Micronutrients Flashcards

1
Q

why do we need micronutrients? / role of micronutrients?

A

micronutrients act as:

  • *1. co-factors:** compound required for a proteins biologal activity
  • *2.** co-enzymes: help enzymes catalyse a reaction
  • *3. antioxidants:** inhibits the oxidation of other molecules. counteracts free radicals
  • *4. control of gene expression**
  • *5. structure:** e.g phosopholipids causes complexes with Mg & Ca
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2
Q

what are the different types of sources that free radicals can be derived from? (2)

what can they have an adverse reaction on?

A

endogenous sources: mito, peroxisomes, ER

exogenous sources: pollution, alcohol, tobacco, paracetemol

adverse reactions on: nucleic acids, lipids & proteins :(

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3
Q

how does an antioxidant work?
e.g.?s (5)

A

antioxidant:

  • free radicals cause chain reaction of oxidation causing damage
  • antioxidants: neutralise free radicals by ‘lending; an electron to stabilise damaged atoms

examples:
vitamin A, C, E & copper, zinc & selenium

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4
Q

which micronutrient is important in imprinting home to the gut mucosa from peyers patches?

how does it occur (2)

A

vitmain A: precursor for retinoic acid !

  • gut dendritic cells use retinoic acid to inform the niave T cells
  • causes niave T cells to change transcription to express CCR9 & a4B& to do gut honing
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5
Q

which population are micronutrients most important in?
WHY? (3)

A

most important in paediatric population: (body growth & development; energy supply; healthy infants have 3x energy per kg body weights than adults)

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6
Q

which micronutrient helps to improve childrens learning ability and cognitive development? WHY? (1)

A

iron helps to improve childrens learning ability and cognitive development: Fe helps Hb to carry oxygen to neurons in brain

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7
Q

if someone is malnourished, what is going to be impaired? (7)

A
  • impaired wound healing
  • reduced fertlitliy
  • impaired immune response - predisposes to infection
  • reduced muscle strength
  • depression
  • increased risk to post-op complications
  • inactivity - pressure sorees
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8
Q

what are vegans likely to be deficient in? (2)

A
  • *vitamin D: (**oily fish, dairy products)
  • *vitamin B12 (**meat and dairy food)
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9
Q

what are fat-soluble vitamins (4?)
which are water-soluble vitamins? (2)

which can be stored / which normally excreted? what does this mean as a consequence?

A

fat soluble: A D E K -> can be stored in liver (but can be toxic in XS)
- absorbed with fats (readily absorb in micelles & chylomicrons)

water soluble: B & C -> normally excreted

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10
Q

why is commensal bacteria gut overgrowth clinically significant regarding vitamins?

A

commensal bacteria: providers AND consumers of B vitamins** & **vitamin K.

overgrowth: likely to have B12 deficiency & high B9

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11
Q

vitamin deficiency in deveoloped countries is likely from two overarching categories. what are they?

A

**decreased intake

decreased absorption**

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12
Q

what are main causes of vitamin deficieny in developed countries are

  • *decreased intake:**
  • alcohol:
  • vegans:
  • elderly w. poor diet:
  • anorexia:
  • *decreased absorption:**
  • malabsorbative state e.g. coeliac disease:
  • ileal diease:
  • liver & biliary tract disease:
  • intestinal bacterial overgrowth:
  • oral antibiotics:

what are they likely to be deficient in?

A
  • *decreased intake:**
  • alcohol: B vitamins
  • vegans: Vit D & Vit B12
  • elderly w. poor diet: Vit D & folate
  • anorexia: folate
  • *decreased absorption:**
  • malabsorbative state e.g. coeliac disease: folate (B9)
  • ileal diease: only B12
  • liver & biliary tract disease: fat soluble vitamins (bc bile helps absorb fat !)
  • intestinal bacterial overgrowth: b12
  • oral antibiotics: vit K
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13
Q

what are the clinical features of deficiences in

vitamin A

vitamin D

vitamin E

vitamin K

(fat soluble vitamins)

A

vitamin A: eyes -> xeropthalmia (Xerophthalmia refers to the spectrum of ocular disease caused by severe Vitamin A deficiency (VAD))

vitamin D: rickets (in adults = osteomalacia)

vitamin E: peripheral neuropathy

vitamin K: coagulopathy

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14
Q

what are the clinical features of deficiences in

  • vit c
  • B1
  • B2
  • B3
  • B4
  • B6
  • B12
  • folate?
A
  • vit c: scurvy
  • B1: beri beri
  • B2: angular stomatitis
  • B3: pellagra
  • B4: anemia
  • B6: anemia
  • B12: anemia (but also lots of neurological disorders)
  • folate: anemia
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15
Q

trace element deficiencies?

calcium?
phosphorous?
iron?
selenium
zinc
copper

A

calcium: bone problems ! osteoporosis, muscle spasms
phosphorous: bone pain, pseudofractures
iron: anemia, muscle problems
selenium: cardiomyopathy
zinc: growth retardation, congenital deformation
copper: ​growth retardation

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16
Q

iron metabolism:

  • absorbed where in GI?
  • function in the body? (2)
  • stored where (2) and as what (1)?
A

iron metabolism:

  • absorbed where in GI: duodenum (and proximal jejunum)
  • function in the body: oxygen transport with Hb (1) myoglobin function in skeletal muscle
  • stored: liver (1) & macrophages (1) as ferratin (1)
17
Q

deficiency in iron can cause? (4)
excess in iron can cause? (5)

