Respiratory Flashcards

Question

Secondary (Post primary) Pulmonary TB - in sensitised hosts

Answer 1

Chronic cough (>2 weeks) - dry/productive Low grade fever - remittent (appears late afternoon & fades out) Anorexia Weight Loss Night Sweats Progressive pulmonary involvement - increasing amounts of sputum Haemoptysis (advanced) - agressive disease (invasion of blood vessels) Pleuritic chest pain

Answer 2

Primarily based on history, signs and symptoms and radiographic findings 1.Sputum direct smear for acid fast bacilli Stained in bright red with Ziehl Nielson stain Need 3 sputum samples - early morning sample is best Most commonly used method Cannot differentiate between species Cannot test antibiotic sensitivity 2.Mycobaterial culture Need only 1 sputum sample Can differentiate between species Takes 4-12 weeks to bet result 3. PCR Rapid detection Can detect antibiotic resistance genes 4. Mantoux test - screening method

Answer 3

Infection/Inflammation of the lungs

Answer 4

Impaired pulmonary defence makes an individual more susceptible to getting pneumonia

Answer 5

Bacteria “translocate” to normally sterile distal airway - bacteria from URT that has either came in quickly or colonised for a while are micro-aspirated into lower lung Resident host cells become overwhelmed Develop an inflammatory response – neutrophils and inflammatory exudate fill alveolar space Resolution phase – when bacteria cleared Inflammatory cells removed by apoptosis Resolution phase leads to complete recovery In pneumonia you see: Fluid filled alveoli Bronchoconstriction Increase in mucus secretion Consolidation: process that fills the alveoli with fluid, pus, blood, cells resulting in lobar diffuse opacities

Answer 6

Lobar pneumonia Broncho pneumonia

Answer 7

Bronchopneumonia affects patches throughout both lungs Infection spreads along airway and finally reaches distal areas Tendency for secretion to graduate to longer lobes

Answer 8

If greater than 2, needs to be hospitalised

Answer 9

Community Acquired pneumonia Hospital acquired pneumonia Aspiration pneumonia Chronic pneumonia

Answer 10

Lung abscess complication: Extention to pleural cavity Haemorrhage Brain abscess Meningitis Secondary amylodosis

Answer 11

1. Chest X Ray Patchy "bronchopneumonia" Consolidation "lobar" 2. Sputum testing (Gram Stain) To identify bacteria MCS 3. Urine antigen testing Identify bacteria: strep pneumonia or legionella 4. Blood testing FBC: WBC increase/decrease indicates severity. Neutrophilia indicates bacteria. Haemolytic anaemia suggests mycoplasma EUC testing: Urea high indicates severity LFT: Abnormal if basal pneumonia inflames liver

Answer 12

1. Oxygen: All patients with tachypnoea, hypoxemia, hypotension or acidosis Cardinal signs of Pneumonia: Chest Pain Dyspnoea Exudate (sputum) Fever 2. Intravenous fluids: Severe patient, elerly. Increase in vomitng 3. Pain: NSAIDs, opiods 4. Antibiotics

Answer 13

Pneumocystis pneumonia is most common in HIV patients

Answer 14

One of the most common autosomal recessive disease Cystic fibrosis is a disease resulting from abnormality in the cystic fibrosis conducting regulator Clinical Manifestation: Pancreatic dysfunction, Lung disease, and salty sweat

Answer 15

The clinical presentation of cystic fibrosis defer in infants and children. Infants Meconium ileus (bowel obstruction due to poo) Rectal prolapse Children - Mainly failure to thrive and recurrent upper respiratory tract infection Chronic cough and wheezing FTT Pancreatic insufficiency (symptoms of malabsorption such as steatorrhea) Alkalosis and hypotonic dehydration Neonatal intestinal obstruction (meconium ileus)/Nasal polyps Clubbing of fingers/Chest radiograph with characteristic changes Rectal prolapse Electrolyte elevation in sweat, salty skin Absence or congenital atresia of vas deferens Sputum with S. aureus or P. aeruginosa (mucoid) Remember Cystic Fibrosis usually presents in childhood as recurrent lung infections that become persistent and chronic

