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Finals Club (Dundee Medicine Master Summary Deck) > Year 3: Haematology > Flashcards

Year 3: Haematology Flashcards

Everything you need to know to pass for Haematology in Dundee Medical School

1
Q

Reduced amount of Hb in blood

A

Anaemia

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2
Q

Too much Hb in blood

A

Polycythaemia

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3
Q

Reduced platelets in blood

A

Thrombocytopenia

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4
Q

Too many platelets in blood

A

Thrombocytosis

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5
Q

Too much iron in blood

A

Haemochromatosis

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6
Q

Circulating iron

A

Transferrin

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7
Q

Stored iron

A

Ferritin (in the liver)

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8
Q

Functional iron

A

Hb

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9
Q

Haematocrit

A

% of Hb in blood

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10
Q

The production of cells derived from pluripotent stem cells

A

Haematopoiesis

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11
Q

The two lineages of a multipotential haematopoietic stem stell (Haemocyoblast)

A

Left: Common Myeloid Progenitor

Right: Common Lymphoid Progenitor

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12
Q

Extended lineage of the myeloid family

A
  • Megakaryocyte
  • Erythroblast
  • Mast Cell
  • Myeloblast
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13
Q

A megakaryocyte becomes

A

Thrombocytes (Platelets)

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14
Q

A myeloblast gives lineage to?

A
  • Basophil
  • Neutrophil
  • Eosinophil
  • Monocyte
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15
Q

An erythroblast gives rise to an

A

Erythrocyte (RBC)

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16
Q

A monocyte becomes

A

Macrophage

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17
Q

Extended lineage of the lymphoid family

A
  • Natural Killer cell (NK)
  • Small lymphocyte
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18
Q

A small lymphocyte becomes

A
  • T cell lymphocyte
  • B cell lymphocyte
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19
Q

A B cell lymphocyte becomes

A

Plasma cell

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20
Q
  • Segmented nucleus
  • Neutral staining granules
A

Neutrophil

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21
Q
  • Bi-lobed nucleus
  • Bright orange granules
A

Eosinophil

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22
Q
  • Large deep purple granules (containing histamine)
  • Associated with IgE
A

Basophil

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23
Q
  • Single large nucleus
  • Faintly staining granules
  • Vacuolated
A

Monocyte

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24
Q
  • Large nucleus
  • Rim of cytoplasm
A

Lymphocyte

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25
Q

Neutrophils usually indicated

A

Bacterial infection

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26
Q

Lymphocytes usually indicate

A

Viral infection

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27
Q

Eosinophils usually indicate

A
  • Allery/ Atopy
  • Parasitic infection
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28
Q

Basophils can indicate

A
  • Polycythaemia Rubra Vera
  • Chronic myeloid Leukaemia
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29
Q

Granular leukocytes

A

WBC that contain granules

  • Neutrophils
  • Basophils
  • Eosinophils
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30
Q

Agranular Leukocytes

A

WBC that contain a single nucleus and have few/no granules

  • Monocytes
  • Lymphocytes
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31
Q

The process of producing RBCs

A

Erythropoiesis

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32
Q

Haemoglobin is made out of

A
  • Haem (porphyrin ring and Fe2+)
  • Globins
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33
Q

Adult Haemoglobin: HbA

A
  • 2 x Alpha chain globins
  • 2 x beta chain globins

97% of Hb

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34
Q

Variant of adult haemoglobin: HbA2

A
  • 2 x alpha chain globins
  • 2 x delta chain globins

2.5% of Hb

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35
Q

Foetal haemoglobin: HbF

A
  • 2 x alpha chain globins
  • 2 x gamma chain globins

0.5% of Hb

However is very high in foetus and 1st year of life

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36
Q

Haemoglobin life span

A

120 days

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37
Q

Thrombocyte life span

A

7-10 days

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38
Q

Neutrophil life span

A

7-8 hours

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39
Q

Haematopoiesis in an embryo takes place in

A
  • Yolk sac (until week 10)
  • Liver (starts week 6)
  • Bone Marrow (starts week 16)
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40
Q

Haematopoiesis at birth takes place in

A
  • Bone marrow
  • Liver
  • Spleen
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41
Q

Haematopoiesis in an adult takes place in

A

Bone marrow of:

  • Skull
  • Ribs and sternum
  • Pelvis
  • Proximal femur
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42
Q

As you get older your bone marrow turns from red to

A

Yellow ( as it’s more fatty)

