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AC1 > Blood > Flashcards

Blood Flashcards

1
Q

Which blood type is the most common in all ethnicities?

A

O

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2
Q

Which blood type is the most rare in all ethnicities?

A

AB

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3
Q

What type of antibodies are ABO antibodies?

A

IgM constitutively expressed

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4
Q

In a patient with A serum antibodies, exposure to A antigen will cause what?

A

Agglutination

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5
Q

What type of antibodies are anti rhesus antibodies? And what is the significance of this?

A

IgG so can cross placenta

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6
Q

What is the dominant rhesus haplotype?

A

CDe - rhesus D

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7
Q

What needs to happen in order for anti rhesus D antibodies to be expressed?

A

Need to be exposed to RhD

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8
Q

What cells are present in a blood transfusion?

A

Packed RBCs

No plasma

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9
Q

What are the principles of blood donation relating to antigens and antibodies?

A

Selection of donor is based on antigens present on their RBCs
Recipient can only receive blood which does not express antigens they have antibodies to

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10
Q

What is the universal donor blood group?

A

O negative

No antigens

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11
Q

What is the universal recipient blood group?

A

AB positive

No antibodies

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12
Q

Describe the process of cross matching

how long does it take?

A

Blood group recipient determined
Screen for abnormal recipient antibodies
Each unit tested against patients blood
Takes 1 hour

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13
Q

Describe the process of group and save

How much time does it save from cross matching?

A

Blood group recipient determined
Screen for abnormal recipient antibodies
Takes 45 mins but means that first steps of cross matching are complete so rest of process can be done in 15 mins

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14
Q

How long are group and save records kept?

A

7 days

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15
Q

What steps should be taken for taking blood for pre transfusion testing in order to ensure that it is safe?

A

Positively identify patient at bedside
Label sample tube and complete request form after pt identity confirmed
Do not label or write forms in advance

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16
Q

What safety steps should be done when administering blood in a transfusion?

A

Positively identify patient at bedside
Ensure identity of each blood pack matches patient
Check ABO and RhD of each pack compatible with patient
Check each pack for damage
If in doubt, return to blood bank
Complete forms to document transfusion of each pack

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17
Q

What records should be kept in relation to transfusion?

A 
Record in notes: reason for transfusion
Product given
Dose
Adverse effects 
Clinical response
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18
Q

What observations should be performed when a transfusion is performed?

A

BP, pulse and temp before and 15 mins after each pack
If conscious, further monitoring only if adverse reaction
If unconscious, pulse and temp at regular intervals

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19
Q

What percentage of transfusion errors are avoidable?

A

50%

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20
Q

Give some clinical problems with transfusions

A 
Haemolysis
Other immune responses: TRALI (transfusion related acute lung injury), anaphylaxis
Infection
Volume overload
Endotoxaemia
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21
Q

How many genotypes and phenotypes are generated by the ABO system?

A

6 genotypes

4 phenotypes

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22
Q

What are the contents of the normal LFT panel?

A

Bilirubin
Alkaline phosphatase (ALP)
Alanine transaminase (ALT)
Serum Albumin

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23
Q

What tests of liver function could be requested?

A 
Clotting tests e.g. Prothrombin time (PT), APTT 
Gamma glutamyl transferase (GGT)
Iron studies 
Hepatitis serology 
Auto-antibodies
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24
Q

What can be analysed from an LFT panel?

A

Hepatocellular damage
Cholestasis
Biliary excretion
Liver synthetic function

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25
Q

What could cause a raised ALP result?

A

Damage to bile ducts, e.g. obstruction, cholestasis, infiltrative liver disease
Release from bone turn over, e.g. fracture healing, bony metastasis,
Paget’s disease
Highest in third trimester of pregnancy

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26
Q

Where is ALP produced?

A

Bile ducts
Bone
Placental tissue

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27
Q

Where is gamma GT produced?

A

Relatively specific to damage to the liver ducts

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28
Q

What could cause a raised gamma GT result?

