Nutrition

Oh lordy. What do eat? KALE. AND LEGUMES.

VITAMINS YO.
The widespread use of vitamins as tonics is unnecessary and should be
discouraged; toxicity from fat soluble vitamins is occasionally seen.

Name
RDA/RNI
Sources
Uses

Absorption/Metab
olism

Pathology- def
and OD

Vitamin A/Retinol [Beta Carotene is a precursor]

NB 6 micrograms of Beta carotene= 1 of retinolfood labelling beware.
LIVER; milk, butter, cheese, egg yolk, fish oil, added
to margarine in the UK. Beta-carotene is found in
green veg, carrots and other yellow andred fruits.
Rhodopsin/Iodopsin {cones} light= change to trans
isomer- memb pot change brain.
Control of cell proliferation
Cofactor in the synthesis of most gps containing
MANNOSE
Beta carotene acts as an antioxidant
Beta carotene- cleved in intestinal mucosa by
carotene dioxygenase RETINALDEHYDE[red to]
retinol. 1/3 dietary vitA derived from retinoid direct.
Absorbed with LC f.as.
Liver stores [stellate cells in space of Disse?]
Plasma bound to retinol binding protein [alpha
globulin]
WW def is major cause of blindness in young people:
XEROPTHALMIA- Imp adaptation followed by night
blindness, then conjunctival xerosis [dryness and
thickening]. Bitots spot [<-keratin. NB can also be
caused by exposure]. Corneal softening, ulceration
and dissolution [keratomalacia] late stage +/superimposed infection = blindness. Relative vitA
def can occur in PEM as red alpha globulin [RBP].
Beta carotene and CVD:
Hypervitaminosis A: Liver+ bone damage [as
retinoic acid supresses OB activit and stimulates OC,
so inc bone turnoverhypercalcaemia, OP], hair
loss, double vision, V, H + more abn. At doses of
300mg a/h, 100mg c/h. In infants can cause
softening of the skull bone craniotabes, and bulging
fontanelle, ^ICP.
Teratogenicc- >3mg/d preg f inc incidence birth
defects. DOES NOT INC BETA CAROTENE. In
organogenesis, disrupts neural cell activitybrain/heart defects, microcephaly, hydrocephaly.

Foot note

Other carotenoids, lycopene, lutein are probably of

little quantitative importance as dietary precursors
of vitamin A, and although beta carotene is not

teratogenic, it can cause cartodermia. No not use

vitA for acne in pregnant females
See chapter 11 allso for vitamin D. Links to C??

Name
RDA/RNI
Sources
Uses

Absorpti
on/Meta
bolism
Patholog
y

DDx
Inv and
Mx

Name

Vitamin K
Leafy greens, dairy, rapeseed and soya been oil.
Coagulation: CF II, VII, IX, X of the EXTRINSIC P/W. protein C and S.
P-s: Cofactor for P-c in inact of Va and VIIIa when free.
Bone: Osteocalcin [G1a residues bind to hydroxyapatitie, leading to
bone mineralisation], matrix G1a protein, protein S- bone matrix
formation.
Intestinal bacteria can synthesis another major form of vitK than
can be utilised, in th terminal ileum. It is absorbed as a fat soluble
vitamin in the upper small intestine, and the mannequinones [K2]
bacteria produced must also be abs as this is the major form of vitK
Found in the liver.
DEF-> NN most prone- poor placental transfer, little in breast milk,
no hepatic stores of menaquinone due to no S.I m.o. Leads to
haemorrhagic disease of the nb; prophylactic phytomenadion 1mg
i.m to all NN, as vitK def can occur at anyage but in NN they are
most at risk of bleeding.
Cholestasis- red abs as is FAT SOLUBLE. E.g PBS, stone, stricture,
chronic pancreatitis. anything than causes chronic cholestasis.
BONE- seems to have no effect other than on rapidly growing bone;
imp act of bone matrix protein osteocalcin and imp bone P by
reducing OB func.
Mass blood transfusion can also cause def!
Deficiency presents differently in infants, but in adults vitK can go
unnoticed until hypoprothrombinaemia occurs: Bleeding to minor
trauma, epistaxis, petechiae, haematoma, gastrointestinal bleeding,
menorrhagia, haematuria and bleeding from gums.
Hypervitaminosis K ofcourse would cause the opposite- thrombosis,
and possible sudden death from clots to brain/<3
Be aware that Warfarin is a vitamin K antagonist, and
colestyramine, salicylates, rifampicin, isoniazid and barbiturates are
Rx ass w/ vitK def
Consider vitK as a possible cause of any bleeding disorder;
Leukaemia, DIC, dysfibrinogenaemia, ITP, scurvy, TTP, vWF ds.
Bleeding time, PT, aPTT all elevated.
Antibody test for high level of des-gamma carboxy prothrombin
protein in vitamin K absence [DCP PIVKA]
Plasma vitK reduced
Mx- Fresh frozen plasma [if severe] then vit K as phytomenadione
[water sol] IV slowww [AVOID bronchospasm and peripheral
vascular collapse]. IM injection can lead to sever haemotoma at
injection site due to imp clotting.

Vitamin E
No exact requirement set as varies widely w/ ind dietary intake of

Sources
Uses

Absorpt
ion/Met
abolism
Patholo
gy

DDx
Inv and
Mx

polyunsaturated fatty acids [PUFA], i.e the larger the intake of PUFA,
the more vitE required
pt.co.uk says 30mg a day
Vegetables and seed oils, cereals and nuts. Infant formulations.
Contributes to membrane stability. Antioxidant: Protects cellular
structures agains damage from some highly ROS inc H2O2,
superoxide. MAY also affect cell proliferation and growth
??Animal data- prevent formation and reduce size of atheromatous
plaque
Fat soluble, LDL transport in blood.

