nutrition pdf - غير معروف

vitamins

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
vit12 and vitA need years to deplete the stores
folate and tiamine need weeks stores

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. TPP is involved in the oxidative decarboxylation of

acetyl CoA in mitochondria.

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

decarboxylation of α-ketoacid.

Has role in peripheral nerve conduction(unknown mech.)

Thiamin (vitamin B1)

Source

many foodstuffs:
cereals, legumes, pork, as well as beef meat.
Coffee ,tea, raw fish (

thiaminase

) decrease the vitam.

milled and polished rice have little vitB1

Body stores are small and signs of deficiency quickly develop

with inadequate intake. (1 month)

Deficiency:

1. Cells cannot metabolize glucose aerobically ; this is

likely

to affect the nervous system .

2 .There is accumulation of pyruvic and lactic acids,

which produce vasodilatation and increased cardiac

output.

Causes:

1. poor diatary itake, in severe prolonged hyper -

emesis gravidarum .

3 . where the only food consumed is polished rice .
2 . In chronic alcohol-dependent patients ( absorption)
4. Chronic illness as cancer

Clinical feature

• Non specific at early stage : anorexia, fatigue, irritability

• Dry beriberi

1. Symmetrical peripheral neuropathy: Sensory and motor

pain and parasthesia

2.Cerebral involvement :

Wernicke-encephalopathy

. This syndrome, which

consists of mental impairment, cerebellar ataxia,

ophthalmoplegia and horizontal nystagmus .

Korsakoff syndrome

: loss of new memory

,confabulation

• Wet beriberi

high output failure (3 months)
peripheral neuropathy

Diagnosis :

measurement of the circulating thiamin concentration

enzymatic assay of transketolase activity.

Treatment :

• In acute thiamine deficiency with either cardiovascular or

neurologic signs, 100 mg/d of thiamine should be given
parenterally for 7 days, followed by 10 mg/d orally until there
is complete recovery. Cardiovascular and ophthalmoplegic
improvement occurs within 24 h.

• Other manifestations gradually clear, Wernicke-Korsakoff

syndrome may be permanent or persist for several months.

• NB. 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

milk, dairy products , cereals(main

source)

Meat , fish , egg , legumes(good source)

Diagnosis :

serum or urinary level

Deficiency :

Almost is dietary

Riboflavin (B2 )

Deficiency cause:

mucocutaneous lesion

1. Angular stomatitis or cheilosis
2. red, inflamed tongue
3. seborrhoeic dermatitis, particularly involving the face (around

the nose) and the scrotum or vulva.

4.Conjunctivitis with vascularization of the cornea .
5. Anemia
6. Personality changes

Treatment

Riboflavin 10 mg daily, usually given as the vitamin B complex.

Niacin (B3)

• This is the name for the two chemical forms, nicotinic acid and

nicotinamide .

• Many oxidative steps in the production of energy and in DNA

repair

source

• Niacin is found in many foodstuffs, including plants, meat and

fish. Niacin can be synthesized in humans from Eggs and milk

contain tryptophan.

Niacin (B3)

Causes of deficiency

1. Dietary deficiency (corn based diet).

2. In generalized  malabsorption (rare).

3. In Hartnup's  disease. (Tryptophan renaland git. absorp.

Defect)

4. In alcohol-dependent patients who do not eat.

5. In the carcinoid syndrome and, tryptophan is needed for

serotonine.

6.Isoniazid therapy can lead to a deficiency of vitamin B6, which

is needed for the synthesis from tryptophan.

Clinical features

Pellagra :

dermatitis

diarrhoea

and

dementia

early non specific symptoms anorexia, weakness, irritability
bright red glossitis and angular stomatitis

Dermatitis.

Scaling pigmented skin rash exposed to sunlight,

casal s necklace

Diarrhea.

Due to proctitis. esophagitis and dysphagia(non

infective inflammation)

Dementia

. This occurs in chronic disease. In milder cases

there are symptoms of depression.

Hallucinations and acute psychosis are seen

with more severe cases.

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Niacin (B3)

Diagnosis



this is based on the clinical features with assesing the urinary

excretion of the 2 pyridone and 2 methyl nicotinamide.

Treatment



Nicotinamide (approximately 300 mg daily by mouth) with a

maintenance dose of 50 mg daily.



