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phase2a medicine > haematology > Flashcards

haematology Flashcards

Haematological diseases and their risk factors, pathology, clinical signs, diagnosis, and treatment.

1
Q

causes of microcytic anaemia

A

iron deficiency
chronic disease
thalassaemia
vitamin B6 deficiency

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2
Q

how many menstruating women get iron deficiency anaemia?

A

15%

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3
Q

microcytic anaemia blood film

A

small erythrocytes

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4
Q

pathology of microcytic anaemia

A

low MCV
blood loss
malabsorption
hookworm

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5
Q

clinical sign of microcytic anaemia

A

koilonychia (spoon nails)

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6
Q

diagnosis of microcytic anaemia

A

blood film - microcytic
ferritin test
gastroscopy

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7
Q

treatment of microcytic anaemia

A

oral iron/ferrous sulfate

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8
Q

normal Hb range for males

A

131 - 166 g/L

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9
Q

normal Hb range for females

A

110 - 147 g/L

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10
Q

complications of anaemia

A 
myocardial fatty change
fatty change in liver
angina
claudication 
skin and nail atrophy
CNS cell death
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11
Q

normal MCV

A

80-100 fl

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12
Q

how many men are affected by normocytic anaemia?

A

44% of men over 85

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13
Q

causes of normocytic anaemia

A

acute blood loss
chronic disease
combined haematinic deficiency

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14
Q

pathology of normocytic anaemia

A 
normal MCV
acute blood loss
anaemia secondary to chronic bone disease
bone marrow failure
renal failure
hypothyroidism 
haemolysis
pregnancy
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15
Q

diagnosis of normocytic anaemia

A

normal MCV but decreased haemoglobin and haematocrit

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16
Q

causes of macrocytic anaemia

A

B12/folate deficiency
alcohol (liver disease)
hypothyroid
haematological (rare) - genetic disease

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17
Q

diagnosis of macrocytic anaemia

A

high MCV on blood film
Schilling test
IF/coeliac antibodies

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18
Q

causes of folate deficiency

A 
poor diet
malabsorption
increased demand (e.g. pregnancy)
medications
high exposure to UV
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19
Q

clinical sign of folate deficiency

A

macrocytosis

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20
Q

symptoms of folate deficiency

A 
loss of appetite
weight loss
weakness
heart palpitations
megaloblastic anaemia
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21
Q

diagnosis of folate deficiency

A

blood film

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22
Q

treatment of folate deficiency

A

improve diet
oral vitamin supplements
treat specific cause if secondary

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23
Q

complications of folate deficiency if pregnant

A

neural tube defect in baby

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24
Q

risk factors for sickle cell anaemia

A 
family history (recessive autosomal)
African descent
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25
Q

pathology of sickle cell anaemia

A

HbS polymerises when deoxygenated
deformation of erythrocytes
blockage of small vessels

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26
Q

signs of sickle cell anaemia

A

microvascular occlusion

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27
Q

symptoms of sickle cell anaemia

A

muscle and bone pain
strokes
vaso-occlusive crisis - pain
triggered by cold

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28
Q

treatment of sickle cell anaemia

A 
transfusion in aplastic crisis
hydroxycarbamide (increase in HbF)
prophylactic active artificial immunity
antibiotics
genetic counselling
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29
Q

complications of sickle cell anaemia

A 
aplastic crisis
chronic renal failure
sequestration crisis (atrophic spleen)
splenic infarction (immune-compromisation)
sickle cell chest syndrome
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30
Q

causes of autoimmune haemolytic anaemia

A

broadly idiopathic

can be secondary to another disease

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31
Q

pathology of autoimmune haemolytic anaemia

A

antibody mediated phagocytosis of erythrocytes

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32
Q

signs of autoimmune haemolytic anaemia

A

breathlessness

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33
Q

diagnosis of autoimmune haemolytic anaemia

A

rule out other causes of anaemia
evidence of haemolysis
serological tests
Coomb’s test

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34
Q

treatment of autoimmune haemolytic anaemia

A

blood transfusion
splenectomy
immunosuppressant (e.g. rituximab)
if secondary, treat primary illness

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35
Q

type of antibodies involved in autoimmune haemolytic anaemia

A

IgG and IgM

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36
Q

causes of thrombosis

A

Virchow’s triad:
changes in vessel surface
changes in blood flow
changes in blood constituents

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37
Q

why is thrombosis more likely after surgery or an MI?

