Respiratory Flashcards

Question

Why do rises or modest falls in pO2 from 13kPa e.g. in hyperventilation or mild hypoventilation, causes little change in arterial O2 content?

Answer 1

As dissociation curve is flat in this region, so Hb is fully saturated with O2 from around a pO2 of 8.5kPa, so small changes in the pO2 still correspond with around 97% saturation with O2.

Answer 2

By-product of glycolysis that promotes T state of Hb, so shifts dissociation curve to the right, decreasing affinity of Hb for O2 so O2 is more readily released to the tissues. 2,3BPG increased in anaemia and at high altitude.

Answer 3

O2 store in tissues. Composed of a single haem group attached to a single globin chain, no cooperative binding so dissociation curve is hyperbolic and far to the left of HbA. High affinity for O2 means O2 store only released when local pO2 is severely reduced, e.g. in heavy exercise.

Answer 4

pH=pKa+log([HCO3-]/(pCO2x0.23)) pKa=6.1 | That pH of plasma and hence ECF depends on the ratio of pCO2 to [HCO3-].

Answer 5

By the mediastinum, extending from the vertebral bodies behind to the sternum in front?

Answer 6

Azygos vein, thoracic aorta, oesophagus, vagus nerve, sympathetic trunks

Answer 7

Heart, pericardium, roots of great vessels, main bronchi

Answer 8

Restrictive: problem with inspiration. FEV1.0 proportion doesn't change, still > or equal to 70% of FVC, but FVC much less as less air inspired in the first place. FEV1.0 less aswell but both affected to same proportion as all of expiration is affected to the same extent. Obstructive: problem with expiration, e.g. airway narrowing, e.g. in asthma, COPD. FVC relatively normal, but FEV1.0 markedly reduced as increased resistance to air expiration, so air comes out more slowly.

Answer 9

- diffusion resistance - SA for diffusion - Concentration gradient

Answer 10

The pCO2 as the solubility is fixed (solubility constant of 0.23)

Answer 11

The ratio of [HCO3-] to pCO2. This is normally about 20:1

Answer 12

The arterial pO2 and the concentration of Hb.

Answer 13

Appropriate O2 content in arterial blood and an adequate CO and adequate local perfusion of tissues.

Answer 14

rima glottidis

Answer 15

The 2 true vocal cords and the aperture between them

Answer 16

Runs from spinous process of T2 to costal cartilage of 6th rib. Sepatates upper and lower lobes of lung.

Answer 17

Found along the 4th rib, from the mid axillary line, on the right side.

Answer 18

Dome shape of diaphragm means periphery attached to inferior margin of thoracic cage but dome extends upwards in expiration to level of 5th rib on right side and level of 5th intercostal space on left side so organs in the upper abdomen e.g. liver, spleen, stomach and the kidneys, can be damaged in a perforating thoracic wound.

Answer 19

breathing more than required for your metabolic state.

Answer 20

Hypocapnia- pCO2 decreases. This can cause lethal tetany.

Answer 21

Expiring more so removing more CO2 from alveloi than produced, so pCO2 decreases, increasing the pH of the blood- respiratory alkalosis, and calcium is relatively insoluble in alkaline conditions so as calcium unable to dissolve in blood, it us uptaken by bone and binds to proteins, so its free ionised concentration is reduced to life-threateningly low levels. Muscles go into involuntary spasms, may cause airway obstruction.

Answer 22

As on flat part of dissociation curve, Hb remains 100% saturated with O2 from around 8 kPa so decreases in pO2 from 13.3kPa can be as much as 4-5kPa and Hb will still be 100% saturated.

Answer 23

pH of blood is returned to normal by altering the other variable ( the concentration of HCO3-),rather than the variable which was disturbed (the pCO2), because pH depends on the ratio between the concentration of HCO3- and the pCO2. Important as ventilation can't really change in certain problems e.g. respiratory infection.

Answer 24

A fall in [HCO3-] in the blood

Answer 25

By breathing

Answer 26

peripheral chemoreceptors

Answer 27

- increase in breathing - changes in HR - diversion of b.flow to brain via changes in resistance vessels.

Answer 28

Changes in pH of CSF.

Answer 29

Choroid plexus cells, so [HCO3-] is fixed in the short term, but in persisting changes in pH, choroid plexus cells correct this by changing [HCO3-].

Answer 30

They might stop breathing as they have type 2 respiratory failure, so their pCO2 is persistently highm meaning CSF acidity is corrected by choroid plexus cells increasing [HCO3-] to maintain normal pH, and so the central chemoreceptors 'reset' to higher CO2 level as they lose their stimulation due to pH correction, so reduced resp drive, and this is now driven by hypoxia so if O2 given, they'll be no resp drive!

Answer 31

increase in haemoglobin in blood

Answer 32

Carotid and aortic bodies

Answer 33

In the medulla

Answer 34

Type 1 respiratory failure: ventilation/perfusion mis-match: O2 poorly soluble in liquid in inflammatory exudate, hyperventilation will try and increase O2 but affected alveoil consolidated, and those unaffected by pneumonia won't be able to increase O2 in blood as Hb already 100% saturated. But CO2 diffusion isn't limited in those alveoli unaffected by consolidation, so it is able to diffuse easily from the blood into the alveoli unaffected by consolidation when hyperventilating.

Answer 35

Boyles law states that pressure is inversely proportional to volume. When we inspire, our diaphragm flattens, our ribs are pulled upwards and ourwards, so the vertical, transverse and AP diameters of our thoracic cavity are increased, hence volume is increased, so pressure is markedly reduced, allowing air to flow into the lungs down a pressure gradient.

Answer 36

Mixing of inspired and expired air in trachea.

Answer 37

a potential space between the parietal pleura adhering to the thoracic wall and the visceral pleura covering the lungs. The cavity is lined by a single layer of flat cells-mesothelium-simple squamous epithelium, and associated supporting CT, which together form the pleura. Cavity normally contains a thin film of serous fluid. Visceral pleura continuous with parietal at lung hilum.

Answer 38

Cervical, costal, diaphragmatic and mediastinal

Answer 39

Somatic afferent fibres. Costal part innervated by IC nerves, and diaphragmatic and mediastinal innervated by phrenic nerves- pain in these areas would be referred to C3, C4 and C5 dermatomes, so lateral neck and supraclavicular region of shoulder.

Answer 40

region between inferior part of lung and inferior part of pleural cavity. Occurs between costal and diaphragmatic pleura. Deepest after forced expiration and shallowest after forced inspiration.

Answer 41

Autonomic innervation- visceral sensory afferents.

Answer 42

- mucosal oedema - bronchial wall thickening as inflammatory cell infiltration - mucus over prod. and abnorma - smooth muscle contraction - shed epithelium- incorporated into thick mucus

Answer 43

Relievers and preventers. - Short and long-acting Beta 2 agonists - Inhaled corticosteroids - Oral steroids - Leukotriene receptor antagonsits - Xanthines - Muscarinic antagonists

Answer 44

``` pulse>110 RR>25 Can't complete sentences No wheeze PEFR 35-50% predicted ```

Answer 45

Bronchial inflammation, fibrosis, and mucus hypersecretion characteristic of obstructive bronchitis, and destruction of alveoli seen in emphysema. Both implicated in progressive airflow obstruction.

Answer 46

Cigarette smoke= primary RF for COPD related mortality. Among those with COPD, those who continue to smoke have more symptoms, a faster decline in lung function and a higher death rate than those who stop smoking.

Answer 47

Alpha 1 antitrypsin deficiency

Answer 48

This tells you the max volume of air exhaled in first s of a forced expiration from a position from a full inspiration, but only weak correlation exists between objective measures of airflow obstruction and patient important outcomes such as mortality and risk of future exacerbations. Some patients are better able to cope with same degree of airway obstruction, so their QOL will be better, and they may be better able to carry out exercise and live for longer.

Answer 49

Reduced PEFR with scooped-out (sharply concave) appearance of expiratory limb.

Answer 50

Current or former smokers over age of 35 who have history of progressive and persistent exertional dyspnoea with or without chronic cough and sputum production. History of frequent episodes of winter bronchitis, wheezem and fatigue common.

Answer 51

According to FEV1.0 as a percentage of the predicted normal value as adjusted for sex, age, height, and race.

Answer 52

post-bronchodilator FEV1.0/FVC ratio of less than 70%

Answer 53

``` sat. O2 less than 92% pCO2 rising or normal Exhaustion Altered state of consciousness Silent chest PEFR less than 33% predicted ```

Answer 54

- pharmacologic therapy - education of patient and their family - avoidance of triggers - dealing with environmental factors

Answer 55

- pre- and post- bronchodilator spirometry, large response to bronchodilators suggestive of asthma e.g. >15% increase in FEV1.0. - serial peak flow measurements using a peak flow meter- asthma suggested when diurnal or day to day variability exceeds 20%.

