ENT specific pathologies Flashcards
1
Q
Cerumen, perforation, and middle ear fluid, will increase the _______ gap between ______ conduction
A
cerumen, perforation, middle ear fluid will increases the air-bone gap between the air and bone conduction
2
Q
Damage to the inner ear (cochlea) or auditory nerve (CN VIII), leads to … ?
A
Sensorineural Hearing Loss
3
Q
What is the primary etiology of temporomandibular joint (TMJ) disorder?
A
TMJ disorder is multifactorial, including trauma, poor cervical spine posture, bruxism (teeth grinding), stress, malocclusion, and excessive jaw movements.
4
Q
What are the primary clinical symptoms of TMJ disorder?
A
Patients experience jaw pain, limited jaw mobility, clicking or popping sounds, ear pain, headaches, and facial tenderness.
5
Q
What distinguishes TMJ disorder from other causes of facial pain?
A
TMJ disorder is often aggravated by jaw movements (e.g., chewing, yawning) and may present with jaw deviation or malalignment.
6
Q
How is TMJ disorder diagnosed?
A
Diagnosis is clinical, based on history and physical exam findings such as jaw tenderness, limited mouth opening, and clicking/popping sounds. Imaging (MRI or CT) is reserved for severe or refractory cases.
7
Q
What is the initial treatment for TMJ disorder?
A
Conservative management includes patient education, behavioral therapy, jaw exercises, physical therapy, NSAIDs, and warm compresses.
8
Q
What are additional treatment options for persistent TMJ pain?
A
Bite splints, muscle relaxants, intra-articular corticosteroid injections, and botulinum toxin injections may be considered.
9
Q
When is surgery indicated for TMJ disorder?
A
Surgical intervention (arthroscopy, arthroplasty) is reserved for severe, refractory cases with structural abnormalities or joint degeneration.
10
Q
What are potential complications of untreated TMJ disorder?
A
Chronic pain, worsening malocclusion, dental wear from bruxism, and progressive joint degeneration.
11
Q
How does stress contribute to TMJ disorder?
A
Stress-induced bruxism (teeth grinding) and clenching can exacerbate TMJ symptoms by increasing tension in the jaw muscles.
12
Q
What is the role of physical therapy in TMJ disorder management?
A
Physical therapy focuses on jaw exercises, posture correction, and muscle relaxation techniques to reduce pain and improve mobility.
13
Q
What is sialolithiasis and what are its risk factors?
A
Sialolithiasis is the formation of calculi (salivary stones) in the parotid, submandibular, or sublingual glands. Risk factors include dehydration, use of anticholinergic drugs, and trauma.
14
Q
How does sialolithiasis present clinically?
A
Patients present with pain and swelling of the affected salivary gland, which worsens with eating due to increased salivary flow.
15
Q
What is the treatment for sialolithiasis?
A
Hydration, gland massage, sialogogues (e.g., lemon drops), NSAIDs for pain relief, and in some cases, surgical removal of the stone.
16
Q
What is sialadenitis and how is it related to sialolithiasis?
A
Sialadenitis is an infection of the salivary glands, often secondary to sialolithiasis or poor oral hygiene.
17
Q
What are the common causes of sialadenitis?
A
Most commonly caused by Staphylococcus aureus (bacterial) or viral infections like mumps.
18
Q
How does sialadenitis present clinically?
A
Painful, swollen, erythematous salivary gland with tenderness and fever. May have purulent discharge from the salivary duct.
19
Q
What is the treatment for sialadenitis?
A
Hydration, warm compresses, sialogogues, and antibiotics (e.g., dicloxacillin, clindamycin) for bacterial cases.
20
Q
What is sialadenosis and what conditions is it associated with?
A
Sialadenosis is a benign, non-inflammatory, bilateral enlargement of the salivary glands, associated with autonomic dysfunction.
21
Q
How does sialadenosis present clinically?
A
Painless, bilateral swelling of the salivary glands, often seen in patients with liver disease (alcoholic or non-alcoholic cirrhosis), diabetes, or bulimia.
22
Q
What is pleomorphic adenoma and what are its characteristics?
