A presentation made about Sickle cell disease by Yara Mostafa, Yasser Osama, Yaser Mostafa ,Ain shams university, Medicine faculty, first year students.
This a series of notes on hematology useful for undergraduate and postgraduate medical and paramedical students. Notes are prepared from standard texts and are easy to reproduce in exams.
This a series of notes on hematology useful for undergraduate and postgraduate medical and paramedical students. Notes are prepared from standard texts and are easy to reproduce in exams.
This Presentation of Hemolytic Anemia try to cover important Hemato-pathological aspects of Red cell membrane disorders ( Hereditary Spherocytosis, others ) , Enzymopathies ( G6PD deficieny, others ) and Hemoglobinopathies ( Thallasemia, SCA) and their differentiation. References includes Robbins pathology, Wintrobes atlas and text, and others
Fetal hemoglobin and rh incompatibilityrohini sane
A comprehensive presentation on fetal hemoglobin & Rh incompatibility for undergraduate medical, dental, biotechnology & pharmacology students for self-learning .Presentation has physical & chemical properties of fetal hemoglobin along with its function. Binding affinity for O₂ of HbF and oxygen dissociation curve for HbF elucidated with suitable diagrams. Molecular constitution of Embryonic Hb ( Grover I &Grover II )with electrophoretic patterns are presented here . Importance of Kleihauer staining for detection of fetal cells is described briefly.
Diagrammatic representation of Rh- incompatibility is done for complete understanding of the concept. Signs & symptoms Kernicterus are presented diagrammatically.
Direct and indirect Coomb’s Test for Rh- incompatibility for diagnosis of Erythroblastosis Fetalis is illustrated. Biochemical aspects of Hemolytic Disease of Newborn (HDN) and Physiological /Neonatal Jaundice are presented. Comparison of Causes & biochemical findings for Hemolytic Jaundice along hepatic and obstructive jaundice is done in this presentation.
Molecular mechanism involved in biosynthesis of Hb Bart and Hb H along with their electrophoretic patterns for their detection are illustrated.
Hereditary persistent fetal Hb( HPFH ) & Point mutations causing HPFH are described in lucid manner. Google images are used for intense impact of the subject.
Sickle cell anemia is a genetic diseases where red blood cells can take shape of a crescent or a sickle . And this allows them to be more easily destroyed – causing anemia and other complexities
This Presentation of Hemolytic Anemia try to cover important Hemato-pathological aspects of Red cell membrane disorders ( Hereditary Spherocytosis, others ) , Enzymopathies ( G6PD deficieny, others ) and Hemoglobinopathies ( Thallasemia, SCA) and their differentiation. References includes Robbins pathology, Wintrobes atlas and text, and others
Fetal hemoglobin and rh incompatibilityrohini sane
A comprehensive presentation on fetal hemoglobin & Rh incompatibility for undergraduate medical, dental, biotechnology & pharmacology students for self-learning .Presentation has physical & chemical properties of fetal hemoglobin along with its function. Binding affinity for O₂ of HbF and oxygen dissociation curve for HbF elucidated with suitable diagrams. Molecular constitution of Embryonic Hb ( Grover I &Grover II )with electrophoretic patterns are presented here . Importance of Kleihauer staining for detection of fetal cells is described briefly.
Diagrammatic representation of Rh- incompatibility is done for complete understanding of the concept. Signs & symptoms Kernicterus are presented diagrammatically.
Direct and indirect Coomb’s Test for Rh- incompatibility for diagnosis of Erythroblastosis Fetalis is illustrated. Biochemical aspects of Hemolytic Disease of Newborn (HDN) and Physiological /Neonatal Jaundice are presented. Comparison of Causes & biochemical findings for Hemolytic Jaundice along hepatic and obstructive jaundice is done in this presentation.
Molecular mechanism involved in biosynthesis of Hb Bart and Hb H along with their electrophoretic patterns for their detection are illustrated.
Hereditary persistent fetal Hb( HPFH ) & Point mutations causing HPFH are described in lucid manner. Google images are used for intense impact of the subject.
Sickle cell anemia is a genetic diseases where red blood cells can take shape of a crescent or a sickle . And this allows them to be more easily destroyed – causing anemia and other complexities
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
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!
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. Sickle Cell Disease
• RBCs disorder that causes
the sickling of biconcave
shaped RBCs.
• There are many types:
*Sickle cell Anemia.
*Sickle cell Trait.
4. Brief Medical History
1910 – First Description of Sickle-Shaped
Blood Cells by Dr James Herrick.
1917 – Genetic basis for SCD were discovered
by Dr. V. Emmel.
