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FFCP haematology Flashcards

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1
Q

What type of anaemia is iron deficiency?

A

hypochromic, microcytic

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2
Q

What will you see on blood tests for IDA?

A

decreased MCV, decreased ferritin, increased total iron binding capacity and decreased transferrin saturation

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3
Q

What anaemia in B12 deficiency?

A

macrocytic anaemia

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4
Q

What might you see on blood test for b12 deficiency?

A

increased mean corpuscular value, decreased b12 and increased methylmalonic acid (bc whenb12 low ability to convert this to suuccinylcoA is compromised)

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5
Q

Main inheritance of hereditary spherocytosis?

A

mainly autosomal dominant

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6
Q

How do patients with moderate hereditary spherocytosis tend to present?

A

With anaemia, jaundice and splenomegaly. (but mild cases will be asymptomatic)

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7
Q

What is the direct Coombs test?

A

A test used to test for autoimmune haemolytic anemia

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8
Q

What would you see on blood tests for hereditary spherocytosis?

A

increased reticulocytes, increased LDH, increased unconjugated bilirubin, decreased haptoglobin (markers of haemolysis)

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9
Q

How can EMA test help diagnose hereditary spherocytosis?

A

flurescent dye that binds to membrane proteins, uses flow cytometry. People with HS show less EMBA labelled RBC membrane proteins

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10
Q

Treatment of HS?

A

Folic acid supplementation, splenectomy in those severely affected and reliant on transfusions. EPO might be needed in young infants

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11
Q

What will you see on blood film of autoimmune haemolytic anaemia?

A

spherocytes lacking central pallor

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12
Q

What are the three forms of G6PD deficiency?

A

acute intermittent haemolytic anaemia, chronic haemolytic anaemia, no risk of haemolytic anaemia

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13
Q

What might you see on G6PD blood smear?

A

Heinz bodies - inclusions within the RBCs of denatured haemoglobin

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14
Q

Inheritance of G6PD?

A

X-linked recessive

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15
Q

What happens in aplastic anaemia?

A

You get reduction or absence of haemopoietic precursors of all 3 cell lineages eg erythrocytes, leukocytes and thrombocytes due to failure of haematopoietic stem cells

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16
Q

How is aplastic anaemia confirmed?

A

bone marrow biopsy which typically reveals a hypocellular marrow with fatty infiltration where there should be bone marrow cells

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17
Q

Pathophysiology of sickle cell?

A

mutation in HBB gene - glutamate is substituted by valine in position 6 of beta globin gene causing the presence of HbS

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17
Q

inheritance of sickle cell?

A

autosomal recessive

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18
Q

Gold standard for diagnosing sickle cell?

A

haemoglobin electrophoresis. Can also do sickle solubility test

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19
Q

Management of acute chest syndrome?

A

analgesia, incentive spirometry, o2 therapy (non invasive ventilation), fluid management, antibiotics, transfusion

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19
Q

What virus can precipitate aplastic crises?

A

paravirus B10

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20
Q

Where do you find mutation is beta thalassemia?

A

mutations in the HBB gene on chromosome 11 (autosomal recessive)

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21
Q

Gold standard to assess iron status to avoid iron overload?

A

cardiac/liver MRI

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22
Q

in alpha thalassemia what do the excess beta chains form?

A

haemoglobin H compromising 4 beta chains - non functional and haemoglobin bart’s compromising 4 gamma chains

