Haematology Otago 4Th Year Medicine

Front 1

Three mechanisms that cause Anaemia

Back 1

Breakdown (Haemolysis)

Decreased production

Sequestration in the spleen (Hypersplenism)

Front 2

Symptoms of Anaemia

Back 2

Tiredness, decreased exercise tolerance, SOBOE, palpitations, headaches

Front 3

Signs of Anaemia (remember the difference between symptoms and signs!)

Back 3

Tachycardia

Heart Murmurs

Retinopathy (if long term)

Front 4

What are some common causes of Anaemia?

Back 4

Iron deficiency

B12/Folate deficiency

Chronic Disease

Bleeding

Bone Marrow Infiltration

Autoimmune Haemolytic Anaemia

Front 5

What are some causes of Microcytic Anaemia?

Back 5

Remember the big three:

Iron Deficiency

Thalassemia

Anaemia of Chronic Disease

Then you have the others

Myelodysplasia

Lead Poisoning

Front 6

What is the daily requirement of iron for Men?

Back 6

1mg

Front 7

What is the daily Iron requirement for premenopausal women?

Back 7

2mg

Front 8

What are some causes of Iron Deficiency?

Back 8

Dietary lack

Malabsorption

Increased demand

Increased loss

Front 9

What are symptoms of Iron Deficiency?

Back 9

Anaemia symptoms listed previously +

Painful mouth

Dysphagia

Pica

Increased infections

Impaired growth

Front 10

What are some signs of Iron Deficiency?

Back 10

Glossitis

Blue Sclera

Angular Stomatitis

Koilonychia (spoon nails)

Front 11

In Iron deficiency, what would be the findings on a blood film?

Back 11

Smaller, lighter RBCs (microcytic, hypochromic anaemia), poikilocytes (pencil cells), target cells, increased platelets

Front 12

What would be the results from iron studies in iron deficiency? (Ferritin, Serum Iron, Iron Saturation, Transferrin)

Back 12

Ferritin, Serum Iron and Saturation goes down, Transferrin goes up

Front 13

Upon suspicion of Iron Deficiency, what are some important points to investigate in history?

Back 13

Menstrual history, GIT abnormalities, obvious bleeds.

Basically, BLEEDS.

Remember, always try to find the CAUSE of the iron deficiency. Don't want to get screwed over in court if you don't.

Front 14

What are some causes of Macrocytic Anaemia?

Back 14

B12 and/or Folate deficiency, Drugs (causes of Megaloblastic Anaemia)

Newborns

Alcoholism, liver disease

Hypothyroidism

Haemolysis

Marrow Disorders

And of course, Idiopathic

Front 15

What does the Anaemia of Chronic Disease look like on a blood film?

Back 15

Hypochromic, Normocytic anaemia

Front 16

How can you distinguish between Anaemia of Chronic Disease and other anaemias?

Back 16

History

Blood Film

Anaemia of Chronic Disease tends to be less severe

Front 17

What is Anaemia of Chronic Disease associated with?

Back 17

Infection

Chronic Inflammation

Cancer

Front 18

Describe the pathogenesis of the Anaemia of Chronic Disease

Back 18

Decreased RBC survival

Decreased EPO secretion

Decreased marrow response to EPO

Iron limited Erythropoiesis

Front 19

What are some clinical features of Megaloblastic Anaemia?

Back 19

Angular Stomatitis, Glossitis, Anaemia, Purpura, Infection, Jaundice, Malabsorption and thus weight loss

Front 20

What will a Blood Film reveal in Megaloblastic Anaemia?

Back 20

Macrocytosis

Neutropenia

Hypersegmented Neutrophils

Thrombocytopenia

Oval Macrophages

Front 21

What other investigations (other than a FBC and Blood Film) would you order for investigation of Megaloblastic Anaemia?

Back 21

Serum B12 and Folate

Bone Marrow Aspirate

Front 22

Why might a Cervical Smear look abnormal in Megaloblastic Anaemia?

Back 22

B12 and Folate are needed for DNA replication, so in deficiency, any replicating cells will be affected.

Front 23

Where in the bowel is Folate absorbed?

Back 23

Proximal Small Bowel

Front 24

What are some common causes of Folate Deficiency?

