DHYG 314 Review Questions PDF

**[DHYG 314 REVIEW QUESTIONS]** **INTRODUCTION TO PRELIM DIAGNOSIS** 1. **What does the diagnostic process include** a. Requires gathering of information that is relevant to the client and the lesion being evaluated b. Usually one area alone will not provide sufficient informa...

**[DHYG 314 REVIEW QUESTIONS]** **INTRODUCTION TO PRELIM DIAGNOSIS** 1. **What does the diagnostic process include** a. Requires gathering of information that is relevant to the client and the lesion being evaluated b. Usually one area alone will not provide sufficient information to make a diagnosis c. The strength of the diagnosis if often a combination of data collected. 2. **What are the 8 categories that play a role in the final diagnosis** d. Clinical diagnosis e. Radiographic diagnosis f. Historical diagnosis g. Laboratory diagnosis h. Microscopic diagnosis i. Surgical diagnosis j. Therapeutic diagnosis k. Differential diagnosis/findings 3. **How does a clinician make a diagnosis** l. The clinician can establish a diagnosis for some lesions on the basis of colour, shape, location and history. 4. **How do you know whether a referral is necessary** m. When a 'clinical diagnosis' can be made on the basis of the above unique features, biopsy or surgical intervention is not necessary 5. **What historical data do we need from the client when making a clinical diagnosis** n. Historical data is an important component in every diagnosis. o. Personal history, family history, past and present medical and dental histories, history of presenting disease or lesion, history of drug ingestion can all provide information necessary for the final diagnosis 6. **How can the lab help with a clinical diagnosis** p. Clinical lab tests, including blood chemistry and urinalysis, can provide information helpful to a diagnosis 7. **How do you get a good surgical diagnosis** q. The strength of the surgical diagnosis comes from surgical intervention 8. **What is the differential diagnosis** r. This is the point in the diagnostic process when the practitioner decides which test or procedure is required to rule out the conditions originally suspected and to establish the definitive or final diagnosis 9. **What are the 7 components of a differential diagnosis** s. Clinical, historical, radiographic, laboratory, microscopic, surgical, therapeutic 10. **What are the 6 observations implying a more benign condition** t. Nonulcerated lesion u. Bilateral involvement v. Sharply demarcated borders w. Multiple areas of involvement x. Elevated, soft, and moveable y. Lesions that have a direct cause-and-effect relationship 11. **What are the 8 observations implying a malignant of aggressive lesion** z. Paresthesia -- numbness or tingling a. Single area of involvement -- not bilateral b. Poorly defined and ragged borders c. Flat, indurated, and fixed lesions d. Alteration of the periodontal ligament space and/or the lamina dura e. Mixed red and white lesions; velvety red lesions f. Lesions on the lateral borders of the tongue, soft palate, floor of the mouth, and lip g. Radiographic evidence of bone expansion or root erosion, displacement, or resorption 12. **The dental hygienist\'s ability to effectively obtain information from the patient depends on many factors (list the 3)** h. Showing genuine concern i. Having a non- judgmental attitude j. Asking the right questions in the right way. 13. **What is a differential diagnosis** k. A differential diagnosis is a listing of all the probable causes of a particular disease manifestation or group of manifestations. 14. **What are the 5 steps of making a differential diagnosis** l. Describe the abnormality in clinical terms m. Determine the list of diseases/conditions that present with similar manifestations n. Eliminate some of the possible causes already on your list by adding other factors that could be involved with the abnormality. Such as chronic health condition, medications, age, and whether the patient has any other manifestations that are inconsistent with any of the listed possibilities. o. Rank the remaining possible causes according to the probability they are the causative agent p. Decide what additional information might be necessary to eliminate more of the possibilities, such as blood work, biopsy, diagnostic radiographs, cultures of oral microbes, and medical consultations. 15. **Describe how we can determine the cause of the lesion if it is only temporary** q. We may determine that the lesion is most likely caused by an irritant, like eating spicy or sour foods/candy. If the patient stops eating them, and the lesion or condition clears up, then it is resolved, and the cause-effect is known 16. **What happens if the definitive diagnosis is not determined** r. If the definitive diagnosis is not determined, then the list of conditions that remains is the differential diagnosis. And necessary referrals will be needed. 17. **How do we determine the definitive diagnosis** s. This is determined when all of the suspected causes on our list except one have been eliminated. - That one is the definitive diagnosis. 18. **When we need to refer, who do we refer to** t. In many cases we will need to refer to: i. An oral surgeon for a biopsy; ii. General dentist office for biopsy, exfoliative smear, cytology, or brush biopsy **INTRO TO GENERAL AND ORAL PATHOLOGY INCLUDING DIFFERENTIAL DIAGNOSIS** 1. **Describe 3 things to consider when going through the diagnostic process** a. Requires gathering of information that is relevant to the client and the lesion being evaluated b. Usually one area alone will not provide sufficient information to make a diagnosis c. The strength of the diagnosis if often a combination of data collected. 2. **What are the 8 categories that play a role in the final diagnosis?** d. Clinical diagnosis e. Radiographic diagnosis f. Historical diagnosis g. Laboratory diagnosis h. Microscopic diagnosis i. Surgical diagnosis j. Therapeutic diagnosis k. Differential diagnosis/findings 3. **What basis does the clinician (dental hygienist) use to diagnose some lesions? Are biopsies or surgical interventions necessary? Give examples?** l. on the basis of colour, shape, location and history. m. When a 'clinical diagnosis' can be made on the basis of the above unique features, biopsy or surgical intervention is not necessary i. Fordyce granules, fissured tongue, herpetic ulcers 4. **Tru** **WEEK 3: NEOPLASIA** 1. **Define Neoplasia** a. New growth b. Cells exhibit uncontrolled and abnormal proliferation c. is an uncontrolled abnormal process, the cells are abnormal and the proliferation of cells are unlimited and uncontrolled 2. **Define Neoplasm** d. A mass of such cells 3. **Define a tumor** e. Means swelling, but is often used as a synonym for neoplasm 4. **What is oncology** f. The study of tumors or neoplasms 5. **What needs to happen for a Neoplasia to occur** g. An irreversible change must take place in the cells h. This change must be passed on to new cells i. Which results in uncontrolled cell manipulation 6. **Define Hyperplasia** j. normal cells proliferate in a normal arrangement in response to tissue damage. The proliferation stops when the stimulus is removed 7. **Compare a neoplasia to a hyperplasia** k. Neoplasia i. Abnormal cells ii. Uncontrolled proliferation iii. Does not normally stop growing l. Hyperplasia iv. Cells appear normal v. Does not permeate into other systems vi. Stops when stimulus removed 8. **List the characteristics of a benign neoplastic growth** m. Slow growth. n. Expands into tissues, usually encapsulated. o. Cells are well differentiated. p. Do not metastasize (spread). 9. **List the characteristics of a malignant neoplastic growth** q. Variable growth rate, depends on the level of cell differentiation. r. Invades surrounding tissues by infiltration, not encapsulated. s. Undifferentiated cells may not resemble cells of origin. t. Metastasizes to distant tissues. 10. **Define Carcinogenesis** u. The development or process of cancer growth; genetic damage or mutation is the foundation of carcinogenesis. 11. **What are the 5 etiology of genetic damage** v. Inherited traits/influences w. Chemicals x. Environmental insults/agents y. Viral infections z. Immune system defects 12. **What is a carcinoma in situ** a. cancer in waiting because there is change in the cells but they haven't proliferated to the extent of cancerous cells, but when it does, it will stay local to the area 13. **What are 3 systems in which the body can metastasize** b. Lymph system---most common method; cells enter lymph vessel, travel to regional lymph nodes, and establish secondary tumor; eventually, cells enter circulating blood through venous drainage of lymph system. c. Blood system---more complicated because tumor cells must first invade the vessel and circulate until finding a place to attach to vascular endothelium. Then, cells must breach the endothelium again before multiplying. d. Seeding---body cavities provide avenue for tumor metastasis; cancer cells growing in abdominal organs or lungs may break off and travel through spaces to grow in adjacent organs. 