سرماخوردگي Nasopharyngitis اهميت 1-شايعترين عفونت بچه ها 2-...

سرماخوردسرماخوردگي گي

NasopharyngitisNasopharyngitis

اهميتاهميت

ها- 1 بچه عفونت شايعترين

فراوانيعوارض- 2

به- 3 زمان ،سينوسها Nasopharyn Xگسترشهمگوشمياني ،

اتيولوژي

بيشاز- ) 1 ( 150ويروسها بخصوص Rhinoنوعyirous

گروه- 2 بخصوصاسترپتوكوك اوليه باكتريهايA باكتريها ساير

My coplasma. P , C.Diphtheriaشامل :

Neisseria.M , Neisseria. G

ميشوند- 3 ظاهر ثانويه بصورت باكتريهائيكهاستافيلوكوك H.Influengaمانند ، پنوموكوك

، اتيت باعثسينوزيت غالبا; كه طالئي . پنومونيميشوند و آدنيت ، استوئيديت

Inoculation by virus

Invqsion of epithelium of nasopharynx, sinuses, and upper

respiratory tract

Release of inflammatory mediators in nasal secretions

Cellular damage of nasopharynx

Cholinergic stimulation

Increased meucus production

Increased vascular permeability

Mucosal edema

Nasal stufiness Rhinorrhea Postnasal

drip Cough

Sore

throat

Bronchial constriction

اپيدميولژي

از- 1 سرايت دوره ويروسي نوع درتا ساعتقبل عالئم 1-2چند از بعد روز

. باشد مي

باز- 2 بخصوصزمان فصولسرد در. است تر مدارسشايع شدن

سال- 3 در بچه مي 5-8هر مبتال بارزمان ترين شايع و اول 2شوند سال

. است عمر

4 -Malnutrition هم و باعثشيوع هم . افزايشعوارضميشود

پاتولژي

زير- 1 ناحيه در عروق گشادي و ادم ابتدامخاط

سپس- 2 و مونونوكلئر انفيلتراسيون بعدمحل در نوكلئر پولي

ها- 3 مژه عملي و تغييراتساختماني . ميشود آنها كار اختالل باعث

تليان- 4 اپي سلولهاي شدن كندهسطحي

ابتدا- 5 كه موكوسي افزايشترشحات. چركيميشود غليظو بعد رقيق

عالئم باليني

3زير ماه

تا 3 ماه

سال 3

باالي 3

سال

از- 1 شديتر شيرخواران در بيماري شدتبزرگترها

تب- 2 بدون سرماخوردگي عالئم

من- 3 با سينوزيت بجز عوارضچركي . نسبتعكسدارد

1. باشد- مي عطسه و بيقراري تب، با شروع

مي- 2 خوردن شير مانع كه بيني گرفتگي و ترشحشود.

گوش- 3 پرده پشت مايع گاهي و قرمزي

بين- 4 و 3تبشديد تا 3ماه ساعت چند و 3سال. كشد مي طول روز

و- 1 بيني سوزشدر ، خشكي بيماري شروع در. دارد وجود حلق

درد- 2 احساسسرما، ، ساعتعطسه چند پسازبيني ترشح عضالني

تبخفيف- 3 و اشتهائي بي ، بيحالي ، سردرد

حاد- 4 دوره سرفه، بينيو ترشح 2-4غليظشدن. است روز

تشخيص

افتراقي

عوارض

1 -، هپاتيت اطفال، فلج ، سرفه سياه سرخك، شروعاست بيماري مسبب اريون

آترزي- 2 و بيني خارجي جسم ديفتري، با ترشج دواماول هفته در كوان

آلرژيك- 3 رنيت

جوانان- 4 در اعتياد

1 : كه- اتيتگوشمياني ، سينوزيت ميكربييا لوزه در و سلوليت استوئيديت، است، شايعترين

چشم دور

2 : پنوموني L.T.Bويروسي- ، برونشيت

بعلت- 3 آسم Reactive Airwayعالمتشبيه

پيشگيري

درمان

ندارد- 1 وجود اي وسيله هيچ

ايزوالسيون- 2 توان نمي بيماري علتشيوع بهدر بجز كرد برقرار

بهتر زياد عارضه بعلت كه كوچك شيرخواران. شوند ايزوله است

ندارد- 1 وجود اختصاصي درمان

بر- 2 تب و مسكن

بيني- 3 براي بخور و فيزيولوژي سرم

بيني- )4 ( 4-5قطره روز

بزرگ- 5 هاي بچه براي خوراكي احتقان ضد

اسيدوز- 6 براي عسل مانند شيرين مواد دادن

TABLE 2. Classic features: acute streptococcal TABLE 2. Classic features: acute streptococcal pharyngitispharyngitis

Sudden onset Sudden onset Age 5-11 yearsAge 5-11 yearsLate winter- early spring Late winter- early spring HeadacheHeadacheFever Fever Sore throat Sore throat Abdominal pain, nausea and vomitingAbdominal pain, nausea and vomitingTender, enlarged anterior cervical nodes Tender, enlarged anterior cervical nodes Pharyngeal erythema and exudation Pharyngeal erythema and exudation Palatal petechiae Palatal petechiae Tonsillar hypertrophy Tonsillar hypertrophy Lack of cough, rhinorrhea, hoarsenessLack of cough, rhinorrhea, hoarseness

