Benign Head and Neck Neoplasms
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1 Benign Tumors of Head and Neck Dr. Billones
Erik 14
References: Source: Cor Christi batch 2009 and 2011, past powerpoint, recording, past-e Guys, this is based on batch 2012 ppt. Ayaw kasi bigay ni doc ung new ppt nya. Items that came out in the past-e‟s are Emphasized. I encourage everyone to read other references na rin, remember mahirap maging pula ulit ung Evals results nating lahat. That‟s all I ask of you. God bless! BENIGN TUMORS OF HEAD AND NECK I. SURGICAL ANATOMY OF THE NECK Anterior Submandibular Carotid Muscular Submental Lateral Occipital Supraclavicular The neck is divided into specific triangles: anterior triangle and postero-lateral triangles. The sternocleidomastoid will divide . the neck into anterior and posterior triangle.
A. TRIANGLES OF THE NECK Knowing the anatomy is important so that you will know what structures to look for when presented with masses in these particular areas. And based on what is under those triangles, more or less it will give us an idea of what structures are involved: Location Anterior
Posterolateral
Triangle
Boundaries
Components
submandibular triangle
digastric muscles
floor of the mouth, submandibular gland and LN, facial vessels, carotids, IJV, vagus nerve
carotid
digastric and omohyoid
carotid artery, IJV, hypoglossal and laryngeal nerve
muscular
omohyoid and hyoid
midline structures; thyroid, strap muscles, larynx, traches, esophagus
submental
digastric and hyoid
submental nodes
Occipital
SCM, traps, inferior belly of omohyoid
nerves spinal nerve
Supraclavicular
SCM, inferior belly of omohyoid, clavicle
low and middle trunk of brachial plexus,EJV, subclavian artery, nerve to subclavius
lymph
such as accessory
contains the cervical parts of the aerodigestive tract: larynx and trachea, hypopharynx and esophagus, thyroid and parathyroid glands, carotid sheath and the large neurovascular structures contained therein, and suprahyoid and infrahyoid strap muscles, and associated neurovascular and lymphatic structures. bounded by the borders of the sternocleidomastoid and trapezius and the middle third of the clavicle. Contains fibrofatty lymphatics,, CN XI, cervical nerve plexus, and small vascular bundles, hence known as “bloody gulch”
B. CERVICAL LYMPHATICS Cervical lymphatics are important in localization of the sites because this will give an idea on what primary sites to look for. Superficial lie near the surface of the neck along the external jugular vein Superficial anterior and Superficial lateral perforate the first layer of cervical fascia to empty into the deep cervical lymphatic chain Although frequently involved by metastasis, especially during the late stages, the superficial lymph nodes are nevertheless of little significance from a practical standpoint of surgical treatment. The reason is that if superficial lymphatics are involved with cancer they cannot be removed without resection of large areas of skin. Deep –more important since they receive lymph from the mucous membranes lining the mouth, pharynx larynx, and major salivary and thyroid glands, as well as the skin of the head and neck. Accompany the internal jugular vein and their branches or lie within the major salivary glands Anterior Submandibular (I) preglandular interglandular prevascular and retrovascular submental (IB) Anterior Compartment Group (VI) Pre-tracheal Para-tracheal Pre-laryngeal Jugular chain (II, III, IV) -> related to IJV superior jugular (Subdigastric) (II) o junctional nodes of Finch middle (III) inferior (IV) o prescalene nodal masses Lateral (Spinal accessory group) (V) Upper Middle Inferior o supraclavicular group Left Thoracic duct climbs upward and left lateral arch behind the carotid sheath, receives tributaries from the neck, enters the venous junction between the internal jugular and subclavian veins Virchow’s nodes-enlarged, hard, left supraclavicular nodes that may indicate abdominal malignancy Multiple lymphatic ducts drain the right side which also drains to the venous system in the right. Right Multiple lymph vessels (right lymphatic duct)
II. BENIGN TUMORS OF HEAD AND NECK
