BUKU PANDUAN PRAKTIKUM ANATOMI

BLOK 10
SISTEM PENGLIHATAN

LABORATORIUM ANATOMI
PROGRAM STUDI PENDIDIKAN DOKTER
FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH PURWOKERTO
2019
 BUKU PANDUAN PRAKTIKUM ANATOMI
BLOK X
SISTEM PENGLIHATAN

LABORATORIUM ANATOMI
FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH PURWOKERTO
2019

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Buku Panduan Praktikum Anatomi Blok 10
(Pegangan Mahasiswa)

Sistem Penglihatan

Blok 10 Edisi 1
@2017 Laboratorium Anatomi
Fakultas Kedokteran Universitas Muhammadiyah Purwokerto

Penyusun :

Asisten Mahasiswa Anatomi

Staff Pengajar :

dr. Abdul Hakim Nitiprodjo, SH, Sp.KF

dr. Rizka Adi Nugraha Putra, M.Sc
Andi Muh. Maulana, M.Sc

Editor :

Asisten Mahasiswa Anatomi 2016

Buku ini digunakan untuk kalangan sendiri.

Dilarang mengutip atau memperbanyak sebagian atau seluruh dari isi buku ini
tanpa seizin tertulis dari TIM ANATOMI Laboratorium Anatomi Fakultas
Kedokteran Universitas Muhammadiyah Purwokerto.

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 KATA PENGANTAR

Anatomi merupakan ilmu yang mempelajari struktur tubuh dan hubungannya dengan
bagian tubuh lain manusia secara makroskopis. Ilmu anatomi akan menunjang ilmu kesehatan
lainnya hubungannya dengan manusia sebagai subjek kegiatan ilmu kesehatan. Dalam
menjalankan kegiatan rutinnya yang berkaitan dengan tindakan terhadap pasien, seorang
dokter, perawat dan paramedis lainnya butuh penguasaan dan pengetahuan dalam
mengidentifikasi struktur tubuh manusia. Sehingga dengan demikian, kesalahan dalam
pelaksanaan kegiatan kemedisan saat melaksanakan tindakan dapat diminimalisasi bahkan
dihindari.
Anatomi merupakan ilmu kedokteran yang memiliki karakteristik penggunaan bahasa
latin dalam istilah-istilah organ dan struktur organ baik istilah posisi maupun nama organnya.
Tujuan penggunaan bahasa latin ini untuk menyamakan persepsi anggota tim medis dalam
mengerti dan menghindari kesalahan persepsi terutama saat pencatatan dan dokumentasi
tindakan medis. Selain itu, tim medis lain dapat mengerti persepsi yang sama jika catatan
harus dipindah tangankan ke anggota tim medis lainnya dalam rujukan.
Peranan anatomi yang penting dalam kegiatan medis inilah yang melatarbelakangi
pembuatan modul anatomi Laboratorium Anatomi. Modul Blok 10 ini diharapkan
mempermudah kegiatan pembelajaran anatomi di laboratorium sehingga praktikan dapat
mengefisienkan waktu praktikum. Selain memudahkan praktikan, hal ini juga mempermudah
asisten laboratorium anatomi.

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 STRUKTUR ORGANISASI LAB
ANATOMI FK UMP

1. Kepala Laboratorium : dr. Abdul Hakim Nitiprodjo, SH, Sp.KF

2. Staff Pengajar Dosen : 1. dr. Rizka Adi Nugraha Putra, M.Sc

2. Andi Muh. Maulana, M.Sc

3. Asisten Mahasiswa : 1. Ni’matur Rabiu’ul Ula

2. Siti Hartini Nur Aissyah

3. RD. Selma Rachmawaty Bey

4. Lintang Suroya

5. Ajikwa Ari Widiyanto

6. Shofia Hilmi Abdillah

7. Alifia Putri Karomah B

8. Nida Rizqi Amalia

9. Ari Febriyan

10. Firdha Afghani

4. Laboran : Imam Santoso, S.T

5. Pembantu Pelaksana : Mistam

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 VISI DAN MISI
PROGRAM STUDI PENDIDIKAN DOKTER
FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH PURWOKERTO

VISI PROGRAM STUDI

Pada tahun 2025 menghasilkan dokter yang mampu bersaing di tingkat global, unggul di bidang
kedokteran herbal dan selalu mengikuti perkembangan ilmu dan teknologi kedokteran terkini,
beretika sesuai dengan nilai-nilai Islami.

