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respiratory diseases Flashcards

1
Q

Condition describing patients with features of both COPD & asthma.

A

Asthma COPD overlap syndrome, e.g. COPD + reversibility + eosinophilia + steroid responsive.

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2
Q

Acute condition, worked in a shipyard, fever, chest pain & bloody pleural effusion.

A

Acute asbestos pleuritis.

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3
Q

Preceded by common cold which “goes to the chest”. Usually self-limiting, but increased morbidity in patients with chronic lung disease.

Symptoms: productive cough, possible fever.
Signs: normal chest exam, normal CXR, may have transient wheeze.

A

Acute bronchitis.

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4
Q

Life-threatening airway obstruction (in children). Inflamed epiglottis (often due to haemophilus influenza B -HiB).

Symptoms: acute onset of sore throat + drooling, severe croup/stridor & fever.

Treated with Ceftriaxone.

A

Acute epiglottitis.

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5
Q

Preceded by common cold + purulent nasal discharge. Usually self-limiting & resolves in approx. 10 days.

A

Acute sinusitis.

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6
Q

Acute/chronic inflammation of nasal mucosa due to allergen inhalation (^IgE which binds to mast cells & basophils). Allergen re-exposure causes mast cells & basophil degranulation.

Symptoms: acute sneezing, itching, rhinorrhoea, nasal congestion (due to mediator release e.g. histamine).

Delayed lymphocyte & eosinophil recruitment to nasal mucosa increases congestion.

A

Allergic Rhinitis

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7
Q

A condition affecting the lungs that may result from autoimmune disease (e.g. SLE, polyarteritis, Wegener’s Churg-Strauss, Bechet’s), or drugs (amiodarone, methotrexate, gold, bleomycin).

Typically causes alveolar thickening, and decreased O2 levels in blood.

A

Alveolitis.

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8
Q

Treatment: IV adrenaline/epinephrine + IV antihistamine + IV corticosteroid + high flow O2 + nebulised bronchodilators + endotracheal intubation.

A

Severe anaphylaxis.

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9
Q

High risk factors: miners, construction workers, ship-builders, car workers.

Straight fibres (amphibole) - dangerous. Curved fibres (serpentine) are less so.

Many related lung disorders: benign pleural plaques, acute X pleuritis, pleural effusion and diffuse pleural thickening, malignant mesothelioma, pulmonary fibrosis & bronchial carcinoma.

A

ASBESTOS

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10
Q

Occurs as a result of prolonged exposure to asbestos.

Signs: diffuse pulmonary fibrosis & restrictive defects. Asbestos bodies may be seen in sputum & lung biopsy.

A

Asbestosis pulmonary fibrosis.

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11
Q

A fungal chest infection caused by inhalation of fungal spores.

In the immunocompromised/immunosuppressed: severe pneumonia & invasive disease.

In the immunocompetent: localised pulmonary infection & aspergilloma in pre-existing chest cavities.

Diagnosis: BAL, fungal culture, PCR & histopathology.

Treatment: Amphotericin B, voriconazole or surgery.

A

Aspergillus.

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12
Q

Chronic inflammatory disease of the airways. Genetic pre-disposition + triggers causes eosinophilic inflammation (-> TH2 cytokines)

A

Asthma

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13
Q

immediate phase of an asthma attack, consisting of early phase bronchospasm & acute inflammation.

Involves mast cells, mononuclear cells, chemotaxins & chemokines. Causes bronchospasm.

A

Type 1 hypersensitivity reaction.

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14
Q

Delayed phase of asthma attack, consisting of late phase bronchospasm & delayed inflammation.

Results in epithelial damage, airway hyper-responsiveness, wheeze, mucus hyper-secretion &cough.

A

Type 4 hypersensitivity reaction.

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15
Q

Type of asthma involving crosslinking of IgE receptors to stimulate Ca2+ entry into mast cells, & Ca2+ release from intracellular stores causing spasmogen release, e.g. histamine, leukotriene, & smooth muscle contraction.

A

Allergic asthma.

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16
Q

Difficulty breathing: diurnal variability & often in response to triggers e.g. allergens or exercise.

May hear a widespread due to turbulent airflow when auscultating.

Normal FVC, normal TLCO.
Reduced FEV1 and PEFR.
FEV1/FVC <75%.
B2-agonist delivers >15% improvement in FEV1/FVC.

A

Asthma

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17
Q

Normal FVC, normal TLCO.
Reduced FEV1 and PEFR.
FEV1/FVC <75%.

A

Asthma

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18
Q

the fixed abnormal dilation of the bronchi, usually due to fibrous scarring from infection, but can also be seen with chronic obstruction.

Dilated airways accumulate purulent secretions.

A

Bronchiectasis.

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19
Q

Abnormal fixed dilation of bronchi.

Treatment involves smoking cessation + vaccination + antibiotics (clarithromucin/azithromycin for pseudomonas) + an anti-inflammatory.

A

Bronchiectasis.

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20
Q

Chronic inflammation of bronchi & bronchioles.

Patients present with gradually increasing breathlessness. Chronic cough, productive of sputum. Infective exacerbations produce purulent sputum.

Chronic neutrophilic inflammation, mucus hypersecretion, mucociliary dysfunction, altered lung microbiome, smooth muscle spasm and hypertrophy, & partial reversibility.

A

Chronic bronchitis.

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21
Q

Form of chronic bronchitis that occurs due to inhalation of coal dust + smoking.

Simple: abnormal CXR, but no impairment in lung function.
Complicated: progressive massive fibrosis, restrictive PFTs and breathlessness.

A

Coal workers pneumoconiosis.

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22
Q

Acute (typically viral) infection of nasal passages, usually accompanied by a sore throat + mild fever.

Typically due to adenovirus, rhinovirus, coronavirus & respiratory syncytial virus.

A

Common cold (coryza).

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23
Q

Most common cause of immunodeficiency, leading to recurrent respiratory infections.

A

Common variable deficiency.

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24
Q

Airway epithelial cells receive a stimulus, alveolar macrophages produce cytokines IL8 & LTB4, causing lung inflammation.

Cytokines activate neutrophils to produce CD8+ T cells & macrophages. These cause release of matrix metalloproteinases, free radicals & proteases which breakdown connective tissue of lung parenchyma.

A

COPD pathology

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25
Q

COPD pathology causing alveolar wall destruction, and which disease?

A

Emphysema

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26
Q

COPD pathology causing mucus hypersecretion, and which disease?

A

Chronic bronchitis

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27
Q

Multicomponent disease process of mucociliary dysfunction, inflammation & tissue damage.

