Finals - Fall 2018 Flashcards
Primer does what?
Increases surface tension of dentin to allow for bonding agent to reach collapsed collagen.
Vitrebond is a
RMGI
No need to use GLUMA if you are using —- or if you are using ——
VitreBond liner
ScotchBond Universal adhesive
- Typically refers to Commercial plans
- Estimate - No guarantee of payment
- Allows verification of benefits letting the patient know how much they need to pay, and the College know how much to collect.
Pre-Determination: (Could take 4-6 weeks)
- For ALL Medicaid/Agency related plans. (Month to month eligibility)
- Payer requires approval in advance of starting a procedure to ensure they will pay for the procedure.
- College receives a preauthorization approval number for the specific CDT Code and we have to include that on the bill for payer.
Preauthorization: (Could take 4-6 weeks)
Dx occlusal adjustment of the mounted casts to:
Provide —– at the recorded —- (grinding list to record the reductions in order)
Determine the correct and desirable —-.
maximum intercuspation
CR
OVD
mounted in CR:
- restoring all posterior teeth in one or both arches
- restoring all teeth in one arch
- complete dentures
- occlusal equilibration
Post height = crown length
Guarded
3/4 of root length > crown length
Good prognosis
May be best for extremely tapered, funnel
shaped canals.
Cast post
For post, endo will tell you
….
1. The color which will indicate the size
(red, blue, black or red)
2. The length to which they removed gutta
percha. (Should be a reference-i.e.
buccal cusp, remaining lingual portion of
tooth etc.
Paracore etch:
No need for this.
Five-minute exposure to 21.3% AlCl3 - hemodent
. Complete smear layer removal and noticeable dentin etching, some tubules remain partly occluded
Gluma is made of —- in water and helps to reduce hypersensitivity of dentin and reduce the incidence of post-operative sensitivity in restorative dentistry procedures.
5% glutaraldehyde and 35% HEMA (hydroxyethyl methacrylate)
The —– in Gluma works by blocking the dentinal tubules, thereby preventing the flow of fluid and decreasing sensitivity. —– forms deep resin tags and then occludes the dentinal tubules.
glutaraldehyde
HEMA
If the tooth is vital and asymptomatic, stop excavating after you are —% through dentin to avoid pulp exposure.
75
SDF: • Diamine ~
Ammonia (8%) o Stabilizer
o Vaporizes at body temperature
SDF: • Silver (25%)
o Antimicrobial: denatures proteins, breaks cell walls and membranes, inhibits DNA replication
curing light inhibitis
deep penetration of SDF into dentin
Gingiva effects to SDF
o Short-term: transient inflammation (24 h)
o Long-term: reduces plaque and gingival inflammation where it is applied (antimicrobial)
• Composite and Glass Ionomer bond strength —- by SDF
unaffected
SMART –
silver modified atraumatic restorative technique
Fluoride toxicity
5mg/kg is PTD
Colophony aka
rosin is a resin obtained from pine trees and other coniferous plants
dental materials contain colophony
Root canal sealers, cements
Colophony has been known to cause —– in affected individuals
—–
ALLERGIC CONTACT DERMATITIS
Type IV Hypersensitivity
Colophony tx
Oral antihistamine
Diphenhydramine
5mg/kg/day, four divided doses
Max dose 300mg/day
Type I:
Anaphylactic/Atopy Ex: Food allergies, eczema
Type II:
Cytotoxic/Antibody dependent
Ex: Autoimmune hemolytic anemia, myasthenia gravis
Type III:
Immune Complex
Ex: Systemic lupus erythematosus, rheumatoid arthritis
Type IV:
Delayed type/Cell-Mediated Ex: TB Mantoux test, contact dermatitis
Make sure that balls given to children younger than three are at least —” in diameter
1.75
• differs from chronic inflammatory enlargement • fibrous, firm and pale pink, w/ little tendency to bleed • occurs slowly • occurs 1st in papilla • spreads to gingival margin • may cover & interfere w/ eruption or occlusion • may improve or resolve when medication discontinued • genetic component to susceptibility • severity affected by adequacy of oral hygiene • severity affected by gingival concentration of the medication
Drug-induced gingival overgrowth
Prominent max frenum - tx
Treatment usually delayed until permanent incisors & cuspids erupted to allow natural closure of diastema
• If orthodontic treatment planned, postpone surgical treatment until diastema has been closed
