Hematinics are substances used to treat and prevent anemia. Megaloblastic anemias are caused by vitamin B12 or folate deficiencies and are characterized by large, abnormal red blood cells. Vitamin B12 is essential for two metabolic reactions and acts as a coenzyme. It is absorbed in the ileum with intrinsic factor and stored in the liver. Deficiencies can be detected using the Schilling test which evaluates vitamin B12 absorption. Treatment involves cyanocobalamin injections or oral methylcobalamin supplements.
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
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
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
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
Iron poisoning (physical appearance, sources- dietary and environmental, uses- industrial and biological, usual fatal dose, toxicokinetics, mode of action, clinical features, diagnosis, treatment, autopsy features
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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!
2. Hematinics: Hematinics are the substances
used in the prevention and treatment of
anemia.
Anemia: Reduced oxygen carrying capacity
of blood due to various reasons including
reduced Hb content or reduced number of
RBCs or abnormal RBCs.
3. Measurements of Anemia
Hemoglobin = grams of hemoglobin per 100
mL of whole blood (g/dL)
Hematocrit = percent of a sample of whole
blood occupied by intact red blood cells
RBC = millions of red blood cells per microL of
whole blood
MCV = Mean corpuscular volume
If > 100 → Macrocytic anemia
If 80 – 100 → Normocytic anemia
If < 80 → Microcytic anemia
4. The mean corpuscular hemoglobin (MCH), or
"mean cell hemoglobin" (MCH), is the
average mass of hemoglobin per red blood
cell in a sample of blood. The normal MCH
level is between 26 and 33 picograms of
hemoglobin per red blood cell.
5. Causes of Anaemia
1. Deficiency of substance
a. Exogenous substances
b. Endogenous substances
2. Reduced (hypoplastic) or absent synthesis (aplastic)
including disease and drug induced.
3. Excess destruction (haemolysis) including disease and
drug induced.
4. Genetic abnormalities
5. Excess loss of blood
6. Drug induced
7. Other causes
6. Iron in diet and body
The normal daily diet contains about 10 to 20 mg
of iron, mostly in the form of heme.
About 20% of heme iron and only 1% to 2% of
non heme iron) is absorbable.
The total body iron content is normally about 2
gm in women and as high as 6 gm in men divided
into functional and storage pools.
About 75% of the functional iron is found in
hemoglobin; myoglobin and iron-containing
enzymes such as catalase and the cytochromes
contain the rest.
The storage pool (hemosiderin and ferritin)
contains about 25% of total body iron.
7. iron requirements are:
Adult male 0.5-1 mg (13 µg/kg)
Adult female 1-2 mg (21 µg/kg)
(menstruating)
Infants 60 pg/kg
Children 25 pg/kg
Pregnancy 3-5 mg (80 pg/kg)
(last 2 trimesters)
Dietary sources of iron
Rich : Liver, egg yolk, dry beans dry fruits, wheat
germ, yeast.
Medium : Meat, chicken, fish, spinach, banana, apple.
Poor : Milk and its products, root vegetables
8. Iron Distribution in Healthy Young Adults
(mg)
Pool Men Women
Total 3450 2450
Functional
Hemoglobin 2100 1750
Myoglobin 300 250
Enzymes 50 50
Storage
Ferritin, hemosiderin 1000 400
9. Iron Absorption
• Diet – 10 to 20 mg – absorbed from all over
the Intestine (more from upper part)
• 2 forms – haeme and Inorganic
• Factors increasing absorption – ???
• Factors impending absorption – ???
• Mucosal block: from ferritin the iron is very
slowly released into the plasma. So iron (as
ferritin) will be in the mucosal cell for a long
time
10. Iron – Transport, storage etc.
• In plasma immediately converted to Fe3+
form –
complexed with transferrin (Tf) –
• Transported to RBCs by transferrin receptors (TfRs) –
endocytosis – Iron dissociates from TfR in acidic pH of
vesicles
• Iron utilized for Hb synthesis – TfRs return to surface
• In Iron deficiency – TfRs increase
• Storage – RE cells in Liver, spleen, bone and muscles
as ferritin and haemsiderin
• Excretion – 0.5 to 1 mg/day – exfoliation in GI mucosal
cells, RBCs and in Bile …. Also in skin, urine and sweat
12. Preparation
Oral Preparations
ferrous sulfate, contains 20 % ( hydrated salt) and 32
% elemental iron. It is the oldest and cheapest iron
preparations.
Ferrous gluconate: contains 12 % elemental iron and is
less gastric irritant.
Ferrous fumarate contains 33 % elemental iron.