A
Pleomorphic adenoma is a benign mixed tumor that is the most common salivary gland neoplasm, composed of epithelial and myoepithelial elements. Those who are 30-40 years of age and who have a history of repeated head and neck radiation are at higher risk of developing pleomorphic adenoma. The incidence is also twice as likely in individuals assigned female at birth than it is in individuals assigned male at birth. Other risk factors include smoking, alcohol misuse, diets rich in cholesterol, and certain occupations (e.g., rubber manufacturing, asbestos mining, and plumbing). The signs and symptoms of pleomorphic adenoma typically include the growth of a smooth, painless mass on one side of the face that gradually enlarges over time. It typically begins as a painless lump at the back of the jaw, just below the earlobe. As the adenoma swells, it can affect the facial nerve and make it difficult for an individual to move one side of their face. Over time, hearing impairment, difficulty chewing, difficulty swallowing, and muscle weakness of the face can occur. Depending on the size of the tumor, the person may have a hard time opening the mouth widely. Diagnosis is with physical exam, imaging (US, CT, MRI) followed by biopsy.
23
Q
What is mucoepidermoid carcinoma and how does it present?
A
Mucoepidermoid carcinoma is the most common malignant salivary gland tumor, consisting of mucinous and squamous components. Can present as a painless, slow-growing mass.
24
Q
What is Warthin tumor and what are its histological features?
A
Warthin tumor (papillary cystadenoma lymphomatosum) is a benign cystic tumor with germinal centers, strongly associated with smoking.
25
What is the preferred treatment for salivary gland malignancies?
Superficial or deep parotidectomy depending on the extent of the tumor, with radiation therapy in high-grade malignancies.
26
What condition causes an infection in the floor of the mouth that causes the tongue to be pushed up and back, eventually obstructing the patient’s airway?
Ludwig’s angina
Clinical findings include fever, dysphagia, odynophagia, and drooling.
The most common cause of this abscess is infection in the teeth. This is a rapidly progressive cellulitis of the bilateral submandibular and sublingual spaces, most often arising from an infected mandibular molar.
27
What is the treatment for cellulitis of the sublingual and submandibular space ... ?
The treatment for Ludwig’s angina requires incision and drainage of the abscess along with Abx.
28
Ludwig’s angina requires use of what type of Abx?
Antibiotic coverage should include oral cavity anaerobes.
Commonly used Abx are Amp-Sulbactam or Clindamycin and Vancomycin if MRSA is suspected or know to be present.
29
What if the principle cause for a patient's Ludwig's angina is from infected 2nd or 3rd molars?
Since the mylohyoid line on the inner aspect of the body of the mandible descends on a slant, and the tips of the roots of the second and third molars are behind and below this line, if these teeth are abscessed, the pus will go into the submandibular space and may spread to the parapharyngeal space. Usually, the infected tooth is not painful.
Patients with these infections present with unilateral neck swelling, redness, pain, and fever.
Treatment is incision and drainage over the submandibular swelling.
30
What if the principle cause for Ludwig's angina is from infected 1st molar or forward?
Tooth roots that are above the mylohyoid line, as they are from the first molar forward, the infection will enter the sublingual space, above and in front of the mylohyoid. The infection will cause the tongue to be pushed up and back and these patients usually will require an awake-tracheotomy, as the infection can progress quite rapidly and produce airway obstruction. The firm tongue swelling prevents standard laryngeal exposure with a laryngoscope blade, so intubation should not be attempted. Even if there is no airway obstruction on presentation, it may develop after you operate and drain the pus. This results from post- operative swelling, which can be worse than the swelling on initial presentation.
31
How is acute angioneurotic edema managed?
Acute angioneurotic edema is dramatic swelling of the tongue, pharyngeal tissues, and the supraglottic airway and urgently requires a surgical airway.
Angioneurotic edema, can either familial or due to a functional or quantitative deficiency of C1-esterase inhibitor, can also result in swelling can progress rapidly, and oral intubation may quickly become impossible, which is why this condition urgently requires a surgical airway.
Common medical treatments are IV steroids, and H1 and H2 histamine blockers.
32
A fungal infection of the sinonasal cavity that occurs in immunocompromised hosts is called ... ?
