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YEAR 4 CANCER CARE > Anaemia + Complications > Flashcards

Anaemia + Complications Flashcards

1
Q

What is Anaemia?

A
  • low level of haemoglobin
  • result of underlying disease
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2
Q

What is
1. microcytic anaemia
2. normocytic anaemia
3. macrocytic anaemia

A

1.Low Hb with low mean cell volume
2. Low Hb with normal mean cell volume
3. Low Hb with high mean cell volume

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3
Q

Cause of Microcytic anaemia?

A

Mnemonic TAILS
T- Thalassaemia
A- Anaemia of chronic disease
I- Iron deficiency anaemia
L-Leas poisoning
S-Sideroblastic anaemia

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4
Q

Normocytic anaemia causes?

A

3As and 2Hs

A- Acute blood loss
A-Anaemia of chronic disease
A-Aplastic anaemia
H-Haemolytic anaemia
H-hypothyroidism

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5
Q

Types and causes of Macrocytic anaemia?

A
  • Megaloblastic anaemia: B12 deficiency and Folate deficincy
  • Normoblastic macrocytic anaemia: Alcohol, Reticulocytosis (usually from haemolytic anaemia or blood loss), Hypothyroidism, Liver disease,Drugs such as azathioprine
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6
Q

Symptoms of anaemia?

A
  • Tiredness
  • Shortness of breath
  • Headaches
  • Dizziness
  • Palpitations
  • Worsening of other conditions such as angina, heart failure or peripheral vascular disease
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7
Q

Symptoms of iron deficiency anaemia?

A
  • Pica describes dietary cravings for abnormal things such as dirt and can signify iron deficiency
  • Hair loss can indicate iron deficiency anaemia
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8
Q

Signs of anaemia?

A
  • Pale skin
  • Conjunctival pallor
  • Tachycardia
  • Raised respiratory rate
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9
Q

Signs of anaemia?

A
  • Pale skin
  • Conjunctival pallor
  • Tachycardia
  • Raised respiratory rate
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10
Q

Specific signs of iron deficiency anaemia?

A
  • Koilonychia- spoon shaped nails
  • Angular chelitis
  • Brittle hair and nails
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11
Q

Bloods for anaemia?

A
  • Haemoglobin
  • Mean Cell Volume (MCV)
  • B12
  • Folate
  • Ferritin
  • Blood film
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12
Q

What is Haemolytic anaemia?

A
  • where there is destruction of red blood cells leading to anaemia
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13
Q

What causes haemolytic anaemia?

Think of broad classifications and then give examples of the conditions

A

Inherited
* Membrane: Hereditary spherocytosis/elliptocytosis
* metabolism: G6P deficiency
* Haemoglobinopathies: sickle cell, thalassaemia
Acquired
Immune (Coombs-positive):
* Autoimmune: warm/cold
* Alloimmune incl. transfusion reaction, haemolytic disease newborn
* Drug: methyldopa, penicillin

Non-immune (Coombs negative)
* Microangiopathic haemolytic anaemia: TTP/HUS, DIC, malignancy, pre-eclampsia
* Prosthetic heart valves
* paroxysmal nocturnal haemoglobinuria
* infections: malaria
* drug: dapsone
* Zieve syndrome

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14
Q

What is Zieve syndrome?

A
  • rare clinical syndrome of Coombs-negative haemolysis, cholestatic jaundice, and transient hyperlipidaemia associated with heavy alcohol use, typically following a binge
  • typically resolves with abstinence from alcohol
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15
Q

What happens to haemaglobin in intravascular haemolysis?

A
  • Free haemoglobin is released which then binds to haptoglobin
  • As haptoglobin becomes saturated haemoglobin binds to albumin forming methaemalbumin (detected by Schumm’s test).
  • Free haemoglobin is excreted in urine as haemoglobinuria, haemosideriuria
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16
Q

Cause of intravascular haemolysis?

