Pulmonary Disorders Flashcards

1
Q

What is Community Acquired Pneumonia and what are the 2 most common causes?

A

1. acquired outside of the hospital setting & patient is not a resident of a long term care facility OR

2. patient that was ambulatory prior to admission who develops pneumonia within 48 hours of initial hospital admission

1. Streptococcus pneumoniae

2. Haemophilus influenzae

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2
Q

What is Hospital Acquired (nosocomial) Pneumonia?

A

pneumonia occurring > 48 hrs after hospital admission

often caused by Pseudomonas, MRSA

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3
Q

Atypical Pneumonia Organisms: Mycoplasma

A

MYCOPLASMA:** ear pain, **bullous myringitis, erythematous pharynx or TM. Persistent nonproductive cough

Send _serum cold agglutins_ as part of the diagnostic workup

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4
Q

Atypical Pneumonia Organisms: Chlamydophila

A

hoarseness, fever ⇒ respiratory symptoms after a few days

send IgM, IgG titers

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5
Q

Atypical Pneumonia Organisms: Legionella

A

Legionella: associated with GI Sx, î LFTs, hyponatremia

send legionella urine antigens + PCR

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6
Q

Chest XRAY of typical pneumonia** vs. **atypical pneumonia

A

typical pneumonia: lobar pneumonia

atypical pneumonia: diffuse, patchy interstitial or reticulonodular infiltrates

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7
Q

Diagnostic Workup of Pneumonia

A

A. CXR/CT Scan: CXR resolution may lag behind clinical improvment for weeks. A pleural effusion may be present (usually exudative)

  1. abscess formation ⇒ S. aureus, Klebsiella, anaerobes
  2. Upper lobe (especially R upper lobe) with bulging fissure, cavitations ⇒ Klebsiella

B. Sputum (gram stain/culture): utility debated. Gross sputum may reveal clues to pathogen

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8
Q

Physical Exam of Pneumonia

A

dullness to percussion

INCREASED fremitus

Bronchial breath sounds, EGOPHONY*

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9
Q

Treatment for CAP outpatient

A

Macrolide or Doxycycline 1st line**

Fluoroquinolones are only used first line if comorbid conditions/recent Abx use

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10
Q

Treatment for CAP, inpatient

A

ß lactam + macrolide (or doxycycline)

OR

broad spectrum FQ

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11
Q

What is the PCV13 Pneumococcal conjugate vaccine? (Prevnar)

A
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12
Q

What is Asthma?

A

reversible hyperirritability of the tracheobronchial tree ⇒ airway inflammation & bronchoconstriction

MC chronic childhood disease (10%)

1/2 develop < 10 y of age, another 1/3 by 40 yo

atopy is a risk factor*

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13
Q

What is Samter’s Triad?

A

1. asthma

2. nasal polyps

3. ASA/NSAID allergy

associated with atopic dermatitis

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14
Q

Pathophysiology of asthma

A

1. AIRWAY HYPERREACTIVITY:

extrinsic (allergic); associated with increased IgE

intrinsic (idiosyncratic): nonallergic triggers: infection (viral, URI), pharmacologic, occupational, exercise, emotional, cold air

2. BRONCHOCONSTRICTION: airway narrowing secondary to smooth muscle constriction, bronchial wall edema, and thick mucus secretion, collagen deposition, smooth muscle/mucosal hypertrophy

(brochoconstriction leads to air trapping)

decreased expiratory airflow

3. INFLAMMATION: secondary to cellular infiltration (T lymphocytes, neutrophils, eosinophils) & their pro-inflammatory cytokines (leukotrienes)

increased histamine from mast cells

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15
Q

Clinical Manifestations of Asthma

A

Classic Triad

1. dyspnea 2. wheezing 3. cough (esp @ night)

Physical Examination

1. prolonged expiration with wheezing, hyperresonance to percussion, decreased breath sounds, tachycardia, tachypnea, accessory muscle use

