This document discusses the morphological changes that occur in the optic nerve head and retinal nerve fiber layer in glaucoma. It describes the various patterns of glaucomatous optic nerve damage including focal notching, concentric cupping, saucerization, and advanced cupping. Features that indicate glaucomatous damage include neuroretinal rim thinning, disc hemorrhages, and changes in the retinal vasculature around the optic disc. Evaluation of the optic nerve head is important for early detection of glaucoma before visual field loss occurs.
Most retinal surgeons are trained to create formal retinal drawings of the fundus.
Retinal drawings are useful to document pathology, although more and more people now prefer fundus photographs.
Can be used for serial follow up of patients to document changes in the pathology.
Most retinal surgeons are trained to create formal retinal drawings of the fundus.
Retinal drawings are useful to document pathology, although more and more people now prefer fundus photographs.
Can be used for serial follow up of patients to document changes in the pathology.
A systematic approach with practical tips to diagnose and manage optic disc pallor. Disc pallor is often encountered in the routine clinical practice and remains a diagnostic enigma for most ophthalmologist. I illustrate the relevant practical points to be looked out for to deal with disc pallor.
A systematic approach with practical tips to diagnose and manage optic disc pallor. Disc pallor is often encountered in the routine clinical practice and remains a diagnostic enigma for most ophthalmologist. I illustrate the relevant practical points to be looked out for to deal with disc pallor.
Evaluating the optic nerve head in glaucomaRiyad Banayot
The best method readily available to the clinician for performing this examination is high plus lens fundus biomicroscopy. Optimal magnification can be achieved by using a +60D lens which provides 1.5 times the magnification of a 90D lens. During this examination the patient's pupils must be maximally dilated with a combination of mydriatic agents such as 1% Tropicamide and 2.5% Phenylephrine.
Gonioscopy and optic nerve head evaluationAhmedfaik
this is a simple presentation copy paste from kanski clinical ophthalmology about gonioscopy and optic nerve head changes in glaucoma... hope you get benefit
thesis statement is a sentence that sums up the central point of your paper or essay. It usually comes near the end of your introduction.
Your thesis will look a bit different depending on the type of essay you’re writing. But the thesis statement should always clearly state the main idea you want to get across. Everything else in your essay should relate back to this idea.
Example: Thesis statement
Despite Oscar Wilde’s Aestheticist claims that art needs no justification or purpose, his work advocates Irish nationalism, women’s suffrage, and socialism.
You can write your thesis statement by following four simple step
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.
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.
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.
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.
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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
- 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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
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.
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
2.
Glaucoma is defined as heterogeneous group of
disorders which manifests as chronic progressive optic
neuropathy characterized by specific morphological
changes at optic nerve head and retinal nerve fibre layer
with resultant loss of retinal ganglion cells which results
in loss of visual fields.
3.
For many years , the diagnosis of glaucoma was
based on :
1. raised intraocular pressure
2. visual field changes
3.optic nerve head evaluation
5.
Raised IOP is not a diagnostic criteria but a risk
factor for glaucoma and patients with normal IOP
may develop glaucomatous disc changes.
It has been proved that 20-40% of ganglion cells are
lost before visual field defects develop in patients of
glaucoma on standard automated perimetry.
6.
Pre perimetric glaucoma is a new terminology to describe
glaucomatous optic neuropathy before development of
visual field defects.
It is detected by evaluating and documenting the optic
nerve head changes and retinal nerve fibre layer defects.
In one study fifty five percent of patients of ocular
hypertension converted to treatment group based on
optic disc changes without field changes.
Another study showed that sixty percent of ocular
hypertensives have RNFL defects up to 6 years before
they developed visual field defects on standard
automated perimetry.
Pre perimetric glaucoma
7.
Neuroretinal rim
The neuro retinal rim (NRR) is the tissue between the
outer edge of the cup and the optic disc margin.
The normal rim has an orange or pink colour and a
characteristic configuration in most healthy eyes: the
inferior rim is the broadest followed by the superior,
nasal and temporal (the ‘ISNT’ rule).
The cardinal feature of glaucomatous optic
neuropathy is a loss of NRR from the inner edge of
the rim.
Normal optic nerve head
9.
Features that should raise suspicion that
glaucomatous damage has already occurred
include:
1. notching of the rim
2. hemorrhage crossing the rim
3. undercutting of rim
4. asymmetry of rim width between eyes in
absence of asymmetry of disc size
5. an abnormally thin rim in one or two sectors.
10.
An approximate rule is that a vertical cup-disc ratio
of >0.7 or loss of rim to the disc margin anywhere
outside the temporal sector strongly suggest
glaucoma . This rule may not apply if the disc is
extremely large or very tilted.
12.
Optic disc size is important in deciding if a cup-disc (C/D)
ratio is normal.