A
  • mismatched blood transfusion
  • G6PD deficiency
  • red cell fragmentation: heart valves, TTP, DIC, HUS
  • paroxysmal nocturnal haemoglobinuria
  • cold autoimmune haemolytic anaemia*
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17
Q

Extravascular haemolysis causes?

A
  • haemoglobinopathies: sickle cell, thalassaemia
  • hereditary spherocytosis
  • haemolytic disease of newborn
  • warm autoimmune haemolytic anaemia
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18
Q

Features of haemolytic anaemia?

A
  • Anaemia- fatigue, breathlessness, palpitations
  • Splenomegaly- as spleen becomes filled with destroyed RBC
  • Jaundice- as bilirubin is released during destruction of RBCs
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19
Q

Investigations for haemolytic anaemia?

A
  • Bedside: ECG- if pt has palpitations
  • Bloods: FBC- normocytic anaemia
    Blood film- schistocytes, reticulocytosis
    If immune cause- positive coombs test
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20
Q

What is Hereditary Spherocytosis?

A
  • Autosomal dominant condition
  • Causes sphere shaped RBC- fragile and break down when passing through the spleen
  • Most common hereditary haemolytic anaemia in people of northern European descent
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21
Q

Presentation of Hereditary spherocytosis?

A
  • failure to thrive
  • jaundice, gallstones
  • splenomegaly
  • aplastic crisis precipitated by parvovirus infection
  • degree of haemolysis variable
  • MCHC elevated
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22
Q

Diagnosis of Hereditary Spherocytosis?

A
  • Diagnosis: Positive fhx, clinical features, typical lab investigations (spherocytes, increased reticulocytes, raised MCHC)- if this is all present, no additional tests are needed
  • If diagnosis is ambiguous: EMA binding test and the cryohaemolysis
  • atypical presentation: electrophoresis analysis of erythrocyte membranes
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23
Q

Managment of Hereditary spherocytosis?

A
  • Folate replacement
  • Splenectomy
  • Acute haemolytic crisis:
    treatment is generally supportive, transfusion if necessary
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24
Q

What is G6PD deficiency?

A
  • Defect in red blood cell enzyme G6PD
  • More common in Mediterranean and African patients
  • X linked recessive
  • Causes crises that are triggered by infections, medications (anti-malarials) or fava beans
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25
Q

How does G6PD deficiency present?

A
  • Neonatal jaundice
  • Gallstones
  • Anaemia
  • Splenomegaly
  • Heinz bodies on blood film
    *
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26
Q

How do you diagnose G6PD deficiency?

A
  • G6PD enzyme assay
  • measure the activity of the enzyme
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27
Q

What do you seen on blood film of G6PD deficiency?

A
  • Heinz bodies
  • Bite and blister cells may also be seen
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28
Q

When do you perform the enzyme assay for G6PD deficiency?

A
  • around 3 months after an acute episode of haemolysis
  • This is because during haemolysis the most severly affected RBC without G6PD will have hemolysed there fore will not be measured in the assay–> false negative results
  • Therefore need to wait 3 months
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29
Q

What can precipitate a crisis in G6PD?

A
  • Infection
  • Fava beans
  • Drugs: anti-malarials e.g. primaquine, ciprofloxacin, sulph groups (sulphonamides, sulphasalazine, sulfonylureas)
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30
Q

What is autoimmune haemolytic anaemia?

A
  • Antibodies are created against the patients RBC
  • This leads to the destruction of rbc
  • 2 types- warm and cold
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31
Q

What are the investigation findings in autoimmune haemolytic anaemia?

A

General features of haemolytic anaemia:
* anaemia
* reticulocytosis
* low haptoglobin
* raised lactate dehydrogenase (LDH) and indirect bilirubin
* Blood film: spherocytes and reticulocytes
Specific features of autoimmune haemolytic anaemia:
Positive coombs test

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32
Q

What is Warm Autoimmune haemolytic anaemia (AIHA) ?

A
  • The antibody (IgG usually) causes haemolysis best at body temp
  • haemolysis tends to occur in extravascular sites e.g. spleen
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33
Q

Causes of warm AIHA?

