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Oral Pathology Exam 1 > 4. Physical and Chemical injury > Flashcards

4. Physical and Chemical injury Flashcards

1
Q

Where do most Traumatic Bone Cysts occur?

A

Mandible

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2
Q

What population is effected by Traumatic Bone Cysts?

A

Males 10-20 y.o.

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3
Q

What is the Pathogenesis of Traumatic Bone Cysts?

A

Intramedullary Hemorrhage

  • Instead of healing by organization of the clot with bone fill, the clot dissolves leaving an empty hole, rather than organizing with granulation tissue & bone fill
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4
Q

What are the unproven Etiologies of Traumatic Bone Cysts?

A
  • Trauma not proven, but reported in 50%
  • Vascular infarct that causes the bone to dissolve
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5
Q

What is the Radiographic appearance of Traumatic Bone Cysts?

A
  • Small to large, well-defined pure RL with sclerotic border (rim of RO around border)
  • Scalloped upper margin interdigitates bwtn tooth roots
    • “Tooth floating in bone”
  • Lower border of the lesion is above the mandibular canal
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6
Q

What are some surgical findings associated with Traumatic Bone Cysts? (3)

A
  • Aspiration yeilds - air OR serous/bloody non-clotting fluid
  • Empty hole at surgery
  • No epithelial lining, just a thin fibrous membrane
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7
Q

What is the Treatment protocol for Traumatic Bone Cysts?

A
  • Eventually heals spontaneously without tx
  • Surgery induces hemorrhage which speeds healing
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8
Q

Where is a Hematopoietic (Osteoporotic) Bone Marrow Defect found?

A

Posterior Mandible

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9
Q

In what population does Hematopoietic (Osteoporotic) Bone Marrow Defect typically occur in?

A

Females (5:1)

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10
Q

What is the pathogenesis of Hematopoietic (Osteoporotic) Bone Marrow Defect?

A
  • Healing defect – following an extraction
    • Red bone marrow fills socket instead of bone
    • Left with a RL
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11
Q

What is the etiology of a Hematopoietic Bone Marrow Defect?

A

Iatrogeneic - follows extraction of a tooth

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12
Q

What is the Radiographic appearance of a Hematopoietic Bone Marrow Defect?

A
  • Small, ill-defined RL in a former extraction site, usually mandibular molar area
  • Lobulated with trabecular pattern
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13
Q

What is the Histology of a Hematopoietic Bone Marrow Defect?

A
  • Normal red bone marrow
  • Pleomorphic looking cells with fat cells & megakaryocytes (large cells with abundant pink cytoplasm, look like they are multinucleated)
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14
Q

What is the Treatment for a Hematopoietic Bone Marrow Defect?

A
  • Innocuous = Leave Alone
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15
Q

What is the location of a Surgical Ciliated Cyst?

A

ONLY in Posterior Maxilla

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16
Q

What is the Pathogenesis/Etiology of a Surgical Ciliated Cyst?

A
  • Iatrogenic = antral surgery or when a dental extraction perforates the sinus & fragments of sinus lining becomes entrapped in the maxilla, fragments drop into alveolar bone & proliferates into a cyst
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17
Q

What is the clinical presentation of a Surgical Ciliated Cyst?

A
  • Vague maxillary pain/swelling or discomfort
  • History of extraction or oral-antral surgery
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18
Q

What is the Radiographic presentation of a Surgical CIliated Cyst?

A

Well-defined RL in Posterior Maxilla approximating the sinus

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19
Q

What is the Histology of a Surgical Ciliated Cyst?

A

Normal sinus lining = pseudostratified ciliated columnar epithelium with goblet mucous cells

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20
Q

What is the Treatment for a Surgical Ciliated Cyst?

A

Remove and Biopsy

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21
Q

Where is a Pulse Granuloma found?

A

Mandibular 3rd Molar Extraction Site

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22
Q

What is the Pathogenesis of a Pulse Granuloma?

