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Year 5 😊✌🏼 > Path: Haem > Flashcards

Path: Haem Flashcards

1
Q

Differences betwen CLL and SLL?

A

CLL is primarily seen in the BM

SLL (small lymphocytic lymphoma) seen in the LNs

otherwise they are essentially the same disease process

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2
Q

Complications of CLL

A

anaemia
hypogammagobulinaemia leading to recurrent infections
splenomegaly
warm AIHA
transformation to high grade lymphoma (Richter’s transformation)

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3
Q

What is Richter’s transformation?

A

occurs when leukemia cells enter the LN and change into a high-grade, fast-growing non-Hodgkin’s lymphoma.

Patients become unwell very suddenly.

can happen CLL -> DLBC lymphoma

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4
Q

What do smear cells indicate?

A

CLL

remember: SMEAR C(e)LL(s)

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5
Q

Features of CLL on blood Ix

A

persistently mildly raised lymphocyte count
smear cells and small/medium size lymphocytes on blood film

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6
Q

epidemiology of CLL

A

commonest leukemia in adults
>65 yo

(median 65-70)

M>F

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7
Q

Clinical features of CLL

A

can be asymptomatic (in 80% diagnosed in routine bloods)

  • symmetrical painless lymphadenopathy
  • BM failure (anaemia, thrombocytopaenia, RECURRENT INFECTIONS (50% deaths))
  • B sx (weight loss, low grade fever, night sweats)
  • splenomegaly +/- hepatomegaly
  • associated with autoimmunity (Evan’s syndrome) - AIHA (w>c), ITP -> it is a disease of immune cells so you also get AID
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8
Q

Which clincial finding helps differentiate CLL and CML?

A

lymphadenopathy more in CLL

(generally helps differentiate lymphoid from myeloid malignancy)

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9
Q

How commonly is CLL an incidental finding?

A

80% diagnosed in routine bloods

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10
Q

buzzword for DLBC lymphoma

A

sheets of large lymphoid cells

can be as a result of Richters transformation CLL -> DLBC

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11
Q

DLBC

A

diffuse large B cell (lymphoma)

-> aggressive

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12
Q

Mx of DLBC lymphoma

A

Rituximab - CHOP

auto-SCT or CAR-T for relapse

R-CHOP = rituximab + cyclophosphamide + doxorubicin + vincristine + prednisolone

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13
Q

who is affected by DLBC lymphoma?

A

middle aged and elderly

can be transformed from CLL (Richter’s transformation) or from low grade lymphoma

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14
Q

Ix findings for CLL

A
  • high WCC with lymphocytosis >5 (high % of WBC composed of lymphocytes, small, mature)
  • low serum Ig
    flow cytometry: confirms monoclonal population (normally CD5+ CD23+)
  • SMEAR CELLS on blood film
  • abnormal BM - lymphocytic replacement
  • mutation status: TP53 mutation - worse; IGHV rearrangement: better
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15
Q

Flow cytometry in CLL

A

confirms monoclonal population

usually CD5+ and CD23+

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16
Q

What mutation status is associated with a better and worse prognosis in CLL?

A

TP53 mutation - worse

IGHV rearrangement: better

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17
Q

Prognostic fx for CLL

A

good:
- hypermutated Ig gene
- low ZAP-70 expression
- 13q14 deletion

bad:
- LDH raised
- CD38+ve
- 11q23 deletion
- beta 2 microglobulin level elevated
- older age

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18
Q

Staging for CLL

A

Binet (A-C) or Rai (0-IV)

Binet
Stage A:
- high WCC
- <3 groups of enlarged LNs
- usually no treatment required

Stage B:
- >3 groups of enlarged LNs

Stage C:
- anaemia or thrombocytopaenia

RAI
0 - isolated lymphocytosis - low risk

I - lymphocytosis plus lymphadenopathy - intermediate risk
II - plus H/S-megaly - intermediate risk
III - plus anaemia (<11g/dL) - high risk
IV - plus thrombocytopaenia (<100 000 / mL) - high risk