A

Chronic alcohol abuse

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29
Q

Where is ALT produced?

A

Mainly liver

Also heart, muscles, kidneys, pancreas

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30
Q

What could cause a raised ALT result?

A

Damage to hepatocytes: hepatitis, chronic liver disease, drug induced liver damage

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31
Q

What does total bilirubin measure?

A

Combination of conjugated and unconjugated bilirubin

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32
Q

What are the 3 categories of causes of raised total bilirubin?

A

Prehapatic e.g Haemolysis
Hepatic e.g. Liver disease
Post Hepatic e.g. Bile duct obstruction

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33
Q

What may cause reduced serum albumin?

A

Sepsis, chronic disease states and cirrhosis

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34
Q

Where is AST produced?

A

Liver parenchyma, kidneys, heart, brain and skeletal muscle

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35
Q

What does prothrombin time measure?

A

Extrinsic pathway of coagulation, main rate limiting step is
availability of Factor VII, which is produced by liver, hence increased PTT is an indirect measure of liver function

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36
Q

What can cause an increase in transferrin saturation?

A

Haemachromatosis

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37
Q

What can cause a decrease in transferrin saturation?

A

Iron deficiency anaemia

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38
Q

What can cause a raised serum ferritin?

A

Iron overload
Liver disease (reflecting damage to ferritin containing hepatocytes)
Inflammation
Malignancy

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39
Q

What secondary blood tests would commonly be requested to look at the underlying cause of intrinsic liver disease?

A

Hepatitis serology

Auto-antibodies

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40
Q

List key features to check in the history of a patient you suspect of having an acute liver disease

A 
Pruritus 
Jaundice 
Oedema  
Abdominal pain 
Fever 
Changes to urine and stool  
Drug and sexual hx 
Foreign travel 
Recent food poisoning 
Fatigue 
Family Hx
Previous Hx - gallstones
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41
Q

List key features to check in the history of a patient you suspect of having chronic liver disease

A 
Weight changes – gains as well as losses
Anorexia 
Jaundice 
Changes to urine and stool  
Alcohol consumption 
Gynaecomastia 
Easy bruising 
Arthralgias 
Family Hx
Mental state changes 
Haematemesis 
Previous hospital admissions
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42
Q

Excluding Hepatitis virus A, B, C, D & E list three other infectious causes of hepatitis

A

Glandular fever/EBV
Amoebic/parasite infections
CMV

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43
Q

In pre hepatic jaundice, what colour will urine and stools be? What pattern of hyperbilirubinaemia is this?

A

Urine normal
Faeces normal/darkened
Unconjugated hyperbilirubinaemia: not water soluble
More bilirubin produced than can be conjugated and excreted

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44
Q

What will the urine and stool colour be in hepatic jaundice? What pattern of hyperbilirubinaemia is this?

A 
Urine darker
Stools lighter 
Mixed hyperbilirubinaemia 
Hepatocytes function poorly, so have difficulty conjugating and 
excreting bilirubin
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45
Q

What colour will urine and stools be in post hepatic jaundice?
What pattern of hyperbilirubinaemia is this?

A

Urine dark
Stools light
Conjugated hyperbilirubinaemia, water soluble
Biliary obstruction: conjugation occurs, but bile cannot be excreted, as outflow is blocked

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46
Q

When does jaundice become clinically apparent?

A

When bilirubin levels rise >40unol/L

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47
Q

What is the normal process of bilirubin metabolism?

A

Bilirubin is conjugated in liver
Released into intestine
Converted to urobilogen (colourless)
Oxidized by bacteria in bowel to stercobilin (dark brown pigment)

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48
Q

What are the possible mechanisms underlying the change in stool colour seen in certain types of jaudice?

A

Pale stool is due to absence of stercobilin in stool, due to blockage of passage of bile, or failure bilirubin conjugation in liver
Hepatic picture: decreased production of conjugated (water soluble) bilirubin, but there may also be a decreased excretion due to inflammation blocking bile caniculae, less bilirubin getting
into bowel, hence lighter stool

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49
Q

How does a head of pancreas tumour lead to jaundice?