2. _severe asthma and status asthmaticus:_ inability to speak in full sentences, PEFR < 40% predicted, altered mental status, pulsus paradoxus (inspiratory, decreased SBP > 10), cyanosis, “tripod” position, “silent chest” (no air exchange)

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16
Q

Diagnostic Studies for Asthma

A

A. PULMONARY FUNCTION TEST: GOLD STANDARD

reversible obstruction (decreased FEV1, decreased FEV1/FVC)

B. Bronchoprovocation: methacholine challenge test (> 20% decrease in FEV1) + Bronchodilator challenge test ( > 12% increase in FEV1)

C. Peak Expiratory Flow Rate (PEFR): best and most objective way to assess asthma exacerbation severity & patient response in ED (PEFR > 15% from initial attempt = response to treatment)

D. Pulse Oximetry: < 90% indicative of respiratory distress

E. ABG

F. CXR: usually not helpful but can be used to rule out other etiologies

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17
Q

Management of Asthma: Quick Relief of Acute Exacerbation (Rescue Drugs)

A

1. Short Acting ß2 agonists (SABA): 1st line treatment

Albuterol

MOA: bronchodilator

SE: ß1 cross reactivity: tachycardia/arrhythmias, muscle tremors, CNS stimulation, hypokalemia

2. Anticholinergics

Ipratropium

MOA: central bronchodilator, inhibits nasal mucosal secretions

SE: thirst, blurred vision, dry mouth, urinary retention, dysphagia, acute glaucoma, BPH

3. Corticosteroids

predniose, methylprednisolone, prednisolone

MOA: anti-inflammatory. all but the mildest exacerbations should be discharged on a short course of oral corticosteroids (3 - 5 days)

SE: immunosuppression, catabolic, hyperglycemia, fluid retention, osteoporosis, growth delays

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18
Q

Management of Asthma: Long-Term (chronic control) maintenance

A

1. Inhaled Corticosteroids (ICS)

beclomethasone, flunisolide, triamcinolone

  • Drug of choice for long term persistent asthma*
  • MOA: cytokine & inflammation inhibition*
  • SE: thrush*

2. Long-Acting ß2 Agonists (LABA)

Salmeterol, ICS/LABA Combo:Symbicort (Budesonide, Formoterol), Advair diskus (Fluticasone/ Salmeterol)**

  • long acting ß2 agonists added to steroids ONLY if persistent asthma is not controlled with ICS alone*
  • NOT used in acute exacerbations and LABAs are NOT used alone*

3. Mast Cell Modifiers

Cromolyn, Nedocromil

MOA: inhibits mast cell and leukotriene-mediated degranulation. used as prophylaxis only

inhibits acute phase response to cold air, exercise, sulfites

4. leukotriene modifiers/receptor antagonists (LTRA)

montelukast, zafirlukast, zileuton

useful in asthmatics with allergic rhinitis/aspirin induced asthma. prophylaxis only

SE: minimal, increased LFTs, HA, GI myalgias

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19
Q

Management of Asthma: adjuncts

A

IV Magnesium

bronchodilator

(decreased Ca2+-mediated smooth muscle contraction)

Heliox

decreases airway resistance because helium + oxygen is lighter than room air

Ketamine

IV anesthetic that has sedative, analgesic, and bronchodilator effects. may be useful as an induction, sedative agent in young, otherwise healthy population of intubated patients

OMALIZUMAB:

anti-IgE antibody** (inhibits IgE inflammation) **used in severe, uncontrolled asthma

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20
Q

Classification of Mild Persistent Asthma

A
  • Sx > 2 days/week (but not daily)
  • SABA use > 2 days/week (but not more than 1x per day)
  • nighttime awakenings 3 - 4x per month
  • minor limitation with activity
  • FEV1 > 80% predicted
  • FEV1/FVC normal

Management: inhaled SABA prn + low dose ICS

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21
Q

Classification of Moderate Persistent Asthma

A
  • Sx daily
  • SABA use daily
  • nighttime awakenings > 1x/wk (but not nightly)
  • some limitation with activity
  • FEV1 60 - 80% predicted
  • FEV1/FVC reduced by 5%