Answer 56

Programme normally lasting 6 wks involving exercise training, disease education, psychiatric counselling, and behavioural/nutritional instruction. It improves exercise capacity, reduced admissions to hospital, improves health-related QOL and symptomatic breathlessness.

Answer 57

Bronchodilators. Inhaled corticosteroids not given alone and should be used only in combination with ling acting bronchodilators in those with a FEV1.0 less than 60% predicted. Potential risk of pneumonia with use of inhaled corticosteroids- anti-inflammatory.

Answer 58

Airflow obstruction causes hypoxia, which leads to pulmonary hypertension as a result of hypoxic pulmonary vasoconstriction, AND pulmonary capillary destruction occurs with emphysema, so R heart must work harder to pump blood through a higher pressure pulmonary circulation as increased resistance, so impaired R heart function as filling pressure increased, which can then back up into the systemic circulation, with a raised CVP and *peripheral oedema, subsequently leading to cor pulmonale- fluid retention/HF secondary to lung disease.

Answer 59

A daily morning cough and excessive mucus production most days for 3 mnths in 2 successive yrs, in absence of airway tumour, acute/chronic infection or uncontrolled cardiac disease. So based on clinical history

Answer 60

Alpha 1 antitrypsin is an anti-protease which inhibits the action of proteases released from bacteria and neutrophils which degrade proteins e.g. elastin, so if deficiency, there is a predisposition to elastin disruption in airways.

Answer 61

A chronic, slowly progressive disorder characterised by airflow obstruction which does not change markedly over several months. Encompasses chronic bronchitis and emphysema.

Answer 62

Bronchodilators as inhibit breakdown of cAMP so more around, and also anti-inflammatory.

Answer 63

-cardiac arrythmias -CNS function impaired -hypoxic pulmonary vasoconstriction -central cyanosis Peripheral chemoreceptors will increase ventilation.

Answer 64

- cor pulmonale - polycythaemia - increase 2,3-BPG - renal correction and increased ventilation

Answer 65

- breathlessness - impaired CNS function - cardiac arrythmias - cerebral vasodilatation - peripheral vasodilatation

Answer 66

- CSF compensation, central chemoreceptors reset to higher pCO2, problem with administering O2 and may reduce patient's breathing - renal compensation

Answer 67

increased resp. rate e.g. where increased central drive in resp.failure

Answer 68

Excessive bronchoconstriction reduces ventilation to particular alveoli, resulting in ventilation/perfusion mismatch and hypoxia. PaCO2 falls as attack worsens as peripheral chemoreceptor and pulmonary receptor stimualtion produce reflex increase in ventilation despite increased work of breathing.

Answer 69

Chronic- near-normal pH as compensation by choroid plexus cells of brain. Acute- arterial pH decrease as renal adjustments slow

Answer 70

Lose hypoxic pulmonary vasoconstriction, increasing ventilation perfusion mismatch

Answer 71

All need arterial blood gas analysis as severity difficult to assess clinically. Chest X-ray Lung function tests Airway maintenance, O2 therapy, mechanical ventilation, clearance of secretions bronchodilators and antibiotics Treat problems with CO, Hb conc and fluid balance

Answer 72

Chronic develops gradually so time for compensatory mechanisms to occur- hypoxia and hypercapnia tolerated better

Answer 73

the primary (Ghon's focus)- sub-pleural focus of tubercles, and the draining lymph (hilar) nodes together.

Answer 74

Probably not as patient usually quite sick and information not particularly useful

Answer 75

During inspiration, inflamed pleura moves against the thoracic wall, causing pain.

Answer 76

Opacities visible, may be one opacity-lobar pneumonia, or more patchy opacification-bronchopneumonia

Answer 77

infection of lung parenchyma with consoldation, involving distal airways and with resultant inflammatory exudation

Answer 78

mild to moderate= amoxicillin | severe= co-amoxiclav

Answer 79

Vibration of intra-thoracic airway wall at site of flow limitation. More pronounced in expiration as intrathoracic airways narrower than in inspiration, with increased pressure on very small airways, so become compressed, and narrowing worsened.

Answer 80

smoke, cold air, exercise

Answer 81

pollen, HDM faeces

Answer 82

Bronchial provocation tests- inhale increasing dosages of histmaine or methacholine until FEV1.0 reduces by 20%.

Answer 83

Beta 2 adrenergic agonists acitvate Beta 2 receptors, resulting in stimulation of Na+ pump, increasing K+ uptake into cells.

Answer 84

H.influenzae | Moraxella catarralis

Answer 85

Patient will be on immunosuppressive medication to prevent rejection of transplant by her IS.

Answer 86

An acid-fast bacillus-requires ziehl neelsen staining e.g. of sputum sample- 3 samples taken. Bacilli slow-growing- 4 to 6 wks. BM or CSF culture may confirm diagnosis of miliary TB

Answer 87

Diagnostic test of TB which is strongly +ve in post-primary TB and often -ve in military TB (reduced host response) and HIV- reduced cellular immunity. Injection of tuberculin into skin, inflammatory reaction development

Answer 88

May have been haematogenous spread of M.TB to the meninges, resulting in bacterial meninigits.

Answer 89

``` often asymptomatic mild fever erythema nodosum small pleural effusions wheeze may result from bronchial compression by lymphadenopathy ```

Answer 90

Rifampicin, isoniazid, pyrazinamide and ethambutol for 2 mnths, followed by rifampicin and isoniazid for 4 mnths. ethambutol given if drug resistance suspected. Corticosteroids occasionally improve results in severe pulmonary TB.

Answer 91

Peripheral neuropathy

Answer 92

BCG vaccination of non-immune subjects | Adequate living space

Answer 93

Cigarette smoking Asbestos-mesothelioma* Radon gas

Answer 94

Small cell and non-small cell- majority

Answer 95

Release of PTH-related peptide- increases release of calcium from bone, reduces renal Ca2+ excretion and reduces renal phosphate reabsorption, BUT doesn't increase renal 1 alpha-hydroxylase activity, so doesn't increase calcitriol, unlike PTH.

Answer 96

TNM staging

Answer 97

Surgical resection Chemotherapy Radiotherapy Only palliative care suitable for stage 4 disease-incurable.

Answer 98

Side effect of rifampicin drug

Answer 99

- Resp failure - rising pCO2 - worsening metabolic acidosis - hypotension despite fluid resucitation

Answer 100

Early -staph. aureus, H.influenzae | Later- pseudomonas aeruginosa

Answer 101

Opportunistic. Pneumocystis jirovecii- fungus, produces spores which enter lungs and cause acute alveolitis. May not detect on specimens. Induced sputum, bronchoalveolar lavage, lung biopsy- silver stain?, PCR to detect fungus, DNA. High dose cotrimoxazole

Answer 102

polycythaemia pulmomary hypertension with RHF (cor pulmonale) CO2 retention- flapping tremors, warm hands, bounding pulse

Answer 103

Give non-invasive ventilator support as well as O2.

Answer 104

- goblet cell hyperplasia in epithelium, so increased mucus prod. - reduced cilia as ciliated cells lost, preventing mucus sweep up - mucous gland hypertrophy in SM, resulting in mucus hypresecretion and bronchial wall swelling.

Answer 105

Increased mucus and bronchial wall swelling narrow airways by reducing lumen calibre, causing airway obstruction.

Answer 106

Progressive alveolar wall destruction with air space enlargement and reduction in capillary bed as pulmonary capillaries lost.

Answer 107

Permanent destructive enlargement of airspaces distal to terminal bronchiole

Answer 108

Neutrophil

Answer 109

Spirometry- VC, TV, FEV1.0 and FVC, and ratio, and flow volume loops. Body plethysmography and/or helium dilution for lung vol measurements e.g. TLC, RV and FRC TLCO- transfer factor of lung, to measure diffusion

Answer 110

Hyperinflated lungs- large, blunting of costophrenic angles and flattened hemidiaphragms Elevated ribs and loss of rib curvature, >6 ribs seen anteriorly Narrowed and elongated heart shadow Low, flat diaphragm Narrow mediastinum

Answer 111

