ABO-Rh Isoimmunisation in that The Basics of Blood, antibody can Be Detected,ABO Blood Group System,Rh Blood Group System,Pathogenesis Of Rh Isoimmunisation, Prevention and Management of ABO incompatibility in PPT
ABO-Rh Isoimmunisation in that The Basics of Blood, antibody can Be Detected,ABO Blood Group System,Rh Blood Group System,Pathogenesis Of Rh Isoimmunisation, Prevention and Management of ABO incompatibility in PPT made By Sonal Patel
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
Similar to ABO-Rh Isoimmunisation in that The Basics of Blood, antibody can Be Detected,ABO Blood Group System,Rh Blood Group System,Pathogenesis Of Rh Isoimmunisation, Prevention and Management of ABO incompatibility in PPT
MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(ISBT001) and RH(ISBT004)MAJOR BLOOD GROUPS, ABO(
This presentation aims to help medicine undergraduates and post graduates in the department of Pathology and Department of transfusion medicine for better understanding of various blood grouping systems, sub groups, RBC antigens and corresponding antibodies. It also covers the practical aspect of blood grouping and cross matching.
Similar to ABO-Rh Isoimmunisation in that The Basics of Blood, antibody can Be Detected,ABO Blood Group System,Rh Blood Group System,Pathogenesis Of Rh Isoimmunisation, Prevention and Management of ABO incompatibility in PPT (20)
Breast & it's problems and treatment made by sonal Patelsonal patel
Breast & it's problems and treatment - Anatomy of Breast and Physiology of lactation , Breast Diseases - 1. bening breast problems, Breast Cancer, bening neoplastic lump made by sonal Patel
Antenatal Care Guideline- gestational Age Assessment,Early USG, Nutritional ...sonal patel
Antenatal Care Guideline- gestational Age Assessment,Early USG, Nutritional Supplements,, Food Acquired Infections,medicine, alcohol,smoking, Sexual Intercose avoid, Exercise, Clinical Screening in PPT made by sonal patel
methods of Chromosomal Evaluation in Amniocentesis- Define, Time for test, C...sonal patel
methods of Chromosomal Evaluation in Amniocentesis- Define, Time for test, Complications,and Chorionic Villus sampling ( CVS) , Risk of Procedure, Steps of Procedure in PPT -Define, Time for test made By sonal Patel
Amenorrhea - Define, Cause, Sign and Symptoms, Type- Pathological and Physiol...sonal patel
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Abruptio placenta- Define, cause, sign and symptoms, Risk Factors, Incidence,pathology, Classification, Prevention and Treatment, management in PPT made by sonal Patel
Dysfunctional uterine Bleeding is type of Abnormal bleeding from the genital ...sonal patel
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Birth defect system according to System wise in that Respiratory System Birth...sonal patel
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Embryology-all basic definition,Stage wise development of fetus,development o...sonal patel
Embryology-all basic definition,Stage wise development of fetus,development of Zygote stage ,development of Embrionic Stage ,development of Fetus Stage all are according week development,Amnione,chorion,Fetal layer, Umbilical Cord developmentmade By sonal Patel
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
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.
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
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
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
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.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
Ocular injury ppt Upendra pal optometrist upums saifai etawah
ABO-Rh Isoimmunisation in that The Basics of Blood, antibody can Be Detected,ABO Blood Group System,Rh Blood Group System,Pathogenesis Of Rh Isoimmunisation, Prevention and Management of ABO incompatibility in PPT
2. The Basics Of Blood
2
ANTIGEN
>400 Agglutinogens on the cell
membrane
W.B.C. & Platelet R.B.C. Plasma
ANTIBODY
Natural & Immune
Agglutinins/
Isoantibodies
Antigen-Antobody reaction on the
cell surface Hemolysis
3. The Basics Of Blood
• Controlled by genes at unknown No. of
chromosomal loci.
• Appearance by 40 days of I.U. Life- unchanged
till death.
• Also present in tissues & tissue fluids.
• Blood group system: A group of antigens
controlled by a locus having a variable no of
allele genes.
3
Antigens: -
4. The Basics Of Blood
• > 15 blood group systems are recognised :
– ABO, Rh, Kell, Duffy, MN, P, Lewis, Lutheran, Xg,
Li, Yt, Dombrock, Colton, Public antigens & Private
antigens.
• Blood type- means individual antigen phenotype
which is the serological expression of the
inherited genes
• Most of these blood group antigens have been
found to be associated with hemolytic disease.
• However– ABO & Rh account for 98%
4
Antigens: -
5. The Basics Of Blood
5
Alloantibodies / Agglutinins
Natural
IgM
Iso / immune antobodies
IgG
Formed in response to
foreign R.B.C. or soluble
blood group substance.
Antibodies: -
6. The Basics Of Blood
• Antibodies are formed against most of the major group
antigens & present in almost all individuals when the antigen
is absent.
• In most other minor systems, natural antibodies to the
antigens are found occassionally but as their anitgenicity is
low, the immune antibodies are also rare ( except –Kell &
Duffy)
• Mostly of them are IgM type.
