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Haematology Flashcards

1
Q

What are the components of blood

A 
Plasma 
Cells - RBC, WBC, platelets 
Clotting factors - fibrinogen
Glucose
Electrolytes - sodium and potassium 
Protein - immunoglobulins and hormones
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2
Q

What are pluripotent haematopoietic stem cells

A

Undifferentiated cells that have the potential to become a variety of blood cells

  • Myeloid
  • Lymphoid
  • Dendritic cells
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3
Q

How do red blood cells develop

A

Reticulocytes from the myeloid stem cells

Survive up to 3 months

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4
Q

How do platelets form?

A

Megakaryocytes

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5
Q

How are white blood cells formed

A

Myeloid stem cells become promyelocytes that become monocytes, neutrophils, eosinophils, mast cells, basophils
Lymphocytes from lymphoid stem cells and become B or T cells
B lymphocytes become plasma cells or memory B cells
T lymphocytes become CD4/CD8/ Naturasl killer cells

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6
Q

What is anisocytosis and what does it mean

A

Variation in size of RBC

Myelodysplastic syndrome and anaemia

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7
Q

What are target cells and what do they signify

A

Central pigmented area surrounded by pale area surrounded by thick ring of cytoplasm

Iron defiency anaemia and post splenecotmy

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8
Q

What are Heinz bodies and where are they seen

A

Individual blobs inside RBC - denatured globin

G6PD and alpha thalassaemia

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9
Q

What are Howell Jolly bodies and where are they seen

A

Individual blobs of DNA material seen inside RBC, normally the DNA material is removed by the spleen during RBC circulation

Post splenectomy or in severe anaemia

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10
Q

What are reticulocytes and where are they seen

A

Immature RBC - slightly larger than standard RBC and have RNA material in them
Reticular mesh inside

Haemolytic anaemia

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11
Q

What are schistocytes and where are they found?

A

Fragments of RBC
Indicate RBC physically damaged by trauma during their journey through the blood vessels
Indicate clots in small vessels

HUS
DIC
TTP
Metallic heart valves
Haemolytic anaemia
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12
Q

What are sideroblasts and where are they found

A

Immature RBC with blobs of iron
Occur when bone marrow unable to incorporate iron into Hb molecule

Myelodysplastic syndrome

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13
Q

What are smudge cells and where are they found

A

Ruptured white blood cells that occur in the process of preparing blood film due to aged or fragile white blood cells

CLL

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14
Q

What are spherocytes and what do they indicate

A

Spherical RBC without normal bi-concave shape

Autoimmune haemolytic anaemia or hereditary spherocytosis

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15
Q

List the causes of microcytic anaemia

A 
Thalassaemia 
Anaemia of chronic disease
Iron deficiency anaemia 
Lead poisoning
Sideroblastic anaemia
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16
Q

List the causes of normocytic anaemia

A 
Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
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17
Q

List the causes of macrocytic anaemia

A

Megaloblastic anaemia - B12 deficiency and folate deficiency

Normoblastic anaemia - Alcohol, reticulocytosis. hypothyroidism, liver disease, Drugs (azathioprine)

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18
Q

List some symptoms of anaemia

A 
Tired
Breathless
Headache
Dizzy 
Palpitations
Worsen of other conditions - angina, HF and PVD 
Pica - dietary cravings for abnormal things such as dirt 
Hair loss
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19
Q

List some signs of anaemia

A 
Pale skin 
Tachycardia
Raised respiratory rate
Conjunctival pallor 
Koilonychia - spoon shaped nails 
Angular cheilitis 
Atrophic glossitis - smooth tongue due to atrophy of the papillae and can indicate iron deficiency
Jaundice 
Brittle hair and nails 
Bone deformities - thalassaemia
Oedema, HTN, excoriations - CKD
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20
Q

How do you investigate anaemia

A 
Hb
MCV
B12
Folate
Ferritin 
Blood film
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21
Q

What further investigations may you do for someone with anaemia and unclear cause

A

OGD and colonoscopy 0 GI blood loss

Bone marrow biopsy

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22
Q

Where and how is iron absorbed

A

In the duodenum and jejunum

Relies on stomach acid to keep it in its soluble Fe2+ form instead of Fe3+ (ferric)

