ICS_RESP_MSII

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soren101
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ICS_RESP_MSII
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2011-09-02 01:48:34
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ICS Respiratory MSII
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ICS Respiratory MSII
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  1. COMPONENTS OF ABG
    ABG -- ARTERIAL BLOOD GAS

    • pH: 7.4
    • -- <ACIDEMIC
    • -- >ALKALEMIC

    • PaO2: 90mmHg
    • USED TO DETECT HYPOXEMIA
    • DECREASES WITH AGING (75mmHg BY AGE 90). <=56-60 SIG HYPOXIA

    • PaCO2: 40mmHg
    • REFLECTION OF ACID/BASE BALANCE.
    • HYPERCAPNIA >=45-50mmHg
  2. COMPLIANCE
    CHANGE IN VOLUME DIVIDED BY CHANGE IN PRESSURE

    MEASURE OF EASE AT WHICH LUNGS EXPAND

    • REDUCED:
    • PULM FIBROSIS
    • PULM EDEMA
    • ARDS

    • INCREASED:
    • EMPHYSEMA
  3. EQUATION FOR ARTERIAL O2 CONTENT
    CaO2 = (1.36 x Hgb x SaO2) + (0.003 x PaO2)

    SaO2 IS SATURATION ... FRACTION OF BOUND Hg

    CaO2 DEPENDS PRIMARILY ON Hg CONC AND O2 SAT OF ARTERIAL BLOOD, NOT THE ARTERIAL PARTIAL PRESSURE OF O2
  4. AIRWAY RESISTANCE EQUATION AND IMPLICATION IN DISEASE
    R = 8 N L / pi r^4

    • N = VISC
    • L = LENGTH

    RESISTANCE = PRESSURE DIFF / FLOW

    • TURBULENT FLOW:
    • --HIGH FLOW
    • --HIGH GAS DENSITY
    • --LARGE RADIUS
    • --ONE OF ABOVE OR ALL 3

    --25-40% IN UPPER AIRWAYS; GREATEST IN MEDIUM-SIZED BRONCHI

    • LAMINAR:
    • --ONLY IN SMALLEST AIRWAYS

    • INCREASED RES:
    • --ASTHMA
    • --COPD
    • --EMPHYSEMA
    • --CHRONIC BRONCH

    • NORM RES:
    • --ARDS
    • --ILD (INTERSTITIAL LUNG DISEASE)
    • --PNEU
  5. RISK OF HIGH Fi02
    OXY TOXICITY -- DIFFUSE ALVEO DAMAGE PATTERN IN LUNG = ARDS

    ABSORPTIVE ATELECTASIS (LACK OF NITROGEN IN ALVEO GAS ALLOWS OXY TO BE ABS AND ALVEO TO COLLAPSE
  6. DISEASES SEEN IN INC AIRWAY RESISTANCE
    ASTHMA

    COPD (EMPHYSEMA & CHRON BRONCHITIS)

    • NORMAL RESISTANCE:
    • --ARDS
    • --ILD
    • --PNEUMO
  7. ALVEOLAR VENTILATION AND ALVEOLAR AIR EQUATION
    VENT = TIDAL VOL (TV) x RESP RATE IN 1 MIN

    NORM PaCO2 = 40 torr

    PAO2 = FiO2 (Pb_atm - P_H2O) - (Pa_CO2 / R)

    • SIMPLIFIED STANDARD: sea level breathing room air
    • --FiO2 = .21
    • --Pb_atm = 760mmHg
    • --Pb_H2O = 47mmHg
    • --PaCO2 = 40
    • --R = 0.8

    PAO2 = 150 - (PaCO2 / 0.8)
  8. A-a GRADIENT AND CAUSES OF DISREGULATION
    EFFICIENCY OF LUNG

    PAO2 - PaO2

    NORMAL IS 3-16 mmHg

    VARRIES ACCORDING TO AGE

    • ELEVATED:
    • --V/Q MISMATCH
    • --RIGHT/LEFT SHUNTS
    • --IMPAIRED DIFFUSION

    • NORMAL:
    • --HIGH ALTITUDE
    • --ALVEO HYPOVENT
  9. FUNCTIONAL RESIDUAL CAPACITY (FRC)
    VOL GAS REMAINING IN THE LUNGS AT END OF NORMAL TIDAL EXPIRATION