MISI PROGRAM STUDI

Untuk mencapai visi tersebut maka misi Program Studi Pendidikan Dokter adalah:
1. Menyelenggarakan program studi pendidikan dokter yang mampu menghasilkan dokter
berkualitas dan memiliki keunggulan di bidang kedokteran herbal
2. Menyelenggarakan penelitian berdasar ilmu pengetahuan dan teknologi kedokteran sesuai
perkembangan zaman
3. Menyelenggarakan pengabdian masyarakat di bidang kedokteran yang dapat dirasakan
manfaatnya oleh masyarakat
4. Mengimplementasikan nilai-nilai keislaman dalam bidang kedokteran
5. Membina dan mengembangkan jaringan kerjasama dibidang pendidikan, riset, dan pengabdian
masyarakat dengan lembaga dalam dan luar negeri

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 TATA TERTIB
PEMAKAIAN LABORATORIUM ANATOMI
FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH PURWOKERTO

A. Ketentuan Umum

1. Sebelum pelaksanaan, minimal satu jam sebelum praktikum laboran menyiapkan

peralatan yang diperlukan untuk proses praktikum
2. Praktikan hadir 10 menit sebelum acara praktikum dimulai. Keterlambatan >10
menit, praktikan tidak diperkenankan untuk mengikuti praktikum kecuali dengan izin
khusus.
3. Praktikan sudah mempelajari materi yang akan dipraktikumkan dirumah.
4. Praktikan memasuki dan atau keluar laboratorium dengan seijin asisten
mahasiswa/dosen secara tertib dan tenang.
5. Praktikan meletakkan tas dan barang-barang yang tidak diperlukan saat praktikum
ditempat yang telah disediakan.
6. Selama praktikum, praktikan wajib :
- Menghormati guru besar (Cadaver) dalam melakukan praktikum Anatomi.
- Mengecek jumlah, jenis dan kondisi torso yang akan digunakan dalam praktikum.
- Mengenakan sepatu selama praktikum, jas praktikum dilengkapi tanda pengenal
secara benar dan rapi, memakai dan melepaskan jas praktikum harus diluar
ruangan.
- Praktikan pria berambut pendek disisir rapi dan perempuan mengenakan jilbab.
- Praktikan wajib berprilaku sopan, santun dan saling menghargai antara praktikan
dengan praktikan, praktikan dengan dosen, praktikan dengan asisten dan praktikan
dengan laboran.
- Tiap kelompok menghadapi 1 meja preparat (cadaver atau preparat lepas atau
manequin).
- Menjaga attitude, ketenangan dan ketertiban jalannya acara praktikum.
- Menonaktifkan atau men silent HP/alat komunikasi lainnya.
- Menjaga keutuhan, kelengkapan dan kebersihan torso dan kadaver praktikum
yang digunakan.

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 - Memperhatikan dan melaksanakan acara praktikum sesuai dengan petunjuk dan
arahan asisten mahasiswa/dosen.
- Melaporkan kepada asisten apabila selama praktikum terjadi kecelakaan (alat
hilang/rusak/pecah).
- Mengembalikan torso yang telah digunakan sesuai dengan jumlah kondisi awal
sebelum praktikum.
- Menjaga kebersihan laboratorium, tempat cucian, dan lingkungan disekitar
laboratorium.
- Setelah praktikum selesai, pastikan gas, api, kran air, dan listrik sudah dalam
keadaan mati.
7. Selama praktikum, praktikan dilarang :
- Memakai kaos oblong.
- Dilarang berkuku panjang.
- Makan, minum, merokok dan melakukan aktivitas yang tidak ada kaitannya
dengan acara praktikum.
- Melakukan aktivitas yang dapat membahayakan diri sendiri maupun oranglain.
- Mengganggu jalannya acara praktikum baik dalam skala kelompok maupun
rombongan praktikum.
- Menggunakan alat-alat laboratorium selain yang digunakan untuk praktikum yang
bersangkutan.
- Membuang bahan/zat berbahaya (korosif, mudah terbakar) kedalam bak cucian.
- Menghilangkan, mengambil, merusak atau memecahkan peralatan dan
kelengkapan laboratorium.
8. Praktikan berhak untuk mengajukan pertanyaan dan meminta petunjuk kepada asisten
mahasiswa/dosen apabila dalam pelaksanaan praktikum ada hal-hal yang kurang jelas.
9. Praktikan wajib mengganti alat yang hilang, rusak/pecah sesuai dengan spesifikasi
alat yang sama.
10. Praktikan wajib mematuhi peraturan yang berlaku yang dibuat oleh laboratorium
Anatomi Fakultas Kedokteran Universitas Muhammadiyah Purwokerto.
11. Praktikan yang melanggar tata tertib ini akan dikenakan sanksi mulai dari teguran
sampai tidak diperbolehkan mengikuti praktikum.

