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Phase 2a Peer Teaching > Haematology Peer Teaching > Flashcards

Haematology Peer Teaching Flashcards

1
Q

how much of blood is plasma and how much is cellular

A

55% is plasma

45% is cellular

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2
Q

what is eryptosis and where does it occur

A

it is the apoptosis of RBCs and occurs in the spleen, liver and bone marrow

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3
Q

which white blood cells are granulocytes

A

neutrophils

basophils

eosinophils

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4
Q

what are platelets derived from?

A

they are derived from megakaryocytes

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5
Q

what are the functions of thrombin

A
  • convert fibrinogen to fibrin (major component of a clot)
  • activates factors
    • V
    • VIII
    • XI
  • this causes positive feedback on more thrombin production
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6
Q

which clotting factors are vitamin k dependent

A

2

7

9

10

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7
Q

what are the two reasons that the liver is important for clotting

A

produces bile salts which are important for vitamin K absorption

the liver synthesises clotting factors

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8
Q

draw the clotting cascade

A
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9
Q

5 things included in an FBC

A

red blood cell volume

white blood cell volume

platelet volume

Hb concentration

mean corpuscular volume

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10
Q

what is the reticulocyte count and what can it tell you

A
  • the reticulocyte count is a blood test that enables you to see how quickly the bone marrow is producing new RBCs
  • low RC:
    • something is preventing RBCs from being produced
    • e.g. haematinic deficiency
  • high RC:
    • indicates that rbcs are being lost or destroyed so more RBCs are being made to compensate
    • e.g. bleeding/haemolytic anaemia
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11
Q

what is haematinic defiiciency

A

it is anaemia that is caused by deficiency in the constituents of blood cells

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12
Q

what is serum ferritin and what does it mean if it’s high or low

A

ferritin is the major iron storage protein in the body

it can be used to indirectly measure iron levels in the body

it’s also an acute phase protein so can be raised in inflammation and malignancy

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13
Q

why would you choose a THICK blood film

A

this allows the examination of a large amount of blood for the presence of parasites

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14
Q

why would you choose a THIN blood film

A

this allows observation of RBC morphology, inclusions and intracellular and extracellular parasites

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15
Q

how much O2 can each haemoglobin carry

A

there are two alpha chains and two beta chains

each can carry a molecule of O2

so overall, each molecule of haemoglobin can carry 4O2

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16
Q

what is anaemia

A

it is a decrease in haemoglobin below reference range

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17
Q

when is it microcytic, normocytic or macrocytic

A

microcytic - MCV <80

normocytic - MCV 80-100

macrocytic - MCV >100

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18
Q

nearly all anaemia presents with the same 5 symptoms

what are they

A
  1. Fatigue
  2. Lethargy
  3. Dyspnoea
  4. Palpitations
  5. Headache
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19
Q

nearly all anaemia presents with the same 3 signs

what are they

A
  1. Pale skin
  2. Pale mucous membranes
  3. Tachycardia
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20
Q

what are the 3 main causes of microcytic anaemia

A

thalassaemia

iron deficiency anaemia

anaemia of chronic disease

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21
Q

where in the digestive system is iron absorbed

A

in the duodenum

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22
Q

what are 4 signs specific to iron deficiency anaemia

A
  • brittle hair and nails
  • kolionychia - spoon shaped nails
  • atrophic glossitis - inflamed tongue with depapillation
  • angular stomatitis - inflammation of corners of mouth
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23
Q

name 5 things that can cause iron deficiency anaemia

A

low iron diet

blood loss

breastfeeding

malabsorption

hookworm

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24
Q

what does hypochromic mean

A

that red blood cells are paler than usual due to a deficiency of Hb

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25
Q

Ix for iron deficiency anaemia and what you will find

A
  • FBC: hypochromic microcytic anaemia
  • serum ferritin: low
  • reticulocyte count: low
  • endoscopy: possible GI bleed
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26
Q

treatment for iron deficiency anaemia and 5 SEs

A
  • Ferrous Sulphate or Ferrous Fumarate
  • SEs:
    • black stools
    • constipation
    • diarrhoea
    • nausea
    • epigastric abdo pain
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27
Q

