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Finals Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

What are causes of microcytic anaemia?

A 
Thalassaemia
Iron deficiency
Sideroblastic anaemia 
Late stages of anaemia of chronic disease
Lead poisoning
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2
Q

What are the causes of normocytic anaemia?

A 
Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
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3
Q

What are the causes of macrocytic anaemia?

A

B12 deficiency
Folate deficiency
Reticulocytosis
Alcohol-induced anaemia

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4
Q

What are the causes of iron deficiency anaemia?

A
  1. Blood loss
  2. Reduced iron intake
  3. Increased demand e.g. pregnancy, malignancy
  4. Reduced absorption e.g. PPIs, IBD, coeliac
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5
Q

What haematinics would you expect in IDA?

A

Low ferritin
Low transferrin saturation
Increased transferrin concentration
Increased total iron binding capacity

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6
Q

What is pernicious anaemia?

A

Cause of B12 deficiency anaemia
Autoimmune condition with ab being produced against gastric parietal cells or intrinsic factor

Intrinsic factor is produced by gastric parietal cells and allows B12 to be absorbed in the distal ileum.

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7
Q

What is the gold standard test to look for pernicious anaemia?

A

Intrinsic factor antibody testing

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8
Q

How can B12 be replaced in anaemia?

A

In dietary deficiency: oral cyanocobalamin

Pernicious/malabsorptive: IM hydroxycobalamin 3x weekly for 2 weeks and then 3 monthly

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9
Q

If B12 and folate deficiency exist together, which should you replace first?

A

B12

Folate can increase development of subacute degeneration of the cord.

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10
Q

What are examples of inherited haemolytic anaemia?

A 
Spherocytosis (autosomal dominant)
Elliptocytosis (autosomal dominant)
Thalassaemia (autosomal recessive)
Sickle cell anaemia (autosomal recessive)
G6PD deficiency (X-linked recessive)
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11
Q

What are examples of acquired haemolytic anaemia?

A

Warm/cold autoimmune HA
Paroxysmal nocturnal haemoglobinuria
Microangiopathic HA (small vessels cause destruction of RBCs)
Prosthetic valve haemolysis

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12
Q

What triad of features suggests haemolytic anaemia?

A

Anaemia
Splenomegaly
Jaundice

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13
Q

Which tests suggests an autoimmune cause of haemolytic anaemia?

A

Direct Coombs test = positive

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14
Q

What can trigger an aplastic crisis in hereditary spherocytosis?

A

Parvovirus infection

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15
Q

What can trigger an aplastic crisis in G6PD deficiency?

A 
Infection
Fava/broad beans
Ciprofloxacin 
Sulphonylureas
Anti-malarials
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16
Q

Which blood film finding is classic of G6PD deficiency?

A

Heinz bodies

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17
Q

How is sickle cell anaemia diagnosed?

A

Heel-prick test in newborns
Pregnant women tested
Haemoglobin/genetic testing

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18
Q

What would you see on a blood film in sickle cell?

A

Sickle-shaped cells,
Howell-Jolly bodies,
presence of nucleated red blood cells,
cell fragments can be seen on the blood smear

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19
Q

How is sickle cell generally managed?

A 
Avoid dehydration
Ensure up to date with vaccinations
Prophylactic penicillin V 
Hydroxycarbamide to stimulate the production of HbF
Blood transfusion
Bone marrow transplant
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20
Q

What can trigger sickle cell crises?

A 
Infection
Dehydration
Cold
Stress
Significant life events
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21
Q

What are the signs and symptoms of thalassaemia?

A 
Anaemia
Splenomegaly
Jaundice and gallstones
Poor growth and development
Pronounced forehead and cheekbones
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22
Q

How is thalassaemia diagnosed?

A
  1. FBC: microcytic anaemia
  2. Hb electrophoresis
  3. Genetic testing
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23
Q

What are the three types of Beta thalassaemia and their genotypes?

