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66 Cards in this Set
- Front
- Back
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COPD definition
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– a disease state characterized by airflow limitation that is not fully reversible
Both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases |
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COPD pathophysiology
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lumen occlusion by mucus secretion - chronic bronchitis
too many goblet cells, cause wrinkles thickening of walls increase in lymphatic, cause more wrinkling breaking of alveoli walls - emphysema increased neutrophils, macrophages, t lymphocutes, eosinophils inflammation stays around even if you stop smoking ciliary dysfunction - destroyed and loss of beat frequency increased mucus secreting cells Structural changes – fibrosis Destruction of alveolar walls – emphysema Vascular changes – pulmonary hypertension, cor pulmonale Systemic inflammation Poor nutritional status Reduced BMI Impaired skeletal muscle – weakness and wasting Multicomponent disease – mucociliary, airway inflammation, structural changes, systemic component, airflow limitation |
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COPD dx
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FEV1/FVC < 0.70
And FEV1 <80% TLC elevated Elevated RV Decreased DLCO |
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COPD staging
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Staging:
Mild FEV1/FVC <0.70 FEV1 >80% Moderate: Fev1/FVC <0.70 Fev1 50-80% Severe fev1 30-50% Very severe – need oxygen |
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tx of COPD
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Tx. Bronchodilators
Inhaled steroids Oxygen Surgery Smoking cessation – best thing to do for a COPD patient Prophylaxis Long term bronchodilator Pneumovax Fluvax Bone densitometry for women and men Management – pulmonary rehabilitation Supplemental oxygen Surgery Inhaler – do not develop resistance to steroid |
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CF genetics
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chromosome 7
F508 most common Results in: Impact on periciliary layer hydration Normal: sodium, chloride and water with ciliary movement to clear mucus Abnormal: failed secretion of chloride, coupled with abnormal sodium absorption from airway lumen causes thickened layer and thus impaired clearance |
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childhood presentation and common infections of CF
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Childhood:
Respiratory most common Chronic cough Recurrent pneumonia Staphylococcal pneumonia Pseudomonas aeruginosa Nasal polyposis Upper lobe bronchiectasis Sinusitis Digital clubbing Gatrointestinal: Meconium ileus Pancreatic insufficiency Rectal prolapsed Biliary cirrhosis Distal intestinal obstruction syndrome Hypoproteinemic edema Recurrent pancreatitis Liver disease: Decreased bile flow, biliary obstruction, increased toxic bile acids, biliary fibrosis |
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CF dx
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Dx.
Positive sweat test Genetic analysis compatible with CF Newborn screening Newborn Screening: Immunoreactive trypsinogen is elevated in cystic fibrosis Confirm with two IRT tests in some states or in others IRT and DNA test Benefit – improved nutritional intervention and outcomes in 1st years of life Slows progression of lung disease Factors affecting long term outlook: Genetic mutations Medical interventions Environmental exposures |
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CF tx
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Therapies – replace gene, modify CFTR, modify ion transport, augment clearance, antibacterial therapy, reduce inflammation, replace damaged lungs
Bacterial colonization: Early years – more likely Staphylococcus aureus By age 8 – pseudomonas aeruginosa most common Antibacterial Therapy: (1)intermittent use of systemic antibiotics (2)intermittent and chronic use of inhaled antibiotics Choice guided by culture of sputum Infection and the accompanying inflammation is the cause of lung damage. Once infection is established it can be controlled but not eradicated. Intermittent flare-ups of infection occur (pulmonary exacerbations). They are treated with discrete courses of antibiotic therapy Exacerbation: Increased cough Change in sputum production Hemoptysis Change in appetite or weight Change in activity Exercise intolerance Fever uncommon Increased respiration rate Change in chest sounds (increased crackles) Retractions or accessory muscle use Decreased weight Change in spirometry |
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rhDNAse for CF
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(B) Augment Airway clearance
Chest percussion, flutter valve, high frequency chest wall oscillation, positive expiratory pressure valve, autogenic drainage, active cycle of breathing rhDNAse – neutrophil-released DNA increases viscoelasticity and adhesiveness of CF sputum breaks down extracellular DNA, improving clearability Complications of CF: Hemoptysis Pneumothorax Allergic bronchopulmonary aspergillosis Cor pulmonale Chronic respiratory insufficiency Lung Transplantation: Survival – 85% in 1 year but only 50% by 5 years Trade CF lung disease for transplant disease – leads to bronchiolitis obliterans |
