Haematology Flashcards

1
Q

Hodgkin lymphoid lineage

A

Crippled B cell -> Reed Sternberg within inflammatory picture

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2
Q

Myeloma cells

A

Malignancy of plasma cells. Natural home is bone marrow not the lymph node

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3
Q

Making and numbers of RBCs

A

In adult made in bone marrow - restricted to pelvis, sternum, vertebrae and ends of long bones
Adults ave approx 4x10^12 red cells/L of blood
Cell lifespan approx 120 days
Control of RBC production controlled by hypoxaemia detection in corticomedullary interstitium (in renal cortex, via HIF pathway), then stimulating Epo synthesis -> incr RBC synthesis in the marrow

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4
Q

Lab clue that anaemia due to haemolysis or haemorrhage

A

Increased reticulocyte count (marrow response), poss consequently causing slight macrocytosis

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5
Q

Iron deficiency anaemia causes

A

Insufficient intake: tea and toast, vegans, pregnancy
Inadequate absorption (in duodenum): coeliac disease, gastrectomy (HCl needed to solubilise iron)
Incr loss: GI bleeding, gynae bleeding

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6
Q

Characteristic haematinics in iron deficiency anaemia

A

Low MCV
Low MCH
Variation in size and shape -> anisocytosis and poikilocytosis
Not v high retic count
low serum iron
incr serum rtansferrin
Low serum ferritin (but is acute phase protein so will rise in infection/inflammation)

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7
Q

B12 deficiency cuases

A

Insufficient diet: tea and toast, vegans, pregnancy
Insufficient absorption: pernicious anaemia (no intrinsic factor), fastrectomy or atrophic gastritis, pancreatic disease, pancreatectomy, Crohn’s, ileal resection
(requirees both intrinsic factor produced in stomach, and absorption of complex in terminal ileum)

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8
Q

Findings in B12 deficiency anaemia

A

High MCV anaemia
Neutrophil and platelet count also may be reduced
Not v high retics
Hypersegmented neutrophils
Glossitis
Peripheral neuropathy
Dorsal column degen
Anti-intrinsic factor Ab if pernicious anaemia

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9
Q

findings in folate deficiency

A

Anaemia
High MCV
White count and platelet may be low
Hypersegmented neutrophils
Confirm w serum folate assay

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10
Q

Features of anaemia of chronic disease

A

Often a mild anaemia
typically normal MCV
Often low serum iron, high/normal ferritin and low transferrin

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11
Q

Clinical features of haemolysis

A

Pallor, icteric sclerae, jaundiced skin, splenomegaly

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12
Q

Lab results with intravascular haemolysis

A

Red cell fragmentation on film
LDH v high
Free haemoglobin in circulation
Low serum haptoglonin
Haemoglobinuria
Haemosiderinuria

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13
Q

Lab features extravascular haemolysis

A

Spherocytes on film
LDH less high
No haemoglobinuria, no haemosiderinuria

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14
Q

S&S of acute transfusion reaction

A

Fever, flushing, chillls
Urticaria
Rigors
Tachycardia
Hypotension
Collapse
Respiratory distress

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15
Q

What is acute haemolytic transufsion reaction

A

life threatening
Acute intravascular haemolysis often with renal failure and DIC
Urgently need help
Due to ABO incompatabiltiy

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16
Q

Transfusion anaphylaxis

A

often rapid onset after starting
rash, swelling of face/lips progressing to airway compromise or hypotension
Need urgent help, ABC
Stop transfusion, resuscitate, IV chlorphenamine and hydrocortisone
May need IM adrenaline

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17
Q

Febrile non-haemolytic transfusion reactions

A

Relatively common and not serious
Due to cytokines in transfused blood
temp rarely rises >2 degrees aboce baseline
continue transfusion but monitor carefully

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18
Q

TRALI

A

Transfusion related acute lung injury
Usually from plasma products with abx against HLA
looks like ARDS with capillary leak and so pulomnary oedema
Supportve management
Ban the donor

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19
Q

TACO

A

Transfusion associated circulatory overload
Cardiogenic pulmonary oedema
JVP raised
treat w diuretics
Prevent by cautious transfusion practiceH

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20
Q

Haemolytic disease of the newborn

A

RhD negative mother and RhD+ve fetus in first pregnancy, when red cells enter maternal circ at delivery then mother immunised
In 2nd pregnancy, IgG agains RhD potentially cross placental and haemolyse fetal cells

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21
Q
A
22
Q

polycythaemia vera management

A

Aspirin (reduce risk of VTE)
Cenesection
Chemotherapy (2nd line): hydroxyurea, phosphorus 32 therapy
5-15% progress to myelofibrosis. 5-15% progress to acute leukaemia

23
Q

TUmour lysis syndrome biochemistry

A

High potassium, high phosphate, high uric acid, low calcium

24
Q

Prevention of tumour lysis syndrome

A

IV fluids
If at higher risk receive allopurinol or rasburicase (recominant urate oxidase). One of not both

25
Q

Richter transformation

A

CLL transformation into high grade fastr growing non-Hodgkin’s lymphoma. patients often become unwell very suddenly having been absolutely fine for years/
Sympt: lymph node swelling, fever without infection, weight loss, night sweats, nausea, abdo pain

