Most Important Chapters in Biology, Physics and Chemistry for NEET/AIIMS Exams

Most Important Chapters in Biology, Physics and Chemistry for NEET/AIIMS Exams

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Azeem Farooqui

TOPICS WHICH ARE ASKED OUTSIDE TH£ NCERT IN NEET cl AIIMS

VITAMINS (Vital Amines)

 Vitamins

Vitamins are a group of chemically diverse organic compounds that an organism requires for normal metabolism. Apart from a few exceptions (e.g., vitamin D), the human body cannot synthesize vitamins on its own in sufficient amounts and must, therefore, ensure a steady supply through the diet. Vitamins are micronutrients that do not provide energy (like macronutrients) but instead have very specific biochemical roles: They are coenzymes in various reactions (B vitamins, vitamins A and K) and antioxidants that protect the cell and its membranes from free radicals (vitamins C and E), enable cell signaling (vitamin A) and gene transcription (vitamins A and E), and serve hormone-like functions (e.g., vitamin D). Vitamins are classified as fat-soluble vitamins, which the body can store, and water-soluble vitamins, which, with the exception of vitamins B9 (folate) and B12, cannot be stored in the body over significant lengths of time and therefore require continuous intake. A balanced diet typically supplies the body with all the vitamins it requires, and deficiencies occur mainly due to malnutrition, malabsorption disorders, or restrictive diets (e.g., vitamin B12 in a vegan diet).
Overview of vitamins
• Classification: according to solubility
• Fat-soluble vitamins: vitamin A, vitamin D, vitamin E, vitamin K
• Water-soluble vitamins: vitamin B1, vitamin B2, vitamin B3, vitamin B5, vitamin B6, vitamin B7 (biotin), vitamin B9(folate), vitamin B12, vitamin C
• Sources
• Diet
• Produced in the body: Vitamin D is the only vitamin that the human body is capable of synthesizing in significant amounts.
• Intestinal flora: Vitamins K, B7, B9, and B12 are synthesized in small amounts by human intestinal flora (although vitamin B12 is produced in the large intestine, it is absorbed in the ilium. Therefore, consumption of vitamin B12 rich products is necessary)
• Recommended daily intake (RDI): While there are standard recommendations, the amounts required are highly dependent on individual factors.
• Functions
• Coenzymes (e.g., B vitamins, vitamins A and K)
• Hormone (vitamin D)
• Antioxidants (e.g., vitamins C and E)
• Cell signaling (e.g., vitamin A)
• Gene transcription (e.g., vitamins A and E)
• Deficiency
• Malnutrition, restricted diet (e.g., lactose-free or vegan diet)
• Malabsorption disorders
• Genetic disorders
• Excess
• Oversupplementation
• Almost exclusively from fat-soluble vitamins, which accumulate in the body.


To view flow chart for both vitamins like Fat soluble and Water soluble,Please open this link

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Vitamins

Summary

Vitamins are a group of chemically diverse organic compounds that an organism requires for normal metabolism. Apart from a few exceptions (e.g., vitamin D), the human body cannot synthesize vitamins on its own in sufficient amounts and must, therefore, ensure a steady supply through the diet. Vitamins are micronutrients that do not provide energy (like macronutrients) but instead have very specific biochemical roles: They are coenzymes in various reactions (B vitamins, vitamins A and K) and antioxidants that protect the cell and its membranes from free radicals (vitamins C and E), enable cell signaling (vitamin A) and gene transcription (vitamins A and E), and serve hormone-like functions (e.g., vitamin D). Vitamins are classified as fat-soluble vitamins, which the body can store, and water-soluble vitamins, which, with the exception of vitamins B9 (folate) and B12, cannot be stored in the body over significant lengths of time and therefore require continuous intake. A balanced diet typically supplies the body with all the vitamins it requires, and deficiencies occur mainly due to malnutrition, malabsorption disorders, or restrictive diets (e.g., vitamin B12 in a vegan diet).

