Encephaloceles are rare birth defects associated with skull defects characterized by partial lacking of bone fusion leaving a gap through which a portion of the brain sticks out (protrudes).
Neural tube defects (myelomeningocele) | spina bifida NEHA MALIK
NTDs occur when the neural tube does not close properly. The neural tube forms the early brain and spine. These types of birth defects develop very early during pregnancy, often before a woman knows she is pregnant. The two most common NTDs are spina bifida (a spinal cord defect) and anencephaly (a brain defect).
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Encephaloceles are rare birth defects associated with skull defects characterized by partial lacking of bone fusion leaving a gap through which a portion of the brain sticks out (protrudes).
Neural tube defects (myelomeningocele) | spina bifida NEHA MALIK
NTDs occur when the neural tube does not close properly. The neural tube forms the early brain and spine. These types of birth defects develop very early during pregnancy, often before a woman knows she is pregnant. The two most common NTDs are spina bifida (a spinal cord defect) and anencephaly (a brain defect).
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Neural tube defects are the most common congenital abnormality in India which can be easily prevented with due information and better nursing practices. Neural Tube Defects can be prevented with intake of folic acid.
Hydrocephalous is a serious disease of the central nervous system which has both congenital and aquired subtypes. the congenital variety affects the children and is a considerable burden especially is the developing countries. I tleads to long term morbidity and high rates of mortality
Neural tube defects are the most common congenital abnormality in India which can be easily prevented with due information and better nursing practices. Neural Tube Defects can be prevented with intake of folic acid.
Hydrocephalous is a serious disease of the central nervous system which has both congenital and aquired subtypes. the congenital variety affects the children and is a considerable burden especially is the developing countries. I tleads to long term morbidity and high rates of mortality
All about Spina Bifida:
Definition
7 Types
Causes
Health Status
Incidence and epidemiology
Prevention
Social impact
Management
Detection
Diagnosis
Treatment
Antibiotics
Careful observation
Physical therapy
Neural tube defects are birth defects of the brain, spine, or spinal cord. They happen in the first month of pregnancy, often before a woman even knows that she is pregnant. The two most common neural tube defects are spina bifida and anencephaly.
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.
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.
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
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.
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.
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.
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
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
- 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
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Failure of normal fusion of the neural plate
to form neural tube during the first 28 days
following conception .
Neural tube defects (NTDs) are one of the
most common birth defects, occurring in
approximately one in 1000 live births in the
United States.
3. Prevalence
Increased incidence in families of Celtic and Irish
heritage .
Increased incidence in minorities (genetic or
environmental?)
Increased incidence in families
Neural tube defects (NTDs) are among the
most common birth defects that cause infant
mortality (death) and serious disability .
5. Combination of environmental and genetic
causes .
Teratogens :
- Drugs
-Rdiation
Infection and maternal illnesses.
Nutritional deficiencies . - notably, folic acid
deficiency
6. All pregnancies are at risk for an NTD.
However, women with a history of a previous
pregnancy with ( NTD).
women with first degree relative with(NTD)
women with type 1 diabetes mellitus
women with seizure disorders on Na valproic
acid.
women or their partners who themselves
have an NTD.
7. Two types of NTDs:
1- Open NTDs ( most common) :
- occur when the brain and/or spinal cord are
exposed at birth through a defect in the skull
or vertebrae.
Spina bifida
Anencephaly
Encephalocele
8. 2- closed NTDs (Rarer type ):
- occur when the spinal defect is covered by
skin.
lipomyelomeningocel
lipomeningocele
tethered spinal cord.
9. What are the common Neural Tube Defects
(NTDs) ?
Spina Bifida - 60%
Anencephaly - 30%
Encephalocele - 10%
10. - A midline defect of the :
bone,
skin,
spinal column, &/or
spinal cord.
11. Spina Bifida is divided into two subclasses :
1 - Spina Bifida Occulta(closed ) :
- mildest form ( meninges do not herniate
through the opening in the spinal canal )
2 -Spina Bifida Cystic ( open) :
- meningocele and myelomeningocele .
12.
13. Failure of fusion of the vertebral arch .
The meninges do not herniate through the bony defect.
This lesion is covered by skin.
Symbtoms :
Difficulties controlling bowel or bladder .
weakness and numbness in the feet
recurrent ulceration .
In Diastematomylia neurological deficits increase with
growth.
Signs :
Overlying skin lesion :
tuft hair - lipoma - birth mark or small dermal sinus
Usually in the lumbar region .
15. The 2 major types of defects seen here are
myelomeningoceles and meningoceles.
lumobosacral regions are the most common
sites for these lesions .
Cervical and thoracic regions are the least
common sites.
16.
17. The spinal cord and nerve roots herniate into
a sac comprising the meninges.
This sac protrudes through the bone and
musculocutaneous defect.
18. Certain neurologic anomalies such as :
- hydrocephalus
- Chiari II malformation
19. myelomeningoceles have a higher incidence
of associated :
- orthopedic anomalies of their lower
extremities ( why).
- Intestinal malformations.
- Cardiac malformations.
- esophageal malformations.
- renal and urogenital anomalies.
20. - Variable paralysis of the legs.
