More diseaess-Kerr, Dry mouth Flashcards

(100 cards)

1
Q

Erythroplakia

Treatment

A

○ Biopsy required for diagnosis

○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal

○ Complete excision

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

What is this clinical presentation?

A

Erythroplakia.

Well-circumscribed red patch on the
posterior lateral hard and soft palate

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

What is this clinical presentation?

A

Erythroplakia.

Erythematous macule on the right
floor of the mouth.

Biopsy–

Turned out to be early invasive squamous cell
carcinoma.

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

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv

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

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Mild. A soft, fissured,
gray-white lesion of the lower labial mucosa located in the area of
chronic snuff placement.

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

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC

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

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

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

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

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

What is this clinical presentation?

A

Pemphigus Vulgaris.

Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.

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

What is this clinical presentation?

A

Pemphigus Vulgaris.

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

What is this clinical presentation?

A

Pemphigus vulgaris

● Multiple, chronic, mucocutaneous ulcers
● Many patients also have

● Relatively non‐specific
● Very superficial, only in epithelium
● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal,
genital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is this clinical presentation?

A

Pemphigus vulgaris

PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)

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

What is this clinical presentation?

A

Pemphigus vulgaris

usually suffer from Desquamative
gingivitis (DG)

More superficial erosion of the marginal gingiva, typically with an
intense erythema and inflammation, and very often in the absence of
local factors that would typically cause a gingivitis

o Hurts to brush their teeth

Immediately look for areas where there are no local factors and look for
inflammation there
o To check the possibility of systemic factors causing local
gingivitis

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

What is this clinical presentation?

A

Pemphigus vulgaris

Combination of PV
inflammation and
gingival inflammation
accumulating local
factors can result in
advanced loss of
attachment and tooth
loss

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

Pemphigus vulgaris

Etiology

A

Pemphigus vulgaris is not fully understood.

Experts believe that it’s triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug.

In some cases, pemphigus vulgaris will go away once the trigger is removed.

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

Pemphigus vulgaris

Treatment

A

Treatment has 3 stages:
● Stage 1: Control
○ Suppress inflammation / lesion activity with Systemic Corticosteroid: Remains initial / 1st‐line treatment…
○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control
● Stage 2: Consolidation
○ Reducing auto‐antibody production with the addition of Immunosuppressants
○ Assessed by the lack of development of NEW lesions
● Stage 3. Remission / Maintenance:
○ achieving complete remission of lesion activity OFF medication is the GOAL
○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications
○ RITUXIMAB has become the FIRST CHOICE treatment after
○ the consolidation phase to achieve DISEASE REMISSION

● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS
○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease
○ outcome (lesions) and not the systemic illness / pathologic antibody production
○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)

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

What is this clinical presentation?

A

Mucous membrane pemphigoid

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

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

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

What is this clinical presentation?

A

Mucous membrane pemphigoid

Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis

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

What is this clinical presentation?

A

Mucous membrane pemphigoid

REMEMBER:

▪ Plaque and calculus can be the consequence of painful MMP lesions
▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mucous membrane pemphigoid

Etiology

A

Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations

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

Mucous membrane pemphigoid

Treatment

A

o Approach is similar to PV – but generally not as aggressive unless
hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated
▪ NON‐immunosuppressive treatments uniquely effective:

  • *o** Dapsone
  • *o Tetracycline + nicotinamide**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MMP & PV BIOPSY

A

take two different sites
○ For H&E, still must be perilesional
○ If you get only ulcer just because the clinician thinks
○ that is the pathology → there is no epithelium!
○ The sample is useless and no diagnosis can be made

