BLOK SISTEM INDERA

TUTOR :
Dyah Fauziah, dr, Sp.PA(K)
Composed by
Group 1 :
Nadhif Rashesa Brahmana 011611133007
Nur Ilma Asrianti 011611133112
M. Fitra Ramadhan 011611133139
Fariz Augusta 011611133143
Muftihana Hanin Nuha 011611133210
Fiequira Asri Ersyana 011611133217
Kevin Yuwono 011711133001
Zsa Zsa Ollyvia 011711133002
Roy Bagus Kurniawan 011711133003
Ulfa Dwi Karisma 011711133004

FACULTY OF MEDICINE

AIRLANGGA UNIVERSITY

2019
 TABLE OF CONTENTS

Cover
Table of Contents
Scenario
Objective
CHAPTER I
1.1 Main Problem
1.2 Keywords
1.3 Additional Questions and Information
1.4 Early Hypothesis
1.5 Early Concept Mapping
1.6 Learning Issues 1
CHAPTER II
2.1 Cognitive Strategy
2.2 Answer of Learning Issue 1
2.3 Logic and Critical Analysis of Problems in Scenario according to Refference
2.4 Obstacle
2.5 Learning Issues 2
CHAPTER III
3.1 Methods and Steps in Finding Information
3.2 Answer of Learning Issues 2
3.3 Final Hypothesis
3.4 Analysis
3.5 Group Opinion
3.6 Final Concept Mapping
Refferences
Critical Appraisal
 SCENARIO

A 55-year-old man came to the doctor with decreased visibility in both eyes

OBJECTIVE
After learning the sensory system ,5th semester student are able to explain physiology aspect
and biochemical system of sensory , pathophysiology and basic treatment of decrease of
awareness based on SKDI 2012.
CHAPTER I
1.1 Main Problem
Decreased visibility in both eyes.
1.2 Keywords
1. A man
2. 55 years old
3. Decreased visibility
4. Both eyes
1.3 Additional Questions and Information
Additional Question with Reasoning and Additional Information

Question Reason Answer

Anamnesis / History Taking

Identity

What is the patient’s To determine identity No data

name?

How old is the To determine identity 55 years old

patient?
What is his job? To determine risk factors Farmer

Where does he live? To determine risk factors No data

What is his marital To determine identity Married

status?

History of present
illness

How long has he had To determine the etiology of the Last 7 months
this illness? illness

Are there any other To determine the conditions of the Gradual vision loss
complaints? patients which related to main
Cloudy vision
complaints

Diplopia (Double vision)

To find out the cause of the patient's

Any pain around the No pain
disease
eye?

To find out the cause of the patient's

Red eye? No red eye
disease
 To find out the cause of the patient's
Hypertension No data
disease

Past Medical
History &

Family Disease

Has he ever To determine the etiology of the No data

experienced this illness
illness before?

Any consumption of No data

drugs before?

To find out the cause of the patient's No data

Is there any family
disease
disease history?
Is there a history of Might be related to present illness No data
Diabetes Mellitus

Is there a history of Might be related to present illness No data

trauma?

Psychosocial

To find out the cause of the patient's

How is his habit? No data
disease

Smoking, alcohol Might be related to present illness No data

history?

Last education No data

Physical
Examination

General To know about his condition from first No data

appearence
What is general
assessment of the first
glance?
 Vital Sign To determine the status of his body’s No data
vital functions
What are his vital
sign?

Examination Results

Examined Result

Vision Dextra : 6/20

Sinistra : 3/60

Ishihara Color vision deficiency

Intra-okuli pressure Dextra & sinistra : 17,3mmHg

Additional Questions, Reasons, and Answers

Question Reason Answer

What is the patient’s To find out the patient’s identity
Mr. S
name?

Where does the patient To find out socioeconomic conditions

Pujon Malang
live?

What is the patient’s last

High School
education?

Does the patient feel To know how bad is the condition

Yes, it is glare when
sensitive to light?
exposed to light

Does the patient wear To know the patient’s eye condition Reading glasses
glasses before? before

Are there diabetes To know the possible eye disorder due Drug controlled
mellitus and to systemic disease
hypertension?

What is the patient’s

To know the genetic factors Diabetes Mellitus
family history?

Does the patient smoke

One of the risk factors for eye No
and consume alcohol?
deficiency

What is the general

To know the patient’s awareness Normal
condition of the patient?
 What are the patient’s
Determination of a normal baseline can
vital sign?
ensure a standard comparison when
Normal
emergencies occur during treatment

Are there a result from the

Confirm whether there is a visual field Visual field
patient’s field check?
narrowing deficiency but not
specific

Are there a results of a

To know the structure of the posterior Detailed positive
funduscopic examination?
part of the eye reflect fundus
difficult to evaluate

What is the strength of the

To find out if the size of glasses is S +2.50 for close
patient’s reading glasses
increasing range reading
lens?

Does the patient have a

Can cause/accelerate the occurrence of No
history of taking drugs
cataracts
(such as steroids)?

What is the patient’s

Knowing that there is an existence of Height : 165 cm
weight and height?
obesity in patients or not
Weight : 60 kg

1.4 Early Hypothesis

1. Vision decreases at the age of 55 due to structural disorders.
2. Vision decreases at the age of 55 due to degenerative disorders.
3. Vision decreases at age 55 due to metabolic disorders.
4. Vision decreases at age 55 due to functional impairment.
1.5 Early Concept
Mapping

1.6 Learning Issues 1

1. Explain the anatomy and physiology of the eye!

2. What are the general eye examinations?
3. What is the pathophysiology of visual impairment due to:
a. Anterior structural
b. Posterior structural
c. Degenerative
d. Metabolic
e. Functional
4. What is the definition, pathophysiology, diagnosis, and type of cataract?
 CHAPTER II
2.1 Cognitive Strategy
To enrich cognitive thinking ability based on scenarios and problems that have been
given. The learning issue can be an encouragement to each member. We can get a lot of
knowledge and information which can be obtained through journals, e-books, printed books,
or lesson that has been explained by lecturers. All knowledge and information can be connected
and put together so as to produce a solution to the existing scenarios or problems. It helps us
learn how to think quickly and critically which is needed in the clinical phase or after becoming
a real doctor.
2.2 Answer of Learning Issue 1
2.2.1 Anatomy and Physiology of The Eye
A. Anatomy of the Eye
Each eye is composed of three concentric tunics or layers (Mescher, 2018):
1. A tough external fibrous layer consisting of the sclera and the transparent cornea;
2. A middle vascular layer consisting of choroid, ciliary body, and iris; and
3. An inner sensory layer, the retina, which communicates with the cerebrum through the
posterior optic nerve

Figure 2.1 Internal Anatomy of the Eye (Mescher, 2018)

This following table summarizes the components contained and its particular
function of the three tunics of the eye (Mescher, 2018).
 Figure 2.2 Tunics of the Eye, its components and functions. (Mescher, 2018).
Not part of these layers, the lens is a perfectly transparent biconvex structure
held in place by a circular system of zonular fibers that attach it to the ciliary body and
by close apposition to the posterior vitreous body. Partly covering the anterior surface
of the lens is an opaque pigmented extension of the middle layer called the iris, which
surrounds a central opening, the pupil (Mescher, 2018).
Located in the anterior portion of the eye, the iris and lens are bathed in clear
aqueous humor filling both the anterior chamber between the cornea and iris and the
posterior chamber between the iris and lens. Aqueous humor flows through the pupil
that connects these two chambers (Mescher, 2018).
The posterior vitreous chamber, surrounded by the retina, lies behind the lens
and its zonular fibers and contains a large gelatinous mass of transparent connective
tissue called the vitreous body (Mescher, 2018).
Lens
The lens is a transparent biconvex structure suspended immediately behind the
iris, which focuses light on the retina. Derived from an invagination of the embryonic
surface ectoderm, the lens is a unique avascular tissue and is highly elastic, a property
that normally decreases with age. The lens has three principal components (Mescher,
2018):
1. A thick (10-20 μm), homogeneous lens capsule composed of proteoglycans and
type IV collagen surrounds the lens and provides the place of attachment for the
fibers of the ciliary zonule.
2. A subcapsular lens epithelium consists of a single layer of cuboidal cells present
only on the anterior surface of the lens
3. Lens fibers are highly elongated, terminally differentiated cells that appear as
thin, flattened structures. The cytoplasm becomes filled with a group of proteins
called crystallins, and the organelles and nuclei undergo autophagy. Lens fibers
are packed tightly together and form a perfectly transparent tissue highly
specialized for light refraction.
 Figure 2.3 Histology Structure of the Lens, consisting of lens capsule (LC),
lens epithelium (LE), differentiating lens fiber (DLF), and mature lens fiber
(MLF) (Mescher, 2018)