14. **Describe 3 ways in which disease can spread locally.** e. Mechanical pressure---pressure on normal cells weakens or destroys them by disrupting nutrient supply, allowing cancer cells access to surrounding tissues. f. Enzymes---enzymes destroy collagen and weaken extracellular substances holding normal tissue cells together, allowing cancer cells to spread. g. Lack of adhesion---cancer cells (especially epithelial) do not adhere to each other well allowing them to break apart and move through tissues. 15. **What are 4 ways you can screen for cancer** h. Physical exams (visual/palpation) i. Radiographs (mammography) j. Pap smear k. Oral screening devices (brush biopsy and others) 16. **What are the symptoms of cancer** l. Related to the area or tissue involved vii. Ulceration of epithelial tissues, enlargement of tissues impinging on structures. viii. Endocrine tissues may overproduce hormones. ix. Nervous system cancers may cause loss of memory, balance, and pain. x. Bone fractures, pain, or growths. 17. **How can a laboratory be used to screen for cancer** m. Blood tests and saliva tests n. Tumor markers---chemicals produced by specific types of cancer cells; elevated level of these requires further testing to rule out presence of cancer. 18. **What is a Biopsy** o. microscopic evaluation of cells is the only definitive method for determining if a lesion is benign or malignant. 19. **How can you prevent oral cancer** p. Stop the use of tobacco products q. Proper nutrition xi. Eat a variety of fruits and vegetables every day xii. Reduce the amount of refined grains and sugars consumed xiii. Reduce the amount of high-fat red meat consumed r. Maintain a healthy weight throughout life xiv. Stay physically active s. Limit alcohol consumption t. Limit sun exposure, use sunscreen, or other protection 20. **What does nonmelanoma mean** u. Cancer that does not start in the cells but rather in the skin 21. **What does melanoma mean** v. Cancer that starts in the melanocytes. 22. **What is the etiology and pathogenesis of Basal cell carcinoma** w. Pathogenesis---UV exposure causes accumulation of genetic defects over time; lesion exhibits slow growth x. Etiology---UV light, genetic factors, immunosuppression 23. **What is the most common form of skin cancer** y. Basal cell carcinoma 24. **What are the characteristics of basal cell carcinoma** z. most found in head and neck area, classic lesion appears nodular with depressed center and rolled pearly borders often with capillaries seen throughout the border area, alternative presentations a. Nodular without ulceration b. Pigmented like a nevus c. Flat scar-like 25. **What are the dental implications of basal cell carcinoma** d. Any unidentified lesion should be investigated. e. Refer for definitive diagnosis if lesion is suspicious. 26. **What is the treatment for basal cell carcinoma** f. surgical excision, laser surgery, cryosurgery (freezing with liquid nitrogen), electrodesiccation (burning), and radiation therapy g. Radiation therapy---large tumors, those involving areas difficult to access, or other surgical problems such as tumors on the eyelids h. The earlier these cancers are identified, the less invasive the procedures will have to be. 27. **What is the etiology and pathogenesis of squamous cell carcinoma** i. Etiology---UV light, burned areas, genetics, and HPV 28. **What is the second most common skin cancer** j. Squamous cell carcinoma 29. **What are the characteristics of squamous cell carcinoma** k. painless, nonhealing, rough, red scaly papule that eventually becomes ulcerated and crusted as it enlarges 30. **What is the treatment for squamous cell carcinoma** l. surgical excision, m. laser surgery, n. cryosurgery (freezing with liquid nitrogen), o. electrodesiccation (burning), p. radiation therapy and photodynamic therapy (PDT), q. chemotherapy used to treat metastatic SCC, r. radiation therapy used for small tumors or to delay growth of large tumors or for areas where surgery is difficult or contraindicated. 31. **What are the risk factors of melanoma** s. UV radiation t. Artificial tanning u. Nevi (macule) /moles v. Immunosuppression w. Personal and/or family history of skin cancer and/or melanoma x. Physical characteristics (fair skin, hair, etc.) y. History of blistering sunburns 32. **What is the epidemiology of melanoma** z. Less than 1% of all skin cancers a. Cause the majority of skin cancer deaths xv. Leading cause in women age 25 to 30 xvi. Second leading cause in women age 30 to 35 b. Most found in Caucasian men over age 50 33. **What is the pathogenesis of melanoma** c. Develops within melanocytes or preexisting nevus d. Two stages of growth depending on type of melanoma xvii. Horizontal---may not breach basement membrane for years xviii. Vertical---breaches the basement membrane and spreads to local and distant sites e. Metastasis occurs through circulatory or lymphatic systems 34. **What are the characteristics of melanoma** f. Wide range of color possibilities xix. Shades of brown and black xx. Red xxi. Skin colored or nonpigmented g. Change in sensations h. Large flat multicolored macules i. Firm dome-shaped shiny lesions -- when it starts to grow 35. **What are the ABCDEs of melanoma** j. A: asymmetry k. B: border irregularity l. C: colour m. D: diameter n. E: evolving 36. **What are the dental implications of a melanoma** o. Students should not be afraid to look at the exposed skin of their patients and note the presence of nevi and other skin lesions or conditions. A record of the location, size etc., should be recorded in the record and the patient should be referred if **[ANY]** suspicious areas are found. 37. **What is the treatment for a melanoma** p. Surgery is treatment of choice with very large margins. q. All nodes in the area must be removes if even one node is involved. r. Radiation and chemotherapy are used to lengthen life and improve quality of life in those with distant metastasis. WEEK 3: NEOPLASIA PART 2 1. **What is a Lipoma** a. benign tumor of fat cells 2. **What is a Osteoma** b. benign tumor of bone 3. **What is a carcinoma** c. malignant tumor of epithelium 4. **What is a sarcoma** d. malignant tumor of CT 5. **What is a squamous cell carcinoma** e. malignant tumor of squamous cells 6. **What is osteosarcoma** f. malignant tumor of bone 7. **Describe what a papilloma** g. Benign h. Small, exophytic i. Pedunculated or sessile growth j. Composed of numerous papillary projections that may be either white or the normal colour of mucosa 8. **What does a papilloma look like? Where is it most often found? What age does it occur?** k. Often described as cauliflower like in appearance l. Most often on the soft palate or tongue m. Can occur at any age 9. **How is a papilloma treated** n. A papilloma is treated by surgical excision, which must include the base of the growth. Usually will not reoccur 10. **What are the 3 types of premalignant lesions** o. Leukoplakia, erythroplakia, epithelial dysplasia 11. **What is a leukoplakia** p. Defined as a white plaque-like lesion of the oral mucosa that can't be rubbed off and cannot be diagnosed clinically as a specific disease 12. **What is a idiopathic leukoplakia** q. etiology of the lesion is unknown 13. **How do most leukoplakias occur?** r. Most leukoplakias are the result of hyperkeratosis (a thickening of the keratin layer) Or A combination of epithelial hyperplasia (thickening of the prickle cell or spinous layer) And Hyperkeratosis 14. **Where are leukoplakias mostly found in the mouth?** s. floor of the mouth, tongue, soft palate, and lip is more likely to represent epithelial dysplasia or squamous cell carcinoma than leukoplakia 15. **What should you do when a white lesion is identified in the oral cavity?** t. When a white lesion is identified in the oral cavity, the first goal is to ***identify the cause***. u. Any associated irritation should be removed v. If the lesion does not resolve-- a biopsy and microscopic examination of the tissue MUST be done 16. **What does the treatment of leukoplakia depend on?** w. The treatment of leukoplakia depends on the microscopic diagnosis 17. **What is an erythroplakia** x. Is a clinical term used to describe an oral mucosal lesion that appears as a ***smooth red patch or granular red and velvety patch*** 18. **What is a speckled leukoplakia** y. A lesion that shows a mixture of red and white areas 19. **Where do most erythroplakias occur?