Respiratory Flashcards
(207 cards)
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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).
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.
13
Q
COPD
What protease inhibitor can be inactivated by smoke?
A
- Alpha-1-antitrypsin + this can lead to emphysema.
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.
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).
16
Q
COPD
What are the symptoms of COPD?
A
- Chronic cough.
- Sputum.
- Dyspnoea.
- Fatigued.
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).
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.
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.
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.
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.
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.
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.
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.
25
ASTHMA
| What cells are increased in the bronchial wall + mucous membranes in asthma?
- Mast cells, eosinophils, T lymphocytes + neutrophils.
26
ASTHMA
| What is the pathophysiology of allergic asthma?
- Allergen is inhaled + IgE binds to mast cells causing vasoactive substances like histamine to be released causing bronchoconstriction, oedema, bronchial inflammation + mucous hypersecretion.
27
ASTHMA
| What is the aetiology of asthma?
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.
28
ASTHMA
| What is the epidemiology of asthma?
- Commonly starts in childhood 3–5y/o.
- May either worsen/improve during adolescence.
- Non-allergic often presents middle-aged.
29
ASTHMA
| What exacerbating factors + occupational risks are there with asthma?
- Cold air, exercise, stress, smoking (passive too), beta-blockers, aspirin can all exacerbate.
- Paint sprays (fume exposure, animal handlers + welders.
30
ASTHMA
| How can asthma be differentiated to COPD?
- COPD is a later disease, predominately of smokers, more relentless progressive dyspnoea, less diurnal variation.
31
ASTHMA
| What are the symptoms of asthma?
- Intermittent dyspnoea.
- Wheeze.
- Cough (often nocturnal).
- Diurnal variation (symptoms worse in morning).
32
ASTHMA
| What are the signs of asthma?
- Tachypnoea.
- Audible wheeze.
- Hyperinflated chest.
33
ASTHMA
| What is the diagnostic criteria for acute severe asthma?
- RR>25.
- HR>110.
- PEFR 35–50% predicted.
- Cannot complete sentence in one breath.
34
ASTHMA
| What are the investigations for asthma?
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.
35
ASTHMA
| What does Peak Expiratory FLow Rate (PEFR) test and how?
- 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.
36
ASTHMA
| What are the RCP3 questions for?
Testing severity...
- Recent nocturnal waking?
- Usual asthma symptoms during day?
- Interference with ADLs?
37
ASTHMA
| What is the treatment for acute severe asthma?
- Nebulised salbutamol w/ oxygen.
| - IV corticosteroids + Abx if infection.
38
ASTHMA
| What is the lifestyle advice for asthma?
- Stop smoking.
- Avoid allergens + stress.
- Keep healthy.
39
ASTHMA
| What is the aim of asthma treatment?
- Stepped approach to control disease so no day/night symptoms, no exacerbations + normal lung functions (FEV1 or PEFR ≥ 80%).
40
ASTHMA
| What is the medical treatment for asthma?
```
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.
```
41
LUNG CARCINOMAS
| What are the two main types of lung carcinomas?
- Non-small cell lung carcinomas (NSCLC)
| - Small-cell lung carcinomas. (SCLC).
42
LUNG CARCINOMAS
| What are the different types of NSCLC?
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.
43
```
LUNG CARCINOMAS
What type of NSCLC...
i) more common with non-smokers?
ii) strongly associated with smokers?
iii) strongly associated with asbestos exposure?
```
i) Adenocarcinoma.
ii) Squamous.
iii) Adenocarcinoma.
44
LUNG CARCINOMAS
| What is the pathophysiology of SCLC?
- 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.
45
LUNG CARCINOMAS
| What is the aetiology of lung carcinomas? What is the 5 year lung cancer survival rate + why?
- Smoking.
- Occupational (asbestos/radon/coal tar/chromium).
- 5 year lung cancer survival rate 8–10% as people often present late so treatment limited.
46
LUNG CARCINOMAS
| What are the symptoms as a result of local effect of lung carcinoma?
- Cough.
- Haemoptysis.
- Dyspnoea.
- Chest pain.
- Recurrent/slowly resolving chest infections.
47
LUNG CARCINOMAS
| What are the symptoms as a result of metastases of lung carcinoma?
- Bone tenderness.
- Hepatomegaly.
- Neurological deficit like seizures, headache, confusion.