A
  • Leguminous vegetable material (pulse) enters extraction site & evokes chronic foreign body inflammatory rxn
    • Cellulous can’t be digested
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23
Q

What is the Clinical Presentation of a Pulse Granuloma?

A
  • Months after an extraction of mandibular 3rd molars the pt gets a dull ache in the area
    • Surgical Ciliated Cysts also has the symptom of a dull/vague pain, but they are location in the posterior maxilla
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24
Q

What is the Radiographic appearance of a Pulse Granuloma?

A

ill-defined RL

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25
Q

What is the Histology of a Pulse Granuloma?

A
  • Spherical bodies surrounded by a foreign body giant cell rxn
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26
Q

Where would a Lipid Granuloma (myospherulosis) be found?

A

Mandibular 3rd Molar Extraction Site

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27
Q

What is the Pathologenesis of a Lipid Granuloma?

A
  • Oily foreign body enters or is placed in an extraction site (mand 3rd molars)
    • Topical Antibiotic Swab that contains Petroleum
    • The lipid causes the foreign body giant cell response
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28
Q

What is the histology of a Lipid Granuloma?

A
  • Clear (lipid) Vacuoles surrounded by a Foreign Body - Giant Cell Rxn
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29
Q

What is the Treatment for a Lipid Granuloma?

A

Remove and Biopsy

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30
Q

What are the 3 possible ways you can get an Air Emphysema?

A
  1. Opening up a laceration in the oral cavity
    • Air/water syringe shoots air into the oral cavity
    • Some of the air gets trapped in the laceration & enters soft tissues of face then enters mediastinum
  2. Blowing lots of air into laceration that has potentially infectious debris from oral cavity
  3. Using an air syringe during RCT, where a blast of air gets to the tip of the apex

*

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31
Q

What is the Clinical Presentation of an Air Emphysema?

A
  • Pt may have a swollen eye/puffy face
  • Feeling of Crepitus = CLASSIC DIAGNOSTIC SIGN!!!
    • Feel bubbles of air between fingers as you palpate
    • Might hear a crackle
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32
Q

What is the Treatment for an Air Emphysema?

A
  • Reassure the pt it will reabsorb & go away
    • May require hospital if it gets into the mediastinum
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33
Q

What are the Iatrogenic Etiologies of an Amalgam Tattoo? (3)

A
  1. Soft tissue laceration during placement OR removal of amalgam
  2. Fractured amalgam during extraction enters socket
  3. Apicoectomy with retrofil
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34
Q

What is the Non-Iatrogeneic Etiology of an Amalgam Tattoo?

A
  • Trauma when flossing thru recent proximal amalgams
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35
Q

What is the Radiographic appearance of an Amalgam Tattoo?

A
  • May show RO Particles, if taken with a low Kvp X-Ray
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36
Q

What is the Histology of an Amalgam Tattoo?

A
  • Fine to coarse pigmented granules in CT
    • Black, brown or olive green
  • Distributed along reticulin fibers appearing as “loose tobacco strands”
  • Typically elicits NO inflammatory rxn
    • If there is an inflammatory rxn it is probably not totally from amalgam, but maybe the other junk from procedure (tooth fragments, base, composite)
  • Occasionally evokes Fibrosis or Giant Cell Rxn
  • Can enlarge in size b/c macrophages gobble up amalgam and move throughout tissue
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37
Q

How does an Injection Hematoma occur?

A
  • During a PSA Block or Displaced Mandibular Block
    • ​Went laterally into buccal fat pad and hit the Pterygoid Plexus
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38
Q

What is the Clinical Presentation of an Injection Hematoma?

A

Looks really scary, but it is harmless

Can Mimic Child Abuse

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39
Q

What is the Etiology of Anesthetic Necrosis?

A
  • Large Volume Injection = forcing fluid into a tight space
    • Worse is Epinephrine is used
  • Intra-ligamentary Injection
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40
Q

What are the dermal fillers that can cause a Foreign Body Rxn?