** z. Most cases of erythroplakia occur in the floor of the mouth, tongue, and soft palate 20. **What do most erythroplakias demonstrate on a microscopic level and what should we do if they are found?** a. Microscopically- 90% of erythroplakia demonstrate epithelial dysplasia or squamous cell carcinoma -- send for a consult for them to have a biopsy. b. Because of this, it is considered a more serious clinical finding than leukoplakia c. A biopsy must be performed to establish a definitive diagnosis d. Treatment depends on the microscopic diagnosis 21. **What is a epithelial dysplasia** e. A microscopic diagnosis that indicates *disordered growth* f. Considered a premalignant condition 22. **What do lesions that microscopically exhibit epithelial dysplasia frequently precede?** g. squamous cell carcinoma 23. **What does epithelial dysplasia look like clinically** h. May present clinically as erythematous (red) lesion, a white lesion (leukoplakia) or a mixed red and white lesion (speckled leukoplakia) 24. **Where are most epithelial dysplasias found in the mouth?** i. Lesions often arise in the floor of the mouth or tongue 25. **What do epithelial dysplasias look like microscopically?** j. Microscopically- abnormal maturation of epithelial cells with disorganization of the epithelial layers k. Epithelial cells with enlarged and hyperchromatic nuclei l. Hyperplasia of the basal cells 26. **How does epithelial dysplasia differ form SCC** m. that there is no invasion of the abnormal epithelial cells through the basement membrane into the underlying tissue 27. **What is carcinoma-in-situ** n. severe dysplasia involving the full thickness of epithelium but NOT through the basement membrane 28. **How should all dysplastic lesions be dealt with?** o. All dysplastic lesions should be surgically excised 29. **What is Verrucous Carcinoma** p. Is actually a form of SCC that is separated from other SCC since it has a much better prognosis 30. **What is the clinical appearance of Verrucous carcinoma** q. Slow exophytic tumor with a pebbly white and red surface. 31. **What does a verrucous carcinoma look like histologically?** r. Many papillary epithelial proliferations s. Spaces between proliferations filled with keratin t. Epithelium is well-differentiated, does not contain atypical cells u. Basement membrane is intact v. Does not show invasion through the basement membrane 32. **What is the treatment for verrucous carcinoma** w. Surgical excision x. Usually does not metastasize, therefore has a favorable prognosis y. If not treated, may cause extensive local damage 33. **Common places where verrucous carcinoma** z. verr.jpg 34. **What is a neoplasm** a. refers to a mass that has developed due to abnormal cell or tissue growth. Neoplasia refers to various types of growths including non-cancerous or benign tumors, precancerous growths, carcinoma in situ and malignant or cancerous tumors 35. **What is a non-neoplasm** b. refers to the abnormal and disordered production of cementum and bone 36. **What are the 3 types of cemento-osseous dysplasia (non neoplastic disease of bone)** c. Peripheral d. Florid e. Focal 37. **What is an Paget Disease of Bone** f. A chronic metabolic bone disease i. Characterized by resorption, osteoblastic repair, and remineralization of involved bone ii. Unknown cause -- may be due to a virus iii. Most commonly occurs in men over age 50 iv. The maxilla is more commonly affected than the mandible. 38. **What are the clinical and radiographic features of paget disease of bone** g. Clinical and radiographic features v. Enlargement is common; the patient often complains of pain. vi. Spaces may increase between teeth as bone enlarges. h. Radiographic vii. A patchy radiolucency and radiopacity, "cotton wool" viii. Hypercementosis, loss of lamina dura, and obliteration of the periodontal ligament may occur. 39. **What is the diagnosis and treatment of paget disease of bone** i. Diagnosis and Treatment ix. The serum alkaline phosphatase level is significantly elevated in active disease. x. Histologic examination reveals bony trabeculae surfaced with numerous osteoclasts and osteoblasts. xi. Prominent reversal lines may create a pattern known as mosaic bone. 40. **What is Giant cell Granuloma** j. Composed of well-vascularized connective tissue containing many multinucleated giant cells xii. Occurs within bone xiii. (Peripheral GCG-Chapter 2) k. Usually in anterior areas of bone. l. May cause displacement of teeth. m. Uni/Multilocular radiolucency in bone. n. Surgical removal, may recur. 41. **What are some of the differential diagnosis of central giant cell granuloma** o. [ameloblastoma](http://en.wikipedia.org/wiki/Ameloblastoma), p. [odontogenic myxoma](http://en.wikipedia.org/wiki/Odontogenic_myxoma), q. hemangioma, 42. **What is a Osteomalacia** r. A disease of bone that develops over a long period of time xiv. The result of calcium deficiency xv. In young children, it is usually caused by a deficiency of vitamin D (rickets). xvi. In adults, it may be related to various health disorders.(drugs, liver, kidney) 43. **What is the clinical and radiographic features of Osteomalacia** s. Clinical and radiographic features xvii. May be associated with delayed tooth eruption and periodontal disease 44. **What is the treatment for a Osteomalacia** t. Based on identification of the cause **WEEK 4: SKIN LESIONS** 1. **Who are at a higher risk for skin cancer** a. Patients who wear metal frame glasses -- draws sun rays b. Light skinned c. People how have blue or green eyes d. People who spend time in the sun, under sun lamps, or tanning beds 2. **What rate is melanoma in terms of skin cancers** e. The melanoma rate is 2% of skin cancers. 3. **What group is mostly likely to experience cancer?** f. Melanoma is the most common cancer in women age 20 to 29 years. 4. **What does melanoma in the nail look like? Who is more common to experience this** g. Dark steaks, red, brown or black ridges h. Dark skinned individuals 5. **Describe the dangers of tanning beds** i. Increases the chance of melanoma. j. Are often unregulated k. Bulbs in devices are often not regulated. l. Protective glasses are not used. m. Children as young as 10 to 11 years are allowed in many. 6. **Describe basal cell carcinoma** n. Usually occurs on the upper 2/3 of the face o. Rolled borders with a waxy-type appearance p. Pearly iridescent-type surface 7. **True or false, Basal cell and squamous cell carcinoma account for most of the skin cancers** q. True 8. **There is a 90% cure rate of basal cell and squamous cell if detected early** r. True 9. **Describe squamous cell carcinoma** s. May occur on any skin surface. Lower lip is a prime area. t. Vermillion border is lost---no definition. u. Small lines running from the lips are increased from sun damage. 10. **Describe Actinic Keratosis** v. Most common type of precancerous skin lesion. w. May appear as an early melanoma. x. Referral to a dermatologist is needed. 11. **Describe Actinic Cheilitis** y. Caused by solar damage. Also called **solar cheilitis**. z. Smoking is a risk factor. a. Scaling, peeling appearance. 12. **Describe Acrochordon -- benign** b. Skin tag c. Stalk-like or pedunculated d. Flesh coloured - same as person's skin tone e. Can be found anywhere 13. **Describe Comedones -- benign** f. Dilated hair follicles i. Inflammed hair follicle g. Filled with keratin, bacteria, and sebum h. Blackened mass of epithelial debris 14. **Describe Eczema -- benign** i. Inflammatory response of the skin to multiple agents j. Dryness, pruritus, and inflammation k. May need topical steroids 15. **Describe Keloid -- benign** l. More common in dark skinned women m. Hyperplastic scar tissue n. Caused by an injury, 16. **Describe Solar lentigo** o. Benign macules caused by sun exposure. AKA: liver spots and age spots. p. They are lighter in colour compared to skin cancer patches 17. **Describe Milia -- benign** q. Milia (plural of milium) r. Subepidermal keratinous cysts (inclusion cysts  18. **Describe Psoriasis -- benign** s. Red, plaque-like lesions covered with a white thin scale, appearing pearly, iridescent appearance t. Etiology: genetic, environmental, and trauma 19. **Describe Rhinophyma -- benign** u. Called "hammer nose." v. Increased fibrosis and vascularity. w. Nose may appear enlarged and capillaries may be increased in number. 