A

Thalassaemia minor: heterozygous deletion, one normal copy

Thalassaemia intermedia: 2 defective genes or 1 mutation and 1 deletion

Thalassaemia major: homozygous gene deletion

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24
Q

How is thalassaemia major managed?

A

Regular blood transfusions, iron chelation and splenectomy

Bone marrow transplant can be curative

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25
Q

What is the main risk of recurrent transfusions in thalassaemia?

A

Iron overload

Causes fatigue, liver cirrhosis, reduced fertility, osteoporosis, diabetes, HF, arthritis

Rx: iron chelation

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26
Q

How is leukaemia diagnosed?

A

FBC: anaemia, thrombocytopenia, neutropenia, ?^ lymphocytes
Blood film / peripheral blood smear
LDH often raised
Bone marrow biopsy = main definitive investigation
CXR + more detailed imaging for staging

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27
Q

In which populations are ALL most common?

A

children aged 2-5

Adults > 45

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28
Q

Which leukaemia is most associated with Downs and Klinefelter’s syndrome?

A

ALL

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29
Q

Which leukaemia is most common in adults?

A

CLL

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30
Q

Which leukaemia is most associated with causing warm AIHA + transforming into lymphoma?

A

CLL

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31
Q

What is seen on blood film in CLL?

A

Smear/smudge cells

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32
Q

Which leukaemia is currently INCURABLE?

A

CLL
Slow growing so often don’t need treating straight away
Can induce emission but will eventually relapse

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33
Q

In which population is AML most common?

A

> 70s

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34
Q

What is seen on blood film in AML?

A

Auer rods, myeloid blast cells

35
Q

Which leukaemia is most likely to present with splenomegaly and sweating rather than anaemia and infection?

A

CML

36
Q

What biologic agent is most used in CML?

A

Imatinib

37
Q

What are the features of tumour lysis syndrome?

A

Hyperuricaemia
Hyperkalaemia
Hyperphosphataemia
Secondary hypocalcaemia

38
Q

What management is used in tumour lysis syndrome?

A 
Cardiac monitoring
Aggressive fluid resuscitation
Calcium glutinate, insulin, dextrose, salbutamol etc
Rasburicase for hyperuricaemia
Phosphate binders
39
Q

Which cells do leukaemia affect?

A

Cancer of the white blood cells, affecting both myeloid and lymphoid cell lineages.

40
Q

What cells are affected by lymphoma?

A

Lymphocytes of the lymphatic system

41
Q

What are risk factors for Hodgkin’s lymphoma?

A

HIV, EBV, Family history, Autoimmune conditions e.g. sarcoid, RA

42
Q

What symptoms are associated with lymphoma?

A

Lymphadenopathy: usually non-tender, rubbery, tender when drinking alcohol
Fever, weight loss, night sweats
Fatigue, cough, SOB
Recurrent infection, itching, abdominal pain

43
Q

How is lymphoma diagnosed?

A

Bloods: FBC, LDH
FBC may show anaemia / neutropenia / thrombocytopenia but not always
Lymph node USS and biopsy
CT/MRI/PET staging scans

44
Q

How can you differentiate Hodgkin’s and non-hodgkin’s lymphomas?

A

Hodgkins: presence of Reed-Sternberg cells on lymph node biopsy
Abnormally large, multinucleated B cells with nucleoli

45
Q

Which conditions are associated with Burkitt’s lymphoma?

A

EBV
HIV
Malaria

Starry sky appearance on biopsy

46
Q

Which lymphoma is associated with H. Pylori infection ?

A

MALT lymphoma

47
Q

What staging system is used in lymphoma and what is it?

A

Ann-Arbour staging

1- confined to one region
2- more than one region affected but on the same side of the diaphragm
3- regions affected on either side of the diaphragm
4- Widespread involvement, including organs

48
Q

What is myeloma?

A

Cancer of the plasma cells (antibody-producing B cells)

49
Q

What are the features of myeloma?

