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Medicine Year 2 2 > Haematology > Flashcards

Haematology Flashcards

1
Q

LEUKAEMIA

What is Leukaemia?

A

Malignant neoplasms of hemopoietic stem cells, characterised by replacement of bone marrow with cells that often spills into the blood

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2
Q

LEUKAEMIA

What are the 4 different types of Leukaemia?

A
  • Acute Lymphoblastic (ALL)
  • Acute Myeloid (AML)
  • Chronic Myeloid (CML)
  • Chronic Lymphocytic (CLL)
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3
Q

LEUKAEMIA

What is the genetic abnormality in acute myeloid leukaemia?

A

t(15;17)

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4
Q

LEUKAEMIA

What is the genetic abnormality in chronic myeloid leukaemia?

A

t(9;22)

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5
Q

LEUKAEMIA

What may be the causes of Leukaemia?

A

1) Benzenes
2) Ionising Radiation
3) Alkylating Agents (chemo)
4) Pregnancy

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6
Q

LEUKAEMIA

What does Acute Myeloid Leukaemia involve and what age group is it found most commonly in?

A
  • Proliferation of myeloblasts

- Middle aged- old ADULTS

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7
Q

LEUKAEMIA

What does Acute Lymphoblastic involve and what age group is it found most commonly in?

A
  • Proliferation of lymphoblast’s

- usually CHILDREN

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8
Q

LEUKAEMIA

What are the Acute Symptoms and Signs?

A
  • Bone Marrow failure
    (Anaemia= low Hb. Infection= low WCC, bleeding= low platelets)
  • Infiltration (hepatosplenomegaly, lymphadenopathy, organomegaly)
  • Weight Loss
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9
Q

LEUKAEMIA

What tests would you do for a patient with Leukaemia symtpoms?

A

1) FBC (Anaemia)
2) Peripheral blood film
3) Bone marrow aspirate ( characteristic blast cells seen)
4) Lumbar puncture

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10
Q

LEUKAEMIA

What would be found if someone had AML?

A

In AML, auer rods are the diagnostic finding

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11
Q

LEUKAEMIA

what is Phase 1 treatment?

A
  • Induction (99% of leukemic cells killed)
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12
Q

LEUKAEMIA

What is Phase 2 Tretament?

A

Maintenance (remaining 1% of cells killed and maintaining remission)

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13
Q

LEUKAEMIA

Treatment

A
  • Phase 1 and 2

- Chemotherapy and Bone marrow transplant

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14
Q

CHRONIC LEUKAEMIA

What age group is CML most commonly found and where is the genetic defect?

A

Middle aged adults

Philadelphia chromosome t(9;22)

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15
Q

CHRONIC LEUKAEMIA

What is Chronic Leukaemia?

A

proliferation of mature myeloid cells

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16
Q

CHRONIC LEUKAEMIA

What are the clinical features of CML?

A

1) Weight loss
2) Tired
3) Fever
4) Sweating
5) Hepatosplenomegaly
maybe anaemia and bleeding

SYMPTOMS PROGRESS SLOWLY BUT DEVELOP INTO AML AND RAPID DEATH

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17
Q

CHRONIC LEUKAEMIA

What would you test for in suspected CML?

A
  • Bloods (anaemia and high WCC)

- Bone marrow aspirate (shows hypercellular marrow, increased in myeloid cells)

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18
Q

CHRONIC LEUKAEMIA

What is the treatment for CML?

A

Imatinib (Tyrosine kinase inhibitor- PREVENTS FORMATION OF PHILADELPHIA CHROMOSOME)

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19
Q

CHRONIC LEUKAEMIA

What is CLL?

A

Incurable disease of the elderly, with uncontrolled proliferation of mature B lymphocytes

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20
Q

CHRONIC LEUKAEMIA

What are the symptoms of CLL?

A

Usually indolent but may have marrow failure symtpoms (anaemia, infections, bleeding)

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21
Q

CHRONIC LEUKAEMIA

What tests would you do for CLL?

A
  • Bloods (anaemia, high WCC, low platelets)thrombocytopenia= low platelets
    lymphocytosis= high WCC

Bone marrow= heavy infiltration of lymphocytes

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22
Q

What is Anaemia?

A

Decreased level of Hb in blood, so fall in haematocrit, increased plasma volume

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23
Q

What is a Haematocrit?

