Primer Rhinitis And Sinusitis/aaaai Dvd

Front 1

URI of ess than 7 days caused by?

Back 1

Viral illness - viral rhino sinusitis

Front 2

Acute bacterial is most likely

Back 2

Beyond 7-10 days

Front 3

Three types of sinusitis are

Back 3

1) CRS wo NP
2) CRS w NP
3). AFRS

Front 4

Percent with rhinitis and sinusitis in western society?

Back 4

10-25%

Front 5

What percent of patients with rhinitis are no allergic

Back 5

30-50%

Front 6

Seasonal AR is found in what percent of population ?

Back 6

10-20% of general population, with greater prevalence in kids

Front 7

What kind of cells line the nasal cavity and turbinates?

Back 7

Pseudo stratified columnar ciliated epithelium

Front 8

What impairs mucociliary clearance?

Back 8

Infections, allergic inflammation

Front 9

Allergic rhinitis is commonly caused by?

Back 9

Proteins and glycoproteins in airborne dust mites, roach, animal dander, molds and pollens

Front 10

Are rhinitis and asthma interrelated?

Back 10

Yes they are associated

Front 11

How does house dust mite contribute to airway inflammation?

Back 11

Der p 2 mimics MD-2, the LPS-binding component of TLR -4 signaling complex and facilitates TLR 4 signaling and Th2 type inflammation

Front 12

How are allergens usually processed in the nose?

Back 12

Processed by APC (DC expressing CD1a CD11c and macs) in the nasal mucosa with presentation of peptides by MHC class II molecules to TCR on CD 4 in LN. T cell is stimulated and release IL 4, 3, 5, 13. This promotes b cell isotype switching to IgE

Front 13

Immediate allergic response?

Back 13

Caused by release of histamine, trptase, LT C, D, E and prostaglandin D2 causes mucus production, sneezing itching rhinorrhea

Front 14

Late phase response?

Back 14

Nasal congestion, usually occurs 4-8 hours, mediated by cytokines that promote expression of adhesion molecules like ICAM 1, E-selectin, vascular adhesion molecule 1 that promote eos to come in to endothelial cells.

Front 15

Priming effect?

Back 15

Decreasing amts of allergen are needed to elicit an immediate response, is associated with mucosal hyper responsive to nonantigenic triggers such as strong odors and cig smoke

Front 16

Sensitivity to pollen is associated with what?

Back 16

Ocular symptoms

Front 17

True or false? Treatment with intranssal steroids in patients with allergic asthma and rhinitis decreases seasonal bronchial hyperreactivity.

Back 17

True

Front 18

Examples of non allergic rhinitis without eosinophilia

Back 18

Aka idiopathic rhinitis
1) vasomotor rhinitis - caused by change in temp, emotions alcohol

Front 19

Examples of non allergic rhinitis with eos (NARE)

Back 19

Perennial nasal symptoms, pruritus, loss of smell! Nasal smears have eos 5-20%, no evidence of IgE mediated to environmental allergens. You can see mast cells with bound IgE and increased tryptase levels
Common in middle-aged adults, not childhood
May be early predictor of Nasal polyposis
Are at risk for OSA

Front 20

What is the order of development of the sinuses?

Back 20

MEFS (my early frontal sinuses)
maxillary, ethmoid, frontal and sphenoid

Front 21

What is the name of the artery that supplies upper 2/3 of the nasal septum?

Back 21

Sphenopalatine artery, called Little's artery

Front 22

What is the priming effect?

Back 22

Amt of allergen needed to elicit an immediate response becomes less when allergen challenges are given repeatedly. That explains why people have continuing symptoms despite allergy season going down.

Front 23

What is local allergic rhinitis?

Back 23

When people have nasal symptoms, likely has local IgE, but SPT and RAST is negative.

Front 24

Which mediators cause acute symptoms of AR?

Back 24

Histamine, PGD2, LT, kinins

Front 25

which mediators are in the late allergic response of AR?

Back 25

infiltration with basophils, eos and infiltrating lymphocytes, esp Th2 CD4 T lymphocytes. IL-3, IL-5, IL-4, IL-13, GM-CSF (eosinophil growth factor) and stem cell factor, eotaxin and RANTES. Nasal congestion and mucus production.

Front 26

What are some culprit medications associated with rhinitis?

Back 26

ASA, NSAIDs,
Vasodilators (Sildenafil, Tadalafil, Vardenafil
ACE inhibitors
Calcium channel blockers
OCP
antihypertensives
psychotropics
Decongestants

Front 27

True or False: AR is a risk factor for asthma?

Back 27

True

Front 28

AR and pregnancy: Avoidance of decongestants during pregnancy b/c it could lead to what complication during the first trimester?

Back 28

Gastroschisis

Front 29

When does rhinitis of pregnancy begin?

Back 29

Starts usually in the 2nd or 3rd trimester
lasts 6 or more weeks
Resolves within 2 weeks post-delivery
intranasal corticosteroids are not effective

Front 30

What is vasomotor rhinitis?

Back 30

AKA irritant rhinitis
Caused by irritants, cold, perfume, odors, dry air
Azelastine may be beneficial

Front 31

What is gustatory rhinitis?

Back 31

A form of vasomotor rhinitis but is caused by spicy foods. Can treat with atrovent

Front 32

What is atrophic rhinitis?

Back 32

Caused in elderly, may be from frequent sinus surgery,
typically caused by kelbsiella Ozaenae (found in arid countries and in female during puberty)
Paroxysmal nasal congestion and pain

Front 33

What is the ARIA classifications for rhinitis?

Back 33

Intermittent if < 4 day/week and < 4 weeks
Persistent if > 4 days per week and > 4 weeks

Front 34

T or F: greater sleep complaints in AR and there is a risk factor for sleep apnea?

Back 34

True

Front 35

What is the function of H4?

Back 35

H4 are histamine receptors that may be involved in pruritus esp in AD and in inflammation. It causes the chemotaxis of inflammatory cells.

Front 36

What is Birch cross reactive with in PFAS?

Back 36

(apple, cherry, apricot, pear, plum) and Apiaceae vegetables (eg, celery, carrot)
The primary allergens causing PFAS in birch-sensitized patients are Bet v 1-cross-reactive antigens and profilins

Front 37

What is the major foods cross reactive with Mugwort?

Back 37

celery, onion, mustard and cabbage

Front 38

What are the fruits and veggies cross reactive with ragweed?

Back 38

banana, cucumber, canteloupe, watermelon and zucchini

Front 39

What is NAREs?

Back 39

AR, with eos, no specific IgE testing that is positive, prone to nasal polyps and this may be a prodrome to AERD. Are at risk for obstructive sleep apnea.

Front 40

What is Profilin?

Back 40

profilins are now known to be ubiquitous cross-reactive plant allergens

Front 41

Hormone induced rhinitis may be associated with which disease?

Back 41

Hypothyroidism

Front 42

If neutrophils are found in nasal polyps, you need to remember what?

Back 42

CF

Front 43

When d o you think of a nasopharyngeal carcinoma?

Back 43

bleeding in an adolescent male, nasal pain, typically unilateral think Juvenile angiofibromas.

Front 44

Which sinuses drain through the osteomeatal complex?

Back 44

Frontal, anterior ethmoid, maxillary

Front 45

What drains into the sphenoethomiodal recess?

Back 45

Ethmoid and sphenoid sinuses

Front 46

What types of nasal polyps are found in those with AERD and asthma?

Back 46

Bilateral eosinophilic polyps
High levels of LTC4 synthase and IL-5
Increased cysLT receptors on inflammatory cells in the nasal polyps
Upregulation of CysLTs, LXA4 and PGD2
Treatment: Avoidance of ASA, leukotriene receptor antagonists, steroids and ASA densitizations.

Front 47

What are some other causes of CRS with nasal polyposis other than asthma and AERD?

Back 47

DM allergy, AFRS, eosinophils

Front 48

Is CRS with nasal polyposis usually associated with bacteria?

Back 48

Not typically except for local production of staph enterotoxins in NPs which may increase local IgE production and eosinophilic inflammation via Th2 skewing.

Front 49

Neutrophils found in nasal polyps is associated with what?

Back 49

CF, PCD and CSS

Front 50

What types of transcription factors are found in CRS with NP?

Back 50

Increase in GATA3 and Tbet. There is decrease in FOXP3 cells and therefore lack of Treg cells.

Front 51

Describe the difference between these
1) Acute rhinosinusitis < 10 days, > 10 days

Back 51

1) < 10 days is typically viral
2) > 10 days is typically bacteria, esp if getting worse after 5 days. These are acute so lasts < 12 weeks.

CRS is > 12 weeks

Front 52

What is the microbiology of Acute bacterial rhinosinusitis?

Back 52

1) Strep pneumo
2) H flu

These are the 2 most common

Front 53

What is the microbiology of acute bacterial rhinosinusitis in children?

Back 53

1) moraxella catarhallis
2) strep pneumo
3) H influ

Front 54

How can a Haller cell lead to CRS?

Back 54

Haller cells can block the osteomeatal complex

Front 55

What inflammatory mediators are associated with acute rhinosinusitis?

Back 55

IL-1B, IL-6 and IL-8

Front 56

What inflammatory mediators are associated with chronic rhinosinusitis?

Back 56

IL-3, GM-CSF, ECP

Front 57

What inflammatory mediators are associated with nasal polyposis?

Back 57

IL-5, IgE and Eotoaxin

Front 58

Patients with CCRS with NP have low levels of what?
High levels of what?

Back 58

Low of PGE2, high of LTC4, D4 and E4

Front 59

what inflammatory mediators are highest in ASA with NP? What is lowest?

Back 59

LTC4, LTD4 and LTE4
Lowest is PGE2

Front 60

Which type of CRS has the highest levels of Lipoxin?

Back 60

CRS-NP and CRS-ASNP (asp sensitivity)

Front 61

What types of changes do you see in CRS with NP in terms of IL?

Back 61

IL-5, IL-13 and see decreased TGF beta.
Mediators linked to eosinophil activation are impt such as GM-CSF, IL-3 and IL-5

This is a Th2 cyokine profile

Front 62

What is CRS without Nasal polyps profile look like?

Back 62

Th1 cytokine profile. Increased IFN gamma and TFGB and birosis.
Inflammation is neutrophilic due to increase in IL-1B, TNF-alpha, and IL-8

Front 63

What are the current treatment regiments for AOM?

Back 63

1) If < 6 months, treat with antibiotics
2) Between 6 months to 2 years, if dx is certain, treat if treat if severe (>39 C and otalgia) . If dx is uncertain, then can observe for 48-72 hours
3) If greater than 2, antibacteria therapy if severe (> 39 and otaliga). If non severe, observation. If uncertain dx observation

Front 64

what is considered a certain diagnosis of AOM?

Back 64

1) rapid onset, 2) signs of middle ear effusion 3) signs and symptoms of middle ear inflammation

Front 65

Otitis media with effusion carries what characteristics?

Back 65

Presence of fluid in the middle ear without signs and symptoms of acute infection. May occur spontaneously due to poor eustacean tube function or after AOM.
-90% of children with OME before school age
- 30-40% of children have recurrent OME
-5-10% of children have OME > 1 year

Front 66

Otitis media with effusion means what in children and what in adults?

Back 66

In children it can be common, it can be an incidental finding, often resolves within 3 months. Rarely seen in adults and if present, could indicate a structural abnormality such as a tumor.

Front 67

Is there a link between OME and atopic disease?

Back 67

Yes, there is suggestion that allergic rhinitis could be a cause for this.

Front 68

What is the leading cause of hearing loss in children?

Back 68

OME and it may be associated with language delay in children under 10 years of age. The average hearing loss from OME is 25 dB.

Front 69

A flat tympanogram can indicate what?

Back 69

OME or a perforated tympanic membrane, cholesteotoma or there is a tube in

Front 70

A left sided shift in the tympanogram indicates what?

Back 70

Serous OM, acute resolution of OM

Front 71

Those with AR are at risk for otitis media with effusion?

Back 71

True

Front 72

What is the management of OME? When does it become surgical?

Back 72

Monitor every 3 months, baseline hearing test. Indications for tympanostomy tube is OME with structural damage, persistent OME of at least 4 months with physical and behavior problems and reduced child quality of life, hearing loses of 40 db or greater. If repeat surgery is needed, and adenoidectomy should be included plus myringotomy

Front 73

What are risk factors for OME that makes it more likely a child will need an intervention?

Back 73

Permanent hearing loss independent of OME
Speech or language delay
Down syndrome
Carniofacial disorders that include speech, cognitive and laugage delays
Blindness
Cleft palate
DD

Front 74

What are complications with OME?

Back 74

Hearing loss
Atelectasis
Retraction
Cholesteatoma- the most serious complication.

Front 75

What is a cholesteatoma?

Back 75

It is a destructive and expanding keratinizing squamous epithelium in the middle ear and or mastoid process. Causes conductive hearing loss, with potential for ossicle destruction. Untreated may lead to deafness, mastoiditis, brain abscess, meningtis and rarely death.