Management: Low dose ICS + LABA

or

Increase ICS dose (medium)

  • or*
  • Add LTRA*
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22
Q

Classification of Severe Persistent Asthma

A
  • Sx throughout the day
  • SABA use several times a day
  • nighttime awakenings often, usually nightly
  • extremely limited activity
  • FEV1 < 60%
  • FEV1/FVC reduced by > 5%

Management: High dose ICS + LABA

+ Omalizumab (anti-IgE drug)

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23
Q

Step Down/Step Up System for Asthma

A
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24
Q

What is a pneumothorax?

A

air in the pleural space

increasingly positive pleural pressure causes collapse of the lung

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25
Q

Types of Pneumothorax: Spontaneous

A

atraumatic and idiopathic. due to bleb rupture

1. Primary: no underlying lung disease*. mainly affects _t_all, thin men 20 - 40 yo, smokers, + family history of pneumothroax

2.

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26
Q

Types of Pneumothorax: traumatic

A
  • iatrogenic: during CPR, thoracentesis, PEEP (ventilation), subclavian line placement
  • other trauma: car accidents, etc.
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27
Q

Types of Pneumothorax: Tension

A

any type of pneumothorax in which the positive air pressure pushes lungs, trachea, great vessels & heart to the CONTRALATERAL SIDE

  • immediately life-threatening*
  • MC seen during trauma, mechanical ventilation or resuscitative efforts*
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28
Q

Clinical Manifestations of Pneumothorax

A
  1. Chest pain: usually _pleuritic, unilateral,_ non-exertional & sudden in onset; Dyspnea
  2. PHYSICAL EXAM
  • Hyperresonance to percussion, decreased fremitus, decreased breath sounds over affected side
  • unequal respiratory expansion, tachycardia, tachypnea
  • tension pneumothorax: increased JVP, pulsus paradoxus, hypotension
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29
Q

Diagnosis of Pneumothorax

A

CXR with expiratory view preferred

– decreased peripheral lung markings (due to collapsed lung tissue)

+ companion lines (visceral pleural line running parallel with the ribs)

– deep sulcus sign on supine chest radiograph (air collection basally and anteriorly)

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30
Q

Management of Pneumothorax

A
  1. Observation: in primary spontaneous if small ( < 15 - 20% the diameter of the hemithorax or < 2 - 3 cm between the chest wall & lung on CXR). Observe at least 6 hours with repeat CXR to affirm no progression + 24 - 48 hour F/U. often spontaneously resolves w/i 10 days
    * – O2 shown to increase air resorption 3 - 4x faster than 1.25% every day*
    * 2.* Chest tube placement (thoracostomy): if large or severe sx
  2. Needle aspiration: if tension pneumothorax* followed by chest tube placement. Needle placed in 2nd ICS @ midclavicular line on the affected side
    * avoid pressure changes ex: high altitudes, smoking, unpressurized aircraft & scuba diving
31
Q

What is Pertussis? (whooping cough)

A

highly contagious infection secondary to Bordatella pertussis

  • rarely seen due to widespread vaccination. Gram negative coccobaccillus.*
  • MC seen in children < 2 yo*
32
Q

Clinical Manifestations of Pertussis (whooping cough)

A

catarrhal phase ⇒ paroxysmal phase ⇒ convalescent phase

1. catarrhal phase: URI Sx lasting 1 - 2 weeks. most contagious during this phase

2. paroxysmal phase: severe paroxysmal coughing fits with inspiratory whooping sound after fits

+** **post coughing emesis

may develop subconjunctival hemorrhage from the increased pressure due to coughing fits

3. convalescent phase: resolution of cough (coughing stage may last up to 6 wks)

33
Q

Management of Pertussis (whooping cough)

A

supportive treatment mainstay* oxygenation, nebulizers, mechanical ventilation as needed

antibiotics used to decrease contagiousness within the 1st 7 days of Sx onset–also often given to exposed contacts

Macrolides: erythromycin, azithromycin

34
Q

Diagnosis of Pertussis (whooping cough)

A
  1. PCR of nasopharnygeal swab: GOLD STANDARD. performed in the first 3 wks of Sx onset
  2. Lymphocytosis* 60 - 80% lymphocytes on differential. WBC count may be as high as 50,000
35
Q

What is acute bronchiolitis?

