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GI II Midterm > Chapter 16 > Flashcards

Chapter 16 Flashcards

1
Q

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

A

Caries
Tooth decay
Tooth degradation due to mineral dissolution - acids released by oral bacteria during sugar fermentation

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2
Q

What are the signs and symptoms of Caries?

A

Pain
Weight loss/Nutrition problems
Loss of self confidence/esteem
Potential life-threatening infections

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3
Q

What is gingivitis?

A 
Soft tissue inflammation of the squamous mucosa and tissue around teeth
Erythema
Edema
Bleeding
Gingival degeneration 
Contributes to caries
REVERSIBLE DISEASE
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4
Q

What results in gingivitis?

A

Poor oral hygiene ->
Dental plaque - sticky, colorless, biofilm with mixture of bacteria, salivary proteins, and desquamated epithelial cells
Unresolved plaque -> calculus (tartar)

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5
Q

Patients that gingivitis is most prevalent and severe?

A

Adolescence

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6
Q

What is Periodontitis?

A

Inflammatory process that affects the supporting structures of the teeth (periodontal ligaments), alveolar bone, and cementum
Leads to eventual loss of teeth

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7
Q

Periodontitis-associated plaque contains what organisms?

A

Anaerobic and microaerophilic gram-negative flora

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8
Q

Clinical presentation of Periodonitis

A

Typically presents without any associated disorders - poor oral hygiene
Can be a component of systemic diseases: AIDS, Leukemia, Crohn disease, Diabetes, Down syndrome, Sarcoidosis, Neutrophil defect

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9
Q

Often recurrent, exceedingly painful, superficial, shallow oral mucosal lesion, with mononuclear infiltrate that is most common in the first 2 decades of life

A

Aphthous Ulcers (canker sores)

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10
Q

Aphthous Ulcer Patient history

A

Familial
Recurrent ulcers may be associated with Celiac disease, IBD, and Behcet disease
non viral
Resolution spontaneously in 7-10 days

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11
Q

Fibrous proliferative lesions, benign or malignant?

A

Benign

Traumatic fibroma and progenitor granuloma

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12
Q

Traumatic/irritation fibromas

A

Occur along bite line
Smooth pink exophytic nodule on buccal mucosa (squamous mucosa)
Benign

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13
Q

Pyogenic granuloma

A

Highly vascular, Gingival mass
Growth is alarmingly rapid
Can regress, mature into dense fibrous masses, or develop peripheral ossifying fibroma
Benign

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14
Q

Pyogenic granuloma commonly seen in what pts?

A

Children, young adults, and pregnant women (pregnancy tumor)

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15
Q

What infections classically cause cold sores? Describe how they heal

A

Herpes simplex virus (HSV-1 and -2)
Vesicles heal spontaneously in a few weeks, virus becomes dormant
Reactivation driven by trauma, infection or immune suppression (vesicles clear in a few days)

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16
Q

HSV1 infection can be associated with what additional clinical symptoms?

A

Lymphadenopathy, fever, anorexia, and irritability

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17
Q

Morphology of HSV infections and diagnostic test

A

Lesions: vesicles, large bullae, or shallow ulceration (rupture)
Eosinophilia intranuclear inclusions
Multinucleate polykarons (giant cells)
Tzanck test

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18
Q

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

A

Candida albicans - part of normal oral flora in half the population

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19
Q

Clinical presentation of Oral candidiasis and pt history

A 
Pseudomembranous form (thrush): Superficial gray-white inflammatory membranes composed of fibrinosuppurative exudates (can be scrapped off) 
Occurs in setting of broad-spectrum antibiotics, diabetes, neutropenia, or immunodeficiency 
Remains superficial unless immunosuppressed
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20
Q

What fungal infections have a predilection for the oral cavity and head and neck region? Also include key features of fungus

A

Histoplasmosis - Bats, birds, caves
Blastomycosis - Broad based budding yeast
Coccidioidomycosis - San Joaquin valley fever complex
Aspergillosis
Cryptococcosis
Zygomycosis (DM and mucormycosis)

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21
Q

What is the key predisposing factor of deep fungal infections?

