Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
239 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Apthous Ulcer:
|
- Most common oral mucosal disorder.
- 40% RAS people have 1st relatives with RAS - Acute painful usually involves non-ketatinized oral mucosa - Minor major or herpetiform |
|
|
|
Describe characteristics of Minor RAS
|
- 75-85% of cases
- less than 10mm. - shallow round oval yellow. - no scarring - 7-14 days |
|
|
|
Describe characteristics of Major RAS
|
- 10-15% cases.
- More than 10mm - irregiular borders - weeks to month for healing. - May have malaise or fever. - Often leaves scars. |
|
|
|
Describe characteristics of Herpetiform RAS
|
- 5-10% of all cases
- Crops of ulcers <5mm - No treatment - resolves in 7-14 days with no scaring. - Tongue mucosa. |
|
|
|
What is the Etiology of RAS (Apthous Ulcer)
|
- Trauma
- salivary gland dysfunction -- bacterial (streptococci) - vitamin B deficiencies - behcets disease - crohn’s disease - HIV/aids - magic syndrome - stress - Systemic lupus erythematous - T-cell dysfunction |
|
|
|
RAS Events:
|
Presentation of antigens to mucosal immune cells triggers a cytotoxic cascade.
|
|
|
|
List some causes of RAS:
|
- HIV-associated Aphthous cd4 counts <100 cells/mm
- Crohns and ulcerative colitis causes aphthous ulcers - Alcohol can cause it. - Dry Mouth and oral hygiene practices/products such as alcohol |
|
|
|
Can anything prevent RAS?
|
Smoking prevent RAS. WOW!
|
|
|
|
List treatments for RAS in order of least to most potent, (from non to presciption)
|
- Treatment may include sodium laural free toothpaste
- more spit remove sharp teeth. - Rx: Topical treatment: Cautery = Dedacterol = chemical cautery use for 5-10 seconds - Kenalog in Orabase, apply a thin film over ulcer. Intermediate strength corticosteroid - Potent corticosteroid = lidex gel fluocinonide 0.05%, apply thin layer over ulcer - Decadron Elixir (dexamethasone 0.5mg/ml) rinse with 5ml for 5 minutes. - Ultra potent: clobetasol 0.05% thin layer over ulcer. No more than two weeks. - Prednisone = glucocorticoid and immunosuppressant, decreases inflammation by suppressing the chemotaxis of PMN and reduces capillary permeability. Dose .5-1.0 mg a day for 1-2 weeks , if no response increase .25 mg/kg increments a day until lesions respond. Max 2.0 to mg/kg. Long term use has multiple problems. |
|
|
|
What to look for with vesiculo bullous disorders
|
Prior occurance
Freq Number Texture or border Size Associated events Behavior Duration Pain |
|
|
|
For any lesion ask:
|
1. How Many? Single ort multiple
2. How long? Acute or Chronic 3. Had it before? Primary or recurrent 4. Anywhere else? Local or General |
|
|
|
Chronic single lesion usually caused by:
|
Trauma
Infection Malignancy |
|
|
|
Chronic multiple lesions usually caused by:
|
Lichen planus
Pemphigus Pemphigoid |
|
|
|
Types of immunologic lichenoid lesions
|
- Idiopathic oral lichen palnus
- Oral lichenoid contact lesion (dental restore etc…) - Oral Lichenoid drug reaction (ace inhibitor, NSAIDS etc…) - Oral Lichenoid Lesion of graft vs host disease |
|
|
|
Lichen Planus:
DDX? DX? |
DDX= pemphigoid, pemphigus, SLE, trauma, lichenoid Rxn
DX = done by biopsy H&E |
|
|
|
Characteristics of Pemphigus Vulgaris are:
|
- Multiple chronic mucocutaneous ulcers
- Autoimmune disease characterized by intra epithelial blisters (bullae), non healing. - Onset 4th and 6th decade. - Most common form, any mucosal or skin surface - Circulating IgG, C3 directed against desmoglian on keratinocyte surface causes loss of desmosomal attachments. - ( + Nikolsky sign ) - Usually starts in the mouth 67% |
|
|
|
Pemphigus Vulgaris
DDX? DX? |
The DDX should always be erosive lichen planus, pemphigus, pemphigoid.
Pemphigus vulgaris DX: History and physical exam looking for multiple chronic mucocutaneous ulcerations or bullae. On biopsy find Tzank cells(rounded singler cells). Direct immunofluorescence from peri-lesional tissue reveals suprabasilar intraepithelial reaction product. |
|
|
|
Pemphigus Vulgaris TX?
|
TX= systemic corticosteroids to reduce antibody production and inflammation response. Prednisone. Or Prednisone(1mg/kg/day) + cyclophosphamide(2.5mg/kg/day).
|
|
|
|
Describe Pemphigoid:
|
Mucocutaneous autoimmune disease characterized by sub-epithelial bullae, onset usually after 45. 70% oral lesions before skin, +/- nikolsky sign. Multiple shallow ulcerations. Get shit in eyes = symblephron.
|
|
|
|
Pemphigoid DX:
|
history, physical exam. Biopsy H&E = sub basilar clefting and lymphocyctic infiltration. Direct immunofluorescence reveals linear sub-basilar deposition.
|
|
|
|
Pemphigoid TX:
|
Topical for limited disease (colbetesol) and prednisone 1mg/kg for systemic
|
|
|
|
Candida is a type of
|
Oral Fungal Infection
|
|
|
|
Path (causes) to candida infection :
|
Path to candida infection :
Hyposalivation Innate immunity T-cell mediated immunity Change in bacterial flora Dentures |
|
|
|
Different types of candida:
|
Pseudomembranous candida
Erythematous candida Denture stomatitis Hyperplastic candidiasis Angular cheilits Median rhomboid glossitis Hairy Leukoplakia |
|
|
|
Factors that cause candidiasis:
|
• Dentures
• Hyposalivary • Antibiotic therapy • Corticalsteroid therapy • Leukemia, lymphoma, multiplemyeloma • HIV • T-lymphocytedeficiency |
|
|
|
Candida (Candidiasis) DX:
|
H&E shows hyphae
|
|
|
|
Candida (Candidiasis) TX:
|
• Nystatin= topical disp 240ml, wipe lesion with gauze, hold teaspoonful in mouth for 5 min 4x day spit or swallow.
