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Haematology Flashcards

1
Q

What is the definition of anaemia?

A

Low concentration of haemoglobin

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2
Q

Give two signs of anaemia

A

Tachycardia
Dyspnoea
Pallor
Angina

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3
Q

What is the structure of haemoglobin A (HbA)?

A

4 Globular subunits
2 Alpha + 2 Beta

An Fe is bound to each subunit

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4
Q

How does foetal Hb differ from adult Hb in structure?

A

Foetal Hb has 2 Alpha and 2 Gamma subunits.

[vs. 2 Alpha and 2 Beta for adult]

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5
Q

True or false, adults have no foetal haemoglobin?

A

False. Around 2-4% of adult Hb is foetal Hb.

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6
Q

Give two causes of micro, normo and macrocytic anaemia

A

Micro: Thalassaemia, Iron deficiency, Chronic disease

Normo: Blood loss, Haemolysis.

Macro: B12/Folate deficiency, Alcohol.

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7
Q

Hypothyroidism is always macrocytic, true or false?

A

False. It can be normocytic or macrocytic.

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8
Q

In iron deficiency what happens to ferritin and transferrin levels? Which is the gold standard test?

A

Ferritin - Low
Transferrin - High

Ferritin is the best diagnostic test

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9
Q

True or false, infection or inflammation can cause Ferritin levels to increase

A

True

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10
Q

What inheritance pattern does Sickle Cell Disease follow?

A

Autosomal Recessive

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11
Q

Which species of malaria does Sickle Cell make people resistant to?

A

P falciparum

P vivax

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12
Q

What is the amino acid change caused by the SCD mutation?

A

A –> T
Glutamine –> Valine

[End up with TV]

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13
Q

Give an investigation you would perform to diagnose sickle cell disease?

A

Blood film
Reticulocyte count
FBC

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14
Q

Give two managements for acute sickle cell crisis

A

Analgesia (paracetamol/ibuprofen)

Oxygen

Foetal Hb

Fluids

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15
Q

Give two signs of Sickle Cell Disease

A 
Priapism
Frequent infection
Anaemia (normocytic)
Jaundice
Visual loss
Haematuria
Splenomegaly
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16
Q

What is TACO?

A

Transfusion Associated Circulatory Overload

Acute dyspnoea, hypertension and oedema caused by blood transfusion.

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17
Q

What is the long term treatment for sickle cell disease?

A

Regular blood transfusions to keep sickle Hb <30%.

Hydroxyurea (reduces the frequency of crises)

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18
Q

What kind of anaemia does thalassaemia cause?

A

Microcytic

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19
Q

What inheritance pattern does Thalassaemia follow?

A

Autosomal Recessive

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20
Q

What investigations are done to diagnose thalassaemia?

A

FBC

Electrophoresis

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21
Q

What is the treatment for thalassaemia?

A

Blood transfusions +iron chelation to prevent TACO

Bone marrow transplant

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22
Q

True or false, thalassaemia provides some protection against malaria?

A

True.

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23
Q

Name two cell types of myeloid origin and two of lymphoid

A

Myeloid

  • Basophils
  • Eosinophils
  • Monocytes
  • Neutrophils
  • Erythrocytes
  • Megakaryocytes

Lymphoid (learned immunity)

  • B/T lymphocytes
  • NK cells
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24
Q

How big is a red blood cell?

A

5-10 microns in diameter

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25
Q

True or false, reticulocytes are smaller than mature red blood cells?

A

False. They are larger.

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26
Q

What is the life span of a red blood cell?

A

120 days

4 months.

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27
Q

What hormone stimulates the production of red blood cells? Where is it produced?

A

Erythropoietin (EPO)

Kidney in response to low O2 levels.

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28
Q

What deficiency is present in pernicious anaemia?

A

B12 + Folate (B9) deficiency caused by autoimmune destruction of parietal cells in the stomach which reduces levels of intrinsic factor, thereby reducing absorption of B12/9.

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29
Q

How do you treat pernicious anaemia?

