Respiratory Flashcards

Question

What are the characteristic chest signs of pneumonia?

Answer 1

Bronchial breath sounds = harsh breath sounds equally loud on expiration and inspiration caused by consolidation of the lung tissue around the airway Focal coarse crackles = air passing through sputum in the airways Dullness to percussion due to lung tissue collapse and/or consolidation

Answer 2

CURB 65, CXR, FBC, U+Es, CRP Sputum cultures, blood cultures, legionella and pneumococcal urinary antigens

Answer 3

0-1 = mild, only admit if social circumstances or single worrying feature 2 = moderate, admit to hospital 3-5 = severe, admit and monitor closely 4-5 = consider admission to critical care unit

Answer 4

0=0.7% 1=2.1% 3=9.2% 4-5=15-40%

Answer 5

Mild CAP = 5 day course of oral antibiotics (amoxicillin or macrolide) Moderate - severe CAP = 7-10 day course of dual antibiotics (amoxicillin and macrolide)

Answer 6

sepsis, pleural effusion, empyema, lung abscess, bronchiectasis, death

Answer 7

An algorithm for assessment of pneumonia severity C - confusion (new disorientation in person, place or time) U - urea >7 R - respiratory rate ≥ 30 B - blood pressure <90 systolic or ≤ 60 diastolic 65 - age ≥ 65

Answer 8

autosomal recessive genetic condition affecting mucus glands which has multi-systemic effects

Answer 9

Caused by a mutation of the CF transmembrane conductance regulatory gene on chromosome 7 (CFTR) There are many variants of this mutation, the most common being delta-F508 mutation which codes for cellular channels, particularly a type of chloride channel

Answer 10

FHx Caucasians

Answer 11

Thick pancreatic and biliary secretion which cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections Congenital bilateral absence of the vas deferens in males

Answer 12

Meconium ileus (seen in 20% of babies with CF) Recurrent lower respiratory tract infections Failure to thrive (poor weight and height gain) Pancreatitis Chronic cough Thick sputum production Recurrent respiratory tract infections Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes Abdo pain and bloating

Answer 13

Very salty sweat Nasal polyps Finger clubbing Crackles and wheezes on auscultation Abdominal distension

Answer 14

Newborn blood spot testing GS: Sweat test (pilocarpine patch and electrodes used to test chloride concentration) - >60mmol/L = CF Genetic testing CFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling

Answer 15

Chest physiotherapy (multiple times daily) Exercise → improved resp function + reserve, helps clear sputum High caloric diet CREON tablets to digest fats in patients with pancreatic insufficiency Prophylactic flucloxacillin Treat chest infections Bronchodilators (salbutamol inhalers) Nebulised DNase (enzyme which breaks down DNA material in secretions → easier to clear) Nebulised hypertonic saline Vaccinations for pneumcoccal, influenza, varicella Lung transplant in ESRespF Liver transplant in liver failure Fertility treatment involving testicular sperm extraction for infertile males

Answer 16

S. aureus H. influenzae P. aeruginosa

Answer 17

90% CF patients develop pancreatic insufficiency 50% develop diabetes 30% develop liver disease Most males are infertile due to absent vas deferens

Answer 18

permanent dilation of bronchioles (+ excessive mucus in them)

Answer 19

Recurrent pulmonary infection leads to progressive bronchial damage Post infectious (18% of adult patients) COPD (15% of adult patients) Asthma (7%) Connective tissue disorders (9%) Allergic bronchopulmonary aspergillosis (5%) Immunodeficiency (5%) Aspiration or inhalation injury (4%) Genetic IBD Focal bronchial obstruction Idiopathic (29%) Other (e.g. Marfan, Ehlers-Danlos…)

Answer 20

Post infection (e.g. TB, pneumonia) CF HIV ABPA (allergic bronchopulmonary aspergillosis - fungal infection of lung) Congenital airway disorders

Answer 21

Irreversible dilation, loss of cilia + mucus hypersecretion ↑risk of infection (as ↓mucociliary clearance)

Answer 22

Productive cough with lots of sputum + dyspnoea Fever Fatigue Haemoptysis Wheezing

