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CP3 @ UoN - Medicine & Surgery > The White Cell > Flashcards

The White Cell Flashcards

1
Q

What cell types are included in a WC differential?

A 
Neutrophils
Lymphocytes
Eosinophils
Monocytes
Basophil
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2
Q

What is the function of Neutrophils?

A

Ingest/kill bacteria, fungi, cellular debris

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3
Q

What is the function of Lymphocytes?

A

Produce antibodies for cell-mediated immunity

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4
Q

What is the function of Eosinophils?

A

Role in allergic reactions, defence of parasitic infection

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5
Q

What is the function of Monocytes?

A

Precursor to tissue macrophages

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6
Q

What is the function of Basophils?

A

Release histamine in inflammatory reactions

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7
Q

What is Leukocytosis?

A

Increase in WCC

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8
Q

What are the causes of a neutropenia?

A 
Viral infection
Severe sepsis
Neutrophil antibodies (SLE)
Bone marrow failure
Hypersplenism
Cytotoxic drugs
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9
Q

What are the causes of a neutrophilia?

A 
Bacterial infection
Inflammatory reactions
Disseminated malignancy
Stress
Myeloproliferative conditions
Corticosteroid therapies
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10
Q

What is agranulocytosis, and what drug causes it as a s/e?

A

Complete absence of circulating neutrophils

Carbimazole

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11
Q

What are the causes of a lymphopenia?

A 
Bone marrow failure
Corticosteroid therapies
SLE
Uraemia
HIV infection
Cytotoxic drugs
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12
Q

What are the causes of a lymphocytosis?

A

Viral infections
Chronic infections
Myeloproliferative conditions

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13
Q

What are leukaemias?

A

Malignant proliferations of blood forming cells

  • acute/chronic
  • myeloid/lymphoid
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14
Q

Describe the difference b/w myeloid/lymphoid cell lineages?

A

Haemopoietic stem cell –> common myeloid/lymphoid progenitor

  • common myeloid –> erythrocytes, mast cells, megakaryocytes (form platelets), myeloblasts
  • common lymphoid –> NK cells, T/B lymphocytes
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15
Q

What cell lines do myeloblasts go on to form?

A

Monocytes
Basophils
Neutrophils
Eosinophils

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16
Q

What are the myeloproliferative conditions?

A

Myelofibrosis
Myelodysplasia
Polycythaemia vera
PRE-LEUKAEMIC

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17
Q

What is Acute Lymhoblastic Luekaemia (ALL)?

A

Malignancy of lymphoid cells (T/B cells) leading to uncontrolled proliferation of immature blast cells
-eventual bone marrow failure & tissue infiltration

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18
Q

What is the aetiology of ALL?

A

Most common childhood malignancy

  • 3-7yrs average age of dx
  • 80% of childhood leukaemias
  • rare in adults
  • more common in certain syndromes (e.g. Downs)
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19
Q

What is the prognosis of ALL?

A

Children (<10yrs) = good, cure rates >80%

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20
Q

What are poor prognostic factors in ALL?

A 
Older age of presentation
Male sex
B-cell disease
Presence of Philadelphia chromosome
   -9:22 translocation
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21
Q

What is Acute Myeloid Leukaemia (AML)?

A

Malignancy of blast cells from marrow myeloid elements

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22
Q

What are the risk factors for AML?

A 
Can be de novo OR
Myeloproliferative conditions
Previous chemo
Ionising radiation
Genetic syndromes
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23
Q

What is the aetiology of AML?

A

Median age of presentation at 65 yrs

  • can occur at any age
  • incidence increases w/ age
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24
Q

What is the prognosis of AML?

A

Rapidly progressive

20% 3yr survival after chemo

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25
Q

How do acute leukaemias present?

A

B sx
Bone pain
Sx of marrow failure
Hepatomegaly/splenomegaly

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26
Q

What are B sx?

