Pneumology
🇬🇧
In English
In English
Practice Known Questions
Stay up to date with your due questions
Complete 5 questions to enable practice
Exams
Exam: Test your skills
Test your skills in exam mode
Learn New Questions
Popular in this course
Learn with flashcards
Manual Mode [BETA]
Select your own question and answer types
Other available modes
Complete the sentence
Listening & SpellingSpelling: Type what you hear
multiple choiceMultiple choice mode
SpeakingAnswer with voice
Speaking & ListeningPractice pronunciation
TypingTyping only mode
Pneumology - Leaderboard
Pneumology - Details
Levels:
Questions:
428 questions
| 🇬🇧 | 🇬🇧 |
| What is acute bronchitis? | It is an infection involving large airways (bronchi) without evidence of pneumonia and COPD, occurs with viruses and some bacteria, usually self-limited |
| What is pneumonia? | Infection of pulmonary parenchyma, divided into community acquired (CAP) and nosocomial (could be hospital acquire (HAP) or ventilator acquired (VAP)) |
| Talk about the epidemiology of pneumonia? | CAP is most common encountered condition in clinical practice and is the second cause of hospitalization and most common infectious cause of death |
| What are the risk factors for developing CAP? | Old age, chronic comorbidities (COPD, diabetes, heart disease), Viral illness, smoking, alcohol, Immunocomprimised. |
| What are the most common microbiological causes of pneumonia? | Strep pneumonia, respiratory viruses |
| What are the pneumoniogenic bacteria? | S.pneumonia, haemophilus influenza, Moraxella cattarrhalis, Staph aureus (typical) Atypical: Legionella, mycoplasma pneumonia, chlamydia pneumonia |
| What respiratory viruses cause pneumonia? | Influenza A and B, Rhinoviruses, Parainfluenza virus, Adenovirus |
| What is the current situation regarding bacterial/ viral detection causing pneumonia? | Pneumococcus is declining, but still the nb one cause rarely do we identify the pathogen causing pneumonia (50% of the time) There is also antimicrobial resistance patterns and risk factors to be known in order to know the selection for empiric CAP antibiotic tx. |
| How is the pathogenesis of pneumonia? | Transmission by droplets and to a lesser extent aerosols (legionella) Pathogens colonize nasopharyx and reach alveoli by microaspiration, when inoculum size is sufficient immune defense is impaired resulting in an infection. then replication and inflammation occurs damaging parenchyma causing pnuemonia |
| What is the clinical presentation of pneumonia? | Vary from mild cough and fever to sepsis and respiratory failure. Most common respiratory symptoms are cough (dry or with sputum), dyspnea, and pleuritic chest pain General symptoms are fever, chills, fatigue and hypotension |
| What is the physical exam findings for pneumonia? | Tachypnea, increased work of breathing, crackels in bronchi Tectile fremitus, egophony and dullness percussion |
| How do we diagnose pneumonia? | Clinically compatible symptoms with X ray finding of infiltrates (PA imaging), we see consolidations/ cavitations We also use CT scan for immunocomprimised pt and pt with normal X ray We can also perform labs CBC, CRP and BUN levels Maybe blood and sputum culture, urinary Ag, PCR (viruses) |
| How do we assess the severity of pneumonia? | Use one of the scores, either pneumonia severity index or CURB-65 |
| When do we treat pneumonia? | Pt with oxygen saturation <92%, intermediate scores (CURB>1 / PSI>III) unable to take oral drugs with impaired cognition should be hospitalized Respiratory failure pt should be ventilated and ones with sepsis enter the ICU |
| What is the treatment for pneumonia? | First Abx dose is <4 hours - least possible time to get the dose (depends on severity of condition) Macrolide if resistance <20 percent , if >25 beta lactam w/ macrolide or doxycyclin/ only give fluoroquinolone (if no suspicion of MRSA or pseudomonas If pseudomonas sus (antipseudomonas beta lactam and quinolone ICU pt both beta lactam and fluorquinolone for 5-7 days and stop when pt is afebrile and improving for 2 days Chest radiography required after 4-6 weeks for pt >50 years smokers |
| What is pleura? | It is the space between parietal and visceral pleura, contains 0.3ml/kg of hypo-oncotic fluid, which is all the time changed, produced by parietal pleura from up and gets reabsorbed from down Exception where visceral pleura forms it is in case of heart failure, increasing hydrostatic pressure and thus forming liquid from plasma in capillaries. |