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methacholine challenge
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Methacholine Challenge
Asthma suspected Normal spirometry Nonspecific bronchial provocation Give until 20% reduction in FEV1 |
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cardiopulmonary exercise testing
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Cardiopulmonary Exercise Testing
Maximal stress test Measures the ability to perform work Takes into account all organ systems Relies on the cohesive integration Can discriminate differential diagnosis Lead to a change in therapeutics When you max out oxygen delivery, you begin doing anaerobic exercise…creating more CO2 Need to breathe more to exhale CO2 Measure inhaled and exhaled gases Do it to measure actual physiology, not just lung volumes |
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V/Q
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high - dead space problem
low - shunt |
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endobronchial ultrasound
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Endobronchial Ultrasound:
Adjunct to bronchoscopy Look for abnormalities outside of airway tract Use for tumor biopsy Indications: Guide to biopsy of peripheral lung lesions Evulation of mediastinum Evaluate carcinoma in siute Go after small (1 cm or less) Go for things that are PET positive |
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electromagnetic navigation
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Electromagnetic Navigation
Small peripheral lesions Tattoo the lesion for thoracic resection Fiducials for gamma knife radiation Cross reference CT with MRI to navigate |
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Thoracic Ultrasound
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look for PE
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Tumor debulking techniques
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Laser – occluded the blood supply to a tumor
Argon Plasma Coagulation – APC is a thermal energy mechanism to stop blood supply Cryotherapy – freeze Does not kill blood supply Good for sticking to things Or lesions that aren’t going to bloody Photodynamic therapy Targeted destruction of cancer tumor Give a specific radiosensitizer that accumulates in cancer tissue Target radiosensitizer to kill tumor Use for HPV in airways Stenting Use removable and non-terminal stents for collapsed lung segments |
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asthma advanced therapy
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Bronchial thermoplasty – “cook” airway to decrease smooth muscle
Causes remodeling of asthma to go away |
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emphysema advance therapy
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Smoking-centrilobular emphysema
Insert one-way valve to collapse and decrease volume of lungs Intentionally collapse part of lung |
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malignant effusions advance treatment
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Lung and breast, lymphoma
Fluid builds up around lung Tx options: Repeat draining Indwelling catheter Inject scarring agent like talc Binds pleura together so no potential space Inject catheter so patient can drain – PleurX Catheter |
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asthma prevalence
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Higher percentage of children have it, but more total number of adults have it
African Americans more common More African Americans die from it Rising increase in African Americans Children tend to grow out of it F>M in adults In children M>F Men tend to outgrow |
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asthma pathology
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Pathology:
Allergen causes acute inflammation and it becomes chronic inflammation Chronic inflammation can cause remodeling Allergen activates mast cell Releases histamine, tryptase, prostaglandins CD4 T cells activated, release IL4/LF5 to get eosinophils Eosinophils release ECP and MBP that destroy epithelial membrane Also get neutrophils Chronic – adhesion molecules in lung are susceptible to repeated allergen exposure Airways remodeling: Epithelial layers are denuded Loose ciliated border, changes in cells so they are no longer protective of infection Subendothelial thickening Smooth muscle hypertrophy Collagen deposition Mucus hypersecretion |
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flow volume loops of asthma
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Flow volume loops: (Spirometry)
Asthmatic has a curve Collapse in flow volume from remodeling Narrowed lumen Spirometry: FVC remains the same but FEV1 falls Cant breathe out During attack Methlycoline challenge – induces asthma attack |
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asthma tx
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Tx.