• Clotrimazole= dispense 60to 70 troches, dissolve in mouth 5x day for 10-14 days • Fluonazole= take 2 tabs (200mg)on day 1 then 1 per day for 1.2 weeks • Angular cheilitis Tx= clotrimazole vag cream 1% on edges of mouth |
|
|
|
Different types of Hemotologic disorders:
|
1. Lymphoid Hyperplasia
2. Neutropenia 3. Cyclic Neutropenia 4. Agranulocytosis 5. Leukemias 6. Chronic leukemias 7. Lymphoma 8. Multiple myeloma: |
|
|
|
How does Lymphoid Hyperplasia present itself?
|
Increased size of lymphoid tissue
– Waldeyer’s Ring – Lymphadenopathy |
|
|
|
What disease is known for a (Adult) Decrease in number of circulating neutrophils below 1500mm3
|
Neutropenia
|
|
|
|
Neutropenia:
Define give implication and list causes |
• Definition: (Adult) Decrease in number of circulating neutrophils below 1500mm3
• Increase susceptibility to bacterial infections • Drugs may affect neutrophil production • Vitamin B12 and Folate deficiencies may affect neutrophil production • Some viral infections reduce production and enhance destruction |
|
|
|
What is a regular periodic reductions in neutrophil production called?
|
Cyclic Neutropenia
|
|
|
|
Describe Cyclic Neutropenia:
|
• Regular periodic reductions in neutrophil production
• Mutation in neutrophil elastase (ELA2) gene • 21 day cycle • Recurrent fever, anorexia, cervical lymphadenopathy, malaise, pharyngitis, oral mucosal ulcerations • Gingival ulceration and bone loss • Ulcers resemble aphthous ulcers |
|
|
|
Cyclic Neutropenia DX:
|
cdc neutrophil count less than 500mm3 for 3-5 days
|
|
|
|
What disorder has Granulocytes (really neutrophils) which are absent caused by HIV or chemo. Looks like depp punched-out ulcerations of the buccal mucosa and gingiva. Looks like ANUG.
|
Agranulocytosis
|
|
|
|
A disease involving abnormal clotting. Less than 100,000, petechiae, hematoma, easy gingival bleeding
|
What is Thrombocytopenia?
|
|
|
|
Describe Agranulocytosis
|
Granulocytes (really neutrophils) are absent caused by HIV or chemo. Looks like depp punched-out ulcerations of the buccal mucosa and gingiva. Looks like ANUG.
|
|
|
|
Define Thrombocytopenia
|
A disease involving abnormal clotting. Less than 100,000, petechiae, hematoma, easy gingival bleeding
|
|
|
|
What are Leukemias?
|
Neoplasm of hempatopoietic stem cells that originate in the bone marrow characterized by excessive number of malignant WBCs in blood.
|
|
|
|
Types of leukemias:
|
• Acute leukemias
• Chronic leukemias |
|
|
|
What are the types of Acute leukemias? Describe them, list clinical features, causes and TX
|
• Acute leukemias
– Acute lymphoblastic leukemia (Lymphocytes) – Acute non-lymphoblastic leukemias (granulocytes, monocytes, erythrocytes. Immature cells, rapid and fatal is not treated, sudden, mostly affects children. Good prognosis with treatment. – Clinical features = fatigue due to anemia, fever due to infection, bleeding due to thrombocytopenia. – Causes gingival enlargement due to infiltration of gingival tissues with leukemic cells, oral infection, bleeding, and toothache due to leukemic infiltration of the dental pulp. – DX= CDC followed by id of malignant cells. |
|
|
|
What are the types of Chronic leukemias? How do they present themselves? clinical features? DX?
|
– Chronic lymphocytic leukemia
– Chronic granulocytic (myeloid) leukemia – Slow onset , primary affects adults, Dx = cbc – Clinical features = slow onset, fatigue, infection due to neutropenia, bleeding due to thrombocytopenia. |
|
|
|
What is Malignant tumor of lymphoid tissue originating in the lymph nodes or extranodal lymphoid tissue.
|
What is Lymphoma:
|
|
|
|
What are the different types of Lymphomas?
|
• Hodkin’s lymphoma:
• Non-hodgkin’s lymphomas • Burkitt’s lymphoma |
|
|
|
Describe Hodkin’s lymphoma
|
o less common the non-hodgkin’s
o EBV associated o b-cells involved begins in lumph nodes o age 15-35 o Reed-sternberg cells are the distinctive atypical cells o looks like purple fried egg. |
|
|
|
Describe Non-hodgkin’s lymphomas
|
- involved b lymphocytes and t lymphocytes.
- Arise within the lymph nodes or extranodal lymphoid tissue. - Mostly in adults, slow growing mass, that spreads to other lymph node areas. - The primary tumor may be in the oral cavity. |
|
|
|
Describe Burkitt’s lymphoma
|
- malignant B lymphocytes and is EBV associated.
50-70% of Burkitt’s lymphomas arise in jaw and usually effects kids. - Histologically appears as starry sky due to macrophages. |
|
|
|
What is malignant proliferation of plasma cells. Produce abnormal circulating immunoglobulin, causes destructive lesions in bone.
|
Multiple myeloma:
|
|
|
|
Describe Multiple myeloma:
What does it cause. What are the lab findings? (blood n urine) |
malignant proliferation of plasma cells. Produce abnormal circulating immunoglobulin, causes destructive lesions in bone. Most patients are over 40 , have bone pain, multiple punched out radiolucencies. Causes fatigue, infection and bleeding.
Lab finding for MM include (CBC) circulating plasma cells, creatinine elevated, protein elevated, Bence Jones protiens in urine |
|
|
|
Types of Premalignant oral epi lesions and SCC
|
• Clinical leukoplakias = epithelial dysplasia
• Granular or Rough Leukoplakias = early SCC • Erytholeukoplakia (red and white) = CIS • Erythoplakia = SCC • Actinic Chelitis • SCC • Verrucous Carcinoma |
|
|
|
Low Power Microscopic tissue charateristics of Dysplasia:
|
• Bulbous or teardrop-shaped rete ridges
• Lack of progressive maturation toward the surface • Keratin pearls (focal round collections of keratinized cells) • Loss of typical epithelial cell cohesiveness • Crowding and disorganization |
|
|
|
High Power Micro Cellular Characterisatic of Dysplasia:
|
• Enlarged nuclei and cells
• Large and prominent nucleoli • Increased nuclear-to-cytoplasmic ratio • Hyperchromatic nuclei • Pleomorphic nuclei and cells • Dyskeratosis (premature keratinization of individual cells) • Increased mitotic activity • Abnormal mitotic figures |
|
|
|
Describe Actinic Chelitis:
What causes it? What can it progress to? |
• Aka actinic cheilosis
• Common premalignant alteration of the lower lip vermilion • Results from long-term or excessive exposure to the ultraviolet component of sunlight • Equivalent to actinic keratosis of skin • SCC develops in about 10% of cases |
|
|
|
Describe the progression of SCC:
|
• Infiltration of tumor cells through the basement membrane into the underlying connective e tissue
• Keratin formation, keratin pearls. • Cells with large hyperchromatic nuclei • Numberous mitotic figures |
|
|
|
What looks like looks like cottage cheese in mouth, highly ketatinized. No invasion of tumor cells through the basement membrane.
