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Oral Pathology Exam 2 > 6. Acute Oral Ulcers > Flashcards

6. Acute Oral Ulcers Flashcards

1
Q

What is the etiology of Aphthous Ulcers (canker sores)?

A

Undetermined Etiology

  • Thought to represent a Type IV T8 Cell Cytotoxic Rxn to an antigen
  • Especially when mucosal barrier is compromised OR there is a hyper-immune response
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2
Q

Aphthous Ulcers are ALWAYS…

A

Acutely Painful or tender

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3
Q

Where do Aphthous Ulcers develop?

A

Labial, NON-keratinized mucosa (moveable) then heal

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4
Q

What do Aphous Ulcers spare/not develop?

A
  • Gingiva
    • If pt says its the gums, its probs the alveolar mucosa
  • Hard Palate
  • Dorsal Tongue
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5
Q

What is the histology of Aphtous Ulcers?

A

Non-specific, non-diagnostic Ulcer

no need for biopsy for dx

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6
Q

What is the most common type (20-60%) of aphtous ulcer?

A

RAU minor

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7
Q

What aphtous ulcer is ocasionally seen, with most cases in females?

A

Herpetiform apthae

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8
Q

What type of aphtous ulcer is rare?

A

RAU Major

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9
Q

What is the clinical presentation of RAU minor?

A
  • 1-5 small (3mm < 1cm) well demarcated, circular ulcers surrounded by a red border
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10
Q

What is the clinical presentation of Herpetiform aphthae?

A
  • Numerous (6-100) crops of small, irregular ulcers that can coalesce and become larger ulcers
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11
Q

What is the clinical presentation of RAU major?

A
  • Several large (1-3cm), deep (into muscle), ragged ulcers
  • Painful enough to encourage suicide
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12
Q

Where is RAU minor located?

A
  • Confined to labile mucosa or oral cavity
  • NEVER on gingiva or hard palate
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13
Q

Where is Herpetiform aphthae located?

A
  • Mostly on labial mucosa
  • RARELY on hard palate or gingiva
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14
Q

Where is RAU major located?

A
  • Can occur anywhere including pharynx (pretty common location for them)
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15
Q

What is the frequency of RAU minor?

A
  • Episodes Every Few Months
  • Triggered by trauma (cheek biting, tooth brushing, after CPR training, trauma from ortho), stress, foods, meds
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16
Q

What is the frequency of Herpetiform aphtae?

A
  • Frequent episodes (every couple weeks)
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17
Q

What is the frequency of RAU major?

A
  • Almost always present (as 1 heals another 1 starts)
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18
Q

What is the healing time for RAU minor?

A

Heal w/o scars in 1-2 wks

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19
Q

What is the healing time for Herpetiform aphthae?

A

Heal w/o scars in 1 wk

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20
Q

What is the healing time for RAU major?

A
  • Heal with SCARS in 2-6 wks
  • Constriction of the oral cavity; Microstomia
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21
Q

What is the preferred treatment for RAU minor?

A

Chemical Cautery

eradicates the pain but won’t prevent new ones

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22
Q

What is the preffered treatment for Herpetiform aphthae?

A

Topical or Systemic Steroids

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23
Q

What is the prefered treatment for RAU major?

A
  • Systemic Steroids
  • Intralesional Steroid Injection, around the base of the ulcer
  • Dangerous Drugs
    • Bone marrow consequences
    • Birth defects
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24
Q

What are the features of Behcet Syndrome?

A
  • Systemic vasculitis that features multiple aphtous ulcers of various size in 90% ALONG WITH:
    • Genital Ulcers (75%)
    • Inflammatory Eye and Conjunctival Lesions (80%)
      • Blindness (25%)
    • Neurologic Sxs (10-20%)
      • Assoc with poor prognosis, dementia and paralysis
    • Arthritis (common but mild)
    • Varied skin lesion
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25
Q

What is the etiopathogenesis of Behcet Syndrome?

