This document discusses red blood cell membrane defects and osmotic fragility testing. It begins by introducing the structure and components of the red blood cell membrane, including integral proteins, lipids, and peripheral proteins that make up the cytoskeleton. Key membrane defects are then described, such as hereditary spherocytosis caused by weakened interactions between membrane proteins, and hereditary elliptocytosis caused by defects in spectrin. The document concludes by explaining how the osmotic fragility test measures red blood cell resistance to lysis in saline solutions of varying concentrations to evaluate membrane stability and defects.
This presentation is focused on diagnostic utility of Red blood cell indices which will be very useful for undergraduate and postgraduate of medical field.
I have listed out the LE cells structure and Microscopical examinaton of LE CELLS, Difference between tart cells and le cells, clinical symptoms and diagnostic procedure.
This presentation is focused on diagnostic utility of Red blood cell indices which will be very useful for undergraduate and postgraduate of medical field.
I have listed out the LE cells structure and Microscopical examinaton of LE CELLS, Difference between tart cells and le cells, clinical symptoms and diagnostic procedure.
Hijama (Arabic: حجامة lit. "sucking") is the Arabic term for wet cupping, where blood is drawn by vacuum from a small skin incision for therapeutic purposes.The practice has Greek and Persian origin and is mentioned by Hippocrates.
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.
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.
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.
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
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.
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.
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.
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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
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
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Osmotic fragility & rbc membrane defects 050916
1. Osmotic Fragility &
RBC Membrane
Defects
Dr Anwar H Siddiqui
Ph.D. Scholar
Department of Physiology, J N Medical College, AMU, Aligarh
Physiology Presentation
05-09-2016
2. Meet The Red Cell
Shaped like a flattened, bilaterally
indented sphere, a biconcave disc
In fixed, stained blood smears,
erythrocyte appears circular, with a
diameter of about 7 to 8 μm and an area
of central pallor.
Average values for the mean cellular
volume in normal subjects range from 80
to 100 fl.
Highly elastic and deformable.
The normal mature erythrocyte as
visualized by the scanning electron
microscope (×9,800). (Courtesy of Dr.
Wallace N. Jensen.)
The erythrocyte can pass through a vessel of about 3 μm in maximum
diameter
3. Meet The Red Cell
► Durability of Red cell is remarkable
► No nucleus to direct regenerative
processes
► No mitochondria available for efficient
oxidative metabolism
► No ribosomes for regeneration of lost
or damaged protein
► No de novo synthesis of lipid
Images of red blood cells
(top) and a human hair
(bottom) taken with a
confocal microscope
Still survives for 120
days!!!
4. Red Cell Membrane Structure
Erythrocyte membrane that is normal in structure and
function is essential to survival of red cell
Accounts for the cell's antigenic characteristics
Maintains stability and normal discoid shape of cell
Preserve cell deformability
Retain selective permeability
5. Red Cell Membrane Structure
► The red cell membrane consists of:
Proteins 52%
Lipids 40%
Carbohydrates: 8%
Laminated structure consisting of an outer lipid bilayer and a
two dimensional network of spectrin-based cytoskeleton.
Cytoskeleton through linking proteins interacts with
cytoplasmic domains of membrane proteins.
6. The Red Cell Membrane
Integral Proteins
Lipid Bilayer
Anchoring
Proteins
Cytoskeletal
Proteins
7. The Membrane Lipids
Virtually all of the lipids in the mature erythrocyte are
found in the membrane.
Refrence: Wintrobes Hematology
8. The Membrane Lipids
The 5 major phospholipids are
asymmetrically disposed, as shown
below:
Outer monolayer
Phosphatidylcholine (PC);
Sphingomyelin (SM).
Inner monolayer
Phosphatidylethanolamine (PE)
Phosphoinositol (PI).
Phosphatidylserine (PS);
9. The Membrane Lipids• Macrophages recognize
and phagocytose red cells that
expose PS at their outer surface.
• An exposure of PS can potentiate
adhesion of red cells to vascular
endothelial cells.
• PS can regulate membrane
mechanical function, due to their
interactions with skeletal proteins
such as spectrin and protein 4.1R.
The maintenance
of an asymmetric
phospholipid
distribution in the
bilayer is critical.
Premature destruction of thallassemic and sickle red cells has been linked to
disruptions of lipid asymmetry leading to exposure of PS
10. Membrane Proteins
Integral proteins
• Embedded in membrane via hydrophobic interactions with lipids.