• React poorly at body temp. ( except anti-A & anti-B), but
agglutinate R.B.C.s at 5-20°C
• Usually do not cross placenta.
6
Natural Antibodies: -
7. The Basics Of Blood
• In contrast the immune or isoantibodies are IgG.
• Best react at body temp. & readily cross
placenta.
• Most antibodies are complement binding notable
exceptions being Rh & MN.
7
Immune Antibodies: -
8. Antibodies Can Be Detected by: -
a. Saline agglutination test (SAT).
b. Tests using cells suspended in colloid media.
c. Tests using enzyme-treated cells- Rh &
occasional antobodies.
d. Indirect antiglobulin ( Coomb’s test) - wide
spectrum.
• Antibodies may be Complete / Incomplete
IgM IgG
Detected by SAT b, c, d
8
9. ABO Blood Group System
• ABO system is controlled by allelic genes A1, A2, B, O
located on the long arm of chromosome 9
• The loci of ABO & H are not genetically linked
• A1 & A2 genes perform same function but have a
different rate constant
• The O gene is an amorph & functionaly silent
• The H antigen is a precursor to A & B
• Secretors & nonsecretors – Se & se genes control the
production of a flucosyl transferase, which controls the
production of H, A & B antigens in tissues
9
10. ABO Blood Group System
Genotype
(Genes)
Phenotype
(Blood type)
Antigens in
R.B.C.
Antibody In plasma
A1 A1 , A1 A2
A2 A2, A2 O
A1 (23-25%)
A2 (6-10%)
A1, (H)
A2, (H)
anti-B, anti-H
Anti-B, anti-A1
BB, BO B(8-17%) B,(H) Anti-A/A1
A1B
A2 B
A1B(3%)
A2B(1%)
A,A1,B
A,B,H
Anti-H
Anti-A1
O,O
H,h
O(43-50%)
Oh Bombay
H
None
Anti-A,-A1,-B
Anti-A,-A1,-B,-H
10
11. ABO System & Pregnancy
• Majorities of hemolytic diseases are due to ABO
incompatibility
• Foetus inherits one gene from each parent.
– O + O = O, O + A= O or A, O + B= O or B, O + AB=
A or B.
• There is a 20% chance of ABO incompatibility of
mother & foetus
• Only 5% chance of developing hemolytic disease
only in type A & B infants of type O mothers, that
too only of milder forms
11
12. ABO System & Pregnancy
• In foetus & newborn, RBCs have a decreased No.
of H, A & B reactive sites
• The foetal immunoglobulin production is low, so
the plasma contains very little of anti-A & B
agglutinins
• Anti-A & B produced in the mother being natural
are IgM molecules & so do not cross placenta.
• In some type O adults, much of the anti-A & B
and anti-AB (a cross reacting antibody, also called
anti-C) isoagglutinins are of IgG class.
12
13. ABO System & Pregnancy
• There is no adequate method of antenatal
diagnosis.
• Direct Coomb’s antiglobulin test may be negative
in ABO haemolytic disease.
• ABO haemolytic disease is frequently seen in
infants of primigravidae & the chance of
recurence is 87%.
• The risk of stillbirth is not increased & no
antenatal treatment is necessary.
• Only 67% of affected infants will need any
treatment.
13
14. Rhesus Blood Group System
• First demonstrated by testing human blood with
rabit anti sera against red cells of Rhesus monkey
& classifying Rh negative & Rh positive.
• However the underlying biochemical genetics is
not well understood and the genotyping &
phenotyping remains little confused
• The genotype is determined by the inheritance of
3 pairs of closely linked allelic genes situated in
tanderm on chromosome 9 & named as D/d, C/c,
E/e (Fisher- Race theory)
14
16. Rhesus Blood Group System
• 12 sets of combinations & 78 genotypes are
possible. Most frequent genotypes are –
– Cde/cde(33%), Cde/cDe(18%), Cde/cDE(12%)
cDE/cde(11%), cde/cde(15%), cdE/cde(1%),
Cde/cde(1%)
• Though several Rh genotypes and phenotypes
have been described, for clinical & all practical
purposes it is enough to know whether one is
Rh POSITIVE or NEGATIVE against anti D
sera.
16
17. Rhesus Blood Group System
• Incidence of Rh negative varies in different races:
– Mongoloids- nil, Chinese & Japanese- 1-2%, Indians-5%,
Africans-5-8%, Causcasians-15-17% & Basques-30-35%.
• The antigenic expressions of these genes are dependent
on an interaction between R.B.C. membrane protein &
phospholipid molecules resulting in a set of antithelical
epitopes, the coresponding antigens, consisting of C/c,
D/d, E/e.
• The antigenic determinants form an intrinsic part of the
red cell membrane protein structure.
17
18. Rhesus Blood Group System
• C/c & E/e are weak antigens and impractical to
match.
• ‘D’ is by far the most immunogenic in the Rh
system excepting those that have the natural
antibodies.
