Respirology Flashcards

Question

What causes hypoxemia with a normal Aa gradient and normal PaCO2?

Answer 1

Low FiO2 (eg altitude)

Answer 2

- shunt - atelectasis - intraalveolar filling (eg pulmonary oedema, pneumonia) - intra cardiac shunt - vascular shunt within lungs

Answer 3

``` V/Q mismatch Airway disease (asthma, COPD) Interstitial lung disease Alveolar disease Pulmonary vascular disease ```

Answer 4

Asthma is a chronic inflammatory disorder of the airways resulting in episodes of reversible bronchi spasm causing airflow obstruction. It is associated with reversible airflow limitation and airway hyperresponsiveness to endogenous or exogenous stimuli. Px with dyspnoea, wheezing, chest tightness, cough, sputum, respiratory distress and symptoms worse at night. There is an improvement of >12% of FEV after giving bronchodilators.

Answer 5

Asthma, COPD, bronchiectasis, cystic fibrosis and inhalation of a foreign body

Answer 6

COPD is the progressive development of airway obstruction that is not completely reversible. Patients typically have periodic exacerbations characterised by weight loss, lung hyperinflation, and gas trapping. There are 2 subtypes characterised by chronic bronchitis and emphysema. These subtypes usually coexist to various degrees. There is a gradual decrease in FEv1 over time with episodes of acute exacerbations.

Answer 7

Chronic bronchitis is a productive cough on most days for at least 2 consecutive years. The obstruction is due to the narrowing of the airway lumen by mucosal thickening and excess mucous.w

Answer 8

Emphysema is the dilation and destruction of air spaces distal to the terminal bronchiole without obvious fibrosis. There is decreased elastic recoil of the lung parenchyma causing decreased expiratory driving pressure, airway collapse, and air trapping. There are two types of emphysema. Centracinar emphysema is when the respiratory bronchioles are predominantly affected. The typical form seen in smokers primarily affects upper lung zones. Panacinar emphysema is where the respiratory bronchioles, alveolar ducts, and alveolar sacs are affected. This accounts for less than 1% of emphysema cases such as in a1 antitrypsin deficiency, and primarily affects the lower lobes.

Answer 9

Bronchitis presents with 'blue bloater' signs and symptoms - chronic productive cough with purulent sputum and heamoptysis - initially only mild dyspnoea - cyanosis (hypoxemia and hypercapnia) - peripheral oedema for RVF (Cor pulmonale) - crackles, wheezes - prolonged obstructive expiration - frequently obese

Answer 10

Emphysema typically presents with symptoms of a 'pink puffer' - dyspnoea (+/- exertion) - tachypnoea and decreased excercise intolerance - minimal cough - pink skin - pursed lip breathing and acessory muscle use - cachetic appearance due to anorexia and increased work of breathing - hyperinflation/barrel chest, hyperresonant percussion - decreased breath sounds - decreased diaphragmatic excursion

Answer 11

COPDERS C- Inhaled corticosteroids (poor response in COPD) O- Oxygen. Home oxygen prevents Cor pulmonale and can decrease mortality P- Prevention (vaccines for pneumococcus and influenza, smoking cessation) D- Dilators. No mortality benefit. LAch (triotropium bromide) & SACh (ipratropium bromide) >SABA, LABA, E- Experimental: lung volume reduction, lung transplant R- Rehabilitation: patient education, eliminate irritant/allergens, excercise rehabilitation to improve physical endurance

Answer 12

Chronic hypoxemia, pulmonary hypertension from vasoconstriction, and or pulmonale

Answer 13

An acute exacerbation of COPD is a sustained worsening of dyspnoea, cough, or sputum production leading to an increased use of medications. Acute exacerbations of COPD may be triggered by a viral URTI, bacterial infection, air pollution, CHF, PE, or an MI.

Answer 14

Give oxygen. For CO2 retainers target 88-92% Bronchodilators SABA + ACh Systemic corticosteroids eg prednisone Give antibiotics if sputum is purelent. Rehabilitation for post exacerbation. Consider ICU admission for life threatening exacerbations and ventilatory support (NIPPV, BiPAP, mechanical ventilation)

Answer 15

Modified medical research scale for dyspnoea

Answer 16

Bronchiectasis is irreversible dilatation of the airways due to destruction of the airways wall resulting from persistently infected mucous. The most common pathogen to cause this is pseudomonas aueroginosa. Bronchiectasis usually affects the medium sized airways.

Answer 17

- Obstruction: tumour, foreign body, thick mucous - Post Infection: pneumonia, TB, measles, pertussis, allergic bronchopulmonary aspergillosis, mycobacterium avian complex (MAC) - Impaired Defences: Cystic Fibrosis, Ciliary Dysfunction (Kartagener's syndrome:situs inversus, bronchiectasis, sinusitis), hypogammaglobiaemia, defective leukocyte function