Answer 23

Crackles, high pitched inspiratory squeaks and rhonchi (low pitched wheezes)

Answer 24

Non-curative conservative : chest physio (+stop smoking) Drug: bronchodilators Consider abx if infection

Answer 25

Collection of fluid in the pleural cavity which can be exudative (high protein count >35g/L) Or transudative (lower protein count <35g/L)

Answer 26

Exudative causes are related to inflammation which leads to protein leakage out of tissue into the pleural space: Lung cancer Pneumonia Rheumatoid arthritis Tuberculosis

Answer 27

Transudative causes relate to fluid moving across into the pleural space: Congestive cardiac failure Hypoalbuminemia Hypothyroidism Meigs syndrome

Answer 28

SOB Dullness to percussion over the effusion Reduced breath sounds Tracheal deviation away from the effusion if it’s massive

Answer 29

Reduced chest wall expansion Quiet breath sounds Stony dull percussion Reduced tactile/vocal fremitus Mediastinal shift away from affected side

Answer 30

CXR (blunting of costophrenic angle, fluid in the lung fissures, larger effusions have a meniscus, tracheal and mediastinal deviation) Thoracocentesis (sample of pleural fluid, pH, lactate, WCC, microscopy, transudate or exudate)

Answer 31

Blunting of costophrenic angle Fluid in the lung fissures Larger effusions have a meniscus Tracheal and mediastinal deviation

Answer 32

measurements of a number of factors including protein used to show whether pleural effusion is transudative or exudative)

Answer 33

Straw coloured/clear - transudate/exudate turbid /foul smelling - empyema/parapneumonic effusion Milky - chylothorax Blood stained - trauma/cancer/PE Food particles - esophageal rupture

Answer 34

Conservative ; small effusions will resolve with treatment of the underlying cause Pleural aspiration (needle into lungs to remove fluid) Chest drain (drain the effusion, prevents recurrence)

Answer 35

infected pleural effusion - suspected when the patient has improving pneumonia but new or ongoing fever - plueral effusion shows pus, acidic pH, low glucose and high LDL

Answer 36

chest drain to remove pus 6 weeks antibiotics

Answer 37

depends on symptoms, treatment for underlying cancer and prognosis drain + pleurodesis --> chest drain (talc via drain), thoracoscopy (spray talc) if recurrent and problematic --> indwelling pleural catheter

Answer 38

blood in pleural cavity

Answer 39

trauma, post-operative, bleeding disorders, lung cancer, PE, aortic rupture, thoracic endometriosis

Answer 40

large bore chest drain, possible vascular intervention, surgical opinion

Answer 41

air and fluid in pleural space

Answer 42

iatrogenic, gas forming organisms, thoracic trauma

Answer 43

where air from the lungs/trachea/oesophagus escapes into neck/face and abdomen

Answer 44

surgical emphysema/pneumothorax oesophageal rupture (Boerhaave's syndrome)

Answer 45

related to asbestos exposure following infection/empyema/chest trauma/haemothorax cancer (consider if nodular /1 cm depth)

Answer 46

excess air accumulation in the pleural space, causing ipsilateral collapse

Answer 47

Can be primary (spontaneous (rupture of apical pleural bleb), no underlying cause) or secondary (to trauma or pathology) Secondary pathological causes: Known lung disease -60% COPD -Asthma/ILD/CF/Lung cancer -Cystic lung disease Infection -PCP/TB -lung abscess Genetic predisposition -Marfan’s syndrome, Birt-Hogg Dube -LAM - Lymphangioleiomyomatosis Catamenial Pneumothorax Traumatic causes: Penetrating chest wall injury Puncture from rib Rupture bronchus/oesophagus

Answer 48

male, smokers, tall, age 20-40yrs, previous occurrence

Answer 49

Pleural space is normally a vacuum (no air) Breach in pleura (trauma/CT disorders) e.g. subpleural bullae burst –> fistula between pleural space + airways → air in the pleural space THis causes intrapleural pressure to be negative which leads to air being sucked into cavity leading to partial or total lung collapse