A 
Fatigue
Wt loss
Night sweats
Fevers
Pruritis
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27
Q

What are the sx of marrow failure?

A

Anaemia (SOB on exertion, weakness)
Leukopenia (recurrent infections)
Thrombocytopenia (bleeding & brusing)

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28
Q

What is important to remember about the leukopenia in acute leukaemias?

A

Pts have leukocytosis BUT immature cells so present as leukopenia

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29
Q

What investigations are appropriate in suspected acute leukaemia?

A 
FBC
Blood film 
CXR (T-cell ALL, ?mediastinal widening)
Bone marrow aspiration
PET scanning (?mets)
U&amp;Es, LFTs, cardiac function testing
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30
Q

What are the general principles of managing acute leukaemias?

A

Supportive care

Use of antibiotics

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31
Q

What supportive care should be given in acute leukaemia?

A 
Nurse w/ full barrier nursing
Hickman line inserted
High-calorie diet
Frequent blood/platelet transfusions
Allopurinol (prevent tumour lysis syndrome)
Frequent bloods/obs
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32
Q

When should antibiotics be given in acute leukaemia?

A

Temp >38o on 2 occassions >1hr apart

  • assume sepsis
  • start broad spectrum a/b until afebrile for 72 hrs
  • often cephalosporin + gentamycin
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33
Q

What specific management steps are taken in ALL?

A 
High dose chemo to induce remission
   -consolidation w/ high/med dose blocks over months
   -2 yrs maintenance therapy
Consider marrow transplant
   -necessary if Philadelphia chromosome
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34
Q

What specific management steps are taken in AML?

A 
Intensive chemo
If poor prognosis
   -allogenic marrow transplant from HLA-matched siblings
   -allows further high dose chemo
If intermediate prognosis
   -autologous marrow transplants
   -further, lower dose chemo
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35
Q

What is the aetiology of Chronic Myeloid Leukaemia (CML)?

A

Rare in childhood
Most common 40-60yrs
Philadelphia Chr present in 95%
-better prognosis

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36
Q

What are the sx of CML?

A 
Insidious B sx, detected by chance (30%)
Gout (purine breakdown)
Abdo discomfort (splenomegaly)
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37
Q

What are the signs of CML?

A

Splenomegaly
Hepatomegaly
Anaemia/thrombocytopenia

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38
Q

What investigations are appropriate in suspected CML?

A 
FBC (WCC inc)
Blood film (myeloid cells inc)
Bone marrow biopsy
CT/PET
Cytogenic analysis of blood/marrow for Philadelphia Chr
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39
Q

What are the management options for CML?

A 
Imatinib chemo
   -response rate >90%
Stem cell transplantation
   -only treatment to achieve remission
   -significant mortality/morbidity
40
Q

What is the prognosis of CML?

A

Median survival 6yrs

41
Q

What are the three stages of CML?

A 
Chronic phase
   -few sx, lasts for yrs
Accelerated phase
   -inc sx, difficulty controlling counts
Blast transformation
   -features of AML, death
42
Q

What is the aetiology of Chronic Lymphocytic Leukaemia (CLL)?

A

Most common leukaemia
2x as common in males
Median age of presentation 70yrs

43
Q

What is the underlying pathophysiology of CLL?

A

Accumulation of mature B-cells (escaped apoptosis)

Inc mass of immune-incompetent cells –> Bone marrow failure

44
Q

What are the sx of CLL?

A

Asymptomatic, incidental finding on FBC
Anaemic/infection prone
B sx (if severe)

45
Q

What are the signs of CLL?

A

Enlarged, non-tender lymph nodes

Hepatosplenomegaly

46
Q

What investigations are appropriate in suspected CLL?

A 
FBC (inc WCC, AI haemolysis later)
Blood film (smudge cells)
47
Q

What is the rule of 1/3s for CLL?

A

W/o treatment

  • 1/3 will never progress
  • 1/3 will eventually progress
  • 1/3 will progress from diagnosis
48
Q

What are the management options for CLL?