Progressive, fixed airflow obstruction leads to impaired alveolar gas exchange causing type II respiratory failure.

Progressive reduction in lung function, increasingly breathless & worsening quality of life. May cause pulmonary hypertension, RV hypertrophy/failure, & eventually death.

A

COPD

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28
Q

Reduced FVC, FEV1, PEFR.
FEV1/FVC <75%.
B2 agonist shows <15% improvement to ratio.

A

COPD

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29
Q

Acute exacerbations usually preceded by URTI. Result in increased sputum production and purulence, more wheezy &breathless.

Examination: respiratory distress, wheeze, coarse crackles, cyanosis & ankle oedema.

A

COPD

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30
Q

Right heart disease secondary to pulmonary hypertension due to lung disease e.g. COPD.

Causes fluid retention due to hypoxia (+/- RHF).

Signs: RV hypertrophy & dilation. RH failure (swollen legs/oedema), liver congestion.

A

Cor pulmonale

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31
Q

Precipitated by various viruses.
Symptoms: harsh cough/stridor.
If mild, may be treated with humidification.
If requiring admission, then steroids are needed.

A

Croup/acute laryngotracheobronchitis.

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32
Q

Inherited autosomal recessive condition. Most common genetic condition of Caucasians (1 in 25 carry the gene).

Causes mutated CFTR gene, blocking of the airways by abnormally thick, viscous mucus. Some affected children are born with meconium ileus.

A

Cystic fibrosis.

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33
Q

Chronic cough, wheeze, diarrhoea, recurrent chest infections, failure to thrive. Possible diabetes due to pancreatic failure.

Colonisation with staph. aureus, H. influenza, strep. pneumonia, pseudomonas aeruginosa etc.

Portal hypertension & TIPSS (transjugular intrahepatic portosystemic shunt) may occur due to blocking of liver ducts.

A

Cystic fibrosis.

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34
Q

Group of interstitial lung diseases caused by disease of alveolar structures, resulting in impaired alveolar gas exchange, decreased PaO2 & SaO2. However, CO2 exchange is unimpaired.

Symptoms: breathless on exertion, cough w/o wheeze.
Signs: finger clubbing, inspiratory lung crackles, central cyanosis & possible pulmonary fibrosis (end-stage).

CXR: bilateral diffuse alveolar infiltrates.
High res. CT: ground glass appearance.

A

Diffuse parenchymal lung diseases.

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35
Q

Life-threatening condition caused by toxin production. Presents with a characteristic pseudo-membrane, no longer seen in UK due to vaccination.

A

Diphtheria.

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36
Q

Risk factors include: thrombophilia, contraceptive pill, smoking, HRT, pregnancy, pelvic obstruction, trauma, surgery, immobility (long-haul), malignancy, pulmonary hypertension/vasculitis & obesity.

symptoms: swollen, hot & red, tender leg/calf.

A

DVT

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37
Q

Investigation may involve ultrasound Doppler scan of leg, CT scan of ileofemoral veins, IVC & pelvis.

Prevention involves: early mobilisation post-op, compression stockings, calf muscle exercises, subcutaneous low mol. wt heparin post op, anticoagulant (dabigatran. rivaroxaban, apixaban).

A

DVT

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38
Q

Distension & damage to alveoli results in destruction of acinial pouching in alveolar sacs. Results in impaired gas exchange, loss of bronchial support & is irreversible.

Increased air space due to alveolar destruction e.g. by neutrophil elastases or imbalance of proteases & anti-proteases.

Expiratory flow volume curve is of reduced magnitude & more rounded.

A

Emphysema.

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39
Q

Pus in the pleural space, high-mortality rate.
CXR: “D-SIGN” - loculated pleural fluid bulging out from chest wall.

Treatment includes: amoxicillin + metronidazole until cultured bacteria suggest otherwise.

A

Empyema

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40
Q

Hypersensitivity pneumonitis Type 3 reaction (with a lil bit of type IV). Inhalation of a substance, e.g. mould, bird droppings, chlorine, or medication e.g. sulphasalazine can cause the reaction.

Flu-like illness, involving cough, breathlessness, fever, myalgia & joint pain.

There may be crackles upon auscultation, but no wheeze & a patient may be hypoxic.

CXR: widespread pulmonary infiltrates.

A

Acute Extrinsic allergic alveolitis.

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41
Q

Chronic form of a hypersensitivity type 3 pneumonitis reaction due to recurrent allergen exposure. Results in gradual breathlessness & cough, lung scarring, crackles and pulmonary fibrosis of the upper lobes.

Restrictive PFTs - low FEV1 and FVC, but a high/normal ratio. TLCO will be low.

Lung biopsy & precipitins (IgG for antigen) can confirm diagnosis.

A

chronic extrinsic allergic alveolitis

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42
Q

A rare condition that increases the risk of both acute & chronic infections.

A

Hypogammaglobulinaemia.

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43
Q

Common condition which increases the risk of acute respiratory infections.

A

IgA deficiency.

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44
Q

An immunoglobulin deficiency which can cause myeloma, lymphoma & metastatic malignancy.

A

Immunoparesis/immunodeficiency.

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45
Q

Acute onset of fever, malaise, myalgia, headache, cough & fatigue. Self-limiting. Viral infection.

Complications include primary influenza pneumonia, secondary bacterial pneumonia, bronchitis, otitis media.

A

Influenza

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46
Q

General term describing any disease process affecting interstitium of the lung. Interference in gas transfer & restrictive lung patterns are characteristic.

Examples: sarcoidosis, extrinsic allergic alveolitis, idiopathic pulmonary fibrosis etc.

Symptoms generally vary, but typically include breathlessness and dry cough.

A

Interstitial lung disease.

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47
Q

Usually preceded by illness, e.g. pneumonia, virus, inhalation of foreign body. High mortality when untreated.

Symptoms: weight loss, lethargy, fatigue, cough, sputum production.

A

Intrapulmonary abscess.

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48
Q

Treatment may involve removal of a foreign body/ treating an underlying cause, e.g. anaphylaxis.

Administration of mask bag ventilation with high flow O2, cricothyroidotomy & tracheostomy.

A

Laryngeal obstruction.

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49
Q

Acute bronchitis, acute exacerbation of chronic bronchitis, pneumonia & influenza all have what in common?

A

They are infections of the LRT.

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50
Q

Weight loss, haemoptysis, breathlessness, recurrent pneumonia & hoarseness may suggest what?

A

Lung cancer.

