This document discusses seizures in neonates. It begins by defining seizures, convulsions, and epilepsy. It then notes that seizures are most common in neonates, occurring in 0.5-0.8% of term babies and 6-12% of babies under 1500g. Common causes of neonatal seizures include hypoxic ischemic encephalopathy, intracranial hemorrhage, infections, inborn errors of metabolism like hypoglycemia and hypocalcemia, and epilepsy syndromes. The immature neonatal brain is more excitable and prone to seizures due to reduced connectivity, an imbalance toward excitatory processes, and the excitatory effect of GABA in some regions. The document describes different seizure types and discusses
Neonatal seizures, dr amit vatkar, pediatric neurologistDr Amit Vatkar
In the presentaion i will give you a brief idea to apprach, diagnosis and management of neonatal seizures.
The most prominent feature of neurologic dysfunction in the neonatal period is the occurrence of seizures. Determining the underlying etiology for neonatal seizures is critical. Etiology determines prognosis and outcome and guides therapeutic strategies.
Neonatal seizures, dr amit vatkar, pediatric neurologist
Neonatal seizures, dr amit vatkar, pediatric neurologistDr Amit Vatkar
In the presentaion i will give you a brief idea to apprach, diagnosis and management of neonatal seizures.
The most prominent feature of neurologic dysfunction in the neonatal period is the occurrence of seizures. Determining the underlying etiology for neonatal seizures is critical. Etiology determines prognosis and outcome and guides therapeutic strategies.
Neonatal seizures, dr amit vatkar, pediatric neurologist
Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of hypoxic ischemic encephalopathy (HIE) . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Presentation with extensive details of neonatal seizure. Covering its etiology, diagnosis and treatment . Neonatal seizure is one of the commonest clinical situation faced by any one working in a neonatal unit. Furthermore it is a favourite topic of many examiners in MD/DCH/DNB Pediatrics exams.
Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of hypoxic ischemic encephalopathy (HIE) . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Presentation with extensive details of neonatal seizure. Covering its etiology, diagnosis and treatment . Neonatal seizure is one of the commonest clinical situation faced by any one working in a neonatal unit. Furthermore it is a favourite topic of many examiners in MD/DCH/DNB Pediatrics exams.
Seizure disorder is one of the important topic in children and adult also. here i explained the seizure disorder in pediatrics, include all most content for nurses level
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.
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
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.
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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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.
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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.
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
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
2. SEIZURES: A seizure is a transient occurrence
of signs and/or symptoms resulting from
abnormal excessive or synchronous neuronal
activity in the brain.
CONVULSIONS: Motor component of seizures.
EPILEPSY: It is a disorder of the brain
characterised by an enduring predisposition
to generate seizures and by the
neurobiologic, cognitive, psychological and
social consequences of this condition.
3. Seizures occur more frequently in the
neonatal period than at any other time of life.
Neonates are at risk for development of
seizures because, metabolic, toxic, structural
& infectious diseases are more likely to
manifest during this period.
Incidence: 0.5-0.8% in term babies & 6-12%
in babies weighing < 1500g
85% occur during first 15 days with 65%
between 2-5th day of life.
4. The immature brain has many differences
from the mature brain that render it more
excitable and more likely to develop seizures.
1. REDUCED CONNECTIVITY OF NEONATAL BRAIN-
GENERALISED TYPE OF SEIZURES RARE.
Arborization of axons and dendritic process as
well as myelination is incomplete.
Neonatal cortex has near complete neuronal
component but relative paucity of dendrites and
synaptic connections.
5. Neuronal membranes are leaky & allow Na+ and
K+ to move easily across cell membrane. Thus they
remain hyperpolarized, making it more difficult for
the epileptic neuron to have rapid and repetitive
firing and to permit recruitment of other neurons
for synchronous discharge.
2. THE BALANCE OF EXCITATORY AND INHIBITORY
PROCESSES IN IMMATURE BRAIN IS MORE TOWARDS
EXCITATION.(More glutamate synapses with
increased NMDA and AMPA receptor density.)
6. 3. IN SOME REGIONS OF THE NEONATAL BRAIN,
GABA TEMPORARILY ACTS AS AN EXCITATORY
NEUROTRANSMITTER.
8. Seizure with consistent EEG event:
Focal clonic, focal tonic and some myoclonic seizures.
They are clearly epileptic and are likely to respond to
treatment
Clinical seizures with inconsistent EEG events:
All GTCS, subtle seizures and some myoclonic seizures.
