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Digestive > Micronutrients > Flashcards

Micronutrients Flashcards

1
Q

Requirements of normal erythopoiesis

A

Iron
Folate
B12

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2
Q

Low B12 symptoms

A

Tingling in extremities
Concentrations problems
Macrocytosis

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3
Q

Reasons for low B12

A

Diet
Malabsorption
Abnormal acid, IF, pancreatic secretions and ileal absorptive function

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4
Q

Pernicious anaemia

A

Autoimmune disorder where individual develops antibodies against intrinsic factor and/or parietal cells causing decreased IF. Not enough to bind B12 so it can’t be absorbed in the terminal ileum.

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5
Q

B12 malabsorption due to small intestinal issues

A

B12 binds IF normally but abnormal terminal ileum i.e. through surgical removal or Crohns inflammation means it is not absorbed in the small intestine

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6
Q

Pernicious anaemia diagnosis

A

Antibodies to parietal cells of IF detected in blood test

Gastric biopsies can provide evidence of autoimmune gastritis, low acid output or other autoimmune diseases

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7
Q

Pernicious anaemia treatment

A

High doses of B12 required every week for 4-6 months then every 3 months
Response to treatment must be monitored to ensure B12 levels are high, haemoglobin and reticulocytes are responding and neurological symptoms have abated

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8
Q

Loss of specialised receptors on terminal ileum leads to:

A

Failure to absorb B12
Failure to reabsorb bile salts
Bile salts lost through colon causing irritation and secretory diarrhoea. Decreased bile salts means less fat emulsification and impaired fat absorption.

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9
Q

Mechanism by which partial gastrectomy can lead to low B12

A

No antrum = no G cells = no gastrin
No gastrin = less gastric acid, less B12 released from food
No pylorus = bile reflux = stomach atrophy
Atrophy = decreased parietal cells = decreased IF therefore less B12 absoprtion

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10
Q

Low B12 in celiac disease

A

Loss of small intestine villi therefore loss of endocrine cells that secrete secretin and CCK involved in pancreatic stimulation

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11
Q

Schilling test

A

Radioisotope test used to determine if patient has lack of IF
Rarely used now - time consuming, involves radioisotopes and results can be difficult to interpret

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12
Q

B12 is also known as:

A

Cobalamin

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13
Q

Steps of vitamin B12 absorption

A

1) B12 in food released during peptic digestion
2) Parietal cells secrete haptocorrin
3) Parietal cells secrete IF which binds released B12
4) B12-IF uptaken by brush border receptors in small intestine
5) B12-IF cleaved. IF taken back into enterocyte. 80% B12 binds haptocorrin, 20% B12 binds holotranscobalamin
6) B12-haptocorrin goes to liver, B12-holotranscobalamin taken up by all cells for DNA synthesis
7) Pancreatic proteases degrade B12-haptocorrin (currently stored in liver)

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14
Q

Megaloblastic anaemia

A

Slightly larger and irregularly shaped blood cells than normal

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15
Q

Water soluble vitamins

A

Vitamin C
All the Bs
Folic acid
Biotin

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16
Q

Fat soluble vitamins

A

Vitamin A
Vitamin D
Vitamin E
Vitamin K

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17
Q

Absorption of water soluble vitamins

A

Partly digested by mucosal hydrolyses
Absorbed into mucosal cell and transported to hepatic portal vein
Stored in liver

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18
Q

Absorption of fat soluble vitamins

A

Form minor components of micelles
Uptake into mucosal cells
Export into lymphatics and then plasma as chylomicrons
Stored in body lipids

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19
Q

Factors affecting bioavaliability

A 
Efficiency of digestion
Nutrient intake
Foods consumed simultaneously
Food preparation method
Synthetic or natural nutrient
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20
Q

Vitamin B1

A

Thiamin

Metabolism of energy yielding

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21
Q

Vitamin B2

A

Riboflavin

Intermediates via redox reactions

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22
Q

Vitamin B3

A

Niacin

23
Q

Vitamin B6

A

Pyridoxine

Transamination

24
Q

Vitamin B12

A

Cobalamin

Transmethylation

25
Q

Vitamin B9

A

Folate/folic acid

26
Q

Vitamin B5

A

Pantothenic acid

Constituent of coenzyme A

27
Q

Vitamin B7

A

Biotin

Carboxylation using coenzyme A

28
Q

Sources of thiamin

A

Whole grain, fortified and enriched products

Pork

29
Q

Thiamin defincieny

A

Wet (heart) and dry (neuro) beriberi
Wernickes encephalopathy
Caused by alcoholism