Answer 50

SOB One sided sharp pleuritic chest pain Decreased breath sounds Hyperresonant percussion ipsilaterally (increased air) Can be asymptomatic

Answer 51

Often no clinical signs except in severe cases Tachypnoea Hypoxia Unilateral chest wall expansion Reduced breath sounds Hyper-resonant percussion note Red flags (tension pneumothorax) Deviated trachea Surgical emphysema Distended neck veins Cardiovascular compromise

Answer 52

Small = self-resolving Larger - needle decompression (remove air with syringe), chest drain Surgical (if recurrent) - pleurodesis (insertion of a mildly irritant drug into pleural space to close space and prevent further collection of air or fluid)

Answer 53

air can flow into pleural space but can't leave --> intrapleural pressure increases with every breath (can even press on heart --> cardiac disorder symptoms)

Answer 54

tracheal deviation away from side of pneumothorax, reduced air entry to affected side increased resonance to percussion on affected side, tachycardia, hypotension

Answer 55

insert large bore cannula into 2nd intercostal space at the midclavicular line, needle decompress and then chest drain

Answer 56

The 5th intercostal space (inferior nipple line) Mid-axillary line (or the lateral edge of the latissimus dorsi) Anterior axillary line (lateral edge of the pectoralis major)

Answer 57

Resting mPAP >25mmHg measure with right heart catheterisation *often results in RHS heart failure; cor pulmonale

Answer 58

Pre-capillary → pulmonary emboli, primary pulmonary hypertension Capillary + lung → COPD, asthma Post-capillary → LV failure Chronic hypoxemia → COPD, altitude

Answer 59

Increasing the pressure and resistance in the pulmonary arteries causes strain on the right side of the heart trying to pump blood through the lungs which also causes a back pressure of blood into the systemic venous system → RVH + dilated pulmonary arteries

Answer 60

SOB Syncope Tachycardia Raised JVP Hepatomegaly Peripheral oedema

Answer 61

ECG (RVH→ larger R waves (V1-V3) and S waves (V4-V6), right axis deviation, RBBB) GS: CXR (dilated pulmonary arteries, RVH) NT-proBNP blood test (raised) Echo

Answer 62

Primary: IV prostanoids (e.g. epoprostenol) Endothelin receptor antagonists (e.g. macitentan) Phosphdiesterase-5 inhibitors (e.g. sildenafil) Secondary: Treat underlying cause Supportive treatment for complications e.g. resp failure, arrhythmias and heart failure

Answer 63

30-40% 5yr survival rate

Answer 64

thickening or scarring of the lung tissue, the most common interstitial lung disease

Answer 65

Smoking Occupational (e.g. dust) Drugs (methotrexate) Viruses (EBV, CMV)

Answer 66

Exertional dyspnoea Dry unproductive cough

Answer 67

Spirometry = restriction (FEV1:FVC >0.7) but FVC ↓ (<0.8 normal) High res CT (chest) → ground glass lungs + traction bronchiectasis

Answer 68

Smoking cessation + vaccines pirfenidone , nintedanib Surgery (lung transplant)

Answer 69

Idiopathic granulomatous inflammatory disease

Answer 70

Female 20-40yrs Afrocaribbean

Answer 71

Granulomas are nodules of inflammation full of macrophages which can occur in almost any organ in the body (most commonly lungs) Symptoms vary dramatically from asymptomatic (up to 50%) to severe + life-threatening

Answer 72

fever , fatigue Resp = dry cough; dyspnoea Other = eye lesions (uveitis), lupus pernio (blue + red nodules on nose + cheeks)

Answer 73

A specific presentation of sarcoidosis characterised by: Erythema nodosum, lymphadenopathy, polyarthralgia

Answer 74

CXR (staging 1-4) → bilateral hilar adenopathy + pulmonary infiltrates GS: Lung biopsy → non-caseating granuloma ↑Serum Ca2+, ↑serum ACE, hypercalcaemia

Answer 75

Tuberculosis, lymphoma, hypersensitivity pneumonitis, HIV, toxoplasmosis, histoplasmosis

