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Cardiorespiratory 2 > Microcytic and haemolytic anaemia > Flashcards

Microcytic and haemolytic anaemia Flashcards

1
Q

why is vitamin B12 called cobalamin

A
  • it contains cobalt metal
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2
Q

Is vitamin B12 water soluble or not

A
  • water soluble
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3
Q

what can prolonged deficiency of vitamin B12 cause

A
  • Prolonged vitamin B12 deficiency can cause severe and irreversible nervous system damage
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4
Q

what can only slightly lower than normal levels of B12 cause

A
  • a range of symptoms such as fatigue, lethargy, depression, poor memory, breathlessness, headaches, and pale skin may be experienced, especially in elderly people
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5
Q

what is the function of B12

A
  • production of myelin
  • assits in DNA synthesis
  • Methionine synthase is an enzyme which uses B12 to transfer a methyl group from 5-methyltetrahydrofolate to homocysteine, thereby generating tetrahydrofolate (THF) and methionine
  • THF plays an important role in DNA synthesis so reduces the availability of te THF results in ineffective production of cells with rapid turnover in particular RBC
  • THF can be obtained from folate in the diet – this can compensate from the blood problems but not he brain problems
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6
Q

what anaemia does B12 cause

A
  • macrocytic
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7
Q

what are the two types of anaemia

A

megaloblastic and non-megaloblastic anaemia

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8
Q

how can B12 deficiency be measured

A
  • B12 deficiency can be measured clinically as an increased serum methylmalonic acid (MMA) level.
  • Unfortunately, this is not a foolproof test as not all who have increased MMA actually have B12 deficiency.
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9
Q

what part of B12 deficiency can be cured by folate

A
  • The reduced DNA synthetic effects of B12 deficiency can be resolved if sufficient dietary folate is present
  • However the reduced myelin synthesis seen with B12 deficiency is NOT cured by folate.
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10
Q

define megaloblastic anaemia

A

is macrocytic anaemia that results from inhibition of DNA synthesis during red blood cell production

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11
Q

describe vitamin B12

  • water soluble?
  • what food is it found in
  • is it destroyed by cooking
  • is deficiency indistinguishable from folate deficiency
  • require
  • store
  • absorption
A
  • Water soluble vitamin
  • Found in Meat, eggs, cheese animal protein
  • Not destroyed by cooking
  • Deficiency initially indistinguishable from folate deficiency
  • Requires – 1 ug/d
  • Store – 1000ug (3 years)- body stores B12 efficently therefore a temporary loss doesn’t effect as you can have a long store
  • Absopriton – binds to intrinsic factor in the ileum
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12
Q

describe vitamin B9 (folate)

  • water soluble?
  • what food is it found in
  • is it destroyed by cooking
  • is deficiency indistinguishable from B12 deficiency
  • require
  • store
  • absorption
A
  • Water soluble vitamin
  • Liver, greens, yeast
  • Destroyed by cooking* - prolonged boiling or deep frying
  • Deficiency mostly indistinguishable from B12 deficiency
  • Require – 150ug/d
  • Store – 4 months
  • Absorption – duodenum and jejunum
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13
Q

why does vitamin B12 or folate deficiency lead to cell failure

A
  • This leads to DNA synthesis impaired
  • Cells then fail to divide in the proerythroblast stage and therefore they get to big
  • Cannot get through capillary in the muscles and other tissues
  • Increased rate of destruction of red cells as they are too big therefore they lysis
  • Then you get Anaemia signs and symptoms
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14
Q

how is B12 absorbed

A
  • Vitamin B12 is usually bound to protein in foods and is released by stomach acid.
  • Following its release, B12 is absorbed in the ileum when binding to intrinsic factor (IF).
  • The intrinsic factor-B12 complex is absorbed by receptors on the ileum epithelial cells.
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15
Q

what produces intrinsic factor

A

Intrinsic factor is produced by parietal cells* of the gastric mucosa

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16
Q

What is anaemia caused by B12 malabsorption characterised

A
  • Pernicious anaemia characterized by B12 deficiency is often caused by the absence or reduction of intrinsic factor(may be due to autoimmune disease).
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17
Q

how is the ileum separated from the cecum

A
  • It follows the jejunum and is separated from the cecum by the ileococal valve (ICV) at the ileo-cecal junction
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18
Q

how long is the ileum

A

2-4m

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19
Q

what do B12 an folate deficiencies share in blood tests

A
  • low haemoglobin
  • high MCV
  • low WBC and platelets
  • macrocytes
  • hypersegemetned neutrophils
  • increased lactate dehydrogenase
  • increased bilirubin
20
Q

what does it mean if lactate dehydrogenase and bilirubin increases

A
  • test for haemolytic anaemia
21
Q

what is a hypersegemented neutrophil

A
  • this is a neutrophil with an increased number of lobes, it has more than 6 lobes
22
Q

what are the main causes of a B12 deficiency

A
  • Nutritional – poor vegan diet

Malabsorption
– either gastric due to pernicious anaemia and surgical gastrectomy
- intestinal – ileal disease such as crohnS

