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Haematology Flashcards

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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
Clinical features of multiple myeloma
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)
26
Causes of splenomegaly
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
27
HYPERSPLENISM
Enlarged spleen causing decrease in pancytopenia | often accompanied by compensatory hyperplasia of bone marrow - situation rectified by splenectomy
28
What can cause splenic infarcts?
Emboli from heart - can be septic if associated with IE Local thrombosis - eg sickle cell, malignant infiltrates
29
Causes macrocytic anaemias
``` Megaloblastic anaemias (B12/ folate deficiency) Haemolytic anaemias (new immature RBCs are large) ```
30
Causes normocytic anaemias
anaemia of chronic disease | hypoplastic anaemias
31
Causes microcytic anaemia
Fe deficiency | thalassaemia
32
Crises of sickle cell disease
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
33
Common sites of infarction in SCD
Femoral head spleen skin (ulcers)
34
Clinical features of chronic haemolysis in SCD
Anaemia Jaundice + gallstones Fe overload
35
Blood group types in UK (most common to least common)
O A B AB
36
Clinical features of ABO incompatibility
Massive intravascular haemolysis leading to collapse, hypotension, lumbar pain DIC may be triggered
37
Store reserves for Vit B12 and folate
Folate: 50-100 days B12: several years
38
Where is B12 and folate absorbed?
B12: terminal ileum (after binding to IF) Folate: Jejunum
39
Causes B12 deficiency
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
Causes of folic acid deficiency
Malnutrition Malabsorption Increased requirements: pregnancy, lactation, haemolysis, malignancy, extensive psoriasis Drugs (anticonvulsants, methotrexate)
41
Clinical features of Fe-deficiency anaemia
``` Anaemia Angular cheilitis Atrophic glossitis Oesophageal webs hypochlorhydia Koilonycia Brittle nails Pica ```
42
Causes DIC
``` Infection: sepsis, viral, malaria Malignancy Obstetric complications: amniotic embolus, placental abruption, retained fetus Anaphylaxis Burns, major surgery, major trauma Liver disease ```
43
How is Fe transported/ stored?
Transported on transferrin, stored bound to ferritin
44
Neurological manifestations of B12 deficiency
Peripheral neuropathy Subacute combined degeneration of the cord Dementia
45
Causes of congenital haemolysis Presentation
Hereditary spherocytosis Thalassaemia SCD G6PD Pallor, jaundice, splenomegaly
46
What is hereditary spherocytosis?
AD transmission | Defect in cell membrane causing increased cell fragility
47
What is G6PD?
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
Inheritance of haemophilias
X-linked recessive Girls carry Boys suffer
49
Signs and symptoms of polycythaemia
facial plethora, bleeding, splenomegsaly, bruising | headaches, dizziness, pruritus after bathing, LOC, gout
50
What cancerous transformations can result from polycythaemia?
Myelofibrosis, AML
51
What is myelofibrosis vs myelodysplasia?
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
Signs of myelofibrosis | Management
Pallor, bruising, massive splenomegaly, oral thrush, systemic symptoms Supportive: blood transfusion Can also use hydroxycarbamide, thalidomide, splenectomy
53
Signs of myelodysplasia | Management
features of anaemia, bacterial infection, bleeding supportive: transfusions, abx in young patients can consider allogenic bone marrow transplant which can be curative
54
Type I hypersensitivity
Immediate, eg anaphylaxis
55
Type II hypersensitivity
cytotoxic
56
Type III hypersensitivity
immune complex disorders
57
Type IV hypersensitivity
Delayed hypersensitivity
58
What is serum?
Plasma without clotting factors
59
Sites of haematopoeisis
Bone marrow | Extramedullary: liver, spleen
60
Stem cell lineages
