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.
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.
challenges in interpreting abnormal hemoglobin study- the key is to correlate with patient age, ethnicity,RBC indices & morphology findings. Two tier approach for correct characterization of abnormal hemoglobins of HPLC &/or capillary electrophoresis.
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.
challenges in interpreting abnormal hemoglobin study- the key is to correlate with patient age, ethnicity,RBC indices & morphology findings. Two tier approach for correct characterization of abnormal hemoglobins of HPLC &/or capillary electrophoresis.
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.
It is fluid which is present
in the pericardial cavity of
heart b/w parietal pericardium n visceral pericardium.
The pericardial cavity is a
potential space lined by
mesothelium of the visceral n parietal pericardium.
This presentation is focused on diagnostic utility of Red blood cell indices which will be very useful for undergraduate and postgraduate of medical field.
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.
It is fluid which is present
in the pericardial cavity of
heart b/w parietal pericardium n visceral pericardium.
The pericardial cavity is a
potential space lined by
mesothelium of the visceral n parietal pericardium.
This presentation is focused on diagnostic utility of Red blood cell indices which will be very useful for undergraduate and postgraduate of medical field.
Neonatal jaundice occurs in 60% of term and 80% of preterm babies. Despite Neonatal jaundice is one of the commonest neonatal conditions, there are no national practice guidelines for its management in our country. Lack of uniform guidelines and standard practice parameters for diagnosis and management of neonatal jaundice often leads many babies to develop unnoticed hyperbilirubinemia causing kernicterus and long term poor neurological sequelae. This review after briefly discussing the epidemiology and pathophysiology of neonatal jaundice provides evidence-based pragmatic guidelines for the diagnosis and management of neonatal jaundice in resource-limited countries like Afghanistan
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
Biotin (vitamin b7) biological functions, clinical indications and its techn...rohini sane
An illustrative presentation on Biotin (Vitamin B7), clinical indications and technological applications for Medical, Dental, Pharmacology & Biotechnology students to facilitate easy- learning.
An illustrative and lucid presentation on Scurvy (deficiency of vitamin C) for Medical, Dental, Pharmacology & Biotechnology students to facilitate easy- learning.
An illustrative presentation on Vitamin C (Ascorbic acid) and Scurvy for Medical, Dental, Pharmacology & Biotechnology students to facilitate easy- learning.
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
Urinalysis for detection of abnormal constituentsrohini sane
An illustrative presentation on Urinalysis for detection of abnormal constituents for medical ,dental , pharmacology and biotechnology students to facilitate easy-learning.
Urinalysis for detection of normal inorganic and organic constituentsrohini sane
An illustrative presentation on urinalysis for detection of normal inorganic and organic constituents for medical, dental , pharmacology and biotechnology students to facilitate easy-learning.
Biochemical kidney function tests with their clinical applicationsrohini sane
An illustrative presentation on Biochemical kidney function tests with their clinical applications for medical ,dental, pharmacology and biotechnology student to facilitate easy-learning.
A comprehensive presentation on Total parenteral nutrition(TPN) to facilitate easy -learning for medical , dental , pharmacology and biotechnology students.
Nutritional management of clinical disordersrohini sane
A lucid presentation Nutritional management of clinical disorders to facilitate easy-learning for medical , dental , pharmacology and biotechnology students.
Nutritional importance of vitamins and mineralsrohini sane
A lucid presentation on Nutritional importance of vitamins and minerals for medical , dental , pharmacology and biotechnology students to facilitate easy-learning.
A lucid presentation on Basal metabolic rate ( BMR) and nutrition for medical ,dental ,pharmacology and biotechnology students to facilitate easy-learning.
Physical activity of the human body and nutritionrohini sane
A lucid presentation on Physical activity of the human body and Nutrition for medical ,dental ,pharmacology and biotechnology students for easy learning.
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.
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.
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
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
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
2. Fetal hemoglobin ( Hb F )
Hb 2 Alpha (α )chains & 2 Gamma(γ ) or Delta (δ ) chains ( delta chain 146
amino acids , 39amino acids differ from beta chain –embryonic hemoglobin)
Physical chemical properties of Hb F :
1. Increased solubility of Deoxy HbF
2. slower electrophoretic mobility
3. Increased resistance of Hb F to alkali denaturation
4. Decreased interaction with 2,3 BPG
5. Hereditary persistence of HbF ( HPF ) increased HbF without Thalassemia,
no DELTA BETA gene switching
6. Kleihauer staining for Hb F detection
3. Fetal hemoglobin ( HbF )
• HbF has two γ globin chains carrying less positively charged amino acids.
• Therefore HbF exhibits weak binding affinity towards 2,3 BPG ( negatively
charged ).
• HbF has higher affinity for O₂ compared to adult Hb.
• Binding affinity for O₂ of HbF > HbA (This property of HbF helps to transfer
of O₂ from maternal blood to fetus as HbFO ₂)
• Delivery of O₂ to fetus is important function of fetal hemoglobin .
