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Formative Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

What is different between serum and plasma?

A

Plasma- liquid with clotting factors
Serum- liquid without clotting factors

(both without RBCs)

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2
Q

Which part of skeleton produces most blood products in adults?

A

Axial skeleton

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3
Q

In what state can iron bind oxygen?

A

Ferrous, Fe2+

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4
Q

In what state is iron useless at binding oxygen?

A

Ferric, Fe3+

Ferric, DICK, we don’t like

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5
Q

How does Ferrous iron become Ferric iron?

A

Oxidisation, removing of electron

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6
Q

Why is the RBC membrane like a tent?

A 
Made up of:
Lipid bilayer (waterproof canvas tent) &
Protein spars (tent poles)
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7
Q

Which glycoprotein do the terms ‘haematopoietin’ and ‘haemopoietin’ refer to?

A

Erythropoietin

This is a shit flashcard

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8
Q

When is erythropoietin released?

A

When blood oxygen is low

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9
Q

Why is Ferric iron dangerous?

A

Doesn’t bind oxygen, allowing oxygen radicals to form & damage RBCS

Ferric, DICK, we don’t like

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10
Q

What biochemical step prevents Ferrous iron becoming Ferric iron?

A

Reduction

NADH sacrifices electron to prevent oxidisation

Remember this happens to Ferric, DICK, we don’t like

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11
Q

What happens to NADH after it prevents oxidisation of ferrous iron?

A

Becomes NAD-

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12
Q

Where does the body get NADH from?

A

Byproduct of ATP synthesis

you’d know if you listened in higher biology lol

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13
Q

What do enzymes do to oxygen radicals?

A

React to form hydrogen peroxide then water

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14
Q

What reduces hydrogen peroxide to water?

A

Glutathione

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15
Q

What does glutathione do?

A

Prevents RBC damage form oxidative stress, eg by forming water with hydrogen peroxide

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16
Q

What reduces glutathione to its useful state?

A

NADPH

kevin bridges: glutaPHione reduced by NADPH

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17
Q

What does NADPH do to glutathione?

A

Reduces it (to useful state)

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18
Q

What is NADPH generated by?

A

G6PD

Like a like a G6 Police Department

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19
Q

Relevance of G6PD to keeping blood cells healthy? (3 steps)

A

G6PD generates NADPH

NADPH reduces Glutathione to useful state

Glutathione reduces hydrogen peroxide/ oxygen radicals to water

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20
Q

Who gets problems with G6PD?

A

Mainly boys, as its X linked
In F much more unlikely as need 2 faulty copies

Like a G6- song has one female singer, four males

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21
Q

What food should G6PD deficiency sufferers avoid?

A

Fava beans lmao

Pythagoras made all his bros swear off beans

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22
Q

Red cell appearance seen in G6PD deficiency?

A 
Bite cells (degmacytes)
Blister cells

Shouldn’t take a BITE of fava beans or you will not be fly like a G6 (you will get blisters..?)

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23
Q

Red cell inclusion classically seen in G6PD deficiency?

A

Heinz body

Can you actually believe the disease that stops you eating beans has Heinz bodies as a feature HA HA HA

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24
Q

Explain difference between Thrombocytosis and Thrombophilia

A

Thrombocytosis- loadsa platelets

Thrombophilia- tendency to clot, excessive to stimulus

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25
Q

What is a reticulocyte?

A

Baby RBC just released into blood

wook at the wittle weticulocyte (vomit)

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26
Q

Differences between reticulocyte and RBC? (2)

A

Reticulocytes- larger and have some RNA

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27
Q

What does erythropoietin do?

A

Causes erythroid hyperplasia in bone marrow

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28
Q

What does low ferritin mean?

A

Iron deficiency

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29
Q

What is best treatment for iron deficiency?

A

Oral ferrous fumarate

but treat the underlying cause as GI bleed etc can be masked by symptomatic tx

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30
Q

Where is iron absorbed?

