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Phase 3 > Week 3 - Haematology > Flashcards

Week 3 - Haematology Flashcards

1
Q

What is haemopoiesis?

A

The production of blood cells.

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2
Q

Where does haemopoiesis occur in the foetus, infants and adults?

A

Foetus - yolk sac, then liver and spleen, then bone marrow.
Infants - bone marrow (all bones).
Adults - bone marrow (ends of femurs, pelvis, sacrum, vertebrae, ribs, sternum, skull.) Think central skeleton.

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3
Q

Haemopoiesis begins with a pluripotent stem cell. This then differentiates into two different types of stem cells which give rise to all blood cells. What are the name of these two stem cells?

A

Myeloid stem cell and lymphoid stem cell.

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4
Q

What cells does the lymphoid stem cell go on to produce?

A

Lymphocytes, plasma cells, NK cells.

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5
Q

What cells does the myeloid stem cell go on to produce?

A

Erythrocytes, platelets, neutrophils, basophils, eosinophils, monocytes, macrophages, mast cells

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6
Q

Name 4 characteristics of haemopoietic stem cells.

A

Ability to self-renew
Unspecialised
Ability to differentiate
Quiescent

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7
Q

In what 3 places can haemopoeitic stem cells be found?

A

Bone marrow, peripheral blood after treatment with G-CSF, umbilical cord blood.

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8
Q

What are the three possible fates of a haemopoietic stem cell?

A

Self-renewal, apoptosis, differentiation.

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9
Q

With regards to division of haemopoietic stem cells, what is assymetrical division? What is symmetrical division?

A

When the stem cell divides into one stem cell and one differentiated cell.
When the stem cell either self-renews to form two more stem cells or divides to from two differentiated cells.

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10
Q

Stroma is the bone marrow microenvironment which supports the developing haemopoietic cell. Which cells make up the stroma?

A

Macrophages, fibroblasts, endothelial cells, fat cells, reticulum cells.

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11
Q

Bone marrow stromal cells are supported by an extracellular matrix containing what 5 proteins?

A

Laminin, collagen, proteoglycans, fibronectin, haemonectin.

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12
Q

Name 3 heriditary conditions affecting bone marrow function.

A

Thalassaemia
Sickle cell anaemia
Fanconi anaemia

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13
Q

Name 3 acquired conditions affecting bone marrow function.

A

Leukaemia, metastatic malignancy, myelodysplasia

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14
Q

In leukaemogenesis, at what level of differentiation are the neoplastic cells?

A

Haemopoetic stem cells or early myeloid or lymphoid cells.

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15
Q

Can leukaemic cells differentiate?

A

No they proliferate to produce clones.

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16
Q

What are myeloproliferative disorders (MPD)?

A

Clonal disorders of haemopoiesis leading to increased numbers mature blood progeny of myeloid lineage.

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17
Q

Name 3 classical MPDs.

A

Polycythaemia rubra vera
Essential thrombocytosis
Myelofibrosis

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18
Q

MPDs are associated with what two gene mutations? What condition do MPDs have the potential to transform into?

A

JAK2V617F and calreticulin

Acute myeloid leukaemia

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19
Q

Essential thrombocytosis is on a continuum with PRV. What is it? What are some of the clinical features?

A

Increased platelet count.

Thrombotic complications, haemorrhagic complications, splenomegaly

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20
Q

How is essential thrombocytosis treated in low risk and intermediate risk individuals?

A

Low risk - aspirin/anti-platelet agent

Intermediate risk - aspirin + hydroxycarbamide

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21
Q

How is essential thrombocytosis treated in high risk individuals? (i.e. over 60 or high risk features)

A

First line - aspirin + hydroxycarbamide
Second line - anagrelide + aspirin

IFN-α
Busulphan
32P
JAK inhibitors e.g. ruxolitinib

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22
Q

What is the main side effect of JAK inhibitors?

A

Thrombocytopenia

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23
Q

Define Myelodysplastic syndromes (MDS). What kind of cancer treatment can MDS be secondary to? What condition can MDS progress to?

A

Syndromes characterised by dysplasia and ineffective haemopoiesis in 1 or more of the myeloid series.
Chemotherapy and radiotherapy.
Acute Myeloid Leukaemia

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24
Q

MDS are often associated with acquired cytogenic changes such as… (name 2)

A

monosomy 5 or monosomy 7

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25
Q

What do 70-80% of people with MDS present with? In what other ways can MDS present?

