Resp Flashcards

Question

Define and explain the difference between: o Oxygen saturation (SaO2, ‘Sats’) ArterialPaO2(partialpressureofoxygen) o Oxygencontentofblood

Answer 1

% Oxygen saturation of Hb in arterial blood Arterial partial pressure of oxygen (PaO2) in the blood is a function of the amount of dissolved oxygen. Note: PAO2 is alveolar partial pressure of O2. Oxygen content = oxygen bound to haemoglobin and the amount of oxygen dissolved in the blood

Answer 2

2 alpha & 2 beta subunits Each subunit has one haem group that can bind one oxygen molecule forming oxyhaemoglobin. changes shape based on the number of oxygen molecules bound to it. change in shape also alters its affinity to oxygen - inc binding = inc affinity = cooperativity No O2 = Tense state (T-state) Bind = Relaxed state

Answer 3

Fall pH= right Inc temp = right Inc 2-3 DPG = right - 2,3-DPG binds to the beta chains of haemoglobin, so increased 2,3-DPG levels results in it binding to haemoglobin

Answer 4

Hypoxia – low oxygen levels relative to the need in body or tissues 1Shock - reduces blood flow - peripheral vasoconstriction causes peripheral hypoxia 2Tissues using O2 faster than it is delivered 3Secondary to anaemia Anaemia - O2 sat and PaO2 will be normal - Hb levels low. Oxygen content low.

Answer 5

pulmonary embolism causes hypoxaemia by causing V/Q mismatch with V>Q at the site of the embolism (the clot blocks perfusion), and also by diverting blood to other alveoli and creating V

Answer 6

Bluish colouration due to unsaturated haemoglobin (< 85 or 90%) Deoxygenated haemoglobin is less red than oxygenated Can be peripheral (hands or feet) due to poor local circulation Or central (mouth, tongue, lips, mucous membranes) due to poorly saturated blood in systemic circulation Can be difficult to detect • Poor lighting • Skin colouration - darker skin need to look at nail beds for peripheral cyanosis • Shoes

Answer 7

Fatal if CO-Hb is > 50% Does not decrease PaO2 Children at inc risk Symptoms: Headache Nausea Vomiting Slurred speech Confusion Higher affinity so less O2 transport Increases affinity of unaffected subunits for oxygen - Left shift in dissociation curve - dec oxygen release to peripheral tissues

Answer 8

Pulse oxi: Detects level of Hb saturation – non-invasive Detects difference in absorption of light between oxygenated and deoxygenated Hb Only detects pulsatile arterial blood levels Can’t detect tissue oxygen levels or non-pulsatile venous blood Can’t give information about Hb levels Less accurate in darker coloured skin ABG: Partial pressure of PO2 - depends on dissolved O2. Also data on PCO2 and pH and bicarbonate Invasive - blood sample from radial artery

Answer 9

Shunt = 0 VQ mismatch = no. other than 0

Answer 10

In plasma: CO2 + H2O <-> H2CO3 <-> H+ + HCO3- Slow because little CA in plasma Negligible amount of bicarbonate formed In Hb: CO2+H2O->H2CO3->H+ + HCO3- H+ + Hb- ->HbH Happens when Hb in deoxygenated state CA present so rapid Mainly bicarbonate produced (H+ taken up by Hb) Goes into plasma in exchange for Cl- Carbon dioxide also reacts directly with the protein part of haemoglobin, forming Carbamino compounds. This is at low O2 and high CO2 conc. The Haldane effect - low O2 conc inc CO2 carrying capacity of Hb because release of O2 from Hb promotes binding of CO2.

Answer 11

the pH of plasma is determined by the ratio of [HCO3-]: pCO2 which is normally about 20:1.

Answer 12

Hypoxia Hypoxaemia - Falls in arterial pO2 below normal Hyper and hypocapnia- rise or fall in arterial pCO2 Hypoventilation - Removal of CO2 from lungs is less rapid than its production. Hyperventilation. Removal of CO2 from alveoli is more rapid than its production.

Answer 13

Dorsal respiratory group of neurones - dorsal surface of the medulla - basic rhythm of respiration - inspiratory neuron action potentials to spinal nerves innervating the diaphragm and external intercostal muscles - spontaneously and continuously fire. (Preventing over inflation of lung - Stretch receptors located in the walls of bronchi and bronchioles transmit information via the vagus nerve back to the brainstem.) the ventral group located on the ventral-lateral surface of medulla - expiration the pontine - pneumotaxic centre of neurons, located dorsally on the pons - inspiratory off switch. Limits phrenic nerve, dec tidal vol and resp rate.

Answer 14

Peripheral chemoreceptors detect changes in arterial pO2 (also change in pH and arterial pCO2) Located in carotid and aortic body. Afferent impulses travel via the glossopharyngeal nerves to the medulla oblongata and the pons in the brainstem. Changes made: Respiratory rate and tidal volume are increased Blood flow is directed towards the kidneys and the brain Cardiac Output is increased to maintain blood flow, and therefore oxygen supply to tissues Central chemoreceptors Located in the ventral medulla oblongata of brainstem. They detect changes in the arterial partial pressure of carbon dioxide (pCO2). Receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation. Get reset to higher value in prolonged hypercapnia. pH Control of CSF Stimulated by dec pH in CSF CO2 freely diffuses from the arterial blood supply into the CSF. CO2 reacts with H2O, producing carbonic acid, which lowers the pH - stimulates respiratory centres to increase ventilation. However if pCO2 levels stay abnormal for a long period of time, choroid plexus cells within the blood brain barrier allow HCO3– ions to enter the CSF. Alters the pH which in turn resets the pCO2 to a different value.

Answer 15

Normal = 7.35-7.45 Hypoventilation- Removal of CO2 from lungs is less rapid than its production. Resp acidosis - more CO2 in lungs. The alveolar pCO2 rises, so dissolved CO2 rises more than HCO3- producing a fall in plasma pH Compensated - kidneys respond to the low pH by reducing excretion of HCO3-. Full = normal pH Partial = abnormal pH, but opp process is trying to get it back to normal Hyperventilation - Removal of CO2 from alveoli is more rapid than its production. Resp alkalosis - Alveolar CO2 falls - plasma pH rises Compensated - kidneys respond by excreting HCO3- and plasma pH normal. But buffer base concentration is reduced.

