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Y4 Cancer care > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the first line medication for neutropenic sepsis?

A

Tazocin- needs to be given within the first half an hour
If penicillin allergic- give Meropenem
Ideally get the cultures first, but need first dose of antibiotics first

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2
Q

Where do you take blood cultures?

A

Need to take cultures from peripheral vein and indwelling lines

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3
Q

Common infection in patients with haematological malignancies?

A

Diarrhoea- perianal infections

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4
Q

What should you consider in patients with neutropenia if they are not responding to antibiotics?

A

Atypical infections- especially fungal infections

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5
Q

What biomarkers would indicate fungal disease?

A

B-D glucan
Galactomannan
Aspergillus PCR

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6
Q

With neutropenic sepsis, if patient is still not recovering what should you consider?

A

Vancomycin for gram positive cover
If BP dropping- could give Gentamicin (gram negative sepsis, usually from urine/gut)

Contact ITU and get your senior involved

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7
Q

How long do blood cultures take to come back?

A

48 hours

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8
Q

Prophylactic medication

A

Aciclovir- varicella and herpes reactivation
Posaconazole- prevent fungal infection
Co-trimoxazole- prevent PCP

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9
Q

What to give people who are going on chemotherapy to reduce neutropenia

A

G-CSF (granulocyte colony stimulating factor)

Bone pain (femur), headache, fatigue and nausea

Often used in prophylactic lymphoma where neutropenia is expected

Do NOT give in Leukemia- stem cell disease (AML/CML)

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10
Q

What would make you suspicious of a thrombosis in the PICC line? What symptoms?

A

Swelling
Erythema
Normally upstream of the line. A week or two after it has been put in

Investigate?- doppler ultrasound

Management= Enoxparin (LMWH)

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11
Q

What is the complication we are trying to prevent with irradiated blood products?

A

Transfusion associated graft vs host disease

You might accidentally transfuse lymphocytes.

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12
Q

Common chemotherapy in chronic lymphocytic leukemia

A

Fludarabine (purine analogue)

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13
Q

When is cryoprecipitate used?

A

To replace fibrinogen
DIC or major hemorrhage

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14
Q

What is tumor lysis syndrome?

A

Any patient with haematological malignancy can get TLS
Potassium, phosphate and uric acid rises
Calcium is low because phosphate binds to calcium
Cells are full of potassium and uric acid
Release all of those cellular components

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15
Q

How can you prevent TLS?

A

Patient is given lots of IV fluids!!
Strict input/output monitoring

Allopurinol
Xanthine oxidase inhibitor
Xanthine oxidase makes uric acid

Also
Rasburicase (urate oxidase)a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys
generally preferred now for patients at a higher risk of developing TLS

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16
Q

What can you give women who are about to undergo chemotherapy to stop their periods?

A

Norethisterone used to stop menstruation (synthetic oral progestin)

Do NOT give COCP- increase thrombotic risk

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17
Q

How to preserve fertility before chemotherapy?

A

Egg collection (have to wait for a cycle, hormone treatment) if it cancer doesn’t need immediate treatment
Sperm storage in men- cryopreserved

Can give gnrh blockers- shuts down system and reduces damage to eggs

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18
Q

How to prevent mucositis

A

Mouth care is very important
Can get serious impairing ability to eat

Chlorhexidine
Difflam (pain relief)

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19
Q

What is the difference between acute and chronic in blood cancers?

A

Chronic= mature cells (more differentiated)
Acute= higher up the chain in hemopoesis (less differentiated)

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20
Q

Symptoms in blood cancers?

A

Can be non-specific and widely spread across the body:
Weight loss
Infections
Run down
Weak

Picked up on a blood film

Lymphoma= B symptoms
- Night sweats
- Weight loss
- Fever

Can also find unexplained itching with Lymphoma

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21
Q

What are the common infectious causes of lymphadenopathy?

A

Viral: Epstein-Barr virus (EBV), Cytomegalovirus (CMV), HIV.
Bacterial: Staphylococcus aureus, Streptococcus pyogenes, Mycobacterium tuberculosis.
Parasitic: Toxoplasma gondii.

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22
Q

List three common neoplastic causes of lymphadenopathy

A

Lymphoma: Hodgkin and non-Hodgkin lymphoma.
Leukaemia: Chronic lymphocytic leukaemia (CLL), acute lymphoblastic leukaemia (ALL).
Metastatic cancer: Breast, lung, or gastrointestinal carcinomas

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23
Q

What are the common autoimmune causes of lymphadenopathy

A

Systemic lupus erythematosus (SLE): Generalised lymphadenopathy.
Rheumatoid arthritis: Chronic inflammation-related.
Sarcoidosis: Non-caseating granulomas affecting lymph nodes.

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24
Q

How to investigate haematological malignancy?

A

Routine bloods
- FBC, UE, LFT, CRP, Ca2+
- Haematinics, retics, Blood film

Special bloods
- LDH, urate, B2M (beta 2 microglobulin), PV (plasma viscocity)
- Ig +/- SFLC
- PB immunophenotyping

Imaging
- CT scan
- PET scan (lymphoma/myeloma)
- MRI spine/pelvis (myeloma)

Invasive
- Tissue biopsy
- BM aspirate and trephine

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25
Q

Types of Leukaemia

A
  • Acute myeloid leukaemia- Auer rod blood film (buzz word)
  • Acute Lymphoblastic leukaemia
  • Chronic myeloid leukaemia- Philadelphia chromosome translocation
  • Chronic lymphocytic leukaemia
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26
Q

Types of Myeloproliferative neoplasms

A

Still cancers but softer. Not the same as acute leukaemias.

Essential thrombocythaemia- biggest risk is thrombosis

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27
Q

What are some advantages of central venous acess?

A

More than one drug at a time (multi lumen)
Continuous infusion (>24 hours)
Can give nutrition via central catheters
Less invasive for frequent treatment
Home treatment
Long term (over months) therapy
Reduced risk of extravasation (vesicants)

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28
Q

What are some disadvantages of central venous access?

A

Risk of pneumothorax during insertion
Infection (insertion and use)
Bleeding (during procedure of insertion)
Thrombosis of line
Misplacement (could go arterial or into jugular vein), CXR to check, use ultrasound when inserting

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29
Q

What is neutropenic sepsis defined as?

