Pulmonary 2 Flashcards
Laryngotracheobronchitis etiology?
Parainfluenza virus type I (60% of cases) also types II-IV
adenovirus; respiratory syncytial virus RSV; rhinovirus; coxsackie virus; echovirus
Laryngotracheobronchitis SSxs?
prodrome - mild URI with coryza, nasal congestion, sore throat, cough, low-grade fever
then – developing hoarse voice and harsh, brassy, seal bark-like cough with possible stridor (often at night)
Laryngotracheobronchitis PE?
distress from minimal to severe respiratory failure due to airway obstruction
Mild cases: examination at rest usually is normal; may be mild expiratory wheezing
More severe cases: inspiratory stridor at rest with nasal flaring, suprasternal and intercostals retractions.
Lethargy or agitation from hypoxemia
Tachypnea, tachycardia out of proportion to fever, lethargy, pallor
Course: usually peaks over 3-5d, resolves in 4-7d.
Laryngotracheobronchitis Labs/Imaging?
leukocytosis with left shift
A-P X-ray of the C-spine shows “steeple sign”
Prognosis: self-limited disease, but can very rarely result in death from complete airway obs
Laryngotracheobronchitis DDX?
Other causes of SOB with stridor:
Epiglottitis - hot potato voice, high fever (emergency, don’t try to visualize!)
foreign body - no hx URI or fever
retropharyngeal abscess - swelling at back of throat, see on lateral xray
diphtheria - grayish membrane over pharynx/larynx
Acute bronchitis Etiology?
Influenza A and B, parainfluenza, coronaviris (types 1-3), rhinovires, RSV
Rarely: H flu, Mycoplasma pneumoniae, Chlamydophila pneumoniae, Pertussis
Acute bronchitis SSxs?
Cough > 5 days with sputum production (often starting with URI sx)
Sputum may be purulent from sloughing tracheobronchial and inflammatory cells
Acute bronchitis PE?
Generally afebrile or low grade fever
Wheezing suggests bronchospasm
Rhonchi indicates mucus in upper airways, clear with cough
Normal percussion, no changes in transmitted voice tests
Acute bronchitis DDX?
chronic bronchitis, pneumonia, post-nasal drip, GERD, asthma
Pneumonia pathophysiology stages?
congestion
red hepatization
gray hepatization
resolving
Community acquired pneumonia pathogens?
VIRAL: RSV, parainfluenza virus, Influenza A/B, adenovirus
BACTERIAL: S pneumoniae, H flu, S aureus, Group A strep, M catarrhalis, Klebsiella pneumoniae (rare) Legionella spp., M pneumoniae, Chlamydophila pneumoniae, P. aeruginosa,
Hospital acquired pneumonia pathogens?
E coli, Klebsiella, enterobacter spp, P aeruginosa, MRSA, H flu
Bacterial pneumonia SSxs?
cough with thick greenish or rust-colored mucus
SOB
rapid breathing
sharp pleuritic pain–worse with deep breaths
abdominal pain
severe fatigue
May be profuse sweating and mental confusion..
Bacterial pneumonia PE?
Patient looks sick high fever tachypnea tachycardia or bradycardia cyanosis bronchial breath sounds wheezes, rhonchi, and/or crackles positive egophony increased tactile fremitus dullness to percussion pleural friction rub (possible) pallor altered mental status in severe cases
Bacterial Pneumonia workup?
CXR (dense shadow with well-demarcated borders), CBC, CMP, CT, bronchoscopy, thoracentesis
What conditions should be considered if pneumonia is unresolving?
Comorbidities: alcoholism, COPD, CHF, CKD, Malignancy, DM, HIV, Advancing age >65
Aggressive organism: Klebsiella, Legionella, S Aureus
Drug-resistant organism: eg S pneumoniae
Non-bacterial agents: TB, fungi
Underlying neoplastic dz
Misdiagnosis of: connective tissue dz, sarcoidosis, pulmonary embolism, pulmonary edema, drug-induced lung dz
What are possible complications of pneumonia?
lung abscess, pleural effusion, empyema
Streptococcus pneumoniae characteristics?
