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Phase 4 Medicine > Respiratory > Flashcards

Respiratory Flashcards

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.

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2
Q

Define vital capacity

A

The total volume of air that can be expelled from the lungs after a maximum inhalation

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3
Q

What is the vital capacity equal to?

A

The sum of inspiratory reserve volume, tidal volume and expiratory reserve volume

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4
Q

Define forced vital capacity

A

The total amount of air that can be forcible expired

(low FVC indicates airway restriction)

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5
Q

Define Forced Expiratory Volume (FEV1)

A

The total volume of air expired in one second

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6
Q

What is the typical FEV and FEV1:FVC for a patient with COPD?

A

FEV<80% and FEV1:FVC <0.7 (<70%)

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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.

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8
Q

What is the most common pathogen causing infective exacerbations in COPD?

A

Haemophilus influenzae

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9
Q

Name 3 types of COPD

A

Emphysema

Chronic Bronchitis

Alpha-1-antitrypsin deficiency

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10
Q

What is the pattern of inheritance for alpha 1 antitrypsin deficiency?

A

Autosomal recessive

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11
Q

Alpha 1 antitrypsin deficiency is caused by a mutation in what?

A

SERPINA1

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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

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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.

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14
Q

Give 4 causes of COPD

A

Smoking (major cause)

Pollution

Occupational exposure to noxious gasses

Genetics - AAT deficiency

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15
Q

Give 5 clinical features of COPD

A

Cough +/- Sputum

Wheeze

Tachypnoea (rapid breathing)

Dyspnoea (shortness of breath)

Hyperinflation (decreased cricosternal distance)

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16
Q

Give 5 complications of COPD

A

Acute exacerbations +/- infection

Polycythemia

Pneumothorax

Cor Pulmonale (right sided heart failure)

Lung carcinoma

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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

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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)

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19
Q

Describe type I respiratory failure in terms of O2 and Co2

A

Low O2 and Normal/Low Co2

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20
Q

Describe type II respiratory failure in terms of O2 and Co2

A

Low O2 and High Co2

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21
Q

Give 4 causes of Type I respiratory failure

A

High altitude
Hypoxaemic hypoxia (low atrial O2)
Pulmonary embolism
Pneumonia

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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

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23
Q

What score is used to assess symptoms of COPD. Describe the criteria

A

mMRC dyspnoea score (1-5).

  1. Dyspnoea only with strenuous exercise
  2. Dyspnoea on hurrying or walking up-stairs/slight hill.
  3. Walks slowly or has to stop for breath
  4. Stops for breath after <100yrs or after a few minutes.
  5. Too breathless to leave the house or breathless when dressing
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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%

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25
Q

What signs would you see on a chest x ray for a patient with COPD?(4)

A

Increased anteroposterior diameter

Flattened diaphragm

Increased intercostal spaces

Hyperlucent lungs

(Also important to exclude lung cancer)

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26
Q

Describe the general management of COPD (4)

A

Smoking cessation (main)

Pulmonary Rehabilitation and Exercise

Vaccinations (influenza and Streptococcus pneumoniae)

Review 1/2 times per year

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27
Q

What vaccinations should COPD patients receive?

A

Annual influenza vaccine

One off pneumococcal vaccination

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28
Q

What medications can be used to help smoker quit in COPD? (2)

A

Bupropion or Varenicline (partial nicotinic agonists)

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29
Q

In which patients should Bupropion be avoided and why?

A

Epileptic patients

As it reduces seizure threshold

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30
Q

What is the 1st line bronchodilator therapy for COPD?

A

1st line - Salbutamol (SABA) or Ipratropium Bromide (SAMA)

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31
Q

What determines whether a COPD patient requires 2nd line bronchodilator therapy?

A

Whether the patient has asthmatic features/features suggesting steroid responsiveness.

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32
Q

What features are used to determine whether a COPD patient has asthmatic/steroid responsiveness? (4)

A

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%)

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33
Q

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?

A

2nd line - ADD Salmeterol (LABA) + Tiotropium (LAMA)

(If already taking SAMA, discontinue and switch to SABA)

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34
Q

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?

A

2nd line - Add Salmeterol (LABA) + Beclometasone (ICS)

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35
Q

If a COPD patient with asthmatic features/features suggesting steroid responsiveness remains breathlessness or has exacerbations following 2nd line therapy, what should be offered?

A

3rd Line - Triple Therapy - Salmeterol (LABA) + Tiotropium (LABA) + Beclometasone (ICS)

If taking SAMA, discontinue and switch to SABA.

Use combined inhalers where possible.

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36
Q

What should be offered to COPD patients who cannot use inhaled therapy or who have had trials of short/long acting bronchodilators?

A

Oral Theophylline

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37
Q

When should the dose of theophylline be reduced in COPD?

