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PA MS > Haematology PAS > Flashcards

Haematology PAS Flashcards

1
Q

What are the Principal subtypes of leukaemia

A

Acute: Acute lymphoblastic leukaemia (ALL),
Acute myeloid leukaemia (AML).
Chronic:
Chronic lymphocytic leukaemia (CLL), Chronic myeloid leukaemia (CML)

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2
Q

What is the approach to a patient with Leukocytosis?

A

Review smear (are abnormal cells present?) and obtain differential count.

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3
Q

What is the approach to patients with complaints of non-specific confusion/drowsiness?

A

do blood
cultures, FBC, U&E, LFT, Ca2+
, glucose, and clotting. Consider CNS bleeding—CT if in
doubt.

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4
Q

Explain neutropenic regimen ?

A
  • Full barrier nursing in a side room and hand wash.
    *Avoid IM injections.
  • Look for infection and Take swabs.
    *blood ≈3—peripherally
    ± Hickman line
    *Check vital signs 4-hrly
    *Wash perineum after defecation
    *Oral Candida and other infections prophylaxis are important.
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5
Q

What is the risk and management of of Hyperviscocity syndrome ?

A

leukostasis in heart, vessels and leukocytic thrombi in brain and other organs.
TX is hydroxycarbamide or leukapheresis.

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6
Q

Definition of DIC ?

A

DIC is defined as the release of procoagulants into the circulation causing widespread activation of coagulation, consuming clotting factors and platelets and increasing risk of
bleeding.

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7
Q

Signs of DIC ?

A

Bruising, bleeding, renal failure.

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8
Q

Laboratory markers of DIC ?

A

*Decreased Platelets
* Prolongation of PT; APTT due to consumption of coagulation factors.
* Decreased fibrinogen (correlates with severity)
*Increased fibrin degradation products (D-dimers).

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9
Q

Histology of DIC ?

A

*schistocytes

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10
Q

Treatment of DIC ?

A
  • Replace platelets to overcome thrombocytopenia.
    /L
  • cryoprecipitate to replace fibrinogen.
    *FFP to replace coagulation factors
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11
Q

The commonest leukaemia with highest risk of DIC is acute pro myelocytic leukaemia: How is it treated?

A

all-transretinoic
acid (ATRA)

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12
Q

How to prevent sepsis in Leukaemia?

A

*Fluoroquinolone (eg ciprofl oxacin) before neutropenia gets
serious.
*Granulocyte colony stimulators (G-CSF) can increase the production of WBCs
(granulocytes) Careful during Chemotherapy.
*Herpes, pneumocystis, and CMV prophylaxis

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13
Q

Definition of Acute Lymphoblastic Leukaemia ?

A

A malignancy of lymphoid cells, affecting B- or T-lymphocyte cell lineages, arresting
maturation and promoting uncontrolled proliferation of immature blast cells, with
marrow failure and tissue infiltration

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14
Q

Risk factor for Acute Lymphoblastic Leukaemia ?

A
  • Ionizing radiation during pregnancy.
    *Down’s syndrome
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15
Q

The most common paediatric leukaemia ?

A

Acute Lymphoblastic Leukaemia ( CNS involvement is common)

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16
Q

Morphological classification of ALL?

A

L1, L2 and L3

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17
Q

L1 type ALL histology

A

Small
blasts with scanty cytoplasm

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18
Q

Histology of L2 subtype ALL?

A

Larger
blast cells with greater morphological variation and more abundant cytoplasm.

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19
Q

Histology of L3 subtype ALL?

A

Blasts with vacuolated basophilic cytoplasm.

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20
Q

What are the immunological classification of ALL?

A

Surface markers are used to classify ALL into:
*Precursor B-cell ALL
* T-cell ALL
* B-cell ALL.

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21
Q

What is the utility of cytogenic or chromosomal analysis based classification of ALL ?

A

To predict disease prognosis and recurrence.

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22
Q

Signs and symptoms of acute Lymphoblastic Leukaemia ?

A
  • Marrow failure: anaemia (<Hb), Infection (< WBC), Bleeding (<platelets)
    *Infiltration: Heapato and or splenomegaly, Lymphadenopathy, orchidomegaly.
  • CNS involvement: cranial nerve palsies and meningism.
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23
Q

Common infections in ALL?

A

*Bacterial septicaemia,
*zoster, CMV, measles,
*candidiasis, Pneumocystis pneumonia

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24
Q

Lab test in ALL are

A
  • CBC look for blast cells and WBC count.
  • CXR and CT chest to rule out mediastinal lymphadenopathy.
  • LP to look for CNS involvement.
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25
Q

Management of ALL?

