Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Oral Med > Oral ulceration > Flashcards

Oral ulceration Flashcards

1
Q

define ulcer

A

lesion wherein there is a full thickness breach of the epithelial continuity mucosa leaving connective tissue exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is it if there is not a full breach of epithelial continuity

A

it is erosion or abrasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

clinical appearance of an ulcer

A

yellow sloughing base with erythematous halo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

types of ulcers

A
  • Primary = direct formation of an ulcer (ie trauma)
  • Secondary = ulcer tht commenced as another lesion eg blister/vesicle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what salient history details do you need for an ulcer? (9)

A
  • recurrent / persistent
  • nature of initial lesion
  • time and sequence
  • ulcer / blister
  • age of onset - SCC usually age 60+
  • extra-oral involvement (genitals, skin, scalp, nails)
  • pain - controversial (white + pain = bad)
  • medical / social history
  • systemic disease / drug therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do you look at in the examination of an ulcer? (10)

A
  • Base (yellow, homogenous = fine, speckled, heterogenous = worry)
  • granularity
  • margin
  • rolled
    erythematous halo = aphthous
  • regularity of outline
  • texture
  • induration = hard = malignancy
  • site and distribution
  • associated features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

causes of ulcers (7)

A
  • Traumatic = mechanical/chemical/thermal
  • drug induced
  • idiopathic = recurrent aphthous stomatitis
  • associated with systemic disease = Behcet’s/Crohn’s/Coeliac/Paget’s
  • associated with dermatological diseases = LP, DLE, MMP, PV
  • Infective = bacterial/viral/fungi
  • Neoplastic = SCC - non healing ulcer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the most common cause of oral ulceration?

A

Traumatic ulcer caused by
- ill-fitting dentures
- orthodontic appliances
- sharp cusps
- self-induced
lip biting
aspirin burn
- erythema multiforme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do long stading ulcers get

A

keratotic edges → raised + rough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a chronic traumatic ulcer

A

takes a while to heal → white halo
- Once identifying and removing cause, should take ~10days to heal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of traumatic ulcers (4)

A

Remove cause
Difflam spray (LA)
Keep clean (CHX)
Review – improvement should be seen in 2 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what drug’s can cause drug induced ulcers?

A
  • Nicorandil (K-channel activator)
  • NSAID’s (aspirin ibuprofen)
  • Bisphosphonates (alendronate)
  • SSRI (sertraline)
  • Chemotherapy agents (methotrexate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Nicroandil and drug induced ulcers

A

Nicorandil = K-channel activator
- used for heart problems
- vasodilators
- treatment for angina
- often affects palate
- normally seen with an increase in dose, not when first starting drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

management of drug-induced ulcer

A

CHX, review 2/52

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the characteristic pattern of recurrence for recurrent aphthous stomatitis (RAS)?

A

History of recurrent oral ulcers in otherwise healthy person – lesions normally come and go (not constantly present)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the typical gender and age of onset for recurrent aphthous stomatitis (RAS)?

A

RAS has a slight female predominance and usually begins in childhood or adolescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does smoking influence recurrent aphthous stomatitis (RAS)?

A

RAS is uncommon in tobacco smokers. smokers have Hyperkeratotic mucosa which thins when they stop smoking, potentially leading to the development of RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does RAS ulceration look like

A
  • yellow base
  • erythematous halo
  • round/oval
  • soft on palpation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the typical appearance of a minor RAS ulcer

A
  • Most common (80%)
  • Non-keratinised mucosa
  • 2-10 ulcers
  • <1cm diameter
  • Heal within 7-14 days
  • No scarring
  • Painful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does major RAS differ from minor RAS in terms of ulceration and healing?

A
  • Uncommon (10%)
  • 1-3 ulcers
  • > 1cm diameter
  • Slow healing – 1-2 months
  • Possible scarring
  • Non-keratinised or keratinised mucosa
  • Often on soft palate/ uvula
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the appearance and behaviour of herpetiform RAS ulcers?

A
  • Uncommon (10%)
  • Non-keratinised and keratinised mucosa
  • Multiple ulcers
  • 1-2mm diameter
  • Heal variably, may scar (can coalesce and get bigger, then scar)
  • Mimic HSV, but H-RAS are primary ulcers but HSV are secondary ulcers formed from vesicles bursting.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can you differentiate between herpes simplex virus (HSV) ulcers and herpetiform RAS ulcers?

A

HSV vesicles pop → ulcers
H-RAS has inflamed gums
HSV systemically unwell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What investigations might be conducted to assess recurrent aphthous stomatitis (RAS)?