Response rapid(24h)



NB. vitB3 used in RX of hyperlipidemia

Vitamin B6

•

Vitamin B6 exists as pyridoxine, pyridoxal and

pyridoxamine.

•

cofactor of many enzymes involved in the metabolism of

many amino acids.

•

neurotransmitters synthesis

•

heme synthesis.

•

Vitamine metabolism as niacin

Source:

is found widely in plant and animal foodstuffs.

Vitamin B6

Cause of deficiency:

Dietary deficiency

is extremely rare.

Some drugs

(e.g. isoniazid,

hydralazine,methyldopa,

penicillamine) interact

with pyridoxal phosphate,

producing B6

deficiency.

Vitamin B6

Clincal features

: mucsal changes

The peripheral neuropathy occurring after isoniazid

usually responds to vitamin B6. personality changes

,depression, confusion.

Microcytic hypochromic anaemia occasionally responds

to vitamin B6 .

Treatment:

a daily dose of 100 mg should not be exceeded.

NB. vitB6 used as antiemetic especially in the pregnancy

Vitamin B12

The main function of B12 is the methylation of homocysteine to

methionine with the demethylation of methyl THF

polyglutamate to THF.

Source:

• humans are ultimately dependent on animal sources. It is

found in meat, fish, eggs and milk, but not in plants.

• The average adult stores some 2-3 mg, mainly in the liver, and

it may take 2 years or more after absorptive failure before B12

deficiency develops.

Deficiency:

Low dietary intake

, Vegans

Impaired absorption

• Stomach : Pernicious anaemia ,Gastrectomy ,Congenital

deficiency of intrinsic factor

• Small bowel: Ileal disease or resection ,Bacterial overgrowth

Fish tapeworm (Diphyllobothrium latum)

Abnormal utilization

:Congenital transcobalamin II

deficiency

Clinical features

1. Anaemia of megaloblastic type
2. A red sore tongue (glossitis) and angular stomatitis are

sometimes present.

3. The neurological changes,
a.

polyneuropathy progressively

involving the peripheral

nerves

b. the posterior and eventually the lateral columns of the

spinal cord

(subacute combined degeneration

)

symmetrical paraesthesiae in the fingers and toes,
early loss of vibration sense and proprioception, and ataxia

progressive weakness and Paraplegia may result.

Dementia, psychiatric problems

, e.g. depression,

hallucinations, delusions, and optic atrophy also

occur.

Investigations

Haematological findings show the features of a megaloblastic

anaemia

2. Bone marrow shows the typical features of megaloblastic

erythropoiesis

( .

3. Serum bilirubin may be raised as a result of ineffective

erythropoiesis.

4. Serum vitamin B12 is usually well below 160 ng/L, which is

the lower end of the normal range.

Treatment

Hydroxocobalamin 1000 μg can be given intramuscularly.
improvement of the polyneuropathy may occur over 6-12

months,

but long-standing spinal cord damage is irreversible.

Folates

• are present in food as in the reduced dihydrofolate or

tetrahydrofolate (THF).

• act with vit B12 as 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 .

Causes of folate deficiency

Nutritional

major cause

  Poor intake
• Old age
• Poor social conditions
• Starvation
• anorexia
  Gastrointestinal disease,
•  partial gastrectomy
•  small bowel disease , coeliac disease, Crohn's disease
  Antifolate drugs
• Anticonvulsants :

– phenytoin

• Methotrexate

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)

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).

Treatment of folate deficiency

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

body stores.

• Any underlying cause, e.g. coeliac disease, should be treated .

• Prophylactic folic acid is recommended for all women

planning a pregnancy. ( neuronal tube defect)

• Prophylactic folic acid is also given in chronic haematological

disorders where there is rapid cell turnover.

Vitamin C Ascorbic acid

• 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.

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

• Per follicular hemorrhages
• Swollen, spongy gums with bleeding and

superadded infection

• Spontaneous hemorrhage(git, joint,

peritoneum)

• Failure of wound healing

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Diagnosis

• Plasma ascorbic acid is very low in obvious deficiency and a

vitamin C level of less than 11 μmol/L indicates vitamin C
deficiency.

Treatment

Initially the patient is given 200 mg of ascorbic acid daily and

encouraged to eat fresh fruit and vegetables.

