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Finals > Haem > Flashcards

Haem Flashcards

1
Q

What is the epidemiology of iron deficiency anaemia (4)

A
  • Most common cause of anaemia
  • Seen in 14% of menstruating women
  • Develops on inadequate iron for Hb synthesis
  • Microcytic
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2
Q

What are the causes of iron deficiency anaemia (4)

A
  • Bleeding
  • Poor diet
  • Malabsorption
  • Inc. demand eg. growth/pregnancy
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3
Q

How might iron deficiency anaemia present (6)

A
  • Fatigue, Headache, Syncope
  • Palpitations/chest pain
  • Anorexia
  • Shortness of breath
  • Brittle nails/hair
  • Mouth ulcers
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4
Q

How do you diagnose iron deficiency anaemia (6)

A
  • FBC and blood film
    • Decreased MCV
    • Decreased Hb
    • Hypochromic
    • Decreased serum Ferritin/iron (diagnostic)
    • Increased Transferrin receptors
    • Decreased reticulocytes
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5
Q

How do you treat iron deficiency anaemia

A
  • Oral iron (ferrous sulphate)
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6
Q

What is the epidemiology of anaemia of chronic disease (2)

A
  • 2nd most common cause

- Can be normocytic or microcytic (and hypochromic)

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7
Q

What can cause anaemia of chronic disease (3)

A
  • Decreased erythropoetin release
  • Decreased Fe release from bone marrow to erythroblasts
  • Increased RBC death
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8
Q

How might anaemia of chronic disease present (5)

A
  • Headache, fatigue, syncope
  • Chest pain/palpitations
  • Anorexia
  • Breathlessness
  • Chronic disease (fucking obviously)
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9
Q

How would you diagnose anaemia of chronic disease (4)

A
  • FBC and blood film
    • Decreased Hb
    • Decreased or normal MCV
    • Low iron
    • Normal or high transferrin (inflammation)
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10
Q

How do you treat anaemia of chronic disease

A
  • Treat underlying cause

- EPO in kidney or inflammatory disease

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11
Q

What can cause normocytic anaemia (3)

A
  • Pregnancy
  • Acute blood loss
  • Chronic disease
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12
Q

What are the risk factors for B12 deficiency anaemia (4)

A
  • Lack of intrinsic factor (pernicious)
  • Vegan (B12 found in meat, dairy, fish but not plants)
  • Blue eyes, fair hair
  • Thyroid disease
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13
Q

Describe the pathophysiology of pernicious anaemia

A
  • Intrinsic factor binds to B12 to absorb it
  • In pernicious anaemia there is autoimmune attack of parietal cells that secrete intrinsic factor
  • This leads to B12 deficiency
  • B12 is required for thymine hence protein synthesis
  • So due to slowed protein synthesis RBCs mature for longer hence macrocytic and less are produced
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14
Q

How might someone with B12 deficiency present (4)

A
  • Normal anaemia symptoms
  • Lemon coloured skin (mild jaundice due to body breaking down large RBC as they are abnormal and pallor)
  • Big red beefy tongue
  • Mouth ulcers
  • Focal neurology if B12 is very low
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15
Q

How do you diagnose B12 deficiency anaemia (4)

A
  • FBC and blood film
    • Decreased Hb
    • Increased MCV
    • Decreased B12
    • May be raised bilirubin
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16
Q

How do you treat B12 deficiency anaemia (2)

A
  • If dietary dive oral B12 supplements

- If malabsorption eg. pernicious give injections (hydroxocobalamin)

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17
Q

What can cause Folate deficiency anaemia (2)

A
  • Malabsorption (eg. crohns or coeliac)

- Poor diet (folate found in green vegetables)

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18
Q

Describe the pathophysiology of folate deficiency anaemia

A
  • Folate is also required for protein synthesis

- So due to slowed protein synthesis RBCs mature for longer hence macrocytic and less are produced

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19
Q

How might folate deficiency present

A
  • Normal anaemia symptoms
  • Lemon coloured skin (mild jaundice due to body breaking down large RBC as they are abnormal and pallor)
  • Big red beefy tongue
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20
Q

