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
presented by HAFIZ M WASEEM
university of education LAHORE Pakistan
i am from mailsi vehari and studied in lahore
bsc in science college multan
msc from lahore
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
presented by HAFIZ M WASEEM
university of education LAHORE Pakistan
i am from mailsi vehari and studied in lahore
bsc in science college multan
msc from lahore
this is a series of notes on hematology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
Anemia- a decrease in total amount of RBC or hemoglobin in blood
can be caused due to blood loss, iron or vitanminB12 deficiency
thalassemia
hemolysis-destruction of red blood cell
hemolytic anemia- a disorder where RBBC are destroyed faster than they are made.
1st year MBBS
Autoimmune hemolytic anemia (AIHA) is a type of normochromic normocytic anemia that is caused by autoantibodies that are produced in the patient against his/her own blood cells, particularly against RBCs. As a result hemolysis occurs leading to anemia.
Autoantibodies are produced secondary to autoimmune diseases, lymphoproliferative disorder (LPDs), certain infections or immunodeficiency syndromes.
In this presentation AIHA is under consideration on a broader scale, with only basic information and concepts.
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
the presentation will allow you to identify the different state maturation of RBC and to see the the different abnormally including the cell membrane abnormality , the inclusion bodies may appear in RBC ,and other cell abnormality.
this is a series of notes on hematology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
Anemia- a decrease in total amount of RBC or hemoglobin in blood
can be caused due to blood loss, iron or vitanminB12 deficiency
thalassemia
hemolysis-destruction of red blood cell
hemolytic anemia- a disorder where RBBC are destroyed faster than they are made.
1st year MBBS
Autoimmune hemolytic anemia (AIHA) is a type of normochromic normocytic anemia that is caused by autoantibodies that are produced in the patient against his/her own blood cells, particularly against RBCs. As a result hemolysis occurs leading to anemia.
Autoantibodies are produced secondary to autoimmune diseases, lymphoproliferative disorder (LPDs), certain infections or immunodeficiency syndromes.
In this presentation AIHA is under consideration on a broader scale, with only basic information and concepts.
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
the presentation will allow you to identify the different state maturation of RBC and to see the the different abnormally including the cell membrane abnormality , the inclusion bodies may appear in RBC ,and other cell abnormality.
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.
anemia is a condition in which you lack enough healthy red blood cells to carry adequate oxygen to your body's tissues. Having anemia, also referred to as low hemoglobin, can make you feel tired and weak. There are many forms of anemia, each with its
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
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.
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.
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.
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.
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
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
- 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
2. Hemolytic anemia
• Decreased levels of erythrocytes in
circulating blood (anemia) because of
their acclerated destruction
(hemolysis)
• A red blood cell survives 90 to 120
days (on average) in the circulation,
therefore about 1% of human red
blood cells break down each day.
3. • The spleen (part of the reticulo-endothelial
system) is the main organ which removes old
and damaged RBCs from the circulation.
• In health, the breakdown and removal of RBCs
from the circulation is matched by the
production of new RBCs in the bone marrow.
4. • When the rate of breakdown
increases, the body compensates by
producing more RBCs, but if
compensation is inadequate clinical
problems can appear and so anemia
can develop.
5. • The breakdown products of
hemoglobin will accumulate in the
blood causing jaundice and be
excreted in the urine causing the
urine to become dark brown in
colour.
6. Signs of hemolytic anemia: History
• Onset/ duration (hereditary versus
acquired)
• History of fatigue or jaundice
• Abdomen pain (chronic hemolysis)
• Medications or food /ie fava bean/(may
exacerbate enzyme deficiencies)
7. • Travel (consider infection)
• Blood loss or sequestration (increases
reticulocytes in the absence of
hemolysis)
• Discolored urine (intravascular
haemolysis)
• Complete family history (jaundice,
gallbladder disease, splenectomy)
8. Signs of hemolytic anemia: Physical
• Symptoms of anemia
• Jaundice
• Pallor
• Splenomegaly / hepatosplenomegaly
9. Laboratory findings:
Peripheral blood smear microscopy:
• Fragments of the red blood cells
("schistocytes") can be present
• Spherocytes
• Increased reticulocytes
• Normoblasts can be present.