|
Verrucous Carcinoma
|
|
|
|
Similarities and difference between SCC and Verrucous Carcinoma?
|
They are both ketatinized, they are both cancerous. Difference is that SCC tumor cells have infiltrated throught basement membrane into underlying connective tissue, Verrucous Carinomal tumor cells have not.
|
|
|
|
HIV oral lesions
|
• Candidiasis and Angular cheilitis
• Oral Candidiasis = pseudomembranous type • PAS stain shows candida hypae |
|
|
|
Factors the increase the risk of Oral Candidiasis
|
• Dentures
• Xerostomia • Abx • Corticosteroids • DM • Leukemia, lymphoma, multiplw myeloma • HIV infection • T-lymphocytic deficiency |
|
|
|
More diseases associated with HIV
|
• Hairy Leukoplakia
• Viral Papillomas • Koilocytes are characteristic cells of HPV (enlarged cells with clear halos around shrunken nucleus. • Kaposi’s sarcoma: blue/purple swelling in mouth • Cytomegalovirus Ulceration • Lymphoma • Major Aphthous like ulcers • SCC • Gingival/Periodontal disease • Swollen Parotid • Oral Lesions in HIV people are associated with low cd4 lymphocyte counts |
|
|
|
Define Candida Endocarditis
|
Large vegetations on the valves of the heart, can embolize to brain. Increased risk with injected drug use or indwelling catheters
|
|
|
|
characteristics of your wife
|
Cute, smart, adorable
|
|
|
|
Clinical types of oral candidiasis:
|
• Pseudomembranous Candidiasis = Thrush, white plaque with underlying erythematous mucosa, burning and metallic taste.
• Erythematous Candidiasis = on any mucosa on dorsum of tongue with patchy depapilation, painful to asymptomatic. • Denture Stomatitis = erythema and petechiae • Hyperplasitc Candidiasis = white plaques that cannot be wiped off. • Angular Cheilitis • Medial Rhomboid Glossitis |
|
|
|
what disease causes Thrush, white plaque with underlying erythematous mucosa, burning and metallic taste.
|
Pseudomembranous Candidiasis
|
|
|
|
Presents itself on any mucosa on dorsum of tongue with patchy depapilation, painful to asymptomatic.
|
Erythematous Candidiasis
|
|
|
|
erythema and petechiae are a symptom of:
|
Denture Stomatitis
|
|
|
|
white plaques that cannot be wiped off is:
|
Hyperplasitc Candidiasis
|
|
|
|
What are types of Viral infections?
|
- Herpes Simplex Virus = most common
- Primary Herpetic Gingivostomatitis - Secondary Herpes Infection - Varicella Zoster Virus Infection - Human Cytomegalvirus - Epstein-Barr Virus - Kaposi sarcoma - Human Papillomavirus - Verruca vulgarous - Condyloma acumminatum = type 6 and 11, are pink and sessile and happen in clusters - Focal Epithelial hyperplasia= types 13 and 32. Eskimos, native American and Ricans get this. - Florida papillomatosis = HIV people and down syndrome - Measles = paramyxovirus |
|
|
|
What's the most common type of viral infection
|
Herpes Simplex Virus
|
|
|
|
What presents itself as (first time you get it). Crusty sores on lips or inside mouth
|
Primary Herpetic Gingivostomatitis
|
|
|
|
Primary Herpetic Gingivostomatitis TX:
|
force fluids, maintain nutrition, rest avoid touching lesions
|
|
|
|
Primary Herpetic Gingivostomatitis meds:
|
• topical anesthetics, Lidocaine 2% viscous solution. Rinse for 10 ml for 2 mins and spit. Disp: 100ml bottle
• mucosal coating agents, • analgesics Tylenol or ibuprofen • antiviral agents: acyclovir |
|
|
|
1. Describe characteristics of Secondary Herpes Infection:
2. What triggers it? 3. What it looks like |
• Hides in sensory ganglion of trigeminal
• Comes out with stress , wind, sunlight, trauma. • Looks like vesicleson the lipswhich rupture and crust over could happen intraorally on keratinized tissue and rupture forming painful ulcers. |
|
|
|
Tx of Herpes labialis:
|
Ice
L-lysine Topical antivirals = penciclovir = dab lesion every 2 hours for 4 days. Systemic Valacyclovir (FDA approved) Disp 4 tabs. Take 2 PO and then 1 every 12 hours |
|
|
|
What is the 2 day course of valacyclovir as a prophylactic for suppression of dental induced RHSV:
|
• Take 2g 1 hr before dental tx
• 2 g taken same evening • 1g taken BID for next day. |
|
|
|
What is the CDC recommended regimens for treatment of recurrent herpes infection:
|
Valacyclovir 500mg orally bid for 5 days.
|
|
|
|
CDC recommendation for daily suppression of recurrent herpes infection:
|
Valacyclovir 250mg orally bid
|
|
|
|
What is the Varicella Zoster Virus Infection:
|
• Primary VZV = chicked pox
• Secondary infection = shingles. |
|
|
|
Human Cytomegalvirus:
DX: |
Dx: Immunocompromised patients
– Chronic ulcerations – Biopsy • Immunohistochemistry • In situ hybridization – ELISA of antibody titers |
|
|
|
What conditions are associated with Epstein-Barr Virus:
|
• Infectious mononucleitis
• Hairy leukoplakia • Nasopharyngeal carcinoma • Burkitt’s lymphoma • Transmitted through saliva, children get nothing, adults get fever lymphadenopathy, tonsillitis |
|
|
|
Mechanism of Transmission for Epstein-Barr Virus:
|
Infected B cells shed in saliva, virus genome circulates in nucleus.
|
|
|
|
Hairy Leukoplakia features:
Caused by? Associated with what disease? Looks like? DX? TX? |
• Caused by EBV
• Occurs mostly in HIV people • Looks like white corrugated lesions on lateral border of tongue (bilateral). • Non-wipeable. • DX includes H&E showing characteristic EBV infected cells which are balloon like. • Tx= no specific tx. |
|
|
|
Kaposi sarcoma histological features:
|
• Edema
• Vascular slits • Lymphocytic infiltration • Spindle cells |
|
|
|
What is the most active antiviral against HSV-1 and does not affect human cell growth
|
Acyclovir
|
|
|
|
HSV-1 treatment
|
Acyclovir is the most active antiviral against HSV-1 and does not affect human dell growth. It stops the replication of herpes virus DNA by being a competitive inhibitor of viral DNA polymerase.
