Chronic Liver Disease in pediatric: a case presentation and discussionDr Abdalla M. Gamal
A presentation from a tutorial about an interesting case that came to the Pediatric Department of Sebha Medical Center and was imaged by the Radiology Department.
The tutorial was a joint effort between Dr Zeinab Salem Ali (from Pediatric Department) and me (from Radiology Department). In her slides, Dr Zeinab presented the case history, examination, investigations, differential diagnosis and discussed the clinical presentation, investigations and management for chronic liver diseases in pediatric patients.In my slides, I discussed the definition, etiology, natural history of this condition and explained the role of imaging in its diagnosis.
These are my slides after some modifications. I added an aknowlegement page to illustrate Dr Zeinab effort and to thank Dr Khaled Aljasem from Pediatric Department for his effort in revising the original presentations and the constructive feedback he provided which improved the quality of the presented material. Then I added a summary for the parts Dr Zeinab has presented to make this powerpoint presentation complete.
This presentation was presented by Dr Zeinab Salem (from Pediatric Department) and me in a joint tutorial between Pediatric Department and Radiology Department of Sebha Medical Center.
Chronic Liver Disease in pediatric: a case presentation and discussionDr Abdalla M. Gamal
A presentation from a tutorial about an interesting case that came to the Pediatric Department of Sebha Medical Center and was imaged by the Radiology Department.
The tutorial was a joint effort between Dr Zeinab Salem Ali (from Pediatric Department) and me (from Radiology Department). In her slides, Dr Zeinab presented the case history, examination, investigations, differential diagnosis and discussed the clinical presentation, investigations and management for chronic liver diseases in pediatric patients.In my slides, I discussed the definition, etiology, natural history of this condition and explained the role of imaging in its diagnosis.
These are my slides after some modifications. I added an aknowlegement page to illustrate Dr Zeinab effort and to thank Dr Khaled Aljasem from Pediatric Department for his effort in revising the original presentations and the constructive feedback he provided which improved the quality of the presented material. Then I added a summary for the parts Dr Zeinab has presented to make this powerpoint presentation complete.
This presentation was presented by Dr Zeinab Salem (from Pediatric Department) and me in a joint tutorial between Pediatric Department and Radiology Department of Sebha Medical Center.
Neuroprotection in preterm infants: hope or utopy?MCH-org-ua
International conference «Actual approaches to the extremely preterm babies: International experience and Ukrainian realities» (Kyiv, Ukraine, March 5-6, 2013)
one of the common pathology of pregnancy which if not get treated in time can lead to death ! Thanks for all the references from where i have made this slides . Most of them are from standard textbooks
This is a presentation detailing facts about abdominal tuberculosis. Intended for healthcare professionals and medical students
Dr Manoj K Ghoda
Gujarat Gastro Group
This lecture is for undergraduates and post graduates. It is a case based discussion, taking the audience from definition of ascites and spontaneous bacterial sepsis to its symptomatology, physical findings, diagnostic algorithm and management of ascites and bacterial peritonitis
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
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.
- 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
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
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
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.
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.
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
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.
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.
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
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Neonatal cholestasis
1. Approach to a case of neonatal Cholestasis
Dr Arif Vora
3rd year resident, B J Medical college
Dr Manoj K Ghoda
2. 2 months old female
Referred for persistent jaundice.
1st by order of birth
FTNVD
No consanguinity
Noted to have jaundice by parents
@ 15 days or so
Reassured by treating pediatrician
Progressive deepening of jaundice
FTT
3. O/E: Deeply jaundice,
No edema or ascites
Liver ++ 2 fingers bellow costal margin
Splenic tip palpable
No visible veins
Diapers were stained yellow,
Stool color on personal inspection was
yellow
4. S. Bil: 10.2, 70% conjugated
ALT: 376 i.u.
GGT: 240 i.u.
ALP: 357 i.u.