A

If a macrolide (azithromycin) or fluoroquinolone Abx is co-prescribed

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38
Q

What should patients with persistent exacerbations of COPD be offered?

A

Azithromycin prophylaxis

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39
Q

What adverse effects can azithromycin have?

A

Can prolong QT interval

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40
Q

What other medication can also be used to reduce the risk of COPD exacerbations in patients with severe COPD or hx of frequent exacerbations?

A

Phosphodiesterase 4 inhibitors (PDE-4) - Roflumilast

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41
Q

When do NICE recommend giving PDE-4 inhibitors (such as roflumilast) to COPD patients? (2)

A

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

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42
Q

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?

A

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)

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43
Q

Give an example of a SABA and a LABA and describe their MOA

A

Salbutamol (SABA). Salmeterol (LABA)

Beta 2 agonists.

Relax airway smooth muscle

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44
Q

Give 3 possible side effects of SABA/LABAs

A

Tachyarrhythmias

Hypokalaemia

Tremor/anxiety

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45
Q

Give an example of a SAMA and LAMA and describe their moa (3).

A

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.

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46
Q

Define emphysema. What is a nickname for these patients?

A

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.

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47
Q

What is the principle cause of emphysema? Describe the pathophysiology

A

Smoking

Smoking inactivates alpha-1 antitrypsin > increased elastase activity > alveolar wall breakdown > loss of alveolar elasticity and destruction of alveoli

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48
Q

In emphysema, what does the loss of alveolar elasticity and destruction of alveoli result in? (2)

A

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

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49
Q

Give 5 clinical features of emphysema

A

Typical symptoms of COPD (cough, wheeze, dyspnoea, tachypnoea, sputum ect)

Pursed lips on expiration

Barrel chest (hyperventilation)

Cachexia

Use of accessory respiration muscles

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50
Q

Why do patients with emphysema purse their lips on expiration?

A

Increases airway pressure and prevents airway collapse during expiration.

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51
Q

What examination finding would be indicative of air trapping in a patient with ? emphysema

A

Hyper resonant percussion

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52
Q

Describe the results of pulmonary function tests in a patient with emphysema (3)

A

Decreased DLCO (Diffusing capacity of the lung for carbon dioxide)

Raised TLC (total lung capacity)

Raised RV (residual volume)

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53
Q

Define chronic bronchitis. What is their nickname?

A

Defined clinically as a cough and sputum production most days for 3 months of 2 consecutive years.

Blue blotters - As they’re usually cyanosed

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54
Q

How is chronic bronchitis characterised physiogically?

A

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.

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55
Q

Why do patients with chronic bronchitis find it difficult to clear secretions?

A

Occurs due to poor ciliary function.

Ciliated columnar cells are replaced by squamous epithelial cells in response to inflammation/toxins from smoking.

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56
Q

Give 4 clinical features of chronic bronchitis

A

Typical features of COPD (cough, wheeze, dyspnoea, tachypnoea, sputum ect)

Sputum production

Cyanosis

Cor Pulmonale (right sided heart failure)

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57
Q

What would an ABG show for a patient with chronic bronchitis?

A

Low O2 and Increased Co2 - Type II respiratory failure

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58
Q

What would an ABG show for a patient with emphysema

A

Normal O2 and Normal Co2

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59
Q

Define lung cancer

A

Describes a group of malignant epithelial tumours that arise from cells lining the lower respiratory tract (trachea, bronchi, bronchioles and alveoli)

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60
Q

Name 2 categories of lung cancer

A

Non-small cell lung cancer (80%) (inc squamous cell carcinoma, adenocarcinoma, large cell carcinoma)

Small cell lung cancer (aka oat cell)

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61
Q

What type of lung cancer is most aggressive?

A

Small cell lung cancer.

70% of patients have distant metastasis at presentation.

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62
Q

Describe the histology of small cell lung cancers

A

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.

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63
Q

Where do small cell lung cancers arise from? What does this result in?

A

Arise from pulmonary neuroendocrine cells (Enterochromaffin cells, Kulchitski cells, K cells)

Results in paraneoplastic syndromes as these cells secrete polypeptide hormones

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64
Q

Name 3 paraneoplastic syndromes caused by small cell lung cancers

A

SIADH

Ectopic Cushing’s Syndrome (ectopic ACTH production)

Lambert Eaton Myasthenic Syndrome (Abs against voltage gated calcium channels)

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65
Q

Describe Lambert Eaton Myasthenic Syndrome and describe it’s features. (3)

A

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).

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66
Q

What are the 3 main histological types of Non Small Cell Lung Cancer? Which is the most common?

A

Squamous cell carcinoma

Adenocarcinoma (most common)

Large cell carcinomas

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67
Q

Describe the behaviour of squamous cell carcinomas of the lung. What is this type of cancer associated with? (3)

A

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

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68
Q

What chemical are adenocarcinomas of the lung associated with?

