This document discusses several vitamin deficiencies including vitamins A, D, C, and B1. It provides details on the roles of these vitamins, signs and symptoms of deficiencies, diagnostic testing, and treatment approaches. Vitamin A is important for vision, growth, and reproduction. Vitamin D deficiency can cause rickets, a softening of the bones. Scurvy is caused by vitamin C deficiency and results in issues with collagen production. Beriberi is a thiamine (vitamin B1) deficiency that can impact the heart or nerves. Treatment for the deficiencies involves supplementation with the respective vitamins.

1. VITAMIN
DEFICIENCY
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2. VITAMIN A
oVitamin A is a fat soluble vitamin
oRequired for vision, repair, reproduction and growth
oThis occurs in two form  1, retinol in animal foods 2. b carotene in
plant food
oCarotene is converted into retinol in the intestine, which is then
absorbed and stored in the liver as retinol palminate
oRainbow revolution is cultivating and consuming green, yellow, orange ,
red (GYOR) vegetables and fruits to reduce micronutrient malnutrition.
oDue to deficiency of vitamin A  night blindness
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3. VITAMIN D- RICKETS
oRickets is a disease of the growing skeleton.
oIt is characterised by failure of normal mineralisation, seen prominently
at the growth plates, resulting in softening of the bones and
development of deformities
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4. Types of rickets
TYPES 1
a) Due to a deficiency of vitamin D
• Diminished intake e.g., malnutrition
• Diminished absorption e.g.,
◦ – Mal-absorption syndrome
◦ – Gastric abnormalities
◦ – Biliary diseases
• Lack of exposure to sunlight
b) Due to disturbance in vitamin D metabolism
• Hepatic factor e.g.,
◦ – lack of 25 hydroxylation of vitamin D
◦ – Increased degradation of vitamin D in patients on prolonged anti-convulsant therapy
• Renal factor e.g.,
◦ – Lack of 1 hydroxylation (autosomal recessive)
• Unresponsiveness of target cells to 1-25 dihydroxy vitamin D
• Renal osteodystrophy
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5. TYPE 2
a) Defective absorption of phosphates through renal tubules
• Hypophosphataemic rickets (x-linked dominant)
• Fanconi syndrome
• Renal tubular acidosis
• Oncogenic rickets
b) Diminished intake or absorption of phosphates
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7. CLINICAL FEATURES
Nutritional rickets occurs in children about 1 year old.
• Craniotabes: This is the manifestation of rickets seen in young infants. Pressure
over the soft membranous bones of the skull gives the feeling of a ping pong ball
being compressed and released.
• Bossing of the skull: Bossing of the frontal and parietal bones becomes evident
after the age of 6 months.
• Broadening of the ends of long bones, most prominently around wrists and knees.
It is seen around 6-9 months of age.
• Delayed teeth eruption is noticed in infants.
• Harrison's sulcus: A horizontal depression, along the lower part of the chest,
corresponding to the insertion of diaphragm.
• Pigeon chest: The sternum is prominent.
• Rachitic rosary: The costo-chondral junctions on the anterior chest wall become
prominent, giving rise to appearance of a rosary.
• Muscular hypotonia: The child's abdomen becomes protruberant (pot belly)
because of marked muscular hypotonia. Visceroptosis and lumbar lordosis occurs.
• Deformities: Deformities of the long bones resulting in knock knees or bow legs is
a common presentation of rickets, once the child starts walking.
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9. RADIOLOGICAL FEATURES
Early radiological changes are observed in the lower ends of the radius and ulna. X-
rays of both wrists and knees – antero-posterior views are used for screening a
patient suspected of rickets
• Delayed appearance of epiphyses.
• Widening of the epiphyseal plates: Normal width of the epiphyseal plate is 2-4
mm. In rickets it is increased
• Cupping of the metaphysis: Normally, the metaphysis meets the epiphyseal plate
as a smooth line of sclerosis (zone of provisional calcification). In rachitic bones, this
line is absent and the metaphyseal end appears irregular
• Splaying of the metaphysis: The end of the metaphysis is splayed because of the
pressure by the cartilage cells accumulating at the growth plate.
• Rarefaction of the diaphysial cortex occurs late.
• Bone deformities: Knock knees, bow legs and coxa vara are common deformities in
older children.
