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phase 3b > Haematology > Flashcards

Haematology Flashcards

1
Q

What is hodgkins lymphoma?

A

malignant tumour of lymphatic system - characterised histologically by Reed Sternburg Cells

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2
Q

Describe the histology of Hodgkin’s lymphoma

A

Reed Sterburg cells (multinucleated giant cells)

abnormal and smaller mononuclear cells originating from B lymphocytes

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3
Q

Risk factors for Hodgkins lymphoma

A

EBV

previous mononucleosis

HIV

immunosuppression

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4
Q

Presentation of Hodgkins lymphoma

A
  • enlarged but asymptomatic lymph node in lower neck or supraclavicular region (pain with alcohol)
  • cyclical fever
  • chest discomfort - cough dyspnoe (mediastinal lymph node involvement)
  • B symptoms - night sweats, fever, weight loss
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5
Q

Staging of Hodgkins lymphoma

A

Ann Arbor

  1. one lymph node region or structure (spleen, thymus, waldeyers ring)
  2. >1 lymph node region on same side
  3. involvement both sides
    1. splenic, hilar, coeliac or portal
    2. para-aortic iliac or mesenteric
  4. extranodal
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6
Q

Modifying features of Hodgkins lymphoma

A

A: no symptoms

B: night sweats, fever, weight loss

X: > 1/3rd mediastium widening or >10cm diameter of mass

E: extranodal site

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7
Q

Potential examination findings of Hodgkins lymphoma

A

Lymphadenopathy

Hepatomegaly

Splenomegaly

Superior VC syndrome (facial swelling associated with SOB)

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8
Q

Hodgkins lymphoma investigations

A

FBC (leukamia, mono)

ESR (>70 bad prog)

LFT (low albumin bad prog)

HIV

CXR (lymphadenopathy and mediastinal expansion)

Lymph node and bone marrow biopsy (staging)

CT thorax and abdo (staging)

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9
Q

ABVD chemo

A

Doxorubicin

Bleomycin

Vinblastine

Dacarbazine

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10
Q

BEACOPP chemo

A

Bleomycin

Etoposide

Doxorubicin

Cyclophosphamide

Vincristine

Procarbazine

Prednisolone

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11
Q

What can additional things can you give with chemo

A
  • Abx to any pt with severe neutropenia
  • Recombinant human granulocyte colony - stimulating factor stimulates neutrophil production so could reduce duration of chemo induced neutropenia reducing incidence of associated sepsis
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12
Q

Management of Hodgkins lymphoma

A

Early: ABVD then radio (preceeded by BEACOPP in unfavourable prog)

Advanced: ABDV/BEACOPP

ASCT= autologous stem cell transplant

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13
Q

follow up for Hodgkins lymphoma

A

OPD 2-5 years

TFT if radio to neck and upper mediastinum

made aware theyre increased risk of secondary mags, CVD, pulmonary disease and infertility

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14
Q

Prognosis of Hodgkins lymphoma

A

80-90% patients achieve permanent remission

poor prognostic indicators

  • increasing age
  • male
  • B symptoms
    *
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15
Q

Patho behind non-hodgkins lymphoma

A

Genetic mutation causes B/T cells to divide uncontrollably producing a neoplastic cell.

This can be

1) nodal lymphoma

2) extranodal lymphoma
- GI tract
- Bone Marrow
- Spinal cord

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16
Q

What types of B cell lymphoma are there?

A

Indolent : follicular lymphoma

aggressive e.g. Diffuse large B cell lymphoma
mantle cell lymphoma

highly aggressive e.g. Burkitts lymphoma (chromosomal translocation 8->14) associated with EBV

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17
Q

Types of T cell lymphoma

A

adult T cell lymphoma

mycosis fungoides

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18
Q

Non-Hodgkins lymphoma symptoms

A

gastric MALT: GORD + constitutional symptoms

Burkitts: abdo swelling, nausea and diarrhoea

small bowel T cell: associated with coeliac

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19
Q

NHL investigations

A

Lymph node biopsy

Burkitts starry sky on hisology

CT - staging

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20
Q

NHL Management

A

localised - Radiotherapy

High grade - R-CHOP

Rituximab
Cyclophosphamide
Hydroxydaunomycin
Vincristine
Prednisolone

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21
Q

Which cancer is associated with coeliac disease?