A

volume percentage of red blood cells in blood. It is normally 47% ±5% for men and 42% ±5% for women.

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24
Q

Name some types of Microcytic Anaemia?

A

1) Iron- deficiency
2) Chronic disease
3) Thalassaemia
4) Sideroblastic

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25
Q

What does microcytic anaemia have in terms of MCV?

A

Microcytic anaemia has a low mean corpuscle volume

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26
Q

What does MCV mean?

A

mean corpuscle volume is the size of the RBC

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27
Q

Normocytic Anaemia has a normal MCV, name some types of Normocytic Anaemia

A

1) Acute blood loss
2) Chronic disease
3) Combined deficiency (malabsorption)

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28
Q

Name some types of macrocytic anaemia

A

1) B12/ folate deficiency
2) Alcohol
3) Hypothyroidism

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29
Q

What does macrocytic anaemia have in terms of MCV?

A

Macrocytic anaemia has a high mean corpuscle volume

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30
Q

ANAEMIA

General symptoms of anaemia?

A
  • Fatigue
  • Breathless
  • Dyspnoea
  • Faint
  • Headache
  • Anorexia
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31
Q

ANAEMIA

General signs?

A

Hyperdynamic circulation:

tachycardia
systolic flow murmur
pale skin
cardiomegaly

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32
Q

IRON- DEFICIENCY ANAEMIA

What is it?

A

Decrease in mean corpuscular Hb concentration

decrease in (MCHC, MCH, MCV)

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33
Q

IRON- DEFICIENCY ANAEMIA

Cause?

A
  • Blood loss (menorrhagia/ GI bleed)
  • Malabsorption ( poor diet, increased demand such as pregnancy)
  • WORLDWIDE= hookworm (GI Blood loss)
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34
Q

IRON- DEFICIENCY ANAEMIA

What is Microcytosis?

A

Reduced Hb content in RBCs

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35
Q

IRON- DEFICIENCY ANAEMIA

What are specific features of IDA?

A

1) Angular Stomatitis (red/ sore corners of the mouth/lips)
2) Koilonychia (brittle, concave nails)
3) Atrophic glossitis (depapillation and sore tongue)

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36
Q

IRON- DEFICIENCY ANAEMIA

What do RBC’s look like on blood film if someone has IDA

A
  • Hypochromic and microcytic RBC’s
  • Anisocytosis (change in size)
  • Poikilocytosis (change in shape)
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37
Q

IRON- DEFICIENCY ANAEMIA

Investigations?

A
  • Colonoscopy (GI bleed)

- Coeliac serology

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38
Q

IRON- DEFICIENCY ANAEMIA

Treatment?

A

Oral iron (ferrous sulphate)

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39
Q

ANAEMIA OF CHRONIC DISEASE

Causes?

A

-RA, Crohns, SLE, TB, CKD

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40
Q

ANAEMIA OF CHRONIC DISEASE

Pathology?

A

Inflammatory cytokines reduce the sensitivity of bone marrow to EPO and results in failure of iron to be incorporated into RBC’s

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41
Q

ANAEMIA OF CHRONIC DISEASE

Stages of pathology

A

1) Poor use of iron in erythropoiesis
2) Cytokine induced shortening of RBC survival
3) Decreased production of/ response to EPO

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42
Q

ANAEMIA OF CHRONIC DISEASE

Tests?

A

blood film- normocytic/ normochromic anaemia

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43
Q

ANAEMIA OF CHRONIC DISEASE

Treatment?

A

give EPO

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44
Q

Why isn’t ferritin always accurate?

A

Ferritin is an acute phase protein like CRP so can increase in states of inflammation

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45
Q

what is ALPHA THALASSAEMIA?

A

disorder of haemoglobin chain- decreased alpha chains

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46
Q

BETA THALASSAEMIA

What is it?

A

Decreased number of beta haemoglobin chains

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47
Q

BETA THALASSAEMIA

how are more HbA2 and HbF chains formed?

A
  • No beta chains = more alpha to compensate

- These alpha chains combine with any available alpha,beta or gamma chains available so produce more HbA2 and HbF.

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48
Q

BETA THALASSAEMIA

WHat is minor BT?

A

heterozygous

mild anaemia

RBC’s are hypochromic/ microcytic

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49
Q

BETA THALASSAEMIA

What is intermedia BT?