B. Physiology of the Eye

The sensory receptors for vision are photoreceptors, which are located on the
retina. There are two types of photoreceptors, rods and cones (Table 3.4). Rods have
low thresholds, are sensitive to low-intensity light, and function well in darkness. The
rods have low acuity and do not participate in color vision. Cones have a higher
threshold for light than the rods, operate best in daylight, provide higher visual acuity,
and participate in color vision. The cones are not sensitive to low-intensity light
(Costanzo, 2018).
Information is received and transduced by photoreceptors on the retina and then
is carried to the CNS via axons of retinal ganglion cells. Some optic nerves cross at the
optic chiasm, and others continue ipsilaterally (Costanzo, 2018).
Photoreception
Photoreception is the transduction process in rods and cones that converts light
energy into electrical energy (Costanzo, 2018).
Rhodopsin, the photosensitive pigment, is composed of opsin (a protein
belonging to the superfamily of G protein–coupled receptors) and retinal (an aldehyde
of vitamin A). When light strikes the photoreceptors, retinal is chemically transformed
in process called photoisomerization, which begins the transduction process (Costanzo,
2018).
 Figure 2.4 Steps in Photoreception
Axons from retinal ganglion cells form the optic nerves and optic tracts, synapse
in the lateral geniculate body of the thalamus, and ascend to the visual cortex in the
geniculocalcarine tract (Costanzo, 2018).
Notice that the temporal visual fields project onto the nasal retina, and the nasal
fields project onto the temporal retina. Nerve fibers from each nasal hemiretina cross
at the optic chiasm and ascend contralaterally. Nerve fibers from each temporal
hemiretina remain uncrossed and ascend ipsilaterally. Thus fibers from the left nasal
hemiretina and fibers from the right temporal hemiretina form the right optic tract and
synapse on the right lateral geniculate body. Conversely, fibers from the right nasal
hemiretina and fibers from the left temporal hemiretina form the left optic tract and
synapse on the left lateral geniculate body. Fibers from the lateral geniculate body form
the geniculocalcarine tract, which ascends to the visual cortex (area 17 of the occipital
lobe). Fibers from the right lateral geniculate body form the right geniculocalcarine
tract; fibers from the left lateral geniculate body form the left geniculocalcarine tract
(Costanzo, 2018).
 Figure 2.5 Optic pathways of the eye

2.2.2 What are the general eye examinations?

There are several general eye examinations to take note;
 1. Visual Acuity
Measure of the spatial resolution of the visual processing system. VA is tested
by requiring the person whose vision is being tested to identify so-called
optotypes from a set viewing distance. A reference value above which visual
acuity is considered normal is called 6/6 vision, At 6 metres or 20 feet, a human
eye with that performance is able to separate contours that are approximately
1.75 mm apart. Vision of 6/12 corresponds to lower, vision of 6/3 to better
performance. Normal individuals have an acuity of 6/4 or better.
In the expression 6/x vision, the numerator (6) is the distance in metres between
the subject and the chart and the denominator (x) the distance at which a person
with 6/6 acuity would discern the same optotype. Thus, 6/12 means that a person
with 6/6 vision would discern the same optotype from 12 metres away (i.e. at
twice the distance). This is equivalent to saying that with 6/12 vision, the person
possesses half the spatial resolution and needs twice the size to discern the
optotype.
2. Confrontation Visual Field Testing
Confrontation visual field testing involves having the patient looking directly at
your eye or nose and testing each quadrant in the patient's visual field by having
them count the number of fingers that you are showing. Visual field testing
should be carried out in each eye separately. During binocular viewing, the
fields of the two eyes substantially overlap. Consequently, a visual field defect
in one eye will still register as having normal vision when both eyes are open.
The same holds true for binocular defects that occupy different positions in
space. Such defects will go undetected by the examiner unless the fields are
evaluated one eye at a time. As noted above, the eye not being tested should be
covered, either by placing a patch over it or by having the patient hold an
occluder over it. If a patch is used, position it diagonally and apply it so that it
bows slightly outward, which keeps the underside of the patch from rubbing on
the patient’s eyelashes.
3. Pupillary Examination
An examination of pupilary function includes inspecting the pupils for equal
size (1 mm or less of difference may be normal), regular shape, reactivity to
light, and direct and consensual accommodation. A thorough clinical
examination of the pupils requires only simple, inexpensive tools: a bright,
 even, handheld light source (such as a halogen transilluminator); a pupil-
measuring gauge, preferably in half-millimeter increments; neutral density
filters in 0.3, 0.6, and 0.9 log unit values to quantitate relative afferent pupillary
defects; and an examination room in which background illumination is easily
controlled.
In evaluating pupil size, the clinician shines a handheld light obliquely from
below the nose for indirect illumination and a clear view of the pupils in both
darkness and room light. To avoid accommodative miosis, the patient is
instructed to fix on a distant target, and the examiner should be careful not to
block the patient’s fixation. The pupils are measured 5–10 seconds after changes
in illumination to avoid pupillary fluctuations.
4. Motility and alignment examination
The examination of the ocular motor system generally consists of the
assessment of
(1) fixation and gaze-holding ability
(2) range of monocular and binocular eye movements
(3) ocular alignment
(4) performance of versions (saccades, pursuit)
In addition, depending on the findings of the basic examination, it may be
appropriate to test the vestibulo-ocular and optokinetic reflexes to differentiate
between supranuclear and nuclear or infranuclear disorders.
In a normal, awake person, the eyes are never absolutely still. Fixation is
interrupted by three distinctive types of miniature eye movements including
microsaccades, continuous micro drift, and microtremor. Square-wave jerks—
spontaneous, horizontal saccades of about 0.5 degrees, followed about 200 msec
later by a corrective saccade and occurring at a rate of less than 9 per minute—
can also be observed during fixation in most normal individuals.
When no efforts are being made toward ocular fixation or accommodation, the
eyes are said to be in a “physiologic” position of rest. With total
ophthalmoplegia, there is usually a slight divergence of the visual axes, and this
position usually also occurs during sleep, deep anesthesia, and death.
In patients complaining of intermittent diplopia, visual confusion, or
strabismus, tests of sensory fusion (e.g., stereoacuity) and fixation should be
 performed before the eyes are dissociated by tests of monocular visual function
(e.g., visual acuity, color vision, visual fields).
5. Ophthalmoscopy
Ophthalmoscopy is a test that allows a health professional to see inside the
fundus of the eye and other structures using an ophthalmoscope The pupil is a
hole through which the eye's interior will be viewed. Opening the pupil wider
(dilating it) is a simple and effective way to better see the structures behind it.
Therefore, dilation of the pupil (mydriasis) is often accomplished with
medicated eye drops before funduscopy. However, although dilated fundus
examination is ideal, undilated examination is more convenient and is also
helpful (albeit not as comprehensive), and it is the most common type in primary
care.
It is of two major types:
1. Direct ophthalmoscopy one that produces an upright, or unreversed, image
of approximately 15 times magnification.
2. Indirect ophthalmoscopy one that produces an inverted, or reversed, image
of 2 to 5 times magnification.
Ophthalmoscopy is done as part of a routine physical or complete eye
examination.It is used to detect and evaluate symptoms of various retinal
vascular diseases or eye diseases such as glaucoma.In patients with headaches,
the finding of swollen optic discs, or papilledema, on ophthalmoscopy is a key
sign, as this indicates raised intracranial pressure (ICP) which could be due to
hydrocephalus, benign intracranial hypertension (aka pseudotumor cerebri) or
brain tumor, amongst other conditions. Cupped optic discs are seen in
glaucoma.In patients with diabetes mellitus, regular ophthalmoscopic eye
examinations (once every 6 months to 1 year) are important to screen for
diabetic retinopathy as visual loss due to diabetes can be prevented by retinal
laser treatment if retinopathy is spotted early.In arterial hypertension,
hypertensive changes of the retina closely mimic those in the brain and may
predict cerebrovascular accidents (strokes).
6. External Examination
An eye examination is a series of tests performed by an ophthalmologist
(medical doctor), optometrist, or orthoptist, optician, assessing vision and
ability to focus on and discern objects, as well as other tests and examinations
pertaining to the eyes. External examination of eyes consists of inspection of
the eyelids, surrounding tissues and palpebral fissure. Palpation of the orbital
rim may also be desirable, depending on the presenting signs and symptoms.
The conjunctiva and sclera can be inspected by having the individual look up,
and shining a light while retracting the upper or lower eyelid. The position of
the eyelids are checked for abnormalities such as ptosis which is an asymmetry
between eyelid positions.
1. Alignment, position of the eyes, the conjunctiva, and sclera:
In evaluating alignment, shine a light into the eyes and evaluate the reflection
of light on the pupil or iris. The normal reflection should be symmetric. If the
reflex on one eye is more medial, the patient may have exotropia; if more lateral,
the patient may have esotropia. To evaluate position, inspect for outward
deviation, called exophthalmos. In evaluating the conjunctiva and sclera, note
the color of the palpebral conjunctiva (looking for unusual paleness signifying
anemia), the color of the sclera (noting blueness, yellowness, redness), the
vascular pattern, or the presence of nodules. In evaluating the cornea and iris
look for opacities of the cornea or lens and for abnormal bowing forward of the
iris. Also note the symmetry of the palpebral fissures, which provide a clue for
evaluating exophthalmos or ptosis.
2. Pupils:
In evaluating the pupils, inspect the size, shape, symmetry and reactivity of the
pupils. Normal pupillary size is between 3-5 mm with less than 0.5mm size
difference between the two. Pupillary inequality is termed anisocoria. If one or
both pupils are particularly large or small, be sure that reactivity to light is
normal and symmetric. If this is not the case, you need to decide which is the
abnormal pupil. If reactivity seems impaired, be sure that the room has been
fully darkened and a bright light has been used. If reactivity still seems
impaired, test pupillary near reaction.
3. Extraocular movements:
Normally, the eyes move together and are controlled by six muscles (four rectus
and two obliques). There are six cardinal directions that allow you to test the
function of each muscle and the supplying nerve. If one of the muscles is weak
or paralyzed, the eye will deviate from its normal position. In testing extraocular
 movements note normal conjugate movements or deviations from normal,
including the presence of nystagmus, or lid lag.
2.2.3 Pathophysiology of visual loss
Pathophysiology of visual loss due to impairment in anterior segment of the eye
1. Conjunctiva
The conjunctiva is a transparent and thin mucous membrane that encloses the
posterior surface of the eyelid (palpebral conjunctiva) and the anterior surface of the
sclera (bulbary conjunctiva). The conjunctiva borders the skin on the palpebral edge
and with the corneal epithelium in the limbus.
2. Sclera
Sclera is a connective tissue that is flexible and gives shape to the eye. This tissue is
the outermost part that protects the eyeball. The front part of the sclera is called the
cornea which is transparent which allows light to enter the eyeball.
3. Cornea
Cornea is the clear membrane of the eye, the translucent membrane of the eye is a
layer of tissue that covers the front of the eyeball. This cornea is inserted into the
sclera of the limbus, a circular indentation at this joint called the scleral sulcus
The adult cornea has an average thickness of 550 μm at its center (there is variation
according to race); the horizontal diameter is about 11.75 mm and the vertical is 10.6
mm.
From anterior to posterior the cornea has five layers, namely:
1. 1) Epithelium
The thickness of this epithelium is 50 μm. The corneal epithelium has five layers of
hornless epithelial cells consisting of basal cells, polygonal cells, and flat cells.
2. 2) Membrane Bowman
The Bowman membrane is located under the basal membrane of the corneal
epithelium
which is collagen which is arranged irregularly like stroma and
comes from the front of the stroma.
3. 3) Stroma
The corneal stroma makes up about 90% of the thickness of the cornea. Stroma
consists of lamel which is a collagen arrangement that is parallel to one another. On
the surface, visible regular matting is in the peripheral part and collagen is branched.
4. 4) Descemet membrane
 Descemet membrane is an acellular membrane and is
back limit of the corneal stroma.
5. 5) Endothelial
Endothelium comes from the mesothelium, one layer, hexagonal shape, and thickness
of 20-40 μm. This layer plays a role in maintaining the detachment of the corneal
stroma.
4. Pupils
Is the hole in the middle of the iris as regulating the amount of light entering the ball
by miosis and mydriasis
Miosis is a state of contraction (contraction) of the pupil (said to be smaller when the
diameter is less than 2mm)
Migration is a state of dilation (dilation) of the pupil said to be widening when the
diameter is more than 6mm
5. Trabeculum
Is a network that resembles a mesh/filter that is located in the corner of the anterior
camera oculi (COA), functions as an outlet Aqueous humor from the aqueous
trabeculum and then channeled into the scheme canal and then into the veins (veins)
Uvea tissue consists of Iris, Corpus Siliaris, Choroid
6. Uvea
Uvea is a vascular layer in the eyeball and is protected by the cornea and sclera which
consists of three parts, namely:
1) Iris
Iris is an extension of the ciliary to the anterior body
a relatively flat surface with a rounded gap in the middle, called a pupil. Iris can
regulate the amount of light that enters the eyeball automatically by shrinking
(miosis) or dilating (mydriasis) pupils. 19
2) Ciliary body
The ciliary body is a circular arrangement of muscles that function
change the lens capsule voltage so that the lens can focus on near and far objects in
the field of view. The ciliary body consists of
corrugated anterior zone, pars plicata (2 mm) which forms the aqueous humor, and
flat posterior zone, pars plana (4 mm) .19
3) Choroid
The choroid is the posterior segment of the uvea located between the retina
 and sclerosis, which contains large numbers of blood vessels, serves to nourish the
retina in the outer part beneath.19
7. Lenses
The lens is a biconvex structure, avascular, colorless, and almost perfectly
transparent. About 4 mm thick and 9 mm in diameter. On the anterior lens, there is
aqueous humor, on the posterior, there is vitreous humor.
The lens capsule is a semipermeable membrane that will allow water and electrolytes
to enter. In the front, there is a layer of subcapsular epithelium. The lens nucleus is
harder than the cortex. The nucleus and cortex are formed from long concentric
lamellae.
The lens is held in place by the suspensory ligament known as the Zinii zonula, which
is composed of many fibrils that originate from the surface of the ciliary body and
insert into the lens equator.

