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Phase 2a LM > Haematology Diseases > Flashcards

Haematology Diseases Flashcards

1
Q

What is anaemia

A

Reduced RBC mass +/- reduced Hb conc in plasma

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2
Q

What is the lifespan of RBCs

A

120 days

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3
Q

What are the 3 causes of microcytic anaemia

A

Iron deficiency
Thalassaemia
Anaemia of chronic disease

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4
Q

Why might someone be iron deficient

A

Not enough in diet
Haemorrhage - heavy periods
Breast milk iron def
Hookworm

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5
Q

What are the 3 causes of normocytic anaemia

A

Combined haematinic deficiency - B12 and iron
Acute blood loss
Chronic disease

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6
Q

What are the 4 causes of macrocytic anaemia

A

B12/folate def
Hypothyroidism
Excess alcohol consumption/liver disease
Haematological - cancer, bone marrow failure

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7
Q

What is polycythaemia

A

Too many RBCs

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8
Q

What is the main cause of polycythaemia (and other causes)

A

Smoking

Lung disease
Cyanotic heart disease
Polycythaemia rubra Vera (PRV)

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9
Q

What is neutrophilia

A

Too many neutrophils

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10
Q

What are the main causes of neutrophilia

A

Bacterial infection
Inflammation
Malignancies
Chronic myeloid leukaemia

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11
Q

What is the term for too many WBCs

A

Lymphocytosis

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12
Q

What are the causes of lymphocytosis

A

Infection inflammation malignancy

Chronic lymphocytic leukaemia

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13
Q

What is the term for high platelets

A

Thrombocytosis

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14
Q

What are the causes of thrombocytosis

A 
Infection inflammation malignancies 
Essential thrombocythaemia (over active bone marrow)
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15
Q

What is thrombocytopenia

A

Low platelets

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16
Q

What is the term for low neutrophils

A

Neutropaenia

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17
Q

What are the underproduction and increased removal causes of neutropaenia

A

Underproduction = marrow failure/infiltration/toxicity

Increased removal = autoimmune, felty’s syndrome, cyclical

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18
Q

When the endothelium is damaged, what do platelets adhere to it via

A

Collagen and vWF

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19
Q

What does the binding of platelets to collagen/vWF stimulate

A

Cytoskeleton shape change -> ‘spread out’

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20
Q

When platelets are activated by a change in shape, granules are released containing what?

A

ADP, fibrinogen, thrombin, calcium

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21
Q

Activated platelets are cross linked, and aggregation occurs by what molecule

A

Fibrin

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22
Q

What is the lifespan of platelets

A

7-10 days

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23
Q

What are the clinical features of platelet dysfunction

A

Mucosal bleeding - gums, nose, large menstruation
Easy bruising
Petechial, purpura
Traumatic haematomas

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24
Q

Give some causes of thrombocytopenia due to decreased production

A

Congenital = reduced/malfunctioning megakaryocytes
Infiltration of BM = leukaemia, myeloma, lymphoma, mets
Reduced platelet production by BM = low B12/folate, reduced TPO

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25
Q

Give some causes of thrombocytopenia due to increased destruction

A

Autoimmune = immune thrombocytopenia
Hypersplenism = portal HTN, splenomegaly
Drug related = heparin induced thrombocytopenia
Consumption of platelets = DIC, HUS, major haemorrhage

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26
Q

Name 3 types of medication affecting platelets

A 
Aspirin = inhibit COX 1
Clopidogrel = blocks P2Y12
Tirofiban = blocks Gp IIb/IIIa
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27
Q

How many globin chains does a normal Hb molecule have

A

4: 2 alpha and 2 beta

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28
Q

What is the amino acid substitution in sickle cell

A

Valine -> glutamine

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29
Q

What is a carrier of sickle cell protected against

A

Falciparum malaria

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30
Q

Where is the DNA is the mutation in sickle cell

A

Beta globin gene on chromosome 11

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31
Q

What are the disease modifying Tx for sickle cell

A

Transfusion
Hydroxycarbamide
Stem cell transport

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32
Q

What is thalassaemia

A

Reduced production of alpha or beta globin chains

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33
Q

What are the main deletions and mutations in thalassaemia

A

Deletions - alpha thalassaemia
Mutations - beta thalassaemia
(Mainly)

34
Q

What are the 3 categories of thalassaemia

A

Thalassaemia major - require transfusions to survive
Thalassaemia intermedia - can survive without transfusion
Thalassaemia carrier - asymptomatic

35
Q

Are membranopathies autosomal recessive or dominant

36
Q

Give one example of an enzymopathy

A

Glucose-6-phosphate dehydrogenase deficiency

37
Q

What is leukaemia

A

Cancer of the bone marrow with abnormally high levels of white blood cells

38
Q

What cell/cells are affected in acute myeloid leukaemia

A

Myeloblasts

39
Q

What do myeloblasts differentiate into

A

Neutrophils, eosinophils, basophils, monocytes

40
Q

What are the cell/cells affected in chronic myeloid leukaemia

A

Any of: basophils, eosinophils, neutrophils

41
Q

What are the cell/cells affected in acute lymphoblastic leukaemia

A

Lymphoblasts

42
Q

What do lymphoblasts differentiate into

A

T lymphocyte

B lymphocyte

43
Q

What is the cell/cells affected in chronic lymphocytic leukaemia

A

B lymphocytes

44
Q

What are the 3 signs/presentation of bone marrow problems

A

Anaemia - fatigue, SOB
Thrombocytopaenia - rash, bruises, spots
Infections - fever, rigors