A

Asbestos

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69
Q

Describe the behaviour of adenocarcinomas.

A

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

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70
Q

Which type of lung cancer is associated with gynaecomastia and why?

A

Adenocarcinoma

Can secrete HcG.

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71
Q

Which type of non-small cell lung cancer carries the worst prognosis?

A

Large Cell Carcinoma

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72
Q

What are the most common cancers to metastasize TO the lungs? (4)

A

Kidney Cancer (most common) - Renal cell carcinoma

Breast Cancer

Bowel Cancer

Bladder Cancer

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73
Q

Give 6 clinical features of lung cancer

A

Cough

Haemoptysis

Dyspnoea

Chest pain

Recurrent/slow resolving pneumonia

Anorexia and weight loss

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74
Q

Give 4 complications of lung cancer

A

Recurrent laryngeal nerve palsy (voice hoarseness)

Superior Vena Cava obstruction (face swelling, distended neck veins, dyspnoea)

Horners Syndrome (pancoast tumour)

Paraneoplastic stbdromes

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75
Q

What type of tumour is Horner’s syndrome associated with? What is the triad for Horner’s syndrome?

A

Pancoast tumour (invades the sympathetic plexus)

Triad;
Ptosis (drooping eyelid)
Miosis (excessive constriction of pupil)
Ipsilateral Anhidrosis (inability to sweat)

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76
Q

What is the 1st line investigation for patients with suspected lung cancer? What may this show? (4)

A

Chest X-Ray

May show;
Hilar enlargement
Consolidation/collapse
Coin lesions
Plural effusion

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77
Q

What imaging tool is used to stage lung cancer?

A

Contrast enhanced CT

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78
Q

What test should be conducted in all lung cancer patients anticipated to undergo surgery? Why?

A

Pulmonary Function Tests (PFTs)

To assess any post-operative loss of lung function

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79
Q

Describe mesothelioma

A

Describes a high grade tumour of mesothelial cells. Commonly affecting the right lung, usually occurring in the pleura.

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80
Q

What is mesothelioma development strongly associated with?

A

Asbestos exposure.

(Latent period between exposure to onset can be 45 years)

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81
Q

Give 5 clinical features of mesothelioma

A

History of asbestos exposure

Age between 60-85

Chest pain, dyspnoea

Weight loss

Finger clubbing

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82
Q

What is a chest x-ray/CT likely to show for a patient with mesothelioma? (4)

A

Unilateral pleural effusion

Irregular pleural thickening

Reduced lung volumes

Parenchymal changes related to asbestos exposure (interstitial fibrosis)

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83
Q

Give 2 examples of Type 1 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology

A

IgE mediated

Asthma + Anaphylaxis

IgE binds to and primes mast cells > mast cell degranulation > releasing histamine, leukotrienes and prostaglandins

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84
Q

Give 2 examples of Type 2 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology

A

IgG mediated

Autoimmune disease or blood transfusion rejection

Characterised by antibodies targeting antigens present on the surface of cells.

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85
Q

Give an example of a Type 3 Hypersensitivity Reactions and state what mediates it. Briefly describe the pathophysiology

A

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).

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86
Q

Give 2 examples of Type 4 Hypersensitivity Reactions and state what mediates them. Briefly describe the pathophysiology

A

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.

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87
Q

Define asthma

A

Asthma is characterized by recurrent episodes of dyspnoea, cough and wheeze caused by reversible airway obstruction.

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88
Q

What type of hypersensitivity reaction of Asthma? What is it mediated by?

A

Type 1 hypersensitivity reaction. IgE mediated.

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89
Q

What 3 factors contribute to airway narrowing in asthma?

A

Bronchial smooth muscle contraction

Mucosal swelling/inflammation (due to mast cell/neutrophil degranulation releasing histamine)

Increased mucus production

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90
Q

Describe the epidemiology of asthma

A

Commonly presents in childhood (peaks at 5 years) with symptoms resolving/improving with age.

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91
Q

How is asthma subclassified?

A

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)

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92
Q

Atopic asthma patients may also display symptoms of what? (2)

A

Atopic dermatitis (eczema)

Allergic Rhinitis (hay fever)

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93
Q

Give 6 environmental factors associated with non-allergic/non-eosinophilic asthma

A

Smoking

Pollution

Stress

Isocyanates (occupational asthma)

Exercise

Cold air

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94
Q

What is the most common cause of occupational asthma?

A

Isocyanates (found in spray paints)

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95
Q

Describe acute and chronic asthma, state what mediates each.

