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Oral Pathology > White Lesions > Flashcards

White Lesions Flashcards

1
Q

Leukodema and white spongy nevus commonality

A 
Both have 
- can not be rubbed off
- bilateral cheek
- in young patients
- asymptomatic
-hyperkeratosis and acanthisis
- intracellular edema of prickle cells 
Cells with clear cytoplasm and small pyknotic nuclei
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2
Q

Leukodema And white spongy nevus differences

A 
-wsn
..folded 
..spongy
..extra oral manifestations
Vaginal esophageal and conjunctival mucosa 
..in 👅 
.. hydropic degeneration in superficial cells of prickle layer
..eccentric nucleus 
.. perinuclear cytoplasm condensation 
-leukoedema
..dissappear if stretched unless advanced
.. common in negros
.. grayish white 
Milky white 
Diffuse
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3
Q

Derrier’s disease / follicular keratosis clinical

A

50 % oral manifestation
Skin
..symmetrical popular lesions on trunk and face
..thickening of skin of palm and sole
Oral
..on pharynx and nasopharynx difficulty swallowing
..on keratinized mucosa

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4
Q

Witkop disease HBID clinical

A

-bilateral eye conjunctival hyperemia
-intraoral folded keratosis on every mucosa except sulcus
عدد
-appears first year of life

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5
Q

Follicular keratosis histology

A

o Acantholytic epithelial cells (loss of adhesion () cells due to cutting of desmosomes).

o Supra basal vertical clefts.

o Supra basal bullae.

o Corps ronds and arains:

o/Round cells with small pyknotic nuclei, a perinuclear clear halo and eosinophilic cytoplasm.

o Compressed cells with elongated nuclei.

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6
Q

HBID histology

A

Acanthosis, parakeratosis.

o Hydropic degeneration within stratum spinosum layer.

o Dyskeratotic cells →→ enlarged, hvaline, waxy

H/P

eosinophilic cells.

Dyskeratotic cells may be surrounded by adjacent cells producing (cell within cell appearance),

o Few inflammatory cell infiltrate in C.T.

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7
Q

Etiology of thrush

A
  • newborns older than 6m and elderly

- immunocomporomised –hiv leukemia and diabetes

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8
Q

Site of oral thrush

A

Anywhere mainly

-palate dorsum of tongue or buccal mucosa

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9
Q

Acute atrophic candidiasis caused by

A
  • corticosteroids and antibiotics prolonged use
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10
Q

Median rhombus glossitis is it symptomatic

A

No

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11
Q

تقسيمة الcandida

A

-oral thrush
-erythematous candidiasis
..med rhomboid
..acute atrophic candidiasis
..angular chelitis
..chronic multi focal candidiasis
- chronic atrophic candidiasis
- muco cutaneous candidiasis
-chronic hyperplastic candidiasis

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12
Q

Chronic multifold candidiasis site

A

Dorsum
Angle of mouth
Junction of hard and soft palate

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13
Q

Angular chelitis

A

Predisposing factors for angular cheilitis include nutritional deficiencies in vitamin B. folic acid and iron
If it was reported in dentuolus loss young patient it’s an indication of HIV infection

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14
Q

Denture stomatitis

A

Rarely symptomatic

Can be caused by allergy from denture material or poorly cured denture

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15
Q

Sites of candidal leukoplakia

A

-bilateral anterior buccal mucosa triangle tapering posterior
Dorsum of tongue

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16
Q

Risk of candidal leukoplakia

A
  • 50% of cases has sognes of dysplasia

- speckled are more risky

17
Q

Mucocutaneus candidiasis

A
  • severe form happening in immunocompromised
  • nails scalp and oral
  • thick white oral plaques can’t be rubbed off
18
Q

Histology of candidiasis

A
  • candida shown by special stains of koh 10:20% and PAS
  • hyper para keratosis
  • Acanthosis
  • hyphea in keratin layer
  • mico abscess in superficial spinous layer and keratin layer
  • long rete pegs
  • chronic inflam.cells in ct
19
Q

In frictional keratosis what might make you think its idiopathic leukoplakia

A

-areas of induration
- ulceration
Redness

20
Q

Sites of frictional keratosis

A
  • areas that our Commonly traumatised
    Buccal mucosa at the level of occlusal plane
    Lip and edentulus ridge
21
Q

Why tobacco cause white lesion and is it dysplastic

A
  • carcinogenic material like nitroson and nicotin
  • high pH of 8.2 to 9.3 buffered slightly by saliva

Yes

22
Q

Site of nicotinic stomatitis

A

-posterior palate

23
Q

Histology of NS

A

Squamous Metaplasia of excretory ducts with keratin formation
Hyper k and acanthosis
Chr.inflm inflt at gland

24
Q

One of the most common oral forms of

keratosis.