Vitc in large amount used in upper respiratory tract

infection

Vitamin A(retinol)

• Metabolites

: are retinaldehyde and retinoic

acid

• Function:

retinaldehyde

is important of vision

retinoic acid

for the cell growth and

differentiation

retinoids

synthetic molecule

also plays a role in

iron utilization

humeral immunity

T cell–mediated immunity

natural killer cell activity

phagocytosis

Vitamin A(retinol)

Metabolism:

• The

liver

contains 90% of the vitamin A is bound to retinol-

binding protein

transthyretin

trimolecular

complex

specific cell-surface receptors

bound to a series of cellular retinol-binding proteins, function
as transporting agents as well as co-

ligands

for enzymatic

reactions.

• Retinoic acid

is a ligand for certain nuclear receptors that act

as transcription factors.( retinoid-mediated gene
transcription)

Vitamin A(retinol)

• Retinoids

receptors for cell proliferation and

differentiation

used

in : promyelocytic leukemia

cystic acne

• Dietary source:

animal source

: liver and fish(excellent source)

plant source

: dark-green vegetable and fruits

Vitamin A(retinol)

Deficiency:
1.

chronic dietary deficit

(developing countries) In

Southern Asia, Sub-Saharan Africa, some areas of Latin America

inadequate intakes of animal food sources seasonal unavailability of
vegetables, colored fruits.

More than

125 million

preschool-age children with vitamin A deficiency,

4 million

have an ocular manifestation of deficiency .

At least a

quarter

of a million children each year developed blindness.

Vitamin A(retinol)

2. Malabsorption:

(developed countries)

celiac disease, short bowel syndrome

3. Zinc deficiency:

interfere with vitA mobilization from the liver

4. Alcohol :

interfere with conversion of retinol to retinaldehyde

in the retina (dehydrogenase)

5. Drugs :

interfere with the absorption of vitA

neomycin, cholestyramine

Vitamin A(retinol)

Clinical features

• Milder stages of

night blindness

(loss of dark adaptatio)

• conjunctival xerosis

(dryness)

(xerophalmia)

• Bitot's spots

(white patches of keratinized epithelium

appearing on the sclera)

• Keratomalacia

(softening of the cornea) leads corneal

ulceration and necrosis result in corneal scarring that
blinds.

• increased risk of mortality from diarrhea, dysentery,

measles, malaria, and respiratory disease.

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Vitamin A(retinol)

Diagnosis:

1. Serum retinol level
2. Test of dark adaptation
3. Impression cytology of the conjunctiva
4. Store assessment by liver BX

Vitamin A(retinol)

Treatment:

30mg IM

or 60mg orally then

60mg

of vitA after 6 months

15mg

orally for 1 month in patient with malabsorp.

Vitamin A supplementation can markedly reduce risk of child

mortality (23–34%) where deficiency is widely prevalent.

NB.

Used in patient with M3 leukemia and cystic acne

Vitamin D

Synthesis and Metabolism:

• steroid

hormone

involved in mineral ion homeostasis regulation,

can be synthesized endogenously In response to ultraviolet
radiation of the skin, a photochemical cleavage from 7-
dehydrocholesterol.

• In the United States and Canada

animal sources

(vitD3) dairy products, fish oils, egg

yolks.

plant sources

(vitamin D

)

cereals

Vitamin D

Causes of the deficiency :

Vitamin D deficiency

  Impaired cutaneous production
  Dietary absence
  Malabsorption

Accelerated loss of vitamin D

Increased metabolism (barbiturates, phenytoin,

rifampin)

Impaired enterohepatic circulation

Causes of decrease action
Impaired 25-hydroxylation

Liver disease
Isoniazid

Impaired 1-hydroxylation

  Hypoparathyroidism
  Renal failure
  Ketoconazole
   1-hydroxylase mutation
   X-linked hypophosphatemic rickets

Target organ resistance

Vitamin D receptor mutation

Phenytoin

Vitamin D

Clinical features:

1. Mild to moderate deficiency is

asymptomatic

Osteomalacia

(defective bone mineralization)

  Muscle and bone pain
  Malaise
  Fragility fracture( pseudofractures)
  Proximal myopathy ( wadling gait, diff. climbing stairs)
  Bone tenderness

3.

