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163 Cards in this Set
- Front
- Back
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an area of reversible collapsed or non expanded lungs |
atelectasis |
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Terms used for colapse of lung due to resorption of air distal to an obruction |
Resorption/obstruction atelectasis |
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Signs in symptoms of resorption /obstruction atelectasis |
Fever, absent tactile fremitus, dullness to percussion, absent breath sound,ipsilateral tracheal deviation |
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most common causes of resorption atelectasis |
COPD and postoperative procedure |
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Due to fluids, tumor, blood or air in the pleural cavity that cause atelectasis |
Compression atelectasis |
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Deviation of trachea |
contralateral tracheal deviation |
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MC common causes |
CHF or cancer pts who developed pleural effusion |
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Due to localized or general fibrotic lung changes |
Contraction atelectasis |
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Due to lack of surfactant, as occurs in hyaline membrane disease of newborn or adult respiratory distress sysndrome ARDS |
Patchy atelectasis |
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collateral connections between air spaces through which infection and neosplastic cells can spread |
Pores of kohn |
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Shock lung, diffuse alveolar damage, acute alveolar injury, acute lung injury |
ARDS |
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Non cardiogenic pulmonary edema resulting from alveloalr capillary damage eventually leading to multi organ damage |
ARDS |
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TOP 3 causes of ARDS |
Gram negative sepsis Gastric aspiration Severe trauma |
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Direct Causes of trauma |
Direct lung INJURY - drowning -inhalation injury -pneumonia |
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Indirect Causes of trauma |
Indirect lung injury - Burns - acute pancreatitis -Sepsis -chest trauma - Transfusion |
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Morphology: ARDS |
Short term: - Heavy, firm, red, boggy, lungs -waxy hyaline membrane Long term - Intra-alveolar fibrosis |
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Histological manifestation: ARDS |
Diffuse alveolar damage |
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Pathogenesis |
INcreased vascular permeability and loss of surfactant rendering stiff and resistant to expansion Procoagulation increase while anticoagulation decreases |
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Clinical course of ARDS |
Dyspnea and tachypnea Followed by Cyanosis, hypoxemia, respiratory failure to oxygen therapy Ventilation and perfusion mistmatch |
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Treatment of ARDS |
Low tidal volume ventilation Atleast 6 cc/kg Norma TV= 10-12 cc/kg |
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Clinical presentation |
CXR= diffuse bilateral infiltrate PAWP- < 18 mmHg Pa02:Fi02: <200 mmHg Increased A-a gradient |
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what measurement is used to differentiate CHF from ARDS |
PAWP - Increased in CHF, Dec in ARDS BNP- Increased in CHG, Decreased in ARDS |
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Increased resistance to airflow due to obstruction Reduced Expansion of lung parenchyma with decreased TLC |
Obstructive lung disease Restrictive lung disease |
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Examples of obstructive lung disease |
Emphysema Chronic bronchitis Bronchiectasis Asthma |
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Examples of Restrictive lung disease |
1. Chest wall disorders ( neuromuscular disease, obesity, pleural disease 2. chronic interstitial and infiltrative disease |
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Pulmonary function test in obstructive lung disease |
TLC, RV and A-a gradient will increased FEV1, FVC, FEV1/FVC decreased |
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PFT in restrictive lung disease |
TLV, RV,FEV1, FVC will decrease A-a gradient will increase FEV1/FVC is normal or increased |
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What will maintain the inflammatory response during ARDs |
Macrophage inhibitory factory (MIF) |
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e.g of macrophage derived inflamatory cytokines |
IL1, IL8, TNF |
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Neutrophils during ARDS will Produce |
PAF, Leukotrienes, Protease |
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Sequence in development of ARDS |
Tissue damage Edema fluid accumulation, surfactant inactivation Hyaline membrane formation |
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Mucous gland hyperplasia and hypersecretion secondary to tobacco smoke and air pollution |
Chronic Bronchitis |
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Airway dilatation and scarring due to persistent infection |
Bronchiectasis |