A
  • Hyperimmune rxn to oral bacteria, other infectious or environmental agents
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26
Q

Who has a predisposition for Behcet Syndrome?

A

SILK ROUTE

  • HLA predisposition among Turks, Japanese, Mediterranean’s
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27
Q

How is Behcet Syndrome Diagnosed?

A

Pathergy Test

  • Rxn following skin injection of sterile saline
  • Unique to this disease - Diagnostic
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28
Q

What must be present for the diagnosis of Behcet Syndrome?

A

Must have Oral Ulcers, +2 other lesions (genital, eye, skin lesions), + pathergy test

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29
Q

What is the other name for Reactive Arthritis?

A

Reiter Syndrome

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30
Q

In what populations are Reiter Syndrome more common in?

A
  • Males
  • Young Adults, with proper HLA profile
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31
Q

What are the clinical features of Reiter Syndrome? (3)

A
  • Recurrent lesions:
    • Oral
      • ​Resemble Geographic tongue, BUT widespread
    • Conjunctival
    • Genital
      • Resemble Geographic Tongue
      • Non-gonococcal urethritis (mucopurlulent discharge)
  • Prominent Crippling Arthritis
  • Palmar and Plantar Hyperkeratosis and other skin lesions
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32
Q

What is the etiopathogenesis of Reiter Syndrome?

A
  • Autoimmune Rxn following GI disease or STI in pts with susceptible HLA profile or HIV
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33
Q

What is the most common trigger for Reiter Syndrome?

A

Veneral disease

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34
Q

What do the microscopic lesions of Reiter Syndrome resemble, and what do they show?

A

Psoriasis

show munro micro-abscesses

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35
Q

What are the clinical features of Transient Lingual Papillitis “Lie Bumps”?

A
  • Common condition of Fungiform Papillae
  • One or several papilla become enlarged, red, then ulcerates
    • ​“SALT ON A PRETZEL”
  • Causes sharp pain and tenderness
  • Tends to resolve in days to a week
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36
Q

How is Primary Herpes Simplex 1 (oral) transmitted?

A
  • 80% contact virus (antibodies forming)
    • Kissing, fomites, utensils, ect.
  • 20% never contact virus
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37
Q

What are the Primary Herpes Simplex 1 presentations?

A
  • 1% - Primary Herpetic Gingivostomatitis
  • 99% - Asymptomatic Primary Infection
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38
Q

What is the clinical presentation of Primary Herpetic Gingivostomatitis?

A
  • Multiple painful, 3-7mm vesicles, which burst into ulcers throughout the mouth, may coalesce
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39
Q

What must be present for the diagnosis of Primary Herpetic Gingivostomatitis?

A

Acute, Hemorrhagic Gingivitis

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40
Q

When does Primary Herpetic Gingivostomatitis resolve?

A

2 weeks and will not return in the same form

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41
Q

What is the treatment for Primary Herpetic Gingivostomatitis? (3)

A
  • Appropriate antiviral - if caught early
  • Fluids
    • pts don’t want to eat or drink anything, become dehydrated
  • Pt is Contagious
    • Keep away from others and themselves
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42
Q

What percent of HSV-1 infected people get seconday herpes, due to periodic outbreaks of latent virus?

A

50%

  • 1% Seondary Intraoral Herpes
  • 99% Herpes Labialis (Cold Sore/Fever Blister)
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43
Q

Where does Secondary Intraoral Herpes develop?

A

Gingiva and Hard Palate

mucosa bound down to bone

44
Q

What is the clinical appearance of Secondary Intraoral Herpes? (2)

A
  • Small, short lived vesicles
    • “stabbed with icepick”
    • Little red, inflamed, sore
  • Periodic outbreak
    • Triggers: trauma, dental work, fever, colds, stress
45
Q

When does Secondary Intraoral Herpes resolve?

A

Heals in 7-10 days

46
Q

How does Herpes Labialis occur?