Answer 16

Normal ABG: pH: 7.35-7.45 PaO2: 9.3-13.3 kPa PaCO2: 4.6-6 kPa Bicarbonate(HCO3): 22-26 mmol/L Information from ABG: Lung function: pO2, pCO2 Also pH status through the Henderson-H equation that relates pCO2 to pH. Acid-base status: If pH is <7.35 the person has acidaemia caused by an acidosis process. And vice versa. Metabolic status: metabolism, and kidney function, by providing us with the bicarbonate level. Interpretation: 1. Look at pH. Let’s say it is acidic 2. Look at pCO2. If it is elevated = respiratory acidosis 4. If pCO2 normal and bicarbonate low = metabolic acidosis 5. If pCO2 and bicarbonate are elevated and low pH then metabolic compensation is taking place. If pCO2 low, bicarbonate high and low pH then respiratory compensation. 6. If pH normal and other stuff abnormal then full compensation has happened.

Answer 17

Resp alkalosis High altitude Central Causes eg Head Injury, Stroke Anxiety Hyperthyroidism Pulmonary Embolism Pneumonia Asthma Pulmonary oedema Resp acidosis Conditions that impair CNS respiratory drive (eg, brain stem stroke, medications, drugs, or alcohol) Conditions that impair neuromuscular transmission and other conditions that cause muscular weakness Obstructive, restrictive, and parenchymal pulmonary disorders eg COPD

Answer 18

Peripheral - carotid bodies and aortic bodies. The impulses are carried via the glossopharyngeal nerves and vagus nerve respectively. Sends to brainstem resp centres. Response to O2 - increase in tidal volume and rate of respiration. More blood to brain and kidneys & increased pumping of blood by the heart. Response to CO2 Response to pH - low pH results in an increased respiratory rate and tidal volume.

Answer 19

10% of transported CO2 travels as dissolved CO2, 60 % as bicarbonate 30% as carbamino compounds 1) Tissues produce CO2. The increase in pCO2 causes a little more CO2 to dissolve in venous compared with arterial blood 2) When blood arrives at the tissues oxygen is unloaded from haemoglobin. Hb can now bind with H+. Bicarbonate mostly exported to the plasma. 3) CO2 binds to amino groups on Hb so carbamino products. This stabilises pH– CO2 is unable to leave the blood cell to contribute to changes in pH Bohr Effect – it stabilises the T state of haemoglobin 4)When that mixed venous blood reaches the lungs there is oxygenation of Hb. Less good at holding onto CO2 - Haldane effect H+ driven off Hb react with the bicarbonate to form CO2 which is breathed out.

Answer 20

Location - ventral surface of the medulla Responds to brain extracellular fluid. The pH is determined by plasma PaCO2. Choroid plexus cells pump HCO3- into or out of CSF. If pCO2 rises, ventilation increases, to lower pCO2 again. If this does not occur (eg due to disease of lung) choroid plexus cells will pump more bicarbonate ions into CSF. And vice versa. Adjustment means higher level of CO2 needed to cause acidosis and

Answer 21

Hypoxia is defined as reduced oxygen at the tissue level. Abnormalities occurring at any point on the oxygen supply chain can result in hypoxia. Hypoxaemia is defined as a decrease in the partial pressure of oxygen (pO2) in the blood. The pO2 of the blood is determined by gas exchange in the lung.

Answer 22

Type 1 respiratory failure is characterised by a low pO2 (< 8kPa) with a normal or low PCO2. Type 2 respiratory failure is characterised by a low pO2 (< 8kPa) and a high pCO2 of > 6.7 kPa

Answer 23

Low inspired pO2 e.g. high altitude - pO2= FiO2 x total atmospheric pressure -pO2 falls in alveoli at higher altitude - hypoxaemia - Type 1 respiratory failure. Give O2. V/Q mismatch- alveoli poorly ventilated - caused by pneumonia (exudate), asthma (airway narrowing), COPD (airway narrowing+loss of alveoli) , resp distress syndrome in newborn(alveoli not expanded), PE(perfusion blocked), PO(fluid). Give O2 and treat underlying. Diffusion impairment - lung fibrosis(inc distance), emphysema(dec SA). pO2 low and pCO2 normal as it is more soluble. Intrapulmonary shunts - shunt is perfusion of alveoli that have no ventilation – V/Q ratio = 0 Alveolar filling with pus, oedema fluid, blood or tumour eg ARDS. Right to left shunts (e.g. cyanotic heart disease). Blood from the right side of the heart enters the left side without passing through the lungs and taking part in gas exchange.

Answer 24

Hypoventilation - entire lung poorly ventilated due to inadequate resp rate or reducing alveolar minute ventilation. Low pO2 and high pCO2 in the alveolar air. Hypoxaemia and hypercapnia. Acute Causes - Opiate overdose, Head injury, severe asthma Chronic - severe COPD Central control - opioid OD, hypothyroidism MN - MND, ALS Peripheral neuropathy- GBS Nm junction- MG, Organophosphate toxicity, Botulism Resp muscle weakness and fatigue- Duchennes, malnutrition, asthma, COPD, RDS Chest wall disorders - e.g. Scoliosis, morbid obesity, rib fractures, kyphosis(excessive outward curve of spine). Severe lung fibrosis, or widespread severe airway obstruction (life threatening asthma, late stages of COPD)

Answer 25

Pump failure - as more and more airways become severely narrowed and exhaustion sets in ,so hypoventilation, it becomes type 2 respiratory failure eg asthma, COPD, fibrosis. In fibrosis As disease progresses, restrictive lung disease leads to hypoventilation – which will cause hypercapnia. Causes • Idiopathic pulmonary Fibrosis • Asbestosis • Extrinsic allergic alveolitis • Pneumoconiosis

Answer 26

Acute inflammation affecting alveolar-capillary membrane Inc permeability of membrane Exudate inactivates surfactant so collapse of alveoli and dec SA. alveolar atelectasis. Lungs stiff and vol dec. No hypoxic pulmonary vasoconstriction due to inflammation causing vasodilation. intrapulmonary shunt - no ventilation with respect to perfusion Hypoxaemia Deoxygenated blood goes to left heart Eventually type 2 as hyperventilation fails to keep pace with carbon dioxide production.

