Oral Lesions Flashcards

1
Q

What are corticosteroids and what are they used for?

A

a class of drugs that includes steroid hormones naturally produced by the adrenal cortex; used for things like asthma, COPD, allergic reactions, and autoimmune disease

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2
Q

What are some side effects of corticosteroids (especially with long term use)?

A

adrenal insufficiency, high blood glucose, dementia, and osteoporosis

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3
Q

What causes oropharyngeal candidiasis, more commonly known as thrush?

A

caused by normally occuring fungus (in most people) called Candida albicans; local infection occurs when conditions are right for overgrowth (opportunistic)

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4
Q

What are some predisposing factors for thrush?

A

immunucompromised (like HIV and AIDS), infancy, older people with dentures, diabetic, those undergoing chemo or radiation, those taking antibiotics or corticosteroids (topical and systemic)

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5
Q

clinical presentation of thrush

A

sore throat or mouth, oral erythema with OR without white plaques

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6
Q

Will thrush brush?

A

YES! It will brush when compared to leukoplakia (not necessarily when compared to milk)

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7
Q

How is thrush diagnosed?

A

usually diagnosed based on clinical presentation but can be confirmed by a KOH prep – will see budding yeasts with or without pseudohyphae

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8
Q

true hyphae vs. psuedohyphae

A
true = have septa (internal cross walls)
pseudo = not fully septate and are fragile; associated with yeast
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9
Q

What are three medications used to treat thrush?

A

nystatin suspension (topical), clotrimazole (topical), or oral fluconazole (Diflucan)

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10
Q

What is some important patient education for the treatment of thrush?

A

Clean dentures carefully and rinse the mouth after using steroid inhalers!

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11
Q

When would a case of thrush warrant investigation for an underlying disease like diabetes or HIV?

A

if it involves the esophagus, if it is recurrent, or if it occurs without note of predisposing factors

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12
Q

What are some non-infectious causes of pharyngitis/tonsilitis?

A

allergies, smoking, GERD

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13
Q

Is most acute infectious pharyngitis bacterial or viral?

A

viral

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14
Q

What bacteria and viruses can cause acute infectious pharyngitis?

A
viruses = adenovirus, enteroviruses like coxackie A, HSV
bacteria = Strept pyrogenes (a Group A) or GAS, Mycoplasma pneumoniae, Neisseria gonorrhea, Fusobacterium necrophorum, non-group A Strept, Corynebacterium diptheriae, Tularemia
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15
Q

Which is the most common organism involved in bacterial pharyngitis/tonsilitis? What group of people is particularly targeted?

A

Group A Strept

particularly in kids under 3 years old and in adolescents (15-30% of all cases in kids 3-15 years old)

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16
Q

The incidence of GAS pharyngitis peaks in what time of the year?

A

winter and early spring

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17
Q

clinical presentation of GAS pharyngitis

A
  1. pharynx with edema, erythema, and/or exudates
  2. tender anterior cervical nodes
  3. middle grade fever (between 101-103)
  4. absence of usual signs of viral URIs (so no cough or coryza)

may also see palatal petechiae and/or scarlatiniform rash; may be indistinguishable from infectious pharyngitis due to other causes!

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18
Q

What is coryza?

A

cold symptoms, nasal mucous membrane inflammation, congestion

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19
Q

What is scarlet fever and what causes it?

A

illness caused by group A strep; rash starts on torso – moves to arm creases, blanches; illness also associated with sore throat and fever

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20
Q

Centor criteria for GAS pharyngitis (4 things!)

A
  1. tonsillar exudates
  2. tender anterior cervical adenopathy
  3. fever by history
  4. absence of cough
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21
Q

How can we diagnose GAS pharyngitis?

A

throat culture (gold standard) – may take 48 hours; rapid antigen detection test; test only those in whom bacterial pharyngitis is likely (if they have signs and symptoms of bacterial and no signs and symptoms suggestive of viral)

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22
Q

What would you do if you suspected GAS pharyngitis but the rapid strep test was negative?

A

perform a throat culture to confirm, along with any other indicated testing

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23
Q

Do rapid strep tests and throat culture tell us anything about distinguishing between acute infection and colonization?

A

Nope!

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24
Q

What does the IDSA recommend when deciding to treat or test adults for GAS pharyngitis?