A

Treatment only indicated if symptomatic/markers of poor prognosis
Chemo/radio

49
Q

What is the prognosis of CLL?

A

Depends on Rai stage, anywhere from 1yr to 13yrs mean survival
-death usually due to infection/Richter’s syndrome

50
Q

What is Richter’s syndrome?

A

Transformation of CLL to aggressive lymphoma

-usually diffuse large B cell lymphoma

51
Q

What is myeloma?

A

Malignant clonal proliferation of plasma cells (derived from B lymphocytes)

52
Q

What is the monoclonal band/paraprotein of myeloma?

A

Single clone of plasma cells produce single immunoglobulin

-seen on serum/urine electrophoresis as monoclonal band

53
Q

What is the aetiology of myeloma?

A

Average age presentation 70yrs

More common in Afro-Carribean populations

54
Q

What are the core clinical features of myeloma?

A

CRAB

  • calcium (hypercalcaemia)
  • renal (impairment)
  • anaemia (bone marrow failure)
  • bone (osteolytic lesions due to osteoclast activation)
55
Q

What are the presenting sx of myeloma?

A 
Backache
Pathological fractures
Hypercalcaemia (bones, stones, moans, groans)
Infection
Anaemia
Bleeding
Renal impairment (20% at dx)
56
Q

What investigations are appropriate in suspected myeloma?

A 
FBC (normochromic, normocytic anaemia, WCC dec)
Blood film (rouleaeux)
ESR (raised)
U&amp;Es (deranged)
Ca (raised)
Alk Phos (norm)
Serum/urine electrophoresis
Urine Bence-Jones protein (+ve)
Skeletal XR (lytic lesions)
Bone marrow biopsy
57
Q

What are the management options for myeloma?

A

Supportive therapy
Chemotherapy
Radiotherapy
Bone marrow stem cell transplants if <70

58
Q

What are the complications of myeloma?

A

Hypercalcaemia
Spinal cord compression
Hyperviscosity
Acute renal failure

59
Q

What is the prognosis of myeloma?

A

Original cell v. resistant, often returns
Med survial 3-4yrs
Death from renal failure/infection

60
Q

What are lypmhomas?

A

Malignant proliferations of lymphocytes, usually B-cells

  • commonly accumulate in peripheral lymph nodes
  • can accumulate in peripheral blood/infiltrate organs
61
Q

What are the two main types of lymphoma?

A

Hodgkin’s (15%)

Non-Hodgkin’s (85%)

62
Q

What is the defining characteristic of Hodgkin’s lymphoma?

A

Presence of Reed-Sternberg cells

-binucleate ‘mirror cells’ on biopsy

63
Q

What is the aetiology of Hodgkin’s lymphoma?

A

Peak incidence at 20-35yrs & 50-70yrs

More common in males (2:1)

64
Q

What are the risk factors for Hodgkin’s lymphoma?

A

Affected sibling
EBV
SLE
Obesity

65
Q

What are the sx of Hodgkin’s lymphoma?

A

B sx, w/ profuse night sweats (25%)
Lymph node pain induced by alcohol
SVC/bronchial obstruction
Pleural effusion

66
Q

What are the signs of Hodgkin’s lymphoma?

A

Enlarged, non-tender, rubbery lymph nodes (cervical)
Lymphaenopathy
Hepato-splenomegaly (50%)
Cachexia/anaemia

67
Q

What is the prognosis of Hodgkin’s lymphoma?

A

Slow growing, localised, rarely fatal

Better in lymphocyte predominant disease

68
Q

What is the aetiology of Non-Hodgkin’s lymphoma?

A

All lymphomas w/o Reed-Sternburg cells

Peak incidence at 70yrs

69
Q

What are the two main classifications of Non-Hodgkin’s lympoma?