A

Acute (30 mins) - Mast Cell Mediated

Chronic (12 hours) - T helper 2 (Th2) cell mediated

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96
Q

Describe the pathophysiology of Acute Asthma

A

Mast cell degranulation > release of histamine, leukotrienes, prostaglandins > widespread vasodilation, bronchoconstriction and increased permeability of vascular endothelium > asthma symptoms

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97
Q

Describe the pathophysiology of chronic asthma

A

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

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98
Q

What structural changes are seen in airway remodelling in chronic asthma? (4)

A

Subepithelial fibrosis

Increased smooth muscle mass

Epithelial cell hyperplasia

Mucus production

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99
Q

What cell type is responsible for the acute pathology of asthma

A

Mast Cells

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100
Q

Name 3 chemicals produced by mast cells

A

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)

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101
Q

Give 4 differentials for Asthma

A

Pulmonary oedema

COPD

Large airway obstruction

Pneumothorax

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102
Q

What type of variation is seen in Asthma?

A

Diurnal variation (fluctuations in symptoms throughout the day)

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103
Q

Give 3 symptoms of Asthma

A

Dyspnoea

Wheezing

Cough +/- sputum (often nocturnal)

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104
Q

Give 5 clinical signs of asthma

A

Tachypnoea/Tachycardia

Audible wheeze/Widespread polyphonic wheeze

Hyperinflated chest

Recurrent URTIs

Nasal polyps

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105
Q

What is the primary diagnostic test for Asthma? What is the expected result? What can be done in addition?

A

Spirometry (FEV1:FVC) + FeNO testing

Result = FEV1/FVC <80% predicted

Can additionally perform a bronchodilator reversibility test to evaluate effectiveness of SABA

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106
Q

Describe the general management of asthma

A

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)

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107
Q

Describe the treatment ladder for Asthma

A
  1. Salbutamol (SABA)

2 Salbutamol (SABA) + Beclometasone (ICS)

  1. Salbutamol (SABA) + Beclometasone (ICS) + Montelukast/Zafirlukast (LTRA)
  2. Salbutamol (SABA) + Beclometasone (ICS) + Salmetarol (LABA) +/- LTRA (depending on pts response)
  3. Maintenance and reliever therapy (MART) + SABA +/- LTRA (Combined ICS + LABA in single inhaler)
  4. Salbutamol (SABA) +/- Montelukast (LTRA) + Medium dose ICS MART
  5. Salbutamol (SABA) +/- LTRA + Increased ICS OR LAMA/theophylline/Specialist Advice
108
Q

What is the precursor to theophylline?

A

Aminophylline

109
Q

What is the moa of theophyline?

A

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
Q

What drug can increase the risk of theophylline toxicity? Why?

A

Ciprofloxacin

Inhibits hepatic metabolism of theophilline, increasing risk of toxicity.

111
Q

Name 2 leukotriene receptor antagonists. What is their moa?

A

Montelukast and Zafirlukast

Block the effects of cysteinyl leukotrienes by antagonising the CystLT1 receptor.

112
Q

Define Moderate Acute Asthma (4)

A

PEFT 50-75%

Speech normal

RR <25

HR <110

113
Q

Define Severe Acute Asthma (4)

A

PEFR - 33-50%

Can’t complete sentences

RR >25

Pulse >110

114
Q

Define Life-Threatening Acute Asthma (7)

A

Any one of CHEST

PEFR - <33%

SpO2 <92%

C - Cyanosed
H - Hypotension
E - Exhaustion/Confusion
S - Silent Chest
T - Tachy/brady/arrhythmias

115
Q

What test should be performed on patients with acute asthma with O2 sats of <92%?

A

ABG

116
Q

Describe the management of Acute Asthma (severe/life-threatening)

A

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
Q

How long should a patient receive oral prednisolone following an acute exacerbation?

A

5 days after exacerbation or until patient recovers from attack.

118
Q

What are the criteria for discharge following an acute asthma attack? (3)

A

Being stable on their discharge medication (no nebulisers/oxygen) for 12-24 hours

Inhaler technique checked and recorded

PEF >75%

119
Q

Define pneumonia

A

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
Q

Give 2 anatomical classifications of pneumonia. How are they characterised?

A

Bronchopneumonia - Characterised by patchy consolidation throughout both lungs.

Lobar pneumonia - Characterised by consolidation of a single lobe

121
Q

Name 4 categories of pneumonia

A

Community Acquired Pneumonia (CAP)

Hospital Acquired Pneumonia (HAP)

Aspiration

Immunocompromised (HIV)

122
Q

Define CAP

A

Describes acute infection of lung tissue acquired from the community or within 48 hours of hospital admission.

123
Q

What are the most common pathogens causing CAP? (3)

A

Streptococcus pneumoniae (most common)

Haemophilus influenzae (most common in COPD patients)

Mycoplasma pneumoniae

124
Q

Define HAP

A

Describes acute infection of the lung that occurs in a patient >48 hours after hospital admission.