Answer 27

bluish discolouration due to presence of 4 to 6 gm/dl of deoxyhaemoglobin Central - Seen in oral mucosa, tongue, lips. Indicates hypoxaemia Peripheral - In fingers, toes

Answer 28

Effects of Hypoxaemia and/or Hypoxia: • Impaired CNS function – lethargy, confusion, irritability • Cardiac arrhythmias and ischaemia • Hypoxic vasoconstriction of pulmonary vessels • Central cyanosis • Initially tachycardia but as condition persists worsens bradycardia will develop. Tachypnoea. Effects of Hypercapnia: • Respiratory acidosis • Impaired CNS function: drowsiness, confusion, coma, flapping tremors, seizures, and if severe and persistent respiratory arrest • Peripheral vasodilatation –warm hands, bounding pulse • Cerebral vasodilation – headache – if severe and persistent will cause cerebral oedema

Answer 29

Obstruction of a pulmonary artery or one of its branches, usually by DVT (deep vein thrombosis- venous thromboembolism), which has become dislodged and been carried to the lungs by the blood stream. Consequences: Hypoxaemia due to V/Q mismatch Rise in pulmonary artery pressure - right ventricular strain - drop in the cardiac output - vasoconstriction of pulmonary vessels to maintain BP so even more strain on right heart. Can lead to death because of cardiogenic shock with circulatory failure / cardiac arrest due to arrhythmias. If they have patent foramen ovale then shunting then hypoxia. Also paradoxical embolization – clot passes into left heart & systemic circulation -> stroke Pulmonary infarction - alveolar haemorrhage & infarction Causes haemoptysis, pleuritis, small pleural effusion

Answer 30

Risk factors: Immobility • Recent long distance travel • Malignancy, • Inherited hypercoagulable states, • Pregnancy, • Obesity • Recent surgery • Hormone replacement therapy or oral contraceptives Symptoms - pleuritic chest pain, • coughing • dyspnea, syncope, Haemoptysis, Unilateral leg pain/swelling Signs - Tachypnoea and tachycardia, fever up to 39, cyanosis, crackles Investigation Imaging - Detection in CT pulmonary angiography (CTPA) (V/Q scan for pregnant), Chest x-ray - might have peripheral wedge shaped opacification due to infarction Arterial blood gas shows respiratory alkalosis with low pO2, low CO2 D-dimer levels can rule out PE if -ve in low risk patients. ECG = sinus tachycardia Treatment: O2 Anticoagulants - LMW heparin (Heparin-Induced Thrombocytopenia - antibodies form and platelets activate and clump. Thrombi form. Stroke, MI, limb ischaemia). Thrombolytic agents or thrombectomy, resp and haemo support for massive PE. Vena cava filters if high bleeding risk or recurrent PE. Prevention: Early mobilisation post-surgery or during long airplane flights DVT prophylaxis in high-risk patients Postoperative anticoagulation Avoid certain medications (e.g., OCPs) in patients with thrombophilia (e.g., factor V Leiden) or smokers (elevated risk DVT). Falls prevention AES stockings

Answer 31

Fat Embolism Syndrome traumatic fracture of femur, pelvis, tibia. pelvic and knee arthroplasty. massive soft tissue injury, severe burn, bone marrow biopsy etc acute pancreatitis, fatty liver etc Triad - petechial rash, decreased level of consciousness, and shortness of breath. Amniotic fluid embolism - presents as sudden maternal collapse associated with hypotension, hypoxaemia, and DIC. It occurs when amniotic fluid or other debris enter the maternal circulation. Most cases occur during labour or immediately after delivery. Air emboli

Answer 32

Inc EPO secreted by kidney - raised Hb (Polycythaemia) Increased 2,3, DPG – shifts Hb/O2 saturation curve to the right so oxygen released more freely Increased capillary density Chronic hypoxic vasoconstriction of pulmonary vessels results in- • Pulmonary hypertension • Right heart failure • Cor pulmonale

Answer 33

1. Correction of hypoxia removes pulmonary arteriole hypoxic vasoconstriction a. leads to increased perfusion of poorly ventilated alveoli - more CO2 in blood. b. diverting blood away from better ventilated alveoli – i.e worsens V:Q mismatch (V

Answer 34

COPD is a disease state characterised by: airflow limitation that is not fully reversible Persistent respiratory symptoms It encompasses both emphysema and chronic bronchitis The airflow limitation is usually progressive Associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

Answer 35

Tobacco smoking = 90% Air pollution and occupational exposure Alpha-1 antitrypsin deficiency (anti protease so deficiency means destruction of alveolar walls and emphysema)

Answer 36

Host response to noxious substance Chronic inflammatory process: • Enlargement of mucus-secreting glands of the central airways • Increased number of goblet cells (which replace ciliated respiratory epithelium) • Ciliary dysfunction These are all chronic bronchitis • Elastin breakdown leading to destruction of alveolar walls and structure, and loss of elastic recoil - emphysema • Formation of larger air spaces with reduction in total surface area available for gas exchange • Loss of capillaries with loss of the alveolar-capillary membrane secondary to destruction of elastin • Vascular bed changes leading to pulmonary hypertension.

Answer 37

1. Luminal airflow obstruction due to secretions due to airway inflammation and there is airway fibrosis so inc airway resistance AND Narrowing of bronchioles that are kept open by radial traction (exerted on their walls by outward pull of elastin in surrounding alveoli). 2. Elastase break down so destruction of alveolar walls so less lung recoil 3. Less expiration force 4. Hyperinflation of lungs 5. Dec gas exchange as old air trapped in lungs so dec con gradient of O2 6. Air trapping flattens the diaphragm and thus reduces its force upon contraction – dec inspiration force. 7. Hypoxia causes pulmonary vasoconstriction so pulmonary hypertension and R heart failure. Also, thickening of vascular smooth muscle. 8. Hypercapnia

Answer 38

Clinical signs History - gradual, older people with long history of smoking, occupation, pollution Physical: Tachypnoea: to compensate for hypoxaemia and hypoventilation. Use of accessory muscles of respiration Barrel chest (increased antero-posterior diameter of the chest) is due to hyperinflation Purse lip breathing Hyper- resonance on percussion due to hyperinflation and air trapping Reduced intensity breath sounds caused by hyperinflation and loss of lung parenchyma. Dec air entry - secondary to loss of lung elasticity Wheezing on auscultation Late: Central cyanosis – hypoxaemia and tissue hypoxia Flapping tremors - hypercapnia Signs of right-sided heart failure (distended neck veins, hepatomegaly, and ankle oedema). Symptoms Cough - morning but becomes constant, productive but not purulent (not green or yellow) Dyspnoea on exertion then rest

Answer 39

Lifestyle • Smoking cessation • Pulmonary rehabilitation: many COPD patients avoid exercise because of breathlessness = muscle weakness =worsening symptoms. Need exercise, disease education and nutritional advice. • Patient weight, nutrition, physical activity– obesity also impairs lung function. First • Pneumococcal, Influenza, Covid19 vaccination • Bronchodilators • Inhaled corticosteroid Second • If severe- long acting anti-muscarinic agent inhalers Long term oxygen treatment Surgical interventions: such as removal of large bullae, lung volume reduction, and lung transplant).