S. Alb: 2.81
S. Glob: 2.45
INR: 1.9, corrected to 1.2 after
vit K
Hb: 9.8, normochromic
normocytic picture
WCC: 10,200 with 65% polys
Plt: 150,000
RFT: urea 32, creat: 0.9
HBsAg: Non reactive
HAV: Non reactive
HEV Non reactive
USG: Mild hepatomegaly,
slightly altered
parenchymal pattern,
PV and SV were normal in
size,
Spleen mildly enlarged
GB distended
CBD and IHBR seen and
not dilated
10. Conjugated hyperbilirubinemia in
Neonates and infants: Etiology based
approach
• Pregnancy related
• Structural defects
• Metabolic Diseases
• Viral diseases other than those related to pregnancy
• Unknown
11. Jaundice in Neonates, infants and children:
Approach based on age of onset
• Present at birth
• Appearing sometime after birth and progressively
increasing with or without decompensation,
• Appearing in infancy or early childhood
• Appearing in late childhood
Each category has certain diseases which are
peculiar to that category
12. Based on stool colour
•Creamy white from birth
•Normal yellow at birth and then creamy white
•Intermittently yellow and white
•Yellow all the time
Based on Liver status
•Early decompensation
•Late decompensation
13.
14. So when you see a patient with jaundice, you may
have to process information simultaneously
Jaundice soon after birth….. Progressively increasing…… coagulopathy..
Ascites…. Edema…stool yellow
Jaundice detected after a few days, progressively increasing…pale
stool..no edema, no ascites…no FTT
Jaundice detected after a few days, progressively increasing…initially
yellow but now pale stool..no edema, no ascites…some FTT
Jaundice…..developed in late infancy … no failure to thrive….severe
itching….coagulopathy reversible with vitamin K stool intermittently
yellow and white
15. Indian Pediatrics - August 2000, Vol. 37, Number 8
Consensus report on Neonatal Cholestasis Syndrome
Sick child means toxic look, FTT, tachycardia, tachypnea,, vomiting, altered sensorium, edema, ascites
Galactosemia screen
Sugar TORCH
Plasma aminoacids
Urinary organic acids
Ammonia
Urea
Lactate
16. What is your experience with HIDA scan,
which I am sure is our audience is using
quite often?
In next 24 hours it
could rain or it may
not rain. To be sure
look at the sky and
decide for your self.
17. HIDA scan consistently fails to differentiate
between neonatal cholestasis and biliary atresia.
This doesn’t help if there is failure to excrete
dye; you will invariably need second
investigation to confirm the diagnosis before
surgery which is not a minor undertaking.
Liver biopsy with USG and clinical history is what
we use. Laparoscopic operative cholangiogram
where you can also take liver biopsy is also
available to us.
Our main use is therefore before surgery that a
wrong indication is not subjected to surgery
18. Do all metabolic diseases present identically
with jaundice ?
•They differ in their presentation
•Galactosemia and chronic variety of tyrosinemia primarily
could present with neonatal hepatitis and soon develop
features of decompensation which is progressive if not
treated
•FAOD and UCD may present with other symptoms and
during work-up are found to have liver dysfunction
19. Is Liver biopsy safe in this age group? Does
it tell everything
•Safe
•Needs good interpreter
•Not good for a metabolic diseases
21. •USG: Structural defects, biliary Atresia, spontaneous perforation of bile
duct
•TORCH+ Viral markers: For viral etiology
•Septic screen: For Cholestasis of inflammation
•Galactosemia and Tyrosinemia screen
•TMS and Acyl carnitine profile: FAOD, UCD, Tyrosinemia
•ECHO: PPH
•Fundus examination, X-ray spine for butterfly vertebrae
•Liver biopsy
•Lap/op cholangiogram
22. Coming back to our case….
Cytomegalo IgM : Positive
GALIPUT: Within normal range
Alpha feto protein was not significantly elevated
Fundus: Normal
ECHO: Normal
23. Should a pediatrician accept this as evidence of
Cytomegalo virus infection as the cause of hepatitis
in this patient?