125
Q

What pathogen most commonly causes early onset HAP (<5 days after hospital admission)

A

Streptococcus pneumoniae

126
Q

What pathogens commonly cause late onset HAP (>5 days after hospital admission)? (2)

A

Pnseudomonas aeruginosa, E.coli, Klebsiella pneumoniae (Aerobic gram negative bacilli)

Staphylococcus aureus

127
Q

Define aspiration pneumonia

A

Describes pneumonia occurring secondary to inhalation of colonized oropharyngeal contents into lower airways.

128
Q

Who would be considered high risk for aspiration pneumonia? (5)

A

Stroke

Myasthenia

Bulbar palsies

Loss of consciousness

Poor dental hygiene

129
Q

What pathogen is associated with Aspiration Pneumonia? What is a classic characteristic of this?

A

Klebsiella pneumoniae

Red-Currant Jelly Sputum

130
Q

Anatomically, where is the aspiration of gastric contents likely to lodge?

A

Right lung (lower lobe)

131
Q

Give 6 clinical features of pneumonia

A

Wheeze

Cyanosis, Tachypnoea, Tachycardia

Hypotension

Signs of consolidation (reduced expansion)

Pleural rub

Crackles on auscultation

132
Q

What pathogen most commonly causes cavitating pneumonia in the upper lobes of diabetics and alcoholics?

A

Klebsiella pneumonia

133
Q

What diagnostic tests are important to conduct when investigating pneumonia? (3)

A

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
Q

What pathogen commonly causes pneumonia in undiagnosed HIV patients?

A

Pneumocystis jirovecii

135
Q

What score is used to determine CAP severity? State the criteria for this.

A

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
Q

Define CURB-65 in terms of severity

A

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
Q

What is the treatment for mild CAP (CURB-65 1-0)?

A

Amoxicillin (Or Clarithromycin if amoxicillin contraindicated)

5 day course of antibiorics

138
Q

What is the treatment for moderate CAP (CURB-65 >2)?

A

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
Q

What is the treatment for severe CAP (CURB-65 >3)?

A

IV co-amoxiclav + clarithromycin
(or erythromycin in pregnancy)

140
Q

When should all cases of pneumonia have a repeat chest X-ray?

A

6 weeks after clinical resolution

141
Q

How is mild HAP treated?

A

Oral Co-Amoxiclav (offer doxycycline if penicillin allergy)

142
Q

How is severe HAP managed?

A

IV Piperacillin + Tazobactam

Start within 4 hours of diagnosing HAP

143
Q

How is Aspiration pneumonia managemed?

A

Co-amoxiclav

144
Q

How may atypical pneumonia present?

A

Unusual insidious symptoms;
- Low grade fever
- Unproductive cough
- Extra-respiratory symptoms (myalgia, sore throat)

(may also have unremarkable auscultatory findings)

145
Q

Name 2 organisms that can cause atypical pneumonia

A

Legionella pneumoniae

Mycoplasma pneumoniae

146
Q

Give 5 complications of pneumonia

A

Respiratory failure (type I)

Hypotension (dehydration + vasodilation due to sepsis)

Atrial fibrillation (common in elderly)

Pleural effusion

Empyema (pus in pleural space)

147
Q

What pathogens cause TB? (2)

A

Mycobacterium tuberculosis (most common)

Mycobacterium bovis (found in unpasteurised milk)

148
Q

Describe the epidemiology of TB (2)

A

Majority of cases seen in Sub-Saharan Africa and Asia (india/china)

Common co-infection seen in HIV patients.

149
Q

How is TB spread?

A

Spread via inhalation of infected aerosolized droplets

150
Q

How do TB causing mycobacterium evade phagocytosis?

A

Their cell wall has a high mycolic acid content, making the outer capsule difficult to destroy.

151
Q

Describe the pathophysiology of primary TB

A

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
Q

What is the Ghon Focus? How is it characterised?

A

A small area of granulomatous inflammation seen in primary TB.

Typically characterised by lung lesions and Hilar (pulmonary) lymphadenopathy.

153
Q

What does primary TB resemble clinically?

A

Acute bacterial pneumonia

154
Q

Describe latent tuberculosis (3)

A

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
Q

Describe secondary tuberculosis

A

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
Q

What type of hypersensitivity reaction is seen in TB? What is this mediated by?

A

Type 4 hypersensitivity reaction.

Mediated by T-cells.

157
Q

Give 2 risk factors for TB

A

High incidence country (Sub-Saharan Africa/Asia)

Immunosuppression;
HIV, Organ Transplantation, Corticosteroids, Drug use, Low socioeconomic status ect.

158
Q

Give 5 systemic features of TB

A

Low grade fever

Anorexia

Malaise

Night Sweats

Clubbing (bronchiectasis)

159
Q

Give 5 pulmonary symptoms of TB

A

Cough +/- Sputum

Haemoptysis

Pleurisy (tissue between lungs and ribs becomes inflamed)

Pleural effusion

Aspergilloma/mycetoma may form in TB cavities

160
Q

Give 5 extrapulmonary features of TB

A

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
Q

What is the main technique used to screen for Latent Tuberculosis?

