General Basic knowledge of Brain tumour explained in brief of classification, pathogenesis, clinical features, CT, MRI, management, Radiotherapy. Best for MBBS and PG preparation student.
non-skeletal mesodermal tissues: adipose tissue, fibrous tissue, muscle, blood vessels and peripheral nerves (despite neuroectodermal origin)
benign, malignant and intermediate (low-grade malignant – locally aggressive, can recur, no metastatic potential)
originate from primitive mesenchymal stem cells
classification according to differentiation lines (e.g. liposarcoma is not a tumor arising from adipose tissue but exhibiting lipoblastic differentiation)
General Basic knowledge of Brain tumour explained in brief of classification, pathogenesis, clinical features, CT, MRI, management, Radiotherapy. Best for MBBS and PG preparation student.
non-skeletal mesodermal tissues: adipose tissue, fibrous tissue, muscle, blood vessels and peripheral nerves (despite neuroectodermal origin)
benign, malignant and intermediate (low-grade malignant – locally aggressive, can recur, no metastatic potential)
originate from primitive mesenchymal stem cells
classification according to differentiation lines (e.g. liposarcoma is not a tumor arising from adipose tissue but exhibiting lipoblastic differentiation)
Explains about different types of brain tumor and its symptoms, treatments and surgical procedures. The Brain & Spine Centre Uttar Pradesh gives all the latest way to treat the brain tumor even if it is cancerous or non cancerous tumors.
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Radiotherapy in low grade gliomas benefit with local control advantage
Patients with high risk factors need immediate radiation after surgery
RT dose of 50-54 Gy in 2 Gy/Fr
Fractionated radiosurgery in optic nerve glioma and small volume disease
I give this lecture on cell adhesion and cell migration in the Cell Biology and Genetics course for first-year veterinary students. The core material comes from Molecular Biology of the Cell, Fifth Edition, but I have added multiple clinical examples and placed the material in the context of the translational medicine component of the course.
This is a free ebook in pdf format. This book will serve as a rapid reference guide for medical undergraduate and postgraduate students during Pathology practical classes and also as a rapid reference during exams.
This is a free ebook in pdf format. This book will serve as a rapid reference guide for medical undergraduate and postgraduate students during Pathology practical classes and also as a rapid reference during exams.
Dermoid cysts, capillary hemangiomas, and rhabdomyosarcoma are the most common paediatric orbital tumours.
Retinoblastoma is the most common malignant ocular tumour in children.
Neuroblastoma can involve the orbit via metastases and is the most common metastatic tumor to the orbit in children.
Lymphoid tumors, cavernous hemangiomas, and meningiomas are the most common orbital tumours in adults.
Other tumors include those of the lacrimal gland, tumors from the surrounding sinuses, metastatic tumors such as breast cancer in women, and neural-based tumors
Presentation about the the second most common type of ovarian tumors which have a very unique property of being similar to the testicular germ cell tumors.
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
12. • M/E-
• Elongated Bipolar cells
( elongated hair like
processes)
• Rosenthal fibers with
eosinophilic protein droplets
• mural nodule may be
highly vascular; often
calcifications
• Vascular changes are
common –
glomeruloid vascular
proliferation and vascular
hyalinization
15. • Positive stains
• GFAP (strong), PTAH, PAS (protein droplets), alpha-1-antichymotrypsin (protein
droplets)
• Neoplastic astrocytes have intermediate cytoplasmic filaments. These filaments, has protein-glial
fibrillary acidic protein (GFAP), can be detected by I/H/C
• GFAP- positive
17. • Pleomorphic xanthoastrocytoma
• WHO grade II
• Occurs in temporal lobes of children and young adults
• Gross
• Usually cystic
• M/E-
• Pleomorphic cells (occasional xanthomatous change),
• Perivascular lymphocytic cuffing, scattered eosinophilic granular bodies,
reticulin rich network
• No necrosis and no mitosis.