Use inhaled steroids and long acting beta2 agonist for controller Leukotriene modifier Used every day Use short acting beta2 agonist as needed (reliever) Some have anti-cholinergic Severity Class: Step 4 – severe persistent Symptoms all the time Step 3 – moderate persistent Daily symptoms Need low to medium inhaled steroid + LABA beta2 agonist Step 2 – mild persistent On a steroid, low dose Weekly Step 1 – mild intermittent Monthly Step 1 – normal lungs Maybe symptoms during allergies Need just a reliever and not a controller Treatment based upon severity Inhaled steroids – reduce hospitalizations and risk of death Patient compliance: poor Lack of understanding, education, and skills Symptoms correlate poorly with FEV1 And patient’s assessment of their symptoms |
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asthma monitoring...noninvasive
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Give patients a spirometry to help monitor asthma symptoms
• Persistent asthma should be treated with daily long-term controller medications • Inhaled corticosteroids are the most potent anti-inflammatory therapy • Stepwise approach to pharmacological therapy is recommended to gain and maintain control • Frequent reassessment of patients: STEP-UP or STEP-DOWN • Referral to asthma specialist is recommended for difficult-to-control patients Non-invasive biomarkers for inflammation Measure sputum eosinophilia Exhaled NO Better than standard guidelines for control Goals Reduce discomfort and impairment Identify and avoidance of triggers |
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Allergic Rhinitis
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Allergic Rhinitis
IgE mediated inflammatory reaction of the nasal membranes Itching, sneezing, rhinorrhea, and nasal congestion High rate of asthma patients have rhinitis “Allergic march” rhinitis progresses to asthma Th2: central regulator cell of response Mast cell – has tryptase and PGD/LT and cytokines Degranulates by R1 receptors Get release of these factors sets of cascade Get involvement of eosinophils in lung and upper airway Upper airway – get basophils Allergens: Important in rhinitis and asthma Perennial: Dust mites, cockroaches, pets Seasonal allergens: pollens, molds Allergens – innate properties that enhance uptake by dendritic cells and exacerbate allergic disease Can have proteolytic activity that allows cleaving of tight junctions and can enter epithelium easier…get to APC faster Dust mite: can activate TLR 4 Pollens have NADPH oxidase activity increasing oxygen species in airway - inflammation Chitins up regulate chemokine release - inflammation Point is that allergens have innate ability to elicit immune response |
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Sinusitis
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Sinuses:
Sinusitis: inflammation of paranasal sinuses Not often due to infection Acute sinusitis: usually due to infection Chronic sinusitis: often not infection With inflammation: occluding of ostiomeatal unit leads to infection Hypoxic environment, anerobic bacteria grow Sinus cavities filled with psuedostratified ciliated columnar epitheliam, goblet cells Cilia sweep mucus towards ostial opening If obstruction, mucous impaction, then purulent drainage, decerasd o2 levels, anaerobic environment, bacterial growth favored Acute Sinusitis: Infectious etiology Viral most common If bacterial: S. pneumonia h. influenza m. catarrhalis Nosocomial – gram neg enteric or gram positive cocci Antibiotics: after 7-10 days Adjunctive agents for symptomatic relief Chronic sinusitis: Chronic rhinosinusitis Inflammation varies in subtypes CRS without nasal polyps CRS with nasal polyps Allergic fungal sinusitis |
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Chronic Sinusitis
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(1)CRS without nasal polyps:
Cause: Structural, infectious, allergic PMNs, mononuclear, some eosinophils Glandular hyperplasia, submucosal fibrosis Tx. antibiotics (2)CRS with nasal polyps Not infection – superantigen effect of staph enterotoxins is the cause Can activate T cell without APC Broader activation of T cells and inflammation Eosinophil infiltrates Associated with nasal polyposis, atopy, aspirin sensitivity, asthma (3)Allergic Fungal sinusitis (AFS) Most common form of fungal sinusitis Occurs in immunocompotent patients Hypersensitivity response to saprophytic fungi as aspergillus Depends on geographic areas |
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Type II hypersensitivity response
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antibody response
Type II – Antigen on tissue, get antibodies on antigen, Fc activates compliment to destroy tissue Goodpastures: Anti-glomerular basement membrane Pulmonary hemorrhage and hemoptysis Alveolar infiltrates M>F Young adults Therapy includes plasmapheresis with high dose of corticosteroids |
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Type III hypersensitivity response
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compliment mediated (immune mediated)
Type III – Immune complex mediated tissue injury Immune complexes deposited and nearby tissue gets destroyed with complex Vasculitis Systemic Lupus Erythematosus Pleurisy, coughing, dyspnea Abnormal pulmonary function tests Sometimes normal CXR Pleural effusion |
