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phase 2a clinical > haematology > Flashcards

haematology Flashcards

1
Q

plasma cell dycrasias

A

a spectrum of progressively more severe monoclonal gammopathies in which a clone or multiple clones of pre-malignant or malignant plasma cells over-produce and secrete an abnormal monoclonal antibody into the blood stream

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2
Q

2 examples of monoclonal gammopathy of undetermined significance (MGUS)

A

plasmacytomas:

  • tumours consisting of abnormal plasma cells
  • myeloma
  • solitary, multiple solitary or extramedullary plasmacytoma

Waldenstrom’s macroglobulinaemia:
-IgM related

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3
Q

MGUS

A

myeloma protein (abnormal antibody) is found in the blood
MIg <30g/L
no significant increase in bone marrow plasma cells
no organ impairment
CAN LEAD TO MULTIPLE MYELOMA

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4
Q

multiple myeloma

A

neoplastic proliferation of bone marrow plasma cells

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5
Q

multiple myeloma: characteristics

A

monoclonal protein in serum or urine
lytic bone lesions
excess plasma cells in bone marrow
CRAB end organ damage- calcium, renal, anaemia, bone

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6
Q

multiple myeloma: pathogenesis

A
  • accumulation of malignant plasma cells in bone marrow causes it to fail
  • the malignant cells produce excess of one type of immunoglobulin (IgG=55%, IgA=20%)
  • low variety of Ig causes immunosuppression
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7
Q

multiple myeloma: epidemiology

A

average age of diagnosis =70
more common in afro-caribbeans
1% of all cancers
13% of haem cancers

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8
Q

multiple myeloma: incidence/prevalence

A

incidence= 40/million/year

prevalence 180-279/million

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9
Q

multiple myeloma: presentation OLD CRAB

A

old age
Calcium elevated
Renal failure, proteinuria
Anaemia- neutropenia or thrombocytopenia causes infection, bleeding, fatigue and pallor
Bone lytic lesions- back pain and fractures

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10
Q

multiple myeloma: FBC investigation

A

normocytic normochromic anaemia
raised ESR
rouleaux formation of blood film

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11
Q

multiple myeloma: U&E investigation

A

high calcium
high alkaline phosphatase
bence-jones protein present

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12
Q

multiple myeloma: imaging investigations

A

lytic lesions
pepper-pot skull
fractures
osteoporosis

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13
Q

multiple myeloma: bone marrow biopsy

A

increased plasma cells

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14
Q

multiple myeloma: cure or treatment

A

incurable disease

aim of treatment is to achieve plateau phase, control the symptoms and supportive measures

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15
Q

multiple myeloma: treatment

A

chemotherapy, steroids and bisphosphonates

treat end organ damage and infections

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16
Q

leukaemia

A

presence of rapidly proliferating immature blood cells (precursors of white or red) in the bone marrow that are non-functional

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17
Q

what does leukaemia cause

A

wasting energy on non-functioning cells
space taken up in bone marrow
bone marrow unable to produce normal cells
when bone marrow is filled, leukaemia cells enter blood

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18
Q

leukaemia: types

A
  • Acute lymphoblastic leukaemia (ALL)= small lymphocyte that becomes B and T cells
  • Acute myeloid leukaemia (AML)= myeloblast
  • Chronic myeloid leukaemia (CML)= basophil, neutrophil, eosinophil
  • Chronic lymphatic leukaemia (CLL)= B cells
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19
Q

leukaemia: risk factors

A

congenital- very rare, down’s syndrome (1-2% get AML)

environmental= radiotherapy, chemo, benzene/other chemicals

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20
Q

acute lymphoblastic leukaemia: epidemiology

A

common between 2-4 years old
most common cancer in childhood
if proliferation is all B cells- children
all T cells- adults