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.
26
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Early presetation: Smooth, blotchy, pale, dry areas Diffuse, irregular white plaque around line of the lip Crusted, Scaly **​**
27
**Actinic cheilitis** malignant transformation
Actinic cheilitis has **2 times** of risk for developing SCC of the lip. SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body
28
**Actinic cheilitis** Etiology
due to chronic ultraviolet light exposure.
29
**Actinic cheilitis** Treatment
* avoid sun exposure * Laser ablation is preferred for severe actinic cheilitis * surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia * Lip Shaving” (Vermilionectomy) * can also use cryotherapy, electrodesiccation It requires long term follow up and **prognosis is good if caught early**
30
What is this clinical presentation?
**_SCC_** arising from **Actinic Cheilitis**
31
What is this clinical presentation?
**Oral Melanoma** a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
32
What is this clinical presentation?
**Oral Melanoma** an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.
33
What is this clinical presentation?
**Oral Melanoma** patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient's fingers are depicted.)
34
What is this clinical presentation?
**Oral Melanoma** Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.
35
What is this clinical presentation?
Amalgam tattoo This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .
36
What is this clinica presentation?
Oral melanoacanthoma. the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.
37
What is this clinical presentation?
**Oral melanotic macule** an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
38
Oral Melanoma ## Footnote **Etiology**
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma **Acute sun damage** can cause it more than chronic exposure
39
Oral Melanoma Risk Factors
Fair skin A history of sunburn Excessive ultraviolet (UV) light exposure. Living closer to the equator or at a higher elevation Having many moles or unusual moles A family history of melanoma Weakened immune system.
40
**Oral Melanoma** Treatment
* Surgical excision * Radiotherapy * Chemotherapy
41
What is this clinical presentation
Oral Melanoma
42
What is this clinical presentation
Oral Melanoma
43
What is this clinical presentation
Oral Melanoma
44
What is this clinical presentation?
Traumatic ulcer caused by sharp or puncturing food stuff
45
What is this clinical presentation?
Traumatic ulcer a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis
46
What is this clinical presentation?
Traumatic ulcer Post-anaesthesia traumatic ulcer on lower lip.
47
What is this clinical presentation?
Traumatic ulcer Most often on tongue, lips, buccal mucosa Any sites that may be injured by dentition
48
What is this clinical presentation?
Traumatic Granuloma
49
What is this clinical presentation?
Traumatic Granuloma (traumatic ulcertaive granuloma)
50
What is this clinical presentation?
**Traumatic Granuloma** | ( Traumatic Ulcerative Granuloma)
51
Traumatic ulcer/Traumatic ulcerative granluoma Etiology
**Etiology** * typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep. * Chronic mucosal trauma from adjacent teeth * Some adjacent source of irritation
52
Traumatic ulcer/Traumatic ulcerative granluoma Treatment
**Remove cause of irritation** Topical anesthetic or film for pain relief If there is no obvious cause then ► **biopsy**
53
What is this clinical presentation?
Squamous cell carcinoma on the buccal mucosa)
54
What is this clinical presentation?
**Erythroplakia and Squamous Cell Carcinoma** Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia
55
What is this clinical presentation?
Leukoplakia and Squamous Cell Carcinoma Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).
56
squamous cell carcinoma Risk factors
**HPV + SCC** Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue) Younger pts, 3:1 Males to females ratio, high socio-eco status Incidence is decreasing less aggressive → higher survival rates ( Better than HPV negative SCC) **HPV - SCC** The chief risk factors for oral squamous cell carcinoma are Smoking (especially \> 2 packs/day) Alcohol use Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men. ( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva) mostly men, low socio-economic factors Incidence is decreasing Very aggressive → lower survival rates
57
SCC treatment
Early stage: Radiation and/or Surgical removal Late stage : combination of surgery, radiation therapy, or chemotherapy
58
What is this clinical presentation?
