Branched Retinal Vein Occlusion (BRVO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of BRVO.
Also encompasses salient points for PGMEE
Central Retinal Vein Occlusion (CRVO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRVO.
Also encompasses salient points for PGMEE
Central Retinal Vein Occlusion (CRVO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRVO.
Also encompasses salient points for PGMEE
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system by thrombus formation and may involve the central, hemi-central or branch retinal vein.
The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
updating in diabetic macular edema including old and new approach era, including DRCR protocol
how to approach, how to treat, when to surgery
plus knownledge about anti-VEGF therapy up to date
Retinoblastoma for undergraduate MBBS Students.
Covers the basics of Aetiology, Genetics, pathophysiology, clinical features, Classification and management of Retinoblastoma.
Also encompasses salient points for PGMEE
Hypertensive Retinopathy (HTN-R) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, Classification and management of HTN-R.
Also encompasses salient points for PGMEE
Diabetic Retinopathy (DR) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, Classification and management of DR.
Also encompasses salient points for PGMEE
Central Retinal Artery Occlusion (CRAO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRAO.
Also encompasses salient points for PGMEE
Optic Neuritis for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of optic neuritis.
Features of Multiple sclerosis and demyelinating optic neuritis have been detailed.
Also encompasses salient points for PGMEE
Optic Atrophy for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types and associated conditions of optic atrophy.
Also encompasses salient points for PGMEE
Papilloedema for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, stages and associated conditions of optic disc edema, pseudopapilloedema and papilloedema.
Also encompasses salient points for PGMEE
Retinoscopy for undergraduates and post-graduates.
salient points covering examinations and PGMEE.
Detailed discussion of the technique of retinoscopy and its utility in deducing refractive errors.
Use of cycloplegic refraction and subjective refraction has been discussed.
"Sturm's Conoid" for undergraduate MBBS Students.
Covers the basics of Sturm's Conoid, including the ray diagram and explanation of Sturm's interval and circle of least confusion.
it's application in Astigmatism has been covered.
Also encompasses salient points for PGMEE
"APHAKIA" for undergraduate MBBS Students.
Covers the basics of Aphakia and its management.
typical problems associated with spectacle correction of Aphakia have been detailed.
Also encompasses salient points for PGMEE
Management of Cataract for undergraduate MBBS Students.
Covers the basics of diagnosis of cataract, evaluation of a case of cataract and various modalities of treatment of cataract.
Also encompasses salient points for PGMEE.
Overview of Cataract for undergraduate MBBS students.
Covers the aetiology, clinical features, associations and management of cataract in detail.
Also includes salient points for PGMEE.
congenital cataract for undergraduate MBBS Students.
Also covers salient points for PGMEE.
Aetiology, clinical features and management discussed in detail.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
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 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
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
2. Retinal Vein Occlusion
• Retinal vein occlusion is the second
most common cause of visual loss due
to retinal vascular disease1-3
• Types:
– Branch retinal vein occlusion (BRVO)
– Hemi-retinal vein occlusion (HRVO)
– Central retinal vein occlusion (CRVO)
• BRVO is the most common3
– Five-year incidence of 0.6% (21/3558) for
BRVO and
– 3x m/c than CRVO3
• Persistent macular edema causes VA
loss
1. Yau et al. Intern Med J. 2008; 2. RCO RVO guidelines. 2009; 3. Klein et al. Trans Am Ophthalmol Soc. 2000.
HRVOBRVO
2
3. EPIDEMIOLOGY
Definition : a segmental
intraretinal haemorrhage
not exceeding midline
caused by obstruction in
one of the branches of the
main vein draining the
corresponding retinal area
first
described by
Leber in 1877
Age
incidence :
more than
90% cases
>50yrs
No sex/race
predilection
usually
unilateral,
bilateral
only in 9%
3
4. CLASSIFICATION
• one of the
major branch
retinal veins is
occluded
Major
BRVO
• one of the
macular venules
is occluded
Macular
BRVO
4
66% : Superotemporal quadrant
5. THEORIES OF AETIO-PATHOGENESIS
1.Arterio-venous
Crossing
2.Degenerative Changes of
Vessel Wall
3.Hematological Disorders
4.Resistance to Activated
Protein C and Deficiency of
Protein C or Protein S
5.Deficiency of Antithrombin and
Mutation in the Prothrombin
Gene
6.Anti-Phospholipid Antibodies
and Hyperhomocysteinemia
5
8. Pathogenesis of Macular Edema in
BRVO
Vascular occlusion/hypoxia
Increased VEGF / IL-6 secretion
damage to the tight junctions of
capillary endothelial cells
BRB Breakdown
Fluid flux from vessels to tissue
according to Starling's law
8
9. BRVO : C/F
Major BRVO
• can be asymptomatic or
• with visual blurring usually
involving the sector of visual
field corresponding to the
area of the retina involved.
