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128 Cards in this Set
- Front
- Back
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External ear problems are usually disorders or skin diseases cause by... |
foreign bodies, fungus, or irritation |
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External ear problems have greater significance ___ than ____. |
otologically audiologically |
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Disorders of the pinna are commonly caused by irritation reactions from... |
insect bites, poor hearing aid fitting/rubbing, exposure to chemical substances or foreign material |
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Repeated trauma to the pinna can cause ____. Which is a result of ___. |
cauliflower ear
blood collecting near the cartilage skeleton of the ear |
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The most common sign of trauma to the ear canal or TM |
hematoma |
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Pinna irritation can occur from |
constant rubbing, foreign objects, improperly fitting ear molds |
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What do keloids represent? When do they occur? |
unregulated proliferation of fibrous tissue after cutaneous injury.
Occur commonly after trauma to the skin (i.e. ear piercing) |
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Temperature effects the external ear by causing ___, ____, and ____. |
Frostbite, Skin Eruption, and Chilblains |
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Chilblains |
-Occur in above freezing temperatures -Usually in areas that are not prone to cold weather -Red/Purple bumps appear of skin of extremities -Result of constriction of blood vessels -Results are not permanent |
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Frostbite |
-Occurs in temperatures below freezing - Swelling and blood filled blisters as well as skin discoloration - Blood vessels constrict to send more blood to vital organs, but as the body's temperature becomes colder Hunter's Response begins - Severe frostbite results in tissue death in affected area |
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Hunter's Response |
Blood vessels dilate (widen), then constrict again
When blood vessels permanently constrict, frostbite begins |
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What is Seborrheic Dermatitis? |
-Chronic itching of ear canal -Absence of, or very little cerumen (loose protective barrier and acidic pH -Extremely vulnerable to otitis externa -Can treat itchiness with steroids |
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What is Allergic Dermatitis? |
-Response to exogenous material in ear canal -Swelling of ear canal and pain -Fluid secretion, serosanguinous (consisting of both blood and serous- pale yellow and transparent and benign fluid) secretion -Treatment: remove what's causing reaction |
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Lupus Vulgaris |
ulcer like wounds that are hard to heal
treated with antibiotics |
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Tuberculosis |
mainly affects lungs, but also CNS, bones, joints, skin
Caused by mycobacterium tuberculosis or bovid |
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What is the most common condition affecting the EAM |
Otitis Externa |
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Acute Diffuse |
External Bacterial Otitis (cause by pseudomonas aeruginosa) |
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Acute Localized Otitis Externa- Furuncle |
Infection of a hair follicle, usually from staphylococcus aureus
Tender and self resolving |
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Acule Localized Otitis Externa- Bullous myringitis |
Localized viral infection of TM and deep EAM, can result in blood blisters
Painful and self resolving, most of the time |
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Treatment for otitis externa |
Antibiotics- usually neomycin
Drugs that re-acidify ear canal |
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External Bacterial Otitis |
Infections of tissues of the ear canal caused by bacteria
inflammation, subepithelial edema, intense pain, tenderness, erythema
Most caused by pseudomonas aeruginosa
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Chronic Otitis Externa |
Due to chronic reaction to an irritant or allergen
Ear canal appears dry and flaky
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Chronic Otitis Externa: Eczematous |
Dermatitis condition: Itching, red and scaly skin, not much of pain
Complications: stenosis (complete blockage of ear canal; monomeric membrane, conductive hearing loss) |
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Malignant or Necrotizing OE |
Osteomyelitis of temporal bone (bone infection caused by bacteria)
Symptoms: bone pain, fever, discomfort, uneasiness, ill-feeling, local swelling, redness
Usually seen in elderly
Caused by pseudomonas aeruginosa |
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Stenosis |
narrowing of the ear canal |
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Fungal infections (otomycosis) |
Fungal growth usually occurs on any dead material sitting in the ear canal
also can be caused when person is taking too many antibiotics, steroids, immune supplements
Most common fungi: aspergillus fumigators |
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Herpes infection |
begins with burning pain in the affected ear
infection usually involves the facial never but extends to labyrinth and 8th nerve |
