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3rd Year > Haematology > Flashcards

Haematology Flashcards

1
Q

What does haematopoiesis?

A

Production of blood cells.

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2
Q

Where are blood cells produced in embryos?

A

Yolk sac then spleen

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3
Q

What part of the skeleton makes blood in adults?

A

Axial skeleton - skull, ribs sternum, pelvis, proximal femur

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4
Q

What is a megakaryocyte and how does it present on film?

A

The production of platelets - the nucleus and cytoplasm get bigger.

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5
Q

What increases the number of neutrophils?

A

infection, trauma, infarction

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6
Q

What do eosinophils fight against?

A

parasitic and allergic reactions

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7
Q

What do monocytes become and how?

A

They circulate for a week and enter tissues to become macrophages.

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8
Q

Why do RBCs have high oncotic pressure and o2 rich?

A

full of haemoglobin

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9
Q

What shape is the structure of haemoglobin?

A

tetrameric globular protein

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10
Q

What does an erythropoietin (EPO) do?

A
  1. Stimulates red cell production
  2. Epo levels reduce
  3. Hypoxia is sensed by kidneys
  4. Cycle continues
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11
Q

Where are RBCs usually destructed, at what age and by what cell?

A

spleen and liver - 120 days
macrophages take up aged ones to take it out of circulation

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12
Q

After the destruction of RBCs what happens to the haem?

A
  1. Haem is broken down to iron and bilirubin
  2. Bilirubin taken to the liver and conjugated
  3. Then excreted in bile (e.g. faeces and urine)
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13
Q

How do RBCs generate energy?

A

glycolysis - ATP

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14
Q

How is Fe2+ prevented from becoming Fe3+?

A

In glycolysis NADH acts as an electron donor preventing this from happening.

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15
Q

What are the catalysts which are raw materials for cell division of blood cells?

A

iron, B12, folate

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16
Q

How do RBCs prevent oxidative damage to cellular enzymes?

A

Reactive oxygen species which have unpaired free radicals.

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17
Q

How does co2 get from tissues to the lungs?

A

10% - dissolved
30% - bound to Hb
60% - as bicarbonate which the RBCs generate

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18
Q

What is the Bohr effect and what causes it?

A

A curve shift to the right.
Caused by increase in co2, 2,3-dpg, temp. and decrease in pH

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19
Q

What do reticulocytes indicate?

A

increased red cell production

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20
Q

Why are reticulocytes purple in colour?

A

They still have remnants of RNA.

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21
Q

How do you calculate the haematocrit (measures the proportion of red blood cells in your blood) ?

A

No. of cells x size

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22
Q

What causes loss of RBCs?

A

bleeding / haemolysis

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23
Q

Where does hb synthesis occur?

A

cytoplasm

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24
Q

How is haemoglobin synthesised?

A
  1. Iron combines with the porphyrin ring
  2. Generation of haem
  3. Combines with globin
  4. Transported to the cytosol
  5. Globin subunits combine with the haem to form the tetramic hb
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25
Q

What are the causes of microcytic anaemia?

A

T – Thalassaemia (globin defect)
A – Anaemia of chronic disease
I – Iron deficiency anaemia (for erythropoiesis)
L – Lead poisoning (probs. with porphyrin synthesis)
S – Sideroblastic anaemia (haem defect)

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26
Q

Explain transferrin vs ferritin

A

Transferrin is the main iron transporting protein in the circulation.
Ferritin concentrations reflect the body’s iron stores.

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27
Q

What units are used for MCV?

A

femolitres (1fl = 10-15L)

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28
Q

What precursors of a RBC have a nucleus?

A

erythroblasts / normoblasts

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29
Q

What are the causes of megaloblastic anaemia?

A

B12 deficiency, folate deficiency, others

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30
Q

Where does b12 absorption occur?

A

distal ileum

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31
Q

Which drugs can cause folate deficiency?

A

anticonvulsants

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32
Q

Where is folate absorbed?

A

jejunum

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33
Q

What are the laboratory findings of b12 / folate deficiency?