A

Fatigue due to anaemia
Bleeding or infections
Incidental finding on FBC

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26
Q

In what ways can MDS be managed?

A 
Supportive care - blood and platelet transfusion 
Growth factors - EPO and G-CSF
Immunosuppression
Low dose chemotheapy - hydroxycarbamide 
Demethylating agent 
Intensive chemotherapy
Allogenic stem cell transplantation
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27
Q

Fanconi anaemia is a genetic condition accounting for 10-20% of aplastic anaemia cases. What is the pattern of inheritance?

A

Autosomal recessive

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28
Q

What do the majority of people with fanconi anaemia go on to develop?

A

Bone marrow failure and malignancy

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29
Q

What are some of the clinical features of fanconi anaemia?

A 
Microphthalmia 
Short stature 
Short pinkies and absence of thumbs 
GU malformations 
GI malformations 
Mental disability 
Hearing loss 
Hydrocephalus
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30
Q

How is fanconi anaemia treated? How could it possibly be treated in the future?

A

Allogeneic stem cell transplant is gold standard.
Life time surveillance of secondary tumours.

Gene therapy where faulty FANC gene is replaced.

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31
Q

What is an autologous stem cell transplant? What is an allogeneic stem cell transplant?

A

Autologous: the patient’s own blood stem cells are used.
Allogeneic: the stem cells come from a donor.

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32
Q

What are the different types of allogeneic transplant?

A

Syngeneic Transplant - between identical twins.
Allogeneic Sibling - HLA identical.
Haplotype identical - A half matched family member. (usually a parent or a half matched sibling.)
Volunteer Unrelated (VUD)
Umbilical cord blood

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33
Q

What would be the main indications for autologous stem cell transplant?

A

Relapsed hodgkin’s disease

non-hodgkins’s lymphoma and myeloma.

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34
Q

In autologous stem cell transplantation, patient’s receive a growth factor to make the stem cells leave the bone marrow so they can be collected from the blood. What is the name of the growth factor?

A

G-CSF

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35
Q

In allogeneic transplantation where can the blood stem cells be taken from? What are the main indications for allogeneic transplant?

A

Peripheral blood, bone marrow or umbilical cord blood.

Acute and chronic leukaemias, relapsed lymphoma, aplastic anaemia, heriditary disorders.

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36
Q

“Graft versus host” and “graft versus leukaemia” can occur with a patient receives a allogeneic transplant. Explain these two terms.

A

GvH - when the immune cells of the donor’s blood attacks the host’s body cells.
GvL - when the immune cells of the donor’s blood attacks the leukaemia cells.

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37
Q

What is the purpose of Donor lymphocyte infusion (DCI)?

A

Used after stem cell transplant, induces graft vs leukaemia effect to prevent or treat a relapse.

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38
Q

How is non-myeloablative stem cell transplant different from a normal stem cell transplant?

A

Lower dose chemotherapy, and use of immunosuppression to allow donor cells to engraft while graft vs leukaemia eradicates the cancer.

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39
Q

What is the advantages and disadvantages of umbilical cord blood transplant?

A

Advantages - more rapidly available than VUD, less rigorous matching required as baby’s immune system naive.
Disadvantages: only small amounts, may require two transplants. Slower engraftment, if relapse, cant go back for DLI.

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40
Q

How does graft vs host disease present? What is the difference between acute and chronic GvH? How is GvH treated?

A

Jaundice, rash, diarrhoea.
Acute: occurs within first 100 days after transplant.
Chronic: occurs after 100 days.
Immunosuppression.

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41
Q

Name 5 problems with stem cell transplant?

A 
Limited donor availability 
Mortality 10-50% 
GvH disease
Immunosuppression 
Infertility in both sexes
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42
Q

What 4 things are required for normal red cell production?

A

Erythropoietin
Genes for erythropoeisus
Vitamins minerals - vit B12, folate, iron
Functioning bone marrow

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43
Q

Define anaemia.

A

A reduction in the quantity of haemoglobin in the blood.

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44
Q

What is the role of the RBC in gas transfer?