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23
what chromosome is the gene for alpha globlin on?
chromosome 16
24
What is haemoglobin H disease?
when three alpha globlin genes are affected
25
What is alpha thalassaemia major?
when four alpha globin genes are affected - incompatible with life causes hydrops fetalis
26
What chromosome is the gene for beta globin on?
chromosome 11
27
When does delayed haemolytic reaction to transfusion tend to occur?
7-10 days after transfusion
28
If someone experiences a fever during transufsion what should you do?
If not having severe symptoms, likley due to febrile non-haemolytic transfusion reaction, give paracetamol and slow transfusion
29
Virchow's triad?
blood flow, blood coaguability, vessel wall damage
30
How does heparin work?
It binds to enzyme inhibitor antithrombin III that results in its activation. The activated AT then inactivates thrombin, Xa and other proteases
31
How does fondaparinux work?
It binds to antithrombing causing the neutralisation of factor Xa
32
What kind of drug is dabigatran?
direct thrombin inhibitor (DOAC)
33
What kind of drugs are rivaroxaban, apixaban and edoxaban?
factor Xa inhibitors (DOACs)
34
What kind of drug is warfarin?
Vitamin K antagonist, so prevents formation and secretion of vit K dependent clotting factors
35
When should warfarin be avoided?
in pregnancy, but its okay for breastfeeding
36
Treatment of VTE?
Apixaban or rivaroxaban but if neither suitable then LMWH for at least five days followed by dabigatran or edoxaban
37
How do AML and ALL often present?
With signs of bone marrow failure: low Hb, tiredness, SOB, infections bleeding abd bruising
38
In what illness do you see Auer rods?
AML (red staining, needle like bodies)
39
What would be diagnostic of AML in bone marrow biopsy?
Greater than 20% myeloblasts
40
What is leukostasis?
an oncological emergency, occurs in AML and CML when high white blood cell count results in increased blood viscosity. Symptoms headache, stroke, confusion
41
What metabolic disturbances do you get in tumour lysis syndrome?
hyperkalemia, hyperphosphatemia, hypocalcemia and hyperuricemia
42
How do you treat tumour lysis syndrome?
fluids, allopurinol, rasburicase
43
What is given to stem cell donor for 4 days prior to donation?
G-CSF (granulocyte colony stimularing factor) which increases number of haematopoietic stem cell transplantation
44
What is inotuzumab ozogamicin used to treat?
Acute lymphoblastic leukemia
45
How does inotuzumab ozogamicin work?
It consists of a humanised monoclonal antibody against CD22 which are expressed on B cells in ALL so it enters the cell where the ozogamicin is cleaved delivering chemo into cell
46
What cells do you see on blood smear in chronic lymphocytic leukaemia?
Smear cells - lymphocytes whose cell membranes have ruptured in preparation of smear (bc of increased fragility)
47
What kind of drug is ibrutinib?
BTK inhibitor - inhibits B cell receptor pathway (treat CLL)
48
What does venetoclax attach to? (used to treat CLL)
Bcl-2
49
What is Philadelphia chromosome?
Reciprocal translocation of chromosomes 9 and 22 creating bcr-abl fusion gene
50
Why does the BCR-ABL fusion gene cause malignancy?
bc ABL is a tyrosine kinase so after the fusion, the oncogene has uncontrolled tyrosine kinase activity
51
How does imatinib work?
binds close to the ATP binding site of bcr-abl inactivating it semi competitively
52
What is myelodysplastic syndrome?
dysplasia of blood cells due to problem with haematopoietic stem cells in one, two or three main cell lines in bone marrow
53
What is azacytadine for MDS?
It is a DNA demethylating agent
54
What symptoms do you get in myeloma?
hyperCalcemia Renal dysfunction Anemia Bone lesions
55
What can ibrutinib be used to treat?
slow low grade malignancies - myeloma, low grade lymphomas. (It is a small molecule drug that inhibits B cell proliferation by binding tyrosine kinase).
56
targeted immunotherapy drug for myeloma?
daratumumab
57
What drugs compose CHOP for treatment of high grade lymphomas?
cyclophosphamide, doxorubicin, vincristine and prednisone
58
What age group do you tend to get acute myeloid leukaemia?
older people
59
What is the most common childhood cancer?
acute lymphoblastic leukaemia - peak incidence 2-4 years
60
What is TACO?
transfusion associated circulatory overload - pulmonary oedema due to volume overload, occurs within 12 hours of transfusion
61
What is Transfusion associated acute lung injury?
hypoxia due to bilateral pulmonary infiltrates that happens within 6 hours of transfusion. Happens as anti-leucocyte antibodies in donor react with recipient WBCs
62
What translocation do you get in APML? (acute promyelocytic leukemia)
t(15;17) known as PML-RARA fusion
63
How is PML-RARA fusion related APML treated?
With ATRA (all-trans retinoic acid)
64
What does the A indicate in Ann Arbor staging?
the absence of B symptoms - fever, night sweats and unexplained weight loss
65
Causes of macrocytic normoblastic anaemia?
alcohol, liver disease, hypothroidism, pregnancy, reticulocytosis, drugs eg cytotoxics
66
Causes of normocytic anaemia?
Anaemia of chronic disease, CKD, aplastic anaemia, haemolytic anaemia, acute blood loss
67
What do shistocytes on a blood smear indicate?
A haemolytic process - such as disseminated intravascular coagulation or thrombotic thrombocytopenic purpura.
68
What is DAT/ Coobs test?
direct antiglobulin test - detects antibodies against red cell antigens, used to diagnose autoimmune haemolytic anaemia
69
How many points on two level Wells score makes DVT likely?