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21
Q

acute lymphoblastic leukaemia: presentation

A
  • marrow failure (anaemia, thrombocytopenia, infection)
  • bone marrow infiltration causes bone pain
  • liver/spleen infiltration results in hepatosplenomegaly
  • node infiltration causes lymphadenopathy
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22
Q

acute lymphoblastic leukaemia: investigations

A

FBC/blood film
CXR/CT to see for mediastinal and abdo lymphadenopathy
Lumbar puncture to see for CNS involvement

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23
Q

acute lymphoblastic leukaemia: treatment

A 
blood/platelet transfusions
treat infections
IV fluids
chemo
marrow transplant
ALLOPURINOL- prevents tumour lysis syndrome
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24
Q

acute myeloid leukaemia: epidemiology

A

most common leukaemia in adults
associated with radiation and Down’s syndrome
Progresses rapidly with death in 2 months if untreated

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25
Q

acute myeloid leukaemia: presentation

A

gum hypertrophy
hepatomegaly and splenomegaly
marrow failure- anaemia, thrombocytopenia, infection

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26
Q

acute myeloid leukaemia: diagnosis

A

WCC raised but can be low or normal

diagnosis depends on bone marrow biopsy but differentiation from ALL is based on microscopy and immunophenotyping

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27
Q

acute myeloid leukaemia: complications

A

infection is the major issue- septicaemia

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28
Q

acute myeloid leukaemia: treatment

A 
blood/platelet transfusions
treat infections
IV fluids
chemo
marrow transplant
ALLOPURINOL- prevents tumour lysis syndrome
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29
Q

chronic myeloid leukaemia: epidemiology

A

exclusively a disease of adults
mainly occurs between 40-60 years old
slight male predominance
80% have Philadelphia chromosome which has tyrosine kinase activity- stimulates cell division

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30
Q

chronic myeloid leukaemia: presentation

A 
symptomatic anaemia
splenomegaly- abdo discomfort
weight loss
palor
fever
gout due to purine breakdown
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31
Q

chronic myeloid leukaemia: diagnosis

A

blood count- high WCC, low Hb, low platelets

bone marrow aspirate- hypercellular

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32
Q

chronic myeloid leukaemia: treatment

A

stem cell transplant

oral imatinib- specific tyrosine kinase inhibitor

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33
Q

chronic lymphocytic leukaemia: epidemiology

A

most common leukaemia
mainly occurs late in life
genetic mutations influence risk
pneumonia can also be a triggering event

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34
Q

chronic lymphocytic leukaemia: presentation

A

often no symptoms
may be anaemic
if severe- weight loss, sweats, anorexia
enlarged, rubbery, non-tender nodes

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35
Q

chronic lymphocytic leukaemia: diagnosis

A

blood count- raised WCC with high lymphocytes

blood film- smudge cells seen in vitro

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36
Q

chronic lymphocytic leukaemia: complications

A

autoimmune haemolysis
increased infection due to low IgG
marrow failure

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37
Q

chronic lymphocytic leukaemia: progression

A

death is often due to complication of infections

may transform into aggressive lymphoma- Richter’s syndrome

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38
Q

chronic lymphocytic leukaemia: treatment

A

blood transfusion
stem cell transplant
chemo/radiotherapy
human IV immunoglobulins

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39
Q

chronic lymphocytic leukaemia: prognosis

A

rule of thirds
1/3 never progresses
1/3 progresses slowly
1/3 progresses quickly

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40
Q

lymphoma

A

disorder caused by malignant proliferations of lymphocytes

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41
Q

lymphoma: locations

A

accumulate in lymph nodes causing lymphadenopathy

can also be found in blood, bone marrow, liver and spleen

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42
Q

lymphoma: aetiology

A

most cases unknown
immunodeficiency- primary (e.g. ataxia telangiectasia) or secondary (e.g. HIV, transplants)
infections
autoimmune disorders