    RV + ERV
  10. INSPIRATORY CAPACITY vs. TLC vs. VC
    IC = MAX VOL GAS INHALED AFTER NORMAL TIDAL EXHALE

    TLC = VOL GAS INHALED AFTER MAX EXHALE (INCLUDING RV)

    VC = (TLC - RV)
  11. PFTs ARE ADJUSTED FOR:
    AGE, SEX, HEIGHT, ETHNICITY
  12. NORMAL %PREDECTED FVC
    FVC >= 80%

    FEV1 >=80%

    FEV1/FVC >= 70-75%

    TLC 80-120%

    RV 80-120%

    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%
  13. NORMAL %PREDICTED FEV1
    FVC >= 80%

    FEV1 >=80%

    FEV1/FVC >= 70-75%

    TLC 80-120%

    RV 80-120%

    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%
  14. NORMAL %PREDICTED TLC
    FVC >= 80%

    FEV1 >=80%

    FEV1/FVC >= 70-75%

    TLC 80-120%

    RV 80-120%

    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%
  15. NORMAL %PREDICTED FEV1/FVC RATIO
    FVC >= 80%

    FEV1 >=80%

    FEV1/FVC >= 70-75%

    TLC 80-120%

    RV 80-120%

    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%
  16. NORMAL %PREDICTED RV
    FVC >= 80%

    FEV1 >=80%

    FEV1/FVC >= 70-75%

    TLC 80-120%

    RV 80-120%

    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%
  17. NORMAL %PREDICTED DLCO AND CAUSES OF LOW DIFFUSION
    • DLCO (DIFFUSION CAPACITY IN L OF CO)
    • 80-100%

    • CAUSES:
    • --THICKENING OF ALVEO-CAPIL MEM (PULM FIBROSIS, ILD, INTERSTITIAL OR ALVEO EDEMA)

    --DEC SURFACE AREA (EMPHYSEMA, TUMORS, LOW PULM CAPIL BLD VOL

    --DEC ERYTH UPTAKE (ANEMIA)

    --V/Q MISMATCH
  18. OBSTRUCTIVE PFTs AND DISEASES
    IMLPY REDUCED ABILITY TO GET AIR THROUGH COND AIRWAYS AND OUT LUNGS

    FEV1/FVC RATION < 75% (COPD AT <70%)

    • DISEASES:
    • --COPD (EMPH & BRONCHITIS)

    --BRONCHIECTASIS (POST INF AND CYCSTIC FIBROSIS)

    --ASTHMA

    OFTEN ASTHMA & COPD WILL SHOW HYPERINFLATION (TLC > 120%) AND AIR TRAPPING (RV > 120%)

    • RESTICTIVE:
    • --PULM FIBROSIS
    • --ILD
    • --INFILT LUNG DISEASE ( MALIG LYMPH SPREAD)
    • --PLEURAL DISEASE
    • --NEUROMUSC
    • --OBESITY
    • --CHEST WALL DEFORMITIES (KYPHOSIS, PECTUS EXCAVATUM)
  19. DRUGS THAT CAUSE ILD
    BLEOMYCIN -- CHEMO DRUG --> PRE-OP TO 100% SAT CAUSING OXYGEN RADIACALS

    AMIODARONE -- CARDIAC AGENT

    METHOTREXATE -- IMMUNOSUPPRESSANT

    CRACK/COCAINE
  20. RESTRICTIVE PFTs AND ASSOC DISEASES
    INABILITY TO GET AIR INTO LUNGS AND MAINTAIN NORMAL LUNG VOL

    AIR FLOW NOT AFFECTED

    --DEC TLV <80% PREDICTED. GOLD STANDARD

    --LOW FVC <80%

    --NORMAL FEV1/FVC RATIO IS SUGGESTIVE OF RESTRICTIVE PHYS, BUT MUST CONF BY GETTING LUNG VOLS (TLC)

    --CANNOT Dx WITH SPIROMETRY ALONE

    • DISEASES:
    • --PULM FIBROSIS
    • --ILD
    • --INFILTRATIVE LUNG DISEASE (MALIG SPREAD THRU LYMPH)
    • --PLEURAL DISEASE
    • --NEUROMUSC DISEASE
    • --OBESITY
    • --CHEST WALL DEFORMITIES (KYPHOSIS, PECTUS EXCAVATUM)
  21. ALGORITHMS FOR OBSTRUCTIVE vs. RESTRICTIVE
    LOW FEV1 or FVC = OBST or REST