48
LUNG CARCINOMAS
| What are the local complications due to lung carcinomas?
- Left recurrent laryngeal nerve palsy = hoarse voice.
- Spread to brachial plexus = shoulder/arm pain.
- Spread to sympathetic ganglion = Horner's syndrome.
49
LUNG CARCINOMAS
| What paraneoplastic changes can occur in SCLC?
- PTH, ACTH, ADH secretion leading to, Cushing's syndrome, SiADH.
50
LUNG CARCINOMAS
| What is the treatment for NSCLC?
- Lobectomy (open or thoracoscopic) with curative intent.
- Radical radiotherapy.
- Chemotherapy ± radiotherapy if more advanced.
51
LUNG CARCINOMAS
| What is the treatment for SCLC?
- 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.
52
PULMONARY EMBOLISM
| What is the pathophysiology of PE?
- 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.
53
PULMONARY EMBOLISM
What are the consequences of..
i) small-medium, peripheral PE?
ii) massive, central PE?
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.
54
PULMONARY EMBOLISM
| What are the risk factors for PE?
Thrombotic...
- Surgery, immobility, leg fracture.
- Oral contraceptive, HRT, pregnancy.
- Genetic predisposition (inherited thrombophilia).
- Long haul flights = rare.
55
PULMONARY EMBOLISM
| What is the preventing for PE?
```
Mechanical...
- Hydration + early mobilisation.
- Compression stockings + foot pumps.
Chemical...
- LMWH.
```
56
PULMONARY EMBOLISM
| What is the clinical presentation of small-medium PE?
- Dypsnoea.
- Pleuritic chest pain.
- Haemoptysis if infarction.
- May be tachypnoeic, pleural rub + exudative pleural effusion.
57
PULMONARY EMBOLISM
| What is the clinical presentation of massive PE?
- Severe central chest pain.
- Pale + sweaty.
- Shock.
- Raised JVP, RV heave, tachypnoea.
- Hypotensive + tachycardic.
58
PULMONARY EMBOLISM
| What are the investigations for PE?
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.
59
PULMONARY EMBOLISM
| What is the treatment of PE?
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)
60
PNEUMONIA
| What is pneumonia?
- Acute lower respiratory tract infection + when severe can lead to excessive inflammation, lung injury + failure to resolve.
61
PNEUMONIA
| What is the pathophysiology of pneumonia?
- Bacteria translocate to the normally sterile distal airway.
- Resident host defence becomes overwhelmed.
- Macrophages, chemokines + neutrophils produce an inflammatory response.
62
PNEUMONIA
| What are the classifications of pneumonia?
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.
63
PNEUMONIA
| What are the common aetiologies of community acquired pneumonia?
- Streptococcus pneumoniae, gram+ve cocci chain most common.
- Haemophilus influenzae, gram-ve bacilli.
- Enteric gram-negative bacilli like E.coli, klebsielle pneumoniae.
64
PNEUMONIA
| What are the atypical aetiologies of community acquired pneumonia +
Associated with water cooler/air conditioner...
- Mycoplasm pneumoniae.
- Chlamydophila pneumoniae.
- Legionella pneumophilia (Spain/Portugal).
65
PNEUMONIA
| What are the aetiologies of hospital acquired pneumonia?
- Gram-egative bacilli enterobacteria like pseudomonas aeruginosa, E.coli + klebsiella pneumoniae.
- S. Aureus including MRSA.
66
PNEUMONIA
| What are the precipitating + risk factors for pneumonia?
- Smoking, alcohol abuse, underlying lung disease.
| - Elderly + children, co-morbidities (DM, COPD, bronchiectasis), immunocompromised, nursing home residents.
67
PNEUMONIA
| What type of pneumonia is most common in HIV patients?
- Pneumocystis jiroveci pneumonia (PCP).
68
PNEUMONIA
| What are the symptoms of pneumonia?
- Purulent sputum – atypical = non-productive cough.
- Haemoptysis.
- Pleuritic chest pain.
69
PNEUMONIA
| What are the signs of pneumonia?
- Signs of lung consolidation (reduced expansion, dull percussion).
- Tachypnoea/cardia.
- Pyrexia.
- Pleural rub.
70
PNEUMONIA
| What are the complications with pneumonia?
- Parapneumonic effusions + empyema (pockets of pus).