A
  1. macrocytic anaemia
  2. pancytopenia - low RBCs, WBCs & platelets
  3. blood film show macrovalocytes and hypersegmented neutrophils
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34
Q

What are the causes on non-megaloblastic macrocytosis?

A

alcohol, liver disease, hypothyroidism, marrow failure

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35
Q

What is meant by spurious macrocytosis?

A

The volume of red cells is normal but MCV is high.

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36
Q

What is reticulocytosis (cause of spurious mac.)?

A

An increase in reticulocytes in response to blood loss. (false mcv interpretation)

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37
Q

Why is jaundice a symptom of macrocytic anaemia?

A

RBCs die prematurely and release hb and LDH which convert hb into bilirubin.

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38
Q

Where is iron best absorbed?

A

duodenum (goes along with calcium)

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39
Q

Why does vitamin C help with iron absorption?

A

It is a reducing agent.

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40
Q

How would you treat pernicious anaemia and why?

A

IM b12 because there is a problem with absorption in the gut.

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41
Q

Other than pernicious anaemia what are some common causes of b12 deficiency?

A

diet, nitrous oxide (anaesthetic), PPIs, gastrectomy, Crohn’s

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42
Q

What does blood group A and B code for?

A

It codes for transferases - which modify the precursor ‘H’ on the red cell membrane.

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43
Q

What is Landsteiner’s law?

A

If someone lacks A or B antigen the corresponding antibody is produced in the plasma (e.g. babies). IgM plays a part in this.

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44
Q

What is the purpose of antisera?

A

It is a reagent with known antibody specificity to identify antigens on red cells.

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45
Q

What is the indication for blood transfusion?

A

Major blood loss
Sx anaemia - Hb <70g/L (<80g/L for cardiac disease)

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46
Q

When is platelet transfusion needed?

A

Prophylaxis for bone marrow failure.
Thrombocytopenia

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47
Q

When is FFP used?

A

Patient with a coagulopathy prior to surgery.

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48
Q

What the 2 main groups of haemoglobinopathies (autosomal recessive)?

A
  1. Thalassaemia = decreased rate of globin chain synthesis
  2. Structural haemoglobin variants = normal production but abnormal globin chain
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49
Q

What is a consequence of thalassaemias and why?

A

Inadequate Hb production which leads to microcytic hypochromic anaemia.

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50
Q

What is alpha thalassaemia?

A

Deletion of one or both alpha genes on chromosome 16.

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51
Q

Why is iron normal in alpha thalassaemia?

A

It is a globin synthesis problem.

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52
Q

What HbH disease?

A

Only have 1/4 alpha genes.

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53
Q

What are iron chelating drugs (e.g. desferrioxamine)?

A

Chelators bind to iron which is then excreted to try prevent iron overload in those who require regular blood transfusion.

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54
Q

What is the treatment for sickle crisis (blocked blood vessel) ?

A
  1. strong analgesia
  2. hydration
  3. rest
  4. o2
  5. antibiotics - if needed
  6. red cell exchange transfusion (severe)
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55
Q

Explain the pathophysiology behind sickle cell anaemia.

A

Sickle cell anaemia is autosomal recessive where there is an abnormal gene for beta-globin on chromosome 11.

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56
Q

Why is hydroxycarbamide used as a long term tx for sickle cell?

A

Used to stimulate production of fetal haemoglobin (HbF). Fetal haemoglobin does not lead to sickling of rbcs.

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57
Q

What problems can arise from haemolysis (2)?

A

Erythroid hyperplasia - increased bone marrow red cell production
Excess red cell breakdown products - excess bilirubin

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58
Q

What is the problem with extravascular haemolysis?

A

Normal products but in excess.

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59
Q

What causes intravascular haemolysis?

A
  1. ABO incompatibility
  2. G6PD deficiency - breaks down blood cells faster
  3. Severe falciparum malaria
  4. PNH, PCH - rare
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60
Q

What is coomb’s test?

A

To test if you have antibodies that act against your red blood cells.

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61
Q

What are the two types of autoimmune haemolytic anaemia (acquired) and explain them?