60-80% of bacterial pneuomia
Sxs – rigors, severe shaking, pleuritic chest pain, blood/rust colored sputum
Prognosis: overall mortality 5%
Aged 2 years to 50 years- 90-95% survive
if < 1 yr., > 60 yr., positive blood culture, 2 or more lobes involved, use aggressive tx
Complications: meningitis, endocarditis
REFER if: BUN >70, WBC <5000, other underlying dz. (heart, COPD)
Klebsiella pneumoniae characteristics?
Gram negative bacilli causes aggressive necrotizing lobar pneumonia
Risk factors: alcoholism, malnutrition, DM, recent tx with antibiotic, COPD, >40yo, hospitalization
Prognosis: 40-60% if untreated
Sx: Cough, fever, pleuritic chest pain, dyspnea; spreads quickly
Extremely viscid exudates that can’t be expectorated—“currant jelly” sputum
Relative bradycardia: pulse rate does not increase as much with fever (usually with every degree in temp rise is inc 10 in heart rate)
Haemophilus influenza pneumonia characteristics?
Most commonly arises in the winter and early spring
Risk factors: asthma, COPD, smoking, immunocompromised
Sxs – green sputum
Staphylococcus aureus pneumonia characteristics?
Most common in IV drug abusers and other individuals with debilitations infx often spread hematogenously to the lungs from contaminated injection sites.
Legionella pneumophila pneumonia characteristics?
gram negative bacterium - “Legionnaire’s disease”
outbreaks from aerosolized organisms from air conditioning system or contaminated shower heads, more often in hotels and hospitals
common in elderly, smokers, immune compromised, alcoholics, pt. with pre-existing cardio-pulmonary, neoplastic, or renal dz (esp pts with renal transplant)
unlike other pneumonias, Legionella pneumonia has associated GI symptoms >50% of the time (anorexia, nausea, vomiting, and diarrhea)
Common viral pneumonia pathogens?
influenza virus, RSV, parainfluenza virus, adenovirus, paramyxovirus, CMV, varicella-zoster virus, HSV, EBV, Hantavirus, and coronavirus (SARS-CoV)
SSxs of viral pneumonia?
malaise headache myalgia cervical LA chest pain sore throat cough with scant sputum
PE findings of viral pneumonia?
Some patients have few, if any, physical findings other than mild fever, while other patients may have respiratory/multi-organ failure Other findings include: tachypnea and/or dyspnea tachycardia wheezing, rhonchi, crackles sternal or intercostal retractions decreased breath sounds pleurisy
SARS characteristics?
Coronavirus with new mutation
Global epidemic in 2003; approx 800 related deaths
Airborne droplet transmission
SSx: high fever (>100.4C), dry cough, nasal congestion, dyspnea, chest pain, localized chest pain, ms and joint pain, diarrhea, headache
Dx: Rapid Polymerase Chain Reaction (PCR) or ELISA
CXR with patchy infiltrates
Complications: organ failure, osteoporosis, depression
~25% of pts with SARS have residual pulmonary fibrosis.
Hantavirus characteristics?
2012, 8 cases from exposure to mice droppings in Yosemite park, 3 deaths
Sx: initially looks like Flu, then worsens quickly leading to pulmonary edema
Mycoplasma Pneumonia characteristics?
“Walking pneumonia”
SSxs:
benign, slow progression, looks like URI (sore throat, fever, headache, malaise) and usually resolves without any treatment.
May be violent attacks of coughing with scant mucus, chills/fever; occ. N/ V
dry cough can persist for as long as a month; some pts can have a protracted illness/weakness lasting as long as 6 weeks.
PE: nontoxic general appearance
erythematous tympanic membranes or bullous myringitis in patients > 2 years
mild pharyngeal erythema but no exudate: minimal or no cervical LA
Auscultation: no findings early, but rhonchi, crackles, and/or wheezes several days later
Other possible findings: otitis media, rash
Diagonsis: Polymerase Chain Reaction (PCR) detects organism DNA
EIA serology
NO bacteria found on gram-stained sputum sample
CXR may have no findings or some diffuse infiltrate
Prognosis: most resolve after several weeks as pt regains their strength
Pneumocystis jirovecii pneumonia characteristics?