``` cigarette smoke environmental pollutants smoke from cooking fires where poor ventilation and no chimneys coal mining alpha 1 antitrypsin deficiency ```

Answer 112

loss of radial traction of lung so pressure collapsing airways greater than lung elastic recoil, airways can't be held open on expiration loss of lung elastic recoil reduced SA for GE

Answer 113

Residual vol. of lung increased as air trapping, and FRC increased, so will be breathing close to total lung volume, and lung hyperinflated, so reduced compliance of lung as breathing in from a more expanded position, so larger change in intrathoracic pressure necessary to produce lung volume change.

Answer 114

Low pCO2 results in vasoconstriction, which can cause blackouts, paraesthesia and chest pain.

Answer 115

``` Oral candidiasis- immunosuppressive Hypertension Central obesity Bruising Skin thinning Osteoporosis Adrenal suppression ```

Answer 116

Requires Ziehl-Neelsen staining as lipid-rich cell wall retains some dyes, resisting decolourisation with acid. Also resistant to gastric acid in stomach.

Answer 117

Coxsackie, polio, hepatits A

Answer 118

Phagocytosed by alveolar macrophages but resulting phagosome prevented from fusing with lysosome by cell wall lipids of bacterium, so MTB excapes into cytoplasm and multiplies.

Answer 119

Often asymtomatic, may cause mild febrile illness, erythema nodosum, small pleural effusions.

Answer 120

Immunocompromised people: DM, HIV, corticosteroid therapy, Vit D deficiency, chronic kidney disease Lifestyle: alcohol/drug- IV-HIV abuse, homelessness Contact: travelling to high incidence areas

Answer 121

Because of HIV prevalence

Answer 122

Rifampicin drug used in treatment induces liver enzymes, so oral contraception will not be effective

Answer 123

Mediastinal, cervical, axillary and intra-abdominal nodes. | Metastases to liver, bone, adrenal glands and brain.

Answer 124

Central tumours occlude large airways resulting in lung collapse and breathlessness on exertion. Many patients have co-existent COPD-obstructive-airways resistance Phrenic nerve involvement- diaphragm paralysis pleural effusions

Answer 125

Airway occlusion- bronchial wall hypertrophy and excess mucus secretion. Reduced SA for gas exchange Small airway collapse as loss of elastic tissue in alveolar walls

Answer 126

L recurrent laryngeal nerve compression by invading tumour into mediastinal lymph nodes or direct mediastinal invasion. Nerve innervates intrinsic laryngeal muscles controlling vocal cord movement?

Answer 127

Non-caseating granulomata

Answer 128

Late stage presentation so few are operable, age of patient presenting and their co-morbidities e.g. IHD and COPD

Answer 129

Accumulation of triglyceride-rich lymph in pleural space, generally as result of damage to thoracic duct, causing leakage into pleural space e.g. as result of trauma or carcinoma.

Answer 130

Blood within pleural cavity

Answer 131

``` Infective- pneumonia, TB Lunc cancer Lung infarction-PE Pulmonary hypertension- pulmonary oedema Colagulopathies- thrombocytopenia Trauma/foreign body ```

Answer 132

imbalance in Starling's forces, protein-poor fluid (<30g/L), often bilateral, not assoc. with fever, pleuritic pain or tenderness to palpation. Most common cause= congestive HF. May also be result of cirrhosis with ascites, hypoalbuminaemia, nephrotic syndrome, pericardial disease or peritoneal dialysis, sepsis increasing capillary permeability.

Answer 133

imply disease of pleura or adjacent lung, protein-rich fluid (more than 30g per litre). May be result of infection e.g. TB, pneumonia, maliganancy e.g. of pleura, or secondary e.g. breast cancer, lung, AI disease- RA, SLE, maybe abdominal disease e.g. pancreatitis causing an inflamed diaphragm

Answer 134

By re-opening of small airways , during inspiration, which have become occluded during expiration

Answer 135

``` High nuclear to cytoplasmic ratio Hyperchromatic Prominent nucleoli Pleomorphic- irregular in shape Frequent/abnormal mitoses ```

Answer 136

``` Ulceration Necrosis Infiltrative margins Vascular invasion Poorly circumscribed Reaction in surrounding tissue/stroma Little resemblance to normal tissue= anaplastic ```

Answer 137

ERV=FRC-RV

Answer 138

By parietal pleura, and is absorbed from parietal lymphatic vessels

Answer 139

elastic recoil of lungs

Answer 140

A projection of superior lobe of left lung

Answer 141

Bronchi, pulmonary vessels and LNs

Answer 142

Vascular abnormality or mediastinal mass

Answer 143

Heart magnification as heart located anteriorly, so if heart larger than normal, would be unable to say whether the heart was actually enlarged

Answer 144

polysaccharide capsule- anti-phagocytic

Answer 145

Many different capsule serotypes- different antigens

Answer 146

Sickle-cell disease patient will have functional asplenia as a result of multiple small infarcts, causing the spleen to function less efficiently, and the spleen is necessary for the removal of encapsulated bacteria e.g. S.pneumonia. RBC become sickled when low pO2 causes them to become insoluble and polymerise, and their shape is unable to be accomodated in small blood vessels, so they obstruct splenic vessels, resulting in tissue infarction.

Answer 147

Prophylactic antibiotics- penicillin or erythromycin | Vaccination- pneumococcal 13 valent conjugate vaccine

Answer 148

A bluish discolouration seen when there is more than 5g/dl of desaturated Hb (which has a darker colour) in the capillary blood

Answer 149

The total amount of Hb in the blood, the extent of desaturation of Hb and state of capillary circulation

Answer 150

Central: discolouration of tongue or oral mucosa. Result of arterial hypoxia, detected when O2 sat. below 90% and hence pO2 of 8 kPa. May result from poor oxygenation in lungs or cyanotic heart disease Peripheral: cyanosis is limited to the extremities (eg hands, feet,). It is usually due to poor peripheral circulation, as may happen in cold weather due to vasoconstriction of skin vessels; or poor arterial circulation (eg due to peripheral vascular disease or heart failure). In these circumstances the increase in tissue oxygen extraction → increased deoxygenated Hb in the capillaries→ cyanosis. All patients with central will have peripheral

Answer 151

Hypoxia resulting in lactic acidosis as tissues have insufficient O2 for aerobic respiration- pyruvate converted to lactate via lactate dehydrogenase