Aggressive perio - localized affects ——, gernalized affects —-
young pts, young adults
Localized aggressive (formerly “juvenile”) periodontitis (LAP / LJP)
- characterized by loss of attachment & bone around permanent incisors & 1st permanent molars
- attachment loss is rapid, occurring at 3X rate of adult onset disease
LAP
• At least some cases appear to be inherited as an autosomal dominant trait
Treatment of LPP
• Antibiotic therapy combined with debridement
• Tetracyclines, commonly used to treat LJP,
contraindicated for LPP because of potential
for staining of developing permanent teeth
• Metronidazole&amoxicillinor
• Azithromycin
Hypophosphatasia
• geneticdisorderin which the enzyme, —— is deficient or defective
bone alkaline phosphatase
Leukocyte adhesion deficiency (LAD) • group of rare, recessive genetic syndromes • severity variable • affects how --------- • susceptibility to -------`
- absence of pus at infection sites
- recurrent ———–
- periodontal disease symptoms manifested in —— dentition
- inflammation & bone loss
- scrupulous oral hygiene measures needed
- adequate compliance may be difficult to achieve
- —— can be curative
white blood cells (leukocytes) respond & travel to site of
wound or infection
bacterial infections
otitis media, & other bacterial infections of soft tissues
primary
bone marrow transplant
Papillon-LeFèvre syndrome
• rare genetic disorder
• onset of —— in primary or transitional dentition
• severe inflammation & rapid bone loss characteristic
• easily identified ——- of the palms of the hands and soles of the feet
severe
periodontitis
hyperkeratosis
Langerhans Cell histiocytosis
• Diagnosed by —–
biopsy
—-, but not usually —-, may present w/ gingival enlargement caused by infiltrates of leukemic cells
AML
ALL
Max Dose Lidocaine =
4.4mg/kg
• Max Dose Articaine =
7mg/kg
Odontogenic facial cellulitis
- bacteria from tooth
* alpha-streptococci
- skin or mucous membrane trauma
- sinus bacteria
- Hemophilis influenzae
- Hib vaccine lowered incidence
Nonodontogenic facial cellulitis
- bactericidal
- narrow but appropriate spectrum for milder infections
- resistance possible
- amoxicillin has less frequent dosage schedule and better taste
• Penicillin or amoxicillin
- oral Augmentin (amoxicillin and clavulanate) • IV Unasyn (Ampicillin and Sulbactam)
- resistance unlikely
- bactericidal
penicillins w/ b-lactamase inhibitor
Addition of —— to penicillin or amoxicillin • covers anaerobes, so broader spectrum
metronidazole
less resistance
• bacteriostatic
clindamycin oral or IV •
- erythema
- induration
- tenderness of periorbital tissues
- rarely progresses to orbital cellulitis
• “Pre-septal cellulitis”
- more common in children • bulging eye (proptosis)
- loss of vision
- pain in eye
- brain abscess
• Orbital cellulitis
• blood pressure maintained by increased cardiac work
• rapid pulse
• not indefinitely
sustainable
compensated shock
- blood pressure can no longer be maintained
* emergency
uncompensated shock
Veau lip Class I :
Unilateral notching of the vermillion
border, not extending into lip (microform)
Veau lip Class II:
– Class II : UL cleft extending into the lip (incomplete)
Veau lip Class III:
– Class III : UL cleft involving the floor of the nose (complete)
Veau lip Class IV:
– Class IV: Any bilateral cleft of the lip
Veau Cleft PALATE
– Class I :
Isolated soft palate cleft only
Veau Cleft PALATE
– Class II :
UL soft and hard palate cleft
Veau Cleft PALATE
– Class III :
UL cleft involving soft/hard palate through the alveolus (usually involves lip too)
Veau Cleft PALATE
– Class IV:
Same as class II but BILATERAL
CleftLip:
Causedbypartialorcompletelackof fusion of the maxillary prominence with the medial nasal prominence
Etiology of CLP • Environmental -------- exposure to ionizing radiation (suspected) • Genetic ---------
– Maternal smoking
– Teratogens (e.g. alcohol, anticonvulsants)
– Maternal obesity, nutrition, infection, hyperthermia,
– IRF6, 8q24 locus, VAX1 (confirmed)
Etiology of CLP • Environmental -------- exposure to ionizing radiation (suspected) • Genetic ---------
– Maternal smoking
– Teratogens (e.g. alcohol, anticonvulsants)
– Maternal obesity, nutrition, infection, hyperthermia,
– IRF6, 8q24 locus, VAX1 (confirmed)
The ones that really, really, really need tx NOW are:
Permanent tooth avulsions (!!!)