Etiology: ubiquitous unicellular eukaryote, P jirovecii (usu. dormant in a host lung)
frequent cause of morbidity and mortality in persons who are immunocompromised, may be AIDS-defining diagnosis. Rare in general population
SSxs: usually insidious onset of malaise, weight loss, night sweats and low-grade fever associated with a dry cough (sputum is too viscous to expectorate)
may be more severe: dyspnea cyanosis, respiratory distress, chest pain, productive cough
Complications: spontaneous pneumothorax and hypoxemia Can also affect the liver, spleen and kidney.
Coccidioidomycosis characteristics?
(San Joaquin Valley fever or desert rheumatism)
Etiology: Coccidioides immitis, a soil fungus particularly adapted to arid conditions (Southwest US, Mexico, S. America)
Spores become airborne with soil disruption: construction, farming, quakes
SSxs: self-limited respiratory tract infection, occurs 1-3 weeks after exposure.
most cases subclinical, never reaching the attention of a physician
common complaints are nonspecific: fever, cough, chest pain, fatigue, dyspnea, headache, arthralgias, and/or myalgias
May disseminate to other body systems in those immunocompromised
PE: Pulmonary findings are generally nonspecific: crackles, pleural rubs, wheezing, and decreased breath sounds from effusions
Disseminated disease:
- Dermatologic - erythema nodosum
- CNS - disseminated CI may lead to meningitis - fever, headache, meningismus, nausea, vomiting, and altered mental status.
- Cardiovascular - endocarditis (rare but serious if involved)
- Musculoskeletal - osteomyelitis, septic arthritis, and synovitis.
Work-up:
CBC - leukocytosis with eosinophilia, lymphocytosis, or monocytosis.
CXR: Infiltrates can range from segmental or lobar to diffuse reticulonodular
Skin testing - delayed-type hypersensitivity reactions may become pos in 1-3 wks.
Serology tube precipitin assays for IgM may detect acute infection.
Sputum culture results are usually delayed (5- to 7-day incubation period)
Dx: clinical suspicion and history of possible exposure or travel to an endemic area.
Prognosis: General good, but poor if the patient is immunocompromised
Allergic bronchopulmonary aspergiliosis characteristics?
Eosinophilic pneumonia - Type I/II allergic rx. to Aspergillosis nigra or fumigatus
Fungus found in soil, decaying vegetation, dust, water
Typical patient already has asthma- then develops cough, wheezing, dyspnea worse than normal, low-grade fever
Sputum- extremely tenacious, forms plugs with brown flecks filled with aspergillosis
Labs/Imaging: CBC - diff. > 50% eosinophils, increased IgE, pos RAST skin test to aspergillosis
CXR shows bronchiectasis, infiltrates (Alveoli packed with eosinophils)
Histoplasmosis characteristics
“Spelunker’s Lung”
Etiology: Histoplasma capsulatum, a fungus found in soil enriched with bird or bat droppings (caves)
In US: Ohio and Mississippi river valleys, and Southeast. (Up 80 % of persons living in these areas have a positive skin test)
Spores inhaled into alveolar spaces, budding yeast seen within cells
Infection varies in symptoms and seriousness (short-term, treatable infection to a disseminated disease)
SSxs:
Acute (short term, mild) - fatigue, fever, chills, chest pain, dry cough (~10 d post exp)
Chronic (long term, serious) - like TB; occurs mostly in those with prev lung dz
It can progress/relapse over mos or yrs, leading to lung scarring.
Disseminated histoplasmosis leads to serious symptoms, multiple body organs
PE: related to the extent and duration of infection.
- Acute pulmonary histoplasmosis
Lung auscultation: crackles or wheezes (rarely)
Heart auscultation: may be pericardial friction rub (~5% of pts develop pericarditis)
Skin: erythema multiforme or erythema nodosum(~5-6% of pts develop)
- Chronic pulmonary histoplasmosis:
Lung auscultation: crackles, wheezes
- Chronic progressive disseminated histoplasmosis:
Mouth: ulcers on the buccal mucosa, tongue, gingiva, and larynx.
