Week 3 Flashcards
(103 cards)
1
Q
What is the lifespan of a neutrophil?
A
7-8 hours
2
Q
What key factor separates haemopoietic stem cells from myeloid and lymphoid progenitor cells?
A
Haemopoietic stem cells are able to self-renew
3
Q
What are the main sites of haemopoiesis at each of the following ages?
- conception
- week 6
- week 16
- adults
A
Conception - yolk sac
Week 6 - liver
Week 16 - bone marrow
Adults - marrow WITHIN THE AXIAL SKELETON, PELVIS AND PROXIMAL LONG BONES
4
Q
Describe the bone marrow ‘sinus’
A
Arterioles within the bone drain into ‘sinuses’ - wide venous vessels which open into larger central sinuses
Importantly, sinuses have a discontinuous basement membrane and the presence of adventitial cells adjacent to these sinuses (which contain smooth muscle filaments) allow for the sinuses to open up upon contraction
This allows the release of mature red cells from the marrow into the circulation
5
Q
What is the difference between red and yellow marrow?
A
Red marrow - haemopoietically active
Yellow - fatty and inactive.
At birth, all bone marrow is red. Amount of yellow marrow increases with age, resulting in a reduction in marrow cellularity in older individuals. Middle aged adults have about 50% red and 50% yellow marrow
6
Q
What is the myeloid:erythroid ratio?
What might cause this ratio to increase?
A
M:E ratio is the relationship of neutrophils and precursors to the proportion of nucleated red cell precursors
M:E ratio is increased in anaemia (e.g. due to blood loss) and in haemolysis (basically anything that causes loss of red cells)
7
Q
What molecule regulates neutrophil precursor maturation?
A
Granulocyte-colony stimulating factor (G-CSF)
8
Q
What molecule regulates platelet growth and development (via megakaryocytes from their precursors)?
A
Thrombopoietin
9
Q
When assessing haemopoeisis and examining blood, how are the following assessed?
- non-lymphoid cells
- lymphoid cells
A
Non-lymphoid - blood count/morphology is usually sufficient
Lymphoid - cannot be distinguished from one another by morphology (except plasma cells!), so antigen expression is studied via immunophenotyping
10
Q
Where do B cells mature?
Where do T cells mature?
A
B cells - bone marrow
T cells - thymus
11
Q
Which of the following are primary lymphoid tissues and which are secondary?
- Bone marrow
- Lymph nodes
- Spleen
- Thymus
- Tonsils (Waldeyer’s ring)
- Epithelio-lymphoid tissues
A
Primary
- Bone marrow
- Thymus
Secondary
- Lymph nodes
- Spleen
- Tonsils
- Epithelio-lymphoid tissues
- Bone marrow
12
Q
What complications could occur in the event of…
- surgical removal of lymph nodes
- damage to the central lymphatics system (cisterna chyli) e.g. trauma/obstruction
A
Surgical removal - Lymphoedema
Damage to central lymphatics - Chylous ascites
13
Q
What marker can be used to identify…
- B cells
- T cells
A
B cells - CD20
T cells - CD3
14
Q
After stimulation of an immune reaction within a lymph node, what might the following responses indicate?
- Predominant B cell response
- Predominant phagocytic response
- Predominant T cell response
A
Predominant B cell response - autoimmune conditions or infection
Predominant phagocytic response - draining a tumour site
Predominant T cell response - viral infections or certain drugs e.g. phenytoin
*NB - this is just a general guide and not entirely specific
15
Q
Is a diseased spleen more or less likely to rupture? Is this serious?
A
More likely, and yes it is serious! Surgical emergency due to being a very vascular organ, patients can bleed out very quickly
16
Q
Describe the ‘red pulp’ and ‘white pulp’ of the spleen
A
Red pulp - contains sinusoids and cords
- Sinusoids are fenestrated, lined by endothelial cells and supported by hoops of reticulin
- Cords contain macrophages, some fibroblasts and cells in transit (RBCs, WBCs etc.)
White pulp - comprises the peri-arteriolar lymphoid sheath (PALS)
- PALS is expanded by lymphoid follicles and may show reactive change
- APCs in the white pulp present antigen to immune reactive cells, and T and B cell responses may occur as a result.
17
Q
What is the triad of components that makes up hypersplenism (overactive spleen)?
