Ch. 16 Flashcards

1
Q

if a pt presents w. targets/raised edematous papules distributed acrally w/ involvement of one or more mucus membrane.. what kind of reaction is this

A

=erythema multiforme = type IV hypersensitivity

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2
Q

what are aphthous ulcers associated with?

A

celiac dz

IBD

behcet dz

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3
Q

when does dental plaque biofilm form?

A

when microorganisms adhere to the surface of some object in a moist environment and begin to reproduce

-microorganisms form an attachment to surface of the object by secreting slimy, glue like substance

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4
Q

what do the oral lesions for melanotic pigmentation present

A

(see in addison dz)

hemochromatosis

fibrous dysplasia of bone (albirght syndrome)

& Peutz-jegher syndome (pic) - genetic disorder; develop polys & dark spots that appear on various parts of body - greater risk for CA

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5
Q

what is the most common fungal infxn of the oral cavity?

what influences the infxn?

A

Candidiasis. (also most most freq of human fungal infxns)

influenced by :

  • strain of C. albicans
  • compostition of normal flora
  • immune status of pt -
    • neutrophils, macrophages & Th17 = imp protection against Candida
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6
Q

what is gingivitis

what population is the most prevalent and severe

A

inflamof the oral mucosa surrounding the teeth caused by accumulation of dental plaque and calculus

plaque => sticky, colorless, biofil that collects btn & on the surface of teeth (AKA dental plaque) –> if not removed - becomes calculus

plaque beneath gumline –> gingivitis (can contribute to development of caries)

*adolescence*

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7
Q

What population is are these typically found in?

A

=pyogenic granuloma

gingiva of children, young adults & pregnant women (“pregnancy tumor”)

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8
Q

What population presents with torus palatinus the most?

what are characteristics of torus palatinus

A

F>M

= asymp bony outgrowth (exostoses) bc genetics or environment

=localized, benign benign protrusions

no cartilage involement

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9
Q

periodontits may be apart of systemic and/or immunodeficiency syndromes

which ones??

A

AIDS

Leukemia

Crohns

Diabetes

Down syndrome

Sacoidosis

syndromes w/ defects in neutrophils

infective endocarditis

pul or brain abscess

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10
Q

what is the etiology of SCC

A

1. HPV

2. tobacco/alc

3. betel quid/paan (india/asia) = combo of betel leaf, areca nut and slacked lime (aka gutka)

  1. a__ctinic radiation (sunlight) & esp in pipe smokers (lower lip)
  2. seen a rise in oral SCC (esp tongue) in < 40 y/o who doesnt smoke or have HPV - No known risk factors
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11
Q

How do you differentiate aspergillus fumigatis from mucor

A

aspergillus - septated 45 degree uniform branches

mucor- nonseptated 90 degree branches

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12
Q

What is the etiology of sialadenitis

A

etiology = inflam (-itis) of salivary gland

  1. trauma - mucocele (MC) & ranula
  2. autoimmune dx - sjogrens
  3. viral- mumps = MCC
  4. bacterial- staph aureus/strep viridins
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13
Q

what is the range of differentiation for SCC

A

range from well-differentiated keratinizing neoplasms

to

anaplastic, maybe sarcomatoid tumors

& also range in growth - slow to rapidly growing lesions

*degree of histological differentiation (determined by degree of keratinization) IS NOT correlated w/ behavior

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14
Q

what do the oral lesions look like in myeloid neoplasms ( tumors w/ monocytic differentiation)

A

=AML w/ monocytic maturation - nonspecific esterase (+); see monoblasts/mature monocytes in blood

infiltrate the skin (luekemia cutis) & gingiva

present before pancytopenia presents

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15
Q

a pt w/ DM presents complaining of facial pain and numbness w/ progressive conjunctival suffusion and blurry vision. after looking at the noncontrast CT which shows complete opacification of the lumen of the right maxillary sinus w/ bony erosion, what is on your DDx

what are you worried about?

