Brainscape's Knowledge GenomeTM

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


See full index

Oral Pathology Exam 2 > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Which papillae are involved in transient lingual papillitis?

A

Fungiform papillae

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

6 causes of transient lingual papillitis

A 
Local irritation
Stress
Hormonal imbalances
GI disease
Viral infection
Local hypersensitivity rxn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 patterns of transient lingual papillitis

A
  1. A few on anterior dorsal tongue
  2. Most of papillae on tip/lateral tongue
  3. Diffuse + hyperkeratotic (papulokeratotic variant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common oral non traumatic ulcer

A

Aphthous stomatitis (canker sores)

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

6 etiological factors for aphthous stomatitis

A 
Immune
Genetic
Microbiologic
Nutrition
Stress
Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What appears to be the key to the development of aphthous stomatitis?

A

Mucosal barriers

Disruption = increased ulcers
Increased barrer = less ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3 examples of mucosal barrier disruption associated with increased incidence of aphthous stomatitis ulcers

A

Trauma
Unattached mucosa
Smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Smoking is associated with increased or decreased incidence of aphthous stomatitis?

A

Decreased

Smoking increases the mucosal barrier

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

Aphthous stomatitis typical locations

A

UNATTACHED MUCOSA such as:

Tongue
Vesibule
Buccal mucosa

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

Herpetiform aphthae

A

Form of aphthous stomatitis

Multiple small ulcers NOT preceded by vesicles + show NO virus infected cells

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

5 features of major aphthous stomatitis

A 
> 1 cm
Deep
Forms scars
6-8+ weeks
Severe pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

5 features of minor aphthous stomatitis

A 
< 1 cm
Shallow
No scarring
10-14 days
Uncomfortable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3 differences between canker + cold sores

A

Canker = intraoral, unattached (movable) mucosa, crateriform

Cold = lip, attached mucosa, vesicular

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

Aphthous stomatitis NEVER begin as ___

A

Vesicles

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

3 features of the clinical appearance of aphthous stomatitis

A

Round ulcers
Red halo
Fibrin coat

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

Aphthous stomatitis lesions are coated with?

A

Fibrin

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

What kind of immunologic response is assoc. with aphthous stomatitis

A

T-cell mediated

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

The (T cell mediated) immune response assoc with aphthous stomatitis produces which cytokine?

A

TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the immunologic response in apthous stomatitis

A

Increase # of CD8 T-suppressor cells (relative to CD4 T-helper cells)

Cytokine TNF-alpha produced - targets oral mucosa for destruction by CD8 T suppressor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Simple canker sores usually only require palliative tx unless quality of life is altered, in which case there are 4 different tx options:

A

NSAID (Aphthasol)
Silver nitrate
Acid (Debacterol)
Protective coatings (Orobase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 tx options for diffuse minor or herpetiform canker sores

A

CORTICOSTEROIDS:

  1. Dexamethasone rinse (.5mg/mL)
  2. Betamethasone dipropionate (or Flucinonide) gel .05%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Tx for resistant cases of major aphthous stomatitis

A

Systemic steroids: Prednisone

Oral suspension (swish + swallow) preferred over tablets

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

6 tx methods for major aphthous stomatitis

A
  1. Triamcinolone acetonide injections (in lesion)
  2. Clobetosol proprionate gel .05%
  3. Halobetasol propionate ointment .05%
  4. Triamcinolone tablets (dissolved directly on ulcers)
  5. Beclomethosone dipropionate spray (hard to reach areas)
  6. Systemic steriods - Prednisone (resistant cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the GENERAL plan of attack for tx of severe (+ major) apthtous cases

A

Break cycle + clear with systemic corticosteroids (high dose, short burst)

Prevent recurrence w topical corticosteroids

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

Are aphthous stomatitis ulcers associated with systemic conditions different from those seen in healthy pts?