Answer 18

Bronchiectasis may be difficult to differentiate from chronic bronchitis. Signs and symptoms include: -clubbing - chronic cough purelent sputum, heamoptysis (can be massive) - recurrent pneumonia -local crackles (inspiratory and expiratory) - wheezes

Answer 19

Diffuse hyoerinflation with flattening of the diaphragms, increased retro sternal space, bullae (Lucent, air containing spaces that have no vessels and are not perfused), and enlargement of the PA/RV (Cor pulmonale). Findings do not correlate well with pathology and PFTs or high resolution CT are more informative (CT can differentiate between different types eg pan lobular, intra lobular, paraseptal)

Answer 20

Obstructive pattern on PFTs CXR: non specific findings. Increased marking, linear atelectasis, loss of volume in affected areas, cysts or tram tracking High resolution CT: "signet ring" dilated bronchi with thickened walls where diameter bronchus >diameter of the accompanying artery. Also take sputum cultures, serum Ig levels,

Answer 21

Vaccination for pneumococcal and influenza, Antibiotics for exacerbations Inhaled corticosteroids Oral corticosteroids for acute major exacerbations Chest physiotherapy Excercise Pulmonary resection for focal bronchiectasis.

Answer 22

Interstitial lung disease is an inflammatory or fibrosing process that occurs in the alveolar walls causing thickening and possible destruction of pulmonary vessels and fibrosis of interstitium leading to: - decreased lung compliance (increased or normal FEV1/FVC) - decreased lung volumes (decreased TLC, decreased VC, decreased RV) - impaired diffusion(decreased DLCO) - hypoxia usually without hypercapnia due to V/Q mismatch - pulmonary HTN and Cor pulmonale occur with advance disease secondary to hypoxia and blood vessel destruction

Answer 23

FASSTEN Farmer's lung (hypersensitivity pneumonitis) Anklylosing spondylitis Sarcoidosis Silicosis TB Eosinophilic granuloma (langerhans histiocytosis) Neurofibromas oasis

Answer 24

BAD RASH Bronchiolitis obliterates with organising pneumonia (BOOP) Asbestosis / silicosis / pneumoconiosis / berylliosis Drugs (amiodarone, methotrexate, nitrofurantoin, chemo) Rheumatological disease (RA, SLE, polymyositis, dermatomyositis) Aspiration Scleroderma Idiopathic pulmonary fibrosis

Answer 25

- SOB especially on exertion - dry crackles - non productive cough - cyanosis - clubbing (especially in IPF and asbestosis) - features of Cor pulmonale - signs and symptoms vary with each type of ILD

Answer 26

CXR/ HRCT: may be normal or show decreased lung volumes, reticular, nodular, or reticule doulas patterns, Kerley B lines, hilar/mediastinal adenopathy Lines and ground glass appearance in early IPF, this progresses to honey combing in later disease PFTs: decreased lung volume and compliance, normal or increased FEV/FVC. DLco decreased due to V/Q mismatch (less surface area for gas exchange) and pulmonary vascular disease. ABGs: hypoxia and decreased CO2 May also do a bronchoscope, bronchi alveolar lavage, lung biopsy, cANCa(Wegeners) antiGbM (Goodpastures), ESr, ANA (lupus) RF, serum precipitating antibodies to inhaled organic antigens (hypersensitivity pneumonitis)

Answer 27

IPF is a diagnosis of exclusion. IPF is also known as cryptogenic fibrosing alveolitis, or usual interstitial pneumonitis.mit commonly presents over the age of 50, with the incidence rising with age, and is more common in males than females. Pts present with dyspnoea on exertion, non productive cough, constitutional symptoms, late inspiratory fine crackles at the lung bases, and clubbing. Investigations you would order include ESR, ANAs, RF CXR, high resolution CT, and biopsy to exclude granulomas.

Answer 28

Oxygen and steroids. Lung transplantation, mean survival is 3-5 years after diagnosis.

Answer 29

Sarcoidosis is an idiopathic non infectious granulomatous multi system disease other lung involvement in 90% of cases. It is characterised by non caseating granulomas. Proposed triggers include infectious, allergic, and environmental exposures, sarcoidosis typically affects young and middle aged patients. There is a higher incidence among black North Americans.

Answer 30

Asymptomatic, or cough, dyspnoea, fever, arthralgia, malaise, erythema nodosum, chest pain Chest exam usually normal Common extra pulmonary manifestations include: - cardiac (arrhythmias, sudden death) - eye involvement (anterior uveitis) - skin involvement (skin papular, erythema nodosum, lupus) - peripheral lymphadenopathy - arthralgia - hepatomegaly

Answer 31

