Physical and Chemical Injuries Flashcards
(53 cards)
1
Q
Iatrogenic Injury
(4)
A
- Cotton roll injury
- Dental thermoplastic compound
- X-ray film trauma
- Lacerations
2
Q
Factitial Injury
A
Self-inflicted injury caused
by the patient
3
Q
Munchausen syndrome -
A
a psychiatric disorder in which the patient finds
disease or illness in order to draw attention or sympathy to themselves.
4
Q
Familial Dysautonomia
(3)
A
- Autosomal recessive,
Ashkenazi Jewish heritage - Lack of response to painful
stimuli results in injuries - Absence of fungiform
papillae
5
Q
Complications of Piercings
(3)
A
- Infections – acute bacterial,
hepatitis, HIV, infective
endocarditis - Chipped, fractured teeth
- Periodontal lesions
6
Q
Electrical Burns
(3)
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
7
Q
Thermal Burns
(4)
A
Hot foods or beverages -
microwave ovens
* Palate, posterior buccal mucosa
* Erythema and ulceration
* Resolve without treatment
8
Q
Epithelial Desquamation
(2)
A
- Toothpaste detergents - sodium lauryl sulfate – SLS
- Listerine
9
Q
Drug-Associated Intrinsic Discoloration of Teeth
(2)
A
- Certain drugs may be
incorporated into
developing tooth structure
and produce clinically-
evident discoloration - The severity of the
effects depend on stage of
tooth development and the
dose/duration of the drug
administration
10
Q
Tetracycline Staining of Teeth
* Avoid use of
tetracyclines during
pregnancy and in
children under —
years of age
A
8
11
Q
Minocycline (Minocin)
(3)
A
- Derivative of tetracycline
commonly used for acne,
rheumatoid arthritis and for
periodontal disease - May produce intrinsic discoloration
of developing teeth and fully-
developed teeth - Also discolors bone, skin, sclera,
conjunctiva
12
Q
Minocycline Staining of Erupted Teeth
(3)
A
- Drug binds to pulpal
collagen - Oxidation produces
discoloration - Occurs in 5% of users
within 1 month to 1 year of
use
13
Q
Smoker’s Melanosis
(2)
A
- Oral pigmentation increased
significantly in heavy smokers - Exposure to polycyclic amines
stimulates melanin production
by melanocytes
14
Q
skipped
Drug-Related Mucosal Pigmentation
(7)
A
- Anti-malarials
- Tranquilizers
- Chemotherapeutics
- Laxatives
- Antibiotics
- Birth control pills
- Anti-retrovirals
15
Q
Zidovudine (Azidothymidine, AZT) Pigmentation
A
- AZT, an anti-retroviral agent, may produce
pigmentation of mucosa and nails
16
Q
Hydroxychloroquine (Plaquenil) Pigmentation
A
- Plaquenil, an anti-malarial
drug is often used in lupus
erythematosis
17
Q
Heavy Metal Toxicity
(3)
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)
18
Q
Lead Poisoning – Plumbism (Pb)
(4)
A
- Environmental sources
- Gasoline additive
- Lead-based paints
- Water supply - lead solder in plumbing
19
Q
Lead is chemically similar to
— and is deposited in
developing bone and teeth
forming bands of increased
density at metaphyses of
growing tubular bones
A
calcium
20
Q
Lead Poisoning – Variable Presentation
(3)
A
- Anemia -
- Renal dysfunction
- Non-specific signs and
symptoms -
21
Q
skipped
* Anemia -
A
hypochromic
microcytic with basophillic
stippling
22
Q
skipped
* Non-specific signs and
symptoms -
A
fatigue,
irritability, weakness,
abdominal and
musculoskeletal pain,
headache (cerebral edema in
acute poisoning)
23
Q
Oral Manifestations of Lead Poisoning
(4)
A
- Gingival lead line (Burton
line) - - Ulcerative stomatitis,
advanced periodontal
disease - Tongue tremor
- Metallic taste and
excessive salivation
24
Q
Gingival lead line (Burton
line) -
A
bacterial H2S forms
lead sulfide in gingival
crevice, producing a bluish
line at marginal gingiva.
