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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is haemoglobin

A
  • protein found in red blood cells. It is responsible for picking up oxygen in the lungs and transporting it to the cells of the body
  • Made from iron
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2
Q

Causes of microcytic anaemia

A 
T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia
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3
Q

Causes of normocytic anaemia

A 
A – Acute blood loss
A – Anaemia of Chronic Disease
A – Aplastic Anaemia
H – Haemolytic Anaemia
H – Hypothyroidism
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4
Q

What is macrocytic anaemia

A
  • can be megaloblastic or normoblastic
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5
Q

What is megaloblastic anaemia

A
  • the result of impaired DNA synthesis preventing the cell from dividing normally
  • Rather than dividing it keeps growing into a larger, abnormal cell.
  • This is caused by a vitamin deficiency
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6
Q

Examples of a megaloblastic anaemia

A

B12 deficiency

Folate deficiency

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7
Q

Examples of a Normoblastic macrocytic anaemia

A 
Alcohol
Reticulocytosis (usually from haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease
Drugs such as azathioprine
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8
Q

What are the generic 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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9
Q

Signs of specifically, iron deficient anaemia

A
  • Pica: dietary cravings for abnormal things such as dirt

- Hair loss

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10
Q

Generic, systemic signs of anaemia

A

Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate

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11
Q

peripheral stigmata of anaemia

A
  • Koilonychia
  • Angular chelitis
  • Atrophic glossitis
  • Brittle hair and nails
  • Jaundice: haemolytic anaemia
  • Bone deformities: thalassaemia
  • Oedema, hypertension and excoriations on the skin: CKD
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12
Q

What investigations should you do to investigate anaemia

A 
Haemoglobin
Mean Cell Volume (MCV)
B12
Folate
Ferritin
Blood film
? OGD/Colonoscopy for IDA
? bone marrow biopsy
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13
Q

Why do we need iron

A
  • Bone marrow requires iron to produce Hb

- Iron is mainly absorbed in the duodenum and jejunum

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14
Q

Why might patients be iron deficient

A
  • Insufficient dietary iron
  • Iron requirements increase (e.g. pregnancy)
  • Iron is being lost (e.g. slow bleeding from a colon cancer)
  • Inadequate iron absorption
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15
Q

Why do PPIs and antacids cause iron deficient anaemia

A
  • acid from the stomach keeps the iron in the soluble ferrous (Fe2+) form.
  • When the acid drops it changes to the insoluble ferric (Fe3+) form so it can’t be absorbed
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16
Q

Causes of iron deficient anaemia

A
  • Blood loss (most common cause in adults e.g. menorrhagia)
  • Dietary Insufficiency (most common cause in growing children)
  • Poor iron absorption (inflammation of bowel)
  • Increased requirements during pregnancy
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17
Q

What is Total iron binding capacity (TIBC)

A

is directly related to the amount of transferrin in the blood which is the carrier protein for ferric ions (Fe3+)

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18
Q

What is Transferrin saturation

A
  • good indication of the total iron in the body

- Normal adults about 30%

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19
Q

In iron deficient anaemia, what do transferrin levels & TIBC do

A

Increase

decrease in iron overload

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20
Q

What is ferritin

A
  • form that iron takes when it is deposited and stored in cells
  • marker of inflammation
  • Low in iron deficient anaemia
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21
Q

What is a normal serum ferritin level

A

41 – 400 ug/L

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22
Q

What is a normal Total Iron Binding Capacity

A

45 – 80 μmol/L

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23
Q

What is a normal transferrin saturation

A

15 – 50%

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24
Q

What is the management of iron deficient anaemia

A 
- If unclear cause OGD & colonoscopy
If symptomatic:
- Blood transfusion
- Iron transfusion (avoid during sepsis, iron feed bacteria)
- Oral iron: ferrous sulphate
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25
Q

How quickly does the Hb rise when treating an IDA

A

10 grams/litre per week.

