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Haematology Sem 1 > 4. White blood cells in health and disease > Flashcards

4. White blood cells in health and disease Flashcards

1
Q

What are the two types of immune defence?

A

Innate (non-specific) and acquired (specific)

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2
Q

Tell me about the two types of immune defence

A

innate is first response and attacks foreign bodies (micro organisms in wounds, wood splinters). Its preexisting and is first line of defence (early response). It is why medical prothesis need to be tested before use

Acquired immune response is a later reponse that takes <5 days. Quickly proliforate if had contact with specific foreign cell before but if not it can take a while. It has specific memory. It is why there can be a late response to transfusion reactions

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3
Q

What are leukocytes?

A

White blood cells

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4
Q

What are the two types of leukocytes?

A

Polymorphnuclear cells and lymphocytes

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5
Q

What kind of immunity are polymorphnuclear (PNM) cells provide?

A

Innate immunity

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6
Q

What processes do PNM cells destroy pathogens?

A

Phagocytosis

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7
Q

What are monocytes produced by?

A

Granulopoesis

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8
Q

What kind of cells are monocytes?

A

Phagocytic cells

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9
Q

What is the most abundant type of PNM cell?

A

Nuetrophils

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10
Q

What are the nucleus in neutrophils held together by?

A

Heterochromatin

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11
Q

Tell me 6 ways in which neutrophils respond as first line defence?

A

(1) They are the first to respond at site of infection
(2) Bone marrow responds to the increased production of cytokines so their numbers rapidly increase when infection detected
(3) They are responsible for creating pus or inflammation
(4) They are present in both blood and tissue so they can reach site of action easily
(5) They are phagocytic so can ingest bacteria
(6) Their granules destroy bacteria

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12
Q

What other cells are polymorphonuclear cells?

A

Basophils, monocytes, eoisinophils

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13
Q

How do Basophils monocytes and eoisinophils act as first response?

A

Basophils - trigger inflammation
Monocytes - phagocyctic. They increase with nuetrophils during infections
Eoisinophils- fights parasitic infection

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14
Q

What kind of cells are acquired immunity?

A

B and T cells

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15
Q

What is nuetrophilia? Range? Cause?

A

Increased number of neutrophils >7.5 x10^9/L
Caused by cancer and as a reaction to certain drugs
Causes severe infection due to all cells in bone marrow (myeloid cells) be at different stage of development within the bone marrow. (Left shift in production of neutrophils - too many are immature). The granules in the neutrophils are too plentiful and are toxic due to acidic microsubstances

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16
Q

What is neutropenia? Range? Cause? Symptoms?

A

Decreased number of neutrophils >2.0 x10^9/L
Caused by drugs, post viral, TB, HIV but can be idiopathic or hereditary.
Symptoms: infection of mouth and throat, skin ulceration, septicaemia.
Patients must be isolated for their own safety if levels drop below 0.5 x10^9/L

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17
Q

What is eosinophilia? Range? Causes?

A

Increased number of eoisinophils. >0.4 x10^9/L. Caused by parasitic infection, allergic disease, skin disease and drugs

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18
Q

What is basophilia? Range? Cause?

A

Increased number of basophils >0.1x10^9/L

Caused by mixoderma, small pox, chicken pox and ulcerative collitis

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19
Q

What is the name given to an increased number of monocytes? Causes?

A

Monocytosis. Monocytes increase when number of neutrophils increase. Causes: systematic neutrophil erythmatosis (SLE), rhematoid artheritis, protozoal infection.

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20
Q

What is the name given to an increased number of lymphocytes? range? causes?

A

lymphocytosis. >3.0x10^9/L. Seen in healthy children. Also seen in infectious mononucleoisis - glandular fever, whooping cough, viral infection, measles, mumps, HIV, TB

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21
Q

What is the name given to a decrease in the number of lyphocytes? Causes?

A

Lymphopaenia. Causes: viral infections, drugs, bone marrow failure

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22
Q

What is infectious mononucleolis? Tell me about it

A

It is glandular fever. Called kissing disease as it is spread through saliva. It affects 15-20 year olds mostly and is a benign lymphoproliforative disorder caused by the epstien-barr virus (EBV). It is sero-positive in 90% of adults although symptoms will not manifest in all of them.

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23
Q

What are the symptoms of infectious mononucleolis?

A

Abnormally sized lymph nodes (lymphadenopathy), ore throat, stiff neck, rash, lethargy, headaches, dry cough, mild/severe fever, splenamegaly, jaundice, severe anaemia

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24
Q

What are the lab findings of infectious mononucleolis?

A

Haemolytic anaemia. moderately raised blood cells (10-20 x10^9/L…demonstrates absolute lymphocytosis). atypical lymphocytes in peripheral blood. Paul bunnel antibodies. Positive monospot test and positive EBV test. Increased biliruben levels due to haemolytic anaemia and low Hb.

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25
Q

How is infectious mononucleolis treated?

A

Treatment usually not required and the virus will pass after 4 -6 weeks. Corticosteriods used in extreme cases and sometimes antibiotics (if there is streptaccocal infection)

26
Q

What is haemopoeitic malignancy?