Normal median vertical diameter for non-glaucomatous
discs is 1.50 mm in a Caucasian population.
Optic disc size
13. The C/D ratio indicates the diameter of the cup expressed as
a fraction of the diameter of the disc; the vertical rather than
the horizontal ratio is generally used in clinical practice.
The NRR occupies a relatively similar cross-sectional area in
different eyes.
1. Small discs have small cups with a median C/D ratio of
about 0.35
2. Large discs have large cups with a median C/D ratio of
about 0.55
3. Only 2% of the population have a C/D ratio greater than 0.7.
4. In any individual, asymmetry of 0.2 or more between the
eyes should also be regarded with suspicion, though it is
critical to exclude a difference in overall disc size.
Cup–disc ratio
14.
Disc diameter(in mm) Mean cup-disc ratio
<1.0 0.26
1.2 0.33
1.4 0.39
1.6 0.45
1.8 0.5
>2.0 0.55
Normal vertical cup-disc ratio for vertical disc diameter
15.
Disc size is extremely variable. It can be measured by
using the small size spot of a direct
ophthalmoscope. This spot size can be used to
estimate whether a disc is large or smaller than
average.
Disc size can also be evaluated using conventional
photographic means with overlay grid as well as
optic nerve head analysis.
17.
Certain features of highly myopic discs interfere
with interpretation of NRR and cupping:
Relatively large disc area
Oblique insertion of optic disc which distorts the
view of temporal rim.
A temporal gray crescent which could result in
physiologic rim being misinterpreted as
pathologically thin in that area.
A shallow cupping which masks the deepening of
cup in glaucoma.
Optic nerve head in
myopia
18.
Oblique insertion of optic nerve heads in myopic eyes can obfuscate the
interpretation of the neuroretinal rim and creates a wide temporal
peripapillary crescent. In this case, the asymmetry and loss of the superonasal
rim of the right eye corresponds to glaucomatous damage
19.
Retinal nerve fiber layer(RNFL) is seen as striations
in the light reflexes from the bundles of nerve fiber
commonly seen with red free light either on direct
ophthalmoscope or on fundus camera.
RNFL is seen better at the posterior pole in the
peripapillary region where they reach a critical
thickness especially at the vertical poles of optic
nerve head.
Peripapillary retina
20.
Scleral lip
It is seen as thin even white rim outside disc margin
It represents anterior extension of sclera between the
choroid and the optic nerve.
Peripapillary
pigmentation
23.
it is seen within peripheral tissues of optic nerve head
Scleral lip is seen peripheral to the gray crescent.
It is often bilateral and it is usually located along temporal
or infero-temporal disc margin.
Grey crescent is due to internal extension of Bruch's
membrane in the peripapillary scleral ring.
At times in evaluation of optic nerve head ,the grey
crescent can be taken as peripapillary tissue and not NRR
resulting in falsely small optic disc and small NRR area.
Grey crescent
25.
It is seen between peripheral NRR and zone alpha.
It represents a retraction of retinal pigment
epithelium from the disc margin due to atrophy of
RPE.
Sclera and large choroidal vessels are visible due to
RPE atrophy.
It is more frequent and more extensive in patients
with POAG and NTG.
Location and extent of zone beta atrophy correlates
with visual field loss.
It indicates that the area has poor perfusion.
Zone beta
26.
It is better detected at the temporal disc margin
On the inner side ,it is bounded by zone beta or
peripapillary scleral ring and on the outer side by
retina.
It is seen as irregular hyperpigmentation and
hypopigmentation.
It is due to parapapillary crescent of RPE irregularity
close to the margin of Bruch's membrane.
It is present in almost all normal eyes.
Zone alpha
28.
The spectrum of disc damage in glaucoma ranges
from highly localized tissue loss with notching of the
NRR to diffuse concentric enlargement of the cup.
The optic nerve head changes in glaucoma
29.
Glaucomatous damage results in characteristic signs
involving
(a) the optic nerve head
(b) the peripapillary area
(c) the retinal nerve fibre layer
Morphology of glaucomatous optic atrophy
30.
Selective loss of neural rim tissue in glaucoma occurs
primarily in the inferotemporal region of optic disc and
less commonly in superotemporal sector in early
glaucoma resulting in enlargement of cup in vertical or
oblique direction.
In early glaucomatous eyes ,the inferotemporal neural
rim area is smaller than superotemporal area so that the
vertical cup disc ratio is more than horizontal cup disc
ratio.
Focal atrophy
33.
As the glaucomatous process continues, temporal neural
rim is involved after vertical poles, with nasal quadrant
being the last to be destroyed.
The focal atrophy of the neural rim begins as small
discrete defect , usually in inferotemporal quadrant,
which is known as polar notching or focal notching or
pit-like changes.
34. When the local thinning
of neural rim tissue
reaches the disc margin , a
sharpened rim is
produced .