Other preparations are ferrous choline citrate, ferric
ammonium citrate
SE: GIT upset, blackened stool, teeth stain
Form: tablet, liquid, sustained-release
13. Parenteral preparations
Iron sorbitol citric acid complex: given i.m.
Iron dextran : commonly used parenteral
preparations and can be administered i.v.
and i.m.
Sodium ferric gluconate: recently approved
preparation for i.v. use, has a much lower risk
of anaphylactic reaction than iron dextran.
15. Interactions
Iron chelates in the gut with tetracyclines,
penicillamine, methyldopa, levodopa, carbidopa,
ciprofloxacin, norfloxacin and ofloxacin;
it also forms stable complexes with thyroxine,
captopril and biphosphonates.
Ingestion should be separated by 3 hours.
↑absorption: vit C
↓absorption: desferrioxamine, tea (tannins) , Zn,
and bran
16. Unwanted effects of iron
Dose related, include nausea, abdominal cramps and
diarrhoea.
overcome : ↓dose or by taking the tablets after or with meals
Acute iron toxicity
Ingestion of large quantities of iron salts.
Result: severe necrotising gastritis with vomiting,
haemorrhage and diarrhoea collapse
Treatment : gastric lavage with NaHCO3, iron
chelating agent, and treatment of causes.
Chronic iron toxicity
Caused by conditions other than ingestion of iron salts,
Cause pancreatic damage and leading to diabetes.
17. Iron chelators
Used for treatment of iron toxicity
Desferrioxamine(Desferal) (t1/2 6 h)
Injected 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/hr, max 75 mg/kg in a day till serum iron falls
below 300 g /dl.ϥ
In severe poisoning: slow IV too fast: hypotension
forms a complex with ferric iron, excreted in the urine.
18. Iron Summary
Present as haemoglobin; myoglobin, cytochromes and other enzymes.
Absorption: Ferric iron (Fe3+
) ferrous iron (Fe2+
)
active transport into mucosal cells in jejunum and upper ileum
transported into plasma and/or stored intracellularly as ferritin.
Iron loss occurs mainly by sloughing of ferritin-containing mucosal
cells; iron is not excreted in the urine.
Iron in plasma is bound to transferrin, and most is used for
erythropoiesis. Some is stored as ferritin in other tissues. Iron from time-
expired erythrocytes enters the plasma for re-use.
The main therapeutic preparation is ferrous sulfate
Unwanted effects include gastrointestinal disturbances. Severe toxic
effects occur if large doses are ingested; these can be countered by
desferrioxamine, an iron chelator.
20. What is Megaloblastic anemia?
Megaloblastic anemias are characterized by
the presence of abnormally large developing
red cells in the bone marrow.
Anemia is based on ineffective
erythropoiesis.
These red cells are large in shape
21.
22. Vit B12 deficiency causes damage to myelin in
the peripheral nerves, spinal cord & brain
Folate deficiency: weight loss, nervous instability
but damage to myelin is doubtful
Other causes of macrocytic anemias: Liver
disease, myxedema, Leukemia & certain
hemolytic states
23. Diet of Megaloblastic
Anaemia
Sources of B-12: Animal products: Meat,
eggs, milk , Vitamin supplements
Sources of folic acid:
Legumes, nuts, whole grain cereals, yeast
Green vegetables, broccoli, asparagus, okra,
cauliflower, and brussel sprouts. Oranges,
carrots.
24. Vit B12
Vit B12 acts as a coenzyme in certain
metabolic pathway.
Methyl cobalamin (methyl B12)
5’ deoxyadenosylcobalamin (DAB12)
Homocysteine methyl B12 methionine
Methylmalonyl CoA DAB12 Succinyl CoA
25. VITAMIN B12....
Essential in two reactions:
1. Conversion of methylmalonyl-coenzyme A to
Succinyl-CoA
2. Conversion of Homocysteine to Methionine
The second reaction is linked to folic acid
metabolism and synthesis of deoxythymidylate
(dTMP)
dTMP is a precursor for DNA synthesis
29. Vitamin B12 binds to Intrinsic factor (secreted by gastric
parietal cells)
It prevents digestion of B12
In bound state ,it binds to receptors on brush border of mucosa
These receptors are located in ileum
Bound intrinsic factor and B12 are absorbed with pinocytosis
DISTRIBUTION:
Vitamin B12 is distributed to various cells bound to a plasma
glycoprotein,Transcobalamin II
STORAGE:
Excess vitamin B12 (upto 300-500 microgram) is
stored in liver
30.
