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75 Cards in this Set
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(H/P) = rhinorrhea (i.e., nasal congestion & increased secretions), nonproductive cough; nasal and throat irritation, sneezing, possible fever, no exudates or productive cough
Labs = negative throat culture |
Upper respiratory infections (URI)
Inflammation of the upper airways most commonly caused by rhinovirus, coronavirus, or adenovirus |
Treatment = rest, analgesia, treat symptoms; antibiotics are NOT helpful |
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H/P = sore throat, tonsillar exudates (more common w/ bacterial infection), lymphadenopathy, possible nasal congestion; fever, red and swollen pharynx,
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Pharyngitis
Pharyngeal infection caused by group A β-hemolytic streptococci (“strep throat”) or common cold virus Complications = untreated infection can cause rheumatic heart disease or glomerulonephritis (characterized by a high antistreptolysin O titer) |
Labs = throat culture grows streptococcal species, and rapid streptococcal Ag test is + for strep throat; - culture suggests viral etiology Treatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time |
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H/P = similar to streptococcal pharyngitis, tonsillar exudates; ear pain, difficulty swallowing; possible high fever.
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Tonsillar infections
Spread of streptococcal pharyngitis to palatine tonsils leading to tonsillar inflammation (i.e., tonsillitis) Complications = airway compromise; abscess (requires intravenous [IV] antibiotics and surgical incision and drainage followed by tonsillectomy after resolution to prevent recurrence) |
Treatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time |
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H/P = myalgias, vomiting, diarrhea; high fevers (typically >100°F/37.8°C and can reach up to 106°F/41°C), arthralgias, sore throat, nasal congestion, nonproductive cough, nausea, lymphadenopathy
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Viral influenza
Generalized infection with URI symptoms caused by one of several influenza viruses |
Labs = serologic tests are definitive, but rarely required for diagnosis Treatment = treat symptoms; fluid intake important to replace losses from vomiting and diarrhea; self-limited (several days) but amantadine may shorten course of disease; elderly patients, health care workers, immunocompromised patients, and patients with lung disease should receive annual vaccine to reduce risk of infection |
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pain over infected sinuses, purulent nasal discharge, maxillary toothache pain; pain on palpation of affected sinuses, illumination test (i.e., light held close to sinuses) may detect congestion in frontal of maxillary sinuses, but is unreliable
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Sinusitis
Sinus (most maxillary)infection associated w/ allergic rhinitis, barotrauma, viral infection, prolonged nasogastric tube placement, or asthma Acute sinusitis is usually caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, viral infection Acute sinusitis can spread to CNS & cause meningitis if untreated. Chronic sinusitis (lasting >3 months) is usually caused by sinus obstruction, anaerobic infection; patients with diabetes mellitus (DM) predisposed to mucormycosis |
Radiology = radiograph shows opacification and fluid levels in affected sinuses; computed tomography (CT) is diagnostic; frequently radiologic tests are not needed because of clinical diagnosis Treatment = treat symptoms; amoxicillin × 2 weeks in acute cases and for 6–12 weeks in chronic cases; surgical drainage or correction of anatomic obstruction may be required for full cure |
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H/P = productive cough, sore throat; fever, wheezing, tight breath sounds
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Acute bronchitis
Inflammation of trachea and bronchi caused by spread of URI or exposure to inhaled irritants |
Labs = sputum culture only performed in persistent cases and is most commonly -; Radiology = chest x-ray (CXR) may show only mild congestion Treatment = self-limited if viral (most cases); patient groups with an increased risk of bacterial infection (e.g., smokers, elderly, patients with other lung disease) may be given antibiotics (e.g., fluoroquinolones, tetracycline, or erythromycin) |
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H/P = pleuritic chest pain; decreased breath sounds, dullness to percussion, tachypnea, productive or nonproductive cough, dyspnea, chills, night sweats, rales, wheezing, egophony (i.e., change in voice quality heard during auscultation over a consolidated region of lung), tactile fremitus
Labs = increased white blood cell count (WBC) (slight increase with viral cause, significant increase with bacterial or fungal cause) with left shift (more immature forms); + sputum culture |
Pneumonia
Infection of the bronchoalveolar tree can be caused by common nasopharyngeal bacteria (i.e., typical pneumonia) or bacteria, viruses, or fungi from the surrounding environment (i.e., atypical pneumonia); common causes vary by age group |
Treatment = viral pneumonia is self-limited and only requires supportive care; bacterial and fungal pneumonias require antibiotics (started as broad coverage and changed to pathogen-specific therapy as culture results become available Admission=elderly, multiple medical comorbidity, significant laboratory abnormalities, multilobar involvement, signs of sepsis |
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H/P=a non-productive cough be used for influenza A virus
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Viral Pneumonia
Viral (influenza, parainfluenza, adenovirus, cytomegalovirus, respiratory syncytial virus) Most common pneumonia in children; common in adults |
Treatment=Self-limited; amantidine may |
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H/P=pneumonia, high fevers, pleuritic pain, productive cough
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Streptococcus pneumoniae Most common pneumonia in adults; higher risk of infection in sickle cell patients
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Treatment=β-lactams, macrolides(azithromycin, clarithromycin, erythromycin) |
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H/P=pneumonia, slower onset
Patients with COPD; higher risk of infection in patients with sickle cell disease |
Haemophilus influenzae
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Treatment=β-lactams, TMP-SMX |
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H/P=pneumonia, abscess formation
Nosocomial pneumonia, immunocompromised patients |
Staphylococcus aureus
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Treatment=β-lactams |
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H/P=pneumonia, “Currant-jelly” sputum;
Alcoholics, patients with high risk of aspiration, patients staying in the hospital for extended amounts of time, sickle cell patients |
Klebsiella pneumoniae
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Treatment=Both cephalosporins and aminoglycosides (gentamicin, tobramycin) |
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H/P=pneumonia, Young adults, possible rash; + cold-agglutinin test
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Mycoplasma pneumoniae
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Treatment=Macrolides (azithromycin, clarithromycin, erythromycin) |
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H/P=pneumonia, rapid onset
Chronically ill and immunocompromised patients, patients with cystic fibrosis, nosocomial pneumonia |
Pseudomonas aeruginosa
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Treatment=Fluoroquinolones (ciprofloxacin), aminoglycosides, generation 3rd-cephalosporins |
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H/P=pneumonia Slow onset, nausea, diarrhea, confusion, or ataxia
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Legionella pneumophila
Associated with aerosolized water (air-conditioners) |
Treatment=Macrolides, fluoroquinolones |
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H/P=pneumonia, Slow onset, frequent sinusitis
More common in very young and elderly |
Chlamydia pneumoniae
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Treatment=Doxycycline, macrolides |
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H/P=pneumonia, Respiratory distress, lethargy
Neonates and infants |
Group B Streptococcus
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Treatment=β-lactams |
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H/P=pneumonia
Nosocomial pneumonia, elderly patients |
Enterobacter sp.
