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MedEd > Blood Cancers/Disorders > Flashcards

Blood Cancers/Disorders Flashcards

1
Q

Breakdown of chronic and acute leukaemias?

A

Acute = rapid increase in immature blood cells which crowd out the marrow. Abnormal differentiation and excessive proliferation

Chronic = excessive build-up of abnormal but relatively mature. Normal(ish) differentiation proliferation. Mainly in older people

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2
Q

Features of acute myeloid leukaemia?

A

Rapid proliferation of myeloblasts -> neutropenia, anaemia and thrombocytopaenia

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3
Q

Rfs and presentation of AML?

A

RFs: incidence increases with age, Downs, irradiation and anti-cancer drugs

Bone marrow failure: infection, bleeding, pallor

Tissue infiltration: mild splenomegaly and swollen gums

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4
Q

Ix for AML?

A

Sudan black to show Auer rods

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5
Q

What is acute promyelocytic leukaemia?

A

Hyper aggressive subtype of AML

Genetic translocation 15:17 fuses PML with RAR-alpha

Faggot cells on cytology with lots of AUer rods

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6
Q

RFs and presentation of ALL?

A

Most common childhood. Genetics (Downs/NF), radiation, influenza.

Thrombocytopaenia, neutropaenia and anaemia so bone marrow failure = pallor, bleeding, infections

Tissue infiltration = lymphadenopathy, hepatosplenomegaly, swollen testes and tender bones

B symptoms = fever, night sweats and weight loss

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7
Q

Ix for ALL?

A

> 20% lymphoblasts on bone marrow biopsy

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8
Q

CML features?

A

Hyperproliferation of granulocyte precursosrs = bone marrow failure, hypermetabolism and hyperviscosity.

Has chronic phase, accelerated phase and blast phase.

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9
Q

Rfs and presentation of CML?

A

Rfs: M1.4:1F
Philadelphia Chr 9:22 BRC-ABL1 fusion gene

50% asymptomatic
90% massive splenomegaly
Hypermetabolic syndrome: weight loss, malaise, sweating

Bone marrow failure: anaeia, bleeding, infections

Hyperviscosity syndrome: thrombotic events, headaches

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10
Q

CLL features?

A

Progressive accumulation of functionally incompetent lymphocytes =-> occasional features of bone marrow failure and hypermetabolism

Caused by a failure of apoptosis

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11
Q

Rfs and presentation of CLL?

A

M:F 2:1
Genetic risk factors

50% asymptomatic, occasaionaly non-tender lymphadenopathy, occasional bone marrow failure

Usually diagnosed by routine bloods = lymphocytosis and smear/smudge cell on blood films

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12
Q

What are the general investigations for leukaemia?

A

FBC, LDH, blood smear

Bone marrow aspirate for biopsy

Immunophenotyping or CXR

LDH is often elevated in cancer

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13
Q

What is Lymphoma?

A

A group of blood cancers which develop from lymphocytes and the tumours are mainly found on lymph ndes

Often present with a lump/systemic B symptoms

Hodgkins, non hodgkins -> Burkits

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14
Q

Rfs and presentation of Hodgkins?

A

Bimodal age 20-30 and >50
50% EBV associated

Painless enlarging neck mass, which can be painful after alcohol

Neutrophilia

B symptoms

Non-tender, firm and rubber lymphadenopathy with splenomegaly +- hepatomegaly

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15
Q

Ix for Hodgkins?

A

Reed-sternberg cells on lymph node biopsy = bi-nucleate lymphocytes

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16
Q

Rfs and presentation of NHL?

A

More common that hodgkins (85% b cell, 15% T cell or NK)

RFs: EBV, HIV, sjogrens. Incidence increases with age

Painles enlarging mass in neck, axilla or groin

B symptoms (less common than HL)

Neutropaenia
Skin rashese.g. mycosis fungoides, headache, hepatosplenomegaly (more common than HL)

NO REED STERNBERG CELLS

17
Q

Features of Burkitts lymphoma?

A

Strong EBV association, chronic malaria reduces resistance to EBV infection ( Papua new guinea, Equatorial africa and brazil), HIV

Rapidly enlarging lymph node in the jaw

18
Q

Ix for Burkitts?