A

High grade

Low grade

70
Q

Describe high grade Non-Hodgkin’s lymphoma

A

Divide rapidly
Present w/ rapid onset lymphadenopathy
Aggressive
Better prognosis if identified/treated

71
Q

Describe low grade Non-Hodgkin’s lymphoma

A

Divide slowly
Present insidiously
Widely disseminated at dx
Often incurable

72
Q

What are the sx of Non-Hodgkin’s lymphoma?

A 
Nodal disease (lymphadenopathy in 75%)
Extranodal disease (25%)
   -oropharynx, skin, CNS, gut or lung
B sx (wt loss if disseminated)
Bone marrow failure
73
Q

What are the appropriate investigations in Non-Hodgkin’s lymphoma?

A

Bloods - FBC, ESR, LFT, U&Es, LDH, Ca
Lymph node excision biopsy
Image guided biopsy
Staging CT

74
Q

What are the management options for Non-Hodgkin’s lymphoma?

A

Chemotherapy
Radiotherapy
Chemo-radiotherapy

75
Q

What is the prognosis for Non-Hodgkin’s lymphoma?

A 
Survival variable
Poor prognostic signs are
   ->60yrs
   -disseminated disease
   -raised LDH
76
Q

How are Non-Hodgkin’s lymphomas stages?

A

Ann-Arbor system

77
Q

What are myeloproliferative disorders?

A

Disease where clones of haemopoetic stem cells proliferate in the marrow, but retain the ability to differentiate

78
Q

What are the common myeloproliferative disorders?

A

Essential thrombocytosis
Myelofibrosis
Polycythaemia rubra vera

79
Q

What is essential thrombocytosis?

A

Clonal proliferation of megakaryocytes –> persistently raised platelets
-often asymptomatic

80
Q

What are the sx of essential thrombocytosis?

A

Often asymptomatic
Microvascular occlusion
Bleeding sx
Arterial/venous thrombosis

81
Q

What is Polycythaemia rubra vera (PCV)?

A

Malignant proliferation of a clone derived from one pluripotent marrow cell
-not requiring EPO to avoid apoptosis

82
Q

What are the common sx of PCV?

A

Asymptomatic

Arterial/venous thrombosis (>60yrs)

83
Q

What are the main complications of PCV?

A 
Serum hyperviscosity (excess RBCs &amp; WCs)
Thrombotic complications (excess platelets)
84
Q

How is PCV diagnosed?

A

Increased red cell mass

Investigation for JAK 2 mutation

85
Q

What are the rarer presentations of PCV?

A

Vague hyperviscosity sx (headache, dizziness, tinnitus, facial plethora, erythromelagia)
Splenomegaly
Gout

86
Q

How is PCV managed?

A

Repeated venesection

Low dose aspirin

87
Q

What is erythrromelagia?

A

Burning sensation in fingers/toes

88
Q

What is Primary Myelofibrosis?

A

Hyperplasia of megakaryocytes

  • produces excess platelet derived growth factor
  • marrow fibrosis & metaplasia
  • 2o haematopoiesis in spleen
89
Q

What are the sx of Primary Myelofibrosis?

A

B sx
Abdo discomfort (massive splenomegaly)
Bone marrow failure

90
Q

What is the main risk of essential thrombocytopenia & PCV?

A

May progress to myelofibrosis OR AML

-risk relatively rare

91
Q

What is aplastic anaemia?

A

Stem cell disorder leading to pancytopenia/hypoplastic marrow

92
Q

What are the causes of aplastic anaemia?

A

Autoimmune (drugs, viruses, irradiation as triggers)

Inherited (Fanconi)

93
Q

What are the sx of aplastic anaemia?

A

Bone marrow failure

Pancytopenia

94
Q

How is aplastic anaemia diagnosed?

A

Bone marrow biopsy

95
Q

How is aplastic anaemia managed?

A 
Blood product transfusion
Immunosuppression in AI
Allogenic bone marrow transplant
   -curative
   -only in younger pts

CP3 @ UoN - Medicine & Surgery (135 decks)

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