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MRCP Master > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Medications that increase risk of VTE

A
  1. combined oral contraceptive pill: esp 3rd generation
  2. hormone replacement therapy: the risk of VTE is higher in women taking oestrogen + progestogen preparations
  3. raloxifene and tamoxifen

4.antipsychotics (esp. olanzapine)

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2
Q

‘tear-drop’ poikilocytes, massive splenomegaly, dry tap

A

Myelofibrosis

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3
Q

What is Bombesin is a tumour marker for

A

small cell lung carcinomas

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4
Q

Most common tumour causing bone metastases

A

Prostate
Breast
Lung

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5
Q

Sickle cell how does acute chest syndrome present

A

dyspnoea, CP, pulmonary infiltrates on chest x-ray, low pO2
transfusion: improves oxygenation

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6
Q

4 Heme disorders

A

Sideroblastic- ala synthase / vit b6

Acute intermittent porphyria - mutation porphobilinogen demainase

Lead poisoning - ala dehydratase & ferrochelarase

Porphyria cutanea tarda- decrease uroporphyinogen decarboxylase

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7
Q

Ix sideroblastic anemia & rx

A

Blood letting
Deferoxamine
Severe bm or liver transplant

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8
Q

Causes of lead poisoning

A
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9
Q

Sx lead poisoning

A
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10
Q

Dx and rx lead poisoning

A
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11
Q

Cause of acute intermittent porphyria and triggeres

A

Build up of Ala & porphobilinogen

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12
Q

Sx & rx of AIP

A

Raised urinary porphobilinogen (btwn attack)
Raised delta aminolaevulinic acid

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13
Q

Causes of Porphyria cutanea tarda

A
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14
Q

Sx & rx of PCT

A

Rx: avoid triggers. Phlebotomy, hydroxychloroquine

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15
Q

Difference between PCT & AIP

A

AIP urine = raised urinary prophobiliogen
PCT= Uroporphyrinogin

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16
Q

What happens when HbS is deoxygenated?

A

Sickling an polymerisation of hb

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17
Q

Blood markers of hemolysis

A

Haptoglobin mop up Hema = reduced haptaglobin = unconjugated bilirubin a

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18
Q

How does sickle cell affect bones

A
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19
Q

How does sickle cell effect the spleen

A

Fibrosis
Sequestration of blood —> infarction
Increases susceptibility

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20
Q

How does sickle cell effect kidney & penis

A
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21
Q

What are the long term rx of sickle cell?

A

Hydroxyurea - increasing HbF prevents crisis
Every 5 years pneumococcal vaccine

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22
Q

Explain the genetics of sickle cell

A

Glutamic acid is swapped with valine on chrom 11 = decrease HbA and increase hbs
AR
Carrier state exists

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23
Q

What is the most common cause of death in Sickle cell

A

acute chest syndrome

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24
Q
A
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25
Q

What causes increased HbA2
Target cells & anisopoikilocytosis ?

A
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26
Q

Why does parvovirus cause aplastic anemia in beta thalassmia and sickle cell

A

Suppresses rbc production = crisis

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27
Q

What is the main difference btwn Acute & Chronic Leukemias

A

acute leukemias,-cells don’t mature at all, =“blast” form; tend to progress rapidly.

chronic leukemias-caused by the increased proliferation of immature leukocytes,
Progress slowly; CLL,CML,HCL

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28
Q

Where do abnormal Leukemias cells deposit?

A
  • liver and spleen = hepatosplenomegaly,
  • lymph nodes = lymphadenopathy,
  • skin causing purple or flesh colored plaques or nodules = leukemia cutis.
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29
Q

Lymphomas vs Leukemias typically form

A

Lymphomas solid - tumors in lymphatic tissue such as lymph nodes, thymus, or spleen.

Leukemias - bone marrow or blood.

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30
Q

What are the differences in translocations in AML & ALL

A

ALL - children- need to not sent to school @ 9:22 or picked up 12;21

AML - adults pick up at 15:17

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31
Q

What can cause acute leukaemias
Translocation
Both Ass w/ - RAD
Only AML

A
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32
Q

Most common type of AML
What is its translocation
What is rx

A

APL 15;17
Vit A & arsenic

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33
Q

I’m ALL what cells are abnormal?

A

Can be
Bcells in 80% of cases
Or
T cells

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34
Q

Which leukaemias are ass with Philadelphia chrom?