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10. OTHER INVESTIGATION
1. Serum calcium is usually normal or low
2. Serum phosphate is low
3. Serum alkaline phosphatase is high
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11. TREATMENTS
Medical treatment:
oAdministration of vitamin D 6,00,000 units as a single oral dose induces
rapid healing  Repeat Xray within 3-4 weeks  same dose may
repeated
oIf responding with the dose then  400 IU of vitamin D is given per day
oIf not responding with 2nd dose  diagnosis of refractory rickets is
made.
oSuch patients are evaluated in detail by multi speciality team of
nephrologist, endocrinologistand physician.
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12. Orthopaedic treatment: It is required for the correction of deformities
by conservative or operative methods.
a) Conservative methods: Mild deformities correct spontaneously, as
rickets heals. Some surgeons use specially designed splints
(mermaidsplints) or orthopaedic shoes for correction of knee
deformities.
b) Operative methods: Moderate or severe deformities often require
surgery. This can be performed any time after 6 months of starting the
medical treatment. Corrective osteotomies, depending upon the nature
of deformities, are performed.
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13. VITAMIN-C SCURVY
oThis disease is caused by deficiency of vitamin C (ascorbic acid). The
result is decreased production and poor quality collagen.
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14. AETIOLOGY
Due to deficiency of vitamin C.
1. Age – usually from 6 months to 2 years.
2. Diet – more common in artificially fed infants.
3. Precipitated by febrile disease, infections, or diarrhoea
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15. SIGN & SYMPTOMS
Onset –
(a) Usually gradual – Fretfulness and increasing pallor or tenderness of legs which
causes child to cry whenever touched, anorexia and loss of weight.
(b) Rarely sudden onset, the first symptom being inability of the child to use his
legs
.
oIn adults,
•It presents with swollen gums, gingivitis and abnormal bleeding tendencies
typically producing perifollicular haemorrhages over the lower part of the thighs.
•Petechial haemorrhages and spontaneous bruises may occur anywhere in the
body but usually first in the lower extremities.
oIn infantile scurvy,
•features are lassitude, anaemia, painful limbs due to sub-periosteal haematoma
and scorbutic rosary (bead like thickening of the ribs due to calcified sub-
periosteal haematomas).
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17. INVESTIGATIONS
X-RAY
Generalized decrease in bone density of shaft and epiphyses (ground glass
appearance).
Pencilled cortex – Cortex is thinned out appearing only as a pencil streak.
Halo sign of Wimberger – due to pencilling effect produced by the
epiphysis
Subperiosteal hematomas – Soft tissue densitie due to lifting off of the
periosteum from the underlying bone
Joint effusions – causing bulging of joint capsule or the flat planes around
the joint.
Subluxation of epiphysis may occur in very severe cases.
Scorbutic rosary/zone – Step-like subluxation of costochondral joints
Plasma ascorbic acid level – very low.
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19. TREATMENT
Treatment  supplementation with vitamin C.
Vitamin C –
 (i) 3 to 4 ounces of fresh orange juice or tomato juice daily.
 (ii) Ascorbic acid – 100 mg or more orally or parenterally twice or thrice daily.
Pain lessens and alertness increases within 24 hours.
X-ray changes take 15–21 days to resolve  Continue treatment for 10–
15 days.
IV vitamin C is mainly excreted in urine.
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20. VITAMIN-B BERIBERI
The disease caused in the body by the deficiency of vitamin B1 is
known as beriberi.
As vitamin B1 is also known as thiamine, it is also known as thiamine
deficiency.
Beriberi is a life-threatening disease, causing inflammation of nerves
and heart failure.
Due to deficiency of vitamin B (thiamine)
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21. 2 types of beriberi  DRY & WET
WET BERIBERI
1. Symptoms of cardiac involvement.
2. Heart enlarged, Tachycardia, Tenderness of calf muscles and
blunting of sensation.
3. Oedema firmer than that of nephrosis and does not involve
scrotum.
4. Absent or sluggish deep reflexes.
5. Decreased urinary output of thiamine.
DRY BERIBERI
Neurological features – Peripheral neuropathy, ataxia and burning
paraesthesia (e.g. burning mouth syndrome).
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23. TREATMENT
Beriberi can be treated by increasing the level of thiamine in the body.
The doctor may suggest oral supplements and injections of thiamine.
In some cases, intravenous fluid rich in thiamine can also be suggested
to the patient.
◦ Thiamine-rich food to be included in the diet to prevent its deficiency. Beans,
legumes, seeds, nuts, meat, seafood, whole grains, cereals, vegetables like
spinach, beet grains, asparagus, and dairy products are rich in thiamine
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