Otosclerosis

Otosclerosis is a primary disease of the bones of hearing and bone labyrinth capsule. Otosclerosis is a disease of bone in the middle ear especially the stirrup caused new bone formation spongiosus and around the window so it can ovalis fixation resulted in an the stirrup. (Brunner & Sudarth, 2001)

Etiology
a. The cause of otosclerosis is still not clear (idiopathic)
b. Opinions are generally inherited autosomal dominant.
c. Scientific evidence which states that measles virus infection affect otosclerosis.
d. Some argue that chronic measles infection in the bone predisposes affected patients to otosclerosis. virus material can be found in osteoblasts in sclerotic lesions.

 

Pathophysiology of otosclerosis is very complex. The primary key of the lesion otosclerosis is the presence of multifocal areas of sclerosis between the bone endokondral temporal. There are two phases of the identifiable pathological this disease are:

 
a. The initial phase otospongiotic
Histological features: composed of histiocytes, osteoblasts, osteocytes are is the most active group of cells. Osteocytes begin to get into the center of the bone around the blood vessels that causes dilation of blood vessel lumen and dilatation of the circulation. These changes can be seen as a picture of redness on the tympanic membrane. 

Schwartze sign is associated with increased vascular lesions that reached the periosteal surface. with the involvement of osteocytes are more and more, this area is rich in substance basic structure of amorphous and lack of mature collagen and result in the formation of spongy bone. The invention of this histological with haematoxylin and eosin staining known as the Blue Mantles of Manasse. 

b. The final phase of otosclerotic
Otosclerotic phase begins when the osteoclasts are slowly replaced by sclerotic bone osteoblasts and deposited in areas of soft resorption before. When this process occurs in the footplate will causes the stapes fixation on fenestra ovale so that disrupted the movement of the stapes and therefore transmission of sound to cochlear blocked. The end result is the occurrence of conductive deafness.
If it involves only the footplate otosclerosis, only slightly fixation to occur. Things like this are called biscuit footplate. The occurrence of sensorineural deafness in otosclerosis associated with possible release of toxic metabolic result of injuries neuroepitel, nearby blood vessels, a direct relationship with otosclerotic lesion to the inner ear. All this led to changes in electrolyte concentration and mechanism of the basement membrane.

Signs and Symptoms
a. Progressively decreased hearing
b. Tinnitus (ringing in the ears)
c. vertigo
d. Deafness 30-40 db (desible)

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Mastoiditis

Mastoiditis is any inflammatory process in the mastoid cells located in the temporal bone is inadequate. Mastoiditis is a secondary disease of untreated otitis media.

Mastoiditis occurred due to Streptococcus ß hemoliticus / pneumococcus. Also lacking in the hygiene of the ear such as entry of water into the ear and bacteria that enter and nesting that can cause respiratory tract infections. On examination of the ear will show that there is a foul-smelling pus due to respiratory tract infections. Mastoiditis is the result of a long infection of the middle ear, bacterial mastoiditis usually obtained in the same bacteria found in middle ear infections. Gram-negative bacteria and Streptococcus aureus is a bacterium most often found in these infections. As mentioned above, that the circumstances which led to a decrease of the immunological system of the person also may be a predisposing factor mastoiditis. In some recent research, almost half of children suffering from mastoiditis, do not have the disease previous middle ear infection. Bacteria play a role in patients with these children is S. Pnemonieae.

Clinical manifestations of mastoiditis is:
1. Febrile / subfebris
2. Pain in the ear
3. Loss of sensation of hearing

4. Sometimes even the ringing sound occur on one side of the ear (the ear can also be on the other side)

5.Kemerahan the mastoid complex
6. Discharge either clear or in the form of mucus.
7. The demise of the hard tissues (bone, cartilage).
8. The existence of an abscess (collection of dead tissue and pus)

Complications of mastoiditis include damage to the abducens and facial cranial nerves (cranial nerves VI and VII), decreased ability to look towards the client side / lateral (cranial nerve VI) and causes the mouth oblique, as if to the side (cranial nerve VII). Other complications include vertigo, meningitis, brain abscess, otitis media and chronic purulent wound infections.

Treatment with drugs such as antibiotics, anti-pain, anti-inflammatory and others are the first line in the treatment of mastoiditis. But the selection of anti-bacteria must precisely match the test results of culture and resistance results. More invasive treatment is surgery on the mastoid. Surgery is performed in the form of open surgery, this is done if the treatment can not be helped restore to normal function. Common symptoms are usually managed, treated with antibiotics, sometimes required myringotomy. If there is a relapse due to persistent tenderness, fever, headache, and ears may be necessary mastoidektomi. 