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23
Q

List some causes of iron deficiency anaemia

A

Medication - PPI (interfere with absorption)
Blood loss
Dietary insufficiency
Increased requirement - pregnancy

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24
Q

In what form does iron travel round the body

A

Ferric Fe3+ form bound to carrier protein transferrin

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25
Q

What is the total iron binding capacity

A

Total space on the transferrin molecules for the iron to bind

Related to the amount of transferrin in the blood

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26
Q

What is ferritin

A

Form iron takes when it is deposited and stored in cells

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27
Q

What causes release of ferritin

A

Inflammation - infection and cancer

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28
Q

What happens to ferritin in iron deficiency anaemia

A

Can be low or normal

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29
Q

What is transferrin saturation

A

Good indication of the total iron in the body
Normal = 30%

Transferrin saturation = serum iron/total iron binding capacity

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30
Q

How is iron deficiency anaemia managed

A

Blood transfusion
Iron infusion - cosmofer
Oral iron - ferrous sulphate 200mg tds - slowly corrects iron

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31
Q

Give some side effects of ferrous sulphate

A

Black stool

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32
Q

When is iron infusion avoided

A

Sepsis - feeds bacteria

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33
Q

How much of a rise in Hb can you expect per week when correcting iron deficiency with oral iron

A

10g/L/week

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34
Q

Describe B12 absorption

A

Gastric parietal cells secrete intrinsic factor

Intrinsic factor essential for absorption of B12 in ileum

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35
Q

What is pernicious anaemia

A

Autoimmune condition where antibodies form against the parietal cells or intrinsic factor
Lack of intrinsic factor prevents absorption of vitamin B12 and the patient becomes vitamin B12 deficient

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36
Q

Describe the neurological symptoms caused by Vitamin B12 deficiency

A

Pins and needles - peripheral neuropathy
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes

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37
Q

Describe the test for pernicious anaemia

A

Intrinsic factor antibody

Gastric parietal cell antibody - less helpful

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38
Q

Describe the management of pernicious anaemia

A

Oral replacement with cyanocobalamin
if dietary deficiency B12
If pernicious anaemia - 1mg hydroxocobalamin IM 3 times weekly for 2 weeks then every 3 months

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39
Q

Why is it essential to treat B12 deficiency before treating folate deficiency if a patient has both

A

Subacute degeneration of the cord

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40
Q

What is haemolytic anaemia

A

Destruction of red blood cells leading to anaemia

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41
Q

List some inherited haemolytic anaemias

A 
Hereditary spherocytosis
Hereditary elliptocytosis
Thalassaemia 
Sickle cell disease
G6PD deficiency
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42
Q

List some acquired haemolytic anaemias

A

Autoimmune haemolytic anaemia
Alloimmune - transfusion reaction and haemolytic disease of newborn
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolytic anaemia

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43
Q

Describe the features of haemolytic anaemia

A

Anaemia
Splenomegaly
Jaundice

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44
Q

Describe the investigations for haemolytic anaemia

A

FBC - normocytic anaemia
Blood film - schistocytes (fragments of RBCs)
Direct Coombs test - autoimmune haemolytic anaemia

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45
Q

What is the inheritance pattern of hereditary spherocytosis

A

Autosomal dominant

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46
Q

How does hereditary spherocytosis present

A

Jaundice
Gallstones
Splenomegaly
Aplastic anaemia in prescence of parvovirus

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47
Q

How is hereditary spherocytosis diagnosed

A

FH
Blood film - spherocytes
Mean corpuscular haemoglobin concentration (MCHC) is raised on a FBC
Reticulocytes will be raised due to rapid turnover of RBC

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48
Q

How is hereditary spherocytosis treated

A

Folate supplements
Splenectomy
Cholecystectomy if gallstones is a problem

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49
Q

What is the inheritance pattern for G6PD deficiency

A

X linked recessive

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50
Q

Who is G6PD deficiency more common in

A

Mediterranean and African

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51
Q

List some triggers for haemolytic anaemia crises in G6PD deficiency

A

Fava beans
Infection
Medication - antimalarials (primaquine), ciprofloxacin, sulfonylureas, sulfalazine and other sulphonamide drugs

