This document discusses various abnormalities and birth defects that can occur in fetal development of the digestive system, including cleft lip and palate, facial clefts, esophageal atresia, Hirschsprung's disease, anal atresia, and abnormalities of the liver and bile ducts. It provides detailed descriptions and diagrams of the pathogenesis of different defects arising from failures of fusion or recanalization during development of structures derived from the pharyngeal arches, foregut, midgut and hindgut.
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
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
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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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
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
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
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.
2. FACIAL ABNORMALITIES
• most frequent congenital anomalies (1:1000 newborns),
often occurring with other anomalies.
• play a role : environmental & genetic factors
3. CHEILOSCHISIS (CLEFT LIP)
• disorder during the fusioning of the maxillary process with the
prolabium (both globular processes of the medial nasolateral
process).
• can occur unilaterally or bilaterally
• 1=Eye anlage
2=Ear anlage
3=Nasal sac
• The arrows point to the locations of the missing epithelial
bridges between the globular and maxillary processes that lead
to a unilateral or bilateral cleft lip.
4. CHEILOGNATHOSCHISIS (CLEFT LIP
AND JAW)
• besides the soft tissue fusion disorder of the upper lip,
the fusing of the lateral edges of the primary palate with
the two anterior edges of the secondary palate is also
disturbed.
• can occur unilaterally or bilaterally.
5. CHEILOGNATHOPALATOSCHISIS (CLEFT LIP, JAW
AND PALATE)
• fusion disorder of the left and right portions of the secondary
palatine lamina.
• it is not possible for an infant to suck and thereby take in nourishment, a
surgical separation between the nasal and oral cavities must be
undertaken as quickly as possible.
• 1=Fusion locations between maxillary
and globular processes of the
medial nasal lamina
2=Fusion locations between the
primary and secondary palates
3=Fusion locations between the
two palatal processes
• In all cleft face and lip abnormalities fusion disorders occur, i.e.,
no epithelial bridges are formed.
6. FACIAL CLEFT
• disorders that affect the whole face seldom.
• oblique facial cleft deficient fusion of the epithelium of the
lacrimonasal duct a fissure runs from the lower lid edge to the
lower edge of the nasal opening.
• unilaterally or bilaterally or combined with a cleft lip-jaw-palate.
• 1=Eye
2=Ear anlage
3=Nasal sac
no epithelial bridges
have been formed.
7. FACIAL CLEFT
• middle cleft face disorder of the bringing to the front of
the nose and eyes, no flattening of the medial facial
furrows occurs, e.g., between the two globular processes
• comes from an inhibition of tissue proliferation in this
region
• 1=Eye
2=Ear anlage
3=Nasal sac
8. FACIAL CLEFT
• transversal cleft face disorder of cheek formation and
a survival of the early, primitive oral fissure (macrostomia)
that extends into the anlage region of the ears (between
the 1st and 2nd pharyngeal arches).
• 1=Eye
2=Ear anlage
3=Nasal sac
9. PATHOLOGY OF THE HEADGUT
• In the region headgut abnormalities pharyngeal arches,
clefts and pouches
• Connected with the pharyngeal arches are hypoplasias in the
region of the first mandibular arch. Cysts and fistulas result
from persisting pharyngeal pouches (among others). Ectopic
glandular tissue of the thyroid, of the thymus or the
parathyroids can be explained by remaining tissue residuals
along their descent.
• Abnormalities can also result from disorders of the migration
or development of neural crest tissue in this region.
10. CERVICAL FISTULAS, CYSTS AND
SINUS
• This group of abnormalities derived from persisting pharyngeal
pouchesor longitudinal cervical grooves.
Cysts closed cavities with an epithelial lining.
Sinuses cavities that remain open towards the outside or towards
the pharynx and
fistulas connections between the pharynx and outer surface of the
neck.
• 1=Sternocleidomastoid muscle
• Frequent locations for lateral
cervical cysts, sinuses and fistulas.
Roman numbers corresponding
pharyngeal groove.
11. PIERRE ROBIN SYNDROME (PRS)
• combines extreme micrognathia, cleft palate and
abnormalities of the ears
• relative macroglossia (in relation to a very small lower
jaw) is present the tongue fall backwards into the
throat air passage constrictions
12. PERSISTING THYREOGLOSSAL
DUCT
• Ectopic thyroid tissue can be found along descent of the
thyroid gland from the foramen cecum to the isthmus of the
normal thyroid below the larynx.
