RESPIRATORY Flashcards
1
Q
Define pneumonia
A
Inflammation of the substance of the lungs .
It is an acute lower respiratory tract infection
2
Q
How can pneumonia be anatomically classified?
A
- Bronchopneumonia = diffuse, patchy infection of different lobes
- Lobar pneumonia = localised consolidation of a single lobe
3
Q
How can pneumonia be aetiologically classified?
A
- Community acquired pneumonia = person with no underlying immunosuppression or malignancy
- Hospital acquired pneumonia = >48 hours after hospital admission
- Aspiration pneumonia = acute aspiration of gastric contents into lungs
4
Q
Briefly describe the pathophysiology of pneumonia
A
- invasion and overgrowth of a pathogen in lung parenchyma
- overwhelming of host immune defences
- production of intra-alveolar exudates
5
Q
What can cause pneumonia to be severe?
A
- Excessive inflammation
- Lung injury
- Resolution failure
6
Q
Name 3 groups of people who might be at risk of pneumonia
A
- Elderly
- Children
- COPD patients
- Immunocompromised people
- Nursing home residents
- alcoholics
- IV drug users
7
Q
Name 3 pathogens that can cause community acquired pneumonia (CAP)
A
- Streptococcus pneumoniae (most common)
- Haemophilus influenzae
- Mycoplasma pneumoniae
8
Q
Name 3 pathogens that can cause hospital acquired pneumonia (HAP)
A
mainly gram negative
- Pseudomonas aeruginosa
- E.coli
- Klebsiella penumoniae
- Staphylococcus aureus
9
Q
which pathogen can cause pneumonia in immunocompromised patients
A
pneumocystis jiroveci
10
Q
What symptoms might you see in someone with pneumonia?
A
SOB cough sputum fever pleuritic chest pain delirium
11
Q
What signs might you see in someone with pneumonia?
A
- increased resp rate and HR
- hypotension
- decreased O2 saturation
- dull to percuss
- increased tactile fremitus
12
Q
What investigations might you do on someone you suspect has pneumonia?
A
- FBC, U&E, CRP– increased WCC, urea and CRP
- Sputum culture - MC+S
Chest X ray: localised/widespread consolidation, effusion, abscesses, empyema
Multi-lobar – strep pneumoniae, s. aureus
Multiple abscesses – s. aureus
13
Q
How can you assess the severity of community acquired pneumonia?
A
CURB65 score (1 point for each)
- Confusion
- Urea (>7 mmol/L)
- Respiratory rate (> 30/min)
- BP (<90/60 mmHg)
- Age >65
Scores 0-1 = mild (outpatient treatment) 2 = admit to hospital 3-4 = severe, admit and monitor closely 5 = ITU transfer
14
Q
How can pneumonia be prevented?
A
polysaccharide pneumococcal vaccine - protests against 23 serotypes
Smoking cessation
15
Q
What is the treatment for someone with mild CAP (CRUB65 score 0-1)?
A
oral amoxicillin at home
16
Q
What is the treatment for someone with moderate CAP (CRUB65 score 2)?
A
consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin)
17
Q
What is the treatment for someone with severe CAP (CRUB65 score 3-5)?
A
consider ITU,
IV Co-Amoxiclav + macrolide (clarithromycin)
18
Q
What is the treatment for someone with Legionella pneumoniae?
A
Fluoroquinolone + clarithromycin
19
Q
What is the treatment for someone with Pseudomonas aeruginosa pneumonia?
A
IV ceftazidime + gentamicin
20
Q
A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L
a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient
A
a) Their CURB65 score is 5
b) This patient should be treated in hospital and admitted to critical care
c) The patient should be given IV co-amoxiclav and clarithromyocin
21
Q
Give 3 potential complications of pneumonia
A
- Respiratory failure
- Hypotension
- Empyema
- Lung abscess
22
Q
Define bronchiectasis
A
Chronic infection of the bronchi/bronchioles leading to permanent dilation and thinning of the airways
23
Q
Describe the pathophysiology of bronchiectasis
A
Failed mucociliary clearance and impaired immune function means microbes easily invade and cause infection
This causes inflammation and progressive lung damage
Bronchitis –> bronchiectasis –> fibrosis
24
Q
What can cause bronchiectasis?
A
- Congenital = Cystic fibrosis
- Idiopathic (50%)
- Post infection - (most common)
- pneumonia,
- TB,
- whopping cough
- Bronchial obstruction
- RA
- Hypogammaglobulinaemia
25
Which bacteria might cause bronchiectasis?
1. Haemophilus influenza (children)
2. Pseudomonas aeruginosa (adults)
3. Staphylococcus aureus (neonates often)
26
Give 3 symptoms of bronchiectasis
1. Chronic productive cough
2. Purulent sputum
3. Intermittent haemoptysis
4. Dyspnoea
5. Fever, weight loss
27
Give 3 signs of bronchiectasis
1. Finger clubbing
2. Coarse inspiratory crepitate (crackles)
3. Wheeze
28
What investigations might you do on someone to determine whether they have bronchiectasis?
CXR = kerley B lines, dilated bronchi with thickened walls, multiple cysts containing fluid
High resolution CT = bronchial wall dilation
Spirometry = obstructive lung disease
Sputum culture - h.influenzae is most common
29
Describe the treatment for bronchiectasis
1. Antibiotics
2. Anti-inflammatories (azithromycin)
3. Bronchodilators (nebulised salbutamol)
4. Chest physio - physical training
5. Surgery = lung resection or transplant
30
Give 3 possible complications of Bronchiectasis
1. Pneumonia
2. Pleural effusion
3. Pneumothorax
31
A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?
Bronchiectasis
32
Describe the pathogenesis of Cystic fibrosis
Autosomal recessive defect in chromosome 7 coding CFTR protein (F508 deletion = most common mutation)
- Cl- transport affected
- Decreased Cl secretion and increase Na reabsorption this causes an increase H2O reabsorption --> thickened mucus secretion
- in the lungs, this leads to dehydrated airway surface liquid, mucus stasis, airway inflammation and recurrent infection
- this leads to progressive airway obstruction and bronchiectasis
33
What are the main systemic consequences of CF?
Pancreatic insufficiency = dehydrated secretion --> enzymes stagnation
GI = intraluminal water deficiency --> concentrated bile
Resp = thick mucus can't be cleared --> infection risk and inflammatory damage
34
How is CF passed on?
Autosomal recessive condition
35
How does neonate present with CF?
- Failure to thrive
- Meconium ileus - bowel obstruction due to thick meconium
- Rectal prolapse
36
How do children/young adults present with CF?