Pathophysiology of visual loss due to impairment in posterior segment of the eye

1. vitreous humor - viterous opacities (eye floaters). Vitreous opacities are conditions
where your eyes have floaters. That is why this condition is more commonly known as eye
floaters. When you have floaters on your eyes, your vision will be blocked by small patches.

Posterior vitreous detachment (PVD) is defined as separation of the posterior vitreous cortex
from the inner limiting membrane of the retina. Most commonly associated with aging, PVD
results from gel liquefaction and concurrent dehiscence of vitreoretinal adhesion.1 In the
absence of vitreoretinal dehiscence, gel liquefaction causes anomalous PVD, which can place
traction on the peripheral retina, resulting in rhegmatogenous sequelae; can pull on the macula,
optic disc, retinal blood vessels, or a combination therefor can create premacular membranes
(via vitreoschisis) that contribute to macular pucker and holes through tangential traction.

2. Choroidal dystrophy is an eye disorder that involves a layer of blood vessels called
the choroid. These vessels are between the sclera and retina. In most cases, choroidal dystrophy
is due to an abnormal gene, which is passed down through families. It most often affects males,
starting in childhood.The first symptoms are peripheral vision loss and vision loss at night. An
eye surgeon who specializes in the retina (back of the eye) can diagnose this disorder.

3. Optic nerve - retrobulbar neuritis is a form of optic neuritis where inflammation of

the nerve is located behind the eye. The inflammatory area is located between the back of the
eye and the brain. The optic nerve contains nerve fibers which deliver visual information from
retinal nerve cells to nerve cells in the brain. The retina contains photoreceptor cells, which are
cells that are activated by light and connect to other retinal cells called ganglion cells. Then it
sends a projection signal called an axon into the brain. Through this route, the optic nerve sends
visual impulses to the brain. So that when the nerve is inflamed, the visual signal delivered to
the brain becomes disturbed and vision becomes weak

4. Retina - retinal detachment

There are two main types of division :

a. Non-Rhegmatogenous Retinal Ablation

Occurs because of the accumulation of fluid under the sensory retina layer. For example in:

Ocular inflammation: Voght Koyanagi Harada Disease, choroiditis

- Ocular vascular disease: Coat's disease

- Systemic vascular disease: Malignant hypertension

- Intraocular tumors: choroid melanoma, hemangiomas

b. Rhegmatogenous Retinal Ablation

Is the most common form of retinal detachment. Characterized by the existence of a tear / hole
that causes the entry of vitreous fluid through the tear earlier into the subretinal space, so that
the retina is pushed out of the pigment epithelium. For example in: ocular trauma, vitreo-retinal
abnormalities, myopia, afakia, and diabetic retinopathy.

 Pathophysiology of visual loss due to Degenerative Disorder

1. Concretions (lithiasis)
Incidence
It is common in the elderly persons. There is accumulation of epithelial cells and
inspissated mucus in Henle’s glands. They never become calcified so the term ‘lithiasis’ or
‘stone’ is a misnomer.
Symptoms : Foreign body sensation and irritation are common complaints.
Signs :1. There are minute hard yellow spots seen in the palpebral conjunctiva.
2. They project from the surface rubbing against the lid or the cornea.
2. Pinguecula

It is a triangular yellow patch on conjunctiva near the limbus in the palpebral aperture.
Etiology : It commonly occurs in elderly persons exposed to strong sunlight, dust, wind, etc.
Signs : There is a triangular yellow patch, seen first on the nasal side.
• It is situated near the limbus in the palpebral aperture.The base is always towards the limbus
and the apex away from cornea.
Pathology : There is hyaline infiltration and elastotic degeneration of submucous tissue. It is
considered to be precursor of pterygium.
3. Pterygium
 Pterygium is a Greek word-meaning wing of a butterfly, like the butterfly it has got a
head, neck and body. A pterygium is a triangular sheet of fibrovascular tissue which invades
the cornea. It consists of three parts: a head or apex, i.e. the part which rests on the cornea, a
neck and a body.
Etiology :
• It frequently follows a pinguecula.
• It is common in dry sunny (ultraviolet rays) climate with sandy soil as in Australia, South
Africa, Texas or the Middle East.
Incidence : The nasal side is affected first but it may be bilateral.
Symptoms : 1. It is usually symptomless.

2. There is cosmetic disfigurement.

3. Vision is impaired due to astigmatism or if the pupillary area is covered by the
progressive pterygium.

4. Rarely, diplopia (seeing double objects) may be present due to limitation of ocular
movements nspecially in postoperative cases (due to injury to medial rectus
muscle).

Signs : 1. There is a triangular encroachment of the conjunctiva on the cornea from the inner
canthus in the palpebral aperture. Pterygium is loosely adherent to the sclera in its whole length.

2. Numerous small opacities, i.e. deposits of iron (Stocker’s line) may lie in front of the blunt
apex of pterygium.
3. There may be limitation of inward ocular movements occasionally.

Pathology
1. It is a degenerative condition of the sub- conjunctival tissue which proliferates as
vascularized granulation tissue.
2. It invades the cornea and destroys the super-ficial layers of stroma and Bowman’s mem-
brane.

 Pathophysiology of visual loss due to metabolic eye disease or disorder

Metabolic syndrome is becoming a worldwide medical and public health challenge as its
prevalence around the world and over the years has increased, many of them have well
established associations with some eye disease. Those disease such as cataract, age-related
macular degeneration (AMD), diabetic retinopathy (DR), and glaucoma. The main cause of the
increasing prevalence is due to aging population, increasing life expectancy and impact of risk
factors such as smoking, diabetes, and hypertension.