20. **Describe Seborrheic Keratoses -- benign** x. Benign but may appear as melanoma or warts y. Caused by overproduction of sebum by the sebaceous glands z. Part of it is flat/raised a. Has darker areas and can grow. b. Important to check because they resemble melanoma  21. **Describe Xanthelasma -- benign** c. Found in lower eyelids in the corner of the eye d. Flat, yellow to orange plaques e. Heavy lipid plaques. The patient should be checked for cholesterol levels since this is an indication of high production of lipids. f. 22. **Describe Erythema Multiforme -- benign** g. Iris lesion, target lesion, bull's-eye h. May be caused by HSV, mycoplasma, tuberculosis, histoplasmosis, and medications i. Show up on the finger nails 23. **Describe Graft Versus Host Disease** j. Occurs in association with organ or bone marrow transplantation. k. The oral cavity may be involved in 80% of cases. l. Grafted bone marrow recognizes the tissue as foreign and attacks them. GVHD occurs in up to 45% of bone marrow patients, and most of the time (80%) the oral tissues are involved. m. The changes in tissue can occur at any time: immediately or years later. Loss of pigmentation occurring in a patch-like appearance. 24. **Describe Impetigo** n. Caused by *Staphylococcus aureus* and streptococci organisms o. Cortisone cream or antibiotic is used to clear it up. p. Day care centers have high rates and also any facility where children are in close proximity. Highly contagious. Dental procedures should be postponed so that the clinician does not spread the disease. 25. **Describe Lichen Planus** q. Lichen planus of the lips. r. Lichen planus may be oral or cutaneous. s. Polygonal, purple, pruritic, plaques. t. Some corticosteroids may thin the lip tissue, and good results have been found with aloe vera gel from an aloe vera plant. u. Skin lesions. v. Women should let their gynecologist know that they have oral lichen planus. They may also have vaginal lichen planus. w. Pain or difficulty in swallowing may also indicate esophageal lichen planus. -- means lichen planus has spread to the esophagus x. Lichen planus may affect any lining mucosa. 26. **Describe Lupus Erythematosus** y. Autoimmune z. Systemic/discoid lupus a. Multisystem---affects vital organs b. Ulcers and erosive oral lesions c. Discoid lupus d. Butterfly rash ii. Bridge of nose, tops of cheeks e. Skin and scalp may be involved. 27. **Describe Scleroderma** f. Sclerodactyly---skin becomes hardened and thickened g. The skin becomes hardened and thickened. This is especially problematic in the hands, fingers, and mouth. The areas may become constricted enough to limit function. Raynaud's is found in conjunction with numbness and pallor of fingers, toes, and nose due to intermittent lack of blood flow. Many organs are affected with fibrosis h. Abnormality in calcium metabolism causes a deposition of calcium salts in the tissues that is called calcinosis and may lead to thickening and tightening of the skin and the extremities. i. This may make dexterity limited. Morphea is firm, hardened patches of skin. Raynaud's is localized ischemia caused by spasm of the arteries. Esophageal dysmotility is tightening of the mouth and esophagus that may cause hoarseness and wheezing. Sclerodactyly is localized scleroderma of the digits. Telangiectasia is permanent dilation of small blood vessels. 28. **Describe Vitiligo** j. Vitiligo is an autoimmune disease that destroys or alters the melanocytes. The skin has a patch that is much lighter due to the loss of pigmentation. The etiology may be exposure to a chemical or an unidentified problem in melanocyte growth factor. Skin sensitivity and sun sensitivity are a problem, and patients should be encouraged to stay out of the sun and to wear a sunscreen with a high SPF factor. k. Lip balms with sun protection are recommended. 29. **What should be noted when doing an EO/IO** l. Any abnormal discoloration or change in tissue should be noted. 30. **Who do we refer to** m. Referral to the proper specialist is needed such as a dermatologist or other specialist. This may even be a cardiologist or a gastroenterologist. **WEEK 4: DEVELOPMENTAL** 1. **Define developmental** a. Disturbance in the development of the fetus 2. **Define Hereditary** b. Passed from one generation to another 3. **Define Congenital** c. Present at or around the time of birth d. May be developmental or genetic in nature 4. **What are developmental disorders** e. A failure during the process of cell division and differentiation into various tissues and structures 5. **What causes developmental abnormalities (and list some examples)** f. Teratogenic agents i. Alcohol or tobacco ii. Prescription drugs iii. Illegal drugs iv. Microorganisms v. Nutritional deficiencies vi. Maternal disease 6. **What is the etiology and pathogenesis of fetal alcohol syndrome** g. Consumption of alcohol during pregnancy h. Alcohol crosses the placental barrier 7. **What are extraoral characteristics of Fetal Alcohol Syndrome** i. Growth deficits, facial features, neurodevelopmental problems 8. **What are the facial features of Fetal alcohol syndrome** j. Narrow eyes with epicanthal folds k. Short nose with a turned-up end l. Thin upper lip with an indistinct flat philtrum area m. Facial features become less obvious with age 9. **What are the dental implications of fetal alcohol syndrome?** n. Recognition/referral. -- refer back to medical doctor o. Education about teratogenic effects of alcohol. p. Identify medical conditions such as congenital heart defects and evaluate for prophylactic antibiotics. q. Identify medications and determine side effects, etc. r. Educate about the importance of good oral health. 10. **What is the etiology of TORCH syndrome?** s. T---Toxoplasmosis t. O---Other infections such as syphilis, tuberculosis, and varicella--zoster virus u. R---Rubella v. C---Cytomegalovirus w. H---Herpesvirus 11. **What is the epidemiology of TORCH syndrome** x. 1 in 5 live births 12. **What are the extraoral characteristics of TORCH syndrome** y. Premature birth z. Microcephaly, encephalitis, hydrocephaly a. Mental deficiency b. Hearing loss, visual impairment c. Bleeding disorders d. Congenital heart defects 13. **What are the intraoral characteristics of TORCH syndrome** e. Congenital syphilis f. Perinatal herpes---vesicular lesions 14. **What will congenital syphilis cause on the primary teeth** g. Hutchinson incisors h. Mulberry molars 15. **What are the dental implications of TORCH syndrome** i. Treatment modifications j. Education 16. **What is the treatment for TORCH syndrome.** k. Prevention l. Dental care 17. **Describe Osteogenesis Imperfecta** m. Dentinogenesis imperfecta--like condition n. Microdontia o. Teeth appear opalescent or translucent but darken with age p. Enamel is lost because of abnormal dentin 18. **Describe torus mandibularis** q. An autosomal-dominant inheritance pattern with variable expression and marked penetrance 19. **Describe maxillary exostosis** r. An autosomal-dominant inheritance pattern s. Occurs on the buccal aspect of the maxilla t. May be single, multiple, unilateral, or bilateral 20. **What is Amelogenesis Imperfecta** u. A group of inherited conditions affecting the enamel of teeth with no associated systemic defects 21. **Describe Dentinogenesis Imperfecta** v. Multiple types w. Associated with osteogenesis imperfecta x. Hereditary opalescent dentin y. No pulp chambers or root canals are seen z. Roots are short and thin with periapical radiolucencies 22. **Describe pegged or absent maxillary lateral incisors** a. An autosomal-dominant inheritance pattern with variable expression vii. Lateral incisors may be small, peg shaped, or congenitally missing 23. **List inherited disorders affecting the gingiva and periodontium** b. Cyclic neutropenia c. Papillon-Lefèvre syndrome d. Focal palmoplantar and gingival hyperkeratosis e. Gingival fibromatosis f. Laband syndrome g. Gingival fibromatosis with hypertrichosis, epilepsy, and mental retardation syndrome h. Gingival fibromatosis with multiple hyaline fibromas 24. **What are genetics** i. : The inheritance and expression of inherited traits 25. **What is a syndrome** j. A distinctive association of signs and symptoms occurring together 26. **What is a phenotype** k. The physical, biochemical, and physiologic traits of an individual 27. **What is a gene** l. The hereditary units transmitted from one generation to another 28. **Describe molecular abnormalities (from a chromosomal abnormalities POV)** m. Occur at the DNA level n. Not detectable microscopically o. Most inherited disorders are at the level of one or both allelic genes 29. **Describe gross abnormalities (from a chromosomal abnormalities POV)** p. Can be observed in a karyotype: A photographic representation of a person's chromosomal constitution 30. **Describe how genetic abnormalities can occur in chromosomes and genes (DNA)** q. Cytogenetics or the study of chromosomal disorders viii. Abnormal number of chromosomes ix. Abnormal structure of chromosomes r. Genetic (DNA) defects x. Single gene defect xi. Multiple gene defects 31. **Describe how Mosaicism** s. Error in early embryonic cell division leads to the development of two or more different cell lines. t. Genetic error will be passed to each daughter cell. u. Number of abnormal cells and location depend on how early the error occurred. v. Conditions thought to have significant mosaics. xii. Turner syndrome, Klinefelter syndrome, Down syndrome w. Can be passed to children if the gametes are affected. 