0-15
Frequency distribution by age, causative group and location 16-40 >40
CONGENITAL Vascular lesions (AT) Branchial cyst (AT) Thyroglossal cyst (M) Dermoid (M)
CONGENITAL Branchial cyst (AT) Thyroglossal cyst (M) Dermoid (M)
NEOPLASTIC Metastatic Carcinoma Thyroid
INFLAMMATORY ADENITIS Bacterial (AT/PT) Viral (AT/PT) Granulomatous (PT/AT)
INFLAMMATORY ADENITIS Viral (AT/PT) Bacterial (AT/PT) Granulomatous (PT/AT)
INFLAMMATORY ADENITIS Viral (AT/PT) Bacterial (AT/PT) Granulomatous (PT/AT)
NEOPLASTIC Lymphoma (AT/PT) Thyroid Ca (M) Sarcoma (AT/PT)
NEOPLASTIC Lymphoma (AT/PT) Thyroid Ca (M) Salivary (AT) Metastatic (AT/PT) Vascular (AT/PT) Neurogenic (AT)
CONGENITAL Branchial cyst (AT) Thyroglossal cyst (M)
AT – anterior triangle PT – posterior triangle M – midline younger group (0-15) -> Congenital (more common in this group) > inflammatory adenitis > neoplastic(least to think of) ***middle age group (16-40) -> most present with congenital ***older age group (>40) -> (think of) neoplastic > inflammatory adenitis > congenital (least to think of) A. BENIGN VASCULAR LESIONS 1. HEMANGIOMAS a. Classification of Vascular Anomalies Tumors (proliferative)- grow by cellular or endothelial hyperplasia, regress or persists
Juvenile hemangioma Rapidly involuting congenital hemangioma Noninvoluting congenital hemangioma Kaposiform hemangioendothelioma Tufted angioma
Vascular malformations (structural anomalies)- quiescent morphogenesis, never regress High-flow o Arteriovenous malformation Low-flow Venous malformation o Lymphatic malformation o Lymphatic-venous malformation o Capillary (or venular) malformation
endothelium,
local
defects
b. Description overproliferation of vascular entities due to abnormal changes in angiogenesis characterized histologically by high endothelial cell turnover compared with vascular malformation which have normal endothelial cell turnover and abnormal gross vascular anatomy clinical "life cycle“ includes proliferative, plateau, and involution 30% are visible at birth, 70% become visible within one to four weeks after birth; majority are visible a month after birth
of
occur 5 times more often in females than in males, predominantly in Caucasians low birth weight infants (less than 2.2 pounds) have a 26% chance of developing a lesion usually involute in time (30% will resolve by 3 years of age, 50% by 5 years of age, and 80%-90% by 9 years of age) -> so do watchful waiting and manage conservatively composed of proliferating, plump endothelial cells with limited basement membranes which eventually form vascular spaces and channels tissue inhibitors of metalloproteinases(TIMPs), along with interferon and transforming growth factor produced by the mast cells, terminate the endothelial cell proliferation and passively induce involution by senescence of endothelial cells cause nor the cell of origin of infantile hemangiomas has not been definitively elucidated Theories on the cell of origin:
- placental tissue- cell markers (GLUT- 1, merosin, Lewis Y) - endothelial progenitor cells (EPCs) - mesenchymal stem cells
visible lesion on the face or neck may signify presence of another internal hemangioma or may be part of a syndromic complex o o o o o
PHACES Posterior fossa structural brain abnormalities Hemangioma Arterial Lesions Cardiac abnormalities/Coarcatation Eye abnormalities
over one-half of hemangiomas heal with an excellent cosmetic result without treatment hemangiomas are proliferative lesions as compared to arteriovenous malformations which are vessel malformations Superficial
flat lesions which appear reddish in color
deep beneath the skin and bluish in color
both deep and superficial
Deep Compound
c. Clinical Presentations:
Cavernous
compressible globular, bright red or deep purple involving deep structures
plaque-like lesions, slightly elevated, more superficial
flat, capillary type, mostly in dermis
Capillary Port-wine stain
Strawberry marks
capillary type with cavernous component
Spider telangiectasia Senile hemangiomas/ruby spots d. Indications for treatment: (PAST E) ***usually just do “watchful waiting” and inform the parents/px that it will involute in time because chances are, it will.