    LOW FEV1/FVC = OBST

    nL FEV1/FVC w LOW TLC = REST

    ----------------------------------------

    nL FVC & FEV1 >= 80%

    nL FEV1/FVC >= 75%

    nL TLC & RV >80% & < 120%
  22. WHAT IS ARF
    INABILITY TO MAINTAIN EITHER NORM DELIVERY OF OXY OR NORM REMOVAL OF CO2

    • CAUSES:
    • --HYPOXEMIA (PaO2 <= 50-60mmHg)
    • --HYPERCAPNIA (PaCO2 >= 45-50mmHg)

    • OFTEN PATIENS IN "50/50 CLUB"
    • --HYPOXIMIA (PaO2 <= 50-60mmHg)
    • --HYPERCAPNIA
  23. ESTIMATING LUNG FUNCTION
    P/F RATION

    PaO2/FiO2

    USED IN Pt WITH SUPP OXY

    nL RATIO ~ 500 (100mmHg/0.21

    ACUTE LUNG INJURY ALI = P/F <= 300

    ARDS <= 200
  24. DEGREES OF LUNG INJURY
    • ACUTE LUNG INJURY (ALI)
    • --NON-CARDIOGENIC PULM EDEMA WITH PaO2/FiO2 <= 300mmHg

    ARDS <= 200mmHg
  25. SHUNTS
    EXTREME V/Q MISMATCH

    • DEAD SPACE VENTILATION, NO PERFUSION
    • --MASSIVE PULM EMBOLISM
    • --CARDIAC SHUNTS

    ONLY CAUSE OF HYPOXEMIA NOT CORRECTED WITH SUPP O2
  26. MANAGING PATIENTS WITH ARF
    SUPPORTIVE

    --1st "THE ABCs" AIRWAY, BREATHING, CIRC

    --THEN SPECIFIC TREATMENTS DIRECTED AT UNDERLYING DESEASE. GENERALLY, PaO2 ~ 60mmHg USUALLY CORRESPONDING TO SaO2 ~ 90% IS ADEQUATE TARGET
  27. DIFFERENTIAL Dx OF HYPOXEMIA / RESP FAILURE
    CLINICAL CLASSIFICATION BASED ON CHEST X-RAY -- WHITE OR BLACK

    • WHITE:
    • --PNEUMONIA
    • --ARDS
    • --CARDIOGENIC PULM EDEMA: CHF
    • --ILD

    • BLACK:
    • --OBST LUNG DISEASE
    • --PULM EMBOLI
    • --PLEURITIC PAIN, HEMOPTYSIS, RISK FACTORS OF DVT
    • --MICRO ATELECTASIS
    • --SHUNT
  28. PNEUMONIA: DIFFERENTIAL HYPOX / RESP FAILURE
    --WHITE CXR

    --INFILTRATES WITH SUPP CLINICAL FEATURES (FEVER, LEUKOCYTES, SPUTUM PROD)

    --ELDERLY Pt OVER 65 LACK PULM SYMP 50% OF TIME AND MANY PRESENT w CONF AND LETHARGY & FATIGUE
  29. ARDS: DIFFERENTIAL HYPOX / RESP FAILURE
    --WHITE CXR

    --NON-CARDIOGENIC PULM EDEMA

    • --MOST Pt WITH ARDS HAVE ONE OF THE COMMON PRECIP FACTORES LEADING TO DISORDER
    • ----SEPSIS
    • ----HYPOTEMSION
    • ----MASSIVE TRAUMA
    • ----TRANSUFIONS

    • LESS COMMON:
    • --PANCREATITIS
    • --DRUG OVERDOSE
    • --POST CARDIO-PULM BYPASS SURGERY
  30. CARDIOGENIC PULM EDEMA -- CHF: DIFFERENTIAL HYPOXIA / RESP FAILURE
    --WHITE CXR

    --PULM CAPILL WEDGE PRESSURE >18mmHg

    --USUALLY IN SETTING OF MYOCARDIAL INFARCT, SEVERE HYPERTENSION, VALVE DISEASE
  31. ILD DIFFERENTIAL HYPOXIA / RESP FAILURE
    --WHITE CXR (DOTS AND LINES OR RETICULONODULAR PATTERN)