A

Obstruction of the common bile duct by pancreatic neoplasm

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50
Q

What classification system is commonly used to assess liver failure?

A

Child-Pugh Classification: used to determine degree of liver failure and need for transplantation

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51
Q

What is an enzyme inducer?

A

Increases metabolic activity of an enzyme, either through
activation or upregulation of gene expression
Impact on other medications metabolized through same pathway, by increasing their breakdown, thus requiring dose adjustments

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52
Q

Give some example of enzyme inducers

A

Rifampicin
Carbamazepine
Tobacco
isoniazid

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53
Q

What is an enzyme inhibitor?

A

Reduces activity of an enzyme
Normally through binding to enzyme
Break down of medications through that pathway is slowed, potentially causing overdoses

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54
Q

Give examples of enzyme inhibitors

A 
Erythromycin 
Fluoxetine 
Amiodarone 
Fluconazole 
Diltiazem
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55
Q

David Smith is a 56 year old man with known lung cancer. He attends for his routine oncology review. He has been feeling a bit low and has constipation, anorexia and nausea. What are the differentials?

A 
Chemotherapeutics
Paraneoplastic syndrome
Depression
Cerebral metastasis
Biochemical abnormalities: hypercalcaemia, hypokalaemia
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56
Q

How does parathyroid hormone affect calcium levels?

A

Increase levels of serum calcium

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57
Q

What disease processes leads to primary hyperparathyroidism?

A

Abnormality in parathyroid glands

Common causes: parathyroid adenoma or parathyroid gland hyperplasia

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58
Q

What are the common non-PTH mediated causes of hypercalcaemia?

A

Malignancy: haematopoietic or solid organ with mets or ectopic hormone secretion
Elevated vitamin D: vitamin D intoxication, sarcoidosis, HIV or other granulomatous disease
Thyrotoxicosis
Drug induced: Lithium, thiazide diuretics

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59
Q

What is the basis for the appearance of metastasis on a radionucleotide bone scan?

A

Performed with technetium-99m–labeled diphosphonates
Compounds accumulate rapidly in bone, degree of radiotracer uptake depends blood flow and rate of new bone formation reflecting osteoblastic activity

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60
Q

How can malignancy cause hypercalcaemia?

A

Osteolytic metastases with local release of cytokines (including osteoclast activating factors)
Extopic secretion of parathyroid hormone-related protein (PTHrP)
Ectopic production of active vitamin D

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61
Q

What are the common symptoms of acute leukaemia? How do they relate to the underlying pathological abnormality?

A

Evidence of failure of tri-lineage haematopoiesis:
Anaemia: tiredness, shortness of breath, pallor
Thrombocytopaenia: easy bleeding and bruising
Luekopaenia: increase infections

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62
Q

What are the major types of acute leukaemia?

A

Acute myeloid leukaemia- commoner in adults

Acute lymphoblastic leukaemia- commoner in children

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63
Q

What is the major acute complication of chemotherapy in a patient who has an acute leukaemia, with a high proportion of cells proliferating?

A 
Tumour lysis syndrome, reflecting the breakdown of a high number of cells, which are in the cell cycle
Hyperkalaemia 
Hyperphosphataemia 
Hypocalcaemia 
Hyperuricaemia 
Lactic acidosis
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64
Q

What can be given prophylactically to reduce risk of tumour lysis syndrome in acute lymphoblastic leukaemia chemotherapy?

A

Allopurinol is usually given to cover against the renal impact

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65
Q

What is the mechanism of action of allopurinol?

A

Competitive xanthine oxidase inhibitor that reduces amount of uric acid produced by inhibiting conversion of hypoxanthine to xanthine and xanthine to uric acid
Reduced uric acid secretion leads to an increase in urinary excretion of hypoxanthine

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66
Q

What are the 3 most common neoplasms that are associated with cerebral metastases?

