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4TH YEAR - CSIM2 > Blood Disorders > Flashcards

Blood Disorders Flashcards

1
Q

What are the constituents of a red cell count?

A 
Hb
MCV
Reticulocyte count
Red cell count
Haematocrit
MCH
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2
Q

What is the reticulocyte count? What does it mean if its high?

A

The concentration of immature RBCs

High: increased blood loss and haemolytic anaemia because the bone marrow works harder to replace lost cells

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3
Q

What is the haematocrit?

A

Volume percentage of RBCs in the blood

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4
Q

What causes a microcytic anaemia?

A 
Iron deficiency anaemia
Thalassemia
Sideroblastic anaemia (production of ringed abnormal RBCs)
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5
Q

What causes a normocytic anaemia?

A

Acute blood loss
Haemolytic anaemia
Chronic disease
Multiple myeloma

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6
Q

What causes a macrocytic anaemia?

A 
B12/folate deficiency
Alcohol
Reticulocytosis
Liver disease
Pregnancy
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7
Q

What is a physiological cause of normocytic/macrocytic anaemia?

A

Pregnancy

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8
Q

What tests are included in a haematinics study?

A

B12/folate

Ferritin

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9
Q

What does a high/low ferritin tell us?

A

High - not useful as ferritin is an acute phase protein so rises with any inflammation

Low - iron deficiency

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10
Q

What causes iron deficiency anaemia? What are the signs?

A
  • Chronic blood loss (menstrual/GI/urinary)
  • Increased demand
  • Decreased absorption (coeliacs - do tTg), gastrectomy)
  • Poor intake

SIGNS - koilonychia, angular stomatitis, glossitis

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11
Q

How is iron deficiency anaemia treated?

A

Ferrous sulphate tablets

Transfusion if Hb<70

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12
Q

How is B12 absorbed?

A

Binds to intrinsic factor, allowing it to be observed in the terminal ileum

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13
Q

What causes B12 anaemia?

A
  • Pernicious anaemia
  • Malabsorption
  • Not enough meat/fish etc
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14
Q

What causes folate deficiency anaemia?

A
  • Increased requirements
  • Dietary (not enough green veg)
  • Malabsorption
  • Drugs (trimethoprim, phenytoin)
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15
Q

What are some heritable causes of haemolytic anaemia?

A

Haemoglobinopathies: sickle cell
Membrane defects: hereditary spherocytosis, elliptocytosis
Enzyme defects: G6PD deficiency, pyruvate kinase deficiency

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16
Q

What are some acquired causes of haemolytic anaemia

A

Autoimmune (DAT+) - drug induced

Non-immune: DIC, TTP, infection

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17
Q

What is Coombs test for?

A

Autoimmune haemolytic anaemia - DAT direction antiglobulin test

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18
Q

What is polycythemia?

A

Increased number of RBCs in the blood

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19
Q

What are the primary and secondary causes of polycythemia?

A

Primary - polycythemia vera (all cell lines increased)

Secondary - increased epo or chronic hypoxia (just RBC increased)

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20
Q

What causes a high/low neutrophil count?

A

High - bacterial infection, inflammation, steroids, malignancy, stress

Low - chemo, agranulocytosis 4Cs (carbamazepine, clozapine, colchicine, carbimazole)

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21
Q

What causes a high/low lymphocyte count?

A

High - viral infection, CLL, chronic infections

Low - viral infection, HIV, chemo, bone marrow failure

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22
Q

What causes a high/low monocyte count?

A

High - bacterial infection, autoimmune disease, leaukemia

Low - acute infection, steroids, leukemia

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23
Q

What causes a high/low eosinophil count?

A

High - allergy, parasite, drug reactions

Low - n/a

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24
Q

What causes a high/low basophil count?

A

High - leukaemia, hypersensitivity, myeloproliferative disorders

Low - n/a

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25
Q

What causes thrombocytopenia?

A

Decreased production - bone marrow failure, megaloblastic anaemia

Increased destruction - DIC/TTP/ITP/SLE/CLL/viruses/drugs

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26
Q

What causes thrombocythemia?

A

Primary - myeloproliferative disorders

Secondary - bleeding, inflammation, infection, malignancy

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27
Q

What is a myeloproliferative disorder?