A

moderate anaemia but no trasnfusions needed

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50
Q

BETA THALASSAEMIA

What is major BT?

How does it present?

What does it require

A
  • severe microcytic anaemia

Presentation
1st year= Hypertrophy of ineffective BM

  • increased size of facial bones (skull bossing)
  • Hepatosplenomegaly

Treatment = Transfusion

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51
Q

BETA THALASSAEMIA

tests

A

bloods= hypochromic, microcytic anaemia and increased reticulocytes

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52
Q

BETA THALASSAEMIA

management?

A
  • blood transfusions (2-4 weeks)
  • folate supplements
  • iron chelation- prevent Fe overload (deferasirox)
  • bone marrow transplant
  • may die due to HF in 2nd decade
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53
Q

SIDEROBLASTIC

What is it?

A

microcytic hypochromic anaemia where bone marrow produces ringed sideroblasts instead of RBC’s

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54
Q

SIDEROBLASTIC

Cause?

A

enough iron but cant be incorporated into Hb

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55
Q

SIDEROBLASTIC

Diagnosis and treatment?

A

presence of sideroblasts on blood film

treat with pyridoxine and folic acid

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56
Q

MACROCYTIC ANAEMIA

Name the two types of Macro Anaemia

A
  • megaloblastic (B12/folate)

- non megaloblastic (alcohol)- alcohol causes lipid deposition in RBC membranes

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57
Q

MACROCYTIC ANAEMIA

Causes of B12/folate deficiency?

A
  • pernicious anaemia
  • poor intake (diet, old age, alcohol)
  • poor absorption (coeliac/ crohns)
  • excess utilisation (pregnancy/ malignancy)
58
Q

MACROCYTIC ANAEMIA

What is pernicious anaemia?
How is it tested/diagnosed?

A

when there is not enough intrinsic factor which is required for B12 absorption.

tested for by:
Intrinsic factor antibodies
anisocytosis/ poikilocytosis on blood film
Hb low/ MCV high

59
Q

MACROCYTIC ANAEMIA

What can B12 deficiency cause?

A
  • mild jaundice
  • polyneuropathy
  • dementia (subacute degeneration of spinal cord)
60
Q

MACROCYTIC ANAEMIA

Tretament of B12/folate deficiency?

A
  • B12 supplements (hydroxocobalamin)

- folate (green veg, kidney, nuts yeast, liver)

61
Q

MACROCYTIC ANAEMIA`

Signs of folate deficiency

A
  • anaemia and red cell folate/ serum folate is decreased
62
Q

MACROCYTIC ANAEMIA

treatment of folate deficiency

A

oral folic acid 5mg daily

63
Q

SICKLE CELL ANAEMIA

How is it caused?

A

Substitution of glutamine for valine in beta haemoglobin gene leads to production of HbS instead of HbA.

64
Q

SICKLE CELL ANAEMIA

How does tissue infarction occur?

A

1) HbS POLYMERISES WHEN DEOXYGENATED= haemolytic anaemia

2) irreversibly sickled cells causes obstruction to microcirculation which results in TISSUE INFARCTION

65
Q

SICKLE CELL ANAEMIA

Why does it take 6 months to manifest?

A

because foetal haemoglobin (HbF) works fine

66
Q

SICKLE CELL ANAEMIA

Symptoms?

A

kids- occlusion in hands/feet= dactylitis= severe pain
adults- same but also affects long bones

  • often asymptomatic as HbS offloads 02 better than normal Hb
  • pulmonary HTN
67
Q

SICKLE CELL ANAEMIA

What causes a decrease in Hb?

A

1) Splenic Sequestration= sickle cells trapped in spleen= enlargement
2) Bone marrow aplasia due to parvovirus B19= decreased Hb

68
Q

SICKLE CELL ANAEMIA

Long term effects?

A

1) Growth problems due to avascular necrosis of bones = short bones
2) increased risk of infection due to splenic atrophy
3) Priapism due to sequestration of RBC in corpus callosum

4) Gallstones due to chronic haemolysis
5) leg ulcers
6) sickle chest syndrome

69
Q

SICKLE CELL ANAEMIA

Investigations?

A
  • Hb electrophoresis shows HbS
  • increased reticulocytes
  • sickle cells on blood film
70
Q

SICKLE CELL ANAEMIA

Management?

