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Ulcers Flashcards

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1
Q

What are the clinical features of acute viral stomatitis?

A

Prodrome, vesicle formation, ulcers, pain, increased salivation, and virus dissemination.

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2
Q

How do vesicles in viral stomatitis transform into ulcers?

A

Vesicles rupture due to humidity, mechanical irritation, and high temperature, forming small, shallow ulcers.

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3
Q

What are the primary treatments for viral stomatitis?

A

Symptomatic treatment, bed rest, supportive therapy, analgesics, topical anesthetics, antipyretics, and antiviral drugs in severe cases.

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4
Q

Why are corticosteroids contraindicated in viral infections?

A

They decrease body resistance and can lead to the dissemination of the viral infection.

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5
Q

What are the main herpes viruses that infect humans?

A

HSV type 1, HSV type 2, Varicella-Zoster Virus (VZV), Cytomegalovirus, and Epstein-Barr Virus (EBV).

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6
Q

What are the characteristics of herpes simplex virus (HSV) latency?

A

The virus remains latent in ganglia after primary infection and can reactivate to cause recurrent infections.

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7
Q

What distinguishes primary herpetic gingivostomatitis from recurrent herpetic lesions?

A

Primary infection occurs with no prior immunity, while recurrent lesions are due to the reactivation of latent virus.

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8
Q

What are the key clinical features of acute herpetic gingivostomatitis (AHGS)?

A

Prodrome, acute marginal gingivitis, vesicles, excessive salivation, and self-limiting course.

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9
Q

How is AHGS diagnosed?

A

Case history, clinical examination, cytological smear, HSV isolation, antibody titer, and leukocyte count.

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10
Q

What is the recommended treatment for severe AHGS?

A

Acyclovir, along with symptomatic treatments such as bed rest, analgesics, and antiseptic mouth rinses.

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11
Q

What are the symptoms of herpetic whitlow?

A

Itching, pain of the infected fingers, deep vesicles that may coalesce.

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12
Q

What are common predisposing factors for recurrent herpes labialis (cold sores)?

A

Trauma, common cold, sun exposure, stress, and immune suppression.

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13
Q

How should recurrent herpes labialis be treated?

A

Sun blocker, acyclovir ointment, and in immunocompromised patients, oral acyclovir.

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14
Q

How do recurrent intraoral herpes lesions typically present?

A

Vesicles on keratinized mucosa that rupture into painful ulcers surrounded by erythema.

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15
Q

What makes herpes simplex virus infections aggressive in immunocompromised patients?

A

The lesions are more severe, larger, and last longer, often involving multiple sites.

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16
Q

What are the clinical features of chickenpox (varicella)?

A

Mild fever, successive waves of vesicular rash, and oral lesions.

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17
Q

How is chickenpox treated in healthy children versus immune-compromised patients?

A

Healthy children: Self-limiting; Immune-compromised patients: Acyclovir.

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18
Q

What distinguishes herpes zoster from chickenpox?

A

Herpes zoster is a reactivation of latent VZV causing unilateral vesicular rash along a dermatome.

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19
Q

What are common complications of herpes zoster?

A

Post-herpetic neuralgia, generalized herpes zoster, motor nerve involvement, secondary infections, and ophthalmic involvement.

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20
Q

How is herpes zoster treated in healthy patients versus immunocompromised patients?

A

Healthy patients: Acyclovir ointment or oral acyclovir; Immunocompromised: IV acyclovir.

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21
Q

What is Ramsay Hunt Syndrome and its main clinical feature?

A

Herpes zoster affecting the facial nerve, presenting with ear pain, vesicles, and facial paralysis.

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22
Q

How should Ramsay Hunt Syndrome be treated?

A

Acyclovir plus prednisone or ACTH, and carbamazepine for pain management.

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23
Q

What are the key diagnostic features of herpes zoster?

A

Unilateral vesicular rash along the course of an affected nerve, often with prodromal pain.

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24
Q

What is the significance of the viral culture and cytology in diagnosing herpes simplex?

A

To confirm HSV infection when clinical manifestations are unclear.

