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A final year of medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Causes of bone pain/tenderness?

A
  1. Trauma/fracture (steroids increase risk)
  2. Myeloma and other primaries e.g. sarcoma
  3. Secondaries
  4. Osteonecrosis
  5. Osteomyelitis/periostitis
  6. Osteosclerosis e.g. from Hep C
  7. Paget’s disease of bone
  8. Sickle cell anaemia
  9. Renal osteodystrophy
  10. CREST/Sjogrens
  11. Hyperparathyroidism
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2
Q

What is MGUS?

A

Monoclona gammopathy of uncertain significance. Paraprotein in serum, but no other disease or Bence-Jones, fewer than 10% plasma cells in marrow. Some may get lymphoma or myeloma, refer to haem for biopsy

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3
Q

What is a Bence-Jones protein?

A

Immunoglobulin light chains in the urine

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4
Q

What is a PCD?

A

A plasma cell dyscrasia (abnormal proliferation of plasma cells or lymphoplasmacytic cells leading to secretion of immunoglobulin or immunoglobulin fragments causing organ dysfunction)

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5
Q

What is a paraprotein?

A

Or M protein; abnormal immunoglobulin fragment produced in excess to give M band on electrophoresis

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6
Q

Classifying myeloma?

A

Based on Ig product: 2/3 IgG, 1/3 IgA, or presence/absence of Bence Jones proteins in urine

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7
Q

Clinical features of myeloma?

A

CRABI

  1. Hypercalcaemia [lesions caused by osteoclast activity signalled by myeloma cells]
  2. Renal impairment [light chain deposition in LoH]
  3. Anaemia/neutropenia/thrombocytopenia (marrow infiltration by plasma cells)
  4. Osteolytic bone lesions [backache, pathological fractures, vertebral collapse]
  5. Recurrent bacterial infections [immunoparesis, chemotherapy, neutropenia]
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8
Q

What is immunoparesis in myeloma?

A

Low levels of other Ig due to excessive production of paraprotein

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9
Q

Blood film in myeloma?

A

Get rouleaux!

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10
Q

Investigations in myeloma?

A

Screening with serum/urine electrophoresis. Bloods show normocytic anaemia, raised ESR, raised urea and creatinine, alk. phos. usually normal. Bone marrow biopsy (shows many plasma cells), xrays show lytic lesions

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11
Q

How do lytic lesions manifest in myeloma?

A

Pepper pot skull, vertebral collapse, fractures

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12
Q

Treatment of myeloma?

A

Supportive & chemotherapy. Supportive is analgesia for bone pain, bisphosphonates, local radiotherapy, orthopaedic procedures, correct anaemia with transfusion & epo, rehydrate/dialysis to address renal failure, treat infections.
Chemotherapy and autologous stem cell transplantation.

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13
Q

Diagnosis of myeloma?

A
  1. Monoclonal protein band in serum or urine electrophoresis
  2. Raised plasma cells on bone marrow biopsy
  3. Evidence of end-organ damage from myeloma (hypercalcaemia, renal failure, anaemia)
  4. Bone lesions (skeletal survey)
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14
Q

Complications of myeloma?

A
  1. Hypercalcaemia
  2. Spinal cord compression
  3. Hyperviscosity (presents with visual abnormalities, reduced cognition, bleeding; treated with plasmapheresis
  4. AKI
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15
Q

What is paraproteinaemia?

A

Presence in the circulation of immunoglobulins produced by a single clone of plasma cells

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16
Q

Six major categories of paraproteinaemia?

A
  1. Multiple myeloma
  2. Waldenstroms macroglobulinaemia
  3. Primary amyloidosis
  4. MGUS
  5. Paraproteinaemia in lymphoma or leukaemia
  6. Heavy chain disease
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17
Q

What is amyloidosis?

A

Group of disorders characterised by extracellular deposits of a protein in abnormal fibrillar form, resistant to degradation

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18
Q

Features of primary amyloidosis?