Answer 40

Event characterised by acute worsening of resp symptoms eg dysponea, cough, sputum. Result in additional therapy. Monitoring for hypoxaemia and hypercapnia, using Pulse oximetry and ABG analysis. Acute infectious exacerbations = severe dysponea, fever, chest pain, purulent sputum. Give antibiotics, bronchodilators, oral steroids, O2, ventilation.

Answer 41

Spirometry shows an obstructive pattern with FEV1/FVC ratio <70%. CXR: Hyper inflated lungs may result in flattened diaphragm, hyperlucent lungs and an increased antero-posterior diameter of the chest (seen on lateral chest x-ray only). May show complications of COPD, such as pneumonia and pneumothorax Mandatory to exclude other diagnoses. Lung function tests ABG analysis for hypoxaemia and hypercapnia for suspicion of resp failure. Alpha-1 antitrypsin level - atypical history

Answer 42

• Recurrent pneumonia • Pneumothorax: Occurs because of lung parenchyma damage with sub-pleural bulla formation and rupture • Respiratory Failure – acute (higher risk for this) or chronic • Cor pulmonale (Right heart failure)

Answer 43

Chronic, irreversible dilatation of bronchi due to destruction of the elastic and muscular components of the bronchial wall. Causes: Post infective: whooping cough, TB, measles Immune deficiency: Hypogammaglobulinaemia Genetic / Mucociliary clearance defects: o Cystic fibrosis o Primary ciliary dyskinesia, Young’s syndrome(triad of bronchiectasis, sinusitis, reduced fertility) o Kartagener syndrome (triad - bronchiectasis, sinusitis, situs inversus) o Yellow Nail Syndrome - triad of yellow nail, pulmonary problems and lower limb lymphoedema Obstruction eg tumour

Answer 44

Cough Sputum production (can be bloody) Crackles, high pitched inspiratory squeaks and ronchi Dyspnoea Fever Risk - Cystic fibrosis, immunodeficiency, previous infections, IBD, alpha1-antitrypsin def Investigate: High resolution CT scan - bronchus is more dilated than the adjacent blood vessel and bronchial wall thickening. Classically show the ‘Signet Ring sign’ - a very dilated bronchus and smaller pulmonary artery are seen in close association. Treat underlying cause • Physiotherapy – daily mucus clearance • Antibiotics according to sputum cultures • Supportive – vaccine, bronchodilators • Pulmonary Rehab

Answer 45

Sounds: Diminished in COPD Rhonchi, inspiratory squeaks and crackles in B Chest CT: May be normal or show emphysema in COPD Thickened, dilated airways with or without air fluid levels in B Pathogens: Haemophilae influenzae, Strep pneumoniae and moraxella catarrhalis in COPD HI, MC, Pseudomonas aeruginosa, fungi (aspergillus, candida), non-tuberculous mycobacteria, Staphylococcus aureus in B However, patients with COPD may also develop bronchiectasis.

Answer 46

What = common cause of bronchiectasis, autosomal recessive where CFTR is mutated. Diagnosis = history of CF in sibling or +ve newborn screening test result AND Inc NACL in sweat 2 CF mutations Or abnormal nasa epithelial ion transport Management = No smoking Avoid people with colds Avoid Jacuzzis (pseudomonas) Avoid stables,compost–riskof aspergillus fumigatus inhalation o influenza vaccine o strep pneumoniae vaccination oNaCl tablets in hot weather/exercise

Answer 47

Defect on Long arm of Chromosome 7 Leads to Cystic Fibrosis Transmembrane Conductance Regulator mutation Leads to ineffective cell surface chloride transport Leads to thick, dehydrated body fluids in organs which have CFTR

Answer 48

1. Meconium ileus: in CF infants the bowel is blocked by the sticky secretions. Signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium. 2. Intestinal malabsorption - The main cause is a severe deficiency of pancreatic enzymes. 3. Recurrent Chest infections, Pneumothorax, Respiratory failure, Cardiac failure 5. Osteoporosis 6. Male infertility

Answer 49

Complications: 1.Respiratory Infections Treatment = antibiotics and lung physio Prophylactic antibiotics to maintain health 2. Low Body Weight o if needed give pancreatic enzyme replacement therapy o high calorie intake + extra supplements o may need NG or PEG feeding 3. Distal Intestinal Obstruction Syndrome (DIOS) o DIOS vs constipation–faecal obstruction in ileo- caecum vs whole bowel o Due to intestinal contents in the distal ileum and proximal colon (thick, dehydrated faeces) o Due to insufficient pancreatic enzymes or salt deficiency o Palpable right iliac fossa mass (faecal) o Do abdominal XR demonstrating faecal loading at junction of small and large bowel 4. CF Related Diabetes o exocrine pancreatic duct inflammation affects the endocrine portion thus destroying insulin producing beta cells.

Answer 50

TB bacilli are aerobic, rod-shaped, non-motile Can be demonstrated on smears stained by the Ziehl-Nielsen method 2-6 weeks to form colonies on cultures Long chain fatty acids and glycolipids in cell wall = structural rigidity, acid alcohol fast bacilli (resist decolorisation by acids).

Answer 51

Transmission = infected droplets formed from sputum with MTB being released into the air. Need long periods of contact - more than 8hrs so more likely to get from co-worker or family 1. Alveolar macrophages infected as deposition of TB bacilli in the alveoli. 2. Phagocytose MTB 3. T helper cells (Th1 cells or CD+4 cells) activate macrophages enabling them to become bactericidal with enhanced ability to kill MTB. 4-6 weeks 4. Interferon – (IFN-gamma) produced by lymphocytes is critical to activating macrophages 5. Granuloma with central caseous necrosis (tubercles) surrounded by epithelioid macrophages, Langhans giant cells, lymphocytes (eg dendritic cells), neutrophils, foamy macrophages. 6. Development of tubercles called Ghon’s focus. Occurs in subpleural airways in the lower part of the upper lung or the upper part of the lower lobes. 7. MTB bacilli drain from the Ghon’s focus into the hilar lymph nodes. Ghon’s focus and draining lymph nodes = primary Gohn complex. Possible host response: 1) Immediate clearance of the organism through mucosal barriers 2) Complete clearance of infection via innate immunity 3) Complete clearance of infection via innate and adaptive immunity: no MTB + immune system remembers the infection 4) Primary infection contained to latent infection 5) Primary (active) disease - immediate symptoms 6) Post-Primary TB (or Secondary TB) - The onset of an active disease years after a period of latent infection.

