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Minerals Metabolism for MBBS Students.

This document discusses mineral metabolism, focusing on essential minerals like calcium and phosphorus, their functions, metabolism, and related disorders. It outlines calcium homeostasis, deficiency effects, and the relationship between calcium and phosphorus, along with the biochemical importance of various minerals in the body. Additionally, it provides case studies illustrating conditions such as tetany and hypercalcemia, along with learning objectives and FAQs relevant to medical students.

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Smita Pakhmode Lec-1 MINERAL METABOLISM Dr. Smita Pakhmode, Associate Professor Department of Biochemistry NKPSalve Medical College &RC
Smita Pakhmode Competencies No Competency Domain level Core Method BI 6.9 Describe the functions of various minerals in the body, their metabolism and homeostasis. K KH Y Lecture, Small group discussion BI 6.10 Enumerate and describe the disorders associated with mineral metabolism. K KH Y Lecture, Small group discussion
Smita Pakhmode Biomedical Importance of MINERALS Calcification of teeth & Bone Blood coagulation factors Neuromuscular activation Acid base equilibrium Osmotic equilibrium Acts with enzyme ( Metalloenzyme,Cofactor) Integral part of compounds (Hb,Thyroxin,Insulin, Vit B12)
Smita Pakhmode Classification Minerals Principle 60-80% > 100mg/day Ca,P,Na,K,Mg,Cl,S, TRACE ELEMENTS <100mg/day Essential Fe,Cu,I,Mn,Zn,Mb, Co,Fl & Se Possibly Essential Cr,Ni, Va,Cd, Barium Non essential Al.Pb,Hg,Boron, Silver Bismuth
Smita Pakhmode • Introduction & Classification of minerals, • Calcium: • Functions, • Sources, & RDA, • Factors affecting absorption • Calcium Homeostasis • Disease Manifestations of Calcium metabolism • Phosphorus • Functions, • Sources, & RDA, • Factors affecting absorption • Disease Manifestations of phosphorus metabolism Learning Objectives
Smita Pakhmode Frequently asked questions(MBBS) • Factors involved in the regulation of blood calcium levels. (4M) • Biochemical functions of calcium. (4M) • Regulation of serum Calcium(4M) • Functions and deficiency manifestation of Calcium. (4M) • Hormones regulating serum Calcium.(4M) • LAQ: Write in detail about the factors influencing calcium absorption in the body. Write its function (8M) • Case study: Tetany
Smita Pakhmode CALCIUM Total content : 1-1.5 Kg 99% Bones & Teeth 01% Miscible “Ca” pool ( ECF)
Smita Pakhmode Functions of Calcium 1. Bone & teeth calcification • Hydroxyapatite crystals • Bones :Reservoir of Ca • Regulators: Osteoblasts and PTH 2.Blood coagulation factors • Activator of factor IV • EDTA: Chelates Ca Anticoagulant 4.Nerve conduction Releases neurotransmitters at presynaptic & post synaptic terminals 3.Secondary messenger: Glucagon & Epinephrine Tertiary messenger with Cy AMP: ADH
Smita Pakhmode Functions of Calcium 6 Muscle contraction Interaction of Ca & Troponin C Activation of ATPase ↑Actin Myosin Interaction Facilitate excitation contraction coupling 5.Activation of enzyme • Calmodulin mediated • Direct Action Ca2+ + Calmodulin Ca-Calmodulin Complex Kinase. Active Kinase Enzyme. P-Enzymes Biological effects Enzymes activated with Calmodulin Adenylate cyclase, PL C Ca dependent Protein Kinase Gly synthase, Phosphorylase Kinase, G3PDH, Py. Carboxylase, PDH, Myosin kinase Directly Activated Enzyme Pancreatic Lipase Coagulation enzymes Rennin Deficiency of Ca: Tetany
Smita Pakhmode Functions of Calcium 7.Release of hormones from endocrine glands- insulin, PTH, calcitonin 8. Myocardium: Prolongs Cardiac systole ( Caution: IV administration of Ca. Gluconate) 10.Contact Inhibition: maintains Cell to cell adhesion 9. Secretory Process: Microtubule & microfilament mediated functions- endocytosis, exocytosis and cell motility
Smita Pakhmode Adults 800 mg Preg. /Lact .: 1500 mg Growing children 800-1200 mg DAILY REQUIREMENTS Sources Rich: Milk & Milk products Medium: Egg, Fish Vegetable, Beans, Leafy vegs. Poor but major: cereals.
Smita Pakhmode FACTORS AFFECTING ABSORPTION OF CALCIUM • Its an Active process. • Occurs in first and & Second part of duodenum. • Carrier protein helped by Calcium dependent ATPase ↑↑Ca absorption Calcitriol (Active form Of Vit D) Parathyroid hormone → ↑Vit D synthesis Acidity/Low pH lactose Lysine, arginine High protein Intake
Smita Pakhmode Factors decreasing Ca absorption: • Phytates, oxalates • High PO4 content Ideal Ca : P Ratio 1:2 - 2:1 • Impaired fat abs: free fatty acids +calcium---calcium soaps • High pH(ALKALINE PH) • High fiber FACTORS AFFECTING ABSORPTION OF CALCIUM
Smita Pakhmode PLASMA CALCIUM 50% 10% 40% BLOOD CALCIUM Ionized Anion bound protein bound (5 mg/dl ) (1mg/dl) 4mg/dl. DIFFUSIBLE NONDIFFUSIBLE
Smita Pakhmode Homeostasis of Calcium Factors which regulate Ca levels in blood 1Hormones: 1.Calcitriol 2.Parathyroid hormone 3.Calcitonin 2.Concentration of phosphorus: reciprocal relationship Ionic product of ( Cal X Po4= 40) Renal insufficiency: Excretion of Ca leads to tetany 3.Serum proteins: Hypoalbunemia (1gm/dl)⍺ ↓Ser. Cal (0.8mg/dl) - levels of ionized form is normal. 4.Alkalosis and acidosis: Alkalosis favors binding of calcium with proteins Acidosis favors ionization
Smita Pakhmode Blood Calcium N level: 9-11mg/dl Role of Vit D ( Calcitriol) Intestine Bone Kidneys Induces synthesis of “Calcium Binding Protein”[CBP] ↓ • ↑ intestinal abs. of Ca & P (in intestinal cells) Stimulates osteoblasts ↑ ALP (↑ Phosphate level) Promotes calcification of bones ↑ Reabsorption of Calcium & phosp from renal tubules Increases Calcium Level With PTH: Stimulates osteoclasts Mobilizes Ca & Po4 from bone
Smita Pakhmode Low Blood Calcium Role of Parathyroid hormone Intestine Bone Kidneys PTH: Stimulates osteoclasts ↑ Prophosphatase. Lactate. Collagenase Reabsorption & solublization of bone matrix Mobilizes Ca & Po4 from bone ↑ hydroxylation of Vit D to form Calcitriol ↑ Ca2+ Reabsorption ( rapid action ) ↓ excretion of Ca from renal tubule ↑ excretion of Po4 Induces synthesis of “Calcium Binding Protein”[CBP] ↓ • ↑ intestinal abs. of Ca & P (in intestinal cells) Vit D Increases Calcium Level Negative feed back regulation Action last for 1 hour
Smita Pakhmode Raised Blood Calcium Gastrin, Glucagon & Biological amine Role of Calcitonin Bone Kidneys ↑ osteoblasts ↓ osteoclast Inhibit reabsorption of bones ↓ blood calcium level ↑ excretion of Po4 - decreases Calcium Level Antagonist to PTH Significance of Calcitonin Tumor Marker 1) Medullary Ca of Thyroid 2) Lung & Bronchus Malignancies
Smita Pakhmode TEETH CALCIUM NOT SUBJECT TO REGULATION When to check Calcium levels??  Neurological symptoms, irritability  Urinary Calculi  Ectopic Calcification  Suspected Malignancies  Polyurea, Polydypsis  Chronic Renal failure  Prolong treatment with drugs which cause Hypercalcemia ( Vit D, Thiazide Diuretics)
Smita Pakhmode DISORDERS OF CALCIUM METABOLISM • Hypercalcemia : Etiology: 1. Hyperparathyroidism ( Adenoma/ Ectopic PTH tumor) 2. Multiple Myeloma, Paget’s disease, Metastatic Ca 3. thyrotoxicosis, Addison's disease, 4. Prolong Immobilization 5. TB, Leprosy & Sacrcoidosis 6.Drugs: Thiazide, Vit D, IV calcium, Lithium Therapy
Smita Pakhmode DISORDERS OF CALCIUM METABOLISM • Hypercalcemia : Effects: Serum ↑Ca , ↓PO4 Urine ↑Ca , ↑PO4 Ionized serum Ca ↑(6-9mg/dl), Raised Alkaline phosphatase urinary calculi & osteoporosis s/s– Polyurea, polydipsia, confusion, depression , psychosis, Pathological fracture, renal stone, ectopic calcification & Pancreatitis T/t: Adequate hydration, IV frusemide, Steroids. T/t of underlaying cause.