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Treatment=TMP-SMX |
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H/P=pneumonia, Less severe symptoms; subacute disease for initial history
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Fungi
Travelers to southwest U.S. (coccidioidomycosis), caves (histoplasmosis), or Central America (blastomycosis) |
Treatment=Antifungal agents (amphotericin B, ketoconazole) |
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H/P=pneumonia, Slow onset, GI symptoms
Immunocompromised patients (HIV) (CD4 count <200) |
Pneumocystis carinii (fungi-like)
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Treatment=TMP-SMX |
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H/P = cough, hemoptysis, dyspnea, weight loss, night sweats; fever, rales
Risk factors = immunosuppression, alcoholism, lung disease, DM, advanced age, homelessness, malnourishment, crowded living conditions, and close proximity to infected patients Radiology = CXR may show apical fibronodular infiltrates (reactivated disease), lower-lobe infiltrates (primary lesion), and calcified granulomas/lymph nodes (Ghon complexes) |
Tuberculosis (TB)
Pulmonary infection caused by Mycobacterium tuberculosis Following primary infection, disease enters inactive state; untreated infections can become reactivated (most active cases) and extend to extrapulmonary sites (i.e., miliary TB) |
Labs = + purified protein derivative (PPD) tuberculin skin test is screening test for exposure (followed by a CXR to look for signs of TB), anergy test (subcutaneous Candida preparation) in addition to a PPD to check for an appropriate immune response; + sputum acid-fast stain, + culture (may take weeks, so not useful in planning therapy); 1 bronchoscopy is considered equal to 3 sputum samples for specimen collection Treatment = respiratory isolation for any inpatient; report all diagnosed cases to local and state health agencies; multidrug treatment initially w/ isoniazid (INH), rifampin, pyrazinamide, & ethambutol followed by INH & rifampin for a total of 6 months; give vitamin B6 w/ INH to prevent peripheral neuritis (INH competes with vitamin B6 as a cofactor in neurotransmitter synthesis, so supplemental vitamin B6 helps offset this competition); give prophylactic INH to patients with an asymptomatic positive PPD who are immunocompromised, have a history of IV drug abuse (IVDA), are <35 years of age, a history of close contact with TB-infected people, or are indigent patients (reporting is unnecessary unless TB is diagnosed); monthly sputum acid-fast tests should be performed during therapy to confirm adequate treatment |
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H/P = acute dyspnea and pulmonary decompensation in setting of serious underlying condition; cyanosis, tachypnea (begins within 48 hours of initial insult), wheezing, rales, rhonchi
Labs = arterial blood gas (ABG) shows respiratory alkalosis, decreased O2 (caused by impairment of O2 transfer to pulmonary capillaries by pulmonary edema), decreased CO2 (caused by hyperventilation); other tests should reflect underlying pathology; Swan-Ganz catheterization shows wedge pressure <18 mm Hg; Pao2:Fio2 ratio will be <200 during mechanical ventilation |
Acute respiratory distress syndrome (ARDS)
Acute respiratory failure caused by sepsis, trauma, aspiration, near drowning, drug overdose, shock, or lung infection that is characterized by refractory hypoxemia, decreased lung compliance, and pulmonary edema, and carries a high mortality Etiology=ARDS: Aspiration/Acute pancreatitis/Air or Amniotic embolism, Radiation, Drug overdose/Diffuse lung disease/DIC/Drowning, Shock/Sepsis/Smoke inhalation. |
Radiology = bilateral pulmonary edema and infiltrates Treatment = treatment in intensive care unit with mechanical ventilation frequently required; mechanical ventilation should include positive end-expiratory pressure (PEEP), increased inspiratory times, and Fio2 adjusted to maintain O2 saturation (Sao2) >90%; underlying cause must be treated; keep fluid volumes low to prevent pulmonary edema; use of extracorporeal membrane oxygenation (ECMO) may improve outcome in severe cases |
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H/P = prolonged expiratory duration, accessory muscle use, cough, dyspnea, wheezing, chest tightness; tachypnea, tachycardia, decreased breath sounds, wheezing, possible pulsus paradoxus; cyanosis, decreased arterial O2 saturation (Sao2) on pulse oximetry, or difficulty talking in severe attacks
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Asthma
Reversible airway obstruction secondary to bronchial hyperactivity, acute airway inflammation, mucous plugging, and smooth muscle hypertrophy Exacerbations (i.e., sudden bronchoconstriction and airway inflammation) are triggered by allergens (e.g., dust, smoke, pollen, fumes, pet dander), URI, exercise, stress, β-antagonist drugs, aspirin (rare), and sulfites (rare) Risk factors = family history of asthma, allergies, atopic dermatitis, low socioeconomic status Disease can be worse in childhood and improve with age |
Labs = peak expiratory flow rate (PEFR) decreased and used along with clinical symptoms and frequency of medication use to classify disease as mild intermittent, mild persistent, moderate persistent, or severe (see Table 2-8); PFT show decreased FEV1, normal/elevated DLco Radiology = CXR shows hyperinflation Treatment=Inhaled short-acting β2-agonist IV corticosteroids if persistent during exacerbation. daily corticosteroid inhaler (+long long-acting β2-agonist, considerleukotriene inhibitor or theophylline) from Mild Persisent up |
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prolonged, nonresponsive asthma attack
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Status asthmaticus
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Treatment=aggressive bronchodilator therapy, corticosteroids, O2, and, possibly, intubation |