TABLE 1. Possible causes of recurrent TABLE 1. Possible causes of recurrent streptococcal pharyngotonsillitisstreptococcal pharyngotonsillitis

Insufficient penicillin V concentration at focus of infection Insufficient penicillin V concentration at focus of infection

Poor patient compliance Poor patient compliance

Poor absorption in the intestinePoor absorption in the intestine

Poor penetration into tonsillar tissue Poor penetration into tonsillar tissue

Duration of treatment period insufficient Duration of treatment period insufficient

Penicillin tolerance Penicillin tolerance

Lowered resistance due to ecologic disturbancesLowered resistance due to ecologic disturbances

Lack of bacterial interference Lack of bacterial interference

Reinfections )“ping-pong” infections(Reinfections )“ping-pong” infections(

Immunologic defectsImmunologic defects

TABLE 1. Streptococcal carrier us. Repeated TABLE 1. Streptococcal carrier us. Repeated episodes of GABHS pharyngitisepisodes of GABHS pharyngitis

Repeated episodes of GABHS pharyngitis Repeated episodes of GABHS pharyngitis Signs and symptoms consistent with GABHS Signs and symptoms consistent with GABHS Seasonal clustering Seasonal clustering Marked clinical response to antibiotics Marked clinical response to antibiotics No GABHS between episodesNo GABHS between episodesASO or ADB response ASO or ADB response Different serotypes of GABHSDifferent serotypes of GABHS

ASO, anti-streptolysin O; ADB, anti-deoxyribonuclease B.ASO, anti-streptolysin O; ADB, anti-deoxyribonuclease B.

TABLE 1. Streptococcal carrier us. Repeated TABLE 1. Streptococcal carrier us. Repeated episodes of GABHS pharyngitisepisodes of GABHS pharyngitis

Streptococcal carrier Streptococcal carrier

Signs and symptoms of viral infection Signs and symptoms of viral infection

Wrong season Wrong season

Little clinical response to antibiotics Little clinical response to antibiotics

GABHS present between episodes GABHS present between episodes

No ASO or ADB response No ASO or ADB response

Same serotype of GABHSSame serotype of GABHS

TABLE 3. Treatment of group A streptococcal TABLE 3. Treatment of group A streptococcal pharyngitispharyngitis

DosageDosage

Penicillin Penicillin 500 mg (800 000 units) in 2 500 mg (800 000 units) in 2 doses for 10 daysdoses for 10 days

Benzathine penicillin G imBenzathine penicillin G im600 000 units (<60 lb); 1 200 600 000 units (<60 lb); 1 200 000 units(>60 lb) 000 units(>60 lb)

Erythromycin estolateErythromycin estolate50 mg/kg in 2-4 doses for 10 50 mg/kg in 2-4 doses for 10 daysdays

Azithromycin (>15 years) Azithromycin (>15 years) 500 mg day 1 and 250 mg for 4 500 mg day 1 and 250 mg for 4 daysdays

CefadroxilCefadroxil30 mg/kg/day in 1 dose for 10 30 mg/kg/day in 1 dose for 10 daysdays

سينوزيتسينوزيت

سينوزيت سينوزيت جفتسينوس جفتسينوس چهار كه Paranasal Paranasal چهار دارد كه وجود دارد وجود

و تشكيلشده تولد بدو در فونتال بجز و همگي تشكيلشده تولد بدو در فونتال بجز همگيعفونتشوند دچار توانند عفونتشوند مي دچار توانند ..مي

از از عبارتند و ، ، Maxillar Maxillar عبارتند خلفي و قدامي و اتموئيد خلفي و قدامي اتموئيد..اسفنوئيداسفنوئيد