A
  • Idiopathic
  • autoimmune disease e.g. SLE
  • Neoplasia e.g. lymphoma or CLL
  • Drugs e.g. methyldopa
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34
Q

Causes of warm AIHA?

A
  • Idiopathic
  • autoimmune disease e.g. SLE
  • Neoplasia e.g. lymphoma or CLL
  • Drugs e.g. methyldopa
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35
Q

Management of warm AIHA?

A
  • Treatment of underlying disorder
  • Steroids +/- rituximab are generally used first line
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36
Q

What is cold Autoimmune haemolytic anaemia?

A
  • antibody usually IgM
  • Causes haemolysis best at 4 degrees
  • Mediated by complement
  • more commonly intravascular
  • Features may incl symptoms of raynauds and acrocyanosis

Pt responds less wel to steroids

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37
Q

What is cold Autoimmune haemolytic anaemia?

A
  • antibody usually IgM
  • Causes haemolysis best at 4 degrees
  • Mediated by complement
  • more commonly intravascular
  • Features may incl symptoms of raynauds and acrocyanosis

Pt responds less wel to steroids

38
Q

Causes of cold AIHA?

A
  • Neoplasia e.g. lymphoma
  • Infections e.g. mycoplasma, EBV
39
Q

What is Paroxysmal Nocturnal Haemoglobinuria?

A
  • RARE
  • Specific genetic mutation in haematopoitic stem cells in bone marrow- occurs during pts lifetime
  • Mutation results in loss of the proteins on the surface of red blood cells that inhibit the complement cascade
  • Loss of protection against the complement system–> results in activation of complement cascade on the surface of RBC—> destruction of RBC
40
Q

Presentation of Paroxysmal Nocturnal Haemoglobinuria?

A
  • Red urine in the morning containing haemoglobin and haemosiderin
  • Anaemia due to haemolysis
  • Predisposed to thrombosis and smooth muscle dystonia (oesophageal spasm and erectile dysfunction)
41
Q

Managment of Paroxysmal Nocturnal Haemoglobinuria?

A
  • Eclizumab- monoclonal antibody that targets C5 causing suppression of the complement system
  • Bone marrow transplantion can be curative
42
Q

What can cause Microangiopathic Haemolytic Anaemia?

A
  • Haemolytic Uraemic Syndrome (HUS)
  • Disseminated Intravascular Coagulation (DIC)
  • Thrombotic Thrombocytopenia Purpura (TTP)
  • Systemic Lupus Erythematosus (SLE)
  • Cancer
43
Q

Management of Prosthetic valve haemolysis?

A

Monitoring
Oral iron
Blood transfusion if severe
Revision surgery may be required in severe cases

44
Q

Diagnosis of Paroxysmal Nocturnal Haemoglobinuria?

A
  • Flow cytometry of blood to detect low leverls of CD59 and CD55
45
Q

What is anaemia of chronic disease?

A
  • Anaemia due to chronic inflammation
  • Functional problem: body has the iron but cannot use it
  • Caused by malignancy, chronic infections, RA
46
Q

Pathophysiology of Anaemia of Chronic disease?

A
  • Chronic disease leads to chronic inflammation which causes IL-6 and IL-1 to be released
  • high levels of IL-6 stimulated hepcidin release from liver–> hepcin inhibits iron absoprtion as it decreases the activity of ferroportin (iron channel on gut enterocytes and plasma membrane of reticuloendothelial cells- macrophages)
  • This means that there is a reduction of plasma iron
  • This causing inhibition of erythropoiesis in bone marrow
47
Q

What are the blood results in Anaemia of Chronic disease?

A
  • FBC- normochromic, normocytic anaemia (this progresses to microcytic, hypochromic type)
  • Low TIBC
  • High ferritin
  • Low transferrin saturation
48
Q

What is thrombocytopenia?

A
  • Low platelet count
  • Normal platelet count: 150-450 x 10^9/L
49
Q

What conditons affects platelet production?

Resulting in thrombocytopenia ?