Smita Pakhmode • Hypocalcaemia( < 8.8mg/dl) mostly due to hypo PTH Other Causes: 1. Deficiency of Vit D 2. Medullary Ca of Thyroid (↑ Calcitonin) 3. Malabsorption disorders, Acute Pancreatitis, Alkalosis(↓Ca ) 4. Renal failure, RTA, Phosphate infusion (↑PO4) S/S: Muscle cramps, paresthesia, neuromuscular irritability, muscle twitching, Accidental removal Autoimmune DISORDERS OF CALCIUM METABOLISM
Smita Pakhmode Mild deficiency of Calcium Chronic Ca deficiency Cause: Dietary deficiency of Vit D or Ca Renal insufficiency Mg deficiency White patches on nails Deformities of weight bearing bones Treatment: Oral Ca & Vit D supplementation T/t of underlying cause
Smita Pakhmode • TETANY (<7.5 mg/dl) • Serious life threatening disorder S/o: neuromuscular irritability, Spasm & convulsions • mostly due to accidental or autoimmune removal of Parathyroid Gland • Dignostic signs TETANY (<7.5 mg/dl) Serum ↓Ca , ↑PO4 Urine ↓Ca , ↓ PO4 T/t—Severe cases—IV Ca Gluconate (10ml of 10% Calcium glucaonate over 10 min) Imp Note: VIT D Deficiency will never cause Tetany Severe Calcium deficiency: TETANY
Smita Pakhmode Carpopedal Spasm: Flexion of wrist Flexion MPJ & Extension IP joints Adduction of thumbs & fingers Trousseu’s sign: Inflation of BP cuff for 3 min will cause carpopedal spasm Chvostek’s Sign: Tapping over facial muscle causes facial muscle contraction Other Signs: Laryngeal stridor, Prolong QT interval Signs of Tetany
Smita Pakhmode Relationship of Calcium & Phosphorus • RDA Ratio of 1:1 Ca : P ( i.e. 800 mg /day) • Diet: • optimum Ca: P ratio 1:2 - 2:1 • Favors absorption • Blood: • Ionic product of CaXP (10X4)= 40 • Ratio is important for the calcification of Bone • High Ratio: mineralization of Bones Children- 50 • Low ratio: Ricket (<30)
Smita Pakhmode Case • A 54 years years old grossly overweight women presented with the complaints of cramps and spasms of both hands. She was depressed and positive Trasseau’s sign & Chovestek’s sign. Past medical history reveals thyroidectomy for Grave’s disease. The laboratory findings are as follows: Serum Ca: 4.1 mg%; Sr. Creat: 1.0mg%, Sr. Po4 :5.9mg%; Sr Alb:4.0mg% • What is the diagnosis? Tetany What is probable cause for the disease? Hypoparathyroidism due to removal of PTH glands • Interpret laboratory finding and corelate with diagnosis ? hypocalcemia& Hyperphosphatemia with N Creat & Alb • What additional test to be done for conclusive diagnosis? • Estimation serum PTH level & Alk Po4 level. Low PTH & High ALP
Smita Pakhmode Case • A 10 year old boy presented with the complaints of muscle pain , stiffness ,cramps of both hands & feet. He was strict vegetarian & even did not consume milk & dairy products. On examination no signs of rickets were found. He had positive Trousseau’s sign & Chovestek’s sign. Serum Calcium level is as low as 4mg%. • What is the diagnosis? • Tetany • What is probable cause for the disease? • Hypoparathyroidism Or Chronic renal Failure • How would you investigate the case to confirm diagnosis ? • KFT( Urea, Creat,Electrolyte & Urinary Ca & Po4 ratio: CRF • Estimation serum PTH level & Alk Po4 level: Low PTH & High ALP • Estimation of Vit D
Smita Pakhmode Case • A 42 year old lady presented with the complaints of vague abdominal discomfort, fatigue & bone pain. She had frequent episodes of urinary track infection and episodes of urinary stone. Her physical examination was within normal limits.On investigations patient had N CBC, Electrolyte: High Ca & low Po4. • What is the diagnosis? • HyperCalcemia & Hypophosphatemia :Hyperparathyroidism • What is probable cause for the disease? • Primary Hyperparathyroidism(stone,moans,groans,bones) • How would you investigate the case to confirm diagnosis ? • Estimation serum PTH level • Estimation of Vit D
Smita Pakhmode PHOSPHORUS Total Body content = 1 Kg 80% Bones & teeth 10% Muscles , blood 10% chemical compounds Functions 1. Bones and teeth 2. High energy compounds ( ATP , GTP, Cr-P ) 3. Phospholipids, Phosphoproteins, Nucleic acids(DNA/ RNA) 4. Nucleoside Coenzymes NAD+ , NADP+ ,Pyridoxal PO4 5. Activation of Proteins and enzymes by phosphorylation 6. Phosphate buffers system( Na2HPO4/NaH2Po4 =4:1) 7. Formation of phosphate esters. G 6 P,PL, phosphoprotein
Smita Pakhmode Absorption Absorption in jejunum ↑by - Calcitriol - optimum Ca: P ratio 1:2 - 2:1 - Acidity ↓by Phytates ( cereal rickets ) RDA : Ratio of 1:1 Ca : P ( i.e. 800 mg /day) Infants 2:1 ( Milk ) Sources Milk , eggs, meat, fish ,cereals, leafy vegetables, cheese, beans, PHOSPHORUS
Smita Pakhmode Factors Regulating Phosphorus in Blood: Vit D & PTH Excretion: 500 mg / day in urine Renal threshold → 2 mg /dl PTH → Inhibits reabsorption of PO4 by RT Conc. In Blood: Serum Level: Total 3-4 mg / dl Whole blood - 40 mg /dl ( ↑content RBC, WBC’s) Fasting > Post meal Distribution: 40% free ions 10% protein bound 50% bound to cations (Ca2+ / Mg2+ / Na+ /K+ )
Smita Pakhmode Disorders of phosphate Hyperphosphatemia: ↑ absorption of the phosphate: ↑ Vit D/ Po4 infusion ↑ Cell lysis: Cancer chemotherapy, Bone secondaries, ↓ excretion : Renal Impairment, Hypoparathyroidism, Acidosis Drugs: Chlorthiazide, Nifedipine, Frusemide
Smita Pakhmode Disorders of phosphate • Hypophosphatemia: • ↓ absorption of the phosphate: • Malnutrition, Malabsorption, Chr. Diarrhea, Vit D deficiency. • Intracellular shift: Insulin therapy, Renal rickets • ↑ urinary excretion of phosphate: Hyper parathyroid hormone, hypophosphatemic rickets. Hypercalcemia, Chronic alcoholism, Drugs • Drugs: Antacids, Diuretics, salicyclate
Smita Pakhmode RDA Males – 350 mg/day Females – 300 mg/day Sources Cereals, nuts, beans, vegetables { cabbage, cauliflower}, meat, milk & fruits Magnesium (Macroelement) Total content in the body : 20 g 70 % bones & teeth 30% soft tissue & body fluids Absorption Upto 50% ( carrier mediated ) ↑↑ by PTH Ca , P, Alcohol - ↓Mg Absoption Excretion Mostly → Intestine Partly→ Kidneys Serum levels Total 2-3 mg / dl 60% - Ionised 10% - bound to anions 30% - Protein bound
Smita Pakhmode Functions • Bone and teeth • Cofactor for ATP requiring enzymes • e.g. hexokinase , PF kinase , glucokinase, adenylate cyclase • Neuromuscular functions • Improves glucose tolerance . • Reduces BP & prevents stroke • Clinical applications: • When given in large doses (parenterally ) • CNS depressant • (Hence anesthetic / anticonvulsant )
Smita Pakhmode Disorders: Hypomagnesemia( low serum Mg ): •Renal tubular necrosis, Liver Cirrhosis, Toxemia of pregnancy ,Malnutrition , C/F – Neuromuscular irritability weakness convulsions Magnesium Toxicity : Magnesium containing Antacids/ Laxatives C/F - Drowsiness Lethargy Weakness
Smita Pakhmode Sulphur Most important component of body proteins. Sources: S – AA Vegetable & Cereals No specific RDA Excretion: 1gm/day through urine 1. Inorganic sulphate 2. Ethereal sulphate 3. Unoxidized sulphate
Smita Pakhmode Functions of Sulphur 1. Mitochondrial cellular respiration Component of Fe-S Containing protein 2.Stabilize the protein structure: Insulin, Immunoglobulins 3. Part of different coenzyme: Thiamine, Biotin, Lipoic Acid, Coenzyme A 4. Part of fibrous proteins: Keratin of hair & Nail 5.Part of different metabolically active compounds: Glutathione, heparin, Chondrotin Sulphate, taurocholic acid 6. Detoxification reactions: Phosphoadenosine Phosphosulphate (PAPS) 7. Transmethylation Reaction: S- Adenosine Methionine
Smita Pakhmode Sodium Major CATION in ECF 70%- ECF 4-5%-ICF 20%-soft tissues, bone teeth Requirement: 5-10 gm/day as NaCl Source : Common Salt Cereals, legumes, leafy vegetables, nuts, eggs, milk Absorption : 99% in GIT
Smita Pakhmode Functions of Sodium: 1. Maintains ECF volume 2. Osmotic pressure & fluid balance 3. Acid-base balance: 4. Component of Na K pump 5. Absorption of glucose, galactose, amino acids 6. Nerve muscle conduction.