A

B12 and B9 supplementation

[Must give them together as giving folate without B12 can cause degeneration of the spinal cord]

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30
Q

Where is unconjugated bilirubin conjugated and by what enzyme? What is the purpose of conjugation?

A

Liver (in the hepatocytes)

Uridine-diphosphoglucuronic glucuronosyltransferase (UDPGT aka UGT)

Converts it to glucoronic acid.

Purpose is to make bilirubin soluble in water so it can pass into bile.

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31
Q

Where is conjugated bilirubin converted into urobilinogen? What causes this conversion?

A

The small bowel.

Gut bacteria.

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32
Q

What does urobilinogen (produced in the gut) become?

A

80% –> Stercobilin (faeces)
2% –> Urobilin (urine)
18% –> Enterohepatic circulation

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33
Q

What is unconjugated bilirubin bound to in circulation?

A

Albumin

When unconjugated it is only lipid soluble not aqueous soluble.

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34
Q

What is Gilbert’s sydrome and what blood result would you expect?

A

Liver disorder affecting 5% of people. Involves dysfunction of UGT enzyme in hepatocytes.

This means bilirubin cannot be conjugated. So there is a high level of unconjugated bilirubin in the blood.

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35
Q

What are the terms for high and low platelets?

A

High:

  • Thrombocytosis
  • Thrombocythemia

Low:
- Thrombocytopenia

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36
Q

From which progenitor are platelets formed?

A

Megakaryocytes

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37
Q

What hormone stimulates the production of platelets? Where is it produced?

A

Thrombopoietin

Liver

[Liver damage can cause thrombocytopenia]

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38
Q

Give a cause of underproduction and of destruction of platelets

A

Underproduction:

  • B12/Folate deficiency
  • Liver failure (low thrombopoietin)

Destruction:

  • Idiopathic thrombocytopenic purpura (ITP)
  • Thrombotic Thrombocytopenic Purpura (TTP)
  • Haemolytic Uraemic Syndrome (HUS)
  • Systemic Lupus Erythemaotosus (SLE)

[Low platelets can also result from sequestration in the spleen]

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39
Q

What test is used to diagnose autoimmune haemolytic anaemia?

A

Coomb’s Test

IgG/M against RBC

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40
Q

In haemolytic anaemia what would you expect to happen to the levels of reticulocytes, spleen size, unconjugated bilirubin, and MCV?

A

Reticulocytes: Raised
Spleen: Enlarged
Unconj: Raised
MCV: Macrocytic

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41
Q

What is the treatment for immune/idiopathic thrombocytopenic purpura?

A

Prednisolone (1st line)

Rituximab (2nd line)

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42
Q

What is the pathophysiological cause of Thrombotic Thrombocytopenic Purpura?

A

Autoimmune inhibition of enzyme ADAMTS13 –> excessive Von Willebrand Factor (not broken down) which results in excessive clotting.

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43
Q

What is the treatment for Thrombotic Thrombocytopenic Purpura?

A

Plasma exchange

Immune Suppression

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44
Q

Which is more common type A or B haemophilia?

A

Type A is 5x more common.

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45
Q

What inheritance pattern does haemophilia follow?

A

X-linked recessive

Males affected, females carry

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46
Q

Which factors are affected in type A and B haemophilia?

A 
A = 8
B = 9
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47
Q

Give two signs of haemophilia?

A

Bleeding/Bruising
Arthralgia/Arthropathy
Palsies (haematomas)

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48
Q

What is the treatment for haemophilia?

A

Blood transfusions
Clotting factors
Analgesia (not NSAIDs!)

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49
Q

Which clotting pathway is affected in haemophilia? Consequently what would you expect to happen to PT and aPTT and platelets?

A

Intrinsic pathway (12, 11, 9, 8)
aPTT prolonged
PT normal
Platelets normal

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50
Q

Which clotting factors are in the intrinsic clotting pathway? Which are in the extrinsic?

A

INT: 12, 11, 9, 8

EXT: 7

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51
Q

What causes Fibrinogen to form Fibrin?