Hypersensitivity pneumonitis is also known as extrinsic allergic alveolitis. It is caused by intense/repeated inhalation and sensitisation to certain organic agents. There is non IgE mediated inflammation of the lung parenchyma, lymphocytic inflammation and granulomas present. Exposure is usually related to occupation or hobby. Farmers lung = thermophillic actinomyces Bird breeders/bird fanciers lung= chlamydia psittaci Humidifier's lung: aureobasidium pullulans Sauna takers lung: aureobasidium spp.

Answer 32

Pneumoconiosis is an acute reaction to inhaled organic dusts that are 0.5- 5 micrometers in size. There is no effective treatment, therefore prevention of exposure through the use of PPE is the key intervention.

Answer 33

Insulation workers, shipyard workers, pipe fitters, plumbers, construction workers and brake lining workers. Also the spouses of these workers who may have handled their clothing.

Answer 34

Asbestosis is a slowly progressive diffuse interstitial fibrosis from dose related inhalation of asbestos. Usually involves >10 -20 years of of exposure. May develop with heavier but shorter exposure. Typically there is a prolonged period between exposure and clinical manifestation of disease.

Answer 35

Insidious in onset. SOB on exertion usually the first symptom with increased dyspnoea as disease progresses. Paroxysmal, non productive cough, fine end inspiratory crackles increased at the bases, and clubbing (more lie,ly in asbestosis the silicosis or pneumoconiosis) oedema, jugular venous distension. Affects the lower lobe more than the upper lobe. CXR: early shows fibrosis and streaking, later shows cysts and honey combing. Asbestos exposure can cause pleural and diaphragmatic plaques (+\- calcification ), pleural effusion, and round atelectasis.

Answer 36

Microscopic examination of asbestosis shows ferruginous bodies of yellow brown shaped rod structures which represent asbestos fibres coated in macrophages.

Answer 37

Asbestosis, mesothelioma, and bronchi genie cancer.

Answer 38

Removal of exposure, smoking cessation, proper nutrition, excercise, home oxygen PRN, treatment of respiratory infections, annual influenza, and pneumococcal vaccinations

Answer 39

Sandblasters, rock miners, stone cutters, quarry and highway workers. It generally requires >20 years worth of exposure but may develop with a much shorter and heavier exposure.

Answer 40

Dyspnoea, cough, and wheezing. CXR affects upper lobe >lower lobe. Early changes show nodular disease with normal lung function. Late changes show nodules that coalesce into masses (progressive massive fibrosis) there is possible hilar lymphadenopathy that is frequently calcified, especially 'egg shell' calcification,. Complications include mycobacterium infection (eg TB). Treat with prevention, removal from exposure, supportive measures (bronchodilators, oxygen), and lung transplant

Answer 41

Pulmonary hypertension is a mean pulmonary arterial pressure of >25 mmHg at rest and >30 mmHg with exercise, or a systolic pulmonary artery pressure of >40 mmHg. In the past, pulmonary hypertension was classified as primary or secondary pulmonary hypertension but is has since been modified.

Answer 42

Pulmonary arterial hypertension Pulmonary hypertension due to left heart disease Pulmonary hypertension due to lung disease and/or hypoxia Chronic thromboembolic pulmonary hypertension Pulmonary hypertension with unclear multifactorial mechanisms

Answer 43

Idiopathic pulmonary arterial hypertension occurs in young women aged 20-40 with no demonstrable cause. Presents with exertion all dyspnoea, fatigue, syncope, exertion all chest pain, ray aids phenomenon. There is a mean survival rate of 2-3 years from time of diagnosis

Answer 44

Symptoms include Dyspnoea, fatigue, substernal chest pain, syncope, symptoms of underlying disease. Signs include a loud palpable P2, a RV heave, right sided S4, systolic murmur (tricuspid regurg) If RVF; increased JVP, peripheral oedema, TR

Answer 45

Calcium channel blockers (nifedipine or diltiazem, but not verapramil) Vasodilators: oral phosphoritesase inhibitors (eg sildafenil), endothelin receptor antagonists, and parenteral prostaniods Oxygen therapy Consider anticoagulants Sometimes diuretics

Answer 46

Venous stasis Endothelial cell damage Hypercoagulable states

Answer 47

A pulmonary embolus is a lodging of a blood clot in the pulmonary arterial tree with a subsequent increase in pulmonary vascular resistance, impaired V/Q matching, and possibly reduced pulmonary blood flow. Thrombus generally comes from the proximal leg (popliteal, femoral, or iliac veins). Fewer than 30% of patients have clinical evidence of DVTs. . Always expect a PE if a patient develops sudden dyspnoea, chest pain, or collapse 1-2 weeks after surgery.

Answer 48