Smita Pakhmode Distribution of Na in body 4000meq 75% Exchangable ECF 70% ICF 4% 25% Non Exchangable Bone, teeth & soft tissue Normal level = 135-145 meq/L-ECF 35 meq/L-ICF
Smita Pakhmode Regulation of Sodium Decrease in BP Rennin Angiotensinogen1 Angiotensin1 Angiotensin II AngiotensinII Aldosteron Na+ Retention Excretion of K+ & H+ ANF Aldosterone system ↑ BP ↑GFR…….. ↑Na+ excretion ↑Urine out put ↓ in Na Conc
Smita Pakhmode Factors affecting serum Sodium levels: Aldosterone : ↑↑ Na + reabsorption ADH : ↑↑ water reabsorption Edema: ↑ water, Na+ content Diuretics: → ↑Na+ excretion, water excretion Excretion: by Kidneys & sweating 800 gm/day Na+ filtered 99% of this is Reabsorbed Na Homeostasis
Smita Pakhmode Hyponatremia Method of Estimation: Flame photometry /Ion selective electrode Symptoms: Muscle cramps, Headache & Nausea Long term complication Sign: B.P.& Circulatory Failure, Edema
Smita Pakhmode Causes of Hyponatremia Hyponatremia ↓osmolality Hypervolemia CCF, Cirrhosis, Nephrotic Syndrome Euvolemia SIADH Pneumonia, Pulm. TB, Ca Bronchus Hypovolemia Extra renal Diarrhoea, vomiting Sever Sweating Renal ↓ADH, Aldosteron (addisons disease) RTA Diuretcs
Smita Pakhmode Hypernatremia Hypernatremia Blood volume Hypervolemic Cushing’s Syndrome Prolong steroid therapy Pregnancy Excess of Mineralocorticoid Euvolemic Diabetes Insipidus Hypovolemic Dehydration Diarrhoea, vomiting With reduced fluid intake Diuretics
Smita Pakhmode POTASSIUM Major intracellular cation Total Body content: 3500 meq 75% in muscles & ICF RDA : 3-4 gm/day Sources : Bananas, oranges, apples, almonds, dates, beans, potatoes, coconut water, beans , chicken and liver Normal level = 3.5-5meq/L (ECF) 50meq/L (ICF) Daily Intake: 20-200 meq/ Day Excretion: Urine Aldosterone: ↑ excretion of K+
Smita Pakhmode Functions •Intracellular osmotic pressure & volume. •Component of Na K pump •Acid-base & Water balance •Imp in depolarization & contraction of cardiac muscles •Nerve impulse transmission •Enzyme Pyruvate Kinase Activity •Protein Biosynthesis
Smita Pakhmode Regulation of Potassium Serum K Redistribution Of K Insulin Acidosis Increased Excretion ↑Aldosterone ↑Corticosteroid
Smita Pakhmode HYPOKALEMIA (<3 meq/L) Symptoms: Vomiting, Diarrhea, Weakness, Anorexia Irritability, Muscle weakness, Arrhythmias, Cardiac arrest, ECG changes: Flattened /lowering/ inversion of T wave ST seg depression, prominent U wave Arrythmia
Smita Pakhmode Hypokalemia Hypokalemia Redistribution Of K Insulin therapy T/t Aciodocis Meta. Alkalosis Catecholamine B adrenergic drugs Periodic Paralysis True loss of K through Urine K Excretion> 25 Meq/Day RTA A TN ↑Aldosterone ↑Corticosteroid K Excretion < 25 meq/Day Diarrhoea Fistula Extensive surgery
Smita Pakhmode Hyperkalemia Hyperkalemia Pseudo Hemolysis Thrombocytosis Redistribution Of K Insulin Deficiency Meta Acidosis K Retention Massive Blood transfusion Renal transplant Obstructive nephropathy Addison's Disease SLE/ SCD
Smita Pakhmode HYPERKALEMIA: (> 5.5 meq/L) Symptoms: s/o depression of CNS Weakness, decreased Deep tendon reflexes numbness bradycardia , Cardiac arrest. ECG changes: prominent T wave widening of QRS complex Prolong PR interval
Smita Pakhmode Lec-2 MINERAL METABOLISM Dr. Smita Pakhmode, Associate Professor Department of Biochemistry NKPSalve Medical College &RC
Smita Pakhmode Commonly asked questions(MBBS) • Absorption & function of iron.(4M) • Mechanism of iron absorption from the intestine. (4M) • Write a note on intestinal absorption of Iron. (4M) • Factors affecting intestinal absorption of Iron. (4M) • Case on Iron deficiency Anemia (4M) • Explain the defect in Wilson’s disease, state the clinical manifestations (4M) • Functions of Copper(4M) • Case on Wilson’s Disease.(4M)
Smita Pakhmode IRON: • Functions, • Sources, & RDA, • Factors affecting absorption of iron • Regulation of Absorption of Iron • Disease Manifestations of Iron metabolism • Copper • Distribution & Functions, • Sources, & RDA, • Biochemical functions • Disease Manifestations Learning Objectives
Smita Pakhmode IRON 3-5gm • • Requirements- Daily allowance (ICMR) Adult man: -10mg /day Mensturating women: 18mg/day Pregnancy/Lactation- 40mg/day Children (13-15yrs)-30mg/day 75% -blood 20% - liver, bone marrow 5%muscles Absorption: 10% (1-2mg absorbed) ↑↑ Iron deficiency Anaemia, Growing children
Smita Pakhmode • Heme: – Hb , Myoglobin, Cytochromes, Tryptophan Pyrrolase , catalase,peroxidase • Fe-S: – complex III Fe-S, succinate DH, Xanthine Oxidase • Non-heme iron: Ferritin, Transferrin, Hemosiderin IRON CONTAINING PROTEINS:
Smita Pakhmode Functions of Iron: • Hb /Myoglobin: Transport of O2 & CO2 •Cytochrome: ETC & Detoxification •Peroxidase: Present in Lysosome, catalyzes phagocytosis of bacteria by neutrophils. • Immunocompetence of the body
Smita Pakhmode SOURCES- • Rich source: Organ Meat( Liver,heart & Kidney) • Good source: Leafy Vegs., Pulses ,Cereals, , Jaggery, fish ,Apples,Dried fruits • Poor source: Milk, wheat , polished rice • Absorption- • Upper duodenum & Proximal Jejunum Fe2+ Fe3+ Ferroxidase/Ceruloplasmin Ferroreductase Transport form Storage form
Smita Pakhmode
Smita Pakhmode • ↑↑ by - • HCL, • Ascorbic acid, Cysteine, -SH gps of proteins • Iron deficiency Anaema(10 Times ) • ↓↓ by- Phytic acid (cereals) Oxalic acid(vegetable), PO4 Alkaline pH Malabsorption disorders(steatorrhoea) Total or Partial Gastrectomy Diet: Fe3+ + Oragnic acids/Pr. HCl Fe3+ Vit C, Cyst Fe2+ Factors affecting Absorption of Iron:
Smita Pakhmode GIT Lumen Diet: Mucosal cell Blood Fe3+ + Oragnic acids/Pr. HCl Fe3+ Vit C, Cyst Fe2+ DMT Fe2+ Fe3+ Ferroxidase Apoferritin Mucosal Ferritin Fe3+ Ferrireductase Ferroportin Fe2+ Fe3+ Ferroxidase Ceruloplasmin Apotransferrin Plasma (Fe3+) Transferrin Heme Pr. Hb, My, Cyt Ferritin Fe3+ Hemosiderin Hepcidin Liver, spleen, BM Absorption storage and utilization of food Iron. DMT= Divalent Metal transporter Mucosal block theory for the regulation of iron absorption ↑↑Ferritin
Smita Pakhmode Total iron binding capacity • Transferrin: Glycoprotein • 1mol Of Transferrin-2 atoms of Fe3+ • N TIBC Plasma: 250mg/dl-400 mg of Iron/dl • Normal condition 1/3 of transferrin is saturated • TIBC grossly increased in Iron deficiency Anaemia.
Smita Pakhmode • Ferritin: • In liver , spleen, BM( as ferritin) • (Apo-ferritin has 24 subunits (MW5,00,000) • Can take up 4,500 Iron atoms/ molecules to become ferritin • Ferritin: 25% Iron by weight. • In Iron toxicity , ferritin Increased is seen in plasma IRON STORAGE(Permanent) Hemosiderin: 35% of iron by its weight. Accumulate in liver, spleen whenever there is excess of demand of iron.
Smita Pakhmode Iron is one way compound • Once entered in the body, can not be excreted. • It acts in close circuit. • Utilized & reutilized • Not excreted in urine • < 1mg/day excreted through bile salt, sweat. • It gets deposited in the body in form Hemosiderin. Iron loss Feces: Major loss of unabsorbed iron Menstruating women (up to menopause)- 25-30 mg /day Skin →cells lost
Smita Pakhmode Iron is reutilized RBC Lysis Globin removed HB: HB- Haptoglobin complex taken up by liver kuffers cells Iron reutilized Heme: Heme Hemopexin complex Taken up by hepatocyte Porphyrin ring opened. Bilirubin Iron. → Iron transferrin → storage. Iron reutilized Iron reutilized Renal insufficiency leads to iron deficiency due to loss of haptoglobin, hemopexin & deficiency of erythropoietin
Smita Pakhmode • Most common nutritional deficiency disorder • 30% world population • 85% pregnant women • 15 % maternal deaths • In children → irreversible impairment in learning ability IRON DEFICIENCY ANAEMIA
Smita Pakhmode Iron deficiency Anaemia Causes: • Hookworm infestation • Iron deficiency in diet • Repeated pregnancy (1gm/delivery) • Chr. Bloods loss ( piles/ Uterine hemorrhage) • Renal defect (loss in urine) • Lack of abs ( Subtotal gastrectomy, achlorhydria) • Symptoms: • “Microcytic Hypochromic Anaemia” (< 12gm/dl) • Apathy, sluggish, • atrophy of gastric epithelium ↓abs of iron achlorhydria • Chronic deficiency → impaired attention /irritability ↓memory poor school performance
Smita Pakhmode TREATMENT • 100 mg iron + 500 µg Folic Acid - Preg women • 20 mg iron + 100 µg FA - children IRON TOXICITY • Haemosiderosis Haemosiderin→ golden brown granules ↓ (spleen, liver) Complexes of partially denatured ferritin ( 25% iron)
Smita Pakhmode 1)Primary Haemosiderosis • Abnormal gene on chr 6 (short arm) • ↑abs of iron • Excess iron deposit 2) Secondary Haemosiderosis • Secondary to repeated blood transfusions (hemophilia) • Bantu tribes (Africa) Iron vessels + low PO4 ( corn-staple diet)
Smita Pakhmode Hemochromatosis:- Direct iron deposition in tissues Cirrhosis – liver Diabetes – Pancreas Yellow Brown Skin – Skin : Bronze Diabetes Treatment : Repeated Phlebotomy + Desferrioxamins
Smita Pakhmode
Smita Pakhmode COPPER(CU)….100MG Plasma Cu 100-200 mg/dl 95% 5% Ceruloplasmin Albumin 25-50 mg/dl 0.34% Cu 95% in RBCs as colourless erythrocuprein Rest as Ceruloplasmin in plasma (serum ferroxidaseII )
Smita Pakhmode RDA Sources 1.5- 3 mg/day Cereals, nuts, Meat , Liver, Kidney, egg yolk, Green leafy vegetables (Milk poor source ) Absorption Duodenum Metallothionein pr facilitates abs Phytate,Zinc,& Mo
Smita Pakhmode Biochemical Function of Copper Tyrosinase, uricase, catalase, cytochrome oxidase, Monoamine oxidase, Superoxide dismutase, ascorbic acid oxidase, phenol oxidase, • Essential constituent Enzymes: •ALA synthase: For Hb synthesis •Lysyl oxidase : cross linking of collagen & elastin •Ceruloplasmin (Ferroxidase) : Fe+2 to Fe+3 – (Transferrin) transported in plasma •Tyrosinase: • Synthesis of Melanin & phospholipids • For Bone& nervous system(melanin) dev.