Answer 52

Primary infection - first exposure to MTB. Primary active TB - immediate onset of active disease in the individual. 5% Post primary TB - disease in a previously infected host. Can occur due to re-activation of latent infection, re-exposure with weakened host immunity or large inoculum. 5%. Cavity formation: liquefaction of the caseous material discharged into bronchus results in cavity formation. Fibrous tissue forms around periphery. Haemorrhage - extension of caseous process into vessels in the cavity →causes haemoptysis Spread to involve rest of the lung Pleural Effusion: Seeding of TB bacilli in the pleura can result in this.

Answer 53

Extra pulmonary TB - Haematogenous spread of primary TB or reactivation of latent TB in sites other than the lungs. Eg lymph nodes, bones (osteomyelitis), CNS (tuberculous meningitis), GI tract, urinary tract and adrenal glands (addison’s). Miliary TB - MTB draining through the lymphatic system enter venous blood and circulate back to the lung. Small foci of infection (resembling millet seeds) are visible throughout the lungs.

Answer 54

Latent TB -Primary infection contained to latent infection. dormant bacteria present in body but no symptoms Active TB - have symptoms

Answer 55

The onset of active TB is gradual over weeks or months. Tiredness, malaise, weight loss, fever, sweats and cough. The cough may be dry or productive of mucoid sputum, and haemoptysis may occur. Crackles may be present. Cavitation, fibrosis or a pleural effusion present.

Answer 56

CXR shows pulmonary shadowing, which may be patchy solid lesions, cavitated solid lesions, streaky fibrosis with flecks of calcification hilar adenopathy.

Answer 57

ACTIVE lung disease = acid-fast smear and cultures of sputum should be obtained (for drug susceptibility). May have false -ve skin/IGRA test. LATENT TB, or screening for TB = IFN-gamma assays (IGRA) or tuberculin skin test. Positive tests = T cell mediated immunity to mycobacterial antigens BUT does not differentiate between infection and active disease.

Answer 58

TB is treated using a combination of antibiotics over several months. 4 drugs - rifampicin, isoniazid (INAH), pyrazinamide, ethambutol - wild MTB strain has drug resistant organisms arising from mutations. However, the likelihood of such organisms being resistant to all 4 drugs is highly unlikely. To prevent peripheral nerve damage pyridoxine (vitamin B6) must be given along with INAH.

Answer 59

Anti MTB antigens present. Adaptive immunity. Will be +ve in tuberculin skin test.

Answer 60

People who have come from countries with a high rate of TB – may be related to immigration, work, tourism Children of parents whose country of origin has a high rate of TB People with weakened immune system due to disease or treatment eg HIV People who are homeless or living in overcrowded conditions People who are undernourished People have been in prison People who are addicted

Answer 61

HIV = weakened immune system = risk factor for TB Interferon γ producing CD4-T cells are key components of the immune response against MTB. HIV infection causes CD4 T-cell depletion = increased susceptibility to TB disease.

Answer 62

Definition: Asthma is a chronic inflammatory disorder of the airways. Asthma is characterized by a triad of bronchial smooth muscle contraction, airway inflammation, and increased secretions. Result in Airflow obstruction and an increase in airway responsiveness.

Answer 63

• Genetic susceptibility • Often associated with atopy • Sensitisation to an allergen Macrophages present antigens to T lymphocytes. Activates Th2 cells (CD4+). Th2 cells release cytokines, which activate inflammatory cells. Th2 cells also activate B cells, which produce IgE. 2-phase response: Immediate response (20 mins)- type 1 hypersensitivity. It is caused by interaction of the allergen (eg pollen, Fumes, NSAIDS and beta blockers) & specific IgE antibodies. Lead to mast cells degranulation and release of mediators (histamine, prostaglandin, leukotriene) which cause bronchoconstriction. 2. The Late Phase Response - type IV. It involves inflammatory cells, eg eosinophils (release Leukotriene C4 and causes shedding of epithelial cells), mast cells, lymphocytes, & neutrophils, which release mediators and cytokines, which cause airway inflammation.

Answer 64

The airway inflammation causes reduced airway calibre due to: • Mucosal swelling (oedema) due to vascular leak • Thickening of bronchial walls due to infiltration of by inflammatory cells • Mucus over production; the mucus is also abnormal - slow-moving- dry,white sputum cough. Airways can have mucus plugs. • Smooth muscle contraction • The epithelium is shed and is incorporated into the thick mucus hyper-responsiveness of airways - non- allergic stimuli like cold air & fumes can also trigger attacks. Long-term asthma can lead to airway remodelling. The irreversible changes include: • hypertrophy & hyperplasia of smooth muscle, • hypertrophy of mucus glands • thickening of the basement membrane.

Answer 65

Type 1 resp failure due to hyperventilation so dec CO2 and O2. increasing pCO2 is a sign of life-threatening Asthma - complete blockage of some airways and exhaustion - require mechanical ventilation. Dec ventilation of the affected alveoli → ventilation / perfusion mismatch in the affected area.

Answer 66

Investigation: Peak flow and spirometry(shows obstructive pattern) Treatment: • Patient education • Drug treatment using the BTS stepwise approach. Bronchodilators and steroids • Up to date vaccinations Exacerbations: • Oxygen – keep sats 94-98% • Bronchodilators inhaler - Salbutamol, Ipratropium and anti-inflammatory inhaler (Steroids) • If severe- Magnesium sulphate IV, Aminophylline IV • antibiotics

Answer 67

Onset of asthma is typically in early life. COPD older. A personal or family history of allergy, rhinitis, and eczema is often present. COPD history of smoking. Symptoms may be episodic with obvious triggering factors. COPD - gradual worsening. Wheezing and lung function tests responds to bronchodilators. after bronchodilators the airway Obstruction in COPD is not fully reversible. Both can have Tachypnoea and Use of accessory muscles of respiration COPD - chronic bronchitis + emphysema so narrowing of airways and destruction of alveoli. There is hyperinflation so barrel chest and signs of right sided heart failure.