A
  • Hydroxycarbamide increases HbF
    -vaccines to prevent infection
    folic acid for haemolysis
71
Q

GLUCOSE-6-PHOSPHATE DEHYDROGENASE (G6PD) DEFICIENCY

what is the function of G6PD

A

Maintains glutathione in reduced state, this prevents RBC from oxidative injury

72
Q

GLUCOSE-6-PHOSPHATE DEHYDROGENASE (G6PD) DEFICIENCY

tests and treatment?

A
  • direct enzyme measurement
  • avoid precipitants (quinine/ fova beans)
  • transfusions if severe
73
Q

HAEMOLYTIC ANAEMIA

Types?

A

1) Thalassaemia
2) sickle cell
3) G6PD deficiency

these all increase reticulocytes

74
Q

APLASTIC ANAEMIA

Causes?

A

Decrease in pluripotent stem cells and faults in those remaining

75
Q

APLASTIC ANAEMIA

What is it?

A

Pancytopenia with hypocellularity of bone marrow

76
Q

what is hypocellularity?

A

when bone marrow stops making cells

77
Q

APLASTIC ANAEMIA

Symptoms?

A
  • bleeding
  • anaemia
  • infections
78
Q

APLASTIC ANAEMIA

Signs?

A
  • epitaxis (nose bleeds)
  • bleeding gums
  • bruising
79
Q

APLASTIC ANAEMIA

Investigations?

A

FBC and bone marrow aspirate

Pancytopenia/ absent reticulocytes

marrow is hypocellular

80
Q

APLASTIC ANAEMIA

Treatment?

A
  • withdraw offending agent
  • BM transplant
  • support blood count
81
Q

MYELOMA

What is it?

A
  • Malignant neoplasm of a plasma cell.

- clonal proliferation of BM cells, capable of producing monoclonal immunoglobulins, IgA or IgG

82
Q

MYELOMA

What causes dysfunction to organs?

A

excessive quantities of one type of Ig

83
Q

MYELOMA

What can be found in urine?

A

Excretion of bence-jones protein/ M protein

84
Q

MYELOMA

Symptoms?

A
  • Bone destruction due to increased osteoclast activity
    1) back pain 2) spinal cord compression 3)hypercalcaemia
  • bone marrow infiltration
    1) Anaemia 2) Infection 3) Bleeding
  • height and weight loss and fatigue
85
Q

MYELOMA

What is an easy acronym to remember symtpoms of myeloma?

A

calcium
renal
anaemia
bone pain

CRAB

86
Q

MYELOMA

Diagnosis and tests?

A

FBC- anaemia, thrombo/leukocytopenia, ESR increased
BIOCHEM- decreased renal function and hypercalcaemia

1) monoclonal protein in urine electrophoresis
2) X-rays- bone lesions
3) plasma cell increase on BM biopsy
4) evidence of end organ damage

(hypercalcaemia, renal insufficiency and anaemia)

87
Q

MYELOMA

Treatment?

A

1) Analgesia for back pain
2) FLuids for kidney failure
3) EPO for anaemia
4) bisphosphonates- reduce the risk of fracture

specific= CHEMO

average survival = 5 years

88
Q

LYMPHOMA

What is it?

A
  • malignant neoplasm of lymphocytes. Accumulates in lymph nodes not the blood

(lymphadenopathy)

89
Q

LYMPHOMA

What is the difference between Hodgkin’s and non- Hodgkin’s lymphoma?

A

Hodgkin’s lymphoma involves the presence of Reed-Sternberg cells. Non hodgkins lymphoma is B cells, which is more common and known as:

(diffuse large B cell lymphoma DLBCL)

90
Q

LYMPHOMA

Features?

A
  • Large, painless, non-tender lymph nodes (cervical)

- B symptoms (weight loss, night sweats, pyrexia-‘fever’)

91
Q

LYMPHOMA

Signs?

A
  • Lymphadenopathy
  • cachexia
  • anaemia
  • hepatosplenomegaly
92
Q

LYMPHOMA

Tests?

A

Biopsy (presence of reed-Sternberg cells)
bloods (increased ESR/LDH, decreased Hb)

blood films, BM aspirate

93
Q

LYMPHOMA

Treat?