26
Q

Management of sickle cell crises

A

analgesia eg opiates
rehydrate
oxygen
consider abx if evidence infection
blood transfusion if: severe/symptomatic anaemia, pregnancy, pre-op.
Exchange transfusion if: acute vaso-occlusive crisis (stroke, acute chest syndroem, multiorgan failure, splenic sequestration crisis) = actually rapidly reduces % of HbS containing cells

27
Q

VonWillebrand disease Ix results

A

Prolonged bleeding time
APTT may be prolonged
Factor VIII levels may be moderately reduced (Acts as carreir for)
Defective platelet aggregation with ristocetin

28
Q

management of vonwillebrand

A

TXA for milf bleeding
Desmopressin induces release of vWF from cells
Factor VIII concentrate

29
Q

Dabigatran

A

Direct thrombin inhibitor
Excretion majority renal
Reverse: idarucizumab

30
Q

Rivaroxaban

A

Direct factor Xa inhibitor
excretion majority liver
reversal: andexanet alfa

31
Q

Apixaban

A

Direct factor Xa inhibitor
Excreted majority faecal
Reverse w andexanet alfa

32
Q

Edoxaban

A

Mechanism: direct factor Xa inhibitor
Excretion majority faecal
No reversal agent

33
Q

Symptoms of chronic lymphocytic leukaemia

A

Often none, may be picked up from incidetal lymphocytosis
Constitutional: anorexia, weight loss
Bleeding, infections
Lymphadenompathy more marked than CML

34
Q

Causes of massive splenomegaly

A

Myelofibrosis
CML
Visceral leishmaniasis
Malaria
Gaucher’s syndrome

35
Q

Chronic myeloid leukaemia genetics

A

Philadelphia chromosome
translocation between chromosome 9 and 22 generating the BCR-ABL fusion protein with a lot of tyrosine kinase actiity

36
Q

Presentation of CML

A

60-70 year olds
Anaemia: lethargy
weight loss
sweating
marked splenomegaly causing abdo discomfort
increase in granulocytes at different stages of maturation
decr leukocyte alkaline phosphatase
may undergo blast transformation, mostly to AML

37
Q

Management of CML

A

Imatinib= tyrosine kinase inhibitor and is first line

38
Q

Features of G6PD deficiency

A

Neonatal jaundice often
Intravascular haemolysis
Gallstones common
Splenomegaly maybe
Heinz bodies on film, bite and blister cells also possible

39
Q

Drugs causing haemolysis in G6PD

A

Anti malarials eg primaquine
Ciprofloxaacin
Sulph group drugs: sulphonamides, sulphasalazine, sulfonylureas
Infection may precipitate haemolysis
Also broad beans

40
Q

Risk factors for non-Hodgkin’s lymphoma

A

Elderly
Caucasians
History of viral infection, partic EBV
Family history
Cerain chemicals eg pesticides/solvents
history of chemo/radiotherapy
Immunodeficiency (transplant, HIV, DM)
Autoimmune disease (SLE, Sjogren’s. coeliac)

41
Q

Symptoms of non-hodgkins lymphoma

A

Painless lymphadenopathy (non-tender, rubbery, asymnetrical)
Constitutional B symptms (fever, weight loss, night sweats, lethargy)
extra nodal disease (gastric, bone marrow, lungs, skin CNS) (much more common than in Hodgkin’s)

42
Q

Signs of non-hodgkin’s lymphoma

A

Weight loss
lymphadenopathy (typically cervical, axillary or inguinal)
palpable hepatomegaly, splenomegaly or lymph nodes
testicular mass
feverI

43
Q

investigations for non-hodgkins lymphoma

A

Excision biopsy
CT -CAP
HIV test
FBC and film (normocytic anaemia)
ESR (prognostic indicator)
LDH (ditto)

44
Q

Management for non hodgkins lympoma

A

Dependent on subtype and asometimes watchful waiting
Or chemotherapy eg R-CHOP
Radiotherapy
Flu/pneumococcal vaccines

45
Q

Features of lead poisoning

A

ABdominal pain
Peripheral neuropathy
neuropsychiatric features
fatigue
constipation
blue lines on gum margin (fairly rare)

46
Q

Management of lead poisoning

A

Various chelating agents eg dimercaptosuccinic acid
D-penicillamine
EDTA
dimercaprol

47
Q

what roughly is myelofibrosis

A

Myeloproliferative disorder
from hyperplasia of abnormal megakaryovytes
release of platelet derived growth factor thought to stimulate fibroblasts in bone marrow
Haaematopoiesis happens in liver and spleen

48
Q

presentation of myelofibrosis

A

Elderly person presenting with symptoms of anaemia eg fatigue
Massive splenomegaly
Hypermetabolic symptoms: weight loss, night sweats etc

49
Q

Lab findings of myelofibrosis

A

Anaemia
High WBC and platelets early on in disease
Tear drop poikilocytes on blood film
Dry tap bone marrow biopsy
high urate and LDH (incr cell turnover)

50
Q
A