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19
Q

Mx of CLL

A
  • watchful waiting if asymptomatic with slowly progressing disease (1/3 pts never need treatment)
  • supportive treatment with transfusions, infection prophylaxis (early abx, vaccines, IVIG if recurrent inf`)
  • anti-CD20 (rituximab or obinutzumab) with chemotherapy
  • oral BTK inhibitors (ibrutinib)
  • BCL2 inhibtor (venetoclax)

allogenic HSCT is currently the only curative treatment option and is not routinely performed

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20
Q

What type of AIHA is CLL associated with?

A

warm AIHA

(remember: CLL is not cool - therefore warm AIHA)

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21
Q

What antibody type causes warm AIHA and cold AIHA?

A

warm: IgG

cold: IgM

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22
Q

causes of warm AIHA

A

mainly primary idiopathic
lymphoma
CLL
SLE
methyldopa

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23
Q

Mx of warm AIHA

A

steroids
splenectomy
immunosuppression

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24
Q

What does blood film in warm AIHA show?

A

spherocytes

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25
Q

what temp is associated with warm and cold AIHA?

A

WAIHA 37

CAIHA <37

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26
Q

Mx of cold AIHA

A

treat underlying condition
avoid the cold
chemotherapy if lymphoma

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27
Q

What causes CAIHA?

A

primary idiopathic
lymphoma
infections
EBV
mycoplasma

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28
Q

What feature is often also seen with cold AIHA/cold agglutinin disease?

A

Raynaud’s

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29
Q

What is aplastic anaemia and what can be seen on Ix? How do patients present?

A

inability of BM to produce adequate blood cells

HSC numbers are reduces in BM trephines (hypocellular BM)

AA typically refers to anaemia but these patients can have a pancytopaenia as well.

Signs and symptoms relate to each cytopaenia, typically present with bleeding problem.

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30
Q

At what age are patients affected by aplastic anaemia?

A

at any age

peak at
i. 15-24
ii. >60

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31
Q

What conditions is aplastic anaemia linked to?

A

leukemia, paroxysmal nocturnal hemoglobinuria(PNH)

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32
Q

Classification of aplastic anaemia

A

Primary:
- 70% idiopahtic (vast majority unexplained pathology, increasingly seeing mutations with NGS)
- 10 % inherited (Fanconi anaemia, deskeratosis congenita, Schwachmann-Diamond Syndrome, Diamond Blackfan syndrome

Secondary (10-15%)
- malignant infiltration of BM
- radiation
- drugs (incl. chemotherapy)
- viruses (e.g. parvovirus B19)
- autoimmune (e.g. SLE)

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33
Q

Management of aplastic anaemia

A

supportive: transfusions, abx, iron chelation

cessation of causative agent if applicable

drugs: to promote marrow recovery (e.g. growth factors and oxymethalone (androgen)).

immunosuppressants in idiopathic AA

SCT (esp. in young patients)

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34
Q

Inherited causes of aplastic anaemia / BM failure syndrome

A

Fanconi anaemia
Dyskeratosis Congenita
Schwachmann-Diamond syndrome
Diamond-Blackfan Syndrome

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35
Q

Fanconi anaemia - inheritance pattern

A

AR

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36
Q

What does Fanconi anaemia cause?

A

pancytopaenia

also:
skeletal abnormalities (radii (forearm), thumbs, renal malformations, microopthalmia, short stature, skin pigmentation (cafe au lait spots))

No abnormalities in 30%

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37
Q

Complications of fanconi anaemia

A

MDS (30%)
AML risk (10% progress)

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38
Q

At what age does Fanconi anaemia present

A

5-10y

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39
Q

incidence of aplastic anaemia cases

A

2-5 / million / year (globally)

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40
Q

criteria to assess severity of AA

A

Camitta criteria

  1. reticulocytes < 1% or <20 x 10^9/L
  2. neutrophils <0.5 x 10^9/L
  3. Platelets < 20 x 10^9/L

Bone Marrow <25% cellularity

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41
Q

Commonest form of inherited aplastic anaemia?

