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Y5 Pathology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Anaemia definition in men

A

Hb <135g/L (13.5g/dL)

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2
Q

Anaemia definition in women

A

Hb <115g/L (11.5g/dL)

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3
Q

3 causes of anaemia

A

Reduced production of RBCs
Increased loss of RBCs (haemolytic anaemias)
Increased plasma volume (pregnancy)

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4
Q

Microcytic anaemias

A

IDA
Anaemia of chronic disease
Sideroblastic anaemia
Thalassaemia

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5
Q

Normocytic anaemias

A 
Acute blood loss
Anaemia of chronic disease
Bone marrow failure
Renal failure
Hypothyroidism
Haemolysis
Pregnancy
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6
Q

Macrocytic anaemias

A 
Fetus (pregnancy)
Antifolates (e.g. phenytoin)
Hypothyroidism
Reticulocytosis (release of larger immature cells e.g. haemolysis)
B12/folate deficiency
Cirrhosis (EtOH excess/liver disease)
Myelodysplastic syndromes
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7
Q

Symptoms of anaemia

A

Tiredness, shortness of breath, palpitations, headache, tinnitus, anorexia

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8
Q

Signs of anaemia

A

Pallor, in severe hyperdynamic circulation (tachycardia + flow murmurs (ejection-systolic loudest over apex), heart failure)

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9
Q 
Koilonychia
Brittle hair and nails
Atrophic glossitis
Angular cheilosis
Post-cricoid webs (Plummer-Vinson syndrome)
=?
A

IDA

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10
Q

IDA blood film

A

Microcytic, hypochromic
Anisocytosis (varying size)
Poikilocytosis (varying shape)
Pencil cells

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11
Q

Clinically considered cause of IDA

A

Bleeding until proven otherwise, menorrhagia in young women

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12
Q

5 classifications of IDA

A 
Blood loss
Increased utilisation
Decreased intake
Decreased absorption
Intravascular haemolysis
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13
Q

Blood loss-related causes of IDA

A

Gastrointestinal loss of blood

  • peptic ulcers/gastritis
  • polypa/colorectal cancer (>50)
  • menorrhagia (W <50)
  • Meckel’s diverticulum (children)
  • hookworm infestation (developing countries)
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14
Q

Increased utilisation-related causes of IDA

A

Pregnancy/lactation

Growth - infants/children

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15
Q

Decreased intake-related causes of IDA

A

Prematurity - loss of iron each day foetus isn’t in utero

Infants/children/elderly - suboptimal diet

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16
Q

Decreased absorption-related causes of IDA

A

Coeliac disease - absence of villi in duodenum

Post-gastric surgery - rapid transit so less acid to aid iron absorption

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17
Q

Intravascular haemolysis-related causes of IDA

A

Microangiopathic Haemolytic anaemia

PNH (paroxysmal nocturnal haemoglobinuria)

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18
Q

Investigations for IDA

A

Identify cause

If no obvious cause then OGD + colonoscopy, urine dip, coeliac Ix

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19
Q

IDA treatment

A

Treat the cause
Oral iron (ferrous sulphate)
IV iron if severe + symptomatic
If septic then blood transfusion instead of iron (fuels infection)

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20
Q

Anaemia of chronic disease causes

A

Chronic infection (e.g. TB, osteomyelitis)
Vasculitis
Rheumatoid arthritis
Malignancy etc (long-standing illness)

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21
Q

Mechanism of cause for anaemia of chronic disease

A

Cytokine-driven inhibition of RBC production
1 - Inflammatory markers reduce EPO receptor production (and thus EPO synthesis) by kidneys
2 - Iron metabolism dysregulated, IL6/LPS stimulate production of hepcidin by liver decreasing iron absorption by inhibiting transferrin and causing iron accumulation in macrophages

OR renal failure (EPO deficiency)

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22
Q

Ferritin (intracellular protein indicating iron store) status in ACD

A

Raised due to iron storage in macrophages

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23
Q

Aetiology of sideroblastic anaemia

A

Ineffective erythropoiesis - iron loading (accumulation of iron in body) causing haemosiderosis (endocrine, liver, cardiac damage due to iron deposition)

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24
Q

Diagnostic feature for sideroblastic anaemia

A

Ring sideroblasts seen in marrow

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25
Q

Ring sideroblast description

A

Erythroid precursors with iron deposited in mitochondria in a ring around nucleus

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26
Q

Sideroblastic anaemia causes

A 
Myelodysplastic disorders
Post-chemo
Irradiation
!!Alcohol excess
Lead excess
Anti-TB drugs
Myeloproliferative disease
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27
Q

Sideroblastic anaemia treatment + drug

A

Remove cause

Pyroxidine (vit B6 to promote RBC production)

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28
Q

Plasma iron study categories (3)

A

Serum iron
TIBC (total iron binding capacity)
Ferritin

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29
Q

Iron study results - Dx?

