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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is…

i) FEV1?
ii) FVC?

and give the normal values for both.

A

i) Forced expiratory volume in 1 second, max inspiration + exhale as fast as possibly, ≥80% predicted.
ii) Forced vital capacity, total volume of air forcible expired.

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2
Q

What is the pleura? What are the two components to it?

A
  • Double membrane which surrounds the lungs.
  • Parietal = contact with chest wall.
  • Visceral = contact with the lungs.
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3
Q

What are the functions of the pleura?

A
  • Visceral pleura produces + reabsorbs pleural fluid (proteins, mesothelial cells, monocytes, lymphocytes).
  • Allows movement of lung against chest wall.
  • Cushioning.
  • Lubrication.
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4
Q

Is FEV1 or FVC a better assessment of lung health? What are the abnormal values?

A
  • FEV1 is more reproducible.

- FEV1 or FVB < 80% predicted.

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5
Q

What is the FEV1/FVC ratio and what can it show?

A
  • Proportion of FVC exhaled in 1st second.
  • FEV1/FVC < 0.7 = airway OBSTRUCTION.
  • FEV1/FVC > 0.7 = airway RESTRICTION with FEV1 + FVC being low respectively.
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6
Q

Give examples of obstructive + restrictive respiratory diseases.

A

Obstructive…
- Asthma (variable airflow obstruction, reversible).
- COPD (fixed airflow obstruction).
- Bronchiectasis.
Restriction…
- Means lung volumes are small + most breath out in first second like interstitial lung disease (fibrosis + sarcoidosis).

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7
Q

What is type 1 + 2 respiratory failure? Give examples.

A 
Type 1 = 1 change.
- PaO2 low, PaCO2 low/normal.
- Pulmonary embolism (V/Q mismatch).
Type 2 = 2 changes.
- PaO2 low, PaCO2 high
- Hypoventilation.
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8
Q

What would the ABG results for pH, CO2 + HCO3- be in somebody with…

i) Respiratory acidosis.
ii) Respiratory alkalosis.
iii) i) with metabolic compensation
iv) ii) with metabolic compensation

A

i) Low, high, normal.
ii) High, low, normal.
iii) Normalising, high, high.
iv) Normalising, low, low.

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9
Q

COPD

What is chronic obstructive pulmonary disease (COPD)?

A
  • Common progressive disorder characterised by airway obstruction with poor reversibility.
  • It includes chronic bronchitis + emphysema.
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10
Q

COPD

What is the pathophysiology of emphysema?

A
  • Destruction of lung tissue distal to terminal bronchioles cause a loss of elastic recoil which usually allows airways to remain open following expiration so there is air trapping.
  • There is inability to oxygenate + so hyperventilation.
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11
Q

COPD

What is the pathophysiology of chronic bronchitis?

A
  • Exposure to irritants/chemicals (smoke) leads to hypertrophy + hyerplasia of mucous secreting glands in bronchial tree + excess mucous causing an obstruction.
  • Neutrophil + macrophage involvement + increased inflammatory mediators leading to bronchial wall becoming inflamed.
  • Less oxygen can get into alveoli + less carbon dioxide can get out + so V/Q mismatch > hypoxia (cyanosis).
  • Obstruction causes increasing residual lung volume (bloating).
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12
Q

COPD

How can cor pulmonale develop in chronic bronchitis?

A
  • Capillary bed intact + compensatory vasoconstriction which increases CO in attempt to shunt blood to better ventilated alveoli leads to pulmonary HTN > RHF (oedema) > cor pulmonale.
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13
Q

COPD

What protease inhibitor can be inactivated by smoke?

A
  • Alpha-1-antitrypsin + this can lead to emphysema.
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14
Q

COPD

What are the pink puffers + blue bloaters?

A

Pink puffers (emphysema)…
- Have increased alveolar ventilation with a near normal PaO2 + normal/low PaCO2.
- They are breathless but not cyanosed, dyspnoea main issue.
Blue bloaters (chronic bronchitis)…
- Decreased alveolar ventilation with low PaO2 + high PaCO2.
- Cyanosed but not breathless.
- Respiratory centres are relatively insensitive to CO2 + so rely on hypoxic drive to maintain respiratory effort – hypoventilation main issue.

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15
Q

COPD

What is the aetiology of COPD?

A
  • Generall older presentation with no variation in their symptoms.
  • Smoking.
  • Occupational irritans.
  • Alpha-1-antitrypsin deficiency (early-onset emphysema).
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16
Q

COPD

What are the symptoms of COPD?

A
  • Chronic cough.
  • Sputum.
  • Dyspnoea.
  • Fatigued.
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17
Q

COPD

What are the signs of COPD?

A
  • Tachypnoea.
  • Use of accessory muscles of respiration (sternocleidomastoid, scalene muscles).
  • Hyperinflated barrel shaped chest.
  • Wheeze (expiration due to narrowed airways).
  • Thin with loss of muscle mass (unable to exercise).
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18
Q

COPD

What is the diagnostic criteria for chronic bronchitis?

A
  • Cough + sputum production on most days for 3 months of 2 successive years.
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19
Q

COPD

What are the investigations for COPD?

A 
Spirometry...
- Obstructive + air-trapping. FEV1 < 80%, FEV1/FVC < 0.7
CXR...
- Hyper-inflated lungs with reduced peripheral lung markings.
CT chest...
- Bronchial wall thickening.
- Scarring
- Air space enlargement.
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20
Q

COPD

What are the non-pharmacological treatments for COPD?

A
  • Smoking cessation, keep healthy (reduced infection risk).

- Pulmonary rehabilitation to increase exercise capacity + improve general wellbeing.

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21
Q

COPD

What is the pharmacological treatment for COPD?

A 
1st line...
- SABA like salbutamol OR SAMA like ipratropium.
2nd line...
- LABA like salmeterol.
3rd line...
- LAMA like tiotropium.
4th line...
LABA + inhaled corticosteroid like beclometasone (ICS) ± LAMA.
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22
Q

COPD

What is the treatment for acute exacerbations of COPD?

A
  • Oxygen therapy (88–92%)
  • LABA/LAMA/ICS.
  • Systemic steroids (prednisolone.
  • Abx if dyspnoea + sputum production.
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23
Q

ASTHMA

What is asthma and what is it characterised by?

A

A restrictive obstruction of airways + an inflammatory disease characterised by…

  • Airflow obstruction (usually reversible spontaneously or with treatment).
  • Airway hyper-reactivity to variety of stimuli.
  • Bronchial inflammation with inappropriate smooth muscle contraction.
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24
Q

ASTHMA

What are the histological changes in asthma?

A
  • Basement membrane thickening.
  • Epithelium metaplasia leading to increased goblet cells + mucous hypersecretion.
  • Increase in inflammatory gene expression on many cell types.
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25
Q

ASTHMA

What cells are increased in the bronchial wall + mucous membranes in asthma?