1. Cataract

Most of the observational studies have shown an association between metabolic syndrome and
cataract, some of them are diabetes, impaired glucose tolerance, obesity, lipid abnormality, and
also hypertension. The main mechanism involved in the formation of cataract from those
metabolic syndrome are oxidative stress, osmotic imbalance, and non enzymatic protein
glycation, where metabolic syndrome alters those physiological mechanism. More on cataract
will be explained in the next learning issues.

2. Diabetic retinopathy (DR)

As the name suggest, hyperglycemia has been shown to be the biggest risk factor of DR. In
metabolic syndrome, several mechanisms such as the increasing of oxidative stress resulting
from the production of reactive oxygen species (ROS), insulin resistance and inflammation
have been shown to contribute to the development and progression of DR. So first,
hyperglycemia induced overproduction of superoxide and the mitochondrial electron transport
chain accelerates oxidative stress. As ROS exceeds cellular antioxidant capacity, there is an
increasing damage to membrane structure and function leading to increased permeability of
those cells, and modification to DNA and protein which lead to apoptosis, mutation, and stiff
aged protein.

Second mechanism is that individuals with metabolic syndrome release a higher level of insulin
to maintain glucose homeostasis in order to counteract insulin resistance. This increase leads
to reactive leukocyte accumulation in retinal vessels which eventually causes capillary
plugging. Many inflammatory cytokines have also been implicated in the pathogenesis of DR,
which they accumulate in retinal vessels. Those mechanism can cause DR which manifested
to vision impairment.

3. Age-related macular degeneration (AMD)

The mechanism of how metabolic syndrome leads to AMD is not well established, but it was
found that elevated norepinephrine may be a common etiological factor for both of these
diseases, in which chronic inflammation and immune system dysregulation could be the
mechanisms involved, but may differ among these 2 disease, this disease is already been
described in the previous learning issue.

4. Glaucoma

Although there has not been an established association between metabolic syndrome and
glaucoma, there were clear links seen in patients with diabetes and hypertension. Diabetes can
lead to glaucoma via increase in intra ocular pressure (IOP) or direct damage. Diabetic-induced
autonomic dysfunction and corneal stiffening from glycation-induced corneal collagen cross-
linking have been shown to increase IOP.

It is postulated that hypertension causes open angle glaucoma (OAG) through an increase in
the ciliary artery perfusion which leads to an increase aqueous production. A second possibility
is that atherosclerotic vessels that supply the optic nerve may lead to glaucomatous changes.
Lastly obesity may be associated with OAG as the excessive orbital fat and increased viscosity
of blood may increase episcleral venous pressure and reduce aqueous outflow and thus raising
intra-ocular pressure.

4. Cataract
A.Definition
Cataracts are lens opacities. Cataracts have varying degrees of density and can be
caused by various things, but are usually related to aging. Cataract is a condition where the lens
of the eye which is usually clear and clear becomes cloudy. The origin of the word cataract
from the Greek word cataracta which means waterfall. This is because cataract patients seem
to see something like being covered by a waterfall before their eyes. So it can be concluded,
cataract is a clouding of the lens that is normally transparent and passes light to the retina,
which can be caused by various things that cause vision damage.
 B.Pathophysiology
A normal lens is a posterior iris structure that is clear, transparent, shaped like a shirt
button and has a great refractive strength. The lens contains three anatomical components. In
the central zone there is a nucleus, in the periphery there is a cortex, and which surrounds both
are the anterior and posterior capsules. With increasing age, the nucleus changes color to
yellowish brown. Around opacity there are densities such as thorns in the anterior and posterior
nuclei. Opacity in the posterior capsule is the most significant form of cataract, looking like
snow crystals on a window. Physical and chemical changes in the lens result in a loss of
transparency. Changes in multiple fine fibers (zunula) that extend from the ciliary body to
around the area outside the lens, for example, can cause vision to experience distortion.
Chemical changes in the lens protein can cause coagulation, thus blurring the view by blocking
the passage of light to the retina. One theory is that the breakdown of the normal lens protein
occurs along with the influx of water into the lens. This process breaks the strained lens fibers
and interferes with the transmission of light. Another theory says that an enzyme has a role in
protecting the lens from degeneration. The amount of the enzyme will decrease with age and
is absent in most patients who suffer from cataracts.
D. Types
Basically, cataract can be divided to be acquired and congenital cataract. Furthermore,
the complete explanations will be shown below (Kanski and Bowling, 2016).

1. Acquired Cataract

1.1 Age-Related Cataract

Subcapsular cataract

Anterior subcapsular cataract lies directly under the lens capsule and is associated with fibrous
metaplasia of the lens epithelium. Posterior subcapsular opacity lies just in front of the posterior
capsule and has a granular or plaque-like appearance on oblique slit lamp biomicroscopy, but
typically appears black and vacuolated on retroillumination; the vacuoles are swollen
migratory lens epithelial cells (bladder or Wedl), similar to those commonly seen
postoperatively in posterior capsular opacification. Due to its location at the nodal point of the
eye, a posterior subcapsular opacity often has a particularly profound effect on vision. Patients
are characteristically troubled by glare, for instance from the headlights of oncoming cars, and
symptoms are increased by miosis, such as occurs during near visual activity and in bright
sunlight.

Nuclear sclerotic cataract

Nuclear cataract is an exaggeration of normal ageing change. It is often associated with myopia
due to an increase in the refractive index of the nucleus, resulting in some elderly patients being
able to read without spectacles again (‘second sight of the aged’); in contrast, in the healthy
ageing eye (and in occasional cases of cortical and subcapsular cataract) there is mild
hypermetropic shift. Nuclear sclerotic cataract is characterized by a yellowish hue due to the
deposition of urochrome pigment, and is best assessed with an oblique slit lamp beam. When
advanced, the nucleus appears brown or even black, the latter being typical of marked post-
vitrectomy opacity.

Cortical cataract

Cortical cataract may involve the anterior, posterior or equatorial cortex. The opacities start as
clefts and vacuoles between lens fibres due to cortical hydration. Subsequent opacification
results in typical cuneiform (wedge-shaped) or radial spoke-like opacities, often initially in the
inferonasal quadrant. As with posterior subcapsular opacity, glare is a common symptomps.

Christmas tree cataract

Christmas tree cataract, which is uncommon, is characterized by polychromatic needle-like

formations in the deep cortex and nucleus.

Cataract maturity

• Immature cataract is one in which the lens is partially opaque.

• Mature cataract is one in which the lens is completely opaque.

• Hypermature cataract has a shrunken and wrinkled anterior capsule due to leakage of water
out of the lens.

• Morgagnian cataract is a hypermature cataract in which liquefaction of the cortex has

allowed the nucleus to sink inferiorly.

1.2 Cataract in Systemic Disease

Diabetes mellitus

Hyperglycaemia is reflected in a high level of glucose in the aqueous humour, which diffuses
into the lens. Here glucose is metabolized into sorbitol, which accumulates within the lens,
resulting in secondary osmotic overhydration. In mild degree, this may affect the refractive
index of the lens with consequent fluctuation of refraction in line with the plasma glucose level,
hyperglycaemia resulting in myopia and vice versa. Cortical fluid vacuoles develop and later
evolve into frank opacities. Classic diabetic cataract, which is actually rare, consists of
snowflake cortical opacities occurring in the young diabetic; it may mature within a few days
or resolve spontaneously. Age-related cataract occurs earlier in diabetes mellitus. Nuclear
opacities are common and tend to progress rapidly.

Myotonic dystrophy

About 90% of patients with myotonic dystrophy develop fine iridescent cortical opacities in
the third decade, sometimes resembling Christmas tree cataract; these evolve into visually
disabling wedge-shaped cortical and subcapsular opacities, often star-like in conformation by
the fifth decade. Later, the opacities may become indistinguishable from typical cortical
cataract.

Atopic dermatitis

About 10% of patients with severe atopic dermatitis develop cataracts in the second to fourth
decades; these are often bilateral and may mature quickly. Shield-like dense anterior
subcapsular plaque that wrinkles the anterior capsule is characteristic. Posterior subcapsular
opacities may also occur.

Neurofibromatosis type 2

Neurofibromatosis type 2 is associated with early cataract in more than 60% of patients.
Opacities are posterior subcapsular or capsular, cortical or mixed, and tend to develop in early
adulthood

1.3 Secondary Cataract

A secondary (complicated) cataract develops as a result of other primary ocular disease.

Chronic anterior uveitis

Chronic anterior uveitis is the most common cause of secondary cataract, the incidence being
related to the duration and intensity of inflammation. Topical and systemic steroids used in
treatment are also causative. The earliest finding is often a polychromatic lustre at the posterior
pole of the lens. If inflammation persists, posterior and anterior opacities develop. Cataract
appears to progress more rapidly in the presence of posterior synechiae.

Acute congestive angle closure

Acute congestive angle closure may cause small anterior greywhite subcapsular or capsular
opacities, glaukomflecken, to form within the pupillary area. These represent focal infarcts of
the lens epithelium and are almost pathognomonic of prior acute angle-closure glaucoma.

High myopia

High (pathological) myopia can be associated with posterior subcapsular lens opacities and
early-onset nuclear sclerosis, which ironically may increase the myopic refractive error.

Hereditary fundus dystrophies

Hereditary fundus dystrophies such as retinitis pigmentosa, Leber congenital amaurosis, gyrate
atrophy and Stickler syndrome, may be associated with posterior and, less commonly, anterior
subcapsular lens opacities. Cataract surgery may improve visual function even in the presence
of severe retinal change.

1.4 Traumatic Cataract

Trauma is the most common cause of unilateral cataract in young individuals.