A

*SUpportive: blood and platelet transfusion. IV fluids, Alopurinol to prevent tumor lysis syndrome.
* Infections: immediate IV antibiotics + Neutropenic regimen + infection prophylaxis.

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26
Q

Chemotherapy for ALL remission induction?

A

vincristine, prednisolone, L-asparaginase + daunorubicin

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27
Q

Chemotherapy for remission consolidation in ALL?

A

HIgh to medium remission induction chemo in blocks.

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28
Q

What is the CNS prophylaxis of ALL ?

A

intrathecal (or high-dose IV) methotrexate ± CNS irradiation

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29
Q

Maintenance chemotherapy in ALL?

A

mercaptopurine (daily), methotrexate (weekly), and vincristine + prednisolone (monthly) for 2yrs.

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30
Q

what is meant by haematological remission of ALL ?

A

No evidence of leukaemia in blood + recoverning blood cells + <5% blasts in regenerating Marrow.

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31
Q

Prognosis of ALL?

A
  • 70 to 90% cure in children
  • 40% cure in adults, poor prognosis if t(9,22) philadalphia ALL .
  • CNS presentation, low HB, significant leukocytosis or B cell ALL has poor prognosis.
  • poor in philadelphia negative ALL relapse.
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32
Q

Acute myeloid leukaemia (AML) definition ?

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements. It progresses rapidly (death in ~2 months if untreated; ~20% 3yr survival after Rx).

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33
Q

Incidence of Acute myeloid leukaemia (AML)?

A

Most common acute leukaemia in adults 1/ 10,000 per year.

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34
Q

Risk factors for AML ?

A
  • Prior radiation and Chemotherapy
  • Down syndrome and Bloom syndrome.
  • Myelodysplastic syndromes and aplastic syndromes.
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35
Q

Morphological classification of AML ( based on WHO histological classification, cytogenetics, and
molecular genetics)?

A

1)AML with recurrent genetic abnormalities
2) AML multilineage dysplasia
3) AML, therapy related
4)AML, other (subclassified as M0–M7 by maturation)

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36
Q

Signs and symptoms of AML?

A

Marrow failure and infiltration of brain, spleen, liver etc causing organomegaly and leukocytic thrombi. CNS involvement at presentation is rare.

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37
Q

Diagnosis in AML?

A

Low or increased or normal WBC + blasts at least 20%

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38
Q

AML itself can cause ___

A

Fever

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39
Q

Septicemia organism prediction in AML ?

A

Common organisms rarely and rare orgnaisms such as candidia and aspergilus causes sepsis commonly.

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40
Q

Remission chemotherapy in AML ?

A

5 cycles of daunorubicin and
cytarabine in one week blocks to induce remission.

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41
Q

what mutation enhances sensitivity to Cytarabine ( 20% of patients )

A

RAS.

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42
Q

ALL histology

A

TdT , t(12, 21) in children, t(9,22) in adults) with Philadelphia +.

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43
Q

Specific markers of ALL of Lymphoid cells of T cell origin ?

A

CD3

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44
Q

Specific markers of ALL of Lymphoid cells of B cell origin ?

A

CD19, CD20, and CD22

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45
Q

Bone marrow transplant (BMT) in AML ?

A

*Pluripotent haematopoietic stem cells are collected from the marrow. Allogeneic transplants from HLA-matched donors are indicated in refractory or relapsing disease.

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46
Q

Steps of Bone marrow transplant in AML?

A

1) destroy leuk aemic cells and the immune system by, eg cyclophosphamide + total body irradiation.
2) repopulate the marrow with donor cells infused IV.
Note: Ciclosporin ± methotrexate to prevent GVHD.

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47
Q

Complications of BMT in AML

A
  • GVHD, opportunistic infections, relapse of AML and infertility.
    *~ 10% mortality.
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48
Q

AML causes gum ?

A

Hypertrophy

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49
Q

AML causes increased plasma urate from ?

A

Tumor lysis syndrome.

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50
Q

How is AML is differentiated from ALL based on bone marrow biopsy?

A

bone marrow biopsy shows Auer rods which are azurophilic cytoplasmic inclusions also seen in ApML, high grade myelodysplastic syndromes and not in ALL.

51
Q

what is the definition of Myelodysplastic syndromes?

A

These are a heterogeneous group of disorders that manifest as marrow failure with risk of life-threatening infection and bleeding.