– All permanent tooth luxations
– Permanent tooth Class II and Class III fractures
Class II Fractures
Emergency Treatment
Permanent teeth
- Do nothing?
- Bond fragment if available
- Composite/GI “Band-Aid” – then monitor for symptoms
- Restore with composite/GI
Class II Fractures Follow-Up Care Permanent teeth • 6-8 weeks: • 1 year:
clinical and radiographic exam – If emergency tx was provisional restoration,
consider definitive restoration
clinical and radiographic exam
• No matter how minor the injury, we’re always concerned about loss of vitality
• Continue to monitor for signs and symptoms
Class III Fractures
Emergency Treatment
Permanent teeth
• Young tooth with open apex or closed apex
– Direct pulp cap
– Partial pulpotomy (Cvek technique)
Class III Fractures
Emergency Treatment
Permanent teeth
Mature tooth with closed apex
– Pulpectomy
– (Direct pulp cap and partial pulpotomy are also options)
Cvek Partial Pulpotomy Technique
Using a diamond or 330 bur, access the pulp chamber to a depth of 1- 2mm
• Extend the preparation to allow for sufficient access, but keep it in dentin
Obtain hemostasis
• Use a moist cotton pellet to apply firm pressure to the pulp
– Moisten with chlorhexidine or sterile water
– Apply pressure for 5 minutes
After 5 minutes, reassess the tooth
– There should be no more oozing of blood from the pulp chamber
• If bleeding continues:
– Apply further pressure
– Reassess and consider deeper preparation to amputate pulp further
Placemedicament
• Condenseasufficient thickness of dry calcium hydroxide powder or Biodentine to densely fill the preparation
– At least 1mm in depth, avoiding cavosurface margin
– Biodentine preferred over MTA for faster setting time and lack of staining
• Apply vitrebond directly over the medicament
– Apply up to the cavosurface margin
– Avoid placing vitrebond over enamel
• Compositeband-aid placed over fractured tooth
– Etch, Bond, Flowable
• Buildupcompletedat later date after healing confirmed
– Prefer to keep tooth out of occlusion to prevent further trauma
Cvek Partial Pulpotomy Technique - barium
Barium added for radiopacity; Do not add any liquid
1:3 Ratio of Barium:Calcium Hydroxide
Cvek partial pulpotomy criteria for success:
– No clinical signs or symptoms—no pain, no
mobility, no fistula
– No radiographic pathology
– Continued development of immature roots
– Formation of calcific barriers
– Sensitivity to electrical stimulation
– The tooth is vital!
Restoration can occur after success of Cvek has been ascertained
– Typically after — weeks
– Strip crown or composite buildup
6-8
Mostcriticalfactor for permanent tooth avulsion
– Maintaining an intact and viable PDL on the root surface
Avulsion
Emergency Treatment
Permanent Teeth
• Reimplantassoonaspossible.Everyminute counts! The person who is holding the tooth is the person to put it back in.
• Flexiblesplintfor2weeks
• Medications
– Systemic antibiotics-–best choice depends on age
– Chlorhexidine mouth rinse
– Ibuprofen: pain + inhibits bone resorption
Avulsion
Follow-Up
Permanent Teeth
• Closed apex:
remove pulp and fill with CaOH within 7-10 days
• Splint removal after 2 weeks (4 weeks if dry time >60 minutes)
• Complete gutta percha fill in 2-12 months
– No need to complete endo if it becomes ankylosed
Avulsion Follow-Up Permanent Teeth • What if the tooth is immature? – First, ---- – Our goal is to revascularize the severed pulp
WAIT for signs of necrosis
Avulsion
Follow-Up
Immature Permanent Teeth
• Bestprognosisif replanted within — minutes
20
Avulsion
Follow-Up
Immature Permanent Teeth
Recallevery—- weeks
3-4
Avulsion
Follow-Up
Immature Permanent Teeth
• Ifsignsofnecrosis, —-
extirpate pulp and do revascularization procedure
Revascularization
these are not the specifics
- Stimulate bleeding through apex
- Place MTA on top of clot
- Allows continued root development and root wall thickening
What do you do when the tooth becomes ankylosed?