A

Neutrophil count of 0.5 x 10^9 per litre or lower

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30
Q

Causes of pancytopenia

A

Inherited/acquired

Inherited
- Aplastic anaemia
- Fanconi anaemia
- Diamond-Blackfan anaemia (don’t worry about detail)
- Ataxia pancytopenia syndrome (don’t worry about detail)

Acquired
- Excessive alcohol consumption
- Cancers- leukemia, lymphoma, myeloma, myelodysplastic syndrome, metastatic bone marrow cancer
- Hyposplenism
- PNH (paryxysmal nocturnal haemoglobinuria)
- Chemotherapy- methotrexate

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31
Q

Investigations for pancytopenia

A
  • FBC
    (Macrocytic, normocytic, or microcytic anaemia can suggest different causes (e.g., vitamin B12/folate deficiency, bone marrow failure, etc.)
  • Blood film (Blast cells may indicate acute leukaemia.
    Atypical lymphocytes suggest infections like infectious mononucleosis (EBV).
    Tear-drop cells may indicate myelofibrosis.
    Schistocytes might point to haemolytic anaemia or thrombotic microangiopathies.)
  • Bone marrow aspiration and biopsy (LDH levels are also useful in suspecting a malignancy)
  • Autoimmune test- RA/lupus
  • Infection disease testing- HIV and Hep C can cause pancytopenia. Mono, TB and malaria.
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32
Q

What is pancytopenia?

A

Decrease in all peripheral blood cell lines (Low red blood cells, neutrophils and platelets)

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33
Q

Most common causes for pancytopenia

A

Chemotherapy
Immunosuppressants (steroids don’t tend to cause pancytopenia)
B12/folate deficiency- key for making DNA
Alcoholic liver cirrhosis

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34
Q

What type of bleeding do you get with thrombocytopenia?

A

Epistaxis
Mucosal bleeding
(clotting problems)

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35
Q

What is the difference between clotting and platelet type bleeding?

A

Clotting- bruising, swollen joints
Platelet type bleeding- petechial rash (blood blisters on mucosal membranes and skin), mucosal bleeding

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36
Q

Features of fanconi syndrome

A
  • Cafe au lait spots
  • Curved spine or short stature
  • Learning disabilities
  • Constipation and weakness
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37
Q

Febrile neutropenia vs neutropenic sepsis

A

Febrile neutropenia
- Fever in a patient who is neutropenia

Neutropenic sepsis
- Hypotension, tachycardia
- Acidotic

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38
Q

Importance of LDH

A

Increased cellular turnover
Not specific-

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39
Q

What anaemia does B12 deficiency cause

A

Macrocytosis with hypersegmented neutrophils

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40
Q

Where is B12 absorbed?

A

Terminal ileum

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41
Q

If you administer folate first then the B12 will drop

A

Subacute demyelination of the spinal cord

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42
Q

Why do you have to be careful with transfusing patients with B12 deficiency?

A

1 unit at a time- otherwise will go into heart failure

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43
Q

What test tells you how well the bone marrow is functioning?

A

Reticulocyte count
Lots of reticulocytes, more of a purple colour on a blood film- polychromasia (lots of different colours)

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44
Q

How long are patients under surveillance for before they are discharged with high grade lymphoma?

A

3 years

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45
Q

Can you cure myeloma?

A

No you keep patients under surveillance

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46
Q

What are symptoms of relative (decreased plasma volume) polycythemia vera?

A
  • Dry mucous membranes
  • Decreased skin turgor
  • Orthostatic hypotension
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47
Q

What are types of myeloproliferative disorders?

A

Essential thrombocythemia
Polycythemia vera
Myelofibrosis
Chronic myeloid leukaemia

All of these disorders involve dysregulation at the
multipotent haematopoietic stem cell

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48
Q

What is the genetic mutation in myeloproliferative disorders?

A

Many patients have a specific point mutation in one copy
of the Janus kinase 2 gene (JAK2)
- a cytoplasmic tyrosine kinase on chromosome 9,
which causes increased proliferation and survival of
haematopoietic precursors
We now have specific drugs targeting the aberrant protein

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49
Q

What is a paraprotein?

A

An abnormal monoclonal protein produced by a single clone of plasma cells

Paraprotein/M spike/M protein are all the same thing

We produce polyclonal antibodies to cover all infections- why patients get sick with myeloma because they have immunoparesis (don’t make enough of the other immunoglobulins to cover infection)

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50
Q

What is the most common immunoglobulin found in myeloma?

A

IgG

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51
Q

How can you diagnose myeloma?

A
  • Serum electrophoresis (M spike) M-spike on SPEP: Indicates overproduction of a monoclonal immunoglobulin.
  • Light chain assay with a ratio of 2:1

For the above two just need a normal blood test
- Bone Marrow Biopsy: Confirms diagnosis by identifying ≥10% clonal plasma cells and assessing marrow architecture.
- Additional Testing: Cytogenetics (FISH), CRAB criteria evaluation, and imaging (to detect bone lesions).

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52
Q

What are plasma cells?

A

Mature B lymphocytes

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53
Q

If a patient has high levels of IgM what symptom should you be worried about?

A

Hyper viscosity as IgM immunoglobulins are the largest in size

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54
Q

Should you put down bence jones proteins as an investigation for myeloma?

A

NO
It is no longer being used. If you can find light chains in the serum why look in the urine

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55
Q

What is the main result commonly seen on FBC with myeloma?

A

Anaemia
Don’t commonly see thrombocytopenia and low WCC

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56
Q

What percent of clonal plasma cells need to be seen on biopsy for it to be called myeloma?

A

> 10%

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57
Q

When do you start to treat myeloma?

A

When plasma cells seen are >10%
15g/l
Or there is symptomatic myeloma (CRABBI)

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58
Q

What is MGUS?

A

Monoclonal gammopathy of undetermined significance (MGUS, also known as benign paraproteinaemia and monoclonal gammopathy) is a common condition that causes a paraproteinaemia and is often mistaken for myeloma

Think about it like a spectrum with MGUS on one side and symptomatic myeloma on the other

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59
Q

IMWG guidelines

A

Take a look

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60
Q

If a patient has CRABBI symptoms, what should you make sure you do first?

A

Rule out underlying causes

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61
Q

How do you manage a spinal cord compression and what could be causing it in myeloma?

A

Give 16mg STAT of Dexamethasone straight away while ordering a WHOLE spine MRI
No one will mind if they have one dose of steroids and it turns out to not be a spinal cord compression

Plasmacytoma- can be shrunken with radiotherapy

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62
Q

What two symptoms should you ask about with a lymphoma?

A

Visual changes and headaches (microvascular changes)

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63
Q

Why should you be cautious with giving RBCs for patients with myeloma?

A

Hyper viscous blood
One unit at a time

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64
Q

What is the pathophysiology of amyloidosis?

A

Plasma cells mutate and begin to produce abnormal light chain proteins
Light chains become misfolded
Typically affects the heart and/or kidneys

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65
Q

What staining is done for amyloidosis?