A
  • *Fe deficiency:**
  • microcytic anaemia (smaller than normal size)
  • lethargy & fatigue
  • cognitive impairment in children
  • exacerbation of inflam diseases
  • *Fe XS: haemochromatosis**
  • lethargy & fatigue
  • ab and joint pain
  • reduced libido
  • diabetes
  • cirrhosis
  • cardiomyopathy
18
Q

what is vitamin D deficiency in a) adults called? b) children
how can we actually manufacture vit. D?
- * what is biological activty of Vit D? * (3)

A
  • vitamin D deficiency in a) adults: osteomalacia b) children: rickets
  • vitamind D can be made by SUNLIGHT
  • biological activity:
    i) increases gut Ca2+ absorption
    ii) increases bone calcification
    iii) increases reabsorbtion of calcium
19
Q

(what is the difference between exposure time needed to generate vit D during summer bewteen caucasian & non-causcaisian?)

A

caucasians: 20/30 mins of sunlight x 2/3 week in summer
non-cau: requires 2-10 X this

(also: october -> march insufficient UVB to make Vit D AND sunscreens block dermal Vit D synthesis)

20
Q

what are rickets and osteomalacia characterised by?

A

children- rickets:

  • occurs prior to epiphyseal fusion (It is the part of a long bone where new bone growth takes place)
  • growth retardation
  • *- expansion of growth plate**

adults: osteomalacia:

  • **reduced bone strength
  • increased fracture
  • bending of bones
  • bone pain
  • waddling gate
  • looser zones of bones**
21
Q

which lifestyle factors can also contribute to vit D deficiency? (6)
what are disease factors that can contribute to vit D (3)

A
  • *lifestyle factors:**
  • obesity
  • smoking
  • alcohol
  • exercise (too much)
  • exclusive breast feeding
  • lack of sun
  • *disease factors:**
  • reduced skin synthesis
  • drug-related interference
  • reduced bioavailbility (from obesity)
22
Q

B1 (aka thiamine)

  • absorbed where?
    * - function? (3) *
  • deficency leads to which diseases? (3)
A

B1

absorbed: jejuneum

function:

  • glycolysis & krebs cycle - if not present **causes build up of lactate !
  • BCAA (** branch chain a.a. met)
  • pentose phosphate cycle

deficiency leads to:

  • *- Beri-Beri
  • Wernicke’s Enceophalopathy
  • Korsakoffs Physchosis**
23
Q

what are the 3 clinical presentations of beri beri?

A

**Beri-beri - shutting down krebs and ox-phosph.

i) wet:**
cardiac: enlarged heart, tachycardia, high output, peripheral oedema (wet !); neurological: peripheral neuritis

ii) dry: peripheral neuropathy (motor & sensory)

iii) shoshin: cardiac failure & lactic acidosis

24
Q

what are consequences of Wernicke’s & korsakoffs syndrome by?
caused by a lack of WHAT?

A

**B1 deficiency !

Wernickes’ encephalopathy:**

  • rapid & repititive eye movement (horizontal nystagmus)
  • opthalmoplegia (paralysis of eye)
  • cerebellar ataxia (inflamede cerebellum)
  • *Korsakoff syndrome = chornic neurological sequel of wernicke’s enceph.**
  • mentail impairment
  • irreversible !!
25
Q

pellagra is caused by a deficiency in ?

A

B3 !

26
Q

B3 (niacin):

  • absorbed where?
  • forms which two important molecules? !! roles?
  • deficiency causes?
A

B3 - niacin

  • absorbed: jejunum
  • forms: NAD & NADP -> imporant hydrogen acceptors. when reduced forms: hydrogen donors
  • deficiency causes: pellegra
27
Q

* if the diet is deficinet in niacin (B3), cells can manufacture it from WHAT? *

A

tryptophan can make B3 !

28
Q

why may u be deficient in B3? (50

A
  • vegetarian diets
  • alcholism
  • Hartnups disease: cant make trpytophan
  • Carcinoid syndrome: increased conversion of tryptophan to serotonin
  • Isoniazid use (for TB) - inteferses with met.
29
Q

what are the late stage symtpoms of pellegra?
what is problem with B3 treatment?

A
  • casal necklace
  • vaginitis
  • oesophagitis
  • *4Ds:** dermatitis, diarrhoea, dementia and death

B3 treatment: * B3 can be toxic in xs!!!! *

30
Q

what is folate (B9) needed for? what happens if deficient?

A
  • folic acid is needed by rapidly dividing cells: used for closure of neural tube during development - why you need it in pregnancy !!!
  • deficiency: leads to spina bifida & other develompment syndromes
31
Q

B12:

absorbed where?
how?

A
  • B12: absorbed only in terminal ileum, after being complexed with stomach-derived intrinsic factor
  • *absorptive pathway:**
  • bound to dietary protein
  • first dissociated by HCl and pepsin, in stomach
  • reattaches itself via haptocorrin (from saliva thats now in stomach)
  • dissociated from haptocorrin and binds with stomach-derived intrinsic factor
  • absorbed only in terminal ileum in enterocytes (although 60-80% still goes into faeces)
  • reassociates with transcobalamin and then goes to portal circulation
  • cofactor for methionine synthase & methlymalony CoA synthase: produces methionine & succinyl co-A
32
Q

what can lead to B12 defiency? (4)

A
  • inadequate intake - vegans
  • disorders of terminal ileum
  • defective release of cobalamin from food
  • inadequate production of intrinsic factor