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VITAMIN B12

PRESENTED BY: NAINCY

ROLL NO 123
POINT OF DISCUSSION
1. DIETARY SOURCE AND ITS STRUCTURE
2. ABSORPTION,TRANSPORT AND
STORAGE
3. FUNCTIONAL ROLE OF B12
4. CAUSE OF VITAMIN B12 DEFICIENCY
5. DEFICIENCY MANIFESTITION
6. ASSESSMENT AND TREATMENT
Vit B12/cobalamine/extrinsic factor of
castle/antipernicious anemia factor
1. water soluble vitamin
2. RDA 1 microgram /day
 structure
 SOURCE

Source vasudevan
Absorption , transport and storage of vitamin B12

Source vasudevan
Functional role of vitamin B12
Cause of vit B12 deficiency
1.NUTRIENT DEFICIENCY 3.INCREASED DEMAND
2.MALABSORPTION
Deficiency manifestation
1. MEGALOBLASTIC ANEMIA

2. FOLATE TRAP
3. SUBACUTE COMBINED DEGENERATION
ASSESSMENT OF VIT B12 TREATMENT
DEFICIENCY
1. Macroblastic anemia
1. Serum B12 are treated with folate
2. Schilling test and vitamin B12
combinedly
3. Peripheral smear
2. Therapeutic dose of Vit
B12 by intramuscular
injection
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Hypervitamino
sis
Presented by: Nyasa

Roll No. 125

 Hypervitaminosis
• Abnormally high storage levels of vitamins
which can lead to toxic conditions.

• Primarily affects fat soluble vitamins as

these are stored for longer periods.
• Generally caused by high supplement intake
or large intake of highly fortified food.
 Hypervitaminosis A

•Dry skin, enlarged

and cirrhotic liver,
raised intracranial
pressure.

• Amount exceeding 7.5 mg/day should be

avoided.
 Hypervitaminosis D
• Excess exposure to sunlight does not result in
toxicity .
• Loss of appetite, nausea, thirst and weakness.

• Causes hypercalcemia
 Hypervitaminosis E
• Least toxic

• At doses above 1000 IU/day it may cause

tendency to hemorrhage as it is a mild
anticoagulant.
 Hypervitaminosis K
• Can produce hemolytic anemia and
jaundice in infant because of its toxic
effects on RBC membrane.
 Pyridoxine toxicity
• Vitamin B6 is only water soluble vitamin with
significant toxicity.

• Neurological
symptoms (sensory
neuropathy) occurs
at intake above
500mg/day.
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ONE CARBON
METABOLISM

Presented by: Nazneen

Roll No. :126
One carbon metabolism

• One carbon group plays a pivotal role

in donating carbon for synthesis of
different types of compounds.
 “One carbon pool”
1.Formyl group
2.Formimino group
3.Methenyl group
4.Hydroxymethyl group
5.Methylene group
6.Methyl group
 Generation of one-carbon group
1.Serine to glycine=methylene THFA
2.Glycine=methylene
3.Histidine=N5-formimino THFA
4.Tryptophan=formyl-THFA
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Vitamin Deficiency
due to
alcoholism
Presented by : Neeraj
Roll no : 127
How does alcoholism affect vitamin
depletion?

There are multiple ways:

1. Limitation of food intake:
As the primary share of their calories is from alcohol .

2. Gastrointestinal obstruction:
Excessive alcohol consumption has negative impacts the
lining of GIT .
Depletion of Vitamins can lead to :

