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2A week 1 - anaemia, RBC metabolism etc. > haematinic physiology and pharmacology > Flashcards

haematinic physiology and pharmacology Flashcards

1
Q

3 basic components needed for a mature functioning RBC

A
  1. iron;
  2. amino acids (make globin chains);
  3. blasts (DNA synthesis, diving cells etc.)
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2
Q

how much iron is in an average man + woman and what forms is it in

A

around 4g in men and 30-45% less in women (around 2.5g);
65% stored as haemoglobin, 20-30% as ferritin (some as haemosiderin), remainder in myoglobin, catalase and other enzymes

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3
Q

what is the iron status in the body regulated by

A

absorption

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4
Q

how is iron excreted from the body

A

passively through the gut, skin, faeces

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5
Q

iron intake requirements for men, women, growing children and pregnant people

A

men: 0.5-1.0mg/d
women: 1.0-2.0mg/d
growing children: 1.1-2.0mg/d
pregnancy: 1.5-3.0mg/d

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6
Q

8 key players in iron metabolism and what they do

A
  1. DMT-1 (divalent metal transporter) - involved in enterocyte uptake of Fe2+;
  2. Ferritin - intracellular storage;
  3. transferrin - ferric-ion delivery to the organs;
  4. transferrin receptor - uptake into target cells;
  5. haemosiderin - an iron-storage complex that is composed of partially digested ferritin and lysosomes;
  6. ferroportin - transfers Fe2+ out of enterocyte;
  7. hepcidin - regulates iron levels, acts as a feedback signal;
  8. HFE - regulates hepcidin production this controlling uptake into immature enterocytes
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7
Q

consumption -> store -> tissue iron pathway (draw this out! see lect)

A

consumption -> non haem iron (if haem-iron then goes straight into cell) -> Fe3+ –(ferric reductase)–> Fe2+ -> DMT-1 allows it to enter the enterocyte -> can be stored as ferritin (Fe3+) in the cell -> otherwise binds to binding protein -> transported out of the cell via ferroportin 1 -> Fe2+ –[o]–> Fe3+ -> transferrin -> target tissue

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8
Q

what causes increased absorption of iron (8)

A

Fe2+; haem iron; acids; absorbate; soulubilizing agents (sugars, amino acids etc.); pregnancy; increased erythroppoiesis; haemochromatosis; increased DMT-1 and ferroportin

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9
Q

how does hepcidin work

A

binds to ferraportin and causes its removal/destruction from enterocytes -> this means that iron is trapped in the storage cells and cant be removed (usually seen in anaemia of chronic disease)

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10
Q

what causes decreased absorption of iron (11)

A

Hepcidin; Fe3+; non-organic iron; alkalis; phytates/phosphates; tea; tetracyclines; high-iron diet; infections; high body iron stores

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11
Q

4 causes of iron deficency

A

inadequate diet; increased requirements (pregnancy, growth); malabsorption; blood loss (menstrual, GO, lung, Urinary)

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12
Q

who should GI investigations be considered in initially (if presenting with iron deficency anaemia)

A

all men; post menopausal women

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13
Q

what GI investigations should be done for IDA (5)

A

take drug Hx; tissue transglutaminase antibody (tTg); imaging of upper + lower GI tracts; check stools for paracites; faecal haemoglobin (not yet in practice)

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14
Q

what are some GI causes of iron deficency anaemia

A

hookworm infection; oesophago-gastric cancer; coeliac disease; crohn’s disease; gastritis; peptic ulceration; oesophagitis; gastrectomy; NSAID enteritis; meckel’s diverticulum; colon cancer; colitis etc.

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15
Q

with what frequency should iron supplements be given for max absorption

A

once a day

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16
Q

what are the typical iron replacement therapies

A

ferrous sulphate (3 month post Hb-normalisation); ferrous gluconate; sodium ironedetate; ferric maltol

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17
Q

what is given if parenteral iron is required (2)

A

ferric carboxymaltose; ferric derisomaltose

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18
Q

where is folic acid found naturally

A

green vegetables; offal

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19
Q

what is folic acid synthesized by

A

bacteria

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20
Q

what does folic acid require for biological activity

A

B12

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21
Q

what kind of molecule is biologically active folic acid

A

polyglutamate

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22
Q

why is folic acid non-absorpable in the GI tract

A

due to its polar nature (carboxyl group) it cannot pass through the lipid membranes of the cells

23
Q

how is folic acid absorbed into the body

A

the polyglutamate molecule is deconjugated in the jejenum into monoglutamate -> these are smaller, less polar molecules and so can be absorbed

24
Q

folic acid metabolism pathway (consumption -> liver)

A

consumed in polyglutamte form -> broken into monoglutamate form -> absorbed by jejenum -> converted into tetrahydrofolic acid (THF) -> methylated into methyl-THF -> enters blood stream -> either stored in liver or metabolised in tissue

25
Q

what is the main role of folic acid in the body + pathway for this (CH3-TFH -> thymidine)

A

Folic acid is used to synthesize DNA precursors, which is essential for DNA replication and cell division

methyl-THF -> enters targets cells via FAT receptors -> methyl-THF transfers its methyl group to vitamin B12 -> forms methylcobalamin and free THF -> serine provides a methylene group to THF -> methylene group quickly transfered to the nucleotide d-UMP -> d-UMP becomes d-TMP -> converted to thymidine (DNA nucleotide)