A

Congo red staining with green apple colouring if positive

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66
Q

What is Waldenstrom’s macroglobulinaemia?

A

Waldenström’s macroglobulinaemia (WM) is a type of blood cancer where abnormal B-cells produce excessive amounts of IgM paraprotein. This IgM protein is larger than other immunoglobulins, leading to hyperviscosity (thickened blood), which can cause circulation problems like headaches, blurred vision, and dizziness.

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67
Q

What should you tell patients when they are diagnosed with myeloma?

A

It is an incurable disease but it is very treatable

(Essentially you keep trying treatment after treatment, will not be unusual for a patient to be on the 6th line)

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68
Q

When should you be suspicious of fractures?

A

Takes minimal effort to fracture (sneezing and vertebral fracture)

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69
Q

Should you do a skeletal survey?

A

NO
Whole body MRI instead
You have to lose a lot of cortical bone for it to show up (lytic lesion)

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70
Q

What surgeries can take place without disruption to anticoagulants?

A

Minor skin surgeries, cataract surgeries and dental extractions

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71
Q

What are the three main broad symptoms you can ask about with a patient presenting with lymphoma/leukemia

A

Pancytopenia

Fatigue- low RBCs
Fever- low neutrophils
Bleeding- low platelets

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72
Q

What drug is given to patients with chronic myeloid leukemia?

A

Key Points of Relationship:
Philadelphia chromosome (BCR-ABL1 fusion) is the genetic hallmark of CML.
Imatinib directly targets the abnormal protein (BCR-ABL1) produced by the Philadelphia chromosome, thereby controlling the disease.
Imatinib therapy represents a targeted treatment approach, demonstrating the success of molecularly targeted therapies in haematological malignancies.
In summary, the Philadelphia chromosome is the genetic abnormality responsible for CML, and imatinib is the targeted therapeutic agent that specifically inhibits the pathogenic effects of the BCR-ABL1 fusion protein.

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73
Q

What are the three categories of polycythaemia?

A

Relative
- Dehydration
- Stress (Gaisbock syndrome)

Primary (abnormal proliferation of erythroid precursors)
- Polycythaemia rubra vera

Secondary (increased EPO)
- COPD
- Altitude
- OSA
- Excessive EPO- tumour secretion

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74
Q

What are symptoms/signs of polycythemia vera? (EPO low)

A
  • Pruritis
  • Erythromelagia
  • Headaches/visual disturbance
  • Sweats
  • Gout
  • Thrombosis
  • Subconjuntival suffusion
  • Ruddy complexion
  • Tinnitus
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75
Q

Investigations for suspected polycythemia vera

A

FBC- RBC, raised hematocrit, raised haemoglobin, raised red cell mass with low/low-normal plasma volume
History of secondary causes
EPO level (low)
JAK2- if negative consider sleep studies (other causes)
USS abdomen (splenomegaly, renal masses, uterine masses (secondary polycythaemia through increased blood loss)

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76
Q

Management for polycythaemia

A

Aims??
Reduce the risk of thrombotic events
Manage symptoms and address underlying causes

Therapeutic phlebotomy

Low-dose aspirin

Cytoreductive therapy (hydroxyurea) In those patients who are high risk (>60, cardiovascular risk factors)

Venesection in the acute phase

Lifestyle modifications- smoking cessation, weight control, BP control

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77
Q

What is the difference between cytoreductive therapy and venesection?

A

Venesection is a quick fix that removes blood to lower cell counts temporarily.

Cytoreductive therapy is a long-term treatment that uses medication to reduce blood cell production and manage the disease at the source.

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78
Q

Complications of polycythaemia vera?

A

Ischaemic stroke
Myocardial infarction
Pulmonary embolism
Progression to myelofibrosis or acute myeloid leukaemia
Gastrointestinal haemorrhage
Budd-Chiari syndrome

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79
Q

What is graft versus host disease?

A

A type 4 sensitivity reaction

A donor transplant containing a high number of T lymphocytes (usually bone marrow or liver transplants) is given to the patient. The patient can’t overcome the attack of the donor T lymphocytes

Common complications are
- Diarrhoea
- Abdominal pain
- Hepatosplenomegaly
- Jaundice
- Maculopapular rash

80
Q

What is thrombocytosis?

A

A platelet count greater than 450 x 10^9/L

81
Q

What are the three myeloproliferative disorders?

A
  • Primary myelofibrosis
  • Polycythaemia vera
  • Essential thrombocythaemia
82
Q

What would a blood film look like with myelofibrosis?

A

Teardrop-shaped red blood cells
Anisocytosis (varying sizes of red blood cells)
Blasts (immature red and white cells)

83
Q

What are the two main causes of thrombocytosis and how do you differentiate between them?

A

Primary
- Polycythaemia rubra vera
- Chronic myeloid leukaemia
- Essential thrombocythaemia
- Primary myelofibrosis

Increased tendency to bleed
Vasomotor symptoms/bleeding
Splenomegaly

Secondary (reactive)
- Bleeding
- Haemolysis
- Iron deficiency
- Hyposplenism

Bone marrow biopsy normal
JAK2 mutation negative
Raised ESR/CRP

84
Q

How do you treat thrombocytosis?

A
  • Low dose aspirin
  • Hydroxycarbamide to reduce platelet count
  • Interferon alpha for younger patients
  • Anagrelide= specialsit platelet lowering agent
85
Q

Why do you get paradoxical bleeding with thrombocytosis?

A

Very high platelet count
Acquired vWD
In acquired von Willebrand disease, despite having a high number of platelets, the bleeding occurs because there is not enough functional von Willebrand factor to help the platelets stick together and adhere to blood vessel walls. This results in weak or ineffective clots, leading to bleeding problems.

VWF gets used up

86
Q

What test can GPs request to find out whether a lymphoma is B or T cell?

A

Flow cytometry

87
Q

What is the relationship between steroids and neutrophils?

A

People who are on steroids generally have a neutrophila

88
Q

What is a key distinguishing feature between reactive vs malignant lymphadenopathy?

A

Waiting! Persistent lymph nodes more likely to be malignant.

Weeks to months

89
Q

What is a ruddy face more common with?

A

SVCO to do with lung cancer
Don’t get the same with lymphoma

90
Q

Is lymphoma curable?

A

NO but it is treatable

91
Q

Why do you need to administer intrathecal chemo?

A

So it crosses the blood brain barrier

92
Q

Questions when you suspect SVCO?