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Signs and symptoms differentiation of Chronic bronchitis vs bronchiectasis |
Both will present with cough, sputum production Bronchiectasis is more associated with fever |
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smooth muscle hyperplasia, excess mucus, inflammation with immunologic cause |
asthma |
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Airspace enlargement, wall destruction of ACINUS usually caused by smoking |
Emphysema |
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Inflammatory scarring/obliteration of the bronchiole |
small airway disease/ bronchilolitis |
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COPD |
Chronic bronchitis and emphysema |
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how do distinguish asthma from COPD |
Presence of revesible bronchospasm in asthma |
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Irreversible enlargement of the air space distal to the terminal bronchioles (Respiratory unit) |
Emphysema |
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Centriacinar/Centrilobular emphysema |
affected area: Central or proximal part of respiratory unit ( i.e ACINUS) Upper lobes and apices Smoking |
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Panacinar emphysema |
Uniform destruction of all parts of the respiratory unit Lower basal lobes A1 antitrypsin deficiency |
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Distal (Paraseptal) emphysema |
Distal acinus Near the pleura and adjacent to fibrosis Spontaneous pneumothorax |
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Irregular emphysema |
Airspace enlargement with fibrosis MC type Clinically insignificant |
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Pathogenesis of emphysema |
Elastase-anti elastase mechanism - Imbalance between pulmonary proteases and their inhibitors |
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Elastase not inhibited by a1 antitrypsin |
Macrophage elastase |
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Description of samll airways |
Bronchioles less than 2 mm |
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Emphysema Morphology |
Alveorlar spaces enlarged, with thin septal, septal capillaries compressed and bloodless Alvolar wall rupture may produce Blebs and Bullae |
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Most common symptoms |
Dyspnea Other signs and symptoms Classical barrel chest with prolonged expiration in spirometry Patients overventilate hence and are well oxygenated at rest (Pink puffers) |
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When will signs and symptoms in emphysema appears |
when 1/3 of lung parenchyma is affected |
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Death in severe Emphysema is due to |
RHF, Respiratory acidosis and coma, massive collapse of lungs due to pneumothorax |
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Other forms of emphysema |
compensatroy hyperinflation after loss of pulmo parenchyma (e.g Surgical lobectomy) withot septal wall destruction Obstructive hyperinflation- Subtotal obstruction, ball valve Interstitial emphysema- due to alveolar tears |
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Persistent cough with sputum for at least 3 months in at least 2 consecutive years in the absence of any identifiable cause |
Chronic bronchitis |
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Thickness of mucus gland layer/thickness of the wall between the epithelium and cartilage and trachea and bronchi (reid index) |
Chronic bronchitis > 0.4 Normal< 0.4 |
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Pathogenesis in Chronic Bronchitis |
Mucus gland hypertrophy and hypersecretion Goblet cell metaplasia |
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Old patient, 50 to 75 years old, with severe early dyspnea, Decreased pa02, Normal to increased paCO2, Without cyanosis, scanty sputum, Hyperinflation and small heart on chest xray |
emphysema
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40-45 year old, mild dyspea, decreased pa02 with increased pCO2, with cyanosis, copious sputum, commonly with infection, prominent vessels, large heart on xray |
Bronchitis |
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Chronic relapsing inflammatory disorder, with paroxysmal reversible bronchospasm due to smooth muscle hyper reactivity |
Asthma |
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Unremitting ASTHMA attack |
Status asthmaticus |
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two major forms of asthma |
Atopic asthma- Classic type 1 hypersensitivity non-atopic asthma- without atopic family history |
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Drugs that can increased asthma |
Drugs that blocks Cox (nsaids) because they tip the balance towards leukotriene vasoconstrictor |
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Pathogenesis |
T-cell differentiation is skewed to produce TH2 type cells TH2 cell predominates over TH1 IL4 and IL5 overproduction by TH2 cause increased eosinophil to increase |
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Mediators of acute asthma attack |
1. Putative mediators - Leukotriene D4, E4, And acethylcoline 2. Scene of the crime mediators - Histamine, PGD2, PAF, 3. Suspects( inconsistently seen) - IL1, IL6, TNF, eotaxin, NO, Bradykinin, Endothelin |