Mucormycosis
Typically it appears in patients receiving bone marrow transplantation or chemotherapy. It is a devastating disease, with a significant associated mortality. Mucor is a ubiquitous fungus that can become invasive in susceptible patients, classically those with diabetes with poor glucose regulation who became acidotic. If there is any other system failure (e.g., renal failure), mortality goes up significantly. The fungus grows in the blood vessels, causing thrombosis and distal ischemia and, ultimately, tissue necrosis. This also leads to an acidic environment in which the fungus thrives.
The primary symptom is facial pain, and physical exam will show black turbinates due to necrosis of the mucosa. Diagnosis is made by biopsy. Acutely branching nonseptate hyphae are seen microscopically. Usually the infection starts in the sinuses, but rapidly spreads to the nose, eye, and palate, and up the optic nerve to the brain. Treatment is immediate correction of the acidosis and metabolic stabilization, to the point where general anesthesia will be safely tolerated (usually for patients in diabetic ketoacidosis who need several hours for rehydration, etc.). Then, wide debridement is necessary, usually consisting of a medial maxillectomy but often extending to a radical maxillectomy and orbital exenteration (removal of the eye and part of the hard palate) or even beyond. Amphotericin B is the drug of choice. Many patients with mucormycosis also have renal failure, which precludes adequate dosing. Newer lysosomal forms of amphotericin B have been shown to salvage these patients by permitting higher doses of drugs. If the underlying immunologic problem cannot be arrested, survival is unlikely. In patients who are neutropenic, unless the white blood cell count improves, there is no chance for survival.
33
What condition is marked by fullness of the anterior tonsillar pillar, uvular deviation towards one side, a “hot potato” voice, and, in some patients, trismus (difficulty opening the jaws)?
This is most likely a peritonsillar abscess, which is caused by purulence in the space between the tonsil and the pharyngeal constrictor. Patients can also have unilateral lymphadenopathy. This typically occurs when the patient has a history of untreated sore throat (tonsillitis or pharyngitis) for several days, which has now gotten worse on one side. The diagnosis is usually clinical. Treatment includes drainage or aspiration, adequate pain control, and antibiotics. Tonsillectomy may be indicated, depending on the patient’s history. The choice antibiotics are ampicillin-sulbactam or clindamycin.
34
What is a retropharyngeal abscess?
A deep neck space infection in the retropharynx with high risk of spreading to the mediastinum via the danger space.
35
What are common causes of retropharyngeal abscess?
Trauma to the retropharynx (e.g., fishbone injury, penetrating trauma), spread from local pharyngitis, dental infections.
36
Which age group is most commonly affected by retropharyngeal abscess?
Children under 5 years old (children aged 6 months to 4 years). Upper respiratory infections, pharyngitis, and direct trauma (e.g., instrumentation, foreign body ingestion) can lead to abscess formation in this age group.
37
What are the most common bacterial causes of retropharyngeal abscess?
Streptococcus pyogenes, Staphylococcus aureus (including MRSA), and anaerobes like Fusobacterium.
38
What are the key clinical symptoms of a retropharyngeal abscess?
Neck pain, fever, odynophagia, drooling, muffled voice, and limited neck movement.
39
What is the significance of the danger space in retropharyngeal abscess?
It allows spread of infection from the retropharynx to the mediastinum, causing life-threatening complications.
40
What are the key airway symptoms that necessitate urgent intervention?
Drooling, stridor, hypoxia, respiratory distress, and use of accessory breathing muscles.
41
Which imaging study is preferred for diagnosis of a retropharyngeal abscess?
CT with contrast is the preferred imaging modality.
42
What is the classic finding on a lateral neck X-ray in a retropharyngeal abscess?
Widening of the prevertebral space.
43
What is the treatment for a small, non-fluctuant retropharyngeal abscess?
IV antibiotics such as ampicillin-sulbactam or clindamycin.
44
When is surgical drainage required for a retropharyngeal abscess?
If the abscess is >2.5 cm, causing airway compromise, or not responding to antibiotics.
45
What are the complications of a retropharyngeal abscess if untreated?