A

CRAB

Hypercalcaemia
Renal disease
Anaemia
Bone pain

Hyperviscosity is also a feature of myeloma- easy bruising + bleeding, eye vessel disease, purple palmar erythema, heart failure

50
Q

What is myeloma bone disease?

A

Reduced osteoblast activity and increased osteoclast activity, causing lytic lesions to form in bones
Most commonly affects skull, spine, long bones and ribs

This leads to hypercalcaemia as a result of increased osteoclast activity

51
Q

How is myeloma diagnosed?

A

FBC: anaemia, neutropenia, thrombocytopenia
Ca 2+, ESR + plasma viscosity all raised
Urine electrophoresis: presence of bence jones proteins
Serum protein electrophoresis, light chain assay and immunoglobulins

X-ray- punched out, lytic lesions, raindrop skull

Bone marrow biopsy to confirm diagnosis

Whole body MRI

52
Q

How is myeloma managed?

A

Combination chemotherapy
Stem cell transplants in clinical trials currently
VTE prophylaxis important due to increased viscosity - aspirin/LMWH

Bisphosphonates for osteoclast suppression
Radiotherapy can help with bone pain
Orthopaedic surgery to stabilise bones/fractures

Management of renal impairment.

53
Q

What is a myelodysplastic syndrome?

A

Condition whereby myeloid cell lineages don’t mature properly, leading to the production and release of immature blood cells. This causes low levels of the cell affected: neutropenia, anaemia, thrombocytopenia.

These conditions are most common in the over 60s or those who have previously had chemo/radiotherapy.

Blood films will show blast cells, then diagnosis is confirmed with bone marrow aspiration and biopsy

54
Q

What is myelofibrosis?

A

Often the result of a myeloproliferative disorder. Where cell line proliferation causes bone marrow fibrosis in response to cytokine production e.g. fibroblast growth factor. This leads to anaemia and leukopenia, meaning haematopoiesis has to occur in the liver and spleen to compensate.

This results in splenomegaly, hepatomegaly and portal hypertension.

55
Q

What are signs of polycythaemia vera?

A

Conjunctival plethora (redness)
Ruddy complexion
Splenomegaly

Headache
Pruritus
Abnormal bleeding
Fatigue, night sweats and bone pain
Redness of palms, fingers, soles and toes
56
Q

How would you investigate myelofibrosis?

A

FBC: may show polycythaemia, thrombocythaemia or primary myelofibrosis (anaemia + either raised or low WCC/platelets)
Blood film: poikiloctes (teardrop-shaped red blood cells)

Bone marrow biopsy = diagnostic test
Dry bone marrow aspiration

Genetic testing: JAK2, MPL and CALR mutations associated

57
Q

How is polycythaemia vera managed?

A

Venesection
Aspirin
Chemotherapy

58
Q

How is primary myelofibrosis managed?

A

Allogenic stem cell transplant
Chemotherapy
Supportive treatment of portal HTN, anaemia and splenomegaly

59
Q

What are the causes of thrombocytopenia?

A

Decreased production:
Sepsis, B12/folate deficiency, liver failure (low thrombopoietin production), leukaemia, myelodysplastic syndrome

Increased destruction:
ITP, TTP, HITT, HUS
Medication: sodium valproate, methotrexate, PPO, isotretinoin

60
Q

What is ITP?

A

Immune thrombocytopenia

Isolated thrombocytopenia in the absence of any identifiable cause.
Most common in children following a preceding viral infection.

61
Q

What is the treatment for ITP?

A

Prednisolone, IVIG
Rituximab
Splenectomy in refractory

Important to monitor platelet count and educate r.e. symptoms of spontaneous bleed
BP control, suppress menstruation

62
Q

What is TTP?

A

Thrombotic thrombocytopenic purpura
Tiny clots form in the small vessels, using up the platelets and causing bleeding under the skin.
Dysfunctional ADAMTS13 protein causes overactivity of vWF
Can be inherited or autoimmune

63
Q

What are features of TTP?

