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Integrated Care Phase 1 > Haematology > Flashcards

Haematology Flashcards

1
Q

How long is the lifespan of a RBC?

A

120 days

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2
Q

Why is this long life of red blood cells advantageous to us, in terms of tests?

A

It allows for calculation of HbA1c to show diabetic control over 2-3 months

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3
Q

What is HbA1c?

A

Glycosolated haemoglobin

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4
Q

How does HbA1c work? Why is this good?

A

Concentration of glucose bound to Hb is proportionate to the blood glucose levels at the time the cell was made, so HbA1c gives the avergae amount of glucose bound over 3 months, not just at that moment in time (cap blood glucose).

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5
Q

Who is HbA1c not accurate in?

A

Haemolytic patients due to shorter lifespan of RBCs.

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6
Q

What is the lifespan of a platelet? Why is this clinically relevant?

A

10 days - this is why pts on aspirin/clopidogrel etc need to come off it a week prior to surgery

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7
Q

What is the lifespan of a neutrophil?

A

2-4 days

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8
Q

What is the lifespan of a lymphocyte?

A

Very variable - days or years depending on the subtype/function of that lymphocyte

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9
Q

Where are the 2 areas that haematopoiesis occur in early gestation?

A
  • Weeks 1-6 of gestation in the yolk sac

- Week 6 to month 6 of gestation in the liver and spleen

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10
Q

Where does haematopoiesis occur from month 6 of gestation throughout life?

A

Bone marrow

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11
Q

Which bones in children contribute to haematopoiesis?

A

All of them!

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12
Q

Which bones in adults contribute to haematopoiesis?

A 
Pelvis
Sternum
Skull
Ribs
Vertebrae
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13
Q

Due to the areas that contribute to haematopoiesis in adults, where are most bone marrow aspirations/biopsies performed?

A

Anterior iliac crest

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14
Q

When do you get haematopoiesis occuring outside the bone marrow?

A

In haemoglobinopathies and myeloproliferative disorders.

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15
Q

What group of hormones drives haematopoiesis?

A

Cytokines

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16
Q

Which cytokines drive haematopoiesis?

A 
Erythropoietin
Thrombopoietin
G-CSF
GMCSF
Interleukin 6
Others also
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17
Q

What does Erythropoietin stimulate?

A

Red blood cell production

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18
Q

Where is Erythropoietin made?

A

Kidneys

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19
Q

What does thrombopoietin stimulate?

A

Platelet production (via megakaryocytes)

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20
Q

Where is thrombopoietin made?

A

Liver and kidney

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21
Q

What does G-CSF stimulate?

A

Production of granulocytes and stem cells (Granulocyte colony stimulating factor)

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22
Q

What is GMCSF and what does it stimulate?

A

Granulocyte-macrophage colony stimulating factor.

Stimulates neutrophil, eosinophil, and basophil production

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23
Q

What causes the kidney to release erythropoietin?

A

Hypoxia/anaemia

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24
Q

What does erythropoietin act on in the bone marrow?

A

E-progenitor cells

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25
Q

How is iron concentration in the body regulated?

A

By absorption from the gut

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26
Q

Where does iron come from, and how do we lose it?

A

Diet

Loss of blood, sloughing of mucosal epithelial cells, and pregnancy

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27
Q

Can we have too much iron?

A

Yeep

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28
Q

What happens in iron overload?

A

Fe2+ produces hydroxyl and lipid radicals -> damage lipid membranes, nucleic acids and proteins.

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29
Q

How are thalassaemias and myelodysplasias treated?

A

Regular transfusions

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30
Q

Other than iatrogenic, how else can a pt become iron overloaded?

A

Hereditary haemochromatosis

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31
Q

Tell me about hereditary haemochromatosis…

A

Autosomal recessive
Increased gut absorption
Iron deposited in liver, heart, pancreas, testicles, and skin.

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32
Q

What does iron deposition in these organs cause?

A 
Cirrhosis
DM
Cardiomyopathy
Arthritis
Hypogonadism
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33
Q

How is hereditary haemochromatosis treated?

A

Desferal or regular venesection

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34
Q

How is iatrogenic iron overload caused and treated?

A

Regular transfusions

Iron chelating agents given e.g. desferal/desferrioxamine

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35
Q

What process are vit B12 and folate needed for?

A

DNA synthesis

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36
Q

Why are RBCs macrocytic in b12 or folate deficiency?

A

They can’t leave G2 stage of replication, so mitosis doesn’t occur, and cell growth continues without division.

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37
Q

What are the clinical signs of b12/folate deficiency?

A

Glossitis
Angular cheilosis/stomatitis
Jaundice

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38
Q

What kind of anaemia results from b12 deficiency?

A

Pernicious anaemia

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39
Q

Where is B12 absorbed from, and therefore who is at risk of developing pernicious aneamia?

A

Terminal ileum

Pts who have had ileal resection, Crohns pts, coeliacs, UC pts (backwash ileitis)

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40
Q

What is folate deficiency caused by?

A

Reduced absorption or increased utilisation

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41
Q

What diseases cause less folate absorption?