Suspect if WCC/CRP don't settle, pain on deep inspiration, pleural collection – drain.
- Brain abscess.
- Peri/myocarditis.
71
PNEUMONIA
| What are the investigations for pneumonia?
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.
72
PNEUMONIA
| How is the severity of pneumonia assessed?
CURB-65...
- Confusion.
- Urea >7mmol/L.
- Resp rate ≥30/min.
- BP <90/60mmHg.
- 65 ≤ age.
73
PNEUMONIA
| How does CURB-65 determine how you treat pneumonia?
```
0-1 = oral amoxicillin in the community.
2 = oral amoxicillin + clarithromycin in the hospital.
≥3 = IV co-amoxiclav + clarithromycin, consider ITU.
```
74
PNEUMONIA
| What is the generic treatment for pneumonia?
- Maintain oxygen sats.
| - Analgesia like paracetamol/NSAIDs for pleuritic pain
75
PNEUMONIA
| What are the specific antibiotic regimes for Legionella species pneumonia?
- Fluoroquinolone like ciprofloxacin + clarithromycin.
| - Inform Public Health England.
76
PNEUMONIA
| What are the preventative measure for pneumonia?
- Polysaccharide pneumococcal vaccine (PPV) for children.
- Influenza vaccine for those ≥65y/o, immunocompromised or with medical co-morbidities.
- Smoking cessation.
77
TUBERCULOSIS
| What is the pathophysiology of TB?
- 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.
78
TUBERCULOSIS
| What is the pathogenesis of TB?
- 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.
79
TUBERCULOSIS
| What is the epidemiology of TB?
Majority cases in Africa/Asia (India, China).
80
TUBERCULOSIS
| What are the risk factors for TB?
- Living in high prevalence area.
- IV drug users.
- Homeless (immune stresses).
- Alcoholics.
- HIV +ve.
81
TUBERCULOSIS
| What is the clinical presentation of TB?
Systemic...
- Weight loss, night sweats, anorexia, malaise.
Pulmonary...
- Cough (>3/52), chest pain, dyspnoea, haemoptysis.
82
TUBERCULOSIS
| What is the natural history of TB?
- 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.
83
TUBERCULOSIS
| What are the complications of TB?
Spread...
- Bone + joints = pain + swelling.
- Lymph nodes = swelling + discharge.
- CNS = TB meningitis.
- GU TB = haematuria, frequency.
- Haematogenous dissemination = miliary TB.
84
TUBERCULOSIS
| What may a CXR show in TB?
- Consolidation.
- Collapse.
- Pleural effusion.
85
TUBERCULOSIS
| What are the investigations for active + latent TB?
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
TUBERCULOSIS
| What is the treatment for TB?
- Rifampicin (6m).
- Isoniazid (6m).
- Pyrazinamide (2m).
- Ethambutol (2m).
- NOTIFY PUBLIC HEALTH ENGLAND IMMEDIATELY.
87
TUBERCULOSIS
| What are the complications with TB drugs?
- R= red urine, hepatitis + drug interactions as enzyme inducer.
- I = hepatitis, neuropathy.
- P = hepatitis, gout, rash.
- E = optic neuritis.
88
TUBERCULOSIS
| Why is compliance so crucial in TB treatment? How can drug resistance occur?
- 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
TUBERCULOSIS
| What is the prevention for TB?
- Active case finding, reduce infectivity.
- Detect + treat latent TB.
- Vaccination – BCG.
90
PHARYNGITIS/TONSILLITIS
| What is the pathophysiology of pharyngitis/tonsillitis?
- Both are infections in the throat that cause inflammation.
| - If throat primarily affected it's pharyngitis, if tonsils it's tonsillitis.
91
PHARYNGITIS/TONSILLITIS
| What is the aetiology of pharyngitis/tonsillitis?
- Viral = adenovirus (most common), rhinovirus, EBV.
| - Bacteria = Streptococci pyogenes.
92
PHARYNGITIS/TONSILLITIS
| What is the clinical presentation of pharyngitis/tonsillitis?
- Tender gland in neck.
- Large tonsils with exudate.
- Fever, sore throat.
- Oropharynx + soft palate reddened.
93
PHARYNGITIS/TONSILLITIS
| What is the treatment of pharyngitis/tonsillitis?