Answer 16

Failure to thrive Asthma Coeliac Disease GORD Immunodeficiency disorders

Answer 17

Infant have a Heel prick - Immunoreactive Trypsinogen (IRT) to detect cystic fibrosis Side note Heel prick is performed to screen for metabolic disease of the newborn inlcuding: galactosemia, cystic fibrosis, phenylketouria, sickle-cell disease and congenital hypothyroidism Sweat test - first line for diagnosis >60mmol/L Genetic screening - Type of CFTR mutation

Answer 18

Aetiology A mutation of the CFTR gene on the long arm of chromosome 7 is the cause of cystic fibrosis. The mutation of the CTFR gene results in a mutated CFTR protein which is a transported for Cl- ions. The severity of cystic fibrosis depends on the type of mutation found on the CFTR gene.

Answer 19

Pathophysiology Cystic Fibrosis is caused by mutated CTFR protein. The CFTR protein is found on the apical surface of many hollow tissues notably the lungs, pancreas, gastrointestinal tract and sweat glands. The CTFR protein is a transporter for Cl-. A mutated CFTR protein can not transport Cl- properly and as a result this causes a disregulated ion distribution. Whereever Cl- exists Na+ will follow because of the electrochemical gradient. When Na+ move water tends to follow. This basic principle is the cause of the signs and symptoms seen in Cystic Fibrosis Remember Cystic Fibrosis is characterized by the triad of chronic obstructive pulmonary disease, pancreatic exocrine deficiency, and abnormally high sweat electrolyte concentrations.

Answer 20

Management of meconium illeus performed after delivery. General High fat, high calorie diet Pancreatic enzyme supplement Vitamin supplementation (ADEK) Salt supplementation Pulmonary care physiotherapy shaking chest jackets Long-term antibiotics (inhaler) Bronchodilator Ongoing management Management of upper respiratory tract infection Oral Antibiotics IV antibiotics Management of non-pulmonary complications Remember patients with CF are at risk of having recurrent URTI which can be caused by S. aureus, H. Influenzae, P. aerugenosa.

Answer 21

Irreversible dilation of the airways due to inflammatory destruction of airway walls resulting from persistently infected mucus P.aureginosa is the most common pathogen Clinical manifestations include: chronic cough copious mucopurelent expectoration Common in patients with cystic fibrosis

Answer 22

Cystic fibrosis Host immunodeficiency Previous infections Congenital disorders of the bronchial airways Primary ciliary dyskinesia Alpha-1 antitrypisn deficiency Connective tissue disease Inflammatory bowel disease Aspiration or inhalation

Answer 23

Remember Massive haemoptysis is >500ml blood loss in 24hrs Examination: Percussion resonant, mixed predominant coarse crackles, often additional polyphonic wheeze. Presence of of high pitch inspiratory squeals and rhonchi

Answer 24

COPD Asthma Pneumonia Chronic sinusitis

Answer 25

Gold Standard - CT

Answer 26

Essentially the different causes of bronchiectasis with impaired respiratory defences/ immunodeficiency will trigger an inflammatory process, recurrent infections that will result in the pathological changes seen bronchiectasis. There will be bronchiole dilatation, immune cells infiltration into the tissue (lymphocytes), bronchial ulceration and oedema, smoother muscle hypertrophy and neovascularization. Patients with bronchiectasis gets recurrent infection. Common causes of infections are p. aureginosa, s. pneumoniae, h. influenzae, s. aureus. Infection can trigger exacerbations.