A

A group of neoplastic disorders involving the bone marrow cells that produce RBCs, platelets or fibroblasts (everything except WBCs)

  1. Essential thrombocythemia
  2. Chronic myeloid leukemia
  3. Polycythemia vera
  4. Myelofibrosis
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28
Q

What is essential thrombocythemia and how does it present?

A

Overproduction of platelets by bone marrow

- asymptomatic, headache, dizziness, bruising, thrombosis

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29
Q

What do investigations show for ET?

a) bloods
b) genetics

A

B: Isolated rise in platelets
G: JAK2, CALR or MPL mutation

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30
Q

How is ET treated?

A
  1. Aspirin to reduce clot risk
  2. Cytoreductive surgery
  3. Hydroxycarbamide
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31
Q

What is chronic myeloid leukemia and how does it present?

A

Neoplastic disease of mature myeloid cells in the bone marrow, involving basophils, eosinophils and neutrophils
- incidental finding, fever, night sweats, splenomegaly, weight loss, bleeding, petechia, gout, hyper-viscosity syndrome

3 clinical phases:

  1. Chronic
  2. Accelerated
  3. Blast crisis (symptoms of AML)
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32
Q

What do investigations show for CML?

a) bloods
b) cytogenetics (most important test)

A

a) increased myeloid cells, myeloblasts

b) translocation(9:22) involving the ABL:BCR genes - PHILADELPHIA CHROMOSOME

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33
Q

How is CML treated?

A
  • Tyrosine kinase inhibitor (Imatinib)
  • PCR monitoring of BCR:ABL
  • Stem cell transplant
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34
Q

What are the side effects of Imatinib?

A

Pleural effusion, rash, cramps, vomiting, oedema

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35
Q

What is polycythemia vera and how does it present?

A

Overproduction of RBC by the bone marrow cells, causing the blood to thicken

  • thrombosis, splenomegaly, often asymptomatic
  • itch particularly after a hot shower
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36
Q

How is polycythemia investigated?

a) bloods
b) genetics

A

a) all cell lines high, low epo

b) JAK2 mutation

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37
Q

How is polycythemia vera treated?

A
  1. Aspirin to reduce clot risk
  2. Cytoreductive surgery
  3. Hydroxycarbamide
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38
Q

What is multiple myeloma and how does it present?

A 
Neoplastic disease of plasma cells (B cells that produce antibodies.
CRAB presentation
- Calcium increased
- Renal impairment
- Anaemia 
- Bony lesions

BACK PAIN!!!

These are due to paraprotein clogging up various sites

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39
Q

What ethnicity have a higher proportion of patients with multiple myeloma?

A

African descent

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40
Q

What is the pathophysiology of multiple myeloma?

A

Plasma cells proliferate and produce paraprotein, a faulty monoclonal antibody.

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41
Q

How is multiple myeloma diagnosed?

A

Serum paraprotein (immunoglobulin electrophoresis)
Serum free light chain blood test
Blood film rouleax - increased plasma viscosity due to overproduction of immunoglobulins

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42
Q

How is multiple myeloma treated?

A
  • Chemo
  • Bisphosphonates
  • Stem cell transplant
  • Stop nephrotoxic drugs
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43
Q

What are the symptoms of iron deficiency?

A

Fatigue, leg cramps and craving ice

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44
Q

What are the symptoms of iron overload/haemochromatosis?

A

Chondrocalcinosis, iver cirrhosis, diabetes, cardiomyopathy, arthritis ‘bronzed diabetes’

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45
Q

What is the pathophysiology of primary haemochromatosis?

A

Mutation in HFE gene, so hepcidin isnt produced and too much iron is absorbed from the blood.
It is then stored in the liver and heart, where it causes cirrhosis and cardiomyopathy

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46
Q

What causes secondary haemochromatosis?

A

Chronic haemolysis, multiple transfusion, excess dietary

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47
Q

How is haemochromatosis treated? What investigation should you do to look for complications?

A
  1. Phlebotomy
  2. DFO/DFP (bind iron)

MRI for liver and heart

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48
Q

What is myelofibrosis?