• Maintain it as long as possible
– This will depend on the patient’s age
• When it starts to submerge and become an esthetic issue, decoronate + flipper
Extrusion Emergency Treatment Permanent teeth • Reposition with digital pressure • Flexible splint for ---- weeks • Rx -----
2
chlorhexidine mouth rinse
Extrusion
Follow-Up
Permanent teeth
• Closed apex:
likely pulp necrosis. Remove pulp and fill with CaOH when indicated.
Extrusion
Permanent teeth
• Complete gutta percha fill in —– if no inflammatory resorption
2 months
Intrusion Emergency Treatment Permanent teeth • Openapex,----- :spontaneouseruption • Openapex,-------:orthodonticor surgical repositioning • Closedapex,-------:spontaneouseruption • Closedapex,-------:orthodonticorsurgical repositioning • Closedapex,-------:surgical repositioning
upto7mm
morethan7mm
upto3mm
3-7mm
morethan7mm
Intrusion
Follow-Up Care
Permanent teeth
• Closed apex: —–
remove pulp and fill with CaOH within 2-3 weeks
• Complete gutta percha fill in 2 months if no inflammatory resorption
Intrusion Emergency Treatment Primary teeth • Which way did the tooth go? • If tooth was displaced -----, then allow spontaneous re-eruption • If tooth displaced -----, then extract
labially
into developing tooth bud
– Developmental mucocutaneous conditions
Ectodermal dysplasia • Hypohidrotic ectodermal dysplasia • (polygenetic oligodontia) – White sponge nevus – Peutz-Jeghers syndrome – Hereditary hemorrhagic telangiectasia
• Immune-mediated
– Pemphigus vulgaris – Mucous membrane pemphigoid – Bullous pemphigoid – Erythema multiforme – Erythema migrans (geographic tongue) – Lichen planus • Cutaneous lichen planus • Oral lichen planus – Lichenoid mucositis – Lupus erythematosus • Chronic cutaneous (CCLE) • Systemic (SLE) – Systemic sclerosis – CREST syndrome
– Ectodermal dysplasia
• Group of inherited disorders in which — or more —— structures do not develop normally or fail to develop (hypoplasia or aplasia)
two
ectodermally derived
• Clinical features: –Hypoplasia or aplasia of: • Skin • Hair • Nails •Teeth • Sweat glands
– Ectodermal dysplasia
– Ectodermal dysplasia • Clinical features: Hypohidrotic ectodermal dysplasia –One of the best known types –------ – lack of ------ –Features often more pronounced in -----
–Fine, ——–
Teeth: –——
–------- hyperpigmentation –Protuberant -------- –Prominent ------ –Varying degrees of ----- –Dystrophic or brittle -----
Heat intolerance
sweat
glands
males than females
sparse blond or light color hair, eyebrows, eyelashes
Hypodontia –Oligodontia (lack of development of 6 or more teeth) –Conical roots –Abnormally-shaped crowns (conical, tapered, pointed, smaller)
Periocular
lips (midface hypoplasia)
forehead
xerostomia
nails
• Polygenetic oligodontia – This is not an —-
–Dental findings can mimic ——
ectodermal dysplasia
White sponge nevus
• occurs Due to a defect in the —-
normal keratinization of the oral mucosa
• Genodermatosis – genetically determined skin disorder
White sponge nevus
• ——- – genetically determined skin disorder
Genodermatosis
– White sponge nevus
• Clinical features:
–Relatively rare
–Autosomal —- with variable expressivity
–Appears at ——, sometimes adolescence
–Asymptomatic
–Thick, —– appearance of buccal mucosa bilaterally
–Other oral sites may be affected
–——– mucosa may be involved
dominant
birth or early childhood
white
Nasal, esophageal, laryngeal, anogenital
– White sponge nevus • Histopathologic features: –------- sometimes more diagnostic than scalpel biopsy –-------- (thickening of spinous layer) –------- of cytoplasm is pathognomonic
Exfoliative cytology
Parakeratosis with acanthosis
Perinuclear eosinophilic condensation
– White sponge nevus • Treatment: –------ but cosmetic concern –------- reported to help –Reassure the patient that this is a harmless condition –------ prognosis
None necessary
Tetracycline rinses
Good
Peutz-Jeghers syndrome
• Clinical features:
–Rare, but well-recognized, usually noted
in childhood
–Usually inherited, autosomal —— (~ 35% new mutations)
–—— gene mutation allowing uncontrolled cell growth
–—— polyps of gastrointestinal tract, esp. jejunum and ileum
–Can cause ——
–Bowel problems become evident in the
—— (i.e. 20’s)
–High risk of developing cancer — times greater than control population (GI tract, pancreas, male and female genital tract, ovary, breast)
–—— of lips and oral mucosa (also can occur around eyes, nostrils, anus, hands, feet), may fade with age
–~ 1 in 100,000-200,000 births, although more frequent by some reports
dominant
STK11
Benign hamartomatous
bowel obstruction due to intussusception (“telescoping” of proximal segment into distal segment)
3rd decade
18
Hyperpigmented macules
– Peutz-Jeghers syndrome
• Histopathologic features: –—— are not
precancerous
• Benign growths of —–
Gastrointestinal polyps
intestinal glandular epithelium
– Peutz-Jeghers syndrome • Treatment: –Genetic counseling, parents and patient –Monitor for -----
intussusception and for tumor development
Peutz-Jeghers syndrome
• Prognosis:
–—— may self-correct or may require surgery to prevent ischemic necrosis
–If cancer develops, treat appropriately
Intussusception
– Hereditary hemorrhagic telangiectasia (HHT)
• Clinical features:
–Telangiectasia – small collection of
dilated capillaries
–Uncommon autosomal —— –~ 1 in 10,000
–Mutation of one of two genes which are responsible for ————
–Frequent spontaneous —— – may be
initial clue to diagnosis
–Numerous ——- red papules blanch with diascopy
–Telangiectasias may be seen on —–
Oral, oropharyngeal, nasal, genitourinary,
conjunctival mucosa and GI mucosa
–Arteriovenous fistulas may affect the —-
–Oral lesions often most dramatic and
most easily identified • Vermilion zones
• Tongue
• Buccal mucosa
dominant
blood vessel wall integrity
epistaxis
1 mm – 2 mm
mucosa and skin, including hands and feet
lungs (30% of patients), liver (30%) or brain (10-20%)
– Hereditary hemorrhagic telangiectasia (HHT)
• Diagnosis HHT requires 3 of 4 features:
–Recurrent spontaneous ——-
–Telangiectasias of mucosa and skin
–——- involving the lung, liver or brain
–Family history of HHT
epistaxis
AV malformation
– Hereditary hemorrhagic telangiectasia (HHT)
• Histopathologic features:
–Collection of thin-walled blood vessels in the —–
superficial connective tissue
– Hereditary hemorrhagic telangiectasia (HHT) • Treatment: –Genetic counseling, parent and patient –Mild HHT – ---- –Moderate HHT – -------- –Severe – -------
no treatment
selective cryotherapy or electrocautery bothersome lesions
septal dermoplasty to prevent epistaxis
– Hereditary hemorrhagic telangiectasia (HHT)
• Prognosis:
–Generally good, 1-2% mortality sometimes noted due to complications related to blood loss
–If —– develops, 10% mortality can be anticipated, despite early diagnosis and appropriate treatment
brain abscess
– Pemphigus vulgaris (PV)
• —– etiology
• Inappropriate production of —– by the host directed against host tissue (autoantibodies)
–Damage to host by host’s own immune response
Autoimmune
antibodies
– Pemphigus vulgaris (PV)
• In PV —– destroy —–
autoantibodies
desmosomes
– Pemphigus vulgaris (PV)
• Clinical features:
–Relatively rare, ~ — cases per million diagnosed each year in general population
–Average age — y.o. –No gender predilection
5
50
– Pemphigus vulgaris (PV)
• Clinical features (con’t):
– Oral lesions
“first to show, last to go”
• In other words – the oral lesions often are the initial manifestation of the disease and the most difficult to resolve with treatment
– Pemphigus vulgaris (PV) • Clinical features (con’t): • Flaccid -----, ---- on skin; rarely seen intact intraorally • + Nikolsky sign - inducing a ---- by applying firm, lateral pressure to normal appearing skin
vesicles
bullae
bulla
– Pemphigus vulgaris (PV)
• Biopsy
–Normal tissue adjacent to ulceration or erosion should be sampled for direct —— (in Michel’s solution) and for light microscopic evaluation