A
  • diet diary
  • full blood cell count (Hb so anaemia testing)
  • haematinics (ferritin, B12, red cell folate) – will be a lack of
  • coeliac disease in pts > as RAS rare in this age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are some common triggering factors for recurrent aphthous stomatitis (RAS)?

A

stress
trauma
certain foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is RAS diagnosed

A

by exclusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how is recurrent aphthous stomatitis (RAS) managed?

A
  • Correct underlying systemic problems if present
  • Topical antimicrobials: CHX 0.2% mouthwash/1% gel, tetracycline mouthwash
  • Topical anti-inflammatory: Difflam mw/spray
  • Topical steroids: prednisolone mw, betnesol mw (less potent, tablets that dissolve as used as mouthwash), fluticasone propionate (more potent), clobetasol mw
  • Systemic treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the recommended use for chlorhexidine mouthwash in treating RAS?

A

Chlorhexidine mouthwash (0.2%) is used as a rinse, with 10ml used twice daily for 1min. A 300ml bottle is typically prescribed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How should benzydamine mouthwash (Difflam) be used?

A

Benzydamine mouthwash (0.15%) should be used by rinsing or gargling with 15 ml every 1.5 hours as needed. A 300 ml bottle is typically prescribed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the dosage and application for benzydamine oromucosal spray (Difflam)?

A

Benzydamine oromucosal spray (0.15%) should be sprayed 4 times onto the affected area every 1.5 hours. A 30 ml bottle is typically prescribed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is Behcet’s disease and how does it present?

A

Multisystemic inflammatory autoimmune disorder predominated clinically by:
- recurrent oral ulceration
- recurrent genital ulceration
- uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

multisystemic Behcet’s disease

A
  • Cardiovascular
  • Skeletal (arthritis)
  • Mucocutaneous - (painful red lesions, typically on legs)
  • Neurological
  • Gastrointestinal
  • Ocular
    Found in people who live along the silk road (esp high in Turkey)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Treatment of Behcet’s disease

A
  • Multidisciplinary
  • Systemic steroids
  • Anti-TNF therapy (Biologics)
  • Oral lesions: colchicine, topical steroids, topical antimicrobials
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

first signs of Crohn’s

A

First sign often oro-facial granulomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

aetiology of Crohn’s and where it affects

A
  • Aetiology unknown, autoimmune (inflammatory bowel disease)
  • Can affect any part of gastrointestinal tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is crohn’s characterised by

A

abdominal pain
diarrhoea
weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

oral signs of crohn’s

A
  • Linear/aphthous ulcers
  • Buccal cobblestoning
  • Orofacial (eg lips) swelling – can do intralesional steroid injections (triamcinolone 10mg/ml) to decrease swelling → OFG - to reduce swelling Tacrolimus
  • Angular cheilitis
  • Tissue tagging
  • Hyperplastic gingivitis (full thickness gingival hyperplasia)
  • Perioral erythema
  • Lip swelling leading to fissure ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what can be seen on a biopsy for crohn’s

A

Granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is coeliac?

A
  • Autoimmune disease triggered by gluten
  • Can present any time in life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Coeliac symptoms

A

GI disturbances, steatorrhea, fatigue, oral ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Which antibody is commonly present in patients with Coeliac disease

A

tTGA (anti-tissue transglutaminase antibody)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does a biopsy of the duodenum show in coeliac disease?

A

Biopsy of duodenum shows flattening of villi → malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the treatment for coeliac disease

A

lifelong gluten-free diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is lichen planus

A

Common chronic dermatological disease involving skin and mucous membranes (oral/genital mucosa, skin, scalp, nails)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Who is lichen planus most likely to affect?

A

F>M, middle aged patients, uncommon in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what can clinically be seen with lichen planus

A

can be removed by scrapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Aetiology of lichen planus

A

Unknown aetiology (immunopathogenesis) →
Chronic T cell mediated autoimmune mucocutaneous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what lesions do you get with lichen planus

A

extraoral and intraoral lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what t=do the extraoral lesions in lichen planus present like

A

pruritic purple papules on skin (3 P’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what do the intraoral lesions in lichen planus present like

A

Wickham’s striae mostly in buccal mucosa, also in other sites but uncommon in floor of mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what systemic diseases are associated with lichen planus

A
  • liver disease
  • graft vs host disease
  • immunodeficiency
  • diabetes/hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what can cause lichenoid reactions?