 Chronic fatigue
 Pain
 Dehydration
 Bone loss
 Depression,etc
Vitamins Depleted due to Alcoholism:
 Deficiency of Thiamine :
1.Most common upto 80%
2.Decreases phosphorylation of Thiamine pyrophosphate
cofactor
 Deficiency of Pyridoxine:
1.Found in about 50%
2.lowering plasma levels of pyridoxal 5’-phosphate
 Deficiency of Folate :
1.About 1/3 rd of alcoholic patients
2.Alcohol impairs folate absorption, hepatic uptake and renal
conservation.
 Deficiency of Vitamin A:
1. Liver is the site for Vitamin A storage
2. Alcohol consumption lowers vitamin A
levels in liver
 Deficiency of Vitamin K :
Production of abnormal prothrombin
 Deficiency of Vitamin D:
Lowers the level of 25-hydroxyvitamin D
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 Role of Vitamin K in
differentiation of Hepatic
and
Post hepatic jaundice
Presented By: Neha
 Vitamin K overview
• It is present in green vegetable.
• It is synthesized in gut by luminal bacteria.
• Vitamin K is essential co factor for
synthesis of pro-coagulant fat soluble
factors II, VII, IX, X. as well as anti
coagulant factors protein C protein S and
anti thrombin III.
• Liver synthesis all vit-K dependent
procoagulant and anticoagulant
factors
• In obstructive jaundice , deficiency
of Vitamin K results in
hypoprohtrombinaemia and fall in
concentration of other vit-k
dependent pro and anticoagulant
factors.
 Prevention
• Although the predominant effect is
hypocoaguable state with obstructive
jaundice is malabsorption of Vitamin K.
• Prevention is achieved by administering
Vit-K which will correct deficiency in
those without chronic liver disease.
 Hypervitaminosis K
• Administration of large doses of vitamin K
• produces hemolytic anaemia and jaundice
particularly in infants.
• The toxic effect is due to increased
breakdown of RBC.
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VITAMIN - D
SYNTHESIS AND
FUNCTION
By: Nidhi Chaudhry
Roll No.
130
 Characteristics
Fat soluble vitamin
Also known as Anti- Rachitic factor.
 In diet occur in two forms:
 1.) Vitamin D2 (Ergocalciferol)
 2.) Vitamin D3 (Cholecalciferol)
Nutritional Requirement
RDA for Vitamin D is
 Action of Calcitriol on Intestine

Increases the intestinal absorption

of calcium and phosphorus.
By increased synthesis of calcium
binding proteins Calbindins.
Action of Calcitriol on Bone
Promotes the mineralization of
bone.(Anabolic)(At low doses)
D3 along with PTH stimulates the
mobilization of calcium and
phosphorus from bone.
(Catabolic)(At high doses)
Action of Calcitriol on Kidneys

Increased reabsorption of
calcium and phosphorus.
Decrease excretion of
calcium and phosphorus.
Regulation of Calcitriol
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Vitamin D
Deficiency Disorder
Presented By: Nisha Jha

Roll No. 131

The optimal concentration of 25-
hydroxy D3 is > 30 ng/mL, where as
20–29 ng/mL is considered insufficient
and 10–19 ng/mL is deficient.

A level below 10 ng/mL indicates

severe deficiency
The deficiency diseases are
rickets in children and
osteomalacia in adults.
Hence vitamin D is known
as antirachitic vitamin.
Causes for Vitamin D Deficiency
i.Deficiency of vitamin D can occur in people
who are not exposed to sunlight properly,
e.g. inhabitants of northern latitudes, in
winter months, in people who are bedridden
for long periods, or those who cover the
whole body (purdah).

ii.Nutritional deficiency of calcium or

phosphate may also produce similar clinical
picture.
iii. Malabsorption of vitamin (obstructive
jaundice and steatorrhea). High phytate
content in diet may also reduce the absorption
of vitamin.

iv. Abnormality of vitamin D activation. Liver

and renal diseases may retard the
hydroxylation reactions.

v. Deficient renal absorption of phosphates

Clinical Features of Rickets
i.Rickets is seen in children. There is insufficient
mineralization of bone. Bones become soft and
pliable. The bone growth is markedly affected.
ii. The classical features of rickets are bone
deformities. Weight bearing bones are bent (Fig.
36.11). Continued action of muscles also cause bone
malformations.
iii.The clinical manifestations include bow legs,
knock-knee, rickety rosary, bossing of frontal bones,
and pigeon chest.
iv. An enlargement of the epiphysis at
the lower end of ribs and costochondral
junction leads to beading of ribs or
rickety rosary.