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51
Q

Cough of long duration, haemoptysis, smoking, breathlessness, weight loss, fatigue, recurrent infection, chest pain, dysphagia to solids & hoarseness are all red flags of which disease?

A

Lung cancer.

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52
Q

Breathlessness, atrial fibrillation & pericardial effusion can be caused by invasion of which structure?

A

Invasion of pericardium.

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53
Q

Dysphagia for solids suggests invasion of which structure?

A

Oesophagus

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54
Q

Weakness of the hands/arms suggests invasion of which structure?

A

Brachial plexus (most probably by pancoast’s tumours).

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55
Q

Breathlessness and large volumes of pleural effusion suggests invasion of which structure?

A

Pleural space.

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56
Q

Puffy eyelids, headache and vein distension suggests invasion of which structure?

A

The SVC - obstructs blood drainage from arms and head.

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57
Q

Chest pain made worse by movement and at night suggests invasion of which structure?

A

The chest wall, i.e. ribs.

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58
Q

Sudden death due to massive haemoptysis suggests invasion of which structure?

A

Tumour encasing and eroding an artery,

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59
Q

Slow onset weakness, visual disturbance, headaches (worse in morning) & fits suggests invasion of which structure?

A

Metastasis to the brain.

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60
Q

Localised pain worse at nigh, and fractures sustained due to trivial mechanical stress suggests invasion of which structure?

A

Bone

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61
Q

Brain, liver, bone, adrenal glands, lungs, skin have what in common?

A

They are common metastatic sites of lung cancer.

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62
Q

Which investigation would be used if there was a suspected tumour in the central area of the bronchial tree?

A

Bronchoscopy

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63
Q

Which investigation would be used if there was a suspected tumour of the pleural surfaces?

A

Thoracoscopy (deflate lung, visualise & biopsy).

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64
Q

Which investigation would be used if there was a suspected tumour in the hilar/mediastinal structures, & nearby lymph nodes?

A

endobrachial ultrasound - also enables lymph node sampling.

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65
Q

Which investigation would be used if you wanted to diagnose lung cancer or guide biopsy of suspected peripheral tumours?

A

CT scan. Assesses tumour size & shows intercranial metastases.

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66
Q

Which investigation would be used if you wanted to stage a cancer, and detect nodal & distant metastases? Or, outline a tumour within areas of lung collapse?

A

PET scan. Often results in upstaging.

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67
Q

Which investigation would be used if you wanted to avoid use of IV contrast, & required good soft tissue contrast?

A

MRI. It is however, costly, time consuming and better spatial resolution is achieved with CT.

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68
Q

Treatment of small cell lung cancer

A

chemotherapy

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69
Q

Treatment of non-small cell lung cancer?

A

Surgery or radical radiotherapy. Less responsive to chemo.

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70
Q

Most common type of lung cancer seen in non-smokers?

A

Adenocarcinoma.

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71
Q

Symptoms: runny nose, malaise, dry cough, fever.

Signs: red eyes, Koplik’s spots (white spots with red areola on buccal mucosa), maculopapular rash beining behind the ears & gradually descending.

Complications are more common in the imnmunocompromised & malnourished, and include bacterial pneumonia, bacterial otitis media & encephalitis.

A

Measles

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72
Q

An uncommon, malignant tumour of pleural lining due to asbestos exposure. Often takes 30-40 years to develop. Incurable.

Breathlessness, chest pain, weight-loss, fever, sweating & cough.

Pleural effusion.

A

Mesothelioma. Care is palliative, you can pleurodese effusions, radiotherapy/surgery/chemotherapy, but fatal within 2 years.

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73
Q

Massive seeding of mycobacteria via the bloodstream, untreated it is rapidly fatal.

A

Military tuberculosis.

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74
Q

Acute/chronic rhinitis without IgE involvement (eosinophilia syndrome may be present). Can result from infection, hormone imbalance, vasomotor disturbances & medications.

A

Non-allergic rhinitis.

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75
Q

Treatment of non-allergic rhinitis.

A

glucorticoids (inflammation) + H1 & CysLT1 receptor antagonists (block mediator receptors) + vasoconstrictors (reduce nasal blood flow) + sodium cromglycate (anti-allergic) + muscarinic receptor antagonists.

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76
Q

Snoring, dramatic drop in tidal volume and PO2, and an increase in pCO2 that may cause CO2 retention headaches in the morning are symptoms of which syndrome?

(clue - person is overweight).

A

Obesity hypoventilation syndrome.

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77
Q

Intermittent collapse of upper airways when sleeping, causing recurrent, episodic arousals. Results in poor quality sleep, daytime drowsiness, & early morning headaches.

Risk factors: obesity, enlarged tonsils, hypothyroidism, alcohol, opiates & benzodiazepines.

A

Obstructive sleep apnoea.

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78
Q

Treatment of obstructive sleep apnoea.

A

Remove underlying causes, e.g. alcohol & obesity. Continuous positive airway pressure machine when sleeping.

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79
Q

May be a simple or complicated parapneumonic effusion, or even empyema.

Treat with antibiotics +/- drainage +/- surgery.
Discuss nutrition,

A

Pleural infection.

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80
Q

Identify the type of parapneumonic effusion:

+ve gram stain, pH <7.2, low glucose, septations & loculations present.

A

Complicated parapneumonic effusion.

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81
Q

Identify the type of parapneumonic effusion: no +ve gram stain, pH>7.2, normal glucose, no septations or loculations present (ALL MUST APPLY).

A

Simple parapneumonic effusion, does not have ANY characteristics of complicated.

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82
Q

An occupational, restrictive lung disease caused by the inhalation of mineral dust. Fibrogenic causes: asbestos & silicon. Non-fibrogenic causes: iron (siderosis), tin (stenosis) & barium (baritosis).

A

Pneumoconiosis.

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83
Q

A non-expanding collection of air in the pleural cavity, with no shift of the heart or mediastinal structures. May result from penetrating injury to the parietal pleura/ rupture of visceral pleura.

Lung tissue recoils towards the hilum.

A

Pneumothorax.

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84
Q

Increased incidence in tall thin males, smokers (inc. cannabis), and those with underlying lung disease.

Can occur secondary to pulmonary disease or chronic cough causing pleural rupture.

A

Pneumothorax.

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85
Q

Short of breath, acute onset pleuritic chest pain. Primary are often asymptomatic.

May be hypoxic, tachycardic, chest percussion is hyper-resonant. Chest expansion may be reduced, and trachea will deviate. Reduced ipsilateral breath sounds. Hamman’s sign (pleural click) may occur - rare.