Overview of vitamins

• Classification: according to solubility
  • Fat-soluble vitamins: vitamin A, vitamin D, vitamin E, vitamin K
  • Water-soluble vitamins: vitamin B1, vitamin B2, vitamin B3, vitamin B5, vitamin B6, vitamin B7 (biotin), vitamin B9(folate), vitamin B12, vitamin C
• Sources
  • Diet
  • Produced in the body: Vitamin D is the only vitamin that the human body is capable of synthesizing in significant amounts.
  • Intestinal flora: Vitamins K, B7, B9, and B12 are synthesized in small amounts by human intestinal flora (although vitamin B12 is produced in the large intestine, it is absorbed in the ilium. Therefore, consumption of vitamin B12 rich products is necessary)
• Recommended daily intake (RDI): While there are standard recommendations, the amounts required are highly dependent on individual factors. 
• Functions
  • Coenzymes (e.g., B vitamins, vitamins A and K) 
  • Hormone (vitamin D)
  • Antioxidants (e.g., vitamins C and E)
  • Cell signaling (e.g., vitamin A)
  • Gene transcription (e.g., vitamins A and E)
• Deficiency
  • Malnutrition, restricted diet (e.g., lactose-free or vegan diet)
  • Malabsorption disorders
  • Genetic disorders
• Excess
  • Oversupplementation
  • Almost exclusively from fat-soluble vitamins, which accumulate in the body

Fat-soluble vitamins

Fat-soluble vitamins are nonpolar molecules that require lipids for resorption. Since the body can store them for long periods of time, mainly in the liver and adipose tissue, excess accumulation is possible and may cause toxicity. While toxicity occurs mainly in industrialized countries due to oversupplementation, most deficiencies are a health concern mainly in developing countries (vitamin D being the notable exception). Treatment of deficiency involves oral supplementation, dietary adjustment (e.g., if due to restricted diet), or causal treatment of the underlying disease (esp. malabsorption disorders). For further information on etiology, diagnostics, and differential diagnoses, see the learning card on “Malabsorption.”

• Resorption and transport of fat-soluble vitamins
  1. Bile salts combine with lipids and fat-soluble vitamins in aqueous environments to form micelles.
  2. Micelles are resorbed in the intestinal tract (esp. in the duodenum) and packed to form chylomicrons.
  3. Chylomicrons are released into the lymphatic system and transported into circulation via the thoracic duct.
  4. Transport to liver
  5. Transport from liver to target cell with the aid of specialized transport proteins

The fat cat is in the ADEK (pronounced “attic”).

Vitamin A

Chemistry

• Fat-soluble vitamin
• Synonyms: retinol
• Substance class: retinoids
• Inactive precursors (provitamins): carotenoids (esp., alpha-carotene, beta-carotene, gamma-carotene)
• Active forms
  • Vitamin A
  • Retinol (alcohol) 
  • Retinal (aldehyde)
  • Retinoic acid (carboxylic acid)
  • Retinyl esters

Physiology

• Sources
  • Plant sources: as inactive provitamin in yellow and leafy vegetables (e.g., spinach, kale, carrots)
  • Animal sources: in storage form, e.g., in liver, fish, eggs, butter
• Activation: The carotinoid is cleaved into two retinal molecules. Retinal can be reversibly reduced to retinol and reversibly oxidized to retinoic acid.
• Transport:
  • As other fat-soluble vitamins (see “Fat-soluble vitamins” above)
  • Via transport proteins (in the form of retinol):
    • Retinol-binding protein: retinol transport vehicle in serum 
    • Cellular retinoic acid-binding (CRAB) protein: selectively binds retinoic acid
• Storage: in hepatic stellate cells 
  • Storage form: retinyl ester (e.g., retinyl palmitate)
• Excretion: via bile and urine

Functions

• Vision: component of rhodopsin as 11-cis-retinal
• Gene transcription:
  • All-trans retinoic acid (ATRA) binds to its nuclear receptors (retinoic acid receptors– RAR, and retinoid X receptors– RXR) → receptor dimerization (RAR:RXR dimerization) → binding to DNA → loosening of DNAchromatin → exposure of promoter regions of genes → transcription factors binding to promoter → initiation of transcription and cell differentiation
  • Regulation of various genes responsible for cell growth, cell differentiation, apoptosis, reproduction , and embryonic development 
• Tissue maintenance and cell differentiation
  • Mainly retinoic acid
    • Skin and mucous membranes
    • Bone and connective tissue
    • Prevents squamous metaplasia

Retinal plays a major role in vision, while retinoic acid and retinol are involved mainly in gene transcriptionand tissue maintenance!