A
  • Mast cells, eosinophils, T lymphocytes + neutrophils.
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26
Q

ASTHMA

What is the pathophysiology of allergic asthma?

A
  • Allergen is inhaled + IgE binds to mast cells causing vasoactive substances like histamine to be released causing bronchoconstriction, oedema, bronchial inflammation + mucous hypersecretion.
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27
Q

ASTHMA

What is the aetiology of asthma?

A

Allergic (extrinsic), eosinophilic…
- Allergens + atopy, often accompanied by eczema.
- Type 1 hypersensitivity IgE mediated (mast cells).
Non-allergic (intrinsic), non-eosinophilic…
- Idiopathic but triggers.
- Exercise, cold air + stress.

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28
Q

ASTHMA

What is the epidemiology of asthma?

A
  • Commonly starts in childhood 3–5y/o.
  • May either worsen/improve during adolescence.
  • Non-allergic often presents middle-aged.
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29
Q

ASTHMA

What exacerbating factors + occupational risks are there with asthma?

A
  • Cold air, exercise, stress, smoking (passive too), beta-blockers, aspirin can all exacerbate.
  • Paint sprays (fume exposure, animal handlers + welders.
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30
Q

ASTHMA

How can asthma be differentiated to COPD?

A
  • COPD is a later disease, predominately of smokers, more relentless progressive dyspnoea, less diurnal variation.
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31
Q

ASTHMA

What are the symptoms of asthma?

A
  • Intermittent dyspnoea.
  • Wheeze.
  • Cough (often nocturnal).
  • Diurnal variation (symptoms worse in morning).
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32
Q

ASTHMA

What are the signs of asthma?

A
  • Tachypnoea.
  • Audible wheeze.
  • Hyperinflated chest.
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33
Q

ASTHMA

What is the diagnostic criteria for acute severe asthma?

A
  • RR>25.
  • HR>110.
  • PEFR 35–50% predicted.
  • Cannot complete sentence in one breath.
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34
Q

ASTHMA

What are the investigations for asthma?

A

Bloods – FBC for eosinophils.
Lung functional tests…
- PEFR tests reversibility.
- Obstructive pattern FEV1 < 80%, FEV1/FVC < 0.7
Skin prick tests to identify allergic triggers, test atopy.
CXR – distinguish from other factors.

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35
Q

ASTHMA

What does Peak Expiratory FLow Rate (PEFR) test and how?

A
  • Reversibility.
  • Diary of measurements on waking before bronchodilators + before bed after bronchodilator.
  • Should show diurnal variation.
  • Diagnosis by >15% improvement in FEV1/PEFR following bronchodilator.
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36
Q

ASTHMA

What are the RCP3 questions for?

A

Testing severity…

  • Recent nocturnal waking?
  • Usual asthma symptoms during day?
  • Interference with ADLs?
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37
Q

ASTHMA

What is the treatment for acute severe asthma?

A
  • Nebulised salbutamol w/ oxygen.

- IV corticosteroids + Abx if infection.

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38
Q

ASTHMA

What is the lifestyle advice for asthma?

A
  • Stop smoking.
  • Avoid allergens + stress.
  • Keep healthy.
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39
Q

ASTHMA

What is the aim of asthma treatment?

A
  • Stepped approach to control disease so no day/night symptoms, no exacerbations + normal lung functions (FEV1 or PEFR ≥ 80%).
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40
Q

ASTHMA

What is the medical treatment for asthma?

A 
1st line = SABA like salbutamol.
2nd line = ICS (low dose) like beclometasone.
3rd line = LABA like salmeterol.
4th line = increase ICS dose.
5th line = oral prednisolone.
Hospitalisation.
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41
Q

LUNG CARCINOMAS

What are the two main types of lung carcinomas?

A
  • Non-small cell lung carcinomas (NSCLC)

- Small-cell lung carcinomas. (SCLC).

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42
Q

LUNG CARCINOMAS

What are the different types of NSCLC?

A

Squamous…
- Most present as obstructive lesion > infection.
- Ocassionally cavitates, commonly has local spread with widespread metastases.
Adenocarcinoma…
- Local + distant metastases.
Large cell…
- Poorly differentiated, metastases.

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43
Q 
LUNG CARCINOMAS
What type of NSCLC...
i) more common with non-smokers?
ii) strongly associated with smokers?
iii) strongly associated with asbestos exposure?
A

i) Adenocarcinoma.
ii) Squamous.
iii) Adenocarcinoma.

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44
Q

LUNG CARCINOMAS

What is the pathophysiology of SCLC?

A
  • Referred to as oat cell.
  • Arise from Kulchitsky (endocrine) cells.
  • Often secretes polypeptide hormones resulting in paraneoplastic syndromes.
  • Grows rapidly, highly malignant, metastases, worst prognosis.
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45
Q

LUNG CARCINOMAS

What is the aetiology of lung carcinomas? What is the 5 year lung cancer survival rate + why?

A
  • Smoking.
  • Occupational (asbestos/radon/coal tar/chromium).
  • 5 year lung cancer survival rate 8–10% as people often present late so treatment limited.
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46
Q

LUNG CARCINOMAS

What are the symptoms as a result of local effect of lung carcinoma?

A
  • Cough.
  • Haemoptysis.
  • Dyspnoea.
  • Chest pain.
  • Recurrent/slowly resolving chest infections.
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47
Q

LUNG CARCINOMAS

What are the symptoms as a result of metastases of lung carcinoma?

A
  • Bone tenderness.
  • Hepatomegaly.
  • Neurological deficit like seizures, headache, confusion.
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48
Q

LUNG CARCINOMAS

What are the local complications due to lung carcinomas?

A
  • Left recurrent laryngeal nerve palsy = hoarse voice.
  • Spread to brachial plexus = shoulder/arm pain.
  • Spread to sympathetic ganglion = Horner’s syndrome.
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49
Q

LUNG CARCINOMAS

What paraneoplastic changes can occur in SCLC?

A
  • PTH, ACTH, ADH secretion leading to, Cushing’s syndrome, SiADH.
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50
Q

LUNG CARCINOMAS

What is the treatment for NSCLC?

A
  • Lobectomy (open or thoracoscopic) with curative intent.
  • Radical radiotherapy.
  • Chemotherapy ± radiotherapy if more advanced.
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51
Q

LUNG CARCINOMAS

What is the treatment for SCLC?

A
  • Surgery with limited stage disease.
  • Chemotherapy ± radiotherapy if well enough if not palliative radiotherapy.
  • Supportive measures = endobronchial therapy like tracheal stenting to treat airway narrowing, analgesia, steroids, anti-emetics.
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52
Q

PULMONARY EMBOLISM

What is the pathophysiology of PE?

A
  • Venous thrombi, usually from DVT (iliofemoral vein common) pass into the pulmonary circulation + block blood flow to the lungs.
  • Thromboembolism blocks the RV outflow + so suddenly increases pulmonary vascular resistance > acute RHF.
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53
Q

PULMONARY EMBOLISM
What are the consequences of..
i) small-medium, peripheral PE?
ii) massive, central PE?