A

Immunosuppression

  • HIV/AIDs
  • Organ transplant
  • Cancer therapy
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22
Q

Scarlet fever

A

Group A hemolytic strep
Fiery red tongue with prominent papillae (raspberry tongue)
White-coated tongue with papillae (strawberry tongue)

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23
Q

Measles

A

Spotty enanthema in oral cavity before skin rash
Koplik spots
coryza, conjunctiva, cough in a kid
Paramyxovirus
Warthin finkeldey - multinucleated giant cell found in LN early in course of measles

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24
Q

Infectious mononucleosis (mono)

A 
LN enlargement 
Fatigue, sore throat (acute pharyngitis and tonsillitis) 
Gray-white exudative membrane 
Hepatosplenomegaly 
EBV
Palatial petechiae
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25
Q

Diphtheria

A

Gray, fibrinosuppurative, tough, inflammatory membrane in back of mouth before any signs or symptoms
Corynebacterium diphtheriae

26
Q

HIV gives predisposition to what opportunistic oral infections?

A

Herpesvirus, Candida, and other fungi; oral lesions of Kaposi sarcoma and hairy leukoplakia

27
Q

Pt comes in unconscious to the ED. Open mouth and find a striking fibrous enlargement of the gingivae. What can you suspect?

A

Phenytoin ingestion - Dilantin for seizure disorder

28
Q

Hairy Leukoplakia presentation and typical pts

A

Distinctive oral lesion on lateral border of the tongue
Usually seen in immunocompromised pts and is caused by EBV
White patches of hyperkeratosis; superimposed candidiasis infections can augment the “hairiness”
Micro - Balloon cells
CANT SCRAP OFF!

29
Q

What is the most common antecedent for Leukoplakia and Erythroplakia?

A

Tobacco use

30
Q

What is Leukoplakia? How many people are affected?

A 
White plaque on oral mucosa
Cant be removed by scraping
Cant be classified as another disease entity 
3% of population 
Precancerous
31
Q

What should leukoplakia be considered until proven otherwise?

A

Precancerous
Up to 25%
Biopsy all of them

32
Q

What is Erythroplakia

A

Red, velvety, relatively flat, eroded lesion
Less common that leukoplakia
Greater risk of malignant transformation (ominous)
Anywhere in oral cavity
Intermediate forms: speckled leukoerthroplakia

33
Q

Leukoplakia and Erythroplakia are typically seen in what type of patient?

A

40-70
Male
Tobacco users

34
Q

95% of head and neck cancers are what histologic type?

A

Squamous cell carcinoma

35
Q

What are the risk factors of oral SCC ?

A

Tobacco and Alcohol - classic (middle aged)
HPV-16 (oropharynx)
Actinic radiation - sunlight (Lip)
Younger than 40, no known risk factors - ?
Betel Qid and Paan, tobacco concoction (India/Asia)

36
Q

70% of oropharyngeal SCC are HPV related mostly to what type?

A

16

37
Q

What patients have a greater long-term survival if they have SCC?

A

HPV positive tumors do better than HPV negative

38
Q

Rate of development of second primary tumors is higher in what location compared to any other malignancy? What is the theory behind this?

A

Oral cavity
Theory of Field cancerization: multiple individual primary tumors develop independently in the upper aerodigestive tract as a result of years of chronic exposure of the mucosa to carcinogens

39
Q

What are the cancer hallmarks of SCC?

A

Resistance to cell death
Increased proliferation
Induction of angiogenesis
Ability to invade and metastasize

40
Q

What is the classic molecular defect of SCC?

A

TP53 - tumor suppressor gene on chr 17
NOTCH transmembrane receptor protein
P63 protein

41
Q

What are the HPV molecular defects of SCC?

A

p16 overexpression - tumor suppressor protein encoded by CDKN2A gene
P53 protein (E6 and E7)
RB - tumor suppressor protein (E6 and E7)

42
Q

Describe the clinical presentation of classic oral SCC

A

Preceded by a precancerous lesion

Location: ventral tongue, floor of mouth, lower lip, soft palate, gingiva (look under dentures)

43
Q

What are favored sites of metastasis in Classic SCC?

