week 8- resp 3 Flashcards
What is involved in Diffuse Parenchymal Lung dz?
o alveolar epithelium, pulm capillary epithelium, basement membrane, perivascular and perilymphatic tissues, surrounding tissue
• what are the General clinical features of ILD?
o Insidious/Progressive dyspnea -> limited physical activity
o Persistent non-productive cough
o Mb hemoptysis
o Hx of occupational exposure?
o Mb extrapulm sx: MS pain, weakness, fatigue, fever, photosens
• What is found on PE for ILD?
o crackles
o heart exam in advanced cases: pulm HTN
o general: clubbing, skin rashes, joint nodules
o PFT: restrictive ventilatory pattern (reduced TLC and FVC)
• What is hypersensitivity pneumonitis?
o “extrinsic allergic alveolitis”
o Inhale organic dusts/chemicals in sensitized patient -> granulomatous inflammation of alveolar epithelium
o Delayed reaction 4-6 hrs after exposure
• What are clues that strongly suggest dx of hyper. Pneum?
o hx of recurrent pneumonia (esp regular/pattern)
o resp sxs after move to a new home/school/etc
o water damage to the patient’s home/school/etc
o hx w/ birds: “bird fancier’s lung”
o hot tub, sauna, swimming pool
o exposure to others at home/school w/ similar sxs
o improved sxs on vacation
• what is etiology of hyper. Pneum?
o inhaled organic dusts—fibers (cotton, flax) bagasse (sugar cane), hemp, coffee, bean dust, animal dander, mold, cheese, hay, maple bark, cedar oil, birds, moldy saw dust, wheat flour, brewer’s yeast, mites, compost, detergent, paints/resins
• what are ssx of hyper. Pneum?
o often non-specific
o chronic or recurrent cough and SOB or hx of recurrent episodes/exacerbations of acute resp sxs w/o definite infectious triggers.
• What are the 3 types of hypersensitivity pneumonitis?
o Acute: acute onset, usually w/i 4-6 hrs after exposure; fever, chills, dry cough, chest tightness, malaise, headache, ill appearance; tachypnea, crackles (often at lung base), dyspnea, often NO wheezing; resolves w/i 12 hrs to days after the antigenic exposure is eliminated
o Subacute: gradual onset (less severe, lasts longer); cough (mb productive), dyspnea, fatigue, anorexia, weight loss, ill appearance, tachypnea, crackles
o Chronic: insidious onset; cough, progressive dyspnea, fatigue, weight loss, and exercise intolerance; crackles, possible digital clubbing, and an inspiratory squawk in some patients
• What is the work-up for hyper. Pneum?
o CBC, allergy testing, PFT (restrictive changes) o BAL (broncho-alveolar lavage) shows lymphocytosis
• What imaging is done/found for hyper pneum?
o may show irreversible pulm fibrosis.
o Acute: diffuse interstitial micronodular “ground-glass” opacities
o Subacute: micronodular or reticular opacities
o Chronic: loss of lung volume, alveolar destruction (“honeycombing”)
o HRCT: ground-glass opacities
o Lung biopsy
• What are complications of hyper pneum?
o permanent lung damage with pulm fibrosis
o subpleural blebs may rupture -> spontaneous pneumothorax
o chronic resp insufficiency can lead to cor pulmonale and premature death
• what are eosinophilic pulm d/os? Risk?
o allergic response with accumulation of eosinophils in lung interstitium (alveoli possibly)
o obtain a careful travel hx to assess the risk of fungal or parasitic infx. Areas endemic for parasites (e.g., Asia, Africa, Latin America, South America, SE US)
• what is etiology of eos pulm d/os?
o Allergic reaction to filaria, drug rx (abx, phenytoin, L-tryptophan), intestinal parasites (ascaris lumbricoides roundworm) Candida albicans, Aspergillus fumigata (allergic bronchopulm aspergillosis) inhaled toxins (eg cocaine)
• What are the eosinophilic pulm d/os?
o Acute or chronic eosinophilic pneumonia
• What is acute eos pneumonia? Ssx? Work-up?
o unknown etiology, does not recur
o rapid eosinophilic infiltration of lung interstitium
o Ssx: < 7days of fever, dry cough, dyspnea, malaise, myalgia, night sweats, pleuritic chest pain. Tachypnea, crackles,. Possible pleural effusion. May progress to resp failure.
