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macrocytic and haemolytic anaemia Flashcards

1
Q

is vitamin b12 soluble?

A

yes

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2
Q

what are symptoms of mild b12 deficiency?

A

fatigue, lethargy, depression, poor memory, breathlessness, headaches, pallor – esp in elderly people

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3
Q

what does prolonged vitamin b12 deficiency cause?

A

severe and irreversible nervous system damage

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4
Q

why is vitamin b12 deficiency common in alcoholics?

A

they get their calories from alcohol not food

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5
Q

what can cause megaloblastic macrocytic anaemia?

A

B12/B9 deficiency which causes inhibition of DNA synthesis during RBC production

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6
Q

what clinical test shows B12 deficiency?

A

increased serum methylmalonic acid (MMA)

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7
Q

why is testing MMA levels not a foolproof way of testing for B12 deficiency?

A

because not everyone who has increased MMA has a B12 deficiency

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8
Q

what are the uses of B12?

A
  • myelin synthesis in the nervous system

- DNA synthesis - needed in cell metabolism esp RBCs

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9
Q

what is methionine synthase?

A

an enzyme which uses B12 to transfer a methyl group from 5-methyltetrahydrofolate to homocysteine

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10
Q

what is THF needed for?

A

DNA synthesis

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11
Q

how can you get THF?

A

from folate in the diet

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12
Q

how does taking folate supplements help in B12 deficiency?

A

fixes the lack of DNA synthesis but won’t fix the reduced myelin synthesis

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13
Q

is folate water soluble?

A

yes

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14
Q

what foods are rich in vitamin b12?

A

meat, eggs, cheese, animal protein

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15
Q

can vitamin b12 be destroyed by cooking?

A

no

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16
Q

what foods are rich in folate?

A

liver, greens, yeast

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17
Q

can folate be destroyed by cooking?

A

yes apart from brief cooking e.g. stir frying

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18
Q

why doesn’t a b12 deficiency show signs and symptoms immediately?

A

because the body stores b12 efficiently so temporary loss of B12 doesnt result in immediate symptoms

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19
Q

how does b12/folate deficiency result in anaemia?

A

reduced DNA synthesis –> cells fail to divide –> overly large RBCs –> increased rate of destruction of RBCs –> signs and symptoms of anaemia

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20
Q

where and how is folate absorbed?

A

duodenum and jejenum

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21
Q

how is b12 absorbed?

A
  • released from food protein by stomach acid

- binds to IF from parietal cells of gastric mucosa and gets absorbed by receptors of ileum epithelial

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22
Q

where are parietal cells found?

A

gastric mucosa

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23
Q

what cells absorb b12?

A

ileum epithelial cells

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24
Q

what causes pernicious anaemia characterised by b12 deficiency?

A

caused by the absence/reduction of intrinsic factor (may be due to autoimmune disease)

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25
Q

what type of drug is omeprazole?

A

proton pump inhibitor

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26
Q

how can PPIs cause anaemia?

A

PPIs reduces the amount of acid in the stomach
impacts b12 and iron absorption
leads to anaemia

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27
Q

why do parietal cells release HCl in vesicles?

A

pass through the bicarbonate barrier lining the stomach then burst when they reach inside

28
Q

what separates the ileum and the cecum?

A

the ileocecal valve at the ileocecal junction

29
Q

what is the risk of a resection of the bowel?

A

risk of anaemia

30
Q

what does the blood count of someone with b12 or folate deficiency look like?

A

decreased Hb, increased MCV (>120), decreased WBC and platelets

31
Q

what does the blood film or someone with b12/folate deficiency look like?

A

oval macrocytes and hypersegmented neutrophils (more than 6 lobes)

32
Q

what does the biochemistry of someone with b12/folate deficiency look like?

A

increased lactase dehydrogenase (LDH), increased bilirubin

33
Q

why do people with b12/folate deficiency have increased LDH?

A

RBCs don’t have mitochondria, so they use LDH in glycolysis to turn pyruvate into lactate and vice versa
if RBCs burst open in anaemia then they release LDH –> high levels of LDH in anaemia

34
Q

why might people with b12/folate deficiency have jaundice?

A

its removed from old senescent cells by splenic macrophages

increased haemolysis = increased bilirubin = jaundice

35
Q

what are the main causes of b12 deficiency?

A

nutritional - poor diet e.g. vegans
malabsorption - pernicious anaemia
gastric - surgical gastrectomy
intestinal - ileal disease e.g. crohn’s

36
Q

what is crohn’s disease?

A

IBD that can affect any part of the GI tract
cause unknown
causes body’s immune system to attacj the GI tract possibly directed at microbial antigens

37
Q

what is pernicious anaemia?