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Type IV hypersensitivity
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delayed type - T cell mediated
Type IV Delayed type hyerpsensitivity APC presents antigen to T cell, leads to production of cytokines and inflammation Can involve different types of lymphocytes – leads to different types of inflammatory responses |
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ABPA (allergic bronchopulmonary aspergillosis)
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Complex Allergic Response
Allergic Bronchopulmonary Aspergillosis (ABPA) Get in association with asthma Antibody and cell mediated mechanisms Findings: eosinophilia Asthma, fleeting pulmonary infiltrates, total serum IgE, specific IgE/IgG for aspergillus, preciptans of IgG, can identify aspergillus Stages: I – acute, II – remission, III- reexacerbation, IV – corticosteroid dependent, V – fibrosis Management: slower taper of prednisone, follow total serum IgE levels |
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IPF/UIP
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IPF:
Very common 50-70 onset m>f smoking risk factor symptoms – progressive dyspnea, cough for months to year (avg = 2 years) signs = Velcro rales on exam, cyanosis HRCT – Lower lobes most common Subpleural articulations and honeycomb changes Cysts are thick walled Get dilation of airways in lower lobes Dx. Gold standard is lung biopsy Thorascopy or thoracotomy Cant do bronchoscopy or bronchoalveolar lavage because samples are too small Biopsy in younger patients with atypical presentation Prognosis Poor Tx. Lung transplantation best option Mucomist, prednisone (steroids) |
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non-specific interstitial pneumonia (NSIP)
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Non-specific Interstitial Pneumonia (NSIP)
Dyspnea, cough Bilateral infiltrates or consolidation without much honeycombing Ground glass opacities Occurs in association with hypersensitivity, resolving infection, collagen vascular disease Desquamative Interstitial Pneumonitis and Respiratory Bronchiolitis Associated ILD (DIP/RBILD) Usually associated with smoking Cough and dyspnea PFTs show obstruction or restriction DIP usually restrictive, RBILD usually obstructive If you stop smoking, may or may not get better |
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Hypersentivity Pneumonitis
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Hypersensitivity Pneumonitis
Acute and chronic forms Acute: inhalation of antigen followed by mailase, fever, cough…mimics viral pneumonia Chronic: present like UIP, can lead to end stage lung disease Causes: thermophilic bacteria, molds, other bacteria, amoebi, insect products and chemicals Chronic: farmers, bird fanciers Honeycombing Tx. Remove causative agent Three types of presentation, acute, subacute, chronic Similar symptoms to UIP/IPF Granuloma formation with lymphocytes |
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sarcoidosis
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Sarcoidosis:
Idiopathic 20-40 years F>M African Americans >>>Caucasians Symptoms: 1/3 asymptomatic 2/3 dyspnea and dry cough Extrapulmonary symptoms – multiple organs CXR: stage I – bilateral hilar adenopathy Stage II – bilateral hilar nodes and apical reticulonodular infiltrates Stage III – apical infiltrates Stage IV – fibrosis of apices with hilar retraction and honeycomb changes Prognosis: 30% resolve 30% with treatment 30% no resolution Tx. Asymptomatic – observe Severe – treat with corticosteroids, methotrexate, infliximab |
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Asbestosis
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Asbestosis:
At least 10 year latency The longer since first inhalation, more likely First work exposures most important Interstitial lung disease Fine reticular nodular markings – very fine Starts in lung bases Latency often >20years Pleural plaques Parietal Posterior-lateral 6-9th ribs Bilateral 20 years latency Do not affect lung function Scarring in base of lungs Earliest finding – benign pleural effusion After 10 years May be bloody Get blunting of phrenic angles Thickening of visceral pleural Plaques can calcify – parietal pleural |
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mesothelioma
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Mesothelioma:
Exposure hx 70-80% 30-40 yr latency Risk not dose dependent 3 types – epithelial, sarcomatous, desmoplastic Epithelial has best survival Desmoplastic – difficult to diagnose Gene and environment interaction Families tend to get any kind of cancer – genetic predisposition Pleural effusion common Bloody Cytology rarely dx – need tissue Symptoms – pleuritic, dyspnea, cough, weight loss Tumor encases lung Smoking and asbestos exposure = 50-100% likely hood of bronchogenic cancer Cell types are equal to smoking induced…all types increased |
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occupational asthma
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Occupational Asthma: variable airways narrowing that is causally related to exposure at work