Mediastinitis, sepsis, airway obstruction, jugular vein thrombosis, Lemierre's syndrome. Lemierre’s syndrome is a rare but life-threatening septic thrombophlebitis of the internal jugular vein, most commonly caused by Fusobacterium necrophorum, an anaerobic, gram-negative bacillus. It typically follows an oropharyngeal infection (e.g., pharyngitis, tonsillitis, dental infections) that spreads into the parapharyngeal space and then to the internal jugular vein, leading to bacteremia and septic emboli.
46
Which differential diagnoses should be considered with a retropharyngeal abscess?
Epiglottitis, peritonsillar abscess, Ludwig’s angina, bacterial tracheitis, deep neck space infections.
47
What vitamin deficiencies are associated with glossitis (glossy tongue)?
Vitamin B2 (riboflavin), B3 (niacin), B6 (pyridoxine), B12 (cobalamin), iron deficiency.
48
What are the key characteristics of oral candidiasis?
Scrapable white plaques on the tongue and oral mucosa, commonly seen in immunocompromised patients and those using inhaled corticosteroids. Treated with oral nystatin or fluconazole.
49
What are the risk factors for oral candidiasis?
Immunosuppression (HIV, diabetes, chemotherapy), inhaled corticosteroid use, antibiotic use, denture wearing.
50
How do you manage oral candidiasis in HIV patients?
First-line treatment is fluconazole; HIV screen or consider ART optimization.
51
How does leukoplakia differ from oral hairy leukoplakia?
Leukoplakia: Premalignant hyperplasia of squamous epithelium, strongly associated with smoking and alcohol; white patches that cannot be scraped off. Oral hairy leukoplakia: Caused by EBV, occurs in immunocompromised patients (especially HIV), found on the lateral tongue, not easily scraped off.
52
What is the most common risk factor for leukoplakia?
Smoking and alcohol use.
53
What is the treatment for leukoplakia?
Tobacco and alcohol cessation; biopsy if suspicious for malignancy.
54
What is the treatment for oral hairy leukoplakia?
Typically self-limited; consider antiretroviral therapy in HIV patients.
55
What is aphthous stomatitis (canker sores)?
Painful, shallow, round ulcers with a gray base; typically self-limited, treated with symptomatic control such as topical corticosteroids or analgesic gels.
56
How does Behçet’s disease differ from aphthous stomatitis?
Behçet’s disease is a systemic vasculitis characterized by recurrent oral and genital ulcers, uveitis, and skin lesions, often seen in Middle Eastern and Mediterranean populations.
57
What are the distinguishing features between pemphigus vulgaris and bullous pemphigoid?
Pemphigus vulgaris: Intraepithelial blistering due to desmosome autoantibodies, positive Nikolsky sign, oral mucosal involvement. Bullous pemphigoid: Subepidermal blistering due to hemidesmosome autoantibodies, tense blisters, negative Nikolsky sign, no oral involvement.
58
What autoimmune condition is associated with desmoglein autoantibodies?
Pemphigus vulgaris.
59
What is the treatment for pemphigus vulgaris?
Systemic corticosteroids and immunosuppressants like rituximab or azathioprine.
60
What is amyloidosis of the tongue?
A rare condition in which amyloid protein deposits lead to macroglossia (enlarged tongue), associated with systemic amyloidosis.
61
What systemic disease can cause macroglossia?
Amyloidosis, hypothyroidism, acromegaly, Down syndrome.
62
Often the only sign of early nasopharyngeal carcinoma in adults is ... ?
Unilateral OME
Later in the disease process, the tumor metastasizes to the cervical lymph nodes and extends into the skull base, causing cranial neuropathies. In the past, nasopharyngeal examination was performed with mirrors, but most otolaryngologists now routinely use rigid or flexible endoscopic instrumentation.
63
What are the primary types of head and neck cancers?
Squamous cell carcinomas (SCCs) originating from the mucosal linings of the oral cavity, pharynx, and larynx.
64
What are the major risk factors for head and neck cancer?
Tobacco use, alcohol consumption, HPV infection (especially HPV-16 for oropharyngeal cancer), EBV infection (nasopharyngeal carcinoma), and geographical factors (higher incidence in Southeast Asia for nasopharyngeal carcinoma).
65
What are the common clinical presentations of head and neck cancer?
