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Finals Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

Aetiology of Acute Myeloblastic Leukaemia

A

Malignant proliferation of precursor myeloblasts in bone marrow

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2
Q

Risk factors for Acute Myeloblastic Leukaemia

A

Other haematological disorders, exposure to radiation, chemotherapy, Down’s syndrome, Neurofibromatosis, exposure to Benzene, increasing age

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3
Q

What is the most common Acute Leukaemia in adults?

A

Acute Myeloblastic Leukaemia

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4
Q

Presentation of Acute Myeloblastic Leukaemia

A

Anaemia, leukopenia (infections), thrombocytopenia (bleeding), infiltration of leukaemic cells (hepatosplenomegaly, gum hypertrophy)

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5
Q

Diagnosis of Acute Myeloblastic Leukaemia

A

Bone marrow- blast cells > 20% in blood/bone marrow

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6
Q

Management of Acute Myeloblastic Leukaemia

A

Supportive- fertility cryopreservation, blood products
Chemotherapy
Bone marrow transplant

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7
Q

Prognosis of Acute Myeloblastic Leukaemia

A

50% 5-year survival

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8
Q

What is Acute Lymphoblastic Leukaemia?

A

Malignant proliferation of lymphoblast precursor cells in bone marrow, mostly B cells
Lymphoblast precursor cells proliferate and replace normal cells of bone marrow- spill into peripheral circulation

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9
Q

What is the most common cancer in children?

A

Acute Lymphoblastic Leukaemia

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10
Q

What is the most common age of presentation of Acute Lymphoblastic Leukaemia?

A

Age 2-4 years

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11
Q

Presentation of Acute Lymphoblastic Leukaemia

A

Fatigue, dizziness, palpitations, bone and joint pain, infections, fever, splenomegaly, dyspnoea, thrombocytopenia, pallor, petechiae, lymphadenopathy

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12
Q

Diagnosis of Acute Lymphoblastic Leukaemia

A

Bone marrow- blast cells > 20% in blood/bone marrow

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13
Q

How is Acute Lymphoblastic Leukaemia classified?

A

Into B and T cells

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14
Q

Management of Acute Lymphoblastic Leukaemia

A

Chemotherapy/Radiotherapy, stem cell transplant

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15
Q

Prognosis of Acute Lymphoblastic Leukaemia

A

80% cured

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16
Q

What is Chronic Lymphoblastic Leukaemia?

A

Malignant proliferation of mature lymphocytes, usually B cells

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17
Q

Presentation of Chronic Lymphoblastic Leukaemia

A

Lymphocytosis in blood
Lymphadenopathy
Splenomegaly

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18
Q

Management of Chronic Lymphoblastic Leukaemia

A

Chemotherapy

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19
Q

What is Chronic Myeloid Leukaemia?

A

Proliferation of mature myeloid cells

- neutrophils, basophils, eosinophils

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20
Q

Which genetic mutation is linked to Chronic Myeloid Leukaemia?

A

Philadelphia chromosome t9;22 chromosomal translocation

–> tyrosine kinase activity

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21
Q

Management of Chronic Myeloid Leukaemia

A

Imatinib is a tyrosine kinase inhibitor

Cured by bone marrow transplant

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22
Q

Which age group is affected by Chronic Myeloid Leukaemia?

A

Middle aged to elderly

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23
Q

Where is lymphoma found?

A

Mostly in lymph nodes, but also in blood, bone marrow, spleen, liver

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24
Q

Aetiology of lymphoma

A

Cancer of lymphatic system- malignant growth of lymphocytes (WBCs)

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25
Q

Which age groups are affected by Hodgkin’s Lymphoma?

A

Young adults + Elderly

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26
Q

Presentation of Hodgkin’s Lymphoma

A

Painless lymphadenopathy, hepatosplenomegaly, B symptoms, anaemia
Lump in neck painful on alcohol consumption

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27
Q

Investigation of Hodgkin’s Lymphoma

A

Lymph node biopsy- Reed Sternberg cells

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28
Q

What is found on lymph node biopsy in Hodgkin’s Lymphoma?

A

Reed Sternberg cells

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29
Q

Management of Hodgkin’s Lymphoma

A

Stage 1-2a: short combo chemotherapy then radiotherapy
Stage 2a-4a: longer combo chemo
Relapse: high dose chemo then autologous bone marrow transplant
Rituximab: anti-CD20

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30
Q

Which group of people are most likely to get Non-Hodgkin’s Lymphoma?