A
  • Collagen
  • Hyaluronic Acid
  • HAP
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41
Q

What is the pathogenesis of a Foreign Body Rxn to Dermal Fillers?

A

They can migrate through soft tissue by gravity or compression, depositing years later in oral soft tissues.

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42
Q

What is the Clinical Presentation of a Foreign Body Rxn to Dermal Fillers?

A
  • Presents as a nodular mass, in labial, buccal or vestibular mucosa
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43
Q

What is the Histology of a Foreign Body Rxn to Dermal Fillers?

A
  • Foreign Body Granuloma
    • looks like spherical granular brown material
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44
Q

What is the Clinical Presentation of Acute Cheek Biting? (3)

A
  • Small erosion/abrasion
  • Heals within a few days
  • Painful, the pt can recall biting their cheek
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45
Q

What is the clinical appearance of Chronic Cheek Biting? (4)

A
  • White rough, torn surface, with or w/o red areas
  • Bilateral Buccal Mucosa limited to areas accessible to teeth
  • NO PAIN
  • Creates tags of parakeratin
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46
Q

What is the Histology of Chronic Cheek Biting? (3)

A
  • Acanthosis (thickening of epithelium) + Vacuolated cells
  • Macerated, hyperkeratosis
  • Blue color on surface of ragged surface from bacteria
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47
Q

What is the Pathogenesis of Linea Alba?

A
  • Constant negative pressure from Cheek Sucking
  • NOT from Cheek Biting
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48
Q

What is TUGSE?

A

A large, deep, chronic, non-healing, non-specific ulcer, usually on the lateral tongue

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49
Q

What is the Pathogenesis of TUGSE?

A
  • Continual low-grade physical trauma, usually from dentition:
    • Sharp, Pointy, Broken, Carious Tooth Edge or Cusp
    • Lingually malposed tooth/missing teeth
    • Xerostomia
    • Parafunctional Habit
    • Pointed Lingual Cusp
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50
Q

What population is most effected by TUGSE?

A
  • Older individual with slow healing response
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51
Q

What does TUGSE resemble in location, history, and appearance?

A

Tongue SCC

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52
Q

What is the Histology of TUGSE?

A
  • Surface ulcer with fibrin coating
  • Deep inflammation into MUSCLE with histiocytes and eosinophils
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53
Q

What can TUGSE resemble histologically?

A

Lymphoma

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54
Q

What differentiates TUGSE from Tongue SCC?

A

There are no eosinophils in SCC

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55
Q

What is the Treatment for TUGSE?

A
  • Look for the cause 1st and eliminate it
  • May not need to biopsy if the cause is eliminated and the lesion resolves
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56
Q

Where is a Pizza Burn most commonly found?

A

Anterior Palatal Rugae

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57
Q

What is and is not Palatal Petechiae?

A
  • Description of a clinical finding, NOT a disease or diagnosis
  • Ruptured Capillaries on Soft Palate (Blood Hemorrhage)
58
Q

What distinguishes Petechiae from Telangiectasia?

A

If it is a Petechiae: If you press on it, it won’t temporarily disappear, becuase it is already in the CT

59
Q

What is in the Differential Diagnosis of Palatal Petechia? (7)

A
  1. Forcible Retching (pregnancy or bulimia)
  2. Forced Fellatio (Child Abuse if in children)
  3. Influenza, Measles, Scarlet Fever
  4. Mononucleosis
  5. Clotting Disorders (von Willibrand Ds, DIC)
  6. Thrombocytopenia (Leukemia, ITP, TTP)
  7. Anticoagulants
60
Q

What is the Clinical Appearance of Riga-Fede Disease?

A
  • Large laceration of the FOM, right in the middle of the lingual frenum
61
Q

What is the Pathogenesis of Riga-Fede Disease?

A
  • Due to tongue thrusting against premature teeth in suckling infants
62
Q

What other disease has a pathogenesis and histology representive of Riga-Fede Disease?