A
  • Dental materials: amalgam, composite
  • Antimalarias: chloroquine
  • Antihypertensives: metildopa, captopril, enalapril, propanalol
  • NSAIDs: ibuprofen
  • PANDDA → penicillin, antimalarials, NSAIDs, diuretics, dental materials, Antihypertensives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Histology of Lichen planus

A

Hey, I blame lichen planus
- Hyperparakeratosis
- Irregular acanthosis → some aread thick, some areas thin → saw-tooth rete ridges
- Band-like lympho-histiocytic infiltrate
- liquefaction of the basal cell layer
- presence of civatte bodies - hyaline bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

types of lichen planus

A
  • reticular = lace-like
  • atrophic = diffuse red lesions
  • plaque-like = white patches (close monitoring, can have malignant transformation)
  • papular = small white patches
  • erosive = extensive areas with ulceration
  • bullous =subepithelial bullae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

chance of malignant transformation in lichen planus?

A

0.1-2% malignant transformation → especially erosive / atrophic + plaque like

55
Q

treatment of lichen planus

A
  • identify and remove potential causes
  • symptomatic relief - difflam mw spray
  • topical steroids - prednisolone, betamethasone, fluticasone propionate (flixonase)
    topical immunosuppressants (tacrolimus 0.1% to start then down to 0.03%)
  • systemic immunosuppressants - prednisolone, axathioprine, dapsone
56
Q

what is pemphigus

A

Autoimmune reaction against desmosomes (anti-desmoglein 3) - holding cells together

57
Q

who gets pemphigus

A

Rare childhood/early manifestations in adults

58
Q

outcome of pemphigus if untreated

A

Fatal if untreated – extensive ulceration, electrolyte loss and infection

59
Q

where does pemphigus usually present first

A

Frequently in mouth first due to subject to trauma
- Fragile bullae – rupture to form irregular, ragged, superficial ulcers
- Slow healing without scarring
- Severe desquamative gingivitis
- Soft palate, buccal mucosa and lips most common

60
Q

what confirms pemphigus

A

Positive Nikolsky’s sign = look at rubbed surfaces now instead – upper epithelial layer sheds with little trauma

61
Q

pemphigus histology

A

Histology – Teeny Tiny Little Blisters Ahhh
- Thin-roofed vesicles/bullae followed by ulceration
- Tzanck cells (acantholytic prickle cells) in blister fluid – swollen, hyperchromatic nucleus
- Little inflammatory infiltration until ulceration
- Basal cells remain attached (tombstone appearance)
- Acantholysis + destruction of desmosomes → suprabasal split

62
Q

how is immunofluorescence used to diagnose pemphigus

A
  • IgG and C3 intercellularly, incubate with fluoresceine
  • Direct method = biopsy
  • Indirect method = blood sample for fragile bullae
  • Pemphigus = fluorescence show net-like pattern in epithelium
  • Pemphigoid = fluorescence in basement membrane
63
Q

Treatment of pemphigus

A

systemic corticosteroids + steroid-sparing agents (methotrexate, omalizumab, ciclosporin), immunosuppressive agents

64
Q

what is mucous membrane pemphigoid (cicatricial pemphigoid)

A

Hemidesmosomes: separation from basement membrane

65
Q

which area is almost always involved in mucous membrane pemphigoid (cicatricial pemphigoid)

A

Mouth almost always affected, sometimes only one side (oral pemphigoid)

66
Q

what is the typical demographic affected by mucous membrane pemphigoid?

A

normally females over the age of 50

67
Q

how do the bullae in mucous membrane pemphigoid differ from those in pemphigus?

A

they are occasionally hemorrhagic and tense, unlike in pemphigus

68
Q

what are the common symptoms after the bullae rupture in mucous membrane pemphigoid?

A

rupture quickly, soreness, bleeding, and pain, with ulcerations healing slowly

69
Q

what serious complication can result from ulceration of the conjunctiva in mucous membrane pemphigoid?

A

scarring on the conjunctiva, (cicatricial) ulceration of eyeball which can lead to blindness

70
Q

what percentage of mucous membrane pemphigoid cases affect the gingiva, and what condition does it cause?

A

90%, causing desquamative gingivitis

71
Q

besides the oral cavity, which other areas can be affected by mucous membrane pemphigoid?

A

ocular, nasal, larynx, pharynx, oesophagus, and genital areas

72
Q

what histological feature characterises mucous membrane pemphigoid?

A

separation of the epithelium from the lamina propria, forming a bulla with a “thick roof”

73
Q

what cellular infiltrations are observed as vesicles develop in mucous membrane pemphigoid?

