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Haemotology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is anaemia?

A

Anaemia is a drop in the haemoglobin level below the normal range
appropriate for the patient as for age, gender and race

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2
Q

What are the general signs of anaemia?

A
  • Fatigue
  • Weakness
  • Pale or yellowish skin
  • Irregular heartbeats
  • Shortness of breath – worse if underlying respiratory or
    cardiac disease
  • Dizziness or light-headedness
  • Chest pain – worse if underlying arterial disease
  • Cold hands and feet
  • Headache
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3
Q

What causes a normochromic, normocytic anaemia?

A

Blood loss - as volume is lost the Hb drops; the blood volume is replaced by non-red cells containing fluids, or plasma expansion
The colour and size of cells is still normal
Haemoglobin is measured as a concentration of red cells in plasma and not an absolute value

Anaemic of chronic disease/secondary anaemia

Anaemia of renal failure - deficiency of erythropoietin

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4
Q

How do we treat anaemia caused by blood loss?

A

If stable and lack of evidence for further bleeding - give patient ferrous sulphate

If patient unstable transfuse

Iron replacement: 1000ml of blood represents a loss of 500mg iron

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5
Q

What causes a macrocytic, normochromic anaemia?

A

B12 deficiency - most common

may also see thrombocytopaenia and neutropaenia - neutrophul hyper-segmentation on blood film

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6
Q

How do we assess acute blood loss?

A

Clinical signs of shock and visible volume of blood:

  • Pale and clammy
  • Pulse
  • BP
  • Level of consciousness
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7
Q

How do we remember if an anaemia is microcytic or macrocytic?

A
  • Erythrocytes get progressively smaller as they divide
  • They stop dividing then a normal mean cell harmoglovin concentration (MCH) is reached and the nucleus is extruded
  • Anything that reduces production of haemoglobin inside the developing erythrocyte encourages fewer divisions (Fe deficiency, thalassaemia) and the erythrocyte will be smaller (microcytic)
  • Anything that DELAYS nuclear development (reduce DNA synthesis: B12, folate deficiencies, chemotherapy) means fewer cell divisions take place before the final MCH is attained - cells end up larger (macrocytes)
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8
Q

What are the haematinic deficiencies?

A
  • Iron
  • B12
  • Folate

Not diseases themselves, they are symptoms of something underlying

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9
Q

What are the hypochromic microcytic anaemias?

A

Iron deficiency

  • Inadequate iron-containing foods in the diet
  • Malabsorption (coeliac disease, milk, tea)
  • Blood loss - from GI tract

Thalassaemia

  • Beta thalassaemia trait - carriers with 1 abnormal gene have beta thalassaemia minor - diagnosed by raised HbA2
  • Beta thalassaemia major has 2 abnormal genes and so has no HbA, only HbF
Alpha thalassaemia has 4 genes:
1 gene deleted = clinically silent
2 genes deleted = alpha thalassaemia trait
3 genes deleted = Haemoglobin H disease
4 genes deleted = Bart's Hydrops fetalis
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10
Q

What are the causes of iron deficiency anemia?

A

Causes:

Physiological:

  • Rapid growth
  • Menarche
  • Pregnancy

Neonatal:

  • Prematurity
  • Low birth weight
  • Blood loss (including early cord clamping)

Diet:
- Cow’s milk is commonest cause in toddlers but not in adults

GI tract:

  • Comonest GI causes include NSAIDS but in an OLDER MALE/POST-MENOPAUSAL FEMALE
  • Colonic and gastric cancers must be considered the likely cause until excluded

Others:

  • Hiatus hernis
  • H. pylori
  • Duodenal/gastric ulcers
  • Oesophageal varices
  • Meckel’s diverticulum
  • Coeliac disease
  • Polyposis coli
  • Milk enteropathy
  • Hereditary haemorrhagic telangiectasia
  • IBD
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11
Q

How is iron deficiency anaemia diagnosed and treated?

A

Diagnosis:

  • Usually easy
  • Low Hb, low MCV, low MCH
  • Ferritin assay#- Serum iron
  • Transferrin sturation
  • Zinc protoporphyrin
  • Gold standard is to give iron and watch for effect
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12
Q

What are the signs and symptoms of iron deficiency?

A
  • General symptoms of tiredness and lethargy
    More specific:
  • Headache, especially with activity
  • Craving for non-food items to eat (pica)
  • Sore or smooth tongue
  • Brittle nails or hair loss
  • Spoon-shaped nails (koilonychia)
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13
Q

What are the causes of an acquired B12 deficiency?

