Albert OMPR 2nd Exam

  1. 3 major risk of cortisol
    • 1 hyperglycemia from gluconeogenesis
    • 2 osteoporosis from calcium mobilization
    • 3 hypertension from Na resorption followed by water retention
  2. Other risk of cortisol
    • *abnormal body morphology (moon face, buffalo hump)
    • - muscle atrophy ( aminoacid mobilization out of muscle)
    • - collagen /connective tissue fragility and poor wound healing
    • - changes of mood (agitated, irritable, and hyperactive sometimes insomnia)
  3. Glucocorticoids duration
    • - Short acting: cortisone 8-12 hr
    • - intermediate acting: prednisone 18-36 hrs
    • - long acting: dexametasone 36-72 hrs
  4. What is the equivalence between cortisol and prednisone
    Prednisone is 4x as potent as cortisol. 5 mg of prednisone equals 20 mg of cortisol
  5. CBC changes associated with long term use of steroids
    • - decreased blood cells (eosinophils, basophils, lymphocyte)
    • - hypercalcemia hypokalemia

    • - Hyperglycemia
    • - Leukocitosis (oportunistic infections like candida, herpes and other latent infection reactivation
  6. Normal and under stress cortisol blood levels
    • 30 mg to support homeostasis
    • 300 mg under threat like injury, infection or stress
  7. What is adrenal crisis and how to manage it?
    A pt taking long term steroids can develop a lazy pituitary gland. To prevent a potential adrenal crisis and HYPOTENSIVE and hypovolemic SHOCK leading to death, it is recommended supplemental steroid dose

    Usually recommended to doble the dose. Pt taking 5 mg prednisone will have to take 10mg

    • The debate comes when a pt is taking 60 mg of prednisone equivalent to 300 mg cortisol which is the maximum amount the body can assimilate under crisis. At this point is it really necessary to doble the dose?
    • The guideline says to Do it. We must follow the rule and beside it won't do any damage
  8. Is antibioprophylaxis recomended for patients taking steroids
    • Nooouu
    • Unless there is a comorbid immune disorder or in some cases is recommended when taking more than 10 mg prednisone a day
  9. What is the treatment of pemphigus and pemphigoid?
    Steroids are always use to control lesión in combination with cellcept, or imuran, or methotrexate (CMC side effects)
  10. Considerations with topical steroids medication
    • - Are helpful in controlling lesion activity
    • - they Never treat the origin of the illness: pathologic antibodies
    • - should be used when disease activity is low and limited
  11. What are the key words in the diagnostic of pemphigus and or pemphigoid lesions
    • - multiple
    • - chronic
    • - non healing
    • - primary (in a sense that is not a recurrent lesión like an afta or a herpes)
    • can be either localized to the oral cavity or generalized with extra oral manifestations
  12. What is pemphigus and pemphigoid
    • Mucocutaneous
    • - autoimmune disease
    • - multiple, chronic non healing, primary blisters (bullae) which rupture to form a large non healing ulceration
    • - onset usually 50 to 60 y.o.
    • - it is considered an ultra orphan disease
  13. Histopathology of pemphigus
    • Mucocutaneous autoimmune disease
    • * INTRA-EPITHELIAL blisters
    • - Acantholisis: loss of intercellular connections. This is not present in pemphigoid

    Note: the test used is direct immunofluorecence. It shows a space between the cell due to the loss of cohesion
  14. How to diagnose pemphigus vulgaris
    • - medical history
    • - physical exam
    • - biopsy (acantholysis)
    • - direct immunofluorescence (Gold standard) from perilesionalntissue
  15. What is the treatment of pemphigus?
    • Control. Consolidation. Maintenance.
    • Star with systemic corticosteroids.
    • Rituximab if there is any remision. This one is showing the best emerging outcomes

    Local treatment to control blisters, not the disease only the manifestation of it. Example: clobetasol, triamcinolone
  16. Mucocutaneous autoimmune disease with sub epithelial blisters
    Mucus membrane pemphigoid

    Separation of epithelium at junction

    Perform an ocular exam. Blindness can be a complication from pemphigoid

    It's a mild disease. Doesn't kill people. Can be managed with topical
  17. Pemphigoid treatment
    • Is a limited disease. Can be treated with potent topical steroids ( clobetazol)
    • Sistemically: Dapsone
  18. Prevalece of herpes simplex
    • HSV type 1 > non Hispanic white and younger adults (is getting more common in genitals due to oral sex)
    • HSV type 2 > non Hispanic blacks (increase with age due to increase of sexual activity)
  19. What kind of virus is HSV?
    Neurotropic. Lives in a sensory ganglia. Haser ganglion of CN V
  20. What is the treatment for secondary intra oral herpes?
    None. I.O. lesions should not be treated because by the time you get to it there is not much you can do about it.