    --USUALLY SLOWLY PROG DISEASE

    --HIST AND OLD CXR VERY HELPFUL
  32. OBSTRUCTIVE LUNG DISEASE: DIFFERENTIAL HYPOXIA / RESP FAILURE
    --BLACK CXR

    --BEDSIDE SPIROMETRY (FEV1/FVC <75%) VERY HELPFUL

    --OFTEN w WHEEZING, PROLONGED EXPIRATION (1:3 OR 1:4) AND DEC BREATH SOUNDS ON PHYSICAL EXAM
  33. PULM EMBOLI: DIFFERENTIAL HYPOXIA / RESP FAILURE
    --BLACK CXR

    --MAY HAVE SIG HYPOX WITH nL CXR

    --MOST PRESENT w ACUTE DYSPNEA

    --PLEURITIC PAIN, HYMOPTYSIS, OR RISK FACTORS OF DVT INC LIKELYHOOD
  34. MICRO-ATELECTASIS: DIFFERENTIAL HYPOXIA / RESP FAILURE
    --BLACK CXR

    --POST-OP Pt OR Pt WHO BREATH SHALLOW FROM PLEURITIC PAIN (RIB FRAC)
  35. SHUNTS: DIFFERENTIAL HYPOX / RESP FAILURE
    --BLACK CXR

    --PULM ARTERIAL-VENOUS MALFORMATIONS (AVM) OR MICRO AVMs IN CIRRHOSIS (SPIDER ANGIOMAS OR LUNG)

    --INTRACARDIAC: Rt TO Lt SHUNTS FROM CONG OR ACQ HRT DISEASE AND/OR PULM HYPERTENSION. Dx BY BUBBLE ECHOCARDIOGRAM
  36. ANATOMIC INFLUENCES IN RESPITATORY FUNC DURING PREGNANCY
    Level of diaphragm rises 4 cm

    Diaphragmatic excursion increases

    Subcostal angle increases

    Transverse diameter of chest increases 2 cm

    • Chest circumference increases 6 cm
    • --------------------------------------

    ELEV OF DIAPHRAGM WITH INC UTERINE SIZE. MAKES RESP PRIM THORASIC AND MINIMALLY ABDOMINAL

    SUBCOSTAL ANGLE INC MAKES RESP MOVEMENTS SHALLOWER
  37. CHANGES IN LUNG VOLUMES DURING PREGNANCY
    • VITAL CAPACITY
    • --PROB SMALL INC (100-200ml)
    • --INSP CAP MAY INC BY 300ml
    • --EXP RESERVE VOL DEC BY 200ml
    • --RV/FUNC RESID CAP DEC BY 20%

    • TIDAL VOLUME:
    • --INC BY 40% (500 --> 700ml)
    • --RESP RATE NOT CHANGED
    • --MIN VENT RISES IN PARALLEL TO INC TIDAL VOL BY 40%

    PREG WOMAN INC VENT BY BREATHING MORE DEEPLY, BUT NOT MORE FREQUENTLY

    VENT CHANGE PRIM BY CENTRAL RESP CONTROL
  38. BLD GASSES AND CENTRAL VENT CONTROL IN PREGNANCY
    INC VENT IN PREG PROVIDES SOME INC OXY, BUT REALLY REMOVES CO2

    -->DROP IN pCO2

    --PROGESTERONE LOWERS THRESH OF RESP CENTER TO pCO2 AND IS THE MECH OF HYPERVENT AND WASH-OUT.

    SMALL pO2 CHANGE bc OF SHAPE OF Hg DISSOCIATION CURVE; THERE IS LITTLE INC IN Hg SAT

    FALL IN pCO2 IS MATCHED BY AN EQUIV FALL IN PLASMA BICARB AND NO CHANGE IN ART pH. LOSS OF BICARB MAKES PREG MORE SUSCEPTIBLE TO ACIDOSIS (LESS BUFFERING)

    VENOUS pH BECOMES SLIGHTLY MORE ALKALOTIC (7.35 --> 7.38)
  39. ABG LEVELS IN NON-PREG AND PREG
    pH______ 7.4 / 7.42

    PaO2___ 100 / 100

    PaCO2__ 35-40 / 30

    BICARB_ 24 / 20
  40. NEONATAL PULM TRANSITION: LUNG MATURITY FACTORS
    • PHYSICAL:
    • immature

    less surface area for gas exchange,

    capillaries far from those units,

    presence and maturity of surfactant

    FLUID REABSORPTION -- NEEDED FOR GAS EXCHANGE

    LOW PVR; HIGH SVR

    INC O2 CAUSES VASODILATION IN PULM ARTERIOLES BY
    enhancement of prod of endothelium-derived vasodilators PROSTOGLANDIN I2 (prostacyclin) and NO.


