Megaloblastic anaemia is a type of anaemia characterized by the formation of unusually large, abnormal and immature red blood cells called as megaloblasts by the bone marrow, which are released into the blood. To know more visit here: www.lazoi.com
Megaloblastic anaemia is a type of anaemia characterized by the formation of unusually large, abnormal and immature red blood cells called as megaloblasts by the bone marrow, which are released into the blood. To know more visit here: www.lazoi.com
anaemia and its classification, blood transfusion, blood group, erythroblastosis foetalis, blood component , use of blood components in human diseases. blood group reaction
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
Anemia is the blood disorder, characterized by the reduction in:
1. Red blood cell (RBC) count
2. Hemoglobin content
3. Packed cell volume (PVC).
This occurs because of
Decreased production of RBC
Increased destruction of RBC
Excess loss of blood from the body
anaemia and its classification, blood transfusion, blood group, erythroblastosis foetalis, blood component , use of blood components in human diseases. blood group reaction
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
Anemia is the blood disorder, characterized by the reduction in:
1. Red blood cell (RBC) count
2. Hemoglobin content
3. Packed cell volume (PVC).
This occurs because of
Decreased production of RBC
Increased destruction of RBC
Excess loss of blood from the body
Roles, Responsibilities and Rules of the Diagnostic Medical SonographersShaista Jabeen
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Roles, Responsibilities and Rules of the Diagnostic Medical Sonographers
Code of Conduct
Code of Ethics
Physiology of Pain (PPT) Nervous System PhysiologyShaista Jabeen
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Physiology of Pain (PPT)
Nervous System Physiology
INTRODUCTION
BENEFITS OF PAIN SENSATION
COMPONENTS OF PAIN SENSATION
PATHWAYS OF PAIN SENSATION
FROM SKIN AND DEEPER STRUCTURES
FROM FACE
FROM VISCERA
FROM PELVIC REGION
VISCERAL PAIN
CAUSES OF VISCERAL PAIN
REFERRED PAIN
DEFINITION
EXAMPLES OF REFERRED PAIN
MECHANISM OF REFERRED PAIN
NEUROTRANSMITTERS INVOLVED IN PAIN SENSATION
ANALGESIA SYSTEM
ANALGESIC PATHWAY
GATE CONTROL THEORY
APPLIED PHYSIOLOGY
Short Notes
pdf ppt
Classification of nerve fibers, Nervous System PhysiologyShaista Jabeen
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Classification of nerve fibers
Nervous System Physiology
BASIS OF CLASSIFICATION
DEPENDING UPON STRUCTURE
DEPENDING UPON DISTRIBUTION
DEPENDING UPON ORIGIN
DEPENDING UPON FUNCTION
DEPENDING UPON SECRETION OF NEUROTRANSMITTER
DEPENDING UPON DIAMETER AND CONDUCTION OF IMPULSE
Short Notes
pdf ppt
Introduction to nervous system, Divisions of Nervous System, Nervous System P...Shaista Jabeen
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Introduction to nervous system, Divisions of Nervous System, Nervous System Physiology
Introduction to nervous system
Divisions of Nervous System
Nervous System Physiology
DIVISIONS OF NERVOUS SYSTEM
CENTRAL NERVOUS SYSTEM
PERIPHERAL NERVOUS SYSTEM
Short Notes
ppt pdf
Immune system physiology, Three Defense Mechanisms of Human BodyShaista Jabeen
Compiled Extensive Notes
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Immune System Physiology (Notes)
Three Defense Mechanisms of Human Body
1. Barriers (Physical, Chemical and Mechanical)
2. Innate Immunity
3. Adaptive Immunity
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
Pharma Pcd Franchise in Jharkhand - Yodley Lifesciences
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
1. „ INTRODUCTION
Anemia is the blood disorder, characterized by the
reduction in:
1. Red blood cell (RBC) count
2. Hemoglobin content
3. Packed cell volume (PVC).
Generally, reduction in RBC count, hemoglobin
content and PCV occurs because of:
1. Decreased production of RBC
2. Increased destruction of RBC
3. Excess loss of blood from the body.
All these incidents are caused either by inherited
disorders or environmental influences such as nutritional
problem, infection and exposure to drugs or toxins.
„ CLASSIFICATION OF ANEMIA
Anemia is classified by two methods:
1. Morphological classification
2. Etiological classification.
„ MORPHOLOGICAL CLASSIFICATION
Morphological classification depends upon the size and
color of RBC. Size of RBC is determined by mean corpus
cular volume (MCV). Color is determined by mean corpus
cular hemoglobin concentration (MCHC). By this method,
the anemia is classified into four types (Table 14.1):
1. Normocytic Normochromic Anemia
Size (MCV) and color (MCHC) of RBCs are normal. But
the number of RBC is less.