A

Rhinocerebral mucormycosis

worried that infxn will spread to the orbits, cause cavernous sinus thrombosis and possibly invade basilar brain

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16
Q

what are characteristics of salivary gland neoplasms

A

relatively uncommon (<2 % of tumors in humans)

adults - F slightly more than male

5% in children < 16 yo

benign tumors - 50s-70s & malignant = later

(ex: pleomorphic adenoma, warthin tumor, mucoepideral carcinoma, adenoid cystic carcinoma)

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17
Q

compare the 5-yr survival rate of :

smoke/alc related SCC (early stage)

smoke/alc related SCC (late stage)

HPV

A

smoke/alc related SCC (early stage): 80%

smoke/alc related SCC (late stage): 20%

HPV-SCC: Better than non-HPV associated

*2nd primary tumor of oral cavity = 3-7% –> higher risk of malignancy

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18
Q

what is the clinical presentation of HNSCC

A

non-specific symptoms - sore throat, ear ache, pain on swallowing, wt loss.

possible metastasis to LN (submandibular & cervical)

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19
Q

If a pt presents w/ gray-white exudative membrane caused by acute pharyngitis/tonsilittis and the underlying cause is a result of EBV.. what does this pt have?

A

infxous mono

-also see cervical LAD and palatal petechiae

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20
Q

Pt w/ positve pregnancy test comes to your office with oral changes. what are these changes?

A

pregnancy tumor=

friable, red, pyogenic granuloma protruding from gingiva

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21
Q

how does HSV orofacial infxn present in adults

A

most = latent HSV-1 in

reactivation = recurrent herpetic stomatitis = at the site of primary inoculation or in adjacent mucosa w/ same ganglion

herpes labialis (pic) = latent in trigeminal ganglion = 1-3 mm vesicles to large bullae - 1st filled w/ clear serous fluid but rapidly rupture to yield painful, red-rimmed shallow ulcerations - clear w/i 3-4 weeks spontaneously

–> intracell and intercell edema (acantholysis)

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22
Q

what are 3 sources of brain abscesses?

A
  1. spread of infxn from pericranial contiguous focus (sinuses, middle ear, dental infxns)
  2. dental infxns, ethmoid/frontal sinusitis
  3. subacute/chronic otitis media/mastoidosis
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23
Q

which bacteria is most associated with periodontitis in adults

A
  • Aggregatibacter (actinobacillus) actinomycetemcomitans
  • Porphyromonas ginginvalis
  • Prevotella intermedia
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24
Q

what is the MCC salivary gland lesion

A

Mucocele

MC in toddlers, young adults and elderly (who are more prone to falling)

= fluid filled on lower lip due to trauma - fluctuant fluid filled lesion (filled w/ mucinous material & lined by organizing granulation tissue)

Tx: complete excision

*NOT A CYST- bc no epithelial lining

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25
Q

The development of SCC is driven by…

A

accumultion of mutations & epigenetics changes –> alter expression & fxn of oncogenes & tumor suppressor genes –> cancer hallmarks

–> cell death, increased prolif, induce angiogenesis and ability to invade/metastasize

genetic alterations have molecular consistency of tobacco carcinogen induced cancers (DNA adducts)

-freq involve p53 path & proteins responsible for squamous differntiation p63 & NOTCH1

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26
Q

explain the genetic alterations identified for cancer development

A
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27
Q

what is the role of p63?

A

TP63 –> instructions for making a p63

=TF - attaches to certain region of DNA and controls the activity of particular genes

present in leukoplakia & SCC

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28
Q

what are histological features of candida albicans

A

pseudohyphae - chain of budding yeast cells joined end to end at constrictions

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29
Q

What is one of the most common dz’s worldwide and main cause of tooth loss before age 35?

how does it occur

A

dental caries!

-focal demineralization of enamel & dentin by acidic metabolities of fermented sugar produced by bacteria

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30
Q

oral lesions can be the first sign of….