A

Proximal small bowel (Duodenum and Jejunum)

Remember DJ Ileum? Now DJ= Iron

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31
Q

Presence of Intrinsic Factor antibodies indicates what?

A

Pernicious anaemia (very specific)

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32
Q

What is Pernicious Anaemia? (3)

A

Autoimmune destruction of gastric parietal cells ∴
Can’t produce Intrinsic Factor ∴
Can’t absorb Vitamin B12

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33
Q

What makes Intrinsic Factor?

A

Gastric parietal cells

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34
Q

What does Intrinsic Factor do?

A

Binds to Vitamin B12 allowing it to be absorbed (in the ileum)

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35
Q

Where is Folate absorbed?

A

Jejunum

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36
Q

Where is B12 absorbed?

A

Ileum

Highest number B vitamin, furthest away in small bowel

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37
Q

How long do B12 stores last?

A

4 years

remember sudden anaemia in vegan after years

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38
Q

How long do Folate stores last?

A

4 months

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39
Q

1st line tx in B12 deficiency?

A

Hydroxocobalamin (B12) IM for life

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40
Q

Causes of spurious macrocytosis? (2)

A 
Reticulocytosis 
Cold agglutins (IgM mediated)
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41
Q

What is reticulocytosis?

A

Increased reticulocyte level (ie normal haemostatic response to bleed)

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42
Q

What is polychromatic blood film?

A

Blood film seen in reticulocytosis
RBCs- red
Reticulocytes- purple

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43
Q

What causes the anaemia in megaloblastic macrocytic anaemia?

A

Those big boys get whacked by apoptosis in marrow

Fewer RBCs released> anaemia

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44
Q

How to assess impact of iron treatment etc on child?

A

Symptomatic improvement

Don’t try and stick excess needles in them they’ll probably run away

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45
Q

What does polychromasia indicate?

A

New RBC production

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46
Q

Define polychromasia

A

High numbers of immature red blood cells leading to diff colours in blood film

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47
Q

Child with:

  • jaundice & anaemia,
  • family history of splenectomy,
  • spherocytes without normal RBCs seen in blood smear.

Diagnosis?

A

Hereditary spherocytosis

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48
Q

Why should the underlying cause of Iron Deficiency Anaemia be investigated before giving Iron?

A

Can mask worrying pathology

GI bleed etc can be masked by symptomatic tx

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49
Q

What type of Immunoglobin is anti-ABO antibody?

A

IgM

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50
Q

When should Fresh Frozen Plasma (FFP) not be given? (2)

A

Absence of bleeding
Without procedure planned

Even in coagulopathy

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51
Q

Patient with coagulopathy, raised Prothrombin time, not bleeding & no planned procedure. Can I give FFP?

A

NO!

Only give FFP in bleeding or with procedure planned, even in coagulopathy

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52
Q

What is raised HbA2 diagnostic of?

A

Beta Thalassaemia trait

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53
Q

What is there none of in Beta Thalassaemia major?

A

Adult haemoglobin (HbA)

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54
Q

How are Alpha Thalassaemia trait & Beta Thalassaemia trait differentiated from Iron Deficiency anaemia?

A

Ferritin normal in the thalassaemia traits

Ferritin low in IDA

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55
Q

Alpha Thalassaemia disease not compatible with life?

A

Hb Barts Hydrops Foetalis Syndrome

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56
Q

Why is there bony overgrowth in Beta Thalassaemia Major?

A

Extramedullary haematopoiesis

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57
Q

What are the endocrine symptoms of Iron Overload? (3)

A

Delayed growth/ puberty
DM
Osteoporosis

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58
Q

How is iron overload managed in Thalassaemia?

A

Iron chelating drugs (can’t venesect as in haemophilia because you just put more blood in)

eg Desferrioxamine

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59
Q

Why does iron overload cause cardiac abnormalities like arrhythmia?

A

Iron in myocardium

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60
Q

What are the Hepatic sequelae of Iron Overload? (2)

A

Cirrhosis

Hepatocellular cancer

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61
Q

How are haemoglobinopathies diagnosed?