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43
Q

What anatomical landmark do you aim for when taking a bone marrow biopsy

A

Posterior Superior Iliac Spine

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44
Q

Describe how erythropoiesis begins

A
  1. Interstitial fibroblasts and the proximal tubule in the kidney sense hypoxia
  2. The kidneys produce erythropoietin (EPO)
  3. EPO then stimulates the bone marrow to produce more RBCs
  4. The increase in O2 levels in the blood causes EPO levels to drop
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45
Q

What is needed for erythropoiesis to take place

A
  • Globins - from amino acids
  • Haem - from iron stores
  • B12
  • Folate

Stimulation by EPO

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46
Q

What is the end cell produced in erythropoiesis

A

Reticulocyte (an immature RBC)

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47
Q

What is the maturation stages of a RBC

A
  1. Pronormoblast
  2. Early normoblast
  3. Intermediate normoblast
  4. Late normoblast
  5. Reticulocyte
  6. Erythrocyte
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48
Q

Hypersegmented nucleus in a neutrophil

(~7-9 segments)

A

This usually means macrocytic anaemia

(Due to an inefficient breakdown of cell)

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49
Q

An erythroblast contains

A

A nucleus

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50
Q

Reticulocytes contain

A

RNA

Hence why they are polychromatic

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51
Q

Reticulocytosis happens

A

In episodes of acute blood loss or haemolytic anaemia

The bone marrow produces RBCs rapidly, to compensate, hence why they are still immature reticulocytes

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52
Q

The destruction and breakdown of RBCs

A

Haemolysis

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53
Q

Site of haemolysis

A

Spleen

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54
Q

Describe Haemolysis

A
  • RBCs are taken out of the circulation by macrophages and taken to the liver
  • Iron is taken to iron stores (becoming ferritin)
  • Porphyrin becomes unconjugated bilirubin and is taken to the liver to become conjugated
  • Globulin chains are recycled into amino acids
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55
Q

During haemolysis, globulins are recycled as

A

Amino acids

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56
Q

During haemolysis, Fe2+ is

A

Recycled to iron stores

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57
Q

During haemolysis, the porphyrin ring is broken down into

A

bilirubin

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58
Q

Haemolysis causes

A

Haemolytic anaemia due to loss of RBC

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59
Q

Signs of haemolysis

A
  • Spherocytes in blood film
  • Reticulocytes
  • Jaundice
  • Fatigue
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60
Q

Two types of haemolytic anaemia

A
  • Extravascular
  • Intravascular
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61
Q

Extravascular haemolysis

A

happens in the liver and spleen by macrophages

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62
Q

Intravascular haemolysis

A

happens in the circulation

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63
Q

Examples of Extravascular haemolysis

A
  • Liver disease
  • Hypersplenism
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64
Q

Signs of extravascular disease

A

Bilirubinuria (dark yellow urine)

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65
Q

Examples of intravascular haemolysis

A
  • HBO transfusion reaction
  • G6PD deficiency
  • Malaria
  • Prosthetic valve
  • Paroxysmal nocturnal haemoglobinuria
  • Autoimmune Haemolytic anaemia
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66
Q

Signs of intravascular haemolysis

A

Haemoglobinuria

“Pink urine, black on standing”

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67
Q

2 types of autoimmune haemolytic anaemia

A
  • Warm
  • Cold
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68
Q

Warm autoimmune haemolytic anaemia is a

A

Delayed reaction

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69
Q

Cold autoimmune haemolytic anaemia is an

A

Immediate reaction

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70
Q

IgG is involved in

A

Warm autoimmune haemolytic anaemia

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71
Q

IgM is involved in

A

Cold autoimmune haemolytic anaemia

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72
Q

Causes of Warm autoimmune haemolytic anaemia

A
  • Autoimmune disorders (SLE)
  • Chronic lymphocytic leukaemia (CLL)
  • Infections
  • Drugs (penicillin)
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73
Q

Causes of cold autoimmune haemolytic anaemia

A
  • Infections (EBV, mycoplasma)
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74
Q

Direct Coomb’s Test

A

Detects antibodies on the RBC surface

Is used to narrow down the cause of haemolysis

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75
Q

Positive Direct Coomb’s Test

A
  • Autoimmune haemolytic anaemia
  • Drug-induced haemolytic anaemia
  • Haemolytic disease of the newborn
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76
Q