A

advises against testing or treating adults with less than 2 Centor criteria

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25
How is GAS pharyngitis treated?
Pen V PO x 10 days, OR benzathine Pen 1.2 million units IM (a big shot!); can also used cefdinir, clindamycin, azithromycin (zithromax)
26
three complications of GAS pharyngitis
acute rheumatic fever post-strep glomerulonephritis (<7 years old) peritonsillar abscess
27
What are two signs of a peritonsillar abscess?
patient's voice may be muffled; uvula displaced away from the abscess
28
How do we treat a peritonsillar abscess and why is it so important to treat?
can be a medical emergency because it can obstruct the airways; treat with incision and drainage plus antibiotics
29
What organism causes most cases of Lemierre's Syndrome?
Fusobacterium necrophorum
30
What is Lemierre's Syndrome and what are its main complications?
a necrotizing tonsillopharyngitis followed by a Fusobacterium bacteremia; leads to septic thrombophlebitis of the internal jugular vein and subsequent metastatic abscesses (often go to lung); serious and life threatening
31
What kind of bacteria is Fusobacterium necrophorum?
Gram negative anaerobe
32
symptoms of Lemierre's Syndrome
high fever, rigors, respiratort symptoms, and unilateral neck swelling/pain; worsening pharyngitis
33
How do we diagnose Lemierre's Syndrome?
no good test but we know the organism is a gram negative anaerobe
34
Lemierre's Syndrome is resistant to what medications?
macrolides
35
What medications are used to treat Lemierre's Syndrome?
PCN and metronidazole, or with Clindamycin
36
A patient presented one week ago with pharyngitis. A rapid strep was negative and a follow up throat culture was done. He was treated empirically with Zithromax. Throat culture came back positive for non-group A streptococci. The patient now returns 10 days later with fever, worsening pharyngitis, and neck swelling. What do we suspect?
Lemierre's Syndrome, a type of bacterial pharyngitis that is very rare (1 in a million!)
37
What would a C. diphtheriae bacterial pharyngitis look like?
RARE; tightly adhering gray membrane in nares and throat
38
Is diptheria common in the United States?
NO!
39
How does a patient acquire Tularemia bacterial pharyngitis? This is rare, but when would we include it on our differential?
include on differential if the patient doesn't respond to PCN; caused by ingestion of poorly cooked wild animal meat
40
What are the findings in a patient with the rare Neisseria gonorrhoae bacterial pharyngitis? How do we culture this?
no pathognomic findings but if a patient is at risk for STDs, this could be possible; requires a special media to culture
41
Mononucleosis usually occurs in what ages?
10 to 35 (but by age 20, most have antibodies)
42
What causes mono?
EBV - Epstein Barr Virus | transmitted via saliva (kissing disease!)
43
How long does saliva remain infectious with mono?
during convalescence (for six months or longer from the time of symptom onset)
44
clinical presentation of mono
like strep throat -- myalgias and no cough
45
diagnosis of mono
throat culture or rapid strep (also a throat swab), mono spot test (blood test), EBV serology
46
treatment of mono
supportive only, and monitor for complications; advise kids to not play sports for at least four weeks
47
An acute HIV infection is also known as what?
acute retroviral syndrome or primary HIV, the initial period of infection
48
Why is an acute HIV infected patient very contagious?
viral load is high -- has not made any antibodies
49
A disproportionate number of new infections are attributable to...
acute HIV
50
What would a routine HIV test show in a patient with acute HIV?
wouldn't show infection so the diagnosis would be missed (as most are)
51
People in what age group account for HALF of HIV cases?
13-34
52
What is the clinical presentation of acute HIV similar to?
it varies but it can look like mono, Strep, or the flu
53
A viral syndrome associated with a rash and/or oral ulcers would be very suspicious for what condition?
acute HIV infection
54
symptoms of acute HIV infection
fever, malaise, RASH, myalgia/arthralgia, PHARYNGITIS, ORAL ULCERS, night sweats, weight loss
55
3 most common symptoms of acute HIV infection
fever, fatigue, rash
56
What tests do you order when suspecting acute HIV after taking a history?
HIV Ab test and a test to detect the virus like an HIV RNA test
57
Acute HIV illness usually subsides within...
14 days
58
Do we refer patients with acute HIV?
YES -- right away, to HIV specialist
59