| What are the abnormalities of pleura? | Pleural effusion (pleurisy ) and pneumothorax. When filtration exceeds maximum pleural lymphatic flow effusion occurs (max flow is 30ml/h to 700 ml/h) |
| What is pleural effusion? | When fluid collects in pleural space |
| What are the symptoms of pleural effusion? | Pleuritic pain (due to parietal pleura interacting with liquid , felt at the site of effusion, knife-like pain increased with breathing and could irritate the shoulder) Dyspnea (correlated with size of effusion) Dry cough (due to lung compression) Orthopnea (impaired sleep) |
| What are the physical exam findings of pleural effusion? | Diminished breath sounds or absence at site of effusion (bu sthetoscope) with basal dullness in percussion Tachypnea may be present with large effusion. Pleural rub may be heard initially with parapneumonic effusion. |
| What are the imaging findings in case of pleural effusion? | X ray (PA and lateral view reveals 200ml effusion (PA) and 50 ml (lateral)) US (very useful, if multiple punctures, guides the pleural tap (decreasing the risk of iatrogenic pneumothorax)) Chest CT (reveals spots not seen on X ray, provides potential causes of the effusion- white spots are atelectasis- damaged alveoli, shouldn't be punctured!) |
| What are the indications for thoracocentesis? | Dx: puncture to discover the type of fluid accumulated Therapeutic: to get better breathing and decompression of lung tissue (for bilateral) Done under guide of US to reduce the risk of iatrogenic pneumothorax Needle is inserted at the upper part of the rib (where no innervation and vascularization) after anesthesia We should get rid of fluid periodically and gradually (max 1L/tap since it may cause ARDS if very rapid) |
| What is the difference between atelectasis and effusion on X ray? | Atelectasis shrinks the mediastinum while effusion doesn't |
| What is the normal pleural fluid? | Hypo oncotic (low protein) More alkaline than blood (pH=7.6) we usually get this fluid and test in labs (culture, TB, cytopathy for cancer) May be transudate or exudate (transudate is more common) |
| What is the difference between transudate and exudate? | Transudate (increased hydrostatic pressure or low plasma onotic pressure, pleural proteins/plasma <0.6) Exudate (increased oncotic pressure due to inflammation of capillaries, pleural proteins/plasma proteins >0.6) This is light criteria (Protein ratio >0.5, LDH concentration in effusion >200 or LDH ratio >0.6) |
| What are the causes of transudate pleural effusion? | Commonly congestive heart failure, nephrotic syndrome or cirrhosis with ascites. Less common are dialysis, urinothorax, atelectasis, pulmonary embolism, myxedema |
| What are the causes of exudate pleural effusion? | Commonly malignancy, parapneumonic effusion, pulmonary embolism, TB, pancreatitis, postcardiac injury Less common infection, sarcoidosis, asbestosis |
| What is malignant pleural effusion? | Lung carcinoma is the most common neoplasma, then breast then lymphomas and ovaries Mesothelioma (asbestosis) |
| What is pneumothorax? What are the types? | Collection of air or gas in pleura, puts pressure on the lung and may collapse it. Types include spontaneous (primary like blip for tall thin individuals in europe, or secondary with underlying disease like COPD) Tension pneumothorax (presses lungs and heart could lead to an arrest and causes hypotension) Traumatic pneumothorax (caused by chest injuries) |
| What are the diseases associated with 2ary spontaneous pneumothorax? | COPD, asthma HIV infection, necrotizing pneumonia, bronchogenic carcinoma, sarcomas, TB, CF, interstitial lung disease, idiopathic fibrosis, sarcoidosis... |
| What are the S&S of pneumothorax? | Sudden dyspnea and pleuritic chest pain (more severe for 2ary sponaneous type) Significant cardiorespiratory symptoms -->check tension pneumothorax. |
| What are the radiological findings in case of pneumothorax? | If lung margin is >2cm from chest wall at hilum-->pneumothorax CT scan more sensitive, US may be helpful also |
| What is the PE findings in case of pneumothorax? | No sound at all with auscultation. |
| How is the management of pneumothorax? | Driven by symptoms, if pneumothorax <2cm --> self-limited. Thoracostomy is imp for tension pneumothorax (chest tube) stop smoking after first episode and cancel flight plans and scuba diving could provide oxygen if needed when no bubbles found on chest tube |
| What is lung cancer? | Leading cause of cancer death worldwide, 5 year survival rate is very low (17%). We are having progress with screening and intervention 2 Types: small cell and non-small cell lung carcinoma |
