respiratory to work on Flashcards
1
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
2
Q
Name 3 pathogens that can cause community acquired pneumonia (CAP)
A
- Streptococcus pneumoniae (most common)
- Haemophilus influenzae
- Mycoplasma pneumoniae
3
Q
Name 3 pathogens that can cause hospital acquired pneumonia (HAP)
A
mainly gram negative
- Pseudomonas aeruginosa
- E.coli
- Klebsiella penumoniae
- Staphylococcus aureus
4
Q
What symptoms might you see in someone with pneumonia?
A
SOB cough sputum fever pleuritic chest pain delirium
5
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
6
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
7
Q
What is the treatment for someone with mild CAP (CRUB65 score 0-1)?
A
oral amoxicillin at home
8
Q
What is the treatment for someone with moderate CAP (CRUB65 score 2)?
A
consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin)
9
Q
What is the treatment for someone with severe CAP (CRUB65 score 3-5)?
A
consider ITU,
IV Co-Amoxiclav + macrolide (clarithromycin)
10
Q
What is the treatment for someone with Legionella pneumoniae?
A
Fluoroquinolone + clarithromycin
11
Q
What is the treatment for someone with Pseudomonas aeruginosa pneumonia?
A
IV ceftazidime + gentamicin
12
Q
Give 3 potential complications of pneumonia
A
- Respiratory failure
- Hypotension
- Empyema
- Lung abscess
13
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
14
Q
What can cause bronchiectasis?
A
- Congenital = Cystic fibrosis
- Idiopathic (50%)
- Post infection - (most common)
- pneumonia,
- TB,
- whopping cough
- Bronchial obstruction
- RA
- Hypogammaglobulinaemia
15
Q
Which bacteria might cause bronchiectasis?
A
- Haemophilus influenza (children)
- Pseudomonas aeruginosa (adults)
- Staphylococcus aureus (neonates often)
16
Q
Give 3 symptoms of bronchiectasis
A
- Chronic productive cough
- Purulent sputum
- Intermittent haemoptysis
- Dyspnoea
- Fever, weight loss
17
Q
Give 3 signs of bronchiectasis
A
- Finger clubbing
- Coarse inspiratory crepitate (crackles)
- Wheeze
18
Q
What investigations might you do on someone to determine whether they have bronchiectasis?
A
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
19
Q
Describe the treatment for bronchiectasis
A
- Antibiotics
- Anti-inflammatories (azithromycin)
- Bronchodilators (nebulised salbutamol)
- Chest physio - physical training
- Surgery = lung resection or transplant
20
Q
Give 3 possible complications of Bronchiectasis
A
- Pneumonia
- Pleural effusion
- Pneumothorax
21
Q
What are the main systemic consequences of CF?
A
Pancreatic insufficiency = dehydrated secretion –> enzymes stagnation
GI = intraluminal water deficiency –> concentrated bile
Resp = thick mucus can’t be cleared –> infection risk and inflammatory damage
22
Q
How do children/young adults present with CF?
A
- Cough and wheeze
- Recurrent infections
- Haemoptysis
- Pancreatic insufficiency
- Malabsorption
- Male infertility
23
Q
What are 3 possible respiratory complications of CF?
A
- Pneumothorax
- Respiratory failure
- Cor pulmonale
- Bronchiectasis
24
Q
Give 3 signs of CF
A
- Clubbing
- Cyanosis
- Bilateral coarse crepitations
25
Name 3 associated conditions with CF
1. Osteoporosis
2. Arthritis
3. Vasculitis
26
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
27
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
28
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
29
Which type of NSCC is most common in smokers?
Squamous cell carcinoma - it is most stronlgy associated with cigarette smoking
30
where does lung cancer commonly metastasise to?
1. Bone
2. Brain
3. Lymph nodes
4. Liver
5. Adrenal
31
Give 4 symptoms of local disease lung cancer
```
Persistent cough
Shortness of breath
Haemoptysis
Weight loss
Chest pain, wheeze, recurrent infections
```
32
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
33
Give 3 examples of paraneoplastic syndromes due to lung cancer
- ↑PTH -> Hyperparathyroidism
- ↑ADH -> SIADH
- ↑ACTH -> Cushing’s disease
34
Name 3 differential diagnosis's of lung cancer
1. Oesophageal varices
2. COPD
3. Asthma
4. Pneumonia
5. Bronchiectasis
35
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
36
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
37
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:
38
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
39
Describe asthma
Chronic, inflammatory condition, causing episodes of reversible airway obstruction, due to:
Bronchoconstriction
Excessive secretion production
40
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
41
What is the mechanism behind hyper-reactivity?