A

chemo and rituximab

low grade= mucosa-associated lymphoid tissue (MALT) lymphoma
high grade= diffuse large B cell lymphoma DLBC lymphoma
highest grade= Burkitt’s lymphoma

94
Q

PLATELET PROBLEMS (thrombocytopenia)

What are the two basic types of platelet problems?`

A
  • Reduced production (leukaemia, lymphoma, myeloma, aplastic anaemia)
  • increased destruction (DIC, ITP, TTP)
95
Q

PLATELET PROBLEMS (thrombocytopenia)

How do we know if it is either increased destruction, or reduced production

A
  • increased megakaryocytes with increased destruction

- decreased megakaryocytes with decreased production

96
Q

PLATELET PROBLEMS

Clinical Features?

A
  • Epistaxis
  • Menorrhagia
  • Gum bleeding
  • Easy bruising
  • Purpura (red blotches on skin)
  • Petachiae (red dots)
97
Q

PLATELET PROBLEMS

What is ITP?

A

Immune Thrombocytopenic Purpura is immune mediated destruction of platelets

(IgG against platelets)

98
Q

Cause of Immune Thrombocytopenic Purpura

A

Kids= virus

Adults= less acute- mainly young women, caused by autoimmune disorders

99
Q

Diagnosis of Immune Thrombocytopenic Purpura

A

Thrombocytopenia with increased megakaryocytes

100
Q

Treatment of Immune Thrombocytopenic Purpura

A
  • steroids
  • IV Ig
  • platelet transfusion
101
Q

What is TTP?

A

Thrombotic Thrombocytopenic Purpura

102
Q

Cause of Thrombotic Thrombocytopenic Purpura

A

Deficiency of ADAMTS13

This normally degrades vWF

103
Q

Pathology of Thrombotic Thrombocytopenic Purpura

A

1) Widespread aggregation of platelets
2) microvascular thromboses
3) thrombocytopenia

104
Q

Treatment of Thrombotic Thrombocytopenic Purpura

A
  • plasma exchange
  • methylprednisolone
  • Rituximab
105
Q

DEEP VEIN THROMBOSIS

What is it

A

Thrombus in valves of veins

Accumulation of red cells and fibrin

106
Q

DEEP VEIN THROMBOSIS

Risks?

A
  • Surgery
  • immobilisation
  • pregnancy
  • cancer
  • oestrogen contraceptive
  • > 60 years
  • Obesity
107
Q

DEEP VEIN THROMBOSIS

Symptoms?

A
  • Swollen red leg
  • tender and warm calf
  • distended leg veins
  • pitting oedema
108
Q

DEEP VEIN THROMBOSIS

Prophylactic Measures?

A
  • compression stockings
  • early mobilisation
  • leg elevation
109
Q

DEEP VEIN THROMBOSIS

Investigations?

A

Low score D-diver: -ve= no DVT

high score: +be= do Doppler/ultrasound

Tests may be unreliable at a late stage for calf DVT so repeat if -ve

110
Q

DEEP VEIN THROMBOSIS

Treatment?

A

AIM= prevent pulmonary embolism

  • LMHW+ Warfarin (stop heparin at INR 2-3)
    2nd: LMHW+ Heparin

Time scale-

If there’s a cause= 3 months
If no cause= 6 months + search for cancer

111
Q

DEEP VEIN THROMBOSIS

How does treatment work?

A

It activates antithrombin III which inhibits factor Xa, so stops coagulation cascade

112
Q

POLYCYTHAEMIA

What is it?

A

Increase in Hb/haematocrit/red cell count

113
Q

POLYCYTHAEMIA

What is PCV?

A

Packed Cell Volume= haematocrit= % by volume of RBC in blood

(These measurements are all in concentrations therefore a decrease in plasma volume may increase RCC)

114
Q

POLYCYTHAEMIA

What is absolute POLYCYTHAEMIA

A

Increase in red cell mass

115
Q

POLYCYTHAEMIA

What is relative POLYCYTHAEMIA

A

Decrease in plasma volume

116
Q

POLYCYTHAEMIA

How does primary polycythaemia occur?

A

1) polycythaemia vera
2) JAK-2 mutation
3) malignant haematopoietic stem progenitor cell

117
Q

POLYCYTHAEMIA

Secondary causes of polycythaemia

A
  • hypoxia (increased EPO)

- EPO secreting tumour

118
Q

POLYCYTHAEMIA

Difference in symptoms of primary and secondary?