A

Pneumothorax.

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86
Q

CXR: absent peripheral lung markings, & visible lung edges.
Chest percussion is hyper-resonant & trachea is deviated to left. Patient is complaining of breathlessness and acute pleuritic chest pain.

A

Pneumothorax.

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87
Q

Emergency - may cause cardiac arrest. Increased pleural pressure pushes other chest organs away from affected side.

Air is permitted into the pleural cavity, but cannot exit. Tracheal deviation and mediastinal shift may occur, or may remain central if pathology is bilateral.

A

Tension pneumothorax.

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88
Q

May cause hypotension, raised JVP, reduced air entry on affected side & requires immediate needle decompression via a large bore venflon in the second intercostal space anteriorly, mid-clavicular line of affected side.

A

tension pneumothorax.

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89
Q

Acute inflammation of the lungs in response to inhalation of bacteria, most commonly strep. pneumonia.

A

Pneumonia.

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90
Q

Inhalation of bacteria which causes alveoli and bronchioles to fill with fibrous exudate. Different causative bacterial, viral & fungal agents. Typically affects lower lobes.

A

Pneumonia.

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91
Q

Signs/symptoms: malaise, anorexia, sweats, rigors, myalgia, arthralgia, headache, confusion, cough, pleurisy, haemoptysis, dyspnoea, preceding URTI, abdo. pain & diarrhoea. Crackles & pleural rub.

CXR: infiltrates (neutrophils, macrophages & fibrin-rich exudative fluid). Lower lung consolidation due to fluid accumulation.

A

Pneumonia

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92
Q

Assessed using CURB65 - confusion, urea >7, resp. rate >30/min, BP<90 or diastolic <61, and aged >65.

A

Pneumonia

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93
Q

An atypical, gram -ve, water-borne bacteria. Common in hotels etc. May lead to acute renal failure. Causes flu-like symptoms, GI upset and shortness of breath.

A

Legionella pneumonia, may cause legionnaire’s disease.

Treat with levofloxacin/rifampicin/moxifloxacin.

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94
Q

Most common bacterial pneumonia in those with AID/immunosuppression. Symptoms include fever, dry cough, shortness of breath & fatigue.
In HIV patients, they may have a sub-acute low grade fever, but the pneumonia will be more severe.

A 
Pneumocystis jiroveccii (PCP).
diagnosis by BAL > sputum > gargle. Immunofluorescence &amp; PCR.

Treat with co-trimoxazole.

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95
Q

Match the treatment to the pneumonia:

  1. amoxicillin/doxycycline/clarithromycin.
  2. Oxygen + fluids + bed rest + no smoking.
A

Mild-community acquired pneumonia, usually strep. pneumonia - gram -ve cocci, alpha-haemolytic.

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96
Q

Match the treatment to the pneumonia:

  1. Co-amoxiclave + clarithromycin
  2. If penicillin allergic - levofloxacin + clarithromycin.
A

Severe community acquired pneumonia.

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97
Q

Match the treatment to the pneumonia:

  1. IV amoxicillin + metronidazole + gentamicin.
  2. If penicillin allergic - IV co-trimoxazole + metronidazole +/- gentamicin.
A

Severe hospital acquired / aspiration pneumonia.

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98
Q
  1. PO amoxicillin + metronidazole.
A

Non-severe hospital acquired / aspiration pneumonia.

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99
Q

May result from rheumatoid disease, SLE, systemic sclerosis, asbestos, amiodarone, methotrexate. Terminal disease with a median survival of 4 years following diagnosis.

Symptoms: progressive breathlessness, dry cough.
Signs: finger clubbing & bilateral fine inspiratory crackles.

A

Pulmonary fibrosis.

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100
Q

CXR: bilateral pulmonary infiltrates.
CT: reticulonodular shadowing, worse at peripheries and lung bases. Possible honey-combing, traction bronchiectasis (irreversible dilation of bronchioles).

A

Pulmonary fibrosis.

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101
Q

Treatment involves O2 if hypoxic, anti-fibrotic drugs e.g. pirfenidone and nintedanib (which will slow progression, but not cure). Lung transplants may be possible in younger patients.

Otherwise, this is a fatal disease.

A

Pulmonary fibrosis.

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102
Q

Lodging of an embolus in the pulmonary artery, blocking it. Massive emboli can cause cardiovascular shock, low BP, central cyanosis & sudden death.

A

Pulmonary embolism.

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103
Q

Pleuritic pain, leg pain/swelling, collapse, haemoptysis & breathlessness.

Patient may experience tachypnoea, tachycardia, cyanosis, fever, pleural rub or effusion, crackles, hypotension.

A

Pulmonary embolism.

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104
Q

CXR: basal atelectasis, consolidation, pleural effusion.
ECG: acute right-heart strain, T-wave inversion in V1-3.
Raised D-dimers
Pleuritic chest pain, SOB and haemoptysis.

A

Pulmonary embolism.

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105
Q

What investigation would you perform if you suspected a pulmonary embolism?

A

CXR and V/Q scan.

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106
Q

What investigation would you perform if you suspected a pulmonary embolism, the patient had a swollen leg but wanted to avoid radiation?

A

Ultrasound of leg for DVT

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107
Q

What investigation would you perform if you suspected a massive pulmonary embolism or the patients CXR is abnormal due to existing lung disease?

A

CTPA

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108
Q

What investigation would you perform if you suspected a pulmonary embolism, but the patient is acutely unwell?

A

Echocardiogram, which will show right heart strain.

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109
Q

Mean pulmonary arterial pressure >25mmHg.

A

Pulmonary hypertension

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110
Q

May be caused by left ventricular systolic dysfunction(LVSD), mitral regurgitation/stenosis, cardiomyopathy.

A

Pulmonary venous hypertension.

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111
Q

May be caused by hypoxia due to COPD/ pulmonary fibrosis/ obstructive sleep apnoea etc. Or may arise from multiple pulmonary emboli, vasculitis, drugs, HIV, cardiac left-to-right shunt e.g. ASD and VSD, or may be primary.

A

Pulmonary hypertension.

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112
Q

The compromisation of blood flow and oxygen to lung tissue resulting in tissue death.

A

Pulmonary infarction.

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113
Q

Risk factors: abnormal host response arising from immunodeficiency or immunosuppression, an abnormal innate host defence (damage bronchial mucosa, abnormal cilia or abnormal secretion & repeated insult).

Chronic examples include: intrapulmonary abscess, empyema, chronic bronchial sepsis, bronchiectasis & cystic fibrosis.