A
  • Swollen limbs- do your rings feel tighter?
  • Cough when lying down (mediastinal mass)
  • Collaterals
  • Changes in vision/hearing
93
Q

Why are iron tablets more effective when taken every other day?

A

Optimises absorption by allowing time for increased iron transporter expression.

94
Q

What is the molecular rationale behind the use of combination chemotherapy in the induction phase for lymphoma?

A

Combination chemotherapy targets different cell cycle phases, increasing cytotoxicity and reducing the likelihood of resistance. This approach aims to induce rapid tumour lysis and remission.

95
Q

What are the key considerations for selecting maintenance therapies in lymphoma post-remission?

A

Maintenance therapies are selected based on patient-specific factors such as molecular subtype, prior response to treatment, and minimising long-term toxicity while sustaining disease control.

96
Q

What biological markers or clinical factors guide the decision to adopt a watch-and-wait strategy in indolent lymphomas?

A

Indicators include low tumour burden, absence of B symptoms, stable biochemical markers (e.g., LDH), and slow progression on imaging, with regular monitoring required to detect early signs of disease transformation.

97
Q

What are the implications of achieving metabolic remission on PET scans in lymphoma treatment, and how does it correlate with long-term outcomes?

A

Metabolic remission indicates a lack of active glycolytic metabolism in residual tumour tissue. This is a strong predictor of durable remission and improved progression-free survival, especially in high-grade lymphomas.

98
Q

What are the pathophysiological mechanisms behind spinal cord compression due to retroperitoneal lymphadenopathy in lymphoma?

A

Compression occurs due to mass effect from enlarging lymph nodes, which can impinge on the spinal cord or nerve roots, leading to neurological deficits, and may require urgent radiotherapy or surgical decompression.

99
Q

What are the risk factors for meningeal spread in lymphoma, and what are the diagnostic approaches?

A

High-risk factors include aggressive histological subtypes (e.g., Burkitt lymphoma), involvement of extranodal sites, and HIV-associated lymphomas. Diagnosis is confirmed via CSF cytology, flow cytometry, or MRI with contrast.

100
Q

What is the significance of detecting bone marrow involvement in lymphoma, and how does it affect prognosis and treatment planning?

A

Bone marrow involvement indicates advanced-stage disease (Stage IV). It often alters treatment intensity and may necessitate haematopoietic stem cell transplantation or more aggressive chemotherapeutic regimens.

101
Q

How do corticosteroids in the R-CHOP regimen enhance the therapeutic effects of chemotherapy, and what are their immunomodulatory actions?

A

Steroids induce apoptosis in lymphoid cells, modulate immune response, and reduce inflammation and oedema around tumour masses, improving chemotherapy penetration.

102
Q

Discuss the pathophysiology of bisphosphonate-induced osteonecrosis of the jaw (ONJ) and its relevance in lymphoma patients.

A

Bisphosphonates inhibit osteoclast activity, impairing bone remodelling, especially in areas with high turnover like the jaw. This risk is exacerbated by poor dental health or trauma (e.g., extractions), necessitating alternative management like calcium and vitamin D supplementation.

Bisphosphonates are avoided with people with bad dental health. Most people along with calcium and vitamin D will be started on bisphosphonates

103
Q

What is the clinical significance of a Deauville score in assessing response to lymphoma treatment via PET-CT, and how does it guide further therapy?

A

The Deauville score quantifies the intensity of FDG uptake in residual tissue compared to mediastinal blood pool and liver, guiding decisions for consolidation therapy, radiotherapy, or further chemotherapy.

104
Q

Why is ferritin a key marker in assessing systemic inflammation or malignancy in lymphoma patients, and what are its limitations in distinguishing iron deficiency from other causes?

A

Ferritin levels rise in response to cytokines (e.g., IL-6) during inflammatory or malignant states, making it a useful biomarker. However, elevated levels can mask concurrent iron deficiency, necessitating additional tests like soluble transferrin receptors.

105
Q

What is the mechanism of action of polatuzumab vedotin when combined with R-CHOP, and why is it particularly effective in B-cell lymphomas?

A

Polatuzumab targets CD79b, a B-cell receptor component, delivering cytotoxic agents directly to the lymphoma cells, enhancing apoptosis in malignant B cells while sparing healthy tissues.

106
Q

Why is monitoring weight critical in lymphoma patients post-chemotherapy, and how does it relate to the risk of refeeding syndrome during recovery?

A

Weight monitoring helps prevent refeeding syndrome, a metabolic disturbance triggered by the reintroduction of nutrition after a prolonged catabolic state, causing electrolyte imbalances and cardiac dysfunction.

107
Q

Explain why chemotherapy leads to muscle mass loss rather than fat loss and the implications for long-term recovery in lymphoma patients.

A

Chemotherapy induces sarcopenia through systemic inflammation, metabolic dysregulation, and decreased physical activity, leading to preferential muscle breakdown and a prolonged recovery period post-treatment.

108
Q

What is the association between T-cell lymphoma and breast implants, particularly in the context of anaplastic large-cell lymphoma (ALCL)?

A

Breast implant-associated ALCL is a rare T-cell lymphoma linked to textured implants, with inflammation potentially playing a role in its pathogenesis. It often presents with seroma or a mass near the implant.

109
Q

Contrast the cellular characteristics and proliferative behaviour of follicular lymphoma and diffuse large B-cell lymphoma (DLBCL).

A

Follicular lymphoma consists of smaller, more mature B cells with low proliferation rates, while DLBCL is characterised by large, rapidly dividing cells with high mitotic activity, leading to more aggressive disease.

110
Q

Define terminal illness in the context of lymphoma and explain the significance of a 6-month life expectancy prognosis.

A

Terminal illness refers to advanced-stage disease with no curative options remaining, where life expectancy is less than 6 months, guiding the focus towards palliative care and quality of life.

111
Q

Why is an hour of hydration important before administering chemotherapy?

A
  • Renal protection
  • Hemorrhagic cystitis
  • Reduction of chemo toxicity
  • Prevention of TLS
  • Optimisation of drug efficacy
112
Q

What are pre-consultation checks before SACT?

A
  • Urine
  • Weight
  • ECG
  • BP
113
Q

How does Intravenous immunoglobulin (IVIg) work in Immune Thrombocytopenic Purpura (ITP)?

A

ITP is a condition where the body’s immune system mistakenly attacks and destroys its own platelets, which are needed for blood clotting.

IVIg contains antibodies from healthy donors. When given to a patient with ITP, it “distracts” the immune system:

The immune system becomes busy dealing with the antibodies in IVIg, so it attacks fewer platelets.
IVIg also blocks the parts of the immune system that are destroying platelets, allowing the platelets to survive longer in the bloodstream.
In summary, IVIg helps by reducing the immune system’s attack on platelets, allowing platelet levels to rise in people with ITP.