If a retinal vessel crosses
the sharpened rim , it will
bend sharply at the edge
of the disc creating
bayoneting at the disc
edge.
Bayoneting
35. Inferotemporal loss of
neural rim in glaucomatous
optic atrophy, creating a
sharpened rim(SR) at the
disc margin, a sharpened
polar nasal edge (SPNE)
along the cup margin,
bayoneting at the disc edge
(BDE) where the vessels
cross the sharpened rim,
and laminar dot sign (LDS)
due to exposure of fenestrae
in lamina cribrosa.
36. In some cases the loss of neural rim begins temporally and
then progresses circumferentially towards the poles
resulting in enlargement of cup in concentric circles with
retention of round shape of cup. This type of
glaucomatous disc damage is referred to as concentric
atrophy and the phenomenon involved is known as
temporal unfolding.
Concentric atrophy
37.
It is difficult to distinguish concentric atrophy from
physiologic cup ,hence it is important
o to compare the cup in fellow eye
o to study serial photographs for evidence of
progressive change.
38. Large physiologic optic nerve head cups that are symmetrical and intact.The
shape of the physiologic cup is roughly correlated with the shape of the disc,
which means that the margins of cup and disc tend to run more or less
parallel. The cup has a horizontally oval shape in most normal eyes; thus, a
vertical CDR greater than the horizontal CDR should be considered
suspicious.
39.
Sometimes a thinning of neural rim may be seen as
crescentic shadow adjacent to the disc margin on
direct ophthalmoscopy.
It is a sign of early glaucomatous disc damage and it
should not be confused with gray crescent in optic
nerve head.
40.
In some cases deepening of cup is predominant
pattern of early glaucomatous disc damage .
It occurs only if the lamina cribrosa is not initially
exposed and it produces overpass cupping, in which
the blood vessels initially bridge the deepened cup
and later collapse into it.
Deepening of cup
41. Continued deepening of cup causes exposure of
underlying lamina cribrosa, which is often recognized
by gray fenestrae of lamina, seen on direct
ophthalmoscope as gray dots. This has been referred to
as laminar dot sign.
42.
In early stages of glaucomatous optic atrophy
enlargement of cup progresses ahead of area of
pallor.
This pattern differs from other types of optic atrophy
in which area of pallor is more than the enlargement
of the cup.
It is important to differentiate area of cupping from
area of pallor either by examining the optic disc with
stereoscopic techniques or by seeing the kinking of
blood vessels at the cup margin.
Pallor cup discrepancy
44.
Pallor–cup discrepancy may occur with focal or diffuse
enlargement of cup.
Saucerization refers to a pattern of early glaucomatous
change in which diffuse shallow cupping extends to the
disc margin with retention of a central pale cup.
Focal saucerization refers to more localized ,shallow
sloping cup, usually in inferotemporal quadrant.
The retention of normal neural rim color in the area of
focal saucerization is known as tinted hollow. As the
glaucomatous process continues, this is replaced either by
grayish hue known as shadow sign or by laminar dot
sign.
46.
Eventual loss of all neural rim tissue results in total
cupping which is characterized by white disc with
bending of all blood vessels at disc margin.
This is also known as bean-pot cupping because the
cross section of a histologic section reveals extreme
posterior displacement of lamina cribrosa and
undermining of disc margin.
Advanced glaucomatous cupping
48.
Optic disc hemorrhages:
Also referred to as splinter hemorrhages or drance
hemorrhages .
They are seen more commonly in patients of normal
tension glaucoma than COAG.
They tend to come and go and reappear at same site
or different site.
They typically cross the disc margin but during
resorption, the papillary portion may disappear first
so that an extra papillary hemorrhage remains.
Vascular signs of glaucomatous
optic atrophy
50.
The most common location of splinter hemorrhage is
the inferior quadrant.
They most often occur in early or middle stages of
glaucomatous optic atrophy and disappear in
advanced stage of glaucomatous optic atrophy with
absent neural rim.
Although not pathognomonic sign of glaucoma,
splinter hemorrhages are a significant finding as they
often precede RNFL defects ,polar notching and
visual field defects.
51.
They are especially suggestive of glaucoma when
associated with high IOP.
They are more commonly seen in diabetic patients
with glaucoma than non-diabetic patients with
glaucoma.
Disc hemorrhages are more commonly associated
with progressive visual field changes and are
suggestive that glaucoma may be out of control.
52.
Tortuosity of retinal blood vessels may seen in
advanced glaucomatous disc damage and they
represent loops of collateral blood vessels in
response to chronic retinal vessel occlusion.
Venovenous anastomoses associated with chronic
branch retinal vessel occlusion and massive flame
shaped hemorrhages also occur with increased
frequency in glaucomatous eyes.
Tortuosity of retinal blood vessels
54.