A

Bone marrow disorder characterised by excessive fibrosis due to proliferation of an abnormal clone of haematopoietic stem cells

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49
Q

What are the primary and secondary types of myelofibrosis?

A

Primary - idiopathic

Secondary - develops from PV or ET (other myeloproliferative disorders)

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50
Q

What are the symptoms of myelofibrosis?

A

MASSIVE SPLENOMEGALY, bone pain, fatigue, bruising, sweats

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51
Q

What investigations should be done in myelofibrosis

a) bloods
b) blood film
c) bone marrow biopsy

A

Bloods - pancytopenia OR pancythemia
Blood film - tear drop poikilocytes/dacrocytes and nucleated RBCs
Biopsy - collagen fibrosis, JAK2/MLP/CALR mutation

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52
Q

How is myelofibrosis managed?

A

Generally incurable, except for stem cell transplant

Symptomatic treatment - transfusion, allopurinol, splenectomy, folic acid, JAK2 inhibitors

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53
Q

What are the symptoms of hereditary spherocytosis?

A

Splenomegaly, jaundice and fatigue, associated with cholecytisis

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54
Q

What is the pathophysiology of hereditary spherocytosis?

A

Patients have abnormally shaped but functioning inherited erythrocytes. The spleen attacks them (and becomes massive), causing anaemia with a high reticulocyte count

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55
Q

What would you expect from macrocytic anaemia and pancytopenia?

A

B12/folate deficiency

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56
Q

How is B12 deficiency managed?

A

If no intrinsic factor is present either, patient will need lifelong IM B12 (oral wont work due to lack of IF)

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57
Q

What factors are involved in the extrinsic pathway, and how is this measured?

A

7

PTT

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58
Q

What factors are involved in the intrinsic pathway, and how is this measured?

A

8,9,11,12

APTT

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59
Q

What factors are vitamin K dependent?

A

2, 7, 9, 10

60
Q

Describe the process of clot formation

A
  1. Vasconstriction of the blood vessel
  2. Platelet activation and plug formation - granules release ADP, TXA2
  3. Endothelial trauma causes VWF release from WP bodies, this creates a bridge between the platelet plug and collagen in the vessel wall, allowing it to attach
  4. This activates the clotting cascade
  5. Production of a fibrin mesh which stabilises the clot
61
Q

What features would you expect in a history of a patient with a bleeding disorder?

A
  • Bleeding from minor wounds
  • Bleeding after surgery
  • Heavy periods
  • Bruising
  • Gum bleeding
62
Q

What is a correction study?

A

A blood test performed if you have a long APTT/PTT. Add normal plasma to the blood sample:

  • If APTT/PTT corrects - it is a clotting factor deficiency, do an assay
  • If it doesnt correct - the blood has an abnormal factor inhibitor
63
Q

Which is the most common clotting factor inhibitor found in the blood?

A

Lupus anticoagulant

64
Q

What are the symptoms of haemophilia?

A

Bleeding, arthropathy (bleeding into joints)

65
Q

What is the pathophysiology of haemophilia A?

A

X linked recessive deficiency in factor 8, causing high APTT.

NB - 30% are do novo mutations so dont always expect a family history

66
Q

What is the pathophysiology of haemophilia B?

A

X linked recessive deficiency in factor 9, causing high APTT

67
Q

How should haemophilia be treated?

A
  • Recombinant factor 8/9
  • Desmopressin
  • Analgesia and joint immobilisation
  • Physio
  • Avoid aspirin/NSAIDS/heparin
68
Q

What is the pathophysiology of Von Willebrand Disorder?

A

Autosomal deficiency in VWF which usually binds:

  • platelets
  • factor 8
69
Q

What are the symptoms of VWF disorder?

A

Mucocutanoues bleeding, bruising

70
Q

What are the the 3 types of Von Willebrand Disorder?

A

Type 1 - asymptomatic (normal VWF not enough)
Type 2 - mild symptoms (abnormal VWF)
Type 3 - Severe, no VWF at all, may have internal bleeding

71
Q

How is VWF diagnosed?

A
  • Do VWF levels and functionality with a Gp1b assay
  • Reduced ristocetin cofactor activity
  • Reduced factor 8, increased APTT

Sometimes bloods won’t show anything!

72
Q

How is VWF managed?

