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1
Q

5 causes of microcytic anaemia

A
  1. thalassaemia
  2. anaemia of chronic disease
  3. iron deficiency
  4. lead poisoning
  5. sideroblastic anaemia
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2
Q

5 causes of normocytic anaemia

A
  1. acute blood loss
  2. anaemia of chronic disease
  3. aplastic anaemia
  4. haemolytic anaemia
  5. hypothyroidism
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3
Q

2 types of macrocytic anaemia

A 
megaloblastic = result of impaired DNA synthesis preventing normal division 
normoblastic = no problem with DNA synthesis
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4
Q

2 causes of megaloblastic macrocytic anaemia

A
  1. B12 deficiency

2. folate deficiency

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5
Q

5 causes of normoblastic (non-megaloblastic) macrocytic anaemia

A
  1. alcohol
  2. reticulocytosis
  3. hypothryoidism
  4. liver disease
  5. drugs e.g. azathioprine
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6
Q

symptoms of anaemia

A
  • tiredness
  • SOB
  • headaches
  • dizziness
  • palpitations
  • worsening of other conditions e.g. angina, HF, PVD
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7
Q

symptoms specific to iron deficiency anaemia

A
  • pica => dietary cravings for abnormal things such as dirt

- hair loss

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8
Q

signs of general anaemia

A
  • pale skin
  • conjunctival pallor
  • tachycardia
  • tachypnoea
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9
Q

signs specific to iron deficiency anaemia

A
  • koilonychia (spoon shaped nails)
  • angular chelitis/stomatitis
  • atrophic glossitis
  • brittle hair and nails
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10
Q

sign specific to haemolytic anaemia

A

jaundice

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11
Q

sign specific to thalassaemia

A

bone deformities

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12
Q

3 ix in anaemia

A
  1. bloods:
    - FBC: Hb, MCV
    - haematinics: B12, folate, ferritin
    - blood film
  2. OGD and colonoscopy under urgent GI cancer referral in unexplained IDA
  3. bone marrow biopsy
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13
Q

4 ways in which you can become iron deficient

A
  1. insufficient dietary intake
  2. increase requirements e.g. pregnancy
  3. loss of iron e.g. bleeding
  4. inadequate absorption e.g. coeliac, crohn’s
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14
Q

where is iron absorbed and what is important for the process

A

duodenum and jejunum
stomach acid ensures iron in soluble form (Fe2+ rather than Fe3+) therefore meds reducing stomach acid can interfere with iron absorption

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15
Q

formula for transferrin saturation

A

serum iron / total iron binding capacity (directly related to transferrin levels)

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16
Q

what is transferrin

A

carrier protein that iron travels around the blood bound to

directly related to total iron binding capacity

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17
Q

level of TIBC in iron deficiency anaemia

A

increased in IDA

-> low iron levels therefore more room left on ferritin for iron to bind

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18
Q

mx options in iron deficiency anaemia

A
  1. blood transfusion
  2. iron infusion (monofer)
  3. oral iron (ferrous sulphate 200mg TDS)
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19
Q

aim for rise in haemoglobin when correcting IDA

A

10g/litre per week

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20
Q

2 causes of b12 deficiency

A

insufficient intake

pernicious anaemia

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21
Q

pathophysiology of pernicious anaemia

A

autoimmune condition where antibodies against parietal cells or intrinsic factor prevent absorption of vitamin b12 in the ileum

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22
Q

presentation of b12 deficiency

A
  • peripheral neuropathy
  • loss of vibration sense or proprioception
  • visual changes
  • mood or cognitive changes
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23
Q

mx of pernicious anaemia

A

IM hydroxycobalamin (can’t use oral replacement due to problem being absorption)

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24
Q

regime for IM hydroxycobalamin tx in pernicious anaemia

A

1mg 3x weekly for 2 weeks then every 3 months

or if neuro sx: 1mg every other day until improvement in sx

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25
Q

tx of vitamin b12 deficiency due to diet

A

oral cyanocobalamin

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26
Q

important consideration in joint b12 and folate deficiency

A

treat b12 deficiency first or risk subacute combined degeneration of the cord

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27
Q

5 causes of inherited haemolytic anaemia

A
  1. hereditary spherocytosis
  2. hereditary elliptocytosis
  3. thalassaemia
  4. sickle cell
  5. g6pd deficiency
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28
Q

