vitamins

9. Beri beri
 Deficiency:- thiamine
 Symptoms:- anorexia , dyspepsia, heaviness and
weakness.
Types :- wet beri beri:- cardiovascular manifestation
 edema of legs, face, trunk, serous cavities and
distended neck veins , weak heart muscles, calf
muscles are swollen, BP increase , fast pulse, death
- Dry beri beri:- CNS manifestations
- Diffculties in walking
- Sensory distrubance
- Paralysis, become bedridden
-infantile beriberi:-infants born to mothers suffering
from thiamine def.

10. Wernicks-korsakoff syndrome
 Known as cerebral beri beri
 Encephalopathy
 Cerebellar ataxia
 Nystagmus
 Psychosis
Polyneuritis :- chronic alcoholics
Sym.- lactic acidosis
Alcohol inhibits absorption of thaimine
Treatment :- needs large doses of thiamine.

13.  Sources :- liver, egg, fish, green leafy
vegetables, milk .
 Synthesize by the intestinal flora
 Requirements :- adults :- 1.5 mg/day
 Pregnancy ,lactation and old age:- 0.2-0.4
mg/day

15.  Angular stomatitis ;-- infected
corners of mouth
 Proliferation of bulbar conjunctival
capillaries

17. 
Sources :- liver, egg, fish, green leafy
vegetables, milk .
 Requirements :- normal = 20 mg/day
 Lactation :- 5 mg/day
 Toxicity :- given orally produces transient
vasodilatation of the cutaneous vessels and
histamine release
 Causes ;- itching, burning, tingling.

23.  Coenzyme ;- PLP
 RDA :- 2-2.2 mg/day
 Sources :- egg yolk, fish, milk ,meat, wheat,
corn , cabbage.
 Drug induced B6 deficiency
- Isoniazid :- for TB
- Penicillamine :- for RA ( rheumatoid arthritis )

25. Vitamin B6
 Vitamin B6 to a family of 3 related
compounds; -
 pyridoxine (alcohol),
 pyridoxal (aldehyde)
 pyridoxamine.
 Coenzyme :- pyridoxal phosphate (PLP).

26.  RDA :- 2-2.2 mg/day
 Sources :- egg yolk, fish, milk ,meat, wheat,
corn , cabbage.
 Drug induced B6 deficiency
- Isoniazid :- for TB
- Penicillamine :- for RA ( rheumatoid arthritis )

29. Biochemical functions
 Transamination
1. These reactions are catalyzed by aminotransferases
transaminases) which employ PLP as the
coenzyme, For example:
 Alanine + alpha ketoglutarate alanine transaminase
Pyruvate + Glutamic acid

31. Decarboxylation
 eg;-
1. Glutamate → gamma aminobutyric acid(GABA).
GABA is an inhibitory neurotransmitter, and
convulsions may occur in B6 deficiency, especially
in children. (convulsion )
2. Histidine → histamine, which is the mediator of
allergy.
3. 5-hydroxy tryptophan → serotonin
4. Cysteine → taurine
5. Serine → ethanol amine

32. . Metabolism of Sulfur-containing
Amino acids
1. Homocysteine + Serine Cystathionine synthase
Cystathionine
2. Cystathionine → Homoserine + Cysteine (Enzyme
Cystathionase)
 Both these reactions require PLP. Hence in vitamin B6
deficiency homocysteine in blood is increased. Therefore,
pyridoxine is used in homocysteinemia.

33.  Heme Synthesis
 Aminolevulinic acid synthase is a PLP-dependent enzyme. So, in B6
deficiency, anemia may be seen.
 Production of Niacin
 Tryptophan PLP Niacin
 (one vitamin is necessary for synthesis of another vitamin).
 3-hydroxykynurenine Kynureninase 3-hydroxyanthranilic acid
 Glycogenolysis
 Phosphorylase enzyme (glycogen to glucose-1-phosphate) requires
PLP.