• Penetrating trauma

• Blunt trauma may cause a characteristic flower-shaped opacity

• Electric shock is a rare cause of cataract, patterns including diffuse milky-white opacification
and multiple snowflakelike opacities, sometimes in a stellate subcapsular distribution

• Infrared radiation, if intense as in glassblowers, may rarely cause true exfoliation of the
anterior lens capsule
• Ionizing radiation exposure such as for ocular tumour treatment may cause posterior
subcapsular opacities; these may not manifest for months or years

2. Congenital Cataract

2.1 Etiology

Congenital cataract occurs in about 3 in 10 000 live births. Two-thirds are bilateral and a
cause can be identified in about half of these. Autosomal dominant (AD) inheritance is the
most common etiological factor; others include chromosomal abnormalities, metabolic
disorders and intrauterine infections. Isolated inherited congenital cataracts carry a better visual
prognosis than those with coexisting ocular and systemic abnormality. Unilateral cataracts are
usually sporadic, without a family history or systemic disease, and affected infants are usually
otherwise healthy.

2.2 Associated metabolic disorders

Galactosaemia

Galactosaemia is an autosomal recessive (AR) condition characterized by impairment of

galactose utilization caused by absence of the enzyme galactose-1-phosphate uridyl transferase
(GPUT). Unless galactose (milk and milk products) is withheld from the diet, severe systemic
complications culminate in early death. ‘Oil droplet’ lens opacity develops within the first few
days or weeks of life in a large percentage of patients. Exclusion of galactose may reverse early
lens changes.

Lowe syndrome

Lowe (oculocerebrorenal) syndrome is an X-linked recessive (gene: OCRL1) inborn error of

amino acid metabolism with neuromuscular, renal and other manifestations. Cataract is
universal, and microphakia may also be present. Congenital glaucoma is present in about half
of patients. Female carriers may have visually insignificant cortical lens opacities.

Fabry disease

Fabry disease is an X-linked lysosomal storage disorder caused by a deficiency of the enzyme
alpha-galactosidase A that leads to abnormal tissue accumulation of a glycolipid. Systemic
features include periodic burning pain in the extremities (acroparaesthesia) and GI tract,
angiokeratomas, cardiomyopathy and renal disease. Ocular manifestations include white to
golden-brown corneal opacities in a vortex pattern (75%) that may be the first feature of the
disease, facilitating early intervention; wedge- or spoke-shaped posterior cataract (Fabry
cataract); conjunctival vascular tortuosity (corkscrew vessels) and aneurysm formation; and
retinal vascular tortuosity

Mannosidosis

Mannosidosis is an AR disorder with deficiency of α-mannosidase. Infantile and juvenile-adult

forms are seen, both of which feature progressive mental deterioration, musculoskeletal and
other abnormalities. Punctate lens opacities arranged in a spoke-likepattern in the posterior lens
cortex are frequent; corneal clouding can also occur but is less common.

Other metabolic disorders

Potential causes include hypo- and pseudohypoparathyroidism, and hypo- and hyperglycaemia

2.3 Associated intrauterine infection

Rubella

Congenital rubella results from transplacental transmission of virus from an infected mother,
and may lead to severe fetal malformations. Pearly nuclear or more diffuse unilateral or
bilateral cataract occurs in around 15%.

Toxoplasmosis

Ophthalmic features of congenital toxoplasmosis include cataract, chorioretinitis,

microphthalmos and optic atrophy.

Cytomegalovirus infection

Systemic features of congenital cytomegalovirus (CMV) infection include jaundice,

hepatosplenomegaly, microcephaly and intracranial calcification. Ocular features apart from
cataract include chorioretinitis, microphthalmos, keratitis and optic atrophy.

Varicella
Systemic features include mental handicap, cortical cerebral atrophy, cutaneous scarring and
limb deformities; death in early infancy is common. Ocular features may include cataract,
microphthalmos, chorioretinitis, optic disc hypoplasia and optic atrophy.

Others

Measles, syphilis, herpes simplex and human immunodeficiency virus (HIV).

2.4 Other systemic disorders

Down syndrome (trisomy 21)

• Systemic features include learning difficulties, stunted growth, distinctive facial and
peripheral features, thyroid

dysfunction, cardiorespiratory disease and reduced life span.

• Ocular features. Cataract of varied morphology (75%); the opacities are usually symmetrical
and often develop in late

childhood. Other features include iris Brushfield spots and hypoplasia, chronic blepharitis,
myopia,

strabismus and keratoconus.

Edwards syndrome (trisomy 18)

• Systemic features. Characteristic facial and peripheral features, deafness, cardiac anomalies,
mental handicap and early death.

• Ocular features apart from cataract include ptosis, microphthalmos, corneal opacity, uveal
and disc coloboma

and vitreoretinal dysplasia.

Miscellaneous

Hallermann–Streiff syndrome features impaired growth and other features, with cataract in
90%; Nance–Horan syndrome is an X-linked condition comprising distinctive dental and facial
anomalies together with congenital cataract and microcornea. Female carriers may show Y
suture opacities.

D. Diagnosis
Cataracts are diagnosed primarily with subjective symptoms. Typically, patients report
decreased visual acuity, glare, and functional impairment to some degree due to loss of vision,
objective findings usually include condensation such as gray pearls in the pupil so that the
retina will not be visible with the ophthalmoscope. When the lens has become opaque, the light
will be radiated and not transmitted sharply into a shadow focused on the retina. The result is
a blurred or dim, annoying blur that is annoying with shadow distortion and hard to see at night.
Pupils that are normally black, will appear yellowish, gray or white. Cataracts usually occur
gradually over many years, and when the cataract has greatly deteriorated, even stronger
correction lenses will not be able to improve vision.

 Functional Visual Loss (Non Organic Visual Loss)

Functional Visual Loss (FVL) is a decrease in visual acuity and/or visual field not caused by
any organic lesion. It is therefore also called “nonorganic visual loss” (NOVL). This entity is
considered within the spectrum of “conversion disorder”, malingering, somatic symptom
disorder, and “factitious disorder”.

NOVL is a decrease in visual acuity and/or visual field not caused by any organic lesion. NOVL
cannot be explained by organic pathology after a complete neuro-ophthalmic examination. The
decrease in visual acuity may involve one or both eyes and may vary from mild blurriness to
complete blindness. The visual field defects may affect one or both eyes. They may include
constricted or tunnel visual fields, and hemianopias, among other complaints or visual findings.
NOVL is often but not always associated with concurrent diagnoses of depression and anxiety.
The diagnosis of NOVL is frequently confirmed at the neuro-ophthalmologist's office after
referral from a general ophthalmologist.

Functional visual loss is a subjectively described visual disorder without an objectively

observed abnormality. It is an unconscious, often subconscious, simulation of a nonexistent
disease. (Synonyms include psychogenic visual loss, conversion, and hysterical visual loss).
The related group of psychogenic ocular disorders includes functional disease, psychosomatic
disease, and artificial eye diseases. Psychosomatic eye disease is initiated by a psychically
triggered (or heavily influenced) organic disease with demonstrable pathological findings, as
for example, in some reported cases of glaucoma, uveitis, or central serous retinopathy.
Artificial eye diseases arise by self-inflicted trauma (autoaggression) and have demonstrable
pathological findings during the eye examination. This type is usually associated with
psychoses or so-called specific personality disorders.

NOVL may be psychogenic, or the result of malingering. Psychogenic visual complaints result
from a disturbance of higher cortical structures occupied with visual awareness, and patients
with this form of NOVL do experience but do not control their visual symptoms. The
malingerer, on the other hand, deliberately feigns visual loss for secondary gain. The term
‘malingering’ is in many ways a moral accusation rather than a clinical diagnosis, and
consequently should only be used with extreme caution. In the vast majority of cases the
distinction between psychogenic visual complaints and malingering is not made, and the term
non-organic visual loss is used.

At all ages, patients were predominlantly female, and one fifth had migraine, facial pain, or
coexistent organic pathology. Concomitant psychosocial events were mainly social in children
and related to trauma in adults. Psychiatric disease was twice as likely in adults. Normalization
of visual function occurred in a majority of patients.

FVL requires a positive diagnosis of normal function through clinical examination or visual
electrophysiology. A substantial proportion of patients have an underlying organic illness that
needs to be identified and treated. Recent updates in Diagnostic and Statistical Manual of
Mental Disorders-5 reflect the observation that many patients with FVL do not have a
recognizable psychological association. A small number of functional neuroimaging studies
suggest that there may be a stress-mediated prefrontal suppression of visual awareness.

