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142 Cards in this Set

  • Front
  • Back
what is a cold sore?
herpes type 1
what % of pop is positive for herpes virus?
80% if all types are included
what happens to most people during primary infection of herpes type 1 through kissing/fomite?
99% are asypmtomatic from PRIMARY infection
1% get acute gigivostomatitis as a PRIMARY infection
of the population that is asymptomatic in the primary infection what can happen next?
50% of the 99% who are asymptomatic during primary infection never develop herpetic lesions
50% of the infected people get periodic outbreaks of secondary herpes due to retention of latent virus
what is the cause and stats of gingivostomatits?
primary herpes sinplex type 1 infection. only occurs in 1% of people who are infected with herpes.
what is the presentation of gingivostomatitis?
primary herpetic gingivostomatitis - Acute, febrile disease with malaise and
cervical adenopathy. Localizing symptoms in mouth as generalized vesicles
and ulcers, 3-7 mm. with associated acute, hemorrhagic gingivitis. Resolves
in 2 weeks. Does not return. Mostly children and young adults.

gingival swelling, vesicals rupture to ulcers
when does herpes labailis occur?
it is a secondary herpes infection. this is how 99% of people who manifest secondary infections present.
what is the presentation of herpes labialis?
localized tingling and swelling followed by a crop of vesicles on lip. Infection contained because of prior antibodies. No fever, adenopathy. Vesicles break, ulcers crust and heal in 2 weeks. All ages affected.

occurs on the LIP not inside the mouth
what triggers herpes labialis?
Latent virus in trigeminal
ganglion is periodically reactivated by colds and fevers, sun, trauma, stress,menstrual periods
what is characteristic biopsy for primary herpes?(biopsy rarely performed)
vesicals seen as pool of fluid and degnerating epithelial cells that rapidly rupture and ulcerate
what is a normal evaluation technique used to diagnose primary herpes infection?
cytologic smear of vesicular fluid shows multinucleated cell with glassy nuclei which is indicative of viral infection.
what is the antibody status for anyone manifesting secondary herpes outbreak?
positive antibody to the herpes simplex virus usually type 1
what is typical duration of secondary herpes outbreak?
14 days
what is another name for (common term) for herpes labialis?
cold sore, fever blister most common presenation of secondary herpes infection
how do you tell primary herpes from other oral ulceration disease?
primary herpes always presents with inflamed markedly red and often swollen gingiva. with hemorrhage not always generalized but always present
what differentiates herpes 1 from herpes 2?
1 above the waste 2 is genital
what is important about the contgiousness of primary herpes(gingivostomatitis) infection?
extremely contagious AND no antibodies present so it is common for patient to spread disease to themselves in other location.

like the eye and this is the most common cause of infection induced blindness

SO DON'T TOUCH THE SORES YOURSELF OR OTHERS
where do herpes virus stay when latent?
tirgeminal ganglion
what is secondary intraoral herpes?
occurs less common than the cold sore type, similar presenation, but in the oral mucosa.
periodic crops of vesicles ulcers
where is the main site of secondary intraoral herpes and almost diagnostic?
gingvia/hard palate
what is herpetic widlow?
herpes that occurs by touching herpetic ulcer on fingers
what is a dangerous possible complication of herpes infection in children?
herpies hepatitis and encephalopathy. can be fatal
what is caversy varicellaform eruption? and what is its cause?
herpies type 1 in a patient with a concurrent skin disease like pemphigus or excema. the herpes virus goes crazy and cause small pox like eruptions that can be fatal.
what is the intranuclear inclusion in herpies type 1 called?
lipshit bodies
what is the cause of hand foot and mouth disease?
coxsackie virus
who commonly get coxsackie virus infection?
children to young adults
what is the presentation seen in hand foot and mouth disease?
Acute outbreak of vesicles and ulcers throughout mouth accompanied by viral constitutional symptoms and cervical adenopathy and concomitant lesions on hands, feet and buttocks. Resolves and does not recur.
what characteristics of coxsackie differentiate it from herpies infections?
lacks gingivitis, has digital lesions, does not recur.
what is herpangina?
coxsakie viral infection that presents with acute fever with small vesicles and ulcers, but is limited to the SOFT PALATE and PHARYNX as oppesed to hard palate and gingiva as in herpes.
does coxsackie have cytologic inclusions?
no
what is varicella zoster or shingles?
secondary infection of varicella, with primary disease being chicken pox. shingles appear after immunity is weakened due to stress or another disease.
what is the common prodrome to shingles outbreak?
pain often in the flank that is so severe that simpley brushing it with clothing can cause severe burning sensation
what is the presentation of shingles?
vesicular eruption followed by redness and ulceration. ALWAYS ALONG NERVE CLUSTER

usually in flank area but can aries in the head and neck along the trigeminal nerve cluster.
what is key feature in often seen in spread of shingles on the face?
stops at halfway mark becuase its following the nerve
what is important about shingles that are found on the tip of the nose?
almost always has eye invovlement. refer to opthamology immediately can lead to blindness
what is the recomendation for people over the age 60 in reference to shingles?
should have shingles shot which is 14 times stronger than chicken pox vacine
what is a dangerous complication of shingles in population over 60?
necrosis in jaw