A

Removal of CO2, delivery of O2 from lungs to tissues.

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45
Q

What enzyme is involved in RBC CO2 removal?

A

Carbonic anhydrase

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46
Q

What are the components of a haemoglobin molecule?

A

4 globin chains (2 alpha, 2 beta) + 4 haem groups

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47
Q

What part of the RBC does O2 reversibly bind to?

A

The haem groups on the haemoglobin

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48
Q

The normal total body content of iron is about 4G. Where in the body is iron stored?

A

Bone marrow and RBCs
RES
Myoglobin
Enzymes i.e. cytochromes

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49
Q

What is the name of the glycoprotein responsible for delivering iron in the plasma to all tissues? How many iron binding domains does it have? Where is it synthesised?

A

Transferrin
2 iron binding domains
The liver

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50
Q

What is the relationship between level of iron in the plasma and amount of transferrin produced?
What is the % saturation of transferrin with iron?

A

The lower the level of iron in the plasma, the more transferrin produced.
30% saturation

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51
Q

How do macrophages of the RES take up iron? How is iron stored in the RES?

A

By ingesting dead RBC.

As ferritin or haemosiderin

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52
Q

What is the name of the protein that stores iron in every cell?

A

Ferritin

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53
Q

Serum ferritin is directly related to the amount of iron in the RES. This means that serum ferritin levels usually indicate overall iron levels. Explain: why is this sometimes not the case?

A

Ferritin is an acute phase protein. This means that sometimes, in the event of inflammation and tissue damage it can be elevated more than the amount in the body stores. This means that serum ferritin can be normal but iron can be low.

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54
Q

There is no excretory pathway to get rid of excess iron. How much iron do males and females lose each day and by what means?

A

Males: 1G/day through shedding of cells in GI tract
Females: 2G/day through shedding of cells in GI tract and through menstrual blood loss/pregnancy

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55
Q

Iron release from enterocytes into the plasma is regulated by the interaction between what two molecules?

A

Ferroportin and hepcidin

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56
Q

What is the role of ferroportin in release of iron from enterocytes into plasma?

A

It is a transmembrane protein that transports iron from inside to outside the cell.

57
Q

What is the role of hepcidin? How does it work?

A

Hepcidin reduces iron levels in plasma.
It binds to ferroportin and degrades it, reducing iron absorption in enterocytes and decreases iron release from the RES.

58
Q

Iron Deficiency Anaemia (IDA) is the most common anaemia in the world. What are the blood film features of IDA?

A

Red blood cells are hypochromic - pale and microcytic - small.

59
Q

What types of anaemia cause hypochromic and microcytic RBCs?

A

IDA, Thalassaemia, ACD (anaemia of chronic disease), sideroblastic anaemia (particularly congenital SA).

60
Q

What is the percentage saturation of transferrin in IDA compared to normal?

A

IDA - 15%

normal - 30%

61
Q

Does low serum ferritin always indicate low RES iron stores?

A

Yes

62
Q

What are some examination features of IDA?

A

Koilonychia (spoon nails), atrophic glossitis (pale, smooth, painless tongue), angular stomatitis (cracking at mouth edges), oesophageal web

63
Q

What is the most likely cause of IDA in males and post menopausal females?

A

GI blood loss until proven otherwise.

64
Q

What is the most likely cause of IDA in young females?

A

Menstrual blood loss/pregnancy

65
Q

What is the treatment for IDA?

A

Iron replacement - ferrous sulphate or ferrous gluconate or IV iron

66
Q

Anaemia of chronic disease (ACD) is the most common form of anaemia in hospital. What is it? What are its causes?

A 
Failure of iron utilisation, iron is trapped in RES. 
Causes:
Infection
Inflammation – RA, Crohn’s
Neoplasia
67
Q 
What lab values would you expect to see in ACD for:
MCV/MCH
ESR
Ferritin 
Iron 
TIBC (transferrin)
A 
MCV/MCH - decreased or normal (normochromic normocytic or 			         hypochromic microcytic RBCs)
ESR - increased
Ferritin - increased/normal
Iron - decreased
TIBC - decreased
68
Q

Rouleaux is a sign which can be seen on blood film. It looks like red cells stacking up on top of one another. What does this sign indicate?