A pulmonary embolus is a lodging of a blood clot in the pulmonary arterial tree with a subsequent increase in pulmonary vascular resistance, impaired V/Q matching, and possibly reduced pulmonary blood flow. Thrombus generally comes from the proximal leg (popliteal, femoral, or iliac veins). Fewer than 30% of patients have clinical evidence of DVTs. . Always expect a PE if a patient develops sudden dyspnoea, chest pain, or collapse 1-2 weeks after surgery.

Answer 49

A d-dimer test measures products of the thrombotic/fibrinolytic process. An ELISA is better than a latex agglutination. D-dimer results are have a good sensitivity and negative predictive value, but a poor specificity and positive predictive value. Consider only in out patients with a low pre test probability, and always use in conjunction with leg dopplers. If a d-dimer is positive, then go on to do a spiral CT scan. However, if there is a high ore test probability of pulmonary embolus, go straight to the spiral CT. D-dimer is elevated in patients with recent surgery, cancer, inflammation, infection, and severe renal dysfunction.

Answer 50

A V/Q scan is very sensitive but has a low specificity. You order a V/Q scan if the CXR is normal, and there is no COPD. You may also consider ordering a V/Q scan if there is a contraindication to CT (contrast allergy, renal dysfunction). You should avoid a V/Q if CXR is abnormal, or they have COPD, they are an inpatient, or you have a high clinical suspicion of PE. If the results are normal, then the diagnosis of a PE is excluded.

Answer 51

A d-dimer, a V/Q scan, a Doppler ultrasound, an ECG, a CXR, a spiral CT.

Answer 52

Admit for observation, provide supplemental oxygen if short of breath or hypoxemic. Pain relief if needed. Give fluids in BP is low. Anticoagulation: stops clot propagation, prevents new clots, and allows the body's fibrinolytic system to dissolve existing thromboembolic over months. Use UFH if no contraindications (easier to get a stable level and quicker to reverse) use LMWH if pregnant. Get a baseline FBC, INR, aPTT, EUC, and LFT. For SC LMWHS give dalteparin or enoxaparin, no lab monitoring Long term anticoagulation: warfarin- start the same day as LMWHS/heparin, overlap with heparin for at least 5 days. Use LmWH for pregnancy, active cancer, or high bleeding risk patients. IV thrombolytic therapy:if the patient has a massive PE (hypotension if clinical right heart failure) and no contraindications. IVC filter can be used if recent proximal DVT and absolute contraindications to anticoagulation. Can also consider an embolecto my

Answer 53

A low thrombosis risk group is medical patients that are fully mobile, or who had surgery for <30 mins and are fully mobile. Prophylaxis used is to have frequent ambulation.

Answer 54

Most general, gneacologic and urological surgery pAtients are at moderate risk of thrombosis. It also includes sick medical patients. Give LmWH or low dose heperin

Answer 55

High thrombosis risk patients include arthroplasty patients, and hip fracture surgery patients. It also includes patients that have undergone major trauma, or spinal cord injury. Treat with LMWH, fondaparinux, warfarin (INR 2-3), or dabigatran.

Answer 56

Wegeners granulomatosus, Churg-Strauss, and Goodpastures disease.

Answer 57

Five T's : Thymoma, thyroid enlargement, teratoma, thoracic aortic aneurysm, tumours (lymphoma, parathyroid, oesophageal angiomas)

Answer 58

The middle compartment is the anterior to posterior pericardium. Causes of a middle compartment mediastinal mass include pericardial cyst, bronchi genie cyst/tumour, lymphoma, lymph node enlargement, aortic aneurysm.

Answer 59

The posterior compartment is the posterior pericardium to the vertebral column. The causes of posterior mediastinal masses include neurogenic tumours, meningocele, enteric cysts, lymphoma. Diaphragmatic hernias, oesophageal tumours, aortic aneurysms.

Answer 60

Mediastinitis is most commonly caused by postoperative complications of cardiovascular or thoracic surgical procedures. It can be a complication of endoscopy (oesophageal perforation providing entry point for infection), oesophageal or cardiac surgery , or tumour necrosis. Signs and symptoms include fever, substernal pain. Pneumo mediastinum, mediastinal compression, and Hamman's sign (an auscultatory 'crunch' during cardiac systole). Treat with antibiotics, drainage, plus or minus surgical closure of the perforation. Chronic mediastinitis is usually a granulomatous process or fibrosis related to previous infection (eg. Histoplasmosis, TB, sarcoidosis, syphilis)

Answer 61

CHF (usually right sided or bilateral), cirrhosis, nephrotic syndrome, pulmonary embolism (may cause transudative but more likely exudative pleural effusion), peritoneal dialysis, hypothyroidism, CF, urinothorax.

