This document discusses nutritional anemia, defining it as a disease caused by malnutrition resulting in low hemoglobin levels. It outlines the main types of nutritional anemia including deficiencies in iron, folate, vitamin B12, and protein. The document provides details on the prevalence, causes, signs, symptoms and treatments of different forms of nutritional anemia with a focus on iron deficiency anemia. It discusses nutritional anemia prevention programs in India that provide iron and folic acid supplementation targeted at pregnant women, lactating women, and children aged 1-12 years.
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Vitamin A-intoduction, functions, sources, storage, WHO statistics, deficiency, treatment, prevention and control of deficiencies, Vit. A deficiency in India, assessment of Vit. A deficiency, recommended allowances, toxicity.
RMNCH+A approach has been launched in 2013 and it essentially looks to address the major causes of mortality among women and children as well as the delays in accessing and utilizing health care and services. The RMNCH+A strategic approach has been developed to provide an understanding of ‘continuum of care’ to ensure equal focus on various life stages.
The RMNCH+A appropriately directs the States to focus their efforts on the most vulnerable population and disadvantaged groups in the country. It also emphasizes on the need to reinforce efforts in those poor performing districts that have already been identified as the high focus districts.
Important maternal and child health parameters to evaluate quality care for the special group. Includes MMR, IMR, SBR, PMR, NMR, PNMR, U5MR. Practical class for UG 4th sem
Vitamin A-intoduction, functions, sources, storage, WHO statistics, deficiency, treatment, prevention and control of deficiencies, Vit. A deficiency in India, assessment of Vit. A deficiency, recommended allowances, toxicity.
Nutritional anemia refers to types of anemia that can be directly attributed to nutritional disorders. Examples include Iron deficiency anemia and pernicious (Vitamin B12 deficiency) anemia.
Journal of Community Medicine & health care is an open access, peer reviewed, scholarly journal dedicated to publish articles covering all community medicine & health care.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
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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
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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.
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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
How to Give Better Lectures: Some Tips for Doctors
Nutritional anemia -Dr JP Singh, Dept, of community medicine, SRMS IMS Bareilly
1.
2. Dr JP Singh,
Assistant Professor,
Dept of Community Medicine,
SRMS IMS Bareilly
NUTRITIONAL ANEMIA
3. NUTRITIONALANEMIA
DEFINITION
It is a disease syndrome caused
by Malnutrition.
Acc to WHO –
A condition in which
haemoglobin content of blood is
lower than normal, as a result of
deficiency of one or more
essential nutrient, specially iron.
5. NUTRITIONAL ANEMIA
Examples: Iron deficiency anemia and
pernicious anemia.
A. Micro-: Iron deficiency anemia
A. Plummer-Vinson syndrome
B. Macro-: Megaloblastic anemia
A. Pernicious anemia
6. ANEMIA
ANEMIA - Insufficient Hb to carry out O2 requirement by
tissues.
WHO definition : Hb conc. 11 gm %
CDC definition : Hb conc. < 11gm % in 1st and 3rd trimesters
and < 10.5 gm% in 2nd trimester
For developing countries : cut off level suggested is 10 gm %
- WHO technical report Series no. 405, Geneva 1968
Centre for disease control, MMWR 1989;38:400-4
7. Adult man 13 gm/dl
Adult woman (non
pregnant)
12 gm/dl
Adult woman (pregnant) 11 gm/dl
Child above 6 yrs 12 gm/dl
Child below 6 yrs 11 gm/dl
WHO CUT OFF CRITERIA OF HB%
(IN VENOUS BLOOD)
8. A) IRON DEFECIENCY ANEMIA
INTRODUCTIÓN
Iron deficiency (ID) is one of the most
frequent nutrition deficiency all round the
world.( In India - 50%)
Its prevalence is higher in children and
childbearing age women.
Iron deficiency anemia (IDA) mainly
affects child behavior and development,
work performance and immunity.
9. WORLD
It is a world wide problem with highest prevalence in
developing countries.
It affect nearly 2/3 of pregnant and ½ of non pregnant.
INDIA-
Overall , 72.7 % of children up to age of 3 year in
urban and 81.2% in rural are anaemic .
It was found that , except for Punjab , all other state
had more than 50% prevalence of anaemia among
pregnant women.