| What are the risk factors of lung cancer? | Most imp is smoking (any smoking type, even passive smokers -second hand) The higher pack years the more risk of getting it Other risk factors are environmental toxins (Asbestosis, metals...), radiation, pulmonary fibrosis, HIV infection, family history and alcohol abuse. |
| What are symptoms associated with lung carcinoma? | Dyspnea, chest pain (parietal pleura involvement/ metastatic pain) Cough and hemoptysis Anorexia, weight loss, fatigue Diffuse pain is possible. important to note that all these may be absent. |
| How is diagnosis and staging of lung cancer? | It is important to answer 2 questions, what cell type and what stage it is. Evaluation done by hx taking and PE, CBC, serum chemistries and CT scan of chest Usually we catch it in a late stage with metastasis to other organs or paraneoplastic syndrome Symptoms of both types are similar. PET scans are useful in assessing unsuspected mediastinal involvement... giving us the right path to go through |
| How to get a definitive dx of lung cancer? | Histopathology, single invasive test may be enough. Strategy depends on size, location, patient condition and expertise to get the definitive dx. Mediastinal and central lesions: bronchoscopy Small peripheral lesions: transthoracic needle aspiration |
| Describe small cell lung cancer. | 15% of total lung cancers, occurs strictly for smokers, typically central airways affected with lymphadenopathy and distant metastasis at dx. Associated with paraneoplastic syndrome (hypoNa - inappropriate ADH, hypertrophic pulmonary osteoarthropathy, inflammatory myopathy, cushing (ectopic hormone secretion) ...) |
| What are the types on non-small cell lung cancer? | Adenocarcinoma (usually occurs with non-smokers, usually located at lung parenchyma as a mass/nodule, metastasizes in other places) Squamous cell carcinoma (Second most common type of NSCLC, occurs for smokers, central airways, present with cough, hemoptysis, post obstructive pneumonia, collapse) Large cell carcinoma (Presents as peripheral mass) |
| How is immunotherapy in non-small cell lung carcinoma? | Testing for EGFR (epidermal GFR), ALK receptor, ROSI... target the mutation kills only cancer cells Example is keritruda mostly for adenocarcinoma |
| How is staging mechanism of lung cancers? | Based on TNM staging system (tumor, lymph node involvement, metastasis) SCLC is limited disease (one hemithorax, ipsilateral lymph node involvement) |
| What are the other types of pulmonary neoplasms? | Carcinoid tumors (1-2%, involve neuro-endocrine cells, smoking not a risk factor, occurs at proximal airways causing obstruction and obstructive symptoms with bleeding, surgical resection) Adenoid cystic carcinoma (salivary gland tumor at lower respiratory tract, surgical resection) Hamartomas (most common benign tumor, calcified, combines fats, proteins, cartilage epithelium..., smooth bordered nodules) |
| What is mesothelioma? | Rare carcinoma metastatic starts at pleura, could be small nodules to confluent sheets that encase the lung. Ass with inhalation of asbestos, advanced disease. Suspected when we see pleural thickening or recurrent exudative pleural effusion with hx of asbestos exposure Dx requires biopsy (cytology study is not sensitive) Tx acc to condition (surgery + chemo + radiation) Very poor prognosis (survival 6-9 months) |
| Where are most common sites of metastasis of lung cancer? | Lymph nodes, brain, bone, liver, adrenals, pleura.. |
| What is the treatment course of action for lung cance? | Depends on cancer type (SCLC usually radio and chemo, others maybe surgery + others...) + symptomatic tx (pain-->anelgesics, oxygen, cough treatment, metastasis tx, pleural drainage, interventional bronchoscopy...) |
| What are pulmonary nodules? | Small radio opacities (<3cm in size) surrounded by normal lung parenchyma. Asymptomatic found incidentally. If larger than 3 cm --> malignant and should be tested. Evaluated by imaging history estimating malignancy. Guidelines according to size, characteristics of the largest nodule (if more than one is present) |
| How should we screen for lung cancer? | Smokers screened annually for 3 years have reduced mortality of lung cancer 20%. Done for aged 50-80 years with no symptoms and at least 20-packyear/ current smokers/ quit less than 15 years ago Done by low-dose CT scan + test if a nodule seen (indeterminate)/ If suspicious further testing and biopsy is needed |