A

Proliferation of plasma cell clone, get amyloidogenic monoclonal immunoglobulins, fibrillar light chain deposition, organ failure, death. Affects kidneys (nephrotic), heart (restrictive cardiomyopathy), nerves (peripheral and autonomic neuropathy), gut (macroglossia, haemorrhage, obstruction), vascular (purpura). Associations with Waldenstroms, lymphoma myeloma.

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19
Q

Features of secondary amyloidosis?

A

Amyloid derived from the acute phase protein amyloid A, reflecting chronic inflammation e.g. RA, IBD, TB. Affects kidneys, liver, spleen, causes proteinuria, nephrotic syndrome, hepatosplenomegaly. Do NOT get macroglossia or cardiac involvement (usually)

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20
Q

Diagnosing amyloidosis?

A

Biopsy of affected tissue and positive Congo Red staining under polarised light. Rectum or sub-cut fat.

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21
Q

How do steroids work in myeloma?

A

Stop WCCs going to areas of the body where myeloma has caused damage

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22
Q

Why give LMWH when starting warfarin?

A

Get initial pro-coagulant state

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23
Q

Which cells come from lymphoid progenitor?

A

NK cells, T cells, B cells, plasma cells (B-cell lineage)

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24
Q

Which cells come from myeloid progenitor?

A

Granulocytes (neutrophils, eosinophils, basophils, mast cells), RBCs, platelets, monocytes

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25
Q

In anaemic and microcytic patient, what confirms diagnosis of IDA?

A

Ferritin below 15

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26
Q

Features of IDA O/E?

A

Skin & mucous membrane pallor, stomatitis, glossitis and koilonychia. If severe, may get tachycardia and systolic murmur

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27
Q

Treating IDA?

A

Ferrous sulfate 200mg TDS for three months then repeat bloods (increases Hb 1g/dL a week)

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28
Q

What if treating IDA and anaemia persistent?

A

Raise suspicion of underlying malignancy

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29
Q

Bloods in combined iron and folate deficiency?

A

Normocytic with low ferritin; supplment both!

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30
Q

Blood film in myelofibrosis?

A

Leukoerythroblastic picture, tear-drop shaped red blood cells [poikilocytes] (also found in advanced prostate cancer)

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31
Q

Causes of thrombocytosis?

A

Bleeding, infection, malignancy, trauma, post-surgery, iron deficiency, chronic inflammation, essential thrombocytosis

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32
Q

Presentation of myelofibrosis?

A

Hypermetabolic (B symptoms, abdominal discomfort due to hepatosplenomegaly, bone marrow failure (anaemia, infections, bleedidng)

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33
Q

Ix in myelofibrosis?

A

FBC shows BM failure, blood film shows leukoerythroblastic picture with poikilocytes, dry tap on BM aspiration. Definitive diagnosis with BM trephine biopsy.

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34
Q

High RDW?

A

Red cell distribution width; higher means large variation (anisocytosis). Can occur in haemolytic anaemia, IDA, after transfusion, in malabsorption.

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35
Q

Two causes of koilonychia?

A

Iron deficiency and Plummer-Vinson (dysphagia, oesophageal webs, iron-def)

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36
Q

Symptoms of B12 deficiency?

A

Anaemia symptoms and neuro (glove and stocking loss of vibration and proprioception, weakness, subacute combined degeneration of spinal cord)

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37
Q

Blood film in B12 deficiency?

A

Hypersegmented neutrophils, megaloblasts, oval macrocytes

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38
Q

Causes of B12 deficiency?

A
  1. Dietary (cobalamin found in meat, fish, dairy)
  2. Malabsorption (lack of IF due to PA or gastrectomy, or terminal ileum [Crohns, tapeworms])
  3. Congenital metabolic errors
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39
Q

Uses of ferritin test?

A

Low = IDA; moderate/high less helpful as is acute phase reactant. Very high may be haemochromatosis

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40
Q

What does TIBC measure and what do the results mean?

A

Ability of blood to hold onto iron; surrogate for transferrin. Higher in pregnancy becase produce more transferrin, high in IDA, low in anaemia of chronic disease (less transferrin) and hereditary haemochromatosis

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41
Q

Transferrin saturation results?