34. Deficiency manifestation
1. Neurological Manifestations
In children, B6 deficiency leads to convulsions due to decreased
formation of GABA. PLP is involved in the synthesis of sphingolipids,
so B6 deficiency leads to demyelination of nerves and consequent
peripheral neuritis.
2. Dermatological Manifestations
niacin deficiency which is manifested as pellagra. Another
manifestation is the irregular indentations in nails.
3. Hematological Manifestations
In adults, hypochromic microcytic anemia may occur due to the
inhibition of heme biosynthesis.
4.Other metabolic disorders
Xanthurenic aciduria and homocystinuria will respond to vitamin B6
therapy.
Ethanol is converted to acetaldehyde, which inactivates PLP. Hence, B6

35. Pantothenic acid
 Anti dermatitis factor
 Metabolic role as COA( coenzyme A)
 Consists of two component :- pantoic acid & β-
alanine
 RDA :- 5-10 mg
 Sources :- egg , liver , meat, milk etc.
 Synth. :- by bacterial flora in intestines

36. Biochemical function
 CHO A.A F.A
 Acetyl COA
TCA cycle TG Cholesterol K.B Detoxication

37. Rxn
 Pyruvate to acetyl COA
 Ketogulatrate to succinyl COA
 Fatty acid to Acyl COA

38. Difciency
 Burning foot syndrome-
 Burning, pain, numbness in the lower
extremities
 Staggering gait
 Sleep disturbances
 Seen in prison camps, chronic alcoholic renal
dialysis patients .

39. Biotin
 Anti-egg white injury factor
 Consist of imidazole ring with thiophene ring
 Act as coenzyme for carboxylation reactions
 Various metabolic Rxn:-
- TCA & gluconeogenesis
- FA synthesis ( acetyl COA to Malonyl COA)
- Propionyl COA to methylmalonyl COA

40.  Coenzyme Activity of Biotin
 Biotin acts as a coenzyme for carboxylation reactions.
 Biotin Requiring CO2 Fixation Reactions
1. Acetyl-CoA Carboxylase
 This is the rate limiting reaction in the biosynthesis of fatty acids
 Acetyl-CoA + CO2 + ATP → Malonyl-CoA + ADP + Pi
2. Propionyl-CoA Carboxylase
 Propionyl-CoA + CO2 + ATP → Methyl malonyl-CoA + ADP +
Pi
3. Pyruvate Carboxylase
 Pyruvate + CO2 +ATP → Oxaloacetate + ADP + Pi
 Biotin-Independent Carboxylation Reactions
• Carbamoyl phosphate synthetase
• Addition of CO2 to form C6 in the purine ring
• Malic enzyme, converting pyruvate to malate.

41.  RDA :- 200-300 mg
 Sources :- bacterial flora of the gut
- liver, yeast, peanut, milk, egg yolk
BIOTIN ANTAGONISTS
- Avidin , protein present in egg white has great
affinity to biotin
- Intake of raw egg may cause biotin deficiency
- Avidin is heat liable and boiling of egg will
neutralize the inhibitory activity.
- One mole. Of avidin can bind with four mole.
Of biotin.

42. Deficiency
 Dermatitis
 Atrophic glossitis
 Hyperesthesia
 Muscle pain
 Anorexia
 Hallucinations
 Split nail

48. Folate trap

49.  RDA ;- 200 microgram/day
 Pregnancy & lactation ;- 300-400
 Dietary sources:- green leafy vegetables ,
whole grains, liver, kidney and eggs

51. Reduced DNA synthesis
In folate deficiency, THFA is reduced and thymidylate synthase
is inhibited. Hence dUMP is not converted to dTMP. So dTTP is
not available for DNA synthesis. Thus, cell division is arrested
Drugs: Anticonvulsant drugs (hydantoin, Dilantin, phenobarbitone)
will inhibit the intestinal enzyme so that folate absorption is
reduced.
Folate trap: The only way for the regeneration of free THFA is the
homocysteine methyl transferase, with the help of vitamin B12.
When B12 is deficient, this reaction cannot take place, leading to
folate deficiency.
. Homocysteinemia
Folic acid deficiency may cause increased homocysteine levels in
blood. Plasma homocysteine levels above 15 mmol/L will
increase the risk of cardiac diseases