A

No - ulcers are identical

But will decrease in frequency + severity following resolution of systemic condition

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

12 systemic conditions assoc w aphthous stomatitis (4 important ones in caps)

A 
BEHCET SYNDROME
CYCLIC NEUTROPENIA
IMMUNOCOMPROMISED PTS (HIV)
INFLAMMATORY BOWEL DISEASE
Celiacs
Nutritional deficiencies
IgA deficiency
MAGIC syndrome
PFAPA syndrome
Reactive arthritis
Sweet syndrome
Ulcus vulvae acutum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

7 nutritional deficiencies assoc with aphthous stomatitis

A 
Iron
Folate
Zinc
B1
B2
B6
B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MAGIC syndrome

A

*assoc with aphthous stomatitis

Mouth + genital ulcers w inflamed cartilage

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

PFAPA syndrome - what do the letters stand for

A

Periodic Fever
Apthous stomatitis***
Pharyngitis
Cervical Adenitis

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

What is Behcet’s Syndrome?

A

Multisystem disease

Abnormal immune process triggered by infectious or environmental antigen —-> systemic vasculitis

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

Triggers for Behcet’s Syndrome (4)

A

Infectious OR environmental

HLA-B51
Bacteria
Viruses
Pesticides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

7 systems that are affected by Behcet’s syndrome (+ assoc symptoms)

A

GI
Cardio
CNS (paralysis, dementia)
Lungs
Eyes (uveitis, conjunctivitis, cataracts, galucoma)
Skin (erythema nodosum, pseudofolliculitis, acneiform nodules)
Genitals (painful ulcers - esp. in men)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does aphthous stomatitis present in Behcet’s Syndrome?

A

Consistent feature

6(+)
High prevalence of MAJOR aphthae

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

Diagnostic criteria for Behcet’s Syndrome

A

Recurrent oral ulceration (minor, major or herpetiform) + 2 of the following:

Recurrent genital ulcers, eye lesions, skin lesions, (+) pathergy test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3 prognostic factors for Behcet’s Syndrome

A

Gender - F better
Age - older better
Eye + CNS involvement = worse

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

What is sarcoidosis

A

Chronic granulomatous disorder

Improper degradation of antigenic material (infectious or env) leading to INAPPROPRIATE DEFENSE RESPONSE with formation of noncaseating granulomatous inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What kind of inflammation is invoved in sarcoidosis

A

Noncaseating granulomatous inflammation

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

4 etiological routes for sarcoidosis

A
  1. Prolonged/heavy antigenic exposure
  2. Immunodysregulation preventing adequate cell-mediated response
  3. Defective regulation of initial immune response
  4. Combo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Does sarcoidosis have a genetic predisposition?

A

Yes

(+) associations w certain HLA types

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

8 triggers (antigens) of sarcoidosis

A 
Epstein-Barre virus
HHV-8
Wood dust
Pollen
Clay
Mold
Silica
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Incidence of sarcoidosis

A

BLACKS 10-17x&raquo_space; whites

Female > (slightly)
Bimodal age distribution (25-35, 45-65)

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

8 acute (days-weeks) symptoms of sarcoidosis

A 
Dyspnea
Dry cough
Chest pain
Fever
Malaise
Fatigue
Arthralgia
Weight loss
43
Q

In sarcoidosis, any organ can be affected but there are 5 predominant sites:

A 
Lungs
Lymph nodes
Skin
Eyes
Salivary glands

*intraosseous lesions also reported

44
Q

Which tissue is involved in almost all cases of sarcoidosis?

A

Lymphoid tissue

45
Q

25% of sarcoidosis cases show cutaneous manifestations - what are the 2 examples of this?

A

Lupus pernio (widespread violaceous (purple) indurated lesions)

Erythema nodosum (tender erythematous on lower legs)

46
Q

Lupus pernio

A

Cutaneous manifestation of sarcoidosis

Widespread violaceous (purple) indurated lesions

47
Q

25% of cases of sarcoidosis have ocular involvement - what are the 2 presentations?

A

Anterior uveitis

Keratoconjunctivitis sicca (lacrimal gland involved)

48
Q

Sarcoidosis can minic _____ syndrome because it can show which 3 symptoms?

A

Sjogren’s syndrome

Enlarged salivary glands
Xerostomia
Keratoconjunctivitis sicca

49
Q

What are the 2 syndromes associated with acute sarcoidosis?