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H/P = productive cough, recurrent respiratory infections, dyspnea; wheezing, rhonchi
history of productive cough for 3 months of the year for >2 years |
Chronic bronchitis
Chronic bronchial inflammation associated with tobacco use (common) or chronic asthma (uncommon); occurs in continuum with emphysema as chronic obstructive pulmonary disease (COPD) “blue bloaters,” because secondary development of cor pulmonale causes cyanosis and peripheral edema; Complications = emphysema frequently results without smoking cessation |
Labs = PFTs show gradually worsening signs of obstructive disease as condition progresses Treatment = tobacco cessation, antibiotics given for URI because of the greater incidence of a bacterial etiology; bronchodilators during exacerbations |
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H/P = dyspnea, possible productive cough, morning headache; barrel-chested, pursed-lip breathing, prolonged expiratory duration, decreased heart sounds, decreased breath sounds, wheezing, rhonchi, accessory muscle use, jugular venous distension (JVD); exacerbations present with worsening symptoms
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Emphysema (later stage—COPD)
Long-term tobacco use leads to chronic bronchoalveolar inflammation associated with release of proteolytic enzymes by neutrophils and macrophages; destruction of alveoli and bronchioles results with panacinar airspace enlargement and a decreased capillary bed Less common form (appears at younger age) caused by α1-antitrypsin deficiency common form of emphysema has a centrilobular distribution, whereas the form associated with α1-antitrypsin deficiency has a panlobular distribution. |
Labs = PFTs show decreased FEV1, decreased FEV1/FVC, increased total lung capacity (TLC), decreased PEFR; ABG during acute exacerbations shows decreased O2, increased CO2 (beyond a baseline increase already seen in these patients) Radiology = CXR shows flat diaphragm, hyperinflated lungs, subpleural blebs and bullae (i.e., small fluid-filled sacs), and decreased vascular markings Treatment = smoking cessation; supplemental O2; inhaled, short-acting β2-agonists; inhaled anticholinergics; inhaled corticosteroids and long-acting β2-agonists may be useful in severe cases; antibiotics given for respiratory infections; pneumococcal and influenza vaccines important to reduce infection risk; enzyme replacement may have a role in α1-antitrypsin deficiency therapy; lung transplant may be an option in late severe disease |
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H/P = copious sputum, persistent, productive cough; hemoptysis, frequent respiratory infections, dyspnea; wheezing, rales, and hypoxemia
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D. Bronchiectasis
Permanent dilation of small and medium bronchi because of destruction of bronchial elastic components Occurs secondary to chronic airway obstruction, chronic tobacco use, TB, fungal infections, severe pneumonia, or cystic fibrosis Complications = cor pulmonale, massive hemoptysis, abscess formation |
Radiology = multiple cysts and bronchial crowding seen on CXR; CT shows dilation of bronchi, bronchial wall thickening, bronchial wall cysts Treatment = pulmonary hygiene (e.g., hydration, sputum removal), chest physical therapy; antibiotics given when sputum production increases; inhaled β2-agonists and corticosteroids may reduce symptoms; resection of severely diseased regions of lung indicated for hemorrhage, substantial sputum production, or inviability |
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H/P = possibly asymptomatic; hemoptysis, cough, dyspnea, pleuritic chest pain, fatigue, weight loss, frequent pulmonary infections;
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Lung cancer
Most frequently associated with tobacco use (~90% of cases); also can be caused by occupational exposures (e.g., smoke, asbestos) Complications = poor prognosis (~10% 5-yr survival); recurrence common for primary tumors |
Radiology = initially seen on CXR or CT as pulmonary nodule; bronchoscopy with biopsy and brushings or fine needle aspiration of lesion are diagnostic Treatment = use of surgical resection, chemotherapy, and/or radiation therapy based on type of lung cancer (large cell, squamous cell, or adenocarcinoma vs. small cell) and staging of disease (based on local extension, lymph node involvement, and presence of metastases) (see Table 2-11) |
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miosis, ptosis, and anhidrosis
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Horner's syndrome
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Horner's syndrome plus brachial plexus involvement
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Pancoast's syndrome
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obstruction of venous drainage through superior vena cava and associated head swelling and CNS symptoms
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Superior vena cava syndrome
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Lung Cancer, Central
Cavitary lesions; direct extension to hilar lymph nodes Paraneoplastic Syndromes= Hypercalcemia, Dermatomyositis |
Squamous cell carcinoma
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Treatment=Chemotherapy as primary, Radiation Therapy as adjuvant |
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Lung Cancer,Peripheral
Wide metastases; can be caused by asbestos; pleural effusions show increased hyaluronidase levels; bronchiolar cancer is subtype that is low grade and occurs in single nodules Paraneoplastic Syndromes= DIC, Thrombophlebitis,, Microangiopathic hemolytic anemia Dermatomyositis |
Adenocarcinoma
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Treatment for all non-small: no lymph node involvement beyond ipsilateral hilar nodes, No mediastinal invasion, no metastases->Surgical resection, radiation as primary or postop adjuvant, chemo as adjuvant |