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26
Q

What is Penicious anaemia

A
  • Autoimmune vitamin B12 deficiency where antibodies are created against the parietal cells in the stomach which produce intrinsic factors which allows Vitamin B12 to be absorbed in the ileum
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27
Q

What neurological symptoms can a vitamin B12 deficiency cause

A

Peripheral neuropathy with numbness or paraesthesia (pins and needles)
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes

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28
Q

Which autoantibodies should you test for if suspecting pernicious anaemia

A
  • Intrinsic factor antibody: first line

- Gastric parietal cell antibody: can be tested but is less helpful

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29
Q

What is the management of Vitamin B12 deficiency due to dietary issues

A

oral replacement with cyanocobalamin

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30
Q

What is the management of pernicious anaemia

A
  • 1mg of intramuscular hydroxycobalamin 3 times weekly for 2 weeks, then every 3 months
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31
Q

Why must you always treat a folate deficiency AFTER a vitamin B12 deficiency is treated, why?

A

Treating patients with folic acid when they have a B12 deficiency can lead to subacute combined degeneration of the cord.

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32
Q

What is haemolytic anaemia

A
  • destruction of red blood cells (haemolysis) leading to anaemia
  • Can be inherited fragility of RBC leading to faster break down (chronic haemolytic anaemia)
  • Can be acquired increased break down of RBC
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33
Q

Example of inherited haemolytic anaemia

A 
Hereditary Spherocytosis
Hereditary Elliptocytosis
Thalassaemia
Sickle Cell Anaemia
G6PD Deficiency
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34
Q

Examples of acquired haemolytic anaemias

A 
Autoimmune haemolytic anaemia
Alloimmune haemolytic anaemia (transfusions reactions and haemolytic disease of newborn)
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolysis
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35
Q

What are the key features of RBC break down

A
  • Anaemia: reduction in circulating red blood cells
  • Splenomegaly: spleen becomes filled with destroyed RBCs
  • Jaundice: bilirubin is released during the destruction of RBCs
36
Q

What investigations should be done if suspecting a haemolytic anaemia

A

FBC: shows a normocytic anaemia
Blood film: schistocytes (fragments of red blood cells)
- Direct Coombs test: positive in autoimmune haemolytic anaemia

37
Q

What is Hereditary Spherocytosis

A
  • most common inherited haemolytic anaemia in northern Europeans
  • autosomal dominant condition
  • sphere shaped red blood cells that are fragile and easily break down when passing through the spleen.
38
Q

What is the presentation of Hereditary Spherocytosis

A
  • jaundice
  • gallstones
  • splenomegaly
  • aplastic crisis in the presence of parvovirus.
39
Q

How do you diagnose Hereditary Spherocytosis

A
  • FBC
    • mean corpuscular haemoglobin concentration (MCHC)
      raised
    • Reticulocytes: raised
  • Blood film: spherocytes
  • FH
40
Q

How do you treat hereditary spherocytosis

A
  • folate supplementation
  • splenectomy
  • Cholecystectomy if gallstones
41
Q

What is Hereditary Elliptocytosis

A
  • very similar to hereditary spherocytosis except that the red blood cells are ellipse shaped.
  • autosomal dominant
  • Presentation and management are the same.
42
Q

What is G6PD Deficiency

A
  • defect in the red blood cell enzyme G6PD.
  • common in Mediterranean and African patients
  • X linked recessive
  • causes crises that are triggered by infections, medications or fava beans (broad beans).
43
Q

Presentation of G6PD Deficiency

A
  • jaundice (usually in the neonatal period)
  • gallstones
  • anaemia
  • splenomegaly
44
Q

How do you diagnose G6PDDeficiency

A
  • Heinz bodies on blood film

- G6PD enzyme assay.

45
Q

Which medications trigger haemolysis in G6PD deficiency

A
  • primaquine (an antimalarial)
  • ciprofloxacin
  • sulfonylureas
  • sulfasalazine and other sulphonamide drugs
46
Q

What is Autoimmune Haemolytic Anaemia (AIHA)

A
  • antibodies are created against the patient’s RBCs & destroys them
  • There are two types based on the temperature at which the auto-antibodies function to cause the destruction of red blood cells - Warm and cold
47
Q

What is Warm type autoimmune haemolytic anaemia

A
  • More common type
  • Haemolysis occurs at normal or above normal temperatures
  • Usually idiopathic, meaning that it arises without a clear cause.
48
Q

What is the Management of autoimmune haemolytic anaemia

A

Blood transfusions
Prednisolone (steroids)
Rituximab (a monoclonal antibody against B cells)
Splenectomy