A

Starry sky appearance under microscopy

19
Q

How to stage lymphoma>

A

Ann Arbour stagings

20
Q

What is tumour lysis syndrome?

A

Metabolic abnormalities from cancer treatment = especially leukaemias and lymphomas

Phosphate -> forms calcium phosphate crystals = kidney failure and hypocalcaemia

Hyperkalaemia = arrhythia

Uric acid = gout and uric acid renal stones

21
Q

WHat is multiple myeloma?

A

Proliferation of plasma cells so production of monoclonal immunoglobulin (IgG or IgA)

22
Q

features of MM?

A

Rfs: >70, afrocarribean
Ionising radiation, agricultural work, HIV

CRAB
Hypercalcaemia
Renal impairments: 20%, worse prognosis
Anaemia = due to crowding, frequent infections
Bone lesions = increased osteoclast = back/rib pain

23
Q

Ix for MM?

A

Bloods = raised ESR/CRP, irea, Cr, Ca, normal ALP

Rouleaux on blood film

Bence jones proteins in serum/urine electrophoresis

Bone marrow aspirate shows increased plasma cells >10%

24
Q

WHat is MGUS?

A

Monoclonal Gammopathy of unknown significance:

Pre-malignant condition with accumulation of some monoclonal plasma cells

1% acquire additional mutations -> MM

Absent CRAB features

25
Q

What is myelodysplasia?

A

Def: group of syndromes where the immature blood cells do not mature normally

Primary = intrinsic bone marrow problem 
Secondary = previous chemo/radiotherapy

Causes chronic pancytopaenia

Breakdown = refractory anaemia. refractory anaemia with ringed sideroblasts, refractory anaemia with excess blasts, refractory anaemia with excess blasts in transformation, chronic myelomonocytic leukaemia

26
Q

Ix for myelodysplasia?

A

Bone marrow apsirate is hypercellular due to ineffective erythropoeisis

27
Q

Breakdown of normal wound healing?

A

Primary haemostasis = platelet aggregation and plug formation depednign on patelets and vWF. Disorders are superficial bleeding

Secondary haemostsis = fibrin formation to stabilise the platelet plug. Depends on clotting gfactors and disroders are deep bleeding and bruising

28
Q

What is haemophilia?

A

Inherited disorder of clotting factor deficiency/

secondary and xling recessive

a = 8 and b = 9

29
Q

Presentation and Ix for haemophilia?

A

Haemarthrosis, haematoma and excessive bleeding and haematuria

Prolnged APTT and factor assay to confirm diagnosis

30
Q

What are the roles of vWF?

A

Platelet adhesion between endothelium and platelets (GP1b)

Platelet aggregation

factor 8 stabilisation

31
Q

Breakdown of vWF syndrome?

A

1 = reduced level of normal vWF and autosomnal dominant

2 = adequte levels of defective vWF = autosomnal dominant

3= complete lack of vWF and high reduced factor 8

Autosomnal recessive

32
Q

presentation of vWF syndrome?

A

Superficial bleeding, bruising, epistaxis, menorrhagia, prolonged gum bleeding after dental procesures, prologned bleeding from minor wounds

Type 3 = deep bleeding into joints and soft tissue due to factor 8

33
Q

Diagnosis of vWF syndrome?

A

Prolonged bleeding time
Prolonged APTT and normal PT
Reduced vWF
Normal platelets

34
Q

Breakdown of DIC?

A

Acute overt = emergency and life threatening. lots of bleeding

Chronic non-overt = slower rate with time for compensatory response and hypercoagulable but less bleeding

35
Q

DIC MOA?

A

Endothelial damage causes increased TF -> coagulation cascade activation = depleation of clotting factors and platelets. Concomitant activation of fibrinolysis causes bleeding into subcut tissues, mucous membraes and skin

Fibrin deposits in microcirculation -> MAHA and ischaemic organ damage

36
Q

DIC presentation?

A

Signs of underlying pathology e.g. sepsis

ACUTE = bleeding issues, petechiae, ecchymosises, purpura, epistaxix, resp distress

CHRONIC = clotting issues = signs of DVT or arterial thombosid

37
Q

Diagnoss of DIC?

A

FBC = low platelets adn Hb

Clotting = low fibrinogen, high fibrin degradation products, prolonged OT + APTT

Blood film = shistocytes

MedEd (32 decks)

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