52. . Histidine load test or FIGLU excretion test
Histidine is normally metabolized to formiminoglutamic
acid (FIGLU) from which the formimino group is
removed by THFA. Therefore, in folate deficiency,
FIGLU is excreted in the urine. This test is rarely done
nowadays
Folic Acid Therapy
In macrocytic anemia, the therapeutic dose is 1 mg of folic
acid per day orally. Folic acid alone should not be given
in macrocytic anemia; because it may aggravate the
neurological manifestation of B12 deficiency. So, folic
acid and vitamin B12 are given in combination to
patients.

53.  Reduced DNA synthesis:-
 ( macrocytic anemia;- peripheral blood picture
in folate deficiency
- Magaloblastic anemia:- vita. B12 deficiency
Hyper-homocystenemia :- homocysteine level
above 15 mmol/l
-Increase risk of coronary artery disease.
Faliure to convert homocysteine to methoinine .
Folic acid therapy :- 1mg folic acid /day

54. Folate antagonists

55. Folate antagonists
Sulfonamides:- Sulfa drug has structural similarity with para-
aminobenzoic acid (PABA) which is a constituent of folic acid. So
sulfa drugs will competitively inhibit the synthesis of folic acid in
bacteria.
Pyrimethamine;- is an antimalarial drug
 Aminopterin and Methotrexate
- Inhibit dihydrofolate reductase & block the formation of THF
- So, synthesis of purines and DNA impaired
- Blockage of cell proliferation occur.
- Used for the treatment of cancer.

58.  Absorption of B12 requires the intrinsic factor .
 Otherwise used as extrinsic factor becoz.
Derived from external sources .
 IF is secreted from parietal cells.
- One mole. Of IF is attached with 2 mole. Of
B12.

59. Absorption of Vit. B12

62.  Sub acute combined degeneration
-damage to nervous system
Demyelination :- affecting cerebral cortex as well
as spinal cord. so., sensory & motor tracts
affected.
Assessment :- serum B12
Peripheral smear
homocystinuria

63.  Treatment :- 100- 1000 microgram by
intramuscular injections.
 RDA :- 1-2 mcg/day
 Sources :- liver , curd.

67.  Tryptophan metabolism
 Tyrosine metabolism
 Iron ”
 Hb & folic acid metab.:- increase iron
absorption by keeping it in the ferrous form.
 Help in the formation of ferritin( storage form)&
mobilization of iron.
 Help in reconversion of metHb to Hb
 Steroid synthesis:- syn. Of corticosteroid.
 Antioxidant property , sparing action of other
vitamin like A, E & some B-complex.
 Cataract :- concentrated in the lens of eye.

69.  Anemia :- microcytic , hypochromic anemia
- Causes ;- loss of blood by hemorrhage
- Decreased absorption of iron
- Infantile scurvy :- Barlow’s disease
- b/w 6-12 months of age

71. What is the difference between fat-
soluble and water-soluble vitamins?
 Fat-soluble are stored in the liver and fatty
tissues. These are not readily excreted from
the body.
 Water-soluble vitamins travel in the blood and
are stored in limited amounts. These are
readily excreted from the body through urine.

72. What does RDA mean?
 Recommended Dietary Allowances
 These are suggested levels of essential
nutrients considered adequate to meet
nutritional needs of healthy individuals.