• 1=Tongue
2=Foramen cecum
3=Epiglottis
4=Hyoid cartilage
5=Thyroid cartilage
6=Thyroid gland
7=Thyreoglossal duct
13. CATCH 22 SYNDROME
• The CATCH 22 syndrome = a developmental defect of the
3rd and 4th pharyngeal pouches.
• The symptoms :
• hypo- or aplasia of the thymus with defective T-cells and weak
immunity
• hypoplasia of the parathyroid with hypocalcaemia and tetanic
cramps
• cardiac defects (predominately conotruncal defects)
• facial dysmorphisms (hypertelorism; short lid axes; epicanthus;
wide, short nose with everted nasal base levels; short philtrum;
small, pointed mouth; microretrogenia; low-placed, dysmorphic ears
with enlarged anteroposterior diameter).
14. CATCH 22 SYNDROME
• Genetics:
• Most represent sporadic but there are also families, corresponding to
a dominant inheritance pattern with variable expressivity.
• The main cause microdeletion 22q11 (partial monosomy 22q11)
that can be detected in around 95% of the affected children.
• Other chromosomal disorders or a teratogenic genesis (maternal
diabetes mellitus, alcohol abuse, retinoids) have also been
described.
• 15 - 20% of the affected have inherited the microdeletion 22q11 from
a healthy parent. This healthy deletion carrier frequently has facial
microsymptoms associated with the monosomy 22q11.
• Frequency:
Entire population: CATCH 22 syndrome: 1/20000
Entire population: Partial monosomy 22q11: 1/5000
15. MISSING DESCENT OF THE PHARYNGEAL POUCH
DERIVATES
• migration parathyroid and thymus during their
development tissue remnants can also remain and
survive at ectopic locations
• do not give rise to functional disorders
16. PATHOLOGY OF THE FOREGUT
• in the lower foregut
region fistulas, stenosis and ectopic tissue also
form the main class of the abnormalities.
17. ABNORMALITIES IN THE
ESOPHAGUS REGION
• Most frequent Fistulas or atresias of esophagus ≈ abnormalities developing respiratory
tract.
• A=Atresia of the esophagus with a
beginning fistula
B=Atresia of the esophagus
C=Atresia of the esophagus with
fistula of the lower esophagus a section to the trachea
D=Atresia of the esophagus with
fistula of the upper esophagusa section to the trachea
1=Trachea
2=Esophagus
• Seldom stenosis of the esophagus result
from a missing recanalization during development.
• Atresias or stenosis of the esophagus fetus cannot swallow and reabsorb amniotic fluid,
leading to a polyhydramnion.
18. PYLORIC STENOSIS
• = hyperplasia of the pyloric sphincter muscle leads to
sudden and convulsive vomiting, can be rectified by
a longitudinal incision of the pyloric sphincter
muscle.
• relatively frequent, mainly in male newborns.
20. PATHOLOGY OF THE MIDGUT
• Disorders due to the large changes in shape during
the embryonic period in this region
21. MECKEL'S DIVERTICULUM
• 2-4% of the population
exhibits Meckel's
diverticulum.
• a sac with a dead end that
lies ca. 50 cm cranial to
the iliocecal valve and
represents the remnant of
the omphalomesenteric
duct
• usually it is discovered
accidentally but can become
infected or exhibit ectopic
tissue.
22. OMPHALOCELE
• omphalocele intestinal loops remain in the umbilical coelom and are
not repositioned into the abdominal cavity, coated with amnion
and peritoneum.
• In an omphalocele intestinal
loops are visible outside the
body and skin and musculature
are absent
• DD/ with umbilical hernia = a weak abdominal musculature that is
not able to hold back the intraperitoneal contents of the abdominal
cavity
• umbilical hernia is always covered with skin.
23. MALROTATION AND COECAL
ELEVATION
• Sometimes, when the intestinal loops return back into
the abdominal cavity, no or an incomplete
rotation occurs
• can remain asymptomatic or lead to a volvulus or other
form of strangulation.
24. ATRESIAS
• incomplete recanalization of the intestinal lumen can
also occur in the other regions of the intestines after the
first trimester of the pregnancy.
25. AGANGLIONIC MEGACOLON
(HIRSCHSPRUNG'S DISEASE)
• frequency = 1:5000, boys >>
• Hirschsprung's disease ( congenital megacolon) = a congenital
defect of ganglion cells in the large intestine.