Answer 27

Remember to treat the underlying cause as well (ie. cystic fibrosis, Rheumatoid arthritis, Inflammatory bowel disease)

Answer 28

Massive haemoptysis Respiratory failure Cor pulmonale

Answer 29

Accumulation of fluid in the pleural space

Answer 30

Mechanisms: Increase pleural fluid formation: 1. Increase in permeability (inflammation) 2. Increase venous pressure 3. Decrease plasma oncotic pressure (hypoproteinaemia) 4. Decrease pleural pressure Pleural fluid protein is not altered by clearence of fluid of lymphatics Decrease pleural fluid clearance 1. Cancer invasion 2. Blockage of lymphatic stoma 3. Mechanical compression (granuloma) 4. Injury from chemotherapy/radiation therapy

Answer 31

Gold Standard: Ultrasound

Answer 32

Used to differentiate exudative vs transudate pleural effusion

Answer 33

Ultrasound "gold standard" + thoracocentesis thoracocentesis (pleural fluid analysis: lactate dehydrogenase. protein) Light criteria

Answer 34

Causes of transudative pleural effusion: Increase in peural BNP 1. Congestive Heart Failure 2. Liver Cirrhosis 3. Nephrotic syndrome Causes of exudative pleural effusion: Pleural culture. pleural fluid cell differentiation + glucose 1. Infective 2. Malignancy 3. Pulmnary embolism 4. Gastrointestinal pathology 5. Connective tissue disease

Answer 35

Abnormal collection of air in pleural space -Disrupts negative intrapleural pressure + presence in air and pressure -> Lung size will decrease and collapse

Answer 36

1. Outside: through chest wall 2. Inside: ruptured lung and pleura Types: 1. Traumatic- cause by trauma Blunt vs Penetrating Iatrogenic (result of invasive procedure): result of positive pressure mechanical ventilation 2. Non-traumatic - spontaneous Primary Spontaneous Pneumothorax (PSP): Normal lung, no known cause Secondary Spontaneous Pneumothorax (SSP): Lung with underlying disease (COPD, Asthma, TB, fibrosis, Cancer, pneumonia) Classification: Simple (No mediastinal shift) vs Tension (mediastinal shift) Open (Open wound chest wall. Air in & out. "Sucking Chest wall") vs Closed (Chest Wall intact)

Answer 37

Chronic progressive fibrotic interstitial lung disease Primarily occurs in older adults

Answer 38

Heart Failure COPD

Answer 39

Patchy fibrosis of interstitium, minimal or absent inflammation, acute fibroblastic proliferation and collagen deposition.

Answer 40

Pulmonary Function Test: Decreased FVC and TLC Diffusing capacity of carbon monoxide: Decreased Chest X-ray: Bilateral reticular infiltrates Hazy opacities Decreased Inspiratory volume High resolution CT chest: Gold Standard Bilateral reticulation Honeycombing: Changes are lower lobe predominant Traction bronchiectasis

Answer 41

Multisystem inflammatory disease of unknown aetiology Predominantly affects: lungs, intrathoracic lymph nodes, non-caseating granulomas Characterised by an exaggerated immune response against an unrecognised antigen

Answer 42

Non-caseating granulomata form at various sites in the body, particularly the thoracic cavity, skin and eyes. Bilateral hilar lymphadenopathy and/or pulmonary infiltrations. Contain: Langhans giant cells and non-caseating granulomas

Answer 43

Radiological stage by chest radiography at presentation inversely correlates with likelihood of spontaneous resolution. Stage 0: normal Stage I: bilateral hilar lymphadenopathy Stage II: bilateral hilar lymphadenopathy plus pulmonary infiltrates Stage III: pulmonary infiltrates without hilar lymphadenopathy Stage IV: extensive fibrosis with distortion. Typically shows bilateral hilar adenopathy.

Answer 44

Acute Respiratory failure causes hypoxia and/or impaired ventilation with hypercapnia, leading to severe hypoxemia and rapid deterioration. Two main types of respiratory failure

Answer 45

Type 1:Hypoxaemia (PaO2<60mmHg) without hypercapnia. Caused by conditions affecting oxygenation: right-to-left shunts or V/Q mismatch Acute Respiratory Failure Type II: Chronic Respiratory Failure Type I respiratory failure (non-hypercapniec respiratory failure) Primarily from failure of oxygenation (PaO2 <60mmHg) Normal or low CO2 pH 7.5 Usually responds to Oxygen therapy Type II respiratory failure (hypercapniec respiratory failure): Hypoxaemia with hypercapnia (PaCO2>50mmHg). Increased CO2 (PaCO2 >50mmHg) Normal or low O2 pH <7.3 Failure of ventilation as well as oxygenation Requires ventilator support as well as supplemtntal oxygen

