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
Q

How is GAS pharyngitis treated?

A

Pen V PO x 10 days, OR benzathine Pen 1.2 million units IM (a big shot!); can also used cefdinir, clindamycin, azithromycin (zithromax)

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26
Q

three complications of GAS pharyngitis

A

acute rheumatic fever
post-strep glomerulonephritis (<7 years old)
peritonsillar abscess

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27
Q

What are two signs of a peritonsillar abscess?

A

patient’s voice may be muffled; uvula displaced away from the abscess

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28
Q

How do we treat a peritonsillar abscess and why is it so important to treat?

A

can be a medical emergency because it can obstruct the airways; treat with incision and drainage plus antibiotics

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29
Q

What organism causes most cases of Lemierre’s Syndrome?

A

Fusobacterium necrophorum

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30
Q

What is Lemierre’s Syndrome and what are its main complications?

A

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

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31
Q

What kind of bacteria is Fusobacterium necrophorum?

A

Gram negative anaerobe

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32
Q

symptoms of Lemierre’s Syndrome

A

high fever, rigors, respiratort symptoms, and unilateral neck swelling/pain; worsening pharyngitis

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33
Q

How do we diagnose Lemierre’s Syndrome?

A

no good test but we know the organism is a gram negative anaerobe

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34
Q

Lemierre’s Syndrome is resistant to what medications?

A

macrolides

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35
Q

What medications are used to treat Lemierre’s Syndrome?

A

PCN and metronidazole, or with Clindamycin

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36
Q

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?

A

Lemierre’s Syndrome, a type of bacterial pharyngitis that is very rare (1 in a million!)

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37
Q

What would a C. diphtheriae bacterial pharyngitis look like?

A

RARE; tightly adhering gray membrane in nares and throat

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38
Q

Is diptheria common in the United States?

A

NO!

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39
Q

How does a patient acquire Tularemia bacterial pharyngitis? This is rare, but when would we include it on our differential?

A

include on differential if the patient doesn’t respond to PCN; caused by ingestion of poorly cooked wild animal meat

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40
Q

What are the findings in a patient with the rare Neisseria gonorrhoae bacterial pharyngitis? How do we culture this?

A

no pathognomic findings but if a patient is at risk for STDs, this could be possible; requires a special media to culture

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41
Q

Mononucleosis usually occurs in what ages?

A

10 to 35 (but by age 20, most have antibodies)

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42
Q

What causes mono?

A

EBV - Epstein Barr Virus

transmitted via saliva (kissing disease!)

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43
Q

How long does saliva remain infectious with mono?

A

during convalescence (for six months or longer from the time of symptom onset)

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44
Q

clinical presentation of mono

A

like strep throat – myalgias and no cough

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45
Q

diagnosis of mono

A

throat culture or rapid strep (also a throat swab), mono spot test (blood test), EBV serology

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46
Q

treatment of mono

A

supportive only, and monitor for complications; advise kids to not play sports for at least four weeks

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47
Q

An acute HIV infection is also known as what?

A

acute retroviral syndrome or primary HIV, the initial period of infection

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48
Q

Why is an acute HIV infected patient very contagious?

A

viral load is high – has not made any antibodies

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49
Q

A disproportionate number of new infections are attributable to…

A

acute HIV

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50
Q

What would a routine HIV test show in a patient with acute HIV?

A

wouldn’t show infection so the diagnosis would be missed (as most are)

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51
Q

People in what age group account for HALF of HIV cases?

A

13-34

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52
Q

What is the clinical presentation of acute HIV similar to?

A

it varies but it can look like mono, Strep, or the flu

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53
Q

A viral syndrome associated with a rash and/or oral ulcers would be very suspicious for what condition?

A

acute HIV infection

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54
Q

symptoms of acute HIV infection

A

fever, malaise, RASH, myalgia/arthralgia, PHARYNGITIS, ORAL ULCERS, night sweats, weight loss

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55
Q

3 most common symptoms of acute HIV infection

A

fever, fatigue, rash

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56
Q

What tests do you order when suspecting acute HIV after taking a history?

A

HIV Ab test and a test to detect the virus like an HIV RNA test

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57
Q

Acute HIV illness usually subsides within…

A

14 days

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58
Q

Do we refer patients with acute HIV?

A

YES – right away, to HIV specialist

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59
Q

What does a qualitative DNA PCR do?

A

detects cell associated proviral DNA

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60
Q

What test confirms HIV?

A

HIV Ab

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61
Q

T/F. Most HIV-infected individuals will not substantially reduce sexual behaviors that transmit disease once diagnosed.