A

The Mantoux Test

162
Q

What investigations would you perform to diagnose active TB? (3)

A

Chest X-Ray

Sputum Smear (Ziehl Neelsen Stain) (rapid and inexpensive)

Sputum Culture (Lowenstein-Jensen Media) (Gold Standard) (can take 1-3 weeks)

163
Q

What may a chest x-ray show in a patient with Active TB? (2)

A

Upper lobe cavitation (Fibronodular opacities)

Bilateral hilar lymphadenopathy

164
Q

Describe the use of a sputum smear test for active TB (3)

A

3 specimens are needed 8 hours apart.

Is a rapid and inexpensive test

Uses a Ziehl Neelsen Stain

165
Q

Describe the use of a Sputum Culture in diagnosing active TB (4)

A

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
Q

How should active TB be managed from a public health perspective? (2)

A

Notify Public Health England

Begin contact tracing.

167
Q

Describe the treatment for active TB

A

RIPE;

Rifampicin - for 6 months
Isoniazid - for 6 months
Pyrazinamide - for first 2 months
Ethambutol - for first 2 months

168
Q

Give 3 side effects of Rifampicin

A

Red-orange body secretions

Hepatitis

Drug interactions - Enzyme inducer (warfarin, phenytoin and oestrogens)

169
Q

Give 2 side effects of Isoniazid

A

Neuropathy (paraesthesia in hands and feet)

Hepatitis

170
Q

Give 3 side effects of Pyrazinamide

A

Arthralgia/gout

Rash

Hepatitis

171
Q

Give 1 side effect of Ethambutol

A

Optic neuritis/visual impairment

172
Q

What additional drug should be given alongside Isoniazid? And why?

A

Pyridoxine (vitamin B6)

To help prevent Isoniazid Induced Peripheral Neuropathy

173
Q

What is the moa for Rifampicin?

A

Inhibits bacterial DNA dependent RNA polymerase, preventing transcription of DNA into mRNA

174
Q

What is the moa of Isoniazid?

A

Inhibits mycolic acid synthesis

175
Q

What is the moa of Pyrazinamide?

A

Converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase I (FAS)

176
Q

What is the moa of Ethambutol?

A

Inhibits the enzyme arabinosyl transferase which polymerases arabinose into arabinan

177
Q

Define Dalton’s Law

A

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
Q

Define Fick’s Law

A

States that the rate of diffusion is proportional to surface area and concentration difference and inversely proportional to membrane thickness

179
Q

State the Law of LaPlace

A

The magnitude of the inward directing collapsing pressure is directly proportional to surface tension and inversely proportional to the radius of the bubble

180
Q

Define Tidal volume

A

The volume of air entering or leaving the lung during a single breath

181
Q

Define inspiratory reserve volume

A

The volume of air that can be maximally inspired over and above the typical tidal volume

182
Q

Define inspiratory capacity

A

The maximum volume of air that can be inspired at the end of a normal expiration

183
Q

Define residual volume

A

The volume of air left in the lung after a maximal expiration

184
Q

Define vital capacity

A

The maximum volume of air that can be expired after a maximal inspiration

185
Q

How is pulmonary ventilation calculated?

A

Tidal volume x respiratory rate

186
Q

Define V/Q mistmatch

A

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
Q

What would a high V/Q ratio indicate? (3)

A

Dead space;

Comes as a result of lots of ventilation but limited perfusion.

Can indicate pulmonary embolism (occlusion of blood vessels = less perfusion)

188
Q

What can a low V/Q ratio indicate? (4)

A

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
Q

Define Goodpastures Syndrome

A

AKA Anti-glomerular basement membrane disease (GBM)

Describes a rare small vessel vasculitis associated with both pulmonary haemorrhage and progressive glomerulonephritis.

190
Q

What causes Goodpastures Syndrome?

A

Anti-glomerular basement membrane antibodies against Type IV collagen.

Type IV collagen is principally found in the basement membranes of alveoli and glomeruli.

191
Q

Give 2 features of Goodpastures Syndrome

A

Pulmonary haemorrhage

Rapidly progressive glomerulonephritis (proteinuria and haematuria - rapid onset AKI)

192
Q

Give 3 clinical features of Goodpastures Syndrome

A

Haemoptysis (due to pulmonary haemorrhage)

Reduced urine output (proteinuria and haematuria)

Oedema

193
Q

How is Goodpastures syndrome diagnosed? (3)

A

Renal biopsy - Shows IgG deposits along the basement membrane

Increased DLCO (increases during haemorrhage)

Anti-glomerular basement membrane antibody titre (confirmatory diagnostic test)

194
Q

How is Goodpastures Syndrome treated? (3)

A

Oral corticosteroids - Prednisolone

Plasmapheresis - Until GMB antibodies are no longer present

Cyclophosphamide

195
Q

Describe the pleural cavity

A

Describes a potential space between the pleurae (visceral - inner and parietal - outer) of the pleural sac surrounding each lung.