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Acute phase mediators |
Primary (leukotriene) Secondary (Cytokines) |
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Acute phase of asthma is characterized by |
Bronchospasm, edema, mucus secretion, leukocyte recruitement |
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Late phase asthma is characterized by |
Eosinophils, neutro, lympho, mono Persistent bronchospasm and edema, leukocytic infiltration, epithelial damage and loss |
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repeated bouts of asthma causes |
Airway remodelling |
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Characteristic morphology in asthma |
whorled mucus plugs (Curshmann spirals) Crystalloid made up of eosinophil membrane protein (Charcot leyden crystals) |
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Abnormal permanent dialtation of bronchi and bronchioles due to destruction of the muscle and elastic tissue associated with necrotizing infection |
Bronchiectasis |
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Causes |
Congenital/hereditary conditions (e.g Cystic fribrosis, Kartagener's sydrome Post infections (e.g Staph-MCC, pseudomonas, virus, aspergillus, HIV, fungi Bronchial obstruction Other inflammatory states |
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major etiologies of Bronchiectasis |
Infection and obstruction |
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morphology of bronchiectasis |
-More severe changes occurs in the lower lobes -airways dilated up to 4X -present with necrotizing acute and chronic inflammation |
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Clinical course of bronchiectasis |
- Severe persistent cough with foul smelling sputum, hemoptysis, digital clubbing, dyspnea |
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Heterogenous groups of disorders characterized by inflammation and pulmonary interstitial tissue fibrosis particularly the alveolar wall |
Restrictive lung diseas/ Interstial lung disease/ infiltrative lung disease |
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Chest xray in Restrictive lung disease |
Diffuse infiltration by small nodules, irregular lines, or ground glass shadows |
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End result of restrictive lung disease |
End stage lung/Honey comb lung or cor pulmonale |
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Sing and symptoms |
Dry cough, exertional dyspnea, Late inpiratory crackles in lower lung field, lung volume and capacity equally decreased RESPIRATORY ALKALOSIS- Tachypnea |
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Chest xray findings in Restrictive lung diseas |
Diffuse bilateral reticulonodular infiltrates |
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Selected examples |
Idiopatic pulmonary fibrosis pneumoconiosis Sarcoidosis Hypersensistivity pneumonia |
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Fibrosing diseases |
Idiopathic pulmonary fibrosis Nonspecific interstial pneumonia Cryptogentic organizing pneumonia Sarcoidosis Pneumoconiosis |
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Disorder of unknown cause characterized by progressive pulmonary interstitial fibrosis |
idiopathic pulmonary fibrosis |
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Histologic pattern of fibrosis |
Usual interstitial pneumonia |
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repeated cycles of alveolitis by some unidentified agent leading to fibrosis |
Idopathic pulmonary fibrosis
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Hallmark of Idiopathic pulmonary fibrosi |
Patchy interstitial fibrosis which varies in intensity and time |
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Treatment for idiopathic pulmo fibrosis |
Lung transplant |
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Non neoplastic lung response to inhaled organic or inorganic aerosols |
Pneumoconosis |
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Size of most dangerous particles |
1-5 micrometers (Can reach Terminal alveoli) |
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Pneuconeosis development depends on |
-amount of retained dust - Size, shape and particle buoyancy - physiochemical reactivity (toxity) -Particle solubility >highly soluble= rapid toxity > Non soluble= Fibrosis -Additional effects of other irritants |
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Coal |
Antrachosis (simple coal workers pneumoconeosis or progressive massive fibrosis- compromised lung function) |
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Large blackened collagenous scar with central necrosis replace portion of the lung secondary to coal |
Progressive massive fibrosis |
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Cause of Silicosis |
Crystaline forms of silica ( more fibrogenic than amourphous form)
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Asbestos |
Commonly cause LUng carcinoma, mesothelioma, asbestosis |
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Iron oxide |
siderosis |
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Barium sulfate |
baritosis |
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Tin oxide |
stannosis |