A

Infiltrate locally before metastasis
Local: submandibular and cervical nodes
Distant: mediastinal nodes, Lungs, Liver, Bones

44
Q

Describe the clinical presentation of HPV oral SCC

A

NO preceding/precancerous lesion
Originate in tonsillar crypts, base of tongue, oropharynx
Difficult cancers to diagnose
Non specific symptoms: sore throat, ear ache, pain on swallowing (odynophagia), weight loss

45
Q

Where are the sites of metastasis in HPV oral SCC?

A

Deep cervical nodes

46
Q

Describe Odontogenic cysts and tumors

A

Derived from remnants of odontogenic epithelium present within the jaw
Either inflammatory or developmental
potentially aggressive
Pts with multiple odontogenic keratocysts merit evaluation of nevoid basal cell carcinoma syndrome - Gorlin

PTCH tumor suppressor gene

47
Q

Odontogenic keratocysts

A 
Aggressive behavior 
10-40
Males
Posterior mandible
80% of lesions solitary 
Multiple -> Gorlin syndrome: PTCH gene mutations on chr 9
48
Q

What is xerostomia?

A

Dry mouth

49
Q

What are causes of xerostomia ?

A 
Most common - Medications 
Other diseases-> Sjogren syndrome (aka keerotoconjuctivitis sicca), HIV, AD, PD, DM
Cancer therapy (chemo and radiation) 
Trauma/Nerve (parasympathetic) damage
Stroke
Lifestyle-> tobacco
Aging (70% of pts over age 70)
50
Q

What are the complications of Xerostomia

A

Increased caries, candidiasis, and difficulties with swallowing and speaking
Tongue fissuring, ulceration, and salivary gland enlargement can occur

51
Q

What is Sailadenitis?

A

Salivary gland inflammation

52
Q

What can sailadenitis be induced by?

A

Trauma, viral (mumps), or bacterial infection, or autoimmune disease (sjogren syndrome)

53
Q

What is the most common type of inflammatory salivary gland lesion?

A

Mucoceles: ductal blockage or rupture with saliva leakage into surrounding stroma
Most often on lower lip
Typically result from trauma (toddlers, young adults, and elderly - prone to falls)
Blue hue

54
Q

Neoplasms in the salivary gland typically occur in what patients?

A 
Adults
Slight female predominance
5% in children younger than 16 
Benign tumors most often appear in 5th to 7th decades of life 
Malignant appears later
55
Q

Which salivary gland accounts for the majority of salivary gland neoplasms?

A

Parotid

56
Q

Pleomorphic adenoma

A 
Benign tumors - PLAG1
60% of all parotid tumors 
Mixed epithelial and mesenchymal differentiation
Hx of radiation?
Well demarcated masses of varying size
Can recur if not completely excised 
Malignancy can arise the longer they remain untreated (poor prognosis) 
Mobile, painless, slow-growing masses
57
Q

The likelihood of a salivary gland tumor being malignant is associated to what?

A

Size
More or less inversely proportional to the size of the gland
The smaller it is the greater chance it is malignant

58
Q

What tumor is seen almost exclusively in the parotid?

A

Warthin tumor

Papillary cystadenoma lymphomatosum

59
Q

Warthin tumor typical pt and morphology

A 
Males
50-70s
Smoking increases risk (8x) 
Benign tumor of unknown histogenesis 
10% multifocal, 10% bilateral 
Packed with mitochondria - oncocytic 
Follicular germinal center
Eosinophilic epithelial cells
60
Q

What is the most common primary malignant salivary tumor?

A

Mucoepidermoid carcinoma - 15% of all salivary gland neoplasms

61
Q

Describe mucoepidermoid carcinoma

A

Majority parotid; also minor salivary glands
Translocation (11,19)
Survival is grade dependent
MECT1 and MAML2 genes

62
Q

Adenoid cystic carcinoma

A

Relatively uncommon - 5%
Half in minor salivary glands
Slow growing but unpredictable
Grow along nerves (perineural) so pain is common symptom
50% disseminate decades after primary tumor removal
Minor salivary glands - poorer prognosis

GI II Midterm (5 decks)

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