A

9:22 ALL & CML

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35
Q

In CML what does the fusion of 9(abl) & 22 (BCR) cause ?
What is rx for cml

A

BCR-ABL = continuous cell division = blast crisis
BCL- ABL inhibitors

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36
Q

CCL
Cell type
Ix of choice
Labs
Blood flim
Rx

A

B-cells

Immunophenotyping

Smudge cells

ITP + autoimmune haemolytic anemia

FCR : fludarabine, cyclophosphamide, rituximab

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37
Q

What chronic leukaemia is ass w/ BRAF gene
What effect does this have on the bone

A

Hairy cell
Bm fibrosis = pancytopenia + severe spleenomegally

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38
Q

How can you differentiate CML to a leukamoid rnx & what is leukaemoid rnx

A

Leukaemiod rnx is the presence of immature cell in the peripheral blood because push out of the bone marrow.
Which can happen in infections, hemolysis, hemorrhage, ca often indicated by a neutrophilia

CML will have Low Alkaline phosphatase score

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39
Q

CML ix

A

Cytogenetics - Philadelphia chrom

Lukocyte alkaline phosphatase - low (differs from other myeloproliferative disorders
BM aspiration- to qualify blast & fibrosis

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40
Q

How can you differentiate aml from ALL as on BM aspiration shows >20% blast cell (bm or peripheral bl)

A

Myloblasts have aura rods
Immunophenotyping

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41
Q

Dx Hairy cell

A
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42
Q

Rx ALL

A

vincristine, corticosteroids, and anthracycline (daunorubicin, doxorubicin, rubidazone, idarubicin), with or without cyclophosphamide or cytarabine
Maintenance : daily 6-mercaptopurine and weekly methotrexate

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43
Q

Poor prognosis in ALL

A

FAB L3 type
* T or B cell surface markers
* Philadelphia translocation, t(9;22)
* age < 2 years or > 10 years
* male sex
* CNS involvement
* high initial WBC (e.g. > 100 * 109/l)

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44
Q

most valuable test to confirm CLL

A

Immunophenotyping - shows circulating clonal B lymphocytes expressing particular antigens (CD5, CD19, CD20 and CD23).

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45
Q

Compare IX of choice in CLL & CML

A

CLL - Immunophenotyping + Smudge cells more likely to have Lymphadenopathy

CML-
Cytogenetics - Ph chromosome; BM aspiration & biopsy - material for cytogenetic. Also to quantify the % of blasts & degree of fibrosis
**leukocyte alkaline phosphatase test ** LOW
More likely to have hepatosplenomegaly

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46
Q

Compare IX of choice in Acute Luekimas

A

Both classification requires 20% or greater amount of blasts in BM or peripheral blood
AML - will have aura rods esp in PML

ALL- glycogen granules, Immunophenotyping for B vs T cells

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47
Q

Poor prognosis CLL

A

Poor prognostic factors (median survival 3-5 years)

  • male sex
  • age > 70 years
  • lymphocyte count > 50
  • prolymphocytes comprising more than 10% of blood lymphocytes
  • lymphocyte doubling time < 12 months
  • raised LDH
  • CD38 expression positive
  • TP53 mutation
    (del 17p) are seen in around 5-10% of patients =poor prognosis
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48
Q

Leukimas that causes enlarged thymus

A

TALL
ALL

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49
Q
  1. What is it call when a leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma.
  2. Which leukaemia does this happen
A

Richter’s transformation
Ass w/ CLL

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50
Q

Rx CLL

A

Rx: fludarabine, cyclophosphamide and rituximab

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51
Q

Compare HL to NHL
Cells
Spread
Extra nodal
Age

A

Hodgkin lymphoma
-Reed-Sternberg
- arise from B-cells and
- spread in a contiguous manner,
-rarely involve extranodal sites.
-Bimodal age distribution-20 y.o > 60 years of age.
Think: Older wiser owl cells(Reed-Sternberg) orderly (contiguous ) and quite (Not extra nodal)

NHL
No Reed-Sternberg cells
- sometimes spread non-contiguously,
- Can involve extranodal sites: skin, GI & brain.
-children and adults

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52
Q

Name the 5 B-cell subtypes in NHL

A
  1. Follicular -BCL2 gene t(14;18), waxing and weaning neck swelling. Prevent cell death
  2. Diffuse large B-cell- (most common in adults) aggressive, most common BCL 2&6
  3. Burkitt -myc – ass EBV, extra Nodal (ileocecal or jaw ) , starry sky appearance;
  4. Mantel- Aggressive more common in male, translocation bcl1
  5. Marginal zone lymphoma :Malt- extra nodal,
  6. lymphoplasmacytic lymphoma- leads to Waldenstrom macroglobulinemia
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53
Q

Dx CLL

A
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54
Q

2 main subtypes of HL

A

Classical has CS 15 & CD 30 expressed

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55
Q

In HL what are the 4 subtypes of classical HL
Which has the best or worst prognosis
Which 2 are ass with Immcompromised

A
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56
Q

Which HL is ass with popcorn cells ?