How do you diagnose folate deficiency anaemia

A
  • FBC and blood film
    • Low Hb
    • High MCV
    • Low folate
    • May be high bilirubin
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21
Q

How do you treat folate deficiency anaemia

A
  • Oral folate tablets (be wary of B12 levels)
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22
Q

Describe the pathophysiology of the thalassaemias

A
  • Alpha and Beta
  • Genetic disease causing underproduction of A or B chain
  • This results in RBC precursor death (decreased erythropoesis)
  • Also results in increased haemolysis due to A and B chain imbalance
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23
Q

How might Beta thalassaemia present (6)

A
  • Normal anaemia symptoms
  • Leg ulcers
  • Increased infections
  • Splenomegaly
  • Gallstones
  • Bone deformity
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24
Q

How do you diagnose Beta thalassaemia

A
  • FBC and Blood film
    • Microcytic hypochromic
    • Raised reticulocytes
    • Raised serum iron
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25
Q

How would you treat Alpha/Beta thalassaemia (3)

A
  • Lifelong blood transfusions
  • Bone marrow transplant
  • Agents to increased iron excretion
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26
Q

What is the epidemiology of sickle cell anaemia (2)

A
  • More common in Africans

- Autosomal recessive

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27
Q

Describe the pathophysiology of sickle cell anaemia

A
  • Adenine to thymine substitution mutation
  • Valine is produced instead of glutamic acid on Beta chain
  • This causes RBCs to become insoluble and polymerise when deoxygenated
  • This leads to the characteristic sickle shape
  • This causes blockage of small vessels leading to infarct and pain and increased haemolysis
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28
Q

How might sickle cell anaemia present (6)

A
  • Acute hand and feet pain
  • Long bone pain
  • Increased infections
  • Pulmonary hypertension
  • Acute chest syndrome
  • Children have growth/development issues
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29
Q

How would you diagnose sickle cell anaemia (2)

A
  • FBC and blood film
    - Normal Hb
    - Sicle shaped cell
  • Gel electrophoresis confirms diagnosis
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30
Q

How do you treat sickle cell anaemia (4)

A
  • Acute attacks
    • Fluids/oxygen
    • Analgesia
  • Stem cell transplant
  • Blood transfusion
  • Oral hydroxycarbamide (increases HbF)
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31
Q

What is polycythaemia

A
  • An increase in Hb, PCV (haematocrit), and red cell count
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32
Q

What can cause polycythaemia (4)

A
  • Primary
    • Polycythaemia Vera
    • EPO receptor mutation
  • Secondary
    • Hypoxia
    • Inappropriate EPO secretion
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33
Q

What is the epidemiology of Polycythaemia vera (2)

A
  • Over 60

- Genetic association

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34
Q

Describe the pathophysiology of polycythaemia vera

A
  • Malignant proliferation of pluripotent stem cell
  • Causes increased production of RBC, WC and platelets
  • Causes hyper viscosity and thrombosis
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35
Q

How might polycythaemia vera present (6)

A
  • Headache
  • Tinnitus
  • Itching (worse on heat)
  • Dizziness
  • Burning in fingers and toes
  • Hepatosplenomegaly
36
Q

How do you diagnose polycythaemia vera (2)

A
  • FBC
    • Raised Hb, RBC, WCC and platelets
  • JAK2 mutation on screening
37
Q

How do you treat polycythaemia vera (2)

A
  • Venesection

- Low dose aspirin

38
Q

What is the epidemiology of DVT (3)

A
  • Occurs in 25-50% of surgical patients
  • 65% are asymptomatic
  • Commonly occur after periods of immobilisation
39
Q

What can cause DVT (4)

A
  • Immobilisation
    • Surgery
    • Plane journey
    • Leg fracture
  • Genetic
40
Q

When is DVT a concern

A
  • When it is above the knee (can be fatal)

- Below the knee is not too much of a concern

41
Q

What are the risk factors for DVT (7)