A

Immunodeficient- drugs, HIV

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31
Q

How is Non-Hodgkin’s Lymphoma classified?

A

Cell of origin: T or B

Stage of lymphatic maturation- high grade or low grade

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32
Q

What are high grade Non-Hodgkin’s Lymphomas?

A

Diffuse large B cell lymphoma

Burkitt Lymphoma

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33
Q

What are low grade Non-Hodgkin’s Lymphomas?

A

Follicular Lymphoma

Splenic marginal zone lymphoma

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34
Q

Presentation of Non-Hodgkin’s Lymphoma

A

Painless superficial lymphadenopathy, B symptoms, pancytopenia
Extra-nodal disease: Gastric MALT, small bowel lymphomas, skin, bone, oropharynx, CNS, lung

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35
Q

Aetiology of Multiple Myeloma

A

Malignant proliferation of plasma cells in bone marrow

  • B cells that produce Ig
  • Bone marrow destruction + failure from infiltration
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36
Q

What is the spectrum of pre-malignant conditions for Multiple Myeloma?

A

MGUS (Monoclonal Gammopathy of Undetermined Significance)

  • -> Asymptomatic Myeloma
  • -> Multiple Myeloma
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37
Q

What is the peak age for Multiple Myeloma?

A

Age 70

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38
Q

How is Multiple Myeloma classified?

A

By antibody

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39
Q

Which is the most common type of Multiple Myeloma?

A

IgG

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40
Q

Features of Multiple Myeloma

A

CRAB:

  • hyperCalcaemia due to bone resorption
  • Renal failure- deposition of light chains in renal tubules
  • Anaemia (normocytic)
  • Bony lesions- pain or pathological fractures
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41
Q

X-ray findings in Multiple Myeloma

A

Lytic bone lesions eg pepper-pot skull
Vertebral collapse
Fractures
Osteoporosis

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42
Q

Management of Multiple Myeloma

A 
Chemo then autologous bone marrow transplant 
Correct anaemia
Fluids for renal failure
Manage infection
Analgesia/radiotherapy for bone pain
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43
Q

How are MGUS, Asymptomatic myeloma and Multiple myeloma differentiated?

A 
MGUS:
- <10% plasma cells
- +ve monoclones
- Asymptomatic
Asymptomatic myeloma:
- >10% plasma cells
- +ve monoclones
- Asymptomatic
Multiple myeloma:
- >10% plasma cells
- +ve monoclones
- Symptomatic
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44
Q

What is Systemic Sclerosis?

A

Autoimmune production of antibodies –> abnormalities in small blood vessels, fibrosis of skin and internal organs due to excessive collagen production and deposition, immune activation

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45
Q

Types of Systemic Sclerosis

A

Diffuse or Limited

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46
Q

Presentation of limited Systemic Sclerosis

A

CREST

  • Calcinosis
  • Raynaud’s
  • oEsophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
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47
Q

Which antibodies may be present in Systemic Sclerosis?

A

Anti-topoisomerase I
Anti-centromere (ACA) - limited
Anti-RNA polymerase III - diffuse

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48
Q

Management of Systemic Sclerosis

A

Symptomatic treatment

Immunotherapy- Methotrexate

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49
Q

Mechanism of action of Heparin

A

Binds to antithrombin + increases its activity, indirect thrombin inhibitor

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50
Q

How can Heparin be monitored?

A

APTT

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51
Q

How is LMW Heparin excreted?

A

Renally excreted

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52
Q

Mechanism of action of aspirin

A

COX inhibitor, inhibits thromboxane formation –> inhibits platelet aggregation

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53
Q

Mechanism of action of Clopidogrel

A

Inhibits ADP-induced platelet aggregation

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54
Q

Mechanism of action of Warfarin

A

Prevents synthesis of Factor 2, 7, 9, 10; antagonises vitamin K, prolongs PT

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55
Q

How can Warfarin be monitored?

A

INR- target 2-3

Also prolongs PT

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56
Q

How can Warfarin be reversed?

A

Vitamin K or FFP

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57
Q

What is target INR for somebody on Warfarin therapy?

A

2-3 (normal < 1)

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58
Q

Mechanism of action of DOACs

A

Direct Oral Anticoagulants
Anti-IIa and Anti-Xa inhibitors
- Rivaroxaban + Apixaban- Xa
- Dabigatran- direct thrombin inhibitor

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59
Q

How can DOACs be reversed?