- Self-limiting, symptomatic treatment with rest, paracetamol.
- Persistent/severe tonsillitis use phenoxymethylpenicillin.
94
SINUSITIS
| What is the pathophysiology + aetiology of sinusitis?
- Infection of paranasal sinuses.
| - Bacterial = streptococcus pneumoniae or haemophilus influenzae.
95
SINUSITIS
| WHHat is the clinical presentation + treatment of sinusitis?
- Facial pain w/ tenderness, purulent rhinorrhoea, fever.
| - Nasal decongestants + broad spectrum antibiotics like co-amoxiclav.
96
EPIGLOTTITIS
| What is the pathophysiology, clinical presentation + treatment for epiglottitis?
- Inflammation of epiglottis due to haemophilus influenza B infection.
- High fever, severe airflow obstruction, sore throat, inspiratory stridor.
- Urgent endotracheal intubation + IV Abx.
97
WHOOPING COUGH
| What is the pathophysiology + aetiology of whooping cough?
- Humans are the natural host + reservoirs of infection.
| - Bordetella pertussis (gram-ve bacilli).
98
WHOOPING COUGH
| What is the clinical presentation + investigations for whooping cough?
- Chronic cough, inspiratory 'whoop' through partially close vocal cords.
- Culture of nasopharyngeal swab diagnostic on Bordet Gengou agar.
99
WHOOPING COUGH
| What is the treatment for whooping cough?
- Prevention with vaccination – dTaP vaccine (8,12,16w + 3–4y/o).
- Clarithromycin.
100
CROUP
| What is the pathophysiology of acute laryngotracheobronchitis (croup)
- 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
CROUP
| What is the clinical presentation + treatment for croup?
- Voice becomes hoarse with barking cough (croup), audible stridor.
- Nebulised adrenaline short-term, corticosteroids.
102
INFLUENZA
| What is the pathophysiology of influenza?
- 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
INFLUENZA
| What is the clinical presentation of influenza?
- Abrupt onset of fever.
- Generalised aching of limbs.
- Severe headache, sore throat + dry cough.
104
INFLUENZA
| What are the investigations for influenza?
- Viral PCR/rapid antigen testing.
| - Viral culture of clinical samples (throat/nasal swab).
105
INFLUENZA
| What is the treatment for influenza?
- Symptomatic = bed rest, paracetamol, fluids.
- Abx to prevent secondary infection in people with co-morbidities.
- If untreated > pneumonia.
106
RHINITIS
| What is the pathophysiology of rhinitis?
- Sneezing attacks, nasal discharge or blockage occurring for >1h on most days.
107
RHINITIS
| What are the two types of rhinitis?
- Seasonal/hayfever = limited time period of year, summer months.
- Perennial = throughout the whole year, may be allergic or non-allergic.
108
RHINITIS
| What are the allergens/triggers in perennial rhinitis.
- Allergens similar to asthma.
| - Triggers cold air, smoke, perfume.
109
RHINITIS
| What is the clinical presentation of rhinitis?
- Seasonal = itching of eyes + soft palate.
| - Perennial = some develop nasal polys.
110
RHINITIS
| What are the investigations + treatment of rhinitis?
- 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
```
ACUTE CORYZA (COLD)
What is the pathophysiology of the common cold?
```
- Spread by droplets/close personal contact with rhinovirus infection.
112
```
ACUTE CORYZA (COLD)
What is the clinical presentation + treatment for the common cold?
```
- Malaise, slight pyrexia, sore throat + watery nasal discharge which becomes mucopurulent after a few days.
- Symptomatic – bed rest, paracetamol, fluids.
113
PULMONARY FIBROSIS
| What is the pathophysiology of pulmonary fibrosis?
There is patchy fibrosis of the interstitium + minimal/absent inflammation, acute fibroblastic proliferation + collagen deposition.
- It's a restrictive defect.
114
PULMONARY FIBROSIS
| What are the symptoms of pulmonary fibrosis?
- Non-productive cough.
| - Exertional dyspnoea.
115
PULMONARY FIBROSIS
| What are the signs of pulmonary fibrosis?
- Cyanosis.
- Finger clubbing.
- Fine inspiratory basal crackles.
116
PULMONARY FIBROSIS
| What are the complications of pulmonary fibrosis?
- Respiratory failure.
- Pulmonary HTN.