A

i) Impacts in a terminal, peripheral pulmonary vessel + may be clinically silent unless pulmonary infarction.
Lung tissue ventilated but not perfused leading to impaired gas exchange, alveolar dead space > infarction.
ii) Resistance to flow which can result in RHF, syncope, ischaemia + death.

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54
Q

PULMONARY EMBOLISM

What are the risk factors for PE?

A

Thrombotic…

  • Surgery, immobility, leg fracture.
  • Oral contraceptive, HRT, pregnancy.
  • Genetic predisposition (inherited thrombophilia).
  • Long haul flights = rare.
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55
Q

PULMONARY EMBOLISM

What is the preventing for PE?

A 
Mechanical...
- Hydration + early mobilisation.
- Compression stockings + foot pumps.
Chemical...
- LMWH.
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56
Q

PULMONARY EMBOLISM

What is the clinical presentation of small-medium PE?

A
  • Dypsnoea.
  • Pleuritic chest pain.
  • Haemoptysis if infarction.
  • May be tachypnoeic, pleural rub + exudative pleural effusion.
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57
Q

PULMONARY EMBOLISM

What is the clinical presentation of massive PE?

A
  • Severe central chest pain.
  • Pale + sweaty.
  • Shock.
  • Raised JVP, RV heave, tachypnoea.
  • Hypotensive + tachycardic.
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58
Q

PULMONARY EMBOLISM

What are the investigations for PE?

A

Revised Geneva score to predict probability of PE…
- If low, D-dimer > CT pulmonary angiogram if positive (diagnostic).
ABG shows Type 1 resp failure.
ECG may show sinus tachy, RBBB, S1Q3T3 (prominent S wave in lead I, Q wave + inverted T in lead III).
CXR shows decreased vascular markings + raised hemidiaphragm.
Echocardiogram diagnostic for massive PE + bedside test.

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59
Q

PULMONARY EMBOLISM

What is the treatment of PE?

A

Acute…
- Oxygen, analgesia, LMWH.
- Thrombolysis with alteplase if haemodynamically unstable.
Long-term…
- Anti-coagulation with DOAC like rivaroxaban/apixaban or warfarin (continue LMWH until INR >2)

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60
Q

PNEUMONIA

What is pneumonia?

A
  • Acute lower respiratory tract infection + when severe can lead to excessive inflammation, lung injury + failure to resolve.
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61
Q

PNEUMONIA

What is the pathophysiology of pneumonia?

A
  • Bacteria translocate to the normally sterile distal airway.
  • Resident host defence becomes overwhelmed.
  • Macrophages, chemokines + neutrophils produce an inflammatory response.
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62
Q

PNEUMONIA

What are the classifications of pneumonia?

A

Community-acquired…
- May be primary or secondary to underlying disease.
Hospital-acquired…
- Defined as >48h after hospital admission.
- Seen in elderly, ventilator associated + post-operative.
Aspiration…
- Acute aspiration of gastric contents into lungs.
- Seen in stroke, myasthenia + loss of consciousness.

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63
Q

PNEUMONIA

What are the common aetiologies of community acquired pneumonia?

A
  • Streptococcus pneumoniae, gram+ve cocci chain most common.
  • Haemophilus influenzae, gram-ve bacilli.
  • Enteric gram-negative bacilli like E.coli, klebsielle pneumoniae.
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64
Q

PNEUMONIA

What are the atypical aetiologies of community acquired pneumonia +

A

Associated with water cooler/air conditioner…

  • Mycoplasm pneumoniae.
  • Chlamydophila pneumoniae.
  • Legionella pneumophilia (Spain/Portugal).
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65
Q

PNEUMONIA

What are the aetiologies of hospital acquired pneumonia?

A
  • Gram-egative bacilli enterobacteria like pseudomonas aeruginosa, E.coli + klebsiella pneumoniae.
  • S. Aureus including MRSA.
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66
Q

PNEUMONIA

What are the precipitating + risk factors for pneumonia?

A
  • Smoking, alcohol abuse, underlying lung disease.

- Elderly + children, co-morbidities (DM, COPD, bronchiectasis), immunocompromised, nursing home residents.

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67
Q

PNEUMONIA

What type of pneumonia is most common in HIV patients?

A
  • Pneumocystis jiroveci pneumonia (PCP).
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68
Q

PNEUMONIA

What are the symptoms of pneumonia?

A
  • Purulent sputum – atypical = non-productive cough.
  • Haemoptysis.
  • Pleuritic chest pain.
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69
Q

PNEUMONIA

What are the signs of pneumonia?

A
  • Signs of lung consolidation (reduced expansion, dull percussion).
  • Tachypnoea/cardia.
  • Pyrexia.
  • Pleural rub.
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70
Q

PNEUMONIA

What are the complications with pneumonia?

A
  • Parapneumonic effusions + empyema (pockets of pus).
    Suspect if WCC/CRP don’t settle, pain on deep inspiration, pleural collection – drain.
  • Brain abscess.
  • Peri/myocarditis.
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71
Q

PNEUMONIA

What are the investigations for pneumonia?

A

Bloods – FBC (WCC raised), ESR/CRP raised, U+E.
Sputum + blood culture with antibiotic sensitivities, serology (atypicals).
Urinary antigen test.
CXR may show multi-lobar infiltrates, multiple abscesses, upper lobe cavity, pleural effusion.

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72
Q

PNEUMONIA

How is the severity of pneumonia assessed?

A

CURB-65…

  • Confusion.
  • Urea >7mmol/L.
  • Resp rate ≥30/min.
  • BP <90/60mmHg.
  • 65 ≤ age.
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73
Q

PNEUMONIA

How does CURB-65 determine how you treat pneumonia?

A 
0-1 = oral amoxicillin in the community.
2 = oral amoxicillin + clarithromycin in the hospital.
≥3 = IV co-amoxiclav + clarithromycin, consider ITU.
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74
Q

PNEUMONIA

What is the generic treatment for pneumonia?

A
  • Maintain oxygen sats.

- Analgesia like paracetamol/NSAIDs for pleuritic pain

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75
Q

PNEUMONIA

What are the specific antibiotic regimes for Legionella species pneumonia?

A
  • Fluoroquinolone like ciprofloxacin + clarithromycin.

- Inform Public Health England.

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76
Q

PNEUMONIA

What are the preventative measure for pneumonia?

A
  • Polysaccharide pneumococcal vaccine (PPV) for children.
  • Influenza vaccine for those ≥65y/o, immunocompromised or with medical co-morbidities.
  • Smoking cessation.
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77
Q

TUBERCULOSIS

What is the pathophysiology of TB?

A
  • Primary TB is caused by aerosol transmission of Mycobacterium tuberculosis where they are inhaled in the upper region of lung, often apex due to more air + less blood supply (so less immune cells).
  • Bacilli settle in the lung apex + macrophages + lymphocytes mount an effective immune response that encapsulates + contains the organism.
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78
Q

TUBERCULOSIS

What is the pathogenesis of TB?