30
Q

Folate deficiency

A

Macrocytic anaemia
Poor growth and neural tube defects
Caused by alcohol intake, pregnancy, some drugs

31
Q

Sources of folate

A

Leafy greens

Legumes, seeds, fortified cereals

32
Q

Sources of vitamin D

A

Oily fish
Raw mushrooms
Eggs

33
Q

Vitamin D deficiency

A

Rickets

Osteomalacia

34
Q

Vitamin D absorption

A

UV light from sun + precursor in liver made from cholesterol makes previtamin D3
+ foods = Vitamin D3 (inactive)
In liver, vitamin D3 hydroylated
In kidneys, hydroxylated again to active form

35
Q

Folate absorption

A

Folate occurs as polyglutamate in food. When digested, glutamate breaks off and CH3 added.
Folate absorbed and delivered to cells

36
Q

Seven major minerals

A 
Calcium
Phosphorous
Potassium
Sulfur
Sodium
Chloride
Magnesium
37
Q

Iron homeostasis

A

1 g stored in body
300 mg in myoglobin and respiratory enzymes
2.5 g in RBCs
2 mg taken in from diet
1 - 2 mg lost in feces
20 - 25 mg recycled daily for RBC formation

38
Q

Iron recycling

A

Haemoglobin containing iron in RBCs carries oxygen
Bleeding = loss
Liver and spleen dismantle RBCs, package iron into transferrin and store excess iron in ferritin
Sweat, skin and urine = loss
Transferrin carries iron in blood
Some delivered to myoglobin of muscle cells
Bone marrow incorporates iron into haemoglobin of RBCs and stored excess iron in ferritin

39
Q

Iron absoprtion

A

Iron in food
Mucosal cells in the intestine (duodenum) store excess iron in mucosal ferritin
If the body needs iron, mucosal ferritin releases iron to mucosal transferrin which hands iron to another transferrin that travels through the blood to the rest of the body
If the body doesn’t need iron, it’s excreted in shed intestinal cells

40
Q

Heme iron

A

25% absorbed
Haemoglobin and myoglobin from animal products
5 - 10% dietary iron

41
Q

Non-heme iron

A

Vegetable, pulses, supplements

17% absorbed

42
Q

Absorption of heme iron

A

Absorbed into mucosal cell as intact porphyrin complex

Affected by iron deficiency but not composition of meal and gastrointestinal secretions

43
Q

Absorption of non-heme iron

A

Must be present in duodenum in soluble form
In stomach, ionised by gastric juice and neutralised
Ferric iron precipitated and is uptaken at the brush border into the cell by membrane iron binding protein
Affected by meal composition

44
Q

Vitamin C is important for iron absorption because:

A

It is a dietary reducing agent. DMT1 (iron membrane receptor) can only uptake Fe+2 so Fe+3 from non-animal products needs to be reduced

45
Q

Haem oxygenase

A

Enzyme that cleaves haemoglobin from iron in animal products freeing up Fe+2 for storage

46
Q

Hepcidin protein

A

Peptide hormone from liver that regulates iron

47
Q

Haemochromatosis

A

Chronic disorder involving excess absorption and inappropriate storage of iron

48
Q

Factors affecting heme iron absorption

A

Iron status of subjects

Heme iron present in meat

49
Q

Factors affecting non-heme iron absorption

A

Iron status of subjects
Amount of bioavailable non-heme iron
Balance between dietary factors enhancing and inhibiting iron absorption

50
Q

Factors enhancing iron absorption

A

Vitamin C
Meat and fish (meat factor protein)
Organic acids

51
Q

Factors inhibiting iron absorption

A 
Phylates
Iron binding polyphenols
Dietary fibre
Tannins
Calcium
52
Q

Factors decreasing iron absorption

A

Intestinal motility

Steatorrhoea

53
Q

3 stages of iron deficiency

A

1) Depleted storage iron - low serum ferritin
2) Iron restricted erythopoiesis - low serum transferrin saturation
3) Iron deficiency anaemia - low haemoglobin

54
Q

Importance of iron

A

Myelination
Neuronal growth and differentiation
Neurotransmitter regulation
Blood brain barrier closes off to iron at about 2 years old so intake critical in iron deficient populations before this age

Digestive (9 decks)

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