- Cor pulmonale.
117
PULMONARY FIBROSIS
| What are the investigations for pulmonary fibrosis?
- 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
PULMONARY FIBROSIS
| What is the treatment for pulmonary fibrosis?
- 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
SARCOIDOSIS
| What is the pathophysiology of sarcoidosis?
- Distinct cellular infiltrates + extracellular matrix deposition in lung distal to terminal bronchiole – diseases of the alveolar/capillary interface.
120
SARCOIDOSIS
| What do typical sarcoid granulomas consist of?
- Focal accumulations of epithelioid cells, macrophages + lymphocytes (mainly T cells).
121
SARCOIDOSIS
| What is the pulmonary clinical presentation of sarcoidosis?
- Dry cough.
- Progressive dyspnoea with decreased exercise tolerance.
- Chest pain.
122
SARCOIDOSIS
| What are the other clinical presentations of sarcoidosis?
- Erythema nodosum on skin.
- Uveitis on eyes.
- Arthralgia on bone.
- Bell's palsy.
- Hypercalcaemia.
- Hepatosplenomegaly.
123
SARCOIDOSIS
| What are the investigations of sarcoidosis?
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
SARCOIDOSIS
| What is the treatment for sarcoidosis?
- Hilar lymphadenopathy spontaneously resolves.
- Bed rest, NSAIDs.
- Steroids.
125
BRONCHIECTASIS
| What is bronchiectasis?
- Abnormal + permanent dilatation of the central + medium-sized airways (bronchi + bronchioles).
126
BRONCHIECTASIS
| What is the pathophysiology of bronchiectasis?
- 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
BRONCHIECTASIS
| What is the aetiology of bronchiectasis?
Cystic fibrosis.
Post-infectious bronchial damage (pneumonia, whooping cough, TB)...
- S. aureus, H. influenzae, Strep. pneumoniae.
Bronchial obstruction (inhaled foreign body, tumour).
128
BRONCHIECTASIS
| What are the symptoms of bronchiectasis?
- Persistent cough.
- Copious purulent sputum (thick, foul-smelling, green).
- Intermittent haemoptysis.
129
BRONCHIECTASIS
| What are the signs of bronchiectasis?
- Finger clubbing.
- Coarse inspiratory crackles.
- Wheeze.
130
BRONCHIECTASIS
| What are the investigations for bronchiectasis?
- 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
BRONCHIECTASIS
| What are the non-pharmacological treatments + preventions for bronchiectasis?
- Smoking cessation + physiotherapy for sputum clearance.
| - Prevention of exacerbations via annual influenza vaccination, pneumoccocal vaccination.
132
BRONCHIECTASIS
| What is the treatment for bronchiectasis?
```
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
CYSTIC FIBROSIS
| What is the pathophysiology of cystic fibrosis?
- 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
CYSTIC FIBROSIS
| What is the effect of the mutation in cystic fibrosis?
- 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
CYSTIC FIBROSIS
| What is the epidemiology + aetiology of cystic fibrosis?
- Less common in Afro-Caribbean + Asian people.
| - Autosomal recessive condition, 1/25 carriers, most common mutation is DF508.
136
CYSTIC FIBROSIS
| What is the neonatal presentation of cystic fibrosis?
- Failure to thrive.
- Rectal prolapse.
- Meconium ileus (small bowel obstruction from thick intestinal secretions).
137
CYSTIC FIBROSIS
| What is the adult respiratory clinical presentation of cystic fibrosis.
- Recurrent infections > inflammation leads to progressive bronchiectasis + so airflow limitation + respiratory failure.
- Finger clubbing.
- Cyanosis.
138
CYSTIC FIBROSIS
| What are the other clinical presentations of cystic fibrosis?
- Gallstones.
- DM due to pancreatic insufficiency.
- Salty sweat.
- Nasal polyps, sinusitis.
139
CYSTIC FIBROSIS
| What are the complications of cystic fibrosis?
- Infertility.
- Pancreatitis.
- Respiratory tract infections.
- Bronchiectasis.
140
CYSTIC FIBROSIS
| What are the investigations for cystic fibrosis?
```
Sweat test...
- Sweat Na+ + Cl- >60mmol/L.
Genetic screening...
- For common CF mutations.
Bacteriology...
- Cough swab, sputum culture.