Persistent sore throat, dysphagia, odynophagia, hoarseness, unexplained weight loss, non-healing ulcers in the oral cavity, referred otalgia, and cervical lymphadenopathy.
66
What is referred otalgia and why is it significant in head and neck cancer?
Ear pain without primary ear pathology due to shared neural pathways, often an early sign of malignancy.
67
What imaging modality is preferred for head and neck cancer diagnosis?
Contrast-enhanced CT or MRI of the head and neck to assess tumor extent and regional spread.
68
How is definitive diagnosis of head and neck cancer made?
Biopsy of the primary lesion.
69
What is the diagnostic approach for cervical lymphadenopathy with an unknown primary?
Panendoscopy (esophagoscopy, bronchoscopy, and laryngoscopy) to locate the primary tumor.
70
What is the management for early-stage head and neck cancer (Stages I and II)?
Single-modality therapy with surgery or radiation.
71
What is the management for advanced-stage head and neck cancer (Stages III and IV)?
Combination of surgery, radiation, and chemotherapy.
72
Why do HPV-positive oropharyngeal cancers have a better prognosis?
They respond better to treatment and have lower recurrence rates compared to HPV-negative cases.
73
What are the key clinical features of nasopharyngeal carcinoma (NPC)?
Nasal obstruction, epistaxis, serous otitis media due to Eustachian tube obstruction, cranial nerve palsies, and cervical lymphadenopathy.
74
Which virus is strongly associated with nasopharyngeal carcinoma?
Epstein-Barr virus (EBV).
75
What is the primary treatment for nasopharyngeal carcinoma?
Radiation therapy, often combined with chemotherapy in advanced cases.
76
What is the most common site of anterior epistaxis?
The Kiesselbach plexus.
77
What is the most common site of posterior epistaxis?
The sphenopalatine artery, a branch of the maxillary artery.
78
What are the risk factors for epistaxis?
Trauma, coagulopathy, platelet disorders, vascular lesions, tumors, dry air, and nasal irritants like cocaine.
79
What is the first-line treatment for epistaxis?
Tamponade and topical alpha-1 adrenergic agonists like oxymetazoline.
80
What is the next step if anterior epistaxis is refractory to initial measures?
Cautery with silver nitrate or nasal packing.
81
What is the risk of posterior epistaxis?
Can be severe and may require posterior nasal packing or embolization.
82
What are the common causes of nasal septal perforation?
Trauma, cocaine use, post-rhinoplasty, and autoimmune diseases like granulomatosis with polyangiitis (Wegener's).
83
What is the presentation of nasal septal perforation?
Whistling noise during breathing, nasal congestion, epistaxis, and crusting.
84
How do you treat nasal septal perforation?
Humidification, nasal emollients, and septal button placement; surgical repair if severe.
85
What is the etiology of nasal septal deviation?
Congenital or acquired (trauma).
86
What are the clinical features of nasal septal deviation?
Nasal obstruction, congestion, snoring, and recurrent sinus infections.
87
When must this condition be corrected?
When the obstruction involves the nasal pyramid, it, too, must be corrected by rhinoplasty.
Rhinoplasty involves controlled chisel cuts of the bones (osteotomies) on either side of the nose and placement of the bones into the correct position. A splint is used to hold this position for a week after surgery. Rhinoplasty can be combined with trimming of the nasal cartilage to subtly change the contour of the tip of the nose. When the obstruction involves the softer, cartilaginous middle third of the nose and/or the nostril openings, then nasal valve repair may be indicated. This surgery may entail placing cartilage grafts to widen or strengthen the lateral wall of the nasal cavity to relieve the nasal obstruction. This surgery can be performed concomitantly with a septoplasty or rhinoplasty.
88
What is the treatment for nasal septal deviation?
Septoplasty if symptomatic.
89
What is the acute management of a nasal fracture?
Apply ice, elevate the head, and reduce the fracture if displaced.
90
What is a septal hematoma, and why is it a concern?
A traumatic complication that can lead to necrosis of the septum and septal perforation if untreated.
91
What is the treatment for septal hematoma?
Urgent drainage to prevent necrosis, followed by nasal packing and antibiotics to prevent infection.