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Hearing Disorders Due to Noise

Definition

Noise is a sound or noise that bothers or undesirable. From this definition suggests that the actual noise is very subjective, depending on each individual, time and place of occurrence of noise. While in audiology, noise is a mixture of pure tone sound with different frequencies.
Hearing disability caused by work (occupational deafness / noise induced hearing loss) is the loss of the entire hearing sebahagian or someone who is a permanent, on one or both ears caused by the continuous noisy workplace environment. In industrial environments, the higher the intensity noise and the longer time noise exposure experienced by the workers, the more severe hearing loss inflicted on these workers. 

Etiology
Factors that affect the noise exposure:
1. The intensity noise
2. frequency noise
3. The length of time noise exposure
4. individual susceptibility
5. gender
6. age
7. Abnormalities in the middle ear

Distribution
In general, the effect of noise on hearing can be divided into two categories namely:
1. Noise Induced Temporary Threshold Shift (TTS)
2. Noise Induced Permanent Threshold Shift (NIPTS)

NOISE INDUCED TEMPORARY THRESHOLD SHIFT (NITTS)
Someone who was first exposed to loud noise will experience a variety of changes, which at first appears is taller hearing thresholds at high frequencies. In the audiometric picture appears as " notch "which is steep on the frequency of 4000 Hz, which is also called acoustic notch. At the initial level of hearing threshold shift is temporary, which is also called NITTS. If the rest outside the noisy environment usually can return to normal hearing.

INDUCED PERMANENT NOISE THRESHOLD SHIFT (NIPTS)
In everyday practice often found in cases of hearing loss due to noise, and this is called "occupational hearing loss" or loss of hearing due to work or any other names noise induced deafness industri. It is said that to change the time required NITTS be NIPTS noisy work environment for 10 - 15 years, but this depends also to:
1. noise level
2. person's sensitivity to noise
 

NIPTS usually occur around the frequency of 4000 Hz and slowly frequency increased and spread to surrounding areas. NIPTS initially without complaint, but if it has spread to the lower frequencies (2000 and

3000 Hz) complaints will arise. At first a person would have difficulty to hold a conversation in a crowded place, but when it is spread to a lower frequency will give rise to difficulty in hearing the voice very weak. Notch starts at frequencies 3000 - 6000 Hz, and after some time picture of a flat audiogram at frequencies more high. Frequency hearing loss at 4000 Hz will continue to grow and settled after 10 years and later development into a more lambat.

Pathogenesis

Deafness due to noise affecting the organ of Corti in the cochlea, especially the cells the hair. The first area affected is the outer hair cells that show the degeneration which increases with the intensity and duration of exposure. Stereosilia on outer hair cells become less rigid, thereby reducing response to stimulation. With increasing intensity and duration of exposure will be found more damage like loss stereosilia. areas that first exposed to the basal region. With the loss stereosilia, hair cells die and be replaced by scar tissue. The higher intensity of exposure sound, hair cells in and supporting cells are also damaged. with the growing extent of damage to the hair cells, can occur in nerve degeneration can also be found in the brainstem auditory nuclei. 

Clinical features
Deafness due to noise can affect discrimination in speech (Speech discrimination) and social functioning. Disturbances at high frequencies can cause difficulties in receiving and distinguishing consonant sounds. sound with a high tone, like a baby crying or a ringing phone can not be heard at all. Deafness is usually bilateral. Additionally tinnitus is symptoms are frequent complaint and may eventually interfere with the sharpness hearing and concentration.
In general overview on deaf deafness due to noise (noise induced hearing loss) are:
1. is sensorineural
2. Almost always bilateral
3. Rarely cause a very severe degree of deafness (profound hearing loss) The degree of hearing loss ranging between 40 s / d of 75 dB.
4. If the noise exposure is stopped, no longer found a decrease Significant hearing.
5. Ear damage in the first place on the frequency 3000, 4000 and 6000 Hz, where the most severe damage occurred on the frequency of 4000 Hz.
6. With constant exposure to noise, frequency deafness in 3000, 4000 and 6000 Hz will reach a maximum level in 10-15 years.
 

Besides the effect on hearing (auditory), excessive noise also has a non-auditory effects such as the influence of communication speech, impaired concentration, sleep disturbances due to stress triggers hearing loss who terjadi.

Management
In accordance with the causes of deafness, the patient should be transferred works from noisy environments. If not impossible to remove the tool can be used ear protectors that form the ear plugs (ear plugs), closed ear (ear muffs) And protective headgear (helmet).
Therefore, noise induced deafness is the cochlear nerve deafness that are settled (irreversible), when the hearing loss has resulted in difficulties communicate with the volume of ordinary conversation, can be tried installation of equipment hearing aids (ABD). If the hearing has been so bad, so using ABD was not able to communicate adequately, it is necessary done so that patients can receive psychotherapy situation. exercise hearing (auditory training) can also be done so that patients can use of residual hearing with ABD efficiently assisted by speech lip reading (lip reading), expression and movement of limbs and sign language to be berkomunikasi.