A
  • Sepsis
  • B12 or folic acid deficiency
  • Liver failure causing reduced thrombopoietin production in the liver
  • Leaukaemia
  • Myelodysplastic syndrome
50
Q

What causes platelet destruction?

Resulting in thrombocytopenia?

A
  • Medications
  • Alcohol
  • Immune thrombocytopenia purpura
  • Thrombotic thrombocytopenia purpura
  • Heparin-induced thrombocytopenia
  • Haemolytic uraemia syndrome
51
Q

Presentation of thrombocytopenia?

A
  • Mild: may be asymptomatic and found incidentally
  • Below 50 x 10^9: easy or spontaneous bleeding, prolonged bleeding times, nosebleeds, bleeding gums, heavy periods, blood in urine or stool
  • Below 10 x 106^9 : high risk for spontaneous bleeding. Spontaneous intracranial haemorrhage and GI bleeding are concerning
52
Q

Ddx of abnormal/ prlonged bleeding time?

A

Thrombocytopenia
Haemophillia A and haemophillia B
Von Willebrand disease
DIC

53
Q

What is Immune thrombocytopenia (ITP)?

A
  • Immune mediated reduction in platelet count
  • Antibodies against glycoprotein IIb/IIIa or Ib-V-IX complex
54
Q

How does ITP differ in adults and children?

A
  • Children have an acute thrombocytopenia that may follow infection or vaccination
  • Adults tend to have a more chronic condition
55
Q

Who gets ITP in adulthood?

A
  • Older females
  • associated with autoimmune haemolytic anaemia
56
Q

How does ITP present in adults?

A
  • may be detected incidentally following routine bloods
    symptomatic patients may present with:
  • petechiae, purpura
  • bleeding (e.g. epistaxis)
  • catastrophic bleeding (e.g. intracranial) is NOT a common presentation
57
Q

Investigations for ITP in adults?

A
  • FBC- isolated thrombocytopenia
  • Blood film
58
Q

Management of ITP?

A
  • First line: oral prednisolone
  • IVIG (pooled normal human immunoglobulin) may also be used- raised platelet count quicker so may be used if active bleeding or urgent invasive procedure required
59
Q

What is Evan’s syndrome?

A
  • ITP in association with autoimmune haemolytic anaemia
60
Q

What are the chains of haemoglobin called?

A
  • 2 alpha chains
  • 2 beta chains
61
Q

What is alpha thalassaemia?

A
  • caused by defects in alpha- globulin chains
  • Gene coding for this is on chromosome 16
62
Q

What is the severity of alpha thalassaemia dependent on?

A
  • If 1 or 2 alpha globulin alleles are affected then the blood picture would be hypochromic and microcytic, but the Hb level would be typically normal
  • If are 3 alpha globulin alleles are affected results in a hypochromic microcytic anaemia with splenomegaly. This is known as Hb H disease
  • If all 4 alpha globulin alleles are affected (i.e. homozygote) then death in utero (hydrops fetalis, Bart’s hydrops)
    *
63
Q

Management of alpha thalassaemia?

A
  • Monitoring the full blood count
  • Monitoring for complications
  • Blood transfusions
  • Splenectomy may be performed
  • Bone marrow transplant can be curative
64
Q

What is beta thalassaemia?

A
  • Defect in Beta globin chains
  • gene coding for this on chromosome 11
65
Q

What are the types of B thalassaemia and why is this the case?

A

Thalassaemia Minor
Thalassaemia Intermedia
Thalassaemia Major

  • this is due to the gene defect consisting of abnormal copies that retain some function or deletion genes (no function in the beta-globin protein at all)
66
Q

What is the Beta thalassaemia trait?

A
  • SAME AS MINOR
  • Autosomal recessive condition characterised by mild hypochromic, microcytic anaemia
  • Usually asymptomatic
67
Q

What are the features of beta thalassaemia minor/ trait?

A
  • mild hypochromic, microcytic anaemia - microcytosis is characteristically disproportionate to the anaemia
  • HbA2 raised (> 3.5%)
68
Q

What is thalassaemia intermedia?