    The treatment is for cold sore (herpes labialis) fluid filled blisters
  21. Treatment of herpes labialis( cold sore)
    • Depends on severity/ frequency.
    • - remove precipitating factors
    • - antivirals agents / steroids combination agents. Valacyclovir 1g. Famciclovir 500 mg
    • - ice
    • - dessicants
  22. Which viral infection is found predominantly in pregnant/ neonates, immonocompromised patiens.
    Causes hearing loss at birth and early childhood?
    • Cytomegalovirus
    • The diagnosis is based on clinical and lab findings ELISA IgG antibodies to CMV. It resolves spontaneously. Treatment only for immunocompromiced patients
  23. Previous exposure to EBV characterized by a yellowish crypt exudate. Also hyper plastic pharyngeal tonsillitis
    Infectious mononucleosis (kissing disease)
  24. Related to HHV 8. Involve bone causing tooth mobility. Erithematous blue/brown macule that do not blanch with pressure
    • Kaposi's Sarcoma
    • Oral form associated with immunosuppression AIDS
  25. Characteristic cells of HPV infected lesions?
    Koilocites
  26. Soft, painless usually pedunculated, exophytic white lesions with finger like projections. Any age but common in 3rd and 5th decade
    • Viral papilloma
    • Types 6 and 11
    • Benign low risk
  27. Contagious, frequently seen in children. Anterior part of the mouth. Soft painless pedinculated exophitic white lesion with many fingerlikenproyections
    • Oral verruca vulgaris
    • Hpv 2, 57
    • Benign HPV induced focal hyperplasia of stratified squamous epithelium
  28. Sessile, non tender, exophytic pink mass with short blunted surface projections. Contagious.
    • Condyloma acuminatum. Type 6 and 11. Considered a sexually transmitted disease. Oral lesion usually anterior part of the mouth.
    • Tends to be larger than papilloma or verruca vulgaris
    • Characteristic clustering of multiple lesions.
  29. Koplik's spots. Bluish white punctuate mucosal macular surrounded by a rim of erithema. Resemble sprinkled salt
    • Measles
    • Paramyxovirus
  30. Inhalation of organisms. Ulcerated lesion resemble squamous cell carcinoma. Most common systemic fungal infection
    • Histoplasmosis
    • Can be acute: self limited pulmonary infection
    • Chronic: lung infection similar to tuberculosis
  31. Pulmonary infection: inhalations of spores. More frequent in men. Cutaneous lesions are verrucous plaques
    • Blastomycosis
    • Histology: thick cell wall
  32. Second to candidiasis as the most common OPPORTUNISTIC fungal infection. Spores releases and inhaled
    • Aspergillosis
    • - immunocompromised pt
    • - uncontrolled diabetes
    • - maxillary sinus infection
    • - may follow tooth extraction

    Nosocomial infection: you go to the hospital to treat a disease and you end up with this infection
  33. Fungal infection with a predilection for nasal, eyes and head and neck area. Invades and destroys blood vessels causing necrosis on the head area. Predilection for uncontrolled diabetes pt.
    Zygomycosis / Mucoycosis

    Grow is enhanced by iron. Diabetes ketoacidosis increases iron serum levels
  34. Inhalation of microorganism contained in pigeons and bat droppings. Most common systemic fungal infections in HIV pt causing meningitis
    Cryptococcosis
  35. Management of deep fungal infections
    • Diagnosis (biopsy)
    • Risk factors: immunosuppression, HIV, uncontrolled diabetes
    • Systemic anti fungal treatment: ketokonazole, Amphotericin B
  36. C. Albicans response to changes in micro environment
    Transformation from yeast to hyphae (filaments) which is a more pathogenic form. It can invade the epithelial surface
  37. Factors that predispose humans to candidiasis
    • Local: - xerostomia
    • - epithelial changes
    • - changes in comensal flora
    • Systemic: - diabetes
    • - altered hormone state
    • - hypo hyper thiroidism
    • - adrenal suppression
    • - immunosuppression
  38. Curd like white plaques that can always be wiped off (often revealing underlying erythema)
    Pseudomembranous Candidiasis

    Often asymptomatic. Sometimes pt can have a burning sensation. This is an acute form of oral candidiasis.
  39. Clinical types of oral candidiasis
    • - Pseudo membranous Candidiasis (wipeable)
    • - Denture stomatitis
    • - Angular cheilitis
    • - Median rhomboid glossitis
    • - Erythematous candidiasis ( associated with burning sensation)
    • - Hyperplastic Candidiasis ( associated with leukoplakia) areas of non wipeable white plaques
  40. Diagnosis of oral candidiasis
    • - clinical appearance
    • - favorable response to anti-fungal agents.
    • - cytological smear followed by microscopic evaluation
    • - biopsy
  41. Management of mild candidiasis
    • Clotrimazole trches
    • Miconazole mucoadhesive buccal