1922 – Disease was named “sickle cell
anaemia” by Vernon Mason .
1927 – Hahn and Gillespie elaborated on
Emmel’s work by demonstrating that the
sickling effect was linked to de-oxygenation.
Dr James B. Herrick
5. Pathophysiology
• Deoxy Hb S polymer forms with
low O2, depends on Hgb S
concentration, low pH, high
temperature, high 2,3-DPG
• Membrane is damaged so RBCs
accumulate calcium, lose
potassium & water and
become rigid & irreversibly
sickled
• Sickle cells hemolyze within 10-
20 days
6. Genetics
•It’s autosomal recessive blood disease.
•It’s not contagious “You can’t catch it”.
•You inherit it from your parents.
*The gene defect is a known mutation of a
single nucleotide.
*The person that receives the defective
gene from both his parents will develop
Sickle-cell disease.
*The person who receives only one
defective gene from either one of his
parents will develop Sickle-cell trait.
7. Sickle Cell Trait (AS)
*A person has one abnormal allele of the hemoglobin
beta gene.
*Those who are heterozygous for the sickle cell allele
produce both normal “HbA” and abnormal hemoglobin
“HbS” (the two alleles are co-dominant).
* HbA : 60%, HbS: 40% , HbF:<2%
*Asymptomatic :Don’t show severe symptoms as in Sickle
cell Anemia.
*People with sickle cell who exercise heavily, such as
athletes and those who are exposed to dehydration or
altitude extremes, may sometimes experience sickle cell
anemia symptoms.
*They act as carriers and can transmit the disease to their
off springs.
8. *It has been suggested that sickle cell trait is linked to two other
medical problems that may elicit health and performance concerns.
These include:
1) Exercise-related rhabdomyolysis 2) Exercise-associated sudden death
(skeletal muscle breakdown)
* Occur in normal, healthy individuals *Sickle cell trait deaths occurred
following strenuous exercise. predominantly in football players.
*Sickle cell trait individuals might be at *Athletes with the trait experienced
greater risk for developing the syndrome noninstantaneous collapse with
than those without this trait. gradual but rapid deterioration, ie,
* This syndrome can result in renal dyspnea, fatigue, weakness, and
failure and sudden death. muscle cramping.
9. Diagnosis
Sickle test
solubility tests
hemoglobin electrophoresis test
Screening test for newborns DNA Analysis
10. Sickling Test
Method:
1) A sample of venous blood or capillary blood may be collected for this test.
*Venous blood from the arm.*Capillary blood from the finger tips or ear lobes and in
infants from the heel of the foot.
2) Mixing blood with the reducing agent, sodium metabisulphite, will induce sickling in
susceptible cells.
3) the results can be viewed under a microscope after 20 minutes.
Negative Test This test is simple and quick, used Positive Test
HbA to identify the presence of HbS. HbS
Normal RBC Sickled RBC
*Positive sickling test associated
with a normal haemoglobin is likely
to indicate a patient with sickle cell
trait.
11. Sickle Solubility Test (SST)
•A rapid and inexpensive technique used to screen for the presence of sickling
hemoglobins, can be used at home.
•A positive result must be confirmed by another method (HPLC or electrophoresis) to
confirm the presence of Hb S and to distinguish Hb AS (carrier state) from Hb SS
(sickle cell disease).
•Disadvantage: Other insoluble hemoglobins, such as Hb C-Harlem, will also give a
positive result.
Method: Depend on phosphate solubility
1) Erythrocytes are lysed by saponin.
2) The released hemoglobin is reduced by
sodium hydrosulfite in a phosphate buffer.
The presence of HbA under The resulting tactoids of HbS
3) Reduced HbS is characterized by its very
these same conditions results causes the solution to remain
low solubility andred solution. of
in a clear the formation turbid.
neumatic liquid crystals (tactoids).
12. Hemoglobin Electrophoresis test
* Haemoglobin electrophoresis will differentiate between homozygous and
heterozygous conditions.
* Hemoglobin types have different electrical charges and move at different speeds.
*HbAS: Has both HbA and
HbS.
Shows 2 bands
*HbSS: Is less negative by 2
compared to HbA .
Migrates slower than HbA
13. Newborn screening
• It is performed via the most sensitive Hb isoelectric
focusing or HPLC fractionation and identifies the
specific types of hemoglobin present.
•In newborns who carry the sickle cell gene, fetal
hemoglobin F will predominate, but a small
amount of hemoglobin S will also be present.
•There also may be a small amount of hemoglobin
A if they have sickle cell trait.