A
  • Bacilli + macrophage combine to form a granuloma, the Ghon/primary focus.
  • The mediastinal lymph nodes enlarge, primary focus + mediastinal lymph nodes = Ghon complex.
  • As the granuloma grows, it develops into a cavity which is full of TB bacilli which are expelled when the patient coughs.
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79
Q

TUBERCULOSIS

What is the epidemiology of TB?

A

Majority cases in Africa/Asia (India, China).

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80
Q

TUBERCULOSIS

What are the risk factors for TB?

A
  • Living in high prevalence area.
  • IV drug users.
  • Homeless (immune stresses).
  • Alcoholics.
  • HIV +ve.
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81
Q

TUBERCULOSIS

What is the clinical presentation of TB?

A

Systemic…
- Weight loss, night sweats, anorexia, malaise.
Pulmonary…
- Cough (>3/52), chest pain, dyspnoea, haemoptysis.

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82
Q

TUBERCULOSIS

What is the natural history of TB?

A
  • Primary infection leads to primary or progressive primary disease (organ specific or disseminated).
  • Latent TB until post-primary disease (wherever dormant bacilli were hiding, often lung).
  • Re-infection leads to new disease with latent TB until death.
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83
Q

TUBERCULOSIS

What are the complications of TB?

A

Spread…

  • Bone + joints = pain + swelling.
  • Lymph nodes = swelling + discharge.
  • CNS = TB meningitis.
  • GU TB = haematuria, frequency.
  • Haematogenous dissemination = miliary TB.
84
Q

TUBERCULOSIS

What may a CXR show in TB?

A
  • Consolidation.
  • Collapse.
  • Pleural effusion.
85
Q

TUBERCULOSIS

What are the investigations for active + latent TB?

A

Active…
- Micrbiology with sputum culture (3x), Ziehl-Neelsen red if TB.
- Biopsy specimen.
- Histopathology caseating granuloma.
Latent…
- Tuberculin skin test ‘Mantoux’ (stimulates type 4 delayed hypersensitivity reaction).
- Interferon gamme release assays (IGRAs).

86
Q

TUBERCULOSIS

What is the treatment for TB?

A
  • Rifampicin (6m).
  • Isoniazid (6m).
  • Pyrazinamide (2m).
  • Ethambutol (2m).
  • NOTIFY PUBLIC HEALTH ENGLAND IMMEDIATELY.
87
Q

TUBERCULOSIS

What are the complications with TB drugs?

A
  • R= red urine, hepatitis + drug interactions as enzyme inducer.
  • I = hepatitis, neuropathy.
  • P = hepatitis, gout, rash.
  • E = optic neuritis.
88
Q

TUBERCULOSIS

Why is compliance so crucial in TB treatment? How can drug resistance occur?

A
  • Resistance + relapse likely.
  • TB treatment is 6m to ensure all dormant bacteria eradicated.
  • Drug resistance if previous treatment, live in high risk area, contact with resistant TB or poor response to therapy.
  • TB is more difficult to treat, medication course >20m + increased risk of side effects + relapse rate.
89
Q

TUBERCULOSIS

What is the prevention for TB?

A
  • Active case finding, reduce infectivity.
  • Detect + treat latent TB.
  • Vaccination – BCG.
90
Q

PHARYNGITIS/TONSILLITIS

What is the pathophysiology of pharyngitis/tonsillitis?

A
  • Both are infections in the throat that cause inflammation.

- If throat primarily affected it’s pharyngitis, if tonsils it’s tonsillitis.

91
Q

PHARYNGITIS/TONSILLITIS

What is the aetiology of pharyngitis/tonsillitis?

A
  • Viral = adenovirus (most common), rhinovirus, EBV.

- Bacteria = Streptococci pyogenes.

92
Q

PHARYNGITIS/TONSILLITIS

What is the clinical presentation of pharyngitis/tonsillitis?

A
  • Tender gland in neck.
  • Large tonsils with exudate.
  • Fever, sore throat.
  • Oropharynx + soft palate reddened.
93
Q

PHARYNGITIS/TONSILLITIS

What is the treatment of pharyngitis/tonsillitis?

A
  • Self-limiting, symptomatic treatment with rest, paracetamol.
  • Persistent/severe tonsillitis use phenoxymethylpenicillin.
94
Q

SINUSITIS

What is the pathophysiology + aetiology of sinusitis?

A
  • Infection of paranasal sinuses.

- Bacterial = streptococcus pneumoniae or haemophilus influenzae.

95
Q

SINUSITIS

WHHat is the clinical presentation + treatment of sinusitis?

A
  • Facial pain w/ tenderness, purulent rhinorrhoea, fever.

- Nasal decongestants + broad spectrum antibiotics like co-amoxiclav.

96
Q

EPIGLOTTITIS

What is the pathophysiology, clinical presentation + treatment for epiglottitis?

A
  • Inflammation of epiglottis due to haemophilus influenza B infection.
  • High fever, severe airflow obstruction, sore throat, inspiratory stridor.
  • Urgent endotracheal intubation + IV Abx.
97
Q

WHOOPING COUGH

What is the pathophysiology + aetiology of whooping cough?

A
  • Humans are the natural host + reservoirs of infection.

- Bordetella pertussis (gram-ve bacilli).

98
Q

WHOOPING COUGH

What is the clinical presentation + investigations for whooping cough?

A
  • Chronic cough, inspiratory ‘whoop’ through partially close vocal cords.
  • Culture of nasopharyngeal swab diagnostic on Bordet Gengou agar.
99
Q

WHOOPING COUGH

What is the treatment for whooping cough?

A
  • Prevention with vaccination – dTaP vaccine (8,12,16w + 3–4y/o).
  • Clarithromycin.
100
Q

CROUP

What is the pathophysiology of acute laryngotracheobronchitis (croup)

A
  • Acute larngitis is an occasional complication of URT infections, particularly those caused by parainfluenza viruses + measles.
  • Causes progressive airway obstruction due to inflammatory oedema.
  • Common in children.
101
Q

CROUP

What is the clinical presentation + treatment for croup?

A
  • Voice becomes hoarse with barking cough (croup), audible stridor.
  • Nebulised adrenaline short-term, corticosteroids.
102
Q

INFLUENZA

What is the pathophysiology of influenza?

A
  • Surface of virion coated with haemagglutinin (H) + neuraminidase (N) which are necessary for attachment to host respiratory epithelium.
  • Human immunity develops against H + N antigens.
  • Influenza A can undergo antigenic shift with major changes in the H/N antigens leading to pandemic infections.
  • Virus exists in two forms, A+B.
103
Q

INFLUENZA

What is the clinical presentation of influenza?

A
  • Abrupt onset of fever.
  • Generalised aching of limbs.
  • Severe headache, sore throat + dry cough.
104
Q

INFLUENZA

What are the investigations for influenza?

