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90 Cards in this Set
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What is the common epidemiology and natural history of non-influenza respiratory viruses? Think rhinovirus, RSV, etc
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1. Repeated infection due to many serotypes or poor immune response
2. tendency for severe, lower respiratory infection in young pts, milder URIs in adults (w/ small airway dysfunction) 3. Severe in elderly, can be life threatening especially in HSCT pts |
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Common pathogenesis and immunology of non-influenza viruses infecting respiratory system?
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1. mucosal damage or frank necrosis of infected epithelium
2. Inflammatory response causing edema/secretions 3. each agent can cause upper, middle, or lower infections |
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what's croup (laryngotracheobronchitis)? What are the most common agents that cause croup?
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acute viral infection of upper airway in children (like laryngitis in adults) with characteristic "barking" stridor and cough (typically found in <3yo). often with fever, at night, progression to obstruction rare. steeple sign on CXR sometimes.
Common causes: parainfluenza, adenovirus, influenza. |
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what are the "classic" common cold signs/symptoms?
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CLASSIC cold symptoms: nasal irritation, congestion, sneezing, rhinorrhea, mild sore throat, afebrile usually
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What has symptom resolution been associated with in common cold/URIs?
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INTERFERON PRODUCTION. no consistent clearcut clinical benefit of antihistamines, decongestants, immunologic mediators.
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What is bronchiolitis?
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distinctive clinical syndrome seen in infants in the 1 st year or two of life
– URI with development of progressive cough, may get wheezing, tachypnea, poor feeding – Exam will show tachypnea and retractions; auscultation: wheezes and rales. – CXR: hyperinflation ± pneumonia – RSV is the most common cause |
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What is Reye's syndrome?
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Rare complication of Influenza
– Mitochondrial dysfunction affecting liver and brain – Associated with use of aspirin during influenza, flu B > flu A (also w/ varicella) |
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Name the hallmark URI viral syndromes and their characteristic symptoms and causative agents.
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• Hallmark syndromes
– URI “common cold”: rhinovirus – Mid-respiratory infection: croup (paraflu, adeno, influenza) – Bronchiolitis: RSV – “Flu”: influenza A or B |
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what factors should prompt TB to be included in your differential?
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-History of positive PPD or known disease.
-Contact with known or suspected TB case -fibrotic lung lesions or upper lobe scars compatible with inactive TB -immigration from country with high TB incidence • Advanced age • Medically underserved populations • Alcohol or other drug use • Institutional exposure (congregate living) • Known or suspected HIV infection • Other immunosuppressed states |
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What are the principles of anti-TB therapy?
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-high organism burden in patients with active disease (10^8 in 1 cavity)
-mutation rate is 1/10^6 to rifampin and isoniazid -administration of both drugs leads to 1/10^12 |
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what are 1st line TB agents?
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Isoniazid, Rifampin, Ethambutol, Pyrazinamide, aminoglycoside - RIPE
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Classic signs of pulmonary TB?
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chronic cavitary disease, progression from primary infection to reactivation, apices most often involved, pos sputum AFB (contagious), hemoptysis, fibrosis and scarring, hilum retraction
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how can you differentiate type of TB (primary, reactivated, old) on CXR?
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• invaluable diagnostic and screening test
• primary TB -lower lobe infiltrate with hilar LN adenopathy • Reactivated TB -fibrotic and cavitary infiltrates in the apical segment of the upper lobe and superior segment of the lower lobes • Old TB - apical parenchymal scars or calcified granulomas |
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what is Tuberculous pleural
effusion? |
• often with simultaneous hilar
adenopathy • Usually a variant of the primary complex or progressive primary disease • PPD usually + within 6-8 wks • pleural fluid: high protein, low glucose, +bloody, many lymphocytes • low yield on culture, need biopsy of pleura |
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TB symptoms?
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• fever
• night sweats • anorexia • weight loss • elevated sedimentation rate • anemia (of chronic disease) remember rare pericarditis complication, hematogenous or via mediastinal nodes. |
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histological findings in TB
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caseating (necrotic) granulomas, giant cells (macrophages joined), millet seed granuloma pattern
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Characteristics of miliary TB?