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unkwnown cause, characterized by non caseating granulomas in virtually all tissuse but especially lungs, eye and skin |
sarcoidosis
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Morphology of sarcoidosis
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Shaumann bodies- laminated concretion of calcium and protiens
Asteroid bodies- Stellate inclusions inside the giant cell Hilar lymphadenopathy |
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earliest sign of sarcoidosis |
Dyspnea |
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Lab findings |
Increased ACE, hypercalcemia CXR- enlarged hilar and mediastinal LN " potato nodes" |
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Ingested fibers coated by iron containing proteinaceous material to form characteristic beaded, dumbell-shaped fibers |
Asbestos bodies |
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Pulmonary embolism most common cause |
Deep vein thrombosis |
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Most common risk factor in PE |
Immobililization others: Primary Hypercoagulable state (hyperhomocysteinemia, APAS) Secondary hypercoagulable state: Obesity, Pregnancy, cancer, OCP, recent surgery) |
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Pulmonary infarct/embolism morphology |
Usually in patients with preexisting heart/lung disease, lower lobes, wedge shaped apex towards hilus classicaly hemorrhagic |
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Large emboli which causes death in PE |
Saddle emboli |
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CHest xray in PE |
Wedge shaped infiltrate (hampton's hump) |
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D-dimer testing |
Rule out test |
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Other test for PE |
Spiral CT-scan, Pulmonary angiography(Diagnosis) |
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Treatment of PE |
Anticoagulation if without associated hemodynamic compromise add thrombolytics if with hemo compromise |
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Prevention of PE |
Early ambulation Elastic and compression stocking anticogulant for high risk patient (e.g pregnant) Insertion of IVC filter |
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Increased pulmonary artery pressure secondary to to increased vacular resistance or blood flow. Mean pulmo pressure> 1/4 systemic levels |
Pulmonary hypertension |
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Causes of pulmo HPN |
COPD, intestitial lung disease
Congenital or aqcuired heart disease Recurrent thromboemoli Autoimmune disorder |
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Morphology of Pulmo HPN |
-Medial hypertrophy and intimal fibrosis -Plexogenic pulmonary arteriopathy >network and web of dilated thin walled, small arteries |
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Most common signs and symptoms |
Exertional dyspnea OThers: Accentuated P2, fatigue, anginal type pain |
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Localized collections of neutropils (pus) and necrotic pulmonary parenchyma |
LUng abscess |
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Etiology of Lung abscess |
Aspiration- mc cause, usually the right lower lobe and typically has Mixed oral flora Pneumonia epecially one due to S. aureus or kliebsiella Postobstructive septic emboli |
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Single, lung abscess seen most commonly on the right lung lobe is mostly cuased by |
Aspiration |
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Mutiple, diffusely scattered lung abscess is mostly associted with |
Pneumonia, bronchiectasis |
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Cardinal histologic change in Lung Abscess |
Suppurative destruction of lung within a central are of cavitation |
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Clinical findings |
Fever, foul smelling sputum CXR- Cavitation with airfluid level |
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Aspiration sites |
MC. Site- superior segment of the R lower lobe Sitting, standing: Posterobasal segment of the R lower lobe Supine: superior segment right lower lobe Right sided position- R middle lob or posterior segment of R upper lobe |
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acute inflammation and consilidation (solidification) of the lung are due to a bacterial agent |
Bacterial Pneumonia |
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Patients present with fever and chills, productive cough with yellow-green (pus) or Rusty sputum, pleuritic chest pain, decreased breath sounds, rales and dullness |
bacterial pneumonia |
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Chest xray findings in acute pneumonia |
Lobar or segmental consolidation or opacification or bronchopneumonial show patchy opacification |
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Lab results in Acute pneumonia |
Elevated WBC with a left shift (More band neutrophils) |
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Classic phase of pneumonia |
Congestion (active hyperemia and edema) Red hepatization (Neutrophils and hemorrhage) Grey hepatization (Degradation of RBC) Resolution (healing) |
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MC common cause of cap, Lancet shaped diplococci, Treated With PENICILLIN |
Strep pneumo |