- Cough and wheeze
- Recurrent infections
- Haemoptysis
- Pancreatic insufficiency
- Malabsorption
- Male infertility
37
What are 3 possible respiratory complications of CF?
1. Pneumothorax
2. Respiratory failure
3. Cor pulmonale
4. Bronchiectasis
38
Give 3 signs of CF
1. Clubbing
2. Cyanosis
3. Bilateral coarse crepitations
39
Name 3 associated conditions with CF
1. Osteoporosis
2. Arthritis
3. Vasculitis
40
What investigations might you do to diagnose cystic fibrosis?
heel prick test - newborns
Sweat test = Na and Cl < 60 mmol/L
Genetic screening for common mutations
Faecal elastase - tests pancreatic enzyme function
Absent vas deferent and epididymis (males)
Microbiology - for infections
Spirometry
41
What is the management of CF?
1. Physical therapies (airway clearance) and surveillance
2. Antibiotics for infections and prophylaxis
3. Bronchodilators
- B2 agonist (SALBUTAMOL) and inhaled corticosteroids (BECLOMETASONE)
4. Pancreatic enzymes replacement (creon)
5. ADEK vitamin supplements
6. Screening for consequent conditions - osteoporosis
7. Bilateral lung transplant
- must not have m. abscessus
8. Vaccinations - flu and pneumococcal
9. high calorie, high fat diet
42
Infection with a gram negative bacteria is a particular concern in patients with CF. What is this organism and how can infection be prevented?
- Pseudomonas Aeruginosa
| - Nebulised anti-pseudomonal antibiotic therapy and regular sputum cultures
43
Malignant bronchial tumour can be divided into 2 groups, what are they?
1. Non small cell lung carcinoma (80%)
| 2. Small cell lung carcinoma (20%)
44
What type of malignant bronchial tumour tends to have a worse prognosis?
Small cell lung carcinomas - often metastasise
45
From what cells are small cell carcinomas derived from and what is the significance of this?
Neuroendocrine cells
| Can secrete peptide hormones - ACTH, PTHrP, ADH, HCG
46
Give the cell types the make up non-small cell lung cancers
1. Squamous cell (20%) - arise from epithelial cells + associated with keratin production
2. Adenocarcinoma (40%) - originate from mucus-secreting glandular cells
3. Large cell
4. carcinoid tumours
47
what are the risk factors of lung cancer
1. Smoking = main cause
2. Asbestos
3. Radon exposure
4. Coal products
5. pulmonary fibrosis
6. HIV
7. genetic factors
48
Which type of NSCC is most common in smokers?
Squamous cell carcinoma - it is most stronlgy associated with cigarette smoking
49
Which type of malignant bronchial tumour fits into TNM staging?
Non small cell carcinoma
50
What does TNM stand for in lung cancer?
```
T = size/invasion = T1 (<3cm) --> T2 (>3cm) --> T3 (chest wall/diaphragm) --> T4 (heart + vessels)
N = nodal involvement = N1 (hilar) --> N2 (ipsilateral mediastinal) --> N3 (contralateral mediastinal)
M = metastases = M0 (no metastases) --> M1 (metastases)
```
51
where does lung cancer commonly metastasise to?
1. Bone
2. Brain
3. Lymph nodes
4. Liver
5. Adrenal
52
which cancers most commonly metastasise to the lungs?
breast
bowel
kidney
bladder
53
Give 4 symptoms of local disease lung cancer
```
Persistent cough
Shortness of breath
Haemoptysis
Weight loss
Chest pain, wheeze, recurrent infections
```
54
Give 4 symptoms of lung cancer that has metastasised
1. Bone pain
2. Headaches
3. Abdominal pain
4. Seizures
5. Neuro deficit - Confusion
6. Weight loss
55
What are paraneoplastic syndromes?
they are conditions which occur as a side effect of the tumour and occur in 10% of patients
56
Give 3 examples of paraneoplastic syndromes due to lung cancer
- ↑PTH -> Hyperparathyroidism
- ↑ADH -> SIADH
- ↑ACTH -> Cushing’s disease
57
Name 3 differential diagnosis's of lung cancer
1. Oesophageal varices
2. COPD
3. Asthma
4. Pneumonia
5. Bronchiectasis
58
What investigations might you done on someone to determine whether they have lung cancer?
First line:
- CXR - central mass, hilar lymphadenopathy, pleural effusion
(a negative CXR does not rule out cancer)
- CT chest, liver & adrenal glands – for staging
- Sputum cytology - malignant cells in sputum
(high specificity but mixed sensitivity)
diagnostic = biopsy + histology
59
What is the treatment for NSCLC?
* Surgical excision for peripheral tumours with no metastatic spread
* Curative radiotherapy is an alternative if respiratory reserve is poor - complications include radiation pneumonitis + fibrosis
* Chemotherapy +/- radiotherapy for more advanced disease e.g. with monoclonal antibodies e.g. CETUXIMAB
60
What is the treatment for SCLC?
Limited disease = chemo + radio
Extensive = palliative chemo + care
• Superior vena cava stent + radiotherapy + dexamethasone for superior
vena cava obstruction
• Endobronchial therapy - used to treat symptoms of airway narrowing:
61
Give 4 possible complications of lung cancer
1. SVC obstruction
2. ADH secretion --> SIADH
3. ACTH secretion --> Cushing's
4. Serotonin secretion --> carcinoid
5. Peripheral neuropathy
6. Pathological fractures
7. Hepatic failure
62
Describe asthma
Chronic, inflammatory condition, causing episodes of reversible airway obstruction, due to:
Bronchoconstriction
Excessive secretion production
63
What are the 3 characteristic features of asthma?
* Airflow limitation - usually reversible spontaneously or with treatment
* Airway hyper-responsiveness
* Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation
64
what are the causes of asthma?
Hypersensitivity of the airways, triggered by various factors:
Cold air,
exercise
Cigarette smoke
Air pollution
Allergens: pollen, cats, dogs, horses, mould
Time of day: early morning, night
65
What is the mechanism behind hyper-reactivity?
Neurogenic inflammation
66
Describe neurogenic infalmmation
Sensory nerve activation initiates impulses which stimulates CGRP (pro-inflammatory)
this activates mast cells and innervates goblet cells
67
Describe the process of airway remodelling in asthma
1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen
2. Deposition of collagen below the BM thickens the airway wall
3. metaplasia occurs with an increase in number of mucus-secreting goblet cells
68
What type of T cell is involved in asthma?
CD4+
69
What 2 categories can asthma be divided into?