Haemolytic anaemia in infants. Deficiency is seen only in children

with abetallpoproteinaemia and in pts with LT parenteral nutrition.
Severe neurological deficit- Gross ataxia.
Hypervitaminosis E- >1g/kg/day. Bruising, bleeding, raised PT, due to
inhibition of vitK dependant carboxylase. Imp immunity with
secondary necrotising enterocolitis has been obs in premmies given
vitE to prevent retrolental fibroplasia [a retinopathy leads to
blindness]
Rare- Vitamin E is the vitamin in search of a deficiency as it is
present in so many foods.
Inv- alpha tocopherol levels and a clotting screen.
Prevent gross ataxia with vitE injections. Plasma or serum levels of
aloha tocopherol [one of the forms of VITE] m. and corrected for lvl of
plasma lipids- therefore vitE lvls expresses as milligrams PER
MILLIGRAM OF PLASMA LIPID.
Hypervitaminosis- reversed by administering vitK.

Name
RDA/RNI
Sources
Uses

Absorption/Metab
olism

Thiamin/B1
0.4mg PER 1000KCAL NB
more is required in ahigh
carb diets
Cereal, grains, beans,
nuts, pork and duck.
Essential cofactor in
carbohydrate metabolism
in oxidative respiration
[KC].
Water soluble. NB Water
sol vits are non toxic and
relatively cheap so can
be given in large amts if
deficiency present. Once
absorbed, thiamine is
found in many body
tissues but is chiefly
stored in the liver.
HJowever body stores are

Riboflavin/B2

Dairy, offal and leafy

vegetables
Riboflavin is a
flavoprotein that is a
cofactor for many
oxidative processes in
cells

Pathology

small so a deficiency
de3velops quickly with
inadequate intake
Deficiency- Beriberi,
Wernicke-Korsakoffs.
Alcohol dependency is
ass with deficiency of B
vits chiefly, esp thiamine.
Beriberi is pretty much
confined to south east
asia and is due to eating
a diet of purely rice. It
presents as dry beriberi
with peripheral
polyneuropathjy, or wet
with oedemka.

Name

Niacin

RDA/RNI

6.6mg per 1000 kcal

Sources

Plants, meat esp offal

and fish, added toi cereal
and white bread in
developed world.
Tryptophan 60mg can be
converted to 1mg of
niacin. Foods that contain
tryptophan inc eggs,
cheese and leafy green
veg, and the enzymes for
this conversion are
riboflavin and B6
dependent, hence
deficiency in these
vitamins can also cause
pellagra
Act as hydrogen
acceptors in many
oxidative reactions and in
their reduced formsNADH and NADPH act as
hydrogen donors in many
reactions. Necesasary for
hexose monophosphate
shunt for generation of
NADPH which is
necessary for f.a
synthesis.

Uses

There is no definitive
deficiency but it does
tend to produce:
angularstomatis or
cheilosis [fissuring at the
angles of the mouth], a
red ifm tongue,
seborrhoeic dermatitis
est around nose, scrotum
and vulva. Riboflavin
5mg/d can be prescribed
for def, usually in
compelx with other B vits

Vit B6 [pyridoxine,
pyridoxal, pyridoxamine]
15micrograms per gram
of dietary protein

Cofactor in the metab of

many a.a.

Absorption/Metab
olism
Pathology

Pellagra- this is rare and

usually only found in
people who only eat
maize such as in parts of
Africa. Some of the
symptoms of pellagra
may be due to def in
other vitamins and
protein deficiency
Dermatitis in areas of
skin exposed to sunlight;
DIARRHOEA AND
dementia. Be aware that
pellagra can also occur
rarely in generalised
malabsorption; Isoniazid
therapy, Hartnups
disease[a rare inborn
error where some
essential a.a cannot be
abs from the gut inc
tryptophan, and the
same a.a are los inm
urine]m very low prot
diets for renal ds,
carcinoid syndrome and
phaeochromocytoma.

Biotin and pantothenic acid Biotin involved in a number of

carboxylase reactions, found in many foods, small dietary req so def
extremely rare- people who consume rare eggs [as contains biotin
antagonist]
Vitamin c acts as an antioxidant- inactivate oxygen FRs that would
otherwise damage dna, cell memb and cell structures
Water sol- B1, B2, B6, B12, C, FA and niacin
Vitamins are organic nut not synthesised by the body but are vital for
normal metab and maintainance of growth, act as coenzymes. Do not
provide energy or use as building materials
Summary table of vit defs:

Vitamins

Deficiency State

Symptoms/Signs

A (Retinol)

Blindness

Night-blindness

D (Cholecalciferol)

Osteomalacia/rickets

Proximal weakness of limbs

E (Tocopherol)

Anaemia/neuropathy

Haemolytic anaemia - jaundice

K (Phytomenadione)

Defective clotting

Bruising

Beri beri

Wet beri beri oedema, high output left

Fat Soluble

Water Soluble
B1 (Thiamine)

Dry beri beri motor/sensory neuropath

B2 (Riboflavin)

Sore tongue and mouth

B6 (Pyridoxine)

Dermatitis/Anaemia

Skin rash affecting eye/nose and sore to

B12 (Cobalamin)

Pernicious anaemia

Tiredness/ fatigue/pale conjunctivae

C (ascorbate)

Scurvy

Bent/coiled body hair, bruising, gingivitis

Folate

Megaloblastic anaemia

Tiredness/ fatigue/pale conjunctivae

Niacin

Pellagra

Dermatitis, fatigue, insomnia, glossitis, d

psychosis