Respiratory Notes set 3 Flashcards

1
Q

Eosinophilic Pulmonary Disorders

A

Accumulation of eosinophils in lung interstitial or alveoli.
Considered an allergic response, usu. to drugs. Maybe parasites.

Acute & Chronic forms.

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2
Q

Acute Eosinophilic Pneumonia

A

*Does NOT recur.

  • Rapid eosinophilic infiltration of lung interstitium.
  • SSx: less than 7 days of fever, dry cough, dyspnea, malaise, myalgia, night sweats, pleuritic chest pain (if occurring at the edge of the lung). Tachypnea, crackles, and possible pleural effusion, which may progress to respiratory failure.
  • Work Up: CT, CBC (eos.), pleural fluid analysis (eos, high pH), CXR (opacities, Kerley-B lines), Bronchioscopy (eos seen).
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3
Q

Chronic Eosinophilic Pneumonia

A

*May recur.

  • Abnormal chronic accumulation of eosinophils in lung interstitium.
  • SSx: fever, wt loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort.
  • *Clinical picture may lead to misdiagnosis of community-acquired pneumonia
  • Work Up: CBC (eos), CXR shows opacities in mid/upper lobes.
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4
Q

Idiopathic Interstitial Pneumonias

A
  • Interstitial lung diseases with unknown etiologies (happen to be very common in smokers)
  • all present similarly, suspect based on Hx. Lead to restrictive lung changes seen on CXR
  • Hx: family hx, tobacco use, drug use, home & work environments
  • SSx: Cough, dyspnea, tachypnea, reduced chest expansion, bibasilar crackles

-Dx: CXR or CT. Pulmonary function tests usually restrictive, but can be obstructive. Lung biopsy shows “specific” histological patterns

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5
Q

Drug-Induced ILD

A
  • Many drugs/drug categories have direct toxic pulmonary effects leading to respiratory sx, CXR changes, decreased respiratory fxn)
  • Examples: antibiotics, chemotherapy, anti-arrytmics, statins, illicit drugs (cocaine, heroin, methadone), anticoagulants.
  • Dx: based on response to withdrawl of the suspected drug
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6
Q

Environmental causes of ILD

A
  • Group of diseases with replacement of normal lung tissue by abnormal tissue. Restrictive pulmonary changes ensue. *Want complete occupational/exposure hx.
  • Sx: insidious onset of dyspnea, exercise limitation, dry cough (unless there is a secondary infection)
  • PE: mid-late inspiratory crackles, tachypnea. Late findings: cyanosis, pulmonary htn leading to cor pulmonale
  • Work Up: CXR shows patchy, subpleural, bibasilar interstitial infiltrates, cystic radiolucencies, and “honeycombing”
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7
Q

Types of ILD

A
  • Pneumoconiosis
  • Occupational Asthma
  • Irritant Gas Inhalation Injury
  • Air-Pollution Related Illness
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8
Q

Types of Pneumoconiosis

A
  • Asbestosis
  • Silicosis
  • Anthracosis
  • Berylliosis
  • Miscellaneous sources
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9
Q

Asbestosis

A
  • Caused by inhalation of asbestos fibers from mining, milling, manufacture (insulation), which leads to pulmonary fibrosis; a dose-dependent pleural thickening.
  • Can also lead to: bronchogenic carcinoma (10x greater risk in non-smokers, 60-90x in smokers).
  • Malignant pleural mesothelioma* can be seen on CXR and staged with chest CT
  • Sx: insidious onset of dyspnea, may also have coughing & wheezing
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10
Q

Silicosis

A
  • From inhalation of silica particles from mining, pottery, sand-blasting, brick-making, foundries, and glass makers.
  • *occurs 5-20 years post-exposure, worse in smokers.
  • SSx: dry cough, dyspnea, tachypnea, later wt loss, hemoptysis*
  • Imaging: CXR shows 1cm nodules in upper lobes and eggshell calcification of hilar nodes.
  • DDx: COPD, lung cancer
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11
Q

Anthracosis

A

“Black Lung” from over 15 yrs of exposure, worse in smokers

  • SSx:May be no respiratory sx, productive cough sometimes.
  • More severe state leads to progressive massive fibrosis
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12
Q

Berylliosis

A

Mineral beryllium dust from old fluorescent light bulbs, ceramics, electronics, aerospace industry.

-SSx: dyspnea, cough, wt loss

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13
Q

Miscellaneous causes of pneumoconiosis

A
Talc
Iron oxides
Tin oxide
Titanium 
Cadmium
Aluminum
Iron
Cotton
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14
Q

Occupational Asthma

A

Asthma caused by workplace materials. Type 1 hypersensitivity affecting the bronchi.

  • Compounds could include castor bean, grain, detergent, red cedar wood, formaldehyde, antibiotics, epoxy resin and others.
  • SSx: dyspnea, chest tightness, wheezing, cough, perhaps sneezing, rhinorrhea, tearing. *May not occur until several hours after exposure.
  • Can be detected using Peak Flow Meter AT work.
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15
Q

Irritant Gas Inhalation Injury

A

Inhaled gasses enter the fluid of the respiratory tract and release acidic or alkaline radicals -> inflammation of trachea, bronchi, bronchioles, alveoli, etc.