1. Allergic asthma (extrinsic), atopic, IgE and mast cell involvement
2. Non allergic asthma (intrinsic)
70
Define atopy
The tendency to develop IgE mediated response to common aeroallergens
71
What is allergic asthma?
When an innocuous allergen triggers an IgE mediated response
Immune recognition processes are faulty --> increase IgE, IL3,4,5, production
72
What is non-allergic asthma?
Airway obstruction induced by exercise, cold air and stress
it is associated with both smoking/non-smoking
it is also associated with obesity
73
Extrinsic asthma: what happens when IgE binds to mast cells?
Vasodilative substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion
74
Name 4 factors that can exacerbate asthma
1. Allergens
2. Viral infection
3. Cold air
4. Exercise
5. Stress
6. Cigarette smoke
7. Drugs - NSAIDs/BB
75
What occupations can be associated with an increase risk of developing asthma?
1. Paint sprayers
2. Animal breeders
3. Bakers
4. Launder workers
76
What other atopic conditions are associated with asthma?
Eczema
| Hayfever
77
What are the symptoms of asthma?
1. Episodic cough
2. Expiratory wheeze
3. SOB
4. often worse at night (and in the morning)
5. Chest tightness
6. dyspnoea
78
What are the signs of asthma?
1. Tachypnoea - rapid breathing
2. Audible wheeze
3. Widespread polyphonic wheeze
4. Cough
79
What are the signs of an acute asthma attack?
1. Can't complete sentences
2. HR > 110 bpm
3. RR > 35/min
4. PEF < 50% predicted
80
What are the signs of a life threatening asthma attack?
1. Hypoxia = PaO2 <8 kPa, SaO2 <92%
2. Silent chest
3. Bradycardia
4. Confusion
5. PEFR < 33% predicted
6. Cyanosis
81
Give 3 differential diagnosis's of asthma
1. COPD
2. Bronchial obstruction
3. Pulmonary oedema
4. Pulmonary embolism
5. Bronchiectasis
82
What investigations might you do someone to determine whether they have asthma?
1. PEFR
2. Spirometry with reversibility testing (>5 years)
- Obstructive pattern:
- FEV1 <80% of predicted normal (reduced)
- FVC = normal
- FEV1/FVC ratio <0.7
Peak flow measurement (reduced)
3. CXR
4. Atopy = skin prick, RAST
5. Bloods = high IgE, Eosinophils
83
What is the long-term guideline mediation regime for asthma?
1. SABA
2. SABA + ICS
3. SABA + ICS + LTRA
4. SABA + ICS + LABA continue LTRA if needed (stop LTRA in children)
84
Give 3 possible complications of asthma
1. Exacerbation
2. Pneumothorax
3. Pneumonia
85
Define COPD
Progressive obstructive disorder (FEV1/FC < 70%) that is irreversible
long-term deterioration in air flow through the lungs, caused by damage to lung tissue (almost always due to smoking)
86
What can COPD be sub-divided into?
1. Chronic bronchitis
| 2. Emphysema
87
What is the clinical diagnosis of chronic bronchitis?
Cough/sputum for >3 months in 2 consecutive years
88
Describe the pathophysiology of chronic bronchitis
Airway inflammation --> fibrosis and luminal plugs --> decreased alveolar ventilation
89
Would a patient with chronic bronchitis be a 'pink puffer' or a 'blue bloater'?
Blue bloater
Patient have low PaO2 and high PaCo2 --> cyanosis --> cor pulmonale
Cyanosis = blue
90
Describe the pathophysiology of emphysema
Dilation and destruction of the lung tissue distal to the terminal bronchioles
Enlarged alveoli + loss of elastic recoil = increased alveolar ventilation
91
Would a patient with emphysema be a 'pink puffer' or a 'blue bloater'?
Pink puffer
Breathless but not cyanosed
Type 1 respiratory failure
Normal or near normal PaO2 and normal or low PaCO2
92
What are the main cells responsible for inflammation in COPD?
Neutrophils and macrophages
93
What type of T cell is involved in COPD?
CD8+
94
What can cause COPD?
1. Genetic = alpha 1 antitrypsin deficiency
2. Smoking = major cause
3. Air pollution
4. Occupational factors = dust, chemicals
95
Name 4 symptoms of COPD
1. Dyspnoea
2. Cough +/- sputum
3. Expiratory wheeze
4. Weight loss
5. SOB
96
Give 4 signs of COPD
1. Tachypnoea
2. Barrel shaped chest
3. Hyperinflantion
4. Cyanosis
5. Pulmonary hypertension
6. Cor pulmonale
97
Give 3 differential diagnosis's for COPD
1. Asthma
2. HF
3. Pulmonary embolism
4. Bronchiectasis
5. Lung cancer
98
What investigations might you do to diagnose someone with COPD?
```
Spirometry = FEV1:FVC < 0.7
CXR = hyperinflation, bullae, flat hemi-diaphragms, large pulmonary arteries
CT = Bronchial wall thickening, enlarged air spaces
ECG = RA and RV hypertrophy
ABG = decreased PaO2 +/- hypercapnia
```
99
Give 3 factors that can be used to establish a diagnosis of COPD
1. Progressive airflow obstruction
2. FEV1/FVC ratio < 0.7
3. Lack of reversibility
100
What are the treatments for COPD?
general:
- stop smoking (refer to cessation services)
- pneumococcal vaccine
- annual flu vaccine
step 1:
- SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)
step 2:
- If no asthmatic / steroid response:
- LABA (salmeterol)
- LAMA (tiotropium)
- If asthmatic / steroid response:
- LABA (i.e. salmeterol)
- ICS (i.e. budesonide)
step 3:
- long term oxygen therapy
101
Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?
Advantages
1. Improve QOL
2. Improve lung function
3. Reduce the likelihood of exacerbations
Disadvantages:
1. There is an increased risk of pneumonia
102
Give 3 possible complications of COPD
1. Exacerbations
2. Infection
3. Respiratory failure
4. Cor pulmonale
5. Pneumothorax
103
Define exacerbation of COPD
An acute event characterised by worsening symptoms beyond normal day to day variation
104
Give 2 potential consequences of exacerbations of COPD/asthma
1. Worsened symptoms
2. Decreased lung function
3. Negative impact of QOL
4. Increased mortality
5. Huge economic cost
105
What is the likely cause for an exacerbation of COPD?
Viral URTI
| Bacterial infections
106
What are the aims of treatment for exacerbations of COPD?
1. Minimise the impact of the current exacerbation
| 2. Prevent subsequent exacerbations
107
What is the treatment for an exacerbation of COPD?