    • FORAMEN OVALE; DUCTUS ARTERIOSUS

    SUSTAINED BREATING -- CNS

  41. PULM TRANSITION OF NEONATE: FLUID REABSORPTION
    •In utero, lungs are chloride secreting. During the last weeks of a normal pregnancy and during onset of labor, hormonal changes facilitate reabsorption of fluid. “Vaginal squeeze” of minimal importance.

    •Rapid fluid clearance mediated by transepithelial sodium reabsorption through amiloride-sensitive sodium channels in alveolar epithelial cells.

    •Must go via lymphatics to venous system.

    •Failure of clearance quite common, esp. in elective c-section, prematures.

    •Retained fetal lung fluid causes Transient Tachypnea of the Newborn (TTN), exacerbates RDS, pneumonia.
  42. WHY ARE PREMATURE NEWBORNS AT HIGHER RISK FOR ABNORMAL TRANSITION?
    •POSSIBLE SURFACTANT DEFICIENCY

    •DECREASED DRIVE TO BREATHE

    •RAPID HEAT LOSS, POOR TEMPERATURE CONTROL

    •POSSIBLE INFECTION

    •SUSCEPTIBLE TO BRAIN HEMORRHAGE

    •SUSCEPTIBLE TO HYPOVOLEMIA SECONDARY TO BLOOD LOSS

    •WEAK MUSCLES MAKE SPONTANEOUS BREATHING DIFFICULT

    • •IMMATURE TISSUES MAY BE DAMAGED BY
    • EXCESSIVE OXYGEN
  43. PULMONARY SURFACTANT
    •HETEROGENEOUS MIXTURE OF PHOSPHOLIPIDS AND PROTEINS SECRETED BY TYPE II PNEUMOCYTES

    •PRESENT IN SECRETORY ORGANELLES AT 24 WEEKS

    • •SURFACTANT LIPIDS NOT DETECTABLE IN
    • AMNIOTIC FLUID UNTIL AROUND 30 WEEKS

    •MAJOR COMPONENTS - DPPC, PG, APOPROTEINS (SP-A, SP-B, SP-C, SP-D)

    • •EXOGENOUS SURFACTANT AVAILABLE AS
    • TREATMENT; GIVEN VIA ENDOTRACHEAL TUBE
  44. Extrathoracic Airway Obstruction Presentations
    • SYMPTOMS
    • --STRIDOR,
    • --SNORING,
    • --APNEA,
    • --HOARSENESS,
    • --BRASSY COUGH

    • COURSE
    • --ACUTE
    • --RECURRENT
    • --CHRONIC
    • --PROGRESSIVE

    • EXAM
    • --INSPIRATORY = STRIDOR- SUPRAGLOTTIC

    --EXPIRATORY = STRIDOR- LOWER TRACHEA

    --BIPHASIC = GLOTTIC OR SUBGLOTTIC

    --VOICE CHANGES = LARYNGEAL
  45. LARYNGOMALACIAs
    --MOST COMMON CAUSE OF NONINFECTIOUS, RECURRENT OR PERSISTENT STRIDOR IN INFANTS

    --PRESENTS FIRST 6 WKS LIFE. IMPROVES WITH AGE, RESOLVES BY 1- 2YRS.

    • --COLLAPSE OF SUPRAGLOTTIC STRUCTURES (ARYTENOID CARTILAGE AND EPIGLOTTIS) DURING INSPIRATION
    • -------------------------

    • CLINICAL
    • --WORSE
    • IN SUPINE, WITH INCREASED ACTIVITY, CRYING , URI, FEEDINGS, +/- GERD

    --CLINICAL DIAGNOSIS – SUPPORTIVE MEASURES AND REASSURANCE, RARELY LIFE THREATENING.