Answer 152

``` Clubbing of fingers weight loss anaemia wheeze/stridor pleural effusion pneumonia neurological ACTH/ADH/PTH ```

Answer 153

Hilar LNs Mediastinal LNs- occasionally causes oesophageal obstruction Pericardium- causing effusion Pleura- causing effusion RLN- hoarseness of voice, doesn't improve as with laryngitis Phrenic nerve- diaphragm paralysed on affected side, sudden breathlessness as reduced capacity of lung to fully expand on inspiration Bronchus- causing obstruction and lung collapse distal to obstruction

Answer 154

Paraneoplastic syndrome- syndrome of inappropriate ADH secretion- stimulating AQP-2 insertion in apical membrane of CD cells, so increasing water reabsorption, reducing concentration of Na+ in blood

Answer 155

Central, highly invasive and rapidly metastasises. | Very cellular, apoptotic bodies, nuclear moulding, often necrosis and lots of mitoses

Answer 156

Caseous necrosis occurs with granuloma formation. Inflammatory material may leak out into vessels, leaving a space behind where the material was- cavity.

Answer 157

o Is patient’ general health good? o Is pulmonary function adequate to cope with major surgery and pulmonary resection? o Is surgery technically feasible (depends on exact site of tumour)? o Is there evidence of local spread? o Is there evidence of distant metastases?

Answer 158

Some adenocarcinomas of lung show EGFR mutations- receptors work via tyrosine kinase

Answer 159

Finger clubbing in fibrosing alveolitis, never present in extrinsic allergic alveolitis

Answer 160

LFTs- spirometry- restrictive pattern for alveolitis with small lung volumes, and obstructive for asthma with possible lung hyperinflation

Answer 161

Extrinsic allergic alveolitis

Answer 162

Erythema nodosum

Answer 163

Trachea, oesophagus, SVC, aortic arch, thymus, phrenic nerve, L recurrent laryngeal nerve, thoracic duct

Answer 164

Fat, lymph vessels and nodes

Answer 165

Lungs, pleura and chest wall

Answer 166

Ventilation, diffusion and perfusion

Answer 167

Insidious onset- slow and progressive with no symptoms at 1st, tend to accomodate for changes and don't realise anything is wrong, progressive dyspnoea- exertional dyspnoea and dry cough- non-productive, reduced exercise tolerance Bilateral inspiratory crackles May be clubbing (not in extrinsic allergic alveolitis) Hypoxaemia and R sided HF in advanced disease Tachypnoea, tachcardia, bilateral reduced chest movement, cyanosis

Answer 168

Exclude other diseases e.g. malignancy, and increase in inflammatory cells indicates alveolitis and correlates with ground glass opacification

Answer 169

Mechanical support of alveoli

Answer 170

Lubricates, allows movement of lung and chest wall together as visceral and parietal pleura are able to move over one another Chest wall and lung coupled, inward lung recoil and outward chest recoil, surface tension of fluid keeps lung in contact with chest wall so expansion of thoracic cavity allows expansion of lung aswell so it can fill with air

Answer 171

Somatic, S+PNS nerves, phrenic and IC nerves

Answer 172

Devoid of somatic innervation

Answer 173

Parietal: IC and internal mammary lymph vessles Visceral: pulmonary lymphatics

Answer 174

Parietal- costal- IC and internal mammary artery Mediastinal- bronchial, upper diaphragmatic and internal mammary arteries Pleural dome- subclavian artery Venous drainage- peribrochial and vena cavae Visceral- bronchial arteries and pulmonary circulation Pulmonary venous circulation

Answer 175

Parietal pleura- capillary filtration(Starling's forces)

Answer 176

Lymphatic drainage, parietal pleura lymphatics via stomata on parietal pleural surface (mainly mediastinal and diaphragmatic regions)

Answer 177

Increased production- lung interstitial fluid increase, hydrostatic pressure increase e.g. HF, permeability increase e.g. inflammation, malignancy, oncotic pressure decrease e.g. LF, peritoneal fluid, thoracic duct disruption. Decreased absorption- lymphatic blockage, elevated sytemic venous pressures

Answer 178

Pleura are serous membranes with a single layer of mesothelium and thin layer of underlying CT= serosa (both epithelium and CT).

Answer 179

Any collection of extra fluid in the pleural space

Answer 180

Xerstomia- dry mouth as reduced saliva production. Saliva production altogether stops as destruction of salivary glands

Answer 181

Increased accumulation of serous fluid in the pleural cavity

Answer 182

Fistula, trapped lung, fibrothroax, functional restriction

Answer 183

Lung, breast, kidneys, bowel

Answer 184

Primary pleural malignancy. Due to asbestos exposure 20-40 yrs before malignancy. Typically males ageed 50-70, insidious dyspnoea. Pain- aching chest, breathlessness. Effusion- exudate, mediastinal pleural enhancement Chemotherapy, palliative and radical surgery Poor prognosis- 12-24 mnths survival CXR usually show unilateral pleural effusion

Answer 185

Sharp, localised pain arising from any disease of pleura. Made worse by deep inspiration and coughing.

Answer 186

Pleural fibrosis- with restriction, decreasing lung volumes and reduced lung compliance

Answer 187

Consolidation (opacification) of lung, with or without cavitation, pleural effusion, or thickening/widening of mediastinum as hilar or paratracheal adenopathy. Urgent case if miliary shadowing. Upper lobe shadowing suggestive.

Answer 188

Rifampicin- heptaitis, rash, flu-like syndromes, orange urine, shock, thrombocytopenic purpura Isoniazid- peripheral neuropathy, hepatitis, rash Pyrazinamide- rash, hepatitis, arthralgia Ethambutol- optic neuritis

Answer 189

Rifampicin and pyrazinamide can cause liver dysfunction

Answer 190

Monitor colour vision

Answer 191

Long course of treatment and many drugs. If non-comply, multi-resistant strains of M.TB can develop, which are very difficult to eradicate

Answer 192

Screening test for identifying TB. Strongly +ve in post-primary TB (>5mm skin induration with 10 units of intradermal tuberculin, read at 3 days). Also +ve in latent infection. Often -ve in miliary TB as reduced host response, and HIV as reduced cellular immunity.

Answer 193

Upper: lower PEFR Lower: scalloping of the curve When exhaling, initially, the lungs and airways are stretched. Therefore, the diameter of the upper airways are the most limiting factor - they are splinted with cartilage and cannot dilate further. The small airways stretch, but ultimately all of the alveolar gas must pass through the trachea, which is the limiting factor. As expiration progresses, and the intrathoracic pressure increases, the small airways gradually collapse and become limiting. Therefore, abnormalities in early expiration are due to upper airways problems, those in late expiration are due to lower airways problems. Larger airway obstructions will often affect inspiration more than small airways obstruction.

Answer 194

Gas Exchange: The lungs are adapted to perform gas exchange; they have a rich blood supply and large surface area across which gaseous exchange may occur. Metabolism: A number of drugs are metabolised (ACE Inhibitors) and eliminated (anaesthetic vapours) via the lungs Acid base regulation: The lungs do provide some regulation of acid-base - for example by compensation for a metabolic acidosis. Filtration and immune presentation:The rich blood supply (supply driven) means that the entire cardiac output passes through the lungs. Protection: The function of goblet cells in the secretion of mucus, cilia and macrophages in the removal of pathogens provides protection against infection

Answer 195

The ventilation and GE of the lungs

Answer 196

Measures the volume of gas passing into and out of the lungs in unit time

Answer 197

On inspirtation, the airways expand, and so the obstruction is gotten rid of, whereas in expiration, the airways are compressed, and so become more obstructed and prone to collapse

Answer 198

