Many women experience some minor disorders during pregnancy.
Every system of the body may be affected during pregnancy. These disorders, however , are not minor to the pregnant woman.
Many women experience some minor disorders during pregnancy.
Every system of the body may be affected during pregnancy. These disorders, however , are not minor to the pregnant woman.
Hydatidiform Mole (HM) is a rare mass or growth that forms inside the uterus at the beginning of a pregnancy. It is a type of gestational trophoblastic disease (GTD).
When a normal sperm cell fertilizes one of these oocytes, the resulting embryo has only one set of chromosomes. Because the embryo has no genes from the mother, the pregnancy cannot develop normally, resulting in a hydatidiform mole.
This ppt is made by Mr. arkab khan pathan under guidance of Mrs. RAKHI GOAR. this ppt contain the detail and all the lecture notes of HEG.
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Arkab khan
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
Hydatidiform Mole (HM) is a rare mass or growth that forms inside the uterus at the beginning of a pregnancy. It is a type of gestational trophoblastic disease (GTD).
When a normal sperm cell fertilizes one of these oocytes, the resulting embryo has only one set of chromosomes. Because the embryo has no genes from the mother, the pregnancy cannot develop normally, resulting in a hydatidiform mole.
This ppt is made by Mr. arkab khan pathan under guidance of Mrs. RAKHI GOAR. this ppt contain the detail and all the lecture notes of HEG.
THANK YOU.
Arkab khan
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
IUGR
Intrauterine growth restriction is said to be present in those babies whose birth weight is below the tength percentile of the average for gestational age.
INCIDENCE
Dysmaturity comprised about one third of low birth weight babies.
In developed countries , its overall incidence is about
3-10%
Term babies (5%)
Post term babies (15%)
CAUSES OF IUGR
The causes of IUGR can be grouped as
Maternal causes
Fetal causes
Placental causes
Uterine and Environmental causes.
MATERNAL CAUSES
Pregnancy weight of mother influences the fetal size
Chronic maternal disease condition
Renal disease condition
Malnutrition
Multiple pregnancy
Hypertensive disorders of pregnancy
Severe anemia
Previous baby suffered iugr etc.
FETAL CAUSES
Chromosomal anomalies
Exposure to an infection
German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
Birth defects
(cardiovascular, renal, anencephally, limb defect, etc).
• Placenta or umbilical cord defects.
PLACENTAL FACTORS
Uteroplacental Insufficiency
Fetoplacetal Insufficiency
Abruptio placenta
Placenta previa
Post term pregnancy
UTERINE CAUSES
Septate uterus
Fibroid/ myoma uterus
ENVIRONMENTAL CAUSES
High altitude - lower environmental oxygen saturation
Toxins
PATHOPHYSIOLOGY
Due to maternal and placental causes
Decrease in placental transfer of nutrients and oxygen to the fetus
Resulting in reduced fetal body store of lipids, glycogen
Causes neonatal hypoglycemia
Lack of oxygen
Chronic hypoxia that leads to erythropoietin production
Polycythemia etc
CLASSIFICATION OF IUGR
Based On Pathological Processes
I)Type I- Symmetrical
II)Type II- Asymmetrical
SYMMETRICAL
Symmetric IUGR: (33 % of IUGR Infants)
height, weight, head circumference proportional
early pregnancy insult:
commonly due to congenital infection, genetic disorder, or intrinsic factors
reduced no of cells in fetus
normal ponderal index
low risk of perinatal asphyxia
low risk of hypoglycemia
ASYMMETRICAL
later in pregnancy:
commonly due to utero placental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors
low ponderal index
cell number remains same but size is small
increased risk of asphyxia
increased risk of hypoglycemia
CLINICAL FEATURES OF BABY WITH IUGR AT BIRTH
Weight deficit
Large head circumference
Old man look
Cartilaginous ridges on pinna
Dry wrinkled skin
Length remain unaffected
Open eyes
Well defined creases
Alert and active
Normal reflexes Normal cry
Thin umbilical
Scaphoid abdomen
Signs of recent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumference • Signs of long term growth failure - Widened skull sutures, large fontanelles - shortened crown – heel length - delayed development of epiphyses
Normal reflexes Normal cry
Thin umbilical
Scaphoid abdomen
Biochemical changes in pregnancy, Physiological changes in pregnancy, maternal and fetal health assessment, assessment of complications in pregnancy, hormonal changes and physiological evaluations in pregnancy
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
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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.
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.
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
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
- 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
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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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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.
6. Stages
• Stage I (Hyperplasia)
- 4 to 20 weeks
- Rapid mitosis
- Increase of DNA content
7. Stages
• Stage II (Hyperplasia & Hypertrophy)
- 20 to 28 weeks
- Declining mitosis.
- Increase in cell size.
8. Stages
• Stage III ( Hypertrophy)
- 28 to 40 weeks
- Rapid increase in cell size.
- Rapid accumulation of fat, muscle and
connective tissue.
• 95% of fetal weight gain occurs during last
20 weeks of gestations.
13. FETAL FACTORS
• A Chromosome Defect In second trimester 20% SGA fetuses have
chromosomal abnormality
Triploid is most common under 26 wks.
