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General practice > Haem II > Flashcards

Haem II Flashcards

1
Q

Leukaemia likelihood by age

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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2
Q

Features of AML

A 
Anaemia 
Neutropenia 
Thrombocytopenia 
Splenomegaly 
Bone pain
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3
Q

Differential diagnosis of petechiae

A 
Leukaemia
Meningococcal septicaemia
Vasculitis
HSP
ITP
Non-accidental injury
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4
Q

What is acute lymphoblastic leukaemia

A

Acute proliferation of a single type of lymphocyte, usually B-lymphocytes

Excessive proliferation of these cells causes them to replace the other cell types being created in the bone marrow, leading to a pancytopenia

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5
Q

Syndrome associated with ALL

A

Downs syndrome

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6
Q

What does a blood film show in ALL

A

Blast cells

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7
Q

Genetic mutation associated with CML

A

Philadelphia chromosome (t(9:22) translocation)

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8
Q

What is CLL

A

chronic proliferation of a single type of well differentiated lymphocyte, usually B-lymphocytes. This usually affects adults over 55 years of age

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9
Q

Presentation of ALL

A

Often it is asymptomatic but it can present with infections, anaemia, bleeding and weight loss.

It can cause warm autoimmune haemolytic anaemia.

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10
Q

What is richter’s transformation

A

CLL can transform into high-grade lymphoma

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11
Q

What does a blood film show in CLL

A

“smear” or “smudge” cells. These occur during the process of preparing the blood film where aged or fragile white blood cells rupture and leave a smudge on the film.

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12
Q

Phases of CML

A

Chronic
Accelerated
Blast

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13
Q

What is the chronic phase of CML

A

The chronic phase can last around 5 years, is often asymptomatic and patients are diagnosed incidentally with a raised white cell count.

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14
Q

What is the accelerated phase of CML

A

Abnormal blast cells take up a high proportion of the cells in the bone marrow and blood (10-20%).

In the accelerated phase patients become more symptomatic, develop anaemia and thrombocytopenia and become immunocompromised.

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15
Q

What is the blast phase of CML

A

Follows the accelerated phase and involves an even high proportion of blast cells and blood (>30%).

This phase has severe symptoms and pancytopenia. It is often fatal.

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16
Q

Cytogenic change in CML

A

The cytogenetic change that is characteristic of CML is the Philadelphia chromosome, which is a translocation of genes between chromosome 9 and 22: it is a t(9:22) translocation.

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17
Q

Most common acute leukaemia in adults

A

AML

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18
Q

What might a blood film show in AML

A

High proportion of blast cells. These blast cells can have rods inside their cytoplasm that are named Auer rods.

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19
Q

Mx of Leukaemia

A

Chemotherapy and steroids

Radiotherapy
Bone marrow transplant
Surgery

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20
Q

Complications of chemotherapy

A 
Failure 
Stunted growth and development in children 
Infections 
Neurotoxicity 
Infertility 
Tumour lysis syndrome
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21
Q

What causes tumour lysis syndrome

A

Caused by the release of uric acid from cells that are being destroyed by chemotherapy

The uric acid can form crystals in the interstitial tissue and tubules of the kidneys and causes acute kidney injury.

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22
Q

Other chemicals released in tumour lysis syndrome

A

Potassium and phosphate are also released so these need to be monitored and treated appropriately.

High phosphate can lead to low calcium, which can have an adverse effect, so calcium is also monitored.

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23
Q

Complications of CLL

A

Anaemia
Hypogammaglubulinaemia(recurrent infections)
Warm autoimmune haemolytic anaemia
Richter’s transformation

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24
Q

Mx of CML

A

Imatinib first line(tyrosine kinase inhibitor)

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25
Q

Mx of tumour lysis syndrome

A

IV allopurinol or IV rasburicase

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26
Q

What is myeloma

A

cancer of the plasma cells. These are a type of B lymphocyte that produce antibodies

Large quantities of a single type of antibody produced

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27
Q

What is monoclonal gammopathy of undetermined significance

A

excess of a single type of antibody or antibody components without other features of myeloma or cancer

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28
Q

What is smouldering myeloma

A

progression of MGUS with higher levels of antibodies or antibody components. It is premalignant and more likely to progress to myeloma than MGUS

29
Q

What is waldenstrom’s macroglobulinemia

A

type of smouldering myeloma where there is excessive IgM specifically

30
Q

Most common type of antibody produced by myeloma

A

More than 50% of the time this is immunoglobulin type G (IgG)

31
Q

What is the bence jones protein

A

can be found in the urine of many patients with myeloma and is actually a part (subunit) of the antibody called the light chains.

32
Q

Why is there anaemia in myeloma

A

plasma cells invade the bone marrow(infiltration) and cause suppression of development of other blood cell lines –> anaemia, neutropenia and thrombocytopenia

33
Q

Features of myeloma bone disease

A

Skull, spine, long bones and ribs commonly affected

Osteolytic lesions - pathological fractures

Vertebral fractures

Hypercalcaemia

34
Q

What are plasmacytomas

A

individual tumours made up of the cancerous plasma cells. They can occur in the bones, replacing normal bone tissue or can occur outside bones in the soft tissue of the body.