DNA analysis
• This test is used to investigate alterations and mutations in the genes that produce
hemoglobin components.
•It may be performed to determine whether someone has one or two copies of the
Hb S mutation or has two different gene mutations.
•Genetic testing is most often used for prenatal testing: The usual tests offered are
chorionic villus sampling (CVS) or amniocentesis “14 to 16 weeks”.
14. Globin Gene Family
Chromosome 16
1 Zeta
Alpha Family
2 Alpha
Globin Gene
1 Epsilon
Family
2 Gamma
Beta Family
1 Beta
Chromosome 11
1 Delta
15. HbF
*If fetal hemoglobin remains the predominant form of hemoglobin after birth, the
number of painful episodes decreases in patients with sickle-cell disease.
*The fetal hemoglobin's reduction in the severity of the disease comes from its ability to
inhibit the formation of hemoglobin aggregates within the red blood cells also containing
hemoglobin S.
*A form of treatment of Sickle cell
anemia is hydroxyurea that promotes
the production of fetal hemoglobin
16. Signs and Symptoms
• Infection, dehydration, and acidosis act as
triggers but in most instances no predisposing
cause is identified.
• They usually appear after 4 months of age.
• Most common signs are linked to Anemia and
Pain.
18. Vaso-oclusive crisis
• Ischemia
• Pain
• Necrosis
• Often leads to organ damage
• Management
– Severe: analgesics, Opioid
– Mild: NSAIDs
– New treatment involving
*Adenosine A2a receptor
agonists. These medicines may
reduce pain-related
complications.
19. Splenic squestration crisis
• Acute, painful enlargements of the spleen,
caused by intrasplenic trapping of red cells
• Caused by intrasplenic trapping of red cells
• Die within 1-2 hours due to circulatory failure
• Autosplenectomy
20. Aplastic crisis
• Paravirus B19
– Divides in RBCs precursors and destroys them
– Stops erythropoiesis for two or three days
– Causes reticulocytopenia
– Disappears within one week with management and
blood transfusions
Hemolytic crisis
• Common in patients with G6PD deficiency
21. Complications
*Hand-Foot syndrome Pain,
Fever, Swelling.
*Overwhelming post-splenectomy
infection (OPSI) treated
with antibiotics and supportive care.
*Acute chest Syndrome Chest
pain, Shortness of breath, Fever.
*Stroke Learning problems,
Long term disability, Brain damage,
Paralysis, Death.
*cholelithiasis (gall stones) & Cholecytitis
Nausea, Vomiting, Jaundice,
Sweating, Clay-coloured stool.
22. Complications
*Priapism Damge to the Penis and
Impotence.
*Retinopathy Blindness.
* Sickle cell nephropathy Chronic
renal failure.
*Pulmonary hypertension Fatigue,
Shortness of breath.
*In pregnancy spontaneous abortion.
*Aseptic bone necrosis.
23. Management
• Blood transfusions:
– Acute chest crisis OH
O
– Decreases the risk for strokes
– Defrasirox: iron chelator
• Folic acid daily intake N N
• Penicillin N
*
• Malaria chemoprophylaxis OH
* *
HO
Fe
24. Treatment
• Hydroxyurea.
– Reactivates fetal Hb production
– Decreases severity of attacks
– Increases life span
– More effective with Erythropoietin.
• Bone marrow transplant during childhood.
• 5-HMF. This natural compound binds to red blood cells and
increases their oxygen. This helps prevent the red blood cells
from sickling.
25. Prevention
• You can’t prevent sickle cell
anemia, because it’s an inherited
disease.
• If a person is born with it, steps
should be taken to reduce
complications.
• Genetic Counseling should be
considered.
• A counselor can explain the risk of
having a child who has the disease
and can help explain the choices
that are available.
26. Prognosis
*New and aggressive treatments for sickle cell disease are prolonging life and
improving its quality.
*Recently as 1973, the average lifespan for
people with sickle cell disease was only 14
years.
*Currently, life expectancy for these
patients can reach 50 years and over.
*Women with sickle cell live longer than
their male counterparts.
*The median age at death :
-Males : 53years
-Females: 58 years
*As children with sickle cell disease live longer, older patients are now facing medical
problems related to the long-term adverse effects of the disease process.
27. Malaria
• Parasitic infection: Plasmodium falciparum
• Two stages in the human body:
– Exoerythrocytic stage in liver (8 to 30 days)
– Erythrocytic stage
28. Sickle cell gene and malaria
• Heterozygous individuals are tolerant to
malaria
• Homozygous individuals are less tolerant to
malaria because of the common functional
asplenia