9 mo Tx: Rifampin & Isoniazid (INH) 6 mo Tx: Rifampin & Isoniazid (INH) & Pyrazanamide NB: IF Resistant strain or recurrent pt: ADD Ethambutol or Streptomycin
How do you diagnose latent TB?
Positive Mantoux only
When do you treat latent TB?
-Anyone <35; -Recent intimate exposure -HIV POS -If >15 mm Mantoux induration -Previous NEG Mantoux & now converted POS
Latent TB pharmacotherapy regimen
9 mo Isonizid (INH)
Lung abscess etiology & diagnosis
Drinkers pass out, oral bacteria make way into lungs; Look for poor dentition, purulent cough and halitosis-- Confirm with CXR or bronchoscopy
Why is lung CA often well-progressed before identified?
There is no sensory innervation of the lungs, so patient may be asymptomatic until tumor mass interferes with pulmonary function
Lung CA signs and symptoms
Cough, Hemoptysis, Dyspnea. Metastatic S/s: Invasion of neighboring tissue, Distant neoplasia, paraneoplastic syndromes (eg, Cushing's or Phaeochromocytoma)
Indications of local invasion by lung tumors
Cardiac tamponade, dysphagia, bronchial occlusion
The mathematics of mutation: What is the statistical impact of smoking? Of asbestos exposure?
Smoking (Benzpyrene) multiplier: 9X Asbestos multiplier: 5X Both smoking/asbestos: 50X
The two broad classes of lung CA
Small cell, Non-small cell
Etiology of SCLC [Small Cell Lung Cancer]
Arise from neuroendocrine cells.
Lung CA diagnostic tools
Chest film (poor) CT (better): allows visualizing lymph nodes in area Bronchoscopy (variable success)
The prognostic assumption that must always be made with small cell lung cancer.
SCLC is always assumed to be malignant.
Lung cancer staging using TNM classification of CA
1: Tumor confined to the lung, no evidence of node involvement or metastasis. 2: Tumor confined to the lung, Hylar lymph node involvement, but no metastasis. 3a. Tumor confined to the lung, Hylar and ipsilateral mediastinal adenopathy but no metastasis 3b: Tumor may be invading adjacent structures, w/ hilar & contralateral mediastinal adenopathy 4: Distant metastasis
When to deny resection of small cell lung cancer.
1. If class 3B or 4; 2. If FEV1 is already low & you predict it will be reduced by ANOTHER 20% (to below 800 ml) as a result of surgery.
Treatment of NSCLC [non-small cell lung cancer]
1. Resection preferred- if you're sure you'll get it all 2. Radiation- provides symptomatic relief, no increased survival 3. Chemo: almost useless in NSCLC
Treatment of SCLC (small cell lung cancer]
1. Assume malignant at discovery 2. Chemotherapy (Methotrexate or Etoposide) 3. Radiation to primary site 4. Surgery is controversial, only used for limited disease
Lung CA survival & recurrence at 5 yrs by stage
Stage 1: 50% @ 5 yr Stage 2: 30% @ 5 yr Stage 3: 15% @ 5 yr Small Cell: If recurs, won't respond to radiation a 2nd time.
Carcinoid tumors etiology
Neuroendocrine tumors with low malignancy, usually in GI; 28% occur in respiratory system
Carcinoid signs and symptoms
Catecholamine effects: Flushing, Palpitations, Diarrhea, Wheezing, Abdominal cramps; Respiratory effects occur only if pulmonary site, and include: Cough, Hemoptysis, Recurrent PNA, Airway obstruction
1. 24-hr Urine for Hydroxyindole Acetic Acid (5-HIAA, a serotonin metabolite) 2. Serotonin (plasma) 3. Biopsy
Resection Ablation by laser Octreotide
Appearance on CXR and CT of lung nodules. Frequency of malignancy.
Measure 3-6 cm and reside entirely within lung. 20% malignant
Four management strategies for COPD
1. O2 if PaO2< 55 torr 2. Mucous clearing (Guaifenisin & hydration) 3. Exercise! 4. Surgery- lung volume reduction is last resort
Pathogenesis and diagnostic criteria of chronic bronchitis
Pathogenesis: Hypertrophy & hyperplasia of mucous glands in bronchial mucosa, (often with submucosal inflammation) Diagnostic criteria: Productive cough of at least 3 months duration for @ least two consecutive years.