A

FALSE! They will.

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62
Q

What two things must happen in order for you to suspect HIV and order a test?

A
  1. patient has the signs of an acute HIV infection

2. history of potential HIV exposure in past six weeks

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63
Q

What happens if we test an HIV-suspect patient and the antibody comes back negative, and RNA is not detected?

A

Retest in three months.

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64
Q

What happens if we test an HIV-suspect patient and the antibody comes back negative/indeterminate, and the RNA IS detected?

A

Treat as acute HIV and refer to specialist.

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65
Q

What happens if we test an HIV-suspect patient and the antibody is detected and the RNA is detected?

A

Treat as established HIV and refer to specialist.

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66
Q

Other than mono and HIV, what other things can cause viral pharyngitis?

A

HSV, Cocksackie, Adenovirus, influenza

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67
Q

What is the most common clinical manifestation of primary HSV infection in childhood?

A

herpetic gingivostomatis

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68
Q

precipitating factors for HSV-1

A

sun, trauma, stress

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69
Q

How is HSV-1 transmitted?

A

direct contact during viral shedding

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70
Q

T/F. Viral shedding of HSV can occur with or without lesions.

A

T

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71
Q

What are three tests we could use to diagnose HSV?

A

Viral culture
Serology – HSV-1 antibodies
Tzanck smear - scraping ulcer base to look for Tzanck cells (multinucleated giant cells)

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72
Q

What are Tzank cells and when are they found?

A

multinucleated giant cells, found in HSV but also found in varicella, CMV, pemphigous

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73
Q

How is HSV treated?

A

ASAP, at the onset of prodrome! Topical aciclovir and oral meds like acyclovir, valacyclovir (Valtrex), famciclovir

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74
Q

What is the etiology of hand foot and mouth disease?

A

coxsackie A-16 virus

75
Q

Hand foot and mouth disease most commonly occurs in…

A

kids

76
Q

How does Hand Foot and Mouth disease present?

A

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
Q

treatment of hand foot and mouth disease

A

supportive (analgesics, maintain hydration)

78
Q

How long does hand foot and mouth disease last?

A

2-3 days

79
Q

herpangia vs. hand foot and mouth disease

A

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
Q

How would you differentiate between lesions in HSV and hand foot and mouth disease?

A

Unlike HSV, the lesions in hand foot and mouth disease usually spare the gingiva and lips

81
Q

Herpangia usually occurs in what ages?

A

3-10 years

82
Q

clinical presentation of herpangia

A

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
Q

What is the treatment for herpangia?

A

Supportive!

84
Q

Herpangia usually resolves within…

A

a week

85
Q

Pleurodynia is what?

A

chest pain

86
Q

Pleurodynia, orchitis, aspetic meningitis, and nonspecific pericarditis are associated with what?

A

coxsackie virus!

87
Q

T/F. Most viral infections & many bacterial infections will resolve without complication – not necessary to identify & treat.

A

T

88
Q

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?

A

Rapid strep, Mono spot, HIV RNA test

89
Q

Aphthae are also called…

A

oral ulcers or canker sores

90
Q

____ is the most common cause of mouth ulcers in N. America.

A

Recurrent aphthous stomatitis is the most common cause of mouth ulcers in N. America

91
Q

Recurrent aphthous stomatitis affects what percent of people?

A

affects ≈ 25% of the population

92
Q

Aphthae may be associated with alterations in…

A

cell-mediated immunity

93
Q

predisposing factors for aphthae

A

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
Q

How do aphthous ulcers present, and how are they diagnosed?

A

painful, small, gray on an erythematous base – single or multiple

diagnosed clinically

95
Q

How are aphthous ulcers treated?

A

usually supportive; triamcinolone acetonide (steroid) in Orabase may be used; Lysine

96
Q

A patient presents with RECURRENT oral and genital aphthae at multiple sites. What could be the diagnosis?

A

Behcet’s

97
Q

What is the diagnosis criteria for Behcet’s?

A

Recurrent oral ulcers ≥ 3 x per year + 2 other clinical findings (eg. recurrent genital ulcers, eye lesions, or skin lesions)

98
Q

How do we treat Behcet’s?

A

Refer to rheumatologist!

99
Q

Is leukoplakia painful?

A

No!

100
Q

What is leukoplakia?

A

Benign but precancerous oral, white lesion

101
Q

How can leukoplakia progress to cancer?