32. **Describe the etiology and epidemiology of Trisomy 21 (down syndrome)** x. one extra or partial copy of chromosome \#21 y. occurs in approximately 1 in 700 live births xiii. Incidence increases with increasing age of the mother. 33. **Describe the extraoral characteristics of Trisomy 21 (down syndrome)** z. Mild to severe mental deficiency a. Short, poor muscle tone, simian crease b. Congenital heart defects c. Hearing impairment d. Characteristic close set, upward slanting eyes, epicanthal fold e. Increased risk of infection 34. **Describe the perioral and intraoral characteristics of Trisomy 21 (Down syndrome)** f. Midface hypoplasia g. Open mouth posture, mouth breathing h. High narrow palate, cleft lip/palate common i. Malocclusion, anterior open bite, crowding j. Delayed eruption both primary and secondary k. Tooth and root abnormalities l. Early periodontal disease 35. **What are the dental implications of Trisomy 21 (down syndrome)** m. Review history for heart defects and other medical problems. n. Educate the patient and caregivers about proper home care and importance of reducing risk of infections. o. Avoid excessive aerosol production during treatment. 36. **What is the etiology and pathogenesis of Klinefelter syndrome** p. E - one or more extra X chromosomes q. Altered male and female hormone levels. r. Each additional X chromosome increases severity of syndrome 37. **What are the extraoral characteristics of Klinefelter syndrome** s. Tall with long arms and legs t. Lacks sexual development, infertile, gynecomastia u. Mitral valve prolapse common v. Normal intelligence but may see deficits with multiple additional X chromosomes 38. **What are the perioral and intraoral characteristics of Klinefelter syndrome** w. Maxillary hypoplasia x. Tooth and root abnormalities xiv. Taurodontism (40%) xv. Short roots 39. **What are the dental implications of Klinefelter syndrome** y. Discuss risk of endocarditis related to oral infection and stress excellent oral hygiene. 40. **What is the treatment for Klinefelter syndrome** z. Treatment focuses on replacing missing hormones and modifying levels of female hormones. xvi. Monitor for osteoporosis and breast cancer. 41. **What is the etiology for Turner syndrome (monosomy x)** a. Error in paternal contribution caused by nondisjunction. b. Most are mosaics or missing only a portion of the X chromosome. c. 1 in 2,000 live births 42. **What are the extraoral characteristics turner syndrome** d. Short stature (under 5 feet) e. Webbed neck, low hairline f. Wide chest, widely spaced nipples g. Systemic conditions 43. **What are the oral characteristics of turner syndrome** h. short roots, thin enamel, less dentin, simple crown morphology 44. **What are the dental implications** i. review medical history carefully for indications of cardiac defects, hypertension, and endocrine disorders, modify treatment as indicated, discuss the potential for infective endocarditis in the presence of oral infection and the need for excellent home care, refer for early orthodontic evaluation and intervention, observe young patients for characteristics of this disorder, and refer for evaluation. 45. **What is the treatment for turner syndrome** j. growth hormone and estrogen therapy timing is extremely important so early diagnosis is crucial, correction of cardiac defects and medical treatment for other systemic conditions 46. **What is multifactorial inheritance** k. a process reflecting additive effects of a number of genes and environmental factors. 47. **What is our genetic makeup determined by** l. Most of what we are is not determined by single genes but by the complex interaction of many genes and the environment. m. Environmental triggers or exposures. 48. **What is the etiology of cleft lip/ and or palate** n. Multifactorial inheritance o. Linked to genes on most chromosomes 49. **What is the transmission of cleft lip/ and or palate** p. 30% associated with genetic syndromes q. 70% nonsyndromic 50. **What is the epidemiology and pathogenesis of cleft lip and or palate** r. Occurs in 1 of every 500 to 550 live births in the United States s. Occurs during weeks 6 to 8 of development 51. **What are the oral characteristics of cleft lip and or palate** t. Major types xvii. Cleft lip, cleft palate, cleft lip and palate, submucosal clefts u. Bone defects xviii. Nasal defects xix. Alveolar ridge deformities v. Hypodontia and malformed teeth w. Malocclusion 52. **What are the dental implications of cleft lip and or palate** x. Prevention and education 53. **What is the treatment for cleft lip and or palate** y. Surgical z. Nonsurgical a. Team of various health care professionals **WEEK 5: ENDOCRINE DISORDERS** 1. **Where on the face are systemic disease manifested** a. Oral mucosa, maxilla, and mandible 2. **Describe how endocrine disorders occur?** b. The endocrine system consists of a group of integrated glands and cells that secrete hormones i. The amount of hormone circulating in blood triggers factors that control production c. Diseases may result from conditions in which too much or too little hormone is produced d. Diseases may result from gland dysfunction e. Diseases may result from a problem with hormone control and production 3. **Describe hyperpituitarism** f. Excess hormone production by the anterior pituitary gland g. Caused most often by a benign tumor, a pituitary adenoma, that produces growth hormone h. Gigantism results if it occurs before the closure of long bones i. Acromegaly results when hypersecretion occurs during adult life 4. **What are the physical manifestations of hyperpituitarism and who does it mostly effect** j. Poor vision k. Light sensitivity l. Enlargement of hands and feet m. Increase in rib size 5. **What are the facial changes present in those who have hyperpituitarism?** n. Enlargement of maxilla and mandible may cause separation of teeth and malocclusion o. Frontal bossing (pronounced forehead) and an enlargement of nasal bones p. Enlargement of maxillary sinus leads to voice deepening 6. **What will we see orally in someone who has hyperpituitarism?** q. Thickened lips and macroglossia 7. **How do we diagnose hyperpituitarism?** r. Diagnosis involves measurement of growth hormone 8. **Define acromegaly** s. When the growth hormone does not decrease and grows abnormally 9. **What is the treatment of hyperpituitarism** t. Pituitary gland surgery u. Medical management v. Radiation therapy w. Untreated: Diabetes, cardiovascular diseases, respiratory diseases, colon cancer 10. **What is hyperthyroidism and what 2 disease cause it?** x. Excess production of thyroid hormone ii. More common in women than men, in 30s and 40s iii. Most common cause is Graves disease y. Graves disease is an autoimmune disorder in which antibodies, thyroid-stimulating immunoglobulins (THIs), stimulate thyroid cells iv. The thyroid gland enlarges v. Too much thyroid hormone is produced vi. Increase in patient's metabolism 11. **What are the clinical features of hyperthyroidism** z. Thyroid enlargement (goiter) a. Rosy complexion b. Erythema of the palms c. Excessive sweating d. Fine hair e. Softened nails 12. **What are the oral manifestations of hyperthyroidism** f. May lead to premature exfoliation of deciduous teeth in children and premature eruption of permanent teeth g. Osteoporosis may affect alveolar bone h. Caries and periodontal disease may appear and develop more rapidly in these patients i. Burning tongue 13. **What is the treatment of hyperthyroidism** j. Surgery k. Medications to suppress thyroid activity l. Administration of radioactive iodine m. Clinical mismanagement of hyperthyroidism may lead to hypothyroidism 14. **What is hypothyroidism and what is it called in children and in adults** n. Cretinism: Infancy and childhood hypothyroidism o. Myxedema: Hypothyroidism in older children and adults 15. **What are the causes of hypothyroidism** p. Developmental disturbances q. Autoimmune destruction of thyroid: Hashimoto thyroiditis r. Iodine deficiency s. Drugs t. Treatment for hyperthyroidism 16. **What are the oral manifestations of hypothyroidism in infants and adults** u. Infants vii. Thickened lips viii. Enlarged tongue ix. Delayed eruption of teeth v. Adults x. Enlarged tongue 17. **What is hyperparathyroidism** w. Results from excessive secretion of parathyroid hormone (PTH) from the parathyroid glands x. PTH plays a role in calcium and phosphorus metabolism y. May be the result of hyperplasia of parathyroid glands, a benign tumor of one or more parathyroid glands, or a malignant parathyroid tumor 18. **What is hypercalcemia?