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Lung Cancer, Central
Rapidly growing; early distant metastases; several paraneoplastic syndromes Paraneoplastic Syndromes= Cushing's syndrome, Syndrome of inappropriate ADH secretion (SIADH), Ectopic growth hormone and ACTH secretion, Peripheral neuropathy, Subacute cerebellar degeneration, Eaton-Lambert syndrome (similar presentation to myasthenia gravis), Subacute sensory neuropathy, Limbic encephalitis, Dermatomyositis |
Small cell carcinoma
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Treatment for all non-small: has extension to ipsilateral mediastinal nodes, No mediastinal invasion or metastases->radiation as primary, surgery if tumor shrinik, chemo as induction for surgery or adjuvant |
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Lung Cancer, Peripheral
Late distant metastases, early cavitation Paraneoplastic Syndromes=Gynecomastia, Dermatomyositis |
Large cell carcinoma
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Treatment for all non-small: Mediastinal invasion, distant nodes, and/or metastases-> chemo or radiation as palliative |
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H/P = hoarseness that worsens with time (over several weeks), dysphagia, ear pain, hemoptysis; laryngoscopy may visualize mass and airway obstruction
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Laryngeal cancer
Squamous cell cancer of the larynx associated with tobacco and alcohol use |
Labs = biopsy is diagnostic Radiology = magnetic resonance imaging (MRI) or CT with contrast detects soft tissue mass; PET may be useful for detecting lesions earlier in disease course Treatment = partial or total laryngectomy used to remove lesions confined to larynx; radiation therapy can be used in conjunction with surgery or as sole therapy in extensive lesions; advanced cases may require combination of surgery, radiation, and chemotherapy to resect lesion while preserving surrounding structures |
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H/P = progressive exercise intolerance, dyspnea; dry crackles, JVD, tachypnea, and possible digital clubbing
patients >50 years of age Labs = PFT will show restrictive lung disease characteristics (e.g., FEV1/FVC normal, decreased FVC, decreased TLC, decreased compliance); bronchioalveolar lavage shows increased polymorphonuclear (PMN) cells; lung biopsy demonstrates extensive fibrosis and loss of parenchymal architecture Radiology = CXR shows reticulonodular pattern and “honeycomb” lung in advanced cases; CT will show lung fields with “ground glass” appearance |
Idiopathic pulmonary fibrosis (IPF)
Inflammatory lung disease causing lung fibrosis; Complications = progressive lung fibrosis with frequent mortality within 5 years; most patients do not survive sufficiently long to receive a lung transplant |
Treatment = corticosteroids combined with either azathioprine or cyclophosphamide are helpful in some patients (follow PFTs to evaluate effectiveness); worsening PFTs should indicate need to change drug regimen; lung transplant is frequently indicated |
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H/P = cough, malaise, weight loss, dyspnea, arthritis (knees, ankles), chest pain; fever, erythema nodosum (i.e., tender red nodules on shins and arms), lymphadenopathy, vision loss, cranial nerve palsies
Labs = increased serum angiotensin-converting enzyme (ACE), increased calcium, hypercalciuria, increased alkaline phosphatase, decreased WBC, increased erythrocyte sedimentation rate (ESR); PFT show decreased FVC, decreased DLco Radiology = CXR shows bilateral hilar lymphadenopathy, pulmonary infiltrates (ground glass appearance) |
Sarcoidosis
Systemic disease characterized by noncaseating granulomas, hilar adenopathy, pulmonary infiltrates, and skin lesions; unknown etiology Risk factors = blacks > whites; females > males; most frequently occurs between 10 and 40 years of age Patients with sarcoidosis frequently show anergy (no reaction) to a skin test or PPD. |
Treatment = occasionally self-resolving; corticosteroids in chronic cases; cytotoxic drugs can be used with failure of steroid therapy; lung transplantation is rarely required (only in severe cases) |
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H/P = symptoms begin when significant pulmonary fibrosis has occurred (several years between exposure to onset of symptoms is common); cough, dyspnea on exertion, heavy sputum production; rales and wheezing are heard on auscultation, digital clubbing
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Pneumoconioses
Interstitial lung diseases that result from long-term occupational exposure to substances that cause pulmonary inflammation |
Labs = PFT show a restrictive pattern Radiology = CXR shows multinodular opacities; CT shows signs of pulmonary fibrosis Treatment = usually, no successful treatments are available for these conditions; prevention (e.g., proper air filters, following safe-handling recommendations) is vital to avoiding disease |
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H/P = hemoptysis, dyspnea, recent respiratory infection
Labs = + anti-GBM Ab; PFT show restrictive pattern, but increased DLco (caused by the presence of Hgb in alveoli); urinalysis shows proteinuria and granular casts; renal biopsy shows crescentic glomerulonephritis and IgG deposition along glomerular capillaries |
Goodpasture's syndrome
Progressive autoimmune disease of lungs and kidneys caused by anti-glomerular basement membrane (anti-GBM) antibodies and characterized by intra-alveolar hemorrhage and glomerulonephritis |
Radiology = CXR shows bilateral alveolar infiltration Treatment = plasmapheresis to remove auto-antibodies; corticosteroids and immunosuppressive agents |
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H/P = ulcerations of nasopharynx, fever; hemoptysis, dyspnea, myalgias, chronic sinusitis; additional symptoms from renal (e.g., mild hematuria), CNS (e.g., hearing loss, sensory neuropathy, cranial nerve dysfunction), ophthalmologic (e.g., conjunctivitis, proptosis, corneal ulceration, diplopia), and cardiac (e.g., arrhythmia) involvement