A

Nodular lymphocytic predominant HL

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57
Q

How is NHL divided?

A

B cell & T cell

58
Q

Name the two T cell NHLs

A

Adult T cell
Mycosis fungoides

59
Q

Which T cell NHL causes sezary syndrome what is it ?

A
60
Q

Useful prognostic indicator in lymphoma

A

ESR

61
Q

How are NHL B & T differ

A

B cells have CS 20 expressed

62
Q

NHL B-cell: Follicular lymphoma
Translocation causes over express of what gene

A

Think afternoon give follicles/ zits

63
Q

NHL B-cell: most common & aggressive in adults

A

diffuse large cell lymphoma
BCL 2&6

64
Q

NHL B-cell lymphoma: burkitts
Ass w/ virus
Translocation &gene
African presentation outside Africa

A

Starry skys in New York

65
Q

NHL B-cell: mantle cell
Translocation & gene

A

Think pic should be mantle of els Brith

66
Q

NHL B-cell: marginal zone lymphoma associated with

A
67
Q

Which b cell lymphoma is ass with Waldenstorm macroglobinemia ?

A
68
Q

Which NHL Tcell lymphoma is ass with HTLV ?

A
69
Q

Ix of choice for lymphoma?

A

Excisional lumph node biopsy

70
Q

Describe staging of NHL lymphoma

A

Ann Arbor system.

Stage 1 - One node affected

Stage 2 - More than one node affected on the same side of the diaphragm

Stage 3 - Nodes affected on both sides of the diaphragm

Stage 4 - Extra-nodal involvement e.g. Spleen, bone marrow or CNS
The stage is combined with the letter A or B to indicate the presence of ‘B’ symptoms. With the letter A indicating no B symptoms present and B indicating any of the beta symptoms present. For example, a patient with a single node affected and no ‘B’ symptoms would be stage 1A.

71
Q

Name the 3 plasma cell disorders and what do they all produce ?

A
  1. multiple myeloma,
  2. monoclonal gammopathy of unknown significance or MGUS(em-gus),
  3. Waldenström’s macroglobulinemia.

Each of them produce a monoclonal or M-protein,

72
Q

Discuss lymphoma

A
73
Q

Discuss lymphoma

A
74
Q

Sx of MM

A
75
Q

What M protein is produced in MM

A

most common IgG, followed by IgA, and these immunoglobulins have both a heavy and light chain.

Rarely, the myeloma cells can only make the kappa or lambda light chain of the immunoglobulin=the Bence-Jones protein.

76
Q

what is Bence-Jones protein

A

kappa or lambda light chain** of the immunoglobulin

77
Q

Ix MM
BM aspiration
Peripheral smear
Type of amemia
Serum & protein electrophoresis

A
78
Q

Ix MM
BM aspiration
Peripheral smear
Type of amemia
Serum & protein electrophoresis

A
79
Q

How does MGUs an MM differ

A
80
Q

How does MM, Mgus and Waldenström’s macroglobulinemia differ
Serum Electrophoresis
skeletal survey
BM

A

MM
Sx CRABBI SPEP
Serum Electrophoresis: IgG /IgA OR NEG But urine = Bence-Jones protein.
skeletal survey - lytic lesions.
BM: >10% lymphoplasmacytic cells

MGUS- asymptomatic
Serum Electrophoresis: IgG
No lytic lesions
BM: <10% lymphoplasmacytic cells

Waldenström’s macroglobulinemia:
Sx hyperviscosity or autoantibodies
Serum Electrophoresis: IgM
BM: >10% lymphoplasmacytic cells.

81
Q

SX of Waldenström’s macroglobulinemia

A

May be Asymptomatic

Hyperviscosity syndrome, = mucosal bleeding from the nose &gums.

Eyes-distension of retinal veins = retinopathy or blurring and loss of vision.