** z. Elevated blood levels of calcium 19. **What is hypophosphatemia?** a. Low levels of blood phosphorus 20. **What are the clinical features of hyperparathyroidism?** b. Mild cases may be asymptomatic, or may cause joint pain or stiffness c. Lethargy and coma may occur with severe disease d. Kidney stones e. Affects skeletal system and gastrointestinal system 21. **What are the oral manifestations of hyperparathyroidism** f. Bone changes: Loosening of teeth g. Well-defined unilocular or multilocular radiolucencies h. "Ground glass" appearance, loss of lamina dura i. Microscopically, lesions appear to be central giant cell granulomas (CGCGs) 22. **What is the diagnosis and treatment of hyperparathyroidism** j. Measurement of PTH blood levels, to include serum calcium and phosphorus measurements k. Treatment is directed at correcting the cause of increased hormone production (tumors, renal disease, kidney failure, vitamin D deficiency) 23. **What is diabetes mellitus** l. A chronic disorder of carbohydrate metabolism characterized by abnormally high blood glucose levels m. Hyperglycemia: High blood glucose levels n. Results from a lack of insulin, defective insulin that does not work to lower blood glucose levels, or increased insulin resistance caused by obesity 24. **Describe how the body normally regulates glucose and what happens if the production is out of whack** o. Normally, glucose signals the beta cells of the pancreas to make insulin. This hormone is then secreted directly into the bloodstream to facilitate the uptake of glucose into fat and skeletal muscle cells. In the presence of insulin, fat and skeletal muscle cells can use glucose as an energy source. When insulin is lacking, these cells are starved of energy. Without insulin to meet the body\'s demand for carbohydrate, tissues are broken down (catabolism), and weight loss occurs, as well as severe hyperglycemia that can lead to diabetic coma. 25. **What is ketoacidosis** p. Production of ketone acid that lowers the blood pH q. Ketone bodies, including acetone, can lower the pH of the blood (ketoacidosis), an acute condition that can lead to coma and death. White blood cell function is also affected in patients with diabetes mellitus. Phagocytic activity of macrophages is reduced, chemotaxis of neutrophils is delayed, and lymphocyte function (T lymphocytes) is adversely affected. These changes increase a patient\'s susceptibility to infection. In addition, collagen production is abnormal, thus affecting the healing process. With chronic hyperglycemia, collagen and other proteins become tagged with carbohydrate. 26. **Describe how the complications of insulin dependent diabetes mellitus (type 1)** r. Damage to blood vessels s. Complications with organ systems xi. Eyes: Blindness xii. Kidney: End-stage kidney failure xiii. Nerves: Paresthesia or numbness in the extremities. t. Atherosclerosis of large and medium-size blood vessels: Macrovascular disease xiv. Abdominal aortic aneurysm xv. Thrombi xvi. Myocardial infarction xvii. Stroke or cerebrovascular accident 27. **What is the diagnostic criteria for diabetes** u. Fasting blood glucose greater than or equal to 126 mg/dL v. A random blood glucose greater than or equal to 200 mg/dL in a symptomatic patient w. A 2-hour blood glucose greater than or equal to 200 mg/dL after drinking a glucose solution of 75 grams x. A glycosylated hemoglobin level greater than or equal to 6.5% 28. **What is the diagnostic criteria for prediabetes** y. Fasting blood glucose between 100 and 125 mg/dL z. Two-hour blood glucose between 140 and 199 mg/dL after the OGTT a. Glycosylated hemoglobin level between 5.7% and 6.4% 29. **Describe type 1: insulin-dependent diabetes mellitus** b. Thought to be an autoimmune disease c. Associated with Addison disease, Graves disease, pernicious anemia d. Insulin-producing cells of the pancreas are destroyed xviii. Three percent of all diabetic patients have this type xix. Can occur at any age; the peak is at 20 years xx. 3% of all diabetic patients have type 1 30. **What are the three primary signs of type 1 diabetes** e. Polydipsia: Excessive thirst and intake of fluid f. Polyuria: Excessive urination g. Polyphagia: Excessive appetite 31. **What is the current approach to manage type 1 diabetes?** h. The current approach to management of these patients involves multiple insulin injections and proper diet, exercise, and frequent determination of blood glucose levels 32. **Define hypoglycemia** i. Low blood sugar 33. **Define severe hypoglycemia** j. Insulin shock 34. **Define brittle diabetes** k. Uncontrolled blood glucose levels 35. **What are the 4 alternative methods of treatment for type 1 diabetes?** l. Oral hypoglycemic medications m. Transplantation of pancreatic beta cells into the liver n. Stem cell infusion o. Insulin pump 36. **Describe type 2: Non--Insulin-Dependent Diabetes Mellitus (NIDDM) and its characteristics** p. Characterized by insulin resistance xxi. Ninety-seven percent of all diabetic patients have this type of diabetes xxii. Gradual onset xxiii. Usually occurs in patients 35 to 40 years of age or older 37. **What is the role of dental hygienists when it comes to type 2 diabetes.** q. Patient education r. Diabetes (Type 2) -- Infographic \| CardioSmart -- American College of Cardiology 38. **Describe how obesity relates to type 2 diabetes?** s. Obesity decreases the number of receptors for insulin binding in fat and muscle (why obesity increases the chance of having diabetes) 39. **What are adipokines** t. Hormones from fatty tissue 40. **What is Gestational diabetes** u. Occurs during pregnancy v. Disappears after pregnancy w. Increased birth weight of child: Macrosomia x. Mother and child have higher risk of developing type 2 diabetes later in life 41. **What are the clinical features of NIDDM (type 2 diabetes)** y. Vascular system adversely affected z. Decreased resistance to infection a. Skin infections: Furuncles b. Urinary tract infections (UTIs) c. Tuberculosis 42. Describe atherosclerosis d. Atherosclerosis, a thickening of the blood vessel wall from fibrofatty plaques, can lead to impaired circulation, causing impaired oxygenation and nutrition in tissue xxiv. This increases the risk of ulceration and gangrene of the feet, high blood pressure, kidney failure, stroke 43. **What are the oral complications of NIDDM** e. Oral candidiasis (oral fungal infection) f. Mucormycosis: A rare oral fungal infection that affects the palate and maxillary sinuses g. Bilateral asymptomatic parotid gland enlargement h. Xerostomia i. Periodontal disease j. Accentuated response to plaque k. Slow wound healing l. Increased susceptibility to infection 44. **How might periodontal disease by affected by diabetes** m. Perio xxv. Significant complication of diabetes xxvi. Aggravates the control of diabetes xxvii. Significant prognostic or predictive clinical marker for diabetes xxviii. Uncontrolled diabetes = uncontrolled periodontal conditions 45. **What is Addison disease and what are its causes?** n. Insufficient production of adrenal steroids o. Causes of adrenal gland destruction include: xxix. Malignant tumor xxx. Tuberculosis xxxi. Deep fungal infections xxxii. HIV infection xxxiii. Autoimmune disease 46. **What are the clinical features of Addison disease** p. **Stimulation of melanocytes** xxxiv. **Bronzing of the skin** xxxv. **Melanotic macules on oral mucosa** 47. What is the treatment for Addison disease q. **Steroid replacement therapy** 48. **Describe hypercortisolism (cushing syndrome)** r. Caused by sustained increase in glucocorticosteroid levels s. Signs develop slowly t. Weight gain is the most significant and obvious clinical feature 49. **What are 4 signals of hypercortisolism (cushing syndrome)** u. Hypertension v. Hyperglycemia w. Mood alterations x. Decreased ability to respond to stress **WEEK 6: GASTROINTESTINAL, NEUROLOGICAL** 1. **What is the etiology and extraoral characteristics of Dysphagia** a. Etiology i. Physical obstruction (tumors, diverticula) ii. Muscular/neurological disorder (stroke) iii. Normal aging b. Extraoral characteristics iv. Aspiration of food/oral fluids, pneumonia v. Regurgitation vi. Malnourishment 2. **What are the intraoral characteristics and the dental implications for dysphagia?