H&N: Cancer/Salivary Gland Disease/Endocrine Flashcards
In what compartment does the deep lobe of parotid sit?
prestyloid.
What two veins form the retromandibular vein?
internal maxillary vein and superficial temporal vein
Stenson’s duct: relationship to the masseter? where does it open into the oral cavity (by what tooth)?
lateral to the masseter; opens by the second molar
Nerve roots for the greater auricular nerve?
C2-C3
Parasympathetic innervation to the parotid gland?
V3 auriculotemporal by way of otic ganglion (inferior salivary nucleus -> IX ->lesser petrosal nerve -> otic ganglion -> V3
Prestyloid tumors vs poststyloid tumors?
Prestyloid tumors largely deep lobe of parotid. Poststyloid neurogenic or vascular.
Bilateral parotid cysts — suggests what diagnosis?
HIV
Parotid vs submandibular gland saliva: basal rate vs stimulated? proteinaceous/watery/serous vs high mucin?
Parotid: stimulated, proteinaceous/watery/serous. Submandibular: basal rate, high mucin
Name 3 etiologies of xerostomia. Name two classes of drugs a/w xerostomia.
drug induced, autoimmune, postradiation. Antihistamines, anticholinergics.
What is necrotizing sialometaplasia?
Lesion of the hard palate - benign but looks like cancer.
Name 3-5 potential causes of sialoadenitis.
infectious (bacterial, TB), autoimmune (Sjogrens or granulomatous), sialolithiasis, viral (mumps parotitis, HIV)
Sjogren’s patients are at increased risk of what type of cancer?
non-Hodgkin’s lymphoma/MALT lymphoma in the parotid gland
Size “cutoff” for sialolith removal via sialoendoscopy?
5mm cutoff.
How does lithotripsy work for sialoliths and what percentage will have alleviation of symptoms?
Lithotripsy uses sound waves to break up the stones; 75-90% will have alleviation of symptoms, 50% will have resolution of stones
Pediatric parotid disorders: a) What is recurrent parotitis of childhood? b) Work type I vs type II branchial cleft cysts?
a) young boy keeps having cyclical enlargement of the parotid but otherwise is fine. Treatment is antibiotics with coverage of Staph and dilation of stenson’s duct. b) type I involves EAC, type II does not.
Ranula: a) treatment? b) location of plunging ranula relative to mylohyoid?
ranula = mucocele associated with a sublingual gland. Resection of ranula and associated gland. b) plunging ranula is deep to mylohyoid
Hemangioma vs lymphangioma: a) time of presentation? b) time of involution? c) treatment? d) sclerosing agent for lymphangioma?
a) hemangioma at birth, lymphangioma 2-5mo. b) hemangioma involute by 1 year, lymphangioma does not involue. c) hemangioma usually propranolol; lymphangioma sclerosing agent, poss surgery d) OK-432
Rate of malignancy in solid parotid tumors for peds vs adult?
50% in kids, 20% in adults
“Pathology name” (non eponym) for wharthin’s tumor?
papillary cystadenoma lymphomatosum
Name 2-3 indications for level I-V neck dissection in parotid malignancy.
neck dissection: high grade mucoepi, salivary ductal carcinoma, facial nerve invasion, positive lymph node, extraglandular extension.
Name 2-3 indications for postop radiation in parotid malignancy.
postop radiation: adenoid cystic, residual tumor on facial nerve, positive margins, perineural invasion, positive nodes, high grade tumor, recurrent low grade tumor
Most common parotid malignancy in adults? In children?
Mucoep most common in adults and kids.
Most common malignant tumor for non-parotid salivary glands? What site is most common for that malignancy?
Most common non-parotid = adenoid cystic. Palate most common.
Name 2-3 risk factors for SCC metastasis to the parotid gland.
cutaneous SCC anterior to the imaginary coronal plane through the EAC; SCC or melanoma of the cheek, preauricular skin. depth >4mm, diameter > 2cm
Numbering scheme for teeth? (where is 1, where is 32)
teeth get numbered top right to top left, bottom left to bottom right. So #1 is your top right molar and #32 is your bottom right molar
4 intrinsic muscles of the tongue?
intrinsic muscles: superior and inferior longitudinal, transverse, vertical.
4 extrinsic muscles of the tongue?
Extrinsic muscles: genioglossus, hyoglossus, palatoglossus, styloglossus.
4 muscles of mastication?
Mastication: medial and lateral pterygoids, masseter, temporalis
Sensory innervation of the tongue?
V3 for sensation and VII for taste anteriorly. IX for sensation and taste posteriorly
Motor innervation of the soft palate?