Smita Pakhmode • Fe Absorption and incorporation into Hb • Co factor for Vit C in hydroxylation reaction • Component of Cu containing non enzymatic proteins e.g. Hepatocuprein, Cerebrocuprein Hemocuprein Biochemical Function of Copper
Smita Pakhmode Deficiency : -Microcytic Normochromic Anaemia -Weakening of walls of major vessels- fragility of arteries -demineralization of bones, demyelination of neural tissue, myocardial fibrosis, -Hypopigmentation ( tyrosinase) Greying of hair
Smita Pakhmode Deficiency of Cu: Menke’s disease
Smita Pakhmode Menke’s disease : -X linked disorder • Cu is absorbed by intestine but can not be transported to blood. • Absence of intracellular copper binding ATPase. • Cu may be trapped by metallothionein in the intestinal cells • Not mobilized to other tissues. S/S decreased Cu in plasma & urine Anemia, De pigmentation of hair Kinky ,twisted brittle hair( Cu catalyzed S-S bond formation) Seizurs & Metal retardation
Smita Pakhmode Wilson’s disease Defective ATP 7A gene: Cu Binding ATPase ↓Excretion of Cu through intestine from bile ↑ Absorption of Cu from Kidney ↓hepatic incorporation of copper in ceruloplsmin Free Cu accumulates in the organs Liver Hepatic cirrhosis Brain necrosis Renal damage: ↑excertion of AA, Glu,peptide & Hb. ( hepatolenticular degeneration) AR, 1:5000
Smita Pakhmode Symptoms of Wilson’s disease Hepatolenticular degeneration
Smita Pakhmode Treatment • diet low in copper •Penicillamine -Cu chelating agent ↓ excretion of cu in urine
Smita Pakhmode Copper toxicity • Diarrohea • Blue green saliva • Hemolysis • Hb-uria • Proteinuria • Kidney failure
Smita Pakhmode Case study • A 13 year old boy reported with jaundice, fatigue, muscle stiffness, tremors and behavioural changes. Examination revealed an enlarged liver and spleen, Kayser – ring noted. • i) What is the probable diagnosis? • Wilson’s Disease(Hepatolenticular degenerations) • ii) Which organs are affected? • Liver, CNS, Spleen, Eye. • iii) What are the causes for the disease? • Increased accumulation Cu in above organs leading Hepatic Cirrhosis and Cerebral necrosis. • iv) What is the treatment suggested • Low copper diet & D Penicillamine(Chelating agent)
Smita Pakhmode Case Study: A Patient in the hospital had seizures and usually appear weak and tired. Physical finding was deposition of copper in eyes as green ring round the cornea and hepatomegaly • i) What is probable disease? • ii) What is biochemical problem in this disease? • iii) What is treatment to this disease? • iv) Name any four copper containing enzymes.
Smita Pakhmode FLUORINE • Sources: drinking water Req:<2 ppm (one part of fluorine:in one million parts of drinking water) Should not exceed 3ppm
Smita Pakhmode Functions • prevent dental caries: fluoroapatite with hydroxyapatite of enamel forms protective covering. ↓ bacterial enzymes ⇢↓ production of acids • normal bone development • Enzyme Inhibitors: Sodium fluoride- enolase(glycolysis) Fluoroacetate - aconitase(TCA)
Smita Pakhmode Disease States • Dental Caries: (<0.5 ppm) • T/t: Flouridation of Water • Use of flouride toothpaste • Fluoride toxicity – • Dental Fluorosis :(>2ppm,particularly >5 ppm) mottling of enamel, discoloration of teeth Weak, rough, brown yellow patches •
Smita Pakhmode Skeletal Fluorosis(>20 ppm) Hypercalcification of Bone & Ligaments Joint stiffness and Bone density. Neurological disturbances Advanced Flurosis: Stiff Joints crippling state- genu valgum
Smita Pakhmode IODINE • - Sources: Salts(Iodine fortified), Sea foods, drinking water, vegetables, fruits. High altitudes: areas deficient in iodine content in water as well as soil Iodine is added to drinking water or to table salt in these regions TOTAL BODY CONTENT- 20 mg 80% Thyroglobulin 20%Muscle , salivary glands, ovaries
Smita Pakhmode Dietary retirements Adults: _100-150 ug/day Pregnant woman – 200 ug/day
Smita Pakhmode Synthesis of Thyroid Hormone • Synthesis of thyroglobulin precursor: • Tg Glycoprotein, Dimer. Synthesized in follicular cells of glands • Iodine uptake by gland. • Uptake from blood, active process, needs Na-K pump • Follicular cell I2 content > then Blood • Iodination of Thyroid residue: • Formation of mature TG(organification of Iodine) • Peroxidase enz. Imp • Coupling: • MIT + DIT = T3 • DIT + DIT = T4 • Hydrolysis of thyroglobulin: To release Thyroid precursor • Secretion & transport of T4 & T3: Free form < Bound with Alb & TBG • Peripheral conversion of T4 to T3: • Enzyme deiodinase • T4 T3
Smita Pakhmode Synthesis of Thyroid hormone
Smita Pakhmode Regulation of thyroid Hormone
Smita Pakhmode Functions of Thyroid glands • Development of CNS • Regulation of Normal body growth: Promote general body growth Calcification of Bone • Regulations of BMR • Regulations of fuel Metabolism: Amplifiers of cellular metaboilic activity Increase uptake of LDL Cholesterol Actions are opposite to the insulin
Smita Pakhmode Function • Synthesis of thyroid hormones • Thyroxine(T4) ,Triiodothyronine(T3) plasma iodine – 4-10 mg/dl Bound with PBI(Plasma Bound Iodine Disease states Simple goiter Toxic goiter
Smita Pakhmode Zinc RDA Sources Absorption Blood levels 10- 15mg/day Grains, beans nuts, cheese, Meat, fish, eggs, milk etc duodenum (by phytates , Ca, Cu, Fe) Stored in liver (metallothionein) excretion via Pancreatic juice and sweat 100mg/dl TB : 2 gm Prostate gland –very rich(100mg/g)
Smita Pakhmode Functions • More than 300 enzymes Carboxypeptidase , CA, Alk. Phos, , Ethanol DH, SOD , RNA Polymerase • Maintains level of Vit A:Retinol BP Synthesis • Wound healing • ↑cell growth, division,stabilizes membrane • Reproduction • Immunological function • Storage & secretion of insulin in  cells of pancreas • Gusten ( saliva) - taste sensation
Smita Pakhmode Zinc Deficiency ( Chronic Alcoholism ) •Growth retardation •Poor wound healing •Skin lesions •( hyperkeratosis , alopecia , dermitis ) •Depression •Dementia •Loss of appetite •Loss of taste sensation, •Impaired spermatogenesis •anemia
Smita Pakhmode Acrodermatitis enteropathica Rare inherited metabolic disease of Zn deficiency Defect in the absorption of zinc from intestine • Inflammation around mouth nose & fingers • Diarrhea • Alopecia • Hypogonadism Zinc Toxicity Acute - ( Welder’s fumes- Zn oxide) Excess salivation , Fever , headache ,Leucocytosis Chronic – Gastric ulcer , Pancreatitis , Anemia , Nausea, Pulmonary fibrosis
Smita Pakhmode SELENIUM • Soil content • Requirement : 50-200 µg / day • Sources- organ meats , sea foods Antioxidant Mineral Acts with Vitamin E
Smita Pakhmode Functions With vit E prevents hepatic necrosis & muscular dystrophy Maintain structural integrity Lipid peroxidation Heavy metals(Hg, Cd) Selenocystiene -Glutathione peroxidase - Antioxidant enzyme 5’deiodinase [ T4 →T3 ] Thioredoxin reductase(purine meta) is a selenoprotein
Smita Pakhmode • KESHAN DISEASE ( China) Soil deficient in selenium Endemic cardiomyopathy • Cardiovascular disease & various cancer Toxicity SELENOSIS 900 mg/ day ( Metal Polishes , antirust) hair loss , falling nails ,emotional disturbances, diarrhea, weight loss garlic odor in breath ( dimethyl selenide)
Smita Pakhmode Manganese(Mn) Functions • Cofactor –arginase, puruvate carboxylase, isocitrate dehydrogenase, SOD & peptidase • Bone development, reproduction, Normal functioning of nervous system • Hb synthesis • Inhibits lipid peroxidation • Cholesterol biosynthesis
Smita Pakhmode Disease states In animals • Retarded growth, bone deformities, sterility • Accumulation of fat in liver • Increased activity of serum alkaline phosphatase • Diminished activity of B-cells of pancrease
Smita Pakhmode MOLYBDENUM xanthine oxidase, Requirement not clearly known Widely distributed in natural foods Molybdenosis
Smita Pakhmode Cobalt • Constituent of vitamin B12 • Stimulates production of erythropoietin • Prolonged administration leads to polycythemia
Smita Pakhmode Chromium TB – 6 mg • utilization of glucose with insulin • Component of protein chromodulin • binding of insulin to cell receptor sites • lipoprotein metabolism • Decreases LDL & increases HDL • Transport of AA into the cells • Yeast, grains, cereals, cheese & meat • Deficiency- carbohydrate , lipid, protein metabolism • Toxicity- liver & kidney damage
Smita Pakhmode Commonly asked questions for MBBS Commonly asked questions in university exams • Sources, RDA ,disease manifestation of iron (8m) • Absorption of iron (4m) • Iron toxicity (4m) • Heme containing protein (4m)
Smita Pakhmode References: Text book of biochemistry Vasudevan: 9th Edition Text book of biochemistry by Pankaja Naik: 5th Edition Text book of biochemistry by Rafi: 4th Edition Biochemistry by Satyanarayana Harpers Biochemistry
Smita Pakhmode 113 Dr. Smita Pakhmode Asso. Prof. Biochemistry. NKP SIMS & RC, Nagpur

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Minerals Metabolism for MBBS Students.

  • 1.
    Smita Pakhmode Lec-1 MINERAL METABOLISM Dr.Smita Pakhmode, Associate Professor Department of Biochemistry NKPSalve Medical College &RC
  • 2.
    Smita Pakhmode Competencies No CompetencyDomain level Core Method BI 6.9 Describe the functions of various minerals in the body, their metabolism and homeostasis. K KH Y Lecture, Small group discussion BI 6.10 Enumerate and describe the disorders associated with mineral metabolism. K KH Y Lecture, Small group discussion
  • 3.
    Smita Pakhmode Biomedical Importance of MINERALS Calcificationof teeth & Bone Blood coagulation factors Neuromuscular activation Acid base equilibrium Osmotic equilibrium Acts with enzyme ( Metalloenzyme,Cofactor) Integral part of compounds (Hb,Thyroxin,Insulin, Vit B12)
  • 4.
    Smita Pakhmode Classification Minerals Principle 60-80% > 100mg/day Ca,P,Na,K,Mg,Cl,S, TRACEELEMENTS <100mg/day Essential Fe,Cu,I,Mn,Zn,Mb, Co,Fl & Se Possibly Essential Cr,Ni, Va,Cd, Barium Non essential Al.Pb,Hg,Boron, Silver Bismuth
  • 5.
    Smita Pakhmode • Introduction& Classification of minerals, • Calcium: • Functions, • Sources, & RDA, • Factors affecting absorption • Calcium Homeostasis • Disease Manifestations of Calcium metabolism • Phosphorus • Functions, • Sources, & RDA, • Factors affecting absorption • Disease Manifestations of phosphorus metabolism Learning Objectives
  • 6.