```
141
CYSTIC FIBROSIS
| What is the treatment for cystic fibrosis?
- 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
PLEURAL EFFUSION
| What is a pleural effusion?
Build-up of fluid in pleural space.
143
PLEURAL EFFUSION
| What are transudates and exudates?
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
```
PLEURAL EFFUSION
What is...
i) chylothorax?
ii) empyema?
iii) haemothorax?
```
i) Chyle (lymph with fat) in pleural space.
ii) Pus in pleural space.
iii) Blood in pleural space.
145
PLEURAL EFFUSION
| What is the aetiology of transudates?
- Disruption of hydrostatic + oncotic forces operating across pleural membranes.
- Increased venous pressure (cardiac failure, fluid overload).
- Hypoproteinaemia (nephrotic syndrome, cirrhosis)
146
PLEURAL EFFUSION
| What is the aetiology of exudates?
- 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
PLEURAL EFFUSION
| What are the symptoms of pleural effusion?
- Small = asymptomatic.
| - Dyspnoea, pleuritic chest pain.
148
PLEURAL EFFUSION
| What are the signs of pleural effusion?
- Decreased expansion.
- Diminished breath sounds on affected side.
- Stony dull percussion.
149
PLEURAL EFFUSION
| What are the investigations for pleural effusion?
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
PLEURAL EFFUSION
| What is the treatment for pleural effusion?
- 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
PNEUMOTHORAX
| What is a pneumothorax?
- Air in the pleural space leading to partial or complete collapse of the lung.
152
PNEUMOTHORAX
| What are the types of pneumothorax?
Traumatic.
Primary/secondary spontaneous.
Iatrogenic.
Tension pneumothorax.
153
PNEUMOTHORAX
| Typically, how does primary spontaneous pneumothorax present?
- Young men, typically tall + thin as the result of rupture of pleural bleb.
154
PNEUMOTHORAX
| What is the pathophysiology of a tension pneumothorax?
- 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
```
PNEUMOTHORAX
What is the aetiology of...
i) primary spontaneous
ii) secondary spontaneous
iii) traumatic
iv) tension
```
pneumothorax?
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
PNEUMOTHORAX
| What is the clinical presentation of pneumothorax?
- 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
PNEUMOTHORAX
| What are the investigations for pneumothorax?
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
PNEUMOTHORAX
| What is the treatment of tension pneumothorax?
Immediate needle decompression with chest drain insertion.
| - 2nd intercostal space, mid-clavicular line until audible release of air.
159
PNEUMOTHORAX
| What is the treatment for pneumothorax in general?
- Needle aspiration to remove air ± chest drain insertion if aspiration unsuccessful.
- Oxygen for support.
- Surgery for persistent pneumothorax.
- Smoking cessation reduces recurrence.
160
PULMONARY HYPERTENSION
| What is the pathophysiology of pulmonary HTN?
- 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
PULMONARY HYPERTENSION
| What is the aetiology of pulmonary HTN?
- 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
PULMONARY HYPERTENSION
| What are the early clinical presentations of pulmonary HTN?
- Exertional dyspnoea.
| - Lethargy + fatigue (inability to increase CO with exercise).
163
PULMONARY HYPERTENSION
| What are the clinical presentations as right heart failure develops?
- Peripheral oedema.
| - Abdominal pain (hepatic congestion).
164
PULMONARY HYPERTENSION
| What are the investigations for pulmonary HTN?
- CXR = enlarged proximal pulmonary arteries which taper distally.
- ECG = RVH + P pulmonale.
- Echocardiography shows RV dilatation ± hypertrophy.
165
PULMONARY HYPERTENSION
| What is the initial treatment for pulmonary HTN?
- Oxygen.
- Warfarin (higher risk of intrapulmonary thrombosis).
- Diuretics.
- CCBs as pulmonary vasodilators.
166
PULMONARY HYPERTENSION
| What is the advanced treatment for pulmonary HTN?
- Reduce pulmonary vascular resistance with oral endothelin receptor antagonists + prostanoid analogues.
- In primary pulmonary HTN, progressive deterioration = heart + lung transplant.
167
HYPERSENSITIVITY PNEUMONITIS
| What is the pathophysiology of hypersensitivity pneumonitis?
- In sensitised individuals, repetitive inhalation of allergens provokes an allergic response which involves both cellular immunity + deposition of immune complexes (type 3 hypersensitivity).