A

Breast
Lung
Bowel/GU

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67
Q

What is the normal intra cranial pressure?

A

Opening pressure of the CSF is 10-20 cm H2O

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68
Q

How do cerebral metastases cause raised intra-cranial pressure?

A

Presence of a physical space occupying lesion
Haemorrhage into or around the met
Oedema into or around the met
Obstruction of flow of CSF

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69
Q

What is the most significant potential consequence of raised intra-cranial pressure?

A

Herniation leading to cardiorespiratory arrest

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70
Q

What are the major types/sites of herniation of the brain?

A

Subfalcine
Uncal (transtentorial)
Cerebellar tonsillar

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71
Q

What 3 factors are required for successful haemostasis?

A

Vessel wall
Platelets
Coagulation factors

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72
Q

What is DIC?

A

Disseminated intravascular coagulation
Pathological process, widespread activation of clotting cascade that results in formation of blood clots in small blood vessels
Compromise of tissue blood flow, can lead to multiple organ damage
Consumes clotting factors and platelets, normal clotting is disrupted and severe bleeding can occur from various sites

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73
Q

How are endothelial cells anti thrombotic in health?

A

Physical barrier to the pro-thrombotic sub-endothelial tissue
Produce: Prostacyclin and Nitric Oxide, Protein C activator (thrombomodulin), Tissue plasminogen activator (TPA)

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74
Q

How are prostacyclin and nitric oxide anti thrombotic?

A

Vasoldilation and inhibition of platelet aggregation

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75
Q

How is thrombomodulin anti thrombotic?

A

Binds to protein C and inhibits coagulation

76
Q

How is tissue plasminogen activator anti thrombotic?

A

Activates fibrinolysis

77
Q

Where is von willebrand factor made and what activates it?

A

Made by endothelial cells and is activated by ADAMTS13 (plasma protease)

78
Q

What factor is von willebrand factor associated with in plasma?

A

Factor VIII

79
Q

What is the role of tissue factor in the coagulation cascade?

A

Bind platelets and initiatethe coagulation cascade in response to endothelial damage

80
Q

For platelets to form a primary plug they need to…

A

Attach to the injured tissue
Activate: Change shape, Degranulate
Aggregate

81
Q

What factor controls the production of platelets?

A

Thombopoietin

82
Q

Which factor allows attachment of platelets to von willebrand factor?

A

Glycoprotein 1b

83
Q

What does GPIIb/IIIa bind?

A

vWF and fibrinogen so allows plt to plt attachment and clot stabilisation

84
Q

Why is it important for platelets to have a large surface area?

A

Coagulation factors are adsorbed onto surface
Activation fibrinogen
Thrombin activation

85
Q

Where is ADP released from in haemostasis and what is its function?

A

Granule

Plt activation and aggregation

86
Q

Where is serotonin released from in haemostasis and what is its function?

A

Granule

Vasoconstriction

87
Q

Where are fibrinogen and other clotting factors released from in haemostasis and what is their function?

A

Granule

Promotion clotting cascade and secondary plug formation

88
Q

Where is thromboxane A2 released from in haemostasis and what is its function?

A

From phospholipid via arachidonic acid pathway
Promotes release reaction, plt activation and aggregation and
vasoconstriction

89
Q

Where is platelet activation factor released from in haemostasis and what is its function?

A

Granule

Plt aggregation

90
Q

What does the coagulation cascade consist of and where are they made?

A

Pro-enzymes and pro-cofactors that are produced by the liver

91
Q

What initiates the coagulation cascade?

A

Tissue factor is activated (on injured cells) and binds to factor VII forming TF-VIIa complex

92
Q

How do platelets contribute to the coagulation cascade?

A

Provide phospholipid surfaces for the coagulation factors to react on

93
Q

What is the role of thrombin?