Labs = + cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA); biopsy shows noncaseating granulomas; renal biopsy detects vasculitic process |
Wegener granulomatosis
Rare disease with granulomatous inflammation and necrosis of lung and other organ systems Caused by systemic vasculitis that mainly affects lung and kidney causing formation of noncaseating granulomas and destruction of lung parenchyma Complications = rapidly fatal if untreated |
Treatment = cytotoxic therapy (e.g., cyclophosphamide), corticosteroids |
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Pneumoconioses
Working with insulation, construction, demolition, building maintenance, automobiles |
Asbestosis
Complications=Increased risk of malignant mesothelioma and lung cancer; synergistic effect with tobacco |
Labs=pleural biopsy show asbestos fibers Radiology= Multinodular opacities, pleural effusions, blurring of heart/diaphragm; chest CT shows linear pleural/parenchymal fibrosis |
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Pneumoconioses
Mining, pottery making, sandblasting, cutting granite |
Silicosis
Complications=Increase risk of TB infection; progressive fibrosis |
Radiology=Small apical nodular opacities; hilar adenopathy |
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Pneumoconioses.
Coal mining |
Coal worker's disease
Complications=Progressive fibrosis |
Radiology=Small apical nodular opacities |
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Pneumoconioses
Electronics, ceramics, tool, die manufacturing |
Berylliosis
Complications=Increased risk of lung cancer; |
Labs=Pulmonary edema, diffuse granuloma formation Radiology=Diffuse infiltrates; hilar adenopathy Treatment=may need chronic corticosteroid treatment to maintain respiratory function |
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H/P = sudden dyspnea, pleuritic chest pain, cough, syncope, hemoptysis, feeling of impending doom; fever, tachypnea, tachycardia, cyanosis, loud S2, decreased breath sounds over regions of effusion
Labs = increased A-a gradient; increased D-dimer; ABG shows increased CO2, decreased O2 (<80 mm Hg), ventilation-perfusion scan (V/Q scan) may show areas of mismatch ECG = tachycardia, may show S wave in lead I and T-wave inversion in lead V3 |
Pulmonary embolism (PE)
Occlusion of pulmonary vasculature by a dislodged thrombus Increasing pulmonary artery pressure caused by occlusion leads to right-sided heart failure, hypoxia, and pulmonary infarction Risk factors = 7 Hs: Heredity (genetic hypocoagulability), History (prior DVT or PE), Hypomobility (fracture, prolonged travel, surgery, obesity), Hypovolemia (dehydration), Hypercoagulability (cancer, smoking), Hormones (pregnancy, oral contraceptive pill [OCP] use), and Hyperhomocysteinemia. |
Radiology = CXR may be normal or may show pleural effusion or wedge-shaped infarct; pulmonary angiography is diagnostic, but a higher risk study; spiral CT may detect proximal PE; ventilation-perfusion (V/Q) scan can detect areas of ventilation-perfusion mismatch A positive or negative V/Q scan is diagnostic or rules out PE, but an equivocal scan indicates need for angiography Treatment = supplemental O2 to maximize saturation; IV fluids or cardiac pressors as needed for hypotension; anticoagulate initially with either low molecular weight heparin (LMWH) or unfractionated heparin (titrated for PTT 1.5–2.5 times normal); patients treated with unfractionated heparin need to be converted to either LMWH or warfarin (given to achieve goal international normalized ratio [INR] 2 -3) for 3–6 months; inferior vena cava filter can be placed if anticoagulation is contraindicated; thrombolysis may be considered for patients with massive PE or those with no cardiac contraindications, recent trauma, or surgery |
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H/P = dyspnea, fatigue, deep chest pain, cough, syncope, cyanosis; digital clubbing, loud S2, JVD, hepatomegaly
Labs = increased red blood cell count (RBC) and WBC ECG = right ventricular hypertrophy Radiology = CXR shows large pulmonary artery and large right ventricle; echocardiogram useful for measuring pulmonary artery pressure noninvasively and detecting valvular disease; cardiac catheterization is the gold standard test for measuring pressures, but carries greater risks than other studies; PFTs may be useful in diagnosing underlying pulmonary disease |
Pulmonary hypertension
Increased pulmonary artery pressure caused by PE, valvular disease, left-to-right shunts, COPD, or idiopathic causes Idiopathic pulmonary hypertension has a high mortality rate within a few years of diagnosis |
Treatment = treat underlying condition; supplemental O2 helps maintain blood oxygenation; vasodilators indicated for idiopathic and pulmonary causes to decrease pulmonary vascular resistance; anticoagulants indicated in patients with idiopathic, embolic, or cardiac causes to decrease risk of pulmonary thrombus formation |
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H/P = orthopnea, paroxysmal nocturnal dyspnea, dyspnea; tachycardia, frothy sputum, wheezing, rhonchi, rales, dullness to percussion, peripheral edema, S3 or S4 heart sound, hypertension
Labs = increased brain natriuretic peptide (BNP) or abnormal cardiac enzymes help elucidate a cardiac cause ECG = T-wave abnormalities or QT prolongation are common changes and can occur suddenly with acute onset |
Pulmonary edema
Increased fluid in lungs caused by increased pulmonary venous pressure and hydrostatic leak of fluid from vessels Caused by left-sided heart failure, myocardial infarction (MI), valvular disease, arrhythmias, ARDS(pulmonary wedge pressure <18 mm Hg). A pulmonary wedge pressure measured with a Swan-Ganz catheter is suggestive of a cardiac cause for pulmonary edema if >18 mm Hg |