A
- splenomegaly
- fall in one or more cellular components of blood
- correction of cytopenias by splenectomy
18
Q
Name some conditions that may result in hyposplenism
A
Coeliac disease
Sickle cell disease
Sarcoidosis
Iatrogenic
Chronic folate deficiency
19
Q
What histological sign might indicate a damaged or absent spleen?
A
Howell-Jolly bodies - basophilic nuclear remnants in erythrocytes that would usually be removed by a healthy spleen
20
Q
What scoring system is used in patients with AF to determine their risk of stroke and need for anticoagulation?
What are the components of this scoring system and a score above what would indicate the need for treatment?
A
CHA2DS2VASc score
- Congestive heart failure (1)
- Hypertension (1)
- Age equal to or greater than 75 (2)
- Diabetes mellitus (1)
- Prior stroke, TIA or thromboembolism (2)
- Vascular disease e.g. PAD, MI, aortic plaque etc. (1)
- Age 65-74 (1)
- Sc, female sex (1)
Score of 2 and above indicates recommendation for treatment
21
Q
When advising a patient on anticoagulation options, why might it be beneficial for a clinician if the patient opts for Warfarin?
A
Warfarin requires regular monitoring for INR - allows clinician to check for compliance
22
Q
What does the mneumonic ‘CRAB’ stand for in relation to myeloma symptoms?
A
Calcium (raised)
Renal function (decline)
Anaemia
Bones (pain)
23
Q
What are the causes of autoimmune haemolytic anaemia?
Which antibodies are implicated?
A
Warm antibody Haemolytic Anaemia (IgG, mainly)
Cold antibody Haemolytic Anaemia, aka Cold Agglutinin Disease (IgM, mainly)
24
Q
What molecule is present on the cell surface of stem cells and can be used to identify them during immunophenotyping?
A
CD34
25
How does the mechanism of disease differ between acute and chronic leukaemias?
Acute leukaemias - proliferation of abnormal progenitors **with a block in differentiation/maturation**. Lots of cells that look similar
Chronic leukaemias - proliferation of abnormal progenitors but **NO differentiation/maturation block**. Increased number of cells but they all look different
26
One of the ways in which haematological malignancies develop is through somatic mutations in regulatory genes i.e. driver mutations vs passenger mutations. How do driver mutations influence 'clones' in haemopoiesis?
Clone: population of cells derived from a single parental cell. Parent cells have a genetic marker that is shared by daughter cells.
Normally, clones can diversify but will contain a similar genetic backbone.
**Driver mutations can select clones, meaning that malignant haemopoiesis is usually MONOCLONAL**, as opposed to normal haemopoiesis which is polyclonal
27
Why are driver mutations selected by cells during the evolution of cancer?
Because they confer growth advantages
28
How can haematological malignancies be classified?
1. based on lineage e.g. myeloid or lymphoid
2. based on developmental stage (precursor) within lineage e.g. acute lymphoblastic (problem with progenitor cell) vs chronic lymphocytic (problem with daughter cell)
3. based on the anatomical site involved e.g. myeloma (plasma malignancy in marrow), lymphoma (lymph nodes), leukaemia (blood involvement)
29
Which of the following are included in the sites of acute lymphoblastic leukaemia?
- blood
- bone marrow
- lymph nodes
Blood and bone marrow
## Footnote
**Lymph nodes are NOT included in acute leukaemias**
30
How do high-grade lymphomas and acute leukaemias compare to low-grade lymphomas and chronic leukaemias in terms of aggression?
What are some of the characteristic histological signs of a more aggressive malignancy?
High-grade lymphomas and acute leukaemias are **MORE aggressive**
Characteristic features include...
- large cells
- high nuclear-cytoplasmic ratio
- prominent nucleoli due to increased RNA and protein
- open chromatin
- rapid proliferation
31
What cell type is affected in myeloma?
Plasma cells in the bone marrow
32
How is acute leukaemia defined and what are the two main types?
Rapidly progressive clonal malignancy of the marrow/blood with **maturation defects**. Results in an **increased number of blasts** in either the peripheral blood or bone marrow
There is also **always a decrease in the normal haemopoietic reserve**
Two types: **Acute Myeloid Leukaemia (AML)** and **Acute Lymphoblastic Leukaemia (ALL)**
33
Which age groups are most commonly affected by a) AML and b) ALL?
ALL - **most common childhood cancer**
AML - **most common in the elderly (\>60 years)**
34
How does ALL present?
Disease of primitive (lymphoblastic) progenitor cells
Most commonly presents in children
Symptoms are...
