Respiratory Flashcards
(265 cards)
1
Q
Define COPD
A
Chronic Obstructive Pulmonary Disease
Describes a common progressive disorder characterised by airway obstruction and tissue destruction (alveoli) that is not fully reversible.
2
Q
Define vital capacity
A
The total volume of air that can be expelled from the lungs after a maximum inhalation
3
Q
What is the vital capacity equal to?
A
The sum of inspiratory reserve volume, tidal volume and expiratory reserve volume
4
Q
Define forced vital capacity
A
The total amount of air that can be forcible expired
(low FVC indicates airway restriction)
5
Q
Define Forced Expiratory Volume (FEV1)
A
The total volume of air expired in one second
6
Q
What is the typical FEV and FEV1:FVC for a patient with COPD?
A
FEV<80% and FEV1:FVC <0.7 (<70%)
7
Q
Describe the impact of chronic inflammation in COPD
A
Chronic inflammation causes airway narrowing/obstruction and decreased lung recoil (due to elastin degradation), typically resulting in exhalation difficulty, resulting in hyperventilation.
8
Q
What is the most common pathogen causing infective exacerbations in COPD?
A
Haemophilus influenzae
9
Q
Name 3 types of COPD
A
Emphysema
Chronic Bronchitis
Alpha-1-antitrypsin deficiency
10
Q
What is the pattern of inheritance for alpha 1 antitrypsin deficiency?
A
Autosomal recessive
11
Q
Alpha 1 antitrypsin deficiency is caused by a mutation in what?
A
SERPINA1
12
Q
Describe the pathophysiology of Alpha 1 antitrypsin deficiency
A
AAT protects the body from the enzyme neutrophil elastase which is released from WBCs to fight infection.
When AAT is deficient, neutrophil elastase is free to degrade elastase in the walls of the alveoli, leading to emphysema
13
Q
What vaccines must patients with alpha 1 antitrypsin deficiency be given? and why?
A
AAT deficiency is linked to liver disease.
Patients should be given Hepatitis A and B vaccines.
14
Q
Give 4 causes of COPD
A
Smoking (major cause)
Pollution
Occupational exposure to noxious gasses
Genetics - AAT deficiency
15
Q
Give 5 clinical features of COPD
A
Cough +/- Sputum
Wheeze
Tachypnoea (rapid breathing)
Dyspnoea (shortness of breath)
Hyperinflation (decreased cricosternal distance)
16
Q
Give 5 complications of COPD
A
Acute exacerbations +/- infection
Polycythemia
Pneumothorax
Cor Pulmonale (right sided heart failure)
Lung carcinoma
17
Q
Give 4 DDx for COPD
A
COPD patients do NOT tend to present with clubbing or haemoptysis.
Pneumothorax
Pulmonary Oedema
Pulmonary Embolism
Asthma
18
Q
What tests are used to diagnose COPD? (6)
A
Spirometry - FVC <80%, FEV1:FVC <0.7
Chest X-ray
ECG/Echo (cor pulmonale)
FBC
ABG (respiratory failure)
Pulmonary function tests (distinguishing between emphysema and chronic bronchitis)
19
Q
Describe type I respiratory failure in terms of O2 and Co2
A
Low O2 and Normal/Low Co2
20
Q
Describe type II respiratory failure in terms of O2 and Co2
A
Low O2 and High Co2
21
Q
Give 4 causes of Type I respiratory failure
A
High altitude
Hypoxaemic hypoxia (low atrial O2)
Pulmonary embolism
Pneumonia
22
Q
Give 4 causes of type II respiratory failure
A
Inadequate alveolar ventilation
Increased airway resistance (COPD/Asthma)
Reduced gas exchange surface area (Chronic Bronchitis)
Deformed (Kyphoscoliosis) or Damaged chest wall
23
Q
What score is used to assess symptoms of COPD. Describe the criteria
A
mMRC dyspnoea score (1-5).
- Dyspnoea only with strenuous exercise
- Dyspnoea on hurrying or walking up-stairs/slight hill.
- Walks slowly or has to stop for breath
- Stops for breath after <100yrs or after a few minutes.
- Too breathless to leave the house or breathless when dressing
24
Q
Describe how COPD is categorised based on severity
A
Mild - FEV1 >80%,
Moderate - FEV1 50-79%
Severe - FEV1 30-49%
Very severe - FEV1 <30%
25
What signs would you see on a chest x ray for a patient with COPD?(4)
Increased anteroposterior diameter
Flattened diaphragm
Increased intercostal spaces
Hyperlucent lungs
(Also important to exclude lung cancer)
26
Describe the general management of COPD (4)
Smoking cessation (main)
Pulmonary Rehabilitation and Exercise
Vaccinations (influenza and Streptococcus pneumoniae)
Review 1/2 times per year
27
What vaccinations should COPD patients receive?
Annual influenza vaccine
One off pneumococcal vaccination
28
What medications can be used to help smoker quit in COPD? (2)
Bupropion or Varenicline (partial nicotinic agonists)
29
In which patients should Bupropion be avoided and why?
Epileptic patients
As it reduces seizure threshold
30
What is the 1st line bronchodilator therapy for COPD?
1st line - Salbutamol (SABA) or Ipratropium Bromide (SAMA)
31
What determines whether a COPD patient requires 2nd line bronchodilator therapy?
Whether the patient has asthmatic features/features suggesting steroid responsiveness.
32
What features are used to determine whether a COPD patient has asthmatic/steroid responsiveness? (4)
Any pervious, secure diagnosis of asthma or of atopy
A higher blood eosinophil count
Substantial variation in FEV1 over time (at least 400ml)
Substantial diurnal variation in peak expiratory flow (at least 20%)
33
How should a patient, with COPD, who has not responded to 1st line treatment and who has no asthmatic features or features suggesting steroid responsiveness, be managed?
2nd line - ADD Salmeterol (LABA) + Tiotropium (LAMA)
(If already taking SAMA, discontinue and switch to SABA)
34
How should a patient, with COPD, who has not responded to 1st line treatment and who HAS asthmatic features or features suggesting steroid responsiveness, be managed?
