Brain tumours: Analysis of a potential brain tumors
Relative prevalence of brain tumors in children. Metastases, anaplastic astrocytoma, and glioblastoma multiforme are rare. Pilocytic astrocytoma and PNETs are more common compared to adults
Three grades of tumours are recognized:
(1) pineocytoma, the most common of all pineal parenchymal tumors
(2) pineal parenchymal tumor of intermediate differentiation
(3) pineoblastoma, the rarest but most malignant parenchymal cell tumor
Brain tumours: Analysis of a potential brain tumors
Relative prevalence of brain tumors in children. Metastases, anaplastic astrocytoma, and glioblastoma multiforme are rare. Pilocytic astrocytoma and PNETs are more common compared to adults
Three grades of tumours are recognized:
(1) pineocytoma, the most common of all pineal parenchymal tumors
(2) pineal parenchymal tumor of intermediate differentiation
(3) pineoblastoma, the rarest but most malignant parenchymal cell tumor
Update on Neoplasm of Nervous system in Livestock and their DignosiRahul Kadam
World Health Organization classification of nervous system tumor is based on origin of cell. Most primary tumors of neuroepithelial origin from malignant transformation of astrocytes, ependymocytes, and oligodendrocytes in this Gliomas are most common. some are from Arise from astrocytes . some tumor are Metastases more likely than primary CNS tumor in patient with known systemic malignant disease. there are different verities explain in this seminar
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.
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.
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
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.
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 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
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.
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
2. The principle cells of the CNS :
1. Neurons- functional units of the CNS, about 10¹¹
in human brain.
2. Glial cells-
- Astrocytes
- Oligodendrocytes
- Ependymal cells
- Choroid plexus epithelium
- Microglia.
3. Cells that compose of meninges.
4. Blood vessel elements.
2
3.
4. 10% of all tumors.
Commonest solid cancers in children.(2nd to
Leuk for all malignancies)
Age: double peak 1st & 6th decade
Adults - 70% supra-tentorial
Children - 70% infra-tentorial
No/very rare extraneural spread.
Metastasis most common.
4
5. I. TUMOURS OF NEUROGLIA (GLIOMAS)
1. Astrocytoma
2. Oligodendroglioma
3. Ependymoma
4. Choroid plexus papilloma
II. TUMOURS OF NEURONS
1. Neuroblastoma
2. Ganglioneuroblastoma
3. Ganglioneuroma
III. TUMOURS OF NEURONS AND NEUROGLIA
Ganglioglioma
IV. POORLY-DIFFERENTIATED AND EMBRYONAL TUMOURS
1. Medulloblastoma
2. Neuroblastoma
3. PNET
V. TUMOURS OF MENINGES
1. Meningioma
2. Meningeal sarcoma
5
6. VI. NERVE SHEATH TUMOURS
1. Schwannoma (neurilemmoma)
2. Neurofibroma
3. Malignant nerve sheath tumour
VII. OTHER PRIMARY INTRAPARENCHYMAL TUMOURS
1. Haemangioblastoma
2. Primary CNS lymphoma
3. Germ cell tumours
VIII. MISCELLANEOUS TUMOURS
1. Malignant melanoma
2. Craniopharyngioma
3. Pineal cell tumours
4. Pituitary tumours
IX. TUMOUR-LIKE LESIONS
(epidermal cyst, dermoid cyst, colloid cyst)
X. METASTATIC TUMOURS
carcinomas of the lung, breast,skin (malignant melanoma), kidney and the
gastrointestinal tract and choriocarcinoma.
6
8. 1. Neuron: Gangliocytoma, ganglioglioma
medulloblastoma
2. Astrocyte: Astrocytoma, glioblastoma
3. Oligodendrocyte: Oligodendroglioma
4. Ependymal cell: Ependymoma
5. Microglial cell: Tumors derived from microglial
cells have not been described.
6. Meningeal cell: Meningiomas are derived from
arachnoidal cells and are usually dural-based.
10. 2 major divisions
a) Diffusely infiltrating astrocytoma
i.Diffuse astrocytoma(WHO Grade-II)
Ii. Anaplastic astrocytoma (WHO Grade-III)
Iii. Glioblastoma (WHO Grade-IV)
b) Circumscribed astrocytoma
i. Pilocytic astrocytoma (WHO Grade-I)
Ii.Pleomorphic xantho astrocytoma
Iii.Subependymal giant cell astrocytoma
10
11. 10-15% of astrocytic tumors, peak incidence at
ages 30 & 40.
Involves any region of CNS. Frontal and temporal
lobes.
Slow growing tumor.
p53 mutation is seen in >60% of patients.
