How to interpret the visual field printout
Learn basic terms of visual field analysis
How to diagnose glaucomatous field defect
How to diagnose neurological field defect
How to interpret the visual field printout
Learn basic terms of visual field analysis
How to diagnose glaucomatous field defect
How to diagnose neurological field defect
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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 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
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.
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.
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
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
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.
2. Retina is a multi layered tissue with each
layer having a different reflectance pattern
thus by this principleOCT permits
recognition of multiple retinal layers in vivo.
6. Horizontal
Structures
• Inner and Outer
Plexiform layer
• Inner and Outer
Limiting Membrane
• Pigment epithelium
Vertical
Structures
• Müllers fibres
• Cell chains
containing of
photoreceptor to
bipolar and ganglion
cells
7.
8. Imaging with OCT is based on Michelson's
Interferometer and includes complex analysis
of reflections of LOW COHERENCE LIGHT
from the ocular tissue ( low coherence
interferometry)
11. The
reflected
light from
the retinal
tissue and
reference
mirror
interacts
to form an
Step 3
Distance
between
the light
source
and
reference
mirror
Step 2
Distance
between
the light
source
and retinal
tissue
Step 1
INTERFERENCE PATTERN
This interference pattern is processed into a signal
12. The signal is analogous to that obtained with
A Scan Ultrasonography.
A 2D image is built as the light source is
moved across the retina and then the series
of stacked and aligned A scans produce a
2dimensional cross sectional image
resembling a HISTOLOGIC SECTION
13. Transverse scanning at multiple
sequential points (A-Scans)
2 Dimensional data collection
Generation of Cross sectional map
Display in pseudo colours
14. The infrared image has a field of 30˚ .
OCT operates like a fundus camera but
resolves like a USG machine .
USG OCT
Source Sound waves Infrared light
waves
Resolution 150µ 10µ
Patient Contact Needed Non- Invasive
20. Time-domain devices can provide 400 A
scans per second with a maximal axial
resolution of 8-10µm
High quality images require longer time to
create.Therefore time is the major limitation
of this technique.
21. Absence of movable mirror speeds up the
image acquisition up to 50 times.This
technique enables to obtain large numbers of
A-scans that allows creating high resolution
images.
SD devices can provide 20.000-52.000 A-scan
per second with a 5-7µm resolution
Such a speed reduces the eye movement
artefacts.
22.
23. TIME DOMAIN OCT SPECTRAL DOMAIN OCT
RESOLUTION : 10µ 5-7µm
2 Dimensional images 2 D and 3 D
Low coherence Interferometry Low coherence interferometry
Uses fixed wavelength Broad wavelength spectrum
Lower speed 400-512 A scan/sec High speed : 52000 A scans/ sec
24.
25.
26. Scan Utility
Line Multiple line scans can be obtained
without returning to main window
Radial Lines Determines entire macular thickness/
volume
Raster lines Entire area of pathology can be scanned
Repeat scan Monitoring change during follow-up
Macular thickness Determines entire macular thickness/
volume
Fast macular thickness Allows comparative thickness/ volume
analysis
31. Deep:
1. Drusen
2. RPE Hyperplasia
3. Scarring , atrophy
4. Sub retinal neovascular membrane
5. Deep pigmented lesion e.g. Nevus
32. Low reflectivity: ( Black and Blue)
1. Gross separation of cellular elements and
fluid present either in form of cystoid spaces
2. Neurosensory detachment
3. RPE detachment
results in decreased reflectivity
33. Shadowing:
Dense highly reflective elements produce a
kind of blockage of light waves by
attenuation
This appears a shadow that conceals the
element lying behind it
E.g. Haemorrhage's, Hard exudates, cotton
wool spots, dense pigmented lesion or scar,
retained foreign body.
34. Age related Macular Degeneration
a) Dry / non-neovascularAMD: Drusen
b) Wet / neovascularAMD: CNV and PED
Epiretinal Membrane
FullThickness Macular Hole
Central Serous Chorioretinopathy
Cystoid Macular Edema
35. Degenerative disorder affecting macula
Clinical classification of AMD:
Category Definition, based on lesion ( within 2DD of fovea)
No apparent
ageing change
No drusen
No AMD pigmentary abnormalities
Normal ageing
changes
Only druplets
No AMD pigmentary abnormalities
Early AMD Medium drusen (>63 µm - < 125 µm)
No AMD pigmentary abnormalities
Intermediate AMD Large drusen (>125µm)
Any AMD pigmentary abnormalities
Late AMD Neovascular AMD and/or any geographic atrophy
36. Extracellular deposits located at the interface
between the RPE and Brusch membrane.
Derived from immune mediated and metabolic
processes in RPE.