A

Fanconi anaemia

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42
Q

Features of dyskeratosis congenita

A

Triad:
- skin pigmentation
- nail dystrophy
- leukoplakia

+ BM failure

(have marrow failure, cancer predisposition, somatic abnormalities)

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43
Q

Inheritance pattern of dyskeratosis congenita

A

X-linked recessive trait (most common - mutated DKC1 gene - defective telomerase)

AD trait (mutate TERC gene)

AR trait (gene not found yet)

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44
Q

Is one gene responsible for Fanconi anaemia?

A

no

multiple genes appear to be responsible for this illness

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45
Q

What is Kostmann syndrome?

A

AR disorder

causes severe neutropenia

classical form of mutation in HCLS-1 assocaited protein X-1 (HAX-1)

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46
Q

Schwachmann-Diamond Syndrome - inheritance pattern

A

AR

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47
Q

Schwachmann-Diamond Syndrome - what does it cause?

A

Primarily neutropenia +/- others

skeletal abnormalities + SHORT STATURE
endocrine and pancreatic dysfunction (2nd commonest cause of pancreatic insufficiency following CF)
hepatic impairment

AML risk

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48
Q

Which of the inherited causes of BM faliure causes mainly a neutropenia?

A

Schwachmann-Diamond Syndrome

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49
Q

What malignancy are children/patients with Schwachmann-Diamond syndrome

A

AML

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50
Q

What is Diamond Blackfan syndrome

A

pure red cell aplasia
(red progentor cells are affected)

normal WCC and platelets

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51
Q

Which inherited BM failure disorder affects red cells?

A

Diamond-Blackfan syndrome

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52
Q

At what age do patients with Diamond Blackfan syndrome usually present?

A

in the 1st year of life

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53
Q

Inheritance pattern of diamond blackfan syndrome

A

AD

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54
Q

Which drugs can cause aplastic anaemia? (5 categories)

A
  1. Predictable (dose-dependent, common)
    -> cytotoxic drugs
  2. idiosyncratic (NOT dose dependent, rare)
    -> Phenylbutazone (NSAID), gold salts
  3. Abx
    -> chloramphenicol
    -> sulphonamide
  4. diuretics
    -> thiazides
  5. antithyroid drugs
    -> carbimazole
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55
Q

What is more common, HL or NHL?

A

NHL (80%)

HL is 20%

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56
Q

young person with bilateral lymphadenopathy, B sx and pain in LNs when drinking alcohol - dx?

A

Hodgkin’s lymphoma

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57
Q

Name myeloproliferative disorders

A

(‘philadelphia chromosome +ve’)
CML

(‘philadelphia chromosome -ve’)
polycythaemia vera
(primary)myelofibrosis
essential thrombocythaemia

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58
Q

what are myeloproliferative disorders?

A

a group of disorders characterised by a proliferation of malignant haematopoetic stem cells of the myeloid lineage

clonal proliferation of one or more haemapoietic component (i.e. increased production of mature cells)

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59
Q

What mutation are philadelphia chromosome -ve myeloproliferative disorders associated with?

A

JAK2 mutations (esp. PV - >95%)

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60
Q

What age group is affected by CML?

A

middle aged typically (40-60yo)

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61
Q

How do patients with CML present?

A

often diagnosed on routine bloods (large number of differentiated neutrophils)

or present with generally feeling unwell, weight loss, infections, bruising, fevers, fatigue, night sweats

o/e splenomegaly (often massive)

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62
Q

What is the remission rate in CML treated with imatinib?

A

95%

63
Q

Mx of CML

A

1st line: imatinib -> 95% remission

64
Q

what kind of medication is imatinib?