V3 for tensor veli palatini; X for everything else (levator, palatoglossus, palatopharyngeus, musculus uvulae)
What muscle is deep to the palatine tonsils? (Eg what muscle are you separating your tonsillar capsule from)
superior constrictor
5 arteries supplying the tonsil?
ascending pharyngeal, tonsillar branch of facial, tonsillar branch of dorsal lingual, lesser palatine, tonsillar branch of ascending palatine
What is passavant’s ridge?
mucosal horizontal line that occurs during elevation of the soft palate – represents superior border of the superior constrictor
What do each of the constrictor muscles originate from?
superior constrictor: pterygoid plate, mandible, base of tongue; middle constrictor: hyoid/stylohyoid; inferior constrictor: thyroid cartilage.
Function of the medial and lateral pterygoid muscles?
Medial pterygoid elevates/deviation away from midline, lateral pterygoid depresses/deviation towards midline/protrusion
Location and significance of a Killian’s dehiscence with respect to cricopharyngeus? Location of a Killian-Jamieson dehiscence? What artery passes through this space? What nerve is at risk with a Killian-Jamieson diverticulum resection?
Killian’s is above cricopharyngeus, Killian-Jamieson is inferior to the cricopharyngeus and the inferior thyroid artery branches passes through that space. RLN is at risk during K-J resection.
Auerbach vs Meissner’s plexus?
Auerbach is implicated in achalasia; myenteric/between muscle + mucosa. Meissner’s is submucosal.
Descriptions, malignant potential, and treatment for: a) Lichen planus b) Leukoplakia c) erythroplakia
a) lichen planus = reticular/lacy. low malignant potential. topical steroids. b) leukoplakia = hyperkeratotic white lesion, ~10-15% malignant potential. c) erythroplakia 50% malignant potential
Most common head and neck site for Ewing’s sarcoma?
mandible
Origin of ameloblastoma?
enamel of tooth
Potential therapy for each of the following etiologies for dysphagia: a) tongue base weakness b) oral dysfunction c) pharyngeal sensory loss d) vocal cord paresis e) vocal cord paralysis f) failure of UES opening
a) pharyngeal/swallow exercises b) tongue exercises c) texture/thickness/consistency adjustments d) injection e) medialization f) cricopharyngeal myotomy
What is plummer vinson syndrome? What hypopharyngeal subsite cancer are they at increased risk for?
iron deficiency anemia, glossitis, esophageal webs. post cricoid space SCC
Most common type of TEF?
blind sac in the esophagus with distal fistulous connection to the trachea
Where does the subclavian arise from in dysphagia lusoria? Where should it arise from?
arises from descending aorta. Should arise from the innominate
Distance to stomach/LES from incisors? Distance to cricopharyngeus?
40cm; 16cm
When is the esophagus weakest following an esophageal burn?
4-7 days
When do fibroblasts arrive in a healing wound?
2-5 days
When does collagen appear in the wound bed of a healing wound?
8-12 days
Embryologic origin for parafollicular C cells? For thyroid lobes?
neural crest cells for C cells. ultimobranchial body for thyroid lobes.
SLN internal vs external branch functions and course?
internal SLN - sensation to pharynx/supraglottis. external branch - cricothyroid, inferior constrictor
RLN functions: motor, sensory, and parasympathetic?
RLN - motor all intrinsic muscles except cricothyroid, also inferior constrictor. Parasympathetic to upper esophagus. Sensory to TVF
T3 vs T4: a) which one is active form? b) where does conversion to active form occur? c) half life of each / timing of reassessment for levels after dose change in exogenous form? d) which one is produced in higher amounts by thyroid gland?
a) T3 is active. b) peripheral tissues. c) half-life of T3 is 1-2 days, needs 1-2 weeks to clear before checking levels. half-life of T4 is 5-6 days, needs 4-5 weeks to clear. d) T4 is produced in higher amounts
TFTs, pattern of TSH/T3/T4 for: a) subclinical hypothyroidism b) subclinical hyperthyroidism c) hyperthyroidism d) hypothyroidism e) states of high thyroglobulin (eg pregnancy)? f) states of low thyroglobulin (eg anabolic steroids, hypoproteinemia)
a) TSH high but T3/T4 normal. b) TSH low but T3/T4 normal. c) TSH low, T3/T4 high. d) TSH high, T3/T4 low. e) TSH normal, T4 high, T3 low. f) TSH normal, T4 low, T3 high.
MOA for PTU and methimazole?
PTU and methimazole decrease organification of iodine.
Black box warning for PTU for what devastating side effect? What notable toxicities are associated with methimazole?
PTU a/w liver failure, methimazole with birth defects and agranulocytosis.
How to manage PTU/methimazole administration in pregnancy?
Plan for PTU in first trimester, switch to methimazole after.
What is Lugol’s solution and why do people give it?
super saturated iodine, though to decrease vascularity of the thyroid prior to surgery for grave’s disease
Graves: pathophysiology and management?
anti-TPO/autoantibodies activating TSH receptors. antithyroid meds vs total thyroidectomy vs RAI.