    Smita Pakhmode Frequently askedquestions(MBBS) • Factors involved in the regulation of blood calcium levels. (4M) • Biochemical functions of calcium. (4M) • Regulation of serum Calcium(4M) • Functions and deficiency manifestation of Calcium. (4M) • Hormones regulating serum Calcium.(4M) • LAQ: Write in detail about the factors influencing calcium absorption in the body. Write its function (8M) • Case study: Tetany
  • 7.
    Smita Pakhmode CALCIUM Total content: 1-1.5 Kg 99% Bones & Teeth 01% Miscible “Ca” pool ( ECF)
  • 8.
    Smita Pakhmode Functions ofCalcium 1. Bone & teeth calcification • Hydroxyapatite crystals • Bones :Reservoir of Ca • Regulators: Osteoblasts and PTH 2.Blood coagulation factors • Activator of factor IV • EDTA: Chelates Ca Anticoagulant 4.Nerve conduction Releases neurotransmitters at presynaptic & post synaptic terminals 3.Secondary messenger: Glucagon & Epinephrine Tertiary messenger with Cy AMP: ADH
  • 9.
    Smita Pakhmode Functions of Calcium 6Muscle contraction Interaction of Ca & Troponin C Activation of ATPase ↑Actin Myosin Interaction Facilitate excitation contraction coupling 5.Activation of enzyme • Calmodulin mediated • Direct Action Ca2+ + Calmodulin Ca-Calmodulin Complex Kinase. Active Kinase Enzyme. P-Enzymes Biological effects Enzymes activated with Calmodulin Adenylate cyclase, PL C Ca dependent Protein Kinase Gly synthase, Phosphorylase Kinase, G3PDH, Py. Carboxylase, PDH, Myosin kinase Directly Activated Enzyme Pancreatic Lipase Coagulation enzymes Rennin Deficiency of Ca: Tetany
  • 10.
    Smita Pakhmode Functions ofCalcium 7.Release of hormones from endocrine glands- insulin, PTH, calcitonin 8. Myocardium: Prolongs Cardiac systole ( Caution: IV administration of Ca. Gluconate) 10.Contact Inhibition: maintains Cell to cell adhesion 9. Secretory Process: Microtubule & microfilament mediated functions- endocytosis, exocytosis and cell motility
  • 11.
    Smita Pakhmode Adults 800mg Preg. /Lact .: 1500 mg Growing children 800-1200 mg DAILY REQUIREMENTS Sources Rich: Milk & Milk products Medium: Egg, Fish Vegetable, Beans, Leafy vegs. Poor but major: cereals.
  • 12.
    Smita Pakhmode FACTORS AFFECTINGABSORPTION OF CALCIUM • Its an Active process. • Occurs in first and & Second part of duodenum. • Carrier protein helped by Calcium dependent ATPase ↑↑Ca absorption Calcitriol (Active form Of Vit D) Parathyroid hormone → ↑Vit D synthesis Acidity/Low pH lactose Lysine, arginine High protein Intake
  • 13.
    Smita Pakhmode Factors decreasingCa absorption: • Phytates, oxalates • High PO4 content Ideal Ca : P Ratio 1:2 - 2:1 • Impaired fat abs: free fatty acids +calcium---calcium soaps • High pH(ALKALINE PH) • High fiber FACTORS AFFECTING ABSORPTION OF CALCIUM
  • 14.
    Smita Pakhmode PLASMA CALCIUM 50% 10% 40% BLOODCALCIUM Ionized Anion bound protein bound (5 mg/dl ) (1mg/dl) 4mg/dl. DIFFUSIBLE NONDIFFUSIBLE
  • 15.
    Smita Pakhmode Homeostasis ofCalcium Factors which regulate Ca levels in blood 1Hormones: 1.Calcitriol 2.Parathyroid hormone 3.Calcitonin 2.Concentration of phosphorus: reciprocal relationship Ionic product of ( Cal X Po4= 40) Renal insufficiency: Excretion of Ca leads to tetany 3.Serum proteins: Hypoalbunemia (1gm/dl)⍺ ↓Ser. Cal (0.8mg/dl) - levels of ionized form is normal. 4.Alkalosis and acidosis: Alkalosis favors binding of calcium with proteins Acidosis favors ionization
  • 16.
    Smita Pakhmode Blood Calcium Nlevel: 9-11mg/dl Role of Vit D ( Calcitriol) Intestine Bone Kidneys Induces synthesis of “Calcium Binding Protein”[CBP] ↓ • ↑ intestinal abs. of Ca & P (in intestinal cells) Stimulates osteoblasts ↑ ALP (↑ Phosphate level) Promotes calcification of bones ↑ Reabsorption of Calcium & phosp from renal tubules Increases Calcium Level With PTH: Stimulates osteoclasts Mobilizes Ca & Po4 from bone
  • 17.
    Smita Pakhmode Low BloodCalcium Role of Parathyroid hormone Intestine Bone Kidneys PTH: Stimulates osteoclasts ↑ Prophosphatase. Lactate. Collagenase Reabsorption & solublization of bone matrix Mobilizes Ca & Po4 from bone ↑ hydroxylation of Vit D to form Calcitriol ↑ Ca2+ Reabsorption ( rapid action ) ↓ excretion of Ca from renal tubule ↑ excretion of Po4 Induces synthesis of “Calcium Binding Protein”[CBP] ↓ • ↑ intestinal abs. of Ca & P (in intestinal cells) Vit D Increases Calcium Level Negative feed back regulation Action last for 1 hour
  • 18.
    Smita Pakhmode Raised BloodCalcium Gastrin, Glucagon & Biological amine Role of Calcitonin Bone Kidneys ↑ osteoblasts ↓ osteoclast Inhibit reabsorption of bones ↓ blood calcium level ↑ excretion of Po4 - decreases Calcium Level Antagonist to PTH Significance of Calcitonin Tumor Marker 1) Medullary Ca of Thyroid 2) Lung & Bronchus Malignancies
  • 19.
    Smita Pakhmode TEETH CALCIUMNOT SUBJECT TO REGULATION When to check Calcium levels??  Neurological symptoms, irritability  Urinary Calculi  Ectopic Calcification  Suspected Malignancies  Polyurea, Polydypsis  Chronic Renal failure  Prolong treatment with drugs which cause Hypercalcemia ( Vit D, Thiazide Diuretics)
  • 20.
    Smita Pakhmode DISORDERS OFCALCIUM METABOLISM • Hypercalcemia : Etiology: 1. Hyperparathyroidism ( Adenoma/ Ectopic PTH tumor) 2. Multiple Myeloma, Paget’s disease, Metastatic Ca 3. thyrotoxicosis, Addison's disease, 4. Prolong Immobilization 5. TB, Leprosy & Sacrcoidosis 6.Drugs: Thiazide, Vit D, IV calcium, Lithium Therapy
  • 21.
    Smita Pakhmode DISORDERS OFCALCIUM METABOLISM • Hypercalcemia : Effects: Serum ↑Ca , ↓PO4 Urine ↑Ca , ↑PO4 Ionized serum Ca ↑(6-9mg/dl), Raised Alkaline phosphatase urinary calculi & osteoporosis s/s– Polyurea, polydipsia, confusion, depression , psychosis, Pathological fracture, renal stone, ectopic calcification & Pancreatitis T/t: Adequate hydration, IV frusemide, Steroids. T/t of underlaying cause.
  • 22.
    Smita Pakhmode • Hypocalcaemia(< 8.8mg/dl) mostly due to hypo PTH Other Causes: 1. Deficiency of Vit D 2. Medullary Ca of Thyroid (↑ Calcitonin) 3. Malabsorption disorders, Acute Pancreatitis, Alkalosis(↓Ca ) 4. Renal failure, RTA, Phosphate infusion (↑PO4) S/S: Muscle cramps, paresthesia, neuromuscular irritability, muscle twitching, Accidental removal Autoimmune DISORDERS OF CALCIUM METABOLISM
  • 23.
    Smita Pakhmode Mild deficiencyof Calcium Chronic Ca deficiency Cause: Dietary deficiency of Vit D or Ca Renal insufficiency Mg deficiency White patches on nails Deformities of weight bearing bones Treatment: Oral Ca & Vit D supplementation T/t of underlying cause
  • 24.
    Smita Pakhmode • TETANY(<7.5 mg/dl) • Serious life threatening disorder S/o: neuromuscular irritability, Spasm & convulsions • mostly due to accidental or autoimmune removal of Parathyroid Gland • Dignostic signs TETANY (<7.5 mg/dl) Serum ↓Ca , ↑PO4 Urine ↓Ca , ↓ PO4 T/t—Severe cases—IV Ca Gluconate (10ml of 10% Calcium glucaonate over 10 min) Imp Note: VIT D Deficiency will never cause Tetany Severe Calcium deficiency: TETANY
  • 25.
    Smita Pakhmode Carpopedal Spasm: Flexionof wrist Flexion MPJ & Extension IP joints Adduction of thumbs & fingers Trousseu’s sign: Inflation of BP cuff for 3 min will cause carpopedal spasm Chvostek’s Sign: Tapping over facial muscle causes facial muscle contraction Other Signs: Laryngeal stridor, Prolong QT interval Signs of Tetany
  • 26.
    Smita Pakhmode Relationship ofCalcium & Phosphorus • RDA Ratio of 1:1 Ca : P ( i.e. 800 mg /day) • Diet: • optimum Ca: P ratio 1:2 - 2:1 • Favors absorption • Blood: • Ionic product of CaXP (10X4)= 40 • Ratio is important for the calcification of Bone • High Ratio: mineralization of Bones Children- 50 • Low ratio: Ricket (<30)
  • 27.
    Smita Pakhmode Case • A54 years years old grossly overweight women presented with the complaints of cramps and spasms of both hands. She was depressed and positive Trasseau’s sign & Chovestek’s sign. Past medical history reveals thyroidectomy for Grave’s disease. The laboratory findings are as follows: Serum Ca: 4.1 mg%; Sr. Creat: 1.0mg%, Sr. Po4 :5.9mg%; Sr Alb:4.0mg% • What is the diagnosis? Tetany What is probable cause for the disease? Hypoparathyroidism due to removal of PTH glands • Interpret laboratory finding and corelate with diagnosis ? hypocalcemia& Hyperphosphatemia with N Creat & Alb • What additional test to be done for conclusive diagnosis? • Estimation serum PTH level & Alk Po4 level. Low PTH & High ALP
  • 28.