2.3 Logic and Critical Analysis of Problems in Scenario according to Reference

A 55-year-old man came with complaints of decreased vision in both eyes. Several
hypotheses have been made, including reduced vision due to abnormalities in the anterior
structure, posterior structure, degenerative, metabolic, and functional. At the first tutorial we
look for important keywords related to problems in the scenario and determine the reasons
that might cause decreased vision in both eyes in the patient. We also get photos of the
physical examination of the patient, which is the cloudy eyes was found in both eyes.
Furthermore, additional questions are sent to the PBL to get additional data that supports
diagnosis and excludes the available differential diagnosis. In the second tutorial, after
getting additional data and exposure to the learning issue that we have been looking for, we
can conclude a initial analysis. With the physical examination photo results obtained, showed
that there is a turbidity or cloudy eyes of the lens that leads to the alleged a cataract. And also
with the presence of several risk factors that the patient has. There are the work of patients as
farmers where exposure to sunlight is very high, patients suffering from diabetes mellitus that
controlled by taking medication, and patients aged more than 50 years are the risk factors for
cataract. Based on discussion above, the results of our group initial analysis were cataract due
to degenerative and metabolic aspect.
2.4 Obstacle
1. Difficulty to find relevant up to date journals and references
2. Lack of information about patient
3. Overlapping characteristics of possible disease
4. Difficulty on choosing the best diagnosis for the patient among many possibl;e
diagnoses
2.5 Learning Issues 2
1. Pathophysiology of Senile Cataract
2. Risk factors of Cataracts
3. Complication of Cataracts
4. Treatment of Cataracts

CHAPTER III

3.1 Methods and Steps in Finding Information

Method that used in finding information is by inquiry method. Inquiry is a form of student-
centered approach. Inquiry learning provides space for students to develop this potential
because they are stimulated to seek and find answers to their questions. Related to this, the task
of the tutor is to provide space to provide opportunities for students to develop their hypothesis
and openly prove the truth of the proposed hypothesis. Discussion activities are optimized for
open exchange of information and opinions openly so that answers to proposed issues can be
discussed with other students. Here are some steps that we used in finding information:
1. Identify the main problems and other information that already available.
2. Determine the initial hypothesis about the mechanism of the occurrence of the problem.
3. Ask as many questions as possible related to the initial hypothesis to be submitted to the
tutor.
4. Formulate various items of questions which the answers are the necessary knowledge.
5. Arrange the flow of the questions.
After determining the questions related to the main problem, we search for the answer by
utilizing the search engine on the internet. In the steps of finding information using search
engines, we need to assess the information presented according to the criteria of reliable
information that are the author of the information should be clear, the information presented
is up-to-date, the information presented must be in accordance with the actual reality, the
quality of the information must be reliable, and also the perspective (point of view) of the
information itself can provide a purpose. After all information has been collected, re-
evaluation is needed to determine which information is important and which is not, so that
the final hypothesis can be determined appropriately/accurately.

3.2 Answer of Learning Issues 2

3.2.1 Pathophysiology of Cataracts and Senile Cataract
Pathophysiology
a. Genetics
Many inherited genetic syndromes and metabolic disorders are associated with
cataracts, and at least 42 genes and loci have been found to underlie Mendelian
inherited forms of isolated or primary cataract. Increasing evidence exists that several
genes underlying rare forms of inherited cataract also can influence susceptibility to the
much more prevalent forms of age-related cataract. These observations raise the
possibility of molecular genetic links between lens development and aging. Age-
related cataracts are inherited as a multifactorial or complex trait. Determining the
genetics of age-related cataracts is difficult because only a small proportion of the genes
involved have been identified, similar gene mutations result in different cataract
phenotypes, and cataract epigenetics is complex (Yanoff & Duker, 2018).
b. Metabolic Disturbance
Reduced binding of Ca2+ by membrane proteins increases cell membrane permeability
and causes a rise in intracellular Ca2+ levels, the formation of calcium oxylate crystals,
binding of Ca2+ to insoluble lens proteins, increased light scattering, and nuclear
cataract formation. Increased intracellular Ca2+ levels also affect lens epithelial cell
differentiation, causing posterior subcapsular cataracts. Corticosteroids have been
 shown to mobilize intracellular Ca2+ in other tissues, which can increase Ca2+ levels.
In the future, Ca2+-regulating drugs may be developed to prevent cataracts (Yanoff &
Duker, 2018)
c. Protein Modification
Additive modifications of lens proteins (e.g., crystallins) include methylation,
acetylation, carbamylation, glycation in diabetics, and binding of ascorbate, which may
be the cause of lens discoloration. These additions occur especially in disease and can
alter the function or properties of a protein. Diabetes (reducing sugars), renal failure
(cyanate generated from urea), aging (photooxidation products), and corticosteroid use
(ketoamines) have been linked to cataracts. Additive modifications can make proteins
more susceptible to photooxidation by ultraviolet (UV) light (Yanoff & Duker, 2018)
d. Oxidation
Oxidation is a key feature in the pathogenesis of most cataracts. Low oxygen levels
(O2) are important for maintaining a clear lens. Free radicals and other oxidants,
including reactive oxygen species (ROS) are derived from both endogenous sources
(mitochondria, peroxisomes, endoplasmic reticulum, phagocytic cells, etc.) and
exogenous sources (pollution, alcohol, tobacco smoke, heavy metals, transition
metals, industrial solvents, pesticides, and certain drugs like halothane, paracetamol,
and radiation) (Yanoff & Duker, 2018)
Senile Cataract
a. Subcapsular cataract
Anterior subcapsular cataract lies directly under the lens capsule and is associated with fibrous
metaplasia of the lens epithelium. Posterior subcapsular opacity lies just in front of the posterior
capsule and has a granular or plaque-like appearance on oblique slit lamp biomicroscopy, but
typically appears black and vacuolated on retroillumination; the vacuoles are swollen
migratory lens epithelial cells (bladder or Wedl), similar to those commonly seen
postoperatively in posterior capsular opacification. Due to its location at the nodal point of the
eye, a posterior subcapsular opacity often has a particularly profound effect on vision. Patients
are characteristically troubled by glare, for instance from the headlights of oncoming cars, and
symptoms are increased by miosis, such as occurs during near visual activity and in bright
sunlight (Bowling, 2016).
b. Nuclear sclerotic cataract
Nuclear cataract is an exaggeration of normal ageing change. It is often associated with myopia
due to an increase in the refractive index of the nucleus, resulting in some elderly patients being
able to read without spectacles again (‘second sight of the aged’); in contrast, in the healthy
ageing eye (and in occasional cases of cortical and subcapsular cataract) there is mild
hypermetropic shift. Nuclear sclerotic cataract is characterized by a yellowish hue due to the
deposition of urochrome pigment, and is best assessed with an oblique slit lamp beam. When
advanced, the nucleus appears brown or even black, the latter being typical of marked post-
vitrectomy opacity (Bowling, 2016).
c. Cortical cataract
Cortical cataract may involve the anterior, posterior or equatorial cortex. The opacities start as
clefts and vacuoles between lens fibres due to cortical hydration. Subsequent opacification
results in typical cuneiform (wedge-shaped) or radial spoke-like opacities often initially in the
inferonasal quadrant. As with posterior subcapsular opacity, glare is a common symptom
(Bowling, 2016).

3.2.2 Risk Factors of Cataract

A. Age
The cumulative effect of many environmental factors (UV light, x-irradiation, toxins,
metals, corticosteroids, drugs, and diseases, including diabetes) causes age-related
cataracts. Gene expression changes result in altered enzyme, growth factor, and other
protein levels. Protein modification, oxidation, conformational changes, aggregation,
formation of the nuclear barrier, increased proteolysis, defective calcium metabolism,
and defense mechanisms occur with increasing age. Compromised ion transport leads
to osmotic imbalances and intercellular vacuolation. Age-related abnormal cellular
proliferation and differentiation also produce opacities. There is also an increased
incidence of diseases such as diabetes that causes cataracts (Yanoff & Duker, 2018)
B. Sunlight and Irradiation
UV-B light causes oxidative damage, which is cataractogenic. The level of free UV
filters in the lens decreases with age, and breakdown products of the filters act as
photosensitizers that promote the production of reactive oxygen species and oxidation
of proteins in the aging lens. The risk of cortical and nuclear cataract is highest in those
with high sun exposure at a younger age. Exposure later in life was more weakly
associated with these cataracts. Wearing sunglasses, especially when younger, has
some protective effect (Yanoff & Duker, 2018)
C. Smoking and Alcohol
 Smoking causes a threefold increase in the risk of developing nuclear cataracts, and
cessation of smoking reduces this risk. Smoking also may be associated with posterior
subcapsular cataracts. Smokers are more likely to have a poor diet and high alcohol
consumption, which also are risk factors for cataract. Smoking causes a reduction in
endogenous antioxidants. Tobacco smoke contains heavy metals such as cadmium,
lead, and copper, which accumulate in the lens and cause toxicity. No association
between passive smoking and cataract has been demonstrated.19,20 Alcohol use has
little, if any, association with cataract risk, and study reports are mixed (Yanoff &
Duker, 2018)
D. Body Mass Index
A number of health-related factors—diabetes, hypertension, and body mass index
(BMI)—are associated with various forms of lens opacity, and they may be interrelated.
A high BMI increases the risk of developing posterior subcapsular and cortical
cataracts.20 A high BMI also is associated with diabetes and hypertension, which are
associated with cataracts. Severe protein-calorie malnutrition is a risk factor for
cataracts. Therefore, a moderate calorie intake may be optimal to reduce the risk of
developing cataracts (Yanoff & Duker, 2018)
E. Myopia
After controlling for age, gender, and other cataract risk factors (diabetes, smoking, and
education), posterior subcapsular cataracts are associated with myopia, deeper anterior
chambers, and longer vitreous chambers (Yanoff & Duker, 2018)
F. Trauma
Blunt trauma that does not result in rupture of the capsule may allow fluid influx and
swelling of the lens fibers. The anterior subcapsular region whitens and may develop a
characteristic flower-shaped pattern or a punctate opacity.
Electric shocks as a result of lightning or an industrial accident cause coagulation of
proteins, osmotic changes, and fernlike, grayish white anterior and posterior
subcapsular opacities.22 Ionizing radiation, such as from X-rays, damages the capsular
epithelial cell DNA, affecting protein and enzyme transcription and cell mitosis (Yanoff
& Duker, 2018)
G. Systemic Disorder
In uncontrolled type 1 diabetes mellitus in young people, hyperglycemia causes glucose
to diffuse into the lens fiber, where aldose reductase converts it to sorbitol. The cell
membrane is impermeable to sorbitol, and therefore it accumulates. The osmotic effect
 draws water into the lens fibers, which swell and then rupture. The cataract progresses
rapidly with the development of white anterior and posterior subcapsular and cortical
opacities (Yanoff & Duker, 2018)
In type 2 diabetic adults, an early onset age-related type of cataract occurs and is more
prevalent with longer duration of the diabetes. Many mechanisms are involved and
include sorbitol accumulation, protein glycosylation, increased superoxide production
in the mitochondria, and phase separation. During hyperglycemia, glucose is reduced
to sorbitol, depleting antioxidant reserves, and less glutathione is maintained in the
reduced form, which causes other oxidative damage. Levels of lens Ca2+ also are
elevated, which activates calpains, causing unregulated proteolysis of crystallins. The
cataracts are usually cortical or posterior subcapsular or, less frequently, nuclear and
progress more rapidly than age-related cataract (Yanoff & Duker, 2018)