A
  • latent virus in trigeminal ganglion periodically reactivated by lowered systemic or tissue resistance:
    • ​Colds/fever, UV or cold exposure, trauma, menstration, and stress
47
Q

How does Herpes Labialis clincal presentation begin?

A
  • Prodrome of lip tingling and swelling
  • Followed in a day by localized crop of small vesicles
48
Q

When does Herpes Labialis resolve, and what occurs during this period?

A

7-10 days

  • Day 1 - vesicles
  • Day 2 - vesicles with inflammtion
  • Day 4 - weeping crusted ulcer
  • Day 7 - dries up, will go away
49
Q

What percent of the total population NEVER gets a herpetic lesion, with or without contact with the virus?

A

60%

50
Q

What are 2 other lesions caused by HSV-1?

A

HSV-1 can occur anywhere above the waist

  • Herpetic Whitlow
  • Kaposi Varicelliform Eruption
51
Q

What is Kaposi Varicelliform Eruption?

A

Herpes complicating Eczema

  • Looks like chickenpox
  • If untreated can be Fatal
52
Q

What test is used for the Diagnosis of HSV-1 and HSV-2?

A

Tzanck Smear

  • Cytologic exam of the fluid or base of an intact vesicle
    • Shows acantholytic cells
  • Also shown in Pemphigus
53
Q

What is histologically diagnostic for HSV-1 and HSV-2?

A

Lipshutz Bodies

  • Cells are multinucleate
  • Contain intra-nuclear viral inclusions

Pemphigus does not have Lipshutz bodies, but is confirmed with a Tzanck Smear

54
Q

What diseases have an etiology of HHV-3 Varicella-Zoster Virus?

A

Chickenpox

Zoster/Shingles

55
Q

How is chickenpox spread?

A

Primary infection with varicella virus

  • Droplet infection
  • Contact with lesions and fomites
56
Q

What is the incubation period for chickenpox?

A

2 weeks, then generalized flulike symptoms

57
Q

What is the clinical appearance of chickenpox?

A
  • Vesicles fold onto themselves becoming umbilicated pustules and then crusts
  • Oral lesions common
58
Q

Where does the varicella-zoster virus remain latent?

A

Nerve ganglia

59
Q

What are the complications of chickenpox? (3)

A
  • Reye Sx (aspirin)
  • Encephalitis
  • Pneumonia
60
Q

How is chickenpox prevented?

A

Immunization with Varivax

61
Q

What is the treatment for chickenpox?

A

Antivirals = Valtrex or Famvir

  • if caught early, they help shorten the duration and decrease number of lesions
62
Q

How does zoster/shingles occur?

A
  • Reactivation of latent chickpox virus occuring when resistance is lowered:
    • Stress, HIV, Internal Malignancy (Lymphoma/Leukemia), debilitating ds, old age
63
Q

What is the clinical presentation of Zoster/Shingles? (5)

A
  • Intense prodromal pain followed by painful coalescing vesicles
    • DON’T CROSS MIDLINE
  • Post-Herpetic Neuralgia
    • Can be incapacitating and last years after the rash and clisters disappear
  • Jaw and Pulpal Necrosis
    • ​Zoster affects the blood supply
  • May cause Facial Paralysis
  • Involvement of tip of nose predicts Eye Involvement
    • ​Can cause blindness
64
Q

What is the treatment for Zoster/Shingles?

A
  • If tx early with Valtrex or Famvir - can abort the lesions
  • Vaccine for pts > 60 yrs
    • Dire consequences over age 60
65
Q

What is caused by Herpes 6, 7?

A

Roseola (childhood disease)

66
Q

What is caused by HHV8?

A

Kaposi Sarcoma

opportunistic for severe immunosuppression

67
Q

What occurs in Ramsey Hunt Syndrome?

A
  • Herpes in geniculate ganglion
  • Will cause Bell’s Palsy
68
Q

How is Herpes Labialis (Cold Sores/Fever Blisters) prevented?