A

Nutritional:

  • Vegan
  • Poor diet
  • Pregnancy

Malabsorption:

  • Gastric: surgery, pernicious anaemia (IF and gastic parietal cell antibodies)
  • Intestine: ilieal resection, fish tapeworm, tropical sprue
  • Malabsorption but not deficiency: Crohn’s, coeliac, CF
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14
Q

What are the causes of an acquired folate deficiency syndrome?

A
  • Nutritional: poor diet, goat’s milk only
  • Intestinal: coeliac, jejunal resection
  • Excessive requirement: pregnancy, prematurity
  • Increased turnover: chronic haemolysis, severe skin disease
  • Drugs: methotrexate, anticonvulsants
  • Excess loss: dialysis
  • Miscellaneous: alcohol (beer is a good source of folate though)
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15
Q

What are the specific signs and symptoms of B12 deficiency?

A

B12

  • Insidious onset
  • Mild jaundice and anaemia
  • Glossitis (inflammation of the tongue)
  • Angular cheilitis (inflammation of corners of mouth)
  • Neuropathy: peripheral neuropathy, subacute degeneration of the cord (SADC), optic neuropathy, dementia
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16
Q

What are the specific signs and symptoms of a folate deficiency?

A

Folate

    • Insidious onset
  • Mild jaundice and anaemia
  • Glossitis (inflammation of the tongue)
  • Angular cheilitis (inflammation of corners of mouth)
  • Neuropathy: SENSORY peripheral neuropathy
  • Deficiency in pre-conception is associated with increased incidence of neural tube defects
17
Q

What are some causes (other than B12 and folate deficiencies) of macrocytic anaemia?

A
  • Alcohol
  • Pregnancy
  • Drugs (chemotherapy (antifolates, antipurines)
  • Anti HIV drugs
  • Liver disease
  • Raised reticulocyte count
  • Hypothyroidism
  • Myelodisplasia, including acuired sideroblastic anaemia
  • Aplastic anaemia and red cell aplasia
  • Hypoxia
  • Meyloma and other paraproteinaemias
18
Q

What is a haemolytic anaemia and how do we test for it?

A

Haemolytic anaemias
- Anaemia due to the destruction, rather than the underproduction, or RBC

Investigations:

  • FBC with reticulocytes
  • Blood film - essential
  • Bilirubin/lactic dehydrogenase (LDH)

Specific:

  • Coomb’s tests (DAT)
  • EMA-binding
  • Glucose-6-phosphate dehydrogenase level
  • Haemoglobin indentification (HPLC)
19
Q

What are the congenital and acquired haemolytic anaemias?

A

Congenital:

  • RBC membrane (hereditary elliptocytosis, hereditary spherocytosis)
  • RBC enzyme deficiencies (G6PD, pyruvate kinase)
  • RBC haemoglobin disorders (thalassarmias, sickle cells diease)

Acquired:

  • Autoimmune haemolydid (AIHA)
  • Microangiopathic haemolytic anaemia (HUS, TTP, DIC)
  • Drugs, infections, toxins
  • Copper deficiency (Wilson’s disease)
20
Q

What is hereditary spherocytosis and how is it diagnosed?

A

Hereditary spherocytosis

  • Commonest inherited red cell disorder in northern Europeans
  • Inherited abnormalities of red cell membrane proteins (spectric, actin)
  • Autosomal dominant
  • Micro-spherocytes and polychromatic macrocytes
  • Neonatal jaundice
  • Chronic haemolysis
  • Jaundice
  • Gallstones

Diagnosis:

  • Family history (positive in 75%)
  • FBC
  • Reticulocyte count
  • Blood film

If family history + FBC results + film examination are typical = no further investigations needed
If not: use EMA-Binding (specific test)

Treatment:

  • Give folic acid regularly
  • Often need splenectomy
21
Q

What is Glucose-6-Phosphate Dehydrogenase deficiency?

A 
Clinical findings:
- X-linked
- Usually well between attacks
- Often family history or history of neonatal jaundice
Sudden onset of:
- Feeling unwell and lack energy
- Become pale and yellow in colour
- Backache
- Dark coloured urine
Avoid:
BEANS: fava and broad beans
Drugs: 
- anti-malatials
- large doses of aspirin
- Chloramphenicol
- Dapsone
- Phenylhydrazine
- Nalidixic acid
- Nitrofurantoin
- Vitamin K
  • Moth balls??
22
Q

What is Sickle Cell disease?