2nd line - Add Salmeterol (LABA) + Beclometasone (ICS)
35
If a COPD patient with asthmatic features/features suggesting steroid responsiveness remains breathlessness or has exacerbations following 2nd line therapy, what should be offered?
3rd Line - Triple Therapy - Salmeterol (LABA) + Tiotropium (LABA) + Beclometasone (ICS)
If taking SAMA, discontinue and switch to SABA.
Use combined inhalers where possible.
36
What should be offered to COPD patients who cannot use inhaled therapy or who have had trials of short/long acting bronchodilators?
Oral Theophylline
37
When should the dose of theophylline be reduced in COPD?
If a macrolide (azithromycin) or fluoroquinolone Abx is co-prescribed
38
What should patients with persistent exacerbations of COPD be offered?
Azithromycin prophylaxis
39
What adverse effects can azithromycin have?
Can prolong QT interval
40
What other medication can also be used to reduce the risk of COPD exacerbations in patients with severe COPD or hx of frequent exacerbations?
Phosphodiesterase 4 inhibitors (PDE-4) - Roflumilast
41
When do NICE recommend giving PDE-4 inhibitors (such as roflumilast) to COPD patients? (2)
If;
The disease is severe (FVC <50%)
AND
Person has 2 or more exacerbations in past 12 months, despite triple therapy with LAMA, LABA and ICS
42
If a patient with COPD experiences an infective exacerbation causing Type 2 respiratory failure and they are already on maximal medical treatment, what is the most appropriate management?
BiPAP (as it features inspiratory positive airway pressure, inflating the lungs to a larger volume to help the clearance of CO2)
(Extra CO2 clearance is necessary, hence why BiPAP is used over CPAP)
43
Give an example of a SABA and a LABA and describe their MOA
Salbutamol (SABA). Salmeterol (LABA)
Beta 2 agonists.
Relax airway smooth muscle
44
Give 3 possible side effects of SABA/LABAs
Tachyarrhythmias
Hypokalaemia
Tremor/anxiety
45
Give an example of a SAMA and LAMA and describe their moa (3).
Ipratropium bromide (SAMA) and Tiotropium (LAMA)
Muscarinic Antagonists
Relax airway smooth muscle be blocking muscarinic receptors, inhibiting the action of acetyl choline and this preventing smooth muscle contraction.
46
Define emphysema. What is a nickname for these patients?
Defined histologically as enlarged air spaces (alveoli) distal to terminal bronchioles with destruction of alveolar walls.
Pink Puffers - As patients have difficulty breathing but are well perfused.
47
What is the principle cause of emphysema? Describe the pathophysiology
Smoking
Smoking inactivates alpha-1 antitrypsin > increased elastase activity > alveolar wall breakdown > loss of alveolar elasticity and destruction of alveoli
48
In emphysema, what does the loss of alveolar elasticity and destruction of alveoli result in? (2)
A decrease in alveolar and capillary surface area, which decreases gas exchange.
Air trapping - Air is trapped in alveoli due to reduced elastic recoil during exhalation, leading to hyperventilation
49
Give 5 clinical features of emphysema
Typical symptoms of COPD (cough, wheeze, dyspnoea, tachypnoea, sputum ect)
Pursed lips on expiration
Barrel chest (hyperventilation)
Cachexia
Use of accessory respiration muscles
50
Why do patients with emphysema purse their lips on expiration?
Increases airway pressure and prevents airway collapse during expiration.
51
What examination finding would be indicative of air trapping in a patient with ? emphysema
Hyper resonant percussion
52
Describe the results of pulmonary function tests in a patient with emphysema (3)
Decreased DLCO (Diffusing capacity of the lung for carbon dioxide)
Raised TLC (total lung capacity)
Raised RV (residual volume)
53
Define chronic bronchitis. What is their nickname?
Defined clinically as a cough and sputum production most days for 3 months of 2 consecutive years.
Blue blotters - As they're usually cyanosed
54
How is chronic bronchitis characterised physiogically?
Characterised by airway narrowing/obstruction as a result of hypertrophy, hyperplasia and hypersecretion of mucus by goblet cells in the epithelial layer of the bronchial tree.
This occurs 2nd to bronchial wall inflammation, 2nd to inhalation of toxins or infection.
55
Why do patients with chronic bronchitis find it difficult to clear secretions?
Occurs due to poor ciliary function.
Ciliated columnar cells are replaced by squamous epithelial cells in response to inflammation/toxins from smoking.
56
Give 4 clinical features of chronic bronchitis
Typical features of COPD (cough, wheeze, dyspnoea, tachypnoea, sputum ect)
Sputum production
Cyanosis
Cor Pulmonale (right sided heart failure)
57
What would an ABG show for a patient with chronic bronchitis?
Low O2 and Increased Co2 - Type II respiratory failure
58
What would an ABG show for a patient with emphysema
Normal O2 and Normal Co2
59
Define lung cancer
Describes a group of malignant epithelial tumours that arise from cells lining the lower respiratory tract (trachea, bronchi, bronchioles and alveoli)
60
Name 2 categories of lung cancer
Non-small cell lung cancer (80%) (inc squamous cell carcinoma, adenocarcinoma, large cell carcinoma)
Small cell lung cancer (aka oat cell)
61
What type of lung cancer is most aggressive?
Small cell lung cancer.
70% of patients have distant metastasis at presentation.
62
Describe the histology of small cell lung cancers
Tend to develop in a central location, near bronchi.
Tumour cells tend to be small, poorly differentiated and densely packed in character, with scant cytoplasm and absence of nucleoli.
63
Where do small cell lung cancers arise from? What does this result in?
Arise from pulmonary neuroendocrine cells (Enterochromaffin cells, Kulchitski cells, K cells)
Results in paraneoplastic syndromes as these cells secrete polypeptide hormones
64
Name 3 paraneoplastic syndromes caused by small cell lung cancers
SIADH
Ectopic Cushing's Syndrome (ectopic ACTH production)
Lambert Eaton Myasthenic Syndrome (Abs against voltage gated calcium channels)
65
Describe Lambert Eaton Myasthenic Syndrome and describe it's features. (3)
Describes autoimmune disorder of the neuromuscular junction, in which antibidies are produced against voltage gated calcium channels.