A

small bowel T cell lymphoma

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22
Q

What is bacteria is assoicated with Burkitts lymphoma?

A

H. pylori

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23
Q

how do you treat h.pylori?

A

PPI

clarithromycin

metronidazole or amoxicillin

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24
Q

What are the possible causes of a mediastial tumour?

A

Terrible lymphoma (Hodgkins)

Teratoma

Thymoma

Thyroid Mass

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25
Q

Which groups of patients have a higher risk of acute lymphoblastic leukaemia?

A

Children

Downs Syndrome

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26
Q

Which cell line is affected in ALL?

A

Small lymphocyte

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27
Q

How does ALL present?

A

Bone marrow failure

RBC: anaemia, dyspnoea, fatigure, dizziness

WBC: more infections

Platelets: bleeding

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28
Q

Which investigations would you do in suspected ALL?

A

FBC: anaemia, neutropenia, thrombocytopenia

Blood film: Blast cells >=20%

Increase LDH (lactic dehydrogenase) due to increased cell turnover

LP- CNS involvement

Imaging to assess mass

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29
Q

What are poor prognostic indicators in ALL

A

Philadelphia Chromosome

adult

male

CNS signs

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30
Q

What is the management of ALL?

A
  • chemo
  • SCT if poor prog
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31
Q

How does AML present?

A

Bone marrow failure

RBC: anaemia, dyspnoea, fatigue dizziness, palps

WBC: infections

Platelets: Bleeding Gum hypertrophy and bleeding

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32
Q

AML investigations

A

FBC: anaemia, neutropenia, thrombocytopenia

Blood film: blast cells Auer Rods

increased LDH

BM aspiration/biopsy: >=20 blast cells

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33
Q

Management of patient with AML

A

Induction: cytarabin and daunoribicine

SCT

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34
Q

What is the cell line affected in acute myeloid leukaemia

A

myeloblasts

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35
Q

Chronic myeloid leukaemia cell line affected

A

Basophils, neutrophils, eosinophils

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36
Q

What chromosome is assoicated with CML and what does it do?

A

Philadelphia t(9;22)

Activates tyrosine kinase

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37
Q

How does CML present?

A

1) chronic stage: constititional symptoms
2) accelerated: anaemia, thrombocytopenia, neutropenia
3) Blast cell crisis (AML): no mature cells left, terminal

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38
Q

How do you manage CML?

A

Tyrosine kinase inhibators - imatinib

SCT

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39
Q

Which cell line is affected in chronic lymphocytic leukaemia?

A

B-lymphocytes

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40
Q

CLL pathology

A

gradual build up of B lymphocytes that evade immune system - dont die

Build up in blood/bone marrow, lymph nodes and spleen

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41
Q

How does CLL present?

A

Often asymptomatic

Bone marrow failure

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42
Q

Which infection is associated with CLL?

A

SHingles

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43
Q

What investigations would you do in suspected CLL?

A

Blood film: Smudge cells

FBC: anaemia, neutropenia, thrombocytopenia

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44
Q

How would you manage a patient with CLL

A

watch and wait

chemo

rituximab

Bone marrow transplant

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45
Q

Which other cancer can develop in patients with CLL?

A

Richter’s syndrome - NHL, high grade

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46
Q

what is the patho of myeloma?

A

Basically increase in plasma cells which:

1) Accumulation in BM -> failure
2) produce IgG and IgA and paraproteins (bence jones) -> renal failure
3) | increase osteoclast and inhib osteoblasts -> hypercalcaemia, bone destruction

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47
Q

How does myeloma present?