A

Beriplex

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60
Q

Name the 4 blood groups

A

A, B, AB, O

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61
Q

What type of immunoglobulin crosses the placenta in rhesus disease?

A

IgG anti-D

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62
Q

What coagulation disorder does bleeding into muscles and joints suggest?

A

Haemophilia

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63
Q

How do mucocutaneous bleeding disorders present?

A

Easy bruising, prolonged bleeding, epistaxis, gum bleeding, GI blood loss

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64
Q

What is the function of Neutrophils?

A

Phagocytose and kill bacteria

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65
Q

What is the function of Monocytes?

A

Produced in bone marrow and enter tissues as macrophages, some become dendritic cells which present antigens to the immune system

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66
Q

What is the function of Basophils?

A

Migrate to tissues and become mast cells, contain granules of histamine, surface IgE

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67
Q

What is the function of Eosinophils?

A

Protection against parasites, role in inflammation and allergy

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68
Q

What is the function of Lymphocytes?

A

Immunity, generate antibodies against foreign antigen, some have memory –> vaccination

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69
Q

Risk factors for Arterial thrombosis

A

Smoking, hypertension, diabetes, obesity, stress, hyperlipidaemia

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70
Q

How does Arterial thrombosis present?

A

MI
CVA
PVD

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71
Q

Management of Arterial thrombosis

A

Thrombolytics- alteplase, streptokinase

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72
Q

How does Venous thrombosis present?

A

PE

DVT

73
Q

Investigations for Venous thrombosis

A

D-dimer, Doppler, CTPA

74
Q

Risk factors for Venous thrombosis

A

Surgery, immobilisation, oestrogens, malignancy, Factor V Leiden, Antithrombin deficiency, Protein C/S deficiency

75
Q

Management of Venous thrombosis

A

LMW Heparin initially

Then oral Warfarin for 3-6mths (depending on provoked vs unprovoked)

76
Q

Prevention of Venous Thrombosis

A

Prevention: LMWH, TEDs hydration, early mobilisation

77
Q

Hazards of blood transfusion

A

Early: ABO incompatibility reaction, fluid overload, febrile/urticarial reaction, bacterial/malarial reaction
Late: RhD/Antibody sensitisation, delayed transfusion reaction, Hep B/C, HIV, CJD, iron overload

78
Q

Indications for FFP transfusion

A

Liver disease, DIC, dilutional coagulopathy

79
Q

Indications for Platelet transfusion

A

To correct bleeding due to thrombocytopenia

80
Q

Why does liver disease cause bleeding disorders?

A

Liver is the site of synthesis of coagulation factors and fibrinogen
–> Prolonged bleeding + PT time

81
Q

Why does vitamin K deficiency cause bleeding disorders?

A

Vitamin K is needed for synthesis of coagulation factors 2, 7, 9 and 10
Deficiency –> prolonged bleeding and PT time

82
Q

How is vitamin K deficiency prevented?

A

Subcut vitamin K injection in all newborn babies

83
Q

How is Haemophilia inherited?

A

Sex-linked: males affected, female carriers

84
Q

Which type of Haemophilia is more common?

A

A is more common than B

85
Q

Which blood test is abnormal in Haemophilia?

A

Raised APTT- as measures factor 8+9

86
Q

What is deficient in i) Haemophilia A and ii) Haemophilia B?

A

A: deficiency of factor 8
B: deficiency of factor 9

87
Q

Presentation of Haemophilia

A

Severe bleeding disorder- bleed into muscles and joints

88
Q

Management of Haemophilia

A

Recombinant factor 8 (A) or 9 (B)

89
Q

What is the inheritance pattern of Thalassaemia?

A

Autosomal recessive

90
Q

Aetiology of Thalassaemia

A

Decreased or absent of 1 or more polypeptide chains (a or B) that form Hb
–> reduced Hb in red cells –> anaemia

91
Q

How does Thalassaemia trait present?

A

Asymptomatic

92
Q

How does Alpha thalassaemia present?

A

Lethal in utero

93
Q

How does Beta thalassaemia major present?

A

Anaemia- ‘Cooley’s anaemia’

94
Q

When is Thalassaemia screened for?

A

Conceptual screening

95
Q

How is Thalassaemia diagnosed?

