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- FINALS > Haematology > Flashcards

Haematology Flashcards

1
Q

MCV?

A

Average cell size

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2
Q

RDW?

A

Red cell distribution width - measure of the range of variation of red blood cell volume

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3
Q

Reticulocytes?

A

Immature red cells

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4
Q

TIBC?

A

Total iron binding capacity - blood’s capacity to bind iron with transferrin

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5
Q

Haematocrit?

A

How many red cells in blood volume (% red cells) - if it decreases with Hb then it suggests decrease is dilutional

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6
Q

Mnemonic for remembering absorption?

A

DUDE IS JUST FEELING ILL BRO

Duodenum = iron
Jejunum = folate
Ileum = B12
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7
Q

Causes of micro, normo and macro-cytic anaemias

A 
Micro = iron, thalassaemia
Normo = chronic disease, sickle cell
Macro = B12/folate, ETOH, pregnancy
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8
Q

Signs of IDA?

A

Pallor
Severe –> hyperdynamic circulation (tachy, flow murmurs, cardiac enlargement, rectal bleeding)
Chronic –> koilonychia, atrophic glossitis, angular stomatitis, post-cricoid webs

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9
Q

Investigations in IDA?

A 
High = TIBC (clinging on to iron)
Low = Hb, MCV, ferritin, serum iron, transferrin saturation

Ferritin = acute phase reactant

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10
Q

Management of IDA?

A

Ferrous sulphate/ferrous fumerate TDS

3 wks to 1 month - should increase Hb by 20 - continue for 3 months

SEs = constipation, black stools, abdo pain, nausea

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11
Q

Causes of macrocytic anaemia?

A

DIETARY
Lack of intake, alcohol

MALABSORPTION
Stomach - pernicious anaemia –> no intrinsic factor. Also post gastrectomy.
Terminal ileum - Crohn’s disease

PREGNANCY

ANYTHING THAT KNACKS UP BONE MARROW

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12
Q

Signs in macrocytic anaemia?

A

Lemon tinge to skin (pallor + haemolysis)

Glossitis, angular stomatitis

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13
Q

Complications of macrocytic anaemia?

A

Neuropsychiatric - irritability, depression, psychosis, dementia
Neurological - paresthesia, peripheral neuropathy, subacute combined generation of spinal cord

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14
Q

Investigations in macro anaemia?

A 
High = MCV
Low = Hb, WCC, platelets, serum B12, reticulocytes (because production is impaired)
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15
Q

Intrinsic causes of haemolytic anaemias?

A

RBC membrane - hereditary spherocytosis/elliptocytosis

Hb synthesis - sickle cell disease, thalassaemia

RBC enzymes - G6PD deficiency, pyruvate kinase deficiency

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16
Q

Extrinsic causes of haemolytic anaemia?

A

Immune - incompatibility (newborn, transfusion), AI haemolytic anaemia

Non-immune - infections (malaria, black water fever, Clostridium welchii), chemicals (lead, drugs, toxins)

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17
Q

Investigations in haemolytic anaemia?

A

High = reticulocytes, bilirubin, LDH

Low = Hb, haptoglobin (what Hb binds to)

Others = Coomb’s test (AI causes)

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18
Q

Management of haemolytic anaemia

A

HAEMATOLOGY

Folic acid, steroids, rituximab, IVIG (IV immunoglobulins)
Transfusion therapy
EPO

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19
Q

Pathophysiology of sickle cell disease?

A

Normal Hb = 2 alpha 2 beta –> 1 deficient beta chain

Autosomal recessive - heterozygotes = sickle cell trait
homozygotes = SC disease

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20
Q

Investigations in sickle cell?

A

Hb = 60-90
MCV normal
RBC breakdown –> high reticulocytes and bilirubin

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21
Q

Presentation of SC disease?

A

Anaemia + vaso-occlusive crisis (precipitated by hypoxia, infection, dehydration, cold)

Pain crisis, splenic infarct, stroke, priapism

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22
Q

Management of sickle cell crisis?

A

O2, morphine, treat cause (fluid/abx)

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23
Q

Pathophysiology of thalassaemia?

A

Normal globin chains, but not enough - autosomal recessive
Alpha/Beta, Trait/Major

Homozygous = major (disorder) - 2 chains deleted
Heterozygous = trait (healthy carrier) - 1 chain deleted

Alpha major = death in utero (b/c only have fHb)
Beta major = severe anaemia

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24
Q

Presentation of thalassaemia?