Involvement of a vital organ, like the eye or ear, or windpipe Bleeding (recurrent) Ulceration Crusting or infection Rapid growth and deformity (that will compromise function; e.g airway)of the surrounding tissues
e. Diagnosis and Treatment: CT scan, MRI for deep and large lesions Ultrasonography with color flow is cost effective but is operator dependent and does notaccurately depict the relation of the lesion to other anatomic structures for fairly small areas and not on the face, intralesional injection with steroids with or without liquid nitrogen cryosurgery Pulsed dye laser can be used to reduce the superficial component along with the steroid injection Larger hemangiomas require oral steroids usually given during the proliferative phase, inhibits vascular endothelial growth factor (VEGF) Alpha-interferon is recommended for lesions not responding to steroids and if the lesion is problematic or life threatening (Spastic dysplegia has been associated in 10-12% of the children taking this drug) Surgical excision -> could be very bloody (since it is a vascular lesion) so plan the surgery well to prevent blood loss Embolization 2. LYMPHANGIOMAS a. Description represents tumors, malformations or hamartomas of the lymphatic system collections of lymph vessels filled with serous fluid soft lesions with ill-defined borders 50% apparent at birth, 90% appear before age 2 years reflects a failure of lymph ducts to connect with the venous system during embryogenesis, abnormal sequestration of lymphatic structures, or both found in patients with syndromic conditions (Turner, Klinefelter and Noonan’s syndromes) b. Types
Lymphangioma circumscriptum confined to superficial skin, forming small, vesicle-like lesions Cavernous tongue, cheek, floor of mouth, lips, nose Cystic Hygroma most common in the neck (posterior triangle behind the SCM) but may extend to the head, face, axilla or mediastinum Multicystic tend to spread along vital structures and high incidence of recurrence
c. Diagnosis and Treatment CT Scan, MRI for large and deep lesions Wide surgical excision, staged excisions in localized disease, a conservative period of watchful waiting is appropriate if the lesion causes no immediate compromise to life functions fewer than 15% of lesions spontaneously regress some surgeons believe that if the lesion has not spontaneously regressed by age 5 years, surgical intervention is warranted excision should be performed sooner to avoid complications (e.g. infection) multistage operation for diffuse disease
B. BENIGN SALIVARY GLAND TUMORS most (70%) salivary gland tumors originate in the parotid gland (PAST E) remaining tumors arise in the submandibular gland (8%) and minor salivary glands (22%) 75% of parotid gland tumors are benign, slightly more than 50% of tumors of the submandibular gland and 60-80% of minor SGTs are found to be malignant classic presentation of a benign SGT is a painless, slow-growing mass on the face(parotid), angle of the jaw (parotid tail, submandibular), or neck (submandibular) or a swelling at the floor of the mouth (sublingual). freely mobile, no facial nerve involvement- PAST E sudden increase in size may be indicative of infection, cystic degeneration, hemorrhage inside the mass, or malignant degeneration 1. BENIGN EPITHELIAL TUMORS Pleomorphic Adenoma (Benign Mixed Tumor) most common tumor of the salivary gland originate from intercalated duct cells and myoepithelial cells most often located in the tail of the parotid gland when in the minor salivary glands, the hard palate is the site most frequently involved, followed by the upper lip contains epithelial and connective tissue components Case Example: A 45 yr old female, right pre-auricular mass, firm, well-circumscribed, movable, nontender w/ no facial nerve deficit. Warthin’s Tumor (Cystadenolymphoma) smooth, soft, parotid mass, well encapsulated and contains multiple cysts has a heavy lymphoid stroma tends to be bilateral (10% of cases) Intraductal papilloma small, tan, fairly smooth lesion, usually found in the submucosal layer rare Oxyphil adenoma (oncocytoma) manifest as small ( soft with straw-colored fluid upon aspiration surgical excision with preservation of the vital structures is the treatment of choice rarely cause symptoms of airway obstruction and excision is usually for cosmetic reasons
Lipoma relatively uncommon in a major salivary gland derived from fat cells appear grossly as smooth, well-demarcated, bright-yellow masses consists of mature adipose cells with uniform nuclei.