  • Causes: industrial accidents, mixing ammonia & bleach (chloramine)
  • Directly toxic: cyanide, carbon monoxide
  • Indirectly toxic: methane, carbon dioxide (displace O2 -> asphyxiation)
  • Others: Chlorine, sulfur dioxide, hydrogen sulfide, nitrogen dioxide, ammonia
  • SSx: severe burning of eyes nose, trachea, bronchi, with cough, hemoptysis, wheezing, retching, dyspnea (severity depending on extent of exposure). May lead to ARDS or Bronchiolitis obliterates (accumulation of granulation tissue in bronchioles & alveolar ducts.
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16
Q

Air-Pollution-Related Illness

A

Airway hypersensitivity to pollutants: oxides of nitrogen & sulfur, ozone (irritant & oxidant), carbon monoxide, lead, volatile organic cmpds (methane), chlorofluoro carbons, particulates

  • Trigger exacerbations in asthmatics, COPD
  • Most vulnerable: elderly, kids, underlying lung dz
  • Can cause airway inflammation, bronchoconstriction, possibly permanent decrease in lung fxn
17
Q

Pulmonary Vasculidites (vsculitis

A

Inflammatory leukocytes in pulmonary & other blood vessels cause reactive damage leading to hemoptysis, ischemia, and necrosis.

Conditions:

  • Wegener’s granulomatosis
  • Churg-Strauss syndrome
18
Q

Wegener’s granulomatosis

A

Autoimmune condition affecting lungs, nose, kidneys. Causes pulmonary infiltrates, rhinosinusitis, alveolar hemorrhage, and glomerulonephritis.

SSx: cough, dyspnea, hemoptysis, pleuritic pain
Lab: hematuria, protinuria

19
Q

Churg-Strauss syndrome

A

Allergic granulomatosis and angiitis - allergic rhinitis, asthma, and alveolar hemorrhage

20
Q

Connective Tissue Disorders w/Pulmonary Manifestations

A

Goodpasture’s syndrome (also autoimmune)
Rheumatoid Lung dz
Lupus (SLE)

21
Q

Goodpasture’s syndrome

A

Pulmonary hemorrhage w/severe progressive glomerulonephritis. Often in young men, present with severe hemoptysis and secondary iron deficiency, dyspnea & rapidly progressive renal failure

22
Q

Rheumatoid Lung dz

A

Assoc. w/rheumatoid arthritis

  • Autoimmune dz of joints (pain, stiffness, deformity), skin (nodules), lungs, kidneys, usually in a pt with zero-positive rheumatoid factor.
  • Pulmonary SSx: pleuritic chest pain
  • CXR: pleural effusion nodules in lungs, interstitial fibrosis, vasculitis
23
Q

Lupus (SLE)

A

Autoimmune dz of blood, heart, joints, skin, lungs, liver, kidneys

  • Pulmonary SSx: pleuritic chest pain, cough, dyspnea, recurrent URI, hemoptysis
  • CXR: decreased lung volume
24
Q

Pulmonary Amyloidosis (rare-ish)

A

Amyloid protein deposition in lung, heart, spleen, intestine, and kidney. Cause unknown.

  • 3 main types: tracheobronchial, nodular pulmonary, alveolar septal
  • *Pulmonary SSx: chronic & mild fever, dyspnea, cuogh, hemoptysis
  • CXR: multiple pulmonary nodular opacities, low density, irregular contours
  • Biopsy to confirm
25
Q

Sarcoidosis (general)

A

Chronic dz of unknown cause affecting multiple systems. *Characterized by non-caseating granulomas (filled w/macrophages), leading to inflammation of the involved tissues

  • *Lungs are the first area to be affected, may lead to pulmonary fibrosis
  • Incidence: worldwide in all races, M=F, except the direct contradiction that young women of African descent 10-20:1 over Caucasian, also prone are Scandinavians, Northern European & Puerto Rican ethnicities.
  • Age: 20-40 yrs, F>M
  • SSx: mild, moderate, or severe; begins with fever, wt loss, joint pain, dypsnea, persistent cough. Other sx: erythema nodosum on legs. Conjunctivitis, tearing, blurry vision & photophobia, rarely blindness. Also brain, nerves, heart, liver, and endocrine systems can be involved.
26
Q

Sarcoidosis findings: Skin, Neuro, Ocular, Musculoskel., HENT, Cardiac, Abdominal

A
  • Skin: (skin involvement common in dark phenotypes) erythema nodosum (most common), plaques, subcutaneous nodules
  • Neuro: CN VII involvement uni/bi-laterally, Bell’s palsy, basal granulomatous meningitis, peripheral neuropathy
  • Ocular: Uveitis, glaucoma
  • Musculoskeletal: myositis, polyarthritis: spondyloarthropathy assoc. w/+ HLA-B27, back or SI pain
  • Head, neck, upper respiratory: crackles on lung auscultation, tonsillitis, parotitis, epiglottitis (hoarseness, stridor, or cough), non-tender lymphadenopathy
  • Cardiac: Cor pulmonale (most common), complete heart block, arrhythmias, bundle branch block (BBB), myocarditis, pericarditis, CHF
  • Abdominal: splenomegaly, helpatomegaly (elevated LFTs), nephrolithiasis (hypercalcemia & hypercalciuria)
27
Q

Sarcoidosis - Labs, imaging, Dx, Course & DDx

A

-Labs: PFT, CBC, CMP (calcium serum levels), gr
-Imaging: CXR, CT, Bronchoscopy
-Dx: biopsy of granuloma during bronchoscopy. 90% show characteristic non-caseating granuloma on CXR, hilar adenopathy. CBC reveals anemia, eosinophilia or leukopenia, PFTs restriction & obstruction in advanced dz
-Course: 2/3 disappears, 20-30% have permanent lung damage (fibrosis), death can occur if serious damage to an organ.
DDx: TB, aspergillosis, histoplasmosis, RA, lymphomas, Wegener’s granulomatosis, hypersensitivity pneumonitis.