A
  • Desmopressin
  • Pooled plasma concentrates containing VWF

Often treatment only needed before surgery/dental procedures

73
Q

What is the most common bleeding disorder?

A

Von Willebrand Disorder

74
Q

What is the mechanism behind excessive bleeding in renal disease?

A

Uraemia leads to reduced platelet aggregation and associated bleeding

75
Q

What is the mechanism behind excessive bleeding in liver disease?

A

Impaired production of clotting factors

76
Q

What is haemorrhagic disease of the newborn?

A

All babies are born vitamin K deficient so there is impaired production of 2 7 9 and 10 and protein C/S

77
Q

What is DIC?

A

Widespread activation of coagulation from release of procoagulants. Eventually these factors get used up, leading to bleeding

78
Q

How is DIC diagnosed?

A

Low platelets
High PT/APTT
High fibrinogen degradation products
High D dimer

79
Q

What causes DIC?

A

Sepsis
Malignancy
Obstetric catastrophe
Major haemorrhage

80
Q

How is DIC managed?

A
  • Treat underlying cause

- Resuscitate with red cells, plasma, platelets, cryoprecipitate and blood warmers

81
Q

What is cryoprecipitate rich in?

82
Q

How is the clotting cascade initiated?

A

Factor 7 and tissue factor form a complex which activates factor 10.

83
Q

What is a lymphoma?

A

A neoplastic disorder of mature lymphocytes in lymphoid tissue, in which abnormal lymphocytes collect in lymph nodes, particularly in the armpits, groing and neck.

84
Q

What are the symptoms of lymphoma?

A
  • Painless, rubbery LNs

- B symptoms - pel ebstein fever, weight loss, night sweats, pruritus

85
Q

Why should you ask about contact with cats in a lymphoma history?

A

Cat scratch fever gives you generalised lymphadenopathy

86
Q

In what cases should enlarged LNs be refered?

A

6 week history of a node over 1.5cm
OR
6 week history of generalised lymphadenopathy

87
Q

What blood tests should be done in lymphoma and what would they show?

A

Bloods - FBC, U&E, LFT, ESR (usually normal!!, low Hb and high ESR indicate worse prognosis)
Monospot - EBV is a reactive cause of lymphadenopathy
Viral screen - HIV is associated with lymphoma
Blood film
LDH

88
Q

What is the diagnostic test for lymphoma? What would it show for Hodgkins?

A

EXCISION NODE/CORE BIOPSY

- shows Reed Sternburg ‘owl cell’

89
Q

What special tests should be done in lymphoma and what do they show?

A

Genetic sequencing - FISH
PET - increased glycolytic tissue in malig

Bone marrow sampling rarely used as the disease is in the nodes

90
Q

How can lymphoma be classifed?

A

Grade - Low grade vs High grade

Histology - Hodgkins vs Non-Hodgkins

91
Q

What is the difference between low grade and high grade?

A

Low grade - slow growing but incurable, treat if symptomatic

High grade - fast growing but cured with chemotherapy

92
Q

Describe Hodgkins lymphoma

A
  • Reed sternburg cell
  • Months-years survival if untreated
  • Curable
93
Q

Describe Non-Hodgkins lymphoma

A

Over 60 types but split into
Indolent - incurable, survival years
Aggressive - chemo, survival months
Very aggressive - chemo, survival weeks

94
Q

Give an example of an indolent, aggressive and very aggressive NHL

A

Indolent - follicular
Aggressive - DLBCL
Very aggressive - Burkitts

95
Q

How should follicular lymphoma be managed?

A

Usually stage IV at presentation but only treat if symptomatic with:

  • Chlorambucil and steroids
  • Rituximab
  • Bone marrow transplant
96
Q

Describe the severity of diffuse large B cell lymphoma?

A

Can develop from CML or follicular

Severity determined by age, stage, extranodal involvement, performance status and LDH

97
Q

How should DLBCL be treated?

A 
R-CHOP
Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Vincristine (oncovin)
Prednisolone
98
Q

How is lymphoma staged?

A 
Ann Arbour
1 - 1LN
2- >2LN on same side of diaphragm
3 - >2LN on different sides of diaphragm
4 - Disseminated

A - no B symptoms
B - weight loss, fever, night sweats

99
Q

What are the complications of lymphoma, and how are the managed briefly?