PROBLEM STATEMENT
10. Vulnerable groups % of Population with
Anemia
Adult male 20
children 40
Adolescent girls 56
Adult female 60
Pregnant mothers 80
% OF IDA IN INDIA IN VULNERABLE GROUPS
11. PREVALANCE % PUBLIC HEALTH
PROBLEMS
Less than 5 % Not a problem
5-19.9 Low magnitude (Mild)
20-39.9 Moderate magnitude (Moderate)
40 and above High magnitude (Severe)
MAGNITUDE OF IDA
12. SOURCES OF IRON
Animal- meat, liver, kidney, egg yolk.
Veg.- pulses, beans, peas, green vegetables and
fruits
Milk- Human milk -0.29- 0.45mg/dl
(Cow’s milk –poor source with 0.01 – 0.38mg/dl)
13. CAUSES OF IDA
1. Diminished stores
2. Diminished intake: d/t cereals & pulse based diet
3. Diminished absorption
4. Increased demands: During pregnancy & infections
5. Defective metabolism
6. Infections: Ankylostomiasis, PU, Ulcerative colitis, hemorrhoids
14. 1. Pregnancy: Increases risk of maternal & fetal
morbidity & mortality (INDIA: 19% maternal
deaths).
2. Infection: Anemia can be caused by infections
(malaria, intestinal parasites) and may increase
susceptibility to infections.
3. Decreased work capacity.
4. Growth failure among children
DETRIMENTAL EFFECTS OF IDA
21. II. LABORATORY INDICES
1. Low Hemoglobin
2. Low Hematocrit
3. Low Mean Corpuscular Volume
4. Serum Ferritin <10ng/ml
5. Transferrin Saturation<15%
6. TIBC>350µg/dl
7. Increased free erythrocyte
protoporphiryn
22. 1. Adequate nutrition
2. Nutrition education to improve
dietary habit
3. Breast feeding and appropriate
weaning diet
4. Iron rich food
5. Increase ascorbic acid
6. Health education
7. Periodical deworming specially
among children and at least once
during IInd trimester of pregnancy
8. Nutritional supplementation
9. Foot wear use
10. Safe drinking water
1. Food fortification
2. National nutritional anemia
prophylaxis program (NNAPP)
3. National nutritional anemia
control program (NNACP):
The elemental iron was
increased from 60 mg to 100
mg per tablet in 1992
I. HEALTH PROMOTION II. SPECIFIC PROTECTION
PREVENTION OF NUTRITIONAL ANEMIA
23. 1. Infants b/w 5-12 months should also be included as
beneficiaries for iron supplementation, under ICDS
Scheme.
2. Liquid formulations to be prepared, each ml containing 20
mg of iron & 100 mcg of folic acid
3. For children b/w 6-10 yrs, 30 mg of iron and 250 mcg of
folic acid.
4. For children b/w 10-18 yrs (adult dose) also to be included
as beneficiaries for iron supplementation.
NEW RECOMENDATIONS
24. BENEFICIERIES:
A. Pregnant mothers
B. Lactating mothers &
C. Children b/w 1-12 yrs
BENEFITS: Iron & folic acid (IFA) tabs are distributed
free of cost.
BENEFICIERIES & BENEFITS
25. • Iron & Folic Acid (IFA) supplementation: National Nutritional Anemia
Prophylaxis Programme (NNAPP):
• Eligibility criteria: Hb level 10-12 receives IFA tablets; <10 referred to
PHC (MO).
• Dosage:
1. Mothers: One IFA tablet (100 mg elemental iron + 500 μgm folic acid) X 2-
3 months after Hb level returned to normal.
2. Children: Screening for anemia at 6 mths, 1 yr & 2 yrs of age.
3. Children upto 6 yrs: One IFA tablet (20 mg elemental iron + 100 μgm folic
acid) X 100 days.
4. Children 6-10 yrs: One IFA tablet (30 mg elemental iron + 250 μgm folic
acid) X 100 days.