A

Infiltration by neutrophils, eosinophils, and perivascular infiltration mainly by lymphocytes

74
Q

how do we manage vesiculo-bullous disroders and desquamative gingivitis

A
  • oral hygiene essential
  • regular hygienist appointments
  • avoid SLS toothpast
  • topical steroids
75
Q

what is desquamative gingivitis

A
  • descriptive term, not a diagnosis
76
Q

what does desquamative gingivitis look like

A
  • shiny gingiva, smooth and thinned as a result of epithelial desquamation
  • may involve free or attached gingiva
77
Q

conditions which have desquamative gingivitis?

A

HomiPDL
- Hypersensitivity
- OLP (oral lichen planus)
- MMP (mucous membrane pemphigoid)
- (linear) IgA (linear IgA disease)
- PV (pemphigus vulgaris)
- DLE (discoid lupus erythematosus)
- LP again (lichen planus)

78
Q

what is erythema multiforme

A

an acute blistering condition resulting in extensive shallow erosion, which may affect the oral mucosa alome or other mucosal sites, especially ocular and genital mucosa

79
Q

what is the severe form of erythema multiforme called and why is it significant?

A

Stevens-Johnson Syndrome: it can occasionally be life threatening

80
Q

What is the suspected immunological mechanism behind erythema multiforme?

A

it probably represents a type 3 hypersensitivity reaction (immune complex mediated)

81
Q

What are the common symptoms of erythema multiforme?

A

the condition is typically recurrent and may mimic primary herpes, which can lead to diagnostic difficulties

82
Q

What is a distinctive cutaneous feature of erythema multiforme?

A

the presence of “target” lesions on the skin

83
Q

What are the possible causes of erythema multiforme?

A
  • drug reactions (e.g. penicillin, trimethoprim, cotrimoxazole, aspirin, alcohol)
  • Herpes simplex
  • mycoplasma pneumoniae
84
Q

What is a common but often unsatisfactory treatment for erythema multiforme?

A

systemic steroids , such as acyclovir

85
Q

can erythema multiforme affect only one type of mucosal site?

A

Yes, it may affect the oral mucosa alone or involve other mucosal sites as well

86
Q

What are the two types of viruses associated with herpetic stomatitis or primary gingivostomatitis?

A

HSV-1 and HSV-2 (herpes simplex virus types 1 and 2)

87
Q

What percentage of people are infected with herpes simplex virus, and how many experience recurrent infections?

A

80% of people are infected, and 1/3 of them experience recurrent infections

88
Q

How is herpetic stomatitis typically spread, and who is most commonly affected?

A

It is spread through contact or droplets and is most common in children (rarely under 6 years old) and young adults

89
Q

what are the possible presentations or primary herpetic gingivostomatitis?

A

It can present as subclinical or mild pharyngitis, or symptomatic gingivostomatitis

90
Q

what are the prodromal symptoms of gingivostomatitis and how long is the incubation period

A

The incubation period is approximately 5 days. Prodromal symptoms include malaise, fever, irritability, headaches, pain while swallowing, and regional lymphadenopathy

91
Q

what happens after 1-2 days of prodromal symptoms in gingivostomatitis?

A

numerous vesicles appear on the mucosa and lips, which typically resolve within 2 weeks

92
Q

What happens to the vesicles that form during herpetic stomatitis?

A

The vesicles ulcerate, may become secondarily infected, leading to regional lymphadenitis, and crust over with coagulated serum

93
Q

What are the potential extra-oral lesions associated with herpetic stomatitis?

A
  • drooling = lesions on the chin
  • finger sucking = herpetic whitlow
  • rubbing eyes = herpetic keratosis, which can lead to blindness if not treated with antiviral medication
94
Q

how long is herpetic stomatitis considered infective?

A

until all the lesions have disappeared

95
Q

What is the primary infection caused by the Varicella Zoster Virus (VZV)?

A

Chickenpox, characterised by small blisters and ulcers that can appear in the oral mucosa and palate, preceding the skin rash

96
Q

What is the reactivation of varicella zoster virus known as?

A

Herpes-zoster, commonly known as shingles

97
Q

how does Herpes-zoster typically present on the body?

A

It infects only one side of the body (unilateral)

98
Q

What causes the reactiveness of VZV leading to shingles?

A

A decrease in host resistance allows the latent virus in sensory ganglia to reactivate

99
Q

What are the initial symptoms of Herpes-zoster and what follows?

A

Prodromal symptoms are followed by unilateral vesicle eruptions that are painful and rupture, leaving ulcerated areas

100
Q

which division of the trigeminal nerve is most commonly involved in Herpes-zoster?