A
  • Increasing age
  • Surgery
  • Immobilisation
  • Cancer
  • Past DVT
  • Obesity
  • Pregnancy
42
Q

How might DVT present (3)

A
  • Pain, warm, red, swollen
  • Oedema
  • Cyanosis
43
Q

How would you diagnose DVT (2)

A
  • Plasma D dimer
    • Clot breakdown product
    • Raised if not diagnostic but normal rules our
  • Compression ultrasound
44
Q

How do you treat DVT

A
  • LMW heparin (SC. enoxaparin)
  • Low dose aspirin
  • Compression stockings and mobility
  • IVC filter to decrease risk of PE
45
Q

What can cause thrombocytopenia (2)

A
  • Decreased production

- Increased destruction

46
Q

What is immune thrombocytopenia purpura (ITP)

A
  • Autoimmune destruction of platelets leading to thrombocytopenia
47
Q

Describe primary ITP (3)

A
  • Acute, usually in ages 2-6
  • Muco-cutaneous bleeding, rarely haemorrhage
  • Sudden onset purpura
48
Q

Describe secondary ITP (2)

A
  • Chronic, usually in adults

- Muco-cutaneous bleeding/purpura

49
Q

How might someone with ITP present (5)

A
  • Easy bruising
  • Heavy nose bleed
  • Menorrhagia
  • Purpura
  • Gum bleeding
50
Q

How do you diagnose ITP (2)

A
  • FBC low platelets

- Bone marrow biopsy

51
Q

How do you treat ITP

A
  • Prednisolone
  • IV IgG
  • Splenectomy (2nd line)
52
Q

What are the 4 types of leukaemia

A
  • Acute lymphoblastic
  • Acute myeloid
  • Chronic myeloid
  • Chronic lymphocytic
53
Q

What is the epidemiology of acute lymphoblastic leukaemia (3)

A
  • Most common childhood cancer
  • B-cell precursors = children, T-cell precursors = adults
  • Most common between 2-4
54
Q

Describe the pathophysiology of acute lymphoblastic leukaemia

A
  • Malignancy (uncontrolled proliferation) of B/T cell precursors called lymphoblasts
  • Most commonly the B cell precursors
55
Q

How might acute lymphoblastic leukaemia present (4)

A
  • Marrow failure
    • Anaemia (standard symptoms)
    • Infection (low WC)
    • Bleeding (low platelets)
  • Metastases (lymphadenopathy etc.)
56
Q

How do you diagnose acute lymphoblastic leukaemia (2)

A
  • FBC
    • (high lymphocytes, low WC), low RBC/platelets
  • Bone marrow biopsy
57
Q

How would you treat acute lymphoblastic leukaemia (5)

A
  • Bone marrow transplant
  • Chemotherapy
  • Blood and platelet transfusion
  • Prophylaxis
  • Allopurinol
58
Q

Describe the epidemiology of acute myeloid leukaemia (4)

A
  • Neoplastic proliferation of myeloid precursor cells
  • Myeloid precursor cells give rise to eosinophils neutrophils and basophils
  • Most common acute leukaemia in adults
  • Associated with radiation and downs
59
Q

How might acute myeloid leukaemia present (4)

A
  • Marrow failure
    • Anaemia (standard symptoms)
    • Infection (low WC)
    • Bleeding (low platelets)
  • Hepatosplenomegaly
60
Q

How would you diagnose acute myeloid leukaemia

A
  • Bone marrow biopsy
61
Q

How would you treat acute myeloid leukaemia (5)

A
  • Bone marrow transplant
  • Chemotherapy
  • Allopurinol
  • Prophylaxis
  • Blood and platelet transfusion
62
Q

What is the epidemiology of chronic myeloid leukaemia (4)

A
  • More common in adults
  • Uncontrolled proliferation of myeloid cells
  • Associated with Philadelphia chromosome
  • Males, 40-60
63
Q

How might chronic myeloid leukaemia present (5)

