Anemia is a condition where blood lacks healthy red blood cells (RBC), decreasing the competence of blood to carry oxygen to tissues.
In clinical medicine, it refers to decrease in the normal concentration of Haemoglobin (Hb). Anemia is caused by either – 1. A decrease in the production of RBCs (decreased erythropoiesis) or haemoglobin.
2. An increase in loss of blood.
3. Destruction of red blood cells (haemolytic anaemia).
Hemolytic anemia is decreased level of Erythrocytes in circulating blood (anemia) caused because of their accelerated destruction (haemolysis) extravascularly or intravascularly either due to intrinsic or extrinsic factors.
anaemia and its classification, blood transfusion, blood group, erythroblastosis foetalis, blood component , use of blood components in human diseases. blood group reaction
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
anaemia and its classification, blood transfusion, blood group, erythroblastosis foetalis, blood component , use of blood components in human diseases. blood group reaction
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
A presentation made about Sickle cell disease by Yara Mostafa, Yasser Osama, Yaser Mostafa ,Ain shams university, Medicine faculty, first year students.
A presentation made about Sickle cell disease by Yara Mostafa, Yasser Osama, Yaser Mostafa ,Ain shams university, Medicine faculty, first year students.
In this presentation I've tried to summarize classification of hemolytic anemia and in depth review of rbc membrane disorders like hereditary spherocytosis, hereditary elliptocytosis, enzymopathies of hemolytic anemia like g6pd disorder, pyruvate kinase disorders, hemoglobinopathies related to hemolytic anemia like thalassemia, sickle cell anemia and especially pathophysiology and mechanism of hemolysis either extravascular or intravascular. Hope it helps you understand the entity better.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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!
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Phone Us ❤85270-49040❤ #ℂall #gIRLS In Surat By Surat @ℂall @Girls Hotel With...
Haemolytic anemia
1. PRESENTED BY –
VIOLINA BHUYAN
4TH SEMESTER,
M.SC, LIFE SCIENCE
BANGALORE UNIVERISITY
DEPARTMENT OF LIFESCIENCE
BANGALORE UNIVERSITY
HEMOLYTIC ANEMIA
3. INTRODUCTION
❖ Anemia is a condition where blood lacks healthy red blood cells (RBC), decreasing the
competence of blood to carry oxygen to tissues.
❖ In clinical medicine, it refers to decrease in the normal concentration of Haemoglobin (Hg).
❖ Anemia is caused by either –
• a decrease in the production of RBCs (decreased erythropoiesis) or haemoglobin.
• an increase in loss of blood.
• destruction of red blood cells (haemolytic anaemia).
❖ Hemolytic anemia is decreased level of Erythrocytes in circulating blood (anemia) caused
because of their accelerated destruction (haemolysis) extravascularly or intravascularly either
due to intrinsic or extrinsic factors.
4. FATE OF ERYTHROCYTES
contains fluid with dissolved substances
▪ An anucleate, biconcave disc shaped cell that
and
millions of hemoglobin molecules.
▪ Hemoglobin is a pigment protein that transports
O2 and CO2 to and from tissues.
▪ Heme is an iron containing porphyrincompound.
What is an Erythrocyte ?? What happens to RBC after 100 days??
▪ Life span of a normal RBC is 100-120 days. An old RBC becomes rigid,
fragile and their Hb begins to degenerate.
▪ The dying RBCs are engulfed by the macrophages. This is commonly
known as Eryptosis or Apoptosis.
▪ The macrophage destroys the RBC and hemoglobin is breakdown to
globin and heme.
▪ Globin chains are broken down to amino acids which are re-used for
protein synthesis.
▪ The protoporphyrin ring is opened up - CO is released and excreted
though expired air and iron (Fe3+) is transported back to bone marrow to
continue haematopoiesis.
5. What happento the rest of
the component???
▪ Biliverdin present in the heme isconverted to
unconjugated free bilirubin by biliverdin
reductase.
▪ The conjugated bilirubin is excreted in bilegiving
itayellow green colour.
▪ Most of the bile secretedin the small intestine is
reabsorbed and transported back to liver.
▪ Remaining bilirubin converted to stercobilinogen
which gets excreted in faecal matter.
Thus in Hemolytic anemia, the total bilirubin
in the blood serum, urobilinogen in urine,and
stercobilinogen in faecal matter are mildly
increased.
6. HAEMOLYSIS
▪ When the compensation of RBC removal by new RBC
production is inadequate, clinical problems can appear and so
thus anemia develops.
▪ Haemolysis may be caused due to –
1. Intrinsic factors
1. Extrinsic factors
Why and how haemolysis occur???
▪ Hemolytic anemia is the destruction (haemolysis) of
erythrocytes, decreasing the hemoglobin concentration in blood
thus decreasing oxygen level in the tissues.
Genetic
disposition
Antigen/antibody
mediated
Drugs
Viruses
Bacteria
Parasites
Injury/trauma
7. General features of hemolytic disorders
CRITERIA FEATURES
Generalexamination Jaundice,pallor bossingof skull
Physicalfindings Enlargedspleen
Hemoglobin From normal toseverly reduced
Reticulocytes Increased
Bilirubin Increased(mostlyunconjugated)
LDH Increased
Haptoglobulin Redused to absent
9. HEMOGLOBINOPATHIES
▪ The mutations lead to either abnormality in the structure (or)
synthesisof the hemoglobin molecule.
1. Qualitativedefect =Haemoglobinopathy/ Hemoglobin
variants.Ex:Sicklecell diseases.
2. Quantitative defect =Thalassemias.
Hemoglobinopathy V/S Thalassemias
▪ Haemoglobinopathies are a group of recessively inherited
genetic conditions affecting the hemoglobin structure of blood
(due to a genetic change in the hemoglobin gene) leading to
hemolytic anemia.