Valacyclovir is more efficiently absorbed than acyclovir and is rapidly converted to acyclovir. Bioavailability is great when administered as valacyclovir |
|
|
|
What is more efficiently absorbed than acyclovir? The HSV-1 treatment
|
Valacyclovir is more efficiently absorbed than acyclovir and is rapidly converted to acyclovir. Bioavailability is great when administered as valacyclovir
|
|
|
|
Human Papillomavirus
|
Oncogenic = 16 and 18 (it’s bad at the age girls turn bad). Ex. Lichen planus, scc,
Benign = 2, 6, 11. Ex. Viral papilloma, verruca vulgais, condyloma accuminatum (genital herpes), focal epithelial hyperplasia, HIV associated florid papillomatosis |
|
|
|
Characteristic cells of HPV is
|
koilocytes
|
|
|
|
Describe Viral Papilloma of the mouth
|
type 6, 11. Usually a proliferation of keratinized stratified epithelium arranged in fingerlike projections.
|
|
|
|
wart and can happen in mouth, caused by hpv 2, 57. Contagious, usually pedunculated.
|
What is Verruca vulgarous
|
|
|
|
Describe Condyloma acumminatum
|
type 6 and 11, are pink and sessile and happen in clusters
|
|
|
|
types 13 and 32. Eskimos, native American and Ricans get this
|
What is Focal Epithelial hyperplasia
|
|
|
|
HIV infected and individuals with down syndrome get:
|
What is Florida papillomatosis
|
|
|
|
looks like grains of salt sprinkled on an erythematous background
|
What is Measles = paramyxovirus
|
|
|
|
Anti – HPV meds
|
interferon alpha
|
|
|
|
Lichen Planus DDX:
|
linchen planus, lichenoid rnx, systemic lupus erythematosis, hepatitis C infection, graftvs Host disease.
|
|
|
|
Describe LP: symptoms
|
LP has a lacy (wickham striae), burning and sensitivity to spicy foods, usually bilateral, 25% of peeps get extra oral lesions
|
|
|
|
DX of oral LP:
|
Incisional biopsy, biopsy whites change on non-keratinized mucosae, not red nor ulcerated areas.
|
|
|
|
Histophath of LP:
|
• Dense subepithelial lymphocyctic infiltrate
• Epithelial basal cell destruction • Clefts between epithelium and connective tissue because hemidesmosomes are dispupted |
|
|
|
OLP TX:
|
• Topical corticosteroids
• Systemic corticosteroids |
|
|
|
Oral Lichenoid Drug Reaction Tx:
|
• Stop taking the freaking drug, but it may take months to see change
|
|
|
|
Graft vs Host disease tx:
|
• 1st use topical corticosteroid
• 2nd calcineurin inhibitor as an adjust to systemic therapy (Protopic) • Or use systemic agent like Prednisone |
|
|
|
What is type 1 hypersensitivtyrnx involving the skin
|
Urticaria = hives
|
|
|
|
What is diffuse edematous swelling of soft tissues, rapid onset, itching is common
|
What is Angioedema?
|
|
|
|
Angioedema tx:
|
oral antihistamine, intravenous corticosteroid and antihistamines
|
|
|
|
Tx of contact stomatitis:
|
• ID and removal of antigen
• Antihistamine therapy • Topical steroid application |
|
|
|
Erythema Multiforme caused by:
|
• Herpes simplex infection
• Mycoplasma pnumoniae • Drug exposure |
|
|
|
Describe Erythema Multiforme oral lesions
|
lesions look diffuse, erythematous areas that evolve into large superficial erosions and ulcers. You get bloody crusty lips, desquamative gingivitis-like lesions.
EM gives skin lesions that look round erythematous and evolve into bullae with necrotic centers (target lesion) |
|
|
|
EM DX:
|
• Necrotic basal cell
• Mixed inflammatory infiltrate, neutron, eosin, lymphocytes. • Direct and indirect immunofluorescenes to rule out vesiculobullous diseases |
|
|
|
EM DDX:
|
primary herpes simplex infection, pemphigus vulgaris
|
|
|
|
EM TX:
|
systemic corticosteroids, discontinue of causative agents, hydration .
|
|
|
|
Types of OLP:
|
• Reticular form
• Erosive form = superficial ulcerated areas surrounded by white striae • Tongue = keratotic plaques with atrophy of papilla • Desquamative gingivitis |
|
|
|
LP tx:
|
No symptom = no treatment
Topical (fluocinonide) or systemic corticosteroids May need antifungal meds to counter the candidiasis the corticosteroids will give. |
|
|
|
What is Lichenoid Mucositis :
|
• Simlar to lichen planus
• Doesn't respond to topical or systemic steroids |
|
|
|
What are the types of lichenoid mucositis:
|
• Lichenoid contact stomatitis from dental restoration
• Lichenoid drug rnx |
|
|
|
What are the different types of Elevated Lesions? Describe each type (size)
|
1. Fluid-filled
• – Vesicle <5mm diameter • – Bulla >5mm diameter • – Pustule <or>5mm diameter (containing pus) • 2. Solid • – Papule <5mm diameter • – Nodule >5mm but <2 cms diameter • – Tumor >2cms diameter • – Plaque >5mm diameter and almost flat |
|
|
|
List Corticosteroids actions:
|
• Carb and protein metab, increases blood glucose
• Lipid metab, redistribution of fat • Water balance, increase ca2 excression in kidney • Cardiovascular, cause hypertension • Atrophy of skeletal muscle • CNS, euphporia • Blood, increase # of PMN but decrease lymphocytes, eosinophils, monocytes, and basophiles • Anti-inflammatory and immunosuppression |
|
|
|
Indications for topical steroids in dentistry:
|
• Aphthous stomatitis
• Oral LP • Vesiculo-erosive disease • Contact stomatitis |
|
|
|
What are the Strongest topical steroids?
