Respiratory Case Based Learning – Flashcards

-58 YO man comes to see GP with 6 month history of increasing dyspnoea. - Coughs sputum most mornings and has done so for several years. - He has never seen doctor because he though it was linked to smoking. -He has smoked for 43 years on average 25 cigarettes per day.

Suspicions: COPD, Asthma, Cardiac Failure. - Heart Failure=Pinky frothy sputum because of Pulmonary oedema-Could also have pedal oedema and SOB when lying flat at night -Colour of sputum (Chronic, Acute=change in sputum colour, Asthma=yellow pus cells, Fluid in airways=clear sputum, Pink frothy sputum) -Diurnal Variation- Daily variation in symptoms- Asthma is worse at night-there is diurnal variation in bronchial diameter. COPD has fixed airway obstruction. -Wheazing-stethoscope- feature of both but confirms diagnosis. -Chronic Coughing up phlegm-not common in asthma -Progressive-Compare to 12 months-COPD is progressive whereas COPD is not- If worse over this period. -Age- Asthma below age of 35 more common than COPD -Smoking- 95% of cases of COPD caused by smoking other Alpha 1 Antitrypsin deficiency, occupational exposure to dust.

Peak Flow- e.g. 400 litres per minute- isn't helpful for distinguishing between asthma and COPD but tells us about severity. -Useful for monitoring of diurnal variation thus differentiates between two -not used in COPD for monitoring as no diurnal variation in COPD Spirometry- The shape of the graph is different in obstructive and restrictive disease. -Spirometry used for COPD but not Asthma -FEV1/FVC;80% in Obstructive disease-COPD COPD-Fixed airflow limitation-tighter bronchi- FEV1 reduced- chronically thickened bronchial wall. Mucus cell hyperplasia, Mucus hyper secretion. Asthma-Spirometry not useful structurally normal.

-Mucociliary dysfunction -Airflow limitation (obstructive so FEV1;80%) -Structural changes-Parenchymal damage -Systemic component-Osteoporosis and loss of weight is common.

-Generally smoking-sets off inflammatory pathway parenchymal damage and mucus hypersecretion Protease digests lung tissue. -Could be A1 Alpha Antitrypsin deficiency -Could be occupational exposure to irritant/pollutant

COPD- Umbrella Term for disorders that are characterized by obstruction of the airways and limitation to airflow. People with COPD have trouble breathing and shortness of breath generally have a chronic productive cough. •emphysema - destruction of the air sacs -air spaces become enlarged due to increased compliance and destruction of the alveolar walls. -Proteolysis of connective tissue components, including elastic fibers, within the alveolar walls increases the compliance of the walls. -Neutrophils secrete a variety proteases that digest connective tissue fibers and their increased numbers and activity in alveoli are thought to trigger destruction of the alveolar walls. •chronic bronchitis -inflammation of the bronchial tubes -In chronic bronchitis there is mucous hypersecretion with enlargement of tracheo-bronchial submucosal glands and a disproportionate increase of mucous acini. - Marked narrowing of bronchioles due to goblet cell metaplasia, mucus plugging, chronic inflammation and fibrosis -Obliteration of the lumen due to fibrosis may be seen in severe cases.

Big Blue Bloaters (Chronic Bronchitis) •In the chronic bronchitis group, classic symptoms include the following: ?Patients may be obese. ?Frequent cough and expectoration are typical. ?Use of accessory muscles of respiration is common. ?Coarse rhonchi and wheezing may be heard on auscultation. ?Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis. ?Because they share many of the same physical signs, COPD may be difficult to distinguish from congestive heart failure (CHF). One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation Cocectic Pink puffers (Emphysema) •In the emphysema group, the history is somewhat different and may include the following set of classic symptoms: ?Patients may be very thin with a barrel chest. ?They typically have little or no cough or expectoration. ?Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. ?The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant. ?Overall appearance is more like classic COPD exacerbation.

-Airways occluded by tenacious plugs of exudate and mucus (released from tight junctions) -Fragility of airway surface epithelium - Thickening of the reticular layer beneath the epithelial basal lamina and bronchial vessel congestion and oedema -There is increased inflammatory infiltrate comprising 'activated' lymphocytes and eosinophils - enlargement of bronchial smooth muscle particularly in medium sized bronchi.