A

Hb electrophoresis

96
Q

Investigations in Thalssaemia

A

Hb electrophoresis for diagnosis
Conceptual screening
Skeletal survey

97
Q

What are the findings in a skeletal survey in Thalassaemia?

A

Skull x-ray: hair-on-end appearance
Deformed ribs, long bones + flat bones
CXR: Cardiomegaly + cardiac failure

98
Q

How is Thalassaemia staged?

A

Stage 1-3 based on symptoms, transfusions, echo + ECG

99
Q

Management of Thalassaemia

A

Thalassaemia intermedia- occasional transfusions

Thalassaemia major- regular hypertransfusion, iron chelation- Desferrioxamine to avoid overload

100
Q

Which blood test result can be skewed in Thalassaemia?

A

HbA1c

101
Q

Aetiology of Von-Willebrand’s disease

A

Congenital (type 1, 2 or 3) or Acquired (lymphoproliferative/myeloproliferative disorders)
vWF assists platelet plug formation by attracting platelets to site of damage, binds to factor 8 to prevents its clearance from plasma
–> Platelet dysfunction
–> Deficience of Factor VIII

102
Q

Management of Von-Willebrand’s disease

A

Educate to bleeding risk, avoid NSAIDs, anti-platelets
Tranexamic acid for minor bleeding
Desmopressin increases factor 8 + vWF temporarily by releasing endothelial stores
COCP/IUCD for menorrhagia

103
Q

What is the aetiology of Immune thrombocytopenia?

A

Autoimmune disorder with reduced platelets
Antibodies bind to platelet antigens
–> platelet destruction and inhibition of platelet production

104
Q

Causes of Immune thrombocytopenia

A

Secondary to anti-phospholipid syndrome, SLE, viral infections (CMV, HIV, HCV), H pylori, lymphoproliferative disorders
Following immunisations in children

105
Q

How is persistent and chronic Immune thrombocytopenia defined?

A

Persistent: 3-12mths
Chronic: > 12 months

106
Q

Prognosis of immune thrombocytopenia

A

Usually recovers after 6-8 weeks

107
Q

Presentation of immune thrombocytopenia

A

Asymptomatic or petechiae, bruising, epistaxis, haematuria, GI bleeds, menorrhagia, intracranial bleeds

108
Q

Management of Immune thrombocytopenia

A

Trauma prevention, avoid NSAIDs + aspirin

Prednisolone, anti-D, immunisations, IVIg

109
Q

Aetiology of Disseminated Intravascular Coagulation

A

Systemic activation of blood coagulation, which generates fibrin –> thrombosis of medium and small vessels –> organ dysfunction
Simultaneous bleeding and microvascular thrombosis

110
Q

Causes of Disseminated Intravascular Coagulation

A

Sepsis, eclampsia, leukaemia, major trauma, transplant rejection, surgery, recreational drugs, transfusion reaction

111
Q

Presentation of Disseminated Intravascular Coagulation

A

Bleeding from unrelated sites, large bruises, confusion, fever, petechiae/purpura, haemorrhagic bullae, thrombosis

112
Q

How is Disseminated Intravascular Coagulation staged/scored?

A

International society of thrombosis and haemostasis score based on blood tests

113
Q

Management of Disseminated Intravascular Coagulation

A

Treat the cause

Platelet transfusion, FFP, LMW Heparin- all based on symptoms

114
Q

What level of Hb is classed as anaemia?

A

125 in men

115 in women

115
Q

How is anaemia classified?

A

By MCV:

  • < 80 = Microcytic
  • 80-100 = Normocytic
  • > 100 = Macrocytic
116
Q

Causes of microcytic anaemia

A

Iron deficiency
Thalassaemia
Chronic disease

117
Q

Causes of normocytic anaemia

A

Acute bleeding
Haemolysis
Aplastic anaemia
Chronic disease

118
Q

Causes of Macrocytic anaemia

A

Vit B12/Folate deficiency
Hypothyroidism
Pernicious anaemia eg Addison’s/Graves

119
Q

Causes of Polycythaemia

A

True:
- Epo driven- COPD, cysts/tumours
- Epo independent- Polycythaemia rubra vera
Not true- volume depletion

120
Q

Aetiology of Polycythaemia Rubra Vera

A

Too many RBCs produced in bone marrow

JAK-2 mutation

121
Q

Presentation of Polycythaemia Rubra Vera

A

Fatigue, pruritus (worse after hot shower), splenomegaly, thrombosis, peptic ulceration, bleeding, erythromelalgia (burning pain and redness in body), cyanosis with high Hb