• There is a rare type of Rh negative called Rh null
who lack all known Rh antigens.
• ‘D’ antigen has no natural antibody while C & E
have the coresponding natural antibodies, though
weak & found infrequently.
18
19. Rhesus Blood Group System
• A single transfusion of + ve blood to a – ve
person has a 50% chance of forming anti Rh D
antibodies (IgG)
• Anti Rh antibodies are of three categories-
– 1st order – saline / bivalent / complete antibodies
– 2nd order - albumin active / univalent / incomplete
antibodies
– 3rd order – atypical / antiglobulin active /
incomplete antibodies
19
20. Pathogenesis Of Rh Iso-immunisation
20
Rh Negative Women Man Rh positive (Homo/Hetero)
Fetus
Rh Neg Fetus
No problem
Rh positive Fetus
Rh+ve R.B.C.s enter
Maternal circulation
Mother previously sensitized
Secondary immune response
? Iso-antibody (IgG)
Non sensitized Mother
Primary immune response
Fetus unaffected, 1st
Baby usually escapes.
Mother gets sensitised?
Fetus
Haemolysis
?
21. Pathogenesis Of Rh Iso-immunisation
• Chances of T.P.H/F.M.H. are only 5% in 1st
trimester but 47% in 3rd trimester, many
conditions can increase the risk.
• Chances of primary sensitization during 1st
pregnancy is only 1-2%, but 10 to 15% of patients
may become sensitized after delivery.
• ABO incompatibility and Rh non-responder status
may protect.
• Amount of antibodies that enter the fetal
circulation will determine the degree of
haemolysis
21
22. Pathology Of Iso-immunisation
22
HAEMOLYSIS IN UTEROAFTER BIRTH
BILLIRUBIN
ANAEMIA
MAT. LIV NO
EFFECT
HEPATIC
ERYTHROPOESIS
& DYSFUNCTION
PORTAL & UMBILICAL VEIN
HYPERTNSION, HEART FAILURE
BIRTH OF AN AFFECTED INFANT - Wide spectrum of presentations. Rapid
deterioration of the infant after birth. May contiune for few days to few months.
Chance of delayed anaemia at 6-8 weeks probably due to persistance of anti Rh
antibodies.
Jaundice
Kernicterus
Hepatic Failure
DEATH
ERYTHROBLASTOSIS
FETALIS
IUD
23. Prevention of Rh Incompatibility
• Premarital counseling? Ambitious?
• Proper matching of blood particularly in
women before childbearing.
• Blood grouping must for every woman, before
1st pregnancy.
• Rh+ve Blood transfusion- 300mcg
Immunoglobulin (minimum).
• Proper management of unsensitised Rh
negative pregnancies.
23
24. Management of Unsensitised
Pregnancy
• Blood typing at 1st visit, If negative husband’s
typing. If husband is also negative then no
treatment
• If husband is positive, if possible, Homo/Hetero?
• Do Indirect Coomb’s test of mother –
– Negative-good.
– Repeat ICT at 28 weeks – Negative- ICT at 35 weeks -
Negative- Observe
– Positive Sensitised - 300mcg Rh immunoglobulin
24
25. Management of Unsensitised
Pregnancy
• In Abortion, Ectopic, CVS-
– Pregnancy < 12 weeks- 50mcg Anti D
– Pregnancy >12 weeks- 300mcg Anti D
• APH, IUD, Amniocentesis, Abdominal trauma,
Foetal-maternal hemorrhage -300mcg Anti D
• At birth- cord blood for ABO & Rh typing
• Baby Rh negative – Be happy
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26. Management of Unsensitised
Pregnancy
• If Rh positive- Test mother’s blood for ICT &
Infant’s for DCT
– Negative or weakly reactive- 300mcg
immunoglobulin
– Positive – Sensitised–Hb & Bilirubin Estimation of
the infant -Treat the infant
• ?Prophylactic Anti D administration during
antenatal period to all negative mothers at
28weeks and again at 34 / 36 weeks.
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27. Management of Sensitized Pregnancy
• Causes of sensitization-
– Misinterpretation of maternal Rh type
– Rh +ve blood transfusion
– Unprotected preg. & labour
– Inadequate dose / improper use of IgG on
previous occasions
– Immunization to cross-reacting antigen
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28. Management of Sensitized Pregnancy
• Careful planning during antepartum,
intrapartum & neonatal period
• Father’s blood type & Rh antigen status
• Knowledge of maternal antibody titer to the
specific antigen
• Intrauterine foetal monitoring with repeated
ultrasound examination, cordocetesis /
amniocentesis
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29. Management of Sensitized Pregnancy
• Fetus Rh Negative: - Observation
• Fetus Rh Positive: -
– Intrauterine transfusion of ‘Rh Neg’ blood as
indicated
– Timely delivery any time after 32 weeks
– Management of the infant up to 8 weeks
• In cases of severely sensitized women,
consider medical termination of pregnancy and
sterilization .
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