**Graphite tattoo** Most common location on the palate and gingiva Gray, black, or blue-ish macule
59
What is this clinical presentation?
**Graphite tattoo** Gray, black, or blue-ish macule
60
Graphite tattoo Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
61
Graphite tattoo Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
62
What is this clinical presentation?
Traumatic ulcer of the tongue.
63
What is this clinical presentation?
**Hemangioma of Infancy** a relatively common benign proliferation of blood vessels that primarily develops during childhood. display a rapid growth phase with endothelial cell proliferation, followed by gradual involution.
64
What is this clinical finding?
Hemangioma of Infancy
65
**Hemangioma of Infancy** Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
66
What is this clinical finding?
Necrotizing Sialadenometaplasia an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands. *Here it is on the palate*
67
What is this clinical finding?
**Necrotizing Sialadenometaplasia** *we see two ulcers on the palate* *Mostly ● Palatal salivary glands ○ Possible for parotid ● 75% of case on posterior palate ● Hard\>Soft palate ● 2/3rd are unilateral*
68
**Necrotizing Sialadenometaplasia** _Etiology_
*The cause is uncertain, although the hypothesis of ischemic necrosis after vascular infarction seems acceptable.*
69
**Necrotizing Sialadenometaplasia** _Treatment_
No Treatment Needed but we need to biopsy to rule out other diseases
70
What is this clinical finding?
**Frictional Keratosis.** There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”), because this area is now edentulous and becomes traumatized from mastication. **Such frictional keratoses should resolve when the source of irritation is eliminated and should not be mistaken for true leukoplakia.**
71
What is this clinical finding?
**Frictional Keratosis** **the white surrounding a a traumatic ulcer** Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.
72
**Frictional Keratosis.** Differential Diagnosis
Leukoplakia Linea alba Chronic cheek chewing (bite injury) Candidiasis Oral Lichen planus Squamous cell carcinoma
73
What is this clinical finding?
Frictional keratosis on the tongue
74
**Frictional Keratosis** **Etiology**
* Trauma from Sharp cusp & ortho appliance * Chronic mechanical irritation (chronic biting) * Masticatory function * Normal hyperplastic response * Dentures/missing teeth
75
**Frictional Keratosis** **Treatment**
* Remove the cauative factor that caused the trauma * observe large lesion regularly excellent prognosis
76
What is this clinical presentation?
**dry‐mouth** patient a classic example **• Classic fissuring • depapillation of the tongue papilla • some white changes on the tongue.**
77
What is this clinical presentation?
**dry‐mouth** from radiation Note the Ropy, frothiness on the palate. - The tissues are red and irritated due to candida infection as well.
78
What is this clinical presentation?
**dry Mouth** Cervical caries related to radiation. The patient is a smoker and coffee drinker --\> explains the staining
79
What is this clinical presentation?
dry Mouth Incisal caries in a radiation patient: **Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction**
80
What is this clinical finding?
**Xerostomia-related Caries** **Or** **Dry Mouth** . Extensive cervical caries of mandibular dentition secondary to radiation-related xerostomia.
81
**Dry mouth** Subjective vs Objective
**Xerostomia** The subjective experience of a dry mouth (ie a symptom) **Salivary Hypofunction** The objective measurement of a reduction in salivary flow (a sign)
82
What is the normal rate for **Stimulated Saliva Production**
**Stimulated Saliva Production** **▪ 200+ ml/day ▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min** o “Normal” range is very wide
83
What is the normal rate for Unstimulated Saliva Production
**300 ml/day ▪ Flow rate: mean 0.3 ml/min**
84
What are Factors affecting unstimulated flow include?
* **Dehydration** * **Medical conditions** * **Body posture** * **Lighting conditions** * **Circadian/circannual rhythm (lowest during)** * **Medications** Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).
85
What are Factors affecting stimulated flow include:
* **Mechanical stimuli** * **Vomiting** * **Gustatory/olfactory stimuli (acid/smell)** * **Gland size** Age is an independent factor for whole saliva (but not for parotid and minor gland secretions)
86
What causes dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the higher centers of the brain.
87
● What causes xerostomia in absence of measurable salivary hypofunction?