A

Converts plasma fibrinogen to fibrin
Amplifies production of coagulation molecules: Activates factor XI, Cleaves factor VIII from vWF, Activates factor V to Va
Helps stabilise the clot by activating factor XIII
Encourages platelet aggregation
Binds to thrombomodulin to activate protein C (inhibits coagulation)

94
Q

What does antithrombin inhibit?

A

Thrombin, Xa, IXa and XIa

95
Q

What does tissue factor pathway inhibitor inhibit?

A

Tissue factor/VIIa

Xa

96
Q

What do activated protein c and protein s inhibit?

A

Factor Va and VIIIa

97
Q

What is antithrombin activated by?

A

Heparin

98
Q

What are protein c and protein s dependent on?

A

Vitamin K

99
Q

What activates protein c?

A

Thrombin-thrombomodulin complex

100
Q

What factors of the coagulation cascade does prothrombin time measure?

A

VII, X, V, II and fibrinogen

101
Q

What may cause an abnormal prothrombin time?

A

DIC, Liver disease, Warfarin

102
Q

What factors of the coagulation cascade does activated partial thromboplastin time measure?

A

XII, X, IX, VIII, V, II, fibrinogen

103
Q

What may cause an abnormal activated partial thromboplastin time?

A

DIC, Liver disease, haemophilia A and B

104
Q

What factor does the thrombin time measure?

A

Fibrinogen

105
Q

What may cause an abnormal thrombin time?

A

DIC, heparin, fibrinolysis

106
Q

What does a D dimer test measure?

A

Fibrinogen break down products. Positive test if accelerated or increased break down

107
Q

What is Hereditary haemorrhagic telangiectasia?

A

Autosomal dominant inherited condition, with dilated microvascular swellings in mucous membranes and possible arterio-venous malformations in organs due to abnormal blood vessel formation
Easy bruising and spontaneous bleeding from mucosa

108
Q

What will blood test results show in a patient with hereditary haemorrhagic telangiectasia?

A

Blood tests will be normal

109
Q

What are treatment options for hereditary haemorrhagic telangiectasia?

A

Symptomatic, Tranexamic acid helps to reduce bleeding

110
Q

What is Ehlers-Danlos syndrome?

A

Collection of inherited conditions of connective tissue
Joint hypermobility
Stretchy skin
Fragile skin tissue

111
Q

What is Marfans?

A

Genetic disorder of connective tissue
Defects of heart valves
Long limbs
Misfolding of fibrillin-1, glycoprotein which forms elastic fibers in connective tissue and contributes to cell signaling activity by binding to and sequestering TGF-β

112
Q

What are some inherited causes of vessel wall abnormalities?

A

Hereditary haemorrhagic telangiectasia
Ehlers-Danlos syndrome
Marfans

113
Q

What are some acquired causes of vessel wall abnormalities?

A 
Vitamin C deficency (impaired collagen production)
Steroid therapy
Senile purpura
Amyloid in blood vessels
Immune complex deposition
Vasculitis e.g. Henoch-Schonlein purpura
114
Q

What is Henoch-Schonlein purpura?

A

Rare condition of vasculitis resulting in a rash and joint and abdo pain
Can affect people of any age, but majority of cases in under 10s
Blood vessels throughout body become irritated and swollen, so bleeding into skin and problems affecting kidneys and bowel

115
Q

What (broadly) are problems due to platelets which lead to abnormal bleeding?

A

Low platelet numbers: thrombocytopenia, symptomatic around 10x10(9)/L
Disordered platelet function

116
Q

What clinical features would you expect to see with abnormally reduced platelet function/numbers?

A

Easy bruising of the skin, often with petechiae, purpura and ecchymoses
Muscosal bleeding

117
Q

What are some congenital causes of abnormally low platelets?

A

Aplastic anaemia: pancytopenia caused by bone marrow loss
Wiscott-Aldrich syndrome: rare X-linked recessive disease, eczema, thrombocytopenia, immune deficiency, and bloody diarrhoea
Infection e.g. rubella

118
Q

What are some acquired causes of abnormally low platelets?

