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Medicine > Haematology > Flashcards

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
Q

microscopy myeloma

A

Rulo - red cells coated with immunoglobulin, chain appearance,Rouleaux formation refers to the stacking of 4 or more red blood cells.

26
Q

BJ proteins

A

free light chains filtered by the kidney excreted in urine, their presence in urine suggest myeloma
•Serum free light chains XS, -

27
Q

Myeloma

A

Lymphoid disorder,

•Malignant plasma cells,memory b cells in bone marrow, which with secrete IgG

28
Q

lymphoma staging system

A

Ann arbor

29
Q

Microscopy Burkitt lymphoma

A

Starry sky appearance

Tingible bodies - macrophages that have eaten neoplastic cells

30
Q

Pel Ebstein fever

A

high-grade fever that keeps rising and falling every 7-10 days or so
associated with hodgekins

31
Q

Microcytic anaemia causes - TAILS:

A

Thalassaemia
Anaemia of chronic disease (though usually normocytic)
Iron deficiency
Lead poisoning
Sideroblastic anaemia

32
Q

Normocytic anaemia causes

A

normo - 3As and 2Hs
acute blood loss, anaemia of chronic disease, aplastic anaemia
haemolytic anaemia, hypothyroidism

33
Q

Macrocytic anaemia causes

A

Macro - FAT RBC
folate, alcohol, hypothyroid, reticulocytotic, B12, cytotoxics

34
Q

Idiopathic thrombocytopenia purpura

A

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
Q

Idiopathic thrombocytopenia purpura epidemiology

A

children under 10 years old. Often there is a history of a recent viral illness

36
Q

Ix for ITP

A

condition can be confirmed by doing an urgent full blood count for the platelet count. Other values on the FBC should be normal

37
Q

ITP mx

A

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
Q

Advice about ITP

A

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
Q

Vaccinations normally given a few weeks prior to splenectomy include:

A

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
Q

Thrombotic thrombocytopenic purpura

A

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
Q

Thrombotic thrombocytopenic purpura epidemiology

A

30-50

42
Q

TTP presentation

A

fever, neurological signs, renal failure, microangiopathic haemolytic anaemia

43
Q

causes of massive splenomegaly

A

CML
Myelofibrosis
Malaria

44
Q

Warm autoimmune haemolytic anaemia (AIHA) pathophysiology

A

IgG mediated extravascular haemolytic disease in which the spleen tags cells for splenic phagocytosis

45
Q

Causes of warm AIHA

A

Idiopathic
Lymphoproliferative neoplasms (CLL and lymphoma)
Drugs including methyldopa
SLE

46
Q

Cold autoimmune haemolytic anaemia (AIHA) pathophysiology

A

IgM-mediated haemolytic disease in which IgM fixes complement causing direct intravascular haemolysis (also known as cold agglutinins)

47
Q

Causes of the cold AIHA:

A

Idiopathic
Post-infectious haemolytic anaemias: occurring 2-3 weeks after infection (examples include EBV and mycoplasma)

48
Q

direct Coombs test

A

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
Q

Clinical features of Beta thalassaemia major

A

Severe symptomatic anaemia at 3-9 months
failure to thrive
Frontal bossing
Maxillary overgrowth
Extramedullary hematopoiesis (hepatosplenomegaly).
microcytic anaemia

50
Q

Beta thalassaemia

A

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
Q

Management of Beta thalassaemia

A

regular blood transfusions.
iron chelating agents (e.g. desferrioxamine)

52
Q

Clinical presentation Polycythaemia rubra vera

A

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
Q

Treatment polycythaemia ruba vera

A

phlebotomy (venesection), antiplatelet therapy e.g. Aspirin and cytoreductive therapy such as hydroxycarbamide.
Avoid iron replacement

54
Q

Sickle cell

A

*autosomal-recessive
*Mutation in haemoglobin beta chain
*glutamic acid is replaced by valine on the 6th position of the β chain.

55
Q

Complications of sickle cell

A

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
Q

Management of chronic sickle cell

A

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
Q

Haemophilia A

A

deficiency in factor VIII

58
Q

Haemophilia B (also known as Christmas disease)

A

deficiency in factor IX.

59
Q

Blood test results in haemophilia

A

prolonged APTT ( intrinsic pathway measure)
normal bleeding time, thrombin, prothrombin

60
Q

Warfarin prevents the action of clotting factors

A

Factors II, VII, IX and X - 2 + 7 makes 9 not 10

61
Q

Hereditary spherocytosis

A

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
Q

Clinical features of Hereditary spherocytosis

A

neonatal or childhood onset jaundice/anaemia, and splenomegaly.

Medicine (72 decks)

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