Haematology Flashcards
Causes of microcytic anaemia
Inadequate intake, thalassaemia, anaemia of chronic disease
causes of normocytic anaemia
Anaemia of chronic disease, acute blood loss, bone marrow disorder, haemolysis, combined B12/Fe deficiency
Causes of macrocytic anaemia
B12/folate deficiency, myelodysplasia, alcohol excess, haemolysis, DNA synthesis defect (e.g. chemo), hypothyroidism
Haemolysis investigation
High LDH, low haptoglobin, high bilirubin.
Direct antigen test (DAT) may be positive
Iron absorption
In duodenum, promoted by gastric HCl.. Ferritin (soluble) storage, transferrin (insoluble) transports around body
Iron deficiency causes
Inadequate intake, increased requirement (pregnant), coeliac, gastrectomy, chronic haemorrhage (GI bleed/menorrhagia)
Iron deficiency investigations
Blood film (hypochromic, microcytic, pencil cells) Ferritin levels (but increases in inflammation and malignancy, so can be normal/raised) transferrin saturation (reduced in IDA)
Post menopausal women and men should get referral for endoscopy or coloscopy
Treating IDA
Oral preps if ferritin <25, or TF sat <20. Continue for 3 months.
Start on od, then titrate up due to ADEs (constipation)
If not absorbing then can use IV
B12 absorption
Pepsin releases B12 from protein in stomach, but needs parietal cell IF for absorption in terminal ileum. Stores for 2 years.
B12 deficiency causes
Inadequate intake, Pernicious anaemia (against IF and/or gastric parietal cells), gastrectomy, Malabsorption (Crohns/ileal resection)
Can also APPEAR low in COC use or HRT use
B12 diagnosis
Raised MCV
Blood film : hypersegmented (5+ segments) neutrophil, oval macrocyte, tear drop cell.
Low B12
IF antibodies
Gastric parietal cell antibodies (but can be FP in 10%)
B12 Management
Can use oral supplements, but if PA then IM hydoxocobalamin for life
Folate absorption
Absorbed in duodenum and jejunum. Body has 5-6 month stores
Folate deficiency causes
Inadequate intake, increased requirement (pregnancy, Haemolytic anaemia), malabsorption (coeliac disease, jejunal reabsorption)
Folate investigations
Raised MVC
Blood film : Macrocytes, hypersegmented neutrophils
Reduced folate (serum is more sensitive to short term imbalance, but red cell folate is more reliable assessment)
Management of folate deficiency
5mg daily for 3 months
ABO antibodies
Present against antigens the person doesn’t have. Uses IgM. Present from 3 months
ABO antigens
Present at 6 weeks gestation, so from birth too
Rhesus antibodies
IgG (small) antibodies. Only occur in Rhesus negative individuals if exposed to Rh+ blood/platelets by transfusion or from a D+ fetus
Group and Screen/Save
Test blood group
Screen with coombs reagenent (antiglobulin that binds to human immunoglobulins) for serum screen (look for agglutination)
Then final test against donor RBCs with recipient serum
Electronic cross match
Uses previous ABO and RhD testing as well as negative antibody screen for electronic match against blood bank
Transfusion reactions
Almost always patient ID failure
Reaction activates complement pathway, causes intravascular haemolysis and release of inflammatory cytokines. Can cause shock, renal failure, DIC and death
Frequency of White cells
Neutrophil Lymphocytes monocytes Eosinophils Basophils
Never let monkeys eat bananas
Neutrophilia causes
Acute: Reactive (infection/inflammation, neoplasia, bleeding, infarction, smoking, burns, drugs (glucocorticoids)
Chronic: reactive, drugs, high BMI, metabolic syndrome, haematological disorder (myeloproliferative or CML)
Isolated neutropoenia
Viral infection
Drugs (carbimazole (thyrotoxicosis), chemo)
B12/folate (but often affects other lineage)
Autoimmune/Felty’s syndrome in RA
Cyclical neutropoenia
Haematological malignancy (acute leukaemia, myelodysplasia)
Hereditary (african origin)
Congenital bone marrow failure syndrome (Lostmann’s syndrome)
Neutropoenia levels
1.0-1.7 (mild neutropnoea, but ~ethnicity)
0.5-1.0 mod
<0.5 is severe, infection risk
Neutropoenic sepsis
Fever >38
Neutrophils <1.0
Emergency, urgent admin, broad spec IV abx
Lymphocyte distrubution
80% T (thymus derived, circulate in blood - little cytoplasm, few ribosome/ER)
20% B lymphocytes (plasma cells have more rough ER), mainly in lymph nodes
NK cells
Lymphocytosis primary causes
lymphoid malignancy (CLL, lymphomas, monoclonal B lymphocytosis)
Lymphocytosis Reactive and chronic
Viral (EBV, CMV, HSV, VZV)
Whooping cough
TB
Brucellosis
Stress lymphocytosis (drug induced (e.g. phenytoin), septic shock, MI, trauma)
Chronic: cigarette smoking, autoimmune disorder, chronic inflammation, sarcoid, raised BMI/metabolic syndrome
Lymphocytosis managment
Consider haematological cancer, more concerning if clonal than polyclonal
Monocytosis causes
Atypical infections (e.g. TB)
Inflammation
Autoimmune disease
Haematological malignancy (Chronic myelomonocytic leukaemia - CMML)
Eosinophils
parasites. React to complement, antibodies and histamine
Eosinophilia causes
Parasitic infections, asthma, drugs, eczema, haematological malignancies (Hodgkins disease, CML)
Basophil
Granules enclosed by membrane Allergy symptoms (heparin and histamine secretion, histamine causes vasoconstriction, bronchoconstriction and intestinal constriction). Gives parasitic immunity
Basophilia
Very rare, usually only in CML
Abnormal WCC urgent referral criteria
WCC>50
Blood film featues of CML/CMML
Mention of blasts on film
Neutrophils <0.5
Abnormal WCC, consider referral
Chronic neutrophilia (>20) Lymphocytosis (>10) Chronic monocytosis (>1) Chronic eosinophilia (>2) Persistent basophilia (May be CML) Neutrophils <1.0 with no clear cause
Leukostasis
High WCC causes occlusion in vessels. Needs urgent chemotherapy to reduce WCC.
See papilloedema, retinal venous distension, may get pulmonary oedema.
Can be complication of AML and blast phase of CML
CML
Raised WCC, pancytopaenia, immature myelocytes and metamyelocytes in blood (instead of marrow only)
Philadelphia chromosome (9-22).
Insidious onset. splenomegaly
Aplastic anaemia
Pancytopoenia.
Can be due to autoimmmune disorder, toxins, radiation, infections (EBV, HIV)
Glandular fever
EBV infection of B cells, circulate in blood (normally only see T cells circulating). Confirm with monospot test (detects heterophile antibodies)
B cells are EBV reservoir, cna reactivate during immune suppression (causing B cell malignancy)
Acute leukaemia vs chronic
No differentiation, see primative blasts.
In chronic, see normal differentiation into mature white cells
Children almost always get acute leukaemia, and generally ALL.
AML>ALL in adults. CLL>AML in adults.
CLL is most common leukaemia in adults
Features of acute leukaemia
May have symptoms over 1-2 weeks, but can have fatigue for longer (may then have antecedent haematological disorder e.g. MDS). Symptoms of bone marrow failure : aenaemia, neutropoenia, thrombocytopoenia.
Lab features: anaemia Low/high WCC thrombocytopnoenia Pancytopoenia blasts on film