Anemia
Chapter
14
„ INTRODUCTION
„ CLASSIFICATION
„ SIGNS AND SYMPTOMS
2. Macrocytic Normochromic Anemia
RBCs are larger in size with normal color. RBC count is
less.
3. Macrocytic Hypochromic Anemia
RBCs are larger in size. MCHC is less, so the cells are
pale (less colored).
4. Microcytic Hypochromic Anemia
RBCs are smaller in size with less color.
„ ETIOLOGICAL CLASSIFICATION
On the basis of etiology (study of cause or origin),
anemia is divided into five types (Table 14.2):
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Nutrition deficiency anemia
4. Aplastic anemia
5. Anemia of chronic diseases.
TABLE 14.1: Morphological classification of anemia
Type of anemia
Size of RBC
(MCV)
Color of RBC
(MCHC)
Normocytic normochromic Normal Normal
Normocytic hypochromic Normal Less
Macrocytic hypochromic Large Less
Microcytic hypochromic Small Less
2. Section 2 t Blood and Body Fluids
90
1. Hemorrhagic Anemia
Hemorrhage refers to excessive loss of blood (Chapter
115).Anemiaduetohemorrhageisknownashemorrhagic
anemia. It occurs both in acute and chronic hemorrhagic
conditions.
Acute hemorrhage
Acute hemorrhage refers to sudden loss of a large quan
tity of blood as in the case of accident. Within about 24
hours after the hemorrhage, the plasma portion of blood
is replaced. However, the replacement of RBCs does
not occur quickly and it takes at least 4 to 6 weeks. So
with less number of RBCs, hemodilution occurs. How
ever, morphologically the RBCs are normocytic and
normochromic.
Decreased RBC count causes hypoxia, which
stimulates the bone marrow to produce more number of
RBCs. So, the condition is corrected within 4 to 6 weeks.
Chronic hemorrhage
It refers to loss of blood by internal or external bleeding,
over a long period of time. It occurs in conditions like
peptic ulcer, purpura, hemophilia and menorrhagia.
Due to continuous loss of blood, lot of iron is lost
from the body causing iron deficiency. This affects the
synthesis of hemoglobin resulting in less hemoglobin
content in the cells. The cells also become small. Hence,
the RBCs are microcytic and hypochromic (Table 14.2).
2. Hemolytic Anemia
Hemolysis means destruction of RBCs. Anemia due
to excessive hemolysis which is not compensated by
increased RBC production is called hemolytic anemia. It
is classified into two types:
A. Extrinsic hemolytic anemia.
B. Intrinsic hemolytic anemia.
A. Extrinsic hemolytic anemia: It is the type of anemia
caused by destruction of RBCs by external factors.
Healthy RBCs are hemolized by factors outside the
blood cells such as antibodies, chemicals and drugs.
Extrinsic hemolytic anemia is also called autoimmune
hemolytic anemia.
Common causes of external hemolytic anemia:
i. Liver failure
ii. Renal disorder
TABLE 14.2: Etiological classification of anemia
Type of anemia Causes Morphology of RBC
Hemorrhagic anemia
Acute loss of blood Normocytic, normochromic
Chronic loss of blood Microcytic, hypochromic
Hemolytic anemia
Extrinsic hemolytic anemia:
i. Liver failure
ii. Renal disorder
iii. Hypersplenism
iv. Burns
v. Infections – hepatitis, malaria and septicemia
vi. Drugs – Penicillin, antimalarial drugs and
sulfa drugs
vii. Poisoning by lead, coal and tar
viii. Presence of isoagglutinins like anti Rh
xi. Autoimmune diseases – rheumatoid arthritis
and ulcerative colitis
Normocytic normochromic
Intrinsic hemolytic anemia: Hereditary disorders
Sickle cell anemia: Sickle shape
Thalassemia: Small and irregular
Nutrition deficiency
anemia
Iron deficiency Microcytic, hypochromic
Protein deficiency Macrocytic, hypochromic
Vitamin B12 Macrocytic, normochromic/hypochromic
Folic acid Megaloblastic, hypochromic
Aplastic anemia Bone marrow disorder Normocytic, normochromic
Anemia of chronic
diseases
i. Noninfectious inflammatory diseases –
rheumatoid arthritis
ii. Chronic infections – tuberculosis
iii. Chronic renal failure
iv. Neoplastic disorders – Hodgkin’s disease
Normocytic, normochromic
3. Chapter 14 t Anemia 91
The βthalassemia is very common among these
two.
