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F1/ Part 1 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is HITT syndrome?

A

Heparin-induced thrombocytopenic thrombosis

platelet antibodies cause plts to thrombose vessels: loss of limb or life

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2
Q

Types of disease associated with B cell deficiencies

A

Defective antibody response = increased susceptibility to opportunistic infections caused by extracellular organisms

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3
Q

Types of disease associated with T cell deficiencies

A

Defective cell-mediated immunity = increased susceptilibity to opportunistic infections caused by intracellular organisms

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4
Q

Commonest immunodeficiency

A

IgA (1 in 700 Caucasians)

patients prone to sinopulmonary infections and bowel colonisation with Giardia, Salmonella, other enteric organisms

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5
Q

Example primary B cell deficiency

A

IgA deficiency

lots of weird congenital ones

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6
Q

Example primary T cell deficiency

A

DiGeorge (thymic hypoplasia)

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7
Q

Example primary mixed T and B deficiency

A

SCID (severe combined immune deficiency)

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8
Q

Example secondary B cell deficiency

A

Myeloma

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9
Q

Example secondary T cell deficiency

A

AIDS
Hodgkin’s and Non-Hodgkin’s lymphoma
Drugs, eg steroids, ciclosporin, azathioprine

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10
Q

Example secondary mixed B and T cell deficiency

A 
CLL
Post-bone marrow transplantation
Post-chemo/ radiotherapy
Chronic renal failure
Splenectomy
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11
Q

What is amyloidosis?

A

the pathological deposition of abnormal extracellular fibrillar protein (amyloid) in tissues

can’t be broken down

can be systemic or localised
can be inherited (rare)

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12
Q

Figures for neutropenia

A

lower than 2.5 (1.5 if black/ Middle Eastern)

severe is termed ‘agranulocytosis’
vulnerable to opportunistic infection (Gram-positive skin organisms and Gram-negative gut infections)

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13
Q

Causes of neutropenia

A

Reduced granulopoiesis

Accelerated granulocyte removal: autoimmune, SLE, Felty’s, infection

Drug-induced neutropenia

Part of a general pancytopenia

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14
Q

B symptoms

A

weight loss, pyrexia, night sweats

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15
Q

What is Hodgkin’s characterised by

A

Painless lymphadenopathy + presence of large binucleate cells within them (Reed-Sternberg cells)
lymph nodes often within upper half of body (then spreads via lymphatic sx to below diaphragm)

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16
Q

Incidence of Hodgkins

A

15-20 years, then 40-60 years

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17
Q

Incidence NHL

A

Middle/later life

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18
Q

Difference acute and chronic leukaemias

A

Acute: numerous immature blast cells - rapid disease progression

Chronic: large numbers of precursor cells that are more differentiated than blast cells - slower disease progression

Then differentiated into myeloid (granulocytes) or lymphocytic leukaemia

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19
Q

Main features of leukaemias

A

Bone marrow failure: anaemia, haemorrhage, infection

Gout (increased cell turnover)

Metastasis

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20
Q

Incidence of acute leukaemia

A

ALL: most common in children (also occurs in middle-age - worse prognosis)

AML: more common in adults

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21
Q

What is the Philadelphia chromosome associated with?

A

CML

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22
Q

Stages of CML

A

Chronic phase: anaemia + splenomegaly - responsive to chemo

Accelerated phase: more difficult to control - emergence + dominance of a more malignant clone of myeloid cells

Blast crisis phase: transformation to acute leukaemia, usually AML - often rapidly fatal (timing unpredictable)

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23
Q

Difference in presentation of AML and CML

A

In CML the neutrapenia, lymphopenia and thrombocytopenia are uncommon - so not haemorrhaging or infection

Ditto in CLL not common until later stages

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24
Q

Most common leukaemia in adults

A

CLL

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25
Q

Clinical features of multiple myeloma

A

Bone pain, esp backache and pathological fractures

Anaemia

Repeated infections: deficient antibody levels and bone marrow failure

Abnormal bleeding tendency

Renal impairment (Bence-Jones or hypercalcaemia)

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26
Q

Causes of splenomegaly

A

Infection

Congestion
Pre-hepatic: thrombosis of hepatic, splenic or portal vein
Hepatic: longstanding portal hypertension
Post-hepatic: raised venous pressure, eg RHF

Neoplasm (usually secondary)

Haematological disorders

Immune disorders: Felty’s, amyloidosis, sarcoidosis

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27
Q

HYPERSPLENISM

A

Enlarged spleen causing decrease in pancytopenia

often accompanied by compensatory hyperplasia of bone marrow - situation rectified by splenectomy

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28
Q

What can cause splenic infarcts?