A

tyrosine kinase inhibitor

(first generation)

65
Q

What are the different types of tyrosine kinase inhibitors used in CML?

A

1st generation: imatinib (indicated in low-risk CP-CML patients)

2nd generation: dasatinib, nilotinib: usually indicated in AP-CML

3rd generation: ponatinib: especially effective in patients with additional mutations

66
Q

What is known as the philadelphia chromosome?

A

translocation (9;22)

67
Q

in what % CML is (9;22) seen?

A

philadelphia chromosome is seen in 80% CML

68
Q

How do you detect the philadelphia chromosome and how was this done in the past?

A

Now: FISH (fluorescence in situ hybridization)

in the past via karyotyping

69
Q

what does FISH stand for?

A

fluorescence in situ hybridization

70
Q

What are the different phases of CML?

A
  1. Chronic phase
  2. Accelerated phase
  3. Blast phase / Blast crisis
71
Q

Summarise the chronic phase in CML

A

<5% blasts in BM/blood
WBC increases over years

  • often subclinical
  • can persist for up to 10y
72
Q

How do you manage CML in the chronic phase?

A

Imatinib (1st generation tyrosine kinase inhibitor)

OR

dasatinib/nilotinib for resistance

EXTREMELY effective and well tolerated

treatment started immediately after dx confirmation regardless of symptoms

73
Q

molecular remission in CML

A

in some patients CML treatment with imatinib is considered to be in molecular remission when the BCR-ABL gene transcripts are no longer seen on PCR.

74
Q

What happens with t(9;22)?

A

Fusion gene formation

in t(9;22) the BCR-ABL gene is formed and encodes a BCR-ABL non-receptor tyrosine kinase with increased enzyme activity

-> inhibits physiologic apoptosis and increases mitotic rate -> uncontrolled proliferation of functional granulocytes

75
Q

When can you see spherocytes?

How do they look?

A

hereditary spherocytosis
AIHA
haemolytic transfusion reaction

sphere shaped RBCs; often a little smaller.

76
Q

Summarise the accelerated phase of CML

A

> 10% blasts seen in BM/Blood
increasing manifestations such as splenomegaly, lasting up to a year
less responsive to therapy*

*AMBOSS: second generation TKIs such as dasatinib or nilotinib can be used.
Consider systemic chemotherapy or HSCT if pt is eligible.

77
Q

How do you manage AP-CML?

A

imatinib can be used at any stage?

second generation TKIs such as dasatinib or nilotinib can be used.
Consider systemic chemotherapy or HSCT if pt is eligible.

less responsive to treatment compared to CP-CML

78
Q

Summarise the blast phase in CML?

A

> 20% blasts seen in BM/blood

resembles acute leukemia
sx: +/- weight loss, night sweats, lethargy

timeframe = months

treatment: similar to AML (aggressive systemic chemotherapy in combination with a TKI), possibly with allogenic SCT for young patients

79
Q

What cytokine therapy can be used in CML?

A

IFN-alpha

can be used to reduce leukocyte count

80
Q

Haematological causes of acquired antibody deficiency

A

malignancy: CLL, MM
post BM transplant

-> cause secondary (acquired) Ab deficiency

81
Q

What diseases is chronic ITP associated with?

A

associated with AI disease
CLL
HIV
hepatitis

82
Q

who is affected by acute and chronic ITP?

A

acute: children

chronic: adults

83
Q

Causes of CML

A

idiopathic (most commonly)

ionising radiation
aromatic hydrocarbons (esp. benzene)

84
Q

What is the commonest leukemia in the western world

A

CLL

85
Q

When is CD5 normally expressed?

A

transiently expressed in early stage of B-cell maturation before release into the blood

86
Q

Outcomes of CLL

A

1/3 never progress
1/3 treated effectively, die of other cause
1/3 die of CLL (require multiple lines of CLL rx, refractory disease)

87
Q

Should you avoid any vaccines in CLL?