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B. Ketentuan Khusus atau Akademik

1. Apabila nilai pretest kurang dari 70 wajib keluar meninggalkan ruang anatomi untuk
tidak ikut praktikum anatomi atau belajar dirumah.
2. Praktikan wajib mempunyai nilai minimal pretest 70 agar dapat mengikuti praktikum
anatomi.
3. Nilai pretest dan postest praktikan jika dijumlah dan dibagi dua harus minimal 70.
4. Nilai praktikum praktikan yang kurang dari 70 wajib mengikuti inhal.

C. Ketentuan Lain

1. Peserta praktikum wajib mematuhi peraturan yang berlaku yang dibuat oleh
Laboratorium Anatomi Fakultas Kedokteran Universitas Muhammadiyah Purwokerto.
2. Peserta praktikum yang melanggar ketentuan tersebut tidak diperbolehkan mengikuti
praktikum.

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 Innervasi

- Nervus opticus (NII) (utama)

- Nervus lacrimalis cabang dari
nervus trigeminus
- Nervus frontalis
- Nervus trochlearis
- Nervus occulomotorius
- Nervus abducens

Vaskularisasi

Arteri opthalmica bercabang

menjadi A. centralis retina(dekat n.
optici), rami musculares, A. ciliaris
anterior (bola mata dekat limbus
cornea), A. ciliaris posterior (dekat n.
A. Organ: optici), A. lacrimalis (glandula
lacrimalis). Sedangkan aliran vena
Orbita/Bulbus Occuli/Eyes/Mata
adalah dari vena opthalmica superior
Organ mata adalah organ berbentuk dan inferior bermuara ke sinus
spheris dengan ukuran rata-rata cavernosus.
24mm. Mata terletak di dalam cavitas
orbitalis berbentuk piramid dengan Arteri carotis interna
apeks didepan dan basis dibelakang.
Atapnya dibentuk oleh os frontalis A.
pars orbitalis. Dasarnya dibentuk oleh opthalmica
os maxillaris lamina orbitalis.
A. ciliaris A. centralis
Terbagi menjadi dua ruangan oleh anterior retina
lensa dan corpus ciliaris:
rami
A. lacrimalis
musculares
- Cavitas anterior
Terbagi oleh pupil menjad
Camera anterior bulbi dan Camera
posterior bulbi. Terisi oleh aquosus B. Organ assesorius
humor (cairan jernih). a. Palpebra
- Cavitas posterior - Palpebra Superior
Terisi oleh corpus vitreous - Palpebra Inferior
(transparent gel ). • Separatedby canthus
medial and lateral canthus
Aliran Humor Aquosus • Fissurapalpebra : pemisah
palpebra superior dan
Processes ciliaris -> camera bulbi
inferior, tempat masuk ke
posterior->pupil ->camera bulbi
saccus conjunctivae
anterior ->canalis schlemm ->vena.
- Canthus medialis