3 main causes of normocytic anaemia

A

acute blood loss

combined haematinic deficiency (iron and B12)

anaemia of chronic disease

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28
Q

4 conditions that can cause anaemia of chronic disease

A
  • any that causes a shortening of red blood cell like or reduces red blood cell proliferation
    • CKD
    • Rheumatoid Arthritis
    • Lupus
    • Cancer
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29
Q

what are the three main causes of macrocytic anaemia

A

B12 deficiency (pernicious anaemia)

Folate deficiency

Alcohol excess

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30
Q

what is megaloblastic anaemia

A

this is what B12 and folate deficiency anaemia are sometimes called

it means that there has been an inhibition of DNA synthesis

the red blood cell continues to grow without mitosis causing macrocytosis

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31
Q

where is folate absorbed

A

it is absorbed in the jejunum

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32
Q

what are the main causes of folate deficiency

A

poor folate diet

malabsorption

pregnancy

anti-folate drugs (methotrexate)

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33
Q

investigation for folate deficiency anaemia

A

blood film: macrocytic anaemia

erythrocyte folate level: indicates reduced body stores

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34
Q

what is the treatment for folate deficiency anaemia

A

the treatment is folic acid supplementation and treatment of the underlying cause

consider prophylactic supplementation in pregnancy

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35
Q

what is the dietary source of folate

A

leafy greens and spinach

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36
Q

where is vitamin B12 absorbed

A

in the terminal ileum

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37
Q

what is pernicious anaemia

A

it is when there is no intrinsic factor commonly due to autoimmune destruction of parietal cells that produce it or against IF itself

intrinsic factor is required for vitamin B12 to bind and be absorbed

this leads to a B12 deficiency that causes anaemia

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38
Q

4 causes of pernicious anaemia

A

atrophic gastritis

gastrectomy

crohns

coeliac

these all either affect the production of intrinsic factor or absorption in the ileum

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39
Q

investigations for pernicious anaemia

A

blood film: macrocytic red cells

autoantibody screen: there may be IF antibodies

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40
Q

treatments for pernicious anaemia

A

vitamin B12 (Hydroxycobalm) injections

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41
Q

complications of pernicious anaemia

A

heart failure

angina

neuropathy

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42
Q

how are red blood cells removed from the circulation

A

after ~120 days they are removed by macrophages present in the red pulp of the spleen

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43
Q

what is haemolytic anaemia

A

this is when rbcs are destroyed before their 120 day lifespan is up

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44
Q

draw the rbc breakdown diagram

A
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45
Q

How does haemolytic anaemia present

A
  • normal anaemia presentation
  • jaundice (from excess bilirubin)
  • gallstones (from excess bilirubin)
  • signs of underlying disease (SLE Malar rash)
  • leg ulcers
  • splenomegaly
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46
Q

what are the two broad categories of causes of haemolytic anaemia

A

inherited

acquired

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47
Q

three inherited auses of haemolytic anaemia

A

membranopathies

enzymopathies

haemoglobinopathies

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48
Q

three acquired causes of haemolytic anaemia

A

autoimmune

infections

secondary to systemic disease

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49
Q

what is the treatment of haemolytic anaemia

A

treatment of the underlying cause

folate and iron supplementation

immunosuppressives if autoimmune

splenectomy if severe

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50
Q

what are the investigations for haemolytic anaemia

A
  • FBC: reduced haemoglobin
  • Reticulocyte count: increased
  • Blood film: presence of schistocytes
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51
Q

what is bone marrow failure

A

this is where a reduction in the number of pluripotent stem cells causes a lack of haemopoiesis

the reduced number of new RBCs replacing the old ones causes anaemia

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52
Q

4 causes of bone marrow failure

A

congenital

acquired: i.e. aplastic anaemia

cytotoxic drugs/radiation

infections

malignant infiltration

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53
Q

what are some causes of aplastic anaemia

A

radiation

chemotherapy

infection

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54
Q

specific signs and symptoms of bone marrow failure

A

increased susceptibility to infection

increased bruising

increased bleeding (from nose and gums especially)

