This document discusses various haematinics including iron, vitamin B12, folic acid, and erythropoietin. It covers their roles in red blood cell formation, daily requirements, dietary sources, absorption and transport, deficiency states, preparations used to treat deficiencies, and therapeutic uses to treat conditions like iron deficiency anemia and megaloblastic anemia. It provides details on the pharmacokinetics and pharmacology of administering these substances.
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
The current slide include the pharmacology og cephalosporins.
Contents
Introduction to Cephalosporins
Classification of Cephalosporins
Cefazolin
Cephalexin
Cefuroxime
Cefuroxime axetil
Cefotaxime
Cefixime
Cefpodoxime proxetil
Cefepime
Adverse effects of Cephalosporins
Uses of Cephalosporins
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
The current slide include the pharmacology og cephalosporins.
Contents
Introduction to Cephalosporins
Classification of Cephalosporins
Cefazolin
Cephalexin
Cefuroxime
Cefuroxime axetil
Cefotaxime
Cefixime
Cefpodoxime proxetil
Cefepime
Adverse effects of Cephalosporins
Uses of Cephalosporins
Lecture slides for Medical Undergraduate teaching in Pharmacology. Study material is based on Essentials of medical pharmacology by KD tripathi and Katzung. Figures are obtained from google image search and above mentioned textbooks.
Lecture slides for MBBS Undergraduate Medical students. Study material was taken from Essentials of pharmacology by KD Tripathi. Figures were searched from google.
Lecture slides for undergraduate MBBS class in Pharmacology on " Drugs for Diarrhoea" . It includes various treatment modalities which are used in the management of Diarrhoea. Basic source of information for preparing this slides is" Essentials of Pharmacology by KD tripathi, 7th Edition". Images are searched with the help of google images.
This lecture slides are prepared for Refresher course for pharmacist. Essential Medicines, Rational use of drugs and Self medication, These are the topics covered in this ppt.These slides are also useful for other medical undergraduates and post graduates students.
Lecture slides for undergraduate Medical students (MBBS) for Pharmacology class. Presentation includes some important historical milestones followed by introduction to general anesthesia. Stages of general anesthesia, Inhalational and intravenous anesthetic agents with their pros and cons and uses. Complications of general anesthesia and pre anesthetic medication is in the last part of presentation.
This slides are prepared for undergraduate medical (MBBS) class for teaching pharmacology. Materials for slides are taken from Essentials of Pharmacology, KD Tripathi 7th ed, Medical Pharmacology, SK Shrivastav and Sharma & Sharma. Pictures are obtained from google.
Presntation prepared for MBBS pharmacology teaching on Thyroid Hormones and Antithyroid drugs. These slides focuses on Thyroid hormone synthesis along with its regulation and pharmacological actions. treatment of Hypothyroidism and hyperthyroidism is covered.
Medical Undergraduate Lecture slides on Pharmacotherapy of HIV-AIDS. These slides include life cycle of HIV. Classification of available drugs based on target site. Individual Drugs with Mechanism of action, PK, AE and drug interactions. Treatment principles and guidelines for HIV-AIDS based on NACO(National Aids Control Organisation, India) Guidelines.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Presentation for Medical undergraduates for teaching pharmacology. It deals with Physiology of steroid hormones and their action along with agents which are used therapeutically with their action, adverse effects and therapeutic uses.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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4. Anaemia
■ Blood loss
■ Impaired red cell formation – Iron,Vit B12, folic
Acid deficiency
■ Bone marrow depression
■ Erythropoietin deficiency
■ Haemolytic anaemia
5. Distribution of iron
Protein Tissue Iron (mg)
Haemoglobin Erythrocytes 2600
Myoglobin Muscles 400
Enzymes Liver 25
Transferrin Plasma and ECF 8
Ferritin and
Hemosiderin
Liver,
Spleen,
Bone marrow
410
48
300
6.
7. Iron
■ Stored on as ferric form with apoferritin.