    Smita Pakhmode Case • A10 year old boy presented with the complaints of muscle pain , stiffness ,cramps of both hands & feet. He was strict vegetarian & even did not consume milk & dairy products. On examination no signs of rickets were found. He had positive Trousseau’s sign & Chovestek’s sign. Serum Calcium level is as low as 4mg%. • What is the diagnosis? • Tetany • What is probable cause for the disease? • Hypoparathyroidism Or Chronic renal Failure • How would you investigate the case to confirm diagnosis ? • KFT( Urea, Creat,Electrolyte & Urinary Ca & Po4 ratio: CRF • Estimation serum PTH level & Alk Po4 level: Low PTH & High ALP • Estimation of Vit D
  • 29.
    Smita Pakhmode Case • A42 year old lady presented with the complaints of vague abdominal discomfort, fatigue & bone pain. She had frequent episodes of urinary track infection and episodes of urinary stone. Her physical examination was within normal limits.On investigations patient had N CBC, Electrolyte: High Ca & low Po4. • What is the diagnosis? • HyperCalcemia & Hypophosphatemia :Hyperparathyroidism • What is probable cause for the disease? • Primary Hyperparathyroidism(stone,moans,groans,bones) • How would you investigate the case to confirm diagnosis ? • Estimation serum PTH level • Estimation of Vit D
  • 30.
    Smita Pakhmode PHOSPHORUS Total Bodycontent = 1 Kg 80% Bones & teeth 10% Muscles , blood 10% chemical compounds Functions 1. Bones and teeth 2. High energy compounds ( ATP , GTP, Cr-P ) 3. Phospholipids, Phosphoproteins, Nucleic acids(DNA/ RNA) 4. Nucleoside Coenzymes NAD+ , NADP+ ,Pyridoxal PO4 5. Activation of Proteins and enzymes by phosphorylation 6. Phosphate buffers system( Na2HPO4/NaH2Po4 =4:1) 7. Formation of phosphate esters. G 6 P,PL, phosphoprotein
  • 31.
    Smita Pakhmode Absorption Absorption injejunum ↑by - Calcitriol - optimum Ca: P ratio 1:2 - 2:1 - Acidity ↓by Phytates ( cereal rickets ) RDA : Ratio of 1:1 Ca : P ( i.e. 800 mg /day) Infants 2:1 ( Milk ) Sources Milk , eggs, meat, fish ,cereals, leafy vegetables, cheese, beans, PHOSPHORUS
  • 32.
    Smita Pakhmode Factors RegulatingPhosphorus in Blood: Vit D & PTH Excretion: 500 mg / day in urine Renal threshold → 2 mg /dl PTH → Inhibits reabsorption of PO4 by RT Conc. In Blood: Serum Level: Total 3-4 mg / dl Whole blood - 40 mg /dl ( ↑content RBC, WBC’s) Fasting > Post meal Distribution: 40% free ions 10% protein bound 50% bound to cations (Ca2+ / Mg2+ / Na+ /K+ )
  • 33.
    Smita Pakhmode Disorders ofphosphate Hyperphosphatemia: ↑ absorption of the phosphate: ↑ Vit D/ Po4 infusion ↑ Cell lysis: Cancer chemotherapy, Bone secondaries, ↓ excretion : Renal Impairment, Hypoparathyroidism, Acidosis Drugs: Chlorthiazide, Nifedipine, Frusemide
  • 34.
    Smita Pakhmode Disorders ofphosphate • Hypophosphatemia: • ↓ absorption of the phosphate: • Malnutrition, Malabsorption, Chr. Diarrhea, Vit D deficiency. • Intracellular shift: Insulin therapy, Renal rickets • ↑ urinary excretion of phosphate: Hyper parathyroid hormone, hypophosphatemic rickets. Hypercalcemia, Chronic alcoholism, Drugs • Drugs: Antacids, Diuretics, salicyclate
  • 35.
    Smita Pakhmode RDA Males– 350 mg/day Females – 300 mg/day Sources Cereals, nuts, beans, vegetables { cabbage, cauliflower}, meat, milk & fruits Magnesium (Macroelement) Total content in the body : 20 g 70 % bones & teeth 30% soft tissue & body fluids Absorption Upto 50% ( carrier mediated ) ↑↑ by PTH Ca , P, Alcohol - ↓Mg Absoption Excretion Mostly → Intestine Partly→ Kidneys Serum levels Total 2-3 mg / dl 60% - Ionised 10% - bound to anions 30% - Protein bound
  • 36.
    Smita Pakhmode Functions • Boneand teeth • Cofactor for ATP requiring enzymes • e.g. hexokinase , PF kinase , glucokinase, adenylate cyclase • Neuromuscular functions • Improves glucose tolerance . • Reduces BP & prevents stroke • Clinical applications: • When given in large doses (parenterally ) • CNS depressant • (Hence anesthetic / anticonvulsant )
  • 37.
    Smita Pakhmode Disorders: Hypomagnesemia( lowserum Mg ): •Renal tubular necrosis, Liver Cirrhosis, Toxemia of pregnancy ,Malnutrition , C/F – Neuromuscular irritability weakness convulsions Magnesium Toxicity : Magnesium containing Antacids/ Laxatives C/F - Drowsiness Lethargy Weakness
  • 38.
    Smita Pakhmode Sulphur Most importantcomponent of body proteins. Sources: S – AA Vegetable & Cereals No specific RDA Excretion: 1gm/day through urine 1. Inorganic sulphate 2. Ethereal sulphate 3. Unoxidized sulphate
  • 39.
    Smita Pakhmode Functions ofSulphur 1. Mitochondrial cellular respiration Component of Fe-S Containing protein 2.Stabilize the protein structure: Insulin, Immunoglobulins 3. Part of different coenzyme: Thiamine, Biotin, Lipoic Acid, Coenzyme A 4. Part of fibrous proteins: Keratin of hair & Nail 5.Part of different metabolically active compounds: Glutathione, heparin, Chondrotin Sulphate, taurocholic acid 6. Detoxification reactions: Phosphoadenosine Phosphosulphate (PAPS) 7. Transmethylation Reaction: S- Adenosine Methionine
  • 40.
    Smita Pakhmode Sodium Major CATIONin ECF 70%- ECF 4-5%-ICF 20%-soft tissues, bone teeth Requirement: 5-10 gm/day as NaCl Source : Common Salt Cereals, legumes, leafy vegetables, nuts, eggs, milk Absorption : 99% in GIT
  • 41.
    Smita Pakhmode Functions ofSodium: 1. Maintains ECF volume 2. Osmotic pressure & fluid balance 3. Acid-base balance: 4. Component of Na K pump 5. Absorption of glucose, galactose, amino acids 6. Nerve muscle conduction.
  • 42.
    Smita Pakhmode Distribution ofNa in body 4000meq 75% Exchangable ECF 70% ICF 4% 25% Non Exchangable Bone, teeth & soft tissue Normal level = 135-145 meq/L-ECF 35 meq/L-ICF
  • 43.
    Smita Pakhmode Regulation ofSodium Decrease in BP Rennin Angiotensinogen1 Angiotensin1 Angiotensin II AngiotensinII Aldosteron Na+ Retention Excretion of K+ & H+ ANF Aldosterone system ↑ BP ↑GFR…….. ↑Na+ excretion ↑Urine out put ↓ in Na Conc
  • 44.
    Smita Pakhmode Factors affectingserum Sodium levels: Aldosterone : ↑↑ Na + reabsorption ADH : ↑↑ water reabsorption Edema: ↑ water, Na+ content Diuretics: → ↑Na+ excretion, water excretion Excretion: by Kidneys & sweating 800 gm/day Na+ filtered 99% of this is Reabsorbed Na Homeostasis
  • 45.
    Smita Pakhmode Hyponatremia Method ofEstimation: Flame photometry /Ion selective electrode Symptoms: Muscle cramps, Headache & Nausea Long term complication Sign: B.P.& Circulatory Failure, Edema
  • 46.
    Smita Pakhmode Causes ofHyponatremia Hyponatremia ↓osmolality Hypervolemia CCF, Cirrhosis, Nephrotic Syndrome Euvolemia SIADH Pneumonia, Pulm. TB, Ca Bronchus Hypovolemia Extra renal Diarrhoea, vomiting Sever Sweating Renal ↓ADH, Aldosteron (addisons disease) RTA Diuretcs
  • 47.
    Smita Pakhmode Hypernatremia Hypernatremia Blood volume Hypervolemic Cushing’sSyndrome Prolong steroid therapy Pregnancy Excess of Mineralocorticoid Euvolemic Diabetes Insipidus Hypovolemic Dehydration Diarrhoea, vomiting With reduced fluid intake Diuretics
  • 48.
    Smita Pakhmode POTASSIUM Major intracellularcation Total Body content: 3500 meq 75% in muscles & ICF RDA : 3-4 gm/day Sources : Bananas, oranges, apples, almonds, dates, beans, potatoes, coconut water, beans , chicken and liver Normal level = 3.5-5meq/L (ECF) 50meq/L (ICF) Daily Intake: 20-200 meq/ Day Excretion: Urine Aldosterone: ↑ excretion of K+
  • 49.
    Smita Pakhmode Functions •Intracellular osmoticpressure & volume. •Component of Na K pump •Acid-base & Water balance •Imp in depolarization & contraction of cardiac muscles •Nerve impulse transmission •Enzyme Pyruvate Kinase Activity •Protein Biosynthesis
  • 50.
    Smita Pakhmode Regulation ofPotassium Serum K Redistribution Of K Insulin Acidosis Increased Excretion ↑Aldosterone ↑Corticosteroid
  • 51.
    Smita Pakhmode HYPOKALEMIA (<3 meq/L) Symptoms: Vomiting,Diarrhea, Weakness, Anorexia Irritability, Muscle weakness, Arrhythmias, Cardiac arrest, ECG changes: Flattened /lowering/ inversion of T wave ST seg depression, prominent U wave Arrythmia
  • 52.
    Smita Pakhmode Hypokalemia Hypokalemia Redistribution Of K Insulintherapy T/t Aciodocis Meta. Alkalosis Catecholamine B adrenergic drugs Periodic Paralysis True loss of K through Urine K Excretion> 25 Meq/Day RTA A TN ↑Aldosterone ↑Corticosteroid K Excretion < 25 meq/Day Diarrhoea Fistula Extensive surgery
  • 53.
    Smita Pakhmode Hyperkalemia Hyperkalemia Pseudo Hemolysis Thrombocytosis Redistribution Of K InsulinDeficiency Meta Acidosis K Retention Massive Blood transfusion Renal transplant Obstructive nephropathy Addison's Disease SLE/ SCD
  • 54.