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52
Q

What is found on a blood film in G6PD deficiency

A

Heinz bodies

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53
Q

What are the two types of autoimmune haemolytic anaemia

A

Warm

Cold

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54
Q

Describe warm autoimmune haemolytic anaemia

A

Antibodies against the RBC produced and work at normal or above nomral temperatures

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55
Q

What causes warm autoimmune haemolytic anaemia

A

Idiopathic

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56
Q

Describe cold autoimmune haemolytic anaemia

A

Cold agglutin disease
At lower temperatures the antibodies against RBC attach themselves to the RBC and cause them to clump together - agglutination
This results in the destruction of the RBC as the immune system is activated against them and gets fikltered and destroyes in the spleen

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57
Q

What is cold haemolytic anaemia secondary to

A

Lymphoma
Leukaemia
SLE
Infection - EBV, HIV, CMV, mycoplasma

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58
Q

How is autoimmune haemolytic anaemia treated

A

Blood transfusion
Prednisolone
Rituximab - CD20 monoclonal antibody
Splenectomy

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59
Q

Describe prosthetic valve haemolysis

A

Haemolytic anaemia as a complication of prosthetic heart valves

Can be bio prosthetic and metallic
Turbulence around the valve and collision of RBC with the implanted valve

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60
Q

Describe the management of prosthetic valve haemolysis

A

Monitoring
Oral iron
Blood transfusion or revision surgery if severe

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61
Q

Describe the normal chains in normal Hb

A

2 alpha and 2 beta globin chains

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62
Q

What is thalassaemia

A

Genetic defect in the protein chains which make up haemoglobin

RBC more fragile and break down easily

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63
Q

Describe the inheritance pattern of thalassaemia

A

Autosomal recessive

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64
Q

List some signs and symptoms of thalassaemia

A 
Splenomegaly
Pronounced forehead and malar eminences - bone marrow expands to produce extra RBC
Microcytic anaemia
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly 
Poor growth and development
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65
Q

How is thalassaemia diagnosed

A

FBC - microcytic anaemia
Haemoglobin electrophoresis - globin abnormalities
DNA testing - genetic abnormality
Pregnant women screened at booking

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66
Q

Describe iron overload in thalassaemia and its management

A

Faulty creation of RBC, recurrent transfusion and increased absorption of iron in response to anaemia

Symptoms - fatigue, joint pain, liver cirrhosis, infertility and impotence, heart failure, arthritis, osteoporosis and diabetes

Serum ferritin levels checked to monitor for iron overload

Management - iron chelation and limit transfusions

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67
Q

Describe the management of alpha thalassaemia

A 
FBC monitoring
Complication monitoring
Blood transufsions
Splenectomy
Bone marrow transplant may be curative
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68
Q

Which chromosome si the faulty alpha globin gene located

A

16

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69
Q

Which chromosome is the faulty beta globin gene located

A

11

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70
Q

Name the 3 types of beta thalassaemia

A

Minor
Intermedia
Major

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71
Q

Why do multiple types of beta thalassaemia exist

A

Gene defects either consist of abnormal copies that retain function or deletion genes with no function

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72
Q

What is the management for thalassaemia minor

A

No active treatment - just monitoring

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73
Q

Describe the management of thalassaemia intermedia

A

Monitoring

Transfusions and maybe Iron chelation

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74
Q

Describe the management of thalassaemia major

A

Regular transfusions, iron chelation and splenectomy

Bone marrow transplant may be curative

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75
Q

Describe the pathophysiology of sickle cell disease

A

At 6 weeks of age fetal haemoglobin is replaced by HbA
In sickle cells disease abnormal HbS causes cells to be sickle shaped
Autosomal recessive defect of beta globin on chromosome 11

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76
Q

Why do people in Africa, India, Caribbean and the middle east have high proportion of sickle cell trait

A

Selective advantage to malaria - reduces severity

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77
Q

Describe how sickle cell disease is diagnosed

A

Pregnant women at risk of being carriers are tested during pregnancy
Heel prick test on newborn at day 5 of age

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78
Q

List some complications of sickle cell disease

A 
Anaemia 
Infection
Stroke
Avascular necrosis of the hip 
Pulmonary hypertension 
Priapism 
CKD
Sickle cell crises 
Acute chest syndrome
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79
Q