Answer 62

- Infectious: para pneumonic effusion (associated with bacterial pneumonia, lung abscess), and empyema (bacterial, fungal, TB pleuritis, viral infection. - Malignancy: lung carcinoma (35%), lymphoma (10%), metastases (breast, overly, kidney), mesothelioma - Inflammatory: RA, SLE, pulmonary embolism, post coronary artery bypass surgery, drug reaction. - Intrabdominal: subphrenic absess, pancreatic disease (elevated pleural fluid amylase), Meig's syndrome (ascites and hydro thorax associated with ovarian fibroma or other pelvic tumour) - Intrathoracic: oesophageal perforation (elevated pleural fluid amylase) - Trauma: chylothorax (occurs when the thoracic duct is disrupted), heamothorax due to rupture of a blood vessel, pneumothorax

Answer 63

A pleural effusion is an excess amount of fluid in the pleural space (normally up to 25mL). It is caused by a disruption of the normal equilibrium between pleural fluid formation/entry and pleural fluid absorption/ exit. It can be classified as transudative or exudative, traditionally using Light's criteria.

Answer 64

In transudative pleural effusions there may be an increased capillary hydrostatic pressure or an decreased plasma oncotic pressure. In exudative processes there is increased permeability of pleural capillaries or lymphatic dysfunction. Lights Criteria: To be a transudative effusion: protein (pleural/serum) <0.5, LDH (pleural/serum) <0.6, and pleural LDG <2/3rds of upper limit of N serum LDH. To be an exudative effusion, one of these criteria must be met. Protein (pleural/serum)>0.5, LDH >0.6, and pleural LDH >2/3 upper limit of normal serum LDH.

Answer 65

Pleural effusions are often asymptomatic. However, they may present with dyspnoea and pleuritic chest pain. Trachea may deviate away from the effusion, there may be ipsilateral decreased expansion,. There may be decreased tactile fremitis, or dullness. Auscultation may show decreased breath sounds, bronchial breathing, and a pleural friction rub.

Answer 66

CXR PA and lateral. In a decubitus fluid will shift unless it is loculated. Thoracocentesis: indicated if pleural effusion is a new finding (risk of re-expansion pulmonary oedema if >1.5 L of fluid is removed). Analyse fluid for colour, protein, LDH, gram stain, cell count differential, cytology, glucose, RF, ANA, amylase, pH, blood, triglycerides.

Answer 67

A complicated pleural effusion is persistent bacteria in the pleural space, but fluid is non-purelent. There are neutrophils, pleural fluid acidosis, and high LDH. Often no bacteria is grown, since it is rapidly cleared from the pleural fluid. There is a fibrin layer that can lead to loculation of pleural fluid. Treat with antibiotics and drainage. Treat as an empyema.

Answer 68

An empyema is pus in the pleural space, or an effusion with organisms seen on a gram stain or culture (eg. Pleural fluid is grossly purelent). A positive culture is not required for diagnosis.

Answer 69

An empyema is generally caused by contiguous spread from lung infection (most commonly anaerobes), or infection through the chest wall (eg trauma, surgery). Signs and symptoms include fever, and pleuritic chest pain. Investigations include a CT chest, thoracocentesis, or PMNs +\- visible organisms on gram stain. Treat with antibiotic therapy for at least 4-6 weeks (rarely effective alone), complete pleural drainage with a chest tube. If loculated, it may be more difficult to drain, and may require surgical drainage.

Answer 70

Atelectasis is when there is decreased volume of all or part of the lung. It can be due to obstruction causes,or non obstructive causes. Obstructive causes include mucous trapping, tumour, or foreign body aspiration. Non obstructive causes include pleural effusion, empyema, or pneumothorax. They also include a loss of surfactant, compression by a space occupying lesion, or replacement of parenchymal tissue by scarring or malignant infiltration.

Answer 71

Symptoms are often absent in chronic atelectasis, but in acute atelectasis they can include dyspnoea, pain, cyanosis, hypotension, and tachycardia. Signs can include decreased breath sounds, a dullness to percussion, and shifting of the trachea towards the side of the atelectasis.

Answer 72

A pneumothorax is the presence of air in the pleural space. A pneumothorax can be asymptomatic. It may also present with chest pain, dyspnoea, tachypnoea, tachycardia, contralateral tracheal deviation, ipsilateral diminished chest expansion, decreased tactile/vocal fremitis, hyperresonance, ipsilateral dimished breath sounds.

Answer 73