122
Q

Diagnostic criteria for Polycythaemia Rubra Vera

A

Hb, JAK-2, Bone marrow biopsy, erythropoeitin

123
Q

Management of Polycythaemia Rubra Vera

A 
Long-term phlebotomy
Low dose aspirin
JAK2 inhibtiros- Ruxolitinib
Anti-histamines for pruritus
Cytoreductive treatments- Hydroxycarbamide
124
Q

Causes of secondary immunodeficiency

A

Malignancy, drugs (cytotoxic), HIV, malnutrition, protein loss (nephrotic syndrome)

125
Q

Features of immunodeficiency

A

Infections- opportunistic eg PCP
FTT, diarrhoea
Vasculitis, arthritis
Gastric carcinoma, Liver disease

126
Q

Management of Immunodeficiency

A

Healthy lifestyle, dental checks
Live vaccines contraindicated in T cell deficiency
Prophylactic antibiotics/antivirals for some
IV/Subcut Ig replacement
T cell deficiency –> bone marrow transplant

127
Q

What is Aplastic Anaemia?

A

Pancytopenia with hypocellular bone marrow in the absence of abnormal infiltrate or marrow fibrosis

128
Q

At what age groups does aplastic anaemia peak?

A

10-25 and over 60s

129
Q

Causes of Aplastic Anaemia

A 
Majority idiopathic
Congenital eg Fanconi's anaemia
Acquired infection eg EBV
Drugs eg Naproxen
Toxic exposure
Pregnancy
Sickle cell aplastic crisis
130
Q

Features of Aplastic Anaemia

A

Anaemia, thrombocytopenia, infection

131
Q

Diagnosis of Aplastic Anaemia

A

Hb < 100
Platelets < 50
Neutrophils < 1.5

132
Q

Management of Aplastic Anaemia

A 
Haematopoeitic stem cell transplant
Immunosuppressants
Blood/platelet transfusion
Iron chelation
Prophylactic antibiotics + antifungals
133
Q

What is the inheritance pattern of G6PD deficiency?

A

X-linked

134
Q

Aetiology of G6PD deficiency

A

Low G6PD –> low glutathione –> increased red cell susceptibility to oxidative stress –> Neonatal jaundice, intravascular haemolysis, gallstones, splenomegaly

135
Q

Presentation of G6PD deficiency

A

Neonatal jaundice
Intravascular haemolysis
Gallstones
Splenomegaly

136
Q

What is seen on blood film in G6PD deficiency?

A

Heinz bodies

Bite + blister cells

137
Q

How is G6PD deficiency diagnosed?

A

G6PD enzyme assays

138
Q

What is G6PD?

A

Glucose-6-phosphate dehydrogenase, deficiency can lead to haemolytic anaemia

139
Q

Which drugs can trigger haemolysis in G6PD deficiency?

A

Primaquine, Ciprofloxacin, Sulphonamides, Sulfasalazine, Sulphonylureas

140
Q

Causes of iron deficiency anaemia

A

Reduced intake
Increased requirement: pregnancy, childbirth, coeliac disease
Chronic blood loss- GI/menorrhagia

141
Q

Management of iron deficiency anaemia

A

Treat the cause
Ferrous sulphate 200mg oral TDS until Hb normal then 3 months to rebuild stores
Consider IV if caused by malabsorption

142
Q

Causes of B12 deficiency

A

Lack of intrinsic factor- pernicious anaemia (gastrectomy)

Failure of absorption in terminal ileum- resection, Coeliac

143
Q

Management of B12 deficiency anaemia

A

Parenteral Hydroxocobalamin (B12)

144
Q

What other problem can B12 deficiency cause other than anaemia?

A

Peripheral neuropathy

145
Q

What is folate necessary for in the body?

A

DNA synthesis

146
Q

Causes of folate deficiency

A

Dietary, malabsorption (Coeliac)

Increased requirement- pregnancy, drugs, psoriasis

147
Q

Management of Folate deficiency

A

Oral folate 5mg daily

148
Q

Causes of Haemolytic anaemia

A

Congenital: hereditary spherocytosis, G6PD deficiency, sickle cell, thalassaemia
Acquired: haemolytic disease of the newborn, blood transfusion reaction, SLE, trauma, DIC, haemolytic uraemic syndrome, liver disease

149
Q

Presentation of Haemolytic Anaemia

A

Severe anaemia

Gallstones, haemoglobinuria, splenomegaly

150
Q

What is found on blood tests in Haemolytic Anaemia?