عوامل مساعد

كننده سينوزيت

بخصوصرنيت- 1 آلرژي

و- 2 ها مژه اشكال سينوسبعلت درتاژ در اختاللبيني انحراف

مجراي- 3 ostiaانسداد

غلظتموكوس- 4 و افزايشترشح

چركي حاد چركي سينوزيت حاد سينوزيت

عالئم بالين

ي

موضعي- 2تب- 1 ناحيه- 5سردرد- Tenderness 4- 3درد ادم

درد- 2 سر

با- 3 معمولي سرماخوردگي از شديدتر صورتعالئم درچشم دور ادم و صورت درد

بيشاز- 4 سرماخوردگي عالئم روز 10طوالنيشدن

در- 5 ترشحاتچركي بيني Meatusديدن يا

طوالني- 6 سرفه

-a زير ناحيه در اسفنوئيد عفونت درoccipital

-b اتموئيد اسفنوئيد عفونت درچشم باالي قدامي

-c در خلفي اسنفوئيد عفونت دراستوئيد ناحيه

-d maxillar اندامها درد

تشخيص تشخيص

1 -Trans Illumination

زير- 2 كه است .12راديوگرافي مشكل ماه

3 -CT.scan . باشد مي نياز مورد كمتر

تشخيصمي- 4 قطعي راه كشت سينوسو آسپيراسيونپولي. الم بوسيله باشد

ميشود ديده انوزينوفيلها يا نوكلئر

شيوع ميكرب

ي

پنوموكوك- 1

2 -Branhamela cattar Halis

3 -Nonty pable H.Influenza

عوارض

Subduralيا Epiduralآبسه- 1

مننژيت- 2

سينوسكاورموس- 3 ترمبوز

اپتيك- 4 نوريتعصب

اطراف- 5 يا چشم آبسه و سلوليتچشم

استئوميليت- 6

باشد- 1 متفاوت اگر و داده Cegaclarيا Cotriآمپيسيلين. ميشود

و- 2 هيستامين . Dicongestantآنتي نيست مؤثر

جواب- 3 صورتعدم شستشويسينوسدر و رناژ . ميشود عوارضالزم وجود يا بدرمان

درمان

Croup Croup

GroupGroup

اتيولژي

1 -عفوني

2 -مكانيك

ي

آنژيو آلرژيك- : 3 آدمنوروتيك

1 -H.ingluenza 4 -استرپتوكوك

2 -S.Aureus 5 -پنموكوك

3 -C.Diphtheria 6- M.Tubercolosis

1 -باكتريال

ويرال- 2

1 -Para Influenza Type 1,2,3

Herpes- 6آدنوويروسها- 2

مايكوپالسما- 7آنتروويروسها- 3

4 -R.S.Virus 8 -اسپاسموديك الرنژيت

سرخك- 5

خارجي- 1 جسم

اعمال- 2 بدنبالجراحي

و- 3 ها تودهتومورها

انواع Group

ويروسي- 1

اپي- 2گلوتيت

3 -Tracheitis

الرنژيت- 1

الرنژيت- 2اسپاسموديك

3 -L.T.B

پاتوژنيكروپ ويروسي

عفونت- 1

2 -Reactive Aereway

Respiratory failure

Upper aiway obstruction

Increased resistance to airflow

Upset

High negative intrathoracic pressures

Dynamic collapse of upper airway

Figure 16-5. Dynamic demonstration of the vicious cycle in acute upper airway obstructive diseases.

Table 16-4 infectious and noninfectious causes Table 16-4 infectious and noninfectious causes of acute upper airway obstructionof acute upper airway obstruction

InfectiousInfectiousLaryngotracheobronchitLaryngotracheobronchit

is is Epiglottitis Epiglottitis Bacterial tracheitis Bacterial tracheitis Diphtheria Diphtheria Retropharyngeal abscess Retropharyngeal abscess Peritonsillar abscessPeritonsillar abscessNonin’fectiousNonin’fectiousForeign body Foreign body Trauma Trauma Angioneurotic edema Angioneurotic edema Hypocalcemic tetany Hypocalcemic tetany Caustic burns Caustic burns

Table 16-1. Etiologic agents in acute upper Table 16-1. Etiologic agents in acute upper airway infectionsairway infections

Bacterial Bacterial Haemophilus influenzae type B Haemophilus influenzae type B Staphylococcus aureus Staphylococcus aureus Corynebacterium diphtheriae Corynebacterium diphtheriae Group A streptococcus Group A streptococcus Neisseria sp. Neisseria sp. Escherichia coli Escherichia coli Klebsiella sp. Klebsiella sp. Pseudomonas sp.Pseudomonas sp.Chlamydia trachomatis Chlamydia trachomatis

FungalFungal Candida aldicansCandida aldicans

Viral Viral Parainfluenza types 1,2,3Parainfluenza types 1,2,3

Influenza A, BInfluenza A, B

Adenovirus Adenovirus

Respiratory syncytian virus Respiratory syncytian virus

Enterovirus sp.Enterovirus sp.

MeaslesMeasles

Table 16-1. Etiologic agents in acute Table 16-1. Etiologic agents in acute upper airway infectionsupper airway infections

عالئم باليني

1 -خفيف

2 -شديد

استريدوز- 1 خشك، سرفه

باليني- 2 پيشرفتعالئم

ديسپنه- 3

4 -Rctraction تنفسي عضالت

يا- 5 ساعت چند پساز بهبوديروز

بيشتر- 1 شدت با باال عالئم

2 -Drooling – Dysphagia

3 -hypoventilation

بيقراري- 4 و عطشهوا

ضعف- 5 و كاهشتعويضهواعمومي

يا- 6 پريدگي رنگ با همراه شوكسيانوز

درمان

هوا- 1 راه نگهداشتن باز

2 -، مرطوب هواي ، آزاد هواياستفراغ

بوسيله- 3 نفرين اپيNebulaget

كورتن- 4

سرم- 5 مايعاتو

اكسيژن- 6

بخش- 7 آرام داروهاي

ترياك- 8 تركيبات

9 -Intubation

اثركورتناثركورتن

پيش گيري

غشاء- 1 Lysosomeاستحكام

كاپيلوها Permeabilityكاهش- 2

محل- 3 به سلولهايسفيد كاهشانتقالديده صدمه

مفيد- 4 سلولهاي كاهشهضم

T.cellsكاهشفعاليت- 5

كاهشتب- 6

به كمكبهبودي

بهبودي- 1 باعث روز چند تا ساعت چند بينميشود

2. آماس- مولد فعاليتعوامل قطع

بطريق- 3 بهبودي سرعت به سپسكمكزير:

oَ(a آمينه اسيدهاي انتقال بوسيله شايد

(b چربي و قندي مواد انتقال بوسيله شايد

(c كاتابوليسم اثر شايد

Otitis media Otitis media

TABLE 1. Classification of otitis mediaTABLE 1. Classification of otitis media Suppurative Suppurative