Give some general management options for sickle cell disease

A 
Avoid dehydration
Vaccination
Antibiotic prophylaxis - Pen V
Hydroxycarbamide - stimulates fetal haemoglobin production and has a protective effect against crises and acute chest syndrome
Blood transfusion 
Bone marrow transplant
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80
Q

Describe sickle cell crises

A

Umbrella term

Can occur spontaneously or be triggered by stresses such as infection, dehydration, cold or significant life events

81
Q

How are sickle cells crises managed

A 
Low threshold for admission 
Treat any infection
Keep warm
IV fluids
Simple analgesia
Penile aspiration in priaprism
82
Q

Describe vaso-occlusive crises

A

Sickle shaped blood cells clog capillaries and cause distal ischaemia

Associated with dehydration and raised haematocrit

Symptoms are pain, fever, triggering infection, priaprism

83
Q

Describe splenic sequestration crisis

A

RBC block blood flow in spleen

Acutely enlarged and painful spleen

Pooling of blood - severe anaemia and hypovolaemic shock

Management with blood transfusion and fluid resus

Splenectomy prevents sequestration crisis

Recurrence leads to splenic infarction and infection

84
Q

Describe aplastic crisis

A

Temporary loss of creation of new blood cells
Triggered by parvovirus B19 infection

Significant anaemia
Supportive blood transfusion and spontaneously resolves in 1 week

85
Q

Describe acute chest syndrome

A

Fever or resp symptoms and new infiltrates on CXR

Due to infection or non infective cause

Management with ABx or antivirals, blood transfusions, incentive spirometry that encourages dep breathing, artificial ventilation

86
Q

What is leukaemia

A

Cancer of the cells of the bone marrow

87
Q

How does leukaemia cause pancytopenia

A

Excess production of one form of cells leads to suppression of other cell lines and underproduction of other cell types

88
Q

Describe the presentation of leukaemia

A 
Fatigue
Fever
Failure to thrive
Pallor due to anaemia
Petechiae and abnormal bruising due to thrombocytopenia 
Abnormal bleeding 
Lymphadenopathy
Hepatosplenomegaly
89
Q

How is leukaemia diagnosed

A 
FBC 
Blood film - abnormal cells and inclusions
Lactate dehydrogenase 
Bone marrow biopsy - iliac crest, LA, sample may be aspirated (fluid of cells) or trephine (solid core sample) 
CXR
Lymph node biopsy 
Lumbar puncture if CNS involvement 
CT/MRI/PET
90
Q

What are the differentials for petechiae

A 
Leukaemia
Meningococcal septicaemia
Vasculitis 
Henoch-schonlein purpura 
Idiopathic thrombocytopenia purpura
Non accidental injury
91
Q

Describe acute lymphoblastic leukaemia

A

Malignant change to one of the lymphocyte precursor cells

Acute proliferation of B lymphocytes

92
Q

Which chromosomal abnormalities is ALL associated with

A 
Downs syndrome 
Philadelphia chromosome (t9:22) translocation - 30%
93
Q

What age is affected by ALL

A

2-4yrs and >45

94
Q

Describe chronic lymphocytic leukaemia

A

Chronic proliferation of single type of B lymphocyte

95
Q

What age is most often affected by CLL

A

> 55

96
Q

What does blood film of CLL show

A

Smudge or smear cells
Occur in the process of preparing the blood film where aged or fragile white blood cells rupture and leave a smudge on the film

97
Q

What can CLL transform into?

A

Richters transformation - high grade lymphoma

98
Q

What additional symptoms may CLL present with

A

Warm haemolytic anaemia
Infection
Bleeding
Weight loss

99
Q

Describe the 3 phases of CLL

A

Chronic phase - lasts 5 yrs, asymptomatic and patients diagnosed accidentally with raised WCC

Accelerated phase - abnormal blast cells take up a high proportion of the cells in the bone marrow and blood., more symptomatic, anaemia and thrombocytopenia

