Disorders of Special Senses.pdf presentation

It's a great ppt on disorders of special.semses

1. DISORDERS OF
SPECIAL SENSES
GENERIC BSN –BATCH IV –SEMESTER IV
PATHOPHYSIOLOGY II
PRESENTED BY –SYED MUHAMMAD HASAN
Presented by -Syed Muhammad Hasan 1

2. KEY HIGHLIGHTS OF THIS CHAPTER
•Reviewing the Anatomy and Physiology of ear.
•Discussion of the pathophysiology of Tinnitus & Hearing Loss.
•Understanding the Anatomy and Physiology of eye in terms of vision
and accessory structures.
•Explanation of the pathophysiology of Glaucoma.
2Presented by -Syed Muhammad Hasan

3. •The ear is an engineering marvel because its sensory receptors can transduce sound
vibrations as small as 0.3nminto electrical signals1000 times faster than
photoreceptors.
•Besides containing receptors for sound waves, the ear performs critical functions for
maintaining equilibrium.
•The ear is divided into three principal regions:
•External ear –Collects sound waves and channel them inwards.
•Middle ear –Convey sound vibrations to the oval window.
•Internal ear –Houses the receptors for hearing and equilibrium.
THE ANATOMY OF EAR
3Presented by -Syed Muhammad Hasan

4. ANATOMICAL
REPRESENTATION
OF THE HUMAN
EAR
4Presented by -Syed Muhammad Hasan

5. •Components–Auricle, External Auditory Canal and Eardrum.
•Auricle–Also known as Pinna. A flap of elastic cartilage covered by skin. The rim of auricle
is helix while the inferior portion is called lobule.It is attached to the head by ligaments
and muscles.
•External Auditory Canal –Curved tube about 2.5cm long that lies in the temporal bone and
leads from the auricle to the eardrum.
•Eardrum (Tympanic membrane) –Thin semitransparent partition between external
auditory canal and middle ear.
•It is covered by epidermis and composed of collagenand elastin. Contains hairs and
sebaceous (oil) glands called ceruminous glands that secrete earwaxor cerumen. It
prevents dust and foreign objects from entering the ear.
THE EXTERNAL (OUTER) EAR
5
Presented by -Syed Muhammad Hasan

6. •Themiddle earlies within thetemporalbone, and extends from the tympanic membraneto
the lateral wall of the inner ear.
•The middle ear can be divided into three parts:
•Tympanic Cavity–Located medially to the tympanic membrane.It contains three small
bones known as the auditory ossicles: the malleus, incusand stapes. They transmit sound
vibrations through the middle ear.
•Epitympanic Recess–Space superior to the tympanic cavity, which lies next to themastoid
air cells. The malleus and incus partially extend upwards into the epitympanic recess.
•Ear Muscles (Tensor Tympani and Stapedius) andEustachian (Auditory) tube.
6
THE MIDDLE EAR
Presented by -Syed Muhammad Hasan

7. Presented by -Syed Muhammad Hasan 7
ANATOMICAL
REPRESENTATION
OF AUDITORY
OSSICLES IN
MIDDLE EAR

8. 8
THE MIDDLE EAR -OTITIS MEDIA
Presented by -Syed Muhammad Hasan

9. •The inner ear is the innermost part of the ear, and houses the vestibulocochlear organswhich
performs three main functions:
•Convertmechanicalsignals from the middle ear intoelectricalsignals.
•Transfer information to the auditory pathway in the brain.
•Maintainbalance bydetectingpositionandmotion.
•The inner ear has two main components:
•Bony Labyrinth-Composed of the cochlea, vestibuleand three semi-circular canals. All these
structures are lined internally with periosteumand contain a fluid called perilymph.
•Membranous Labyrinth–Lies within thebony labyrinth. It consists of the cochlear duct, semi-
circular ducts, utricleand the saccule. The membranous labyrinth is filled with fluid called
endolymph.
9
THE INNER EAR
Presented by -Syed Muhammad Hasan

10. Presented by -Syed Muhammad Hasan 10
BONY AND MEMBRANOUS LABYRINTH IN THE INNER EAR

11. Presented by -Syed Muhammad Hasan 11
THE
AUDITORY
PATHWAY

12. •Tinnitus is the perception of abnormal ear or head noises, not produced by an
external stimulus.
•It may be described as buzzing, ringing, roaring, whistlingorhissingand is
sometimes variable andcomplex sounds in the ear.
•Tinnitus is most noticeable in quiet environments and in the absence of
distracting stimuliand, thus, frequently seems worse at bedtime.
•Tinnitus may be intermittentor continuous. Continuous tinnitus is at best
annoyingand is often quite distressing.
12
TINNITUS
Presented by -Syed Muhammad Hasan