52
Q

Median survival range of myelodysplastic syndromes ?

A

6 months to 6 years.

53
Q

What percent of Myelodysplastic syndrome progress to acute leukaemia ?

A

30%

54
Q

Laboratory findings in Myelodysplastic syndromes ?

A
  • Pancytopenia with reduced reticulocyte count.
  • Increased Marrow cellularity due to ineffective haematopoiesis.
  • Ring sideroblasts in bone marrow.
55
Q

What is the treatment of myelodysplastic syndromes ?

A

*Multiple transfusions of red cells or platelets as needed
* Erythropoietin ± G-CSF lower transfusion requirements.
* Allogeneic stem cell transplantation
*thalidomide analogues and hypomethylating agents to improve QL

56
Q

Definition of Chronic myeloid Leukaemia ?

A

CML is characterized by an uncontrolled clonal proliferation of myeloid cells.
It accounts for 15% of leukaemias.

57
Q

what is the age and gender predominance in CML ?

A

40–60yrs, Male Predominance.

58
Q

Philadelphia chromosome (Ph) is present in what percentage of CML ?

A

> 80%

59
Q

What is Philadelphia chromosome (Ph)?

A

A hybrid chromosome translocation of t(9,22) chromosomal long arms,giving raise to BCR/ABL fushion gene on chromosome 22.

60
Q

Philadelphia chromosome (Ph)___ activity ?

A

tyrosine kinase

61
Q

Those without Ph have ?

A

worse prognosis

62
Q

Symptoms of CML

A

*Mostly chronic and insidious: <weight, tiredness, fever, sweats.
*features of gout
* Bleeding due to platelet dysfunction
*abdominal discomfort (splenic enlargement).
* ~30% are detected by chance.

63
Q

SIgns of CML

A
  • Splenomegaly >75%
  • Hepatomegaly, anaemia, bruising
64
Q

Laboratory findings in CML

A
  • Leukocytosis with whole spectrum of myeloid cells, ie neutrophils, monocytes, basophils, eosinophils
  • Low Hb
  • variable platelets
  • Bonemarrow hypercellularity
  • increased urate and B12.
  • Philadelphia chromosome in blood or bone marrow.
65
Q

Survival in CML

A

Variable (5 to 6 years)

66
Q

Phases of CML transformation?

A
  • Chronic lasting months or years with little to no symptoms.
    *Accelerated phase- increasing symptoms, spleen size, and difficulty in controlling counts
  • Blast transformation, with features of acute leukaemia ± death
67
Q

Treating CML

A
  • First line: BCR-ABL tyrosine kinase inhibitor.
    *dasatinib has been used in imatinib-resistant blast crisis.
    *Dasatinib and nilotinib allow more patients to achieve deeper,
    more rapid responses.
    *Those with lymphoblastic transformation may benefit from treatment as
    for ALL.
    *Stem cell transplantation. Allogeneic transplantation from an HLA-matched sibling or unrelated donor offers the only cure, but carries significant morbidity and
    mortality
68
Q

What is the Hallmark of CLL?

A

The hallmark of CLL is progressive accumulation of the malignant clones of functionally incompetent
B cells. Mutations, trisomies, and deletions increases risk.

69
Q

What is the epidemiology of CLL

A

CLL is the commonest leukaemia (>25%; incidence: ~5/100 000/yr). M:F≈2:1

70
Q

What is the staging of CLL?

A

Stage 0= Lymphocytosis alone Median survival >13yrs
Stage 01= Lymphocytosis + lymphadenopathy median surivial 8 years.
Stage 02= Lymphocytosis + spleno- or hepatomegaly, median survival 5 years.
Stage 03= Lymphocytosis + anaemia (Hb <110g/L) median survival 2 years.
Stage 04= Lymphocytosis + platelets <100 ≈ 109/L, median survival 1 year.

71
Q

Symptoms of CLL?

A

Often none, presenting as a surprise finding on a routine FBC. Patients
may be anaemic or infection-prone, or have ,<weight, sweats, anorexia if severe.

72
Q

Signs of CLL ?

A

Enlarged, rubbery, non-tender nodes+ Hepato or hepatosplenomegaly.

73
Q

Complications of CLL?