A

Thrombin

[Produced from Prothrombin (II) by activated factor X]

52
Q

Which clotting factors are affected by vitamin K deficiency?

A

10
9
7
2

[1972]

53
Q

How many vitamins are there? Which are fat soluble?

A

13 (A, C, D, E, K)
+ 8 B vitamins

Fat soluble = A D E K

54
Q

True or false, the body can synthesise both vitamin D and K?

A

True.
D via skin
K via bacteria in intestines

55
Q

What are the four types of laukaemia? Which is most common in adults and which is most common in children?

A

Acute Lymphoblastic (Kids)
Chronic Lymphoblastic
Acute Myeloid (Adults)
Chronic Myeloid

56
Q

Give two risk factors for luekaemia

A 
Previous cancer
Chemical exposure e.g. benzenes
Smoking
Down's syndrome 
FHx
57
Q

What is the typical blood result indicative of leukaemia?

A

Pancytopenia + raised WCC

[Raised blast cells (immature cells) indicates AML]

58
Q

What is the difference between autographic and allographic stem cells?

A

Autographic are taken from the patient prior to treatment.

Allographic are taken from someone else.

59
Q

Which leukaemia is the philadelphia chromosome mutation associated with?

60
Q

In Disseminated Intravascular Coagulopathy (DIC) what happens to PT, APTT, Fibrin?

A

PT: Prolonged
APTT: Prolonged
Fibrin: Reduced

This is because the excessive clotting uses it all up the clotting factors.

61
Q

What happens to phosphate, potassium and calcium levels in tumour lysis syndrome?

A

Phosphate and Potassium are released from the lysed cancer cells and so are raised.

Calcium gets bound to phosphate and deposits in tissues. Therefore calcium in the blood decreases! Often deposits in kidneys causing renal failure.

62
Q

What is the treatment for Tumour Lysis Syndrome?

A

Allopurinol (prophylaxis) as it inhibits xanthine oxidase (thus reducing uric acid levels).

Rasburicase in acute TLS, which breaks down uric acid.

63
Q

Which clotting pathway does warfarin affect?

A

Extrinsic

Prolongs PT

64
Q

True or false, warfarin is contraindicated in pregnancy?

A

True. It is teratogenic

65
Q

Based on INR when do you stop warfarin/use Vit K, and when do you restart it?

A

1) Major Bleeds = stop! Give Vit K (+Factors 2, 7, 9, 10)
2) INR >8 = Stop + Vit K. Restart when <5.
3) INR 5-8 = Stop and restart when <5.

66
Q

Name two thrombolytic drugs. How do they work?

A

Alteplase
Streptokinase

Increase plasminogen which converts to plasmin (breaks down clots).

67
Q

Name a genetically caused thrombophylic condition

A

Factor V Leiden

Factor V enhanced which results in FX activation and clotting.

68
Q

How much of blood is fluid?

A

55% (Fluid component / plasma)

Cellular component = 44% RBC and 1% WBC/platelets.

69
Q

What is normal haematocrit?

A

44%

Volume of RBC in blood

70
Q

If you have blood loss, what will happen to the haematocrit?

A

Remain the same.

It is a proportional measure. i.e. the % of blood that is RBC.

71
Q

Which leukocyte has multi-lobed nucleus, phagocytoses bacteria, is granular and represents around 70% of WBCs?

A

Neutrophils

72
Q

Which leukocyte has bilobed nucleus, is granular, is active in parasitic infections, makes up 5% of WBCs, and neutralises the effects of histamine?

A

Eosinophils

73
Q

Which leukocyte makes up 0.5% of WBCs, has a multilobed nucleus and acts with mast cells to release histamine?

74
Q

Which leukocyte has a kidney shaped nucleus?

75
Q

Where do B and T lymphocytes mature?

A 
B = Bone marrow
T = Thymus
76
Q

What is the difference between CD4+ and CD8+ lymphocytes?

A 
CD4 = Helper
CD8 = Cytotoxic
77
Q

What is the most common plasma protein in blood?