13. •For clinical purpose, Tinnitus is subdivided into:
•Objective Tinnitus –Rare case, sound is perceived by observer. Etiological
factors involve:
•Vascular abnormalities (sounds generated by turbulent blood flow = arterial
bruits or venous humps) producing a pulsating sound.
•Neuromuscular abnormalities in ear muscles.
•Subjective Tinnitus –Perception of sound without external stimuli.
•Etiological factors include stimulation of abnormal nerve activity in the
auditory cortex however mechanism is still unknown.
Presented by -Syed Muhammad Hasan 13
TYPES OF TINNITUS

14. Presented by -Syed Muhammad Hasan 14
REPRESENTATION
OF ARTERIAL AND
MUSCULAR
DISTRIBUTION IN
HUMAN EAR

15. •Subjective Tinnitus is caused by abnormal neuronal activity in the auditory cortex.
•This activity results when input from the auditory pathway (cochlea, auditory nerve,
brain stem nuclei, auditory cortex) is disrupted or altered.
•This disruption may cause loss of suppression of intrinsic cortical activity and
perhaps creation of new neural connections.
•Conductive hearing loss (eg, caused by cerumen impaction, otitis media, or
eustachian tube dysfunction) may also be associated with subjective tinnitus, by
altering sound input to the central auditory system.
15
SUBJECTIVE TINNITUS –PATHOPHYSIOLOGY
Presented by -Syed Muhammad Hasan

16. Presented by -Syed Muhammad Hasan 16

17. 17
•Acoustic trauma (noise-induced sensorineural hearing loss)
•Presbycusis(with aging)
•Ototoxic drugs (Ear Poisoning) –Includes aminoglycosides, chemotherapeutics.
•Meniere disease (Episodes of vertigo and hearing loss)
•Infectionsand CNSlesions(eg, caused by tumor, stroke, multiple sclerosis) that
affect auditory pathways also may be responsible.
SUBJECTIVE TINNITUS -ETIOLOGY
Presented by -Syed Muhammad Hasan

18. •Usually involves noise from vascular flow, which causes an audible pulsating sound
synchronous with the pulse. The causes include:
•Turbulent flow through the carotid artery or jugular vein.
•Highly vascular middle ear tumors.
•Muscle spasms of the middle ear (stapedius, tensor tympani) may cause perceptible
noise, typically a rhythmic clicking.
•Such spasms may be idiopathic or caused by tumors, head trauma, and infectious or
demyelinating diseases (eg, multiple sclerosis).
18
OBJECTIVE TINNITUS –PATHOPHYSIOLOGY
Presented by -Syed Muhammad Hasan

19. •History of present illness (which ear, duration and is it constant or
intermittent).
•Review of neurological systems.
•Past medical history (exposure to loud noise, sudden pressure change during
air travel etc.)
•Physical examination of the ear.
•Inspection of ear canal for discharge, inflammation, foreign body and
cerumen.
19
TINNITUS –DIAGNOSTIC EVALUATION
Presented by -Syed Muhammad Hasan

20. •Treatment measures are designed to treat the symptoms rather than cure including:
•Elimination of drugs and foods containing monosodium glutamate, that are
suspected of causing tinnitus. (Excitatory neurotransmitters which stimulate
Tinnitus).
•Use of external noise generators or tinnitus masking devices which mask or inhibit
Tinnitus.
•Psychological interventions to deal with stress and manage distractions.
•Use of Tinnitus Retraining Therapy which include low noise generators to facilitate
auditory adaptation.
•Surgical interventions such as cochlear nerve section and vascular decompression
are used as a last resort.
Presented by -Syed Muhammad Hasan 20
TINNITUS –TREATMENT

21. •Hearing loss represents impairment of the ability to detect & perceive sound.
•It can range from mild, affecting sounds of different tones and intensities, to
moderate or profound.
•Hearing loss is classified as:
•Mild(26 to 40 dB), moderate(41 to 55 dB), severe(71 to 90 dB), or profound
(91 dB or greater).
•Profound deafness is defined as hearing loss greater than 90 dB in adults or
70 dB in children.
Presented by -Syed Muhammad Hasan 21
HEARING LOSS

22. •Conductive–Occurs when auditory stimuli are not adequately transmitted through
the auditory canal, tympanic membrane, middle ear, or ossicle chain to the inner
ear.
•Etiology–Impacted earwax, otitis externa, otitis media, tumors, otosclerosis.
(abnormal bone growth).
•Sensorineural–Irreversible, occurs with disorders that affect the inner ear, auditory
nerve, or auditory pathways of the brain. Sound waves are transmitted towards the
inner ear but are not channeled towards CNS.
•Etiology–Trauma, meningitis, presbycusis (age related hearing loss), tumors,
ototoxic drugs, genetic or idiopathic.
Presented by -Syed Muhammad Hasan
22
TYPES OF HEARING LOSS