Back 24

Pregnancy

Decreased intake (Food faddism, cooking, chronic illness, alcohol, poverty)

Increased cell proliferation

Malabsorption (esp Coeliac disease)

Drugs (anticonvulsants, OCP, antibiotics, methotrexate)

Front 25

Where in the bowel is B12 absorbed?

Back 25

Terminal Ileum

Front 26

What are some common causes of B12 deficiency?

Back 26

Pernicious anaemia

Veganism

Gastrectomy

Intestinal disorders

Front 27

What investigations would you order if you suspect B12 deficiency?

Back 27

FBC

Serum B12

Intrinsic Factor Antibodies

Front 28

In Haemolytic Anaemia, what will you see on investigation?

Back 28

Signs of RBC breakdown, so:

Anaemia

Increased bilirubin

Increased LDH

Decreased Haptoglobin

Also signs of increased RBC production:

Reticulocytes

Marrow Hyperplasia

Front 29

(I found this useful to know) What is Haptoglobin?

Back 29

Protein in the blood that binds to free Haemoglobin outside RBCs

Front 30

What measure is used to determine Haemolytic Anaemia?

Back 30

Urinary Haemosiderin

Front 31

What are the two divisions of the causes of Haemolytic Anaemia?

Back 31

Intravascular

Extravascular

Front 32

What are the Extravascular causes of Haemolytic Anaemia further divided into?

Back 32

Spherocytic and Non-spherocytic anaemia

Front 33

What is the normal composition of Adult Bone Marrow?

Back 33

50% Haematopoietic tissue and 50% fat

Front 34

What are 3 potential problems with the bone marrow?

Back 34

Anaplastic Anaemia

Leukaemia infiltrating the bone marrow

Toxicity destroying the marrow

(surely there are more but these re 3 from the notes)

Front 35

Differential Diagnosis for Pancytopenia?

Back 35

Anaplastic Anaemia, Bone Marrow Infiltration, Myelodysplasia, Megaloblastic Anaemia, Hypersplenism, Miscelaneous e.g. alcohol, infection

Front 36

What will a Bone Marrow aspirate reveal in Anaplastic anaemia?

Back 36

fat cells of the Bone Marrow, but no haematopoietic tissue

Front 37

What may cause Anaplastic Anaemia?

Back 37

An intrinsic defect in the stem cells (either they are dysfunctional, or have reduced production)

Extrinsic damage to stem cells (immune or toxins)

Most common: idiopathic (most likely immune) or drugs

Front 38

Why is Anaplastic Anaemia a medical emergency?

Back 38

Can get infection (reduced WBC) or die from bleeding (thrombocytopenia)

Front 39

How do you manage a patient with Anaplastic Anaemia?

Back 39

ADMIT

Give Antibiotics within 1 hour of admission

Give platelets and RBC transfusion

If cause is immune, immunosuppress

If younger: consider stem cell transplant

If older: the problems are co-morbidities, and Graft Vs Host disease (more common in elderly)

Front 40

What are Haematopoietic Stem Cells?

Back 40

Multipotent cells residing in the bone marrow. Can form any of the blood cell lineages, depending on the cytokines they are exposed to.

Only viable in bone marrow, and have the power of self renewal in the bone marrow

Front 41

Name some Haematopoietic cytokines (don't think these are really too important. Wouldn't spend too much time on them)

Back 41

EPO

Thrombopoietin

G-CSF (neutrophil production)

GM-CSF

Stem cell factor

IL3

Front 42

In what clinical events are Acute Phase Reactant levels altered?

Back 42

Infection

Malignancy

Inflammatory state

Tissue injury

Front 43

Which acute phase reactants increase in infection, malignancy, inflammation or injury?

Back 43

Fibrinogen, Haptoglobin (decreases in haemolytic anaemia), CRP,

vWF, complement, Factor VIII, Ferritin

Front 44

Which acute phase reactants decrease in infection, malignancy, inflammation or injury?

Back 44

Albumin

Prealbumin

Transferrin

Front 45

What are 2 commonly used investigations that test for Acute Phase Reactants?

Back 45

ESR and CRP

Front 46

When is the ESR test used?

Back 46

Diagnostic aid in uncertain circumstances

For monitoring specific diseases e.g. Temporal Arteritis, Polymyalgia Rheumatica, Rheumatoid Arthritis

NOT used as an asymptomatic screen

Front 47

What are the limitations of the ESR?