A

Pulmonary infection.

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114
Q

Accumulation of fluid in the lung (interstitium & alveolar spaces) causing a restrictive PFT pattern.

May be due to increased hydrostatic pressure, injury to alveolar cells e.g. pneumonia, ARDS.

A

Pulmonary oedema.

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115
Q

CXR: possible cardiomegaly, upper lobe venous distension, pleural effusion, Kerley b lines, bat-wing opacity (peri-hilar patchy opacification).

A

Pulmonary oedema.

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116
Q

Due to a relative surfactant deficiency, more common in premature babies.

A

Neonatal respiratory distress syndrome.

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117
Q

In infants, complications include: sudden deterioration, absent breath sounds.
It is due to a deficiency in surfactant (type 2 alveolar lining cells). Neonates thus require increased effort to expand their lungs, causing physical damage to cells.

A

Neonatal respiratory distress syndrome.

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118
Q

In adults: may arise from sepsis, diffuse infection (virus/mycoplasma), severe trauma, oxygen. It results in either resolution and fibrosis, or death.

Due to a relative surfactant deficiency.

A

Adult respiratory distress syndrome.

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119
Q

Conditions which cause hypoxia, e.g. pneumonia, asthma, pneumothorax, PE, pulmonary fibrosis.

A

Type 1 respiratory failure

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120
Q

Conditions which cause hypercapnia, e.g. COPD, respiratory muscle weakness & pulmonary oedema.

A

Type 2 respiratory failure

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121
Q

Occurs when gas exchange in the lungs is insufficient to meet metabolic demand. Type 1 and 2.

A

Respiratory failure.

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122
Q

Intrapulmonary abscess, empyema, chronic bronchial sepsis, bronchiectasis & cystic fibrosis are examples.

A

Respiratory infection.

123
Q

PEFR and FEV1/FVC ratio is normal.

However, FEV1 and FVC are reduced.

A

Restrictive lung disease

124
Q

Reduced static lung volume (e.g. reduced TLC), when given a B2-agonist there is no response.

A

Restrictive lung disease.

125
Q

Signs: central cyanosis if hypoxic, oedema, raised JVP with V-waves, RV heave at left parasternal edge, tricuspid regurgitation, loud P2.

Liver may be enlarged and pulsatile.

A

Right heart failure.

126
Q

Multi-system disease, usually self-limiting.

Signs: lymphadenopathy, erythema nodosum, uveitis, arthritis, parotitis, fever, myocarditis and neuropathy.

A

Sarcoidosis.

127
Q

Chronic form of multi-system disease.

Signs: lung infiltrates (alveolitis), skin infiltrations, peripheral lymphadenopathy, hypercalcaemia, impact on organs (kidneys, heart, brain, liver, spleen).

A

Sarcoidosis.

128
Q

CXR: bilateral hilar lymphadenopathy, lung infiltrates.

Histology shows non-caseating granuloma.

A

Sarcoidosis.

129
Q

Treatment of the chronic form of the condition requires steroids & immunosuppression e.g. azathioprine, methotrexate and anti-TNF therapy.

CXR and pulmonary function should be monitored for several years.

A

Sarcoidosis.

130
Q

Occurs in right-sided endocarditis, infected DVT and septicaemia.

Common in IV drug users who inject into the groin -> DVT + infection.

A

Septic emboli, i.e. PE + abscess.

131
Q

typically occurs following 15-20 years of quartz exposure, e.g. miners & glass workers.

Simple: CXR egg-shell calcification of hilar nodes.
Chronic: restrictive PFT pattern & pulmonary fibrosis.

A

Silicosis.

132
Q

Occurs due to the relaxation of pharyngeal dilator muscles during sleep, causing the upper airway to narrow and turbulent airflow. Results in vibration of the soft palate and tongue base.

A

Snoring

133
Q

Condition caused by mycobacterium tuberculosis, an acid-alcohol-fast-bacilli, with a thick waxy coat.

Usually develops into latent infection, with only 10% causing immediately active infection.

A

Tuberculosis.

134
Q

Delayed type IV hypersensitivity reaction. Caseating granulomas with necrosis. Condition which usually affects the upper lobes.

A

Tuberculosis.

135
Q

Closely associated with HIV, all HIV patients should be offered a test to check for this disease, and all patients with this disease should be offered a HIV test.

A

Tuberculosis.

136
Q

Reactivation of this latent disease may be caused by steroids or use of immunosuppressants.

Imumunity and hypersensitivity occur, sometimes together.
Immunity: T-cell responds by enhancing macrophage ability to kill mycobacteria.
Hypersensitivity: T-cell responds by causing granulomatous inflammation, tissue necrosis & scarring.

A

Tuberculosis.

137
Q

Cough, chest pain, haemoptysis, weakness/fatigue, weight loss, fever, chills & night sweats.

Crackles in upper zones.

A

Tuberculosis.

138
Q

Investigation of this disease involves: microscopy of sputum/tissue (ZN stain, mycobacterium stain pink/red).

Histological: may see multi-nucleate giant cell granulomas, caseating necrosis, possible visible mycobacteria.

A

Tuberculosis

139
Q

to test for previous exposure, you can use interferon gamma release assay or mantoux (tuberculin) skin test.

A

Tuberculosis.

140
Q

CXR: dense consolidation of upper lobe(s), cavity formation, tissue destruction, scarring, shrinkage and healing with calcification.

A

Tuberculosis.

141
Q

Treatment of this condition involves 2 months of rifampicin + isoniazid + pyrazinamide + ethambutol. Followed by 4 months of rifampicin and isoniazid.

Note: rifampicin and isoniazid may disturb liver function.

A

Tuberculosis

142
Q

you should avoid injecting steroids into solitary arthritic joint without first confirming it is not which disease?

A

Tuberculosis

143
Q

Headaches, drowsiness, fits, abdo. pain, back pain.

Signs: bowel obstruction/perforation, peritonitis, spinal deformity, paraplegia, lymphadenopathy, cold abscess formation (pus w/o pain or inflammation).

A

Tuberculosis

144
Q

Coryza, pharyngitis, sinusitis and epiglottitis are all examples of what?

A

URT conditions.

145
Q

Caused by bordetella pertussis, a gram -ve coccobacillus.

A

Whooping cough (pertussis)/ acute tracheobronchitis.

146
Q

Cold-like symptoms, paroxysmal coughing, violent exhalations, inspiratory “whoop” and vomiting.

A

Pertussis

147
Q

Headaches, confusion, thirst & constipation.

Common sign of cancer.