A

Deficient platelet production: bone marrow problem, cytotoxic drugs
Accelarated platelet destruction: Autoimmune, drugs (heparin), DIC, TTP (thrombotic thrombocytopenic purpura), hypersplenism

119
Q

What is autoimmune thrombocytopenia?

A

Autoimmune antibodies directed at platelets which are prematurely destroyed
Can present in childhood or adulthood

120
Q

What is childhood autoimmune thrombocytopenia?

A

Often follows a viral illness
Initially presents like leukaemia
Autoimmune antibodies directed at platelets
Platelets are prematurely destroyed

121
Q

What is the prognosis for childhood autoimmune thrombocytopenia?

A

80% regress spontaneously and have mild clinical symptoms

20% develop severe chronic immune thrombocytopenia

122
Q

What treatment is available for childhood autoimmune thrombocytopenia?

A

Those with severe symptoms e.g. GI bleed may require immune support i.e. steroids or immunoglobulins

123
Q

What are causes of adult onset autoimmune thrombocytopenia? And who is most likely to get it?

A

Normally chronic, M:F= 1:4, autoantibody may be detectable in plasma
Idiopathic
Secondary to malignancy e.g. chronic lymphocytic leukaemia, infection e.g. EBV, HIV or connective tissue diseases e.g. SLE

124
Q

What are treatment options for adult onset autoimmune thrombocytopenia?

A

Depends on level of platelets and clinical symptoms
Prednisolone
Intravenous Ig
Immunosuppressives e.g. rituximab or chemotherapy
Synthetic thrombopoietin analogues
Chronic symptoms + Non-response to therapeutics = SPLENECTOMY

125
Q

How can quinine and heparin lead to adult onset autoimmune thrombocytopenia?

A

Drug + plasma protein= antigen
Antibody formed to antigen
Antigen- Antibody complex forms in plasma
Ag-Ab complex adsorbed onto platelet surface which targets them for destruction

126
Q

Describe what happens in thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome

A

Thrombosis in small blood vessels
RBC fragmentation and haemolytic anaemia
Thrombocytopenia

127
Q

What can be complications of thrombotic thrombocytopenic purpura?

A

Fever, CNS deficits and liver dysfunction

128
Q

What can be complications of haemolytic uraemic syndrome?

A

Renal failure, hypertension, seizures

129
Q

What is thrombotic thrombocytopenic purpura?

A

Rare disorder of coagulation system, extensive microscopic thombi to form in small blood vessels throughout body which can damage kidneys, heart and brain
Associated with autoimmune, pregnancy and infection
Most cases arise from inhibition of ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor into smaller units. Increase in circulating multimers of vWF increase platelet adhesion to areas of endothelial injury, particularly at arteriole-capillary junctions

130
Q

What is haemolytic uraemic syndrome?

A

Characterized by haemolytic anemia, acute kidney failure (uremia), and thrombocytopenia
Predominantly affects children. Most cases preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from contaminated water supply, caused by E. coli, Shigella, Campylobacter and some viruses

131
Q

What would you expect to see on blood tests for thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome?

A

Lactate dehydrogenase raised
PT and APTT normal
FBC: Haemolytic anaemia, low platelets
Plasma bilirubin

132
Q

What are treatment options for thrombotic thrombocytopenic purpura?

A

Plasma exchange with fresh frozen plasma
Antiplatelet drugs
Immunosuppressives

133
Q

What are some causes of abnormal function of platelets?

A

Inherited: Defective GP1b ie. Berard-Soulier
Defective GPIIb/IIIa i.e. Glanzmann thrombasthaemia
Storage pool diseases
von Willebrand Disease
Acquired: drugs e.g. Aspirin and other NSAIDS

134
Q

What blood test results might you expect with abnormally functioning platelets?

A

FBC: normal platelet counts
Abnormal PFA-100 (platelet function analyser)
Disordered platelet aggregation

135
Q

Which factor is affected in haemophilia A?

A

VIII

136
Q

What type of inheritance does haemophilia A have?