| What are the virshow's triad in pathogenesis of venous pulmonary embolism (VTE)? | Alteration of blood flow (like stasis) Vascular endothelial injury Alterations in blood constituents (hypercoagulable state) |
| What are the risk factors of deep venous thrombosis and pulmonary embolism? | Age >60, cancer and myeloproliferative neoplasm, chemotherapy (bevacizumab, thalidomide), hormonal modulation (estrogen receptors/ exogenous estrogen/ testosterone), heart failure, Immobilization, infection, nephrotic syndrome, obesity, pregnancy |
| What are the inherited causes of pulmonary embolism? | Inherited thrombophilia (factor V leiden mutation, prothrombin gene mutation, protein S and C and Antithrombin deficiency, dysfibrinogenemia) |
| What are the acquired causes of pulmonary embolism? | OCPs with 3rd generation progestins are most important cause of thrombosis in young women (increases within 4 months of using, and decreases 3 months after the cessation) Contraceptive transdermal patches and rings as well Immobilization, congestive failure, medications (tamoxifen, bevaczumab, thalidomide...), antiphospholipid antibody syndrome, myeloproliferative disorder, polycythemia vera...) IBD, nephrotic disease, macroglobulinemia, multiple myeloma leukocytosis, SCA, HIV |
| What are the pt most eligible to get thromboembolism? | 50% inherited thrombophilia associated with presence of an acquired risk factor (surgery, immobilization, OCP) |
| How is the outpatient treatment of PE/DVT? | Most pt with DVT treated without hospitalization / come with excellent prognosis, treated with anticoagulation (acute VTE requires unfractionated heparin, LMWH, fondaparinux, warfarin, or direct oral anticoaugulant (DOAC)) |
| What are the objectives of DVT treatment? | To prevent further clot extension, and acute pulmonary embolism so pt are treated with anticoagulants if they are symptomatic proximal DVT with a risk of PE |
| What treatment options other than AG are used for treating DVT? | When there is a contraindication for AG, we use inferior vena caval filter (also indicated for pt with recurrent thromboembolism despite AGs, pulmonary HTN or conccurrent pulmonary embolectomy |
| How is the diagnosis of pulmonary embolism? | CT angiography and D dimer test (may be unnecessary for outpatients) We can use well's criteria score according to risk factors present A score <2 low proba, between 2 and 6 moderate and >6 high proba If low or intermediate score we look at D dimer level to get positive or negative result Then use multidetector CT to see if there is a PE or not to treat it |
| How is PE classified? | Acute or chronic massive or submassive |
| How is prognosis of PE? | MR: 30% if untreated recurrent PE but if dx and treatment with AG 2-8% |
| How is the pathophysiology of PE? | Deep venous thrombus of lower extremity (usually) (mostly iliofemoral veins) 50-80% originate below popliteal vein and propagate proximally, or within proximal veins Most calf vein thrombi resolve spontaneously only 20% go into proximal veins Thrombus travel to lungs may lodge to bifurcation of pulmonary artery cause hemodynamic compromise Smaller thrombi may go more distally and cause pleuritic chest pain by initiating inflammatory response |
| What are the percentages of pulmonary infarctions and multiple emboli? | 10% only cause pulmonary infarction in patients with cardiopulmonary disease lower lobes being involved in majority of cases |
| What are the symptoms of PE? | Dyspnea at rest or with exertion (within seconds or minutes) Pleuritic pain, cough, >2 pillow orthopnea, calf or thigh pain or swelling, wheezing |
| What does ABG in PE reveal? | Hypoxemia, hypocapnia, respiratory alkalosis However it and pulse oximetry are of limited diagnostic role |
| What are the EKG findings in PE? | Tachycardia with ST-T wave abnormalities. S1Q3T3 (s lead I ...) RBBB (abrupy RV size or hypertrophy with chronic PE) Right axis deviation and P pulmonale with T wave inversion V1->V4 |
| What is the duration of PE treatment? | Depends on risk factors can range from 3 months to lifelong therapy (if transient risk factors or durable ones) |
| What are the prevention measures of PE? | Low dose unfractionated heparin, low molecular weight heparin, warfarin, fondaparinux, DOAG, compression devices and elastic compression stockings. IMP for bedbound patients and undergoing surgery |
| What are the six classifications of sleep disorders? | Central hypersomnolence, Circadian rhythm wake disorders, sleep related breathing disorders, parasomnias, sleep related movement disorders, insomnia. |