A

TUGSE

63
Q

What is the counterpart lesion of Riga-Fede Disease seen in adults?

A

Forcible cunnilingus

64
Q

What is a Benign Hyperkeratosis?

A

Appears without obvious cause as a nondescript clinical white lesion.

65
Q

What do 98-99% of white lesions in low risk areas represent?

A

Irritational Keratosis

(they don’t rub off)

66
Q

What is Ridge Keratosis?

A
  • Common Reactive Hyperkeratosis of:
    • Retromolar Pad
    • Edentulous Ridge
67
Q

What is the pathogenesis of Ridge Keratosis?

A
  • Constant low grade occlusal trauma from:
    • Opposing tooth
    • Ill-fitting denture
    • After a 3rd molar extraction
68
Q

When confirmed clinically, the white lesions of Ridge Keratosis are …

A

99% Non-Premalignant

Justifies not doing a biopsy

69
Q

What is the Treatment for Ridge Keratosis?

A

Trauma should be reduced and the lesion observed on periodic recall

70
Q

Where is Nicotine Stomatitis found?

A

Almost Exclusively on the Hard Palate of PIPE Smokers

71
Q

What is the Pathogenesis of Nicotine Stomatitis?

A
  • Heat of Pipe causes Reactive Hyperkeratosis
    • Keratin builds up to protect against the heat
72
Q

What is the Clinical Appearance of Nicotine Stomatitis?

A

White-fissured palate with multiple papules having central red spots (cantaloupe rind)

73
Q

What are the papules on the palate from Nicotine Stomatitis?

A

Inflamed minor salivary ducts

74
Q

How long post cessation of pipe smoking does it take for Nicotine Stomatitis to subside?

A

2 weeks

75
Q

What is the location of Mucoceles?

A

Almost alwasy lower lip

76
Q

What popultion are mucoceles most common in ?

A

Children

77
Q

What is the Etiopathogenesis of a mucocele?

A
  • Laceration of lower lip, tears salivary duct (recently erupted Max Inc)
  • Gland continues to pump saliva that enters CT (mucus extravasation), and is walled off by granulation tissue
  • Grows bigger and burst at surface
78
Q

What is the clinical appearance of a mucocele?

A
  • Soft, pink or blue, submucosal mass
  • Fluctuant - tends to get bigger and smaller as it rupters and refills
79
Q

What is the Histology of a mucocele?

A
  • Cystic pool of pink mucus, located within submucosa and surrounded by a wall of granulation tissue
80
Q

What is the treatment for a mucocele?

A
  • Surgery must remove ENTIRE mucus sac and underlying minor salivary gland
  • If the gland and severed duct remain lesion may recur
81
Q

Where is a Ranula located?

A

Mucocele of the FOM (bigger)

82
Q

What is the Etiology of a Ranula?

A
  • Tearing of sublingual or Wharton’s Duct
83
Q

What is the clinical appearance of a Ranula?

A
  • Soft, fluctuant, pink, translucent, or blue mass in the FOM, off the midline
    • ​Frog Belly
84
Q

Why is it important to biopsy all lesions of the FOM?

A
  • Ranula DD is a Salivary Gland Tumor, which is most often malignant in FOM
85
Q

What is the Etiology of a Pyogenic Granuloma?

A
  • Low grade, persistent, irritation that stimulates the healing rxn to produce EXCESSIVE Granulation Tissue
    • Instead of causing an inflammatory response
86
Q

Where are Pyogenic Granuloma’s found?

A
  • Reactive lesion of Gingiva (75%)
  • Also on Lips and tongue
87
Q

What is the Clinical Appearance of a Pyogenic Granuloma?

A
  • Soft – granulation tissue has no collagen in it (fibroblasts haven’t produced it yet)
  • Red, exophytic, sessile mass
  • Painless - no nerve endings in gt
  • Bleeds Easily - made up of young capillaries
88
Q

What is the tx for Pyogenic Granuloma?