23
Q

What is crohns disease

A
  • chronic inflammatory disorder which the bodies immune system attacks the GI tract
  • possibly directed at microbial antigens
24
Q

describe the features of pernicious anaemia

A
  • An autoimmune disorder
  • Incidence is 1-2% in population > 60 years
  • F > M
  • Associated with fair hair, blue eyes, blood group A
  • Due to an Autoantibody against parietal cells and intrinsic factor (IF)
  • Leads to gastric atrophy, ↓ acid + ↓ IF secretion
25
Q

what are the clinical features of pernicious anaemia

A 
•	Insidious (gradual onset but fatal if untreated)
•	Anaemia
•	Glossitis (inflammation of tongue)
•	Mild jaundice
•	Neurological Symptoms
–	Peripheral neuropathy
–	Damage to Sensory and Motor tracts
–	Dementia
–	Optic atrophy
–	Pins and needles parathethesia 
–	treatment: intramuscular  B12 every 3 months for life
26
Q

what do the lab tests show for pernicious anaemia

A
  • microcytic anaemia
  • hypersegemented neutrophils
  • decreased serum B12
27
Q

what are the causes of folate deficiency

A
  • nutritional – old age, poverty, alcoholism
  • malabsorption – coeliac, crohns
  • excess utilization – pregnancy, lactation, haemolytic anaemia, psoriasis
  • others – anticonvulsants
  • Folate deficiency clinical features are same as for pernicious anaemia but without neurological symptoms.
28
Q

what is the treatment for folate deficiency

A
  • oral folic acid
29
Q

what is haemolytic anaemia

A
  • this is when the RBC has a lifespan of less than 120 days
30
Q

what does increased bilirubin cause

A

jaundice

31
Q

what can long standing haemolysis cause

A

gall stones

32
Q

what is haemosiderin

A

it is a ferritin that is denatured and therefore cannot release the iron

33
Q

what are the tests for haemloysis

A

tests in the urine for
1, urobilinogen
2, haemosidirin

34
Q

what is the presentation of haemolytic anaemia

A
  • Pallor and signs/symptoms of anaemia
  • Jaundice
  • Gallstones
  • Splenomegaly
  • Levels of bilirubin in blood are normally below 17umol/L but here levels are over 34-51 umol/L which typically result in jaundice
35
Q

what are three causes of haemolytic anaemia

A
  • Membrane
  • Haemoglobin
  • Enzymes
36
Q

describe membrane as an haemolytic cause of anaemia

A
  • Hereditary spherocytosis – stay as a sphere, and don’t shrink to there adult form
  • Oxidising agetns
  • Antibodies against RBC membrane
  • Autoantibodies
  • Alloantibodies – transfusion rxn – happens if you give someone the wrong blood
37
Q

describe haemoglobin as an haemolytic cause of anaemia

A
  • Abnormal structure such as sickle cell disease

- Imbalance in Alpha and Beta synthesis such as in thalassaemia

38
Q

describe enzymes as a haemolytic cause of anaemia

A
  • Glucose-6-phosphate dehydrogenase
  • Haemoglobin & other RBC proteins become oxidised over time due to high PO2 – eventually they are converted to methaemoglobin
  • G6PD prevents/reverses oxidation of Hb, membrane etc; prolongs lifetime of RBC.
39
Q

what is hereditary spherocytosis caused by

A
  • This is caused by a defect in the proteins of the red blood cell cytoskeleton. Because of this defect, the blood cell contracts to its most surface-tension efficient and least flexible configuration, a sphere
  • they have smaller surface area and can perform adequately to maintain a healthy oxygen supply but they have high fragility and therefore are prone to physical degradation when they pass through capillaries
40
Q

what are the clinical features of hereditary spherocytosis

A
  • Autosomal dominant
  • Chronic haemolytic anaemia
  • Spherocytes visible in peripheral blood film
  • ↓ Hb, ↑ LDH, ↑ unconjugated serum bilirubin
41
Q

describe Glucose 6-phosphate dehydrogenase genetic features

A
  • 400 million people worldwide have deficiency
  • Tropical Africa, Middle East, subtropical Asia, Mediterranean
  • X-linked
  • 400 different mutations
42
Q

what would show in a lab result if there is increased red cell breakdown

A
  • Increased serum unconjugated bilirubin
  • Increased urinary urobilinogen
  • Increased lactate dehydrogenase
43
Q

what would show in a lab result if there was increased red blood cell production

A
  • Reticulocytes in the blood

- Increased RBC in marrow

44
Q

What things trigger a G6PD symptoms to show

A
  • Carriers of the underlying mutation do not show any symptoms unless their RBC are exposed to certain triggers which are
  • 1) foods (fava beans is one of them),
  • 2) Bacterial or viral infection
  • 3) Drugs eg dapsone, cotrimoxazole and primaquine
45
Q

how can an autoimmune condition cause haemolytic anaemia

A
  • IgG antibodies are present in blood that react with RBC membrane proteins
  • IgG antibody attaches to RBC and labels for destruction
  • Labelled RBCs then removed by spleen (Extravascular haemolysis)
46
Q

how do you check if there is an antibody on red cell

A
  • take a blood sample from a patient with immune mediated haemolytic anaemia
  • patients washed RBC are incubated with antihuman antibodies (Coombs reagent)
  • RBC agglutinate, antihuman antibodies form links beween RBCs by binding to the human antibodies on the RBCs

Cardiorespiratory 2 (43 decks)

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