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Haematology Flashcards

1
Q

Aetiology of microcytic anaemia

A

Iron deficiency
Thalassaemia
Sideroblastic
Chronic disease (can be normocytic)

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2
Q

Aetiology of normocytic anaemia

A 
Acute blood loss
Anaemia of chronic disease
Bone marrow failure
Renal failure
Hypothyroidism
Haemolysis
Pregnancy
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3
Q

Aetiology of macrocytic anaemia

A 
B12 or folate deficiency (or anti-folate drugs)
Alcohol excess or liver disease
Reticulocytosis 
Cytotoxic drugs 
Myelodysplastic syndromes
Marrow infiltration 
Hypothyroidism
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4
Q

When is transfusion in acute anaemia indicated?

A

<70g/L

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5
Q

How is red cell distribution width RDW useful in anaemia

A

If simultaneous pathology is occurring such as poor absorption of iron and folate (coeliac disease) then this may be shown in a greater volume distribution

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6
Q

Signs of chronic iron-deficiency anaemia

A

Koilonychia
Atrophic glossitis
Angular stomatitis
Post-cricoid webs (Plummer-Vinson)

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7
Q

Pathophysiology of anaemia of chronic disease

A

1) Poor use of iron in erythropoiesis
2) Cytokine induced shortening of RBC survival
3) Decreased production of and response to erythropoietin

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8
Q

Microcytic anaemia not responding to iron think

A

Sideroblastic anaemia

Ineffective erythropoiesis

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9
Q

Howell-Jolly bodies

A

Seen post-splenectomy and in hyposplenism

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10
Q

Causes of hyposplenism

A 
Sickle-cell disease
Coeliac diseaase
Congenital
IBD
Myeloproliferative disease
Amyloid
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11
Q

Reticulocytes

A

Young, large, immature RBC
Indicate active erythropoiesis
Increased in haemorrhage, haemolysis

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12
Q

Schistocytes

A

Fragmented RBCs in intravascular haemolysis- DIC, haemolytic anaemic syndrome, thrombotic thrombocytopenic purpura TTP, pre-eclampsia

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13
Q

Spherocytes

A

Autoimmune haemolytic anaemia or hereditary spherocytosis

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14
Q

When are target cells seen (Mexican hat cells)

A

Liver disease
Hyposplenism
Thalassaemia

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15
Q

Cabot rings

A

Pernicious anaemia
Lead poisoning
Bad infections

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16
Q

Macrocytic megaloblastic causes of anaemia

A

B12 and folate deficiency

Nuclear maturation is delayed compared with the cytoplasm

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17
Q

Non-megaloblastic macrocytic anaemia

A 
Alcohol excess
Reticulocytosis 
Liver disease
Hypothyroidism
Pregnancy
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18
Q

Antibodies in pernicious anaemia

A

Parietal cell antibodies in 90%

IF antibodies- more specific but less sensitive

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19
Q

When is the indirect Coombs test used?

A

Pre-natal testing to see if there are antibodies against RBCs that are free in the serum

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20
Q

Causes of haemolytic anaemia

A 
Acquired
Immune mediated- Coomb's +
Coomb's -ve
Microangiopathic haemolytic anaemia
Infection- malaria
Paroxysmal nocturnal haemoglobinuria 
Hereditary
Enzyme defects- G6PD deficiency 
Hereditary spherocytosis 
Hereditary elliptocytosis 
Haemoglobinopathy- sickle cell disease, thalassaemia
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21
Q

Warm AIHA

A

IgG mediated

Lymphoproliferative disease- CLL, lymphoma

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22
Q

Cold AIHA

A

IgM mediated, bind at lower temperatures
Often following infection
Associated with chronic anaemia, Raynaud’s

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23
Q

Haemolytic anaemia that is coomb’s direct test positive

A

AIHA
Drug-induced- penicillin, quinine
Acute transfusion reaction
Haemolysis of the newborn