A
  • Anaemia
  • Weight loss
  • Malaise
  • Fever and sweats
  • Bleeding
64
Q

How do you diagnose chronic myeloid leukaemia (2)

A
  • FBC
    • Raised WBC, low RBC and platelets
  • Bone marrow biopsy
65
Q

How do you treat chronic myeloid leukaemia

A
  • Stem cell transplant

- Imatinab

66
Q

What is the epidemiology of chronic lymphoblastic leukaemia (3)

A
  • Most common leukaemia
  • Mature B-cells escape cell death and proliferate
  • Later life
67
Q

How might someone with chronic lymphoblastic leukaemia present (4)

A
  • Usually asymptomatic
  • Anaemia
  • Sweats, anorexia, weight loss if severe
  • Hepatosplenomegaly
68
Q

How do you treat chronic lymphoblastic leukaemia (4)

A
  • Stem cell transplant
  • Chemotherapy
  • Blood transfusion
  • IV immunoglobulins
69
Q

What is lymphoma

A
  • A malignant proliferation of lymphocytes that accumulate in the lymph nodes but may be found in the blood or organs
70
Q

What are the two types of lymphoma

A
  • Hodgkins lymphoma
    • Characteristic cells (Reed-Sternberg)
  • Non-Hodgkins lymphoma
    • No characteristic cells
    • Low, high and very high grades
71
Q

What is the epidemiology of Hodgkins lymphoma (3)

A
  • Teenagers and elderly
  • EBV association
  • More common in males
72
Q

What are the risk factors for Hodgkins lymphoma (6)

A
  • Elderly/teenager
  • EBV
  • Sibling with it
  • SLE
  • Obesity
  • Immunosupression
73
Q

How might someone with Hodgkins lymphoma present (2)

A
  • Painless rubbery lymphadenopathy

- Malaise, weight loss, sweats

74
Q

How do you diagnose Hodgkins lymphoma (2)

A
  • Lymph node excision

- CT/MRI for staging

75
Q

What staging is used for Hodgkins lymphoma

A
  • Ann-Arbor staging
  • I one lymph node
  • II 2+ nodes above diaphragm
  • III nodes above and below diaphragm
  • IV systemic spread
  • A or B where A is no systemic symptoms and B is systemic symptoms
76
Q

How do you treat Hodgkins lymphoma (2)

A
  • ABCD combo chemotherapy

- Radiotherapy

77
Q

What is the epidemiology of non-hodgkins lymphoma (2)

A
  • 80% B-cell, 20% T-cell

- Not all centre of lymph nodes

78
Q

How might someone with non-Hodgkins lymphoma present (3)

A
  • Lymphadenopathy
  • Fever, weight loss, night sweats
  • Pancocytopenia
79
Q

How would you diagnose non-Hodgkins lymphoma (2)

A
  • Lymph node excision

- CT/MRI for staging

80
Q

What is the treatment for non-Hodgkins lymphoma (2)

A
  • R-CHOP

- Radiotherapy

81
Q

What is the epidemiology of Myeloma (2)

A
  • > 70

- More common in Afro-Caribbeans

82
Q

Describe the pathophysiology of Myeloma

A
  • Malignant proliferation of plasma cells in the bone marrow
  • Secrete Immunoglobulins
    • 55% IgE
    • 20% IgA
    • IgD and IgM
  • Deficiency in non-secreted IG leads to infection
83
Q

How might Myeloma present

A 
- OLD-CRAB
OLD
Calcium high
Renal failure (Ig deposits)
Anaemia (Pancocytopenia)
Bone lesions (back pain)
84
Q

How do you diagnose Myeloma (4)

A
  • Bone marrow biopsy
  • Bloods (raised calcium, Urea and Cr, low Hb)
  • X-ray shows bone lesions
  • Proteinurea
85
Q

How do you treat Myeloma (5)

A
  • Analgesia
  • Biphosphonates to reduce bone fracture
  • Transfusion for anaemia
  • Chemotherapy
  • Stem cell transplant

Finals (11 decks)

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