5 causes of acquired haemolytic anaemia

A
  1. autoimmune haemolytic anaemia
  2. alloimmune haemolytic anaemia (transfusion reaction or haemolytic disease of the newborn)
  3. paroxysmal nocturnal haemoglobinuria
  4. microangiopathic haemolytic anaemia
  5. prosthetic valve related haemolysis
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29
Q

3 key features of haemolytic anaemia

A
  1. anaemia
  2. splenomegaly
  3. jaundice
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30
Q

3 ix in haemolytic anaemia

A
  1. FBC -> normocytic anaemia
  2. blood film -> schistocytes
  3. direct coombs test -> +ve in autoimmune haemolytic anaemia
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31
Q

genetics of hereditary spherocytosis

A

autosomal dominant

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32
Q

presentation of hereditary spherocytosis

A
  • jaundice
  • gallstones
  • splenomegaly
  • aplastic crisis (in presence of parvovirus)
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33
Q

what is haemolytic anaemia

A

low haemoglobin due to abnormal breakdown of RBC (can be caused by various pathologies)

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34
Q

what is hereditary spherocytosis

A

most common inherited haemolytic anaemia in northern europe

sphere shaped RBCs which are fragile and break down when passing through spleen

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35
Q

key findings on ix in hereditary spherocytosis

A
  • FHx (AD)
  • spherocytes on blood film
  • MCHC (mean corpuscular concentration) is raised on FBC
  • reticulocytes raised (high turnover of RBC)
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36
Q

tx of hereditary spherocytosis/elliptocytosis

A

folate supplementation + splenectomy

cholecystectomy may be required if problematic gallstones

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37
Q

what is hereditary elliptocytosis

A

autosomal dominant inherited condition where the RBCs are ellipse shaped and fragile meaning they break down easily when passing through the spleen

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38
Q

what is G6PD deficiency

A

defect in the RBC enzyme G6PD - causes haemolytic crises which are triggered by infections, medications or fava beans (broad beans)

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39
Q

presentation of G6PD deficiency

A
  • jaundice (usually in neonatal period)
  • gallstones
  • anaemia
  • splenomegaly
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40
Q

ix in G6PD deficiency

A
  • blood film shows Heinz bodies

- G6PD enzyme assay is diagnostic

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41
Q

medications which can trigger G6PD haemolysis

A

primaquine (antimalarial)
ciprofloxacin
sulfonylureas
sulfasalazine

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42
Q

what is autoimmune haemolytic anaemia

A

antibodies created against own RBC leading to destruction of RBC

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43
Q

classification of autoimmune haemolytic anaemia

A

depends on temperature of when the autoantibodies work and cause haemolysis

  • cold
  • warm (more common)
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44
Q

pathophysiology of cold autoimmune haemolytic anaemia

A

at temperatures <10c, autoantibodies attach themselves to RBCs and cause agglutination (clump together) resulting in destruction of RBCs

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45
Q

aetiology of cold autoimmune haemolytic anaemia

A

secondary to lymphoma, leukaemia, SLE, infection (mycoplasma, EBV, CMV, HIV)

46
Q

aetiology of warm autoimmune haemolytic anaemia

A

idiopathic

47
Q

mx of autoimmune haemolytic anaemia

A
  • blood transfusions
  • prednisolone
  • rituximab
  • splenectomy
48
Q

what is alloimmune haemolytic anaemia

A

foreign RBCs or foreign antibody circulating causing an immune reaction leading to destruction of RBCs (haemolysis)

49
Q

2 scenarios that can lead to alloimmune haemolytic anaemia

A
  1. transfusion reactions

2. haemolytic disease of the newborn

50
Q

what is microangiopathic haemolytic anaemia

A

small blood vessels have structural abnormalities causing haemolysis of blood cells travelling through them

51
Q

aetiology of microangiopathic haemolytic anaemia

A

normally secondary to another condition:

  • haemolytic uraemic syndrome
  • DIC
  • thrombotic thrombocytopaenic purpura
  • SLE
  • cancer
52
Q

mx of prosthetic valve haemolysis

A
  • monitoring
  • oral iron
  • blood transfusion if severe
  • revision surgery may be required in severe cases
53
Q

genetics of thalassaemia

A

autosomal recessive

54
Q

presentation of thalassaemia

A
  • microcytic anaemia
  • fatigue
  • pallor
  • jaundice
  • gallstones
  • splenomegaly
  • poor growth and development
  • pronounced forehead and cheekbones (expanded bone marrow)
55
Q

dx of thalassaemia

A
  • FBC -> microcytic anaemia
  • Hb electrophoresis to diagnose globin abnormalities
  • DNA testing
56
Q

when is thalassaemia screening offered

A

booking appointment in pregnancy (UK)