v. Harrison’s sulcus is a transverse

depression passing outwards from the
costal cartilage to axilla. This is due to
the indentation of lower ribs at the site
of the attachment of diaphragm
Different Types of Rickets
1.The classical vitamin D deficiency rickets can
be cured by giving vitamin D in the diet.
2.The hypophosphatemic rickets mainly result
from defective renal tubular reabsorption of
phosphate. Supplementation of vitamin D along
with phosphate is found to be useful.
3.Vitamin D resistant rickets is found to be
associated with Fanconi syndrome, where the
renal tubular reabsorption of bicarbonate,
phosphate, glucose, and amino acids are also
deficient.
4. Renal rickets: In kidney diseases, even if
vitamin D is available, calcitriol is not
synthesized. These cases will respond to
administration of calcitriol.

5. End organ refractoriness to 1, 25-DHCC

will also lead to rickets. Either a decrease in
the number of cytosolic receptor or a
structurally abnormal receptor is noticed.
The bone disease has been found to respond
to megadoses of calcitriol (35 mg/day)
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Vitamin A Deficiency
Disorders
Presented By: Nishtha Arya

Roll No. 132 Ni

R
Functions of Vitamin A
The main role of Vitamin A is in the following-
Vision

Cellular differentiation and Growth

Skeletal Growth
Antioxidant Function
Reproduction

Glycoprotein Synthesis
Recommended Dietary Allowance
For an adult male : 2500-3500 I.U./day or 800-900
micrograms/day
For an adult female : 2000-2500 I.U./day or 700-800
micrograms/day
[1 I.U. = 0.3 micrograms of retinol]
Deficiency of Vitamin A
Decreased level of serum Vitamin A levels (normal levels –
30-60 micrograms/Dl)
Causes
Poor nutritional intake – particularly of colored fruits
and vegetables which are rich in carotene
Malabsorption of fats – because of Vitamin A is a fat
soluble vitamin and is absorbed with fats
Lipoprotein abnormalities such as defective chylomicron
synthesis which transport Vitamin A along with the fats
Liver Diseases – leading to inadequate storage and
formation of bile needed for absorption of Vitamin A
 Clinical Manifestations

OCULAR EXTRAOCULAR
MANIFESTATIONS MANIFESTATIONS

 Nyctalopia - Night  Follicular Hyperkeratosis

Blindness of skin
 Xerophthalmia – Dryness  Keratinization of skin and
of Conjunctiva mucous membranes
 Bitot’s Spots  Bone thickening and
 Keratoconus abnormal remodeling
 Keratomalacia  Gonadal dysfunction
 Ocular Manifestations
 Nyctalopia – It is the typical visual defect and is more commonly
referred to as night blindness. Vision in dim light is reduced.
 Dark adaption time is increased.
 Xerophthalmia – dryness of conjunctiva. It occurs due to the
improper formation and differentiation of tissue forming
conjunctiva.
 Bitot’s spots – Greyish white spots on the conjunctiva.

Xerophthalmia Bitot’s spots

 Keratoconus – due to improper cornea formation, it
becomes cone shaped and leads to difficulty in vision.

 Keratomalacia – it refers to the softening and

necrotic dissolution of cornea in the later stages
 Extraocular Manifestations
On skin and mucous membranes
 Follicular hyperkeratosis of skin – it occurs due to
increased keratin formation in follicle and leads to coarse,
rough and dry skin.
 Keratinization of the respiratory, genitourinary tracts and
intestinal mucous surfaces, leading to frequent infections.

Follicular
hyperkeratosis
Bone thickening and abnormal remodeling

 occurs specially in infants and children

thickening of the skull bones takes place + reduced remodeling

increased intracranial pressure

vomiting, seizures and unconsciousness

Gonadal dysfunction
decreased spermatogenesis and increased abortions are known
to be associated with Vitamin A deficiency. This could lead to
infertility.
 Treatment
 For mild deficiency with night blindness but without
eye changes, it is sufficient to give 15 mcg/day of
an oral micellar preparation of retinol capsule for 1
month

 For deficiency associated with eye changes, 60 mcg

of Vitamin A capsule orally or 30 mg of Vitamin A by
intramuscular injection are to be taken for long
duration to replenish body stores as well.
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