Eyes: May be vision loss
Abdomen: hepatosplenomegaly is possible
Work-up: sputum culture for the organism
positive histoplasma skin test, useful only for outbreak investigations
PCR to identify DNA
CXR - calcified hilar lymph nodes, lung scarring seen in chronic forms
Prognosis:
acute pulmonary histoplasmosis is associated with a good outcome
chronic progressive disseminated histoplasmosis has a protracted course, lasting up to years, with long asymptomatic periods. If untreated may result in death
Other fungal organisms: blastocystis hominis, candida
Aspiration pneumonia characteristics?
Etiology: aspiration due to esophageal dz., seizures, chronic hiccups, CNS dz., while under general anesthesia, after surgery, alcoholism, drug abuse, disturbances of consciousness, vomiting
Also Lipoid aspiration (fat or oil) from nasal ointments, nose drops, furniture polish into lungs, causing inflammation, secondary infection
very severe, high mortality
diagnosis based on history
SSXs: acute: fever, cough, oil droplets in sputum, chronic wt loss, night sweats
CXR reveals infiltrates throughout lung
Tx: suction of aspirate
Lung abscess characteristics?
Sequestration of anaerobic bacteria leading to necrosis of lung parynchema, typically as a complication of aspiration pneumonia, or severe bacterial pneumonia
SSxs: history of unresolving pneumonia, fever, cough, sour-tasting sputum for > 2wks; night sweats, weight loss, hemoptysis, pleurisy
Work-up: Seen as cavitation on CXR and CT
Pulmonary TB incidence? Groups of higher prevalence?
- US, Canada: ~ 25,000 cases/yr (40% in immigrants from endemic countries), ~ 650 deaths/yr
- Worldwide: on the top 10 list for all-cause, all-age mortality, ~2 billion people infected, 9 million new cases/yr; ~2 million deaths/yr
Groups with higher prevalence of TB: - Homeless or marginally housed person
- Foreign-born or freq travel to endemic areas
- Persons in correctional facilities, shelters
- Elderly
- Health care workers serving high risk grps
- Medically underserved, low income
- Children exposed to adults at high risk
- Groups with higher risk of progression to active TB:
- Those infected within 2 previous years
- Kids < 4 yrs
- Persons with history of untreated/undertreated TB
- Immunocompromised: HIV, CA, organ transplant, corticosteroid use
- Underlying medical conditions: silicosis, DM, CKD, gastrectomy, underweight
Pulmonary TB transmission?
Transmission occurs mainly person-to person, inhalation of airborne droplet nuclei, (from sneezing, coughing from infected person). To be at risk, exposure to the organisms must be constant– living or working in close quarters with someone with active TB (eg Contact 8h/d x 6 mos or 24h/d x 2mos = 50% chance of infection
Primary TB infection?
Organism enters lungs, inflammatory reaction holds organisms in check
Only 10% of people infected with TB will develop active disease. Remaining 90% will show no signs of infection, nor will they spread the disease to others (latent TB)
Active TB SSxs and PE?
SSxs: Chronic productive cough (>3 wks duration) - yellow-green sputum – usu in AM (late in dz) hemoptysis (late in dz) malaise, fatigue norexia, wt loss low grade fever coming on in late afternoon night sweats Note: classic symptoms are often absent, esp in patients who are elderly or immunocomp PE: Fever cachexia hypoxia tachycardia lymphadenopathy abnormal lung sounds May progress to TB Pleurisy - Pleuritic chest pain, fever, SOB( exudative pleural effusion)
Active TB labs/imaging?
Lab:
PPD test
Acid fast stain of sputum
culture takes 3-6 wk. to grow
gastric aspirates after a 6 hr fast better than sputum (esp non-HIV pts)
WBC usually normal; may see normochromic, normocytic anemia
Imaging Studies:
Radiographic findings consistent with active primary TB are similar to those of lobar pneumonia with ipsilateral hilar adenopathy, often accompanied by atelectasis,
typically in upper lobes
Note: CXR consistent with TB indicates active disease in the symptomatic patient even in the absence of a diagnostic sputum smear result. Similarly, normal chest radiography in the symptomatic patient does not exclude TB, particularly in an immunosuppressed person
Course: 14% of cases can progress to Miliary TB - Hematogenous and lymphatic spread to target organs—kidneys, bones, meninges, pericardium, liver, GI tract, skin, adrenals—with resultant sx
Latent TB/Reactivation TB?