2 points or more
70
If DVT considered likely by Wells score what should be done?
a proximal leg vein ultrasound within 4 hours. If can't be done in 4hours a D-dimer should be performed and anticoag administered whislt waiting
71
If a proximal leg ultrasound is neg but d-dimer positive what should be done?
stop interim anticoag, offer a repeat ultrasound 6-8 days later
72
If neither apixaban or rivaroxaban are suitable then what should be used instead for DVT?
Either LMWH followed by dabigatran or edoxaban OR LMWH followed by vit K antagonist ie warfarin
73
What will FBC of someone with beta-thalassemia trait show?
a microcytic anaemia with normal to low Hb, low MCH, low MCV
74
What will haemoglobin eletrophoresis show in patients with beta-thalassaemia trait?
HbA2 higher in carriers about 3.6-3.7% whereas HbA2 levels between 2.2-3.2% in unaffected people
75
symptoms of beta thalassemia major?
hypersplenism, gallstones, anemia, developmental delay, leg ulcers, organ failure, expansion of bone marrow causing craniofacial abnormalities
76
What virus may precipitate transient red cell aplasia causing severe anaemia in patients with sickle cell?
Parvovirus B19
77
What infections are more common in patients with sickle-cell anaemia?
encapsulated bacterial infections ie streptococcus pneumoniae, haemophilius influenzae and Neisseria meningitidis due to splenic infarctions
78
What is the gold standard for diagnosing sickle cell?
haemoglobin eletrophoresis - predominance of HbS and decrease or absence of HbA
79
How can sickling test help diagnose sickle-cell anaemia?
identifies HbS but doesnt differentiate between sickle cell trait and sickle cell disease
80
preventing infections in sickle cell??
in infancy until at least five years old prophylactic penicillin should be given to prevent pneumococcal infections
81
How is pre natal testing done for sickle cell?
chorionic villus sampling 10-14 weeks, analysed by PCR
82
Inheritance of haemophillia?
X-linked recessive
83
Haemophillia A caused by what deficiency?
Factor VIII deficiency (accounts for 80-85%) of cases
84
What deficiency causes haemophillia B?
Factor IX deficiency
85
Pathophys of how haemophillia causes increased bleeding?
the factor VII/ or IX deficiency interferes with intrinsic pathway, decreased activation of X, reduces generation of thrombin which is critical for converting fibrinogen to fibrin
86
How can clotting studies help diagnose haemophilia?
prolonged activated partial thromboplastin time (aPTT) one of the hallmarks, also a normal prothrombin time PT can rule out extrinsic and common coag pathologies that could present similarly
87
How do VWD and haemophillia tend to differ?
VKD affects mucusal membranes and both genders whereas haemophillia cuases more internal bleeding into joints and muscles
88
What pain relief shouldnt be given to haemophilia patients?
aspirin and NSAIDs due to increased risk of bleeding
89
What do Howell-Joly bodies indicate?
absent or deficient spleen function - they are basophilic inclusions within RBCS and under normal circumstances would be removed
90
What does having a Philadelphia chromosome positive ALL mean?
associated with poor prognosis but responds well to tyrosine kinase inhibitors
91
what does thrombocytopenia mean?
low platelet count
92
What is the only slight clinical difference between AML and ALL?
ALL has predisposition for testicular and CNS involvement, whereas AML predisposition to skin and hums
93
What quantity of blasts in bone marrow or blood warrants an ALL or AML diagnosis?
More than 20%
94
what is the most common childhood cancer?
acute lymphoblastic leukaemia
95
What chemo is often used in ALL?
chemo with CNS directed treatment - vincristine, prednisolone, daunorubicin, asparaginase
96
What proliferates in CLL?
monoclonal proliferation of B-lymphocytes
97
What is the peak age in which CLL occurs?
60-70
98
How does CLL often present?
no symptoms and disease detected during routine blood tests
99
What happens to platelets, fibrinogen, PT and APTT, and fibrinogen degradation products in disseminated intravascular coagulation?
decreased platelets, decreased fibrinogen, increased PT and APTT and increased fibrinogen degradation products and prolonged bleeding time
100
Reversal agent for dabigatran?
Idarucizumab
101
What will bloods for multiple myeloma reveal?
anaemia, renal failure in urea and electrolytes, hypercalcaemia
102
What will protein electrophoresis show for multiple myeloma?
raised concs of IgA/IgG proteins in serum (in the urine they are known as Bence Jones proteins)
103
What does cyrpoprecipitate contain?
factor VIII, fibrinogen, von Willebrand factor, factor XIII
104
What does Richter's transformation refer to?
CLL transforming to high-grade non-Hodgkin's lymphoma
105
What is tumour lysis syndrome?
life threatening complication that can happen when chemo is started in highly proliferative malignancies like Burkitt's lymphoma. The rapid cell death releases intracellular contensts which are metabolished to uric acid and causes symptoms within 24-48 hours
106
What can myelodysplasia progress to?
acute myeloid leukaemia (1/3 of cases)
107
In a non-urgent scenario how quickly should RBCs be transfused?
over 90-120 minutes
108
What can polycythaemia vera transform to?
myelofibrosis or acute leukaemia in particular AML. The bone marrow blast cell count can help to differentiate, if its higher more likely to be AML
109
Reversal agent for dabigatran?
Idaruxizumab
110

Year 3 (14 decks)

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