| What is excessive daytime sleepiness disorder? | Difficulty staying awake in daytime, it is different from fatigue, just sleepiness, and lack of self-recognition is common as the pt may sleep whilst driving or operating. |
| What are the causes of excessive daytime sleepiness disorder? | May be extrinsic (circumstatial) like not getting adequate sleep causing CVD, obesity, glucose intolerance..., or endogenous causes (disease-related) |
| How to assess excess sleep disorder? | Thorough history (sleep hygiene, sleep environment, time and duration...) 1-2 week diary of sleep-wake schedule (self-realization), or by a wrist actigraph-a device. Epworth questionnaire. May be narcolepsy or idiopathic hypersomnia --> sleep laboratory testing |
| What are the conditions that disrupt circadian rhythm? | Jet lag and Shift work sleep disorder |
| What is jet lag? | Internal sleep clock is out of sync from the local time after going to another time zone, occurs for 1 or 2 days after travel (may include neuropsychiatric issues and insomnia). Going eastwards is harder than westwards. For short travels it is better to stay on same time, for longer ones adaptation is better There are measures taken pre and post flight, and hypnosis during flight has a risk of parasomnia (sleep walking) |
| What is shift work sleep disorder? | Many experience excessive sleepiness, mood perturbation, neurocognitive dysfunction lasting for 3 months. Pt are asked to see if they can edit their sleep schedule, if not feasible they look for ways to adapt like decreasing or increasing light exposure, melatonin... Hypnosis is not very useful as it may have effects (carryover effects into nighttime work period) |
| What is obstructive sleep apnea? | OSA, sleep interruption due to repetitive upper airway narrowing or collapse. Breathing events seen during sleep testing (apneas or hypopneas) may be divided by total sleep seen with apnea-hypopnea Index (AHI) AHI [5-14] / hour -->mild OSA AHI [15-30] / hour -->moderate OSA AHI >30 / hour --> severe OSA But sleepiness degree is not always correlated with AHI |
| How is the pathophysio of obstructive sleep apnea? | Pharyngeal muscles relax causing redundancy of soft tissues lining the airway. Snoring, supination may cause tongue displacement narrowing the airway. Most disordered breathing occurs during REM (rapid eye movement) cycle of sleep (all muscles are atonic except diaphragm and extraocular muscles). Could cause arousal or microarousal (repetitive arousal is associated with developing excessive daytime sleepiness and neurocognitive symtoms of OSA (oxyhemoglobin desaturated) |
| What are the risk factors of obstructive sleep apnea? What are the symptoms? | Most important one is obesity. Symptoms include choking or gasping (most sensitive pretest indicator), overnight awakening, nocturia, morning headaches, unrefreshing sleep and excessive daytime sleepiness in addition to neuropsychiatric symptoms (mood alteration, difficulty concentrating, problems completing tasks) |
| How is the testing for OSA? | Polysomnography (may be home tested for less costly) Strongest suggestion of OSA is excessive daytime sleepiness that resolves with treatment of OSA. |
| How do we treat OSA? | Positive airway pressure therapy (splinting open upper airway, reduces AHI to zero) No effective pharmacology to treat it Weight loss improves it severely, reducing alcohol intake before bedtime, avoiding sedator medication, and supine posture CPAP therapy (positive airway pressure) oral appliance (exerting traction of mandible) Upper airway surgery (maxillomandibular advancement improves AHI, patients not tolerating CPAP, maybe soft palatal procedure, tonsillectomy...) |
| What are central sleep apnea syndromes? | Pauses of airflow caused by loss of output of central respiratory generators in brainstem --> lack of respiratory effort. Cheyen-stokes breathing is associated with heart failure, it is a crescendo decrescendo pattern of ventilation. Risk factor fro CSA is atrial fib, in addition opioids destabilizing ventilation, strokes, brainstem lesions, kidney injury. |
| What are sleep related breathing disorders? | Associated with advanced COPD, obesity, restrictive lung diseases, neuromuscular disorders. Impaired gas exchange that is compromised with sleep (in REM) Hallmark of obesity hypoventilation is daytime hypercapnia, PCo2>45mmHg |
| What is parasomnia? | Sleep walking, terrors and talking (partial arousals from sleep) Undesirable physical events occur during initiation of sleep, more common for children but may occur at any age. Occurs for individuals 5-25 years with family history, discovered by other individuals or injury (NREM movement) REM movement is action consistent with dream awakes the sleeper and recalls the event NREM are outgrown no treatment, while REM are associated with degenerative brain disease |