31. Storage sites
Total amount of vitamin in body is 2-5 mg
( adequate for 3 years )
Major site : liver
Excreted through the bile and shedding of
intestinal epithelial cells
Most of the excreted vitamin B12 is again
absorbed in the intestine (enterohepatic
circulation)
32. SCHILLING TEST
For evaluation of absorption of vitamin B12 in the
GIT
Performed in 2 parts – part 1 and part 2
Part 1 :
0.5 to 1 µg of radiolabelled vitamin B12 is given orally
After 2 hrs IM dose (1000 µg) of unlabelled vitamin B12
is given [ saturates binding sites of TC I and TC II and
displaces any bound radiolabelled vitamin B12 (thus
permitting urinary excretion of absorbed radiolabelled
vitamin B12 )
33. Radioactivity is measured in subsequently
collected 24 hr urine sample and expressed as a
% of total oral dose
In normal persons, > 7% of the oral dose of
vitamin B12 is excreted in urine
If excretion is less than normal it indicates impaired
absorption, which may be due to either lack of IF or
small intestinal malabsorption
Part 2 performed if part 1 of test is abnormal
34. Part 2 : patient is orally administered
radiolabelled vitamin B12 along with IF while
remainder of test is carried out out as in part 1
Excretion becomes normal – lack of IF
Excretion remains below normal – defective
absorption in small intestine
35. preparations
Cyanocobalamin, hydroxycobalamin and
methylcobalamin.
Cyanacobalamin is the preparation of choice and is
given through i.m. or s.c. route. The dose of
cobalamin is 100 mcg i.m. once a week for 8 weeks
followed by 1000 mcg i.m. every month life long.
Oral methylcobalamin has been used in the
treatment of trigeminal neuralgia, multiple sclerosis
and other neuropathies.
In alcohol and tobacco amblyopia weekly injections
of hydroxycobalamin is given for 10 weeks
37. FOLIC ACID.....
ABOSRPTION:
Form:
Dietary folates in polyglutamate forms; first undergo
hydrolysis by conjugase (present in brush border of
intestinal mucosa) and form monoglutamate
Site:
Proximal jejunum
Only modest amounts of folic acid are stored in
body, therefore a decrease in diet will lead to
anemia in few months
38. Folic acid
Distribution:
Widely distributed through out the body via
blood stream
Storage:
Normally, 5-20 mg is stored in liver and other
tissues
Elimination:
Excreted in urine and stool, and also destroyed
by catabolism
39. Transport storage and fate:
Orally given folic acid appears in 30 min as
circulation it circulates as N5
Methyl THF
Majority is loosely bound to albumin from
where it is easily taken up by cells
Inside the cells converted to THF by
cobalamine dependent enzyme methionine
synthetase
Vit C protects THF from destruction
Total folate in body = 5 to 20 mg (1/3 in liver
as methyl folate)
40. Metabolic functions
Folic acid DHFA THFA (Active
form)
folate DHF
synthetase reductase
THFA mediates number of one Carbon tranfer
reactions
Conversion of homocysteine to methionine
Generation of thymidylate
Conversion of serine to glycine
Purine synthesis
Histidine metabolism
43. Unwanted effects
do not occur even with large doses of folic
acid
except possibly in vitamin B12 deficiency,
the blood picture may improve and give the
appearance of cure while the neurological lesions
get worse.
Important to determine whether a megaloblastic
anaemia is caused by a folate or a vitamin B12
deficiency.
44. Preparations and dose:
Folic acid tab 5 mg ; dose = 5 to 20 mg
Prophylaxis 0.5 mg/day
Parenteral form available in combination only
Folinic acid: N5 Formyl THFolinic acid
(Citrovorum factor) 3 mg/mL Inj
45. Uses:
1. Megaloblastic anemia
2. Prophylaxis
3. Methotrexate toxicity: Folinic acid used as it is
an active no need to reduced by DHFR before it
can act, Methotrexate is DHFR inhibitor, its
toxicity not reversed by folic acid
4. Citrovorum factor rescue: Methotrexate high
dose IV then half to 2 hr later 1-3 mg folinic acid
IV to rescue normal cells
46. CLINICAL USES OF VIT B12 AND
FOLIC ACID
These are used in anemia (megaloblastic). 1-5 mg daily and
continued for about 3-4 months.
Pernicious anemia ( Vitamin B12, basically IF)
Prophylaxis for neural tube defects (folic acid
0.5 mg/ day is given from the 1st
trimester)
Neuropathy (Vitamin B12)
Cancer chemotherapy
Certain drug therapies lead to deficiency of folic
acid so replacement is required
47. VITAMIN B12 PREPARATIONS
Tablet and syrup forms:
Cyanocobalamin, Hydroxycobalamin
Parenteral:
I/M, I/V.
Use:
To corrects major depletion of B12 quickly
If patient is unable to take orally
Required in patients with pernicious anemia (IF deficiency)
Parenteral therapy can lead to pain at injection site