Presents as; muscle weakness of the lumbs, hyporeflexia and dry mouth,
Muscle strength tends to improve with activity (unlike fatigable conditions such as myasthenia gravis).
66
What are the 3 main histological types of Non Small Cell Lung Cancer? Which is the most common?
Squamous cell carcinoma
Adenocarcinoma (most common)
Large cell carcinomas
67
Describe the behaviour of squamous cell carcinomas of the lung. What is this type of cancer associated with? (3)
Tend to be centrally located, spread locally and metastasize late.
Associated with;
Secreting Parathyroid Hormone Related Protein (PTHrP) leading to hypercalcaemia (and polyuria)
Finger clubbing and hypertrophic pulmonary osteoarthropathy (HPOA)
Hyperthyroidism due to ectopic TSH production
68
What chemical are adenocarcinomas of the lung associated with?
Asbestos
69
Describe the behaviour of adenocarcinomas.
Tumours tend to be peripherally located (but can also be central) and arise from mucus secreting glandular cells.
Commonly metastasize to extrathoracic regions early (pleura, lymph nodes, brain, bones, adrenal glands)
Associated with gynecomastia (enlargement of male breast) due to ectopic secretion of human chorionic gonadotrophin
70
Which type of lung cancer is associated with gynaecomastia and why?
Adenocarcinoma
Can secrete HcG.
71
Which type of non-small cell lung cancer carries the worst prognosis?
Large Cell Carcinoma
72
What are the most common cancers to metastasize TO the lungs? (4)
Kidney Cancer (most common) - Renal cell carcinoma
Breast Cancer
Bowel Cancer
Bladder Cancer
73
Give 6 clinical features of lung cancer
Cough
Haemoptysis
Dyspnoea
Chest pain
Recurrent/slow resolving pneumonia
Anorexia and weight loss
74
Give 4 complications of lung cancer
Recurrent laryngeal nerve palsy (voice hoarseness)
Superior Vena Cava obstruction (face swelling, distended neck veins, dyspnoea)
Horners Syndrome (pancoast tumour)
Paraneoplastic stbdromes
75
What type of tumour is Horner's syndrome associated with? What is the triad for Horner's syndrome?
Pancoast tumour (invades the sympathetic plexus)
Triad;
Ptosis (drooping eyelid)
Miosis (excessive constriction of pupil)
Ipsilateral Anhidrosis (inability to sweat)
76
What is the 1st line investigation for patients with suspected lung cancer? What may this show? (4)
Chest X-Ray
May show;
Hilar enlargement
Consolidation/collapse
Coin lesions
Plural effusion
77
What imaging tool is used to stage lung cancer?
Contrast enhanced CT
78
What test should be conducted in all lung cancer patients anticipated to undergo surgery? Why?
Pulmonary Function Tests (PFTs)
To assess any post-operative loss of lung function
79
Describe mesothelioma
Describes a high grade tumour of mesothelial cells. Commonly affecting the right lung, usually occurring in the pleura.
80
What is mesothelioma development strongly associated with?
Asbestos exposure.
(Latent period between exposure to onset can be 45 years)
81
Give 5 clinical features of mesothelioma
History of asbestos exposure
Age between 60-85
Chest pain, dyspnoea
Weight loss
Finger clubbing
82
What is a chest x-ray/CT likely to show for a patient with mesothelioma? (4)
Unilateral pleural effusion
Irregular pleural thickening
Reduced lung volumes
Parenchymal changes related to asbestos exposure (interstitial fibrosis)
83
Give 2 examples of Type 1 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology
IgE mediated
Asthma + Anaphylaxis
IgE binds to and primes mast cells > mast cell degranulation > releasing histamine, leukotrienes and prostaglandins
84
Give 2 examples of Type 2 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology
IgG mediated
Autoimmune disease or blood transfusion rejection
Characterised by antibodies targeting antigens present on the surface of cells.
85
Give an example of a Type 3 Hypersensitivity Reactions and state what mediates it. Briefly describe the pathophysiology
IgG mediated
Rheumatoid Arthritis
Mediated by formation of antigen-antibody aggregates (immune complexes) which precipitate in various tissues (i.e in synovial fluid in RA).
86
Give 2 examples of Type 4 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology
T effector cell mediated
TB granulomas + Contact Dermatitis
Characterised by T cell-antigen interactions that cause activation and cytokine secretion.
This requires sensitized lymphocytes that respond 24-48 hours after exposure to a soluble antigen.
87
Define asthma
Asthma is characterized by recurrent episodes of dyspnoea, cough and wheeze caused by reversible airway obstruction.
88
What type of hypersensitivity reaction of Asthma? What is it mediated by?
Type 1 hypersensitivity reaction. IgE mediated.
89
What 3 factors contribute to airway narrowing in asthma?
Bronchial smooth muscle contraction
Mucosal swelling/inflammation (due to mast cell/neutrophil degranulation releasing histamine)
Increased mucus production
90
Describe the epidemiology of asthma
Commonly presents in childhood (peaks at 5 years) with symptoms resolving/improving with age.
91
How is asthma subclassified?
Subclassified based on inflammatory pattern;
Allergic/eosinophilic asthma (70%) - Associated with personal or FH or atopy (genetic tendency to develop allergic diseases)
Non-allergic/Non-eosinophilic (30%) - Characterised by airway inflammation with the absence of eosinophils. More associated with environmental factors (i.e smoking)
92
Atopic asthma patients may also display symptoms of what? (2)
Atopic dermatitis (eczema)
Allergic Rhinitis (hay fever)
93
Give 6 environmental factors associated with non-allergic/non-eosinophilic asthma
Smoking
Pollution
Stress
Isocyanates (occupational asthma)
Exercise
Cold air
94
What is the most common cause of occupational asthma?
Isocyanates (found in spray paints)
95
Describe acute and chronic asthma, state what mediates each.