A

Haemolytic anaemia + thrombocytopenia
Usually pentad of : fever, renal failure, haemolytic anaemia, thrombocytopenia, and neurological changes
Blood film shows: fragmented red blood cells (schistocytes) and thrombocytopenia.

64
Q

What is HITT?

A

Antibodies produced against platelets in response to heparin treatment.
AB target platelet factor 4, bind to platelets and activate clotting mechanisms

This causes a hypercoagulable state + thrombosis, followed by platelet breakdown.

Diagnosed by testing for HITT antibodies

65
Q

What is the most common inherited bleeding disorder?

A

von Willebrand disease

66
Q

What is the inheritance pattern of von Willebrand disease?

A

Autosomal dominant

67
Q

What are the types of vWD?

A

Can be type 1-3
type 1: partial deficiency of vWF
type 2: mutation causes defective vWF to be produced
type 2b: mutation causes overactivity of vWF
type 3: almost total deficiency of vWF (most serious)

68
Q

What tests are used to diagnosed vWD?

A 
FBC= normal
PT= normal
APTT = prolonged
vWF antigen = low
vWF function assay= reduced in t2
69
Q

How is vWD managed?

A

No day-to-day treatment.

In haemorrhage: desmopressin, vWF infusion +/- Factor VIII

For menorrhagia: tranexamic/mefanamic acid, norethisterone, COCP/mirena, hysterectomy

70
Q

What are the two types of haemophilia and what are their inheritance pattern?

A

Haemophilia A = deficiency in factor VIII
Haemophilia B = deficiency in factor IX

Both inherited via x-linked recessive pattern

71
Q

How is haemophilia diagnosed?

A

FBC: normal or may be anaemic if history of bleeding
PT: normal
APTT: prolonged

Mixing studies: APTT corrected on mixing with normal blood

72
Q

How is haemophilia managed?

A

IV infusions of deficient factor: can be in response to bleed or prophylactic

In a bleed, desmopressin and TXA often also given

73
Q

What coagulation results would you expect in vitamin K deficiency?

A

Prolonged PT and APTT

74
Q

What drug is used for iron chelation?

A

desferrioxamine

75
Q

What do howell-jolly bodies indicate?

A

Hyposplenism

Can occur in coeliac disease

76
Q

What are potential complications of blood transfusion?

A

Non-haemolytic febrile reaction - slow/stop transfusion + paracetamol
Minor allergic reaction- temporarily stop + antihistamine
Anaphylaxis- stop, IM adrenaline
Acute haemolytic reaction- stop, send sample for Coomb’s test, fluids
Transfusion associated circulatory overload- slow/stop, IV furosemide
Transfusion associated lung injury- stop, oxygen, supportive

77
Q

What is factor V leiden?

A 
Inherited thrombophilia (hypercoagulable state)
Gain of function mutation
78
Q

What is Fanconi anaemia + what are its features?

A

Autosomal recessive.

Features
haematological:
aplastic anaemia
increased risk of acute myeloid leukaemia
neurological

skeletal abnormalities:
short stature
thumb/radius abnormalities
cafe au lait spots

79
Q

Which triad describes the pathophysiology of VTE?

A

Virchow’s triad:

hypercoagulability, stasis of blood flow, endothelial injury

80
Q

What is the management of suspected VTE?

A

LMWH

81
Q

What is long-term management for VTE?

A

DOAC, LMWH, warfarin
LMWH first line in pregnancy and malignancy, otherwise apixaban often first line

3m treatment if obvious or reversible cause
6m treatment if active cancer, unprovoked, recurrent or irreversible cause

82
Q

What is Budd-Chiari syndrome?

A

Thrombus in the hepatic vein, blocking the outflow
Associated with hypercoagulable states + can cause acute hepatitis

Triad: abdo pain, hepatomegaly and ascites

83
Q

What do hypersegmented neutrophils on blood film indicate?

A

Megaloblastic anaemia

Finals Revision (23 decks)

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