A

Normal in anaemia of chronic disease (less transferrin), low in IDA (less iron), low in pregnancy (more transferrin), high in HFE!

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42
Q

Genetics in hereditary haemochromatosis?

A

AR, HFE mutation. Mainly Celtic origins.

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43
Q

Serum iron use?

A

Not much: low in IDA, low in AoCD (iron stored IC), normal in pregnancy, raised in HFE

44
Q

Reticulocytosis interpretation?

A

RBC precursor; pushed into peripheral blood (left shift) in haemolysis/bleeding; sign of healthy marrow so may be absent in deficit or BM failure

45
Q

Investigating hereditary haemo?

A

Do ferritin (raised), transferrin sat (high), decreased TIBC, HFE genotype. Do biopsy from affected origins to show iron deposition. MRI liver and heart show damage.

46
Q

Manifestations of hereditary haemochromatosis?

A

Iron into joints (arthropathy), into skin (bronzed skin), B cells of pancreas (DM), liver (cirrhosis/HCC), heart (HF/arrhythmia), pituitary (hypogonadotrophic hypogonadism)

47
Q

Secondary causes of haemochromatosis?

A

Severe chronic haemolysis, multiple frequent transfusions, excess dietary/parenteral iron

48
Q

Treating haemochromatosis?

A

Venesection and iron chelation therapy

49
Q

Sickle-cell anaemia patho?

A

AR mutation in B-chain of Hb to give HbS not HbA; can be SS or Ss (trait). When deoxygenated, HbS polymerises, causes sickling. Sickle cells haemolyse and cause vascular occlusion

50
Q

Significance of sickle cell trait?

A

Causes no disability but can get symptomatic sickling in hypoxia e.g. anaesthesia

51
Q

Investigations in sickle-cell anaemia?

A

Bloods show low Hb, raised reticulocytes, raised bilirubin.
Blood film shows sickle cells and target cells. Sickle solubility test positive in SS and Ss. Diagnose with Hb electrophoresis

52
Q

Three ways sickle-cell anaemia can present?

A
  1. Vaso-occlusive crisis (severe pain triggered by cold/dehydration/infection/hypoxia; get mesenteric ischaemia, CNS infarction, AVN, leg ulcers, priapism [low flow])
  2. Aplastic crisis (transient, precipitated by parvovirus B19, sudden reduction in marrow production)
  3. Sequestration crisis (blood pools in spleen and liver, only occurs in children as adults have splenic atrophy secondary to infarction). Get severe anaemia, hypotension, hepatosplenomegaly and need urgent transfusion as can be fatal.
53
Q

Do adults with sickle cell get splenomegaly?

A

No, usually children because get infarcts during childhood and atrophy

54
Q

Complications of sickle cell anaemia?

A

Splenic infarction (and therefore encapsulated infection so need vaccines), poor growth, renal failure, gallstones, retinal disease, lung fibrosis and pulmonary HTN secondary to hypo)

55
Q

Managing sickle cell crisis?

A

Prompt analgesia, O2 if needed, sepsis screen, bloods (FBC, X-match, reticulocytes), IVT, broad spec Abx if needed. Blood transfusion if Hb falls and EXCHANGE TRANSFUSION if severe chest crisis, CNS event)

56
Q

Acute chest syndrome in sickle-cell anaemia?

A

Manifestation of sickle cell crisis with emboli to lungs (fat from BM or infectious. Get pain, wheeze, tachypnoea. Give O2, Abx, bronchodilators, transfuse if needed.

57
Q

Three phases of CML?

A
  1. Stable phase (can last years, few symptoms)
  2. Accelerated phase (increasing symptoms, spleen size, BASOPHILIA)
  3. Blast transformation (transforms to AML/ALL, death)
58
Q

Presentation of CML?

A

Mostly chronic and insidious (weight loss, fever, sweats). May be gout, bleeding, abdo discomfort from splenomegaly (a cause of massive splenomegaly), or incidentally (30%). Can present with hyperviscosity (get CVA etc.); may need leukapheresis in emergency

59
Q

Treating CML?