Rickets

( growth retardation, bone deformities)

Vitamin D

Diagnosis:

1. Biochemical tests

decrease serum 25(OH)D (< 37 nmol/L)

low or normal s. Ca. , ph.

increasing PTH levels

increase alkaline phosphatase

2. Radiological tests

of oteomalacia

decrease in cortical thickness

osteopenia of the skeleton

pseudofractures, or Looser's zones in the ribs and pelvis
and long bones and vertebra

3. Bone biopsy

Vitamin D

Treatment:

(

50,000 IU

weekly for 3–12 weeks), followed by maintenance

therapy (800 IU daily). Calcium supplementation should
include 1.5–2.0 g/d of elemental calcium

Daily intake of

(400 IU)

is often insufficient to prevent

deficiency.

800 IU of vitamin D

, with calcium supplementation,

decreases the risk of hip fractures in elderly women. .

Vitamin E ( tocopherols)

Function:

• acts as

antioxidant

and radical

scavenger

, which protects

low-density lipoproteins (LDLs) and polyunsaturated fats
in membranes from oxidation.

Absorption and Metabolism:

• After absorption, vitamin E is taken up from

chylomicrons

by the liver, and a hepatic tocopherol transport protein
mediates intracellular vitamin E transport and
incorporation into very low-density lipoprotein

(VLDL)

Vitamin E ( tocopherol)

Dietary source:

• The RDA for vitamin E is 15 mg/d

• widely distributed in the food supply

high

in sunflower oil, soybean and corn oils.

meats, nuts, and cereal grains

small amounts

in fruits and vegetables.

• Vitamin E pills

containing doses of 50–1000 mg are

ingested by a large fraction of the U.S. population.

Vitamin E ( tocopherol)

Causes of the deficiency:

Dietary deficiency

of vitamin E does not exist.

2. severe and prolonged

malabsorptive diseases

celiac disease, small-intestinal resection.

3. prolonged

cholestasis

may develop vitamin E

4. Children with

abetalipoproteinemia

cannot absorb or

transport vitamin E.

5. A

familial form

of isolated vitamin E deficiency (defect

in the tocopherol transport protein).

Vitamin E ( tocopherols)

Clinical features:

axonal degeneration of the large myelinated axons and results

posterior column

and

spinocerebellar

symptoms.

  Peripheral neuropathy
  ataxic gait (Decreased vibration and position Sensations)

Ophthalmoplegia

skeletal myopathy
pigmented retinopathy

Diagnosis

: of low blood levels of tocopherol

Vitamin E ( tocopherols)

Treatment

• 800–1200

mg of tocopherol per day.

• Vitamin E

has been suggested to increase sexual

performance, and to slow the aging process, but evidence
for these properties

is lacking

• High doses (60–800 mg/d)

of vitamin E have been shown

in controlled trials to improve parameters of immune
function and to reduce colds in nursing home residents.

• but intervention studies using vitamin E to prevent

cardiovascular disease or cancer have

not

shown efficacy.

Vitamin k

Function:

• vitamin K

phylloquinone, from vegetable and animal

sources

• vitamin K

, menaquinone, which is synthesized by

bacterial flora and found in hepatic tissue.

• required for the

carboxylation

of glutamic acid, which is

necessary for calcium binding to -carboxylated proteins
such as prothrombin (factor II); factors VII, IX, and X;
protein C; protein S).

• Warfarin

preventing the conversion of vitamin K to its

active hydroquinone form.

Vitamin k

Dietary Sources:

•

green leafy vegetables

(spinach)

also present in margarine and liver.

vegetable oils rich :olive, soybean oils.

• The average daily intake by Americans is estimated to be

approximately

100 Mg/d

Vitamin k

Causes of the deficiency

1. chronic

small-intestinal disease

(e.g., celiac disease,

Crohn's disease).

cholestatic

liver disease.

3. Broad-spectrum

antibiotic

treatment.

drug

therapy, the antiobesity drug orlistat

Vitamin k

The diagnosis:

• elevated

prothrombin time

or reduced clotting factors,

• vitamin K may also be measured directly.

Treatment:

• Vitamin K deficiency is treated using a parenteral dose of

mg.

• For patients with chronic malabsorption,

1–2 mg/d

of vitamin K should

be given orally, or

1–2 mg/week

can be taken parenterally .