A

Crohn’s disease

Coeliac disease

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42
Q

What drugs can decrease folate levels?

A

Methotrexate
Trimethoprim
(Some others, used less frequently)

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43
Q

What can folate deficiency cause in pregnancy?

A

Neural tube defects

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44
Q

What clinical signs can B12 deficiency cause?

A

Peripheral neuropathy
Optic atrophy
Confusion
Reduced cognition

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45
Q

Name 2 haemoglobin abnormalities.

A

Thalassaemia

Sickle cell disease

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46
Q

What is a thalassaemia?

A

A reduced rate of synthesis of either alpha or beta globin chains so the ratio is no longer 1:1

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47
Q

What does thalassaemia cause?

A

Ineffective haematopoiesis and haemolysis ->

Anaemia, jaundice, splenomegaly

48
Q

How does sickle cell disease occur?

A

Autosomal recessive point mutation -> Beta chain abnormality that changes the shape of the haemoglobin

49
Q

What does the sickle cell mutation change in the protein coding?

A

Glutamic acid -> valine

50
Q

What is sickle cell trait?

A

Carrier of the sickle cell gene causing sickles cell changes in some blood cells

51
Q

What does full blown sickling lead to?

A

Chronic haemolysis and episodic tissue infarction
Chronic anaemia
Jaundice

52
Q

Why are the symtpoms of anaemia in sickle cell patients milder than you would expect?

A

The adjusted shape of the sickle cell causes a sift in the oxygen dissociation curve to the right

53
Q

What is a sickle cell crisis?

A

Sickling causes microcirculation infarction -> tissue ischaemia

Can cause various crises throughout the body

54
Q

What can trigger sickle cell crisis?

A 
Hypoxia
Infection
Cold
Dehydration
Stress
55
Q

What is an aplastic crisis?

A

Temporary cessation of red cell production. Because of the markedly shortened red cell survival time in patients with sickle cell disease, a precipitous drop in hemoglobin occurs in the absence of adequate reticulocytosis -> sever anaemia.

56
Q

What is a sequestration crisis?

A

Pooling of blood in the liver or spleen -> organomegaly, anaemia, and hypotensive shock

57
Q

What complication to do with the spleen can sickle cell lead to?

A

Hyposplenism -> asplenia.

Repeated insult to spleen leaves it unable to function

58
Q

What infections are pts with hyposplenia more susceptible to?

A

All of them, but especially from encapsulated bacteria

59
Q

What are the encapsultaed bacteria that asplenic patients need to look out for?

A

Gram negatives mostly, such as E. coli, Salmonella, Neisseria meningitidis, and Klebsiella pneumonias.

Some gram positives also such as strep pneumoniae, strep pyogenes, and staph epidermidis.

60
Q

Other than infection and hyposplenism, what other complications can develop due to sickle cell disease?

A 
Pulmonary hypertension
Renal Impairment
Ulcers and poor wound healing
Priapism
Pigment gallstones
Osteomyelitis and AVN
61
Q

How do we manage sickle cell disease?

A

Avoid triggers for crises
Give vaccinations and prophylactic abx
Give folic acid

62
Q

How do we manage a sickle cell crisis?

A

The usual, treat the ABCDE as it comes. Analgesia, rest, fluids, warmth, LMWH, O2, ?transfusion, treat the cause.

63
Q

With a thalassaemia, if i said alpha thalassaemia does that mean an alpha or beta gene copy/copies is missing?

A

Alpha copy is missing in alpha thalassaemia

64
Q

How does a thalassaemia get more serious?

A

The more genes are missing, the worse it gets.

65
Q

Who has alpha thalassaemia trait?

A

Anyone with one or 2 inactive alpha chain genes

66
Q

If you have alpha thalassaemia trait, what will I see on your blood work?

A

Lowered MCV and Mean cell Hb

67
Q

Can you live with 3 or 4 missing alpha chain genes?

A

Yes to 3, no to 4.

68
Q

Tell me about only having 1 alpha chain.

A

Compatable with life, causes Haemoglobin H disease where Hb=70-110, decreased MCV and MCH, hypersplenism.

69
Q

Tell me about only having no alpha chains.

A

Fatal in early life as an alpha chain is essential. Called Hydrops fetalis.

70
Q

How many copies are there of the beta Hb chain gene?

A

2

71
Q

When one beta chain gene is missing, what does the pt have?

A

Beta thalassaemia trait

72
Q

When both beta chain genes are missing, what does the pt have?

A

Beta thalassaemia major

73
Q

What are the features of beta thalassaemia major?

A

Severe anaemia for first 6 months of life.
Hepatosplenomegal
Bone marrow hyperplasia
Osteoporosis

74
Q

Aside from regular blood transfusions, how do we treat thalassaemias?

A 
Iron chelating agents so we don't cause iatrogenic iron overload
Folic acid suppliments
Splenectomy
Immunisation and prophylaxis
Treat any resulting endocrine disorders
75
Q

Do we need to treat thalassaemia trait?

A

Not usually, as asymptomatic.