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Eardrum Hemorrhagic Blister |
rare condition
can be seen with trauma, severe bacterial infections and viral infections |
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Obstructions of the Ear Canal |
Collapsed Ear Canal
Wax impactions |
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Neoplasms ("New Tissue") |
can be malignant or benign
Benign: Exostoses, Osteomas, Granulomas, Hemangiomas, Hygromas
Malignant: Basal Cell carcinoma, Squamous Cell Carcinoma |
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Osteomas |
Tumor composed of bone tissue |
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Granulomas |
Tumor composed of sand line granule tissues
Occurs when PE tube is in and granulation grows into tube and blocks it |
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Hemangomas |
Blood filled tumors |
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Hygroma |
Water filled tumors |
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Exostoses |
Periosteal outgrowth
new bony growth in the osseous portion of the external auditory canal |
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Karatosis Obturans |
Increased production of skin cells
Cells aren't expelled at increased rate
increase in keratin protein production that then mixes with wax |
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Cholesteatoma |
benign growth of skin in the EAM |
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Ear Maggots |
insect that has lodged itself into patients ear and laid eggs |
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Ear Canal Fistula |
ear canal mastoid fistula is a hole between the ear canal and the mastoid cavity
rare surgical complication |
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Ontogeny |
refers to the development of the individual which repeats or follows the development of the species
Proceeds in two directions 1. cephalocaudal (head to tail) 2. Proximodistal (near to far) |
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anlage |
foundation or precursor, initial clustering of embryonic cells that serves as a foundation from which a body part develops
Certain structures develop from the same anlage |
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Development of the Ear |
begins 3-4 week gestation involves ectoderm, mesoderm, and endoderm
Sensory component (hair cells) develop by 20 weeks
accessory structures develop by 32 weeks |
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READ DEVELOPMENT SECTION IN POWERPOINT! |
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Malformation |
Poor or inappropriate formation of a structure |
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Deformation |
caused by mechanical interference like a small uterus or wrong fetal position |
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Endemic |
present in a community at a high wrist (due to consanguineous marriages) |
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Epidemic |
attacks many people in a community but not continuously present (flu)
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Syndrome |
collection of anomalies or symptoms resulting from a single pathogenic process or cause (a recognizable pattern of malformations) |
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Sequence |
a series of anomalies not from one defect but due to a consequence of another event (chain of events that may have different beginnings but which all end with the same conclusion) |
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Association |
a collection of anomalies that occur together but have no sequence or symptom, no anlage associate here (which mess that the malformations occur together more often than could be explained by chance) |
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Treatment Options for Structural Abnormalities |
plastic surgery: rebuild, cosmetic Reconstruct ear canal Bone conduction HA |
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Syndromes Associated with external ear abnormalities |
Treacher Collins Syndrome Crouzon's Osteogenesis Inperfecta Pierre Robin |
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Treacher Collins Syndrome |
Also called mandibulofacial dystosis Dominant mode of inheritance
symtoms: microtia, atresia, notch or gap in lower eyelid (coloboma), TMJ, Sclerosis of ME (hardening of ME bones) |
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Crouzon Syndrome |
Also called craniofacial disorder or canal dystosis
Features atresia without microtia ME bone affected Exophthalamus: bulging of eyes Hypertelorism: increased distance between eyes Strabismus: Crossed eyes Anomalies of nose and maxilla |
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Apert Syndrome |
Same abnormalities as Crouzon syndrome combined wit abnormalities of hands and feet |
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Pierre Robin Syndrome |
Micrognathia (very small jaw) Tongue normal size, but too big for jaw
Symptoms: cleft soft palate, high arched palate, natal teeth, recurrent ear infections, small opening in the roof of the mouth |
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Osteogenesis Imperfecta |
characterized by bones that easily break without reason
Genetic defect affecting collagen (extra cellular protein in skin, bone, cartilage) production
Sclera: tinge to whites of eyes (grayish, purple, pink, blue) |
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TM perforations are caused by |
