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322 > Lecture 14: Absorption > Flashcards

Lecture 14: Absorption Flashcards

1
Q

What is a vitamin?

A

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

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2
Q

What are the two classes of vitamins?

A

Water soluble and fat soluble

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3
Q

What are the water soluble vitamins?

A

Vitamin C and Vitamin B complexes

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4
Q

What are the fat soluble vitamins?

A

Vitamin A, D, E, K

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5
Q

What is the other name for vitamin A?

A

Retinol

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6
Q

What is the other name for vitamin D?

A

cholecalciferol

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7
Q

What is the other name for vitamin E?

A

Tocopherol

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8
Q

What is the other name for vitamin B12?

A

Cobalamin

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9
Q

Where is vitamin B12 synthesised from?

A

Microorganisms

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10
Q

Where do ruminants obtain vitamin B12 from?

A

The foregut

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11
Q

What is the only source for humans for vitamin B12?

A

Food of animal origin eg meat, fish, dairy products

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12
Q

What is the daily dietary requirement for vitamin B12?

A

1-2.5 microgram a day

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13
Q

How much vitamin B12 does the western daily diet contain?

A

5-30 micrograms

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14
Q

What are the two mechanisms of vitamin B12 absorption?

A
  • Passive absorption
  • Active transport
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15
Q

What is passive absorption?

A

A small fraction of vitamin B12 is absorbed without the involement of intrinsic factor

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16
Q

Where does passive absoprtion occur?

A

Through buccal, duodenal and ileal mucosa

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17
Q

What is active transport?

A

The normal physiological mechanism B12 is absored. It involves intrinsic factor

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18
Q

How much B12 is absorbed through active transport?

A

Around 70%

19
Q

Where does active transport occur?

A

Through the ileum

20
Q

How is B12 absorbed through active transport?

A
  1. Released from food
  2. Binding to salivary heptocorrin
  3. Pancreatic enzymes and intrinsic factor
  4. Receptor mediated uptake in the terminal ileum
  5. Internalization and transport into the blood stream
  6. Tissue uptake
21
Q

Where is intrinsic factor produced?

A

Pariatal cells

22
Q

What happens in the absence of intrinsic factor?

A

Inadequate amounts of B12 are absorbed

23
Q

What happens if inadequate amounts of B12 is absorbed?

A

Megaloblastic anamia

24
Q

What is the result of an absmce of intrinsic factor?

A

Pernicicous anaemia

25
Q

What is megaloblastic anaemia?

A

Impaired maturation of red blood cells, leading to the production of abnormally large and immature cells. It is primarily caused by a deficiency of either vitamin B12 or folate (vitamin B9), which are essential for DNA synthesis and red blood cell production.

26
Q

What is pernicious anaemia?

A

autoimmune response that targets and destroys the gastric parietal cells in the stomach, which are responsible for producing intrinsic factor—a protein required for the absorption of vitamin B12.

27
Q

What are the causes of B12 deficiency?

A
  • Inadequate dietary intake
  • Loss of gastric parietal cells or intrinsic factor
  • Functionally abnormal intrinsic factor
  • Bacterial overgrowth in intestine eg stagnant loop syndrome
  • Disorders of ileal mucosa eg resection, absence of receptor on ileal cells
    -Disorders of plasma transport eg transcobalamin II deficiency
    -Dysfunctional uptake and use of vitamin B12 by cells
28
Q

What drugs cause B12 deficiency?

A
  • PPI and H2 antagonists
  • Oral contraceptives
  • Metformin
  • Cholchicine
29
Q

How do PPI and H2 antagonists cause a B12 deficiency?

A

Stomach acid helps to seperate B12 from food, a reduction in stomach acid, reduces the separation of B12 from food

30
Q

How do oral contraceptives and HRT cause a B12 deficiency?

A

thought to be due to a reduction in the B12 carrier transcobalamin

31
Q

How does metformin cause a B12 deficiency?

A

Metformin interferes with B12 absorption

32
Q

How does cholchicine cause a B12 deficiency?

A

impairs or inhibits receptors in terminal ileum.

33
Q

What are the consequences of a B12 deficiency?

A
  • Megaloblastic anaemia
  • Parasthesia in hands and feet
  • Sensory loss
  • Gait ataxia
  • Weakness in legs
  • Subacute combined degeneration (SCD) of the spinal cord
  • Hunters glossitis
  • Angina
  • Venous thromboembolic disease
  • Infertility
34
Q

What are the vitamin B12 derivatives?

A
  • cyanocobalamin
  • hydroxycobalamin
  • deoxyadenosylcobalamin
  • methylcobalamin
35
Q

What are the active forms of the vitamin?

A
  • Deoxyadenosylcobalamin
  • methylcobalamin
36
Q

What is the treatment of vitamin B12 deficiency?

A
  • Oral cobalamin: cyanacobalamin
  • Parenteral cobalamin: hydroxycobalamin
37
Q

When is parenteral cobalmin given?

A

in the case of gastric intrinsic factor deficiency (pernicious anaemia) or total gastrectomy.

38
Q

What are the sources of B9?

A

Dark green vegetables eg broccoli, lettuce, Brussel sprouts and spinach, dried legumes eg beans lentils and chickpeas. Fruit and fruit juices. Meat, seafood, poultry and eggs. Fortified cereal and bread.

39
Q

What is the daily requirement of B9?

A

200 micrograms a day, 400 in pregnancy

40
Q

How is folate absorbed?

A
  • In the diet folate exists in a polyglutamate form, which needs to be converted to a monoglutamate form for absorption
  • Natural folate are conjugates to a polyglutamyl chain.
  • During digestion, the polyglutamate form of dietary folate is broken down into monoglutamates by enzymes in the small intestine, this mainly occurs in the duodeum and jejunum
  • The monoglutamate forms of folate are then transported across the intestinal cells through an active transport mechanism. This process requires specific carrier proteins located on the brush border of the intestinal cells. Hydrolysed by folylpoly-g-glutamate carboxypeptidase.
  • Once inside the intestinal cells, folate is converted into its active form, called 5-methyltetrahydrofolate (5-MTHF). This conversion is facilitated by enzymes in the intestinal cells.
41
Q

What are the causes of folate deficiency?

A
  • Inadequate dietary intake
  • congenital defects in the uptake system eg Proton coupled transported
  • intestinal disease eg coeliac disease, IBD, tropical sprue
  • drug interaction e.g. cholestyramine, sulfasalazine, trimethoprim, methotrexate, metformin)
  • Chronic alcohol use
  • increased cellular requirement (e.g. pregnancy)
42
Q

What are the symptoms of folate deficiency?

A
  • Sore tongue (glossitis) and pain upon swallowing, GI symptoms (nausea, vomiting, abdominal pain diarrhoea, especially after meals), Neurologic (cognitive impairment, dementia, and depression), When severe it results in megaloblastic anaemia.
43
Q

What are the treatments for folate deficiency?

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

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