A

yes, avoid live vaccines

88
Q

What is the commonest cause of lymphocytosis in the elderly?

A

CLL

89
Q

Is there a genetic component in CLL?

A

relatives are 7x more likely to develop it

90
Q

what ethnicity is at higher risk of CLL?

A

caucasian

91
Q

How high is the risk of Richters transformation in CLL?

A

1% risk / year

92
Q

What type of supportive care in CLL?

A

early abx

if low IgG can give IVIG for recurrent infections

vaccinations (e.g covid, flu, pneumococcal - avoid live)

93
Q

Meds to treat CLL

A

combination immuno-chemotherapy: being suspended by targeted tx

targeted therapy:
BTK inhibitors (ibrutinib)
BCL2 inhibitors (venetoclax)

cellular therapy only for relapsed high risk cases:
allogenic SCT
CAR-T

94
Q

What is the risk of starting venetoclax in CLL management?

A

tumour lysis syndrome when initiating therapy -> can be fatal

95
Q

Indications to treat CLL

A

progressive lymphocytosis
- >50% increase in 2/12
- lymphocyte doubling time <6/12

progressive BM failure
- Hb <100
- platelets < 100
- neutrophils <1

massive/progressive H/Smegaly

systemic sx (B sx)

AI cytopenias (mx with immunosuppresion, not chemo)

96
Q

Normal B-cell markers

A

CD20+
CD19+
CD5- (it is transiently expressed before released into the blood)

97
Q

CML - detecting disaese approaches

A

molecular - most sensitive (%BCR-ABL transcripts)

cytogenetic analysis - follows (on 20 metaphases, partial 1-35% Ph +ve, complete 0% Ph +ve)

haematological response (WCC)

-> you can imagine, it is more senistive to measure the BCR-ABL transcripts by PCR than looking at 20 metaphases and seeing what % has Ph Chr

98
Q

What is the reversal agent for dagibatran?

A

idarucizumab

99
Q

What type of medication is dagibatran?

A

direct thrombin inhibitor

100
Q

What is the commonest NHL in the UK?

A

diffuse large B cell lymphoma (40% of total lymphoma cases)

101
Q

Red cell abnormalities that may be seen in coealiac disease

A

Target cells
Howell-Jolly bodies

(hyposplenism)

102
Q

Why is Factor VIII reduced in von Willebrand disease?

A

vWF prevents the degradation of F8

103
Q

What is von Willebrand disesaasae?

A

most common inherited b leading disorder

caused by qualitative or quantitative deficiency in vWF.

104
Q

Types of von Willebrand disease

A

Inherited
- type 1 (AD) - low levels of vWF
- type 2 (AD) - poorly functioning vWF
- type 3 (AR) - absent vWF

Acquired
- myelo-/lymphoproliferative d/o
- AID e.g. SLE
- drug SE (e.g. valproate)
- hypothyroidism
- cardiovascular defects (VSD, AS)

105
Q

How does von Willebrand disease present?

A

Varying phenotype, from complete deficiency to asymptomatic mild deficiency

bleeding indicative of platelets d/o e.g. mucocutaneous bleeding but can also present with bleeding indicative of coagulation disorders.

106
Q

What is the commonest inherited bleeding disorder?

A

von Willebrand disease

107
Q

What proportion of people is affected by von Willebrand disease?

A

1 in 10 000

108
Q

Lab findings in vWD

A

(mildly) high APTT (may also be normal)
normal PT/INR
low FVIII
low vWF Ag (or normal Ag level with reduced function in type 2)
normal platelet count

-> can be difficult to diagnose and necessitate haem input

109
Q

Mx of vWD

A

prophylaxis indicated in some patients

treatment of bleeds (TXA(antifibrinolytic), desmopressin, combined vWF and F8 concentrates

cOCP can be used in menorrhagia

110
Q

How does desmopressin work in von Willebrand disease? Which types of the disease does it work in?