A

Sickle cell disease

  • Beta globin variant
  • Co-dominant
  • Carriers (HbAS) normal
  • Usually HbSS
  • Auto-infarction of spleen with increased infection risk

Crises:

  • Painful
  • Chest
  • Abdominal
  • Stroke
23
Q

What is the long-term management of sickle cell disease?

A

Simple measures reduce indicidence of painful crises and infections:

  • Keep warm
  • Keep hydrated
  • Keep regular hours
  • Eat well
  • Take Penicillin and Folic acid

Penicillin and pneumovax

  • Pneumonia - important in UK
  • Malaria
  • Africa - death <5yr
24
Q

What are the complications of sickle cell disorder?

A

Complications of Sickle Cell

  • Stroke: blood supply to part of brain is cut off
  • Increased vulnerability to infection
  • Acute chest syndrome - lungs suddenly lose ability to breathe in oxygen (often due to infection)
  • Pulmonary hypertension - where the blood pressure inside blood vessels that connect the heart to the lungs becomes dangerously high
25
Q

How do we prevent stroke in sickle cell disease?

A

Stroke in sickle cell disease

Primary stroke prevention

  • Detect using transcranial doppler
  • Start regular transfusions

Secondary stroke prevention

  • Following a stroke or finding evidence of previous strokes(s) on MRI
  • Start regular blood transfusions

For both consider stem cell transplant

26
Q

What considerations should be taken when a patient with sickle cell disease has surgery?

A

Propensity to hypoxia:

  • Pre-existing anaemia
  • Pre-op dehydration
  • Anaesthesia
  • Operative blood loss

Stress of the surgery predisposes to crises

  • Fever
  • Post-op hypoxia
  • Post-op infection

These predispose to development of:

  • Painful crises
  • Acute chest syndrome
27
Q

What is the neonatal screening for sickle cell and thalassaemia?

A
  • Diagnose by 2 months of age
  • Show how to palpate the spleen and ask to take child to hospital if unwell and enlarged spleen
  • Prophylactic penicillin
28
Q

What is beta thalassaemia major?

A

Beta thalassaemia major

  • Inheritance of two abnormal beta thalassaemia genes
  • Severe anaemia fro 4-6 months of age (less foetal haemoglobin)
  • Management is based on long term blood transfusions and iron chelation or stem cell transplantation
  • Don’t start chelation too early - wait til Ferritin >1000 ug/L to avoid neuro and skeletal toxicity
29
Q

What is iron chelation?

A
  • Desferrioxamine
  • Desferal
  • > 12 hours of subcutaneous infusion up to 5 times a week
  • Painful
  • Often local inflammation
  • Efficacious in vitro but not in vivo - 1997 study?
  • Poor compliance
  • Potential neuro and skeletal toxicity
30
Q

What is Desferasirox (Exjade)?

A
  • Oral dissolvable preparation
  • Once daily usage
  • Minor GI tract side effects
  • Tolerated well
  • No neuro/skeletal toxicity
  • So good complicant
  • 24 hour chelation
  • First line >6years of age
  • Second line >2 years to <6 years
  • Expensive
31
Q

What is autoimmune haemolytic anaemia?

A

Acquired haemolytic anaemia - autoimmune

  • Two basic types (warm and cold) depending aon thermal range when antibody is actuve
  • Diagnosis is made by confirming haemolysis as usual but blood firm is usually critical in making the diagnosis
  • Followed by finding a positive direct antiglobulin test (DAT or Coomb’s)
  • DAT is positive for IgG in warm AIHA and for complement in cold AIHA
Warm:
- Idiopathic
- Secondary:
Rheumatoid disease (SLE etc)
Lymphoma
Chronic lymphatic leukaemia
Drugs (cephalospprins
Ovarian teratoma
Cold:
- Idiopathic
- Secondary:
EBV infection
Mycoplasma pneumoia
Ulcerative colitis
32
Q

How do we treat sickle cell crises?

A
  • Admit to hospital
  • Analgesia
  • IV fluids
  • Antibiotics
  • May need blood transfusion
  • Severe cases: red-cell exchange transfusion
33
Q

What are the two types of antiglobulin tests used for looking for antibodies to red blood cells?

A

Two types of Coomb’s test:

  1. Direct antiglobulin test
    Antibody in patient’s serum
    Used to cross match blood for transfusion suitability
    Positive test means tested donor red cells are incompatible and should not be given
  2. Direct antiglobulin test (DAT)
    Test is done much less often and detects antibody to patient’s own serum, causing an autoimmune haemolytic anaemia

Haemotology (2 decks)

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