|
#1 clobetasol 0.05, disp 15g tube apply thin layer over area bid, do not use for more than 2 weeks
#2 fluocinonide0.05 % thin layer over area bid, no more than 2 weeks #7 hydrocortisone |
|
|
|
When would you use systemic steroids?
|
When there is a poor response from topical
|
|
|
|
Prednosone: Describe dosing protocol, actions and any causes
|
• Start with .5 to 1.0mg/kg for 1 to 2 weeks, if no response increase in .25mg/kg increments a day with a max of 2.0 to 2.5 mg/kg until you get response
• Increases PMN • Decreases lymphocytes, monocytes and eosinophils • Increases BP and hypokalemia • Causes cushingoid habitus, weight gain, diabetes, osteoporosis |
|
|
|
What is the normal saliva production per day?
|
500-600 ml
|
|
|
|
less than 500-600 ml of saliva produced per day is considered?
|
Dry mouth
|
|
|
|
What will cause temp salivary dysfunction?
|
2+ Gy of radiation
|
|
|
|
What will cause perm salivary dysfunction?
|
26+ Gy of radiation
|
|
|
|
Which saliva gland is more more radiosensitive than the submandibular saliva gland?
|
the Parotid saliva gland
|
|
|
|
autoimmune exocrinopathy, dry mouth and eyes are symptoms of:
|
Sjogren syndrome
|
|
|
|
reduced enjoyment of eating, altered taste
|
Dysgeusia
|
|
|
|
Meds for xerostomia:
|
Pilocarpine 5-7.5 mg tid
Cevimeline 30mg tid |
|
|
|
What are some Inflammatory bowel diseases:
|
• Crohns disease:, oral manifestations = diffuse nodular swelling of the oral and perioral tissue, cobblestone look on mucosa, deep and aphthous ulcers. Crohns could effect the whole gi tract.
• Ulcerative colitis: only the colon, rectum and mucosa of mouth. Aphthous like ulcers • Lupus Erythematosus: oral lesions resemeble lichen planus or aphthous ulcers. • Sjogrens syndrome = lymphocyctic infiltration of salivary glands o Antibodies found in Sjogrens syndrome: Anti-ss-a and anti-sss-b |
|
|
|
Which disease presents itself with diffuse nodular swelling of the oral and perioral tissue, cobblestone look on mucosa, deep and aphthous ulcers. Could affect the whole GI Tract
|
Crohns disease
|
|
|
|
Describe Crohns disease - (Actions)
|
diffuse nodular swelling of the oral and perioral tissue, cobblestone look on mucosa, deep and aphthous ulcers. Could affect the whole GI Tract
|
|
|
|
This disease only affects the colon, rectum and mucosa of mouth. Aphthous like ulcers
|
What is Ulcerative colitis
|
|
|
|
oral lesions resemeble lichen planus or aphthous ulcers.
|
What is Lupus Erythematosus
|
|
|
|
Describe Ulcerative colitis: (where and what)
|
only the colon, rectum and mucosa of mouth. Aphthous like ulcers
|
|
|
|
Lupus Erythematosus:
|
oral lesions resemeble lichen planus or aphthous ulcers.
|
|
|
|
which oral lesions resemeble lichen planus or aphthous ulcers.
|
Lupus Erythematosus
|
|
|
|
Sjogrens syndrome
|
lymphocyctic infiltration of salivary glands
o Antibodies found in Sjogrens syndrome: Anti-ss-a and anti-sss-b |
|
|
|
Disease characterized by Anti-ss-a and anti-sss-b antibodies
|
Sjogrens syndrome
|
|
|
|
What are some Precancerous conditions?
|
• Submucos fibrosis
• Actinic keratosis • Lichen planus • Discoid lupus erythematosus • HPV 16 |
|
|
|
When testing for malignancy how fast should you request the test results?
|
Lower risk malignancy dx in 5 weeks
High risk malignancy dx in 2 weeks 2 weeks |
|
|
|
What's the difference between UC and crohn ‘s?
|
the distribution of affected sites
|
|
|
|
List the Oral bacterial infections:
|
- Streptococcal sore throat
- Noma - Actinomycosis - Syphilis - Tuberculosis |
|
|
|
What is Streptococcal sore throat: What causes it, how is it contracted, symptoms, DX
|
• Group A, B hemolytic streptococci
• Person to person contact nasal or oral, yeah bitch! • Sudden sore throat • Fever • Dysphagia • Erythema of oropharynx and tonsils • Cervical lymphadenopathy • DX = rapid strep test confirm with culture |
|
|
|
Streptococcal TX:
|
• Self limiting resolves in 4 weeks
• Sensitive to penicillin, cephalosporins and erythromycin |
|
|
|
Streptococcal complications:
|
• Scarlet fever
• Rheumatic fever( could get rheumatic heart disease, increased risk of bacterial endocarditis or valve damage) • Post streptococcal glomerulonephritis ( basement membrane get covered in antibody-antigen complexes and basement membrane no longer acts as a filter. |
|
|
|
Define Noma? age?
|
• Destructive fast infection caused by components of oral microflora that become pathogenic with compromised immune statue, like AIDS, malnutrion, poor oral hygiene or ANUG
• Key players Fusobacterium and prevotella • Mostly in kids under 10 and adults with AIDS • Your face gets eaten off, think Seal |
|
|
|
Noma Tx:
|
• Debridement of necrotic tissue
• Antibiotics like penicillin, metronidazole • Reconstruction after healing |
|
|
|
What is Actinomycosis?
|
• Normal component of oral microflora
• Acute or chronic • Slow spreading • Organism enters tissue through area of prior trauma • Sulfur granules • Does not involve lymphatics |
|
|
|
Actinomycosis DX:
|
• Culture
• Sulfur granules • Biopsy |
|
|
|
Actinomycosis TX:
|
• Penicillin or amoxicillin high dose prolonged
• Adscess drainage • Excision of sinus tract |
|
|
|
What is Syphilis: Discuss Stages, histological features, etc.
|
Treponema pallidum
• 3 stages= chancre (primary), skin rash or oral lesion (secondary. Gumma (tertiary) • Leave snail track pattern in oral mucosa • Microscope ID of spirochetes to ID using silver stain or darkfield. • Causes fucked up teeth in kids if transmitted by mom |
|
|
|
Tuberculosis: Define, Describe different types. Is oral manifestation primary or secondary?