Acute suppurative otitis media Acute suppurative otitis media Chronic suppurative otitis mediaChronic suppurative otitis media

Nonsuppurative )otitis media with effusion( Nonsuppurative )otitis media with effusion( Acute otitis media with effusionAcute otitis media with effusionChronic otitis media with effusion )“glue ear”( Chronic otitis media with effusion )“glue ear”(

Specific Specific Tuberculous otitis media Tuberculous otitis media Syphilitic Syphilitic

Adhesive Adhesive Adhesive otitis media Adhesive otitis media Tympanosclerosis Tympanosclerosis

TABLE 4. Symptoms of 363 children TABLE 4. Symptoms of 363 children with acute otitis mediawith acute otitis media

%%

Fever Fever 5555

EaracheEarache4747

Irritability Irritability 5656

Feeding difficultiesFeeding difficulties5050

RestlessnessRestlessness6464

RhinitisRhinitis9090

CoughCough7878

oّFrom Arola 37

TABLE 5. Appearance of the tympanic membrane in 528 TABLE 5. Appearance of the tympanic membrane in 528 inflamed ears of 636 children with acute otitis mediainflamed ears of 636 children with acute otitis media

%%

Position Position

Full or bulgingFull or bulging8989

Normal Normal 1111

ColorColor

RedRed4646

CloudyCloudy5252

YellowYellow2424

InjectedInjected5757

Fluid levelFluid level3333

Bullous myringitisBullous myringitis66

From Arola et al.4

TABLE 1. Acute otitis media in relation to feeding pattern TABLE 1. Acute otitis media in relation to feeding pattern Only infants with information on feeding pattern and AOM were Only infants with information on feeding pattern and AOM were

included in this analysisincluded in this analysis . .

AgeAge

(Months)(Months)

FeedingFeeding

PatternPattern

Total No.Total No.

of Infantsof Infants

AOMAOM

1-31-3Breast-fedBreast-fed3043042(1)2(1)

Mixed- fedMixed- fed60603(5)3(5)††

Weaned Weaned 36362(6)2(6)


Mixed-fedMixed-fed22322315(7)15(7)

WeanedWeaned13113118(14)18(14)††


Mixed-fedMixed-fed70709(13)9(13)

WeanedWeaned30630660(20)60(20)††

Numbers in parentheses, Percent.

†P<0.05 compared with breast- fed infants.

TABLE 2. Increase in resistance of Streptococcus TABLE 2. Increase in resistance of Streptococcus Pneumoniae )MIC>0.1 m/liter( in the paris area Pneumoniae )MIC>0.1 m/liter( in the paris area

between 1988 and 1993between 1988 and 1993

YearYearResistance Resistance

(%)(%)

198819886.76.7

198919898.58.5

1990199014.814.8

1991199120.320.3

1992199234.034.0

1993199358.058.0

Submitted to the Interscience Conference on Antimicrobial Agents and Chemotherapy, 1993. Reference P. Gehanno3

MIC, Minimum inhibitory concentration

TABLTABLE 2. Spontaneous cure rates in E 2. Spontaneous cure rates in mild-to-moderate acute otitis mediamild-to-moderate acute otitis media

ReferenceReferencePatientsPatients

(N)(N)

Patients Age Patients Age (Years) (Years)

Spontaneous Cure Spontaneous Cure Rate (%)Rate (%)

Halsted et al.,1968Halsted et al.,1968393927270-30-38181

Laxdal et al., 1970Laxdal et al., 1970404048480-140-144646

Howie and Ploussard, 1972Howie and Ploussard, 197229291161160-2.50-2.51414

Mygrind et al., 1981Mygrind et al., 1981313177771-101-106969

Van Buchem, 1981Van Buchem, 1981303076762-122-127373

Thalen et al., 1986Thalen et al., 198641411581582-152-158888

Engelhard et al., 1989Engelhard et al., 1989333335350.3-10.3-12323

TABLTABLE 2. Spontaneous cure rates in E 2. Spontaneous cure rates in mild-to-moderate acute otitis media mild-to-moderate acute otitis media

ContCont . .

ReferenceReferencePatientsPatients

(N)(N)

Patients Age Patients Age (Years) (Years)

Spontaneous Cure Spontaneous Cure Rate (%)Rate (%)

Burke et al., 1991Burke et al., 199134341181183-103-108686

Appelman et al., 1991Appelman et al., 1991353554540.5-120.5-128181

Kaleida et al., 1991Kaleida et al., 199142422732730.5-120.5-126363††

86860.5-120.5-125252‡‡

Asymptomatic with normal otoscopic results at 10 to 14 days after diagnosis.

† Mild.

‡ Moderate.