* **May be a reduction in baseline sialometry which is still above “normal.”** * *If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.* * **Saliva film thickness** * *Palatal mucous gland secretions?* * *Anterior dorsum of tongue?* * **Relative contributions by glands** * Mucins, proteins? * **Alterations in sensory perception?** * **Mental status/central inhibition?**
88
What cause Salivary Hypofunction?
**● Dehydration ● Medications (Rx & OTC)** * *Direct damage to glands* * *Head and neck radiotherapy* * *As a result of radiation it’s irreversible damage to the glands* * *Chemotherapy (reversible)* * *Autoimmune diseases* * *Primary vs Secondary Sjögren’s Syndrome, GVHD* * *HIV disease* **● Decreased mastication (tooth loss, soft diet) ● Conditions affecting the CNS:** * Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
89
To have dry mouth xerostomia what is the rate of Unstimulated and Stimulated Salivary flow **USFR** and **SFR**
**Abnormal unstimulated USFR= \<0.1–0.2ml/min** **Abnormal stiumated SFR = \<0.5ml/min**
90
Severity of patients with xerostomia using objective measures
91
How to manage with normal USFR and SFR?
* Salivary stimulation (OTC) to stimulate their glands * Salivary lubrication ( to improve it) * Humidification ( like a humidifier in the room at night) * Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a * diuretic and lead to dehydration). * Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else 􀀀 we want to follow them over time)
92
How to manage with abnormal USFR and normal SFR? (respond to stimulated) Abnormal unstimulated USFR= \<0.1–0.2ml/min
* Look for possible causes (major cause will be medications & can dehydration or others) * Restore chewing function (Masticatory issues) * Reduce medication‐induced salivary hypofunction * Prescribe Salivary stimulation OTC, Rx medications, others * Prescribe Salivary lubrication * Humidification ‐use humidifiers * Hydration/prevent dehydration (ie avoid alcohol, caffeine) * Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
93
How to manage with abnormal USFR and abnormal SFR? Abnormal unstimulated USFR= \<0.1–0.2ml/min Abnormal stiumated SFR = \<0.5ml/min
* If dehydrated ► rehydrate or treat underlying condition * People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back. * All we can do is offering Salivary substitutes (sprays, gels, rinses ) * For patients with high dose radiation treatment ► makes sure they get the INRT * Minimizing damage to salivary glands ( there are other strategies for that) * Prevention and treatment of oral complications
94
**What are the** **Prescription Medications** for people with low USFR and some oral signs, but responds to stimulation ? (abnormal USFR, Normal/improved SFR) **(include dosage and usage)**
– Muscarinic agonists: – **Pilocarpine** 5‐7.5mg tid & qhs (can go as high as 10mg qid) – **Cevimeline** 30mg tid (can go as high as 60mg tid) _Contradicated for_ : **CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma** **Pilocarpine affects M1 & M3** _side effects_ (sweating, flushing, rhinitis, increased urination, weakness and some experience the shakes. ) **Cevimeline affects M3 only** fewer side effects
95
What is this clinical presentation?
**SJÖGREN’S SYNDROME** Autoimmune exocrinopathy Marked bilateral parotid gland enlargement in a patient with primary Sjögren syndrome Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary glands due to retrograde infections.) **increased risk of lymphoma (MALT type)**
96
What is this clinical presentation?
**SJÖGREN’S SYNDROME** _Dry Mouth_ very severe cervical disease & very dry lips
97
What is this clinical presentation?
Depapillated & Fissured Tongue ## Footnote **SJÖGREN’S SYNDROME**
98
What is this clinical presentation?
a patient with a **_bacterial sialadenitis_** who has **_SJÖGREN’S SYNDROME_** When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.
99
**SJÖGREN’S SYNDROME** **Management**
These patients **LOW USFR, no response to stimulation (aka abnormal USFR/SFR)** * Rehydrate if dehydrated * Treat underlying conditions (i.e. DM) * Salivary substitutes (glycerin) * Minimize damage to glands from radiation * Prevention of complications & palliative treatment * Optimal hygiene * Restore caries * Smooth sharp edges in oral cavity * Fluoride therapy * Antifungals * Chlorhexidine rinses w/o alcohol * Sialendoscopy * Salitron - salivary pacemaker * ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
100
What is this clinical presentation?
**Sjögren Syndrome** * bilateral enlargement of the submandibular glands * angular cheilitis, dry and cracked lips and fissured and despapilated tongue * severe ocular lesions.