A

Low Hb

High reticulocytes

151
Q

Management of Haemolytic Anaemia

A

Folic acid
Discontinue causative drugs
Iron therapy
Splenectomy

152
Q

What is the inheritance pattern of Hereditary spherocytosis?

A

Autosomal dominant

153
Q

What is Hereditary spherocytosis?

A

Autosomal dominant defect of the RBC cytoskeleton

154
Q

Presentation of Hereditary spherocytosis

A

FTT, jaundice, gallstones, splenomegaly, aplastic crisis, haemolysis

155
Q

Investigations in Hereditary spherocytosis

A

Blood film- spherocytes

Cryohaemolysis test + EMA binding

156
Q

Management of Hereditary spherocytosis

A

Folate replacement + Splenectomy

157
Q

What is the inheritance pattern of Sickle Cell Disease?

A

Autosomal recessive

158
Q

Aetiology of Sickle cell disease

A

Forms abnormal Hb molecule
Sickled cells have reduced deformability and are easily destroyed –> occlusion of microcirculation + chronic haemolytic anaemia

159
Q

In which region is Sickle Cell Disease most prevalent?

A

Sub-Saharan Africa

160
Q

When does Sickle Cell Disease present?

A

Symptoms appear at 3-6 months when HbF is falling

161
Q

Presentation of Sickle Cell Disease

A

Anaemia, jaundice, pallor, lethargy, growth restriction, infections, splenomegaly, delayed puberty, priapism

162
Q

How is Sickle Cell Disease diagnosed?

A

Blood films, sickle solubility test, Hb analysis

163
Q

How is Sickle Cell Disease screened for?

A

Neonatal blood spot, preconceptual, preop, prenatal

164
Q

What genotype is Sickle cell trait?

A

Heterozygous HbAS

165
Q

What genotype is Sickle cell anaemia?

A

Homozygous HbSS

166
Q

How does Sickle cell trait present?

A

Usually asymptomatic

Haematuria, renal papillary necrosis, splenic infarction, renal medullary cancer, exercise-related sudden death

167
Q

How is Sickle cell trait diagnosed?

A

Presence of HbAS on Hb electrophoresis

168
Q

Management of Sickle cell trait

A

Adequate hydration, avoid exertion/heat

169
Q

Name the Sickle cell crises

A
  • Vaso-occlusive crisis
  • Aplastic crisis
  • Sequestration crisis
  • Acute chest syndrome
  • Hyperhaemolytic crisis
170
Q

Aetiology of Vaso-occlusive crisis in Sickle Cell Disease

A

Obstruction of micro-circulation by sickled cells

Precipitated by cold, infection, dehydration, exertion, ischaemia

171
Q

What can Vaso-occlusive crisis in Sickle Cell Disease be precipitated by?

A

Cold, infection, dehydration, exertion, ischaemia

172
Q

Presentation of Vaso-occlusive crisis in Sickle Cell Disease

A

Swollen painful joints, tachypnoea, neuro signs, abdominal distension, pain, stroke, placental infarction

173
Q

Aetiology of Aplastic crisis in Sickle cell disease

A

Temporary cessation of erythropoeisis

Usually precipitated by Parvovirus 19

174
Q

What is Aplastic crisis in Sickle cell disease usually precipitated by?

A

Parvovirus 19

175
Q

Presentation of Aplastic crisis in Sickle cell disease

A

Severe anaemia

176
Q

Aetiology of Sequestration crisis in Sickle cell disease

A

Sudden enlargement of spleen

–> reduced Hb concentration, circulatory collapse and hypovolaemic shock

177
Q

What is Acute chest syndrome in Sickle cell disease?

A

Vaso-occlusive crisis affecting the lungs

178
Q

Management of Sickle Cell Disease

A
  • Monitoring, educational, psychological
  • Folic acid + zinc supplements
  • Penicillin prophylaxis, pneumococcal vaccine, malaria chemoprophylaxis
  • Blood transfusions
  • Hydroxycarbamide to increase HbF
  • Bone marrow transplant
  • Annual transcranial doppler
179
Q

What annual screening test needs to be done in Sickle cell disease?

A

Annual transcranial doppler

Finals Revision (13 decks)

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