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MP322 > absorption and what goes wrong > Flashcards

absorption and what goes wrong Flashcards

1
Q

vitamins

A

organic compounds that required in small quantities for a variety of biochemical functions

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2
Q

water soluble vitamins

A
  • B complexes
  • C or ascorbic acid
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3
Q

fat soluble vitamins

A
  • A or retinol
  • D or cholecalciferol
  • E or tocopherol
  • K
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4
Q

sources of vitamin B12 (cobalamin)

A
  • synthesised solely by microorganisms
  • only source for humans is - meat, fish, dairy products
  • vegetables, fruits and other foods of non-animal origin are free from B12 unless contaminated by bacteria
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5
Q

dietary requirement of vitamin B12

A
  • western daily diet contains 5-30 microgram
  • body stores2-5 milligram
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6
Q

passive absorption of vitamin B12

A
  • through buccal, duodenal and ileal mucosa
  • rapid but extremely inefficient
  • <1% of an oral dose is absorbed
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7
Q

active transport of vitamin B12

A
  • normal physiological mechanism is active transport
  • occurs through ileum
  • mediated by gastric intrinsic factor
  • 70& of ingested amount is absorbed
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8
Q

absorption of vitamin B12

A
  • vitamin B12 is released from the food and bound to haptocorrin (transcobalamin I)
  • haptocorrin is produced by salivary glands
  • intrinsic factor (glycoprotein) is secreted by parietal cells
  • haptocorrin is degraded in the duodenum releasing B12
  • B12 is captured by intrinsic factor
  • intrinsic factor-bound vitamin B12 is endocytosed by cubam in the terminal ileum
  • inside the enterocyte intrinsic factor is degraded releasing B12
  • ABC transporter releases B12 into the blood
  • vitamin B12 binds to transcobalamin II
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9
Q

plasma transport of vitamin B12

A
  • vitamin B12 is transported in the plasma bound to transcobalamin I, II, III
  • vitamin B12 bound to transcobalamin II is most important for cellular uptake
  • internalisation occurs in complex with transcobalamin receptor (CD320) via endocytosis
  • the transcobalamin is degraded releasing vitamin B12
  • excess vitamin B12 is sent to liver for storage
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10
Q

cellular role of vitamin B12

A
  • essential co-enzyme for 2 enzymes in the body
  • homocysteine –> methionine irreversible reaction first step
  • tetrahydrofolate essential for DNA and RNA
  • methylmalonyl-CoA mutase enzyme that require vitamin B12 found in mitochondria
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11
Q

role of intrinsic factor in absorption

A
  • produced in the parietal cells
  • in the absence of intrinsic factor inadequate amounts of vitamin B12 are absorbed
  • resulting in megaloblastic anaemia
  • when due to absence of intrinsic factor it is pernicious anaemia
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12
Q

pernicious anaemia

A
  • autoimmune atrophic gastritis
  • destruction of gastric parietal cells and lack of intrinsic factor
  • immune response is directed against H/K/ATPase
  • also causes achlorhydria (low production of gastric acid)
  • can also be caused by antibodies against intrinsic factor
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13
Q

aetiology of vitamin B12 deficiency

A
  • inadequate dietary intake
  • loss of gastric parietal cells or intrinsic factor
  • functionally abnormal intrinsic factor
  • bacterial overgrowth in intestine (stagnant loop syndrome)
  • disorders of ileal mucosa (transcobalamin II deficiency)
  • dysfunctional uptake and use of vitamin B12 by cells
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14
Q

drug induced vitamin B12 deficiency

A
  • proton pump inhibitors and H2 antagonists - reduction in stomach acid reduces separation of B12 from food)
  • oral contraceptives and hormone replacement therapy - thought to be due to a reduction in transcobalamin
  • metformin (reduces vitamin B12 absorption)
  • colchicine (impairs or inhibits receptors in the terminal ileum)
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15
Q