Steroids (hydrocortisone / prednisolone)
+
nebulised bronchodilators (salbutamol / ipratropium bromide)
+
antibiotics
Physiotherapy → sputum clearance
If severe:
IV aminophylline (bronchodilator),
NIV (CPAP / BIPAP)
108
Give 3 ways in which subsequent exacerbations of COPD can be prevented
1. Smoking cessation
2. Vaccination
3. LABA/LAMA/ICS
109
A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?
Asthma
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people
110
An older person presents to you with breathlessness, wheeze and cough. There appears to be inflammation and fibrosis of the airways and also alveolar disruption. You ask the patient to do a peak flow diary and the results of this are all abnormal. Is the patient likely to have asthma or COPD?
COPD
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are consistently abnormal is a large indication that this person has COPD; in asthma there would be diurnal variation. Fibrosis and alveolar disruption are also signs of COPD and the fact that the patient is an older patient also makes COPD the more likely diagnosis
111
Give 3 functions of pleura
1. Allows movement of the lung against the chest wall
2. Coupling system between the lungs and chest wall
3. Clearing fluid from the pulmonary interstitium
112
What does the pleural fluid contain?
Protein - albumin, globulin, fibrinogen
| Mesothelial cells, monocytes and lymphocytes
113
How much fluid is contained within the healthy pleural space?
15ml
114
What produces and reabsorbs pleural fluid?
Parietal pleura
115
Name 3 diseases associated with the pleura
1. Pleural effusion
2. Pneumothorax
3. Pleural plaques
116
Define pleural effusion
Excess accumulation of fluid in the pleural space
117
Name the types of pleural effusion
1. Transudate = extravascular fluid with low protein content (<25 g/L)
2. Exudate = protein rich fluid (>35 g/L)
3. Chylothorax = lymph in pleural cavity
118
what are the causes of a transudate pleural effusion?
fluid movement (systemic causes)
1. Heart failure
2. fluid overload
3. Peritoneal dialysis
4. Constrictive pericarditis
5. hypoproteinaemia
- cirrhosis
- hypoaluminaemia
- nephrotic syndrome
119
Name 3 causes of a exudate pleural effusion
inflammatory (local causes)
1. Pneumonia
2. Malignancy
3. TB
4. pulmonary infarction
5. lymphoma
6. mesothelioma
7. asbestos exposure
8. MI
120
How does a pleural effusion present?
- SOB especially on exertion
- Dyspnoea
- Pleuritic chest pain
- cough
- Loss of weight (malignancy)
- Chest expansion reduced on side of effusion
- In large effusion the trachea may be deviated away from effusion
- Stony dull percussion note on affected side
- Diminished breath sounds on affected side
- Decreased tactile vocal fremitus (vibration of chest wall when speaking)
- Loss of vocal resonance
121
How might you diagnose a pleural effusion?
1st line: CXR =
blunt costophrenic angles, fluid in lung fissures, meniscus, tracheal and mediastinal deviation
USS - identify pleural fluid
aspiration (thoracentesis/pleural tap)
- purulent = empyema (pus)
- turbid (cloudy) = infected
- milky = chylothorax
122
How would you treat a pleural effusion?
Dependent on cause
Fluid overload or congestive HF - diuretic
Infective - antibiotics
Large effusions often need aspiration or drainage
123
What can you do if recurrent pleural effusions occur?
Pleurodesis (stick pleura together)
124
What is a pneumothorax?
Accumulation of air in the pleural space which can lead to partial or complete lung collapse
125
How can pneumothorax be classified?
```
Spontaneous pneumothorax
Traumatic pneumothorax
Iatrogenic pneumothorax
Lung Pathology
Tension pneumothorax
```
126
How does a pneumothorax present?
- Sudden onset dyspnoea and pleuritic chest pain
- as the pneumothorax enlarges the patient becomes more breathless and may develop pallor and tachycardia
- Reduced expansion
- Hyper-resonant percussion
- Diminished breath sounds
127
What investigation might you do in someone you suspect to have a pneumothorax?
CXR = translucency and collapse
ABG = in dyspnoeic patients check for hypoxia
128
What is the treatment for a pneumothorax?
- Small primary spontaneous PTX (visible rim ≤ 2cm) and not SOB
- Consider discharge and follow up CXR in review
Large primary spontaneous PTX (visible rim >2cm) and/or SOB
- Needle aspiration
If not <2cm on repeat CXR insert chest drain and supplemental O2 if needed, admit.
- Secondary Pneumothorax – requires chest drain if large/ needle aspiration if small, admission and high flow O2
129
Name a possible complication of a pneumothorax
Tension pneumothorax
130
Describe the pathophysiology of a tension penumothorax
Pleural tear creates 1 way valve - air only goes into cavity --> increased unilateral pressure --> respiratory distress, shock and cardiac arrest
131
What is the treatment for a tension pneumothorax?
```
Put out cardiac arrest call
Start high flow O2
Immediate decompression
Unless tension PTX due to trauma:
“Insert a large bore cannula into the pleural space through the second intercostal space in the mid-clavicular line”
```
Hiss sound confirms diagnosis
132
Define interstitial lung diseases
Distant cellular infiltrate and extracellular matrix deposition in lung distal to the terminal bronchioles - disease of the alveolar/capillary interface
133
What are 5 major categories of interstitial lung disease
1. Associated with systemic disease - rheumatological
2. Environmental aetiology - fungal, dusts
3. Granulomatous disease - sarcoidosis
4. Idiopathic - idiopathic pulmonary fibrosis
5. Other
134
What are the 4 major features of interstitial lung disease?
1. Cough
2. Dyspnoea
3. Restirictve spirometry
4. Abnormal CXR/CT
135
Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?
Restrictive
| Decreased gas transfer and a reduction in PaO2
136
What is the pathology of interstitial lung disease?
Increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion
137
What kind of disease is sarcoidosis?
Granulomatous disease - type of interstitial lung disease
138
Describe the pathophysiology of sarcoidosis
Chronic inflammation --> non-caseating granuloma in various body sites
Typical sarcoid granulomas consist of focal accumulations of epithelioid cells, macrophages and lymphocytes - mainly T cells
139
Describe the epidemiology of sarcoidosis
Women > men
Aged 20-40 years old
African-Caribbean's are affected more frequently and more severely than Caucasians
140
Give 3 pulmonary symptoms of sarcoidosis
1. Dry cough
2. Progressive SOB
3. Wheeze
4. Chest pain
141
What is the effect of sarcoidosis on the skin?
Erythema nodosum
142
What is the effect of sarcoidosis on the eyes?
Uveitis
143
What is the effect of sarcoidosis on the bone?