    --IMAGING - ONLY IF FEEDING ISSUES, SEVERE STRIDOR, SLEEP APNEA, DYSPNEA, FTT
  46. CROUP
    VIRAL CROUP-LARYNGOTRACHEOBRONCHITIS: EDEMA IN THE SUBGLOTTIC SPACE, INFLAMMATION OF ENTIRE AIRWAY.

    • EPIDEMIOLOGY-
    • --6MONTHS- 3 YEARS
    • --MALES 2X > FEMALES
    • --FALL & WINTER (OCT-MAY)
    • --PARAINFLUENZA TYPE 1,2,3,
    • --RSV, ANDENOVIRUS, INFLUENZA,
    • --MYCOPLASMA (ESP > 5 YR),
    • --RUBEOLA.
  47. BRONCHIOLITIS
    •CLINICAL PRESENTATION

    • –SYMPTOMS: RHINORRHEA, CORYZA,
    • COUGH, IRRITABILITY, POOR FEEDING, EMESIS

    • –EXAM:
    • •TACHYPNEA, WHEEZING, LABORED
    • RESPIRATIONS, USE OF ACCESSORY MUSCLES, AND/OR NASAL FLARING, HYPOXIA, WHEEZES / CRACKLES ON EXAM

    • •CXR- HYPERINFLATION, SUBSEGMETAL
    • ATELECTASIS, PERIHILAR STREAKING

    –COURSE- 2-4 WEEKS

    • –1/3 INFANTS WILL HAVE RECURRENT
    • WHEEZING

    • –TREATMENT LARGELY SUPPORTIVE-
    • OXYGEN, CLEARING SECRETIONS, SUPPORT OF HYDRATION/NUTRITION.

    –PREVENTION- IMMUNOPROPHYLAXIS FOR HIGH RISK INFANTS

    • --------------------------------------
    • VIRAL INFECTION OF THE LRT

    •EPIDEMIOLOGY

    • –MOST COMMON SERIOUS ACUTE
    • RESPIRATORY ILLNESS IN INFANTS/CHILDREN UNDER 2YRS.

    • •NINETY PERCENT OF CHILDREN ARE
    • INFECTED WITH RSV IN THE FIRST 2 YEARS OF LIFE

    • •INFECTION WITH RSV DOES NOT GRANT
    • PERMANENT OR LONG TERM IMMUNITY. REINFECTIONS ARE COMMON AND MAY BE EXPERIENCED THROUGHOUT LIFE

    • –WINTER /EARLY SPRING
    • (DECEMBER-MARCH)

    • –RSV, ADENOVIRUS, PARAINFLUENZA,
    • INFLUENZA, PNEUMOVIRUS, HUMAN METAPNEUMOVIRUS

    •PATHOGENESIS

    –CONTACT AND DROPLET DISPERSION

    CHARACTERIZED BY ACUTE INFLAM, EDEMA AND NECROSIS OF EPITHELIAL CELLS LINING SMALL AIRWAYS, AND INCREASED MUCUS PRODUCTION.
  48. THE WHEEZY INFANT
    •NOT ALL WHEEZY BABIES HAVE ASTHMA OR GO ON TO BE WHEEZY ADULTS!

    •BRONCHIOLITIS = COMMON VIRAL LRTI

    •BRONCHOCONSTRICTION INC MUCUS PRODUCTION = SMALLER AIRWAY CALIBER

    •INCREASED CHEST WALL COMPLIANCE AND INCREASED ELASTIC RECOIL → DECREASED RESIDUAL VOLUME (SO MORE QUICKLY SYMPTOMATIC)

    • •DIFFERENTIAL DIAGNOSIS: CONGENITAL
    • ANOMALIES/MALFORMATION OF THE AIRWAYS, CF, GER, IMMUNE DEFECT

    •$$$ IMPLICATIONS
  49. GENETICS OF CISTIC FIBROSIS
    • CYSTIC FIBROSIS TRANSMEMBRANE
    • CONDUCTANCE REGULATOR (CFTR)

    LOCATED IN SWEAT GLANDS, RESPIRATORY EPITHELIUM, PANCREAS, INTESTINE, LIVER, REPRODUCTIVE TRACT

    MEMBRANE SPANNING CHANNEL THAT CONTROLS CHLORIDE MOVEMENT

    CHROMOSOME 7

    –>1000 KNOWN MUTATIONS

    DF508-MOST COMMON MUTATION

    –MODIFIER GENES PLAY A ROLE

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