A
  1. Warm IgG - is more common and happens at normal/raised temps, usually idiopathic.
  2. Cold IgM - in lower temps causes agglutination of the antibodies and rbcs. Usually secondary to another condition.
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62
Q

What are the 2 types of alloimmune (rejection) haemolysis (acquired)?

A
  1. Haemolytic transfusion reaction
  2. Passive transfer of antibody - haemolytic disease of the newborn (mothers antibodies target the antigens on the foetus rbcs)
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63
Q

What are the membrane defects that cause acquired haemolysis? (rare)

A

Paroxysmal nocturnal haemoglobinuria - the specific mutation causes a loss of the proteins on the surface of red blood cells that inhibit the complement cascade.
Vit E deficiency
Liver disease

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64
Q

What is the most common congenital cell membrane defect?

A

Hereditary spherocytosis - is an autosomal dominant condition which causes sphere shaped rbcs to be fragile and easily break down when passing through the spleen.

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65
Q

What is a cause of congenital abnormal haemoglobin?

A

Sickle cell disease - HbS, thalassaemia

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66
Q

What is the function of the divalent metal transporter (DMT)?

A

Transports ferrous iron into duodenal enterocytes (duodenal epithelial cells).

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67
Q

How is iron absorption regulated?

A

Hepcidin - produced in the liver in response to increased iron, binds to ferroportin and causes degradation which traps it in the duodenal cells.

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68
Q

What is the difference between holotransferrin and apotransferrin?

A

Holotransferrin = iron bound to transferrin
Apotransferrin = unbound transferrin

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69
Q

What is meant by anaemia of chronic disease (AOCD)?

A

Iron misutilisation

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70
Q

What is the pathophysiology behind AOCD?

A
  1. Increased transcription of ferritin mRNA stimulated by inflammatory cytokines = increase in ferritin synthesis
  2. Increased plasma hepcidin blocks ferroportin-mediated release of iron
  3. Impaired iron supply to marrow erythroblasts and hypochromic red cells
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71
Q

What is the mechanism behind sideroblastic anaemia and how does it present on film?

A

Excess iron build up in mitochondria due to failure to incorporate iron to into haem - blue granules around nucleus.

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72
Q

What are the normal components of the haemostatic system?

A
  1. formation of platelet plug - primary
  2. formation of fibrin clot - secondary
  3. fibrinolysis
  4. anticoagulant defences
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73
Q

What is the lifespan of platelets?

A

7-10 days

74
Q

What do endothelial cells release when damaged?

A

Collagen and Von Willebrand Factor (VWF)

75
Q

What are sign and symptoms of platelet plug formation failure?

A

spontaneous bruising and purpura, mucosal bleeding (e.g. epistaxis, conjunctival), ICH, retinal haemorrhage

76
Q

Why are platelets positively charged?

A

Ca2+ on the surface - phospholipid (-ve) on the inside of a platelet.

77
Q

How do you test for clotting deficiencies and where do they show a problem?

A

~ prothrombin time = extrinsic pathway (rare)
~ activated partial pathway = intrinsic pathway

78
Q

What are the types of shock?

A
  1. Hypovolaemic - acute haemorrhage, volume depletion (reduced SVR)
  2. Cardiogenic - pump failure, reduced HR & SV, ischaemia
  3. Obstructive - e.g. PE, tamponade, tension pneumothorax
  4. Distributive/vasoplegic - “hot shock”, abnormal vascular autoregulation and vasodilation (e.g. sepsis, anaphylaxis)
  5. Endocrine - severe uncorrected hypothyroidism, addison’s crisis
79
Q

Why is nitric oxide needed?

A

Important for the regulation of blood flow, coagulation, neural activity and immunity.

80
Q

What are the clinical presentations for the different types of shock?

A

All - hypotension
Cardiogenic - Signs of myocardial failure

Obstructive: - Raised JVP
- Pulsus paradoxus
- Signs of cause

Distributive: - Septic: pyrexia, vasodilation, rapid capillary refill
- Anaphylaxis: profound vasodilation, erythema, bronchospasm, oedema

Hypovolaemia - Pale, cold skin, prolonged capillary refill

81
Q

What is the gold standard test for measuring CO?

A

Thermodilution with a PA catheter, pulse contour analysis and doppler US.