Arthralgia
144
What is the effect of sarcoidosis on the liver?
Hepatosplenmeagly
145
What investigations might you do in someone who you suspect to have sarcoidosis?
Bloods = increase ESR, lymphopenia, increase CAE, raised LFTs
Bronchoalveolar lavage = increased lymphocytes
Lung tissue biopsy = diagnostic = non-caseating granulomata (increased lymphocytes in active disease and increased neutrophils in pulmonary fibrosis)
CXR = staging
146
How can you stage sarcoidosis?
Using CXR
Stage 1 = bilateral hilar lymphadenopathy (BHL)
Stage 2 = pulmonary infiltrates with BHL
Stage 3 = pulmonary infiltrates without BHL
Stage 4 = progressive pulmonary fibrosis, bulla formation and bronchiectasis
147
How do you treat acute sarcoidosis?
NSAIDs and bed rest
148
How do you treat sarcoidosis?
do not treat symptomatic stage 1, and asymptomatic stage 2 or 3
patients with BHL do not need treatment - most recover spontaneously
acute = bed rest and NSAIDs
prednisolone orally
if severe = IV methylprednisolone
if steroid resistant = methotrexate (requires close monitoring)
lung transplant in severe cases
149
Give 2 possible differential diagnosis's for sarcoidosis
1. Lymphoma
| 2. Pulmonary TB
150
What is idiopathic pulmonary fibrosis?
Progressive fibrosis in the alveoli that limits the patients ability to respire
Formation of scar tissue in lungs with no known cause.
151
Describe the pathophysiology of idiopathic pulmonary fibrosis
repetitive injury to the alveoli epithelium causes wound healing mechanisms to become uncontrolled
this leads to fibroblast over-production and increased fibrosis
this leads to a loss of elasticity and ability to perform gas exchange is impaired -> restrictive lung disease and progressive respiratory failure
152
what are the risk factors of idiopathic pulmonary fibrosis?
- cigarette smoking
- infectious agents - CMV, Hep C, EBV
- occupational dust exposure
- drugs - methotrexate, imipramine
- GORD
- genetic predisposition
153
what are the clinical features of idiopathic pulmonary fibrosis
1. Dry cough
2. SOB on exertion
3. Systemic = malaise, weight loss, arthralgia
4. Cyanosis
5. Finger clubbing
6. bibasal crackles (Inspiratory crackles/crepitus)
7. dyspnoea
154
What investigations might you do in someone you suspect to have idiopathic pulmonary fibrosis?
ABG = type 1 respiratory failure
Bloods = raised CRP, immunoglobulins and check autoantibodies
CXR/CT = degreased lung volume + honeycomb lung
High resolution CT = ground glass appearance
Spirometry = restrictive
Lung biopsy = confirmation
155
What is the treatment for idiopathic pulmonary fibrosis?
Pharmacological: Pirfenidone, nintedanib - antifibrotic
Non pharmacological: Smoking cessation, physiotherapy, vaccines up to date
Lung transplantation last resort
156
what are the possible complications of idiopathic pulmonary fibrosis
1. Respiratory failure
| 2. Cor pulmonale
157
Define pulmonary hypertension
A disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR)
Increase in mean pulmonary arterial pressure >25 mmHg and secondary right ventricular failure
158
What can cause an increase in mPAP?
Increase resistance to flow
| Increased flow rate
159
what are the causes of pulmonary hypertension
- pre-capillary
- multiple small PE's
- left-to-right shunts
- primary
- capillary
- emphysema
- COPD
- Post-capillary
- backlog of blood causes secondary hypertension
- LV failure
- chronic hypoxaemia
- living at high altitude
- COPD
160
what is the clinical presenation of pulmonary hypertension
initial features - due to an inability to increase cardiac output
- exertional dyspnoea
- lethargy and fatigue
- ankle swelling
- Accentuated pulmonic component to the 2nd heart sound
- Tricuspid regurgitation murmur
- peripheral oedema, cyanosis
- cor pulmonale
161
What investigations might you do in someone to determine whether they have pulmonary hypertension?
Initial tests:
- CXR - Enlarged main pulmonary artery, enlarged hilar vessels and pruning.
- ECG - right ventricular hypertrophy, right axis deviation, right atrial enlargement. (A normal ECG does not rule out the presence of significant pulmonary hypertension)
- TTE - (trans-thoracic echocardiogram)
Diagnostic test: Right heart catheterisation
162
Describe the treatment of pulmonary hypertension
```
General supportive therapy:
Treat underlying cause
- Oral anticoagulants - WARFARIN
- diuretics for oedema
- oxygen
- oral CCBs
- Supervised exercise training
Avoiding pregnancy
```
In treatment-resistant patients:
Balloon atrial septostomy - produces right-to-left shunting that decompresses the right atrium and right ventricle, increases systemic cardiac output, and decreases systemic arterial oxygen saturation
Lung transplantation
163
Give a possible complication of pulmonary hypertension
Cor pulmonale (RS HF) --> pleural effusion + death
164
what are the features of mycobacterium tuberculosis bacteria?
- Aerobic, non-motile, non-sporing, slightly curved bacilli with a thick waxy capsule
- Acid-fast bacilli – turns red/pink with Ziehl-neelsen stain
- Slow growing
- Resistant to phagolysosomal killing and able to remain dormant
165
What mycobacterium can cause abdominal tuberculosis?
Mycobacterium bovis
| - found in unpasteurised milk
166
How is TB transmitted?
Aerosol transmission
167
Describe pulmonary infection of TB
Bacilli settle in lung apex
| Macrophages and lymphocytes mount an effective immune response that encapsulate and contains the organism forever
168
Describe the pathogenesis of pulmonary TB disease
TB spread via respiratory droplets as it is an airborne infection
1. Alveolar macrophages ingest bacteria and the rods proliferate inside.
2. Drain into hilar lymph nodes 🡪 present antigen to T lymphocytes 🡪 cellular immune response.
3. Delayed hypersensitivity reaction 🡪 tissue necrosis and granuloma formation: caseating.
- Primary Ghon Focus
- Ghon Complex – Ghon focus + lymph nodes
169
Describe the disease course of TB
Primary infection --> latent TB --> reactivation/immunocompromised
170
Where in the lung is granuloma cavity most likely to develop in TB?
Apex of the lung = more air and less blood supply and less immune cells
171
Give 3 risk factors for TB
1. Living in a high prevalence area
2. IVDU
3. Homeless
4. Alcohol
5. HIV +ve
172
What systemic symptoms might you see as a result of TB?
1. Weight loss
2. Night sweats
3. Anorexia
4. Malaise
5. low grade fever
173
What pulmonary symptoms might you see as a result of TB?