10. H
E
M
O
G
L
O
B
I
N
O
P
A
T
H
YI
N
H
E
R
I
T
A
N
C
E
▪ Haemoglobinopathy carrier/trait
▪ Haemoglobin disorder
Globin polypeptidegene No.of
variant
s
α-1andα-2 globin gene 424
β-globin gene 571
δ-globin gene 69
Aγ-globin gene 38
Gγ-globingene 58
Hemoglobinopathies are found world wide but occursmost commonly in
African blacks and ethnic groups from Mediterranean basin and southeastasia.
11. SICKLE
CELL
DISEASES
▪ Sickle cell disease is agroup of inherited, autosomal recessive red blood celldisorder that
affects the quality and structure of hemoglobinmolecule.
▪ The types of sickle cell disease include the following:
▪ HemoglobinSC
▪ Hemoglobin Sβ+thalassemia
▪ HemoglobinC syndrome
▪ HemoglobinD
▪ HemoglobinE
▪ HemoglobinSS and many more….
▪ The Hemoglobin SS(HbS)is the Sickle cell anemia, that requires the inheritance of two sickle
cell genes(recessive).
Sickle cell anemia is causedby amutation (GAG → GTGconversion) in the HBBgene (hemoglobin β gene).
β6(A3)Glu →Val
15. THALASSEMIAS
Thalassemia is a group of inherited disorders resulting from mutation in one or more of
the globin genes of hemoglobin, causing decreased or absent synthesis of the
corresponding globinchains.
Consequences of the mutation depend on the particular chain affected and the amount
of globinchain produced.
decreased production of normalHg
synthesis of abnormalhemoglobins
ineffective erythropoiesis
unbalanced synthesis ofα and non- α globin chains and
Symptoms include anemia, hepatosplenomegaly, infections, gallstones, and bone
deformities that alter facial features
FETAL
HEMOGLOBIN
HEMOGLOBINA2
HEMOGLOBINA
2α
and
2β
>95%
2α
and
2δ
3-4%
2α
and
2γ
<1%
17. PATHOPHYSIOLOGY
In normal human body, the maturing erythrocyte produces α-chain to β-chain in equal
ratio of1:1.
Although excessβ and γchains can combine astetramers (β4, γ4) to form abnormal
hemoglobins, but α-chains do not.
• Excess of β-chain
α-chain
synthesis
decreasedor
absent
• Excess of α-chain
β-chainsynthesis
decreased or
absent
α-chainsare
highly insoluble
Precipitatesout Fessasbodies
Apoptosisof
erythrocytes
Ineffective
erythropoiesis
Chronic
extravascular
hemolysis
Combines toform
tetramers(β4)
Hemoglobin H(HbH) High affinity for oxygen Unstable
EXCESSOF α-CHAINS
EXCESSOF β-CHAINS
EXCESS OF γ-CHAINS Combines ofform
tetramers(γ4)
Hemoglobin
Bart’s (HbBart’s)
Highoxygen
affinity
18. ALPHA-THALASSEMIAS
▪ α-Thalassemia is agroup of four disorders characterized by decreased synthesis of α-chains.
▪ Mutations can affect one or more of the α genes. The amount of α-chains synthesized is somewhat proportional to the number of
affected alleles.
α-Thalassemia is found primarily in
people ofMediterranean, Asian, and
African ancestry. In particular, it is
commonly seenin blacks, Indians,
Chinese, and Middle Easternpeople
19. BETA-THALASSEMIAS
▪ There are only two β-globin genes, one located on eachchromosome 11
▪ Twoclassification systems are currently usedfor this diverse group of diseases-
▪ Genotypic system – 6 genotypes based on zygosity.
▪ Phenotypic system – 4 categories based on severity.
▪ When the 3gene designations, β0 , β+, and βSCare combined with the normal allele (β), and the 2 possible zygosity patterns
(homozygous and heterozygous) are considered, 8 possible genotypes emerge
The most severe mutation (β0 ) is found
more frequently in the Mediterranean
regions of northern Italy, Greece,Algeria,
SaudiArabia andSoutheastAsia.
The more severe version is observed in the
Mediterranean region, the Middle East, the
Indian subcontinent, and SoutheastAsia.
21. SUMMARY
▪ Hemoglobin synthesis requires adequate production of heme and globin. Inadequate amounts of either can result in
anemia. Out of many causes of hemolytic anemia, structural defects in Hg molecule that are considered to be the most
common hereditary disease in humans. More than 330,000 infants worldwide are born each year with inherited
hemoglobin disorders such as Sickle cell and Thalassemia.
▪ Hemoglobinopathies are a group of chronic hemolytic anemias caused by qualitative and quantitative defects in the globin
chains of hemoglobin.
▪ The mutations can affect the hemoglobin molecule’s solubility, stability, or function (oxygen affinity), decreased or absent
synthesis of the corresponding globin chains, resulting in unbalanced synthesis of α and β- globin chains and ineffective
erythropoiesis.
22. REFERENCES
C.Hatton, N. Hughes-Jones, D. Hay, D. Keeling(2013)9th edition, Haematology
Lecture Notes,Wiley-Blackwell, UK
GamalA.Hamid(2013),Clinical Hematology,ResearchGate,DOI:
10.13140/RG.2.1.1477.1683,pg-49-61
Shirlyn B.McKenzie,J.Williams(2015)3rd.edition.,Clinical Laboratory
Hematology,Pearson.New Jersey,pg-chp13,14.
https://www.nhlbi.nih.gov/health-topics/sickle-cell-disease
https://www.gov.uk/government/publications/handbook-for-sickle-cell-and-
thalassaemia-screening/understanding-haemoglobinopathies