** c. Intraoral vii. Pain after swallowing viii. Oral malodor ix. Increased risk of infections d. Dental implications x. Patient positioning xi. Caries risk management xii. Home care modifications 3. **What is the treatment for dysphagia?** e. Main objectives: maintain nutrition and hydration, eliminate pain, and prevent aspiration of substances 4. **What is the etiology and pathogenesis of GERD** f. Etiology xiii. Weak or transient relaxation of lower esophageal sphincter allows back flow of gastric acids into the esophagus. xiv. Associated with foods, tobacco, position, and others. g. Pathogenesis xv. Exposure to acids causes mucosal erosions/ulcers, may lead to permanent tissue/cellular damage. 5. **What are the extraoral and intraoral characteristics of GERD** h. Extraoral xvi. Heartburn xvii. Belching xviii. Wheezing, chronic cough, hoarseness xix. Chest pain (also, throat, shoulder, or back) i. Intraoral xx. Dysphagia xxi. Enamel erosion xxii. Increased risk for pharyngeal cancers 6. **What are the dental implications for GERD** j. Intraoral examination k. Chair positioning l. Patient education xxiii. Cancer self-examination xxiv. Caries prevention xxv. Erosion prevention/management xxvi. Tobacco cessation 7. **What is the tx for GERD** m. Medications n. Diet modifications o. Behavior modifications p. Management of oral effects 8. **What is the etiology of crohn disease** q. Multifactorial: strong genetic, environmental, and host factors 9. **What is the pathogenesis of crohn disease (6)** r. Chronic inflammation leads to formation of ulcers involving all layers of GI mucosa. s. Chronic injury causes scarring and malabsorption. t. Ulcers progress to form deep fissures and then fistulas. u. Fistulas communicate with other organs or area of GI tract, bladder, vagina, or skin. v. Abscesses common with fistula formation. w. Increased risk of colon and GI cancer. 10. **What are the extraoral characteristics of crohn disease (7)** x. Diarrhea and abdominal pain y. Vitamin/mineral deficiencies z. Weight loss a. Fatigue b. Low-grade fevers c. Growth retardation or failure to thrive in children d. Blood loss from ulcers and anemia 11. **What are the Perioral and intraoral characteristics (6)** e. Oral manifestations are first sign of CD in 5--10% of patients. f. Multiple recurrent aphthous-like ulcers. g. Swelling of labial and buccal mucosa with cobblestoning or fissuring. h. Indurated mucosal tags. i. Midline lip fissuring. j. Glossitis, angular cheilitis, and gingival hypertrophy 12. **What are the dental implications of crohn disease** k. Prevention education. l. NSAIDs and aspirin are contraindicated for pain management. 13. **What is the Tx for crohn disease** m. Control inflammation. n. Eliminate nutritional deficiencies. o. Prevent complications. p. Therapy xxvii. Medications xxviii. Supplements xxix. Stem cell transplant xxx. Surgery 14. **What is the etiology peutz-jeghers syndrome** q. **Autosomal dominant condition** xxxi. **Mutation of *STK11* tumor suppressor gene on chromosome 19** 15. **What is the pathogenesis of peutz-jeghers syndrome** r. Mutation inactivates the gene that controls the production of kinase leading to an increased risk for cancers of the stomach, colon/rectum, breast, lung, pancreas, gonads, and thyroid. 16. **What is the extraoral characteristics of peutz-jeghers syndrome** s. Brown or dark blue macules on skin of face, hands, fingers, feet, and toes that may lighten with age. t. Intestinal polyps and increased risk for GI cancers. u. About 93% will develop cancer of some type by age 65. 17. **What are the dental implications of peutz-jeghers?** v. Dental professional may be first to suspect. w. Refer for definitive diagnosis. 18. **What is the tx for peutz-jeghers?** x. Identification y. Lifetime cancer surveillance z. Therapy for cancer when identified 19. **What is malabsorption syndromes** a. Inability to absorb specific nutrients/substances through the GI tract. 20. **What are the most frequent causes of malabsorption syndrome** b. Chronic intestinal disease c. Surgical removal of part of the intestine d. Enzyme deficiencies e. Bile acid deficiency 21. **What are the symptoms of maslabsorption syndrome** f. Nutritional deficiencies g. Chronic diarrhea, pain, bloating, etc. 22. **What is the tx for malabsorption syndrome** h. Many treated by diet modifications. 23. **What is the etiology of celiac disease** i. Complex genetic disorder j. Symptoms caused by an immune response to gluten found in many grains (wheat, barley, rye, triticale) 24. **What are the extraoral characteristics of celiac disease** k. Diarrhea, fatty stools, flatulence, bloating, pain, etc. l. Excessive bleeding m. Osteoporosis n. Weight loss, growth retardation in children, or failure to thrive o. Weakness and fatigue p. Skin lesions 25. **What is are the dental implications and tx for celiac disease** q. Dental implications xxxii. Correlate oral findings with the history of associated physical symptoms. xxxiii. Refer to MD for evaluation. r. Tx xxxiv. Total elimination of gluten from the diet xxxv. Corticosteroids if necessary 26. **What is the etiology of Bell Palsy** s. Birth trauma t. Accidental trauma u. Infections v. Diabetes w. Hyperthyroidism x. Hypertension 27. **What is the pathogenesis of bell palsy** y. Paralysis may result from demyelination of nerve sheath. z. Necrosis of neurons a. Partial or total paralysis 28. **What is the extraoral characteristics** b. Facial numbness c. Keratoconjunctivitis sicca d. Posterior auricular pain e. Hyperacusis 29. **What is the intraoral characteristics of bell palsy** f. Not able to smile g. Drooling h. Slurred speech i. Impaired swallowing, mastication, gag reflex j. May have decreased salivary flow k. Sensory loss xxxvi. Dysgeusia xxxvii. Accidental trauma xxxviii. Infections 30. **What are the dental implications of bell palsy** l. Appointment modifications xxxix. Patient safety 1. During appointment 2. After local anesthetics m. Patient education xl. Caries prevention 3. Xerostomia 4. Diminished sensory input xli. Periodontal disease xlii. Home care modifications 31. **What is the tx for bell palsy** n. Spontaneous recovery o. Medication p. Surgical procedures 32. **What are the OM considerations** q. Patients presenting with undiagnosed unilateral facial paralysis should be referred immediately for emergency medical care and definitive diagnosis. -- they may have also had a stroke. 33. **What is the etiology of trigeminal neuralgia?** r. Etiology xliii. Classic---unknown or pressure from normal artery xliv. Symptomatic---vascular abnormalities, neoplasms, inflammation 34. **What is the pathogenesis of trigeminal neuralgia?** s. Pathogenesis xlv. One theory is that demyelination of the nerve allows uncontrolled pain impulses to travel along the nerve. xlvi. Second and third divisions affected most often. xlvii. Usually unilateral. xlviii. Considered a chronic condition with remissions and relapses. 35. **What are the extraoral, perioral, intraoral characteristics of trigeminal neuralgia** t. No clinically observable signs of the disorder u. Pain described as lighting-like and debilitating xlix. Leaves lingering sensation in tissues v. Initiated by various stimuli may involve skin or mucous membranes l. Touch li. Temperature change lii. Foods 36. **What are the dental implications of trigeminal neuralgia** w. Patients may avoid home care procedures. x. Avoid obtaining dental care. y. Dental health care workers need to identify and avoid triggers. z. Home care modifications. liii. Based on individual patient needs 37. **What are the Tx and OM considerations of trigeminal neuralgia** a. OM considerations liv. Referral for management of chronic pain lv. Referral for medical and psychological evaluation b. Treatment lvi. Pain prevention lvii. Medication 5. Carbamazepine 6. Botox lviii. Surgery 38. **What is the etiology of migraine** c. Strong genetic component thought to be inherited as autosomal dominant trait. 39. **What is the pathogenesis of migraine** d. Neural dysfunction causes vasodilation of meningeal vessels. e. Triggers include stress, lack of sleep, medications hormone changes, smoking, bright lights, motion sickness, foods, and more. 40. **What are the extraoral characteristics of migraine** f. May be preceded by aura. g. Unilateral pain may last for hours or days. h. Nausea, vomiting, photophobia, noise sensitivity. 