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 - Canthus lateralis - Abduksi: m. rectus lateralis
- Glandula ciliaris/ Zeis
(minyak)
- Glandula Moll (keringat) Origo: annulus tendinosus
- Glandula tarsalis (Meibom) communis
- Apparatus lacrimalis
➢ Innervasi: N.III, N.IV, N.VI
Glandula lacrimalis
➢
Ductus lacrimalis
➢
Canaliculi lacrimalis d. Osteologi terkait
➢
Ductus nasolacrimalis - Fissura orbitalis superior
- Plica semilunaris Canalis opticus
- Caruncula lacrimalis - Cavum orbita
- Lacus lacrimalis - Incisura supra orbita
- Lapisan fibrosa: - Fossa glandula lacrimalis
→ - Ductus nasolacrimalis
Septum orbitale
→ - Meatus nasi inferior
Lamina tarsalis (tarsus) - Concha nasalis inferior
sebagai pita jaringan ikat
padat penguat palpebra
C. Struktur Organ:
Innervasi: a. Tunica bulbi/ Lapisan bulbi
- Palpebra superior 1. Tunica Fibrosa
→ - Cornea
n.Supraorbitalis
• Limbus Cornea
- Palpebra inferior
→ • Angulus iridocornealis
n. Infraorbitalis
• Spatium anguli
b. Conjunctiva iridocornealis
- Conjunctiva palpebra et • Innervasi: nn. ciliares n.
bulbi ophthalmicus (Nervus V
- Fornix conjunctiva superior cabang I)
et inferior - Sclera
- Saccus conjunctivalis
2. Tunica vaskulosa
c. Musculus occuli externus - Iris
• M. sphincter pupillae
- Elevasi: m. rectus superior
Inervasi: ganglion ciliare
+ m. obliquus inferior
nn. ciliares breves
- Depresi: m. rectus inferior + (parasimpatis)
m. obliquus superior
• M. dilatator pupillae
- Intorsi: m. rectus superior + Inervasi: C8-T4 (ganglion
m. obliquus superior cervicale superius)
- Ekstorsi: m. rectus inferior
+ m. obliquus inferior - Corpus cilliaris
- Adduksi: m. rectus medialis • Proc. ciliaris

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 • Zonula ciliaris (lig.
suspensorium lentis)
• M. ciliaris
• Innervasi: ganglion
ciliares (parasimpatis)
- Choroidea
- Pupil
3. Tunica nervosa/ Retina
- Stratum pigmentosa
- Stratum nervosa
- Macula lutea, fovea centralis
(Gelber spots)
- Pars optica, pars ciliaris, pars
iridica
- Ora serrata
- Discus nervioptici (papilla
nervioptici and excavation
disci)
D. Fisiologi Penglihatan
Nervus opticus terdiri dari
jutaan serabut saraf yang
mengandung akson yang berasal
dari inner ganglion cell layer pada
retina. Serabut-serabut saraf ini
akan melewati lamina cribrosa
pada sclera lalu berjalan melalui
canalis opticus membentuk
chiasma opticum. Serabut-serabut
dari retina nasal menyilang pada
chiasma. Pengaturan pada chiasma
opticum ini membuat akson
temporal retina kiri dan akson nasal
retina kanan akan berjalan menjadi
tractus opticus kiri. Karena lapang
pandang nasal jatuh ke retina
temporal dan lapang pandang
temporal jatuh ke retina nasal,
maka susunan ini menyebabkan
hemisfer otak kiri menerima
informasi visual dari sisi kanan
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(kontralateral). Begitu juga
sebaliknya. Akson temporal retina
kanan dan akson nasal retina kiri
akan berjalan di tractus opticus
kanan, sehingga hemisfer otak
kanan akan menerima input visual
dari sisi kiri. Setelah melewati
chiasma opticum, akson sel
ganglion retina ini akan berjalan
pada tractus opticus, yang
membawa akson ke corpus
geniculatum lateral (CGL) dan ke
colliculus superior. Dari masing-
masing CGL, akson akan berlanjut
secara ipsilateral melalui radiatio
optica menuju cortex calcarina
pada lobus occipitalis. Sehingga,
separuh kanan dari tiap retina
(separuh kiri visual field)
terproyeksi melalui radiation optica
ke lobus occipitalis kanan, dan
sebaliknya. Radiatio optica atau
geniculocalcarine fibers
membawa impuls dari CGL
menuju cortex visual. Meyer’s
loop merupakan radiatio optica
yang melengkung di sekitar
ventrikel lateral, melewati lobus
temporalis, sebelum mencapai
cortex calcarina. Meyer’s loop
membawa serabut radiatio optica
yang merepresentasikan bagian
atas/upper part dari lapang pandang
kontralateral. Jadi, Meyer’s loop
kanan membawa input seperempat
lapang pandang bagian kiri atas.
Sedangkan colliculus superior akan
terproyeksi ke medulla spinalis
melalui tractus tectospinal, yang
mengontrol gerakan reflek kepala,
leher, dan mata sebagai respon
terhadap stimulus visual
 - Visual Pathway