A

Emboli from heart - can be septic if associated with IE

Local thrombosis - eg sickle cell, malignant infiltrates

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29
Q

Causes macrocytic anaemias

A 
Megaloblastic anaemias (B12/ folate deficiency)
Haemolytic anaemias (new immature RBCs are large)
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30
Q

Causes normocytic anaemias

A

anaemia of chronic disease

hypoplastic anaemias

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31
Q

Causes microcytic anaemia

A

Fe deficiency

thalassaemia

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32
Q

Crises of sickle cell disease

A

Sequestration crises: pooling of RBCs in liver and spleen - death from rapid fall in Hb

Infarctive crises: brain, retinopathy, ARDS, cor pulmonale, haematuria, bone necrosis

Aplastic crises: infection with parvovirus B19 which targets erythrocyes and lyses them - rapid fall in Hb

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33
Q

Common sites of infarction in SCD

A

Femoral head
spleen
skin (ulcers)

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34
Q

Clinical features of chronic haemolysis in SCD

A

Anaemia
Jaundice + gallstones
Fe overload

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35
Q

Blood group types in UK (most common to least common)

A

O A B AB

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36
Q

Clinical features of ABO incompatibility

A

Massive intravascular haemolysis leading to collapse, hypotension, lumbar pain

DIC may be triggered

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37
Q

Store reserves for Vit B12 and folate

A

Folate: 50-100 days
B12: several years

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38
Q

Where is B12 and folate absorbed?

A

B12: terminal ileum (after binding to IF)
Folate: Jejunum

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39
Q

Causes B12 deficiency

A

Pernicious anaemia: autoimmune atrophic gastritis

Congenital lack of IF

Surgical gastrectomy

Surgical removal or disease of terminal ileum

Bacterial overgrowth (competes for B12)

Veganism: rare

40
Q

Causes of folic acid deficiency

A

Malnutrition
Malabsorption
Increased requirements: pregnancy, lactation, haemolysis, malignancy, extensive psoriasis
Drugs (anticonvulsants, methotrexate)

41
Q

Clinical features of Fe-deficiency anaemia

A 
Anaemia
Angular cheilitis
Atrophic glossitis
Oesophageal webs
hypochlorhydia
Koilonycia
Brittle nails
Pica
42
Q

Causes DIC

A 
Infection: sepsis, viral, malaria
Malignancy
Obstetric complications: amniotic embolus, placental abruption, retained fetus
Anaphylaxis
Burns, major surgery, major trauma
Liver disease
43
Q

How is Fe transported/ stored?

A

Transported on transferrin, stored bound to ferritin

44
Q

Neurological manifestations of B12 deficiency

A

Peripheral neuropathy
Subacute combined degeneration of the cord
Dementia

45
Q

Causes of congenital haemolysis

Presentation

A

Hereditary spherocytosis
Thalassaemia
SCD
G6PD

Pallor, jaundice, splenomegaly

46
Q

What is hereditary spherocytosis?

A

AD transmission

Defect in cell membrane causing increased cell fragility

47
Q

What is G6PD?

A

glucose-6-phosphate dehydrogenase deficiency

X-linked

normally generates NADPH, needed for maintaining healthy Hb so can withstand stress

need to avoid drugs that precipitate haemolysis

48
Q

Inheritance of haemophilias

A

X-linked recessive
Girls carry
Boys suffer

49
Q

Signs and symptoms of polycythaemia

A

facial plethora, bleeding, splenomegsaly, bruising

headaches, dizziness, pruritus after bathing, LOC, gout

50
Q

What cancerous transformations can result from polycythaemia?

A

Myelofibrosis, AML

51
Q

What is myelofibrosis vs myelodysplasia?

A

MYELOFIBROSIS: clonal proliferation of haematopoietic stem cells, leading to bone marrow fibrosis

MYELODYSPLASIA: clonal disorder of bone marrow, producing morphologically/functionally abnormal cells - worse prognosis with 1/3 turning to AML

52
Q

Signs of myelofibrosis

Management

A

Pallor, bruising, massive splenomegaly, oral thrush, systemic symptoms

Supportive: blood transfusion
Can also use hydroxycarbamide, thalidomide, splenectomy

53
Q

Signs of myelodysplasia

Management

A

features of anaemia, bacterial infection, bleeding

supportive: transfusions, abx
in young patients can consider allogenic bone marrow transplant which can be curative

54
Q

Type I hypersensitivity

A

Immediate, eg anaphylaxis

55
Q

Type II hypersensitivity

A

cytotoxic

56
Q

Type III hypersensitivity

A

immune complex disorders

57
Q

Type IV hypersensitivity

A

Delayed hypersensitivity

58
Q

What is serum?

A

Plasma without clotting factors

59
Q

Sites of haematopoeisis

A

Bone marrow

Extramedullary: liver, spleen

60
Q

Stem cell lineages

A 
MYELOID STEM CELLS
Proerythroblasts > erythrocytes
Megarkaryocytes > platelets
Myeloblasts > neutrophils, eosinophils, basophils
Monoblasts > monocytes

LYMHOID STEM CELLS
NK cells
Lymphocytes T, B

61
Q

How to manage mild allergy to blood transfusion?

