Mouth and Throat Dz Flashcards
Stomatitis
etiologies (5)
nutritional deficiencies
chemotherapy
nicotine
systemic autoimmune disease
infection
thrush (def. and common pathogen)
infection of buccal mucosa by candidiasis
commonly C. albicans
populations with thrush
infants and neonates
abx or steroids (inhalation)
endocrine disorders
underlying immune dysfunction
denture wears w/poor oral hygiene
clinical appearance of thrush
shedding of epithelial cells
lumpy/bumpy white
pseudomembranous easily peeled but leaves red erosion
thrush treatment
topical nystatin
pral fluconazole
HIV can’t be missed here
systemic diseases associated with aphthous ulcers (6)
HIV
Behcet syndrome
Celiac disease
SLE
IBD
Neutropenia
aphthous ulcers
aka canker sores
last 7-10 days
usually less than 5 mm
small, red, round/oval spots, prodromal tingling/burning
pain usually dissipates 3-4 days later
possible etiologies of aphthous ulcers (6)
genetics
medications
nutrient deficiencies
stress
allergy/sensitivity
trauma
aphthous ulcers treatment
avoid spicy food, citrus, hot foods, smoking and EtOH
topical analgesic can be used
antimicrobial mouthwashes
workup indicated if aphthous ulcers don’t heal
CBC ESR serum iron studies B6 B12 folate
transmission of herpes labials
primarily caused by HSV-1
non sexual contact in childhood
herpes labials lesions
vesicular lesions that rapidly rupture and ulcerate
acquire virus without clinical illness
buccal mucosa first, then disease is usually on the lips in keratinized skin
herpes labials treatment
acyclovir or famciclovir
most effective early in course of illness to shorten duration of illness and infectivity
herpes labials outbreak onset
stress, illness, trauma, menses or other irritants can provoke it
prodromal burning/tingling
leukoplakia
pre malignant condition that is the result of inflammation
hyperplasia of epithelium
leukoplakia occurs where
areas of trauma or in areas of significant carcinogen/chemical exposure
leukoplakia more common in which population
smokeless tobacco users
associated with HPV
most significant prognostic indicator of leukoplakia
degree of dysplasia
send pt to ENT physician
erythroplakia
red patches adjacent to normal mucosa
clinical term but not dx
appearance of atrophic glossitis
tongue appears smooth, glossy and with the loss of papillae
etiologies of atrophic glossitis
nutritional deficiencies (B12 or iron)
sick and Sjogren’s syndrome
celiac disease
oral candiaisis
PCM
black tongue appearance
hyperpigmentation of tongue and oral mucosa
commonly seen in darker skin individuals
black tongue causes
drugs (tetracyclines, line solid, antidepressants, proton pump) and addison’s disease
black hairy tongue
condition caused by antibiotics, candida infection, or poor oral hygiene
elongated filiform papillae and yellowish white to brown dorsal tongue surface
black hairy tongue treatment
brush area of the tongue with a soft bristle toothbrush and toothpaste two to three times per day
head and neck cancers include tumors where? (5)
oral cavity
pharynx
larynx
nasal cavity and paranasal sinuses
major and minor salivary glands
risk factors for CA of head and neck
tobacco use
alcohol use
HPV
pathogenesis of Head and Neck CA
mostly squamous cell origin
multiple genetic mutations
field carcinogenesis
exposure everywhere when exposing head and neck to cancer causing agents
reminds us that cancer in this area can develop a second PRIMARY tumor (2, genetically different cancers)
common symptoms of head and neck cancers
pain
sores that won’t heal
hoarseness/voice change
cough
dysphagia
neck mass
endoscopic visualization
used to evaluate cancers of deeper tissues
image studies used to diagnose head and neck CA
CT scan w/wo IV contrast
MRI scan w/wo IV contrast
PET scan
local invasion
CA remains at site of primary tumor
grows out of organ to invade neighboring tissue
lymph node involvement
lymphatic drainage can follow spread
gives easy access
distant mets
far away from site
second primary cancer
totally genetically different cancer found in the same spot
cancer can’t be confirmed until
tissue dx is obtained
sequence of events in evaluating head and neck CA
H and P –> imaging –> tx
most common sites of head and neck CA metastasis
lungs, liver bone
most common second primaries in head and neck CA
head and neck CA
lung CA
esophageal CA
treating early head and neck CA
early head and neck cancer
treated surgically or with definitive radiation therapy
follow up with patients in head and neck CA
surveillance for recurrence for next 5 years at least
most recurrences occur within first 2-4 yrs