82
Q

How is shock managed?

A

ABCDE and fluids (not to overload as more at risk of pulmonary oedema).

83
Q

What types of fluid are there?

A

Crystalloids, colloids, blood.

84
Q

What pharmacological options are there for shock management?

A

~ noradrenaline = first line
~ adrenaline
~ vasopressin
~ dopamine
~ dobutamine

85
Q

What are acquired causes of thrombocytopenia?

A
  1. Reduced production - marrow prob.
  2. Increased destruction
86
Q

What causes increases destruction of platelets?

A

~coagulopathy = disseminated intravascular coagulation
~AI
~hypersplenism (overactive spleen)

87
Q

What causes platelet functional defects?

A

~drugs (aspirin, NSAIDS, steroids)
~renal failure

88
Q

What hereditary reason causes reduced platelets?

A

VWF deficiency

89
Q

What causes multiple factor deficiencies?

A

Liver failure, Vit k def./warfarin therapy, complex coagulopathy

90
Q

Which coagulation factors require vit k?

A

Factors II, VII, IX, X

91
Q

What causes vit k deficiency?

A

-poor diet intake
-malabsorption
-obstructive jaundice
-vit k antagonists (warfarin)
-haemorrhagic disease of the newborn

92
Q

What is disseminated intravascular coagulation (DIC)? [3]

A

~excessive and inappropriate activation of the haemostatic system
~microvascular thrombus formation
~clotting factor consumption (e.g. bruising)

92
Q

What is the pathway of fibrinolysis?

A

fibrinogen - fibrin -(combining with plasmin)- FDPs / d-dimers [end products]

93
Q

How do you treat DIC?

A
  1. Treat underlying cause
  2. Replacement therapy - platelet, plasma transfusion / fibrinogen replacement
94
Q

What is haemophilia?

A

An x-linked hereditary disorder with abnormally prolonged bleeding.

95
Q

Describe haemophilia A vs B.

A

A = factor VIII def. (more common)
B = factor IX def.

96
Q

What investigation is done for haemophilia?

A

Prolonged activated partial thromboplastin time

97
Q

How do you treat an arterial thrombosis (platelet rich thrombosis)?

A

Aspirin and other AP

98
Q

How is a venous thrombosis treated?

A

heparin/warfarin/other AC

99
Q

What is the MOA of heparin?

A

By inactivating thrombin and factor Xa.

100
Q

What are the potential mechanisms of thrombophilia?

A

~decreased anticoagulant activity
~decreased fibrinolytic activity
~increased coag. activity

101
Q

What naturally occurring ac inhibits factor V/Xa?

A

PC and PS

102
Q

What are examples of hereditary thrombophilia?

A

-factor V leiden
-prothrombin 20210 mutation
-protein c def.
-protein s def.

103
Q

What causes acquired thrombophilia?

A

antiphospholipid antibody syndrome - bigger risk than hereditary ones

104
Q

What is the pathogenesis behind antiphospholipid antibodies?

A

Conformational change in b2 glycoprotein which leads to activation of both primary and secondary haemostasis.

105
Q

What factor does LMW heparin turn off?

A

factor X

106
Q

What test is best to monitor when on heparin?

A

APTT

107
Q

What is a long term complication of heparin?

A

osteoporosis, HIIT (monitor fbc)

108
Q

How long does warfarin (coumarin ac) take to work?

A

a week

109
Q

Name 4 components of vit k.

A

~fat soluble
~absorbed in upper intestine
~requires bile salts for absorption
~final carboxylation of factors II (prothrombin), VII, IX, X

110
Q

What is INR used for?

A

To measure prothrombin in a patient on warfarin.

111
Q

What is the MOA of warfarin?

A

Inhibits vit k which is required for the final carboxylation of factor II, VII, IX, X.

112
Q

Why are new anticoagulants used?

A

Direct activated factor X inhibitors (e.g. edoxaban, rivaroxaban, apixaban).

113
Q

Where are rbcs destroyed in pernicious anaemia?

A

in the bone marrow

114
Q

What is myelopoiesis?

A

Development on neutrophils.