Acute (30 mins) - Mast Cell Mediated
Chronic (12 hours) - T helper 2 (Th2) cell mediated
96
Describe the pathophysiology of Acute Asthma
Mast cell degranulation > release of histamine, leukotrienes, prostaglandins > widespread vasodilation, bronchoconstriction and increased permeability of vascular endothelium > asthma symptoms
97
Describe the pathophysiology of chronic asthma
T Helper 2 cells release IL-3, IL-4 and IL-5 > promotes recruitment of mast cells, eosinophils and B cells > airway remodelling > airway narrowing and epithelial damage
98
What structural changes are seen in airway remodelling in chronic asthma? (4)
Subepithelial fibrosis
Increased smooth muscle mass
Epithelial cell hyperplasia
Mucus production
99
What cell type is responsible for the acute pathology of asthma
Mast Cells
100
Name 3 chemicals produced by mast cells
Histamine (causes bronchoconstriction and inflammation) (released in seconds)
Tryptase (only found in mast cells - so good indicator of activity)
Cysteinyl leukotrienes (more potent than histamine) (released in minutes)
101
Give 4 differentials for Asthma
Pulmonary oedema
COPD
Large airway obstruction
Pneumothorax
102
What type of variation is seen in Asthma?
Diurnal variation (fluctuations in symptoms throughout the day)
103
Give 3 symptoms of Asthma
Dyspnoea
Wheezing
Cough +/- sputum (often nocturnal)
104
Give 5 clinical signs of asthma
Tachypnoea/Tachycardia
Audible wheeze/Widespread polyphonic wheeze
Hyperinflated chest
Recurrent URTIs
Nasal polyps
105
What is the primary diagnostic test for Asthma? What is the expected result? What can be done in addition?
Spirometry (FEV1:FVC) + FeNO testing
Result = FEV1/FVC <80% predicted
Can additionally perform a bronchodilator reversibility test to evaluate effectiveness of SABA
106
Describe the general management of asthma
TAME
T- Technique for inhaler use
A - Avoid exacerbations (allergens, smoking, dust ect)
M - Monitor - Keep peak flow rate diary
E - Educate (how to alter mediation according to severity, what to do in an emergency, when to liaise with a specialist nurse)
107
Describe the treatment ladder for Asthma
1. Salbutamol (SABA)
2 Salbutamol (SABA) + Beclometasone (ICS)
3. Salbutamol (SABA) + Beclometasone (ICS) + Montelukast/Zafirlukast (LTRA)
4. Salbutamol (SABA) + Beclometasone (ICS) + Salmetarol (LABA) +/- LTRA (depending on pts response)
5. Maintenance and reliever therapy (MART) + SABA +/- LTRA (Combined ICS + LABA in single inhaler)
6. Salbutamol (SABA) +/- Montelukast (LTRA) + Medium dose ICS MART
7. Salbutamol (SABA) +/- LTRA + Increased ICS OR LAMA/theophylline/Specialist Advice
108
What is the precursor to theophylline?
Aminophylline
109
What is the moa of theophyline?
Competitively inhibits phosphodiesterase 3/4, increasing cAMP. cAMP inhibits myosin light chain kinase, an enzyme which coordinates muscle contraction.
Inhibition of myosin light chain kinase reduces bronchoconstriction.
110
What drug can increase the risk of theophylline toxicity? Why?
Ciprofloxacin
Inhibits hepatic metabolism of theophilline, increasing risk of toxicity.
111
Name 2 leukotriene receptor antagonists. What is their moa?
Montelukast and Zafirlukast
Block the effects of cysteinyl leukotrienes by antagonising the CystLT1 receptor.
112
Define Moderate Acute Asthma (4)
PEFT 50-75%
Speech normal
RR <25
HR <110
113
Define Severe Acute Asthma (4)
PEFR - 33-50%
Can't complete sentences
RR >25
Pulse >110
114
Define Life-Threatening Acute Asthma (7)
Any one of CHEST
PEFR - <33%
SpO2 <92%
C - Cyanosed
H - Hypotension
E - Exhaustion/Confusion
S - Silent Chest
T - Tachy/brady/arrhythmias
115
What test should be performed on patients with acute asthma with O2 sats of <92%?
ABG
116
Describe the management of Acute Asthma (severe/life-threatening)
1st line;
Oxygen - If hypoxemic (maintain 94-98%)
High Dose SABA (Salbutamol/Terbutaline) (pressuried metered dose inhaler or oxygen driven nebuliser in life-threatening)
Oral Prednisolone - 40-50mg daily (continued for at least 5 days or until patient recovers from attack)
2nd line (ADD);
Ipratropium Bromide (SAMA) - If pt unresponsive to 1st line
IV Magnesium Sulphate
117
How long should a patient receive oral prednisolone following an acute exacerbation?
5 days after exacerbation or until patient recovers from attack.
118
What are the criteria for discharge following an acute asthma attack? (3)
Being stable on their discharge medication (no nebulisers/oxygen) for 12-24 hours
Inhaler technique checked and recorded
PEF >75%
119
Define pneumonia
Describes any inflammatory condition affecting the alveoli of the lungs.
As pneumonia affects the alveoli, it is considered to be an Acute Lower Respiratory Tract Infection
120
Give 2 anatomical classifications of pneumonia. How are they characterised?
Bronchopneumonia - Characterised by patchy consolidation throughout both lungs.
Lobar pneumonia - Characterised by consolidation of a single lobe
121
Name 4 categories of pneumonia
Community Acquired Pneumonia (CAP)
Hospital Acquired Pneumonia (HAP)
Aspiration
Immunocompromised (HIV)
122
Define CAP
Describes acute infection of lung tissue acquired from the community or within 48 hours of hospital admission.
123
What are the most common pathogens causing CAP? (3)
Streptococcus pneumoniae (most common)
Haemophilus influenzae (most common in COPD patients)
Mycoplasma pneumoniae
124
Define HAP
Describes acute infection of the lung that occurs in a patient >48 hours after hospital admission.