73. Digesting and Absorbing Water-
Soluble Vitamins

74.  All absorption takes place in the small intestine
 Fat-soluble vitamins
 Are absorbed in the duodenum
 Storage
 Vitamin A is mainly stored in the liver
 Vitamins K and E are partially stored in the liver
 Vitamin D is mainly stored in the muscle tissue
Vitamin Absorption and Storage

76. RDA
 Three components :- retinol, retinal ,retinoic acid
 Children
2000 – 3500 I.U.
 Men
5000 I.U.
 Women
4000 I.U.

78. Sources
 Animal Sources
 Eggs
 Meat
 Cheese
 Milk
 Liver
 Kidney
 Cod
fish oil
Plant sources
•Carrots
•Sweet Potatoes
•Apricots
•Broccoli
•Spinach
•Pumpkin

79.  Hypervitaminosis A leads to toxic
symptoms:
Dry, itchy skin
Headaches and fatigue
Hair loss
Liver damage
Blurred vision
Loss of appetite
Skin coloration

80. Wald’s visual cycle

83. Functions
 1. visual cycle :- vit. A is component of the
visual pigments of rod and cones cells.
-

84. Vitamin A and vision
 Vit. A is necessary to form rhodopsin (in
rodes, night vision) and iodopsins
(photopsins, in cones – color vision) -
visual pigment.
 Retinaldehyd is a prosthetic group of
light-sensitive opsin protein.
 In the retina, all-trans-retinol is
isomerized to 11-cis-retinol → oxidized to
11-cis-retinaldehyd, this reacts with opsin
(Lys) → to form the holoprotein
rhodopsin.
 Absorption of light → conformation
changes of opsin → photorhodopsin.

85. The Visual Cycle

88. Dark adaption mechanism
 Person shifts from bright light to dim area- leads
difficulty in seeing .
Due to resynthesis of rhodopsin & vision is improved.
 Increased in vita. A dificiency.
 Red light bleaches rhodopsin to a lesser extent.
 photosensitive cells
 Rods cones
( for dim light vision) ( bright light & color vision)

89. Causes
 Decreased intake
 Obstructive jaundice
 Cirrhosis of liver
 Severe malnutrition
 Chronic nephrosis
Investgation :-
Dark adaption test
Vitamin A
Normal level:- 25-50mg/dl

90.  Deficiency of vitamin A: Deficiency leads to a variety of
disorders of the eyes and this affect the vision, some of the
disorders are –
 1)Night blindness: The person cannot see the objects in
dim light and in nights.
 Bitot’s spot:- seen as greenish white triangular plaques
adherent to conjuctiva.
 2)Xeropthalmia : conjuctiva becomes dry, thick, wrinkled.
 Losses its transperancy.
 Dryness spreads to cornea.
3) Keratomalacia( softening of the cornea) :- Xeropthalmia
persists for long time , leads Keratomalacia .
Occur degeneration of corneal epithelium

92.  4)Skin become scaly, rough and is
covered with papillae (Small eruptions).
 5)Reproductive functions may also be
effected in vitamin ‘A’ deficiency.
 National Institute of Nutrition, Hyderabad
has evolved a method giving a large dose
(5 – 6 drops) of Vitamin-A once in six
months to prevent blindness in children

95.  RDA
 Children = 10 mcg/day
 Adult = 5-10 mcg/day
 Pregnancy = 10mcg/day

96. Vitamin D3 can be obtained in diet, or derived from cholesterol in a reaction
that requires UV light. Active form :- calcitriol
UV light
spontaneous
liver enzyme
25-hydroxylase
Vitamin D3
calcitriol

99. calcium
PTH

100. Why it is called prohormone
 Synthesized in one tissue and is transported in
blood to act on other tissues.
 It include autocrine and paracrine actions
 Its effect in kidney can be act as autocrine.