23. 23
COCHLEAR IMPLANTS
A cochlear implant is a small electronic device
that electrically stimulates the cochlear nerve
(nerve for hearing).
The implant has external and internal parts.
The external part sits behind the ear. It picks up
sounds with a microphonewhich then processes
the sound and transmits it to the internal part of
the implant.
The internal part is placed under the skin behind
the ear during an outpatient surgery. A thin wire
and small electrodes lead to the cochlea, which is
part of the inner ear.
The wire sends signals to the cochlear nerve,
which sends sound information to the brain to
produce a hearing sensation.
Presented by -Syed Muhammad Hasan

24. •The human eye is a paired sense organ that reacts to light and allows vision. Rod and cone
cellsin the retina are photoreceptive cells which are able to detect visible light and convey
this information to the brain.
•Eyes signal information is used by the brain to elicit the perception of color, shape, depth,
movement, and other features. The eye is part of the sensory nervous system.
•More than half of the sensory receptors in the human body are located in the human eyes,
and a large part of cerebral cortex is devoted to visual processing.
•A normal human eye can see about 10 million different colors. The accessory structures of
the human eye include the eyelids, eyelashes, eyebrows, the lacrimal (tearing) apparatus
and extrinsic eye muscles.
24
VISION AND ACCESSORY STRUCTURES OF THE HUMAN EYE
Presented by -Syed Muhammad Hasan

25. 25
ANATOMICAL
REPRESENTATION
OF HUMAN EYE

26. •The adult eyeball measures about 2.5cm in diameter. Of its total surface
area, only the one sixth portion is exposed, the remainder is recessed and
protected by the orbitinto which it fits.
•The eyeball is covered by three types of layers which are:
•Fibrous Tunic –Superficial layer, consists of cornea and sclera.
•Vascular Tunic–Middle layer, consists of choroid, ciliary body and iris.
•Retina–Innermost layer, houses optic nerve & photoreceptors (Rod and
Cone cells)
26
ANATOMY OF EXTERIOR EYEBALL
Presented by -Syed Muhammad Hasan

27. •Superficial layer of the eyeball and is composed of anterior cornea and
posterior sclera.
•Cornea
•Transparent curved coat that covers the colored iriswhich help focus light on
to the retina. It is avascularand made up of collagen fibers and fibroblasts.
•Sclera (White of the eye)
•Gives shape to the eyeball, makes it more rigidand protectsits inner parts. It
is made up of denseconnective tissue, collagen fibers and fibroblasts.
27
FIBROUS TUNIC
Presented by -Syed Muhammad Hasan

28. •Middle layer of the eyeball and consisting of choroid, ciliary body and iris.
•Choroid–Posterior portion of the vascular tunic, provides nutrients to the posterior
portion of the sclera.
•Ciliary body –The choroid becomes ciliary body in the anterior portion of the vascular
tunic, consisting of ciliary processes (vascularized and secrete aqueous humor) and
ciliary muscles (alters the shape of lens adapting to near and far vision)
•Iris(Colored portion of the eye)–Regulate the amount of light entering eyeball
through pupil(hole in the center of iris). Also consists of circular muscles (contract in
response to bright light) and dilator muscles (dilate in response to dim light) with
assistance from autonomic nervous system.
28
VASCULAR TUNIC
Presented by -Syed Muhammad Hasan

29. •Third and innermost layer of the eyeball and is the beginning of the visual pathway.
•It consists of three parts which include:
•Optic disc -Site of exit for optic nerve.
•Pigment epithelium -Contain melaninthat absorbs stray light rays and prevents scattering
and reflection of light within the eyeball resulting in sharp and clear image.
•Neural portion -Consisting of photoreceptor cells (Rods & Cones) and neurons.
•The retina also contains macula lutea, a small flat spot in the posterior portion of the retina
which contains central fovea, that is the area of highest visual activity (sharpness of vision).
29
RETINA
Presented by -Syed Muhammad Hasan

30. •Two types of photoreceptor cells are specialized to transduce light rays into
receptor potentials; rodsandcones cells.
•Each retina has about 6 million cones and 120 millions rods.
•Rods–Have a low threshold that allows us to see in dim light (moonlight).
They do not provide color vision(scotopic vision).
•Cones–Have a brighter threshold that produce color vision.
•Most of our visual experiences are mediated by Cones, the loss of which
produces legal blindness.
30
PHOTORECEPTOR CELLS
Presented by -Syed Muhammad Hasan