A

Electrophoresis
Prenatal screening based on parent genotype

(High Performance Liquid Chromatography in the past)

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62
Q

Long term management of hyposplenism? (2)

A

Vaccinate

Prophylactic penicillin

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63
Q

Name a drug that increases the production of foetal haemoglobin (HbF)

A

Hydroxycarbamide

Also known as Hydroxyurea, it’s same thing

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64
Q

What does Hydroxycarbamide do?

A

Increases the production of foetal haemoglobin (HbF)

Useful in sickle cell disease

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65
Q

What does Hepcidin do? (2)

A

Decreases iron absorption

Inhibits iron release from macrophages and enterocytes

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66
Q

When is Hepcidin decreased?

A

If body iron is low

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67
Q

What channel does Hepcidin bind to, to inhibit iron transport?

A

Ferroportin

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68
Q

When is Ferritin raised? (3)

A

Too much iron
Malignancy
Tissue damage/inflammation

It’s an acute phase protein too!

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69
Q

Why is Ferritin level increased in inflammation, malignancy and tissue damage?

A

It is an acute phase protein

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70
Q

In what type of anaemia does iron build up in the mitochondria due to failure to incorporate it into haeme?

A

Sideroblastic anaemia

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71
Q

Why is Anaemia of Chronic Disease hypothesised to occur?

A

To starve pathogens of iron- they need it too!

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72
Q

What gene is mutated in haemochromatosis?

A

HFE

Haeme For Ever!!

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73
Q

Treat haemochromatosis?

A

Weekly venesection to deliberately exhaust iron stores

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74
Q

What is the main thing that happens in primary homeostasis?

A

Formation of platelet plug

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75
Q

What is the main thing that happens in secondary homeostasis?

A

Formation of Fibrin clot

76
Q

What factors are Vitamin K dependant?

A

2, 7, 9, 10

BLOODy sunday happened in 1972
count 1 as 10

77
Q

What does Vitamin K do?

A

Makes Koagulation factors

Originally named in Danish!

78
Q

What factor is deficient in Haemophilia A?

A

Factor VIII

A- Eight- 8

79
Q

What factor is deficient in Haemophilia B?

A

Factor IX

We know factor Eight is deficient in type A
B comes after A, Nine comes after Eight

80
Q

Boy with repeated bleeding into load bearing muscles and joints. Diagnosis?

A

Haemophilia

81
Q

What is a ‘target joint’ in haemophilia?

A

Joint with recurrent bleeds

Leads to fused joint with loss of joint space

82
Q

Sequelae of untreated ‘target joint’ in haemophilia? (2)

A

Fused joint

Loss of joint space

83
Q

Prevalence of Haemophilia A vs B?

A

A 5:1 B

ABrAcAdABrA (not QUITE magic cos there’s an extra B)

84
Q

How is Haemophilia treated?

A

Intravenous clotting factor (whichever is missing)

85
Q

Give some indications for longterm anticoagulation in Venous Thrombosis (4)

A

Previous thrombosis
Spontaneous (eg can’t identify trigger, no surgery etc)
Foetal loss
Arrhythmia

86
Q

What mode of inheritance is seen in Haemophilia?

A

X linked recessive

87
Q

Mechanism of Warfarin?

A

Vitamin K inhibitor

88
Q

What is Vitamin K soluble in- fat or water?

A

Fat

89
Q

The production of what is inhibited by Warfarin? (6)

A

Clotting factors 2, 7, 9, 10

Protein C and S

90
Q

Why must LMWH be given with Warfarin? (3)

A

Warfarin inhibits protein C and S production (not just clotting factors)

C and S have shorter half life than clotting factors, so are cleared faster

There is a period of time where anticoagulating effects of C and S are removed, allowing unopposed coagulation by factors 2, 7, 9, 10

LMWH makes up the difference in this gap!

91
Q

How is response to heparin monitored?