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• "millet-seed" pattern of granulomata,
particularly as seen on chest x-ray • multiorgan involvement and prominent systemic symptoms • fever of unknown origin • hematological problem (pancytopenia or leukemoid reaction) • Meningitis develops in about 10% • Liver frequently involved - incr alk phos biopsy granuloma in 60-90% • Bone marrow - any kind of disturbance possible. Biopsy positive for granuloma in 30-40% COMMON in AIDS pts in TB endemic areas |
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what is granulomatous meningitis? what can cause it/
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CSF with aseptic pattern, TB can cause
• 100-1000 WBC - mostly lymphs • low glucose-progressive fall over time • increased protein • Acid fast bacilli rarely seen on smear • culture multiple samples of cerebrospinal fluid • have to make therapeutic decision on clinical grounds |
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what is GU TB?
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• Urinary: Kidneys involved by
hematogenous spread, structures down-stream by urinary or hematogenously carried bacilli • Local symptoms outweigh systemic, resemble urinary tract infection or stones: dysuria, gross hematuria, flank pain, pyuria. • "sterile" (really abacteriuric) pyuria or microscopic hematuria on lab studies • Diagnosis by culture from urine • Radiological findings – bilateral calyceal deformity – "Beaded" or "pipestem" ureter – renal calcifications • Male genital tract - palpable mass • Female genital tract - salpingitis |
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What are common presentation of TB besides pulmonary?
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CNS TB (meningitis), small abscesses Brain, genitourinary, osteomyelitis, intestinal (mimics Crohn's), adrenals
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what is latent TB?
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presence of MTB without symptoms or radiographic evidence of TB disease. interferon gamma assays, TST.
controlled by immune system. NOT infectious |
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Risk factors for progression of latent TB to active disease?
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HIV, previous TB, substance abuse, corticosteroid or immunosuppression therapy, organ transplant, silicosis, DM, kidney disease, cancer,
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What is tx for latent TB?
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Isoniazid daily for 9 months. Or Rifampin daily for 4 mos or isoniazid/rifapentine weekly for 12 doses
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what does the term infiltrate mean?
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filling of airspaces with fluid (pulmonary edema), inflammatory exudates (white cells, protein), etc.
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what are effusion and empyema?
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Effusion is excess fluid in pleural. empyema is pus in infected pleural cavity.
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Predisposing Factors to CAP
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• Smoking and COPD*, asthma
• Congestive heart failure, cirrhosis, DM, EtOH* • Altered mentation, EtOH • Age (pneumonia = “old man’s friend”) >65* • Immunocompromised*(HIV, CLL, asplenia, etc.) • Prior viral infection, esp., influenza. • Past CAP* • Solid Organ Transplantation* |
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define the following terms, common causes, how to test:
Rales, crackles, crepitations, Rhonchi, Stridor, Egophony, whispered pectoriloquy |
Rales=crackles=crepitations - inhalatory sound caused by "popping open" of collapsed alveoli (due to fluid, exudate, lack of aeration, lack of surfactanct). many causes: pneumonia, atelactasis, PF, acute bronchitis, bronchiectasis, PE from CHF.
Rhonchi - low pitched, continuous snoring sounds. caused by secretions in bronchial airways, partial obstruction. COPD or bronchitis Stridor: high pitched wheezing sound, turbulent upper airway flow. can be inspiratory or expiratory or both. many causes. Egophony: increased resonance due to enhanced transmission of high frequency sounds. lung consolidation or fibrosis. E to A transition test or "99" Whispered pectoriloquy: increased loudness of whispered words, caused by lung consolidation. "whisper 99 or toy boat, auscultate loudness" |
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Epi, presentation, diagnosis, prognosis of H. influenza CAP?