On OCT:
Medium sized and large drusen are seen as hyper
reflective irregular nodules beneath the RPE
37. • Small drusen/ Hard drusen
• Well defined , whitish yellow lesion
• < 63 µm
• Fairly well defined yellow white focal
deposits
• Measuring between 63 µm - 125 µm
Intermediate
Drusen
• Large drusen/ Soft drusen
• Less well delineated yellow white deep
retinal lesion
• >125µm
39. Types: Classified according to Macular
Photocoagulation Study (MPS): Based on FA
Classic CNV (20%): well defined lacy pattern
during early transit of dye subsequently
leaking to sub retinal space.
Occult CNV (80%): Limits cannot be fully
defined on FA
Predominantly / Minimally classic CNV:
Classic element is grater or less than 50 % of
total lesion
40. On OCT:
CNV is shown as
1. thickening and fragmentation of RPE and
Choriocapillaries
2. Sub retinal, Sub-RPE fluid,
3. Blood and scarring
are demonstrated.
41.
42. Thickened and dysfunctional Brusch
membrane impending movement of fluid
from RPE towards the choroid PED.
On OCT :
PED shows
Separation of RPE from the Brusch membrane
by an optically empty area
Clinically:Orange dome shaped
lesion
FA:Well demarcated Hyperfluroscent
pooling
ICGA: Hypofluroscence
OCT: Optically empty area below
RPE
43. Sheet like fibro cellular structure that
develops over surface of retina.
Proliferation of cellular component and
contraction of membrane leads to visual
symptoms.
On OCT-
o Highly reflective surface layer associated
with retinal thickening.
o Useful to exclude significantVMT .
44.
45. Pathogenesis:
The vitreofoveal traction is central to
development of a full thickness macular hole.
Gass: Proposed that contraction of
prefoveolar cortical vitreous results in
tangential traction
46. Classification:
1. Gass classification scheme on
Biomicroscopy,
2. New OCT based classification- IVTS-
(InternationalVitreomacularTraction Study)
52. Idiopathic
Characterised by local serous detachment of
the sensory retina at the macula secondary to
leakage from choriocapillaries through one or
more hyper permeable RPE sites
Affects young , middle aged men
Risk factors: Steroid administration,Cushing
syndrome, H. Pylori infection, pregnancy,
psychological stress, sleep apnoea.
53. On OCT:
Optically empty neurosensory elevation,
Other findings – one or more smaller RPE
detachments , precipitates on posterior surface
of detached retina , thickened choroid.
On FA:
Hyperfluroscent spot that enlarges- Ink Blot
Vertical column- Smoke stack
54.
55. Accumulation of fluid in outer plexiform layer
and inner layers of retina with formation of
tiny cyst like cavities.
Fluids may initially accumulate intracellularly
in Müller cells with subsequent rupture.
57. On OCT:
Retinal thickening with cystic hypo reflective
spaces, and loss of foveal depression.
Lamellar holes may be demonstrated in
advanced cases.
On FA:
A petalloid pattern is seen due to dye
accumulation in microcytic spaces in outer
plexiform layer
58.
59. Various newer OCT systems are:
1. Ultra high resolution OCT
2. Doppler OCT
3. CAS OCT-Visante OCT
4. Combined FFA and en-faceOCT
5. IntraoperativeOCT
60. Axial resolution of 3 µm
Transverse resolution of 15-20 µm
Useful for visualization of
a) External limiting membrane
b) Ganglion cell layer
c) Photoreceptor layer
61. Technique that combines laser doppler
velocimetry and OCT for imaging the depth ,
diameter flow rate, retinal haemodynamic
characteristic
Only possible in larger vessels
Not well suited for angiography of retinal and
choroidal microvasculature, where vessels
are nearly perpendicular to the OCT beam.
62. Surgical microscope integrated with OCT to
perform simultaneous imaging and en face
visualization
Uses are:
Macular hole surgery,
ERM peeling,
Sub retinal surgery
Zeiss OPMI LUMERA® 700 and RESCAN™ 700
63. Doppler OCT uses the Doppler phase shift to
quantify blood flow in larger vessels and
measure total retinal blood flow
OCTA is more concerned about separating
moving scatters from static background
tissue to create angiograms.
64.
65.
66.
67.
68. Principles and Practices of Ophthalmology,Vol. 2 ,
Third edition, Albert and Jacobiec’s.
RETINA,Vol.1 , Fifth edition, Ryan.S.J.
Kanski’s Clinical Ophthalmology, 8th edition,
Bowling B.
Practical Handbook of OCT , Lumbroso.B, Rispoli M.
Step by Step Optical CoherenceTomography.