A

underlying systemic conditions

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31
Q

which one is reversible, gingivitis or periodontitis?

A

BOTH!

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32
Q

what is the relationship of salivary gland tumor size and malignancy

A

malignancy = inversely proportional to size of gland

NO RELIABLE clinical criteria to diff btn benign and malignant - have to Bx

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33
Q

describe the gross and histological findings for pyogenic granulomas

A

surface = ulcerate, red-purple; growth may be rapid (worry about malignancy)

histologically - highly vascular proliferation of organizing granulation tissue

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34
Q

what is the fxn of salivary glands

A

produce saliva

  • digestion (ptyalin/salivary amylase)
  • lubrication for swallowing

protection (IgA, lactoferrin, lysozome)

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35
Q

explain the process of formation of dental caries

A

health-associated streptococci –> [poor oral hygiene, high sugar diet, salivary/immunologic/microbial factors] –>

  1. S. mutans- glucan production, biofilm formation, acid tolerant/producing
  2. late colonizers - acid tolerate & producing

–> dental caries

(picture also lists how to prevent!)

36
Q

What are some conditions assocaited w/ compromise immune state that may predispose the pt to Candida infxns

A

AIDs

HIV (*if pt present w/ candida and no obv cause -test for HIV!)

DM

newborns

kids on oral steriods for asthma

organ/BM transplant

pregnant

broad spectrum ABx

37
Q

what population are peripheral ossifying fibromas most common?

presentation?

treatment?

A

young/teenage females

= red, ulcerated & nodular lesions of gingiva

complete surgical excision down to the periosteum

38
Q

what provides the simplest and rapid diagnostic test for Candida species?

A

wet mount - vaginal discharge

Candida vaginitis - DM women, or on OC

=intense itching, thick, curdlike discharge

39
Q

what do you see on histology slides of pts w/ hairy leukoplakia

A

hyperkeratosis & acanthosis w/ “balloon cells” in upper spinous layer

40
Q

what are characteristics of erythoplakia

A

red, velvety, eroded areas w/i oral cavity that usually remains level w/ or may be slightly depressed in relation to surrounding mucosa

less common but more ominous bc almost always associated w/ dysplasia/carcinoma in situ (CIS = has not broken basal membrane yet)

41
Q

what oral changes are seen in pts w/ HIV

A

predisposition to opportunistic oral infxn, particulary

herpes virus

candida

kaposi sarcoma

hairy leukoplakia

42
Q

compare the oral changes in pemphigus vs bullous pemphigoid

A

pemphigus - vesicles & bullae prone to rupture, leaving hyperemic erosions covered w/ exudates

bullous pemphigoid - orally look like pemphigus lesions- need to differentiate via histology

43
Q

what strep infxn can cause dental infxn/periodontitis/caries?

A

Viridans group strep

-microaerophilic

also cause endocardititis –> so life threatening!

44
Q

what is the MC cancerous lesion of the head/neck

A

SCC = 95%

= 6th MC neoplasm in the world

(have high rate of multiple primary tumors)

45
Q

What oral manifestations may a pt w/ measles present w/

A

spotty exanthema before skin rash

koplik spots = made by ulcerations on buccal mucosa about stensen duct

(cough, coryza, conjunctivitis)

46
Q

what are histological features for pleomorphic adenomas

A

great heterongenity

epithelial elements in ductal formations, acini, irregular tubules, strands or sheets

mesenchymal foci of cartilage, bone, fat in myxoid stroma

47
Q

what is the role of cyclin D1

A

= protein required for progression thru G1 phase of cell cycle; in G1-phase -made rapidly and accumulated in nucleus and is degraded as the cell enters S-phase