SEVERE pain. so severe and long lasting people commit suicide even after the outbreak is resolved due to continueing pain.
what does ANUG stand for?
acute necrotizing ulcerative gingivitis
also known as trench mouth.
what is the cause of ANUG?
anerobic, fusopriochetal bacterial infection.
what is presentation of ANUG?
Anterior gingiva are painful and swollen with punched out necrotic ulcers of gingival papillae. Foul odor. Sialorrhea. Fever, malaise and lymphadenopathy present.
what are the predisposing factors of ANUG?
poor oral hygiene (plaque and calculus)
what is used to differentieate ANUG from herpies?
necrosis of papillae, not common in children, the ulcers are only on the ginigiva. REALLY BAD smell.

gingival papillae=area between teeth
how is ANUG treated?
dental prophalaxis, and antibiotics
like penicillin
no antivirals
what kind of infection is it that causes ANUG?
endogenous. these are common bacteria of the mouth that only act up due to poor hygiene.
what is steven johnson syndrome also known as?
erythema multiforme that affects the mouth, eyes, skin and genital mucosa.
what is the pathologic process involved in steven johnson syndrome?
cytotoxic T cell mediated, type IV delayed hypersensitivity reaction
what are the common triggers of steven johnson syndrome?
recent herpes outbreak, medication, URI, lymphoma

often we don't know what the cause is but these are the ones we do recognize
who gets steven johnson syndrome most often and when?
young adult males, with seasonal recurrence in spring and fall
what is the presentation of steven johnson syndrome?
Acute onset of debilitating, confluent oral ulcers producing bloody, crusted lips. Typically spares the gingiva. Skin lesions are red macules, papules, blisters and TARGETOID LESIONS of palms and soles. Resolves in 1 month.
what are some thing that differentiate steven johnson syndrome from herpies?
spares gingiva, confluent slough, skine an dother mucosal lesions.
what is the normal treatment for steven johnson syndrome?
steroids
what is the most extreme version of erythema multiforme?
lyle disease
what occurs in lyle disease?
skin falls off all over

from this you lose fluid and electrolytes constantly

extremely vulnerable to infection

often fatal
what is the classic lesion triad of erythema multiforme?
oral lesions
ocular lesions
gential lesions
what is the appearance of erythema multiforme lesions?
can be many different way erythemous
vesicular, ulcers, plaques etc

the main one is TARGETOID lesions
often seen on PALMS and FEET
when would you not use steroids in erythema multiforme?
lyle disease it would encourage infection
what is another name of recurrent apthous ulcers?
canker sores
what is protective against apthous ulcers?
smoking if you quite it can develop even later in life when its less common
what percent of pop gets apthous ulcers?
20%
treatment? cause? of apthous ulcers?
hypersensitivity maybe?
stress, trauma, certain foods, mentration.

no decent treatment
what differentiates apthous ulcers from herpies?
almost never occurs on hard palate or ginvia. no vesicular formation first
what are the causes of Red, white and speckled mucosal lesions?
lichens planus
cicatricicial pemphigoid(BMMP)
geographic tongue
candida
snuff patch
nicotine stomatitis
dysplasia/carcninoma in situ
oral cancer
what is the cause of lichen planus?
immune-mediated disease in which there is a T cell response to basal cells.
what is usually true about the skin and mucosal lesions of lichens planus?
they rarely present together.
what is the epidemiology of lichens planus?
2% of women over age 40
what is the clinical presenation of lichens planus?
chronic lesions that wax and wane, may burn
a. lacy white striae of buccal mucosa sometimes with atrophic red background;
b. diffuse, red, shiny, atrophic, burning gingiva;
c. large, soft, well-demarcated serpiginous yellow ulcers on a red/white background
d. atrophic, bald plaque-like white dorsal tongue
e. skin lesions when present are pruritic plaques on wrists-ankles
what is seen on hystology for lichens planus?
hyperkeratosis, band-like lymphocytes infiltrating and hugging the basal layer. liquefaction of basal cells, saw toothing of th rete ridges, exocytosis
what is appearance of skin lesions with lichens planus?
pruritic(itchy) plaques on wrists-ankles
what is the classic case of lichens planus?
bilateral presentation of lacy white striae that dont rub off called whichums stria
what is atypical lichens planus examples and usually mistaken for?
erosive
atrophic-plaque like