A

Albumin (54% of plasma protein)

78
Q

Apart from albumin, name another plasma protein

A

Globins (A, B, and G)

  • Iron transport
  • Fat soluble vitamins
  • Immunoglobulins (G)

Fibrinogen
- Clot formation

79
Q

What is the mechanism of action of aspirin?

A

Blocks Cyclo-oxygenase 1 enzyme which suppresses prostaglandins and thromboxane A2 (preventing platelet aggregation).

80
Q

What does clopidogrel/prasugrel act on?

A

Blocks ADP P2Y12 receptors which stops platelet activation

81
Q

What does ABCiximab act on?

A

Blocks glycoprotein IIb / IIIa receptors which stops platelet aggregation.

82
Q

Give an example of where the 5 types of collagen are used?

A

1) Skin/Bone
2) Cartilage
3) Reticulin (organ structure)
4) Basement membrane
5) Placenta

83
Q

Basement membranes are made of what type of collagen?

84
Q

What is the predominant type of collagen in skin?

A 
Type 1 (90%)
Type 3 (10%)
85
Q

What type of muscle contains multiple nuclei, is striated and had fused myoblasts (syncitium)?

A

Skeletal muscle

86
Q

Which tool/score is used to assess the bleeding risk in patients taking anticoagulants?

A

HAS-BLED

Hypertension
Abnormal liver/renal function 
Stroke
Bleeding
Labile INR
Elderly >65
Drugs/Alcohol
87
Q

What score is used to assess the risk of VTE?

A

Well’s score

Active cancer
Calf swelling
Previous DVT
Localised tenderness
Bedridden 3+ days
Paralysis/Immobilisation
No alternative Dx. more likely

{3+ = significant. 5+ = CTPA!]

88
Q

If a patient scores 5 on the Well’s score what do you need to do?

A

CTPA

LMWH or Fondaparinux if CTPA is delayed.

89
Q

Is Fondaparinux a direct or indirect inhibitor of Factor X?

A

Indirect (just like LMWH)

Potentiates Antithrombin III
This inhibits Factor X

90
Q

Is D-Dimer a test of inclusion or exclusion?

A

Exclusion.

If its -ve you can rule out a VTE. If its +ve you need to do more tests. It is sensitive but not specific.

91
Q

What is virchow’s triad?

A

Major factors contributing to thrombus formation.

  • Stasis
  • Hypercoagulability
  • Endothelial injury
92
Q

Give two risk factors for varicose veins

A 
Age
Female
Pregnancy
FHx
Long time standing/sitting
93
Q

What 2 investigations must you do before giving a patient compression stockings?

A

Duplex US to ensure good venous circulation and Ankle Brachial Pressure Index (arterial supply).

94
Q

How are varicose veins treated?

A
  • Compression stockings
  • Endothermal ablation
  • Surgical ligation
  • Foam sclerotherapy (irritant foam causes local inflammation which closes the veins).
95
Q

What is the 1st line treatment for a continuous nosebleed?

A

Nasal Packing (cotton wool + vasoconstrictor + local anaesthetic)

Once stopped cauterise with silver nitrate stick.

96
Q

What is the first line treatment for haemochromatosis?

A

Blood letting

Deferoxamine (2nd line)

97
Q

What mutation is responsible for 95% of cases of primary polycythaemia?

A

JAK2

Results in the proliferation of erythroid progenitor cells

98
Q

Give two causes of secondary polycythaemia

A

Smoking
Cyanosis
COPD
Polycystic Kidney Disease

99
Q

True or false, in polycythemia you find macrocytosis of RBCs?

A

False. You find microcytosis due to iron depletion resulting from overproduction.

100
Q

Give two signs of multiple myeloma

A

[CRAB]

HyperCalcaemia
Renal impairment
Anaemia
Bone lesions (pepper potting)
\+ Hyperviscosity
101
Q

What would you expect to see on the bone marrow aspirate of a patient with multiple myeloma?

A

Monoclonal bands of IgG

102
Q

Give two key investigations you would do in a patient suspected of multiple myeloma

A

Bone marrow aspirate
Skeletal survey
MRI spine (if compression)
Serum electrophoresis for para protein (light chains).