A

Hypercalcaemia.

148
Q

CO2 retention.

CO2 retention headache: characteristically on wakening, doesn’t change with posture, feels like a thick head, similar to a hangover. May feel drowsy/dizzy, increased HR and BP, sweaty.

A

Hypercapnia.

149
Q

Altered mental state, cyanosis, dyspnoea, tachypnoea, arrhythmias. May arise as a result of what?

A

Hypoxaemia.

150
Q

If you were to give a patient with this condition high concentrations of inspired oxygen, they would quickly develop hypercapnia and become acidotic.

A

Chronic Type 2 respiratory failure COPD patients - sensitive to high conc. of inspired oxygen.

151
Q

The abnormal collection of fluid in the pleural space, secondary to another disease.

A

Pleural effusion.

152
Q

straw-coloured pleural effusion suggests?

A

Cardiac failure or hypoalbuminaemia

153
Q

Bloody pleural fluid suggests?

A

trauma, malignancy, infection or infarction.

154
Q

Milky/turbid pleural fluid suggests?

A

empyema or chylothorax

155
Q

Foul smelling pleural fluid suggests?

A

Anaerobic empyema

156
Q

Food particles present in pleural effusion suggests?

A

Oesophageal rupture.

157
Q

Which type of pleural effusion?
Protein <30g/l. May arise due to HF, liver cirrhosis, hypoalbuminaemia, atelectasis, peritoneal dialysis and hypoproteinaemia.

A

Transudate

158
Q

Which type of pleural effusion?
Protein >30g/l. May arise due to malignancy, infection inc. TB and pneumonia, malignancy, pulmonary infarct, asbestos & connective tissue disease.

A

Exudate

159
Q

LVF, PTE, drugs & systemic pathology produce which type of pleural effusion?

A

Bilateral pleural effusion.

160
Q

The presence of lymphocytes in recently developed pleural effusion is suggestive of what?

A

Tuberculosis or malignancy, BUT any long-standing effusion will eventually become lymphocytic.

161
Q

The presence of neutrophils in pleural effusion is suggestive of what?

A

An acute process, e.g. trauma.

162
Q

How would you treat pleural effusion due to left ventricular failure?

A

diuretics.

163
Q

How would you treat pleural effusion due to infection?

A

Drain, antibiotics, possibly surgery.

164
Q

How would you treat pleural effusion due to malignancy?

A

Drain, pleurodesis & a long term pleural catheter.

165
Q

A coarse audible wheeze due to difficulty inhaling. Worrying as it is a possible symptom of cancer.

A

Stridor.

166
Q

Predominantly an inspiratory wheeze due to obstruction of large airways (larynx/trachea/major bronchi).
Main causes in children: infection, foreign body inhalation, anaphylaxis/angioneurotic oedema, burn etc.

A

Stridor.

167
Q

Predominantly an inspiratory wheeze due to obstruction of large airways (larynx/trachea/major bronchi).
Main causes in adults: neoplasm, goitre, trauma, bilateral vocal cord palsy etc.

A

Stridor.

168
Q

Anaemia, emphysema, ILD, pulmonary oedema, bronchiectasis, pulmonary emboli and any other condition affecting alveolar surface area all have what effect on TLCO?

A

TLCO = transfer carbon monoxide factor (describes extent to which oxygen may pass from the air sacs of the lungs, into the blood.

They may reduce it.

169
Q

Forced expiratory flow rate (spirometry) is an example of what?

A

Effort dependent pulmonary function tests.

170
Q

Relaxed vital capacity (spirometry) is an example of what?

A

Effort independent pulmonary function tests.

171
Q

Whole body plethysmography is an example of what?

A

Effort independent pulmonary function tests.

172
Q

Impulse oscillometry is an example of what?

A

Effort independent pulmonary function tests.

173
Q

Exhaled breath nitric oxide is an example of what?

A

Effort independent pulmonary function tests.

174
Q

Helium/N2 washout static lung volumes is an example of what?

A

Effort independent pulmonary function tests.

175
Q

Volume dependent expiratory airway closure diseases, producing graphs of normal shape, but reduced magnitude.

A

Asthma and chronic bronchitis.

176
Q

Pressure dependent expiratory airway closure disease. Expiratory flow volume curve is more rounded and significantly reduced in comparison to the normal curve.

A

Emphysema

177
Q

The volume of air forcibly exhaled in one second following a full inspiration.

A

Forced expiratory volume in 1 second (FEV1)

178
Q

Whole body plethysmography and impulse oscillometry are methods of measuring what?

A

Airway resistance.

179
Q

Maximum speed of expiration measured with a peak flow meter. Measures airflow through the bronchi & thus the degree of airway obstruction.

A

Peak expiratory flow rate (PEFR).

180
Q

Analyses tissue uptake of glucose causing tissues with high metabolic activity to light up. Assesses function rather than structure.

A

PET scan

181
Q

Pulmonary function gas diffusion tests (there are 3)?

A
  1. CO transfer factor.
  2. ABGs at rest.
  3. SaO2 during exercise
182
Q

Which muscarinic (cholinergic) receptors enhance cholinergic transmission?

A

M1

183
Q

Which muscarinic (cholinergic) receptors inhibit acetyl choline release?

A

M2

184
Q

Which muscarinic (cholinergic) receptors mediate bronchoconstriction & mucus secretion?

A

M3

185
Q

Where are the cell bodies of postganglionic fibres found in the respiratory system?

A

Embedded in the walls of the bronchi & bronchioles.

186
Q

Stimulation of parasympathetic postganglionic cholinergic fibres causes bronchial smooth muscle contraction mediated by which muscarinic receptors and where?

A

M3 muscarinic ACh receptors on airway smooth muscle cells.

187
Q

Stimulation of parasympathetic postganglionic cholinergic fibres causes increased mucus secretion mediated by which muscarinic receptors?

A

M3 muscarinic ACh receptors on goblet cells.

188
Q

Phosphorylation of MLC in the presence of elevated intracellular Ca2+ and ATP causes what?

A

Smooth muscle contraction.

189
Q

De-phosphorylation of MLC by myosin phosphatase causes what?

A

Smooth muscle relaxation.

190
Q

Substance composed of phospholipids and apo-proteins. A deficiency results in atelectasis & impaired gas exchange. Its production is stimulated by steroids,

A

Pulmonary surfactant.

191
Q

Sympathetic stimulation causes bronchial smooth muscle relaxation via which adrenoceptors and where?

A

B2-adrenoceptors of airway smooth muscle cells.