Traumatic: penetrating or non penetrating injuries. Iatrogenic: Central venous catheter, thoracocentesis, mechanical ventilation with barotrauma Spontaneous : primary (no underlying lung disease) normally in young tall healthy males caused by rupture of a sub pleural blob of lung into pleural space. Secondary (underlying lung disease).

Answer 74

Severe respiratory distress., tracheal deviation to the contralateral side, distended neck veins (increased JVP), hypotension.

Answer 75

A small pneumothorax can resolve spontaneously (breathing 100% oxygen can speed up the resorption of air). A small intercostal tube with a Heinrich valve can be used for most spontaneous pneumothoraces. Large pneumothoraces require the placement of a chest tube connected to an underwater seal plus or minus suction. Treat underlying cause.

Answer 76

Mesothelioma is a primary malignancy of the pleura. Persistent chest pain, dyspnoea, cough, bloody pleural effusion, weightloss. Note: asbestos exposure can also results in a benign exudative pleural effusion, and pleural plaques that are usually calcified are a marker of exposure and are usually an asymptomatic radiological finding.

Answer 77

Respiratory failure is an impairment of gas exchange between ambient air and circulating blood. Hypoxeamix is <60mmHg, hypercapnia is >50 mmHg. Signs of hypoxemia include restlessness, confusion, cyanosis, coma, Cor pulmonale. Signs of hypercapnia include headache, dyspnoea, drowsiness, asterixis, warm periphery, plethora, increased ICP (secondary to vasodilation)

Answer 78

- Low FiO2 (altitude) - Hypoventilation - Shunting (alveolar collapse, intra-alveolar filling (pneumonia, oedema) intra cardiac, intra pulmonary AVM - Low mixed venous O2 content (aneamia, low cardiac output, hypermetabolism) - V/Q mismatch (airway disease/asthma/COPD, alveolar disease/pneumonia/oedema, vascular disease/PE)

Answer 79

- high inspired CO2 - low total ventilation - high dead space ventilation - high CO2 production (fever, sepsis, seizure, acidosis, CHO load) Alveolar hypoventilation: COPD, asthma, CF, chest wall disorder, rapid shallow breathing.

Answer 80

ARDS is a clinical syndrome that is characterised by severe respiratory distress, hypoxemia, and non cardiogenic pulmonary oedema. The American European consensus conference criteria for ARDS includes: - acute onset - bilateral infiltrates on CXR - Pulmonary capillary wedge pressure <18 or no evidence of increased left atrial pressure. - PaO2/FiO2 <200

Answer 81

ARDs may result from direct or indirect lung injury: - Airway: aspiration (gastric contents, drowning), pneumonia, gas inhalation (oxygen toxicity, nitrogen dioxide, smoke) - Circulation: sepsis, shock, trauma, pancreatitis, DIC, blood transfusion, embolism (fat, amniotic fluid), drug overdose (narcotics, sedatives, TCAs) - Neurogenic: head trauma, intracranial haemorrhage.

Answer 82

A disruption of alveolar capillary membranes leads to leaky capillaries, which leads to interstitial and alveolar pulmonary oedema, which leads to reduced compliance, which leads to reduced compliance, V/Q mismatch, shunt, hypoxemia, and pulmonary hypertension.

Answer 83

The exudative phase occurs in the first 7days after exposure to the ARDs precipitant. The alveolar capillary endothelial cells and type 1 pneumocytes are injured, resulting in a loss of the normally tight alveolar barrier. Patients develop dyspnoea, tachypnoea, and increased work of breathing. This results in respiratory fatigue and eventually in respiratory failure.

Answer 84

The proliferative phase of ARDs occurs between days 7-21. The dyspnoea, tachycardia, fatigue, and hypoxemia may still last into this phase. Some patients will develop fibrotic lung disease, most patients clinically improve and are able to wean off their medications. The fibrotic phase occurs only for some patients. These patients may require long term support on supplemental oxygen or even mechanical ventilation.

Answer 85

Treat underlying cause. Provide mechanical ventilation using low tidal volumes to recent barotrauma. Use fluids and inotropic therapy (dopamine, vasopressin) if cardiac output is inadequate.

Answer 86

- Barotrauma: pneumothorax, tension pneumo, pneumo mediastinum, subcutaneous emphysema - Ventilator assisted pneumonia (nosocomial pneumonia): patient intubated >72 hours at risk, commonly gram negative rods, anaerobes, S. aureus. - Hypotension (decreased Cardiac Output): increased Intrathoracic pressure with decreased venous return - Tracheal stenosis - laryngeal dysfunction

Answer 87

A pulmonary nodule is a round or oval, sharply circumscribed radio graphic lesion up to 3-4 cm which may or may not be calcified, and is surrounded by the normal lung.

Answer 88

The corona radiata sign is highly associated with malignancy.there are fine strait ions that extend linearly from a nodule in a speculated fashion.

Answer 89