A

Raised ESR

69
Q

What are the different causes of ACD? (think mechanisms)

A

RES Iron blockade - iron trapped in macrophages, raised levels hepcidin
Reduced EPO response
Depressed marrow activity

70
Q

How is ACD treated?

A

By treating the underlying condition.

71
Q

Vitamin B12 and Folate are required for DNA synthesis and nuclear maturation. Does deficiency cause macrocytic anaemia or microcytic?

A

Macrocytic anaemia (large RBC)

72
Q

Deficiency of vitamin B12/folate causes megaloblastic anaemia.
What is the cause of this? How would this appear on a blood film?

A

Results from inhibition of DNA synthesis during RBC production. There would be large immature and dysfunctional RBCs (megaloblasts) present.

73
Q

What are dietary sources of vitamin B12?

A

Meat (especially liver and kidney) and dairy products.

74
Q

What factor does vitamin B12 bind to in the stomach? Where is vitamin B12 absorbed in the GI tract? What factor must it bind to in order to be absorbed? How long is it stored for?

A

Intrinsic factor.
The terminal ileum.
Transcobalamin
3-4 years

75
Q

What are dietary sources of folate? Where is folate absorbed? How long is it stored for?

A

Green vegetables
Small bowel
Only a few days

76
Q

With vitamin B12/folate deficiency, what would you expect bilirubin and LDH levels to be?

A

Raised bilirubin, raised LDH

77
Q

B12/folate deficiency causes megaloblastic anaemia which causes leucopenia and thrombocytopenia. Define these two words.

A 
Leucopenia = lack of WBC
Thrombocytopenia = lack of platelets
78
Q

Vitamin B12 deficiency causes some neurological manifestations. Name two.

A

Bilateral peripheral neuropathy or demyelination of tracts of the spinal cord.

79
Q

What effect can folate deficiency have on the developing foetus in the first 12 weeks?

A

Neural tube defects i.e. spina bifida.

80
Q

How do patients with vitB12 or folate deficiency present?

A

Symptoms of anaemia/cytopenia - tiredness, easy bruising
Mild jaundice
Neurological problems

81
Q

What are the causes of vitamin B12 deficiency?

A

Dietary insufficiency
Pernicious anaemia
Gastrectomy
Terminal ileum i.e. crohn’s, resection.

82
Q

What are the causes of folate deficiency?

A

Dietary
Extensive small bowel disease - crohn’s, coeliac
Increased cell turnover - i.e. skin disorders, haemolysis

83
Q

Name 2 other causes of macrocytosis.

A

Reticulocytosis

Liver disease

84
Q

What are haemoglobinopathies?

A

Lack of normal haemoglobin due to absent or variant genes.

85
Q

The genes that code for alpha and beta globin chains are found on what chromosomes?

A

Alpha - chromosome 16

Beta - chromosome 11

86
Q

Adult haemoglobin is made up of 2 alpha and 2 beta globin chains. What about foetal haemoglobin?

A

2 alpha and 2 gamma

87
Q

If a person has a problem with their alpha globins, when will the condition be present from? If the problem is with beta, when will be condition be present from?

A

Alpha - from birth

Beta - from 3-6 months

88
Q

What is the genetic basis of thalassaemias?

A

Relative lack of globin genes.

89
Q

What would be the clinical significance of alpha thalassaemia when:

  • 1 gene is missing.
  • 2 genes are missing
  • 3 genes are missing
  • 4 genes are missing
A

1 - mild microcytosis
2 - microcytosis, increased RBC count, sometimes very mild asymptomatic anaemia
3 - Significant anaemia and bizarre shaped small red cells (HbH disease)
4 - incompatible with life

90
Q

How are the globin chains abnormal in HbH disease?

A

There are 3 alpha genes missing so the lack of alpha chains results in excess beta chains.

91
Q

Beta thalassaemia is an autosomal recessive condition causing significant dyserythropoiesis. What is the abnormality?

A

Missing both beta globin genes.

92
Q

What is the management of beta thalassaemia major? Why do people with this condition have a reduced life expectancy?

A

Blood transfusions required from early life.

Iron overload has a major effect on life expectancy.

93
Q

What is the genetic basis of sickle cell disease?

A

Single amino acid substitution on B globin gene at position 6 on chromosome 11.