If symptomatic, usually hypochromic and microcytic anaemia that presents like iron deficiency. Don’t want to iron overload them!

76
Q

What is MCV important in?

A

Determining the cause of anaemia

77
Q

What is the haematocrit?

A

Packed cell volume i.e. volume % of red blood cells in blood

78
Q

Who is a raised haemaocrit often seen in and why?

A

COPD pateints or those who live at altitude due to chronic hypoxia.

79
Q

What is a reticulocyte?

A

Young erythrocyte/rbc

80
Q

When are reticulocytes raised?

A

Anameia

81
Q

When are reticulocytes lowered?

A

Haematinic deficiency or bone marrow failure

82
Q

What is anisocytosis?

A

Increased variability in size of RBCs

83
Q

What is dimorphism of RBCs?

A

2 distinct red cell populations

84
Q

What can spiculated red cells be called?

A

Echinocytes
Acanthocytes
Keratoncytes
Schistocytes

85
Q

What is a myeloproliferative disorder?

A

Overproduction of one or several blood elements with dominance of a transformed clone

86
Q

What can a myeloproliferative disorder lead to?

A

Acute leukaemia

87
Q

What is the difference between lymphoma and leukaemia?

A

Leukaemia starts in the bone marrow and then spreads to the lymphatic tissues

Lymphoma starts in the lymphatics due to abnormal lymphocytes

88
Q

How do myeloproliferative disorders come about?

A

Myeloid stem cell becomes damaged so it ignores apoptotic signals, rapidly divides, and produces more myeloid cells

89
Q

What gene is responsible for myeloproliferative disorders?

A

JAK2 (mutated)

Janus kinase 2

90
Q

What is a myelodysplastic syndrome?

A

Dysplastic changes in blood cells leading to increased numbers of abnormal precursor cells

91
Q

What is myelofibrosis?

A

Proliferation of an abnormal cell type leading to damage and fibrosis of bone marrow

92
Q

What is multiple myeloma?

A

Bone marrow based cancer affecting plasma cells

93
Q

What is pancytopaenia?

A

Anaemia, thrombocytopaenia and neutropenia combined - global lack of blood cells

94
Q

What are the 2 mechanisms that can lead to pancytopaenia?

A

Global problem with blood production

Process destroying all blood products

95
Q

What could cause pancytopaenia via bone marrow decreased production of blood cells?

A

-Aplastic anaemia
-Myelodysplastic syndrone
Myelofibrosis
-Bone marrow failure
-Iatrogenic bone marrow suppression secondary to radiotherapy and chemotherapy

96
Q

What could cause pancytopaenia via increased blood product destruction?

A

Autoimmune haemolytic anaemia

97
Q

What are the 4 types of leukaemia?

A

Acute myeloid leukaemia
Chronic myeloid leukaemia
Acute lymphoid leukaemia
Chronic lymphoid leukaemia

98
Q

What is myeloid leukaemia?

A

Excess granulocyte production

99
Q

What is lymphoid leukaemia?

A

Excess lymphocyte production

100
Q

What characterises acute leukaemia?

A

Abundance of blast/progenitor cells in bone marrow and on blood films

101
Q

What characterises chronic leukaemia?

A

Abundance of fully differentiated cells

102
Q

Who gets acute lymphocitic leukaemia?

A

Children

103
Q

Who gets chronic lymphocitic leukaemia?

A

Adults.

M:F 2:1

104
Q

Who gets acute myeloid leukaemia?

A

Adults

105
Q

Who gets chronic myeloid leukaemia?

A

People 20-50

Children can get this rarely

106
Q

How does acute myeloid leukaemia present?

A

Symptomatic anaemia
Mucosal and internal bleeding
Increased susceptibility to infection

107
Q

How does acute lymphoblastic leukaemia present?

A 
Symptomatic anaemia
Greater tendency to illness
Bruising and bleeding
Bone or lung pain
Failure to thrive
108
Q

How does chronic myeloid leukaemia present?

A 
Symptomatic massive splenomegaly
Symptomatic anaemia
Hyperviscousity of blood and clots
Bone pain
Hypermetabolism
109
Q

How does chronic lymphocytic leukaemia present?

A

Asymptomatic or unspecific symptoms
LAD
Hepatosplenomegaly

110
Q

What are the classifications of lymphoma?

A

Hodgkins
Non Hodgkins

High grade vs low grade
B cell vs T cell
Systemic vs localised

111
Q

Who is Hodgkin lymphoma common in?

A

Young adults

112
Q

What is Hodgkins lymphoma?

A

Idk *****

113
Q

Do more on lymphoma

A

Ok

114
Q

What are non Hodgkins lymphomas?

A

Any malignant solid tumours of lymphoid tissue not characterised as Hodgkins lymphoma

115
Q

What is multiple myeloma?

A

Bone marrow based cancer affecting plasma cells

116
Q

What are the most common symptoms of multiple myeloma and how do we remember them?

A

CRAB

Calcium raised
Renal failure
Anaemia
Bone pain

Integrated Care Phase 1 (8 decks)

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