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Year 2 Respiratory > Exam I, sinonasal tract, Gomez > Flashcards

Exam I, sinonasal tract, Gomez Flashcards

1
Q

What are the basic structures in the sinonasal tract

A

nasal cavity, rhinosinuses

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2
Q

what are the basic structures of the pharynx

A

nasopharynx
oropharynx
hypopharynx

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3
Q

what are the major funcitons of upper airway

A 
conduit air to and from lungs
heat/humidify air
particle removal
immune surveillance
smell and speech
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4
Q

What are the 3 types of epithelial cells in sinonasal resp mucosA

A

ciliated psudeostratified columnar cells
mucin-containing goblet cells
basal (reserve) cells

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5
Q

what are the 2 characteristics of lamina propria

A

prominent vascularity

subepithelial seromucous glands

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6
Q

what is acute infectious thinitis

A

common cold- coryza

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7
Q

How is common cold trasmitted

A

conatc with contaminated sin, contaminated environmental surface, aerosolization

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8
Q

What can acute rhinitis progress to

A

pharyngitis, sinusitis, otitits media

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9
Q

up to 40% adult colds are due to what viruses

A

rhino (picorna, ss-RNA, genus enterovirus)

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10
Q

what are the other cold causing viruses that are not rhino

A

adeno, echo, corona, parainfluenza, respiratory syncytial

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11
Q

What are signs of allergic rhinitis

A

watery rhinorrhea, sneeing, nasal congestion and itching

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12
Q

what are the classifications for allergic rhinitis

A

seasonal: symptoms typically occur at a particular time of the year
perennial: occur year round
episodic: bouts of Sx occur at irregular intervals

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13
Q

What are the early spring pollens

A

tree pollens, oak, maples, elms, birches

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14
Q

what are the spring pollens

A

grass: ryegrass, bluegrass, bermuda grass

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15
Q

What type HS is allergic rhinitis

A

type I

IgE mediated

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16
Q

describe type I HS reaction

A

allergens timulates TH2 responses and IgE prodcution
IgE binds to Fc R on mast cells and then continuous exposure to allergin will activate mast cells to release histamine and other mediators

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17
Q

What is definition of chronic rhinitis

A

> 1 mo Sx:

sneezing, rhinorrhea, nasal congestions, postnasal drainage

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18
Q

What is major distinction of chronic rhinitis thatn alergic

A

onset after age 20

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19
Q

What is a problem with nasal polyps

A

recurrent attachs of rhinitis, most patients are not atopic
multiple
may acuse bostruction or become secondarily infected

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20
Q

What are types of sinusitis

A

acute- less than 4 weeks
empyema of sinue
subacute 4-12 weeks
chronic greater than 4 weeks

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21
Q

what is a mucocele of sinue

A

mucus accumulation no bacterial involvement

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22
Q

what are major findings of sinusitis

A 
facial pain/pressure
nasal obstruction/blockage
nasal discharge/discolored postnasal drip
hyposmia/anosmia
facial congestion/fullness
purulence in nasal cavity
fever
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23
Q

what are the minor findings in sinusitis

A

HA, halitosis, fatigue, dental pain, cough, ear pain, pressure, fullness, fever

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24
Q

what are serious complications of sinusitis

A

spread to orbit
osteomyelitis
cranial vault extension
septic thromboplebitis of dural venous sinus

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25
Q

What is ARS

A

acute infectiou sinusitis

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26
Q

what is presentation of acute sinusitis

A

purulent rhinorrhea, nasal congestion and/or facial pain

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27
Q

what is AVRS

A

acute viral sinusitis assoc withc ommon cold and cleras in 7 days or less

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28
Q

what can cause AVRS

A

rhinoviruses, influenzavirus, parainfluenza

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29
Q

what is ABRS

A

acute bacterial sinusistis

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30
Q

what are causes of ABRS

A

strep pneumoniae
Haem influenzae
morazella catarrhalis

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31
Q

What are signs of ABRS

A

Sx for more than 7 days
Sx initially improve and then worsen
sinusitis associated with dental disease

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32
Q

what are anatomic predisposing factors to chronic obstructive sinusitis

A

deviated septum, trauma, foreign body, sinonasal mass/neoplasm
previous sinus surgery

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33
Q

what are the fenetic medical predisposing factors to chronic obstructive sinusitis

A 
ASA triad
immunodeficiency
immotile cilia cyndrome
cystic fibrosis
DM
intensive care unit
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34
Q

What is the ASA triad

A

aspirin induced chronic rhinosinusitis, nasal polyps, severe bronchial asthma

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35
Q

what is kartagener syndrome

A

defective ciliary action and situs inversus

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36
Q

what are the environmental predisposing factors to chronic obstructive sinusitis

A

allergic rhinitis, nonallergic rhinitis microorganisms
sick building syndrome
smoking, pollutants, dry indoor heating

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37
Q

majority of chronic sinusitis is:
reccurent acute
obstructive
fungal sinus disorders?