49
Q

What is cold type autoimmune haemolytic anaemia (cold agglutinin disease)

A
  • <10ºC the antibodies against RBCs attach themselves to eachother & cause them to clump together - agglutination
  • agglutination results in the destruction of the red blood cells as the immune system is activated against them and they get filtered and destroyed in the spleen.
  • Often secondary to something else
50
Q

What other conditions may trigger cold type autoimmune haemolytic anaemia

A
  • lymphoma
  • leukaemia
  • systemic lupus erythematosus
  • infections e.g. mycoplasma, EBV, CMV and HIV.
51
Q

What is Microangiopathic Haemolytic Anaemia (MAHA)

A
  • small blood vessels have structural abnormalities that cause haemolysis of the blood cells travelling through them. Imagine a mesh inside the small blood vessels shredding the red blood cells.
  • This is usually secondary to an underlying condition:
52
Q

What underlying condition can result in Microangiopathic Haemolytic Anaemia (MAHA)

A

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

53
Q

What is Prosthetic Valve Haemolysis

A
  • Haemolytic anaemia due to prosthetic heart valves
  • occurs in both bioprosthetic and metallic valve replacement
  • caused by turbulence around the valve and collision of red blood cells with the implanted valve.
54
Q

What is the management of prosthetic valve haemolysis

A

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

55
Q

What is sickle cell anaemia

A
  • genetic condition that causes sickle (crescent) shaped red blood cells
  • Fetal haemoglobin is replaced with Sicke haemoglobin instead of adult around 6 weeks
  • This makes the red blood cells fragile and more easily destroyed leading to an haemolytic anaemia
56
Q

What type of genetic inheritance is sickle cell disease

A
  • automsal recessive
  • abnormal gene for beta-globin on chromosome 11
  • One copy of the gene results in sickle-cell trait (usually asymptomatic)
57
Q

Whta is sickle cell disease thought to give an advantage against

A
  • Malaria

- More common in people from Africa, India, the Middle East and the Caribbean

58
Q

What are the complications of sickle cell disease

A 
Anaemia
Increased risk of infection
Stroke
Avascular necrosis in large joints such as the hip
Pulmonary hypertension
Painful and persistent penile erection (priapism)
CKD
Sickle cell crises
Acute chest syndrome
59
Q

How do you diagnose sickle cell disease

A
  • Blood film
  • High risk patients offered screening during early pregnancy
  • newborn screening heel prick test at 5 days of age.
60
Q

What is the general management of Sickle cell disease

A
  • Avoid dehydration and other triggers of crises
  • Ensure vaccines are up to date
  • Antibiotic prophylaxis: phenoxymethypenicillin
  • Hydroxycarbamide: stimulate production of fetal haemoglobin (HbF).
  • Blood transfusion for severe anaemia
  • Bone marrow transplant can be curative
61
Q

Why do patients with sickle cell disease get given Hydroxycarbamide

A
  • stimulates production of fetal haemoglobin (HbF)
  • Fetal Hb does not lead to sickling of red blood cells
  • protective effect against sickle cell crises and acute chest syndrome.
62
Q

What is a sickle cell crisis

A
  • Umbrella term for an acute crisis related to the condition
  • Can be mild to life threatening
  • Triggered by various things
63
Q

What can cause a sickle cell crisis

A

Can occur spontaneously or be triggered by stresses:

  • infection
  • dehydration
  • cold
  • significant life events.
64
Q

What is the management of a sickle cell crisis

A
  • low threshold for admission to hospital
  • Treat any infection
  • Keep warm
  • Keep well hydrated (IV fluids may be required)
  • Simple analgesia such as paracetamol and ibuprofen
  • Penile aspiration in priapism
  • Avoid NSAIDs where there is renal impairment
65
Q

What is a Vaso-occlusive Crisis (AKA painful crisis)

A
  • sickle shaped blood cells clogging capillaries causing distal ischaemia
  • associated with dehydration and raised haematocrit. y
66
Q

What are the symptoms of a Vaso-occlusive Crisis (AKA painful crisis)

A
  • Pain
  • fever
  • symptoms of infection
  • Priapism
67
Q

What is priapism

A

trapping blood in the penis causing a painful and persistent erection. This is a urological emergency and is treated with aspiration of blood from the penis.