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55
Q

investigations for aplastic anaemia

A
  1. FBC: pancytopaenia
  2. Reticulocyte count: low
  3. Bone marrow biopsy: increased fat spaces where stem cells were
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56
Q

treatment for aplastic anaemia

A

removal of causative agent

blood/platelet transfusion

bone marrow transplant

immunosuppressive therapy

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57
Q

what is the definition of polycythaemia

A

it is an increase in haemoglobin, PCV and RBCs

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58
Q

primary causes of polycythaemia

A
  • these are causes that increase the sensitivity of bone marrow to EPO
    • Polycythaemia rubra vera
      • mutation in JAK2 gene
    • Primary familial congenital polycythaemia
      • mutation in EPOR gene
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59
Q

secondary causes of polycythaemia

A
  • these are causes where there are more RBCs due to incresed circulating EPO
    • chronic hypoxia
    • poor oxygen delivery (e.g. high altitude)
    • abnormal RBC structure
    • tumours that release EPO
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60
Q

symptoms of polycythaemia

A

may be asymptomatic

may present with easy bleeding/bruising, fatigue, dizziness, headaches

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61
Q

what are the Ix for polycythaemia

A
  • FBC: increased PCV, RBC and Hb
  • Genetic testing for JAK2 and EPOR gene
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62
Q

treatments for polycythaemia

A

primary: blood letting and aspirin
secondary: treat the underlying cause

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63
Q

risk factors for a DVT or embolism

A
  • age
  • obesity
  • varicose veins
  • long haul travelling
  • immobility/bed rest
  • plasminogen deficiency
  • thrombophilia
  • pregnancy
64
Q

what is Virchow’s triad

A

Virchow’s triad of hypercoagulability, venous stasis, and injury to the vessel wallprovides a model for understanding many of the risk factors that lead to the formation of thrombosis

65
Q

symptoms of DVT

A

calf pain and swelling

ankle oedema

calf warmth

pitting oedema

66
Q

DVT Ix

A

D-Dimer test for EXCLUSION ONLY

Coagulation screen

FBC including platelets

US doppler

WELL’S SCORE

67
Q

differential diagnosis for DVT

A

cellulitis

68
Q

treatment for DVT

A

start LMWH and Warfarin immediately

stop LMWH when INR is 2-3

then either continue on warfarin or swap to a NOAC like rivaroxaban

69
Q

how does LMWH work?

A

it inactivates factor Xa

70
Q

how does warfarin work

A

it antagonises vitamin K dependent clotting factors

these are 2, 7, 9 and 10

71
Q

what is the prevention of DVT

A

stockings

mobilisation

hydration

leg elevation

72
Q

name 5 things on the well’s score and what the threshold is for likely vs unlikely DVT

73
Q

three categories of red cell disorder and an example of each

A
  • haemoglobinopathy
    • sickle cell disease
    • thalassaemia
  • membranopathy
    • spherocytosis
  • enzymopathy
    • glucose-6-phosphate deficiency
74
Q

what is the inheritance pattern of sickle cell disease

A

autosomal recessive

commoner in afrocarribean populations

75
Q

what is the mutation in sickle cell disease

A

it is apoint mutation of the B globin gene with valine changed to a glutamine

this produces HS variant

76
Q

what happens in sickle cell disease

A

under stress, i.e. cold, infection, dehydration, the RBCs become deoxygenated which causes HS to polymerise

this makes the RBCs rigid and sickled

77
Q

carriers of sickle cell trait are protected from what

A

falciparum malaria

78
Q

acute and chronic complications of sickle cell disease

A
  • acute
    • painful crisis
    • sickle cell chest crisis
    • haemolytic crisis
    • mesenteric ischaemia
  • chronic
    • renal impairment
    • pulmonary hypertension
    • joint damage
79
Q

Ix for sickle cell disease

A
  • screen neonates: blood/heel prick test
  • FBC: Hb and reticulocyte count
  • Blood film: sickled erythrocytes
  • Hb electropharesis for Dx shows HbSS to be present
80
Q

management of sickle cell disease

A
  • supportive
    • agressive analgesia (i.e. opiates)
    • treat underlying cause of crisis (Abx)
    • fluids
    • folic acid
    • transfusion if falling Hb
  • stem cell transplant
  • if hyposplenic
    • prophylactic Abx
    • pneumococcal and meningococcal vaccination
81
Q

what is the inheritance pattern of thalassaemia

A

autosomal recessive

82
Q

what is hyposplenism

A

it is when there is reduced spleen functuion and you get increased risk of serious infections

it can occur in sickle cell anaemia as well as coeliac

83
Q

what populations in thalassaemia most common in

A

mediterranean, middle eastern and asian

84
Q

what is the normal makeup of HbA (adult haemoglobin)