Variants-
Fibrillary astrocytoma
Gemistocytic astrocytoma
Protoplasmic astrocytoma.
11
12. 12
Gross
Enlargement and
distortion of involved
area with blurring of
gross anatomical
boundaries.
Cystic areas and focal
calcifications are
common.
13. Most frequent variant.
Diagnostic criterion is nuclear atypia- enlarged,
cigar shaped, irregular and hyperchromatic with
coarse chromatin.
Cytoplasm is scanty.
Dyscohesive growth pattern.
Fibrillary matrix, microcysts containing mucinous
fluid are seen.
Mitotic activity, necrosis and microvascular
proliferation are absent.
IHC: GFAP, vimentin, S100.
13
17. 17
Rare variant
Composed of
homogenous cell
population of astrocytes.
Round to oval nuclei,
short and delicate
cytoplasmic processes in
an abundant eosinophilic
matrix.
Mucoid degeneration and
microcyst formation are
common.
Mitotic activity absent.
IHC: Low
immunoreactivity for
GFAP.
18. Diffusely infiltrating malignant astrocytoma.
Mean age at dx 45yrs.
May arise de-novo or from diffuse astrocytoma.
Tendency to progress to glioblastoma, mean time
interval 2 yrs.
Histo:
Increased cellularity, nuclear atypia and mitotic
activity.
Multinucleated tumor cells and abnormal mitosis
may be present.
Microvascular proliferation and necrosis are absent.
18
20. Most frequent and most malignant primary brain
tumor.
Most common between 45 and 75 years.
Subcortical white matter of cerebral hemispheres is
the most common site.
May arise de novo or through progression from
diffuse astrocytoma or anaplastic astrocytoma.
May spread to the contralateral hemisphere
(butterfly glioma) or may metastasize via CSF.
20
21. 21
Gross:
Poorly delineated.
C/S- peripheral
grayish tumor mass
and central areas of
yellowish necrosis.
Foci of hemorrhage
and cystic areas may
be seen.
22. Histo:
Poorly differentiated, pleomorphic astrocytic tumor
cells with marked atypia.
Prominent microvascular proliferation with
glomeruloid tufts like appearance.
Pseudopalisading pattern of necrosis.
Tumor cells accumulating around neurons, blood
vessels and subpial region of cortex.
Mitotic activity.
Multinucleated tumor giant cells.
Large cells with granular, PAS + cytoplasm may be
scattered.
Adenoid and squamous metaplasia may be seen .
Perivascular lymphocytic cuffing may be seen.
22
24. 5-6% of all gliomas.
Most common glioma in children.
First two decades of life.
Most common sites: Cerebellum, 3rd ventricular/
hypothalamic region, anterior optic pathway.
24
26. Histo:
Low to moderate cellularity with biphasic pattern-
Compacted bipolar cells with Rosenthal fibers.
Elongated, cytologically bland nuclei with long hair
like processes.
High content of refractile eosinophilic fibrils,
strong positivity for GFAP.
Loose textured multipolar cells with microcysts and
granular bodies/ hyaline droplets.
Round to oval, cytologically bland nuclei.
Small cell body and short, cobweb-like precesses.
Fibril poor and weak GFAP +ve.
26
27. Mitoses are rare.
Hyalinized and glomeruloid vascular proliferation
common.
Infarct-like and non-palisading necrosis seen.
Perivascular lymphocytic infiltration.
27
32. Syncytial (Meningotheliomatous)
meningioma
i. Lobular microarchitecture
ii. Cells having delicate round/oval nuclei,
inconspicuous nucleoli,lightly eosinophillic
cytoplasm and indistinct cytoplasmic border
iii. Tumor cells arranged in tight whorls
iv. Nuclear clearing and pale nuclear
pseudoinclusion containing invaginated
cytoplasm.
v. Psammoma bodies
32
37. Mixed(transitional) M
Psammomatous M
Angiomatous M
Microcystic M
Lymphoplasmacyte-rich M
Metaplastic M
Choroid M
Clear cell M
Rhabdoid M
Atypical M
Anaplastic M
37
38. 3 tiers of increasing biologic potential
Meningioma WHO Gr-I
Atypical Meningioma WHO Gr-II
Anaplastic Meningioma WHO Gr –III
Atypical Meningioma define as
A)4/more MF/10 HPF
B)At least 3 of i)Hypercellurarity
ii)Paternless sheet like growth
iii) Macronucleoli
iv) Small cell with high N/C ratio
v) Necrosis
Anaplastic Meningioma
i) 20 or more MF/10HPF or
ii) Exibiting loss of differentiated features resulting
in CA, Melanoma,Sarcoma like appearance
38