In normal hemoglobin, number of α and β polypeptide
chains is equal. In thalassemia, the production of these
chains become imbalanced because of defective
synthesis of globin genes. This causes the precipitation
of the polypeptide chains in the immature RBCs, leading
to disturbance in erythropoiesis. The precipitation also
occurs in mature red cells, resulting in hemolysis.
α-Thalassemia
αthalassemia occurs in fetal life or infancy. In this
αchains are less, absent or abnormal. In adults, βchains
are in excess and in children, γchains are in excess.
This leads to defective erythropoiesis and hemolysis.
The infants may be stillborn or may die immediately after
birth.
β-Thalassemia
In βthalassemia, βchains are less in number, absent
or abnormal with an excess of αchains. The αchains
precipitate causing defective erythropoiesis and
hemolysis.
3. Nutrition Deficiency Anemia
Anemia that occurs due to deficiency of a nutritive
substance necessary for erythropoiesis is called nutrition
deficiency anemia. The substances which are necessary
for erythropoiesis are iron, proteins and vitamins like
C, B12 and folic acid. The types of nutrition deficiency
anemia are:
Iron deficiency anemia
Iron deficiency anemia is the most common type of
anemia. It develops due to inadequate availability of
iron for hemoglobin synthesis. RBCs are microcytic and
hypochromic.
Causes of iron deficiency anemia:
i. Loss of blood
ii. Decreased intake of iron
iii. Poor absorption of iron from intestine
iv. Increased demand for iron in conditions like
growth and pregnancy.
Features of iron deficiency anemia: Features of iron
deficiency anemia are brittle nails, spoonshaped nails
(koilonychias), brittle hair, atrophy of papilla in tongue
and dysphagia (difficulty in swallowing).
Protein deficiency anemia
Due to deficiency of proteins, the synthesis of hemoglobin
is reduced. The RBCs are macrocytic and hypochromic.
iii. Hypersplenism
iv. Burns
v. Infections like hepatitis, malaria and septicemia
vi. Drugs such as penicillin, antimalarial drugs and
sulfa drugs
vii. Poisoning by chemical substances like lead,
coal and tar
viii. Presence of isoagglutinins like antiRh
ix. Autoimmune diseases such as rheumatoid
arthritis and ulcerative colitis.
B. Intrinsic hemolytic anemia: It is the type of anemia
caused by destruction of RBCs because of the defective
RBCs. There is production of unhealthy RBCs, which are
short lived and are destroyed soon. Intrinsic hemolytic
anemia is often inherited and it includes sickle cell
anemia and thalassemia.
Because of the abnormal shape in sickle cell anemia
and thalassemia, the RBCs become more fragile and
susceptible for hemolysis.
Sickle cell anemia
Sickle cell anemia is an inherited blood disorder,
characterized by sickleshaped red blood cells. It is also
called hemoglobin SS disease or sickle cell disease. It
is common in people of African origin.
Sickle cell anemia is due to the abnormal hemoglobin
called hemoglobin S (sickle cell hemoglobin). In this,
αchains are normal and βchains are abnormal. The
molecules of hemoglobin S polymerize into long chains
and precipitate inside the cells. Because of this, the
RBCs attain sickle (crescent) shape and become more
fragile leading to hemolysis (Fig. 14.1). Sickle cell anemia
occurs when a person inherits two abnormal genes (one
from each parent).
In children, hemolyzed sickle cells aggregate and
block the blood vessels, leading to infarction (stoppage of
blood supply). The infarction is common in small bones.
The infarcted small bones in hand and foot results in
varying length in the digits. This condition is known as
hand and foot syndrome. Jaundice also occurs in these
children.
Thalassemia
Thalassemia is an inherited disorder, characterized by
abnormal hemoglobin. It is also known as Cooley’s
anemia or Mediterranean anemia. It is more common
in Thailand and to some extent in Mediterranean
countries.
Thalassemia is of two types:
i. αthalassemia
ii. βthalassemia.
4. Section 2 t Blood and Body Fluids
92
FIGURE 14.1: A. Normal RBC; B. Hypochromic anemia; C. Sickle cell anemia; D. Thalassemia;
E. Megaloblastic anemia (Courtesy: Dr Nivaldo Medeiros).
5. Chapter 14 t Anemia 93
Pernicious anemia or Addison’s anemia
Pernicious anemia is the anemia due to deficiency of
vitamin B12. It is also called Addison’s anemia. It is due
to atrophy of the gastric mucosa because of autoimmune
destruction of parietal cells. The gastric atrophy results
in decreased production of intrinsic factor and poor
absorption of vitamin B12, which is the maturation factor
for RBC. RBCs are larger and immature with almost
normal or slightly low hemoglobin level. Synthesis of
hemoglobin is almost normal in this type of anemia. So,
cells are macrocytic and normochromic/hypochromic.