114
Q

Why is hydroxycarbamide useful in sickle cell disease?

A

Hydroxycarbamide essentially makes your red blood cells bigger, stay rounder and more flexible.

115
Q

What are some clinical features that suggest transfusion associated graft vs host disease?

A

These include fever, rash, diarrhoea, abdominal pain, pancytopenia and abnormal liver function tests.

116
Q

What is involved in a phase 1 trial?

A
  • Small numbers, small dose
  • Healthy volunteers
  • Safety signals, toxicity
  • PK studies, bioavailability
  • First in humans
  • Dose escalation study
  • Phase 1b- first in patients
117
Q

What is involved in a phase 2 trial?

A
  • A few tens or hundreds
  • Patients
  • Safety signal
  • Start to look for efficacy
  • Modelling statistics
  • Begin to inform larger scale studies
118
Q

What is involved in a phase 3 trial?

A
  • Hundreds
  • Expensive
  • Period of years
  • Placebo controlled
  • Blinded (participants/doctors don’t know what the drug is, bias).
  • Open label
  • Efficacy over standard
  • Licensing and market authority
119
Q

What is involved in a phase 4 trial?

A
  • No longer ‘investigational’
  • Post licensing studies
  • Long term safety

Real world evidence
- Often gathered by consortia of interested clinicians
- Usually retrospective

120
Q

What is the purpose of patient and public involvement groups?

A
  • Play a crucial role in clinical trials, providing input to ensure research is relevant, practical, and patient-centred.
  • Study design
  • Participant experience
  • Recruitment strategies
  • Ethical oversight
121
Q

What is assent in a clinical trial?

A

In a clinical trial involving children, assent is the child’s voluntary agreement to participate, after being provided with age-appropriate information, while formal consent is given by a parent or guardian.

Not the same as informed consent

122
Q

Risk factors for VTE

A
  • Surgery
  • Pregnancy & postpartum
  • Obesity
  • Age over 60
  • Smoking
  • Pacemakers, fractures
  • Sepsis
  • Vasculitis
  • Radiation
  • Immobility
  • Heart failure
  • Venous insufficiency
  • Factor V leiden
  • Dehydration
  • Cancer and treatment
  • Oestrogen containing HRT and contraceptives
  • Heparin (HIT)
123
Q

How a cancer causes VTE

A
  1. Release of procoagulant substances (tissue factor- activates the clotting cascade)
  2. Chronic inflammation cytokines which activate the clotting cascade
  3. Tumours can aggregate platelets
124
Q

Cancer specific related risk factors for VTE

A

Cancer type
- Advanced stage
- High tumour burden
- Radiotherapy- causes inflammation
- Surgery- immobility
- Chemotherapy- damages endothelial cells

125
Q

Cancers with highest risk for VTE

A
  • Brain
  • Pancreas
  • Ovarian
  • Lung
  • Renal
  • Lymphoma
126
Q

Definition for active cancer as defined by NICE

A
  • Receiving antimitotic treatment
  • Diagnnsed in past 6 months
  • Recurrent, metastatic or inoperable cancers
127
Q

How long does anticoagulation need to be given for after VTE in cancer?

A

Needs to be given for 3-6 months
6- recurrent VTE, palliative chemo, patients who have undergone radical treatment but remain at very high risk of recurrence

Continue with the duration that the risk factor will be present for. Metastatic malignancy- carry on with anticoagulation, if there is increased risk of bleeding then stop the anticoagulation.

128
Q

Cautions with VTE medications and cancer

A
  • Renal function (<30ml/kg)
  • Weight
  • Drug-drug interactions
  • Bleeding risk (avoid DOAC, LMWH is a better choice)
  • Cancer type
129
Q

Management for obstruction of the biliary tree

A
  • CT scan
  • MRCP
  • Percutaneous biliary drainage
  • ERCP- stent placed in bile duct
130
Q

Why is there a high risk of bleeding in cancer patients with DOACS?

A

LMWH- shorter duration of action, clearance is better (as long as renal function is normal)
Can be stopped 24 hours before surgery
Luminal malignancies- genitourinary/GI bled more on DOACs
Non-luminal malignancy- DOAC.

131
Q

Why not use Warfarin for cancer patients?

A
  • INR will not be in the range
  • Impact on quality of life
  • Will have to come in for frequent blood tests
132
Q

What anticoagulation is preferential with renal impairment?

A

LMWH more preferential for renal impairment

133
Q

Can you take the PICC line out straight away if there is a thrombosis?

A

Stabilise the clot first- LMWH for 5 days before PICC line is removed

134
Q

Side effects of LMWH?

A
  • Osteoporosis
  • Haematoma at site of injection
  • HIT
135
Q

When is Apixaban not recommended?

A
  • Patients with brain cancer or acute leukemia
  • Unresected GI/GU cancer or upper GI surgery
136
Q

Patient factors for CAT (cancer associated thrombosis)

A
  • Mobility
  • Dehydrated
  • Clotting disorders
  • Prior VTE
  • Presence of varicose veins
  • Medical comorbidities (CCI >3)
137
Q

Indications for IVC filters

A

Times when you can’t anticoagulate a patient- surgery (urgent) or bleeding risk
Temporary- can become fibrosed
Filter should come out in three months

138
Q

Tumour related risk factors for VTE

A
  • Stage of cancer
  • Stomach, pancreas, brain (very high)
  • Histological grade
  • Time since cancer diagnosis
139
Q

Treatment risk factors for VTE in cancer patients

A
  • Platinum based and other chemotherapy
  • Anti-angiogensis agents
  • Hormonal therapy
  • Surgery
  • Radiotherapy
  • Blood transfusion
  • Central venous catheters
  • Immobolity and hospitalization
140
Q

What is the CCI?