A

In secondary there is no hepatosplenomegaly and no increased WCC

119
Q

POLYCYTHAEMIA

Symptoms and signs?

A
  • Facial plethora
  • Headache
  • Dizziness
  • Tinnitus
  • Angina
  • Intermittent claudication (pain in legs due to clocked arteries)
  • Visual disturbances
  • Pruritis
120
Q

POLYCYTHAEMIA

Investigations and diagnosis?

A
  • increase WCC, increased RCC, increase Hb/PCV

- Possible JAK-2 mutation

121
Q

POLYCYTHAEMIA

Treatment?

A
  • Low dose aspirin
  • Venesection

Secondary Treatment:

Remove EPO secreting tumour
02 if hypoxic

122
Q

DISSEMINATED INTRAVASCULAR COAGULATION

WHat is it?

A

Over activation of clotting cascade

Widespread:
1) generation of fibrin within vessels,
this leads to  
2) consumption of platelets/coagulation factors 
Leads to
3) widespread bleeding
123
Q

DISSEMINATED INTRAVASCULAR COAGULATION

Causes?

A
  • Burns
  • major trauma
  • sepsis
  • surgery
  • advanced cancer
  • acute promyelocytic leukaemia- due to generation of procoagulant substances
124
Q

DISSEMINATED INTRAVASCULAR COAGULATION

Signs?

A

Vary from none to complete haemostatic failure

125
Q

DISSEMINATED INTRAVASCULAR COAGULATION

Diagnosis?

A
  • Severe thrombocytopenia

- fragmented RBC in blood film

126
Q

DISSEMINATED INTRAVASCULAR COAGULATION

Treatment?

A

Underlying cause treated

-give platelets, RBC’s and clotting factor

127
Q

MALARIA

What is it?

A

It is a protozoan parasite widespread in tropics and subtropics

128
Q

MALARIA

How is it transmitted?

A

Through the bite of infected female Anopheles mosquito

129
Q

MALARIA

What is the most fulminating strain of malaria

A

P falciparum

130
Q

MALARIA

Pathogenesis?

A

1) infective form of parasite passed through skin, into the blood to the liver
2) many enter hepatocytes and after a few days cause rupture. They are then released into the blood, enter erythrocytes and cause rupture of red cells.
3) rupture of red cells contributes to anaemia and cause fever
4) RBCs containing P falciparum adhere to endothelium of small vessels, cause occlusion and severe organ damage
5) some strains stay latent in liver and this is how relapse occurs

131
Q

MALARIA

Clinical features?

A
  • fever
  • anaemia and hepatosplenomegaly
  • cerebral malaria
  • blackwater fever
  • diarrhoea
132
Q

MALARIA

Diagnostic tests?

A

Thick and thin blood smears

All types of blood test to see any complications

Rapid antigen tests

133
Q

MALARIA

Treatment?

A

Uncomplicated falciparum=
Oral riamet/ oral quinine

Complicated falciparum=
IV artesunate/ quinine

Non falciparum malaria=
Oral chloroquine

134
Q

What is prothrombin time?

A

Measures how long it takes to blood to clot. Expressed as INR (international normalised ratio)

135
Q

What is activated partial thromboplastin time?

A

Tests for the intrinsic system of coagulation

136
Q

What is thrombin time?

A

Thrombin is added to plasma to convert fibrinogen to fibrin-Time taken for blood to form a clot in plasma of a blood sample containing an anti-coagulant and an excess of thrombin

137
Q

What is bleeding time?

A

Tests haemostasis. Done by making two small incisions into arm. Rarely done

138
Q

What is the 3 roles of vWF in clotting?

A

1) to bring platelets intoccontact with exposed subendothelium
2) to make platelets bind to each other
3) to bind factor VIII, protecting it from destruction in the circulation

Deficiency leads to defective platelet function as well as factor VIII deficiency

139
Q

What is Plasmin?

A

Enzyme that destroys blood clots by attacking fibrin. (Stops occlusion problems arising)

140
Q

What foods are high in folate?

A

green veg, kidney, nuts yeast, liver

141
Q

What is Vit B12 and folate required for?

A

DNA synthesis

Medicine Year 2 2 (15 decks)

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