Before knowing the cause of this anemia, it was
very difficult to treat the patients and the disease was
considered to be fatal. So, it was called pernicious
anemia.
Pernicious anemia is common in old age and it is
more common in females than in males. It is associated
with other autoimmune diseases like disorders of
thyroid gland, Addison’s disease, etc. Characteristic
features of this type of anemia are lemon yellow color
of skin (due to anemic paleness and mild jaundice)
and red sore tongue. Neurological disorders such as
paresthesia (abnormal sensations like numbness,
tingling, burning, etc.), progressive weakness and
ataxia (muscular incoordination) are also observed in
extreme conditions.
Megaloblastic anemia
Megaloblastic anemia is due to the deficiency of another
maturation factor called folic acid. Here, the RBCs are
not matured. The DNA synthesis is also defective, so the
nucleus remains immature. The RBCs are megaloblastic
and hypochromic.
Featuresofperniciousanemiaappearinmegaloblastic
anemia also. However, neurological disorders may not
develop.
4. Aplastic Anemia
Aplastic anemia is due to the disorder of red bone
marrow. Red bone marrow is reduced and replaced
by fatty tissues. Bone marrow disorder occurs in the
following conditions:
i. Repeated exposure to Xray or gamma ray
radiation.
ii. Presence of bacterial toxins, quinine, gold salts,
benzene, radium, etc.
iii. Tuberculosis.
iv. Viral infections like hepatitis and HIV infections.
In aplastic anemia, the RBCs are normocytic and
normochromic.
5. Anemia of Chronic Diseases
Anemia of chronic diseases is the second common type of
anemia(nexttoirondeficiencyanemia).Itischaracterized
by short lifespan of RBCs, caused by disturbance in iron
metabolism or resistance to erythropoietin action.Anemia
develops after few months of sustained disease. RBCs
are normocytic and normochromic.
Common causes anemia of chronic diseases:
i. Noninfectious inflammatory diseases such
as rheumatoid arthritis (chronic inflammatory
autoimmune disorder affecting joints).
ii. Chronic infections like tuberculosis (infection
caused by Mycobacterium tuberculosis) and
abscess (collection of pus in the infected tissue)
in lungs.
iii. Chronic renal failure, in which the erythropoietin
secretion decreases (since erythropoietin is
necessary for the stimulation of bone marrow to
produce RBCs, its deficiency causes anemia).
iv. Neoplasticdisorders(abnormalanddisorganized
growth in tissue or organ) such as Hodgkin’s
disease (malignancy involving lymphocytes)
and cancer of lung and breast.
RBCs are generally normocytic and normochromic
in this type of anemia. However, in progressive disease
associated with iron deficiency the cells become
microcytic and hypochromic.
„ SIGNS AND SYMPTOMS OF ANEMIA
„ SKIN AND MUCOUS MEMBRANE
Color of the skin and mucous membrane becomes pale.
Paleness is more constant and prominent in buccal and
pharyngeal mucous membrane, conjunctivae, lips, ear
lobes, palm and nail bed. Skin looses the elasticity and
becomes thin and dry. Thinning, loss and early grayness
of hair occur. The nails become brittle and easily
breakable.
„ CARDIOVASCULAR SYSTEM
There is an increase in heart rate (tachycardia) and
cardiac output. Heart is dilated and cardiac murmurs are
produced. The velocity of blood flow is increased.
„ RESPIRATION
There is an increase in rate and force of respiration.
Sometimes, it leads to breathlessness and dyspnea
(difficulty in breathing). Oxygenhemoglobin dissociation
curve is shifted to right.
6. Section 2 t Blood and Body Fluids
94
„ DIGESTION
Anorexia, nausea, vomiting, abdominal discomfort and
constipation are common. In pernicious anemia, there is
atrophy of papillae in tongue. In aplastic anemia, necrotic
lesions appear in mouth and pharynx.
„ METABOLISM
Basal metabolic rate increases in severe anemia.
„ KIDNEY
Renal function is disturbed. Albuminuria is common.
„ REPRODUCTIVE SYSTEM
In females, the menstrual cycle is disturbed. There
may be menorrhagia, oligomenorrhea or amenorrhea
(Chapter 80).
„ NEUROMUSCULAR SYSTEM
Common neuromuscular symptoms are increased
sensitivity to cold, headache, lack of concentration, rest
lessness, irritability, drowsiness, dizziness or vertigo
(especially while standing) and fainting. Muscles become
weak and the patient feels lack of energy and fatigued
quite often and quite easily.