TABLE 7. Antimicrobials for treatment of TABLE 7. Antimicrobials for treatment of acute otitis mediaacute otitis media

TABLE 1. Indications for alternative TABLE 1. Indications for alternative antimicrobial agents for acute otitis mediaantimicrobial agents for acute otitis media

Initial treatment failure Initial treatment failure

Persistent infection at 10 to 14 daysPersistent infection at 10 to 14 days

Culture-positive susceptible organism Culture-positive susceptible organism

Prior treatment failures Prior treatment failures

Compliance features Compliance features

High incidence of resistant organisms in High incidence of resistant organisms in communitycommunity

TABLE 1. Factors that may be relevant in identifying TABLE 1. Factors that may be relevant in identifying patients who may progress to recurrent otitis mediapatients who may progress to recurrent otitis media

The host The host Male gender Male gender Ethnic origin )greater incidence in Native Americans, Alaskan and Ethnic origin )greater incidence in Native Americans, Alaskan and

Canadian Eskimos(Canadian Eskimos(Sibling or parental history of severe or recurrent ear infection Sibling or parental history of severe or recurrent ear infection Early age for initial episode of acute otitis media Early age for initial episode of acute otitis media Not breast- fedNot breast- fedIn group day care In group day care Altered host defenses: anatomical, physiologic or immunologic Altered host defenses: anatomical, physiologic or immunologic Exposure to environmental antigens )allergy( or pollutants )smoke( Exposure to environmental antigens )allergy( or pollutants )smoke( Abnormal multifrequency hearing lossAbnormal multifrequency hearing lossBilateral infection Bilateral infection Presence of upper respitatory tract infections )90% have cough(Presence of upper respitatory tract infections )90% have cough(

TABLE 1. Factors that may be relevant in identifying TABLE 1. Factors that may be relevant in identifying patients who may progress to recurrent otitis mediapatients who may progress to recurrent otitis media

Behavioral changes recognized by carersBehavioral changes recognized by carersThe organismThe organismAntibiotic- resistant strains )patient or local epidemiologic data(Antibiotic- resistant strains )patient or local epidemiologic data(Beta-lactamase-producing strains Beta-lactamase-producing strains Streptococcus pneumoniae persistenceStreptococcus pneumoniae persistenceViral etiology alone )5-10%(Viral etiology alone )5-10%(Coinfection with virusesCoinfection with virusesInfection severity Infection severity The antibiotic The antibiotic Activity against pathogen )probability of incorrect empiric dosage( Activity against pathogen )probability of incorrect empiric dosage( ? Altered distribution of antibiotic in some infections ? Altered distribution of antibiotic in some infections Multiple antibotic coursesMultiple antibotic coursesNoncompliance Noncompliance Prophylactic antimicrobialsProphylactic antimicrobials

TABLE 2. Complications of otitis mediaTABLE 2. Complications of otitis media

Intratemporal Intratemporal Mastoiditis Mastoiditis Petrositis Petrositis Facial palsy Facial palsy Labyrinthitis Labyrinthitis Intractanial Intractanial Extradural abscessExtradural abscessSubdural abscessSubdural abscessSigmoid sinus thrombophlebitis Sigmoid sinus thrombophlebitis Meningitis Meningitis Cerebral abscess Cerebral abscess Otitis hydrocephalusOtitis hydrocephalus

آسم آسم

What is known about asthmaWhat is known about asthma ? ?

Unfortunately Unfortunately Asthma is one of the most common chronic Asthma is one of the most common chronic

diseases worldwide, the prevalence of diseases worldwide, the prevalence of asthma symptoms in children varies from 1 asthma symptoms in children varies from 1 to more than 30 percent in different to more than 30 percent in different population and is increasing in most population and is increasing in most countries, especially among young children countries, especially among young children

What is known about asthma? What is known about asthma? )cont.()cont.(

FortunatelyFortunately Asthma can be effectively treated and most Asthma can be effectively treated and most

patients can achieve good control of their patients can achieve good control of their disease. When asthma is under control disease. When asthma is under control children can. children can.


Avoid troublesome symptoms night and day Avoid troublesome symptoms night and day Use little or no reliever medication Use little or no reliever medication Have productive , physically active lives Have productive , physically active lives Have )near ( normal lung function Have )near ( normal lung function Avoid seious attacks Avoid seious attacks


Asthma causes recurring episodes of Asthma causes recurring episodes of wheezing, wheezing, breathlessness, chest tihghtnessbreathlessness, chest tihghtness, and , and coughingcoughing, , particularly at night or in the early morning. particularly at night or in the early morning.

Asthma is a Asthma is a chronic inflammatory disorderchronic inflammatory disorder of the of the airways. Chronically inflamed airways are airways. Chronically inflamed airways are hyperresponsivehyperresponsive, they become obstructed and , they become obstructed and airflow is limited )by bronchoconstriction , mucus airflow is limited )by bronchoconstriction , mucus plugs, and increased inflammation( when airways plugs, and increased inflammation( when airways are exposed to various risk factors are exposed to various risk factors


Common Common risk factorsrisk factors for asthma symptoms for asthma symptoms include exposure to allergens )such as those include exposure to allergens )such as those from house dust mites, animals with fur, from house dust mites, animals with fur, cockroaches , pollens, and molds( , cockroaches , pollens, and molds( , occupational irritants tobacco smoke occupational irritants tobacco smoke respiratory )viral (infections, exercise, respiratory )viral (infections, exercise, strong emotional expressions , chemical strong emotional expressions , chemical irritants and drugs )such as aspirin and irritants and drugs )such as aspirin and beta blockers(. beta blockers(.