168
HYPERSENSITIVITY PNEUMONITIS
| What initially happens in hypersensitivity pneumonitis and how can this develop?
- 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
HYPERSENSITIVITY PNEUMONITIS
| What is the aetiology of hypersensitivity pneumonitis?
- Farmer's lung = fungus in mouldy/poorly stored hay.
| - Bird fancier's lung = handling pigeons, proteins in bird faeces.
170
HYPERSENSITIVITY PNEUMONITIS
| What is the clinical presentation of hypersensitivity pneumonitis?
Acute... fever, malaise, dry cough.
| Chronic... finger clubbing, increasing dyspnoea, weight loss
171
HYPERSENSITIVITY PNEUMONITIS
| What are the investigations for hypersensitivity pneumonitis?
- Bloods show raised WCC, ESR.
- Serum antibodies.
- Lung function tests show reversible restrictive (FEV1/FVC > 0.7 but FVC + FEV1 < 80%)
172
HYPERSENSITIVITY PNEUMONITIS
| What is the treatment for hypersensitivity pneumonitis?
- Remove/avoid allergen.
- Oxygen.
- Corticosteroids like prednisolone.
173
PNEUMOCONIOSIS
| What is the pathophysiology of pneumoconiosis?
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
PNEUMOCONIOSIS
| Describe the pathophysiology of coal worker's pneumoconiosis.
- Coal is ingested by alveolar macrophages (dust cells) which aggregate around the bronchioles.
- Macrophages die + release their proteolytic enzymes causing fibrosis.
175
PNEUMOCONIOSIS
| What is the difference between macular CWP + nodular CWP?
- Macular = aggregates of dust laden macrophages with no significant scarring.
- Nodular = nodules >10mm in background of extensive macular CWP, with no significant scarring.
176
PNEUMOCONIOSIS
| What are the clinical features + investigations for coal worker's pneumoconiosis?
- 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
PNEUMOCONIOSIS
| What is the pathophysiology of silicosis? What occupations is it seen in?
- 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
PNEUMOCONIOSIS
| What is the clinical presentation of silicosis?
- Progressive dyspnoea.
- Increased incidence of TB.
- CXR shows diffuse upper lobe nodular pattern.
179
PNEUMOCONIOSIS
| What is the pathophysiology of asbestosis? What occupations is it seen in?
- 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
PNEUMOCONIOSIS
| What is the clinical presentation + consequences of asbestosis?
- Progressive dyspnoea, clubbing, fine end-inspiratory crackles.
- Increased risk of lung cancer + mesothelioma, diffuse pulmonary/pleural fibrosis.
181
PNEUMOCONIOSIS
| What is the clinical presentation of byssinosis and what occupations is it seen in?
- Symptoms begin once returning to work + get better during week.
- Tight chest, cough, dyspnoea.
- Common in cotton mill workers.
182
PNEUMOCONIOSIS
| What is the clinical presentation of berylliosis and what occupation is it seen in?
- Beryllium is inhaled + causes a systemic illness with progressive dyspnoea + pulmonary fibrosis.
- Beryllium is a copper alloy used in aerospace industry.
183
PNEUMOCONIOSIS
| What are the investigations + treatment for pneumoconiosis?
- PEFR at work, Hx to see symptoms worse at work, serum immunology looking for IgE to specific workplace antigens.
- Avoid exposure, claim compensation.
184
PNEUMOCONIOSIS
| What is the prevention of pneumoconiosis?
- Risk assessment.
- Legal requirement under COSHH.
- Prevent + minimise exposure to harmful substances.
- Monitor worker's health to identify problems early.
185
GOODPASTURE'S SYNDROME
| What is the pathophysiology of goodpasture's syndrome?
- 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
GOODPASTURE'S SYNDROME
| What is the aetiology + clinical presentation of goodpasture's syndrome?
- Autoimmune, strong genetic link to HLA-DRB1.
| - Cough, haemoptysis, dyspnoea + anaemia (may result from persistent intrapulmonary bleeding).
187
GOODPASTURE'S SYNDROME
| What are the investigations for goodpasture's syndrome?
- Bloods = presence of antiglomerular basement membrane (anti-GBM) membranes.
- CXR = infiltrates due to pulmonary haemorrhage.
