Assignment: Tympanic Membrane

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Assignment: Tympanic Membrane

Assignment: Tympanic Membrane


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Assignment: Tympanic Membrane and Thyroid Gland

Using the South University Online Library or the Internet, research the tympanic membrane and the thyroid gland. Based on your findings, create a 5- to 6-page Microsoft Word document that includes:

  • Information about a minimum of two health assessment histories.
  • The possible findings for the tympanic membrane.
  • Information on how to examine the thyroid gland using both the anterior and posterior methods.
  • A concise note in the subjective, objective, assessment, and plan (SOAP) format with each patient’s encountered findings.
    • For a review of SOAP notes:
    • Information about laboratory tests that may be used for screening clients and the expected normal levels for each test.

Support your responses with examples.

On a separate references page, cite all sources using APA format.

  • Use this as a convenient reference for properly citing resources.
  • This handout will provide you the details of .
  • You may create your essay in this .
  • Thyroid hormone is critical for auditory development and has well-known actions in the inner ear. However, less is known of thyroid hormone functions in the middle ear, which contains the ossicles (malleus, incus, stapes) that relay mechanical sound vibrations from the outer ear to the inner ear. During the later stages of middle ear development, prior to the onset of hearing, middle ear cavitation occurs, involving clearance of mesenchyme from the middle ear cavity while the immature cartilaginous ossicles attain appropriate size and ossify. Using in situ hybridization, we detected expression of Thra and Thrb genes encoding thyroid hormone receptors α1 and β (TRα1 and TRβ, respectively) in the immature ossicles, surrounding mesenchyme and tympanic membrane in the mouse. Thra+/PV mice that express a dominant-negative TRα1 protein exhibited deafness with elevated auditory thresholds and a range of middle ear abnormalities including chronic persistence of mesenchyme in the middle ear into adulthood, markedly enlarged ossicles, and delayed ossification of the ossicles. Congenitally hypothyroid Tshr−/− mice and TR-deficient Thra1−/−;Thrb−/− mice displayed similar abnormalities. These findings demonstrate that middle ear maturation is TR dependent and suggest that the middle ear is a sensitive target for thyroid hormone in development.

    Deafness can arise in developmental thyroid disorders and may reflect both sensorineural and conductive hearing loss (, ). In rodent models, thyroid hormone has a well-documented role in the development of the cochlea in the inner ear (–), but less is known concerning the middle ear (ME). The ME, an air-filled chamber, contains the malleus, incus, and stapes, the articulated ossicle bones that transmit sound from the outer ear to the cochlea (). Sound waves cause vibration of the tympanic membrane at the interface of the outer ear canal and the ME. These vibrations are transmitted and amplified by precise lever- and piston-like motions of the ossicles to the oval window of the cochlea, which in turn stimulates the cochlear hair cells and the transduction of sound into neural impulses.

    In many mammals, such as mice, the ME is nonfunctional at birth and matures during postnatal life (). This maturation can be a limiting step in the onset of hearing (, ). In the early embryonic ME, the ossicles arise from mesenchymal condensations and initially form as cartilaginous structures (, ). In mice, the ossicles ossify postnatally, while surrounding mesenchyme in the ME cavity is cleared and replaced by air before the onset of hearing at approximately 2 wk of age (–). The mechanisms that control mesenchyme clearance, also known as cavitation or pneumatization, are poorly understood. In humans, ME abnormalities are a cause of hearing loss (), and residual mesenchyme has been associated with otitis media, inflammation of the ME, a common childhood ailment (, ).

    Although little is known of the factors that promote ME maturation, pituitary and thyroid hormones have been implicated. ME abnormalities have been reported in Snell dwarf mice, which have combined pituitary hormone deficiency () and in hypophysectomized rats (, ). In addition, ME infections and conductive hearing loss have been noted in human thyroid diseases (, ). Here we report detection of expression of Thra and Thrb thyroid hormone receptor (TR) genes in the immature ME in mice. We also report that Thra+/PV mutant mice () display ME abnormalities with enlarged ossicles, delayed ossification of the ossicles, and retention of mesenchyme in adulthood. Hypothyroid Tshr−/− mice () and TR-deficient Thra1−/−;Thrb−/− mice () display related phenotypes, further supporting the conclusion that TR signaling is required for ME cavitation and ossicle growth.

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