A

autoimmune disorder

38
Q

who is more at risk of pernicious anaemia?

A

females

associated with fair hair, blue eyes and blood group A

39
Q

what causes pernicious anaemia?

A

autoantibody against parietal cells and IF

40
Q

what problems can pernicious anaemia cause?

A

gastric atrophy
decreased acid
decreased IF secretion
B12 deficiency

41
Q

which part of the body does autoimmune gastritis affect?

A

the parietal cells of the fundus but not the antrum

42
Q

why does pernicious anaemia lead to iron deficiency and B12 deficiency?

A

because parietal cells produce acid (iron absorption) and intrinsic factor (B12 absorption)

43
Q

what are the clinical features of pernicious anaemia?

A

insidious (gradual onset but fatal if untreated
anaemia
glossitis
mild jaundice
Neurological symptoms; peripheral neuropathy, damage to sensory and motor tracts, dementia, optic atrophy

44
Q

what is the treatment of pernicious anaemia?

A

intramuscular B12 every 3 months for life

45
Q

what do lab investigations show in someone with pernicious anaemia?

A

macrocytic anaemia
hypersegmented neutrophils
decreased serum B12

46
Q

what are the causes of folate deficiency?

A
  • Nutritional – old age, poverty, alcoholism
  • Malabsorption – Coeliac, Crohn’s
  • Excess utilisation – pregnancy, lactation
  • Others – anticonvulsants
47
Q

what are the clinical features of folate deficiency?

A

same as for pernicious anaemia but without neurological symptoms:
insidious (gradual onset but fatal if untreated
anaemia
glossitis
mild jaundice

48
Q

what is the treatment for folate deficiency?

A

oral folic acid

49
Q

what causes haemolytic anaemia?

A

shortened RBC survival

50
Q

what is a sign of haemolytic anaemia?

A

jaundice without itching

51
Q

what can long standing haemolysis cause?

A

gall stones which can obstruct the common bile duct

52
Q

how does haemolytic anaemia present?

A

pallor, signs/symptoms of anaemia, jaundice, gallstones and splenomegaly

53
Q

what are the normal levels of bilirubin in the body?

A

normally less than 17 micromoles/litre

54
Q

what bilirubin levels cause jaundice?

A

Levels of over 34-51 cause jaundice

55
Q

what are the three sites where pathology may be present in haemolytic anaemia?

A
  • Membrane – hereditary spherocytosis (where immature RBCs don’t shrink down to adult size), oxidising agents, antibodies against RBC membrane (autoantibodies, alloantibodies)
  • Haemoglobin - Abnormal structure (sickle cell disease); Imbalance in α:β synth (thalassaemia)
  • Enzymes - Glucose-6-phosphate dehydrogenase def.
56
Q

what do the lab investigations show in haemolytic anaemia?

A
  • Red cell breakdown; increased serum unconjugated bilirubin, urinary urobilinogen, lactate dehydrogenase
  • Increased RBC production; increased reticulocytes in blood and RBCs in marrow
57
Q

what causes hereditary sphreocytosis?

A

Caused by a defect in proteins of RBC cytoskeleton bc of this the RBC contracts to its most surface-tension efficient and least flexible configuration (a sphere)

58
Q

why is it bad that spherocytes are v fragile?

A

prone to physical degradation (e.g. when passing through capillaries)

59
Q

what are the clinical features of hereditary spherocytosis?

A

autosomal dominant, chronic haemolytic anaemia, spherocytes visible in peripheral blood film, decreased Hb, increased LDH, increased unconjugated serum bilirubin

60
Q

what is the function of glucose-6-phosphate dehydrogenase?

A

prevents/reverses the oxidation of Hb, membrane etc; prolongs the lifetime of RBCs

61
Q

where is G6PD deficiency common?

A

Tropical Africa, Middle East, subtropical Asia, Mediterranean

62
Q

when do G6PD carriers show symptoms?

A

when RBCs are exposed to certain triggers. can be of 3 main types;
o Foods – e.g. fava beans
o Bacterial or viral infection
o Drugs e.g. dapsone, cotrimoxazole, primaquine

63
Q

how does autoimmune haemolytic anaemia work?

A
  • IgG antibodies in the blood react with RBC membrane proteins
  • IgG antibody attaches to RBC and labels for destruction
  • Labelled RBCs then removed by spleen (extravascular haemolysis)
64
Q

what is the coombs test?

A

a test for autoimmune haemolytic anaemia

65
Q

how do you do the coombs test?

A
  • take a blood sample from the patient - antibodies are shown attached to antigens on the RBC surface
  • RBCs are washed and incubated with antihuman antibodies
  • RBCs agglutinate; antihuman antibodies form links between RBCs by binding to the human antibodies on the RBCs

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