192
Q

What is the transmitter that causes bronchial smooth muscle relaxation and what releases it?

A

Adrenaline. The adrenal gland.

193
Q

What impact does sympathetic stimulation have upon mucus secretion? What are its receptors and where?

A

Decreased mucus secretion. B2-adrenoceptors of goblet cells.

194
Q

What impact does sympathetic stimulation have upon mucociliary clearance? What are its receptors and where?

A

Increased mucociliary clearance. B2-adrenoceptors of airway epithelial cells.

195
Q

What effect does sympathetic stimulation have upon vascular smooth muscle contraction?

A

Increases vascular smooth muscle contraction (a1-adrenoceptors of vascular smooth muscle cells).

196
Q

Loratidine, cetirizine and fexofenadine are example of what?

A

Anti-histamines (H1 receptor antagonists). May be orally or nasally administered.

197
Q

What is the purpose of anti-histamines?

A

To reduce the effects of mast cell derived histamine.

198
Q

Omalizumab is an example of what?

A

Anti-IgE/ humanised monoclonal IgE antibodies. EXPENSIVE.

199
Q

What are anti-IgE antibodies used for?

A

Severe eosinophilic asthma.

200
Q

How do anti-IgE antibodies work?

A

They suppress the mast cell response to allergens, require IV administration.

201
Q

Mepolizumab and reslizumab are examples of what?

A

Anti-IL5.

202
Q

what are anti-IL5 used for?

A

Inhibiting eosinophilic inflammation in asthma. Used in treating severe refractory asthma that perseveres despite max. therapy. They reduce exacerbations & are steroid sparing.

203
Q

How are anti-IL5 administered?

A

Injection every 4 weeks.

204
Q

Salbutamol is an example of what?

A

Short acting B2-agonist

205
Q

Salmeterol, formeterol and the combination inhalers symbicort and seratide are examples of what?

A

Long acting B2-agonist

206
Q

Substances which act as antagonists of smasmogens, causing airway smooth muscle relaxation and relieving bronchospasm.

A

B2-adrenoceptor agonists.

207
Q

When would Salbutamol be used in the treatment of asthma?

A

First line in mild intermittent asthma.

208
Q

These act rapidly to relax bronchial smooth muscle and have maximal effect within 30 minutes, which persists for 3-5hours. They increase mucus clearance and decrease mediator release from mast cells and monocytes.

A

SABA e.g. salbutamol.

209
Q

These are used in nocturnal asthma. They should never be used alone, but in combination with a glucocorticoid.

A

LABA e.g. salmeterol and formeterol or combo. inhalers.

210
Q

What is the brown inhaler? What is it used for?

A

Beclometasone diproprionate. Used in preventing an attack of asthma.

211
Q

What is the blue inhaler? What is it used for?

A

Ventolin i.e. salbutamol. Used for relief in an attack.

212
Q

Sodium cromoglycate is an example of what?

A

A cromoglycate.

213
Q

When are cromoglycates used?

A

Prophylactically in allergic asthma in children.

214
Q

Why are cromoglycates not commonly used?

A

They are capable of reducing both phases of an asthma attack, but efficacy can take weeks to develop and they require frequent dosing.

215
Q

Oral montelukast and zafirlukast are examples of what?

A

CysLT1 (cysteinyl leukotriene) / leukotriene receptor antagonists

216
Q

When are leukotriene receptor antagonists used?

A

As add on therapy in bronchospasm of mild, persistent asthma. They may be used in combination, e.g. with ICS in more severe asthma.

217
Q

Side effects of leukotriene receptor antagonists?

A

Headaches and GI upset.

218
Q

How do leukotriene receptor antagonists work?

A

CysLTs are derived from mast cells and eosinophils (inflammatory cells) which cause smooth muscle contraction, mucus secretion and oedema. LTRA act as competitors at the CysLT1 receptor to block them, relaxing bronchial smooth muscle.

219
Q

How do leukotriene receptor antagonists work in rhinitis?

A

Reduces CysLTs effects on nasal mucosa.

220
Q

This tuberculosis drug may cause optic neuritis.

A

Ethambutol.

221
Q

Beclometasone, budesone and fluticasone are examples of what?

A

Glucocorticoids/corticosteroids that can be used as maintenance monotherapy anti-inflammatory drugs in asthma.

222
Q

Use of glucocorticoids/corticosteroids in asthma?

A

Efficacy develops over several days, to resolve & prevent inflammation. Can be used as effective long-term treatment options (+LABA) in mild/moderate asthma as preventers.

223
Q

Use of glucocorticoids/corticosteroids in eosinophilic COPD exacerbations?

A

May be used in combination with a LABA to reduce eosinophilic COPD exacerbations.

224
Q

Why does prednisolone differ from the other glucocorticoids/corticosteroids?

A

It has a low therapeutic ratio and should not be used as maintenance monotherapy in asthma, but in acute exacerbations only (also severe chronic).

225
Q

Side effects of corticosteroids?

A

Dysphonia and oropharyngeal candidiasis.

226
Q

Why is cortisol itself not used in asthma?

A

IT has no direct bronchodilator effects, so is ineffective at relieving acute bronchospasm, therefore synthetic derivatives, i.e. corticosteroids, are used instead.

227
Q

How do corticosteroids work?

A

Reduce production of TH2 cytokines and mast cells, prevent Ig production and Fc expression. Also prevent allergen influx into the lungs.

228
Q

Steroids, azathioprine, methotrexate, monoclonal antibodies (e.g. infliximab) are examples of what?

A

Immunosuppressants.

229
Q

Oral theophylline and aminophylline are examples of what?

A

Methylxanthines.

230
Q

What is the purpose of methylxanthines?

A

They are bronchodilators and anti-inflammatories, used 2nd line in asthma in combo. with B2-adrenoceptor agonist & glucocorticoids.

231
Q

How do methylxanthines work?

A

Inhibitor mediator release from mast cells, increase mucus clearance & diaphragmatic contractility. They also reduce fatigue and are thought to potentiate the anti-inflammatory action of glucocorticoids.

232
Q

Side effects of methylxanthines?

A

hypotension, dysrhythmias, seizures, nausea, vomiting, abdo. discomfort and headaches.

233
Q

Methylxanthines have numerous drug interactions, but with which group of antibiotics in particular?

A

Those that inhibit CYP450s.

234
Q

Enzyme responsible for phosphorylation of dephosphorylated MLC.

A

Myosin light chain kinase.

235
Q

Oral carbocisteine and erdosteine are examples of what?

A

Mucolytics.

236
Q

What are mucolytics used for?