= regulatory subunit of CDK4 & CDK6

expressed in both leukoplakia and SCC

48
Q

how can infxns occur in the resp, GI, GU tract in healthy ppl

A

virulent microorganisms with ability to damage or penetrate the epidermis/mucosal epithelium

transfer via contact (direct/indirect), resp route, fecal-oral, sex, vertical transmission, insect/arthropod vectors

infxn if virulence factros overcome host defense or if host is compromised

49
Q

what are complications of dental caries

A

pain - affects daily living

wt. loss/nutritional probs

loss of self confidence/esteem

potential life-threatening

50
Q

what are characteristics of pleomorphic adenoma/mixed tumors

A

pleomorphic adenoma =well demarcated mass (vary in size) benign tumor that consists of mixture of ductal (epithelial) & myoepithelal cells (histologically = mixed tumor)

parotid > submandibular >>> minor

RF = ionizing radiation

reoccur is not completely excised

invasive to acini - malignancy arise as long as they are untreated

PLAG1 gene rearrangement- overexpression

51
Q

What are characteristics of Ranula

A

due to trauma

=cyst of sublingual gland - usually intra-oral but can bulge out

Tx: excise completely - if not may reoccur

52
Q

what do all these have in common:
focal fibrous hyperplasia (traumatic fibroma)

pyogenic granuloma (pregnancy tumor)

peripheral ossifying fibroma

peripheral giant cell granuloma

A

ALL BENIGN!

53
Q

if a pt presents w/ a fiery red tongue w/ prominent papillae, what could be the underlying cause?

what are other ways it could present

A

= raspberry tongue –> scarlet fever

could present w/ white coated tongue through which hyperemic papillae project (strawberry tongue)

(group A beta hemolytic - strep pyogenes)

54
Q

which deep fungal infxns have a predilection for the oral cavity & head/neck?

What is the predisposing factor

A

predisposing factor: immunosuppression

histoplasma, blastomycosis, coccidiodomycosis

aspergillosis

cryptococcosis

zygomycetes - mucor, absidia, rhizopus

55
Q

Label this

A
56
Q

What does HPV demonstrate tropism for? explain the process

A

HPV - tropism for lymphod assocaited structures of the oropharynx (including palatine & lingual tonsils)

in oropharynx- HPV gains access to basal kertinocyte progenitors via fenestrations in retuculated epithelium of tonsil crypts

infxn of tonsillar epithelium –> aberrant basal cell differntiation, dysplasia, carcinoma in situ & invasive carcinoma

57
Q

what is the MC orofacial herpetic infxn & what population does it present in most

A

HSV-1 (but HSV-2 possible)

primary infxn MC in kids 2-4 (often asymptomatic)

58
Q

what oral manifestations will a pt w/ diptheria present w/

A

dirty white, fibrinosuppurative, tough, inflam membrane over the tonsils & retropharynx

59
Q

What are characterisitics of Warthin tumors (papillary cystadenoma lymphomatosum)

A

almost always parotid

M > F

10% multifocal & 10% bilateral

=smokers 8x greater risk

distinctive double layer of neoplastic epithelial cells resting on a dense lymphoid stroma, sometimes bearing germinal centers

60
Q

Describe this lesion

What is it and what is the presentation

A

single ulceration w/ an erythematous halo around a yellowish fibropurulent membrane

=aphthous ulcer (canker sore)- single/multiple shallow, hyperemic ulceration covered by thin exudate & rimmed w/ narrow zone of erythema

painful, superficial oral mucosal ulceration of UNKNOWN ETIOLGY; resolves spontaneously in 7-10 days

61
Q

what are traumatic/irritation fibromas

A

aka focal fibrous hyperplasia

=submucosal nodular mass of fibrous CT stroma on bucal mucosa along bite line or gingiva (could be sessile or pedunculated)

=reactive prolif bc of trauma

remove w/ complete surgical excision

62
Q

what is the association of HPV and oropharyngeal SCC (OPSCC)