A

lesion/hyperplasia → dysplasia → squamous cell carcinoma in situ

102
Q

Leukoplakia has an association with what virus?

A

HPV

103
Q

Besides HPV, leukoplakia can be seen in association with…

A

inflammatory or autoimmune conditions or chronic inflammation/irritation

104
Q

What are the risk factors for leukoplakia?

A

tobacco (especially smokeless) and alcohol

105
Q

Does leukoplakia brush?

A

No!

106
Q

What causes oral hairy leukoplakia? Is it benign?

A

EBV and associated with HIV; it is not cancerous or premalignant

107
Q

A definitive clinical diagnosis for leukoplakia requires what?

A

biopsy and ENT evaluation

108
Q

What percent of erythroplakia are dysplastic/carcinoma?

A

90

109
Q

How do we treat leukoplakia?

A

Avoid the irritant and monitor…if it becomes dysplastic, it needs to be removed surgically.

110
Q

Is lichen planus common?

A

Yes! Up to 2% of the population gets it.

111
Q

T/F. Lichen planus is an acute, inflammatory, autoimmune disease.

A

F. It is a CHRONIC, inflammatory, autoimmune disease.

112
Q

How does lichen planus present?

A

like lacy leukoplakia but may be erosive, difficult to diagnosis

113
Q

How do you diagnose lichen planus?

A

exfoliative cytology or biopsy (ENT referral)

114
Q

How do you treat lichen planus?

A

Manage the pain by using corticosteroids (topical or systemic).

115
Q

Which has more of a chance of maligant transformation to squamous cell carcinoma – leukoplakia or lichen planus?

A

leukoplakia

116
Q

Ulcers or masses in the oral cavity that DO NOT HEAL are likely…

A

squamous cell carcinoma

117
Q

Tobacco and alcohol account for up to __% of the squamous cell cancers of the head and neck.

A

80

118
Q

How will you diagnose squamous cell carcinoma (SCC)?

A

ENT referral for biopsy

119
Q

What bacterium causes syphillis?

A

Treponema palladium

120
Q

How does syphillis present?

A

painless chancre

121
Q

How is syphillis diagnosed?

A

Rapid Plasma Reagin (RPR) blood test

122
Q

Who do we report syphillis to?

A

County Health Dept.

123
Q

What medication and dosage do we give to treat syphillis?

A

Benzathine PCN G, 2.4 mu IM, one time

124
Q

What are mucoceles?

A

fluid filled cavities with mucous glands lining the epithelium

125
Q

Mucoceles are generally seen after…

A

mild oral trauma

126
Q

What other body part can mucoceles show up on besides in the mouth?

A

labia

127
Q

The diagnosis for mucoceles is ___

A

clinical

128
Q

How are mucoceles treated?

A

Most rupture spontaneously, but they can be removed by cryotherapy or excision

129
Q

Is black hairy tongue benign?

A

Yes!

130
Q

What factors are associated with black hairy tongue?

A

antibiotic use, candida, chemo, radiation, poor oral hygiene

131
Q

The diagnosis for black hairy tongue is __.

A

clinical

132
Q

What is the treatment for black hairy tongue?

A

brush the affected area with toothbrush and toothpaste 2-3 times a day

133
Q

Geographic tongue is also known as…

A

benign migratory glossitis

134
Q

What is the cause of geographic tongue?

A

unknown

135
Q

How does geographic tongue/benign migratory glossitis present?

A

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
Q

What is the treatment for geographic tongue?

A

Reassurance!

137
Q

___ must be included in differential and ruled out for any oral pigmented lesion with any features of cutaneous melanoma.

A

Melanoma

138
Q

What can we confuse with a melanoma?

A

an analgam tattoo – a blue-black macule seen in area adjacent to amalgam dental filling

139
Q

Stevens Johnson syndrome is also known as…

A

erythema multiforme major

140
Q

What is the background and etiology of Stevens Johnson syndrome?

A

Hypersensitivity reaction
Usually a drug reaction [sulfa, NSAIDs, phenytoin (Dilantin), others]
Also assoc. with HSV, other infections, may be idiopathic

141
Q

Is Stevens Johnson a life-threatening condition?

A

YES!

142
Q

clinical presentation of Stevens Johnson

A

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
Q

Intraoral bullae in Stevens Johnson suggest…

A

severe disease

144
Q

How is Stevens Johnson diagnosed?

A

clinical picture first, then biopsy

145
Q

How is Stevens Johnson treated?

A
  1. discontinue the inciting medication

2. use corticosteroids like prednisone (but there isn’t a lot of good data to support this)

146
Q

When should you admit a person with Stevens Johnson?