104. Rickets
 Insufficient mineralization of bone
 Bones become soft
 Weight bearing bones are bent
 Bow legs, knock knees , pigeon chest.
 Type :- Renal rickets
 Loss of hair (alopecia)
 Osteomalcia :- seen in adult
 bones are softened due to mineralization
 Increased osteoporosis
Bone fractured

105. Hypervitaminosis D
 Symptoms:-
 Weakness
 Hypertension
 Weight loss
 Polyuria
 Hypercalacemia

108. RDA
 Males = 10mg/day
 Females = 8 mg/day
 Pregnancy = 10mg/day

109.  For absorption bile salts requires ,occur in
small intestine , transported in plasma.
 Function :-
 Antioxidant
 Anti – atherogenic – oxidation of LDL & in the
development of atherosclerosis.
 Antisterility

110.  Protects cell membranes and other fat-soluble parts of
the body (LDL cholesterol) from oxidation
 May reduce the risk of heart disease
 May also discourage development of some types of cancer
 Promotes normal growth and development
 Promotes normal red blood cell formation
 Acts as anti-blood clotting agent
 Plays some role in the body’s ability to process glucose
 Also been known to aid the process of wound healing
role

111. Role of Vit E as antioxidant
 Act as natural antioxidant by scavenging free
radicals and molecular oxygen.
 Prevent peroxidation of PUFA in cell
membrane.
 Protection of RBC membrane from oxidants.
 Prevent oxidation of LDL. Oxidised LDL is
more atherogenic than native LDL.
 Terminate free radical lipid peroxidation.

113.  Neurological deficiency :- neuropathy,
demyelization of nerves , cerebellar ataxia
 retinal pigment degeneration
 A betalipoproteniemia .

118.  Absorption :- require bile salt.
 Transported in blood in chylomicrons
& VLDL.
 Stored in liver.( less amount)

120. Role of γ-carboxylate glutamate
in clotting factors
 γ-carboxyl group of clotting factors such as
prothrombin chelates Ca++ ions & so helps
in binding of blood clotting factors to platelet
cell membrane through –ve charged
phospholipids .
 In vitamin K deficiency , this carboxylation
does not occur & leads to coagulation
failure .

122. Causes
 Premature infants & new born babies
- Unable to store vitamin K
- chronic liver diseases
- malabsorption from intestine
- Prolonged use of antibotics
- Prolonged use of warfarin ( anticoagulant drug)

125. LIPOIC ACID
 Vitamin like compound, perform many
important functions.
 Sulphur containing fatty acid called 6,8-
dithiooctanoic cid( Alpha lipoic acid).
 Fat and water soluble.
 Metabolic role: As a coenzyme of Pyruvate
dehydrogenase complex(PDH Complex).
 As a coenzyme of Alpha keto glutarate
dehydrogenase complex.
 Also required for the action of enzyme sulfite

126. Antioxidants
 Group of compounds that neutralizes free
radicals, helping to counteract the oxidation
that takes place in cells
 Includes
 Vitamins E
 Vitamins C
 Selenium
 Flavonoids
 Carotenoids

127.  Defn: Substances that fight off free-radicals in
our bodies.
 Free radicals are compounds within our bodies
that may lead to chronic disease and/or are
involved in cell tissue damage.
 Examples of vitamins that contain antioxidants
are… C, E, and Beta Carotene.

128. Free Radicals

129.  Antioxidants, such as vitamin E and C,
selenium, flavonoids, and carotenoids, help
counteract the damaging effects free-radicals
 Oxidative stress occurs when free radicals
accumulate faster than the body can neutralize
them
 Contribute to chronic disease and conditions
 Fruits, vegetables, and whole grains are
excellent sources of antioxidants

130. Antioxidants proprties
.
 May be useful in prevention of myocardial
infarction and stroke.
 Can mop up free radicals in brain tissue and
thus can prevent conditions like multiple
sclerosis, Alzheimer's disease.
 Helps in reducing LDL.
 Stimulate production of glutathione.