| What is nightmare disorder? | Recurrent nightmares, causing anxiety and prolonged awakening, associated with psychopathology inversed by mental well-being (antidepressants, antihypertensives, dopamine receptors agonists. Common for acute stress disorder or PTSD in NREM or REM |
| What are the manifestations of restless leg syndrome? | Urge to move legs in sleep, sensations beginning with resting (after lying or sitting for a period), relief with movement, worsening of symptoms in evening (NIGHT), nighttime leg twitching (periodic limb movement of sleep) |
| What are the causes of restless leg syndrome? | Peripheral neuropathy (DM and alcoholism) iron deficiency, kidney failure, spinal cord condition, parkinson's |
| What is narcolepsy? | Severe and persistent drowsiness causing functional impairment, very rare, disrupts sleep-wake, excesive daytime sleepiness. Cataplexy is sudden loss of muscle control (NT1) happens in response to a suddent emotion like laughter or excitement |
| What is insomnia? | Most common sleep disorder, trouble falling asleep, staying asleep or getting good quality of sleep. Can lead to excessive daytime sleepiness, short-term may be caused by stress and can last days or weeks. Long-term (chronic) lasts 3 months and occurs 3 times nightly, fully explained by another health problem |
| What are the symptoms of insomnia? | Trouble falling asleep, trouble staying asleep, unwanted early morning wakening, resistance of bedtime sleep, daytime symptoms of sleep loss (fatigue, impaired attention and memory, negative mentally, irritabiltity... |
| How do we diagnose insomnia? | Hx, sleep diary (week or more) Pittsburgh sleep quality index, sleep study (may be ordered) |
| What is the treatment of insomnia? | Acc to type of insomnia (if associated with a condition or event) support sleep hygeine, CBT (relieves anxiety), sleep medication, homeopathic treatment (melatonin or dietary supplements yoga, hypnosis, aromatherapy with no scientific evidence) |
| What are healthy sleep habits? | Set sleep schedule, dedicated sleep space, mindful of substance use, control light exposure, keep sleep-related anxiety in check, adjust eating habits. |
| What are the most common clinical presentations in lung disease patients? | Cough (most common) and dyspnea Hemoptysis and chest pain are less common (more for cardio) |
| How to assess the dyspnea of a presenting patient? | Determine time course, if acute (<days) [could be caused by airway (bronchospasm), parenchyma (pleural edema, respiratory tract infection), pleura (pneumothorax) and vascular (emboli)] If subacute (days till 3 weeks) [airway (exacerbation), parenchyma (infectious, Wegne's, pneumonia, cyrptogenic), neuromuscular (Guillain-Barre, myasthenia), pleura (pleural disease or effusion)] If Chronic (>3 weeks) [airway (asthma and COPD), parenchyma (multiple disease with slow progression causing fibrosis)] |
| How to assess cough in patient presenting with respiratory disease? | See if dry or productive, sputum suggests airway disease (asthma, bronchitis, excess bronchiactasis |
| How to assess hemoptysis? | Can be due to airway, parenchyma or vasculature, most commonly due to bronchitis (coughing causes bruising of airway) Can be neoplasm (inflammatory) or localized (TB, pneumonia) or diffuse (goodpasture's hemosiderosis). Could be vascular (pulmonary emboli and AV malformation) |
| How to assess chest pain? | From parietal pleura, usually affected with inspiration, pleural neoplasm, inflammatory disorder, parenchymal disorders (pneumonia/ emboli) |
| What are other things necessary to see in history of pt? | Smoking history (pack year, how many packs per day * nb of years of smoking / second hand smoking) Occupation (inorganic dust (asbestos), organic (pollen))) Contact with infectious persons (TB) Comorbidities (RA, neoplasm, AIDS) Meds (radiation, chemo, b-blockers, ACEi) Family history (asthma, CF, a1 antitrypsin) |
| What are the inspection targets in assessing a pt? | Evaluate rate and pattern of breathing. Tachy/ bradypnea/ agonal breathing. Use of accessory muscles, paradoxical breathing, asymmetric expansion, chest wall deformities (scoliosis) |
| What are the palpation targets in assessing a pt? | See breathing symmetry, and transmission of vibratory sounds (decrease in case of obstruction or pleura effusion , increased in case of consolidation) |