35
Q

Features of myeloma renal disease

A

High levels of immunoglobulins (antibodies) can block the flow through the tubules
Hypercalcaemia impairs renal function
Dehydration
Medications used to treat the conditions such as bisphosphonates can be harmful to the kidneys

36
Q

Risk factors for multiple myeloma

A 
Older age
Male
Black African ethnicity
Family history
Obesity
37
Q

Initial ix in multiple myeloma

A 
FBC (low white blood cell count in myeloma)
Calcium (raised in myeloma)
ESR (raised in myeloma)
Plasma viscosity (raised in myeloma)

urgent serum protein electrophoresis and a urine Bence-Jones protein test.

38
Q

Testing specifically for myeloma - BLIP

A

B – Bence–Jones protein (request urine electrophoresis)
L – Serum‑free Light‑chain assay
I – Serum Immunoglobulins
P – Serum Protein electrophoresis

39
Q

Imaging for myeloma

A

Whole body MRI
Whole body CT
Skeletal survey (xray images of the full skeleton)

40
Q

X-ray signs in myeloma

A

Punched out lesions
Lytic lesions
“Raindrop skull” caused by many punched out (lytic) lesions throughout the skull that give the appearance of raindrops splashing on a surface

41
Q

Mx of myeloma

A

Chemotherapy first one

Stem cell transplantation

VTE prophylaxis

42
Q

1st line chemotherapy for multiple myeloma

A

Bortezomid
Thalidomide
Dexamethasone

43
Q

Mx of myeloma bone disease

A

Bisphosphonates
Radiotherapy
Orthopaedic surgery
Cement augmentation

44
Q

complications of myeloma

A 
Infection 
Renal failure 
Anaemia 
Peripheral neuropathy 
SCC
Hyperviscosity
45
Q

Presentation of von willebrand disease

A

Bleeding gums with brushing
Nose bleeds (epistaxis)
Heavy menstrual bleeding (menorrhagia)
Heavy bleeding during surgical operations

46
Q

Diagnosis of von willebrand disease

A

Bleeding assessment tools
History
Family history

47
Q

Mx of von willebrand disease

A

Only if major bleeding or trauma

Desmopression
VWF infusion
Factor VIII infusion

48
Q

Mx of VMD in women with heavy periods

A 
Tranexamic acid
Mefanamic acid
Norethisterone
Combined oral contraceptive pill
Mirena coil

Hysterectomy in severe cases

49
Q

What is haemophilia A caused by

A

Deficiency in factor VIII

50
Q

What is haemophilia B caused by

A

Deficiency in factor IX

51
Q

Inheritance of haemophilia A and B

A

X linked recessive

52
Q

Presentation of haemophilia A and B

A

Abnormal bleeding - gums, GI tract, joints(can lead to damage and deformity)

Haematuria

53
Q

Mx of haemophilia

A

Replacement of clotting factors by IV infusion

Desmopressin to stimulate VWF release

Tranexamic acid

54
Q

Diagnosis of haemophilia

A

bleeding scores, coagulation factor assays and genetic testing

55
Q

Signs and symptoms of thalassaemia

A 
Low MCV 
Fatigue 
Pallor 
Jaundice 
Gallstones 
Splenomegaly
56
Q

Diagnosis of thalassaemia

A

FBC
Haemoglobin electrophoresis
DNA testing

57
Q

What needs to be monitored in thalassaemia

A

Serum ferritin - iron overload due to faulty RBCs, recurrent transfusions and increased absorption of iron in response to anaemia

58
Q

Mx of alpha thalassaemia

A

Monitor FBC
Blood transfusions
Splenectomy
Bone marrow transplant(curative)

59
Q

Mx of beta thalassamia

A

Regular transfusions
Iron chelation
Splenectomy
Bone marrow transplant

60
Q

Complications of sickle cell anaemia

A 
Anaemia 
Stroke 
Avascular necrosis 
Pulmonary HTN 
Priapism
61
Q

Renal complication of sickle cell anaemia

A

CKD

62
Q

Neurological complication of sickle cell anaemia

A

Stroke

63
Q

Mx of sickle cell anaemia

A 
Avoid dehydration 
Up to date vaccinations 
Antibiotic prophylaxis(Pen V) 
Blood transfusion 
Bone marrow transplant
64
Q

Mx of sickle crises

A 
Admission 
Treat infection 
Keep warm 
IV fluids 
Simple analgesia 
Penile aspiration in priapism
65
Q

Presentation of splenic sequestration crisis

A

Acutely enlarged and painful spleen –> severe anaemia and circulatory collapse

66
Q

Mx of splenic sequestration crisis

A

supportive with blood transfusions and fluid resuscitation to treat anaemia and shock

Splenectomy in recurrent crises

67
Q

what can trigger aplastic crisis in sickle cell anaemia

A

Parvovirus B19

Leads to significant anaemia

68
Q

Diagnosis of acute chest syndrome in sickle cell anaemia

A

Fever or respiratory symptoms with

New infiltrates seen on a chest xray

69
Q

Mx of acute chest syndrome in sickle cell anaemia

A

Antibiotics or antivirals for infections
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Artificial ventilation with NIV or intubation may be required

General practice (26 decks)

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