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Haematology Flashcards

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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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22
Q

polycythaemia vera management

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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

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A

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

24
Q

Prevention of tumour lysis syndrome

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A

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

25
Richter transformation
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
Management of sickle cell crises
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
VonWillebrand disease Ix results
Prolonged bleeding time APTT may be prolonged Factor VIII levels may be moderately reduced (Acts as carreir for) Defective platelet aggregation with ristocetin
28
management of vonwillebrand
TXA for milf bleeding Desmopressin induces release of vWF from cells Factor VIII concentrate
29
Dabigatran
Direct thrombin inhibitor Excretion majority renal Reverse: idarucizumab
30
Rivaroxaban
Direct factor Xa inhibitor excretion majority liver reversal: andexanet alfa
31
Apixaban
Direct factor Xa inhibitor Excreted majority faecal Reverse w andexanet alfa
32
Edoxaban
Mechanism: direct factor Xa inhibitor Excretion majority faecal No reversal agent
33
Symptoms of chronic lymphocytic leukaemia
Often none, may be picked up from incidetal lymphocytosis Constitutional: anorexia, weight loss Bleeding, infections Lymphadenompathy more marked than CML
34
Causes of massive splenomegaly
Myelofibrosis CML Visceral leishmaniasis Malaria Gaucher's syndrome
35
Chronic myeloid leukaemia genetics
Philadelphia chromosome translocation between chromosome 9 and 22 generating the BCR-ABL fusion protein with a lot of tyrosine kinase actiity
36
Presentation of CML
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
Management of CML
Imatinib= tyrosine kinase inhibitor and is first line
38
Features of G6PD deficiency
Neonatal jaundice often Intravascular haemolysis Gallstones common Splenomegaly maybe Heinz bodies on film, bite and blister cells also possible
39
Drugs causing haemolysis in G6PD
Anti malarials eg primaquine Ciprofloxaacin Sulph group drugs: sulphonamides, sulphasalazine, sulfonylureas Infection may precipitate haemolysis Also broad beans
40
Risk factors for non-Hodgkin's lymphoma
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
Symptoms of non-hodgkins lymphoma
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
Signs of non-hodgkin's lymphoma
Weight loss lymphadenopathy (typically cervical, axillary or inguinal) palpable hepatomegaly, splenomegaly or lymph nodes testicular mass feverI
43
investigations for non-hodgkins lymphoma
Excision biopsy CT -CAP HIV test FBC and film (normocytic anaemia) ESR (prognostic indicator) LDH (ditto)
44
Management for non hodgkins lympoma
Dependent on subtype and asometimes watchful waiting Or chemotherapy eg R-CHOP Radiotherapy Flu/pneumococcal vaccines
45
Features of lead poisoning
ABdominal pain Peripheral neuropathy neuropsychiatric features fatigue constipation blue lines on gum margin (fairly rare)
46
Management of lead poisoning
Various chelating agents eg dimercaptosuccinic acid D-penicillamine EDTA dimercaprol
47
what roughly is myelofibrosis
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
presentation of myelofibrosis
Elderly person presenting with symptoms of anaemia eg fatigue Massive splenomegaly Hypermetabolic symptoms: weight loss, night sweats etc
49
Lab findings of myelofibrosis
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

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