A
  • Protection from elements
  • Prophy antivirals prior to exposure to elements
  • L-lysine 1000mg supplement and avoid arginine (chocolate, nuts, dried fruit)
    • Have to take it min 1 month
    • Vegans are typically deficient in this EAA
    • Herpes virus needs arginine to replicate
    • L-lysine competes with arginine
69
Q

What is the treatment for Herpes Labialis?

A
  • Denavir cream
  • Famvir or Valtrex @ onset of outbreak
70
Q

What is the treatment for Primary Herpes (chickenpox) or Zoster?

A
  • Famvir or Valtrex capsules as soon as clinical diagnosis is made
    • Will not prevent post-herpetic pain, but it will reduce the duration of it and the lesions
71
Q

What is shown in the histology of Varicella-Zoster Virus diseases?

A

Viral inclusion bodies

72
Q

What is caused by Coxsackieviruses? (3)

A
  • Hand, Foot, and Mouth Disease
  • Herpangina
  • Acute Lymphonodular Pharyngitis
73
Q

What is shown in the histology of coxsackieviruses?

A

NO viral inclusion bodies

unlike HSV-1, HSV-2, HHV-3

74
Q

What is the clinical presentation fo HFM Ds?

A
  • Multiple, acute oral vesicles breaking into ulcers
    • ​Resemble Primary Herpes, but NO GINGIVITIS
  • Ulcer Stage, resembles Herpetiform Aphthae, ​but NO RECURRENCE
    • Hand/foot lesions present but may be delayed
    • Also get lesions on buttocks
  • aka primary herpes but include lesions on hands, feet, and butt
75
Q

What is the clinical presentation of Herpangina?

A
  • Small number of acute oral vesicles & ulcers confined to Soft Palate and Pharynx
    • Pharynx is a common location for RAU major, but it will have several lesions
76
Q

What is the clinical presentation of Acute Lymphonodular Pharyngitis?

A
  • Soft, shiny, yellow/red, nodules on soft palate
    • Representing inflamed lymphoid tissue
77
Q

What is the etiopathogenesis of Necrotizing Ulcerative Gingivitis (NUG)?

A
  • Opportunistic fuso-spirochetal anaerobic infection
  • Triggered by: poor oral hygiene in a setting of stress, smoking, debilitation
78
Q

What does NUG affect?

A

Gingival Papillae

79
Q

What is the diagnostic triad of NUG?

A
  • Pain
  • Bleeding
  • Necrotic ulceration of inter-dental papillae
    • “punched out” papillae
    • doesn’t look like gingivitis at all
80
Q

What symptoms/signs occur in NUG in addition to the diagnositc triad?

A
  • Excessive salivation
  • Metallic taste (from blood)
  • Fever and Lymphadenopathy
81
Q

What are the complications of NUG?

A
  • HIV-association NUG (much worse)
  • Noma
    • Lack of treatment of NUG leads to the spread of infection into soft tissue sites
    • Causing extensive intraoral destruction, which can expose alveolar bone and teeth
    • Palatal destruction
82
Q

What are the similarities between NUG and Primary Herpetic Gingivostomatitis (primary herpes)? (3)

A
  • Children/young adults
  • Painful ulcers
  • Fever and lymphadenopathy
83
Q

What are the differences between NUG and Primary Herpetic Gingivostomatitis (primary herpes)? (4)

A
  • Acute Hemorrhagic Gingivitis must be present for herpes dx, so the papillae will be swollen (inflammation vs. necrosis)
  • Contact virus vs. bacterial infection
  • Throughout the mouth vs. gingival papillae (generalized vs. localized)
  • NUG is non-contagious
84
Q

What is the etiology of Measles?

A

Paramyxovirus

85
Q

How is measles spread?

A

Droplets, very contagious

86
Q

What is the incubation period of Measles?

A

10-12 days, followed by flu-like symptoms

87
Q

What is the 1st lesion shown in measles?