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25
Why is acyclovir most effective when used early in the disease process?
It inhibits viral replication effectively in the early stages, reducing resistance and improving outcomes.
26
How does varicella-zoster virus (VZV) spread in chickenpox?
Through respiratory droplets or direct contact with skin lesions.
27
What are common oral manifestations of herpes zoster?
Painful ulcers that heal with scar formation, often involving one or more branches of the trigeminal nerve.
28
How do complications like post-herpetic neuralgia arise in herpes zoster?
From inflammation and fibrosis of the affected nerve, causing persistent pain even after the rash has healed.
29
What are the differences between herpes zoster and herpes simplex infections?
Herpes zoster is unilateral and follows a dermatome; herpes simplex is more localized and may recur in the same area.
30
What is the causative virus for herpangina and hand, foot, and mouth disease?
Coxsackie virus A
31
How is Coxsackie virus primarily transmitted?
Contaminated saliva, air-borne spread, and oro-fecal contamination
32
What age group is primarily affected by Coxsackie virus infections?
Children and occasionally adults
33
What are the common oral lesions of herpangina?
Bilateral vesicles on soft palate, uvula, and pharynx that rupture to form shallow ulcers
34
What extraoral lesions are seen in hand, foot, and mouth disease?
Macules, papules, and vesicles on the skin of hands and feet
35
What is the typical clinical presentation of erythema multiforme simplex?
**Macules, papules, and vesicles** on hands, feet, elbows, knees, face, and neck with **target** lesions
36
What distinguishes Stevens-Johnson syndrome from erythema multiforme simplex?
Stevens-Johnson syndrome involves skin, oral mucosa, eyes, and genitals with systemic manifestations
37
How is toxic epidermal necrolysis (TEN) managed?
Hospitalization, skin grafting, and correction of fluid and electrolyte imbalances
38
What are the primary oral manifestations of erythema multiforme?
Large, irregular ulcers with red halo, often starting as bullae on an erythematous base
39
How can erythema multiforme be differentiated from acute herpetic gingivostomatitis?
EM ulcers are larger, irregular, and more likely to involve lips, whereas AHGS ulcers are smaller and more uniform
40
What causes oral ulcers secondary to cancer chemotherapy?
Direct damage to oral epithelial cells by drugs like methotrexate and indirect effects through immune suppression
41
How do oral ulcers from chemotherapy typically resolve?
They resolve within 2-3 weeks after cessation of therapy
42
What is a common feature of chronic multiple ulcers?
Persistent lesions due to conditions like pemphigus vulgaris or subepithelial bullous dermatoses
43
What is the mechanism of pemphigus vulgaris?
Autoantibodies against desmosomal glycoproteins causing loss of cell-to-cell adhesion
44
What is the typical age and sex demographic for pemphigus vulgaris?
Middle-aged individuals, with a higher prevalence in females
45
What is the key clinical feature of pemphigus vulgaris?
Thin-walled flaccid bullae that rapidly break to form shallow, bleeding ulcers
46
What is Nikolsky’s sign and how does it relate to pemphigus vulgaris?
Lateral pressure causes peeling of the epithelium or appearance of bullae, indicating acantholysis
47
How is pemphigus vulgaris diagnosed definitively?
Biopsy showing Tzanck cells, direct immunofluorescence, and indirect immunofluorescence
48
What treatment options are used for pemphigus vulgaris?
Systemic corticosteroids, azathioprine, topical steroids, systemic antibiotics, and antifungals
49
What is mucous membrane pemphigoid?
A chronic autoimmune disease affecting mucous membranes, leading to ulceration and scarring
50
What are common oral manifestations of mucous membrane pemphigoid?
Erosions or intact bulla that rupture to form ulcers with scar formation
51
How can mucous membrane pemphigoid be distinguished from pemphigus vulgaris?
MMP has thicker walled bullae and is slower developing, with smaller, less extensive lesions compared to PV
52
What is the typical age and sex for mucous membrane pemphigoid?
Over 50 years old, with a higher prevalence in females
53
What is bullous lichen planus?
A form of oral lichen planus presenting as chronic, **multiple irregular** ulcers surrounded by **Wickham’s** striae
54
How is bullous lichen planus differentiated from other forms of oral lichen planus?
It involves subepithelial bullae and is characterized by chronic, irregular ulcers
55
What is the common treatment for subepithelial bullous dermatoses?
Topical **steroids**, **scaling and root** planing, and sometimes **systemic corticosteroids**
56
How are oral ulcers secondary to chemotherapy managed?
**Antiseptic** mouth rinses, topical **anesthetics**, and **antibiotics** for secondary infections
57
What are the clinical signs of erythema multiforme major forms?
Stevens-Johnson syndrome shows generalized vesicles and systemic symptoms; TEN results in extensive skin sloughing
58
What is recurrent aphthous stomatitis (RAS)?
RAS is a disorder characterized by recurring ulcers confined to the oral mucosa.
59
What are the three categories of RAS?
Minor ulcers, Major ulcers, and Herpetiform ulcers.
60