A

Charleston Comorbidity Index

141
Q
A

Postpoerative thromboprophylaxis with LMWH for 4 weeks in patients undergoing

142
Q

Superficial vein thrombophlebitis

A
  1. Close Proximity to Deep Vein (<3cm)
    Risk: If the SVT is located within 3 cm of a deep vein (e.g., saphenofemoral junction), there is a higher risk of progression to a deep vein thrombosis (DVT) or pulmonary embolism (PE).
    Management: Treat as you would a DVT with a DOAC or other anticoagulation for at least 3 months, as there is a significant risk of thromboembolism.
  2. More than 3cm from Deep Vein and >5cm in Length
    Risk: Larger SVTs (>5 cm) carry an increased risk of clot extension and complications such as DVT.
    Management: Interim anticoagulation with a DOAC (e.g., rivaroxaban or apixaban) for 6 weeks.
  3. Smaller than 5cm in Length and More than 3cm from a Deep Vein
    Risk: Smaller SVTs (<5 cm) and those located away from deep veins pose a lower risk of progression.
    Management: NSAIDs, compression stockings, mobilisation, and warm compresses can also be helpful adjuncts.
143
Q

Enoxaparin dose

A

1.5mg/kg OD

1mg/kg TDS- patients with more risk factors- obesity, cancer, recurrent VTE or proximal thrombosis

UHL connect for all trust guidelines

144
Q

Inx for anaemia

A

Serum ferritin- stored iron (don’t rule out if normal/high as acute phase protein) (most important test to do on bloods)
Ferritin of 12 is NOT normal
Serum iron
Total iron binding capacity- low in anaemia of chronic disease (inflammation
Transferrin saturation- low is iron deficiency anaemia
B12/folate- lead to megaloblastic anaemia, long term chemotherapy (methotrexate)
Retics- low is problem in making RBCs, high in blood loss/hemolytic anaemia
Bone marrow biopsy- hypercellular (aplastic anaemia), MDS, infiltration of cancer cells
EPO levels- CKD would be low
LFTs- chemotherapy are damaging to the liver
LDH/haptoglobin- hemolytic anaemia. High LDH= high cell turnover, low haptoglobin- binds to free heme
Blood smear- morphology of blood cells, hypochromic, macrocytic, shiscocytes, blast cells

145
Q

Microcytic anaemia

A

TAILS
Sideroblastic- dysfunction in heme production, iron build up in the bone marrow, immature blood cells
Thalassemia- decreased/absent heme production
Anaemia of chronic disease- hepcidin, reduces absorption of iron. CKD, heart failure.
Lead poisoning

146
Q

Normocytic

A

Hemorrhagic anaemia
Hemolytic anaemia
G6PHD deficiency- fava beans, malaria drugs
Sickle cell
Leukemia
Severe burns
MDS- fibrosis of the bone marrow
Aplastic anaemia- primary failure of the bone marrow

147
Q

Macrocytic anaemia

A

Megaloblastic or non megaloblastic
Megaloblastic
- Large, immature RBCs,
- Segmented RBCs
- Problem with DNA production
- Pernicious anaemia

Non-megaloblastic
- large mature
- chronic alcohol use
- hyperthyroidism

148
Q

Hemolytic anaemia

A
  • Cephalosporins, levodopa, nitrofurantoin
  • Sickle cell- hydroxyurea, vaccinations, blood exhanges
  • Steroids in AIHA
149
Q

Types of blood products

A

Packed red cells (2 hours)
- Acute blood loss
- Chronic anaemia
- Symptomatic anaemia
- 1 unit increases Hb by 10

Platelets- 30 minutes
- thrombocytopenia
- hemorrhagic shock
- platelet levels by 20-40

FFP (30 minutes)
- DIC
- Hemorrhage due to liver disease

150
Q

Special requirements

A

CMV negative
- Women during pregnancy
- Intrauterine
- Neonates up to 28 days old

Irradiated
- Graft vs host disease
- 1st/second
- Hodgkin
- Stem cell transplant
- Fludarabine
- Intra-uterine transfusions

151
Q

Blood transfusion reactions

A

Acute- up to 24 hours
Delayed- couple of weeks

152
Q

What amendments should be made to the drug chart in acute bleeding?

A
  1. Stop anticoagulant drugs
153
Q

Why give IV iron instead of oral?

A
  • Tolerability of oral
  • Patient can’t swallow, GI dysfunction
  • Quicker onset (surgery, pre-op anaemia clinics, bowel cancer, pregnant women- close to when you think a woman is going to deliver)
154
Q

Blood test commonly used in renal clinic

A

CHR- reticulocyte hemoglobin

155
Q

Risk of IV iron transfusion

A

Iron that leaks into the skin- permanent
Risk of extravasation
Anaphylaxis- more likely to get it from iron than blood (make sure its given in a healthcare setting where people are equipped to deal with anaphylaxis)

156
Q

Hb level to transfuse

A

How symptomatic a patient is
Likely cause
How do we treat the cause

157
Q

Signs of B12/folate deficiency

A

Low reticulocyte count (bone marrow can’t do what it needs to do)
The cells that are being made are useless- jaundice
Jaundice is common and high LDH- cell turnover. LDH of over 1000 with B12 deficiency (don’t necessarily have cancer)

Important to have a structure when ordering blood tests

158
Q

Order of investigations for anaemia

A
  1. Ferritin
  2. Haematinics
  3. Reticulocytes
159
Q

Other signs of bone marrow failure

A
  • Low white blood cells
  • Low platelets
160
Q

Where do you get vitamin B12 from?

A

Only get it from animal, dairy or fortified products

161
Q

Causes of B12 deficiency

A
  • Poor intake
  • Malabsorption- gastric band/gastrectomy (will not produce intrinsic factor) Atrophic gastritis- kills of parietal cells
  • Pernicious anaemia- antibodies against parietal cells
  • IBD, bowel resection- terminal ileum
  • Metformin
162
Q

Main indications for giving vitamin B12 IV

A
  • Pregnant women
  • Gastric resection
  • Peripheral neuropathy
163
Q

Explain to me really simply why you get a low serum iron level and high ferritin level in anaemia of chronic disease?

A

Serum iron is low because iron is trapped in storage and not available in the bloodstream due to the effects of hepcidin.
Ferritin is high because it reflects both increased iron storage and the body’s inflammatory response as an acute-phase reactant.

164
Q

Why do you need folate supplements if you have sickle cell disease?

A

Patients with sickle cell disease require folic acid supplements to support the increased production of red blood cells due to their shortened lifespan and to prevent folate deficiency, which is critical for effective RBC synthesis and overall health.

165
Q

What are common triggers for sickle cell crises?

A

Menstrual cramps
Dehydration
Stress
Infection
Anxiety

166
Q

What prophylaxis can be considered in patients with sickle cell to prevent infections?

A

Penicillin V

167
Q

Why is IV cyclizine contra-indicated in patients with sickle cell?

A

IV cyclizine is contra-indicated in sickle cell patients primarily due to its potential for vasoconstriction, which can exacerbate the risk of vaso-occlusive crises. Safer alternatives should be used to manage symptoms in this vulnerable population.

168
Q

Example of a presentation of CML

A

On-going cellulitis that wasn’t clearing for 2 years.
Recently felt reflux symptoms, LUQ pain due to splenomegaly

169
Q

Bloods done for investigation of CML

A

Purpose: To assess the overall blood cell levels, including white blood cells (WBCs), red blood cells (RBCs), and platelets.
Findings: CML is often characterised by elevated WBCs, especially basophils and myeloid precursors.