Nervus Opticus

Chiasma opticus

Tractus Opticus

Lateral geniculate
nucleus of thalamus

Radiatio Optici
(Tortora,2012)
Area visual primer cortex cerebri
area 17

1. Hordeolum
A stye, or external hordeolum, is an abscess of gland Zeis at the lid margin (Figure
A). An internal hordeolum is an infection within the meibomian gland deeper in the tarsus
(Figure B). Both are acute, painful lid nodules, tender to the touch, which produce lid
swelling and redness and which may point as the abscess localizes. Hordeola typically
respond to warm compresses within several days. Occasionally, incision and drainage are
necessary.

Figure : Stye of the upper eyelid. B: Hordeolum pointing on

the inner aspect of the lid and at the meibomian gland opening
at the lid margin. (Ilyas,2005)

2. Kalazion
Eyelid has a thin layer of skin , while at the rear there is a mucous membrane called
tarsal conjunctiva . In the petals there are parts in the form of the glands and muscles.
Glands that found on the eyelids are Moll glands or sweat glands , Zeis glands at the base
of the hair , and the Meibomian glands on the tarsus which leads to the border of the eyelid
. (Vaughan,2000)

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 ll gland or sweat glands

sebum ( oil ) .

Glands :
Chalazion is a mass in the eyelid resulting from chronic non-infectious inflammation
of the meibomian gland granulomatosa . Chalazion with infection of Meibomian gland
resulting mild chronic inflammation . This disorder usually begin with blockage of the
gland, infection and scarring more. (Ilyas,2005)

3. Ptosis
Ptosis is drooping eyelid. Ptosis is a condition where the upper eyelid cannot open or
cannot lifted to the top so the gap of eyelid becomes smaller than normal. The grade of
ptosis are:
a. Mild : about 2 mm

b. Moderate : about 3 mm

c. Severe : more than 3 mm

The classification of ptosis are:

a. Unilateral ptosis

b. Bilateral ptosis

c. Complete bilateral ptosis

Signs and symptomps ptosis requires a careful history to determine the age of onset,
familial insidence, rate of progression, variability/fatigability, and association with other
occular findings. The treatment of ptosis is surgical. The preferred method of repair is an
external lid crease incision with reattachment or advancement of the levatoraponeurosis to
the tarsal plate. (Mansjoer,2005)

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4. Cataract
A. Causes Cataract
The eye functions much like a camera. Light rays enter the eye, passing
through the cornea, the aqueous humor -- transparent fluid in the front of the eye --
and then the pupil and into the lens. The lens bends the light rays to focus objects onto
the retina lining the back of the eye. From there, the image passes through the retinal
cells, into the optic nerve, and finally to the back of the brainwhich process the
images.
Cataractsoccur when there is a buildup of protein in the lens that makes it
cloudy. This prevents light from passing clearly through the lens, causing some loss
of vision. Since new lens cells form on the outside of the lens, all the older cells are
compacted into the center of the lens resulting in the cataract

Types of cataracts include:

Age-related cataracts. As the name suggests, this type of cataract develops as

a result of aging.

Congenital cataracts. Babies are sometimes born with cataracts as a result of an

infection, injury, or poor development before they were born, or they may
develop during childhood.

Secondary cataracts. These develop as a result of other medical conditions, like

diabetes, or exposure to toxic substances, certain drugs (such as corticosteroids
or diuretics), ultraviolet light, or radiation.

Traumatic cataracts. These form after injury to the eye.

Other factors that can increase a person's risk of developing cataracts include
cigarette smoke, air pollution, and heavy alcohol consumption

B.Symptoms of Cataracts
Cataracts usually form slowly and cause few symptoms until they noticeably block
light. When symptoms are present, they can include:

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 although their distance vision is deteriorating, they may no longer need reading
glasses.

(like a superimposed
image).