A

Blistering
Mucosal involvement interferes with hydration and nutrition
If extensive skin denudation, may need treatment in burn unit

147
Q

Pemphigus is a rare, ___ blistering disease.

A

autoimmune

148
Q

prevalence of pemphigus

A

0.75 to 5 per millon in US

149
Q

Before antibiotics and steroids, pemphigus was fatal within __ years.

A

5

150
Q

In pemphigus, autoantibodies cause ___.

A

acantholysis

151
Q

What is acantholysis?

A

seen in pemphigus, when autoantibodies cause separation of epidermal cells from each other, forming a blister

152
Q

What is the cause of pemphigus?

A

unknown, but drug induced in some cases

153
Q

In what age groups does pemphigus commonly occur?

A

middle age

154
Q

What is the onset of pemphigus like?

A

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
Q

What is an early site of involvement in pemphigus?

A

scalp

156
Q

In pemphis vulgaris, where do lesions first appear?

A

oral mucous membranes

157
Q

Nikolsky’s sign

A

seen in pemphigus; rubbing cotton swab or finger laterally on surface of uninvolved skin causes superficial skin to slip free from deeper layers

158
Q

In pemphigus vulgaris, the immune system attacks __ in the skin.

A

proteins

159
Q

A patient with pemphigus may present only with lesions. Why is that?

A

bullae are fragile and rupture easily

160
Q

How is pemphigus diagnosed?

A

Biopsy, Microscopy – acantholysis is hallmark finding (loss of intercellular connections)*
Urgent Derm evaluation

161
Q

How is pemphigus treated?

A

systemic (oral) corticosteroids and immunosuppressive agents, plus antibiotics for secondary infection; if severe, hospitalization

162
Q

What are three complications of pemphigus?

A
  1. fluid and electrolyte disturbance
  2. decreased nutritional intake
  3. secondary infection
163
Q

What is the most frequent cause of death in pemphigus patients?

A

secondary infection with Staph aureus, causing septicemia

164
Q

T/F. The course of pemphigus tends to be acute in most patients.

A

F. CHRONIC

165
Q

What is bullous pemphigoid?

A

autoimmune blistering disease

166
Q

How does bullous pemphigoid compare to pemphigus?

A

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
Q

cause of bullous pemphigoid

A

autoimmune, unknown (may be drug induced)

168
Q

Who is affected more by bullous pemphigoid?

A

People over 60, and men > women

169
Q

What is bullous pemphigoid characterized by?

A

tense blisters in flexural areas; may be preceded by uticaria (hives) or edematous lesions for months

170
Q

1/3 of bullous pemphoid patients also have ___.

A

oral lesions

171
Q

Which is more common – bullous pemphigoid or pemphigus vulgaris?

A

bullous pemphigoid (2x)

172
Q

The combination of __ and __ is characteristic of bullous pemphigoid.

A

bullous lesions and urticarial plaques

173
Q

How is bullous pemphigoid diagnosed?

A

biopsy, light microscopy – shows epidermal blister; derm referral

174
Q

How is bullous pemphigoid treated?

A

corticosteroids, immunosuppressive agents

175
Q

T/F. Bullous pemphigoid is characterized by exacerbations and remissions.

A

T

176
Q

Which is more rare and serious – bullous pemphigoid or pemphigus vulgaris?

A

pemphigus vulgaris

177
Q

Which has oral lesions – bullous pemphigoid or pemphigus vulgaris?

A

oral lesions are common in pemphigus vulgaris, and only in a third of patients with bullous pemphigoid

178
Q

How do the methods of diagnosis compare in bullous pemphigoid or pemphigus vulgaris?

A

bullous pemphigoid = biopsy and epidermal blister; pemphigus vulgaris = Nikolsky’s sign and biopsy

179
Q

How do the treatment methods of bullous pemphigoid and pemphigus vulgaris compare?

A

Both are treated with corticosteroids and immunosuppressive agents.

180
Q

If a patient presents with blisters and no history of burn, what would you suspect?

A

Take it seriously! Could be Stevens Johnson, pemphigus, or bullous pemphigoid!

181
Q

bullae

A

large blister or skin vesicle

182
Q

denudation

A

removal of protective layer

183
Q

exanthem

A

rash associated with an infection / inflammation, eg. the rash associated with measles is an exanthem

184
Q

corticosteroids

A

class of drugs that includes steroid hormones naturally produced by the adrenal cortex; strong anti inflammatories