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Oral medicine > Ulcers > Flashcards

Ulcers Flashcards

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
Q

Why is acyclovir most effective when used early in the disease process?

A

It inhibits viral replication effectively in the early stages, reducing resistance and improving outcomes.

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26
Q

How does varicella-zoster virus (VZV) spread in chickenpox?

A

Through respiratory droplets or direct contact with skin lesions.

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27
Q

What are common oral manifestations of herpes zoster?

A

Painful ulcers that heal with scar formation, often involving one or more branches of the trigeminal nerve.

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28
Q

How do complications like post-herpetic neuralgia arise in herpes zoster?

A

From inflammation and fibrosis of the affected nerve, causing persistent pain even after the rash has healed.

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29
Q

What are the differences between herpes zoster and herpes simplex infections?

A

Herpes zoster is unilateral and follows a dermatome; herpes simplex is more localized and may recur in the same area.

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30
Q

What is the causative virus for herpangina and hand, foot, and mouth disease?

A

Coxsackie virus A

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31
Q

How is Coxsackie virus primarily transmitted?

A

Contaminated saliva, air-borne spread, and oro-fecal contamination

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32
Q

What age group is primarily affected by Coxsackie virus infections?

A

Children and occasionally adults

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33
Q

What are the common oral lesions of herpangina?

A

Bilateral vesicles on soft palate, uvula, and pharynx that rupture to form shallow ulcers

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34
Q

What extraoral lesions are seen in hand, foot, and mouth disease?

A

Macules, papules, and vesicles on the skin of hands and feet

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35
Q

What is the typical clinical presentation of erythema multiforme simplex?

A

Macules, papules, and vesicles on hands, feet, elbows, knees, face, and neck with target lesions

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36
Q

What distinguishes Stevens-Johnson syndrome from erythema multiforme simplex?

A

Stevens-Johnson syndrome involves skin, oral mucosa, eyes, and genitals with systemic manifestations

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37
Q

How is toxic epidermal necrolysis (TEN) managed?

A

Hospitalization, skin grafting, and correction of fluid and electrolyte imbalances

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38
Q

What are the primary oral manifestations of erythema multiforme?

A

Large, irregular ulcers with red halo, often starting as bullae on an erythematous base

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39
Q

How can erythema multiforme be differentiated from acute herpetic gingivostomatitis?

A

EM ulcers are larger, irregular, and more likely to involve lips, whereas AHGS ulcers are smaller and more uniform

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40
Q

What causes oral ulcers secondary to cancer chemotherapy?

A

Direct damage to oral epithelial cells by drugs like methotrexate and indirect effects through immune suppression

41
Q

How do oral ulcers from chemotherapy typically resolve?

A

They resolve within 2-3 weeks after cessation of therapy

42
Q

What is a common feature of chronic multiple ulcers?

A

Persistent lesions due to conditions like pemphigus vulgaris or subepithelial bullous dermatoses

43
Q

What is the mechanism of pemphigus vulgaris?

A

Autoantibodies against desmosomal glycoproteins causing loss of cell-to-cell adhesion

44
Q

What is the typical age and sex demographic for pemphigus vulgaris?

A

Middle-aged individuals, with a higher prevalence in females

45
Q

What is the key clinical feature of pemphigus vulgaris?

A

Thin-walled flaccid bullae that rapidly break to form shallow, bleeding ulcers

46
Q

What is Nikolsky’s sign and how does it relate to pemphigus vulgaris?

A

Lateral pressure causes peeling of the epithelium or appearance of bullae, indicating acantholysis

47
Q

How is pemphigus vulgaris diagnosed definitively?

A

Biopsy showing Tzanck cells, direct immunofluorescence, and indirect immunofluorescence

48
Q

What treatment options are used for pemphigus vulgaris?

A

Systemic corticosteroids, azathioprine, topical steroids, systemic antibiotics, and antifungals

49
Q

What is mucous membrane pemphigoid?

A

A chronic autoimmune disease affecting mucous membranes, leading to ulceration and scarring

50
Q

What are common oral manifestations of mucous membrane pemphigoid?

A

Erosions or intact bulla that rupture to form ulcers with scar formation

51
Q

How can mucous membrane pemphigoid be distinguished from pemphigus vulgaris?

A

MMP has thicker walled bullae and is slower developing, with smaller, less extensive lesions compared to PV

52
Q

What is the typical age and sex for mucous membrane pemphigoid?

A

Over 50 years old, with a higher prevalence in females

53
Q

What is bullous lichen planus?

A

A form of oral lichen planus presenting as chronic, multiple irregular ulcers surrounded by Wickham’s striae

54
Q

How is bullous lichen planus differentiated from other forms of oral lichen planus?

A

It involves subepithelial bullae and is characterized by chronic, irregular ulcers

55
Q

What is the common treatment for subepithelial bullous dermatoses?

A

Topical steroids, scaling and root planing, and sometimes systemic corticosteroids

56
Q

How are oral ulcers secondary to chemotherapy managed?

A

Antiseptic mouth rinses, topical anesthetics, and antibiotics for secondary infections

57
Q

What are the clinical signs of erythema multiforme major forms?

A

Stevens-Johnson syndrome shows generalized vesicles and systemic symptoms; TEN results in extensive skin sloughing

58
Q

What is recurrent aphthous stomatitis (RAS)?

A

RAS is a disorder characterized by recurring ulcers confined to the oral mucosa.

59
Q

What are the three categories of RAS?

A

Minor ulcers, Major ulcers, and Herpetiform ulcers.