A

2 alpha and 2 beta chains

85
Q

how many genes produce alpha chain and beta chain of Hb

A

4 genes produce alpha

2 genes produce beta

86
Q

what is thalassaemia

A

thalassaemia is the decreased production of one or more globin chain in red cell precursors or mature red cells

alpha thalassaemia: decreased alpha chain synthesis

beta thalassaemia: decreased beta chain synthesis

87
Q

what happens in thalassaemia

A
  • precipitation of globin chains in red cell precursors inhibits erythropoiesis
    • there is reduced production of red cells
  • precipitation of globin chains in mature red cells causes haemolysis

so overall you get faulty production and premature destruction of RBCs

88
Q

what happens in alpha thalassaemia

A
  • 4 genes control alpha chain production and symptoms vary depending on the number of mutations
    • all 4 affected: invariably fatal in utero
    • 3 affected: commmon in parts of asia. patients have severe haemolytic anaemia and splenomegaly. they’re sometimes dependent on transfusions
    • 2 deletions: asymptomatic with possible mild anaemia
    • 1 deletion: blood picture is normal

CARRIERS ARE PROTECTED FROM FALCIPARUM MALARIA

89
Q

What is HbA

A

it is made up of two alpha and two beta chains

90
Q

what is HbA2

A

it is made up of two alpha chains and two delta chains

91
Q

what is HbF

A

it is made up of 2 alpha and 2 gamma chains

92
Q

what are the clinical syndromes of B thalassaemia

A

beta thalassaemia minor

beta thalassaemia intermediate

beta thalassaemia major

93
Q

what is the beta thalassaemia minor like

A

it is an asymptomatic heterozygous carrier state

there is mild or absent anaemia (low MCV and MCH)

iron stores and ferritin are normal

94
Q

what is the presentation of beta thalassaemia intermediate

A

it is moderate anaemia

doesn’t require transfusions

there is often splenomegaly, bone abnormalities and recurrent leg ulcers and gallstones

95
Q

what happens in beta thalassaemia major

A

aka cooley’s anaemia

presents in first year of life with severe anaemia, failure to thrive and chronic infections

there may be bony abnormalities like skull bossing and thalassaemic facies

they may have hepatosplenomegaly

96
Q

investigations for beta thalassaemia

A
  • FBC and blood film will show hypochromic microcytic anaemia
  • there will be irregular and pale RBCs
  • there are increased reticulocytes and nucleated RBCs
  • diagnosis is by Hb electrophoresis
97
Q

treatment of beta thalassaemia

A
  • regular blood transfusions are the mainstay of treatment
    • risk of iron overload and deposition in major organs like liver, spleen, pancreas and heart
      • iron chelation needed (desferrioxamine reduces iron overload)
      • ascorbic acid increases urinary excretion of iron
  • promote fitness and healthy diet
98
Q

what is the aetilogy of membranopathy and what are the two types

A

this is an autosomal dominant condition that leads to a deficiency in a protein for the RBC membrane

deformed cells get trapped in the spleen

spherocytosis is where they have vertical deformity

elliptocytosis is where they have a horizontal deformity

99
Q

symptoms of membranopathy

A

neonatal jaundice and haemolytic anaemia

this is exacerbated during infection

there’s excess bilirubin which can cause gallstones

100
Q

investigation for membranopathy

A

FBC and reticulocyte count

Blood film: osmotic fragility tests (RBCs show fragility in hypotonic solutions)

101
Q

treatment for membranopathy

A

folic acid and splenectomy

102
Q

what is the inheritance pattern of glucose-6-phosphate deficiency

A

it is x linked but can affect women

103
Q

who does glucose-6-phosphate deficiency mainly affect

A

mainly affects men from mediterranean, africa, and middle east

104
Q

what are the symptoms of glucose-6-phosphate deficiency

A
  • it is rarely symptomatic!
  • there can be oxidative crisis
    • precipitated by drugs (nitrofurantoin) or illness
    • Henna is also a precipitant
    • rapid haemolysis –> jaundice –> anemia
105
Q