Answer 68

Recurring/variable symptoms • Wheeze • Cough • Chest tightness • Breathlessness Dry cough Atopic features • Eczema, Rhinitis, Nasal polyps Periods of increased symptoms - exacerbations Examination: Tachypnoea • Tachycardia • Hypoxia • Unable to speak full sentences • Accessory muscle use • Silent chest • Altered conscious level Can mimic other conditions: • Psychosocial factors - Anxiety, panic disorder • Inducible Laryngeal Obstruction - Abnormal closing of vocal cords Breathing Pattern Disorder (BPD)

Answer 69

RIPE (for image quality) Rotation The medial aspect of each clavicle should be equidistant from the spinous processes The spinous processes should also be vertically orientated against the vertebral bodies. Inspiration 5-6 anterior ribs, the lung apices, both costophrenic angles and lateral rib edges should be visible Projection AP vs PA film Tip- if there is no label, then assume it’s a PA. Also, if the scapulae are not projected within the chest, it’s PA. Exposure Left hemidiaphragm should be visible to the spine. vertebrae visible behind heart

Answer 70

INTERPRETATION (ABCDE) Airway Is the trachea significantly deviated from its normal position? If so is anything pushing or pulling? Pushing eg pleural effusion or tension pneumothorax. Pulling eg consolidation with lobar collapse Paratracheal masses / lymphadenopathy • The trachea is normally located centrally or just slightly off to the right Look at Carina and bronchi, Hilar structures Breathing Lungs, Pleura Cardiac Heart size Heart borders Diaphragm Costophrenic angles Location diaphragm in relation to ribs/chest Everything else Bones, Soft tissues Air beneath the diaphragm Pacemaker, Wires/ Central access devices

Answer 71

Shadowing/ opacification in lung field = pneumonia Evaluating symptoms (cough, chest pain, etc), signs (hypoxemia or pulmonary exam), lines, tubes and pacemakers, effects of treatment

Answer 72

Common Viridans streptococci, Neisseria spp, Anaerobes Candida Less common Streptococcus pneumoniae Streptococcus pyogenes Haemophillus influenzae Other Pseudomonas, Escherichia coli Lungs are not sterile Alveolar microbiota Aspiration Blood stream spread Direct spread

Answer 73

Acute bronchitis: infections causing inflammation in the bronchial airways - virus, smokers, usual symptoms, CXR normal Bronchiectasis: Bronchiectasis is a permanent dilatation and thickening of the airways associated with chronic cough, sputum production, bacterial colonisation, and recurrent infection Bronchiolitis: Bronchiolitis is a viral infection of the bronchioles, commonly caused by respiratory syncytial virus and commonly occurs in children younger than 12 months Empyema: Empyema is a collection of pus in the pleural cavity, usually with pneumonia but also after thoracic surgery or trauma Lung Abscess: localised collection of pus within lung that leads to cavity formation with a thick wall. Commonly when microbial infection causes necrosis of the lung parenchyma; if they communicate with an airway they may lead to purulent cough. imaging typically demonstrates the presence of air-fluid levels in the cavity ( air rises above a fluid in a contained space + flat surface at the "air-fluid" interface).

Answer 74

Pneumonia is a general term denoting inflammation of the lung parenchyma due to infection. The common feature of pneumonias is a cellular exudate in the alveolar spaces. localized to a particular lobe/s of the lungs –"lobar pneumonia" diffuse and patchier –"bronchopneumonia".

Answer 75

Community acquired Pneumonia (CAP) symptoms and signs consistent with a lower respiratory tract infection. no other explanation for the illness. commonest causative organism = Streptococcus Pneumoniae - split immunoglobin (IgA) Others: • Haemophilus influenzae, • Moraxella catarrhalis, Above 2 common with COPD • group A streptococci, • Staphylococcus aureus. Atypical: • Mycoplasma pneumoniae (commonest, lacks a peptidoglycan bacterial cell wall)-shear off cilia • Chlamydia pneumoniae (obligate intracellular pathogen) - ciliostatic factor • Legionella pneumophila (intracellular pathogen) - contaminated water sources

Answer 76

Hospital acquired pneumonia: occurring > 48 hours after admission and was not incubating at the time of admission. Causative organisms include aerobic gram-negative bacilli, such as: • Pseudomonas aeruginosa, • Escherichia coli, • Klebsiella pneumoniae, • Acinetobacter species Gram-positive bacteria = Staph aureus(MRSA) Patients with poor immune response are susceptible to a range of organisms, such as Pneumocystis jiroveci, Aspergillus, Cytomegalovirus.

Answer 77

cough with mucopurulent sputum, dyspnoea, pleuritic chest pain, myalgia Signs in community - Crackles, Decreased breath sounds, Dullness to percussion, Wheeze, Increased vocal resonance over area consolidation, Tachypnoea, Fever Chest x-ray - shadowing in lung field. in patients at risk for malignancy - obtain an initial chest x- ray. Then, request a repeat chest x-ray during recovery for patients with persisting symptoms or higher risk of underlying malignancy (smokers, ex-smokers, age >50 years). Microbiology: Gram stain and culture of sputum, blood culture, nose and throat swabs for viral PCR, urine antigen test for strep p and legionella). FBC, U & E, CRP, ABG Complications of pneumonia include: • Pleural effusion, Empyema, Lung abscess formation. Pathology: Acute inflammatory response Exudation of fibrin rich fluid - consolidation on CXR Neutrophil and macrophage infiltration Prevention - vaccine, chemoprophylaxis

Answer 78

Persistent dry cough that does not resolve with time = atypical pneumonia caused by Mycoplasma pneumoniae or Chlamydophila pneumoniae Pneumonias may be of very rapid onset, particularly if pneumococcal or staphylococcal

Answer 79

Assessing severity of pneumonia in hospital setting: CURB 65 score - presence of 2 or more of the features is an indication for hospital treatment. C – New mental confusion U – Urea > 7 mmol/L R – Respiratory rate > 30 per minute B – blood pressure (SBP < 90 or DBP <60) Age > 65 years In community to decide whether to hospitalize: C – New mental confusion (no U) R – Respiratory rate > 30 per minute B – blood pressure, Age > 65 years

Answer 80

Presentation Atypical - more prolonged prodromal period with symptoms lasting for several weeks. Factors to consider to find organism = age, community or hospital, chronic lung disease, smoking, immunosuppression, pet. Management for both: General measures: maintain good oral fluid intake to avoid dehydration. Anti-pyretic drugs (e.g. paracetamol) with analgesics for pleural pain. More severe illness may require intravenous fluids and oxygen. Treatment: community-acquired - target is Pneumococcus which is usually sensitive to Amoxycillin. Atypical - do not respond to ‘cell wall antibiotics’. So antibiotics that act on protein synthesis such as macrolides (erythromycin/clarithromycin/azithromycin) or tetracyclines (doxycycline). hospital acquired pneumonia - gram negative so e.g. IV Co-Amoxiclav.

