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?

_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

what are the clinical features of deficiences in - vit c - B1 - B2 - B3 - B4 - B6 - B12 - folate?

- 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

Micronutrients Flashcards by patrick ellis

why do we need micronutrients? / role of micronutrients?

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

what can they have an adverse reaction on?

endogenous sources: mito, peroxisomes, ER

exogenous sources: pollution, alcohol, tobacco, paracetemol

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

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

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

how does it occur (2)

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

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

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

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

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

*vitamin D: (**oily fish, dairy products)
*vitamin B12 (**meat and dairy food)

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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?

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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why is commensal bacteria gut overgrowth clinically significant regarding vitamins?

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

overgrowth: likely to have B12 deficiency & high B9

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

**decreased intake

decreased absorption**

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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?

*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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what are the clinical features of deficiences in

vitamin A

vitamin D

vitamin E

vitamin K

(fat soluble vitamins)

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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what are the clinical features of deficiences in

vit c
B1
B2
B3
B4
B6
B12
folate?

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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trace element deficiencies?

calcium?
phosphorous?
iron?
selenium
zinc
copper

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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iron metabolism:

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

Study These Flashcards

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)

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

Study These Flashcards

*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

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)

Study These Flashcards

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

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

Study These Flashcards

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)

what are rickets and osteomalacia characterised by?

Study These Flashcards

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**

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

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*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)

B1 (aka thiamine)

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

Study These Flashcards

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**

what are the 3 clinical presentations of beri beri?

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**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

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

Study These Flashcards

**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 !!

**pellagra is caused by a** deficiency in ?

B3 !

B3 (niacin): - absorbed where? - forms which two important molecules? !! roles? - deficiency causes?

**B3 - niacin** - absorbed: **jejunum** - forms: **NAD & NADP -\> imporant hydrogen acceptors. when reduced forms: hydrogen donors** - deficiency causes: **pellegra**

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

**tryptophan** can make B3 !

why may u be deficient in B3? (50

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

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

- casal necklace - vaginitis - oesophagitis * *4Ds:** **dermatitis, diarrhoea, dementia and death** B3 treatment: \* **B3 can be toxic in xs!!!! \***

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

- 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**

B12: absorbed where? how?

- 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_**

what can lead to B12 defiency? (4)

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

Micronutrients Flashcards

(32 cards)