A

X linked

1:5000 males

137
Q

What factor is affected in haemophilia B/Christmas disease?

A

IX

138
Q

How is haemophilia B inherited?

A

X linked

1:30000 males

139
Q

How is von willebrand disease inherited?

A

Autosomal dominant

140
Q

If a female carrier of haemophilia A and a normal male have children, what are the probabilities those children will have haemophilia A?

A

50% chance daughter carrier

50% chance son has disease

141
Q

What are clinical features of haemophilia A?

A

Normally presents in childhood

Bleeding into joints and muscles common, can cause disability (haemarthrosis)

142
Q

What would blood tests show in a haemophilia A patient?

A 
APTT- prolonged
PT- Normal
PFA-100- Normal
Reduced Plasma FVIII
DNA analysis can be useful in carrier detection or for antenatal screening
143
Q

What are treatment options and things that should be put into place for haemophilia A patients?

A

Infusions of FVIII- 20-50% normal for everyday

Register with Haemophilia Centre and carry card

144
Q

What should haemophilia A patients avoid?

A

Antiplatelet drugs

Intramuscular injections

145
Q

What can occur as a result of giving haemophilia A patients factor VIII infusions?

A

Some patients develop neutralising antibody to FVIII

146
Q

What would blood test results show in a patient with haemophilia B?

A 
APTT- prolonged
PT- Normal
PFA-100- Normal
Reduced Plasma F IX
DNA analysis can be useful in carrier detection or for antenatal screening
147
Q

What factors are affected in von willebrand disease?

A

vWF and FVIII (carried by and stabilised by vWF in plasma)

148
Q

What would blood test results look like in von willebrand disease?

A 
APTT- prolonged
PT- Normal
FVIII and VWF levels reduced
PFA- 100 prolonged
Reduced platelet aggregation
FBC- may see mild thrombocytopenia
DNA analysis can be useful in carrier detection or for antenatal screening
149
Q

What are treatment options for von willebrand disease?

A

vWF and FVIII concentrates

Fibrinolytic inhibitors e.g. tranexamic acid

150
Q

What blood clotting test results might you expect to see in liver disease?

A 
PT: increase 
APTT: increase 
TT: normal/increase 
Platelets: reduced 
Other: dysfibrinaemia
151
Q

What blood clotting test results would you expect to see in DIC?

A 
PT: increase 
APTT: increase 
TT: increase 
Platelets: reduced 
Other: D dimer increase, RBC fragments
152
Q

What blood clotting tests would you expect to see in vitamin K deficiency?

A

PT: increase
APTT: increase or normal
TT: normal
Platelets: normal

153
Q

What blood clotting test results would you expect to see in someone taking oral anticoagulants?

A

PT: increase
APTT: increase
TT: normal
Platelets: normal

154
Q

What blood clotting test results would you expect to see in someone taking heparin?

A 
PT: increase 
APTT: increase 
TT: increase 
Platelets: normal 
Other: anti Xa reduced
155
Q

What clotting abnormalities does liver disease result in?

A

Reduced synthesis of vitamin K dependent factors
Impaired synthesis of other coagulation factors
Thrombocytopenia and abnormal platelet function
Impaired fibrinolysis
Reduced protein C and S and antithrombin
Dysfibrinogenaemia

156
Q

What is Virchows triad?

A

Abnormal flow
Abnormal endothelium
Abnormal coagulation

157
Q

What tends to be the cause of arterial thombus formation?

A

Abnormal endothelium

158
Q

What tends to be the cause of venous thrombus formation?

A

Abnormal flow

159
Q

What are the different fates of thrombi?