Radiology = CXR shows fluid throughout lungs, cephalization of vessels (i.e., increased vascular markings in upper lung fields), Kerley B lines (i.e., prominent horizontal interstitial markings in lower lung fields) Treatment = treat underlying condition; diuretics, salt restriction, O2, morphine, vasodilators; nesiritide improves outcomes in cases with a cardiac cause; pressors may be required to improve cardiac output if perfusion is inadequate; Swan-Ganz catheter placement useful for monitoring response to therapy |
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H/P = possibly asymptomatic; dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophony
Radiology = CXR shows blunting of costophrenic angles; decubitus CXR can demonstrate whether fluid is loculated or free flowing; CT is useful for measuring pleural thickness, distinguishing a discrete collection from a diffuse one (e.g., abscess vs. empyema) |
Pleural effusion
Serous or lymphatic fluid collection in pleural space is classified according to protein and lactate dehydrogenase (LDH) content and is caused by changes in hydrostatic and oncotic pressure (transudative), inflammation (exudative), or lymphatic duct rupture (lymphatic) 1/4 of pleural effusions are associated with neoplasm |
Labs = pleural fluid analysis used for protein and LDH levels (i.e., transudate vs. exudates), glucose (low in TB, malignancy, autoimmune diseases), pH (acidic in malignancy, TB, empyema), amylase (high in pancreatitis, esophageal rupture, some malignancies), triglycerides (high in thoracic duct rupture), complete blood cell count (CBC), Gram stain, and cytology Treatment = treat underlying condition; relieve pressure on lung with thoracocentesis and chest tube placement; for cases with empyema (i.e., effusion of pus due to infection), a chest tube is required; if recurrent malignant effusion occurs, use pleurodesis (talc or other irritant) to scar the pleural layers together |
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Pleural effusion
Pleural: Serum Protein Ratio <0.5; Pleural: Serum LDH Ratio <0.6; Total Pleural Protein <3 g/dL |
Transudate
etiology=CHF, cirrhosis, kidney diseases (nephrotic syndrome) |
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Pleural effusion
Pleural: Serum Protein Ratio >0.5; Pleural: Serum LDH Ratio >0.6; Total Pleural Protein >3 g/dL |
Exudate
etiology=Infection, cancer, vasculitis |
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H/P = unilateral chest pain, dyspnea; decreased chest wall movement, unilateral decreased breath sounds, increased resonance to percussion, decreased tactile fremitus; respiratory distress, decreased Sao2, hypotension, JVD, or tracheal deviation suggest tension pneumothorax
Radiology = CXR shows lung retraction and mediastinal shift away from affected side; tension PTX will demonstrate tracheal deviation |
Pneumothorax (PTX)
Collection of air in pleural space that predisposes patient to pulmonary collapse Can occur spontaneously (less common) or secondary to trauma or a pulmonary medical condition (more common) |
Treatment Small (<15% lung field) PTX may resolve with supplemental O2 only Larger (>15%) PTX requires chest tube placement Open PTX with small wound is treated with chest tube and occlusive dressing Open PTX with larger wounds should be treated with attempted closure and should carry a low threshold for intubation Tension pneumothorax requires immediate needle decompression (4th or 5th intercostal space at the maxillary line) and chest tube placement Recurrent pneumothorax may require pleurodesis |
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H/P = dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophony
Labs = thoracocentesis shows bloody effusion |
Hemothorax
Collection of blood in pleural space caused by trauma, malignancy, TB, or pulmonary infarction Complications = thrombi formation, fibrosis can occur if blood is not drained from pleural space |
Radiology = CXR resembles that for pleural effusion (i.e., lung retraction, mediastinal shift from affected side) Treatment = supplemental O2; chest tube placement; treat underlying cause |
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H/P = nonpleuritic chest pain, dyspnea; dullness to percussion over lung bases, palpable chest wall mass, scoliosis toward lesion
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Malignant mesothelioma
Uncommon tumor occurring on visceral pleura or pericardium with very poor prognosis Increased incidence with asbestos exposure (occurs 20 years after exposure) |
Labs = pleural biopsy is usually diagnostic; thoracocentesis of an associated pleural effusion can be used for cytology studies Radiology = CXR shows pleural thickening, pleural effusion; chest CT can display extent of local disease; PET scan can be used to detect extrathoracic disease Treatment = extrapleural pneumonectomy with adjuvant chemotherapy and radiation therapy; chemotherapy alone used for unresectable disease |
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H/P = fatigue, daytime sleepiness, snoring, gasping or choking during sleep, morning headaches or confusion, impaired daytime function because of sleepiness; obesity common, anatomic abnormalities of palate or pharynx may be visible
Labs = Epworth sleepiness scale is useful for predicting likelihood of sleep apnea as cause for daytime somnolence (score >10 common in sleep apnea); polysomnography is definitive test that measures Apnea Index (AI, average apneic episodes per hour), Sao2, and number of arousals |
Sleep apnea
Episodic cessation of airflow during sleep leading to desaturations and frequent arousals Types Obstructive: obstruction of upper airway during sleep with continued respiratory effort; most often associated with obesity or abnormal pharyngeal anatomy Central: loss of central respiratory drive leads to cessation of airflow and respiratory effort Mixed: combines both obstructive and central characteristics Risk factors = obesity, sedative use; males more than females Etiology is unknown, but may be linked to abnormal feedback control during sleep or decreased sensitivity of upper airway muscles to stimulation |