Neurogenic inflammation
42
Describe neurogenic infalmmation
Sensory nerve activation initiates impulses which stimulates CGRP (pro-inflammatory)
this activates mast cells and innervates goblet cells
43
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
44
What type of T cell is involved in asthma?
CD4+
45
Extrinsic asthma: what happens when IgE binds to mast cells?
Vasodilative substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion
46
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
47
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
48
What are the signs of asthma?
1. Tachypnoea - rapid breathing
2. Audible wheeze
3. Widespread polyphonic wheeze
4. Cough
49
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
50
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
51
Give 3 differential diagnosis's of asthma
1. COPD
2. Bronchial obstruction
3. Pulmonary oedema
4. Pulmonary embolism
5. Bronchiectasis
52
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
53
What is the long-term guideline mediation regime for asthma?
1. SABA
2. SABA + ICS
3. SABA + ICS + LTRA
4. SABA + ICS + LTRA/LABA + MART
54
Give 3 possible complications of asthma
1. Exacerbation
2. Pneumothorax
3. Pneumonia
55
Describe the pathophysiology of chronic bronchitis
Airway inflammation --> fibrosis and luminal plugs --> decreased alveolar ventilation
56
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
57
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
58
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
59
What are the main cells responsible for inflammation in COPD?
Neutrophils and macrophages
60
What type of T cell is involved in COPD?
CD8+
61
What can cause COPD?
1. Genetic = alpha 1 antitrypsin deficiency
2. Smoking = major cause
3. Air pollution
4. Occupational factors = dust, chemicals
62
Name 4 symptoms of COPD
1. Dyspnoea
2. Cough +/- sputum
3. Expiratory wheeze
4. Weight loss
5. SOB
63
Give 4 signs of COPD
1. Tachypnoea
2. Barrel shaped chest
3. Hyperinflantion
4. Cyanosis
5. Pulmonary hypertension
6. Cor pulmonale
64
Give 3 differential diagnosis's for COPD
1. Asthma
2. HF
3. Pulmonary embolism
4. Bronchiectasis
5. Lung cancer
65
What investigations might you do to diagnose someone with COPD?
```
Spirometry = FEV1:FVC < 0.7
CXR = hyperinflation, bullae, flat hemi-diaphragms, large pulmonary arteries
FBC = exclude secondary polycythaemia
```
```
CT = Bronchial wall thickening, enlarged air spaces
ECG = RA and RV hypertrophy
ABG = decreased PaO2 +/- hypercapnia
```
66
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
67
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
68
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
69
Give 3 possible complications of COPD
1. Exacerbations
2. Infection
3. Respiratory failure
4. Cor pulmonale
5. Pneumothorax
70
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
71
What is the likely cause for an exacerbation of COPD?
Viral URTI
| Bacterial infections
72
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)
73
Give 3 ways in which subsequent exacerbations of COPD can be prevented
1. Smoking cessation
2. Vaccination
3. LABA/LAMA/ICS
74
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
75
What does the pleural fluid contain?
Protein - albumin, globulin, fibrinogen
| Mesothelial cells, monocytes and lymphocytes
76
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
77
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
78
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
79
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
80
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
81
How can pneumothorax be classified?
```
Spontaneous pneumothorax
Traumatic pneumothorax
Iatrogenic pneumothorax
Lung Pathology
Tension pneumothorax
```
82
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
83
What investigation might you do in someone you suspect to have a pneumothorax?
CXR = translucency and collapse
ABG = in dyspnoeic patients check for hypoxia
84
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
85
Name a possible complication of a pneumothorax
Tension pneumothorax
86
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
87
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
88
Define interstitial lung diseases
Distant cellular infiltrate and extracellular matrix deposition in lung distal to the terminal bronchioles - disease of the alveolar/capillary interface
89
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
90
What are the 4 major features of interstitial lung disease?
1. Cough
2. Dyspnoea
3. Restirictve spirometry
4. Abnormal CXR/CT
91
What is the pathology of interstitial lung disease?
Increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion
92
What kind of disease is sarcoidosis?
Granulomatous disease - type of interstitial lung disease
93
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
94
Give 3 pulmonary symptoms of sarcoidosis
1. Dry cough
2. Progressive SOB
3. Wheeze
4. Chest pain
95
What is the effect of sarcoidosis on the skin?