LTBI-Most common clinical form, in elderly or debilitated pt, up to 90% of those infx
Asymptomatic, bacteria are alive but inactive (latent) in walled-off tubercles.
Reactivation risk greatest in first few yrs after initial infx, in childhood, adolescence, in immunocompromised
Lab: QuantiFERON-TB Gold or PPD (positive in 80%)
Imaging: Chest X-ray: on routine chest film may see small tubercle- healed over area
Pulmonary lesions are often located in the posterior segment of the RUL, apicoposterior segment of the LLL, and apical segments of the Lower Lobes.
TB testing
PPD (purified protein derivative) skin test
Interpretation (48 – 72 hrs) based on diameter of induration (palpable, raised, firm swelling)
5 mm is considered positive in HIV infected, contact of known TB, hx prev TB, those with organ transplants; those taking immunosuppressant drugs
10mm positive in recent immigrants, IV drug user, workers/residents in congregate settings, kids< 4 yo, children with exposure to high risk adults
15mm considered positive in any person
Falsely positive in those who have received the TB vaccine
Falsely negative in those with sarcoidosis, non-Hodgkin’s lymphoma, malnutrition
Clinical evaluation and additional tests (such as a chest radiograph, acid-fast sputum smear, and culture) are needed to differentiate between a diagnosis of active TB or latent TB
QuantiFERON-TB Gold QFT-G (an IGRA—interferon gamma release assay)
whole-blood test used in diagnosing Mycobacterium tuberculosis infection, including latent tuberculosis infection (LTBI)
Advantages of the test are:
Requires a single patient visit to draw a blood sample.
Results can be available within 24 hours.
Does not boost responses measured by subsequent tests, which can happen with tuberculin skin tests
Is not subject to reader bias that can occur with skin tests
Is not affected by prior BCG (bacille Calmette-Guérin) vaccination
Drug resistant TB?
Develops in the course of TB treatment, with inappropriate doses or incomplete dosing
More common in immunocompromised, indigent populations. Mortality rate up to 80%
Typical first-line anti TB meds (isoniazid, rifampacin) are insufficient to kill 100% of organisms. Tx is using 4 different antibiotics over 18-24 mos
TB vaccine: bacillus Calmette-Guèrin (BCG)
Immunity decreases after 10 years
DDx for TB: pneumonia, lung abscess, pulmonary mycosis, CA, non-TB mycobacterium, histoplasmosis, coccidioidomycosis, silicosis, sarcoidosis
Pleurisy etiology?
Inflammation of the pleura, may lead to pleural effusion (fluid in pleural space)
Layers of pleura rub with inhalation, causing sharp pain ie “pleuritic chest pain”
Etiology:
infections: bacterial, TB, fungus, parasites, or viruses (most common)
inhaled chemicals or toxic substances
collagen vascular diseases: lupus SLE, rheumatoid arthritis RA
cancers - spread of lung cancer or breast cancer to the pleura
tumors of the pleura – mesothelioma (from asbestos exposure) or sarcoma
congestion: heart failure (CHF)
pulmonary embolism (PE)
obstruction of lymph channels - as a result of centrally located lung tumors
trauma - rib fractures or irritation from chest tubes used to drain air or fluid from the pleural cavity in the chest
drugs that can cause lupus-like syndromes (eg Hydralazine, Procaine, Dilantin)
abdominal conditions such as pancreatitis, cirrhosis of the liver
lung infarction: lung tissue death due to lack of oxygen from poor blood supply
Pleurisy SSxs?
usually sudden onset of pain (vague or sharp stabbing pain)
pain with coughing or deep breathing leads to rapid, shallow breathing, holding breath, splinting of chest
pain may be referred to shoulder or diaphragm
SOB, painful cough
may have sore throat
when there is effusion- pain usu. subsides, increased dyspnea
Pleurisy PE?
fever if infectious cause
Pleural friction rub is characteristic, may not hear until 24-48 hrs after onset of pain (Compared to Pericardial friction rub rub will be constant, have pt hold breath and the sound will persist)
tachycardia
limited chest motion on that side
decreased breath sounds
With pleural effusion, decreased or absent breath sounds, percussion dullness, decreased tactile fremitus, egophony at upper border of fluid
Pleurisy Labs/Imaging?