Peripheral proteins
• Located on cytoplasmic surface of lipid bilayer, constitute membrane skeleton.
• Anchored via integral proteins
• Responsible for membrane elasticity and stability.
11. Integral Proteins
The red blood cell membrane proteins organized according to
their function:
Transport Proteins Cell Adhesion Protein Structural Proteins
AE1- the anion-exchange
protein, (formerly knows as Band 3)
ICAM-4- interacts with
integrins
Glycophorins - Imparts a
negative charge to the cell,
reducing interaction with
other cells/ endothelium.
•Glycophorin A carry M/N,
Gerbich blood group.
•Glycophorin C and
GlycophorinA, important for P
falciparum invasion of RBC.
Aquaporin 1 – water
transporter, defines
the Colton Blood Group
Glut1 – glucose and L-
dehydroascorbic
acid transporter
Kidd antigen protein – urea
transporter
BCAM – a glycoprotein that
defines the Lutheran blood
groupRhAG – gas transporter
defines Rh Blood Group
ATPase, co transporter &
exchangers
13. Peripheral Proteins
Names Definition Function
1. Spectrin
2. Actin
3. Ankyrin
4. Protein 4.1
5. Protein 4.2
cytoskeletal protein that lines the
intracellular side of the plasma
membrane.
Two subunits:
–Alpha and beta, entwined to form
dimers.
Abundant protein in cell membrane
family of adaptor protein
is a major structural element.
is an ATP-binding protein
Responsible for biconcave
shape of RBC
participates in more protein-
protein interactions
Interacts with band 3 protein
and spectrin to achieve linkage
between bilayer and skeleton.
Stabilises actin-spectrin
interactions.
Regulate the association of
Band 3 with ankyrin.
14. Interactions of RBC Membrane Protein
And Lipids
Disturbed vertical interactions, i.e. disturbed anchoring and membrane
cohesion,
Proteins include: Ankirin, Band 3 ,Glycoporin and Protein 4.2 etc
15. Interactions of RBC Membrane Protein
And Lipids
Disturbed horizontal interactions
Proteins include: Spectrin , Actin
16. Membrane Defects
• Hereditary Spherocytosis
Vertical
Interactions
• Hereditary elliptocytosis Syndrome
• Hereditary elliptocytosis
• Hereditary Pyropoikilocytosis (HPP)
• South East Asian Ovalocytosis
Horizontal
Interactions
17. Hereditary Spherocytosis
HS is a hemolytic disorder characterized by anemia,
intermittent, jaundice, splenomegaly
Most common inherited anemia in Northern European
descent
Prevalence 1/1000-2500
75% autosomal dominant fashion
25% Rarely autosomal recessive
Loss of membrane surface area relative to intracellular
volume
spherical shape decreased deformability splenic destruction
21. Hereditary spherocytosis. A typical Wright-stained peripheral blood smear from a
patient with autosomal dominant hereditary spherocytosis is shown. Small, dense,
round, conditioned spherocytes that lack central pallor are visible throughout
22.
23. Hereditary Elliptocytosis
Syndrome
The HE syndromes are a family of genetically
determined erythrocyte disorders characterized by
elliptical red cells on the peripheral blood smear.
Inheritance of HE is autosomal dominant (except
HPP)
the HE variants occur with an estimated frequency of
1:1,000 to 5,000.
HE has a worldwide distribution, but is more
common in malaria endemic regions with prevalence
approaching 2% in West Africa.
24. The mechanistic basis for decreased membrane
mechanical stability in HE is weakened “horizontal”
linkages in membrane skeleton due either to defective
spectrin dimer-dimer interaction or a defective spectrin-
actin-protein 4.1R junctional complex.
The mechanism by which these protein defects result in
elliptocyte formation is not clear.
26. A B
C
A: Common Hereditary elliptocytosis
B: Hereditary pyropoikilocytosis. Red
cell budding and fragmentation.
C: Southeast Asian ovalocytosis
27. Osmotic Fragility Test
The osmotic fragility test is a measure
of the ability of the red cells to take up
fluid without lysing.
It is a test to measures red blood cell
(RBC) resistance to hemolysis when
exposed to a series of increasingly
dilute saline solutions.
28. The primary factor affecting the osmotic fragility
test is the shape of the red cell, which, in turn,
depends on the
1. Volume
2. Surface area
3. Functional state of the red blood cell
membrane.