Blast phase - high proportion of blast cells and blood, often fatal

100
Q

Which genetic abnormality is associated with CML

A

Philadelphia chromosome - Chromosome 9 and 22 translocation

101
Q

Describe AML

A

Acute myeloid leukaemia
Most common leukaemia in adults
Middle age and onwards
Transformation from myeloproliferative disorders such as polycythaemia rubra vera and myelofibrosis
Blood film shows high proportion of blast cells with Auer rods in their cytoplasm

102
Q

Describe leukaemia treatment

A

Chemotherapy and steroids
Radiotherapy
Bone marrow transplant
Surgery

103
Q

List the complications of chemotherapy

A 
Failure
Stunted growth and development in children
Infection - immunosuppression 
Neurotoxicity 
Infertility 
Secondary malignancy 
Cardiotoxicity 
Tumour lysis syndrome
104
Q

What causes tumour lysis syndrome

A

Release of uric acid from the cells being destroyed by chemotherapy

Forms crystals in the interstitial fluid and renal tubules and causes AKI

Potassium and phosphate are also released

High phosphate causes a low calcium

105
Q

What drugs can be given to reduce the uric acid from tumour lysis syndrome

A

Allopurinol and Rasburicase

106
Q

What is the preferred treatment for CML

A

Imatinib (tyrosine kinase inhibitor)

107
Q

What is the preferred treatment for non-hodgkins lymphoma

A

R-CHOP - rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone

108
Q

What is the preferred treatment for CLL

A

FCR - fludarabine, cyclophosphamide and rituximab

109
Q

What is a Rouleaux formation on blood film associated with

A

Myeloma

110
Q

What are Reed-Sternberg cells on blood film associated with

A

Hodgkins lymphoma

111
Q

What are lymphomas

A

Cancers that affect the lymphocytes inside the lymphatic system - proliferate inside lymph nodes causing lymphadenopathy

112
Q

Name the two types of lymphoma

A

Hodgkin’s

Non-Hodgkin’s

113
Q

What is Hodgkin’s lymphoma

A

Proliferation of lymphocytes

114
Q

List some risk factors for Hodgkin’s lymphoma

A

HIV
EBV
Autoimmune conditions - RA and sarcoidosis
FH

115
Q

Describe the presentation of Hodgkin’s lymphoma

A

Bimodal age distribution 20 and 75yo

Lymphadenopathy - non-tender and rubbery, axilla, groin, neck. pain when drink alcohol

B symptoms - fever, weight loss, night sweats

Fatigue
Itching
Cough
SOB
Abdominal pain 
Recurrent infection
116
Q

Describe the investigations for Hodgkin’s lymphoma

A

Lactate dehydrogenase - non specific
Lymph node biopsy - diagnostic - reed Sternberg cells (abnormally large B cells with multiple nuclei and nucleoli) - owl eyes
CT/MRI/PET - staging and diagnosis

117
Q

Describe the Ann-Arbor staging system

A

Used for both Hodgkins and non-hodgkins lymphoma

Puts importance on wether the affected nodes are above or below the diaphragm

Stage 1 - confined to one region of lymph nodes
Stage 2 - in more than one region but on the same side of the diaphragm
Stage 3 - affects lymph nodes above and below the diaphragm
Stage 4 - widespread involvement including non-lymphatic organs such as the lungs and liver

118
Q

Describe the management of lymphoma

A

Chemo - risk of leukaemia and infertility

Radiotherapy - risk of cancer, damage to tissues and hypothyroidism

119
Q

Describe Burkitt lymphoma

A

Associated with EBV, HIV, malaria

120
Q

Describe MALT lymphoma

A

Mucosa associated lymphoid tissue
Usually around the stomach
Associated with Hpylori

121
Q

Describe diffuse large B cell lymphoma

A

Rapidly growing painless mass in patients over 65

122
Q

List some risk factors for non-hodgkins lymphoma

A 
HIV
EBV
H.pylori
Hep B or C
Exposure to pesticides - trichloroethylene
FH
123
Q

Describe the management of non-hodgkins lymphoma

A 
Watchful waiting 
Chemo
Monoclonal antibodies - rituximab 
Radiotherapy 
Stem cell transplantation
124
Q

What is myeloma

A

Cancer of plasma cells - B lymphocyte

Excess production of antibodies

125
Q

What is multiple myeloma

A

Myeloma affecting multiple areas of the body

126
Q

What is monoclonal gammopathy of undetermined significance

A

Excess of a single type of antibody or antibody compenets without myeloma or cancer