A

CRABI

  • *C**alcium high
  • *R**enal impairment
  • *A**naemia
  • *B**oney lesions - pepper pot skull

Infections +

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48
Q

what oncology emergency could be caused by myeloma?

A

Spinal cord compression

hyperviscosity of blood -> soft tissue swelling

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49
Q

How would you investigate suspected myeloma

A

FBC: bone marrow failure

hypercalaemia

serum protein electrophoresis: monoclonal plasma cells

urine protein electrophoresis: monoclonal antibodies - Bence Jones proteins

X-ray: pepper pot skull

50
Q

What are the diagonstic criteria for myeloma?

A

1) monoclonal plasma cells in bone marrow
2) monoclonal antibodies in urine (bence jones protein)
2) symptom from CRAB - end organ failure

51
Q

How would you manage a patient with myeloma?

A
  • chemo: bortezomib, thalidomide, dexomethasone
  • SCT
  • other: radio, bisphosphonates, infection prophylaxis
52
Q

68 yo male pt with enlarged lymp nodes neck, axillae, groin.

low Hb, high WBC

Blood film: 60% white cells are small mature lymphocytes

diagnosis

A

CLL

53
Q

What is the most commonly inherited thrombophilia?

A

Activated protein C resistance (Factor V Leiden)

54
Q

What is Thromobotic thrombocytopenic purpura?

A

lack of enzyme that cleaves vWF so you have more vWF

Mini thrombi form which use up platelets/clotting factors -> clotting

55
Q

What are the symptoms of TTP?

A

The Terrible Pentad

  1. Anaemia
  2. Thrombocytopenia
  3. Fever
  4. Renal problems
  5. CNS involvement
56
Q

What investigation findings would confirm TTP?

A

Schistocyes on blood film

low platelets

57
Q

How would you manage a patient with TTP?

A

plasmapheresis

+rituximab

+corticosteroids

58
Q

What is disseminated intravascular coagulation?

A

systemic activation of blood coag, initally form clots but then no more platelets -> bleeding

59
Q

how does DIC present?

A

bleeding

petechiae

purpura

60
Q

What causes DIC

A

systemic: infection, trauma, leukaemia

61
Q

How would you investigate ?DIC

A

D dimer high (fibrin degradation)

High PT/APTT

Low platelets

62
Q

How would you manage a pt with DIC

A

bleeding: platelet transfusion, FFP, fibrinogen conc

Not bleeding: heparin

63
Q

what is idiopathic thrombocytopenic purpura?

A

antibodies that bind to platelets and destoy them, diagnosis of exlusion

64
Q

How would a patient with ITP present?

A

Bruising, petechiae

Bleeding: gums, GI, nose, menorrhagia

65
Q

How would you investigate a pt with ?ITP

A

Low platelets

serology: Antibodies

66
Q

How would you manage a patient with ITP?

A

1st: pred + IVIG
2nd: splenectomy

67
Q

What is haemolytic uraemic syndrome

A

Infection with E.Coli causing platelet destruction

  • haemolytic anaemi
  • thrombocytopenia
  • AKI
68
Q

How does HUS present?

A

Bloody diarrhoea

abdo pain, fever, vomiting

69
Q

How would you investigate a pt with ?HUS

A

Stool sample: E.coli
Increased: Cr, LDH, WCC
Decreased: platelets

70
Q

how would you manage a pt with HUS?

A

supportive

fluids and electrolytes

*notifiable disease*

71
Q

what is von willebrands disease

A

Low vWF leads to defective platelet plug formation and decreased factor VIII

72
Q

How does vWD present?

A

bruising

bleeding: post surgery, mucosal, GI epistaxis

73
Q

What would bloods show in a person with vWD?

A

High APTT

Low: vWF, VIII

74
Q

How would you manage a patient with vWD?