Answer 81

mucins lining the surface of the airways trap micro-organisms that are then cleared by ciliary movement, up respiratory tract; expelled as cough or swallowed- mucociliary escalator. ciliated epithelial cells and mucus-secreting goblet cells. Secretory IgA surfactant has some anti-microbial activity alveolar macrophages - neutrophils migrate out of capillaries into the airspaces and phagocytose. Lymphoid follicles of the pharynx and tonsils, Lungs infection 1. alveolar macrophage fails to stop the pathogen 2. cytokines recruit more macrophages 3. inflammation = increased permeability 4. more neutrophils/lymphocytes/antibodies to aid macrophages • Outside the lungs 1. cytokines/chemokines into systemic circulation 2. activates bone marrow /more cardiac output /raised body temp 3. dysregulation - signs of tissue injury/organ injury caused by pathogen, Host factors, Drugs

Answer 82

Aspiration of food, drink etc can lead to pneumonia. due to anaesthesia alcohol or drug abuse swallowing-related problems due to neuromuscular or oesophageal disease or after a CVA with loss of the gag reflex. Causative organisms include oral flora & anaerobes, though in-hospital aspiration increases risk for pseudomonas aeruginosa infection. Common with neurological dysphagia - epilepsy, alcoholics etc Co-amoxiclav

Answer 83

nose clip is worn so that breathing is through the mouth sterile mouthpiece attached to the spirometer is used for breathing. With the mouth forming a tight seal around the mouthpiece, the patient is instructed to perform various breathing manoeuvres by inhaling and exhaling. few cycles of quiet inspiration and expiration. Then forced vital capacity is performed. Involves taking a maximal inspiration followed by breathing out as hard and fast as possible.

Answer 84

Peak Flow Meters (in L/s) - measures the highest velocity of airflow that can be achieved during forced expiration Normal: ≥ 80% of the predicted average value based on: height, gender & age, ethnic group. Baseline determined when patient is asymptomatic Useful in monitoring people with asthma

Answer 85

Diffusing Capacity Carbon Monoxide Test lets us determines how much oxygen travels from alveoli of lungs to bloodstream by measuring CO diffusion Provides information on alveolar-capillary membrane Can be decreased in Emphysema, Pulmonary fibrosis, idiopathic pulmonary arterial hypertension, chronic thrombo-embolic disease of lung

Answer 86

Forced expiratory volume in 1 second (FEV1): maximum volume of air can be forcefully expired within 1 second after maximal inspiration Forced vital capacity (FVC): total amount of air exhaled after maximal inspiration during entire FEV test – occurs over 6 seconds FEV1/FVC: represents proportion of patient’s forced vital capacity that they can expire in first second of forced expiration

Answer 87

Obstructive defect: During expiration (esp forced) the small airways are compressed, increasing flow resistance, until no more air can be driven out of the alveoli. If airways are narrowed then expiratory flow is compromised EARLIER in expiration - 'obstructive' deficit. Eg COPD, bronchiectasis, asthma This means FEV1 will be reduced markedly FVC is nearly normal though may decrease as disease progresses if there is air trapping. FEV1/FVC ratio is <0.7 Restrictive defect: Total lung capacity is reduced - defined by this FVC is reduced FEV1 is reduced proportionately FEV1/FVC ratio is normal or higher (due to reduced compliance) Eg diffuse lung fibrosis, muscle weakness dec inspiratory effort

Answer 88

Volume of air moved as a function of time - Volume-time plot Rate of airflow as a function of volume of air in lungs – Flow-volume loop Measures: Lung volumes Rate of airflow Gas exchange (alveolar/vascular membrane) • Diagnose patients with respiratory symptoms • Establish severity and progression of lung disease • Assess treatment response • Monitor patients on meds with lung toxicity

Answer 89

expiratory flow rate is plotted against lung volume. Obstructive: Start of expiration lungs are expanded and airways are open - expiratory flow is max - Peak Expiratory Flow Rate (PEFR) When small airways are narrowed there is early fall in expiratory flow rate so dec PEFR and SCALLOPING of curve (this is main consequence- more severe means more scalloping, not dec PEFR). Restrictive: Reduction in FVC and TLC so narrow flow volume loop PEFR is not significantly reduced as there is no airways obstruction. Narrow & tall flow volume loop.

Answer 90

Restrictive: Reduced TLC Normal or Reduced FEV1 Reduced FVC Ratio FEV1:FVC normal Parenchymal lung diseases - restrictive pattern on spirometry AND abnormal DLCO eg pulmonary fibrosis Lung diseases related to abnormalities in chest wall – restrictive pattern on spirometry, normal DLCO, abnormal CXR eg kyphoscoliosis Lung disease related to neuromuscular disease – restrictive pattern on spirometry, normal DLCO eg myasthenia gravis Pulmonary hypertension – normal spirometry, normal CXR, but abnormal DLCO Obstructive: – Reduced FEV1 – FEV1:FVC ratio <0.7 – In late/severe COPD FVC also falls – but still less than the fall in FEV1 – Asthma reversible + response to bronchodilator; COPD not

Answer 91

leading cause of cancer-related deaths worldwide. Lung cancer is the commonest male cancer 2nd most common in women

Answer 92

Around 90% of lung cancers in men and 80% in women are caused by smoking. Other aetiological factors include exposure to asbestos and radon. Genetic and dietary factors also influence individual susceptibility.

Answer 93

Primary tumour: Cough: 3-week cough Dyspnoea - central tumours may occlude airways resulting in lung collapse. pleural effusions may also present with dyspnoea. Haemoptysis: occurs typically because of tumour erosion into an airway. Wheeze: may occur secondary to partial airway obstruction caused by a lung tumour. • Weight Loss • Lethargy/Malaise Regional metastases Hoarse voice: mediastinal nodal or tumour invasion resulting in compression of the recurrent laryngeal nerve (RLN), left RLN more often. • Chest / shoulder pain - parietal pleural involvement Dysphagia (oesophageal compression) Bloated face (SVC obstruction) Distant metastases • Bone pain/fractures • CNS symptoms (headache, double vision, confusion etc.) Metabolic • Thirst (hypercalcaemia) • Constipation (hypercalcaemia) • Seizures (hyponatraemia– SIADH, small cell)

Answer 94

SVC Obstruction: dyspnoea and/or difficulty swallowing, stridor and a swollen and oedematous face, plethora, neck venous congestion and dilated veins on the upper chest and arms. Caused by tumour or enlarged lymph nodes compressing or invading the SVC. Medical emergency. Brachial plexus nerve and/or sympathetic nerve chain compression: Pancoast tumours – tumours occurring in the lung apex (superior sulcus) of the lung- may invade the brachial plexus causing C8/T1 palsy with small muscle wasting in the hand and weakness, as well as pain radiating down the arm. If the sympathetic chain is also compressed then an ipsilateral Horner’s syndrome may occur( miosis, ptosis and anhidrosis). Recurrent lung infections: related to partial airway obstruction and resultant post-obstructive pneumonias – post-pneumonia chest X-ray in high-risk patients. Cachexia • Pale conjunctiva • Cervical lymphadenopathy • Liver enlargement • Skin metastases

Answer 95

Paraneoplastic Syndromes: Arise from secretion of functional peptides or hormones from the tumour, or inappropriate immune cross-reaction between host cells and tumour cells. Humoural hypercalcaemia by squamous cell carcinoma of the lung - PTH-related protein (secreted from tumour) or Ectopic PTH production. Or Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) by small cell lung cancer. Also can cause Cushing’s syndrome. Paraneoplastic neurological syndromes: lung cancer associated myasthenic syndrome. Haematological - Anaemia - Thrombocytosis

Answer 96

Histology - divided broadly into non-small cell lung cancer (more common) or small cell lung cancer. For NSCLC, adenocarcinomas + squamous-cell carcinomas are most common.