Cataracts occur when there is a buildup of protein in the lens that makes it cloudy.
This prevents light from passing clearly through the lens, causing some loss of vision.
Since new lens cells form on the outside of the lens, all the older cells are compacted
into the center of the lens resulting in the cataract..
Other factors that can increase a person's risk of developing cataracts include
cigarette smoke, air pollution, and heavy alcohol consumption.(Remington,2012)

5. Refractive Disorder

Nearsightedness (myopia) occurs when the eyeball is too long for the refractive
power of the cornea and lens. Because of the relatively long size, light is focused in front
of (rather than directly on) the retina, and the person has trouble clearly seeing distant
objects. In children, nearsightedness frequently increases until children stop growing.
Farsightedness (hyperopia) occurs in some people when the eyeball is too short for
the refractive power of the cornea and lens. Because of the relatively short size, light is
focused behind the retina. Children and young adults who are mildly farsighted may be
able to see clearly if their lens is flexible enough to properly refocus light on the retina.
However, with aging, the lens stiffens. Thus, as farsighted adults age, seeing near objects

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 clearly becomes more difficult and seeing distant objects also becomes more difficult.
Blurring of nearby objects is worse in dim light.
Astigmatism is an imperfectly shaped cornea or lens (not perfectly round or
spherical), which may cause objects to appear blurred at any distance.
Presbyopia occurs as people age. As people reach their early or mid 40s, the lens
becomes increasingly stiff. The lens does not change shape easily, so it cannot focus on
nearby objects. As adults age, they often notice difficulty seeing nearby objects. This
difficulty occurs because the lens loses its ability to change shape.
Aphakia is the absence of a lens resulting from a birth defect, eye injury, or eye
surgery for removal of a cataract. If a person has had a lens removed to treat cataracts but
has not had a lens implant, objects look blurred at any distance.

Symptoms
A person who has a refractive error may notice that vision is blurred for distant
objects, near objects, or both. For example, a child who becomes nearsighted may have
difficulty seeing the chalkboard in school. People may sometimes have headaches caused
by squinting or frowning. In children, frowning when reading and excessive blinking or
rubbing of the eyes may indicate the child has a refractive error. Occasionally, when a
person stares for a long time trying to read something, the eyes can dry out and become
itchy, red, and irritated. (Vander,2015)

6. Synechia
Iris synechia is an abnormal attachment between the iris surface and another
structures. In a posterior synechia, the posterior iris surface is adherent to the anterior lens
surface. In an anterior synechia, the anterior iris surface is adherent to the corneal
endothelium or the trabecular meshwork. Synechia can occur as a result of a sharp blow to
the head or a whiplash-type movement that brings the two structures forcefully together.
Alternatively, cells and debris from a uveal infection that are circulating in the aqueous
humor can make the surface “sticky” and so cause synechia (Remington, 2012).
If a posterior synechia involves a large portion of the pupillary margin, aqueous will
accumulate in the posterior chamber. Continual production of aqueous causes the pressure
in the posterior chamber to increase, which in turn causes the iris to bow forward in a
configuration called iris bombé. This can push the peripheral iris against the trabecular
meshwork, setting the stage for a dramatic increase of intraocular pressure (IOP). A drug-
induced dilation usually will break a posterior synechia. The break usually occurs between
the epithelial layers, leaving remnants of the posterior epithelium on the anterior surface of
the lens (Remington, 2012). An anterior synechia usually occurs at the iris periphery and
involves the meshwork. It is called a peripheral anterior synechia (PAS). Aqueous outflow
is impeded by a PAS, causing an increase in IOP if the adhesion occupies a considerable
amount of the trabecular meshwork (Remington, 2012).

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 Picture 1.Anterior synechia (left); posterior synechia (right) (Slatter, 2002).

7. Glaucoma
Most of the time in glaucoma, damage occurs when the optic nerve, or certain parts
of the retina, get compressed as a result of high pressure inside the eye. If the optic nerve
is damaged, it cannot send electrical impulses to the brain to produce a proper image
(CNIB, 2008)

Classification of Glaucoma
A. Open-angle glaucoma
Open-angle glaucoma is by far the most common form of the disease. It occurs
when fluid in the eye passes too slowly through a spongy meshwork connecting the
cornea and the iris. This causes a buildup of pressure that damages the optic nerve
(CNIB, 2008).

Picture.Open-angle glaucoma (CNIB, 2008).

B. Normal tension glaucoma

In normal tension glaucoma, damage to the optic nerve may occur even without a
buildup of pressure in the eye (CNIB, 2008).

C. Closed-angle glaucoma

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 In closed-angle glaucoma, the distance between the cornea and the iris closes
completely, stopping fluid from draining from the eye (CNIB, 2008).

