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PATH II > physical and chemical injury > Flashcards

physical and chemical injury Flashcards

1
Q

iatrogenic

A

caused by provider

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2
Q

examples of iatrogenic injury

A
  • Cotton roll injury
  • Dental thermoplastic compound
  • X-ray film trauma
  • Lacerations
  • suction
  • post anesthetic lip chewing
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3
Q

Factitial Injury

A

Self-inflicted injury caused
by the patient
* Munchausen syndrome

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4
Q

Munchausen syndrome -

A

a psychiatric disorder in which the patient finds disease or illness in order to draw attention or sympathy to themselves.

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5
Q

inheritence, demo, absence of what strucutre?

Familial Dysautonomia/
Riley-Day Syndrome

A
  • Autosomal recessive, Ashkenazi Jewish heritage
  • Lack of response to painful stimuli results in injuries
  • Absence of fungiform papillae
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6
Q

complications of body piercings

A
  • Infections – acute bacterial,
    hepatitis, HIV, infective endocarditis
  • Chipped, fractured teeth
  • Periodontal lesions
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7
Q

where are these seen? initially present as? tx?

electrical burns

A
  • Commissures of lips of young children under 4 years from chewing through a live wire
  • Initially a painless charred area with little or no bleeding. Edema after several hours, followed by necrosis and sloughing by day 4 (monitor for bleeding)
  • Minimize scar contracture with
    microstomia prevention appliance
    for 6 to 8 months
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8
Q

where in mouth? present as? tx?

thermal burns

A
  • Hot foods or beverages -microwave ovens
  • Palate, posterior buccal mucosa
  • Erythema and ulceration
  • Resolve without treatment
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9
Q

giving neck and oral trauma

A

Palatal Ecchymosis Secondary to Fellatio

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10
Q

cunnilingus trauma

A

Lingual Frenum Trauma Secondary to Cunnilingus, thickened frenum

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11
Q

french kissing trauma

A

frenum affected

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12
Q

aspirin burns

A

chemical burn due to aspirin in vestibule, presenting as a white sloughing in the mouth, usually gone within 24hrs

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13
Q

Epithelial Desquamation
Chemical Slough presentation/ causes

A
  • Toothpaste detergents - sodium lauryl sulfate – SLS
  • Listerine
    present as removable sloughs of mucosa
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14
Q

Drug-Associated Intrinsic Discoloration of Teeth

A
  • Certain drugs may be incorporated into developing tooth structure and produce clinically-evident discoloration
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15
Q

severity of drug indcued tooth discoloration depends on?

A

The severity of the effects depend on stage of tooth development and the dose/duration of the drug administration

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16
Q

when to avoid tetracyclines

A
  • Avoid use of tetracyclines during pregnancy and in children under 8
    years of age
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17
Q

tetracycline staining seen as

A

bands of discoloration

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18
Q

commonly used for?

Minocycline (Minocin)

A

Derivative of tetracycline commonly used for acne, rheumatoid arthritis and for periodontal disease

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19
Q

minocycline staining

A

May produce intrinsic discoloration of developing teeth and fully-developed teeth
* Also discolors bone, skin, sclera, conjunctiva

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20
Q

Minocycline Staining of Erupted Teeth mechanism

A
  • Drug binds to pulpal collagen
  • Oxidation produces discoloration
  • Occurs in 5% of users within 1 month to 1 year of use
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21
Q

Smoker’s Melanosis

A
  • Oral pigmentation increased
    significantly in heavy smokers
  • Exposure to polycyclic amines
    stimulates melanin production
    by melanocytes
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22
Q

Drug-Related Mucosal Pigmentation drug types

A
  • Anti-malarials
  • Tranquilizers
  • Chemotherapeutics
  • Laxatives
  • Antibiotics
  • Birth control pills
  • Anti-retrovirals
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23
Q

Zidovudine (Azidothymidine, AZT) Pigmentation

A
  • AZT, an anti-retroviral agent, may produce pigmentation of mucosa and nails
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24
Q

Hydroxychloroquine (Plaquenil) Pigmentation

A

Plaquenil, an anti-malarial drug is often used in lupus erythematosis can cause pigmentation of skin

25
Q

Antimalarial Drug Pigmentation

A

can cause pigmentation in various regions

26
Q

how metals interact with us? acute vs chronic? tx?

