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Block 34 - Metabolic > Anaemias > Flashcards

Anaemias Flashcards

1
Q

Define anaemia.

A

Anaemia is defined as a Hb level 2 standard deviations below the normal for age and sex.

Reference ranges for Hb are:

Male = 130-180g/L
Female = 115-165g/L
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2
Q

What are the following classifications of anaemia defined as:

1) Microcytic
2) Normocytic
3) Macrocytic

A

These are categories based upon the MCV of a cell.

1) Microcytic = <80fL
2) Normocytic = 80-100fL
3) Macrocytic = >100fL

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3
Q

1) As well as EPO, what two other hormones aid in the production of RBCs?
2) What are the main characteristics of a megaloblastic anaemia?
3) What are megalocytes?

A

1) Thyroid hormones and andreogens.
2) There is the presence of megalocytes and hyperhsegmented neutrophils.
3) Immature cells with large nuclei occurring due to abnormal DNA synthesis.

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4
Q

Name the 5 causes of microcytic anaemia.

A 
Thalassaemia
Anaemia of chronic disease (initially normocytic but eventually microcytic)
Iron deficiency anaemia
Lead poisoning
Sideroblastic

**Use the mnemonic TAILS.

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5
Q

How can the following classes of anaemia be further categorised:

1) microcytic
2) normocytic
3) macrocytic

A

1) Using iron studies
2) Reticulocyte count (hyper proliferative/ hypo proliferative)
3) Megaloblastic and non-megaloblastic.

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6
Q

Name 7 causes of microcytic anaemia.

A 
B12 deficiency
Folate deficiency
Drug induced anaemia
Alcohol abuse
Hypothyroidism
Pregnancy
Myelodysplastic syndromes
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7
Q

Name 5 causes of normocytic anaemia.

A 
Haemolytic anaemias
Haemorrhage
Leukaemia
Aplastic anaemia
Pure red cell aplasia
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8
Q

How can hyper proliferative or hypoproliferative normocytic anaemias be identified?

A

By using the reticulocyte count:

> 2% reticulocytes = hyperproliferative
<2% reticulocytes = hypoproliferative

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9
Q

1) Name the normocytic anaemias which are hypoproliferative.

2) Name the normocytic anaemias which are hyperproliferative.

A

1) Leukaemias, aplastic anaemias, pure red cell aplasia.

2) Haemolytic anaemias, haemorrhage.

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10
Q

Which of the causes of microcytic anaemias cause:

1) Megaloblastic anaemia.
2) Non-Megaloblastic anaemia.

A

1) B12 deficiency, Folate deficiency and drug induced anaemia (Methotrexate).
2) Alcohol abuse, pregnancy, hypothyroidism and myelodysplastic syndromes.

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11
Q

What would iron studies show in iron deficiency anaemia?

A

LOW serum iron
LOW ferritin
HIGH transferrin/ TIBC

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12
Q

What would iron studies show in anaemia of chronic disease?

A

LOW serum iron
NORMAL/HIGH ferritin
LOW transferrin/ TIBC

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13
Q

State 10 potential signs or symptoms which could occur in a patient presenting with anaemia.

A 
SOB/SOBOE
Fatigue
CPx/ palpitations
Syncope
Pallor/ conjunctival pallor
Headaches
Abdominal pain (hepatosplenomegaly)
Angular chelitis
Glossitis
Koilonychia
Pica
Neurological symptoms
Scleral icterus

**There may also be signs or symptoms of a disease which is causing the anaemia.

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14
Q

1) Where is iron absorbed?
2) How does iron travel in the blood?
3) Where and how is iron stored?
4) How is iron destroyed?
5) What are iron levels regulated by?

A

1) Duodenum.
2) Bound to transferrin.
3) Stored in the liver bound to ferritin.
4) Destroyed by reticuloendothelial macrophages, often in the spleen.
5) Hepcidin which is made in the liver and regulates iron absorption.

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15
Q

What are the 4 categories of causes for iron deficiency anaemia?

A

Decreased intake
Decreased absorption
Increased loss
Increased demand

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16
Q

1) What is the most common cause of iron deficiency anaemia worldwide?
2) In whom does iron deficiency anaemia tend to occur due to decreased intake?

A

1) Decreased intake.
2) In infants as breast milk is low in iron. In vegetarians whose iron intake is mainly non-ahem iron which is much harder to absorb.