3. SALIVARY GLAND TUMORS DIAGNOSTIC PROCEDURES the utility of FNAB has been well established with a reported accuracy rates of 74-90% procedure is somewhat operator dependent it is generally regarded as safe, simple to perform, and relatively inexpensive and results in low morbidity controversy exists about whether FNAB is warranted for masses in the superficial lobe of the parotid gland, as it is not likely to change the management because you end up still removing the superficial lobe CT scan or MRI for deeper lesions Management of benign SGTs includes complete removal with an adequate margin of tissue To avoid recurrences Surgical Complications - recurrence from inadequate excision or innoculation bleeding seroma formation nerve injury (facial, lingual, hypoglossal nerves) salivary fistula Frey Syndrome – gustatory sweating caused by aberrant connection of parasympathetic fibers of the salivary gland to sweat glands of the skin. (PAST E) C. BENIGN ODONTOGENIC TUMORS ODONTOGENIC CYSTS AND TUMORS derived from tissues of developing teeth
1. ODONTOGENIC CYSTS (Inflammatory) Radicular Cyst
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most common odontogenic cyst (65%) thought to arise in response to inflammation originate in preexisting periapical granulomas painless when sterile but painful when infected xray shows pulpless, nonvital tooth with small well-defined periapical radiolucency at its apex
Tx: extraction of the affected tooth and its periapical soft tissue
Paradental Cyst Due to inflammation of the gingiva overlying a partly erupted third molar.
2. ODONTOGENIC CYSTS (Developmental) Dentigerous Cyst nd
developmental cyst, 2 most common (24%) originate via the accumulation of fluid between reduced enamel epithelium and a completed tooth crown usually found in the mandibular third molars, maxillary canines, maxillary third molars most are asymptomatic, but large lesions can cause displacement or resorption of adjacent teeth and pain xray shows a unilocular radiolucency with well defined sclerotic margins encircling the crown of an unerupted tooth -> may clinically present the same as a radicular cyst but is different radiographically (PAST-E) enucleation or decompression followed by enucleation if large.
Break Bati:
Odontogenic Keratocyst rd
-
3 most common “scalloping” on x-rays great mimic (e.g. ameloblastoma, dentigerous cyst) diagnosis is a histologic one aggressive and can be difficult to remove can grow quite rapidly, with frequent recurrences - 40% of OKCs appear in a dentigerous relationship, 9% of dentigerous cysts are OKCs when the histology is examined
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Lateral Periodontal cyst -
well-circumscribed unilocular radiolucency along the lateral periodontal are arises from cystic degeneration of clear cells of the dental lamina most frequent location is at the level of the mandibular premolars but it has been reported occurring in other areas clinically silent and is usually discovered during routine radiologic examination
Residual Cyst -
an odontogenic cyst that remains within the jaw after the removal of the tooth with which it was associated Gingival Cyst of the Newborn- Bohn's nodules
-
few or many, white to yellowish, round to oval, nodes in the maxillary and/or mandibular gingiva and alveolar ridge of newborns – (PAST-E) cystic degeneration of epithelial rests of the dental lamina (rests of Serres). majority of these cysts break by themselves, a few days after birth exuding the keratin. In some babies they may remain for a period of several months, in such cases surgical opening is indicated.