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43
Q

lymphoma: symptoms

A

loss of appetite
loss of weight
night sweats

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44
Q

lymphoma: signs

A

hepatosplenomegaly

lymph node enlargement

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45
Q

lymphoma: investigations

A

blood film and bone marrow
lymph node biopsy
immunophenotyping
imaging

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46
Q

lymphoma: assessing a patient

A 
history/exam
bloods
CXR
echo
PFTs
performance status
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47
Q

lymphoma: WHO performance status

A

0= asymptomatic
1=symptomatic but only restricted by strenuous activity
2= symptomatic <50% in bed during day
3= symptomatic >50% in bed but not bed bound
4=bed bound
5= death

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48
Q

lymphoma: subtypes

A

hodgkin’s

non-hodgkin’s

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49
Q

hodgkin’s lymphoma: presentation

A

painless
lymphadenopathy
(B symptoms) sweats, weight loss

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50
Q

hodgkin’s lymphoma: diagnosis

A

reed-sternberg cell: 4 histological subtypes

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51
Q

hodgkin’s lymphoma: stages

A

1= one place
2= 2 areas or more, same side of diaphragm
3= lymph nodes on both sides of diaphragm
4 spread to multiple places

A= absence of B symptoms
B=presence

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52
Q

hodgkin’s lymphoma: treatment

A

depends on stage
ABVD- adriamycin, bleomycin, vinblastine, dacarbazine
relapse responds to marrow transplant

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53
Q

hodgkin’s lymphoma: treating stage 1-2A

A

short course combo of chemo followed by radiotherapy

70-80% prolonged disease free survival

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54
Q

hodgkin’s lymphoma: treating stage 2B-4

A

combination chemotherapy

50-70% prolonged disease free survival

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55
Q

hodgkin’s lymphoma: late effects

A 
infertility
cardiomyopathy (anthracyclines) 
lung damage (bleomycin)
peripheral neuropathy (vinca alkaloids)
psychological issues
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56
Q

non-hodgkin’s lymphoma (NHL)

A

presentation, subtypes, treatments and outcomes have a much larger variety

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57
Q

low grade/indolent NHL

A

e.g. follicular lymphoma
slow growing
usually advanced at presentation
average survival is 9-11 years

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58
Q

low grade/indolent NHL: treatment

A 
do nothing!
alkylating agents
purine analogues
combination chemo
monoclonal antibodies
radiotherapy
bone marrow transplant
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59
Q

high grade/aggressive NHL

A

e.g. diffuse large B cell lymphoma
usually nodal presentation but 1/3 have extranodal involvement
patients usually unwell with short history

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60
Q

high grade/aggressive NHL: treatment

A

early= short course chemo+radiotherapy

advanced= combination chemo and monoclonal antibodies

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61
Q

monoclonal antibodies

A

rituximab

anti-CD-20 targets CD20 expressed on cell surface of B cells

minimal side- effects

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62
Q

lump in the neck- differential diagnosis

A

infected or inflamed lymph nodes
malignant lymph nodes
thyroid
embryologic remnant

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63
Q

anaemia

A

reduced haemoglobin levels

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64
Q

normal haemoglobin ranges

A

male= 131-166g/L

female=110-147g/L

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65
Q

anaemia: acute consequences

A

reduced oxygen transport
tissue hypoxia
compensation- increased perfusion, oxygen transfer and red cell production

66
Q

anaemia: pathological consequences

A

myocardial fatty change
fatty change in liver
skin and nail atrophic changes
CNS cell death

67
Q

normal red blood cell cycle

A

produced in bone marrow
life span 120 days
removed in spleen, liver, bone marrow or blood loss

68
Q

types of anaemia

A

microcytic
normocytic
macrocytic

69
Q

anaemia: mean corpuscular volume

A

the size of red blood cells, used to determine the type of anaemia

normal: male=81.8-96.3fl, female= 80-98.1fl

70
Q

microcytic anaemia

A

small, often hypochromic red blood cells

low MCV

71
Q

microcytic anaemia: causes

A

iron deficiency
chronic disease
thalassaemia

72
Q

microcytic anaemia: iron deficiency

A

tests= ferritin or iron studies

treat this with iron supplements (ferrous sulphate)