``` Infectious granuloma (TB, histoplasmosis, atypical mycobacterium) Other infections (bacterial abscess, PCP, aspergilloma) Benign neoplasms (heamatomas, lipoma, fibroma) Vascular (AV malformation, pulmonary varix) Developmental (bronchogenic cyst) Inflammatory (wegener's granulomatosus, rheumatoid nodule, sarcoidosis) Other (heamatoma, infarct, pseudo tumour,rounded atelectasis, lymph nodes, amyloidoma) ```

Answer 90

- Bronchogenic carcinoma: adenocarcinoma, squamous cell carcinoma, large cell carcinoma, small cell carcinoma. - Metastatic lesions: breast, head and neck, melanoma, colon, kidney, sarcoma, germ cell tumours - Pulmonary carcinoid

Answer 91

<3cm, round, regular. Smooth margin Calcified pattern. Central 'popcorn' pattern if heamatoma, usually no cavitation, if cavitated the the wall is thin and smooth, with no other lung pathology.

Answer 92

A malignant pulmonary nodule is >3cm, irregular and spiculated. There is an ill defined or notched margin. A malignant nodule is usually not calcified, and if it is calcified then the pattern is eccentric. There are no satellite lesions, cavitation with a thick wall. There may be pleural effusions, and lymphadenopathy.

Answer 93

Less than 5% of lung tumours are benign. However, of those that are benign, 90% of them are bronchial adenomatous and heamartomas Less common benign neoplasms of the lung include fibromas, lipomas, leiomyomas, hemangiomas, papillomas, chondromas, teratoma, and endometriosis.

Answer 94

Can present with a cough, wheezing, heamoptysis, recurrent pneumonia, and atelectasis. It may also present as an asymptomatic pulmonary nodule.

Answer 95

A hamaetoma is comprised of the tissues usually present in the lung (fat, epithelium, fibrous tissue, and cartilage), but they exhibit disorganised growth. The peak incidence is at age 60, it is more common in men, and they usually occur in the periphery, are clinically silent, and benign in behaviour. On CXR, they have a clustered 'popcorn' pattern of calcification that is pathognmonic for a hamaetoma.

Answer 96

Bronchogenic cancers Lymphomas Secondary metastases: breast, colon, prostate, kidney, thyroid, stomach, cervix, recto, testes, bone, melanoma

Answer 97

Bronchogenic cancer makes up 90% of all lung cancer. Bronchogenic lung cancer can be classified into small cell lung cancer, , bronchioalveolar cancer (BAC), and non small cell lung cancer. The types of non small cell lung cancers include adenocarcinoma, squamous cell carcinoma, large cell carcinoma.