94
Q

How is sickle cell disease diagnosed?

A

Through looking at a blood film and seeing the sickle shaped RBCs.

95
Q

What is the clinical result of sickle cell disease?

A

Reduced red cell survival - haemolysis

Vaso-occlusion - tissue hypoxia/infarction

96
Q

Sickle cell disease is a multi-system disease. What is the effect of the disease on the following organs:

  • brain
  • lungs
  • spleen
  • bones
  • eyes
A 
brain - stroke 
lungs - acute chest syndrome 
spleen - hyposplenic
bones - osteonecrosis 
eyes - vascular retinopathy
97
Q

What is the treatment for sickle cell disease?

A
  1. Prevent crises
    - hydration, analgesia, prophylactic vaccination and antibiotics, folic acid.
  2. Prompt management of crises
    Oxygen, fluids, analgesia, antibiotics, specialist care, transfusion, red cell exchange.
  3. Bone marrow transplantation.
98
Q

What is haemolytic anaemia?

A

Anaemia related to reduced RBC lifespan. It is not related to blood loss or haematinic deficiency.

99
Q

What is the normal lifespan of a RBC? What is the lifespan of a RBC in compensated haemolytic state? What is the lifespan of a RBC in haemolytic anaemia?

A

120 days
20-100 days
<20 days

100
Q

What are some of the causes of congenital haemolytic anaemia?

A
  1. Abnormalities of RBC membrane - i.e. hereditary spherocytosis
  2. Haemoglobinopathies
  3. Abnormalities of RBC enzymes
101
Q

Hereditary spherocytosis is an autosomal dominant condition which causes congenital haemolytic anaemia. What would you see on a blood film and what are some of the clinical features?

A

RBCs spherocytic and polychromatic, jaundice, splenomegaly.

102
Q

Abnormalities of RBC enzymes can cause congenital haemolytic anaemia. Deficiency in what two enzymes can cause this?

A

Pyruvate kinase, glucose 6 phosphate dehydrogenase

103
Q

What are the three types of acquired haemolytic anaemia?

A
  1. Autoimmune - cold type (IgM) and warm type (IgG)
  2. Isoimmune - haemolytic disease of the newborn (HDN)
  3. Non-immune - fragmentation haemolysis
104
Q

Cold Autoimmune Haemolytic Anaemia (AIHA) is mediated by an IgM autoantibody. What would be seen on a blood film?

A

Agglutinations due to the structure of IgM.

105
Q

Warm Autoimmune Haemolytic Anaemia (AIHA) is mediated by an IgG auto-antibody. What would be seen on a blood film?

A

Spherocytic and polychromatic RBCs.

106
Q

Name a drug than can induce Autoimmune Haemolytic Anaemia (AIHA) causing mild haemolysis.

A

Hapten

107
Q

What is the purpose of a Direct Coombs Test? A positive test could indicate what 2 conditions?

A

To detect antibodies on the RBC surface.
AIHA
HDN (haemolytic disease of the newborn.)

108
Q

What is the purpose of a Indirect Coombs Test?

A

To detect RBC antibodies in the plasma prior to a blood transfusion.

109
Q

How do you treat cold AIHA? How do you treat warm AIHA?

A

Cold - keep warm

Warm - stop drugs, immunosuppression, steroids, splenectomy

110
Q

What factors does Prothrombin Time (PT) depend on?

A

Factors in extrinsic and common pathway i.e. factor 7 and factors 1 (fibrinogen), 2, 5 and 10

111
Q

What factors does Activated partial thromboplastin time (APTT)?

A

Factors in intrinsic and common pathways i.e. factors 8, 9, 11 and 12 and factors 1 (fibrinogen), 2, 5 and 10.

112
Q

What does Thrombin Clotting time (TCT) depend on? What could TCT be prolonged by?

A

Amount of fibrinogen in plasma and how well the fibrinogen functions.
Inhibitors of thrombin i.e. heparin

113
Q

What are the three different classes of anti-thrombotic agents and their general mechanism?

A

Anti-coagulants - inhibit components of the coagulation cascade.
Fibrinolytic agents - enhance lysis of the fibrin clot.
Anti-platelet agents - inhibit platelet activity.

114
Q

Heparin is an anti-coagulant drug. What is the mechanism of action? Is the half life relatively long or short? How is it administered?