A

Remove completely and remove etiology or it will return

89
Q

What is the Histology of Pyogenic Granuloma?

A
  • Exophytic mass of inflammed granulation tissue, with surface ulceration
  • High power view may show capillary bv with scattered inflammation
90
Q

What is the Pathogenesis of Pregnancy Tumor?

A
  • Increased levels of hormones cause angiogenesis
  • Gingiva becomes more susceptible to minor irritants
91
Q

What is the tx for pregnancy tumor?

A
  • Remove AFTER Birth
    • Will not go away without surgery
92
Q

How does Epulis Granulomatosum occur?

A
  • Granulation tissue wells up in a recent extraction site due to irritant (potentially bone left in socket)
93
Q

What is the tx for Epulis Granulomatosum?

A

Remove and BIOPSY
cancer in an area near an extraction site will present the same

94
Q

Where are Fibromas found?

A
  • Favors Buccal Bite Line
  • Lip, Gingiva, Tongue
95
Q

What is the clinical appearance of a Fibroma?

A
  • Smooth surfaced, light pink, soft or firm, Fixed pea-like nodule
    • ​Mucocele and Ranula are fluctuant
96
Q

What is the histology of a Fibroma?

A
  • Mass of dense bundles of collagen in a non-functional arrangement
  • Replaces submucosa
97
Q

What is the Etiology/Pathogenesis of Peripheral Ossifying Fibroma?

A
  • Between that of a reactive and neoplastic lesions of periodontal or periosteal origin
  • Initiated by an irritant, then enlarges independently
98
Q

Where is a Peripheral Ossifying Fibroma found?

A

Only on GINGIVA

  • Mostly tooth-bearing
  • Mostly crestal region/ridge
99
Q

In what population do Peripheral Ossifying FIbromas occur?

A

2/3 in Females in the 2nd decade

100
Q

What is the Histology of Peripheral Ossifying Fibroma?

A
  • Derived from PDL
  • Spindly cellular fibrous stroma forming bone and/or cementum
  • Fibroblasts
101
Q

What is the clinical appearance of a Peripheral Ossifying Fibroma?

A

Firm, pink mass that may Displace Teeth

102
Q

What is the radiographic appearance of Peripheral Ossifying Fibroma?

A
  • Some RO
  • Cupping or triangulation of crestal bone
    • with extension along root, it wedges down PDL
103
Q

What is the tx for Peripheral Ossifying Fibroma?

A
  • Complete Removal including origins along PDL
  • Eliminate irritant
  • 8-16% recurrence rate
104
Q

How does Peripheral Giant Cell Granuloma differ from POF in clinical appearance?

A
  • Typically Anterior
  • Purple to dull magenta, soft, painless mass that bleeds easily
    • ​Resembles a big Pyogenic Granuloma, but they have different etiologies
  • Mostly young BUT can be at any age
105
Q

What is the Histology of Peripheral Giant Cell Granuloma?

A
  • Cellular spindly stroma containing clusters of foreign body giant cells, vessels and hemorrhage
    • Pyogenic Granuloma will not have Giant Cells
    • POF will form bone or cementum
106
Q

What is the DD for red, soft, gum bumps that bleed easily?

A
  • Pyogenic Granuloma
    • ​More common
    • 75% on Gingiva, also on lips and tongue
    • Low grade trauma stimulated the healing rxn to produce excessive granulation tissue
  • Peripheral Giant Cell Granuloma
    • ​Only on Gingiva (anterior and tooth-bearing)
    • Slight preponderance for young females
    • Low grade trauma to Gingival PDL of Periosteum
107
Q

What is the DD for Pink, Firm, Gum Bumps that Don’t Bleed Easily?

A
  • Peripheral Ossifying Fibroma
    • ​Gingiva
    • Female in 20s
  • Fibroma
    • ​Buccal Bite Line
108
Q

What is the Etiopathogenesis of Traumatic (Amputation) Neuroma?

