ANATOMYS MODUL

10th BLOK

LABORATORY
ANATOMY MEDICAL
FACULTY
MUHAMMADIYAH UNIVERSITY OF
PURWOKERTO 2016
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Tim Editor:

Rosmayda Ria Julianti (1413010002)

Nadya Ratu Aziza Fuady (1413010031)
Tyas Ratna Pangestika (1413010030)
Dewandaru Istighfaris A. B (1413010044)
Mahidin (1413010006)

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 ORBITA
In general, the orbita is divided into two parts, namely eye assesorius organ and
eyeball ( occuli ) .

1. Organ Assesorius
a. Palpebra (eyelid)
Palpebra Superior
Palpebra Inferior
Separated by canthus medial and lateral canthus
Fissurapalpebra : hole between the superior and inferior palpebral place
enter into saccus conjunctivae
b. Conjunctiva (epithelial)
Conjunctiva Fornix
Conjunctiva Palpebra (indicators of anemia)
Conjunctiva Bulby (identification of red eyes)
Apparatus Lacrimalis
Glandula lacrimalis
Ductus lacrimalis:
Lacus lacrimalis
Punctum lacrimalis
Canaliculi lacrimalis
Caruncula lacrimalis
Sacus lacrimalis
Ductus nasolacrimalis
c. Musculus occuli externus (musculus Mover eyeball)

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 M.Rectus Superior

M.Rectus Inferior

M.Rectus Media

M.Rectus lateral

M.Obliquus superior

M.Obliquus inferior

d. Cilia (eyelashes)

e. Glandulatarsalia

f. Supercilia(eyebrows)

2. Bulbus Occuli (Eyeball)

Divided into two rooms by a lens clan corpus ciliaris
a. Cavitas anterior
Contains aquosus humor ( the clear liquid )
Divided 2 slices den room by pupi
o Camera anterior bulbi
o Camera posterior bulbi
b. Cavitas posterior
Contains corpus vitreous ( transparent gel )

3. Tunica bulbi (Layer of the eyeball)

a. Tunica Fibrosa
Cornea
Sclera
Limbus
b. Tunica vaskulosa
Iris
Corpus cilliaris
Choroidea
Pupil
M. Cilliaris

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 c. Tunica nervosa/ Retina
Stratum pigmentosa
Stratum nervosa
Macula lutes, fovea centralis (Gelber spots)
Discus nervioptici (papilla nervioptici and excavation disci)

4. Lens cristalina/lens
Hanged pads corpus ciliaris by the suspensory ligament lentis( ZonulaZinn )

5. Flow of humor aquosus

Processes ciliaris camera bulbi posterior pupil camera bulbi anterior
canalis schlemm vena.

Clinical applications : the intraocular pressure , serves to maintain the balance

Table 1. Extraocular Muscles of Orbit

Osteology -related
Cavum orbita
Fissura orbitalis superior
Canalis opticus

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 Incisura supra orbita
Fossa glandula lacrimalis
Ductus nasolacrimalis
Meatus nasi inferior
Concha nasalis inferior

Clinical Application
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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 Glands
:
Sebaceous glands
Moll gland or sweat glands
Zeis glands at the base of the hair, associated with hair follicles
and produce sebum
Meibomian gland ( glandtarsalis ) contained in the tarsus . These
glands produce sebum ( oil ) .
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

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 preferred method of repair is an external lid crease incision with reattachment or
advancement of the levatoraponeurosis to the tarsal plate. (Mansjoer,2005)

4. Cataract

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.

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 Types of cataractsinclude:

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

Symptoms of Cataracts

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

Vision that is cloudy, blurry, foggy, or filmy

Progressive nearsightednessin older people often called "second
sight" because although their distance vision is deteriorating, they
may no longer need reading glasses.
Changes in the way you see color because the discolored lens acts as
a filter.
Problems driving at night such as glare from oncoming headlights.
Problems with glare during the day.
Double visionwhile looking through the eye with a cataract (like a
superimposed image).
Sudden changes in glasses prescription.

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,

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 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

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 farsighted adults age, seeing near objects 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

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 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 bomb. 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).

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).

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 Picture.Normal and damage optic nerve (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

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

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 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 isnt 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).

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):
Severe eye pain
Headaches (especially in dim light)
Blurred vision
Nausea
Redness in the eye
Haloes around lights

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

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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. Other problems with the retina are also more likely, such as:

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)

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

b. Headaches Sudden symptoms are a medical emergency.

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

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 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.

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.

Diabetic retinopathy affects blood vessels in the light-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.
Diabetic macular edema (DME). A consequence of diabetic retinopathy,
DME is swelling in an area of the retina called the macula.

Diabetic eye disease also includes cataract and glaucoma:

Cataract is a clouding of the eyes lens. 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.
Glaucoma is a group of diseases that damage the eyes optic nervethe
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.

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Diabetic Retinopathy

What 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 retinas 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.
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
detachmentthe pulling away of the retina from underlying tissue,

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 like wallpaper peeling away from a wall. Retinal detachment can
lead to permanent vision loss.

What is 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.

Who is at 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

What are the symptoms of diabetic retinopathy and DME? 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

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 vision.

(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

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 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)

Picture.1 Retinal Detachment

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Remington Lee Ann. 2012. Clinical Anatomy and Physiology of the Visual System. 3rd
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