A

blood flow is slower

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38
Q

thrombus definition

A

solid mass of blood constituents formed within the vascular system in life

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39
Q

venous thrombosis is most commonly due to

A

stasis

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40
Q

why are immobile patients more likely to get thrombosis?

A

muscular pressure decreases –> venous return also decreases

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41
Q

thrombophlebitis

A

the inflammatory reaction when a vein is thrombosed

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42
Q

phlebothrombosis

A

when an inflamed vein forms a thrombus

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43
Q

pathology of arterial thrombosis

A

usually superimposed on atheroma

generates turbulence –> loss of intimal cells –> clot formation with fibrin deposition and platelet clumping

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44
Q

propagation

A

thrombi grow in the direction of blood flow

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45
Q

signs of thrombosis

A

local pain and local inflammation

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46
Q

treatment of thrombosis

A

anticoagulants (aspirin, warfarin)

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47
Q

complications of arterial thrombosis

A

distal tissue infarction

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48
Q

complications of venous thrombosis

A

oedema

embolism

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49
Q

leukaemia risk factors

A

smoking
ionising radiation
Down’s syndrome
prior chemotherapy

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50
Q

who does acute myeloid leukaemia tend to affect?

A

older people who have had treatment for other cancers

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51
Q

who does ALL tend to affect?

A

young children

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52
Q

what does leukaemia come from?

A

haematopoietic stem cells

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53
Q

subtypes of leukaemia

A

acute lymphoblastic leukaemia
chromic lymphoblastic leukaemia
acute myeloid leukaemia
chronic myeloid leukaemia

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54
Q

which mutation is associated with chronic myeloid leukaemia?

A

Philadelphia translocation

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55
Q

where does tumorigenesis occur in leukaemia?

A

bone marrow

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56
Q

signs of leukaemia

A 
petechiae (easy bruising)
enlarged spleen/liver
fever
pale skin
low platelet count
anaemia
immune suppression (--> sores and opportunistic infection)
neurological symptoms
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57
Q

acute leukaemia diagnosis

A

> 20% of WBCs in marrow are blasts

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58
Q

what can indicate leukaemia relapse before anything else?

A

MRD testing

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59
Q

diagnosis of leukaemia

A

lymph node biopsy
XR and MRI
FBC
bone marrow biopsy

60
Q

treatment for acute myeloid leukaemia

A

chemotherapy

61
Q

what can be used to treat some variations of leukaemia?

A

tyrosine kinase inhibitors

62
Q

treatment for leukaemia

A

chemotherapy
bone marrow transplant
targeted therapy

63
Q

differential diagnosis for acute leukaemia

A

post operative changes

sepsis

64
Q

who does Hodgkin’s lymphoma affect?

A

bimodal peak (young and old)

65
Q

risk factors for lymphoma

A

HIV
EBV
HTLV-1
H.pylori

66
Q

what cells are present in Hodgkin’s lymphoma?

A

Reed-Sternberg cells

67
Q

lymphoma

A

cancerous proliferation of lymphocytes predominantly in lymph nodes, but can present anywhere in the body

68
Q

signs of lymphoma

A

compression syndromes

69
Q

symptoms of lymphoma

A 
fatigue
lump
nodal disease
night sweats
weight loss
70
Q

diagnosis of lymphoma

A 
lymph node biopsy
bone marrow biopsy
flow cytometry 
immune-phenotyping
blood films
PET scan 
blood test
71
Q

first line treatment for lymphoma

A

watch and wait

72
Q

treatment for Hodgkin’s lymphoma stage 1-2

A

combination chemotherapy and radiotherapy

73
Q

treatment for Hodgkin’s lymphoma stage 3-4

A

long term combination chemotherapy

74
Q

treatment for low grade non-Hodgkin’s lymphoma

A

radiotherapy and monoclonal antibodies

75
Q

treatment for high grade non-Hodgkin’s lymphoma

A

combined chemotherapy and monoclonal antibodies (rituximab or zevalin)

