Disorders of Nutrition:

Vitamin deficiencies-1

Dr. Mehzabin Ahmed

Vitamins

1) Lipid Soluble Vitamins - A, D, E & K

2) Water Soluble Vitamins - B complex & C

 Vitamin A

• It is made by the body from carotene in red and yellow vegetables and
fruits
• It exists as retinol, retinal, retinoic acid
• Stored in the liver and shuttles it around on retinol-binding protein *
– * formerly called "prealbumin" or "transthyretin".
• After 25-hydroxylation in the liver, it is completely activated by 1-
hydroxylation in the kidney.
• Vitamin A is responsible for maintaining the differentiation of certain
special kinds of epithelium (including many ducts), and in the deficiency
state, epithelial surfaces of all kinds tend to undergo squamous metaplasia
and hyper-keratinize.
 Functions of Vitamin A

A. Maintaining normal vision in reduced light A component of

visual pigment

B. Potentiating the differentiation of specialized epithelial cells,

mainly mucus-secreting cells

C. Enhancing immunity to infections, particularly in children.

Resistance to infection

D. Regulates gene expression of growth factors and cell receptors

E. Nuclear transcription factor

 Clinical manifestations of vitamin A deficiency
NIGHT BLINDNESS-impaired vision, particularly in reduced light

RHODOPSIN
Squamous metaplasia causes the following complications:

– Xerophthalmia

– Secondary pulmonary infections,

– Renal and urinary bladder stones.

– follicular or papular dermatosis.

 Clinical manifestations of vitamin A deficiency
• Xerophthalmia (dry eye).
– Xerosis
• dryness of the conjunctivae as the
normal lacrimal and mucus-secreting
epithelium is replaced by keratinized
epithelium.
– Bitot spots
• build-up of keratin debris in small
opaque plaques
– Keratomalacia
• erosion of the roughened corneal surface
with softening and destruction of the
cornea
– Total blindness
 Immune deficiency

• Another consequence of avitaminosis A is immune deficiency.

– This impairment of immunity leads to higher mortality rates from

common infections such as measles, pneumonia, and infectious
diarrhea.
 Vitamin D.

• The major function of vitamin D is the maintenance of normal plasma

levels of calcium and phosphorus.

– Normal mineralization of bone

– Vitamin D maintains the correct concentration of ionized calcium in

the extracellular fluid compartment required for normal neural
excitation and relaxation of muscle.
Vitamin D precursor is available in the diet, or from the action of ultraviolet
light on 7-dehydrocholesterol in the skin.

• Women in countries where they

are required to remain veiled
when they go outdoors are at
greatly increased risk for rickets
Osteomalacia/
Rickets
 Vitamin D deficiency

• Rickets in growing children

• Osteomalacia in adults
• Hypocalcemic tetany
– Insufficient ionized calcium in
the extracellular fluid results in
continuous excitation of
muscle, leading to the
convulsive state, hypocalcemic
tetany.
Palisade of cartilage is lost and some of
the trabeculae are old well formed bone
with excessive uncalcified osteoid
 Osteomalacia

• In adults, the lack of vitamin D deranges the normal bone remodeling that

occurs throughout life. The newly formed osteoid matrix laid down by

osteoblasts is inadequately mineralized, thus producing the excess of

persistent osteoid characteristic of osteomalacia.

• Although the contours of the bone are not affected, the bone is weak and

vulnerable to gross fractures or microfractures, which are most likely to

affect vertebral bodies and femoral necks.

 Rickets

• The changes that occur in the growing

bones of children with rickets, however,
are complicated by inadequate provisional
calcification of epiphyseal cartilage
deranging endochondral bone growth.
• The basic derangement in rickets is an
excess of unmineralized matrix.
– This is because bone matrix or
osteoid continues to form but cannot
be calcified
– The accumulation of this non
calcified osteoid results in the
irregular appearance of the
metaphysis.
Rickets

• Craniotabes
• Frontal bossing
• Pigeon breast deformity
• Enlarged costochondral junction
(rachitic rosary)
• Harrison groove
• Lumbar lordosis
• Bowing of the legs
 Rickets - Deformity of cranial bones

• During the nonambulatory stage of infancy, the head and chest sustain the

greatest stresses.

• The softened occipital bones may become flattened, and the parietal bones

can be buckled inward by pressure; with the release of the pressure, elastic

recoil snaps the bones back into their original positions (craniotabes).

• An excess of osteoid produces frontal bossing and a squared appearance

to the head.
 Rickets - Chest wall deformities

• Deformation of the chest results from overgrowth of cartilage or osteoid

tissue at the costochondral junction, producing the "rachitic rosary."
• The weakened metaphyseal areas of the ribs are subject to the pull of the
respiratory muscles and thus bend inward, creating anterior protrusion of
the sternum (pigeon breast deformity).
• The inward pull at the margin of the diaphragm creates Harrison's
groove, girdling the thoracic cavity at the lower margin of the rib cage.
 Rickets - Bony deformities

• The pelvis may become deformed.

• When an ambulating child develops rickets, deformities are likely to affect

the spine, pelvis, and long bones (e.g., tibia), causing, most notably,

– lumbar lordosis and

– bowing of the legs

Rickets – X ray findings

• On plain film there is

characteristic flaring, cupping,
expansion and irregularity of the
metaphysis.
 Vitamin K.

• Vitamin K is a required cofactor for a liver microsomal carboxylase that is

necessary to convert
carboxylase
• Glutamyl residues γ-carboxyglutamates
(certain protein precursors)

• Clotting factors VII, IX, and X and prothrombin all require

carboxylation of glutamate residues for functional activity.

• The major consequence of vitamin K deficiency (or of inefficient use of

vitamin K by the liver) is the development of a bleeding diathesis.
 Vitamin K deficiency

• In neonates, it causes hemorrhagic disease of the newborn.

– Its most serious manifestation is intracranial hemorrhage, but
bleeding may occur at any site, including skin, umbilicus, and
viscera.
• In normal full-term infants, by 1 week of age, endogenous flora provide
sufficient vitamin K to correct any lingering deficit.
• In adults suffering from vitamin K deficiency or decreased synthesis of
vitamin K-dependent factors, a bleeding diathesis may occur, characterized
by hematomas, hematuria, melena, ecchymoses, and bleeding from the
gums.