196
Q

Define pleural effusion. How can this be characterised? (2)

A

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
Q

Give 4 risk factors for pleural effusion

A

Congestive Heart Failure

Pneumonia

Malignant Mesothelioma

Recent coronary artery bypass graft surgery

198
Q

What are the 2 classifications of pleural effusion?

A

Transudate (transparent - less protein) (Effusion protein <25g/L)

Exudate (effusion protein >35g/L)

199
Q

Describe transudative pleural effusion. Give 3 causes

A

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
Q

Describe exudative pleural effusion. Give causes.

A

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
Q

Define cystic fibrosis

A

Describes an autosomal recessive disorder causing increased viscosity of secretions (lungs and pancreas)

202
Q

What is the pattern of inheritance in Cystic Fibrosis?

A

Autosomal Recessive

203
Q

Cystic fibrosis arises from a mutation in what gene? What does this gene code for?

A

CFTR gene

Encodes for a cAMP regulated chloride channel

204
Q

Where chromosomally is the gene mutation in the majority of cystic fibrosis cases?

A

Delta F508 on the long arm of chromosome 7

205
Q

Name 3 organisms which may colonise CF patients

A

Staphylococcus aureus

Pseudomonas aeruginosa

Aspergillus

206
Q

What test is used to diagnose CF? Is this reliable?

A

Sweat test - CF patients have abnormally high sweat chloride

Can cause false positives in;
Malnutrition
Adrenal insifficiency
Nephrogenic diabetes insipidus
Hypothyroidism
Hypoparathyroidism

207
Q

Give 4 presenting features of CF

A

Neonatal period - Meconium ileus

Recurrent chest infections

Malabsorption; steatorrhoea, failure to thrive

Liver disease

208
Q

Give 5 features of cystic fibrosis

A

Short stature

Diabetes mellitus

Delayed puberty

Rectal prolapse (due to bulky stools)

Nasal polyps

209
Q

How is cystic fibrosis managed?

A

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
Q

Name 1 drug that can be used to treat cystic fibrosis. What is it’s MOA?

A

Orkambi.

Increases number of CFTR proteins transported to cell surface.

211
Q

Define bronchiectasis

A

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic inflammation or infection

212
Q

Give 5 causes of bronchiectasis

A

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
Q

Give 4 clinical features of bronchiectasis

A

Persistent productive cough (large volumes of sputum)

Dyspnoea (breathlessness)

Haemoptysis

Coarse crackles/wheeze on auscultation

214
Q

What is the best diagnostic tool for bronchiectasis in adults?

A

High resolution chest CT

215
Q

What sign would be seen on a chest CT for a patient with bronchiectasis?

A

Signet Ring Sign (bronchi larger than their adjacent pulmonary artery)

216
Q

What may a chest x-ray show for a patient with bronchiectasis? (2)

A

Dilated and thickened airways

Tram lines

217
Q

What is the most common organism to infect patients with bronchiectasis?

A

Haemophilus influenzae

218
Q

How is bronchiectasis managed? (6)

A

Treat underlying cause

Physical training (inspiratory muscle training)

Postural drainage

Antibiotics for exacerbations + long-term rotating antibiotics (severe cases)

Bronchodilators

Immunisations

219
Q

Describe acute bronchitis

A

A typically self-limiting chest infection that results from inflammation of the trachea and major bronchi.

220
Q

How long does it typically take for acute bronchitis to resolve?

A

3 weeks

221
Q

When does acute bronchitis typically occur?

A

Autumn or winter

222
Q

Give 5 clinical features of acute bronchitis

A

Cough (+/- sputum)

Sore throat

Rhinorrhoea

Wheeze

Low grade fever

223
Q

How can acute bronchitis be differentiated from pneumonia? (2)

A

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
Q

How is acute bronchitis diagnosed? And what guides whether antibiotics are required?

A

Diagnosed clinically

CRP testing guides whether antibiotic therapy is needed

225
Q

When should antibiotic therapy be considered in cases of acute bronchitis (3)

A

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
Q

Describe how CRP testing guides antibiotic use in acute bronchitis.

A

If patient has a CRP of 20-100mg/L - Offer delayed prescription

If patient has CRP of >100mg/L - Offer antibiotics immediately

227
Q

What are the 1st line and 2nd line antibiotics for acute bronchitis (if needed)

A

1st line - Doxycycline

2nd line - Amoxicillin (if child or pregnant)

228
Q

Describe sarcoidosis

A

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
Q

How does acute sarcoidosis often present? (4)

A

Swinging fever

Bilateral hilar lymphadenopathy (Lofgren’s Syndrome)

Erythema nodosum

Polyarthralgia

230
Q

What is Lofgren’s syndrome associated with?