Answer 97

Treatments include surgery, chemotherapy, radiotherapy, and palliative therapy. Prognosis 5-year survival for patients with stage I NSCLC is roughly 80%, and patients with stage II to stage III disease have a 5-year survival of 13–60%. The standard of care for patients with stage I, stage II, and some stage IIIA NSCLC disease is surgical resection.

Answer 98

All Chest Xray Staging chest CT Some: PET-CT Head CT Pelvic CT MRI -various Bone Scan Ultrasound

Answer 99

Tissue for diagnostic purposes is usually obtained by bronchoscopy and needle biopsy of the lung or pleura. • Cervical lymph node fine needle aspiration (FNA) • Can do biopsy of various structures such as Adrenal, • Skin • Bone • Brain • Lymph nodes

Answer 100

irritation of cough receptors. vagus nerve to medulla. efferent signal down vagus, phrenic, and spinal motor nerves to musculature. deep breath in, closure of the glottis, inc intra-thoracic pressure. Glottis suddenly opens, so excursion of air. Muscles of expiration are required. duration: Acute – less than 3 weeks Sub-acute - cough persisting for 3-8 weeks Chronic- more than 8 weeks Productive, where and when it occurs. Most common cause = URTI - maybe has sputum, is tired and has fever. Pain and discharge localised to ENT or sinus. Acute: Covid Acute bronchitis - with wheeze Pneumonia Pneumothorax- sudden pleuritic pain PE Sub-acute: Post-infectious Chronic: Upper airway cough syndrome ACEi cough Asthma GORD

Answer 101

COPD - History: progressive dyspnoea. Pursed lip breathing, prolonged exhalation. Asthma - episodic wheezing, prolonged expiratory phase. attack may include: severe breathlessness. Investigations: peak expiratory flow rate (PEFR): may be reduced; FEV1/FVC ratio dec Pneumonia o Exam: crackles asymmetric chest expansion, bronchial breathing for consolidation signs focal dec breath sounds, increased vocal resonance for signs of effusion Pulmonary embolism o History: sudden-onset dyspnoea and chest pain; o Exam: tachypnoea • Pleural effusion o Exam: asymmetrical chest expansion, decreased tactile fremitus, decreased vocal resonance and absent breath sounds Pulmonary tumours o History: hoarseness; o Exam: may be unilateral wheeze and decreased breath sounds in large airway lesions. crackles and rhonchi may be present in post-obstructive pneumonia. • Bronchiectasis o Exam: prolonged expiratory phase, crackles, rhonchi, and wheeze o Investigation: pulmonary function tests: obstructive ventilatory deficit”

Answer 102

Pneumothorax is the presence of air in the pleural space -pleura has a hole - air moves down pressure gradient. Pleural seal is broken and lungs collapse due to inward elastic recoil. Simple • Not expanding pneumothorax • Air goes in and out Primary spontaneous pneumothorax - most commonly in young, tall, thin males with no predisposing lung disease or history of trauma. Rupture of an underlying sub pleural bleb (small air- containing spaces) or bulla (permanent, air-filled space at least 1 cm in size) is thought to be responsible. Risk factor - smoking Secondary spontaneous pneumothorax occurs secondary to an underlying lung problem e.g., COPD or Asthma. Iatrogenic - caused by invasive medical procedures e.g. - central vein cannulation Tension pneumothorax - any pneumothorax causing mediastinal shift and cardiovascular collapse.

Answer 103

Tension: Air can enter pleural cavity during inspiration but cannot leave during expiration. Inc in intrapleural pressure. Cause the mediastinum to shift and compress other lung + cardiac venous return. Veins of the body rely on the low intrathoracic pressure to return blood to the heart. Dec preload. impaired gas exchange (from the loss of lung volume). reduced cardiac output results in the hypoxaemia and haemodynamic compromise. Tachycardia to inc CO. Also, tachypnoea, tracheal shift, elevated JVP, and hypotension for tension. • History: sudden onset of pleuritic stabbing chest pain and dyspnea. Worse on breathing deeply. One side. • Examination: on the affected side, chest movement are reduced, percussion is hyper resonant and breath sounds are reduced in intensity. Vocal resonance is also reduced.

Answer 104

Loss of lung markings. Pleura moved away from lungs.

Answer 105

Investigations: Obs ECG FBC CXR If air is in the pleural space that should not be there Let it out by: ▪ Needle aspiration -2nd intercostal space, mid clavicular ▪ Intercostal chest drain Where do chest drains go in? ▪ THE TRIANGLE OF SAFETY - lateral borders of pec major, lattismus dorsi and 5th intercostal space, mid-axillary Reduced chance of damage Above the rib How do we prevent air entering the drain? - Water Seal, Hickman Valve

Answer 106

Pleural fluid is secreted by the parietal pleural and drained through the lymphatics of the parietal pleura. maintained via a balance of hydrostatic and oncotic pressures and lymphatic drainage. keeps the visceral and parietal pleura connected, lubricant. may result from disruption of the balance between hydrostatic and oncotic pressures, or disrupted lymphatic drainage. collection of extra fluid in the pleural space = pleural effusion. If blood = haemothorax; if chyle (from the lymphatic system) = chylothorax if pus = empyema.

Answer 107

Simple effusion categorised on protein content Transudates – have a low protein content Causes 1. Due to increased pleural capillary hydrostatic pressure – Congestive cardiac failure 2. Due to decreased capillary oncotic pressure- low serum albumin levels – cirrhosis; nephrotic syndrome Exudates - have a high protein content Due to increased capillary permeability (e.g., inflammation, malignancy) 1. Bronchial Carcinoma 2. Pneumonia associated with three types of pleural effusion: Simple parapneumonic effusion→complicated parapneumonic effusion→empyema 3. Tuberculosis 4. Pulmonary infarction from pulmonary embolism 5. Metastases (most common) – Cancers that very commonly metastasise to the lung include bladder, colon, breast, prostate, germ cell tumours and head and neck squamous carcinomas. require drainage by therapeutic pleural aspiration or intercostal chest tube drainage.

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