consequences of vitamin B12 deficiency

A
  • normal serum concentration of vitamin B12 is 115-1000 mmol/L
  • megaloblastic anaemia is the hallmark of symptomatic vitamin B12 deficiency
  • in advanced causes anaemia may be severe with haematocrit as low as 10-15% (normal: 40% women; 45% men)
  • may be accompanied by leucopoenia and thrombocytopaenia and hypersegemented neutrophils
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16
Q

neurological symptoms of vitamin B12 deficiency

A
  • paraesthesia (pins and needles) in hands and feet
  • sensory loss
  • gait ataxia
  • weakness in legs
  • subacute combined degeneration of spinal cord
17
Q

digestive symptoms of vitamin B12 deficiency

A
  • hunter’s glossitis
18
Q

cardiovascular symptoms of vitamin B12 deficiency

A
  • angina
  • venous thromboembolic disease
19
Q

gynaecological symptoms of vitamin B12 deficiency

A
  • infertility
20
Q

vitamin B12 derivatives

A

human serum has:
0-10% cyanocobalamin
8-15% hydroxocobalamin
22-39% deoxyadenosylcobalamin
36-62% methylcobalamin
- deoxyadenosylcobalamin and methylcobalamin are active forms of the vitamins in humans

21
Q

treatment of vitamin B12 deficiency

A
  • oral cyanocobalamin and parenteral hydroxocobalamin
  • must be parenteral in the case of gastric intrinsic factor deficiency (pernicious anaemia)
  • lifelong treatment is necessary
22
Q

sources of vitamin B9 (folate/folic acid)

A
  • dark green vegetables (broccoli, lettuce, brussels, sprouts, spinach)
  • dried legumes (beans, lentils, chickpeas)
  • fruits and fruit juices
  • meat, seafood, poultry and eggs
  • fortified cereals and bread
23
Q

recommended daily dose of vitamin B9

A
  • 200 microgram
  • 400 microgram during pregnancy
24
Q

absorption of folate

A
  • natural folates are conjugated to a polyglutamyl chain
  • folates are absorbed in the monoglutamate form
  • hydrolysed by folypoly-y-glutamate carboxypeptidase
  • N5-methyltetrahydrofolate (5-MTHF) is main dietary folate
  • most absorption occurs in proximal small intestine (duodenum/jejunum) some absorption in colon
  • folate is absorbed from the lumen by proton-coupled folate transporter (PCFT)
  • absorption is also via a reduced folate carrier (RFC) with folate being exchanged for organic phosphate
  • enterocytes have folate receptors
  • folate can be exported without further metabolism or reduced to 5-MTHF
  • both forms of folate are exported from enterocyte by an organic anion transporter
25
Q

plasma transport of folate and cellular uptake

A
  • most is transported as monoglutamyl derivative
  • most folate circulates free in the blood (some bound to albumin)
  • plasma concentration is 10-30 nmol/L
  • cellular uptake is by the same three mechanisms as for enterocytes (PCFT, RFC and folate receptor)
  • intracellular folates exist primarily (75%) as polyglutamate conjugates
26
Q

aetiology of folate deficiency

A
  • inadequate dietary intake
  • congenital defects in the uptake system
  • intestinal disease (coeliac, IBD, tropical sprue)
  • drug interaction (cholestyramine, sulfasalazine, trimethoprim, methotrexate, metformin)
  • chronic alcohol use
  • increased cellular requirement (pregnancy)
27
Q

symptoms of folate deficiency

A
  • sore tongue (glossitis) / pain upon swallowing
  • nausea/vomiting
  • abdominal pain
  • diarrhoea
  • cognitive impairment/dementia
  • depression
  • if severe results in megaloblastic anaemia
28
Q

treatment of folate deficiency

A
  • oral folic acid for 1-4 months
  • oral route is sufficient even in those with malabsorption
  • treated until haematological recovery occurs

MP322 (18 decks)

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