88-92% so that we don't reduce the hypoxic drive to breathe

Answer 199

Influenza Parainfluenza RSV Adenovirus

Answer 200

3 spontaneous sputum samples- stain with Ziehl Neelsen CXR Blood test- HIV Mantoux skin test Blood test- interferon gamma assay- prod. by macrophages to contain the infection Biopsy

Answer 201

Body's repsonse to malignancy= inflammation as a mechanism of protection, so increased vessel permeability, proteins move out, water follows as reduce oncotic pressure in blood.

Answer 202

Homogeneous dense opacity- uniformly white | Meniscus sign- top of white area concave

Answer 203

Hypoalbuminaemia- reduce oncotic pressure- fluid moves from capillaries into interstitium- increase ECF volume, fluid can then move into pleura. Proteins don't move into interstitium as no inflammation, so no increase in vessel wall permeability.

Answer 204

Due to effects of gravity

Answer 205

L main bronchi divides into L upper and lower lobe bronchi. R main bronchi divides into R upper love bronchus, and an intermediate bronchus, which then divides into a middle lobe bronchus and a R lower lobe bronchus.

Answer 206

Replacement of alveolar air by fluid, cells, pus or other material e.g.in pneumonia

Answer 207

Middle lobe

Answer 208

Lingula (part of upper lobe)

Answer 209

An inspiratory sound due to partial obstruction of upper airways e.g. foreign body, oedema, a goitre

Answer 210

TB | Malignancy e.g. lymphoma

Answer 211

May be on ACE inhibitors- ACE breaks down bradykinin, so with ACEIs, there is more bradykinin around, which causes coughing.

Answer 212

May be on ACE inhibitors- ACE breaks down bradykinin, so with ACEIs, there is more bradykinin around, which causes coughing.

Answer 213

PE, trauma, or bleeding into a lung cavity

Answer 214

The volume of air in the conducting airways, into and including the terminal bronchiole.

Answer 215

The volume of air in alveoli which is not taking part in GE e.g. due to loss of alveolar perfusion-PE

Answer 216

The sum of anatomical and alveolar dead space

Answer 217

- Lack of surfactant means increased surface tension, so the lungs are harder to inflate and fill with air as reduced lung compliance. - There will be many collapsed alveoli as smaller alveoli collapse into larger ones due to lack of surfactant meaning increased surface tension and hence pressure, especially in the smaller alveoli as they have a smaller radius so increased pressure, so many alveoli can't take part in GE, there is ventilation/perfusion mismatch, resulting in arterial hypoxia.

Answer 218

Phagocytose inhaled microbes and p[articles that have evaded innate defences proximal to the alveoli. Key to removing material as no cilia present on alveolar epithelium. Also clear surfactant proteins, and suppress uneccessary immune responses by producing anti-inflammatory cytokines e.g. IL-10. But, can initiate immune responses in more severe infections, release chemoattractents e.g. LKT-B4, so promote neutrophil infiltration from plasma

Answer 219

- opsonises antigenic particles | - prevents adherence of microbes to mucosa

Answer 220

- respiratory depression- stop breathing | - paCO2 increase further- potentially fatal

Answer 221

Can't reverse it. But want to ease symptoms, slow disease progression (airway decline) and prevent acute exacerbations. Smoking cessation Bronchodilators- Beta 2 agonists, and anticholinergics. Xanthines Inhaled corticosteroids in severe disease Pulmonary rehabilitation O2 therapy May give replacement therapy in alpha 1 antitrypsin deficiency Prevention of acute exacerbations- pneumococcal and influenza vaccination Antibiotics

Answer 222

Infection Acute respiratory failure Pulmonary embolus Cardiac arrhythmia

Answer 223

Residual volumes refer to air that is never breathed out, and so can't be measured with spirometry. Instead, we use helium dilution

Answer 224

Low pO2 in alveolar gas | impaired transfer of O2 to arterial blood

Answer 225

If peripheral chemoreceptors in carotid and aortic bodies stimulate increased ventilation

Answer 226

pCO2 normally controls urge to breathe, rather than O2, as the pO2 can decrease by quite a large amount and Hb will still remain fully saturated as Hb exhibits positive cooperativity in terms of binding O2, producing a sigmoidal curve, where there is a large range of pO2 values contributing to the flat part of the curve, where Hb remains 97% saturated. So peripheral chemoreceptors only respond to O2 when it is less than 8kPa. Central chemoreceptors detect raised pCO2 as CSF acidity increased by CO2 diffusion across BB barrier, and subsequently stimulate an increase in ventilation to exhale more CO2, and so return the blood pH to normal.

Answer 227

'Virchow's node' - if enlarged, indicative of GI malignancies e.g. gastric cancer

Answer 228

The transfer coefficient (KCO) is an expression of gas transfer standardised for the alveolar volume.

Answer 229

Mouldy hay- farmer's lung- microbial Pigeon/Budgies/Parrot- bird fancier's lung- animal Paint- isocyanate alveolitis- chemical

Answer 230

CT scan can identify changes before they are apparent on a CXR

Answer 231

Haemoptysis- bright red coloured blood, may be frothy | Haematemesis- dark coloured blood as altered by gastric acid

Answer 232

Cotrimoxazole

Answer 233

Tension pneumothorax with lung collapse | Large pleural effusion

Answer 234

lung collapse from central airway obstruction | localised fibrosis

Answer 235

Can increase ventilation with chronic hypoxia in type I as renal compensation means pH returned to normal so can breathe more CO2 out and therefore be allowed to breathe, but can't increase ventilation in type II as ineffective resp. effort.

Answer 236

Diaphragm- phrenic nerve-C3,C4,C5 | External intercostals- IC nerves- A rami of nerves T1-T11

Answer 237

passive process

Answer 238

Scalene, sternocleidomastoid, pec major-lateral and medial pectoral nerves, serratus anterior- long thoracic nerve

Answer 239

Anterior abdominals- rectus abdominis, external and internal oblique- thoracoabdominal nerves* Internal intercostals- IC nerves

Answer 240

Down a partial pressure gradient, hence diffusion can occur passively

Answer 241

Gases diffuse through gases at a rate inversely proportional to their molecular weight, so CO2 slower than O2, but gases diffuse through liquids at rate proportional to their solubility, so CO2 diffuses 21X as fast.

Answer 242

Because pCO2 of alveolar gas determines blood pH, so if atmo. air entered alveoli, blood would be alkaline on inspiration, and acidic on expiration.

Answer 243

NO This is air which can never be breathed out, and though it doens't participate in ventilation, it does communicate with ventilated space. Measured using helium dilution

Answer 244

the vol. of air in the lungs at resting expiratory level (after expelling a tidal breath). =ERV + RV

Answer 245

Volume of air moved into and out of a space per min. =TVxRR 8L/min at rest

Answer 246

PVR- (RR x dead space volume= dead space ventilation rate)

Answer 247

Destruction of elastic tissue in alveolar walls reduces elastic recoil of lungs so easier to stretch

Answer 248

Tracheal deviation to left | heart shifted to left

Answer 249

superior laryngeal nerve

Answer 250

muscarinic antagonists only inhibit action of parasympathetic nerve stimulation, whereas B2 agonists cause bronchodilation irrespective of the factors causing the bronchoconstriction

Answer 251

involved with creating sound resonance

Answer 252

rich vascular network of lamina propria, so inhaled air warmed by blood flowing through

Answer 253

stratified squamous | protects mucosa from abrasion caused by rapidly moving air stream

Answer 254

move larynx during swallowing

Answer 255

at sternal angle

Answer 256

lamina propria | to maintain opening of lumen so prevent tracheal collapse, and prevent oesophageal collapse

Answer 257

by firbroelastic CT and trachealis muscle

Answer 258