■ Major storage – Reticuloendothelial cells
■ Parenchymal iron in Enzymes
14. Mucosal Block
■ Ferritin curtain
■ Erythropoiesis and iron status of body
govern absorption
■ Larger % absorbed during deficiency
■ In gross excess, mucosal block fails
15. Transport and Utilization
■ On entering plasma iron is immediately
converted to the ferric form
■ Complexed with a glycoprotein transferrin (Tf)
■ Transported into cells through transferrin which
binds withTransferrin receptors
■ Iron dissociates at acidic pH, and utilized.
16. Storage
■ Stored in RE cells of Liver, Spleen and bone
marrow & Hepatocytes and Myocytes.
■ Apoferritin synthesis is regulated by iron status
of the body
■ Low – Less apoferritin and moreTf produces
■ High – More apoferritin synthesis
17. Excretion
■ Highly conserved (one way substance)
■ Excreted by Shedding of mucosal cells, bile,
Desquamated skin, urine and sweat.
■ Menstruation – (0.5 – 1 mg/day)
■ Excess iron requirement in pregnancy.
20. Oral iron
■ Preferred route
■ Ferrous salts preferred – cheap, high iron
content, better absorption
■ Gastric irritation and constipation depends on
quantity of iron
■ Elemental iron
21. Oral iron preparations
■ Ferrous sulphate – 20 % in hydrated form, 32 %
in dried salt
■ Ferrous Gluconate – 12 % elemental iron
■ Ferrous fumarate – 33 % elemental iron,
tasteless.
■ Carbonyl iron – Powder form, better gastric
tolerance, less bioavailability
22. Oral iron
■ SR preparation costly and irrational
■ Liquid formulation stain the teeth
■ 200 mg elemental iron divided into 3 doses
■ Better absorption on empty stomach – irritateGI mucosa
■ Larger dose after meal / smaller dose in between meals
23. Adverse effects
■ Epigastric pain, Heartburn, Nausea,Vomiting
■ Bloating, staining of teeth, metallic taste
■ Start with low dose and gradually increase the dose
■ Constipation is more common than diarrhoea
28. Iron Dextran
■ High molecular weight colloid
■ Only preparation given by IM and IV
■ Dextran is allergic – Anaphylactic reaction
■ Small test dose for sensitivity testing
29. ■ By IM, circulates through lymphatics without
transferrin
■ Dose needs to be adjusted in IM due to local
binding
■ 2 ml daily/ alternate day/ 5 ml on each side
■ Given in gluteal region, deep IM by Z technique
30. ■ IV bolus given slowly over 10 minutes daily
■ Total dose diluted in saline over 5-6 hours under
observation
■ Infusion terminated if giddiness, paresthesias or
chest tightness
32. Ferrous Sucrose
■ Iron hydroxide with sucrose
■ Highly alkaline, so only given by IV over 5
minutes daily
■ Total dose can’t be given by infusion
■ Safer than older preparation, less antigenic
33. Ferric Carboxymaltose
■ Rapidly taken up by RE cell, liver and spleen on IV
■ 100 mg daily /1000 mg in 100 ml saline slowly IV
■ Rapid increase in Hb and stores
■ Less antigenic
■ Pain@ injection site, rashes, Headache, nausea,
hypotension
■ Not recommended < 14 years
35. Iron DeficiencyAnaemia
■ Treatment of cause
■ Oral iron preferred
■ 0.5-1 g/dl Hb ↑ desired, rate decreases later
■ Continue till Normal level, 2-3 months
thereafter t0 replenish stores
41. Vitamin B12 (COBALAMIN)
■ Synthesised by microorganism
■ Dietary sources – Liver, kidney, Sea fish, egg yolk, meat
■ Vegetables, fruits lacks cobalamin unless contaminated
by microorganism
■ Daily 1–3 μg, Pregnancy and lactation : 3–5 μg./day
■ Present in food as protein conjugates is released by
cooking or by proteolysis
42. ■ Intrinsic factor (a glycoprotein) secreted by stomach
forms a complex with B12
■ attach to specific receptors present on intestinal
mucosal cells at the ileum.
■ Absorbed by active carrier mediated transport
■ Transported in blood in combination with a β
globulin, transcobalamin II (TCII).