92
Which autoimmune disease can cause nasal septal perforation?
Granulomatosis with polyangiitis (Wegener's granulomatosis).
93
How does granulomatosis with polyangiitis (Wegener's) affect the nose?
It can cause chronic sinusitis, nasal septal perforation, and saddle-nose deformity.
94
What is the initial diagnostic approach for recurrent epistaxis?
Check for underlying coagulopathy, platelet dysfunction, or vascular abnormalities.
95
What are the signs of a posterior nasal bleed?
Profuse bleeding, difficulty stopping with anterior measures, and potential need for posterior nasal packing or embolization.
96
When a patient has nasal polyps, they should also be evaluated for ... ?
Allergies
Polyps that are associated with chronic, grape-like swellings that protrude into the lumen, obstruct and cause anosmia are often associated with asthma.
97
What is the condition when a patient presents with extremely edematous nasal or sinus mucosa?
Nasal polyps
These growths are localized, extremely edematous nasal or sinus mucosa, and are a frequent cause of nasal blockage. Microscopically, they are essentially full of water. They can enlarge while in the nose, and obstruct either the nose or the ostia through which the sinuses drain.
98
How are nasal polyps normally treated?
Polyps usually respond very well to a course of systemic steroids followed by continuous intranasal steroid sprays. Surgery may be indicated if the polyps recur frequently or do not respond to treatment.
99
How are nasal polyps that are also associated with asthma treated?
Inhaled nasal steroids as well as short bursts of systemic steroids often produces good long-term control of the disease. Surgical removal provides relief, but unfortunately, recurrence is common.
100
Unilateral nasal polyps may be a manifestation of ... ?
Neoplasms.
Unilateral nasal polyposis associated with unilateral sinusitis suggests tumor (most commonly inverted papilloma, a benign growth caused by human papilloma virus).
101
Nasal polyps in children ought to warrant a workup for ... ?
CF (they are usually uncommon in children)
102
What is the most common nasal mass?
By far the most common nasal masses encountered by physicians are nasal polyps.
Other types of intranasal masses include inflammatory etiologies, such as pyogenic granuloma, Wegener’s granulomatosis, and sarcoidosis. Neoplasms, including inverting papilloma, juvenile nasopharyngeal angiofibroma, esthesioneuroblastoma, sinonasal undifferentiated carcinoma, adenocarcinoma, and other malignancies, are fortunately not as common.
103
Samter’s triad consists of (3):
asthma, an allergy to aspirin, and nasal polyposis
104
What is the most common cause of acute laryngitis?
Viral upper respiratory infection; lasts <3 weeks and is self-limited.
105
What is the next step in evaluation for hoarseness lasting more than 3 weeks?
Laryngoscopy to evaluate for malignancy or other structural causes.
106
Hoarseness and chest tightness in a patient with a history of smoking is likely ... ?
vocal cord polyps.
107
What are the most common benign causes of hoarseness?
Vocal cord polyps, nodules, and papillomas.
108
What are the risk factors for vocal cord nodules?
- Smoking
- GERD
- vocal overuse (singers, teachers)
- chronic irritation
109
What is the most common benign lesion of the vocal cords?
**Polyps**, which are benign lesions that develop in response to vocal fold irritation in the anterior one-third of the vocal fold. They tend to arise in younger adults between 30 and 50 years and more commonly affect females. The known etiologies are from voice overuse (e.g., teachers, professional singers), smoking, GERD, and anticoagulant use. Patients clinically present with low-pitched, whispery voice and hoarseness. Diagnosis requires a laryngoscopy revealing a unilateral fluid filled spherical lesion in the superficial lamina propria of the vocal fold. Histologically, polyps tend to also contain fibrin. Treatment is with surgical removal.
110
Where do **vocal cord nodules** most commonly occur?
Vocal cord nodules most commonly occur at the junction of the anterior and middle thirds of the true vocal cords.
111
What is the histological characteristic of vocal cord nodules?
Vocal cord nodules are benign lesions that are caused by frequent microtrauma (e.g., voice overuse) to the vocal cords, which leads to edematous swelling and development of fibrotic scars caused by a fibrotic scar (vocal fold nodule) of the superficial lamina propria. Histologically they appear as myxoid degeneration and squamous hyperplasia.