3. ODONTOGENIC TUMORS Ameloblastoma most common odontogenic tumor (PAST-E) benign but locally invasive neoplasm (acts like a malignant lesion) derived from odontogenic epithelium multicystic (86%), unicystic (13%) and peripheral (extraosseus –1%) may arise from the lining of a dentigerous cyst but more often arises independently of impacted teeth progressive growth rate and may reach enormous proportions symptoms may include a painless swelling, loose teeth, malocclusion, or nasal obstruction. maxillary tumors frequently perforate into the antrum and may grow freely, with extension into the nasal cavity, ethmoid sinuses, and skull base they can exhibit cytologic features of malignancy with squamous differentiation (< 1%) -> malignant degeneration unilocular – often confused with odontogenic cysts radiograph shows multilocular radiolucency with a predilection for the posterior mandible, wellcircumscribed, soap-bubble appearance –(PAST E) Dx: biopsy Tx: complete excision, including adequate zone of normal-appearing bone around the main tumor mass; mandibular reconstruction Calcifying Epithelial Odontogenic Tumor Adenomatoid Odontogenic Tumor Squamous Odontogenic Tumor Calcifying Odontogenic Cyst
4. RELATED JAW LESIONS FIBROOSSEUS LESIONS Fibrous dysplasia replacement of medullary bone with fibrous tissues, leading to expansion and weakness of the involved bone likely due to gene mutation found in the proximal femur, tibia, humerus, ribs, and craniofacial bones (aside from the head & neck) monostotic, polyostotic (different bone involvement), McCune-Albright syndrome (polyostotic fibrous dysplasia occurs with pigmented skin lesions or "cafe au lait" spots and hormonal abnormalities radiography shows a ground glass appearance- PAST E bone scan (particularly for polyostotic lesions) to evaluate entire skeleton CT scan conservative management, tend to mature -> when they mature, they harden contouring or resection with reconstruction -> for cosmetic purposes D. SOFT TISSUE TUMORS 1. FIBROMATOSES non metastasizing, locally invasive fibroblastic or myofibroblastic lesions Desmoid fibromatosis deep-seated, benign, slowly growing Greek word "desmos“ - band or tendon-like intraabdominal or extraabdominal usually at the supraclavicular fossa at head and neck may develop along surgical scars locally aggressive, but do metastasize tumor-related destruction of vital structures and/or organs can be fatal, particularly when they arise in patients with familial adenomatous polyposis (FAP, Gardner's syndrome) CT Scan, MRI, biopsy high rate of recurrence with surgery alone Systemic therapy include antiinflammatory agents, hormonal agents (eg, tamoxifen), and cytotoxic chemotherapy Radiotherapy Fibromatosis Colli (Sternocleidomastoid Tumor) produces torticollis (wry neck) usually develops several weeks after birth, slowly increase in size over 2-3 months, then regresses and disappears in 4-6 months olive-shaped or oval tumor mass in the lower third of the SCM high incidence of difficult labor and breech presentation CT Scan, MRI, biopsy conservative managament, stretching exercises surgery for progressive torticollis at an older age
2. NEUROGENIC TUMORS Neurilemoma (Schwannoma) encapsulated neoplasms from Schwann cells slow-growing tumor, present for several years pain and neurologic symptoms are uncommon unless the tumor is large or, by virtue of a deep-seated location, is impinging on neighboring structures.
waxing and waning of the tumor size may be noted due to fluctuations in the amount of cystic change and high vascularity common along lateral neck region exact nerve of origin may be impossible to determine CT Scan, MRI, biopsy Surgical excision
Neurofibroma affects all neural crest cells (schwann cells, melanocytes, endoneural fibroblasts genetically inherited, autosomal dominant usually arise from subcutaneous tissues(ill-defined and unencapsulated) but may also occur deeper in head areas (circumscribed and encapsulated)
tend to be multiple (associated with café-au-lait spots, von Recklinghausen’s disease)
significant risk of developing malignant neurogenic tumors if with multiple neurofibromatosis frequently found in the head rather than neck
CT Scan, MRI, biopsy Surgical excision
3. PARAGANGLIOMAS arise from the glomus cells (chemoreceptors located along blood vessels that have a role in regulating blood pressure and blood flow) found in the abdomen (85%), thorax (12%), and head and neck (3%) unlike paragangliomas of the abdomen, head andneck paragangliomas rarely secrete catecholamines most occur as single tumor when occuring at multiple sites they are usually found as a part of a heritable syndrome such as multiple endocrine neoplasia types II-A and II-B MEN Type IIA Medullary Ca Pheochromocytoma Parathyroid
MEN Type IIB Pheochromocytoma Medullary Ca Mucosal Neuromas Marfanoid habitus
Typical locations for paragangliomas of the head and neck 1) Carotid body tumor - from the carotid body, a baroreceptor and chemoreceptor, at the bifurcation of the common carotid,(PAST-E) may extend to the skull base, pharynx, or along cranial nerves 2) Glomus vagale - from the paraganglia of the vagus nerve, may compress the internal jugular, displace the carotid vessels anteromedially, or pushe the pharyngeal wall medially
3) Glomus tympanicum - from paraganglia along the tympanic branch of the glossopharyngeal nerve, also known as Jacobsen's nerve, or the auricular branch of the vagus nerve, also known as Arnold's nerve. It is often seen at the dome of the jugular bulb or submucosally at the cochlear promontory. By definition it remains confined to the middle ear and mastoid air cells.