|
• Mycobacterium tuberculosis
• Oral lesion are secondary infection from pulmonary lesions • Scrofula is the involvement of cervical lymph nodes from drinking contaminated milk. • Primary tb is usually asysmptomatic • Secondary tb = fever malaise, night sweats, weight loss, productive couch, wasting syndrome • Chronic non-healing progressively enlarging, indurated ulcers • Nodular granulomatous proliferation, usually painless |
|
|
|
Tuberculosis DX:
|
PPD skin test and chest xray, biopsy and acid fast stain show presence of bacilli
|
|
|
|
Tuberculosis TX:
|
multi-agent therapy for several months using isoniazid, rifampin, pyrazinamide
|
|
|
|
What are the different types of Inflammatory/reactive lesions:
|
• Mucocele
• Necrotizing sialometaplasia • Sialadenitis • Mumps |
|
|
|
Which lesion involves the salivary gland duct that is severed, pseudocyst, lined by granulation tissue, lumen filled wirg foamy macrophages and inflammatory cells
|
Mucocele
|
|
|
|
Which lesion manifests as local destructive inflammatory condition caused by local trauma, palatal injection, or previous surgery. Associated with pain, within 2-3 weeks tissue sloths off and becomes a crater like ulcer. No treatment it spontaneously resolves in 6-10 week. Happens in the palete.
|
Necrotizing sialometaplasia
|
|
|
|
Describe Sialadenitis, Discuss causes
|
acute or chronic inflammation in major or minor salivary gland due to blocked salivary gland duct, infection or decreased salivary flow. In the parotid gland it is known as parotitis. Causes are viral (mumps), bacterial (staph aureus) most common, or fungal (candida). Non-infectious causes are sjogren syndrome, sarcoidosis. In acute you get PMN, in chronic you get lymphocytes, plasma cells, macrophages and salivary gland is replaced by fibrous connective tissue.
|
|
|
|
Sialadenitis TX:
|
TX= antibiotics, rehydration, surgical drainage, surgical removal.
|
|
|
|
paramyxovirus, affects primarily parotid gland, transmitted in urine, saliva or resp drops. 2-3 weeks incubation period, fever, headache, malaise and chills, swelling of salivary glands. Orchitis are serious complications
|
What is Mumps?
|
|
|
|
Mumps DX:
|
Mumps IgM or IgG titers
|
|
|
|
Mumps TX:
|
palliative for fever and pain.
|
|
|
|
Clinical features of Mucocele:
|
o Fluctuant swelling, bluish hue
o Lower lip most common |
|
|
|
Clinical features of Ranula:
|
o Fluctuant swelling
o Floor of the mouth |
|
|
|
Clinical features of Sialolithiasis:
|
o Major glands: Episodic pain and swelling of the affected gland
o Minor glands: Asymptomatic/local swelling or tenderness o If superficial, firm to palpation and yellowish color |
|
|
|
Clinical features of Necrotizing sialometaplasia:
|
o Initial painful swelling, later necrotic ulcer
o Posterior lateral hard palate and soft palate |
|
|
|
Clinical features of Sialodenosis:
|
o Painful swelling of affected gland
o Purulent discharge if acute infection |
|
|
|
Clinical features of Benign Lymphoepithelial Lesion:
|
• Usually unilateral
• Women > men • 85% of cases in the parotid |
|
|
|
Sialodenosis associated with :
|
• DM
• Hypothyroid • Prego • Malnutrition • Alcoholism • Anorexia nervosa • Bulima |
|
|
|
Bilateral salivary gland enlargement is associated with:
|
• Sjogrens syndrome
• Alcoholism • DM • Prego • Drugs • Malnutrition • HIV |
|
|
|
What are the two types of Salivary Gland tumors:
|
- Benign (adenoma)
- Malignant (adenocarcinoma) |
|
|
|
List the different types of Benign (adenoma) Salivary Gland Tumors:
|
• Encapsulated, freely movable, slow growing, non- tender
• Pleomorphic adenoma (benign mixed tumor). Mostly in superficial lobe of parotid gland and palate. Encapsulated, duct formation, epithelial. Tx= surgical excision, occasional recurrence in major glands. Malignant transformation can occur. Look like a big bump on palate or neck. • Monomorphic adenoma. Upper labial mucosa, buccal mucosa, occurs in adults. Slow growing, painless. Tx= surgical excision. Histo look like coral or brain. • Warthin tumor. Exclusively in the parotid gland, ebv smoking, slow painless mass of parotid sometimes bilateral. Looks like huge bumps on parotid, ridiculous. |
|
|
|
Which Benign (adenoma) Salivary Gland Tumors isMostly in superficial lobe of parotid gland and palate. Encapsulated, duct formation, epithelial.
What is the TX: |
• Pleomorphic adenoma (benign mixed tumor).
Tx= surgical excision, occasional recurrence in major glands. |
|
|
|
Which Benign (adenoma) Salivary Gland Tumors is of the Upper labial mucosa, buccal mucosa, occurs in adults. Slow growing, painless.
What is the TX: |
Monomorphic adenoma.
Tx= surgical excision |
|
|
|
Which Benign (adenoma) Salivary Gland Tumors is . Exclusively in the parotid gland, ebv smoking, slow painless mass of parotid sometimes bilateral.
|
Warthin tumor.
|
|
|
|
What does the Warthin tumor look like?
|
Looks like huge bumps on parotid, ridiculous.
|
|
|
|
What does Pleomorphic adenoma look like?
|
Looks like a big bump on palate or neck.
|
|
|
|
What does Monomorphic adenoma histo look like?
|
Histo look like coral or brain
|
|
|
|
What are characteristics of Malignant (adenocarcinoma) Salivary Gland tumors:
|
Infiltrative, fixed rapid, or slow, larger, can cause pain or paresthesia, ulcerated overlying mucosa
|
|
|
|
What are the different types of
Malignant (adenocarcinoma) Salivary Gland tumors: |
- Mucoepidermoid Carcinoma= most common
- Adenoid Cystic Carcinoma (cylindroma) - Carcinoma ex Pleomorphic Adenoma - Other adenocarcinomas |
|
|
|
Which Malignant (adenocarcinoma) Salivary Gland tumors most common salivary gland malignancy, slow growing mass. Lump on neck, tongue or palete.
|
Mucoepidermoid Carcinoma
|
|
|
|
+++Mucoepidermoid Carcinoma - describe, histo, low grade, high grade TX and prognosis
|
• +++Mucoepidermoid Carcinoma= most common salivary gland malignancy, slow growing mass. Lump on neck, tongue or palete. Low grade TX surgery, mimics neoplasm, prognosis good. Histo has abundant mucous cells and cyst formation. This was on exam. High grade tx is surgery plus radiation, and prognosis poor
|
|
|
|
Which Malignant (adenocarcinoma) Salivary Gland tumors is slow growing tumor, rare in kids, prognosis = recurrence common
|
Adenoid Cystic Carcinoma (cylindroma)
|
|
|
|
Which malignant Salivary Gland Tumor transformation of a pleomorphic adenoma, slow growing pleomorphic ademona which suddenly enlarges fast, become painfull:
What is the TX: |
What is Carcinoma ex Pleomorphic Adenoma.