Answer 98

Adenocarcinomas are a type of bronchogenic cancer. They are malignant. Adenocarcinomas are the most common bronchogenic carcinoma, and are slightly more common in women than men. There is a weak correlation with smoking. They are located peripherally, and come from the mucin producing glandular tissue. Adenocarcinomas metastasis early, and go to distant sites.

Answer 99

Squamous cell carcinomas are the second most common type of bronchogenic cancer. They have a strong correlation with smoking. Squamous cell carcinomas are located centrally, and develop from keratin and intercellular bridges. They metastasise by local invasion and distant spread, and may cavitate.

Answer 100

Small cell lung cancers are a type of bronchogenic lung cancer that are strongly correlated with smoking.they are located centrally and develop from oat cells or neuroendocrine cells. Whilst they originate from endobronchial cells, they are often disseminated at presentation.

Answer 101

Large cell lung cancers are the least common type of bronchogenic lung cancers. They have a strong correlation with smoking. Large cell lung cancers occur peripherally and are a aplastic and undifferentiated. They metastasise early to distant locations.

Answer 102

``` Smoking Asbestos exposure Radiation from Radon or uranium Exposure to arsenic, chromium, or nickel. Genetic damage Parenchymal scarring: granulomatous disease, fibrosis, scleroderma Passive exposure to cigarette smoke HIV ```

Answer 103

Cough (particularly beware of a chronic cough that changes in character) Dyspnoea Chest pain Heamoptysis Other pain Clubbing Constitutional symptoms (anorexia, weight loss, fever, aneamia)

Answer 104

SVC syndrome occurs when there is obstruction of the superior vena cava. This causes neck and facial swelling, as well as dyspnoea, and a cough. Other symptoms include hoarseness, tongue swelling, epistaxis, and heamoptysis. Physical findings include dilated neck veins, increased number of collateral veins, covering the anterior chest wall, cyanosis, oedema of the face, arms, and chest. Pemberton's sign (facial flushing, cyanosis, and distension of neck veins upon raising both arms over head). There are milder symptoms if the obstruction is above the azygous vein.

Answer 105

Squamous cell carcinoma has the best (25%), then Adenocarcinoma (12%), and large cell carcinoma (13%). Small cell carcinoma has the worst (1%).

Answer 106

Surgery is not usually performed for small cell carcinoma as it is not curable. However, the preferred treatment for stage 1 and 2 NSCLC is resection with curative intent. Advanced NSCLC is often palliated and or radiation. Contraindications for surgery include spread to contralateral lymph nodes or distant sites. There is no role for chemotherapy alone, only in combination with other treatments. Radiotherapy is also used.

Answer 107

Bronchioalveolar carcinoma is a adenocarcinoma that grows along e alveolar wall in the periphery. Bronchioalveolar cancer may arise at sites of previous lung scaring. The clinical presentation of bronchioalveolar cancer is similar to bronchogenic cancer. It spreads within the lungs, but extra pulmonary metastases occurs late. Solitary lesions are respectable and have a survival rate of 69%. Overall five year survival rate is 25%.

Answer 108

Apnoea is the absence of breathing for >10 seconds.

Answer 109

Hypopnea is an excessive or decreased rate of breathing (>50% reduction rate in ventilation).

Answer 110

Sleep apnoea is episodic decreases in airflow during sleep. Quantitatively measured by the apnoea/hypopnea index= # of apneic and hyponeic events per hour of sleep. Sleep apnoea is generally accepted to be present if AHI>15.

Answer 111

Sleep apnoea can either be obstructive, central or mixed. Obstructive apnoea is caused by transient, episodic obstruction of the upper airway, or by absent or reduced airflow despite persistent respiratory efforts. Central sleep apnoea is caused by transient episodic decreases in the CNS drive to breath. There is no airflow because there is not respiratory effort. Mixed sleep apnoea has features of both OSA and CSA. There is a loss of both hypoxic and hypercapnic drives to breath secondary to 'resuscitative breathing'. Resuscitative breathing is overcompensatory hyperventilation upon awakening from OSA induced hypoxia.

Answer 112

Obesity, upper airway abnormality, neuromuscular disease, hypothyroidism, alcohol/sedative use, nasal congestion, sleep deprivation.

Answer 113

Cheyne stokes respiration is a form of CSA in which central apnoea so alternate with hyperneas to produce a crescendo-decreascedo pattern of tidal volume that is seen in severe LV dysfunction, brain injury and many other settings.

Answer 114

LV failure, brain stem lesions, encephalopathy, encephalitis, myxoedema, high altitude.

Respirology Flashcards

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