Back 47

Will increase the faster the RBC drop

Will increase with Rouleaux effect

Front 48

Describe the C Reactive Protein

Back 48

Synthesized in the liver

Part of the Innate Immune System

Binds to surface of dying cells and bacteria, activating compliment for phagocytosis

Rises within 6 hours after the stimulus

No diurnal variation or effect from drugs

Front 49

When is the CRP test used?

Back 49

To monitor patients at risk of infection

Front 50

What are some causes of Neutrophilia?

Back 50

Inflammation, Cancer, Blood Disorders, Infections, Acute bleeding, Acute Haemolysis, Physiological

Front 51

What feature on blood film indicates infection?

Back 51

Left Shift

Front 52

Describe the toxic changes in Neutrophils

Back 52

Increased granules

Increased Vacuoles

Dohle bodies

Nuclear clumping

Occur due to switch to protein synthesis

Front 53

What is Virchow's Triad?

Back 53

Triad of changes causing increased risk of thrombosis

Changes to Blood

Changes to Blood Vessels

Changes to Flow

Front 54

What are some causes of change in blood?

Back 54

Decreased Fibrinolysis

Increased vWF, Factor VIII, Fibrinogen

Front 55

What are some causes of change in blood flow?

Back 55

Surgery

Immobilization

Anaesthesia

Local Pressure

e.g.velocity is reduced when standing and further on sitting.

Sitting also increases pressure the popliteal fossa

Front 56

What are some causes of change in vessel wall?

Back 56

Burns

Endotoxin

Hypoxia

Direct trauma

Front 57

What are signs of Venous Thromboembolism in the leg?

Back 57

Redness, swelling, tenderness, dilated veins

Front 58

What are the more common causes of primary (inherited) hypercoagulable state?

Back 58

Factor V leiden, Prothrombin Gene Mutations

Front 59

What are some causes of secondary hypercoagulable state?

Back 59

Malignancy, Pregnancy, Surgery, Trauma, Stasis, Myeloproliferative Disorders, Antiphospholipid disorders, Age, Dehydration => Viscosity, Drugs

Front 60

Janine, 63, is flying from Auckland to San Francisco in December. What risk factors for Venous Thrombosis will you look for in her before she departs

Back 60

Hormonal Therapy (increased Oestrogen causes slight hypercoagulable state), Surgery, Malignancy, Immobilization, Obesity, Previous VTE, Significant family history, Pregnancy (unlikely in this patient)

Front 61

Janine, 63, is flying from Auckland to San Francisco in December. What will protect her from VTE onboard her flight?

Back 61

Aisle Seats

Compression Stockings

Front 62

Janine, 63, is flying from Auckland to San Francisco in December. She asks you about using Aspirin for VTE prophylaxis, because she saw it on a forum website on Google. What will you tell her?

Back 62

Aspirin is not such a good idea: Increased risk of upper GI bleeding. LMWH a better drug (but of course you aren't going to jump straight to meds before anything else and if she is not particularly concerning)

Front 63

Describe Polycythaemia

Back 63

An increase in total RBC mass

Can be spurius: an example is dehydration

Front 64

How does Polycythaemia lead to an increase in Thrombosis risk?

Back 64

increased haematocrit therefore increased blood viscosity

Front 65

What causes primary Polycythaemia?

Back 65

Myelodysplasia

Front 66

What causes secondary Polycythaemia?

Back 66

Driven by EPO metabolism, anything that lowers O2 concentration. Causes can be normoxic (renal diseases e.g. RCC, renal stenosis, liver disease, tumors, esp. posterior cerebellar tumors) or hypoxic (high altitude, pulmonary disease, abnormal Hb, cyanotic heart disease, hypoventilation syndromes)

Front 67

What are symptoms of Polycythaemia rubra vera?

Back 67

Headache, weakness, pruritis, dizziness, sweating

Front 68

What are signs of Polycythaemia rubra vera?

Back 68

Hepatosplenomegaly, flushed appearence, skin and conjunctival plethora

Front 69

What will investigation produce in Polycythaemia rubra vera?

Back 69

Low EPO

High RBC, neutrophils, platelets, Hb

Hypercellular Bone Marrow

Front 70

Most common cause of death in Polycythaemia Rubra Vera is...

Back 70

thrombotic event

Front 71

How would you treat someone with Polycythaemia Rubra Vera?