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17
Q

Describe the two causes of iron deficiency anaemia which occurs due to decreased absorption.

A

1) Any disease affecting the duodenum (IBD, coeliac) as these cause inflammation and destruction of duodenal cells.
2) Gastrectomy as after this surgery there is a decrease in stomach acid.

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18
Q

Describe what might cause iron deficiency anaemia to occur through increased loss.

A

1) Menorrhagia (14% women get IDA due to menstruation).

2) Haemorrhage (GI ulcer, malignancy or hookworm) which causes chronic slow bleeding.

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19
Q

When might iron deficiency anaemia occur due to increased demand?

A

1) In children and adolescents due to rapid growth and increasing blood volume.
2) Can happen during pregnancy due to increased iron requirements for foetal development.

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20
Q

Describe the 4 important pieces of NICE guidance which must be adhered to with regards to certain patient groups receiving a diagnosis of iron deficiency anaemia.

A

1) All men with IDA get a GI referral.
2) All people >50 with IDA get a GI referral.
3) People >60 with IDA get 2ww referral to gastro.
4) People <50 with PR bleeding get a 2ww referral to gastro.

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21
Q

Name 3 signs or symptoms which can be specific to iron deficiency anaemia.

A 
Koilonychia
Atrophic glossitis
Angular chelitis
Hair loss
Pica
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22
Q

What is often first line management for patients with iron deficiency anaemia?

A

Oral iron supplements (after advice about increased dietary intake).

Prescribe all people with iron deficiency anaemia oral ferrous sulfate 200 mg tablets two or three times a day — treatment should continue for 3 months after iron deficiency is corrected to allow stores to be replenished.

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23
Q

What treatment options are available for patients with iron deficiency anaemia if oral ferrous sulphate is not tolerated?

A

1) Different preparation of iron (Ferrous fumarate/ ferrous gluconate).
2) IV iron
3) Blood transfusion

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24
Q

How should patients with IDA on oral supplements be monitored?

A

Recheck haemoglobin levels (full blood count) after 2–4 weeks of iron supplement treatment to assess the person’s response. The haemoglobin concentration should rise by about 2 g/100 mL over 3–4 weeks.

Continue treatment for 3 months once FBC normal.

Then monitor FBC 3 monthly for a year, and then check after a further year.

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25
Q

1) What is the second most common type of anaemia worldwide?

2) What does anaemia of chronic disease tend to be caused by?

A

1) Anaemia of chronic disease (this is also the most common type of anaemia seen in hospital inpatients).
2) Continuous systemic inflammation occurring due to chronic disease.

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26
Q

Name 4 potential causes of anaemia of chronic disease.

A

1) Infections
2) Malignancy
3) DM
4) Autoimmune disorders (RA/ SLE)

**Can also be due to renal failure and vasculitis.

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27
Q

1) What happens in thalassaemia?
2) What is the inheritance pattern of thalassaemia?
3) How does thalassaemia cause anaemia?
4) When does thalassaemia often present?

A

1) There is an abnormality in the production of Hb chains.
2) Autosomal recessive inheritance pattern.
3) Due to ineffective erythropoiesis and early cell destruction.
4) In childhood as there is a congenital abnormality.

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28
Q

What happens in Sideroblastic anaemia?

A

RBCs cannot integrate iron into haemoglobin and so the iron remains in the cell cytoplasm, causing the RBC to be dysfunctional.

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29
Q

1) How does sideroblastic anaemia appear histologically?

2) What does sideroblastic anaemia present very similarly to?

A

1) With ringed sideroblasts on a blood smear (iron-engorged perinuclear mitochondria).
2) Haemochromatosis.

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30
Q

1) What organ does lead poisoning mainly affect?
2) Which form of anaemia can lead poisoning cause and how?
3) Where might a patient be exposed to lead occupationally?

A

1) The brain.
2) Sideroblastic anaemia: lead poisoning denatures enzymes which can result in sideroblastic anaemia.
3) Manufacturing radiation shields, ammunition or surgical equipment and in plumbing.

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31
Q

Why can ferritin sometimes be raised in a patient with anaemia of chronic disease?

A

Because ferritin is an inflammatory marker and anaemia of chronic disease is often caused by long-running inflammatory conditions.