    Smita Pakhmode HYPERKALEMIA: (>5.5 meq/L) Symptoms: s/o depression of CNS Weakness, decreased Deep tendon reflexes numbness bradycardia , Cardiac arrest. ECG changes: prominent T wave widening of QRS complex Prolong PR interval
  • 55.
    Smita Pakhmode Lec-2 MINERAL METABOLISM Dr.Smita Pakhmode, Associate Professor Department of Biochemistry NKPSalve Medical College &RC
  • 56.
    Smita Pakhmode Commonly askedquestions(MBBS) • Absorption & function of iron.(4M) • Mechanism of iron absorption from the intestine. (4M) • Write a note on intestinal absorption of Iron. (4M) • Factors affecting intestinal absorption of Iron. (4M) • Case on Iron deficiency Anemia (4M) • Explain the defect in Wilson’s disease, state the clinical manifestations (4M) • Functions of Copper(4M) • Case on Wilson’s Disease.(4M)
  • 57.
    Smita Pakhmode IRON: • Functions, •Sources, & RDA, • Factors affecting absorption of iron • Regulation of Absorption of Iron • Disease Manifestations of Iron metabolism • Copper • Distribution & Functions, • Sources, & RDA, • Biochemical functions • Disease Manifestations Learning Objectives
  • 58.
    Smita Pakhmode IRON 3-5gm • • Requirements- Dailyallowance (ICMR) Adult man: -10mg /day Mensturating women: 18mg/day Pregnancy/Lactation- 40mg/day Children (13-15yrs)-30mg/day 75% -blood 20% - liver, bone marrow 5%muscles Absorption: 10% (1-2mg absorbed) ↑↑ Iron deficiency Anaemia, Growing children
  • 59.
    Smita Pakhmode • Heme: –Hb , Myoglobin, Cytochromes, Tryptophan Pyrrolase , catalase,peroxidase • Fe-S: – complex III Fe-S, succinate DH, Xanthine Oxidase • Non-heme iron: Ferritin, Transferrin, Hemosiderin IRON CONTAINING PROTEINS:
  • 60.
    Smita Pakhmode Functions ofIron: • Hb /Myoglobin: Transport of O2 & CO2 •Cytochrome: ETC & Detoxification •Peroxidase: Present in Lysosome, catalyzes phagocytosis of bacteria by neutrophils. • Immunocompetence of the body
  • 61.
    Smita Pakhmode SOURCES- • Richsource: Organ Meat( Liver,heart & Kidney) • Good source: Leafy Vegs., Pulses ,Cereals, , Jaggery, fish ,Apples,Dried fruits • Poor source: Milk, wheat , polished rice • Absorption- • Upper duodenum & Proximal Jejunum Fe2+ Fe3+ Ferroxidase/Ceruloplasmin Ferroreductase Transport form Storage form
  • 62.
  • 63.
    Smita Pakhmode • ↑↑by - • HCL, • Ascorbic acid, Cysteine, -SH gps of proteins • Iron deficiency Anaema(10 Times ) • ↓↓ by- Phytic acid (cereals) Oxalic acid(vegetable), PO4 Alkaline pH Malabsorption disorders(steatorrhoea) Total or Partial Gastrectomy Diet: Fe3+ + Oragnic acids/Pr. HCl Fe3+ Vit C, Cyst Fe2+ Factors affecting Absorption of Iron:
  • 64.
    Smita Pakhmode GIT Lumen Diet: Mucosalcell Blood Fe3+ + Oragnic acids/Pr. HCl Fe3+ Vit C, Cyst Fe2+ DMT Fe2+ Fe3+ Ferroxidase Apoferritin Mucosal Ferritin Fe3+ Ferrireductase Ferroportin Fe2+ Fe3+ Ferroxidase Ceruloplasmin Apotransferrin Plasma (Fe3+) Transferrin Heme Pr. Hb, My, Cyt Ferritin Fe3+ Hemosiderin Hepcidin Liver, spleen, BM Absorption storage and utilization of food Iron. DMT= Divalent Metal transporter Mucosal block theory for the regulation of iron absorption ↑↑Ferritin
  • 65.
    Smita Pakhmode Total ironbinding capacity • Transferrin: Glycoprotein • 1mol Of Transferrin-2 atoms of Fe3+ • N TIBC Plasma: 250mg/dl-400 mg of Iron/dl • Normal condition 1/3 of transferrin is saturated • TIBC grossly increased in Iron deficiency Anaemia.
  • 66.
    Smita Pakhmode • Ferritin: •In liver , spleen, BM( as ferritin) • (Apo-ferritin has 24 subunits (MW5,00,000) • Can take up 4,500 Iron atoms/ molecules to become ferritin • Ferritin: 25% Iron by weight. • In Iron toxicity , ferritin Increased is seen in plasma IRON STORAGE(Permanent) Hemosiderin: 35% of iron by its weight. Accumulate in liver, spleen whenever there is excess of demand of iron.
  • 67.
    Smita Pakhmode Iron isone way compound • Once entered in the body, can not be excreted. • It acts in close circuit. • Utilized & reutilized • Not excreted in urine • < 1mg/day excreted through bile salt, sweat. • It gets deposited in the body in form Hemosiderin. Iron loss Feces: Major loss of unabsorbed iron Menstruating women (up to menopause)- 25-30 mg /day Skin →cells lost
  • 68.
    Smita Pakhmode Iron isreutilized RBC Lysis Globin removed HB: HB- Haptoglobin complex taken up by liver kuffers cells Iron reutilized Heme: Heme Hemopexin complex Taken up by hepatocyte Porphyrin ring opened. Bilirubin Iron. → Iron transferrin → storage. Iron reutilized Iron reutilized Renal insufficiency leads to iron deficiency due to loss of haptoglobin, hemopexin & deficiency of erythropoietin
  • 69.
    Smita Pakhmode • Mostcommon nutritional deficiency disorder • 30% world population • 85% pregnant women • 15 % maternal deaths • In children → irreversible impairment in learning ability IRON DEFICIENCY ANAEMIA
  • 70.
    Smita Pakhmode Iron deficiencyAnaemia Causes: • Hookworm infestation • Iron deficiency in diet • Repeated pregnancy (1gm/delivery) • Chr. Bloods loss ( piles/ Uterine hemorrhage) • Renal defect (loss in urine) • Lack of abs ( Subtotal gastrectomy, achlorhydria) • Symptoms: • “Microcytic Hypochromic Anaemia” (< 12gm/dl) • Apathy, sluggish, • atrophy of gastric epithelium ↓abs of iron achlorhydria • Chronic deficiency → impaired attention /irritability ↓memory poor school performance
  • 71.
    Smita Pakhmode TREATMENT • 100mg iron + 500 µg Folic Acid - Preg women • 20 mg iron + 100 µg FA - children IRON TOXICITY • Haemosiderosis Haemosiderin→ golden brown granules ↓ (spleen, liver) Complexes of partially denatured ferritin ( 25% iron)
  • 72.
    Smita Pakhmode 1)Primary Haemosiderosis •Abnormal gene on chr 6 (short arm) • ↑abs of iron • Excess iron deposit 2) Secondary Haemosiderosis • Secondary to repeated blood transfusions (hemophilia) • Bantu tribes (Africa) Iron vessels + low PO4 ( corn-staple diet)
  • 73.
    Smita Pakhmode Hemochromatosis:- Direct irondeposition in tissues Cirrhosis – liver Diabetes – Pancreas Yellow Brown Skin – Skin : Bronze Diabetes Treatment : Repeated Phlebotomy + Desferrioxamins
  • 74.
  • 75.
    Smita Pakhmode COPPER(CU)….100MG Plasma Cu 100-200mg/dl 95% 5% Ceruloplasmin Albumin 25-50 mg/dl 0.34% Cu 95% in RBCs as colourless erythrocuprein Rest as Ceruloplasmin in plasma (serum ferroxidaseII )
  • 76.
    Smita Pakhmode RDA Sources 1.5-3 mg/day Cereals, nuts, Meat , Liver, Kidney, egg yolk, Green leafy vegetables (Milk poor source ) Absorption Duodenum Metallothionein pr facilitates abs Phytate,Zinc,& Mo
  • 77.
    Smita Pakhmode Biochemical Functionof Copper Tyrosinase, uricase, catalase, cytochrome oxidase, Monoamine oxidase, Superoxide dismutase, ascorbic acid oxidase, phenol oxidase, • Essential constituent Enzymes: •ALA synthase: For Hb synthesis •Lysyl oxidase : cross linking of collagen & elastin •Ceruloplasmin (Ferroxidase) : Fe+2 to Fe+3 – (Transferrin) transported in plasma •Tyrosinase: • Synthesis of Melanin & phospholipids • For Bone& nervous system(melanin) dev.
  • 78.
    Smita Pakhmode • FeAbsorption and incorporation into Hb • Co factor for Vit C in hydroxylation reaction • Component of Cu containing non enzymatic proteins e.g. Hepatocuprein, Cerebrocuprein Hemocuprein Biochemical Function of Copper
  • 79.
    Smita Pakhmode Deficiency : -MicrocyticNormochromic Anaemia -Weakening of walls of major vessels- fragility of arteries -demineralization of bones, demyelination of neural tissue, myocardial fibrosis, -Hypopigmentation ( tyrosinase) Greying of hair
  • 80.
    Smita Pakhmode Deficiency ofCu: Menke’s disease
  • 81.
    Smita Pakhmode Menke’s disease: -X linked disorder • Cu is absorbed by intestine but can not be transported to blood. • Absence of intracellular copper binding ATPase. • Cu may be trapped by metallothionein in the intestinal cells • Not mobilized to other tissues. S/S decreased Cu in plasma & urine Anemia, De pigmentation of hair Kinky ,twisted brittle hair( Cu catalyzed S-S bond formation) Seizurs & Metal retardation
  • 82.
    Smita Pakhmode Wilson’s disease DefectiveATP 7A gene: Cu Binding ATPase ↓Excretion of Cu through intestine from bile ↑ Absorption of Cu from Kidney ↓hepatic incorporation of copper in ceruloplsmin Free Cu accumulates in the organs Liver Hepatic cirrhosis Brain necrosis Renal damage: ↑excertion of AA, Glu,peptide & Hb. ( hepatolenticular degeneration) AR, 1:5000
  • 83.
    Smita Pakhmode Symptoms ofWilson’s disease Hepatolenticular degeneration
  • 84.
    Smita Pakhmode Treatment • dietlow in copper •Penicillamine -Cu chelating agent ↓ excretion of cu in urine
  • 85.