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1. Epidemiology
Causes 5% CAP. COPD or smokers will have non-typable H.flu, and children (formerly) had hemophilus influenza type B strains. 2. Clinical Presentation Fever, productive cough, empyema, and pleural effusion are less common than with staphylococcus, more common than with pneumococcus. 3. Diagnosis Sputum gram stain and culture. Chest x-ray: bronchopneumonia typical. 4. Prognosis Mortality roughly 33%--highest in those with advanced age/COPD. |
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Epi, presentation, diagnosis, prognosis of anaerobic CAP?
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Epidemiology
Occurs in individuals at risk for aspiration, or with periodontal disease, or bronchial obstruction (e.g., cancer). Clinical Presentation Ranges from gradual onset of foul smelling sputum, weight loss, and fever, to necrotizing pneumonia with pulmonary abscesses (cavities with air/fluid levels) and empyema. Diagnosis Culturing anaerobes such as Bacteroides, Fusobacterium, peptostreptococcus, and peptococcus—very difficult. CXR small infiltrate early, multiple small cavities in 1 or more lung lobes in late necrotizing pneumonia; lung abscess; empyema. Prognosis and therapy 5% to 20% mortality depending on form of the illness. Clindamycin or addition of metronidazole to CAP regimens (above). |
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likely causative agent of pneumonia in young adults? symptoms?
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MYCOPLASMA, spreads within families.
tracheobronchitis/pharyngitis, 3-10% clinically apparent pneumonia, insidious onset, headache, malaise, fever over 2-4 days, followed by dry cough |
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typical vs atypical pneumonia presentation.
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classic is abrupt onset with fever, chills, pleuritic pain, tachycardia, consolidation, effusion, sputum production caused by Strep pneumo, H influenzae, Staph aureus, klebsiella.
Atypical is gradual and with rarely symptoms of classic pneumonia (mycoplasma, legionella, viruses, chlamydia) |
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epidemiology and clinical presentation of Staph aureus CAP
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Epidemiology
• 2-5% of CAP--postinfluenza, or hematogenous (endocarditis). (also healthcare associated) Clinical Presentation • Severe illness: pleurisy, productive cough, and fever are common--may progress rapidly. • Complications are common: Bacteremia in 50%: can produce endocarditis, CNS, kidney, bone, or joint infections. |
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treatment for Staph pneumonia?
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Vancamycin until prove beta-lactam susceptibility
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consequences of pneumonia
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Lung abscess (usually due to Staph. aureus, anaerobes, Pseudomonas)
• Cavitation • Empyema • Recurrent pneumonia • Acute respiratory failure • Superinfection (associated with increased mortality) • Complications of bacteremic pneumococcal pneumonia (meningitis, pericarditis) |
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contrast treatment of choice for CAP outpatient and in hospital?
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Outpatient: azithromycin 500po or doxycycline 200po
Inpatient: Azithromycin 500 AND Ceftriaxone with aspiration add clindamycin or metronidazole with influenza add oseltamavir |
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Azithromycin MOA, ADME, agents active against
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A member of the macrolide group
of antibiotics that inhibits protein synthesis by binding to the 23S subunit of the bacterial ribosome. • 37% bioavailable (so PO~IV). Half- life 40-68 h. Urinary excretion 6%. No dose adjustment in renal/hepatic failure. Concentration in WBCs 10X times that of serum. • Adverse effects: GI upset, rash, hepatotox, ototox (reversible), long QT, active against legionella, chlamydia, intracellular pathogens (ie mycoplasma), hemophilus, moraxella. resistance a problem in GAS and pneumococ |
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Recurrent themes in antibiotic resistance?
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1. efflux from cell,
2. target alteration, 3. drug modification, 4. decreased access |
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Ceftriaxone MOA, ADME, agents active against
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• Beta lactams, e.g., cephalosporins and penicillins, inhibit the final steps in peptidoglycan synthesis
leading to cell wall formation. • Third-generation cephalosporins are stable against most plasmid-encoded beta-lactamases, but not extended spectrum, or AmpC, beta-lactamases. • Half-life of 8 hours allows Q24H dosing for many diseases ((50mg/kg up to 2GM) Q12H for meningitis). • 50% urinary and 50% biliary excretion. side effects: allergic rxns including epidermal necrolysis Stevens Johnson Syndrome), nephritis, hepatitis, leukopenia, hemolytic anemia, fever, diarrhea, active against: strep, MSSA, enteric gram negs: ecoli, klebsiella, hemophilus, moraxella, most salmonella shigella |
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Different pathogenesis types of pleural effusion?