A

avoid: NSAIDS, aspirin, IM injections

  • tranexamic acid + desmopressin - increase VIII and vWF from endothelial stores
  • Type 3: vWF concentrates
  • screening
75
Q

What is haemophilia A/B

A

X linked recessive condition resulting in deficiency in factor VIII (A) or IX (B)

76
Q

How would a patient with haemophilia present?

A
  • bruising
  • bleeding: after small trauma, into small joints
77
Q

What woudl bloods show in haemophilia?

A

Increased APTT

decreased VIII or IX

78
Q

how would you manage haemophilia?

A

recombinant VIII or IX

79
Q

Which factors are vitamin K dependent?

A

2, 7, 9, 10

80
Q

What is coombs test?

A

antibody added to blood sample

+Ve = immune system causing RBC destruction

81
Q

What is MCV and MCH

A

Mean corpuscular volume: Size of RBC

Mean corpuscular hb: Hb content of average RBC

82
Q

What are causes of normocytic anaemia?

A

Haemolytic

aplastic

83
Q

What are causes of microcytic anaemia?

A

Iron def

thalassaemia

84
Q

What are causes of macrocytic anaemia?

A

Pernicious

Folate def

85
Q

How does haemolytic anaemia present?

A

Asymptomatic unless severe

  • weakness
  • angina
  • jaundice
  • tachy
  • dyspnoea
86
Q

What would investigations show in haemolytic anaemia

A

Hb: low
MCV: normal
Reticulocytes: high (increased production)
UCB/LDH: high (break down of RBC)
+ve coombs if immune mediated

Blood film: spherocytes

87
Q

How do you manage haemolytic anaemia?

A

Corticosteroids

folic acid

transfusion if necessary

88
Q

What causes haemolytic anaemia?

A

Genetic: SCA, thalassaemia, G6PD def

Aquired: Haemolytic disease of the newborn, SLE, CLL, trauma

89
Q

What is aplastic anaemia?

A

Pancytopenia with hypocellular BM

90
Q

How would a patient with aplastic anaemia present?

A

General: pallor, fatigue, oedema, palps, headache

Post hep: 2-3 months jaundice

Congential: short stature, cafe au lait spots, skeletal abnorms

91
Q

What would you see on investigations for aplastic anaemia?

A

Hb: low
Platelets: low
Neutrophils: low
Reticulocytes: low
Viral studies

92
Q

How would you manage a pt with aplastic anaemia?

A

non severe: immunosups - ATG + ciclosporine or alemtuzumab

severe: haematopoietic SCT

Blood/platelet transfusion

93
Q

What causes Aplastic anaemia?

A

Idiopathic

Infection: post hepatitis

Viral: EBV, HIV

congenital/inherited

94
Q

Causes of Iron def anaemia

A

Blood loss: GI, menorrhagia, NSAID use
Dietary inadequacy: growing children and elderly
Malabsorption: tetracyclines, PPIS, coeliac, H. Pylori
Increased need: growth, preg

95
Q

How does iron def anaemia present

A

Fatigue, SOB, palps, headache

OE: pallor, koilnychia (spoons shaped)

angular chelitis, atropic glossitis

96
Q

What would you expect to see on investigations of pt with Iron def anaemia ?

A

Hb: low
MCV: low, microcytic
MCH: low, hypochromic
Ferritin: low

Film: varying size and abnormal shaped RBC

males/post meno fems : endoscopy
coeliac screening

97
Q

How do you manage Fe def anaemia>

A

Ferrous sulphate tablets

98
Q

what are the side effects of ferrous sulphate tablets?

A

Constipation, nausea, black stools

99
Q

What is thalassemia?

A

Autosomal recessive condition where either ɑ or β chains on haemoglobin are absent or decreased resulting in reduced hemoglobin in RBC

100
Q

How does thalassaemia present?

A

Normally asympotmatic

Severe: pallor jaundice, HF

101
Q

What would you expect to see on investigations for ?thalassaemia?