131. MINERAL METABOLISM

132.  Inorganic elements
Classification:-
 Macrominerals- required >100mg/day
 Microminerals- required < 100mg/day

133. Classification
 Macrominerals  Microminerals
 Sodium
 Potassium
 Calcium
 Phosphorus
 Magnesium
 Sulphur
 Chlorine
 Chromium
 Cobalt
 Copper
 Fluoride
 Iodine
 Iron
 Manganese
 Molybednum
 Selenium
 Zinc

134. Metabolism of sodium, potassium
and chlorine
They grouped together because they
maintain:-
 Electrical neutrality
 Osmotic pressure
 Water and acid-base balance.
 Sodium- Extracellular fluid(cation)
 Potassium- Intracellular fluid(cation)

135.  Sodium: 135-145mEq/L
 Chloride: 95-105mEq/L
 Potassium: 3.5-5.5mEq/L
Normal levels ( electrolytes )

136. Sodium
 Sodium is the principal cation present in
extracellular fluids
 Total body sodium-4000mEq
 50% in bones, 40% in ECF, 10% in soft tissues
 Major cation in blood & plasma.
 Extracellular conc. Is maintained by Na-K ATPase
pump.
 Mainly present as NaCl or NaHCO3.
 Higher conc. In blood than in cells.

137.  Sources:- Tabel salt(NaCl) is major source
 Other sources- vegetables, nuts, eggs and milk.
 Readily absorbed in GIT, by active transport
in epithelial cells.
 Excretion:- kidney is the major source of
excretion
 About 800gm/day is filtered by Glomerulus in
that 99% is reabsorbed by tubules.
 Reabsoprtion is controlled by Aldosterone

138. Regulation of Sodium in Blood

139.  functions include:
osmotic equilibrium
acid-base balance
carbon dioxide transport
cell membrane permeability
muscle irritability

140. Disorders
Hyponatremia: ↓ sodium levels
Causes:-
 Use of Diuretics
 Excessive sweating
 Chronic renal failure
 Renal tubular acidosis
 Congestive heart failure
 Addisson disease(adreno-cortical insufficiency)
 Diarrhoea, Vomiting

141. Mild: Headache, Muscle cramps
Moderate to Severe: Low blood pressure and
Circulatory failure
Clinical features

142. Hypernatremia: ↑ sodium levels
Causes:-
 Cushing syndrome ( excess aldsterone)
 Prolonged adminstration of steroids
hormones( ACTH/Cortisone/Sex hormones)
 Severe dehydration(only water)
(Burns, Diabetes insipidus)
 Excess sodium intake
 C/F:- Increased blood volume and
Hypertension.

143. Potassium (K)
 Total body potassium-3500mEq
 75% in skeletal muscle
 Major Intracellular cation
 Daily requirement: 3-5gm/day
 Sources- vegetables, fruits(Banana, Orange),
meat, legumes and milk
 Tender coconut water(major source)

144. Absorption and Excretion
 Readily absorbed in GIT, by passive
transport in epithelial cells.
 Normal level: 3.5-5.5mEq/L
 Excretion:- three routes- GIT, skin and
urine(major route)
 During absorption of sodium there is
obligatory loss of potassium.

145. Factors that enhances the transport of
potassium in to the cell are:-
 Insulin
 Aldosterone
 Alkalosis
Factors causing potassium to move out of
cell:
 Acidosis
 Lack of insulin
 Severe cell damage

146.  Maintain osmotic pressure and water
balance.
 Maintain acid-base balance.
 Involved in neuromuscular activity of
cardiac and skeletal muscle.
 Involved in transmission of nerve impulses.
 Involved in biosynthesis of Proteins.
 Pyruvate Kinase needs potassium
Function

147. Hypokalemia: ↓ potassium levels
Causes:-
 Prolonged Vomiting and severe Diarrhoea
 Renal tubular acidosis
 Conn’s syndrome ( excess aldosterone causes K loss)
 Cushing syndrome
 Alkalosis
 Administration of Steroids
 C/F:- Muscle cramps, ECG changes, Vomiting, fatigue,
respiratory failure .
Disorders

148. Hyperkalemia: ↑ potassium levels
Causes:-
 Cell damage
 Addison’s disease ( deficiency of aldosterone)
 Diabetes mellitus
 Violent muscle contraction
 Acidosis
 Renal failure
 C/F:- Cardiac arrest, Cardiac arrhythmia, Muscle
weakness, ECG changes, CNS toxicity.