A

Nicotinic stomatitis

25
Q

Etiology of actinic chelitis

A

Represents accelerated tissue

degeneration of the lips (especially the lower lip) secondary to regular and

prolonged exposure to sunlight.

26
Q

Histo of solar chelitis

A

Epithelium atrophic with hyperkeratosis,

Hyperchromatic basal cell layer.

Basophilic change in submucosa due to degeneration of collagen

bundles.

27
Q

Etiology and pathogenesis of lichen

A

T-Lymphocytes secrete Gamma-interferon which:

:

Epithelial basal cells are the primary target in lichen planus.

o Related to 2 factors:

External factor→ 95% of cases associated with psychological disturbance. (2) Internal factor (HLA-DR) major histocompatibility complex.

The mechanism of basal cell damage appears to be related to a cell-mediated immune process involving Langerhans cells, macrophages and T-lymphocytes.

Langerhans cells & macrophages contact and recognize an antigen in epithelium →→ secrete Langerhans cells/macrophages lymphokines (“interleukin-1” IL-1) which Attract T-lymphocytes to the area stimulating it to secrete IL-2 causing Proliferation of T-lymphocytes which is cytotoxic to basal cells.

Induces keratinocytes (basal) to express the class II histocompatibility

antigen (HLA-DR).

Increase rate of differentiation ( thickness of epithelium).

Degeneration of the basal layer leads to liberation of a factor analogous to IL-1 →stimulation and proliferation of T-lymphocytes.

28
Q

Lichen
Is it uni or bi
Male or female
Steady or not

A

Bi in 90%

has periods of remission and exacerbation.

29
Q

Reticular lichen clinically

A

The most common type

Numerous interlacing white keratotic lines (Wickham’s strale) in a lacy or annular pattern.

Mainly in buccal mucosa.

(2) Lateral side of tongue. Less frequently in lip & gingiva

Asymptomatic

30
Q

Plaque/ hypertrophic lichen clinically

A

Elevated and smooth plaques (raised patches). Resemble leukoplakia clinically.

Mainly on the dorsum of the tongue.

Posterior part of buccal mucosa.
Asymptomatic

31
Q

Atrophic lichen clinically

A

May be seen with reticular or erosive variant.

> The surface is granular and erythematous & at margins of the atrophic zones, whitish keratotic striae are usually evident, radiating and blending into surrounding mucosa.

Attached gingiva in a so-called

Symptomatic (burning

“desquamative gingivitis” pattern.

32
Q

Erosive lichen clinically

A

The surface is brightly erythematous.

Keratotic component peripheral to site of erosion with either reticular or finely radiating keratotic striae.

Burning

33
Q
  1. The bullous variant clinically
A

The most unusual form.

The buline or vesicles range from a few mm to several cm in

diameter.

  1. The bullous variant

> Bullae are short-lived rupture leave 1 ulcerated,

extremely painful surface.

18uccal mucosa, (posterior and inferior

regions adjacent to the third malars). 2. Lateral margin of the tongue

Extremely painful after rupture of bullae.

  1. Rarely on the gingiva and along the inner aspect of the lips
34
Q

Do of lichen

A
  • leukoplakia
  • drug eruptions
    Dle
    Sq.c.c
    Atrophic candidiasis

On gingiva — mmp

35
Q

Skin lesions of lichen appears in …% and where

A

20:60%

Flexor surface

36
Q

Is there candidiasis in lichen why?

A

Yes
50%
Altered cellular immunity

37
Q

Ttt of lichen

A
  • symptomatic
    Topical and sys corticosteroids
    -asymptomatic
    Vit a as it regulates epi differentiation

Oral Pathology (21 decks)

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