    Smita Pakhmode Copper toxicity •Diarrohea • Blue green saliva • Hemolysis • Hb-uria • Proteinuria • Kidney failure
  • 86.
    Smita Pakhmode Case study •A 13 year old boy reported with jaundice, fatigue, muscle stiffness, tremors and behavioural changes. Examination revealed an enlarged liver and spleen, Kayser – ring noted. • i) What is the probable diagnosis? • Wilson’s Disease(Hepatolenticular degenerations) • ii) Which organs are affected? • Liver, CNS, Spleen, Eye. • iii) What are the causes for the disease? • Increased accumulation Cu in above organs leading Hepatic Cirrhosis and Cerebral necrosis. • iv) What is the treatment suggested • Low copper diet & D Penicillamine(Chelating agent)
  • 87.
    Smita Pakhmode Case Study: APatient in the hospital had seizures and usually appear weak and tired. Physical finding was deposition of copper in eyes as green ring round the cornea and hepatomegaly • i) What is probable disease? • ii) What is biochemical problem in this disease? • iii) What is treatment to this disease? • iv) Name any four copper containing enzymes.
  • 88.
    Smita Pakhmode FLUORINE • Sources:drinking water Req:<2 ppm (one part of fluorine:in one million parts of drinking water) Should not exceed 3ppm
  • 89.
    Smita Pakhmode Functions • preventdental caries: fluoroapatite with hydroxyapatite of enamel forms protective covering. ↓ bacterial enzymes ⇢↓ production of acids • normal bone development • Enzyme Inhibitors: Sodium fluoride- enolase(glycolysis) Fluoroacetate - aconitase(TCA)
  • 90.
    Smita Pakhmode Disease States •Dental Caries: (<0.5 ppm) • T/t: Flouridation of Water • Use of flouride toothpaste • Fluoride toxicity – • Dental Fluorosis :(>2ppm,particularly >5 ppm) mottling of enamel, discoloration of teeth Weak, rough, brown yellow patches •
  • 91.
    Smita Pakhmode Skeletal Fluorosis(>20ppm) Hypercalcification of Bone & Ligaments Joint stiffness and Bone density. Neurological disturbances Advanced Flurosis: Stiff Joints crippling state- genu valgum
  • 92.
    Smita Pakhmode IODINE • - Sources: Salts(Iodinefortified), Sea foods, drinking water, vegetables, fruits. High altitudes: areas deficient in iodine content in water as well as soil Iodine is added to drinking water or to table salt in these regions TOTAL BODY CONTENT- 20 mg 80% Thyroglobulin 20%Muscle , salivary glands, ovaries
  • 93.
    Smita Pakhmode Dietary retirements Adults:_100-150 ug/day Pregnant woman – 200 ug/day
  • 94.
    Smita Pakhmode Synthesis ofThyroid Hormone • Synthesis of thyroglobulin precursor: • Tg Glycoprotein, Dimer. Synthesized in follicular cells of glands • Iodine uptake by gland. • Uptake from blood, active process, needs Na-K pump • Follicular cell I2 content > then Blood • Iodination of Thyroid residue: • Formation of mature TG(organification of Iodine) • Peroxidase enz. Imp • Coupling: • MIT + DIT = T3 • DIT + DIT = T4 • Hydrolysis of thyroglobulin: To release Thyroid precursor • Secretion & transport of T4 & T3: Free form < Bound with Alb & TBG • Peripheral conversion of T4 to T3: • Enzyme deiodinase • T4 T3
  • 95.
  • 96.
  • 97.
    Smita Pakhmode Functions ofThyroid glands • Development of CNS • Regulation of Normal body growth: Promote general body growth Calcification of Bone • Regulations of BMR • Regulations of fuel Metabolism: Amplifiers of cellular metaboilic activity Increase uptake of LDL Cholesterol Actions are opposite to the insulin
  • 98.
    Smita Pakhmode Function • Synthesisof thyroid hormones • Thyroxine(T4) ,Triiodothyronine(T3) plasma iodine – 4-10 mg/dl Bound with PBI(Plasma Bound Iodine Disease states Simple goiter Toxic goiter
  • 99.
    Smita Pakhmode Zinc RDA SourcesAbsorption Blood levels 10- 15mg/day Grains, beans nuts, cheese, Meat, fish, eggs, milk etc duodenum (by phytates , Ca, Cu, Fe) Stored in liver (metallothionein) excretion via Pancreatic juice and sweat 100mg/dl TB : 2 gm Prostate gland –very rich(100mg/g)
  • 100.
    Smita Pakhmode Functions • Morethan 300 enzymes Carboxypeptidase , CA, Alk. Phos, , Ethanol DH, SOD , RNA Polymerase • Maintains level of Vit A:Retinol BP Synthesis • Wound healing • ↑cell growth, division,stabilizes membrane • Reproduction • Immunological function • Storage & secretion of insulin in  cells of pancreas • Gusten ( saliva) - taste sensation
  • 101.
    Smita Pakhmode Zinc Deficiency (Chronic Alcoholism ) •Growth retardation •Poor wound healing •Skin lesions •( hyperkeratosis , alopecia , dermitis ) •Depression •Dementia •Loss of appetite •Loss of taste sensation, •Impaired spermatogenesis •anemia
  • 102.
    Smita Pakhmode Acrodermatitis enteropathica Rareinherited metabolic disease of Zn deficiency Defect in the absorption of zinc from intestine • Inflammation around mouth nose & fingers • Diarrhea • Alopecia • Hypogonadism Zinc Toxicity Acute - ( Welder’s fumes- Zn oxide) Excess salivation , Fever , headache ,Leucocytosis Chronic – Gastric ulcer , Pancreatitis , Anemia , Nausea, Pulmonary fibrosis
  • 103.
    Smita Pakhmode SELENIUM • Soilcontent • Requirement : 50-200 µg / day • Sources- organ meats , sea foods Antioxidant Mineral Acts with Vitamin E
  • 104.
    Smita Pakhmode Functions With vitE prevents hepatic necrosis & muscular dystrophy Maintain structural integrity Lipid peroxidation Heavy metals(Hg, Cd) Selenocystiene -Glutathione peroxidase - Antioxidant enzyme 5’deiodinase [ T4 →T3 ] Thioredoxin reductase(purine meta) is a selenoprotein
  • 105.
    Smita Pakhmode • KESHANDISEASE ( China) Soil deficient in selenium Endemic cardiomyopathy • Cardiovascular disease & various cancer Toxicity SELENOSIS 900 mg/ day ( Metal Polishes , antirust) hair loss , falling nails ,emotional disturbances, diarrhea, weight loss garlic odor in breath ( dimethyl selenide)
  • 106.
    Smita Pakhmode Manganese(Mn) Functions • Cofactor–arginase, puruvate carboxylase, isocitrate dehydrogenase, SOD & peptidase • Bone development, reproduction, Normal functioning of nervous system • Hb synthesis • Inhibits lipid peroxidation • Cholesterol biosynthesis
  • 107.
    Smita Pakhmode Disease states Inanimals • Retarded growth, bone deformities, sterility • Accumulation of fat in liver • Increased activity of serum alkaline phosphatase • Diminished activity of B-cells of pancrease
  • 108.
    Smita Pakhmode MOLYBDENUM xanthine oxidase, Requirementnot clearly known Widely distributed in natural foods Molybdenosis
  • 109.
    Smita Pakhmode Cobalt • Constituentof vitamin B12 • Stimulates production of erythropoietin • Prolonged administration leads to polycythemia
  • 110.
    Smita Pakhmode Chromium TB –6 mg • utilization of glucose with insulin • Component of protein chromodulin • binding of insulin to cell receptor sites • lipoprotein metabolism • Decreases LDL & increases HDL • Transport of AA into the cells • Yeast, grains, cereals, cheese & meat • Deficiency- carbohydrate , lipid, protein metabolism • Toxicity- liver & kidney damage
  • 111.
    Smita Pakhmode Commonly askedquestions for MBBS Commonly asked questions in university exams • Sources, RDA ,disease manifestation of iron (8m) • Absorption of iron (4m) • Iron toxicity (4m) • Heme containing protein (4m)
  • 112.
    Smita Pakhmode References: Text bookof biochemistry Vasudevan: 9th Edition Text book of biochemistry by Pankaja Naik: 5th Edition Text book of biochemistry by Rafi: 4th Edition Biochemistry by Satyanarayana Harpers Biochemistry
  • 113.
    Smita Pakhmode 113 Dr. SmitaPakhmode Asso. Prof. Biochemistry. NKP SIMS & RC, Nagpur

Editor's Notes

  • #10 BCCI MEN Have Heart. B-Bone & Teeth, C- Muscle contraction, C- Coagulation, I: Integrity & Permiability of cell memb, E- Enzyme activation Have- Hormone release Heart_ Cardiac Systole
  • #21 Calcium acts as antagonist to the ADH
  • #25 CATS: Convulsions, Arrythmias, tetany Spasm/striodor
  • #28 Alb: 3.7 to 5.3 mg/dl, Po4: high(N: 3-4mg/dl)
  • #31 Gly Synthase Active Dephospho form Gly Phosphorylase: Active in phosphorylated form Phos Proteins: Casein
  • #33 Fasting > Post meal becoz after ingestion of glucose all phosphate is used for the formation of ATP. PTH : increases Ca & Po4 release from the bone & resorption Ca & po4 from the urine.
  • #37 Neuromuscular functions: Low levels leads NM irritability. Improves glucose tolerance : Increases utilization of glucose by enhancing Glycolysis
  • #38 Magnesium containing Antacids/ Laxatives Symptoms are same as Calcium Deficiency
  • #39 Inorganic sulphate: proportional to the protein Intake Ethereal/ Organic sulphate : Conjugated sulphate, represents putrification activity in intestine, Increased in Intestinal stasis & its consumption unOxidized sulphate: 10% of total , S containing AA, Thiocynate, Urochrome , Does not vary with diet, Increased A Aacidurea .
  • #41 Hypertension history-5g Pt of HT : 1 g/day
  • #42 1. NACL exerts osmotic pressure & resposnsible for distribution of blood volume in various compatments 3. NaHCo3 is the part of bicarbonate buffer to maintain blood pH Na H exchanger presnt in renal tubule, it is part of renal mechanism of acid base balance. 4. Exchanges Na Imp for maintenance of cell volume, maintainance of action potential around the memeb 5. Absorption through intestine & Renal Tubular absorption. 6. Closing and opening of Na K channel helps in proper nerve conduction/
  • #59 ICMR: Indian council of Medical research.
  • #90 Fluroappetite forms resistance layers over hydroxyappetite of enamel