26
Q

secondary role of folic acid + pathway (intracellular CH3-THF -> methionie)

A

lowering the levels of homocysteine in the body, too much of which can be harmful

methyl-THF transfers its methyl group to vitamin B12 -> forms methylcobalamin and free THF -> methylcobalamin transfers its methyl group to homocysteine -> converted into an essential amino acid called methionine

27
Q

what is the consequence of a folate/B12 deficency

A

new DNA cannot be made (Hb can be made but not the cells!); build up of homocystien

28
Q

what can folic acid easily be degraded by

A

cooking for too long

29
Q

structure of B12

A

corrin ring (similar to haem) with a colablt complex centre

30
Q

role of folic acid in foetal development

A

needed for the closure of the anterior neuropore of the neural tube during the 23rd day, and posterior neuropore during the 26th day of gestation - This is a crucial step in the development of the central nervous system

31
Q

where is B12 stored

A

liver

32
Q

what reaction is vit B12 involved in

A

co-enzyme for methyltransferase reactions (homocysteine ->methionine) i.e. essential to folate metabolism

33
Q

what are some key players in B12 metabolism

A

R-binders; gastric parietal cell; gastric acid; intrinsic factor; pancreatic secretion; ileal receptor; Transcobalamin-I/II/III

34
Q

where is B12 naturally obtained from in the diet

A

meat

35
Q

vit B12 absorption pathway

A

B12 consumed -> R factors (haptocorrin) in saliva + gastric juice bind -> intrinsic factor secreted from parietal cells -> HCO3- secreted by pancreas as move towards ileum (increasing pH) -> B12-R split by IF -> B12-IF absorbed when reaches terminal ileum

36
Q

why can B12 only be absorbed in the terminal ileum

A

this is the only place receptors where expressed

37
Q

what cells are most vulnerable to folate/B12 deficency

A

rapidly dividing cells e.g. bone marrow precursors, gut epithelium

all cells are affected tho

38
Q

what are 2 specific signs of B12 deficeincy

A

neuropathy and optic atrophy

39
Q

what may folate/B12 deficiency cause in elders

A

confusion

40
Q

what investigations should be done for suspected magaloblatic anaemia (4)

A
  1. blood film (unusually large, structurally abnormal, immature red blood cells- megaloblasts);
  2. B12/red cell folate levels;
  3. bone marrow biopsy;
  4. check methylmalonic acid and homocysteine levels
41
Q

what does megaloblastic anaemia indicate

A

there is a bone marrow problem

42
Q

6 causes of megaloblastic anaemia

A
  1. B12 deficiency;
  2. folate deficiency;
  3. combined deficiency;
  4. abnormal folate metabolism (e.g. due to Mtx);
  5. abnormal DNA synthesis;
  6. myelodysplasia
43
Q

why does cell size increase in non-megaloblastic macrocytic anaemia

A

cells get bigger due to lipid deposits

44
Q

causes of non-megaloblastic macrocytic anaemia (8)

A
  1. just macrocytosis;
  2. pregnancy;
  3. liver disease;
  4. alcoholism (classic example);
  5. reticulocytosis;
  6. hypothyroidism;
  7. drugs;
  8. marrow infiltration;
45
Q

what is given to treat B12 deficiency

A

hydroxycobalamin

46
Q

what does parenteral mean

A

administered or occurring elsewhere in the body than the mouth and alimentary canal

47
Q

when might B12 prophylaxis be given

A

after a total gastrectomy/ileal resection -> given parenterally (IM usually), oral replacement can be given if absorption intact

48
Q

when are folic acid supplements given as prophylaxis (3)

A

pregnancy + preconception (reduced risk of neural tube defects); haemolyis; Mtx therapy

49
Q

5 causes of folate deficiency

A
  1. diet - anorexia, children, alcoholic, elderly;
  2. increased utilisation - physiological (growth, pregancy), pathological (cancers, haemolysis, inflammation);
  3. malabsorption - small bowel disease;
  4. urinary loss (haemodialysis);
  5. drugs (Mtx, sulfasalazine etc.)
50
Q

what can cause a B12 deficiency (6)

A
  1. diet -vegans;
  2. gastric disease - autoimmune gastritis, major gastrectomy;
  3. ileal disease - resection, inflammation;
  4. infections - small bowel, fish tapeworm;
  5. pancreatic disease;
  6. transcobalamin-II deficiency;
  7. B12 destruction (NO)
51
Q

how to test for B12 absorption

A

57/58Co labelled-B12 tracking; can be +/- intrinsic factor; urinary excretion sampled

52
Q

what autoantibodies can be tested for in B12/folate deficiencies

A

B12 - anti parietal cell, anti intrisic factor;
folate - anti gliadin, anti endomysial

53
Q

what is addisonian pernicious anaemia

A

a relatively rare autoimmune disorder that causes diminishment in dietary vitamin B12 (cobalamin) absorption due to destruction of specialise gastric body mucosa (mucosal atrophy), resulting in B12 deficiency and subsequent megaloblastic anemia

2A week 1 - anaemia, RBC metabolism etc. (5 decks)

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