Macular BRVO
• there is always a central
visual disturbance with
normal peripheral vision
•asymptomatic/Sudden painless loss of Vn
•Vision loss at presentation is related to the extent of macular damage
from intraretinal oedema, haemorrhage or capillary non-perfusion
9
10. OPHTHALMOSCOPIC FEATURES
Acute RVO Chronic RVO
Intra-retinal haemorrhages : flame shaped
& dot - blot
Cystoid macular edema
Hard exudates RPE atrophy
Cotton wool spots ERM / sheathing of vessels
Optic disc edema Shunt vessels/ venous collaterals
Macular edema NVD/NVE/NVI
Dilated , tortuous retinal veins in
segmental distribution
Late complications :
VH
RD
NVG
10
11. Infero-temporal brvo in female aged 53years :
dilated , tortuous veins.
soft exudates and hemorrhages 11
14. a sheathed supero temporal vein.
Haemorrhages and cotton wool
spots in supero-temporal acute
BRVO
14
15. The characteristic fluorescein
angiographic findings in BRVO include
ACUTEPHASE
• Delayed venous
filling/emptying
• Areas of Capillary
non-
perfusion/closure :
• A. Perfused
BRVO— <5DD
• B. Non-perfused
BRVO : >5DD
• Macular oedema :
perfused, non-
perfused or mixed
LATEPHASE
• micro vascular
abnormalities
• Late staining
and leakage
from the
affected veins is
seen
• particularly useful
in determining the
extent of ME and
Ischemia
• Blocked
fluorescence d/t
hemorrhages seen
through all phases
• Dilated capillaries,
microaneurysms
and telangiectatic
changes seen
15
16. Blocked fluorescence & non-perfusion
Late staining
Leakage around blocked vessel
late staining
16
23. • Current treatment options focus on the
sequelae of the occluded venous branch, such
as ME, NV, VH , TRD .
• The complex pathogenesis of this disease
requires investigation and treatment of all risk
factors (hypertension, diabetes mellitus, blood
lipid disorders, hematological disorders).
23
24. Intravitreal Corticosteroids
• In various studied doses from 4 to 25 mg,
triamcinolone acetonide (TA) has been
reported to be effective
• complications are raised intra-ocular pressure,
infectious endophthalmitis, post-injection
steroid-induced cataract, retinal detachment.
24
25. OZURDEX™
(dexamethasone intravitreal implant)
• OZURDEX® : FDA-approved t/t for macular edema
following BRVO.
• Injectable, biodegradable intravitreal implant contains 0.7 mg (700 μg)
dexamethasone in NOVADUR™ solid polymer DDS (preservative-free).
preloaded in sterile, single-use, applicator
• Poly (D,L-lactide-co-glycolide) PLGA biodegradable polymer matrix : slowly degrades to
lactic acid and glycolic acid as dexamethasone is gradually released. 25
27. Humanized monoclonal IgG
antibody against VEGF-A
1.25 to 2.5 mg
monthly x 6 months
Off-label use
M/c a/e : conjunctival
hyperemia and subconjunctival
hemorrhage at injection site.
1.BEVACIZUMAB
(AVASTIN)
27
28. 2.RANIBIZUMAB
( LUCENTIS )
Fab fragment of parent
molecule of bevacizumab
Designed for intra-ocular
use.FDA approved
0.5 or 0.3 mg
monthly x 6months
10-25 x more costly
28
29. Macular Grid Laser
Photocoagulation
MLG is recommended as an effective treatment to reduce the ME in BRVO :
after a period of 3 to 6 months after onset
and following absorption of the majority of hemorrhage
if VA is 20/40 or worse.