o Work-up: CT, CBC (eos), pleural fluid analysis (eos, high pH), CXR (opacities, Kerley-B lines), Bronchoscopy (eos seen)
• What is chronic eos pneumonia? Ssx? Work-up? Ddx/mis-dx?
o unknown etiology, mb recurrent
o abn chronic accumulation of eosinophils in lung interstitium
o ssx: fever, weight loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort
o Work-up: CBC (eos), inc ESR, CXR shows characteristic opacities in mid/upper lobes
o NOTE: Clinical picture may lead to misdiagnosis of community acquired pneumonia
• What are the idiopathic interstitial pneumonias? Ssx? Hx? Dx?
o Interstitial lung dzs with unknown etiologies, (but very common in smokers!) present similarly, suspect on history, lead to restrictive lung changes, seen on CXR
o 6 histological subtypes
o Common SSX: cough, dyspnea, tachypnea, reduced chest expansion, bibasilar crackles
o Hx: family hx, tobacco use, drug use, home and work environments
o DX: CXR or CT, PFTs (restrictive, though may be obstructive as well), Lung biopsy show specific histological patterns
• What are the 6 histological subtypes of idiopathic interstitial pneumonias?
- -Idiopathic pulm fibrosis: most common, M smokers, gradual onset, poor px
- -non-specific interstitial pneumonia: 30 yo smokers; pigmented M0s in distal airways
- -acute interstitial pneumonia: healthy M & F >40; abrupt fever, cough, dyspnea. Poss resp failure
• What is drug-induced ILD?
o over 150 drugs or categories have toxic pulm effects leading to: resp sxs, CXR changes, dec resp fxn, histological changes
o Mechanism not known: Abx, chemo, anti-arrythmics, statins, illicit drugs (cocaine, heroin, methadone), anticoagulants
o Dx based on response to w/d of suspected drug
• What are the ILDs due to environmental causes?
o group of dzs from various inhalants, causing replacement of normal lung tissue by abn tissue. Restrictive pulm changes.
o Get clear and complete occupational/exposure hx!
o Pneumoconiosis; occupational asthma; irritant gas inhalation injury; air pollution-related illness
• What is ssx, PE, work-up for environmental caused ILDs?
o SSX: insidious onset of dyspnea, exercise limitation, dry cough (unless 2° infx)
o PE: mid to late inspiratory crackles, tachypnea; late findings: cyanosis, pulm HTN leading to cor pulmonale
o Work-up: CXR shows patchy, subpleural, bibasilar interstitial infiltrates, cystic radiolucencies, “honeycombing”
• What is pneumoconiosis? Types?
o Caused by the inhalation of inorganic “mineral” dusts
o Asbestosis; silicosis; anthracosis; berylliosis; miscellaneous sources
• What is asbestosis? Consequences? Ssx?
o Inhale asbestos fibers: mining, milling, manufacture (insulation)
o -> pulm fibrosis - dose dependent, pleural thickening
o May -> bronchogenic carcinoma (10x > risk in non-smokers; 60-90x in smokers); malignant pleural mesothelioma (seen on CXR and staged with chest CT)
o Ssx: insidious onset of dyspnea; may also have coughing and wheezing
• What is silicosis? Ssx? Ddx?
o Inhale very fine silica particles: mining, pottery, sand-blasting, brick-making, foundries (cast metals), glassmakers etc.
o occurs 5-20 yr. after 1st exposure, ≥1 cm nodules in upper lobes seen on CXR, eggshell calcification of hilar nodes
o smoking or mycobacterium infx increase effect
o SSx: dry cough, dyspnea, tachypnea, later weight loss, hemoptysis
o DDx: COPD
• What is anthracosis?
o (anthracite=coal) “black lung” >15 yr. exposure, worse in smokers
o SSx: may be no resp. sxs, productive cough possible
o More severe state -> progressive massive fibrosis
• What is berylliosis? Ssx?
o (mineral beryllium dust)
o Source: older fluorescent light bulbs, ceramics, chemical plants, electronics, aerospace industry
o SSx: dyspnea, cough, wt. loss
• What are miscellaneous sources of pneumoconiosis?