A

Lofgren’s syndrome

Heerfordt’s syndrome (uveoparotid fever)

50
Q

Lofgren’s Syndrome - 4 features

A
  1. Associated with acute sarcoidosis
  2. Erythema nodosum
  3. Bilateral hilar lymphadenopathy
  4. Arthralgia
51
Q

Heerfordt’s Syndrome (uveoparotid fever) - 5 features

A
  1. Associated w acute sarcoidosis
  2. Parotid enlargement
  3. Anterior uveitis
  4. Facial paralysis
  5. Fever
52
Q

In most cases of intraoral sarcoidosis, the oral lesion was the 1st documented clinical manifestation of the disease. What are the 6 most common intraoral sites (in order)?

A 
BUCCAL MUCOSA
Gums
Lips
FOM
Tongue
Palate
53
Q

Histological features of sarcoidosis

A

Schaumann bodies

Asteroid bodies

54
Q

What enzyme will be elevated in sarcoidosis pts? (Diagnosic feature)

A

Angiotensin converting enzyme (ACE)

55
Q

What should be biopsied to diagnose sarcoidosis and avoid misdiagnosing Sjogrens?

A

Posterior superficial parotid lobe

93% success rate

56
Q

Etiology of orofacial granulomatosis (+ cheilitis granulomatosa)

A

Idiopathic but probs represents abnormal immune rxn

57
Q

Orofacial granulomatosis affects _____ MUCH more than any other mucosa

A

Lips (= cheilitis granulomatosis)

58
Q

Cheilitis granulomatosis

A

Non-tender persistent swelling of lips

Appears alone or as part of orofacial granulomatosis

59
Q

Histology of orofacial granulomatosis + cheilitis granulomatosa

A

Non-caseating granulomatous inflammation

60
Q

Describe the lesions of orofacial granulomatosis in:

Buccal mucosa
Gingiva
Tongue
Palate
Vestibular sulcus
A

Buccal mucosa = cobblestone pattern + submucosal swelling

Gingiva = swelling, erosions, erythema, pain

Tongue = fissures, edema, erosions, altered taste

Palate = papules

Vestibular sulcus = linear hyperplastic tissue + erosions

61
Q

Melkersson-Rosenthal Syndrome - 3 features

A
  1. Fissured tongue
  2. Facial paralysis
  3. Orofacial (cheilitis) granulomatosa
62
Q

3 local processes that can present as orofacial granulomatosis

A

Chronic oral infection
Foreign material
Allergy

63
Q

Wegener’s Granulomatosis

A

Uncommon, abnormal immune response to an inhaled environmental or infectious agent

NECROTIZING granulomatous process of respiratory tract, necrotizing glomerulonephritis, + systemic vasculitis of small arteries + veins

64
Q

Incidence of Wegener’s Granulomatosis

A

Wide age range (most cases in elderly pts but 20% in <20 yrs)

90% White

65
Q

Generalized/Classic Wegener’s granulomatosis

A

Upper + lower respiratory + renal

66
Q

Limited Wegener’s granulomatosis

A

Respiratory lesions WITHOUT renal involvement

67
Q

Superficial Wegener’s granulomatosis

A

Skin/mucosal lesions + slow development of systemic lesions

68
Q

Wegener’s granulomatosis - upper respiratory symptoms (8)

A 
Purulent nasal drainage
Sinus pain
Nasal ulceration + congestion
Fever
Ear ache
Sore throat
Epistaxis (nose bleed)
Saddle-node deformity (progressive disease)
69
Q

Wegener’s granulomatosis - lower respiratory symptoms (4)

A

Dry cough
Hemoptysis
Dyspnea
Chest pain

70
Q

Wegener’s granulomatosis - most common cause of death

A

Glomerulonephritis

71
Q

Oral lesions present in 2% of cases of Wegener’s granulomatosis. What are the 3 features of the lesions?

A

STRAWBERRY GINGIVITIS
Ulceration
Major salivary gland enlargement

72
Q

What is the most useful diagnostic tool of Wegener’s granulomatosis?

A

Blood test for antineutrophil cytoplasmic antibodies (specifically PR3-ANCA)

73
Q

Prognosis of Wegener’s granulomatosis

A

Most pts die within 5 mo if untx

74
Q

5 reasons why the oral mucosa is much LESS sensitive than the skin

A
  1. Contact is short
  2. Saliva dilutes, digests, removes antigens
  3. Limited keratinization = harder antigen building
  4. Increased vascularity = faster antigen removal
  5. Less antigen presenting cells = allergen not recognized
75
Q

Perioral dermatitis is idiopathic but associated with what 3 things

A

Topical corticosteroids
Fluorinated toothpaste
Cosmetics

76
Q

Perioral dermatitis rashes are worsened by what 3 things

A

UV
Heat
Wind

77
Q

3 clinical presentations of perioral dermatitis lesions/rashes

A

Erythematous papules
Papulovesicles
Pustules (sometimes)

78
Q

What is the gold standard for treating perioral dermatitis?

