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Oral Med > White and Red patches > Flashcards

White and Red patches Flashcards

1
Q

What to do with a white patch?

A

try to scrape off
- scrapes off = typical debris or thrush
- does not = thickened keratin → severe conditions
ask a thorough history
investigations = biopsy, blood test, immunofloresence

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2
Q

What is candida albicans in the oral cavity under normal conditions?

A

A harmless commensal organism

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3
Q

Under what circumstances can candida albicans become pathogenic?

A

When there is a disturbance of the oral flora or a decrease in immune defenses

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4
Q

What local factors should be ruled out first when diagnosing oral candida?

A
  • denture-related issues (friction, not removing at night, denture stomatitis)
  • smoking
  • xerostomia
  • antibiotics use
  • topical steroids therapy (e.g. steroid inhalers)
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5
Q

What systemic factors can predispose a person to oral candidiasis

A
  • uncontrolled diabetes
  • haematinic deficiencies (iron, folate, B12)
  • immunosuppression
  • certain drugs
  • endocrinopathies (e.g. diabetes, thyroid issues)
  • HIV
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6
Q

What are the clinical variants of oral candidiasis?

A
  • acute pseudomembranous candidiasis - commonly known as thrush
  • acute atrophic candidiasis - associated with inahaler use
  • chronic atrophic hyperplastic candidiasis: white pathces that cannot be wiped away, often extending to angular cheilitis. Seen in smokers, AIDS patients, and those with immunosuppression. Required fluconazole treatment.
  • chronic erythematous candidiasis (median rhomboid glossitis): associated with a kissing lesion, often seen in smokers and inhaler users
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7
Q

what is chronic hyperplastic candidiasis, and why is it significant?

A

It is a form of candidiasis where white patches cannot be wiped away and has an increased potential for malignant transformation. It is often seen in smokers, AIDS patients, and those with immunosuppression

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8
Q

what is the treatment of choice for chronic hyperplastic candidiasis?

A

fluconazole

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9
Q

what is chronic mucocutaneous candidiasis associated with?

A

angular cheilitis, especially in cases with dentures that are too large or in elderly patients with reduced OVD (occlusal vertical dimension)

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10
Q

what deficiency is commonly associated with angular cheilitis

A

vitamin B12 deficiency

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11
Q

what are the characteristic features of acute pseudomembranous candidiasis in the oral cavity?

A

white papules with a milky appearance on the surface of the oral mucosa, which can be wiped off to leave a red, raw base

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12
Q

What are the local causes of acute pseudomembranous candidiasis?

A
  • antibiotic use
  • steroid use
  • xerostomia
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13
Q

what are the systemic causes of acute pseudomembranous cadidiasis?

A
  • systemic disease
  • malignancy
  • immunosuppression
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14
Q

what is the first step in treating acute pseudomembranous candidiasis

A

Remove any contributing factors, such as stopping or reducing use of antibiotics, steroids, or addressing xerostomia

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15
Q

what topical antifungals are used to treat acute pseudomembranous candidiasis

A
  • nyastatin oral suspension (4 times a day)
  • miconazole gel 2% (can be applied to denture fit surfaces or the corners of the mouth for denture stomatitis)
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16
Q

What are the systemic antifungals used for acute pseudomembranous candidiasis?

A
  • fluconazole
  • itraconazole
  • voriconazole
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17
Q

Which antifungals used for treating acute pseudomembranous candidiasis can interact with warfarin and simvastatin, and what are the possible effects?

A

Miconazole and fluconazole can interact with warfarin and simvastatin, leading to very painful muscle cramps and wasting

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18
Q

What are the primary symptoms of acute atrophic candidiasis

A

a burning sensation in the mouth, which can be painful

19
Q

What are the common causes of acute atrophic candidiasis

A
  • use of asthma inhalers
  • broad spectrum antibiotics
  • deficiencies in B12, folate and ferritin
20
Q

Where does chronic atrophic candidiasis (denture stomatitis) typically occur?

A

On the denture-bearing areas of the oral mucosa

21
Q

Is chronic atrophic candidiasis (denture stomatitis) usually symptomatic or asymptomatic

A

It is typically asymptomatic

22
Q

Which types of dentures are associated with chronic atrophic candidiasis

A

Both acrylic and Co-Cr dentures, especially chronic denture wearers.

23
Q

What are Newton’s three types of chronic atrophic candidiasis (denture stomatitis)?

A

Type 1: Pinpoint (localized) erythematous areas
Type 2: Diffuse erythematous areas
Type 3: Erythema associated with granular or multinodular mucosa (indicative of chronic inflammatory papillary hyperplasia)

24
Q

What are the clinical features of chronic hyperplastic candidiasis (candidal leukoplakia) ?