- effects of **marrow failure** - anaemia, infections, bleeding
- **leukaemic effects** - high count with obstruction of cells, meaning **involvement of areas outside the marrow and blood e.g. CNS, testis etc.**
- **Bone pain**
35
How does AML present?
More common in elderly patients
Similar marrow failure presentation to that seen in ALL (anaemia, infections, bleeding etc.)
Subgroups may have characteristic presentation...
- **DIC**
**- gum infiltration**
36
Acute leukaemia - investigations
1. FBC followed by blood film (looking at cell morphology and presence of primitive cells) - there will be a **reduction in normal** and **presence of abnormal**
2. Coagulation screen
3. Bone marrow aspiration - morphology and immunophenotyping
37
What telltale histological sign may be seen on blood film that allows differentiation between AML and ALL?
**Auer rods** are seen in acute myeloid leukaemia
38
Morphologically, bone marrow aspiration samples of AML and ALL may look identical. How else could they be separated?
Using **immunophenotyping via flow cytometry**
39
How does treatment of ALL compare to AML?
ALL - can last up to 2-3 years with different phases of varying intensity
AML - normally intensive with 2-4 cycles of chemo (5-10 days followed by 2-4 weeks recovery). Requires prolonged hospitalisation
40
What is one of the main complications to be aware of regarding bone marrow suppression in the treatment of acute leukaemias?
**Neutropenia** meaning increased severity and duration of infections
This could also result in **gram-NEGATIVE bacteria causing fulminant life-threatening sepsis**
Also **anaemia** and **thrombocytopenia** (causing bleeding in the form of pupura and petechiae)
41
What are some of the complications and side effects associated with chemotherapy?
Nausea and vomiting
Hair loss
Liver and renal dysfunction
Tumour lysis syndrome (during the first course of treatment)
Infection - **bacterial, fungal and protozoan**
Later effectss - loss of fertility, cardiomyopathy associated with anthracyclines
42
What should be done as soon as a patient undergoing chemotherapy develops neutropenic fever?
**Begin empirical treatment with broad spec. antibiotics** - especially covering gram negative bacteria.
Begin the treatment quickly and don't wait for results to come back before commencing
43
What is the prognosis for children being treated for ALL?
How about adults with AML?
Children with ALL - Very good! **\>85-90% cure rates**
Adults with AML - Not as good... **if under 60, 40-50%, if over 60 then 10% or less**
44
What are B symptoms?
Associated with lymphoma
**- PAINLESS LYMPHADENOPATHY**
**- Night sweats**
**- Weight loss**
**- Fever**
45
What are some of the things on your list of differentials when you see a patient with lymphadenopathy?
'Reactive' lymphadenopathy
Bacterial infection causing **regional** swelling
Viral infection causing **generalised** swelling
Metastatic malignancy
Lymphoma
46
Should you be worried/what is the likely diagnosis?
Non-tender nodes, rubbery/soft texture, smooth surface, no skin inflammation and not tethered
Yes - presentation is that of **lymphoma**
47
Should you be worried/what is the likely diagnosis?
Non-tender nodes, hard, irregular surface, no skin inflammation and tethered to underlying structures
Yes - presentation is that of **metastatic carcinoma**
48
Can CT be used to diagnose lymphoma?
No - can't differentiate between lymphoma and metastatic disease
49
What investigations can be used to investigate lymph node pathology?
Histological appearance
Immunohistochemistry (looking at expressed proteins), done on solid sample
Immunophenotyping, similar to the above but uses a fluid blood/marrow sample
Genetic analysis
Molecular analysis
50
What pathology are Reed-Sternberg cells indicative of?
**Hodgkin's Disease**
RS cells cause inflammatory response and resulting nodular sclerosis
51
What CD molecule is expressed on B cells and would indicate the presence of a non-Hodgkin's lymphoma when performing immunohistochemistry?
**CD20**
52
What CD molecule is seen on Reed-Sternberg cells in Hodgkin's Lymphoma?
**CD30**
53
What lab test is useful in determining the pattern of CD numbers in cells, and as such is useful in identifying various leukaemias and lymphomas involving the marrow?
How does this investigation work?
**Immunophenotyping**
Cells are tagged with antibodies and emit a specific colour of light when a laser is shone on them
Useful for identifying **Burkitt's Lymphoma (t 8:14)**
54
Regarding treatment aims, how do Hodgkin's Lymphoma/High grade NHL and Low grade NHL differ?
Hodgkin's Lymphoma/High grade NHL - **can be cured**
Low grade NHL - **cannot be cured**, aim is to make the disease indolent
55
How does the treatment for Burkitt's lymphoma differ from standard chemo given in other forms of lymphoma?
Burkitt's is very aggressive and requires specialised treatment
Chemo is given **every day for several days,** rather than having breaks
56
Non-Hodgkin's Lymphoma can be classified into B cell and T cell types. What are some examples of each?
Which is most numerous in practice?
B-NHL
* precursor B-ALL
* B-ALL, lymphoblastic NHL
* Burkitt's
* DLCL
* Mantle cell lymphoma
* Follicular lymphoma
* MALToma
T-NHL
* precursor T-ALL, lymphoblastic lymphoma
* T-PLL
* T-cell LGL
* ATLL
* CTCL
* ........
In practice, **B cell NHLs are by far the most common (both low and high grade)**
57
What is pancytopenia?
Deficiency of blood cells of all lineages
Importantly, it is **not a diagnosis and doesn't always mean bone marrow failure**
58
Generally, causes of pancytopenia can be broken down into increased destruction or reduced production.
What can reduced production further be broken down into?
Inherited syndromes (incredibly rare)
Acquired (either primary or secondary)
59
Give an example of an inherited syndrome of marrow failure.
How does this condition present?
**Fanconi's anaemia** - inherited cause of reduced production of all cells
Short stature
Skin pigment abnormalities (cafe au lait spots)
Hypogenitalia
Endocrinopathies
GI,cardiovascular, renal and haematological defects
60
What associated haematological abnormalities are seen in someone with Fanconi's anaemia?
Bone marrow failure (aplasia) - 84% of patients by 20 years
Leukaemia - 52% of patients by 40 years
61
What is the main mechanism of pathophysiology in Fanconi's anaemia?
Inability to correct inter-strand cross-links (DNA damage)
62
What are some examples of acquired primary bone marrow failure?
Idiopathic aplastic anaemia
Myelodysplastic syndromes (MDS)
Acute leukaemia
63
What is the (believed) mechanism behind idiopathic aplastic anaemia?
Autoimmune attack against haematopoietic stem cells - INF-gamma and TNF-alpha damage the stem cell compartment, especially the myeloid branch
64
Myelodysplatic syndromes are a form of acquired primary bone marrow failure and subsequent pancytopenia.
What are the key features of myelodysplastic syndromes? What does it have a propensity to evolve into?
Dysplasia (disordered development of blood cells)
Hypercellular marrow + increased apoptosis of progenitor and mature cells = **ineffective haemopoiesis**
**Propensity for evolution into AML**
65
How does acute leukaemia cause pancytopenia?
1. **Proliferation of abnormal cells (blasts) from leukaemia stem cells** \> failure to differentiate or mature into normal cells
2. **Prevention of normal haemopoietic stem/progenitor cells** development by "**hijacking**" the haemopoeitic niche and marrow microenvironment
66
What are the clinical features of pancytopenia?
**Anaemia** - fatigue, SoB, cardiovascular issues
**Neutropenia** - infections with increased severity and duration
**Thrombocytopenia** - bleeding (petechiae and purpura)
67
In a patient with pancytopenia, if a marrow biopsy was done what would the following suggest?
- hypocellularity
- hypercellularity
Hypocellular = **aplastic anaemia**
Hypercellular = **MDS, B12/Folate deficiency, hypersplenism**
68
What investigations would you perform in a patient presenting with pancytopenia?
History, including family, as well as clinical exam
FBC and blood film
B12/Folate, LFTs, virology, autoantibody tests
Bone marrow examination (aspiration of trephine biopsy)
69
What is the shape of the following immunoglobulins?
- IgG
- IgE
- IgD
- IgA
- IgM
IgG, IgE and IgD = **monomer**
IgA = **dimer**
IgM = **pentamer**
70
What are paraproteins?
What are they a marker of?
Monoclonal immunoglobulins all derived from clonal expansion of a single B-cell
Have identical structure and specificity (size and charge)
**Marker of an underlying CLONAL B cell disorder**
71
Serum electrophoresis can be used to detect immunoglobulins and abnormal proteins, with separated serum proteins appearing as distinct bands.
Within which region to all immunoglobulins appear?
How does this region appear normally (i.e. polyclonally)?
Immunoglobulins appear within the **gamma region**
This is a broad region that, if polyclonal, shows a diffuse stain with no specific areas of banding
72
What procedure is then done following serum electrophoresis to classify the abnormal bands?
**Immunofixation**
73
What is a Bence Jones protein and what condition(s) might its appearance suggest?
BJ proteins are **excess** **immunoglobulin light chains** that are detected in the **urine** with electrophoresis
Their presence is particularly associated with **Multiple myeloma** (and also **Waldenstrom's macroglobulinaemia**)
74
What is the most common cause of paraproteinaemia?
**MGUS** (monoclonal gammopathy of undetermined significance)
75
Describe the progression of development from normal plasma cells to myeloma
Normal plasma cells pick up a "genetic hit" and **MGUS** develops (benign/pre-malignant)
MGUS picks up more genetic hits and becomes **Asymptomatic myeloma** (malignant, but with no organ damage)
Asymptomatic myeloma picks up even more genetic hits and develops into overly malignant **myeloma**
76
Myeloma affects the body through both direct tumour cell effects and paraprotein-mediated effects. What are some of the direct tumour cell effects?
Bone lesions
Increased calcium
Bone pain
Replacement of normal bone marrow and subsequent marrow failure
77
Myeloma affects the body through both direct tumour cell effects and paraprotein-mediated effects. What are some of the paraprotein-mediated effects?
Renal failure
Immune suppression
Hyperviscosity
Amyloid accumulation
78
Myeloma is classified by the type of antibody produced. Which is the most commonly produced antibody?
**IgG** (59%)
79
What are some of the clinical signs and symptoms of hypercalcaemia?
Stones (kidney)
Bones
Abdominal groans (N+V, constipation, indigestion)
Psychiatric moans (lethargy, fatigue, memory loss, depression)
Thirst
Dehydration
Renal impairment
80
What major organ in the body is commonly affected in patients with myeloma?
How has it become damaged?
The **kidneys** - 30% of patients present with renal impairment at diagnosis
Causes
* Tubular cell damage by light chains
* Light chain deposition, "cast nephropathy"
* Sepsis
* Hypercalcaemia and dehydration
* Drugs, NSAIDs
* Hyperuricaemia
* Amyloid deposition
81
How is myeloma treated and what is used to measure response?
**Combination chemo** is the mainstay of treatment (+symptom control)
- Corticosteroids: dexamethasone or prednisolone
- Alkylating agents: cyclophosphamide, melphalan
- 'Novel' agents: thalidomide, bortezomib, lenalidomide
- High dose chemo/autologous stem cell transplant in patients that are fit enough
**Paraprotein levels** are used to monitor response to treatment
82
What is MGUS (monoclonal gammopathy of undetermined significance)?
"Everything that myeloma is not"
Paraprotein is present, but in small amounts (**\<30 g/l**)
Bone marrow plasma cells are **\<10%**
No evidence of myeloma/organ damage
- normal Ca
- normal renal function
- normal Hb
- no lytic lesions
83
What antibody is associated with Waldenstrom's macroglobulinaemia?
How does this condition present?
**IgM** paraprotein is seen
Tumour Effects
* Lymphadenopathy
* Splenomegaly
* Marrow failure
Paraprotein Effects
* Hyperviscosity - fatigue, visual disturbance, confusion, coma
* Neuropathy
**B symptoms - night sweats, weight loss**
84
Myeloproliferative disorders and acute leukaemia are both _clonal haematopoietic stem cell disorders_ with an increased production of one or more types of haemopoietic cells. How do MPD and acute leukaemia differ?
In contrast to acute leukaemia, **maturation is relatively preserved in MPDs**
Cells in acute leukaemia are monomorphic, while cells in MPDs will appear at various stages of maturation i.e. not monomorphic
85
MPDs can be classified into one of two subtypes based on whether they are **BCR-ABL1 positive** or **BCR-ABL1 negative**
Provide examples of both
BCR-ABL1 positive
* **Chronic Myeloid Leukaemia (CML)** - overproduction of granulocytes, associated with the Philadelphia chromosome
BCR-ABL1 negative
* **Polycythaemia Rubra Vera** - overproduction of red cells
* **Idiopathic Myelofibrosis**
* **Essential Thrombocythaemia** - overproduction of platelets
86
What features on a blood count might make you suspect a MPD?
High granulocytes
+/-
High red cell count/haemoglobin
+/-
High platelet count
+/-
Eosinophilia/Basophilia - **especially in CML**
Splenomegaly
Thrombosis in unusual places
87
What types of cells do you see in excess in chronic myeloid leukaemia (CML)?
Proliferation of myeloid cells, meaning both **granuloctes and their precursors,** but also other lineages (**platelets**)
88
What are some of the clinical features of Chronic Myeloid Leukaemia?
May be asymptomatic
Splenomegaly and associated symptoms
Hypermetabolic symptoms e.g. weight loss, night sweats, fatigue
Gout (due to high cellular turnover)
Miscellaneous other problems related to hyperleucocytosis ('sludging up' of small vessels) e.g. eye pathology, priapism etc.
89
What would be the main differences if you compared a blood screen in a patient with MPD (CML) with a patient that had reactive change e.g. infection?
In both, WBCs, platelets and granulocytes would be raised.
However, in CML the rise in granulocytes (and their precursors, myelocytes) and WBCs would be considerably higher (especially eosinophils/basophils)
90
What chromosome is the hallmark of CML?
What does this result in and why is it clinically very important?
**Chromosome 22** (the Philadelphia chromosome) - translocation with chromosome 9
Results in a new chimaeric gene: **BCR-ABL1**
This gene produces tyrosine kinase which causes abnormal phosphorylation, resulting in the haematological changes seen in CML. This one mutation means that only one pathway is affected, and so giving a **tyrosine kinase inhibitor** (such as **imatinib**) provides a very good response
91
What is Polycythaemia rubra vera (PRV)?
What other conditions is it important to distinguish it from?
PRV - high haemoglobin/Hct accompanied by erythrocytosis, but may also have excessive production of other lineages. Results in the blood becoming thicker
Important to distinguish from **secondary polycythaemia** (chronic hypoxia, smoking, EPO-secreting tumours etc.) and **pseudopolycythaemia** (dehydration, diuretic therapy, obesity)
92
What test can be performed to distinguish between true and pseudopolycythaemia?
Centrifugation of whole blood to give packed red cells and plasma, then leave to sit
93
What are some of the clinical features of Polycythaemia rubra vera (PRV)?
Those common to MPD (increased cellular turnover, splenomegaly, marrow failure, thrombosis)
Headache, fatigue
**Itch (aquagenic pruritis - worse in warm water)**
94
What investigations might you perform if you suspected PRV?
What mutation in particular might you look for?
History (exclude secondary polycythaemia)
Examination (look for signs of splenomegaly)
FBC and blood film
Test for the **JAK2 mutation** (strongly associated with PRV, present in over 95% of cases)
95
How is PRV treated?
Venesect to Hct of \<0.45
Aspirin
Cytotoxic oral chemotherapy (e.g. hydroxycarbamide)
96
What is Essential Thrombocythaemia (ET)?
**Uncontrolled production of abnormal platelets**
Abnormal platelets have abnormal function, meaning more likely to cause **thrombosis** and at higher leels can also cause bleeding due to acquired vW Disease)
97
When a patient presents with possible Essential Thrombocythaemia, what condition should be ruled out initially?
Why might this condition present?
Need to rule out **Reactive Thrombocytosis**
Seen with blood loss, inflammation, malignancy and iron deficiency
98
The appearance of teardrop-shaped RBCs in peripheral blood would indicate which condition?
Myelofibrosis
99
How might myelofibrosis present?
Bone marrow fibrosis - anaemia, bleeding, infection
Extramedullary haemopoiesis causing hepatosplenomegaly - LUQ pain, portal hypertension
Clinical hallmarks are **leukoerythroblastosis** and **splenomegaly**
100
What are the causes of a leukoerythroblastic blood film (3)?
Reactive (sepsis)
Marrow infiltration
Myelofibrosis
101
Reactive causes of high cell counts are much more common than myeloproliferative disorders. What are some of the reactive causes of raised granulocytes?
Infection
Physiological e.g. post-surgery, use of steroids
102
Reactive causes of high cell counts are much more common than myeloproliferative disorders. What are some of the reactive causes of raised platelets?
Infection
Iron deficiency
Malignancy
Blood loss
103
Reactive causes of high cell counts are much more common than myeloproliferative disorders. What are some of the reactive causes of raised red cells?
Dehydration (+ use of diuretics) resulting in pseudopolycythaemia
Secondary polycythaemia e.g. hypoxia, smoking, EPO-secreting tumours