Raynaud

IgMs can also inappropriately act as autoantibodies against
RBC = autoimmune hemolytic anemi

Or attack sheaths of nerves = peripheral neuropathy.

lymphadenopathy, splenomegaly, and hepatomegaly

82
Q

Rx MM

A

lenalidomide in combination with dexamethasone, and bortezomib either alone or in combination with pegylated doxorubicin

83
Q

Rx tumour lysis syndrome

A

Rasburicase (a recombinant version of urate oxidase, an enzyme which catalyses the conversion of uric acid to allantoin*)

84
Q

What is tumour lysis sx

A

hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia & AKI

85
Q

Age distribution in Leukaemia

A

ALL -children
CML- Middle age
AML - Older Middle age
CLL- old age

86
Q

Tumour maker: Carcinoembryonic antigen (CEA)

A

Colorectal cancer

87
Q

Tumour maker: S-100

A

Melanoma, schwannomas

88
Q

Tumour maker :Alpha-feto protein (AFP)

A

Hepatocellular carcinoma, teratoma

89
Q

Tumour maker CA125

A

Ovarian

90
Q

Carcinogen Aflatoxin (produced by Aspergillus)

A

Liver - (hepatocellular carcinoma)

91
Q

Carcinogen Aniline dyes

A

Bladder (transitional cell carcinoma)

92
Q

Carcinogen Nitrosamines

A

Oesophageal and gastric cancer

93
Q

Carcinogen Vinyl chloride

A

Hepatic angiosarcoma

94
Q

t(15;17)

A
  • seen in acute promyelocytic leukaemia (M3)
  • fusion of PML and RAR-alpha genes
  • Good prognositic Acute myeloid leukaemia
95
Q

Oncovirus Epstein-Barr virus causes
(4)

A

Burkitt’s lymphoma
Hodgkin’s lymphoma
Post transplant lymphoma
Nasopharyngeal carcinoma

96
Q

Oncovirus Human papillomavirus 16/18

A

Cervical cancer
Anal cancer
Penile cancer
Vulval cancer
Oropharyngeal cancer

97
Q

Oncovirus Human herpes virus 8

A

Kaposi’s sarcoma

98
Q

Oncogenes ABL

A

Chronic myeloid leukaemia

99
Q

Oncogenes BCL-2

A

Follicular lymphoma t(14;18)

100
Q

Oncogenes RET

A

Multiple endocrine neoplasia (types II and III)

101
Q

Oncogenes RAS

A

Many cancers especially pancreatic

102
Q

Oncogenes n-MYC

A

Neuroblastoma

103
Q

Oncogenes

A

gain of function results in an increased risk of cancer

104
Q

Tumor suppressor genes

A

loss of function results in an increased risk of cancer

105
Q

RX HL

A

ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine): considered the standard regime

BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone): alternative regime with better remission rates but higher toxicity

106
Q

pentad of fever, neuro signs, thrombocytopenia, haemolytic anaemia and renal failure

A

TTP
ADAMTS13

107
Q

Rx Methaemoglobinaemia

A

NADH methaemoglobinaemia reductase deficiency: ascorbic acid

acquired: IV methylthioninium chloride (methylene blue)

108
Q

Rx cyanide poisoning

A

Dicobalt edetate & hydroxocobalamin

109
Q

leukaemia that often presents as DIC

A

AML
Acute promyelocytic leukaemia

110
Q

HbAS indicates

A

sickle cell trait

111
Q

Hb SC indicates

A

is a milder form of sickle disease

112
Q

Protein C deficiency + warfarin

A

=skin necrosis

113
Q

deletions of part of the short arm of chromosome 17 (del 17p) in which leukaemia is associated with a poor prognosis

A

CLL

114
Q

Low haptoglobin indicates

A

haemolytic anaemias

115
Q

most common inherited thrombophilia

A

Activated protein C resistance (Factor V Leiden)

116
Q

Haemolytic anaemias:
Intravascular haemolysis: causes

A

mismatched blood transfusion
G6PD deficiency*
red cell fragmentation: heart valves, TTP, DIC, HUS
paroxysmal nocturnal haemoglobinuria
cold autoimmune haemolytic anaemia

stay inside as it a cold night for a meditarainin

117
Q

Extravascular haemolysis causes

A

haemoglobinopathies: sickle cell, thalassaemia

hereditary spherocytosis

haemolytic disease of newborn

warm autoimmune haemolytic anaemia

118
Q

Hereditary angioedema screening

A

C4 are low

119
Q

Hereditary angioedema to confirm the diagnosis

A

serum C1-INH levels

120
Q

aromatase inhibitors Example and function & SE

A

Anastrozole and letrozole

reduces peripheral oestrogen synthesis

Adverse effects
osteoporosis
hot flushes
arthralgia, myalgia
insomnia

121
Q

Hereditary spherocytosis what is it
genetic inheritance
decent
Triggers
Blood film
Choice Ix