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32
Q

1) What is a main condition which is harmful which can cause a normocytic anaemia?
2) What FBC abnormalities might aplastic anaemia cause?
3) What FBC abnormalities might pure red cell aplasia cause?

A

1) Bone marrow failure.
2) A pancytopenia.
3) Anaemia (shouldn’t affect other myeloid cell production).

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33
Q

1) Name a condition which can lead to aplastic anaemia.

2) Name a condition which can lead to pure red cell aplasia.

A

1) Fanconi’s anaemia.

2) Diamond black fan anaemia.

34
Q

In a patient with normocytic anaemia, what do you need to check and why?

A

Reticulocyte count.

If reticulocyte count is elevated, this shows that the marrow is functioning properly.

If reticulocyte count is not elevated, then this is a sign that the marrow is not functioning properly and could suggest bone marrow failure.

35
Q

Name and describe the 3 main causes of B12 deficiency.

A

1) Malabsorption: pernicious anaemia and IBD.
2) Poor dietary intake: veganism (only get B12 from meat and dairy).
3) Gastrectomy/ gastric bypass: food passes through the stomach too quickly so intrinsic factor cannot bind to B12.

**Pernicious anaemia is the main cause of B12 deficiency.

36
Q

Name and describe the 4 main causes of folate deficiency.

A

1) Poor dietary intake: elderly and alcoholics.
2) Increased demand: haemolysis and pregnancy.
3) Malabsorption.
4) Antifolate drugs: for example, methotrexate.

**Folate deficiency is mainly caused by dietary problems. Can be caused by decreased dietary intake for >6 weeks.

37
Q

Where are the following dietary components absorbed?

1) B12
2) Iron
3) Folate

A

1) Terminal ileum.
2) Duodenum.
3) Jejunum.

38
Q

1) What is B12 used for?
2) Name the group of symptoms which can occur specifically in patients with B12 deficiency.
2a) Give examples of some of these symptoms.

A

1) Used to synthesis thymidine which is needed for DNA.
2) Neurological symptoms.
2a) Confusion, drowsiness, poor concentration and poor memory.

**Can also cause psychosis, depression and irritability.

39
Q

How can neurological impairment happen in patients with B12 deficiency?

A

In B12 deficiency, there are increased levels of methylmalonic acid which builds up in the myelin sheaths of neurons. This slows down communication between neurons, causing neurological impairment.

40
Q

Why does glossitis occur in patients with b12 deficiency?

A

Because the normally fast dividing epithelial cells of the tongue mucosa aren’t replaced after normal wear and tear, leading to inflammation.

41
Q

What causes atherosclerosis to occur in patients with B12 deficiency?

A

There are increased levels of homocysteine which binds to blood vessel endothelium. This causes inflammation and attracts leukocytes which leads to atherosclerosis.

42
Q

What happens pathophysiologically in patients with pernicious anaemia?

A

There is increased production of IgA antibodies against intrinsic factor/ parietal cells.

43
Q

1) Presence of which type of antibodies would suggest pernicious anaemia?
2) How would B12 deficiency with a dietary cause be treated?
3) How should B12 deficiency with a malabsorptive cause be treated?

A

1) Anti-intrinsic factor antibodies.
2) B12 supplements.
3) With very high dose oral B12 to encourage passive diffusion or IM B12 injections for a couple of months.

44
Q

What is the classic triad or signs/ symptoms associated with subacute degeneration of the spinal cord?

A

1) Extensor plantars (UMN)
2) Absent knee jerk reflexes (LMN)
3) Absent ankle jerk reflexes (LMN)

45
Q

In subacute degeneration of the cord:

1) Which senses are often affected first?
2) What causes LMN signs?
3) What causes UMN signs?
4) Why do pain and temperature sensation remain intact?

A

1) Joint position and vibration senses, leading ataxia.
2) Posterior dorsal column loss causes sensory and LMN signs.
3) Corticospinal tract loss causes motor and UMN signs.
4) Because the spinothalamic tract is preserved.

46
Q

1) How do the effects of folate deficiency vary between age groups?
2) What is folate required for in a foetus?

A

1) Can cause anaemia in all age groups, or neural tube malformation in a foetus.
2) Closure of the anterior and posterior neuropores of the neural tube on 23rd and 26th days of gestation.

47
Q

What conditions can result if:

1) the anterior pore of the neural tube in a foetus doesn’t close?
2) the posterior pore of the neural tube in a foetus doesn’t close?

