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Haematology Flashcards

1
Q

poikilocytes/ tear drop rbc associated with

A

myelofibrosis

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2
Q

Lymphoid disorders are cancer derived

A

from b and t lymphocytes

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3
Q

Myeloid disorders are derived from

A

neutrophils, red blood cells and platelets

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4
Q

progressive ages of the different leukaemia

A

“ALL CeLLmates have CoMmon AMbitions”

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

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5
Q

Acute myeloblastic leukaemia

A

clonal expansion of myeloid blasts in the bone marrow, peripheral blood, or extramedullary tissues. most common acute leukaemia in adults.

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6
Q

Causes of Acute myeloblastic leukaemia

A

idiopathic, result of a transformation from a myeloproliferative disorder
RF include radiation, Downs syndrome

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7
Q

Microbiology Acute myeloblastic leukaemia

A

high proportion of blast cells which have Auer rods inside. Auer rods are aggregates of myeloperoxidase only found in myeloblasts.Stain positive for MPO
high WCC, Anaemia, neutropenia, thrombocytopenia

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8
Q

Acute promyelocytic leukaemia is associated with

A

Coagulopathy, can have fatal haemorrhage,

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9
Q

Treatment Acute promyelocytic leukaemia

A

Sensitive to ATRA ( all trans retinoic acid derivative of vitamin A) and arsenic trioxide. ( can be treated without cytotoxic- chemotherapy)

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10
Q

Treatment of non-APL AML

A

•Remission induction using fairly intensive chemotherapy in combination with anthracycline / cytarabine arabinoside.

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11
Q

Acute Lymphoblastic Leukaemia

A

acute proliferation of a single type of lymphocyte, usually B-lymphocytes.most common cancer in children.associated with Downs, congenital bone marrow failure syndromes.

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12
Q

Acute Lymphoblastic Leukaemia ALL clinical features

A
  • Constitutional symptoms.
  • Organomegaly.
  • Lymphadenopathy.
  • CNS involvement
  • Mediastinal mass
  • Hyperleukostasis- extremely elevated blast cell count and symptoms of decreased tissue perfusion
  • (some types) Hyperuricaemia + tumour lysis syndrome.
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13
Q

Philadelphia chromosome

A

t(9:22) BCR:ABL

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14
Q

Treatment Acute Lymphoblastic Leukaemia ALL

A

chemotherapy with intrathecal methotrexate as induction and for CNS prophylaxis.

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15
Q

Chronic Lymphocytic Leukaemia

A

indolent lymphoproliferative disorder in which monoclonal B cells lymphocytes are predominantly found in peripheral blood.

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16
Q

Microscopy Chronic lymphocytic leukaemia CLL

A
  • Abnormal lymphocytes

* Smash cells - smear/smudge cells

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17
Q

Treatment Chronic lymphocytic leukaemia CLL

A

Combination of cytotoxics and monoclonal antibody

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18
Q

Richter’s transformation.

A

sudden transformation of the CLL/SLL into a significantly more aggressive form of large cell lymphoma

CLL can transform into high-grade lymphoma.

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19
Q

Chronic myeloid leukaemia CCML

A

abnormal expansion of myeloid cells in the bone marrow and peripheral blood. Affects granulocytes ( neutrophil, basophil, eosinophil)
Characterised by Philladelphia chromosome (t9:22), producing constitutive activation of Abl kinase. Induces abnormal proliferation

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20
Q

Treatment Chronic myeloid leukaemia CML

A 
•Tyrosine kinase inhibitors:
Imatinib
Nilotinib
Dasatanib
Posnatinib
Bosutinib
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21
Q

B symptoms

A

fever,
night sweats ( drenching, they will wake up and have to change sheets/clothes)
profound lethargy
lymphadenopathy

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22
Q

hodgkin lymphoma strongly associated with

A

EBV

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23
Q

Reed-Sternberg cells ( bi nuclear cells in lymph nodes or affected tissue)

A

Hodgkin lymphoma

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24
Q

Clinical presentation myeloma

A

C- calcium ( raised) cytokines can increase osteoclast activity
R- renal failure ) because of calcium/protein deposition/stones/raised uric acid)
A- anaemia
B- bone pain (bone marrow working hard, osteoclast actiivty
B- bleeding
I - Infection