A

Augments the activity of endogenous anti-thrombin, especially anti-2a and anti-10a.
Short half-life.
Administered parenterally.

115
Q

What are some of the side effects of heparin?

A

HIT (heparin induced thrombocytopenia), osteoporosis, hyperkalaemia.

116
Q

What is the benefit of LMWH in comparison to UFH?

A

Safer side effect profile, clinical efficacy possibly better, can be used in outpatients, more predictable dose response.

117
Q

What are the indications for using heparin?

A

Acute DVT or PE, during cardiac bypass surgery, ACS, post VTE and prophylaxis against VTE, medical and post-op patients, obstetric patients.

118
Q

Why would heparin be suitable for use in obstetric patients?

A

It doesn’t cross the placenta.

119
Q

How are heparin, warfarin and DOACs different in terms of how long they take to have an effect and how long the effect lasts?

A

Heparin and DOACs - immediate action and short acting.

Warfarin - takes longer to have an effect and longer acting.

120
Q

What is the mechanism of action of warfarin?

A

Vitamin K antagonist and inhibits factors 2, 7, 9, 10.

121
Q

Warfarin has a narrow therapeutic window. What is the target INR for warfarin?

A

2-3

122
Q

What conditions would warfarin be effective in managing?

A
  • atrial fibrillation
  • acute DVT or PE
  • prosthetic heart valve
123
Q

Name 3 different Direct Oral Anti-Coagulants (DOACs) and state their mechanism of action. (they end in ‘ban’)

A

Dabigatran - factor 2a inhibitor
Rivaroxaban - Factor 10a inhibitors
Apixaban

124
Q

Name 2 contraindications for DOACs.

A

Pregnancy/breastfeeding, liver disease with cirrhosis.

125
Q

Why are DOACs preferable drugs than warfarin?

A

Greater efficacy, lower bleeding risk, less drug and food interactions, requires less review.

126
Q

What are the two main classes of fibrinolytic dugs? Give two examples of each class.

A

Kinases - streptokinase, urokinase.

Tissue plasminogen activators (tPA) - alteplase, tenecteplase.

127
Q

How do tPA derivatives work in enhancing fibrinolysis?

A

They activate plasminogen to plasmin to break down fibrin.

128
Q

How do kinases work?

A

They bind to plasminogen, releasing plasmin and enhancing the breakdown of fibrin.

129
Q

Which of the two classes of fibrinolytic drugs; kinases and tPA derivatives carries a greater bleeding risk? Why is this?

A

Kinases have greater bleeding risk because they cause systemic fibrinogenolysis but tPAs cause minimal unwanted fibrinogenolysis.

130
Q

tPA derivatives have a very short half life of 4-5 minutes. What would the indications for tPA derivatives be?

A

Acute myocardial infarction for patients not suitable for PCI.
Ischaemic stroke
Massive PE

131
Q

What are some of the potential serious complications of tPA derivatives?

A

Haemorrhage, particularly haemorrhagic stroke.

132
Q

What is the benefit of catheter directed thrombolysis? When would this be used?

A

Administered directly into thrombotic vessel so less systemic effect.
Acute limb ischaemia, massive DVT.

133
Q

Clopidogrel and ticlopidine are anti-platelet agents. How does they work?

A

They inhibit ADP mediated platelet aggregation and decrease expression of GPIIb/IIIa.

134
Q

Abciximab and tirofiban are anti-platelet agents. How do they work?

A

Monoclonal antibodies that antagonise GPIIb/IIIa, reducing platelet aggregation.

135
Q

Aspirin is an anti-platelet agent. What is its mechanism of action?

A

Irreversible binding of cyclo-oxygenase which leads to reduced platelet activation.

136
Q

Phosphodiesterase III inhibitors are anti-platlet agents. How do they work?

A

By inceasing the platelet concentration of cAMP, reducing aggregation.

137
Q

What type of drugs are picotamide and ifetroban?

A

Thromboxane synthetase inhibitors and thromboxane receptor blockers.

138
Q

What would be the indications for anti-platelet drugs?

A

CV disease, acute MI, cerebrovascular disease (without AF), acute stroke/TIA, peripheral vascular disease.

Phase 3 (14 decks)

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