A

lower respiratory tract infection of the small ariways ⇒ proliferation/necrosis of the bronchiolar epithelium produces obstruction from the sloughed epithelium. increased mucus plugging & submucosal edema leading to peripheral airway narrowing & variable obstruction

36
Q

What is the MC cause of acute bronchiolitis?

A

respiratory synctial virus (RSV) (50 - 70%) RSV part of parayxovirus family*

other: adenovirus, influenza, parainfluenza, + mycoplasma pneumonia, chlamydia trachomatis

37
Q

What are the risk factors for acute bronchiolitis?

A

infants < 2 yo MC affected (esp ~ 2 months)

  • < 6 months of age exposure ot cigarettes, lack of breastfeeding, premature (< 37 wks gestation) & crowded conditions*
  • MC in fall and spring*
38
Q

Clinical Manifestations of acute bronchiolitis

A

fever, URI Sx 1 - 2 days ⇒ repiratory distress

(wheezing, tachypnea, nasal flaring, cyanosis, retractions + rales)

39
Q

Diagnosis of acute bronchiolitis

A

CXR: hyperinflation, peribroncbial cuffing, etc.

nasal washings using monoclonal Ab testing

pulse ox single best predictor of disease in children (< 96% ⇒ ADMIT TO HOSPITAL)

40
Q

Management of acute bronchiolitis

A

1. supportive: humidified O2 mainstay of treatment

delivered by mask, tent, or hood. IV fluids. Acetaminophen/ibuprofen for fever. mechanical ventilation if severe.

2. Medications:** **play a limited role

+ ß agonists, + nebulized racempic epi

corticosteroids NOT indicated unless history of reactive airway disease

3. Ribavarin + administered if severe lung or heart disease or in immunosuppressed patients

41
Q

Prevention for Acute Bronchiolitis

A

Palivizumab prophylaxis may be used in increased risk groups

HAND WASHING

RSV is highly contagious and is transmitted via direct contact with secretions and self-inoculation by contaminated hands

42
Q

What is acute epiglottitis?

A

inflammation of epiglottitis that may interfere with breathing

medical emergency

43
Q

Causes of acute epiglottitis

A

HAEMOPHILUS INFLEUNZAE TYPE B (Hib) MC***

reduced incidence due ot Hib vaccination. may rarely be caused by Streptococcus pneumoniae, S. aureus, GABHS

  • MC in children 3 mnths - 6 yrs*
  • Males 2x MC*
  • DM is a risk factor in adults…*
44
Q

Diagnosis of acute epiglottitis

A
  • Laryngoscopy: definitive Dx** provides direct visualization but may provoke spasm

Cherry red epiglottits with swelling

  • Lateral cervical radiograph: THUMB SIGN
    • if high suspicion, do not attempt to visualize the epiglottits with a tongue depressor in children
45
Q

Clinical Manifestations of acute apiglottitis

A

3 Ds - Dysphagie, Drooling, Distress

fever, odynophagia, inspiratory stridor, dyspnea, hoarseness, muffled voice, _tripoding_

suspect in pt with rapidly developing pharyngitis, muffled voice & odynophagia (painful swallowing) out of proportion to physical findings

46
Q

Management of acute epiglottitis

A

1. Maintaining the airway & supportive management is the mainstay of Tx

place child in a comfortable position

dexamethasone to reduce airway edema

tracheal intubatiodn to protect the airway in severe cases

2. Antibiotics: 2nd/3rd cephalosporins: ceftriaxone or cefotaxime

+ add PCN, ampicillin, or anti-staphylococcal coverage

47
Q

What is laryngotracheitis (croup)?