A

Tumour lysis syndrome - allopurinol/rasburicase + hydrate

Spinal cord compression - MRI/steroids/surgery

Hypercalcemia - IV bisphosphonates

100
Q

How do patients with bone marrow failure present?

A

Bruising, fatigue, pallor, organomegaly, SOB, infection

101
Q

Why do patients get organomegaly in anaemia?

A

Increased demand induces extramedullary haemoatopoiesis in the liver and spleen

102
Q

What do blood tests show in bone marrow failure?

A

Pancytopenia - bone marrow failure is the leading cause of pancytopenia

103
Q

What can cause pancytopenia?

A

Increased destruction - sepsis, immune, splenomegaly

Decreased production - bone marrow failure

104
Q

What investigations should be done in anyone with pancytopenia?

A

Reticulocyte count, B12/folate, abdo USS, temperature

105
Q

What are the 3 categories of causes of bone marrow failure

A
  1. Aplastic anaemia
  2. Megaloblastic anaemia
  3. Infiltration of the bone marrow with malignancy
106
Q

What is aplastic anaemia?

A

A rare stem cell disorder involving pancytopenia and hypoplastic bone marrow, due to drugs (benzene, chemo, gold, suphonamide), congenital or idiopathic

107
Q

How is aplastic anaemia managed?

A
  • Treat underlying cause
  • Supportive care - infusions, infection check
  • Stem cell transplant from HLA matched sibling
108
Q

What is megaloblastic anaemia?

A

Production of large, abnormal immature RBCs by the bone marrow, usually due to B12 or folate deficiency.

109
Q

How is megaloblastic anaemia treated? What should you not do?

A

Give B12/folate replacement (IM)

DONT give Hb transfusion as the patient has adapted to the anaemia overtime and overload will lead to heart fialure

110
Q

Which blood cancer commonly presents with bone marrow failure. What are the symptoms?

A

Acute leukemia - sweats, weight loss, flu, anaemia, bleeding etc

111
Q

What is acute leukemia?

A

Neoplastic disorder of the IMMATURE myeloblasts or lymphoblasts in the bone marrow

112
Q

What investigations should be done in a patient with suspected acute leukemia and what would they show?

A

Bloods - anaemia, pancytopenia, high number of blasts
Tissue biopsy - huge nuclei
Bone marrow biopsy - blast cells

113
Q

What causes acute leukemia?

A
  • Genetic predisposition - eg. Downs syndrome
  • Haematological disease
  • Irradiation
  • Chemotherapy
114
Q

What are the features of ALL? What important investigation must be done?

A 
Affecting lymphocytes (80%B, 20%T), more common in children
BUZZ WORDS - blast cells, parotids/testicles, extra medullar involvement

Do lumbar puncture to assess for CNS involvement

115
Q

What are the features of AML? What is the characteristic finding on cytology?

A

Affecting neutrophils, RBCs, platelets, more common in adults
BUZZ WORDS - downs syndrome, NF1, male, risk of DIC, previous MDS/CML

Auer rods

116
Q

How is acute leukemia managed?

A
  1. Supportive - transfusions, IV fluid, allopurinol
  2. Infection - assess risk, start empirical abx
  3. Discussion about sperm banking precehmo
  4. Chemotherapy + LP if CNS mets suspected (as chemo cant cross BBB_
  5. Allogeneic marrow transplant
117
Q

What are the features of CLL?

A

Often asymptomatic and diagnosed incidentally eg. before an operation
Found in the elderly, no treatment usually required

118
Q

What does a CLL blood film look like?

A

Lots of small, mature lymphocytes

119
Q

Name 7 conditions that cause thrombosis?

A 
Factor V leiden
DVT/PE
Antiphospholipid syndrome
Cerebral sinus thrombosis
Arterial embolus
Metallic heart valves
Ventricular pace maker
120
Q

What is factor V leiden?

A

A point mutation in factor V gene, leading to slow inactivation of Va and hence a tendency to form clots - this is one of the most common causes of inherited procoagulant states

Usually this would be inactivated by protein C

121
Q

What are the RF for thrombosis?