Prognosis
Because this type of deafness caused by exposure to noise is deaf cochlear nerve sedentary nature, and can not be treated as medical or surgery, the prognosis is less good. Therefore the most important is the prevention of deafness.

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ANATOMY OF EAR

The ear is divided into 3 parts, the outer ear, middle and deep.

a. Outer ear
The outer ear consists of the ear, ear canal to the tympanic membrane. The auricle consists of cartilage and skin elastin. S-shaped ear canal, with a framework of cartilage in the outer third, while two-thirds of it consists of bone, its length is approximately 2 ½ - 3 cm. In the outer third of the ear canal skin there are a lot of cerumen glands (modified sweat glands = cerumen glands) and hair. Sweat glands found in the skin of the ear canal. In two-thirds of the cerumen glands are not found.

b. Middle ear
Cube-shaped middle ear tympanic membrane with the outer border; front boundary eustachius tuba; lower limit jugular vein (bulbus jugularis); rear boundary aditus ad antrum, facial canal pars vertikalis; upper limit of the tegmen tympani (meninges / brain) and the boundary in a row from top to bottom horizontal semicircular canal, facial canal, casement oval (oval window), casement round (round window) and the promontory.
In the middle ear hearing bones are composed from the outside in, namely the malleus, incus and stapes. Bone loss in the middle ear are interconnected. Processus longus malleus attached to the tympanic membrane, malleus attached to the incus, and stapes incus attached. Stapes lies in dealing with the oval windows of the cochlea. Relations between the bones of a joint hearing. While tubal eustachius included in the middle ear that connects the nasopharynx to the middle ear.

c. ear in
The inner ear consists of the cochlea (the cochlea) in the form of two half-circles and vestibular consisting of 3 pieces of the semicircular canals. End or top of the cochlea called helikotrema, connecting perilimfe tympanic scale with the scale vestibuli. Semicircular canals are not fully interconnected. Scale vestibuli and scale tympani contains perilimf, whereas media containing endolimf scale. Ions and salts contained in different perilimf endolimf. It is important for hearing. Basic scale vestibuli called vestibuli membrane (Reissner membrane) while the medium-scale basis is the basement membrane. At this membrane lies the organ of Corti.
On a scale of media there is a section called the tongue-shaped membrane tektoria, and the basement membrane attached to the hair cells of the hair cells, outer hair cell and the canal of Corti, which form the organ of Corti.

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Skin disease Impetigo

DEFINITION
Impetigo is a skin infection that causes the formation of small blisters containing pus (pustules). Impetigo most often affects children, especially the cleanliness underweight and could appear in any body part, but is most often found on the face, arms and legs. In adults, impetigo can occur after other skin diseases. Impetigo may also occur after an upper respiratory tract infection (eg flu or other viral infections).

CAUSE
Staphylococcus or Streptococcus bacteria. Impetigo can occur after an injury or a condition that causes a tear in the skin (eg fungal infections, because the sun burns or insect bites). Impetigo can also attack normal skin, especially on the limbs of children.

SYMPTOMS
Impetigo begins as an open wound that causes itchy, and blistered, remove the contents lepuhannya then dry up and eventually form a scab. Impetigo is a contagious disease, which is transmitted through the liquid that comes from lepuhannya. The amount of blisters varies, ranging from the size of a pea to the size of a large ring. These blisters contain yellowish carian accompanied by intense itching. Can occur swollen lymph nodes around the infected area.

DIAGNOSIS
Diagnosis based on symptoms. To ensure that the cause is staphylococcal or streptococcal, can be breeding the infected tissue samples in the laboratory.

TREATMENT
For a mild infection, given an antibiotic ointment (such as erythromycin or dicloxacillin). Antibiotics by mouth (swallowed) may speed healing. To remove the scab, the skin should be washed with antibacterial soap several times / day.

PREVENTION
Infection can be prevented by maintaining cleanliness and health agencies. Minor scratches or abrasions should be washed thoroughly with soap and water, if necessary, spread with anti-bacterial substances.
# To prevent transmission: Avoid contact with fluid from blisters on the skin
# Avoid sharing towels, razors or clothing with an infected person
# Always wash hands after handling the skin lesions.

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Irritant Contact Dermatitis

Definition

DKI is an inflammatory skin reaction nonimunologik, where damage occurs directly without any prior skin sensitization process. Irritant contact dermatitis (DKI) is an inflammation of the skin which manifests as erythema, mild edema and cracked. DKI is a non-specific response against chemical damage direct skin that release inflammatory mediators, mostly from epidermal cells.

