Nutrition pdf - د. رباح

Vitamins

organic substances with key roles in certain

metabolic pathways; they are required in small
amounts in food because they are not
synthesized in the body .

body stores

is varied

vit.B

and vit.A need years to deplete their

stores.

Folate (vit.B

) and thiamine (vit.B

) need

weeks to deplete their stores.

Vitamins

Vitamins are

fat-soluble

(vitamins A, D, E and K)

water-soluble

(vitamins of the B

complex group and vitamin C).

Thiamin (vitamin B1)

Function

thiamin pyrophosphate (TPP), is an essential

cofactor in carbohydrate metabolism.

1. Involved in the oxidative decarboxylation of

acetyl CoA in mitochondria.

2 .In the Krebs cycle, is the key enzyme for the

decarboxylation of α-ketoacid.

3. Has role in peripheral nerve conduction (unknown

mech.)

Thiamin (vitamin B1)

Source

many foodstuffs

 cereals, legumes

 pork, as well as beef meat.

 Coffee and tea (have anti-thiamine factors),

and raw fish (has thiaminase), all decrease
the vitamin .

 milled and polished rice have little vit.B

Thiamin (vitamin B1)

Deficiency

1. Cells cannot metabolize glucose aerobically

this likely to affect the nervous system .

2 .There is accumulation of pyruvic and lactic

acids, which produce vasodilatation and

increased cardiac output.

Thiamin (vitamin B1)

Causes

1. poor dietary intake, in severe prolonged

hyper -emesis gravidarum

3 . where the only food consumed is polished

rice

2 . In chronic alcohol-dependent patients

4. Chronic illness as cancer

Thiamin (vitamin B1)

Clinical feature

Body stores are small and signs of deficiency

quickly develop with inadequate intake.

• Non specific at early stage : anorexia, fatigue,

irritability

• Two clinical forms

Dry beriberi

Wet beriberi

Thiamin (vitamin B1)

• Dry beriberi

1. peripheral neuropathy:

Sensory and motor

pain and parasthesia

2.Cerebral involvement :

Wernicke-encephalopathy

mental impairment

cerebellar ataxia

ophthalmoplegia

horizontal nystagmus

Thiamin (vitamin B1)

Korsakoff syndrome

loss of new memory

confabulation

• Wet beriberi

high output failure (3 months)
peripheral neuropathy

Thiamin (vitamin B1)

Diagnosis

 measurement of the circulating thiamin

concentration

 enzymatic assay of transketolase activity.

Thiamin (vitamin B1)

Treatment

• 100 mg/d of thiamine given parenterally for 7

days, followed by 10 mg/d orally until
complete recovery.

• Cardiovascular and ophthalmoplegic

manifestations improve within 24 h .Others
gradually clear

• Wernicke-Korsakoff syndrome may be

permanent or persist for several months.

• VitB1 must be replaced in alcoholic patient

after feeding

Riboflavin (B2 )

• Riboflavin is a flavoprotein that is a cofactor for

many oxidative reactions in the cell for energy
production.

Source

widely distributed all plant and animal sources

(main source) cereals, milk, dairy products

(good source) legume, Meat , fish , egg

Riboflavin (B2 )

Deficiency causes

almost is dietary with other VitB

Clinical manifestations

1. Mucocutaneous lesion

angular stomatitis or

cheilosis

red inflamed tongue

2. Seborrhoeic dermatitis

(face around the nose)

scrotum or vulva.

Riboflavin (B2 )

3.Conjunctivitis with vascularization of the

cornea .

4. Anemia

5. Personality changes

Diagnosis

serum or urinary level

Treatment

Riboflavin 10 mg daily, usually given as the

vitamin B complex.

Niacin (B3)

two chemical forms, nicotinic acid, nicotinamide

Function

Many oxidative steps in the production of

energy and in DNA repair

source

   many foodstuffs: plants, meat and fish.

  can be synthesized in humans from Eggs,

and milk contain tryptophan.

Niacin (B3)

Causes of deficiency

1. Dietary deficiency (corn based diet)

2. In malabsorption (rare)

3. In Hartnup's  disease. (Tryptophan renal, or GIT

absorption defect)

Niacin (B3)

4. In alcohol-

dependent patients (who don’t eat)

5. In the carcinoid syndrome (tryptophan is

needed for serotonin).

6.Isoniazid therapy ( lead to a deficiency of

vitamin B6, which is needed for the synthesis
of nicotinamide from tryptophan).

Niacin (B3)

Clinical features

Pellagra :

dermatitis

diarrhoea

and

dementia

1. early non specific symptoms anorexia,

weakness, irritability

2. bright red glossitis and angular stomatitis

Niacin (B3)

3. Dermatitis

Scaling pigmented skin rash

exposed to sunlight

(casal s necklace)

4. Diarrhea

proctitis

esophagitis

(non infective)

5. Dementia

milder cases cause depression.

severe cases cause hallucinations and

acute psychosis

Niacin (B3)

Diagnosis



assesing the urinary excretion of the 2 pyridone
and 2 methyl nicotinamide.

Treatment



Nicotinamide 300 mg daily by mouth with a
maintenance dose of 50 mg daily



. VitB3 used in RX of hyperlipidemia

Vitamin B6

• Vitamin B6 exists as pyridoxine, pyridoxal and

pyridoxamine.

