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YEAR 5: Haematology AS > Haem: anaemia > Flashcards

Haem: anaemia Flashcards

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1
Q

limits for anaemia in men and women

A

Men: <135 g/L (13.5g/dL), Women: < 115g/L (11.5g/dL)

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2
Q

very general causes of anaemia

A

reduced production of RBCs
increased loss of RBCs (haemolytic anaemias)
increased plasma volume (pregnancy)

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3
Q

symptoms of anaemia

A

fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, anorexia

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4
Q

Signs of anaemia

A

pallor, in severe anaemia (Hb < 80g/L) → hyperdynamic circulation e.g. tachycardia, flow murmurs (ejection-systolic loudest over apex) → heart failure

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5
Q

causes of anaemia with low MCV

A

fast
Fe deficiency
Anaemia of chronic disease
Sideroblastic anaemia
Thalassaemia

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6
Q

causes of normocytic anaemia

A

acute blood loss
anaemia of chronic disease
bone marrow failure
renal failure
hypothyroidism
haemolysis
pregnancy

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7
Q

causes of macrocytic anaemia

A

FATRBCM
Fetus (pregnancy)
Antifolates
Thyroid (hypothyroidism)
Reticulocytosis (release of larger immature cells e.g. with haemolysis)
B12 or folate deficiency
Cirrhosis (Alcohol excess or liver disease)
Myelodysplastic syndromes

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8
Q

Signs of iron deficiency anaemia

A

Koilonychia, atrophic glossitis, angular cheilosis, post-cricoid webs (Plummer-Vinson syndrome), brittle hair and nails

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9
Q

What might you see on the blood film of iron deficiency anaemia?

A

microcytic
hypochromic
anisocytosis
poikilocytosis
pencil cells

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10
Q

Causes of IDA

A

Blood loss:
Menorrhagia
Meckel’s diverticulum (older children)
Peptic ulcers / Gastritis (chronic NSAID use)
Polyps/colorectal Ca (most common cause in adults >50yrs)
Hookworm infestation (developing countries)

Increased utilisation:
Pregnancy
Growth of children

Decreased Intake:
Prematurity- loss of Fe each day fetus is not in utero
Suboptimal diet

Decreased absorption:
Coeliac: absence in villous surface in duodenum
absorption
Post-gastric surgery: rapid transit, ↓ acid which helps Fe absorption

Intravascular haemolysis:
Microangiopathic Haemolytic anaemia
PNH
Chronic loss of Hb in urine → Fe deficiency

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11
Q

Investigations of IDA

A

if no obvious cause then patients should have OGD + colonoscopy, urine dip, coeliac investigations

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12
Q

Treatment of IDA

A

Treat the cause

Oral iron (SE: nausea, abdominal discomfort, diarrhea/constipation, black stools).
(alternate days almost as quick at improving anaemia and has less toxicity)
IV iron such as Ferrinject / Monofer (anaphylaxis risk)
Indications: poor oral absorption, failure of oral iron trial, or need for rapid rise (e.g. imminent major surgery)

Note: in sepsis and severe infection, iron will not absorb well and can fuel sepsis. Blood transfusions are better in this scenario.

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13
Q

Anaemia of chronic disease causes

A

Cytokine driven inhibition of red cell production

Causes:
* Chronic infection (e.g. TB, osteomyelitis)
* Vasculitis
* Rheumatoid arthritis
* Malignancy etc

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14
Q

Anaemia of chronic disease pathophysiology

A
  • Inflammatory markers like IFNs, TNF and IL1 reduce EPO receptor production (and thus EPO synthesis) by kidneys
  • Iron metabolism is dysregulated. IL6 and LPS stimulate the liver to make hepcidin, which decreases iron absorption from gut (by inhibiting transferrin) and also causes iron accumulation in macrophages
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15
Q

Ferritin levels in anaemia of chronic disease

A

Ferritin (intracellular protein, iron store) high:
Fe sequestered in macrophage to deprive invading bacteria of Fe (unless the patient has co- existing iron deficiency anaemia)

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16
Q

Why does renal failure cause anaemia of chronic disease?

