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CP3 @ UoN - Medicine & Surgery > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is Anaemia?

A

Decreased Hb in the blood such that there is inadequate oxygen delivery to tissues

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2
Q

What are the Hb levels indicating anaemia?

A

Hb <135g/L in men

Hb <115g/L in women

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3
Q

What are the Sx of anaemia?

A 
Can be asymptomatic
Fatigue
Weakness
Headaches
Dyspnoea on exertion
Angina
Intermittent claudication
Palpitations
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4
Q

What are the signs of anaemia?

A

Pallor
Tachycardia
Systolic flow mumur
Cardiac failure

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5
Q

What peripheral signs are indicative of different anaemia types?

A

Koilonychia (IDA)
Jaundice (haemolytic anaemia)
Leg ulcers (sickle cell disease)
Bone marrow expansion (thalassaemia)

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6
Q

What are the three main types of anaemia?

A

Microcytic (<80fl)
Normocytic (80-96fl)
Macrocytic (>96fl)

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7
Q

What are the common causes of microcytic anaemia?

A

Iron deficiency anaemia (commonly blood loss)
Thalassemia
Lead poisoning
Sideroblastic anaemia

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8
Q

What are the common causes of normocytic anaemia?

A 
Acute blood loss
Anaemia of chronic disease
Renal anaemia
Haemolytic anaemia (can be macro)
Marrow failure
Pregnancy
CT diseases
Diamorphic blood film
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9
Q

What are the common causes of macrocytic anaemia?

A 
B12 deficiency
Folate deficiency
Alcohol excess
Myelodysplastic syndromes
Severe hypothyroidism
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10
Q

What are the clinical signs of IDA?

A

Koilonychia
Angular stomatitis
Brittle nails/hair

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11
Q

What are the common causes of IDA?

A 
Blood loss (hookworm, heavy menstruation, GI bleed)
Dec absorption (coeliacs, antacids, post gastrectomy)
Inc demand (growth, pregnancy)
Inad intake (premature infants/prolonged breastfed)
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12
Q

What are the appropriate investigations to confirm IDA?

A

Serum Fe, ferritin, total iron binding capacity
Serum soluble transferrin receptors (increased)
Blood film

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13
Q

What signs of IDA would be present on a blood film?

A

Typically hypochromic
Sideroblasts
Signs of thalassaemia

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14
Q

What further investigations are necessary after confirming IDA?

A

Coeliac serology
GI investigation (OGD, colonoscopy)
Stool microscopy

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15
Q

How is IDA managed?

A

Address underlying cause
Oral ferrous sulphate 200mg t.d.s
Increase dietary Fe intake

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16
Q

What are the common side effects of Ferrous Sulphate?

A

Cramping, bloating
N/V
Constipation
Black stools

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17
Q

What investigations are appropriate in suspected anaemia of chronic disease?

A

Serum Fe (dec)
TIBC (dec)
STR (normal)
Ferritin (inc)

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18
Q

How long should treatment for IDA be continued?

A

Monitor after 1mo
-improvement in sx
-increase of Hb 20g/L
3mo after bloods return to normal

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19
Q

What is the Rule of 10’s?

A

Max rise in Hb in 1wk is 10g/L
If >10g/L decline in 1wk then blood is being lost
When transfusing 1 bag will raise Hb 10g/L

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20
Q

What is Paterson-Brown Kelley (Plummer Vinson) Syndrome?

A 
Rare disease occurring in post-menopausal women
Characterised by
   -dysphagia
   -odynophagia
   -IDA
   -glossitis
   -chelitis
   -oesophageal webs
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21
Q

How is Paterson-Brown Kelley (Plummer Vinson) Syndrome managed?

A

Iron supplementation & mechanical widening of oesophagus

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22
Q

What is Thalassemia?

A

Genetic disorders of Hb synthesis

-deficient a/b chain synthesis

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23
Q

What are the two main types of B-thalassemia?