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Most frequent cause of invasive disease (type B encapsulated), most common cause of Acute COPD excerbation |
H. influenza |
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Causes epiglotitis, pediatric emergency and high mortality rate |
H. Influenza |
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second most common cause of COPD excerbation |
Moraxella catarrhalis |
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Follows viral pneumonia, high incidence of complications (LUng abscess, empyema) Associated with IV drug abusers, also causes nosocomial infection |
Staph Aureus |
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Causes of HCAP |
Staph aureus Kliebsiella pnuemonia pseudomonas |
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Malnourished people, chronic alcoholic with pneumonia presenting with thick and gelatinous sputum |
Klebsiella pneumonia |
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Occurs in cystic fibrosis patients, high propensity to invade blood vessal with consequent extrapulmonary spread, Associated with flor de li pattern |
Pseudomonas aeroginosa |
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Via aerosols or contaminated water, patients predisposing conditions such as prior organ transplantation, requires hospitalization |
legionella pneumonia |
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Pneumonia with insidious onset, low grade fever, non productive cough, chest pain, myalgia, headache with signs of consolidation |
Atypical pneumonia |
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Most common cause of atypical pneumonia |
Mycoplasma pneumonia others: Chlamydia pneumonia Coxiella burnetti |
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Clinical course of Atypical pneumonia` |
Low mortality rate (1 %) except for pandemics and epidemics |
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Presents in patients in Mechanical ventilation, Gram negative rods (Enterobacteriaceae, pseudomonas) and staph aureus are MC cause |
Nosocomial pneumonia |
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Mixed types aerobes > anaerobes, often necrotizing, pursues fulminant clinical course, |
aspiration pneumonia |
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Chronic pneumonia with presence of epitheloid granuloma progressing to coagulative necrosis with cavities, tree bark appearance, may involve apices |
histoplasmosis |
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Chronic pneumonia with suppurative granuloma |
Balstomycois |
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pneumonia in aids |
Pneumocystis jivereci |
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Principles: HIV pulmo disease |
NOt all pulmonary infiltrates are infectious (e.g Kaposi, Pulm NHL, primary lung CA) CD4 count - > 200 Bacterial pneumonia, TB -< 200 Pneumocystis carini -<50 Mycobacterium avium |
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MCC of CAP |
Strep Peumonia |
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MCC of Colds |
Rhinovirus |
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MCC of croup in infants |
Parainfluenza |
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MC viral cause of atypical pneumonia, bronchiolitis in children |
RSV |
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Fever, cough, conjunctivitis, koplik's spots, warthin finkeldey |
Measles |
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MCC of atypical pneumonia |
Mycoplasma pneumonia |
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Gray pseudomembrane |
C. Diptheriae |
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Contains edema factor, lethal factor, protective antigen |
Bacillus anthracis |
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Anaerobe, draining sinuses in jaw, sulfur granules |
Actinomyces |
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Catarrhal pahse, paroxysmal coughing phase, convalescence phase |
Bordetella pertussis |
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Thumbprint sign (epiglotittis) |
H. Influenza |
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MCC of nosocomial pneumonia and pneumonia in CF |
Pseudomonas |
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Currant jelly sputum, alcoholics |
Kliebsiella |
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Pyocyanin, pneumonia associated with infarction due to vessel invasion |
Pseudomonas |
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Budding yeast with narrow based bud, encapsullated |
Cryptococcus |
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narrow angled branching hyphae with septa |
Aspergillus |
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wide angle hyphae without septa |
Mucor
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Most common |
MC cancer in Men Prostate MC cancer in women Breast MC cause of cancer death LUNG MC common type of lung cancer- Metastasis Mc primary lung cancer- adenoca |
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Dietary drugs that was associated with pulmonary hpn |
Pnentermine and Fenfluramine |
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lung cancer may extend via lymphatic and hemogenous route to the following site |
Adrenals (50 %), Liver (30-50%), Brain (20 %), Bone (20%) |