A

Activated Partial Thromboplastin Time (APTT)

92
Q

What type of heparin needs monitored?

A

Unfractionated Heparin

93
Q

What are the two types of heparin?

A

Unfractionated

Low Molecular Weight (LMWH)

94
Q

What anticoagulant has the shortest half life?

A

Unfractionated Heparin

therefore can be titrated right up to last minute before surgery

95
Q

What is the antidote to unfractionated heparin?

A

Protamine Sulphate

96
Q

What is the mechanism of heparin?

A

Potentiates anti-thrombin

97
Q

Rivaroxaban, apixaban, edoxaban inhibit which clotting factor?

A

Factor Xa

rivaroXaban, apiXaban, edoXaban all have Xa in name

98
Q

Which blood test is most raised with Warfarin treatment?

A

PT or INR (both measure same thing, whichever is available)

99
Q

How do we reverse warfarin treatment? (2)

A

Oral Vitamin K (6hr response)

IV Clotting factors (immediate response)

100
Q

What is the blood finding seen in multiple myeloma?

A

Rouleaux formation

RBCs make a wee stack

101
Q

What is suggested by RBCs all in a little stack?

A

This is the Rouleaux formation

Seen in Myeloma

102
Q

What type of poisoning is a cause of Sideroblastic Anaemia?

A

Lead poisoning

103
Q

Causes of vitamin K deficiency? (3)

A 
Dietary insufficiency (commonest)
Malabsorption
Storage problems (liver disease)
104
Q

Best test to confirm haemolysis?

A

Reticulocyte count

105
Q

Why is there macrocytic anaemia in Pernicious Anaemia?

A

No B12> cells don’t mature properly, retain nucleus > macrocytic

They undergo apoptosis due to being abnormal/nucleated > anaemia

106
Q

Why is there hyperbilirubinaemia in Pernicious Anaemia?

A

Breakdown products of increased apoptosis of RBC precursors in marrow

107
Q

What does ‘blast’ refer to in haematology?

A

A nucleated precursor cell

108
Q

What is a Megakaryocyte?

A

Platelet precursor cell

platelets break off from cytoplasm

109
Q

How are platelets produced by a Megakaryocyte?

A

Platelets break off from Megakaryocyte cytoplasm

110
Q

When embryologically does bone marrow become the main site of haemopoiesis?

A

Week 16

111
Q

Where is the main site of embryological haemopoiesis at roughly week 1-3 of development?

A

Yolk sac

112
Q

Where is the main site of embryological haemopoiesis at roughly week 3-16 of development?

A

Liver & Spleen

113
Q

Where is bone marrow biopsy taken in normal healthy adult?

A

Posterior Iliac Crest

114
Q

Where is bone marrow biopsy taken in a small child?

A

Tibial Marrow Cavity

115
Q

Why is bone marrow biopsy not taken from the tibia in normal healthy adult?

A

No red marrow to sample

In adults haemopoiesis occurs in the axial skeleton, ie no haemopoiesis in the tibia

116
Q

What does red bone marrow change to with increasing age?

A

Yellow marrow, ie fat

117
Q

What is Neutrophil maturation stimulated by?

A

Granulocyte-Colony Stimulating Factor (G-CSF)

118
Q

What is stimulated by G-CSF?

A

Neutrophil maturation

G-CSF stands for Granulocyte- Colony Stimulating Factor

119
Q

Define immunophenotyping

A

Study of antigen presentation using specific antibodies

(Antigen expression is unique to each cell lineage, immunophenotyping allows for histologically identical cells to be differentiated from one another)

120
Q

What does immunophenotyping allow us to do?

A

Differentiate histologically identical cells

tests antigen expression using antibodies, this is unique to each cell

121
Q

Generalised lymphadenopathy raises suspicion of which malignancies? (2)

A

Leukaemia

Lymphoma

122
Q

Excess blasts (>20%) suggests what?

A

Acute Leukaemia

123
Q

Two types of Acute Leukaemia?