A A stepwise approachstepwise approach to pharmacologic to pharmacologic treatment to achieve and maintain control treatment to achieve and maintain control of asthma should take into account the of asthma should take into account the safety of treatment , potential for adverse safety of treatment , potential for adverse effects , and the cost of treatment required effects , and the cost of treatment required to achieve control. to achieve control.


Asthma Asthma attacksattacks )or exacerbations ( are episodic, but )or exacerbations ( are episodic, but airway inflammation is chronically present. airway inflammation is chronically present.

For many patients ,For many patients , controller controller medication must be medication must be taken daily to prevent symptoms, improve lung taken daily to prevent symptoms, improve lung function , and prevent attacks. function , and prevent attacks. RelieverReliever medications medications may occasionally be required to treat acute may occasionally be required to treat acute symptoms such as wheezing, chest tightness , and symptoms such as wheezing, chest tightness , and cough. cough.

To reach and maintain asthma control requires the To reach and maintain asthma control requires the development of a development of a partnershippartnership between the person between the person with asthma and his or her health care team. with asthma and his or her health care team.

Asthma is not cause for sham. Olympic athletes, Asthma is not cause for sham. Olympic athletes, famous leaders, other celebrities , and ordinary famous leaders, other celebrities , and ordinary people live people live successfulsuccessful lives with asthma. lives with asthma.

Triggers

Host

Inflamation + Spasm

اتيولوژي؟اتيولوژي؟

آنتي ژن

گياهي- 1

(MITE)انگلي- 2

(MOLD)قارچي- 3

ويروسي- 4

( NO2- SO2)محيطي- 5

شيميايي- 6 مواد(IRITANT)

TABLE 22-2. Conditions of patients that may TABLE 22-2. Conditions of patients that may demonstrate bronchial hyperresponsivenessdemonstrate bronchial hyperresponsiveness

After a viral upper respiratory infection for 6 wk After a viral upper respiratory infection for 6 wk in nonasthma patients in nonasthma patients

In absence of changes in FEVIn absence of changes in FEV11 in patients with in patients with

asthma asthma

Chronic bronchitis Chronic bronchitis

Left ventricular failure Left ventricular failure

Allergic rhinitis in absence of asthmaAllergic rhinitis in absence of asthma

Apparently normal patients Apparently normal patients

TABLE 22-2. Conditions of patients that may TABLE 22-2. Conditions of patients that may demonstrate bronchial hyperresponsiveness demonstrate bronchial hyperresponsiveness

)Cont.()Cont.(

Exposure to irritants Exposure to irritants

Smoking Smoking

In some normal infants In some normal infants

First degree relatives of asthma patients First degree relatives of asthma patients

Sarcoidosis Sarcoidosis

FEVFEV11. forced expiratory volume in 1 second.. forced expiratory volume in 1 second.

TABLE 1. Potential mechanisms in viral TABLE 1. Potential mechanisms in viral indced lower airway obstructionindced lower airway obstruction

Increased Thickness of Increased Thickness of the Airway Wallthe Airway Wall

Increased Luminal Increased Luminal ContentContent

Airway Smooth Nuscle Airway Smooth Nuscle ContractionContraction

Vascular engorgementVascular engorgementIncreased secretions Increased secretions Autonomic nervous Autonomic nervous system dysfunction system dysfunction

Cellular infiltration Cellular infiltration Rheologic changes in Rheologic changes in mucusmucus

Chemical mediator release Chemical mediator release from recruited cellsfrom recruited cells

Mucosal and Mucosal and submucosal edemasubmucosal edema

Epithelial sloughingEpithelial sloughingImpairment of epithelial Impairment of epithelial mediated muscle mediated muscle relaxationrelaxation

Impaired ciliokinesisImpaired ciliokinesisAltered activation Altered activation characteristics of airway characteristics of airway smooth musclesmooth muscle

Inoculation by virus

Invqsion of epithelium of nasopharynx, sinuses, and upper

respiratory tract

Release of inflammatory mediators in nasal secretions

Cellular damage of nasopharynx

Cholinergic stimulation

Increased meucus production

Increased vascular permeability

Mucosal edema

Nasal stufiness Rhinorrhea Postnasal

drip Cough

Sore

throat

Bronchial constriction

AL age 7 years, the groups were set up as followsAL age 7 years, the groups were set up as follows : :

Control Control Children who had never wheezedChildren who had never wheezed

GroupGroup(n=106)(n=106)

Mild wheezy Mild wheezy

Bronchitis Bronchitis

Group: Group:

Children with <5 episodes of Children with <5 episodes of wheezing. Always associated with wheezing. Always associated with bronchitis or apparent respiratory bronchitis or apparent respiratory infection infection

(n=75)(n=75)

Wheezy Wheezy

Bronchitis Bronchitis

Group:Group:

Children with >5 episodes of Children with >5 episodes of wheezing with bronchitis associated wheezing with bronchitis associated with an apparent respiratory infection with an apparent respiratory infection

(n=107)(n=107)

Asthma Asthma

Group: Group:

Children with wheezing unassociated Children with wheezing unassociated with respiratory infectionwith respiratory infection

(n=113)(n=113)

TABLE 137-3 Factors Associated with Risk of TABLE 137-3 Factors Associated with Risk of severe status Asthmaticussevere status Asthmaticus

History History Chronic steroid-dependent asthma Chronic steroid-dependent asthma Prior intensive care admissionPrior intensive care admissionPrior mechanical sentilation for asthma Prior mechanical sentilation for asthma Recurrent visits to emergency unit in past 48 hrRecurrent visits to emergency unit in past 48 hrSudden onset of severe respiratory distressSudden onset of severe respiratory distressPoor compliance with therapy Poor compliance with therapy Poor recognition by patient, family, or physician, of Poor recognition by patient, family, or physician, of

severity of attackseverity of attackFanily dysfunction , crisis Fanily dysfunction , crisis Respiratory arrest Respiratory arrest Hypoxic seizures, encephalopathyHypoxic seizures, encephalopathy

TABLE 137-3 Factors Associated with Risk of TABLE 137-3 Factors Associated with Risk of severe status maticus )Cont.(severe status maticus )Cont.(

Physical Examination Physical Examination Pulsus paradoxus>20 mm HgPulsus paradoxus>20 mm HgHypotension, tachycardia, tachypneaHypotension, tachycardia, tachypneaCyanosis Cyanosis 1-2 word dyspnea1-2 word dyspneaLethargy Lethargy Agitation Agitation Sternocleidomastoid, intercostal , suprasternal Sternocleidomastoid, intercostal , suprasternal

retractions retractions Poor air exchange )e.g., quiet chest with severe Poor air exchange )e.g., quiet chest with severe

distress( distress(


Laboratory testsLaboratory testsHypercarbia Hypercarbia

Hypoxia with supplemental oxygen Hypoxia with supplemental oxygen

FFVFFV11<30% expected: no improvement 1 hr after <30% expected: no improvement 1 hr after

aerosol therapy aerosol therapy

Chest x-ray )pneumothorax, pneumonediastinum(Chest x-ray )pneumothorax, pneumonediastinum(


Therapy Therapy Over –reliance on aerosol, inhaler therapy Over –reliance on aerosol, inhaler therapy

Delayed use of systemic corticosteroids Delayed use of systemic corticosteroids

Sedation Sedation

Delayed admission to hospital or intensive care Delayed admission to hospital or intensive care unit unit

TABLE 248-5 Diffetential diagnssis for TABLE 248-5 Diffetential diagnssis for recurrent wheezing in childrenrecurrent wheezing in children

InfantInfantViral infection, Viral infection, posivtal syndromeposivtal syndrome Respitatorv Syncyfial virus Respitatorv Syncyfial virus Parainfluenza virus type 3Parainfluenza virus type 3Adenovituses Adenovituses Influenza viruses Influenza viruses Asthma or reactive airway diseaseAsthma or reactive airway diseaseCystic fibrosis Cystic fibrosis Congenital heart disease with large left-to-right shuntCongenital heart disease with large left-to-right shuntBronchopulmonary dysplasiaBronchopulmonary dysplasiaAcquited immunodeficiency syndrome Acquited immunodeficiency syndrome Aspitation Aspitation Pharyngeal incoordination Pharyngeal incoordination Gastroesophageal refluxGastroesophageal reflux

TABLE 248-5 Diffetential diagnssis for TABLE 248-5 Diffetential diagnssis for recurrent wheezlng in children )Cont.(recurrent wheezlng in children )Cont.(

Tracheoesophageal fistula Tracheoesophageal fistula Laryngotracheoesophageal cleft Laryngotracheoesophageal cleft Congenital malformation Congenital malformation Vascular anomalies Vascular anomalies Tracheobronchial anomalies Tracheobronchial anomalies Lung cyst Lung cyst Mediastinal lesions )e.g., thymus hyperplasia(Mediastinal lesions )e.g., thymus hyperplasia(TuberculosisTuberculosisHistoplasmosls, other mycotic infections Histoplasmosls, other mycotic infections Hypocalcemia Hypocalcemia Toddlers and preschool-aged children Toddlers and preschool-aged children Asthma or reactive airway diseaseAsthma or reactive airway diseaseEnvironmenial irritants )e.g., environmental tobacco smoke(Environmenial irritants )e.g., environmental tobacco smoke(Viral infection , postviral syndrome Viral infection , postviral syndrome Respiratory syncytial virusRespiratory syncytial virus


Adenoviruses Adenoviruses Parainfluenza virus type 3Parainfluenza virus type 3Influenza virus Influenza virus Foreign-body aspiration Foreign-body aspiration Gastroesophageal refluxGastroesophageal refluxTuberculosisTuberculosisHistoplasmosis, other mycolic infections Histoplasmosis, other mycolic infections Cysilc fibrosis Cysilc fibrosis TumorTumorLeukemia Leukemia Lymphoma Lymphoma Lymphosarcoma Lymphosarcoma Visceral larva migrans Visceral larva migrans Congental heart disease with left-to-right shuntCongental heart disease with left-to-right shuntAspiratioa )less common(Aspiratioa )less common(