112
What is the most common cause of persistent hoarseness in school-aged children?
**Vocal cord nodules**. The differential diagnosis for pediatric hoarseness can be broad. Diagnoses to consider include vocal cord pathology (e.g., vocal cord paralysis), vocal cord lesions (e.g., nodules, cysts, polyps), benign tumors (e.g., laryngeal papillomatosis), congenital lesions (e.g., laryngeal webs), laryngopharyngeal reflux, and functional (nonanatomic) disorders. Most cases of pediatric hoarseness are related to benign lesions or functional disorders. A thorough history that elicits chronicity, impact, and any associated airway symptoms, dysphagia, or reflux symptoms is critical for narrowing the diagnosis and assessing the timing of laryngoscopy. Laryngoscopy enables visualization of the larynx and is imperative to rule out more sinister causes of hoarseness (e.g., laryngeal papillomatosis), allowing for initiation of appropriate treatment. Chronic misuse or overuse of the voice with symptoms of worsening hoarseness throughout the day and voice loss - is classic for vocal cord nodules. These lesions are the most common cause of pediatric voice disorders associated with voice overuse or misuse, particularly in the preschool age group. The nodules result from mechanical trauma that incites inflammation, edema, and eventually fibrosis at the free edge of the vocal cord, ultimately hampering voice production. Vocal cord nodules can be diagnosed via laryngoscopy. Prolonged hoarseness in a preschool-age child with voice overuse and no airway symptoms, dysphagia, or reflux symptoms is likely due to vocal cord nodules that can be diagnosed with laryngoscopy.
113
Obstruction of laryngeal mucus-secreting glands in the larynx leads to ... ?
Vocal fold cysts. Blockage of the mucus glands leads to swellings within the lamina propria. Intracordal cysts lead to hoarseness and saccular cysts can cause airway obstruction and voice changes as they tend to occur in the supraglottic region. Intracordal cysts tend to occur in the middle third of the vocal cord with an area of hyperkeratosis on the opposite cord (likely due to repeated abrasions). Diagnosis is with a laryngoscope. Macroscopically, the lesions are yellow-white lesion with distinct border. Treatment is with surgical removal.
114
What is the most likely cause for this condition?
Reinke edema is most commonly due to smoking (to a lesser degree voice overuse, allergy, chronic URI and GERD). Patients present with hoarseness, a low-pitched, rough voice, and vocal fatigue. Diagnosis is with a laryngoscopy showing bilateral swelling of the true vocal cords secondary to edema within the superficial lamina propria between the epithelium and vocal ligament (Reinke's space). Reinke edema can be managed conservatively with elimination or minimizing the risk factors causing the swelling.
115
Bilateral lesions on the vocal cords (commonly occurring after intubation) most likely is due to ... ?
Vocal cord granulomas. These occur secondary to trauma of the vocal cords. Endotracheal intubation, especially if prolonged, can damage the vocal folds through pressure or friction, which may result in the formation of granulation tissue and subsequently granuloma. This is not to say that the same etiologies are not equally possible (signing, GERD, smoking, etc). Treatment is with surgical removal.
116
Chronic worsening hoarseness leading to acute stridor in a child is most consistent with ... ?
**Respiratory papillomatosis**. Respiratory papillomatosis is the most likely cause of patients chronic hoarseness and acute stridor. Recurrent respiratory papillomatosis (RRP) is caused by infection with human papillomavirus, thought to be acquired in utero, and classically manifests with long-standing hoarseness secondary to the location of the disease on the vocal cords. Unrecognized growth of the papillomas can lead to an obstructive phenomenon and to biphasic stridor and respiratory distress. Definitive diagnosis of RRP can be made with flexible laryngoscopy. Treatment typically consists of surgical debulking and adjuvant therapy, for which there are many options. Patients often need multiple procedures at intervals determined by their symptoms.
117
What is the etiology of vocal cord papillomas?