    7-14 days
  42. Management of moderate to severe candidiasis
    Oral fluconazole 7-14 day.
  43. Most common oral mucosal disorder. Acute and painful
    Recurrent aphthous stomatitis
  44. Canker sore<10 mm, shallow, oval ulcer with slightly raised margin and erythematous halo. No scarring.
    • Minor RAS
    • 75% of all RAS. Resolves without treatment in 7-14 days
  45. Deep ulcer, with irregular borders, healing can take weeks or month. Often leaves scarring
    • Major RAS
    • >10 mm. May be associated with fever or malaise. Predilection for the throat
  46. Crops of ulcers < 5 mm in diameter which may fuse. Resolve without treatment in 7-14 days. No scarring
    Herpetiform RAS
  47. RAS treatment plan
    • Treatment dictated by
    • - associated symptoms
    • - # and location of ulcers
    • - recurrence history
    • - possible underlying cause

    • Consider 5 options
    • 1 no treatment
    • 2 prevention / treatment of/ for possible causes
    • 3 topical therapy
    • 4 systemic therapy
    • 5 referral for severe disease
  48. White changes with lacy appearence, reticular appearance Wickham striae. Most commonly bilateral.
    Oral lichen planus
  49. Diagnosis of lichen planus
    • Biopsy the white changes not the ulcer
    • T cell lymphocytic infiltrate

    T cell mediated response
  50. Amalgam or other metal contact sensitivity. With a systemic cause, lesions may be widespread including extra-orally
    Oral lichenoid reactions

    Biopsy white changes on non keratinized mucosae NOT ulcerated area
  51. Treatment for OLP
    • Topical corticosteroids
    • Clobetazol (don't use for more than 2 weeks)
    • Flucicnonide
    • Dexamethasone

    • Sistemic agents
    • Prednisone
    • Azathioprine
    • Mycophenolate mofetil
  52. Characteristic type 1 hypersensitivity reaction involving skin
    Urticaria. Hives
  53. Localized manifestation of immediate hypersensitivity. Involve the respiratory tract and conjuntivae
    Hay fever
  54. Bronchoconstriction, airway obstruction and circulatory colapse
    Anaphylactic shock
  55. Diffuse edematous swelling of soft tissues. Rapid onset, itching, solitary or multiple areas. Reduction or dysfunction in the inhibitor C1-INH
    Angioedema

    • Treatment.
    • Oral antihistamine
    • Intramuscular epinephrine (interference with breathing)
    • Intravenous corticosteroids and antihistamines
  56. A mucosal response that occurs at the site of contact with an allergen. Acute or chronic forms. More common in female. Type 4 hypersensitivity
    Allergic contact stomatitis

    • Treatment
    • Identification and removal of antigen
    • Antihistamine therapy
    • Topical steroid application
  57. Non-specific vesiculoerosive or apthous-like lesion. Lichenoid drug reaction. Intraoral fixed drug eruptions. Pemphigus-like drug reactions
    Stomatitis medicamentosa

    Diagnosis based on the resolution of lesions with discontinuation of drug
  58. Diffuse, erithematous areas evolve into large, superficial erosions and ulcers. Hemorrhagic crusting of the vermilion (bloody crusted lips). Skin lesions 50% of pt. Target lesion
    Erythema multiforme - Minor
  59. Erythema multiforme treatment
    • Systemic corticosteroids
    • Hydration
    • HSV associated: continuos oral acyclovir can prevent recurrences
  60. Trigger by drugs rather than infections. Ocular or genital involvement in addition to oral mucosa. More sites are involve
    Steven Johnson syndrome. Erithema multiforme major
  61. Multisistem granulomatous disorder of unknown cause. Improper degradation of antigenic materials with formation of non necrotic granulomatous inflammation. Discovered on chest radiograph (pulmonary lesions). Asteroid body in a giant cell
    Sarcoidosis
  62. Necrotizing granulomatous lesions of the respiratory tract. Necrotizing glomerulonephritis. Potentially fatal if not treated. Characteristic gingival lesion: strawberry gingivitis
    Wegener Granulomatosis
  63. Facial butterfly rash. Kidney, heart involvement. Oral lesions. Predilection for women
    Systemic Lupus erythematosus