A

inflammation MC secondary to acute viral infection of the UPPER AIRWAY (larynx, subglottis, trachea)

subglottic larynx/trachea swelling

  • ⇒*
  • stridor, BARKING cough, hoarseness*
48
Q

What is the MC cause of laryngotracheitis (croup)?

A

PARAINFLUENZA type 1 MC cause**

also…adenovirus, RSV, rhinovirus, etc. Diptheria rare

15% of children experience croup in childhood (MC 6 months - 6 yrs)

MC in fall/winter

49
Q

Clinical Manifestations of laryngotracheitis (croup)

A

Barking cough (seal-like, harsh)

stridor both inspiratory and expiratory (worsened by crying or agitating the child)

hoarseness due to laryngitis

dyspnea (especially worse at night) + URI Sx either preceding or concurrent fever

50
Q

Diagnosis of laryngotracheitis (croup)

A

clinical Dx (once epiglottitis and foreign body aspiration are excluded)

Frontal cervical radiograph: STEEPLE SIGN** (subglottic narrowing of trachea) - 50%

51
Q

Management of laryngotracheitis (croup)

A
  1. Mild: (no stridor at rest, no respiratory distress): cool, humidified air mist, hydration

Dexamethasone provides significant relief as early as 6 hours after single dose

  1. Moderate: (stridor at rest with mild to moderate retractions): Dexamethasone PO or IM + supportive treatment + nebulized Epi
    * should be observed for 3 - 4 hours of clinical intervention*
  2. Severe: (stridor at rest with marked retractions) Dexamethasone + nebulized Epi and hospitalization
52
Q

What is influenza?

A

Acute repiratory illnesses caused by Influenza A or B viruses. part of the orthomyxovirus family

A is associated with more severe, extensive outbreaks

spreads primarily via airborne respiratory secretions. outbreaks occur mainly in the fall/winter

53
Q

Clinical Manifestations of influenza

A

usually abrupt onset of a wide range of sx: HA, fever, chills, malaise, URI Sx, pharyngitis, pneumonia

Myalgias MC seen in legs and lumbosacral area

54
Q

Diagnosis of influenza

A

usually clinical

rapid influenza test (nasal swab) or viral culture can be performed

55
Q

Management of influenza

A

1. supportive mainstay tx in healthy patients (acetaminophen, rest)

  1. antivirals usually only needed in patients with high risk of complications

best if initiated within 48 hours of sx onset

A. Neuraminidase Inhibitors–oseltamivir (tamiflu) (vs. A and B)

B. Amantadine and Rimantidine (vs. A, not commonly used)

56
Q

Prevention of Influenza

A
57
Q

What is acute bronchitis?

A

acute bronchitis is defined by a cough which persists for MORE THAN 5 days

(fever is unusual; if your patient has a fever, consider PNA)

95% will be viral cause

58
Q

Although 95% of acute bronchitis is viral, some bacterial causes are…

A

M. Cattarhalis (common bacterial cause of acute bronchitis)

H. influenzae

S. pneumoniae

59
Q

What is the organism for tuberculosis and how can you get it?

A

Mycobacterium tuberculosis

chronic infection leading to granuloma formation

inhalation of airborne droplets ⇒ mycobacterium reaches the alveoli & are ingested by alveolar macrophages

60
Q

classic findings of tuberculosis

A

fever, night sweats, anorexia, weight loss

61
Q

What is secondary (reactivation) TB and where is the MC location?

A

reactivation of latent TB with waning immune defenses

5 - 10% lifetime incidence

MC localized in apex/upper lobes with cavitary lesions

THESE PATIENTS ARE CONTAGIOUS

62
Q

What is the screening test for TB and how is it interpreted?