Heinz bodies indicate

A

G6PD Deficiency Haemolytic Anaemia

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77
Q

Pathophysiology of G6PD deficiency

A

a defect in glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely

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78
Q

Pathophysiology of Paroxysmal Nocturnal Haemoglobinuria

A

Your body thinks your blood is foreign and so it destroys it

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79
Q

Symptom of Paroxysmal Nocturnal Haemoglobinuria

A

Peeing blood

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80
Q

Polycythaemia Rubra Vera

A

A myeloproliferative neoplasm which causes the bone marrow to produce too many red blood cells

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81
Q

Polycythaemia RV is usually due to a default in

A

JAK 2 gene

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82
Q

Polycythaemia RV presents with

A
  • Itch (after hot bath)
  • Patient looks red
  • DVT
  • Splenomegaly
  • Gout
  • Headache
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83
Q

Treatment for Polycythaemia RV

A
  • Hydroxycarbamide (marrow suppression)
  • Venesection
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84
Q

Presentation of haemochromatosis

A
  • Liver disease
  • Heart problems
  • Bronzing of the skin
  • Diabetes (iron deposition kills islet cells)
  • Arthritis
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85
Q

Types of Haemochromatosis

A
  • Primary
  • Secondary
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86
Q

Primary Haemochromatosis

A

Inherited

(decreased hepcidin, so the channels for iron release in the gut open more often, so iron is in serum)

  • High Transferrin (>50%)
  • High Ferritin (>200 (F), >300 (M))

Gradual increase, and so present in their 40s

Causes end-organ damage

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87
Q

Secondary Haemochromatosis

A

More acute

Too many blood transfusions (so iron overload)

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88
Q

Iron in cells can be detected by

A

Perl Staining Prussian Blue

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89
Q

Treatment for Primary haemochromatosis

A

Weekly Venesection in aim of exhausting iron stores

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90
Q

Treatment of Secondary Haemochromatosis

A

Desferrioxamine (Iron-chelating drugs)

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91
Q

Erythropoiesis

A

The production of RBCs

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92
Q

Mechanism of Erythropoiesis

A
  1. Hypoxia is sensed by the proximal tubule in the kidneys
  2. Kidneys produce erythropoietin
  3. Erythropoietin stimulates RBC production in the bone marrow
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93
Q

Role of folate

A
  • Converts uridine to thymidine
  • Needed for DNA synthesis
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94
Q

Daily requirement of Folate

A

Adult: 200 micrograms

Pregnant Women: 400 micrograms

Diabetic Pregnant Women: 5mg

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95
Q

Body store of Folate

A

4 months

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96
Q

Folate absorption takes place in

A

Duodenum and jejunum

“Coz DJs stay up fo-late playing music”

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97
Q

Folate deficiency is often seen in

A

Malnourished (e.g. alcoholics)

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98
Q

Role of B12

A

Is needed to make DNA, RNA, proteins due to S-adenosylmethionine synthesis

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99
Q

Daily requirement of B12

A

1.5 micrograms

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100
Q

B12 body stores last

A

2-4 years

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101
Q

B12 absorption takes place in

A

Ileum

“Because vegans lack B12 and they are ill”

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102
Q

Symptoms of B12 deficiency

A
  • Sore tongue “glossitis”
  • Neurological problems as B12 is associated with myelin development
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103
Q

Don’t prescribe folate without

A

B12 (in healthy people) as it will cause spinal cord problems (due to myelin interaction)

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104
Q

Iron absorption is regulated by

A

Hepcidin

Inhibits iron transport, and so regulates iron

  • High hepcidin: iron accumulated
  • Low hepcidin: iron exported
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105
Q

Iron absorption takes place in

A

Duodenum

“Because you need to iron your denum jeans”

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106
Q

Daily requirement of Iron

A
  • Men: 8.7mg
  • Women: 14.8mg
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107
Q

Chronic disease and inflammation causes

A

Increased hepcidin (due to IL6 and macrophages)

Which causes:

  • Decrease in iron absorption release, and this leads to microcytic anaemia
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108
Q

Glucose-6-phosphate dehydrogenase “G6PD” pathway is responsible for getting rid of

A

H2O2 free radicals

Converts NADP+ to NADPH

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109
Q

What converts Fe3+ to Fe2+

A

NADH

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110
Q

Microcytic anaemia

A
  • Low Hb
  • Low MCV (size of RBC)

Hypochromic RBCs

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111
Q

Causes of microcytic anaemia

A
  • Iron related: GI bleed, Period related, Chronic disease
  • Porphyria related: lead poisoning
  • Globulin synthesis: Thalassaemia
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112
Q