170
Q

Explain the Philadelphia chromosome, BCR-ABL fusion protein in CML

A

Chromosome 9 has the ABL gene
Chromosome 22 has the BCR gene

ABL moves from 9 to 22

22 now has the BCR-ABL fusion protein

It is now called the Philadelphia chromosome

The resulting BCR-ABL gene codes for a fusion protein that has tyrosine kinase activity in excess of normal.

171
Q

What is the difference between FISH and cytogenetics in CML?

A

FISH specifically targets the BCR-ABL fusion gene to confirm the diagnosis of CML.
Cytogenetic analysis provides a broader view of the entire chromosome set, looking for various chromosomal abnormalities.

172
Q

What will be the main blood test finding for CLL and CML?

A

CLL:
Lymphocytosis: An increased number of mature lymphocytes (>5,000 lymphocytes/mm³).
Characteristic appearance of small, mature lymphocytes on the blood smear.

CML:
Leukocytosis: Markedly elevated white blood cell count with a left shift, including immature cells like myeloblasts, promyelocytes, and myelocytes.
Presence of the Philadelphia chromosome and BCR-ABL fusion gene in cytogenetic testing.

173
Q

What is Richter’s transformation?

A

Some patients may transform to Richter’s transformation, where CLL transforms into a more aggressive form of lymphoma (usually diffuse large B-cell lymphoma).

174
Q

What are the three phases of CML?

A

Chronic Phase: Stable phase with <10% blast cells; manageable with treatment.
- May have increased eosinophils and basophils
- Often asymptomatic

Accelerated Phase: Progression with 10-19% blast cells; less responsive to treatment.
- Increased basophils to cause pruritus
- Splenomegaly
- Thrombocytopenia

Blast Phase: Aggressive phase with ≥20% blast cells; resembles acute leukaemia, requiring immediate and intensive treatment.

175
Q

Time frame you would expect with reactive lymphadenopathy

A

4-6 weeks

176
Q

How long do bone marrow biopsies take?

A

4-5 days

177
Q

How would you commence treatment in CML?

A

Start on hydroxyurea to bring WCC count down (Leukostasis (sludging of blood due to high viscosity), which can cause issues like impaired perfusion to the brain, lungs, and other organs.
Increased risk of thrombosis or bleeding.)

Then do Imatinib once bone marrow biopsy has come back

178
Q

General marker for fungal infections

A

B-D glucan
Not specific to any fungal infection
Also raised in chemotherapy

179
Q

What is involved in a myeloma screen?

A

IgG
IgA
IgG
Serum electrophoresis

180
Q

Outline the functions of the red pulp of the spleen (haematological role)

A

Filtration of blood: Removes old, damaged, or abnormal red blood cells.

Phagocytosis: Macrophages in the red pulp engulf and break down defective red blood cells, platelets, and pathogens.

Iron recycling: Recycles iron from haemoglobin of broken-down red blood cells, storing it for reuse.

Storage of platelets: Acts as a reservoir for platelets and can release them when needed.

Blood reservoir: Stores blood, which can be mobilised during times of acute blood loss or stress (though less significant in humans).

181
Q

Outline the functions of the white pulp of the spleen (immune role)

A

Immune surveillance: Detects pathogens and antigens in the blood, initiating an immune response.

Lymphocyte activation: Contains T lymphocytes and B lymphocytes. T cells help in recognising antigens, while B cells produce antibodies.

Antibody production: B cells in the white pulp produce antibodies against pathogens, especially encapsulated bacteria.

Phagocytosis of antigens: The white pulp contains macrophages that engulf and destroy pathogens and present antigens to lymphocytes.

182
Q

Causes of hyposplenism

A

Splenectomy- Most common cause is iatrogenic (e.g blood vessels are damaged during cholecystectomy)​

​

Sickle-cell- Repeated vaso-occlusion and infarction due to trapped sickle cells casing progressive fibrosis. ​

​

Alcoholic liver disease- Alcoholic liver disease causes hyposplenism due to congestion and fibrosis in the liver, leading to portal hypertension (splenomegaly). ​

​

Essential thrombocythaemia - Essential thrombocythaemia causes hyposplenism due to splenic infarctions from clots. ​

​

Coeliac disease- Coeliac disease causes hyposplenism due to autoimmune damage and lymphocytic infiltration.​

​

Grave’s disease- Grave’s disease causes hyposplenism due to autoimmune-related splenic atrophy (immune system mistakenly attacks the spleen)

183
Q

Management of hyposplenism

A

Patients are at a higher risk of infections from encapsulated bacteria. ​

​

Vaccinations​

Pneumococcal vaccine​

Haemophilus influenzae type b (Hib) vaccine​

Meningococcal vaccine (MenACWY and MenB)​

Annual influenza vaccine​

​

Antibiotic Prophylaxis​

Lifelong antibiotic prophylaxis (e.g., Penicillin V) ​

​

Other Measures​

Medical alert bracelet​

Patient education: Being alert with signs of infection, animal/insect bites (lyme disease) and travel (anti-malarial drugs)

184
Q

Causes of massive splenomegaly

A

CML

Myelofibrosis- extramedullary hematopoiesis

Malaria- excessive phagocytosis

Leishmaniasis- accumulation of macrophages

185
Q

Causes of moderate splenomegaly

A

Infection (EBV, endocarditis, TB)-

Portal hypertension (liver cirrhosis)- splenic congestion

Connective tissue disease (RA, SLE)

186
Q

What are the common clinical features of Hodgkin Lymphoma (HL)?

A

Painless lymphadenopathy, usually in the neck, underarms, or groin.

B symptoms: Fever, night sweats, and unexplained weight loss.

Fatigue: Generalised tiredness and weakness.

Pruritus (itching): May be severe, without skin lesions.

Alcohol-induced lymph node pain: Rare but characteristic feature.

Mediastinal mass: Can cause cough, chest pain, or dyspnoea.

187
Q

What are the common clinical features of Non-Hodgkin Lymphoma (NHL)?

A

Painless lymphadenopathy, often diffuse and involving multiple sites.

B symptoms: Fever, night sweats, weight loss (less common than HL).

Fatigue: Generalised tiredness.

Extranodal involvement: May affect organs outside the lymphatic system (e.g., GI tract, CNS, skin).

Splenomegaly: Can cause abdominal discomfort or fullness.

188
Q

How do the disease courses of Hodgkin Lymphoma (HL) and Non-Hodgkin Lymphoma (NHL) differ?