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-Increased hydrostatic pressure (CHF fluid moves across interstitium then across mesothelial layer into pleural space)
-Decrease in oncotic pressure (malnourished and liver sclerosis/ascites have low albumin, fluid leaves intravascular compartment into pleural space) -Increase permeability (pneumonia) -Impaired drainage (malignancy) -Fluid from abdomen (cirrhosis) |
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common malignancies causing malignant pleural effusions?
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breast (28%), lung (22%), lymphoma (12%), other (39%)
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What are the differences between exudates and transudates? How are the 2 distinguished?
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exudates are thick, viscous, colored green or yellow, can be malignant cells. caused by inflammation.
transudates are watery and colorless. caused by fluid leak due to hydrostatic and oncotic pressure problems. Distinguished by light's criteria (gross appearance, types of cells, protein content, serum enzymes (LDH) a pleural effusion is likely exudative if at least one of the following exists:[10] 1.The ratio of pleural fluid protein to serum protein is greater than 0.5 2. The ratio of pleural fluid LDH and serum LDH is greater than 0.6 3. Pleural fluid LDH is greater than 0.6 [6] or ⅔[10] times the normal upper limit for serum. |
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what are some common causes and associations of pneumothorax?
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trauma (penetrating -> tension PTX = emergency), apical subpleural blebs, secondary to diagnostic procedures, secondary to bullous lung disease (COPD), eosinophilic granuloma, CF, fungal infxn, rheumatoid disease, LAM
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histology of pneumothorax
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the same regardless of cause:
-mesothelial proliferation (normally 1 layer, no accumulation, cuboidal, cells pile up) -papillary tufts -fibrin deposition and fibrosis -multinucleated giant cells |
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What are pleural plaques??
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Localized regions of fibrous thickening of pleura usually on parietal surface more than viscera, parallel to ribs, may mimic mesothelioma, basket weave pattern, acellular, no asbestos bodies.
typically asymptomatic, may be markers of asbestos exposure. usually detected by CXR or seen at autopsy. |
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what is pneumoconiosis?
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"dusty lungs" - term for fibrotic rxn of lung due to mineral or inorganic dust inhalation.
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you see clubbing in a patient with occupational exposure to toxins. what do you suspect?
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ASBESTOSIS
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You observe bibasilar end-inspiratory crackles in a patient who works in construction. what do you suspect?
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asbestosis or hypersensitivity pneumonitis (HPS)
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a patient wheezes but only at work. you suspect?
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occupational asthma, reactive airway dysfunction syndrome (RADS), HPS
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a patient has interstitial markings and pleural plaques on CXR you suspect?
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asbestosisz
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A patient has pulmonary nodules and eggshell calcification of hilar lymph nodes, you suspect?
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silicosis
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what occupational diseases would typically present as restrictive on PFTs? As obstructive?
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restrictive: silicosis, asbestosis, HSP
obstructive: OA, RADS |
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what is silicosis? who is at risk? treatment? prevention?
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chronic lung disease caused by inhalation of dusts with free crystalline silicon dioxide.miners, sandblasters, stonecutters, pottery workers (ABRASIVE BLASTING)
causes nodules of lung and LNs, and fibrosis. A few types: low level exposure for >20 yrs, acute onset after few weeks of high level exposure, high level accelerated after 5 yrs? Higher risk of lung cancer and TB associated with bronchitis, airflow limitation, mucous hypersecretion, emphysema. no treatment, prevention not fully effective by masks. |
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pathophysiology of silicosis
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Pathophys-- bronchial lumen distortion / narrowing by nodules. Also large airway compression by hypertrophy / scarring of lymphoid tissue -> obstruction, restriction or both by PFT
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What is asbestosis?