Lab Values & CXR in chronic bronchitis
Labs NORMAL CXR will only show other comorbidities (eg, emphysema)
Chronic bronchitis treatment
Quit Smoking! Mucous clearance (Guaifenisin and hydration) If active infection exists (which you should not assume) Azithromycin, 5d
You want 'em LARGE- Thin COPD's have exaggerated inflammatory response
Why COPD patients may develop pneumothorax
Dead space--> Bullae--> Pneumothorax develops if bullae burst
Bronchiectasis definition and etiology
IRREVERSIBLE dilation of the medium & large bronchi caused by DESTRUCTION OF ELASTIC TISSUE in the airway. Usual causes include: PYOGENIC infectiion, cystic fibrosis, Kartagener's syndrome, Aspergilliosis
Crackles Clubbing Cyanosis "Ground Glass" on CXR [should be even distribution in both lungs] Honeycombing
Interstitial lung disease pathognomic finding and its specificity
"Honeycomb" lung with cross-hatching & nodules on HR CT; 85-90% specific
Interstitial lung disease spirometry and lung test findings
1. DLCO Decreases persistently. This is the most sensitive test. 2. O2 desaturates 15 Torr on exercise 3. Lung volumes & flow rates decrease 4. FEF increases 25-75%
Interstitial lung disease treatment
None is effective in reversing the disease. Prednisone or Prednisolone may be used to suppress inflammation (only little to start)
Differences between non-silicosis interstitial lung disease (NSILD) and ILD
NSILD is more inflammatory- has better response to corticosteroids; Associated with autoimmune disorders: SLE, RA, Polymyositis, BOOP (Bronchiolitis obliterans organizing PN)
Sarcoidosis pathonogmic finding
Lymphatic disease that spreads to form non-caseating granulomas. May appear in ANY organ, but 94% of patients have in lungs (73% Lymph nodes, 32% Skin, 21% Eyes...)
30% pts are symptomatic; SOB, Cough, Hemoptysis
0. Normal 1. Hilar lymphadenopathy 2. Hilar LA + Lung infiltrates 3. Substantial lung infiltrates + fibrosis 4. End stage fibrosis [honeycomb scarring]
Two key Sarcoidosis extra-pulmonary concern
1. Granulomatous Uveitis (red, photophobia --> glaucoma) 2. Hypercalcemia [10-20%] because activated macrophages in the lung and lymph nodes produce calcitriol [vitamin D] independent of PTH -->Cardiomyopathy
1. Goodpastures: Associated w/ idiopathic alveolar hemorrhage & destruction of the glomerular basement membrane. 2. Wegner's Granulomatosis: Associated w/ vasculitis & autoimmune attack by ANCAs [Anti-Neutrophil Cytoplasmic Antibodies] against small and medium-size blood vessels in the lungs & kidney.
Virchow's Triad & what it most often contributes to
Stasis, Injury & Hypercoagulability; Appears as DVT and emboli
Doppler US Impedance Plethysmography Venography
120K cases/yr 50% Untreated Symptomatic are fatal
TWO serious problems PE creates
1. Shunt: (no air, lotsa blood), so hypoxia occurs; 2. Blocked pulmonary vessel raises P-BP to over 40 mm Hg (usual 20/8); NOTE: Shunts don't respond to O2
Dyspnea, Anxiety, Syncope, Chest pain; D-C-3: DVT, S3 gallop & Crackles are pathognomic when together
The two Pulmonary Embolism tests you must perform
1) D-Dimers: [Positive is 90-95% sensitive] 2) EKG: To rule out MI & check for RBBB
PE Gold Standard
Pulmonary Angiography: Way low risk, Way high value; BUT: Spiral CT is better
1. Heparin followed by warfarin 2. Thrombolytics (tPA or Streptokinase) REAL LIFE: DON'T give THROMBOLYTIC- Risks Intercranial hemorrhage
Normal mean Pulmonary Blood Pressure & Pulmonary Hypertension values
Normal is 20/8, so mean is [0.5] + 8 = 18 mm of Hg Pulmonary Hypertension is defined = 25 mm of Hg
Normal causes of P-HTN & why
Ischemic heart dz or LVH/LCHF; (Left side weak, right backs up)
S/s of RV failure & P-HTN
Pedal edema; Increased JVP; S3 (RV "heave")
Diagnosis of pulmonary hypertension
1. Echo; 2. Heart catheterization 3. Pulmonary capillary wedge pressure 4. Spirometry to rule out lung disease mimics
Primary: Warfarin, Vasocilators (CCB or Prostacycline); Secondary: Tx the underlying Dz & correct hypoxia
Two types of Pleural Effusion
Transudate: Low protein/pus Exudate: High protein/pus/blood
Causes of transudates
Non-infectious sources of pulmonary hypertension: CHF, Cirrhosis, Renal failure, Hypothyroid
Causes of exudates; Special classes high in blood or fat
PN, Ix, Malignancy, PE; Hemothorax & chylothorax
Exudate Test values
Protein: >0.5 LDH: >0.6 Also run Glu & pH
Accumulation of air in pleural cavity & sources of air
Pneumothorax; Sources: Lung, Chest wall, Esophagus, Bacterial metabolism in Ix
Most likely pneumothorax pts
Young, thin men 20-40 yrs. Pleural blebs burst
Pneumothorax Tx (clever, really)
Inject doxycycline-- Irritates pleural membranes, and they fuse during inflammatory response.
Who should get 'flu vaccine?
1) 65 years and over 2) All health care workers 3) Chronic pulmonary morbidities [COPD, Asthma, ILD, also DM] 4) 2nd and 3rd trimester pregnancy
Who should get pneumococcus vaccine?
1. All Chronic pulmonary morbidities (COPD< Asthma, ILD) every 5 yrs until 65