Pulmonary hemosiderosisPulmonary hemosiderosisAcquired immunodeficlency syndrome Acquired immunodeficlency syndrome School-aged and adolescent childrenSchool-aged and adolescent childrenAsthmaAsthmaStnoking, drug useStnoking, drug useViral infection Viral infection Adenoviruses Adenoviruses InfluenzaInfluenzaGastroesophageal reflux Gastroesophageal reflux Tubercuiosis Tubercuiosis Histoplasmosis, other mycotic infections Histoplasmosis, other mycotic infections TumorTumorLeukemia Leukemia LymphomaLymphomaLymphosarcomaLymphosarcoma


Cyslic fibrosis Cyslic fibrosis

Kartagener syndrome Kartagener syndrome

Hypersensitivity pneumonitls Hypersensitivity pneumonitls

Vocal cord dysfunction Vocal cord dysfunction

Angioneurotic edemaAngioneurotic edema

عوارضكورتن عوارضكورتن

Inhibition or arrest of growth can result Inhibition or arrest of growth can result from the administration of relatively small from the administration of relatively small doses of glucocorticoids to children, and it doses of glucocorticoids to children, and it cannot be overcome with exogenous human cannot be overcome with exogenous human growth hormone. The widespread inhibitory growth hormone. The widespread inhibitory effect of the glucocorticoids on DNA effect of the glucocorticoids on DNA synthesis and cell division discussed above is synthesis and cell division discussed above is apparently responsible. apparently responsible.

TABLE 22-12. Treatment of status asthmaticusTABLE 22-12. Treatment of status asthmaticus

1.1. Culoereula tnerapy )give immedlately in the office or Culoereula tnerapy )give immedlately in the office or emergency department( Hydrocortisone )Solu-Cortef(4 mg/kg emergency department( Hydrocortisone )Solu-Cortef(4 mg/kg intravenously every 4-6 h or methylprednisolone )Solu-intravenously every 4-6 h or methylprednisolone )Solu-Medrol(0.5-1.0 mg/kg inrtavenously every 4-6 h or prednisone 1 Medrol(0.5-1.0 mg/kg inrtavenously every 4-6 h or prednisone 1 mg/kg orally every 4-6 hmg/kg orally every 4-6 h

2.2. B-Adrenergic agonists B-Adrenergic agonists Choice of approaches available.Choice of approaches available.

Epinephrine 0.01 mL/Kg of 1:1000 solution, subcutaneously not Epinephrine 0.01 mL/Kg of 1:1000 solution, subcutaneously not to exceed 0.3-0.5 mL in adults; may repeat twice at 20-min to exceed 0.3-0.5 mL in adults; may repeat twice at 20-min intervals then at reduced freqency intervals then at reduced freqency

Terbutaline 0.25 mg subcutaneously; may be repeated in 30 min Terbutaline 0.25 mg subcutaneously; may be repeated in 30 min , then in 4 h, then in 4 h

Aerosolized therapy; albuterol , metaproterenol, terbutaline, or Aerosolized therapy; albuterol , metaproterenol, terbutaline, or other agent; repeat in 30 min , then at reduced frequency other agent; repeat in 30 min , then at reduced frequency

If a patient does not respond to steps 1 or 2 )above( try, step 3; if If a patient does not respond to steps 1 or 2 )above( try, step 3; if a patient does does not respont to step 3, try step 1a patient does does not respont to step 3, try step 1

TABLE 22-12. Treatment of status asthmaticus TABLE 22-12. Treatment of status asthmaticus )cont.()cont.(

3.3. HospitalizeHospitalize4.4. Laboratory studies Laboratory studies WBC with differential WBC with differential Chest roentgenogram Chest roentgenogram Pulest roentgenogram Pulest roentgenogram Serum electrolytes and chemistries Serum electrolytes and chemistries Sputum Gram stain , culture, and sensitivitiesSputum Gram stain , culture, and sensitivitiesBedside spirometer may be useful, but not essential Bedside spirometer may be useful, but not essential ElectrocardiogramElectrocardiogram5.5. Oxygen therapy Oxygen therapy 6.6. Correct dehydrationCorrect dehydration2-3 L/min nasal cannula )best guided by arterial blood gas 2-3 L/min nasal cannula )best guided by arterial blood gas

determination( determination(

TABLE 22-12. Treatment of status asthmaticus TABLE 22-12. Treatment of status asthmaticus )cont.()cont.(

7.7. Aminophylline therapy )controversial( Aminophylline therapy )controversial(

Check theophylline concentration if chronic therapy; adjust Check theophylline concentration if chronic therapy; adjust therapy based on Tables 22-9 and 22-10; administration therapy based on Tables 22-9 and 22-10; administration is optional because efficacy has been questioned during is optional because efficacy has been questioned during emergency use emergency use

8.8. Antibiotic therapy Antibiotic therapy

When indicated for purulent rhinitis, bronchitis, or sinusitis When indicated for purulent rhinitis, bronchitis, or sinusitis

9.9. Impending or acute respiratgry failure Impending or acute respiratgry failure

Repeat B-adrenergic agonisis Repeat B-adrenergic agonisis

Endotracheal intubation with essisted or controlled Endotracheal intubation with essisted or controlled ventilationventilation

WBC, white blood cell count.WBC, white blood cell count.

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