A

*Autoimmune haemolysis
*increased Infection due to hypogammaglobulinaemia (= low IgG), bacterial, viral especially herpes zoster.
* Marrow failure

74
Q

Treatment of CLL

A
  • Drug therapy tailored to symptoms
    *Fludarabine + rituximab ± cyclophosphamide is 1st line (there is synergism)
  • Radiotherapy
    helps lymphadenopathy and splenomegaly.
    *Supportive care: Transfusions, IV human immunoglobulin if recurrent infection.
    *Stem-cell transplantation may have
    a role in carefully selected patients
75
Q

Natural Hx of CLL

A

*⅓ never progress (or even regress), ⅓ progress slowly, and ⅓ progress actively.
*CD23 and beta 2 microglobulin correlate with bulk of disease and rates of
progression.
*Death is from Richter’s syndrome.

76
Q

What are Lymphomas ?

A

Lymphomas are malignant proliferation of Leukocytes that occur within the Lymph nodes as opposed to it in bone marrow as in in Leukemias.

77
Q

What are the broad classification of lymphomas

A

Hodgkins lymphoma and non-hodgkins lymphoma.

78
Q

What is the histological hallmark of Hodgkin’s Lymphoma ?

A

Reed-Sternberg cells in lymph node biopsy.

79
Q

Epidemiology of Hodgkins Lymphoma ?

A

Two peaks: 15 to 24 years and elderly
Male to female ratio: 2:1

80
Q

Risk factors for Hodgkin’s Lymphoma ?

A

An affected sibling; EBV, SLE; post-transplantation.

81
Q

Symptoms of Hodgkin’s Lymphoma ?

A
  • Enlarged, non-tender, Rubbery lymph nodes ( 60-70% cervical)
  • 25% may have fever, weight loss,
    night sweats, pruritus, and lethargy.
    *alcohol-induced lymph node pain.
    *Mediastinal lymph node involvement can cause mass effect,
    *direct extension, eg causing pleural effusions.
82
Q

Signs of H lymphoma ?

A

*Lymphadenopathy
*cachexia, anaemia, spleno- or hepatomegaly.

83
Q

What is the tissue diagnosis in H lymphoma ?

A

Lymph node excision biopsy if possible. Image-guided needle biopsy, laparotomy, or mediastinoscopy may be needed.

84
Q

What should be the blood test in Hodgkin’s’ Lymphoma ?

A

FBC, film, ESR, LFT,
LDH, urate, calcium.

85
Q

Imaging in H lymphoma

A

CXR, CT/PET of thorax,abdo, and pelvis.

86
Q

Ann Arbor staging of Hodgkin’s Lymphoma ?

A

Done by imaging ±marrow biopsy :
* 1 Confined to single lymph node region.
*2 Involvement of two or more nodal areas on the same side of the diaphragm.
*3 Involvement of nodes on both sides of the diaphragm.
*4 Spread beyond the lymph nodes, eg liver or bone marrow.

87
Q

Ann Arbor staging of Hodgkin’s Lymphoma A or B classification.

A
  • each stage is classified to A ( stage 01 A), if there is only Pruritus as associated symptom.
  • Each stage is classified to B, if there are associated symptoms like weight lose, unexplained fever. B has worse prognosis.
88
Q

Chemotherapy in Hodgkin’s disease ?

A

*Radiotherapy + short courses of chemotherapy for stages
I-A and II-A.
*Longer courses of chemotherapy for II-A with >3 areas involved through to IV-B.

89
Q

Drugs used in Hodgkin’s disease?

A

Adriamycin (doxorubicin), Bleomycin, Vinblastine, Dacarbazine cures ~80% of patients.

90
Q

what is the treatment of Hodgkin’s Lymphoma ?

A

High-dose chemotherapy followed by autologous stem cell transplantation.

91
Q

Emergency presentation of Hodgkin’s Lymphoma ?

A

Infection; SVC obstruction— elevated JVP, sensation of fullness
in the head, dyspnoea, blackouts, facial oedema

92
Q

What are the subtypes of Hodgkin’s Lymphoma ?

A

*Nodular sclerosing (70%) Good
Mixed cellularity (20–25%) Good
*Lymphocyte rich (5%) Good
Lymphocyte depleted (<1%) Poor

93
Q

5 year survival in Hodgkin’s lymphoma ?

A
  • depends of stage and grade.
    *>95% in I-A lymphocyte predominant disease.
    *<40% with IV-B lymphocyte-depleted.
94
Q

what are non Hodgkin’s Lymphomas ?

A

All lymphomas without Reed-sternberg cells are grouped as non hodgkin’s lymphomas.

95
Q

Most Non-Hodgkin’s Lymphoma’s are derived from?

A

B cells.

96
Q

The most common Non-Hodgkin’s Lymphoma is ?