DOSES
26. GRADE (WHO) DEGREE OF
ANMIA
TREATMENT
11-14 gm/dl Normal Nothing required
9-11 gm Mild Oral iron therapy
required
7-9 gm Moderate Parenteral iron
therapy
Less than 7 gm Severe Blood transfusion
GRADING & T/T OF ANEMIA
27. TREATMENT OF IDA
1. Treat underlying cause (hook worm etc)
2. Oral iron therapy: 3-6mg/kg in 3 divided doses ( Hb rises
by 0.4g/day)
3. Vit C, empty stomach or in between meals: For 6-8 wks
after Hb is normal
4. Parental iron therapy ( Iron in mg=wt in kg× Hb deficit in
gm/dl×4)
5. Blood transfusion –rarely when Hb<4gm/dl, CCF, severe
infection with poor iron utilisation
28. B) FOLIC ACID DEF
1. Necessary for DNA synthesis.
2. SOURCES: Liver, soya bean, dark green leafy
vegetables
3. CAUSES: Strict vegetarian, Tape worm anemia,
Repeated Pregnancy, Chronic diarrhea, malabsorption
and recurrent infections
4. Cooking destroys folic acid
5. Deficiency disease: Megaloblastic anemia in children &
pregnant mothers
6. Treatment with phenytoin / antimetabolites
7. T/T: Folic acid 2-5 mg/day
8. RDA: 500 mcg/day for pregnant mother
29. C) B12 DEFICIENCY
Necessary for DNA synthesis.
SOURCES: Foods of animal origin only (fish, egg, meat)
DISEASES: Megaloblastic anemia, parasthesia of fingers & toes.
It is observed in breast fed infants of vit. B 12 deficient mother &
delayed weaning child
RDA: Vit. B12 1µg/day
30. CLINICAL FEATURES
1. Pale
2. Very sick
3. Irritable
4. Severe anorexia
5. Failure to thrive
6. Knuckle pigmentation (hands and nose)
7. Tremor and developmental regression
Introduction
Despite the fact that iron is the fouth most common element on earth, Iron deficiency (ID) is one of the most frequent nutrition deficiency all round the world, in developing as well as in developed countries,
its prevalence, which is arround 50% in developing and 10% in developed countries,
the higher prevalence in children and childbearing age women, and
the consequences of Iron deficiency anemia (IDA) on child behaviour and development, work performance and immunity,
make IDA a very important problem from a public health perspective.
Assessment of IDA
Several indices have been applied in assessing nutrition Iron status. They can be classified as Clinical and Laboratory indices.
Laboratory indices are the most common methods used to assess iron nutrition status.
Hemoglobin: Hemoglobin concentration varies considerably with age. Even when hemoglobin is related to iron deficiency and the definition of IDA is based on hemoglobin concentration, some authors have stated that it is not an adequate indicator when it is applied as the only measurement, specially in populations with low prevalence (it will be discussed later).
Transferrin Saturation: corresponds to plasma iron divided by plasma total iron-binding capacity X 100. Percentages below 16% in adults and children and below 12% in infants suggest insufficient iron delivery to the hematopoietic tissues
Serum Transferrin receptors: Serum transferrin receptors reflect the number of receptors in immature red blood cells and thus the level of erythropoiesis. It is unaffected by infection or inflammation what makes Serum Transferrin receptors concentration be an accurate index of Iron nutrition status.
Erythrocyte protoporphyrin: protoporphyrin combines with iron to form heme. Under ID conditions, the lack of iron determines an increase in erythrocyte protoporphyrin, which can not combined with Iron.
Increased values of erythrocyte protoporphyrin indicate impaired erythropoyesis due to iron deficiency. Values greater than 100 ug/dl and 120 ug/dl have been used as cutoff points
Pallor of the conjunctiva, tongue, nail bed and palm can be used as clinical indices of ID what is due to the low hemoglobin concentration in areas with high vascularization. Even when they are easily and inexpensively obtained, subjectivity is the main problem of clinical indicators.
Mean corpuscular volume: It depends on hemoglobin content in the red blood cell, so in absence of other conditions a decrease in hemoglobin is associated with a decrease in MCV.
Ferritin: Even when ferritin is present within cells, a small amount circulates in plasma and permits estimation of total ferritin, been the earliest indicator of ID.
As it has been mentioned before, Serum Ferritin expresses Iron Stores. During infancy Serum Ferritin concentration below 10 ng/ml are considered as the expression of depleted iron stores (Siimes et al, 1974; Thomas et al, 1977; Dallman et al, 1981). During infection or inflammation Serum Ferritin increases like other acute phase proteins, and then SF is not an accurate indicator in such situations.