Treatment Obstructive = consider weight loss (possibly bariatric surgery) and stop sedative use; continuous positive airway pressure (CPAP) is helpful in chronic cases to maintain airway patency; surgical correction of tonsillar hypertrophy, polyp removal, correction of congenital upper airway deformities, or tracheostomy may be necessary in severe or refractory cases Central = respiratory stimulants; phrenic nerve pacemaking may be needed in severe cases Bariatric surgery is associated with resolution of sleep apnea in 86% of cases. |
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H/P = asymptomatic if mild or slow development; pleuritic chest pain, dyspnea; fever, decreased breath sounds, dullness to percussion over affected area
Radiology = CXR will show fluffy infiltrates in mild cases and lobar collapse in cases of airway obstruction |
Atelectasis
Localized alveolar collapse; common after surgery (especially abdominal) and anesthesia (generally not clinically serious); can also occur in asthmatics, after foreign body aspiration, or from mass effect (e.g., tumors, pulmonary lesions, or lymphadenopathy) If atelectasis lasts >72 hr, pneumonia is likely to develop. |
Treatment = inspiratory spirometry, ambulation, and inpatient physical therapy are important for prevention in the hospital and postoperatively; severe cases require upper airway suctioning or bronchoscopy with deeper suctioning |
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Mechanical Ventilation
Use=General anesthesia, overdose Patient=No effort |
Mode=Controlled mechanical ventilation (CMV)
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Machine Determines and automatically delivers tidal volume (TV) and rate |
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Mechanical Ventilation
Use=Weaning patient from ventilator Patient=Can breathe spontaneously between mechanical breaths |
Mode=Intermittent mandatory ventilation (IMV)
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Machine Determines and automatically delivers TV and rate |
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Mechanical Ventilation
Use=More comfortable for patient because of attempted synchronization; frequently used in place of IMV Patient=Can breathe spontaneously between mechanical breaths |
Mode=Synchronized intermittent mandatory ventilation (SIMV)
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Machine Machine tries to synchronize rate with patient-initiated breaths; automatically delivers TV and rate |
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Mechanical Ventilation
Use=Used when patient is more awake and in progressive weaning Patient driven unless no attempts to breathe (backup rate) |
Mode=Assist-control ventilation (AC)
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Machine senses patient's attempt to breathe and delivers full preset TV; backup rate if no spontaneous breaths |
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Mechanical Ventilation
Use=Used when patient relies less on ventilator; intubation not required Patient does all breathing |
Mode=Continuous positive airway pressure (CPAP)
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Machine maintains airway patency to decrease work of breathing |
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H/P = barking cough, inspiratory stridor, dyspnea, nasal congestion; fever, mild pharyngeal erythema, lymphadenopathy; respiratory distress in severe cases
Radiology = neck radiographs may show subglottic narrowing of airway (i.e., steeple sign) |
Croup
Acute inflammation of larynx caused by parainfluenzae virus type 1; less commonly, by parainfluenzae virus types 2 and 3, respiratory syncytial virus (RSV) influenza virus, rubeola, adenovirus, or Mycoplasma pneumoniae 3 Ss: Seal-bark cough, Subglottic swelling, and Stridor. |
Treatment = supportive care (e.g., hydration, humidified air, rest, analgesia); aerosolized epinephrine and inhaled corticosteroids can be used in severe cases to decrease pharyngeal inflammation; with concerns for respiratory distress, the child should be admitted for observation If child develops stridor at rest, hospitalization and respiratory monitoring is needed. |
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H/P = dysphagia, muffled voice, drooling, soft stridor, anxiety from symptoms; sudden high fever, inspiratory retractions; child may lean forward with hands on knees to aid breathing; erythematous and swollen epiglottis
Radiology = neck radiographs show swollen opacified epiglottis that partially obstructs the airway (i.e., thumbprint sign); laryngoscope (only used in controlled situations) can visualize red and swollen epiglottis |
Epiglottitis
Rapidly progressive infection of epiglottis and surrounding tissues that can cause airway obstruction Most common in children from 2–7 years of age Caused by Haemophilus influenzae type B (Hib) infection; can also be caused by streptococcal or other H. influenzae bacteria |
Labs = culture from swab of epiglottis can determine causative bacteria (should only be performed if patient intubated) Treatment = keep child calm; admit for close observation and respiratory monitoring; unless airway obstruction is mild, intubate (nasotracheal) to maintain airway patency; antibiotics for 7–10 days; airway obstruction preventing intubation requires emergent tracheostomy In cases of suspected epiglottitis, examine the patient's throat only in a setting in which prompt intubation is possible because examination of the patient's throat can lead to additional throat irritation and resulting occlusion. |
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H/P = nasal congestion, cough, respiratory distress; wheezing, fever, tachypnea, crackles, prolonged expiration, hyperresonance to percussion