A

Myeloblastic

Lymphoblastic

124
Q

Commonest childhood cancer?

A

Acute Lymphoblastic Leukaemia (ALL)

125
Q

Which organs does Acute Lymphoblastic Leukaemia affect much more than Acute Myeloblastic Leukaemia? (2)

A

CNS

Testes

126
Q

Surface protein on Hemopoietic Stem cells and Progenitor Cells?

A

CD34

+34 is Spain’s dialling code, where the BLOOD runs HOT and RED because they have lots of CD34 (idk)

127
Q

Auer rod cell inclusion suggests what?

A

Acute Myeloblastic Leukaemia

AML>Anti Money Laundering 👮‍♂️
Au> gold 🥇

128
Q

Test to differentiate AML and ALL?

A

Immunophenotyping

129
Q

Life threatening feverish infection with marrow suppression. Causative organism?

A

Gram Negative bacteria

130
Q

Neutropenic patient is feverish. Treatment?

A

Broad-spectrum antibiotics STAT
(covering gram negative bacteria)

Do not wait for culture/microbiology (emergency)

131
Q

Neutropenic patient is feverish, and hasn’t responded to broad-spectrum antibiotics. Causative organism?

A

Fungus

132
Q

Low levels of what type of blood cell makes a patient more susceptible to Pneumocystis Jirovecii pneumonia?

A

Neutrophils

133
Q

Mega side effects of anthracycline chemotherapy?

A

Cardiomyopathy

134
Q

Painful lymph nodes after drinking alcohol. Classic symptom of what?

A

Hodgkin’s Lymphoma

135
Q

Best node biopsy for lymphoma?

A

Excisional biopsy

Core biopsy is a bit shit as can’t see cellular architecture

136
Q

Which is better for ?lymphoma- excisional or core biopsy?

A

Excisional biopsy

Core biopsy is a bit shit as can’t see cellular architecture

137
Q

Reed Sternberg cells suggest what?

A

Hodgkin’s Lymphoma

138
Q

Tests to identify spread of Lymphoma? (2)

A

CT

PET

139
Q

Main drug in Hodgkin’s Lymphoma?

A

Bleomycin

140
Q

Bleomycin used to treat what?

A

Hodgkin’s Lymphoma

141
Q

Characteristic cell seen in Hodgkin’s Lymphoma?

A

Reed Sternberg cells

142
Q

Cellular inclusions classically seen in Acute Myeloid Leukaemia?

A

Auer bodies

AML>Anti Money Laundering 👮‍♂️
Au> gold 🥇

143
Q

What virus is Hodgkin’s Lymphoma strongly associated with?

A

Epstein Barr Virus

144
Q

At what age is Hodgkin’s Lymphoma most commonly seen?

A

20s

145
Q

Name a common high grade Non-Hodgkin’s Lymphoma

A

Diffuse Large B-Cell (Lymphoma)

146
Q

Non-Hodgkin’s Lymphoma with a propensity for extra-nodal disease? (2)

A

T Cell Non-Hodgkin’s Lymphoma

Burkitt Lymphoma

147
Q

Rituxumab targets what surface protein?

A

CD20 on B cells

Useful in B Cell Non-Hodgkin’s Lymphomas

148
Q

Brentuximab targets what surface protein?

A

CD30 on T cells

Useful in T Cell Non-Hodgkin’s Lymphomas

149
Q

CD20 seen on the surface of which cells?

A

B Cells

150
Q

CD34 seen on the surface of which cells? (2)

A

Hemopoietic Stem cells
Progenitor Cells

+34 is Spain’s dialling code, where the BLOOD runs HOT and RED because they have lots of CD34

151
Q

Fastest growing human tumour?

A

Burkitt lymphoma

152
Q

Endemic Burkitt lymphoma is associated with which infections? (2)

A

EBV (most)

Malaria

153
Q

Chromosomal translocation seen in Burkitt Lymphoma?

A

c-myc

154
Q

c-myc chromosomal translocation is seen in what haematological malignancy?