One study suggested that presence of cilioretinal
arteries in glaucomatous eyes was associated with
larger cup-disc ratio and progressive visual field
defects.
Another study suggested that presence of cilioretinal
arteries was associated with retention of central
visual field for longer duration.
Cilioretinal arteries
55.
Overpass cupping
Baring of circumlinear vessel
Nasal displacement of blood vessels
Vertical eccentricity of central retinal vessel trunk
Generalized arterial narrowing
Location of retinal blood
vessel in relation to cup
56. Overpass cupping is due to deepening of cup where a
blood vessel bridges the cup and then collapse into it.
Baring of circumlinear vessel:
a. In many normal optic discs, one or two blood vessels
curve the outline of a portion of physiologic cup. With
glaucomatous enlargement of the cup, these circumlinear
blood vessel may be bared from the margin of the cup.
b. This sign is not pathognomonic of glaucoma but it’s
presence in glaucoma suspect patients is associated with
visual field loss.
59.
Earlier thought to be related to glaucomatous disc
changes, nasal displacement of blood vessels in
now no longer considered diagnostic of glaucoma.
However vertical eccentricity of central retinal
vessel trunk may be related to course of
glaucomatous optic atrophy.
Neural rim loss was more likely to occur in the
vertical quadrant further away from the central
retinal vessel trunk.
60.
Generalized arterial narrowing outside optic nerve
head is seen in some patients of chronic open angle
glaucoma but it is a nonspecific finding also seen in
patients of anterior ischemic optic neuropathy.
62.
• The loss of axonal bundles in glaucoma lead to
loss of neural rim tissue
visible defects in retinal nerve fibre layer.
These defects appear as
a. Dark stripes or wedge shaped defects in
peripapillary region
b. Diffuse loss of retinal striations.
They often follow disc hemorrhages and correlate
highly with visual field defects and lost neural rim
tissue.
Retinal nerve fibre bundle defects
63. RNFL defects are also seen in
o many neurological disorders
o ocular hypertension
o healthy eyes.
Diffuse RNFL loss occurs in following order of
decreasing frequency:
COAG > ocular hypertension > normotensive
individuals.
RNFL defects either localized or diffuse may be the
initial sign of glaucomatous disc damage
64.
Retinal nerve fibre bundle defects
Superotemporal wedge shaped defect Same defect in red free light
65.
These changes are nonspecific for glaucoma as they also
occur in myopia and ageing.
Peripapillary atrophy occur more frequently and it is
larger in glaucomatous eyes than normal eyes.
It enlarges with progression of glaucoma and correlate
with the quadrant of greater neural rim loss.
Absence of peripapillary atrophy may be associated
with decreased progression of glaucomatous damage in
patients of ocular hypertension.
Peripapillary pigmentary changes
67.
1.Normal variation in physiological cup
2.Optic disc coloboma
3.Optic pit
4.Morning glory syndrome
5.Tilted disc syndrome
6.Optic disc hypoplasia
7. Arteritic type of anterior ischemic optic
neuropathy
8.Intra cranial aneurysms
Differential diagnosis of glaucomatous optic
atrophy
68.
Optic disc coloboma
Colobomas of the optic nerve heads can simulate glaucomatous
cupping. This patient would appear to have nearly total cupping
and pallor, and yet the IOP was low normal and the visual fields
were full with normal central vision.
74.
Qualitative assessment
1. Direct ophthalmoscopy
2. Indirect ophthalmoscopy
3. Slit lamp biomicroscopy using
o 90 d lens
o 78 d lens
o 60 d lens
4. Fundus camera photography
Various techniques of optic
disc evaluation
76.
Optic disc can be assessed clinically as follows:
1. A narrow slit beam is focussed on the disc using a
fundus biomicroscopy lens
2. The height of the beam is adjusted until it matches the
distance between the superior and inferior limits of the
NRR (not the scleral rim surrounding the neural tissue)
and the diameter in mm read from the slit-lamp
graticule.
3. A correction factor may be necessary, dependent on the
lens used Refractive error affects measurement only
minimally, although myopia above −8 dioptres may
distort the result.
Slit lamp biomicroscopy
77.
Lens Correction factor
Volk 60 D × 0.88–1.0
Nikon 60 D Around 1.0
Volk 90 D ×1.3
Volk 78 D ×1.1
Goldman 3-mirror ×1.27
Correction factors for estimating optic
disc diameter
78.
Careful detailed drawing of the optic disc should be done on every
visit.
Following structures should be always documented
1. Size and shape of the optic nerve head.
2. Size and shape of the cup.
3. Neuroretinal rim thinning at the vertical cup
4. Disc hemorrhages
5. Position of blood vessel as they cross the cup margin.
6. Scleral crescent
7. Peripapillary atrophy
8. Nerve fiber layer defects
9. Tortuosity of blood vessel
10. Arteriolar narrowing
Disc recording