Iron deficiency anemia (IDA) is the most common form of anemia worldwide. It can be caused by blood loss or impaired iron absorption. The body needs iron to produce hemoglobin for red blood cell production. Treatment involves treating the underlying cause and replenishing iron stores, usually with oral iron supplements. Parenteral iron may be used for patients unable to tolerate or absorb oral iron. Complications of iron overload include organ damage, so excess iron intake must be avoided.
A presentation about Iron deficiency anemia (IDA) or (Hypochromic anemia) and its diagnose, causes, treatments, cautions - subjected to a task for biochemistry lecture - postgraduation study - Soran University
by Mahmood Khaleel Pirani
mahmoud_pirani@yahoo.com
mahmud.khalil.p@gmail.com
+964 (0) 750 412 8959
A presentation about Iron deficiency anemia (IDA) or (Hypochromic anemia) and its diagnose, causes, treatments, cautions - subjected to a task for biochemistry lecture - postgraduation study - Soran University
by Mahmood Khaleel Pirani
mahmoud_pirani@yahoo.com
mahmud.khalil.p@gmail.com
+964 (0) 750 412 8959
Anemia - Types, Pathophysiology, Clinical Manifestations, Etiology, TreatmentMd Altamash Ahmad
Anaemia can be defined as a reduction from normal of the quantity of haemoglobin in the blood.
It is not one disease, but a condition that results from a number of different pathologies.
The World Health Organisation defines anaemia in adults as haemoglobin levels less than 13g/dL for males and less than 12g/dL for females.
The low haemoglobin level results in a corresponding decrease in the oxygen-carrying capacity of the blood.
Anaemia is possibly one of the most common conditions in the world and results in significant morbidity and mortality, particularly in the developing world.
Anemia - Types, Pathophysiology, Clinical Manifestations, Etiology, TreatmentMd Altamash Ahmad
Anaemia can be defined as a reduction from normal of the quantity of haemoglobin in the blood.
It is not one disease, but a condition that results from a number of different pathologies.
The World Health Organisation defines anaemia in adults as haemoglobin levels less than 13g/dL for males and less than 12g/dL for females.
The low haemoglobin level results in a corresponding decrease in the oxygen-carrying capacity of the blood.
Anaemia is possibly one of the most common conditions in the world and results in significant morbidity and mortality, particularly in the developing world.
General Pharmacology Lecture Slides on Essential Drugs and Rational use of Medicines by Sanjaya Mani Dixit Assistant Professor of Pharmacology at Kathmandu Medical College
Dental Pharmacology Lecture Slides on Sialogogues and Antisialogogues by Sanjaya Mani Dixit Assistant Professor of Pharmacology at Kathmandu Medical College
Pharmacology Lecture Slides on Autonomic Nervous System Introduction by Sanjaya Mani Dixit Assistant Professor of Pharmacology at Kathmandu Medical College
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
3. Iron Deficiency Anemia
• Iron deficiency anemia (IDA) is the most
common form of anemia worldwide.
• In men and postmenopausal women the
commonest cause of IDA is blood loss from
lesions in the gastrointestinal tract, making it a
common cause of referral to gastroenterologists.
• Causes of IDA relate either to
blood loss, or
iron mal-absorption
4. Iron deficiency Anemia
• The body needs iron to produce the Hb
necessary for RBC production.
• In general, most people need just 1 milligram
of iron daily.
• Menstruating women need double the dose
5. Iron Deficiency
Successive Stages of Iron Deficiency
• Iron-deficient erythropoiesis,
– or functional iron deficiency
• Depletion of iron stores
• Iron-deficiency anaemia
Grosbois B, et al. Bull Acad Natl Med. 2005;189:1649.
6. Beris P, Tobler A. Schweiz Rundsch Med Prax. 1997;86:1684.
Reprinted from Lambert JF, et al. In C Beaumont, P Beris, Y Beuzard, C Brugnara, eds. Disorders of iron homeostasis,
erythrocytes, erythropoiesis. Forum service editore, Genoa, Italy, 2006 page 73 figure 1, by permission of European
School of Haemotology.
Main Causes of Anaemia
Haemolysis
17.5%
Others
9%
Iron Deficiency
29%
Chronic Disease
27%
Acute
Bleeding
17.5%
8. Iron Deficiency—Iron loss
• In physiologic conditions
– Menstruation
• In pathologic conditions
– Surgery, delivery
– Haemoglobinuria,haemoptysis
– Gastrointestinal tract pathology
• In therapeutic procedures
– Phlebotomy
• In blood donation
9.
10.
11. Iron Deficiency
Clinical Manifestations
• Fatigue
• Decreased exercise tolerance
• Tachycardia
• Dermatologic manifestations
• Decreased intellectual performance
• Dysphagia
• Depression, increased incidence of infections
• Restless legs syndrome
Hoffman, ed. Hematology: Basic Principles and Practice, 4th ed. 2005.
Trost LB, et al. J Am Acad Dermatol. 2006;54:824.
12. Iron Deficiency Anemia
• The CVS adaptations of chronic anemia can worsen the
condition of patients with underlying cardiovascular
disease and include:
– Tachycardia
– Increased cardiac output
– Vasodilation
• In the absence of adequate iron, small erythrocytes with
insufficient hemoglobin are formed, giving rise to
microcytic hypochromic anemia.
13. Management
of IDA
• Treatment of iron deficiency anemia consists of correcting the underlying
etiology and replenishing iron stores.