19. • Positive stains
• GFAP and S100
• Reticulin, class III beta tubulin (73%)
• Variable expression of neuronal markers including synaptophysin
20. • D/D-
• Glioblastoma and giant cell glioblastoma
• Malignant fibrous histiocytoma
• Other cystic lesions, especially those with a cyst-mural nodule
architecture (pilocytic astrocytoma and ganglioglioma
21. Infiltrative astrocytoma
• Site-
Infiltrative astrocytomas are usually found in the cerebral
hemispheres,
• Age-
most common in patients between 30 and 60.
• Presentation-
Patients most commonly present with seizures, headaches, and
focal neurologic deficits (depending on where the tumor is).
23. • Diffuse astrocytoma
• Most common adult tumor.
• 80% of adult primary brain tumors
• Location: Usually supratentorial
• Age-4th to 6th decades
• MRI-
• Ill defined, non enhancing lesion with mass effect and variable peritumoral
edema.
24. • Gross-
Poorly defined infiltrative
tumor that distorts
the brain.
C/S-
Firm / soft & gelatinous, Cystic degeneration
25. • M/E-
• Mild to moderate glial
cellularity
• Variable nuclear
pleomorphism
• Fibrillary background
due to astrocytic process
28. • Anaplastic astrocytoma
• Grading: WHO grade III/IV
● Age and sex: mean age 45 years; male predominance
● Site: usually supratentorial, but can be anywhere in CNS;
● MRI:
• Usually heterogeneous or
patchy enhancement
29. Gross-
Anaplastic astrocytoma
predominantly
occupying the right temporal lobe.
The tumour is ill-defined and
appears as a homogeneous mass.
Note the large cyst in the periphery
of the neoplasm and shift of
midline structures
towards the left hemisphere.
30. This astrocytoma
had densely cellular
areas with back-to-
back nuclei,
moderate nuclear
pleomorphism, and
increased mitotic
activity. However,
necrosis or
endothelial
proliferation - the
two hallmarks of
Glioblastoma - were
absent.
31. • M/E-
• Increase in cellularity
• Nuclear pleomorphism
• Hyperchromasia
• May have mitosis
• No necrosis
32. • D/D-
● Anaplastic oligodendroglioma:
• hypercellular with loosely cohesive and single cells, moderate
pleomorphism, vacuolated background, mitotic activity
● Anaplastic oligoastrocytoma:
• conspicuous oligodendroglioma and astrocytoma components
• Glioblastoma
33. • Anaplastic astrocytoma Glioblastoma
• Increase in cellularity Dense cellularity
• Nuclear pleomorphism
• Hyperchromasia
• May have mitosis Mitosis
• No necrosis Necrosis & vascular proliferation
34. Gemistocytic astrocytoma
Dense eosinophilic cytoplasm & eccentrically
displaced nucleus.
Gemistocytes are frequently
found in other fibrillary
astrocytomas &
oligodendrogliomas. Some
authors require at 20% of
tumor cells to be gemistocytic
before using the designation of
gemistocytic astrocytoma.
This tumor appears to be
composed of an almost
pure population of gemistocytic cells.
36. • D/D-
• Gliosis:
• Hypertrophy of cells rather than hyperplasia, even distribution
• Subependymal giant cell tumor: intraventricular, larger nuclei,
non-infiltrative
• Ganglioglioma: neoplastic neurons
37. • Glioblastoma
• WHO grade IV
• "Multiforme" due to variegated gross appearance (firm white areas, yellow necrotic
areas, hemorrhagic areas and cystic areas) as well as diverse histological features
• Sites
• Usually supratentorial;
• Either primary (de novo, with with p53 mutation) or secondary (transformed from
grade II/III astrocytoma)
• MRI
• Contrast enhancing (ring pattern),
• large surrounded by peritumoral edema.
• (parietal lobe)
38. • Gross-
glioblastoma is a poorly defined
intra-axial mass with variegated
(multiform) appearance due to
necrosis and hemorrhage.