greater angle of bronchus as more vertical than left

Answer 259

cartilage rings replaces by crescenteric cartilgae plates

Answer 260

continuous layer of smooth muscles in musacularis externae

Answer 261

by elastic tension of alveolar walls

Answer 262

larger- pseudostratified ciliated columnar | smaller- simple ciliated columnar, then simple cuboidal in terminal bronchioles

Answer 263

mucus would reduce effective GE, no mucus- no need for cilia, instead have alveolar macrophages

Answer 264

found in termianl brochioles and respiratory bronchioles. secrete a surfactant lipoprotein- prevents luminal adhesion, espec. on expiration. also secrete clara cell secretory protein- can be measured in bronch-alveolar lavage, if reduced indicates lung damage

Answer 265

located in skull bones

Answer 266

in the nasal cavity

Answer 267

by the median nasal septum

Answer 268

elongated airways, formed from the confluence openings to alveoli, have almost no walls

Answer 269

spaces surrounded by alveoli clusters

Answer 270

primary site of GE, terminal air space

Answer 271

8 in l lung, 10 in right

Answer 272

pulmonary lobule

Answer 273

alveolar septum

Answer 274

the same fraction of total pressure as the volume fraction of the gas in the mixture

Answer 275

an area of lung supplied by its own segmental bronchus and segmental branches of pulmonary artery and vein

Answer 276

degree of elasticity to allow movement of chest in respiration

Answer 277

diaphragm- responsible for 70% of chest expansion. As contracts, central tendon of diaphragm pulled down, increasing the vertical diameter/. external intercostals contract- ribs are elevated in bucket handle type movement, increasing AP diameter and transverse diameter

Answer 278

the 5th rib as lies above the liver, whereas L dome extends to 5th IC space

Answer 279

heimlich manouver

Answer 280

severely deficient O2 supply to body as unable to breathe normally

Answer 281

To assess for meningitis- may be TB meningitis, can look for bacteria in CSF e.g. Ziehl-Neelsen staining for M.TB

Answer 282

opposing forces acting on the static lung

Answer 283

when diaphrgam can't be moved easily into the abdomen e.g. pregancy and obesity, so difficult to increase vertical diameter of thoracic cavity

Answer 284

when alveolar pressure has increased to atmospheric pressure

Answer 285

remains -ve (subatmoshperic) throughout. At resting expiratory level, -ve as lungs and chest wall are recoiling in opposite directions. On inspiration, pressure becomes more -ve as chest wall expands outwards, and returns to its original -ve pressure as lung returns to resting expiratory level in quiet expiration- passiv process due to lung's natural elastic recoil

Answer 286

surface tension and elastic properties of lungs and chest wall

Answer 287

CT deposition

Answer 288

*TOB | coiled protein

Answer 289

volume change per unit pressure change/ starting vol. of lung

Answer 290

when the lungs are deflated, not when fully inflated, so little breaths are easy

Answer 291

this is produced by type II pneumocytes of the alveoli. It is a mixture of phospholipids and proteins, with detergent properties- so it can get between the water molecules and reduce the forces between them. hydrophilic end sin fluid, and tails in alveolar gas, so float on the surface of the lining fluid REDUCES SURFACE TENSION- LACK IN RESPIRTATORY DISTRESS SYNDROME OF NEWBORN SO LUNG COMPLIANCE REDUCED AND SMALL ALVEOLAR COLLAPSE

Answer 292

as surfactant molecules are closer together in small alveoli, which reduces the surface tension more than if they are spread further apart as in larger alveoli

Answer 293

= surface tension X 2 / radius, so larger alveoli would have a smaller pressure, and smaller alveoli and larger pressure, so as air flow from higher to lower pressure, small alveoli would collapse into larger ones but surfactant increases surface tension in large alveoli so the pressure remains high

Answer 294

as when an alveolus increases in size, both the radius and surface tension is increased

Answer 295

facilitates lung expansion at birth increases lung compliance by reducing surface tension stabilises the lungs by preventing small alveoli collapsing into larger ones prevents surface tension in alveoli creating a suction force tending to cause transudation fluid from pulmonary capillaries

Answer 296

work done to stretch the lungs- as work must be done against elasticity of lungs and thorax, and surface tension of alveoli and work is done against airways resistance

Answer 297

cartilage would cause the diffusion resistance to be too high for GE necessary to provide O2 and remove CO2 at a rate appropriate for the metabolism of our tissues. surface tension of alveoli reduced by surfactant, which therefore increases our lung compliance

Answer 298

incomplete posteriorly where trachealis muscle bridges the incomplete ends, as this allows are small degree of tracheal collapse in swallowing to food to pass down the oseophagus

Answer 299

lung mechanical function, airways resistance and diffusion across alveolar membrane, in a non-invasive way

Answer 300

vitalograph trace

Answer 301

this is when the airways are maximally expanded, and so at their least resistance, before the airways are subsequently compressed

Answer 302

can use a peak flow meter, but very insensitive, dependent of effort exerted by patient

Answer 303

The subject first fully exhales, then takes a rapid and full inspiratory vital capacity of a gas mixture composed of air, containing a tiny fraction of CO and a fraction of an inert gas such as helium (helium is to make an estimate of the total lung volume- allows correction for diluting effecr of RV when measurement begins). The breath is held for 10 seconds. Gas is collected during mid-expiration, as an alveolar sample, for analysis of the concentration of CO and of the inert gas. CO=very high affinity for Hb, so almost all entering blood binds Hb, plasma CO taken as 0. so conc gradient between alveolar pCO and the capillary pCO is maintained for whole time blood in contact with alveolar gas, so amount of CO transferred not affected by factors like blood flow rate From these measurements the The Carbon Monoxide Transfer factor is calculated.

Answer 304

continuous O2 diffusion between alveoli and the blood

Answer 305

by ensuring that the rate at which ventilation bring O2 and removes CO2 from alveolar air in in equilibrium with rate at which O2 diffuses into the blood and CO2 diffuses out

Answer 306

becomes +ve

Answer 307

re-seal pleural cavity and remove air from lungs- aspirate using a needle and large syringe, or leave if minor, treat secondary symptoms- give painkillers

Answer 308

reduced lung compliance as lack of surfactant to reduce surface tension in alveoli Normally as the chest wall expands during inspiration, the pleural pressure becomes more negative, and this causes the lungs to expand. When the lungs are stiffer due to reduced compliance, the lung resists expansion. This leads to greater inspiratory effort and the greater negative intra pleural pressure tends to suck in the chest wall, giving rise to intercostal recession (indrawing of intercostal spaces during inspiration) as well as subcostal recession, suprasternal and supra clavicular recessions during inspiration.

Answer 309

to reduce resistance to air flow and to reduce anatomical dead space as gas here does not undergo GE

Answer 310

vagus nerve

Answer 311

cricothyroid muscle | innervated by superior laryngeal nerve

Answer 312

effort dependent: FEV1 and FVC can be underestimated normally repeated at least three times to ensure reproducibility. spirometry can only be used on children old enough to understand and follow the instructions given not suitable for patients who are unconscious, sedated, etc. Other types of lung function tests must be used in these circumstances

Answer 313