57
Q

how does iron overload occur in thalassaemia

A

faulty RBC creation, recurrent transfusions and increased absorption of iron in response to anaemia

58
Q

common complication in thalassaemia

A

iron overload

59
Q

monitoring for iron overload in thalassaemia

A

monitoring of serum ferritin levels

60
Q

mx of iron overload in thalassaemia

A

limiting transfusions

iron chelation

61
Q

complications of iron overload in thalassaemia

A
  • fatigue
  • liver cirrhosis
  • infertility and impotence
  • heart failure
  • arthritis
  • diabetes
  • osteoporosis and joint pain
62
Q

chromosome responsible in alpha thalassaemia

63
Q

chromosome responsible in beta thalassaemia

64
Q

mx of alpha thalassaemia

A
  • monitoring FBC
  • watch for complications
  • blood transfusions
  • splenectomy
  • bone marrow transplant -> can be curative
65
Q

types of beta thalassaemia and difference

A
  • thalassaemia major => both deletion genes
  • thalassaemia intermedia => both defective or one defective + one deletion
  • thalassaemia minor => only one abnormal (deletion or defective)
66
Q

disease course in thalassaemia minor

A

causes mild microcytic anaemia

pts usually only require monitoring and no active tx

67
Q

disease course in thalassaemia intermedia

A

causes more significant microcytic anaemia

pts require monitoring and occasional blood transfusions +/- iron chelation to avoid overload

68
Q

disease course in thalassaemia major

A

causes severe microcytic anaemia, splenomegaly and bone deformities

69
Q

mx of beta thalassaemia major

A
  • regular transfusions
  • iron chelation to avoid overload
  • splenectomy
  • bone marrow transplant (potentially curative)
70
Q

what is sickle cell anaemia

A

genetic condition causing sickle (crescent) shaped RBCs when deoxygenated meaning they are more fragile and susceptible to destruction -> haemolytic anaemia

71
Q

genetics of sickle cell anaemia

A

autosomal recessive condition where there is an abnormal gene for beta-globin on chromosome 11
one copy = trait, usually asymptomatic
two copies = disease

72
Q

how is sickle cell related to malaria

A

sickle cell is more common in patients from traditionally malaria affected areas
-> sickle cell trait (one copy) reduces severity of malaria therefore more prevalent through evolution

73
Q

when is sickle cell tested for

A

pregnancy in those at risk of being carriers

newborn screening heel prick test at 5 days old

74
Q

complications of sickle cell

A
  • anaemia
  • increased infection risk
  • stroke
  • avascular necrosis
  • pulmonary hypertension
  • painful and persistent erection (priapism)
  • CKD
  • sickle cell crises
  • acute chest syndrome
75
Q

lifestyle mx of sickle cell

A
  • avoid dehydration and other triggers

- vaccination

76
Q

medication mx of sickle cell

A
  • abx prophylaxis (pen v)

- hydroxycarbamide to stimulate production of foetal haemoglobin (doesn’t sickle)

77
Q

procedural mx options in sickle cell

A
  • blood transfusion in severe anaemia

- bone marrow transplant (may be curative)

78
Q

what is meant by sickle cell crises

A

spectrum of acute crises related to the condition which can be mild to life-threatening. may be spontaneous or triggered by stresses.

79
Q

stresses which may trigger sickle cell crises

A

infection
dehydration
cold
significant life events

80
Q

mx of sickle cell crises

A

supportive mx:

  • low threshold for admission
  • tx infection
  • keep warm
  • hydration
  • simple analgesia
  • penile aspiration in priapism
81
Q

4 examples of sickle cell crises

A
  1. vaso-occlusive crisis (painful crisis)
  2. splenic sequestration crisis
  3. aplastic crisis
  4. acute chest syndrome
82
Q

what is vaso-occlusive crisis

A

sickle cell crisis where sickle shaped RBCs clog capillaries causing distal ischaemia

83
Q

sx of vaso-occlusive crisis

A

pain
fever
sx of triggering infection
may cause priapism

84
Q

triggers for vaso-occlusive crisis

A

dehydration
infection
raised haematocrit

85
Q

what is splenic sequestration crisis

A

sickle cell crisis where RBCs block blood flow within spleen causing acutely enlarged and painful spleen
can lead to severe anaemia and hypovolaemic shock