31. •Just posterior to the pupil and iris and within the cavity of the eyeball is the
avascular lens.
•Proteins called crystallinsare arranged like the layers of onion make up the
lens which normally is perfectly transparent.
•It is enclosed by connective tissues and held in position by suspensory
ligamentswhich are attached to ciliary process.
•The function of lens is of critical importance because it fine tunes incoming
light radiationsand focus them on to the retina to facilitate clear vision.
31
LENS
Presented by -Syed Muhammad Hasan

32. 32
THE COMPLETE
ANATOMY OF
EXTERIOR
EYEBALL
Presented by -Syed Muhammad Hasan

33. •The interior of the eyeball is divided by the lens into two cavities; the anterior cavity
and the vitreous chamber.
•The Anterior Cavity –Filled with aqueous humor (watery fluid) that is continuously
filtered from blood capillaries which nourishes the lens and the cornea.
•Vitreous Chamber –Filled with vitreous body (jelly like substance) that assist in
image formation in retina, contains phagocytic cells that remove debristo avoid
obstructed vision.
•Intraocular Pressure -Pressure inside the eyes, mainly because of the presence of
aqueous humor and partly vitreous body which is about 16mm Hg.
33
ANATOMY OF INTERIOR EYEBALL
Presented by -Syed Muhammad Hasan

34. Presented by -Syed Muhammad Hasan 34
THE VISUAL PATHWAY

35. •Glaucoma comprises a group of conditions that produce an elevation in intraocular
pressure.
•If left untreated, the pressure may increase sufficiently to cause ischemic and
compressive degeneration of the optic nerve, leading to progressive blindness.
•It is one of the leading causes of blindness worldwide, and is second only to age-
related macular degenerationas the leading cause of blindness in North America.
•The condition is often asymptomatic, and a significant loss of peripheral vision may
occurbefore medical attention is sought.
35
GLAUCOMA
Presented by -Syed Muhammad Hasan

36. •Glaucoma–Results from congenital or acquired lesions of the anterior segment of the eye
that mechanically obstruct aqueous outflow. (Normal range 9 to 21 mmHg).
•It is classified as open angle (i.e., wide-angle) or angle-closure(i.e., narrow-angle)
glaucoma, depending on the location of the compromised outflow, and may occur as a
primary or secondary disorder.
•Primaryglaucoma –Occurs without evidence of preexisting ocular or systemic disease.
•Secondary glaucoma –Results from inflammatory processes that affect the eye, from
tumors, or from blood cells of trauma-produced hemorrhage.
•In glaucoma, temporary or permanent impairment of vision results from degenerative
changes in the retina and optic nerveand from corneal edemaand opacification.
Presented by -Syed Muhammad Hasan
36
CLASSIFICATION OF GLAUCOMA

37. 37
PATHOGENESIS
OF GLAUCOMA
Presented by -Syed Muhammad Hasan

38. Presented by -Syed Muhammad Hasan 38

39. Presented by -Syed Muhammad Hasan 39
STAGES OF VISION
LOSS IN GLAUCOMA

40. •Patients (and those with any risk factors) should be referred to an
ophthalmologist for a comprehensive examination that includes:
•Thorough family history.
•Examination of the optic disks (preferably using a binocular examination
technique)
•Formal visual field examination.
•Tonometry(measurement of IOP).
•Measurement of central corneal thickness, optic nerve and/or retinal nerve
fiber layer imaging (usingoptical coherence tomography).
40
GLAUCOMA -DIAGNOSIS
Presented by -Syed Muhammad Hasan

41. •Diagnostic methods include tonometry, ophthalmoscopic visualization of the optic nerve,
and central visual field testing.
•Drugs used in management of glaucoma are applied topically which lowers the production of
aqueous humor and increases its output. They are:
•β-adrenergic antagonists –Timolol, Betaxolol, Levobunolol, Carteolol etc.
•Prostaglandin analogs –Pilocarpine, Latanoprost.
•Adrenergic agonists –Brimonidine and Apraclonidine.
•Carbonic anhydrase inhibitors –Dorzolamide and Brinzolamide.
•Traditional incisional surgeries & guarded filtration procedures [trabeculectomy], glaucoma
drainage implant devices [tube shunts] create a new drainage pathway between the
anterior chamber and subconjunctival space.
Presented by -Syed Muhammad Hasan
41
GLAUCOMA –TREATMENT

42. Presented by -Syed Muhammad Hasan 42
REFERENCES
GERARD. J TORTORA / BRYAN DERRICKSON
PRINCIPLES OF ANATOMY & PHYSIOLOGY –15
TH
EDITION

43. Presented by -Syed Muhammad Hasan 43