A

Trait = often asymptomatic

B major = severe anaemia at 4-6 months (babies have HbF)
Characteristic facial features, splenomegaly, pallor, failure to thrive, stunted growth, HF

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25
Q

Presentation and treatment of haemochromatosis?

A

Iron overload (symptoms develop in middle age, later in females because of periods)

Bronze diabetes –> bronze deposits in skin, hepatic dysfunction, diabetes, gonadal dysfunction, cardiac problems

Treatment = venesection (once a week –> every few months)

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26
Q

Too little and too many white cells?

A

Too little = leucopenia (99% neutropenia)

Too many = leucocytosis

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27
Q

Definitions of neutropenia?

A 
<1.5 = neutropenia
<1 = infection
<0.5 = immediate review
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28
Q

Causes of neutropenia?

A

REDUCED PRODUCTION
Marrow aplasia/infiltration, viral infections, TB, drugs (antimetabolites, sulphonamides, carbimazole, sulfasalazine)

INCREASED CONSUMPTION
Septicaemia (neutrophils used up), hypersplenism (neutrophils destroyed), autoimmune destruction of neutrophils (SLE, Felty’s syndrome)

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29
Q

Presentation of neutropenic sepsis?

A

7-10 days post-chemo

Fevers, rigors, malaise, hypothermia, hypotension, tachycardia, dizziness, reduced urine output

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30
Q

What is the MASCC risk score?

A

Assesses risk of complications during febrile neutropenic episode

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31
Q

What is involved in a neutropenic sepsis screen?

A 
Bloods - FBC, LFT, U+E, CRP, lactate
Cultures - line and peripheral cultures
Swabs, viral swabs
Sputum culture
Urine analysis and culture
Stool analysis and culture
CXR
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32
Q

Management of neutropenic sepsis?

A

Empirical antibiotic therapy - TAZOCIN or VANC/AZTREONAM

?G-CSF

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33
Q

Differentials for leucocytosis?

A

Primary haem problem (cancer) or a secondary response (infection)

NEUTROPHILIA
Infection (rarely >30), CML (>200, really high), others (steroid use, post-op, MI, DKA)

LYMPHOCYTOSIS
Viral (infectious mono), CLL/ALL/NHL

LEUCOSTASIS
Emergency –> ischaemia

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34
Q

Too little and too many platelets?

A

Too little = thrombocytopenia

Too many = thrombocytosis

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35
Q

Definition of thrombocytopenia?

A

<100

in reality…
For surgery - should be over 100
>30 asymptomatic
<10 worrying

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36
Q

Causes of thrombocytopenia?

A

IMMUNE - ITP, drug induced (HEPARIN - 5-10 days after), SLE, post-transfusion

Dilutional
Haemolytic uraemic syndrome
Cancer
DIC
Decreased production (low numbers megakaryocytes - radiation)
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37
Q

Presentation of thrombocytopenia?

A

Bleeding tendency - spontaneous purpura/ecchymoses, mucous membrane bleeding, nose bleeds, menorrhagia, PPH

Rare (< 30) - retinal/subconjunctival haemorrhage, GI bleeding, intracranial bleeding

38
Q

Thrombocytosis?

A

Differentiate between primary cause or secondary reactive cause

Primary = myeloproliferative neoplasm
Secondary = acute phase reactant (rarely >1000)
39
Q

Rough definition of leukaemias, lymphomas, myeloma?

A

Leukaemia = malignant cells in marrow

Lymphoma = malignant cells in LNs

Myeloma = plasma cell malignancy

Myelodysplasias = not enough cells, Myeloproliferative = too many cells

40
Q

Acute myeloid leukaemia?

A

Older adults (65-70) - 80% under 50 get complete remission, 30% cure with chemo post-remission

Symptoms of anaemia, thrombocytopenia, neutropenia
Infections (bacterial/fungal)
Fever
DIC
Infiltration of extramedullary sites (lymphadenopathy, hepatosplenomegaly, CNS involvement, gingival infiltration)

41
Q

Acute lymphoblastic leukaemia?

A

Kids (most commonly) - Philadelphia chromosome (Ph1) –> poor outcome. Good remission/cure rates.

Acute illness over several days, tiredness or non-specific aches over several weeks/months.

BONE MARROW FAILURE –> anaemia, thrombocytopenia (bleeding), bacterial infection

ACCUMULATION OF LEUKAEMIC CELLS –> bone/joint pain, hyperleukocytosis –> CNS involvement; tissue deposits of leukaemic cells –> gum hypertrophy, stomatitis; hepatosplenomegaly, lymphadenopathy, bone tenderness

42
Q

Chronic myeloid leukaemia?