• Oral ferrous iron salts are the most economical and effective form
• Ferrous sulfate is the most commonly used iron salt
• Better absorption and lower morbidity have been claimed for other iron
salts
• Toxicity is generally proportional to the amount of iron available for
absorption
• Reserve parenteral iron for patients who are either unable to absorb oral
iron or who have increasing anemia despite adequate doses of oral iron
• Reserve transfusion of packed RBCs for patients who are experiencing
significant acute bleeding or are in danger of hypoxia and/or coronary
insufficiency
14. IRON
Iron is among the abundant minerals on earth.
Of the 87 elements in the earth’s crust, Iron
constitutes 5.6% and ranks 4th
behind Oxygen
(46.4%), Silicon (28.4%) and Aluminum (8.3%).
In soil, Iron is 100 times more than Ca, Na & Mg and
1000 times more than Zinc and 100,000 times more
than Iodine.
15. Dietary iron:
Iron is present in food as ferric hydroxides (ferric-protein
complexes and hem-protein complexes).
-meat, liver
-vegetables, eggs.
-The average diet contains 10-15mg and only 5-10% is normally
absorbed.
Iron requirements:
It varies depending on sex and age:
Male/female 0.5-1 mg/day
Pregnant female 1-2 mg/day
Children 0.5 mg/day
16. IRON
• Total body iron in a 70-kg man is 4 g.
• Although the body only absorbs 1 mg daily to
maintain equilibrium, the internal requirement
for iron is greater (20-25 mg).
• An erythrocyte has a lifespan of 120 days so
that 0.8% of red blood cells are destroyed and
replaced each day. A man with 5 L of blood
volume has 2.5 g of iron incorporated into the
hemoglobin, with a daily turnover of 20 mg for
hemoglobin synthesis and degradation and
another 5 mg for other requirements.
• Most of this iron passes through the plasma for
reutilization.
• Iron in excess of these requirements is
deposited in body stores as ferritin or
hemosiderin.
17. Iron transport and metabolism
• The average adult iron intake is 10–15 mg per day of which 1–2
mg is absorbed by duodenal enterocytes.
• Ingested iron then undergoes enzymatic reduction from ferric
iron (Fe3 + ) to the more readily absorbed ferrous iron (Fe2 + )
by brush border ferrireductase with the help of low gastric pH.
• Divalent metal transporter 1 (DMT1) on duodenal epithelium
transfers iron across the apical membrane where it is either
transferred across the basolateral membrane to reach plasma
bound to transferrin or stored as ferritin and eventually
excreted as the enterocyte is sloughed.
18. Uses of Iron
• Iron deficiency anemia
• Prophylaxis in pregnancy
• Megaloblastic anemia
• Astringent in throat paint
19. Iron preparations
Oral iron
1. Ferrous sulfate:
Hydrated salt 20% iron,
Dried salt 32% iron 200 mg tab
2. Ferrous gluconate (12% iron) 300 mg Tab
3. Ferrous fumarate (33% iron) 200 mg Tab
4. Ferrous succinate (35% iron)
5. Ferric citrate is an oral iron that has shown efficacy and
gained FDA approval for treatment of iron deficiency
anemia in adults with CKD and not on dialysis.
20. Adverse Effects of Oral Iron
• Epigastric pain,
• heartburn,
• nausea, vomiting,
• Staining of teeth,
• metallic taste,
• bloating,
• Colic
21. Iron preparations
Iron therapy by injection is indicated only when:
1. Oral iron is not tolerated: bowel unset is too
much.
2. Failure to absorb oral iron
3. Non-compliance to oral iron.
4. In presence of severe deficiency with chronic
bleeding
22. PARENTERAL IRON THERAPY
• For patients who cannot be maintained with oral iron
alone, in conditions including:
– Various postgastrectomy conditions
– Previous small bowel resection
– IBD involving the proximal small bowel
– Malabsorption syndromes
– Advanced chronic renal disease including hemodialysis and
treatment with erythropoietin
24. Adverse Effects of parenteral Iron
Local
• Pain at site of i.m. injection, pigmentation of skin,
• sterile abscess- especially in old and debilitated
patient.
Systemic
• Fever, headache, joint pains, flushing,
• palpitation, chest pain, dyspnoea,
• lymph node enlargement.
25. CHRONIC IRON TOXICITY
• Aka Iron overload and hemochromatosis.
• Results when excess iron is deposited in the heart, liver, pancreas, and
other organs. It can lead to organ failure and death.
• Most common in patients with inherited hemochromatosis, a disorder
characterized by excessive iron absorption, and in patients who receive
many red cell transfusions over a long period of time.
• In the absence of anemia, it is most efficiently treated by intermittent
phlebotomy where One unit of blood can be removed every week or so
until all of the excess iron is removed.
• Parenteral deferoxamine is much less efficient as well as more
complicated while oral iron chelator deferasirox as effective as
deferoxamine at reducing liver iron concentrations and is much more
convenient.
26. Poisonings
Seen in infants and children (> 60 mg/kg iron)
Precipitates as
• vomiting, abdominal pain,hematemesis,
• diarrhoea, dehydration, acidosis,
• lethargy, cyanosis,convulsions;
• finally shock, cardiovascular collapse
• and death
Antidote: Desferrioxamine (chelating agent)
27. Poisoning-Management
A. Supportive measure: maintain the fluids
& electrolyte balance, vital support & O2
therapy
B. Preventive measure: Induce vomiting by
syrup ipecac or gastric lavage with
sodium bicarbonate or phosphate
solution to render iron insoluble; Egg yolk &
milk to complex
28. Poisoning-Management
C. Pharmacological measure:
• Desferrioxamine [specific antidote]:
binds to remove the iron already absorbed.
• 1 g stat then 500 mg every 4 hours for two
doses orally. Intravenous for the patient with
shock
• Diazepam or phenytoin iv to control
convulsions