Back 71

Phlebotomy, Anti-platelet agents, Marrow suppressing agents

Front 72

What genetic mutation causes polycythaemia rubra vera? (doubt this is important)

Back 72

JAK2 gain of function. Codes for tyrosine kinase signal trandsucer for EPO receptors

Front 73

What causes Iron Overload?

Back 73

Haemochromatosis, transfusion

Front 74

Describe the genetics of Haemochromatosis

Back 74

Variable penetrance

C282Y (most common and potent), and H63D (doubt these are important)

Front 75

What organs does Iron Overload affect?

Back 75

Liver: cirrhosis and hepatocellular cancer

Pancreas: Diabetes

Joints

Testes

Heart

Skin

Front 76

What would the results of blood tests look like in Iron Overload?

Back 76

High Ferritin

Fasting transferrin saturation over 45%

Front 77

What further investigations would you order for Iron Overload?

Back 77

Liver Biopsy and Quantitative Fe MRI

Front 78

How do you treat Iron Overload?

Back 78

Phlebotomy

Front 79

What are Myeloproliferative disorders?

Back 79

A primary clonal proliferation of Myeloid cells, that can affect any of the three cell lineages.

Front 80

What is the most common cause of Myeloproliferative disorders in outpatients?

Back 80

Iron deficiency

Front 81

When are increased platelets most commonly seen?

Back 81

After Surgery or Trauma

Front 82

What does Leukoerythroblastosis imply?

Back 82

Disturbance of the blood/marrow barrier

Front 83

What do you see on blood film in Leukoerythroblastosis?

Back 83

Nucleated RBCs and immature neutrophils

Front 84

What are some causes of Leukoerythroblastosis?

Back 84

Immaturity of bone marrow, toxicity, hypoxia, mechanical damage, tumor, septicaemia, respiratory failure, haemolysis, extramedullary haematopoiesis

Front 85

What is Extramedullary Haematopoiesis?

Back 85

Making cells outside the bone marrow (no blood marrow border).

Common in myeloproliferative disorders, especially Myelofibrosis.

Front 86

What are common sites for Extramedullary Haematopoiesis?

Back 86

Spleen, Liver. There is always splenomegaly.

Front 87

What are symptoms in Chronic Granulocytic Leukaemia?

Back 87

Fatigue, bleeding, weight loss, splenomegaly.

May be an incidental finding.

Front 88

What would be the blood count, bone marrow aspirate and biochemistry results in Chronic Granulocytic Leukaemia?

Back 88

High WBC. Anaemia, High platelets,

Hyperplastic Bone Marrow full of WBCs

High Uric Acid due to high cell turnover

Front 89

What mutation is Chronic Granulocytic Leukaemia associated with?

Back 89

Philadelphia Translocation (Reciprocal 9:22 translocation)

Front 90

How would you treat Chronic Granulocytic Leukaemia?

Back 90

Hydroxyurea (slows time course but doesn't cure) and imatinab

Other options:

Interferon

Bone Marrow Transplant

Front 91

Describe the progression of Chronic Granulocytic Leukaemia.

Back 91

Three phases: Chronic, Accelerated, Blast Transformation (blast transformation is acutely aggressive and rapidly fatal)

Time course is usually around 3 years

Front 92

Describe Chronic Idiopathic Myelofibrosis

Back 92

Slow onset condition, in which marrow fills up with Collagen and Scar tissue

Front 93

30% of cases of Chronic Idiopathic Myelofibrosis are preceded by...

Back 93

Polycythaemia vera

Front 94

Describe the signs and symptoms of Chronic Idiopathic Myelofibrosis

Back 94

Anaemia symptoms

Weight Loss

Night Sweats

Massive Hepatosplenomegaly, causing problems e.g. early satiety

Splenic infarcts causing lots of pain

Front 95

There is massive splenomegaly and painful splenic infarcts in Chronic Idiopathic Myelofibrosis. How can we reduce the size of the spleen?

Back 95

Surgery, radiotherapy, or chemotherapy

Front 96

What are findings on blood count, blood film and bone marrow aspirate in Chronic idiopathic myelofibrosis?

Back 96

Anaemia, WBC and platelets high early and low late

Tear drop RBCs

Collagen fibrosis in bone marrow

Front 97

How do you treat Chronic idiopathic myelofibrosis?