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24
Q

Sickle cell vaso-occlusive crises precipitated by

A

Hypoxia
Cold
Dehydration
Infection

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25
Q

Hereditary haemorrhagic telangiectasia

A

Osler-Weber-Rendu syndrome

Abnormal blood vessel development in the cutaneous tissue and mucous membranes

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26
Q

Haemophilia A inheritance

A

X-linked recessive
50% of sons affected
50% of daughters carriers

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27
Q

Christmas disease

A

Haemophilia B

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28
Q

Liver disease bleeding pathology

A

Decreased synthesis of clotting factors
Decreased absorption of vit K
Abnormalities of platelet function

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29
Q

Alteplase MOA

A

Recombinant tissue plasminogen activator
Converts plasminogen into plasmin
Degrading fibrin cross-linking
Bind fibrin so localise to the area of the clot

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30
Q

Immune thrombocytopenia

A

Anti-platelet antibodies

IV immunoglobulin may be used to temporarily raise the platelet count- ie for pregnancy or surgery

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31
Q

PT factors tested

A

Extrinsic and common

I, II,V,VII,X

32
Q

APTT factor tested

A

I, II, V, VIII, IX, X, XI, XII

33
Q

How should crossmatch blood be taken?

A

From one patient at a time and labelled immediately

34
Q

When is Fresh Frozen Plasma used?

A

To correct clotting defects

DIC, TTP, liver disease, when vitamin K would be too slow

35
Q

Complications of transfusion

A

Early- within 24 hours
Acute haemolytic reactions, anaphylaxis, bacterial contamination, febrile reactions, allergic reactions, fluid overload, transfusion related acute lung injury

Delayed- after 24 hours
Infections, iron overload, post-transfusion purpura, potentially lethal fall in platelet count

36
Q

What is a massive blood transfusion?

A

Replacement of an individuals entire blood volume within 24 hours

37
Q

What is autologous blood transfusion?

A

Patients blood is stored pre-op for their own use later

38
Q

TRALI management

A

STOP the transfusion
Give 100% oxygen
Treat as ARDS with respiratory and circulatory support and close monitoring for sepsis
Donor should be removed from donor panel

39
Q

LMWH

A

Preferred preventative anticoagulant
Inactivated factor Xa but not thrombin
Half life 2-4 fold longer than standard heparin and response is more predictable

40
Q

Unfractioned heparin MOA

A

Binds antithrombin- increasing ability to inhibit thrombin, factor Xa and IXa
Rapid onset and short half-life

41
Q

How often do DOACs need monitoring?

A

Every 3 months an assessment and an annual blood test

42
Q

Target INR for warfarin for PE/DVT/AF/aortic valve replacement

A

2-3

43
Q

Target INR for warfarin for mitral valve replacement

A

2.5-3.5

44
Q

INR 5-8, no bleed

A

Withhold warfarin and restart at lower dose once <5

45
Q

INR 5-8 minor bleed

A

Stop warfarin and admit for urgent IV vit k

Restart warfarin <5 INR

46
Q

INR >8 no bleed

A

Stop warfarin

Haematology advice

47
Q

INR >8 minor bleed

A

Stop warfarin and admit for urgent IV vit k
Restart warfarin <5 INR
Daily check of INR

48
Q

Any major bleed on warfarin

A

STOP warfarin
Give Prothrombin Complex Concentrate and IV vit K
Discuss with haematology

49
Q

Types of leukaemia

A

Chronic lymphoblastic leukaemia
Chronic myeloid leukaemia
Acute lymphoblastic leukaemia
Acute myeloid leukaemia

50
Q

Commonest cancer of childhood

A

Acute lymphoblastic leukaemia

51
Q

Signs and symptoms of ALL

A

Marrow failure- anaemia, infection and bleeding
Infiltration- hepatosplenomegaly, lymphadenopathy- superficial or mediastinal, orchidomegaly, CNS involvement- cranial nerve palsies, meningism

52
Q

Treatment for ALL

A

Educate and motivate patient to get involved with treatment
Support- blood/platelet transfusion, IV fluids, allopurinol (tumour lysis syndrome prevention)
Infections- immediate antibiotics and start neutropenic regimen
Chemotherapy

53
Q

Philadelphia chromosome

A

Reciprocal change of information between 22 and 9
Results in chronic myeloid leukaemia and is associated with some forms of ALL
22t(9:22)

54
Q

What are myelodysplastic syndromes?