• A 9.0 cm tumor with foci of
hemorrhage and necrosis
involving the left temporal lobe.
40. • M/E-
• Densely cellular with nuclear
pleomorphism
• Necrosis in a serpentine pattern
• Tumour cells crowded along the
edges of necrosis - pseudopalisading
• When vascular cell proliferation
is extreme, the tuft forms a ball-like
structure, the glomeruloid body
41. • Besides necrosis with nuclear pseudopalisading, the presence of endothelial
proliferation is another histologic hallmark of glioblastomas.
44. • Gliomatosis Cerebri-
• WHO Grade- III/IV
• Neoplastic astrocyte infiltrates
• the multiple region of brain or
• in some cases the entire brain .
• H/P-
• Largely composed of elongated,
hyperchromatic glial cells
Mitosis.
No necrosis or
microvascular proliferation
46. Oligodendroglioma
• WHO grade- II/IV
• Gross
• well-circumscribed, gelatinous,
gray masses, often with cysts,
focal hemorrhage,
& calcification
47. • M/E-
• Sheets of regular cells with
spherical nuclei & perinuclear halo
(fried egg)
(perinuclear halo artifact due to fixation,
and is not present in frozen sections)
• Calcifications-90% cases,
• Arborizing thin capillaries
• (chicken
wire pattern)
48.
49. • Positive stains
OLIG2, Leu7, S100, MAP2 (strong)
• D/D-
• Clear cell ependymoma: enhancing, well-circumscribed, perivascualr
pseudorosettes, dot- or ring-like EMA+
• Clear cell meningioma: extra-axial, enhancing, PAS+, EMA+
• Metastatic clear cell carcinoma: enhancing, well-circumscribed,
EMA+, CK+; molecular testing for 1p/19q deletion may be helpful, but some
oligodendrogliomas are negative for the deletion
• Pituitary adenomas: chromogranin+, pituitary hormone+
52. Ependymoma
• Slowly growing tumor of ependymal cells arising from walls of
ventricles or spinal canal
• Grade II/!V
• MRI-
• Well circumscribed lesions
with variable enhancement
56. • D/D-
Glioma:
• no true rosettes,
• no cell-cell junctions,
• no intracytoplasmic microvilli-lined lumina
57. Anaplastic Ependymoma
• Grade- III /IV
• Rare; usually infants and children
• Cerebrum/ cerebellum of children / young adults, but all ages and locations
• M/E-
Marked hypercellularity,
nuclear atypia
high mitosis &
necrosis
58. Myxopapillary ependymoma
• Grade - I / IV
• M/E-
• Well differentiated Cuboidal to elongated tumor cells arranged around the
papillary cores with a myxopapillary appearance.
• Usually no atypia,
• no/low mitotic activity
59. MOLECULAR CHANGES IN ASTROCYTOMA-GLIOBLASTOMA
• Isocitrate dehydrogenase (IDH)
• IDH is a citric acid cycle enzyme that catalyzes that convert isocitrate to a-
ketoglutarate.
• IDH1 and IDH2 are frequently mutated in gliomas.
• IDH1 mutated in 70-80% of grade II and III astrocytomas,
oligodendrogliomas, oligoastrocytomas, & in secondary but not primary
glioblastomas.
• IDH2 mutations are more common in oligodendrogliomas
• Detection of IDH1 mutations by I/H/C is an important tool in the diagnosis of
gliomas.
60. • Tumor Protein 53 (TP53)
• It repairs DNA damage and induces apoptosis when damage
cannot be repaired. Its mutation promotes tumor formation
• TP53mutations common in diffuse astrocytoma, anaplastic
astrocytoma, and secondary glioblastoma, and help distinguish
glioma from gliosis.
• Mutations can be detected by I/H/C shows strong nuclear
staining for p53.
61. • Epidermal Growth Factor Receptor (EGFR)
Overexpression of EGFR, on 7p, occurs in 40 % of glioblastomas
(more commonly primary ones) and less frequently in lower
grade astrocytomas .