125
What pathogen most commonly causes early onset HAP (<5 days after hospital admission)
Streptococcus pneumoniae
126
What pathogens commonly cause late onset HAP (>5 days after hospital admission)? (2)
Pnseudomonas aeruginosa, E.coli, Klebsiella pneumoniae (Aerobic gram negative bacilli)
Staphylococcus aureus
127
Define aspiration pneumonia
Describes pneumonia occurring secondary to inhalation of colonized oropharyngeal contents into lower airways.
128
Who would be considered high risk for aspiration pneumonia? (5)
Stroke
Myasthenia
Bulbar palsies
Loss of consciousness
Poor dental hygiene
129
What pathogen is associated with Aspiration Pneumonia? What is a classic characteristic of this?
Klebsiella pneumoniae
Red-Currant Jelly Sputum
130
Anatomically, where is the aspiration of gastric contents likely to lodge?
Right lung (lower lobe)
131
Give 6 clinical features of pneumonia
Wheeze
Cyanosis, Tachypnoea, Tachycardia
Hypotension
Signs of consolidation (reduced expansion)
Pleural rub
Crackles on auscultation
132
What pathogen most commonly causes cavitating pneumonia in the upper lobes of diabetics and alcoholics?
Klebsiella pneumonia
133
What diagnostic tests are important to conduct when investigating pneumonia? (3)
Chest X-ray - Showing consolidation (required for diagnosis)
Blood culture - (if CURB-65 is >2) before antibiotics are given.
Sputum culture - (if CURB-65 is >3) or if CURB >2 have not yet had antibiotics.
134
What pathogen commonly causes pneumonia in undiagnosed HIV patients?
Pneumocystis jirovecii
135
What score is used to determine CAP severity? State the criteria for this.
C - Confusion
U - Urea (>7mmol/L)
R - Respiratory Rate (>30 breaths/min)
B - Blood pressure (<90mmHg systolic and/or 60mmHg Diastolic)
65 - Age >65
136
Define CURB-65 in terms of severity
0-1 - Mild - can be treated at home with oral antibiotics
2 - Moderate - patients require hospital therapy
>3 - Severe - indicated mortality 15-40%. Consider ITU
137
What is the treatment for mild CAP (CURB-65 1-0)?
Amoxicillin (Or Clarithromycin if amoxicillin contraindicated)
5 day course of antibiorics
138
What is the treatment for moderate CAP (CURB-65 >2)?
Dual oral antibiotic therapy;
1st line; Amoxicillin + Clarithromycin (or Erythromycin in pregnancy)
2nd Line: Doxycycline (if penicillin allergy)
7-10 day course is recommended
139
What is the treatment for severe CAP (CURB-65 >3)?
IV co-amoxiclav + clarithromycin
(or erythromycin in pregnancy)
140
When should all cases of pneumonia have a repeat chest X-ray?
6 weeks after clinical resolution
141
How is mild HAP treated?
Oral Co-Amoxiclav (offer doxycycline if penicillin allergy)
142
How is severe HAP managed?
IV Piperacillin + Tazobactam
Start within 4 hours of diagnosing HAP
143
How is Aspiration pneumonia managemed?
Co-amoxiclav
144
How may atypical pneumonia present?
Unusual insidious symptoms;
- Low grade fever
- Unproductive cough
- Extra-respiratory symptoms (myalgia, sore throat)
(may also have unremarkable auscultatory findings)
145
Name 2 organisms that can cause atypical pneumonia
Legionella pneumoniae
Mycoplasma pneumoniae
146
Give 5 complications of pneumonia
Respiratory failure (type I)
Hypotension (dehydration + vasodilation due to sepsis)
Atrial fibrillation (common in elderly)
Pleural effusion
Empyema (pus in pleural space)
147
What pathogens cause TB? (2)
Mycobacterium tuberculosis (most common)
Mycobacterium bovis (found in unpasteurised milk)
148
Describe the epidemiology of TB (2)
Majority of cases seen in Sub-Saharan Africa and Asia (india/china)
Common co-infection seen in HIV patients.
149
How is TB spread?
Spread via inhalation of infected aerosolized droplets
150
How do TB causing mycobacterium evade phagocytosis?
Their cell wall has a high mycolic acid content, making the outer capsule difficult to destroy.
151
Describe the pathophysiology of primary TB
Describes first contact with mycobacterium.
Primary TB is usually localised to the upper-middle portion of the lungs (Apex) causing a small area of granulomatous inflammation known as the Ghon Focus
152
What is the Ghon Focus? How is it characterised?
A small area of granulomatous inflammation seen in primary TB.
Typically characterised by lung lesions and Hilar (pulmonary) lymphadenopathy.
153
What does primary TB resemble clinically?
Acute bacterial pneumonia
154
Describe latent tuberculosis (3)
In most individuals, the Ghon Focus enters a state of dormancy (latency).
Patients are infected but show no clinical or x-ray signs of TB.
This may persist for years and patients are non-infectious.
155
Describe secondary tuberculosis
TB is an opportunistic infection and can reactivate during periods of immunosuppression.
Mycobacterium promotes recruitment of macrophages, leading to the formation of granulomas and epithelioid cells.
Can result in granulomatous necrosis and cavitation.
156
What type of hypersensitivity reaction is seen in TB? What is this mediated by?
Type 4 hypersensitivity reaction.
Mediated by T-cells.
157
Give 2 risk factors for TB
High incidence country (Sub-Saharan Africa/Asia)
Immunosuppression;
HIV, Organ Transplantation, Corticosteroids, Drug use, Low socioeconomic status ect.
158
Give 5 systemic features of TB
Low grade fever
Anorexia
Malaise
Night Sweats
Clubbing (bronchiectasis)
159
Give 5 pulmonary symptoms of TB
Cough +/- Sputum
Haemoptysis
Pleurisy (tissue between lungs and ribs becomes inflamed)
Pleural effusion
Aspergilloma/mycetoma may form in TB cavities
160
Give 5 extrapulmonary features of TB
Lymph node - Cervical Lymphadenopathy
GI - Colicky abdominal pain and vomiting
Bone - Vertebral collapse and Pott's vertebra
Skin - Lupus Vulgaris (jelly-like nodules)
Adrenal - Addison's disease
161
What is the main technique used to screen for Latent Tuberculosis?