patients with recurrent head and neck CA treatment
pallative care, support
components of salivary system
2 parotid glands
2 submandibular glands
hundreds of minor salivary glands
acute sialadenitis
aka parotitis
infection of the salivary gland
may be bacterial or viral
sialolithiasis
stones in the salivary duct resulting in obstruction
stone formation
bacterial sialadenitis s/s
unilateral parotid glands
- unilateral swelling of the gland
- exquisite localized pain
- dysphagia or trismus (lockjaw)
- systemic symptoms
bacterial sialadenitis pathophysiology
stasis of saliva in the duct
therefore oral bacteria spread into the gland
bacterial sialadenitis
salivary stasis is facilitated by
obstruction (stone, tumor, growth)
decreased salivary flow (dehydration)
medication (anticholinergics, diuretics, opioids)
bacterial sialadenitis
bactieral culture suspected
polymicrobial (gram positive and anaerobes) – esp staph aureus
if hospitalized - gram neg. (klebsiella, enterobacter)
culture material from the duct (not just swob) but typically just empirically treat
bacterial sialadenitis
diagnostic working
Ultrasound *** detects abscess (I&D)
Contrast ct is best to distinguish cellulitis from abscess
elevated serum amylase w/o concurrent pancreatitis
bacterial sialadenitis
treatment
hydration
promotion of salivary flow (lemon drops or other mints)
IV ABx (vancomycin + metronidazole) 10-14 days
if abscess - I & D
bacterial sialadenitis
complications
massive swelling of neck = air way obstruction
osteomyelitis
septic phlebitis (jugular)
sepsis
sialithiasis s/s
pain and swelling over gland before or during eating
may be possible to feel stone or milk it (duct may be tender)
sialithiasis
dx
NON contrast CT of face
sialithiasis
tx (conservative)
moist heat
sialogogues
good hydration ‘
milking duct
NSAIDS for pain
sialithiasis
tx (procedural)
lithotripsy
wire basket retrieval via endoscopy
surgery
untreated/chronic sialithiasis
saliva production ceases and gland then becomes firm
infection/irritation of pharynx or tonsils
pharyngitis/tonsillitis
pharyngitis/tonsillitis
etiologies
infectious (typically viral)
trauma, toxins, allergy, neoplasm
infectious pharyngitis/tonsillitis
if bacterial: typically caused by GAS (group A strep)
but most often viral
symptoms associated with bacterial pharyngitis/tonsillitis
fever ( <102) white spots (pus) cervical LAD sudden, systemic illness sick contact
4-7 y.o., vomiting and HA, petechiae
symptoms viral pharyngitis/tonsillitis
SUB ACUTE onset
hoarseness, coryza, myalgia
cough, conjunctivitis, rhionrrhea
unreliable pharyngitis/tonsillitis symptoms that don’t help us distinguish b/t viral and bacterial
fever (or lack of)
tonsillar or pharyngeal exudates
Centor criteria (list)
- fever to 101
- anterior cervical lymphadenopathy
- tonsillar exudate
- absence of cough
centor criteria interpretation
if 4 present - high likelihood of GAS, give aBX
if 2-3: preform rapid strep test
if 1: probably viral, symptomatic management
tests used to diagnose step
rapid strep testing
throat culture (takes longer but sure that it is strep)
what is our biggest concern in missing a GAS pharyngitis/tonsillitis diagnosis?
rheumatic fever
but we shouldn’t be concerned bc the strains that cause it are not in America
viral pharyngitis treatment
symptomatically
NSAIDs/tylenol, salt water, hot showers/steam inhalation, lozenges
GAS pharyngitis/tonsillitis treatment
self limited
s/s can resolve spontaneously 3-4 days
empiric ABX treatment of GAS pharyngitis/tonsillitis
penicillin (first line)
can give amoxicillin in young kids
erythromycin if PCN allergy
severe complications of strep
- scarlet fever
- rheumatic fever
- strep glomerulonephritis
scarlet fever
epidemiology
occurs in < 10% of strep throat cases
typically follows untreated/poorly treated strep
pathophysiology of scarlet fever
TOXIN produced by strep causes pathognomonic rash and other s/s
scarlet fever
rash
orange/red coarse sandpaper textured rash
- starts on head/center and moves out and down
- blanches may be puritic
- intensifies on flexor creases and facial flushing
- 12-48 hrs following fever
desquamation of skin 7-10 days later
scarlet fever
other s/s
rash +
strawberry tongue (white coating and red papillae, until white peels away)
high fever (103,104)
abdominal pain
scarlet fever management
HIGHLY contagious
PCN still drug of choice
rheumatic fever
pathophys
autoimmune inflammatory response
molecular mimicry causes inflammatory tissue injury persisting beyond acute GAS infection
body can’t distinguish b/t strep and self