Picture. Closed-angle glaucoma (CNIB, 2008).

In the acute form of closed-angle glaucoma, this happens suddenly, often in a
matter of hours. In chronic closed-angle glaucoma, this can take weeks or even years
(CNIB, 2008).

Glaucoma symptoms

Open-angle glaucoma and chronic closed-angle glaucoma begin without any

symptoms. There is no pain, and vision loss isn’t noticeable at first. If left untreated,
glaucoma causes a growing area of vision loss on the periphery of vision (CNIB,
2008).

Picture.Normal vision and vision with glaucoma (CNIB, 2008).

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 Over time this can expand to “tunnel” vision or even complete vision loss.
Acute closed-angle glaucoma is a medical emergency and has a sudden onset of
symptoms (CNIB, 2008):

8. Retinophaty
A. Retinophaty Hypertension

Hypertensive retinopathy is damage to the retina from high blood pressure.

The retina is the layer of tissue at the back part of the eye. It changes
a. Damage to the nerves in the eye (ischemic optic neuropathy), due to poor blood
flow

b. Blockage of the blood supply in the arteries to the retina (retinal arteryocclusion)

c. Blockage of the veins that carry blood away from the retina (retinal veinocclusion)

Light and images that enter the eye into nerve signals that are sent to the brain.
Causes High blood pressure can damage blood vessels in the retina. The higher the
blood pressure and the longer it has been high, the more severe the damage is likely to
be. You have a higher risk of damage and vision loss when you have diabetes, high
cholesterol level, or you smoke. Rarely, blood pressure readings suddenly become
very high, but when they do, it can cause severe changes in the eye.

Symptoms
Most people with hypertensive retinopathy do not have symptoms until late in
the disease.Symptoms may include:
a. Double vision, dim vision, or vision loss

Exams and Tests

Your health care provider will use an ophthalmoscope to look for narrowing
of the blood vessels and signs that fluid has leaked from blood vessels. The degree of
damage to the retina (retinopathy) is graded on a scale of 1 to 4: a. Grade 1: You may
not have symptoms

b. Grades 2-3: There are a number of changes in the blood vessels, leaking from blood
vessels, and swelling in other parts of the retina
c. Grade 4: You will have swelling of the optic nerve and of the visual center of the
retina (macula). This swelling can cause decreased vision.

Fluorescein angiography may be used to examine the blood vessels.

Treatment :
The only treatment for hypertensive retinopathy is to control high blood pressure.

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B. Retinophaty Diabeticum

Diabetic eye disease can affect many parts of the eye, including the retina,
macula, lens and the optic nerve. Diabetic eye disease is a group of eye conditions
that can affect people with diabetes.

-sensitive tissue called the

retina that lines the back of the eye. It is the most common cause of vision loss
among people with diabetes and the leading cause of vision impairment and
blindness among working-age adults.

swelling in an area of the retina called the macula.

Diabetic eye disease also includes cataract and glaucoma:

s. Adults with diabetes are 2-5 times more
likely than those without diabetes to develop cataract. Cataract also tends to
develop at an earlier age in people with diabetes.

—the bundle of
nerve fibers that connects the eye to the brain. Some types of glaucoma are
associated with elevated pressure inside the eye. In adults, diabetes nearly doubles
the risk of glaucoma

All forms of diabetic eye disease have the potential to cause severe vision loss and
blindness.

Causes diabetic retinopathy

Chronically high blood sugar from diabetes is associated with damage to the
tiny blood vessels in the retina, leading to diabetic retinopathy. The retina detects light
and converts it to signals sent through the optic nerve to the brain. Diabetic
retinopathy can cause blood vessels in the retina to leak fluid or hemorrhage (bleed),
distorting vision. In its most advanced stage, new abnormal blood vessels proliferate
(increase in number) on the surface of the retina, which can lead to scarring and cell
loss in the retina.
Diabetic retinopathy may progress through four stages:
1. Mild nonproliferative retinopathy. Small areas of balloon-like swelling in the
retina’s tiny blood vessels, called microaneurysms, occur at this earliest stage of
the disease. These microaneurysms may leak fluid into the retina.