```
Productive cough
Haemoptysis
Cough >3 weeks (dry or productive)
Breathlessness
Sometimes chest pain
```
174
Name 3 places where TB might spread to?
1. Bone and joint = pain and swelling
2. Lymph nodes = pain and discharge
3. CNS = TB meningitis
4. Biliary TB = disseminated
5. Abdominal TB = ascites, malabsorption
6. GU TB = sterile pyuria, WBC in GU tract
175
What investigations might you do to determine whether someone has TB?
Inflammatory markers = raised CRP, hyperalbuminaemia, thromobocytosis, high B cell count
CXR = consolidation, collapse, pleural effusion
Microbiology - sputum/biopsy = Ziehl-Neelson stain and culture
176
A special culture medium is needed to grow TB, what is it called?
Lowenstein Jenson Slope
177
What test might you do to diagnose latent TB?
Tuberculin skin test (Mantoux)
Intradermal injection --> stimulates type 4 hypersensitivity reaction
interferon gamma release assay -> detect response of WBC to TB antigens
(rapid results and less likely to give false positives)
178
What might a lymph node biopsy from someone with TB show?
Caseating granuloma
179
What is the drug treatment commonly used for TB?
RIPE
RI = 6 months
PE = for first 2 months
```
R = rifampicin
I = isoniazid
P = pyrazinamide
E = ethambutol
```
180
Give 2 potential side effects of Rifampicin
1. Red urine
2. Hepatitis
3. Drug interaction - it's an enzyme inducer
181
Give 2 potential side effects of Isoniazid
1. Hepatitis
| 2. Neuropathy
182
Give 2 potential side effects of Pyrazinamide
1. Hepatitis
2. Gout
3. Neuropathy
183
Give a potential side effect of Ethambutol
Optic neuritis
184
Why is compliance so important when taking TB medication?
Resistance and relapse likely if non-compliant
185
Why does TB treatment need to last 6 months?
Ensure all dormant bacteria have 'woken up' and been killed
186
Give 2 factors that can increase the risk of drug resistance in TB
1. If the patient has had previous treatment
2. If they live in a high risk area
3. If they have contact with resistant TB
4. If they have a poor response to therapy
187
How can TB be prevented?
1. Active case finding
2. Detect and treat latent TB
3. Vaccination = BCG
188
What is Whooping cough caused by?
Bordatella pertussis (gram -ve coccobacilli) - rod
189
Describe the disease course of whooping cough
7-10 day incubation --> 1-2 week catarrhal stage --> 1-6 week paroxysmal stage
190
What are the symptoms of whooping cough?
Paroxysmal cough - sudden and severe
| Vomiting after cough
191
What is the treatment of whooping cough?
Clarithromycin - in catarrhal or early paroxysmal stages
- have little effect on disease course in paroxysmal stage
192
How can you prevent whooping cough?
Pertussis vaccination
| 8, 12 and 16 weeks and a pre school booster
193
Give 2 possible complications of whooping cough
1. Pneumonia
2. Encephalopathy
3. Sub-conjunctival haemorrhage
194
What is the difference between bronchitis and bronchiolitis?
```
Bronchitis = inflammation of bronchi epithelium due to irritant and chemical
Bronchiolitis = Inflammation of bronchioles and increased mucus secretion due to RSV infection
```
195
A patient presents with breathlessness. On examination they have absent breath sounds and their chest produces a stony dull sound on percussion. They have a PMH of heart failure. What is the likely cause of their symptoms?
Pleural effusion
196
what is the epidemiology of cystic fibrosis?
• One of the most commonest lethal autosome RECESSIVE conditions in
CAUCASIANS, 25% condition and 50% carrier risk
- Much less common in Afro-Caribbean and Asian people
- Multi-system disease although respiratory problems are usually the most prominent
- Most people with CF also have pancreatic insufficiency
197
what are the risk factors for cystic fibrosis?
- Family history
| - Caucasian
198
what is CFTR and what is it's function?
• Transport protein on membrane of epithelial cells that acts as a chloride
channel
• Transports chloride ions
• Normally; it actively exports NEGATIVE IONS especially Cl- and Na+ passively follows causing an osmotic gradient and movement of water out of the cell and into the mucus
199
what is the clinical presentation of the alimentary effects of cystic fibrosis?
• Thick secretions
• Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
• Pancreatic insufficiency (diabetes mellitus & steatorrhoea (fatty stools
since enzymes not released to digest fat)
• Distal intestinal obstruction syndrome - bowel obstruction (equivalent of
meconium ileus) resulting in reduced GI motility
• Reduced bicarbonate (HCO3-)
• Maldigestion & malabsorption thus poor nutrition (associated with
pulmonary sepsis)
• Cholesterol Gallstones (in increased frequency) & cirrhosis
• Increased incidence of peptic ulcers & malignancy
200
what is transudate pleural effusion?
- transparent (less protein)
• Pleural fluid protein is less than 30g/L since vessels are normal so only
fluid is able to leak out and not protein
• Occurs when the balance of hydrostatic forces in the chest favour the accumulation of pleural fluid i.e. increased pressure due to the backing up of blood in left sided congestive heart failure
201
what is exudate pleural effusion?
- exudes proteins
- Pleural fluid protein is more than 30g/L since endothelial cells of vessels are more apart meaning fluid and protein is able to leak out
- Occurs due to the increased permeability and thus leakiness of pleural
space and or capillaries usually as a result of inflammation, infection or
malignancy
202
what is the epidemiology of pleural effusion?
- Seen in adults and less commonly in children
- Recurrent pleural effusions are seen malignant mesothelioma
- Pleural effusions are transudates or exudates
203
what are the risk factors for pleural effusion?
- Previous lung damage
| - Asbestos exposure
204
what are the risk factors for pneumothorax?
```
Smoking
Family history
Male
Tall and slender build
Young age
Presence of underlying lung disease
```
205
what is the pathophysiology of pneumothorax?
Normally intrapleural pressure is negative
When there is a bridge between alveoli and pleural space or atmosphere and pleural space
Flow of air in until communication closed or gradient closed.
206
what is the clinical presentation of a tension pneumothorax?
```
Cardiopulmonary deterioration:
Hypotension – imminent cardiac arrest
Respiratory distress
Low sats
Tachycardia
Shock
Severe chest Pain
```
207
what are the clinical features of a tension pneumothorax?
Tracheal deviation to contralateral side
Ipsilateral reduced breath sounds
Hyperresonance on percussion
Hypoxia
208
what is the epidemiology of pneumothorax?