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diffuse slowly progressive fibrotic lung disease caused by inhalation of asbestos fibers (straight fibers worse).
insterstitial fibrosis with UIP, asbestos bodies, pleural plaques and effusions. symptoms 20-30 yrs after exposure. serious complications: respiratory failure, malignancy. |
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Reactive Airway Dysfunction Syndrome (RADS), tell me about it. is it RAD?
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persistent asthma like illness >3mos after high single exposure to irritant.
symtpom onset within 24hrs, nonimmunologic. Not reproducible by methacholine challenge. most recover with no long term deficit, proportion have asthma like illness bronchodilators not as useful, typical tx is steroids |
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hard metal disease
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uncommon group of diseases related to very specialized compounds, typically alloys of tungsten and cobalt (the toxic component).
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Coal worker's pneumoconiosis
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similar to silicosis, caused by deposition of coal dust in lungs and tissue reaction
dust laden macrophages coalesce -> nodules -> masses -> progressive massive fibrosis. Alveolar walls become weak -> COPD, bronchioles collect dust and become inflammed and scarred -> obstruction no specific symptoms MTB, MOT, silicosis complicate |
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What are the effects of pneumothorax on the body?
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-pressure gradient from alveolus to pleural space.
-increase volume of thoracic cage and lung collapse -decr VC, VQ mismatch, decr PaO2, incr Aa gradient, shunting w large PTX -in tension PTX rapid deterioration due to intrapleural pressure > atmospheric pressure, decreased CO and venous return. |
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what are light criteria for transudate?
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The classical Light criteria for a transudate include all of the following:
1) a pleural fluid to serum total protein ratio < 0.5, 2) a pleural fluid to serum lactate dehydrogenase (LDH) ratio < 0.6, and 3) a pleural fluid LDH that is < 2/3 of the upper limits of normal for the serum LDH |
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Define the following:
PAO2 PaO2 SaO2 CaO2 FiO2 |
PAO2 - partial pressure of oxygen in alveoli
PaO2 - partial pressure of oxygen in arterial blood SaO2 - oxygen saturation of hemoglobin, % of hemoglobin molecules bound by oxygen. Often measured in arterial system by pulse oximetry. CaO2 - Directly reflects the total number of oxygen molecules in arterial blood (both bound and unbound to hemoglobin) FiO2 - fraction inspired oxygen (0-1.0) |
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What factors determine rate of flow movement in pulmonary edema?
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[Formation of Fluid(hydrostatic driving pressure) - (oncotic driving pressure)] - Drainage (lymphatics)
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etiologies of ARDS?
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Infections (sepsis, pneumonia), hemodynamic (shock), Trauma(fat emboli), drugs (cocaine, heroin), inhaled toxins (smoke inflammation, oxygen), misc (lung contusion, aspiration, massive blood transfusion, pancreatitis)
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What is the pathogenesis of ARDS?
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PERMEABILITY EDEMA, NONCARDIOGENIC EDEMA
characterized by DAD refractory hypoxemia results from shunting lung compliance leads to airway pressures Treatment: supportive, PEEP |
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what are the big 3 infections for upper respiratory infections like epiglottitis, sinusitis, otitis media.
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Streptococcus pneumoniae (aka pneumococcus), Hemophilus influenzae B, Moraxella(Branhamella) catarrhalis
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what is the rule of 3s of otitis media?
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By age of 3:
1/3 children have had 3 or more episodes 1/3 of children have had 1-2 episodes 1/3 of children have had 0 episodes |
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what is otitis media and how is it diagnosed?
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inflammation and fluid in middle ear. Inflammation causes pain, erythema of TM, fever, cold symptoms.
Bacterial OM characterized by bulging eardrum with purulent fluid behind and drainage after perforation |
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are decongenstants and antihistamines effective for preventing otitis media?
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NO
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Common agents causing otitis media?
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35% Pneumococcus
20% H. influenzae 12-14% Moraxella |
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etiology and epi of sinusitis, what agents?
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Strep pneumo, H. influenzae, Moraxella, also Staph from roots of teeth
Seen at all ages, frequent consequence of viral URI, if not improving in 1 week probably bacterial. |
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most common causes of nonexudative pharyngitis?