A

obstructive

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38
Q

what are common Sx of chronic obstructive sinusitis

A

facial pain, pressure fullness
nasal obstruction/congestion
nasal drainage/postnasal drip
decreased sense of smell

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39
Q

what are the types of obstructive sinusitis

A

non-infected (mucocele)

suppurative(empyema)

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40
Q

what are the common bacterial agents to cause chronic obstructive sinusitis

A

staph aureus, gram neg rods

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41
Q

describe allergic fungal sinusitis

A

recurrent sinusitis, possibly nasal polyps

eosinophilic mucus charco-leyden cyrstals; with fungi

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42
Q

how do you Tx allergic fungal sinusitis

A

surgical debridment and possibly systemic steroids

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43
Q

describe fungus ball

A

mass lesion by X ray in one sinus cavity

fungal organisms with scant mucus and little inflammation

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44
Q

what is Tx for fungus ball (mycetoma)

A

surgical debridement

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45
Q

desribe invasive fungal sinusisits

A

severe, sometimes neuro deficit

the fungal organisms invade tissue vessels

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46
Q

what is Tx for invasive fungal sinusitis

A

aggressive surgical debridement; post-op anti-fungal drugs

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47
Q

What are vascular necrotizing lesions of upper airways

A

granulomatosis with polyangiitis
cocaine
churg strauss syndrome

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48
Q

what are infectious causes of necrotizing lesions of upper airways

A

rhinocerebral mucormycosis/ rhinocerebral zygomycosis

hansen disease/leptromatous leprosy

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49
Q

what lymphoma can cause necrotizing lesions in upper airways

A

extranodal NK/T cell lymphoma

50
Q

what causes rhinocerebral mucormycosis and what patients is it seen in

A

saprophytic mold fungi

usually in uncontrolled DM with ketoacidosis

51
Q

What population is affected by nasopharyngeal angiofibromas?

Sx?

A

young males
onset 10-20 “juvenile NA”
Sx: unilateral nasal obstruction and epistaxis. can also cause swelling of face, eye and cheek

52
Q

histo of nasopharyngeal angiofibroma

A

posterolateral wall fibromuscular stroma origin

benign, 10-20% locally aggressive

53
Q

What is Tx for nasopharyngeal angiofibroma

A

surgery, hemorrhagic complications no uncommon

pre-op ateriogram with pre surgical embolization

54
Q

prognosis of nasoparhyngeal angiofibroma depends on what

A

extent of resectability

55
Q

What are schneiderian benign neoplasms derived from and 3 types

A

from embrologic schneiderian membran that coverys cavity and sinuses
Exophytic- septal and squamous
Inverted- lateral and squamous
oncocytic- lateral and cylindrical/columnar

56
Q

what papilloma is more common thatn schneiderian mucosa tumors

A

squamous papilloma of nasal vestibule

(verruca vulgaris or wart

57
Q

Exophytic sinonasal papilloma occurs in what population

A 
20-50 y.o
male more likkel ythan female
HPV 6/11 in 60%
recurrence
rarlery develops invasive carcinoma
58
Q

inverted sinonasal papillma occurs in what pipulation

A

40-70 y.o
male more likely than female
HPV 6/11 in 40%
5-10% develop invasive carcinoma within 5 years

59
Q

oncocytic sinonasal papilloma occurs in what population

A

> 50 y/o
M:F 1:1
some may develop invasive carcinoma
oncocyte-abundant bright pink cytoplasm (mitochondria)