inflammatory lesions of joints, heart, subcutaneous tissue, central nervous system
s/s of rheumatic fever
Arthritis (75%) - SYMMETRIC lg joints (knees, shoulder)
Carditis (30-60) pericarditis, valvular injury, myocarditis- esp. younger
sydenham chorea (little girls, near and psych features)
fever
abdominal pain
erythema marginatum (non-puritic, painless, serpiginous eruption) - RARE
Jones criteria of rheumatic fever
pancarditis (CV issues)
polyarthritis
syndham chorea
subcutaneous nodules
erythema marginatium
rheumatic fever
treatment
PCN and anti inflammatories
following diagnosis patients are placed on long term PCN to prevent recurrence
rheumatic valvular disease
causes mitral valve stenosis
more common in women `
increased risk for clotting issues, dental problems, procedures and fluid adminstarion
streptococcal glomerulonephritis
occurs 1-2 weeks after strep (throat or impetigo)
urinary (hematuria, oliguria or anuria) edema (face, arms, eyes, feet, ankles) hypertension abdominal pain back pain
deep neck infections
infections of the deep fascial layers of the neck
bad bc they can cause airway obstruction
deep neck infections
bacterial etiologies
typically polymicrobial (Gram pos. + anaerobes_)
deep neck infections
presenting s.s
may not have distinct fluctuant mass
dysphagia
swelling
trismus
pooling of saliva
deep neck infections
historial questions
likely source of infection
recent hospital or ECF
prior surgery
deep neck infections
imaging
CT scan of neck w/wo contrast
must be done quick bc of airway problems
deep neck infections
treatment options
vancomycin/zosyn
hospital admission
ENT + I and D consult
PTA/cellulitis
infection of tonsils that has extended into soft tissue of neck
not quite as deep but on way
result of contiguous spread (cellulitis -> phlegm -> abscess
pTA mc in which population
adolescents and young adults
PTA bacterial etiology
often poly microbial
GAS, MSSA/MRSA, respiratory anerobes
PTA symptoms
severe sore throat muffled voice drooling trismus systemic symptoms
PTA signs
enlarged, s wollen and fluctuant tonsil
bulging or fullness of soft palate
deviation of uvula
PTA work up
labs not great but imaging is diagnostic
CT scan of neck w/and w/o IV contrast
pta Differential
epiglottis
other deep neck infections
severe tonsillopharyntitis
PTA management
hospitalization
airway management
drainage
ABX (gram + and anaerobe cvg) - Unasyn, cleocin, vanco 14 days
typically full recovery
stridor
high pitched whistling produced from narrowed air way
above the cords = inspiratory, below cords = expiratory
why is PEEP important?
keeps a little bit of air inside the lungs so that alveolar cells are still open
decreases stress and allows easier gas exchange
epiglottitis bacterial causes
H. flu (we have vaccine now)
now it is mostly viral
must control bc airway compromise
epiglottitis s.s (young kids)
Abrupt onset of:
respiratory Distress
Dysphagia
Drooling
tripod or sniffling posture (CHIN thrust forward) to maximize airway
epiglottitis s/s (adults)
sore throat, fever, muggled voice, drooling
onset is more gradual and compromise is less common
not sniff posture bc airway is larger
epiglottitis exam
be careful in exam bc may provoke laryngospasm and constriction of air way
ENT consult and lateral neck radiographs
epiglottitis treatment
- airway management
- supplemental oxygen
- monitoring in ICU, ent consult
+/- corticosteroids, bronchodilators
laryngitis
hoarseness persisting for one or more weeks
treatment is voice rest
abnormal adduction of vocal cords during respiratory cycle that produces air flow obstruction at larynx
vocal cord dysfunction (VCD)
vocal cord dysfunction (VCD)
epidemiology
can occur at any age
MC in females, 20-40
vocal cord dysfunction (VCD)
risk factors
GERD, occupational exposure, swimming, strenuous exertion, allergies, psychiatric
vocal cord dysfunction (VCD)
pathoneumonic finding
paradoxical vocal cord adduction with posterior glottic chink during inspiration
vocal cord dysfunction (VCD)
symptoms
sudden onset of dyspnea cough throat tightness wheezing stridor
exam findings in VCD
harsh stridor and may have radiation of wheezing into upper chest
patients are often dx and tx for asthma with no or little response
vcd v. asthma
both have wheezing, cough, dyspnea BUT VCD has
for response to inhaled beta agonists or ICS
absence of nocturnal awakening
absence hypoxemia
INSPIRATORY stridor and wheezing
vocal cord dysfunction (VCD) diagnosis
direct observation via laryngoscopy while symptomatic
vocal cord dysfunction (VCD)
treatment
speech therapy
psychotherapy