2. Moderate nonproliferative retinopathy. As the disease progresses, blood vessels

that nourish the retina may swell and distort. They may also lose their ability to
transport blood. Both conditions cause characteristic changes to the appearance of
the retina and may contribute to DME.

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 3. Severe nonproliferative retinopathy. Many more blood vessels are blocked,
depriving blood supply to areas of the retina. These areas secrete growth factors
that signal the retina to grow new blood vessels.

4. Proliferative diabetic retinopathy (PDR). At this advanced stage, growth factors

secreted by the retina trigger the proliferation of new blood vessels, which grow
along the inside surface of the retina and into the vitreous gel, the fluid that fills the
eye. The new blood vessels are fragile, which makes them more likely to leak and
bleed. Accompanying scar tissue can contract and cause retinal detachment—the
pulling away of the retina from underlying tissue, like wallpaper peeling away
from a wall. Retinal detachment can lead to permanent vision loss.

Diabetic macular edema (DME)

DME is the build-up of fluid (edema) in a region of the retina called the
macula. The macula is important for the sharp, straight-ahead vision that is used for
reading, recognizing faces, and driving. DME is the most common cause of vision
loss among people with diabetic retinopathy. About half of all people with diabetic
retinopathy will develop DME. Although it is more likely to occur as diabetic
retinopathy worsens, DME can happen at any stage of the disease.

Risk for diabetic retinopathy

People with all types of diabetes (type 1, type 2, and gestational) are at risk for
diabetic retinopathy. Risk increases the longer a person has diabetes. Between 40 and
45 percent of Americans diagnosed with diabetes have some stage of diabetic
retinopathy, although only about half are aware of it. Women who develop or have
diabetes during pregnancy may have rapid onset or worsening of diabetic retinopathy.

Symptoms and Detection

The same scene as viewed by a person normal vision (Top) and with (Center)
advanced diabetic retinopathy. The floating spots are hemorrhages that require prompt
treatment. DME (Bottom) causes blurred vision.
The early stages of diabetic retinopathy usually have no symptoms. The
disease often progresses unnoticed until it affects vision. Bleeding from abnormal
retinal blood vessels can cause the appearance of “floating” spots. These spots
sometimes clear on their own. But without prompt treatment, bleeding often recurs,
increasing the risk of permanent vision loss. If DME occurs, it can cause blurred
vision.

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 (Khurana,2007)
9. Ablatio Retina / Retinal Detachment
A retinal detachment is a separation of the sensory retina from theunderlying retinal
pigment epithelium (RPE). There are numerous variations in the basic pathogenesis of a
retinal detachment. They include developmental factors (e.g., myopia and Marfan
syndrome) that affect the overall size and shape of the globe vitreoretinal disorders (e.g.,
coloboma and retinal dysplasia), metabolic disease (e.g., diabetic retinopathy), vascular
disease (e.g., sickle cell disease), trauma, inflammation, degenerative conditions, and
neoplasms. Retinal detachments can be classified as rhegmatogenous or
nonrhegmatogenous.

a. Rhegmatogenous Retinal Detachment

The most common type of retinal detachment, rhegmatogenous, results from a
break in the sensory retina. The break is most often caused by vitreous traction on the
surface of the retina. This traction physically pulls a small section of the sensory
retina away from the pigment epithelium, resulting in what is called a "retinal tear."
Traction at the site of a tear can initiate retinal detachment surrounding the tear by
pulling on the surface of the adjacent retina. The break in the retina may also allow
fluid from the vitreous cavity to percolate into the potential subretinal space. Thus, a
rhegmatogenous retinal detachment caused by a retinal tear is the result of both
vitreous traction and fluid ingress between the sensory retina and the pigment
epithelium.
b. Nonrhegmatogenous Retinal Detachment
The second type of retinal detachment, nonrhegmatogenous, usually results
from the accumulation of exudate or transudate in the potential subretinal space,
rather than from a retinal break. Sometimes a nonrhegmatogenous retinal detachment
is caused by sheer traction, without the production of a retinal tear. Other etiologies of
this type of detachment include chorioretinitis, metastatic choroidal tumor, choroidal
effusion, retinal angioma, Harada's disease, pars planitis, sympathetic ophthalmia,
eclampsia, and trauma. (William,2004)

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Asisten Mahasiswa Anatomi Fakultas Kedokteran Universitas Muhammadiyah Purwokerto | 23
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