``` reversibility widespread, variable air flow obstruction chronic inflammatory process airways hyperresponsiveness susceptibility ```

Answer 314

increased prevalence of astham in developed countries with westernised lifestyles- living conditions facilitate HDMs, and atmoshperic pollution

Answer 315

increased as lung architecture in utero is altered by pre-natal smoke exposure

Answer 316

aspirin- NSAID, can be given after MI to inhibit thromboxane A2 prod. hence platelet aggregation. But also inhibits PG synthesis and shifts arachidonic acid met. towards lipoxygenase pathway and prod. of leukotriene C4 and D4- inflammatory mediators

Answer 317

may be in remission, bronchi may become unresponsive | chronic, severe asthma- poorly reversible- airways remodelling

Answer 318

premature a.way closure so air trapping towards end of maximal expiration as increased smooth muscle tone, inflammation and oedema of airway walls, and abnormal secretions, some loos of elastic recoil, may increase FRC and TLC

Answer 319

identify extrinsic factors, development of a wheal around prick site indicates allergen sensitivity, blood IgE levels to specific aeroallergens.

Answer 320

usually normal, but used to exclude other diseases e.g. FB obstruction, or pneumothorax during severe acute exacerbations

Answer 321

immediate- type 1 hypersensitivity, max. reached in 20 mins, allergen interaction with specific IgE, causing mast cell degranulation and mediator release e.g. histmaine and LKTs, causing bronchial SM contraction, bronchoconstriction and increased mucus prod. and vascular leak late phase- 3-12 hrs later- type IV hypersensitivity- primarily result of inflammation- T helper 1 cells prod. IF gamma?, eosinophils recruited by TH2 cells- release LKTs, major basic proteins, eosinophilic cationic protein, and platelet-activating factor, MBP and ECP- epithelial cell damage- increased permeability to allergens, epithelial cells shredded. Also mast cells, lymphocytes and neutrophils.

Answer 322

eosinophils

Answer 323

beclometasone

Answer 324

bronchodilation- relief of acute symptoms, also reduce mast cell activation

Answer 325

main preventors- reduce eosinophil no.s and macrophage and lymphocyte activity

Answer 326

SEs e.g. may inhibit growth

Answer 327

adverse effect danger is greater

Answer 328

bronchodilate and reduce mucus secretion

Answer 329

british thoracic society

Answer 330

in the abdominal muscles as floating ribs, do not attach to sternum anteriorly

Answer 331

% of amount of O2 bound at saturation, and are independent of pigment concentration

Answer 332

at those partial pressures found in the tissues, so small decreases in pO2 when metabolising tissues results in O2 being readily released to the tissues as each dissociation of O2 reduces affinity of remaining haeme groups for bound O2

Answer 333

2 dimeric subunits each with 1 alpha and 1 beta globin chain, the 2 subunits are linked weakly, and O2 binding state alters strength of association T state- subunits held together rigidly

Answer 334

3 sites- in venous blood

Answer 335

as extra O2 in blood not normally used, about 27% of O2 in blood normally given up to tissues, so in exercise can be used by skeletal muscle, so about 55% of O2 in blood taken off

Answer 336

deoxyHB and stabilises it- T state

Answer 337

2 gamma chains- these weakly bind 2,3BPG so deoxyHb not stabilised

Answer 338

if lengthened diffusion pathway from alveolus to blood, or reduced SA available for diffusion

Answer 339

buffer function of CO2 controlling pH of ECF

Answer 340

reaction in red cell | very small amount produced in plasma as little carbonic anhydrase

Answer 341

ratio of [HCO3-] to pCO2 is 20:1, so 20 times as much HCO3- dissolved in plasma as CO2

Answer 342

buffering capacity of HB in red cell | variable HCO3- excretion by kidneys

Answer 343

dissolved CO2 reacts with H20 much more rapidly, so CO2 can be converted to H2CO3 as fast as it enters cells, so maintains strong aprtial pressure gradient between tissues and blood, driving CO2 diffusion. H+ binds to Hb, so 1 of products removed, lots of CO2 is reacting to form lots of HCO3-

Answer 344

Hb binds H+ as amine groups of globin in Hb have -ve charge so bind H+, so CO2 and H20 reaction keeps trying to replace H+, so HCO3- amount made depends on how much H+ bound to Hb

Answer 345

via Cl-HCO3- exchanger

Answer 346

rbc membrane relatively impermeable to H+, buffered by Hb as H+ accumulates with O2 release- Hb undergoes conformational change favouring H+ binding, so H+ and HCO3- in cell kept low favouring forward reaction

Answer 347

as reactions of CO2 in red cell producing most of HCO3- in blood are determined by how much H+ binds to Hb

Answer 348

H+ reacts with HCO3- in blood, pushing reaction frward with CO2 prod.- travels in venous blood to lungs where breathed out.

Answer 349

reacts with amine groups, so can bind directly with protein part of so when Hb binds H+= more favourable substrate for carbamino compound formation- haldane effect.

Answer 350

as pCO2 is higher- waste product of metabolism

Answer 351

Hb lost O2 so binds H+ more readily, so increase HCO3- prod., a little more CO2 dissolves in venous blood as waste prod. so both pCO2 and [HCO3-] increase. when blood reached lungs, O2 binds, H+ given up, reacts with HCO3-, prod. CO2- exhaled.

Answer 352

21.5mmol/L

Answer 353

23.5mmol/L

Answer 354

difference between venous and arterial CO2 content | 2mmol/L of CO2 carried to lungs in each L if venous blood, in addition to 21.5mmol/L

Answer 355

linear relationship between pCO2 and CO2 content in blood, but O2 curve reaches plateauy- Hb already 100% sat.

Answer 356

lung transplant

Answer 357

hyperventilating, PCO2 low so removes chemical drive to breathing

Answer 358

assoc. with increase in mortality, independent of disease severity ``` harmful effects:hypertension osteoporosis skin thinning brusing central obesity glucose intolerance adrenal suppression ```

Answer 359

main bronchus  airway obstruction, - (Monophonic wheeze) - Pneumonia in the lung distal to the obstruction can occur - If complete obstruction occurs, the lung collapses, as the air in the lung distal to the obstruction is gradually absorbed Pulmonary vessels (artery and vein) Bronchial vessels (artery and vein) Lymph vessels and lymph node  enlarged lymph nodes Nerves  compression of recurrent laryngeal nerve on the left side  paralysis of intrinsic laryngeal muscles  hoarseness of voice

Answer 360

SVC obstruction Left Recurrent laryngeal nerve – hoarseness Phrenic nerve palsy – paralysis of affected hemi diaphragm  breathlessness

Answer 361

squamous cell carcinoma

Answer 362

surgical resection if tumour can be accessed

Answer 363

metastasis from previous cancer, micrometastases- malignant cells lodge at a site distant from origin and start off being unable to grow or only grow to a very small size, but may grow in future

Answer 364

aspirate pleural fluid: 1) Protein estimation (transudate or exudate?) (2) microscopy and culture. (3) cytology – for malignant cells.

Answer 365

1st and part of 2nd costal cartilages

Answer 366

part of 2nd, and 3rd-7th costal cartilages

Answer 367

sternal angle

Answer 368

head-2 articular facets neck tubercle- 1 articular facet shaft- costal groove- protect IC vessels and nerves in NVB

Answer 369

costovertebral joints: joint of the rib head, costotransverse joint

Answer 370

parietal pleura and overlying skin, intercostal muscles

Answer 371

each space has an anterior IC artery (except from last 2) which anastomoses with a posterior intercostal artery

Answer 372

internal thoracic artery (branch of subclavian (R and L), and its continuation the musculophrenic artery

Answer 373

aorta and the superior IC artery- from costo-cervical trunk, a branch of the subclavian

Answer 374

2 anterior and 1 posterior IC vein anterior drain via internal thoracic into subclavian posterior drain via azygos on R and hemiazygos on L, into SVC

Answer 375

A rami of thoracic spinal nerves (T1-T12), supply IC muscles, parietal pleura and overlying skin

Answer 376

internal and innermost IC muscles

Answer 377

as dome of diaphragm means thoracic cavity much smaller than bony thorax would suggest and so abdominal organs e.g. liver, parts of stomach, spleen and upper kidneys in abdominal cavity are covered by the ribs and so can be damaged by a chest injury R dome of diaphragm lies at level of 5th rib, L dome at 5th IC space

Answer 378

vertebral part: from crura and arcuate ligaments, crura= strong tendons attached to AL surfaces of the upper 3 L VBs, R crus from bodies and IV discs of L1,2,3, L from L1,2. arcuate ligaments= thickenings of fascia, media= thickening over psoas major muscle, lateral= over quadratus lumborum muscle costal part: from inner aspects of 7-12 costal cartilages sternal part: from deep surface of xiphisternum

Answer 379

by the mediastinum

Answer 380

sternal angle | angle between these bronchi=carina-at T4/T5

Answer 381

R= shorter, wider, and more vertical | L passes below arch of aorta, anterior to the descending aorta and oesophagus

Answer 382

can be isolated and removed without much bleeding or air leakage, or interfering with other bronchopulmonary segments

Answer 383

bronchoscopy

Answer 384

supply bronchi from carina up to the respiratory bronchioles, visceral pleura and CT 2 on L side from aorta, 1 on R from 3rd IC artery (branch of aorta)

Answer 385

superficial group- drain visceral pleura and bronchi in hilar region to azygos vein on R and accessory hemiazygos on L deep group- drain rest of bronchi deep in lung into main pulmonary vein or directly into L atrium.