The Mantoux Test
162
What investigations would you perform to diagnose active TB? (3)
Chest X-Ray
Sputum Smear (Ziehl Neelsen Stain) (rapid and inexpensive)
Sputum Culture (Lowenstein-Jensen Media) (Gold Standard) (can take 1-3 weeks)
163
What may a chest x-ray show in a patient with Active TB? (2)
Upper lobe cavitation (Fibronodular opacities)
Bilateral hilar lymphadenopathy
164
Describe the use of a sputum smear test for active TB (3)
3 specimens are needed 8 hours apart.
Is a rapid and inexpensive test
Uses a Ziehl Neelsen Stain
165
Describe the use of a Sputum Culture in diagnosing active TB (4)
Is the gold standard investigation for active TB
Can take 1-3 weeks.
Can be used to assess drug sensitivities
Uses a Lowenstein-Jensen Media
166
How should active TB be managed from a public health perspective? (2)
Notify Public Health England
Begin contact tracing.
167
Describe the treatment for active TB
RIPE;
Rifampicin - for 6 months
Isoniazid - for 6 months
Pyrazinamide - for first 2 months
Ethambutol - for first 2 months
168
Give 3 side effects of Rifampicin
Red-orange body secretions
Hepatitis
Drug interactions - Enzyme inducer (warfarin, phenytoin and oestrogens)
169
Give 2 side effects of Isoniazid
Neuropathy (paraesthesia in hands and feet)
Hepatitis
170
Give 3 side effects of Pyrazinamide
Arthralgia/gout
Rash
Hepatitis
171
Give 1 side effect of Ethambutol
Optic neuritis/visual impairment
172
What additional drug should be given alongside Isoniazid? And why?
Pyridoxine (vitamin B6)
To help prevent Isoniazid Induced Peripheral Neuropathy
173
What is the moa for Rifampicin?
Inhibits bacterial DNA dependent RNA polymerase, preventing transcription of DNA into mRNA
174
What is the moa of Isoniazid?
Inhibits mycolic acid synthesis
175
What is the moa of Pyrazinamide?
Converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase I (FAS)
176
What is the moa of Ethambutol?
Inhibits the enzyme arabinosyl transferase which polymerases arabinose into arabinan
177
Define Dalton's Law
States that in a mixture of non-reacting gasses, the total pressure exerted is equal to the sum of all the partial pressures of the individual gasses.
178
Define Fick's Law
States that the rate of diffusion is proportional to surface area and concentration difference and inversely proportional to membrane thickness
179
State the Law of LaPlace
The magnitude of the inward directing collapsing pressure is directly proportional to surface tension and inversely proportional to the radius of the bubble
180
Define Tidal volume
The volume of air entering or leaving the lung during a single breath
181
Define inspiratory reserve volume
The volume of air that can be maximally inspired over and above the typical tidal volume
182
Define inspiratory capacity
The maximum volume of air that can be inspired at the end of a normal expiration
183
Define residual volume
The volume of air left in the lung after a maximal expiration
184
Define vital capacity
The maximum volume of air that can be expired after a maximal inspiration
185
How is pulmonary ventilation calculated?
Tidal volume x respiratory rate
186
Define V/Q mistmatch
Describes when perfusion of the blood in the capillaries is not matching the ventilation of the alveoli
V = Ventilation (air you breath in)
Q = Perfusion (blood flow)
187
What would a high V/Q ratio indicate? (3)
Dead space;
Comes as a result of lots of ventilation but limited perfusion.
Can indicate pulmonary embolism (occlusion of blood vessels = less perfusion)
188
What can a low V/Q ratio indicate? (4)
Shunt
Indicates lots of perfusion but limited ventilation
Can indicate pulmonary oedema.
(apex of the lungs has a high V/Q due to effects of gravity)
189
Define Goodpastures Syndrome
AKA Anti-glomerular basement membrane disease (GBM)
Describes a rare small vessel vasculitis associated with both pulmonary haemorrhage and progressive glomerulonephritis.
190
What causes Goodpastures Syndrome?
Anti-glomerular basement membrane antibodies against Type IV collagen.
Type IV collagen is principally found in the basement membranes of alveoli and glomeruli.
191
Give 2 features of Goodpastures Syndrome
Pulmonary haemorrhage
Rapidly progressive glomerulonephritis (proteinuria and haematuria - rapid onset AKI)
192
Give 3 clinical features of Goodpastures Syndrome
Haemoptysis (due to pulmonary haemorrhage)
Reduced urine output (proteinuria and haematuria)
Oedema
193
How is Goodpastures syndrome diagnosed? (3)
Renal biopsy - Shows IgG deposits along the basement membrane
Increased DLCO (increases during haemorrhage)
Anti-glomerular basement membrane antibody titre (confirmatory diagnostic test)
194
How is Goodpastures Syndrome treated? (3)
Oral corticosteroids - Prednisolone
Plasmapheresis - Until GMB antibodies are no longer present
Cyclophosphamide
195
Describe the pleural cavity
Describes a potential space between the pleurae (visceral - inner and parietal - outer) of the pleural sac surrounding each lung.
196
Define pleural effusion. How can this be characterised? (2)
Describes when fluid collects between the parietal and visceral pleural layers.
Can be characterised by either;
Over production of pleural fluid
Impaired removal of pleural fluid
197
Give 4 risk factors for pleural effusion
Congestive Heart Failure
Pneumonia
Malignant Mesothelioma
Recent coronary artery bypass graft surgery
198
What are the 2 classifications of pleural effusion?
Transudate (transparent - less protein) (Effusion protein <25g/L)
Exudate (effusion protein >35g/L)
199
Describe transudative pleural effusion. Give 3 causes
Effusion protein <25g/L
Vessels are not compromised so accumulation of fluid is driven by increases in hydrostatic pressure (high venous pressure).