Heavy Metal Toxicity

A

Form complexes with biologic molecules that affect protein structure and inactivate enzyme systems
* Acute effects from massive ingestion and chronic effects from slow accumulation
* Treatment with chelating agents (EDTA)

27
Q

sources of Pb

Lead Poisoning – Plumbism (Pb)

A
  • Environmental sources
  • Gasoline additive
  • Lead-based paints
  • Water supply - lead solder in plumbing
28
Q

plumbism presentation
lead similar to? result?
blood?
renal?
s/s?
what happens with acute poisonings?

A
  • Lead is chemically similar to calcium and is deposited in developing bone and teethm forming bands of increased density at metaphyses of growing tubular bones
  • Anemia - hypochromic microcytic with basophillic stippling
  • Renal dysfunction
  • Non-specific signs and symptoms - fatigue, irritability, weakness, abdominal and musculoskeletal pain, headache (cerebral edema in acute poisoning)
29
Q

Oral Manifestations of Lead Poisoning
gingiva, tongue, mucosa, taste, saliva, perio

A
  • Gingival lead line (Burton line) - bacterial H2S forms lead sulfide in gingival crevice, producing a bluish line at marginal gingiva.
  • Ulcerative stomatitis, advanced periodontal disease
  • Tongue tremor
  • Metallic taste and excessive salivation (sialorrhea)
30
Q

absorbed? exposure from?

mercury poisoning

A
  • Elemental mercury poorly absorbed, but mercury salts and vapor well absorbed
  • Occupational exposure
  • Dietary
  • Medications - teething powders, antihelminthics, cathartics
31
Q

acute and chronic exposures

Systemic Manifestations of Mercury Toxicity

A
  • Acute – abdominal pain, vomiting, diarrhea
  • Chronic – gastrointestinal upset, neurologic changes
32
Q

Oral Manifestations of Mercury Poisoning
enlargement of?
discoloration?
bone?
mucosa?
taste?

A
  • Inflammation and enlargement of salivary glands, tongue and gingiva
  • Discoloration of gingiva
  • Periodontal bone destruction -mercuric sulfide
  • Ulcerative stomatitis
  • Metallic taste
33
Q

signs? oral signs?

Acrodynia (Pink Disease, Swift Disease)

A
  • Chronic mercury toxicity in infants and children
  • Painful, pink discoloration of hands and feet
  • Hypersalivation, ulcerative gingivitis, premature loss of teeth
34
Q

systemic Silver intoxication (Argyrosis)
dissemenated?
skin?
other affected tissues?
oral sign?

A
  • Disseminated throughout the body
  • Accumulates in skin producing a diffuse grayish-blue discoloration, especially in sun-exposed areas
  • Sclera, nails, silver line on gingival margin
35
Q

sources of silver for intoxication

A
  • Industrial exposure
  • Prescription medications
  • Topical medications - silver nitrate
  • Over-the-counter drugs - colloidal silver
36
Q

Angioedema
additional names, defined, can affect, common presentation?

A
  • Quincke disease, angioneurotic edema
  • Rapid, recurring, diffuse, edematous swelling of subcutaneous or submucosal soft tissues – frequently the lips
  • May involve gastrointestinal or respiratory tract mucosa
  • The common clinical presentation of a group of conditions with different pathogenesis
37
Q

Allergic Angioedema
hypersensitivy?
mechanism?
stimuli?
responds to?

A
  • IgE-mediated hypersensitivity
  • Type I hypersensitivity reaction
  • Mast cell degranulation and histamine release
  • Contact allergic reaction to drugs, foods, plants, dust, inhalants, cosmetics, topical medications, rubber dam.
  • Physical stimuli such as heat, cold, emotional stress, exercise, solar exposure, vibration
  • Responds to antihistamines
38
Q

ACE-Inhibitor Angioedema
drug names?
mechanism?
does not respond to?
attacks may be precipitated by?