Answer 386

level of 1st rib into neck

Answer 387

convex costal surface separated from concave diaphragmatic surface by sharp inferior border posterior border rounded to fit paravertebral gutter thin anterior border, shows cardiac notch on L side R an L mediastinum groove mediastinal surfaces

Answer 388

main bronchus, pulmonary artery, 2 pulmonary veins, bronchial vessels, nerves and lymphatics

Answer 389

fibres from vagi and sympathetic trunk via pulmonary plexuses situated at hilum parasympathetic fibres from vagus motor to bronchial SM- bronchoconstriction, inhibitory to pulm vessels-vasodilator, and secretomotor to mucous glands vagal afferent fibres for cough reflex and some subserving pain sympathetic efferents bronchodilator and vasoconstrictior

Answer 390

the rich capillary network surrounding the alveoli

Answer 391

the alveoli also, some anastomoses between bronchial and pulmonary arteries at pre capillary and capillary level which maintain blood supply to lung parenchyma after PE

Answer 392

the alveoli | run in intersegmental septa and 2 leave each hilum, draining upper and lower lobes

Answer 393

superficial subpleural plexus- lies deep to visceral pleura and drains lung parenchyma and visceral pleura, drain along surface to hilar LNs deep bronchopulmonary lymphatic plexus- lies in submucosa of bronchi and peribronchial tissue, also drain eventually into hilar LN- bronchopulmonary nodes- in hilum of each lung. efferents from these nodes run to tracheobronchial nodes- enlargement of these can cause widening of angle of the carina

Answer 394

about 3cm above medial part of the clavicle

Answer 395

suprapleural membrane- fasica covering the apical pleura which sometimes deosn't prevent the lung and pleura extending into the neck

Answer 396

subclavian vessels and BP

Answer 397

insertion of a chest drain exposing kidney liver biopsy insertion of a sub-clavicular cannulation line into subclavian vein

Answer 398

neisseria viridans streptococci candida anaerobes

Answer 399

muco-ciliary clearance cough and sneezing reflex resp. mucosal IS- lymphid follicles of pharynx, tonsils-GALT*, alveolar macrophages, secretory IgA and IgG

Answer 400

RSV rhinovirus influenza/parainfluenza coronavirus

Answer 401

``` pharyngtitis rhinitis epiglottitis laryngitis- contrast with non-improvement in hoarse voice in lung cancer sinusitis otitis media tracheitis ```

Answer 402

staph aureus pseudomonas gram -ve enteric e.g. E coli MRSA

Answer 403

``` pneumocystis jirovecii- silver staining on lung biopsy cytomegalovirus candida aspergillus- CGD crytposporidium varicella-zoster virus ``` opportunistic:SPUR

Answer 404

s.pneumoniae- elderly, co-morbidity, pleuritic pain, high fever s.aureus- post-influenza H.influenzae-COPD legionella-recent travel mycoplasma- prior antibiotics, extra-pul involv chlamydia- bird contact klebsiella-thrombocytopenia

Answer 405

oropharyngeal colonisation with enteric gram -ves as immobile, loss of consciousness and instrumentation and gastric acid inhibition subsequent aspiration of nasopharyngeal secretions suspected when new infiltrates on CXR, with infection features- fever >38C purulent sputum, leucocytosis, hypoxaemia

Answer 406

repeated injury from exo.or endog. stimuli e.g. infection-EB virus, or pollutant. increases number of activated macrophages, so cytokine release, attract neutrophils and eosinphils, causing local lung damages with ROS and protease prod, causing tissue destruction and fibrosis, GFs recruit fibroblasts and are prod. by alveolar cells

Answer 407

lymphoma | TB- caseous granuloma- so distinguish by transbronchial biopsy

Answer 408

1: bilateral hilar lymphadenopathy 2: BHL with pulmonary infiltrates 3: infiltrates but no BHL 4: irreversible fibrosis

Answer 409

asbestos fibres penetrate to alveoli, cause alveolitis with macrophage influx coating fibres, producing asbestosis bodies, alveolitis progresses to fibrosis

Answer 410

lung parenchyma involved, not airways airways tend to be helped to be kept open as increased radial traction on airway as more fibrous tissue meaning the airway lumen is anchored to the lung interstitium more stongly

Answer 411

``` radiation methotrexate-RA nitrofurantoin-UTIs amiodarone-arrythmias chemotherapy ```

Answer 412

coal workers pneumoconiosis-coal dust and carbon silicosis-mining and stone working asbestosis

Answer 413

pneumonia | as poor clearance of secretions by coughing so prone to infections

Answer 414

obligate aerobe

Answer 415

droplet nucleus- formed from evaporation of droplets. disperses

Answer 416

macrophages- present TB antigen to T cells- CD4+ T cells? T helper 1 cells release interferon gamma- enhances phagocytosis activity of macrophages activated macrophaes emerge with an enhanced ability to kill M TB, takes about 6wks to develop

Answer 417

contained by IS- T cells- cell-mediated immunity, and hypoxic acidic environment of the granuloma

Answer 418

type IV hypersensitivity reaction

Answer 419

reduced cellular immunity, so less destructive element of TB in lung- CD4+ T cells infected by HIV, and these mediate inflammatory response to TB, with macrophage activation and granuloma formation

Answer 420

when the bacilli is detectable in sputum

Answer 421

macropahges and dendritic- IL-12 | Interferon gamma and TNF alpha- NK and CD4+ T cells

Answer 422

high V/P ratio relative to other parts of lung

Answer 423

pleural effusion- bacilli seed in pleura, or hypersensitivity

Answer 424

``` haemoptysis persistent cough unresolving pneumonia fever malaise weight loss night sweats ```

Answer 425

``` pallor-anaemia- haemoptysis? fever weight loss clubbing palpable cervical nodes ```

Answer 426

primary infection to disease reactivation haematogenous spread with miliary TB exogenous reinfection

Answer 427

contact screening | can reduce transmission and cure

Answer 428

to determine susceptibility to drugs

Answer 429

neck painless enlargement of cervical or supraclavicular no erythema

Answer 430

subchondral bone, spreads to VBs and joitn space, then follows A and P long. ligaments, so may be pus on both sides of spine- paravertebral abscesses chronic back pain ankylosing- spine takes a different course

Answer 431

CT or lumbar puncture

Answer 432

fever malaise weight loss

Answer 433

resistant to both rifampicin and isoniazid

Answer 434

single mutatgenic events cause aa substitutions in drug target proteins

Answer 435

if FH of TB in past 5 yrs

Answer 436

dilated veins in upper chest and arms

Answer 437

``` relatively non-specific chest pain- pleuritic dyspnoea new and unresolving cough weight loss hoarse voice dysphagia haemoptysis recurrent infections lethargy and malaise ```

Answer 438

partial bronchus obstruction, secretions retained, so bacterial overgrowth

Answer 439

``` rounded opacity- mass lesion pleural effusion slow resolving consolidation collapse hilar adenopathy ```

Answer 440

``` CXR CT PET isotope bone scan ultrasonography MRI ```

Answer 441

bronchoscopy needle biopsy surgical biopsy

Answer 442

chemotherapy

Answer 443

no heart magnification | scapulae moved out of the way

Answer 444

bats wing apperance- opacities at hilum of lung due to pulm oedema

Answer 445

consolidation lung collapse massive pleural effusion pneumonectomy

Answer 446

vaccination against H.influenzae

Answer 447

by transverse thoracic plane