A

1) Anencephaly.

2) Spina Bifida.

48
Q

1) What is haemolytic anaemia?

2) What are the two types of haemolytic anaemia?

A

1) Anaemia which occurs due to the premature destruction of RBCs, reducing their lifespan to <100 days.
2) Intravascular or extravascular.

49
Q

1) What is intravascular haemolytic anaemia?
2) What is extravascular haemolytic anaemia?
3) What clinical finding can often be found in patients with intravascular haemolytic anaemia?

A

1) Where RBCs are broken down in the blood vessels.
2) Where RBCs are broken down in the reticuloendothelial system (mainly in the spleen).
3) Haemosiderinuria - brown coloured urine occurring due to the presence of iron from the haem (normally seen 3-4 days after onset of haemolytic conditions).

50
Q

What are the classic blood result findings for a patient with haemolytic anaemia?

A 
HIGH LDH
HIGH globin
HIGH iron
HIGH unconjugated bilirubin
LOW haptoglobin
51
Q

What are the 3 congenital causes of haemolytic anaemia?

A

1) Membrane abnormalities
2) Metabolic machinery abnormalities
3) Haemoglobin molecule abnormalities (haemoglobinopathies).

52
Q

Describe an example of a haemolytic anaemia caused by membrane abnormalities.

A

Hereditary spherocytosis.
These RBCs are destroyed by the reticuloendothelial system because of abnormal morphology.

RBCs are circular. There is low Hb and raised reticulocytes.

53
Q

Describe an example of a metabolic machinery abnormality which can cause haemolytic anaemia.

A

G6PD deficiency.

G6PD normally protects RBCs from metabolic stress. Lack of G6PD = lack of ATP = lack of energy = cells cannot maintain shape or function properly = RBCs broken down.

54
Q

Describe an example of a haemoglobinopathy which can cause haemolytic anaemia.

A

Sickle cell anaemia and Thalassaemia are both haemoglobinopathies.

In SCA, low O2 saturations cause RBCs to sickle.

In Thalassaemia, there is impaired production of alpha or beta Hb chains, causing RBC malformation.

Both these conditions lead to early cell destruction by the RES.

55
Q

How can acquired causes of haemolytic anaemia be further classified?

A

Immune: warm/ cold autoimmune haemolytic anaemia (AIHA).

Non-Immune: Anything which can cause damage to RBCs.

56
Q

1) What can G6PD deficiency be exacerbated by?
2) What is a finding which is pathognomonic of G6PD deficiency?
3) What is the inheritance pattern for G6PD deficiency?
4) When should haemolytic anaemia be suspected in a patient?

A

1) Certain medications.
2) Heinz bodies are specific findings on blood film in G6PD deficiency.
3) X-linked recessive disorder.
4) When a patient presents with signs and symptoms of anaemia AND jaundice.

57
Q

Name 3 causes of acquired non-immune haemolytic anaemia.

A

1) Mechanical trauma: metallic heart valves, MAHA, TTP.
2) Infections: Malaria, clostridium perfringens.
3) Hypersplenism: liver cirrhosis.

58
Q

Describe warm autoimmune haemolytic anaemia.

A

Tends to cause haemolysis at body temperature.
IgG antibodies attack RBC membranes.
Usually indicates a more serious underlying condition.

59
Q

Describe cold autoimmune haemolytic anaemia.

A

Usually occurs at temperatures below normal body temperature.
IgM antibodies induce RBC destruction.
Associated with Raynaud’s disease.

60
Q

Name 3 conditions that warm AIHA can be associated with.

A

CLL
Lymphomas
SLE

61
Q

Name 3 conditions that cold AIHA can be associated with.

A

Mycoplasma pneumoniae
Infectious mononucleosis
Lymphomas

**Most commonly associated with infections.

62
Q

What are the 3 categories of presenting features for haemolytic anaemia?

A

Sx of anaemia
Sx of haemolysis
Sx of the underlying cause

63
Q

Name 3 signs or symptoms of haemolytic anaemia due to haemolysis.

A

Jaundice
Gallstones
Dark urine
Splenomegaly

64
Q

What is sickle cell anaemia?

A

A disease of the RBCs caused by an autosomal recessive single gene defect in the beta chain of Gb, resulting in the formation of HbS.

65
Q

How can SCA lead to infarctions?