- Kidney biopsy = crescentic glomerulonephritis.
188
GOODPASTURE'S SYNDROME
| What is the treatment for goodpasture's syndrome?
- Can spontaneously improve or progress to renal failure.
- Treat shock.
- Vigorous immunosuppressive treatment with plasmapheresis.
189
WEGENER'S GRANULOMATOSIS
| What is the pathophysiology of Wegener's granulomatosis?
- Vasculitis of unknown aetiology, commonly involves upper airway + endo-bronchi.
- Granulomatous with polyangiitis (autoimmune inflammatory condition affecting endothelial cells in nose, sinuses etc).
190
WEGENER'S GRANULOMATOSIS
| What is the clinical presentation of Wegener's granulomatosis?
- Rhinorrhoea.
- Haemoptysis.
- Epistaxis.
- Destruction of nasal septum ('saddle-nose' deformity).
- ?renal disease, with proteinuria/haematuria.
191
WEGENER'S GRANULOMATOSIS
| What are the potential complications with Wegener's granulomatosis?
- AKI.
| - Respiratory failure.
192
WEGENER'S GRANULOMATOSIS
| What are the investigations for Wegener's granulomatosis?
- Bloods = FBC, U+E, raised ESR/CRP.
- Serum c-ANCA + anti-PR3 positive.
- Urinalysis = proteinuria + haematuria indicates renal biopsy.
193
WEGENER'S GRANULOMATOSIS
| What is the treatment of Wegener's granulomatosis?
- Steroids like prednisolone.
- Methotrexate used for maintenance.
- Immunosuppressants with monoclonal antibody like rituximab in severe disease.
194
MESOTHELIOMA
| What is the pathophysiology of mesothelioma?
- 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
MESOTHELIOMA
| What is the aetiology + epidemiology of mesothelioma?
- Occupational (strong association with asbestos inhalation, latent period up to 45 years).
- Genetic risk.
- 3x more common in men, >75y/o.
196
MESOTHELIOMA
| What is the clinical presentation of mesothelioma?
- Chest pain.
- Dyspnoea.
- Finger clubbing.
- Weight loss.
- Recurrent pleural effusions.
197
MESOTHELIOMA
| What are the investigations for mesothelioma?
- CXR/CT scan = pleural thickening/effusion, blood pleural fluid.
- Pleural biopsy.
- Diagnosis via histology following thoracoscopy.
198
MESOTHELIOMA
| What is the treatment for mesothelioma?
- Surgery for extremely localised mesothelioma.
| - Generally resistant to surgery, chemo + radiotherapy.
199
BETA-2-ADRENOCEPTOR AGONISTS
| What are beta-2-adrenoceptor agonists? What are their mechanism?
- Inhaled medications delivered directly to lung via oral/nasal route.
- Bind to beta-2-adrenoceptors causing smooth muscle relaxation + bronchodilation.
200
BETA-2-ADRENOCEPTOR AGONISTS
| How are beta-2-adrenoceptor delivered? Give examples.
- 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
BETA-2-ADRENOCEPTOR AGONISTS
| What are the adverse effects of beta-2-adrenoceptor agonists?
- Hypokalaemia, tremor.
| - Palpitations + muscle cramps.
202
MUSCARINIC ANTAGONISTS
| What is the mechanism of muscarinic antagonists?
- Anticholinergic compounds block the muscarinic receptors (M3) on airway smooth muscle, glands + nerves to prevent muscle contraction, gland secretion + enhance neurotransmitter release.
203
MUSCARINIC ANTAGONISTS
| What are some examples of muscarinic antagonists?
- Atropine = naturall occurring anticholinergic.
| - Short-acting = ipratropium, long-acting = tiotropium.
204
STEROIDS
| What is the mechanism of action of steroids?
- 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
STEROIDS
| What are some examples of steroids? What are the adverse effects?
- Prednisolone, dexamethasone.
| - Osteoporosis (+ subsequent fractures), adrenal suppression, cataracts + increased infection risk.
206
STEROIDS
| What are inhaled corticosteroids used for? Give an example. What is the adverse effect?
- Improves quality of life, lung function + reduces likelihood of exacerbations.
- Beclometasone.
- Increased pneumonia risk.
207
TREATING FIBROSIS
| What 2 drugs can be used for treating fibrosis and what are their mechanisms?
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.