A

If have Ph (better prog) give BCR-ABL TKI (e.g. dasatinib). Also use hydroxycarbamide.
HSCT is only cure (only for young).

60
Q

Signs, symptoms and investigations in CLL?

A
  1. Often asymptomatic, incidental with raised WCC on FBC. May be anaemic, infection prone, or weight loss.
  2. Signs: enlarged, rubbery non-tender nodes, spleno/hepatomegaly
  3. FBC shows lymphocytes elevted. Later get AIH, marrow infiltration and BM failure. Film shows smear cells (fragile cels)
61
Q

Investigations in CML?

A

FBC shows very high WCC with lots of myeloid cells (neuto, baso, mono, eosino). Blood film shows many granulocytes at different maturity ages

62
Q

Differences between CML and CLL?

A

CML usually younger, more B symptoms, get massive hepatosplenomegaly, and blood film shows granulocytes

63
Q

What is TACO?

A

Transfusion associated circulatory over-load; get hypervolaemia. SOB, oedema, HTN. RFs are extremes of age, CKD/lung disease/CVD, low albumin, severe anaemia

64
Q

What is TRALI?

A

Transfusion-related acute lung injury. SOB, hypoxia (similar to ARDS, hypotension (unlike TACO). Immune-mediated. Occurs in first six hours post transfusion. Supportive management with steroids, fluids, vasopressors

65
Q

IDA alongside low albumin and calcium?

A

Suggestive of malabsorption as cause of anaemia e.g. coeliac

66
Q

Autosplenectomy?

A

Occurs in SCA. Spleen initially becomes enlarged with removal of abnormal blood cells. After continuous hypoxic and thrombotic insults, reduced to non-functional, small mass of fibrotic tissue

67
Q

Features of DIC?

A

Triad of thrombocytopenia, rise in PT/APTT/TT, low fibrinogen. Get rise in FDPs (fibrin degradation products)/D-dimer. Blood film may show schistocytes (fragmented red blood cells arising from microangiopathic haemolysis as red cells trapped in fibrin mesh). Get abnormal activation of coagulation and unregulated fibrinogen deposition and lysis, so get bleeding and thrombosis simultaneously

68
Q

Differentiating AoCD and IDA?

A

Ferritin high in AoCD, low in IDA, and TIBC low in AoCD, high in IDA

69
Q

What does plasmin do?

A

Degrades fibrin and fibrinogen to products that inhibit thrombin, preventing over-coagulation. This is why fibrinolytics are used in stroke etc.

70
Q

Three key events in haemostasis?

A
  1. Vasoconstriction
  2. Platelet aggregation to form primary haemostatic plug
  3. Clotting cascade activated to form a fibrin plug
71
Q

Myeloma and stroke?

A

Myeloma predisposes to hypercoagulable state therefore CVA

72
Q

Haptoglobins in haemolysis?

A

These are serum proteins which bind Hb released by RBCs. These complexes (haemoglobin-haptoglobin) and removed by the RES. In haemolysis, get more Hb released so lower serum haptoglobins

73
Q

Hereditary sphero inheritance?

A

Mostly AD, 25% AR

74
Q

Antibodies in pernicious anaemia?

A

90% have parietal cell antibodies, 50% have antibodies to intrinsic factor

75
Q

Features of Fanconi’s anaemia?

A

Defective DNA repair. AshkenaziJews. Abnormal/absent radii or thumbs. Also kidney malformations, microcephaly, hypogonadism, high fetal Hb. Most common cause of inherited aplastic anaemia and is big cause of AML in paeds. Rx is HSCT.

76
Q

Causes of DIC?

A

(Gram negative) sepsis, trauma, haemorrhage, malignancy, vascular abnormalities, hepatic failure

77
Q

What is APLS?

A

Disorder characterised by hypercoagulable state with autoantibodies against phospholipid components inc. cardiolipin (therefore do anti-cardiolipin Abs). Can cause recurrent spontaneous miscarriages. 10% have renal abnormalities

78
Q

Risk factors for AML?