(electrophoresis is preferred to Bence Jones screening now).,

103
Q

If a patient with microcytic anaemia is not responding to iron treatment, what do you suspect?

A

Sideroblastic anaemia
(Microcytic)

Caused by ineffective erythropoesis and iron loading in bone marrow.

104
Q

In sideroblastic anaemia is ferritin increased or decreased?

A

Increased. Poor use of iron results in accumulation of iron in the blood stream as wellas in the bone marrow.

105
Q

What is koilonychia? Give a cause

A

Spooning of the nails

Iron deficiency

106
Q

What are acanthocytes?

A

RBCs with spike projections due to unstable membranes.

Caused by splenomegaly, alcoholic liver disease and spherocytosis.

107
Q

In microcytic anaemia e.g. thalassaemia, iron deficiency and sideroblastic anaemia, do you find hyper or hypochromic RBCs?

A

Hypochromic

108
Q

True or false, steroids can increase the neutrophil count?

109
Q

Name a vitamin deficiency that can cause glossitis?

A

B12
B3 (Pellagra)
Iron
Zinc

110
Q

What would you expect to happen to the MCV in pernicious anaemia?

A

Increased (macrocytic)

Lack of B12

111
Q

What is the treatment for pernicious anaemia?

A

Hydroxocobalamin (B12) IM for 2 weeks

112
Q

What is Coomb’s test for?

A

Autoimmune haemolysis

113
Q

Give two indications for fresh frozen plasma

A

Urgent correction of clotting defect

  • DIC
  • Warfarin OD
  • TTP
  • Liver disease
  • When Vit K too slow
114
Q

What is TRALI?

A

Transfusion related acute lung injury (TRALI)

Acute reaction to a blood transfusion (within 24hrs):

  • Dyspnoea
  • Cough
  • White out on CXR

Tx: Stop infusion! 100% 02 treat ARDS.

115
Q

What legal statutes prevent medics from treating a patient against their consent?

A

Battery - Common Law

‘Degrading act/torture’ - European Convention on Human Rights

116
Q

What diuretic would you give, if a patient was fluid overloaded (tachycardic, dysphnoea, raised JVP etc) following a blood transfusion?

A

100% O2

Furosemide 40mg IV (‘Loop for lungs’)

117
Q

How does LMWH work?

A

Inactivates Factor Xa

[Fondaparinux does the same].

118
Q

How do you bridge a patient onto anticoagulation therapy?

A

Give both warfarin + LMWH

Continue until INR is within therapeutic range (2-3)

119
Q

What causes Hodgkin’s Lymphoma? Which has a worse prognosis, HL or NHL?

A

Malignant proliferation of lymphocytes in the lymph nodes.

HL = Reed Sternberg cells = 15% cases = More treatable

120
Q

What staging system is used to assess Hodgkin Lymphoma?

A

Ann Arbor

1) Single lymph node
2) 2+ lymph nodes (same side of diaphragm)
3) Nodes both sides of diaphragm
4) Beyond lymph nodes e.g. bone marrow

121
Q

What is the RCHOP regimen?

A 
Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Vincristine (Oncovin)
Prednisolone

Used for high grade lymphoma. Low grade may only need radiotherapy.

122
Q

What is agranulocytosis? Give a drug which can cause it

A

When granulocytes e.g. neutrophils, basophils or eosinophils stop being produced. This leaves the patient vulnerable to infection.

Carbimazole
Procainamide
Clozapine

123
Q

Give two treatments for myeloma

A

Analgesia
Bisphosphonates
Chemotherapy
Stem cell transplantation

124
Q

If a patient with myeloma gets spinal cord compression, what is the best investigation and treatment?

A

MRI spine

Dexamethasone + Radiotherapy

125
Q

What condition is considered a precursor to myeloma?

A

Waldenstrom macroglobulinaemia

IgM paraprotein overproduction –> CNS disorder and hyperviscosity.

Haematology (P4) (1 decks)

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