60
Q

What are the typical features of minor aphthous ulcers?

A

Small, shallow, round ulcers with an erythematous halo, healing without scar formation.

61
Q

How do major aphthous ulcers differ from minor ones?

A

Major ulcers are larger, deeper, and painful, often leaving scars.

62
Q

What are herpetiform aphthous ulcers?

A

Small, multiple, painful ulcers that appear in adults and heal without scarring.

63
Q

What genetic factors are associated with RAS?

A

Heredity factors, with a higher chance if parents have RAS; specific HLA antigens.

64
Q

How does serum iron deficiency relate to RAS?

A

Serum iron deficiency is one of the hematologic deficiencies linked to RAS.

65
Q

What immunologic abnormalities are seen in RAS patients?

A

Increased lymphocytoxicity, antibody-dependent cytotoxicity, altered lymphocyte ratios.

66
Q

Name some other etiologic factors for RAS.

A

Trauma, psychological stress, food allergies, hormonal disturbances.

67
Q

How can RAS be associated with gastrointestinal diseases?

A

It may occur with Crohn’s disease and ulcerative colitis.

68
Q

What distinguishes RAS from Behcet’s syndrome?

A

Behcet’s syndrome includes genital ulcers, eye lesions, and a positive pathergy test.

69
Q

How is Behcet’s syndrome diagnosed?

A

By recurrent oral ulcers plus two of the following: genital ulcers, eye lesions, skin lesions, or positive pathergy test.

70
Q

What is the most common skin manifestation in Behcet’s syndrome?

A

Large pustules or lesions precipitated by trauma.

71
Q

What are the typical oral lesions in Reiter’s syndrome?

A

Scalloped white lines surrounding red areas, resembling geographic tongue.

72
Q

What is the first step in managing traumatic oral ulcers?

A

Removal of the source of trauma.

73
Q

How do you differentiate a traumatic ulcer from a malignant ulcer?

A

Traumatic ulcers resolve quickly after removing the cause, while malignant ulcers are persistent and often painless.

74
Q

What are the characteristics of a tuberculous oral ulcer?

A

Irregular, chronic, painful ulcer with indurated base and undermined edge.

75
Q

What is the appearance of primary syphilis in the oral mucosa?

A

A painless, single ulcer (chancre) with an indurated base.

76
Q

What is a key feature of secondary syphilis oral lesions?

A

Mucous patches and condyloma latum.

77
Q

How does tertiary syphilis affect the oral cavity?

A

It can cause gumma affecting the hard palate or tongue, leading to perforation.

78
Q

What is the main adverse effect of glucocorticoids on carbohydrate metabolism?

A

Hyperglycemia, potentially leading to diabetes.

79
Q

How do glucocorticoids affect fat metabolism?

A

They induce lipolysis and redistribute fat to face, abdomen, and shoulders.

80
Q

What is a common side effect of glucocorticoids related to protein metabolism?

A

Muscle wasting and thinning of the skin.

81
Q

What is a major adverse effect of glucocorticoids on salt and water metabolism?

A

Edema, hypertension, and osteoporosis.

82
Q

How do glucocorticoids impact the immune system?

A

They suppress inflammation and immune response, potentially spreading infections.

83
Q

What is a significant side effect of glucocorticoids on the gastrointestinal system?

A

Peptic ulcers due to increased HCl and pepsin production.

84
Q

How do glucocorticoids affect the central nervous system?

A

They can cause euphoria, behavioral changes, or psychosis.

85
Q

What is a common treatment for Reiter’s syndrome?

A

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs).

86
Q

What is a key diagnostic criterion for Behcet’s Syndrome?

A

Recurrent oral ulceration plus two other manifestations such as genital ulcers or eye lesions.

87
Q

How is RAS differentiated from RIOH (Recurrent Intraoral Hyperplasia)?

A

RAS affects non-keratinized mucosa without tissue tags; RIOH affects keratinized mucosa with tissue tags.

88
Q

What laboratory investigations are needed to manage severe RAU?

A

Tests for serum iron, folate, and vitamin B-12 levels.

89
Q

What is the typical healing time for minor aphthous ulcers?

A

Healing usually occurs within 7 to 10 days without scar formation.

90
Q

What treatment is recommended for severe RAU?

A

Intralesional steroid injections or systemic corticosteroids.

91
Q

How are herpetiform aphthous ulcers treated?

A

They are treated symptomatically and heal within 7-10 days without scarring.

92
Q

What are some common drugs tried for RAU management?

A

Colchicine, thalidomide, azathioprine, and pentoxifylline.

93
Q

Why should caustic agents not be applied to RAU lesions?

A

They cause tissue damage, delay healing, and lead to scar formation.

94
Q

What is a distinguishing feature of malignant oral ulcers compared to benign ones?

A

Malignant ulcers are large, deep, and often have everted edges with an indurated base.

95
Q

What is a key feature of a traumatic oral ulcer?

A

It usually resolves within 1 to 2 weeks after removing the cause.

96
Q

How do you diagnose a traumatic ulcer?

A

Based on history, clinical examination, and rapid resolution after removing the cause.

97
Q

What is the treatment for a squamous cell carcinoma of the oral mucosa?

A

Treatment typically involves surgical excision and possibly radiation or chemotherapy.

98
Q

What is a key diagnostic feature of primary syphilis oral ulcers?

A

A painless, single ulcer (chancre) with an indurated base.

99
Q

What are the systemic manifestations of Behcet’s syndrome?

A

Arthritis, central nervous system involvement, and venous thrombosis.

Oral medicine (7 decks)

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