Pulmonary Flashcards
COPD general info
two types: chronic bronchitis and emphysema
CB - clinical dx; chronic, productive cough with sputum for at least 3 months per year for at least two consecutive years.
E - pathologic dx w permanent enlargement of air spaces d/t destruction of alveolar walls
Both often coexist, pure dz of either rare
COPD 4th leading cause of death of US
COPD risk factors and causes
Tobacco smoke (90% of cases) alpha 1 antitrypsin deficiency - risk worse w smoking environmental factors (2nd hand smoke) chronic asthma
COPD pathogenesis
Chronic bronchitis - excess mucus productions narrows airways (productive cough); inflammation and scarring in airways, enlargement in mucous glands, smooth muscle hyperplasia lead to obstruction.
Emphysema - destruction of alveolar walls d/t relative excess in protease (elastase) activity or relative deficiency of anti-protease (alpha 1 antitrypsin) activity in lungs. PMNs + macrophages release elastase and digest human lung.
Tobacco smoke increases # of activated PMNs and macrophages, inhibits antitrypsin, and incr oxidative stress on lung by free radical production.
COPD clinical features
Any combo of cough, sputum production, dyspnea, some patients may live sedentary lifestyles with few complaints, avoiding exertional dyspnea.
prolonged expiratory time
end-expiratory wheezes on forced expiration, decr breath sounds, inspiratory crackles
tachypnea, tachycardia
cyanosis
accessory respiratory muscle use
hyper-resonance on percussion
signs of cor pulmonale
chronic resp acidosis + compensatory metabolic alkalosis
COPD diagnosis
PFT - definitive diagnostic test
obstruction evident - decr FEV1, decr FEV1/FVC ratio < 0.70; incr TLC + incr residual vol + incr FRC = air trapping; decr vital capacity
GOLD staging: FEV1 => 80 of predicted value is mild disease.
FEV1 50% - 80% = moderate disease
30% - 50% = severe disease
< 30% = very severe disease
COPD HPI tips
Hx cardiopulmonary diseases
smoking history ( duration, intensity, current smoker)
family history (COPD, heart disease, asthma)
occupation (industrial dusts, fumes)
overall health
history of resp infections (frequency, severity)
pulmonary medications
pulmonary sxs: dyspnea, cough, sputum production, wheezing
clinical monitoring: serial FEV1, pulse ox, exercise tolerance
COPD treatment
smoking cessation most important - improvement in sxs, slows rate of decline, prolongs survival, does not completely reverse
1. inhaled anticholinergic drugs (ipratroprium bromide): bronchodilators
2. inhaled B agonists (albuterol): bronchodilators, provide sx relief, long-acting (salmeterol) for pts using frequently
OR combo of the two above
3. inhaled corticosteroids (budesonide, fluticasone): anti inflammatory
4. theophylline - controversial
5. oxygen therapy - improves survival and quality of life for those with chronic hypoxemia (PaO2 55 mmhg or O2 sat < 88% or PaO2 55-59 + polycythemia or cor pulmonale, despite max med therapy)
6. pulm rehab
7. vaccination
8. surgery
give systemic steroids and abx for acute exacerbations
BBs contraindicated in acute COPD
COPD tx guidelines
mild - mod dz: bronchodilator MDI +- low dose inhaled glucocorticoids
severe dz: above + continuous O2 (if hypoxemic), pulm rehab, triple inhaler therapy (long-acting B agonist, long-acting anticholinergic, inhaled glucocorticoid)
acute COPD exacerbation: bronchodilators, IV methylprednisolone then taper with oral once improved, abx (azithro, levoquin, doxy), supp O2 (90-93% goal), NPPV, intubate or mechanical vent if above doesn’t stabilize (incr RR, incr PaCO2, worsening acidosis)
COPD complications
acute exacerbations (d/t infxns, cardiac dz, noncompliance)
secondary polycythemia
pulm HTN and cor pulmonale
CAP gen info
Two types: community acquired and nosocomial
CAP
- occurs in community or within 72 hrs of hospitalization
- typical or atypical
MC bacterial pathogen: strep pneumoniae (60%) –> H. flu, reg flu, legionella spp
Nosocomial pna
- occurs during hospitalization after 72 hrs
- MC bacterial pathogen: gram neg rods (Ecoli, pseudomonas) and staph aureus
- if vitals entirely normal in OP, probability of pna < 1%
Two rec prevention methods
- influenza vaccine
- pneumococcal vaccine: >65 yo or young ppl at risk (heart disease, scd, etc)
Typical CAP: common agents, sxs, CXR
Common agents
- strep pneumoniae (60%)
- H flu (15%)
- Aerobic gram-negative rods (6-10%) - klebsiella (& other enterobacteriaceae)
- staph aureus (2-10%)
Symptoms
- sudden shaking chills followed by fever
- cough productive of thick, purulent sputum
- pleuritic chest pain (suggests pleural effusion)
- dyspnea
Signs
- tachycardia, tachypnea
- late inspiratory crackles, bronchial breath sounds, increased tactile and vocal fremitus, dullness on percussion
- pleural friction rub (a/w pleural effusion)
Chest xray
- lobar consolidation
- multilobar consolidation indicates very serious illness
Most cases of CAP result from aspiration of oropharyngeal secretions bc majority of organisms that cause CAP are normal inhabitants of the pharynx.