86
Q

mx of splenic sequestration crisis

A 
emergency:
- blood transfusion to tx anaemia
- fluid resuscitation to tx shock
definitive:
- splenectomy
87
Q

what is aplastic crisis

A

temporary loss of creation of new RBCs causing severe anaemia

88
Q

trigger for aplastic crisis

A

parvovirus B19

89
Q

mx of aplastic crisis

A

blood transfusions if necessary

usually resolves spontaneously within a week

90
Q

what is acute chest syndrome

A

sickle sell crisis:

  • fever or respiratory sx with
  • new infiltrates seen on CXR
91
Q

causes of acute chest syndrome

A

infection (pneumonia, bronchiolitis)

non-infective (pulmonary vaso-occlusion, fat emboli)

92
Q

tx of acute chest syndrome

A

emergency:

  • abx or antivirals
  • blood transfusions
  • incentive spirometry (encourages effective and deep breathing)
  • artificial ventilation (NIV, intubation)
93
Q

5 causes of thrombocytopaenia related to production issues

A
  1. sepsis
  2. b12 or folate deficiency
  3. liver failure (reduced thrombopoietin production)
  4. leukaemia
  5. myelodysplastic syndrome
94
Q

6 causes of thrombocytopaenia related to destruction issues

A
  1. medications
  2. alcohol
  3. immune thrombocytopaenic purpura
  4. thrombotic thrombocytopaenia purpura
  5. heparin-induced thrombocytopaenia
  6. haemolytic uraemic syndrome
95
Q

medications that can cause thrombocytopaenia

A
  • heparin
  • sodium valproate
  • methotrexate
  • antihistamines
  • PPIs
96
Q

presentation of thrombocytopaenia

A
  • incidental finding
  • if count <50: nosebleeds, bleeding gums, menorrhagia, easy bruising, haematuria
  • if count <10: spontaneous IC or GI haemorrhage
97
Q

differentials for abnormal or prolonged bleeding

A
  • thrombocytopaenia
  • haemophilia A or B
  • von willebrand disease
  • DIC secondary to sepsis
98
Q

what is ITP

A

immune thrombocytopaenia purpura

antibodies created against platelets causing an immune response that destroys the platelets

99
Q

4 medical mx options for ITP

A
  • prednisolone
  • IV Ig
  • rituximab
  • splenectomy
100
Q

general mx/advice in ITP

A
  • safety net about concerning bleeding e.g. melaena, persistent headaches
  • control BP
  • suppress periods
101
Q

what is TTP

A

thrombotic thrombocytopaenia purpura
tiny blood clots develop throughout small vessels of body and use up platelets resulting in thrombocytopaenia, bleeding under the skin etc.
= microangiopathy

102
Q

pathophysiology of TTP

A

blood clots develop in small vessels throughout the body in response to a lack of protein ADAMTS13 (normally inactivates vWF to prevent clot formation)
clots lead to haemolytic anaemia and use up platelets causing thrombocytopaenia

103
Q

aetiology of TTP

A
  • inherited gene mutation causing deficiency in ADAMST13 protein
  • autoimmune conditions creating antibodies against ADAMST13 protein
104
Q

tx options in TTP

A
  • plasma exchange
  • steroids
  • rituximab
105
Q

what is von Willebrand disease

A

most common inherited cause of abnormal bleeding due to problem with von Willebrand factor

106
Q

genetics of von willebrand disease

A

autosomal dominant

107
Q

presentation of von willebrand disease

A

hx of easy, prolonged or heavy bleeding

  • bleeding gums
  • nose bleeds
  • menorrhagia
  • heavy bleeding during surgery
  • FHx heavy bleeding or von willebrand disease
108
Q

mx of von willebrand disease

A

only required in response to major bleeding or trauma or in preparation for operations:

  • desmopressin stimulates release of vWF
  • vWF infusion
  • factor VIII
109
Q

mx of menorrhagia in von willebrand disease

A
  • tranexamic acid
  • mefanamic acid
  • norethisterone
  • COCP
  • Mirena coil
110
Q

pentad of symptoms/signs in thrombotic thrombocytopaenic purpura

A
  1. fever
  2. altered mental state
  3. thrombocytopaenia
  4. haemolytic anaemia
  5. renal impairment

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