Answer 76

Early stages are self-resolving Symptomatic patients → corticosteroids 2nd line options: methotrexate or azathioprine

Answer 77

60% spontaneously resolve in 6 months, can progress with pulmonary fibrosis and pulmonary hypertension potentially requiring a lung transplant

Answer 78

Type III hypersensitivity reaction to an environmental allergen which causes parenchymal inflammation and destruction in people that are sensitive to that allergen

Answer 79

Bird fancier’s lung - caused by proteins in bird feathers or droppings Farmer’s lung - caused by mould which grows on hay, straw and grain Hot tub lung - caused by bacteria in water vapour from hot tubs Humidifier lung - caused by fungi and bacteria in humidifiers, heating and air con systems

Answer 80

Over 300 known causes including: Bacteria Moulds and fungi Certain chemicals and metals Animal and plant proteins

Answer 81

Occupation (e.g. farming), bird keeping 50-70 yrs

Answer 82

SOB Dry cough Chest tightness Chills Fatigue Fever Muscle aches

Answer 83

SOB Cough Fatigue Weight loss Finger or toe clubbing

Answer 84

Bronchoscopy + broncheolar lavage (shows lymphocytes and mast cells) Allergy blood tests Imaging (CXR, CT) Lung function tests

Answer 85

Remove allergen, give oxygen and steroids Anti-fibrotic drugs (slow lung scarring) Oxygen therapy Pulmonary rehabilitation Lung transplant

Answer 86

Inflammation of the pharynx +/- exudate

Answer 87

Viral (EBV, adenoviruses) - 70-80% Bacterial (group A B-haemolytic strep (GAS); S. pyogenes) Fungal

Answer 88

Sore throat Fever Viral = + cough + nasal congestion Bacterial = + exudate headache

Answer 89

Rapid antigen test for group A strep Nucleic acid amplification for group A strep

Answer 90

generally self-limiting analgesia OTC medications antibiotics for bacterial

Answer 91

Inflamed mucosa of nasal cavity and nasal sinuses Acute ≤4 weeks Subacute 4-12 weeks Chronic ≥12 weeks Recurrent acute ≥4 episodes per year

Answer 92

Mostly viral (<10 days, non purulent discharge) Sometime bacterial - S.pneumococcus (40%), H. influenzae (30%)

Answer 93

viral URTI allergic rhinitis

Answer 94

Most likely to be caused by the interaction of a predisposing condition (e.g. environmental triggers), a viral infection, and a consequent inflammatory response with the sinonasal mucosa With increased oedema and mucus production, the sinus ostium is obstructed, blocking normal ventilation and drainage of the sinus. With decreased mucociliary clearance, stasis of secretions occurs and a secondary bacterial infection can take place

Answer 95

Purulent nasal discharge Nasal obstruction Facial pain/pressure

Answer 96

Cough Myalgia Sore throat Hyposmia Oedematous turbinate Fever

Answer 97

Generally self-limiting Treatment is primarily symptomatic

Answer 98

Infection involving the middle ear space which is a common complication of viral respiratory illnesses

Answer 99

Young age FHx Native american or native alaskan Lower socioeconomic status Craniofacial anomaly Immunological deficiency

Answer 100

Upper respiratory viruses can infect the nasal passages, eustachian tube and middle ear, causing inflammation and impairing the mucociliary action and ventilatory function of the eustachian tube → development of OM Middle ear effusion develops and nasopharyngeal bacteria contaminate the effusion Suppuration and subsequent pressure against the tympanic membrane lead to pain and fever, which are typical symptoms of OM

Answer 101

Otalgia (ear pain) Preceding upper resp symptoms Bulging tympanic membrane Myringitis

Answer 102

Irritability Sleep disturbance Fever Decreased appetite

Answer 103

Analgesia Some patients may require antibiotic therapy

Answer 104

Infection of the supraglottis which can result in airway compromise

Answer 105

infection of the supraglottis which can result in airway compromise

Answer 106

Most common: H.influenzae Also Strep penumoniae, S. aureus, MRSA

Answer 107

Inflammatory pathways lead to localised oedema of the airway, exponentially increasing airway resistance while narrowing the effective supraglottic aperture The glottis is usually not inflamed or affected as the process affects the supraglottic structures