115
Q

What is meant by a myelocyte?

A

Nucleated precursor between neutrophils and blasts.

116
Q

When does the bone marrow become the site of haemopoiesis?

A

Week 16

117
Q

What is a sinusoid?

A

Sinuses that have a discontinuous basement membrane.

118
Q

How long do neutrophils live?

A

7-8hrs

119
Q

What is G-CSF (granulocyte-colony stimulating factor)?

A

Neutrophil precursor maturation.

120
Q

What does thrombopoietin do?

A

Regulates the growth and development of megakaryocytes from their precursors.

121
Q

How is haemopoiesis assessed?

A

Immunophenotyping - liquid phase to identify patterns of protein (antigen) expression unique to cell lineage by using specific antibodies.

122
Q

What are tear drop cells a sign of on blood film?

A

Anaemia of the bone marrow.

123
Q

Explain hyperplasia vs neoplasia.

A

Hyperplasia - response to stimulus
Neoplasia - absence of stimulus

124
Q

What’s the difference between acute and chronic leukaemia?

A

Acute - proliferation of abnormal progenitors with block in differentiation / maturation.

Chronic - proliferation of abnormal progenitors with no block in differentiation / maturation.

125
Q

What type of cloning is present in malignant haemopoiesis?

A

monoclonal

126
Q

What is a myeloma?

A

Plasma cell malignancy in the marrow.

127
Q

What is acute lymphoblastic leukaemia (ALL)?

A

Disease of primitive lymphoid cells (lymphoblasts).
Most common childhood cancer.

128
Q

What is acute myeloid leukaemia?

A

Similar to ALL but presents mainly in >60yrs.
Coagulation defect - DIC acute promyelocytic leukaemia

129
Q

What disease in a Auer rod on blood film seen?

A

Acute myeloid leukaemia

130
Q

What are the 3 main problems of bone marrow suppression?

A
  1. Anaemia
  2. Neutropenia - infections (gram -ve can be life threatening)
  3. Thrombocytopenia - bleeding
131
Q

What is a side effect of anthracyclines?

A

Cardiomyopathy

132
Q

What is immunohistochemistry used for?

A

Confirms lymphoma and helps subclassify.

133
Q

What kind of cancer is Burkitt’s lymphoma?

A

Fast growing B cell NHL.

134
Q

What virus do patients with Burkitt’s lymphoma present with?

A

EBV

135
Q

What are the 3 characteristics of inherited bone marrow failure in pancytopenia?

A
  1. cancer predisposition
  2. impaired haemopoiesis
  3. congenital anomalies
136
Q

What is Fanconi’s anaemia?

A

A very rare inherited marrow failure which is unable to correct interstrand cross-links (DNA damage).

137
Q

What are the acquired primary causes of bone marrow failure (3)?

A

~ idiopathic aplastic anaemia = AI attack against haemopoietic stem cells
~ myelodysplastic syndromes (MDS)
~ acute leukaemia

138
Q

What is myelodysplastic syndrome likely to evolve into?

A

Acute myeloid leukaemia

139
Q

What causes secondary acquired bone marrow failure?

A

~ drugs (e.g. alcohol, azathioprine, methotrexate)
~ B12 def.
~ infiltrative (e.g. lymphoma, non-haemopoietic malignant infiltration)
~ miscellaneous (e.g. HIV)

140
Q

What causes a polyclonal increase in immunoglobulins?

A

Reactive = infection, AI, malignancy, liver disease

141
Q

What is a paraprotein?

A

Name for a monoclonal immunoglobulin

142
Q

Explain Bence Jones protein.

A

Indicates multiple myeloma by paraproteins in the urine.

143
Q

In myeloma how does the direct tumour affect cells?

A

-bone lesions
-increased calcium
-bone pain
-replace normal bone marrow
- marrow failure

144
Q

In myeloma how does the paraprotein affect the cells?

A

renal failure
immunosuppression
hyperviscosity
amyloid

145
Q

What is the most common classified type of myeloma?

A

IgG

146
Q

What causes normoblastic macrocytic anaemia?

A

Alcohol, liver disease, myelodysplasia, hypothyroidism

147
Q

What do spherocytes indicate?