What does a qualitative DNA PCR do?
detects cell associated proviral DNA
60
What test confirms HIV?
HIV Ab
61
T/F. Most HIV-infected individuals will not substantially reduce sexual behaviors that transmit disease once diagnosed.
FALSE! They will.
62
What two things must happen in order for you to suspect HIV and order a test?
1. patient has the signs of an acute HIV infection | 2. history of potential HIV exposure in past six weeks
63
What happens if we test an HIV-suspect patient and the antibody comes back negative, and RNA is not detected?
Retest in three months.
64
What happens if we test an HIV-suspect patient and the antibody comes back negative/indeterminate, and the RNA IS detected?
Treat as acute HIV and refer to specialist.
65
What happens if we test an HIV-suspect patient and the antibody is detected and the RNA is detected?
Treat as established HIV and refer to specialist.
66
Other than mono and HIV, what other things can cause viral pharyngitis?
HSV, Cocksackie, Adenovirus, influenza
67
What is the most common clinical manifestation of primary HSV infection in childhood?
herpetic gingivostomatis
68
precipitating factors for HSV-1
sun, trauma, stress
69
How is HSV-1 transmitted?
direct contact during viral shedding
70
T/F. Viral shedding of HSV can occur with or without lesions.
T
71
What are three tests we could use to diagnose HSV?
Viral culture Serology – HSV-1 antibodies Tzanck smear - scraping ulcer base to look for Tzanck cells (multinucleated giant cells)
72
What are Tzank cells and when are they found?
multinucleated giant cells, found in HSV but also found in varicella, CMV, pemphigous
73
How is HSV treated?
ASAP, at the onset of prodrome! Topical aciclovir and oral meds like acyclovir, valacyclovir (Valtrex), famciclovir
74
What is the etiology of hand foot and mouth disease?
coxsackie A-16 virus
75
Hand foot and mouth disease most commonly occurs in...
kids
76
How does Hand Foot and Mouth disease present?
Prodrome: low-grade fever, malaise, abdominal pain, upper respiratory symptoms Painful oral lesions (pale papules on erythematous base); may occur on hands, feet, and buttocks
77
treatment of hand foot and mouth disease
supportive (analgesics, maintain hydration)
78
How long does hand foot and mouth disease last?
2-3 days
79
herpangia vs. hand foot and mouth disease
Herpangia is similar but WORSE; also herpangia is caused by ANY Coxackie virus and hand foot and mouth disease is caused by A-16
80
How would you differentiate between lesions in HSV and hand foot and mouth disease?
Unlike HSV, the lesions in hand foot and mouth disease usually spare the gingiva and lips
81
Herpangia usually occurs in what ages?
3-10 years
82
clinical presentation of herpangia
Sudden onset fever (up to 40.6 C / 105.8 F!), sore throat, headache, myalgias, vomiting Papules on soft palate become shallow ulcers in ≈ 3 days, then heal
83
What is the treatment for herpangia?
Supportive!
84
Herpangia usually resolves within...
a week
85
Pleurodynia is what?
chest pain
86
Pleurodynia, orchitis, aspetic meningitis, and nonspecific pericarditis are associated with what?
coxsackie virus!
87
T/F. Most viral infections & many bacterial infections will resolve without complication – not necessary to identify & treat.
T
88
A 15-year-old female presents complaining of a fever, myalgias, and sore throat. Physical exam reveals a temp. of 101.4F, red exudative tonsils, and tender anterior cervical adenopathy. What tests should we run?
Rapid strep, Mono spot, HIV RNA test
89
Aphthae are also called...
oral ulcers or canker sores
90
____ is the most common cause of mouth ulcers in N. America.
Recurrent aphthous stomatitis is the most common cause of mouth ulcers in N. America
91
Recurrent aphthous stomatitis affects what percent of people?
affects ≈ 25% of the population
92
Aphthae may be associated with alterations in...
cell-mediated immunity
93
predisposing factors for aphthae
Stress, hormones, infection, immune irregularity (eg. HIV) Association with celiac disease and inflammatory bowel disease Vitamin and mineral deficiencies, e.g. deficiencies in: B vitamins, iron, folic acid, zinc
94
How do aphthous ulcers present, and how are they diagnosed?
painful, small, gray on an erythematous base – single or multiple diagnosed clinically
95
How are aphthous ulcers treated?
usually supportive; triamcinolone acetonide (steroid) in Orabase may be used; Lysine
96
A patient presents with RECURRENT oral and genital aphthae at multiple sites. What could be the diagnosis?
Behcet's
97
What is the diagnosis criteria for Behcet's?