A

DLBCL

97
Q

What are the causes of Non-Hodgkin’s Lymphomas ?

A
  • high grade Lymphomas from EBV transformed cells.
  • Immunodeficiency: HIV
    *Drugs
    *HTLV-1, H. Pylori
  • Toxins
  • Congenital.
98
Q

Signs and symptoms of Non-Hodgkin’s lymphoma?

A
  • Superficial lymphadenopathy (75% at presentation).
    ** Extranodal disease (50%) Gut (commonest).
99
Q

Gastric MALT is caused by

A

*H. pylori and usually regressess with eradication of the organism.
*MALT usually involves the antrum, is multifocal and metastasizes late

100
Q

What are Non-malt Lymphomas ?

A

Non-MALT gastric lymphomas (60%) are usually diffuse
large-cell B lymphomas—high-grade and not responding well to H. pylori eradication.

101
Q

What are the Non-hodgkin’s Lymphomas presents with diarrhoea, vomiting, abdominal pain, and weight loss + poor prognosis?

A
  • immunoproliferative small intestine
    disease (IPSID)
  • enteropathy/coeliac-associated intra-epithelial T-cell lymphoma (EATCL).
102
Q

what is the pathology of cuataneous Lymphoma ?

A

clonal T cells in mycosis fungoides

103
Q

Second most common type of Lymphoma is

A

cutaneous lymphoma (50% of the NH Lymphomas)

104
Q

What is the oropharyngeal NH-Lymphoma ?

A

Waldeyer’s ring lymphoma causes
sore throat/obstructed breathing.

105
Q

Systemic features of Non-hodgkin’s Lymphoma?

A

It is less common in Non- H lymphomas, when it does it indicates dissemination of the disease and the features are fever, night sweats, weight loss. Pancytopenia from marrow involvement—anaemia, infection,bleeding.

106
Q

Blood test in NH lymphoma ?

A

FBC, U&E, LFT. >LDH ≈ worse prognosis,reflecting > cell turnover.

107
Q

Marrow
and node biopsy in NH lympha

A

for staging based on Ann arbor classification.

108
Q

Low grade NH Lymphomas are ?

A

indolent, often incurable and widely disseminated.

109
Q

Examples of low grade NH Lymphomas are

A

follicular lymphoma, marginal zone lymphoma/MALT, lymphocytic lymphoma

110
Q

Treatment of low grade NH lymphomas

A

They are closely related to CLL and are treated similarly.

111
Q

Waldenström’s macroglobulinaemia is a ?

A

lymphoplasmacytoid lymphoma
and Produces IgM.

112
Q

Examples of high grade Lymphomas are ?

A

They are more aggressive, but often curable. examples are DLBCL, Burkit’s Lymphoma.

113
Q

Treatment of Low grade NH lymphomas ?

A
  • None, if asymptomatic.
  • Curative radiotherpay in localized disease.
  • Remission maintenance therapy with interferon alfa or rituximab.
114
Q

rituximab-refractory NH low grade Lymphomas ?

A

Bendamustine monotherapy or

115
Q

Treatment of HIgh garde NH lymphoma ?

A

*R-CHOP’ regimen: Rituximab, Cyclophosphamide, Hydroxydaunorubicin, vincristine (Oncovin®) and Prednisolone.
*Granulocyte colony-stimulating factors (G-CSFs) help neutropenia.

116
Q

Prognosis of NH Lymphomas ?

A
  • poor prognosis if age >60 +/- Systemic symptoms, Bulky disease (abdominal mass >10cm), high LDH, Disseminated disease.
  • 5 year survival is 30% for high grade and 50% for Low grade.
117
Q

Histopathology of follicular lymphoma may show ?

A

‘buttock cells’ with
cleaved nuclei.

118
Q

histology of Cutaneous T cell lymphomas may show

A

Sézary cells.

119
Q

Rituximab in Follicular lymphoma ?

A
  • Rituximab kills CD20 +ve cells by antibody-directed cytotoxicity ± apoptosis induction.
    *It also sensitizes cells to CDVP( * cyclophosphamide, doxorubicin, vincristine, and prednisolone).
    *It also has a role in maintaining remission, and in relapsed disease.
120
Q

Immunophenotypes of AML ?

A

CD33 or CD13

121
Q

Immunophenotypes of B lineage ALL?

A

CD10 and CD 19

122
Q

Immunophenotypes of T lineage ALL?

A

CD3

123
Q
A

PA MS (44 decks)

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