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viruses or mycoplasma
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most common causes of exudate pharyngitis?
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GAS (only common form where AB therapy indicated), EBV (mono), adenovirus (#1 cause in kids <3 yo),
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why is there very little epiglottitis in the US anymore?
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Hib vaccine
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Classic clinical picture of epiglottitis?
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children 2-6 in winter, rapid onset of sore throat, dysphagia, chin jutted forward, hoarse,
death can occur from obstruction thumb sign on CXR due to inflamed epiglottis almost always caused by Hib, rarely Strep pneumo tx is ceftriaxone |
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Key features of thromboembolus?
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predominantly a complication of lower extremity DVT
Many go undiagnosed 10% die in the first year pathophysiology: thrombi form due to stasis, intimal injury, |
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virchow's triad?
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Stasis, hypercoagulability, endothelial cell injury.
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what is the gold standard for diagnosing pulmonary thromboembolism?
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chest CT with dye (in olden times was pulmonary angiogram)
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tx for thromboembolism
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DVT prevention, anticoagulation( hep, coumadin), IVC filter, thrombectomy
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categories of pulmonary hypertension?
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passive (venous HTN),
hyperkinetic (increased blood flow), obstructive (thromboembolism, vascular disease), obliterative (inflammatory), venoconstrictuve (hypoxia), idiopathic (?) |
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clinical consequences of pulmonary hypertension?
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- Hypoxemia - due to V/Q mismatch + shunting (pulmonary + cardiac)
-First manifestation is generally DOE + decr exercise tolerance (May also have: chest pain, syncope, signs of RV failure) -Regardless of etiology, once pulmonary HTN is sustained, vasculature changes lead to further damage (generally progressive + not reversible) |
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general pathophys of pulmonary htn?
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endothelial injury -> hypertrophy of vascular smooth muscle -> piling of endothelium -> obstruction to pulmonary flow, decreased area of pulmonary vascular bed -> self-perpetuating primary PH
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what process controls ventilation rate and what part of body does this control?
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metabolic rate determines ventilation, processed and controlled in the medulla, which has tight control over PaO2 and PaCO2.
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What are chemoreceptors?
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control receptors in the medulla, sense changes in PCO2 homeostasis (and H+ independently). the response plateaus in the 80-100mmHg range for PaCO2.
Peripheral receptors in carotid (and aortic) bodies sense changes in PO2 but have limited response to PCO2 and pH. Ventilatory effort primarily determined by PaCO2 |
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What are respiratory mechanoreceptors?
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poorly understood stretch receptors located in muscles of inspiration/chest wall, smooth muscle of airways. Limits inhalation. also irritant receptors and justacapillary receptors in interstitium.
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what can decrease sensitivity of central chemoreceptors?
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normal aging, sleep, athletes, DRUGS
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At what PaO2 does it become a significant determinant of ventilatory effort?
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less than 60-70 mmHg
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What's the Haldane Effect?
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giving O2 to patient with low PaO2 unloads CO2 rapidly from Hg, causing a CO2 narcosis that can suppress respiratory drive?
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definition of apnea?
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absence of airflow for >10 seconds.
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what is sleep apnea?
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frequent episodes of apnea while sleepign, condition affecting 2-4% of population, more in males, most of which are overweight.
presents with loud snoring, restless sleep, daytime somnolence. O2 desat -> systemic htn, pulm HTN, dysrhythmia treat with weight loss, nocturnal CPAP |
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definition of respiratory failure
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in absence of R -> L shunt, when PaO2 is < 60 mm Hg or PaCO2 is > 50 mm Hg (dyspnea + acidemia).
Hypoxemic resp. failure generally due to pulm. process (i.e. lung failure) Hypercapnic resp. failure results from severe lung disease or extrapulmonary disorders (i.e. “pump” failure). caused by hypoventilation. |
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how is hypercapnea defined?
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a high CO2 with a low O2. failure of alveolar ventilation. hypoxemia can cause hypercapnea.
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