- muscle imbalance .
- Sensory loss .
- bladder denervation ( neuropathic )
- bowel denervation .
- scoliosis .
- Arnold chiari malformation .
22. Herniation of the cerebellar tonsils through
the foramen magnum .
cerebellar hypoplasia .
caudal displacement
of the hindbrain through .
the foramen magnum .
usually associated with
Hydrocephalus .
23. Hydrocephalus .
Cranial Nerve Palsies .
Visual Deficits .
Pressure from the enlarged ventricles
affecting adjacent brain structures .
Cognitive and perceptual problems.
Motor dysfunction .
25. Fluid-filled sac with meninges involved but
neural tissue unaffected .
The spinal cord and nerve roots do not
herniate into this dorsal dural sac.
The primary problems with this deformity
are cosmetic
26. Neonates with a meningocele usually have
normal findings upon physical examination
and a covered (closed) dural sac.
Neonates with meningocele do not have
associated neurologic malformations such as
hydrocephalus or Chiari II.
May complicted by CSF infection.
27. Lipomeningocele
(lipo = fat)
lipoma or fatty tumor
located over the
lumbosacral spine.
Associated with bowel
& bladder dysfunction
Lipomeningocele
28. Abnormal eye movement
Pressure sore and skin irritations.
Latex allergy.
Bladder and bowel control problems
musculoskeletal deformities (scoliosis).
joint and extremity deformities (joint
contractures, club foot, hip subluxations,
diminished growth of non-weight bearing
limbs)
Osteoporosis.
tethered spinal cord after surgery .
30. Failure of development of most of the
cranium and brain.
Infants are born without the main part of
the forebrain-the largest part of the
cerebrum.
31. The fetus usually blind, deaf and unconscious .
partially destroyed brain, deformed
forehead, and large ears and eyes with often
relatively normal lower facial structures.
Both genetic and environmental insults
appear to be responsible for this outcome.
The defect normally occurs after neural fold
development at day 16 of gestation but
before closure of the anterior neuropore at
24-26 days' gestation.
32. Symptoms
Mom- Polyhydramnios
Baby- absence of brain/skull
Diagnosis
Ultrasound
Treatment
None, incompatible with life
Management
Comfort Measures
Support Parents
33. Extrusion of brain
and meninges
through a midline
Skull defect .
- Often associated
with cerebral
malformation
34. Amniocentesis
AFP - indication of abnormal leakage
Blood test
Maternal blood samples of AFP
Ultrasonography
For locating back lesion vs. cranial signs
37. Treatment of mylomenigocele
- Genetic counseling may be recommended. In some
cases where severe defect is detected early in the
pregnancy, a therapeutic abortion may be considered
After birth - surgery to repair the defect is usually
recommended at an early age. Before surgery, the
infant must be handled carefully to reduce damage
to the exposed spinal cord. This may include special
care and positioning, protective devices, and changes
in the methods of handling, feeding, and bathing.
38. Hydrocephalus:
- Children who also have hydrocephalus may
need a ventricular peritoneal shunt
This will help drain the extra fluid
- Antibiotics may be used to treat or prevent
infections such as meningitis or urinary tract
infections
39. Most children will require lifelong treatment for problems
that result from damage to the spinal cord and spinal
nerves. This includes :
- Gentle downward pressure over the bladder may help drain
the bladder. In severe cases, drainage tubes, called
catheters, may be needed. Bowel training programs and a
high fiber diet may improve bowel function
- Orthopedic or physical therapy may be needed to treat
musculoskeletal symptoms. Braces may be needed for
muscle and joint problems
- Neurological losses are treated according to the type and
severity of function loss
40. - Follow-up examinations generally continue
throughout the child's life. These are done to
check the child's developmental level and to
treat any intellectual, neurological, or
physical problems
41. Treatment of menigocele
The key priorities in the treatment of
meningocele are to prevent infection from
developing through the tissue of the defect
on the spine and to protect the exposed
structures from additional trauma. Most
children with meningocele are treated with
surgery (within the first few days of life) to
close the defect and to prevent infection or
further trauma
42. Management of spina bifida occulta
- can remove fat or fibrous tissues which are
affecting the functioning of the spinal cord
- can drain syrinxes or cysts in the spinal canal
to reduce pressure on the spinal cord and
- can be performed on the legs or feet to
improve their functioning
43. SUMMERY :
Prevention
folic acid 0.4 mg daily pre, 1 mg daily preg
Identify
Prenatal
At birth
Protect pre-op and post-op
Skin integrity to prevent infection
Special handling to reduce nerve damage
Support
Parental coping
Pictures of similar defects corrected
Genetic Counseling
For future pregnancy
In early pregnancy, therapeutic abortion
Complications
Permanent disability
Education
Symptoms of hydrocephalus
Symptoms of meningitis
Follow up for monitoring to assess neurologic damage
44. All women of childbearing age should receive
0.4 mg (400 micrograms) of folic acid daily
prior to conception of planned or unplanned
pregnancies and continue thru 1st trimester
Women with a history of NTD and should
receive daily supplementation of (4000
micrograms) of folic acid starting three
months prior to conception and continuing
thru the 1st trimester