Answer 108

tripoding (leant forard, mouth open + tongue out = max air in) sore throat SOB dysphagia acute distress fever

Answer 109

GS: Laryngoscopy Lateral XR radiograph (thumbprint sign), FBC, cultures of blood/supraglottis

Answer 110

ABC - secure airway Oxygen Intravenous antibiotics Corticosteroids if needed

Answer 111

Complication of upper respiratory tract infection characterised by sudden onset barking cough

Answer 112

Due to viral infection Often accompanies parainfluenza/measles infection

Answer 113

Children 6 months-6years Male Prior intubation

Answer 114

Symptoms result from upper-airway obstruction due to generalised inflammation and oedema of the airways. At the cellular level this progresses to necrosis and shedding of the epithelium Narrowed subglottic region is responsible for the symptoms of seal-like barky cough, stridor (from increased airflow turbulence), and sternal/intercostal indrawing If the upper airway obstruction worsens, respiratory failure can result, leading to asynchronous chest and abdominal wall motion, fatigue, hypoxia, and hypercapnia

Answer 115

Hoarse voice Barking cough Stridor Abrupt onset of symptoms Respiratory distress Fatigue Signs of hypoxia/hypercapnia in severe cases

Answer 116

Single dose of dexamethasone Supportive care

Answer 117

Chronic cough caused by Bordetella pertussis (gram -ve bacillus)

Answer 118

unvaccinated/under-vaccinated <5y/o close contact with infected person

Answer 119

bordatella ↑↑virulence - haemaglutinin + fimbriae adhere to URT - adenylate cyclase toxin inhibits phagocyte chemotaxis - pertussis toxin inhibits alveolar macrphages

Answer 120

Pertussis typically starts with mild coryzal symptoms (low grade fever and mild, dry cough) Paroxysmal cough starts after a week + (sudden and recurring attacks of coughing) Loud inspiratory whooping sound between coughs (forceful sucking in of air) Patient can cough so hard they faint, vomit or even develop pneumothorax Can present with apnoeas rather than cough

Answer 121

Nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks of symptom onset If cough present for 2+ weeks - anti-pertussis toxin immunoglobulin G

Answer 122

supportive care macrolide antibiotics (azithromycin, erythromycin, clarithromycin)

Answer 123

bone, liver, adrenals, brain, lymph nodes

Answer 124

squamous, adenocarcinoma, carcinoid, large cell

Answer 125

malignancy affecting the mesothelial cells of the pleura which is strongly linked to asbestos inhalation

Answer 126

male 50-80 yrs asbestos exposure radiation exposure genetic predisposition

Answer 127

Suggested that exposure to asbestos fibres results in recruitment and activation of alveolar macrophage and neutrophils with subsequent generation of reactive oxygen and nitrogen species Chronic inflammation and oxidative stress may culminate in DNA damage alterations in gene expression, and eventually malignant transformation

Answer 128

Cancer symptoms: weight loss, night pain, fatigue SOB Cough Pleuritic chest pain Haemoptysis Finger clubbing Recurrent pneumonia Lymphadenopathy

Answer 129

CXR + CT (pleural thickening), CA-125 (non-specifically raised in many tumours, sensitive but not specific) GS: lung biopsy

Answer 130

Very aggressive tumour so tx normally palliative If found early can try surgery + chemotherapy (but generally resistant)

Answer 131

Expansion of the lung is reduced due to: 1. altered lung parenchyma 2. pleural disease 3. neuromuscular disease 4. chest wall disease

Answer 132

COPD Asthma Bronchiectasis Cystic fibrosis

Answer 133

shortness of breath or breathlessness

Answer 134

Assessment tool for degree of baseline functional disability due to dyspnoea

Answer 135

0 - no breathlessness except with strenuous exercise 1 - shortness of breath when hurrying on the level or walking up a slight hill 2 - walks slower than people of the same age on the level because of breathlessness or has to stop for breath when walking at own pace on the level 3 - stops for breath after walking about 100m or after few minutes on the level 4 - too breathless to leave the house or breathless when dressing or undressing