A
  • Viral PCR/rapid antigen testing.

- Viral culture of clinical samples (throat/nasal swab).

105
Q

INFLUENZA

What is the treatment for influenza?

A
  • Symptomatic = bed rest, paracetamol, fluids.
  • Abx to prevent secondary infection in people with co-morbidities.
  • If untreated > pneumonia.
106
Q

RHINITIS

What is the pathophysiology of rhinitis?

A
  • Sneezing attacks, nasal discharge or blockage occurring for >1h on most days.
107
Q

RHINITIS

What are the two types of rhinitis?

A
  • Seasonal/hayfever = limited time period of year, summer months.
  • Perennial = throughout the whole year, may be allergic or non-allergic.
108
Q

RHINITIS

What are the allergens/triggers in perennial rhinitis.

A
  • Allergens similar to asthma.

- Triggers cold air, smoke, perfume.

109
Q

RHINITIS

What is the clinical presentation of rhinitis?

A
  • Seasonal = itching of eyes + soft palate.

- Perennial = some develop nasal polys.

110
Q

RHINITIS

What are the investigations + treatment of rhinitis?

A
  • Clinical, skin-prick testing/measurement of specific serum IgE antibody against the particular antigen (RAST).
  • Avoid allergens, anti-histamines, decongestant topic steroids (beclometasone spray).
111
Q 
ACUTE CORYZA (COLD)
What is the pathophysiology of the common cold?
A
  • Spread by droplets/close personal contact with rhinovirus infection.
112
Q 
ACUTE CORYZA (COLD)
What is the clinical presentation + treatment for the common cold?
A
  • Malaise, slight pyrexia, sore throat + watery nasal discharge which becomes mucopurulent after a few days.
  • Symptomatic – bed rest, paracetamol, fluids.
113
Q

PULMONARY FIBROSIS

What is the pathophysiology of pulmonary fibrosis?

A

There is patchy fibrosis of the interstitium + minimal/absent inflammation, acute fibroblastic proliferation + collagen deposition.
- It’s a restrictive defect.

114
Q

PULMONARY FIBROSIS

What are the symptoms of pulmonary fibrosis?

A
  • Non-productive cough.

- Exertional dyspnoea.

115
Q

PULMONARY FIBROSIS

What are the signs of pulmonary fibrosis?

A
  • Cyanosis.
  • Finger clubbing.
  • Fine inspiratory basal crackles.
116
Q

PULMONARY FIBROSIS

What are the complications of pulmonary fibrosis?

A
  • Respiratory failure.
  • Pulmonary HTN.
  • Cor pulmonale.
117
Q

PULMONARY FIBROSIS

What are the investigations for pulmonary fibrosis?

A
  • Bloods = CRP + Igs raised, ABG = low PaO2, high PaCO2 if severe.
  • Spirometry shows restrictive pattern (FEV1/FVC > 0.7 but FVC and FEV1 < 0.8).
  • High-resolution CT chest = bilateral irregular linear opacities with honeycombing.
  • Lung biopsy = usual interstitial pneumonia seen histologically.
118
Q

PULMONARY FIBROSIS

What is the treatment for pulmonary fibrosis?

A
  • Supportive (oxygen, pulmonary rehabilitation, palliative care with opiates).
  • Transplantation is best option for severe cases.
  • Anti-fibrotic (pirfenidone), tyrosine kinase inhibitor (nintedanib).
  • Prognosis is 50% 5yr survival.
119
Q

SARCOIDOSIS

What is the pathophysiology of sarcoidosis?

A
  • Distinct cellular infiltrates + extracellular matrix deposition in lung distal to terminal bronchiole – diseases of the alveolar/capillary interface.
120
Q

SARCOIDOSIS

What do typical sarcoid granulomas consist of?

A
  • Focal accumulations of epithelioid cells, macrophages + lymphocytes (mainly T cells).
121
Q

SARCOIDOSIS

What is the pulmonary clinical presentation of sarcoidosis?

A
  • Dry cough.
  • Progressive dyspnoea with decreased exercise tolerance.
  • Chest pain.
122
Q

SARCOIDOSIS

What are the other clinical presentations of sarcoidosis?

A
  • Erythema nodosum on skin.
  • Uveitis on eyes.
  • Arthralgia on bone.
  • Bell’s palsy.
  • Hypercalcaemia.
  • Hepatosplenomegaly.
123
Q

SARCOIDOSIS

What are the investigations of sarcoidosis?

A

Pulmonary function tests…
- Restrictive lung defect (FEV1/FVC > 0.7 but FVC + FEV1 < 80%).
CXR = bilateral hilar lymphadenopathy in 90%.
Tissue biopsy shows non-caseating granuloma.

124
Q

SARCOIDOSIS

What is the treatment for sarcoidosis?

A
  • Hilar lymphadenopathy spontaneously resolves.
  • Bed rest, NSAIDs.
  • Steroids.
125
Q

BRONCHIECTASIS

What is bronchiectasis?

A
  • Abnormal + permanent dilatation of the central + medium-sized airways (bronchi + bronchioles).
126
Q

BRONCHIECTASIS

What is the pathophysiology of bronchiectasis?

A
  • This leads to impaired clearance of bronchial secretions with secondary bacterial infection + bronchial inflammation + so progressive lung damage – may be localised to a lobe or generalised throughout the bronchial tree.
  • Bronchitis>bronchiectasis>fibrosis.
127
Q

BRONCHIECTASIS

What is the aetiology of bronchiectasis?

A

Cystic fibrosis.
Post-infectious bronchial damage (pneumonia, whooping cough, TB)…
- S. aureus, H. influenzae, Strep. pneumoniae.
Bronchial obstruction (inhaled foreign body, tumour).

128
Q

BRONCHIECTASIS

What are the symptoms of bronchiectasis?

A
  • Persistent cough.
  • Copious purulent sputum (thick, foul-smelling, green).
  • Intermittent haemoptysis.
129
Q

BRONCHIECTASIS

What are the signs of bronchiectasis?

A
  • Finger clubbing.
  • Coarse inspiratory crackles.
  • Wheeze.
130
Q

BRONCHIECTASIS

What are the investigations for bronchiectasis?

A
  • High resolution CT chest (gold standard) = airway dilatation, bronchial wall thickening + cysts.
  • Sputum culture.
  • Obstructive spirometry (FEV1 < 80%, FEV1/FVC < 0.7).
  • CXR shows dilated brochi + thickened bronchial walls.
131
Q

BRONCHIECTASIS

What are the non-pharmacological treatments + preventions for bronchiectasis?

A
  • Smoking cessation + physiotherapy for sputum clearance.

- Prevention of exacerbations via annual influenza vaccination, pneumoccocal vaccination.

132
Q

BRONCHIECTASIS

What is the treatment for bronchiectasis?