Trisomy-18 is common after 26 wks .
Other are 21(Down’s syndrome), 16, 13, xo
(turner’s syndrome).
14. FETAL FACTORS
• Exposure to an infection• German measles (rubella),
cytomegalovirus, herpes simplex,
tuberculosis, syphilis, or toxoplasmosis,
TB, Malaria, Parvo virus
15. FETAL FACTORS
• birth defects
• (cardiovascular, renal, anencephally, limb
defect, etc).
• A primary disorder of bone or cartilage.
• A chronic lack of oxygen during
development (hypoxia
• Placenta or umbilical cord defects.
16. PLACENTAL FACTORS
• Uteroplacental Insufficiency
Resulting From -.
– Improper / inadequate trophoblastic
invasion and placentation in the first
trimester.
– Lateral insertion of placenta.
– Reduced maternal blood flow to the
placental bed.
17. PLACENTAL FACTORS
• Fetoplacetal Insufficiency Due To-.
– Vascular anomalies of placenta and
cord.
– Decreased placental functioning mass-.
• Small placenta, abruptio placenta,
placenta previa, post term pregnancy
20. Environmental Causes of IUGR
• High altitude - lower environmental oxygen
saturation
• Toxins
21. Types of IUGR
• Symmetric IUGR:
(33 % of IUGR Infants)
• Asymmetric IUGR
(55 % of IUGR)
• Combined type IUGR:
(12 % of IUGR)
22. SYMMETRICAL
• height, weight, head circ proportional
• early pregnancy insult:
• commonly due to congenital infection,
genetic disorder, or intrinsic factors
• Reduced no of cells in fetus
• normal ponderal index
• low risk of perinatal asphyxia
• low risk of hypoglycemia
23. PONDERAL INDEX
• The ponderal index is used determine
those infants whose soft tissue mass is
below normal for their stage of skeletal
development.
Ponderal Index =
birth weight x 100
crown-heel length
24. PONDERAL INDEX
• Typical values are 20 to 25.
• Those who have a ponderal index below
the 10th % can be classified as SGA
• PI is normal in symmetric IUGR.
• PI is low in asymmetric IUGR
25. ASSYMETRICAL
• later in pregnancy:
• commonly due to utero placental
insufficiency, maternal malnutrition,
hypoxia, or extrinsic factors
• low ponderal index
• Cell number remains same but size is
small
• increased risk of asphyxia
• increased risk of hypoglycemia
26. • Growth restriction in the stage of
hypertrophy
• Brain sparing effect
• Head growth remains normal but
abdominal girth slows down
27.
28.
29.
30. Newer Classification: 1. Normal Small Fetuses-
Have no structural abnormality,
normal umbilical artery & liquor but
wt., is less.
They are not at risk and do not need any
special care.
31. Abnormal Small Fetuses- have
chromosomal anomalies or structural
malformations. They are lost cases and
deserve termination as nothing can be
done.
Growth Restricted Fetuses- are due to
impaired placental function. Appropriate &
timely treatment or termination can
improve prospects.
36. • Signs of recent wasting
- soft tissue wasting
- diminished skin fold thickness
- decrease breast tissue
- reduced thigh circumference
• Signs of long term growth failure
- Widened skull sutures, large
fontanelles
- shortened crown – heel length
- delayed development of epiphyses
37. PREDICTION OF IUGR
• History
risk factors
last menstrual period - most precise
size of uterus
time of quickening (detection of
fetal movements)
• Examination /
38. MATERNAL SERUM
SCREENING
• AFP
• more for gestation in the absence of fetal
anomaly, there is a 5-10 fold increase in
the risk of FGR
39. • Uterine Artery Doppler Velocimetry
- Notching of the waveform /reduce
EDF
associated 3-fold increase in risk of
FGR.
• Bright or echogenic fetal bowel in the
second trimester is associated with
increase risk of FGR.
40. • Combination of un-explain elevated
maternal AFP is powerful predictor of
adverse perinatal outcome (FGR)
• Increase AFP combine with echogenic
bowel is strong predictor of FGR
41.
42. • DOPPLER OF THE UMBILICAL ARTERY
• Reduced end diastolic flow.
•
Absent end diastolic flow
•
Reversed end diastolic flow( severe
cases)
43.
44. Problems
• Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration
• Thermoregulation
- Hypothermia due to diminished
subcutaneous fat and elevated
surface/volume ratio
45. Metabolic
- Hypoglycemia
- result from inadequate glycogen
stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level,
which stimulate calcitonin excretion
46. • Hematologic
- hyperviscosity and polycythemia due to
increase erythropoietin level sec. to
hypoxia
• Immunologic
- IUGR have increased protein catabolism
and decreased in protein, prealbumin and
immunoglobulins, which decreased
humoral and cellular immunity.
47. • Fetal distress,
• Hypoxia, Acidosis and Low Apgar Score
at birth.
Increased perinatal morbidity and mortality
•
Grade 3-4 intraventricular haemorrhage
•
Necrotizing enterocolitis
57. MEDICAL
• ASPIRIN THERAPY
• Other forms of treatment that have been
studied are
• nutritional supplementation,
• zinc supplementation,
• fish oil,
• hormones and
• oxygen therapy