• Sample at periphery – not the ulcerated center
immunofluorescent
– Pemphigus vulgaris (PV)
• Histopathologic features:
–Microscopically, —— above the basal layer (i.e. within the epithelium)
–—— (breakdown of spinous layer; cells appear to fall apart) – is also usually evident
intraepithelial clefting
Acantholysis
• Direct immunofluorescence (DIF) used to detect
autoantibodies bound to the patient’s tissues
• Indirect immunofluorescence (IIF) used to detect antibodies
circulating in the blood
– Pemphigus vulgaris (PV)
• Immunopathologic features:
–—–) immunofluorescence studies will be positive in pemphigus vulgaris
–Autoantibodies bind —— components (desmoglein 1 & 3)
Both direct (DIF) and indirect (IIF
desmosomal
– Pemphigus vulgaris (PV)
• Treatment:
–——, often with azathioprine or other steroid-sparing agents
–Topical —– have little effect (PV is a systemic disease)
–~ —% resolve on their own after 10 yrs
Systemic corticosteroids
corticosteroids
30
– Pemphigus vulgaris (PV) • Prognosis: –Usually ---- if not treated • *Severe infection • Loss of fluids/electrolytes • Malnutrition due to mouth pain –Prior to corticosteroid therapy, 60-90% mortality
fatal
– Pemphigus vulgaris (PV) • Prognosis (con’t): –Complications of long-term steroid may lead to mortality –Today, ---% mortality, usually due to complications of therapy (side effect of steroids, immune- suppression; azathioprine suppresses bone marrow and is a carcinogen)
5-10
– Mucous membrane pemphigoid (MMP)
Also known as —– • Clinical features:
–Resembles PV due to blister formation (i.e. pemphig”oid”)
–Twice as common as PV
–Older age than PV, average 50 – 60 y.o. –2:1 female predilection
cicatricial (scarring) pemphigoid
– Mucous membrane pemphigoid (MMP)
• Clinical features (con’t):
–Any mucosal surface, occasionally affects
skin –Scarring
• Skin
• —– (conjunctiva) • Scarring on oral mucosa rare
Symblepheron
MMP: –May see intact —- because
the split is —-
intraoral blisters
subepithelial
– Mucous membrane pemphigoid (MMP)
• Clinical features (con’t):
–—– gingivitis – descriptive term: erythema, desquamation, ulceration
• May be seen in several disorders
Desquamative
– Mucous membrane pemphigoid (MMP)
• Most significant aspect of this condition is ocular involvement of symblepheron
–Scarring obstructs the —–
–Dryness leads to —— of the corneal epithelium, leading to blindness
orifices of glands that produce tears, resulting in a dry eye
keratinization
– Mucous membrane pemphigoid (MMP)
• For biopsy:
–Must include generous sample of normal mucosa, —– away from areas of ulceration/erythema, as epithelium easily strips off
–Tissue should be submitted in ——
0.5-1.0 cm
both formalin and Michel’s solution
– Mucous membrane pemphigoid (MMP)
• Histopathologic features:
–—— formation – separation of the epithelium from the connective tissue at the basement membrane zone (BMZ)
Subepithelial cleft
– Mucous membrane pemphigoid (MMP) • Immunopathologic features: –----- deposition of immunoreactants at the BMZ –Positive DIF; negative IIF (only 5-25% of patients will have circulating autoantibodies)
Linear
– Mucous membrane pemphigoid (MMP) • Treatment: –Depends on extent of involvement • Oral lesions alone - --------, tetracycline/niacinamide or dapsone may be sufficient • Frequent dental prophylaxis,----mos. Refer patient to ophthalmologist for exam and follow-up • If ocular involvement, systemic immunosuppressive therapy indicated
topical steroids
q 3-4
– Mucous membrane pemphigoid (MMP) • Prognosis: –Rarely fatal –Condition can usually be controlled –Blindness results in patients with untreated ocular disease –Rarely undergoes -----
spontaneous resolution
Bullous pemphigoid (BP)
• Clinical features:
–Most common of autoimmune blistering
conditions ~ 10 cases per million per year
–Usually older population affected, average age 75 – 80 y.o.