Atypical CAP: common agents, sxs, CXR
Atypical pna - organisms not visible on gram stain & not curable on standard blood agar
Common Agents
- mycoplasma pneumoniae mc
- chlamydia pneumoniae
- chlamydia psittaci
- coxiella burnetti (Q fever)
- legionella spp
- viruses: influenza A or B, adenoviruses, parainfluenza virus, RSV
Symptoms
- insidious onset - sore throat & headache 1st, fatigue, myalgias
- dry cough (no sputum production)
- fevers (chills are uncommon)
Signs
- pulse-temp dissociation; nl pulse in setting of high fever
- wheezing, rhonchi, crackles
CXR
- diffuse reticulonodular infiltrates
- absent or minimal consolidation
CAP diagnosis
1st differentiate lower resp tract infection from upper resp infection and other causes of cough.
- nasal discharge, sore throat, ear pain predominates –> upper
- lower tract infection suss –> differentiate btw pna and acute bronchitis (can’t just with clinical features), need CXR.
CXR, labs (cbc diff, BUN, Cr, glc, lytes or CMP) O2 sat, blood cultures, gram stain/culture, abx therapy)
PA and lat CXR required to confirm dx
- interstitial infiltrates, lobar consolidation, and/or cavitation
- sensitive; if findings not suggestive of pna don’t treat w abx
- false negative cxrs w neutropenia, dehydration, infection w PCP, early dz < 24 hrs
- after treatment, changes on CXR lag behind clinical response (up to 6 wks)
Sputum gram stain (everyone) and culture (hospitalized pts) with cap (low sensitivity + specificity, but done for antimicrobial resistance prob)
- good specimen > 25 [mns and < 10 epithelial cells
Special stains
- acid-fast stain (mycobacterium spp) if TB suss
- silver stain (fungi, p.carinii) for HIV/immunocompromised
Urinary antigen assay for legionella
- very sensitive
- antigen persists in urine for weeks (even after treating)
Consider two blood cultures
CAP pearls
Alcoholics –> klebsiella
Immigrants –> TB
Nursing home residents –> nosocomial pathogen
HIV + –> P. carinii, TB, more likely to have typical infxn
legionella –> organ transplant recipients, renal failure, chronic lung dz, smokers
- presents with GI sxs + hyponatremia
CAP treatment
Hypoxic or hypotensive –> hospitalize (can use PSI, CURB-65 admission if at least 2 points)
Uncomplicated CAP in <60yo, no comorbidities –> macrolide (azithromycin, clarithyromycin) or doxycycline first line
- comorbidities –> FQ
- > 60 yo, comorbidities, or abx tx in last 3 months –> resp FQ (levofloxacin, moxifloxacin) PLUS macrolide or augmentin
OP –> 5 day treatment (don’t stop until patient has been afebrile 48 hrs)
IP –> FQ alone or 3rd gen ceph + macrolide (ceft + azithro)