29. Increased Surface – To – Volume Ratios:
• more resistant to hemolysis and has decreased fragility
• The larger the amount of red cell membrane (surface
area) in relation to the size of the cell, the more fluid the
cell is capable of absorbing before rupturing . As
• Example:
Iron-deficiency anemia
Thalassemia
Sickle cell anemia
Liver disease and any condition associated with the presence of target
cells
30. Decreased Surface – To – Volume Ratios:
• Increased osmotic fragility (decreased
resistance to lysis) is found in
• hemolytic anemias
• hereditary spherocytosis
• And whenever spherocytes are found
31. Apparatus And Materials
Tube Method
Wood or metal test tube rack with 12 clean, dry, 7.5 cm × 1.0 cm
glass test tubes. •Glass marking pencil. •Glass dropper with a
rubber teat.
Sterile swabs moist with alcohol. •2 ml syringe with needle.
Freshly prepared 1 percent sodium chloride solution. •Distilled
water.
Slide Method
Fresh Saline solutions of 0.4%, 0.9% and 4.0% strength.
Sterile swabs moist with alcohol. •2 ml syringe with needle.
Glass slides with cover slips
Microscopes
32. Procedure (Tube Method)
Number the test tubes from 1 to 12 with the glass-marking pencil
and put them in the rack.
Using the glass dropper, place the varying number of drops of 1%
saline in each of the 12 test tubes as shown below. Then add the
number of drops of distilled water to each of the 12 tubes, as
shown
33. Draw 2 ml of blood from a suitable vein and gently eject one
drop of blood into each of the 12 tubes.
Mix the contents gently by placing a thumb over it.
Leave the test tubes undisturbed for few minutes.
Observe the extent of hemolysis in each tube by holding the
rack at eye level, with a white paper sheet behind it.
34. Observation and Result
tube # 1 (normal saline), and tube # 12 (distilled water) will act as
controls, i.e. no hemolysis in normal saline (# 1) and complete
hemolysis in distilled water (# 12).
The test tubes in which no hemolysis has occurred, the RBCs will settle
down and form a red dot (mass) at the bottom of the tube, leaving the
saline above clear.
Some hemolysis, the saline tinged red with Hb, with the unruptured
cells forming a red dot at the bottom.
The test tubes with complete hemolysis, the saline will be equally deep
red with no red cells at the bottom of these tubes.
35. Observation and Result
Express the result in % saline.
Hemolysis begins in ..... % saline.
Hemolysis is complete in ..... % saline.
36. Procedure (Slide Method)
Saline solutions of 0.4%, 0.9% and 4.0% strength are prepared.
One drop of each solution is put on three separate slides and
one drop of blood is put on each drop of the solutions.
Put a coverslip and observe all the slides for the shape of RBC’s
under high power of microscope.
37. Normal Range :Initial hemolysis for normal erythrocytes will begin at
0.45 ± 0.05 % NaCl and hemolysis will be complete at 0.30 ± 0.05 % NaCl
38. When red cells become more fragile, hemolysis may begin at about 0.64%
saline and be complete at about 0.44% saline.
When red cells are less fragile, hemolysis starts and is complete at lower
strengths of saline.
39. Plotting the OF graph
The results of the test may then be graphed, with the percent
hemolysis plotted on the ordinate (vertical axis) and the sodium
chloride concentration on the abscissa (horizontal axis)
Carefully transfer the supernatants to cuvettes and read on a
spectrophotometer at a wavelength of 540 nm.
Set the optical density at 0, using the supernatant in test tube #1,
which represents the blank, or 0% hemolysis. Test tube #14 represents
100% hemolysis.
Calculate the percent hemolysis for each supernatant as follows:
Percent of hemolysis = (O.D. of supernatant/ O.D. supernatant tube
#14) x 100
40.
41. A normal Osmotic Fragility test does not exclude HS
Sensitivity 68% fresh, 81% incubated
42. Other Tests
EMA binding test
Flow cytometry of red cells labeled with eosin-5’-maleimide (EMA)
HS: sensitivity 93%, specificity 99%
Cryohemolysis Increased susceptibility of HS RBCs to rapid cooling
(37 to 4°C) in hypertonic solutions
Sensitivity 95%, Specificity 95-96%
Ektacytometry
RBCs suspended in viscous solution as defined values of shear stress applied
by ektacytometer, a laser-diffraction viscometer
SDS-Page Electrophoresis
Sodium Dodecyl suphate Polyacrylamide gel electrophoresis
Genetic sequencing