25
Sialorrhea -
excessive salivation (ptyalism)
26
Mercury Poisoning
(4)
* Elemental mercury poorly
absorbed, but mercury
salts and vapor well-
absorbed
* Occupational exposure
* Dietary
* Medications - teething
powders, antihelminthics,
cathartics
27
Systemic Manifestations of Mercury Toxicity
* Acute and chronic exposure
28
* Acute –
abdominal pain,
vomiting, diarrhea
29
* Chronic –
gastrointestinal
upset, neurologic changes
30
Oral Manifestations of Mercury Poisoning
(5)
* Inflammation and enlargement
of salivary glands, tongue and
gingiva
* Discoloration of gingiva
* Periodontal bone destruction -
mercuric sulfide
* Ulcerative stomatitis
* Metallic taste
31
Acrodynia (Pink Disease, Swift Disease)
(3)
* Chronic mercury toxicity in infants
and children
* Painful, pink discoloration of hands
and feet
* Hypersalivation, ulcerative
gingivitis, premature loss of teeth
32
Systemic Silver Intoxication
(3)
* 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
33
Systemic Silver Intoxication
(4)
* Industrial exposure
* Prescription medications
* Topical medications - silver nitrate
* Over-the-counter drugs - colloidal silver
34
Angioedema
(4)
* 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
35
Allergic Angioedema
(5)
* 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
36
skipped
ACE-Inhibitor Angioedema
(4)
* 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
37
Hereditary Angioedema
(4)
* 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)
38
Therapeutic Irradiation
(2)
* External source
* Internal source
39
Acute Effects of Radiation Therapy
(2)
* Radiation kills both tumor cells
and normal cells
* Mucositis and dermatitis
40
Chronic Head and Neck Effects of Radiation Therapy
(5)
* Dental anomalies
* Alveolar bone hypoplasia
* Mandibular hypoplasia
* Pituitary dysfunction
* Thyroid dysfunction
41
Chronic Effects of Radiation Therapy
(3)
* Xerostomia and hypogeusia
* Trismus
* Osteoradionecrosis
42
Radiation Damage to Salivary Glands
(4)
* Serous glands are most sensitive
* Mucous glands are more resistant
* Symptomatic xerostomia
* Xerostomia-related caries
43
Saliva in Xerostomia
(3)
Volume
* pH
* Buffering capacity
44
Acute Effects of Chemotherapy
(4)
* 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
45
Chronic Effects of Chemotherapy on Dentition
(3)
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
46
Clinical Definition of Osteoradionecrosis
(2)
* Exposed bone that persists for three
months in an irradiated area
* Rare < 60 Gy
47
Osteoradionecrosis
(2)
* Bone death caused by radiation injury (avascular necrosis of bone)
* ORN is not a primary infection of bone. The infection is secondary.
48
Radiation Effect on Bone
(2)
* Permanent damage to osteocytes and microvasculature
* Bone is hypovascular, hypoxic, hypocellular
49
Pathogenesis of Osteoradionecrosis
(3)
* 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
50
Osteoradionecrosis of Mandible
(3)
* Squamous cell carcinoma of lateral border of tongue
* External beam RT
* Interstitial implants
51
Treatment of Osteoradionecrosis
(3)
* 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
52
Medication-Related Osteonecrosis of the Jaws - BRONJ
(4)
* 53 year-old female
* Spontaneous, bilateral,
asymptomatic ulceration
of edentulous maxilla of 1
month duration
* Breast cancer - 1997
* Radiation therapy – bone
metastases to spine
53
Medication-Related Osteonecrosis of the Jaws - BRONJ
* Medications
(3)
– Bisphosphonate - Zometa
– Anti-estrogen – Arimidex
– Analgesic - Morphine