A

not cytokine driven but due to Erythropoietin (EPO) deficiency (EPO made by kindey)

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17
Q

Mechanism underlying sideroblastic anaemia

A

Ineffective erythropoiesis → iron loading (bone marrow) causing haemosiderosis (endocrine, liver and cardiac damage due to iron deposition)

haemosiderin is a storage product of iron from erythrocyte breakdown found in cells

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18
Q

How is sideroblastic anaemia diagnosed?

A

Ring sideroblasts seen in the marrow (erythroid precursors with iron deposited in mitochondria in a ring around the nucleus)

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19
Q

Causes of sideroblastic anaemia

A

myelodysplastic disorders, following chemotherapy, irradiation, alcohol excess, lead excess, anti-TB drugs or myeloproliferative disease

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20
Q

Treatment of sideroblastic anaemia

A

Remove the cause and consider Pyridoxine (vitamin B6 promotes RBC production). Consider giving EPO

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21
Q

Interpretation of Plasma Iron Studies

A
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22
Q

Investigations for pancytopaenia

A

check for splenomegaly: myelofibrosis and lymphoproliferatives disorders

  • B12/Folate/Iron (note: iron deficiency alone shouldn’t cause pancytopenia)
  • Abdo exam for spleen (myelofibrosis)
  • Reticulocyte count (if low= BM not responding appropriately = BM failure= aplastic anaemia, BMF syndromes)
  • Blood film (abnormal cells i.e. acute leukaemia high WCC but could be low, hairy cell leukaemia, LGL leukaemia, dysplastic changes i.e. myelodysplasia)
  • Myeloma screen (infiltrated bone marrow= pancytopenia)
  • Parvovirus (immunosuppressed patients + blood PCR test)
  • Medications review

Unless there is a clear cause on above tests, patients are likely to require a bone marrow biopsy to diagnose

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23
Q

Macrocytic anaemia causes

A

Megaloblastic: B12 deficiency, folate deficiency, cytotoxic drugs.

Non-megaloblastic: Alcohol (most common cause of macrocytosis without anaemia), reticulocytosis (e.g. in haemolysis), liver disease, hypothyroidism, and pregnancy

Other haematological disease: Myelodysplasia, myeloma, myeloproliferative disorders, aplastic anaemia

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24
Q

Megaloblastic blood film

Study These Flashcards
A

Hypersegmented polymorphs, leucopenia, macrocytosis, anaemia, thrombocytopenia with megaloblasts

Megaloblasts are red cell precursors with an immature nucleus and mature cytoplasm. B12 and folate are required for nucleus maturation