43. ■ ExcessVit B12 is stored in liver cells as
5’- deoxyadenosylcobalamin.
■ Not degraded in the body.
■ It is secreted in bile (normally) or excreted in urine
by glomerular filtration (therapeutic doses).
44. Vitamin B12: Functions
■ Essential for cell growth and replication.
■ Re-arrangement of methylmalonyl CoA to Succinyl
CoA (for fatty acid synthesis in neural tissue)
■ Conversion of homocysteine to methionine.
■ Essential to support folate metabolism
47. ■ Hydroxocobalamin preferred over cyanocobalamin
■ Higher protein binding, Better retention in blood
■ Prophylactic – 3-10 ug/day orally
■ Therapeutic dose - Hydroxocobalamin 1 mg IM/SC
daily for 2 weeks
■ Cyanocobalamin – 100 ug IM/SC daily for 1 week
48. Methylcobalamin
■ Active coenzyme form ofVitamin B12
■ Needed for integrity of myelin
■ Neurological defects in Diabetic Alcoholic and
peripheral neuropathy
50. Folic Acid
■ Contains 2 to 8 molecules of glutamic acid.
■ Humans do not synthesize FA and meet the need from
green leafy vegetables (spinach), egg, meat, milk.
■ Synthesized by gut flora, but this is largely unavailable
for absorption
51. ■ Daily requirement of an adult : 0.2 mg/day.
■ During pregnancy, lactation: 0.8 mg/day.
■ Total body folate in the adult is ~10 mg,
■ Stores are sufficient for only 3–4 months.
52. ■ Folate is transported in plasma about one-third is
loosely bound to albumin, and two-thirds is
unbound.
■ Methyltetrahydrofolate (Me-THF) is the principal
folate congener supplied to cells.
53. ■ Rapidly extracted by tissues and stored in cells
as polyglutamates.
■ Alcohol interferes with release of methyl-THFA
from hepatocytes.
■ Pharmacological doses are excreted in urine.
54. Metabolic functions of Folic acid
■ Conversion of Homocysteine to Methionine:- Me-
THF (vitamin B12 as a cofactor).
■ Conversion of Serine to Glycine
■ Purine synthesis
■ Synthesis of thymidylate
■ Histidine metabolism
58. ■ Prophylaxis
■ Methotrexate toxicity : Folinic acid
■ Citrovorum factor rescue
■ To enhance anticancer efficacy of 5-fluorouracil
59. Erythropoietin (EPO)
■ Secreted by peritubular cells of kidney
■ Kidney cells release EPO in response to anaemia and
hypoxia
■ Stimulates proliferation of colony forming cells of the
erythroid series.
■ Induces haemoglobin formation and erythroblast
maturation.
■ Releases reticulocytes in the circulation.
60. Therapeutic Uses
■ Anaemia of chronic renal failure
■ Hb < 8 mg/dl
■ Epoetin 25–100 U/kg s.c. or i.v. 3 times a week
61. ■ Anaemia due to zidovudine therapy
■ Cancer chemotherapy induced anaemia
■ Before autologous blood transfusion
62. Adverse Effects
■ Increased clot formation in the A-V shunts
■ Hypertensive episodes
■ Serious thromboembolic events
■ Seizures
■ Flu like symptoms
Haemoglobin is a protoporphyrin; each molecule having 4 iron containing haeme residues.
It has 0.33% iron; thus loss of 100 ml of blood (containing 15 g Hb) means loss of 50 mg elemental iron.
To raise the Hb level of blood by 1 g/dl—about 200 mg of iron is needed.
Avg 10-20 mg
Major absorption from upper part of small intestine
- Absorption of haeme iron is better upto 35% compared to inorganic iron which averages 5
The major part of dietary iron is inorganic and in the ferric form. It needs to be reduced to the ferrous form before absorption.
Two separate iron transporters. At the luminal membrane the divalent metal transporter 1 (DMT1) carrys ferrous iron into the mucosal cell.