A

Recanalised, embolised, propagate, dissolve

160
Q

Name some risk factors for thrombosis which cause endothelial cell damage

A 
Hypertension
Smoking
Diabetes
Hyperlipidaemia
Hyperhomocysteine
Polycythaemia
Increased F VIII
Increased fibrinogen
Lupus 
Heparin therapy
161
Q

Name some risk factors for thrombosis which result in abnormal blood flow

A 
Cardiac failure
Oedema
Nephrotic syndrome
Post-operative bed rest
Immobility
Trauma
Obstruction
162
Q

Name some risk factors for thrombosis which result in abnormal coagulation

A

Coagulation factors: Inherited: Factor V Leiden, Deficiency in Protein S or C, Antithrombin deficiency, Prothrombin mutation
Acquired: Hyperoestrogenaemia, Malignancy, Pregnancy, Lupus, Raised homocysteine
Blood cells: Polycythaemia, Thrombocythaemia

163
Q

What is the most common inherited thrombophilia?

A

Factor V Leiden mutation

Activated factor V Leiden is resistant to inactivation by protein C Increases risk thrombosis 80 fold in homozygotes

164
Q

What protein deficiencies can result in thrombophilia?

A

Protein S (PS) or Protein C (APC) deficiency

165
Q

What is the mechanism of action of clopidogrel?

A

Inhibits ADP receptor on platelets so prevents activation and cross linking

166
Q

What is Dipyridamole?

A

Phosphodiesterase inhibitor, raises platelet cAMP levels so prevents platelet aggregation

167
Q

What is abciximab?

A

Glycoprotein IIb/IIIa antagonist so prevents platelet aggregation

168
Q

Name some indications for Antiplatelet drugs

A

Thrombotic episode
Post CABG or stenting
Peripheral vascular disease
Thrombocytosis

169
Q

Describe the mechanism of action of fibrinolytic therapy

A

Enhance conversion of plasminogen to plasmin i.e. degrades fibrin

170
Q

When might you use fibrinolytic therapy?

A

Within 5-7 days of a venous thrombosis

Within hours of an arterial thrombosis e.g. post MI or ischaemic stroke

171
Q

What are contraindications to fibrinolytic therapy?

A

Active GI bleeding
Head injury or recent neurosurgery
Bleeding disorders

172
Q

What are some side effects of fibrinolytic therapy?

A

Bleeding

Anaphylaxis with streptokinase

173
Q

What are the different types of fibrinolytic therapy?

A

Streptokinase: Directly activates plasminogen, Due to antibodies, loading dose is required, Ineffective after 4-10 days
Urokinase: Similar action, can be used when high levels of anti-
streptococcal antibodies present
Acylated plasminogen streptokinase activator complex: Activates streptokinase bound to plasminogen
Recombinant tissue plasminogen activator (rTPA): Causes activation of fibrin bound plasminogen

174
Q

What are indications for anticoagulation?

A

Acute thrombosis (heparin) and chronic reduction in risk (Warfarin)

175
Q

What is Dabigatran?

A

Direct thrombin inhibitor

176
Q

How do you administer heparin?

A

Unfractionated: IV
LMWH: Sub-cut

177
Q

What is tinzaparin?

A

Low molecular weight heparin

Anticoagulant

178
Q

How is warfarin administered?

A

PO (per os, orally)

179
Q

How is heparin use monitored?

A

APTT

180
Q

How is warfarin use monitored?

A

INR (PT)

181
Q

What is rivaroxaban?

A

Factor Xa inhibitor

182
Q

What is bivalirudin?

A

Direct thrombin inhibitor

183
Q

How does warfarin work?

A

Inhibits vitamin K epoxide reductase which inhibits carboxylation activity of glutamyl carboxylase and therefore coagulation factors II, VII, IX, X are not activated

184
Q

How do you monitor the effect of dabigatran?

A

Thrombin time

185
Q

What is the mechanism of action of heparin?

A

Inhibits antithrombin III causing a conformational change resulting in its activation through an increase in flexibility of its reactive site loop
Activated AT then inactivates thrombin and factor Xa

186
Q

Which out of unfractioned and low molecular weight heparin has the least side effects and most targeted effect?

A

Unfractionated heparin greater risk of side effects

LMWH has a more targeted effect

AC1 (18 decks)

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