Chromosome associated with Alpha Thalassaemias

A

16

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113
Q

Chromosome associated with Beta Thalassaemias

A

11

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114
Q

2 types of thalassaemia

A
  • Alpha
  • Beta
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115
Q

Types of Alpha thalassaemias

A
  • a+/a (3 alpha globulin)
  • a0/a+ (1 alpha globulin) = HbH (3/4 betas)
  • a0/a0 (0 alpha globulin) = Major: Hb Barts (4 gammas)
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116
Q

HbH presentation

A
  • Jaundiced
  • Splenomegaly
  • “Golf ball occlusions” on blood film
  • Common in South East Asians
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117
Q

Presentation of Alpha thalassaemia major (Hb Barts)

A
  • Barts Hydrops Fetalis
  • Usually always stillborn
  • Oedema and hypoxic tissues
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118
Q

2 types of Beta thalassaemias

A
  • Trait (b+/b) or (b0/b) = 3 or 2 betas
  • Major (b0/b+) or (b0/b0) = 1 or 0 betas
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119
Q

Beta Thalassaemia Trait

A
  • Increased HbA2

As 2 alpha, 2 delta chains involved

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120
Q

Beta Thalassaemia Major

A
  • HbA2 or HbF
  • Presents 6-24 months (due to loss of HbF), failure to thrive
  • Extramedullary haematopoiesis (large head, spinal cord compression)
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121
Q

How to investigate/diagnose Thalassaemias

A

High Performance Liquid Chromatography

122
Q

Macrocytic Anaemia

A
  • Low Hb
  • Increased MCV
123
Q

3 types of Macrocytic Anaemia

A
  • Megaloblastic
  • Non-megaloblastic
  • False Megaloblastic
124
Q

Megaloblastic Anaemia

A
  • Due to failure of DNA synthesis (caused by B12 and Folate deficiencies)
  • RBC precursors cannot break down into RBCs, hence why they stay large (high MCV) and why there is less Hb (as less of them break down)
125
Q

Pathophysiology of Pernicious anaemia

A

Autoimmune condition resulting in the destruction of gastric parietal cells which leads to B12 deficiency due to malabsorption

126
Q

Non-megaloblastic anaemia

A

There are no reticulocytes etc

Due to liver disease, there is increases cholesterol and so RBCs are bound to fat/cholesterol etc and this is percieved as an increased MCV

127
Q

False megaloblastic anaemia

A

Due to cold agglutination- reticulocytosis occurs and therefore MCV is raised

128
Q

Fanconi Anaemia

A
  • Macrocytic anaemia
  • Increased HbF
  • Bone marrow failure
129
Q

Inheritance of Fanconi Anaemia

A

Autosomal recessive

130
Q

Fanconi Anaemia Presentation

A
  • Child (Usually of Jewish origin)
  • Undeveloped thumbs
  • Eye and ear defects
  • Horseshoe kidney
  • Cafe au lait spots
  • Short stature
131
Q

Fanconi Anaemia sufferers are at risk of

A

Acute Myeloid Leukaemia

132
Q

Types of Sickle Cell Disease

A

Trait or Anaemia

133
Q

Pathophysiology of Sickle Cell Disease

A

Valine takes place of glutamic acid

134
Q

Sickle Cell Trait

A

One normal Beta, one abnormal beta

(B/BS)

Mainly HbA (60%), HbS (40%)

135
Q

Sickle Cell Trait are asymptomatic until

A

Hypoxia

136
Q

HbS protects you against

A

Malaria

137
Q

Sickle Cell Anaemia (HbSS)

A

Two abnormal beta genes

(BS/BS)

HbS >80% the other 20% is HbF/HbA2

138
Q

Inheritance pattern for Sickle Cell Anaemia

A

Autosomal Recessive

More commin in sub-saharan africans

139
Q

Why are HbSS anaemic

A

Due to chronic haemolysis

Shortened RBC

Howell-Jolly bodies are seen on a blood screen

140
Q

Presentation of a sickle cell crisis

A
  • Dactylitis
  • Chest pain
  • A lot of pain everywhere

Due to RBCs clumping together in small veins

141
Q

Investigation of HbSS

A

High performance liquid chromatography

to see HbS globin

142
Q

Treatment of a sickle cell crisis

A
  • Supportive
  • Hydroxycarbamide (induces HbF production)
143
Q

Haemostasis

A

The arrest of bleeding and the maintenance of vascular patency

4 pathways

144
Q

4 pathways to haemostasis

A

Extrinsic pathway (left)

Intrinsic pathway (right)

Common pathway

Fibrinolysis

145
Q

Extrinsic pathway (left side)