14. Rh- incompatibility
• This condition results from incompatibility between maternal & fetal blood
group. Antigen D existing on membrane of fetal RBC (Rh positive fetus)
induces synthesis of antibodies (anti –D ) in Rh negative mother . In Rh
incompatibility ,the first child often escapes . But in second pregnancy , Rh
antibodies will pass from mother to the fetus. Rh antibodies start destroying
fetal red cells even before birth.
• Sometimes ,the child is born with severe hemolytic disease referred to as
Erythroblastosis Fetalis .
• When bilirubin levels are more than 20 mg/dl ,the capacity of albumin to bind
to bilirubin is exceeded.
• Free bilirubin passes through blood brain barrier and enters the brain.
(Kerniecterus)
• Bilirubin gets deposited in brain leading to mental retardation,fits ,toxic
encephalitis & spasticity.
15. Rh- incompatibility
• If the newborn develops hemolytic disease ( HDN ),the child may be
given exchange transfusion along with phototherapy and
barbiturates ( induce bilirubin metabolizing enzymes in liver).
• Phototherapy with blue light ( 440nm wavelength ) isomerize
insoluble bilirubin to more soluble non toxic isomer ( Lumirubin ).
These can be easily excreted through urine without conjugation.( in
contrast to bilirubin which cannot be excreted without conjugation )
16.
17.
18.
19. This condition results from incompatibility between maternal & fetal blood group. Antigen
D existing on membrane of fetal RBC(Rh positive fetus) induce synthesis of antibodies (anti
–D ) in Rh negative mother .In Rh incompatibility ,the first child often escapes .
But in second pregnancy , Rh antibodies will pass from mother to the fetus. Rh antibodies
start destroying fetal red cells even before birth.
Rh- incompatibility:1
20. In Rh positive fetus:
RBC carry Antigen D on their membrane.
Rh- incompatibility:1a
21. In Rh negative mother :
RBC don’t carry Antigen D on their membrane.
Rh- incompatibility:1b
24. Rh- incompatibility:4
In Rh incompatibility : Antigens D on membrane of fetal RBC(Rh positive ) induce synthesis
of antibodies ( anti –D ) in Rh negative mother .
33. Hemolytic Disease of Newborn (HDN )
Rh antibodies will pass from mother to the fetus. Rh antibodies start destroying
fetal red cells even before birth.
34. Hemolytic Disease of Newborn (HDN) unconjugated Hyperbilirubinemia
Incompatibility between maternal & fetal blood groups
Anti antibodies ABO(IgM type cannot be transferred to placenta)
Rh incompatibility
Fetus mother
Rh ( +ve ) Rh ( -ve )
RBC RBC elicit immune response Anti-D ( IgG )
Destruction Anti-D ( IgG )
Of fetal
RBC ← Placenta
Second pregnancy ( before birth of fetus –destruction of fetal RBC ) child is born with severe hemolytic disease
Erythroblastosis fetalis
35. Erythroblastosis Fetalis
• Serum Bilirubin > 20 mg/dl no more bound to Albumin
• Bilirubin Brain (Kernicterus-deposition of bilirubin in brain )
• Basal ganglia mental retardation
• ↓ ATPase mitochondria fits ,spasticity ,toxic encephalitis
• Treatment : (1) phototherapy before age < 1 year
isomerization ZZ ZE
(2 ) Blood transfusion
36. • Hemolytic Jaundice
• Causes –
Rh- incompatibility
Hemolysis due to Malaria
Mismatched blood
transfusion,
sickle cell anemia,
• Liver fails to conjugate
excess of Bilirubin
• Therefore
↑unconjugated bilirubin
↑Urobilinogen
↑ stercobilinogen
(brown color stool )
• SGPT / ALP -Normal
• Absence of bilirubin in
Urine
• Hepatic Jaundice
• Causes –dysfunction of
Liver Hepatitis
al infection
poisons/toxins
cirrhosis/CCF
• ↑unconjugated
bilirubin ↑conjugated
bilirubin
↑Urobilinogen
↑ stercobilinogen
(brown color stool )
↑SGPT / ALP
• Obstructive Jaundice
• Gall stone
stool contains fat
unavailability of bile
salts
• ↑conjugated bilirubin
↑Urobilinogen
↓ stercobilinogen
(pale color stool )
↑SGPT / ALP
37.
38.
39. Physiological /Neonatal Jaundice
• Not a truly genetic defect
• Causes : increased hemolysis of RBC with HbF and immature liver
enzyme system for conjugation of bilirubin
• The activity of the enzyme UDP- glucuronyl transferase is low in the
new born.
• The enzyme deficiency is more serious with increasing degree of
prematurity.
40.
41.
42.
43. Fetal hemoglobin ( Hb F )
• Normal Hb F – (2 α 2 γ )
• If α globin not synthesized then synthesis γ & β chain continues
Tetramers (γ ₄ )—Hb Bart
• β ₄ Tetramers (β ₄ )—Hb H
• HbH lack Heme –Heme interaction
44. Hb H & Hb Bart
Hb lack Heme –Heme interaction
Oxygen dissociation curve -Hyperbolic
No delivery of sufficient oxygen to tissue
Fetal death
45.
46. Hereditary persistent fetal Hb( HPFH )
1. Increase in HbF
2. no clinical symptoms
3. Failure to switch over γ gene to β gene