A

stimulates the release of vWF from endothelial cells.

works in type 1&2 but not in type 3.

111
Q

When is treatment needed in vWD?

A

if symptomatic

prophylactic e.g. before surgery

112
Q

What medications are contraindicated in vWD?

A

Platelet aggregation inhibitors (e.g., aspirin, NSAIDs, clopidogrel) and intramuscular injections are contraindicated in von Willebrand disease because they further increase the risk of bleeding!

113
Q

What chromosomal translocation is seen in mantle cell lymphoma?

A

t(11;14) involving Cyclin D1

Cyclin D1 deregulation (chr 11)

114
Q

What group is affected by mantle cell lymphoma?

A

middle aged men

M>F
middle age

115
Q

Is mantle cell lymphoma an indolent or aggressive lymphoma?

A

aggressive

116
Q

median survival with mantle cell lymphoma

A

3-5 years

117
Q

Histological finding: angular/clefted nuclei - dx?

A

mantle cell lymphoma

118
Q

Mx of mantle cell lymphoma

A

rituximab-CHOP and high dose cytarabine

Auto SCT for relapse

oral options for less fit

119
Q

Mx of mantle cell lymphoma relapse

A

auto SCT

120
Q

Level of disease at presentation in mantle cell lymphoma

A

disseminated

121
Q

Eselsbrücke for Mantle cell lymphooma

A

an aggressive and dysregulated middle-aged man in cycling (cyclin D1) in a ‘Mantel’.

He is not cycling far, 3-5km (mean years life expectancy)

He has two children, aged 11 and 14 (t(11;14)).

He is cycling to R-CHOP some wood.

He has citrus fruit on a karabiner (cytarabine).

The buttons of his mantel are clefted and angular.

if he becomes less fit he will have to eat something (oral therapy for less fit) and if he loses himself again (relapse) he will need to auto-SCT to change.

122
Q

What translocation is seen in Burkitt’s lymphoma and what gene is affected?

A

t(8;14)

c-myc (oncogene overexpression)

123
Q

Histology of Burkitt lymphoma

A

starry sky appearance

Significant infiltrates of homogenous lymphocytes. Macrophages are interspersed between sheets of lymphocytes and clearly contain apoptotic lymphocytes

124
Q

What different types of Burkitt’s lymphoma are there?

A

endemic

sporadic

immunodeficiency

125
Q

Is burkitt’s lymphoma aggressive or indolent?

A

(very) aggressive + fast growing

126
Q

Does Burkitt’s lymphoma respond well to meds?

A

rapidly responsive to rx

127
Q

Mx of Burkitt’s lymphoma

A

Rituximab

& secondary CNS prophylaxis

128
Q

Endemic Burkitt’s lymphoma

A

most common malignancy in equatorial Africa (and South America)
EBV-associated
characteristic JAW INVOVLEMENT
abdominal masses

129
Q

Immunodeficiency Burkitt’s lymphoma

A

In HIV/post-traansplant patients

Non-EBV associated

130
Q

Sporadic Burkitt’s lymphoma

A

EBV assocaited

found outside of Africa
jaw less commonly involved

131
Q

Which lymphomas are low grade and high grade>

A

High grade:
- Burkitt’s (very aggressive)
- Diffuse large B cell (aggressive)
- mantle cell (aggressive)

Low grade:
- Follicular (indolent)
- Marginal Zone (indolent)
- small lymphocytic (indolent)

132
Q

Which lymphoma is associated with pain in the affected LNs following alcohol?

A

Hodgkin’s lymphoma

133
Q

What proportion of lymphoma is HL and NHL ?

A

20% HL

80% NHL

134
Q

Which types of Burkitt’s lymphoma are and are not associated with EBV

A

EBV associated: endemic + sporadic

Not EBV associated -> immunodeficiency BL

135
Q

What is the inheritance pattern of hereditary elliptocytosis?