A

Burkitt Lymphoma

Burkitt was an Irish surgeon
myc sounds like start of an Irish name

155
Q

boobs

A

dleet this card

156
Q

Why should biopsy be performed before giving steroids in ?Burkitt Lymphoma ?

A

Avoids tumour lysis

157
Q

Electrolyte abnormalities seen in Tumour Lysis syndrome

A

Hyperphosphataemia (Ph)
Hyperuricaemia (U)
Hyperkalaemia (K)

Hypocalcaemia (Ca)

PhUK Ca-ncer

158
Q

Causative haematological abnormality in Fanconi Anaemia?

A

Unable to correct inter-strand DNA crosslinks

Macarena, Fanconi, CRISS CROSS

159
Q

Myelodysplastic syndromes tend to evolve into what?

A

Acute Myeloblastic Leukaemia

160
Q

Hyper or Hypocellular marrow seen in aplastic anaemia?

A

Hypocellular

161
Q

Hyper or hypocellular marrow seen in B12 deficiency anaemia?

A

Hypercellular

162
Q

Hyper or hypocellular marrow seen in hypersplenism?

A

Hypercellular

163
Q

Hyper or hypocellular marrow seen in myelodysplastic syndromes?

A

Hypercellular

164
Q

Commonest cause of hypocellular bone marrow?

A

Aplastic Anaemia (idiopathic)

165
Q

Feverish neutropenic patient has had tests sent off to microbiology. What should be done now?

A

Treat with broad spectrum antibiotics
Don’t wait for culture

Gram Negative bacteria can cause fulminant sepsis

166
Q

What happens in Tumour Lysis Syndrome

A

Large number of cancer cells die within a short period, releasing their contents into the blood

167
Q

Type of Acute Leukaemia affecting testes and CNS?

A

Acute Lymphoblastic Leukaemia

168
Q

Which immunoglobin is dimeric?

A

IgA

169
Q

Which immunoglobin is pentameric?

A

IgM

170
Q

Clock face nucleus seen in what cell?

A

Plasma cells

171
Q

What is a paraprotein?

A

Protein produced by underlying B-Cell or Plasma Cell disorder

172
Q

At what age is Myeloma typically diagnosed?

A

65

173
Q

What is MGUS?

A

Monoclonal Gammopathy of Unknown Significance

Paraprotein without myeloma organ damage

174
Q

Vincristine side effect?

A

Neuropathy

175
Q

Philadelphia Chromosome suggests what malignanacy?

A

Chronic Myeloid Leukaemia

176
Q

Emergency Lymphoma treatment?

A

Steroids

Preferably do a biopsy first

177
Q

Suggest haematological malignancies that don’t require treatment (2)

A

Early Chronic Lymphocytic Leukaemia
Low grade Lymphoma

(if no symptoms or cytopenia due to marrow infiltration)

178
Q

How to treat CLL without symptoms or cytopenia due to marrow infiltration?

A

Watchful waiting (ie no treatment)

179
Q

How to treat Low Grade Lymphoma without symptoms or cytopenia due to marrow infiltration?

A

Watchful waiting (ie no treatment)

180
Q

Commonest symptoms of Myeloma?

A

Calcium high
Renal failure
Anaemia
Bone lesions/ pain

a C.R.A.B. called Mylo 🦀

181
Q

CRAB symptoms of Myeloma?

A

Calcium high
Renal failure
Anaemia
Bone lesions/ pain

a C.R.A.B. called Mylo 🦀

182
Q

What is seen on a Leukoerythroblastic Blood Film? (2)

A

Immature granulocytes

Nucleated RBCs

183
Q

Causes of Leukoerythroblastic Blood Film? (3)

A

Haemorrhage
Bone marrow malignancy
G-CSF Administration

184
Q

Smudge Cells indicate?

A

Chronic Lymphocytic Leukaemia

185
Q

Smear Cells indicate?

A

Chronic Lymphocytic Leukaemia

Formative Revision (50 decks)

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