Haematology Flashcards
Hodgkin lymphoid lineage
Crippled B cell -> Reed Sternberg within inflammatory picture
Myeloma cells
Malignancy of plasma cells. Natural home is bone marrow not the lymph node
Making and numbers of RBCs
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
Lab clue that anaemia due to haemolysis or haemorrhage
Increased reticulocyte count (marrow response), poss consequently causing slight macrocytosis
Iron deficiency anaemia causes
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
Characteristic haematinics in iron deficiency anaemia
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)
B12 deficiency cuases
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)
Findings in B12 deficiency anaemia
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
findings in folate deficiency
Anaemia
High MCV
White count and platelet may be low
Hypersegmented neutrophils
Confirm w serum folate assay
Features of anaemia of chronic disease
Often a mild anaemia
typically normal MCV
Often low serum iron, high/normal ferritin and low transferrin
Clinical features of haemolysis
Pallor, icteric sclerae, jaundiced skin, splenomegaly
Lab results with intravascular haemolysis
Red cell fragmentation on film
LDH v high
Free haemoglobin in circulation
Low serum haptoglonin
Haemoglobinuria
Haemosiderinuria
Lab features extravascular haemolysis
Spherocytes on film
LDH less high
No haemoglobinuria, no haemosiderinuria
S&S of acute transfusion reaction
Fever, flushing, chillls
Urticaria
Rigors
Tachycardia
Hypotension
Collapse
Respiratory distress
What is acute haemolytic transufsion reaction
life threatening
Acute intravascular haemolysis often with renal failure and DIC
Urgently need help
Due to ABO incompatabiltiy
Transfusion anaphylaxis
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
Febrile non-haemolytic transfusion reactions
Relatively common and not serious
Due to cytokines in transfused blood
temp rarely rises >2 degrees aboce baseline
continue transfusion but monitor carefully
TRALI
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
TACO
Transfusion associated circulatory overload
Cardiogenic pulmonary oedema
JVP raised
treat w diuretics
Prevent by cautious transfusion practiceH
Haemolytic disease of the newborn
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