A

Clonal disease (immune disease) that is caused by one single cell in the bone marrow undergoing genetic alteration.

27
Q

How is haemopoeitic malignancy classified?

A

2 subcategories:
haemopoeitic lineage: (whether its myeloid (bone marrow stem cells) or lymphoid (lymphatic system)

or whether its acute or chronic

28
Q

Describe (general) acute leukaemia

A

Associated with stem cells or early progenitors. The disease is aggressive and progesses faster and is fatal if left untreated. Immediate treatment required. Caused by increased rate of proliferation and reduced rate of apoptosis, causing accumulation of early haemopoeitic cells in bone marrow (blast cells)

29
Q

Describe (general) chronic leukaemia

A

Associated with mature cells. Progresses slower. Treatment can be delayed depending on stage of disease

30
Q

What are the symptoms of leukaemia?

A

Pallor, lethargy, bone pain, flu-like symptoms, lymphadenopathy (abnormal sized lymph nodes), hepatomegaly, pharyngitis, recurrent infection, easy bruising, pyrexia, night sweats

31
Q

What are the clinical features of leukemia?

A

Bone marrow failure due to accumulation of malignant cells. There will be a rise in opportunistic infections (candida). Anaemia is secondary disorder. Thrombocytopenia (bleeding gums, petichiae), disseminated intravascular coagulation (DIC) which is micro clots in blood vesssels and gum hypertrophy (increase in gum size)

32
Q

How is (general) accute leukemia diagnosed?

A

> 20% blast cells present in blood or bone marrow at clinical presentation.
Lineage of disease determined via microscopy to check the morphology of disease but this can be difficult.
Cells will be immunotyped (flow cytometry) - myeloid is CD13 positive and lymphoid is CD19 positive
Cytogenetic and molecular analysis of bone marrow cells
Cytochemistry less used as its not the most effect type of testing
Karyotyping

33
Q

What will labs check when diagnosing leukaemia?

A

Size of cells: compare the size of RBCs and normal lymphocytes.
Check amount/ colour of cytoplasm around the nucleus
Check the nucleus: check for open/dense chromatin structure. The shape of nucleus might be lobular or indented instead of round.
Check if there is a nuclei in the nucleus (where RNA produced)
Check for granules in the cytoplasm or auer rods

34
Q

What is acute myeloid leukemia? Prevelance? How is it diagnosed? How is it classified?

A

Most common form of leukemia. Mostly 65+ years of age and only 10% of child leukemia. Diagnosed with cytogenetics and the speed of diagnosis and action greatly impacts prognosis.
Classified by specific gene types: 60% have karyotype abnomalities (cytogenetic testing).
Some have normal kayrotypes but gene mutations:FLT3 and CEBPA (molecular testing)

35
Q

What are the 6 types of AML?

A

AML with:
undefferenciated cells
without maturation
with maturation

Acute:
Promyelinated leukemia
Myelomonocytic leukemia
Megaloblastic leukaemia

36
Q

What are the lab findings of AML? How are blasts characterised?

A

Needs to be carried out before treatment
A full blood count showing RBC, low or high WBC, low haemoglobin, low platelets but blast cells present.
Disseminated intravascular coagulation (DIC) positive test
Bone marrow biopsy showing hypercellular marrow due to abnormal proliforation

Blast characterised using:
immunophenotyping
immunoflorecent staining
molecular analysis - karyotyping. CRITICAL FOR DIAGNOSIS

37
Q

If a patient is under the ‘good, intermediate or poor’ category, what is their liklihood for survival? What is their liklihood of relapse?

A

Good:
5 years following diagnosis:70
relapse change:33

Intermediate
5 years following diagnosis:48
relapse chance: 50

Poor
5 years following diagnosis: 15
relapse chance: 80

38
Q

How is AML treated?

A

Aim is to support patient and to bring them to full remission. It is case specific.
Bone marrow only given to ‘poor liklihood of survival’ patients as they are in least favourable risk group
Chemotherapy
Daunorubicin, cytocin, arabinocide and etoposide are myelotoxic drugs that are only given in severe marrow failure
General supportive therapy: frozen plasma (for coagulation), clotting factors (for coagulation) or platelet factors (for coagulation)

39
Q

What is acute promyelocytic leukemia?

A

maturation of WBC stops are promyelocyte stage so they accumulate in the bone marrow
These are not enough other blood cells made because of this (<30% blast cells)
Presence of of t(15:17) mutation (PML/RARA fusion gene)
Targetted treatment is to disassociate the fusion and translocation of the gene so that it can mature
95% survival after 5 years

40
Q

What is chronic myeloid leukemia? Prevelance? Chromosones?

A

Slow progression of AML. Clonal disorder of plutipotent stem cells.
15% of all leukaemias
Occurs at any age
Easily diagnosed due to presence of philadelphia chromosone (Ph): t(9:22) (q34:q11) - oncogene ABR1 translocates to BRC on chromosone 22. ALB1/BRC fusion protein
Conventional karyotyping is labour intensive: PCR better for this

41
Q

What are the clinical findings of CML? Prevelance? Symptoms?