4) Glomus jugulare - within the jugular foramen from the jugular bulb, Jacobsen's nerve, or Arnold's nerve. It may extend through bone into the mastoid air cells and middle ear with an aggressive pattern of bone destruction. Carotid Body Tumor/ Paraganglioma most common head and neck paraganglioma slow-growing, painless neck mass along the anterior edge of the SCM lateral to the tip of the hyoid bone may expand and cause bulging of the pharynx may compress adjacent nerves to cause hoarseness, dysphagia, cord paralysis – Angiography, CT Scan Surgical excision
4. LIPOMAS
most common soft tissue tumor composed of mature adipose cells tend to occur in obese patients or those with recent weight gain smooth, soft, encapsulated, freely movable masses that almost always arise in the subcutaneous tissue presence of capsule differentiates the tumor from simple aggregation of fat deeper lipomas may occur between muscle groups or within muscles that become obvious with muscular contraction Surgical excision with biopsy From the net: Benign Symmetric Lipomatosis or Madelung's Disease and Lanois-Bensaude Syndrome is a metabolic condition characterized by the growth of fatty masses around the face, back of the head, neck, upper arms, abdomen, back and upper leg in a very specific pattern or distribution. Unlike the usual lipoma, these benign, fatty masses are not enclosed within a membranous capsule with very distinct boundaries. (PAST-E)
5. RHABDOMYOMA rare, benign tumor of striated muscles important to differentiate from malignant rhabdomyosarcoma Adult Rhabdomyoma most common subtype, occuring at a mean age of approximately 50 years predilection for head and neck region (larynx, pharynx, and the floor of the mouth) circumscribed mass (usually less than 10 cm), coarse, with a brick-red colour may be multinodular Fetal Rhabdomyoma slow growing mass, usually less than 5cm in size. occurs primarily in the subcutaneous tissues of the head and neck region (common behind ear) usually among infants usually less than 3 years of age CT scan, MRI, section biopsy Surgical excision E. DEVELOPMENTAL NECK MASSES 1. DERMOID CYSTS (PAST E) solitary, or occasionally multiple, hamartomatous tumor containing structures derived from ectoderm covered by a thick dermis-like wall that contains multiple sebaceous glands and almost all skin adnexa may contain substances such as nails and dental, cartilagelike, and bonelike structures occur mostly on the face, neck, or scalp but can be intracranial, intraspinal, perispinal or within the ovary or omentum 2. CERVICAL TERATOMAS midline mass in an infant with airway obstruction Ex. A dyspneic newborn w/ large midline neck mass (PAST E) tumors containing tissue elements derived from all three germinal layers usually discovered at birth, rarely presents after age of 1 year encapsulated, partially cystic sometimes referred to as thyroid teratoma since it is in the midline symptoms develops over time due to progressive pressure, resulting in upper airway obstruction maternal hydramnios has been incriminated as a predisposing factor Ultrasonography, CT scan Surgical excision
3. BRANCHIAL CLEFT REMNANTS lateral cervical lesions arising from congenital developmental defects of the primitive branchial arches,clefts and pouches may take the form of cysts, fistulas, sinuses rarely diagnosed at birth, becomes apparent in childhood or adulthood may become infected, develop abscess, form draining sinuses fistulas and sinuses usually present as a small opening along anterior border of SCM orifice may discharge milky, serous, mucoid or purulent material
First Branchial Cleft Remnants
duplications of membranous EAC ending at a cul-de-sac extend near angle of mandible through parotid Type II substance to the vicinity of EAC Type I
Second Branchial Cleft Remnants most common (PAST E) external opening along anterior border of SCM at the junction of its middle and lower thirds tract follows the carotid sheath crossing over the hypoglossal nerve and coursing between the internal and external carotid arteries, ending at the tonsillar fossa (where it rarely opens into the posterior tonsillar pillar)