A

Koplik Spots

  • Blue-white papules on buccal mucosa
  • Appear and disappear frequently
88
Q

What is the clinical presentation of measles?

A
  • Red maculopapular rash of: face –> trunk –> extremities
  • Accompaning painful gingivitis
89
Q

In what population is measles a very serious disease?

A
  • < 5 yrs
  • > 20 yrs
90
Q

What are the complications associated with measles? (6)

A
  • Fatal Encephalitis
  • Delayed symptoms of CNS disease
  • Pneumonia (can be fatal, especially in children)
  • Appendicitis due to lymphoid swelling
  • Severe, sometimes fatal infections and Noma
  • Vitamin A Deficiencies
    • Can lead to blindness and deafness
    • Fatal
91
Q

What is the prevention for measles?

A

Vaccine

92
Q

What is the classic lesion of Oral Hairy Leukoplakia?

A
  • Bilateral white, ragged, lesions that don’t scape off
  • Classicly on the Lateral Tongue
93
Q

What does Oral Hairy Leukoplakia clinically resemble? (3)

A
  • Tongue Biting
  • Cinnamon Stomatitis
  • Candidiasis
94
Q

What do Oral Hairy Leukoplakia lesions frequently show?

A

Candidiasis, especially in HIV pts

95
Q

What is the prognosis of Oral Hairy Leukoplakia?

A

Not a terrible disease, just an indicator of something serious that is going on

96
Q

What is the treatment for Oral Hairy Leukoplakia?

A

Anti-virals

97
Q

What is the histology of Oral Hairy Leukoplakia?

A
  • Hyperparakeratosis and clusters of koilocytic clear cells with beaded nuclei (dark beads around periphery of nucleus)
98
Q

How can you confirm the diagnosis of Oral Hairy Leukoplakia?

A

With ISH studies, can conclusively identify EBV to confirm ds

99
Q

What is the etiology of Infectious Mononucleosis and how is it spread?

A
  • EBV
  • Spread through intimate contact with saliva
100
Q

What are the signs of Infectious Mononucleosis? (6)

A
  • Kids are usually asymptomatic
  • Fever, cough, runny nose
  • Cerival Lymphadenopathy
  • Whopping Tonsillitis they can get so big that they may touch
  • Painful Pharyngitis
  • 30% get classic Palatal Petechiae
101
Q

How long does it take Infectious Mononucleosis to resolve?

A

4-6 weeks

102
Q

What occurs in those with Infectious Mononucleosis that doesnt resolve?

A
  • Manifests as a systemic disease that likes to grow in liver & spleen
  • In spleen, it gets into & weakens the splenic capsule, causing tenderness
  • Can cause splenic rupture with trauma, which can be fatal
103
Q

How is Infectious Mononucleosis diagnosed?

A

DIAGNOSTIC if peripheral smear shows: > 10% large lymphocytes

(​Lymphocytes are so big they look like monocytes)

  • Test for Paul Bunnell Heterophile Antibody (IgM)
  • Mono Spot Test (rapid results)
104
Q

What are the complications associated with Infectious Mononucleosis? (3)

A
  • Splenic rupture
  • Bell’s Facial Palsy
  • Chronic Fatigue Syndrome
105
Q

What is in the Differential Diagnosis of: Acute, Recurrent Aphthaeform Lesions? (12)

A
  • RAU minor
    • Default dx
  • RAU major
  • Herptiform Apthae
  • Behcet Sx
  • Chron’s Ds
    • GI complaints, and sudden increase/appearance of oral aphthae
  • Ulcerative Colitis
  • HIV
  • Neutropenia
    • Gingival ulcers, so kinda doesn’t fit
  • IgA Deficiency
  • MAGIC Sx
  • Nutritional Deficiency
    • Fe, Zn, B-complex
  • Secondary Intraoral Herpes

Oral Pathology Exam 2 (7 decks)

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