A

TF > Factor VIIa

146
Q

Intrinsic pathway (right side)

A

Factor IXa > Factor VIII

Preceded by XIIa >XIa >IXa

147
Q

Common pathway

A

Prothrombin > Factor Xa/V >Thrombin

Thrombin then converts fibrinogen to fibrin

148
Q

What converts Prothrombin to thrombin

A

Factor Xa/V

149
Q

What converts fibrinogen to fibrin

A

Thrombin

150
Q

Fibrinolysis

A

Plasminogen > Plasmin by tissue plasminogen activator (tPA)

then plasmin converts fibrin to fibrin degredation products

151
Q

Tissue plasminogen activator converts

A

Plasminogen to Plasmin

152
Q

Plasmin converts

A

Fibrin to fibrin degredation products

153
Q

Describe physiology of haemostasis

A

Enothelial wall damage exposes collagen and releases Von Williebrand Factor (VWF), platelets then adhere to the site of injury and secrete thromboxane 2 which leads to the aggregation of more platelets

154
Q

Another name for prothrombin

A

Factor II

155
Q

All coagulation factors are synthesised in

A

The Liver

156
Q

Vitamin K carboxylates factors

A

II, VII, IX, X

As well as proteins S and C

157
Q

Thrombin also

A

Accentuates factors VIII/IXa

158
Q

Primary Haemostasis

A

Platelet plug

159
Q

Secondary haemostasis

A

Fibrin clot

160
Q

Test of primary haemostasis

A

PLT count

161
Q

Test for Secondary haemostasis

A

Prothrombin time (PTT)

Activated Partial Thromboplastin time (APTT)

162
Q

PTT measures

A

Extrinsic pathway

TF and Factor VIIa

163
Q

APTT measures

A

Intrinsic pathway

Factors IX/VIII

“AY PTT = factor AY-TE”

164
Q

Inhibitions of primary haemostasis

A
  • Inhibited thromboxane 2 (COX2)- by NSAIDs (decreases platelet aggregation)
  • Decreased Collagen- elderly people (makes it easier for endothelial walls to break)
  • VWF Disease (stops platelet aggregation and intrinsic pathway from working)
  • Marrow disease (thrombocytopenia)
  • Immune Thrombocytopenic Purpura (ITP)
165
Q

VWF Disease

A

Affects platelet aggregation and Factor VIII

166
Q

Vitamin K is absorbed in the

A

Dueodenum

“Wearing denum is Kool”

167
Q

To be absorbed Vit K needs

A

Bile salts

168
Q

Inhibitions of secondary haemostasis

A
  • Vit K deficiency
  • DIC (used up all of your clotting factors)
  • Haemophilia
169
Q

Disseminated Intravascular Coagulation (DIC)

A
  • Uses up all the clotting factors leading to bleeding, purpura and bruising
  • Leading to microvascular thrombus formation = end organ failure
170
Q

Treatment for DIC

A

FFP

171
Q

Two Haemophilias

A

Haemophilia A: Problem with Factor VIII

Haemophilia B: Problem with Factor IX

“AY = AY-TE”

“Bee=NINE, benign”

172
Q

Haemophilia affects the

A

intrinsic pathway

173
Q

Haemophilia A affects

A

Factor VIII

174
Q

Haemophilia B affects factor

A

IX

175
Q

Which haemophilia is more common

A

Haemophilia A (5 times more common)

176
Q

Presentation of Haemophilias

A
  • Male (X-linked)
  • Swellings in elbows and knees
177
Q

What is prolonged in VWF Disease

A
  • APTT: prolonged (problem with Factor VIII)
  • PTT: normal
  • Bleeding time: increased (problem with platelets)
178
Q

What is prolonged in Vit K deficiency

A
  • APTT: prolonged (due to Factor IX)
  • PTT: prolonged (due to Factor II and Factor VII)
  • Bleeding time: normal (platelets are fine)
179
Q

What is prolonged in Haemophilia

A

APTT: prolonged (due to Factors VIII/IX)

PTT: normal (extrinsic not affected)

Bleeding time: normal (platelets are fine)

180
Q

What is prolonged in DIC

A
  • APTT: Prolonged (Affects intrinsic factors)
  • PTT: (Affects extrinsic factors)
  • Bleeding time: (Affects platelets)
181
Q

Types of Thrombosis

A
  • Arterial
  • Venous
  • Thrombophilia
182
Q

Arterial thrombosis clots are

A

Platelet-rich clot in a high-pressure system

Endothelium breaks off, exposing endothelium leading to a platelet plug quickly fixing the problem