25
sources of B12
meat and dairy
26
Causes of B12 deficiency
Dietary (e.g. vegans) Malabsorption: * Stomach (lack of intrinsic factor produced by gastric parietal cells)→ Pernicious anaemia, post gastrectomy * Terminal ileum (absorption) due to ileal resection, Crohn's disease,bacterial overgrowth, tropical sprue and tapeworms
27
B12 clinical features
* Mouth: Glossitis, angular cheilosis * Neuropsychiatric: Irritability, depression, psychosis, dementia. * Neurological: Paraesthesiae, peripheral neuropathy (loss of vibration and proprioception first, absent ankle reflex, spastic paraperesis, subacute combined degeneration of spinal cord)
28
Pernicious anaemia - what is it
Autoimmune atrophic gastritis → achlorhydria and lack of gastric intrinsic factor Most common cause of a macrocytic anaemia in Western countries (Usually >40yrs)
29
Pernicious anaemia test
Parietal cell antibodies (90%), Intrinsic factor antibodies (50%), Schilling test (outdated)
30
Treatment B12 deficiency
Replenish stores with IM hydroxocobalamin (B12) with 6 injections over 2 weeks. NICE recommend testing for anti-parietal cell / anti-intrinsic factor antibodies as if there is an autoimmune cause rather than dietary, patients will need 3-monthly IM injections
31
Folate sources
DIET - green vegetables, nuts, yeast & liver, synthesized by gut bacteria (low body stores, cannot produce de novo)
32
Causes of folate deficiency
* Poor diet * Increased demand: pregnancy or ↑ cell turnover (haemolysis, malignancy, inflammatory disease and renal dialysis) * Malabsorption: coeliac disease, tropical sprue * Drugs: alcohol, anti-epileptics (phenytoin), methotrexate, trimethoprim
33
Folate deficiency treatment
Give oral folic acid Ensure B12 is checked and replaced prior to folic acid otherwise folic acid may exacerbate the neuropathy of B12 deficiency
34
haemolytic anaemia definition
increased breakdown of red blood cells before their 120 day lifespan
35
lab results in all haemolytic anaemia
high bilirubin high urobilinogen high LDH reticulocytosis (high MCV and polychromasia) pigmented gallstones
36
intravascular haemolytic anaemia lab results
high free plasma Hb low haptoglobin (binds Hb) haemoglobinuria Methaemalbuminaemia (Haem + albumin in blood)
37
what examination finding may you see in haemolytic anaemia
splenomegaly
38
what is erythroid hyperplasia and what risks is it associated with
overproduction of erythroid cells in bone marrow in response to anaemia associated with parvovirus B19 aplastic crisis, iron overload and osteoporosis
39
how does reticulocyte count change in response to anaemia
increases as bone marrow produces more in response
40
causes of inherited haemolytic anaemia
membrane defect: * hereditary spherocytosis * hereditary elliptocytosis enzyme defect: * G6PD deficiency * pyruvate kinase deficiency haemoglobinopathies: * sickle cell diseases * thalassaemia
41
causes of acquired haemolytic anaemia
immune: * autoimmune: warm or cold * alloimmune: haemolytic transfusion reactions non-immune: * mechanical: metal valves or trauma * PNH, MAHA * infection: malaria * drugs
42
hereditary spherocytosis mode of inheritance
autosomal dominant 25% recessive or de novo
43
mechanism underlying hereditary spherocytosis
spectrin or ankyrin deficiency- these are membrane proteins
44
what are individuals with hereditary spherocytosis susceptible to
parvovirus B19 and gallstones
45
diagnosis of hereditary spherocytosis
extravascular haemolysis: splenomegaly spherocytes on blood film high osmotic fragility- lyse in hypotonic solutions -ve DAT/ Coombs flow cytometry EMA binding test
46
management of hereditary spherocytosis
folic acid maybe splenectomy
47
hereditary elliptocytosis mode of inheritance
Almost all forms are autosomal dominant – spectrin mutations Except Hereditary Pyropoikilocytosis (erythrocytes are abnormally sensitive to heat) – autosomal recessive
48
symptoms and diagnosis of hereditary elliptocytosis
asymptomatic usually elliptical on blood film
49
South East Asian Ovalocytosis mode of inheritance
Recessive – heterozygous +/- malaria protection
50
Glucose-6-phosphate dehydrogenase (G6PD) Deficiency mode of inheritance and epidemiology
Commonest RBC enzyme defect – X linked Prevalent in areas of malarial endemicity i.e. African, Mediterranean and Middle Eastern populations
51
Glucose-6-phosphate dehydrogenase (G6PD) Deficiency mode of inheritance and epidemiology
Commonest RBC enzyme defect – X linked Prevalent in areas of malarial endemicity i.e. African, Mediterranean and Middle Eastern populations
52
blood film of G6PDD
bite cells and Heinz bodies (blue deposits, oxidized Hb)
53
G6PDD S/S
attacks - rapid anaemia and jaundice intravascular haemolysis: dark urine
54
what can cause G6PDD
Precipitated by oxidants as G6PD helps RBCs make glutathione which protects them from oxidant damage - - drugs (usually 2-3 days after starting) (e.g. primaquine, sulfonamides, aspirin), broad beans (within 1 day of eating)(favism), acute stressors, moth balls, acute infection
55
diagnosis of G6PDD
Enzyme assay ~2- 3 months after a crisis: young RBCs may have sufficient enzyme so results may appear normal
56
treatment of G6PDD
Avoid precipitants; transfuse if severe, genetic screening (rare subtypes give chronic haemolysis for which splenectomy can be needed)
57
pyruvate kinase deficiency mode of inheritance
Autosomal recessive (but autosomal dominant has been observed with the disorder)
58
pyruvate kinase S/S
Clinical features: can be severe neonatal jaundice, splenomegaly, haemolytic anaemia
59
treatment of pyruvate kinase deficiency
most do not require treatment (can incl blood transfusion or splenectomy)

YEAR 5: Haematology AS (20 decks)

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