A
  • Does not wipe off
  • mainly occurs in smokers
    often on buccal mucosa near the commisure
  • less common on the tongue
  • higher risk of developing squamous cell carcinoma (6-8%)
25
Q

What investigations should be performed for chronic hyperplastic candidiasis?

A

Swab - candida culture
FBC, haematinics, blood glucose
- histopathology after treating with antifungal agents to assess for dysplasia

26
Q

How is chronic hyperplastic candidiasis treated?

A
  • remove risk factors (eg smoking)
  • use chlorhexidine 0.2% mouthwash, 100,000 units/ml, 1ml twice daily for 2 weeks
  • Topical antifungals:
    = Nystatin oral suspension: 100,000 units/ml, 1ml after food four times daily for 7 days, send 30ml
    = miconazole oromucosal gel: 20mg/g, pea-sized amount after four times daily, send 80g tube
  • Systemic antifungals: Fluconazole, Itraconazole, Voriconazole
27
Q

Why is fluconazole first-line treatment for chronic hyperplastic candidiasis?

A

A non-wipeable white patch indicated invasion into epithelial cells, so topical antifungals alone may not be effective. Fluconazole is first-line alongside smoking cessation and biopsy to assess for dysplasia if the lesion persists

28
Q

What are they key features of white sponge naevus?

A
  • needs to be referred - premalignant
  • rare autosomal dominant disease - hereditary so must ask family history
  • soft, white and spongy plaques in the oral muosa
  • early childhood, adolescence
  • benign course
29
Q

How is white sponge naevus managed?

A

Treatment is challenging due to its genetic nature, but options include laser therapy or doxycycline

30
Q

Where is smoker’s keratosis commonly found, and is it premalignant?

A
  • Often found on the hard palate
  • not considered premalignant
  • associated with smoking or long-term drinking of hot beverages
31
Q

What are the characteristic signs of smoker’s keratosis?

A

Pin-prick-like dots on the palate, caused by heat opening the ducts of minor salivary glands

32
Q

What causes frictional keratosis and where is it commonly found?

A
  • very common
  • due to regular friction, mostly from teeth or dentures
  • presents as linea alba in the cheks or buccal mucosa, often bilateral
  • can be a discrete white patch anywhere in the mouth (esp edentulous ridges)
  • should resolve if source or irritation removed
33
Q

What is the management for frictional keratosis?

A
  • Remove the frictional cause
  • symptomatic relief if required
  • biopsy if there is no improvement or if it is very dense to assess for dysplasia
34
Q

What is leukoplakia and how is it disgnosed?

A

Leukoplakia is a clinical term for a white patch that cannot be removed and does not fit into other histological or morphologial diagnosis.
Clincial descriptor, not a diagnosis Diagnosis is made through histopathology to assess for dysplasia.

35
Q

What are the malignant tranformation risk of leukoplakia?

A

4-6% risk

36
Q

What are the clinical risk features of leukoplakia?

A

erythema, density, ulceration, locaation (lateral tongue, floor of mouth), sudden changes, spontaneous pain, hyperplastic margins (exophytic), verrucous keratosis / leukoplakia, pain and speckling

37
Q

What is the management of leukoplakia?

A

Histopathological assessment for dysplasia, regular monitoring, re-biopsy if clinical changes occur, and avoid risk factors like tobacco and alcohol.
- if premalignant needs close monitoring

38
Q

In which condition is hairy leukoplakia most commonly seen?

A
  • most commonly seen in HIV infection
  • may also be seen in other immunodeficient states like T-cell lymphoma and in patients taking ciclosporin
39
Q

What are the clinical features of hairy leukoplakia?

A
  • classically occurs on the lateral borders of the tongue with a corrugated surface, though it can also be smooth.
  • Epstein-Barr virus is the likely cause, and it is not considered premalignant.
40
Q

What is the prognostic significance of hairy leukoplakia in HIV patients?

A

80% of patients with hairy leukoplakia are likely to develop full-blown AIDS within 32 months

41
Q

What viral infections are associated with oral lesions?

A

Hairy leukoplakia: Epstein-Barr Virus (EBV)
Warts and papillomas: Human Papillomavirus (HPV)
Koplik spots: Measles

42
Q

Clinical Risk features of oral lesions?

A
  • Speckling or heterogenous
  • density,
  • uleration
  • location (lateral tongue, floor of mouth),
  • sudden changes
  • spontaenous pain/pain on palpatation,
  • hyperplastic margins/exophytic
  • verrucous keratosis/leukoplakiaappearance
43
Q

What are the differential diagnoses for red patches in the oral cavity?

A

Atrophic or erosive forms of oral lichen planus
Candida infection
Vesiculo-bullous lesions
Erythroplakia or erythroleukoplakia (often associated with squamous cell carcinoma).

Oral Med (10 decks)

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