A

Slow transfusion, antihistamine
(eg rash, itch, urticaria)

occurs immediately

62
Q

How to manage ABO incompatible transfusion

A

Stop transfusion, inform lab, IV fluids
Manage DIC

occurs within minutes

63
Q

How to manage febrile non-haemolytic transfusion

A

Slow transfusion, paracetamol

occurs within hours

64
Q

How to manage bacterial contamination of blood products

A

Stop transfusion, sepsis 6
inform lab

occurs within 24h

65
Q

How to treat TRALI (transfusion-related acute lung injury)

A

stop transfusion, oxygen, treat ARDS

(acute SOB, Cough, normal CVP/ JVP)

occurs within 6-24h

66
Q

How to treat TACO

A

slow transfusion, oxygen, IV furosemide

(acute SOB, raised CVP/ JVP)

occurs within 6-24h

67
Q

What is HSCT

A

Haematopoietic stem cell transplant

Allogenic: usually HLA-matched, requires high-dose chemo (destroys malignant cells + induces temporary immunosuppression)

Autologous: harvested prior to therapy then re-infused post-chemo

68
Q

WHO anaemia

A

below 13 in men

below 12 in women

69
Q

Diagnosing Fe-deficiency anaemia

A

Microcytic anaemia
Ferritin (<12 ng) - although as an acute phase protein could be falsely elevated
Gold standard: Prussian blue staining of bone marrow biopsy

(Consider testing for coeliac)

70
Q

Managing iron-deficiency anaemia

A

Oral supplements: may take 2 months for Hb to normalise

IV iron if not responsive

71
Q

What is sideroblastic anaemia?

A

Excess Fe deposition in RBC precursors, forming ringed sideroblasts in bone marrow
Congenital or acquired (chronic infections, SLE, drugs, lead poisoning)

Clinically indistinguishable from other anaemias but iron studies will show high Fe levels (then bone marrow studies)

Generally supportive treatment/ treat underlying cause
Pyridoxine (B6) may be helpful in treating congenital forms

72
Q

Antifolate drugs

A

methotrexate
phenytoin
trimethoprim

73
Q

What further investigation should be offered when pernicious anaemia is identified?

A

OGD: susceptibility to gastric cancers

74
Q

Replace B12 or folate first?

A

B12: prevent exacerbation of neurological symptoms

75
Q

Diagnosis of aplastic anaemia

A

Hypocellular bone marrow and 2 of:
Hb < 10
Neut < 1.5
Plts < 50

76
Q

Mx hereditary spherocytosis

A

Folate replacement

Splenectomy (usually after age 6)

77
Q

Blood film: G6PD

A

Heinz bodies and Blister (bite) cells

78
Q

Blood film: pyruvate kinase deficiency

A

Prickle cells

79
Q

What is the Coombs test - what are the types?

A

Detects presence of antibodies

DAT (Direct Coombs): haemolytic anaemias, transfusion reactions
detects antibodies bonded to the RBC

IAT (Indirect Coombs): cross-matching, prenatal rhesus testing
Detects antibodies in plasma

80
Q

Classifying bleeding disorders

A

VESSEL WALL DISORDERS

PLATELET DISORDERS: thrombocytopenia or platelet dysfunction

COAGULATION DISORDERS: congenital or acquired

81
Q

Distinguishing clotting and coagulation disorders

A

Clotting (ie platelets): bruising, purpura, mucosal membranes. Occurs spontaneously

Coagulation: generally haemarthroses or haematomas - occurs within hours/ days

82
Q

Understanding the coagulation screen: bleeding times

A

Gives info about platelets: is there platelet dysfunction or vWB disease

83
Q

Understanding the coagulation screen: APTT

A

gives info about the intrinsic pathway

helpful to monitor heparin therapy, haemophilia, DIC

84
Q

Understanding the coagulation screen: PT, INR

A

gives info about the extrinsic pathway

helpful for monotoring warfarin therapy, liver disease, DIC

85
Q

Understanding the coagulation screen: fibrinogen levels

A

final common pathway

helpful in liver disease, DIC

86
Q

Congenital and acquired examples of vessel wall disorders

A

HHT, Ehlers-Danlos

Scurvy, vasclitis (Henoch-Schonlein), infection (meningococcal rash)

87
Q

Difference in LMWH and UFH with heparin-induced thrombocytopenia

A

Much more common in UFH, typically occurs within 5-10 days of commencement

88
Q

HAEMOPHILIA A

A

X-linked

Factor VIII deficiency (intrinsic pathway)

89
Q

Mx haemophilia A

A

Severe bleeds: give factor VIII IV

Mild bleeds: IV or intranasal desmopressin (DDAVP)
stimulates release of vWF > increases Factor VIII levels

90
Q

Things to avoid in haemophilia A

A

contact sports!
NSAIDs
IM injections

91
Q

HAEMOPHILIA B (CHRISTMAS DISEASE)

A

Factor IX

DDAVP has no effect

92
Q

Findings on coagulation test in vWD

A

Both prolonged PT and APTT

93
Q

Smudge cells

A

CLL - fragile lymphocytes

94
Q

The most common indications for irradiated blood products

A
  • Those at risk of transfusion associated with graft versus host disease such as neonates
  • Those receiving purine analogues based chemotherapy
  • Hodgkin’s lymphoma
  • Immunodeficiency states
  • Post bone marrow transplants
95
Q

Blood tests to support assumption that haemolysis was causing jaundice in patient?

A

Low haptoglobin

High LDH

F1/ Part 1 (13 decks)

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