3.2.3 Complication of Cataracts

Cataracts could possibly cause degradation or even loss of vision in a patient suffering from it.
The complications of cataracts mostly arises after an attempt of cataract surgery;
In general, poor vision after cataract surgery is caused by: inadequate correction of
postoperative refractive error (lack of spectacles); failure to detect pre-existing eye conditions,
e.g. macular degeneration or amblyopia (selection); or surgical complications (surgery).
Many things can go wrong during or immediately after cataract surgery, for example, capsular
rupture and vitreous loss. In high-income countries, the incidence of capsular rupture and
vitreous loss appears to be declining and is now in the region of 1–2%. This improvement may
be related to the use of phacoemulsification and to earlier intervention, which means that the
great majority of cataracts are now removed before they are mature. In low- and middle-income
countries, however, the incidence of capsular rupture and vitreous loss appears to be higher.
This is probably due to the greater complexity of many cataract operations in developing
countries, rather than to specific deficiencies of training, expertise, or equipment used. Vitreous
loss also increases the risk of endophthalmitis, the most feared compli-cation of intraocular
surgery. The incidence of endophthalmitis may vary.
With all complications, including capsular rupture and vitreous loss, and even endophthalmitis,
the prognosis is better if the complication is managed effectively. Not every patient who suffers
capsular rupture and vitreous loss experiences a poor outcome. If the complication is managed
well, it is possible for the patient to retain excellent vision.
It is important to collect data in order to identify patients at risk and to monitor their
management before and after surgery. Even where the incidence of complications is low,
regular collection of data helps to identify high-risk patients and to confirm that they are being
managed appropriately.
3.2.4 Treatment of Cataracts
Indications for surgery
1. Visual improvement is by far the most common indication for cataract surgery.
Operation is indicated when the opacity develops to a degree sufficient to cause
difficulty in performing essential daily activities. Clear lens exchange (replacement of
the healthy lens with an artificial implant) is an option for the management of refractive
error (Bowling, 2016).
2. Medical indications are those in which a cataract is adversely affecting the health of the
eye, for example phacolytic or phacomorphic glaucoma; clear lens exchange usually
definitively addresses primary angle closure, but less invasive options are generally
preferred. Cataract surgery to improve the clarity of the ocular media may also be
required in the context of monitoring or treatment of fundus pathology (Bowling, 2016).

Manual Cataract Surgery

When posterior chamber IOLs began to be widely used in the 1980s most surgeons adopted
extracapsular cataract extraction (ECCE), abandoning the older intracapsular technique
(ICCE).
1. In ICCE, a cryoprobe is used to remove the lens complete with its capsule. In ECCE,
after a large anterior capsulotomy is created, an extensive limbal incision (8–10 mm) is
completed and the lens nucleus is expressed following hydrodissection to free its
cortical attachments. Cortical matter is then aspirated, leaving behind a sufficiently
intact capsular bag to support an IOL. Suturing of the incision is required, sometimes
inducing considerable corneal astigmatism (Bowling, 2016).
2. Manual small-incision cataract surgery (MSICS) is a variant of ECCE used to address
the requirement for high-volume surgical throughput of dense cataracts in less affluent
geographical regions; it involves the creation of a small self-sealing sclerocorneal
tunnel, manual onepiece expression of the nucleus, manual aspiration of the cortex and
IOL implantation. Visual rehabilitation is comparable to phacoemulsification but
MSICS is faster and avoids theneed for expensive technology (Bowling, 2016).
3.3 Final Hypothesis
From our findings, we hypothesize the patient’s complaints are caused by immature
senile / age-related cataract, with possible contribution from patient’s systemic disease.

3.4 Analysis

Patient’s History

Mr. S, a 55-year-old man came to the doctor with complaints of having had a decrease of vision.
From anamnesis, we knew the patient lives in Pujon village, Malang, is already married with
2 children, and works daily as a farmer. He is a high-school graduate. His vision decreases
slowly and was apparently started bothering since 7 months ago. It kept on worsening until he
finally decided to go to the doctor. He mentioned having ‘foggy’ vision, with no pain, and no
red eyes. Previous history mentioned no similar symptoms before, and any complaint regarding
vision is he has been using a prescription glasses for reading. He has diabetes and hypertension
but are well controlled with drugs. Family history shows heritage of diabetes, and the patient
denied when asked whether or not he smokes and drink alcoholic beverages. Patient also shows
signs of photosensitivity (dazzled by lights).

From physical examination, we obtained data of normal vital sign. Patients’ general appearance
looked fine and normal. Patient’s body weight is 60 kg and height is 165 cm (sufficient
nutrition). Eye examination shows visual acuity of 6/20 and 3/60 for right and left eye
respectively. Ishihara testing shows slight color blindness. Intraocular pressure is normal, at
17.3 mmHg on both eyes. Slight but unspecific visual field testing abnormality, and normal
fundus examination with positive fundus reflex is observed.

From our findings, we hypothesize the patient’s complaints are caused by senile / age-related
cataract, with possible contribution from patient’s systemic disease.

Diagnosis of Cataract in Mr. S

We can determine the diagnosis of cataract from simple examination. Below is Mr. S eye
examination:
 Figure 3.1 Anterior Segment of Mr. S’s right eye

Figure 3.2 Anterior Segment of Mr. S’s left eye

From the photo above, we can clearly see the opacity in the patient’s anterior eye segment, on
both eyes. Examination of eye’s anterior chamber shows opacity of the structure behind iris,
which lens is the most likely possibility. Keratitis or other corneal disease is excluded through
this observation. Cataract is the most likely diagnosis as classic opacity of the lens is observed

Pathogenesis and Pathophysiology of Cataract in Mr. S

Pathogenesis as to why cataract occur in Mr. S can be multifactorial, which is explained below.
1. Age
Mr. S is a 55-year-old man, with diabetes. His old age might be the cause of many
cataracts, especially age-related cataracts due to cumulative effects of environmental
factors such us UV light, metals, drugs, and contributing diabetes which is directly
proportional to the increasing age. Increasing age is related to compromised ion
 transport and lens osmotic imbalances, with cellular proliferation and differentiation.
In older people, mitochondrial function also diminishes and superoxide production
by the mitochondria increases, resulting in increased nuclear oxygen and superoxide
levels.
2. Sunlight and Irradiation
Mr. S works as a farmer, which makes him susceptible to UV as he is pretty much
exposed by it every time he works in the field. UV-B, especially causes oxidative
damage, and increases the possibility of cataract. This is due to decreasing UV filters
in the lens as age increases, and increasing of reactive oxygen species and oxidation
of proteins in the aging lens.
3. Diabetes Mellitus
We are unsure of which diabetes type Mr. S has, but both type of diabetes are risk
factors for cataracts. Hyperglycemia in diabetes causes glucose to diffuse into the
lens fiber, where aldose reductase converts it to sorbitol. As cell membrane of lens is
impermeable to sorbitol, it accumulates and cataract progresses. Combined with old
age, antioxidant is further depleted and oxidative damage is inevitable.

Major pathophysiology mechanisms of why cataracts occur in Mr. S is explained below.

1. Oxidation
Oxidation is a major key in most of cataracts pathogenesis. Low oxygen (O ) levels
2

are important for maintaining a clear lens. Free radicals and other oxidants, including
ROS (reactive oxygen species).
2. Protein modification
Modifications of lens proteins (crystallins) especially glycation is profound in patient
with diabetes, considering Mr. S also has the same condition. These modifications
make proteins more susceptible to photooxidation by ultraviolet (UV) light.

Symptoms of cataract present in Mr. S are:

1. Decreased visual acuity, as his visual acuity decreases in both eyes. Furthermore. The
patient described his vision as ‘foggy’.
2. Increased glare sensitivity, as patient is described feeling dazzled from lights.
3. Monocular diplopia, which is described as double-vision (diplopia) in only one eye,
that persists even when the other eye is closed. This phenomenon happen due to
cortical opacities which changes the refractive index of the lens.
 As it was quite clear that Mr. S currently suffers from senile cataract, we should also determine
the structure affected and stadium of the cataract.

Lens Structure Affected

Senile cataract most commonly affects either subcapsular, nuclear, or cortical. To further
differentiate between the three, further examination such as slit-lamp biomicroscopy should be
performed. Increased glare and decreased visual acuity are commonly associated with posterior
subcapsular opacity. Nuclear sclerosis is often associated with myopic shifts, which is not
present in Mr. S, and lastly cortical opacity associates with both glare and monocular diplopia.
Lastly, hyperglycemia may possibly have an effect, and most are associated with cortical or
posterior subcapsular. Thus, Mr. S might possibly have cortical or posterior subcapsular
opacity.