What are the typical features of minor aphthous ulcers?
Small, shallow, round ulcers with an erythematous halo, healing without scar formation.
61
How do major aphthous ulcers differ from minor ones?
Major ulcers are larger, deeper, and painful, often leaving scars.
62
What are herpetiform aphthous ulcers?
Small, multiple, painful ulcers that appear in adults and heal without scarring.
63
What genetic factors are associated with RAS?
Heredity factors, with a higher chance if parents have RAS; specific HLA antigens.
64
How does serum iron deficiency relate to RAS?
Serum iron deficiency is one of the hematologic deficiencies linked to RAS.
65
What immunologic abnormalities are seen in RAS patients?
Increased lymphocytoxicity, antibody-dependent cytotoxicity, altered lymphocyte ratios.
66
Name some other etiologic factors for RAS.
Trauma, psychological stress, food allergies, hormonal disturbances.
67
How can RAS be associated with gastrointestinal diseases?
It may occur with Crohn's disease and ulcerative colitis.
68
What distinguishes RAS from Behcet's syndrome?
Behcet's syndrome includes genital ulcers, eye lesions, and a positive pathergy test.
69
How is Behcet's syndrome diagnosed?
By recurrent oral ulcers plus two of the following: genital ulcers, eye lesions, skin lesions, or positive pathergy test.
70
What is the most common skin manifestation in Behcet's syndrome?
Large pustules or lesions precipitated by trauma.
71
What are the typical oral lesions in Reiter’s syndrome?
Scalloped white lines surrounding red areas, resembling geographic tongue.
72
What is the first step in managing traumatic oral ulcers?
Removal of the source of trauma.
73
How do you differentiate a traumatic ulcer from a malignant ulcer?
Traumatic ulcers resolve quickly after removing the cause, while malignant ulcers are persistent and often painless.
74
What are the characteristics of a tuberculous oral ulcer?
Irregular, chronic, painful ulcer with indurated base and undermined edge.
75
What is the appearance of primary syphilis in the oral mucosa?
A painless, single ulcer (chancre) with an indurated base.
76
What is a key feature of secondary syphilis oral lesions?
Mucous patches and condyloma latum.
77
How does tertiary syphilis affect the oral cavity?
It can cause gumma affecting the hard palate or tongue, leading to perforation.
78
What is the main adverse effect of glucocorticoids on carbohydrate metabolism?
Hyperglycemia, potentially leading to diabetes.
79
How do glucocorticoids affect fat metabolism?
They induce lipolysis and redistribute fat to face, abdomen, and shoulders.
80
What is a common side effect of glucocorticoids related to protein metabolism?
Muscle wasting and thinning of the skin.
81
What is a major adverse effect of glucocorticoids on salt and water metabolism?
Edema, hypertension, and osteoporosis.
82
How do glucocorticoids impact the immune system?
They suppress inflammation and immune response, potentially spreading infections.
83
What is a significant side effect of glucocorticoids on the gastrointestinal system?
Peptic ulcers due to increased HCl and pepsin production.
84
How do glucocorticoids affect the central nervous system?
They can cause euphoria, behavioral changes, or psychosis.
85
What is a common treatment for Reiter's syndrome?
NSAIDs (Non-Steroidal Anti-Inflammatory Drugs).
86
What is a key diagnostic criterion for Behcet’s Syndrome?
Recurrent oral ulceration plus two other manifestations such as genital ulcers or eye lesions.
87
How is RAS differentiated from RIOH (Recurrent Intraoral Hyperplasia)?
RAS affects non-keratinized mucosa without tissue tags; RIOH affects keratinized mucosa with tissue tags.
88
What laboratory investigations are needed to manage severe RAU?
Tests for serum iron, folate, and vitamin B-12 levels.
89
What is the typical healing time for minor aphthous ulcers?
Healing usually occurs within 7 to 10 days without scar formation.
90
What treatment is recommended for severe RAU?
Intralesional steroid injections or systemic corticosteroids.
91
How are herpetiform aphthous ulcers treated?
They are treated symptomatically and heal within 7-10 days without scarring.
92
What are some common drugs tried for RAU management?
Colchicine, thalidomide, azathioprine, and pentoxifylline.
93
Why should caustic agents not be applied to RAU lesions?
They cause tissue damage, delay healing, and lead to scar formation.
94
What is a distinguishing feature of malignant oral ulcers compared to benign ones?
Malignant ulcers are large, deep, and often have everted edges with an indurated base.
95
What is a key feature of a traumatic oral ulcer?
It usually resolves within 1 to 2 weeks after removing the cause.
96
How do you diagnose a traumatic ulcer?
Based on history, clinical examination, and rapid resolution after removing the cause.
97
What is the treatment for a squamous cell carcinoma of the oral mucosa?
Treatment typically involves surgical excision and possibly radiation or chemotherapy.
98
What is a key diagnostic feature of primary syphilis oral ulcers?
A painless, single ulcer (chancre) with an indurated base.
99
What are the systemic manifestations of Behcet’s syndrome?
Arthritis, central nervous system involvement, and venous thrombosis.

Oral medicine (7 decks)

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