Ix of glucose-6-phosphate deficiency

A

blood film: bite and blister cells

diagnosis is by enzyme assay

106
Q

management of glucose-6-phosphate deficiency

A

avoid precipitants e.g. henna

transfuse if severe

107
Q

what are two ways to assess someone’s coagulation

A

APTT (Activated partial thromboplastin time) tests the intrinsic pathway

PTT (prothrombin time) tests the extrinsic pathway

108
Q

what is DIC

A
  • disseminated intravascular crisis
    • generation of fibrin within blood vessels and also consumption of platelets/coagulation factors causing secondary activation of fibrinolysis
  • this means there will be initial thrombosis followed by bleeding tendancy
  • this is rare but life threatening
109
Q

causes of DIC

A
  • malignancy
  • septicaemia
  • obstetric causes
  • trauma
  • infections
  • haemolytic transfusion reactions
  • liver disease
110
Q

treatment for DIC

A

treat underlying cause

maintain blood volume and tissue perfusion

may require transfusions

give activated protein C

111
Q

what is thrombocytopenia? what are the two types and which is more common

A

thrombocytopenia is low platelet count

it can be immune thrombocytopenic purpura (ITP) which is more common or thrombotic thrombocytopenic puprura (TTP) which is less common

112
Q

three general causes of thrombocytopenia

A

reduced platelet production in the bone marrow

excessive peripheral destruction of platelets

problems associated with an enlarged spleen

113
Q

ITP physiology

A
  • immune thrombocytopenic purpura
    • often triggered by a viral infection or malignancy
    • there is antibody mediated destruction of platelets
    • may be associated with other autoimmune conditions
    • acute: in kids 2 weeks after infection
    • chronic: mainly in women with fluctuating course
114
Q

ITP clinical features

A

easy bruising

purpura

epistaxis/menorrhagia

115
Q

investigation of ITP

A

reduced platelets so normal/increased megakaryocytes

may be able to detect platelet autoantibodies

116
Q

what is TTP and what is the pathology

A
  • thrombotic thrombocytopenic purpura
    • deficiency in ADAMTS13 protease which usually cleaves von willebrand factor multimers
    • large vwf multimers cause platelet aggregation and fibrin deposition in small vessels
    • this is a haematological emergency due to multi-system thrombotic microangiopathy
117
Q

treatments for ITP

A

corticosteroids like prednisolone

splenectomy

118
Q

what are the clinical features of TTP

A

aki

neurological symptoms e.g headache, palsies, seizure

fever

microangiopathic haemolytic anaemia

119
Q

Ix for TTP

A

reduced platelets so normal/increased megakaryocytes

ADAMTS13 activity

120
Q

what is the treatment for TTP

A

plasma exchange flushes away antibodies and replaces ADAMTS13 protease

corticosteroids like prednisolone

consider retuximab for non-responders r

121
Q

what are the two main types of Haemophilia and what are the causes

also which is more common

A
  • haemophilia A: factor 8 deficiency (more common)
  • haemophilia B: factor 9 deficiency
122
Q

what is the inheritance patterns of haemophilia A and B

A

both are x linked recessive so females are rarely affected

123
Q

will haemophila A and B affect the APTT or the PTT

A

the PPT will be normal but the APTT will be prolonged

this is because factor 8 and 9 are part of the intrinsic pathway not the extrinsic

PTT = extrinsic

APTT = intrinsic

124
Q

who usually gets AML

A

usually older people - there is better survival in young people

125
Q

who usually gets ALL

A

this is the commonest malignancy in childhood and has very good survival

126
Q

investigation for AML and ALL

A

FBC

Blood film

BM aspiration

127
Q

AML and ALL treatment

A
  • supportive
    • blood
    • platelets
    • fluids
    • abx
  • chemo to induce remission
  • bone marrow transplant
  • steroids to maintain and manage GVHD
128
Q