A

The ophthalmic division more often

101
Q

What is post-herpetic neuralgia?

A

A sequela of Herpes-zoster, where sensory nerves become fibrosed, causing pain that persists for more than 3 months

102
Q

What type of pain is associated with post-herpetic neuralgia, and how is it managed?

A

Severe burning or electric shock-like pain in dermatomes supplied by the trigeminal nerve. It is managed with carbamazepine or Amitriptyline

103
Q

What is Ramsey-Hunt syndrome, and what causes it?

A

A complication of VZV characterised by inflammation of the geniculate ganglion of the facial nerve

104
Q

what are the clinical features of Ramsey-Hunt syndrome?

A

Unilateral facial paralysis, loss of taste, oral ulceration, external ear neuralgia, tinnitus, and vertigo

105
Q

What causes measles?

A

The paramyxovirus

106
Q

How was measles described in the pre-vaccination era, and where is it still a significant issue?

A

It was universal and highly contagious, often fatal in developing areas

107
Q

What are the prodromal symptoms of measles?

A

Symptoms resemble a common cold and include the presence of Koplik’s spots

108
Q

What are Koplik’s spots, and where are they found?

A

Small white or blue spots on the buccal mucosa, opposite the molar teeth

109
Q

When do Koplik’s spots appear and disappear in the course of Measles?

A

They appear before the skin rash develops and disappear after the rash appears

110
Q

What are the other diseases caused by the paramyxovirus family?

A
  • Newcastle disease
  • Parainfluenza (4 types)
  • Mumps
111
Q

What are the two common conditions caused by Coxsackie Type A virus?

A

Herpangina and Hand, Foot and mouth disease

112
Q

Who is most commonly affected by Herpangina?

A

Children

113
Q

What are the symptoms of Herpangina?

A

Sore throat, dysphagia, fever, headaches, vomiting, and abdominal pain, mouth blisters

114
Q

What is the incubation period for Herpangina?

A

approximately 4 days

115
Q

Describe the appearance and location of the vesicles in Herpangina

A

Small vesicles (1-2mm) on the tonsils, soft palate, and uvula, which ulcerate to form lesions with a grey base and inflamed periphery

116
Q

How long does Herpangina typically last, and what is its nature?

A

It is self-limiting and typically resolves in about 7 days

117
Q

How is the location of lesions in Herpangina different from those in herpes simplex virus (HSV) infection?

A

Herpagina affects the oropharynx, while HSV causes gingivostomatitis

118
Q

Who is most commonly afffected by Hand, Foot and mouth disease

A

Young children

119
Q

What are the typical clinical features of Hand, Foot and mouth disease?

A

Multiple ulcero-vesicular lesions on the hard palate, tongue, buccal mucosa, and skin.

120
Q

What is the incubation period for Hand, Foot and Mouth Disease?

A

3-6 days

121
Q

How long is Hand, Foot and mouth disease infectious, and when does the contagious period end

A

It is infective until the rash has disappeared

122
Q

What is the typical duration and severity of Hand, Foot and Mouth disease?

A

It is mild, self limiting condition that usually lasts 5-7 days.

123
Q

What is the primary lesion of syphillis called, and where is it typically located?

A

The primary lesion is called a chancre, typically found on the genitalia, but it can also appear on the oral mucosa or lips

124
Q

What are the characteristics of a primary syphilis chancre?

A

A shallow, painless ulcer with an indurated base and associated lymphadenopathy

125
Q

How long does it take for a primary syphilis chancre to heal spontaneously?

A

3-6 weeks

126
Q

What are the main features of the secondary phase of syphilis?

A

Generalised skin rash, mucous patches, and ulceration that may coalesce into “small track” lesions

127
Q

When does the secondary phase of syphilis typically appear?

A

2-3 months after the intial infection

128
Q

What is the main characteristic of tertiary sypilis?

A

Formation of gummas, which are areas of coagulative necrosis and granulation tissue that can cause palate perforation

129
Q

What is a serious complication associated with the white lesions in tertiary syphilis?

A

An increased risk of oral squamous cell carcinoma (OSCC)

130
Q

What are the dental anomalies associated with congenital syphilis?

A

Hutchinson’s incisors and mulberry molars

131
Q

How does syphillis affect the feotus if the mother is infected during pregnancy?

A

It affects the second germ layer, leading to congenital syphilis

132
Q

What is the characteristic oral lesion of tuberculosis?

A

A solitary ulcer, often found on the underside of the tongue

133
Q

How is the ulcer in tuberculosis typically described

A

as a non-specific ulceration

Oral Med (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions