Forme clinice: rinitele alergice pot fi sezoniere sau

perene
Rinita alergica sezoniera (febra de fan) apare intr-o anumita perioada a anului, legata de ciclul biologic al
alergenului. Rinita la polenul de graminee este forma cea mai frecventa de rinita alergica sezoniera
intalnita la noi in tara. Manifestarile caracteristice debuteaza la sfarsitul lunii mai, ating maximul in luna
iunie si cedeaza de regula in iulie. Perioada mai precoce sau mai tardiva a polenizarii depinde de conditiile
meteo si geografice (ploaia reduce concentratia granulelor de polen din atmosfera; vantul, in functie de
directia sa le concentreaza sau le disperseaza).
Rinita alergica perena este prezenta tot timpul anului si este declansata mai ales de pneumalergenii din
habitatul bolnavului si in principal de acarienii din praful de casa. Sensibilizarea poate fi determinata si de
mucegaiuri, pene, peri de animale sau de alergeni din mediul profesional si poate prezenta agravari
sezoniere.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883199/


Astfel, pe lng evaluarea statusului biologic al pacientului
(HLG, IgE), se impune efectuarea unor teste specific in vivo (testare
cutanat) sau in vitro (RAST-Radioallergosorbent Test).



https://www.synevo.ro/profil-astmrinita-intermitenta/

http://www.cdt-babes.ro/articole/rinita_alergica.php


https://www.jniosh.go.jp/en/indu_hel/pdf/IH_46_4_397.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677841/

http://www.archbronconeumol.org/en/rhinitis-and-asthma-one-airway/articulo/13080317/

TESTE
Efectuarea testelor cutanate implica introducerea unor cantitati de allergen si de substante control
in piele.
Testul percutanat e cel mai folosit. Ocazional se fol testul intradermal.Testul intradermal e mai
senzitiv iau testul percutanat e mai specific.
De obicei se fol testul intradermal.
Rinita alergica are un raspuns imediat si unul intarziat. Testarea pe piele ne ofera ambele
raspunsuri.Noi ne dorim sa aflam raspunsul imediat cauzat de eliberarea din mastocite sau bazofile a
mediatorilor specifici igE care ne dau reactii cu semnal luminos si ................ dupa 15 minute.
Raspunsul intarziat apare dupa 8 ore de la expunere si nu e prea folositor in clinica.
Testarea anticorpilor lgE specifici (RAST-radioallergosorbent testing=) e folosit daca testul percutanat
nu poate fi folosit(dc pac ia medicamente care interfereaza cu testarea antihistaminice). RAST e mai
specific dar nu atat de senzitiv.RAST e folosit in principal pt alergenii comuni(polen).
Pentru testarea alergiilor la copii avem nevoie de testul percutanat pt copii de la 3 ani in sus, sau
testul RAST pt orice varsta .Testul ar trebui ales in functie de istoricul bolii.
Testele prin punctionare sau zgariere (percutanate). In aceste teste, care sunt cel mai frecvent intalnite, cantitati foarte mici
de extract alergenic sunt introduse foarte superficial la nivelul pielii. Acest tip de test este de obicei realizat pentru a identifica
alergii la polen, par de animale, acarieni si alimente;-REACTIE IMEDIATA
2. Testele intradermice (intracutanate). Extractele purificate de alergen sunt injectate in piele la nivelul antebratului. Acest tip
de test este de obicei folosit daca medicul suspecteaza ca pacientul este alergic la venin sau la penicilina;-R IMEDIATA
3. Testele cu plasture (epicutanate). Acest tip de test nu foloseste ace. In schimb, alergenul este aplicat pe un plasture, care
este apoi plasat de piele. Acest tip de test este de obicei realizat pentru a identifica substante care determina dermatita de
contact. Acestea includ latex, medicamante, parfumuri, conservanti, vopseluri de par, metale si rasini. INTARZIATA REACTIA
Testele pentru depistarea reactiilor alergice imediate
Sus
Un test cutanat prin punctionare sau zgariere verifica reactia alergica imediata la mai mult de 40 de substante diferite in acelasi
timp. La adult, testul este efectuat de obicei la nivelul antebratului. Copiii sunt testati de obicei la nivelul spatelui superior.

Dupa curatarea locului unde va fi realizat testul cu alcool, asistenta va realiza urme fine la nivelul pielii si apoi aplica o picatura
de alergen pe fiecare urma. Apoi, folosind un obiect ascutit introduce extractul in piele. Un nou obiect ascutit este folosit pentru
fiecare zgarietura pentru a nu se contamina incrucisat cu alergenii. Picaturile sunt lasate pe piele pentru 15 minute, apoi
asistenta verifica locul testarii pentru a detecta semne ale reactiilor alergice.

Pentru a vedea daca pielea reactioneaza asa cum trebuie, asistenta introduce doua substante aditionale in suprafata
pielii:

1. Histamina
La aproape orice persoana, aceasta substanta determina un raspuns cutanat, deci este folosita pentru controlul pozitiv. Daca
pacientul nu reactioneaza la histamina, testul cutanat poate fi foarte dificil sau imposibil de interpretat.

2. Glicerina sau solutie salina
La aproape orice persoana, substanta nu determina nici o reactie. Deci una dintre cele doua sunt folosite pentru controlul
negativ. Daca pacientul reactioneaza la glicerina sau la solutie salina, acesta poate avea o piele foarte sensibila, deci reactia
pielii la extractul alergen trebuie interpretat cu atentie.

Unii pacienti necesita un test pentru reactiile imediate mai sensibil cunoscut si sub numele de test intradermal daca testul
prin punctie sau zgariere nu este foarte clar. In timpul acestui test, asistenta foloseste un ac subtire si o seringa pentru a injecta
o cantitate mica de extract alergenic imediat sub suprafata pielii, la nivelul bratului. Apoi asistenta verifica dupa 15 minute
aparitia unei eventuale reactii cutanate locale.


CE ESTE RINITA?
Ce este rinita alergica ?
Reactiile alergice apar doar la oamenii care au o caracteristica numita atopie - o sensibilitate sau susceptibilitate la alergeni.
Cand se expun la alergenii la care sunt sensibile, persoanele cu atopie dezvolta o reactie alergica sub forma uneia din bolile
alergice, cum este rinita alergica. O persoana atopica dezvolta adesea mai mult de o alergie.
Rinita alergica este o reactie exagerata a sitemului imunitar la particulele din aerul pe care il respirati. Sistemul imunitar in mod
normal protejeaza corpul de virusi si de bacterii prin producerea de anticorpi care sa-i combata. La rinita alergica, sistemul
imunitar incepe lupta cu substantele in fond nedaunatoare, cum este praful, acarienii si polenul (alergeni) ca si cum acestea
incearca sa va atace corpul. Aceasta reactie exagerata (reactie alergica) cauzeaza inflamatie si simptome ce afecteaza in
principal nasul, dar si ochii, urechile, gatul si gura.


ETIOPATOGENIE
Prezenta altor afectiuni alergice, precum dermatita, urticarie, astm;
Polen
parul de animale
gandacii
substantele chimice (latexul)
praful din casa Acarienii sunt gunoierii resturilor tegumentare umane.

COMPLICATII

Rinita alergica va poate afecta calitatea vietii. Congestionarea si suflarea permanenta a nasului poate cauza disconfort si jena
sociala. Insomnia rezultata, oboseala si iritabilitatea pot afecta de asemenea performanta dvs in munca sau la scoala.
Dar rinita alergica poate spori riscul de a dezvolta stari alergice mai serioase cum este astmul, o boala cronica care apare cand
caile respiratorii principale din plamanii dvs, tuburile bronhice, se inflameaza. Rinita alergica si astmul apar adesea impreuna.\
n lipsa unui tratament medicamentos adecvat, rinita alergic poate produce schimbri asupra vieii sociale i profesionale. Astfel, din cauza
crizelor repetate, se poate perturba programul de somn, ceea ce determin o oboseal accentuat, o capacitate de concentrare sczut i o
predispunere la schimbri brute de comportament. Netratat, rinita se poate transforma n astm. Totodat, crete riscul de apariie al unor
afeciuni precum sinuzita, infecii ale urechii, polipi nazali i pot aprea infecii ale cilor respiratorii. \



PROFILAXIE
Evitarea plimbarilor in aer liber dimineata in perioadele de polenizare a plantelor. Persoanele alegice
ar trebui sa evite iesirile la padure sau in zonele cu vegetatie multa si la orele pranzului, cand
concentratia de polen din aer este mai ridicata decat dimineata si seara. Ploaia curata aerul de
alergeni, iar vantul ii rascoleste de la nivelul pomilor si solului. Concentratia de polen din aer este
mai mare in zilele calde comparativ cu cele mai reci. Polenul se depune pe haine, piele si par. Asadar,
dupa o iesire in aer liber trebuie sa faceti dus si sa indepartati hainele purtate afara;


http://www.biomedcentral.com/1471-2466/6/S1/S4
http://books.google.ro/books?id=ehuYVX2-
hWYC&pg=PA1325&lpg=PA1325&dq=asthma+and+rhinitis+DD&source=bl&ots=8eGpRGs2WK&sig=
ewF7XMpnaIojvCDbRns7ACbgEX4&hl=ro&sa=X&ei=PO9RVM_mMILcaO2kgqgJ&ved=0CFkQ6AEwBQ
#v=onepage&q=asthma%20and%20rhinitis%20DD&f=false

file:///C:/Users/Administrator/My%20Documents/Downloads/Documents/1939-4551-5-S3-S210.pdf
https://www.mja.com.au/journal/2006/185/10/6-rhinitis-and-asthma-united-airway-disease























Rhinitis
Rhinitis is defined as inflammation of the nasal mucosa characterised by nasal discharge,
blockage, sneezing and itch, with two or more symptoms occurring for more than 1 hour
on most days. It can be further classified as intermittent (symptoms occurring on less
than 4 days out of 7 or for less than 4 weeks per year) or persistent (symptoms
occurring on at least 4 days out of 7 or for more than 4 weeks per year).
Severity:
Mild: normal sleep and no impairment of daily activities, sport, leisure, work or
school; no troublesome symptoms.
Moderate to severe: one or more of (a) abnormal sleep; (b) impairment of daily
activities, sport or leisure; (c) problems caused at work or school; and (d)
troublesome symptoms.
Asthma
Asthma is a chronic inflammatory disorder of the airway in which many cells and cellular
elements play a role in particular, mast cells, eosinophils, T lymphocytes,
macrophages, neutrophils and epithelial cells. In susceptible individuals, this
inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and
coughing, especially at night or in the early morning. These episodes are usually
associated with widespread but variable airflow obstruction that is often reversible,
either spontaneously or with treatment. The inflammation also causes an associated
increase in existing bronchial hyper-responsiveness to a variety of stimuli.
Severity:
Mild: occasional symptoms, but no nocturnal or early morning symptoms; use of
short-acting -agonists less than twice a week; no previous hospital admission or life-
threatening attack; lung function: FEV1 > 80% of predicted value, morning PFR
> 90% of recent best.
Moderate: symptoms most days, but nocturnal and early morning symptoms less
than once weekly; usually no previous hospital admission or life-threatening attack;
lung function: FEV1 60%80% of predicted value, morning PFR 80%90% of recent
best.
Severe: daily symptoms, with nocturnal and early morning symptoms more than
once weekly; usually previous hospital admissions and/or previous life-threatening
attack; lung function: FEV1 < 60% of predicted value, morning PFR < 80% of recent
best.



VEGETATIILE ADENOIDIENE

Amigdala faringiana Luschka este o masa de tesut limfatic ce captuseste peretele
posterior al rinofaringelui. Ea se afla la intersectia cailor nazale cu cavitatea
faringiana. La nastere aceasta amigdala are dimensiuni de 2-3 mm .

Orice rinita banala sau o afectiune virala a regiunii nazofaringiene poate duce la
inflamatia acuta a acestei amigdale. In cazul infectiilor rinosinusogene sau
rinofaringiene repetate, tratate incorect sau netratate la timp, va avea loc
hipertrofierea (marirea in volum ) a amigdalei faringiene, patologie care poarta
denumirea de adenoidita cronica sau vegetatii adenoida.

In aceste situatii dimensiunile amigdalei faringiene pot sa ajunga la 4-6 mm,
acoperind partial cele doua orificii nazale prin care aerul ajunge din nas in cavitatea
bucala si de aici in caile respiratorii inferioare(bronhii si plamani).






Vegetatiile adenoide sunt mai frecvente la copii cu varsta cuprinsa intre 3-7 ani, dar
pot sa apara si dupa pubertate, cand in mod normal regreseaza (se micsoreaza in
dimensiuni).

Un rol important in aparitia vegetatiilor adenoide il au infectiile repetate
rinofaringiene, deficientele alimentare (hrana necalitativa, avitaminozele ) si
conditiile nefavorabile de mediu (frig, umiditate).

Afectiunea se manifesta prin sindromul de obstructie a foselor nazale: respiratia
nazala este ingreunata, mai ales in timpul eforturilor fizice, somnul este agitat, cu
respiratie preponderant orofaringiana, copilul tine permanent gura deschisa, nu-si
poate sufla nasul mereu infundat.

La copil apare faciesul adenoidian" : fata palida, gura intredeschisa, expresia de
surmenaj a fetei. Copilul este apatic, are dureri de cap si obtine rezultate insuficiente
la scoala.

In caz de vegetatii adenoide apare, de obicei, o hipoacuzie de transmisie (scaderea
moderata a auzului) deoarece amigdala faringiana marita in volum acopera orificiul
nazal al tubei auditive care face legatura dintre nas si ureche.

Daca copilul prezinta aceste simptome, este necesara consultatia unui medic
specialist ORL. El va pune un diagnostic corect si va recomanda tratamentul
corespunzator.

Tratamentul vegetatiilor adenoide este profilactic si chirurgical. Primul se
realizeaza printr-o asistenta medicala buna si asigurarea unor conditii de viata
satisfacatoare.



AMIDALELE
Cnd se scot amigdalele Amigdalele filtreaz bacteriile i alte microorganisme pentru a preveni infectarea organismului. n anumite condiii ns, nu mai fac fa infeciilor,
se nroesc i se umfl, ducnd la amigdalit. Tratamentul medicamentos al amigdalitei vizeaz administrarea de antibiotice timp de zece zile. ns amigdalita recurent
necesit un tratament prelungit, modalitate prin care se poate evita de multe ori intervenia chirurgical de excizie a amigdalelor amigdalectomie). Aceasta este indicat n
caz de mrire n volum a amigdalelor, care afecteaz respiraia, d complicaii cardiopulmonare i/sau dificulti la nghiit, dar i n cazul prezenei unui abces
periamigdalian la care tratamentul medicamentos nu a dat rezultate.

Citeste mai mult: adevarul.ro/sanatate/medicina/afectiuni--sfera-orl-1_50ae40d77c42d5a6639b164b/index.html
Amigdalectomia este o interventie invaziva care necesita anestezie si prezinta riscul
hemoragiei locale , atat in timpul operatiei,cat si post-operator. Lunile cele mai favorabile
pentru interventie chirurgicala sunt: mai-iunie, septembrie-octombrie. La copii, varsta
optima pentru operatie este de 4-5 ani, cand pericolul de hemoragie este minim. Necesitatea
tratamentului chirurgical trebuie stabilita cu mare responsabilitate deoarece exista o
tendinta actuala de exagerare in practicarea acestei interventii chirurgicale.

http://www.sfatulmedicului.ro/amigdalita




BIBLIOGRAFIE
1. Meneghetti A, Upper Respiratory Tract Infection, Dec 2007, http://emedicine.medscape. com
2. Seaton A., Seaton D., Leitch A.G., Acute Infections of the Upper Respiratory Tract, Trachea and
Bronchi, Crofton and DouglasaS Respiratory Diseases, Blacwell Scientific Publications, 1989, 270-285
3. Woodwell DA, Cherry DK. Advance Data from Vital and Health Statistics. In: National Ambulatory
Medical Care Survey: 2002 Summary. No. 346. Hyattsville, Md: National Center for Health Statistics;
August 2004
4. Principles of appropriate antibiotic use for acute pharyngitis in adults: Background. Ann Intern Med.
134: 2001; 509-517.
5. Treatment of rhinosinusitis in the outpatient setting. Am J Med. 118: 2005; 45-50.
6. Management of acute bronchitis in healthy adults. Infect Dis Clin N Am. 18: 2004; 919-937.
7. National Center for Infectious Diseases. Division of Bacterial and Mycotic Diseases. Epstein-Barr virus
and infectious mononucleosis. Centers for Disease Control and Prevention, www.cdc.gov/
ncidod/ebv.htm July , 2006.
8. Mortality associated with influenza and respiratory syncytial virus in the United States. JAMA. 289:
2003; 179-186.
9. Mossad S., Upper Respiratory Tract Infections, http:// www.clevelandclinicmeded.com
10. The economic burden of non-influenza-related viral respiratory tract infection in the United States.
Arch Intern Med. 163: 2003; 487-494.
11. Fagnan LJ. Acute sinusitis: a cost-effective approach to diagnosis and treatment. Am Fam Physician.
Nov 15 1998; 58(8):1795-802, 805-6. sMedlinet
12. Centers for Disease Control and Prevention. Nonspecific upper respiratory tract infection. Centers for
Disease Control and Prevention. Available at www.cdc.gov/drugresistance/
community/files/ads/nurti.htm April 5, 2006.
13. Development of a predictive index for picornavirus infections. Clin Infect Dis. 36: 2003; 253-258.













ASTM SI RINITA
Similarities and Differences Between Nasal and Bronchial Inflammation
In patients with rhinitis or asthma, the inflammatory infiltrate is similar, with the same mediators, T-helper (Th) 2
lymphocyte derived cytokines, and adhesion molecules.
19
Nevertheless, the extent of inflammation may vary. In
patients with moderate to severe asthma, eosinophilic infiltration is more pronounced in the bronchi than in the nose,
whereas patients with mild asthma have a similar degree of inflammation at both sites.
20
As mentioned earlier, nasal
eosinophilic inflammation is present in asthmatic patients with or without nasal symptoms,
7
but airway remodeling
seems to be less extensive in the nasal mucosa than in the bronchial mucosa. Patients with asthma have a thicker
basement membrane, smooth muscle hypertrophy, and greater epithelial desquamation, whereas the nasal epithelium
of those with rhinitis alone is less damaged.
21

Nasal Inflammation and Bronchial Response
A number of clinical and experimental studies have investigated the link between rhinitis and the presence of
inflammation and functional disorders in the lower airway. Bronchial hyperreactivity and changes in lung function
occurred in patients with allergenic rhinitis after nasal provocation with allergen.
22-25
Other studies have described the
presence of systemic allergic inflammation after nasal provocation in both animal models and in humans. McCusker et
al
26
used ovalbumin for nasal provocation in a murine model, and showed that inflammatory changes, as indicated by
elevated interleukin 5 and eosinophils in bronchoalveolar lavage, occurred in both the nasal and bronchial mucosae.
Braunstahl et al
27
studied the expression of adhesion molecules in nasal and bronchial biopsies taken before and 24
hours after nasal provocation with allergen in patients with seasonal rhinitis. They found a significant increase in
eosinophils in the epithelium and the nasal lamina propria, and in the bronchial epithelium at 24 hours. This increase
was directly related to expression of adhesion molecules. They also detected a significant increase in the number of
eosinophils and concentration of interleukin 5 in blood samples obtained at 24 hours. Beeh et al
28
studied
inflammatory markers in induced sputum and in plasma before and 24 hours after nasal provocation with pollen
extracts in allergic patients outside the season for allergies. Inflammatory markers (eosinophil cationic protein and
intercellular adhesion molecules) were found to be elevated in sputum. This increase was related to an increase in
interleukin 5 in plasma.
Other studies have shown bronchial inflammatory response in nonasthmatic patients with allergic rhinitis after natural
exposure to pollen and after repeated provocation at low doses.
29-32

Bronchial Inflammation and Nasal Response
Braunstahl et al
33,34
have also taken the opposite approach and studied nasal inflammatory response after segmental
bronchial provocation with allergens in nonasthmatic patients allergic to pollen. They found that this procedure
induced nasal and bronchial symptoms, and increased peripheral blood eosinophils and eosinophilic and basophilic
infiltration of the nasal and bronchial mucosae.
Response to Exercise (Figure 4)

Figure 4. Exercise-induced nasal dilatation. Nasal geometry (volume and cross-sectional area) of the patient
was assessed by acoustic rhinometry (A), and computed tomographic x-ray assessment (B), before exercise
testing (trace 1 and image 1) and after exercise testing (trace 2 and image 2). Note the increase in nasal
volume (trace 2) in Panel A and the decrease in the size of vascular structures of the nose in Panel B.
The nose and bronchi respond differently to exercise. Forced expiratory volume in 1 second decreases in 40% to 90%
of asthmatic patients during exercise testing. Some authors suggest that this bronchoconstriction may be mediated by
mast cell degranulation resulting from the higher osmolarity of the fluid coating the airways.
35

Unlike the bronchi, the nose is always dilated after exercise. Several studies done both in healthy subjects and in
those with a range of respiratory diseases (nasal septal deviation, rhinitis, asthma, cystic fibrosis)
36-41
have shown that
exercise lowers nasal resistance and increases nasal volume. These changes occur immediately after exercise and
basal values are usually recovered within 30 or 40 minutes.
36-39
Nasal response to exercise is thought to occur
through decreased volume of the venous sinuses as a result of vasoconstriction, which in turn is due to an increase in
sympathetic activity. This hypothesis is supported by the fact that stellate ganglion block and local application of
phentolamine have been shown to impede nasal vasoconstrictive response during exercise.
36

In asthmatic patients, bronchoconstriction after exercise is much more pronounced when subjects breathe through the
mouth (probably because of the lack of conditioning of inspired air),
14
whereas nasal dilatation occurs regardless of
whether the patients are breathing through the nose or through the mouth,
13
and even when their noses are blocked.
Effect of Chronic Rhinosinusitis and Polyposis on Asthma Severity
The main pathologic findings of chronic sinusitis are goblet cell hyperplasia, presence of subepithelial edema, and
infiltration by mononuclear cells and activated eosinophils.
42,43
Eosinophil infiltration is more extensive in patients with
polyps (50% of the inflammatory infiltrate) than in those with no polyposis (2% of the inflammatory infiltrate).
44
This
type of inflammatory infiltrate is similar to that found in asthmatic patients.
The counts of other inflammatory cells such as, for example, mast cells, lymphocytes, macrophages, and, to a lesser
extent, neutrophils, are also increased, and this contributes to the release of proinflammatory mediators, cytokines,
and growth factors.
Some studies suggest that asthma is more prevalent and severe in those with severe rhinosinositis.
2
Bresciani et
al
45
compared the incidence of rhinosinusitis in patients with mild to moderate asthma with that in patients with severe
corticosteroid-dependent asthma. The proportion of patients with nasal symptoms was similar in both groups, whereas
abnormalities of the paranasal sinuses detected by computed tomography were present in all patients with severe
asthma and in 88% of those with mild to moderate asthma. Scores on clinical and tomographic scales were higher in
those with severe asthma.
Acetylsalicylic acid intolerance, which is present in 10% of asthmatic patients
46
and which possibly affects up to 40%
of patients with concurrent chronic rhinosinusitis or nasal polyposis,
47
is another important issue related to disease of
the paranasal sinuses, and therefore, to asthma severity. Asthmatic patients with chronic rhinosinusitis or nasal
polyposis, and acetylsalicylic acid intolerance are said to suffer from the Widal or acetylsalicylic acid triad and, in such
cases, asthma is usually hard to control.