TX = wide surgical excision poor prognosis. |
|
|
|
Salivary Gland Tumors: Summary of Key Points:
|
• Involve both major and minor glands
• Benign and malignant tumors both have similar clinical presentation • Most malignant salivary gland tumors do not show histopathologic characteristics associated with malignancy • Most occur in adults • Warthin Tumor seen in parotid, may be bilateral • Mucoepidermoid carcinoma o Can occur in children o May occur centrally in bone |
|
|
|
Lab Tests for Benign Soft Tissue Tumors
|
• Radiograph
• CT/MRI • Serology cdc • Needle aspiration • Viral/bacterial culture • Biopsy for histo |
|
|
|
Types of Benign Soft Tissue Tumors
|
- Giant cell Fibroma
- Inflammatory papillary hyperplasia - Pyogenic granuloma - Peripheral Giant Cell Granuloma - Peripheral ossifying fibroma - Neuroma - Hemangioma - Lymphangioma |
|
|
|
What is a fibrous bump on tongue or mouth that is a mass of fibrous connective tissue
|
Giant cell Fibroma
|
|
|
|
Describe Inflammatory papillary hyperplasia.
Describe detailed TX |
bumps under denture tx stop using denture, soak denture in nystatin for 5 mins. Then partial or full thickness excision. Remake denture, reline of tissue conditioner.
|
|
|
|
What is a mass in prego women granulation like tissue?
|
Pyogenic granuloma
|
|
|
|
Pyogenic granuloma TX:
|
Tx excisional biopsy send for hist exam and remove irritation like calculus, scale and root plane.
|
|
|
|
Which benign soft tissue tumor displays multinucleated giant cells in gingiva
|
Peripheral Giant Cell Granuloma
|
|
|
|
Peripheral Giant Cell Granuloma TX:
|
excisional biopsy send to hist exam and clean shit up.
|
|
|
|
Peripheral ossifying fibroma tx:
|
cut out send for hist and exam remove irritant
|
|
|
|
What is a Neuroma?
|
bump on tounge that has sharp shooting electrical pain, comes from nerve bundle with densefibrous stuff around it could also be neurofibroma and in extreme cases neurofibromatosis.
|
|
|
|
What is Hemangioma?
|
vascular proliferation forming multiple capillary blood vessels, blue or purple tongue or mucosa or palete.
|
|
|
|
What is a pebbly vesicle like appearance of a tumor of tongue
|
Lymphangioma
|
|
|
|
What are the steps to ask a person with smoking
|
• Ask (if you smoke)
• Advise (to quit) • Assess (wiliness to quit) • Assist (in the quiting attempt) ((((((Presciption)))))) • Arrange (follow up) |
|
|
|
How should a patient attempt to quit smoking?
|
• Less than 10 cigs = refer patient to nyu nurse or NYS quitline
• 10-15 cigs = 14mg patch for 2 weeks or 4 mg gum or lozenge • More than 15 cigs = 21mg + gum 4mg |
|
|
|
Which drugs are prescribed to assist with smoking cessation?
|
• Varenicline
• Bupropion |
|
|
|
a proliferation of granulation tissue at the opening of a fistula
|
What is a Parulis
|
|
|
|
leave brown spots on iris (Lisch Nodules)and on skin (café au lait)
|
What is Neurofibromatosis
|
|
|
|
Describe a Hemangioma:
|
benign vascular tumor, most common on tongue. Hist has lots of capillaries and is cavernous. Bleed easy
|
|
|
|
= rare non-hereditary developmental condition, vascular proliferation involving tissues of the brain and face. Unilateral port wine stains and intracranial calcifications. Intraoral involvement is common.
|
sturge weber angiomatosis
|
|
|
|
“Doughy” to palpation; usually occurs in floor of mouth; occurs commonly in skin
|
What is a Epidermoid or dermoid cyst?
|
|
|
|
Describe the Lymphoepithelial cyst:
|
Usually has yellow color; (little yellow ball filled with keratin )occurs in floor of mouth, ventral & lateral surfaces of tongue, soft palate & tonsillar area; also occurs in anterior cervical lymph node chain.
|
|
|
|
Which Oral soft tissue lesions of palate has a Midline location and is lobulated
|
Torus
|
|
|
|
Which Oral soft tissue lesions of palate is Non-ulcerated and off midline
|
Pleomorphic Adenoma
|
|
|
|
Oral soft tissue lesions of palate which is Indurated, ulcerated and off midline
|
Adenocarcinoma, lymphoma
|
|
|
|
Which Oral soft tissue lesions of palate are seen in HIV-positive individuals
|
Lymphoma, Kaposi’s sarcoma
|
|
|
|
Gingival enlargement cause by :
|
• Dilantin
• Cyclosporine • Calcium channel blockers • Leukemia • Fibromatosis |
|
|
|
Topical Antifungal Treatment:
|
Rx: Clotrimazole 10mg troches,
Disp: 60 troches Label: Dissolve troche (lozenge) slowly in mouth 5 times a day until finished (2-3 days beyond lesion resolution) – 2 weeks for treatment Rx: Nystatin oral suspension 100,000 units/ml Disp: 240 ml Label: wipe lesions with gauze then hold 1 teaspoonful (500,000 u) in mouth for 5minutes, 4 times/day and swallow/or expectorate |
|
|
|
Systemic Antifungals:
|
• Fluconazole
• Disp: 15 tabs • Label: take 2 tabs stat then 1 tab daily until finished |
|
|
|
List the EBV-induced diseases with oral manifestations:
|
o infectious mononucleosis,
o oral hairy leukoplakia, one of the most common oral manifestations of EBV o nasopharyngeal carcinoma most common malignancy associated with EBV occurs in particularly an Asian population o Burkitt’s lymphoma also associated with EBV |
|
|
|
one of the most common oral manifestations of EBV
|
o oral hairy leukoplakia
|
|
|
|
Most common malignancy associated with EBV
(occurs in particularly an Asian population) |
nasopharyngeal carcinoma
|
|
|
|
How is EBV transmitted? What are the symptoms for various age groups
|
Transmitted through saliva
o Childhood exposure- asymptomatic o Adolescent/adult exposure- symptomatic Fever, lymphadenopathy, pharyngitis, tonsillitis Occasionally hepatosplenomegaly |
|
|
|
Paramyxovirus causes what disease
|
measles
|
|
|
|
Multiple Myeloma clinical features are:
|
– Bone pain, pathologic fractures
– Anemia, low platelets (bleeding), low neutrophils (susceptibility to bacterial infections) – Increased serum calcium (hypercalcemia): confusion, weakness, lethargy and constipation – 99% of patients have increased blood immunoglobulin and/or Bence-Jones proteins in urine – Amyloid deposition in various soft tissues – Amyloid - periorbital skin, neck, lips, oral mucosa, tongue (sometimes, macroglossia) |
|
|
|
take up and process microbial antigens to become fully functional antigen-presenting cells.