A

AD

136
Q

What are sources of Vitamin B12?

A

meat and dairy products

137
Q

Causes of vitamin B12 deficiency

A

dietary (e.g. vegans)

malabsorption
- stomach: lack of intrinsic factor which is produced by gastric parietal cells -> pernicious anaemia, post gastrectomy
(can have anti-IF antibodies or anti-parietal cell antibodies)

  • terminal ileum: absorption due to ilial resection, Crohn’s disease, bacterial overgrowth, tropical sprue and tapeworms
138
Q

Where is intrinsic factor produced?

A

in the parietal cells in the stomach

139
Q

what are clinical features of B12 deficiency?

A

Mouth: glossitis, angular cheilosis

Neuropsychiatric: irritability, depression, psychosis, dementia

neurological: paraesthesiae, peripheral neuropathy, (loss of vibration and proprioception first, absent ankle reflex, spastic paraparesis, subacute combined degeneration of the spinal cord)

140
Q

What is pernicious anaemia?

A

autoimmune atrophic gastritis -> achlorhydria and loss of gastric intrinsic factor

141
Q

What is the most common cause of macrocytic anaemia in the western world?

A

pernicious anaemia

142
Q

What age group is affected by pernicious anaemia?

A

usually >40 yo

143
Q

Specific test for pernicious anaemia

A

parietal cell antibodies (90%)
intrinsic factor antibodies (55%)

Schilling test (outdated) - pt swallows radiolabelled B12 and an injection of normal B12(to make sure the radiolabelled vitamin does not bind to sites of depletion).
Levels of radiolabelled vitamin B12 excretion are measured in the urine.

144
Q

management of B12 deficiency

A
  • replenish stores with IM hydroxocobalamin (B12) with 6 injections over 2 weeks

Nice recommends testing for anti-parietal cell / anti-IF antibodies to check for autoimmune rather than dietary causes; here patients would need 3-monthly IM injections.

145
Q

What are the commoner autoantibodies found in pernicious anaemia?

A

anti-parietal cell antibodies (90%)

50% have anti-IF antibodies

146
Q

Sources of folate

A

Diet:
green vegetables
nuts
yeast
liver

synthesised by gut bacteria (low body stores, cannot produce de novo)

147
Q

What are causes of folate deficiency?

A
  • poor diet
  • increased demand: pregnancy or increased cell turnover (e.g. haemolysis, malignancy, inflammatory disease and renal dialysis)
  • malabsorption: coeliac disease, tropical sprue
  • drugs: alcohol, anti-epileptics (phenytoin), methotrexate, trimethoprim
148
Q

Mx of folate deficiency

A

oral folic acid

ensure B12 is checked and replaced prior to folic acid as folic acid may exacerbate neuropathy of B12 deficiency

149
Q

Why should you check B12 levels before starting folic acid replacement?

A

folic acid may exacerbate neuropathy of B12 deficiency

150
Q

What is a megaloblastic blood film?

A

Hypersegmented polymorphs, leucopenia, macrocytosis, aneamia, thrombocytopenia with megaloblasts.

Megaloblasts are red cell precursors with an immature nucleus and mature cytoplasm

b12 and folate are required for nucleus maturation

151
Q

Macrocytosis with megaloblastic blood film ddx

A

b12 def
folate def
cytotoxic drugs

152
Q

macrocytosis with non-megaloblastic blood film ddx

A

alcohol (most common cause of macrocytosis without anaemia)
reticulocytosis (e.g. in haemolysis)
liver disease
hypothyroidism
pregnancy

153
Q

What is the commonest cause of macrocytosis without anaemia?

A

alcohol

154
Q

What haematological diseases can cause macrocytosis?

A

myelodysplasia
myeloma
myeloproliferative disorders
aplastic anaemia

Year 5 😊✌🏼 (53 decks)

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