A
  • Tearing or crushing a peripheral n.
  • nerve twigs attempt to reestablish themselves but become blocked by fibrous scar causing nerve fibers to proliferate in a hyperplastic twisted, tangled mass
109
Q

What are the possible locations for a Traumatic (Amputation) Neuroma to occur?

A
  1. Tongue or Lip after a bite injury
  2. 3rd molar area or mandibular canal after extraction
  3. Mental n. area after ill fitting denture or atrophic ridge
110
Q

What does a Traumatic Neuroma look like clinically?

A
  • Fibroma
    • BUT it is Painful
111
Q

What is the histological difference between a Traumatic Neruoma and a Fibroma?

A
  • Dense fibrous tissue like Fibroma,
  • but with many hyperplastic nerve endings (nerve bundles seen)
112
Q

What is the Direct Theory for Radiation Injury?

A
  • x-ray or gamma-rays damage DNA, particularly cells with high mitotic rate,
  • Destroying chromosomes and the ability to divde
  • Selective value in tx cancer
113
Q

What is the Indirect Theory for Radiation Injury?

A
  • Radiation kills tissue by ionization of H2O forming free radicals that damage cell structures
114
Q

What tissues are Radio-Sensitive, most easily destroyed, they grow fast? (4)

A
  • Hematopoietic
  • Lymphoid
  • Germ Cells
  • GI Epithelium
115
Q

What tissues are Radio-Responsive - reasonably susceptible, but can regenerate? (6)

A
  • Skin
  • Salivary Glands
  • Oral muscosa
  • Osteoclasts, -blasts
  • Growing CT
  • Endothelium of bv
116
Q

What tissues are Radio-Resistant, tissue that is not growing very fast? (6)

A
  • Muscle
  • Mature CT
  • Neutrophil
  • Nerve
  • CNS
  • RBC
117
Q

How many rad is needed to kill malignant tumor cells/ how many per day?

A
  • 4000-7000
    • 4000 for fast growing tumors (lymphomas)
    • 7000 (SCCA)
  • Most Adenocarcinomas and well differentiated tumors are radiation
  • Fractionate doses ~200 rad/day
118
Q

What are the effects of Radiation on Skin?

A
  • Radiation Dermatitis
    • Begins 2 weeks post radiation (kills basal cells)
    • Skin in path appears sunburned
    • Heals in 3 weeks, with permanent atrophy, pigmentation, hair loss, and telangectasia
119
Q

What are the musculoskeletal effects of radiation and how do you treat them?

A
  • Trismus due to fibrosis or a Spasm of muscle and TMJ capsule
  • Rx with Jaw Opening Exercises, so collagen won’t form as strongly
120
Q

What is the effect of radiation on taste buds?

A
  • Hypogeusia several weeks post radiation but often returns > 4 month
  • Some pts are left with permanent hypogeusia or dysgeusia
  • Rx with Zinc helps with tast
121
Q

What is radiation’s effect on Mucosa?

A
  • 180-200 rad 5x day cause mucositis
  • Basal cells damaged immediately
    • Mucosa gets red, sore and sloughs 2-4 wks later (latency)
  • Severe Pain, then heals with atrophy and fibrosis starting in 3 weeks
  • Candida is common due to xerostomia
122
Q

What is radiations effect on Salivary Glands?

A
  • 1000-3000 rad = Reversible
  • >4000 rad = Irreversible
  • Serous Glands most affected, mucosa glands less affected
  • Resulting in Xerostomia with thick, ropy, mucous saliva
123
Q

What is Radiations Effect on Teeth?

A
  • No Effect on Formed Teeth (radio-resistant)
  • Rampant encircling cervical “radiation” caries due to xerostomia
    • Amputates the tooth
    • Seen in Meth Mouth
  • Damages developing tooth buds in path
124
Q

What is Radiations effect on Bone?