73
Q

microcytic anaemia: chronic disease

A

investigate clinically and in a lab

often renal failure or infections

74
Q

normocytic anaemia

A

normal MCV but haematocrit and haemoglobin is low

75
Q

normocytic anaemia: causes

A

acute blood loss
chronic disease
combined haematinic deficiency (iron, B12, folate)

76
Q

macrocytic anaemia

A

red blood cells are larger than normal

bigger MCV

77
Q

macrocytic anaemia: causes

A

B12/folate deficiency
alcohol excess/liver disease
hypothyroid

78
Q

anaemia: B12 deficiency

A

IF antibodies
schilling test
coeliac antibodies

treat with B12 replacement

79
Q

haemoglobinopathies

A

disorders of quality such as sickle cell

disorders of quantity such as thalassaemia

80
Q

sickle cell disorders

A

mutated Hb distorts RBCs into crescent shape at low oxygen levels
arise from homozygous state (SS) or combined heterozygous (SC or Sb)

81
Q

sickle cell pathogenesis

A

Hb S is a variant Hb arising because of a point mutation in the b globin gene

82
Q

sickles cell carriers

A

symptom free

protection against falciparum malaria

83
Q

managing sickle cell disorders

A

acute complications such as sickle chest syndrome or stroke
chronic complications such as renal and joint damage
disease modification- transfusion, stem cell transplant

84
Q

thalassaemia

A

heterogenous disorders- deletions(alpha thal) and mutations (beta thal)
globin chain disorders resulting in diminished synthesis of 1 or more chains
causes a decrease in Hb

85
Q

clinical classification of thalassaemia

A

thal major= transfusion dependent
intermedia= can survive w/o regular transfusions
carrier= asymptomatic

86
Q

thalassaemia major

A

age presented is 6-12 months
severe anaemia
1000 sufferers in UK
220,000 carriers in UK

87
Q

thalassaemia major presentation

A

failure to feed
listless
crying
pale

88
Q

thalassaemia major blood results

A

Hb=40-70g/L
MCV and MCH low
irregular and pale RBCs on film
ferritin normal

89
Q

treating thalassaemia major

A

regular transfusions
iron chelation
endocrine supplementation
bone health

90
Q

monitoring thalassaemia major

A 
ferritin
cardiac and liver MRI
vit D, calcium PTH
thyroid
endocrine testing
91
Q

morbidity and mortality from transfusional iron overload

A
  • thalassaemia results in death during childhood if not treated with transfusions
  • transfusions causes increase in body iron load as no natural means for elimination
  • excess iron is deposited in the liver and spleen causing fibrosis and cirrhosis
  • also deposited on glands and heart= diabetes, heart failure and premature death
92
Q

membranopathies

A

deficiency of red cell membrane proteins
autosomal dominant
spherocystosis( vertical interaction) and elliptocytosis (horizontal) are most common

93
Q

consequences of membranopathies

A

neonatal jaundice
mild to moderate haemolytic anaemia w/ occasional exacerbations during infection
gallstones

94
Q

parvovirus and haemolytic anaemias

A

common infection in children
occurs in epidemics
leads to decreased RBC production
dramatic drop in patients who have reduced red cell lifespan

95
Q

enzymopathies

A

lead to shortened red cell lifespan from oxidative damage

G6PD deficiency and pyruvate kinase deficiency are most common

96
Q

glucose 6 phosphate dehydrogenase deficiency

A

caused by mutations within G6PD gene
most are asymptomatic
X-linked but females also affected
african, middle eastern, mediterranean and south asian

97
Q

glucose 6 phosphate dehydrogenase deficiency consequences

A

haemolysis, jaundice, anaemia
usually self-limiting
symptomatic patients rate

98
Q

primaquine and glucose 6 phosphate dehydrogenase deficiency

A

this drug is used for curing malaria but should not be prescribed to someone with g6pdd as it can react to cause haemolytic anaemia