A

70% OPSCC (esp of base of tongue, tonsils, and pharynx) = associated w/ HPV-16 (oncogenic varient)

highest risk: 35-55 yo, non-smoking, white male

greater survival rate than HPV-neg tumors

63
Q

How do you treat pyogenic granulomas

A

they can regress, mature into dense fibrous masses and form peripheral ossifying fibromas

-complete surgical excision is the definitive Tx

64
Q

What are oral changes are seen in the following hematologic disorders:

  1. pancytopenia
  2. leukemia
  3. monocytic leukemia
A
  1. (agranulocytosis, aplastic anemia) –> severe infxn - gingivitis, pharyngitis or tonsillitis ; may spread to neck = cellulitis (ludwig angina)
  2. (see above) -similar bc neutropenia
  3. leukemic infiltration & enlargement of gingivae w/ periodontitis
65
Q

what viral infxns can involve the oral cavity &/or head/neck region

A

HSV 1 & 2

herpes zoster

EBV (mono, nasopharyngeal carcinoma, lymphoma)

CMV

Enterovirus (herpangina, HFM dz, acute lymphodocular pharyngitis

rubeola

66
Q

what is the prevalence, etiology and complication of xerostoma

A

increase risk w/ age - 20% pt >70 yo

etiology

  1. due to meds (anticholingerics, antidepressant/antipsychotics, diuretic, antiHTN, sedative, M relaxant, analgesics, antihistamines)
  2. sjogrens syndrome
  3. radiation therapy

complication - burning mouth syndrome - may also suggest HYPOfxn of PNS

67
Q

Which genes are mutated in HPV associtated - OPSCC

A

HPV:

E6 –l p53 –> p53 degrades

E7 –l RB

HPV is integrated into host genome

68
Q

what will make erythema multiforme an emergency

A

SJS/TEN

= widespread blisters predom on the trunk & face

= erythematous or pruritic macules

epidermal detachment

69
Q

what are characteristics of oral candidiasis (thrush)

A

= superficial, gray-white inflam membrane made of matted organisms enmeshed in fibrinosuppurative exudate-

can be scraped off to reveal underlying erythematous inflam base

(remain superficial EXCEPT in compromised pt - organ/bone marrow transplant, neutropenia, chemo pt, AIDs, DM)

70
Q

what define and explain dysplastic cells

A

=disordered growth

-loss of uniformity & loss of architectural orientation

may exhibit considerable pleomorphism - often have hyperchromatic nuclei w/ high nuclear-to-cytoplasm ratio

more abundant mitotic figures & seen in all layers

71
Q

Overexpression of which tumor suppressor contributes to HPV-induced SCC

A

p16 = tumor supressor protein encoded by CDKN2A

surrogate marker bc p16 overexpressed in HR-HPV​-(+) OPSCC

72
Q

what does hairy leukoplakia look like?

what population and how does it occur

A

distictive oral lesions on the lateral border of the tongue

seen in immunocompromised pts

caused by EBV

73
Q

what are characterisitics of leukoplakia

A

=white patches/plaques- canNOT be scraped off & canNOT be characterized clinically or pathologically w/ any other dz

3% world pop

25% of lesions = premalignant- until proven otherwise, think of ALL leukoplakia as precancerous

74
Q

describe multilocular keratocytic odontogenic tumors

A

=epithelial lined cyst in mandible & maxilla

need to differentiate from other cysts becuase of its aggressive behavior

seen at any age; but MC 10-40 yo

Males

w/i posterior mandible

75
Q

how do you differentiate hairy leukoplakia from candida infxn

A

hairy leukoplakia - white confluent pathches of “hairy”, hyperkarototic thickening - usually on lateral tongue (canNOT be wiped off-like in Candida)

*but can have a superimposed candida infxn - contributes to “hairiness”

76
Q

what is the oral side effect of phenytoin (Dilantin) ingestion

A

fibrous enlargement of gingiva (gingival hyperplasia)

often due to poor hygiene or side effect of medications (Dilantin- anti-seizure med)