``` MYELOID STEM CELLS Proerythroblasts > erythrocytes Megarkaryocytes > platelets Myeloblasts > neutrophils, eosinophils, basophils Monoblasts > monocytes ``` LYMHOID STEM CELLS NK cells Lymphocytes T, B
61
How to manage mild allergy to blood transfusion?
Slow transfusion, antihistamine (eg rash, itch, urticaria) occurs immediately
62
How to manage ABO incompatible transfusion
Stop transfusion, inform lab, IV fluids Manage DIC occurs within minutes
63
How to manage febrile non-haemolytic transfusion
Slow transfusion, paracetamol occurs within hours
64
How to manage bacterial contamination of blood products
Stop transfusion, sepsis 6 inform lab occurs within 24h
65
How to treat TRALI (transfusion-related acute lung injury)
stop transfusion, oxygen, treat ARDS (acute SOB, Cough, normal CVP/ JVP) occurs within 6-24h
66
How to treat TACO
slow transfusion, oxygen, IV furosemide (acute SOB, raised CVP/ JVP) occurs within 6-24h
67
What is HSCT
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
WHO anaemia
below 13 in men | below 12 in women
69
Diagnosing Fe-deficiency anaemia
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
Managing iron-deficiency anaemia
Oral supplements: may take 2 months for Hb to normalise IV iron if not responsive
71
What is sideroblastic anaemia?
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
Antifolate drugs
methotrexate phenytoin trimethoprim
73
What further investigation should be offered when pernicious anaemia is identified?
OGD: susceptibility to gastric cancers
74
Replace B12 or folate first?
B12: prevent exacerbation of neurological symptoms
75
Diagnosis of aplastic anaemia
Hypocellular bone marrow and 2 of: Hb < 10 Neut < 1.5 Plts < 50
76
Mx hereditary spherocytosis
Folate replacement | Splenectomy (usually after age 6)
77
Blood film: G6PD
Heinz bodies and Blister (bite) cells
78
Blood film: pyruvate kinase deficiency
Prickle cells
79
What is the Coombs test - what are the types?
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
Classifying bleeding disorders
VESSEL WALL DISORDERS PLATELET DISORDERS: thrombocytopenia or platelet dysfunction COAGULATION DISORDERS: congenital or acquired
81
Distinguishing clotting and coagulation disorders
Clotting (ie platelets): bruising, purpura, mucosal membranes. Occurs spontaneously Coagulation: generally haemarthroses or haematomas - occurs within hours/ days
82
Understanding the coagulation screen: bleeding times
Gives info about platelets: is there platelet dysfunction or vWB disease
83
Understanding the coagulation screen: APTT
gives info about the intrinsic pathway helpful to monitor heparin therapy, haemophilia, DIC
84
Understanding the coagulation screen: PT, INR
gives info about the extrinsic pathway helpful for monotoring warfarin therapy, liver disease, DIC
85
Understanding the coagulation screen: fibrinogen levels
final common pathway helpful in liver disease, DIC
86
Congenital and acquired examples of vessel wall disorders
HHT, Ehlers-Danlos Scurvy, vasclitis (Henoch-Schonlein), infection (meningococcal rash)
87
Difference in LMWH and UFH with heparin-induced thrombocytopenia
Much more common in UFH, typically occurs within 5-10 days of commencement
88
HAEMOPHILIA A
X-linked | Factor VIII deficiency (intrinsic pathway)
89
Mx haemophilia A
Severe bleeds: give factor VIII IV Mild bleeds: IV or intranasal desmopressin (DDAVP) stimulates release of vWF > increases Factor VIII levels
90
Things to avoid in haemophilia A
contact sports! NSAIDs IM injections
91
HAEMOPHILIA B (CHRISTMAS DISEASE)
Factor IX | DDAVP has no effect
92
Findings on coagulation test in vWD
Both prolonged PT and APTT
93
Smudge cells
CLL - fragile lymphocytes
94
The most common indications for irradiated blood products
* 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
Blood tests to support assumption that haemolysis was causing jaundice in patient?
Low haptoglobin | High LDH

F1/ Part 1 (13 decks)

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