A
  • 2 abnormal copies of the beta globin
  • 2 defective copies or one defective gene and one deletion gene
69
Q

Features of thalassaemia minor

A
  • more significant microcytic anaemia
  • pts require more monitoring and occasional blood transfusions
  • if they require more transfusions may need iron chelation to prevent iron overload
70
Q

What is beta thalassaemia major?

A
  • Homozygous for the deletion genes
  • No functioning beta-globin genes
  • Most severe form
71
Q

Features of beta- thalassaemia major?

A
  • presents first year of life with failure to thrive and hepatosplenomegaly
  • microcytic anaemia
  • HbA2 & HbF raised
  • HbA absent
72
Q

Management of beta thalassaemia?

A
  • Repeated transfusions–> leads to iron overload–> organ failure
  • Iron chelation therapy is v imp
73
Q

Most common inherited bleeding disorder?

A
  • Von Willebrands Disease
74
Q

What is Von Willebrands Disease?

A
  • Autosomal dominant (classically)
  • VW factor is a large glycoprotein which promotes platelet adhesion to damaged endothelium
  • carrier molecule for factor VIII
  • In this disease, the VWF does not work how it should
75
Q

What are the types of VWD?

A

type 1: partial reduction in vWF (80% of patients)
type 2: abnormal form of vWF
type 3: total lack of vWF (autosomal recessive)

76
Q

Presentation of VWD?

A
  • Bleeding gums when brushing
  • Epistaxis
  • Menorrhagia
  • Heavy bleeding in surgical operations
77
Q

Investigations in VWD?

A
  • Prolonged bleeding time
  • APTT may be prolonged
  • Factor VIII levels may be moderately reduced
  • defective platelet aggregation with ristocetin
78
Q

Management of VWD?

A
  • Tranexamic acid for mild bleeding
  • Desmopressin: raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
  • Factor VIII concentrate
79
Q

Woman presents with very heavy periods with a background of VWD- what are management options for her?

A
  • Tranexamic acid
  • Norethisterone
  • COCP
  • Mirena coil
80
Q

What is Haemophilia?

A
  • X-linked recessive disorder of coagulation
  • up to 30% of the patients have no fhx of the condition
81
Q

Difference between Haemophilia A and B?

A
  • A- due to deficiency of factor VIII
  • B- deficiency of factor IX
82
Q

Features of haemophilia?

A
  • Haemoarthroses
  • Haematomas
  • Prolonged bleeding after surgery or trauma
    Abnormal bleeding can occur in other areas:
  • Gums
  • Gastrointestinal tract
  • Urinary tract causing haematuria
  • Retroperitoneal space
  • Intracranial
  • Following procedures
83
Q

Blood tests in Haemophilia?

A
  • APTT- prolonged
  • Bleeding time, thrombin time and prothrombin time normal
84
Q

Managment of Haemophilia?

A
  • The affected clotting factors (VIII or IX) can be replaced by IV infusions
  • Prophulactically or in response to bleeding
85
Q

Complications of haemophilia treatment?

A
  • Antibodies to the clotting factor–> treatment becomes ineffective
86
Q

Which drugs can cause haemolytic anaemia?

A
  • Methyldopa
  • Penicillin
    *
87
Q

Causes of neutropenia?

A

Severe sepsis
Viral infection
Drugs
Marrow failure (due to malignancy or infiltration
Hypersplenism (less common)
Felty’s syndrome (less common)
SLE (less common)

88
Q

What is feltys syndrome?

A

Triad of:
* splenomegaly
* Rheumatoid arthritis
* neutropenia

89
Q

Causes of lymphocytosis?

A

Acute viral infection (especially EBV and CMV)
Chronic atypical infection (tuberculosis, brucella, toxoplasmosis)
Lymphoproliferative disorders (chronic lymphocytic leukaemia and lymphoma).

90
Q

What haematological side effects can steroids have?

A
  • Raised white cell count?
91
Q

Causes of Leukocytosis?

A
  • ALL specifically
  • Infection
  • Malignancy

YEAR 4 CANCER CARE (22 decks)

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