If FFA reveals macular nonperfusion, MLG not warranted.
Argon MLG is usually used for this purpose. However, diode laser (810 nm) and
krypton red laser (647 nm) also can be used.
29
30. Applied only to the area of leaking
capillaries
cover all areas of leaking
capillaries within 2 DD of
fovea
not extend beyond 2DD from
fovea
not extend within
the FAZ
avoid collateral vessels and
retinal haemorrhages
100 µm spots at 0.1 second
produce medium white burn
•spacing of one half to one burn-width apart
30
31. Scatter Laser
Photocoagulation
significantly reduced the development of retinal
neovascularization and vitreous hemorrhage.
if all eyes with large retinal nonperfusion were treated,
64% of these patients would never develop NV.
If only the eyes that develop NV were treated, the events
of VH decrease from 61% to 29%.
waiting is generally advocated until NV actually develops
before scatter photocoagulation is considered.
31
32. Laser spots spaced one
burn width apart
covering entire involved
segment
extending no closer than 2
DD from fovea
Spot Size : 200-500
microns
Duration : 0.1 s
Medium
white burn
Argon
green/
Ag
blue-
green 32
33. Clinical Trials and Venous
Occlusive Diseases
2010 Anti-VEGF Ranibizumab studies
BRAVO and CRUISE
2009 Steroid studies
SCORE Study Ozurdex Trials
Laser studies
1980s Branch Vein Occlusion Study
(BVOS)
1990s Central Vein Occlusion Study
(CVOS)
33
34. • Perform FA for macular edema, macular non-perfusion, retinal
neovascularization only after retinal hemorrhages have cleared
adequately (3-6 months)
• If macular edema is the cause of a vision less than 6/12,
undertake macular grid photocoagulation.
• If macular non-perfusion is the cause of decreased vision then no
laser treatment should be performed. Follow up these cases every
four months.
• If retinal non-perfusion more than 5 disc areas, follow up for
neovascularization at 4 monthly intervals.
• Undertake laser photocoagulation in the involved quadrant only if
neovascularization develops.
BVOS
34
35. BRVO Summary
BRVO:
• SCORE: Laser better than IVTA
• OZURDEX: Dexamethasone better
than sham (no laser arm)
• BRAVO: Ranibizumab monthly for 6
months better than observation/laser
in BRAVO. Improved VA: 61% vs 29%
eyes gained 15 or more letters
35
36. T/T summary in RVO’s
T/T Modality CRVO BRVO
Erythrocyte/platelet anti-
aggregative therapy
Routine use of ticlopidine / troxerutine for improving VA
or resolution of VH not recommended
Fibrinolysis Limited use in acute CRVO
(<11days): I.V. low dose rt-
PA +Heparin
Routine use not
recommended
Isovolemic hemodilution Routine use for improving VA or resolution of VH not
recommended
Pars plana vitrectomy Routine use not recommended
Intra-vitreal steroids Improve VA /resolve ME TA not sup. to MLG.
A/E >than MLG /anti-
VEGF
Intra-vitreal anti-VEGF Bevacizumab/ranimizumabused effectively for improving
VA , resolving ME & NV.Trials ongoing.
36
37. Modality CRVO BRVO
Grid laser
photocoagulation
Not recommended for t/t
of ME
Indicated in ME and
VA≤20/40 of 3 months
duration.
Not recommended in
macular ischemia .
Scatter laser
photocoagulation
For NV : prophylactic t/t
not recommended if
gonioscopy & dilated
fundus examination
possible every 4 weeks .
If NV +nt : prompt laser to
avoid sec. complications
Recommended if disc /
retinal NV +nt
37
38. Natural Course and Visual Prognosis
Determine the natural course of BRVO
efficiency of the
developing
collateral
circulation
integrity of arterial
perfusion to the affected
sector
Site/degree of
occlusion,
38
39. In general, BRVO has a good prognosis.
50–60% of eyes have a final VA of 20/40 or better even
without any treatment.
Chronic ME and VH d/t neovascularizations account most
frequently for a poor final VA.
Retinal neovascularization and persistent ME develop in
25% and 60% of eyes, respectively.
39