A

Oral tetracycline

*avoid during pregnancy + kids

79
Q

Angioneurotic edema basic etiology

A

Commo allergic rxn caused by mast cell degranulation = histamine release

80
Q

2 causes of angioneurotic edema

A

Hereditary

Acquired

81
Q

What causes aquired angioneurotic edema

A

ACE inhibitors

82
Q

Cause of hereditary angioneurotic edema

A

Deficiency in inhibitor that converts C1 to C1 esterase

C1 esterase cleaved C4 + C2 = edema

83
Q

3 tx methods for angioneurotic edema

A

Antihistamines
Epinephrine IM
IV steroids + antihistamines

84
Q

Simple definition of ectodermal dysplasia

A

2(+) ectodermally derived structures fail to develop

Skin, teeth, nails, hair, sweat glands

85
Q

Etiology of ectodermal dysplasia

A

Inherited

AD, AR, or X linked

86
Q

ectodermal dysplasia is an inherited condition in which only 20% of cases have genes that are IDed. These genes are involved in which 3 processes

A

Cell signaling
Adhesion
Transcriptional regulators

87
Q

What is the best known syndrome assoc w ectodermal dysplasia

A

Hypohidrotic ectodermal dysplasia

88
Q

Hypohidrotic ectodermal dysplasia has what inheritance pattern

A

X linked

89
Q

Incidence of ectodermal dysplasia

A

Men&raquo_space;

Bc can be x linked

90
Q

8 clinical features of ectodermal dysplasia

A
  1. Heat intolerance (less sweat glands)
  2. Fine/sparse hair
  3. Hyperpigmentation + wrinkling in periocular skin
  4. Midfacial hypoplasia
  5. Xerostomia (hypoplastic salivary glands)
  6. Brittle nails
  7. Hypo/oligodontia
  8. Cone incisors, small molars
91
Q

Lyon’s hypothesis

A

Partial expression of hypohidrotic ectodermal dysplasia in women (x linked)

92
Q

White spongy nevus - cause

A

Genetic skin disease (genodermatosis)

Autosomal dominant inheritance

93
Q

White spongy nevus - etiology

A

Defect in normal keratinization of oral mucosa

Mutations in keratin 4 + 13

94
Q

White spongy nevus clinical presentation

A

BILATERAL
SYMMETRICAL
Thick white corrugated velvety diffuse plaques on buccal mucosa

95
Q

Symptoms of white spongy nevus

A

None

96
Q

2 histological features of white spongy nevus

A
  1. Hyperparakeratosis + acanthosis (epi thickening) showing perinuclear clearing of the spinous cells
  2. Perinuclear eosinophilic condensation
97
Q

Tx of white spongy nevus

A

None - benign

98
Q

Inheritance pattern of hereditary benign intraepithelial dyskeratosis

A

Autosomal dominant

99
Q

Incidence of hereditary benign intraepithelial dyskeratosis

A

Descendants of a triracial isolate (Haliwa-Saponi Native American, Black, White) of people originally from North Carolina (Hailfax County)

100
Q

What tissues are affected by hereditary benign intraepithelial dyskeratosis

A

Oral + conjuctival mucosa

101
Q

Clinical presentation of oral lesions of hereditary benign intraepithelial dyskeratosis

A

Similar to white spongy nevus (thick, white, corrugated, velvety, diffuse plaques)

Buccal + labial mucosa

May have secondary candidal infection

102
Q

Describe the eye lesions in hereditary benign intraepithelial dyskeratosis

A

Thick gelatinous opaque plaques in bulbar conjuctiva

103
Q

5 Symptoms of active eye lesions in hereditary benign intraepithelial dyskeratosis

A 
Tearing
Photophobia
Itching
Most active in spring
RARE - blindness
104
Q

Cause of hereditary benign intraepithelial dyskeratosis

A

Associated with duplication in chromosome 4q35

Oral Pathology Exam 2 (1 decks)

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