76
Q

complications of lymphoma treatment

A

infertility

77
Q

rituximab

A

monoclonal antibody that is anti-CD20 (CD20 is found on B cells)

78
Q

multiple myeloma

A

cancerous condition of bone marrow plasma cells

79
Q

risk factors for multiple myeloma

A

MGUS protein in blood

obesity

80
Q

pathology of multiple myeloma

A

cloned malignant plasma cells produce immunoglobulins
high osteoclast activity
light chain deposition in kidneys
clonal expansion –> MGUS –> early myeloma (smouldering myeloma) –> late myeloma and end organ damage

81
Q

symptoms of multiple myeloma

A 
bone pain
bleeding
frequent infections
tiredness
malaise
82
Q

signs of multiple myeloma

A 
CRAB
Calcium (high)
Renal 
Anaemia
Bone disease
83
Q

diagnosis of multiple myeloma

A

Rouleaux stacks - aggregated RBCs in blood film
high ESR
monoclonal protein in blood and urine (Bence Jones protein)
light chain deposition in kidneys
pepper pot skull
evidence of bone marrow plasma cells in excess of 10%

84
Q

treatment of multiple myeloma

A

thalidomide
dexamethasone
stem cell replacement therapy
radiotherapy

85
Q

complications of multiple myeloma

A 
peripheral neuropathy (may be from treatment)
amyloidosis
infection (main cause of death from MM)
86
Q

malaria vector

A

female anopheles mosquito

87
Q

Malaria falciparum causes what percentage of malaria cases?

A

50%

88
Q

signs of malaria

A 
flu-like symptoms
haemolytic anaemia
fever
jaundice
paroxysm (sudden changes between hot and cold)
can be cerebral 
enlarged spleen 
high bilirubin
low platelet count
89
Q

diagnosis of malaria

A

antigen RDT

thick and thin blood films

90
Q

malaria treatment

A

PO quinine

primaquine for hypnozoite clearance (check G6PD/pregnancy status)

91
Q

complication of Malaria malariae

A

quartan fever

92
Q

risk factors for polycythaemia

A 
dehydration 
hypertension
obesity
smoking
hypoxia
altitude
lung disease
cyanotic heart disease
inappropriate increased EPO secretion
93
Q

primary polycythaemia

A

polycythaemia rubra vera

94
Q

95% of cases of polycytheamia are associated with which mutation?

A

JAK2 mutation

95
Q

pathology of polycythaemia

A

clonal proliferation of haematopoietic myeloid stem cells in the bone marrow which retain the ability to differentiate into erythrocytes

96
Q

polycythaemia

A

too many red blood cells

97
Q

relative polycythaemia

A

decrease in plasma volume

normal RBC mass

98
Q

absolute polycythaemia

A

increase in RBC mass
normal plasma volume
can be primary of secondary

99
Q

signs of polycythaemia

A

splenomegaly
facial plethora
thrombosis

100
Q

symptoms of polycythaemia

A 
headaches 
dizziness
tinnitus
burning sensation in fingers and toes
itching
101
Q

diagnosis of polycythaemia

A

raised red cell mass on 51Cr studies and splenomegaly in the setting of a normal PaO2 is diagnostic

decreased serum EPO

102
Q

FBC results for patient with polycythaemia

A 
increased RCC
increased Hb
increased HCT
increased PCV
± increased WBCs and platelets
103
Q

treatment of polycythaemia

A 
aim to keep HCT <0.45 to decrease thrombosis risk 
aspirin
alpha-interferon
venesection
bone marrow suppressive drugs
104
Q

risk factors for haemophilia

A

x-linked inheritance pattern - therefore greater risk for males
30% new mutations