- Occurs spontaneously or secondary to chest trauma
- Spontaneous pneumothorax is most common in young males
- Generally a pneumothorax is MUCH MORE COMMON in MALES
- Often patients are tall and thin
- Caused by the rupture of a pleural bleb/sub-pleural bulla(serous filled blister),
usually apical (top) thought to be due to congenital defects in the connective
tissue of the alveolar walls
209
what are the causes of pneumothorax?
- In patients over 40 years of age the usual cause is underlying COPD
- Other/rarer causes include:
• Bronchial asthma
• Carcinoma
• Breakdown of a lung abscess leading to bronchopleural fistula
• Severe pulmonary fibrosis with cyst formation
• TB
• Pneumonia
• Cystic fibrosis
• Trauma (penetrating or rib fracture)
• Iatrogenic e.g. pacemakers or central lines
210
what is the catarrhal phase of whooping cough?
* Patient highly infectious
* Cultures from respiratory cultures are positive in 90% of cases
* Malaise
* Anorexia
* Rhinorhoea (nasal cavity congested with significant amount of mucus)
* Conjunctivitis
211
what is the paroxysmal phase of whooping cough?
• Begins 1 week later from catarrhal phase
• Coughing spasms
• Classic inspiratory whoop is only seen in younger individuals in whom
the lumen of the respiratory tract is compromised by mucus secretion
and mucosal oedema
• These coughing spasms usually terminate in vomiting
• Cough for more than 14 days
212
what are the investigations for whooping cough?
- Chronic cough and one clinical feature indicated pertussis
- Chronic cough and history of contact or microbiological diagnosis is used
to confirm pertussis
- Suggested clinically by the characteristic whoop and history of contact with
an infected individual
- PCR test
- But culture of a nasopharyngeal swab = definitive diagnosis
213
what is the epidemiology of whooping cough?
Mainly a disease of childhood with 90% of cases occurring below 5 years of age
214
what is the pathophysiology of whooping cough?
- Highly contagious and spread by droplet infection
| - In early stages it is indistinguishable from other upper respiratory tract infections
215
what are the signs of TB?
```
Signs of bronchial breathing
Dullness to percuss
Decreased breathing
fever
crackles
```
216
what is the treatment for pneumonia?
Maintaining O2 Sats between 94-98%
In COPD patients: maintain O2 sats between 88-92%
Analgesia: paracetamol or NSAIDs
IV fluids
217
which bacteria causes rusty sputum in pneumonia?
strep pneumoniae
218
what is atypical pneumonia?
Bacterial pneumonia caused by atypical organisms that are not detectable on Gram stain and cannot be cultured using standard methods.
219
what are the common organisms that cause atypical pneumonia?
Mycoplasma pneumoniae,
Chlamydophila pneumoniae,
Legionella pneumophila
coxiella burnetii
220
what are the characteristic symptoms of atypical pneumonia?
headache
low-grade fever
cough
malaise
221
what is the mechanism of action for rifampicin for TB?
bactericidal - blocks protein synthesis
222
what is the mechanism of action of isoniazid for TB?
bactericidal - blocks cell wall synthesis
223
what is the mechanism of action for pyrazinamide for TB?
bactericidal initially, less effective later
224
what is the mechanism of action for ethambutol
bacteriostatic - blocks cell wall synthesis
225
what antibiotics are used for bronchiectasis?
- pseudomonas aeruginosa = oral ciprofloxacin
- h.influenzae = oral amoxycillin, co-amoxyclav or doxycycline
- staph aureus = flucloxacillin
226
what is the pathophysiology of goodpasture's syndrome?
Specific autoimmune disease caused by a type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often acute kidney injury and chronic kidney disease)
- There are circulating anti-glomerular basement membrane (anti-GBM) antibodies
227
what is the characteristic presentation of COPD?
```
productive cough
white or clear sputum
wheeze
SOB
following many years of smoking
```
228
what are the systemic effects of COPD?
```
hypertension
osteoporosis
depression
weight loss
reduced muscle mass with general weakness
```
229
where does squamous cell carcinoma of the lung arise from?
- epithelial cells typically in the central bronchus
230
what is squamous cell carcinoma associated with the production of?
associated with the production of keratin
231
where does small cell lung cancer arise from?
Arises from endocrine cells typically in the central bronchus
232
what is small cell lung cancer associated with the production of?
Secretes polypeptide hormones
233
which is the most common lung cancer in non-smokers?
adenocarcinoma
234
where does adenocarcinoma arise from?
mucus-secreting glandular cells
235
which is more common, primary lung cancer or metastatic lung cancer from elsewhere?
Cancer metastasising from elsewhere is more common than a primary lung tumour
236
what is the pathophysiology of pulmonary hypertension?
The main vascular changes are:
Vasoconstriction
Smooth-muscle cell and endothelial cell proliferation
Thrombosis
237
what are the different types of emphysema?
centri-acinar emphysema
pan-acinar emphysema
irregular emphysema
238
what is centri-acinar emphysema?
* Distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved
* Extremely common
239
what is pan-acinar emphysema?
* Less common
* Distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae
* Associated with alpha-1 antitrypsin deficiency
240
what is irregular emphysema?
• Scarring and damage that affects the lung parenchyma
| patchily, independent of acinar structure
241
what are the signs of emphysema?
```
Dyspnoea / Tachypnoea
Minimal cough
Pink skin, pursed-lip breathing
Accessory muscle use
Cachexia
Hyperinflation (barrel chest)
Weight loss (due to increased work of breathing and cachexia)
```
242
what are the complications of emphysema?
Pneumothorax due to bullae
243
what are the symptoms of emphysema?
- Chronic productive cough
- Purulent sputum
- Dyspnoea
- Cyanosis (hypoxaemia)
- Can cause secondary polycythemia
- May develop pulmonary hypertension (reactive pulmonary vasoconstriction)
- Peripheral oedema
- Obesity
- Haemoptysis
244
what are the investigations for IE COPD?
ABG
- CO2 retention → acidosis
- Raised pCO2 + low pO2 = T2RF
Chest X-Ray, sputum culture + sensitivities for antibiotic therapy, FBC + U&E
245
what is the epidemiology of asthma?
- Commonly starts in childhood between the ages 3-5 years and may either worsen or improve during adolescence
- Peak prevalence between 5-15 years
- more common in developed countries
246
what is extrinsic (atopic) allergic asthma?
- Occurs most frequently in atopic individuals
| - Childhood asthma often accompanied by eczema
247
what is intrinsic allergic asthma?
- Often starts in middle-aged and attacks are usually triggered by respiratory infections
248
what are the genetic factors for asthma?