Serum iron - lowered
TIBC - raised
Ferritin - lowered

A

IDA

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30
Q

Plasma iron study results - Dx?

Serum iron - lowered
TIBC - lowered
Ferritin - raised

A

Anaemia of chronic disease

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31
Q

Iron study results - Dx?

Serum iron - raised
TIBC - lowered
Ferritin - raised

A

Chronic haemolytic anaemia

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32
Q

Iron study results - Dx?

Serum iron - raised
TIBC - lowered or normal
Ferritin - raised

A

Haemochromatosis

33
Q

Iron study results - Dx?

Serum iron - raised
TIBC - raised
Ferritin - normal

A

Pregnancy

34
Q

Sideroblastic anaemia iron study results

A

Serum iron - raised
TIBC - normal
Ferritin - raised

35
Q

Transferrin saturation calculation + iron deficiency threshold

A

serum iron/TIBC

<20% = Fe deficiency

36
Q

Adjustment to iron study necessary if patient in inflammatory state (e.g. infection/malignancy)

A

Ferritin is raised so check CRP with each ferritin sent and transferrin saturation will be more useful

37
Q

Investigations for pancytopenia

A

B12/folate/iron
Abdo exam to assess spleen (myelofibrosis = splenomegaly)
Reticulocyte count (aplastic anaemia or bone marrow failure syndromes if low)
Blood film (hairy cell leukaemia, dysplasia = myelodysplasia, blasts = acute leukaemia)
Myeloma screen
Parvovirus (can cause this in immunosuppressed)
Some medications may cause this
Bone marrow biopsy

38
Q

Macrocytic anaemia types (3)

A

Megaloblastic
Non-megaloblastic
Other haematological disease

39
Q

Megaloblastic macrocytic anaemia causes

A

B12 deficiency
Folate deficiency
Cytotoxic drugs

40
Q

Non-megaloblastic macrocytic anaemia causes

A 
Alcohol excess (commonest cause of macrocytosis without anaemia as well)
Reticulocytosis
Liver disease
Hypothyroidism
Pregnancy
41
Q

Other haematological diseases that cause macrocytic anaemia (neither megaloblastic/non-megaloblastic)

A

Myelodysplasia
Myeloma
Myeloproliferative disorders
Aplastic anaemia

42
Q

Megaloblastic macrocytic anaemia blood film description

A 
Hypersegmented polymorphs
Leucopenia
Macrocytosis
Anaemia
Thrombocytopenia with megaloblasts
43
Q

Main sources of vitamin B12

A

Meat and dairy

Large body stores

44
Q

Causes of vitamin B12 deficiency

A

Dietary

Malabsorption

45
Q

Causes of vitamin B12 malabsorption

A

Stomach - lack of intrinsic factor produced by gastric parietal cells - pernicious anaemia or post-gastrectomy
Terminal ileum - ileal resection, Crohn’s, bacterial overgrowth, tropical sprue, tapeworms

46
Q

Clinical features of B12 deficiency

A

Mouth - glossitis, angular cheilosis (swelling, fissuring of lips)
Psych - irritability, depression, psychosis, dementia
Neuro - parasthesiae, peripheral neuropathy (loss of vibration/proprioception, absent ankle reflex, spastic paraperesis, subacute combined degeneration of spinal cord)

47
Q

Pernicious anaemia aetiology and physiological consequences

A

Autoimmune atrophic gastritis - achlorydia and lack of gastric intrinsic factor
COMMONEST cause of macrocytic anaemia in Western countries (>40yrs)

48
Q

!!TESTS for pernicious anaemia

A

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

49
Q

Treatment for vit B12 deficiency

A

Replenish stores with !!IM hydroxycobalamin

50
Q

Main sources of folate

A

DIET - green veg, nuts, yeast & liver, synthesised by gut bacteria (low body stores, can’t produce de novo)

51
Q

Causes of folate deficiency

A

Poor diet
Increased demand - pregnancy or increased cell turnover (haemolysis, malignancy, inflammatory disease, renal dialysis)
Malabsorption - coeliac, tropical sprue
Drugs - alcohol, anti-epileptics (phenytoin), methotrexate, trimethoprim