A

Acute Sarcoidosis

231
Q

What is the triad for Lofgren’s syndrome? (3)

A

Erythema Nervosum

Polyarthralgia

Bilateral perihilar lymphadenopathy

232
Q

Give 2 biochemical features of sarcoidosis

A

Hypercalcaemia

Raised ACE

233
Q

Give 5 clinical features of sarcoidosis

A

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
Q

What skin lesion may be seen in sarcoidosis?

A

Lupus pernio (hard purple lesion on cheeks, nose, lips, ears or forehead)

235
Q

What diagnostic test is used to stage sarcoidosis? Describe the stages (5)

A

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
Q

Why does sarcoidosis cause hypercalcaemia?

A

Macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

237
Q

Give 3 indications for steroid use for patients with sarcoidosis

A

Chest X-ray showing stage 2 or 3 in symptomatic patients

Hypercalcaemia

Eye, heart or neuro involvement

238
Q

Give 5 factors of sarcoidosis associated with a poor prognosis

A

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
Q

Give 6 causes of upper zone lung fibrosis

A

CHARTS

C - Coal Worker’s Pneumoconiosis
H - Histiocytosis/Hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation (cancer therapy)
T - Tuberculosis
S - Silicosis/Sarcoidosis

240
Q

List 3 drugs associated with causing lower zone lung fibrosis

A

Amiodarone

Bleomycin

Methotrexate

241
Q

Give 4 causes of lower zone lung fibrosis

A

ACID

A - Asbestosis
C - Connective tissue disorders (Excluding Ankylosing Spondylosis, e.g SLE)
I - Idiopathic
D - Drug induced (amiodarone, bleomycin, methotrexate)

242
Q

Give 4 presenting features of pulmonary fibdosis

A

Progressive exertional dyspnoea

Bi-basal fine end inspiratory crepitations

Dry cough

Clubbing

243
Q

What is the gold standard investigation for diagnosing pulmonary fibrosis?

A

High resolution CT scan

244
Q

What is the 5 step approach to ABG interpretation?

A
  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
Q

On an ABG, a PaCO2 of >6.0kPA would suggest what?

A

Respiratory acidosis (or respiratory compensation for a metabolic acidosis)

246
Q

On an ABG a PaCO2 of <4/7 suggests what?

A

Respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

247
Q

On an ABG a bicarbonate of <22mmol/L suggests what?

A

Metabolic acidosis (or renal compensation for respiratory alkalosis)

248
Q

On an ABG a bicarbonate of >26mmol/L suggests what?

A

Metabolic alkalosis (or renal compensation for a respiratory acidosis)

249
Q

Use the acronym ROME to describe ABG interpretation

A

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
Q

Give 4 key indications for NIV use

A

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
Q

How much oxygen should be given to patients who are critically ill (anaphylaxis, shock ect) and how should it be given?

A

15L/min via reservoir mask

252
Q

What is the oxygen saturation target for acutely ill patients (no COPD)

A

94-98%

253
Q

What is the oxygen saturation target for management of patients with COPD? (2)

A

88-92%

(adjust range to 94-98% if pCO2 is normal)

254
Q

Describe inhaler technique in 5 steps

A
  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
Q

Describe pneumothorax

A

A condition characterised by the accumulation of air in the pleural space, resulting in the partial, or complete, collapse of the affected lung.

256
Q

Name and describe 2 classifications for spontaneous pneumothorax

A

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
Q

What does the classic Primary Spontaneous Pneumothorax patient look like?

A

Tall, thin, young indivuduals

258
Q

Define tension pneumothorax

A

Describes a severe pneumothorax resulting in the displacement of mediastinal structures.

May result in severe respiratory distress and haemodynamic collapse

259
Q

Give 6 clinical features of pneumothorax

A

Acute onset dyspnoea

Acute onset pleuritic chest pain

Reduced breath sounds

Reduce lung expansion

Hyper-resonant lung percussion

Tachypnoea/Tachycardia

260
Q

Give 3 distinctive features of tension pneumothorax

A

Respiratory distress

Tracheal deviation (away from side of pneumothorax)

Hypotension

261
Q

Describe the management for a primary pneumothorax (3)

A
  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
Q

Describe the management for secondary pneumothorax (3)

A
  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.

  1. If pneumothorax is <1cm give O2 and admit for 24 hours.
263
Q

What discharge advice should be given to a patient recovering from a pneumothorax? (3)

A

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
Q

Give 4 causes of respiratory alkalosis

A

Pulmonary Embolism

Pregnancy

Encephalitis

Anxiety

265
Q

List 6 conditions causing upper lobe pulmonary fibrosis

A

CHARTS

C- Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

Phase 4 Medicine (15 decks)

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