Answer 46

Clinical Presentation Increased work of breathing Increased RR Use of accessory muscles Tracheal tug Abdominal recession Increased HR Sweating or clammy skin Anxiety or agitation Exhaution and confusion *Other signs and symptoms depending on cause Signs of Hypoxia Cyanosis Low O2 Arrthymia (from hypoxia) Anxiety, agitation Acidosis (tissue hypoxia) Hypoventilation Vasodilation Headache, fatigue Asterixis Acidosis Obstruction Inability to speak Accumulation of secretion Remember Use pulse oximetry, ECG, ABG and Chest X-ray in the initial assessment

Answer 47

Type I Type II Pneumonia COPD ARDS Life-threatening asthma Interstitial lung Disease Drug Intoxication (opioids) Acute Pulmonary Oedema CVA/trauma Asthma Primary muscles disorders COPD Myasthenia gravis Pneumothorax Poliomyelititis Pulmonary Embolism Kyphoscoliosis Obesity Polyneuropathies Pulmonary hypertension Obesity

Answer 48

V/Q mismatch Pneumonia ARDS Interstitial Lung disease PE Pneumothorax Right-to-left shunt Physiological: Pneumonia, acute pulmonary oedema, atelectasis Anatomical: intra-cardiac shunts (VSD, ASD), pulmonary AVM Low inspired O2 partial pressure (FiO2) High altitude Diffusion impairment Interstitial lung disease - Restrictive Acute pulmonary oedema ARDS Hypoventilation Obesity

Answer 49

Oxygenation (non-invasive) Nasal prongs Simple Mask Venturi mask Treat underlying cause Ventalin - if asthma or COPD to reduce bronchoconstriction Antibiotics – if infection Diuretics – if fluid overload Monitor clinically and with ABG Non-invasive mechanical ventilation CPAP/PEEP Maintain recruitment of collapsed lung Increased functional residual capacity Minimise intrapulmonary shunt BiPAP Invasive mechanical ventilation - if not improving Endotracheal Intubation Tracheostomy Tube

Answer 50

Hypercapnia when alveolar ventilation insufficient to excrete volume of CO2 produced by tissue metabolism due to: Decreased minute ventilation COPD Asthma Heart failure Neurological causes Kyphoscoliosis Obesity Increase in dead space ventilation Increased CO2 production Fever, sepsis, seizure, acidosis, carbohydrate load

Answer 51

Remember aims of treatment here is to achieving safe oxygen concentration without increasing CO2 and acidosis, while identifying precipitating condition Oxygenation (non-invasive) Nasal prongs Simple Mask Venturi mask Treat underlying cause Ventalin - if asthma or COPD to reduce bronchospasm Antibiotics – if infection Diuretics – if fluid overload Monitor clinically and with ABG Non-invasive mechanical ventilation BiPAP Invasive mechanical ventilation - if not improving Intubation Think Becareful using oxygen in COPD. Severe COPD hypoventilate and retain CO2. Giving uncontrolled O2 may increase CO2.

Answer 52

Leading cause of cancer related deaths Cigarettes are the major cause of lung cancer

Answer 53

General Chest X-Ray - opacity Spirometry - if thinking of obstructive or restrictive lung disease CT Investigation Chest x-ray findings can vary in patients with lung cancer and can include pulmonary opacity, hilar enlargement, pleural effusion and collapsed lung. Investigations for staging CT CT- Biopsy PET scan Pleural fluid aspiration Lung biopsy with bronchoscopy Endobronchial ultrasound Sputum MCS

Answer 54

Lung cancer can be broadly divided into either small cell lung carcinoma or non-small cell carcinoma. Non small cell lung carcinoma making up the majority 80% Small cell lung carcinoma (SCLC - 20%) Non-small cell lung carcinoma ( NSCLC - 80%) Adenocarcinoma Squamous cell carcinoma Large cell