HPV 6 and 11 infection most commonly, followed by HPV subtypes 16, 18, 31, and 33. HPV 6 and 11 cause benign papillary tumors on the vocal cords, however HPV 16, 18, 31, and 33 cause can premalignant lesions. These lesions cause hoarseness, dysphonia/aphonia, stridor, chronic cough, dyspnea due to airway obstruction and dysphagia (in advanced disease) are all possible symptoms. Diagnosis is with laryngoscopy showing multiple raspberry-like swellings on the vocal cords. These can be either unilateral or bilateral. There is no definitive cure, so the goal of care is to limit disease spread. Surgical removal (e.g., microdebridement, carbon dioxide lasers) of symptomatic lesions is usually the first treatment approach followed by adjuvant treatment with antivirals (e.g., acyclovir, ribavirin, cidofovir). Papillomas that remain till adulthood are potential precancerous lesions. Although it rarely occurs, papillomas can undergo malignant transformation and become squamous cell carcinoma.
Laryngeal papillomatosis is the most common form of recurrent respiratory papillomatosis (RRP), which develops as a result of human papillomavirus virus (HPV) infection (most commonly HPV 6 and HPV 11). Juvenile-onset RRP usually develops before the age of 5 years and is due to vertical transmission of HPV from the mother during vaginal delivery. Patient's delivered by a mother with a history of a sexually transmitted infection, who did not receive prenatal care, and had a vaginal birth, increase the risk of vertical HPV transmission. The diagnosis is typically established using laryngoscopy, which shows raspberry-like growths located on the vocal cords. There is no definitive treatment for RRP.
Management aims to limit the spread of disease via surgical excision of symptomatic lesions and potentially antiviral adjuvant therapy (e.g., cidofovir, interferon). Complications include malignant transformation into squamous cell carcinoma, airway obstruction, and life-threatening respiratory distress.
118
Children who have progressive hoarseness with recurrence of respiratory symptoms, cough, and dyspnea, should be evaluated using a ...
Laryngoscope. The most severe condition being laryngeal papillomas. Additional symptoms include cough, dysphonia or aphonia, stridor, and dysphagia.
119
What are the clinical features of
Hoarseness, upper airway obstruction, and multiple papillomas in children (juvenile form).
120
What is the treatment for laryngeal papillomas?
Microsurgical excision and possible adjuvant therapy with interferon or cidofovir.
121
What is the most common malignant laryngeal tumor?
Squamous cell carcinoma of the larynx.
122
What are the major risk factors for laryngeal squamous cell carcinoma?
Tobacco, alcohol, HPV infection (especially HPV-16).
123
How does laryngeal squamous cell carcinoma typically present?
Persistent hoarseness, dysphagia, stridor, and possibly weight loss.
124
What is the workup for suspected laryngeal cancer?
Laryngoscopy with biopsy, CT or MRI for staging.
125
What are the treatment options for laryngeal squamous cell carcinoma?
Surgical resection, radiation, and chemotherapy for advanced cases.
126
What neurological conditions can cause hoarseness?
Vocal cord paralysis (recurrent laryngeal nerve injury), Parkinson's disease, myasthenia gravis.
127
What are the causes of recurrent laryngeal nerve injury?
Thyroidectomy, mediastinal masses, aortic aneurysm, or lung cancer invasion.
128
What is the difference between breathy voice, aphonia, and strained voice in hoarseness?
Breathy voice = incomplete vocal cord closure; Aphonia = completely abducted cords; Strained voice = large mass on the cords.
129
What is the management for hoarseness due to GERD?
Lifestyle modifications (weight loss, avoiding acidic foods), proton pump inhibitors (PPIs).
130
How is functional dysphonia treated?
Speech therapy and vocal rehabilitation.
131
What is the first-line treatment for vocal cord nodules?
Voice rest, speech therapy, and vocal hygiene.
132
What conditions can cause vocal cord granulomas?
Intubation trauma, GERD, chronic cough, excessive throat clearing.
133
What is the common presentation of unilateral vocal cord paralysis?
Breathy, weak voice with ineffective cough; may result from recurrent laryngeal nerve injury.
134
What are common causes of bilateral vocal cord paralysis?
Brainstem stroke, surgical trauma, neurological diseases like ALS.
135
What is the most common treatment for vocal cord polyps?
Microsurgical removal, voice therapy.
