic events

Long term anticoagulation ONLY if recurrent thrombotic events

48
Q

Risk factors for Recurrent Thrombosis

A

History of previous thrombosis
Spontaneous thrombosis rather than acquired transient risk factor (eg immobility or surgery)
Family history

49
Q

Antiphospholipid syndrome

A 
Is an acquired thrombophilia
Multi organ disease
Arterial and venous thromboses
Recurrent fetal loss
Mild thrombocytopenia
50
Q

Investigations of Antiphospholipid syndrome

A

Either Lupus anticoagulant or Anti cardiolipin antibodies
APTT usually prolonged
Antibodies may be elevated following surgery, drugs or malignancy

51
Q

Management of Antiphospholipid syndrome

A

Need anticoagulation with INR between 3 and 4 (warfarin and aspirin)

52
Q

Conditions associated with Antiphospholipid Antibodies

A

Autoimmune Disorders
Lymphoproliferative Disorders
Viral Infections
Drugs

53
Q

Complications of thrombosis

A

Thrombosis can block the blood flow in both veins and arteries. Complications depend on where the thrombosis is located. The most serious problems include stroke, heart attack, and serious breathing problems.

54
Q

Risk factors for arterial thrombosis may include:

A 
Smoking
Diabetes
High blood pressure
High cholesterol
Lack of activity and obesity
Poor diet
Family history of arterial thrombosis 
Lack of movement, such as after surgery or on a long trip
Older age
55
Q

Venous thrombosismay be caused by:

A 
Disease or injury to the leg veins
Immobility
A broken bone (fracture)
Certain medicines
Obesity
Autoimmune disorders that make it more likely your blood will clot
56
Q

D-dimer

A

D-dimer is a protein fragment (small piece) that’s made when a blood clot dissolves in your body. Blood clotting is an important process that prevents you from losing too much blood when you are injured. Normally, your body will dissolve the clot once your injury has healed.

Haemotology (9 decks)

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