Back 97

Observation, Chemotherapy, Splenectomy if symptomatic, stem cell transplant if young and chance of a cure

Front 98

What is the mean survival time for Chronic idiopathic myelofibrosis?

Back 98

3-4 years

Front 99

10% of patients with Chronic Idiopathic Myelofibrosis go on to develop...

Back 99

Acute Leukaemia

Front 100

In what age group is Essential Thrombocythaemia most common?

Back 100

Elderly, but seen in all age groups

Front 101

Describe Thrombocythaemia

Back 101

Higher than normal Platelet count.

Cause is either primary or secondary

Front 102

What are some primary causes of Thrombocythaemia?

Back 102

Essential Thrombocythaemia

Another Myeloproliferative disorder

MUST DETERMINE IF THROMBOCYTHAEMIA IS PRIMARY OR SECONDARY

Front 103

What are some secondary causes of Thrombocythaemia?

Back 103

Generally indicates reactive process

Iron Deficiency Anaemia

Haemorrhage

Trauma

Malignancy

Inflammation

Post-splenectomy

Front 104

What does Bone Marrow aspirate reveal in Essential Thrombocythaemia?

Back 104

Increased numbers of enlarged, mature, megakaryocytes.

Front 105

What are some symptoms and signs of Essential Thrombocythaemia?

Back 105

Often Asymptomatic

Patients can present with bleeding (dysfunctional platelets), thrombosis, or splenomegaly (can be similar to presenting symptoms and signs of Polycythemia Vera)

Front 106

What is revealed on blood count and blood film in Essential Thrombocythaemia?

Back 106

Increased platelets, abnormal platelet morphology and function (PFA100), normal or mild increase in WBC, normal or mild iron deficiency anaemia

Front 107

How do you treat Essential Thrombocythaemia?

Back 107

Observation, Aspirin (decrease risk of thrombosis), Anagrilide and Hydroxyurea (decreasing platelet count), Interferon

Front 108

What does Haemostasis involve?

Back 108

It is stopped bleeding. Involves Vasoconstriction, platelet activation and activation of coagulation cascade, leading to conversion of fibrinogen to fibrin.

Front 109

Define Blood Coagulation

Back 109

conversion of Soluble Fibrinogen to Insoluble Fibrin

Front 110

What is the lab test for the intrinsic system of the Coag Cascade?

Back 110

APTT

Front 111

What is the lab test for the extrinsic system of the Coag Cascade?

Back 111

PT/INR

Front 112

What is Thrombin time useful for?

Back 112

Monitoring Dabigatran

Front 113

Which factor converts fibrin to cross-linked fibrin?

Back 113

XIIIa

Front 114

What are some acquired disorders of coagulation?

Back 114

liver disease, DIC, VitK deficiency, Uraemia, Massive blood transfusion, factor inhibitors

Front 115

What are some congenital disorders of coagulation?

Back 115

Haemophilia A and B, von Willibrand disease.

Can get other factor deficiencies but these are extremely rare.

Front 116

What is the role of the liver in Coagulation?

Back 116

Synthesizes a number of coagulation factors, inhibitors, fibrinolytics and carboxylases. REMEMBER VITK

Front 117

What is the end result of DIC?

Back 117

conversion of large amounts of fibrinogen to fibrin

Front 118

Describe the three pathways that lead to DIC

Back 118

Release of tissue Thromboplastin in the vasculature, through trauma, malignancy or major surgery.

Activation of Factor XII in endothelium, occuring in sepsis, burns, anoxia and acidosis

Activation of either factor X or II which occurs in pancreatitis or amnionic fluid emboli

Front 119

How dies DIC cause organ damage? Which organs are most susceptible to this?

Back 119

In DIC, get fibrin deposition in microvasculature and then you get clotting and ischaemic organ damage.

Kidneys and brain are susceptible to this.

Front 120

How does DIC cause microangiographic haemolytic anaemia?

Back 120

Fibrin cross-stranding shreds RBCs causing microangiopathic haemolytic anaemia

Front 121

What will be the result of Blood Tests in DIC?

Back 121

INR and APTT increased, Fibrinogen and Platelets decreased, FDPs increased (D-dimer)

Front 122

How do you manage a patient with DIC?

Back 122

TREAT THE CAUSE

In the meantime, give platelet transfusion, fresh frozen plasma and cryoprecipitate

Front 123

What are some causes of Vitamin K deficiency?