Recurrent oral ulcers ≥ 3 x per year + 2 other clinical findings (eg. recurrent genital ulcers, eye lesions, or skin lesions)
98
How do we treat Behcet's?
Refer to rheumatologist!
99
Is leukoplakia painful?
No!
100
What is leukoplakia?
Benign but precancerous oral, white lesion
101
How can leukoplakia progress to cancer?
lesion/hyperplasia → dysplasia → squamous cell carcinoma in situ
102
Leukoplakia has an association with what virus?
HPV
103
Besides HPV, leukoplakia can be seen in association with...
inflammatory or autoimmune conditions or chronic inflammation/irritation
104
What are the risk factors for leukoplakia?
tobacco (especially smokeless) and alcohol
105
Does leukoplakia brush?
No!
106
What causes oral hairy leukoplakia? Is it benign?
EBV and associated with HIV; it is not cancerous or premalignant
107
A definitive clinical diagnosis for leukoplakia requires what?
biopsy and ENT evaluation
108
What percent of erythroplakia are dysplastic/carcinoma?
90
109
How do we treat leukoplakia?
Avoid the irritant and monitor...if it becomes dysplastic, it needs to be removed surgically.
110
Is lichen planus common?
Yes! Up to 2% of the population gets it.
111
T/F. Lichen planus is an acute, inflammatory, autoimmune disease.
F. It is a CHRONIC, inflammatory, autoimmune disease.
112
How does lichen planus present?
like lacy leukoplakia but may be erosive, difficult to diagnosis
113
How do you diagnose lichen planus?
exfoliative cytology or biopsy (ENT referral)
114
How do you treat lichen planus?
Manage the pain by using corticosteroids (topical or systemic).
115
Which has more of a chance of maligant transformation to squamous cell carcinoma -- leukoplakia or lichen planus?
leukoplakia
116
Ulcers or masses in the oral cavity that DO NOT HEAL are likely...
squamous cell carcinoma
117
Tobacco and alcohol account for up to __% of the squamous cell cancers of the head and neck.
80
118
How will you diagnose squamous cell carcinoma (SCC)?
ENT referral for biopsy
119
What bacterium causes syphillis?
Treponema palladium
120
How does syphillis present?
painless chancre
121
How is syphillis diagnosed?
Rapid Plasma Reagin (RPR) blood test
122
Who do we report syphillis to?
County Health Dept.
123
What medication and dosage do we give to treat syphillis?
Benzathine PCN G, 2.4 mu IM, one time
124
What are mucoceles?
fluid filled cavities with mucous glands lining the epithelium
125
Mucoceles are generally seen after...
mild oral trauma
126
What other body part can mucoceles show up on besides in the mouth?
labia
127
The diagnosis for mucoceles is ___
clinical
128
How are mucoceles treated?
Most rupture spontaneously, but they can be removed by cryotherapy or excision
129
Is black hairy tongue benign?
Yes!
130
What factors are associated with black hairy tongue?
antibiotic use, candida, chemo, radiation, poor oral hygiene
131
The diagnosis for black hairy tongue is __.
clinical
132
What is the treatment for black hairy tongue?
brush the affected area with toothbrush and toothpaste 2-3 times a day
133
Geographic tongue is also known as...
benign migratory glossitis
134
What is the cause of geographic tongue?
unknown
135
How does geographic tongue/benign migratory glossitis present?
Erythematous patches on dorsal tongue with circumferential white borders; lesions can change location, pattern, & size within minutes to hours; may have numerous exacerbations & remissions; the exacerbations are usually asymptomatic but can be uncomfortable
136
What is the treatment for geographic tongue?
Reassurance!
137
___ must be included in differential and ruled out for any oral pigmented lesion with any features of cutaneous melanoma.
Melanoma
138
What can we confuse with a melanoma?
an analgam tattoo -- a blue-black macule seen in area adjacent to amalgam dental filling
139
Stevens Johnson syndrome is also known as...
erythema multiforme major
140
What is the background and etiology of Stevens Johnson syndrome?
Hypersensitivity reaction Usually a drug reaction [sulfa, NSAIDs, phenytoin (Dilantin), others] Also assoc. with HSV, other infections, may be idiopathic
141
Is Stevens Johnson a life-threatening condition?
YES!
142
clinical presentation of Stevens Johnson
90% have mucosal involvement Painful ulcerations at 2 or more sites, may see erythema & edema of the lips Intraoral bullae (maybe) Skin lesions, favor trunk, may be extensive Denudation of skin
143
Intraoral bullae in Stevens Johnson suggest...
severe disease
144
How is Stevens Johnson diagnosed?
clinical picture first, then biopsy