CBC, Arterial blood gases (ABGs)
CXR: may be normal, fluid blunting of costo-phrenic angle if effusion
Ultrasound can detect the presence of pleural fluid
CT scan can be very helpful in detecting trapped pockets of pleural fluid
Pleurisy DDX?
acute abdomen- N/V, abd. Pain
intercostal neuritis- no friction rub
costo-chondritis- hx of trauma?, localized pain, reproducible with palpation
herpes- if no eruptions yet may be difficult to tell!
MI- location of pain, concomitant sx, risk history, cardiac enzymes
pneumothorax- tracheal deviation, R/O by x-ray,
pericarditis- rub with heart beat (constant) instead of breath, precordial pain radiating to neck, shoulders, also < resp, cough, heart sounds are lowered as fluid in sac muffles heart sounds
Pleural effusion - transudate etiology?
- transudate - from increased microvascular pressure or decreased oncotic pressure due to: Congestive heart failure CHF Cirrhosis (hepatic hydrothorax) Atelectasis (malignancy, pulmonary embolism) Hypoalbuminemia Nephrotic syndrome Peritoneal dialysis Myxedema Constrictive pericarditis
Pleural effusion - exudate etiology?
- exudate – local pleural inflammation with increased permeability of pleural space to protein due to: Lung infections Malignancy (carcinoma, lymphoma, mesothelioma) Pulmonary embolism Collagen vascular (RA, SLE) TB Asbestos Chest trauma Esophageal perforation Radiation pleuritis Sarcoidosis
Types of pleural fluid?
Lymph: chylothorax
Pyogenic: empyema
Blood: hemothorax
Serous: hydrothorax
Pleural effusion SSxs/PE?
Dyspnea - related to distortion of diaphragm/chest wall rather than hypoxemia
mild, nonproductive cough
chest pain
PE: do not usually manifest until pleural effusions exceed 300 mL
decreased breath sounds
dullness to percussion
decreased tactile fremitus
egophony (E-to-A change) (at top of fluid)
pleural friction rub with breathing
mediastinal shift away from the effusion (with effusions >1000 mL)
What is a thoracentesis?
- Removal of pleural fluid by thoracentesis is essential in diagnosing pleural effusion (referral to perform) Analysis of fluid color, consistency, and clarity; presence of organisms and/or cancer cells will clarify if it is an “exudate” (high in protein, low in sugar, high in LDH enzyme, and high WBCs; characteristic of a local inflammatory process) or a “transudate” (containing normal levels of these body chemicals, from a systemic problem).
Depending on cause/course, a thoracostomy tube is used to drain accumulating fluid
Pleural Empyema etiology?
infective pneumonia, chest wound, chest surgery, lung abscesses, or a ruptured esophagus - infective organism enters pleural cavity either through the bloodstream or other circulatory system, in secretions from lung tissue, or on the surfaces of surgical instruments or objects that cause open chest wounds.
common organisms: Streptococcus pneumoniae, Haemophilus influenzae, and S aureus.
Pleural empyema SSxs?
symptoms of pneumonia: fever, cough, fatigue, SOB, chest pain, bad breath
In severe cases: may become dehydrated, cough up bloody or greenish-brown sputum, fever as high as 105°F or lapse into coma.
Pneumothorax etiology?
1 - Spontaneous (idiopathic)
Secondary to emphysema, interstitial lung dz., cystic fibrosis, asthma, abscess, TB, Cancer
Tall, thin people are at increased risk of developing
2 - Traumatic
chest trauma, lung biopsy, mechanical ventilation (e.g. anesthesia),
fluid in sac muffles heart sounds
Pneumothorax SSxs/PE?
SSxs: vary from minimal to severe dyspnea
sudden sharp pain (90%), dyspnea (80%), occ. dry, hacking cough at onset
may refer pain to shoulder, or abdomen
PE: decreased vocal fremitus
decreased or NO breath sounds on affected side
tympany on percussion if a lot of air in pleural space
tracheal deviation to the opposite side