    Minimize sun exposure, anti-inflamatories, steroids: prednisone,
  64. Widespread damage to small blood vessels. Progressive interstitial and perivascular fibrosis in skin and multiple organs. Calcinosis cutis. Talangiectasia. Skin felt thickened and tight. Limited mouth opening
    Systemic sclerosis (Scleroderma)
  65. Painful, erythematous gingiva with necrosis of the interdental papillae. Borrelia vincentti, foul odor and lymphadenopathy
    Necrotizing ulcerative gingivitis
  66. Swelling, indurated areas of fibrosis. Draining absces with sulfur granules.
    Actinomycosis

    Caused by actinomyces israelii
  67. Caused by treponema pallidum. Several stages
    • Syphilis
    • Primary: infectious, regional lymphadenopathy, Chancre
    • - 2: infectious. Skin rash, mucus patches
    • -3: non infectious: Gumma. CNS involvement
  68. Hutchinson triad: deafness, keratitis, tooth defects
    Congenital syphilis
  69. Inflammation of bone and bone marrow. Sequestration of dead bone. Resemble a malignancy.
    Osteomyelitis
  70. Lighter pink than surrounding mucosa. Associated with chronic trauma. Exophytic lesion. Feels firm. Microscopical: spindle shape
    • Fibroma
    • Composed of dense scar-like fibrous connective tissue

    Should be removed with excitional biopsy
  71. Soft exophitic lesion. Either sessile or pedunculated. Deep red to purple. Bleeds easily. Soft keratosis and ulcerations. Common in gingiva, but can be present in other areas of the mouth. Develops rapidly and then remain static. Feels soft
    • Pyogenic granuloma
    • Common in pregnant woman
  72. Occurs exclusively on the gingiva. Red blue-purple nodular mass. Feels somewhat firm
    • Giant cell granuloma
    • Surgical excisional biopsy. SRP of the surrounding teeth
  73. Well demarcated lesion that appears to originate from the gingival interdental papilla. Reactive lesion. Frequently seen in younger pt. Feels hard
    Peripheral ossifying fibroma

    Fibrous Proliferation with mineralization areas
  74. Characteristic cells of HPV infected lesions
    Koilocytes
  75. Yellowish-orange mass surfaced by thin overlying epithelium. Surface blood vessels. Feels soft and squishy
    • Lipoma
    • Benign tumor of mature fat cells. Treatment surgical excision. Doesn't recur.
  76. Reactive proliferation of nerve tissue after injury. Related with extraction or other surgical procedure.
    Neuroma (traumatic neuroma)
  77. Multiple mucosal neuromas with multiple tumors and hyperplasia of endocrine glands. Type 2B or 3 associated with oral cavity
    Multiple endocrine neoplasm. MEN
  78. Firm, slow growing, painless, yellowish white nodule. Benign tumor arising from peripheral nerve tissue
    • Neurofibroma
    • Under microscope: serpentiginous neural nuclei. with delicate fibrous background

    Look for extra oral lesion to rule out the possibility of neurofibromatosis
  79. Multiple skin nodules. Cafe au lait. Type 1 most common form. Lisch nodules on the iris of the eye
    • Neurofibromatosis
    • von Recklinghausen's disease
  80. Only neural lesion with a capsule. Microscope: Verocay bodies. Usually found on the tongue.
    Schwanoma
  81. Most common neural lesion usually seen on dorsal tongue. Slow growing, painless firm, submucosal nodule. Yellowish-white
    Granular cell tumor
  82. Present at birth, resembling granular cell tumor
    Congenital epulis
  83. Benign vascular tumor. Rapid grow phase then gradual involution. Proliferation of blood vessels with bluish or redish color.
    • Hemangioma
    • If present at birth and persist throughout life is called venous malformation

    • Can be capillary (small blood vessels). Or it can be cavernous (big blood vessels)
    • Blanching: turns white pale under pressure

    You may feel a pulse when touching the lesion. Never biopsy because of the profuse bleeding that may occur
  84. Vascular proliferation involving tissue of the brain and face. Unilateral distribution along one or more segments of the trigeminal nerve
    Sturge Weber angiomatosis
  85. Benign tumor of lymphatic vessels. IO location: tongue
    • Lymphangioma
    • No treatment. Monitor.
    • Can be capillary
  86. Caused by HHV 8. Palate and maxillary gingiva most common location. AIDS related. Immunosuppressed pt
    Kaposi's sarcoma
  87. What are the tumor of muscle?
    Leiomyoma (benign) leiomyosarcoma (malign) of smooth muscle

    Rhabdomyoma (benign) Rhabdomyosarcoma (malign) of skeletal muscle
Author
albertin1989
ID
326495
Card Set
Albert OMPR 2nd Exam
Description
Bacterial, viral, fungal infection. Soft tissue lesions
Updated