|
What are Langerhans cells
|
|
|
|
Features of Langerhans Cell Disease:
|
• Jaw lesions 10-20%
• Alveolar bone destruction results in loose teeth • Ulcer and/or soft tissue proliferation over the bone lesion • Disseminated disease with skin, bone and internal organ involvement • Ulcer or soft tissue proliferation over the bone lesion |
|
|
|
Langerhans Cell Disease TX:
|
• Surgical - for localized, accessible lesions (curettage)
• Low dose radiation for inaccessible lesions • Chemotherapy for disseminated disease |
|
|
|
How does Thalassemia affect the
Head and neck? |
• Frontal bossing, “hair-on-end” appearance of calvaria
• Enlarged jaws • ‘Honeycomb’ bone pattern • Delayed eruption |
|
|
|
Thrombocytopenia can be caused by:
|
• Stem cell problems: Aplastic anemia; bone marrow infiltration by malignancy (leukemia, metastatic malignancy)
• Defective DNA synthesis: Megaloblastic anemia • Infections: Viral • Alcohol • Drug-induced: Antibiotics, thiazides, cytotoxic drugs, etc. |
|
|
|
What are the different types of Hypersensitive rxns:
|
Type 1 = allergies = IgE, mast cells
Type II = penicillin hyper sensitivity, autoimmune disease Type III = serum sickness, endocarditis = AG-Ab complexes = autoimmune Type IV = contact hypersensitivity = T cell mediated, autoimmune |
|
|
|
Which type of Hypersensitive rxns have contact hypersensitivity = T cell mediated, autoimmune
|
Type IV
|
|
|
|
Which type of Hypersensitive rxns= allergies = IgE, mast cells
|
Type 1
|
|
|
|
Which type of Hypersensitive rxns
has serum sickness, endocarditis = AG-Ab complexes = autoimmune |
Type III
|
|
|
|
Which type of Hypersensitive rxns has penicillin hyper sensitivity, autoimmune disease
|
Type II
|
|
|
|
What is ANUG and what causes it?
|
Necrotizing periodontal disease is caused by a bacterial infection that includes anaerobes such as P. intermedia[3] and Fusobacterium as well as spirochetes, such as Borrelia and Treponema.
|
|
|
|
necrotizing periodontal diseases was originally associated with what disease? and now?
|
In the late 1980s-early 1990s, it was originally thought that necrotizing periodontal diseases were strictly a sequela of HIV, and it was even called HIV-associated periodontitis.[5] It is now understood that its association with HIV/AIDS was due to the immunocompromised status of such patients, and it occurs with higher prevalence in association with other diseases in which the immune system is compromised
|
|
|
|
Clinical features of necrotizing periodontal disease may include:
|
• necrosis and/or punched out ulceration of the interdental papillae ("punched-out papillae")[3] or gingival margin[clarification needed]
• pseudomembranous formation[clarification needed] • painful, bright red marginal gingiva that bleed upon gentle manipulation • halitosis |
|
|
|
necrotizing periodontal TX:
|
Treatment includes irrigation and debridement of necrotic areas (areas of dead and/or dying gum tissue), oral hygiene instruction and the uses of mouth rinses and pain medication. As these diseases are often associated with systemic medical issues, proper management of the systemic disorders is appropriate.[2] Metronidazole is an antibiotic that works well to kill the specific bacteria associated with ANUG; amoxicillin is broad-spectrum penicillin that also works well in treating the acute phase. These are antibiotics that must be taken orally to work their way through the body. Taken together with chlorhexidine, a prescription antibacterial mouthrinse, and saline (mild saltwater) rinses, symptoms should abate within 24 to 48 hours.
|
|
|
|
Describe Oral Melanotic Macule:
appearance, location in order of most frequent, size, and tx: |
• “freckle” (professional term “ephilis”)
• The oral melanotic macule occurs at any age in both men and women • LOWER LIP is the most common site of occurrence (33%), followed by the buccal mucosa, gingiva, and palate. • The typical lesion appears as a solitary (17% are multiple), well-demarcated, uniformly tan to dark-brown, asymptomatic (always) , round or oval macule with a diameter of 7mm or smaller • Lesions generally don’t enlarge over time • Treatment usually NOT required for the, except for aesthetic considerations • All oral pigmented macules of recent onset, large size, irregular pigmentation, unknown duration, or recent enlargement should be submitted for microscopic examination |
|
|
|
Oral Melanotic Macule associated with:
|
o Peutz-Jeghers syndrome
o Addison’s disease |
|
|
|
Types of Oral Melanosis:
|
• Drug-induced melanosis
• Inflammatory/reactive melanosis • Smoker’s melanosis |
|
|
|
Is Oral Melanoma a common or rare metastatic event?
|
rare metastatic event
|
|
|
|
to measure dry mouth
|
Sialometry
|
|
|
|
Describe Sialometry: to measure dry mouth
|
o Difficult to guage since its dependent upon pt’s normal baseline
o Unstimulated flow <0.1ml/minute = abnormal o Stimulated flow <0.5ml/min = abnormal |
|