Back 123

Haemorrhagic disease in newborns, Dietary deficiency, Biliary obstruction (because fat soluble vitamin), Malabsorption, Liver disease, Warfarin, VVitamin E, antibiotics, hyantoids

Front 124

How does Renal Failure affect Haemostasis?

Back 124

causes defective platelets (somehow - PFA100 is prolonged)

Severity of coagulopathy correlates with severity of renal failure

Front 125

How do you treat Haemostasis issues due to Renal Failure?

Back 125

RBC transfusion, Vasopressin

Front 126

How does a massive blood transfusion cause coagulopathy?

Back 126

Only replacing RBCs, not factors, which get diluted.

Front 127

How do you treat coagulopathy due to Massive Blood Transfusion?

Back 127

Give platelets, fibrinogen and FFP

Front 128

What are factor inhibitors?

Back 128

Autoantibodies to factors, usually FVIII or FIX

Front 129

How do you distinguish between simple factor deficiency and an inhibitor? (very important to do this)

Back 129

Do a 1:1 mix. If the coagulopathy corrects, it is a factor deficiency. If not, it is an inhibitor

Front 130

A 14 year old girl comes in with easy bruising. Her APTT is elevated, PFR100 low-ish. What do you suspect?

Back 130

von Willebrand's disease. Do a von WIllebrand screen

Front 131

A 14 year old girl comes in with easy bruising. Her APTT is elevated. PFR is fine. What do you do to further investigate?

Back 131

Suspect Haemophilia.

Test F VIII THEN F IX if VIII is negative(VIII is more common)

If still negative, start testing the other factors, cos this is going to be a rare one.

When you find the problem factor, do a 1:1 mix, to check for inhibitors

Front 132

What is Tranexamic Acid?

Back 132

Antifibrinolytic. Blocks antithrombin

Front 133

How do you treat someone bleeding and having inhibitors, to Factor VIII?

Back 133

Give infusion of F VIIa

Front 134

What is the most common form of adult leukemia?

Back 134

Chronic Lymphoid Leukaemia. Does not require urgent treatment

Front 135

How is Leukaemia categorized?

Back 135

Acute or Chronic. Further divided into Granulocytic and Lymphocytic

Front 136

What is the clinical course for Acute Leukaemia?

Back 136

Rapid onset, rapid demise if not treated

Front 137

What are the symptoms caused by in Acute leukaemia?

Back 137

Either marrow failure or tissue infiltration

Front 138

What other thing associated with Cancers can cause marrow failure and tissue infiltration?

Back 138

Chemotherapy. More of an issue in chronic cases

Front 139

What are the signs of Acute Leukaemia?

Back 139

Anaemia, bleeding, infection (from pancytopenia due to marrow failure)

Hepatosplenomegaly

Lymphadenopathy

Bone pain (more common in children)

Front 140

What tests would you order if you suspect acute leukaemia?

Back 140

FBC, Bone Marrow sample, Cytochemistry, Immunology, Cytogenetics, Molecular Genetics.

Front 141

How do you distinguish between AML and ALL on the bone marrow analysis?

Back 141

In ALL cells in the Bone Marrow all look the same

In AML Auer Rods are a characteristic feature

Front 142

How do you manage a patient with Acute Leukaemia?

Back 142

Supportive care - antibiotics, platelets, blood transfusions

Cytotoxic treatment - at least 2-3 cycles

Hickman line

CNS prophylaxis

Stem Cell Transplant

Front 143

When analysing the bone marrow, what indicates leukaemia?

Back 143

If the blast numbers are over 20%

Front 144

How is remission defined?

Back 144

If the patient is clinically well, with a normal FBC, and the blast cells in the Bone Marrow are down to <5%

Front 145

What is Acute Promyelocytic Leukaemia caused by?

Back 145

a very specific gene translocation

Front 146

How do you manage a patient with Acute Promyelocytic Leukaemia?

Back 146

Give Supportive Care

Treat with ATRA

Front 147

A 17 year old woman comes in to ED due to car accident. Bleeding heaps, naturally, you wonder if she has Haemophilia. You test her FVIII and find it to be increased. Worried, you tell your consultant, and they look at you like you are an idiot. Why do they think you are an idiot?

Back 147

Because you are concerned by that! Factor VIII is an acute phase protein, so of course its gonna be raised! silly!