mistaken for cancer until hystology is seen
what is the pathology of lichens planus?
autoimmune T cells destroy the basal cells
what is the typical case of lichens planus?
bilateral
chronic
white lacey stria(wickens striae)
don't rub off

can ulcerate to cause pain but otherwise asymptomatic
what is the appearance of lichens planus?
raised rhompoid scally plaque
that is pink to purple in color
with white scale on surface
what is the trait of skin lesions of lichens planus?
extremely puritic (itchy)
occur mainly on the wrists and ankles
what is the treatment for lichens planus?
topical or systemic steroids
what is seen on histo for lichens planus?
lymphocytes
saw toothed rete ridges
liquification of basal cells
hyperkeratosis
what is a condition that seems like lichens lichens planus?
geographic tongue
what is geographic tongue
conditions with red and white lesions that comes and goes, its not dangerous but we don't know what causes it. may cause some burning, but may be asymtomatics until you eat something spicy or acidic.
what is the presenation of candidiassis?
red and white lesion on tongue that resembles lichen planus, excepute that it produces white curds that can be scraped off.
what is lost on the tongue with geographic tongue?
the papilla are lost in the erythemoatous areas
when does candidiasis occur?
candida is everywhere espeacially in the mouth, it only manifests when you are imunocomprimised by something like steroid treatment or immunedisfuction
how is candidiassis diagnosed?
scrape lesion
add potassiam hydrate
histo will show psudohyphae with football shaped spores.
how is candidiasis treated?
antifungal meds
What does diagnosis with candidiassis infer?
that patient is immuno compreimsed
such as by antibiotics, steroids, diabetes uncontrolled, lymphoma, AIDS


candidiasis is rarely the primary condition
what are nonimmune related condition that could cause candidiasis?
dry mouth
dentures
presence of other oral lesinos

you should always test for candida if you find another condition like lichens planus?
what is found in patients who use snuff?
snuff patch, known as benign keratosis
not dangerous, will resolve in about a month its rare for cancer to develop in a place that patient uses snuff its takes a long time as well.
what is a white lesion with red dots in it along the top of the hard palat?
nicotinic hyperkeratosis
seen in pipe smokers
benign caused by heat not the carcinognens, resolves in a month
what is the main type of oral cancer/
squamous cell
what are the main causes of oral cancer?
smoking
alcohol will add risk to smoking but wont add risk by itself
what is the main cause of lower lip cancer?
UV light
what is the overall survival for oral cancer?
58%
what is a problem with diagnosising oral cancer?
once they look like cancer its too late. They look like so many other oral conditions when they are still small enough to treat, and its hard to justify biospying all these oral pathches.
What are the high risk areas for cancer of the mouth?
favored areas are lower vermillion of lip, lateral tongue, ventral tongue, floor of mouth, soft palate. Less commonly, buccal mucosa and gingiva.

Rarely, hard palate, dorsal tongue, lip mucosa, upper vermillion
what is the rule of biopsy of mouth lesions?
Management: since early curable dysplasias present as asymptomatic, innocuous red, white and red/white patches as do many other irritational, inflammatory and mucocutaneous disorders, the rule of thumb is if a non-descript white, red or speckled mucosal patch is present for more than 2 weeks without obvious cause or attribution to some specific disease and is in a high risk location for oral cancer - it gets biopsied.
what lesion has the highest chance of being malignant?
red lesion that does not go away after 2 weeks espeacially in high risk area.
what is the metastatic potential and place for oral cancer?
very metastatic even when small, usually metastasize to lymph nodes above the clavicle.
what are the three major glands of the mouth?
parotid
sublingual
submandibular
where are the minor glands?
lips
bucal mucosa
palat
only a few in the tongue
none in the gums
where do most salivary gland tumors occur?
the parotid gland
where in the parotid gland do most tumors occur?
the superfical lobe, which is palpable in front of the ear.
what is the percentages of tumors that occur in all the glands?
parotid-70%
submandibular-10%
sublingual-1%
minor glands-20%
what is the most common site of intra oral salivary tumors?
the palate most common then the lip.

very rare to have salivary tumor of the tongue bc not many glands there
which lip gets the most salivary gland tumors?
the upper lip lower lip is even more rare than tongue.
what is presentation of salivary gland tumors.
painless slow growing free moving, submucosal lumps
females slightlymore common
blacks more than whites
30yo, but children and elderly can also get them.
what is the rule about any free moving lump in the palate?
salivary tumor until proven otherwise, bc its such a common tumor its more common than other type of bumps in that area.
what can you use to differentiate btw benign and malignant salivary gland clinically?
its impossible to distinquish, but if its fast growing, ulcerative, fixed, or has bloodvessels visible in its surface then you may suspect malignant.
which type of salivary gland tumor is always fixed?
tumors in the palate are always fixed.
which locations in the mouth are more commonly malignant than benign.
lower lip and tongue- both very rare but when present usually malignant

behind the pharangeal tonsil is almost always malignant.
what is odd about malignant salivary tumors?
often slow growing
often encapslated and non invasive
often painless
often well differentiated.