A

Purified Protein Dertivative (PPD): examine 48 - 72 hours for transverse induration (redness is NOT considered positive)

POSITIVE IF:

> 5 mm: HIV +, or immunosuppressed (ex. prednisone 15 mg/day > 1 mnth)

close contacts of patients with active TB

CXR consistent with old/healed TB (calcified granuloma)

> 10 mm: all other high risk populations/high prevalence populations (prison, homeless)

> 15 mm: pts with no risk factors

63
Q

Diagnostic Studies in suspected cases of active TB

A

1. (GOLD STANDARD) Acid-fast smear & sputum cultures x 3 days: TB ruled out after 3 negative smears

2. CXR are indicated to excluse active TB (newly + PPD) and used as yearly screening in patients with known + PPD

64
Q

On a CXR where are the MC places for TB to occur? (reactivation, primary, and miliary TB)

A
  • Reactivation: apical (upper lobe)
  • Primary TB: middle/lower lobe
  • Miliary TB (widespread dissemination): CXR shows small millet-seed like nodular lesion (2 - 4 mm)
65
Q

Miliary TB is TB spread outside the lungs. What are some names for this?

A

Potts Dz is Tb to the spine

Scrofula is Tb to the cervical lymph nodes

66
Q

RIPE Treatment for TB

A

Rifampin (RIF) (orange-colored secretions)

Isoniazid (INH) (hepatitis, peripheral neuropathy prevented by pyridoxine B6)

Pyrazinamide (PZA) (hepatitis and hyperuricemia, photosensitive rash)

Ethambutol (EMB) (optic neuritis)

or Streptomycin (STM) (ototoxicity and nephrotoxicity)

INH prophylaxis given to children < 4 yo with exposure to contacts with active disease

67
Q

Mycobacterium avium complex (MAC)

A

Mycobacterium avium and intracellulare

Transmission: soil/water (NOT person to person)

Sx occur RARELY in immunocompetent pts.

seen in HIV when CD4 < 50**

68
Q

Clinical Manifestations of Mycobacterium Avium Complex (MAC)

A
  1. Pulmonary Infection: in immunocompetent: cough with sputum, fever, weight loss, bronchiectasis
  2. Disseminated: (in HIV pts) FUO, sweating, weight loss, fatigue, diarrhea, dyspnea, RUQ pain
  3. Lymphadenitis in children: cervical submandibular/maxillary
69
Q

Diagnosis and Management of Mycobacterium Avium Complex (MAC)

A

Dx: Acid-fast bacillus staining & culture

Management: Clarithromycin + Ethambutol at least 12 months

70
Q

What is another name for enterobiasis?

A

Pinworms!!

71
Q

Clinical Manifestations of enterobiasis (pinworms)

A

perianal itching especially nocturnal

(eggs are laid at night)

72
Q

Diagnosis and Mangement of enterobiasis (pinworms)

A

Dx: scotch tape test (early in AM) to look for eggs under a microscope

Management: Albendazole or Mebendazole

none are used in children < 2 yo

73
Q

What is Cystic Fibrosis?

A

autosomal recessive disorder that results in the abnormal production of mucus by almost all exocrine glands, causing obstruction of those glands and ducts

lungs are generally histologically normal at birth, but most pts develop pulmonary disease beginning in infancy or early childhood

non-pulmonary - pancreatitis and steatorrhea - pts will need supplementation of fat-soluble vitamins

the course is characterized by episodic exacerbations with infection and progressive decline in pulmonary function – mean survival is about 31 years

74
Q

Diagnosis and Management of Cystic Fibrosis

A

elevated quantitative sweat chloride test performed on two different days

increased NaCl > 60 mEq/L

a normal result does not exclude the diagnosis, if strongly suspected, DNA testing can provide definitive Dx

CXR may reveal hyperinflation, mucus plugging and focal atelactasis

Management: in the first few months of life, respiratory infection is common with Staph aureus and Haemophilus influenzae

AFTER THAT Pseudomonas aeruginosa becomes the major causative organism for infections

therapies focus on:

  • clearing the airway of secretions – chest physiotherapy
  • reversing bronchoconstriction
  • treating respiratory infections (treat for pseudomonas)
    *