A 
Abx during exacerbations...
- Flucloxacillin for S.aureus.
- Ciprofloxacin for P.aeruginosa.
Bronchodilators if airflow obstruction.
Corticsteroids.
Mucolytics to treat hypersecretion.
Surgery if localised disease/severe haemoptysis control.
133
Q

CYSTIC FIBROSIS

What is the pathophysiology of cystic fibrosis?

A
  • There is a mutation in a single gene on chromosome 7 that encodes the CF transmembrane conductance regulatory (CFTR) protein, a chloride channel + regulatory protein found in epithelial cell membranes in the lungs, pancreas, GI + reproductive tract.
134
Q

CYSTIC FIBROSIS

What is the effect of the mutation in cystic fibrosis?

A
  • Deranged transport of Cl- ± other CFTR affected ions such as Na+, HCO3- leads to thickening mucous secretions + increased salt content in sweat gland.
  • In the lungs, it leads to dehydrated airway surface lipid, mucous stasis + infection.
135
Q

CYSTIC FIBROSIS

What is the epidemiology + aetiology of cystic fibrosis?

A
  • Less common in Afro-Caribbean + Asian people.

- Autosomal recessive condition, 1/25 carriers, most common mutation is DF508.

136
Q

CYSTIC FIBROSIS

What is the neonatal presentation of cystic fibrosis?

A
  • Failure to thrive.
  • Rectal prolapse.
  • Meconium ileus (small bowel obstruction from thick intestinal secretions).
137
Q

CYSTIC FIBROSIS

What is the adult respiratory clinical presentation of cystic fibrosis.

A
  • Recurrent infections > inflammation leads to progressive bronchiectasis + so airflow limitation + respiratory failure.
  • Finger clubbing.
  • Cyanosis.
138
Q

CYSTIC FIBROSIS

What are the other clinical presentations of cystic fibrosis?

A
  • Gallstones.
  • DM due to pancreatic insufficiency.
  • Salty sweat.
  • Nasal polyps, sinusitis.
139
Q

CYSTIC FIBROSIS

What are the complications of cystic fibrosis?

A
  • Infertility.
  • Pancreatitis.
  • Respiratory tract infections.
  • Bronchiectasis.
140
Q

CYSTIC FIBROSIS

What are the investigations for cystic fibrosis?

A 
Sweat test...
- Sweat Na+ + Cl- >60mmol/L.
Genetic screening...
- For common CF mutations.
Bacteriology...
- Cough swab, sputum culture.
141
Q

CYSTIC FIBROSIS

What is the treatment for cystic fibrosis?

A
  • Management by MDT witih GP, PT, dietician.
  • Surveillance with FEV1 + BMI recordings each time.
  • Avoid smoking, have a good diet (high protein), genetic counselling.
  • PT for airway clearance techniques, bronchodilators, prophylactic Abx.
  • Enzyme + fat soluble vitamin (ADEK) supplements.
142
Q

PLEURAL EFFUSION

What is a pleural effusion?

A

Build-up of fluid in pleural space.

143
Q

PLEURAL EFFUSION

What are transudates and exudates?

A

Transudates (<25g/L)…
- Excessive production of pleural fluid or resorption reduced.
- Extravascular fluid w/ low protein content + low specific gravity.
Exudates (>35g/L)…
- Result from damaged pleura.
- Protein rich fluid w/ cellular elements that oozes out of blood vessels in inflammation + deposited in nearby tissues.

144
Q 
PLEURAL EFFUSION
What is...
i) chylothorax?
ii) empyema?
iii) haemothorax?
A

i) Chyle (lymph with fat) in pleural space.
ii) Pus in pleural space.
iii) Blood in pleural space.

145
Q

PLEURAL EFFUSION

What is the aetiology of transudates?

A
  • Disruption of hydrostatic + oncotic forces operating across pleural membranes.
  • Increased venous pressure (cardiac failure, fluid overload).
  • Hypoproteinaemia (nephrotic syndrome, cirrhosis)
146
Q

PLEURAL EFFUSION

What is the aetiology of exudates?

A
  • Increased permeability of pleural surface and/or capillaries (inflammation).
  • Increased leakiness of pleural capillaries secondary to infection, inflammation or malignancy (bacterial pneumonia, PE, mesothelioma).
147
Q

PLEURAL EFFUSION

What are the symptoms of pleural effusion?

A
  • Small = asymptomatic.

- Dyspnoea, pleuritic chest pain.

148
Q

PLEURAL EFFUSION

What are the signs of pleural effusion?

A
  • Decreased expansion.
  • Diminished breath sounds on affected side.
  • Stony dull percussion.
149
Q

PLEURAL EFFUSION

What are the investigations for pleural effusion?

A

CXR = white (fluid) with blunt costophrenic angles if small.
USS = identify presence of pleural fluid.
Pleural biopsy = tissue diagnosis.
- Thoracentesis, transudate = clear, exudate = cloudy.

150
Q

PLEURAL EFFUSION

What is the treatment for pleural effusion?

A
  • Drainage (slowly, diagnostic tap/intercostal drain).
  • Pleurodesis (injection causes adhesion of pleura to help prevent re-accumulating effusion).
  • Surgery if persistent + increasing pleural thickness.
151
Q

PNEUMOTHORAX

What is a pneumothorax?

A
  • Air in the pleural space leading to partial or complete collapse of the lung.
152
Q

PNEUMOTHORAX

What are the types of pneumothorax?

A

Traumatic.
Primary/secondary spontaneous.
Iatrogenic.
Tension pneumothorax.

153
Q

PNEUMOTHORAX

Typically, how does primary spontaneous pneumothorax present?

A
  • Young men, typically tall + thin as the result of rupture of pleural bleb.
154
Q

PNEUMOTHORAX

What is the pathophysiology of a tension pneumothorax?

A
  • Pleural tear acts as a one-way valve + this allows air into the cavity but not out.
  • Increased intra-pleural pressure leading to severe respiratory distress, shock + cardiorespiratory arrest.
155
Q 
PNEUMOTHORAX
What is the aetiology of...
i) primary spontaneous
ii) secondary spontaneous
iii) traumatic
iv) tension

pneumothorax?

A

i) Congenital defect in connective tissue of alveolar wall like Marfan’s/Ehlers-Danlos syndromes.
ii) Associated with underlying lung disease, esp. COPD.
iii) Stab wound, chest trauma.
iv) Trauma, patients on ventilation.

156
Q

PNEUMOTHORAX

What is the clinical presentation of pneumothorax?

A
  • Sudden onset of pleuritic chest pain + dyspnoea.
  • Large pneumothorax there are reduced breath sounds + hyper-resonant percussion.
  • Tachycardia.
  • Tension leads to tracheal deviation + severe respiratory distress.
157
Q

PNEUMOTHORAX

What are the investigations for pneumothorax?

A

CXR = look for loss of pulmonary markings, peripheral edge of collapsed lung.

  • Large/tension pneumothorax there is tracheal deviation away form pneumothorax.
  • Diaphragm pushed down on same side.
158
Q

PNEUMOTHORAX

What is the treatment of tension pneumothorax?