99
Q

FBC reference ranges

A

HB=131-166
WBC=3.5-9.5
plts=150-400
MCV= 81.8-96.3

100
Q

polycythaemia

A

too many red blood cells

101
Q

polycythaemia causes

A

primary cause or proliferative= polycythaemia ruba vera

secondary/reactive= smoking, lung disease, altitude, cyanotic heart disease

102
Q

polycythaemia ruba vera (PRV)

A

overactive bone marrow
mainly RBCs but also WBCs and Plts
JAK2 mutation is 95%

103
Q

polycythaemia ruba vera (PRV) presentation

A

plethoric appearance
thrombosis
itching
splenomegaly

104
Q

polycythaemia ruba vera (PRV) treatment

A

aspirin
venesection
bone marrow suppression drugs

105
Q

neutrophilia

A

increase in number of neutrophils

106
Q

neutrophilia causes

A 
reactive= infection, inflammation, malignancy
primary= chronic myeloid leukaemia
107
Q

neutropenia

A

abnormally low conc. of neutrophils

108
Q

neutropenia severity

A

normal 1.7-6.5
mild 1-1.7
moderate 0.5-1
severe (major infection risk) <0.5

109
Q

neutropenia caused by underproduction

A

marrow failure
marrow infiltration
marrow toxicity e.g. drugs

110
Q

neutropenia caused by increased removal

A

autoimmune

cyclical

111
Q

lymphocytosis

A

increase in number of lymphocytes, neutrophil number normal

112
Q

lymphocytosis causes

A 
reactive= infection, inflammation, malignancy
primary= chronic lymphocytic leukaemia
113
Q

thrombocytopenia

A

abnormally low levels of thrombocytes

114
Q

thrombocytopenia caused by increased destruction

A

autoimmune
hypersplenism
drug related immune destruction
consumption of platelets

115
Q

thrombocytopenia caused by decreased production

A
  • congenital
  • bone marrow infiltration
  • reduced platelet production by bone marrow
  • dysfunctional production of platelets
116
Q

thrombocytosis

A

excessive number of platelets

117
Q

thrombocytosis causes

A 
reactive= infection, inflammation, malignancy
primary= essential thrombocythaemia
118
Q

platelet physiology

A

anucleate cell, fragments from megakaryocytes

regulated by thrombopoietin

119
Q

platelet tests

A

number- FBC
appearance- blood film
function- PFA, bleeding time
surface proteins- flow cytometry

120
Q

causes of bleeding

A 
injury
vascular disorders
low platelets
abnormal platelet function
defective coagulation
121
Q

clinical features of platelet dysfunction

A 
mucosal bleeding
gum bleeding
easy bruising
purpura
traumatic haematomas
122
Q

causes of low platelets

A 
production failure (drugs, marrow suppression or failure, acquired, congenital)
increased removal (immune, consumption, splenomegaly)
123
Q

congenital impaired platelet function

A

von willebrand disease

platelet disorders

124
Q

acquired impaired platelet function

A

uraemia

drugs

125
Q

immune thrombocytopenia

A

IgG antibodies formed against platelets and megakaryocyte surface glycoproteins

126
Q

primary immune thrombocytopenia

A

may follow viral infection or immunisation

127
Q

secondary immune thrombocytopenia

A

occurs in association with some malignancies such as chronic lymphocytic leukaemia
HIV/Hep C infections

128
Q

immune thrombocytopenia: investigations

A

for the underlying cause

diagnosis of exclusion

129
Q

immune thrombocytopenia: treatment

A

immunosuppression
treat underlying cause
give platelets if bleeding

130
Q

disseminated intravascular coagulation

A

blood clots form throughout the body, blocking small blood vessels

131
Q

disseminated intravascular coagulation: pathophysiology

A

cytokine release in response to systemic inflammatory response syndrome
activates clotting cascade

132
Q

disseminated intravascular coagulation: investigations

A

underlying cause

evidence of organ failure

133
Q

disseminated intravascular coagulation: treatment

A

treat underlying cause

supportive provision of platelets, fibrinogen and clotting factors

134
Q

thrombotic thrombocytopenia purpura

A

spontaneous platelet aggregation in microvasculature (brain, kidney, heart)
reduction in protease enzyme