Erythema nodosum
96
What is the effect of sarcoidosis on the eyes?
Uveitis
97
What is the effect of sarcoidosis on the bone?
Arthralgia
98
What is the effect of sarcoidosis on the liver?
Hepatosplenmeagly
99
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
100
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
101
How do you treat acute sarcoidosis?
NSAIDs and bed rest
102
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
103
Give 2 possible differential diagnosis's for sarcoidosis
1. Lymphoma
| 2. Pulmonary TB
104
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
105
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
106
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
107
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
108
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
109
what are the possible complications of idiopathic pulmonary fibrosis
1. Respiratory failure
| 2. Cor pulmonale
110
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
111
What can cause an increase in mPAP?
Increase resistance to flow
| Increased flow rate
112
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
113
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
114
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
115
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
116
Give a possible complication of pulmonary hypertension
Cor pulmonale (RS HF) --> pleural effusion + death
117
How is TB transmitted?
Aerosol transmission
118
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
119
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
120
Give 3 risk factors for TB
1. Living in a high prevalence area
2. IVDU
3. Homeless
4. Alcohol
5. HIV +ve
121
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
122
What pulmonary symptoms might you see as a result of TB?
```
Productive cough
Haemoptysis
Cough >3 weeks (dry or productive)
Breathlessness
Sometimes chest pain
```
123
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
124
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
125
A special culture medium is needed to grow TB, what is it called?
Lowenstein Jenson Slope
126
What might a lymph node biopsy from someone with TB show?
Caseating granuloma
127
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
```
128
Give 2 potential side effects of Rifampicin
1. Red urine
2. Hepatitis
3. Drug interaction - it's an enzyme inducer
129
Give 2 potential side effects of Isoniazid
1. Hepatitis
| 2. Neuropathy
130
Give 2 potential side effects of Pyrazinamide
1. Hepatitis
2. Gout
3. Neuropathy
131
Give a potential side effect of Ethambutol
Optic neuritis
132
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
133
What is Whooping cough caused by?
Bordatella pertussis (gram -ve coccobacilli) - rod
134
Describe the disease course of whooping cough
7-10 day incubation --> 1-2 week catarrhal stage --> 1-6 week paroxysmal stage
135
What are the symptoms of whooping cough?
Paroxysmal cough - sudden and severe
| Vomiting after cough
136
What is the treatment of whooping cough?
Clarithromycin - in catarrhal or early paroxysmal stages
- have little effect on disease course in paroxysmal stage
137
How can you prevent whooping cough?
Pertussis vaccination
| 8, 12 and 16 weeks and a pre school booster
138
Give 2 possible complications of whooping cough
1. Pneumonia
2. Encephalopathy
3. Sub-conjunctival haemorrhage
139
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
140
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
141
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
142
what are the risk factors for pleural effusion?
- Previous lung damage
| - Asbestos exposure
143
what are the risk factors for pneumothorax?
```
Smoking
Family history
Male
Tall and slender build
Young age
Presence of underlying lung disease
```
144
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.
145
what is the clinical presentation of a tension pneumothorax?
```
Cardiopulmonary deterioration:
Hypotension – imminent cardiac arrest
Respiratory distress
Low sats
Tachycardia
Shock
Severe chest Pain
```
146
what are the clinical features of a tension pneumothorax?
Tracheal deviation to contralateral side
Ipsilateral reduced breath sounds
Hyperresonance on percussion
Hypoxia
147
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
148
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
149
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
150
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
151
what are the signs of TB?
```
Signs of bronchial breathing
Dullness to percuss
Decreased breathing
fever
crackles
```
152
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
153
which bacteria causes rusty sputum in pneumonia?
strep pneumoniae
154
what are the common organisms that cause atypical pneumonia?
Mycoplasma pneumoniae,
Chlamydophila pneumoniae,
Legionella pneumophila
coxiella burnetii
155
what are the characteristic symptoms of atypical pneumonia?
headache
low-grade fever
cough
malaise
156
what is the mechanism of action for rifampicin for TB?
bactericidal - blocks protein synthesis
157
what is the mechanism of action of isoniazid for TB?
bactericidal - blocks cell wall synthesis
158
what is the mechanism of action for pyrazinamide for TB?
bactericidal initially, less effective later
159
what is the mechanism of action for ethambutol
bacteriostatic - blocks cell wall synthesis
160
what antibiotics are used for bronchiectasis?
