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YEAR 5: Haematology AS > Haem: anaemia > Flashcards

Haem: anaemia Flashcards

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

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
Q

sources of B12

A

meat and dairy

26
Q

Causes of B12 deficiency

A

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
Q

B12 clinical features

A
  • 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
Q

Pernicious anaemia - what is it

A

Autoimmune atrophic gastritis → achlorhydria and lack of gastric intrinsic factor

Most common cause of a macrocytic anaemia in Western countries (Usually >40yrs)

29
Q

Pernicious anaemia test

A

Parietal cell antibodies (90%), Intrinsic factor antibodies (50%), Schilling test (outdated)

30
Q

Treatment B12 deficiency

A

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
Q

Folate sources

A

DIET - green vegetables, nuts, yeast & liver, synthesized by gut bacteria (low body stores, cannot produce de novo)

32
Q

Causes of folate deficiency

A
  • 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
Q

Folate deficiency treatment

A

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
Q

haemolytic anaemia definition

A

increased breakdown of red blood cells before their 120 day lifespan

35
Q

lab results in all haemolytic anaemia

A

high bilirubin
high urobilinogen
high LDH
reticulocytosis (high MCV and polychromasia)
pigmented gallstones

36
Q

intravascular haemolytic anaemia lab results

A

high free plasma Hb
low haptoglobin (binds Hb)
haemoglobinuria
Methaemalbuminaemia (Haem + albumin in blood)

37
Q

what examination finding may you see in haemolytic anaemia

A

splenomegaly

38
Q

what is erythroid hyperplasia and what risks is it associated with

A

overproduction of erythroid cells in bone marrow in response to anaemia

associated with parvovirus B19 aplastic crisis, iron overload and osteoporosis

39
Q

how does reticulocyte count change in response to anaemia

A

increases as bone marrow produces more in response

40
Q

causes of inherited haemolytic anaemia

A

membrane defect:
* hereditary spherocytosis
* hereditary elliptocytosis

enzyme defect:
* G6PD deficiency
* pyruvate kinase deficiency

haemoglobinopathies:
* sickle cell diseases
* thalassaemia

41
Q

causes of acquired haemolytic anaemia

A

immune:
* autoimmune: warm or cold
* alloimmune: haemolytic transfusion reactions

non-immune:
* mechanical: metal valves or trauma
* PNH, MAHA
* infection: malaria
* drugs

42
Q

hereditary spherocytosis mode of inheritance

A

autosomal dominant
25% recessive or de novo

43
Q

mechanism underlying hereditary spherocytosis

A

spectrin or ankyrin deficiency- these are membrane proteins

44
Q

what are individuals with hereditary spherocytosis susceptible to

A

parvovirus B19 and gallstones

45
Q

diagnosis of hereditary spherocytosis

A

extravascular haemolysis: splenomegaly
spherocytes on blood film
high osmotic fragility- lyse in hypotonic solutions
-ve DAT/ Coombs
flow cytometry EMA binding test

46
Q

management of hereditary spherocytosis

A

folic acid
maybe splenectomy

47
Q

hereditary elliptocytosis mode of inheritance

A

Almost all forms are autosomal dominant – spectrin mutations

Except Hereditary Pyropoikilocytosis (erythrocytes are abnormally sensitive to heat) – autosomal recessive

48
Q

symptoms and diagnosis of hereditary elliptocytosis

A

asymptomatic usually
elliptical on blood film

49
Q

South East Asian Ovalocytosis mode of inheritance

A

Recessive – heterozygous +/- malaria protection

50
Q

Glucose-6-phosphate dehydrogenase (G6PD) Deficiency mode of inheritance and epidemiology

A

Commonest RBC enzyme defect – X linked

Prevalent in areas of malarial endemicity i.e. African, Mediterranean and Middle Eastern populations

51
Q

Glucose-6-phosphate dehydrogenase (G6PD) Deficiency mode of inheritance and epidemiology

A

Commonest RBC enzyme defect – X linked

Prevalent in areas of malarial endemicity i.e. African, Mediterranean and Middle Eastern populations

52
Q

blood film of G6PDD

A

bite cells and Heinz bodies (blue deposits,
oxidized Hb)

53
Q

G6PDD S/S

A

attacks - rapid anaemia and jaundice
intravascular haemolysis: dark urine

54
Q

what can cause G6PDD

A

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
Q

diagnosis of G6PDD

A

Enzyme assay ~2- 3 months after a crisis: young RBCs may have sufficient enzyme so results may appear normal

56
Q

treatment of G6PDD

A

Avoid precipitants; transfuse if severe, genetic screening (rare subtypes give chronic haemolysis for which splenectomy can be needed)

57
Q

pyruvate kinase deficiency mode of inheritance

A

Autosomal recessive (but autosomal dominant has been observed with the disorder)

58
Q

pyruvate kinase S/S

A

Clinical features: can be severe neonatal jaundice, splenomegaly, haemolytic anaemia

59
Q

treatment of pyruvate kinase deficiency

A

most do not require treatment (can incl blood transfusion or splenectomy)

YEAR 5: Haematology AS (20 decks)

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