Incidental finding

May progress to myeloma - monitor patient

127
Q

What is smouldering myeloma

A

Progression of MGUS with higher levels of antibodies

Premalignant

128
Q

Describe waldenstroms macroglobulinaemia

A

Type of smouldering myeloma where there is excessive IgM

129
Q

What are antibodies made up of

A

2 heavy and 2 light chains

130
Q

Which type of antibody are most myelomas

A

IgG

131
Q

What can be found in the urine of patients with myeloma

A

Bence Jones protein - subunit of antibody (light chain)

132
Q

Describe myeloma bone disease

A

Plasma and stromal cells release cytokines which stimulate osteoclast activity to absorb bone and to decrease osteoblast depositing bone activity.

Skull, spine, ribs, long bones

Osteolytic - predispose to pathological fractures

Hypercalcaemia

133
Q

Describe myeloma renal disease

A

Immunoglobulins block tubule flow
Dehydration
Hypercalcaemia
Nephrotoxic medications - bisphosphonates eg

134
Q

Describe how myeloma affects plasma viscosity and what this results in

A

Increased plasma viscosity - more proteins

Essy bruising, bleeding
Loss of sight due to vascular disease in eye
Purple discolouration of extremeties
Heart failure

135
Q

Give the acronym used to remember features of myeloma

A

Calcium - raised
Renal failure
Anaemia - normochromic, normocytic
Bone lesions and pain

136
Q

List some myeloma risk factors

A 
Old age
Male
Black African 
FH
Obesity
137
Q

List the investigations for myeloma

A 
FBC
Calcium
ESR
Plasma viscosity 
Serum protein electrophoresis - serum immunoglobulins/Serum light chain assay 
Urine bence Jones protein test 
Bone marrow biopsy 
Imaging - whole body MRI, whole body CT, skeletal survey
138
Q

List some X-ray changes of myeloma

A

Punched out lesions
Lytic lesions
Raindrop skull - many punched out lesions that give appearance of raindrops splashing on skull

139
Q

Describe the management of myeloma

A

MDT
Chemotherapy - bortezomid, thalidomide, dexamethasone

Stem cell transplant

VTE prophylaxis

Bone disease - bisphosphonates, radiotherapy, ortho surgery, cement augmentation

140
Q

List some complication of myeloma

A 
Infection
Pain 
Renal failure
Anaemia
Hypercalcaemia
Peripheral neuropathy 
Spinal cord compression 
Hyperviscositiy 
Amyloidosis
141
Q

What are myeloproliferative disorders and give examples

A

Uncontrolled proliferation of single type of stem cell

Primary myelofibrosis - haematopoetic stem cells
Polycythaemia vera - erythroid cells
Essential thrombocythemia - megakaryocytes

142
Q

What do myeloproliferative disorders have the potential to turn into

A

AML

143
Q

Which mutations are associated with myeloproliferative disorders

A

JAK2
MPL
CALR

144
Q

Describe myelofibrosis

A

Where proliferation of cell lines leads to fibrosis of the bone marrow - replaced by scar tissue
Response to cytokines such as fibroblast growth factor
Fibrosis leads to anaemia and leukopenia

When the bone marrow is replaced by scar tissue, the production of blood cells starts to happen in other areas such as the liver and spleen - extramedullary haematopoiesis - hepatomegaly and splenomegaly - portal hypertension and if around the spinal cord can cause spinal cord compression

145
Q

Describe the presentation of myeloproliferative disorders

A

Asymptomatic

Systemic symptoms - fatigue, weight loss, night sweats, fever

Anaemia
Splenomegaly 
Portal hypertension 
Low platelets - bleeding and petichiae
Thrombosis
Raised RBC - red face and thrombosis
Low WBC - infection
146
Q

What are the 3 clinical signs on examination in someone with polycythaemia vera

A

Conjunctival pallor
Ruddy complexion
Splenomegaly

147
Q

What are the FBC findings in polycythaemia vera

A

Raised Hb >185 in men and 165 in women

148
Q

What are the FBC findings in thrombocythemia

A

Raised platelets >600

149
Q

What are the FBC findings in myelofibrosis

A

Anaemia
Leucocytosis or leukopenia
Thrombocytosis or thrombocytopenia

150
Q

What can a blood film in myelofibrosis show

A

Teardrop shaped RBCs, varying in size (poikilocytosis) and immature red and white cells (blasts)