infections and traumas Acute & chronic infections Blast and penetrating traumas
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Pars Tensa vs. Pars Flaccida Perf |
Pars Tensa- Hearing loss will occur Central perf- relatively safe
Pars Flaccida- No hearing loss but good place for cholestiatoma to grow marginal perf |
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TM Retraction |
Type C tymps
Occurs as a result of ET malfunction TM sucked towards ME- can cause damage to ossicles
Long term retraction will cause erosion of the ear canal and forms a deep pocket- pocket may trap skin and form cholesteotoma |
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Tympanosclerosis |
As Tymps
eardrum has calcium plaques as a result of old infections
no significance unless plaques bind the malleus with the ear canal preventing the TM from vibrating |
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Otitis Media |
inflammation of the middle ear
occurs most frequently in children can cause negative implications for speech and language |
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Acute Suppurative Otitis Media |
Suppurative = infection starts with upper respiratory tract infection that leads to impaired ET function
Symptoms: ear pain, fever, malaise, loss of appetite, red and bulging ear drum
treatment- antibiotics |
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Myringotomy Tubes |
Tubes placed in TM to help drain fluid
Minor procedure |
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Acute Serous Otitis Media |
Serous = no infection
most commonly seen in adults as barotrauma -rapid pressure change symptoms: pressure change followed by severe ear pain and hearing loss |
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Chronic Serous Otitis Media |
Also called otitis media with effusion, OME, chronic mutinous otitis media, glue ear
ET dysfunction persists but without acute bacterial infection
causes conductive hearing loss with variable severity |
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Chronic Suppurative Otitis Media |
Suppurative = puss like infection
Two broad forms: 1. tubotymanic: perf of Tm 2. atticoantral: cholesteatoma |
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Tympanoplasty |
surgery of ME to remove disease and reconstruct the hearing mechanism
1. repair TM perf 2. repair TM perf & reconstruction of ossicular chain 3. after disease, tympani remnant is allowed to drape itself onto stapes to encourage direct transmission of sound to oval window 4. Fenestration cavity 5. stapedectomy |
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Atticoantral Disease (cholestiatoma) |
Occurs in patients with glue ear
slowly increase in size as skin cells naturally shed will grow into attic, antrum, and mastoid system
has ability to erode bone and crease HL recurrent infection may lead to otalgia and otorrhea |
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Cholestiatoma and hearing |
Auditory impairment is related to size and position
may produce flat audiogram with thresholds ranging from 35-55 dB, SRT in agreement, good WRS |
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Cholestiatoma treatment |
Modified radical mastoidectomy - drilling out infected mastoid air cells and cholestiatoma - removes incus and malleus head, and excising any involved TM
Combined approach or canal wall up tympanoplasty - preserve anatomy of ear as close to normal as possible
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Neoplasms (Glomus Tumors) |
benign tumors of the middle ear arising from glomus bodies (tiny normal structures in the middle ear that serve as bark receptors)
can occur within the ME, temporal bone, neck or jugular vein
appease as a red mass behind the TM & associated with pulsatile tinnitus |
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Impedance matching of middle ear |
allows a reasonable amount of sound energy to be passed from the air to cochlear fluid
Lever Ratio Areal Ratio |
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Congenital Malformations |
More than 50 different syndromes associated with ME bone anomalies
Anomalies of outer ear should signal problems in the middle ear Anomalies of the middle ear usually require surgical intervention |
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Audiological Considerations with ME |
hearing loss can be up to 55-65dBHL by AC BC testing usually reveals intact cochlear Speech testing will have similar results to AC |
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Chorda Tympani issues |
Chorda tympani is a branch of the facial nerve- serves the taste buds in the front 2/3 of tongue
runs through the middle ear- damage to CT leads to abnormal taste messages to the brain |
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Ossicular Chain Discontinuity |
Causes: - children: necrosis - adults: trauma and previous surgical procedures
Treatment: - ossiculoplasty |
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Otosclerosis |
"hard ears"
irregular growth of vascular spongy bone replaces the normal bone -occurs most often in oval window -extends to stapes footplate and annular ligament -can also spread to cochlea - releases toxic enzymes into the perilymphatic space of the inner ear causing SNHL |
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Symptoms of Otosclerosis |
Autosomal dominant inheritance Genetic but not congenital Most common in females More prevalent in caucasian women Aggravated during pregnancy and menstruation Hearing loss, tinnitus, vertigo, nausea TM can have Schwartze Sign |