135
Q

thrombotic thrombocytopenia purpura: consequences

A

consumption of platelets
microangiopathic haemolytic anaemia
renal/CNS/cardiac impairment

136
Q

thrombotic thrombocytopenia purpura: treatment

A 
plasma exchange
immunosuppression
no platelets- increases thrombosis
90% mortality
10-20% mortality if treatment starts promptly
137
Q

neutropenia and neutropenic sepsis

A

abnormally few neutrophils in the blood leads to increased susceptibility to infection

138
Q

neutropenic sepsis: causes

A

decreased production due to problem with the bone marrow

haematologist- chemo

139
Q

neutropenic sepsis: features

A

fever
rigor
feeling unwell or off
low BP (not as common)

140
Q

neutropenic sepsis: when to suspect

A

if they had chemo in the last 3 months
present with fever
chills/rigor
isolated hypotension

141
Q

neutropenic sepsis: what to do

A

see patient
put in cannula
give antibiotics

142
Q

neutropenic sepsis: early management

A

first dose of antibiotics is important

if in doubt give them antibiotics

143
Q

sickle cell crisis: features

A
  • precipitated by dehydration, cold weather and/or infection
  • gradual onset over a few days
  • then unbearable pain in arms, back, chest or abdo
  • poor prognosis if: chest pain, severe abdo pain or neurological symptoms
144
Q

sickle cell crisis: what to do

A

see patient
control the pain
put in cannula and start fluids

145
Q

sickle cell/acute chest syndrome

A

cycle of hypoxia, sickles and lung infarction

146
Q

acute chest syndrome: features

A

new signs on chest xray

hypoxia

147
Q

acute chest syndrome: what to do

A

see patient
give oxygen, fluids, antibiotics
call haematologist

148
Q

spinal cord compression

A

occurs in any malignancy due to metastases of the spine
particularly prone= myeloma patients
can be caused by plasmacytoma

149
Q

spinal cord compression: symptoms

A 
back pain
neuropathic pain
leg weakness
saddle anesthesia 
loss of sphincter control
150
Q

spinal cord compression: clinical signs

A

decreased power in legs
typically decreased reflexes
decreased sensitivity
decreased anal tone

151
Q

spinal cord compression: what to do

A

keep them in bed
dexamethasone 8mg
urgent MRI

152
Q

spinal cord compression: treatment

A

surgical- avoid in myeloma

medical- radiotherapy and chemo

153
Q

hyperviscosity syndrome

A

malignant plasma cells produce a lot of immunoglobulin which increases the thickness of your blood

154
Q

hyperviscosity syndrome: symptoms

A 
non specific symptoms
headache
neurological
blurred vision
fatigue
mucosal bleeding
confusion
155
Q

hyperviscosity syndrome: examination

A

general=bruising
CVS= pulmonary oedema, evidence of fluid overload
neuro= confusion, ataxia, nystagmus

156
Q

hyperviscosity syndrome: what to do

A

put in cannula
fluids
call haematologist

157
Q

tumour lysis syndrome

A

chemo kills cancer cells- making them release intracellular components
this overwhelms the kidneys causing crystallisation and renal failure

158
Q

tumour lysis syndrome: those at risk

A

large tumour burden= more cells to die= greater risk

aggressive cancer= rapid cell turnover= greater risk

159
Q

tumour lysis syndrome: features

A 
blood tests
hyperkalaemia= first sign
hyperphosphataemia
hyperuricaemia
hypocalcaemia
160
Q

tumour lysis syndrome: prevention

A
  • much easier than treatment
  • give vigorous IV fluids during chemo and days after
  • rasburicase eliminates uric acid
  • monitor bloods and urine output closely
161
Q

tumour lysis syndrome: treatment

A 
fluids
rasburicase
monitor urine output
manage electrolytes
dialysis

phase 2a clinical (8 decks)

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