151
Q

Describe how myeloproliferative disorders are diagnosed

A

Bone marrow biopsy

Genetics - JAK2, MPL, CALR

152
Q

Describe the management of primary myelofibrosis

A

Mild symptoms - monitor and no active treatment
Allogenic stem cell transplantation
Chemotherapy
Supportive management

153
Q

Describe the management of polycythaemia vera

A

Venesection
Aspirin - reduce thrombus formation
Chemotherapy - hydroxycarbamide and interferon (cyto-reductive therapy)

154
Q

Describe the management of essential thrombocythemia

A

Aspirin - reduce thrombus formation

Chemo to control disease

155
Q

Describe myelodysplastic syndrome

A

Myeloid bone marrow cells not maturing properly and not producing healthy blood cells

Anaemia
Neutropenia
Thrombocytopenia

156
Q

What are some risk factors for myelodysplastic syndrome

A

> 60yo

Previous chemotherapy or radiotherapy

157
Q

What is myelodysplastic syndrome associated with

A

AML

158
Q

Describe how myelodysplastic syndromes are diagnosed

A

FBC
Blood film - blasts
Bone marrow aspiration and biopsy

159
Q

Describe the management of myelodysplastic syndrome

A

Watchful waiting
Supportive treatment
Chemo
Stem cell transplantation

160
Q

List the causes of thrombocytopenia

A

Decreased production

  • Sepsis
  • B12/folate defieicny
  • Liver failure
  • Leuakemia
  • Myelodysplastic syndrome

Increased destruction

  • Medication - sodium valproate, methotrexate, isotretinoin, antihistamines PPI
  • Alcohol
  • ITP
  • TTP
  • Heparin induced thrombocytopenia
  • Haemolytic ureamic syndrome
161
Q

Describe the presentation of thrombocytopenia

A

Incidental finding

Platelets <50 - easy, spontaneous bruising and prolonged bleeding time, nosebleed, bleeding gums, heavy periods, easy bruising, blood in the urine or stool

Platelets

162
Q

Describe immune thrombocytopenic purpura (ITP)

A

Antibodies against platelets - creates an immune response against platelets resulting in destruction and low count

163
Q

Describe the management of ITP

A

Oral prednisolone
IV immunoglobulins
Rituximab - monoclonal antibody against B cells
Splenectomy
Monitor platelets
Educate patient about persistent headaches and melaena - when to seek help
Control BP and suppress menstrual periods

164
Q

Describe thrombotic thrombocytopenic purpura

A

Blood clots develop throughout the small vessels of the body using up platelets and causing thrombocytopenia, bleeding under the skin
Microangiopathy
Genetic/autoimmune Defect in ADAMTS13 protein which normally inactivates von Willebrand factor and reduces platelet adhesion to vessel walls and clot formation. Overactivity of von Willebrand factor causes platelets to be used up and blood clots form, these break down causing haemolutic anaemia

165
Q

How is TTP treated

A

Plasma exchange
Steroids
Rituximab

166
Q

Describe heparin induced thrombocytopenia

A

Development of antibodies against platelts in response to exposure to heparin

Antibodies target platelet factor 4 on platelets

Bind to platelets and activate clotting mechanisms causing hypercoagulable state and leads to thrombosis and break down platelets causing thrombocytopenia

167
Q

How is HIT diagnosed

A

HIT antibodies

168
Q

How is HIT managed

A

Stop the use of heparin and switch to alternative anticoagulant

169
Q

What is Von Willebrand disease

A

Most common inherited cause of abnormal bleeding
Autosomal dominant
Deficiency/malfunctioning/absence of glycoprotein Von Willebrand factor

170
Q

How do patients with von Willebrand present

A 
Bleeding gums with brushing
Nose bleeds
Heavy menstrual bleeding
Heavy bleeding during surgery 
FH
171
Q