68
Q

What is a Splenic Sequestration Crisis

A
  • RBCs blocking blood flow within the spleen
  • causes an acutely enlarged and painful spleen.
  • The pooling of blood in the spleen can lead to a severe anaemia and circulatory collapse (hypovolaemic shock)
69
Q

What is the management of a Splenic Sequestration Crisis

A
  • considered an emergency
  • supportive with blood transfusions and fluid resuscitation to treat anaemia and shock.
  • splenectomy if recurrent crises
70
Q

What is an aplastic crisis

A
  • temporary loss of the creation of new blood cells
  • triggered by infection with parvovirus B19
  • Management is supportive with blood transfusions
  • Usually resolves within a week
71
Q

How do you diagnose Acute chest syndrome

A

Must have:

  • Fever or respiratory symptoms with
  • New infiltrates seen on a chest xray
72
Q

What can cause acute chest syndrome

A
  • due to infection (e.g. pneumonia or bronchiolitis)

- non-infective causes (e.g. pulmonary vaso-occlusion or fat emboli).

73
Q

How do you manage Acute chest syndrome

A
  • Medical emergency, high mortality rate
  • Antibiotics or antivirals for infections
  • Blood transfusions for anaemia
  • Incentive spirometry using a machine that encourages effective and deep breathing
  • Artificial ventilation with NIV or intubation may be required
74
Q

What is Thalassaemia

A
  • Genetic defect in the protein chains that make up haemoglobin, either alpha or beta globin chains
  • Both autosomal recessive
  • RBCs are more fragile and break down more easily which are collected in the spleen causing splenomegaly
75
Q

Why are patients with thalassamia more likely to be susceptible to fractures

A
  • bone marrow expands to produce extra red blood cells to compensate for the chronic anaemia.
  • causes a susceptibility to fractures and prominent features such e.g. pronounced forehead and malar eminences (cheek bones).
76
Q

What are the signs and symptoms of thalassaemia

A 
Microcytic anaemia 
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
Poor growth and development
Pronounced forehead and malar eminences
77
Q

How do you diagnose Thalassaemia

A
  • FBC: microcytic anaemia.
  • Haemoglobin electrophoresi: globin abnormalities.
  • DNA testing
  • Full blood count shows a microcytic anaemia.
  • Pregnant woman screened at booking
78
Q

Why do people with Thalassaemia get iron overload

A
  • faulty creation of red blood cells
  • recurrent transfusions a
  • increased absorption of iron in response to the anaemia
  • Therefore, ferritin must be monitored
  • Prevent by limit transfusions and iron chelation
79
Q

What are the signs and symptoms of iron overload

A 
Fatigue
Liver cirrhosis
Infertility and impotence
Heart failure
Arthritis
Diabetes
Osteoporosis and joint pain
80
Q

What is alpha thalassaemia

A
  • defects in alpha globin chains

- gene coding for this protein is on chromosome 16.

81
Q

What is the 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
82
Q

What is beta thalassaemia

A
  • defects in beta globin chains
  • gene coding for this protein is on chromosome 11.
  • Can either be abnormal copies that retain some function or deletion genes where there is no function
  • Three types of beta thalassaemia: Minor, intermedia, major
83
Q

What is Thalassaemia minor

A
  • one abnormal and one normal gene.
  • mild microcytic anaemia
  • usually patients only require monitoring and no active treatment.
84
Q

What is Thalassaemia major

A
  • homozygous for the deletion genes
  • no functioning beta globin genes at all
  • most severe form: severe anaemia and failure to thrive in early childhood.
85
Q

What does thalassaemia major cause

A

Severe microcytic anaemia
Splenomegaly
Bone deformities

86
Q

What is the management of thalassaemia major

A
  • involves regular transfusions
  • iron chelation
  • splenectomy
  • Bone marrow transplant can potentially be curative.
87
Q

What is Thalassaemia intermedia

A
  • Two abnormal copies of the beta globin gene
  • can be either two defective genes or one defective gene and one deletion gene.
  • Causes microcytic anaemia, needs monitoring and may require treatment

Haematology (4 decks)

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