60
Q

What is an esthesionneuroblastoma

A

olfacotry neuroblasotma that arises from neuroendocrine cell in olfactory mucosa

61
Q

what is survival of esthesionneuroblastoma

A

5 yr survival is 40-90% with varying biologic activity

62
Q

What are the 3 divisions of pharynx and coinciding mucosae

A

nasopharynx- 60% non-keratinizing(no cornified layer) squamous. 40% respiratory epithelium
oropharynx
laryngopharynx- 100% NK squamos

63
Q

what are the upper airway lymph structures

A

diffuse submucosal lymphoid aggregates in nasal cavity

tonsils

64
Q

What are some disorders of pharynx that are secondary to lymphoid hyperplasia

A

obstructive sleep apnea

recurrent otitis media(adenoids)

65
Q

describe bordetella pertussis

A

whooping cough
small gram - coccobacilli taht spread in respiratory droplets
have Tdap
Dx with nasopharyngeal swab for culture and PCR or serology

66
Q

what are the stages of whooping cough/pertussis

A

stage 1- catarrhal phase: indistinguishable from common URI, nasal congestion, rinorrhea and sneezing. most infectious stage
stage 2- paroxysmal intense coughing, vomiting
stage 3- covalescent phase
chronic cough which may last for weeks

67
Q

how does whooping cough present in infants younger than 6 mo

A

apneic episodes instead od characteristic whoop

68
Q

what are the 3 histopath types of nasopharyngeal carcinoma

A

keratinzing (squamous cell carcinoma)
nonkeratinizing- squmaous cell
undifferentiated carcinoma with lymphoid component

69
Q

epidemiology of nasopharyngeal carcinoma

A 
EBV related
associated with smoking
common in children in Africa
common in adults in S China
rare in USA
70
Q

What is clinical course of nasopharyngeal carcinoma

A

unresectable at Dx (metastases in 70%)
treat with radiotherapy
5 yr survival is 60%

71
Q

What is NUT midline carcinoma

A

appearance similar to nasopharyngeal and squamous cell carcinoma
mostly in mediastinum and is highly aggressive
assoc with BRD4-BRD3-NUT fusion gene

72
Q

What are typical clinical features of Group A strep

A 
age 5-15
peaks winter-early spring
sore throat with rapid onset fever
strawberry tongue
no cough, hoarseness of conjunctivitis
tender anterior cervical lymph nodes
enlarged tonsils with patchy exudate
73
Q

what is the filamentou anaerobic gram - rod that can cause pharyngitis

A

fusobacgerium necrophorum

>20% in recurring cases and inperitonsillar abscesses

74
Q

what is the bacteria where humans are only known reservoir

A

corynebacterium diphtheriae

75
Q

describe gene of diphtheriae

A

only strains with tox gene casue diphteria

genes are encoded with lysogenic bacteriophage

76
Q

what is clinical course of diphteriae

A

sudden onset exudative pharyngitis that gets worse over 3 days
produces a pseudomembrane

77
Q

What are common viruses that cause pharyngitis

A 
rhinoviruses
adeno- pharynogconjunctival fever
EBV- infecitous mononucelosis
HSV 1 and 2- gigivitis, stomatitis, pharyngitis
influenza- pharyngitis
parainfluenze and coronavirus
entero
CMV and HIV
78
Q

what is Dx test for EBV

A

monospot test

79
Q

What is the most common cause epiglottitis

A

H influenze type b

Hib vaccine

80
Q

What are Sx of acute laryngitis

A

hoarseness, decreased vocal volume, painful speech

81
Q

what are common causes acute laryngitis

A

infections, vocal overuse: Acute- loud yelling
vocal overuse- subacute- lecturing
heavy smokin
direct trauma

82
Q

describe clinical course acute laryngitis

A

abrubt onset, self limited, <3 week duration

ages 3-5 yrs, 18-40 y/o

83
Q

what viruses and bacteria cause acute laryngitis

A

viruses >90% cases: rhino, parainfluenza, RSV, adeno

bacteria: H influenza, S pneumonia

84
Q

what can acute laryngitis lead to in children

A

life-threatening laryngoepiglottisis

85
Q

What is most common cause of inspiratory stridor in children and associated with seal-like barking

A

croup, laryngotracheitis

86
Q

When is “Croup season”

A

3 mo- 5 yr
acute onset
MArch-April

87
Q

what is cause of croup

A

parainfluenza that caues edema and inglammtion in subglottic layrnx and trachea around circoid cartiladge
edema of vocal cords can cause hoarseness

88
Q

What is Tx fro Croup

A

supportive with short term steroids to reduce inflammation

89
Q

What is the steeple sign

A

subglottic narrowing, seen in croup

90
Q

What is reinke edema and population it affects

A

soft gelatninous translucent expansion of cord surfaces from edema
usually in middle aged females who are heavy smokers
develop husky low pitched weak voices

91
Q

where is classic location for vocal cord nodules and polyps

A

junction anterior and middle third of cord

92
Q

What can lead to vocal cord nodules

A

heavy smoking
heavy recurrent voice strain (singers nodules)
HPV types 6/11

93
Q

howlikely are nodules and polyps going to give rise to cacner

A

virtually never

94
Q

how do vocal cord papillomas differ in adults and children

A

single in adults

mutiple in children

95
Q

what are clinical findings or squamous cell carcinoma of larynx

A

prolonged hoarseness, >6 weeks earliest, most consistent symptom

96
Q

epidemiology of squamous cell carcinoma of larynx

A

50 pack years)

ehtanol abuse.dependence

97
Q

what is progression of squamous cell carcinoma of larynx

A

hyperplasia- hyperkeratosis- dysplasia- carcinoma in situ- cancer

98
Q

What are the anatomic locations of laryngeal carincomas and which are most common

A

glottic(true vocal folds) 50-60%
supraglottic 30-40% when Dx usually already stage III or IV
subglottic
transglottic

99
Q

what is best indicator for prognosis of cancer

A

stage

100
Q

What are physical findings of otitis externa

A

marked tenderness after gentle traction of pinna
erythema, swelling, moist debris
peak age 7-12

101
Q

What can cause otitis externa

A 
traumatized ear canal
swimmers ear
bacterial 90%: pseudomonas Sp
Staph Ps
Gram - rods
Fungal: aspergillus, candida
102
Q

what are neoplasms of the external ear

A

squamous and basal cell carcinoma

103
Q

what is middle ear lined by

A

non-keratinizing stratified squamous epithelium

104
Q

what is a cholesteatoma

A

squamous peithelium trapped within temporal bone (middle ear or mastoid)

105
Q

what are sequalle of cholesteatoma

A

hearing loss, facial nerve paralysis, labrynthitis, meningitis, epidural or brain abscess

106
Q

what is Tx for choesteatoma

A

surgical resection to prevent sequellae

107
Q

What are the signs of acute otitis media

A

ear pain, fever, otorrhea(discharge), irritability vomiting and diarrhea
TM opacity, bulding, erythema, effusion and dec mobility

108
Q

What are the most common bacterial caues of acute otitis media

A

S pneumoniae, H influenza, M catarrhalis

109
Q

What are the common causes of chronic otitis media and long term sequellae

A

pseudomonas aeruginos, S aureus

perforation TM, scarring, mastoiditis, bone erosion, cysts and conductive hearing loss common

110
Q

what are the two types of cyst lining in middle ear

A 
squamoud epithelium (cholesteatoma) large amounts keratin
metaplastic columnar epithelium
111
Q

what is etiology of middle ear disorders like otosclerosis

A

> 50% famility Hx

auto dominant, variabl epenetrance

112
Q

what is clinical course otosclerosis

A

begins unilaterally 60-80% become b/l
hearing loss begins late adolescence
progressive ankylosis leading to severe conductive hearing loss

113
Q

Where does the bone thicken in otosclerosis

A

callus of bone accumulates at footplate of the stapes and rim of oval window

114
Q

What are some branchial cleft defects

A

sinus tracts, fistulas, cysts

115
Q

What is a thyroglossal duct cysts

A

cyst in midline
any age
portion of hyoid bone is removed along with cyst and tract

116
Q

What is prototype of parasympathetic tumor

A

carotid body tumor

117
Q

What are effects of carotid body tumor

A

releases NT that increase RR when hypoxic

118
Q

what are Signs of a carotid body tumor

A

bruit on auscultation from obstruction and turbulence

119
Q

What population is carotid body tumor more common in

A

40s
M=F
familial: MEN types 2a and 2b, vHL syndrome, Neurogibromatosis type 1 and 4 distinct paraganalgionic tumor syndromes

120
Q

What is dangerious about carotid body tumors

A

may metastasize to lymph nodes and distant

50% fatal due to infiltrative growth

Year 2 Respiratory (5 decks)

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