How is Von Willebrand diagnosed

A 
Abnormal bleeding 
FH
Bleeding assesssment tools 
Lab investigations
No specific test
172
Q

How is von Willebrand managed

A

Desmopressin - stimulate release of VWF
VWF infusion
Factor 8 alongside VWF infusion

Women with heavy periods - mefenamic acid, tranexamic acid, norethisterone, COCP, Mirena coil and hysterectomy in severe cases

173
Q

What is Haemophilia A a deficiency of

A

Factor 8

174
Q

What is haemophilia B (Christmas disease) a deficiency of

A

Factor 9

175
Q

Describe the inheritance of haemophillia

A

X linked recessive

176
Q

List some signs and symptoms of haemophilia

A 
Spontaenous haemorrhage 
Intracranial haemorrhage 
Haematoma
Cord bleeding
Hemarthrosis 
Bleeding into muscles 
Gum bleeding
GI bleed
Haematuria
Retroperitoneal space bleeding
177
Q

How is haemophilia diagnosed

A

Bleeding scores
Cogulation factor assays
Genetic testing

178
Q

How is haemophilia managed

A

IV infusions of affected clotting factors (8 or 9) - complication is antibodies forming against the clotting factors
Desmopressin - stimulate von Willebrand factor - stimulates clotting
Tranexamic acid - antifibrinolytic

179
Q

What defect would a patient have if a DVT travelled to the brain reuslting in a stroke

A

Atrial septal defect

180
Q

List the risk factors for VTE

A 
Immobiltiy 
Recent surgery 
Long haul flight
Hormone replacement therapy with oestropgen or COCP
Malignancy
Pregnancy
Polycythaemia
SLE
Thrombophilia (antiphispholipid syndrome, protein C/S defieicny), factor V leiden
181
Q

What VTE prophylaxis is given to patients

A

LMWH with enoxaparin

Anti-embolic compression stockings

182
Q

What is the main contraindication to compression stockings

A

Peripheral arterial disease

183
Q

What is the contraindications to LMWH as VTE prophylaxis

A

Anticoagulation or active bleeding

184
Q

Describe the presentation of DVT

A 
Unilateral 
Calf or leg swelling
Dilated superficial veins
Tenderness to the calf
Oedema
Colour change to leg
185
Q

What are the alternatives to a bilateral DVT

A

Chronic venous insufficiency

Heart failure

186
Q

How do you examine for a DVT

A

Measure leg circumference of the calf 10cm below the tibial tuberosity - more than 3cm difference between the calves is significant

187
Q

What does the Wells score predict

A

Risk of a patient presenting with DVT/PE symptoms actually having one

188
Q

How is VTE diagnosed

A

D-dimer if wells score suggests
Doppler USS leg - repeat 1 week after negative USS and positive D-dimer but unlikely wells
PE- CTPA or VQ scan if patient is pregnant or has significant renal impairment

189
Q

List some causes of raised D-dimer

A 
Pregnancy
Malignancy
Heart failure 
Surgery 
Pneumonia
190
Q

Describe the initial management of VTE

A

Apixaban or rivaroxaban

191
Q

Describe long term anticoagulation of those with VTE

A

DOAC, warfarin or LMWH

192
Q

What is first line long term anticoagulation for those with antiphopsolipid syndrome following VTE

A

Warfarin

193
Q

What is the first line anticoagulant in pregnancy

A

LMWH

194
Q

How long do you continue long term anticoagulation following VTE

A

3 months if reversible cause

6 months if recurrent, unclear cause or cancer

195
Q

Describe the use of inferior vena cava filters

A

Used to filter blood and catch clots travelling to the lungs - prevent PES
Used in cases of recurrent PEs or those unsuitable for anticoagulation

196
Q

Describe budd-chiari syndrome

A

Blood clot in hepatic vein blocking outflow of blood

Acute hepatitis
Abdominal pain
Hepatomegaly
Ascites

Management involves anticoagulation and investigating the underlying hypercoagulation and treating the hepatitis

197
Q

Describe the coagulation screen results for DIC

A

Prolonged PT, Prolonged APTT and reduced fibrinogen

198
Q

What so you give to treat DIC when patient is bleeding

A

Platelets
Cryoprecipitate
Fresh frozen plasma

Finals (18 decks)

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