Radiology = CXR shows hyperinflation of lungs and patchy infiltrates |
Bronchiolitis
Viral infection of bronchioles caused by RSV (most cases) or parainfluenzae virus type 3 (less common) Most commonly occurs in winter and spring; usually found in children <2 years of age Complications = increased risk of developing asthma |
Treatment = adequate hydration, humidified air, inhaled corticosteroids and β2-agonists; ribavirin can be used in severe cases to shorten disease course; children with respiratory distress or hypoxemia should be admitted for observation and respiratory monitoring |
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H/P = presentation within 2 days of birth; cyanosis, nasal flaring, expiratory grunting, intercostal retractions, respiratory rate >60 breaths/min, crackles, decreased breath sounds
Radiology = CXR shows bilateral atelectasis with ground glass appearance and decreased lung volumes |
Respiratory distress syndrome of the newborn
Preterm infants (e.g., 24–37 wks' gestation and especially before 30 wks' gestation) have surfactant deficiency because of lung immaturity that leads to decreased lung compliance, atelectasis, and respiratory failure Complications = increased risk of developing asthma in childhood compared with other children |
Labs = ABG shows increased CO2, decreased O2; amniotic fluid analysis (see Figure 2-9) not usually helpful, but may guide treatment between 34 and 37 wks' gestation by determining fetal lung maturity with the amniotic lecithin:sphingomyelin ratio (always treat for <34 weeks, treatment typically unnecessary for >37 weeks) Treatment = maternal administration of corticosteroids before initiation of labor helps to speed fetal lung maturation; neonatal intensive care unit (ICU) admission appropriate for close observation; supplemental O2 and surfactant replacement therapy mainstays of therapy; intubation should be performed for any neonate not responding to treatment or requiring high levels of O2 to maintain adequate Sao2 |
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H/P = meconium stained-amniotic fluid seen during delivery; cyanosis, intercostal retractions; distended chest, tachypnea
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Meconium aspiration syndrome
Aspiration of meconium (i.e., fetal stool passed into amniotic sac) predelivery causing obstruction of airways and pneumonia Complications = pulmonary hypertension can develop if not promptly treated; increased risk of developing asthma during childhood |
Labs = consider blood culture to rule out sepsis Treatment = suction nose, mouth, and upper airway at birth; supplemental O2; intubate for worsening respiratory distress; surfactant therapy may be useful for improving respiratory function; consider empiric antibiotic therapy if concerned for development of pneumonia |
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H/P = recurrent pulmonary infections (e.g., Pseudomonas, S. aureus), dyspnea, hemoptysis, chronic sinusitis, cough, meconium ileus at birth, steatorrhea, failure to thrive; cyanosis, digital clubbing, esophageal varices, rectal prolapse
Labs = decreased serum Na; sweat test shows increased Na and increased Cl (>60 mEq/L in children, >80 in adults); genetic testing can locate mutation in CF transmembrane conductance regulator (CFTR) gene in suspected cases or in carriers of the gene considering pregnancy |
Cystic fibrosis (CF)
Autosomal recessive disorder caused by defect in chloride-pumping channel in exocrine glands; ducts of exocrine glands (e.g., lungs, pancreas, reproductive glands) become clogged with thick secretions Presents in childhood and universally fatal, but proper treatment may allow survival into late 20s or early 30s Affects both pulmonary (recurrent infections, chronic sinusitis) and gastrointestinal systems (pancreatic enzyme deficiencies, malabsorption) Risk factors = whites at higher risk than other races |
Treatment = deoxyribonuclease (DNase) aids in decreasing the viscosity of secretions; chest physical therapy helps to clear secretions; bronchodilators, non-steroidal anti-inflammatory drugs (NSAID), antibiotics for any suspected pulmonary exacerbation or infection; supplemental pancreatic enzymes and vitamins A, D, E, and K given for malabsorption |
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Tidal volume (TV)
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Inspiratory volume during Normal respiratioN
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Inspiratory reserve volume (IRV)
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Air volume beyond normal tidal volume that is filled during maximal inspiration
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Inspiratory capacity (IC)
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Total inspiratory air volumE considering both tidal volume and inspiratory reserve volume (IC = TV + IRV)
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Expiratory reserve volume (ERV)
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Air volume beyond tidal volume that can be expired during normal respiration
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Residual volume (RV)
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Remaining air volume left in lung ollowing maximal expiration
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Functional reserve capacity (FRC)
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Air volume remaining in lungs after expiration of tidal volume (FRC = RV + ERV)
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Functional vital capacity (FVC)
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Maximal air volume that can be inspired and expired (FVC = IC + ERV)
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Total lung capacity (TLC)
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Total air volume of lungs (TLC = FVC + RV)
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