This along with the iron released from haeme is transported across the basolateral membrane by another iron transporter ferroportin (FP).
Acid: by favouring dissolution and reduction of ferric iron
Reducing substances: ascorbic acid, amino acids containing SH radical. These agents reduce ferric iron and form absorbable complexes.
- Meat: by increasing HCl secretion and providing haeme iron.
- Iron reaching inside mucosal cell is either transported to plasma or oxidised to ferric form and complexed with apoferritin to form ferritin
This ferritin generally remains stored in the mucosal cells and is lost when they are shed This is called the ‘Ferritin curtain’.
- When body iron is low or erythropoiesis is occurring briskly, ferritin is either not formed or dissociates soon— the released iron is transported to the blood.
- Free iron is highly toxic.
Iron dissociates from the complex at the acidic pH of the intracellular vesicles; the released iron is utilized for haemoglobin synthesis or other purposes, while Tf and TfR are returned to the cell surface to carry fresh loads.
- In iron deficiency and haemolytic states when brisk erythropoiesis is occurring, erythropoietic cells express more TfRs, but other cells do not.
When it is low—the ‘iron regulating element’ (IRE) on mRNA is blocked—transcription of apoferritin does not occur, while more Tf is produced.
On the other hand, more apoferritin is synthesized to trap iron when iron stores are rich
Only chronic insufficient intake leads to iron deficiency.
Excess iron is required during pregnancy for expansion of RBC mass, transfer to foetus and loss during delivery; totalling to about 700 mg.
This is to be met in the later 2 trimesters.
Ferrous sulphate – Cheapest, Metallic taste (65 mg in 325 mg hydrated, 65 mg in 200mg dried preparation)e -
Ferrous gluconate – 36 mg in 300mg tablets
- Depends on amount of elemental iron, common @ therapeutic doses
- Adverse Drug reaction
Apart from nutritional deficiency, chronic bleeding from g.i. tract (ulcers, inflammatory bowel disease, hookworm infestation) is a common cause.
In few cases death occurs early (within 6 hours), but is typically delayed to 12– 36 hours, with apparent improvement in the intervening period.
The pathological lesion is haemorrhage and inflammation in the gut, hepatic necrosis and brain damage.
i.m. (preferably) 0.5–1 g (50 mg/kg) repeated 4–12 hourly as required, or i.v. (if shock is present) 10–15 mg/kg/hour; max 75 mg/kg in a day till serum iron falls below 300 μg/dl.
DTPA - diethylene triamine penta acetic acid
Body stores are of the order of 2–3 mg, sufficient for 3–4 years if supplies are completely cut off.
The conversion of 5,10-methylen-THF into 5-methyl-THF, which is catalysed by MTHFR, is irreversible. The only way to make further use of 5-methyl-THF and to maintain the folate cycle consists in the vitamin-B12-dependent remethylation of homocysteine to methionine (regenerating THF).
In cases of vitamin-B12 deficiency, it is possible that, in spite of sufficient availability of folates (and 5-methyl-THF), an intracellular deficiency of biologically active THF arises. This situation is called a ‘folate trap’ (or methyl group trap)
- Oral vit B12 is not dependable for treatment of confirmed vit B12 deficiency because its absorption from the intestine is unreliable.
- Folic acid and iron added in case of vit b12 deficiency
- Inadequate dietary intake, Malabsorption, Biliary fistula, Chronic alcoholism, increased demand, Drug induced (phenytoin, phenobarbitone, primidone and oral
Contraceptives)
In certain malignancies, high dose of methotrexate is injected i.v. and is followed within ½ –1 hour with 1–3 mg i.v. of Folinic acid to rescue the normal cells.
t is ineffective if given > 3 hours after methotrexate.
- Folinic acid is now routinely infused i.v. along with 5-FU, because THFA is required for inhibition of thymidylate synthase by 5-FU.
- The recombinant human erythropoietin (Epoetin α, β) is administered by i.v. or s.c. injection and has a plasma t½ of 6–10 hr, but action lasts several days.
- Due to sudden increase in haematocrit, blood viscosity and peripheral vascular resistance