183
Q

Factors that increase arterial thrombosis

A
  • Enothelial damage
  • HTN/smoking
  • Hypercholesterolaemia
  • Diabetes
184
Q

Arterial thrombosis lead to

A
  • CHD
  • Angina
  • MIs
185
Q

Treatments for Arterial Thrombosis

A
  • Aspirin- blocks thromboxane 2 (COX2)
  • Clopidogrel (ADP inhibitor)

COX 2 (leads to platelet aggregation)

ADP (activates platelets to find more platelets)

186
Q

Venous thrombosis clots are

A

Fibrin rich clot in a low-pressure system

187
Q

Factors for venous thrombosis

A

Virchow’s Triad

  • Stasis
  • Vessel Wall damage
  • Hypercoagulability
188
Q

Venous thrombosis lead to

A
  • DVTs
  • PEs
  • Strokes
189
Q

Treatments for venous thrombosis

A
  • Heparin
  • Warfarin
  • DOACs (Rivaroxaban)
  • Thrombin Inhibitors (Dabigatran)
190
Q

Two types of Heparin

A
  • Unfractionated
  • Low Molecular Weight Heparin (LMWH)
191
Q

Mechanism of action of unfractionated heparin

A

Blocks thrombin

192
Q

What should you monitor if on unfractionated heparin

A

APTT

193
Q

Mechanism of action of LMWH

A

Blocks factor Xa

194
Q

What reverses the effects of heparin

A

Protamine sulphate

195
Q

What contraindicated protamine sulphate use

A

Fish allergy

as it’s made from salmon semen

196
Q

Side effects of Heparin

A
  • Heparin-Induced Thrombocytopenia
  • Osteoporosis
197
Q

Mechanism of action of Warfarin

A

Vit K antagonist

198
Q

Problem with warfarin

A

Takes 3 days to work

199
Q

Warfarin is contraindicated in

A

CYP interactions (Grapefruit Juice etc)

200
Q

How do you reverse Warfarin

A
  • Acute: Beriplex/ Prothrombin complex concentrate (clotting factors)
  • In 24 hours: Vitamin K
201
Q

International Normalized Ratio (INR)

A

A test for how well Warfarin is working

202
Q

What should INR be between

A

2 - 3

203
Q

An INR < 2 means

A

At risk of clotting

204
Q

An INR >3 means

A

At risk of bleed

205
Q

Mechanism of action of Direct Oral Anticoagulants (DOACs)

A

Directly inhibit active factor Xa:

  • Rivaroxaban (Ban Xa is in the name)
  • Apixaban
  • Edoxaban

Direct thrombin inhibitor:

  • Dabigatran
206
Q

What is the effect of thrombophilias

A

Deficiency of naturally occurring anticoagulants

Increased risk of clotting

207
Q

Two types of thrombophilias

A
  • Factor V Leiden
  • Antiphospholipid Syndrome
208
Q

Antiphospholipid Syndrome Presentation

A
  • Multiple pregnancy losses
  • Recurrent DVTs
209
Q

Antiphospholipid syndrome pathophysiology

A

Autoimmune disease where antibodies change beta-2-glycoprotein which effects primary and secondary haemostasis

210
Q

Antiphospholipid antibodies

A

aPL autoantibodies

Anti-cardiolipin antibodies

211
Q

Treatment of Antiphospholipid Syndrome

A

Aspirin- primary haemostasis

Warfarin- secondary haemostasis

212
Q

When would you swap warfarin therapy for LMWH

A

During pregnancy as Warfarin is teratogenic

213
Q

Myeloproliferative Disorders

A
  • BCR ABL positive
  • BCR ABL negative
214
Q

Myeloproliferative BCR ABL positive disorder

A

Chronic Myeloid Leukaemia (CML)

215
Q

Myeloproliferative BCR ABL negative disorders

A
  • Polycythaemia Rubra Vera (PVC)
  • Idiopathic Myelofibrosis
  • Essential Thrombocythaemia (ET)
216
Q

Myeloproliferative disorders are

A

Increase in all myeloid lineages’ cells

217
Q

Myeloid disorders present with

A
  • Weight loss
  • Night sweats
  • Fatigue
  • Anaemia
  • Splenomegaly (due to an increase in RBCs)
218
Q

Chronic Myeloid Leukaemia (CML)

A
  • Increased WBC (granulocytes)
  • Increased basophils and eosinophils
219
Q

Philadelphia chromosome indicates

A

Chronic myeloid leukaemia (9:22)