A

Reducing sputum viscosity and aiding sputum expectoration. They reduce COPD exacerbations.

237
Q

Which type of muscarinic cholinergic receptors do muscarinic antagonists block?

A

M3

238
Q

Function of muscarinic antagonists?

A

To relax bronchial smooth muscle and reduce mucus secretion.

239
Q

Ipratropium is an example of what?

A

A short acting muscarinic antagonist.

240
Q

Ipratropium should not be used in conjunction with what?

A

A long acting muscarinic antagonist. It is non-selective.

241
Q

Tiotropium, aclidinium and glycopyrronium are examples of what?

A

Long acting muscarinic antagonists.

242
Q

What type of muscarinic antagonist would be used in acute asthma/COPD?

A

High nebulised doses of ipratropium.

243
Q

what muscarinic antagonist might be used in rhinitis and why?

A

Ipratropium, stops mucus secretion when administered nasally but can dry out nasal membranes.

244
Q

Tuberculosis antibiotic which colours bodily fluids orange.

A

rifampicin

245
Q

Tuberculosis antibiotic that is a potent inducer of cytochrome enzymes, e.g. hormonal contraception.

A

Rifampicin

246
Q

Stony dull to percussion

A

pleural effusion

247
Q

right sided pleuritic chest pain

A

probably pneumonia

248
Q

ground glass appearance on CXR

A

pulmonary fibrosis or neonatal respiratory distress syndrome

249
Q

positive Ziehl-Neelsen stain for acid fast bacilli

A

tuberculosis

250
Q

Caseous necrosis (caseating granulomas with necrosis)

A

tuberculosis

251
Q

Fever, night sweats, anorexia, haemoptysis

A

tuberculosis

252
Q

Apical disease

A

Secondary tuberculosis

253
Q

What is an apical lesion called?

A

Assman focus

254
Q

military tuberculosis is spread via the?

A

bloodstream

255
Q

Military tuberculosis spread via the pulmonary artery deseminates to where?

A

The lung

256
Q

Military tuberculosis spread via the pulmonary vein deseminates to where?

A

Liver, spleen and kidneys.

257
Q

+ve anti-GBM antibodies.

A

Indicator of Goodpasture’s syndrome.

258
Q

Chest infection with a parrot/pigeon as a pet.

A

Chlamydia psittaci

259
Q

mucoid sputum

A

probably Chlamydia psittaci

260
Q

Dry cough, diarrhoea after holiday abroad, some indication of water spread.

A

Legionella pneumonia

261
Q

Tall, thin young man who indulges in marijuana.

A

Probably pneumothorax.

262
Q

Mr. Martin Mitchell/Mr. Snoop Dogg

A

Probably pneumothorax.

263
Q

Bilateral hilar lymphadenopathy

A

Sarcoidosis

264
Q

Erythema nodosum, non-caseating granulomas, fatigue, uveitis and weight loss

A

Sarcoidosis

265
Q

Increased serum ACE and Ca2+

A

Sarcoidosis

266
Q

Signet ring sign

A

bronchiectasis

267
Q

Bronchiole wider than the neighbouring arteriole on CT

A

bronchiectasis

268
Q

D sign on x-ray

A

Empyema

269
Q

Steeple sign on x-ray

A

Croup/laryngotracheobronchitis

270
Q

Child with barking cough

A

croup/laryngotracheobronchitis

271
Q

Pneumocystis pneumonia is a red flag for?

A

HIV

272
Q

Treatment of Pneumocystis pneumonia

A

Co-trimoxazole

273
Q

asthma + nasal polyps + salicylate sensitivity

A

Samter’s Triad: aspirin exacerbated respiratory disease/aspirin sensitive asthma

274
Q

Alcoholic pneumonia (Aspiration)

A

Klebsiella

275
Q

Red jelly sputum

A

Klebsiella pneumonia

276
Q

Rusty sputum

A

Pneumococcal pneumonia

277
Q

Cannonball metastases + weight loss + haematuria.

A

Primary renal cell carcinoma

278
Q

morning headache

A

hypercapnia or side effects of organic nitrates

279
Q

ACTH secreting lung tumour

A

Small cell carcinoma

280
Q

PTH secreting lung tumour

A

Squamous cell carcinoma

281
Q

Eggshell calcification of hilar region

A

silicosis

282
Q

infection & caseous necrosis at lung periphery, beneath the pleura. Found in TB infection.

A

Ghon focus.

283
Q

Heart failure cells seen in alveolar spaces (absorbed macrophages)

A

Haemosiderin

284
Q

Occurs due to cancer spread to intrathoracic nodes/pancoast’s tumour

A

Horner’s syndrome

285
Q

Thumb-print sign on head X-ray

A

Epiglottitis

286
Q

Inspiratory whoop/barking cough

A

Pertussis/whooping cough

287
Q

snow-storm appearance on x-ray

A

baritosis or silicosis

288
Q

non-smoker + lung cancer

A

adenocarcinoma

289
Q

Location of squamous/small cell lung cancers

A

central

290
Q

High D-dimers

A

Suspect PE, send for CTPA or V/Q scan.

291
Q

Large PE treatment

A

thrombolysis

292
Q

Small PE treatment

A

low molecular wt. heparin

293
Q

Low D-dimers

A

exclude PE

294
Q

CXR: alveolar bat wings, Kerley B lines, cardiomegaly, dilated prominent upper lobe vessels.

A

pulmonary oede

295
Q

Hyper expanded chest

A

COPD

296
Q

Stridor

A

upper airway obstruction

297
Q

early onset emphysema

A

alpha-1-antitrypsin deficiency

298
Q

Positive sweat test >60mmol/L NaCl

A

cystic fibrosis

299
Q

swinging fever, copious and foul smelling sputum

A

lung abscess

300
Q

tuberculosis drug causing gout

A

pyrazinamide

301
Q

tuberculosis drug causing hearing problems

A

streptomycin

302
Q

tuberculosis drug causing peripheral neuropathy or hepatitis.

A

Isoniazid

303
Q

Acute management of asthma

A

OSHITMAN

OXYGEN
SALBUTAMOL
HYDROCORTISONE IV or PREDNISOLONE po
IPRATROPIUM BROMIDE nebulised hourly
THEOPHYLLINE or AMINOPHYLLINE IV
MAGNESIUM + call an ANAESTHETIST
304
Q

Acute management of COPD

A

iSOAP

IPRATROPIUM
SALBUTAMOL
OXYGEN
AMOXICILLIN
PREDNISOLONE

General (24 decks)

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