- pseudomonas aeruginosa = oral ciprofloxacin
- h.influenzae = oral amoxycillin, co-amoxyclav or doxycycline
- staph aureus = flucloxacillin
161
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
162
what is the characteristic presentation of COPD?
```
productive cough
white or clear sputum
wheeze
SOB
following many years of smoking
```
163
what are the systemic effects of COPD?
```
hypertension
osteoporosis
depression
weight loss
reduced muscle mass with general weakness
```
164
which is the most common lung cancer in non-smokers?
adenocarcinoma
165
where does adenocarcinoma arise from?
mucus-secreting glandular cells
166
what is the pathophysiology of pulmonary hypertension?
The main vascular changes are:
Vasoconstriction
Smooth-muscle cell and endothelial cell proliferation
Thrombosis
167
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
168
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
169
what is irregular emphysema?
• Scarring and damage that affects the lung parenchyma
| patchily, independent of acinar structure
170
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)
```
171
what are the complications of emphysema?
Pneumothorax due to bullae
172
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
173
what is extrinsic (atopic) allergic asthma?
- Occurs most frequently in atopic individuals
| - Childhood asthma often accompanied by eczema
174
what is intrinsic allergic asthma?
- Often starts in middle-aged and attacks are usually triggered by respiratory infections
175
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
176
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
177
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
178
which drugs can trigger asthma attacks?
NSAIDs and aspirin
| beta blockers - results in bronchoconstriction which results in airflow limitation and potential attack
179
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
180
give 2 examples of SABAs
- salbutamol (partial agonist)
| - terbutaline
181
what is the mechanism of action for SABAs?
- are beta-2 selective
| - bind to B2 receptor causing more cAMP which leads to more bronchodilation
182
give 2 examples of LABAs
- salmeterol
| - formoterol (full agonist)
183
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
184
give an example of a SAMA
ipratropium
185
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
186
give an example of a LAMA
tiotropium
187
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
188
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
189
what are the side effects of ICS?
Loss of bone density
Adrenal suppression
Cataracts
Glaucoma
190
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
191
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
192
what are the risk factors for developing pneumonia?
- under 16 or over 65
- HIV infection
- DM
- CF
- COPD
- smoking
- excess alcohol
- IVDU
- immunosuppressant therapy
193
what is a Ghon complex?
Ghon focus + lymph nodes
194
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
195
what scoring system is used to measure the risk of PE?
Wells score
196
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
197
what is the management for haemodynamic instability caused by a PE?
- IV thrombolysis - alteplase
- catheter directed thrombolysis
- embolectomy
198
what are the most common causes of pharyngitis?
group A strep = most common
| EBV
199
what are the clinical features of pharyngitis?
```
Sore throat → difficulty swallowing
Fever
Headache
Joint pain/ muscle ache
Skin rashes
Swollen lymph nodes in neck
```
200
what are the clincial features of pharyngitis that suggest a viral cause?
runny nose, blocked nose, sneezing, cough
201
what are the clinical features of pharyngitis that suggest a bacterial cause?
fever, pharyngeal exudate, cervical lymphadenopathy, absence of cough + runny nose
202
what are the investigations for pharyngitis?
rapid antigen detection test (RADT)
| throat culture
203
what is the management for pharnygitis?
group A strep = phenoxymethylpenicillin (clarithromycin if allergic to penicillin)
viral = self resolving, supportive care
204
what are the most common causes of sinusitis?
Common infectious agents:
Streptococcus pneumoniae
Haemophilus influenzae
Rhinoviruses
205
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
206
what is the clinical presentation of sinusitis caused by bacteria?
```
symptoms > 10 days
purulent nasal discharge
nasal obstruction
dental/facial pain
headache
```
207
what is the clincial presentation of sinusitis caused by virus?
symptoms < 10 days
clear nasal discharge
fever
sore throat
208
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)
209
what is the clinical diagnosis of chronic bronchitis?
cough/sputum for more than 3 months in 2 consecutive years
210
what are the signs of COPD on CXR?
hyperinflation
bullae
flat hemidiaphragm
211
what are the signs that long term oxygen therapy is required in COPD?
- FEV1 < 30% predicted value
- cyanosis
- polycythaemia
- peripheral oedema
- raised JVP
- O2 less than or equal to 92% on room air
212
what is the treatment for latent TB?
rifampicin
isoniazid
RI for 6 months
I for 3 months