-Coughing -Wheezing -chest tightness -non productive cough

Episodic symptoms of airflow obstruction are present - Airflow obstruction or symptoms but are at least partially reversible -Spirometry with postbronchodilator response should be obtained as the primary test to establish the asthma diagnosis. -Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. - The chest radiograph remains the initial imaging evaluation in most individuals with symptoms of asthma, but in most patients with asthma, chest radiography findings are normal or may indicate hyperinflation. -Serial Peak flow more than diurnal 20% variation for Asthma -Metacoline challenge test -Exhaled Nitric Oxide-High turnover of Nitric Oxide because endothelial cells over activated.

CT Scan-To detect emphysematous disease. MRC-Dyspnoea Score. BODE Index. Other indicators.

COPD with structural lung disease and loss of lung space- increased pulmonary artery pressure transmitted to right heart leads to right ventricular dilation and failure- orthopnia, pedal oedema.

-SABA (beta-2-agonists) -LABA (Long acting beta agonists- Salmetarol) -Long acting muscarinic receptor antagonist -Inhaled Corticosteroids

It is not an indicator of COPD think about other causes... -Lung Cancer -TB (any infection actually) -Pulmonary embolus could cause it

-Classified as an obstructive lung disease along with COPD and Asthma. -Permanent enlargement of parts of the airways of the lung. - Symptoms typically include a chronic cough productive of mucus. -Other symptoms include shortness of breath, coughing up blood, and chest pain - Wheezing and nail clubbing may also occur, although clubbing is uncommon.Those with the disease often get frequent lung infections. -Bronchiectasis may result from a number of infective and acquired causes, including pneumonia, tuberculosis, immune system problems, and cystic fibrosis. -Involves large volume of sticky sputum -Chronic bronchial dilation-Recurrent or chronic infection-poor mucus clearance. (this is a cycle)

1.X-Ray fluffy shadow-infection Rounded shape-Calcified node after TB Malignancy- Spiculated lesion in left upper zone

do CT scan -Contrast-illuminates Blood vessels-tumours have angiogenesis-therefore tumours would light up

-Do a biopsy-determined by anatomy-if sat by a major bronchus then may be able to do it by bronchus otherwise percutaneous -Bronchoscopic washings -Transbronchial biopsy -Video assisted transbronchial surgery -helps target chemotherapy

Non-Small Cell carcinoma-Approximately 85 to 90 percent of lung cancer cases are NSCLC. There are three types of NSCLC: •Adenocarcinoma is a slow-growing lung cancer usually discovered in an outer area of the lung, often before it has a chance to spread. It occurs more often in smokers, but it's the most common form of lung cancer in nonsmokers as well. •Squamous cell carcinoma generally occurs in the center of the lung. It tends to develop in smokers. •Large cell carcinoma occurs anywhere in the lung, and it usually grows and spreads at a rapid rate. Small cell carcinoma- SCLC usually starts near the center of the chest in the bronchi. It's a fast-growing form of cancer that tends to spread in its early stages. It tends to grow and spread much faster than NSCLC. SCLC is rare in nonsmokers.

Used for lung cancer staging Tumour-Size Node-Number of lymph nodes Metastasis-Present or not?

Type 1 respiratory failure: Defined as a low level of oxygen in the blood (hypoxemia) without an increased level of carbon dioxide in the blood (hypercapnia), and indeed the PaCO2 may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. The basic defect in type 1 respiratory failure is failure of oxygenation characterized by: PaO2 decreased (; 8.0 kPa) PaCO2 normal or decreased (;6.7 kPa) PA-aO2 increased Type 2 Respiratory Failure: Hypoxemia (PaO2 6.0kPa). The basic defect in type 2 respiratory failure is characterized by: PaO2 decreased ( 50 mmHg (6.7 kPa)) PA-aO2 normal pH decreased

-Low ambient oxygen (e.g. at high altitude) -Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism) -Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe -Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia or ARDS) -Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right-to-left shunt)

Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated. The underlying causes include: -Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation) -Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) -A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis) -Neuromuscular problems (Guillain-Barré syndrome, motor neuron disease) -Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.[1]

He has type 1 Respiratory failure showing that COPD is not the issue here- he has another underlying problem which needs investigation.

Pneumonia, PE, Pneumothorax?

CT Pulmonary angiogram-will get a filling defect. Risk factors for clot: Malignancy Post operative (sat in bed)