A
  • Damages endothelium causing occlusion of bone vessels and osteoblasts
  • Mature bone is stable until injured, then vascular infarct - Osteoradionecrosis
  • Almost always in Mandible (x24)
  • Unexpected with dose <6000 rad
125
Q

How do mange a radiated pt, and what is the timing of the tx?

A
  • EXTRACT non-restorable or perio involved, Mandibular teeth in Field of Radiation
    • Especially if salivary gland damage is anticipated,
    • Trying to prevent Osteoradionecrosis
  • Best Time is > 1 month before tx
  • NEVER EXTRACT DURING Rad Tx
  • Ok to extract within 4 months of tx but NOT AFTERWARD!
  • Extractions must be atraumatic
    • Give pt Vit. E and pentoxifylline (improves blood flow)
  • Wait on Dentures after FM Extractions
    • Sore Spots = Emergency
126
Q

What does MRONJ preferentially affect?

A

Jaws

127
Q

What does Sanguinaria Rxn cause histologically?

A

Hyperkeratosis and Dysplasia in 20%

128
Q

What are the Oral Manifestations of Heavy Metal Poisioning? (4)

A
  • Heavy metal line on the free gingiva
  • Ptyalism - excessive salivation
  • Metallic Taste
  • Severe Gingivitis and Periodontitis with Generalized Tooth Loss
    • Direct toxic effects from sulfide salts
    • Mercury is the worst - perio destruction and tooth loss
129
Q

What are the 3 classes of medications that cause Drug Induced Gingival Hyperplasia (Fibromatosis)?

A
  1. Anticonvulsants (Dilantin)
  2. Calcium Channel Blocker (Nifidipine)
    • Most likely
  3. Cyclosporine
    • immunosuppressant (anti-rejection drug of transplants)
130
Q

What is the etiology of the Allergic Form of Angio(neurotic) Edema?

A

Type 1 Allergic Rxn

131
Q

What is the clinical presentation of the Allergic Form of Angio(neurotic) Edema?

A
  • Rapid, Painless, Swelling of lips, face, eyelids, tonge, FOM, larynx
  • May have tingling or burning
  • Lasts 24-36 hrs, if left alone
132
Q

What is the etiology of the Non-Hereditary Form of Angio(neurotic) Edema?

A

Allergen

133
Q

What is the etiology of the Hereditary Form of Angio(neurotic) Edema?

A
  • Absence of C1 esterase inhibitor
    • ​Normally inhibits the action of complement cascade
    • If not inhibited - kinin production is unchecked
    • Causes major swelling to minor allergens
134
Q

What is the result of the Hereditary Form of Angio(neurotic) Edema?

A

25% fatal airway obstruction

135
Q

What is the etiology of the ACE Inhibitor Form of Angio(neurotic) Edema?

A
  • Increased Bradykinin
  • May occur spontaneously or be set off by manipulation
136
Q

Which forms of Angio(neurotic) Edema do not respond to antihistamines, epi, or steroids, and may require the airway to be maintained?

A
  • Hereditary Form
  • ACE Inhibitor Form
137
Q

What is the DD of Angio(neurotic) Edema aka other causes of sudden swelling of face?

A
  • Ludwig’s Angina
  • Carvernous Sinus Thrombosis
  • Cervicofacial (Air) Emphysema
138
Q

What systemic drug is most likely to cause Stomatitis Medicamentosa?

A

Antibiotics

139
Q

How does Stomatitis Medicamentosa manifest?

A
  • Acute, confluent ulcers
  • Lichenoid lesions
  • Blisters
140
Q

What does Stomatitis Medicamentosa look like clinically?

A
  • Chemotherapy
  • Radiation Mucositis
141
Q

What is the Diagnostic Histology of Stomatitis Venenata to Cinnamon?

A
  • Lichenoid Rxn (sub-epithelial inflammation)
    • This is also the hallmark of LP
  • But with a distinct Perivascular Infiltrate
    • Also seen in LE, but less prominant

Oral Pathology Exam 1 (8 decks)

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