52
Q

Treatment for folate deficiency

A

Oral folic acid (don’t give if cause of anaemia is unknown as may exacerbate)

53
Q

Definition of haemolytic anaemias

A

Breakdown of RBCs before their normal life span of around 120 days

54
Q

Features present in all haemolytic anaemias

A 
Raised bilirubin (unconjugated)
Raised urobilinogen
Raised LDH (lactate dehydrogenase)
Reticulocytosis (raised MCV and polychromasia)

May have pigmented gallstones

55
Q

Features present in intravascular haemolytic anaemias

A

Raised free plasma Hb
Lowered haptoglobin (binds free Hb)
Haemoglobinuria (dark red urine)
Methaemalbuminaemia (haem + albumin in blood)

56
Q

Main feature of extravascular haemolytic anaemias

A

Splenomegaly

57
Q

Issues patients in erythroid hyperplasia state are susceptible to

A

Parvovirus B19 (aplastic crisis)
Iron overload
Osteoporosis

58
Q

Expected outcome of reticulocyte count if patient is acutely anaemic

A

High reticulocyte count - bone marrow responding appropriately to produce more RBCs

59
Q

Classifications of causes of haemolytic anaemias

A

Inherited

  • membrane defect
  • enzyme defect
  • haemoglobinopathies

Acquired

  • immune
  • non-immune
60
Q

Inherited causes of haemolytic anaemias

A

Membrane defect - hereditary spherocytosis/elliptocytosis

Enzyme defect - G6PD deficiency, pyruvate kinase deficiency

Haemoglobinopathies - sickle cell disease, thalassaemias

61
Q

Acquired causes of haemolytic anaemias

A

Immune - autoimmune (warm or cold), alloimmune (haemolytic reactions to transfusions)

Non-immune - mechanical (e.g. metal valves, trauma), PNH, MAHA, infections (e.g. malaria), drugs

62
Q

Hereditary spherocytosis + elliptocytosis inheritance pattern

A

Autosomal dominant

63
Q

Aetiology of hereditary spherocytosis and susceptibilities

A

Spectrin or ankyrin deficiency (membrane proteins)

Susceptible to parvovirus B19 and gallstones

64
Q

Site of haemolysis in hereditary spherocytosis + clinical sign

A

Extravascular

Splenomegaly

65
Q

Diagnosis method for hereditary spherocytosis

A

Spherocytes on blood film
Increased osmotic fragility (lysis in hypotonic solution)
Negative DAT/Coombs test (not autoimmune Ab mediated)
Flow cytometry

66
Q

Treatment of hereditary spherocytosis

A

Splenectomy

Folic acid

67
Q

Only form of hereditary elliptocytosis that ISN’T autosomal dominant

A

Hereditary pyropoikilocytosis (overly sensitive to heat) - autosomal recessive

68
Q

Severity range of outcomes for hereditary elliptocytosis

A

Hydrops foetalis to asymptomatic

69
Q

Hereditary elliptocytosis appearance on blood film

A

RBCs are elliptical in shape

70
Q

South East Asian Ovalocytosis inheritance pattern + clinical relevance

A

Recessive - heterozygous +/- malaria protection

71
Q

Inheritance pattern for commonest RBC enzyme defect (G6PD def)

A

X-linked

72
Q

Prevalent areas of G6PD def

A

Malarial endemicity (i.e. Africa, mediterranean, middle eastern populations)

73
Q

G6PD def attack clinical features + blood film description

A 
Rapid anaemia + jaundice + dark urine
Bite cells (RBCs with small semicircular part cut out, like a bite) + !!Heinz bodies (blue deposits, oxidised Hb)
74
Q

Causes of G6PD def attacks

A

Oxidants (G6PD usually helps RBCs make glutathione = antioxidant)

  • drugs (2-3 days after starting)
  • broad beans
  • acute stressors
  • moth balls
  • acute infection
75
Q

Diagnosis method for G6PD def

A

Classical signs of anaemia on basic Ix
G6PD def spot test - NON-FLUORESCENT as no NADPH

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

76
Q

Treatment for G6PD def

A

Supportive + folic acid, avoid precipitants
Blood transfusion if severe attack
Genetic screening can be useful

77
Q

Inheritance pattern for pyruvate kinase def

A

Autosomal recessive

78
Q

Clinical features of pyruvate kinase def

A

Severe neonatal jaundice
Splenomegaly
Haemolytic anaemia

79
Q

Management of pyruvate kinase def

A

Most don’t require treatment but can do blood transfusion or splenectomy

Y5 Pathology (4 decks)

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