A

G6PD deficiency
- Male (X-linked recessive
-Descent African + Mediterranean
Triggers : Infection/drugs
Blood filmHeinz bodies
Ix: enzyme activity of G6PD

Hereditary spherocytosis (AD)- Male + female

  • Northern European
    Trigger: infection
    Film Spherocytes (round, lack of central pallor)
    Ix: EMA binding test
122
Q

ECOG score performance status’ scale

A

0 Fully active, able to carry on all pre-disease performance without restriction

1 Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature, e.g., light house work, office work

2 Ambulatory and capable of all selfcare but unable to carry out any work activities; up and about more than 50% of waking hours

3 Capable of only limited selfcare; confined to bed or chair more than 50% of waking hours

4 Completely disabled; cannot carry on any selfcare; totally confined to bed or chair

5 Dead

123
Q

good response to a single dose of adrenaline & complete resolution of symptoms

Resus Council UK recommend how long before discharge

A

2 Hours

124
Q

Resus Council UK recommend how long before discharge :
2 doses of IM adrenaline needed, or
previous biphasic reaction

A

6 hours

125
Q

Resus Council UK recommend how long before discharge :

severe rnx requiring > 2 doses of IM adrenaline

  • pt has severe asthma

possibility of an ongoing reaction (e.g. slow-release medication)
Pt presents late at night

pt in areas litmited access to care may

A

minimum 12 hours after symptom resolution

126
Q

How do you distinguish between
transfusion related lung injury (TRALI ) &
transfusion associated circulatory overload (TACO)

A

TACO presents with HYPERtension often without F and leukopenia,

127
Q

What causes
recurrent bacterial infections (e.g. Chest)
eczema
thrombocytopaenia
low IgM levels

A

Wiskott-Aldrich syndrome
X-linked recessive

127
Q

What are Irradiated blood products and what are they used for

A

depleted of T-lymphocytes and used to avoid transfusion-associated graft versus host disease (TA-GVHD)

✓ Bone marrow / stem cell transplants

✓ Immunocompromised (chemo/congenital)

✓Pts with/previous Hodgkin lymphoma

✓ Granulocyte transfusions

✓ Intra-uterine transfusions

✓ Neonates

128
Q

Polycythaemia rubra vera can progress to

A

myelofibrosis or AML

129
Q

Rx vitamin B12 deficiency no neuro sx and no folate deficiency

A

1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3 months

if a pt is also deficient in folic acid then it is important to treat the B12 deficiency first to avoid precipitating subacute combined degeneration of the cord

130
Q

most common cause of neutropenic sepsis

A

Coagulase-negative, Gram-positive bacteria such as Staphylococcus epidermidis

131
Q

low neutrophils, splenomegaly and rheumatoid arthritis

A

Felty’s syndrome

131
Q

rx smoldering multiple myeloma

A

watch and wait

132
Q

What is the underlying problem in methaemoglobinaemia

A

oxidation of Fe2+ in haemoglobin to Fe3+
normally regulated by NADH methaemoglobin reductase

Rx NADH methaemoglobinaemia reductase deficiency: ascorbic acid
IV methylthioninium chloride (methylene blue) if acquired

133
Q

most common inherited thrombophilia

A

Activated protein C resistance (Factor V Leiden) i

134
Q

Organomegaly with no bone lesions

A

Waldenstrom’s macroglobulinaemia

135
Q

Irinotecan MAO

A

inhibits topoisomerase I which prevents relaxation of supercoiled DNA

Doesn’t iron it out

136
Q

Hodgkin’s lymphoma - best prognosis =

A

lymphocyte predominant

137
Q

CLL Indications for Rx

A

BM failure:- worsening of anaemia and/or thrombocytopenia

lymphadenopathy massive (>10 cm)/ progressive

splenomegaly massive (>6 cm) or progressive

progressive lymphocytosis: > 50% increase over 2 months or lymphocyte doubling time < 6 months

systemic symptoms:
- weight loss > 10% Over 6 mo,
-F >38ºC for > 2 weeks,

extreme fatigue, night sweats
autoimmune cytopaenias e.g. ITP

138
Q

RX CLL

A

fludarabine, cyclophosphamide and rituximab (FCR)

139
Q

best diagnostic test for paroxysmal nocturnal

A

Flow cytometry for CD59 and CD55 is the gold standard test for paroxysmal nocturnal haemoglobinuria

140
Q

What is Rasburicase

A

recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin

MRCP Master (47 decks)

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