41. **What are the perioral and intraoral characteristics of migraine** i. Facial or oral numbness j. Speech or language disturbances 42. **What are the dental implications and tx of migraine** k. Dental implications lix. Side effects of medications 7. Xerostomia lx. Increased risk for dental erosion (nausea, vomiting) l. Treatment lxi. Prophylactic medications lxii. Medications to relieve pain and other symptoms lxiii. Alternative therapies 43. **What is the etiology of burning mouth syndrome (BMS)?** m. True BMS may be a form of trigeminal neuropathy n. Other conditions associated with symptoms of burning mucous membranes 44. **What is the pathogenesis of BMS?** o. Deep burning pain without detectable pathology for at least 6 to 8 months 45. **What are perioral and intraoral characteristics?** p. True BMS has no clinically observable signs. q. Burning sensations often severe and debilitating. r. Less severe in the morning, increase as day progresses. s. Absent during sleep. 46. **What are the dental implications and OM considerations of BMS** t. Dental implications lxiv. Reassure the patient u. OM considerations lxv. Refer for evaluation to rule out other causes, if indicated 8. Neurology 9. Endocrinology 10. Psychology 47. **What is the Tx for BMS** v. Identify the cause and eliminate. w. If BMS is a definitive diagnosis, then treatment options are lxvi. Medication 11. Dopamine agonist, pramipexole 12. Clonazepam and paroxetine lxvii. Cognitive--behavioral therapy and counseling lxviii. Diet modifications 48. **What is the etiology of osteoarthritis** x. Multifactorial degenerative disease lxix. Genetic and environmental factors lxx. Risk factors 49. **What is the pathogenesis of osteoarthrosis** y. Destruction of cartilage z. Bone on bone function a. Cartilage breaks off and floats in joint space b. Formation of osteophytes c. Destruction of bone surface 50. **What is the extraoral characteristics of osteoarthritis** d. Joints most often affected lxxi. Weight bearing lxxii. Knee, hip, cervical and lumbar spine lxxiii. Fingers e. Pain lxxiv. Deep, achy increases with the use of the joint f. Heberden nodes lxxv. Exostosis in joints of fingers lxxvi. Seen more in women than in men 51. **What are the perioral and intraoral characteristics of osteoarthritis** g. Temporomandibular joint dysfunction lxxvii. Pain lxxviii. Crepitus lxxix. Deviation lxxx. Deflection lxxxi. Limitation in function/motion 52. **What are the dental implications and OM considerations of osteoarthritis** h. Dental implications lxxxii. Treatment modifications 13. Appointment scheduling 14. Positioning 15. Excessive bleeding 16. Home care modifications i. OM considerations lxxxiii. Consult with physician regarding current medications lxxxiv. Should not require prophylactic antibiotic coverage for joint replacements 53. **What is the Tx for osteoarthritis** j. Relieve symptoms lxxxv. Anti-inflammatory medications lxxxvi. Sodium hyaluronate injections k. Rehabilitate and strengthen lxxxvii. Exercises lxxxviii. Resistance training l. Surgery lxxxix. Arthroscopic xc. Total joint replacement 54. **What is the pathogenesis of rheumatoid arthritis** m. Autoimmune reaction triggered in susceptible person xci. Inflammatory mediators xcii. Rheumatoid factor n. Inflammation of the synovial membrane xciii. Formation of scar tissue on opposing bony articular surfaces xciv. Calcification of scar tissue 17. Ankylosis and fusion of the bones causing deformity and loss of function xcv. Other organs/skin can be affected. 55. **What are the extraoral characteristics of rheumatoid arthritis** o. Pain, stiffness, swelling, deformed joints. p. Accumulation of fluids around the joint. q. Formation of rheumatoid nodules. r. Deformities may cause nerve entrapment. xcvi. Carpal tunnel syndrome s. Other organ involvement xcvii. Keratoconjunctivitis sicca (secondary Sjögren syndrome) xcviii. Fluid accumulation around the heart and lungs 56. **What are the perioral and intraoral rheumatoid arthritis** t. TM joint is often affected. xcix. Loss or limitation of function c. Pain u. Xerostomia may be associated with RA. ci. Sjögren syndrome 57. **What are the dental implications of rheumatoid arthritis** v. Immunosuppressant drugs---osteoporosis w. Anti-inflammatory drugs---coagulation status x. Should not require prophylactic antibiotic coverage y. Xerostomia z. Appointment modifications cii. Positioning ciii. Bite blocks/mouth props a. Home care modifications civ. Mechanical toothbrush cv. Modify home care implements 58. **What is the Tx for rheumatoid arthritis** b. Slow progression and minimize deformities cvi. Medications 18. DMARDs 19. Biologic response-modifying 20. Anti-inflammatories 21. Corticosteroids cvii. Exercise cviii. Rest c. Surgery cix. Joint fusion and replacement 59. **What is the etiology of osteoporosis** d. Primary cx. Aging and loss of hormones cxi. Unknown, many risk factors (see next slide) e. Secondary cxii. Known cause such as 22. Endocrine disorder 23. Long-term use of corticosteroids 60. **What is the pathogenesis of osteoporosis** f. Defective bone remodeling g. Imbalance between bone resorption and formation creates a decrease in bone density. 61. **What are some risk factors for osteoporosis** h. Female i. Age j. Family history k. Lazy l. White/Asian m. Alcohol abuse n. Drugs 62. **What are the extraoral characteristics of osteoporosis** o. Decrease in height p. Dowager hump q. Lower back pain r. Bone fractures 63. **What are the perioral and intraoral characteristics of osteoporosis** s. Decreased density of maxilla and mandible t. Loss of trabecular detail u. Accelerated bone loss with periodontal infections 64. **Dental implications of osteoporosis** v. Maintain periodontal health w. Precautions for those taking antiresorptive drug therapy cxiii. Medication-related osteonecrosis of the jaw (MRONJ) cxiv. Osteonecrosis of the jaw 65. **What is the Tx for osteoporosis** x. Antiresorptive medications y. Bone-stimulating medications z. Exercise---weight bearing and resistance training a. Calcium and vitamin D supplements 66. **What is the etiology of MRONJ** b. disruption of vascular supply to jaw bone associated with the use of antiresorptive and antiangiogenic agents 67. **What is the pathogenesis of MRONJ** c. **Medications affect normal bone remodeling and formation or decrease the formation and repair of blood vessels** d. **Creates bone that is denser, less vascular and has decreased ability to repair itself** e. **May be asymptomatic and not noticed by patient** 68. **What are the contributing factors or MRONJ** f. **Preexisting oral infection or inflammation** g. **Extractions** h. **Implants** i. **Constant irritation** j. **Microtrauma** 69. **What 3 things do you need to diagnose MRONJ** k. **Current/previous treatment with antiresorptive or antiangiogenic agent** l. **Exposed bone or bone probed through fistula present for longer than 8 weeks** m. **No history of radiation therapy in area or metastatic disease** 70. **What are the characteristics of MRONJ** n. **Pain** o. **Soft tissue swelling** p. **Infection and drainage** q. **Tooth mobility** r. **Exposed bone** s. **Halitosis** t. **Usually preceded by trauma such as tooth extraction** 71. **What are the dental implications of MRONJ** u. **Comprehensive examination before or early in therapy.** v. **Regular dental examinations during therapy.** w. **Maintain healthy oral tissues with good oral hygiene practices.** x. **Advise patients to contact the dentist if problems are observed.** y. **Minimize surgical manipulation.** z. **Perform localized surgery prior to extensive procedures to gauge healing.** a. **Rinse with chlorhexidine.** 72. **What is the Tx for MRONJ** b. **Symptoms without exposed bone** cxv. **Conservative local treatment** cxvi. **Analgesics and antibiotics if indicated** cxvii. **Remove any sources of irritation** cxviii. **Consult with the physician** c. **Exposed bone** cxix. **Antimicrobial mouth rinses** cxx. **Analgesics and antibiotics** cxxi. **Local debridement of area** 73. **What is the etiology of paget disease** d. **Unknown** 74. **What is the pathogenesis of paget disease** e. **Initial resorption of the cancellous bone** f. **Replaced by vascular connective tissue** g. **New bone created at excessively fast rate** cxxii. **Affected bones enlarge** cxxiii. **Abnormal in structure, highly mineralized but weaker** cxxiv. **May result in osteogenic sarcoma** 75. **What are the extraoral characteristics of Paget disease?** h. **Enlargement of affected bones** i. **Pain, tenderness in area of bone lesions** j. **Neurological symptoms** k. **Compression of nerves in foramina** l. **Bowing of femur** m. **Radiographic abnormalities** n. **Cotton-wool appearance** o. **\ \ **