10% all asthma Occupational exposures can worsen pre-existing asthma (different than occupational asthma) Specific to work place – need to remove them from work place environment Metal refinery largest exposures, cotton workers Hx suggests occupational exposures Need period of 1-5 year sensitivity to exposure (latent period of immunologic sensitization) TDI Causes RADS – very acute irritant reaction Overwhelming exposure – high level exposure Nonspecific bronchial hyperreactivity there after Etiologies of occupational asthma: Low weight Isocyanates Woods Glues Colophony Dyes High weight flour Animal handlers Latex Psyllium Crab processing Antibiotics |
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Silicosis
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Silicosis – exposure to stone and sand
Sand blasting most common Findings: Sensation of chest tightness Wheezing Cough/sputum production Spirometry – hard to tell difference with COPD Xray – round large nodules Start in apex May coalesce and calcify – egg shell calcification May calcify in hilar nodes Scarring in apex, and makes lower lobes bullae Bilateral Progressive massive fibrosis and turn into cavity Immunity – can have scleroderma and rheumatoid arthritis High prepotency to have fungal and microbacterium infection Tx. Controversial Prognosis – bad Often die of fungal/mycobacterium diseases |
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Pulmonary hypertension
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Symptoms:
Breathlessness, fatigue, weakness, angina, syncope, abdominal distension PE: Loud P2 Early systolic ejection click TR murmur Right sided fourth heart sound Jugular venous distention Peripheral edema Dx. Need to look for secondary or comorbidities associated with pulmonary hypertension Tests: echocardiogram Right atrial and ventricular hypertrophy Flattening of intraventricular septum Small left ventricle Gold standard – right heart catheterization 1/3 systolic pressure By definition mPAP >25 |
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pulmonary hypertension pathogenesis
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Pathogenesis:
(1)Excess of endothelin This signals through g coupled receptors, more calcium leading to smooth muscle contraction and hypertrophy (2) nitric oxide pathway cGMP and phodiesterase Phosphodiesterase not inhibiting pathway so vasocontstriction (3)prostacyclin pathway deficiency cAMP Endothelial proliferation in small pulmonary arteries (artioles) Plexiform lesion Intimal proliferation, muscular hypertrophy Intimal fibrosis Necrotizing vasculitis |
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pulmonary vasculitis
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wegeners
churg straus syndrome goodpasture's syndrome |
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wegener's granulomatosis
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Wegener’s granulomatosis –
Nasal or oral inflammation Abnormal CXR – ground glass opacities Abnormal urinary sediment Granulomatous inflammation c-ANCA Tx. High dose steroids |
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churg-strauss
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Churg-Straus Syndrome
p-ANCA – see lobes of nucleus eosinophilic granulomatous lesions with necrosis involving pulmonary arteries inflammation granulomatous vasculitis involving heart, lung, kidneys, CNS CXR – transient patchy densities or nodular infiltrates Often with asthma tx. High dose steroids, cyclophosphamide, azathioprine |
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goodpasture's
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Goodpasture’s Syndrome
Anti-glomerular basement membrane antibodies Pulmonary hemorrhage M>F Linear basement membrane 20-30 year olds Smoking history Tx. Plasmapheresis and steroids |
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hypercapnic vs hypoxemic
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(A) Hypercapnic – increased CO2 blood gas
PaCO2>45 mmHg Acute – develops in min to hrs Chronic – develops over several days or more (B) Hypoxemic – too little oxygen PaO2 <55mHG Acute – develops min to hrs Chronic – several days |
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causes of acidosis/alkalosis
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Causes:
(1)Hypoventilation (2)Ventilation perfusion shunt Gross mismatch of capillary blood and capillary airflow (3)impaired diffusion (4)impaired tissue utilization of O2 |
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alveolar gas equation
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PaO2 = PiO2 – (PaCo2/R)
R = 0.8 |
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right to let shunting
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Right to left shunting:
Mixed venous blood goes directly into the arterial circulation without having first been exposed to alveolar gas P(A-a)O2 gradient is increased Three types: Cardiac or great vessel Pulmonary vascular Pulmonary parenchymal |
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d dimer and PE/DVT
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D-dimer:
Good for ruling out, terrible for ruling in |
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PE/DVT dx
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DVT dx.