• The level of unconjugated bilirubin in
the blood is elevated.
• The level of lactate dehydrogenase
(LDH) in the blood is elevated
10. Laboratory findings(2)
• Haptoglobin, hemopexin levels are
decreased
• Iron level in the blood is elevated.
• The direct Coombs test is positive, if
hemolysis is caused by an immune
process.
• Free hemoglobin, methemalbumin
elevated level in the blood.
• hemosiderin in the urine indicates
chronic intravascular hemolysis.
13. Classification of hemolytic anemias
===Acquired===
• ''Immune mediated hemolytic anemia''' (direct
Coombs test is positive)
Autoimmune hemolytic anemia
• Warm antibody autoimmune hemolytic anemia
(Ab binds at 37degree Celsius)
▫ Idiopathic
▫ Systemic lupus erythematosus (SLE)
▫ Evans' syndrome (antiplatelet antibodies
and hemolytic antibodies)
14. • Cold antibody autoimmune hemolytic
anemia
(Ab binds at 4degree Celsius)
▫ Idiopathic cold hemagglutinin syndrome
▫ Infectious mononucleosis and
mycoplasma ( atypical) pneumonia
▫ Paroxysmal cold hemoglobinuria.
(Rare cause seen in children in association with cong
syphilis)
15. Classification of hemolytic anemia
===Acquired===
'
• Alloimmune hemolytic anemia
• Hemolytic disease of the newborn (HDN)
▫ Rh disease (Rh D)
▫ ABO hemolytic disease of the newborn
▫ Anti-Kell hemolytic disease of the newborn
▫ Rhesus c hemolytic disease of the newborn
▫ Other blood group incompatibility (RhC,
Rhe, RhE, Kidd antigen system, Duffy
antigen, MN, P and others)
16. • Alloimmune hemolytic blood transfusion
reactions (ie from a non-compatible blood type)
• Drug induced immune mediated
hemolytic anemia
• Penicillin (high dose)
• Methyldopa
17. Coombs Test
• Typical screening is with broad
spectrum reagent.
• Contains antibodies directed at both
human immunoglobulin and
complement components
32. Hemolytic anemia (complications)
• Clinical course may be complicated with
Crisis:
▫ Hemolytic Crisis: associated with
infection
▫ Aplastic crisis: associated with
Parvovirus infection
33. Differential diagnosis
* ''Ineffective hematopoiesis'' is sometimes
misdiagnosed as hemolysis.
• Clinically these conditions may share many features
of hemolysis
• Red cell breakdown occurs before a fully developed
red cell is released into the circulation.
• Examples: myelodysplastic syndrome, megaloblastic
anemia.
34. Hereditary Spherocytosis
1. Inherited as autosomal dominant
2. red cell membrane protein defects
(Deficiency of Beta Spectrin or Ankyrin)
3. Family history
4. Clinical features: jaundice,
gallstones, splenomegaly.
35. • 5. Laboratory features
- hemolytic anemia
- microspherocytes
- abnormal osmotic fragility test
- negative direct Coombs test
- increased MCHC
39. Hereditary Elliptocytosis
• Equatorial Africa, SE Asia
• AD / AR
• Functional abnormality in one or more anchor
proteins in RBC membrane- Alpha spectrin ,
Protein 4.1
• Usually asymptomatic
• Mx: Similar to H. spherocytosis
• Variant:
3.SE-Asian ovalocytosis:
Common in Malaysia , Indonesia…
Asymptomatic-usually
Cells oval , rigid ,resist invasion by malarial parasites
41. SICKLE CELL ANEMIA
Definition: chronic hemolytic anemia
characterized by sickle-shaped red
cells(RBCs) caused by homozygous
inheritance of Hemoglobin S
42. SICKLE CELL ANEMIA-pathogenesis
- In HbS, valine is substituted for glutamic acid in
the sixth amino acid of the ß chain.
- Deoxy-HbS is much less soluble than deoxy HbA;
it forms a gelatinous network of fibrous polymers that
cause RBCs to sickle at sites of low pO2.