Stages of the Cataract

We suspect the stage of cataract in Mr. S case is still immature, as the opacity is quite clearly
visible, but does not affect the visual acuity bad enough, and funduscopy is still performable
(shown by positive fundus reflex, means not yet mature).

Management of Cataract in Mr. S

As we knew that Mr. S has possibly immature, senile cataract, management is explained below.

1. Additional Examination

Slit-Lamp Biomicroscopy

Slit lamp biomicroscopy is best done to differentiate between the possible structure of the lens
affected in this case of cataract.

2. Treatment

Surgical Correction

Surgical correction can be done without waiting for the cataract to mature. Type of IOL
(intraocular lens) should be adjusted to the power of Mr. S original eyes. After that, many
aspects of surgical correction should be considered, such as:
 1. Anesthesia choice used for cataract surgery
2. Pre-, intra-, and post-operative medications (pupil dilatation, anti-infection
prophylaxis, etc).
3. Surgical method:
a. Manual cataract surgery: ECCE (extracapsular cataract extraction), ICCE
(intracapsular cataract extraction), MSICS (manual small-incision cataract
surgery, a variant of ECCE), etc.
b. Phacoemulsification: a surgical technique to remove the nuclear portion of
a cataractous lens using an aspirating and vibrating ultrasonic handpiece.

3.5 Group Opinion

A 55-year-old man came to the doctor with the main complaint of having a decreased visibility
in both eyes for the last 7 months. From this data we could think of many possibilities that
could lead to his main complaint which is decreased visibility. After we asked our tutor, we
gained more information about the patient’s condition which then we could search and find
more about the patient’s case. Based on those data we have collected in our first tutorial, and
also from the additional questions that we have also asked, our discussion leads us to conclude
that the man is having a cataract. The cataract can be caused by many factors which have been
discussed and presented before this. And knowing our limitations as a general practitioner, we
are trying to find how to treat this patient’s condition from the guideline and also give this
patient the education he needs about his condition to minimalized the risk of getting the
complication of cataract.
3.6 Final Concept Mapping
 REFERENCES

Poh, S., Mohamed Abdul, R., Lamoureux, E., Wong, T. and Sabanayagam, C. (2016).
Metabolic syndrome and eye diseases. Diabetes Research and Clinical Practice, 113, pp.86-
100.

Rahimi, H., Omidtabrizi, A., Ghayour Mobarhan, M. and Sharifi, F. (2014). Ocular
Manifestations of Metabolic Syndrome. Razavi International Journal of Medicine, 2(2).

http://digilib.unimus.ac.id/files/disk1/135/jtptunimus-gdl-andriniest-6717-2-babii(-).pdf

Eye Floaters: Causes, Symptoms, and Treatment. http://www.webmd.com/eye-health/benign-

eye-floaters#1-2. Accessed November 6, 2016. What causes eye floaters? 7 possible
conditions. http://www.healthline.com/symptom/eye-floaters. Accessed November 6, 2016.
Eye floaters.

http://www.mayoclinic.org/diseases-conditions/eye-floaters/basics/definition/con-20033061.
Accessed November 6, 2016

Tozer, K., Johnson, M.W., and Sebag, J. Vitreous aging and posterior vitreous detachment. in:
J. Sebag (Ed.) Vitreous: in Health and Disease. Springer, New York; 2014: 131–150.

Jogi, Renu. (2009). Basic Ophthalmology fourth edition. New Delhi: jitendar P Vij

Mescher, A.L., 2018, Junqueira’s Basic Histology Text & Atlas, Fifteenth Edition, McGraw-
Hill Education.
Costanzo, L.S., 2018, Physiology, Sixth Edition, Elsevier Inc.

Bowling, B., 2016, Kanski’s Clinical Ophthalmology, Eighth Edition, Elsevier.

Yanoff, M., Duker, J. S., 2018, Ophthalmology, Fifth Edition, Elsevier.

Beatty, S., 1999. Non-organic visual loss. Psychogenic medicine. Manchester Royal Eye
Hospital. Postgrad Med J 75: 201-207. Available at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1741186/pdf/v075p00201.pdf

Klosinski, S., T. Chapter 15: Functional visual loss and malingering. Available at:
http://eknygos.lsmuni.lt/springer/585/203-214.pdf
 LEMBAR SCIENTIFIC PAPER APPRAISAL
(TELAAH KRITIS TULISAN ILMIAH)

Nama / kelompok :Kelompok 1

NIM :-
Judul paper : Non-organic visual loss

1. TELAAH KELENGKAPAN FORMAT PAPER

Item telaah Ada / tidak (sebutkan

halamannya)

n Judul (Title) Present (201)

n Abstrak dan/atau Ringkasan (Abstract and or Present (201)

Summary)

n Pendahuluan (Introduction, background) Present (201)

n Bahan dan Cara (Method) Present (201)

n Hasil (Result) Present (207)

n Diskusi (Discussion) Presen (207)

n Daftar Pustaka (Reference) Present (207)

Kesimpulan : format lengkap/tidak lengkap

2. TELAAH VALIDITAS PENELITIAN

Tujuan penelitian :

Metode penelitian

Item telaah Temuan (sebutkan berikut halamannya)

Disain/rancangan (design) Expert’s opinion.

* Tingkatan dalam hierarchy of 5

evidence

Sampel (sample) The sample is the collection of data by the author or

researcher regarding the area of research.

Ukuran sampel (sample size) 1

Kriteria inklusi (eligibility Sample articles, journals, or opinions are made by

criteria) valid people, and published by valid organizations.

Metode penentuan sampel Articles, journals, opinions and more, regarding the
(sampling frame) research topic.

Metode pengumpulan data Qualitative data based on reviewing existing research.

Cara pengukuran (measurement Analyzing multiple journals and articles to assess the
and or assessment) expert’s opinion.
 Instrumen yang dipergunakan Not stated.
(instrument)

Metode randomisasi Not stated.

(randomization)

Intervensi (intervention) Not stated.

Metode analisis / pengolahan Qualitative analysis.

data (analysis method)

Kesesuaian antara disain dan tujuan penelitian : sesuai / tidak

sesuai
Kesesuaian cara pengukuran dan instrument yang dipergunakan : sesuai/tidak
sesuai

Kesimpulan : valid / tidak valid (HANYABERDASARKAN KEDUA KRITERIA DI

ATAS)
CRITICAL APPRAISAL OF JOURNAL ARTICLE
CRITICAL APPRAISAL OF JOURNAL ARTICLE
Source Searching Information Validity Importance Applicability
Method Type Fondation Fondation Fondatiion
│Result │Result │Result
Poh, S., Mohamed Internet Digital Idea │Yes Content of Is it
Abdul, R., Lamoureux, Information applicable?
E., Wong, T. and │Yes │Yes
Sabanayagam, C.
(2016). Metabolic
syndrome and eye
diseases. Diabetes
Research and Clinical
Practice, 113, pp.86-
100.

Internet Digital Idea │Yes Content of Is it

Rahimi, H., Information applicable?
Omidtabrizi, A., │Yes │Yes
Ghayour Mobarhan, M.
and Sharifi, F. (2014).
Ocular Manifestations
of Metabolic
Syndrome. Razavi
International Journal of
Medicine, 2(2).

https://www.researchga
te.net/publication/2627
32138_Ocular_Manifes
tations_of_Metabolic_
Syndrome

Eye Floaters: Causes, Internet Digital Idea │Yes Content of Is it

Symptoms, and Information applicable?
Treatment │Yes │Yes
https://www.webmd.c
om/eye-
health/benign-eye-
floaters#1-
2.%20Accessed%20No
vember%206,%202016
.
What causes eye Internet Digital Idea │Yes Content of Is it
floaters? 7 possible Information applicable?
conditions. │Yes │Yes
http://www.healthline.
com/symptom/eye-
floaters

Beatty, S., 1999. Non- Internet Digital Idea │Yes Content of Is it

organic visual loss. Information applicable?
Psychogenic medicine. │Yes │Yes
Manchester Royal Eye
Hospital. Postgrad Med
J 75: 201-207.
Available at:
https://www.ncbi.nlm.
nih.gov/pmc/articles/P
MC1741186/pdf/v075
p00201.pdf

Book Digital Idea │Yes Content of Is it

Yanoff, M., Duker, J. S., Information applicable?
2018, Ophthalmology, │Yes │Yes
Fifth Edition, Elsevier.
Bowling, B., 2016, Book Digital Idea │Yes Content of Is it
Kanski’s Clinical Information applicable?
Ophthalmology, Eighth │Yes │Yes
Edition, Elsevier.

Costanzo, L.S., 2018, Book Digital Idea │Yes Content of Is it

Physiology, Sixth Information applicable?
Edition, Elsevier Inc. │Yes │Yes

Mescher, A.L., 2018, Book Digital Idea │Yes Content of Is it

Junqueira’s Basic Information applicable?
Histology Text & Atlas, │Yes │Yes
Fifteenth Edition,
McGraw-Hill
Education.

Klosinski, S., T. Chapter Internet Digital Idea │Yes Content of Is it

15: Functional visual Information applicable?
loss and malingering. │Yes │Yes
Available at:
http://eknygos.lsmuni.l
t/springer/585/203-
214.pdf

Tozer, K., Johnson, Internet Digital Idea │Yes Content of Is it

M.W., and Sebag, J. Information applicable?
Vitreous aging and │Yes │Yes
posterior vitreous
detachment. in: J.
Sebag (Ed.) Vitreous: in
Health and Disease.
Springer, New York;
2014: 131–150.
https://www.aaojourn
al.org/article/S0161-
6420(18)31225-
9/fulltext