–Primarily on skin but mucous membrane involvement occurs
No gender predilection
–—– early symptom, followed by the development of multiple, tense bullae, blisters on normal or erythematous skin
–Rupture, crust, heal without scarring
Pruritus
– Bullous pemphigoid (BP)
• Clinical features (con’t):
–Oral involvement uncommon
• —– rupture sooner than on skin (constant trauma?) leaving —–
Bullae
large shallow ulcerations with smooth, distinct margins
– Bullous pemphigoid (BP)
• Histopathologic features: –—– cleft similar to MMP
• Immunopathologic features:
–—- DIF and IIF with immunoreactants deposited at the —-
Subepithelial
Positive
BMZ
Bullous pemphigoid (BP) • Treatment: –Management similar to ----, but most BP cases resolve spontaneously in ---- years
cicatricial pemphigoid
1-2
– Bullous pemphigoid (BP)
• Prognosis:
–Many patients —–
–Problems may develop with use of —- therapy in older population
• Mortality — times higher than age and sex matched population
experience remission
immunosuppressive
3
– Erythema multiforme (EM)
• Etiology:
–Probably —–
• —— stimulated by trigger that produces the disease
immune-mediated
Immunologic derangement
– Erythema multiforme (EM)
• Etiology (con’t):
–50% cases- —- –25% - —–
–25% - ——
unknown
preceding infection;
• *Viral (herpes), • Bacterial (Mycoplasma pneumoniae)
medication-related (antibiotics and analgesics)
– Erythema multiforme (EM)
• Clinical features:
–Acute onset —- disorder skin and
mucous membranes –Young adult , age ——-
ulcerative
20’s – 30’s
– Erythema multiforme (EM)
• Clinical features (con’t):
–—— symptoms ~ 1 week before onset (fever, malaise, headache, cough, sore throat)
–Previous studies showed —– predilection, more recent studies show —- predilection
Prodromal
male
female
– Erythema multiforme (EM) • Clinical features EM minor: –Skin (extremities) –Mucosa (oral, conjunctival, genitourinary, respiratory) »---- crusting of vermilion zones –Skin • Variety of appearances “multiforme” • ------ on skin of extremities • ----- with ------ centers
–Mucosa
• Erythematous patches oral mucosa that undergo —– and result in large, shallow erosions and ulcers with irregular borders
• ——- usually spared
HemorrhagicRound, dusky-red patches - “target lesions”
Bullae
necrotic
necrosis
Gingiva and hard palate
– Erythema multiforme (EM) • Clinical features EM major: –------ mucosal sites in conjunction with skin lesions • Mucosal, lip and skin lesions as seen in EM minor –Ocular involvement can produce ------
2 or more
symblepheron
• Stevens-Johnson syndrome (SJS) –
at least two mucosal sites plus skin involvement
• Toxic epidermal necrolysis (TEN) - (Lyell’s disease) –
diffuse bullous involvement of skin and mucosa
- Difference between SJS and TEN: –Degree of —– involvement and age
- SJS <10% and usually ——
- TEN >30% and usually over
skin
younger patient
60 y.o.
• SJS and TEN almost always triggered by a —–, rather than —-
• SJS and TEN skin lesions begin as ——-
–Within 2 weeks ——- develop
–Patients may appear ——- - usually treated in —–
–Almost all patients have —— involvement, esp. oral
drug
infection
red macules on trunk rather than extremities
skin sloughing and flaccid
bullae
badly scalded
burn unit
mucosal
– EM, SJS and TEN
• Diagnosis:
–Usually based on —–
–DIF and IIF —–, not helpful except to rule-out other immune- mediated condition
clinical
presentation
non-specific
– EM, SJS and TEN • Histopathologic features: –------ vesicles –Necrotic ------ –Mixed inflammatory cell infiltrate –May see ------ inflammation
Subepithelial or intraepithelial
basal keratinocytes
perivascular
– Erythema multiforme (EM)
• Treatment (supportive therapy):
–Discontinue causative drug!
–Systemic or topical steroids early on (benefits controversial)
–—– re-hydration
–Topical anesthetic or analgesic for pain
IV
• Treatment SJS and TEN (con’t):
–—– are avoided in the management of TEN – associated with increased mortality
–IV administration of —— seems helpful in resolution of TEN by blocking apoptosis of epithelial cells
Steroids
pooled human immunoglobulins
– Erythema multiforme (EM)
• Prognosis:
–EM minor and major - —–
–—% of patients get recurrences (esp. spring and autumn)
• If HSV is trigger maintenance antiviral –Not life-threatening except severe cases
self-limiting (2 – 6
weeks)
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