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Medical Treatment of Otosclerosis |
Medical treatment has limited success
Sodium Fluoride- idea was to harden the bone, thus restricting bone growth
Surgical treatment: 1. Fenestration 2. Stapedolysis 3. Stapedectomy |
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Fenestration |
create new oval window - drilled into the lateral semicircular canal at the level of the promontory
Will not lead to complete restoration of hearing |
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Stapedolysis |
involves raising the TM, exposing the contents of the ME, attaching a hook like instrument to the crus of the stapes, and jerk the footplate free from the otosclerotic growth
long term effects are unsuccessful |
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Stapedectomy |
Most common
removal of the stapes and the insertion of a prosthesis |
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Audiological findings in otosclerosis |
Early stages: mild low frequency conductive HL As disease progresses- higher frequencies will be affected
ABG diminishes at 2k
As tymps, early stages can have A type
Elevated SRTs and good WRS initially- poor WRS with advanced disease |
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Chromosomes |
long DNA molecules that have proteins, carry hereditary information, and contains many different kinds of genes
humans have 23 pairs 1-22: autosomes 23: sex chromosomes |
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Gene |
Region of DNA that controls hereditary characteristics |
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Genotype |
gene/allele (DNA sequence) for trains EX: hair color, height |
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Phenotype |
physical expression of gene EX: black hair, brown eyes |
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Penetrance |
manifestation of disorder by gene expression Low penetrance: gene not expressed Incomplete penetrance: person fails to express the train even though they carry the allele
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Variable expression |
expression always present but varies with range |
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Genetic Hearing Loss |
Inherited gene from one of both parents |
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Autosomal recessive |
both parents need to have the abnormal gene |
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Autosomal dominant |
Abnormal genetic programs from one parent is sufficient to produce the disorder |
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Sex linked |
genetic material carried on X chromosome |
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Chromosomal Abnormalities |
Extra or missing chromosome Extra: called trisomy most severe- trisomy 13, 15, 18 Missing: called monosomy (almost always fatal)
Variable expressivity: all characteristics may not show up, or be fully pronounced |
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Mitochondrial Inheritance |
Can cause HL Range in severity & tends to worsen over time
Mutations in DNA within mitochondria of cells
Inherited only through mother
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Aplasia |
Defective development or absence of organ or tissue
All modes of transmission can occur with or without associated abnormalities of the OE, ME, or IE
IE anomalies are generally rare |
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Michel Anomaly |
The most extreme and rare form of IE anomaly
No inner ear & sometimes entire auditory nerve may be absent |
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Scheibe Type |
More common
Have intact bony labyrinth, but with the loss of some of the vestibular and metabolic organs of the IE lost, and atrophy of the organ of corgi |
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Mondini Type |
Tissue of the cochlear duct and its contents is altered
EX: first 1.5 turns of cochlea may be normal and remaining part is absent or malformed |
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A Fourth Type of Aplasias |
bony anatomy may be completely normal but there may be various degrees of damage to the neuro-sensory epithelium (hair cells & spiral ganglia neurons) |
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Gene Mapping & Localization |
Decodes genes responsible for HL
Ultimate goal: therapeutic or preventative intervention in people with genetic hearing loss |
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Congenital HL |
can be syndromic or non-syndromic
present at birth
Nongenetic congenital deafness: ototoxic drugs mother took during pregnancy |
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Post-Natal HL |
Begins after birth (can still be genetic)
Non-genetic acquired HL: not born with condition Tumors, drugs, noise, etc |
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Genetic Hearing Loss |
based on anomalies that can be categorized into four groups
1. integumentary: skin & eye pigmentation 2. Skeletal: craniofacial, vertebral 3. Ocular: vision 4. Other: kidney, legs, limbs, etc |
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Waardenburg Syndrome |
Integumentary disorder Heterochromia iridis: different colored eyes White forelock Hypertelorism: widely spaced eyes Flat nasal bridge Heart shaped mouth Bilateral SNHL
Dominant gene disorder with variable expression |
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Albinism |