* Genes controlling the production of cytokines IL-3,-4,-5,-9 & -13
* ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
249
what are the environmental factors for asthma?
• Early childhood exposure to allergens and maternal smoking has a
major influence on IgE production
• Growing up in a ‘clean’ environment may predispose towards an IgE
response to allergens whereas growing up in a ‘dirtier’ environment may
allow the immune system to avoid developing allergic responses
250
what are the risk factors for developing asthma
- Personal history of atopy
- Family history of asthma or atopy
- Obesity
- Inner-city environment
- Premature birth (low birth weight, not breast-fed)
- Socio-economic deprivation
- exposure to allergens
251
which drugs can trigger asthma attacks?
NSAIDs and aspirin
| beta blockers - results in bronchoconstriction which results in airflow limitation and potential attack
252
what is the acute management of asthma?
1. oxygen
2. salbutamol nebuliser
3. ipratropium bromide nebuliser
4. hydrocortisone IV or oral prednisolone
5. IV magnesium sulfate
6. aminophylline / IV salbutamol
253
give 2 examples of SABAs
- salbutamol (partial agonist)
| - terbutaline
254
what is the mechanism of action for SABAs?
- are beta-2 selective
| - bind to B2 receptor causing more cAMP which leads to more bronchodilation
255
how long do SABAs last for?
4 hours
256
give 2 examples of LABAs
- salmeterol
| - formoterol (full agonist)
257
what is the mechanism of action for LABAs?
- are beta-2 selective
- bind to B2 receptor causing more cAMP which leads to more bronchodilation
- are longer acting since more lipophilic so remain in the body for longer
258
give an example of a SAMA
ipratropium
259
what is the mechanism of action for SAMA?
- Act on airway M3 receptors
| - prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action
260
give an example of a LAMA
tiotropium
261
what is the mechanism of action for LAMA?
- Act on airway M3 receptors
- prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action
- has high affinity and disassociates slowly from muscarinic receptors
262
what is the mechanism of action for ICS?
- They reduce the number of inflammatory cells in the airways
- Suppress production of chemotactic mediators
- Reduce adhesion molecular expression
- Inhibit inflammatory cell survival in the airway
- Suppress inflammatory gene expression in airway epithelial cells
263
what are the side effects of ICS?
Loss of bone density
Adrenal suppression
Cataracts
Glaucoma
264
what is the effect of interaction between beta-2 agonists and glucocorticoids in the treatment of asthma?
- glucocorticoids increase the transcription of B2-receptor gene, resulting in increased expression of cell surface receptors
- Long acting B2 agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids
- Leads to greater overall efficacy and need for lower doses
265
what are the advantages of inhaled drugs?
- lungs are robust -> can handle repeated exposure
- very rapid absorption
- large SA
- fewer drug metabolising enzymes
- non-invasive port of entry
- fewer systemic side effects
266
what are the risk factors for developing pneumonia?
- under 16 or over 65
- HIV infection
- DM
- CF
- COPD
- smoking
- excess alcohol
- IVDU
- immunosuppressant therapy
267
what is a Ghon complex?
Ghon focus + lymph nodes
268
what are the extra-pulmonary manifestations of lung cancer?
Recurrent laryngeal nerve palsy - hoarse voice
Superior vena cava obstruction - facial swelling, distended veins in neck and upper chest, Pemberton’s sign
Horner’s syndrome - ptosis, miosis, anhidrosis
269
what is a PE?
occlusion of a pulmonary artery by an embolic thrombus.
270
what is the pathophysiology of a PE?
clot breaks off from venous thrombus → IVC → RA → RV → pulmonary arteries
271
what are the causes/risk factors of PE?
Increased age
Immobility e.g. post-surgery, long haul flights
Pregnancy
Active malignancy
DVT
Family history of VTE
Congenital and acquired thrombotic disorders
272
what is the clinical presentation of PE?
SYMPTOMS
Acute onset SOB
Cough +/- haemoptysis
Pleuritic chest pain
```
SIGNS
DVT
hypoxia
tachycardia
increased resp rate
low grade fever
haemodynamic instability -> hypotension
```
273
what scoring system is used to measure the risk of PE?
Wells score
274
what are the investigations for PE?
D-dimer
CTPA spiral with contrast
ABG
275
what is the management for PE?
- if investigations are delayed start anticoagulation
1st line = apixaban/rivaroxaban
LMWH for 5 days followed by dabigatran
3 months for provoked
>3 months for unprovoked
IVC filter
276
what is the management for haemodynamic instability caused by a PE?
- IV thrombolysis - alteplase
- catheter directed thrombolysis
- embolectomy
277
what is pharyngitis?
rapid onset of sore throat and inflammation of the pharynx (with or without exudate)
278
what are the most common causes of pharyngitis?
group A strep = most common
| EBV
279
what are the clinical features of pharyngitis?
```
Sore throat → difficulty swallowing
Fever
Headache
Joint pain/ muscle ache
Skin rashes
Swollen lymph nodes in neck
```
280
what are the clincial features of pharyngitis that suggest a viral cause?
runny nose, blocked nose, sneezing, cough
281
what are the clinical features of pharyngitis that suggest a bacterial cause?
fever, pharyngeal exudate, cervical lymphadenopathy, absence of cough + runny nose
282
what are the investigations for pharyngitis?
rapid antigen detection test (RADT)
| throat culture
283
what is the management for pharnygitis?
group A strep = phenoxymethylpenicillin (clarithromycin if allergic to penicillin)
viral = self resolving, supportive care
284
what is sinusitis?
inflammation of the mucous membrane of the nasal cavity and paranasal sinuses - also known as acute rhinosinusitis.
285
what are the most common causes of sinusitis?
Common infectious agents:
Streptococcus pneumoniae
Haemophilus influenzae
Rhinoviruses
286
what are the risk factors for sinusitis?
nasal pathology e.g. septal deviation or nasal polyps
recent local infection e.g. rhinitis or dental extraction
swimming/diving
smoking
287
what is the clinical presentation of sinusitis caused by bacteria?
```
symptoms > 10 days
purulent nasal discharge
nasal obstruction
dental/facial pain
headache
```
288
what is the clincial presentation of sinusitis caused by virus?
symptoms < 10 days
clear nasal discharge
fever
sore throat
289
what are the investigations for sinusitis?
clincial diagnosis
290
what is the management for sinusitis?
Symptom management with analgesia and intranasal decongestants
intranasal corticosteroids considered if symptoms have been present for >10 days
Antibiotic therapy not normally required but may be given for severe presentations (phenoxymethylpenicillin first-line)