These infants tend to be neurologically depressed of
comatose &are associated with HIE. Seizures are non
epileptic in origin and do not Require or respond to
conventional antiepileptics.
Electrical seizures with absent clinical seizures:
May occur in encephalopathic infants not on AED
Persistent electrical changes after initiation of AED
10. Subtle seizures: Most common type of neonatal
seizures. More common in preterms.
Chewing, blinking, nystagmus, peddling,
bicycling, hyperopnea, tachycardia, hypertension
episodes, apnea.
Oral, facial and lingual phenomenon are common due
to advanced maturation of the limbic system.
11. Clonic seizures: focal/ multifocal.
Stereotypic, repeated biphasic movements
with fast contraction & slow relaxation
Unifocal -infarct
-SAH
-metabolic
Multifocal: nonjacksonian, migrating
Generalised clonic seizures are uncommon in
neonatal period.
12. Tonic seizures: Rigid posturing with tonic eye
deviation
Focal :sustained posturing of a limb
Generalized: mimic decorticate / decerebrate
posturing
MC in premature infants with diffuse neurologic
dysfunction or IVH; kernicterus.
Poor prognosis
13. Myoclonic seizures: sudden jerky movements
produced by episodic contractions of a group
of muscles.
Rapid jerks and non rhythmic
Focal: MC flexor group of upper limbs
Multifocal: asynchronous twitching of several
parts of body
Generalized: commonly associated with EEG
changes.
14. Spasms: sudden generalized jerks lasting 1-2
sec.
Distinguished from generalized tonic spells by
their shorter duration and usually associated
with a single, very brief, generalized
discharge.
15.
16. CNS:
Hypoxic ischemic encephalopathy
Intracranial haemorrhage
CNS infections
CNS malformations:
Neuronal migration disorders
Cerebral dysgenesis
Neurocutaneous disorders
Maternal drug withdrawl
Local anaesthetic intoxication into infant scalp
Kernicterus
19. Commonest cause- 50% of the cases
Can be global as in perinatal asphyxia/
focal ischemia (MCA stroke)
In perinatal asphyxia, history s/o difficult
labour, decreased umbilical artery ph, APGAR
score of <5 at 5 mins.
Focal seizures <1 min,very frequent esp in 1st
24 hrs of life.
20. 10 to 15% of the cases
Subarachnoid :
May be the result of trauma, deliveries with
instrumentation.
More common in premature.
Seizures on 2nd day of life
good prognosis.
Intraventricular / parenchymal:
more common among prematures
Tonic type, occur within day 3 of life.
poor prognosis
21. Subdural:
More likely due to trauma in a large baby and
after breech delivery.
Occur due to tear of falx, tentorium, or
superficial cortical veins.
Bleeding occurs during first few days of life.
22. 5% of the cases
Postnatal sepsis:Bacterial/ fungal/viral
TORCH infections
23. Ionised calcium: <4.4mg/dl-term & >1.5kg
<4mg/dl- preterms <1.5kg
Early: <3 days of life
associated with prematurity, IUGR,
asphyxia, infants of diabetic mothers
Late: >10 days of life
may be d/t cow milk feeding,
hypoparathyroidism, DiGeorge syndrome,
hypomagnesemia.
24. Seizures usually occur once the feeds are
introduced.
Convulsions may be intractable to Rx.
H/O affected previous sibling may be present.
Associated features like vomiting, severe
jaundice, Hepatospleenomegaly, virilization &
malodorous urine, hypotonia, metabolic
acidosis ( anion gap) may be present.
HYPERGLYCENEMIA: Myoclonic events
d/t defect in glycine cleavage, glycine
acts as co agonist with glutamate.
25. PYRIDOXINE DEPENDENCY:
Rare cause of Seizure in NB.
Prolonged maternal intake of B6.
decreased levels of Pyridoxal-5-phosphate
in CSF and increased serum pipecolic acid.
Deficiency in binding of coenzyme to GABA
may be the primary cause.
Present as intractable seizures within 1st 12
hrs.(may occur in utero)
Responds to 50-100mg of pyridoxine.
26. BENIGN FAMILIAL NEONATAL SEIZURES
BENIGN INFANTILE NEONATAL SEIZURES-
FIFTH DAY FITS
EARLY MYOCLONIC EPILEPSY
EARLY INFANTILE EPILEPTIC
ENCEPHALOPATHY- Ohtahara syndrome
MALIGNANT MIGRATING PARTIAL SEIZURES IN
INFANCY- Coppola syndrome