Function

• cofactor of many enzymes involved in the

metabolism of many amino acids.

• neurotransmitters synthesis

• heme synthesis.

• Vitamine metabolism as niacin

Vitamin B6

Source

is found widely in plant and animal foodstuffs.

Cause of deficiency

Dietary deficiency

( isolated extremely

rare)

Some drugs

isoniazid

hydralazine

methyldopa

penicillamine

interact with pyridoxal phosphate, producing
the deficiency.

Vitamin

Clinical features

1. mucosal changes

2. The peripheral neuropathy

personality changes

depression, confusion

3. Microcytic hypochromic anaemia

Treatment

100 mg daily should not be exceeded.

. VitB6 used as antiemetic especially in the

pregnancy

Vitamin B12

function

• cofactor for activation of the folate

(demethylation of methyl THF polyglutamate
to THF, with methylation of homocysteine to
methionine).

• Coenzyme for many synthetic reactions

Source

• animal sources meat, fish, eggs and milk, but

not in plants.

• The storage may take 2 years or more after

absorptive failure before

deficiency develops.

(total stored amount in the adult is about 2-5
mg).

Vitamin B12

Deficiency

Low dietary intake

, Vegans

Impaired absorption

• Stomach : Pernicious anaemia

Gastrectomy

Congenital deficiency of

intrinsic factor

• Pancreatic insufficiency
• Small bowel: ilea disease or resection

Bacterial overgrowth

Diphyllobothrium latum (fish

tapeworm).

Abnormal utilization

Congenital

transcobalamin II

deficiency

Vitamin B12

Clinical features

1. megaloblastic anemia

2. glossitis and angular stomatitis.

3. The neurological changes
•

polyneuropathy

• subacute combined degeneration of the

spinal cord

• psychiatric problems
• Dementia
• optic atrophy

•

Vitamin B12

polyneuropathy

symmetrical paraesthesiae in the fingers and

toes

subacute combined degeneration

( posterior, lateral columns of the spinal cord)

• loss of vibration sense and proprioception
• sensory ataxia
• progressive weakness
• Paraplegia may result.

Vitamin B12

psychiatric problems

• depression
• hallucinations

Dementia

optic atrophy

Vitamin B12

Investigations

1. Hematological findings

features of a megaloblastic anemia

2. Bone marrow

features of megaloblastic erythropoiesis

)

3. Serum bilirubin

may be raised

result of ineffective erythropoiesis.

4. Serum vitamin B12

below the normal (160 ng/L)

Vitamin B12

Treatment

Hydroxocobalamin 1000 μg can be given

intramuscularly.

improvement of the polyneuropathy may

occur over 6-12 months,

long-standing spinal cord damage is

irreversible.

Folates

in food as in reduced dihydrofolate or

tetrahydrofolate (THF)

function

• coenzymes in the transfer of single carbon

units in amino acid metabolism and DNA
synthesis.

Source

• Dietary intake Folate is found in green

vegetables

• Cooking causes a loss of 60-90% of the

folate

Folates

Causes of folate deficiency

Nutritional

major cause

Poor intake

• Old age
• Poor social conditions
• anorexia
  Gastrointestinal disease
•  partial gastrectomy
•  small bowel disease as coeliac disease,

Crohn’s disease

Antifolate drugs

• Anticonvulsants:

– Phenytoin, barbiturates

• Methotrexate, , trimethoprim, sulphasalazine

Folate

Excess utilization

Physiological

• Pregnancy
• Lactation
  Pathological

• Haematological disease with excess red cell

production, e.g. haemolysis

• Malignant disease with increased cell turnover
• Inflammatory disease
• Haemodialysis or peritoneal dialysis (loss with

the fluid)

Folate

Clinical features

• asymptomatic
• symptoms of anaemia or of the underlying

cause.

• Glossitis can occur.
• CNS manifestations does not occur .

Investigations

The haematological findings are those of a

megaloblastic anaemia

low levels of serum folate (4-18

μg/L).

Folate

Treatment of folate deficiency

• 5 mg of folic acid daily for about 4 months to

replace body stores.

• Rx (i.e. treatment) of underlying cause, e.g.

coeliac disease

• Prophylactic folic acid is recommended for all

women planning a pregnancy. (neuronal tube
defect)

• Prophylactic folic acid is also given in chronic

haematological disorders (when there’s rapid
cell turnover)

Vitamin C

(Ascorbic acid)

function

• It is involved in the

hydroxylation

of proline to

hydroxyproline, which is necessary for the
formation of

collagen

Source

• Vitamin C is present in all fresh fruit and

vegetables.

Vitamin C

(Ascorbic acid)

Deficiency

1. is seen mainly in the

elderly

and single

people who do not eat vegetables.

  2. Increase need in the trauma, burn infection

  3. drugs as steroid, indomethacin, aspirin,

tetracycline

Vitamin C

Ascorbic acid

Clinical features :

scurvy

• Perifollicular hemorrhages
• Swollen, spongy gums with bleeding and

superadded infection

• Spontaneous hemorrhage (GIT, joint,

peritoneum)

• Failure of wound healing

Vitamin C

Ascorbic acid

Diagnosis

• Plasma ascorbic acid is very low (less than

μmol/L) .

Treatment

200 mg of ascorbic acid daily and

encouraged to eat fresh fruit and vegetables.

Vit.C in large amount used in upper

respiratory tract infection

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