220
Q

Treatment of CML

A

Imatinib (Tyrosine Kinase inhibitor)

221
Q

Idiopathic myelofibrosis is

A

Fibrosis of the bone marrow leading to bad production of cells

Hence:

  • Leukoerythroblastic blood film (nucleated RBCs)
  • Tear-drop shaped RBCs
222
Q

Leukoerythroblastic blood film

(Nucleated RBCs)

A

Myelofibrosis

223
Q

Tear-drop shaped RBCs

A

Myelofibrosis

224
Q

Essential Thrombocythaemia

A

Excessive production of platelets

(>1000)

225
Q

Presentation of Essential thrombocythaemia

A
  • Headache
  • Visual problems
  • Sore digits
  • Bleeds a lot
226
Q

Treatment for ET

A
  • Hydroxyurea
  • Aspirin
227
Q

Lymphoid Cancers

A
  • Acute (problem with precursors)
  • Chronic (problem with mature cells)
228
Q

Acute lymphoid cancers

A
  • Acute Lymphoblastic Leukaemia (ALL)
  • Acute Myeloid Leukaemia (AML)
229
Q

Chronic Lymphoid cancer

A

Chronic Lymphoid Leukaemia

230
Q

Acute Lymphoblastic Leukaemia (ALL) pathophysiology

A
  • An increase in lymphoid progenitors
  • A decrease in myeloid progenitors (because body is so busy making lymphoid progenitors)
231
Q

ALL occurs in

A

Young kids

232
Q

An ALL blood test would show

A

Increased Lymphoblasts

  • Decreased RBCs
  • Decreased PLTs
233
Q

Increased lymphoblasts is a diagnosis of

A

ALL

234
Q

Investigations for ALL

A
  • Gold standard: Bone marrow biopsy
  • Immunophenotyping: Establish specific cells
235
Q

Treatment for ALL

A
  • Vaccinations against gram negatives
  • Antibiotics and antifungals
  • Chemotherapy
236
Q

Acute Myeloid Leukaemia (AML)

A
  • An increase in myeloid progenitors
  • A decrease in lymphoid progenitors (due to over-production of myeloid progenitors)
237
Q

AML occurs in

A

Older adults (age 60ish)

238
Q

A blood test of AML would show

A

Auer rods

Increased Myeloblasts

  • Decreased RBCs
  • Decreased PLTs
239
Q

Auer rods

A

AML

240
Q

Increased myeloblasts is a diagnosis of

A

AML

241
Q

Treatment of AML

A

A lot of chemotherapy

242
Q

Chronic Lymphocytic Leukaemia (CLL)

A

Increased number of Mature B Cells

243
Q

CLL can travel in

A

The blood and the lymph

244
Q

On a CLL blood film you would see

A

Smudge cells

245
Q

Smudge cells

A

CLL

246
Q

CLL can sometimes transform into

A

a Non-Hodgkin’s Lymphoma

247
Q

CLL patients are more likely to get

A

Viral infections (Herpes zoster)

248
Q

Types of Lymphoma

A
  • Hodgkins
  • Non Hodgkins
249
Q
  • Enlarged lymph nodes
  • Chills
  • Fatigue
  • Weight loss
  • Increased LDH
A

Symptoms of Lymphoma

250
Q

Investigations for Lymphomas

A

Lymph node biopsy

251
Q

Lymphoma is associated with

A

EBV

252
Q

Hodgkins Lymphoma

A
  • Reed-Sternberg Cells
  • Painful upon drinking alcohol
  • Itching
  • Asymptomatic painless lymphadenopathy
253
Q

Treatment for Hodgkins Lymphoma

A

Chemotherapy (Brentuximab)

Radiotherapy

254
Q

Non-Hodgkins

A
  • T-Cell
  • B-Cell
255
Q

Prognosis for T-Cell NHL

A

Bad

256
Q

Immature B-cell NHL

A

Low Grade

257
Q

Mature B-cell NHL

A

High grade

258
Q

Treatment for NHL

A

Rituximab

259
Q

Types of high grade B-cell NHLs

A
  • Burkitt’s Lymphoma
  • Mantle Cell Lymphoma
  • Waldenstorm’s Macroglobinaemia
260
Q

Burkitt’s Lymphoma

A
  • Common in Africans
  • Associated with EBV
  • Mandibular/Maxillary Tumours
  • Sometimes intra-abdominal tumours
261
Q

Stary Sky Appearance on blood film

A

Burkitt’s Lymphoma

262
Q

Treatment of Burkitt’s Lymphoma

A

Chemotherapy

  • Can cause tumour lysis syndrome so give with IV allopurinol or IV rasburicase to reduce this risk
263
Q