Answer 136

asthma heart failure myocardial ischaemia COPD interstitial lung disease pneumonia psychogenic disorders

Answer 137

associated with damage to lung tissue which prevents adequate oxygenation of the blood (hypoxaemia) but the remaining normal lung is still sufficient to excrete CO2. => low O2, normal or low CO2, PaO2 <8kPa (low) and normal or low PaCO2

Answer 138

when alveolar ventilation is insufficient to excrete the CO2 being produced. Inadequate ventilation is due to reduced ventilatory effort or inability to overcome increased resistance to ventilation. It affects the lung as a whole and therefore CO2 accumulates => low or normal PaO2 and PaCO2 >6.0kPa (hypercapnia)

Answer 139

dyspnoea, irritability confusion, somnolence, fits tachycardia, arrythmia tachypnoea cyanosis

Answer 140

headache change of behaviour coma papilloedema warm extremities

Answer 141

pulmonary oedema pneumonia COPD asthma acute respiratory distress syndrome chronic pulmonary fibrosis pneumothorax pulmonary embolism pulmonary hypertension

Answer 142

COPD (mc) chest-wall deformities, respiratory muscle weakness CNS depression severe asthma myasthenia gravis muscle disorders obesity hypothyroidism adult respiratory syndrome

Answer 143

Chronic obstructive pulmonary disease = progressively worsening, irreversible airflow limitation

Answer 144

chronic bronchitis emphysema A1AT deficiency

Answer 145

almost always due to smoking patients are susceptible to exacerbations during which there is worsening of their lung function exacerbations are often triggered by infections

Answer 146

SMOKING air pollution genetics occupational exposure age

Answer 147

1. hypertrophy and hyperplasia of mucous glands in response to toxic or infectious stimuli 2. chronic inflammation cells infiltrate bronchi + bronchioles --> luminal narrowing 3. mucous hypersecretion, ciliary dysfunction, narrowed lumen --> infection risk + airway trapping

Answer 148

1. destruction of the elastin layer in alveolar ducts/sacs/respiratory bronchioles 2. elastin keeps the walls open during expiration (Bemouli principle) 3. decreased elastin --> air trapping distal to blockage

Answer 149

centriacinar (respiratory bronchioles affected only) panacinar (rib, alveoli, alveolar sacs) distal acinar irregular

Answer 150

Autosomal dominant inheritance - A1AT normally degrades neutrophil elastase (NE) and protects excess damage to elastin layer in lungs especially - deficiency results in increased NE which causes panacinar emphysema and liver issues

Answer 151

Chronic cough with often purulent sputum (infection risk due to mucus hypersecretion + stasis) Blue bloater (chronic bronchitis) - chronic purulent cough, dyspnoea, cyanosis, obesity Pink puffer (emphysema) - mimics cough, pursed lip breathing, cachectic (muscle wasting), barrel chest, hyperresonant, percussion Most patients a mix of BB/PP

Answer 152

clinical exam/history GS: spirometry (FEV1/FVC ratio <0.7) reversibility testing with B-2 agonists like salbutamol during spirometry testing, CXR, FBC sputum, ECG/echo, serum A1AT

Answer 153

lung cancer, fibrosis, heart failure, asthma

Answer 154

first smoking cessation + vaccines for flu + pneumococcal 1. short acting bronchodilators - B-2 agonists (SABA) (salbutamol/terbutaline) or short acting antimuscarinics (ipatropium bromide) 2. Long acting beta agonist (LABA) + long acting muscarinic antagonist (LAMA) for more severe cases: + nebulisers, oral theophylline, oral mucolytic therapy + long term oxygen therapy is used for severe COPD

Answer 155

chronic reversible airway disease characterised by airway obstruction, airway hyperresponsiveness, inflamed bronchioles +mucous hypersecretion