A

Hereditary spherocytosis / autoimmune haemolytic anaemia

148
Q

What are the precursors for myeloid and lymphoid cancer?

A

myeloid = neutrophils
lymphoid = b cells

149
Q

What are side effects of alkylating agents?

A

Infertility, secondary malignancy

150
Q

What gene is responsible for CML?

A

BCR-ABL1 = tyrosine kinase which causes abnormal phosphorylation

151
Q

What are the 3 main subtypes of myeloproliferative neoplasm (MPN)?

A

Polycythaemia Vera (PV) - RBCs

Essential thrombocythaemia (ET) - platelets

Primary Myelofibrosis (PMF)

152
Q

What are the causes of leuoerythroblasts on blood film?

A
  • reactive (sepsis)
  • marrow infiltration
  • myelofibrosis
153
Q

What does frontal bossing indicate?

A

Beta major thalassaemia

154
Q

When is a dry tap aspirate indicated?

A

myelofibrosis

155
Q

What is the primary treatment for VWD?

A

desmopressin

156
Q

How does haemophilia present?

A

In early life with joint bleeding.

157
Q

What is Waldenström macroglobulinaemia and what does it secrete?

A

It is a low grade lymphoma which secretes IgM.

158
Q

What causes the oxygen curve to shift to the right?

A

Increase in co2, DPG, temp.
Decrease in o2 and ph.

159
Q

Which factor does prothrombin test?

A

VII

160
Q

What does central pallor indicate?

A

hereditary spherocytosis

161
Q

What drug can induce G6P deficiency?

A

nitrofurantoin

162
Q

What conditions has heinz bodies present?

A

G6P def., alpha thalassaemia

163
Q

What is the pentad present for TTP?

A

fever, haemolytic anaemia, thrombocytopenia, acute renal failure, and neurological symptoms

164
Q

What does protamine sulphate do?

A

It reverses the acts of heparin.

165
Q

What is the difference between the MOA of aspirin and NSAIDs?

A

Aspirin = is an irreversible inhibitor of COX (cyclooxygenase) enzyme
NSAIDs = a reversible inhibitor of COX enzyme

166
Q

What drugs can cause folate deficiency?

A

anticonvulsants

167
Q

What is waldenström macroglobulinaemia?

A

A non-hodgkin’s lymphoma classified by IgM paraproteins.

168
Q

What are the specific immunoglobulins for warm and cold haemolytic anaemia?

A

warm - IgG
cold - IgM (intravascular)

169
Q

What should the treatment be for a hb <8?

A

asymptomatic - IV packed rbcs
symptomatic - blood transfusion

170
Q

What is an indicator of tumour lysis syndrome and what is the treatment?

A

Treatment of leukaemias / lymphomas (high uric acid, phosphate, potassium, low ca)

Tx = IV allopurinol / rasburicase

171
Q

What is the treatment for ITP?

A
  1. prednisolone
  2. immunoglobulins
  3. blood transfusion
  4. platelet transfusion
172
Q

What is the physiology behind oedema?

A

Increase in capillary hydrostatic pressure.

173
Q

When does delayed transfusion reaction occur?

A

After 24hrs

174
Q

What does rouleaux formation indicate?

A

multiple myeloma

175
Q

Which immunoglobulin is likely to spike in multiple myeloma?

A

IgG

176
Q

What factor does dabigatran inhibit?

A

thrombin

177
Q

What is a diagnostic test for thalassaemia?

A

haemoglobin electrophoresis

178
Q

What does frontal indicate?

A

beta major thalassaemia

179
Q

Explain the Bohr effect.

A

Shift to the right:
[Increased o2 delivery = low affinity]
- increase temp, co2, 2,3-dpg
- decrease in pH

180
Q

Describe the haldane effect.

A

Shift to the left.
[Decrease in o2 delivery = high affinity]
-increase in pH
- decrease in temp, co2, 2,3-dpg

181
Q

What is the function of 2,3-dpg?

A

It is an allosteric regulator for hb and controls the ease of o2 delivery (which reduces affinity).

3rd Year (7 decks)

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