Integumentary anomaly
Absence of melanin or extremely low pigmentation
Autosomal dominance (most common), recessive, or sex linked
Severe SNHL when HL is present |
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Klippel Feil Syndrome |
Autosomal dominant
Skeletal abnormality, defect (fused or abnormal vertebrae)
Physical Features: short neck & lowered hairline in back
Conductive, mixed or SNHL
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Crouzon Syndrome |
Autosomal dominant inheritance
Physical expression: exopthalmus: bulging eyes hyertelorism: ocular and craniofacial abnormalities
SNHL of varying degrees |
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Usher Syndrome |
Recessive mode of inheritance
Ocular abnormality retinitis pigmentosa: degeneration or retina
MR, epilepsy, vertigo
SNHL of varying degrees |
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Pendred Syndrome |
Part of Mondini Aplasia
Mainly recessive inheritance, may show autosomal dominant inheritance
progressive SNHL and ocular abnormalities
Enlarged thyroid (goiter) |
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Mucopolysaccaridosis |
Group of genetic disorders
Excessive accumulation of mucopolysaccharides Gel like substance
Recessive or X-linked inheritance
7 types
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MPS1--- Hurler Syndrome |
Mixed & severe hearing loss
Autosomal recessive inheritance
MR Osseous and articular deficits Reduced height Large heart Hypertelorism and wide nasal bridge Fatal |
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MPS2 --- Hunter Syndrome |
less severe than hurler syndrome
X-linked inheritance
Normal at birth, reduced growth as aging progresses
Chronic nasal problems ME problems Longer life but early death (30) |
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Alport Syndrome |
X linked, recessive, or dominant inheritance - males more effected and more severe
Renal (kidney problems): nephritis asymptomatic for a while HL in second decade of life
diagnosed later in life |
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Down Syndrome |
Physical characteristics: slanted eyes, small ear canals, retarded growth, flat hypo plastic face, small rounded ear, thick tongue, MR, conductive & mixed HL, prominent epicanthic skin folds, protruding lower lip, short stubby fingers, simian folds across palms
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Nonsyndromic Autosomal Dominant HL |
Genetic analysis 15% of HL in humans
Classified in different ways Groupings of different abnormalities |
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Nongenetic Congenital HL |
Generally viral, sometimes bacterial viral: more serious because it crosses placenta
Prenatal viruses usually cause deafness |
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TORCHS |
toxoplasmosis, rubella, cytomegalovirus, herpes, syphilis
Represents the major non genetic congenital causes of SNHL in neonates |
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Toxoplasmosis |
caused by parasite called toxoplasma gondii asymptomatic in adults detrimental to fetus or immunocompromised person
Symptoms: seizures, hydrocephalus, MR, visual and neuromuscular impairment
HL is progressive and not repairable Calcium deposits in stria vascularis and spiral lig. |
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Rubella |
caused by rubella virus Children now vaccinated mother can be immunized transfer to infant via placenta, birth canal, direct contact, contamination during birthing
can be fatal Corner Audiogram |
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Symptoms of Rubella |
congenital cataract, congenital heart disease/defect, MR, SNHL
Endolabyrinthitis: inflammation of the labyrinth
IE lesions: stria vascularis, Reissner's membrane, Tectorial Membrane
cookie bite audiogram |
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Cytomegalovirus (CMV) |
herpes family Most frequently transmitter parentally to fetus Postnatally it is asymptomatic no long-term consequences but stays in body
High risk groups: unborn child, people who work with children, transplant patients, HIV patients |
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Symptoms of CMV (1) |
hepatospleenomegaly: enlarged liver & speen Hyperbilirubinemia: jaundice Thrombocytopenia: platelets disorder, lack of platelets, abnormal bleeding
Various degrees of CNS involvement - Microcephaly (small head), SNHL |
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Symptoms of CMV (2) |
Children will have subtle neurologic deformities -Auditory neuropathy Normal OAEs, abnormal ABRs, reduced AP skills, mild-moderate SNHL |
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Herpes |
Most common STD Transferred during birthing process
If crosses placenta (not common) leads to spontaneous abortion or severe malformations if baby survives
HL present at birth |
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Syphilis (1) |
Caused by spirochete treponema pallidum
Mother can take antibiotics to prevent fetus from becoming infected -if untreated, disease is transmitted through placenta and can lead to spontaneous abortion or serious injury to fetus
If survives, baby will have rash, anemia, CNS defects, cardiac defects, and HL
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Syphilis (2) |
Penicillin used to treat
congenitally, asymptomatic at birth Vertigo and tinnitus with or w/o HL
Otosyphilis: ME is effected (suppurative OM) Neurosyphilis: affects CNS, will lead to HL |