A

Hodgkin Lymphoma (HL):
Bimodal age distribution: Peaks in young adults and those over 55.
Contiguous spread: Spreads predictably between adjacent lymph nodes.
Good prognosis: High cure rate with treatment.

Non-Hodgkin Lymphoma (NHL):
Occurs more in older adults.
Non-contiguous spread: Can spread randomly, often involving extranodal sites.
Variable prognosis: Indolent forms are incurable but slow-growing, while aggressive forms may be curable with prompt treatment.

189
Q

What are the haematological features of acute leukaemia?

A

Blast cells in peripheral blood: Elevated immature white blood cells (blasts), often >20% of cells in the bone marrow.

Pancytopenia: Reduced red blood cells, white blood cells, and platelets due to bone marrow failure.

Anaemia: Low haemoglobin levels, often causing symptoms of fatigue.

Neutropenia: Low neutrophil count, predisposing to infections.

Thrombocytopenia: Low platelet count, leading to bleeding and bruising.

Hyperleukocytosis (in some cases): Extremely high white cell count, leading to symptoms like shortness of breath or neurological issues due to blood hyperviscosity.

190
Q

What are the common presenting clinical features of acute leukaemia?

A

Fatigue and weakness: Due to anaemia (low red blood cells).

Frequent infections: Resulting from neutropenia (low white blood cells).

Bruising and bleeding: Caused by thrombocytopenia (low platelets), presenting as petechiae, purpura, or mucosal bleeding.

Bone pain: Due to bone marrow expansion.

Fever: Often due to infection or the disease process itself.

Lymphadenopathy and hepatosplenomegaly: May occur in some cases, especially in acute lymphoblastic leukaemia (ALL).

191
Q

What are the haematological features of chronic lymphocytic leukaemia (CLL)?

A

Lymphocytosis: Marked increase in small, mature-looking lymphocytes in the peripheral blood.

Smudge cells: Fragile lymphocytes that break during the preparation of blood films.

Hypogammaglobulinaemia: Reduced immunoglobulin levels, leading to an increased risk of infections.

Anaemia: Often mild at presentation, but may worsen due to bone marrow infiltration or autoimmune haemolytic anaemia.

Thrombocytopenia: Low platelet count, typically in advanced disease stages due to bone marrow infiltration.

Bone marrow infiltration: Lymphocytes infiltrate the bone marrow, suppressing normal haematopoiesis.

192
Q

What are the clinicopathological features of chronic lymphocytic leukaemia (CLL)?

A

Asymptomatic in early stages: Often found incidentally during routine blood tests.

Lymphadenopathy: Painless swelling of lymph nodes, typically in the neck, axillae, or groin.

Hepatosplenomegaly: Enlargement of the liver and spleen, often seen in later stages.

Recurrent infections: Due to immunosuppression and hypogammaglobulinaemia.

Autoimmune complications: Haemolytic anaemia and immune thrombocytopenia may occur.

Indolent course: Slow progression over years, but can transform into a more aggressive form (Richter’s transformation).

193
Q

Distinguishing Features of ET:

A

Clonal disorder: ET is a myeloproliferative neoplasm (MPN) characterised by abnormal proliferation of megakaryocytes, confirmed by the presence of mutations (e.g., JAK2, CALR, MPL).

Persistent thrombocytosis: Platelet counts remain chronically elevated without a secondary cause.

Bone marrow biopsy: Increased megakaryocytes with characteristic morphology, helping to differentiate ET from reactive causes.

194
Q

Distinguishing ET from Reactive (Secondary) Thrombocytosis:

A

Causes of reactive thrombocytosis: Can result from infection, inflammation (e.g., rheumatoid arthritis, inflammatory bowel disease), malignancy, iron deficiency, or following surgery/trauma.

Inflammatory markers: In reactive thrombocytosis, markers such as CRP and ESR are often elevated due to underlying inflammation, which is not typical in ET.

Transient elevation: In reactive causes, the platelet count usually normalises once the underlying cause is treated or resolves, whereas ET shows persistent thrombocytosis.

Iron deficiency: Can cause reactive thrombocytosis; features like low ferritin levels and microcytic anaemia can help identify this cause.

195
Q

Distinguishing ET from Other Myeloproliferative Neoplasms (MPNs):

A

Polycythaemia vera (PV): Often presents with elevated red cell mass and haematocrit, along with thrombocytosis. Erythrocytosis and raised haemoglobin/haematocrit levels help differentiate PV from ET.

Primary myelofibrosis (PMF): Can present with thrombocytosis but also shows features of progressive bone marrow fibrosis, leading to splenomegaly, leucoerythroblastic blood film, and anaemia. Bone marrow biopsy is crucial to differentiate ET from early-phase PMF.

196
Q

What features help distinguish primary myelofibrosis (PMF) from other myeloproliferative neoplasms (MPNs)?

A

Bone marrow fibrosis: The presence of reticulin or collagen fibrosis in the bone marrow biopsy is a key diagnostic feature distinguishing PMF from other MPNs, like polycythaemia vera (PV) or essential thrombocythaemia (ET).

Leukoerythroblastic blood film: Seen in PMF but absent in ET and PV, unless in advanced stages.

Massive splenomegaly: More common and pronounced in PMF compared to PV and ET.

Absence of polycythaemia: In contrast to PV, PMF does not present with elevated red blood cell mass.

Progressive cytopenias: As PMF advances, pancytopenia becomes more pronounced, which is less common in ET and early-stage PV.

197
Q

What are the main laboratory features of primary myelofibrosis (PMF)?

A

Anaemia: Normocytic or macrocytic anaemia, often presenting with teardrop-shaped red blood cells (dacrocytes) on the blood film.

Leukoerythroblastic blood film: Presence of immature white blood cells (myelocytes, promyelocytes), nucleated red blood cells, and teardrop cells in the peripheral blood.

Thrombocytosis or thrombocytopenia: Platelet count can be elevated in early disease but often drops as the disease progresses.

Leukocytosis or leukopenia: White blood cell count may be high early on but can fall with advancing bone marrow failure.

Bone marrow biopsy: Shows fibrosis (reticulin or collagen deposition), megakaryocyte proliferation with abnormal morphology, and reduced normal haematopoietic cells. In later stages, the bone marrow may be “dry” on aspiration (aspiration failure).

JAK2 V617F mutation: Present in ~50-60% of patients. Other mutations, such as CALR or MPL, are found in JAK2-negative cases.

Elevated lactate dehydrogenase (LDH): Reflects increased cell turnover and haemolysis.

Y4 Cancer care (15 decks)

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