45
Q

What is the sign of an acute leukaemia

A

> 20% of bone marrow is blast cells

46
Q

What is the age, the cause and the diagnosing detail of acute myeloid leukaemia

A

Age: 70 yrs (rare in children)
Cause: complication of chemo
Diagnosis: Auer rods in myeloblasts

47
Q

What is the most common paediatric cancer

A

Acute lymphoblastic leukaemia

48
Q

What are some of the signs/symptoms of acute lymphoblastic leukaemia

A

Marrow failure - infection, anaemia, bleeding

Tissue infiltration - lymphadenopathy

49
Q

What is the cause of chronic myeloid leukaemia

A

Philadelphia chromosome

50
Q

What is the Philadelphia chromosome

A

A translocation of chromosome 9 ->22

51
Q

What does the Philadelphia chromosome cause

A

Increase in tyrosine kinase that then increases the number of affected WBCs

52
Q

What age group does chronic myeloid leukaemia typically affect

A

40-60 yr olds

53
Q

What is the most common leukaemia

A

Chronic lymphocytic leukaemia

54
Q

What are the Tx for chronic lymphocytic leukaemia

A

Blood transfusions
Chemo
Rituximab (anti CD20 - found on B lymphocyte surface)

55
Q

What is lymphoma

A

Malignant growth of WBCs - predominantly in the lymph nodes

56
Q

What are most caused by

A

Unknown!
Immunodeficiency - HIV, transplant recipients
Infection
AI

57
Q

What is the difference between Hodgkin’s lymphoma and non-hodgkins lymphoma

A

Hodgkin’s lymphoma has the presence of Reed-Sternberg cells in the lymph node biopsy, but NHL doesnt

58
Q

What is the presentation of Hodgkin’s lymphoma

A

Enlarged and painless nodes

59
Q

What are B symptoms

A

Sweats, weight loss, fever, pruritus and lethargy

Systemic features of cancer

60
Q

What are the 4 clinical stages of Hodgkin’s lymphoma

A 
1= single lymph node region
2= two or more regions on the same side of the diaphragm 
3= nodes on both sides of diaphragm 
4= spread beyond the lymph nodes 
A= absence of B symptoms 
B= presence of B symptoms
61
Q

What is the Tx for Hodgkin’s lymphoma

A

Stage 1-2A: chemo then radio

Stage 2-4B: combined chemo

62
Q

What are the two types of NHL

A

Low grade or high grade

63
Q

What is an example of low grade NHL

A

Follicular lymphoma

64
Q

What is an example of a high grade NHL

A

Diffuse large B cell

65
Q

What are the Tx for the high grade NHL

A

Short course chemo and radio

Combination chemo and monoclonal Abs e.g. Rituximab

66
Q

What is myeloma

A

Cancer of differentiated B lymphocytes known as plasma cells

67
Q

What’s the peak age for myeloma

68
Q

What are the features of myeloma

A

Malignant plasma cells accumulate in the BM- BM failure
Abnormal Ab and short chain (paraproteins) produced by the plasma cells
Renal failure
Osteoporosis

69
Q

How do you diagnose myeloma

A
  1. Monoclonal plasma cells in BM >10%
  2. Monoclonal Ab (paraprotein) in serum or urine (bence jones)
  3. One or more of:
    C- calcium - hypercalcaemia
    R- renal failure
    A- anaemia
    B- bone - lytic lesions, osteoporosis, spinal cord compression
70
Q

Name some chemicals the malignant plasma cells produce in the bone

A

IL3 (stops osteoblasts progenitors developing)
DKK1 (inhibits OPG from stopping RANK-L binding to RANK)
MIP1-alpha (increase osteoclasts activity)
RANK-L (stimulates osteoclasts activity)

71
Q

What is a common source of neutropaenia sepsis

A

Chemo (recently had)

72
Q

What are the symptoms of neutropenic sepsis

A

Fever
Rigors
Generally ‘off’
Low BP

73
Q

What to do is suspect neutropaenic sepsis

A
  1. See patient ASAP
  2. Put cannula in before history
  3. ANTIBIOTICS before history
74
Q

Sickle cell disease crisis patient in agony, what do you do

A
  1. See patient
  2. Control pain
  3. Put cannula in, start fluids and oxygen
75
Q

If sickle cell leads to acute chest syndrome (lung infarction and hypoxia then worse sickle) what do you do

A
  1. See patient
  2. give fluids/Abx and oxygen
  3. Call haem (need RBC exchange)
76
Q

What are the symptoms of the myeloma complication of spinal cord compression

A

Back pain
Neuropathic pain
Leg weakness/numbness
Saddle anaesthesia

77
Q

What to do if suspect spinal cord compression

A
  1. Keep in bed
  2. Large dose of steroid - dexamethasone
  3. MRI
78
Q

Complication of myeloma: hyperviscosity syndrome, symptoms

A 
Non-specific
Headaches
Blurred visions 
SOB
Mucosal bleeding
79
Q

What to do if suspect hyperviscosity syndrome

A
  1. Put cannular in
  2. Fluids
  3. Call haem
80
Q

What is tumour lysis syndrome

A

Where chemo has killed cancer cells, but they release all their intracellular contents and the kidneys become overwhelmed

81
Q

What are the 4 common signs of tumour lysis syndrome

A

Increased potassium
Increased phosphate
Increased Uric acid
Decreased calcium

82
Q

What’s the Tx for tumour lysis syndrome

A

LOTS OF FLUID

Manage electrolytes

Phase 2a LM (7 decks)

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