in all appearances many salivary malignant tumors appear both clinically and histologically benign.

conversely benign cells can appear malignant under microscopic.
what is the standard treatment for parotid glands tumors?
total removal of superficail lobe. reguardless of malignancy or benign.

going in multiple times can damage the nerve
what is the treatment for submandibular?
removal of whole gland reguardless of malignancy
what is the treatment of the intraoral salivary tumors?
depends on type and malignancy.
what is the problem of myoepithelial cells in the parotid glands?
they look and stain like many many other cells, chondrocyte, plasma cells, spindle cells, and clear cells
what are the important benign salivary tumors?
mixed tumor(pleomorphic adenoma)
Warthin's tumors
what are the important malignant salivary?
mucoepidermoid tumor
adenoid cystic carcinoma
acinic cell carcinoma
malignant mixed tumor
polymorphous low grade adenocarcinoma
what is the appearance of warthins tumor?histo
papilary infoldings into a cystic cavity that has a lymphoid stroma
what is the most common malignant salivary tumor?
mucoepidermoid tumor
what is the most dangerous malignant salviary tumor?
adenoid cystic carcinoma(cylindroma)
what is the most common salivary tumor?
benign mixed tumor
where are benign mixed tumors usually found?
parotid, palate, upper lip
what is the origin of benign mixed tumor?
intercalated duct and myoepithelial cells
what is the risk with mixed tumor?
present with a very clean encapsulation but the tumor usually has microscopic buds that penetrate the capsule, so if you only remove the capusle it will usually recur and its not good to have to go in for more than one surgery.

Also 5% undergo malignant transformation.
which mixed tumor salivary usually turn maligant?
ones allowed to grow for a long time and those surgically mismanaged
what is the problem with needle biospy for mixed tumor?
different locations have extremely different appearances due to the myoepithelial cells producing a wide varity of tissue appearances
where do warthins tumors occur
only in the parotid but only 6% of parotid tumors
what is the common cause of warthins tumor?
only salivary tumor that is associated with cigarret smoking
what is the prognosis of warthings?
no recurrance, no malignant transformation, limited growth potential

but it can make you sick primariliy
what is the location of mucoepidermoid tumor?
palate and retromolar pad

can occur in cysts within a tooth
what is the most common salivary tumor in children?
mucoepidermoid
what is the appearance of low grade mucoepidermoid tumor?
"low grade" examples are predominantly cystic and well-differentiated with mucous cell preponderance
what is the appearance of high grade mucoepidermoid tumors?
solid, poorly differentiated and have more intermediate and squamous cells.
what is the prognosis of mucoepidermoid tumors?
Low grade tumors are more common.
e. most are slow growing but infiltrative and have a high recurrence rate. Low grade ones rarely metastasize and when they do, may require up to 20 years to manifest symptoms.
f. 50% (high grade), 92% (low grade) 5 year survival, 15 year survival remain high in low grade tumors but is 0-20% in high grade tumors.
what does mucoepidermoid tumor resemble?
may clinically resemble mucocele because of soft cystic composition - beware of "mucoceles" in unusual sites like retromolar pad
what stain can be helpful in identification of mucoepidermal tumor?
mucicarmen stain for mucous cells
what is metastatic potential of mucoepidermal tumor?
more are low grade rare metastatis sometime local recurrance. high grade rare and medium metastatic potential
what scary about adenoid cystic carcinoma?
slow growing
look benign under microscope
devastatingly infiltrative, showing persistent recurrences and eventual blood-borne metastases up till 20 years.
What is seen on histo for adenoid cystic carcinoma?
swiss cheese pattern of monotonous basaloid cells compartmentalized into ovoid cylinders by hyalinized pink material,
where does adenoid cystic carcinoma arise from?
ductal and myoepithelial cells
what is the prognosis for adenoid cystic carcinoma?
intraoral and submaxillary are more deadly than parotid

overall 5 year survival 70% and 15 year survival of only 20%
where does adenoid cystic carcinoma usually metastasize to?
bone, brain, lung not lymph node
where are adenoid cystic carcinoma found?
not parotid very often

intraoral very common

ALONG NERVES can spread from mouth up nerves into the brain.
how is adenoid cystic carcinoma treated?
wide margin excision
revmoval of bone and never in area all the way up to nearest ganglion
radiation(not very effective but you have to do something)

no need for nodal excision.


if metastasize already debulk tumor to reduce symptoms, otherwise nothing is going to help they are dead already.