Answer 55

Once a patient presents with symptoms or radiographic findings suggestive of lung cancer, the next steps are as follows: 1.Tissue diagnosis to establish malignant diagnosis and histologic type 2.Staging to determine resectability or curative potential 3.Cancer treatment: surgery, radiotherapy, or chemotherapy

Answer 56

NSCLC Post-obstructive pneumonia/hypoxia Superior vena vaca syndrome Paraneoplastic syndromes SCLC Post-obstructive pneumonia/hypoxia Superior vena vaca syndrome Paraneoplastic syndromes Chemothreapy induced hematological toxicity Radiation induced esophageal/lung injury

Answer 57

Cancer arising from mesothelium

Answer 58

Pleural mesothelioma Peritoneal mesothelioma Pericardial mesothelioma

Answer 59

exposure to asbestos

Answer 60

Shortness of breath, dull diffuse chest pain (occasionally pleuritic), weight loss, lethargy. Pleural effusion. History of asbestos exposure, sometimes. Potentially a palpable chest wall mass.

Answer 61

Arises from mesothelial cells (80% pleura, rest are peritoneum and pericardium). Deposition of the asbestos fibres in parenchyma -> penetration of the visceral pleura -> transport of the fiber to the pleural surface -> Development of a malignant plaque (asbestos can apparently facilitate foreign DNA entering the cell -> messing with oncogenes etc)

Answer 62

CXR: Pleural effusion. Potentially rib destruction. Pleural aspiration: Straw coloured or blood stained. Pleural biopsy: Gold standard

Answer 63

Surgical: Ressection (pleurectomy and decortication may relieve pain and effusions) Chemo: Improves survival of patients with unressectable mesothelioma. Radio: Mostly for pain control if at all

Answer 64

COMMON CAUSES OF CHRONIC DYSPNOEA Respiratory Disease Cardiovascular Disease COPD Myocardial Dysfunction (Heart Failure) Asthma Obesity/de-conditioning Interstitial lung disease

Answer 65

High Res CT - gold standard

Answer 66

Inappropriate immune response to an antigen causing inflammation of the lung extrinsic allergic alveolitis Upper Lobe predominance

Answer 67

Increase in blood pressure in the pulmonary circulation Mean arterial pressure >25mmHg

Answer 68

Right sided heart failure

Answer 69

Parainfluenza 1 and 2 Respiratory syncytial virus (Common cause of bronchiolitis) Remember Croup symptoms usually start with flu like symptoms. Croup is caused by viruses, with para-influenza virus (types 1 to 3) as the most common

Answer 70

Classic Tetrad: barking cough, stridor, hoarse voice, and respiratory distress Agitation Inspiratory stridor Barking Cough Hoarse voice Male Young age Tracheal Tug Lethargy Abrupt onset of symptoms Symptoms worse at night

Answer 71

Differentials for stridor Croup (common) Bacterial tracheitis (uncommon) Foreign body Epiglottitis (rare)

Answer 72

Croup is a clinical diagnosis based on early respiratory infections followed by a barking cough Chest X-ray Neck X-ray - steeple sign

Answer 73

Mild Airway Obstruction Barking cough without inspiratory stridor Moderate Airway Obstruction Stridor at rest Tracheal tug Chest wall recession Severe Airway Obstruction Persisting stridor Tracheal tug Chest wall recession Aaethetic/restless Soft stridor, irritability, tachycardia, pallor indicates imminent airway obstruction

Answer 74

A single dose of dexamethasone is recommended in all patients with croup, including those with mild disease. Nebulized epinephrine is an accepted treatment in patients with moderate to severe croup. Mild Airway Obstruction No need for specific treatment Moderate Airway Obstruction Corticosteroids Oral Prednisalone (1mg/kg) Dexamethasone (0.3mg/kg) +/- Nebulised Adrenaline - Budesonide (2mg) Severe Airway Obstruction Oxygen Corticosteroids Oral Prednisalone (1mg/kg) Dexamethasone (0.3mg/kg) +/- Nebulised Adrenaline - Budesonide (2mg) Monitor Remember Antibiotics have no role in uncomplicated croup as it has a viral aetiology