Thiamine, also known as vitamin B1, is an essential nutrient that plays a key role in carbohydrate metabolism. It consists of a pyrimidine ring connected to a thiazole ring. Thiamine acts as a cofactor for several enzymes involved in the breakdown of carbohydrates and the citric acid cycle. Deficiency of thiamine can cause diseases like beriberi, which presents as either "wet" beriberi with edema or "dry" beriberi with neurological symptoms. Treatment involves high doses of thiamine supplementation.

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2. • THIAMINE
•B1
• By
•DR MUSTANSAR

3. • Thiamine was the first of the water soluble
B vitamins to be identified as an essential
nutrient. Chemically, it consists of a
substituted pyrimidine ring (A) and a
thiazole, connected by a methyl group.
The term vitamin B1 encompasses
several compounds with thiamine-like
effects.

4. • Naturally occurring B1 consists mostly of
thiamine phosphates. In pharmaceuticals,
water-soluble thiamine derivatives like
thiamine hydrochloride or nitrate as well
as lipophilic thiamine analogues like
benfo-thiamine or fursulthiamine are used.

6. B1: structure & function

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THIAMINE (VIT B1)
It is also called Anti Beri-Beri factor, Anti
Neuritic factor.
It is colorless basic organic compound
composed of a sulfated pyramidine ring.

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Source
• PLANTCEREALS,
PEAS, BEANS, NUTS
VEGETABLES
• ANIMALLIVER,
KIDNEY, EGGS, PORK
MEAT, MILK

9. Vitamin B1 (Thiamine)
SOURCES
 Cereals
 Pulses
 Oil seeds
 Nuts
 Yeast
 Meat
 Fish
 Egg
 Milk
RDA: Adults 1.2-1.5 mg/day

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Absorption and excretion
It is readily absorbed from both small & large
intestine.
The capacity of human intestine to absorb this
vitamin is limited to about 5mg per day.
Any excess supply of thiamine is excreted in
the urine.

11. BIOCHEMICAL FUNCTIONS: THIAMINE
• TPP [cocaroxylase] being an essential
part of the decarboxylating
dehydrogenases acts as a cofactor in
many important reactions in carbohydrate
metabolism i.e., dehydrogenase [PDH]
complex and α-ketoglutarate
dehydrogenase [αKGDH] complex
i. Oxidative Decarboxylation of α-ketoacids

12. ii. Conversion of α-Ketoglutarate to succinyl-
SCoA
iii. TPP acts as coenzyme in reactions
catalyzed by transketolase
iv. Tryptophan metabolism:
Tryptophan pyrrolase
Tryptophan N-formylkynurenine
O2

13. v. TPP is a coenzyme for mitochondrial
branched chain α-ketoacid
dehydrogenases [decarboxylases] which
oxidatively decarboxylate α-ketoacids
formed in the catabolsim of valine, leucine
and isoleucline.

14. v. In the nervous system: TPP is a cofactor
for the synthesis of acetylcholine.
vi. TPP also acts as a coenzyme [co-
carboxylase] for pyruvate carboxylase in
yeast for non-oxidative decaroxylation of
pyruvate to acetaldehyde.

17. THIAMIN IMPORTANCE

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Functions
Essential for normal growth and development
Essential for maintaining nerves in normal
condition
Nervous tissue – it plays important role in the
normal functioning of the entire nervous
system.
Digestion – it aids in the digestion especially
that of carbohydrates.

19. FUNCTIONS
Essential for normal functioning of nerves
Co-enzymatic activities- carbohydrate,
nucleic acid and energy synthesis

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Daily requirement
Men – 1.3 mg
women – 1.0 mg
Pregnancy and lactation 2mg
Children – 1.1mg.

21. DEFICIENCY
 Beri beri
Earliest symptoms:
anorexia
dyspepsia
heaviness and weakness of legs.
calf tenderness

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Deficiency
Nervous disorders – when cells cannot
metabolize glucose, it affects the nervous
system first, since it depends entirely on
glucose for its energy requirement. & There is
mental depression.

23. Digestive symptoms- it occurs due to
defective hydrochloric acid production in the
stomach patient complains of loss of appetite,
poor digestion, loss of weight.

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PROLONGED DEFICIENCY
BERI BERI
a) DRY BERI BERI
b) WET BERI BERI..
c) INFANTILE BERI BERI
Other diseases which can be associated with it
are
wernickes encephalopathy
peripheral neuritis
korsakoff’s psychosis.

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BERI-BERI
Early symptoms: Irritability, fatigue, restlessness,
decreased appetite.
Later symptoms:
 tingling numbness in the extremities
 dyspnoea
 cyanosis
 unusual behaviour
 seizures
 loss of conscious

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DRY BERI BERI
Clinical features:-
 it is peripheral neuropathy.
 In long standing cases, there is degeneration
and demyelination of both sensory & motor
nerve
INFANTILE BERI BERI
 Vomiting
 Weight loss
 Convulsions

27. Wet beri beri Dry Beri beri
 Oedema of legs, face Progressive muscle weaknes and
trunk and serous cavities. disability
 Calf muscles are swollen and tender Neurological manifestations
 Palpitation and breathlessness
 Low diastolic BP, high systolic.
 Fast pulse
 Heart becomes weaker
and patient dies of heart failure

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Wet beri beri
It is marked by cardiac dilation with four chamber
enlargement, pallor and flabbiness of
myocardium.
Etiology :-
Diet
 Alcoholics- interferes with intestinal absorption
of thiamine

29. Infantile Beri beri
 Infants born to mother with low thiamine in
their breast milk.
 Restlessness and sleeplessness
 Anorexia, vomiting and breathlessness
 cardiac dilatation and failure.
 Sudden death if not treated urgently with
thiamine.

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34. Wernicke-korsakoff psychosis
Seen mostly in chronic alcoholics
Body demand of thiamine increases in
alcoholism
Characterized by:
• Dementia
• Apathy
• Nystagmus

35. Clinical features
 Odema- leg, face.
Anorexia
Dyspepsia
Rapid pulse

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Oral manifestation
There is hypersensitivity of oral mucosa
Pain in tongue, teeth, jaw, and face

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Pathogenesis-
Deficiency
Incomplete metabolism of glucose
Accumulation of pyruvic acid & lactic acid in
tissue & body fluid
Dilation of peripheral blood vessels
Fluid may leak out through capillaries,
producing edema
High cardiac output, heart dilation.

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Management
Complete rest
Thiamine 50mg IM for 3 days then 10mg 3
times daily by oral route.
 Infantile beriberi is treated via mothers milk.
The mother should receive 10,000mcg twice
daily, in addition infant should be given
thiamine in doses of 10,000 to 20,000 mcg IM
once in a day for 3 days