145
How is Stevens Johnson treated?
1. discontinue the inciting medication | 2. use corticosteroids like prednisone (but there isn't a lot of good data to support this)
146
When should you admit a person with Stevens Johnson?
Blistering Mucosal involvement interferes with hydration and nutrition If extensive skin denudation, may need treatment in burn unit
147
Pemphigus is a rare, ___ blistering disease.
autoimmune
148
prevalence of pemphigus
0.75 to 5 per millon in US
149
Before antibiotics and steroids, pemphigus was fatal within __ years.
5
150
In pemphigus, autoantibodies cause ___.
acantholysis
151
What is acantholysis?
seen in pemphigus, when autoantibodies cause separation of epidermal cells from each other, forming a blister
152
What is the cause of pemphigus?
unknown, but drug induced in some cases
153
In what age groups does pemphigus commonly occur?
middle age
154
What is the onset of pemphigus like?
Insidious (slow) onset of tender flaccid bullae – rupture easily In pemphigus vulgaris, lesions appears on oral mucous membranes first, rapidly become erosive Scalp is also early site of involvement
155
What is an early site of involvement in pemphigus?
scalp
156
In pemphis vulgaris, where do lesions first appear?
oral mucous membranes
157
Nikolsky's sign
seen in pemphigus; rubbing cotton swab or finger laterally on surface of uninvolved skin causes superficial skin to slip free from deeper layers
158
In pemphigus vulgaris, the immune system attacks __ in the skin.
proteins
159
A patient with pemphigus may present only with lesions. Why is that?
bullae are fragile and rupture easily
160
How is pemphigus diagnosed?
Biopsy, Microscopy – acantholysis is hallmark finding (loss of intercellular connections)* Urgent Derm evaluation
161
How is pemphigus treated?
systemic (oral) corticosteroids and immunosuppressive agents, plus antibiotics for secondary infection; if severe, hospitalization
162
What are three complications of pemphigus?
1. fluid and electrolyte disturbance 2. decreased nutritional intake 3. secondary infection
163
What is the most frequent cause of death in pemphigus patients?
secondary infection with Staph aureus, causing septicemia
164
T/F. The course of pemphigus tends to be acute in most patients.
F. CHRONIC
165
What is bullous pemphigoid?
autoimmune blistering disease
166
How does bullous pemphigoid compare to pemphigus?
Like pemphigous, it is autoimmune, and it also has an unknown cause and can sometimes be drug induced. It also involves blistering. Unlike pemphigous, acantholysis is not seen. Also, it is a benign prutitic condition.
167
cause of bullous pemphigoid
autoimmune, unknown (may be drug induced)
168
Who is affected more by bullous pemphigoid?
People over 60, and men > women
169
What is bullous pemphigoid characterized by?
tense blisters in flexural areas; may be preceded by uticaria (hives) or edematous lesions for months
170
1/3 of bullous pemphoid patients also have ___.
oral lesions
171
Which is more common -- bullous pemphigoid or pemphigus vulgaris?
bullous pemphigoid (2x)
172
The combination of __ and __ is characteristic of bullous pemphigoid.
bullous lesions and urticarial plaques
173
How is bullous pemphigoid diagnosed?
biopsy, light microscopy -- shows epidermal blister; derm referral
174
How is bullous pemphigoid treated?
corticosteroids, immunosuppressive agents
175
T/F. Bullous pemphigoid is characterized by exacerbations and remissions.
T
176
Which is more rare and serious -- bullous pemphigoid or pemphigus vulgaris?
pemphigus vulgaris
177
Which has oral lesions -- bullous pemphigoid or pemphigus vulgaris?
oral lesions are common in pemphigus vulgaris, and only in a third of patients with bullous pemphigoid
178
How do the methods of diagnosis compare in bullous pemphigoid or pemphigus vulgaris?
bullous pemphigoid = biopsy and epidermal blister; pemphigus vulgaris = Nikolsky's sign and biopsy
179
How do the treatment methods of bullous pemphigoid and pemphigus vulgaris compare?
Both are treated with corticosteroids and immunosuppressive agents.
180
If a patient presents with blisters and no history of burn, what would you suspect?
Take it seriously! Could be Stevens Johnson, pemphigus, or bullous pemphigoid!
181
bullae
large blister or skin vesicle
182
denudation
removal of protective layer
183
exanthem
rash associated with an infection / inflammation, eg. the rash associated with measles is an exanthem
184
corticosteroids
class of drugs that includes steroid hormones naturally produced by the adrenal cortex; strong anti inflammatories