Etiology

Causes of irritant contact dermatitis are materials that are irritants, such as solvents, detergents, lubricating oils, acids alkalis, sawdust, abrasive materials, enzymes, oils, concentrated salt solution, low molecular weight plastic or hygroscopic chemicals. Skin disorder that appears depends on several factors, including factors of the irritant itself, environmental factors and individual patient factors.

Pathogenesis

Skin disorders arising from cell damage caused by chemical irritants through work or physical. Irritants damage the stratum corneum, keratin denaturation, get rid of the fat layer of horn and change the water holding capacity of skin. Mostly irritants (toxin) damage the fatty membrane of keratinocytes but some can penetrate cell membranes and damage the lysosomes, mitochondria or complement the core. Kerisakan membrane activate phospholipase and release of arachidonic acid (AA), diasilgliserida (DAG), platelet actifating factor (PAF) and inositida (IP3). AA is converted to prostaglandin (PG) and leukotrienes (LT). PG and LT induces vasodilatation, increased vascular permeability and thus facilitate the transudation of complement and kinin. PG and LT also act as a strong kemoatraktan for lymphocytes and neutrophils, and activated cells release histamine mas, LT and other PG, and PAF, thereby strengthening the vascular changes.
Second messengers DAG and other mengstimulasi gene expression and protein synthesis, such as interleukin-1 (IL-1) and granulocyt-macrophage colony stimulating factor (GMCSF). IL-1 activates T-helper cells release IL-2 receptor expressing an IL-2 that cause autocrine stimulation and cell proliferation.

 Clinical
A detailed history is needed because the diagnosis of Capital depend on a history of cutaneous irritant exposure on places on the body. Patch tests are also used in cases of severe or persistent to get rid of ACD. Primary subjective symptoms usually include the following:
Adequate history of exposure to skin irritants Onset of symptoms appear within a few minutes to several hours in acute Establishments. In subacute ICD is a hallmark of certain irritants such as benzalkonium chloride (on disinfektak) which brought an inflammatory reaction 8-24 hours after exposure. Onset and the symptoms can be delayed several weeks in Jakarta cumulative. Pain, burning, stinging or uncomfortable feeling in the early phase. Other subjective symptoms include: onset within 2 weeks of exposure and the same complaint adalanya coworkers or other family members. Establishments occupational usually occur on new employees or those who have not learned to protect skin from irritants. Individuals with atopic dermatitis (especially of the hands) were exposed to ICD hand.

Diagnosis

Diagnosis is based ICD thorough anamnesis and clinical observations. Establishments acute easier to detect, because the emergence of faster, so people generally still remember what the cause. Instead Establishments arising chronic slow and have a wide variety of clinical picture, so it is sometimes difficult to distinguish from ACD. This is necessary to patch test with the suspected material.

Management

Treatment efforts are most important irritant contact dermatitis is to avoid exposure to irritants, whether they are mechanical, physical or chemical factors that aggravate and get rid of. When can be done perfectly and without complications, it is not necessary and adequate topical treatment with a moisturizer for dry skin repair.
When it is necessary to overcome the inflammation can be given topical corticosteroids. Use of the adequate protection needed for those who work with irritants as a preventive effort.

a.Acute dermatitis
For acute dermatitis, compresses locally administered physiological saline solution or potassium permanganas 1/10.000 for 2-3 days and after drying was given a cream containing hydrocortisone 1 to 2.5%.
Systemically administered antihistamines (CTM 3x1 tablet.hari) to relieve itching. If the weight / area can be given prednisone 30 mg / day and if there are corrections made tapering. If there is a secondary infrksi antibiotics administered at a dose of 3x500 mg for 5-7 days.
b.Dermatitis chronic
Given topical steroid ointment containing hydrocortisone is more potent as an experienced Fluorination like desoksimetason, diflokortolon. Systemically administered antihistamines (CTM 3x1 tablet.hari) to relieve itching.

Complication The ICD complications are as follows:
Capital increases the risk of sensitization to topical treatment
Skin lesions may develop secondary infections, especially by Staphylococcal aureus
Secondary neurodermatitis (lichen simplex chronic) can occur terutapa in workers exposed to irritants at work or with psychological stress
Hipopignemtasi post inflammatory hyperpigmentation or in areas exposed to Establishments
Scarring appears on exposure to corrosive materials, ekskoriasi or artifacts.

Prognosis
Good prognosis in non-atopic individuals where Establishments diagnosed and treated properly. Individuals with atopic dermatitis are prone to Jakarta. When irritants can not be ruled out completely, the prognosis is not good, where the condition is often the case that the cause is multifactorial chronic Establishments.

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