A

Immediate needle decompression with chest drain insertion.

- 2nd intercostal space, mid-clavicular line until audible release of air.

159
Q

PNEUMOTHORAX

What is the treatment for pneumothorax in general?

A
  • Needle aspiration to remove air ± chest drain insertion if aspiration unsuccessful.
  • Oxygen for support.
  • Surgery for persistent pneumothorax.
  • Smoking cessation reduces recurrence.
160
Q

PULMONARY HYPERTENSION

What is the pathophysiology of pulmonary HTN?

A
  • Defined by a mean pulmonary artery pressure >25mmHg at rest + secondary to RV failure.
  • As blood accumulates in pulmonary artery, the RV experiences greater afterload + works harder to pump blood out + into pulmonary artery so there is RVH + RHF.
161
Q

PULMONARY HYPERTENSION

What is the aetiology of pulmonary HTN?

A
  • Increase in pulmonary vascular resistance/increase in pulmonary blood flow…
  • HIV infection.
  • Congenital heart defects ASD/VSD.
  • Long-term use of cocaine/amphetamines.
  • Left heart disease.
162
Q

PULMONARY HYPERTENSION

What are the early clinical presentations of pulmonary HTN?

A
  • Exertional dyspnoea.

- Lethargy + fatigue (inability to increase CO with exercise).

163
Q

PULMONARY HYPERTENSION

What are the clinical presentations as right heart failure develops?

A
  • Peripheral oedema.

- Abdominal pain (hepatic congestion).

164
Q

PULMONARY HYPERTENSION

What are the investigations for pulmonary HTN?

A
  • CXR = enlarged proximal pulmonary arteries which taper distally.
  • ECG = RVH + P pulmonale.
  • Echocardiography shows RV dilatation ± hypertrophy.
165
Q

PULMONARY HYPERTENSION

What is the initial treatment for pulmonary HTN?

A
  • Oxygen.
  • Warfarin (higher risk of intrapulmonary thrombosis).
  • Diuretics.
  • CCBs as pulmonary vasodilators.
166
Q

PULMONARY HYPERTENSION

What is the advanced treatment for pulmonary HTN?

A
  • Reduce pulmonary vascular resistance with oral endothelin receptor antagonists + prostanoid analogues.
  • In primary pulmonary HTN, progressive deterioration = heart + lung transplant.
167
Q

HYPERSENSITIVITY PNEUMONITIS

What is the pathophysiology of hypersensitivity pneumonitis?

A
  • In sensitised individuals, repetitive inhalation of allergens provokes an allergic response which involves both cellular immunity + deposition of immune complexes (type 3 hypersensitivity).
168
Q

HYPERSENSITIVITY PNEUMONITIS

What initially happens in hypersensitivity pneumonitis and how can this develop?

A
  • In acute phase, the alveoli are infiltrated with acute inflammatory cells.
  • Later there is chronic inflammation + granulomas which can either resolve or progress to fibrosis.
169
Q

HYPERSENSITIVITY PNEUMONITIS

What is the aetiology of hypersensitivity pneumonitis?

A
  • Farmer’s lung = fungus in mouldy/poorly stored hay.

- Bird fancier’s lung = handling pigeons, proteins in bird faeces.

170
Q

HYPERSENSITIVITY PNEUMONITIS

What is the clinical presentation of hypersensitivity pneumonitis?

A

Acute… fever, malaise, dry cough.

Chronic… finger clubbing, increasing dyspnoea, weight loss

171
Q

HYPERSENSITIVITY PNEUMONITIS

What are the investigations for hypersensitivity pneumonitis?

A
  • Bloods show raised WCC, ESR.
  • Serum antibodies.
  • Lung function tests show reversible restrictive (FEV1/FVC > 0.7 but FVC + FEV1 < 80%)
172
Q

HYPERSENSITIVITY PNEUMONITIS

What is the treatment for hypersensitivity pneumonitis?

A
  • Remove/avoid allergen.
  • Oxygen.
  • Corticosteroids like prednisolone.
173
Q

PNEUMOCONIOSIS

What is the pathophysiology of pneumoconiosis?

A

Lung disease caused by inhaled dust with varied reactions…

  • Inert = Coal worker’s pneumoconiosis.
  • Fibrous = asbestosis + silicosis.
  • Allergic = hypersensitivity pneumonitis.
  • Neoplastic = mesothelioma, lung cancer.
174
Q

PNEUMOCONIOSIS

Describe the pathophysiology of coal worker’s pneumoconiosis.

A
  • Coal is ingested by alveolar macrophages (dust cells) which aggregate around the bronchioles.
  • Macrophages die + release their proteolytic enzymes causing fibrosis.
175
Q

PNEUMOCONIOSIS

What is the difference between macular CWP + nodular CWP?

A
  • Macular = aggregates of dust laden macrophages with no significant scarring.
  • Nodular = nodules >10mm in background of extensive macular CWP, with no significant scarring.
176
Q

PNEUMOCONIOSIS

What are the clinical features + investigations for coal worker’s pneumoconiosis?

A
  • Asymptomatic/dyspnoea with productive cough (black sputum).
  • Simple pneumoconiosis = small pulmonary nodules on CXR.
  • Continued exposure = progressive massive fibrosis with large fibrotic masses, upper lobe.
177
Q

PNEUMOCONIOSIS

What is the pathophysiology of silicosis? What occupations is it seen in?

A
  • Inhalation of silica particles which are very fibrogenic as they are toxic to macrophages leading to their death + release of proteolytic enzymes.
  • Sandblasting, ceramic manufacture.
178
Q

PNEUMOCONIOSIS

What is the clinical presentation of silicosis?

A
  • Progressive dyspnoea.
  • Increased incidence of TB.
  • CXR shows diffuse upper lobe nodular pattern.
179
Q

PNEUMOCONIOSIS

What is the pathophysiology of asbestosis? What occupations is it seen in?

A
  • Caused by inhalation of asbestos fibres, degree of exposure relates to degree of fibrosis.
  • long latency period 20–40 years.
  • Insulation (roofing), builders/plumbers/electricians.
180
Q

PNEUMOCONIOSIS

What is the clinical presentation + consequences of asbestosis?

A
  • Progressive dyspnoea, clubbing, fine end-inspiratory crackles.
  • Increased risk of lung cancer + mesothelioma, diffuse pulmonary/pleural fibrosis.
181
Q

PNEUMOCONIOSIS

What is the clinical presentation of byssinosis and what occupations is it seen in?

A
  • Symptoms begin once returning to work + get better during week.
  • Tight chest, cough, dyspnoea.
  • Common in cotton mill workers.
182
Q

PNEUMOCONIOSIS

What is the clinical presentation of berylliosis and what occupation is it seen in?

A
  • Beryllium is inhaled + causes a systemic illness with progressive dyspnoea + pulmonary fibrosis.
  • Beryllium is a copper alloy used in aerospace industry.
183
Q

PNEUMOCONIOSIS

What are the investigations + treatment for pneumoconiosis?