A

B-thalassemia minor (trait)

B-thalassemia major (Cooley’s anaemia)

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24
Q

Describe B-thalassemia minor

A

Carrier state
Usually asymptomatic, mild microcytic anaemia worsening in pregnancy
-HbA2/HbF raised

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25
Q

Describe B-thalassemia major

A

Abnormality in both b-globin genes

Survival possible due to HbF

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26
Q

How does B-thalassemia major present?

A 
In first year with
   -severe anaemia
   -hepatosplenomegaly
   -failure to thrive
Facial deformities (due to extramedullary haematopoiesis)
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27
Q

What are the abnormalities on a blood film in B-thalassemia major?

A

Hypochromic microcytic cells
Target cells
Nucleated RBCs

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28
Q

How is B-thalassemia major managed?

A

Lifelong blood transfusions

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29
Q

What are the main types of a-thalassemia?

A

Major/hydrops fetalis/Bart’s hydrops
HbH disease
Minor
Carrier

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30
Q

Describe a-thalassemia major

A

Deletion of all 4 globin genes

-death in utero

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31
Q

Describe HbH disease

A

Deletion of 3 globin genes

-moderate microcytic anaemia w/ haemolysis

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32
Q

Describe a-thalassemia minor

A

Deletion of 2 globin genes

-asymptomatic carrier w/ reduced MCV

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33
Q

Describe a-thalassemia carrier

A

Deletion of 1 globin gene

-clinically normal

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34
Q

What is sideroblastic anaemia?

A

Bone marrow produces sideroblasts instead of erythrocytes

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35
Q

What causes sideroblastic anaemia?

A

Congenital disorder OR

Acquired in myelodysplastic syndrome

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36
Q

What are the key investigations in a macrocytic anaemia?

A 
Blood film
LFTs/TFTs
Serum B12/folate
   -if B12 low --> anti-parietal Ab, anti-IF Ab, Schilling test
Bone marrow biopsy
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37
Q

What is the Schilling test?

A

Assesses B12 metabolism w/ & w/o IF

Distinguishes b/w pernicious anaemia & small bowel disease

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38
Q

What is the common mechanism by which B12/folate deficiency lead to a megaloblastic anaemia?

A

B12 co-enzyme for activation of folate
Activated folate needed for DNA synth
Deficiency leads to inc erythrocyte development
-large cells
-trapped/destroyed in reticuloendothelial system

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39
Q

What are the dietary sources of B12?

A

Meat
Fish
Eggs
Milk

40
Q

How is B12 absorbed/stored?

A

Binds w/ IF (secreted by gastric parietal cells)
Absorbed in terminal ileum (brush border)
Stored in liver (3yr store)
Excreted in bile (70% reabsorbed)

41
Q

What are the common causes of B12 deficiency?

A 
Chronic low dietary intake (vegans)
Impaired binding (pernicious, congenital IF absence, gastrectomy)
Small bowel disease (resection, Chron's, UC, bacterial overgrowth)
42
Q

What is Pernicious anaemia?

A

Autoimmune disease resulting in severe B12 deficiency

43
Q

What are the three autoantibodies that may be present in pernicious anaemia?

A 
Autoantibodies against parietal cells
Blocking antibodies (stop IF-B12 binding, most common)
Binding antibodies (prevent IF binding to ileum)
44
Q

What is subacute combined degeneration of the cord?

A

Simultaneous post column (LMN) & CST (UMN) loss due to B12 deficiency

45
Q

How does subacute combined degeneration of the cord present?

A 
Peripheral neuropathy
Extensor plantars
Brisk knee jerk but absent ankle jerk
Tone/power normal
Gait ataxic
46
Q

What are the major dietary sources of folate?

A

Leafy green vegetables/offal (as DHF/THF)

-90% lost in cooking

47
Q

How is folate absorbed & stored?

A

DHF/THF converted to folate in upper GI
Absorbed in jejunum
Low stores (3mo)

48
Q

What are the common causes of folate deficiency?