A

Median age 65 yrs. 95% have philadelphia chromosome.
Usually remains stable for years then transforms to more malignant fatal disease. Only bone marrow transplantation is curative.

REALLLY high WCC; splenomegaly, weight loss, sweats, anaemia, bleeding.

43
Q

Chronic lymphocytic leukaemia?

A

Median age 69 years
Insidious onset - when symptoms present disease is advanced

‘B’ symptoms - lethargy, weight loss, fever, night sweats
Infections, anaemia, thrombocytopenia

Symmetrical, non-tender lymphadenopathy
Hepatosplenomegaly
Skin lesions (HZV, pruritis)

44
Q

Histology and spread of Hodgkin’s lymphoma?

A

Histology = polymorphic - Reed-Steenberg cells diagnostic

Spread = predictable - step by step to contiguous LNs, starting in neck usually.

45
Q

Histology and spread of Non-Hodgkin’s lymphoma?

A

Histology = monomorphic - malignant cells most numerous.

Spread = random

46
Q

Aetiology and epidemiology of Hodgkin’s/Non-Hodgkins?

A

Hodgkins = unknown aetiology; bimodal distribution (many are young)

Non-Hodgkins = unknown aetiology (EBV, h.pylori, HIV, hep C); median age = 50, increasing with age.

47
Q

What are B symptoms?

A

Indicate poor prognosis in lymphoma

Fever, night sweats, weight loss

48
Q

Lymphadenopathy in Hodgkin’s?

A

Painless - single group of nodes (cervical/supraclavicular)

49
Q

Lymphadenopathy in non-Hodgkin’s?

A

Painless (generalised; visceral) - typically disseminated at presentation

50
Q

Symptoms in Hodgkin’s

A 
B symptoms (25%)
Pruritis
Chest discomfort/cough/dyspnoea
Anaemia
Immune dysfunction

ETOH-induced LN pain

51
Q

Symptoms in non-Hodgkin’s

A

B symptoms

Anaemia
Infections
Purpura

52
Q

Staging system in Lymphoma?

A

Ann Arbor System

53
Q

Investigations in lymphoma?

A

LN biospsy

Blood - film, FBC/ESR, U+E, LFT, bone profile, LDH (worse prog in non-hodgkin’s), HIV serology

Chest radiography

Staging with contrast (CT neck to pelvis or PET/CT)

Bone marrow biopsy

54
Q

Management of Hodgkin’s?

A

Localised = RTx

Disseminated = high-dose chemotherapy (+/- stem cell transplantation)

55
Q

Management of Non-Hodgkin’s?

A

INDOLENT
Local RTx = first line; watchful waiting if asymptomatic, rituximab, chemo

AGGRESSIVE
Usually HIV +ve; R-CHOP regimen; chemo/radioT; bone marrow/stem cell transplantation

56
Q

What is myeloma?

A

Malignant proliferation of plasma cells

Presence of paraproteins in blood or urine

Associated organ dysfunction

57
Q

What are paraproteins?

A

Abnormal immunoglobulin light chains –> damage kidneys by forming protein casts in renal tubules

58
Q

How does myeloma cause bone pain/hypercalcaemia?

A

Abnormal plasma cells screte factors which activate osteoclasts

Lytic lesions, bone pain, hypercalcaemia

59
Q

Risk factors for myeloma?

A

Age, male, afro-caribbean, +ve FH, obesity, diet

60
Q

Mneominc for myeloma?

A

CRAB

HyperCalcaemia
Renal failure
Anaemia
Bone lesions

61
Q

Presentation of myeloma?

A

Bone pain (spine, ribs, pepper pot skull)

Anaemia/thrombocytopenia (normocytic normochromic)

Renal failure (uraemic symptoms, itching/muscle cramps, SoB/oedema)

Infection

Neurological (hypercalcaemia, hyperviscosity, peripheral neuropathy)

62
Q

Bloods in myeloma?

A

FBC - anaemia, neutropenia, thrombocytopenia
U+E - creatinine, hypercalcaemia
ESR - persistently raised
Blood film - Rouleaux formation

Protein electrophoresis –> bence jones protein (blood and urine)

63
Q

Imaging in myeloma?