Answer 156

allergic (70%) - IgE mediated, extrinsic, T1 hypersensitivity - triggered by pollen, smoke dust, mould, antigens non-allergic (30%) - non-IgE mediated, intrinsic - may present later, harder to treat, associated with smoking (like COPD)

Answer 157

Family History allergies atopic dermatitis hay fever obesity smoking occupational exposure nasal polyps, aspirin sensitivity (+ asthma = Samter's triad)

Answer 158

TH2 cells are overexpressed in airways and when exposed to trigger release cytokines (IL-3,4,5,13), produce IgE antibodies and recruit eosinophils IgE stimulates mast cell degranulation which leads to histamine, leukotriene and tryptase release eosinophilia leads to release of toxic proteins this causes bronchoconstriction, mucous hypersecretion

Answer 159

Wheeze, cough (typically dry), chest tightness, SOB *typically episodic with triggers and diurnal variation * episodes can be classed as moderate (PEF 50-75%), severe (PEF 33-50% - can't finish sentences), life threatening (PEF <33% - decreased consciousness, fatal (hypercapnic pKa>6)

Answer 160

Spirometry - ↑FeNO + spirometry showing obstruction (FEV1/FVC<0.7), FEV1 >12%

Answer 161

1. SABA 2. SABA + ICS 3. SABA + ICS + LTRA (leukotriene receptor antagonist like montelukast) 4. SABA + ICS + LABA +/- LTRA 5. Increases ICS dose

Answer 162

O2 Nebulisers SABA ICS hydrocortisone IV MgSO4 IV theophylline CPAP/BiPAP +/- Abx if infection present

Answer 163

Adenocarcinoma (45% of NSCLC) Squamous cell carcinoma Carcinoid Tumour Large cell carcinoma

Answer 164

Malignant tumour formed from the mucous-producing glandular epithelial cells lining the outside of the lungs - commonly caused by asbestos - mets common --> bone, brain, adrenals, lymph nodes, liver

Answer 165

malignant tumour arising from lung epithelium which forms lesions with central necrosis and may secrete PTHrP--> hypercalcaemia - mostly smokers - late mets, mostly locally spread

Answer 166

serotonin-secreting neuroendocrine tumours which mostly arise in the GIT and sometimes the lungs - associated with genetics, MEN1 mutations and neurofibromatosis

Answer 167

lung cancer in which the cells are large and look abnormal when viewed under microscope - fast growing, aggressive type of cancer

Answer 168

Smoking Asbestos Coal Ionising radiation Lung disease already present COPD Older age

Answer 169

Chest pain (+/- shoulder pain) Cough + haemoptysis Cancer symptoms; weight loss, nausea, fatigue Signs of mets (e.g. hoarse voice Permberton sign, Homer’s syndrome)

Answer 170

Imaging - CXR, CT GS: Bronchoscopy + biopsy MRI - staging (TNM)

Answer 171

If caught early ⇒ surgical excision Metastasised ⇒ chemo +/- radio e.g. mAB therapy cetuximab

Answer 172

Malignant epithelial tumour arising from cells lining the lower respiratory tract

Answer 173

Cigarette smoking Environmental tobacco exposure Radon gas exposure Asbestos exposure Aged 65 to 70 Male

Answer 174

The tumour cells and small and densely packed, with scant cytoplasm, finely granular nuclear chromatin, and absence of nucleoli

Answer 175

Cough Dyspnoea Haemoptysis Chest pain Weight loss Fatigue Hoarseness Nausea

Answer 176

CXR, CT Bronchoscopy and biopsy MRI - staging (TNM)

Answer 177

Most patients present with advanced disease so surgery usually not an option 1st line: chemotherapy +/- radio (often unsuccessful) Metastasised ⇒ palliative

Answer 178

pro-inflammatory cytokines vasodilation impaired cardiac contractility reduced blood pressure impaired organ perfusion tissue hypoxaemia

Answer 179

delerium renal impairment - raised urea increased oxygen demand - high resp rate lactic acid production from anaerobic respiration systolic diastolic BP drop

Answer 180

in the lungs a very thin membrane for gas transfer is needed which also means there is not much space for barriers, immune defence or commensals like in other parts of the body.