• In a certain portion of the large intestine (thinner in this region and
cannot expand very far) nerve cells are absent that normally
stimulate the muscles to contract and transport the intestinal
content. Both Auerbach's and Meissner's plexus are affected.
• Stools remains at this location congenital megacolon.
• frequent accompaniment : absent relaxation of the anal sphincter
muscle
• Characteristic : the abdomens are bloated and hard – they suffer
from vomiting and constipation
• Therapy = a surgical removal
26. PATHOLOGY OF THE HINDGUT
• embryonic hindgut begins already in the transition from
the middle to the last third of the transverse colon, blood
supply by the superior mesenteric artery ceases and
blood supply of the inferior mesenteric artery begins.
• only the abnormalities of the anus will be mentioned
here.
27. MISSING PERFORATION OF THE ANUS,
ANAL ATRESIA, FISTULAS
• The development of the anus can be disturbed in a large
number of ways. The disorder ranges from a simple
membrane at the anal exit (persisting cloacal
membrane) to atresias of various lengths. Every
newborn, therefore, must be examined to see whether
the anus is open. Sometimes the anal atresia is
combined with a fistula, which connects the intestine with
another structure of the original urogenital sinus.
Frequently fistulas form that extend as far as the vagina,
theurethra, the bladder or into the perianal region on
the outside.
28. LIVER ABNORMALITIES
ATRESIAS OF THE BILE PASSAGES
• Many shape variations of the liver and the discharging
bile passages exist but most of them have no functional
importance.
• One serious abnormality is an atresia of the bile
passages. This disorder can occur at any place along
the bile passage, from the tiny canaliculi to the
discharging bile duct. Newborns with an atresia of the
bile passages develop an icterus shortly after birth.
When the cause cannot be corrected, a liver
transplantation is necessary.
29. PANCREAS ABNORMALITIES
• Pancreas abnormalities can affect only its form but also
its function. Form variations are relatively frequent
without there being any influence on function
30. ANNULAR PANCREAS
• very seldom, frequently associated with the Down
syndrome
• pancreas forms a ring around the whole duodenum..
31. CYSTIC FIBROSIS (CF)
• Cystic fibrosis(mucoviscidosis) is the second most
frequent hereditary disease.
• The outflow passages of the exocrine portion of the
pancreas become stopped up due to the viscous mucus
buildup of secretion fibrous tissue throughout the
organ pancreas insufficiency.
32. CYSTIC FIBROSIS (CF)
• CF = a congenital, autosomal recessive, inherited, multi-organ syndrome caused by a deficiency
of CFTR (cystic fibrosis transmembrane regulator), a regulatory protein of chloride transport
through the cellular membrane with consecutive elevation of the viscosity of bodily secretions.
• The defective enzyme on chromosome 7 influencing of the active chloride transport, primarily
from epithelial cells.
• The most severe sequelae : pulmonary (chronic bronchitis) and intestinal.
• Gastrointestinal manifestations meconiumileus, pancreas
insufficiency, maldigestion, prolapse of the rectum, cholestasis, prolonged
icterus,cholestatic hepatic cirrhosis.
• Death before the 1st year of life is almost exclusively due to intestinal complications, later as
the result of pulmonary affection together with heart failure due to the overload of lung
circulation. Life expectancy amounts to 25 - 35 years.
• Diagnosis : Elevated osmolality and elevated NaCl content in sweat.
• only symptomatic treatment available retaining the longest possible organ functions.
At various clinics a sweat test is now performed routinely as a part of newborn screening.
34. DISCUSSION FROM ARTICLE : A METABONOMIC
APPROACH TO ANALYZE THE DEXAMETHASONEINDUCED CLEFT PALATE IN MICE
• In the normal mouse embryo, palate shelves grow
and elevate into a horizontal position by embryonic
day 14 (E14)
• By the day of E17, the process of fusion has
completely finished.
• Some studies incidence of cleft palate may be
closely related to high maternal concentration of
plasma homocysteine OR lower activity of the
glucocorticoids prereceptor metabolizing enzyme
11β-hydroxysteroid dehydrogenase type 2
(11β2HSD2) in placental trophoblastic cells.
35. DAFTAR PUSTAKA
• Embyology.ch
• Article : A Metabonomic Approach to Analyze the
Dexamethasone-Induced Cleft Palate in Mice
• Jornal : Maternal Consumption of Coffee and
Caffeine-containing Beverages and Oral Clefts: A
Population-based Case-Control Study in Norway