Deficiency [1]

• Causes
  • Disorders associated with fat malabsorption: inflammatory bowel disease (e.g., Crohns disease), celiac disease, cystic fibrosis, pancreatic insufficiency, cholestasis [2]
  • Malnutrition
• Symptoms
  • Ocular manifestations
    • Night blindness
    • Retinopathy
    • Xerophthalmia
    • Bitot spots: Gray triangular patches that develop on the bulbar conjunctiva of patients with vitamin A deficiency as a result of keratinization.
  • Keratinizing squamous metaplasia of the bladder (pearl-like plaques on cystoscopy)
  • Xeroderma
  • Poor growth
  • Immunosuppression

Excess

• Causes: Oversupplementation
• Symptoms
  • Acute
    • Nausea
    • Vertigo
    • Fatigue
    • Headache
    • Blurry vision
  • Chronic
    • Alopecia
    • Arthralgias
    • Dry skin
    • Hepatosplenomegaly, hepatic toxicity
    • Pseudotumor cerebri
  • Teratogenic (e.g., microcephaly, cleft palate, skeletal, neurologic, and cardiac abnormalities, fetal death)

Therapeutic uses

• Agent: isotretinoin (13-cis-retinoic acid)
  • Indications:
    • Skin conditions, including acne (e.g., nodulocystic), and rosacea
    • Measles
  • Contraindicated in pregnancy (teratogenic)
• Agent: all-trans retinoic acid (ATRA)
  • Acute promyelocytic leukemia 

Isotretinoin is a strong teratogenic agent. A negative pregnancy test and two forms of contraception are required before prescription in women.

Vitamin A should be given to patients with measles to boost their immune system, especially in countries where vitamin A deficiency is endemic.

References:[3][4][5]

Vitamin D

Chemistry

• Fat-soluble vitamin
• Substance class: steroid hormones, calciferols
• Inactive precursors:
  • Ergocalciferol (vitamin D2)
  • Cholecalciferol (vitamin D3)
  • 7-dehydrocholesterol (provitamin D3)
• Intermediate form: 25-hydroxyvitamin D (25-OH D3, calcidiol; activated vitamin D2)
• Active form: 1,25-dihydroxyvitamin D (1,25-(OH)2 D3, calcitriol; activated vitamin D3)

Physiology

• Sources:
  • Vitamin D2: mushrooms, fortified foods (e.g., milk, breakfast cereals, formula), yeast (from ergosterol)
  • Vitamin D3: synthesized from 7-dehydrocholesterol in the skin (stratum basale), when exposed to UV light; fortified foods (e.g., milk, breakfast cereals, formula), fatty fish (liver), egg yolks
• Vitamin D synthesis 
  1. Liver: cholesterol → 7-dehydrocholesterol (provitamin D3)
     • Enzyme: cholesterol dehydrogenase
  2. Skin
     • Storage of 7-dehydrocholesterol
     • Cleavage of 7-dehydrocholesterol via irradiation with UV light→ cholecalciferol (in the stratum basale of the skin)
  3. Liver: hydroxylation of cholecalciferol to 25-hydroxyvitamin D
  4. Kidneys: 1α-hydroxylase hydroxylates 25-hydroxyvitamin D → 1,25-dihydroxyvitamin D
• Transport to target cells: vitamin D-binding protein (DBP) 
• Storage: mainly in adipose tissue as 25-hydroxycholecalciferol
• Excretion: via bile
• Regulation of vitamin D synthesis: via regulation of 1α-hydroxylase activity 
  • ↓ Calcium, ↓ phosphate, ↑ PTH → ↑ 1α-hydroxylase activity → ↑ 1,25-dihydroxyvitamin D biosynthesis
  • ↑ Calcium, ↑ phosphate, ↑ 1,25-dihydroxyvitamin D → ↓ 1α-hydroxylase activity → ↓ 1,25-dihydroxyvitamin Dbiosynthesis

Vitamin D is the only vitamin that the human body can produce entirely on its own!

Functions

• Calcium and phosphate metabolism (see also calcium homeostasis)
  • Increases resorption of calcium and phosphate in the intestine
  • Increases reabsorption of calcium in the kidney 
• Stimulation of bone mineralization and remodeling
  • Indirectly: through maintenance of serum calcium and phosphate levels
  • Directly: through activation of osteoblasts and promotion of osteoclast differentiation

Vitamin D deficiency [6]

• Causes
  • Lack of sun exposure 
  • Malnutrition (common in alcohol use disorder)
  • Malabsorption disorders (e.g., fat malabsorption, chronic GI disease)
  • Chronic kidney or liver disease: due to the impaired hydroxylation of active vitamin D precursors
  • Breastfeeding without supplementation of vitamin D 
• Symptoms
  • In adults: Osteomalacia
  • In children: Rickets (bone deformities such as genu varum or “bow legs”)
  • Clinical features of hypocalcemia (e.g., tetany)

Excess

• Hypercalcemia
• Hypercalcinuria
• Common in granulomatous disorders (e.g., sarcoidosis)
  • Due to increased 1,25-dihydroxyvitamin D production by epithelioid macrophages

Vitamin E

Chemistry

• Fat-soluble vitamin
• Synonyms: tocopherol, tocotrienols
• Substance class: tocopherols
• Inactive precursors (provitamins): none
• Active form: tocopherol