No.
•CMV is ubiquitous …and not everybody develops manifest
infection.
•False-positive results are common;
•PCR ...to confirm the activity and to ascertain the
magnitude of the viral load ... to initiate therapy,
24. If PCR was high in this case would you treat this
patient?
Treatment criteria
• Immunocompromised are at risk of developing life-threatening
and sight-threatening CMV disease.
25. Or if the patient has Cytomegalo Inclusion Disease (CID)
• IUGR,
• hepatosplenomegaly,
• hematological abnormalities particularly severe
thrombocytopenia, and
• cutaneous manifestations, including petechiae and purpura
The most significant manifestations of CID involve the CNS.
• Microcephaly,
• ventriculomegaly,
• cerebral atrophy,
• chorioretinitis, and
• sensorineural hearing loss
26. •CMV PCR was negative.
•Liver biopsy was carried out which showed giant cell
hepatitis.
•The child was treated with supportive treatment and
eventually recovered
•Is Idiopathic Neonatal Hepatitis a
homogenous entity?
27. •Heterogenous
•It may be a form of hepatitis where there is yet
unidentified group of disorders
•Familial or sporadic
•Outcome varies
•25-30% could have adverse outcome including
death
28. Summary:
Neonatal cholestasis differs from neonatal liver failure; tempo is much
slower
Overlap is possible
Good history, examination of stool color and judicious use of tests are
cornerstone for diagnosis
In our centre, following causes are seen;
•Viral
•Galactosemia
•Tyrosinemia
•Fructosemia
•Allagille
But most of the time we have Idiopathic neonatal hepatitis as the final
diagnosis
More alertness is required
Editor's Notes
One thing in history is consistent that the treating pediatrician kept reassuring. This is very dangerous unless you are absolutely certain that you are dealing with a benign variety.
It is very important that you see the stool colour your self. Urine in the diaper could confuse so obtain stool sample not contaminated with urine.
There was conjugated hyperbilirubinemia with mild transaminitis and correctable coagulopathy. USG showed normal CBD and IHBR thus making EHBA unlikely; viral markers were negative
Different etiologies and different tempo of progression separates this case from previous one.
So at the outset we differentiate if there is decompensation or no decompensation. Of course there will be overlap and also the time at which you see the patient is very important. We focus on non decompensated cases here.
First and foremost, pediatricians need to separate unconjugated from conjugated variety as the two have totally different etiologies and natural history. In this talk we will deal with conjugated variety only which has various underlying causes as mentioned here.
In our experience, conjugated hyperbilirubinemia can be looked at from different angles to get a complete picture.
There are various angles of looking at neonatal jaundice. One of them is as shown above
Some metabolic disorders present themselves at birth. Others present sometimes after birth. Yet other appear late in infancy; the examples are PFIC or AIH in early childhood. Around five years, you start seeing Wilson’s disease, AIH, Drug induced and viral diseases and so on
Armed with information thus obtained, your mind must work like a dual core processor. You have to synthesize all information simultaneously to come to a conclusion.
This another approach by Indian Pediatric Academy. Problem we find here is that it starts at 14 days, by that time many diseases may be far advanced or the patient may already be dead especially in the “sick child category”.
Second concern is stool colour. Now we all now that this could keep changing over a course of few weeks or days.
Third concern is that certain milder variety of metabolic or viral disease could be missed going by this protocol and we feel they should be testes as well (green box). The list in green box is surely going to increase over a period of time
If you rely too much on HIDA scan, you will keep sending patients for “Kasai”.
Surgeon, if equally unaware will operate and mess it up.
For us HIDA scan is no no.
Although metabolic diseases are an important causes, they differ in their presentation and speed of progression.
Based on information gathered using previous strategy We mainly use tests mentioned above. Not all are done at time; more depends upon history, state of liver functions and results of initial investigations.
Many cases will come out from this category like many have come out already.