- Hemolysis - because sickle RBCs are too fragile to
withstand the mechanical trauma of circulation
- Occlusion in microvascular circulation caused by
distorted, inflexible RBCs adhering to vascular
endothelium
43. SICKLE CELL ANEMIA-incidence
- Homozygous - about 0.3% of blacks
in the USA
(have sickle cell anemia)
- Heterozygotes 8-13% of blacks, (are
not anemic, but the sickling can be
demonstrated in vitro)
44. SICKLE CELL ANEMIA-clinical features
IN HOMOZYGOTES
1. Clinical complications due to severe hemolytic anaemia
- slow growth and development in children
- gall bladder stones
- aplastic crisis
- congestive heart failure from chronic anemia and
cardiac overload compensation
2. Consequences of vaso-occlusion of the microcirculations
(tissue ischemia and infarction)
- infarction of spleen, brain, kidney, lung, aseptic
necrosis, central nervous system and ophtalmic vascular
lesions
45. SICKLE CELL ANEMIA
laboratory findinges
1. Anemia-normocytic or slightly macrocytic
2. Leukocytosis (chronic neutrophilia)
3. Thrombocytosis - usually mild
4. Reticulocytosis
5. Peripheral smear: sickle shaped red cells,
polychromatophilia, Howell-Jolly bodies
6. Hb –electrophoresis or high-performance
liquid chromatography (HPLC)
46. Sickle Cell Disease
• Mutation in beta
globin
(6 Glu Val)
• Inherited as
autosomal recessive
• Protection against
malaria
47. Thalasemias
• Thalasemia result from gene (located on
chromosomes 11 and 16) deletion, abnormalities
in transcription and translation and instability of
the mRNA directing globin synthesis or of the
globin itself.
• Result: imbalanced synthesis of normal globin
chain. The unpaired chain accumulates in the
developing erythroid precursor cell, and toxicity
results – ineffective erythropoiesis, hemolysis
and anemia of variable degree.
49. Different forms of thalassemia
• α thalassemia
• β thalasemia: major, minor (trait), intermedia
• δ/β thalassemia
• Hereditary persistentce of fetal hemoglobin
(HPFH)
50. Hemoglobin
Chains Hgb (g/dl) MCV (fl) Analysis
/ Normal Normal Normal
/- 12-14 75-85 Normal
-/- or 11-13 70-75 Normal with Hgb
Barts (4);
--/ Hgb H (4)
--/- 7-10 50-60 Normal with Hgb
Barts (4);
Hgb H (4)
--/-- - - Not viable
Alpha Thalassemia: Laboratory Findings
51. Beta Thalassemia
Clinical Hgb
Syndrome Genotype Hgb (g/dl) Analysi
Minor (Trait) /+
or /° 10-13 Hgb
A2, Hgb F
Intermedia +
/+
7-9 Hgb
A2, Hgb F
Major(Cooleys) +
/° or °/° < 7 Hgb A2,
Hgb F
52. Beta-Thalassemia major
(Cooley anemia)
• Usually homozygous condition
• Is the most severe variant no beta-chains are synthesized
• Clinical features: severe anemia that appears in the first
year of life; jaundice, hepatosplenomegaly (secondary
neutropenia and thrombocytopenia),
• skin pigmentation and chronic leg ulceration,
• expansions of the erythroid marrow with secondary
body changes (including retarded growth, bossing of
skull, expanded maxilla, widened diploe,
• gross skeletal deformities, spontaneous fractures, dental
problem), increased susceptibility to infection,
symptoms of iron overloading
53. Beta-Thalassemia major
laboratory features
• Severe anemia
• Blood film: anisopoikilocytosis, hypochromia,
target cells, basophilic stippling, reticulocytosis
• Bone marrow: marked erythroid hyperplasia,
increased sideroblasts
• Shortened red cell survival
• Fetal hemoglobin > 90%, HbA absent, HbA2
low/normal/high
54. Red Cell Enzymopathies
1. Glucose-6-Phosphate Dehydrogenase (
G6PD ) Deficiency
▫ Pivotal enzyme in HMP Shunt & produces
NADPH to protect RBC against oxidative
stress
▫ Most common enzymopathy -10% world’s
population
▫ Protection against Malaria
▫ X-linked