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25
microscopy myeloma
Rulo - red cells coated with immunoglobulin, chain appearance,Rouleaux formation refers to the stacking of 4 or more red blood cells.
26
BJ proteins
free light chains filtered by the kidney excreted in urine, their presence in urine suggest myeloma •Serum free light chains XS, -
27
Myeloma
Lymphoid disorder, | •Malignant plasma cells,memory b cells in bone marrow, which with secrete IgG
28
lymphoma staging system
Ann arbor
29
Microscopy Burkitt lymphoma
Starry sky appearance | Tingible bodies - macrophages that have eaten neoplastic cells
30
Pel Ebstein fever
high-grade fever that keeps rising and falling every 7-10 days or so associated with hodgekins
31
Microcytic anaemia causes - TAILS:
Thalassaemia Anaemia of chronic disease (though usually normocytic) Iron deficiency Lead poisoning Sideroblastic anaemia
32
Normocytic anaemia causes
normo - 3As and 2Hs acute blood loss, anaemia of chronic disease, aplastic anaemia haemolytic anaemia, hypothyroidism
33
Macrocytic anaemia causes
Macro - FAT RBC folate, alcohol, hypothyroid, reticulocytotic, B12, cytotoxics
34
Idiopathic thrombocytopenia purpura
condition characterised by idiopathic thrombocytopenia causing a purpuric rash (non-blanching rash). type II hypersensitivity reaction. It is caused by the production of antibodies that target and destroy platelets. Can happen spontaneously or after viral infection
35
Idiopathic thrombocytopenia purpura epidemiology
children under 10 years old. Often there is a history of a recent viral illness
36
Ix for ITP
condition can be confirmed by doing an urgent full blood count for the platelet count. Other values on the FBC should be normal
37
ITP mx
Tx may be required if the patient is actively bleeding or severe thrombocytopenia (platelets below 10): Prednisolone IV immunoglobulins Blood transfusions if required Platelet transfusions only work temporarily, sometimes given to these patients in the context of severe life-threatening haemorrhage. Rituximab is increasingly being used in patients with resistant ITP long term immunosuppression with drugs such as Azathioprine. Consideration of splenectomy
38
Advice about ITP
Avoid contact sports Avoid intramuscular injections and procedures such as lumbar punctures Avoid NSAIDs, aspirin and blood thinning medications Advice on managing nosebleeds Seek help after any injury that may cause internal bleeding, for example car accidents or head injuries
39
Vaccinations normally given a few weeks prior to splenectomy include:
HIB vaccine, Streptococcus pneumonia vaccine, Meningococcal A and C vaccine. Pneumoccocal vaccine should be repeated every five years. – splenectomy makes patients at increased risk of bacterial infection with encapsulated organisms e.g. streptococci (rather than viruses)
40
Thrombotic thrombocytopenic purpura
blood disorder that results in blood clots forming in small blood vessels throughout the body. This results in a low platelet count, low red blood cells due to their breakdown, and often kidney, heart, and brain dysfunction.
41
Thrombotic thrombocytopenic purpura epidemiology
30-50
42
TTP presentation
fever, neurological signs, renal failure, microangiopathic haemolytic anaemia
43
causes of massive splenomegaly
CML Myelofibrosis Malaria
44
Warm autoimmune haemolytic anaemia (AIHA) pathophysiology
IgG mediated extravascular haemolytic disease in which the spleen tags cells for splenic phagocytosis
45
Causes of warm AIHA
Idiopathic Lymphoproliferative neoplasms (CLL and lymphoma) Drugs including methyldopa SLE
46
Cold autoimmune haemolytic anaemia (AIHA) pathophysiology
IgM-mediated haemolytic disease in which IgM fixes complement causing direct intravascular haemolysis (also known as cold agglutinins)
47
Causes of the cold AIHA:
Idiopathic Post-infectious haemolytic anaemias: occurring 2-3 weeks after infection (examples include EBV and mycoplasma)
48
direct Coombs test
test for autoimmune haemolytic anaemia (AIHA). Patients with AIHA have antibodies directed against cell surface markers on the red blood cell. The Coombs test uses antibodies against these autoantibodies to cross link and agglutinate the red cells.
49
Clinical features of Beta thalassaemia major
Severe symptomatic anaemia at 3-9 months failure to thrive Frontal bossing Maxillary overgrowth Extramedullary hematopoiesis (hepatosplenomegaly). microcytic anaemia
50
Beta thalassaemia
deficiency in beta globin chain production. Free alpha chains subsequently clump together and damage the erythrocyte cell membrane leading to haemolysis. Prognosis is usually death by heart failure if it goes undiagnosed.
51
Management of Beta thalassaemia
regular blood transfusions. iron chelating agents (e.g. desferrioxamine)
52
Clinical presentation Polycythaemia rubra vera
ruddy complexion Fatigue Headache Visual disturbances Pruritus (typically after a hot bath) Erythromelalgia (a painful burning sensation in the fingers and toes) Arterial thrombosis (such as MI or stroke) Venous thrombosis (such as PE or DVT) Haemorrhage (intracranial or gastrointestinal) Paradoxical increased bleeding risk (due to impaired platelet function) Increased risk of gout Facial redness on examination Splenomegaly
53
Treatment polycythaemia ruba vera
phlebotomy (venesection), antiplatelet therapy e.g. Aspirin and cytoreductive therapy such as hydroxycarbamide. Avoid iron replacement
54
Sickle cell
*autosomal-recessive *Mutation in haemoglobin beta chain *glutamic acid is replaced by valine on the 6th position of the β chain.
55
Complications of sickle cell
Children - delayed growth , aplastic crisis, sequestration crisis, Adult- ARDS, cardio renal problem, avascular necrosis of hip , chronic ulcers, increased stroke risk Vaso- occlusive crisis
56
Management of chronic sickle cell
Patients with frequent crises (3 or more per year) may benefit from oral Hydroxycarbamide (ribonucleotide reductase inhibitor), which increases synthesis of HbF Hydroxyurea- reduction in the incidence of painful crises and acute chest syndrome. Immunisation Prophylactic Phenoxymethylpenicillin – Life Long if asplenic Folic Acid transfusion
57
Haemophilia A
deficiency in factor VIII
58
Haemophilia B (also known as Christmas disease)
deficiency in factor IX.
59
Blood test results in haemophilia
prolonged APTT ( intrinsic pathway measure) normal bleeding time, thrombin, prothrombin
60
Warfarin prevents the action of clotting factors
Factors II, VII, IX and X - 2 + 7 makes 9 not 10
61
Hereditary spherocytosis
autosomal dominant condition, seen in northern European populations spherical distortion of cells (seen as spherocytes on blood film)Eventually, as more membrane is removed, the cells haemolyse (extravascular haemolysis) and are removed from circulation in the spleen.
62
Clinical features of Hereditary spherocytosis
neonatal or childhood onset jaundice/anaemia, and splenomegaly.

Medicine (72 decks)

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