A

Skeletal survey –> x-rays of skull, axial skeleton and proximal long bones (lytic lesions)

64
Q

What is the intrinsic pathway and what measures its time?

A

XII, XI, IX, VIII

aPTT

65
Q

What is the extrinsic pathway and what measures its time?

A

TF + VII

PT

66
Q

What is haemophilia A/B deficiency of?

A 
A = FVIII
B = FIX
67
Q

What is prolonged in haemophilia?

A

aPTT

68
Q

How is haemophilia inherited?

A

X-linked recessive (only affects males - can have female carriers)

69
Q

How does haemophilia present?

A

Haemarthroses and soft tissue bleeds after trauma or spontaneously

70
Q

What is vWD? How is it inherited?

A

Congenital deficiency of vWF

Autosomal dominant

71
Q

What does vWF do? How does vWD present?

A

Is a cofactor essential for platelet adhesion and transport of factor VIII

Prolonged APTT, low levels of factor VIII and IX

Asymptomatic usually, and diagnosed following perioperative bleeding.
Haemarthroses, soft tissue haematomas, epistaxis and menorrhagia.

72
Q

What can liver disease do to bleeding?

A

Increase INR, low platelets

73
Q

What can renal disease do with bleeding?

A

Uraemic bleeding –> affects platelet function

74
Q

Causes of DIC?

A

Malignancy, infection, obstetric complications

75
Q

How does DIC happen?

A

Trigger –> release of THROMBIN –> activation of platelets and clotting factors –> these are used up and form microthrombi

Fibrinolytic system activates in response to thrombi –> unregulated fibrinolysis

THROMBOTIC AND HAEMORRHAGIC FEATURES

76
Q

What is antithrombin III deficiency?

A

AT III inhibits thrombin, fXa, fXIIa, fXIIIa and fIXa

Autosomal dominant deficiency of this –> recurrent thrombosis and thromboembolism

77
Q

What is protein C deficnecy?

A

Protein C = vit K dependent protease which inactivates fVIII and fV and stimulates fibrinolysis

deficiency —> THROMBOPHILIA

78
Q

What is protein S deficiency?

A

Protein S = regulates protein C on surface of endothelial cells (needs Ca2+ as cofactor)

deficiency –> THROMBOPHILIA

79
Q

Packed red cells - how much do they increase Hb and how long over?

A

1 unit lasts 4 hours

1 unit –> Hb increased by 10-15, given over 3 hours

80
Q

Platelets - how much do they increase by and how long over?

A

1 unit –> plts increase by 20, given over 30 minutes.

lasts 24-48 hours in body

81
Q

What are the special requirements for blood?

A

Hep E negative -
CMV negative - transplant patients
Irradiated blood - chemo/prego/immunosuppressed

ALWAYS ASK WHETHER PATIENT HAS ANY SPECIAL REQUIREMENTS

82
Q

Additional treatments in transfusion?

A

Furosemide (if overloaded)

K+ treament –> can increase K+ because is intracellular and can damage cells

83
Q

Name some acute transfusion reactions?

A

Febrile non-hemolytic transfusion reaction (FNHTRs)
Bacterial contamination
Transfusion related acute lung injury (TRALI)
Transfusion-related circulatory overload (TACO)
Allergic/anaphylactic reaction

84
Q

Management of FNHTR?

A

Slow or temporarily stop transfusion
PCM
Monitor closely

Can occur up to 2 hours after. Less common now due to leucodepleted blood.

85
Q

Management of bacterial contamination?

A

Stop transfusion
Urgent supportive care - IV abx
Call haem - send unit back to lab

86
Q

Presentation of TRALI?

A

Antibodies in donor blood react with patients neutrophils, monocytes or pulmonary endothelium

Within 2 hours of transfusion

Severe breathlessness, cough + frothy sputum
Hypotension, fever, rigors

87
Q

Management of TRALI?

A

Stop transfusion
Supportive managment - O2, ICU if required
Remove donor from panel

88
Q

Presentation of TACO?

A

Acute pulmonary oedema

Acute resp distress, tachycardia, hypertensive, positive fluid balance

89
Q

Managment of TACO?

A

Stop/slow transfusion
Oxygen/diuretic therapy
Careful monitoring and critical care if required

90
Q

Management of allergic reaction?

A

Slow transfusion
Antihistamine (oral/IV) - chlorphenamine
Monitor closely

91
Q

Management of anaphylaxis transfusion reaction?

A

STOP TRANSFUSION

Anaphylaxis algorithm

- FINALS (24 decks)

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