A
  • Angiotensin-converting enzyme inhibitors - Captopril, Enalipril, Lisinopril
  • Produces angioedema due to increased levels of bradykinin
  • Swelling does not respond well to antihistamines
  • Attacks may be precipitated by dental procedures in long-term users
39
Q

Hereditary Angioedema

A
  • C1 esterase inhibitor (C1-INH) deficiency
  • Complement cascade triggered after trauma or spontaneously, producing vascular permeability and edema
  • Mimics allergic angioedema, but produces more severe symptoms.
  • Prophylaxis by C1-INH replacement (C1-INH concentrate)
40
Q

danger associated?

forms of therapeutic radiation

A

internal and external
radiation injury possible (burns)

41
Q

Acute Effects of Radiation Therapy

A
  • Radiation kills both tumor cells
    and normal cells
  • Can lead to Mucositis and dermatitis
42
Q

Chronic Head and Neck Effects of Radiation Therapy
* Dental
* Alveolar bone
* Mandibular
* Pituitary
* Thyroid

A
  • Dental anomalies
  • Alveolar bone hypoplasia
  • Mandibular hypoplasia
  • Pituitary dysfunction
  • Thyroid dysfunction
43
Q

Chronic Effects of Radiation on Tissue

A
  • Hypovascularity
  • Hypoxia
  • Hypocellularity - fibrosis
44
Q

Chronic Effects of H/N Radiation Therapy orally

A
  • Xerostomia and hypogeusia
  • Trismus
  • Osteoradionecrosis
45
Q

Onset and Duration of Radiation-Induced Oral Sequellae

A
46
Q

Radiation Damage to Salivary Glands
most/least sensitive glands?
result?

A
  • Serous glands are most sensitive
  • Mucous glands are more resistant
  • Symptomatic xerostomia
  • Xerostomia-related caries
47
Q

Saliva in Xerostomia has what decreased qualities?

A
  • Volume decreased
  • pH decreased
  • Buffering capacity decreased
48
Q

Acute Effects of Chemotherapy
* cells killed
* most affected tissues?
* Oral
* Cytopenias

A
  • Chemotherapy kills both tumor cells and normal cells
  • Tissues with rapid turnover are affected most severely –mucosal surfaces and bone marrow
  • Oral mucositis
  • Cytopenias – thrombocytopenia, neutropenia, anemia
49
Q

Chronic Effects of Chemotherapy on developing Dentition
* less severe than? effects?
* Effects depend on?

A
  • The effects of chemotherapy on the developing dentition are less severe than radiation therapy
  • Hypoplastic enamel defects, discoloration, root hypoplasia
  • Effects depend on stage of tooth development and the dose/duration of the chemotherapy
50
Q

Clinical Definition of Osteoradionecrosis

A
  • Exposed bone that persists for three
    months in an irradiated area
  • Rare < 60 Gy
51
Q

infection?

ORN caused by

A
  • Bone death caused by radiation injury (avascular necrosis of bone)
  • ORN is not a primary infection of bone. The infection is secondary.
52
Q

Radiation Effects on Bone

A
  • Permanent damage to osteocytes and microvasculature
  • Bone is hypovascular, hypoxic, hypocellular
53
Q

Pathogenesis of Osteoradionecrosis

A
  • The irradiated bone has an absence of reserve reparative capacity with limited ability to meet even basic metabolic
    demands
  • Trauma overwhelms reparative
    capacity
  • Trauma may be caused by tooth extraction, pulpal disease, periodontitis, mucosal ulcers or denture-related
    injury produces a chronic non-
    healing wound
54
Q

Osteoradionecrosis of Mandible can be due to?

A
  • Squamous cell carcinoma of lateral border of tongue tx = External beam RT
  • Interstitial implants
55
Q

how would ORN appear histo

A

bac devris present in hypocellualr bone

56
Q

Treatment of Osteoradionecrosis

A
  • Antibiotic therapy
  • Surgical debridement of necrotic,
    infected bone
  • Hyperbaric oxygen therapy (HBO)
    partially reverses cellular alterations of
    radiation and restores the microvasculature to higher level
57
Q

Medication-Related Osteonecrosis of the Jaws - MRONJ
often related to hx of? drugs?

A
  • Spontaneous, bilateral, asymptomatic ulceration of edentulous maxilla

often occurs in those with hx of breast cancer- tx with: RT, Bisphosphonate (Zometa), Anti-estrogen (Arimidex), Analgesic (Morphine)

58
Q

how would MRONJ appeart histo?

A

hypocellular bone with bac debris

PATH II (24 decks)

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