77
Q

how will HNSCC present histologically

A

numerous nests & islands of malignant keratinocytes invading the underlying CT stroma and sk. M

if HPV related - nonkeratinizing SCC formed by basophillic cells w/ indistinct borders & scanty cytoplasm, w/ strong expression of p16

78
Q

what auto. dom. disorder presents w/ multiple congenital aneurysmal telangtasia beneath mucosal surfaces of the oral cavity and lips

A

osler-weber-rendu dz (aka hereditary hemorrhagic telangiectasia- HHT)

-affect blood vessels throughout the body - cause vascular dysplasia –> increase tendency to bleed

MC presentation = recurrent/severe epistaxis –> severe anemia - need transfusions

79
Q

what locations will oral cavity SCC present

what is important to find for long-term survival

A

tumor on ventral tongue, floor of mouth, lower lip, soft palate or gingiva *look under dentures*

premalignant lesions can be heterogenous in presentation & present before classic malignancy (EXCEPT HPV-SCC - no premalignant lesion) ==> early detection of all premalignant lesions critical for long term survival

= firm, pearly plaques that may ulcerate/protrude w/ irregular borders

80
Q

what are characterisitcs of mucoepidermoid carcinoma

A

15% of all salivary gland tumors (MC primary malignancy)

60-70% occur in parotid

balanced chromosomal translocation (11:19)(q21;p13) produces a fusion gene product (MECT1-MAML2)

prognosis dep on grade

= low grade - look normal and tend to grow/spread slowly compared to high-grade

3 diff types of cells - solid epithelial squamous, intermediate celll and mucus producing cells (see on histology w/ mucus stains & cyst like spaces w/ mucus)

81
Q

what is periodontitis?

A

poor oral hygiene w/ resultant change in oral flora (anaerobic/gram (-)) –> inflam process that affects the supporting structures of the teeth (periodontal ligaments) alveolar bone and cementum

–> can lead to complete destruction of ligament –> loosen and lose teeth

82
Q

What are characteristics of adenoid cystic carcinoma

A

relatively uncommon

10% in MINOR salivary glands (palatine gland)= poorer prognosis

slow growing BUT unpredictable

50% disseminate (bone, liver, brain) decades after primary tumor removal

cells = clear cytoplasm but cells someitme solid and other times vacuolated

pain bc grow along nerve (perineural)

83
Q

how does primary infxn of HSV in orofacial region present

A

10-20% acute herpetic gingivostomatitis = abrupt onset of diffuse oral vesicles w/ ulcerations (esp in gingiva) [also have LAD, fever, anorexia and irritability]

84
Q

explain the lympathic drainage of the oral cavity and pharynx

A
  1. upper lip, teeth & submental LN –> submandibular LN –> SDC nodes –>IDC nodes
  2. hard palate & lateral tongue –> submandibular LN –> SDC nodes –> IDC nodes
  3. soft palate –> retropharyngeal nodes –> SDC nodes –> IDC nodes
  4. pharyngeal arches –> SDC nodes –> IDC nodes
  5. tonsils –> jugular diagastric nodes
  6. lateral lip cross over and tip of tongue cross over –> submental LN –> submandibular LN or IDC nodes
  7. middle of tongue cross over –> IDC nodes
85
Q

what is the Tzanck test for HSV

A

= fluid from vessicle on micro slide and stained w/ Wright or Giemsa stain

(+) = acantholytic keratinocytes or multinucleated giant acantholytic keratinocytes (multinucleated polykaryons), or eospinophilc intranuclear viral inclusions

(+) in 75% of early cases (primary or recurrent)

86
Q

what oral changes are associated w/ lichen planus

A

reticulate, lacelike, white keratotic lesions

sometimes ulcerate and rarely form bullae

87
Q

are peripheral ossifying fibromas neoplastic?

how do they form

A

no, most likely = reactive

from pyogenic granuloma or de nova from periodontal ligament cells