Venography is gold standard Compression ultrasound – duplex MRI CT Dx. Pulmonary arteriogram gold standard Expensive Chest CT – better for symptomatic patients Combined CTPA and CT venogram If both negative than patient is likely negative Can use MRA V/Q lung scan – not very specific |
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DVT prevention
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DVT Prevention:
Prevention of thromboembolism Antithrombotic therapy Heparin induced thrombocytopenia Anticoagulants Prevention – heparin and warfarin Should be given for even after hospital stay post surgery |
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prophylaxis for DVT
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Prophylaxis – enoxaparin increases survival rate
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net forces on pleural effusion
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hydrostatic pushes out
oncotic pulls in NET: driving force from parietal pleura drives fluid in Visceral surface – pulmonary veins have less hydrostatic pressure, so there is no net driving force So don’t get fluid pushed from visceral into pleural space |
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transudative vs exudative
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Exudative versus Transudative:
Exudative Protein pleural fluid/Protein serm >= 0.5 LDH pleural/LDH serm >=0.6 LDH pleural >2/3 normal serum |
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causes of transudative vs exudative
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Transudative pleural effusion – alterations in hydrostatic or oncotic pressures and there is movement of fluid in and out of pleural space
Heart failure, liver failure, kidney failure Increased hydrostatic pressure Decreaed pleural pressure Decreased oncotic pressure Tx. – underlying cause Exudative pleural effusion – lung is diseased or inflamed. Hyodrstatic/oncotic pressure are normal, but the vessels are leaky Pleural inflammation Increased capillary permeability Impaired lymphatic drainage Infection Malignancy – metastatic, mesothelioma, lymphatic drainage impaired Problem is on the parietal pleura side |
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malignant pleural effusions
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Malignant Pleural effusions:
Usually bloody, serosanguineous or serous Most commonly breast, lung cancer or lymphoma Mesothelioma is pleural primary Very uncommon |
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complicated parapneumonic
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Complicated parapneumonic:
Effeusion is a pleural effusion associated with pneumonia Empyema is progression to pus in the pleural space Characterstis of complicated: Low glucose <40 Loculatd Positive gram stain Pus ANTIBIOTICS will not cure alone, need drainage <10mm – no need to do thoracentesis Small to moderate – no drainage Large, loculated – drainage needed Gram stain culture positive, pus…must drain WBC count very high Treatment options Systemic antibiotics – if uncomplicated Drainage procedure – if complicated |
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tx for smoking cessation
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Tx for addiction:
Controller + rescue inhaler + behavioral modification Combination therapy has better result than single agents Controller: Patch Bupropion Varenicline Rescue: Inhaler Nasal spray Gum Lozenge Behavioral therapy – identify stressors and triggers Avoid Teaches alternative or coping behaviors Types of counseling Pratical Intra-treatment social support Doctor during appointment Extra-treatment social support Friends and family |
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4 A's of smoking
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ASK about tobacco use
ADVISE to quit ASSESS willingness to make a quit attempt ASSIST in quit attempt ARRANGE for follow-up |
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Sleep Apnea
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m>F
OSA: Apnea – no breath for 10 secodns Hypopnea – flow reduction by 50% AHI – number of apnea hypoxemia events per hour Apneas – Central no effort no flow (nerve) Obstructive – effort, but no flow Mixed – nerve and obstructive |
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risk factors for OSA
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Risk factors:
Reduced airway size – obesity, male Craniofacial features Retrognathia, micrognathia, macroglossia Macroglossia – can be from amyeloid deposition from multiple myeloma Reduced neuromuscular output Gender differences Racial differences – Asian, American Indians African Americans have higher incidence of systemic vascular resistance |
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clinical manifestations of OSA
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Clinical Manifestations:
Restless sleep Snoring Personality changes Morning headaches |
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severity of OSA
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Severity:
AHI greater than 30 Increased cardiovascular risk |
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tx for OSA
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Medical therapy:
CPAP CPAP based on severity and symptoms <5 no CPAP >30 CPAP |