A 
Age
Immobilisation
Surgery
Oestrogen
Air travel
Cancer
Antiphospholipid anti bodies 
Thrombophilia
122
Q

What naturally occurring anticoagulants are deficient in thrombophilia?

A

Protein C
Protein S
Antithrombin

123
Q

What are the symptoms of a VTE?

A

DVT - hot unilateral swollen legs

PE - sudden onset unilateral chest pain

124
Q

What investigations should be done to diagnose a VTE?

A

DVT - bilateral doppler USS
PE - CTPA

D dimer is helpful in exclusion but has a low specificity so should not be used diagnostically.

125
Q

How should a VTE be managed?

A

Anticoagulate with LMWH eg. enoxaparin
Anticoagulate with factor Xa inhibitor eg. fonadparinux
Anticoagulate with warfarin
Thrombolysis with alteplase

126
Q

Describe an anticoagulation regimen post VTE using a LMWH

A

Tinzaparin

- continue for 5 days or until INR >2 for 2 consecutive readings

127
Q

Describe an anticoagulation regimen post VTE using a factor xa inhibitor

A

Rivaroxaban

- continue for 21 days

128
Q

Describe an anticoagulation regimen post VTE using warfarin

A

Warfarin

  • slow onset of action so cover with LMWH during first few days of initiation
  • day 1 (5mg)
  • day 2 (5mg)
  • day 3 (check INR)
  • adjust dose accordingly
129
Q

What are the complications of anticoagulation?

Describe symptoms, and treatment

A

Anticoagulant associated ICH

  • Stroke symptoms within 24-48h of admin
  • Treat with beriplex and vitamin K
130
Q

What score is used to predict likelihood of recurrence of VTE?

A 
DASH score!!
Positive D dimer - 2
Age < 50 - 1
Male - 1
Female/hormone associated VTE - -1

If DASH < = 1, stop anticoagulant

131
Q

What is chronic leukemia?

A

Neoplastic disease of mature WBCs in the bone marrow, to to progressive accumulation of functionally incompetent WBCs

132
Q

What are the symptoms of chronic leukemia?

A

Insidious weight loss, fever, sweats, bleeding.

In CLL in particular, it is often an incidental finding

133
Q

What would tests show for CML?

A

BLOODS - High WCC (neutrophils, basophils, eosinophils) Anaemia
BIOPSY - Philadelphia translocation (9:22) of ABL:BCR

134
Q

How is CML treated?

A

Tyrosine kinase inhibitors - Imatinib
Hydroxycarbamide
Stem cell transplant

135
Q

What would tests show for CLL?

A

BLOODS - High lymphocyte count, anaemia

136
Q

How is CLL treated?

A 
OFTEN NO TREATMENT
Chemo
Radio
Supportive
Stem cell transplant
137
Q

What is the prognosis of chronic leukemia?

A

CML - chronic, accelerated and blast phase (in which it transforms to AML)

CLL - often never progress, better prognosis

138
Q

What may a blood film of someone with iron deficient anaemia show?

A

Elliptocytes and hypersegmented neutrophils

139
Q

What would the FBC look like of a patient with anaemia of chronic disease?

A

Normocytic anaemia
Normal platelets
Increased ferritin
Reduced total iron binding capacity

140
Q

What is the most appropriate measurement of the bodys iron stores?

A

Serum ferritin

141
Q

What is the most common complication of allogeneic bone marrow transplant?

A

Graft versus host disease

142
Q

What is the most common complication of allogeneic bone marrow transplant for aplastic anaemia?

A

Graft failure

143
Q

What is acquired haemophilia?

A

An autoimmune process in which the body starts making antibodies to factor 8 or 9. Often this is due to an occult malignancy

144
Q

What would blood tests show in a patient with acquired haemophilia?

A

Grossly elevated APTT

- no correction with mixed study

145
Q

What are protein C/S deficiencies?

A

Deficiency of vit K dependent natural anticoagulants - gives a 5 fold increase in VTE risk

146
Q

What is the name of the condition in which patients have urine/serum monoclonal antibodies but do not fulfil the criteria for multiple myeloma?

A

Monoclonal gammopathy of uncertain significance

  • 2% risk of transforming into MM

4TH YEAR - CSIM2 (20 decks)

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