A

Poor nutritional intake (diet/alcohol/anorexia)
Malabsorption (Coeliac)
Anti-folate drugs (trimethoprim, methotrexate, anti-convulsants)
Excess physiological use (preg, lact, prematurity)
Excess pathological use (haemolysis, malig, inflam)

49
Q

How should folate deficiency be managed?

A

Folic acid 5mg/day PO for 4mo

-always w/ combined B12

50
Q

How should pernicious anaemia be managed?

A

IM B12 initially then oral B12 for maintenance

51
Q

What is anaemia of chronic disease?

A

Normochromic/hypochromic
-low Fe, high ferritin, low TIBC, normal STR
Rarely severe
Seen in chronic infection, malignancy, CKD, rheumatoid

52
Q

How does bone marrow failure appear on blood tests?

A

Hb, reticulocytes, WCs, platelets all low

Alterations on blood film

53
Q

What are the potential causes of bone marrow failure?

A 
Aplastic anaemia (idiopathic/drugs)
Malignancies
Metastatic disease
Meylofibrosis
Meylodysplasia
Parviovirus infection
54
Q

What is Haemolysis?

A

Breakdown of RBCs before 120days

  • intravascular or extravascular
  • asymptomatic –> haemolytic anaemia
55
Q

What are the intrinsic causes of a haemolytic anaemia?

A

Haemaglobinopathies (sickle cell/thalassemia)
Membranopathies (spherocytosis/eliptocytosis)
Enzymeopathies (G6DP deficiency)

56
Q

What are the extrinsic causes of a haemolytic anaemia?

A

Autoimmune disease (warm/cold)
Alloimmune disease (transfusion/transplant, rhesus)
Drug induced (penicillins)
Paraistes (plasmodium)
Microangiopathic haemolytic anaemia (DIC)

57
Q

What are the investigation results that would indicate increased RBC breakdown?

A 
Anaemia w/ raised MCV
Raised bilirubin (unconjugated, pre-hepatic)
Raised serum LDH
58
Q

What are the investigation results that would indicate increased RBC production?

A

Reticulocyte count >2% OR 100*10^9/L

-will give a raised MCV

59
Q

How can a blood film identify the cause of a haemolytic anaemia?

A 
Hypochromic, microcytic = thalassemia
Sickle cells = SCA
Spherocytes = hereditary spherocytosis/AI haemolysis
Eliptocytes = hereditary eliptocytosis
Heinz bodies = G6PD deficiency
60
Q

What further investigations are indicated in haemolytic anaemia?

A 
Coomb's test (?immune cause)
Hb electrophoresis (haemaglobinopathies)
Enzyme assays
Plasma haptoglobin/urinary haemosiderin
   -indicate intravascular haemolysis
61
Q

What is Sickle Cell Anaemia?

A

Autosomal recessive disorder producing abnormal B-globulin chains

  • HbS rather than HbA
  • more common in african pts
62
Q

What are the two genotypes of SCA?

A

HbSS - sickle cell anaemia phenotype
HbAS - sickle cell trait
-protective against falciparum malaria
-rarely symptomatic, vaso-occlusive crises can occur in hypoxia

63
Q

What is the underlying pathophysiology of SCA?

A

HbS polymerises when deoxygenated –> produces sickle cells

-fragile, haemolyse, block small vessels

64
Q

How is SCA diagnosed?

A

Guthrie card
Sickle cells on blood film
Hb electrophoresis to confirm/distinguish variants

65
Q

What are the sx of SCA?

A

Anaemia in first few months of life
Acute haemolytic crises (bone infarcts/painful dactylitis)
Repeated splenic infarction (CKD, CVA)
Chronic haemolytic anaemia (60-90g/L)

66
Q

What are the potential complications of SCA?

A 
Hyposplenism
CKD
Bone necrosis
Chronic leg ulcers
Fe overload
Long term pulmonary damage
67
Q

What is the long-term management of SCA?

A

Folate supplementation
Pneumococcal vaccination & prophylactic penicillin (hyposplenism)
Hydrocycarbamide (if frequent crises)
Transfusions (2-4/wk) w/ Fe chelators

68
Q

What is the curative treatment for SCA?