A

Occurs in either sex (1.4:1 ratio between males and females)
No presposing factors although large incidence in survivors of Japanese atomic bomb
Symptoms: weight loss, night sweats, lassitude, splenamegaly, features of anaemia, bruising, gout, renal impairment.
Chance finding in 50% of patients

42
Q

What would the lab finding of CML be?

A

Leucoytosis > 50x10^9/L.
Spectrum of myeloid proginator cells
Increased circulating basophils
Noromochromic/normocytic anaemia
Platelent count can be high but can also be normal or low
Hypercellular bone marrow
BCR-ABL1 fusion protein present in 98% of patients

43
Q

What are the 3 phases of CML?

A

Chronic, accelerated phase, blastic transformation phase

44
Q

What phase are 90 of CML patients in?

A

Chronic. 2-3 years

45
Q

What happens during the accelerated phase?

A

Blast cell population increases
WBC population rise steadily during treatment.
Platelet either extremely low (<100x10^9/L.) or extremely low (>1000x10^9/L. )
Hb <8.0g/dl
<10% blasts in peripheral blood
<20% basophils/eoisinophils in peripheral blood
Difficult to treat

46
Q

What happens during the blastic transformation phase?

A

> 30% of blasts in blood or bone marrow
Marked anaemia and thrombopenia
Can transform into AML (1 year prognosis) or ALL (1-2 year prognosis)

47
Q

What is the treatment of the chronic phase of chronic myeloid leukaemia?

A

Imatinib 400mg daily
ABL1-BRC inhibitor
Good response from almost all patients
Bone marrow transplant if imatinib fails

48
Q

What is the treatment of accelerated phase?

A

May be in phase for several months
Less easy to control
Different chromosone abnormalities
must be treated as AML/ALL

49
Q

What is acute lymphoblastic leukaemia

A

Malignent disorder of B progenitor cells which are classified into 3 groups by immunophenotyping
affects mostly children 3-5 years but adults can be affected too
most common child hood cancer
Cause is unknown but likely to be mutated stem cells that cause disorder of the B progenitor cells

50
Q

What would lab findings be of ALL?

A

Variable but abnormal blood count in 90% of cases
platelets low in 70% of cases <100x10^9/L. but are as low as <100x10^9/L. in 15% of cases
white blood cells are abnormal in 50% of cases and above average in 10% of cases
blood film shows presence of lymphoblasts

51
Q

What are the clinical features of ALL?

A

Variable but all associated with bone marrow failure. Lethargy, paleness, weakness due to anaemia.
Petechia or easy bruising due to thrombopenia (low platelet leads to cappillary haemorraging)
Joint pain common in children

52
Q

What are the blood film features of ALL

A 
Blasts are 2x the size of RBC
Sparse cytoplasm
Nucleus round or oval
Homogeneous chromatin
Occasional nuceoli
Vacule present
53
Q

What is the genetic subtyping of ALL?

A

t(12:21) TEL/AML - most comon in childhood
alteration of chromosone numbers:
hyperedipody: over 55 chromosones
hypodipody: less than 44 chomosones

various other t(9,22…1:19…4;11)
genotyping important for treatment and prognosis

54
Q

Treatment of ALL in children?

A

Specific treatment
Chemotherapy -90% of children get into remission and 80-90% of adults
Radiotherapy

Type of treatment changes depending on age, gender,WBC count and production as this changes the risk

Must have maintenance therapy for 2-3 years

55
Q

Treatment of ALL in adults?

A

Challenging as relapse is common. <40% remission after 5 years but drops to 5% if patient over 70
Treatment is mostly supportive (to support failing bone marrow)

56
Q

What is chronic lymphoblastic leukaemia?

A

Most common chronic leukaemia
60-80 years of age
Men are two times more likely to suffer
Unknown is there is a genetic predisposition
Geographical variation
Mature lymphocytes accumulate in the bone marrow, blood, spleen, liver and lymph nodes
25% aysmptotic so chance finding 25%

57
Q

What are the clinical features of CLL>

A

Anaemia, reccurent infection, spenomegaly, bruising, enlargement of cervic and lymph nodes in a symetrical way

58
Q

What are the lab findings of CLL?

A

Lymphocytosis
B cells CD19+, CD20+ and CD5+
normocytic/normochromic anaemia
low platelet count (thrombocytopenia)
auto-immune haemoloyis (destruction of red cells)
CLL lymphocytes are mature and homogenous (same structures) - dense nuclear chromatin and little cytoplasm

59
Q

What is the prognosis for a person with CLL?

A

> 20 yeats following diagnosis depending on age, gender, severity of thromoctyopenia, cytogenetics and other clinical features
cytogenetic abnormalities are major factors on prognosis

60
Q

What is the treatment for CLL?

A 
Some patients may never need treatment due to favourable genetic markers
Radiotherapy
Combination chemotherapy
Immunosupprensant (clyclosporin) 
Splenectomy

Haematology Sem 1 (8 decks)

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