A

Due to the abnormal shape of the sickled cells. They cannot mould to pass through small capillaries, so they clump together and occlude small vessels.

66
Q

Describe the mutation which leads to SCA.

A

There is an amino acid substitution where Glutamine is replaced by Valine.

67
Q

How can sickle cell anaemia present in:

1) infants and children
2) adults

A

1) Dactylitis (painful swollen digits on hands and feet).

2) Vaso-occlusive crises

68
Q

What are 3 ways that sickle cell anaemia can be diagnosed?

A

1) Newborn blood spot screen.
2) Blood smear.
3) Protein electrophoresis.

**Should aim for diagnosis at birth to allow for prompt pneumococcal prophylaxis.

69
Q

What is the most deadly presentation of sickle cell anaemia and what happens?

A

Acute chest syndrome.

Hypoxia leads to necrosis of the lung which leads to pulmonary HTN.

70
Q

1) How is acute chest syndrome diagnosed?

2) How is acute chest syndrome treated?

A

1) Diagnosed in a patient with fever or respiratory symptoms with the presence of new infiltrates on XR in a patient with SCA.
2) Abx, oxygen, blood transfusion, ventilation if necessary.

71
Q

1) What is the most common cause of osteomyelitis in a patient with sickle cell anaemia?
2) What is the most common cause of osteomyelitis in a patient without SCA?

A

1) Salmonella (SCA patients can be more susceptible to encapsulated bacteria).
2) Staphylococcus aureus.

72
Q

1) What treatment can be given to a patient with SCA who suffers frequent crises?
2) Why is this treatment useful?

A

1) Hydroxycarbamide.
2) Because it allows for increased production of HbF which can reduce the frequency of vast-occlusive crises. This is not first line.

73
Q

Describe some of the management steps required when treating a patient with a sickle cell crisis.

A 
Prompt generous analgesia.
X-match blood. 
FBC and reticulocyte count.
Septic screen.
IV fluids.
Keep patient warm.
Consider antibiotics if needed. 
Blood transfusion. 
O2 if needed.
74
Q

In a patient with sickle cell anaemia, how might the following test results look?

1) Hb
2) MCV
3) Reticulocyte count

A

1) Low
2) Normal
3) Raised

75
Q

1) What is the mainstay of treatment for SCA aimed at?

2) State 3 ways that are used to try and prevent sickling.

A

1) Aimed at prophylaxis to stop sickling from occurring.
2) Avoid dehydration, keep vaccines up to date, penicillin V prophylaxis. Essentially help to avoid hypoxia/ acidosis which can exacerbate sickling.

76
Q

What is hereditary haemochromatosis?

A

An iron storage disorder resulting in excessive total body iron and deposition of iron into tissues.

It is a multi-system disease.

77
Q

1) What is the inheritance pattern of hereditary haemochromatosis?
2) What is often the first organ to be affected in patients with hereditary haemochromatosis?
3) How is a definitive diagnosis of hereditary haemochromatosis made?

A

1) Autosomal recessive.
2) The liver is often the first organ to be affected and hepatomegaly is a common clinical finding.
3) HFE genetic testing

78
Q

What happens pathophysiologically in patients with hereditary haemochromatosis?

A

Mutation in human haemochromatosis gene which regulates hepcidin.
Hepcidin regulates absorption of iron from duodenum.
In this condition, hepcidin levels are low and so there is not regulation of iron absorption from the duodenum.
Therefore, the body keeps on absorbing large amounts of iron unnecessarily.

79
Q

What is the classic triad of clinical features for patients with hereditary haemochromatosis?

A

DM
Bronze skin
Hepatomegaly

**Men can have ED because haemochromatosis can cause pituitary dysfunction.

80
Q

1) What is the treatment required for hereditary haemochromatosis?
2) What main conditions do you need to monitor for in patients with hereditary haemochromatosis?

A

1) Venesection.
2) Liver cirrhosis and liver cancer (HH is a big risk factor for these) and this is done through liver biopsy. Also monitor for DM.

81
Q

How might the results for the following tests look in a patient with hereditary haemochromatosis?

1) Serum iron.
2) Ferritin.
3) Transferrin.

A

1) Elevated in 90%.
2) Elevated.
3) Low.

**Transferrin is low as the body doesn’t need to transport iron around as much are there are large quantities of it everywhere.

Block 34 - Metabolic (18 decks)

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