A

Bone marrow transplantation

69
Q

What are vaso-occlusive crises?

A

Occur due to micro-vascular occlusion

  • affect bone marrow, cause severe pain
  • caused by cold, infec, dehydration, hypoxia
70
Q

How do vaso-occlusive crises present?

A 
Usually severe pain
Can be
   -mesenteric ischaemia (acute abdomen)
   -cerebral infarcts
   -priapism
71
Q

What are aplastic crises?

A

Sudden reduction in marrow production due to parvovirus B19

-self limiting (<2wks), may need transfusion

72
Q

What are sequestration crises?

A

Pooling of blood in spleen +/- liver

  • presents w/ organomegaly, severe anaemia, shock
  • typically in children
  • urgent transfusion required
73
Q

How should a sickle cell crisis be managed?

A 
A-E resus, O2, IV fluids
Analgesiaa
FBC, reticulocytes, cross-match
Screen for infec
Prophylactic enoxaparin
Give blood transfusion
74
Q

What is G6PD deficiency?

A

X-linked deficiency of G6PD

  • most common in Africa/mediterranean males
  • females have mild sx
75
Q

How does G6PD deficiency present?

A

Asymptomatic
Oxidative crises (reduced glutathione production)
-rapid anaemia & jaundice
-bite & blister cells on blood film

76
Q

What are the triggers for oxidative crises in G6PD deficiency?

A

Drugs (aspirin, primaquine, sulphonamides)
Broad bean consumption
Illness

77
Q

How is G6PD deficiency diagnosed?

A

Enzyme assay 3mo after crisis

78
Q

How is G6PD deficiency managed?

A

Precipitant avoidance +/- transfusion

79
Q

What is Pyruvate Kinase deficiency?

A

AR condition of reduced ATP production

80
Q

How does PK deficiency present?

A

Neonatal jaundice

Chronic jaundice w/ hepatosplenomegaly

81
Q

How is PK deficiency diagnosed?

A

Enzyme assay

82
Q

How is PK deficiency managed?

A

Well tolerated, no specific therapy needed

-splenectomy may help

83
Q

What is Hereditary Spherocytosis?

A

AD membran defect –> spherical RBCs

-trapped in spleen

84
Q

How does HS present?

A

Haemolysis
Splenomegaly
Jaundice

85
Q

What is Hereditary Eliptocytosis?

A

AD defect

-asymptomatic

86
Q

How are HS/HE managed?

A

Folate
Splenectomy
-curative, saved for severe disease

87
Q

What is the underlying pathophysiology of an autoimmune haemolytic anaemia?

A

Autoantibodies –> extravascular haemolysis & spherocytosis

88
Q

What are the common causes of AHA?

A

Idiopathic

2o to lymphoproliferative disease/other AI conditions

89
Q

What are the two types of AHA?

A

Warm

Cold

90
Q

Describe warm AHA

A 
IgG mediated (binding at 37o)
Treat w/ steroids/immunosuppressants +/- splenectomy
91
Q

Describe cold AHA

A 
IgM mediated (binding at <4o)
Treat w/ cold avoidance +/- chlorambucil
92
Q

What is a microangiopathic anaemia?

A

Mechanical haemolysis caused by physical trauma in the circulation
-shistocytes on blood film

93
Q

What are the common causes of a microangiopathic anaemia?

A 
Malignant HTN/Pre-eclampsia
HUS
Thrombotic thrombocytopenic purpura
Vasculitis
DIC
Mechanical heart valves
94
Q

What are allommune reactions?

A

Immune mediated BUT coomb’s negative reactions linked to transplantation/transfusion/rhesus

95
Q

What screening for anaemia takes place before surgery?

A

Most common abnormality pre-op

  • <60g/L = transfusion
  • <100g/L = transfusion if cardiac risk/high anticipated blood loss

CP3 @ UoN - Medicine & Surgery (135 decks)

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