A

Disorders that manifest as bone marrow failure- life threatening infection and bleeding

55
Q

AML differentiated from ALL

A

Auer rods on biopsy

56
Q

Commonest acute leukaemia in adults

A

AML

57
Q

CML presentation

A

Mostly chronic and insidious- weight loss, tiredness, fever, sweats
Features of gout due to purine breakdown
Bleeding- anaemia and bruising
Abdominal discomfort from splenic enlargement

58
Q

Most common leukaemia

A

Chronic lymphocytic leukaemia

Progressive accumulation of a malignant clone of functionally incompetent B cells

59
Q

CLL presentation

A

Often none- surprise on a routine FBC
Can have constitutional symptoms or anaemic or infection prone
Enlarged, rubbery, non-tender nodes
Hepatosplenomegaly

60
Q

Characteristic Hodgkin’s lymphoma cells

A

Reed-Sternberg cells

61
Q

Risk factors for Hodgkin’s lymphoma

A

Affected sibling
EBV
SLE
Post-transplantation

62
Q

Symptoms and signs of Hodgkin’s lymphoma

A 
Enlarged, non-tender, rubbery, superficial lymph nodes- usually cervical but can be axillary or inguinal
25% have constitutional upset 
Alcohol induced lymph node pain 
Mediastinal lymph node involvement 
Cachexia, anaemia, organomegaly
63
Q

Tests for Hodgkin’s lymphoma

A

Blood- FBC, film, ESR, LFT, LDH, urate, Ca2+

Imaging- CXR, CT TAP

64
Q

Staging system used in Hodgkin’s lymphoma

A

Ann-Arbor system

65
Q

MALT lymphoma

A

Mucosa-associated lymphoid tissue

Gastric is caused by H. pylori

66
Q

Burkitt’s lymphoma

A

Non-Hodgkin’s lymphoma
Childhood disease
Characteristic jaw lymphadenopathy

67
Q

Causes of polycythaemia

A

Relative- low plasma
Absolute- primary- Polycythaemia vera,
secondary- hypoxia or inappropriate erythropoietin secretion

68
Q

Mutation in polycythaemia vera

A

JAK2

>95%

69
Q

Presentation of polycythaemia vera

A

Asymptomatic and detected on FBC
or
Hyperviscosity related- headaches, dizziness, tinnitus, visual disturbance
Itching after a hot both and erythromelalgia (burning sensation in fingers and toes)

Signs
Facial plethora, splenomegaly, gout from increased urate from RBC turnover
Arterial or venous thrombosis may be present

70
Q

Treatment of polycythaemia vera

A

Venesection to keep the risk of thrombosis down
Aspirin 75mg daily
If higher risk (>60 years old or previous thrombosis) then hydroxycarbamide
Alpha-interferon in women of childbearing age

71
Q

Treatment for essential thrombocythaemia

A

Aspirin 75mg daily

72
Q

Clinical features of myeloma

A

Osteolytic bone lesions- backache, pathological fractures, vertebral collapse
Hypercalcaemia- increased osteoclastic activity
Anaemia, neutropenia or thrombocytopenia from marrow infiltration by plasma cells
Recurrent bacterial infections
Renal impairment from light chain deposition in the distal loop of Henle

73
Q

Tests for multiple myeloma

A

FBC, raised ESR, raised urea and calcium, alk phos normal unless healing fracture
Film
Bone marrow biopsy- increased plasma cells
Serum/urine electrophoresis
Xray- lytic lesions, pepperpot skull, vertebral collapse, fractures, osteoporosis

74
Q

Treatment for multiple myeloma

A

Supportive- analgesia (avoid NSAIDs- renal function), bisphosphonate, local radiotherapy
Transfusion for anaemia
Renal failure- rehydration and ensure adequate fluid intake
Rapid infection control
Chemotherapy

75
Q

Causes of massive splenomegaly

A

CML
Myelofibrosis
Malaria
Leishmaniasis

76
Q

Protein C & S action

A

Vitamin K dependent factors that act together to cleave and neutralise factors V and VIII
Deficiency causes thrombophilia

77
Q

Activated protein C resistance/ factor V leiden syndrome

A

Single point mutation in factor 5 so that this clotting factor is not broken down by APC
5 fold increase risk of DVT/PE if heterozygous

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