A

Down syndrome, benzene exposure, previous radiotherapy

79
Q

Rouleax?

A

Stacks of red blood cells, seen in chronic inflammation e.g myeloma and are reason for raised ESR

80
Q

Managing major and minor bleeding in haemophilia A?

A

Minor = desmopressin (encourages factor VIII release) and TXE and supportive.
Major - give recombinant factor 8.

81
Q

Coag in haemophilia A vs VWD?

A

Haemophilia A = long APTT, normal PT and bleeding time. VWD = long APTT and bleeding time, normal PT (and plt).

82
Q

Types of VWD?

A

Types II and II are AD, type III is AR

83
Q

Treating VWD?

A

Give recombinant VWF +/- factor VIII (can become depleted)

84
Q

Role of VWF?

A

Assists platelet adhesion and factor VIII stabilisation (hence why factor VIII needed in severe VWD)

85
Q

How can transfusion lead to heart failure?

A

Can get transfusion haemosiderosis where iron deposits in endocrine organs and the heart, detected by MRI and can cause heart failure. A consideration in repeated transfusion

86
Q

Which patients get treatment in CLL?

A

Must be properly symptomatic e.g. significant B symptoms or complications from lymphadenopathy/splenomegaly/hepatomegaly. Can give rituximab, fludarabine, not HSCT in CLL

87
Q

Target INR for patients who get recurrent VTE while on adequate warfarin therapy?

A

3.5 as are clearly high risk

88
Q

Managing men with unexplained IDA and Hb below 11?

A

Need urgent gastro referral. If also have dyspepsia may get referral with higher Hb

89
Q

Hypochromic RBCs with target cells are seen in?

A

Get central pallor. Seen in Hbopathies e.g. thalassaemia or IDA

90
Q

Pentad of CFs in TTP?

A

Haemolytic anaemia, thrombocytopenic purpura, fever, neurological and renal abnormalities

91
Q

RF for TTP?

A

Female gender, obesity, pregnancy, Afro-Caribbean

92
Q

Patho of TTP?

A

Get low platelet count due to clotting and so get platelets sequestered inside small vessels. First line treatment is plasma exchange with FFP

93
Q

Signs of parvovirus B19 infection?

A

Slapped cheek rash, fever, new purpuric/macular rash on extremities

94
Q

Inheritance of haemophilia A and B?

A

Both are X-linked recessive

95
Q

How does ITP present?

A

Features of thrombocytopenia and reduced ability to achieve haemostasis e.g. epistaxis, prolonged gum bleeding, menorrhagia, PPH, spont. bruising. OE get petechial or purpuric rash and areas of ecchymoses.

96
Q

Treating ITP?

A

Depends on platelet level; steroids if mild, if severe or moderate-severe bleeding may get IVIg or platelet transfusion

97
Q

First-line treatment of thrombocytosis?

A

Hydroxyurea

98
Q

Four characteristic features of essential thrombocytosis?

A

Raised platelets, hyperplasia of megakaryocytes in bone marrow, splenomegaly, episodes of bleeding or thrombosis (can present with either)

99
Q

Most common form of NHL?

A

Follicular lymphoma

100
Q

Features of follicular lymphoma?

A

C’somal transolocation between 14 and 18, over-produce bcl-2. Affects men and women equally, incidence increases with age. Present with painless progressive adenopathy, B symptoms come later. Do LN biopsy.

101
Q

How does ALL present?

A

Hepatosplenomegaly, generalised lymphadenopathy, bruising. Fatigue, joint and bone pain, superimposed infections leading to infections e.g. otitis media

102
Q

What is TdT a marker of?

A

Expressed in immature lymphocytes and lost when matured so can be use to detect immature cells in ALL etc.

103
Q

What are Auer rods and what are they associated with?

A

Intracytoplasmic dark pink rods, found in immature cells in APML

104
Q

What are Howell-Jolly bodies?

A

Features of splenic disruption (along with nucleated red cells) suggestive of SCD

105
Q

What % of blasts in the BM denotes complete remission?

A

<5%

A final year of medicine (20 decks)

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