105
Q

cause of haemophilia A

A

factor VIII deficiency

106
Q

cause of haemophilia B

A

factor IX deficiency

107
Q

symptoms of haemophilia

A

bleeding into joints
severe arthropathy
haematomas

108
Q

diagnosis of haemophilia

A

increased APTT

decreased factor assay

109
Q

treatment of haemophilia

A

genetic counselling
recombinant factors
desmopressin
avoid NSAIDs

110
Q

acquired haemophilia

A

a bleeding diathesis causing big mucosal bleeds

caused by antibodies that suddenly appear and interfere with factor VIII

111
Q

risk factors for Von Willebrand’s disease

A

genetic - autosomal dominant or recessive

112
Q

pathology of Von Willebrand’s disease

A

decreased VWF

113
Q

signs of Von Willebrand’s disease

A

platelet disorder signs
bruising
epistaxis
menorrhagia

114
Q

diagnosis of Von Willebrand’s disease

A

increased APTT
increased bleeding time
decreased clotting factors
decreased VWF

115
Q

treatment or Von Willebrand’s disease

A

desmopressin

VWF concentrate given for surgery

116
Q

risk factors for immune thrombocytopaenia

A 
pregnancy
female
viral infection (primary)
cancer (secondary)
HIV (secondary)
117
Q

immune thrombocytopaenia pathology

A

anti platelet autoantibodies coat platelets

118
Q

who does acute immune thrombocytopaenia affect?

A

children, following an infection

119
Q

who does chronic immune thrombocytopaenia affect?

A

women

120
Q

signs of immune thrombocytopaenia

A

petechiae

121
Q

symptoms of immune thrombocytopaenia

A 
bleeding
epistaxis
menorrhagia
purpura
bruising
haematomas
122
Q

complications of immune thrombocytopaenia

A

subarachnoid haemorrhage

intracerebral haemorrhage

123
Q

diagnosis of immune thrombocytopaenia

A

megakaryocytic in marrow

anti platelet auto-antibodies

124
Q

treatment of immune thrombocytopaenia

A 
IV immunoglobulin (to temporarily raise platelet count)
rituximab
tranexamic acid inhibits breakdown of fibrin (may help with the bleeding)
125
Q

risk factors for thrombotic thrombo-cytopaenic purpura (EMERGENCY)

A

lupus
secondary
often idiopathic

126
Q

pathology of thrombotic thrombocytopenic purpura

A

reduction of a protease which chops VWF in half before entering circulation –> bit bits of VWF stick to platelets –> extensive microscopic clots in small vessels of the body causing low platelet count
results in multi-organ damage

127
Q

signs of thrombotic thrombocytopaenic purpura

A 
fever
changes in mental status
thrombocytopaenia
reduced renal function 
haemolytic anaemia
hypertension
128
Q

symptoms of thrombotic thrombocytopaenic purpura

A 
tiredness
confusion 
headaches
seizures
stroke-like episodes
129
Q

which protease is deficient in thrombocytopaenic purpura?

A

ADAMTS13

130
Q

diagnosis of thrombocytopaenic purpura

A

thrombotic microangiography

genetic tests for abnormal ADAMST13 genes

131
Q

treatment of thrombocytopaenic purpura

A

plasma exchange
glucocorticoids
rituximab
cyclophosphamide

132
Q

complications of thrombocytopaenic purpura

A

sudden death (often within 24hrs)

133
Q

thalassaemia

A

abnormal erythrocytes due to unequal amount of Hb chains

134
Q

what may carriers of thalassaemia have?

A

slightly smaller RBCs

135
Q

risk factors for thalassaemia

A

genetic

136
Q

pathology of thalassaemia

A

unbalanced production of Hb chains - divided into alpha and beta thalassaemia

137
Q

when does beta thalassaemia major present?

A

when the child stops making foetal Hb

138
Q

signs of thalassaemia

A

splenomegaly
yellow skin
slow growth in children
bone problems

139
Q

symptoms of thalassaemia

A

tiredness

pale skin

140
Q

diagnosis of thalassaemia

A 
FBC
MCV
blood film 
HbF
electrophoresis
141
Q

complications of thalassaemia

A

blood transfusions may cause iron overload –> iron deposition in organs –> haemachromatosis

e.g. myocardial siderosis from iron overload (do MRI to diagnose)

142
Q

treatment of thalassaemia

A

blood transfusions
splenectomy
hormonal replacement
marrow transplant (chance of cure)

143
Q

pathology of neutropenia due to underproduction

A

marrow failure
marrow infiltration
marrow toxicity

144
Q

pathology of neutropenia due to increased removal

A

autoimmune
Felty’s syndrome
cyclical

145
Q

common cause of neutropenia

A

chemotherapy

phase2a medicine (53 decks)

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