Tumour Lysis Syndrome can cause

A
  • hyperkalaemia
  • hyperphosphataemia
  • hypocalcaemia
  • hyperuricaemia
  • acute renal failure
264
Q

What Ig is associated with Waldenstrom’s Macroglobulinaemia

A

IgM

Hyperviscosity syndrome

265
Q

Grade I lymphomas

A

1 node group

266
Q

Grade II lymphomas

A

2 nodal groups on 1 side of the diaphragm

267
Q

Grade III lymphomas

A

Nodes involved on both sides of the diaphragm

268
Q

Grade IV

A

Extra nodal disease

269
Q

T cells are produced in the

A

Paracortex

270
Q

B cells are produced in the

A

Follicles

271
Q

Myeloma

A

A plasma cell malignancy in the bone marrow

272
Q

Presentation of Myeloma

A
  • Older patient
  • Bone pain
  • Wedge fractures of vertebrae
  • Bone lesions “Pepperpot skull”- lytic punched out lesions
  • Hypercalcaemia
273
Q

What causes hypercalcaemia in Myeloma

A

IL-6 increases osteoclasts and decreases osteoblasts which leads to the breakdown of bone

274
Q

Treatment of hypercalcaemia

A

Biphosphonates

275
Q

Investigations for myeloma

A
  • Serum electrophoresis: Monoclonal antibodies (IgG/IgA)
  • Urine electrophoresis: Bence-Jones protein
  • Increased ESR
  • X-ray: Rain-drop skull/Pepperpot skull
276
Q

Bence-jones proteins and Monoclonal antibodies

A

Myeloma

277
Q

Treatment for myeloma

A
  • Bortezomib (proteasome inhibitor) + Steroid
  • Thalidomide + Steroid
  • Cyclophosphamide + Steroid
  • Daratuximab + Steroid
278
Q

Monoclonal Gammopathy of Unknown Significance (MGUS)

A
  • Paraprotein <30g/l
  • Low plasma cells in bone marrow
279
Q

Amyloidosis

A
  • Amyloid is laid down everywhere (beta-pleated sheets)
  • Usually associated with Myeloma
280
Q

Muscle biopsy of amyloidosis patient

A
  • Congo red stain
  • Apple-green bifringent under polarized light
281
Q

If a patient has Infectious Mononucleosis (EBV) never give them

A

Amoxicillin - causes rash

Tx: Penicillin G

282
Q

Felty’s Syndrome Triad

A
  • Rheumatoid Arthritis
  • Splenomegaly
  • Neutropenia
283
Q

Howell-Jolly bodies are seen in

A
  • Hyposplenism (splenectomy)
  • Sickle-Cell anaemia
284
Q

Blue gums is a symptom of

A

Lead poisoning

285
Q

RBCs are stored for

A

35 days at 4oC

286
Q

Factors (FFP) are stored for

A

3 years at -30oC

287
Q

PLTs are stored for

A

7 days at 22oC

288
Q

Treatment for Neutropenic Sepsis

A
  • 1st: Piperacillim (Tazobactam if P allergy)
  • Severe: add Gentamicin

Give all patients at risk antifungals (Itraconazole)

289
Q

Rituximab is a

A

Monoclonal antibody

290
Q

Imatinib is a

A

Tyrosine kinase inhibitor

291
Q

Side effects of Vinca Alkaloid (Vincristine) Chemo

A

Neuropathy

292
Q

Side effect of Antracycline (Daunorubicin) Chemo

A

Cardio toxic

293
Q

Side effect of Cis-Platinum Chemo

A

Nephrotoxicity

294
Q

Universal blood donor

A

O-

As they have no antigens

295
Q

Universal receiver

A

AB+

As they have all of the antigens

296
Q

ABO system is defined on chromosome

A

9

297
Q

85% of blood types are

A

RhD+

298
Q

Transfusion-Associated Circulatory Overload (TACO)

A
  • Oedema
  • Respiratory distress
  • HTN
  • Increased JVP

Within 6 hours of blood transfusion

Tx: Diuretics

299
Q

Transfusion-Relate Acute Lung Injury (TRALI)

A
  • Immune-mediated lung injury
  • Hypotension
  • Within 6 hours of blood transfusion
300
Q

Indications for a blood transfusion

A

Hb <70 and symptomatic

Hb <80 and has cardio disease

Finals Club (Dundee Medicine Master Summary Deck) (8 decks)

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