A

Hb: low
MCH/MCV: low
iron: high
ferritin: high
Haemoglobin electrophoresis is diagnostic

102
Q

How do you manage a pt with thalassaemia?

A

Asx: monitor

intermediate: ?blood transfusion
major: regular hypertransfusions to mainly enough Hb
Desferrioxamine, oral chelating agents (deferasirox)
SCT: better outcome when younger

103
Q

what is pernicious anaemia?

A

An autoimmune coniditon which involves gastritis and loss of parietal cells.

For B12 to be absorbed in terminal ileum parietal cells which produce intrinsic factor are required

104
Q

Causes of Pernicious anaemia

A

intake: lack of animal producs
Gastric: H.pylori infection, gastritis
Intestinal: malabsorption, crohns, HIV
Drugs: neomycin, colchicine

105
Q

how would a pt with pernicious anaemia present?

A

Fatigue, lethary

palps and headaches

B12 def: neuro (loss of vibration postion, reflexes) , paraesthesia, numbess, visual changes

OE: pallor, glottis, oral ulceration

106
Q

Investigation findings in pernicious anaemia?

A

Hb: low
MCV: high
Autoab screen: Parietal cell antibodies
Blood film: hypersegmented neutrophils, oval macrocytes and megaloblasts

107
Q

Management of pernicious anaemia?

A

IM hydroxocobalamin

108
Q

What are the causes of folate def?

A

Diet: goats milk, alcohol XS
Malabsorption: coeliac, IBD
Excretion: CHF
Antifolate drugs: nitrofurantoin, anti-c, methotrexate
Increased need: preg
Genetic Disorder

109
Q

What is sickle cell trait and anaemia?

A

Autosomal recessive condition with abnormal HbS

Homozygous= sickle cell anamia

heterozygous (HbA HbS) = sickle cell trait, asx, malaria protec

110
Q

How does sickle cell anaemia present

A

3-6 months old bc decrease in HbF
symptoms triggered by infection

  • anaemia: pallor, lethargy
  • growth restriction
  • jaundice
111
Q

When does a SC patient need hopsital referal?

A

Symptoms: severe pain, haematuria
OE

  • temp >38.5 or <36 in adults
  • temp>38 in kids
  • hypotensive
  • dehydrated
  • low Hb
112
Q

How do you diagnose SCA?

A

Hb electrophoresis

Decreased Hb

Blood film: sickled erythrocytes

113
Q

What are the sickle cell crises?

A
  1. Vasco-occlusive: obstruction of micro-circ by sickled RBC -> anaemia
  2. Aplastic: erythopoiesis cessation due to parvovius B19
  3. Sequestration: sickling in spleen causing pooling of blood
114
Q

What can trigger a vaso-occulsive SC crisis?

A

DICE

Dehydration
Infection/Ischaemia
Cold
Exertion

115
Q

How does a vaso-occulsive SC crisis present?

A
  • Pain
  • dactylitis
  • stroke
  • retinal occulsion
  • tachy
  • abdo distension
116
Q

how you you manage aplastic SC crisis?

A

Transfusion

117
Q

How does a sequestration SC crisis present and how do you u manage?

A

Px: hypovolaemia, splenomegaly

Ix: low Hb, high reticulocytes

Mx: splenectomy if recurrent

118
Q

What is polycythaemia?

A

increased RBC associated with JAK2 mutation which means haematopoietic stem cells keep producing RBC regardless of EPO

119
Q

How does polycythaemia present?

A

1) plethoric stage
- fatigue
- dizziness
- itching (worse when hot)
- facial plethora

2) spent stage
scar tissue formation means BM cant produce RBC - anaemia, thrombocytopenia, leukopenia

120
Q

How would you investigate polycythamia?

A

FBC: high Hb, WCC and platelets,

Genetic: JAK2

Bm: fibrosis, teardrop cells in spent phase

121
Q

How do you manage polycythaemia

A

Venesection

hydroxycarbamide:

CVD prophylaxis: Aspirin

phase 3b (15 decks)

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