who gets CLL

A

incidence increases with age

M>F

white>black

usually with a FH of ALL or CLL

129
Q

what is the cell type affected by CLL

A

it is a malignancy of B cells

130
Q

what is the presentation of CLL

A
  • 50% cases are incidental findings from something unusual on a FBC
  • symptomatic disease is generally associated with later stage disease
    • lymphadenopathy
    • infections
    • hepatosplenomegaly
131
Q

treatment of CLL

A

usually watchful waiting

maube chemo or radio to shrink lymphadenopathy

its chronic and incurabl - patients die with rather than from

132
Q

who gets CML

A

middle aged people

philadelphia chromosome

133
Q

what is the philadelphia chromosome and what is the treatment associated with it

A
  • translocation that produces BCR-ABL1 fusion protein
  • this is a constitutively active tyrosine kinase
  • causes cell proliferation
  • seen in CML
  • treatment is imatinib which is a TK inhibitor
134
Q

what is the age incidence of hodgkin’s lymphoma

A

bimodal - young and old

135
Q

what histology is hodgkin’s lymophoma associated with

A

reed sternberg cells

136
Q

what disease is associated with auer rods

137
Q

what is the system used to stage lymphoma

A

ann arbour system

138
Q

stages 1 - 4 of ann arbor system

which diseases does it apply to

A
  • Stage 1: involvement of single lymph node region
  • stage 2: involvement of two or more lymph node regions on same side of diaphragm
  • stage 3: involvement of lymph node regions on both sides of the diaphragm
  • stage 4: diffuse extralymphatic disease (e.g. in liver or bone marrow)

A and B refers to presence or absense of B symptoms

ann arbor is for both hodgkin and non-hodgkin lymphomas

139
Q

what are B symptoms

A

fever

night sweats

weight loss

140
Q

what is the difference between low grade and high grade lymphoma

A

low grade you won’t cure and median survival is 3-10 years

high grade is more severe but there’s a 30% cure rate

141
Q

what is myeloma

A

it is malignancy of one clone of plasma cells in the bone marrow

there is monoclonal Ig so repeat infections cause no other Ig

bence jones protein (it’s an Ig protein) found in urine

142
Q

does Myeloma affect men or women more

143
Q

clinical features of myeloma

A

cancer symptoms

confusion (maybe due to hyperviscosity and hypercalcaemia)

hypercalcaemia symptoms

repeat infections

pathological fractures

bone pain

renal impairment

144
Q

diagnosis of myeloma

A

monoclonal Ig band seen on electrophoresis

BM aspiration shows excess plasma cells

X-Ray: pepper pot skull

145
Q

treatment for myeloma

A

chemo

supportive care including bisphosphonates

watchful waiting

146
Q

what is tumour lysis syndrome and how can you prevent it

A

this is where chemo is given and cells die and lyse releasign their contents

this leads to hyperkalaemia and release of nucleic acids

this can produce crystals which get deposited in the kidney impairing function

to prevent this give allopurinol

to treat give IV fluid and correct electrolytes

147
Q

what type of organism is responsible for malaria

A

protozoa called Plasmodia falciparim normally

sometimes it’s P. ovale or P. vivax

148
Q

what organism transmits malaria

A

female anopheles mosquito

149
Q

what are the three stages of malaria

A

exo-erythrocytic

endo-erythrocytic

dormant stage (P.ovale and P.vivax)

150
Q

signs and symptoms of malaria

A
  • fever + exotic travel = malaria until proven otherwise
  • chills
  • sweats
  • anemia
  • hepatosplenomegaly
  • fatigue
  • black urine
151
Q

pathogenesis of malaria

A
  • paracite matures in RBC
  • knobs form in RBC surface
  • infected cells bind to eachother and this is called rosetting
  • they also bind to receptors on endothelial cell walls
  • this causes microvascular obstruction which may lead to tissue hypoxia
152
Q

investigations for suspected malaria

A
  • thick and thin blood film
  • rapid diagnostic test (RDT) detects plasmodium antigens in blood
  • RULE OUT MENINGITIS
153
Q

Treatment for malaria

A

quinine and doxycycline

154
Q

what is neutropenic sepsis and what is the management

A

it is temperature >38 and absolute neutrophil count of <0.5 x 10 9/L

Give Abx immediately

155
Q

management for acute sickle cell crisis

A

fluids and pain relief

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