Third Branchial Cleft Anomalies rare opening may also be located in the same place as the second branchial cleft tract extend along the carotid sheath behind the internal carotid artery over the hypoglossal nerve and follows the superior laryngeal nerve internal opening would be at the region of the pyriform sinus
Fourth Branchial Cleft Anomalies
more of a theoretical possibility than reality opening would have to be along the anterior border of SCM in the lower third tract would extend along the carotid sheath into the chest, passing under either the arch of the aorta on the left or the subclavian on the right internal opening would be along the esophagus
Diagnostics: cystogram with contrast Treatment: management of infection with antibiotics and drainage; complete surgical excision
4. THYROGLOSSAL DUCT CYST results from the persistence of the thyroglossal tract midline- NALABAS LAGI SA PAST-E! or paramedian masses tract is intimately related to the hyoid bone and the mass is usually seen below the hyoid may retract on swallowing or tongue protrusion -> just like thyroid gland fistulas may occur spontaneously or secondary to trauma or infection
Diagnosis and Treatment: Ultrasonography Thyroid scintiscans Complete surgical excision with removal of the central portion of the hyoid (Sistrunk)
F. BENIGN SKIN TUMORS 1. EPIDERMAL TUMORS Seborrheic keratosis sharply demarcated, keratotic, usually pigmented lesions, elevated above the level of the adjacent epidermis may be confused with malignant melanoma
Keratoacanthoma develops over several months, assuming an elevated dome-shape configuration with a central keratin plug diagnosis is clinicopathologic
2. ADNEXAL TUMORS Hair Follicle Tumors -> excise and send for histopathology
Pilar Cyst (Trichilemmal Cyst)
Trichoepithelioma
Trichofolliculoma
Pilomatrixom
Sebaceous Gland Tumors
Senile Sebaceous Hyperplasia Apocrine Gland Tumors Eccrine Sweat Gland Tumors
Nevus Sebaceus
Sebaceous Adenoma
3. MELANOCYTIC TUMORS Ephelis – common freckle due to localized increase in melanin pigment Lentigo – nonspecific term for flat, macular hyperpigmented skin lesion, related to sun exposure Melanocytic Nevus – circumscribed new growth of skin of congenital origin junctional – at epidermal-dermal junction intradermal – confined at dermis compound – both junctional and intradermal are present Premalignant Melanocytic Lesions irregular Lentigo maligna – flat, slow-growing, pigmented lesion Atypical intraepidermal melanocytic proliferation – more rapid growth
4. SEBACEOUS CYST (EPIDERMAL CYST; KERATIN CYST; EPIDERMOID CYST)
closed sac found just under the skin, most often arising from swollen hair follicles contains cheesy-looking skin secretions. skin trauma can also induce a cyst to form a sac of cells is created into which a protein called keratin is secreted usually slow- growing, painless, freely movable lumps beneath the skin occur in almost any part of head and neck asymptomatic unless infected management of infection with local heat, antibiotics and drainage surgical excision with meticulous removal of all cyst remnants to prevent recurrence
III. THE SANDS OF TIME (PAST-E Which does not belong to the group? TIP: Marami pa yan. Most of the questions are based on under what heading they are. Some memorize! 1. muscular, carotid, occipital, submandibular, submental triangle 2. MRI, Plain X-ray, UTZ, CT, biopsy 3. digastric, lateral triangle, supraclavicular triangle, trapezius, omohyoid 4. carotid body tumor, glomus vagale, neurofibroma, glomus tympanicum, paraganglioma 5. E. Inclusion cyst, radicular cyst, dentigerous cyst, paradental, residual For the Past-e, Doc seems to „recycle” his questions. Different Questions but same points of emphasis. Know the must knows and ESPECIALLY the group of diseases they are under. ------------------------------------------END OF TRANSCRIPTION------------------------------------------------Hello Christine…
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