Physiology

• Sources: meat, eggs, vegetable oils, leafy vegetables[7]
• Transport: alpha-tocopherol transfer protein (α-TTP)
• Storage: adipose tissue, parenchymal cells of the liver 
• Excretion: via bile

Functions

• Antioxidant: protects sensitive substances, esp. erythrocytes and cell membranes, from free radicals
  • Tocopherol interrupts free radical chains caused by oxidative damage and becomes oxidized itself in the process. 
• Other functions
  • Inhibits platelet aggregation, cell proliferation, and monocyte adhesion
  • Inhibits certain enzymes (e.g., protein kinase C, phospholipase A2)
  • Inhibits transcription of certain genes (e.g., for α-TTP, tropomyosin alpha-1 chain)

Deficiency

• Causes (very rare)
  • Occurs mostly due to defects in genes that code for α-TTP or fat malabsorption disorders[7]
• Clinical features
  • Neurologic dysfunction: demyelination of the posterior column and spinocerebellar tract (similar to vitamin B12 deficiency)
    • Can be differentiated from vitamin B12 deficiency by the lack of hypersegmented neutrophils, megaloblastic anemia, and increased methylmalonic acid levels [8]
  • Hemolytic anemia[7]
    • Vitamin E protects erythrocytes from free radical damage and thus prevents membrane breakdown.
  • Acanthocytosis

Excess

• Toxicity is very rare.
• Causes: Oversupplementation
• Symptoms
  • In children: increased risk of enterocolitis
  • Can alter the metabolism of warfarin → enhanced anticoagulant effect → increased risk of bleeding
  • Studies have linked long-term high-dose supplementation to increased incidence of heart failure and increased risk of fatal subarachnoid hemorrhage and mortality.

References:[9]

Vitamin K

Chemistry

• Fat-soluble vitamin
• Synonyms: phytomenadione, phylloquinone, phytonadione
• Substance class: naphthoquinones
• Inactive precursors (provitamins): none
• Active form: vitamin K hydroquinone

Physiology

• Sources: leafy green vegetables ; synthesized in small amounts by intestinal flora
• Transport: via lipoproteins; no specific protein
• Storage: liver
• Excretion: bile and urine
• Activated by the enzyme epoxide reductase → cofactor for γ-carboxylation of glutamic acid residues on clotting factors → adequate hemostasis

Functions

• Coenzyme for γ-carboxylation of glutamic acid residues in vitamin-K-dependent proteins involved in:
  • Coagulation: factors II (prothrombin), VII, IX, and X; proteins C and S
  • Bone formation: osteocalcin (bone Gla protein), matrix Gla protein

In 1972 vitamin K Killed CSf

Deficiency[10]

• Causes
  • Liver failure (e.g., cirrhosis)
  • Fat malabsorption
  • Prolonged broad-spectrum antibiotic therapy 
  • Vitamin K antagonists (e.g., warfarin) 
  • Neonatal deficiency
    • Vitamin K does not cross the placenta and breast milk does not contain vitamin K. Furthermore, theneonatal liver is incapable of synthesizing the active form of vitamin K and the neonatal intestine is sterile, i.e. has not yet developed flora that could synthesize it. All newborns should receive a vitamin K injection to prevent vitamin K-deficient bleeding.
• Symptoms
  • Hemorrhage (e.g., petechiae, ecchymoses)
    • Coagulation disorders as a result of an overdose of vitamin K antagonists will only become apparent when stores have been depleted (approx. after 3–4 days).
  • Vitamin K deficient bleeding (VKDB)  (↑ PT and aPTT, normal bleeding time)
    • Prophylaxis: Vitamin K injection at birth

Excess

• Causes
  • Toxicity is very rare
  • Oversupplementation
• Symptoms
  • Hemolytic anemia
  • Hyperbilirubinemia
  • Jaundice
  • Kernicterus in infants

Water-soluble vitamins

Water-soluble vitamins are polar molecules that function primarily as coenzymes in various chemical reactions. They are not stored in the body except vitamins B9 and B12, which are stored in the liver. Accumulation and consequent toxicity are exceedingly rare, even with vitamins B9 and B12. Treatment of deficiency involves oral supplementation, dietary adjustment (e.g., if due to restricted diet), and causal treatment of underlying disease (esp. malabsorption disorders). For more information on etiology, diagnostics, and differential diagnoses, see the learning card on “Malabsorption.” Deficiency of B-complex often causes glossitis, dermatitis, and diarrhea.

• Resorption and transport
  1. Resorption in the intestine: active transport and passive diffusion
  2. Transport in the blood: active, via various transport proteins