o talc, Fe oxides, tin oxide, titanium, Cd, aluminum, iron, cotton
• what is occupational asthma? Ssx? Detection?
o Reversible airway obstruction caused by workplace materials: castor bean, grain, detergent, red cedar wood, formaldehyde, antibiotics, epoxy resin etc.
o Type 1 hypersensitivity affecting the bronchi
o SSX: SOB, chest tightness, wheezing, cough and perhaps sneezing, rhinorrhea, tearing—which may not occur until several hours after exposure Temporal association with work
o Can be detected by using Peak Flow Meter at work
• What is irritant gas inhalation injury? Causes? Ssx? Consequences?
o gases dissolve in resp tract fluids, release acidic/alkaline radicals which cause inflammation in trachea, bronchi, bronchioles, alveoli (into interstitium)
o Mb from industrial accidents, mixing household ammonia with bleach (chloramine)
o Directly toxic agents: CN, CO
o Displace O2 leading to asphyxia: methane, CO2
o Others: chlorine, SO2, HS, NO2, NH3
o Ssx: depends on extent and duration of exposure; severe burning of eyes, nose, trachea, bronchi with cough, hemoptysis, wheezing, retching, dyspnea
o May leads to ARDS or Bronchiolitis obliterans (granulation tissue accumulates in bronchioles and alveolar ducts)
• What is air pollution-related illness?
o Airway hypersensitivity to Agents: N and S oxides, O3 (irritant and oxidant), CO, Pb, volatile organic compounds (eg methane), chlorofluoro carbons, particulates
o Triggers exacerbations in asthmatics, COPD
o Most vulnerable: elderly, kids, underlying lung dz
o Airway inflammation, bronchoconstriction, may be permanent decrease in lung fxn
• What are pulm vasculitides? 2 Types?
o Inflammatory leukocytes in pulm (and other) blood vessel walls with reactive damage to mural structures, leading to bleeding (hemoptysis), ischemia and necrosis
o Wegener’s granulomatosis: AI; affects lung, nose, kidneys; Pulm infiltrates, rhinosinusitis, alveolar hemorrhage, glomerulonephritis; Cough, dyspnea, hemoptysis, pleuritic pain, hematuria, proteinuria
o Churg-Strauss syndrome: “Allergic granulomatosis and angiitis”: allergic rhinitis, asthma, alveolar hemorrhage
• What are the 3 connective tissue d/os with pulm manifestations?
o Goodpasture’s syndrome: pulm hemorrhage with severe and progressive glomerulonephritis; M Fe deficiency, dyspnea and rapidly progressive renal failure o Rheumatoid Lung dz: assoc w/ RA; AI dz of joints (pain, stiffness, deformity), skin (nodules), lungs, kidney; usu in pt w/ sero-positive rheumatoid factor; Pulm Ssx: pleuritic chest pain, pleural effusion; CXR shows nodules in lungs, interstitial fibrosis, vasculitis o Lupus (SLE): AI dz of blood, heart, joints, skin, lungs, liver, kidneys; Pulm Ssx: pleuritic chest pain, cough, dyspnea, URIs, dec lung volume, hemoptysis
• What is pulm amyloidosis? Ssx?
o relatively rare; unknown cause
o Amyloid protein deposition in lung (also commonly in heart, spleen, intestine, kidney)
o 3 main pulm types: tracheobronchial, nodular pulm, alveolar septal
o Pulm ssx: (chronic and mild) fever, dyspnea, cough, hemoptysis
o CXR shows multiple pulm nodular opacities, low density, irregular contours; Biopsy will confirm
• What is sarcoidosis?
o chronic dz of unknown cause; affects multiple systems; non-caseating granulomas, (nodules filled with macrophages) leading to inflammation of the involved tissues
o lungs are usually the first area to be affected, may lead to pulm fibrosis
• what is incidence, age, sex of sarcoidosis?
o Incidence: worldwide, in all races and both sexes; young women of African descent (10-20:1 over Caucasian); also prone–Scandinavian, Northern European or Puerto Rican ethnicities
o Age: most common 20- 40yo
o Sex: F>M
• What is etiology of sarcoidosis?
o inflammatory response (T lymphocytes, macrophages, cytokines) to environmental exposure (viral, bact. infx, organic or inorganic agent) in a genetically susceptible person leads to the development of non-caseating granulomas