A
  • PEFR at work, Hx to see symptoms worse at work, serum immunology looking for IgE to specific workplace antigens.
  • Avoid exposure, claim compensation.
184
Q

PNEUMOCONIOSIS

What is the prevention of pneumoconiosis?

A
  • Risk assessment.
  • Legal requirement under COSHH.
  • Prevent + minimise exposure to harmful substances.
  • Monitor worker’s health to identify problems early.
185
Q

GOODPASTURE’S SYNDROME

What is the pathophysiology of goodpasture’s syndrome?

A
  • Co-existence of acute glomerulonephritis + pulmonary alveolar haemorrhage + presence of circulating antibodies directed against an intrinsic antigen to basement membrane of both kidney + lung.
  • Specific autoimmune disease caused by type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis > AKI + CKD.
186
Q

GOODPASTURE’S SYNDROME

What is the aetiology + clinical presentation of goodpasture’s syndrome?

A
  • Autoimmune, strong genetic link to HLA-DRB1.

- Cough, haemoptysis, dyspnoea + anaemia (may result from persistent intrapulmonary bleeding).

187
Q

GOODPASTURE’S SYNDROME

What are the investigations for goodpasture’s syndrome?

A
  • Bloods = presence of antiglomerular basement membrane (anti-GBM) membranes.
  • CXR = infiltrates due to pulmonary haemorrhage.
  • Kidney biopsy = crescentic glomerulonephritis.
188
Q

GOODPASTURE’S SYNDROME

What is the treatment for goodpasture’s syndrome?

A
  • Can spontaneously improve or progress to renal failure.
  • Treat shock.
  • Vigorous immunosuppressive treatment with plasmapheresis.
189
Q

WEGENER’S GRANULOMATOSIS

What is the pathophysiology of Wegener’s granulomatosis?

A
  • Vasculitis of unknown aetiology, commonly involves upper airway + endo-bronchi.
  • Granulomatous with polyangiitis (autoimmune inflammatory condition affecting endothelial cells in nose, sinuses etc).
190
Q

WEGENER’S GRANULOMATOSIS

What is the clinical presentation of Wegener’s granulomatosis?

A
  • Rhinorrhoea.
  • Haemoptysis.
  • Epistaxis.
  • Destruction of nasal septum (‘saddle-nose’ deformity).
  • ?renal disease, with proteinuria/haematuria.
191
Q

WEGENER’S GRANULOMATOSIS

What are the potential complications with Wegener’s granulomatosis?

A
  • AKI.

- Respiratory failure.

192
Q

WEGENER’S GRANULOMATOSIS

What are the investigations for Wegener’s granulomatosis?

A
  • Bloods = FBC, U+E, raised ESR/CRP.
  • Serum c-ANCA + anti-PR3 positive.
  • Urinalysis = proteinuria + haematuria indicates renal biopsy.
193
Q

WEGENER’S GRANULOMATOSIS

What is the treatment of Wegener’s granulomatosis?

A
  • Steroids like prednisolone.
  • Methotrexate used for maintenance.
  • Immunosuppressants with monoclonal antibody like rituximab in severe disease.
194
Q

MESOTHELIOMA

What is the pathophysiology of mesothelioma?

A
  • Tumour of mesothelial cells usually occurs in pleura (others are peritoneum, pericardium).
  • Deposition of asbestos fibres in parenchyma leads to penetration of visceral pleura + transportation of fibre to pleural surface leading to developing of malignant plaque > mesothelioma.
195
Q

MESOTHELIOMA

What is the aetiology + epidemiology of mesothelioma?

A
  • Occupational (strong association with asbestos inhalation, latent period up to 45 years).
  • Genetic risk.
  • 3x more common in men, >75y/o.
196
Q

MESOTHELIOMA

What is the clinical presentation of mesothelioma?

A
  • Chest pain.
  • Dyspnoea.
  • Finger clubbing.
  • Weight loss.
  • Recurrent pleural effusions.
197
Q

MESOTHELIOMA

What are the investigations for mesothelioma?

A
  • CXR/CT scan = pleural thickening/effusion, blood pleural fluid.
  • Pleural biopsy.
  • Diagnosis via histology following thoracoscopy.
198
Q

MESOTHELIOMA

What is the treatment for mesothelioma?

A
  • Surgery for extremely localised mesothelioma.

- Generally resistant to surgery, chemo + radiotherapy.

199
Q

BETA-2-ADRENOCEPTOR AGONISTS

What are beta-2-adrenoceptor agonists? What are their mechanism?

A
  • Inhaled medications delivered directly to lung via oral/nasal route.
  • Bind to beta-2-adrenoceptors causing smooth muscle relaxation + bronchodilation.
200
Q

BETA-2-ADRENOCEPTOR AGONISTS

How are beta-2-adrenoceptor delivered? Give examples.

A
  • Inhaler devices allow drugs to penetrate deep into lung to achieve correct dose.
  • Nebulisers deliver medication in form of aerosols.
  • Short-acting = salbutamol, long-acting = salmeterol.
201
Q

BETA-2-ADRENOCEPTOR AGONISTS

What are the adverse effects of beta-2-adrenoceptor agonists?

A
  • Hypokalaemia, tremor.

- Palpitations + muscle cramps.

202
Q

MUSCARINIC ANTAGONISTS

What is the mechanism of muscarinic antagonists?

A
  • Anticholinergic compounds block the muscarinic receptors (M3) on airway smooth muscle, glands + nerves to prevent muscle contraction, gland secretion + enhance neurotransmitter release.
203
Q

MUSCARINIC ANTAGONISTS

What are some examples of muscarinic antagonists?

A
  • Atropine = naturall occurring anticholinergic.

- Short-acting = ipratropium, long-acting = tiotropium.

204
Q

STEROIDS

What is the mechanism of action of steroids?

A
  • Reduce inflammation by suppressing the production of chemotactic mediators, reduce adhesion molecule expression + inhibit inflammatory cell survival in airway.
  • Suppresses inflammatory gene expression in airway epithelial cells.
205
Q

STEROIDS

What are some examples of steroids? What are the adverse effects?

A
  • Prednisolone, dexamethasone.

- Osteoporosis (+ subsequent fractures), adrenal suppression, cataracts + increased infection risk.

206
Q

STEROIDS

What are inhaled corticosteroids used for? Give an example. What is the adverse effect?

A
  • Improves quality of life, lung function + reduces likelihood of exacerbations.
  • Beclometasone.
  • Increased pneumonia risk.
207
Q

TREATING FIBROSIS

What 2 drugs can be used for treating fibrosis and what are their mechanisms?

A

Antifibrotic (pirfenidone)…
- Reduces fibroblast proliferation, collagen + fibrogenic mediator production.
Tyrosine kinase inhibitor (nintedanib)…
- Inhibits growth factor receptors which are some of the drivers of fibrotic process.

Phase 2a (12 decks)

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