Causes;
Congestive heart failure
Constrictive pericarditis
Fluid overload
200
Describe exudative pleural effusion. Give causes.
Effusion protein >35g/L
Vessels are compromised so have increased mesothelial and capillary permeability, so fluids and proteins are able to leak into the pleural space.
Causes;
Pneumonia
Tuberculosis
Malignancy
201
Define cystic fibrosis
Describes an autosomal recessive disorder causing increased viscosity of secretions (lungs and pancreas)
202
What is the pattern of inheritance in Cystic Fibrosis?
Autosomal Recessive
203
Cystic fibrosis arises from a mutation in what gene? What does this gene code for?
CFTR gene
Encodes for a cAMP regulated chloride channel
204
Where chromosomally is the gene mutation in the majority of cystic fibrosis cases?
Delta F508 on the long arm of chromosome 7
205
Name 3 organisms which may colonise CF patients
Staphylococcus aureus
Pseudomonas aeruginosa
Aspergillus
206
What test is used to diagnose CF? Is this reliable?
Sweat test - CF patients have abnormally high sweat chloride
Can cause false positives in;
Malnutrition
Adrenal insifficiency
Nephrogenic diabetes insipidus
Hypothyroidism
Hypoparathyroidism
207
Give 4 presenting features of CF
Neonatal period - Meconium ileus
Recurrent chest infections
Malabsorption; steatorrhoea, failure to thrive
Liver disease
208
Give 5 features of cystic fibrosis
Short stature
Diabetes mellitus
Delayed puberty
Rectal prolapse (due to bulky stools)
Nasal polyps
209
How is cystic fibrosis managed?
Regular chest physiotherapy and postural drainage
High calorie diet, high fat intake
Minimise contact with other CF patients to reduce cross-infection risk
Pancreatic enzyme supplementation taken with meals
210
Name 1 drug that can be used to treat cystic fibrosis. What is it's MOA?
Orkambi.
Increases number of CFTR proteins transported to cell surface.
211
Define bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic inflammation or infection
212
Give 5 causes of bronchiectasis
Post infective (TB, Whooping Cough, Pneumonia, Measles)
Cystic fibrosis
Bronchia obstruction (lung cancer/foreign body)
Immune deficiency (selective IgA, hypohammaglobulinaemia)
Ciliary dyskinetic syndromes (Kartagner's syndrome, Young's syndrome)
213
Give 4 clinical features of bronchiectasis
Persistent productive cough (large volumes of sputum)
Dyspnoea (breathlessness)
Haemoptysis
Coarse crackles/wheeze on auscultation
214
What is the best diagnostic tool for bronchiectasis in adults?
High resolution chest CT
215
What sign would be seen on a chest CT for a patient with bronchiectasis?
Signet Ring Sign (bronchi larger than their adjacent pulmonary artery)
216
What may a chest x-ray show for a patient with bronchiectasis? (2)
Dilated and thickened airways
Tram lines
217
What is the most common organism to infect patients with bronchiectasis?
Haemophilus influenzae
218
How is bronchiectasis managed? (6)
Treat underlying cause
Physical training (inspiratory muscle training)
Postural drainage
Antibiotics for exacerbations + long-term rotating antibiotics (severe cases)
Bronchodilators
Immunisations
219
Describe acute bronchitis
A typically self-limiting chest infection that results from inflammation of the trachea and major bronchi.
220
How long does it typically take for acute bronchitis to resolve?
3 weeks
221
When does acute bronchitis typically occur?
Autumn or winter
222
Give 5 clinical features of acute bronchitis
Cough (+/- sputum)
Sore throat
Rhinorrhoea
Wheeze
Low grade fever
223
How can acute bronchitis be differentiated from pneumonia? (2)
History; Sputum, wheeze, breathless may be absent in acute bronchitis, whereas at least one tends to be present in pneumonia.
Examination;
No other focal chest signs (dullness on percussion, crepitations or bronchial breathing) are seen in acute bronchitis (except for wheeze).
Systemic features (malaise, myalgia, fever) may also be absent in acute bronchitis, but tend to be present in pneumonia)
224
How is acute bronchitis diagnosed? And what guides whether antibiotics are required?
Diagnosed clinically
CRP testing guides whether antibiotic therapy is needed
225
When should antibiotic therapy be considered in cases of acute bronchitis (3)
Antibiotics should be considered if;
Patient is systemically very unwell
Patient has pre-existing co-morbidities
Patient has a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
226
Describe how CRP testing guides antibiotic use in acute bronchitis.
If patient has a CRP of 20-100mg/L - Offer delayed prescription
If patient has CRP of >100mg/L - Offer antibiotics immediately
227
What are the 1st line and 2nd line antibiotics for acute bronchitis (if needed)
1st line - Doxycycline
2nd line - Amoxicillin (if child or pregnant)
228
Describe sarcoidosis
Describes a multisystem disorder (affecting skin, eyes and lungs) of unknown cause characterised by non-caseating granuloma with multinucleated giant cells in the center.
229
How does acute sarcoidosis often present? (4)
Swinging fever
Bilateral hilar lymphadenopathy (Lofgren's Syndrome)
Erythema nodosum
Polyarthralgia
230
What is Lofgren's syndrome associated with?
Acute Sarcoidosis
231
What is the triad for Lofgren's syndrome? (3)
Erythema Nervosum
Polyarthralgia
Bilateral perihilar lymphadenopathy
232
Give 2 biochemical features of sarcoidosis
Hypercalcaemia
Raised ACE
233
Give 5 clinical features of sarcoidosis
Cough
Dyspnoea
Chest pain
Photophobia, red painful eye, blurred vision (uveitis)
Lupus pernio (hard purple lesion seen on cheeks, nose, lips, ears or forehead)
234
What skin lesion may be seen in sarcoidosis?
Lupus pernio (hard purple lesion on cheeks, nose, lips, ears or forehead)
235
What diagnostic test is used to stage sarcoidosis? Describe the stages (5)
Chest X-ray
Stage 0 = Normal
Stage 1 = Bilateral Hilar Lymphadenopathy
Stage 2 = BHL + Interstitial infiltrates
Stage 3 = Diffuse Interstitial Infiltrates Only (No BHL)
Stage 4 = Diffuse Fibrosis
236
Why does sarcoidosis cause hypercalcaemia?
Macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
237
Give 3 indications for steroid use for patients with sarcoidosis
Chest X-ray showing stage 2 or 3 in symptomatic patients
Hypercalcaemia
Eye, heart or neuro involvement
238
Give 5 factors of sarcoidosis associated with a poor prognosis
Insidious onset, symptoms >6 months
Absence of erythema nodosum
Extrapulmonary manifestations (lupus pernio, splenomegaly)
Chest X-ray showing stage 3-4 features
Afro-Caribbean ethnicity
239
Give 6 causes of upper zone lung fibrosis
CHARTS
C - Coal Worker's Pneumoconiosis
H - Histiocytosis/Hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation (cancer therapy)
T - Tuberculosis
S - Silicosis/Sarcoidosis
240
List 3 drugs associated with causing lower zone lung fibrosis
Amiodarone
Bleomycin
Methotrexate
241
Give 4 causes of lower zone lung fibrosis
ACID
A - Asbestosis
C - Connective tissue disorders (Excluding Ankylosing Spondylosis, e.g SLE)
I - Idiopathic
D - Drug induced (amiodarone, bleomycin, methotrexate)
242
Give 4 presenting features of pulmonary fibdosis
Progressive exertional dyspnoea
Bi-basal fine end inspiratory crepitations
Dry cough
Clubbing
243
What is the gold standard investigation for diagnosing pulmonary fibrosis?
High resolution CT scan
244
What is the 5 step approach to ABG interpretation?
1. How is the patient?
2. Is the patient hypoxaemic (PaO2 on RA should be >10kPa)
3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
4. Respiratory component - What has happened to the PaCO2? (>6.0 = respiratory acidosis) (<4.7 = respiratory alkalosis)
5. Metabolic component: What is the bicarbonate level/base excess (Bicarbonate <22 = metabolic acidosis) (Bicarbonate >26 = metabolic alkalosis)
245
On an ABG, a PaCO2 of >6.0kPA would suggest what?
Respiratory acidosis (or respiratory compensation for a metabolic acidosis)
246
On an ABG a PaCO2 of <4/7 suggests what?
Respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
247
On an ABG a bicarbonate of <22mmol/L suggests what?
Metabolic acidosis (or renal compensation for respiratory alkalosis)
248
On an ABG a bicarbonate of >26mmol/L suggests what?
Metabolic alkalosis (or renal compensation for a respiratory acidosis)
249
Use the acronym ROME to describe ABG interpretation
Respiratory = Opposite
Low pH + High PaCO2 = Acidosis
High pH + Low PaCO2 = Alkalosis
Metabolic = Equal
Low pH + Low Bicarbonate = Acidosis
High pH + High Bicarbonate = Alkalosis
250
Give 4 key indications for NIV use
COPD with respiratory acidosis pH 7.25-7.35
Type 2 respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
Cardiogenic pulmonary oedema unresponsive to CPAP
Weaning from tracheal intubation
251
How much oxygen should be given to patients who are critically ill (anaphylaxis, shock ect) and how should it be given?
15L/min via reservoir mask
252
What is the oxygen saturation target for acutely ill patients (no COPD)
94-98%
253
What is the oxygen saturation target for management of patients with COPD? (2)
88-92%
(adjust range to 94-98% if pCO2 is normal)
254
Describe inhaler technique in 5 steps
1. Remove cap and shake
2. Breath out gently
3. Put mouthpiece in mouth and as you begin to breath in, which should be slow and deep, press canister down and continue to inhale steadily and deeply.
4. Hold breath for 10 seconds (or as long as possible)
5. For a second dose, wait approximately 30 seconds before repeating steps 1-4
255
Describe pneumothorax
A condition characterised by the accumulation of air in the pleural space, resulting in the partial, or complete, collapse of the affected lung.
256
Name and describe 2 classifications for spontaneous pneumothorax
Primary Spontaneous Pneumothorax (PSP) - Occurs without underlying disease, often in tall, thin, young individuals. Associated with rupture of subpleural blebs or bullae
Secondary spontaneous pneumothorax (SSP) - Occurs in patients with pre-existing lung disease (COPD, asthma CF, cancer)
257
What does the classic Primary Spontaneous Pneumothorax patient look like?
Tall, thin, young indivuduals
258
Define tension pneumothorax
Describes a severe pneumothorax resulting in the displacement of mediastinal structures.
May result in severe respiratory distress and haemodynamic collapse
259
Give 6 clinical features of pneumothorax
Acute onset dyspnoea
Acute onset pleuritic chest pain
Reduced breath sounds
Reduce lung expansion
Hyper-resonant lung percussion
Tachypnoea/Tachycardia
260
Give 3 distinctive features of tension pneumothorax
Respiratory distress
Tracheal deviation (away from side of pneumothorax)
Hypotension
261
Describe the management for a primary pneumothorax (3)
1. If the rim of air is <2cm and the patient is NOT short of breath - Discharge
2. Otherwise, aspiration should be attempted
3. If aspiration fails (>2cm or still short of breath) then chest drain should be inserted
262
Describe the management for secondary pneumothorax (3)
1. If patient is >50 and the rim of air is >2cm and/or patient is SOB then insert chest drain.
2 Otherwise, attempt aspiration if rim of air is between 1-2cm. If aspiration fails, insert chest drain and admit for at least 24 hours.
3. If pneumothorax is <1cm give O2 and admit for 24 hours.
263
What discharge advice should be given to a patient recovering from a pneumothorax? (3)
Avoid smoking
No Flying until 2 weeks after successful drainage ( if there is no residual air) Or 1 week after post check x-ray
Avoid scuba diving
264
Give 4 causes of respiratory alkalosis
Pulmonary Embolism
Pregnancy
Encephalitis
Anxiety
265
List 6 conditions causing upper lobe pulmonary fibrosis
CHARTS
C- Coal worker's pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
